Ayu Suci Pratiwi

405140238

PEMICU 4
GI TRACK

LEARNING OBJECTIVE
1. Describe the etiology of acute abdomen ( appendicitis,
ileus
paralitik,
acute
peritonitis,
perforation,
incarcerated/strangulated
hernia,
intussusception,
diverticulitis, infeksi cacing)
2. Describe the pathophysiology of acute abdomen
(potassium imbalance)
3. Analyze the clinical findings of acute abdomen (signs
and symptoms) and laboratory findings, imaging studies
4. Describe the terapeutic management of acute abdomen
(pharmacology,
nonpharmacology,
surgery)
and
prescription
5. Describe the complication and prognosis of acute
abdomen.

LO 1

DESCRIBE THE ETIOLOGY OF ACUTE ABDOMEN

Acute Appendicitis
ACUTE APPENDICITIS

Acute Appendicitis:
Pathogenesis

Its etiology is still not completely understood

Fecaliths, incompletely digested food residue, lymphoid
hyperplasia, intraluminal scarring, tumors, bacteria, viruses, and
inflammatory bower disease have all been associated with
inflammation of the appendix and appendicitis
Although not proven, obstruction of the appendiceal lumen is
believed to be an important step in the development of
appendicitis
In some cases, obstruction leads to bacterial overgrowth and
luminal distension, with an increase in intraluminal pressure
that can inhibit the flow of lymph and blood in some cases
Then, vascular thrombosis and ischemic necrosis with
perforation of the distal appendix may occur
Appendiceal fecaliths (or appendcicoliths) are found in
approximately 50% of patients with gangrenous appendicitis who
perforeate but are rarely identified in those who have simple
disease
When perforation occurs, the resulant leak may be contained by

Acute Appendicitis: Clinical

Manifestations
Non-spesific complaints occur first
Patients may notice changes in bowel habits or malaise
and vague, perhaps intermittent crampy, abdominal
pain in the epigastric or periumbilical region
The pain susequently migrates to the right lower
quadrant over 12-24 h, where it is sharper and can be
difinitively localizes as transmural inflmmation when the
appendix irritates the parietal peritoneum
Patients with appendicitis will most often observe that their
nausea, if present, followed the development of abdominal
pain, which can help distinguish them from patients with
gastroenteritis, for example, where nausea occurs first

Acute Appendicitis: Clinical

Manifestations

Acute Appendicitis: Clinical

Manifestations
Patients with pelvic appendicitis are more likely to present with
dysuria, urinary frequency, diarrhea, or tenesmus. They
may only experience pain in the suprapubic region on
palpation or on rectal or pelvic examination
Patients with simple appendicitis normally only appear mildly ill
with a pulse and temperature that are usually only slightly
above normal
If the temperature is >38.3 C and if there are rigors, the provider
should be concerned about other disease processes beside
appendicitis or the presence of complications such as perforation
Patients with appendicitis will be found to lie quite still to
avoid peritoneal irritation caused by movement, and some
will report discomfort caused by a bumpy car ride on the way to
the hostpital or clinic, coughing, sneezing, or other actions that
replicate a Valsava maneuver

Acute Appendicitis: Clinical

Manifestations

Acute Appendicitis: Differintial

Diagnosis

Acute Appendicitis: Laboratory

Testing
Laboratory testing does not identify patients with
appendicitis but can help the clinician work through the
differintial diagnosis
The white blood cell count is only mildly to
moderately elevated in approximately 70% of
patients with simple appendicitis (with a leukocytosis
of 10,000-18,000 cells/uL). A left shift toward
immature PMN leukocytes is present in >95% of
cases
Serum amylase and lipase levels shoud be measured
Urinalysis is indicated to help exclude genitourinary
conditions that may mimic acute appendicitis

