PROBLEM 4 GI

FORTUNE DE AMOR
405140230
KEL. 14
LEARNING OBJECTIVES

1. MM Etiologi & Faktor Resiko Acute Abdomen

2. MM Patofisiologi Acute Abdomen

3. MM Tanda & Gejala Acute Abdomen

4. MM Pemeriksaan Fisik & Penunjang Acute Abdomen

5. MM Tatalaksana Acute Abdomen

6. MM Komplikasi & Prognosis Acute Abdomen

 ETIOLOGY

Inflammatory – Bacterial (acute appendicitis, diverticulitis)

– Chemical (a perforation of a peptic ulcer)

Mechanical obstructive conditions (intussusception, carcinoma of

the colon)
Neoplastic

Vascular Mesenteric arterial thrombosis, embolism

Congenital Defect Duodenal atresia, diaphragmatic hernia, chronic

malrotation of the intestine
Traumatic
range from stab and gunshot wounds to blunt
abdominal injuries producing such conditions
as splenic rupture
 Causes of Acute Abdomen
In first few years of life In older children- In adolescents – Non- surgical causes of
– abdominal pain –

Congenital Trauma Acute appendicitis Hyperthyroidisin

abnormalities
Incarcerated inguinal Intestinal worm Rupture of ovarian cyst Addison’s disease
hernia infestatioin
Intussuceptioin Primary peritonitis Testicular torsion Porphyria
Intestinal volvulus Meckel’s diverticulum Cholecystitis Diabetic ketoacidosis
(acalculous)
GI perforation Pancreatitis Lead poisoning
NEC in preterm Hypercalcemia
neonates

Non-specific abdominal pain

It is the most common cause of abdominal pain in late childhood and early
adolescence. It is a colicky pain with some localization that becomes worse after
meals. Bowel sounds may be increased and a palpable mass of feces may be
present in right or left iliac fossa. The causes commonly are constipation, irritable
bowel and chronic spasm.
 Causes of Acute Abdominal
emergencies in Baby and infants
History in Patients w it h Acute Abdominal Pain
Question Potential Responses and Indications
Where is the pain? See Fig. 1: Acute Abdomen and Surgical
Gastroenterology: Location of abdominal pain and
possible causes.
What is the pain like? Acute waves of sharp constricting pain that “take the
breath away” (renal or biliary colic)
Waves of dull pain with vomiting (intestinal
obstruction)
Colicky pain that becomes steady (appendicitis,
strangulating intestinal obstruction, mesenteric
ischemia)
Sharp, constant pain, worsened by movement
(peritonitis)
Tearing pain (dissecting aneurysm)
Dull ache (appendicitis, diverticulitis, pyelonephritis)
Have you had it before? Yes suggests recurrent problems such as ulcer
disease, gallstone colic, diverticulitis, or
mittelschmerz
Was the onset sudden? Sudden: “like a light switching on” (perforated ulcer,
renal stone, ruptured ectopic pregnancy, torsion of
ovary or testis, some ruptured aneurysms)
Less sudden: most other causes
How severe is the pain? Severe pain (perforated viscus, kidney
stone, peritonitis, pancreatitis)
Pain out of proportion to physical findings
(mesenteric ischemia)
Does the pain travel to Right scapula (gallbladder pain)
any other part of the Left shoulder region (ruptured spleen,
body? pancreatitis)
Pubis or vagina (renal pain)
Back (ruptured aortic aneurysm)
What relieves the pain? Antacids (peptic ulcer disease)
Lying as quietly as possible (peritonitis)
What other symptoms Vomiting precedes pain and is followed by
occur with the pain? diarrhea (gastroenteritis)
Delayed vomiting, absent bowel
movement and flatus (acute intestinal
obstruction; the delay increases with a
lower site of obstruction)
Severe vomiting precedes intense
epigastric, left chest, or shoulder pain
(emetic perforation of the intra-abdominal
esophagus)
 Surgery
TABLE
Indications for Surgical Consultations in Children with Acute
Abdominal Pain
Severe or increasing abdominal pain with progressive signs of
deterioration
Bile-stained or feculent vomitus
Involuntary abdominal guarding/rigidity
Rebound abdominal tenderness
Marked abdominal distension with diffuse tympany
Signs of acute fluid or blood loss into the abdomen
Significant abdominal trauma
Suspected surgical cause for the pain
Abdominal pain without an obvious etiology
Important Signs In Urgent Abdominal Disorder

