Peritonitis and Intra-abdominal Abscess - Pelvic and
Sub-phrenic
Author’s 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 für 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
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 Murphy’s and Rovsig’s
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 O² 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 post-operative
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 mono-microbial, 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 extra-intestinal 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/mm³.
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 over-emphasized. 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 re-laparotomies 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 co-morbidity.
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 Hartmann’s 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
pre-eminently 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 intra-abdominal abscess stand the test of time and need little revision.
They are a testament to the ongoing value of the handbook.
7. Recommendations
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
(1) King M. Pus in the pleura, the pericardium and the peritoneum.
In: King Meal, editor. Primary Surgery Volume One Non-Trauma. Oxford: Oxford
University Press, 1990: 65-82. http://ps.cnis.ca/wiki/index.php/Main_Page
(2) Schein M. Surgical management of intra-abdominal infection:
is there any evidence?. [Review] [30 refs]. Langenbecks Archives of Surgery
387(1):1-7, 2002. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/34998
(3) Marshall JC. Intra-abdominal infections. [Review] [66 refs].
Microbes & Infection 6(11):1015-25, 2004. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/35064
(4) Levinson M&BL. Peritonitis and Intra-abd Abscesses.
In: Mandell B&D, editor. Principles and Practice of Infectious Diseases.
Churchill Livingstone, 2005.
(5) Gupta S, Kaushik R. Peritonitis - the Eastern experience.
World J Emerg Surg 2006; 1:13. PM:16759427
(6) Adesunkanmi AR, Oseni SA, Adejuyigbe O, Agbakwuru EA. Acute
generalized peritonitis in African children: assessment of severity of illness
using modified APACHE II score. ANZ Journal of Surgery 73(5):275-9, 2003.
(7) Malangoni M, Inui T. Peritonitis - the Western experience.
World Journal of Emergency Surgery 2006; 1(1):25. http://www.wjes.org/content/1/1/25
(8) Thompson AE, Marshall JC, Opal SM. Intraabdominal infections
in infants and children: descriptions and definitions. [Review] [47 refs]. Pediatric
Critical Care Medicine 6(3 Suppl):S30-5, 2005. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/34988
(9) Podnos YD, Jimenez JC, Wilson SE. Intra-abdominal Sepsis
in Elderly Persons. [Review] [56 refs]. Clinical Infectious Diseases 35(1):62-8,
2002. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/34997
(10) Weigelt JA. Empiric treatment options in the management
of complicated intra-abdominal infections. [Review] [59 refs]. Cleveland Clinic
Journal of Medicine 74 Suppl 4:S29-37, 2007. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/35054
(11) Malangoni MA. Contributions to the management of intraabdominal
infections. [Review] [30 refs]. American Journal of Surgery 2005; 190(2):255-259.
http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/35060
(12) Wittmann DH, Schein M, Condon RE. Management of secondary
peritonitis. [Review] [76 refs]. Annals of Surgery 224(1):10-8, 1996. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/35083
(13) Hall JC, Heel KA, Papadimitriou JM, Platell C. The pathobiology
of peritonitis. [Review] [126 refs]. Gastroenterology 114(1):185-96, 1998. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/35081
(14) Farthmann EH, Schoffel U. Epidemiology and pathophysiology
of intraabdominal infections (IAI). [Review] [26 refs]. Infection 26(5):329-34,
1998;-Oct.
(15) Laroche M, Harding G. Primary and secondary peritonitis:
an update. [Review] [79 refs]. European Journal of Clinical Microbiology &
Infectious Diseases 17(8):542-50, 1998. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/35077
(16) Plank LD, Hill GL. Sequential metabolic changes following
induction of systemic inflammatory response in patients with severe sepsis or
major blunt trauma. [Review] [64 refs]. World Journal of Surgery 24(6):630-8,
2000. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/35072
(17) Riquelme A, Calvo M, Salech F, Valderrama S, Pattillo
A, Arellano M et al. Value of adenosine deaminase (ADA) in ascitic fluid for
the diagnosis of tuberculous peritonitis: a meta-analysis. [Review] [34 refs].
Journal of Clinical Gastroenterology 40(8):705-10, 2006. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/35057
(18) Martin RF, Rossi RL. The acute abdomen. An overview and
algorithms. [Review] [8 refs]. Surgical Clinics of North America 77(6):1227-43,
1997.
(19) Soybel D&DR. Acute Abdominal Pain. In: American College
of Surgeons, editor. ACS Surgery: Principles and Practice. 2006.
(20) Lee MJ. Non-traumatic abdominal emergencies: imaging and
intervention in sepsis. [Review] [33 refs]. European Radiology 12(9):2172-9,
2002. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/34996
(21) Cotton M. The acute abdomen and
HIV. [Review] [0 refs]. Tropical Doctor 36(4):198-200, 2006.
