PROBLEM 4

GIT
Aldi Firdaus
405140098
 LEARNING OBJECTIVES
1. Apendisitis
2. Divertikulitis
3. Hernia Inguinal
4. Intususepsi
5. Bowel Obstruksi
6. Akut Peritonitis
7. Ileus  Potasium Imbalance
8. Ascaris Ball
9. Perforasi
 LO 1
Apendisitis
 Acute appendicitis
• Incidence & epidemiology
– The peak incidence of acute appendicitis is in the
second and third decades of life
– perforation is more common in infancy and in the
elderly, during which periods mortality rates are
highest
– Males and females are equally affected, except
between puberty and age 25, when males
predominate in a 3:2 ratio
• Pathogenesis
– occur as a result of appendiceal luminal obstruction
• Obstruction is most commonly caused by a fecalith
• Enlarged lymphoid follicles associated with viral infections
(e.g., measles)
• inspissated barium
• worms (e.g., pinworms, Ascaris, and Taenia)
• tumors (e.g., carcinoid or carcinoma)
– appendiceal ulceration
– Infection with Yersinia organisms may cause the
disease
• Luminal bacteria multiply and invade the appendiceal wall
 venous engorgement and subsequent arterial
compromise  gangrene and perforation occur 
– slow: terminal ileum, cecum, and omentum (localized abscess);
rapid: perforation with free access to the peritoneal cavity
• Clinical manifestations
– abdominal discomfort and anorexia
– The pain is described as being located in the
periumbilical region initially and then migrating to the
right lower quadrant
• resulting from distention of the appendiceal lumen; pain is
carried on slow-conducting C fibers and is usually poorly
localized in the periumbilical or epigastric region
– In general, this visceral pain is mild, often cramping
and usually lasting 4–6 h
– As inflammation spreads to the parietal peritoneal
surfaces  pain becomes somatic, steady, and more
severe and aggravated by motion or cough
– Nausea and vomiting occur in 50–60% of cases
• Differential diagnosis
• Physical findings
– tenderness to palpation will often occur at McBurney's point
– Abdominal tenderness may be completely absent if a
retrocecal or pelvic appendix is present  tenderness in the
flank or on rectal or pelvic examination
• Referred rebound tenderness is often present and is most
likely to be absent early in the illness
– Flexion of the right hip and guarded movement by the
patient are due to parietal peritoneal involvement
– The temperature is usually normal or slightly elevated [37.2°–
38°C (99°–100.5°F)], >38.3°C (101°F)  perforation
– Rigidity and tenderness  more marked as the disease
progresses to perforation and localized or diffuse peritonitis
– Perforation is rare before 24 h after onset of symptoms, but
the rate may be as high as 80% after 48 h
– Any infant or child with diarrhea, vomiting, and
abdominal pain is highly suspect
– Fever is much more common in this age group
– Abdominal distention is often the only physical finding

