Peritonitis and Intra-abdominal Abscess - Pelvic and Sub-phrenic

Authors note: {Primary Surgery Volumes 1 & 2, edited by Maurice King, are recognized as indispensable texts for surgeons in low-income countries. Published in 1990 by Oxford University Press they are now partially available online thanks to the Deutsche Gesellschaft fr Technische Zusammenarbeit at http://www.primary-surgery.org/start.html. They remain surprisingly relevant despite being unrevised for 17 years. Dr. Michael Cotton from Zimbabwe is currently revising Volume 1 Non-trauma. Primary Surgery is also available as a Wikimedia through the Canadian Network for International Surgery at http://ps.cnis.ca/wiki/index.php/Main_Page . (1)} 1. Introduction 2. Etiology/Epidemiology 3. Pathophysiology 4. Peritonitis 4.1. Diagnosis the acute abdomen 4.1.1. Acute abdomen with HIV/AIDS 4.2. Treatment 4.2.1. General measures 4.2.1.1. Antibiotics 4.2.1.2. Peritoneal lavage 4.2.2. Primary Peritonitis 4.2.2.1. Tuberculous Peritonitis 4.2.3. Secondary Peritonitis 4.2.4. Tertiary Peritonitis 4.2.5. Specific conditions 4.2.5.1. Perforated peptic ulcer 4.2.5.2. Typhoid perforation/small bowel 4.2.5.3. Perforated appendicitis 4.2.5.4. Perforated colon 4.2.5.5. Necrotizing Pancreatitis

5. Intra-abdominal Abscess 5.1. Diagnosis 5.2. Treatment 5.2.1. Pelvic Abscess 5.2.2. Sub-phrenic Abscess 6. Review of Primary Surgery on Peritonitis and Intra-abdominal Abscess 7. Recommendations Clinical case: sub-phrenic abscess

1. Introduction Treatment of intra-abdominal infections is without doubt one of the most common and important challenges for surgeons generally and for those who work in low-income countries, in particular. Despite the development of much ancillary diagnostic technology, the diagnosis of peritonitis is still dependent on clinical criteria. Operative management, which may require repeated laparotomies, may tax the skills of the most experienced surgeon. A multi-disciplinary approach to intensive care support of the critically ill patient may be as important to survival as surgery. Controlling the source of infection, removing contamination by peritoneal lavage, antibiotics and physiologic support remain the chief modalities of treatment. (2) Intra-abdominal infections comprise a) infections of specific organ systems, eg. appendicitis and cholecystitis; b) peritonitis resulting from extension of infection into the general peritoneal cavity and c) intra-abdominal abscesses which result from the extension of inflammation beyond the viscus and from incompletely resolved peritonitis. (3) The latter two entities comprise the subject of this Review. 2. Etiology/Epidemiology A wide variety of disease states give rise to intra-abdominal infection. (4) While varying according to age, gender and geography, the three most common causes of generalized peritonitis in low-income countries are probably appendicitis, perforated duodenal ulcer and typhoid perforations, in no particular order. (5) In a study of Nigerian children 50% of patients had typhoid perforation. (6) In women, the complications of pelvic inflammatory disease predominate. Abdominal trauma resulting in intestinal injury is also a significant cause of peritonitis, particularly in low-income countries. In the West appendicitis remains the most common cause of peritonitis, followed by colonic perforation, usually as a result of diverticulitis. (7) Iatrogenic causes, resulting from failure of intestinal anastomosis and inadvertent bowel injuries, need to kept in mind. Certain clinical conditions, primary peritonitis and appendicitis, are more common in children. (8) Intra-abdominal infection has its own features in the elderly. (9) Mortality in secondary peritonitis decreased significantly throughout the last century from 90% to about 20%. (10) It varies significantly depending on the specific cause: from 0.25% for