(22) Saltzman DJ, Williams RA, Gelfand DV, Wilson SE. The surgeon
and AIDS: twenty years later.[see comment]. [Review] [88 refs]. Archives of
Surgery 140(10):961-7, 2005. http://simplelink.library.utoronto.ca/url.cfm/41122
(23) Marshall JC, Innes M. Intensive care unit management of
intra-abdominal infection. [Review] [110 refs]. Critical Care Medicine 31(8):2228-37,
2003. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/35067
(24) Streat SJ, Plank LD, Hill GL. Overview of modern management
of patients with critical injury and severe sepsis. [Review] [68 refs]. World
Journal of Surgery 24(6):655-63, 2000. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/35073
(25) Wong PF, Gilliam AD, Kumar S, Shenfine J, O'Dair GN, Leaper
DJ. Antibiotic regimens for secondary peritonitis of gastrointestinal origin
in adults [Systematic Review]. Cochrane Database of Systematic Reviews 2007;(3).
http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/35061
(26) Bohnen JM. Antibiotic therapy for abdominal infection.
[Review] [36 refs]. World Journal of Surgery 22(2):152-7, 1998. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/35079
(27) Madan AK. Use of ciprofloxacin in the treatment of hospitalized
patients with intra-abdominal infections. [Review] [82 refs]. Clinical Therapeutics
26(10):1564-77, 2004. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/34989
(28) Schein M, Gecelter G, Freinkel W, Gerding H, Becker PJ.
Peritoneal lavage in abdominal sepsis. A controlled clinical study. Archives
of Surgery 125(9):1132-5, 1990.
(29) Savoie PH, Peycru T, Mingoutaud L, Sow A, Biance N, Pauleau
G et al. [Primary peritonitis in Sub-Saharian Africa: a 15 case series]. [French].
Medecine Tropicale 67(2):154-8, 2007.
(30) Koulaouzidis A, Bhat S, Karagiannidis A, Tan WC, Linaker
BD. Spontaneous bacterial peritonitis. [Review] [91 refs]. Postgraduate Medical
Journal 83(980):379-83, 2007. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/35055
(31) Mowat C, Stanley AJ. Review article: spontaneous bacterial
peritonitis--diagnosis, treatment and prevention. [Review] [70 refs]. Alimentary
Pharmacology & Therapeutics 15(12):1851-9, 2001. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/35070
(32) Wiggins KJ, Johnson DW, Craig JC, Strippoli GF. Treatment
of peritoneal dialysis-associated peritonitis: a systematic review of randomized
controlled trials. [Review] [76 refs]. American Journal of Kidney Diseases 50(6):967-88,
2007.
(33) Sanai FM, Bzeizi KI. Systematic review: tuberculous peritonitis--presenting
features, diagnostic strategies and treatment. [Review] [122 refs]. Alimentary
Pharmacology & Therapeutics 22(8):685-700, 2005. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/35058
(34) Pereira JM, Madureira AJ, Vieira A, Ramos I. Abdominal
tuberculosis: imaging features. [Review] [31 refs]. European Journal of Radiology
55(2):173-80, 2005. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/35059
(35) Bosscha K, van Vroonhoven TJ, van der WC. Surgical management
of severe secondary peritonitis.[see comment]. [Review] [85 refs]. British Journal
of Surgery 86(11):1371-7, 1999. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/35076
(36) Pieracci FM, Barie PS. Intra-abdominal infections. [Review]
[85 refs]. Current Opinion in Critical Care 13(4):440-9, 2007. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/34985
(37) Hunter JD, Damani Z. Intra-abdominal hypertension and
the abdominal compartment syndrome. [Review] [64 refs]. Anaesthesia 59(9):899-907,
2004. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/24015
(38) Lamme B, Mahler CW, van Ruler O, Gouma DJ, Reitsma JB,
Boermeester MA. Clinical predictors of ongoing infection in secondary peritonitis:
systematic review. [Review] [66 refs]. World Journal of Surgery 30(12):2170-81,
2006. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/35056
(39) Malangoni MA. Evaluation and management of tertiary peritonitis.
[Review] [25 refs]. American Surgeon 66(2):157-61, 2000. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/35074
(40) Evans HL, Raymond DP, Pelletier SJ, Crabtree TD, Pruett
TL, Sawyer RG. Diagnosis of intra-abdominal infection in the critically ill
patient. [Review] [36 refs]. Current Opinion in Critical Care 7(2):117-21, 2001.
http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/35071
(41) Chambers WM, Mortensen NJ. Postoperative leakage and abscess
formation after colorectal surgery. [Review] [80 refs]. Best Practice &
Research in Clinical Gastroenterology 18(5):865-80, 2004. http://simplelink.library.utoronto.ca/url.cfm/41124
(42) Asgeirsson K&MR. Intra-abdominal Abscesses. Surgery
(Oxford) 2002; 20(5):108-111.
(43) vanSonnenberg E, Wittich GR, Goodacre BW, Casola G, D'Agostino
HB. Percutaneous abscess drainage: update. [Review] [63 refs]. World Journal
of Surgery 25(3):362-9; discussion 370-2, 2001. http://simplelink.library.utoronto.ca.myaccess.library.utoronto.ca/url.cfm/34999
(44) Dunn D&BG. Surgical Infections. In: Brunicardi FC,
editor. Schwartz's: Principles of Surgery. New York: McGraw-Hill, 2005.
Click here to join the Surgery in Africa Discussion Group
