Acute Abdominal Pain in the Tropics

Acute Abdominal Pain in the Tropics
2011 Global Health Missions Conference Louisville, Kentucky Presented by Bruce C. Steffes, MD, FACS, FWACS, FCS(ECSA) Certificate of Knowledge in Clinical Tropical Medicine and Travelers Health (ASTMH) Abdominal pain in the tropics includes many of the same diseases as elsewhere but there are conditions that are unique. Using a case-based approach, some of the more common of the conditions which cause acute abdominal pain will be dressed. Approaches to diagnosis and treatment, especially those which are not obvious to the practitioner from N. America, will be discussed in an interactive style Session Problem: For the uninitiated, abdominal crisis due to tropical diseases and conditions can be frightening. Diagnostic, physiological and treatment principles must be applied in a unique fashion and this session is designed to increase awareness and to give principles which will help in the treatment of these patients. Session Solution: To increase awareness of presentation, diagnosis and treatment of these abdominal conditions which are usually found only (predominantly) in the tropics.

Introduction Surgery in the developing world is different
Different diseases or at least different prevalence Advanced pathology Fewer care givers Limited resources

Diseases seen less commonly in the developing world
Diveriticulitis Acute and chronic cholecystitis Appendicitis Small bowel obstruction due to adhesions

Diseases seen more commonly in the developing world
Primary peritonitis Perforated duodenal ulcers Volvulus Adult intussusception Tuberculous peritonitis Pigbel

What are diagnoses seen in the two-thirds world?
University Hospital in Ghana1 Appendicitis Perforated typhoid Bongolo Mission Hospital, Gabon2 Incarcerated/strangulated hernias Volvulus Adhesive SBO Tenwek Mission Hospital3 Perforated PUD Trauma SBO

Hoof Beats ARE Zebras

Case Presentation 5 yo boy from Papua New Guinea.
Pig feast 5 days before Severe abdominal pain 4 days during with fever, nausea & diarrhea. Intermittent cramps, especially with eating & drinking WBC 14,400 Abdomen initially soft. Dx? Tx? Correction of fluid and electrolyte deficits; hydrate well; correct moderate to severe anemias. Nasogastric drainage Intravenous antibiotics - CMP, Crystalline PCN and Metronidazole/Tinidazole (+/- Gentamicin) Treatment of Ascaris ?treatment of malaria Consider hyperalimentation or TPN if course prolonged Antiserum +/- (Not readily available or effective)

NPO, nasogastric tube and antibiotics
“Dark” NG output, “dark” diarrhea and abdomen became “surgical” Dx? Due to the rapid progression of pigbel, the decision for surgery is often a judgment call by the surgeon based on clinical experience Urgent laparotomy with wide resection of SB to normal margins End-to-end anastomosis vs. Two ostomies Usually cm (2-4 feet) of jejunum need resected Questions that arise: How much bowel to resect? Which patients to do second look?

Pigbel (Enteritis Necroticans, Necrotizing Enteritis) was reported first in medieval Europe and again in Germany after WWII when it was called “darmbrand” (gut-fire). It resurfaced in the early 1960s in Goroka, PNG with culture-positive cases and was the most common cause of death in children >24 months). At one time, Pigbel was the most common cause of acute abdominal pain in the PNG Highlands(Prior to vaccination was the most common cause for abdominal laparotomy in that area)

Incidence of Pigbel Male > Female (2.2:1) – probably because males encouraged to eat more protein for strength 70% between ages 1 – 10. Infants protected by maternal antibodies. Can be seen in young adults (25%) More common in dry season (better weather leads to more frequent pig feasts)

Bacteriology of Pigbel
Clostridium Perfringens Type C (also known as Clostridium welchii) = Anaerobic, gram +, spore-forming rod - found in human stool, pig stool and soil Spores are heat stable up to 95 C (Boiling point of water is 95 in the PNG Highlands) Type A commonly causes food poisoning (botulism). Type C grows in protein-rich chyme and produces a b – toxin).

Effect of the b-toxin b-toxin is rapidly degraded by intestinal proteases (e.g. trypsin) in well-nourished people The toxin attacks the intestinal lining and causes inflammation and necrosis and may also cause arterial thrombosis

How It Comes Together Trypsin has low activity Malnutrition causes a decrease in the pancreatic production of all proteases including trypsin, a key enzyme in the digestion of meat and protein and the toxin Ascaris infestation and diet rich in sweet-potato (kaukau) cause high levels of heat-stable trypsin inhibitors Contamination risk is high Unwashed hands and feet of food handlers Poorly cooked pork/meat or spillage of pig’s bowel contents in mumu preparation Sporadic high protein meals provides growth medium for C.P.