appendicitis to 45% for fecal peritonitis. In general it depends very much on the degree of contamination and the ability to achieve control of the source. (11) The APACHE II physiologic measurements correlate best with mortality. (12) Unfortunately many of the required indices are not available in low-income countries. http://www.sfar.org/scores2/apache22.html#calcul 3. Pathophysiology Peritonitis is an inflammatory response to peritoneal injury. Injury results in an influx of protein rich fluid, activation of the complement cascade, up-regulation of peritoneal mesothelial cell activity and invasion of the peritoneum with polymorphonuclear neutrophils and macrophages. (13) There is stimulation of cytokine and chemokine production. Bacteria are opsonized and killed by white blood cells and cleared through the lymphatics. The anatomic origin of bacterial contamination and microbiological findings are no major predictors of outcome. However, the preoperative physiological derangement, the surgical clearance of the infectious focus and the response to treatment are established prognostic factors. The pathogenesis of intra-abdominal infections is determined by bacterial factors which influence the transition from contamination to infection. Bacterial stimuli, especially endotoxin, lead to an almost uniform activation response which is triggered by reaction of mesothelial cells and interspersed peritoneal macrophages and which also involves plasmatic systems, endothelial cells and extra- and intravascular leukocytes. The local consequences of this activation are the transmigration of granulocytes from peritoneal capillaries to the mesothelial surface and a dilatation of peritoneal blood vessels resulting in enhanced permeability, peritoneal edema and lastly the formation of protein-rich peritoneal exudate.(14) Intra-abdominal adjuvants such as bile, talc, barium and the local host response are additionally important. (15) Sequential metabolic changes occur as a result of induction of the systemic inflammatory response syndrome by severe sepsis or blunt trauma and result in protein catabolism and weight loss. (16) The first line of defense is clearance of noxious agents via the lymphatics of the parietal peritoneum, diaphragm and omentum. The formation of fibrin acts to wall off the infection and is associated with abscess formation. (17) The response to intra-abdominal infection depends on 5 key factors: (a) inoculum size; (b) virulence of the contaminating organisms; (c) the presences of adjuvants within the peritoneal cavity; (d) adequacy of local, regional, and systemic host defenses; and (e) the adequacy of initial treatment. (11) The specific microbial characteristics of different regions of the gut determine the types of infecting organisms found with specific diseases. Secondary peritonitis typically results in polymicrobial infections with gram-negative aerobes and anaerobes. Inflammation within the peritoneal cavity evokes a series of secondary changes that produce the clinical syndrome of peritonitis. These features are part of the Systemic Inflammatory Response Syndrome, whose characteristics include two or more of the following: Temperature >38 C or <36 C; Heart rate >90 beats/min; Respiratory rate <20 breaths/min, or Paco2 <32 mm Hg; WBC >12,000 cells/mm3 or <4000 cells/mm3, or <10% immature (band) forms. While SIRS is caused by a wide variety of conditions, when seen in peritonitis it is called sepsis. Severe sepsis denotes organ dysfunction distant from the site of infection (renal, cardiac, respiratory or brain) or hypotension (systolic < 90mm Hg or mean BP < 70). Septic shock is sepsis with hypotension unresponsive to fluid administration and requiring pressor agents.

The acute inflammatory process within the abdomen results in sympathetic activation, and suppression of intestinal peristalsis, or ileus. Fluid absorption through the wall of the bowel is impaired, and significant amounts of tissue fluid may be sequestered within the lumen of the gut, resulting in systemic hypovolemia. Moreover reduced intestinal peristalsis promotes microbial overgrowth, leading to translocation of bacteria and their products from the gut lumen into regional nodes, the peritoneal cavity, and the portal circulation. (3) 4. Peritonitis Peritonitis is traditionally classified as a) primary, b) secondary and c) tertiary. The form most commonly encountered by surgeons is secondary peritonitis resulting from perforation of a hollow viscus or other abdominal pathology. Primary peritonitis results from spontaneous bacterial infection of the peritoneum, alone or in association with peritoneal dialysis. Tertiary peritonitis is characterized by a class of very ill patients in whom secondary peritonitis fails to resolve despite what appear to be appropriate measures and is associated with multi-organ failure. 4.1. Diagnosis the acute abdomen Abdominal pain is the most common reason for admission to hospital in the USA and correct diagnosis of the acute abdomen remains a challenge for physicians. (18) Acute abdominal pain is defined as acute undiagnosed pain arising relatively suddenly and less than 7 days (usually 48 hours) in duration.(19) A variety of disorders is associated with acute abdominal pain. (Table 1) Since the majority of patients (2/3 in the USA) do not require surgical intervention, it is essential to identify those who do. Proper history taking and physical examinations remain the most important skills leading to correct diagnosis. A complete medical history is appropriate including information on past, family, social, medications, as well as the history of the presenting complaint. Age and gender help to focus the wide panoply of conditions causing the acute abdomen as do the specific features and location of the abdominal pain. Associations with anorexia, nausea, vomiting, bowel activity and menstrual cycle are all important. Physical examination is crucial and must include inspection, auscultation, percussion and palpation, in that order. Rectal, genital and, in women, pelvic examination should always be performed as well as that of extra-abdominal systems. The first sign of peritoniteal irritation is localized tenderness on deep palpation. With increasing severity the signs progress to voluntary guarding, involuntary guarding or rigidity. Rebound tenderness is a useful sign for localized peritoneal irritation. Generalized tenderness and boardlike rigidity are pathgnomonic of generalized peritonitis. Diffuse abdominal tenderness without guarding is unlikely to represent peritoneal irritation. Additional signs, such as Murphys and Rovsigs should be elicited if appropriate. Upon completion of history and physical examination, the surgeon develops a differential diagnosis, with attention to whether the case is non-surgical or surgical and if the latter, the urgency of surgical intervention. An algorithm to assist this has been developed. (Algorithm) In those patients whose diagnosis is uncertain, repeated examination is the most important procedure. Laboratory tests including Hb, WBC, urinalysis and, if available, basic biochemistry including electrolytes, amylase and liver function tests will be helpful. While CT scan has replaced abdominal xrays in many wealthy countries, routine 2 view examination of the supine and upright abdomen is very effective in diagnosing obstructions and free air. (20) While

