Surgery I

Index
Acute abdomen 3

Barrett's esophagus (EB) 16

Enteral and parenteral nutrition 21

Hydroelectrolyte and acid-base equilibrium in the surgical patient 27

The wonderful history of infection in surgery through the centuries 29

Surgical site infections (II) 30

Preparation for intervention and risk factors 35

Chest pain: approach to the causes of greater clinical impact based on the evidence 39

Management of post-operative anemia 45

Prevention of wound infection 48

Lung tumors 52

Esophageal foreign bodies 62

Caustic injuries 71
Accrescimento and ways of diffusion of t. lung 77

Diagnosis of pulmonary tumors (II) and therapy 80

Boerhaave syndrome, Mallory-Weiss lesions, achalasia 83

Diseases of the mediastinum 86

Senological surgery 95

Part I: Obesity surgery 102

Digestive bleeding 105

Lymphology and microsurgery 107

Tumors of the esophagus 109

Functional diseases of the esophagus 114

Preparation for intervention and risk factors for the elderly 120

Notes of:

M. Bagnasco M. Cavelli F. Feta S. Marra G. Spiandorello A.

Vitale

N. Boveri L. Cuniolo F. Forni A. Prey C. Trimmers

S. Buccilli L. Di Tullio E. Hysa F. Rivano M. Tixi

Prof. Campisi 11/11/16

Acute abdomen

'Acute abdomen' is a very generic, non-specific terminology, which is used to indicate a syndrome,
therefore a symptom complex, with its abdominal localization from the subjective and objective point
of view, and which has the peculiarity of having a rapid onset , dominated by a symptom: pain, an
acute pain that can be stabbed, then of a piercing type , or cramp-like or of a colonic type , then with a
peak of painful symptoms that can then regress spontaneously (at least in part) and reappear with as
much acuity at a later stage, even without pharmacological treatment against pain.

Colic pain is a pain of visceral origin, connected to a phenomenon that is the spasm of the bowel, for
example of intestinal origin.
There are other signs that may, due to the intensity, the specificity of the acute, indicate the need for
urgent treatment.
So the characteristics of pain, the objectivity of pain, the anamnesis (always fundamental, enlightens us
on what may be the origin of the symptomatology of acute abdominal syndrome), we will therefore
initially have a very general diagnosis (so much so that we speak of acute abdomen in the most general
and nonspecific sense of the term), then on the guide of the EO and the collection of anamnestic data,
we can put a first diagnostic suspicion in the hope of being able to reach then, with the necessary
laboratory, diagnostic, radiological and instrumental, to a definitive diagnosis.

First of all we must try to verify, in front of a syndromic picture of this type, if the symptomatology,
and the pain in particular, are to refer to the abdomen from the clinical and anatomical-topographical
point of view, or if the abdominal pain with the symptomatology associated can be of non
origin abdominal . It is very important to evaluate for the differential diagnosis of the acute abdomen,
which does not it can be separated from the fact that there can be a painful symptomatology referring
to the abdomen which, however, is not of abdominal origin. For example, myocardial infarction.

So a patient who comes with a syndrome of this type to your observation requires this initial
differential diagnosis.
We usually proceed by exclusion : on the basis of the symptoms and related symptoms, with the help of
investigations that can go from the ECG to the dosage of myocardial necrosis enzymes, up to the chest
radiograph, those findings that, in the meantime, the observation of the blood chemistry tests will
proceed, allowing us to begin a diagnostic-differential screening.

But we must not forget to observe the patient well, in the meantime: observatio et ratio represents a basis
of all the semiotic and clinical methodology. The observation also starts with the immediate inspection of
the patient, beginning with the appearance , the facies and the decubitus , which can be

particularly evocative (in the case of acute pancreatitis, it

will be a rifle dog decubitus ).

Abdominal pain will naturally have a seat in which this subjective

and objective symptomatology will be particularly localized. We
must evaluate the pain: first of all the onset (which may
be sudden , such as stabbing pain of perforated gastroduodenal
ulcer, or it may be more or less

rapidly worsening as in acute appendicitis and acute cholecystitis), to then pass to the type of the pain (to
evaluate if its peculiarities of representation and clinical manifestation can be caused by colic,
then cramping bowel pain - a phenomenon of visceral spasm, with contracture of the smooth musculature of
the visceral wall - or a continuous pain, as can occur
 1

in intestinal ischemia or acute inflammation), the modification of the manifestation of pain in time ,
short-term (eg continuous pain but acute onset, which can be done correctly represent in the drafting of
the medical record - graph 1 -, or the characteristic intermittent pain of the colonic - graph 2 -, or the
continuous and increasing pain - graph 3 -).

We must not neglect the localization and irradiation of pain.

For the localization , the logical reference from the anatomical-topographical point of view is that of the
four abdominal quadrants (upper and lower abdominal quadrants, delimited by the two imaginary xifo-
pubic and transverse umbilical lines) or of the nine topographic areas (starting from the top: the right
hypochondrium, the epigastrium, the left hypochondrium, the region of the right flank, the
mesogastrium, the region of the left flank, the right iliac fossa, the hypogastrium and the left iliac fossa)
in which the abdominal cavity is subdivided.

Then the irradiation of pain, the pain that follows a certain path: a pain that goes from the right
hypochondrium towards the lumbar region and then goes towards the scapula, as happens in the hepato-
biliary colic; or the pain that radiates along the path of the extraction of the urinary tract excretric, then from
the lumbar region anteriorly and medially, even up to radiate to the testis or large lip homolateral to the
colic; irradiation of acute appendicitis pain may extend to the root of the right lower limb. Hence differential
diagnosis between hepato-biliary colic, renal colic and appendicular colic.

If we refer in a practical way to the division into four quadrants, we must keep in mind that each of the
quadrants has a peculiar relationship with certain organs, viscera, parenchymal.
Upper right quadrant: gallbladder, duodenum, pancreas (especially the head), appendix,
colon transverse (right half), right kidney.
Upper left quadrant: stomach, pancreas (especially body and tail), spleen, heart, colon transverse
(left half), left kidney.
Lower right quadrant: appendix, tenuous, right colon (but with possible reference, in cases
not infrequent of dolicocolon , also to the left colon), attached uterine to the right, right ureter and
hernias of the inguinal wall (inguinal, crural, inguino-crurale).
Left lower quadrant: left colon, left uterine appendix, left ureter and hernia of the inguinal wall
(inguinal, crural, inguino-crural).

In the case of appendicitis with an

anatomical position of the appendix in the
retrocecal area , there can be a very
important posterior reference of pain that
can also be located quite precisely at
Neirotti's point (considering the imaginary
extension of the angle-scapular line, where it
meets the Twelfth coast and then up to the
iliac wing: at the middle of this path we find
the Neirotti point, which is considerably
positive in acute retrocecal appendicitis).

Another very important element to consider in the anamnesis and in the EO is the evolution of pain
itself. For example, in hepato-biliary colic, we must first remember the most frequent pathology:
cholelithiasis and acute lithiasic cholecystitis. In this case, colic pain (typical hepato-biliary colic) can
then become continuous.
In the ileum of intestinal occlusion (therefore of mechanical nature - mechanical ileus -), we must consider
that with the passing of time the viscera (usually an intestinal loop) involved in the occlusion, can undergo
an ischemia, so the pain will begin as colic and then become continuous.

Then there is the whole symptom cortege , that is the signs and the associated symptoms: vomit , which
may be according to the cases of reflex, toxic or obstructive nature (of the mechanical ileus), the
alterations of the alve , which may go from diarrhea at the closure of the complete alvo (closure at the
passage of both gas and faeces) and abdominal distension (typical of mechanical intestinal
obstruction); we must never forget the importance of detecting body temperature , which in this case
must be measured in the axillary and rectal region . In fact, if the rectal temperature exceeds by at least
1 ° C the temperature measured in the axillary region isa very important sign to support the diagnosis of
suspicion of an acute peritonitic abdomen (as can occur in acute perforated appendicitis, in acute
appendicitis gangrenous and in the appendicular abscess).

This datum along with the finding from the blood count of a neutrophilic leukocytosis will
naturally further support the diagnostic suspicion.

Equally important, in women of childbearing age menstrual cycle data must be analyzed in order to
rule out the suspicion of an ectopic pregnancy: suspension of menstrual cycles and the duration of such
suspension.

In the area of acute abdominal syndrome, various types of morbid conditions must be differentiated:
there is a distinction between acute abdomen of the hemorrhagic type , of the peritonitis type , of
the occlusive andvascular type .
So with regard to the acute abdomen, we must first evaluate, in relation also to the general anamnestic
and symptomatological framework, subjective and objective, for example if in the syndrome
predominates a picture that is that of shock and that calls attention to itself: l
Acute haemorrhagic abdomen has an abdominal objectivity that is far lower than the acute peritonitic
abdomen, that from intestinal and vascular occlusion, because the scenario of the symptomatology is
dominated by the state of shock (hence from severe hypotension, from the circulatory and metabolic
decompensation that comes to be determined in the context of the shock, for example after an abdominal
trauma - closed or open - like the traumatic rupture of the spleen in a traffic accident). There is therefore
an acute abdominal picture, but the predominant symptomatology is that of shock, whereby the
predominant intervention on the patient, to save his life, will be that of the resuscitator, who associated
the surgical evaluation, must be able to bring the patient in the operating room even without the
possibility (due to lack of time) to perform certain examinations as it could be, in the case of a spleen
rupture, hemoperitoneum, a computerized tomography.

In the case of the acute peritonitis , however , we will have a specific, peculiar abdominal objectivity,
which will be characterized, apart from the general state of suffering of the patient and fever, by
abdominal symptoms with a defense reaction resulting in abdominal contracture , and the maneuver of
Blumberg positive, until reaching total contracture pictures of the abdominal wall that will make
(particularly noticeably in thin subjects, but not only) the abdomen 'a boat' (typical of acute peritonitis
from perforation of an ulcer gastroduodenal peptide, or an acute appendicitis with circumscribed
peritonitis, has rapidly spread and become generalized - as may occur in diabetic, immunosuppressed and
elderly subjects.

The picture of the acute abdomen due to intestinal obstruction is characterized by the increase in abdominal
distension, by the particular tympanism of abdominal distention, which in the case of mechanical occlusion
will be upstream of the mechanical obstacle that has determined the occlusion; with the auscultation you can
feel the presence of borborigmi , which can be appreciated even without the aid of the phonendostetoscope.

With the framework of the acute vascular abdomen we can have, for the fixation, for the rupture or
for the dissection of an abdominal aortic aneurysm, all a symptom cortege that will refer to the
pathology of the abdominal aorta, and therefore obviously also with the 'anemia and a component
say hemorrhagic acute vascular abdomen.
In the critical case of acute mesenteric ischemia, the picture with the passing of the hours can pass to
more or less extensive necrosis of segments of the intestine, in particular of the small intestine.

However, all this does not prevent the combination of the already abducted acute abdomen types: an
example for all is the case of acute necrotic-hemorrhagic pancreatitis , in which the hemorrhagic
component, the occlusion component (paralytic ileus with the anse 'a sentinel ' of acute pancreatitis), the
vascular component (for hemorrhagic necrosis that occurs) and the peritonitic component.

It should also be considered that the diagnosis in the acute abdomen may vary in relation to age and sex :
acute appendicitis is more common in young people; acute cholecystitis, intestinal occlusion, mesenteric
ischemia up to the infarction with intestinal necrosis, diverticulitis (complication of diverticulosis),
tumors, perforation of peptic ulcer disease, rupture of abdominal aortic aneurysms are more frequent in
advanced adulthood and in the elderly.

The signs that we must take into account for an emergency intervention are signs of peritoneal
irritation, and therefore the defense reaction, the positive maneuver of Blumberg, the pain localized,
severe, persistent, invigorating for more than 6 hours, l association of pain with fever, hypotension,
pallor, tachycardia, tachycardia, tachypnea, cold sweating, the significant differential between axillary
and rectal temperature, the presence of metallic noises, the borborigmi all abdominal auscultation,
progressive abdominal distention in the occlusion in particular mechanics and with the passing of the
hours the worsening of the general conditions of the patient.

The acute abdomen requires, for a correct diagnostic-differential and therapeutic approach, an early
diagnosis .

In the past , emergency surgeries were used often in order to prevent the onset of more serious
complications, so the intervention also served from a diagnostic point of view, so much so that often
there was talk oflaparotomy of urgent exploration .

In some cases laparotomies did not give rise to findings that justified emergency surgery, so-
called white laparotomies, exploratory laparotomies that were not necessary.
Today, thanks to the progress we have made in the field of radiological imaging techniques, we
can better select and then perform a more precise, more adequate screening, thanks to the image
diagnostics we have available, in particular the computed tomography, the echotomography and, in some
cases, the magnetic resonance. To these is added a surgical procedure that in the first instance can have a
diagnostic value but can also become a therapeutic approach, that is videolaparoscopy, which can be
dirimente in cases of major doubt and can itself become the pathway of surgical treatment ( minimally
invasive, more conservative).

Looking at the past and evaluating the present, the future aims to perform emergency surgeries that are
increasingly targeted and increasingly less invasive, thanks to the diagnostics we now have available, in
order to reduce the risk of diagnostic error.

4
Despite this, we must bear in mind that there exists a very wide range of conditions of 'false
abdomen acute ' or ' pseudo acute abdomen ' : pain is lacking during the election, the Blumberg
maneuver is negative, there is no defensive contracture of the abdominal wall, a paralytic ileum does not
occur (as for example in the case of intestinal obstruction which in the most advanced phase of
decompensation then becomes predominantly of the paralytic type, or as in the case of mesenteric
intestinal ischemia when it comes to intestinal infarction). Therefore, there are no signs that can support
an objective, effective diagnostic suspicion of an acute abdomen proper.
The main pathologies responsible for pictures of acute abdomen can be surgical pathologies, but for
this reason the intervention is not necessary or is rationally differentiated, but above all under the name of
a false acute abdomen there are medical pathologies for which the abdominal picture is possible but not It
is mandatory, or pathologies that are peculiar to an acute abdominal pattern but are of medical origin
(from hereditary diseases : intermittent acute porphyria, Quinck's angioneurotic edema, Mediterranean
fever, idiopathic hyperlipemia, infectious diseases : mononucleosis , shingles, mesenteric adenitis,
follicular ileitis, infectious hepatopathies,endocrinopathies : diabetes, Addison's disease,
hyperparathyroidism, hyperthyroidism, collagen diseases, Schoenlein-Enoch's purple, acute articular
rheumatism, LES, nodular panarteritis, haematological diseases : malaria, neoplasms of the red and white
series of blood, lymphomas, paroxysmal hemoglobinuria; abdominal pain can be reflected , at a cardiac
start as in the IMA, pericarditis, acute heart failure; charged to the SNC o SNP; at pleuro-pulmonary
starting; at renal or urinary origin; from ganglioplegics, opiates, cases of acute and chronic alcoholism).

Fortunately, it is estimated that a careful anamnestic research alone is capable of solving these diagnostic
problems in 50% of cases.
The objective examination, laboratory investigations, instrumental investigations, including images, in
selected cases also laparoscopy, are usually able to allow a correct diagnosis to be made.
Therefore any surgery in the case of a false, acute abdomen should be forbidden, as it could expose to
unforeseen post-operative complications. In the literature there are described cases of death as a result of
white laparotomies. The exitus, rather than emergency surgery, is due to the serious underlying disease.

The impact on the current state of the false, surgically treated abdomen is the increase in mortality, the
increase in operative morbidity, linked to laparotomy or video laparoscopy performed in urgency, the
increase in discharge with the dispatch to assisted health residences, the the increase in hospitalization
days, the increase in the use of complex diagnostic investigations, the increase in the use of
polypharmacotherapies, with an increase in the risk of side effects and the formation of antibiotic-
resistance. So a significantly significant increase on health care costs.

Acute hemorrhagic abdomen: it is characterized by the impairment of the circulatory system, and
therefore the shock. It can occur in case of closed traumas or open traumas.
In the acute vascular abdomen we consider dissection, fixation, rupture of an abdominal aortic
aneurysm, acute mesenteric ischemia up to intestinal infarction.

The acute abdomen from intestinal occlusion with the mechanical ileus and the paralytic
or adynamic ileus: a paralytic ileus must be carefully evaluated, because acute peritonitis not so
infrequently carries with it a paralytic ileus, which can be of such magnitude induce you to reoperate the
patient, just for its striking symptomatology (abundant gastric stagnation, absence of intestinal
peristalsis, closure of the alvo to gases and faeces).

The acute peritonitic abdomen after all, at least at its onset, has a frame and a dominant symptomatology
that is subjective and very objective, with the defense contracture of the abdominal wall.
 5

Some peculiarities related to pain in acute clinical pictures : pain in acute cholecystitis is localized to
the right hypochondrium, irradiated posteriorly in the right subscapular region; the stomach has a painful
projection prevalent in the epigastrium; the perforated duodenal ulcer in the right hypochondrium and in
the right lumbar region; the pain that originates from the small intestine is typically periumbilical; the
innervation of the cecal appendix is common to that of the small intestine, so it should not be surprising
that the onset of acute appendicitis manifests itself with pain practically in the center of the abdomen, in
the mesogastric region; the symptomatology of the colon often expresses symptoms referred to the lower
quadrants of the abdomen.

The patient should be followed in his / her path and also needs first level laboratory tests (blood count
with leukocyte formula, ionogram, liver function, renal function, glycemia, pancreatic lipase and
amylase enzymes, complete coagulation, proteinemia, albuminemia, B-HCG and urinalysis), second
level in anticipation of transfusion of blood products or sending precautionary for surgical intervention
(the type and screen and group);serological tests (for HBV, HCV, HIV, lue, salmonellosis, brucellosis,
rickettsiosi, exanthematic typhus, immuno-serological
reactions); the markers tumors ; cardiac enzymes (to exclude a heart condition with abdominal
symptoms, like the myocardial infarction that affects the diaphragm wall of the left ventricle, which can
give rise to a false acute abdomen).

The choice of diagnostic procedures : they must naturally be sensitive and specific (reliability), we need
to evaluate the execution time (urgency / election), the patients' compliance with the diagnostic procedures
and the latter with respect to the clinical case, and the invasiveness of the same procedures (eg endoscopic
examinations, angiography with selective catheterization according to the Seldinger method, ..).

Today the instrumental examination that is tended in the first instance to perform, especially for the
study of liver and biliary tract, pancreas, kidney, spleen, prostate and female genital is
the ultrasound , which however has a big limit: the patient in urgency it can arrive with a more or
less accentuated intestinal meteorism (not only in the case of mechanical occlusion, but even if it
consumed a meal shortly before the examination), which can limit the diagnostic value of the
ecotomography.

TC and clismaTC have a high sensitivity and specificity, allow an accurate characterization of
the lesions occupying intra-abdominal space, localization of primary and metastatic tumors, the
differential diagnosis between solid and cystic lesions, the evaluation of vascular alterations if the
examination is performed with contrast agent, differential diagnosis between the mechanical ileum
and the paralytic, but expose the patient to a high dose of radiation. The organs best investigated by
CT scan with the liver, biliary tract (intra- and extra-hepatic), pancreas, spleen, large vessels, kidneys,
adrenals and endopelvic organs.

But also the MRI and, in this case, the angioRM, the lymphangio, the colangioRM, can have their
usefulness and do not expose the patient to radiation. However, there may be absolute contraindications
to the realization of an examination of this type also from the organizational point of view, and not only
for the presence of ferromagnetic endovascular clips, pace-makers, ferromagnetic endoprostheses, and
implantable electrostimulators.MRI has undoubted advantages related to sensitivity and specificity, not
exposure to radiation, specific sequences depending on the question and the organ to be investigated.
Acute appendicitis

Acute appendicitis is an acute inflammatory process of the very frequent appendix it represents

however, the most common cause of acute abdominal pain may require surgical treatment.

The incidence is calculated between 7% and 12% of the population in the course of life, the ages that can
be

all of them are affected, but you can have acute pictures especially during childhood, during adolescence and

then in the elderly.

L 'appendectomy represents 1% of all abdominal surgery.

The obstruction of the lumen occurs on the part of coprolites, hyperplastic lymphatic follicles, or
abnormal angulations of the appendix or the presence of appendix tumors (for example carcinomas).

Infection of the appendix, inflammation has an infectious, bacterial base, mainly via the enterogenic
route , rarely by hematogenous route. The germs are predominantly Gram negative, ie E. coli in
particular, Pseudomonas Aeruginosa, Enterococco faecalis and foecium, bacterioides.

The obstruction of the appendix determines the secondary accumulation of secretions, with an increase
in the intraluminal pressure; we therefore compromise the lymphatic drainage of the appendix and the
vasculature with ischemia of the wall. This is why evolution is towards necrosis, towards gangrene with
perforation. Then the inflammatory process extends, purulent, suppurative, through the layers of the
wall of the bowel, until reaching the peritoneal cavity.

The peritonitis is initially limited, however depending on the conditions of the immune system of the
patient (diabetes, immunosuppressants including patients with AIDS: in these cases the process can
extend more or less rapidly and from a circumscribed peritonitis switch to a diffuse with the framework
then possible further evolution of septic shock).

Acute untreated appendicitis progresses through 4 evolutionary stages :

the first of acute hyperemic-edematous appendicitis (the appendix shows itself lucid, hyperemic) in which,
however, the picture can also spontaneously resolve with adequate medical therapy; the second is that
acute catarrhal appendicitis with micro-
abscesses; the third stage is that of acute
appendicitis phlegmonous with confluence of
abscesses of the acute catarrhal appendicitis,
which invade the meso with consensual
 thrombophlebitis and hemorrhagic
infarction; the fourth stage is finally that of
acute appendicitis gangrenous, with perforation
with circumscribed and / or generalized
peritonitis.

Obviously along with the antibiotic-therapy, that

it must be as wide spectrum as possible but then it can be targeted by taking a sample of liquid

peritonitis from the cavity of the appendiceal abscess, rehydration and water rebalancing are important.

electrolyte, but therapy is fundamentally based on urgent appendectomy.

Some considerations: when the acute appendicitis presents a picture of frank peritonitis (some perform a
preliminary videolaparoscopic approach) it is better to perform a median laparotomy, not the McBurney
cut of the hyperemic-edematous subacute appendicitis.
The cut of McBurney can go well in the early stages of the appendicitis phlegmonous, but when the
appendicitis begins to present a gangrenous picture, it is better to have (if we resort to the exposure of
the abdominal cavity) an exposure as wide as possible. It is not the length of the cut that makes the
difference, but the mastery of the clinical picture with the exploration that laparotomy allows.

Otherwise you make a cut of McBurney a little longer and then you move into the pararectal seat (it's a
middle way).
But if the acute abdominal picture is a frank peritonitis, then confirmed if there was also the possibility
to ultrasound and in particular from CT, it is better to perform an access amplio, where the fingers or the
retractors do not already take away a part of that minimal space that McBurney's cut allows.
A very important fact is that often associated with acute appendicitis is associated, and remains asymptomatic
(even for life), a diverticulum of Meckel: it is good to do then a systematic search of the diverticulum of
Meckel, which should be searched up to about 60 cm from the ileo-caecal valve (and therefore also for this
maneuver it is better to have the necessary space). Meckel's diverticulum (fetal residue of
the onepathicentericous duct ) can be

itself, possibly a source of complication, for hemorrhage, perforation, inflammation.

Today, with the means we have at our disposal, the videolaparoscopic columns, a difficult appendectomy
whose invasiveness we want to reduce, can also be carried out urgently with the use of the
videolaparoscopic approach: in this case we speak of 'appendectomy videolaparo-assisted ' . So the
videolaparoscopy not only acts as a diagnostic confirmation but also reduces the surgical trauma of open
access.

Acute appendicitis can also give rise to very important complications, from circumscribed peritonitis
becoming widespread, generalized, to systemic sepsis, to the formation of pelvic or subphrenic
abscesses, to plephlebite (ie, the portal vein thrombophlebitis) which can lead to piletrombosis
(piletromboflebite), hepatic abscess, early or late intestinal occlusion with the consequent paralytic ileus.

Classification of acute peritonitis: acute primary , secondary and tertiary peritonitis .

The primary acute peritonitis are peritonitis from bacteria, chlamydia, fungi, mycobacteria but in
the absence of perforation of the gastro-intestinal tract.
Then we have secondary , more classic peritonitis , those that are seen more often, secondary to the
spread from an abdominal inflammatory focus (acute cholecystitis → infiltrating cholecystitis →
ganglenous cholecystitis → bile filtration → secondary peritonitis), from perforation of a bowel
(gallbladder, appendice, diverticolo, intestino – da trauma aperto, o chiuso evoluto e non riconosciuto
precocemente -), ischemia e gangrena di un viscere, oppure da deiscenza di una sutura anastomotica
pregressa (complicanze post-chirurgiche).

Therefore in the secondary acute peritonitis there is the contamination of the peritoneal cable by
infected material, pollutant that determines the inflammation.

Finally, we have acute tertiary peritonitis , ie the primary and secondary acute peritonitis that, in spite of
the treatments put in place, relapse and therefore present a higher risk of MOF (multiple organ failure), ie
multi-organ decompensation. They therefore derive from a therapeutic failure, due to an incomplete
surgical control of the infectious focus and are related to the reduction of host defenses (decreased
peritoneal clearance and a lymphatic stasis is present).

Some conditions that simulate acute pediatric appendicitis: an acute inflammation of the mesenteric
lymphatic lymphatic structures, tuberculous caseous necrosis or Yersinia enterocolitica, Yersinia
pseudotubercolosis, streptococcus viridans, staphylococcus aureus, Giardia Lamblia, .. are conditions that
could fall in the framework of the false acute abdomen, because they can be treated with specific medical
and antibiotic therapy.

Then we have pictures of peritonitis that are completely unexpected, even relatively rare, that are
related to pathologies of peripheral lymphatic vessels and lymphatic vessels including organ and
apparatus (such as intestinal lymphatic vessels, mesenteric vessels, the cistern chili and thoracic
duct).

The kilo is the lymph that is enriched with chylomicrons after intestinal absorption of fats, and which
takes on a similar appearance to milk (milky).
If a rapid spread of kilo occurs in the peritoneal cavity, this tends to gather above all in correspondence with
the right parieto-colic region, due to the Laplace law because it is wider, there is more space and therefore
tends to gather in the parietal loggia -alcohol right, in right iliac fossa. Consequently, the resulting symptom
picture, due to the irritation that the kilo determines on the parietal peritoneum as well as visceral, is
precisely that of an acute appendicitis, simulates an acute appendicitis. So the surgeon finds free kilo in the
peritoneal cavity when he opens suspecting acute appendicitis and then believes that this liquid is pus (but
unlike the pus, the kilo is not malodorous, it is not fetid like the typical pus

from E. Coli of acute appendicitis purulent perforated gangrene). So there is an inflammation

from irritation produced by the kilo without infection.
The chyliferous vessels can not be developed, may have the expansions, the ectasia, it is
called 'chilolinfangectasie' , chylous cysts. These alterations, these chilolinfangiodisplasie, can
also affect the intestinal wall, the meso, the retroperitoneal space, not forgetting that all the lymph that
derives from the lower limbs, then together with the lymph that derives from the pelvic organs, from
the intestine, and from the peritoneum , it is conveyed towards the chili tank .

We have three main afferences to the chili cistern: the right lumbar afference, the left lumbar afference
and the mesenteric afference, which is that through which the chylous component of the lymph, together
with all the other lymph of the lower limbs, of the genitals (external and internal), of the urinary
apparatus, of the spleen, of the liver, .. reaches the cistern chili.

The chili cistern is a sort of small saccula, which may be 1-2 cm in length and 0.5-1 cm in diameter,
projecting onto the right transverse process of the second lumbar vertebra, in the retroperitoneum. From
there the thoracic duct branches off, which for a short distance is intra-abdominal, retroperitoneal, then
goes behind the aorta through the hiatus aorticus and goes into the mediastinum, and goes up from right
to left until it reaches the venous corner. left jugular.

Therefore, at multiple levels, the whole path may be affected by traumatic lesions, inflammatory
lesions, more or less marked and severe dysplasias, with ectasias, with a kilo gravitational reflux,
iatrogenic lesions during surgery.

These spreads of kilo are called chiloperitoneum or chylous ascites (improper term because the kilo is a
gelatinous liquid, it is not like the classic ascites of cirrhosis of the liver, there is a component of protein
macromolecules, chylomicrons and also a corpuscular component that it makes it more similar to the
exudate than to the transudate).
The causes can be the most varied: from dysplasias (45%), obstructions of the thoracic duct
(15%), traumas and iatrogenic lesions (15%), while the last 25% may be due to injuries of the
chilified pathways from neoplastic infiltration of abdominal lymphatic-lymphatic
structures, tuberculous infections , or filariasis (in India and less in China and in South America,
especially the north-western region of Brazil; parasitic disease due to the Filaria Bancrofti, a nematode
that is injected through the bite of mosquitoes, in subjects that however live in poor hygienic
conditions, and which goes to deposit the eggs inside the lymphatic vessels, where they run the lymph,
they are able to feed themselves optimally → it follows an obstructive lymphangitis even to the
involvement of the lymph nodes, with possible manifestations that go up to the monstrous
elephantiasis of the limbs with deformation of the limb with the sclero-indurative pachydermitis, then
lymphorrhea, overlapping infections and the possibility that the pathology also affects the external
genitalia and the female genital system with a chylocolpometrorrea, it may affect the intestine with
chyloperitoneum, chylous ascites, the urinary tract with chyluria, ...).
 The lymphangectasies of parietal chiliferous
vessels are considerable dilations in which the
lymph tends to stagnate and then, due to the
considerable hypertension that is determined
inside the dysplastic vessel, the wall is broken
(because there is no function valve: the valves
are incontinent or even missing in the
dysplastic forms) with the spread of kilo in
the peritoneal cavity.

Other times the chiliferous vessels of the

intestinal submucosa are more interested and
then yes

it has the exuding protido-dispersing enteropathy with thickening of the conniving plicas. The kilo in this case
pours into the intestinal lumen, and the patient goes through episodes of diarrhea, not just protein
→ is a steatorrhea in the sense that kilo is eliminated, therefore fat. But with fats are eliminated

also proteins and therefore they are hypoproteinemic patients, hypoalbuminemic, they have a
lymphocytopenia and very low immune defenses. The picture then by gravitational reflux, can also affect the
lower limbs, and these are the lymphanangiographic pictures that can be highlighted in the case of the
pathology of chiliferous vessels.
 The
lymphography
that we still
perform today,
in selected cases
with
complement TC,
isolation,
cannulation of
lymphatic
concealers under
local anesthesia

assisted, the injection of the gradual MdC, manual, not to break the vessels, with particular injectors. The
MdC is ultrafluid lipiodol, we perform an x-ray with preoperative brightness amplifier, a radioscopy, we
see that the contrast medium proceeds in the lymphatic pathways and then accompanies the patient in
radiology for a complement TC. Together with the angioTC and the MRI with the technique of electronic
subtraction of adipose tissue (lymphangioRM), we can study this pathology very well in its various
forms and even more bizarre and rarer expressions.

There is the possibility of septic complications because these patients, when they eliminate the kilo,
obviously there can also be bacteria from the intestine, they are immunosuppressed subjects and then
there can be a bacterial translocation through the kilo in the peritoneal cavity. In itself, they can then go
to septic complications, but then there is also the possibility that by performing the paracentesis to
remove the fluid, the complication is even iatrogenic.

The therapeutic approach of chyroid peritonitis always depends on the cause that causes it.

You can also perform gravitational classical ligatures, ectatic lymphatic correctors, dilated chilifiers,
with valvular incontinence and gravitational reflux, you can use the laser beam, which with
its Welding effect of low voltage welding can seal the vessels, or you can place of devices that
are called ' peritoneal - jugular shunt ' or the Denver valve with a reservoir that the patient himself can
operate resting on the lower part of the rib cage of the affected hemithorax (it is like a small pump on
which the patient can act, sucking liquid from the peritoneal cavity to bring it towards the internal
jugular). In fact the ascending branch is introduced into the internal jugular and the descending branch
instead catches the peritoneum.

But before implanting these devices one thinks well, because the kilo is gelatinous, it forms like
clots, and therefore they can easily get clogged. And of course this is the complication that causes
the device to no longer function, does not exert its drainage functions.
The microsurgical anastomoses which are performed for the treatment of peripheral lymphedema can
also be adapted within the abdominal cavity to retroperitoneal chylei vessels and therefore anastomoses
can be performed at these vessels and tributaries of the superior mesenteric vein or of the inferior
mesenteric vein.

Plastic peritonitis is due to the fibrinous reaction which also determines adhesions between the visceral
peritoneum and the parietal peritoneum.

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THE PERITONE

The peritoneum is a serous membrane that covers the cavity of the abdomen and extends around the
organs it contains.
The peritoneum, like the pleura, is a very important serine of mesenchymal origin, and is divided into
a parietal and a visceral portion. It covers the walls of the abdominal cavity, part of the organs
contained in it, in the adult subject of medium height has a surface of about 2m² and behaves like a
semipermeable membrane.

The structure of the peritoneum is fundamentally connective lapse of mesenchymal origin , covered
by a single line of mesenchymal cells that make up the mesothelium .
As it happens, the importance of the function, but also the structure itself, of the peritoneum is due to
its wealth of lymphatic vessels . The lymphatic structures contained in the peritoneum are divided
into superficial lymphatics (which have a diameter ranging from 20 to 80 μm) and deep lymphatics ,
also called sub- or sub-peritoneal (with a diameter greater than 80 μm).

Both the nets, the superficial and the deep ones, are oriented in such a way as to run parallel to the
connective fibers, lymphatics being strictly adhered to the nearby venules and the nearby arterioles.
Then we must consider it as a sort of matrix (always a cellular substance, a loose connective
tissue) that includes both the lymphatic and the lymph nodes also in the retroperitoneal area.

From this network we arrive at the chili cistern, also called Pecquet cistern . If the surgeon does not
know where he is, he can unintentionally cause serious damage and then you can have very important
post-operative chiloperitoneum pictures. Or the neoplastic infiltration of these structures can give rise to
very important chiloperitoneum paintings.
From the cistern chili, which is projected onto the right transverse process of the second lumbar
vertebra, the thoracic duct branches off, which then enters behind the aorta through the hiatus aorticus in
the mediastinum and then makes all this long path from right to left until to exit into the venous corner
succlav-jugular. The same mouth of the thoracic duct is susceptible of very numerous anatomical
variants.

On the right there is a similar structure, the right lymphatic duct , which however only drains the
emiling of the head, neck, upper right limb and right hemithorax. The most important part of the body's
lymph is carried by the thoracic duct, say for 85%. So all the lymph, including the kilo, is poured into
the blood stream (because to speak of the venous corner, the left jugular succlavio means the origin of
the superior vena cava and therefore of the confluence of the brachiocephalic veins of right and left
(anonymous veins) ).

Then the mouth of the thoracic duct occurs right near the right atrium of the heart, so at each diastole
there is a large suction pump that promotes the progression of the lymph from the thoracic duct to the
upper cavity through the anonymous trunks.
Among other things, the outlet of the thoracic duct in the venous-jugular venous corner is that,
through the studies and experiences of surgery, they have led us to copy this anatomical model for our
lymphangiovenous anastomoses.

PATHOPHYSIOLOGY OF THE PERITONE

We have three lines of defense .

The first is peritoneal clearance, ie being a semipermeable membrane, it is thanks to the wealth of vessels
(the venules and lymphatics) that the clearance is exercised, especially through the venules especially for
toxins and catabolites, and through the lymphatics (peritoneal) for germs and foreign bodies (up to 10 μm in
diameter). Then diaphragmatic lymphatics, since the diaphragm muscle, with its excursions, acts as a suction
pump, makes the sap move from the bottom upwards. Breathing is very important, and it is said

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also to the patients to do this respiratory gymnastics with deep and slow inspirations and
expirations, just to favor lymphatic drainage even after microsurgery.
Diaphragmatic lymphatics also play a fundamental role, active, in peritoneal clearance because they
present, unlike those of the peritoneum, of the areas, the areas that are called stomata , are lacunae
described for the first time in 1863 by von Recklinghausen (that of neurofibromatosis), which may need
to open up in real lymphatic gaps, ie they are lymph storage spaces equipped with an anti-reflux valve.
Therefore they direct the lymph directly and massively towards the lymphatic-lymphatic lymphatic
structures (therefore in an antigravitational sense), thus favoring a more rapid immune-mediated
response.

When operating a patient, in general, it is placed in a supine position; sometimes instead the lower
limbs are raised above the pelvis (under various conditions we need to tilt the bed, especially in video-
laparoscopic surgery, but we must take into account that the best position to keep active peritoneal
clearance during surgery surgical, especially of a certain duration, is the semi-assisi, the so -
called anti-Trendelenburg position (with the pelvis higher than the lower limbs).

This is because the supine position, or even more the position of Trendelenburg, diminishes the
effectiveness of diaphragmatic excursions. It can occur as a result of general anesthesia, antalgic
therapy, so they are all factors that tend to reduce peritoneal clearance.
The second line of defense corresponds to the immuno mediated reaction (cellular and humoral),
which occurs when the fragments of the germs or germs in full reach the lymph nodes, where the
activation of the T-specific immune process takes place and therefore the cellular and humoral
reaction , with lymphocytes and plasma cells.

Finally we have the third line of defense, it is the one that brings us back to the topic we are dealing with:
acute peritonitis. It is the one that causes the peritoneum to have a fibrinous reaction that leads to the
formation of adhesions (the adherent syndrome, the adherent reins); the reaction from fibrinosa
becomes fibrous with the adhesions that then justify the appearance of the positivity of the Blumberg
maneuver. So when peritonitis becomes clinically detectable, thanks to the EO and especially to
the positiveness of the Blumberg maneuver , we have a process that has already reached the third line of
defense, two lines of defense have already been overcome.

ABDOMINAL COMPARTMENTAL
SYNDROME The drama occurs when triggering
mechanisms that lead to MOF ( multi-organ
failure , multi-organ failure ) or MODS ( multiple
organ dysfunction syndrome , multi-
organ dysfunction syndrome).

It represents an extremely severe clinical condition

( abdominal compartiment syndrome) , determined by
the progressive and acute increase of intra-
abdominal pressure values, ie intra-abdominal pressure
increases and therefore we speak of intra-abdominal
hypertension ( intra-abdominal hypertension , IAH). It
can be three degrees : mild ( mild ) but with a rapid
increase from 10 to 20 mmHg,

moderate ( moderate ) from 20 to 35 mmHg and severe ( severe ) above 35 mmHg.

This is the syndrome that practically corresponds to what happens in the limbs in the subfascial spaces
in the presence of compartmental syndrome of the limbs, in compressed trauma of the limbs (in these
cases the fasciectomy is performed).
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2

The evolution towards this multi-organ decompensation, or this syndrome of multi-organ dysfunction, is
fundamental for the prognosis: this is because whenever there is an acute abdomen, especially if peritonitis,
intestinal occlusion, if the intra-abdominal pressure reaches high values ( with the gravity that

it is indeed typical at values above 35 mmHg), mortality ranges from 38 to 100% of cases. This tells us
how important prevention, early recognition of the syndrome and as early treatment as possible, to reduce
the syndrome (and therefore treatment of acute abdominal pathology).

The role of lymphatics is fundamental because it is the primum movens of abdominal compartment
syndrome. The effects of abdominal hypertension on the lymphatics can be direct and indirect .
The direct effects are those due to the high pressure exerted on the wall of the abdominal lymphatic
vessels which therefore can not perform their drainage function (on germs, on foreign bodies, on protein
macromolecules); the indirect effects are due to the release of toxic substances, cytokines, formation of
free radicals, decrease in the production of cellular ATP.
Therefore we have, due to the addition of these direct and indirect effects, the intraddominal lymphatic
block. The abdominal lymphatic insufficiency, which then also becomes thoracic, through the cisterna
chili and the thoracic duct, has this relationship of forces: we have a decrease in inflammatory and
immune responses, an easier bacterial translocation (also due to the fact that the lymphatics do not they
remove the germs more), edema increases (in the abdomen, the edema has an inflammatory component
of lymphatic stasis) and a reduction in the blood flow of the mucosa.
Therefore we have a reduction of the splanchnic-venous flow, insufficiency up to the paralysis of
the peritoneal lymphatics and therefore all the conditions for establishing a MOF or a MODS.
We also have important studies demonstrating the role of lymphatics in the pathogenesis of acute
hemorrhagic pancreatitis , because the mesenteric lymph in acute pancreatitis contains factors that
determine an alteration of red blood cells that manifests itself in a reduced deformability (it has been
demonstrated through the interruption of lymphatic flow from the injured intestine compared to the
adjacent contiguous circulatory district). Ligation of the mesenteric lymphatic duct reduces the red cell
alterations caused by acute pancreatitis.

In acute pancreatitis, therefore, lymphatics determine the transformation of pancreatitis itself from
local or regional disease to systemic disease.
The factors of intestinal derivation, in intestinal lymph, have been shown to cause lung injury,
neutrophil activation, alteration of endothelial cells in guinea pigs affected by hemorrhagic shock.
Every disease has its own lymphatic component.

Also the very evolution of necrotic-hemorrhagic pancreatitis, prognostic factors, are all with reference,
in large part, to the loco-regional lymphatic circulation (pancreatic and peri-pancreatic), including the
thoracic duct. Today, in fact, we start again to propose the interest for the study of lymph samples taken
from the thoracic duct during acute pancreatitis to prepare in the laboratory specific anti-enzymes
(protease-specific inhibitors) for acute pancreatitis of the individual subject, to prevent evolution in
systemic disease.
Imaging diagnostics is also evolving, in particular the MRI with lymphography (lymphangio), which is
even able to highlight the dilated lymphatic structures, filled with intestinal lymph, with particular
techniques without the use of electronic fat subtraction. various types of diseases. For example, in an
acute cholecystitis the dilatation also in correspondence of the cisterna chili, in acute biliary pancreatitis,
..

The use of fluorescence lymphography for the study of lymphatic circulation: these are special infrared
cameras with which one can study various lymphatic networks in the various districts, especially the more
superficial ones. It is especially useful to evaluate the cannulation of the thoracic duct at the outlet in the
venous-jugular venous corner in the most severe cases of abdominal compartment syndrome. Withdrawing
the sap

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from the thoracic duct we can identify those specific proteases of the disease (in the particular case of
acute pancreatitis) and with a more informatic approach then, through this proteomic analysis of the
lymph, identify diagnostic markers of acute pancreatitis and then be able to cure the disease before it
evolves at systemic disease.

Conclusions : the knowledge of the role played by lymphatics in the pathophysiology of abdominal
affections, today can no longer represent a secondary aspect.

Prof. Stabilini 17 November

2016

Barrett's esophagus (EB)

It is a metaplasia (definition: replacement of specialized adult cells with another type of adult cells), in
this case the esophageal mucosa is substituted with intestinal mucosa. It is a finding that affects the
endoscopist, visual finding. Not by any symptoms, it is a clinical finding because it is associated with
greater risk of esophageal adenocarcinoma.
At the base of metaplasia there is a chronic tissue damage, in this case the chronic damage is due to acid
insult given by the reflux. The transformation of squamous cells into columnar cells caused by
inflammatory insult occurs (or we can consider the hypothesis that the development of totipotent
progenitors present at the esophageal level turns into typical cells of the intestinal mucosa, these cells
can derive from the bone marrow or from the stomach or be the embryonic residues in each case
stimulated by the inflammatory insult to transform and to cause EB).
Endoscopy, in general the patient will have a long-standing reflux. Columnar epithelium extending above
the gastroesophageal junction, from the histological point of view there are 3 types: Type 1 (complete
intestinal metaplasia) type 2 (mixed glandular form) and type 3 (only muciparous goblet cells). It is
important to know if there is a 360 degree circular involvement (this is why biopsies are done at different
points in the entire circumference) and to know the length that correlates with the risk of complications.
We distinguish EB short if less than 3 cm or long if longer than 3 cm.
EB is a frequent problem in the population: 5-6%. It has been identified in 15% of patients who have
gastroesophageal reflux especially in those with reflux history for more than 5 years (increased risk in
these patients to develop EB by 3-6 times compared to the normal population). GERD is associated
more frequently with long EB, while EB is not associated with GERD and the causes of onset are not
well known.
Other risk factors for EB (the same as those related to esophageal adenocarcinoma): advanced age,
Caucasian race, male gender, chronic reflux symptomatology, smoking, obesity, family history. We can
identify a pathway of progression from EB to adenocarcinoma that has as its connecting link the
dysplasia that is sought in EB biopsy. Loss of glandular structures, cytoplasmic and nuclear alterations,
positivity for ki67, pluristratification of the columnar epithelium are all factors that allow us to define the
presence of dysplasia within the examined area. The age and length of EB correlate with the probability
of development of dysplasia (3,3% increase in risk for each year after 50 years and each 1 cm extension
over 3 cm leads to a 14% increase in risk of development of adenocarcinoma). There are also protective
factors such as the use of statins, a diet rich in fruits and vegetables, and fans.

The important thing is to identify those at higher risk of transformation. The transition from low-grade
dysplasia to adenocarcinoma is 5.4 per 1000 while it becomes 7 per 100 from high-grade dysplasia to
adenocarcinoma. Because if we know a population at risk even if asymptomatic we can act on the
predisposing condition to reduce the development of the disease. This is why screening for EB was
proposed so we could identify all patients who have dysplasia to prevent it

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progression and reduce the incidence of disease. In fact what we see is that 90% of the patients who
develop the neoplasm do not have EB.
We are in areas where the risk of disease is not so high because many of the risk factors that are more
typical of the Eastern countries are often lacking, where alcohol consumption (chronic insult) and
obesity are more widespread. (In Veneto the screening program may be more effective for the habits of
life) Unlike the colon cancer for which screening has given better results (use of occult fecal blood).

This is why a carpet screening can not be performed but is proposed on a specific population: male, with
reflux for at least 5 years and two other risk factors: abdominal obesity, age over 50, Caucasians, smoking
and patients with first-degree relatives with this pathology. In women not

screening is indicated except in special cases with numerous risk factors (they have more protective
ginoid obesity). It may be indicated, in addition, in patients with risk factors that have age and life
expectancy that would allow treatment of the condition.
Therapeutic Algorithm: important to know subjects with non-dysplastic EB must repeat the test after 3 -
5 years. If low or high grade dysplasia is present or even tumor in situ the patient should be
treated. Biopsy techniques: at a distance of 2 cm in the four quadrants to go up in all the languages of
rosy tissue that are present.
Medical treatment: does not exist. You can control the insult that causes the onset of the B: proton
pump inhibitors and you can do the treatment of the symptoms, the use of NSAIDs does not have a
protective purpose in the PC with EB.
Regarding the treatment of high dysplasia areas or in situ tumors this is an endoscopic treatment:
submucosal dissection of the affected area and its removal.
Remember that a nodulation on eb is very suspicious and should be biopsied or removed by endoscopy
or surgery.
Surgery: interventions to block the reflux are proposed (the damage is now present and it is a chronic
damage that however does not regress), for which it is possible to evaluate the cost benefit compared to
the treatment with pump inhibitors. Esophagectomy with reconstruction with colon or ileal loop.