Pathology Blood and pus in stool (from “sloughing” enteritis of jejunum, ileum and colon) Transmural infection of the bowel (patchy segmental ulcerative necrosis) Gas gangrene, separation of the layers of the bowel wall, pseudomembranes Affects jejunum > ileum > cecum > colon

Types of Pigbel: Mild Diarrheal (type IV) Subacute Surgical (type III)
May go undiagnosed or diagnosed as gastroenteritis (GE) Usually only diarrhea but can progress to Type IV Mortality: Rare Subacute Surgical (type III) Presents later Complication of Type II (See next category) Mortality: 49%

Types of Pigbell Acute Surgical (type II) Acute Toxic (type I)
Present with ileus, small bowel obstruction (SBO), strangulation, perforation, peritonitis Mortality: 42% Acute Toxic (type I) Fulminant toxemia and shock Usually young children (immunologically naïve) Mortality: 85% (Some deaths before hospital)

The Clinical Course Symptoms usually become apparent 48 hours after a large meat or protein meal but can present up to a week later Present with colicky or constant abdominal pain, vomiting with dark emesis (blood flecks), blood in stool, foul flatus, and diarrhea early Tachycardic, febrile, dehydrated, tender & distended upper abdomen with visible bowel, guarding, rigidity, decreased bowel sounds

The Clinical Course Symptoms consistent with ischemia
Pain out of proportion Eating may increase pain Late symptoms: partial SBO, malnutrition, fibrosis, adhesions, malabsorption and strictures (especially with Type III) Mortality due to peritonitis, septicemia, dehydration, electrolyte abnormalities, and shock

Diagnostic Approach High index of suspicion
Early recognition of pigbel and quick action are of utmost importance. The toxin begins attacking the bowel instantly and constantly. Timely recognition and treatment may reduce severity or even prevent death of the child! Early fluid resuscitation, decompression of SB, and appropriate antibiotics may preclude need for laparotomy. If severe, early referral and surgery may prevent death.

Diagnosis of Pigbel Gas in bowel wall or SBO on abdominal x-ray
Bloody NG aspirate or blood in stool Neutrophilic leukocytosis (>/= 20,000) Serological test possible, ? availability (immuno-florescence using type C coated silicon beads) Culture C.P. from stool (anaerobic blood agar) Bloody ascites on ultrasound

Treatment of Pigbel Correction of fluid and electrolyte deficits; hydrate well; correct moderate to severe anemias. Nasogastric drainage Intravenous antibiotics - CMP, Crystalline PCN and Metronidazole/Tinidazole (+/- Gentamicin)

Treatment of Pigbel Treatment of Ascaris ?treatment of malaria
Consider hyperalimentation or TPN if course prolonged Antiserum +/- (Not readily available or effective)

Early Hospital course If improves, wait 24 hours then slowly go from oral rehydration solution (ORS) milk  solids After 48 hours , laparotomy if there if failure to improve: high NG output, persistent SBO by x-ray, persistent peritonitis, high white count, persistent fever Acute decompensation requires emergent surgery Improvement: decreased swelling, pain, fever, pulse, white count, NG aspirate, abdominal tenderness and vomiting; increased hunger; normal bowel movements), Lack of improvement: high NG output, persistent SBO by x-ray, persistent peritonitis, high white count, persistent fever

Surgery Due to the rapid progression of pigbel, the decision for surgery is often a judgment call by the surgeon based on clinical experience Urgent laparotomy with wide resection of SB to normal margins Questions that arise: How much bowel to resect? End-to-end anastomosis vs. 2 ostomies Which patients to do second look? Usually cm (2-4 feet) of jejunum need resected

Surgery Findings Palpable loops of thick bowel
Enlarged mesenteric nodes typical “Tiger Striping” “Skip Lesions” Mucosal Ulcerations Perforations/SBO

Enlarged mesenteric nodes typical

“Tiger Striping”

“Skip Lesions”

Mucosal Ulcerations

Post Op Care Strict I & O, Adequate fluid resuscitation and good nursing care. Attention to the CBC (transfusion is needed) and K+ levels Nutritional supplement

Prevention of Pigbel Type C toxoid immunization. Inactivated toxin: 0.5 cc given at 2, 4 and 6 months of age with the DPT vaccine. Protects 2-4 years Was used from mid 1990’s and cases were 1/5 of pre-immunization levels, When the PNG government felt it was too expensive (and quit paying for it), it became an orphan drug and the manufacturer quit making it. In one recent study, 6 of 25 non-immunized kids had pre-existing antibodies to C.P. type C indicating that the organism is still common.

