Pemicu 5 - GIT

• A 29-year-old male was brought to the emergency department due to sudden non-
colic pain at his left abdomen, which was aggravated by movement. The patient
had a history of a procedure where 􀂳some fluid were put inside his bowels through
his anus􀂴 when he was 6 months old due to abdominal pain and also bloody and
mucous stools. He also had the same procedure 10 years ago when he felt pain in
his right lower abdomen. His family history shows that his brother had a surgery
due to a lump in his left inguinal region and colicky pain, in which during that time
he could not defecate or flatulate and had bloated belly. On physical examination,
his pulse is 118 bpm, temperature is 38.9 C and respiratory rate is 38 x/minute.
There is also tenderness in his left lumbar region with muscle guarding. There are
three barely visible scars seen at his umbilicus and lower abdomen. Laboratory
examination result shows that his leukocyte count is 33.000 /microL, potassium is
2.3 mEq/dL and CRP is 100 mg/dL What can you learn from the problem?
• 1. Acute abdomen pain(definisi,etiologi)
• Patofisiologi dan Cara Penegakan diagnosa(Anamnesa,pemeriksaan
fisik,pemeriksaan penunjang)Tatalaksana farmako dan non
farmako,edukasi(pencegahan),komplikasi,prognosis dan resep(4)
• appendicitis akut
• diverticular disease
• intestinal perforation
• peritonitis akut
• hernia inguinalis dan hernia femoralis inkarserata dan strangulata
• hernia inguinalis dan hernia femoralis(reponibel dan ireponibel)
• umbilical hernia
• umbilical infection
• intususepsi invaginasi
• volvulus
• Illeus obstruktif dan illeus paralitik(ascariasis)
Appendictis
• Acute inflammation of the appendix
• can be due to obstruction by fecalith, inflammation, foreign body,
neoplasm or lymphoid hyperplasia (in children)
• Proximal obstruction of appendiceal lumen produces closed-loop
obstruction  increased intraluminal pressure  stimulation of visceral
afferent nerve fibers at  initial diffuse periumbilical pain 
inflammation extends to serosa and irritates parietal peritoneum
• Pain localized to RLQ/ McBurney point
• Nausea, fever; may perforate  peritonitis
• Treatment: appendectomy
https://healthjade.net/rovsing-sign/

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Signs and symptoms
• begins with vague, often colicky periumbilical or epigastric pain
• Within 12 hours the pain shifts to the right lower quadrant steady ache that is worsened by
walking or coughing
• Nausea
• one or two episodes of vomiting
• Protracted vomiting or vomiting that begins before the onset of pain suggests another diagnosis
• A sense of constipation
• Low-grade fever (below 38°C)  high fever or rigors suggest another diagnosis or appendiceal
perforation
• localized tenderness with guarding in the right lower quadrant can be elicited with gentle
palpation with one finger or light percussion
• When asked to cough precisely localize the painful area peritoneal irritation
Atypical signs and symptoms
• retrocecal appendix  does not touch the anterior abdominal wall
pain remains less intense and poorly localized  psoas sign
• pelvic appendicitis  pain in the lower abdomen, left, urge to urinate
or defecate, no Abdominal tenderness, tenderness on pelvic or rectal
examination the obturator
Lab and imaging
• Leukocytosis and netrophilia
• abdominal ultrasound
• CT scanning (perforation susp)
DD
• A several-hour period of close observation with reassessment
• Viral gastroenteritis  with nausea, vomiting, low-grade fever, and diarrhea 
generalized pain and localized tenderness
• The onset of vomiting before pain not appencitis
• Acute salpingitis or tubo-ovarian abscess  young, sexually active women, fever and
bilateral abdominal or pelvic tenderness
• mittelschmerz  sudden onset of lower abdominal pain in the middle of the menstrual
cycle
• Retrocecal or retroileal appendicitis (often associated with pyuria or hematuria) 
ureteral colic or pyelonephritis
• diverticulitis, Meckel diverticulitis, carcinoid of the appendix, perforated colonic cancer,
Crohn ileitis, perforated peptic ulcer, cholecystitis, and mesenteric adenitis
Complications
• Perforation  pain persisting for over 36 hours, high fever, diffuse
abdominal tenderness or peritoneal findings, a palpable abdominal
mass, or marked leukocytosis
• Abscess suppurative peritonitis with toxicity.