Gastric tumors:

It is a tragically surgical field, any therapy without surgery is not curative, surgery can be curative. When
a patient diagnosed with gastric cancer arrives, I expect there to be histological confirmation, and the
patient has made an endoscopy. So I know the location of the tumor and the histological
characteristic. We must therefore make the staging, or have a cTNM (clinical TNM). To get it I could do
a study with:

• Tc thorax abdomen with intravenous contrast medium and in some cases also per os. (a
suspicious lymph node to be positive to the tc if it is over a centimeter)
• Ecoendo: in the stomach it is not necessary unless it is necessary to do dd between t3 and t4
(operability limit) or between t1 t2 (different type of intervention, t1 can be treated in a much
more conservative way, with mucosectomy or with removal of a gastric portion). (By
definition, a tumor is operable if it is not attached to a viable structure for eg if it does not
infiltrate the aorta)
• Pet: can be used for confirmation of small liver or lung mts (weak point of tc: peritoneal
carcinosis or liver miliary dissemination) however the pet has a limited use because gastric
tumors may not have a high metabolism.

• Diagnostic Laparoscopy: aims to prevent a certain number of useless laparotomies in which we

are faced with peritoneal carcinosis or multiple liver metastases (inoperability criteria). The
therapeutic behavior can vary in 20-30% of cases. They always end with peritoneal lavage and
cell collection to understand if there is a peritoneal microcarcinosis. Not all patients but those
who have a t3 or t4 tumor are subjected to this technique, depending on the results you can
decide to start them to do a preoperative or palliative chemotherapy.

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Therefore, criteria of non-resectability are: invasion of a major vascular structure, third- or fourth-level
lymph node metastases, presence of peritoneal carcinosis or other metastasations. Surgical therapy:

There may be doubt whether to make a gastrorenection or a gastrectomy. It tends to leave the bottom of
the stomach if the tumor is pyloric or present at the level of the antrum, otherwise it will remove the
whole stomach. Numerous studies have been carried out to find out whether gastrorenection or
gastrectomy is preferable for antral tumors, and the results assessed with survival curves show that
survival is overlapping at 5 years and also similar morbidity and mortality. For all other tumors instead a
total gastrectomy is made.

As for the lymph nodes, a conflict arose between east (japan in particular) and west (united states). There are
differences in staging for the classification of N. For Westerners the number of metastatic lymph nodes is an
important prognostic factor in risk stratification, the Japanese do not care much the number of lymph nodes
but consider that more a lymph node is far from the primitive tumor, higher
is the risk that the patient will die in the short term. Both systems have their validity. The Japanese
staging derives from a completely different intervention from ours, divide the lymph nodes into 3 levels:
Level 1 perigastric, Level 2 periceliaci, Level 3 paraortici and the stomach in 3 parts: upper third, middle
and lower. So depending on whether the tumor falls into one of the three parts of the stomach will have a
different type of lymph node removal. They numbered the lymph nodes according to the part of the
organ from which they received lymphatic contribution: distinguishing them in 1,2,3, M for this a
perigastric lymph node but very distant from the primitive tumor can be of level 3 or can also be
considered a metastasis (G1, G2, G3, MTS).Western lymphadenectomy is therefore different from that
of Japanese and for us a patient with only one metastatic lymph node has better prognosis than that
which is recognized by the Japanese who would consider more the type of lymph node involved than the
fact that it is single. For the Japanese the lymphadenectomies are divided into D0 (lymph nodes are not
removed, in the early gastric cancer) D1 (only the first level lymph nodes removed), D2 (first and second
level), D3 (also third) and consider a curative one D higher than the tumor TNM stage.For the Japanese
the lymphadenectomies are divided into D0 (lymph nodes are not removed, in the early gastric cancer)
D1 (only the first level lymph nodes removed), D2 (first and second level), D3 (also third) and consider
a curative one D higher than the tumor TNM stage.For the Japanese the lymphadenectomies are divided
into D0 (lymph nodes are not removed, in the early gastric cancer) D1 (only the first level lymph nodes
removed), D2 (first and second level), D3 (also third) and consider a curative one D higher than the
tumor TNM stage.

A 1987 study comparing Japanese results with Western ones showed that their survival was double or
even triple that of our patients. The Japanese generally showed greater attention to make an organ
removal, compared to the sometimes poorly made gastrectomies that were seen in some cases in the West
and showed that it required at least 15 lymph nodes to say that a lymphadenectomy was well done.
The management of gastric cancer must be as much as possible on the local control of the disease
because the majority of patients present with an already locally advanced disease. 85% of patients have
lymph node metastases and 40-65% have local disease recurrence. In the absence of a screening program,
because in the West the tumor is not endemic as it is in Japan, the prognosis is very bad, 24 months with
20-30% of patients able to have a 5-year survival. Clinical trials have been done also because the great
discrepancies with the results of the Japanese made them think that these were falsified. The two main
trials are called Dutch trial and MRC and they came out roughly in 2000.In particular, the best Japanese
surgeons were called in Holland to teach the Dutch surgeons how to do the lymphadenectomy, the
teaching was also carried out with video recordings of the interventions. Thus they set up two groups of
patients: one group treated with traditional Western intervention and the other with interventions that
followed the modalities taught by Japanese colleagues, for whom the D2 lymphadenectomy was the
fundamental modality. Five years after the start of the trial the results said that survival was almost the
same but morbidity and mortality were higher for the Japanese approach (higher risks intraoperators and
perioperators without giving a real advantage after some time). In 2004 the 10-year curves came out, in
which the results were the same, theonly difference was for patients with n2, favorable trend for the
treated with lymphadenectomy d2.

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The weaknesses of the Dutch trial: there were a large number of EarlyGCs that would be treated by both
approaches, high number of protocol deviations, high morbidity and mortality rates. It was thought that
the Japanese simply had more experience than ours and were therefore better at working because the
complications in the trial Dutch were much more frequent than in Japanese studies. Being unskilled could
be the reason why with the D2 technique, however, they had more deaths than the oriental standards. The
confirmation could be seen from the fact that by removing the male deaths from the trial (more difficult
to operate because more frequently obese) it is highlighted that the women operated showed a benefit if
treated with a d2 rather than a d1. Splenectomy could also be the cause of this problem:effectively
removing the splenectomies d2 was better than d1. In 2005 it was understood that the studies we have
talked about so far had too many limits to be considered reliable.

Since then a first alternative solution came in 2010 from a Japanese study that compares d2 and d3.
They took tumors of the same type and evaluated whether it was better to treat them with d2 or d3.
Results: Slightly smaller overlapping complications with d2, identical mortality, equal survival. It is
shown that there is no reason to do a d3 instead of a d2, but also that the 5-year survival of patients
undergoing lfadenectomy d2 is 70% (very different from the survivals of the mrc and dutch studies in
which it was of 35-40% so dramatically better than standard survival). Still doubt about the removal of
the spleen, for Japanese it is always removed.

However, surgery alone works less than surgery with chemotherapy especially for t3, t4 patients with
lymph node metastases. More recent study of 2014 with xaliplatino and capecitabine data for os shows
that there is advantage to give them after intervention. There is therefore a rationale for postoperative
chemotherapy especially for those patients who have a high risk of relapse.

Furthermore, there is confirmation that it may be very useful to do perioperative chemotherapy.

Perioperative chemo allows to control the disease locally, reduce the size of the preoperative tumor,
improve survival, make a less invasive surgery. (Study of 2006 and recently confirmed called magic
which proves that it may be useful to reduce the size of the preoperative tumor as in rectal cancer,
especially in locally advanced cases) The study included 2 groups, the first (magic group) treated with: 3
preoperative cycles of ECF, surgery 3-6 weeks after the end of the first 3 cycles and then 3 post-
operative cycles of ECF and instead the second group called surg was only surgery. Both groups of 250
patients.In the surg group, 243 patients completed the study, while the magic group only 103, but
analyzing the data showed that there was a survival of more than 13% in subjects receiving
chemotherapy with even 25% less risk of death. So what does it mean? Chemo allows to select those
that have greater benefit from the intervention. So they consider that it is better to lose patient during
chemo than to do an intervention that will not help. So it was concluded that it depends on the biology of
the tumor that is very important and that the chemo controls the size of the disease and reduces it.So
what does it mean? Chemo allows to select those that have greater benefit from the intervention. So they
consider that it is better to lose patient during chemo than to do an intervention that will not help. So it
was concluded that it depends on the biology of the tumor that is very important and that the chemo
controls the size of the disease and reduces it.So what does it mean? Chemo allows to select those that
have greater benefit from the intervention. So they consider that it is better to lose patient during chemo
than to do an intervention that will not help. So it was concluded that it depends on the biology of the
tumor that is very important and that the chemo controls the size of the disease and reduces it.

Instead in cancer where it is not possible to make an R0 resection, the options are chemotherapy alone,
palliative surgery or non-curative surgery. Non-curative and palliative surgery are two completely
different surgeries. In the first part we start with the idea of making a complete resection but then we
realize that it is not possible to remove everything, but still has some more hope than palliation. In
palliative surgery it is already known that it will not be possible to remove all the tumors, but it is
necessary to intervene for a bleeding or an occlusion, to resolve the symptoms and improve the quality of
life, but survival is low, about 8 months .It is not done for other reasons because when you remove a
stomach with a non-curative intervention you are exposed to complications that shorten survival and
worsen the quality of life of the patient and accelerate the suffering. In non-operable metastatic patients
the metal stent for occlusal palliation is used, a complicated operation because the tumor must be placed
in a sufficiently straight area in the stomach to allow placement.

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Subepithelial tumors

They have an absolutely variable behavior. Endoscopic characteristic is the prominence in the lumen
of the organ without affecting the mucosa. The incidence varies from 0.76 to 1%. Those of small size
rarely tend to increase, those that increase in size are those that at diagnosis reach at least 2 cm. There
are two types of subepithelial lesions, submucosal tumors and non-neoplastic forms.

GIST are the most frequent forms. In particular, the symptomatic forms are derived from the
encumbrance of the tumor, for example, early satiety or bleeding, melene or strange anemias. There
are also asymptomatic forms. There are also pictures that are symptomatically concluded, eg patients
presenting the Triad of Carney (gastric gist associated with functioning paragangliomas and
pulmonary chondromes to which they recently added esophageal leiomyomas and adrenal cortical
adenomas in young patients) or the Carney Stratakis Dice (gist) and paragangliomas, but with genetic
association).

For staging a tc with mdc, or nmr. You see well with the pet but it is not a useful exam
preoperatively, if the pc is operable. If it is not, it is a pet because it is also a predictive function of
therapy.
Traditional criteria of malignancy:

• dimensions

• Number of mitoses

• Most favorable gastric gist of one that starts from small intestine. There are nomograms
in

we see survivors: better survival of the gastric gist than the duodenal ones or in general
intestinal ones, they generally have smaller dimensions but are also biologically more
benign. At the autopsy level there is a finding of gastric gist in 10% of patients (subjects
who died for another cause).

Treatment of gastric gist: if operable, surgical therapy, enucleorenection or removal of organ portions is
performed. Do not break the tumor that otherwise tends to spread. No lymph node removal required.
Survival was low before the introduction of imatinib, only 45%. Imatinib has changed everything (blocks
tyrosine kinase and prevents cell proliferation). It is used for gist completely resected, but at high risk of
recurrence, patients are kept in maintenance for 2 or 3 years or even for unresectable gist or recurrences.
For imatinib-resistant gist: there are other drugs specifically produced for mutations in the tumor such as
rivoratinib and sunitinib. First of all, the dosages of imatinib are increased, then if the drug does not
respond, the drug is changed.It was thought to use imatinib even in very extensive and inoperable
preoperative forms. Studies have been done on the gist of the rectum: pre-operative imatinib to improve
the success of the operation, for now it is only used for very invasive procedures. Monitoring of the
therapy is done with the pet, good pet suv is prognostic of a better imatinib response.

Prof. Camerini, 11/21/16

Enteral and parenteral nutrition

If you give a fasting patient 400 calories a day in the form of carbohydrates, you can at least partially
reduce muscle catabolism. However, there are stressful conditions that cause unavoidable muscle
catabolism, first of all burns, then traumas, sepsis and even surgical interventions. In the immediate
post-operative period it is useless to try to stop the increase in energy consumption and therefore the
muscular catabolism, which are inevitable, so for a few days there will be profoundly negative
balances. In the surgical patient it is important to perform a parenteral (intravenous) or enteral (through
the alimentary canal) nutrition because in this way the typical complications of the malnourished patient
are reduced. The enteral pathway, being more physiological, is the best one, but it can not

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be used in patients undergoing abdominal surgery, who have paralytic ileus and therefore require
parenteral nutrition.
Evaluation of nutritional status

There are various ways to evaluate a patient's nutritional status; first of all it is necessary to inquire, through
the anamnesis, on how much the patient eats and consumes. It is very important to evaluate the weight of the
body, because a patient who has involuntarily lost about 10% of the weight is called malnourished. There are
techniques that are not widely used for quantification of fat mass and lean mass and are respectively the
plicometry and the measurement of the circumference of the arm. Also some bio-temporal indexes give
information on the nutritional status of the patient: excretion of creatinine (normal values 15-25 mg / kg / d),
which gives indications on muscle mass and basal metabolism; albumin (normal values 35-50 g / L) and total
proteins; the lymphocytes (normal values 1000- 3700 / μL);transferrin (normal values 200-360 mg / dL),
which is the parameter that moves faster and is therefore very reliable. As for other acute phase proteins, such
as prealbumin or retinol binding protein, they move even faster than transferrin but they do not serve

clinical view since the laboratory does not dose them. Another parameter to evaluate the nutritional
status is the creatinine-height index (CHI) obtained from the ratio between the 24-hour urinary
creatinine and the ideal creatinine for a given height. Ideal creatinine = IBW X 23 mg / kg in male

IBW X 18 mg / kg in the female

IBW = Ideal Body Weight

WHO> 80 slight depletion

60 <CHI <80 moderate depletion

WHO <60 severe depletion

Another method of assessing nutritional status is the calculation of BMI (body mass index).

CLASSIFICATION BMI (kg / m 2 ) OBESITY CLASS

Underweight <18.5
Normal 18.5 - 24.9
Overweight 25.0 - 29.9
Obesity 30.0 - 34.9 THE
Moderate obesity 35.0 - 39.9 II
Extreme obesity > 40 III
Malnutrition

Malnutrition is a condition characterized by an unintentional 10% weight loss associated with a serum
albumin level of less than 3.2 g / dL. There are two types of malnutrition, but they are not clearly
distinct and often border each other: marasmus and Kwashiorkor.
The chaos is characterized by deficiency of proteins and energy, the Kwashiorkor instead of
deficiency mostly of proteins, being the sufficient energy supply.
In the marasmus the insulinemia is low because the patient, besides not ingesting proteins, does not take
simple and complex sugars; for this reason the energy is drawn from the fat, that is from the stocks, with
subsequent increase of free fatty acids in the blood. All this involves an energy homeostasis. On the
other hand, low insulinemia leads to a catabolism of muscle proteins, which represent most of the body's
proteins, with consequent gluconeogenesis and energy production mainly from alanine, as well as a
saving of visceral proteins, from which depends on survival; in this way there is also a protein
homeostasis.

In Kwashiorkor insulinemia is high because the patient introduces sugars, therefore the lipolysis and the
catabolism of muscle proteins can not be performed. This leads to a catabolism of visceral proteins, with
decompensation and the appearance of hypoalbuminemia, responsible for ascites and edema, anemia
and immunosuppression, resulting in infections.

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Specifically for surgical patients, about 40-55% of them have malnutrition. Usually they are also elderly
patients who show sarcopenia, or a loss of skeletal muscle mass over the years (1-2% every year after 50
years, at 80 years you have 50% less muscle mass than at the age of 20, with the same BMI). The loss of
muscle mass is due to reduced physical activity, nutritional deficits, hormonal changes (reduction of sex
hormones), chronic diseases and oxidative stress (accumulation of free radicals).
Criteria for defining sarcopenia: ASM (total appendicular skeletal muscle) index (kg / m 2 ) less than 7.26
kg / m 2 in men and 5.45 kg / m 2 in women. Malnutrition can also be associated with obesity (sarcopenic
obesity), leading to more complications. It is a malnutrition with a high energy intake ("High calories
malnutrition"), caused by low quality of food consumed, wrong eating behaviors and repeated cycles of
diet. Obese patients who undergo bariatric surgery have a probability of preoperative vitamin D
deficiency of 50-80%, of folates of 20-30%, of selenium of 10-20%, of iron of 25-40%. The prevalence
of sarcopenic obesity is 15.4% for men and 21.7% for women.

The four stages of convalescence

First phase : corticometabolic response to surgery, which lasts 3-6 days without complications; there
is albumin reduction and increased PCR.
Second phase : corresponds to the sixth day approximately and is the point of transition from catabolism
to anabolism; diuresis increases because the adrenal hormones secreted in the previous phase had caused
liquids to be retained; there is also a balance of positive potassium.

Third phase : early anabolism, with initial increase in muscle mass and body weight.
Fourth phase : late anabolism, which is completed after months.
The malnourished patient has a 2-3-fold increased chance of developing complications, such as
immunosuppression infections or anastomotic dehiscences due to the difficulty of the healing
process. Therefore, two or three weeks before surgery, it is advisable to give the patient a 1.5-2 times
higher protein intake than usual, vitamins in doses 400 times higher than the daily necessity and an
adequate amount of leucine and valine amino acids. , important for reducing muscle catabolism. The
relationship between carbohydrates, proteins and lipids should be 40:30:30.

Parenteral nutrition

It consists of the intravenous administration of substances with a high energy content, ie carbohydrates,
proteins, lipids and various nutrients. Most of the calories are given in the form of carbohydrates, then
3-5% of the total should be made up of amino acids, 10-15% of lipids, etc. Each patient must receive an
individualized bag according to their needs (age, co-morbidity, etc.). In general, 1 g of protein provides
4 Kcals, 1 g of fat 9 Kcals, 1 g of sugars (dextrose) 3,4 Kcals, 1 g of nitrogen 6.25 Kcals.
IS It is important to know the patient's basal metabolic rate to know how much he has to be fed. There
are various ways to calculate the basal metabolic rate, including the Harris Benedict equation, the indirect
calorimetry (which evaluates how much oxygen is consumed and how much carbon dioxide is produced)
and the direct calorimetry (which measures how much heat the patient produces). Under normal
conditions, 70% of the energy is consumed for the basal metabolism, 20% for physical activity and 10%
for the DIT (energy spent to absorb, digest and store nutrients). In general it is assumed that a
hospitalized patient should receive 25-30 Kcals / Kg per day. If there are complications such as
peritonitis, infections, burns,this value can increase considerably (up to 80 Kcals / Kg per day in case of
severe and extensive burns). In addition, the patient needs 20-40 mL / kg per day of water, 60 mEq of Na
and K, a quantity of nitrogen that must be related to the calories administered (calories: nitrogen = 150:
1) and multivitamin preparations. We need to use formulas that improve the patient's immune situation;
very important nutrients are glutamine, which is almost completely contained in the muscles and which is
a substrate for enterocytes and bone marrow cells, arginine, which promotes the release of growth
hormone and accelerates the healing process, the nucleotides and the omega-3.a quantity of nitrogen that
must be related to the calories administered (calories: nitrogen = 150: 1) and multivitamin preparations.
We need to use formulas that improve the patient's immune situation; very important nutrients are
glutamine, which is almost completely contained in the muscles and which is a substrate for enterocytes
and bone marrow cells, arginine, which promotes the release of growth hormone and accelerates the
healing process, the nucleotides and the omega-3.a quantity of nitrogen that must be related to the
calories administered (calories: nitrogen = 150: 1) and multivitamin preparations. We need to use
formulas that improve the patient's immune situation; very important nutrients are glutamine, which is
almost completely contained in the muscles and which is a substrate for enterocytes and bone marrow
cells, arginine, which promotes the release of growth hormone and accelerates the healing process, the
nucleotides and the omega-3.arginine, which promotes the release of growth hormone and accelerates the
healing process, nucleotides and omega-3.arginine, which promotes the release of growth hormone and
accelerates the healing process, nucleotides and omega-3.
In a patient undergoing parenteral nutrition, the blood chemistry parameters, ions, hepatic profile (increase in
transaminases in case of overnutrition) should be checked; it is also necessary to calculate the revenue and the

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outputs and hydration status, by measuring the central venous pressure, normally between 5 and 10
mmHg. Blood glucose should also be evaluated, which must remain below the renal threshold; if it increases,
the patient may undergo hyperosmolar coma. A sudden drop in blood sugar
it is an early sign of an infection or an abscess, which manifests itself before the onset of fever and
the movement of white blood cells.
Indications for parenteral nutrition:

• Inflammatory bowel disease

• Intestinal obstruction

• Bowel obstruction

• Intestinal fistulae

• Short bowel syndrome (when fasting and ileum measuring less than 1.5 meters
overall)
• Tumor (especially when the patient has to undergo a new cycle of

chemotherapy, so it must be well nourished)

Complications of parenteral nutrition:

• Overload of fluids (particularly dangerous in the case of patients with heart

failure)
• Hyperglycaemia (can cause excessive osmotic diuresis and consequent dehydration,
up to the hyperosmolar coma, so you need to hydrate the patient a lot, you can also put
insulin in the bag in solution with albumin so as not to make it fall)
 • Hypoglycemia rebound (if the patient is not diabetic in the bag and no simple sugars are
given, the patient secretes insulin and a hypoglycemic crisis occurs when the bag is
interrupted)
• Hepatic toxicity (characterized by increased transaminases and typical of the
patient who are given many calories parenterally, may also result in a reduction of
cholecystokinin secretion, due to lack of food in the duodenum, with risk of
gallbladder stones)
• Excess calories (increase in respiratory coefficient and accumulation of carbon
dioxide, especially dangerous in patients with respiratory failure)
• Hypertriglyceridaemia (accumulation of lipid particles in the lungs and consequent
reduction of gaseous exchange at the alveolar level)
• Intestinal atrophy (due to the absence of food transit and reduction of intestinal
clearance, villi lowering and bacterial overgrowth occur, with risk of intestinal bacterial
translocation)

• Intestinal bacterial translocation (passage in the circulation of intestinal bacteria by

altered

permeability of the mucosa)

Modern concepts:
1. Underfeeding: recent studies state that it is better to lightly underestimate the patient,
without reaching the exact level of necessary caloric intake (the so-called Caloric Goals), rather than
overranging it, since this would entail a greater risk of complications and infections.

2. Timing: US and Canadian guidelines suggest to start parenteral nutrition a little later in the
ICU patient, after about a week instead of two or three days later. This would ensure a reduction in
the risk of infections, a lower incidence of cholestasis, a decrease in the number of patients requiring
more than two days of mechanical ventilation and a
lowering costs (parenteral nutrition is very expensive).

Venous access

For parenteral nutrition the peripheral veins can not be used, since most of the calories are administered in the
form of simple sugars, characterized by a high osmolarity, which would involve chemical phlebitis. The
parenteral may be partial (PPN) when the osmolarity is less than 900 mOsm / L, for which the peripheral
veins may also be used, or it may be total (TPN), when the osmolarity ranges from 900 to 3000 mOsm / L and
it is necessary to insert the catheter into the superior vena cava, where the flow is high enough to dissolve the
solutes and avoid chemical phlebitis. The nutrients on which the osmolarity is most dependent are the amino
acids, the dextrose and partly the electrolytes, which have an osmolarity

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respectively 10 mOsm / g, 5 mOsm / g and 2 mOsm / mEq. Lipids, on the other hand, being larger
molecules and therefore having an osmolarity of 1.5 mOsm / g, tend to lower the osmolarity of the
solution.
In general, partial parenteral nutrition is preferable, both because less concentrated solutions are infused,
and because there are no typical risks of central venous access. However, it is sustainable for a
maximum of two weeks and for a still shorter time in a malnourished or sarcopenic patient, after which
it must pass either to natural feeding or total parenteral nutrition, with central venous catheter (CVC).
Total parenteral nutrition allows to supply all the nutrients the patient needs; moreover, thanks to the
use of large-caliber catheters, it is possible, for example, to infuse dextrose up to 25%.

For central venous access at the level of the superior vena cava it is possible to pass through the internal
jugular vein or through the subclavian vein. In the latter case, the vein should be pricked just below the
clavicle periosteum to avoid a pneumothorax or the rarest lesion of the subclavian artery. In any case, at
the end of the procedure performed through the subclavian vein, a radiograph of the thorax should be
performed to verify that no pneumothorax has occurred and that the insertion of the catheter has been
successful. Since the pneumothorax takes some time to become visible at the Rx, the X-ray should not be
done immediately after the maneuver.

In an emergency, for example in a patient in shock, the catheter can also be inserted at the femoral vein
level, with consequent access to the inferior vena cava. This is the easiest access, because once the
pulsation of the artery has been identified, the vein is easily pricked, located medially to it, but we try to
avoid it since it is an area with a rich bacterial contamination. There is a relationship between the size of
the vein used and the diameter of the catheter, measured in French (1 French = 0.33 mm); moreover,
different catheters are used depending on the quantity of solution to be infused. For the measurement of
central venous pressure, a large-caliber catheter should be used, otherwise it would not be able to
transmit the pressure itself.During measurement of central venous pressure the patient, who has central
venous access through the jugular or subclavian, is supine; about 5 cm below the sternum is a graduated
tube with a water column, connected to a closed circuit, which allows to measure precisely the central
venous pressure.

Furthermore, catheters can be characterized by one or more lumens and usually the latter are those that
are more likely to clog. The materials of which they are made are represented by silicone,
polyurethane, carbothane and coated polyurethane.

There are various types of catheters, such as open tip, or open-ended, with which the central venous
pressure can be measured; however, they have the disadvantage of being more frequently affected by
thrombosis, because, due to their conformation, blood regurgitation may occur, therefore they must be
replaced more frequently.
On the contrary, the Groshong catheters, thanks to the presence of a valve, do not show blood reflux
and are therefore less likely to undergo thrombosis; they also allow to avoid gaseous embolism in the
vena cava, a complication that can occur with some types of catheter, having the vena cava a negative
pressure. However, this type of catheter does not allow measurement of central venous pressure.

The type of catheter is chosen taking into account how long it must be maintained; when in fact it is
expected a long stay of the catheter it is better to choose a tunneled, which does not escape exactly at the
point where the vein was pierced, but is characterized by a sort of tunnel to prevent bacteria on the skin
from contaminating the catheter itself and in particular its tip. Then there is the PORT, consisting of a
subcutaneous access equipped with a tank not in contact with the outside that is pierced by the needle; it
can be maintained for a long period of time.
Finally, the PICC is represented by a central venous access inserted in a peripheral vein, above all the
cephalic or the basilica at the level of the arm; this makes it possible to perform a total parenteral
nutrition, since it has access to the superior vena cava. To insert a PICC one can proceed under
ultrasound guidance, in order to highlight the vein. It is a type of access easy to insert, with low risk of
complications and low costs, but the catheter, being long, presents a greater probability of thrombosis.
For insertion of the catheter proceeds under local anesthesia and with the syringe in suction equipped with a
large needle; then with the Seldinger technique the needle with the catheter is replaced by the following
modality: insertion of a metallic guide, removal of the needle and insertion of the catheter on the guide
itself. According to guidelines

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with type 1B evidence, catheter insertion should be performed under ultrasound guidance, as this
will reduce the number of attempts and complications.
Complications related to catheter insertion:

• Artery injury

• Pneumothorax in case of access through the subclavian vein

• arrhythmias

• Gaseous emboli in vena cava

• Hemothorax (rare)

Complications related to catheter maintenance:

• Infection

• Catheter occlusion

• Central venous thrombosis

The infection can occur due to the passage of bacteria (especially S. Aureus and S. Epidermidis) or fungi
present on the patient's skin along the catheter, up to the tip, from which they reach the bloodstream. This
leads to the appearance of fever preceded by shaking chills, up to sepsis if the infected catheter is not removed.
The chances of infection increase with increasing residence time of the catheter: very few if the catheter is
kept less than 3 days, corresponds to 3-5% if it is maintained for 3 to 7 days and reach 5-10% in case of
catheter stay for more than 7 days. Taking these data into account and the fact that any colon or stomach suture
dehiscence occurs in the third or fourth day after surgery,it is good not to exclude that the fever in this period
of time may be caused by a more serious complication, such as a dehiscence,

instead of a catheter infection. Infections can be localized or, if neglected, become systemic (sepsis). For
their resolution a short cycle of antibiotic / antifungal therapy is carried out, in association with the
removal of the catheter and the analysis of the tip of the same. For the prevention of infections it is
advisable to avoid withdrawals from the CVC, a maneuver that may also lead to obstruction of the
catheter or alteration of the result of laboratory tests, such as blood sugar, which may be increased if the
patient is receiving a solution hyperosmolar through the CVC itself. It is also important to perform
dressings correctly and to pay attention to any local signs of infection.

Enteral nutrition

It is more physiological, less expensive and exposes you to a lower risk of complications than
parenteral nutrition.
Indications:

• Neurological disorders (cerebrovascular diseases, hypoxic encephalopathy,

amyotrophic lateral sclerosis, etc.)
• Traumatized patient (especially on the face and neck)

• Neoplasms (in particular of the head-neck district)

The patient can not swallow due to neurological diseases or unconsciousness, so it must be done in one
of the following ways. A usable technique is the insertion of a naso-gastric tube, which however is not
the best method, since this tube can determine erosions of the nasal mucosa and, due to its passage
through the lower esophageal sphincter, gastro-oesophageal reflux, particularly dangerous in a patient in
a coma and not intubated, in which an ab ingestis pneumonia may result. Since currently there is a
tendency to be less and less invasive to allow a reduction of trauma and a more early discharge of the
patient, the probes begin to be used less and less frequently and in any case for a period of time not
exceeding 3 days.
An alternative is represented by the PEG, that is the endoscopic gastrostomy, which is performed by first
illuminating the gastric wall from the inside through endoscopy, then piercing from the outside into the
illuminated spot through Russell introducers. It is a very advantageous method also because it is better to
perform enteral nutrition, usually characterized by a high osmolarity, at the gastric level rather than
intestinal, since the pylorus allows to pass only the osmotically acceptable substances from the intestine
downstream . Thus a lower risk of diarrhea is obtained, which would result in loss of nutrients
administered. However, PEG exposes to 3% more complications:

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3

• Puncture of other viscera (eg the transverse colon)

• Hemorrhages (being a very vascularized stomach)

• pneumoperitoneum

• Moving the tube

An additional alternative is the jejunostomy, which must be carried out as close as possible, immediately
downstream of the Treitz ligament and then at the level of the first or second loop of the fast. For the
jejunostomy you can proceed in laparoscopy or endoscopy, but this second technique is very difficult
because you have to get with the enteroscopy downstream of the Treitz ligament.
Indications for jejunostomy:

• Patient with significant gastro-oesophageal reflux

• Risk of pneumonia ab ingestis

• Difficulty in gastric emptying (eg gastroplegia due to diabetes, or

presence of duodenal ulcer that causes edema of the wall with stenosis first transient
and, following repeated relapses, scarring)
Contraindications to jejunostomy:

• Previous surgery (possible presence of adhesions)

• coagulopathy

• Portal hypertension

• History of peritoneal dialysis

• Severe edema of intestinal wall

• Radiation enteritis

• Inflammatory bowel disease

• Massive ascites or severe malnutrition

• Intestinal ischemia

Various enteral nutrition formulas can be used, individualized according to the clinical context, for
example rich in fibers or alanine or suitable for hepatic, renal or pulmonary diseases.
Contraindications to enteral nutrition:

• Hiatal hernia

• Short bowel syndrome

• Enterocutaneous and enteroenterical fistulas

• Distal intestinal obstruction

• Malabsorption syndromes (celiac

disease, etc.) Adverse effects of enteral nutrition:
• Intestinal distension

• Cramps
 • Impairment of respiratory mechanics

• Intestinal pneumatosis

• Necrosis of the small intestine (caused by intestinal distension that involves

impairment of microcirculation initially lymphatic and then hematic, starting from

venules)
Enteral nutrition should be carefully followed and pumped with a certain number of mL / min. Patients
are fed, at least at the beginning, very gradually, to avoid the aforementioned complications, which are
linked to pathophysiological factors such as hyperosmolarity of enteral solutions, bacterial overgrowth,
the fermentation of the administered substances, the accumulation of catabolism products.
Comparison between parenteral nutrition and enteral nutrition

Benefits of parenteral nutrition:

• It can be used in the case of surgical operations on the abdomen, which involve
paralytic ileus

• It allows to provide the patient, through the CVC, all the nutrients he needs

• It can also be maintained during diagnostic procedures

• It allows an easy achievement of the so-called Caloric Goals (while with the enteral it is

very difficult to overcome 50% of Caloric Goals due to frequent diarrhea)

Benefits of enteral nutrition:

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4

• Low cost

• Few risks

• Beneficial effect on intestinal tropism

In general, parenteral exposure poses a greater risk of bacteremia, sepsis, intra-abdominal abscess,
catheter infection, pneumonia, etc. Often the two methods are integrated for an easier achievement of the
Caloric Goals, through the parenteral, and to avoid intestinal atrophy and bacterial translocation, through
the enteral.

23/11/16
Hydroelectrolyte and acid-base equilibrium in the surgical patient
The patient who undergoes surgery undergoes changes in paraphysiological metabolism, especially in
the catabolic sense: it is necessary, among other things, to rebalance the water and saline losses and to
treat acidosis. Usually the anesthesiologist makes these assessments and prescribes the therapy in an
anesthetic folder at the exit from the room, but then the surgeon will define and adapt it in the following
days.
It is evident that a superficial microsurgery operation does not require the same contribution of a long
open abdominal operation, where the water dispersion is much greater (1000 mL versus 2000 mL)
because the peritoneal surface is very wide; the case of laparoscopic surgery that reduces losses is
different.

The liquids in the human body make up about 60% of the total mass, of these liquids the extracellular is
1/3 and is divided into interstitial (80%) and plasmatic.
Interstitial fluids are formed from the plasma by filtration, which depends on wall permeability and oncotic
and hydrostatic pressures. One part goes into the serous, one part into the cells and the rest is drained by the
lymphatics. Capillary permeability can be increased for example in the obese and during cortisone therapy.

Volume, concentration and composition disorders

Volume

Hypovolemia
Mostly they cause neurological disorders, with variable alterations of consciousness (drowsiness,
apathy, soporific state, coma) and anorexia, hyporeflexia, nausea and vomiting.
Hypotension with tachycardia. Dry skin and hypothermia.
hypervolaemia
Peripheral and central edema, first interstitial pulmonary then completed. Important especially in the
elderly, heart patients with insuff. Respiratory: control quantity and speed of infusion of liquids.

As a rapid assessment we consider hourly diuresis and dryness of skin and mucous membranes. If
central venous access is present, the central venous pressure (PVC) is assessed, which is normal
between 5 and 12 cmH 2 O.

Concentration

Hyponatremia
Hyperreflexia, convulsions, intracranial hypertension (vomiting).

Hypertonic solutions are administered, with NaCl vials dissolved in physiological solution (0.9%).

hypernatremia
Dryness, temperature rise, delirium in severe cases.
Hypothonic solutions 0.45%.
Mixed alterations They occur for profuse diarrhea, for example.
It is NOT glucose. Isotonic salt solution.

--- Wikipedia --- Colloids, critalloids (Ringer), plasma expanders

Colloid: a turbid mixture that does not spread and does not form true solutions, constitutes a
heterogeneous system.
Crystal-like: opposite the colloid, it easily diffuses in solution.
Lactated Ringer: crystalloid with lactate and sodium ions, chloride, potassium, calcium.
Plasma expander: aqueous solution of high molecular weight bio-inert substances (colloid).
 2
5

Composition

Acid-base and potassium, calcium and magnesium ions.

Buffer systems: the main buffers are bicarbonate, phosphate and proteins. Metabolic and respiratory
acidosis, metabolic and respiratory alkalosis. In some interventions it is advisable to provide in
advance with intravenous bicarbonates, evaluating the acidosis with hemogas (chest surgery, for
example).

Assessment of the hydro-salt balance: see usual reference values

Total amount of revenue and expenses:

+ per os
+ IV
+ solid foods
-diuresis
- stools 250 mL
-perspiratio insensibilis, with fever increases 250 mL every ° C

Example:

surgical patient enticed urgently due to intestinal obstruction + fluids /

bags 2000 + albumin phlebs, gastric protectors 500

-diuresi 1500 -drain 300 - nasogastric slide 400 -perspiratio without fever 800
tot. 2500 - 3000 = 500 missing to be administered more

These alterations are responses to traumas for hormone balancing of kidney, adrenal and
pituitary. The operation leads to dehydration, also because it must not drink more from the previous
midnight, without keeping it in prolonged unnecessary fast (eg when you move in the afternoon
remember to tell the patient that he can drink in the morning!). In fast-track can drink up to 3 hours
before and maybe glucose solutions.
Once it was 500 mL before the intervention, now, wrong for the prof., The anesthesiologists do not
do it anymore ... "but how do you go to sleep a dehydrated ... I do not understand ..."
In occluso the liquid is held in third space, therefore excluded from the volemia and not mobilizable,
it should not be diuretic because in reality it is dehydrated, liquids go in the third space.

Infusion rate on infusion or micro-drip pumps: 500 mL / hr in juveniles, hourly diuresis 80 mL / hr.
1-PICC: catheter inserted in the periphery up to the cavity with Seldinger technique, placed by nurses.
2 -Only ultrasound-guided jugular, the axillary was used at one time, but risk of pneumothorax.

23/11/16
 The wonderful history of infection in surgery through the centuries

Stated and adapted for you by prof. Nahum

(Did you all pee? Wash your hands? Good.)

The two Black Beasts of Medicine are infections and tumors.

The surgeon fights just these two, metabolic diseases of course there are but does little. Think of the
wounds, the traumas of the war: amputations are mainly due to the infection that followed. To date,
we amputate due to severe trauma and ischemia with extensive necrosis that can become infected. A
diabetic with severe ischemia in the lower limbs: what germs combine, even in apparently unscathed
tissues, because the infectious state can colonize distant locations!

In my day infectious diseases was a sort of accessory examination, we did not know what the septic
shock was ... Who today can think of graduating without an examination of infectious! THERE IS
NO DISEASE THAT DOES NOT HAVE AN INFECTIVE INVOLVEMENT!

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Two very fast notions.

History dates back to a century and a half ago. It was known that there was an infectious agent but not the
cause, ie the germs. The therapies were empirical. Think about how disinfection was done: a stump cut
with a knife and caustic with a hot iron. This is to sterilize, but sterilize WHAT? !!? YOU DO NOT
KNOW! You know that the research proceeded to jumps, today we can say that it is not so because it is
organized and focused. Sorry for this hat but the arguments must be understood and the container is
fundamental, to understand the contents that it makes melting pot.
Look then that you died of acute appendicitis. Chew your belt and drink the whiskey.
Then analgesia was born, the possibility of anesthetizing.
You could work but then it was bad: because there were infections brought by the bare hands, unsterile
irons. Joseph Listerine is the first to introduce antisepsis. Because others had already identified the
microbes. Louis Pasteur discovers fermentation microbes.

Semmelweis was a Hungarian student in Vienna who understood why in the university gynecological
department there were many more deaths of puerperal sepsis than the hospital: it was students and professors
who carried microbes in the vagina with their hands to explore the cervix and the presentation of the child.

--- here we are wrong about Kocher and Koch: he says that Kocher was French and that he
discovered the acid-resistant bacteria bacteria, while he was Swiss and those bacteria are the
bacilli of Koch, which was German. BAH

W.Halsted starts operating in America with sterile gloves. The practice of using them then spread at
the end of the nineteenth. The basic principles began to develop during the twentieth century and
reduced the fear of surgery. War sharpens ingenuity. Marie Curie goes to the battlefield with a
portable X-ray unit. The surgeon uses antiseptic procedures.
There were still many infections. The '40s sulphonamides and penicillin make it hope that the
infection is beaten. But then we understand the mechanisms of resistance.
We must ensure the patient of the GREAT survival possibilities. Life is prolonged above all for the
hygiene measures put in place.
The immune defenses age and in fact the response of the elderly is much less than the adult.

Synthetic vascular prostheses, not vascularized and therefore do not reach the antibodies, do not
even get infections.

Obviously we must not lose attention to sterilization but rather increase it.

The surgeon must understand that the knowledge of immunology, microbiology and infectious
diseases is fundamental.
Respect for general hygiene rules!

Sometimes the answer to the bacterium itself is deadly. As for the bacterium, virulence and bacterial
load are considered. If it exceeds one million per mL it is high. Bacteria between 10 and 50
microns. Virulence varies from strain to stock.

It happens to observe a swollen wound that is manipulated with forceps and emits pus. Like the Romans
and the Carthaginians in Canne, a massacre. It can affect the superficial fascia, muscle fascias, deep
seats. Prosthetic infections. SI can have empyema and mediastinitis.

Postoperative intra-abdominal abscess, develops because the germs have come out of their
physiological site (saprophytic bacteria and symbionts of the intestine).
Ahh when they started to boil the needles in the kitchen and sometimes they forgot ... Then he
replaced the needle and not the syringe, did not follow the rules of asepsis ... It happened everything
and more.
The empyema is an abscess inside a hollow bowel. The most common event is that the infection is
transmitted from the lung to the pleura. All preformed cavities can be home to empyema, while abscess is
a collection in a tissue. Mediastinites are very serious situations that are not attainable. An empyema
almost always requires drainage surgery. Ubi pus ibi evacua.

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Prof. Nahum, 11/25/16

Surgical site infections (II)

Causes of surgical site infection

1. BACTERIAL FACTORS
Surgical wound infections occur when the combination of number and virulence of the microbial
agents present in the wound is large enough to overcome the host's local defense mechanisms and thus
result in progressive microbial growth. Few microbes do not give problems because the immune system
can eradicate them; if however the number is> 10 ^ 6 / mL of liquid, then the infection is almost
certain, because the defenses are overcome. It should also be remembered that the size of a bacterium is
about 10-40 μm, that of a white blood cell is about 10 times greater and often does not reach the
interstices in which bacteria can settle, for example the prosthesis weave. All surgical
infections postoperative, which occur at the surgical site, are defined surgical site infections
(SSIs):

- superficial incisions : those that develop between the skin and the fascial plane (lining of the
rectus abdominis muscle ); the skin is swollen, red, and dividing the margins of the wound comes out the
pus (serum + interstitial fluids + bacteria + immune cells)

- deep incisionals : involve the fascial and muscular planes;

- of the organ space (involving any anatomical space or organ, in addition to the incision, affected or
opened by surgical manipulation). The SSIs of the organ space include:

• postoperative intra-abdominal abscesses → liquid deposits confined to a tissue or

space
• empyema → is the abscess in the hollow bowel, for example empyema of the
gallbladder, pleural empyema
• mediastinitis → bacterial infection of a precise space; serious, often in need of

surgery.
When an infection occurs, it is drained outside .
The deposition and growth of bacteria in wounds are the necessary condition for the development of
an infection, while the species (and the strain : more or less virulent ) and the bacterial load contribute
significantly to the development or not of the infection itself. The bacterial species is an important factor,
because there are more or less aggressive microbes; the bacterial load is just as important, for example a
charge of 10 ^ 6 bacteria / mL, for example, is a considerable quantity, but can reach quantities even 10 ^
8, 10 ^ 12 and more: when for example a colon has been occluded for days , and therefore retains for
days faeces and liquids inside it, the bacteria develop and can even reach the charge of 10 ^ 15 / mL of
colonic liquid; if this colonic liquid is poured into the abdominal cavity, since there are not the same
defenses there inside the intestinal wall, an infection of great proportions will develop very easily.

The development of the infection is also influenced:

- from bacterial toxins produced;
- from the ability to resist phagocytosis ;

- from the intracellular destruction of the involved micro-organism.

Numerous bacterial species have surface components that contribute to their pathogenicity by inhibiting
phagocytosis, such as the Klebsiella and Streptococcus pneumoniae capsules , and the glycocalytes of
Staphilococci Sp. (Glycocalyx = bacterial surface structures that have the ability to adhere to surfaces,
for example they adhere perfectly to the catheters and here they resist very well).
Gram bacteria - possess surface components (endotoxin or lipopolysaccharide ) that are toxic; other
bacteria, like some clostridia and streptococci, produce powerful exotoxins : the latter allow these
bacteria to provoke invasive and faster infections, even at lower concentrations than other
pathogens. Therefore, while many wound infections do NOT occur clinically within the first five days or
more after surgery, infections due to streptococci or clostridia may present in severe form within the
first twenty-four hours , because exotoxin infections are more rapid to act. , even at more limited
concentrations.

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An example of Streptococcus surgical site infection: safenectomy; the internal saphenous vein (great
saphenous) belongs to the superficial venous circulation of the lower limb, originating at the level of the
medial malleolus and conveying the blood up to the femoral vein (deep). Stripping is performed to
remove this vessel: lower vein isolation at the malleolus, and superior isolation in the inguinal region
before it is inoculated in the femoral; it binds above and below and introduces a long steel wire that
(stripper), is pushed from the bottom upwards until it comes out of the upper part; it is then fixed to the
vein and then the whole is removed from above; therefore a furrow is created, a subcutaneous "tunnel",
which is filled with blood, so at the end ofsurgery a compressive bandage is made in order to limit the
hematoma in the tunnel.

If, however, there is an infection in this tunnel, the patient could show up (in the case cited by Prof. the
patient had presented with streptococcus infection the day after discharge, ie within 24 hours because this
surgery is done in day hospital) with the lower limb flushed, ringonfio, with a streak along the course of
the saphenous vein and blisters, infection expression. This is because microbes from the patient's skin
were conveyed together with the stripper inside the limb, or because the stripper was not sterile (although
today they are single-use), and an infection was generated with consequent collection of pus throughout
the saphenous canal. You can therefore try to remove the infection not so much with antibiotics, but by
evacuating the necrotic, gangrenous and purulent material.

In the sterilization processes some flaws can always occur. The surgeon is the last link in a chain of
organizational events, carried out by qualified personnel, that add up to one another, and which lead to
the presence or absence of sterile materials in the operating field. It is necessary to avoid the presence of
bacteria, or at least to ensure that the bacterial load is not effective, since absolute sterility in the
operating room is practically impossible.

Wounds classified as clean , even healed (NB: if a wound is not clean DOES NOT heal, does not heal
well except by secondary intention!) Generally contain skin bacteria such as Staphilococcus
epidermidis or diphtheroids. In traumatic wounds - contaminated the bacteria most frequently
implicated are Staphylococcus aureus and Streptococcus pyogenes.

With the opening of a hollow bowel, the resident microbial flora becomes potentially pathogenic.

