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More recently, colonic and rectal cancers have been
staged using the TNM system (see Chapter7), and a
simplified version of this is shown below:
T1
The tumour is confined to submucosa.
T2
The tumour invades the muscle wall.
T3
The tumour invades through the muscle wall
into the serosa or pericolic/perirectal tissue.
The tumour invades other organs or has
T4
grown into the surface of the visceral peritoneum.
No regional lymph node involvement.
N0
N1
Tumour involves one to three lymph nodes in
pericolic or perirectal tissue.
Tumour involves more than three lymph
N2
nodes in pericolic or perirectal tissue.
No distant metastasis.
M0
M1
Distant metastasis.
This leads to stages of disease from one to four according to how far the tumour has spread through the
bowel wall (stages 1 and 2), to the draining lymph
nodes (stage 3) or if there is metastatic (distant)
spread (stage 4).
Prognosis
Depends largely on the stage of progression of the
tumour and its histological degree of differentiation
(see Chapter 7). The more advanced its spread and
the more poorly differentiated its cells, the worse the
prognosis.
presenting complaint in about 60% of patients. There
may also be mucus discharge, rectal pain and
tenesmus.
Examination
Abdominal palpation is often normal in early cases, but
careful attention must be paid to the detection of hepatomegaly, ascites or abdominal distension. Other general features that may be detected in more advanced
cases are enlarged supraclavicular nodes, enlarged
inguinal nodes, hepatomegaly or jaundice. Rectal
examination reveals the tumour in many cases.
Special investigations
• Sigmoidoscopy enables the great majority of
tumours to be seen and a biopsy to be taken.
Colonoscopy is indicated to rule out synchronous
•
tumours (5% of tumours in the large bowel are
multiple) or if there is ulcerative colitis or familial
polyposis. CT colonography is indicated when
colonoscopy is not readily available.
• CT of the chest, abdomen and pelvis is performed
for staging in order to detect metastatic spread.
•
Magnetic resonance (MR) imaging of the pelvis is
necessary for preoperative staging of the tumour
and for planning appropriate treatment, including
preoperative radiotherapy and chemotherapy, as
well as subsequent surgery.
Clinical features
The patient may present with:
Local disturbances owing to the presence of the
•
tumour in the rectum.
• Manifestations of secondary deposits (metastases).
The general effects of malignant disease.
•
Effects of secondary deposits and malignant disease
are similar to those of carcinoma of the colon (see
Chapter27) with the addition that, rarely, carcinoma
of the low rectum may spread to the inguinal lymph
nodes as a late phenomenon. With carcinoma at the
anal verge, this more commonly occurs.
Local symptoms
Local symptoms include bowel disturbance (constipation and/or diarrhoea occur in 80% of cases)
and bleeding, which is almost invariable and is the
Differential diagnosis ofa rectal
cancer
Differential diagnosis of a palpable malignant tumour
in the rectum must be made from the following:
•
Benign tumours.
•
Carcinoma of the sigmoid colon prolapsing into
the pouch of Douglas and felt through the rectal
wall.
Secondary deposits (metastases) in the pelvis.
•
•
Ovarian or uterine tumours.
Extension from carcinoma of the prostate or
•
cervix.
• Endometriosis.
• Lymphogranuloma inguinale.
• The rare malignant tumours of the rectum (see
earlier in this chapter).
•
Faeces (these give the classic physical sign of
indentation).
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It may be possible to mistake the normal cervix for a
palpable tumour, and note should be made of the
presence of a ring pessary or tampon in the vagina,
which are readily felt per rectum.
Treatment
Surgery
This may be performed by a traditional open
approach (laparotomy), or by minimally invasive surgery (laparoscopic or robotic). The type of surgery
performed generally depends upon the distance of
the tumour from the dentate line, along with its local
staging evident on MRI scan (Figure28.5).
• Upper third tumours can be resected with restorative anastomosis between the colon and the lower
rectum (anterior resection).
•
Lower third tumours, less than 5cm from the anal
verge and adjacent to the dentate line, may require
treatment by abdominoperineal excision of the
rectum, with a permanent end colostomy. A low
anastomosis can still be possible in carefully
selected cases.