patients who manifest hemodynamic instability usually require emergency surgery and are best resuscitated in the operating room, the majority will benefit from methodical assessment and stabilization prior to surgery. 4.1.1. Acute abdomen with HIV/AIDS The ongoing HIV/AIDS pandemic, with its epicentre in sub-Saharan Africa, has had profound implications for the assessment and treatment of patients with acute abdominal pain and peritonitis. (21) Where available HAART has changed the epidemiology of abdominal pain in HIV/AIDS patients. (22) Presentation with acute abdominal pain occurs in 12-48% of HIV patients. In the absence of anti-retroviral therapy over 50% of these have HIV-related pathology. These are, most commonly, cytomegalovirus (CMV) gastroenteritis, followed by lymphomas, Kaposi sarcoma and TB peritonitis. Specific HIV-related conditions include: primary peritonitis, spontaneous bowel perforation, mesenteric thrombosis, colitis (in adults), necrotizing enterocolitis (in infants), acalculous cholecystitis and intra-peritoneal rupture of splenic or hepatic abscess. (21) The physical examination with peritonitis may be obscured by a neuropathy and a leukocytosis may not be present in those patients with severely depressed CD4 counts. Operation in HIV patients, particularly in the absence of anti-retroviral therapy, is associated with elevated morbidity and mortality rates. This mandates careful evaluation and avoidance of unnecessary operation. Where diagnosis is obscure, laparoscopy has been advised. 4.2. Treatment The recurring themes of treatment in peritonitis are: a) resuscitation, b) antibiotics, c) peritoneal lavage, and d) source control 4.2.1. General measures: Hemodynamic resuscitation, early antibiotics and source control are the hallmarks of peritonitis treatment. Restoration of cardiac and pulmonary function recognized by normalization of blood pressure, urinary output and O saturation through the prompt administration of supplemental oxygen and intravenous fluids are critical to survival. These measures should be instituted immediately on initial assessment of the patient and continued throughout the operative and postoperative period. Septic patients may require invasive monitoring with inotropic support and mechanical ventilation if these are available. (23;24) 4.2.1.1. Antibiotics While antibiotics are imperative in the treatment of peritonitis, there is a lack of evidence to recommend one antibiotic regime over another. (25) While primary peritonitis is often monomicrobial, secondary peritonitis is usually polymicrobial with both gram-negative aerobes and anaerobes predominating. Antibiotics with adequate spectra to cover these organisms are required. Availability, cost, toxicity, local sensitivities and the risks of resistance are all relevant. Weigelt recommends classifying patients into low and high risk classifications on the basis of whether the peritonitis is community (low risk) or hospital-acquired (high risk) and using monotherapy and less broad spectrum agents for lower risk patients. (10) (Table 2). I have used the combination of an aminoglycoside with an anti-anaerobic agent such as clindamycin or metronidazole throughout my career with excellent results. Once-daily aminoglycoside regimes are effective and safe. Renal toxicity needs to be prevented by dose adjustment and ensuring adequate urine output. (26) Fluroquinolones are being used more regularly as primary agents.