– In the elderly, pain and tenderness are often blunted

– the diagnosis is also frequently delayed and leads to a
30% incidence of perforation in patients over 70
– often present initially with a slightly painful mass (a
primary appendiceal abscess) or with adhesive
intestinal obstruction 5 or 6 days after a previously
undetected perforated appendix
• Laboratorium findings
– moderate leukocytosis of 10,000–18,000
cells/microL is frequent
– Leukocytosis of >20,000 cells/microL 
perforation
– Anemia and blood in the stool suggest a primary
diagnosis of carcinoma of the cecum, especially in
elderly individuals
– urine may contain a few white or red blood cells
without bacteria if the appendix lies close to the
right ureter or bladder
– Urinalysis is most useful in excluding genitourinary
conditions that may mimic acute appendicitis
• Radiographs
– opaque fecalith (5% of patients) is observed in the
right lower quadrant (especially in children)
– intestinal obstruction or ureteral calculus may be
present
– Ultrasound  an enlarged and thick-walled
appendix
– CT will include a thickened appendix with
periappendiceal stranding and often the presence
of a fecalith
• Treatment
– early operation and appendectomy as soon as the patient
can be prepared
– A different approach is indicated if a palpable mass is
found 3–5 days after the onset of symptoms  phlegmon
/ abscess
• broad-spectrum antibiotics, drainage of abscesses >3
cm, parenteral fluids, and bowel rest usually show
resolution of symptoms within 1 week
• Interval appendectomy can be performed safely 6–12
weeks later
– antibiotics alone can effectively treat acute, nonperforated
appendicitis in 86% of male patients (higher recurrence
rate)
 LO 2
Divertikulitis
 LO 3
Hernia Inguinal
 Hernia
•  protursion of an organ or part of an organ
through a defect wall of the cavity containing
it, into an abnormal position
• Abdominal wall hernia
– Inguinal (direct or indirect)
– Femoral
– Umbilical & para-umbilical
– Incisional
– Ventral & epigastric
Etiology
– Weakness in the abdominal wall
– Occur at the site of penetration of structures through the
abdominal wall
– The layers of the abdominal wall may be weakened
following a surgical incision
– Poor healing as a result of infection, hematoma formation
– Damage to the nerve  paralysis of abdominal muscles
– Increase of intra-abdominal pressure
• Chronic cough
• Constipation
• Urinary obstruction
• Pregnancy
• Abdominal distention with ascites
• Weak abdominal muscles
Varieties
– Reducible hernia
• Can be replaced completely into the peritoneal cavity
• Presents as a lump that may disappear on lying down, not
painful
• Examination: reveals a reducible lump with cough impulse
– Irreducible hernia
• Adhesions of its contents to the inner wall of the sac
• Painless, absence of cough impulse
– Strangulated hernia
• The hernia constricted on the neck of the sac  circulation
is cut off  perforation & gangrene
• Severe pain of sudden onset, colicky pain, vomitting,
distention, absolute constipation
• Examination: tender, tense hernia, overlying skin become
inflamed, noisy bowel sound
• (femoral, indirect inguinal, umbilical)
 Inguinal hernia
• Indirect inguinal hernia
– Passes through the internal ring, along the canal in front of the spermatic
cord ; if large enough  emerges through the external ring into scrotum
– Features
• Hernia doesn’t reach its full size until patient has been up & around a
little time; doesn’t reduce immediately when lies down
• Distinct tendency to strangulate
– Examination
• Can be felt in the mid-inguinal point
• Direct inguinal hernia
– Pushes its way directly forward through the posterior wall of the inguinal
canal
– Features
• Appears immediately on standing; disappearing at once when lies
down
Treatment
– Herniotomy
• Patent processus vaginalis is ligated & hernial
sac excised at the age of about 1 year and adult
– Shouldice repair
• Excision of the sac & repair of the weakened
inguinal canal by plicating the transversalis
fascia in the posterior wall by nylon suture
– Lichtenstein repair
• Reinforcing the posterior wall with a nylon or
polypropylene mesh
 Femoral hernia
• Hernia passes through the femoral canal
• Clinical features
– Commonly in women (wider female pelvis)
– A non strangulated  globular swelling below &
lateral to the pubic tubercle; it enlarged on
standing, coughing, disappear when lies down
– Hernia enlargement  passes through the
saphenous opening in the deep fascia 
penetration of the great saphenous vein
 Richter’s hernia
• Occur in femoral sac, only part of the wall of
small intestine herniates through the defect
 strangulated
• Knuckle of bowel can become necrotic 
perforate  acute peritonitis
• Treatment
– Repaired with excision of the sac & closure of the
femoral canal because the danger of strangulation
 Umbilical hernia
• Exomphalos
– Failure of all part of the midgut to return to the abdominal
cavity in fetal life
– Bowel is contained within a translucent sac through a
defective anterior wall
– Untreated  rupture  fatal peritonitis (rupture may
occur during delivery)
– Treatment
• Surgical repair immediately
• Congenital umbilical hernia
– Result from failure of complete clossure of the umbilical
cicatrix
– Common in black children
– Treatment
• Not surgical repair (unless the hernia persist when the child is 2 yo
 Para-umbilical hernia
• Acquired hernia that occurs just above or below
umbilicus
• Occurs in obese, multiparous, middle-aged
women
• Neck is narrow, prone to become irreducible or
strangulated
• Treatment
– Sac is excised and the edges of the rectus sheath are
overlapped above and below the hernia (Mayo’s
operation)
 Ventral, epigastric, incisional hernia
• Ventral hernia
– Exist as an elongated gap between the recti
– No treatment is required
• Epigastric hernia
– Consists of one or more small protursions through the defects in
the linea alba above umbilicus
– Contain only extraperitoneal fat, often surprisingly painful
– Treatment
• Suturing the defect
• Incisional hernia
– Occurs through a defect in the scar of a previous abdominal
operation
– Wide neck, strangulation is rare
– Treatment
• Dissecting out and suturing the individual layers of abdominal wall
• If operation is inadviseable  abdominal belt
 LO 4
Intususepsi
 Intussusception
• Is the prolapse of one portion of the intestine
into the lumen of the immediately adjoining
bowel
• 95% occur in infants or young children
– Usually 3-12 months
– Boys are affected twice as often as girls
• Intussusceptum and Intussuscipiens
 Terminology
• Ileocolic : the ileo-ileal intussuception extends
through the ileocaecal valve into the colon
(commonest sort : 75%)
• Ileo-ileal : the ileum is invaginated into the
adjacent ileum
• Ileocaecal : the ileocaecal valve is the apex of
the intussusception
• Colocolic : the colon invaginates into the
adjacent colon
 Etiology
• Hyperplasia of the lymphoid tissues in Peyer’s
patches in the bowel wall.
Acts as foreign body which is then propelled
by peristaltis distally along the gut, dragging
the bowel behind
• Unstable intestine contraction
• Tumour/polyp
 Patophysiology
• The blood supply is cut off by direct pressure
of the outer layer  ileus
• If untreated gangrene will occur
 Clinical features in infants
• Abdominal colic
• Screaming and pallor
• Vomitting
• Pale and anxious
• Palpation : sausage-shaped tumour
• 60% of infants pass a stool containing red blood and
mucus, the currant jelly stool.
• If neglected after 24 hours :
– Abdomen distended
– Faeculent vomitting
– Intensely toxic due to gangrene
– peritonitis
 Diagnosis
• Barium
• X-Ray confirmation

