Acute Abdomen

By : Group 12
Fasilitator : dr. Krisnha Lestadi

FAKULTAS KEDOKTERAN UNIVERSITAS TARUMANGARA

Group 12
Leader : Ferdy Halim 405070082
Secretary : Grace 405070080
Scriber : Gladys Sudiyanto 405070123
Member : Melia Sugiarto 405070009
Arianto Leonardi 405070072
Viencensia 405070090
Wahyu Wijasena Adhi P 405070106
Iman Teguh 405070109
Hadiyanti 405070125
Apolonia Aurensia 405070130
Nazrien 405070133
Diah Permatasari 405070156
Scenario
Caci, a 6 year old girl, came to you with a 2 day history
of abdominal cramp.The pain is located in the lower
abdominal area band is associated with anorexia,
nausea, and four episodes of vomitus. She appears to
be weak and her parents notify a decreased in urination.
There was several episodes of diarrhea, low grade fever
or coughing. She has not passed any stools for the two
days since she was ill. Her past history is significant for
passing large and pink resembling smooth earthworms
twice in the past six months. Her family history is
negative for other family members with similar problems.
Exam :
VS : T 37.0, P110, RR 12, BP 100/60, Ht 103 cm, Wt 14,
both less than the 5th percentile. She is thin and small for
age but not cachectic.
Scenario
She is alert and subdued. She moves without difficulty
but cries episodically because of abdominal cramp.
HEENT : pale conjunctivae, sticky mucous membrane,
sunken eyes, neck is supple, heart and lungs are
normal. She has moderate abdominal distention with
hyperactive bowel sounds, peristaltic rushes and
borborygmi with generalized mild tenderness.she has no
inguinal hernias and her external genitalia is normal. A
rectal exam finds no stool or mass. Her back is non
tender, decreased skin turgor, but her overall skin color
and perfussion are good.
CBC : WBC 11.0 ; Ba/Eo/St/Sg/Ly/Mo : 0/6/2/56/31/5 ;
Hgb 8.9 ; Hct 38.
Abdominal series radiographs show distended ladderlike
large bowel with air / fluid levels and whirlpool
appearance.
Learning Objectives
 Describe about the comparison of normal value.
 Describe about acute abdomen
Definition
Classification
Etiology
Epidemiology
Signs and symptoms
Pathophysiology
Diagnosis
Laboratory findings
Treatment
Complication
Learning Objectives
 Describe about ileus obstructive
Definition
Classification
Etiology
Epidemiology
Signs and symptoms
Pathophysiology
Diagnosis
Laboratory findings
Treatment
Complication
Learning Objectives
 Describe about parasite infection that can make
intestinal obstruction
Definition
Classification
Etiology
Epidemiology
Signs and symptoms
Pathophysiology
Diagnosis
Laboratory findings
Treatment
Complication
Laboratory &
Vital Signs
 Laboratory

Pemeriksaan Hasil Nilai normal Panic Value

Lab
Hb 8,9g/dL 11,5-15,5g/dL <5g/dL, >20g/dL

Leukosit 11.000/μL (4-10)ribu/μL <500mm3, >30.000mm3

Basofil 0% 0-1% -
Eosinofil 6% 1-3% -
Sel batang 2% 2-6% -
Sel segmen 56% 50-70% -
Limfosit 31% 20-40% -
Monosit 5% 2-8% -

Hematokrit 38vol% 36-48% -

Vital signs
Pemeriksaan Hasil Normal

IMT (14/(1,03)2)= 17-23

13,20
Berat badan 14 kg 8+2x6= 20 kg
Tensi 100/60mmHg 120/80mmHg
Nadi 110x/menit 80x/menit
Frekwensi 12x/menit 12-20x/menit
pernafasan
Konjunctiva anemis Tidak anemis
Suhu badan 370C 36-370C
ACUTE ABDOMEN
ACUTE ABDOMEN PAIN

Abdominal pain is pain that you feel

anywhere between your chest and groin.
This is often referred to as the stomach
region or belly.
Stomach pain; Pain - abdomen; Belly
ache; Abdominal cramps (alternative
name)
TYPES ABDOMINAL PAIN