• Septic thrombophlebitis (pylephlebitis) of the portal venous system is
rare and suggested by high fever, chills, bacteremia, and jaundice
Treatment
• laparoscopic appendectomy
• open laparotomy
• Prior to surgery broad-spectrum antibiotics with gram-negative and
anaerobic coverage to reduce the incidence of postoperative infections
• conservative management with antibiotics alone may be considered in
patients with a nonperforated appendicitis with surgical contraindications
• Emergency appendectomy  perforated appendicitis with generalized
peritonitis
• Abscess  percutaneous CT-guided drainage with intravenous fluids and
antibiotics  appendectomy after 6 weeks to prevent recurrent appendicitis
Ileus paralytic
• Neurogenic failure  Intestinal hypomotility without obstruction
constipation and decreased flatus distended/tympanic abdomen
with  decreased bowel sounds
• Associated with abdominal surgeries, severe illnesses, opiates (affect
intestinal motility), hypokalemia, sepsis
• Treatment: bowel rest, electrolyte correction, cholinergic drugs
(stimulate intestinal motility)
Ileus
• mild diffuse, continuous abdominal discomfort with abdominal distention
• minimal abdominal tenderness
• Bowel sounds are diminished
• Serum electrolytes (sodium, potassium), magnesium, phosphorus, and
calcium, should be obtained to exclude abnormalities as contributing
factors
• Xray :
• distended gas-filled loops of the small and large intestine
• Air-fluid levels may be seen
• A CT scan  exclude mechanical obstruction

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Ileus – treatment
• The primary medical or surgical illness should be treate
• Severe or prolonged ileus requires nasogastric suction and parenteral
administration of fluids and electrolytes
• Alvimopan (12 mg PO 2x/d) short term is a peripherally acting mu-
opioid receptor antagonist with limited absorption or systemic activity
that reverses opioid-induced inhibition of intestinal motility
Ileus obstruction
Acute Colonic Pseudo-obstruction (Ogilvie
Syndrome)
• Spontaneous massive dilation of the cecum and proximal colon
• Progressive cecal dilation  spontaneous perforation
• detected in
• postsurgical patients (mean 3–5 days), after trauma, and in medical patients
with respiratory failure, metabolic imbalance, malignancy, myocardial
infarction, heart failure, pancreatitis, or a recent neurologic event (stroke,
subarachnoid hemorrhage, trauma)
• use of opioids or anticholinergic
• manifestation of colonic ischemia
Acute Colonic Pseudo-obstruction (Ogilvie
Syndrome)
• Abdominal distention
• Some patients are asymptomatic
• mild abdominal pain, Nausea and vomiting
• Bowel movements may be absent
• Abdominal tenderness
• signs of peritonitis are absent unless perforation has occurred
• Laboratory findings  Serum sodium, potassium, magnesium, phosphorus,
and calcium should be obtained to exclude abnormalities as contributing
factors
• Significant fever or leukocytosis raises concern for colonic ischemia or perforation
Acute Colonic Pseudo-obstruction (Ogilvie
Syndrome)
• Xray  colonic dilation cecum and proximal colon
• A cecal diameter >10–12 cm  increased risk of colonic
perforation
• small intestinal dilation and air-fluid levels due may be seen