Studies on traumatic wounds in healthy subjects have shown that bacterial contamination with
more than 10 ^ 5 microorganisms / mL frequently causes infection . It follows that:

- normal defense mechanisms are of great importance in preventing the initial stages of infection,
however wound infection is unavoidable when the bacterial load is sufficiently high ;

- since devitalized tissues and foreign bodies are ineluctably present, fewer bacteria are sufficient to
cause wound infections than necessary in healthy tissues. At best, the only foreign bodies present
 are the points, and the only devitalized tissues are those obtained with the use of an electric scalpel
(concentrates the heat exclusively in the cutting area, but minimally destroys the surrounding cells
for diffusion. of the heat: the tissue goes into necrosis even if for infinitesimal quantity!) →
however, even in the best conditions, a pabulum for microbes.

2. LOCAL FACTORS OF THE WOUND

The inhibition of various local defense mechanisms with antimicrobial barrier function is perhaps the
most important cause of wound infections. Furthermore, they all represent factors that increase the risk
of infection:

- The use of foreign bodies , such as suture threads or drainages,

- a deficient recovery of tissue continuity (when you are unable to perfectly reconstruct the
dissected planes)

- the schemia of the tissues themselves due to too tight sutures: if blood does not arrive the suture
will have INFECTION and DEISCENZA (= scar formation and therefore opening of the suture, the
wound does not heal only thanks to the mechanical support of the points, in fact around 4-5 days of
the resistance is conferred only by the scar. very critical situations occur if for example you

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dehiscence of a colonic suture, for this reason the colostomy of protection is done when sutures are
performed on the colon: this is done so that the feces are completely deviated, and that the bacterial
load that comes into contact with the suture is practically nil → not developing infection, nor
traumatism for the transit of feces, the suture heals)

- the presence of necrotic tissue, hematomas or seromas (= accumulation of serum in the wound site,
due to interstitial edema, in such quantities as not to be reabsorbed, for example due to a persistent
infection).
Fortunately, the majority of these factors can be reduced by the use of good surgical technique.

3. PATIENT FACTORS

• Wound infections are more common in pediatric and elderly subjects , perhaps due to

of immaturity or respectively of senescence of defense mechanisms.

•
• Any condition that reduces blood flow in the surgical wound (such as in occlusive
vasculopathies, in hypovolaemic shock or following the use of vasoconstrictors with
local or systemic action) increases the incidence of infection. If the patient is in shock,
the bloodstream is preferentially diverted to the vital organs (heart, brain), and organs
less sprayed at that moment, such as the intestine, can easily go into necrosis and then
puncture.
 •
• The local tissue tension reduction of O2 , caused by reduced blood flow is

from systemic hypoxemia, increases the likelihood and severity of infection.

•
• prevention of intraoperative hypothermia and maintenance of high levels of FIO2
(80%, is the inspired fraction of O2) in the operating room and in the recovery
room can significantly reduce the risk of infection of the surgical site . Hypothermia is
caused by anesthesia (hypothermia of central origin), by the fact that the piece is not
covered by clothes, and also by the fact that, if the piece is opened, there is evaporation
of heat from the viscera; all these factors significantly lower the local immune defenses
and can promote the development of infections, for this reason today in many centers are
used thermal blankets and mattresses in which hot air circulates.

• Furthermore, conditions that reduce vascular reactivity , such as uremia, advanced

age, use of high dose corticosteroids and other drugs, increase the susceptibility to
infections.

• More complex problems that can cause an increase in infections include the

cancer and trauma.

Prevention of wound infection

Premise: "One of the most important factors in preventing wound infection is the constant vigilance of
the entire surgical team and in particular of the surgical surgeon".
1. PREVENTION OF THE BACTERIAL
CONTAMINATION OF ENVIRONMENTAL FACTORS
The two main sources of bacterial contamination of the wound, in the operating room, consist of:
- exogenous source , deriving from technical deficits of the operating team;
- endogenous source , originating directly from the patient's skin and other organs containing
bacteria. Of the two, endogenous contamination causes more infections in all types of wounds except
those classified as "clean". As far as exogenous contamination is concerned, it would certainly be
important to limit the entry and exit traffic from operating theaters, maintain positive pressure, limit
motor activities and talk. Table: classification of surgical wounds based on the risk of infection

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GUY DEFINITION INFECTION INCIDENCE

clean Not traumatic from 1.5 to 2.9%
Absence of technical errors
 Absence of opening of the lines
respiratory, genitourinary,
digestive
Clean - contaminated Opening of the respiratory tract o from 2.8 to 7.7%
digestive in the absence of
significant contamination
Opening of the oropharynx, of the
vagina or genitourinary features e
biliary (uninfected)
Wasteland Major technical error From 6.4 to 15.2%
Important contamination of the
gastrointestinal tract
Traumatic wounds
Opening of the genitourinary
features o
bile in the presence of urine or
bile
infected
dirty Coarse pollution of From 7.1 to 40%
maternal purulent, faecal or
material coming from
from the external environment

Today there are tools that allow the simultaneous incision and suture: you avoid spill and therefore
have greatly reduced infections.
In the case of presence of necrotic or purulent liquid, it is collected and sent to culture; while waiting to
know which antibiotic therapy is necessary, it is possible to start with a broad spectrum therapy to
cover the most probable etiologies. The infectiologist has a fundamental role in the indication to the
specific antibiotic.
If the wound is contaminated or dirty at the start (ie traumatic), the surgeon must declare it, to partially
alleviate his responsibility for any serious complications or death of the patient (which otherwise a
legal authority could allege to the surgeon's misconduct).
Preoperative patient preparation: Patients who are hospitalized for a long period or have chronic
disease sufferers are subject to an increase in resident skin flora, especially in the inguinal region and
at the level of large skin folds.
Trichotomy : the microtrauma caused by shaving promotes the penetration of bacteria from the skin into the
wound. One precaution may be to disinfect the area to be shaved BEFORE shaving, as well as after; if you
use a normal razor, you should take care to depilate at least one day before surgery, so that the microtraumas
can already be largely solved. If, on the other hand, the electric shaver is used, as it is commonly used today
in the operating theaters, one must use one with disposable heads, at the same time as the operation, thus
trying not to traumatize the skin; the electric razor is better from this point of view because it does not
eradicate the hair at the base so it should not create the microtrauma. Preparation of the skin : the skin is an
important source of microorganisms capable of contaminating clean surgical wounds. The validated technique
of skin preparation consists of:

1.washing of the patient's entire operating region for 5-7 minutes with a detergent
and germicidal solution ;
2. application, on the affected area, of an antimicrobial solution based on iodine , iodopovidone
or chlorhexidine (non-toxic or allergenic substances, but caution: do not give it to the wall, because if,
for example, it is applied on the abdomen and the excess goes behind the back, here in contact with the
skin and can create burns).
→ when to dry the antimicrobial liquid from the body surface? Wait at least a few minutes to allow
time for the substance to act; the time of contact with the substance is important, otherwise it is
completely useless!

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3. alternative modality of skin isolation at the incision site: use of an antimicrobial adhesive
sheet applied over the entire surgical field; normally to delimit the field externally surgical instruments
are used sterile towels that have a "sticky" side that allows them to remain firm where they are
applied; the aforesaid antimicrobial adhesive sheet is an extra stratagem, in the sense that this is applied
to cover the operative field itself, and its edges are applied to the edges of the sterile sheets; as a
consequence the incision is made through the plastic, of exposed skin there is none. In addition, the first
incision should always be done with the knife scalpel, the electric one causes burn and often
hypertrophic scar. At the end of the operation, when the deep layers have been assembled and the skin
has to be sutured, the adhesive sheet is moved aside.

2.TEAM OF OPERATING ROOM AND DISCIPLINE

The contamination originates more frequently from the operating team , one of the most important
sources of microorganisms responsible for infections in clean surgery.
Clean clothing, hats, masks. Washing of the hands and forearms with an antimicrobial soap ,
prolonged for at least 5 minutes for the first operation or after each "dirty" operation and for 3 minutes in
subsequent interventions. After a certain number of hours of surgery it would also be advisable for the
surgeon to wash his hands again and change the gloves; this is because, however, after two hours from
even careful washing of the hands, microbial colonization is again present on the skin. An additional
source of contamination is the sterile knobs of the lamps , which can be contaminated by impacts with
the surgeons' heads.

Up to 90% of the operating team's components pit or cut their gloves during a prolonged
surgery. In these cases the gloves must be replaced immediately .

3. ENDOGENIC CONFIGURATION

Endogenous contamination occurs in variable degree at the time of transection of the respiratory tract,
gastrointestinal or genitourinary, whenever it is that a hollow viscera is opened. However, a consistent
effort to minimize the degree of contamination can maintain the incidence of bacterial infection at low
levels.
Before a hollow viscera is opened, the operating area should be isolated from the rest of the
surgical field.
A different set of instruments should be used in this phase of intervention until the closing of the
hollow bowel. Once the hollow bowel has been closed, all the laparotomic instruments, gauze and
drapes, which may have come into contact with the contaminated area, must be removed from the
operating field as well as the sterile gowns and the operating team gloves must be replaced .
In addition to endogenous pollution for substances from the surgical field, other factors are
responsible for wound infection , and in particular:
- the duration of the intervention itself,

- the "physical status score" of the American Society of Anaesthesiology (ASA).

A more recent risk classification system for surgical procedures assigns a point to a given
intervention depending on whether:
- the wound is classified as contaminated or dirty,

- the duration of the surgical time exceeds the 75th percentile for that procedure, or
- the ASA score is 3, 4 or 5.

Therefore a score of 0, 1, 2 or 3 can be assigned to a specific surgical procedure. This score, which is
used by the National Nosocomial Infections Surveillance (NNIS) system of the Center for Disease
Control (CDC), has proven to be much more sensitive in predicting the risk of SSIs compared to the
more obsolete National Research Council (NRC) system.
(continue in the next lesson)

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 29/11/16

Preparation for intervention and risk factors

We can find ourselves in front of outpatients, the patient hospitalized in internal medicine where the
surgeon is called in counseling or the patient observed in emergency (first aid) for suspected surgical
pathology.

We have to consider:

- The nature of the disease (whether it is tumor or not), the acute illness (acute
cholecystitis or other diseases)
- The proposed intervention (I can do a hernia open under local anesthesia with minimal risk or I
can do laparoscopically under general anesthesia and if it is bilateral, I opt for the latter).

- The clinical conditions of the patient. If you are young and need to be operated on the gallbladder,
if you have comorbid or not, age (an elderly person taking antiplatelet medications).
- Evaluation of risk factors (cardiorespiratory, metabolic diseases such as diabetes decompensated
with patients who reach 170 mg / dl of fasting glycemia or with an 8% glycated Hb which are
neglected, haematological).

- Results of diagnostic and therapeutic procedures to improve the general conditions of the patient
(for example an ECG, spirometry and parameters that, depending on the value, entail different
anesthetic risks) (ASA classes we will see later))

- State of preparation for intervention (especially for patients in election)

Understanding if the intervention is necessary or not. The patient normally arrives with a suspected
surgical pathology and investigations to support this suspicion. Evaluating the most relevant clinical
signs, revisiting the clinical history, evaluating laboratory and instrumental investigations (an echo of a
year ago has to be redone because maybe the calculation may no longer exist and opening the patient's
stomach by not finding anything is not the maximum: D). A picture not always to be performed is
appendicitis or a diverticulitis in which one can alternatively perform an antibiotic therapy, cools the
patient and then a parenteral therapy. In diverticulitis you have to perform a resection and an
anastomosis but you do it in election because in urgency the anastomosis may not hold for perivisceritis
(inflammatory peritoneal reaction).So "let's cool the patient's clinical picture" and then in laparo (later)
the resection is done. The exams required for the patient must be checked again! Then we carry out the
prescription of any further diagnostic investigations (for the heart the echocardiogram, the cardiologic
examination, the pressure holter based on the cardiac pathology.For the respiratory system the
spirometry for the respiratory function and the EGA for the oxygen ). Consider possible alternative
treatment options and explain to the patient and any family members explaining the perioperative risk to
them.Then we carry out the prescription of any further diagnostic investigations (for the heart the
echocardiogram, the cardiologic examination, the pressure holter based on the cardiac pathology.For the
respiratory system the spirometry for the respiratory function and the EGA for the oxygen ). Consider
possible alternative treatment options and explain to the patient and any family members explaining the
perioperative risk to them.Then we carry out the prescription of any further diagnostic investigations (for
the heart the echocardiogram, the cardiologic examination, the pressure holter based on the cardiac
pathology.For the respiratory system the spirometry for the respiratory function and the EGA for the
oxygen ). Consider possible alternative treatment options and explain to the patient and any family
members explaining the perioperative risk to them.
These may or may not accept the risk (if the patient is dying in ASA -4 as patients with peritoneal or
peritoneal dialysis peritonitis.) If you bring them into the room, they do not leave.In the peritoneal
dialysis the intestine becomes flabby and risks perforate).

Perioperative planning
Surgical timing. On the basis of urgency, election and priorities, patients with gastroesophageal reflux
candidates for gastroplasty (fundo plicatio). There are patients whose symptoms are controlled by the
therapy or those who have been with Barrett for 20 years.

Place of intervention. Depending on whether we have to do general or spinal anesthesia. There are check-
in and check-out cards in this regard.
Type of anesthesia
Pre-operative preparation. Fasting is the most important. From midnight the day before must not even
take liquids. Way to operate fast and track. As if they had not been operated. They also give him to
drink. Apart from these situations, in which intestinal preparation. Once the clean intestine was
needed. For example in election for the K colon. In videolaparoscopia only the air is bothered by the
antimeteoric drugs (in drops) for 3 days. If the stools are poorly formed, when I do an intestinal resection
... stercoric peritonitis. If they are solid it does not come out so it is advantageous. When I do the
anastomosis, if the faeces are more formed, that slurry does not come out. In video it is much more
advantageous.

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In the pre-operative assessment, what is important is the assessment of comorbidities. For example, in
severe connectivis such as severe rheumatoid arthritis, the tissues are more fragile, so the alterations
in scarring are more important.

If the patient does not tell us about his illnesses, we ask them for the drugs they take and go back to the
disease. Important anamnesis!
A tumor of the esophagus causes dysphagia in the patient and this tends to malnourish with a
consequent state of malnutrition and consequent cachexia. The diagnosis is made when the tumor is in a
fairly advanced stage. Its serum proteins are lowered because the catabolism is directed towards its own
proteins, not having other ones. You can not operate a pc with less than 2 albumin otherwise the
anastomoses do not hold. I have to resect the esophagus and make an esophagoplasty either with the
colon or with the stomach or with the fast. It is necessary to put the piece back in order to avoid that the
surgical risk is too high. A thoracic esophagus-gastric dehiscence gives important mediastinitis.

The evaluation of the surgical risk in the peri-operative phase: intra-operative (up to 48h after) or
post-operative up to 30 days later.
To recapitulate preoperative assessment it is important to identify any co-morbidities that may influence
the outcome of the intervention (history, objective examination, age-related factors, disease
progression). In case of significant co-morbidities or associated pathologues not well compensated, it is
useful to contact internists or reference specialists.
Evaluation of risk factors

We have patients with renal failure, coagulation disorders, thrombocytopenic agents. There are heparins
like fundaparin that does not give thrombocytopenia. We use the Child score to be evaluated in liver
failure. Anemic Pz. As the major intervention gives bleeding. The right colon cancer is found later
because the intestine is wider and becomes large without giving symptoms while in the left they give
alterations of the rectum and rectal bleeding. So the one with K in the right colon bleeds. If it is an atrial
fibrillation, the priority is that it does not bleed. Maybe we replace the dicumarolico with the clexane.
Wait until it stops bleeding and transfuse it. It depends on the type of surgery or when I remove pieces of
fabric quite bulky I lose more blood.
The fourth is at high anesthetic and surgical risk. A K in the stenosing esophagus in patients with
ASA3.5 does not program an esophagectomy but we do palliative therapy because it will not exceed the
intervention. So we use the laser. The tumor remains there (a little smaller than before) but the patient
will have a better quality of life because he will resume eating.

CARDIOLOGICAL RISK ASSESSMENT. NYHA Classes and Goldman Criteria

Based on the clinical history, diagnostic tests, the general state, respiratory and ionogram. The clearance
is given by 3 people: cardiologist, anesthesiologist and the surgeon. The cardiologist writes the increased
risk and then the anesthesia that decides whether to put the patient to sleep or not, also evaluating the
surgical aspect. Because the anesthesiological risk is most important. Once upon a time there were a lot
of gastrorenections, like hernias and gallbladders with the risk of developing a carcinoma of the gastric
stump over time (resections are risk factors for gastric carcinoma)
If the patient had an IMA? For the assessment of ischemic risk, do myocardial scintigraphy to see if
there is a hypoperfusion. From stress or under pharmacological stimulation such as a cycle ergometer
test or dipyridamole which puts the heart under strain. If I have put the stents evaluate the residual
ischemic risk.

EVALUATION OF THE RISK OF RESPIRATORY INSUFFICIENCY

If I do peripheral interventions (varices), it is a risk that interests me less because I do not operate regions
near the diaphragm. But if I do a hog with all the intestinal loops that have lost the right to domicile, if
the piece is overweight and thrown it all in, I get to the neck. (?) Sometimes the patient starts in local and
for complications, the intervention it must be carried out under general anesthesia. For example: for a
hernia I would have operated under local anesthesia, because I did not see a bladder diverticulum in the
pre-operative examinations, what looked like a hernial sac opens and exits a liquid (injured bladder
diverticulum) and therefore the intervention requires the transition to general anesthesia.

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In spirometry they evaluate FEV1 (maximum expiratory volume in the first second, if FEV1 is less than
0.8 L7sec or 30%, high risk), the FVC (forced vital capacity) and the DLCO (diffusion capacity of
carbon monoxide).
We do not do them all. The standard preoperators for all are blood chemistries, coagulation, renal
function, hepatic function, ions, ECG and chest X-ray. All the rest if anamnesis and comorbidities
require further investigation.

Interventions that can reduce respiratory complications are smoking cessation and treating the
underlying disease (with bronchodilators, antibiotic treatment of pre-existing infections, treatment of
asthmatic patients with steroids.

EVALUATION OF THE RISK OF RENAL INSUFFICIENCE

About 5% of the adult population suffers from a certain degree of renal failure (the basic creatinine is
controlled).
Appropriate to identify in these patients possible cardiovascular, circulatory, haematological and
metabolic alterations secondary to renal dysfunction. Careful anamensi and eo
The perioperative period in patients with IR should include:

Potassium can be altered, as well as for renal failure, also for the possible intake of potassium-sparing
diuretics that increase (worsening) plasma levels.
Maintain adequate volemia in patients who may be dehydrated.
Nephrotoxic drugs can be NSAIDs (we choose paracetamol as an alternative), antibiotics used for
surgical prophylaxis (therefore we use others metabolized by the liver), heparin (Clexane) same used
as antithrombotic prophylaxis should be adjusted in dosage (eventually give less ).

EVALUATION OF THE PRE-OPERATIVE RISK IN THE PC WITH HEPATIC INSUFFICIENCY

Child Pugh Scoring System: Albumin, prothrombin time (PT) and INR are always evaluated, a
possible ascites is evident or can be seen with ultrasound and encephalopathy is also clinically
evident. A class A, B, C is given as a function of risk.
We do this in transplant patients! In such a way as to make them in force before the intervention with
any rehabilitative interventions and reduce the risk as much as possible.
EVALUATION OF PRE-OPERATIVE RISK IN PATIENTS WITH ENDOCRINE-
METABOLIC DYSFUNCTION

If the anamnesis suggests it (story of Basedow or maybe other tireopathies), even if they are not
routine, ask for thyroid hormones! Because if they were altered and not checked, after surgery
the patient risks alterations of cardiac function.

Adrenal secreting adenomas (phaeochromocytoma) can give severe hypertensive crises. There are pre
and post operative therapies that monitor adrenal function. Now that the interventions are done in
laparoscopy, the gland is practically not "squeezed" so the risk is less.

In diabetic patients have adequate glycemic control, possibly insulin preoperatively to control the
glycemic situation.

Hyperosmolar sacs for 33% glucose parenteral nutrition used in diabetics and glucose buffering with
insulin in diabetics must be greater with 70, 80 or 90 IU insulin. The insulin units must be bound with
50 cc of albumin because if they precipitate, the insulin goes all in the vein and a major hypoglycemia
at night could kill the patient.
EVALUATION OF THE PRE-OPERATIVE RISK IN THE IMMUNEPRESS

PZ WITH HEMATOLOGICAL ALTERATIONS.

PATIENT EVALUATION WITH HEMATOLOGICAL ALTERATIONS
There are scores such as that of Caprini that according to the score is given antithrombotic prophylaxis.

Eg: with large retroperitoneal hematoma. The surgeon if he can not intervene because if he is affected, he
loses. From angioTC, see if the bleeding is still active. If it is active, the angiographers must embolize the
vase. The surgery can be done even if the angiography can not stop the bleeding because the vessel is heavily
damaged, but at that point it is a very high risk intervention.

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5

Eg: in treatment with dicumarolico falls from the stairs of the cruise, arrives in the emergency room
for a large trauma and strongly anemic. The surgeon operates it and the patient dies. Theoretically, he
would have to wait, make bags, transfusions, coagulation factors and platelets. However, these are
difficult cases.
Ex: young man who is a traffic accident and suffers an important trauma with a large hemorrhage. What
can be done? We can ask the CTO (orthopedic trauma center) to carry out intraoperative blood
retrieval. There is a machine that aspirates all internal bleeding (peritoneal in this case), filters the blood
and is returned with a bag. In urgency it is something that could be required.
Angiographers can put the filter in the groove under the kidneys because if you put on it, a thrombus
can embolize to the kidney and give acute renal failure.
What's the point? The thromboembolic risk is when it is a piece that does not respond to anticoagulant tp
or in which the tp is contraindicated (like the bleeding patient) or despite the therapy, it embolizes. If
you have an important femoropopeal thrombus that is ready to embolize. Temporary filters are placed
just before surgery and then removed after surgery.
The definitive ones are left behind.

Recall that in antithrombotic prophylaxis heparin should be done NOT before 6 hours after
otherwise the patient bleeds. Alternatively, it is done BEFORE the intervention (from 12h before
up to 2h before)

30/11/16

Chest pain: approach to the causes of greater clinical impact based on the evidence

Learning to have an "evidence based" method: follow the guidelines to minimize errors.

Epidemiology : 5% of PS access is attributable to chest pain. Of these, 10% of cardiac origin, but 50%
remains without a diagnosis. Not always acute is required to make a diagnosis, but you need to
understand what are the most serious causes of chest pain that require immediate intervention.

Critical aspects: identifying the critical issues is one that is not able to do google, while the thinking brain
does.
NB: The severity of the symptoms and the severity of the clinical picture do NOT correlate with the
clinical evolution. A PC presenting a clinical picture that apparently makes one think of dismissing it
could evolve into a dramatic picture. Therefore: until a high probability of diagnosis has been reached,
the patient should be considered with chest pain as a risk of acute or even dramatic complications (yellow
or red in PS, but not green).
The early identification of life-threatening frameworks serves to set up an immediate life-saving
treatment.

Main clinical pictures:

• at immediate risk: the pc actually risks his life; myocardial infarction, unstable angina, thoracic
aortic dissection, ruptured thoracic aneurysm, pulmonary embolism, cardiac tamponade
• serious conditions: short-term diagnosis and treatment; pneumothorax (the hypertensive one is
at immediate risk), acute pericarditis, rupture of the esophagus, pleuropneumonia.
• lower-gravity conditions: with deferrable treatment; gastro-oesophageal reflux, biliary pain,
musculoskeletal origin, psychiatric disorders, Herpes Zoster.

The first interventions that we must take are the same for all the patients who enter the PS with chest
pain, regardless of what will then be the diagnosis:

- resting in the supine / seated decubitus, better at 40 ° (provided the conditions allow it →
no traumatized patient , because it is first necessary to rule out any fractures)

- monitor the PA and SO2: two parameters that give us important information on the patient's
hemodynamic conditions .

- guarantee O2 and peripheral venous accesses (usually one is sufficient, but in particular conditions, such
as aortic dissection, must be two, because there is a risk of massive hemorrhage).

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6

- ECG trace: first diagnostic investigation that we can apply to the patient. It is a simple, low-
cost investigation , but it is burdened by a fairly low sensitivity (50%).
All this takes up to 10 minutes.

We divide patients according to the general conditions in:

• stable : accurate history, in-depth objective examination, blood tests / diagnostic tests

• unstable : ABCDE assessment ( A airway - B Breathing - C Circulation - D Disability -

E Exposure. →

resuscitation maneuvers for stabilization)

•
• Acute coronary syndrome (SCA)

• STEMI: elevation of the ST segment; cardiac enzymes moved.

• NSTEMI: absence of elevation or depression of the ST segment; cardiac enzymes moved.

• Unstable angina: absence of elevation or depression of the ST segment, but normal or mild

increase in the dosage of cardiac enzymes

A typical symptomatology (chest pain) is present only in 60% of the patients, 40% have atypical
symptoms (syncope, new onset arrhythmia, dyspnoea, even in total absence of chest pain).
Scores have been developed, such as the Brownwald criteria which identify the probability of having
SCA.

Diagnostic procedure : the first 4 operations are performed (see above).

• The ECG is the most useful exam for the diagnosis of acute myocardial infarction, but, as we
said, it is burdened by a low sensitivity; it is normal in 50% of cases.
• Q waves are the only sure sign of necrosis, but they appear late, so cardiologists have tried to
find "escape":
• elevation ST in v1, v2 and v3> 0.2 or in the other derivations> 0.1.

• elevations of cardiac enzymes: myoglobin is the most precocious, has a good negative
predictive value (if it is missing it is unlikely that there is infarction), but it is nonspecific because
 it is present in all muscle cells; Troponine T and I are the most specific enzymes and appear after
a few hours, the peak is at 24 hours and decrease in 4-10 days; CKMB has an intermediate
specificity, the peak is 18-24 hours and decreases to 36-72 hours.

Therapeutic Iter :
First step:

• oxygen therapy is indicated in those patients who have SO2 <94%, if there is no evidence that it
can benefit.
• Nitroglycerin is indicated for the first 48h after IMA, heart failure, hypertension as it reduces
ischemic pain and acts as a vasodilator of the coronary and peripheral circulation, reducing
cardiac load;

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7

• ASA: reduces mortality by 25%, provided there are no contraindications, therefore hemorrhages in
progress;
• morphine is the analgesic of choice indicated if the pain from IMA is persistent. 2-4 mg ev in doses

refractory.
Second step:
- fibrinolysis and angioplasty. "Time is more important than medication". A fibrinolysis has a certain
sense because it brings a certain advantage to the pc, if done within 60 minutes, intermediate between 60
minutes and 12 hours, practically nil if after 12 hours. Contraindications to fibrinolysis are:
cerebrovascular events in the last year, current hemorrhage, known aneurysm or cerebral MAV,
suspected aortic dissection.
Angioplasty has a high success rate (90%) and has reduced mortality by 20% for IMA, but its
availability is limited (not in all centers do it and this is a problem that arises at the time of arrival of the
ambulance: one must choose where to transfer the patient according to the type of intervention
necessary).
Angioplasty has two conditions: it must be performed no later than 90 minutes after the onset of IMA
(over 90 only if fibrinolysis is contraindicated), and must have an experienced cardiologist. Indications:
STEMI, NSTEMI, unstable angina (reserved for patients with negative evolution, clinical manifestations
of severity and worse prognosis).

Acute aortic dissection

It has a high mortality rate: 50% at 48 hours, 90% at one year, but fortunately the incidence is relatively
rare: 3/100000. The M / F ratio is in favor of the first: 2-5 / 1.
The causes are essentially: collagenopathies in young people (Marfan), hypertension and atherosclerosis
in the elderly.
Classification strongly orients therapeutic intervention: Stenford A → urgent surgical
treatment; Stenford B can be postponed (follow up).
Clinic : the pain is in 90% of the patients (10% no →> diabetics, in which the neuropathy affects the
transmission of pain sensitivity → risk of mis-diagnosis), is generally retrosternal, irradiated in the
interscapular region. An important clinical sign is the pressure difference between the two limbs> 20
mmHg (this is a very rare maneuver, but in this case it could be diagnostic). Other symptoms:
neurological deficits due to carotid dissection (40%), acute ischemia in the lower limbs, when the
dissection has now reached the abdominal aorta.

Diagnostic and therapeutic Iter: first 4 interventions. The ECG can detect abnormalities compatible with
SCA, so it is not diagnostic. Troponins are usually required, but can be moved for other reasons. Then
the chest X-ray is performed (mediastinal widening, tracheal displacement, pleural effusion, aortic
abscess, disappeared aorto-pulmonary space, all nonspecific signs), then the fast TT echocardium (DD
with ischemic heart disease, if the Chinese ventricles is conserved we can exclude that it is SCA, may be
the presence of pericardial effusion and cardiac tamponade), the TE echocardium is the election test in
the unstable PC, trivially because it is invasive. The TC is the definitive exam and the gold standard (in
suffering patients you do as FIRST exam), gives us information about the extension,but the
contraindication is the contrast medium (IRC).

When we suspect DA the therapy must be started BEFORE the definitive diagnosis: ensure a DOUBLE
large-caliber venous access (exception), because the risk of a hemorrhagic shock is very high, so we
must guarantee an adequate volume replacement (internal jugular, subclavian , femoral ..). Control the
pain with boluses of Morphine ev to reassure the patient, important for the next two steps.
Pharmacologically reduce the FC (goal 60 bpm) and the PS (goal 100-120 mmHg) that could cause wall
stress using beta-blockers ev and Nitroprussiato.
Urgent cardiac surgeon is required in type A dissection (ascending tract involvement), whereas type B
(descending aorta only) may deserve only follow-up treatment, or endovascular treatment in selected
cases (persistent chest pain, peritoneal hematoma) ).

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Pulmonary thromboembolism

Incidence increases with age and enticement. Mortality is 30% if not treated, 10% if treated with optimal
therapy. The causes are: hypercoagubility (congenital, major surgery, immobility, FA, neoplasm like
paraneoplastic syndrome, pregnancy, obesity).
The embolic risk in the neoplastic pc is extremely high → anticoagulants.
Clinic : quite varied. The main symptoms are sudden dyspnea and chest pain, but there is a great
variability, also in relation to the size of the thrombus (totally or partially occluding the vessel). Severe
pulmonary embolisms are those in the major pulmonary branches.

Wells Score: being the clinical nuanced, there are these simple questions that identify the risk of
developing EP.
Iter diagnostic : 1st level: EGA (typical finding: hypoxia → exchange prevented by thrombus,
hypocapnic → iperventila), ECG (S1Q3T3 is rare!), Thorax chest (rarely pulmonary infarction, often
non-specific signs). 2nd level: D-dimer (a sign that fibrinolysis is occurring) has negative predictive
value (if negative it is very unlikely that the PC has EP, if it is positive it is not said that it has it).
Perfusion scintigraphy is falling into disuse as it is difficult to interpret if there are concurrent
cardiopulmonary diseases. Used for negative predictive value and as an alternative to TC. TC with
contrast medium is certainly the primary choice and the gold standard because it has high sensitivity and
specificity (> 90%) and is easily interpretable. The echocardiogram is important because it gives us
information about the extent of pulmonary embolism, which,if severe, it has already caused alterations in
the right ventricular chambers (indicated in critical cases for the acute pulmonary heart search).
Compressive echo in the lower limbs → lower limb TVC has positive predictive value, low negative
predictive value.

Therapeutic Iter : anticoagulants (heparin in bolus 80 IU / kg and then in continuous infusion with
syringe pump 18 IU / kg / h, first PTT control after 6 hours). The alternative to heparin is fibrinolytics
(tissue plasminogen activator), but the latest guidelines say they give more bleeding complications. They
are used in patients with Tep during shock, cardiac arrest and cardiac or respiratory failure (10 mg in
bolus, then infusion in 120 minutes in relation to body weight). The reason that makes Heparin an
excellent drug is that it has a direct antidote, protamine sulfate. Low molecular weight heparins are
filtered and modified versions of heparin that do not have an antidote, so you have to wait for their effect
to end.Once the acute phase has been resolved, treatment with oral anticoagulants is started as
maintenance.

Pneumothorax :

the incidence is a little higher than aortic dissection: 18-28 cases / 100,000 people / year (M) 1,2
- 6 cases / 100,000 people / year (F). Mortality is low because it is usually well diagnosed and treated
early, with the exception of p. hypertensive, which can occur as a complication of a p. simple, and, if
not promptly treated, leads to death.

The causes are: bullous dystrophy (young subjects with characteristic facies), COPD, neoplasms, TB,
surgery (eg iatrogenic pneumothorax → central venous subclavian catheter), barotrauma, post-
traumatic.

39

The clinic is variable: chest pain, air hunger, dyspnoea, tachycardia, distension of the neck veins,
cyanosis (late manifestation), hypotension, but the most important are tracheal deviation towards the
opposite side to the lesion, unilateral absence of MV, plessic hyperphonesis, affected and loose
immobile hemitorace.
There are two types of pneumothorax: hypertensive and simple. We talk about hypertension because
it's the condition of
emergency. 4 phases: air in pleural cavity causes lung collapse → contralateral mediastinal shift →
reduction of venous return and contralateral lung compression → reduction of cardiac output and
obstructive shock.
Diagnostic diagnosis : the diagnosis is clinical (because the treatment must be started immediately,
before confirmation
instrumental!). Then confirm with RX (lately also thoracic ECO: sensitivity> to RX). Description
quantitative of the aerial flap:> or <of 2 cm
The therapy consists of pleural decompression through a large-caliber needle in the 2 intercostal
space along the hemiclaviculus of the affected hemitheater. The success of the procedure also
depends on the length of the needle used (5 cm → 100% success, 8 cm → 90%). This is followed by
the placement of a thoracic drainage (see figure: take a needle with a rubber tube over it, make the
incision on the chest, pull the tube out, pull the mandrel out.) The tube must be connected to
something, because if left free, it would let air in. The tube then attaches to a water valve.The air that
is in the pleural cavity exits during expiratory action and gets trapped in a tub of water, the bubbles
come out of a tube connected to the atmosphere;when the patient inhales air fishing until he is able
to negativize his endothoracic pressure; the air comes out but can not enter).
 Take home message:

- Chest pain: extremely common symptom, attributable to numerous clinical conditions.

- Need to exclude potentially fatal causes within the first 10 minutes.

- Implement therapeutic interventions aimed at stabilizing the critical patient through a standardized
approach.

Set up a focused and evidence-based procedure to complete the diagnosis of urgent but different
clinical situations.

Management of perioperative anemia

Once they were blood bags without thinking twice, today we know that these give problems both in the
short and long term.
Transfusion is a common practice in clinical but risky, so the new attitude is to rationalize its use.
So the "PBM: patient blood management" was born = "pay attention to the blood of the patient",
avoiding a too liberal transfusion. It has three pillars:
1) Erythropoiesis optimization

2) Minimization of blood loss

3) Treatment of postoperative anemia

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0

1) Erythropoiesis optimization : "Anemia" is defined as a situation in which Hb is <13 g / dl in

women <12 g / dl in humans. The problem of anemia derives from the fact that there is a mass of red
blood cells not sufficient for adequate tissue oxygenation.
 In the surgical population it is very frequent (20-40%). A normal exchange of O2 is maintained for Hb
from 6-10 g / dl. So in reality an anemia at 10-11 g / dl does not give big problems, but beyond there are
hypoxia and organ dysfunctions.

Anemia is associated with a higher mortality: even close to 70% for patients with Hb <8-7-6 g / dl (Htc
22-23%).
How a preoperative anemia is identified: a patient operand needs a control of the hemoglobin values and
of hematocrit dating back to at least 4 weeks. This is why patients do preoperative examinations
(screening). Four weeks is the time needed to react to any anemia present.
The motivations of preoperative
anemia: or advanced age
or chronic
diseases or nutrit
ional
deficits or blood
loss

or combinations of the previous ones

Martial Deficiency Anemia (It is the most widespread form of nutritional deficiency in the world).

Absolute deficit: reduction in iron deposits. It is typical of the general surgical patient (because he loses
blood or because he is traumatized).
Functional deficiency: the occurrence of iron-deficient erythropoiesis in the presence of normal or even
increased iron stores. The mechanism is a reduction in plasma iron transport. There is a reduction in the
activity of hepcidin-mediated transferrin (hepatic production hormone), which blocks the plasma
transport of iron after duodenal absorption and from macrophages and hepatocytes. We talk about "iron-
deficient" erythropoiesis.

The causes are: chronic inflammation in situations of increased demand for iron (hemoglobinopathies,
hemolytic anemia, use of EPO).
Typical of the patient CARDIOGIRURGICO.
 Treatment strategy :
Martial supplementation:
THE bodily iron stores are of
3-4 gr. The bioavailability of
the
iron 10-15% e

can further decline in the

presence of inflammation,
infection, chronic
disease Oral supplementation :
Optimal, proven efficacy. The
absorption rate is 2-16 mg /
day. It takes 3-6 months to
replace a loss of 1-2 grams of
storage iron. The presence of
malabsorption can frustrate an
oral martial therapy. Obviously
this therapy has side effects:
diarrhea, constipation,
abdominal pain.
For speed, effectiveness and minors
side effects are preferred
instead parenteral supplementation with the vials of iron (2 vials in 15 minutes). Because of the reactions

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1
allergic can be administered only at the hospital level. The caries allow the exposure of the dextran in the oral
cavity that determines the formation of self Ab and anaphylactic shock. Dextran is one of the iron delivery
systems and this is why these reactions can occur. The reactions are a memory of the past linked to dextran
preparations now replaced by safer preparations.

The iron deficiency is calculated with a formula: (16-Hb of the pkg in gr) x 225 / 62.5 = vials to balance
the reserves (9 of Hb →> 20 vials, 10 → 15-16 vials).

Also to solve the problem of perioperative anemia we use Erythropoietin (EPO), historically used in pcs
with IRC, in which the stimulus to the production of red blood cells is missing. At 5 days from the
administration there is a peak in reticulocytes produced at the medullary level. There is favorable
evidence in cardiac surgery and in orthopedics not in general surgery.
Doubts about their use in general surgery
or hypertension
o Thrombotic / ischemic events (surgical patients are already at risk of pulmonary
embolism, therefore increasing the circulating mass does not help).
o Stimulation of tumor growth

2) The second pillar is the minimization of blood loss :

• We know that where we use laparoscopy, robotic surgery, bleeding is minor (if one works
well, the patient does not bleed.) Cit Stabilini).
• The fact that the anesthesiologist is attentive to the blood volume of the PC minimizes the
risks (the lower the volume and the greater the risk that the patient is at risk of organ
dysfunction in case of hemorrhage, the greater the volume and the lower the
risks). Normothermic allows to reduce the loss of blood, in fact keeping the temperature at
the correct values helps the hemostasis.
• The intraoperative management of the blood means evaluating the extent of the losses, the
need for coagulation and other things that do not concern us.

There are ways for surgeons to lose less blood (antifibrinolytic drugs): Tranexamic acid, Aprotinin and
fibrin glue. The first two are direct procoagulants, while the fibrin glues are bonding systems that are
used where bleeding occurs.

In order to minimize losses, intraoperative recovery of the blood is performed. It is indicated when there
is a blood loss greater than 1000 ml, because below there is evidence that it is not cost-effective. Each
200 ml of saved cc correspond to about 1 unit of transfusion red blood cells. Its use leads to a reduction of
about 38% of transfusions in general surgery, 55% in orthopedic surgery. The risks associated with this
procedure, which do not make it universal are: the presence of cancer cells (the one that is recovered is
metastasized around), bacteria (dirty interventions), the need for coagulation factors lost in the process
(there is the risk of establishing coagulation deficits).

How it works: one of the surgeons inhales the blood during the operation that ends in a solution made of
heparin or anticoagulants that prevent the blood from coagulating and ends up in a reservoir; then the
blood is fired in a processor that washes it with saline, placed in a bag and then re-infused through a
previously cannulated vein.
Indication: serious blood loss required. Remember: coint-indications.
One of the major systems is acute normovolemic hemodilution: predeposit of whole blood of the
patient before surgery replaced with crystalloids that maintain stable volemia and the hematocrit at
20-30%.

Purpose: dilution of RBC and plasma components to minimize intraoperative

loss; availability of whole blood to be returned perioperatively.
Benefits: defined as modest; possible higher cost-effectiveness compared to intraoperative recovery. The
advantage is that it is the patient's blood, the problem is that it has never been proven that it can have a
real impact and utility (in the polyglobulic pc, eg obese, yes).

Management of post-operative anemia

Post-operative anemia should be managed to maintain tissue oxygenation with a target saturation> 95%.

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2

A bag of red blood cells provides the ability to transport and deliver O 2 in the presence of a volemia and
effective cardiac function:
↓ erythrocyte mass → compensatory mechanisms
↑ GC (FC and ejection fraction)
↑ Peripheral extraction
right shift of the curve O 2 Hb
↑ Plasma volume
What are clinical situations and the threshold to transfuse?
It depends on the clinical situation.
Administration of 1 bag of red blood cells raises the hematocrit by 2-3%, or 1 point of Hb.

Up to about 15 years ago the rule "10/30" (Hb / Ht) was in force, ie the transfusion was performed every
time Hb <10g / dl or Ht <30%.
Study dated 1999 from the New England Journal of Medicine that divided patients into two groups:
RESTRICTIVE group
418 transfusion patients if Hb <7g / dl - Hb between 7.0 and 9.0 g /
dl LIBERAL Group
420 transfusion patients if Hb <10g / dl - Hb between 10 and 12 g / dl
Results: 30-day mortality was:

• similar globally

• best restrictive group in pcs under 55

• best restrictive group in APACHE II <20

Current indications for blood transfusion :

1. Hb <8 g / dl and in any case the acute loss in otherwise healthy pcs with reduction of O2
and at least 2 of the following signs:
 • estimated loss> 15% of total volume (750 ml)
• Diastolic BP <60 mmHg
• Reduced systolic BP of 30 mmHg from baseline
• FC> 100 bpm
• oliguria
• Alterations consciousness
or
2. Hb <10 g / dl in critical pieces (angina, IMA, severe COPD)
or symptomatic anemia : (tachycardia, alterations of consciousness,
3. ischemia, etc).

Indications inconsistent: ↑ wound healing, ↑ subjective wellbeing Hb between 7 and 10 g / dl in

asymptomatic patient, availability of autologous blood.

The fresh blood taken in toto is centrifuged for 6 hours to separate the corpuscular part (stored at 1-6 ° C)
from the liquid part (plasma and PLT). The latter is further centrifuged to divide the plasma (frozen at -18
° -20 ° C) from the platelets and coagulation factors except VIII. The corpuscular part has a short-term
expiration, the plasma can be kept freezing for years and, once thawed at 4 ° C, the proteins are separated
from the cryoprecipitate.

Indications for plasma transfusion :

• treatment of multiple or specific deficiencies of coagulation factors with severe PT or aPTT

alterations
• specific abnormalities of coagulation factors in the presence of one of:

a. congenital deficiency of ATIII; prothrombin; Factors V, VII, IX, X and XI; protein C
and S; plasminogen or antiplasmin
b. CID, warfarin therapy; severe liver disease, massive transfusion, vitamin K
deficiency. Insubstantial indications: nutrition, volume expansion, hypoalbuminemia.

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3

Indications for transfusion of platelet concentrates:

• PLT <100,000 (checked in 24h) (as prophylaxis)

• PLT <50,000 (checked in 24h) with proven bleeding or in anticipation of invasive

procedure / surgery.
• sudden fall of platelet count and confirmed bleeding

• polytrasfused pc in the operating room (> 10sacks of red blood cells)

 • confirmed platelet dysfunction (15min bleeding time, altered platelet aggregation test)
• Insufficient indications: secondary platelet dysfunction, prophylaxis in thrombotic
thrombocytopenic purpura patients.

Procedures for requesting a blood bag:

• group determination (moment A)

• Type & screen (moment B): determination of ABO and Rh group and identification of Ab
against erythrocyte Ag. If the risk of leaks is <10% the blood is not crossed, if> 10% is crossed.

These two moments (A and B) must be separated.

Transfusion adverse events:

• Transmission of infections: bacterial, viral, protozoal (milestones: 1947 test for syphilis, 1980
discovery HIV test for blood virus, HCV infects about 10% of transfusions between the '70s and'
80s, 1996 SHOT Serious Hazard Of Transfusions, first scheme of haemovigilance).
Bacterial infections are the most frequent and represent the third leading cause of mortality
secondary to transfusion (> Serratia, Yersinia, S. Aureis, Coli and Enterobacter). The symptoms
are: fever, hypotension, tachycardia, possible shock. The measures that must be taken in these
situations are: blood cultures and targeted antibiotic therapy.
Special speech for Hepatitis: the current risk is 0.01%. This necessitates a series of virus screening
screens.
Other viruses: HIV (frequency decreasing since the 80s despite the increase in population

general. Current risk: 1-2 / 1000000), HTLV I and II (risk: 1/650000), CMV (it is not routinely
sought because ubiquity, greater risk for immunodepress).

• Immunological effects: GVHR (mortal in 90%, linked to the introduction of immunocompetent

lymphocytes in immunocompromised patients), immunomodulation (blood transfusion determines
deterioration of the immune response, susceptibility to infections, recurrence of neoplasms,
reactivation of viruses).
• Risk of massive transfusions: replacement with GR of the entire total circulating mass in 24
hours, or transfusion of> 10 pockets of red blood cells in a few hours, causes imbalances: acid-base,
hyperkalaemia, hypocalcemia, hemostasis, fluid overload.
• TRALI ("transfusion related acute lung injury"): estimated incidence of one case per 5000
transfusions. It is the main cause of transfusion death. It is due to antibodies or activated lipids of the
donor which, in sensitized patients, stimulate the release of cytokines by the GBs at the pulmonary
level with an increase in alveolar capillary permeability and fluid exudation. The symptoms are:
dyspnoea, cyanosis, hypotension, fever, pulmonary edema (dd with cardiogenic epa, liquid overload,
ARDS). Treatment: support.

• Haemolytic reactions: acute <24 h, late> 24 h. The most severe forms are related to the non
compatible AB0 transfusions (massive hemolysis). Mechanism: massive hemolysis with peptide
release → hypotension → renal damage → coagulation activation → DIC

Signs: pain, redness on the infused vein, precordialgia, oliguria, fever, hemoglobinemia,
hemoglobinuria.
 Treatment: immediate stop of the transfusion and sending to the CT of the whole infusion system
(agocannula, drip in parallel, bag, etc); forced hydration and diuresis, maintenance of vital
parameters (prognosis worse in the presence of DIC and hypotension).

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4

• Adverse Reactions to Errors: It's something that happens. These are adverse reactions due to
transfusion errors which account for 70% of all adverse events after transfusion. 20% due to AB0
incompatibility. The health ministry says: "the transfusion reaction from AB0 incompatibility can
represent a dramatic adverse event and is always due to error". There must be a culprit, there is no
miracle (see compatibility table).