Acute Abdominal pain Chronic abdominal pain

Characteristics Common Causes Characteristics Common Causes

1. Less than 4-6 1) Urinary tract 1. Three episodes Constipation

weeks (subacute disease over 3 months Lactose intollerance
less than 12 2) Peptic Ulcer 2. Continuous, dull, Mittelschmerz
weeks) Disease vague and diffuse Psychogenic (See
2. Single episode, 3) Inflammatory Abdominal Pain Recurrent Abdominal
self limited and Bowel Disease 3. Recurrent, Pain Syndrome) :
treatable 4) Gastroesophageal Associated with Secondary Gain
3. Episodic Reflux Disease debilitation Sexual abuse
localized pain, School Phobia
sharp, stabbing
DD Acute Abdominal Pain
GENERALIZED/ UPPER LOWER
PERIUMBILICA
L
RIGHT LEFT RIGHT LEFT
Gastroenteritis Hepatitis Pancreatitis Appendicitis Inflammatory
 Obstipation  Biliary colic  Splenic  Inflammatory bowel disease
 Small bowel  Peptic ulcer infarction bowel disease  Diverticulitis
obstruction disease  Pyelonephritis Salpingitis  Salpingitis
 Large bowel  Pyelonephritis Myocardial  Rectus  Rectus
obstruction Acute infarction abdominus abdominus
Mesenteric cholecystitis muscle strain muscle strain
ischemia  Ureteral  Ureteral
 Peritonitis calculus calculus
 Abdominal Ruptured  Ovarian
aortic dissection corpus luteum torsion
Sickle cell cyst  Ruptured
crisis Ruptured corpus luteum
ectopic cyst
pregnancy  Ruptured
Ovarian torsion ectopic
pregnancy
Sigmoid
volvulus
Location of abdominal pain and possible causes.
CAUSE ABDOMINAL PAIN in CHILDREN

Neonatal Infant Child Adolescent (12-18

years)
Colic Intussusception Constipation Appendicitis
Milk Protein Infantile Colic Bowel Lactose Gastroenteritis
Allergy Obstruction Intolerance Constipation
Gastroesophageal Battered Infant Lead Poisoning Gynecologic cause
Reflux Gastroenteritis Helicobacte pylori Testicular Torsion
Malrotation or Constipation Urinary Urinary Tract Drug and Alcohol
midgut volvulus Tract Infection Infection use
Necrotizing Pneumonia Sexual abuse
enterocolitis Pancreatitis Gallbladder disease
Hirschprung's Appendicitis Neoplasm
enterocolitis Mesenteric Inflammatory bowel
lymphadenitis Disease
Gastroenteritis
Intussusception or
volvulus (children
under age 6)
Abdominal trauma
Pharyngitis
(e.g.Strep Throat)
Sickle Cell Crisis
Henoch-Schonlein
purpura
Causes of Acute
Abdominal Pain in
Children
Gastrointestinal causes Genitourinary causes Drugs and toxins
Gastroenteritis Appendicitis Urinary tract infection Erythromycin Salicylates
Mesenteric lymphadenitis Urinary calculi Lead poisoning Venoms
Constipation Abdominal Dysmenorrhea
trauma Intestinal obstruction Mittelschmerz Pelvic Pulmonary causes
Peritonitis Food poisoning inflammatory disease Pneumonia Diaphragmatic
Peptic ulcer Meckel's Threatened abortion pleurisy
diverticulum Inflammatory Ectopic pregnancy
bowel disease Lactose Ovarian/testicular torsion Miscellaneous Infantile
intolerance Endometriosis colic Functional pain
Hematocolpos Pharyngitis Angioneurotic
Liver, spleen, and biliary edema Familial
tract disorders Hepatitis Metabolic disorders Mediterranean fever
Cholecystitis Cholelithiasis Diabetic ketoacidosis
Splenic infarction Rupture of Hypoglycemia Porphyria
the spleen Pancreatitis Acute adrenal insufficiency