Prevention of Pigbel References
Changes in dietary habits (Less reliance on sweet potatoes and more regular protein) Changes in cooking methods (higher temperatures) and better preservation of food Changes in hygiene and food preparation Public Health Education Eradication of Ascaris References Oxford Handbook of Tropical Medicine 2002. Common Medical Problems in the Tropics (Second Edition) 1999. Pathology in the Tropics (Second Edition) 1976. Hamilton Bailey’s Emergency Surgery (Twelfth Edition) 1995. Primary Surgery, Volume 1, King and Bewes, 1993. Manson’s Tropical Diseases (Twenty-first Edition), Cook and Zulma, 2003. Pediatrics for Doctors in Papua New Guinea 2003. PNG Medical Society Abstracts, B7 pg 56, 2005. PNG Medical Journal, “Epidemiological Factors”, reprint Vol. 48, 2005. PNG Medical Journal, “Pathogenesis of Pigbel in PNG”, March 1979, reprint Vol. 48, 2005. Pigbel, Chapter 17, Gregory Lawrence. Papua New Guinea Medical Journal, “A Review of Pigbel (Necrotizing Enteritis) in Papua New Guinea”, PNG IMR, M.W. Davis, Pigbel (Necrotizing Enteritis) in PNG, PNG IMR Monograph #6, Michael Davis, editor; 1980.

Case Study 10 yo Togolese boy presents in the dry season with history of fevers and malaise. He has had intermittent nausea and mild diarrhea. He was treated for malaria. He worsened 48 hours ago and hasn’t eaten since then. Dx, Rx? Typhoid fever is our first topic. Salmonella enterica serovar typhi (previously known as salmonella typhi), is a pathogen specific only to humans. Typhoid fever can also be caused certain non-typhoid salmonella (NTS), particularly Paratyphoid strains A, B, C. Location and Prevalence: million cases per year, almost exclusively in the developing world, with an overall mortality rate of 10%. These waterborne gram negative aerobes are associated with poor sanitation and fecal contamination of water and food supplies.

Typhoid fever Cause: Salmonella enterica serovar typhi
Certain non-typhoid salmonella (NTS), particularly Paratyphoid strains A, B, C. Disease of poor sanitation, often seasonal Typhoid fever is our first topic. Salmonella enterica serovar typhi (previously known as salmonella typhi), is a pathogen specific only to humans. Typhoid fever can also be caused certain non-typhoid salmonella (NTS), particularly Paratyphoid strains A, B, C. Location and Prevalence: million cases per year, almost exclusively in the developing world, with an overall mortality rate of 10%. These waterborne gram negative aerobes are associated with poor sanitation and fecal contamination of water and food supplies.

Typhoid Fever Note that ulceration and perforation occurs 2- 3 weeks into the disease. They will have been ill for a while. Bitar & Tarpley, Reviews of Infectious Diseases 7: , 1985

Clinical Features of Typhoid
Classically a four week disease Weeks one and two: fever, headache, abdominal pain Week three: “typhoidal state” with disordered mentation and toxemia Week four: Defervescence and improvement

Lab in Typhoid Disease:
Leukopenia/thrombocytopenia are common Culture is the best diagnostic tool – but may not be available.

Widal? Widal test: very controversial
Conclusion of a paper by Tupasi et al ([Phil J Microbiol Infect Dis 1991, 20(1):23-26] “Culture isolation of Salmonella typhi from blood and bone marrow should be considered the standard diagnostic test to confirm typhoid fever. A single Widal test in an endemic area is of no diagnostic value. In addition, it should not be used as a screening test in asymptomatic individuals. Neither should a "negative" Widal test rule out the diagnosis of typhoid fever in patients with signs and symptoms of the disease since a "negative" Widal test may be seen early in the course of illness. The Widal test should not also be used as the basis for deciding the duration of antimicrobial therapy.”