Disorder Important Clinical Signs

Early perforation of Abdomen seems scaphoid
Gastrointestinal tract or Tense
other tract Hypoactive bowel sounds
Liver dullness disappears
Pressure pain
Muscular defense
Peritonitis Patient is passive
Bowel sound disappears
Coughing pain
Motility pain
Rebound tenderness
Muscular defense
Common inflammation signs
Body function drops
Infection mass or abscess Mass pain
Punching pain
Local test (psoas)
Common inflammation signs
Intestinal Abdominal distension
obstruction Strong peristlatic ( colic ) seen with naked eye
Borborigmi and felt by the patient
No peritoneum excitation
Paralytic ileus Abdominal distension
Decreased or even no bowel sounds
There’s no local pressure pain
Ischemia or strangulation
Unclear distension
Bowel sounds may be heard
Severe pain
Pressure pain is unclear
There’s possibility that blood may come out
from rectum
Toxic signs
Bleeding Pale
Shock
Probable distension
Pulse is felt if there is aorta aneurysm
Local pressure pain in ectopic pregnancies
Ascites
Anemia
 Diagnosis Age/Sex History Physical Lab Analysis Radiology Treatment
Typical presenting clinical characteristicsExamination
of common abdominal disorders (Abdomen)
in infants and
children
Appendicitis Peak:10-12 Periumbilical - Fever >100.5 Increased X-Ray - IV Fluids,
years M:F=3:2 pain (early) degree F. WBC (> - Concave - Antibiotics,
followed by 10000/cumm) curvature of -
vomiting and - Localized spine to the Antispasmodi
localized right right lower right. cs
lower quadrant quadrant -
pain. peritonitis - Presence of Appendectom
faecolith in 5– y
10 % USG
- Pericolic
/appendicea
fluid and/or
edema.
Intussuception 5 – 9 months - Paroxymal - Fever - - Dehydration X-Ray – - Ba enema /
M:F= 3:2 crampy Distension - Pallor Obstructive Gastrograffin
abdominal pain (late sign) - Later pattern enema, - In
followed by - Right Sided increased USG – severe cases:
periods of calm mass (85%) WBC. "Pseudo Operative
- Nonbilious kidney" and reduction,
vomiting "target" sign Resection and
(early), later Contrast end-to-end
bilious vomiting enema – anastomosis.
- Currant jelly Intussuceptio
stools. n and failure
of
gas/contrast
to reflux in
the small
bowel
Malrotati < 1 Unexpected - Is normal - X-Ray – - Surgical
on / month bilious vomiting in early Dehydratio Distended reduction,
midgut M:F=3:2 in an otherwise stages - n stomach, -
volvulus healthy infant There may - Anemia gasless Adhesionol
be - Increased abdomen ysis
tenderness WBC (late (high
. sign). obstructio
- n). Upper
Distension GL contrast
and Study –
peritonitis Abnormal
may be duodenal
late sweep
features Lower GI
contrast
study –
Caecum in
the left
abdomen
or RUQ
Incarcera <1 year - Irritability, - - Firm, - X-Ray – Surgery
ted F>M Crampy, tender Dehydratio Obstructive and
inguinal abdominal pain. groin or n - Later- pattern hernitomy.
hernia - Early – scrotal Increased
nonbilious mass. - WBC
vomiting, later Abdominal
bilious vomiting. distension
- Previously is seen in
noted groin late stages
mass.
Cholelith All - Associated Minimal Normal USG – Gall Cholecyste
iasis illness >- physical bladder ctomy
Hemolytic findings stones/slu
anemia dge
- Nausea,
vomiting,
- Vague right
upper quadrant
pain
Cholecyst All - Fever - Right - Fever, - - Increased USG – Gall IV Fluids, IV
itis upper quadrant Right LFT, - bladder antibiotics,
pain upper Increased distension, Antispasm
- Nausea, quadrant WBC thickening, odics,
vomiting tenderness stones/slud Cholecyste
- Mass ge - ctomy
Pericholecy
stic fluid
HIDA scan
– Non
functioning
gall
bladder
Intestinal Malrotation
Intestinal Malrotation
 Intestinal Malrotation
• General consideration
– Rotation of midgut is incomplete, the dorsal
fixation of the mesentery is defective and
shortened  bowel from the ligament Treitz to
the mid transverse colon may rotate around its
narrow mesenteric root and occlude the superior
mesenteric artery (volvulus)
 Intestinal Malrotation
Clinical Findings
• Symptoms and signs
Present in the first 3 weeks of life
– Bile-stained vomiting or overt small bowel obstruction
Intrauterine volvulus  intestinal obstruction or perforation
at birth
Neonate
– Ascites or meconium peritonitis
Later
– Intermittent intestinal obstruction, malabsorption, protein-
losing enteropathy or diarrhea
 Intestinal Malrotation
• Imaging
– Upper GI series shows the duodenojejunal
junction and the jejenum on the right side of the
spine
– Barium enema  demonstrate a mobile cecum
located in the midline, RUQ, or left abdomen
 Intestinal Malrotation
• Treatment
– Surgical treatment  Ladd procedure
• Young infants  should be performed even volvulus has not
occurred
– Laparoscopic repair
• Technically difficult
• Never performed in the presence of volvulus
• Complication
– Occlusion of the superior mesenteric artery  bowel
necrosis
• Prognosis
– Prognosis is guarded if perforation, peritonitis, or
extensive intestinal necrosis is present
Intussusception
 Intussusception
one part of the intestine invagination into the
next bowel
The place of Intususpection:
Ileokolik, ileoleal, kolokolik
 Intussusception
• Telescoping of one segment
of bowel into another
– Ileocolic most common
– 6 months – 3 years old
• Progressive course
– Intermittent acute abd. pain
– Vomiting
– Bloody stools (currant jelly)
– Fever, lethargy
– Palpable sausage-shaped
mass in upper abdomen
 Intussusception
• Etiology
– Small bowel polyp
– Meckel diverticulum
– Omphalomesenteric remnant
– Henoch-Schonlein purpura
– Lymphoma
– Lipoma
– Parasites
– Foreign bodies
– Viral enteritis with hypertrophy of Peyer patches
 Intussusception
• Clinical findings
Infant 3-12 months
– Recurring paroxysms of abdominal pain
– Screaming
– Drawing up of the knees
– Vomiting and diarrhea (occur soon)
– Bloody bowel movement with mucus (next 12 hours)
Child
– Lethargic between paroxysms and febrile (+)
– Abdomen is tender and often distended
– A sausage-shaped mass may be palpated (usually in the
upper mid abdomen)
 Intussusception
• Treatment
– Barium enema and air enema
• Barium enema should not be attempted if signs of
strangulated bowel, perforation, or toxicity are present
– Surgery
• Extremely ill patients
• Patients with evidence of bowel perforation
• Patients whom hydrostatic or pneumatic reduction has
been unsuccessful
 Intussusception
• Prognosis
– Relates directly to the duration of intussusception
before reduction
– Mortality rate with treatment is 1-2 %
INTESTINAL OBSTRUCTION
 Definition