The path and the weak points where errors can occur:

• Withdrawal for group determination

• request for blood components that accompanies the sample

• acceptance, registration, provision at the CT

• transfusion at SO, UTI ..

At the time of filling in the request:

• make sure of the identity (double surnames, foreign names, fugitives with false generality,
prostitutes with names of art)
• who makes the withdrawal must write the patient's data on the tube (department, surname,
name, date of withdrawal)
• sign the test tube.

Accompanying paper request: department, surname, name, d / n, type of blood component and quantity,
diagnosis, reason and degree of urgency, date of request.
In the transfusion center: verification of data correspondence (test tube and request), there must be 2
determinations of the patient group performed at different times from two successive samples (only in
election), checking the correspondence between the bag label and the request data.

In the ward, to avoid incompatible transfusions: verification of the patient's data to be transfused (on the
bag, on the copy of the request, on the folder, on the consent and on the group); compatibility check
between the groups of the bag and the patient's group.

In the patient's bed: double check doctor and nurse asking the patient's name by checking the bag.
Attentions to multiple urgency situations (transfuse two patients into two adjacent beds)
Record the successful transfusion in the clinical diary (bag n °, group, start and end time)
Notification of the transfusion to the CT (attached card)
Report any adverse events. Do not transfuse with fever because it could cover the symptoms of an
adverse frequency (unless it is moribund).

Transfusion substitutes:
- autotransfusion
- acute normovolemic hemodilution

- intraoperative recovery
- EPO

- iron supplementation
- synthetic substitutes of the red blood cells (they must be 100% saturable, capable of yielding O2,
purified, free of endotoxins or contaminants)
- perfluorocarbonates

- Hb stromafree

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Nahum 01-12-2016

Prevention of wound infection

We have already seen the classification of wounds in:

• Clean

• Clean-contaminated

• Contaminate-dirty

What other risk factors are there during surgery and what factors determine the occurrence of infections?
The duration of surgery : es appendicectomy in election can last at most half an hour, if it is conducted
cleanly, without opening the bowel or with very limited opening of the bowel (with exposure of the very
short mucosa, for seconds) there are no particular sources of pollution; nevertheless in some rare cases
one can see infection. In any case, the speed of the intervention limits the risk. If, on the other hand, an
operation lasts for example seven hours, the chances of an infection are multiple: from the air, from the
gloves, from nurses who change the shift, from the sheets that are still contaminated by an exogenous
flora present, especially if viscera are wet with washing liquids or if there is an exudation. So time is
always unfavorable: the intervention lasts longer,the more the chances of infection multiply and therefore
the infection is more frequently identified.

Another very important parameter in the frequency of the infection is connected to the health status of
the individual : there are scales that roughly identify the general conditions of the individual, for example
the ASA score (identified by the anesthetists, dates back to 1963). The pc is always classified according to
these parameters by the anesthetist in the preoperative visit, which, next to the examination exams,
evaluates the piece according to this scale:

ASA 1: the pc has no organic, physiological, biological, psychic disturbance (the patient
has normal general conditions, is fine, has a normalizing immune system, is in optimal nutrition
conditions, is autonomous, is oriented, moves all the limbs) .

ASA 2 : with mild systemic diseases that do not involve functional limitations, eg well-
controlled hypertension , uncomplicated diabetes mellitus, which has not caused serious vascular disease
or trophic alterations.

ASA 3 : patients with serious systemic diseases that have resulted in functional impairment, eg
diabetes mellitus with vascular complications, previous AMI, uncontrolled hypertension.
[For people living in the city the risk of heart attack is very low because usually an ambulance arrives
within a reasonable time, the patient is transferred to the emergency room; moreover, today we have the
aid of an ever present cardiac hemodynamics, the pc is subjected to disruption, if there is a coronary
obstruction, and the heart attack is not even produced. In order for the infarct to occur, it is necessary that
the lack of blood and oxygen to the myocardium is prolonged beyond a certain period of time. If the time
is lower and if the myocardium is revascularized within 45 minutes to 1 hour, the heart attack does not
even occur, but there has been only severe ischemia. We know the difference between the two
frameworks: infarction means cell necrosis, which are replaced by connective cells,being able to
determine a long-term sequelae of a ventricular aneurysm or septum. Today this risk is therefore very
reduced for those who live in the city, while people who live in the countryside have arrival times at the
center of reference much greater, moreover there are well-equipped regions, others less so.
Today many have a heart attack but less than the number that existed previously, qu
[Diabetes disappears in the post-operative period because in that context many hormones are produced
against the insular ones, which limit the function of the little insulin present; in addition, the glycemia has
important variations that are difficult to control, especially in the first hours after the operation, when
numerous catecholamines and cortisol are produced as a reaction to the stress: this leads to decreased
sensitivity

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insulin, therefore, often difficult to correct hyperglycemias are seen, and hyperglycemia is a factor that
constitutes a pabulum for germs that increase their multiplication rate, therefore where a bacterial charge
that would not be infecting into a normal subject becomes in the diabetic]
ASA 4 : Severe systemic disease that causes a constant life-threatening, eg congestive heart failure,
unstable angina (eg patients with 35% of ejection fraction and perforated gastric ulcer should be operated,
but is at greater risk, for problems with the circulation: there will be areas of the organism that receive
less blood and therefore less defenses).

ASA 5 : moribund piece believed to survive neither with nor without intervention, es aortic aneurysm in
rupture, cerebral haemorrhage with elevated intracranial pressure.

ASA 6 : PC with declared brain death, whose organs are taken for transplantation

E : needs emergency intervention

Another very important factor: the applied surgical technique : protection or favors infection?

In the different techniques the various operating times (= the various steps that must be taken in the
course of a surgical intervention) are always more or less the same; what changes the most is the attitude
of the surgeon in the execution of these times: there are those who are more scrupulous, some less, those
who are more attentive to the minutiae, who goes on more coarsely.

Pay attention to how the technique is applied:

• For example, it is necessary to avoid that there is a spillage of liquids in the peritoneal cavity, in
order to avoid spreading the infection. If the endoabdominal effusion occurs, it is necessary to
perform large washes, a simple and minimal suction is not sufficient because every cubic
centimeter of remaining liquid can contain numerous bacteria, constituting an important source of
pollution. By washing a lot the bacterial charge is diluted and therefore the infecting charge.

• Perform accurate hemostasis, remove necrotic and devascularized tissues , because they are foci
of potential infection.
• In traumatic injuries must remove foreign bodies.

• The wound should not be sutured if complete cleaning of the operative field is not possible ,
since the foreign bodies remaining inside it reduce by 10,000 times or more the minimum
bacterial load necessary to envelop an infection. Recently it has begun to follow advanced
medication techniques in which the wound, heavily polluted (or in case of strongly ischemic
organs or organs such as the pancreas which is sectioned continues to secrete pancreatic juice, or
in acute pancreatitis), is not sutured, but the abdomen is left open with advanced dressings and
subjected to a continuous suction treatment that removes the secretions; the wound must not be
closed, confined, because otherwise the chances of infection increase. Subsequently there are
techniques to close the abdomen that has been opened and in which there have been tissue
retractions.These techniques are now codified and applied in cases where the indication is very
specific and precise.

• Monofilament sutures are preferred over interwoven threads: the latter are unfavorable because
between a filament and the other there is a tiny space in which the germs can succeed in
proliferating and keeping alive and where the white blood cells can not enter. When the threads
become infected, the infection remains until they are removed, unless they are reabsorbable
threads (in this case you can slowly beat the infection, but within months, when the thread is
completely reabsorbed, and then the germsaranno remained unprotected). The monofilament
threads are made of new materials, eg polypropylene, they are unique, full filaments, they do not
 constitute pabulum for germs, which at most can stick to the surface thanks to glycocalyx, but no
more.This means that even where tension-free techniques are used (retinas in the hernia of the
gauntlets, or for the treatment of large laparoceles) prosthetic materials are used. Until a few
years there was not a prosthetic material that could be completely inert, and therefore easily
inserted. Now these materials have become extensively used. If it is infected they are

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problems, but much less than those caused by interwoven strands. Sometimes, however, you are
forced to remove the prosthetic material but often you can not overcome the infection.

• The best non-resorbable sutures used in contaminated wounds are made of polypropylene and
nylon.
• Also absorbable synthetic suture materials, such as polyglactin910, polyglycolic acid, the
glycolide / lactide copolymer, are protection against infection (Vycril).

What should the surgeon do?

• avoid leaving hematomas (therefore performing extremely accurate hemostasis), serum

collections (limiting their formation), dead spaces or residual cavities (the layers must be
glued together), since they all favor bacterial localization and growth and interfere with
migration and the action of the phagocytic cells.
• In traumatic wounds with additional foreign bodies, avoid getting stuck in their removal.

• Perform drainages and sutures as little as possible: drain when necessary with drains of
various types, but remove them immediately when they are no longer strictly necessary,
leaving them in place as little time as possible.

• In heavily contaminated wounds, the wound must be widely opened by opening skin and
subcutaneous tissue, covered flat with gauze after closing the band. Each febrile episode in
the post-operative patient must involve checking the surgical wound! Then it opens, it is
rinsed and the fever collapses. The wound can then be sutured once it is completely clean (to
verify it is sufficient observation, it is not necessary to do microbiological tests, the important
thing is that the subject's defenses are able to beat the residual infection after we have
reduced the infective charge).

Systemic factors

The resistance of the host organism is reduced in a number of conditions and systemic diseases including
leukemia, diabetes mellitus, uremia, prematurity, burns, trauma, advanced neoplasms, senescence,
obesity, malnutrition and numerous immunodeficiency diseases.

About Immunodeficiency, a pc with HIV can be regularly operated. He is immunodeficient to some

bacterial strains, to many viruses, but serum immunity suffers very little harm from the HIV virus, the PC
continues to produce antibodies directed against the most common germs. As a consequence these
subjects can be operated with a certain tranquility.

Social considerations : infection control is important; one must think that in a surgical ward the
incidence of infections must tend to zero, so we must continue to try to reduce this incidence more and to
minimize the risk. Epidemiological surveillance of what happens in the ward is important: if there is 50%
of the wards of the ward that has infection, it means that there is something wrong.
Today there is a continuous quality control, which is very important; in the face of modest local
epidemics that occur in a lane, you must take the proper precautions, understand that there is some error,
and then make surveillance.

We tend to think that if an infection does not develop in 5 ^ -6 ^ -7 ^ day it will not develop
anymore. This is true in many cases, but there are germs that develop slowly and can cause infection even
after a long time: it can be said that a PC operated is free of infections after 30 days from surgery, and not
to discharge, because more than half of the infections occur after discharge (even if today we try to
discharge the surgery as soon as possible, even when the risk of developing infection is actually still
high).

Important factors to prevent wound infection:

1 Preoperative shower, with antimicrobial soap (for the patient)

2 Tricotomy with depilator, not with razor, just before surgery
3 Control of aseptic technique errors by operating room staff
4 Preventive antibiotic therapy, when indicated: it can be especially useful in anticipation of a highly
contaminated intervention. It is not necessary in clean interventions (where there is no opening of hollow
viscera),

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probably not even in clean-contaminated ones. Some always do it, others try to be a little more selective,
and in endocrine surgery, where thyroidectomy is often done, antibiotic tp is almost never done, and even
if the thyroid is dissected there is no shedding of germs; same speech for a normal appendectomy, or even
cholecystectomy (for which the gallbladder should not be opened, if by mistake it opens, then
immediately at that moment the antibiotic is administered). But if I have a piece with intestinal
obstruction and safe sepsis inside the loops, a situation that involves a resection then a reasoned antibiotic
therapy that covers a wide range of pathogens becomes necessary.

5 Limitation to the use of suture and ligature threads (suture thread is in any case a foreign body)
6 Use of monofilament suture threads
7 Use of closed drainage rather than open drainage: drainage is a tube that comes out of the skin and is
connected to a collection bag, in which the secretions end, the blood and which prevents the reflux of
these and therefore also the germs. When the bag is removed and replaced with a clean one, it is
necessary to use sterile gloves.
8 Synthesis or meticulous suture of the skin
9 High oxygen tension in the intra and post operative period (avoid even small hypoxia situations because
it is pejorative)
10 Maintenance of normothermia during surgery: do not let the PC cool down, trying not to disperse its
heat or trying to heat it, because hypothermia involves many problems, such as metabolic acidosis,
oliguria.

For prevention it is preferable to use bactericidal rather than bacteriostatic antibiotics and to know the
sensitivity of germs present in the hospital environment.
Preventive antibiotic therapy must be limited , an antibiotic can not be given for 5 days because nothing
is prevented. Prevention is obtained by giving the right antibiotic at the right time, breaking down the
germs before they multiply excessively.

Today it has been seen that the use of bactericidal antibiotics in the perioperative period immediately
upon induction of anesthesia, and of epidemiologically tested antibiotics that are suitable for the
nosocomial population of that moment (because this population varies continuously), allows to do good
prevention in association with all measures aimed at limiting the risk of infection. In addition, antibiotic
therapy should not persist for a long time, it is not necessary to prolong it for 10 days, one administration
is sufficient. If an operation lasts several hours or is prolonged, the anesthetist will work to ensure that the
antibiotic is administered within the correct and necessary time limits. A therapy that lasts 5 days is not
prophylaxis, but at most 24 hours.
The
[The professor stopped at this point saying that the rest of the lesson on this topic we can do it
alone using the slides that are on aulaweb]

Nahum 01/12/2016

Lung tumors

They constitute one of the most important and widespread neoplastic diseases, with a high degree of
mortality, epidemiologically very frequent in the context of all the neoplastic pathologies treated.

Classification :
3. Primitive tumors : they are born from the anatomical elements of the lung
4. Secondary tumors : metastases, which reach the pulmonary capillary filter in general by
blood (organs with a thick capillary filter are frequent sites of metastases, as also typically the
liver). The lung is therefore a favorite target of many neoplasms from the point of view of
secondary injuries. [NB They are not haematogenous metastases, because haematogenous can
mean something that originates from the blood tissue! So better to say blood metastases]

Distinct tumors in:

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- benign : rare, are the group of adenomas (which are actually benign up to a certain point,
they are not so much)
 - Malignans : the overwhelming majority of primitive tumors; I'm like:
or epithelial (overwhelming majority)
or connect them (very few)

MALIGNI EPITELIAL Tumors

They are the most frequent. They come from the epithelium covering the bronchi, which is not always the
same, but in the large bronchi the epithelium flattens out, in the small ones it becomes cylindrical; for this
reason there are sub-variants between epithelial tumors with different appearance.

CARCINOMA BRONCOGENO

Neoplasia that originates from the epithelium of the bronchial mucosa.

Probably there are tumors of alveolar origin, but it is under discussion; they probably exist but are less
changeable, much rarer and do not depend on the same causes as those of more common importance.

Epidemiology

Autoptic incidence of the early 1900s: lung tumors were rare diseases (<1 new case / 100,000 inhabitants
/ year). If we go to the 90s in England there were already 90 new cases / 100,000 inhabitants / year. The
incidence today more or less is maintained at these levels.

As for sex, it is more common in male sex. In women, however, it has reached incidence of 18 new cases
/ 100,000 inhabitants / year, with a mortality that has exceeded that which occurs for k breast (this
because women have increasingly taken the male habits such as smoking) (Arab women do not become
ill with lung cancer if not with a negligible incidence, since they are not allowed to smoke)

The frequency of k is higher in the countries with the highest industrialization index (USA, UK, Northern
Europe). In the US it is among the most important health problems, with an incidence now quite similar
between men and women and peak incidence between 55 and 65 years.

Is the incidence increase real or apparent? Is it increased because more diagnoses are made, or because
the average survival age has increased? In reality this increase is real, it is not false: the incidence in
autoptic cases has increased; the frequency of the disease has increased in the specialized centers for the
diagnosis and therapy of bronchopulmonary diseases; the current incidence ratio between males and
females of 4: 1 corresponds to a real increase in neoplasia in the female sex (twenty years ago it was 8:
1).

The peak of incidence is between the fifth and the seventh decade of life.

At the time of the first diagnosis the distribution of the location of the disease is:

• in 30%, localized disease , ie confined, 5-year survival is 50% or higher. They are the only
curable people.
• in 30%, involvement of regional lymph nodes (= intrapulmonary lymph nodes, and of the
ipsilateral mediastinum), with a 5-year survival of 20%. These pieces are operated but with
modest survival.
• in 40%, already distant metastases , 5-year survival is <1 year; these pcs are not typically
operated.

STADIUM
 • Stage 1 and 2 correspond to the initial 30% which is treated with a certain% of success

• Stage 3 corresponds to the other 30%, with palliative interventions

• Stage 4 , the remaining 40%

The staging is preoperative when the patient has surgical indication, then there will be a "real"
postoperative staging.

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Mortality

86% die within 5 years, and most of these survive less than a year. However, the therapies have produced
some significant results: advances in treatment, but above all advances in early diagnosis, allow the
choice and prescription of the best potentially healing tp or palliative palliative optimized to the clinical
picture and to the physiopathological characteristics of the individual patient.

Today the diagnosis is earlier because every "speck" that is detected in the chest is subjected to much
more significant diagnostic investigations, and if you can biopsy (even if you can not do a prevention
such as for the breast or other superficial organs , since the study of the lung involves the execution of a
CT scan, which corresponds to 100 plates of the chest, not to mention the higher cost). However, the
ability to identify and classify pulmonary opacities is greatly increased and therefore the diagnosis is
however earlier and more patients are treated.

TNM

The tumor is evaluated according to these three descriptors.

The size of the tumor is important, but even more so are the values of the descriptor N, compared to the
diameter of the tumor itself. The intrinsic capacity of the tumor to give metastases is more important.
NB Stage IV: any T, any N, but with M1 (5-year survival <1%)

Pathological anatomy

Usually all is known about the tumor's histology, but the macroscopic aspect of the tumor is also very
important, but it is generally given less importance but instead the surgeon must know how to act and
intervene.

The neoplastic tissue is grayish white, compact, sometimes with necrotic striations, sometimes centrally
excavated (sometimes it becomes difficult the DD between tumor excavated and ascissualized and
primary pulmonary abscess), of hard consistency, in any case much higher than that of the pulmonary
parenchyma. healthy surrounding.
The location is very important, because according to the location we will have a different
symptomatology; in addition, the surgical strategy and prognosis also change.
There are 3 main variants:

• ilo-mediastinal , vegetative, inside a large bronchus; it can then cross the wall and infiltrate
the surrounding pulmonary parenchyma; it's at the hilum, so it's central
• middle parenchymal , "ball"; it is in the middle field of the lung, distant from both the hilum
and the pulmonary cortex
• peripheral invasive , in close proximity or already adherent to the chest wall; already born in
the suburbs, quickly overcomes the visceral pleura, attaches to the parietal pleura, generally
causing painful symptomatology
• intermediate forms

Prof Nahum,
12/02/16

Let's go back to the last lesson ... I told you about the macroscopic aspect of the tumor that is
important to know .. It is important the SEAT , we follow exposure according to the SEDE of
the tumor.
We begin to consider neoplasms that insist on ILO, CARCINOMA ILO-MEDIASTINICO we said that they
are born from a bronchial mucosa and then they overcome abundantly the bronchial wall to infiltrate the
surrounding tissues (rather infiltrate rather than invade) it is a central or para-central mass that is leaning
against the lobar bronchi or the main bronchus, cap inside the bronchus is a vegetation that stops the bronchus
at the end. The vegetation can be tiny or very developed to obstruct the lumen: the obstruction of the lumen is
a typical situation that determines a series of complications and overlapping panels downstream of the
obstruction itself, then obstructs the lumen and infiltrates the wall extensively, you can have different
behaviors but it is clear that theorigin which is the fundamental moment of neoplastic development happens in
the mucous field after then behaves in different ways: the vegetative quota can be higher than the infiltration
quota or the opposite or both are realized and

this is the most frequent occurrence. The tumor infiltrates the large central vessels, is there stuck in the lung
or in the para-hilar region, the ilo is a vascular and lymphatic peduncle so that in the lung they penetrate and

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out of the vessels, the airways penetrate the lung and lymphatic vessels emerge from the lung, the ilo
represents a petiole to which the lung adheres. During the evolution infiltrates the large central vessels,
the share of neoplastic infiltration extends outwards; there in the hilum there are the pulmonary arteries
and their dividing branches, the main bronchus or the lobar bronchi, the pulmonary veins. In the most
important and extensive phases of neoplastic invasion it extends to the pericardium, infiltrates
the esophagus by contiguity, the cavity veins upper and lower (there is not much distance between the
superior vena cava and the inferior vena cava: there is the atrium space of a few centimeters) and rises up
along the trachea inside the lymphatic collectors. The tumor then permeates the lymphatic ducts, the
collectors and then goes back along the lymphatic pathways, invades the lymph nodes that are stuck to
the trachea and the esophagus, the neoplasia develops into the lymph nodes and subsequently affects the
most external tissues such as the trachea and l The esophagus then tracheal infiltration and esophageal
infiltration can be mediated by lymph node metastasis. That is, metastasis occurs in the lymph node,the
lymph node is applied to the trachea and from there the metastases exceed the lymph node capsule and
thus affect the surrounding tissues such as the esophagus and trachea.

I told you that it is important the LOCALIZATION of these tumors because the symptoms that
characterize them are different and are determined precisely by the invasion of surrounding structures.
We will have TOSSE for the presence of the tumor in the center that invades the big bronchi, there
is EMOFTOE = blood emission through the sputum, cough, the sputum, the blow of phlegm (a
swallow does not make spring but many swallows spring. .) EMOTHYSIS is the large blood emission
that occurs when there is important vascular erosion typical in the tuberculous cavern, a large vein or a
large artery is broken, then we will have massive hemoptysis. The tumor develops in the large bronchus
and in the lobar bronchi, at the mouth of the lobar bronchi then the neoplastic tissue is CENTRAL is
soon to mix with the sputum that reaches the outside: we see it .

The radiological picture in front of a situation of this kind can be MINIMUM that is, we do not see this
tumor because it overlaps the mediastinal shadows, the mediastinum is loaded with organs so it is opaque
and behind it is the vertebral column therefore the traditional radiological application that does not see the
three-dimensional but is only two-dimensional overlaps the shadows to each other and therefore is not
able to discriminate the presence of the neoplasm when it is strictly hilar: the neoplasm flees to an antero-
posterior plate of the chest because the shadows overlap, you no longer know how to discern what is the
shadow on the slab determined by the vertebral column or by the bronchi or by the aorta that rises or from
the pulmonary:you see the neoplasia then when invades the lateral lung fields but in the center you can
not distinguish exactly the structures then a traditional chest radiology in the postero-anterior position (I
say postero-anterior because the X-ray source is placed behind the patient, yes it always indicates the
position in which the X-ray tube is placed) the X-ray tube is behind and the front plate and the rays
impress or not the plate. A screening mode based exclusively on the AP plate of the thorax is not very
effective, it detects little or nothing in these cases.the position in which the X-ray tube is placed is always
indicated) the X-ray tube is behind and the front plate and the rays impress or not the plate. A screening
mode based exclusively on the AP plate of the thorax is not very effective, it detects little or nothing in
these cases.the position in which the X-ray tube is placed is always indicated) the X-ray tube is behind
and the front plate and the rays impress or not the plate. A screening mode based exclusively on the AP
plate of the thorax is not very effective, it detects little or nothing in these cases.

I remember the case of a neoplasm of the lung in the hilar seat but in the left lower lobe and in front of
the left there is the cardiac silhouette, for months it remained hidden, when it came to our observation
then to us surgeons was already following the suspected diagnostic then he brought a tac then things
were completely different but for months they chased this neoplasm without identifying it because they
made a mistake to request a standard plate in the postero-anterior position without requiring the lateral-
lateral projection that reveals many pathological conditions that remain hidden in the slab AP. So if you
need a radiological examination it is necessary that the projection is twofold, also serves lateral-
lateral projection (the radiological source placed on the side and the plate is on the opposite side).
obviously even if it is in both projections you can see better with the CT but if you want to do screening
tests you can not do all the TC (radiation amount of the screening test and then you wonder if we are
authorized with screening tests to provide such a massive radiation dose and then there are production
costs: the screening would occupy a number of machines that instead are responsible for the diagnosis of
acute lesions usually) is not solved yet this problem in fact a screening test does not actually lead to
Europe while it is realized partly in Japan just with some CT scans but there the neoplasia is present with
high frequency because you know that the Japanese are heavy smokers so they have problems related to
cigarette consumption and consumption of hot tea, they are particularly affected by lung cancer and
tumors ofesophagus as well as in China, Afghanistan and all that band in Central Asia. You understand
that when you want a plate that is more suitable for your diagnostic needs, always start
with a radiological examination of the thorax in TWO PROJECTIONS: that is, the postero-
anterior and the lateral-lateral (in latero-

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lateral we see what has escaped us in the postero-anterior because there are no more shadows and
spine, sternum, lung, heart are dissociated) and the hilar neoplasm if it is of certain dimensions
substantially if it is SUPERIOR to 1 cm becomes visible, as a hilar lymphadenopathy can also occur
and become visible, even if it is still confined and small and invisible to the standard chest X-ray.
We were saying that the radiological picture can be minimal demonstrating only a slight
accentuation of the normal shadow profile which at least in the first phase can remain
undetected. You see this whitish mass these whitish striae that are adherent to the hilum, the
bronchus main and the structures do not see them anymore because they are occupied by a tumor
that infiltrates the structures, here you see again a patent vase, this lung is thickened, is not breathed
there is a cap then we will do a good lesson to see what happens when the bronchi they are plugged.

The other more peripheral topographic situation is constituted by the MEDIUM-POLMONARY

CARCINOMES that usually take on a ball-like appearance , are not starry nummular , rounded masses
with sometimes defined polycyclical limits sometimes not located in full pulmonary parenchyma of
nummular aspect that is as coins (nummus in Latin means coin). The pulmonary node may have a very small
diameter of 0.5-1 cm or so voluminous to occupy the whole hemisphere and I add with little symptoms, the
little one knows, the big one begins to understand that it can exist through symptoms that are not clear
because these are the least diagnosable tumors based on the symptoms. They have net margins, sometimes
polycyclic aspect, lardaceous cut surface, areas of necrosis occasionally central excavation as an abscess
because the central mass goes into necrosis, is not sufficiently vascularized and goes into necrosis, the
expansive growth continues at the periphery,the necrosis is replaced by pus so we have cancer and abscess es
here in this postoperative sample there is big cancer escaved where

pus is present (in this photo missing a measurement is an error, when photographing a sample taken
operationally you must always place a meter, a decimeter, something that indicates the size as a
geographical scale) we can not understand exactly the size anyway it's big because we see that the
surrounding parenchyma is reduced to very little.

PERIPHERAL CARCINOMA -> the invading bronchi are of small caliber, there is a long way from the
small-caliber bronchus to the trachea, the modest loss of blood from the neoplasm stops first, stops in the
bronchial area, it is not emitted, there is no it is the urge to cough, there is no pain . These tumors do not
bring pain because the lung as well as the intestine are not sensitive to painful stimuli, you can
manipulate the lung without the subject feeling anything, he realizes if you manipulate the parietal pleura,
muscles, bones, skin but not notices when you manipulate a pulmonary parenchyma, the liver, the spleen,
a kidney, the intestine. A preter-natural anus is an alternative way of stool emission (faeces are no longer
emitted through normal escretric ways but through a non-natural hole that has been practiced by the
surgeon for various reasons: this is done continuously and are created by the iliac aniices, on the splenic
flexure, on the transverse colon, on the hepatic flexure, on the cecum ..; the technique involves the
manipulation of a loop that is passed through an incision of the wall and is extroflexed to the outside, as
in some situations it is better to wait for the loop to take full coalescence with the surrounding structures
with the skin, the band , the muscles in such a way that when the patient goes out of body the feces come
out of the hole but do not return inside the abdomen because there are spaces, the cicatrization in 4-5
days makes sure that the feces do not fall within the abdomen when issued and then expects a littlebefore
doing the hole outside, when it's time you make a hole you take an electric scalpel and the patient does
not feel anything because the manipulation of the loops is free from pain and has not even tactile
sensitivity, the organism is made well does not put what you do not need what it takes for a loop to feel
pain and be sensitive to touch? Nature does not foresee that a loop is manipulated or that a lung is
manipulated and therefore does not insert in that place the nerve endings apt to feel pain. Pain is
something that allows the defense of one's own structures, a person is defended when he feels pain, if he
did not feel it could easily burn his hand. There are people who, as a genetic anomaly, have agenesis of
the nerve endings of the pain and they happen to them of everything and more, the pain is like a red light
that indicates an aversion but the loop and the lung should not be attacked by anyone.

These tumors grow and no one notices, grow without symptoms until at some point the growth is such
that the symptoms come out either by compression, or by atelectasis, for cough finally the sputum
reaches the major respiratory tract so these are tumors PARTICULARLY INSIDIOUS . An invasive
peripheral carcinoma that is born in the cortex of the lung quickly develops and quickly infiltrates the
pleura, it no longer infiltrates the central vessels, we are

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on the opposite side we are on the other side, so in the growth we meet visceral pleura, then parietal
pleura, it determines a pleural effusion that can be serous or hemorrhagic, rapidly invades the parietal
pleura that yes that hurts when it is offended! Then from the parietal pleura can still infiltrate the
muscular and bone structures (then we will see an example typical carcinoma of the lung apex that causes
pancoast syndrome) that explains the need to understand the TOPOGRAPHIC RELATIONSHIP
with the symptomatology because the symptomatology is completely variable , there are no common
symptoms, if you go to analyze there are no common symptoms between symptoms of tumors that arise
in the center and symptoms of tumors that arise in the periphery, there is no typical symptomatology of
lung cancer. The symptomatology depends on many factors.

What are the organs that infiltrate the pulmonary neoplasm? If it is a cortical peripheral part of the wall
it infiltrates the parietal pleura, then the endothoracic fascia then the ribs then the intercostal muscles and
gradually saying, but if the neoplasm arises on the medial mediastinal side of the lung it will infiltrate
the mediastinal organs and see trachea, vena cava , esophagus, pericardium, can reach the dorsal column
causing large erosions and destructions of the vertebral bodies and can reach the sympathetic
paravertebral ganglia, see how they differ from each other as a peripheral neoplasm but on the
mediastinal side quickly become a mediastinal neoplasia ie produces mediastinal symptoms that are part
of the mediastinal syndrome. Here is a photograph of a neoplasm born in the periphery, this knot cut in
the middle that shows the presence of completely peripheral carcinoma mantellar on the lung cortex.
Here you see well are small peripheral bronchi cut in half along their longitudinal axis, you stick inside
the scissors follow the light and open the bronchial tubes, see how in this bronco the neoplasia obstructs
the bronchus, here they have claimed that it indicates size, neoplasm exceeds 4-5cm in its largest
diameter.

Histologically, we have said the most frequent of all are EPITELIALS that derive from the epithelium
of the mucous membrane of bronchial lining or sometimes from the alveoli, from the alveolar cells; then
there are other lung tumors that originate from different tissues: MESOTELIOMI, LYMPHOMES and
STROMAL tumors (the latter are very rare, less rare the lymphomas, even less rare the mesotheliomas).
Surely though, if we have to talk about frequent tumors, we talk about epitheliomas not of the other types
that are actually less frequent.

This is a very important thing, among the tumors that develop from the epithelium the histotypes are
numerous, lung cancer indicates substantially the epithelioma with numerous variants, with numerous
histotypes and then there are extremely differentiated and totally undifferentiated aspects very atypical
that constitute a negative prognostic factor: the more the neoplasm is the same, because replication times
increase considerably, replication times decrease, the more the cells are undifferentiated, they lose the
original structure and are wild, atypical cells , monstrous, lymphomatous-like.

14 types classified by the WHO but it is an anatomic-pathological stuff but we must remember some aspects:
the flat, squamous appearance that is trivially observed in other types of locations such as esophagus, skin and
squamous epithelioma skin; epidermoid similar to epidermis coating cells, paved, flat; the corneal pearls for
production of keratin or para-keratin or keratin-like substances; next to an extremely differentiated type such
as this one classifies tumors completely undifferentiated to medium and large cells that are distinguished by
the size of the ANAPLASTIC cells therefore worse than the previous ones;

ADENOCARCINOMA that comes out of cells that are apparently glandular-like, which are part of the
epithelium of bronchial coating, are those that make mucus, the mucus is formed there by more or less
activated glandular cells and are distributed more peripherally not in the main bronchi but in the bronchi
a little more peripheral: therefore the adenocarcinoma we will find it above all in the middle-
parenchymal carcinomas, in the middle-parenchymal localization of the lung tumor while the paving
carcinomas will be typical to the hilum much more frequent to the hilus rather than in others lung
regions but this has its own logic. More peripherally still the bronchiolo-alveolar carcinoma or
pulmonary adenomatosis we will see is a somewhat strange thing with a frequency of less than 1% of
cases. Then we have another category of tumors completely different from those described so far that is
the

CARCINOMA A SMALL CELLS or MICROCITOMA is what we used to study with this

description A GRANI D'AVENA oat cell tumor was even thought to be an origin

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epidemic of this tumor because it was similar to an epidemic tumor typical of sheep for this reason the genesis
of this tumor has always remained a little bit unknown until it is understood that it has nothing to do with
tumble-cell tumor because it is a tumor of neuroendocrine origin. Then we talk about other types of rarer
tumors. So here it comes out an important thing from this description that tumors of origin origin of epithelial
origin exception cc have substantially a similar prognosis, the clinical trend is sufficiently predictable, there
are common biological areas, common symptoms, common progression, prognosis sufficiently common that
depends on the staging,the MICROCITOMS have a completely different biological trend so that as they are in
small cells it has been thought to distinguish the microcytomas from the other tumors with this simple
indication: NON-SMALL carcinomas

CELLS that is all the carcinomas except the NON SMALL CELL LUNG CANCER microcytoma
(NSCLC) all those epithelial tumors that do not have the characteristics of the small cell tumor,
instead SMALL CELL LUNG CANCER is a microcitome that has a completely different trend ,
whose prognosis and therapy are totally different from those of NSCLC are not comparable categories,
while the clinical performance of an NSCLC is compared continuously according to the staging of TNM
can be made comparisons, you can make therapeutic exchanges, programs .. with the microcitoma all
this it does not happen ie the two categories are very different and we will also see why and how. Here
we have already mentioned summary tables, appear benign tumors but benign tumors are not so much as
the carcinoid tumor, the mucoid-epidermoid, the adenoid-cystic these are still malignant however are
included in the diction of lung adenomas at least in one first phase, they are very rarely seen a few times
and have very special prognoses.I only remember seeing a cystic adenoid with a very complex
localization, fortunately infrequent at the level of the tracheal bifurcation, invaded the right bronchus, the
left main bronchus was just slightly affected by the neoplasm and had a very difficult therapeutic
program. Beyond those epithelial, mesothelial tumors and other tumors among which appears the
carcino-sarcoma which is a tumor mixed with aspects of carcinomatosis and with mesenchymal aspects,
is a terrible tumor kills very quickly but of rare observation. Then there is melanoma, lymphoma. The
important thing is NSCLC and SCLC. Let's see a little 'one by one these types of tumors.the left main
bronchus was barely affected by the neoplasm and had a very difficult therapeutic program. Beyond
those epithelial, mesothelial tumors and other tumors among which appears the carcino-sarcoma which is
a tumor mixed with aspects of carcinomatosis and with mesenchymal aspects, is a terrible tumor kills
very quickly but of rare observation. Then there is melanoma, lymphoma. The important thing is NSCLC
and SCLC. Let's see a little 'one by one these types of tumors.the left main bronchus was barely affected
by the neoplasm and had a very difficult therapeutic program. Beyond those epithelial, mesothelial
tumors and other tumors among which appears the carcino-sarcoma which is a tumor mixed with aspects
of carcinomatosis and with mesenchymal aspects, is a terrible tumor kills very quickly but of rare
observation. Then there is melanoma, lymphoma. The important thing is NSCLC and SCLC. Let's see a
little 'one by one these types of tumors.The important thing is NSCLC and SCLC. Let's see a little 'one
by one these types of tumors.The important thing is NSCLC and SCLC. Let's see a little 'one by one
these types of tumors.

PAVIMENTOSY CARCINOMA -> flat cells, arranged in cords, very differentiated aspects in
the epidermoid variety, spines and cornea pearls, this variety is usually located in ILARE , in 99% when
you see a hilar tumor I tell you now there are two possibilities separated by a wall of 50%: or are spider-
cellular spider-cell carcinomas epidermoidali or are microcitomi, based on the seat you can hypothesize a
histological type. Hilar seat, originated from large bronchi, can sometimes be located in the middle-
parenchymal site with a ball-like appearance but more rare, usually in the middle-parenchymal with ball
aspect you will see the adenocarcinoma appear. The pathogenesis is strongly linked to SMOKE , is a
common knowledge now universally recognized, then there are lung tumors certainly related to tobacco
smoke and others that have nothing to do with tobacco smoke see the bronchiole-alveolar that are
especially common in females and in relatively young age . The flat carcinoma goes
slowly SLOWLY GROWS , its doubling time is about 200 days, it leaves room, its metastases spread
substantially through the lymph, they prefer the LYMPHATIC VIA and are loco-regional, lobar, hilar,
mediastinal do not skip the lymph node stations , therefore with SLOW behavior and substantially
FORESEEABLE . There are also blood metastases, often present at the time of the first diagnosis in a
specific location: in the SURRENE , they can be ipsilateral or contralateral. This organ affinity is not
clear, it is not well known why it exists but it is common practice to request for this tumor the CT of the
thorax but with extension to the ADHDOME SUPERIORE to assess the presence of adrenal volume
increases that may correspond to metastasis. Metastases depose more frequently by lymphatic, hematic to
the adrenal glands that are the first metastatic site then obviously there are also other sites such as brain
and contralateral lung. In the ipsilateral lung these metastases occur no longer by blood but by
canalicular, ie the cells are emitted in exfoliation from the tumor and they end up in the bronchial way,
they move with the air currents and they end up in the bronchi, they stick to some other part in the lung
itself or they can end up in the contralateral lung . In the images taken from the Netter we see the typical
scaly epidermoid in his manifestation in situ and its invasive manifestation where it overcomes the basic
membrane. Here is the typical example schematized by the Netter of a scaly hilum tumor, probably born
here from a superior lobar bronchus, it grows in the surrounding areas, closes by compression or
infiltration the bronchi

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lobari and will determine a pneumonia called obstructive for primary bronchial obstruction and
peripheral atelectasis; here is here in a plate the hilar tumor in the center, this is a large tumor is not
covered by shadows because the center moves to the periphery and becomes extremely well
distinguishable in the standard plate of the chest.

ANAPLASTIC CARCINOMA -> also its seat is the large-cell lungs , frequent in smokers, are
large "ball" tumors , vegetating in the segmental bronchi, the process towards the hilum of the lung is
rather rapid, so there is metastasis both by lymphatic and by blood . Look in drawing drawn from the
Netter these huge clearly neoplastic polynuclear cells with large amounts of cytoplasm completely
without differentiation and formless anaplasty. Examples of distant metastases in para-tracheal lymph
nodes, here there is the station number 4 according to the numbering of the lymph node structures and
the station number 7 which is the inter-tracheo-bronchial which is actually a station that for its
placement in communication with the counter-lateral lymphatic system, that is, it is in common both on
the right and on the left, thus in fact carrying a metastatic situation on the other side.

ADENOCARCINOMA -> comes from the lining mucosa in the periphery , all in all
a pavement epithelium is a defense epithelium, has a modest function that is, it has no peculiar
functional characteristics; more peripherally more inward this structure becomes less usual, the glands
producing mucus appear and from these glands the so-called adenocarcinomas are born because they
have a GHIANDULAR ASPECT . Nucleus is peripherally pushed by abundant mucus present in the
cytoplasm. While once the frequency of epidermoidal floor carcinoma far exceeded the frequency of all
the other types, more recently the number of adenocarcinomas equaled the number of epidermoid
carcinomas and even exceeded it! The most recent statistics show an increase in adenocarcinoma
compared to epidermoidal carcinoma.

MIXED FORMS Adeno-squamous carcinoma -> variety that demonstrates the minor etiological
relationship with smoking habit, prevalent middle-parenchymal site; here the habits of the tumor
change because their onset is less frequently related to smoking and the modalities of metastasis change
ie the metastases are more frequent for VIA EMATICA , but they are not metastasized by the lymphatic
way but blood metastases are more frequent. Their development is faster, doubling time is higher than
that of epidermoid carcinomas. Here is an important sentence: the onset symptoms may be neurological
due to the presence of cerebra metastasesthe single or multiple ie the tumors become symptomatic for
neurological problems while they are asymptomatic in the lung. These types of tumors as well as
microcytomas can manifest themselves through their metastases especially in the brain and unfortunately
such examples we have all also on the conscience. I remember a case that is me stayed inside of a 36-
year-old mother of two children who had a speck in the right mid-pulmonary site, had an opacity but was
central; we asked ourselves what to do we thought to do a biopsy but it was difficult to do, it was difficult
to reach there in the middle and then it was 1 cm, we did the TC that did not say anything, the PET said
that there was an increased metabolization of glucose but in a structure of 1 cm. We wondered if it was a
tumor or not because it could also be an inflammatory lesion, we decided to wait what would happen in
time thinking if it is a malignant tumor then it will double. 6 months later it was not doubled, 1 year later
it was not doubled and it had not even increased in size it was still 1 cm.At 1 and a half years and still 2
years away. At 2 and a half years begins to increase in size and we are alarmed, while we are alarming
the woman has one Jacksonian crisis ie an epileptic seizure, then we do brain CT: it had 2 brain
metastases! The primary adenocarcinoma was 1 cm and a half. I do not tell you how it ended because it
is rather sad. This case was a direct experience, it is true that we could have operated it but who felt it to
operate it and smash the lung to take away a lower right lobe when there was no type of diagnostic safety
only based on a survey of the Credible PET to a certain extent that moved only after 2 and a half years,
has remained unchanged for a lot of time for which we thought we are riding is not a tumor and instead it
was. This girl had never smoked, she was Calabrese, mother of a family, attached to the family, as much
as possible traditional, absolutely void, non-alcoholic, non-smoker.Evidently what we know does not
cover all possible cases, something escapes us. Even without being anatomopathologists we see that the
macroscopic picture at a glance is completely different from squamous cell carcinoma, we see glandular
appearance, appearance

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typical papillary, stroma, secreting peripheral cells, monstrous nucleus. It is peripheral, mantle . Let's see the
Netter. It is not hilarious, it is peripheral: it may seem hilarious if you see it on a single plane but it is placed
far from the hilum, the shadow seems close to the hilum but it serves horizontal cut of the image to say where
it is placed and then we can evaluate the real distances, serves the third dimension, seems hilarious but not
hilar, is posterior peripheral does not affect the bronchial tree, it is asymptomatic is discovered by chance.

BRONCHIOLO-ALVEOLARE CARCINOMA -> fourth variety, less frequent than

adenocarcinoma, the identification is rare, this tumor is characterized by the lobar extension of the
disease means that it is born in a very peripheral alveolar point then spreads rapidly towards the
bronchioles seems almost a pneumonia, it occupies more and more space invading the surrounding
alveoli, almost with appearance of an inflammatory disease mimicking an inflammatory disease. The
cells have a cubic appearance and cover the alveoli whose septa are free. Rare tumor, poor prognosis. Do
they come from the alveoli? Some say yes, others say no or at least from the extremely peripheral
bronchioles that precede the alveoli. Multifocal genesis agrees all those who support derive from the
alveolar cells and those that support derives from the lining cells of the peripheral bronchioles. It
spreads quickly as if it were an inflammatory disease , even the surgery is poor results, I remember
them horrible those few times that we tried to operate them. Cells propagate from one alveolus to
another.

MICROCITOMA -> cells with poor cytoplasm and large nucleus, simulates lymphocyte that
is modestly small cell , is the smallest of the white blood cells has a nucleus and little cytoplasm, so the
cells of the microcytoma appear. Frequency in surgical cases 10% of all lung tumors; say that 45% is
epidermoidal, 45% adenocarcinoma and the remaining 10% microcitoma , then there are all the
variations we have said before but they are rare. Malignant, no longer treatable at the time of first
diagnosis: not in all cases, because if we are lucky enough to catch them at the beginning of their
progression surgery can even be curative ie completely eliminate the disease but the lucky cases are
sporadic. The other cases consist of cancer that are already inoperable when diagnosed. They have a
completely different biological behavior from tumors originating from the squamous epithelium, the cells
are frequently found in the blood vessels so there is a blood invasion and a blood metastasis, they are
seen at a younger age than the epidermoids. The epidermoid is a typical tumor of the elderly person seen
at 70 years,usually in the person who smokes who maintains a high risk of developing it for many years
even if he quits smoking because the induction of alterations in cell DNA has already been produced,
nicotine is the first of the alkylating agents that transform DNA. also the product of combustion but the
direct action of nicotine on the transformation of DNA has been demonstrated. The microcitome is linked
to the cigarette SMOKE, it appears in smokers just like the epidermoid.direct action of nicotine on DNA
transformation. The microcitome is linked to the cigarette SMOKE, it appears in smokers just like the
epidermoid.direct action of nicotine on DNA transformation. The microcitome is linked to the cigarette
SMOKE, it appears in smokers just like the epidermoid. Its favorite place is the ILO, so when we are
faced with a hilarious mass we always have to find a differential diagnosis at least between epidermoidal
carcinoma and microcitoma. Of course we can not be sure until we have had the tumor biopsied.
Metastasizes lympho-hematic to multiple organs. Histogenesis is no longer controversial today, when the
written these slides was controversial , today we are absolutely certain that it is a tumor of NEURO-
ENDOCRINE ORIGINS , it was hypothesized already since then but today it is certain. See how it
changes substantially the histological aspect compared to the pictures you have seen so far, as the
chromatin has the prevalence in these colors, cytoplasm practically absent because the nucleus is large.
We see in the Netter this large aloe tumor with metastases in the lower lobe of the same lung, metastasis
at the n ° 7 inter-tracheo-bronchial station, at the station 4 which is hilariously disposed between the
trachea and the pulmonary parenchyma and behind the vein azigos that collects blood from lumbar veins
and intercostal veins and throws into the superior vena cava a few inches above the outlet of the superior
vena cava in the heart and just above the emergence of the main bronchus. To be able to do the surgical
reclamation of this station we must always isolate the vein azigos, bind it peripherally,tying it centrally,
removing a segment and, together with the segment, removing the lymphatic stations that surround it and
compress it from the back. Then there are other WDNC tumors but they are extremely specialized things.