•
Mid- third rectal tumours can usually be treated by
low anterior resection, provided satisfactory
distal clearance can be obtained. This can be a
challenging procedure, given the constraints of a
deep and narrow pelvis. A temporary covering
loop ileostomy is often used in order to protect
Primary
end-to-end
anastomosis
Upper
third
Lower
Rectum
third
Figure28.5 Surgical procedures for carcinoma of rectum.
Abdominoperineal
resection
Anterior
resection
End colostomy
Abdominoperineal
resection
Closed perineum
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the anastomosis, with subsequent closure of the
stoma some months later.
Neoadjuvant therapy
Preoperative radiotherapy reduces the risk of local
recurrence, and is commonly combined with chemotherapy (5is typically delivered in the form of external beam,
although brachytherapy (internal radiotherapy) may
be delivered from a source placed in the rectum in
some limited circumstances.
There is increasing evidence that some rectal
cancers completely respond to chemoradiotherapy
and are no longer clinically evident after this treatment (complete clinical response), potentially
negating the need for subsequent surgical resection. National registries are assessing whether this
will become an appropriate routine treatment
option in the future.
fluorouracil or capecitabine). Radiotherapy
Surveillance
After potentially curative treatment, ongoing surveillance will be advised, usually with annual CT scans
and tumour marker (carcinoembryonic antigen –
CEA) blood test to detect locally recurrent or metastatic disease, and colonoscopy at intervals to detect
and remove further benign adenomas in order to
prevent metachronous bowel cancer.
Palliative procedures
Even if there are metastases not amenable to potentially curative treatment, palliation may still be best
achieved by excision of the primary tumour. A colostomy may be necessary for intestinal obstruction, but
this does not relieve the bleeding, mucus discharge
and sacral pain. In cases where surgery is not appropriate, radiotherapy is the palliative treatment option
of choice for local symptoms such as bleeding, and
palliative chemotherapy may be considered if there is
incurable metastatic disease.
Anal cancer
Anal cancer is rare, affecting around 1 500 people a
year in the UK. It is more common in women and the
elderly, and its incidence is increasing. It is most
commonly anal squamous cell carcinoma, and risk
factors include:
Human papilloma virus: around 90% of cases are
•
linked to HPV infection, particular to the type 16
virus.
•
Genital warts and cervical cancer, both conditions
which share the HPV aetiology.
Immunosuppression, whether for organ transplan-
•
tation or as a consequence of disease (e.g. human
immunodeficiency virus [HIV]).
Pathology
The anal canal is lined by squamous epithelium and
anal carcinomas are usually squamous cell carcinomas and manifest as an ulcer near the anal verge.
Rarely, adenocarcinoma, arising from the anal
glands, basal cell carcinoma and melanoma may
occur in this area.
Anal carcinomas spread to the inguinal lymph
nodes as well as those within the pelvis; the anal canal
should always be inspected in patients presenting
with unexplained inguinal lymphadenopathy.
Clinical features
Anal cancers present with the passage of mucus or
blood (similar to rectal cancer), anal pain, a lump at
the anal verge and faecal incontinence. They are
usually best examined under general anaesthetic
when a biopsy can also be taken.
Special investigations
• MRI imaging to assess local invasion and CT scan
to assess for distant spread.
Treatment
Abnormal anal lesions should be excised for histological analysis. Highlesions (HSIL) and their low- grade equivalent (LSIL)
may subsequently develop into malignancy and subsequent surveillance is required. These were previously known as anal intraepithelial neoplasia (AIN).
Anal squamous cell cancers less than 2cm in size
(T1) can be treated by local excision, preserving the
anal sphincter. Larger tumours and those with confirmed or suspected lymph node involvement are
treated by a combination of radiotherapy and chemotherapy. If chemoradiotherapy fails to control the
grade squamous intraepithelial
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disease, a salvage abdominoperineal resection is
performed. Anal adenocarcinomas are treated in the
same manner as rectal carcinomas.
Overall, about 70% of patients will be alive 5 years
after diagnosis and treatment.