• Intestinal obstruction is a partial or complete

blockage of the bowel that results in the
failure of the intestinal contents to pass
through.
 Causes

a. Mechanical obstructions
b. Non-mechanical obstruction (ileus or
paralytic ileus)
COMMON CAUSES OF INTESTINAL
OBSTRUCTION ACCORDING TO AGE
 Gallstone colic Volvulus Diverticulosis

Hernia incarcerate Intussusception Hirschprung’s disease

PATOPHYSIOLOGY
 Intestinal Obstruction
a. Mechanical obstructions
• Occur because the bowel is physically blocked and its
contents can not pass the point of the obstruction.
• 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)
 Intestinal Obstruction
b. Non-mechanical obstruction (ileus or paralytic ileus)
• Occurs because peristalsis stops. Peristalsis is the rhythmic
contraction that moves material through the bowel.
• Causes of paralytic ileus 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 . Example :
chemotherapy drugs such as vinblastine (Velban, Velsar) and
vincristine (Oncovin, Vincasar PES, Vincrex)
Intestinal Obstruction
 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
a. Adult Cancer of the duodenum or head of
pancreas, ulcer disease
b. Neonates Atresia, volvulus, bands, annular
pancreas
Jejunum and Ileum
a. Adult Hernias, adhesions (common), tumors,
foreign body, Meckel's diverticulum,
Crohn's disease (uncommon), Ascaris
infestation, midgut volvulus,
intussusception by tumor (rare)
b. Neonates Meconium ileus, volvulus of a malrotated
gut, atresia, intussusception
 Pathophysiology
A. Mechanical obstruction
Ingested fluid and food, digestive secretions, and gas accumulate
above the obstruction