If Surgery Indicated Emergently
Aggressive resuscitation prior to OR with appropriate antibiotic coverage (triple antibiotics to cover GI flora as well as Salmonella) and sharing of the Gospel Ampicillin and chloramphenicol are no longer the drugs of choice. Fluoroquinolones (?decreasing efficacy) and third generation cephalosporins are probably the best at present.

Typhoid Mary notwithstanding, surgery for the carrier state, i. e
Typhoid Mary notwithstanding, surgery for the carrier state, i.e. cholecystectomy, is NOT a usual indication. Normally, surgery in a typhoid carrier is done only only for chronic cholecystitis per se, largely because it doesn’t always work for carrier state. Hemorrhage % of patients, bleeding usually in 3 or 4th week, usually UGI in type and may be hard to find if in the small intestine) Perforation % of patients, common in the second and third weeks of illness. Some patients perforate without an obvious prodrome. Mortality for perforation is as high as 40%, affected by many factors in these environments.

Indications for Surgery in Enteric Fever
Surgery for carrier state is NOT a usual indication. Normally, do only for chronic cholecystitis per se (doesn’t always work for carrier state) Hemorrhage ( % of patients, bleeding usually in 3 or 4th week, usually UGI in type and may be hard to find if in the small intestine) Perforation (1 - 5% of patients, common in the second and third weeks of illness, but can be much later. Some patients perforate without an obvious prodrome) Mortality for perforation is as high as 40%, affected by many factors in the austere environment.

Indications for surgery:
Pneumoperitoneum on x-ray (may require left lateral film) Persistent palpable mass (especially with erythema of abdominal wall) Diffuse peritonitis or positive peritoneal tap Persistent sepsis/failure to improve on medical therapy Suspicious of abdominal catastrophe but negative x-rays? Do frequent examinations (by the same or equally experienced examiner) and x-rays (q. 6 h at first) until improvement or perforation is evident.

Typhoid – Pneumoperitoneum
Are you suspicious of abdominal catastrophe but have negative x-rays? Do frequent examinations (performed by the same or an equally experienced examiner) and x-rays q. 6 h until improvement or perforation is evident. X-rays may be expensive for the patient but are sometimes more sensitive than abdominal examination and early detection improves survival.

Typhoid – Perforation The perforations are due to necrosis of the Peyer’s patches in the distal small intestine and are often “punched out”. Before taking to the OR, resuscitate aggressively and use appropriate antibiotic coverage. 70% of all perforations are single and should be oversewn with a Lembert or something similar. Need for excision of ulcer edges is debatable. Look for other sites “about to perforate” and consider plication of those questionable areas.

Surgical Approach Multiple perforations Up to 3 or so – oversew
Multiple – consider resection with single anastomosis Aggressive peritoneal debridement and/or irrigation of the peritoneal cavity If there are multiple perforations, it is often quicker and faster to do a resection, especially if they are in the same loop of bowel. Aggressive peritoneal debridement and copious irrigation of the peritoneal cavity have been helpful for me.

Surgical Approach Consider retention sutures
Consider a second-look operation A negative laparotomy is rare and better tolerated than a missed perforation. Some lessons learned by bitter experience: Consider retention sutures Consider a second-look operation A negative laparotomy is rare and better tolerated than a missed perforation.

Typhoid Cholecystitis
Acute cholecystitis – very uncommon Predominance in children Often advanced (gangrene or perforation) because of low index of suspicion Acute cholecystitis due to typhoid is very uncommon but because of its predominance in the children and because they are sick from their typhoid fever, the diagnosis is often delayed and the presentation is advanced. Courtesy, Dr. J. Brown, Cameroon

Typhoid Cholecystitis
Acute cholecystitis – very uncommon Predominance in children? Often advanced (gangrene or perforation) because of low index of suspicion

Bowel Obstruction The differential diagnoses have different probability Examples: Decreased adhesions due to fewer surgeries (except in women where PID increases risk of adhesions) Lower frequency of colon cancer and diverticulitis Increased prevalence of lymphogranuloma venereum stricture At the beginning of this discussion, I mentioned that infectious disease can change the diagnostic and therapeutic algorithms. In N. America, adhesions are the leading cause of bowel obstruction. In a country where surgery is rare, only PID has a significant incidence of adhesion formation. Colon cancer and diverticulitis are uncommon and therefore only rarely cause colonic obstruction. Volvulus is a much more common cause of colon obstruction.