• Enemas and CT scan
Acute Colonic Pseudo-obstruction (Ogilvie
Syndrome)
• The underlying illness is treated
• All drugs that reduce intestinal motility, such as opioids, anticholinergics, and calcium
channel blockers, should be discontinued if possible
• Enemas may be administered judiciously if large amounts of stool are evident on
radiography
• Oral laxatives are not helpful
• Cecal size  assessed by abdominal radiographs every 12 hours
• Intervention should be considered in patients with any of the following:
• no improvement or clinical deterioration after 24–48 hr
• cecal dilation >10 cm for more than 3–4 d
• patients with cecal dilation greater than 12 cm
• Neostigmine injection should be given unless contraindicated  Cardiac monitoring
Chronic intestinal pseudo-obs and
gastroparesis
• Intermittent symptoms and signs of gastric or intestinal obstruction w/o
mechanical lesions
• Etiology  endocrine disorders (diabetes mellitus, hypothyroidism,
cortisol deficiency), postsurgical conditions (vagotomy, partial gastric
resection, fundoplication, gastric bypass, Whipple procedure),
neurologic conditions (Parkinson disease, muscular and myotonic
dystrophy, autonomic dysfunction, multiple sclerosis, postpolio
syndrome, porphyria), rheumatologic syndromes (progressive systemic
sclerosis), infections (postviral, Chagas disease), amyloidosis,
paraneoplastic syndromes, medications, and eating disorders
(anorexia); a cause may not always be identified.
Chronic intestinal pseudo-obs and
gastroparesis
• chronic or intermittent  postprandial fullness (early satiety),
nausea, and vomiting (1–3 hours after meals)
• abdominal distention, vomiting, diarrhea, and varying degrees of
malnutrition
• Abdominal pain is not common
• Bacterial overgrowth in the stagnant intestine  malabsorption
• Colonic involvement  constipation or alternating diarrhea and
constipation.
• Xray  dilation of the esophagus, stomach, small intestine, or colon
resembling ileus or mechanical obstruction
• Endoscopy
• CT
• barium enterography
Treatment
• no specific therapy
• Acute exacerbations  nasogastric suction and intravenous fluids
• Long-term treatment  maintaining nutrition
• small, frequent meals that are low in fiber, milk, gas-forming foods, and fat
• Foods that are well tolerated include tea, ginger ale, soup, white rice, potatoes and sweet
potatoes, fish, gluten-free foods, and applesauce
• may require liquid enteral supplements
• NO opioids, anticholinics
• Treatment of underlying disease
• Metoclopramide and erythromycin
• Gastric electrical stimulation  internally implanted neurostimulators  reduction in
nausea
Ascaris obstruction
• mass of worms  obstruct the bowel lumen acute
intestinal obstruction
• commonly at the ileocecal valve
• Symptoms  colicky abdominal pain, vomiting and
constipation
• Vomitus may contain worms
• PE abdominal mass that changes in size and location
• Complications  volvulus, ileocecal intussusception,
gangrene, and intestinal perforation occasionally result
Patogenesis
• Form large bolus  mechanical obstruction
• worm bolus may intussusception or a pivot in small bowel volvulus
• inhabit the ileocecal valve  neurotoxins prompts small-bowel
contraction can obstruct the intestine.