Hematologic disorders
Sickle cell anemia Henoch-
Schönlein purpura
Hemolytic uremic
syndrome
Extra-Abdominal Causes of Abdominal Pain
Abdominal wall
Rectus muscle hematoma
Infectious
Herpes zoster
Metabolic
Alcoholic ketoacidosis
Diabetic ketoacidosis
Porphyria
Sickle cell disease
Thoracic
Myocardial infarction
Pneumonia
Pulmonary embolism
Radiculitis
Toxic
Black widow spider bite
Heavy metal poisoning
Methanol poisoning
Scorpion sting
Opioid withdrawal
Pathophysiology
Visceral pain
comes from the abdominal
viscera, which are innervated
by autonomic nerve fibers and
respond mainly to the
sensations of distention and
muscular contraction—not to
cutting, tearing, or local
irritation.
Somatic pain Referred pain
comes from the parietal perceived distant from its source
peritoneum, which is and results from convergence of
innervated by somatic nerves, nerve fibers at the spinal cord
which respond to irritation from
infectious, chemical, or other
inflammatory processes

Visceral pain is typically vatigue, Somatic pain is sharp and well Common examples of referred
dull, and nauseating localized. pain are scapular pain due to
biliary colic, groin pain due to
renal colic, and shoulder pain
due to blood or infection
irritating the diaphragm.
Foregut structures (stomach,
duodenum, liver, and pancreas)
cause upper abdominal pain.
Midgut structures (small
bowel, proximal colon, and
appendix) cause periumbilical
pain. Hindgut structures (distal
colon and GU tract) cause lower
abdominal pain.
EXAM
Physical Exam Labs Radiology
Perform in comfortable, Screening Flat and Upright
non-threatening 1) Complete Blood abdominal XRay (KUB)
environment Count Consider
Growth 2) Erythrocyte 1) Barium Enema
Development Sedimentation 2) RUQ Ultrasound
Appearance Rate 3) Pelvic Ultrasound
Vital signs 3) Urinalysis 4) Abdominal CT
Comprehensive exam 4) Urine Pregnancy Skeletal Survey (assess
Abdominal exam Test (Urine HCG) physical abuse)
a) Test rebound as when appropriate Upper GI with small bowel
"Jump on and off 5) Liver Function follow through
table" Tests Upper endoscopy (EGD)
b) Avoid removing 6) Amylase Colonoscopy
hand rapidly (loses 7) Lipase
patient trust) Consider additional testing
Rectal Exam necessary 1) Helicobacter Pylori
titer
2) Ova and Parasites
(e.g. Giardia)
3) Hepatitis
Serologies (A,B,C)
4) Lead Ingestion
Treatments

 Intravenous fluid
 Antibiotic  ampicilin, gentamicin, clindamycin,
metronidazole
 Antispasmodic
 Surgical treatment
Acute Appendicitis
in Children
ACUTE APPENDICITIS IN CHILDREN

 Inflammation (a cellular response to injury or blockage)

of the appendix (a tube of tissue that extends from a
portion of the large intestine, usually along the lower
right-hand side of the abdomen) can cause abdominal
pain and is considered a medical emergency
 appendicitis is rare under 2 years of age and most
commonly occurs between the ages of 10 and 30 years
ETIOLOGY
 Appendicitis is thought to result from obstruction of the
appendiceal lumen, typically by lymphoid hyperplasia,
but occasionally by a fecalith, foreign body, or even
worms.
 The obstruction leads to distention, bacterial
overgrowth, ischemia, and inflammation.
 If untreated, necrosis, gangrene, and perforation
occur.
 If the perforation is contained by the omentum, an
appendiceal abscess results.
SYMPTOMS APENDICITIS
 Dull pain near the navel or upper abdomen that
becomes sharp as it moves to the lower right abdominal
area
 Fever
 Loss of appetite
 Vomiting after the onset of abdominal pain
 Inability to walk normally because of pain, or pain when
asked to cough or jump
 Abdominal swelling
 Constipation (inability to pass feces) or diarrhea
DIAGNOSIS TEST APENDICITIS
 Medical history
 Complete physical examination, including abdominal and
pelvic examinations
 Urine test to exclude a urinary tract infection
 Blood tests to identify an infectious process
 Diagnostic imaging tests, such as CT scans (X-ray
tests) and ultrasound (using sound waves)
TREATMENT APENDICITIS
 If appendicitis is suspected, appendectomy (surgical
removal of the appendix) is the treatment of choice.
 Antibiotics are given prior to surgery, general
anesthesia is used, and the appendix is removed
through a single incision or by laparoscopy (removal of
the organ through a scope).
PROGNOSIS APENDICITIS
 If the appendix has not ruptured, recovery is usually
quick, and children usually leave the hospital one or two
days after surgery.
 Most children can usually return to normal activities in
two to three weeks. If rupture occurs, the recovery
process can be more complicated.
Ileus obstruction
Ileus obstruction
 Obstruction may be partial or complete
and may arise from intrinsic or extrinsic
abnormalities of the gut.
 Obstruction can be further classified as
simple or strangulating.
 Simple obstruction is associated with the
failure of the progression of aboral flow of
luminal contents.
 Strangulating obstruction is associated
with impaired blood flow to the intestine in
addition to obstruction of the flow luminal
contents.
Cause Mechanical and Nonmechanical