Intussusception in an infant. The

obstruction is evident in the proximal
transverse colon. Contrast material
between the intussusceptum and the
intussuscipiens is responsible for the coil-
spring appearance.
 Treatment
• Non-operative :
barium may be completely reduced
hydrostatically by its pressure
• Operative :
Laparotomy
 Prognosis
• Mortality is very low in the first 24 hours
• Very high in the irreducible or gangrenous
cases
• May recur in small percentage of children
 LO 5
Bowel Obstruksi
 LO 6
Akut Peritonitis
 Peritonitis
•  life-threatening event that is often
accompanied by bacteremia and sepsis syndrome
– Pancreas, duodenum, and ascending and descending
colon are located in the anterior retroperitoneal space
– Kidneys, ureters, and adrenals are found in the
posterior retroperitoneal space
– Other organs, including liver, stomach, gallbladder,
spleen, jejunum, ileum, transverse and sigmoid colon,
cecum, and appendix, are within the peritoneal cavity
• Cavity is lined with a serous membrane that can
serve as a conduit for fluids
 Primary (spontaneous) bacterial
peritonitis
• Usually caused by single organism
• Etiology
– Occurs most commonly in conjunction with cirrhosis
of the liver (frequently the result of alcoholism)
– Metastatic malignant disease
– postnecrotic cirrhosis
– chronic active hepatitis & acute viral hepatitis
– congestive heart failure
– systemic lupus erythematosus
– lymphedema
• Clinical manifestation
– Fever (80%)
– Acites  predates infection
– Abdominal pain, an acute onset of symptoms, and peritoneal irritation
(physical examination)
– Nonlocalizing symptoms  malaise, fatigue, or encephalopathy