• A host inflammatory reaction to worm-derived haemolysins,
endocrinolysins, and anaphylatoxins can be severe enough to obstruct
the gut lumen
 PP
• vomitus or stool 
•  X-ray  cigar bundle appearance or "whirlpool" effect, abdominal
distention, dilated bowel loops, multiple air fluid levels  free gas
under diaphragm indicates perforation
• Ultrasonographic  single worm, bundles of worms,
or a pseudo tumour-like (helmenthinoma) appearances
Treatment
• to starve the worms and hydrate the patient promotes their
movement and disentanglement The hypertonic saline enema
• NO anti helmintic   alter the motility of the worms  complications
 intussusceptions, volvulus, haemorrhagic or necrotic bowel and
perforation
• Surgery
Diverticulitis
• Diverticulum  Blind pouch A protruding from the alimentary tract
that communicates with the lumen of the gut
• Diverticulitis  Inflammation of diverticula with wall thickening
• ausing LLQ pain, fever, leukocytosis
• Treat with antibiotics  patogens
• Complications: abscess, fistula (colovesicalfistula pneumaturia),
obstruction (inflammatory stenosis), perforation
PP
• Empiric theraphy  better  colonic evaluation with colonoscopy or
radiologic imaging (CT colonography or barium enema)
• The presence of colonic diverticula and wall thickening, pericolic fat
infiltration, abscess formation, or extraluminal air
• Endoscopy and colonography are contraindicated during the initial
stages of an acute attack because of the risk of free perforation
Complications
• fistula formation that may involve the bladder, ureter, vagina, uterus,
bowel, and abdominal wall
• Stricture of the colon with partial or complete obstruction
Treatment
• mild symptoms and no peritoneal  broad-spectrum oral
• a high-fiber diet is often recommended
• severe diverticulitis (high fevers, leukocytosis, or peritoneal signs) and
patients who are elderly or immunosuppressed or who have serious
comorbid disease  hospitalization acutely
• Intravenous antibiotics should be given to cover anaerobic and gram-
negative bacteria  antibiotics should be continued for 5–7 days,
before changing to oral antibiotics.
Surgical treatment
• do not improve after 72 hours of medical management
• abdominal abscess >4 cm  percutaneous catheter drain
• Indications for emergent surgical management
• generalized peritonitis, large undrainable abscesses, and clinical deterioration
despite medical management and percutaneous drainage
Prognosis
• Diverticulosis is not associated with an increased risk of colorectal
cancer
• colonoscopy is recommended in patients over age 50 who have not
undergone appropriate screening and should be considered in other
high-risk patients, especially those with suspicious radiologic imaging,
diverticulitis with complications or protracted symptoms, or family
history of colorectal cancer
When to Refer
• Failure to improve within 72 hours of medical management
• Presence of significant peridiverticular abscesses (4 cm or larger)
requiring possible percutaneous or surgical drainage
• Generalized peritonitis or sepsis
• Recurrent attacks
• Chronic complications, including colonic strictures or fistulas
When to Admit
• Severe pain or inability to tolerate oral intake.
• Signs of sepsis or peritonitis.
• CT scan showing signs of complicated disease (abscess, perforation,
obstruction).
• Failure to improve with outpatient management.
• Immunocompromised or frail, elderly patient.
SPONTANEOUS BACTERIAL
PERITONITIS
• “Spontaneous” bacterial infection of ascitic fluid w/o intraabdominal
inf
• ascites caused by chronic liver disease (cirrhotic)
• bacteremia from other sites
• monomicrobial infection
• enteric gram-negative bacteria (E coli, Klebsiella pneumoniae)
• gram-positive bacteria (Streptococcus
pneumoniae, viridans streptococci, Enterococcus)
Signs and symptoms
• fever and abdominal pain
• change in mental status  exacerbation or precipitation of hepatic
encephalopathy, or sudden worsening of kidney function
• Physical examination  signs of chronic liver disease with ascites
Lab findings
• abdominal paracentesis cell count with differential, and blood
culture bottles
Intussuseption
• commonly at the ileocecal junction
• Most commonly idiopathic, but may be due to lead poin
• Compromised blood supply  intermittent, severe, abdominal pain often with “currant jelly”
dark red stools Majority of cases in
• infants, unusual in adults
• Most common pathologic lead point:
• Children—Meckel diverticulum
• Adults —intraluminal mass/tumor
• PE  draw their legs to chest to ease pain, sausage shaped mass on palpation.
• Imaging—Ultrasound/CT may show “target sign”
• associated with IgA vasculitis (HSP), recent viral infection
(eg, adenovirus; Peyer patch hypertrophy creates lead point)
Volvulus
• Twisting of portion of bowel around its mesentery can lead to
obstruction and infarction
• Can occur throughout the GI tract
• Midgut volvulus  common in infants and children
• Sigmoid volvulus  common in elderly (coffee bean sign on x-ray)