Obstruction of the bowel may due to:

A mechanical cause, which simply
means something is in the way
Ileus, a condition in which the bowel
doesn't work correctly but there is no
structural problem
Cause Mechanical and Nonmechanical

 Paralytic ileus, also called pseudo-obstruction, is

one of the major causes of intestinal obstruction in
infants and children. Causes of paralytic ileus may
include:
 Chemical, electrolyte, or mineral disturbances (such as decreased
potassium levels)
 Complications of intra-abdominal surgery
 Decreased blood supply to the abdominal area (mesenteric artery
ischemia)
 Injury to the abdominal blood supply
 Intra-abdominal infection
 Kidney or lung disease
 Use of certain medications, especially narcotics
Mechanical causes of intestinal obstruction may include:
 Abnormal tissue growth
 Adhesions or scar tissue that form after surgery
 Foreign bodies (ingested materials that obstruct the
intestines)
 Gallstones
 Hernias
 Impacted feces (stool)
 Intussusception
 Tumors blocking the intestines
 Volvulus (twisted intestine)
Neurogen dan vaskuler
 Paralitic/adinamic
 CNS
 Degeneration
 Neoplasma
 Trauma
 Myasthenia gravis
 Postanastesi
 Reflex peritoneum
 Peritonitis
 The blood of retroperitoneal
 Colic of kidney or fessica felleaa
 Spastic/hyperdinamic M. hirschprung
 Vasculer: Bowel iscemic
INTESTINAL
OBSTRUCTION
INTESTINAL OBSTRUCTION
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
Adults Cancer of the duodenum or head of
pancreas, ulcer disease
Neonates Atresia, volvulus, bands, annular
pancreas
Jejunum and ileum
Adults Hernias, adhesions (common),
tumors, foreign body, Meckel's
diverticulum, Crohn's disease
(uncommon), Ascaris infestation,
midgut volvulus, intussusception by
tumor (rare)
Symptoms and Signs
Obstruction of the small
bowel
abdominal cramps centered
around the umbilicus or in the
epigastrium,
vomiting,
in patients with complete
obstruction—obstipation
partial obstruction may
develop diarrhea
Hyperactive, high-pitched
peristalsis with rushes
coinciding with cramps is
typical
Shock and oliguria are
serious signs that indicate
either late simple obstruction
or strangulation.
Obstruction of the large
bowel
Increasing constipation
leads to obstipation and
abdominal distention
Vomiting may occur
(usually several hours after
onset of other symptoms) but
is not common.
Lower abdominal cramps
unproductive of feces occur
distended abdomen with
loud borborygmi.
no tenderness, and the
rectum is usually empty
Phatophysiology
 Obstruction is typically associated with an
acumulation of ingested food, gas, and
intestinal secretion proximal to the point of
obstruction, leading to distention of the bowel.
 As the bowel dilates, intestinal obstruction
decrease and secretion of fluid and electrolit
increase.
 The gut proximal to the obstruction initially
demontrates an increase in contractile activity,
which is followed by a marked decrease with
hipoactive bowel sounds.
 The combination of fluid acumulation
(distention) and hipomotility is associated with
nausea and vomiting.
ILEUS OBSTRUCTIVE
Management
 Initial treatment must be directed at fluid
resuscitation and stabilizing the patient.
 Nasogastric decompression usually provides
relief of pain and vomiting.
 Patients with strangulation must have
immediate surgical relief before the bowel
infarcts, resulting in gangrene and intestinal
perforation.
 Nonoperative concervative management is
usually limited to children with suspected
adhesion or inflammatory strictures that
mayresult with resolve with nasogastric
decompression or antiinflammatory medications.
Intestinal Worms (Helminths)
 Intestinal worms (helminths) are common cause of diarrhea,
bloating and malnutrition. They may cause severe infection
(infestation), predominantly in children in areas with hot
climates, bad hygiene and poor sewage disposal: in rural parts of
Africa, Middle East, South Asia, Indonesia, and Central and South
America. In Europe and North America, infestations are more
sporadic.
 Pathology of Intestinal Worms
 Adult worms (from 1 millimeter to several meters long) invade the
bowel wall and suck the blood from it or live freely in the intestine
and utilize nutrients from the bowel content. The result are small
intestinal or colonic inflammation and ulcers, anemia, protein, iron
and vitamin (mainly A, C, B12) deficiency. Intestinal obstruction
may occur in severe cases. Larvae may migrate to other organs
(liver, spleen, bladder, muscles, lungs, brain) where they form cysts
and trigger allergic inflammation.
Ascaris lumbricoides
Ascariasis