The proximal bowel distends, and the distal segment collapses

The normal secretory and absorptive functions of the mucosa are
depressed

The bowel wall becomes edematous and congested.

• Severe intestinal distention is self-perpetuating and progressive,

intensifying the peristaltic and secretory derangements and
increasing the risks of dehydration and progression to strangulating
obstruction.
 Pathophysiology
B. Non mechanical obstruction (Ileus)
Ileus is mediated via activation of inhibitory spinal
reflex arcs.
Anatomically, 3 distinct reflexes are involved:
1.Ultrashort reflexes confined to the bowel wall
2.Short reflexes involving prevertebral ganglia
3.Long reflexes involving the spinal cord
 Intestinal Obstruction
Ileus Pseudo-obstruction Mechanical
Obstruction (Simple)
Symptoms Mild abdominal pain, Crampy abdominal Crampy abdominal
bloating, nausea, pain, constipation, pain, constipation,
vomiting, obstipation, obstipation, nausea, obstipation, nausea,
constipation, vomiting, anorexia vomiting, anorexia

Physical Silent abdomen, Borborygmi, tympanic, Borborygmi,

Examination distension, tympanic peristaltic waves, peristaltic waves,
Findings hypoactive or high-pitched bowel
hyperactive bowel sounds, rushes,
sounds, distension, distension, localized
localized tenderness tenderness

Plain Radiographs Large and small bowel Isolated large bowel Bow-shaped loops in
dilatation, diaphragm dilatation, diaphragm ladder pattern,
elevated elevated paucity of colonic gas
distal to lesion,
diaphragm mildly
elevated, air-fluid
levels
 Exams and Tests

• Listening bowel sound

– If the obstruction has persisted for long time or the bowel has been
significantly damaged bowel sounds decrease or silent
– Paralytic ileus decreased or absent bowel sound.
• Tests that show obstruction include:
– Abdominal CT scan
– Abdominal x-ray
– Barium enema
• Barium enema is a special x-ray of the large intestine, which includes the colon
and rectum.
• The liquid called barium sulfate is placed in the rectum that use for contrast
.Contrast highlights specific areas in the body, creating a clearer image.
– Upper GI and small bowel series
• An upper GI and small bowel series is a set of x-rays taken to examine the
esophagus, stomach, and small intestine.
 Treatment
Initial assessment
• The first step in treatment is inserting a nasogastric tube to suction
out the contents of the stomach and intestines.
• The patient is then given intravenous fluids to prevent dehydration
and correct electrolyte imbalances.

Nonsurgical approaches
• In some cases of volvulus, guiding a rectal tube into the intestines
will straighten the twisted bowels.
• In infants, a barium enema may reverse intussusception in 50-90%.
• An air enema is sometimes used instead of a barium enema. The
treatment can relieves the obstruction in many infants.
• In patients with only partial obstruction, a barium enema may
dissolve the blockage.
 Treatment
Surgical treatment
• If these efforts fail, surgery is necessary.
• The obstructed area is removed and part of the
bowel is cut away.
• If the obstruction is caused by tumors, polyps, or scar
tissue, they are removed.
• Hernias, if present, are repaired.
• Antibiotics are given to reduce the possibility of
infection.
 Prevention

• Most cases of intestinal obstruction are not

preventable.
• Surgery to remove tumors, polyps, or
gallstones helps prevent recurrences.
 Prognosis
Mortality
• Delayed diagnosis of volvulus in infants has a mortality rate of 23-33%
with prompt diagnosis and treatment the mortality rate is 3-9%.
• The bowel either strangulates or perforates, causing massive infection.
• With prompt treatment, most patients recover without complications.