Case 8 year old female presents with abdominal swelling, pain and vomiting. WBC 14, % eosinophilia. Hg 8.9 gm%. A sausage-shaped RLQ mass was palpated.

Ascariasis & Volvulus - Xray
The local prevalence of Ascariasis varies widely, depending on climate, cultural customs and hygiene. Children are affected much more common. The examination of these children is that of small bowel obstruction but it is not unusual to feel through the abdominal wall a doughy loop crammed with worms. On plain x-ray, worms may be silhouetted by air present within the lumen of a classic small bowel pattern. Contrast studies may demonstrate them well (including a free UGI for the worms). Anecdotally, water soluble contrast seems to help break up the worm bolus.

Ascariasis These common roundworms only cause problems in two situations When they migrate When they don’t Ascaris in some areas is not only endemic but “over-distributed” in some areas. These common roundworms can cause trouble in only two conditions: when they migrate and when they don’t. They usually begin to migrate because their micro-environment has been changed in some way they don’t like.

Ascariasis – Migrating
Loeffler’s syndrome (non-surgical) Biliary-pancreatic Anastomotic perforation After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10 to 14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . This can create an eosinophilic pneumonitis known as Loeffler’s syndrome. This is not surgical. After infective eggs are swallowed , the larvae hatch in the gut , invade the intestinal mucosa, and are carried via the portal, and then systemic, circulation to the lungs . This can create an eosinophilic pneumonitis known as Loeffler’s syndrome. This is not surgical but it can interfere with your surgical care of some patients.

What is surgical is the tendency for the unhappy worm to migrate – migration up the esophagus into the nose and mouth is not unknown and many times they will migrate through the Ampulla of Vater, causing symptoms in the biliary pancreatic tree. This is a case of acute cholecystitis associated with Ascariasis. I have had one case where worms migrated through my suture line as I watched.

Non-migratory – Bowel Obstruction
Diagnosis – prevalence varies widely by locale and age May have history of recent Antihelminthic treatment Physical examination Plain x-ray Contrast studies – especially with Gastrografin ® Ultrasound and CT scan

Ascariasis – Bowel Obstruction
Diagnosis – local prevalence varies widely Prevalence varies by age group Physical examination Plain x-ray – may see worms superimposed on SBO appearance Contrast studies – especially with water soluble contrast The local prevalence of Ascariasis varies widely, depending on climate, cultural customs and hygiene. Children are affected much more common. The examination of these children is that of small bowel obstruction but it is not unusual to feel through the abdominal wall a doughy loop crammed with worms. On plain x-ray, worms may be silhouetted by air present within the lumen of a classic small bowel pattern. Contrast studies may demonstrate them well (including a free UGI for the worms). Anecdotally, water soluble contrast seems to help break up the worm bolus.

Medical Treatment of Ascariasis
If no peritonitis, rehydration and nasogastric decompression Some prefer no vermicidal treatment at all. Those who treat debate between mebendazole or albendazole versus piperazine. Hypertonic saline enemas? Public health education for all. In treating these patients, decompression of the GI tract and rehydration is appropriate. The argument is over the use of a vermifuge or not and if so, which one. Mebendazole and albendazole are cidal; piperazine causes a partial paralysis. Some feel that the use of medbendazole and albendazole can convert a partial to a complete obstruction. Approximately 75% can be treated medically and avoid surgery. No matter what works, public health education for the village is required.

Treatment Operative vs. nonoperative management
Does the patient have peritonitis? Is the patient toxic? How long has the child had symptoms? Does X-ray suggest complete SBO? Is the child worsening on nonoperative treatment?

Surgical Treatment of Ascariasis
Milk the worm bolus through into colon if possible. If not effective, transverse enterotomy and removal of worm bolus with primary closure. Prevent spills into peritoneal cavity (bacterial infection) Close anastomotic line securely (to prevent worm migration) Ue antibiotic prophylaxis. 1/3 will require resection

Surgery for Ascariasis
If you must operate, use broad spectrum antibiotic prophylaxis in case of enterotomy and subsequent contamination. Milk the worm bolus through into colon if possible. I can’t say that I have ever had much success with that. If not effective, perform a transverse enterotomy and use sponge forceps to remove of worm bolus. Do a primary closure of the intestine. Remember to prevent spills into peritoneal cavity (bacterial infection), and close anastomotic line securely (to prevent worm migration).