Additional resources
Case 72: A pathological anal verge
Case 73: A painful mass at the anal verge
Case 74: Another painful mass at the anal verge
Case 75: A painful anal verge
Case 76: A very painful buttock
Case 77: A patient with recurrent perianal sepsis
Case 78: A prolapsing anal mass
Case 79: An ulcer in the rectum
Case 80: An ulcer at the anal verge
The acute abdomen
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Constantinos Simillis
Learning objective
✓ To know the causes and assessment of the acute abdomen, and the
general principles of treatment.
The patient’s temperature, heart rate, respiratory
Aetiology
An acute abdomen refers to the rapid onset of severe
abdominal pain requiring early diagnosis and treatment. There are many causes for an acute abdomen
and the clinician should be able to consider all possible causes, investigate these accordingly, and provide
the appropriate treatment urgently.
Diagnosis is difficult due to the numerous potential
causes. The causes of an acute abdomen may usefully
be considered in terms of the individual organs and
their pathology (see Box29.1)
Clinical assessment
A detailed history is invaluable in order to guide the clinician through the extensive list of differential diagnoses to the appropriate diagnosis and treatment.
Meticulous physical examination is also important. For
example, the location of abdominal tenderness may
point towards the underlying diagnosis. Examination
of the hernial orifices for incarcerated hernias and the
scrotum for testicular torsion are particularly important areas that are often missed. Scars from previous
surgical procedures may suggest postoperative complications or adhesions causing obstruction.
Ellis and Calne’s Lecture Notes in General Surgery, Fourteenth Edition.
Edited by Christopher Watson and Justin Davies.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
Companion website: www.wiley.com/go/Watson/GeneralSurgery14
rate, oxygen saturation, blood pressure and urinary
output are important to assess the extent of sepsis or
shock, which may necessitate rapid escalation of
treatment.
Special investigations
• Full blood count: to look for anaemia, leucocy tosis,
neutropenia, thrombocytosis and thrombocy-
topaenia.
Urea and electrolytes: to identify acute kidney
•
injury or electrolyte abnormalities. Knowledge of
kidney function allows renaldrugs and selection of appropriate antibiotics.
Liver function tests: alanine transaminase (ALT)
•
and aspartate transaminase (AST) as markers of
hepatocellular injury, alkaline phosphatase (ALP)
and bilirubin as a marker of biliary sepsis e.g.
cholangitis, cholecystitis.
•
Serum amylase and lipase: to identify acute
pancreatitis.
• C- reactive protein (CRP): a marker of infection or
inflammation.
Clotting screen: to identify underlying bleeding
•
risk, and important in anticoagulated patients in
case of surgery.
•
Group and Save: to identify the patient’s blood
group and save serum for future crossmatch, or
crossmatch some blood immediately in readiness
for emergency surgery.
29
dose adjustment of
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Box 29.1 Causes ofan acute abdomen
Oesophagus, stomach andduodenum
•
Gastroesophageal reflux or heartburn.
•
Gastritis or duodenitis.
•
Peptic ulcer or peptic ulcer perforation.
•
Perforated oesophagus.
Intestine
•
Acute appendicitis.
•
Bowel ischaemia.
•
Diverticulitis with or without complications, e.g.
perforation, abscess, obstruction.
•
Meckel’s diverticulitis.
•
Inflammatory bowel disease e.g. Crohn’s disease,
ulcerative colitis.
•
Small bowel obstruction e.g. due to adhesions,
hernia.
•
Large bowel obstruction e.g. due to neoplasm,
sigmoid volvulus.
•
Bowel volvulus e.g. sigmoid volvulus, caecal
volvulus.
•
Irritable bowel syndrome.
•
Constipation.
Liver, biliary tree andpancreas
•
Biliary colic.
•
Cholecystitis.
•
Cholangitis.
•
Gallbladder perforation.
•
Hepatitis.
•
Liver abscess.
•
Pancreatitis.
Abdominal wall hernia strangulation
•
Groin hernia: inguinal and femoral.
•
Other abdominal wall hernias e.g. umbilical,
paraumbilical, incisional, epigastric, spigelian.
Gynaecological causes
•
Ruptured ectopic pregnancy.
•
Ovarian torsion.
•
Ovarian cyst rupture.
•
Pelvic inflammatory disease, e.g. salpingitis,
tubo- ovarian abscess.
•
Endometriosis.
Urological causes
•
Ureteric colic.
