Special forms of peritonitis

Postoperative

The patient is ill, with raised pulse and peripheral circulatory failure. Following an anastomotic dehiscence the general condition of a patient is usually more serious than if the patient had suffered leakage from a perforated peptic ulcer with no preceding operation. Local symptoms and signs are less definite. Abdominal pain may not be prominent and is often difficult to assess because of normal wound pain and postoperative analgesia. The patient’s deterioration may be wrongly attributed to cardiopulmonary collapse which is usually concomitant.

Peritonitis follows abdominal operations more frequently than is realised. The principles of treatment do not differ from those of peritonitis of other origin. Antibiotic therapy alone is inadequate; no antibiotic can stay the onslaught of bacterial peritonitis due to leakage from a suture line, which must be dealt with by operation.

In patients under treatment with steroids

Pain is frequently slight or absent. Physical signs are similarly vague and misleading.

In children

The diagnosis is in some ways more difficult, in other ways easier, than in adults. If a history can be taken it is plain and unembroidered. Any physical signs elicited by a gentle, patient and sympathetic examiner are meaningful.

In senile patients

These can be as fractious as children and unable to give a reliable history. Abdominal tenderness is usually well localised, but guarding and rigidity are less marked because the abdominal muscles are thin and weak.

Bile peritonitis

Unless there is reason to suspect that a bile duct was damaged at an operation, it is improbable that bile as a cause of peritonitis will be thought of until the abdomen has been opened and bile is seen therein. The common causes of bile peritoni­tis are shown in Table 56.6. Unless the bile has extravasated slowly and the collection becomes shut off from the general peritoneal cavity there are signs of diffuse peritonitis. After a few hours a tinge of jaundice is not unusual. Laparotomy (or laparoscopy) should be undertaken with evacuation of the bile and penitoneal lavage. The source of bile leakage should be identified. A leaking gall bladder is excised or a cystic duct ligated. An injury to the bile duct may simply be drained or alternatively intubated; later reconstructive operation is often required. Infected bile is more lethal than sterile bile. A ‘blown’ duodenal stump must be drained as it is too oedematous to repair, but sometimes it can be covered by a jejunal patch. The patient is often jaundiced from absorption of peritoneal bile, but the surgeon must ensure that the abdomen is not closed until any obstruction to a major bile duct has been either excluded or relieved. Post cholecystectomy bile leaks may be dealt with by percutaneous (ultrasound guides) drainage and endoscopic biliary stenting to reduce bile duct pressure. The drain is reduced when dry and the stent at 4—6 weeks.

Meconium peritonitis

Meconium is a sterile mixture of epithelial cells, mucin, salts, fats and bile and is formed when the foetus commences to swallow amniotic fluid. By the third month of intrauterine life the upper third of the small intestine has become filled with meconium; by the fourth month the accumulation has reached the ileocaecal valve; during the remainder of intrauterine life the colon becomes increasingly filled.

Meconium peritonitis is an aseptic peritonitis which develops late in intrauterine life or during, or just after, delivery. Meconium enters the peritoneal cavity through an intestinal perforation and in over 50 per cent of cases the perforation is the result of some form of neonatal intestinal obstruction; in the remainder no cause for the perforation is discernible. When meconium, which is sterile, enters the peritoneal cavity an exudate is secreted that organises rapidly; matting of intestinal loops occurs, and in many cases in a matter of weeks the extruded meconium becomes calcified.

Meconium remains sterile until about 3 hours after birth; thereafter, unless the perforation has become sealed, sterile meconium peritonitis gives place to acute bacterial peritonitis which, unless treated promptly, is rapidly fatal.

Clinical features. Meconium peritonitis should always he considered when a baby is born with a tense abdomen. There is vomiting and failure to discharge meconium. The differential diagnosis between neonatal intestinal obstruction and peritonitis is, in many cases, virtually impossible; indeed in half the cases both are present. Free fluid in the peritoneal cavity is often sufficient to give a fluid thrill. Meconium ileus occurs in 5—10 per cent of newborn babies with cystic fibrosis (mucoviscidosis) who have an inherited autosomal recessive abnormality of mucus secretion. This leads to secondary damage to the pancreas, lungs, liver and small bowel. Bronchial obstruction by mucus plugs can cause fatal pneumonia.

Radiography (Fig. 56.11). Free air in the peritoneal cavity, an abundant quantity of abdominal fluid, fluid levels, calcification (often most distinct on the surface of the liver or the spleen and most readily seen in a lateral view) are characteristic findings, all of which are unlikely to be present in every case. Meconium peritonitis has been diagnosed by radiography of the foetus in utero 2 days before birth.

Treatment. The prognosis is bad, but recovery may follow prompt operation. The greatest chance of survival is in those patients who have an intestinal perforation but no intestinal obstruction, in which case closure of the perforation and drainage of the peritoneal cavity are performed expeditiously. Intestinal lavage can prevent reformation of meconium bolos obstruction and supplements of pancreatic exocrine enzymes are often necessary throughout life. If there is an associated pulmonary problem, the condition requires special treatment (e.g. oxygen, bronchial lavage, nebulisers and long-term use of antibiotics).

Pneumococcal peritonitis

There are two forms of this disease: (1) primary, and (2) secondary to pneumonia.