(27) 4.2.1.2. Peritoneal lavage While peritoneal lavage for peritonitis is universally recommended, remarkably little study has been done on its specifics. While 154 articles on peritoneal lavage in peritonitis are available from 1950 to 2007, none of these is a randomized controlled trial. A small clinical control trial by Schein in 1990, comparing no lavage with intra-operative lavage with and without antibiotics, showed no differences in survival. (28) As a result Schein recommends only swabbing or mopping peritoneal surfaces with moist laparotomy packs. (2) Despite this, intra-operative lavage reamins standard therapy. It is recommended that all fluid be aspirated at the closure of the abdomen as there is evidence that the ongoing presence of fluid decreases macrophage effectiveness. Studies looking at post-operative continuous lavage come mostly from Germany or Russia. Information on these is too limited to allow comment. There is a risk of fistulization with continuous lavage. 4.2.2. Primary Peritonitis Primary peritonitis or spontaneous bacterial peritonitis (SBP) has a number of distinct clinical syndromes. It may occur in children; it occurs in patients with hepatic cirrhosis (usually alcohol) or the nephritic syndrome and ascites, in patients on peritoneal dialysis and in HIV/AIDS. Operation is unnecessary for SBP. In children SBP accounted for 10% of all abdominal emergencies in the pre-antibiotic era. (4) It is now uncommon. Savoie reports 15 cases in children from Senegal over a 3 year period. (29) Gram-negative aerobes were the most common infecting agent, followed by streptococcus. In patients with cirrhosis and ascites, SBP may be prevalent in as many as 7-30% of patients. (30) The pathophysiology appears to be bacterial translocation outside the bowel lumen into extraintestinal sites. E.coli and other gram-negative bacilli predominate. The mortality varies in these patients from 10-40% and over 50% of surviving patients will have a recurrence. Therefore prophylactic antibiotics, Septra or norfloxacin, should be prescribed to all survivors to achieve selective gut decontamination. Patients present with fever, abdominal pain, tenderness and often signs of hepatic decompensation. Diagnosis is confirmed by the presence of PMNL>250/mm. The condition is a reflection of serious hepatic failure and initial survivors have a 2 year mortality rate of 50% in the absence of liver transplantation. (31) In patients undergoing peritoneal dialysis peritonitis remains one of the major complications. (32) Gram positive organisms predominate. Treatment consists of instilling antibiotics into the dialysate. Catheter removal may be necessary. 4.2.2.1. Tuberculous Peritonitis Peritoneal tuberculosis, which might be considered a special case of primary peritonitis, represents a common extra-pulmonary manifestation of tuberculosis. (33) It is associated with HIV infection. The disease has an insidious onset and should be suspected in any case of unexplained ascites. Peritonitis is usually seen in association with other abdominal manifestations. Abdominal pain, fever, weight loss and tenderness are the common presenting features. The indolent nature of the process should assist in distinguishing it from other forms of primary and secondary peritonitis. Analysis of ascitic fluid shows predominance of lymphocytes

