dr. Yudi Susanto sp.

B (K) BD
 Acute inflammation of the vermiform appendix
 The disease is slightly more common in males,
with a male:female ratio of 1.4:1. In a lifetime,
8.6% of males and 6.7% of females can be
expected to develop acute appendicitis.
 Young age is a risk factor, as nearly 70% of
patients with acute appendicitis are less than
30 years of age.

 13. Addiss DG, Shaffer N, Fowler BS, Tauxe RV. The epidemiology of appendicitis and appendectomy in
the United States. Am J Epidemiol 1990;132:910–925 [PubMed: 2239906]
 Wangensteen extensively studied the structure and function
of the appendix and the role of obstruction in appendicitis,
He proposed the following sequence of events to explain
appendicitis:
 (1) closed loop obstruction is caused by a fecalith and
swelling of the mucosal and submucosal lymphoid tissue at
the base of the appendix; (2) intraluminal pressure rises as
the appendiceal mucosa secretes fluid against the fixed
obstruction; (3) increased pressure in the appendiceal wall
exceeds capillary pressure and causes mucosal ischemia; and
(4) luminal bacterial overgrowth and translocation of bacteria
across the appendiceal wall result in inflammation, edema,
and ultimately necrosis. If the appendix is not removed,
perforation can ensue.
 16. Wangensteen OH, Buirge RE, Dennis C, Ritchie WP. Studies in the etiology of acute appendicitis: The significance of the structure and function of the vermiform appendix in
the genesis of appendicitis. Ann Surg 1937;106:910–942
17. Wangensteen OH, Dennis C. Experimental proof of the obstructive origin of appendicitis in man. Ann Surg 1939;110:629–647
Table 29-1 Common Organisms Seen in Patients with Acute
Appendicitis