The fundamental distinction is SCLC and NSCLC , this is the international diction that all pneumologists
and thoracic surgeons understand . At the time of the first diagnosis SCLC, that is, the microcitome more
frequently exceeds the limits of resective surgery and is treated with chemo and radiotherapy, on the
contrary the NSCLC in most cases appears localized and we propose an attempt to cure both with

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resective surgery with both radiotherapy. What can certainly be done to large tumors is to try the route
of restaging, that is, the pre-surgical treatment with chemotherapy, if the tumor is sensitive it reduces its
size until it almost disappears and becomes surgically attackable (ie T3 becomes T1 then we can subject
the patient to surgery because his prognosis will be completely different).

ETIOLOGY -> there is no single aetiological factor, but concurrent multiple causal factors are likely to
be involved . The ascertained factors are certainly:

• the cigarette SMOKE (the first surgeon who put in relation the onset of cancer lung with
smoke smoked cigarette and he died of lung cancer we are talking about 1920)

Cigarette consumption in the world -> 400 million packages / year in 1945, 4 billion packages /
year in 1960, today we are a bit 'downhill in cigarette consumption and is good. The habit of
 smoking has spread to every social state involving women and young people. Mortality is
different according to the number of cigarettes smoked: the incidence of mortality in recent years
is 50 deaths per 100 thousand smokers of 20 cigarettes / day, 150 deaths per 100 thousand
smokers of> 20 cigarettes / day therefore mortality is closely related to the number of smoked
cigarettes. The action of: polycyclic aromatic hydrocarbons, nitrosamines (also causing tumors in
the esophagus), aromatic amines (bladder tumors) and radioactive compounds (come from
fertilizers used in the cultivation of tobacco plants) is carcinogenic.

• the POLLUTION ATMOSPHERIC important not only on the side of respiratory

insufficiency and bronchospasm but also produces an allergic reaction to a foreign body,
granulomatous reactions within the parenchyma, damage to cellular DNA; especially urban
policemen who monitor urban roads near tunnels have higher lung cancer incidence than other
traffic police. Some substances involved are chromium, beryllium, arsenic, nickel, asbestos and
fumes at high temperatures: they are seen above all in mines. Miners' carcinoma is certainly
induced by the presence of heavy metals mixed with the extracted rock and also by radiation
(those that pierce the white mountain are subject to considerable radioactive level, the
radioactivity in these tunnels is always detected).

• the parenchymal SCARS of previous pulmonary diseases , typically lung cancer occurs
on tuberculosis scars . That 1% of the tumors that were seen in the early 1900s were mainly
related to tumors that arose on tuberculous scars, cigarettes did not exist, cigars and pipe smoke
existed (pipe smoking is typically not inspired, it's easier than induces the production of local
tumors of the mouth, tongue, cheeks but less frequently induces lung cancer because the smoke
does not reach the bronchi and alveoli.

• CHRONIC BRONCHITIC subjects especially if they live in humid and misty

areas. Chronic irritation of ulcerated epithelia is a favoring factor (typical example:
gallbladder cancer that often arises in individuals suffering from gallbladder stones because
there is chronic irritation produced by gallbladder stones and remember that it is a tumor that
kills a lot quickly). Chronic inflammation agrees with the onset of neoplasms.

• FATT GENETICI obviously a genetic predisposition is necessary.

However, cigarette smoking remains the most important factor contributing to the onset of
pulmonary neoplasm.

VIE DIFFUSIONE of carcinoma -> by infiltration by contiguity of the surrounding organs and
structures, by lymphatic route, by blood dissemination, by intra-bronchial dissemination.
INFILTRATION FOR CONTIGUITY -> thoracic wall, mediastinum and diaphragm offer poor
resistance to neoplastic infiltration. The pericardium, which is a robust fibrous lamina, is opposed to
neoplastic infiltration and is unlikely to be infiltrated, it is opposed to the progression of the tumor
towards the heart. The tumor follows the wall of the major vessels, ie moves from the periphery towards
the center, continuing for example along the walls of the pulmonary veins and is at some point in front of
the pericardium which resists carcinomatous infiltration, but over time the tumor progresses along the
vascular wall until it reaches the atrium, or in the arterial side it progresses along the pulmonary artery up
to the
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bifurcation, it goes more and more in the mediastinal direction then there becomes a big problem
because as you do to interrupt surgically, to make vascular sutures on a region that is infiltrated by the
neoplasm. The vein wall loses consistency and becomes friable, if it breaks if you connect the veins
without realizing the tumor in them, the wall does not resist the pull of your hook. You can open the
pericardium, follow the infiltration of the veins to the atrium and then directly clamp the atrium, dissect
the veins and suture them (possible very severe hemorrhaging and the subsequent hemostasis is very
difficult). We have said that the pericardium is opposed. There may be Dysphagia from lung cancer, but
I saw it is a rather rare occurrence. The invasion of the chest wall by a tumor of thepulmonary apex (ie
neoplasm of the "sulcus superior") determines the S. of PANCOAST which is subsequent to lung cancer
in 90% of cases (in the remaining 10% of cases it is due to inflammatory lesions of the lung or non-
pulmonary tumors es neurinomas, Hodgkin ). The tumor originates in the postero-medial portion of the
pulmonary apex: it is a typical position, invades the parietal pleura, the endothoracic fascia, the C8-T1-
T2 nerve roots of the brachial plexus and therefore causes great pain in the shoulder (then it is already
extra-pulmonary = we are facing a T4). In this area there is the sympathetic paravertebral plexus -> for
which we have S. of CLAUDE-BERNARD-HORNER (sympathetic deficit symptoms: miosis, palpebral
ptosis, homolateral armpit anhydrosis.of POURFOUR-DU PETIT is caused by irritation of the
sympathetic plexus (has opposite symptoms compared to S.di claude-bernard and that is mydriasis,
exophthalmos and eyelid retraction, ipsilateral hyperhidrosis), I have seen it only once in life and that
time that I saw it was really resounding in a patient who had been operated on for a Pancoast tumor and
had presented vertebral erosions -> is the only case in which these tumors are operated because extra-
thoracic tumors are never operated. They assume a great aggression of the structure and ample
demolitions. This patient had been operated and following the scraping of the vertebrae that had been
invaded by the tumor -> he had manifested an inflammation and had this irritation alteration.It was very
difficult to understand what the diseased part was, whether it was ptotic or miotic on one side or a part of
the myocia because of an irritation syndrome. It was enough to ask which side you were operated on and
he had been operated on the right and right had the symptoms of the irritation syndrome of PORFOUR-
DU PETIT.

Prof. Camerini 1/12/16

Albe P. King in the
North

Esophageal foreign bodies

Materials or objects accidentally or intentionally swallowed

Very often in the emergency room.
- children between 6 months and 6 years.

- disorders of conscience, psychiatric problems, dementia, prisoners, alcoholics often relapses, drugs,
drugs
- structural deficits: poor vision, dental prostheses, pre-existing diseases of the esophagus.

- professional activities (upholsterer, tailor)

- illicit activities (drug dealer, smuggler)
Bones and fishpots, toys, coins, drugs, teeth, button batteries
80% of foreign bodies progress automatically. 1% needs intervention. When they are incarcerated
they give lacerations in 9% of the cases. If they are sharp in 12% of cases, they will give
perforation and require laparotomy.
They stop especially in the proximal esophagus, because here there is a weaker contraction,
where the striated muscle becomes smooth . When incarceration occurs in the thoracic esophagus
or below esophagus should be suspected underlying disease.
Possible underlying diseases:

• reflux esophagitis with stenosis

• engine disorders

• achalasia

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• diverticula

• eosinophilic esophagitis

• pos-operative stenosis

• Schatzki ring (up to 14%) smooth, thin, concentric rings, originating from the protrusion of
esophageal tissues. They can grow with age
 • hiatal hernia

• k

PENETRATION SYNDROME
Difficult swallowing up to dysphagia, pharyngoesophageal pain at the passage of substances,
pharyngeal globe, chest pain, nausea and vomiting, aphias and sialorrhea.

Triad of Chiari:

• hematemesis

• chest pain

• drooling

The site of symptoms does not correspond to the site of occlusion.

Complications:

• tearing (higher frequency)

• ulcer

• drilling

Prognosis of esophageal perforation (<1% of foreign bodies, mortality up to 22%)

• cause (mucosal perforation / direct esophageal wall or indirect perforation caused by

pressure necrosis if the body has been present for a long time)
• dimension

• site (in mediastinum greater probability of mediastinitis / fistulae)

• early recognition (removal in 1-3h)

Prognosis changes radically depending on the timing of the intervention.

Diagnosis
Biplanar Rx (2/3 not recognized with only the anterior-posterior plane).
Opaque objects (glass, metal, bones, dressings), radiolucent (food, fish bones, wood, aluminum) but form
difficult to investigate.
Not indicated Rx with barium because it does not allow endoscopy and risks the penetration of barium in
case of perforation.
TC is effective in 80-100% and is indicated.

Endoscopic management and surgery

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Haslinger's laryngoscope, Jackson's endoscope, flexible endoscope (preferable for lower risk of
perforation).
In 50% of cases the foreign bodies are extracted with biopsy forceps, in 17% with nets, in 15% with
alligator, in 8% pushed into the stomach.
Timing of endoscopic intervention.
If the foreign body is in place for more than 24 hours, the probability of risk is greater than 14 times
compared to a stay of less than 24 hours.
patients who have swallowed small bevel objects may be asymptomatic (except for batteries and
magnets) → monitoring.
Asymptomatic patients who have ingested drug packages are monitored, unless a package rupture or
obstruction is suspected.
Emergency EGDS (within 2-6h) in case of complete obstruction, sharp / pointed objects, batteries.
Emergency EGDS (within 24h) in case of other foreign bodies without complete obstruction.
Non-urgent EGDS (within 72h): foreign bodies also sharp / pointed, magnets, batteries and long or
wide objects in the stomach.
Surgical intervention (0.8%):

• when the foreign body can not be removed

• evident perforation

• hematemesis

- Closure of the perforation in two layers (the perforation is closed

normally)
- Closure with intercostal muscle flaps, pleura or pericardium (perforation of

long period when the flaps are no longer able to hold sutures)
Drainage T-tube (born in the biliary tract), left for 2 months. The esophagus-cutaneous fistula is created
and then closed

- Esophageal exclusion (cervical esophagostomy + stapling distal stump + decompressive gastrostomy

+ jejunostomy for nutrition)

- Partial esophagectomy
-Stent
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Reformation of esophageal continuity through:

• gastric tubulization (formation of 4 cm of new esophagus with gastric tissue)

• Ivor-Lewis esophagectomy (laparotomy + thoracotomy dx → intrathoracic

anastomosis). Better tumor visualization, better dissection of adjacent lymphatics
 • Gray-Turner esophagectomy (laparotomy and "blunt" dissection (without cutting
instruments), cervical anastomosis). Impossible mediastinal exploration and
lymphadenectomy but less invasive.

Diverticolo di Zenker

Sacciform extrfection of the posterior

esophageal wall through an area of
weakness between the inferior
constrictor muscle and the
cricopharyngeal (Killian's triangle),
caused by an action disorder of the
cricopharyngeal muscle. 2 / 100,000,
peak in the seventh and eighth
decade. Risk factors: age, male gender,
hiatal hernia, gastroesophageal reflux.
Symptoms; 80% dysphagia, 60% regurgitation, 20% suffocation, 20% cough, 20% globe sensation, 20%
weight loss, halitosis 20%.

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Associated diseases: pneumonia ab ingestis 40%, diseases of the upper GI 60% (K of diverticulum,
ulceration, perforation, malnutrition), reflux 40%, other comorbidity 50%. Asymptomatic diverticula up
to 2%.

Radiological diagnosis with barium or endoscopy (perforation risk).

Common distal esophagus problems.

Open surgery:

• cricopharyngeal myotomy (if 2-3cm above the hypopharyngeal muscles and 3-4cm
towards the cervical esophagus)
• cricopharyngeal myotomy and diverticulum suspension at the prevertebral fascia (if <3-4cm)

• cricopharyngeal myotomy and diverticulectomy (if> 4cm)

Start to do myotonia away from the diverticulum because the area is not inflamed and the muscular
and subcutaneous planes are well separable.
Endoscopic treatment with rigid endoscope (ENT surgery, currently the most widely used ):
diverticulum > 3cm, 10-15% not executable (ankylosis, cervical kyphosis), persistence of the cul de-
sac.
A linear stapler is used (sews a segment on both sides and cuts in half). The lateral walls of the
diverticulum are sutured with those of the esophagus and the posterior wall of the esophagus is cut so
that the esophageal and diverticular cavities become a single space.

Surgery complications: perforation, mediastinitis, recurrent laryngeal nerve injury

Endoscopy complications: mediastinitis more frequent than surgery (1% vs <0.1%), cervical emphysema
3%. Risk of perforation and injury of the major recurrent laryngeal nerve in surgery.

Endoscopy: operation and hospitalization of short duration, rapid return to food, few complications. 5%
interventions fail. Inadequate myotomy causes recurrence.

Dysphagia

Difficulty in swallowing due to neurological or structural causes. To be distinguished from the

globe: mass sensation in the throat not related to dysphagia or odynophagia and tending to
disappear with food intake.
Dysphagia is not a disease but a symptom of various etiological causes particularly badly affecting
quality of life.
Epidemiology: 14% of hospitalized for acute events. 45% of the pcs after head-neck
radiotherapy. Residents in nursing homes up to 30%. Stroke patients 60-90%.
Swallowing stages:

• oral preparatory phase (chewing, bolus formation, normal breathing through the nose)

• oral stage (bolus pushed back by the tongue and contraction of the buccal muscles, 1-1.5s
of duration Activation of the swallowing reflex Normal breathing with the nose)
• pharyngeal phase: starts when the bolus reaches the tonsils → pharyngeal reflex → pharyngeal
wall and back of the tongue move together and the pharyngeal muscles contract to push the bolus
down the pharynx.The vocal cords close to protect the airway. The upper esophageal sphincter
opens to let the bolus pass. Duration of the phase: 1s. Suspended breathing.

Protective mechanisms: elevation of the soft palate to avoid nasal regurgitation, the pharynx
moves up and forward to reduce the risk of suffocation. Epiglottis closes the larynx. In case the
bolus goes crosswise → tussive reflection.

• esophageal phase: the bolus is pushed into the esophagus by a propulsive wave of
contraction. Duration: 8-20s. Normal breathing.

Dysphagia of making oral preparations

Causes: K head-neck, stroke, parkinso, xerostomia.

Characters: lip closure disorder, chewing problems, increased duration of the phase.

Dysphagia of the oral phase

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Causes: stroke, progressive neurological diseases

Characters: difficulty in moving the bolus posteriorly, delay in propulsion of the bolus.

Dysphagia of the pharyngeal phase (together with the previous, ENT scope)
Causes: K head-neck, neurological disorders
Characters: nasal reflux from soft palate palsy, delayed activation of the pharyngeal reflex, tongue palsy
and pharyngeal muscles, lack of laryngeal elevation (risk of suffocation), inadequate opening of the
upper esophageal sphincter.

Dysphagia of the esophageal phase (gastroenterological field)

Causes: K, reflux.
Characters: structural abnormalities in the esophagus, abnormalities of motility or esophageal
contraction, inadequate opening of the lower esophageal sphincter.
 Symptoms
Body in
throat,

nasal
regurgitation,

cough →
disorder
pharyngeal
block
in the chest
→
disorder
oesophageal
Causes
Oropharyngeal dysphagia

• stroke

• SLA

• Parkinson

• Myasthenia gravis

• dementia

Esophageal dysphagia

• achalasia

• engine disorders

• stenosis
• rings

• GERD

• neoplasms

• diverticula

• foreign bodies

• iatrogenic

• infections

• caustic damage

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4
Signs of possible dysphagia

Recurrent pulmonary infections

Cough during / after swallowing
Rattling / bubbling voice
Nasal regurgitation
Chewing disorders
Weight loss and dehydration
 65

Oropharyngeal dysphagia

It presents with difficulty in the beginning of swallowing and immediate cough, suffocation, nasal
regurgitation. The most common causes are neuromuscular dysfunction . More severe symptoms
for liquid ingestion .
Neurological approach.
Aspiration : food or liquids below the level of the vocal cords in the airways. Modification of
the consistency of the diet. Possible enteral nutrition.
Signs and symptoms of aspiration : nasal secretions and tearing, reddened face, breath
modification, lung sounds, noisy breathing, attempts to free the throat manually, cough, bubbling / wet
voice. Possible silent suction .

Classification
On an etiological, clinical and gravity basis.
Penetration-Aspiration Scale (1- no suction material → 8- suction)
New Zeland Index for Multidisciplinary Evaluation of Swallowing (0- no alteration swallowing →
4-deep alterations)

history

Start, duration, progression, severity of symptoms, types of ingested foods that cause problems,
breeding factors. Examination of the oral cavity, dentition, oropharynx, nasolaryngoscopy, cranial nerve
examination (IX, X, XII), neck for lfn, masses, laryngeal cartilages.
Blood tests: Ca serum when nutrition is deficient or suspected metastasis; thyroid function (goof
dysphagia or neoplasm).

Instrumental examinations

• Bedside swallowing evaluation

• Videofluoroscopic examination (VSE): gold standard

• Endoscopic examination of swallowing with flexible tube (observed pharynx and larynx)

• Echo

• Chest X-ray

• Tc neck, chest, abdomen

• MRI only for neurological causes

VSE : tested with solid and liquid foods mixed with barium by Rx. Best choice for
dysphagia oropharyngeal. It also evaluates aspiration.
Clinical / Bedside swallowing evaluation: during the meal the patient is evaluated clinically by
subjecting different foods to him. If there is aspiration → VSE.

Head-neck tumors

Head and neck tumors can cause dysphagia, as their therapy can cause dysphagia or worsen the existing
one. The medical intervention is to safeguard the swallowing from the neoplasm.

Interventions

• surgical: total or partial removal of swallowing components

• radiant tp: salivation reduction, edema, teeth fall, pain

• chemiotp: nausea, vomiting, asthenia

• tracheotomy: alteration of air exchange, interferes with

swallowing. Structural alterations
• osteophytes of cervical arthritis

• Zenker's diverticulum

• tumors

• scars

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Oropharyngeal dysphagia treatment

Compensatory or restorative approaches. Diet modification or enteral nutrition with nasogastric tube,
gastrostomy, jejunostomy.
Physiotherapy, diet, support in the act of feeding.

Esophageal dysphagia
Difficulty in prophylaxis of the bolus in the esophagus. Structural or functional disorders.
Instrumental examinations
 • Chest X-ray

• barium test

• endoscopy

• manometry

• Tc neck, chest, abdomen

General causes of dysphagia

Related to age

Newborn: cleft lip, unilateral vocal cord paralysis, tracheo-esophageal fistula, esophageal atresia
Children: foreign bodies, malformations
Adults: reflux, hiatal hernia, achalasia, orb

Elderly: K, reflux stenosis, motility disorders associated with neurological disorders

Tied to trauma

Accidental and iatrogenic, penetrating, cranial nerves, cranial traumas

Related to infections

Pharyngitis, tonsillitis, epiglottitis

HSV, candida, CMV

Abscesses

Linked to inflammation

GERD

Collagenopatie (rheumatoid arthritis, scleroderma, Sjogren)

Related to disorders of esophageal motility

Achalasia, scleroderma, widespread esophageal spasm

Related to neoplasms

Oral cavity, pharynx, esophagus

Tumors of the cranial base
leukemia / lymphoma
Mediastinal lymphadenomegaly
Acute onset dysphagia in elderly smoking and / or drinkers who progresses rapidly to solids and
liquids is a sign of malignancy.

Related to neurological neoplasms

Stroke
Paralysis of the recurrent laryngeal nerve
Parkinson
Myasthenia gravis
SM
SLA

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iatrogenic

Esophagitis (tetracyclines, vitamin C, Fe stimulate acid production), broad-spectrum antibiotics and

chemotherapeutics may cause viral ulceration or fungal infections
Stevens-Johnson Sd

Anticholinergics, tricyclic antidepressants, Ca antagonists

Anti-hypertensive, antiemetics, diuretics, opioids
(xerostomia)

Linked to various causes

Presbiodisfagia
Foreign bodies
caustics
Tracheostomy

Prof Camerini, 02/12/2016

Caustic injuries

Caustic injuries began in the early 1900s to be very frequent for the diffusion of caustic soda with
various uses including house cleaning. The injuries are sometimes very dramatic and lead to perpetual
disability, which is why there has been a sensitization movement translated into legislation that
included both adequate labeling and reducing the concentrations of these substances on which the entity
of caustic lesions, and also a suitable packaging (if you have certain bottles you can not open if not
crushing, it all depends on these regulations for which children have less access and less easily can
swallow these substances accidentally) we can say that the incidence of this disease has been quite
reduced.
It has a large incidence in pediatric age (68% in less than 5 years); in adults the caustics
are intentionally hired or for suicidal purposes or in the case of psychiatric patients, there are also
some drugs that have a caustic action if ingested. After the ingestion of caustics a severe injury of the
esophagus is in 10% of cases and in 1-2% of cases it will then hesitate in stenosis. In 40% it is
involved the larynx and this has immediate therapeutic implications very important. In general the
ALCALINE substances are more involved. We report two types of foreign bodies: the pills of drugs that
take mainly the elderly and then other very dangerous foreign bodies are the batteries because they
contain sodium hydroxide and if kept inside the esophagus can free this caustic and cause perforation of
the esophagus , we talk about normal batteries because instead the lithium ones are also dangerous but
they determine a perforation not for the release of the caustic but for the electricity, they are still very
damaging too. The somewhat unresolved and debated issues that we will try to clarify during this chat
are:

• Whether it is useful or not to put the naso-gastric tube

• The risks or benefits of an early endoscopy

• The pharmacological ways we have to prevent strictures

• Timing and surgical techniques

Let's start with an introduction on substances: alkalis and acids. The substances are more damaging the
more we go to the extreme phases of the pH (eg a pH of 12 if we talk about an alkaline substance or 1-2 if
we talk about an acid). The acids most frequently involved are the PHOSPHORIC, OXALIC,
HYDROCHLORIC acid present in the batteries, in the industrial cleaning to clean the pools, to clean the
metal objects from rust and so on. The alkali: caustic soda is present in the products for household
cleaning eg oven.

The severity of the lesion obviously depends on the pH (the more serious the more the ph is extreme),
the concentration (but after that legislation we were talking about by law these substances can not have
more than 10% concentration while previously they could have even 50% and therefore the lesion was
much more serious), the viscosity , is very different that it is solid or liquid (if the caustic substance is
solid

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it will probably have a lesion of the first airways and that's it, if the substance is liquid it will be
circumferential and it will progress more distally), the duration of exposure and obviously the quantity
of ingested caustic.Are alkalis or acids more severe ? THE ALCALS !!! for 2 main reasons:

• first of all because they have a less sour odor and taste for which they are ingested in a
larger quantity
• they cause deeper lesions in the muscular esophagus because they give rise to this

phenomenon of NECROSI LIQUEFATTIVA for which the lesion penetrates very deeply
contrary to the acid which is very pungent and then immediately regurgitated and vomited, if it is
accidental the subject immediately stops the act of swallowing and then determines the phenomenon
of NECROSI COAGULATIVA (it means that a superficial extract is formed immediately which in
some way limits the penetration into depth of the damage). The acids give less esophageal lesions
but more gastric lesions because very early they determine a stenosis functional of the pylorus for
which the stomach is damaged much more by the acid than by the basic substance. The solids are
smaller quantities and cause more gold-pharyngeal and supra-glottic lesions while the liquid damage
is more extensive and above all extends to the entire circumference of the
esophagus. Some medications that can cause caustic lesions are quite common: ascorbic acid,
the Iron sulfate determine a lesion precisely due to their acidity, phenytoin (it's an alkali), iron
sulfate due to an osmolarity problem, fans for intracellular poisoning. Obviously, in order to
determine a caustic lesion, the drug must remain in the esophagus for a long time , so there must
be a concomitant esophageal disease that involves an alteration of the motility or for example if it
slips into a diverticulum.

The injury starts immediately, a few seconds later but we can divide 4 phases :

• 1 ° -2 ° day -> intense inflammation with erythema, edema, cell death and saponification or
eschar formation in case of acid necrosis
• 2 ° -4 ° day -> thrombosis of submucous vessels and a real necrosis and gangrene; bacteria
arrive and there is a bacterial contamination that can cause the presence of intramural
abscesses
• First week after the damage -> lymphocytes arrive, lymphocytic infiltration, angiogenesis and
fibroblasts arrive. There is therefore an inflammatory response with the development of
granulation tissue: this is the phase in which there is the highest risk of perforation (from the 4th
to the 7th day)
• In the next two weeks, neovascularization with collagen deposition and a

from the second week up to the third and then gradually the scar formation: this is the phase in
which the stenoses take over and can arrive.
Where do these injuries happen most if we talk about esophagus? Obviously in places where the
esophagus is narrower : therefore at the level of CRICO-FARINGEO, at the level of the middle
esophagus where there is the relationship with the arch of the aorta and the left bronchus, and
IMMEDIATELY ABOVE THE BURST OF LOWER ESOPHAGE. In the physiological
constrictions, the acid or the alkaline substance stagnates.
When studying any classification I always recommend to know who it is, in this case I have never
been able to understand who this classification is. It is a classification of endoscopists ,
in 3 GRADI , is that which show all the main works. It is very important because it has
implications extraordinary therapeutic and prognostic and correlates the endoscopic vision we have
with the depth of the lesion.

• 1st degree -> the lesion is only of the mucosa, we will see hyperemia and edema
 • 2nd degree -> the lesion crosses the entire wall of the bowel but not the peri-oesophageal
tissue, we will have vesicles, a somewhat hemorrhagic form, exudative with pseudomembrane
formation
• 3rd degree -> with involvement of the peri-oesophageal tissue, with obliteration of the lumen,
edema

massive, the formation of escaping or even the perforation of the bowel.

We are beginning to answer one of the first questions: whether or not it is appropriate to make
an endoscopy early -> many said no but the answer is clearly YES! It must be very early, it must be done by
the fourth day because then the risk of perforation increases: so it must be done first, second or maximum
third day. Endoscopy is important because it gives us all this information, that is, if it is a zero-grade
oophagitis or one we can keep the patient under observation for 12-24 hours and then send it home even as
soon as we have made it autonomous from the point of view of food; if it is grade 2 the situation is a bit 'more
complex, it must be kept in hospital, must be fed with liquids

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clear (some seconds, according to others not) and certainly will have to do in the third week a transit (not
with the barium because when we fear piercing never the barium, always with the Gastrografin ie the
water-soluble contrast agent!); if it's type 3 it's a big problem and now we'll try to develop a little bit of
reasoning. However, when we receive a patient who has had this injury we must try to understand what
he ingested from the anamnesis or the interview with relatives and then evaluate the pH, the
concentration of the harmful substances, if it was liquid or solid, the quantity ingested, the duration
exposure and we must begin to understand which is the most involved organ based on the data I have
told you about the frequency of injuries but also especially based on the patient's symptoms. Clearly we
will have more respiratory symptoms such as stridor and dyspnoea if the laryngeal area has been
affected more ; if the damage was more esophageal we will have dysphagia, odynophagia (we must
keep in mind that dysphagia is not necessarily linked to an anatomical-pathological lesion but in the first
hours after exposure to caustics it can also be linked to an alteration of the motility and are alterations
that last for weeks); if instead the damage is at the gastric level will have abdominal pain, vomiting,
hematemesis and the like. You must start orienting yourself on the history and symptoms to see which
organ is the most affected.

It is also important to try to exclude that the perforation of the bowel has already occurred (even if
it is not typical of the early hours), the symptoms would be completely different with crazy or
abdominal or retrosternal pain, there is a picture of peritonitis, the crackle on the neck due to
emphysema and blood tests show a very high leukocytosis and an important acidosis. In particular, if we
have 20,000 white, ph lower than 7.22 and a base excess of more than 12, we are facing a very serious
situation.

Let's see how the caustic lesion is dealt with immediately and then in the long term. Even if you do the
doctors who run in ambulances you will have to intervene even before being in hospital or if you will
help patients on the street and then in the prehospital you have to say two or three things that you need
to know:

• It can be beneficial to give milk or water to dilute the caustic and therefore to reduce
its aggressiveness but this NOW within 30 minutes because we have said that the
damage begins immediately in a few seconds;
• Do not EVER give BICARBONATE sodium because it develops CO2 and can
increase the risk of perforation, and even emetics because riespongono esophagus
damage therefore should not be administered. Do not give NEUTRALIZING
AGENTS to neutralize alkalinity or on the contrary acidity, produce exothermic
reactions therefore increase the temperature and can increase the risk of perforation as
well as the

GASTRIC LAVENDER ; none of these 4 things should be done, while diluting with
milk or water should be done when possible.
If you are on an ambulance the first thing to do is the evaluation of airway patency , we have seen that
40% of these patients have a larynx or high respiratory tract injury and therefore may need a gold
intubation. tracheal or an incision to ensure airway patency. If we are no longer on the ambulance or
where the event took place but we begin to be in a hospital, first we make a plate that sees very well if
there is air in the mediastinum, if there is a pneumothorax, pleural effusions, if there is free air if the
stomach or the intra-abdominal esophagus is punctured. As a radiological sign: here you see air in the
mediastine that spreads the mediastinum.

The nasogastric tube should be placed or not? Yes, it must be put !! If you can endoscopy , not
blindly. Therefore, the patient must make an endoscopy early within 24-48h and must put the tube
because of all these advantages: first if the injury was severe prevents the adherence between the opposite
walls of the mucosa that prevents them from accollino (in somehow serves as a stent and maintains the
lumen), then it is still a way to guarantee enteral nutrition to the patient (even if it should not be left too
long because to some extent it could facilitate the formation of strictures due to the fibrosis that can be
created around to it. I recommend you to know that traditional plates with Gastrografin have very low
diagnostic reliability over drilling, with very many false negatives so if you have any doubts you should
always make the CT with contrast agent orally. we had made a study when we did gastroplasty for
obesity and the typical complication doing all those sutures on the stomach could be the dehiscence of the
sutures and, we had 4 cases of dehiscence and in all 4 cases the traditional radiology had been negative,
so we concluded by saying that traditional radiology is even "misleading" because the fake negative
is misleading, so do TC with contrast medium for os (even when we look for thedehiscences on high
anastomoses, on esophagus-fasting anastomoses, esophageal anastomoses and so on). If we do not have
to exclude a perforation immediately or 2-3 days after ingestion if

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the lesion was grade 3 according to the classification we talked about, we have to do it to exclude the
stenosis.
This examination is strange, it is not very well known and frankly I do not know its real clinical
importance but it is an interesting examination -> that is a scintigraphy with the technetium that is
carried by sucralfate,the sucralfate goes very well in the burnt areas so to some extent it can affect the
clinical choices (it can also be used in peptic ulcers), I frankly have never used it but I have seen that
there are a few jobs on this. It can be useful as a screening because it is a very non-invasive test to rule
out an important injury and to then see how to manage the patient follow-up. If the injury was very
important then there is no doubt (eg if the patient is in intensive care), if instead it is not important I
have to decide whether to send him home or not, if you do a gastroscopy or not and this could be a
useful exam .

The CT has a very high sensitivity but a specificity not so high in determining the degree of the lesion and
therefore the necessity then of an immediate or late surgical intervention (it is 90% and 40%), and is
confirmed by this work: therefore TC has high sensitivity and low specificity. This is the reason why it is
necessary to take this examination: the esophagus-gastro-duodenum-scopia . In the early hours, as we have
already said. With a pediatric endoscope obviously smaller than we can and being very careful to insufflate
as little as possible. This gives us a lot of information about whether or not we should keep the patient in
intensive care, whether or not he or she has an operation, the potential complications, is an examination that
directs us so much but not

is a banality because until recently the idea of doing an esophagoscopy in a patient who ingested the
caustics would jump on the chair if you proposed it. There are obvious contraindications: for example if
there is an obvious perforation or haemodynamic instability or supraglottic lesions.

It is debated whether ECO-endoscopy can be useful , let's say that at present it has not shown
to condition the therapeutic choices in an exaggerated way but for sure it sees very well how
much muscle tissue has been destroyed: it is an information that gives us in a very precise way .

We did the diagnostics, now we see what drugs we can use because the problem is that to try to avoid the
stenosis in the third phase there were those who proposed the use of corticosteroids (it is reasonable to
think of giving them to reduce the formation of collagen, stenosis, scars): unfortunately as always when
trying to get to the bottom of a problem is the literature that goes in one verse in the other, the studies are
randomized on this 4 and of course they are in conflict with each other so in un primo tempo c'era questo
studio un po' più vecchio pubblicato sul NEJM che diceva che non serviva dare corticosteroidi subito
dopo, però poi sono arrivati almeno altri 2 studi un po' più recenti (del '96 e del 2014) in cui si dice che
se diamo del metil-prednisolone, con anche dell'antibiotico e la ranitidina si riduce la probabilità di
stenosi dal 30-45% al 10-15% quindi non mi sento di dire che non servono del tutto anche se non è così
chiara la questione. There are ongoing studies that say that mitomycin could be used with the same
meaning of reducing collagen deposition.

One of the cornerstones of therapy that has a bit 'wavered lately was the use of broad-spectrum antibiotics
because clearly the infection that occurs mainly in the second stage can increase inflammation and
therefore increase the likelihood of fibrosis and therefore of stenosis, for it is certainly not wrong to give
the pump inhibitors and to administer parenteral nutrition at least initially unless there is a naso-gastric
tube. Let's say that the steroids tend to be used, the mitomycin C I do not say it, the antibiotics we see
later if it's worth giving them or not because here too there are very contrasting studies.

The administration of antibiotics was a surgical myth but never demonstrated, let's say that now the
reason to give them is: if there is an infection at least suspicious, if we are currently administering
steroids or if we are doing the dilatation procedures -> these are the 3 situations in which the antibiotic
is certainly to be given and for the rest this surgical myth of the past is a little questioned.
From which specialists do we show the patient who took the caustics? Of course the endoscopist we
have already said, we will talk about surgery later, let's not forget the psychiatric visit even in children
(not for those of 2 years but for those between 2 and 5 years there are studies that show that even
children can having had some suicidal intentions).
The complications we have already practically all said: fibrosis, stenosis , perforation , fistula and the only
one that we have not yet talked about but that will have to keep the patient in follow-up A VITA is
the CARCINOMA SQUAMOSO because the its probability increases enormously after the ingestion of
caustics.

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We speak of squamous carcinoma, not adenocarcinoma. Even if there are reports of one year and two
years, the rule is 15-20 years later.
How do we behave for strictures? First of all, of course only when there are. How to make? Obviously
very smooth metallic probes were used , generally with a diameter of 1-2 french smaller than the
stenosis, then gradually with the technique of the dilators of Hegar, weekly sessions were increased to
increase the expansion diameter more and more. It is obvious that using a metal dilator that is
introduced causes in some way a force not only circumferential but also longitudinal that can contribute
to perforation because obviously when we do this maneuver what we fear is perforation. So, it seems
that the balloon dilation is safer , that is, the balloon is put inside and dilated and therefore this force
is lost in the longitudinal direction and the perforation is less probable.

These are two relatively modern things, since you can not find the road in a gullet destroyed by edema
and necrosis, you can leave non-absorbable sutures during the dilations that are left as guides and then
used for future dilation or even use a gastrostomy and make the backward dilations if at a certain
point it is no longer possible to pass and therefore it is necessary to use both trans-oral and trans-
gastrostomic access, leaving the guide wires.

There are criteria to understand that the stenosis will not be successful : if it occurs late, if it comes
from a stenosis of the 3rd type, if there are dense stenoses that during the maneuvers of dilatation are like
"crack", if they are longer than 5 cm and if after 9-12 months I have not yet come out -> fortunately this
happens in no more than 10% of the lesions, these are criteria to start the patient at surgery. A relatively
recent novelty is that of the self-expanding prostheses (they can be plastic, metal and so on) that in a
single procedure they put the thing in place. Naturally, the risk we have as always when we use them is
that of migration. Therefore not only dilatation but also endoprosthesis. Arriving at the surgery , we have
to divide it in 2 different situations : one is obviously the immediate surgery I underwent, after 3-4 days,
which is the one linked to the urgency; and the other surgical situation is where I have to deal with the
problem or with carcinoma or stenosis.
In the early one we have already said everything, we are obliged to intervene if we have signs of
peritonitis, of pneumo-peritoneum, of evident perforation or of the clinic or radiology, bleeding or
anyway a patient who is not well (ie patient with a big lesion of type 3 which continues to be in acidosis,
feverish, which meets a MOF). In this sense, we surgeons now have the good fortune to act with very
skilled anesthesiologists in intensive care who are aware of minimal hematochemical details if a patient is
doing badly or well and therefore sometimes we rely on them without having a crazy pneumo-peritoneum
but from signals in blood tests, in respiratory parameters. In these cases we are obliged to do the early
intervention which is a drama:what do I do when I have a broken laundry gullet? You have all the burnt
mediastinum, full of bacteria, you do not get there to take the stomach, tubulize it, do the anastomosis ..

It was said that you had to open all 2 cavities both the chest and the abdomen but it is a disastrous
intervention in terms of aggression, now I can do many of these things even with minimally invasive
access within certain limits. If I can, I must always do a gastrostomy and a jejunostomy to feed the
patient. Another concept that you have to transfer to this situation but to all the other dramatic situations
of the surgery (which are when we are obliged to intervene at 4 weeks in acute pancreatitis for the
infected necrosis, in the massive intestinal infarct) many times now it is since it is better not to do things
done at once but in SECOND LOOK ! Let's take the example of an intestinal infarction: I do not
immediately resemble all that seems to me gone into necrosis, I resecure what is definitely necrotic, then
you make the bogota bag -> you leave your stomach open, you put a urine bag, the is fixed to the band
and put the sterile drape you leave your belly open knowing that the next day we come back but in this
way we see how the lesion is delimited , so we do not unnecessarily take pieces of intestine in case of
intestinal infarction or esophagus in case of burn. So they are interventions that provide a second look. If
I have to make an exclusion of the esophagus it is cervicostomy it's a horrendous thing, that is, it pulls up
the gun-headed esophagus and everything that the patient swallows ends up on the left, does not go into
the mediastinum to worsen a mediastinite. It is engraved on the left, it takes the esophagus and it is pulled
out of it is a horror. The esophagus is completely destroyed, somehow I have to remove it, make a
cervicostomy and then the reconstruction must be done months later, not in this situation with the
unstable patient.

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The organ with which we replace the esophagus: the main one is the stomach because just one
anastomosis is the most vascularized one, it goes everywhere and surely it's an easier surgery but in this
case so many times we can not use the stomach if it is to have drunk especially the acid the stomach is
not usable; we have passed the acute phase with the criteria that we have said, we are in the late
phase and we have to replace the esophagus because of the stenoses we could not manage them
endoscopically or because we have to reconstruct the continuity of the alimentary canal months after the
dramatic event or because there it's a fistula or because there's a carcinoma or whatever; we must think
with which organ to replace the esophagus :this time it is no longer the stomach as for the tumor but
the COLON (it takes 3 anastomoses, it is a much more complex intervention, you can take the
transversus, the descendant or whatever, last choice is always the interposition of fasting because it does
not get to the colon fasting so you have to do some anastomoses vascular to make it arrive). You have to
remember not only what the substitute is but what the road is. If I have a mediastinum completely
destroyed by the burn, so often the first choice is the colon (doing all these techniques .. see in this case a
lower mesenteric is used) we must then make an anastomosis for the colon, a high anastomosis and a
short, 3 anastomosis, it's not a good deal. We had to make one this year which had already been gastro-
resected and had a tumor. THE'other thing you have to remember are the ways in which we pass the
colon : in the normal path that is in the posterior mediastinum however in the acute phase in which
everything is infected, full of bacteria obviously can not be done, but possibly also in the chronic phase
keep in mind that the esophagus can also be left there. I made the cervicostomia, it is rotting fibrous,
removing it may not be trivial, I know it is a possible cancer but I can also decide to leave it there and
with the colon pass either in the front mediastino or even in front of the breastbone (the latter not I've
never seen it done) so either back or ante-sternal.

These were the interventions I had already shown you last year -> when I replace the esophagus with the
stomach the two main ones are GRAY-TURNER and IVOR-LEWIS according to whether or not I open
the thoracic cavity; GRAY-TURNER I make gastric tubulization with the stomach, to make this tubule
with the stomach I have to respect a vessel, only one unfortunately, that is the right gastroepiploic because
all the others bind them ie the short vessels and the left gastric artery then all my tubule will be
vascularized by the right gastroepiploic (so you think that stress when you do this part that if you frigate
this jar you bleed this vase ends the surgery) after which we free everything and with a stapler cuts - more
or less 4 -5 cm we shoot here or in laparoscopy (we have been doing it for a long time in laparoscopy) and
we carry on this tubule that reaches up to the neck. And I can do this, especially theremoval of the
diseased part I can do in this case also blunt that is according to the intervention of Gray-turner that is
without opening the chest (the surgeon passes a little 'from below and then the whole carves and then
brings up the stomach) and is a technique obviously very criticized compared to IVOR-LEWIS because
you do not do the lymphadenectomy for the tumor but if we have to replace a esophagus because it has
had a caustic burn is fine not to open the chest we do not have to do lymphadenectomy apart from
nowfrom below and then the whole scilla and then brings on the stomach) and is a technique obviously
very criticized compared to IVOR-LEWIS because you do not do the lymphadenectomy for the tumor but
in the case where we have to replace a gullet because he had a burn to caustic is fine not open the chest
we do not have to do lymphadenectomy apart from that nowfrom below and then the whole scilla and
then brings on the stomach) and is a technique obviously very criticized compared to IVOR-LEWIS
because you do not do the lymphadenectomy for the tumor but in the case where we have to replace a
gullet because he had a burn to caustic is fine not open the chest we do not have to do lymphadenectomy
apart from that now almost everything we do in laparoscopy (here at San Martino we started with the
abdominal part in video and with the chest still open, and then now we do both parts in minimally
invasive that is the abdominal part that I do and both the part chest that makes a thoracic surgeon).

Nahum, 12/5/16

Growth and diffusion pathways of pulmonary tumors

The routes of diffusion of the lung apical tumor include:

1) INFILTRATION FOR CONTIGUITY

Among the structures that are invaded by the tumor we have the chest wall , the mediastinum and
the diaphragm that offer little resistance to infiltration and destruction of their tissue constituents by
the neoplasm (ribs, mm., Intercostal, diaphragm, after passing the band endothoracic), while
the pericardium , which is composed of a strong fibrous lamina, is opposed, with some effectiveness,
to the spread of the neoplasm that expands in its interior for propagation along the adventitial lining of
the pulmonary vessels; Lung cancer rarely infiltrates the esophagus , which can instead be compressed
by satellite adenopathies.

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In case the tumor originates from the pulmonary apex (postero-medial portion of the lung apex, at the top
of the cost-vertebral shower → Pancoast tumor) rapidly invades the parietal pleura, the endothoracic
fascia and the C8-T1 nerve roots and T2 of the brachial plexus [pain in the neck, shoulder, upper limb ,
amyotrophy of the hand ], the sympatico cervico-thoracic [ S. of Claude-Bernard-Horne r: miosis,
enophthalmos, ptosis palpebral, anhydrosis of the hemifaccia ipsilateral and of the axilla , for paralysis
of the sympathetic plexus, while the S. of Pourfour-Du Petit : mydriasis, exophthalmos, eyelid retraction,
hyperhidrosis of the homolateral hemiface and of the axilla, which can sometimes precede paralysis,
indicates the state of irritation of the sympathetic plexus ]. On the other hand, if the tumor originates
from the postero-lateral portion of the apex or from the anterior portion of the upper lobe, symptoms
related to the infiltration of the succlaval vessels and the phrenic nerve prevail (sob, diaphragm
superelevation and diaphragmatic paralysis) without the characteristic pains appearing irradiated to the
arm of t. of Pancoast: these apex tumors are therefore not considered t. of Pancoast in the strict sense.

2) VIA LYMPHATIC

The affected lymph nodes (lfn) will vary according to the site of the neoplasm and then to the
drainage area where it was formed.
For tumors of the upper territory → LFN PARATRACHEALI OMOLATERALI.
For tumors of the lower territory → INTERTRACHEOBRONCHIAL LFN (station
7) For tumors of the intermediate territory → both previous stations
From the lfn of station n 7 then the lymph node metastases propagate to the contralateral mediastinal
lymph nodes. However, the lymph from a tumor lobe will first pass through the LFN LOBARI and
ILARI STATIONS ( numbered intrapleural lymphs , for staging purposes, from 1 to 14) → STAGE
N1 then for MEDIASTINAL LFN ( extrapleural lfn from 1-9) → STAGE N2 from here to LFN
MEDITATINIAN CONTROLATERALS or LFN OVERLOADED ( extrathoracic lymph )
→ STAGE N3

All the lymph node stations have been classified according to a standard nomenclature and a rigid
anatomical-topographical scheme: these elements allow an objective prognostic evaluation and the
execution of a complete lymphadenectomy at the time of the surgical intervention. An N2 tumor,
which has infiltrated the mediastinal lymph, has an unfavorable prognosis and is not treated
surgically because it offers a low chance of survival, while N0 or N1 tumors have practically the
same prognosis, favorable.
NB ! The infiltration of the station 5 and 6 left causes damage of n. left inferior laryngeal ( bitonal
voice for paralysis of the vocal chord of the left ). Much more rare the involvement of n. right
laryngeal. In the case of bilateral lesion of the inferior laryngeal nerve, often of iatrogenic etiology, we
have a paralysis of the 2/3 post of the vocal cords (medium-low tones) that will result alleged towards
the center with reduction / abolition of the respiratory space.
To evaluate the involvement of the lymph node stations, use:
- Tc with mdc (gold standard) evaluating the diameter of the lfn (cut-off = 15 mm), while
being a rough data allows a rapid evaluation.
However, studies performed on thousands of both autopsy and surgical samples have allowed us to
establish that metastases may be present in lfn. small and absent instead in lfn. increased in volume, in
the lymphatic progression towards the major lymph-venous anastomoses, some successive lymph node
stations (skip) can be "skipped", the presence of lymphatic diffusion of the neoplasia is difficult to
determine with the macroscopic or clinical-instrumental intraoperative observation. The metastatic
invasion of a

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the lymph node may be "intranodal" and the capsule may remain intact (the lymph appears to be mobile
with the surrounding tissues), but later infiltration becomes "extranodal". The capsule is overcome and
the lymph node is fixed to the surrounding tissues, in turn infiltrated extranodal metastases effectively
exclude patients from the surgical indication, while tumors with intranodal metastasis to the lymph.
ipsilateral mediastinal can still be operated with radical intent [importance of pretoracotomy
mediastinoscopy]

- MEDIASTINOSCOPY performed on indication of CT when the presence of paratracheal or pretracheal

lymphadenopathies of d ≥1.5 cm is demonstrated, for the histological confirmation of metastases in them
(N2) in the pre-operative phase. It is performed by carving the jugle and detaching the tissues to the front of
the trachea, inserting a rigid tube equipped with optics and which allows the introduction of various
instruments. The risk is to damage the internal jugular and succlavie that are placed at the front of the
mediastinoscope sliding plane.