• Other examination
– >250 PMNs/L is diagnostic for PBP
– Blood culture
• enteric gram-negative bacilli (Escherichia coli)  most commonly encountered
• gram-positive organisms (streptococci, enterococci, or even pneumococci)  sometimes
found
• Aerobic bacteria
– Contrast-enhanced CT  intraabdominal source for infection
– Chest & abdominal radiography  to exclude free air
• Treatment
– Third-generation cephalosporins (cefotaxime 2 g q8h,
administered IV)  initial coverage in moderately ill patients
– Broad-spectrum antibiotics, such as penicillin/β-lactamase
inhibitor combinations (piperacillin/tazobactam 3.375 g q6h IV
for adults with normal renal function); ceftriaxone (2 g q24h IV)
• Prevention
– Up to 70% of patients experience a recurrence within 1 year
– Antibiotic prophylaxis reduces this rate to <20%
– Prophylaxis agents
• fluoroquinolones (ciprofloxacin, 750 mg weekly; norfloxacin, 400
mg/d)
• trimethoprim-sulfamethoxazole (one double-strength tablet daily)
 Secondary peritonitis
• Develops when bacteria contaminate the peritoneum
as a result of spillage from an intraabdominal viscus 
chemical irritation and/or bacterial contamination
• Found almost always constitute a mixed flora in which
– facultative gram-negative bacilli
– anaerobes predominate, especially when the
contaminating source is colonic
• Early death in this  gram-negative bacillary sepsis
and to potent endotoxins circulating in the
bloodstream
– E. coli, are common bloodstream isolates, but Bacteroides
fragilis bacteremia also occurs
• Clinical manifestation
– local symptoms may occur in secondary peritonitis, ex:
• Epigastric pain from a ruptured gastric ulcer
• Appendicitis  vague, with periumbilical discomfort and nausea;
number of hours  pain localized right lower quadrant
– lie motionless
– knees drawn up to avoid stretching the nerve fibers of the
peritoneal cavity
– Coughing and sneezing  increase pressure within the
peritoneal cavity  sharp pain
• Physical examination
– voluntary and involuntary guarding of the anterior abdominal
musculature
– tenderness, especially rebound tenderness
• Treatment
– antibiotics aimed particularly at aerobic gram-negative
bacilli and anaerobes
– penicillin/β-lactamase inhibitor combinations
(ticarcillin/clavulanate, 3.1 g q4–6h IV); cefoxitin (2 g q4–6h
IV)
– Patients in the intensive care unit  imipenem (500 mg
q6h IV), meropenem (1 g q8h IV), or combinations of
drugs, such as ampicillin plus metronidazole plus
ciprofloxacin
– Surgical intervention + antibiotics (bacteremia) 
decrease incidence of abscess formation & wound
infection; prevent distant spread of infection
 Peritonitis in Patients Undergoing
CAPD
• CAPD (continuous ambulatory peritoneal
dialysis)
• CAPD-associated peritonitis usually involves
skin organisms
• Pathogenesis
– skin organisms migrate along the catheter 
serves as an entry point and exerts the effects of a
foreign body
• usually caused by a single organism
• Clinical presentation
– diffuse pain and peritoneal signs are common

– dialysate is usually cloudy and contains >100 WBCs/L,

>50% of which are neutrophils
– Organisms:
• most common organisms are Staphylococcus spp
• Gram-negative bacilli and fungi such as Candida spp. are also
found
• Vancomycin-resistant enterococci and vancomycin-
intermediate S. Aureus
• Treatment
– should be directed at S. aureus, coagulase-negative
Staphylococcus, and gram-negative bacilli until the results of
cultures are available
– first-generation cephalosporin such as cefazolin (for gram-
positive bacteria)
– fluoroquinolone or a third-generation cephalosporin such as
ceftazidime (for gram-negative bacteria)
– MRSA  vancomysin
– If the patient is severely ill, IV antibiotics should be added at
doses appropriate for the patient's degree of renal failure
– if the patient has not responded after 48 h of treatment,
catheter removal should be considered
 LO 7
Ileus  Potasium Imbalance
 Paralytic Ileus
• Paralytic ileus (adynamic ileus) is temporary
absence of the normal contractile movements
of the intestinal wall

• Ileus commonly occurs for 24 to 72 hours after

abdominal surgery
 CAUSES
• Chemical, electrolyte, or mineral disturbances (such as
decreased potassium levels or high calcium levels)
• Complications of intra-abdominal surgery
• Atherosclerosis that reduces the blood supply to the
intestine
• Intra-abdominal infection
• Use of certain medications, especially narcotics, opioid
analgesics, and anticholinergic drugs
• Kidney or lung disease
• Underactive thyroid gland
 SIGN AND SYMPTOMS
• Abdominal distention
• Abdominal fullness, gas
• Abdominal pain and cramping
• Breath odor
• Constipation
• Diarrhea
• Vomiting
• Loss of appetite
• Few bowel sounds or none at all through a stethoscope
• An x-ray of the abdomen shows bulging loops of
intestine
 DIAGNOSIS
• Abdominal CT scan
• Abdominal X-ray
• Barium enema
• Upper GI and small bowel series
• Physical examination:
– Tympanic percussion with a weak bowel sounds
may not sound even at all
– Palpation: the patient simply stating the uneasy
feeling in his stomach
– Not found any tenderness and rebound
tenderness