Aerobic and Facultative Anaerobic

Gram-negative bacilli Gram-negative bacilli

E. coli Bacteroides fragilis

Pseudomonas aeruginosa Bacteroides species

Klebsiella species Fusobacterium species

Gram-positive cocci Gram-positive cocci

Streptococcus anginosus Peptostreptococcus species

Streptococcus species Gram-positive bacilli

Enterococcus species Clostridium species

 Clinical features:
◦ Pain starts in the umbilical region and consists of
a dull ache or colic.
◦ the pain shifts to the right lower quadrant of the
abdomen as the inflamed appendix irritates the
parietal peritoneum.
◦ Nausea and vomiting are common
◦ Sustained tachycardia, mild pyrexia and
abdominal tenderness. A very high temperature
(> 39°C) indicates probable abscess formation or
some other diagnosis such as a viral illness.
 The diagnosis of acute appendicitis is made largely
on clinical grounds but there are some investigations
that maybe of value:
• WCC;
• plain abdominal X-ray;
• urinalysis;
• ultrasound (especially in females to exclude
acute
gynaecological pathology);
• laparoscopy (especially in female patients in the
reproductive age);
• aspiration cytology;
• CT (selective use for right iliac fossa mass).
 The treatment is appendicectomy.
Prophylactic antibiotics should be used in all
patients. Metronidazole alone, administered
as a suppository, is appropriate. In patients
with perforated appendicitis, appendicectomy
is followed by peritoneal lavage with saline
containing an antibiotic. These patients
require intravenous antibiotics
(metronidazole and cefuroxime) for 5 days
postoperatively.
 Perforated Appendicitis:
◦ It is a commonly held belief that if left untreated,
appendiceal inflammation will progress inevitably to
necrosis, and ultimately to perforation
 A hernia is an outpouching of the parietal
peritoneum through a preformed or secondarily
established hiatus. If the hernia extends beyond
the abdominal cavity and is thus visible on the
surface of the body, it is defined as an external
hernia. If the outpouching is limited to peritoneal
pockets, it is known as an internal hernia.
 An incarcerated hernia occurs when the hernia
contents are trapped in the hernia defect so that
the contents cannot be reduced back into the
abdominal cavity. The tight circumferential
pressure applied by the hernia defect serves to
impede the venous outflow from the hernia
contents, resulting in congestion, edema, and
tissue ischemia. Ultimately, the arterial inflow to
the hernia contents is compromised as well,
resulting in tissue loss and necrosis, termed
strangulation of the hernia.
 • Non-operative: applicable in asymptomatic or
minimally symptomatic hernias.
• Operative: Herniotomy, Herniorraphy,
Herniorraphy
 Adynamic ileus
 Mechanical ileus
I. Pathophysiology
Paralysis of intestinal motility
II. Causes
A. Abdominal trauma
B. Abdominal surgery (i.e. laparatomy)
C. Serum electrolyte abnormality
D. D. Infectious, Inflammatory or irritation (bile, blood)
E. Intestinal Ischemia
F. Skeletal injury
G. Medications
IV. Signs
A. Quiet bowel sounds
B. Abdominal distention
V. Differential Diagnosis
A. Mechanical Ileus
B. Bowel Pseudoobstruction
VI. Radiology: Refractory ileus course
A. Indicated to evaluate for Mechanical Ileus
B. Upper GI series and small bowel follow through
1. May be diagnostic and therepeutic
2. Use gastrograffin instead of barium
3. Barium may further obstruct bowel lumen
4. Gastrograffin may stimulate bowel motility
C. Decompress stomach with Nasogastric Tube
D. Instill gastrograffin via Nasogastric Tube
D. Contrast with Mechanical Ileus
1. Less prominent air fluid levels
2. Generalized involvement of entire GI tract
3. Air filled bowel loops tend not to be distended
VII. Management
A. Initial
1. Limit or eliminate oral intake
2. Intravascular fluid replacement
3. Correct electrolyte abnormalities (e.g. Hypokalemia)
4. Consider Nasogastric Tube placement
B. Refractory Management
1. Consider Prokinatics
2. Consider lower bowel stimulation (e.g. Enema)
VIII. Course
A. Post-operative ileus resolves within 24-48
hours
I. Types
A. Simple mechanical obstruction
B. Closed loop obstruction
C. Strangulated obstruction
II. Causes
A. Most Common Causes: Postoperative
Adhesions (accounts for 50% of cases),
Hernia (25% of cases, especially younger
patients), Neoplasms (10% of cases, esp.
older patients)
A. Intrinsic bowel lesions
1. Congenital anomalies (Pediatric)
a. Atresia
b. Stenosis
c. Bowel duplication
 Symptom
How is it diagnosed?

Evaluation Goals:
• Distinguishing mechanical obstruction from ileus
• Determining the etiology of the obstruction
• Discriminating partial from complete obstruction
• Discriminating simple from strangulating obstruction.

History:
• Prior abdominal operations
• Presence of abdominal disorders (cancer or IBD)
• Last BM and Flatus
• Pediatrics - Ingestion of foreign body

Physical Exam:
• Meticulous Search for Hernias (inguinal and femoral)
• Rectal Exam to look for gross or occult blood.

The diagnosis is usually confirmed by Radiology

Most Specific Finding: The Triad
1. Dilated small-bowel loops (>3 cm in diameter)
2. Air-Fluid levels on upright films
3. Paucity of air in the colon.

Sensitivity is 70 to 80%.

Specificity is low, because ileus and colonic obstruction have similar

appearing findings.