Acute Appendicitis: Imaging

Plain films of the abdomen are rarely helpful and so
are not routinely obtained unless the clinician is
worried about other conditions such as intestinal
obstruction, perforated viscus, or ureterolithiasis
USG findings suggesting the presence of
appendicitis include wall thickening, an increase
appendiceal diameter, and the presence of free fluid
CT findings include dilation with wall thickening, a
lumen that does not fill with enteric contrast, and
fatty tissue stranding or air surrounding the
appendix, which suggests inflammation

Acute Appendicitis:
Treatment
In the absence of contraindications, a patient who has a
strongly suggestive medical history and physical
examination with supportive laboratory findings should
undergo appendectomy urgently
If there is a mass representing a phlegmon or abscess,
such patients are best served by treatment with broad
spectrum antibiotics, drainage if there is an abscess
>3cm in diameter, and parenteral fluids and bowel rest
Laparoscopic appendectomy
Postoperative complications are fever and
leukocytosis. Continuation of these findings beyong 5
days should rise concern for the presence of an
intraabdominal abscess

Peritonitis
ACUTE APPENDICITIS

Acute Peritonitis:
Introduction
Acute peritonitis, or inflammation of
the visceral and parietal peritoneum,
is most often but not always
infectious in origin, resulting from
perforation of a hollow viscus. This is
called secondary peritonitis, as
opposed to primary or
spontaneous peritonitis, when a
spesific intraabdominal source
cannot be identified. In either

Acute Peritonitis: Etiology

Infective organism
Secondary peritonitis most commonly results from
perforation of the appendix, colonic diverticuli, or the
stomach and duodenum
Others: complication of bowel infarction or incarceration,
cancer, inflammatory bowel disease, and intestinal
obstruction or volvulus
Over 90% of the cases of primary or spontaneous
bacterial peritonitis occur in patients with ascites or
hypoproteinemia (< 1 g/L)
Aseptic peritonitis is most commonly caused by the
abdnormal presence of physiologic fluids like gastric
juice, bile, pancreatic enzymes, blood, or urine

Acute Peritonitis: Clinical

Features
The cardinal signs and symptoms of peritonitis are
acute, typically severe, abdominal pain with
tenderness (diffuse/localized) and fever
Bowel sounds are usually absent to hypoactive
Most patients present with tachycardia and signs
of volume depletion with hypotension
Laboratory testing typically reveals a significant
leukocytosis, and patients may be severely
acidotic
Radiographic studies may show dilation of the
bowel and associated bowel wall edema

Acute Peritonitis: Differential

Diagnosis

Acute Peritonitis: Therapy And

Prognosis
Successful treatment depends on
correcting any electrolyte
abnormalities, restoration of fluid
volume and stabilization of the
cardiovascular system, appropiate
antibiotic therapy, and surgical
correction of any underlying
abnormalities

PARALYTIC ILEUS

INTUSSUSCEPTION

Intussusception
Occurs when a portion of alimentary track is
telescoped into a adjascent segment.
Common obstruction for 3 month 6 years old
60% occur < 1yo
80% occur 24 month

http://eradiology.bidmc.harvard.edu/LearningLab/gastro/Daftary.pdf

http://eradiology.bidmc.harvard.edu/LearningLab/gastro/Daftary.pdf

Palpitation
on
abdomen

http://eradiology.bidmc.harvard.edu/LearningLab/gastro/Daftary.pdf

http://eradiology.bidmc.harvard.edu/LearningLab/gastro/Daftary.pdf

Diagnosis
Clinical history &physical findings suggestive of
intussusception performed ultrasound.
Screening
ultrasounds
for
suspected
intussusception
increases
the
yield
of
diagnostic/therapeutic
enemas
and
reduces
unnecessary radiation exposure in children with
negative ultrasound examinations
Contrast enemas demonstrate a filling defect or
cupping in the head of the contrast media where its
advance is obstructed by the intussusceptum
A central linear column of contrast media may be
visible
in
the
compressed
lumen
of
the
intussusceptum, and a thin rim of contrast may be
seen trapped around the invaginating intestine in the
folds of mucosa within the intussuscipiens (coiledspring sign)

http://eradiology.bidmc.harvard.edu/LearningLab/gastro/Daftary.pdf

DIFFERENTIAL
DIAGNOSIS
The bloody stools and abdominal cramps that
accompany enterocolitis can usually be
differentiated from intussusception
in enterocolitis the pain is less severe and less
regular, there is diarrhea, and the infant is
recognizably ill between pains.