Ascariasis is the most common

helminthic infection, with an estimated
worldwide prevalence of 25% (0.8-1.22
billion people).
Usually asymptomatic, ascariasis is
most prevalent in children of tropical and
developing countries, where they are
perpetuated by contamination of soil by
human feces or use of untreated feces as
fertilizer.
Symptomatic
Symptomatic ascariasis may manifest as
growth retardation, pneumonitis, intestinal
obstruction, or hepatobiliary and
pancreatic injury. In developing countries,
ascariasis may exist as a zoonotic
infection in pigs, but little evidence has
shown transmission of porcine ascariasis
to humans.
 Intestinal obstruction — A mass of worms can obstruct
the bowel lumen in heavy Ascaris infection, leading to
acute intestinal obstruction. The obstruction occurs
most commonly at the ileocecal valve.

 Symptoms include colicky abdominal pain, vomiting

and constipation. Vomitus may contain worms.
Approximately 85 percent of obstructions occur in
children between the ages of one and five years.

 Complications including volvulus, ileocecal

intussusception, gangrene, and intestinal perforation
occasionally result.
 CLINICAL FEATURES — The majority of
infections with A. lumbricoides are
asymptomatic. However, the burden of
symptomatic disease worldwide is still relatively
high because of the high prevalence of disease.
Clinical disease is largely restricted to
individuals with a high worm load. When
symptoms do occur, they relate either to the
larval migration stage or to the adult worm
intestinal stage. Pathophysiologic mechanisms
include
Ascaris lumbricoides in small intestine – Intestinal obstruction occurs when
large masses of Ascaris accumulate. Source: Dr. Scott Smith’s lecture on GI
Nematodes for “Parasites and Pestilence,” Stanford University.
Ascaris lumbricoides

• A still colonoscopy picture of a 20cm worm

TAENIA sp.
Biology and life cycle
The worm attaches to the mucosa of the
small intestine by means of hooks and
suckers located in the scolex (head)
It has head (scolex), neck, strobila
(body) that consists of hundreds of
segments (proglottids)
After about 2 months gravid distal
proglottids begin the detach from the
worm and is excreted in the faeces
Biology and life cycle
Eggs contain an embryo that is called an
oncosphere
Action of gastric acid and intestinal
fluids (bile salts) release the embryos
from the eggs
Biology and life cycle
Oncospheres then actively cross the
bowel wall, enter the bloods stream and
migrate to internal organs
Cells within the cyst differentiate into
scolex – mature Taenia Solium larva
Development in the Definitive Host