Ascariasis & Volvulus One last reminder - Although you can usually wait and observe the patient to see if the vermifuge works, always keep in mind the risk of volvulus due to the weight of the worms in the small intestine.

Case Study 29 year old male with 24 hours of marked distension, supraumbilical cramping pain and obstipation. WBC 12, % esosinophilia. No peritoneal signs. Diagnosis? Treatment?

Sigmoid Volvulus - Facts
Wide age range More common in males (most series 2:1) Most common form of GI volvulus

Sigmoid Volvulus - History
Rapid onset of pain and remarkable distention Obstipation Prior episodes Nausea/vomiting as obstruction persists

Diagnosis Massive distention Empty rectum Characteristic X-ray
Massive distention of colon “bent inner-tube” sign (aka “coffee bean sign,” “horse’s butt”. +/- small bowel distention Empty left iliac fossa No rectal gas

Sigmoid Volvulus - Management
Resuscitation of fluid and electrolyte deficits Antibiotics If no peritonitis, urgent rigid sigmoidoscopy with rectal tube placement (sutured) Urgent laparotomy for signs of peritonitis or failed rigid sigmoidoscopy

Sigmoid Volvulus – Surgical Options
Semi-elective laparotomy after successful endoscopic detorsion with placement of rectal tube Sigmoidopexy has a high recurrence rate Low morbidity and mortality rate for semi-elective resection and anastomosis

Cecal Volvulus Clinical characteristics
Similar presentation with sigmoid volvulus More common in females Preoperative diagnosis much more challenging Gangrene of colon is common

Cecal Diagnosis - Diagnosis
X-ray: Suggest obstruction. Only 1 in 5 are diagnostic Barium enema: high rate of accuracy but challenging without fluoroscopy. Bird’s beak seen at point of volvulus. Colonoscopy: difficult in unprepared colon and there is high risk of perforation

Cecal Volvulus Only 1 of 5 x-rays are “classic”
Dilated loop in cecal volvulus tends to end in the right upper quadrant

Cecal Volvulus - Surgical Options
Decompression alone has 50% recurrence Detorsion and cecopexy: May recur if cecopexy is not extensive Detorsion and cecostomy: most authors feel this procedure should be abandoned as complication rates can be 50%

Cecal Volvulus – Surgical Options
If gangrenous, resection required Resection and ileostomy with mucus fistula: choice for septic/unstable patients with comorbid conditions Resection (partial or complete right colectomy) with anastomosis +/- colopexy

Double Volvulus Usually refers to sigmoid volvulus associated with small intestinal volvulus Detorsion is often difficult and confusing. Often presnets with necrotic gut. In that case, detorsion is potentially dangerous. Resection and then sorting it out has been my usual approach

Double Volvulus Ileostomy should be avoided if at all possible
Short gut syndrome is one result but not usual. Second look laparotomy should always be considered for questionable bowel in setting of possible short gut syndrome Lack of immediate improvement after endoscopic detorsion of presumed sigmoid volvulus should lead the surgeon to the OR so as not to miss small bowel volvulus

Double Volvulus

Case Study 9 year old female presents with 24 hours of anorexia, increasing abdominal pain and increasing fever. She has non-localizing rebound and guards in all quadrants. Differential diagnosis?

Primary Peritonitis Occurs in previously health children
Very rare problem in the West Disease of children, especially girls, ages 6-10 Females much more common than males Cause is not understood

Presentation Rapid onset (usually <48 hours)
Fever and leukocytosis with severe abdominal pain Tenderness often most severe in RLQ Very difficult to distinguish from acute appendicitis

Treatment Exploratory laparotomy with appendectomy and washout (nosurgeon wants to sit on a case strongly suggesting acute appendicitis) Laparoscopy with washout (if equipment available) Broad spectrum antibiotics until culture results available Some authors have suggested a paracentesis with strep species or Pneumococcus on Gram stain would obviate the need for laparotomy.

Bacteriology Strep species are most common in most reports E. coli
Mixed aerobe/anaerobe

Summary: Primary peritonitis
A disease causing a rapid onset of an acute abdomen with vomiting and diffuse peritonitis, especially in girls, which usually resolves quickly after surgery for diagnosis and antibiotic therapy.

Intussusception Adults are more common in children in series from Nigeria, Uganda and S. Africa (remembering adult cases are more likely associated with surgical pathology) Colocolic intussusception is uncommon but more common in areas with high rate of amoebiasis

Acute Abdominal Pain in the Tropics

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