Bleeding from Meckel diverticulum is usually

painless
Because intussusception can be a complication
of this disorder, ultrasonography may be
needed to distinguish the conditions

Treatment
Reduction of an acute intussusception is an
emergency procedure and performed immediately
after diagnosis in preparation for possible surgery
patients with prolonged intussusception with signs of
shock, peritoneal irritation, intestinal perforation, or
pneumatosis intestinalis, reduction should not be
attempted.

An ileoileal intussusception is best demonstrated

by abdominal ultrasonography
An ileoileal intussusception is best demonstrated
by abdominal ultrasonography

Prognosis
Untreated intussusception in infants is usually fatal;
the chances of recovery are directly related to the
duration of intussusception before reduction.
Most infants recover if the intussusception is reduced in
the 1st 24 hr.
But the mortality rate rises rapidly after this time,
especially after the 2nd day.
Spontaneous reduction during preparation for operation
is not uncommon.

The recurrence rate after reduction of

intussusceptions is 10%
and after surgical reduction it is 25%;
none has recurred after surgical resection

PERFORATION

Gastrointestinal perforation
Definition
Gastrointestinal perforation is a hole that develops through the
wall of the esophagus, stomach, small intestine, large bowel,
rectum, or gallbladder. This condition is a medical emergency.
Etiology :
Gastrointestinal perforation can be caused by a variety of
illnesses. These include:
Appendicitis
Cancer
Crohn's disease
Diverticulitis
Gallbladder disease
Pepticulcer disease
Ulcerative colitis
https://medlineplus.gov/ency/article/0002

Symptoms

Clinical Assessment

Symptoms may
include:
Severe abdominal
pain
Chills
Fever
Nausea
Vomiting

X-rays of the chest or

abdomen may show air in
the abdominal cavity,
called free air. This is a
sign ofa tear (perforation)
A CT scan of the abdomen
often shows the location
of the perforation
The white blood cellcount
is often higher than
normal

Treatments
Treatment usually involves surgery to repair the
hole (perforation). Occasionally, a small part of
the intestine must be removed. A temporary
colostomy or ileostomy may be needed.
In rare cases, antibiotics alone can be used to
treat patients whose perforations have closed.
This can be confirmed by a physical exam, blood
tests, CT scan, and x-rays.

Prognosis
Surgery is usually
successful,
but
depends
on
the
severity
of
the
perforation and the
length of time to
treatment.

Complications
Bleeding
Infection ( including a
widespread infection
called sepsis, which
can lead to death )
Intra-abdominal
abscess

ASCARIS LUMBRICOIDES

Introduction
A. lumbricoides is the largest intestinal nematode
parasite of humans, reaching up to 40 cm in
length.
Clinical disease arises from larval migration in the
lungs or effects of the adult worms in the
intestines.
Epidemiology :
Ascaris is widely distributed in tropical and
subtropical regions as well as in other humid
areas, including the rural southeastern United
States.
Transmission typically occurs through fecally
contaminated soil and is due either to a lack of
sanitary facilities or to the use of human feces

Morphology & Diagnosis

Stage

Characteristic

Adult
worm

Female: 20-35cm, copulation ring 1/3 anterior, sharp tail

Male: 15-31cm, curved posterior end, spicula
(-) cephalic alae, (+) 3 lips

Fertilized
egg

60x45 um
Inner shell: thick hyaline coat
Outer shell: albuminoid coat (corticated; decorticated: (-)
albuminoid coat), usually stained a golden brown

Unfertilize
d egg

90x40 um
Inner shell: thin hyaline coat
Outer shell: albuminoid coat (corticated), (-) albuminoid
coat (decorticated)
Consisted of rough granules