Recurrence
• As many as 80% of patients whose volvulus is treated without surgery
have recurrences.
• Recurrences in infants with intussusception are most likely to happen
during the first 36 hours after the blockage has been cleared.
• The mortality rate for unsuccessfully treated infants is 1-2%.
EXAMPLES OF CAUSES OF INTESTINAL
OBSTRUCTION

Obstruction due to Obstruction due to Obstruction due

adhesions mesenteric occlusion to hernia

Obstruction due to Obstruction due to Obstruction due to

intussusception tumor volvulus
 Differential diagnosis
Ileus Pseudo-obstruction Mechanical
obstruction (simple)
Symptoms Mild abdominal pain, Crampy abdominal Crampy abdominal
bloating, nausea, pain, constipation, pain, constipation,
vomiting, obstipation, obstipation, nausea, obstipation, nausea,
constipation vomiting, anorexia vomiting, anorexia

Physical Examination Silent abdomen, Borborygmi, Borborygmi,

Findings distention, tympanic tympanic, peristaltic peristaltic waves,
waves, hypoactive or high-pitched bowel
hyperactive bowel sounds, rushes,
sounds, distention, distention, localized
localized tenderness tenderness

Plain Radiographs Large and small bowel Isolated large bowel Bow-shaped loops in
dilatation, diaphragm dilatation, diaphragm ladder pattern,
elevated elevated paucity of colonic gas
distal to lesion,
diaphragm mildly
elevated, air-fluid
levels
 Helminth Infection that
Cause Ileus Obstruction
• Ascaris lumcbricoides
• Taenia saginata
• Diphyllobotrium latum
• Fasciola buski
ASCARIS LUMBRICOIDES
 Ascaris lumbricoides
• 240.000 eggs/ day
• The larvae then migrate via the venous
circulation to the pulmonary circulation and to
the lungs.
Pathophysiology Ascaris Infection
 Diagnosis
• Diagnosis is by microscopic detection of eggs in
stools.
• Occasionally, larvae can be found in the sputum
during the pulmonary phase.
• Eosinophilia can be marked while larvae migrate
though the lungs but usually subsides later in
infection when adult worms reside in the
intestine.
• Chest x-ray during the pulmonary phase may
show infiltrates (Löffler's pneumonia).
 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
 Treatment
• Mebendazole
• Piperazine
• Pyrantel pamoate
• Albendazole
• Thiabendazole
 Treatment
• Prevention
Prevention and Control Efforts on to the cycle of
life and the nature of this worm eggs, following
steps: health counseling on good sanitation,
Family hygiene and personal hygiene such as:
Not using feces as a fertilizer plant.
Preparation of food and to eat, wash hands using
the soap.
For those who consume fresh vegetables (raw) as
Lalapan, washed again with flow water.
Surgery of Ascaris
PERITONITIS
 Definition

Peritoneum inflammation inside the abdominal cavity

that can be caused by infections, autoimmune, and
chemical processes
• Facts :
– Infectious Peritonitis 
• Primary : infectious agent from outside, living inside the
peritoneum through hematogenic and lymphogenic path
• Secondary : Spreads from intra abdominal organ
– Trans placental infection causes peritonitis on neonatus
– Most often infectious and usually related to a perforated
viscus
– Often caused by infection before or after birth
 Etiology
• Ruptured appendix
• Diverticulum
• Perforated peptic ulcer
• Incarcerated hernia
• Gangrenous gall bladder
• Volvulus
• Bowel infarction
• Cancer
• Inflammatory bowel disease
• Intestinal obstruction.
 Signs & Symptoms
• Swelling & tenderness in
the abdomen
• Limited Urine Production
• Fever & Chills
• Inability to pass gas or feces
• Loss of Appetite