on gram stain and a low LDH level. The highest sensitivity and specificity is found with adenosine deaminase ADA measurement. (17) CxR abnormalities are seen in only 38% of cases. The imaging findings are reviewed by Pereira et al. (34) Laparoscopy is recommended as the diagnostic procedure of choice in that it allows inspection and biopsy of the peritoneum. Treatment is pharmacologic. 4.2.3. Secondary Peritonitis Secondary peritonitis is the most common cause of peritonitis. It requires surgical intervention in virtually all cases. The complex and highly demanding character of the surgery has been emphasized. (12;35) As with any abdominal procedure, understanding of the anatomic spaces of the peritoneal cavity is crucial. (Figure 1) A midline incision is the most versatile approach to all areas of the abdomen. Source control, reduction in bacterial contamination and prevention of its recurrence are the hallmarks of surgical treatment. Source control, whether achieved by closure of perforation, resection of disease combined with anastomosis or exteriorization of bowel is best considered in relation to the specific cause. (see 4.2.5. Specific conditions) Its importance cannot be overemphasized. Without it successful treatment of secondary peritonitis is not possible. Source control is possible in 90% of cases. In these, reoperation is necessary in 10% of patients. Where source control fails, reoperation is necessary in 30%. (7) Reduction in bacterial contamination is achieved through opening all contaminated spaces, aspirating the purulent fluid and removing food, feces and foreign debris. The traditional but unproven value of peritoneal lavage has been discussed above (see 4.2.1.2.). Radical debridement of fibrinous exudates is associated with increased risk of bleeding and perforation itself. (2) One trial showed it to be more dangerous than lavage alone and it has been abandoned. Addition of antibiotics to lavage solution also has not been shown valuable. Neither has post-operative continuous lavage or use of drains. (35) Because a single operation is sometimes insufficient to resolve the most severe forms of secondary peritonitis, the question of re-operation, to improve survival and prevent subsequent intra-abdominal abscess, has dominated recent discussions. Various approaches include open management of the abdomen with re-exploration in the intensive care unit; planned relaparotomies versus laparotomy on demand on the basis of deterioration or proven residual sepsis. (36) The presence of an abdominal compartment syndrome prohibits fascial closure. (37) Various low tech solutions such as the Bagota bag may be used as well as absorbable mesh. (2) The omentum should be used to separate the intestine from its temporary coverings. However, routine use of the open abdomen is very labour and resource-intensive. There is a lack of evidence on which to decide between planned re-laparotomy and laparotomy on demand. (38) Lamme has attempted to assess clinical indicators of need for re-laparotomy. Failure to achieve source control correlates with positive re-laparotomy, as does upper GI source, age and comorbidity. Schein stresses that the key to re-laparotomy surgery is be gentle. (2) Great skill is required to determine the extent of any exploration to minimize damage to the edematous and friable bowel. The indications for re-laparotomy are certainly not resolved. 4.2.4. Tertiary Peritonitis Tertiary peritonitis is defined as recurrent infection of the peritoneal cavity after an episode of primary or secondary peritonitis. (39) It occurs when source control, antibiotic therapy or host

immunity are inadequate. Enteroccoci, yeast and antibiotic resistant gram-negative aerobes are more common in recurrent peritonitis. Few patients have significant abdominal symptoms although they will exhibit fever and leukocytosis. Thus imaging, particularly with CT scan plays an important role in detection. The majority of patients require surgical intervention but mortality rates are much higher, up to 50%. (40) 4.2.5. Specific conditions The reader is referred to the following Surgery in Africa Reviews for detailed discussions on the surgical methods to achieve source control for specific causes of peritonitis. 4.2.5.1. Perforated peptic ulcer April 2007 As the incidence of perforated peptic ulcer has decreased in the West, the surgical treatment of those remaining has tended to simple closures rather than resection. (7) 4.2.5.2. Typhoid perforation/small bowel October 2006 Primary closure/anastomosis, even in the face of peritonitis, is standard therapy for small bowel perforations. 4.2.5.3. Perforated appendicitis March 2006 Laparascopic appendectomy is not recommended for perforated appendicitis with generalized peritonitis. (7) 4.2.5.4. Perforated colon July 2005 While Hartmanns procedure after sigmoid resection has been the standard treatment of perforated sigmoid diverticulitis, evidence is accumulating that resection and anastomosis can be undertaken in the presence of perforation as long as the patient is not in shock. (7) Breakdown of a colonic anastomosis with peritonitis may be treated by exteriorization of bowel or by repair and proximal decompression. (41) 4.2.5.5. Necrotizing Pancreatitis September 2007 The treatment of peritonitis from necrotizing pancreatitis is complex. Avoidance of surgery except for proven infectious complications is probably best. 5. Intra-abdominal Abscess Intra-abdominal abscesses, although occasionally primary, usually develop as a result of the localization of peritonitis. The site and frequency of abscesses is therefore determined by the site and frequency of the source of contamination, but also by the mesenteric partitions and peritoneal recesses, gravity and intra-peritoneal pressure gradients. (4) (Figure 2) Appendicitis usually results in right lower quadrant or pelvic abscesses; infections of the female genital tract pelvic abscess; diverticulitis left para-colic and pelvic abscesses; complications of gallbladder disease sub-hepatic and right sub-phrenic abscesses. Pancreatitis may result in lesser sac abscesses. Inadequately resolved or drained peritonitis, anastomotic breakdown and internal fistulae typically cause intra-loop abscesses. The dynamics of flow and intra-peritoneal fluid reabsorption by diaphragmatic lymphatics account for the frequency of sub-phrenic abscesses. 50% of sub-phrenic abscesses in children occur as a result of appendicitis. (4) As with secondary