3) HEMATIC DISSEMINATION

BRAIN, SURRENES, BONE, CONTROLATERAL LUNG, liver etc. It is therefore appropriate to

perform a CT scan and a bone / PET scintigraphy for a complete clinical staging
Sometimes metastasis constitutes and determines the first sign of the disease, when the tumor is
still confined in the parenchymal field (eg: brain metastasis with genesis of epileptic seizures).
4) INTRABRONCIAL DISSEMINATION (endoluminal, rare)

There are two ways:

- vegetative neoplasm fragments are detached and are pushed, with the coughing, in other bronchi or
in the bronchial system of the contralateral lung where they are implanted peripherally
-the neoplastic cells follow the peribronchial lymphatic collectors where, by block or inversion of
flow, they take root in the bronchial wall of another lobe.

Finally, a particular diffusion path, typical of the bronchiolo-alveolar carcinoma, is

the INTRABRONCIAL DISSEMINATION where the cells reproduce very quickly, "by gradually "
papering " , by contiguity, the surface of the surrounding alveoli. The clinical-radiological finding
simulates, at least initially, a subacute inflammatory lesion.

SYMPTOMATOLOGY

In 5-15% of cases, lung cancer is asymptomatic (the diagnostic hypothesis arises from a routine
standard chest X-ray)
Clinical signs, when present, depend on:
-from the volume of the lesion (local expansion)
- from growth in regional lymph nodes (lymphatic dissemination)
- from the site of the neoplasia (invasion or obstruction of thoracic structures)
- from the stage of evolution

- from neoplastic growth in metastasis sites (blood dissemination)

There are also symptoms:

LOCALS
The first local signs are often made up of the generic ones of " bronchial irritation " [dry, persistent,
even nocturnal cough ; modest escreato, feverish . L ' hemoptysis is the most important sign] . When
the tumor comes to block a bronch of a certain caliber, the air trapped is slowly reabsorbed and this
causes pulmonary atelectasis ("parenchymal carnation") with stasis and the establishment of infectious
processes that together outline the clinical picture of " obstructive pneumonia" [area of
atelectasis after obstruction, fever, sputum - productive cough, infectious state, dyspnea] up to
eventual abscess.

The pain indicates the infiltration of the visceral pleura. Its appearance is therefore subordinated to the
tumor site, early or late, if the tumor is cortical or deep
The pleural infiltration (both visceral and parietal) determines the appearance of effusion which is
firstly citrine - reactive - and which in the continuation becomes hemorrhagic. Sometimes the two
pleuses adhere early: in this case the neoplasia quickly infiltrates the thoracic wall. It will be quinid of
extreme importance in a patient with t. pulmonary fluid in which it appears to be going to examine the
liquid

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pleural to search for the presence of any malign cells (if positive, the patient is classified as STADIUM
IV with a worsening of the prognosis regardless of the presence or absence of other symptoms).
If the tumor has a hilar or paraxial site or is located peripherally, but on the mediastinal side of the lung,
infiltrates the mediastinum and the organs contained in it with the genesis of a mediastinal syndrome
characterized by: superimposition of the hemidiaphragm - diaphragmatic paralysis - by infiltration of
the phrenic nerve, two-tone voice, hoarseness - paralysis of the homolateral vocal cord - by infiltration
of the recurrent nerve, dysphagia by invasion of the esophagus, edema of the neck and supraclavicular
regions by infiltration and obstruction of the superior vena cava or anonymous veins, dyspnea, signs of
tracheal obstruction by infiltration of the trachea mediated by metastatic neoplastic localization in the
paratracheal lymph nodes. NB ! Pulmonary collapse is different from atelectasis . The first is a
condition, partly reversible, which occurs when the pressure gradient between pleural and external space
decreases or clears, but the air is free to pass through the bronchial tree, albeit in smaller quantities,
actually preventing collapse of the alveolar walls; the second one is an irreversible condition (once the
"carnation" has occurred) which prevents the passage of air and therefore the alveolar walls collapse.)

GENERAL (weight loss, anorexia, fatigue, anemia with pallor, nausea, asthenia,
insomnia) S.PARANEOPLASTICHE
As such, some symptomatic pictures are defined as having no direct reference to lung cancer. For some
of them, the pathogenesis is recognized as due to the secretion of peptidergic substances by the same
neoplastic cells.
Paraneoplastic syndromes can be collected in five broad categories
1. endocrine disorders : S. of Cushing-like , with hypercalcemia and
gynecomastia; water retention for production and release of adiuretin (ADH-like)

2. neuromuscular disorders : peripheral neuropathies, cortico-cerebellar

degeneration, myelopathy, pseudoasthenic myopathy of Lambert-Eaton
3. anomalies of connective tissues : arthralgia; hypertrophy of the periosteum of the
distal phalanges ("drumstick" fingers + clock nail) → S. by Pierre Marie - Bamberger
4. skin and muscle changes : acanthosis nigricans, dermatomyositis
5. blood and vascular changes : fibrinolytic purpura; endocarditis; myelopriva anemia
(medullary infiltration)
S. from EXTRATORACIC REPETITIONS

Symptoms of distant repetitions are more often cerebral (outbreak symptoms), hepatic or adrenal
(inappetence, weight loss, asthenia). They can precede the diagnosis in 10-15% of cases.

NAHUM 6/12/16
Diagnosis of pulmonary tumors (II) and therapy

The stratigraphic examination (Genoese pride for his invention by Alessandro Vallebona)
has now been replaced by:
CT that has revolutionized imaging diagnostics in the thoraco-pulmonary area. Each area
of different density , with a resolution index of a few millimeters, can be identified and studied,
evaluating the morphological aspect, the location and the relationships.

It then became the essential and specific investigation for the study of pulmonary and
mediastinal lymph node stations, of which it is able to detect any volumetric increase.
By convention, every lymph node is considered pathological whose major Ø is = 1.5 cm and whose minor
Ø is
> of cm 1. However, even the CT is unable to establish whether the increase in volume is due to
inflammation or neoplasm, so the information we obtain is the increase in volume of the lymph nodes
and their site. This is essential for subsequent biopsies, which instead are able to determine the nature of
the lesion and are implemented in various ways:
- biopsy sampling in mediastinoscopy,

- transbronchial or transtracheal agobiopsy,

- TC-guided transparietal biopsy.
A biopsy on a lung is, however, a complicated procedure even with an eco / tc guide and
pneumothorax complications are possible first of all.

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(When a diagnosis is missing even after all the available exams theoretically it would be possible to
proceed with an exploratory thoracotomy.In reality they DO NOT MAKE MORE, limiting their use to
emergency situations because the risks of complications and uselessness of the intervention do not
justify the implementation.)

When thoracic CT is performed, the upper segments of the abdomen are always inclined, as often I
can find metastases in various locations, for example hepatic or adrenal (50% cases of adrenal
metastases at diagnosis).

Brain CT and bone scintigraphy follow for preoperative staging. In some cases even bone marrow
samples can be evaluated for bone marrow involvement.
We are considering the possibility of replacing CT with MRI in the future, as it is less harmful and with
excellent quality of discrimination of the lesion and its diffusion in the organism. Above all, its ability to
highlight infiltration at the pericardium, myocardium, large ilari vessels and to define the progression of
Pancoast tumors towards the supraclavicular fossa is very good. For now, however, the problems of
resonance, that is the high cost and long timings, remain.

In the moment in which the suspicion of lung cancer is present, the achievement of the following
objectives must be pursued:
- diagnostic confirmation of the lesion;

- its anatomo-histopathological characterization;

- stage of diffusion - staging - of the disease;

- possibility of surgical exeresis with intent of radicality vs. possibility of palliation.

Recent experience indicates that with the association of the two most recent diagnostic imaging, spiral
CT and PET (Positron Emission Tomography), a diagnostic sensitivity of 78% and a specificity of 95%
are obtained, while individually considered , the spiral CT shows a sensitivity of 66% and a specificity of
67%, PET a sensitivity of 77% and a specificity of 84%.
Another survey of fundamental importance is BRONCOSCOPY, already known before the biopsy . This
examination explores the bronchial tree up to the segmental and subsegmentary branches, allowing also the
execution of DIRECT biopsies on the tumor (if it protrudes in the lumen) or in TRANSBRACIAL or
TRANSTRACHEAL mode by inserting a needle into the bronchoscope and pricking under CT topographical
guide. With this technique it is possible to collect material both from the tumor and from the LN that seem
interested.

In patients in whom direct endobronchial diagnostic maneuvers are impossible or dangerous, the
diagnosis can in many cases be reached by the research of the neoplastic cells present in the
bronchial secretion. These are obtained in bronchoscopy by brushing or bronchoalveolar lavage.

Cytology can also be done on the sputum, it has a low diagnostic efficacy but as it is not very invasive and
inexpensive it can be an examination that can also be used as SCREENING. The gold standard would be the
CT but we can not undergo all radiation for screening, it would be more inductive than a preventive tumor!

In the presence of a peripheral pulmonary node, near the thoracic wall and NOT endoscopically
attainable, the lesion of the lesion can be obtained reaching the outbreak with a fine needle introduced
from the outside ( FNAB = Fine Needle Aspiration Biopsy), through the thoracic wall , under TC
control. Complications of the method are pneumothorax and hemothorax (and hemoftoe), usually mild
and without dangerous sequelae.

Special techniques less used are:

• PRESCALENIC BIOPSY → pre-clasical LNs are reached, extracted and

examined. Now of rare and limited use.
• MEDIASTINOSCOPIA → incision to the jugulo, getting space in front of the trachea I go down
with the instrument. Remote metastases effectively exclude patients from the surgical indication,
while tumors with intranodal metastases to the ipsilateral mediastinal LNs can still be operated
with radical intent. The mediastinoscopy finds its main indication in all patients with lung cancer
in which the CT shows the presence of ilari and mediastinal LNs of ø> or = 1.5 cm, because it
allows me to directly evaluate the operability or otherwise of the disease .

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While it is very used, above all to operate more than for diagnosis, it is the VIDEO-ASSISTED
TORACOSCOPY (VATS) → the chest opens with a small incision in the antero-lateral area and
the instrument is inserted , the patient is asleep and the lungs to have room for maneuver. It is performed
diagnostically when it has not arrived at certainty previously because the lesion is difficult to achieve
with other investigations. Very often in these cases the resection of the mass is associated in the same
intervention: we practice modest thoracotomic incision + trocars and videos that allow you to insert
instruments in a small space and to see well on screen what you are doing.

Markers are not specific:

NSE (Neuron specific enolase), is a cytoplasmic glycolytic enzyme and is a tumor marker used in
staging, identifying relapses and monitoring the therapy of patients with small cell lung cancer.
It may also be present in medullary thyroid tumors, neuroblastoma and neuroendocrine
tumors. Moreover, small non-stable increases over time may also be present in non-neoplastic lung
diseases!

OPERABILITY CRITERIA

Pts with stages I, II, IIIa are operable with intent of radicality, while IIIb or IV are not subject to
resolutive surgical treatment. To this rule are the exception of the Pancoast T. which are basically
operable even beyond the IIIa (maybe you remove a pair of ribs or a vertebra but you can manage to
operate them). These operability criteria are very important because to date the only treatment considered
as a solution is surgery, the other therapies are palliative. However it is not only the stage that is taken
into consideration but also the quantity of parenchyma to be removed and the state of the remaining
lung, the age, the comorbidities of the patient. The two features that most interest are the respiratory
and the cardiovascular because removing a part or a whole lung sets the stage for a pulmonary
hypertension of the remaining circle, which with a lower vascular bed has to bear the same blood V as
before! The heart can react well and adapt to this situation, or the overload may be excessive, resulting in
a heart failure or atrial fibrillation or other arrhythmia.

So I have an idea of the "tolerability" of the intervention for the PC, I perform tests: spirometry, EGA,
DLCO, ergometric tests, perfusion scintigraphy (then compared with spirometry to predict how much
functioning parenchyma will remain at the PC after surgery!). The residual FEV1 is calculated after
intervention by multiplying the current FEV1 by the lung perfusion%.
They are UNABLE:

→ pz with serious INSUFF. CHRONIC RESTRICTIVE AND / OR OBSTRUCTIVE RESPIRATORY,

→ pz with critical reduction of the capillary bed and the respiratory surface,
→ pz with FEV1 <0.80L (absolute risk), while in the cases with FEV1 <1.20L the risk is relative,

→ cardiopathic or recently infarcted,

→ pz with cirrhosis, IR or insuff. pancreatic,

→ pcs> 70y! I can operate them but do not remove a whole lung.
Pcs with palsy paralysis, limited invasion of the chest wall or Pancoast tumor are operable. THERAPY

In NSCLC the tp is the radical surgical exeresis, therefore LOBECTOMIA,

BILOBECTOMIA OR PNEUMONOMETOMIA (the latter always involves various
complications).
After having resected each bronco it will obviously need to be sutured and if I have resected too close to
the neoplasm, I will still have tumor on the edges: the suture will be badly worn or will not take place →
dehiscence! Therefore it is important to evaluate the exeresis margins under microscopy to confirm that
they have made a correct resection. TRACHEOBRONCOPLASTICA → you can make more limited
resections by suturing the bronchi together! A very used technique is that of SLEEVE LOBECTOMY:
let's say that the tumor is located at the origin of the upper lobar bronchus and involves the main
bronchus, it would be necessary to perform a pneumonectomy. By performing a sleeve resection of the
lobar bronchus comprising a portion of the main bronchus and performing a terminal-terminal bronchial
anastomosis, it is possible to limit theintervention to a lobectomy and obtain the same result from the
oncological point of view of a pneumonectomy!
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8

The problem of sutures between bronchi

is that they are not very vascularized
because already this basic tissue
receives just enough spraying. So when
you make a plastic of this type you have
to try to save the vessels as much as
possible to decrease the risk of
dehiscence, which in this case would
then lead to the development of
EMPIEMA PLEURICO (air enters from
the dehiscence of the bronchus into the
pleural cavity, is a ' air that carries
germs from the oral cavity!). Another
type of bronchial plastic is the

WEDGE LOBECTOMY, in which I do not take a sleeve like a sleeve but a wedge of bronco!
A particular variant of the
SLEEVE is the SLEEVE
CARINAL
LOBECTOMY, in which
the origins of the main
bronchi are affected by the
trachea → I remove the
intersection and re-locks
the two main bronchi to
the stump of the trachea!
 In case of an anonymous
trunk or superior vena cava
invasion it is possible to
draw a BYPASS with
goretex stent (PTFE)
between subclavian or

jugular and right auricle of the heart.

Prof. Camerini -
12/6/16

Boerhaave syndrome, Mallory-Weiss lesions, achalasia

S. of Boerhaave → syndrome caused by barotrauma of the esophagus. They also call

it SPONTANEOUS PERFORATION but in reality it is NOT! In fact, it is linked to a well-defined cause:
an abnormal increase in pressure in the esophagus with loss of release of the upper esophageal sphincter.

Other causes of barotrauma of the esophagus:

• violent abdominal or thoracic trauma (although it is easier to develop diaphragmatic hernia

than rupture of the esophagus)
• epileptic seizures

• childbirth

• defecation.

S. of boerhaave is rare, about 3 cases per 100,000 a year. It happens that subjects under sedatives,
under general anesthesia, under the influence of alcohol or other substances, vomit massively but the
upper esophageal sphincter is not released correctly → increases P in the esophagus → BREAK.

In 80% of cases the lesion is a longitudinal tear of a few cm on the postero-lateral esophageal wall, 2-
6cm above the diaphragm. This area is considered more fragile for two reasons: more relaxed and thin
muscle fibers and place of entry of vessels and nerves, x which is a locus minoris resistentiae.

Possible causes of perforation of the esophagus:

 • barotrauma (15%)

• instruments (endoscopy, dilation, tube, biopsies)

•K

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• caustic substances

• foreign bodies

• surgery (myotomy, vagotomy, fundoplication, pneumonectomy)

• infections.

DIAGNOSIS

Not easy because they are nonspecific symptoms: dyspnea, tachypnea, tachycardia (I think of a
pulmonary picture!), Fever and we get to the signs of shock. They address more the diagnosis of
atrocious low epigastric / thoracic pain, accentuated by swallowing and vomiting. A correct initial
diagnosis is made only in 33% of cases, instead it is important to be quick to intervene within 24 hours
→ after a day doubles mortality, especially for contamination of the pleural cavity with septic insult →
SIRS is established (systemic state of inflammation) and you can get to MOF (multiorgan failure).
At the physical examination there are signs of MEDIASTINITE FULMINANTE with subcutaneous
cervical emphysema in 85% of cases and of MASSIVE PLEURAL VERSUS with
insuff. Respiratory, hypovolaemia and shock.

Only in 60% of cases is the classical triad (TRIADE DI MACKLER) with vomiting, significant chest
pain and subcutaneous emphysema.
The differential diagnosis is with various respiratory diseases, the IMA, the aortic dissection,
the perforated ulcer, the acute pancreatitis, the incarcerated paraesophageal hernia ...
At the chest X-ray we see:

➔ pleural effusion sn (90%)

➔ enlarged medistine

➔ cervical or mediastinal free air

➔ hydropneumothorax sn

➔ pulmonary infiltrates.
Another exam to use is the TC with MDOS per os.

THERAPY
First evaluate the vital parameters and stabilize the patient then ABC.
Then fluids and antibiotics are administered (serious problem of thoracic contamination),
then it goes to the surgery with cleaning of the pleural cavity and closing of the lesion.

A drainage is placed for any residual septic material and if necessary the lungs are reexposed.

the pc is then kept under control, providing nutritional and ventilatory support.

• One of the most used surgical techniques is that of EXCLUSION and DIVERSION of the
esophagus: the lumen is closed with a stapler at the lesion level (in time the passage is opened
again by itself!) And it is joined at the neck level → CERVICOSTOMY . Also since the lesion
is almost always distal I can also associate a fundoplicatio of the stomach that covers the points
and keeps them more "protected" and reduces the possibility of reflux.

• Another procedure involves the use of endoprosthesis in the esophagus, but requires a more
extensive and complicated cleaning of the pleural cavity.
• Drainage with T-tube: this T-tube is endoscopically positioned which has the longest part that
protrudes and drains outside through the fistula while the shorter one, inserted in the lumen,
guides the repair of the tissue. It is removed later.
• Esophagectomy.

MALLORY-WEISS → esophageal lesion, single or multiple, which takes advantage in the mucosa,
maximum in submucosa, for 15-20mm in length and 2-3mm deep in the gastro-esophageal junction or on
the proximal gastric mucosa. In this case the increase of P in the esophagus is related to the lack of
relaxation of the lower esophageal sphincter in case of very frequent vomiting or coughing.
It occurs mostly in alcoholic male patients, suffering from hiatal hernia or who frequently use
NSAIDs. It represents 15% of the high digestive hemorrhages and the main symptoms are:
hematemesis or melena, pain, hypotension. Mortality mostly in alcoholic / cirrhotic pcs.

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In 90% cases it ceases to bleed spontaneously. PPI therapy is associated with (if appropriate) fresh
blood / plasma transfusions / platelets, especially in patients with coagulation abnormalities.
If medical therapy is insufficient: ENDOSCOPY → epinephrine (vasoconstringe), coagulation, clipping.
Almost never ANGIOGRAPHY.

ACALASIA → alteration of motility with esophageal sphincter inf (LES) which is not released when it
should (may or may not be associated with LES hypertonus). Subsequently also the esophageal
peristalsis becomes ineffective. It is called FUNCTIONAL STYOSIS.
Incidence is 1 / 100,000 per year and especially between 30 and 60y. The diagnosis is almost always
late, patients spend years to be taken for crazy.
The etiology is linked to autoimmune inflammatory processes (primitive or secondary to viral diseases
or Chagas-like infections) or neurodegenerative disorders that alter Auerbach's plexus cells, which
would inhibit motility through the production of VIP and NO. Lacking this inhibition on cholinergic
fibers → MOTOR DYSFUNCTION.
Symptoms include:

• dysphagia for solids and liquids (98%)

• regurgitation (78%)

• respiratory complications (cough, night suction)

• chest pain

• epigastric burning

• weight loss.

Chest pain is supported by multiple conditions related to the disease → organ distension, tertiary
contractions, esophagitis. The latter develops for STASI of food and its fermentation which decreases
pH, therefore mucous damage and easier settlement of the candida! In addition there are subjects who
have failed to release the LES but not its hypertonic, so they can also present reflux! In this condition,
poor clearness does not counteract reflux → further contribution to mucosal damage.
DIAGNOSIS
The first step is to exclude pseudoachalasia or anatomical lesions through instrumental investigations
(for pseudoachalasia we mean those conditions that mimic the pathology but are secondary to other, such
as K cardias, K esophagus, Chagas disease, pseudo-transplant after surgery, x eg a fundoplication
according to Nissen too tight.I suspect a pseudo especially when the pc is elderly, dysphagia developed
rapidly and / or there was an important weight loss).
The investigations that are made are:

• baritone meal → highlights dilated and tortuous esophagus, aperistalsis or narrowly distal
esophagus with bird's beak or mouse tail. In addition, 250ml of liquid is emptied in at least 5
minutes. It would be such a typical picture that it does not require anything else! Then in reality
there is always also the manometry. There are 4 radiological classes identified on the basis of
the organ morphology (4 is sigmoid).
• Manometry → sees elevated P of the LES (not always but very often!), Its incomplete
relaxation (always), aperistalsi. In the case of hypertonic waves over 40mmHg of P it is
called vigorous achalasia. At HRM (high-resolution manometry) 3 stages are
distinguished: Type 1 FAILURE contractions and no pressurization with swallowing,

Type 2 PRESSURIZATION of the whole esophagus>

30mmHg, Type 3 contractions SPASTICHE and
PREMIATURES with high P.
• Endoscopy and biopsy → definitive between achalasia and pseudoachalasia.

• Ecoendoscopy → can be used to evaluate thickening of the muscular tunic.

The differential diagnosis as well as with the pseudo is also with other motility disorders such as
diffuse esophageal spasm, scleroderma and presbyophage.

THERAPY → pharmacological, botox, dilatation, surgery.

• Pharmacology includes the use of nitrates to increase NO and guanosine monophosphate,

which promote muscle release; of Ca ++ antagonists; of sildenafil, which blocks the

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fosfodiesterasi5. The data are BEFORE the meal because decreasing the P of the LES improves
the symptoms in 53-83% of the cases. Problem: COLLATERAL EFFECTS !!! Hypotension and
headache type.

• Botox is injected into endoscopy at the point of functional stenosis. It decreases the P of the LES
by 40% and has NO side effects but decreases its action over time: initially effective in 80% of
cases, then falls. This fall in effect is also linked to the subject's production of antibodies against
toxin.

It is also a problem if you later decide to do a myotomy. In fact, the injections cause
microtrauma in the wall → inflammation → fibrosis and adhesions that make it more difficult to
find a cleavage plan for myotomy.

• The dilatation is done with a RIGIFLEX ball and gives good results (80-90%), especially if the
treatment is repeated several times. The best results are in pcs> 40y, women and type 2 of
HRM. However, complications are greater than surgery → PERFORATION in 2%, adverse
events in general in 33% (ab ingestis, fever, hematemesis, mucosal injury, hematoma). Also in
this case it would be complicated to do a subsequent myotomy.

• Surgical → LAPAROSCOPIC MIOTOMY 5cm long on the distal esophagus and 2 on the
proximal stomach (this is the standard but lately we talked about adapting it and calibrating it
on the single piece). The result is very good for dysphagia (90-95% results +).
X avoid reflux, practically certain after this technique, is also associated with the
FUNDOPLATATY according to Dor (front): I take the bottom of the stomach and with 3 rows
of 3 points the attack on the front of the esophagus in which I did the myotomy. It also has
protective effect on a wall that I have deprived of muscles, and therefore thinner.
You do the Dor, NOT the Nissen because it is an aperistal esophagus so it would aggravate the
dysphagia, NOT the Toupet because the protection serves me anteriorly.
If dysphagia develops after surgery it means that either the myotomy has not been done correctly
on the gastric side or the anti-reflux plastic has not been made correctly or there has been an
important scarring of everything.

To predict the progression of the PC after surgery are important: the outcome of the
manometry and the emptying that occurs the day after the operation.
A new surgical technique under development is the POEM → ENDOSCOPIC MYOTOMY BY
ORAL: from inside the lumen on the post surface they get mucous and submucosal, the musculature
 is broken off and the endoscope proceeds to underline down to the LES. Then pick up the endoscope
and put a clip. The endoscopist must be very very good. Since it is posterior and minimally invasive
it can be effective in those in whom the surgery was not successful.

In very rare cases (eg, 4th stage with sigmoid esophagus) a GIANT ESOPHAGUS may be
developed that requires ESOFAGECTOMY.

In acalasico there is an increase in the risk of K of 3.5% → SCREENING for DYSPLASIA → to be done
at 15y from the diagnosis.

07/12/2016
Diseases of the mediastinum

[The information in italics has been skipped by Prof. in the discussion of this
lesson] Il Mediastino
1. Anatomy of the mediastinum and mediastinal syndrome
The mediastinum is the space between the two mediastinal pleurae on the two sides. It is delimited:
a. forward, from the breastbone;
b. back, from the spine;

c. at the top, from an ideal horizontal plane passing through the concavity of
the first right and left ribs → there is no real "anatomical" delimitation.
d. at the bottom of the diaphragm.

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The delimitations from the breastbone and the column determine a rigidity of space; as a consequence,
the injuries, after having occupied it all, must move towards the spaces adjacent to it and in particular
towards the lungs.

To speak of a pathology of "space", and not of that of organ or apparatus, is contrary to custom . This
finds, however, its justification for the mediastinum, in which a series of traumatic, inflammatory
(mediastinal) and tumoral diseases develops that affect very different tissues and organs, normally
contained in it (thymus, thoracic duct, lymph nodes, adipose tissue) ) or migrated in it (gozzi immersed -
goitre plongent "that dives" (fr)).

Being such a confined space, any condition occurring within it causes the appearance of a rather
stereotypical symptomatology and constitutes a "space" syndrome, making it impossible to define, in the
first instance, the organ that causes the pathology.

On the whole, this is a rich pathology, with multiform aspects, which involves vital structures.
The symptoms are many and are related, in general, to infiltration or irritation of the organs contained in
it.

In this category, lesions of the heart and of the large vessels as well as those of the
esophagus are excluded , even if they are related to organs anatomically located in the mediastinum.
They deserve, in fact, a separate treatment, because of their peculiar nature and complexity; also the
diseases of the trachea are closely linked to those of the respiratory system

The traumas are due to external causes or even to iatrogenic lesions during endoscopic examinations;

• Incidents / crushing / earthquakes ... all these major dramatic causes can lead to mediastinal
injuries and, in these cases, there is generally no problem in recognizing the
symptomatology that will already be clear when the patient is examined.
• For iatrogenic causes we can think, for example, esophageal perforations: we will have passage

of the esophageal-gastric content within the mediastinum with serious consequences:

mediastinite production, initially chemical and therefore suppurative.
Endoscopic examinations: ex. dilation intervention → if it is not carried out correctly and
prudently, it can cause a perforation. Esophageal dilatation, can not exceed 4 mm in diameter per
session → repeated sessions will be performed until the desired diameter is obtained. These
dilations are made with soft balloons and are, in general, made to treat functional esophageal
disorders, eg. achalasia.

Organic stenoses, e.g. neoplasia, are instead treated with rigid dilators. This dilatation is often
difficult to do but constitutes a good palliation in the patient who is no longer able to introduce
food (in the last stage is the percutaneous gastrostomy: a stoma is created with a tube that
connects the stomach to the skin and, through this, it will be possible introduce water and
food.There are different types, depending on the diameter of the "tube / catheter" we can provide
the patient food in different ways: for thick tubes → bolts, for very small tubes: nutrition
extended in 24h to avoid clogging the tube.

It is very important to supply the patient with fluids and, at the end of the meal, it will also be
necessary to supply liquids for cleaning the catheters → coca-cola or water and lemon are
excellent for cleaning and unblocking.
NB: if the ostomy is intestinal the administration of foods and liquids must be slow so as not to
induce diarrheal syndromes).

The infections , secondary to esophageal perforations or diagnostic and / or surgical interventions, can
acquire an extreme gravity or, if cronicizzate, can induce consequences of great importance;

• Esophageal es.neoplasia: esophagectomy is done and the esophagus is replaced with the tubular
stomach or loops of the small intestine or colon. There are particular techniques that ensure the
vascularization of the transposed viscera → this is a fundamental condition for the success of the
surgery because, if I do not have good vascularization, the organ will not be able to hold the
suture: there will be no good scarring .

If you have a dehiscence I will see saliva in dranggi or the first meal administered or again, if I am
scrupulous and I do an intestinal transit with non-barred water-soluble MdC I will see that a
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suture level occurs a "sbaffo" of escaping MdC (for distal tumors, in general, under the
mediastinal emergence of the pulmonary veins)
This condition is an important cause of mediastinitis and it is necessary to stop the
administration of any oral food, good drainage and positioning at the point of the esophageal
fistula of suction tubes that keep the bowel as dry as possible. Surgical solutions exist but, in
general, they do not give very good results → they foresee total esophagectomy and a new
organ transposition with a long tube that will go directly to an anastomoses at the pharyngeal
level (→ if I do this, the dehiscence will be in the neck and not in the mediastinum → easier to
treat in any complications).

Tumors are frequent and above all present a considerable variety, both for histogenesis
and for biological behavior.

Finally, there is a group of malformative lesions that must be kept in mind, eg. cyst.

The mediastinal space has the form of a wider parallelepiped at the bottom, and narrower at the top.
or Front and back is bordered by rigid bone structures, the sternum and the column.
or On the sides, the mediastinal pleuras that delimit it, can easily be pushed out by large
volume neoformations, because the lung parenchyma is easily depressed. Sometimes, the
mediastinal masses grow very slowly, expanding into a pleural cavity, without giving
symptoms, until they assume enormous dimensions .

→ the pleurae are those that determine the expansive possibility of the mediastinal
masses which, otherwise, would cause compression of the large vessels with almost
100% mortality. The atelectasis that can be generated by compression of the lung is,
after all, the lesser evil.
The expanding masses make contact and adherence with the lung and often become from

it is inseparable → it is not possible to find cleavage planes for which it is very

difficult to separate them for the surgeon

or At the top and bottom , the mediastinal connective interstices are in continuity
with those of the neck and retroperitoneal abdominis: through the cellular lapse of
these spaces, organs or liquid collections can migrate from one region to another.
In analogy, by the same pathways, it is possible, from the neck or abdomen, to drain
mediastinal spaces or to penetrate them according to well-defined anatomical-surgical
planes.
→ a technique for obtaining significant images of the mediastinum involves introducing
gaseous contrast medium into the retroperitoneum (air) → blow the posterior peritoneum
with air by inserting a needle in an area adjacent to the coccyx. We will manage to
dissociate mediastinal shadows by rising from the gas, obtaining a pneumomediastinum
→ it is not an examination that is often done, it was more often used in the past to
demonstrate the relationships between the various structures.

Contacts with adjacent structures are important because this means that
mediastinal collections can open up within the mediastinum and move to
 contiguous spaces. "Draining": both liquid and semi-solid collections can be
drained.

The mediastinum can be subdivided into regions or compartments, according to conventional ideal
plans. [This is of considerable importance, because every pathological formation has a preferential
seat: the exact localization is therefore an important element of differential diagnosis].
We distinguish one:
i) superior mediastinum and a

ii) lower mediastinum,

separated by a horizontal plane passing through the tracheal bifurcation (always well appreciated
on the radiograph).

On a sagittal plane one can recognize one

i) anterior mediastinum, between the posterior face of the breastbone and the anterior wall of the
trachea;

ii) middle or middle mediastinum, between the anterior and posterior border of the trachea;

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iii) posterior mediastinum , delimited by the posterior wall of the trachea and the vertebral
column. [The posterior neoplasms found or originated in the costovertebral showers (such as tumors
of the sympathetic chain) are included by habit in the posterior mediastinum, even though the
costovertebral showers, from the strictly anatomical point of view, are not part of the mediastinum].

Six compartments are thus delimited :

of the upper mediastinum front- are the thymus, goiters migrated into the
mediastinum (submerged or plongeants), anonymous veins and the superior vena cava, the
ascending aorta and the arterial trunks epiaortic;

d.ii. in the antero-inferior mediastinum , the pericardial sac and the heart ;

D. III. in the medial mediumstinum (upper and lower), the trachea, the tracheal bifurcation,
the pre- and para-tracheal lymph nodes, those of the tracheo-bronchial angle and those
subcarinal / intertracheobronchial (staz 7);

d.iv. in the posterior mediastinum (upper and lower) the esophagus, the descending aorta,
the thoracic duct , the sympathetic thoracic chain.

• this is useful because, especially with regard to neoplasia, we can recognize the preferential
sites of their appearance.
Eg thymic tumor is always available in the mediastinal anteroposterior region
 Eg Posterior inferior mediastine → probably the mass will be a cardiac or paracardiac
lipoma. Eg a tumor of the sympathetic wall will always appear in the posterior mediastinum,
above all in the superior mediastinum.

It helps us to orient ourselves on the pathology.

• NB: the goiter → usually the thyroid descends into the anterior mediastinum (carrying its own
vasculature), but there are "retro vascular" goiters located at the posterior mediastinum.
In the front crawlers, if you are a little expert, it is possible to bring back a goiter in the neck
region that has also fallen for 2-3 cm in the mediastinum.
If the goiter is greater, it will be necessary to intervene with stereotomy.

This anatomical-surgical division in six compartments is fundamental for the localization of any radiological
mass or opacity: it can be identified by observing a chest radiograph in a postero-anterior and lateral-lateral
projection (which is always indispensable for the study of the mediastinum). The hyperdiafana image of the
trachea represents the central axis of this scheme that allows us to trace the ideal subdivision planes of
space → it is the only fixed image that, placed at the center, allows me to divide the space.

In antero-posterior projection I have the overlap and therefore I can not distinguish anything, while in
latero-lateral position the trachea is hyperdiafana → ne distinguish the silouette (the inner trachea of the
trachea appears black, because full of air, while its white profile ).

This is a good boundary, a good element of repere, which immediately places our injury in a
mediastinal space rather than in the other and, based on the location, we can begin to get an idea about
what kind of pathology we can find.

Mediastinum-Semeiotics and special diagnostics

Mediastinal affections are located in a region that is not accessible to physical examination, being
protected by very solid bone structures (sternum, column). The search for objective symptoms with
inspection, palpation, auscultation becomes significant only in the presence of very bulky masses or the
consequences they provoke (eg compression of vascular structures or airways).
The only thing we can achieve, objective, from EO will be through auscultation: heart noises or, if you
are ultra-bright, the transit of a liquid into the esophagus.
With percussion we could identify dullness if there are large masses that reduce the lung's clear lung
sound → they must be very large, to date we often recognize them much earlier starting from the
symptomatology, not from the physical examination. The physical examination is therefore not relevant.

The symptoms, reported by the patient, are always generic (modest pains, cough, fever, dyspnoea,
expectoration) and late so much so that a large part of mediastinal diseases is discovered by chance, in

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followed by mass screening or periodic radiological checks, mandatory for some categories of
people.
The study of the mediastinum therefore requires a series of instrumental investigations, which allow,
first of all, to establish if there is an abnormal mass occupying space, and to define its location, limits
and relationships. It is also necessary to clarify which of the anatomical structures are compromised
(dislocated, compressed, invaded, obstructed or destroyed).
The simplest of instrumental investigations, which takes on specific significance, consists of the standard
radiology of the thorax in two projections, while the pneumomediastinum (see before) and the
stratigraphy (see neoplastic lesions of the lung) have now become obsolete after the introduction in
the clinic of the TC.
Computerized axial tomography (CT) provides very clear images of the thorax section in horizontal
planes and allows to evaluate the density of each point, identifying the physical characteristics of the
formation, whether liquid, adipose or parenchymatous.

With the intravenous injection of contrast medium (contrast medium), vascular structures are very well
defined. Without contrast it gives us some information, possibly, in the study of intracranial
structures; for everything else I need mdc.

Useful information is also provided by ultrasound , to demonstrate above all if a mass is solid or
liquid; however, the ultrasound beam is blocked by the bony structures and the air present in the lung
parenchyma: the examination is therefore only feasible if there is a sufficient "window" to access the
ultrasound to the mass under examination (cervical, abdominal or intercostal).

The acoustic windows are scarce. Among the most used there is the one to perform transacetic
echocardiosis but not always, even in this case, the window is suitable.
The trans-oesophageal echo is much more useful and shows us the region in more detail; now it
has also entered into use in the detection of the presence of lymph node mts at the
paraesophageal level.

Nuclear magnetic resonance imaging (MRI) represented further progress in mediastinal diagnostics. In
the absence of invasive aspects, it allows to precisely define the seat, volume and ratios of a space
occupying space.

The study of individual mediastinal structures and organs includes a series of contrast and
endoscopic examinations.

Contrastographic examinations:

• esophagography with barite meal → I can see esophageal dislocations from medistine mass

• tracheo-bronchography with water-soluble iodine medium → practically never used

• the superior cavity with iodinated contrast medium introduced into the veins of the arms, the
contrast injection must be bilateral and contemporary;
• aortography, by opacifying the aorta and its epiaortic branches through a catheter introduced
through the femoral or brachial arteries (SELDINGER technique) or using a technique

digitized → only highly selected cases.

however, I am going to perform tests if I have any particular suspicions.
es. cavography now replaced by TC with contrast medium.
I'll go do it if I have a big suspicion of the quarry's occlusive painting.
How do I get a cavography? I insert water-soluble mdc into the cavity through a catheter placed in the
brachial vein, bilaterally, with simultaneous introduction of the contrast medium that will thus reach the
groove.

or the lymphography , which leads to the identification and morphological study of the
thoracic duct, obtained by injecting a liposoluble contrast medium into the lymphatic vessels of the
back of the feet. → especially in cases of kilo mediastinum and chiothorax to identify thoracic duct
lesions.
This follows the principle of cavography or aortography: insert the contrast medium into lymphatic
vessels → it is not simple: first of all it is necessary to reach a lymphatic system and to inject the
contrast medium into it. I have to look for ways that surely reach the thoracic duct → because I want
to study this!

The thoracic ducts convolgia especially the lymph that comes from the lower limbs and the digestive
tract → I have to find a peripheral that has manifolds that flow into the thoracic duct: where? In the
subcutis of the back of the foot. Once identified and isolated I can introduce a very thin needle and push
the contrast medium.

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A second problem arises here: the lymphatics are very thin and non-dilatable vessels. While a venous
system is very elastic and can increase its flow rate much, lymphatic no → can not be done → so the
images obtained by injecting the radiolucent contrast medium are extremely fleeting and can not be
used! We need to inject a radiopaque liquid that stays longer in the circulation and can be x-rayed.

In lymphography it is the only case in which the use of a liposoluble mdc substance is useful:
iodine is carried by ultrafluid lipiodol (it is a highly soluble oil) without taking risks of fat
embolization at the level of the large vessels, because they are in the lymphatic system.

At the thoracic duct the lymph is poured into the subclavian vein → right heart → pushed into the lungs.
Then for lymphography individual 2 lymphatics on the right foot back and left and I introduce two thin
needles (24-27G) and through them the lipid mdc is pushed. It is impossible to push it by hand with a
plunger because the resistance of the lymphatic circulation is very high (it can not be dilated) → metal
rack syringes are used, with which I insert small amounts of contrast medium into a shot → this moves
and I allows to see the lymphatic of the leg and lymph node stations up to the thoracic duct that I can
follow up to its outlet in the subclavian left → the image of the thoracic duct appears after about 45 min.
from the injection of the contrast medium at the level of the foot.
The liquid will remain in the lymphatic circle for at least 24-36 hours, afterwards I will be able to find traces
of it. An additional difficulty and risk of the lymphography is the unavoidable appearance of a pulmonary
microembolia → consequence of the lipid mdc → after some hours I find a picture of the ground-glass lung.
If the lymphography is repeated I can lead to a residual pulmonary fibrosis → for this it is repeated to
max 2 times.

Endoscopic examinations:
 or the tracheo-bronchoscopy with which are detected compressions, dislocations or
lesions of the trachea and bronchi;
or the esophagoscopy, with which it is possible to carefully study the esophagus
in all its course;
or esophageal echoendoscopy, for ultrasound exploration especially of the
posterior mediastinum;
or ecobronchoscopy, especially applied to the study of lymph nodes contiguous to the
trachea;
or mediastinoscopy, proposed by the Swedish CARLENS in 1956, which deserves a
specific treatment.

Mediastinoscopy refers to a diagnostic technique that does not exactly identify an endoscopic
examination, because the exploratory instrument is not introduced through an orifice and a natural
conduit, but in a path created by the surgeon detaching the tissues along an anatomical plane of
connective lasso. practically bloodless.
[This is therefore a real exploratory surgical operation performed in the operating room and under
general anesthesia, which involves a few centimeters cutaneous incision, but which allows a much
deeper exploration.]

[The patient is placed in a supine position with the hyperextended head. The skin is incised at the
jugule for a few centimeters; the pretracheal muscles are spread out until reaching the anterior
surface of the trachea. The incision and dissection of the pretracheal fascia allow deep penetration
into the mediastinum, between the aortic arch (in front) and the trachea (behind), a finger, then a
special spatula equipped with illumination (mediastinoscope). It is thus possible to reach the tracheal
bifurcation and conduct biopsies on paratracheal lymph nodes and abnormal pathological masses
The withdrawal must be prudent, always performed after having ascertained that it is not to be
performed on a vascular formation: deep hemorrhages are fearful and, if important, require a wide and
immediate opening of the thorax to suture the injured vessel].

In expert hands this survey often provides data not otherwise obtainable and a reliable histological
diagnosis on the nature of mediastinal adenopathies (lymphomas, sarcoidosis, tuberculosis, silicosis,
etc.).

Other diagnostic tests:

the transmural needle biopsy of mediastinal masses;

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 the biopsy of a pre-native lymph node (Daniels's intervention);


the parasternal biopsy obtained resecting a portion of the 2nd costal cartilage (defined
intervention: mediastinotomy front);

thoracoscopy and videotoracoscopy, performed by introducing a tube equipped
with lenses into a pleural cavity.
While the diagnostic pneumomediastinum is practically abandoned or replaced by CT, other
radiological and endoscopic investigations can contribute, in individual cases, to confirmation of the
diagnosis.
A goiter (thyroid) with mediastinal localization can be identified with certainty by scintigraphy
with 131 I, while a phaeochromocytoma with scintigraphy with 131 metaiodophenylguanidine.

Laboratory data can also provide expressive elements:

or urinary excretion of catecholamines in the pheochromocytoma;
or increase of chorionic β-gonadotropin and of a-fetoprotein in some germination
tumors (corioncarcinoma, yolk sac tumor);
or haematological alterations (erythroblastopriva anemia, acquired
hypogammaglobulinemia) symptomatic of autoimmune syndromes, which must induce
to look for a thymoma.

MEDIASTIN SYNDROME:

set of compressive symptoms resulting from occupation of space.

We do not recognize the nature of the pathology that generates it, we only take note that there is
mediastinal involvement.

Mediastinal diseases have poor, generic, and late clinical symptoms, such as vague pains, irritating
cough, and moderate exertional dyspnea.
However, when an abnormal expansive lesion or a pathological liquid collection reaches a volume that
causes compression on the mediastinal structures , a symptomatological complex due to compression of
the involved viscera manifests: less than 5% are benign lesions (gozzi or venous thrombosis or fibrous
mediastinitis ).

This "symptom complex", which goes by the name of mediastinal syndrome , may be due to the most
diverse causes, inflammatory, tumor, dysplastic.

It is in any case an important syndrome, whose signs, sometimes still not visible, must always be
carefully researched, to then go back to the pathogenesis of the disease.
The first organs affected by an increase in endomediastinal pressure are the most depressible, namely
the superior vena cava and the two left and right anonymous veins that flow into it. They are equipped
with a thin wall and the blood contained in them has almost zero pressure , slightly higher than that of the
right atrium of the heart.
ai Compression on the superior vena cava causes venous hypertension upstream with stasis:
the result is edema, cyanosis, inefficiency (turgor) of visible veins (external jugular) and

formation of a collateral circulation circle with appearance of subcutaneous venous reticulum.

Edema of the face, of the eyelids, of the lips, of the skin of the neck (the
patient can no longer button the collar), of the shoulders, of the upper half
of the thorax, assuming the so-called "edema a mantellina" appearance.

i) The cyanosis is revealed by the bluish discoloration of the facial skin and
mucous membranes; it increases if the patient coughs or bends, lowering his
head to the ground.

(on a practical level: the patient can no longer close the shirt collar)
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ii) The thickening (turgidity) of the veins is well evident in the neck
where the external and anterior jugular veins become ectasic, tense and
tortuous.
(in the image: jugular turgor (it is bilateral → excluding stress thrombosis
because it is unilateral - it is bilateral when the obstruction is low!) + dilated
anterior thoracic venous reticulum that extends to the shoulder

iii) The collateral circulation circle manifests itself with a more evident vein
network in the light and thin skin subjects, in correspondence of the
shoulders, of the anterior and lateral surface of the thorax, of the breast in
women.

(image: we see veins of the arms and neck extremely dilated + venous circles of the thoracic and
abdominal wall → index of an obstruction of the upper cavity at the level of the azygos → blood
exploits the superficial thoraco-abdominal veins to reenter the caval)

The collateral circle represents an effective mechanism through which the

blood of the head and arms, not being able to flow through the superior
vena cava, follows another way to reach the right atrium of the heart.

The azygos vein, a tributary of the superior vena cava and with a
considerable caliber, can represent an important way of compensation.
There are three situations, depending on whether the obstruction is placed:

• above the caval outlet of the azygos vein;

 • below the outlet;

• right next to it.

Obstruction above the outlet of the azygos vein.

The blood flows back from the subclavian vein in the internal mammary and
lateral thoracic veins where the flow is reversed. From these it reaches the
intercostal veins and then the azygos vein, whose flow is increased, but with
normal direction (circle of cava superior to cava superior)
the collateral circle will be quite limited at shoulder level

Obstruction below the outlet of the azygos vein.

The blood of the superior vena cava penetrates into the azygos vein
where the current inverses and through the lumbar veins reaches the
inferior vena cava (upper hollow-azygos-cava inferior circle through
deep collateral-lumbar vessels)

Obstruction at the outlet of the azygos vein . The caval obstruction also
involves the azygos vein and therefore the blood of the head and upper limbs
can reach the inferior vena cava through superficial veins, such as the lateral
thoracic, the epigastric, the intercostal. In this case the subcutaneous
collateral network will be more evident (upper hollow-lower cavity circle
through superficial collaterals)

these situations are extremely rare, the pathology that causes these
kinds of conditions must be "favorable" because if it were

malignant and, consequently, with rapid onset there is no time to see collateral formation:
the first die dies!