•
Pyelonephritis.
•
Urinary tract infection.
•
Testicular torsion.
Vascular causes
•
Abdominal aortic aneurysm rupture.
•
Other arterial aneurysm rupture, e.g. common and
internal iliac arteries.
Trauma
•
Organ injury e.g. splenic rupture, liver laceration,
kidney injury.
•
Haemoperitoneum.
•
Penetrating or blunt injury.
Postoperative complications
•
Iatrogenic injury e.g. bowel perforation, bowel
ischaemia.
•
Anastomotic leak.
Non- surgical causes
•
Diabetic ketoacidosis.
•
Myocardial infarction.
•
Pulmonary embolism.
•
Primary peritonitis or spontaneous bacterial
peritonitis.
•
Basal pneumonia.
•
Adrenal crisis.
•
Sickle cell crisis.
•
Acute intermittent porphyria.
•
Tuberculosis.
• Arterial blood gas (ABG) provides the lactate, pH,
base excess, and some electrolyte concentrations
quickly, as well as assessing oxygenation.
• Glucose: a marker of pancreatitis severity, of hepatocellular failure, and to identify diabetic ketoacidosis.
• Urine dipstick: leucocytes or nitrites may suggest
urinary tract infection; blood may suggest renal
colic; ketones may suggest malnutrition and dehydration or diabetic ketoacidosis; glucose in urine
will suggest poorly controlled diabetes.
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• Pregnancy test: β- human chorionic gonadotropin
HCG) to help diagnose ectopic pregnancy, and
(βalso to rule out pregnancy before exposure to X-
Erect chest X- ray may reveal free gas under the dia-
•
phragm in cases of a perforated abdominal viscus
(seen in 70% of perforated peptic ulcers). It may
also exclude pulmonary infection as a differential
diagnosis.
•
Abdominal X- ray may demonstrate small or large
bowel dilation due to bowel obstruction; free
intraperitoneal gas may also be noted if Rigler’s
1
sign
is present (the bowel wall is outlined by air
both inside and outside). Plain X- rays are less
commonly performed today in favour of a computed tomography scan.
•
Computed tomography (CT): the most important
imaging tool because it provides rapid and accurate diagnostic information. CT is the most sensitive technique for detecting free intraperitoneal
gas or free fluid and is valuable for determining
the cause of the acute abdomen.
– A contrast enhanced CT scan (done with intra-
venous contrast) is the technique of choice, but
it can be done without contrast when investigating possible renal colic or if the patient is in
renal failure.
– CT scan with oral contrast may be requested in
cases of bowel obstruction.
– CT angiogram may be performed to assess the
blood supply to the bowel or identify a bleeding point within the bowel.
•
Ultrasound scan is the investigation of choice for
suspected acute cholecystitis, biliary colic, or
cholangitis. An ultrasound scan is often used to
investigate acute abdomen in children to minimize exposure to ionizing radiation. In children,
or patients with minimal central adiposity, ultrasound may identify the cause of the acute abdomen e.g. acute appendicitis.
Transvaginal ultrasound may be useful when
•
investigating pelvic pain in young female patients
because it can visualize the gynaecological organs
and assess for gynaecological pathology e.g. ovarian torsion, ovarian cyst, salpingitis, tubo- ovarian
abscess.
1
Leo George Rigler (1896–1979); Professor of Radiology,
serially at University of Minnesota and University of
California Los Angeles.
rays.
• Magnetic resonance imaging (MRI) is useful as an
alternative to CT where ionizing radiation
exposure should be avoided, e.g. in children and
pregnant patients.
Principles oftreatment
In this section, only an outline of treatment is given,
as specific causes of acute abdomen may require specific therapy, and these are dealt with in their appropriate chapters. The standard principles of
resuscitation are followed, after an initial assessment
of the patient’s general condition.
Oxygen therapy: Oxygen is required if the patient is
1
hypoxic based on their haemoglobin oxygen saturation or on ABG.
2
Analgesia: Relief of pain with opiates, such as
intravenous morphine.
Nil by mouth: Patient should remain nil by mouth
3
in case they require urgent surgery.