• Nausea & Vomiting

 Classification
• Acute or Chronic in natural history
• Primary or Secondary in etiology
• Localized or Diffuse in location
• Infectious or Aseptic in pathogenesis
 Primary Acute Peritonitis
• Definition :
– Peritoneum cavity infection, with no sign of any intra-abdominal
organ infection
• Facts :
– Most are child that suffers ascites from a nefrotic syndrome or
cirrhosis
– Child < 6 y/o
• Etiologies :
– Pneumococcus
– Streptococcus group A
– Enterococcus
– Staphylococcus
– Bacteria gram (-) – s/a Eschericia coli and Klebsiellapneumoniae
 Primary Acute Peritonitis
• Clinical Manifestations :
– Fever
– Abdominal pain
– Vomiting
– Diarrhea
– Shallow/short & fast breathing (hypotension &
tachycardia)
– Painful and stiff (Abdominal Palpation)
– Hypo/no bowel sound
 Primary Acute Peritonitis
• Diagnosis :
– Leukocytosis with polymorphonuclear cell
– Proteinuria (patient with nefrotic syndrome)
– Large & small intestine dilatation (roentgen)
– Peritoneal fluid pH < 7,35 and an increased lactate
concentration
 Secondary Acute Peritonitis
• Definition :
– Peritoneum inflammation caused by bacterial
infection through damaged abdominal organs
• Etiologies :
– Appendix perforation (most common)
– Torn DiverticullumMeckeli
– Ulcuspepticum
– Traumatic Perforation
– Other intra-abdominal organ damage
 Secondary Acute Peritonitis
• Clinical Manifestation :
– Fever (> 39.5C)
– Nausea
– Vommiting
– tense abdomen, limited movements, hypo/no
bowel sound
– Syok (massive exudation and systemic vasodilator
release)
• Diagnosis :
– Perifer white blood cells 12.000 cell/mm2 w/
polymorphonuclear
– Obstruction, liquid inside the peritoneum, air
inside the peritoneum

• Therapy :
– Antibiotics.
– Surgery.
 Localized Secondary Peritonitis
(Peritoneum Abscess)
• Clinical Manifestation :
– Prolonged Fever
– Loss of appetite
– Vommiting
– Weak
 Patophysiology
• Infectious agents gain access to peritoneal cavity through:
– Perforated viscus
– Penetrating wound of the abdominal wall
– Eternal introduction of a foreign object that is infected (chronic
peritoneal dialysis catheter)
• Aseptic  irritation by abnormal presence of physiologic
– fluids (e.g, gastric juice, bile, pancreatic enzymes, blood, or
urine)
– Foreign bodies (e.g, surgical sponges)
– Lupus erythematosus, porphyria, or familial Mediterranean
fever
 Examination
• Blood Test

• Samples of fluid from the abdomen

• CT Scan

• Chest X-rays

• Peritoneal lavage.
 Therapy
– Relies on rehydration
– Correction of electrolyte abnormalities
– Antibiotics
– Morphine for pain
– Surgical correction of the underlying defect
– Dietary supplements (omega 3, omega 6 fatty
acids, vitamin A, E, C, and zinc)
 Evaluation
• The usual sounds made by the active intestine
and heard during examination with a
stethoscope will be absent, because the
intestine usually stops functioning.
• The abdomen may be rigid and boardlike
• Accumulations of fluid will be notable in
primary due to ascites.
 Prognosis
– Mortality rates <10%, on perforated ulcer or
ruptured appendix or diverticulum
– Mortality rates >40%, on elders, underlying
illnesses, peritonitis has been present for
>48hours
 Appendicitis
Inflammation & obstruction of the vermiform appendix

http://www.privatehealth.co.uk/EasysiteWeb/getresource.axd?AssetID=2683&amp;type=full&amp;servicetype=inline&amp;customSizeId=0
 EPIDEMIOLOGY
• In USA > 250.000 appendectomies/year that
has been done & it is the common abdominal
emergency surgery

• Predilection of age is 5-30 years old

• < 2 years old  its incidens is 70-80% for

perforation & the common peritonitis because
of the delaying diagnostic
 Etiology
• Mucosal ulceration
• Fecal mass
• Stricture
• Infection
 Patophysiology Necrosis
I
f
Mucus, stool, or The blood supply to Perforation
Reduced
parasites the appendix is cut
blood flow
off
Appendicular Peritonitis
Inflammation abcsess

Obstructs the Obstruction of Pressure in

appendix mucus outflow appendix
increases

Multiplying bacteria,
Restricting blood flow inflammation and Appendix
to the organ pressure continue to contracts
increase