Diagnosis:
Larval migration phase: finding larvae in sputum, or in gastric
washings
Intestinal phase: eggs (fertilized or unfertilized) or adult worms in
stool
Radiographic: w/ barium ingestion trolley car lines, to view

Signs and Symptoms

Most patients are asymptomatic. When symptoms
occur, they are divided into 2 categories:
1. Early (larval migration) and
2. late (mechanical effects).
. In the early phase (4-16 d after egg ingestion),
respiratory symptoms result from the migration of
larvae through the lungs. Classically, these symptoms
occur in the setting ofeosinophillic pneumonia (Lffler
syndrome).
Fever
Nonproductive cough
Dyspnea
Wheezing

Signs and Symptoms

In the late phase (6-8 wk after egg ingestion),
gastrointestinal symptoms may occur and are
more typically related to the mechanical effects
of high parasite loads.
Passage of worms (from mouth, nares, anus)
Diffuse or epigastric abdominal pain
Nausea, vomiting
Pharyngeal globus, "tingling throat"
Frequent throat clearing, dry cough
Complications - Biliary and intestinal
obstruction,appendicitis, pancreatitis

Physical Examination
General
Fever
Jaundice (in biliary obstruction)
Cachexia (due to malnutrition)
Pallor (anemia)
Urticaria(early infection)
Pulmonary
Wheezing
Rales
Diminished breath sounds

Physical Examination
Abdominal
Abdominal tenderness, which may be diffuse (in
obstructive infections), or localized to the right lower
(appendicitis) or right upper quadrant (hepatobiliary
infections)
Peritoneal signs in cases of bowel perforation
Obstructive
symptoms
(nausea/vomiting/constipation/distention)
Migrating larva may transmit other organisms,
causing bacterial pneumonia orcholangitis. Rare cases
of airway obstruction have also been reported. Other
much less common presentations include lacrimal
drainage obstruction, small bowel intussusception,
acute interstitial nephritis, and encephalopathy.

Diagnosis
Laboratory Studies
Early infection (larval migration)
Complete blood count (CBC) may show eosinophilia.
Sputum analysis may reveal larvae or CharcotLeyden crystals.
Stool examination findings are typically normal in
absence of previous infection (during the first 40 d).
Ascarisspecific 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.

Diagnosis
Radiologic Findings
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).
ObstructingAscarislesions 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.
Ultrasonography may detect worms in the gallbladder

Treatmen Info
t
Mebendaz
ole

Drug of choice for both children & adults

Albendazol Mechanism:
e
Binds irreversibly to tubulin, blocking
microtubule assembly & inhibiting glucose uptake
by the worm
Drug of choice for ascariasis & other roundworms
(exceps strongyloides)
Side effects: minimal: diarrhea, abd pain,
hypersensitivity (rare)
Pyrantel
Pamoate

Mechanism:
Depolarizes the myoneural junction in the worms,
paralyzing them in a spastic condition
Side effect: headache, dizziness, fever, nausea,
Treatment for obstruction:
vomiting, abd cramps, diarrhea
Surgical or endoscopic removal
Ineffective for strongyloidiasis & trichuriasis
Intestinal obs: treated by nasogastric suction until vomiting is
controlled, 1-2hrs after suction is discontinued, antihelmintic is
administered (eg: piperazine)

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)
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

DIVERTICULITIS

DIVERTICULAR DISEASE
True diverticulum is a saclike herniation of the
entire bowel wall
a pseudo diverticulum involves only a protrusion
of the mucosa and submucosa through the
muscularis propria of the colon.
type of diverticulum affecting the colon is the
pseudodiverticulum.
Commonly affect the left & sigmoid colon
In asia population: 70% of diverticula are seen
in the right colon and cecum as well

Pathophysiology
Diverticulitis : inflammation of a diverticulum.
The diverticula occur at the point where the nutrient
artery (vasa recti) penetrates through the muscularis
propria resulting in a break in the integrity of the
colonic wall.
This anatomic restriction may be a result of the relative
high-pressure zone within the muscular sigmoid colon.
Higher-amplitude contractions + constipated (high fat
content stool within the sigmoid lumen in an area of
weakness in the colonic wall) = the creation of these
diverticula
Consequently, the vasa recti is either compressed or
eroded leading to either perforation or bleeding.