peritonitis, the microbiology of intra-abdominal abscesses is polymicrobial with frequent infection with both aerobes and anaerobes. 5.1. Diagnosis Aside from signs of ongoing sepsis such as fever, leukocytosis, and anorexia, localizing physical signs are often absent in intra-abdominal abscesses. Shoulder tip pain and hiccups may derive from a sub-phrenic abscess. Diarrhoea and urinary frequency may result from pelvic abscess. Hip flexion and pain on extension may indicate psoas abscess. (42) Presence of these signs is helpful. Others include localized mass and tenderness, elevation of the hemidiaphragm, rectal or vaginal mass and tenderness. Ongoing purulent drainage from an operative site or drain may suggest a site. (see clinical case) Sub-phrenic abscesses are particularly obscure. Thus the aphorism: Pus nowhere, pus somewhere pus under the diaphragm. As a result, the diagnosis of intra-abdominal abscess depends greatly on imaging modalities. (20) Sadly many advanced techniques are not easily accessible in low-income countries. Plain radiographs, while not particularly sensitive, may be all that is available and suggest the presence of abscesses in 50% of cases. (4) Sub-phrenic abscesses may show elevation of the hemi-diaphragm, atelectasis and pleural effusion of the adjacent lung. Air-fluid levels, soft tissue masses, displacement of organs and obliteration of psoas shadows are other signs. If partial drainage is already occurring a sonogram may be helpful. (see clinical case) Water-soluble contrast should be used if contact with the peritoneal cavity is suspected. Ultrasound has fairly good sensitivity at detecting sub-phrenic and pelvic abscesses. (20) It is fairly widely available, relatively inexpensive and mobile. It can be combined with aspiration and percutaneous drainage. It has limitations particularly in the presence of intra-abdominal gas. CT scan is the procedure of choice for diagnosing intra-abdominal abscesses. Its sensitivity approaches 90-100%. Its main disadvantages are general lack of availability and access problems in critically ill patients. It is particularly relevant in pancreatic and intra-loop abscesses. Due to the sensitivity of CT scan, radionucleotide scintigraphy has been relegated to a back-up role, even in the West. 5.2. Treatment Drainage is essential for intra-abdominal abscesses. Percutaneous abscess drainage (PAD) under U/S or CT control has revolutionized the treatment of these conditions in the West over the last 25 years. Curative treatment without surgery is possible in 80% of cases, higher when the abscess is unilocular. (43) A wide number of abscesses can be treated in this manner. Probably the only current indications for primary surgical intervention are inaccessibility to percutaneous approach due to bowel or other structures, multiple abscesses and need for source control as in anastomotic breakdown. (44) However, availability of imaging modalities, not to mention catheters and ancillary equipment, is unlikely to exist in low-income countries where surgery for intra-abdominal abscesses remains the more common approach. This redo surgery is notoriously challenging because of patient condition, eradication of tissue planes and adhesive, edematous and friable bowel. An extra-peritoneal approach should be used when possible. (42) 5.2.1. Pelvic Abscess