Severe abdominal pain

Sign and Symptom
 SIGNS AND SYMPTOMS
• Aching pain that begins around your periumbilical and often shifts to your lower
right abdomen
• Pain that becomes sharper over several hours
• Tenderness that occurs when you apply pressure to your lower right abdomen
• Sharp pain in your lower right abdomen that occurs when the area is pressed on
and then the pressure is quickly released (rebound tenderness)
• Pain that worsens if you cough, walk or make other jarring movements
• Nausea
• Vomiting
• Loss of appetite
• Low-grade fever ( 37,2-37.8°C)
• Constipation
• Inability to pass gas
• Diarrhea
• Abdominal swelling
 DIAGNOSIS
• Medical history
• Physical examination
– low grade fever
– Pain at Mc Burney’s point
– Rebound tenderness
– Guarding
– Psoas sign +
• 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
• Surgical removal
• IV fluids and antibiotics (Metronidazole,
Gentacimin,Cefotetan,Cefoxitin)
Appendectomy
 Complication
• Intra-abdominal abscess
• Fecal fistula
• Intestinal obstruction
• Incisional hernia
• Peritonitis
• Death
 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.
 Ascariasis
• Disease :
• Ascariasis, ascariasis infection, roundworm infection.
 Pathophysiological mechanism
 Adult worms move throughout the GI tract and may become incarcerated, leading to
obstructive pathology.
 The worms may die → leading to inflammation, necrosis, infection, and abscess
formation.
 If they migrate through an existing perforation in the bowel wall → secondary to
tuberculosis or typhoid → cause a granulomatous peritonitis.
 Larvae during migration → may be deposited in the brain, spinal cord, kidney, or other
organs → leading to granuloma formation, inflammation, or infection.
 They may become entwined in a bolus and obstruct the small bowel; this is most
common in the terminal ileum, although other, more proximal, sites have been rarely
reported.
 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.
 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, which 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.
HERNIA
 Etiology
Any condition that increases the pressure in the intra abdominal cavity may
contribute to the formation of a hernia, including the following:
• Marked obesity
• Heavy lifting
• Coughing
• Straining with defecation or urination
• Ascites
• Peritoneal dialysis
• Ventriculoperitoneal shunt
• Chronic obstructive pulmonary disease (COPD)
• Family history of hernias[16]
 Pathophysiology
Types of Hernia – Location

• Indirect hernia
An indirect inguinal hernia follows the tract through the inguinal canal. This
results from a persistent process vaginalis. The inguinal canal begins in the intra-
abdominal cavity at the internal inguinal ring, located approximately midway
between the pubic symphysis and the anterior iliac spine. The canal courses down
along the inguinal ligament to the external ring, located medial to the inferior
epigastric arteries, subcutaneously and slightly above the pubic tubercle.

• Direct hernia
A direct inguinal hernia usually occurs due to a defect or weakness in the
transversalis fascia area of the Hesselbach triangle. The triangle is defined
inferiorly by the inguinal ligament, laterally by the inferior epigastric arteries, and
medially by the conjoined tendon.[5]
• Femoral hernia
The femoral hernia follows the tract below the inguinal ligament through the
femoral canal. The canal lies medial to the femoral vein and lateral to the
lacunar (Gimbernat) ligament.

• Umbilical hernia
The umbilical hernia occurs through the umbilical fibromuscular ring, which
usually obliterates by 2 years of age. They are congenital in origin and are
repaired if they persist in children older than age 2-4 years.[2, 5]

• Richter hernia
The Richter hernia occurs when only the antimesenteric border of the bowel
herniates through the fascial defect. The Richter hernia involves only a
portion of the circumference of the bowel. As such, the bowel may not be
obstructed, even if the hernia is incarcerated or strangulated, and the patient
may not present with vomiting. The Richter hernia can occur with any of the
various abdominal hernias and is particularly dangerous, as a portion of
strangulated bowel may be reduced unknowingly into the abdominal cavity,
leading to perforation and peritonitis.[6]
• Incisional hernia
This iatrogenic hernia occurs in 2-10% of all abdominal operations secondary
to breakdown of the fascial closure of prior surgery. Even after repair,
recurrence rates approach 20-45%.