Primary pneumococcal peritonitis is much more common. The patient is often an undernourished girl between 3 and 6 years of age, and it is probable that the infection sometimes occurs via the vagina and Fallopian tubes, for pneumococci have been cultured from patients’ vaginas. At other times, and always in males, the infection is blood-borne from the upper respiratory tract or the middle ear. After the age of 10 years pneumococcal peritonitis is most unusual. Children with nephritis are more liable to this condition than others. During the past 30 years the instance of pneumococcal peritonitis has declined greatly and the condition is now rare.

Clinical features. The onset is sudden and the earliest symptom is pain localised to the lower half of the abdomen. The temperature is raised to 39.80C or more and there is usually frequent vomiting. After 24—48 hours profuse diarrhoea, occasionally blood-stained, is characteristic. There is usually increased frequency of micturition. The last two symptoms are due to severe pelvic peritonitis. Herpes on the lip or nostril is often present. In acute forms of the disease, even in cases where there is no involvement of a lung, there is a tinge of cyanosis of the lips and cheeks and movement of the alae nasi is often discernible. On examination rigidity is usually bilateral but is less than in most cases of acute appendicitis with peritonitis.

Differential diagnosis. A leucocytosis of 30000/mm3 (30 x 109/litre) or more with approximately 90 per cent polymorphs suggests pneumococcal peritonitis rather than appendicitis. Even so, it is often impossible, especially in males to exclude perforated appendicitis. The other condition which is extremely difficult to differentiate from primary peritonitis in its early stage is pneumonia. An unduly high respiratory rate and the absence of abdominal rigidity are the most important signs supporting the diagnosis of pneumonia, which is usually clarified by a chest X-ray.

Treatment. Early operation is always required. After starting antibiotic therapy and correcting dehydration and electrolyte imbalance, a short midline incision is made. The peritoneum is incised. Should the exudate be odourless and sticky, the diagnosis of pneumococcal peritonitis is practically certain, hut it is essential to perform a routine laparotomy to exclude other lesions. Assuming that no other cause for the peritonitis is discovered some of the excudate is removed with a syringe and sent to the laboratory for culture and sensitivity tests. Thorough peritoneal lavage is carried out and the incision closed. The patient is returned to bed, and antibiotic and fluid replacement therapy continued. Nasogastric suction drainage is essential. Recovery is usual.

Primary streptococcal peritonitis of infants and children

Primary streptococcal peritonitis of infants and children is rather more frequent than pneumococcal peritonitis but still uncommon. When a streptococcus is the infecting organism the peritoneal exudate is thin and slightly clouded and contains flecks of fibrin. The clinical presentation and treatment of streptococcal peritonitis in infants and children are similar to those of pneumococcal peritonitis (see above), hut the mor­tality is higher. An intravaginal foreign body should always be looked for in female patients.

Idiopathic streptococcal and staphylococcal peritonitis in adults

Idiopathic streptococcal and staphylococcal peritonitis in adults is fortunately rare, for prior to the antibiotic era it was nearly always fatal and the mortality is still very high. Rightly, in early cases the abdomen is opened, usually on a diagnosis of acute appendicitis. In streptococcal peritonitis the peritoneal exudate is odourless, thin, contains some flecks of fibrin and may he blood stained. In these circumstances pus is remov­ed by suction, the abdomen closed with drainage and nonoperative treatment of peritonitis performed. Recently the use of intravaginal tampons has led to an increased incidence of Staphylococcus aureus infections: these can be associated with toxic shock syndrome’ and disseminated intravascular coagulopathy.

Peritonitis following abortion/patturition

The abortionist has usually pushed an instrument through the uterine vault and streptococcal peritonitis follows. Peritonitis following puerperal infection is more common after first deliveries. Rigidity is seldom much in evidence; this, at any rate in part, is due to the stretched condition of the abdominal musculature. The lochia may he offensive but not necessarily so. Diarrhoea is common.

Treatment. Provided the infection is limited strictly to the pelvis, the correct treatment is to rest the gastrointestinal tract and provide intravenous fluids, the required antibiotics and attention to electrolyte balance. Posterior colpotomy may be necessary if a pelvic abscess forms. If the peritonitis is generalised, the patient is usually extremely ill and drainage is advisable. This may be carried out by making a small suprapubic incision under local anaesthesia and inserting a drain, which can be done with the patient in bed, if necessary.

In the pre antibiotic era the mortality of general peritonitis following parturition or abortion was at least 50 per cent; with antibiotic therapy and timely operation, the mortality has fallen to less than 10 per cent (Brews).

Familial Mediterranean fever (periodic peritonitis)

Familial Mediterranean fever (periodic peritonitis) is characterised by abdominal pain and tenderness, mild pyrexia, polymorphonuclear leucocytosis and occasionally pain in the thorax and joints. The duration of an attack is 24—72 hours, when it is followed by complete remission but exacerbations recur at regular intervals. Most of the patients have undergone appendicectomy in childhood. This disease, often familial, is limited principally to Arabs, Armenians and Jews; other races are occasionally affected. The aetiology is unknown. Usually children are affected hut it is not rare for the disease to make its first appearance in early adult life when females outnumber males by two to one. Exceptionally the disease becomes manifest in patients over 40 years of age. At laparotomy, which may be necessary to exclude other causes, the peritoneum particularly in the vicinity of the spleen and the gall bladder is inflamed. There is no evidence that the interior of these organs is abnormal. Colchicine may prevent recurrent attacks.

Differential diagnosis. Patients with abdominal epilepsy do not have positive physical signs of pyrexia and their attacks are usually controlled by anticonvulsive medication.