4
Intravenous fluid and electrolyte replacement:
intravenous fluids or blood may be required in the
presence of shock to correct hypovolaemia and
improve organ perfusion (see chapter 8). This
should lead to improved blood pressure, heart
rate, and urine output.
Antibiotic therapy to treat the broad spectrum of
5
bowel organisms, for example penicillin and gentamicin together with metronidazole, or coamoxiclav; or in patients who have already been on
antibiotic therapy the addition of an anti- candidal
agent, such as fluconazole, is worthwhile.
Cultures of blood, pus, urine and swabs of the
peritoneal cavity should be taken to identify causative microorganisms and their microbiological
sensitivities in order to guide antibiotic therapy in
conjunction with the microbiology team.
6
Inotropes: If, despite intravenous fluid rehydration
and antibiotics, the patient remains tachycardic,
hypotensive and oliguric, then the patient may
require inotropic support and intensive care
management.
7 Urinary catheter: to monitor urine output as a
measure of the patient’s hydration and to monitor
response to volume replacement.
8 Nasogastric tube: gastric aspiration by means of a
nasogastric tube reduces the risk of inhalation of
vomit (aspiration), prevents further abdominal
distension and helps to ease symptoms of nausea
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and vomiting, hence it is used in bowel obstruction. It will also reduce the risk of aspiration at the
time of induction of anaesthesia should surgery be
necessary.
Drainage: Radiologically guided drainage is an
9
option in order to drain any localized intraperitoneal collection of pus, thus avoiding the risks of surgery especially in highstill be an option if drainage fails, or sepsis recurs.
Non- surgical treatment
Conservative treatment is indicated, at least initially,
when the infection has been localized, for example an
appendix mass, or when the primary focus is irremovable, as in pancreatitis or postpartum infection. It
may also be indicated when the patient is high risk for
surgery or moribund.
Some causes of the acute abdomen may be treated
without surgery, such as acute cholecystitis, urinary tract
infection, pyelonephritis, pelvic inflammatory disease,
uncomplicated diverticulitis and appendix mass. There
are also circumstances when acute appendicitis can be
managed non-
operatively (see chapter26).
risk patients. Surgery may
3
Via the blood stream, e.g. as part of septicaemia (e.g.
Pneumococcus, streptococcus, staphylococcus).
Via the female genital tract, e.g. acute salpingitis or
4
puerperal infection.
Pathology
Peritonitis of bowel origin usually shows a mixed
faecal flora (Escherichia coli, Streptococcus faecalis,
Pseudomonas, Klebsiella and Proteus, together with
the anaerobic Clostridium and Bacteroides).
Gynaecological infections may be chlamydial, gonococcal or streptococcal. Blood- borne peritonitis may
be streptococcal, pneumococcal, staphylococcal or
tuberculous. In young girls, a rare gynaecological
infection is due to Pneumococcus. Peritonitis is characterised by:
Widespread absorption of toxins from the large,
1
inflamed surface.
2
The associated paralytic ileus with the following:
a Loss of fluid.
b Loss of electrolytes.
Loss of protein.
c
3 Gross abdominal distension with elevation of the
diaphragm, which produces a susceptibility to
lung collapse and pneumonia.
Surgery
Surgery is indicated as the definitive treatment for
many causes of the acute abdomen to manage the
source of sepsis, for example the repair of a perforated
ulcer, removal of a gangrenous and/or perforated
appendix, resection of part of the colon for perforated
diverticulitis or repair of a strangulated hernia.
Peritonitis
Aetiology
Peritonitis is localized or generalized inflammation of the
peritoneum, caused by an infection or irritant entering
the peritoneal cavity through one of four portals:
From the exterior, e.g. penetrating wound, peritoneal
1
dialysis.
2 From intra- abdominal viscera, e.g. infected or
perforated viscus.
Clinical features
Peritonitis is usually secondary to a precipitating
lesion, one of the causes of the acute abdomen listed
above, which may have its own clinical features. For
example, there may be features of peptic ulceration
before the ulcer perforates to cause peritonitis.
Peritonitis is characterised by severe pain, exacerbated by movement such that the patient gains relief
by lying still. Irritation of the parietal peritoneum on
the underside of the diaphragm may produce referred
pain to the shoulder tip which, like the diaphragm, is
also innervated by the C3, 4, 5nerve roots. There may
be associated nausea and vomiting, and patients are
usually pyrexial and tachycardic.