In addition to the described circles, there is also the collateral circulation of vertebral veins and
plexuses of the vertebral speculum: this deep circle is not visible, but constitutes a very important
path.

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To highlight the site, the extent and the severity of an obstacle to the venous outflow of the mediastinum,
one uses the cavity with injection of contrast medium through the veins of the two arms. The axillary
axes, succlaves, anonymous left and right and the superior vena cava are opaque.

In this way the presence and the location of an obstacle to the progression of the contrast medium
can be documented. At the same time, moreover, the type and extent of the eventual collateral
circulation can be observed.

The symptomatology from stasis cavale, with the passage of time, tends to become less evident or even
disappear, even if the cause persists. This is due to the fact that the compensation circle becomes
increasingly efficient, because the new outflow ways dilate and allow better drainage of the blood.

Although it can also be caused by benign affections (for example enlarged tuberculous lymph nodes
located against the vena cava), the stasis of the superior caval circulation is mostly a symptom of tumor
affections and therefore represents a sign of alarm and severe prognosis, especially if not tends to
regress spontaneously or with care.

The causes of the superior vena cava syndrome in percentages are in 77.8% of malignant nature (lung
cancer 52.3%, lymphomas 9.3%, breast cancer lung metastasis 8.1%, testicular tumor metastasis 3,
5%, thymic tumors 2,3%, occult cancer metastasis 2,3%);

21.8% of benign nature (mediastinal fibrosis 10.5%, 7% thrombosis, inflammatory lymphadenopathy

2.3%, actinic fibrosis 1%, unknown causes 1%).

Among the mediastinal syndromes it is also worth mentioning the exceptional Mènetrier
syndrome , due to compression of the thoracic duct and consequent lymphatic stasis. It manifests
with lower extremity edema (lymphoedema - not improntabile), in the left upper limb, with thorax
thorax (kilo in the pleural space) and chyloperitoneum.

The second mediastinal structure which, in order of frequency, may undergo compression by an
expansive mass, is the trachea .
a.ii. Although the wall is protected on three sides by the cartilaginous rings, the trachea may first
undergo displacements and angles by extrinsic compression and finally the lumen may be
reduced by anterior-posterior (flat trachea) or lateral-lateral (trachea scabbard)

→ this is a condition that surely determines the framework of tracheomalacia - no longer a

rigid structure, but a spring, as a consequence of the degeneration of the cartilaginous
structure determined by compression. the tracheal structure is maintained by the
surrounding tissues and if I remove them, it will not restore its normal structure with the
consequent risk of collapsing with each inspiratory act.

a.iii. When the lumen, which in the adult has an average diameter of 15-16 mm, is reduced by half or
more, dyspnoea appears after exertion and later tirage (re-entry of the supraclavicular and
jugulal cavities during inspiration, due to increased negativity pleural), irritative cough,
stagnation of secretions, sweating (by accumulation in the blood of CO2 which is eliminated by
perspiration in the form of carbonic acid) and finally cyanosis.

A.IV. It is easy to see patients with tracheal compression syndrome, in whom the diagnosis
of "asthma" was wrongly made.
av For the differential diagnosis we must consider that: the asthma dyspnoea is essentially
expiratory (for spasm of the bronchiolar musculature, therefore distal bronchial obstruction),
 while the tracheal compression dyspnea is inspiratory (therefore proximal obstruction - the
patient fights to let the air in the lungs).
A.VI. A radiographic and stratigraphic examination of the thorax with a search of the
hyperhumanfana image of the trachea in the two orthogonal projections makes it possible to
ascertain the possible reduction of the lumen.

Other mediastinal structures that are more rarely compressed are the nerve trunks .

• the sympathetic chain, with possible appearance of the Claude Bernard-Horner syndrome ;

• the right or left phrenic nerve, to whose infiltration follows a paretic elevation of a hemidiaphragm,
which, during radioscopic examination, appears motionless during deep breathing; → there have
been very important judicial disputes with regard to injury of a phrenic nerve during pulmonary
excision surgery → it can happen → we may have the appearance of

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respiratory failure. Some say that frenicotomy is useful because going up, the diaphragm, occupies
the "empty" space that is left after the lobectomy. Others, on the other hand, reason by considering
that, if the phrenic works, there will be a consequent expansion from the residual lung.
• the vagus nerve and especially its recurrent branch (lower laryngeal), with paralysis of the
homolateral vocal cord and typical dysphonia (two-tone voice) . Of the two recurrent nerves, the
left is more easily affected, because it originates deeply in the mediastinum under the aortic arch,
while the right originates much higher, under the right subclavian artery and is therefore less
interested in mediastinal pathological processes.

Finally, almost never an expansive mass of the mediastinum comes to reduce the lumen of the arteries
(aortic arch and epiaortic trunks), because they have a robust elastic wall and the blood flowing in them
has a pressure of 110-130 mmHg -> in these cases mass will never be practically ever eligible for
surgical removal: it must be very large to compress the arterial structures! In the Sd. Mediastinal rarely
sees arterial compression due to the high pressures in these vessels.

Also extrinsic mass compression on the esophagus is almost never a cause of dysphagia, because the
esophagus, although having a soft and depressible wall, lies in a loose cellular tissue which allows it to
move considerably , without the lumen being reduced.

In some cases, esophagus reveals dislocations of the esophagus by several centimeters without the
patient experiencing disturbances; dysphagia only appears when the wall of the organ is compromised
for at least half the circumference (lumen reduced to a Ø of 8 mm).

The mediastinal syndrome is therefore a "symptom complex" , mainly related to caval and tracheal
compression, present in whole or in part, due to multiple causes, which all have the characteristic of
giving disturbances of a mechanical nature .

There is no relationship between the volume of the expansive mass and the severity of the mediastinal
syndrome. Sometimes huge masses slowly increased, expanding into one or both pleural cavities do
not give a sign of themselves; other times, small hard and sticky knots become an early cause of the
reduction of the lumen of the quarry or trachea with resounding symptoms.
The clinical diagnosis of mediastinal syndrome is generally easy; with all the instrumental exams
available, we try to trace the cause of it and possibly to a bioptic sampling of the expansive mass
occupying space in the mediastinum.
The cure consists of:
A.VII. in the surgical removal or reduction with medical care (cortisone, cytostatics) or
radiant pathological mass, when the exeresis is not possible.
a.viii. In thrombosis caval fibrinolytics are indicated and, in failure, thrombectomy.
a.ix. In the benign or malignant extrinsic cavity obstructions, not otherwise correctable, one
can
perform a (by-pass) assembly between the anonymous trunk and the right earring, using
material

biological (saphenous or pericardium) suitably modeled or synthetic material.

Prof. Friedman 12/12/16

Senological surgery
Epidemiology
Incidence of breast cancer (also in Italy): 1/8 women, increasing for
increasingly effective screening and for early diagnosis with consequent reduction of invasive
techniques such as radical mastectomy.
1 million new cases a year worldwide and due to 500,000 / year.
ANATOMY AND PHYSIOLOGY

From birth to adulthood the breast goes against a simple proliferation , without differentiating
itself. Differentiation and therefore the ability to produce milk only occurs with pregnancy. The
breast is mainly composed of adipose tissue and what is called "mammary tissue", ie the glandular
component, is only 10%.
The gland is in turn made up of lobes, ducts and lymphatic tissue.

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• Lobi: these are the operating units that produce milk during breastfeeding, around 8/10,
are arranged in "daisy petal" around the alveolo-nipple complex. They are in turn made up of
subunits that take the name of lobules which include bulbs , responsible for the production of
milk.
• Ducts : deriving from the confluence of the lobes. They are branched inside the breast
increasing more and more of the caliber and ending with the main ducts inside the nipple
• Lymphatic tissue : present ubiquitely within the breast and draining into three main lymph
node stations → axillary (the one that most interests in the breast), chain
Internal mammary or thoracic (breast's sternal side) and over and under-nasal lymph nodes .
Thus, within the breast, there are 3 tubular structures : ducts, blood vessels and lymphatic vessels.

SIGNS AND SYMPTOMS OF MAMMAL PATHOLOGY

• Appearance of non-painful palpable tumefaction. Pain is little associated with K (<10%). If the patient
has pain, we must reassure him
• Secretions serous, milky, blood, sieroematiche, greenish. If the secretion turns out to be bilateral and
lactescent, an index of greater benignity, probably linked to a hypersecretory condition of PRL
• Modification of the breast contour
• Inversion / retraction of the nipple (only if acquired, not infrequently it is in fact congenital)
• Crusts or ulcerations in the areola (Paget's disease index of an in situ k below)
• Volumetric increase in breast with orange peel skin and redness (lymphatic stasis)
EO MAMMELLA

• Supine and sitting position

• Hand to flat, using fingertips

• Exploration of all quadrants

If we show an injury , we will evaluate:

• Margins

• Mobility compared to floors below and above

• Consistency

benignity Malignancy
EO LESIONE
Multiple injuries Single injury
Soft consistency Hard consistency
Adheres to the superficial and / or deep
Mobile levels
Well defined edges Irregular borders
SECRETARY CAPEZZOLO
Bilateral Unilateral
Multiduttale Monoduttale
milky Serous / serosanguineous
Often related to hyperPRL Spontaneous
Persistent (not linked to the menstrual cycle)
CUTANEOUS CHANGES
No special signs Retraction of the nipple
Edema
Thickening of the skin

Benign injuries
 n
i
n
e
t
y

t
w
o

• Non-proliferative

• Fibrocystic mastopathy

• Simple cysts (vary over time, we can observe a sudden increase in volume due to capillary
rupture in the wall, TP only if symptomatic with aspiration)
• Adenoma

• Fibroadenoma: juvenile injury of the fertile age. Indication surgery if: 1) d> 3-4 cm at the time of
diagnosis, 2) fibroadenoma already known to echo that grows> 5-10 mm in a year. I take it off only
for its marked growth tendency, thus avoiding extensive surgical incisions, 3) difficulties

in the DD, 4) psychological aesthetic reasons at the request of the pc. It can be symptomatic in
relation to the various phases of the menstrual cycle.
• Hyperplasia without atypia

• Epithelial hyperplasia

• Sclerosing adenosis

• Intraductal papilloma

• Hyperplasia with atypia

• LCIS

• DCIS

• Inflammatory / infectious

• Mastitis related to the puerperium. They can also lead to a suspension of breastfeeding

• Mastitis not related to the puerperium, probably due to obstruction of the ducts. Possibly
recurrent
 (some abscesses may rarely need mastectomy).
TP in this case : if possible antibiotic is used, but sometimes surgery with incision and abscess drainage
is necessary .

• Tied to trauma

• Collections and hematomas

Malignant lesions

• 75% ductal K

• 10% lobular K: infectious tumor form, often bilateral and often radiotransparent to
mammography. (RM)
• Mixed

• K tubular

• Mucinous

• Medullary

• Micropapillary

microcalcification

Fine intracellular calcium deposits. They are indirect sign of cells with impaired
metabolism. Depending on the method of deposition, I can distinguish: dystrophic type → involutive
breast tissue (fatty tissue involution with saponification of adipose tissue) or small rod-like groupings,
sunburst, etc., can be linked to cancer still without a real nodule.

A few words of ANATOMY

Observing the section of a learned:

As the epithelium, normally monostratified, inside the ducts becomes hypertrophied (sometimes even
up to the obstruction of the lumen) the passage from an atypical hyperplasia to a k in situ is very thin
→ a limit is therefore the n ° of cellular layers that line a duct.

When tumor cells of an in situ k exceed the basement membrane → microinvasive carcinoma →
metastatic carcinoma
MTS 1st level: locoregional lymph nodes (axillary, internal mammary chain, supra / subclavicular)
MTS 2nd level: bloodstream, filtering organs → bones, liver and
lung The same applies to lobules.

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PROGNOSIS

• Closely related to TNM (no examination

required) Micrometastasis : 0.2 to 2 mm
Macrometastasis: > 2 mm. Important to distinguish them as it will vary the surgical therapy

Survival 5 aa: 0 = 92%, 1 = 87%, 2 = 75%, 3 = 13%, 4 =

0% Other IMPORTANT PROGNOSTIC FACTORS

• Tumor histotype

• ESTR / PRG receptors : positive prognostic factor (the more the tumor resembles the origin
tissue the more it will be differentiated)
• Lymphovascular invasion (negative p-factor)

• Ki67 (proliferation index, if> 15% negative p-factor)

• HER2 negative prognostic factor if expressed (despite her-2 = specific biological TP)

• Tumor genetic profile : especially in the USA, mammaprint is used → defines the risk of
recurrence and therefore tp suitable.

DIAGNOSIS: STANDARD EXAMS

• Mammography (NO INDICATION <40 aa) (I look for masses or calcifications)

• Breast ultrasound (GOLD STANDARD <40 years Yes, if familiarity or symptomatology)
• MRI (exam II / III level with specific indications *)
•Biopsy

* It is likely to see too much with a very high sensitivity. Use mdc. MRI is superstading /
overestimating. Indicated for :

• K lobular which is bilateral frequently

• Multicentric (+ in the same breast) or multifocal (+ in the same quadrant) tumors

• LN mts axillary localizations

• Study of pcs subjected to neoadjuvant CT (serves to destabilize the CT)

• Implanted prosthesis control

• High risk PPCs (10%) = BRCA1 (80% k) BRCA2 (50%, but also k ovaries) familiarity

Once the lesion has been identified, before resorting to surgery → BIOPSIA

• Non-surgical : FNAC, core biopsy (truecut biopsy with tissue carrot, histological and cytological)
• Surgical : incisional biopsy, excisional biopsy
Biopsies are performed according to ultrasound or mammography (the microcalcifications are not
visible to the echo) with a special bed → Pz pron, needle inserted in the breast in a mammographic
guide (VABB). Biopsies under guide rm are possible but very expensive.

MAMMARY TUMOR THERAPY

CHEMOTHERAPY

• Neoadjuvant : has the aim to destabilize the lesion and in triple negative forms (no rec hormonal, Ki67
+ and Her2 +) improves long-term prognosis.
• Adjuvant (classical chemotherapy, hormone with tamoxifen and aromatase inhibitors,
biological as transtuzumab)
RADIOTHERAPY

It is used for conservative surgery or if we have not made an R0 (ie I have more than three axillary LNs
x metastasis.)

HISTORY OF MAMMELLA SURGERY

• Ancient Egyptians (2500 BC), to control mammary tumors locally, used cauterization, an
inevitable remedy of late diagnosis.
• Galen (130-200 AD) attributed the origin of breast cancer to a sort of "morbid melancholy"
and recommended specific diets

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• Throughout the Middle Ages (450-1400A.D.), Exorcisms and topical applications of

various substances were the most used principals
• During the Renaissance, Andreas Vesalius (1514-64), in the treatise "De Humani corporis
fabrica" proposed mastectomy and ligation of blood vessels
• LeDran (1685-1770) was the first to recognize that breast cancer could spread to axillary
lymph nodes and that this was associated with a worse prognosis.
• At the end of the 19th century most of the radical mastectomies were performed for
locally advanced tumors.
• At John Hopkins Hospital, 10-year survival was only 12%, with a relapse rate

30% local
The history of breast cancer is dotted with numerous "conceptual revolutions" .
Since the time when breast cancer was considered an inexorably fatal disease, important progress has
been made.
Since 1920, survival rates have increased from 10% to 50% in 30 years and since then this percentage
has been growing progressively.
Rational of demolitive surgical interventions :
Tumor diffusion occurs exclusively through the lymphatic system → removal of all the main drainage
pathways of the mammary region → Radical mastectomies with removal of the pectoral muscles and of
all the lymph node sites.

HALSTED 1890 (Theory valid until the early 60s)

Based on the idea that breast cancer was a loco-regional disease and that this condition was maintained
for a long time, he thought that:
Timely diagnosis + complete excision (first basic steps x radical mastectomy: LN diffusion and
large and small pectoral removal and all lymph node sites) → definitive cure
So until the 60s elements such as:

• Difficulties in controlling the disease

• The uncertainties about its biology

• Diagnosis often late

They had pushed towards very aggressive treatments according to what was then the " dominant
rule" that is: the maximum tolerable treatment .
The Halstedian theory was largely refuted for the clinical finding of the failure of radical surgical
therapies → so, thanks to Madden , we arrived at the introduction of mastectomies with pectoral
muscle preservation, with survival rates completely overlapping with Halsted practices .

Starting from the 70s there was a cultural change thanks to the best biological knowledge, the greater
precociousness of diagnosis and the introduction of multidisciplinarity.

At the Guy's Hospital in London, the prognosis of patients undergoing a comparison was compared:

Radical mastectomy plus radiotherapy vs extensive tumor resection without lymphadenectomy

plus breast radiotherapy and loco-regional lymph nodes
Finding a disturbing increase in mortality among patients undergoing conservative
surgery. VERONESI
PROPOSAL FOR A TRIAL ON BREAST CONSERVATION (WHO Meeting Geneva, December 1969)
The premises for a conservative treatment are :

1) That the prognosis of breast cancer depends essentially on the development of distant metastases
and to a lesser extent on local treatment with its important and useless mutilations.
2) That the tumor of the mammilla is radiosensitive
ART MILAN 1
Veronesi showed that the prognosis of patients with tumors with a diameter of less than 2 cm underwent:
QUA + DA + RT at appropriate doses (60 Gy) VS mastectomy according to Halsted

It was equivalent → Therefore the failure of the English study was due to
an inadequate radiant dose .
Hypothesis : Diversity of local treatment does not affect survival
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5

• Milan II (1986-1989): Tumorectomy + RT vs Quadrantectomy + RT

• Milan III (1987-1989): Quadrantectomy with or without Radiotherapy

DIFFERENT LOCAL REGIONAL TREATMENTS INFLUENCE LOCAL RECIDIENCE BUT

NOT PROGNOSIS.
Guidelines on surgical therapy of breast cancer
(The Steering Committee on Clinical Practice Guidelines for the Treatment of Breast Cancer, 1998) Do
not contraindicate conservative surgery

• Tumor localized in the central quadrants (level III evidence)

• Axillary lymph node involvement (level I evidence)

• Presence of breast implants (level IV

evidence) Contraindicative conservative surgery
• Factors that increase the risk of local recurrence: extended microcalcifications (level IV
evidence) ; multicentricity (level IV evidence) ; non-free margins (level IV evidence)
• Absolute contraindications to RT: pregnancy (level I evidence); previous breast
irradiation (level I evidence)
• Contraindications related to RT: systemic lupus erythematosus (level III
evidence); scleroderma (level III evidence)
• Physical disabilities that prevent the optimal administration of RT (level I evidence)

• Large tumor volume in relation to the volume of the breast (strongly conditions the decision
between conservative surgery and mastectomy)
• Clear patient preference for mastectomy

BREAST CONSERVATION SURGERY (BCS)

BCS combined with postoperative radiotherapy has become the gold standard treatment for most patients
with early-stage breast cancer, with survival overlapping mastectomy but with improved body image and
quality of life. The success of the BCS is therefore based on the complete removal of the tumor in
"healthy margin" preserving the natural shape and appearance of the breast.

MA limiting factor → amount of tissue removed not in terms of absolute volume but in relation to the
location of the tumor and the relative size of the breasts.
The failure of the classical BCS has stimulated the growth of new advanced techniques during the last
decade. It therefore comes to ONCOPLASTICA (OPS - Oncoplastic surgery)

• It is a surgical approach that allows extensive tissue excision without compromising the natural
shape of the breast
• It is based on the integration between reshaping plastic surgery techniques and extensive
tumor removal
• The oncological effectiveness in terms of the state of local margins and relapses is comparable to
the
 traditional conservative surgery.

The techniques of oncoplastic surgery range from simple remodeling of breast tissue to more
advanced mammoplasty techniques that allow the removal from 20% to 50% of breast volume with
adaptation of the contralateral breast (in the end it is a bilateral intervention that also involves the
breast healthy). NB: k in situ ductal can lead to mastectomy because it is not very worrying but
growing in the ducts and having expanding ducts all over the parenchyma I have to do
mastectomy. In addition to advancing "conservative" techniques, we have also witnessed
the evolution of " conservative mastectomy "

Skin sparing mastectomy (SSM) was first described by Toth and Lappert in 1991.

It was possible to preserve almost completely the envelope and the inframammary furrow, thus obtaining
an improvement of the aesthetic result and a reduction of contralateral remodeling performed to improve
symmetry → reconstruction contextual to the demolition process (preservation of the airfoil complex)
The classical technique involves the use, after mastectomy for carcinoma in situ, of an expander →
temporary prosthesis inserted between the large and small pectoral muscles. It is progressively inflated with
physiological solution until it reaches the same volume of the contralateral breast, in order to guarantee a

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gradual adaptation of mammary tissues. At this point the expander is replaced with a definitive
prosthesis.
NAC (Nipple Areola Complex)

The loss of NAC represents an important body mutilation for women who perform this type of surgery.
The removal of NAC ( NAC sparing surgery ) is based on oncological fundamentals
(obtained from retrospective studies in the forms of k in situ):

• Occult tumor involvement of the NAC: about 20% in retrospective studies with major
cases
• Reduction of this value to 2-6% for lesions located more than 2 cm from the NAC

Study the possibility of conservation of this structure:

Italian Consensus Conference (superimposable to that of the NCCNNational comprehensive Cancer Network)

SURGICAL INDICATIONS (to keep NAC)

• infiltrating or in situ neoplasm that according to preoperative radiological investigations does

not involve the NAC (Imaging negative predictive value of 97% Mx distance nipple lesion> 4
cm, RMN at least 2 cm)

• Mammelle medium-small and with degree of minimal / moderate ptosis

ABSOLUTE CONTRAINDICATIONS

• Clinical or instrumental evidence of NAC involvement

 • Presence of pathological C4-C5 secretion (C4 = presence of tumor cells inside the ducts with risk
of high recurrence, C5 = positive cytology for malignancy)
• Paget's disease of the nipple

• Inflammatory carcinomas

RELATIVE CONTRAINDICATIONS

• Prior RTp or RTp prediction (effects on cutaneous trophism)

• Preoperative surgery peri or retroareolar (if the surgical scar is greater than half of the
circumference of the contralateral breast, I will face a risk of vascular suffering)

• Smoking, diabetes, immune diseases

THEY ARE NOT CONTRAINDICATIONS TO THE CONSERVATION OF THE NAC

• Age

• Proximity of extra NAC skin cancer as long as it is removed

• Preventing neoadjuvant

• Size of the tumor

• Multicentric multifocality

• Histological type

• Lymph node status

SURGICAL TECHNIQUE

At the level of the retroarary region it is advisable to remove all the glandular tissue up to the areola
using preferably a cold-blade scalpel - either to avoid injuries induced by the electrosurgical unit and
to facilitate the observation of the finding by the anatomopathologist.

Sending a disc fragment separately with a diameter corresponding to the diameter of the areola
with a thickness of about 1 cm.
It is a relatively young surgery (less than 10 years) so studies in this regard are still very limited.
ONCOLOGICAL RESULTS → Although there is no very long median follow-up
(Benedictktsson EJSO 2008, it is about 13 aa) the% of real local recurrences, meaning the central ones or
the NAC, are extremely low attesting between 0 and 2%. The oncological safety of the NSM has not
yet been fully demonstrated.

Many authors have compared this technique from the oncological point of view with traditional mastectomy:
the incidence of local recurrences in the two groups was similar for T1, T2 and multicentric tumors.
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Radiation therapy on the NAC could have an alternative role to the removal of the NAC, when at the final
histological examination the margins result unscathed but with a distance less than the suggested safety
distance.

Due to the lack of randomized trials, NSM continues to gain popularity as a prophylactic
procedure in high-risk women.

FUTURE

• The will to move from a "destructive" objective (cut, irradiate, inject cytotoxic) to the
maximum possible conservation, from the maximum tolerable doses to the minimum
effective ones.

• Art. GIULIANO (NYC) Proposal related to axillary surgery → DO NOT perform axillary
dissection in patients with MACROmts in the sentinel lymph nodes in those tumors with a
diameter of less than 2cm (to date this treatment is reserved only for patients with MICROmts
in the sentinel lymph node).
• Axillary ultrasound as staging for small tumors.

• The best results are in the BREAST UNIT - multidisciplinary senology units: they involve the
collaboration of more professionals. In order to be defined as such at European level:
• Each BU must receive at least 150 new annual cases

• At least 50 surgeries must be performed for the surgeon

• At least 500 radiographs by radiologist must be performed

Prof. Camerini, 12/13/16

Part I: Obesity surgery

Restrictive measures: reduce stomach volume: gastric banding, vertical gastroplasty, sliv gastrectomy
Malassorbitive interventions: bilio-pancreatic diversion (conceived by Prof. Scopinaro)

Obesity is a chronic, developmental and relapsing disease, which involves significant co-morbidities
(BMI> 30-35), presents in 11% of the world population, 23% in Europe, 21% in Italy. Life expectancy is
diminished by the obesity of 13 years in men and 8 in women: this is because the fattyroid disposition
increases the cardiovascular risk more than the gynoid one.
Surgery is indicated with BMI> 40 and BMI> 35 in the presence of co-morbidity; if the patient is
diabetic, they are also admitted in obese to BMI of 30-35.
Studies show that surgery is more effective than pharmacological and behavioral therapy in reducing
weight and extending life expectancy. This type of intervention is mostly performed in the United
States and Canada, where there is a high prevalence of obesity in the population.
Most performed interventions to treat obesity:
 • Roux-en-Y gastric bypass 46.6%

• Sleeve gastrectomy 27.8%

• Gastric binding 17%

Diabetes in obese patients is resolved globally in 76.8% of cases; this is because the BMI is so much
higher, so diabetes will depend on insulin resistance; therefore the DM resolves itself more precociously
and efficaciously than obesity.

Gastric resection interventions:

• Vertical gastroplasty: an eyelet was created in the center of the stomach with a circular stapler (as
if the stomach were a donut); a ring was inserted in correspondence with the small curvature, so
that it restricted the transit point between cardias and pyloric cavity; finally, cardias from the
body of the stomach were separated at the bottom, with a linear stapler. The intent was to give a
feeling of early repose. There was also a variant in which the excluded bottom and body part was
cut directly, avoiding gastro-gastric fistulas.

• Adjustable gastric binding: a silicone ring is inserted around the stomach, inflatable with a
tube to the subcutis, with the possibility of adjustment according to the slimming intent.

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• Sleeve gastrectomy: consists of resection with stapling of part of the stomach; in addition to
mechanical intent, there is also the exclusion of the stomach part producing ghrelin (the only
enterormone

orexigenic).
The resection has the problem of not maintaining weight in the long term, since the patient must also
be educated to good eating behavior.
The gastric band gave long-term complications such as esophagitis, esophageal dilatation, gastritis,
peptic ulcer, reservoir infections, stenosis, and intragastric device migration.
In the case series, two years after the bypass operation, there was again an increase in BMI and
survival decreased.
Calorie restriction and weight reduction also improve insulin resistance, making DM improve. The
bandage solves the DM but is less effective than the other procedures developed for the
purpose. Sleeve gastrectomy

It consists of the sleeve, or vertical resection of part of the stomach: in this way we have both restrictive and
malabsorption intent. The only sleeve decreases weight at first but then the weight tends to increase again at
10 years. Another problem is the escape of food ingested by the gastric suture: the leak is a long-term
complication. The sleeve is contraindicated in the case of GERD, because the angle of Hiss is eliminated.
Bilio-pancreatic diversion

It consists of two times:

• the first consists of a real sleeve gastrectomy, saving the pyloric portion and the first duodenal
segments; the gastric volume therefore reaches about 250 ml.
• the second involves intestinal resection and gastro-intestinal reconstruction; consists in joining the
short section of the duodenum with a section of the small intestine previously dissected at about
half of its length between the duodenum and the ileocecal valve. The intestinal tract excluded
from the passage of food is in turn joined with the alimentary tract to about 50 cm
from the ileocecal valve.
The GI tract and the bilio-pancreatic tract (which consists of a dedicated loop on which the choledochus
is anastomosed) meet at 50 cm from the ileo-cecal valve, causing poor digestion of fats and more
complex carbohydrates, which then poorly absorbed.

Advantages:

• Weight loss always present and maintained over time

• 87% of DM healing

• Improvement of hypercholesterolemia due to the lack of reabsorption of the bile salts, which
therefore diminishes the entero-hepatic recirculation and favors the synthesis from scratch
starting from cholesterol

• Decreases the intramyocellular fat already one month after surgery, with the collapse of the
insulin

resistance
Side effects:

• Protein malnutrition

• Malabsorption of vitamins A, D, K (liposoluble)

• Ca ++ malabsorption (carrier-specific absorption up to the first jejunal loop)

• Iron malabsorption

• Stinky stools (rich in fats)

• Increased defecation and flatulence

• Follow-up necessary

Complications:

• Gastric ulcer

• Bone demineralization

• Protein malnutrition
If the operation is too bad for the patient, the common stretch is surgically extended. RYGBP

Gastro-intestinal Y-shaped anastomosis with longer common section and less spacious pocket
compared to DBP; furthermore, the resected residual stomach is left in place.
Mechanisms on which it acts:

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• Neuroendocrine mechanism, so that NPY and GLP1 that induce satiety, are produced
immediately because of stimulation by foods that transit precociously in the intestine
• Mechanism of mechanical satiety, due to reduced gastric volume

We lose 60% of excess weight, but in the long follow-up we increase slightly weight, less than what
happens for the sleeve gastrectomy.
The complications are very low; sometimes the ulcer occurs because the jejunal loop is not used to
gastric juice.
Supplements of calcium, iron and vitamins are necessary, but not with the scrupulous attention needed
in the DBP.
The resolution of the DM thanks to DBP and RYGBP has various hypotheses:

• Weight loss hypotheses

• Hypothesis of ghrelin

• Hypothesis of early stimulation of GLP1 secreting cells, anorectic, stimulating insulin and
antiapoptotic secretion for pancreatic β cells
• Hypothesis of incretin secretion failure, with lowering of blood glucose levels Follow-up:
• one month after the intervention

• every three months in the first year

• every six months in the second year

• annuals after three years from the intervention

In the restrictions, frequent checks help to avoid weight gain.

In diversion, instead, complications of malnutrition are prevented.
Diversion indicated for:

• Superobeses

• Patients with metabolic complications

• Age (very young and very old are not subjected)

 • Previous failed surgical attempts

Part II: Laparoscopic surgery

With the improvement of anesthetic, analgesic and antiseptic techniques, surgery remains a very invasive
act.
Laparoscopic surgery has minimally invasive access. At the beginning there was resistance in using it for
cancer surgery: this was because, previously, when laparoscopy was used for oncological purposes, wall
recurrences were frequently due to aerosolization because the tumor cells were attracted towards the
wall; today we use special precautions that avoid this complication.
Instruments:

• Laparoscope, optical system of lenses, camera and light source

• Insufflator: since the abdomen is a virtual cavity, it must be insufflated with CO2, making it real
and inducing pneumoperitoneum. The air is heated so as not to induce hypothermia. CO2 is
used because it is well absorbed, not very flammable, but it can cause acidosis, tachycardia
and arrhythmias (rarely)
• The Veress needle was previously used to insert the laparoscope and insufflator, but it
allowed blind entry; now we do mini-laparotomy (direct vision)
• Trocars, or shirts with a valve channel, which prevents the insertion of the instruments

lose the pneumoperitoneum. The positioning of the trocars is very important for working at the
right angles.
Benefits for the hospital:

• Reduction of postoperative complications, especially related to trauma of access (laparocele,

wound infections, baseline atelectasis and respiratory failure)
• Reduction of costs for shorter stays (on average 7 to 3 days)

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Benefits for the surgeon:

• Improved vision, often even better than open (eg low rectum and diaphragm dome)

• Increased technical diffusion for the improvement of teaching (eg possibility of projecting the
entire intervention by videoconference thanks to the registration of the laparoscope images)
• Improved dissection (eg between Todd and spontaneous Gerota bands with pneumoperitoneum;

more delicate laparoscopic on peritoneum)

Disadvantages for the surgeon:

 • Altered tactile response

• Two-dimensional vision

• At the beginning, dilated times

• Introduction of a new
technique. Benefits for the patient
• Less pain

• Less peritoneal adhesions

• Less post-operative complications

• Shorter stay

Laparoscopy is indicated if open access is very invasive compared to the region on which it is
going to intervene: for example, in the case of adrenalectomy, laparoscopy is indicated because it
replaces a very invasive open access with respect to the narrowness of the working field .

Today there is also esophagectomy, pacreasectomy, gastrectomy, liver resection.

Emergency surgery is still often performed in open, due to the difficulty of the cases: for example,
intestinal obstruction is impossible to treat in laparoscopy, due to the abnormal distension of intestinal
loops.

The inguinal hernioplasty intervention benefits from laparoscopic surgery because by accessing the
hernia from the inside of the abdominal cavity, the herniae doors can be closed from the inner side and
reinforced by the yielding points of the wall with a prosthesis. However, we must consider the greater
invasiveness of this type of intervention compared to that in open, in which we are going to act from the
outside.
Studies show that the reduction of post-operative complications in major cancer surgery is evident in
minimally invasive surgery, e.g. esophagectomies, hepatectomies and pancreasectomies.
The development of laparoscopic surgery has allowed the development of fast track surgery, which
requires team work, preoperative education, not colon preparation, minimally invasive surgery, no
fluid overload, early removal of the SNG and bladder catheter, less use of drainage, re-feeding and
early mobilization, pain and insomnia treatment.
There are other types of minimally invasive surgery:

• NOTES: surgery through natural orifices (eg stomach or rectal cholecystectomy)

• SILS: only umbilical access

• Robotics: the surgeon can be distance, it is three-dimensional, the robot filters the surgeon's
movements,

unlimited degrees of freedom in the movements of the mechanical arms

These are not techniques, but concepts evolving towards unimaginable surgical fields now. To
evaluate them, three parameters must be taken into consideration: feasibility ("feasibility"),
efficacy ("effectiveness"), effectiveness ("effective applicability").
 12/14/16 Prof
Campisi

Digestive bleeding

They are defined as a loss of blood through the alimentary canal, due to lesions of the digestive system
with different etiology.
A first classification divides them into acute and chronic.
A second classification divides them into:
- upper digestive bleeding

- lower digestive haemorrhages

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The limit to distinguish them is the duodenodigiunal corner of the Treiz : the upper ones are
hemorrhages from the oral cavity up to the Treiz, while the inferior ones are located from the ligament
up to the anus.
Those higher are more frequent, more severe, have a lower tendency to spontaneous resolution and tend
to give more relapses than inferior hemorrhages.
Statistically, the haemorrhages of the small intestine are less frequent.

Regardless of the localization, the haemorrhages are classified as mild, moderate or severe according
to the criteli of the following table:

Etiology: all diseases of the alimentary canal (inflammatory, neoplastic, etc.) and also systemic
diseases.
In general the higher ones are caused more frequently by:

- duedal ulcers
- acute lesions of the mucosa
- esophageal archs
-MRGE
- Sd of Mallory-Weiss.

Less frequently we have neoplasms, hemophilia, vascular and hematological alterations.

The lower ones :

-hemorrhoids
-carcinoma
-Ulcerative colitis
With less frequency they are caused by fissures, diverticulosis and adenoma.
With low frequency angiodysplasia, meckel diverticulum, Chron's disease and neoplastic ulcer of the
rectum.

In relation to age: under 60 years polyps, ulcerative rectocolitis, Chron, infectious enterocolitis and
angiodysplasia are more probable.
Over 60 years the most frequent causes are: diverticulosis, ischemia and neoplasia.

There may have been generalized bleeding :

1) primary: coagulation diseases, platelets, etc.
2) secondary: anticoagulant tp and massive transfusions.

NB: the pcs have no particular tendency to generalized bleeding, apart from pcs with CID.

even if there are coagulation problems, the most probable cause will be specific and localized.

Symptoms more frequently reported: hematemesis, melena, proctorragia and hematochezia.

The history is fundamental: to evaluate previous episodes, familiarity with hemorrhages, alcohol,
weight loss, alterations of the alve, drug intake (salicitate, NSAIDs, anticoagulants, cortisone),
cirrhosis of the liver, portal ipt, neoplasia, MICI, coagulopathies, peptic disease .

We also evaluate previous operations in the stomach and abdominal aorta, episodes of vomiting, trauma,
angina abdominis (functional stress related to the meal, I have pain when I eat → it is similar to the
clavicicatio intermittens in the lower limbs due to the increased demand for blood), infectious causes
(typhus shigellosis, amoebiasis) and finally suspect the sd of mallory weiss for alcoholics and pregnant.

Evaluate bleeding characteristics: entity, location, modalities, specific characteristics.

The upper ones give pain, nausea, vomiting, heartburn and dysphagia.
Those inf: pain, anorexia, asthenia, weight loss, alve alteration and general state impairment.

EO: hemodynamic conditions, skin inspection, gynecomastia; palpation due to tenderness and
lymphadenopathy; percussion, auscultation and rectal exploration.

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For diagnosis it serves nasogastric tube, endoscopy (within 24 hours), rx, scintigraphy with marked
red blood cells, selective angiography.

Distal hemorrhages are needed for rectosigmoidoscopy, colonoscopy (difficult to perform urgently).
We need haemodynamic stability, otherwise angiography is necessary.
Endoscopy makes sense to do it either immediately or at the end of bleeding. It should not be
performed if there is a risk of perforation!
tp proximal haemorrhages : multidisciplinary treatment between surgeon, resuscitator,
gastroenterologist endoscopist and angioradiologist.
- nasogastric riverbed
-H2 antagonist
-ppi
-somatostatine
octreotide
tranexanic acid
-vasopressina
-embolization by superselective way

-haemostasis x endoscopically.

Surgery serves as an alternative of necessity to endoscopic or angiographic tp medicam. Indications

based on clinical monitoring. Recall that surgery has a mortality 3 times higher than the tp of
election!

It can serve a demolition (gastrectomy) or conservative intervention with direct hemostasis (suture,
ulcer excision, selective or superselective truncal vagotomy) and possible pyloroplasty.

tp distal haemorrhages : often self-limiting course and therefore need support tp.
It serves medical tp x inflammatory diseases (cortisone and mesalazine), serves antibiotic tp in the forms
of C.
Hard.

Endoscopic tp is useful for angiodysplasia and polyps (attention to possible complications!)

Angiography in 40-60% of cases due to temporary or permanent arrest.
Surgery is necessary for more or less extensive segmental resection.

Severe is the situation of rupture of varices esophageal: we place hemostatic probe (max 24 hours, it is
used in emergency when the hemorrhage is too high) and are administered vasoactive drugs
(vasopressin). Endoscopic route for sclerosis and ligature of varicose veins, treatment always in
emergency mode.
radiological tp: TIPS.
very high mortality. bad prognosis.
tp surgical: non-selective derivations to reduce portal ipt (harbor-caval, mesenteric-caval), selective
derivation (distal splen-renal), esophageal transection and sugiura surgery.

If after two sessions of sclerosing tp the picture does not resolve, angioradiological treatment or
alternatively the surgical treatment is necessary (only if the patient has an acceptable operative risk,
since the surgery has a very high mortality).

Lymphology and microsurgery

Lymphology does not deal only with lymphedema of the lower limbs: it is only the tip of an
iceberg (there are congenital malformations, or post-tumoral malformations). It serves a
multispecialistic team for the treatment of diseases of the lymphatic system.

Lymphedema can be congenital or acquired (but based on a definitely congenital

predisposition). Lymphedema involves the upper limbs after a radical mastectomy or the lower limbs for
lymphatic stasis in the interstitial space and in the collectors.
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In addition to stasis, there is a gravitational reflux due to insufficient collectors and lymph
nodes. The deficiency of the lymphatic circulation has a mixed etiopathogenesis:
neuroendocrine, post-traumatic, post-inflammatory, post-radiotherapy.

The new classification of 2001 distinguishes:

lad I : lymphangiodysplasia
lad II : linfadenodisplaisia
LAAD : lymphangioadenodysplasia

staging for the prognosis of lymphedema :

IA : latent lymphedema, not visible clinically. we see alternation with

lymphoscintigraphy. immunohistochemical alterations .
IB : initial lymphedema, which disappears with rest and clinostasis. more marked lymphoscintigraphic
alterations.

IIA : invasive lymphedema, with poor lymphatic transport and initial disability, episodes of acute
lymphangitis (because there is excellent environment for development of microbial flora), deposition
of fibrous tissue and then fibroadipose.

IIB : column limb with fibrolymphedema. Lymph-filled vesicles develop.

IIIA : elephantiasis, with scleroindurative pachydermite. disability that significantly compromises the
life of the pc.
IIIB : extreme elephantiasis with total disability.

Until IB is CURABLE pathology!

also to the pathology we see that initially there is hyperplasia of the muscular portion of the lymph
nodes, to increase the physiological "systole" of the lymph nodes for lymphatic drainage. This
hyperplasia reduces in severe forms to leave room for fibrous tissue.

Technically we use ecocolordoppler, but above all lymphoscintigraphy to calculate the drainage time
(transportation index) and microlinfography that uses indocyanine green to underline the fluorescence
to an infrared camera to see alterations of the superficial lymphatic network.

Complicated lymphangiography is used to assess where there is lymphatic reflux (soluble iodate
mdc is used called lipiodol).

The main tp is MLVA (multiple lymphatic anastomoses), performed under an operative

microscope. The negative pressure in the venous segment caused by a downstream block before the
execution of the anastomosis, causes a suction of lymph and works similarly to the outlet of the
thoracic duct into a vein. You can bring the flaps of the veins closer together to make them
continents, in case they were not.
Another technique is the lymphatic-venous-lymphatic plastic ( LVLA ), where venous segments are
taken from the basilic or cephalic vein to reconstruct dysplastic lifetimes.
Lymphatic-lymphatic anastomoses can also be associated with venous anastomoses (mlvl-ll-a).
NB: It is also useful to operate the advanced stages, they can recover some of the functionality and
improve the quality of life!

A single incision has been shown to reduce the risk of infection and it is appropriate that the incision is
proximal, because the infections are more expected distally (due to the lack of mobilization of the
immune cells to the lymph node lymph nodes).

It is also important to use larger gauge veins because they are easier to use for anastomosis.

Protocol:

phase 1: conservative of 6-12 months

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phase 2: lasts one week and includes surgery with (flla-lvsp, i.e. fibrolinfolinfoaspiration with
linphovein sparing procedure)
phase 3: 5-year follow-up with post-operative rehabilitation

The FLLA-LVSP is used in advanced stages, it is used to remove the excess fibroadipose.

We try to save venous lymphatic lesions through lymphoscintigraphy with indocyanine: we mark the
lymphatic path and the canons pass between the signs drawn on the skin before the operation, so that the
lymphatic vessels are not touched by the procedure.

nb: it is not a liposuction, but fibrolinfolipoaspirazione with sparing of the venous and lymphatic
structures, to underline that it is not a cosmetic surgery procedure.

Prof. Gianetta 12/15/2016

Tumors of the esophagus

Anatomy The esophagus is a hollow, tubularized bowel, 25-35 cm long (depending on the constitution)
with a course of S. It serves to propel the food bolus towards the stomach
It goes from C6 (cricoid cartilage) to T11, penetrates the diaphragm joining the stomach.
He stands in front of the aorta and behind the bronchi.
4 segments: pharyngoesophageal-cervical-thoracic-abdominal
3 physiological narrowings: cervical (cricopharyngeal); broncoaortic (aortic arch, main bronco
sn); diaphragmatic
Arterial vascularization: it does not have its own vascular network, so the vessels come from nearby
organs: it then receives branches from the aorta, from the bronchi, from the diaphragm, and the 1/3
receives branches from the left gastric. Venous vascularization: what you must remember is that in the
lower 1/3 there is an anastomosis between the caval system and the portal system, responsible for the
development of the esophageal varices of the submucous veins. Lymphatic drainage: the lymphatic
pathways extend longitudinally. Drena to the peribronchial, wholeortobronchial, celiac, gastric (small
curvature) lymph nodes and the upper 1/3 drains into the cervical ln.

The esophagus is made of layers: Mucosa, Sottomucosa, Muscular layer (internal circular and external
longitudinal)

( serves for propulsion), Adventitia. NO serosa !!! (It is important to remember that it does not have the
serous but only the adventitia because the latter does not protect the neighboring organs from the
invasion)

Benign tumors: benign tumors of the esophagus are very rare (less than 1% of all esophageal neoplasms).

They are:

• Leiomyoma

• Papilloma

• Polyps

they are operated because they give a compressive effect and therefore, they develop dysphagia.

Leiomyoma: (leio = smooth muscle) It is a smooth muscle tumor, is the most common among benign
tumors. As a symptom of dysphagia, which begins to appear when the tumor occupies 2/3 of the
esophageal lumen (occupies space)

It commonly occurs in the distal esophagus as a small oval neoformation.

Rx with barium, leiomyoma is seen in the esophageal lumen, the mucosa is intact,
but for mechanical reasons it can ulcer and bleed

Treatment: ENUCLEATION: you practice a little cut, take it away, and just because
the mucosa is intact we can not enter the lumen of the esophagus, and so do not
have complications such as fistulas.
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Malignant tumors: 1% of all tumors, 3% of tumors of the gastrointestinal tract. K squamous in the past
was the most widespread, because linked to tobacco and alcohol; now there is a draw with
adenocarcinoma. We need to make a distinction between the epidemiology of the north of the world,
where it is more frequent adk, and south of the world, where squamous k is more frequent.
Although the tumor of the esophagus is quite rare, it has a high mortality, it is the sixth cause of death
due to neoplasia in the world.
Squamous K has higher incidence in Black Race Males (socioeconomic conditions affect), Adk more
frequently in White males.

HISTOLOGICAL TYPES:

Squamous cell carcinoma (SCC) and Adenocarcinoma (ADK) →

95% Melanoma, Leiomyosarcoma, Carcinoid, Lymphoma. (they are
exceptional)

PATHOLOGICAL ANATOMY

Macroscopic appearance:

• Vegetation: Irregular excrescence, cauliflower foma, more frequently bleeding

• Ulcerate: hard-edged ulcer with hard edges

• Infiltrating: from place to thickening of the esophageal wall

→ why does the vegetative ulcerate bleed more frequently? Because a lesion that is vegetative must make
neoangiogenesis to develop and the vessels of the tumor are more fragile, moreover the mechanical insult
given by the food can be an ulterior cause of bleeding.

Squamous cell carcinoma: scc originates from the floor epithelium.