• Investigations:
– Plain abdominal: Multiple Air fluid level in the
form of a picture line-up (alignment).
 COMPLICATIONS
• Electrolyte imbalances
• Infection
• Jaundice
• Perforation (hole) in the intestine
 Management:
• Management of paralytic ileus are conservative and
supportive:
– Actions in the form of decompression with
nasogastric tube installation,
– Fluid and electrolyte balance, treating the primary
disease and the provision of adequate nutrition.
– Drugs:
• Sicaprid useful for postoperative paralytic ileus
• Klonidin reported to be useful to overcome the
paralytic ileus due to drugs
 Different
Paralytic ILeus Obstructive ILeus

Bowel sounds minimal Bowel sounds hyperactive

Multiple Air Fluid level Multiple Air fluid level

provides line up provides a step ladder

Not accompanied by a Accompanied by a paroxysmal

paroxysmal colicky abdominal colicky abdominal pain
pain
 Air fluid levels in intestinal obstruction
Plain X-ray abdomen showing multiple air fluid levels (yellow arrows) in a case of
subacute intestinal obstruction.
 Mechanical intestinal obstruction
• Intestinal obstruction is a restriction to the normal passage of
the intestinal contents.
• It may be divided into 2 main groups
– Paralytic
– Mechanical ileus
• Speed of onset: acute, chronic, acute on chronic
• Site: high or low
• Nature: simple versus strangulating, and
• aetilogy
 Speed of onset
• In acute obstruction: the symptoms are
insidious and slowly progressive
• A chronic obstruction :may develop acute
symptoms as the obstruction suddenly
become complete
 Site
• Is classifies into high or low, which is roughly
synonymous with small or large bowel
obstruction
 Nature
• Is divided into simple or strangulated:
– Simple obstruction occurs when the bowel is
occluded without damage to its blood supply
– Strangulating obstruction when the blood
supply of the involved segment of intestine is cut
off
 Etiology
Causes
in the lumen faecal impaction, gallstone’ileus’, food bolus, parasites,
intussusception
In the wall congenital atresia, crohn’s disease, tumours,
divertivculitis of the colon
Outside the wall strangulated hernia, volvulus and obstruction due to
adhesions or bands
Neonatal congenital atresia and stenosis, imperforate anus,
volvulus neonatorum, hirschsprung’s disease,
strangulated hernia and meconium ileus
Infants intussusception, hirschsprung’s disease, strangulated
hernia and obstruction due to meckel’s diverticulum
Young adults and atrangulated hernia, adhesions and bands, crohn’s
middle age disease
The elderly strangulated hernia, carcinoma of the bowel, colonic
diverticulitis, impacted faeces
 Pathology
• The bowel is obstructed by a simple occlusion the
intestine distal to the obstruction rapidly empties
and become collapsed  above the obstruction
become dilated (partly with gas and fluid poured out
by the intestinal wall together with gastric biliary and
pancreatic secretion increased peristalsis in an
attempt to overcome the obstruction  intestinal
colic
• As the bowel distends intestinal wall becomes
impaired and in extreme cases, there may be
mucocal ulceration and eventually perforation
 Pathology
• In strangulating obstruction
– The integrity of the mucosal barrier is lost as
ischemia progresses so bacteria and theirs
toxins can no longer be contained within the
lumen. transudation of organisms into the
peritoneal cavity rapidly take place, with
secondary peritonitis.
– Unrelieved strangulation is followed by gangrene
of the ischemic bowel with perforation
 Clinical features
The four cardinal symptoms of intestinal obstruction are the following
– Colicky abdominal pain’
• Usually the first symptom of the intestinal obstruction and is
colicky in nature
• In small bowel obstruction periumbilical
• In distal colonic obstructionsuprapubic
– Distension
• Is marked in chronic large bowel obstruction and also in
volvulus of the sigmoid colon
– Absolute constipation large bowel obstruction
– Vomiting
• Small bowel obstruction
• Faeculent vomiting obstructed small intestine
• True vomiting faeces  gastrocolic fistula
 CAUSES OF INTESTINAL
OBSTRUCTION
Location Causes
Colon Tumors (usually in left colon), diverticulitis
(usually in sigmoid), volvulus of sigmoid or
cecum, fecal impaction, Hirschsprung's disease
Duodenum Cancer of the duodenum or head of pancreas,