Pelvic abscesses are best drained through the vagina or rectum. A mass with fluctuance indicates the suitability of this approach. One must be assured that there is no bowel intervening between the abscess and rectum or vaginal wall. Pus obtained on aspiration of the mass with a small bore needle is reassuring. Surgical drainage is then carried out; gentle digital exploration of the cavity to remove loculations, irrigation and insertion of a soft drain follow. If the pelvic mass presents as a suprapubic mass it may be drained anteriorly.(1) One aims for drainage of the abscess without disturbance of otherwise sealed peritoneal spaces. 5.2.2. Sub-phrenic Abscess The surgical approach to the sub-phrenic abscess may be anterior or posterior. (see clinical case) Posterior drainage is perhaps more effective, but the abscess must be accessible from behind. On the right side the liver intervenes and sub-divides the space. King provides a good description of the operative technique for sub-phrenic abscess (1) 6. Review of Primary Surgery on Peritonitis and Intra-abdominal abscess Primary Surgery Volumes I & II are unique handbooks of surgery. Produced in the early 1990s, with editorial input by a number of surgical experts from the developing world, they maintain a consistent style through the medium of a single author, Maurice King, who is not himself a surgeon. Designed for surgeons in district hospitals in Africa who are confronted by seldom seen problems, with a minimum of assistance and with little possibility of referral, they remain preeminently practical, cookbooks of surgery, which a generation of surgeons has turned to for guidance. Since these handbooks are now available on the internet as Open Access, it is worthwhile to examine the extent to which the information requires revision. Primary Surgery deals with peritonitis and intra-abdominal abscess in Volume One Non Trauma chapter 6 Pus in the pleura, the pericardium, the peritoneum and the pelvis. (1) In the introductory section on peritonitis, the description of the presentation and the instructions for history taking and physical exam are vivid and complete. The differential diagnosis, brief description of pathophysiology and role of resuscitation are adequate. The cautions concerning adherent bowel and risk of perforation or development of a fecal fistula are very much to the point. The recommendation to add antibiotics in the lavage fluid has not been born out by the literature. The section providing the details of management of generalized peritonitis continues these themes. Investigation is extremely limited in these hospital settings. The technique of aspiration of the abdomen for diagnosis, recommended for pancreatitis, is widely practiced in Africa. Resuscitation is appropriately stressed, recognizing that these hospitals do not have the facilities for advanced cardiac and respiratory support. Recommendations for chloramphenicol or cephalosporin plus metronidazole as the antibiotics of choice are not in themselves wrong, but could be broadened somewhat to account for the increased variety of agents currently available. While aminoglycosides are known to interact with anaesthetic agents, their use has never been a problem in my experience. The section on treating the source recommends exteriorization for all colonic perforations. The current literature would question this, but it is probably a safer choice (unproven) in inexperienced hands. The importance of post-operative care is correctly stressed. Modern practice limits blood replacement to Hb<7gm/dL.

The particular value of these texts is revealed when the section on difficulties is discussed. Primary peritonitis presenting a negative exploration; the problem of residual sepsis and the need for re-exploration; wound infection, and intestinal fistula are all briefly discussed and the reader is referred to appropriate sections in the text. The next section on intra-abdominal abscesses, particularly sub-phrenic and pelvic continues the authoritative, context-relevant information. The main deficiency here is the failure to mention percutaneous approaches to abscess drainage. However, these are unlikely to be available in district hospitals in low-income countries today. The rest of the descriptions on open drainage are expert and complete. They are not widely available in modern surgical texts. Surgeons facing these problems for the first time would do well to follow the stepwise advice. Aside from the minor criticisms above, these important sections on peritonitis and intraabdominal abscess stand the test of time and need little revision. They are a testament to the ongoing value of the handbook. 7. Recommendations 1. Patients presenting with acute abdomen pain should have a complete history and physical examination leading to a differential diagnosis based on non-surgical or surgical management and ranking priority for surgery. 2. All patients diagnosed with peritonitis should be resuscitated immediately after initial assessment with intravenous fluids, supplemental oxygen if hypotensive or 0 saturation is <90%, nasogastric suction and monitored with urinary catheter. 3. In cases of clinical secondary peritonitis, investigations may be limited to Hb, WBC, cross matching blood, urinalysis and basic biochemistry and amylase if available. 4. Peri-operative antibiotics should be prescribed, active against gram-negative aerobes and anaerobes. 5. All patients with secondary peritonitis should be operated via a midline incision. On entering the abdomen, purulent fluid should be aspirated and cultured. 6. Source control is vital for all cases of secondary peritonitis. The injury should be excised, debrided, repaired or if necessary exteriorized. Recommendations for methods of source control for specific conditions should be followed. 7. Peritoneal lavage should be done to remove contamination. Vigorous attempts to remove fibrin should not be carried out. All fluid should be aspirated prior to closure. 8. In cases with evidence of abdominal compartment syndrome, an unstable patient, or where source control is inadequate and the need for further exploration is anticipated; open management of the abdomen may be carried out. The omentum should be placed between the bowel and the temporary abdominal coverings. Respiratory support may be necessary in these patients. 9. Patients with intra-abdominal abscess will benefit from advanced imaging modalities and percutaneous drainage procedures when possible. 10. Referral to appropriate centers should be considered especially in cases of tertiary peritonitis.

Brian Ostrow MD, FRCSC Co-editor Surgery in Africa Monthly Reviews Adjunct Lecturer Office of International Surgery University of Toronto Canada brian@bookshelf.ca Reference List

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