Examination elicits localized or generalised tenderness, depending on the extent and underlying
cause of the peritonitis. The abdominal wall may be
held rigidly or guarding may be present (increasing
resistance to increasing depth of palpation), and
rebound tenderness may be present. Rectal examination may show tenderness in the pouch of Douglas or
pelvis, elicited by moving the examining finger
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anteriorly in the rectum; palpating posteriorly,
against the sacrum, should not elicit pain as it does
not stimulate peritoneum and is a useful ‘control’.
The abdomen may become distended and tympanic.
Depending on the underlying cause of peritonitis, other
relevant signs or symptoms may also be present, for
example, faeculent vomiting in bowel obstruction, or
pain radiating to the back in pancreatitis.
Peritonitis is classified as primary, secondary or
tertiary.
Primary peritonitis
In primary peritonitis, or spontaneous bacterial peritonitis (SBP), there is inflammation of the peritoneal
surface without another intraan identifiable anatomical derangement. It most
commonly occurs in patients with hepatic cirrhosis
and ascites, and less often in patients with ascites
from other causes, such as heart failure and nephrotic
syndrome. Such infections often precipitate hepatic
decompensation in a patient with cirrhosis, resulting
in encephalopathy, ascites and renal failure. The
protein- rich ascitic fluid acts as a culture medium for
organisms in these patients who often have a weakened immune response. Infection occurs when
enteric organisms translocate across the intact bowel
wall from the gut lumen into the ascites.
Bacteria may also gain access to the peritoneal
fluid to cause primary peritonitis through different routes such as haematogenous or lymphatic
dissemination, passing through the fallopian
tubes from the vagina in women, through a peritoneal dialysis catheter or other iatrogenic sources
of contamination. The majority of SBP cases are
of monomicrobial origin. The commonest implicated pathogens are enteric gram- negative rods,
such as Escherichia coli and Klebsiella species.
Asmaller number of cases are due to gram- positive
organisms, such as Streptococcus pneumoniae.
Primary peritonitis may be confirmed by a peritoneal tap rich in leucocytes and a positive bacterial culture. It is managed with antibiotics and
organ support, without surgical intervention.
abdominal process or
Secondary peritonitis
Secondary peritonitis is the most commonly encountered type of peritonitis in surgical patients and is
defined as an infection or inflammation of the peritoneal
cavity secondary to inflammation or infection from
an abdominal viscus, such as appendicitis, diverticulitis, perforated bowel, pancreatitis, cholecystitis,
bowel anastomotic leak, penetrating wound, bowel
ischaemia and many others. The mainstay of treatment for secondary peritonitis is urgent surgery to
achieve surgical control of the source of infection
and reduction of the bacterial load, in conjunction
with appropriate antibiotic therapy and organ support. There are cases of secondary peritonitis, however, not necessarily requiring urgent surgery, such
as pancreatitis. Peritonitis of bowel origin usually
shows mixed faecal flora (Escherichia coli,
Streptococcus faecalis, Pseudomonas, Klebsiella and
Proteus, together with the anaerobic Clostridium and
Bacteroides).
Tertiary peritonitis
Tertiary peritonitis has been defined as a severe
recurrent or persistent intra- abdominal infection 48
hours after apparently successful and adequate surgical source control of secondary peritonitis. For example, development of multiple intraabscesses following an appendicectomy; or development of collections following the surgical management of perforated colonic diverticulitis.
After surgical treatment of secondary peritonitis,
some patients develop persistent intra- abdominal
infection which causes prolonged systemic inflammation leading to a high chance of severe sepsis or
septic shock with multiorgan failure. There is a
significant difference between the microbial flora
in secondary and tertiary peritonitis, and the
causal agents in tertiary peritonitis are mostly
opportunistic and nosocomial facultative pathogenic bacteria and fungi (e.g. enterococci, entero-
bacter, and candida).
The development of multibeen observed in microbes causing tertiary peritonitis due to use of broad- spectrum antibiotic therapy.