Small Bowel Gas Pattern

•Centrally located
•Soft tissue across entire lumen

Colon Gas Pattern

•Peripheral Located
•Mostly not overlapping
•Haustra markings
VIII. Management: Conservative Therapy
A. Fluid replacement
B. Bowel decompression
1. Nasogastric Tube
2. Long intestinal tube (eg. Cantor) offers no advantage
C. Antibiotic
1. Indications (Not for routine use)
a. Surgery planned
b. Bowel ischemia or infarction
c. Bowel perforation
2. Cover Gram Negatives and Anaerobes
a. Second-generation Cephalosporin
IX. Management: surgical intervention
A. Spontaneous resolution often occurs without
surgery
1. Partial small bowel obstruction: 75%
2. Complete small bowel obstruction: up to 50%
A. Predictors of resolution without surgery
1. Early postoperative bowel obstruction
2. Adhesive obstruction (prior laparotomy)
3. Crohn's disease
B. Indications for surgery
1. Inadequate relief with Nasogastric tube placement
2. Persistant symptoms >48 hours despite treatment
(strangulation)
3. Neoplasms
X. Complications
A. Intestinal Ischemia or infarction
B. Bowel necrosis, perforation and bacterial
peritonitis
C. Hypovolemia
D. Complications of surgical intervention if needed
XI. Prognosis: Recurrence of obstruction due
to adhesions
A. Risk after first episode: 53%
B. Risk after more than one episode: 83%
 Peritonitis – inflammation of the peritoneum
which maybe localised or generalised

 Peritonism – refers to specific features found on

abdominal examination in those with peritonitis
 Characterised by tenderness with guarding,
rebound/percussion tenderness on examination
 Peritonism is eased by lying still and exacerbated by any
movement
 Maybe localised or generalised

 Generalised peritonitis is a surgical emergency –

requires resuscitation and immediate surgery
 Infective – bacteria cause peritonitis e.g. due to
gangrene or perforation of a viscus
(appendicitis/diverticulitis/perforated ulcer). This is
the most common cause of peritonitis

 Non-infective – leakage of certain sterile body fluids

into the peritoneum can cause peritonitis.
 Gastric juice (peptic ulcer)
 Bile (liver biopsy, post-cholecystectomy)
 Urine (pelvic trauma)
 Pancreatic juice (pancreatitis)
 Blood (endometriosis, ruptured ovarian cyst, abdominal trauma)
 Note: although sterile at first these fluids often become infected
within 24-48 hrs of leakage from the affected organ resulting in
a bacterial peritonitis
 Pain
 Constant and severe (site will give clue as to cause, or maybe generalised)
 Worse on movement (hence shallow breathing in those with generalised
peritonitis to keep the abdomen still)
 Eased by lying still
 If localised peritonitis – peritonism is in a single area of the abdomen
 If generalised peritonitis – peritonism is all over abdomen with board like rigidity

 Signs of ileus (generalised peritonitis > localised peritonitis)

 Distention
 Vomiting
 Tympanic abdomen with reduced bowel sounds

 Signs of systemic shock

 Tachycardia, tachypnoea, hypotension, low urine output
 More prominent with generalised than localised peritonitis
 Diagnosis most often made on history and examination

 If localised peritonitis
 Investigations are those listed on “investigations for acute abdomen” slide
 All patients get simple investigations
 Complex investigations are requested depending on suspected diagnosis (remember that
some diagnoses do not require complex investigations and are entirely based on history
and examination e.g. Appendicitis)

 If generalised peritonitis
 Surgical emergency – will require emergency operation
 Following investigations should be performed:
 Bloods: FBC, U&E, LFT, Amylase!! (acute pancreatitis can present with generalised peritonitis
and does not require emergency surgery), CRP, clotting, G&S, ABG
 AXR and Erect CXR
 CT scan
 Only if this can be performed urgently and patient is stable
 If this can not be performed urgently or patient is unstable then for surgery without delay
 Does not change management (i.e. Patients will need emergency surgery regardless) but useful as
will identify cause of peritonitis therefore helping to plan surgical procedure
 Other Time consuming complex investigations should not be performed as they will only
delay definitive treatment (emergency surgery) and add very little
 ABC
 Oxygen
 Fluid resuscitation (large bore cannule,
bloods, IVF, catheter)
 IV antibiotics (Augmentin and metronidazole)
 Analgesia
 Surgery (with or without preceeding CT
depending on availability and stability of
patients)