(Adults) ulcer disease
Duodenum Atresia, volvulus, bands, annular pancreas
(Neonates)
Jejunum and ileum Hernias, adhesions (common), tumors, foreign
(Adults) body, Meckel's diverticulum, Crohn's disease
(uncommon), Ascaris infestation, midgut
volvulus, intussusception by tumor (rare)
Jejunum and Ileum Meconium ileus, volvulus of a malrotated gut,
(Neonates) atresia, intussusception
Mechanical Ileus
 Closed loop obstruction
• Increasing distension of a loop of bowel due
to a combination of complete obstruction
distally and a valve-like mechanism proximally
allowing the bowel to fill, but preventing
reflux back.
• Most commonly seen with a left sided colonic
obstruction
• Closed loop obstruction is a specific type of obstruction in
which two points along the course of a bowel are obstructed
at a single location thus forming a closed loop.
• Usually this is due to adhesions, a twist of the mesentery or
internal herniation.
• In the large bowel it is known as a volvulus.
• In the small bowel it is simply known as small bowel closed
loop obstruction.
• Especially in the small bowel the risk of strangulation and
bowel infarction is high with a mortality rate of 10-35%.
 Volvulus
• A twisting of a loop of the bowel around its
mesenteric axis, which result in a combination
of obstruction together with occlusion of the
main vessels at the base of the involved
mesentery
• Most commonly: sigmoid , caecum and small
intestine
 Etiology
• An abnormally mobile loop of intestine
• An abnormally loaded loop
• A loop fixed at its apex by adhesions
• A loop of bowel with a narrow mesenteric
atachment
 Sigmoid volvulus
• Occurs usually in elderly and Constipated
patient
• 4 time more common in men than in women
• More common in Russia, Scandinavia and
central Africa
• The loop of sigmoid colon usually twist
anticlockwise, from one half to three turns.
 Clinical features
• Sudden onset of colicky pain with
characteristic gross and rapid dilatation of the
sigmoid loop
• A plain X-ray enormously dilated oval gas
shadow on the left side ‘ bent inner tube’ sign
• Caecum is usually visible and dilated in the
right lower quadrant, distinguishing it
radiologically from caecal volvulus
 Treatment
• Soft rectal tube
• Laparotomy
 Caecal volvulus
• Associated with a congenital malrotation.
• There is an acute pain in the right iliaca focca
with rapid abdominal distension
• X-ray grossly dilated caecum, which is often
ectopically placed and its frequently located in
the left upper quadrant of the abdomen
• Treatment laparotomy, right hemicolectomy
 Small intestine volvulus in adults
• This may occrus where a loop of the small
intestine is fixed at its apex by adhesions or by
fibrous remnant of the vitellointestinal duct
• Treatment: early operations,
 Neonatal intestinal obstruction
• Intestinal atresia
• Volvulus nenatorum
• Meconimun ileus
• Necratizing enterocolitis
• Hirshcprung’s disease
• Anorectal atersias
 Intestinal atresia
• May be septum, complete or partial or a
complete gap, which may be associated with a
corresponding defect In the mesentery.
• Multiple segments may be involved
• Treatment resection of the stricture and
anastomosis
• High mortality
 LO 8
Ascaris Ball
 Ascariasis
Disease :
• Ascariasis, ascariasis infection, roundworm
infection.
 Risk Factors
• Preschool age or younger
• Eating unsanitary food
• Drinking unclean water
 Symptoms
• Small burdens of worms in the intestine may cause no
symptoms
• The patient may have symptoms of pneumonitis with cough,
dyspnea, wheezing, chest pain and low grade fever during
the migration of the larvae through the liver and lungs.
• In heavy worm burdens the adult worms actively migrate in the
intestine resulting in intestinal blockage, vomiting,
abdominal pain, colic, nausea, anorexia, and intermittent
diarrhea
• A heavy worm burden in children may lead to severe
nutritional impairment and retardation in growth.
• Worms exiting through the nose or mouth
 Laboratory Studies
• Early infection (larval migration)
– Complete blood count (CBC) may show eosinophilia.
– Sputum analysis may reveal larvae or Charcot-Leyden crystals.
– Stool examination findings are typically normal in absence of
previous infection (during the first 40 d).
– Ascaris specific antibodies (not useful in acute infection and not
protective)
– Increases in IgE and later IgG