• Spigelian hernia
This rare form of abdominal wall hernia occurs through a defect in the
spigelian fascia, which is defined by the lateral edge of the rectus muscle at
the semilunar line (costal arch to the pubic tubercle) The two subtypes are
interstitial and subcutaneous, which are best defined using CT and assist with
optimizing the surgical approach when indicated.[7, 8, 9]

• Obturator hernia
This hernia passes through the obturator foramen, following the path of the
obturator nerves and muscles. Obturator hernias occur with a female-to-male
ratio of 6:1, because of a gender-specific larger canal diameter and
predominately in the elderly.
 Differential Diagnoses

• Epididymitis
• Hidradenitis Suppurativa
• Hydrocele
• Lymphogranuloma Venereum
• Testicular Torsion
 Medication
For strangulated hernias, start broad-spectrum antibiotics.
Antibiotics are administered routinely if ischemic bowel is
suspected.

Multiple regimens that cover for bowel perforation and/or

ischemic bowel can be used. Cover for both aerobic and
anaerobic gram-negative bacteria.
 Complications
• If strangulation of the hernia is missed, bowel perforation and
peritonitis can occur.
• Hernias can reappear in the same location, even after surgical
repair.
 Pottasium
• The magnitude of the potassium gradient across cell
membranes determines excitability of nerve and muscle
cells, including the myocardium.
 Rapid or significant changes in the serum potassium
concentration can have life-threatening consequences.
• Evaluation of serum potassium must consider the effects of
changes in serum pH.
1. Serum pH falls  serum potassium rises, because
potassium shifts from the cellular to the vascular space.
2. Serum pH rises  serum potassium falls , because
potassium shifts from the vascular space into the cells.

http://circ.ahajournals.org/content/112/24_suppl/IV-121.full
 Imbalance Pottasium
• Hyperkalemia  serum potassium concentration
>5 mEq/L, it is moderate (6 to 7 mEq/L) and severe
(>7 mEq/L) hyperkalemia that are life-threatening
and require immediate therapy.
• Hyperkalemia is most commonly seen in patients
with end-stage renal disease.
• Signs and symptoms of hyperkalemia include:
weakness, ascending paralysis, and respiratory
failure. A variety of electrocardiographic (ECG)
changes suggest hyperkalemia.

http://circ.ahajournals.org/content/112/24_suppl/IV
-121.full
 Imbalance Pottasium
• Hypokalemia  serum potassium level <3.5 mEq/L.
• The most common causes of low serum potassium: gastrointestinal loss
(diarrhea, laxatives), renal loss (hyperaldosteronism, severe
hyperglycemia, potassium-depleting diuretics, carbenicillin, sodium
penicillin, amphotericin B), intracellular shift (alkalosis or a rise in pH),
and malnutrition.
• The major consequences of severe hypokalemia result from its effects on
nerves and muscles (including the heart).
 The myocardium is extremely sensitive to the effects of hypokalemia,
particularly if the patient has coronary artery disease or is taking a
digitalis derivative.
• Symptoms of mild hypokalemia are weakness, fatigue, paralysis,
respiratory difficulty, constipation, paralytic ileus, and leg cramps; more
severe hypokalemia will alter cardiac tissue excitability and conduction.

http://circ.ahajournals.org/content/112/24_suppl/IV-121.full
 Hypokalemia  Paralytic Ileus
• Mekanisme kontraksi otot polos:
• Otot polos (sel Cajal  BER/irama listrik
dasar)  fluktuasi potensial membran (variasi
pelepasan ion Ca dari RE/penyerapan ion Ca
dari mitokondria sel Cajal)  ada makanan 
capai ambang  potensial aksi aktivasi
saluran ion Ca  influks ion Ca ke sel otot
polos
 References
• Hay WW, Levin MJ, Sondheimer JM, Deterding RR. Current
diagnosis and treatment pediatrics. 19th ed. USA:Mc Graw Hill.
2009. pp.83-4, 583-8, 591, 599-600
• Towsend, Courtney M et al.Abdomen. In:Sabiston Textbook of
Surgery. 18th ed. Saunders Elsevier.2008.
• Chen C, M.C.Kim.Gatrointestinal Imaging in Pediatric Surgery.
In: Pediatic Gastrointestinal Imaging and Intervention. 2nd ed.
• McCance KL, Huether SE, Brashers VL, Rote NS. The Digestive
System. In:Pathophysiology. 6th ed. 2010.
• Reid R, Roberts F. gastrointestinal Tract. In: pathology
illustrated. 6th ed. USA: Saunders Elsevier. 2005. pp. 320-36