Presentation Evaluation and

Management of Diverticular Bleeding
Hemorrhage from a colonic diverticulum is the
most common cause of hematochezia in
patients >60 years.
only 20% of patients with diverticulosis will
have gastrointestinal bleeding.
Increase risk for bleeding:
Tend to be hypertensive.
Have atherosclerosis.
Regularly use aspirin and nonsteroidal antiinflammatory agents.
Bleeding: self limited and stop spontaneously
with bowel rest

Presentation Evaluation and Management of

Diverticular Bleeding

Initial licalization of diverticular bleeding:

Colonoscopy
Angiogram
Nuclear medicine tagged red cell scan.
If the patient stable best managed by angiography
If the bleeding site is localized can be occluded
successfully with a coil (in 80% of cases).
Alternatively, a segmental resection of the colon can be
undertaken to eliminate the risk of further bleeding.
with highly selective coil embolization, the rate of colonic
ischemia is < 10% and the risk of acute rebleeding is <25%.
If the patient is unstable or has had a 6-unit bleed within 24 h
surgery should be performed.
If the bleeding has been localized a segmental resection can
be performed.

Presentation

Diagnosis of diverticulitis
Best made in CT with followig findings:
Sigmoid diverticula
Thickened colonic wall >4mm
inflammation within the periodic fat + the collection of
contrast material or fluid.

Symptoms of irritable bowel syndrome may

mimic those of diverticulitis.
Therefore, suspected diverticulitis that does not meet
CT criteria or is not associated with a leukocytosis or
fever is not diverticular disease.
Colonoscopy considered important in the exclusion
of colorectal cancer

Complicated divertivular
disease
Complicated diverticular disease is
defined as diverticular disease
associated with an abscess or
perforation and less commonly with a
fistula.
Perforated diverticular disease is
staged using the Hinchey
classification system.
To predict outcomes following the
surgical management of complicated

the Hinchey
classificatio
n system.

Treatment medical management

Asymptomatic best managed by diet alteration. eat fiberenriched diet (30 gr of fiber each day)
Supplementary fiber product: metamucil, fibercon, or citrucel.
Complicated diverticular disease increased in patient who
smoking. refrain patient to stop smoking.
Symptomatic uncomplicated w/ inflamation & infection within the
colon treated initially with antibiotics and bowel rest
current recommended antimicrobial coverage is trimethoprim/
sulfa methoxazole or ciprofloxacin and metronidazole targeting
aerobic gram-negative rods and anaerobic bacteria.
Unfortunately, these agents do not cover enterococci, and the
addition of ampicillin to this regimen for non responders is
recommended.
Usual course of antibiotic: 7-10 days

LO 2
DESCRIBE THE PATHOPHYSIOLOGY OF ACUTE
ABDOMEN (POTASSIUM IMBALANCE)

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

Pathogenic mechanisms
Hypokalemia can occur via
the following pathogenetic
mechanisms:
1. Deficient intake
2. Increased excretion
The most common
mechanisms leading to
increased renal potassium
losses include the
following:

Enhanced
sodium
delivery to the collecting
duct, as with diuretics
Mineralocorticoid excess,
as
with
primary
or
secondary
hyperaldosteronism
Increased urine flow, as
with an osmotic diuresis

3. A
shift
from
the
extracellular to the
intracellular space

Hypokalemia caused by a
shift from extracellular to
intracellular space often
accompanies
increased
excretion, leading to a
potentiation
of
the
hypokalemic
effect
of
excessive loss.
Intracellular
shifts
of
potassium
often
are
episodic and frequently
are self-limited, as, for
example,
with
acute
insulin
therapy
for
hyperglycemia.