• Established infection (adult phase):

– Stool examination findings include characteristic eggs. Adult
females lay about 200,000 eggs per day, aiding microscopic
identification of characteristic eggs.
 Imaging Studies

• Early infection (larval migration):

– Chest radiography may reveal patchy infiltrates of eosinophilic
pneumonia.

• Established infection (adult phase)

– Abdominal radiography may reveal adult worms (especially with
contrast).
– Obstructing Ascaris lesions cause cylindrical filling defects on contrast
computed tomography (CT) scans.
– Cholangiopancreatography by endoscopy (ERCP) or magnetic
resonance imaging (MRCP, or magnetic resonance
cholangiopancreatography) may detect adult worms in bile or pancreatic
ducts.8
– Ultrasonography may detect worms in the gallbladder.
 Treatment
• Albendazole
– 400 mg PO once, for all ages
• Mebendazole
– 100 mg bid PO for 3 days or 500 mg PO once for
all ages
• Piperazine citrate
– 150 mg/kg PO initially, followed by 6 doses of 65
mg/kg at 12 hr intervals PO  causes
neuromuscular paralysis of the parasite (the
treatment of choice for intestinal or biliary
obstruction)
 Treatment

• Pyrantel pamoate
– 11 mg/kg PO once, maximum 1 g
• Nitazoxanide
– 100 mg bid PO for 3 days for children 1-3 yrs of age,
– 200 mg bid PO for 3 days for children 4-11 yr
– 500 mg bid PO for 3 days for adolescents and adults
produces cure rates comparable with single-dose
albendazole.
• Surgery may be required for cases with severe
obstruction
 Complications
• Intestinal obstruction - 63%
• Bile duct obstruction - 23%
• Perforation, peritonitis, or both - 3.2%
• Volvulus - 2.7%
• Hepatitic abscess - 2.1%
• Appendicitis - 2.1%
• Pancreatitis - 1%
• Cerebral encephalitis - 1%
• Intussusception - 0.5%
• Other sites of pathology (<0.5%) include Meckel diverticulum, the
gallbladder, ears, eyes, nose, lungs, kidneys, vagina, urethra, heart,
placenta, spleen, thoracic cavity, and umbilicus.
• In endemic regions, ascariasis is a significant part of the differential
diagnosis for intestinal obstruction, appendicitis, biliary tract disease,
pancreatitis, intussusception, and volvulus.
 LO 9
Perforasi
 Perforation
• Perforated Ulcer
– Perforated gastric/duodenal ulcer requires
immediate operative therapy
– Anterior gastric perforations cause peritonitis
– Posterior gastric and duodenal perforations may
not cause peritonitis, and after the acute episode
of pain, the leak may wall off, giving the
impression that the patient is improving
– Free air (80% of perforated ulcers)
 Etiology
• Helicobacter Pylori
• Smoking
• NSAIDs
Patophysiology
 Treatment
• Immediate surgery
• For a perforated duodenal ulcer,may include:
– a highly selective vagotomy, a truncal vagotomy and
pyloroplasty, or vagotomy and antrectomy.
• For a perforated gastric ulcerdepends on the
patient's condition:
– If the patient is moribund, the ulcer is best excised by
grasping it with multiple Allis clamps and using a GIA-
60 linear stapler. Or,can be excised with
electrocautery
– In a stable patient, the ulcer is excised and sent for
frozen section analysis to exclude malignancy
 References
• Kliegman: Nelson Textbook of Pediatrics, 18th ed. 2007
• Fauci. Braunwald. Dkk. Harrison’s Principles of Internal
Medicine. 17th edition. United State: The McGraw-Hills; 2008
• Nelson Textbook of Pediatric, 19th edition
• Evers BM. Small intestine. In: Townsend CM, Beauchamp RD,
Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery. 18th
ed. St. Louis, Mo: WB Saunders; 2008:chap 48.