Altered microbial flora, failure of the immune
response, septic shock and progressive organ dysfunction lead to a high risk of mortality in tertiary
peritonitis. Therefore, it is important to recognize
tertiary peritonitis early in order to minimize complications and improve patient outcomes. Treatment
involves appropriate antibiotics and antifungals,
organ support, radiologically guided drainage of any
source of intra- abdominal sepsis and reoperation if
all other measures fail.
drug resistance has also
abdominal
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Special causes
ofperitonitis
Peritoneal dialysis peritonitis
Patients on peritoneal dialysis are prone to peritonitis
either from organisms entering via the indwelling dialysis catheter (usually, skin flora such as Staphylococcus
species) or from perforation of a viscus, in which case
the flora are generally a mixture of faecal organisms.
Diagnosis is made by the presence of abdominal pain
and turbid dialysate. Single organisms are treated by
intravenous and intraperitoneal antibiotics. Multiple
organisms, particularly gut flora, suggest perforation
and require surgery as well as antibiotics. Once
infected, the peritoneal dialysis catheter may form a
focus for sepsis, in which case it should be removed.
Pneumococcal peritonitis
This may be secondary to the septicaemia accompanying a pneumococcal lung infection, or can originate
from an infected or colonized female genital tract.
Clinically, there is peritonitis of sudden onset accompanied by septicaemia, and the white cell count is elevated. Peritoneal fluid is clear or turbid containing
fibrin flakes without an obvious primary cause within
the abdomen. The peritoneal fluid reveals characteristic gram- positive pneumococci arranged in chains and
pairs. The condition responds to penicillin therapy.
Haemolytic streptococcal
peritonitis
This may occur in children, secondary to streptococcal infection of the tonsils, otitis media, scarlet fever
or erysipelas.
tuberculosis. The majority of cases are due to the
reactivation of dormant peritoneal tuberculous collections. It can also arise as a result of haematogenous spread from a primary active pulmonary focus
or miliary tuberculosis. Less frequently, mycobacteria tuberculosis can enter the peritoneal cavity
directly from the gastrointestinal tract (e.g. after a
bowel perforation or transmurally from infected
small intestine). There have also been cases of lymphatic spread (e.g. through mesenteric lymph nodes).
In some female patients, spread has been noted via
the genital tract (e.g. from primary tuberculous
salpingitis).
Risk factors for tuberculous peritonitis include
patients who are immunosuppressed, either iatrogenic
(e.g. in peritoneal dialysis, chemotherapy or steroid
therapy), or by disease (e.g. human immunodeficiency
virus infection, liver cirrhosis). Lifestyle risk factors
include alcoholism and intravenous drug abuse.
Tuberculous peritonitis is commonly classified into
three types: wet, fixed fibrotic and dry plastic. The
commonest type (>90% of cases) is the wet, or ascitic
type, and it usually results from the haematogenous
spread from a primary lung infection or through reactivation of latent tuberculous peritoneal lesions. As
the name suggests, the wet type is characterized by
large amount of either free or loculated viscous fluid.
The fixed fibrotic type is characterized by large mesenteric and omental masses leading to fixed bowel
loops with loculated ascites. The dry plastic type is the
least common type and is characterized by caseous
mesenteric lymphadenopathy, thickened omentum
and fibrous adhesions.
Clinical features of tuberculous peritonitis include
abdominal distension, night sweats, fevers, abdominal pain and weight loss. Treatment comprises of
anti- tuberculous chemotherapy. Surgery may be
required for complications including bowel perforation, intestinal obstruction secondary to adhesions,
fistulae or abscesses.
Staphylococcal peritonitis
Staphylococcal septicaemia may rarely cause staphylococcal peritonitis, which can be further complicated by intra- abdominal or perinephric abscess
development.
Tuberculous peritonitis
Tuberculous peritonitis is a type of extrapulmonary
tuberculosis affecting the peritoneum. It is frequently
seen in the presence of other types of gastrointestinal
Biliary peritonitis
Biliary peritonitis is caused by perforation of the
gallbladder, bile duct or upper gastrointestinal tract.
This may occur as a result of the following:
•
Traumatic rupture of the gallbladder or biliary
ducts.
• Iatrogenic injury after invasive procedures such as
liver biopsy, percutaneous cholangiography or
endoscopic retrograde cholangiopancreatography (ERCP).
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