More frequent in the middle third (60%), and in the lower third (30%) (in the superior it is less frequent
but still possible)
Four anatomopathological aspects: Mycotic, Ulcerated, Infiltrating, Polypoid.
Adenocarcinoma : Certainly more frequent in the lower third, origins of the glands of
the esophagogastric junction , more frequent in the M, from 1970 to today has had an increase in its
incidence. In the last 20 years we have moved from a squamous cell-adenocarcinoma ratio of 8: 1 to a
current one of 1.2: 1.
Causes: - malignant degeneration of Barret's esophagus
- heterotopic islands of columnar epithelium of 1/3 inferior
- from esophageal submucose glands 8 more rarely)
from this table we can see the recurring factors of scc and adk.
SCC: above all tobacco and alcohol, caustic insults (either for suicidal or by mistake), plus is associated
with
of the rather rare syndromes: one is the palmar plantar hyperkeratosis (also called tylosis), the other is the
Plummer Vinson syndrome
One risk factor that adk and scc have in common is the chest RT for breast carcinoma

( probably because the radiations so close to the esophagus create lesions also to its epithelium). ADK:
Barret's esophagus, gastroesophageal reflux disease, obesity (because it is fdr for reflux because the
stomach is crushed by fat)

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SCC ETIOLOGICAL FACTORS: Like all malignant tumors we can return to the classic pattern
irritation, regeneration, scarring, which continued in the years ago a target cell going crazy that will then
be the cancer stem cell.

-90% of scc is associated with chronic alcohol and

smoking abuse - genetic predisposition: es tilosis
- low social status (subject only has to work and therefore gets drunk and smokes)

- Plummer Vinson syndrome: sideropenic anemia, glossitis and dysphagia because membranes are formed
on the esophagus that cause difficulty in the progression of the bolus. It is linked to iron deficiency)

Smoke carcinogens: aromatic hydrocarbons, which have a carcinogenic action on their own, but since
smoking has a high temperature it exerts an irritating action on the mucosa of the esophagus; it also
reduces the tone of SLE (predisposing to reflux disease), reduces esophageal clearance and is a
predisposing factor for chronic esophagitis.

Spirits: they contain Nitrosamines and nitroso-derived compounds, with a high carcinogenic action (which
are the same as those cooked on the grill) and are suitable for promoting action (even the sulphites are
carcinogenic). They can determine the onset of chronic esophagitis, decrease LES tone.
→ compared to a normal subject, alcohol + smoking combined together, the incidence of esophageal
carcinoma increases by 54%.

ADJ ETIOLOGICAL FACTORS:

• GERD: incidence increased 8 times in pcs with recurrent reflux present> 5aa

• Barret's esophagus: metaplasia-dysplasia of low grade-high grade-CIS dysplasia

• Therapy with beta-blockers, aminophillinics, anticholinergics (because they alter motility and
release LES)
• Obesity

• Secondary thoracic ak mammary RT

PREVENTION: if you stop smoking and drinking within 10 years, the risk level is that of a normal
person (for scc), while quitting smoking does not lower the risk of developing adk, because the risk
factors are different. Dietary change towards carcinogenic foods halves the risk of developing SCC (see
Chinese who move to America, the second-third generation have lower incidence).

Patients suffering from Barret's esophagus have to do annual endoscopy. In the West being a rare
cancer, a screening policy has not been set (as we have for example for the colon, breast or cervix), ie
the mass screening expense is not justified due to the low incidence of this type of carcinoma, while it is
justified in the East, where it is a social disease due to its high incidence → so in China and Japan is
performed endoscopic screening with brushing. In this way, early diagnosis is made: in situ carcinoma,
superficial carcinoma or intramucosal carcinoma.

INVASIVITY CHARACTERISTICS:

High biological aggressiveness: the esophagus does not have a serous cassock but only has the adventitia
that can not protect the neighboring organs from the local invasion.
Diffusion for continuity : infiltrative growth of major mediastinal structures (recurrent-
bitonal voice, bronchial tree, vascular erosion).
Also invades the lymph nodes (those of the chain that we have mentioned before), in particular the tumor
can give skip metastases, ie we can have the jump of one or more lymph node stations (for example k of
the 1/3 average can metastasize to the celiac lymph nodes) .

Hematogenous metastasis: since there is anastomosis between the portal circle and the systemic venous
circle, the mts can go anywhere, with particular tropism for lung and liver, and also adrenal gland,
kidney, brain, bone.

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 STAGING: TNM

CIS / High-grade dysplasia: mucosa

T1: does not exceed muscolaris mucosae => 5 years: 50-80%
T2: does not exceed the muscle itself
T3: overcomes the adventitia, invades periesophageal fat, but not adjacent
structures
T4: invades adjacent structures
N0: no lymph node mts
→ lymph nodes most frequently involved: mediastinal, subcarenal,
paracardial, of small gastric curvature, splenic, 1/3 from metastasis to celiac

SYMPTOMS: often remains asymptomatic for a long time, when symptoms appear is already late
Early stage: retrosternal aspecific discomfort

Advanced stage: Dysphagia (2/3 of the lumen), is present in

95% of the weight loss
Vomiting or regurgitation (prof says that vomiting is a gastric symptom rather than an
esophageal one)
Pain (spasms, infiltration)

Dysphonia or hoarseness (recurrent nerve infiltration) Cough-

pneumonia (infiltration that gave esophagus-bronchial fistula)
Dyspnea

Hiccup (phrenic nerve involvement),

drooling
Halitosis

Bleeding-anemia-melena (in the most advanced stages)

DD: Benign stenosis (benign tumors, extrinsic compressions), Caustic stenosis, Gastric fund
malignancies, Achalasia (intermittent dysphagia), Bronchogenic neoplasms.

DIAGNOSIS: Clinical examination is scarcely useful: positive only when the disease is in an advanced
stage (from the semeiological point of view it is difficult to make a diagnosis with the objective
examination of the esophagus, because it is in the mediastinum)

Every patient who complains of progressive and increasing dysphagia must, until proven otherwise, be
suspected as a possible carrier of k esophageal → EGDS with a possible biopsy. (if pz refuses to start
with a contrast report with bario)

EGDS with biopsy: fundamental, allows to localize the neoplasia, make a diagnosis of nature (tells me
that the tumor is). Multiple and deep biopsies are performed.
CONTRASTIC EXAMINATION WITH BARIUM: complementary to the endoscopic
one. Provides

Information on: Seat, Macroscopic aspect, Extension of the lesion, Presence of possible fistulosis.
EUS (ecoendoscopy): to see infiltration of the tumor (determination of T) is superior to CT for what
concerns the diagnostic accuracy (as regards the determination of infiltration). It has a limit: when there is
an obstructive tumor and the probe can not overcome it. EUS also allows to evaluate the lymph node
extension and allows to make the ultrasound guided biopsy.

In the image: 1 = mucous

2 = muscolaris mucosae

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3 = submucosa
4 = muscle

5 = adventitia

TC: to see if there are any other organs affected by the pathology, it DOES NOT allow to define the
infiltration of the wall, it is accurate for lymph node and distant mts. The abdomen and thorax are
done; sometimes also cerebral Tc (for mts)

PET: it's not always done, but it has specificity for mts, you can see well.

BRONCHOSCOPY
 THERAPY: 3 questions: Is radical intervention possible? Is neoadjuvant therapy useful? If radical
intervention is not possible, how can palliate dysphagia?
Contraindications to surgical therapy: Mts N2 (celiac, cervical,
supraclavicular); Hepatic, pulmonary, bone mts
Invasion adjacent structures (T4)
Serious comorbidity (cardiac, respiratory)

Indications for surgical therapy: Histological diagnosis of k High-

grade dysplasia in Barret's esophagus
Surgical treatment : depends on the site of the neoplasm.

Lower third → distal esophagectomy associated with proximal gastrectomy: the last piece of
esophagus and bottom and small curvature is removed
if the lymph nodes are also involved → Total esophagogastrectomy.

Two / three times: One thoracic, one abdominal, sometimes also cervical. → mixed team with general
surgeons

and thoracic that can do esophageal stripping: unstitch the esophagus and take it out of the neck.

Then the transit must be reestablished: The remaining esophagus is anastomosed to the stomach: gastro
esophagus anastomosis, gastric tubulisation (in the sleeve leave the small curvature, in the tubulization
leave the great curvature, cit Giannetta)

If we no longer have a stomach: Esophagus anastomosis Transposition

colon

Palliative treatment:

CT, RT
Laser surgery
Endoscopic dilation
Dilatation, CT, RT
Stent positioning (the most used because the most durable)

Transluminal dilatation keeps cancer cells at bay with respect to the stent, which hinders them
mechanically. It is placed with a guide wire with a spindle, which allows to spread the stenosis, on this
thread you slide the stent (possibly after dilatation with balloon, as is done for angioplasty: first inflate the
balloon to create space, then retrai balloon and insert stent).

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Ultraflex: another technique for insertion of the stent (but very specific, should not be requested in the
examination).
The stents are not medicated, they are metallic, to be incompressible, in fact they are radiopaque.

60% of Western patients are inoperable for diagnosis, but we can:

→ If locoregional disease: surgery is done followed by Ct and Rt

→ if locally advanced disease: CT and / or RT neoadjuvant, pz is among the operable because the
neoplastic mass decreases → surgery
→ if disseminated disease (t4 and / or mts at a distance): palliative therapy only

Surgical resection is the standard treatment for esophagus k.

In the last decade the 5-year survival has increased thanks to: better staging, increased frequency of
healing resections, reduction of postoperative mortality (thanks to intensive care units)

QUESTION: Is it possible to make mucosectomy in the t1 forms? Answer: no is always eradicated, it is

too dangerous to leave a cancer stem cell, also due to the high mortality of this tumor. We are not
conservative. For low-grade follow-up dysplasia, for high-grade dysplasia, it is a step away from cancer
and you do not know if close to the point where you have biopsied there is already cancer) (quite the
opposite of what Camerini told us last year in gastro ... boh)

K is a degenerative disease, at one point a cell goes crazy.

If the tumor is 1/3 higher, esophagectomy should be performed

if 1/3 lower remove 2/3 of the esophagus and proximal part of the
stomach if 1/3 medium remove from the azygos vein

Functional diseases of the esophagus

The esophagus is subdivided into cervical, thoracic and abdominal. They are distinguished: the
esophageal sphincter
upper (UES: Upper Esophageal Sphincter), the esophageal body, the lower esophageal sphincter (or
LES:
Lower Esophageal Sphincter).
Upper esophageal sphincter: It consists of the cricopharyngeal muscle (innervated by the vagus nerve), to
remember the Killian triangle, positioned on the posterior wall of the esophagus, and is delimited
inferiorly by the cricopharyngeal muscle, superiorly by the inferior constrictor muscle of the pharynx,
which represents the more frequent place of formation of the faringoesophageal diverticula (it is the point
of least resistance). All people have the triangle of Killian, but fortunately not all have the esophageal
diverticulum → this because in order for the diverticulum to form, there must also be a pathology of
esophageal motility.

Body of the esophagus: The passage from the smooth, pale, squamous epithelium of the esophagus (pink-
silver color) in the cylindrical epithelium of the stomach (intense red color) forms a sharp demarcation
line, with a zig-zag pattern, called , in the endoscopic terminology, Z line.

Lower esophageal sphincter: The esophagus-gastric junction is the only area of the digestive system in
which

two types of pressure can coexist: the negative thoracic and the positive one of the abdominal cavity. The
sphincter thanks to its 12-30 mm hg tone makes sure that the gastric contents are not sucked into the
esophagus. An absolute anatomical correspondence of the LES is not recognized but more mechanical
structures are recognized that maintain the sphincter tone:
- the "pinza" action of the right diaphragmatic pillar at the esophageal hiatus (Allison's lasso);
- the acute angle of His: esophagogastric and the gastric bubble;
- the valve action of the "rosettes" of the mucosa (valve of von Gubaroff);

- the brake-esophageal membrane of Bertelli;

- the action of the right gastric artery;

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- the abdominal positive pressure on the sub-diaphragmatic tract of the esophagus.

ESOFAGEI DIVERTICLES: they are out of the esophageal wall, based on a more or less wide implant,
communicating with the lumen of the organ. We distinguish them in:

• true: the whole wall participates in the saccular formation (including the muscular)

• false or pseudodiverticoli: the muscular component is missing and therefore they are formed only
by

mucosa and submucosa.

This classification links the diverticulum structure with the diverticulum formation mechanism itself
As for the location, they can be:
Hypopharyngeal (Zenker)
III ° superior; Parabronchiali /
Middle III; Epiphrenics / III ° inferior.
As for the etiology, they can be: drive and drive.

A typical example of drive diverticulum is the ZENKER diverticulum: it is the most frequent esophageal
diverticulum, in 65% of cases. It is formed at the level of the posterior wall of the esophagus in
correspondence with the Killian triangle (where there is less resistance) by instinct → there is a missed or
inadequate opening of the LES or for increase of peristaltic waves during the swallowing phase, which
causes a pathological increase in intraluminal pressure.
Traction dividerticles, typical example PARABRONCHIAL diverticoli: the force that intervenes is
external,
that draws. They are made for: cicatricial outcomes of previous peribronchial lymphoadenopathies
(species as outcomes of TB processes). In fact, when they are inflamed they stick to the wall of the
esophagus, then when they go to the fibrosis phase they retract and carry the esophagus with them.

They represent 15% of all diverticula of the esophagus and are often asymptomatic.

ZENKER: develops at the level of the posterior wall, initially it is directed towards the lateral position, on
the left, as behind there are the vertebral bodies, and in a second moment, when it is enlarged again, its
axis will go parallel to the greater one of the esophagus, descending towards the mediastinum. Pills will
initially feel dysphagia and halitosis, then when the diverticulum grows it may gradually compress the
esophagus, and when it becomes a sac the symptoms are represented by the pneumonia ab ingestis due to
the reflux of material from the diverticulum into the bronchus; this happens above all in the night when
the tussigenous reflex is less. Then over time diverticulum may undergo the inflammatory complication =
diverticulitis, which can lead to perforation of the diverticulum -> mediastinitis.

PARABRONCHIALS: while the diverticulum of Zenker can reach large dimensions, the parabronchial
ones due to their formation mechanism tend to remain small and can also be multiple.

EPIFRENIC DIVERTICLES: they are not frequent, only 20%, belonging to the type acquired by the
drive: missed or inadequate opening of the cardia, associated with diffused esophageal spasm or distal
spasm, secondary to gastroesophageal reflux.

SYMPTOMS:
It can be found occasionally.
→ Dysphagia: episodic for solids and / or liquids In Zenker there is the so-called dysphagia of the
third bite: after three mouthfuls the diverticulum is filled and the symptoms are felt, he himself with
manual maneuvers manages to continue swallowing.

→ fetor ex hours (fermentation of foods)

→ sialorrhea and sign of the pillow

→ food regurgitation
→ respiratory app: repeated bronchitis due to ab ingestis phenomena

DIAGNOSIS: remember when there is dysphagia you must make sure that the cause is not organic

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Dg is mainly Clinic (especially in Zenker)

Endoscopic (when it is necessary to do biopsies but pay attention to danger of perforations);
Radiological (esophagography: better to associate it with the study of the stomach, to check for the
presence of reflux and / or hernia jatale);
Manometry (document: the absence of primary peristaltic waves, the failure to release the SLE or its
hypothesis), you must discover the underlying cause of diverticulation formation;
pHmetry (documents the presence and duration of an abnormal pH in the esophageal site)

COMPLICATIONS: Complications: Inflammation, Hemorrhage, Perforation

THERAPY: it is recommended if the diverticulum is symptomatic and if it is large, and it is a therapy

CHIRUGICA!
→ Complete longitudinal subdiverticular myotomy with open stapler + Excision of diverticulum
→ endoscopic treatment with stapler (= cut-sew)

This surgery is apparently simple, but it must be taken into account that when the patient arrives at the
surgical treatment, he is defeated because he has not been eating for months.

Achalasia

Altered lower esophageal sphincter (LES) during swallowing, present at all ages but more frequent
between 30 and 50 years, especially in the female sex.
Etiopathogenesis: Primum movens is unknown. A reduction of the myenteric plexus neurons of Meissner
and Auerbach was observed at the LES.
All the motor mechanics of the esophageal wall is altered: absence of primary peristaltic wave, inefficient
tertiary peristaltic waves, lack of opening of the lower esophageal sphincter with obstacle to the normal
transit of the food bolus. At the beginning there is hypertrophy of the esophageal musculature to
overcome the resistance, then later there is a failure of the wall, esophageal dilatation, up to the
megaesophagus:
Phase I: Normal esophageal wall with hypertrophy of the muscular tunic of the lower esophageal
segment
Phase II : Initial dilatation of the esophagus upstream of the hypertrophic tract
Stage III: Massive expansion of the esophagus with thinning of the muscular tunic and of
the mucosa. Until you get to a "tissue paper" esophageal wall.

SYMPTOMS: dysphagia is a cardinal symptom, in 'achalasia dysphagia is paradoxical, ie it is greater for

liquids than for solids, this is because solid foods are able to develop greater pressure on the LES and
then to pass, while the liquids fail. In fact, they tell us that they have to eat and drink together. It is not
said that dysphagia is worsening (dd with neoplasia). There is alternation of periods of exacerbation and
remission, also in relation to the psychic state of the pc.

Another symptom is regurgitation, although it is not always present especially in the initial stages.

At the onset of the disease, dysphagia is often accompanied by odynophagia (strong chest pain, dd with
angina pectoris), but in the more advanced phases when we have the exaggeration of the esophagus, the
odifagia is lost; remains dysphagia that will be increasingly severe and persistent + regurgitation + weight
loss + anemia + signs of respiratory compromise (bronchitis and pneumonia ab ingestis)
Diagnosis
- Chest X-ray: enlargement of the mediastinum

- Esophagography with barite meal: useful in the later stages of the disease: mouse-tailed esophagus and
mega-esophagus (increased diament)
- Esophagoscopy: Reveals the atony and the distension of the wall, It highlights the gravity of an
eventual esophagitis
- Manometry: (first choice test for diagnosis !!) Failure to release the LES, absent primary peristaltic
waves

Complications
Generals: Slimming, Anemia, Caches, Chronic bronchitis, Pneumonia ab ingestis, Abscess
pulmonary,
Local: Esophagitis (→ chronic ulcers → cancer); Bleeding; Perforation (→ mediastinal abscess
paraesofageo)

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Therapy
Medical: Nifedipine: Calcium antagonist that prevents the contraction of LES
Pneumatic expansion: Probe + dilatable balloon that wins the hypertonus. (risk of complications:
laceration of the esophageal wall, cardiac incontinence with reflux oesophagitis)

These work in the early stages of achalasia, when these tp are no longer sufficient to see the type of
patient we have before: if you can tolerate the surgery, if you have long life expectancy, etc.

we can do: Intraparietal infiltration of botulinum toxin: cause flaccid paralysis of SLE, must be repeated
every six months. However, if the patient is young and without significant comorbidity, surgery is the
most appropriate choice: Longitudinal extramucose cardiasmotomy according to Heller + Nissen
antireflux plastic (that is, it affects the muscle so remove the resistance, and to avoid iatrogenic reflux,
make plastic).
Access routes: thoracic, laparotomic, laparoscopic (recommended)
From 2013 in Japan: POEM = catheter in the esophagus, submoducosal tunnel is created, Les cuts, go up
the tunnel, close with metal clips. It seems that the effectiveness of the intervention is comparable to that
of Heller's intervention and without having to add the anti-reflux plastic.
Gastroesophageal reflux disease (GERD)
It is a syndrome, therefore a set of signs and symptoms, caused by the reflux of gastric material in the
esophagus. This in most cases is acidic, but there are also some cases in which it is alkaline (for example
after gastrorenection). Being a syndrome all these pictures are characterized by the same
symptomatology, but the basic pathologies can be varied and it is important to correctly frame in which
situation we find ourselves in order to establish an adequate therapy.

MRGE arises when the physiological balance between aggressive and protective factors is altered in
favor of the former, allowing prolonged contact of the gastric origin material with the esophageal
mucosa.

AETIOLOGY:

• Congenital short esophagus (true Brachiesophagus);

 • Hiatal hernia;

• Primary hypotonia of the SEI (LES);

• iatrogenic insufficiency of the SEI (LES) after cardioplastic and / or corrective myotomies of
achalasia);

• Heterotopic islands of gastric mucosa in the esophagus;

• Scleroderma;

• Obesity;

• Chronic cough;

• Chronic constipation.

• Pregnancy

• Food: tea, mint, dark chocolate

ERNIA IATALE: Commitment of a more or less conspicuous part of the stomach through the
diaphragmatic esophageal hiatus.
Classification:

I) Hernia with brachiesophagus:

True: congenital short esophagus. It is usually a reducible acquired retraction of the esophagus in the
mediastinum.
II) Hernia for rotation (Paraesophageal) : The gastric bottom rotates around the jatus towards the
mediastinum. The cardias remains sub-diaphragmatic, the angle of His is maintained
III) Sliding hernia : Intrathoracic sliding of cardias and gastric bottom. The acute angle of His and the
intra-abdominal esophagus part disappear → the mechanism of continence against reflux is lost.

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Pathophysiology

- Lower esophageal sphincter dysfunction (LES) : Most (60-70%) of reflux episodes are correlated with
transient, spontaneous and inappropriate SLE releases, not evoked by swallowing. Diaphragmatic
straps: The presence of a hiatal hernia prevents the diaphragm pillars from correctly opposing intra-
abdominal pressure increases.
- Esophageal clearance from acid : An insufficient esophageal peristalsis and an alteration of salivary
secretion cause a prolonged contact time between the gastric material and the esophageal
mucosa. Lesensive agents and resistance of the esophageal mucosa

- Lesensive agents and resistance of the esophageal mucosa: Gastric acid, bile salts, pepsin and pancreatic
enzymes cause damage to the esophageal mucosa, causing a diminished efficiency of the epithelial
barrier. Esophageal mucosecernyl glands play a protective role against harmful agents, especially during
sleep.
- Gastric emptying : A delayed emptying of the stomach, with acid retention and food for a long time in
the lumen, is an important factor in the pathogenesis of GERD.
- Gastric duodenum flow: (It is due to an alteration of the antro-pyloroduodenal coordination.The role of
duodenal-gastric reflux is controversial)

COMPLICATIONS:
1) Reflux oesophagitis: (reflux disease is divided into erosive and non-erosive, and the patients with
macroscopically evident lesions are only 20%)
CLASSIFICATION OF SAVARY (endoscopic):
-I ° GRADO: erythemato-edematous esophagitis
-II ° GRADE: ulcer-hemorrhagic esophagitis
-III ° GRADE: scleroprophilic esophagitis
Lesion due to chemical irritation of the esophageal mucosa following contact with gastric and / or
alkaline duodenal acid (for achlorhydria, atrophic gastritis, after gastric surgery, etc.). It is indicative of
MRGE.
2) Barret's esophagus
3) Hemorrhage

4) Stenosis

SYMPTOMS:
Typical symptoms : Pyrosis, Regurgitation, Dysphagia, Chest pain (retrostenal pain), Belching,
Nausea, Odinophagia.
Atypical symptoms: Anemia, Hematemesis, Asthma or respiratory diseases, Hoarseness, Chronic cough,
Laryngitis or laryngospasm, Granulomas of the vocal cords, Loss of dental enamel, Otalgia.
PPIs act well on typical symptoms, but not on atypical ones

DIAGNOSIS:

• endoscopy should always be done not so much to make the diagnosis of reflux but to do biopsies
to rule out the possibility that there are complications.

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• Impedenzometry : tells me the moment when there is fluid passing through the
esophagus. Measure the impedance that is the inverse of the conductivity. You put a catheter in
the esophagus for 24h and when there are liquids in the esogago the impedance collapses.
• pH-metry, documents the presence and duration of abnormal pH in the esophagus. Reeds can be
performed in 24h
• manometry, documents the hypothesis of LES

THERAPY:

• behavioral and dietary tp: if obese lose weight, do not go to sleep before 3 h after meals, sleep with
the head up, avoid the foods that stimulate reflux
• tp medica: PPI → acting on typical symptoms, will be taken for life because the effectiveness in
reducing the symptoms is 90%, but the relapses to 6 months from the suspension occur in 65% of
cases. They are well tolerated drugs, but they can give problems for example to the patients in
renal failure. (other drugs: H2 antagonists, prokinetic)
• tp surgical: it is indicated when: medical tp fails, young people who do not want to take drugs

for life, and for patients who have problems taking medication
NB: criteria of rome 2015: definition of Functional Pyrosis : these are gastroesophageal reflux without
the presence of acid in the esophagus being documented, all the diagnostic tests are negative, and
functional pathology. In these PPI patients do not work and therapy should be performed with tricyclic
antidepressants and serotonin re-uptake inhibitors. These patients should NEVER go to surgery, it would
be useless if not harmful.

SURGICAL INTERVENTIONS: nowadays they are almost always done in Laparoscopy. Plastics can be
total or partial:

• NISSEN (total) there are several variations: creation of a valve that rotates around the esophageal
body of 360 ° to recreate a sphincter continence. Then the transfection of this valve is made to the
esophageal body itself in a space of 5 cm with 5 points
• NISSEN-ROSSETTI: transfection on the gastric bottom and not on the esophageal body

• FLOPPY NISSEN: it is the one you use most today, here the cm is 2 instead of 5.

An important thing to do during these interventions is to use intraesophageal catheters that measure the
pressure before and after the plastic, so as not to tighten too much and thus avoid iatrogenic
dysphagia. The complications of these total plastics are dysphagia and the bloat syndrome (ie the
impossibility of expelling gas with belching). Dysphagia after surgery may be early and late, the early
one usually resolves itself within a month

• TOUPET (partial): plastic 270 ° on three points

• DOR (partial) always on three points, with front access, is the most used by thoracic
surgeons. Complications such as dysphagia and bloat syndrome are less common with partial
plastics.

The therapy of reflective cicatricial stenosis consists in the endoscopic dilatation of the esophageal lumen
(with the associated antireflux plastic intervention) or, alternatively, the transluminal esophagoplasty with
balloon catheter. Barrett's esophagus therapy is anti-reflux plastic. In inoperable cases, or if the pc. refuses
surgery, strict surveillance is required with periodic endoscopic examinations (¾

months) associated with biopsy.

Hiatal hernia is operated when by large symptoms, with anti-reflux plastic.

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16-12-16
Prof.Boccardo

Preparation for intervention and risk factors for the elderly

The surgical risk in the elderly pc (age> 65 years) is a very important issue, considering the increasing
life expectancy, but at the same time, also the possible comorbidities that can present this type of
piece. Surgical risks can be related:
• at the age and therefore the deterioration of pulmonary, cardiovascular, renal, nervous and nutritional
functions
• surgery and medications: - adjustment - postoperative analgesia (the choice must be optimal,
considering, for example, the effect of opioids on the respiratory system) - effects of infusions,
therefore pay attention to the hydro-electrolyte balance - drug administration - effects of intensive care
(increased risk of contracting infections!)
COMPLICANCE PREVENTION

• screening of any cognitive deficits (ask yourself, for example, whether a cognitive deficit is due to a
pharmacological effect or if the patient already had a deficit in the anamnesis); possibly eliminate drugs
that can cause cognitive dysfunction (sedatives for example)

• evaluate nutritional status by providing adequate caloric intake; so-called clear liquids (physiological,
Ringer) should be administered generally for 1-2 days after surgery, then it should be switched to a
parenteral supply or, if the patient is able, even by mouth

• to perform a thromboembolic prophylaxis (antithrombia socks) and intestinal hemorrhage

• insert an antibiotic prophylaxis

• prepare an early physiotherapy (even with simple walking) to avoid respiratory and
cardiovascular complications of entrapment
• early discharge

• adequate home care; possibly rely on structures like the rsa.

In the senior pc it is fundamental to carefully evaluate the real indication to the surgical treatment:
conditions exist, some of which are non-surgical and not intra-abdominal or, if intra-abdominal, not
subject to surgery, which can cause abdominal pain and confuse with an acute abdomen (so-called false
abdomens) There are numerous causes that can lead to a false abdomen:

hereditary diseases infectious diseases acute porphyria intermittent mononucleosis angioneurotic edema
of quinck herpes zoster fever mediterranean adenitis mesenteric idiopathic hyperlipemia hepatopathies
infectious ileitis follicular endocrinopathies collagen diseases diabetes purple schoenlein enoch addison
disease les hyperparathyroidism panarteritis nodosa hyperthyroidism
Hematological affections malaria reflex pain with cardiac starting (ima involving neoplasms of the red
and white series of the ventricle, leaning on the paroxysmal diaphragm hemoglobinuria, can cause
epigastralgia)
at the start of the CNS or SNP at pleuro-pulmonary start (embolism) at renal origin
The clinical features of the false acute abdomen are:
• lack of pain in an elective location
• Negative Blumberg

• lack of defense contracture of the abdominal wall

• not frank paralytic ileus
In contrast, the indications for an urgent surgical intervention are:
• signs of peritoneal infection

• localized, severe or persistent pain from more than 6h or more severe

• association of pain with fever, hypotension, pallor or tachycardia

• significant differential (> 1 degree) between axillary and rectal temperature

• presence of metallic noises at abdominal auscultation

• progressive abdominal distension (referable to a single quadrant for the volvulus or to the entire
abdomen in case of occlusion)
• deterioration of the general conditions
IMPACT OF FALSE ABDOMEN ACUTE SURGICAL TREATMENT •
increased mortality

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• increase in morbidity
• increase in resignation by sending to RSA

• increase in days of hospitalization

• increase in the use of complex diagnostic investigations

• increased use of plifarmacotherapies with possible side effects and antibiotic resistance
Access to the PS for acute abdomen is about 7% of the total. In 42% of patients over 65 it is
actually a false abdomen and of these
1) 37.5% are subjected to an exploratory laparotomy THERAPEUTIC 2) 31% are false abdomens
acute for splanchnic diseases resolved with NON-SURGICAL therapy 3) 32% are false acute abdomens
for NON SPLANCNIC affections

In front of a situation of possible acute abdomen not well framed by the instrumental examinations, the
surgeon can decide to perform an exploratory laparotomy. Exploratory laparotomies can be divided into
3 categories:
• therapeutic or a procedure that confirms the diagnosis and allows the surgical treatment of the
pathology at the base of the acute abdomen
• non-therapeutic or a procedure that allows the diagnosis of the responable pathology of the acute
abdomen, but this condition would not require the intervention
• negative or a procedure at the end of which it is not possible to find any cause that justified
the acute abdomen
The set of non-therapeutic and negative laparotomies is called white laparotomy.

To prevent the elderly patient from the risks of a laparotomy (which could turn out to be white), the
causes of the possible acute abdomen must be correctly and comprehensively investigated, through:
• clinical evaluation (anamnesis and eo)
• laboratory tests

• first level investigations (RX, ultrasound)

• second level investigations: TC (it is essential not to stop at the first level examinations, at least in
doubtful cases); ANGIOTC is used in the suspicion of a mesenteric ischemia
• laparoscopy (also therapeutic)
ERNIE

They represent the spillage of a viscera or part of it, covered by its integuments, from the cavity in which
it is contained through an area of weakness of the wall, an orifice or a natural canal. It is estimated that
about 5% of the population may suffer from this disease, especially elderly subjects (less resistance of the
muscular structures) and in pediatric age (congenital hernias). We can distinguish:
• congenital hernias ---> result from stopping the development of a part of the abdominal wall

• acquired hernias ----> develop in areas of limited weakness as a result of increased intra-
abdominal pressure.
We can also make a further topographic subdivision:
• front hernias: epigastric (also called hernias of the alba line)

inguinal umbilicals 90% cases in the crude male sex 85% cases in the female obturator
• posterioro-lateral hernias:
schiatic lombarii The predisposing causes of
hernia formation:
• congenital malformations (pervency of the peritoneo-vaginal duct)

• pregnancy (especially umbilical hernias due to increased intra-abdominal pressure)

• hereditary factors (abdominal wall weakness)

• rapid weight loss

The determining causes, however, are:

• efforts that increase intra-abdominal pressure (crying, coughing, defecation, weight lifting)
• massive ascites

• chronic respiratory failure

• traumas of the wall

Examining the conformation of a hernia, it is possible to recognize different anatomical portions: the port is
the orifice from which the viscera emerges, whose margins are called pillars; the path is the path that follows
the hernia (if the viscera engages in a channel, the hernia tip is further distinguished if only the inner ring is
engaged, the interstitial hernia if it stops in the canal, the complete hernia if the outer ring is exceeded). The

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sack is the lining of the bowel, extroflection of the peritoneum parietele with adherent accessory
envelopes (muscle tissue, aponeurotic, connective tissue, adipose tissue). In the case in which to herniate
is a viscera partially covered by peritoneum (the cecum, for example) we speak of slipping hernia. The
contents of the hernia can be represented potentially by any organ, except those fixed in the
retroperitoneum.
An important concept is the REDUCIBILITY, or the possibility to reposition the contents of a hernia in
the abdomen; It is possible through the reduction maneuver for Taxis, which provides to exert a gradual
pressure with the fingers on the hernial swelling, starting from the periphery up to the center (the pc can
be both in clino and in orthostatism). On the contrary, IRRIDUCIBILITY may be due to a very large
volume of the hernia or the formation of adhesions between the viscera. We talk about
INCONTINIBILITY if the viscera, repositioned in the abdomen, come out again in orthostatism or after
the minimum effort. We identify the main complications that can affect a hernia:

• incarceration: irreducible following the formation of adhesions between content, bag and hernia

• throttling: can occur after exertion or without apparent cause. It is determined by the constriction of the
vascular pedicle of the herniated viscera in the door, resulting in an obstruction to the blood and lymphatic
circulation ----> the consequence is the gangrene of the content that can lead to phlegone piostercoraceous
and peritonitis. Hernia is irreducible with live and spontaneous pain, mechanical ileus and, with the onset of
peritonitis, a reflex paralytic ileus. They occur more frequently in hernias with a rigid hernia (crural,
umbilical, epigastric). The hernial throttling is an acute event that significantly increases the incidence of
morbidity and pre and postoperative mortality and can be manifested in various ways: 1) strangulation of
afree loop 2) throttling of the antimesenteric wall of the bowel (or Richter's hernia) 3) retrograde or W-
choking involving more non-herniated loops but dependent on the same vascular pedicle 4) throttling of a
sliding hernia NB if we have a complication vascular misunderstood and proceed with a Taxis maneuver, we
can risk to bring back into the abdomen a portion of the intestine that ischemic ----> the risk is the breaking
of the loop with consequent peritonitiswe can risk to bring back a portion of the intestine into the abdomen
which however is ischemic ----> the risk is the breaking of the loop with consequent peritonitiswe can risk to
bring back a portion of the intestine into the abdomen which however is ischemic ----> the risk is the
breaking of the loop with consequent peritonitis

• clogging: accumulation of intestinal contents in the hernia loops that can not progress into the lumen ---

> mechanical occlusion. If it is not reduced with the reduction maneuver according to Taxis, emergency
intervention is indicated
• inflammation: acute (rare) caused by violent or chronic trauma (more frequent) due to small traumas or
bacterial infection
• rupture: rare complication due to severe trauma that can cause a loop to burst.
INGUINAL ERNIES

The inguinal region, shaped like a triangle, is delimited on three sides:

1. from the lateral edge of the rectus abdominis 2. from an ideal line drawn between the
upper anterior iliac spine and the lateral margin
rectal muscle 3. from the inguinal ligament (or Poupart ligament), which extends from the iliac
spine
anterior superior to the pubic tubercle The so-called Malgaigne line corresponds superficially to the
inguinal ligament and divides the inguinal area from the crural area
The inguinal canal is a virtual structure (therefore better called inguinal route) that crosses the abdominal
wall with an oblique course directed in a postero-anterior direction downwards and medially. In the adult
it is about 5 cm, flattened with walls:

• front consisting of the band of the external oblique bar

• posterior constituted by the transversal band

• superior formed by m. internal oblique and m.tasverso (joint tendon)

• lower which corresponds to the upper face of the inguinal ligament The internal inguinal ring is
constituted at the top and laterally by the aponeurosis of the m. transversely and from the internal oblique
point, while the external inguinal ring is formed by the fibers of the aponeurosis of the external oblique.

Inside the inguinal canal, the spermatic cord (surrounded by the external sperm fascia and the cremaster) is
formed in the man: the vas deferens, the deferential artery, the external and internal sparmatic artery, the
pampiniform venous plexus, the lymphatic vessels and the nerves. genito-femoral and ileo-inguinale) that
passes from an intra-abdominal position to a subcutaneous position in the scrotal bag. In its migration through
the inguinal canal, the testis is accompanied by an extroflection of the peritoneum that forms the vaginal
peritoneum duct, whose incomplete obliteration is due to the origin of congenital inguinal hernias and of the
hydrocele.

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In the woman, the round ligament runs and the peritoneum is extracted (Nuck's canal), whose incomplete
obliteration is at the origin of the external oblique congenital hernias and of the Nuck canal cysts. From the
inside of the abdomen, the inguinal region presents 3 folds (residual of the urachus, residual of the
umbilical artery and inferior epigastric vessels) converging from the pelvis towards the navel which delimit
3 dimples:

1. external inguinal (corresponds to the internal inguinal ring) where external oblique inguinal
hernias are formed ----> they can occupy the inguinal canal entirely or only a portion (hernia tip) 2. mean
inguinal where hernias are formed direct inguinal ----> due to the weakness of the back wall of the
inguinal canal in the Hasselbach triangle where the only support is formed by the transversalis fascia. It
usually increases slowly in volume and does not reach large dimensions. Sometimes it is bilateral and
when it is associated with an external oblique ipsilateral hernia, it is called a pant hernia. Since the hernial
gate is wide, it is unlikely to be throttled, however special attention must be paid to the section of
thestrangling ring due to the presence of the epigastric vessels 3. Internal inguinal where internal oblique
inguinal hernias are formed ----> they exit medially to the muscular involvement, are infrequent and
rarely choke; may contain adipose tissue, the bladder or its diverticulum.
SYMPTOMS: swelling that protrudes through the abdominal wall covered with integuments, is neither
painful nor painful, but is described as a sense of weight, strain or discomfort at the site of the swelling.
Sometimes completely asymptomatic and reduced in cavity from which it escapes only after exertion (in
these cases, with a glove introfletto the swelling in the inguinal canal and I ask the patient to cough ---->
I feel an impulse coming from the swelling: in the external oblique hernia I appreciate it with the tip of
the finger, in direct with the first and second phalanx, in the internal oblique the impulse is medial).
DIGNOSIS: on anamnesis and objective examination in orthostatic position and then supine
decubitus. On palpation, if there are no complications, the hernia is of soft consistency and if it contains
intestine, parenchymatous if it contains epiploon. You can also appreciate the continuity of the hernial
gate with the intestinal wall. At percussion, tympanism if the intestine is spread by gas, otherwise
dullness. Arrange an ultrasound for possible differential diagnoses Transillumination: in the adult the
hernia is opaque, unlike the hydrocele which allows the light beam to pass through.
THERAPY: surgical therapy that includes:
• inguinal canal opening

• isolation of the funiculus in humans (no particular attention is required in isolating the round
ligament in the woman)
• isolation of the hernial sac, its opening, verification and reduction of the contents in the abdomen,
binding of the bag to the collar and exeresis of the bag. If the hernia is throttled or clogged, incision and
debridement of the throttling cercine (chelotomy)

• closure of the hernial door Intervention must be done urgently if there is clogging,
choking or breaking of the hernia.

If the viscera have irreversible lesions (ischemia which has been translated into necrosis), resection
should be performed.
SURGICAL TECHNIQUES: according to Bassini: the technique is based on the creation of a triple
layer, consisting of external oblique m, transverse m of the abdomen and transverse fascia, which is
fixed to the inguinal ligament with 4 or 5 stitches. With the first of these points, the upper one, the upper
inguinal ring is reconstructed. Subsequently we proceed to the suture of the aponeurosis of m. external
oblique, which occurs on a more superficial plane and, with the last point, the lower one, the lower
iguinal ring is reconstructed. Other surgeons proposed special techniques (Postemski and Shouldice) up
to the helioplasty, or repair of the hernia with prostheses. Using the inguinal way, Liechtenstein,
beginningto use a polypropylene mesh (net) as a reinforcement for plastic surgery. The next and
definitive step was to completely eliminate the sutures between different muscles and aponeuroses
(cause of tension, responsible for pain and scarring anomalies) leaving them exclusively for anchoring
the net. Thus the concept of tension free hernioplasty was born, because it is based exclusively on the
positioning of a reinforcement prosthetic network. This technique, performed as an outpatient procedure,
reduces recurrences and eliminates the deleterious consequences related to bed hospitalization,
reinserting the patient in his social and working environment. Intervention according to Trabucco: this
author contributed to the further evolution of the inguinal hernia alloplasty by introducing the concept of
"suture less",or complete abolition of sutures. In its technique the mesh is inserted into a pocket obtained
above
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of the transversalis fascia without it being necessary to fix it with stitches. The weak point
corresponding to the internal inguinal ring is closed with a poly plug (plug) always in
polypropylene. Videolaparoscopic hernial plastic is indicated in bilateral and recurrent hernia, but
requires general anesthesia and one day hospitalization, but reduces post-operative pain and a more
rapid recovery. (by laparotomy, local anesthesia can be used or, if the hernia is bilateral, spinal
anesthesia, but the benefits of laparoscopy are lacking)

CRUNAL OR FEMORAL ERNIES

Particularly frequent in the female sex, they occur in the crural region where the abdominal wall is
characterized, for anatomical reasons, by a constitutional weakness. They must be diagnosed
differentially with inguinal hernia, with a crural lymphadenomegaly, with a saphenous varices or a
femoral artery aneurysna. In their path, they appear medially to the femoral vein. The treatment is
surgical: through the crural route with incision on the tumefaction, opening of the sac, reduction of the
viscera, ligation and excision of the same bag, closure of the hernia portya approaching the ligament of
Cooper to the inguinal ligament. Inguinal incision with inguinal incision, inguinal canal opening,
incision of the transversal fascia, reduction ofherniation and closure of the door by suturing the inguinal
ligament to the Cooper ligament.

OMBELICAL ERNIES

They can be presented in neonatal or adult age:

• embryonic hernia or omphalocele due to abdominal wall aplasia due to developmental arrest. The
hernia is present at birth, the viscera are covered by amnios, and the parietal peritoneum is absent (it has
no sac). It is very serious if extensive and it is not possible to reduce the viscera in the abdomen (loss of
the right of residence)

• fetal hernia present at birth appears as a funneling defect of the centric part of the wall; originates from
incomplete closure of the wall, therefore the viscera are covered only by peritoneum.
• Neonatal umbilical hernia is covered by skin and occurs within a few weeks after the fall of the
umbilical cord; It is due to defective adhesion between the cicatricial residues of the cord and the
umbilical ring. It is easily reducible and tends to heal spontaneously by applying a compressive pad,
normally it is asymptomatic.
• Adult umbilical hernia are most often expressed in the upper porzoione of the umbilical ring; small and
asymptomatic, they tend to increase in volume. The overlying skin is thin and shiny, tends to ulcer and
become infected. It tends to get jammed and choked even if it is small. Generally it is a direct hernia, that
is, it engages directly in the umbilical channel.
HARMONIES OF SPIGELIO OR SEMI-SEED

Infrequent, usually acquired, located at the point of least resistance of the posterior fascia of the rectus
muscle (shorter than the anterior fascia), which creates a sort of half-moon. The sac usually remains
below the aponeurosis of the external oblique m edge, confined in the thickness of the wall.

EPIGASTRIC ERNIE
They prefer adult age and male sex, manifesting along the dawn line between the ensiform apophysis and
the navel. They start as a protrusion of fabric in the orifice of passage of a flattened vessel from the age
and the increase of the abdominal pressure. In addition to fat, a hernia containing omentum and
sometimes intestinal loops can come out. They present a complete hernial sac often asymptomatic and
misunderstood. They easily face incarceration and bottleneck.
ERNIE LOMBARI

The male and the right side of the body are more affected. They are very rare hernias of variable
volume that develop in the context of:
• Petit triangle (lower lumbar hernia) delimited by the dorsal m, external oblique m and iliac crest
• Quadrilateral of Grynfelt (lumbar or superior lumbar hernia) delimited by the lateral margin of the
spinal mm, and of the squared m of the loins, from the posterior margin of the external oblique mullion,
from the XII rib and from the inferior margin of the inferior posteratum. They can be congenital or
acquired, making their way into an area of weakness at the point of passage of vessels and nerves. It
may contain omentum or intestine preceded by lipoma. It appears as a swelling and lumbar pain
ERNIE OTTURATORIE

The obturatory channel (osteofibroso duct located under the ileopubic branch) has a length of 2cm and a
diameter of about 1 cm delimited by: superiorly from pubic bone inferiorly from obturator membrane and

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mm shutters. It is a rare hernia that is observed in elderly women (greater amplitude of the pelvis and
obturation canal for pregnancies and hypotonia of the pelvic muscles). A pelvic bowel (bladder, tuba,
ovary, large intestine, large omentum) is contained in the hernia sac. It is usually small with often sudden
symptoms with intestinal obstruction accompanied by pain in the medial side of the thigh, which is kept
bent in an attitude analgesic. Diagnosis is difficult in the uncomplicated forms due to the lack of
pathognomonic local symptoms; if it is choked, the clinical picture of the occlusion appears with
spontaneous pain and palpation of the Scarpa triangle.

ERNIE RARE

Ischial Hernia: the sac exits from the pelvic cavity through the ischial foramen and is projected into the
gluteal region remaining covered by the gluteus maximus m. The content consists of omentum and
intestine and may undergo a peristal Ernie constriction: an abdominal bowel outflow from the pelvic
floor. It makes its way into congenital weaknesses: posterior between m ischiococcygeus and ischial part
of the anus elevator; anterior to the front of the deep perineum transverse m Typically in the woman in
relation to the laxity of the pelvic floor for pregnancy and childbirth Rare the strangulation for the laxity
of the structures surrounding the sac.

INTERNAL ERNIES

Abnormal dislocation of one or more viscera into natural recesses of the peritoneal cavity
• Congenital (make their way through abnormal orifice of ligaments or abdominal months and have no
sack): omental purse hernias
 hernia del recesso duodenodigiunale hernias of the
retrocecal recess hernias of the intersigmoid recesses

• Acquired early or late complication of asymptomatic surgery or with vague abdominal pain,
dyspepsia and irregular brow
Frequent complication is the strangulation with sudden appearance of intestinal mechanical occlusion
incisional hernia

Abdominal viscera spillage through a muscle-aponeurotic breccia of the wall, in correspondence of a

previous surgical wound. Postoperative complication occurring in 2% of laparotomies Frequent after
wound infection (50%) which causes part of the muscle-aponeurotic suture to yield. Possible to occur
also due to lack of surgical technique, or for concomitant metabolic diseases or COPD with violent
cough. Slow and progressive evolution, but it can reach remarkable dimensions. More frequent
localization in longitudinal incisions than lateral and lateral posterior incisions, frequent in colostomy or
ileostomy. The surgery, which once consisted only of rebuilding the muscle fascia, now sees theuse of
prostheses that can be placed directly in contact with the intestinal loops. In videolaparoscopy we
proceed by resecting the adhesions, reducing the incisional hernia and then inserting a prosthesis from the
inside. It is very useful before intervening, to perform a CT scan (with or without contrast medium) to
better identify the contents of the incisional hernia.

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