When a juvenile worm reaches the

small intestine of the definitive host
it excyst, evaginate, or both to
begin its growth and sexual
maturation. The action of digestive
enzymes in the host ‘s gut may be
necessary to at least partially release
the organisms from their cyst.
Temperature is important and
sometimes enough for some worms.
 Persons infected with adult tapeworms will
have eggs in their stool 8 to 12 weeks
after initial infection. The adult tapeworm
can live in the intestine and produce eggs for
more than 30 years.
 Symptoms of cysticercosis may appear from
weeks to ten years or more after infection,
often when the larval cysts are dying.
T. saginata
Taenia Saginata
 Symptomatology in Taenia carriers is vague
and may include abdominal pain, nausea,
dizziness, headache, weight loss, increased
appetite, pruritus ani and excitation.

 Presence of the tapeworm can often be

detected by the carrier after observing
proglottids in the stool or active migration of
segments through the anus. It should be
stressed that many infections may go undetected.
Clinical Manifestations

occasional nausea or vomiting,

appetite loss,
epigastric or umbilical pain,
weight loss.
Moderate eosinophilia may develop.
Rarely, intestinal perforation may occur
from the scolex of Taenia
Treatment
 Niclosamide, is a nonabsorbed oxidative
phosphorylation inhibitor that kills the scolex
and anterior segments on contact, after which
the worm is expelled.
 Praziquantel, a synthetic isoquinoline-pyrazine
derivative, is an equally effective and relatively
nontoxic cesticidal compound. Since the scolex
is usually but not always destroyed, and a new
worm can regenerate if the scolex and a
minute portion of the neck survive, the patient
should be observed for several months, as egg-
bearing segments can reappear in 10-12 weeks.
T. solium
Taenia Solium
The intestinal symptoms of T. solium
infection are similar to infection with T.
saginata. The most important
complication of clinical syndrome is
cysticercosis.
It is the larval stage (metacestode) of
Taenia solium that produces cysticercosis.
Phatophysiology
 The feces of human carriers with the intestinal cestode
T. solium contain mature proglottids, each with several
thousand viable eggs that contaminate the environment
of places without sanitation and vegetables irrigated with
sewage contaminated with human feces.

 Both humans and pigs can become infected by

ingesting water and raw fruit or vegetables
contaminated with Taenia eggs.

 The eggs lose their keratin coat when they come in

contact with the digestive enzymes, and free
oncospheres traverse the intestinal wall and enter
the blood stream, which will carry them to the
nervous system.
Pathology
The hooked scolex of T. solium may
cause greater intestinal disturbance,
pain, and inflammatory
response than that caused by T. saginata,
but symptoms are still generally mild and
the
pathology minor.
Host Defenses
 Cysticercosis elicits considerable host
sensitization due to the systemic migration
and tissue localization of the cysticerci.
However, this response is insufficient to block
the initial infection but
 probably renders the normal host immune to
a subsequent one. Much of the damage from
 cysticercosis is caused by the severe
inflammatory host response that occurs after
the death and
 disruption of the parasite.
Conclucion
In this case, probably caci suffer for ileus
obstructive e.c. ascaris
To get the exact diagnosis, need more
examination.
Suggestion
Food and water sanitation
Adequate therapy
Reference
Netter FH. Atlas of anatomy. 2nd ed.
Canada: Icon Learning System,1997
Fauci AS, Braunwald E, Kasper DL,
Hauser SL, Longo DL, Jameson JL, et al,
editors. Harrison’s principle of internal
medicine. 17th ed. USA: Mc.Graw Hill
medical, 2008.
Reference
Sutanto I, Ismid IS, Sjarifuddin PK,
Sungkar S, editors. Buku ajar parasitologi
kedokteran UI. Edisi ke-4. Jakarta: Balai
penerbit FKUI,2008.
Wyllie R. The digestive system. In :
Kliegman RM, Berhman RE, Jenson HB,
Stanton BF. Nelson’s textbook of
pediatrics. 18th ed. Philadelphia: WB
Saunders Co,2007:1521-645.