Scleroscing encapsulating peritonitis has been classified as primary and secondary based on whether it is idiopathic or has a definite cause.2
The aetiology of the primary form is uncertain with various hypotheses, although it is probably caused by a subclinical peritonitis leading to the formation of a cocoon.1,4,5
Foo et al. detected the condition in 10 young girls with symptoms of bowel obstruction two years after menarche and postulated that a chemical peritonitis was caused by retrograde menstruation, leading to the formation of a cocoon.4
Secondary causes include the placement of Le Veenshunts for refractory ascites,5
continuous ambulatory peritoneal dialysis,6
systemic lupus erythematosis, and the use of povidone iodine for abdominal wash-out,7
as well as the α adrenergic blocker practolol.8
Practolol has been withdrawn from use because it was noted to cause the formation of a peritoneal membrane.
Clinically, most patients with abdominal cocoon syndrome present with features of recurrent acute or chronic small bowel obstruction secondary to kinking and/or compression of the intestines within the constricting cocoon.1,4,5
An abdominal mass may also be present due to an encapsulated cluster of dilated small bowel loops.
Abdominal X-ray findings are non-specific. CECT is a useful tool for preoperative diagnosis of abdominal cocoon. The imaging features are, however, not pathognomic. CT findings of a membrane enveloping loops of small bowel were seen in some paraduodenal hernias, abdominal cocoon, and in peritoneal encapsulation.5
However, the clinical and pathological features of these entities are different.
The final diagnosis of abdominal cocoon is usually based on intra-operative and histopathology findings, with a significant number presenting for emergency treatment without any imaging being performed. In all the reported patients, portions of the small bowel were encased within a fibrous cocoon.
Differential diagnosis includes peritoneal encapsulation, which was described as a developmental anomaly where the whole of the small bowel is encased in a thin accessory membrane. The clinical symptoms of this condition differ from those of the abdominal cocoon syndrome, in that the patients are mostly asymptomatic and the findings are incidental and late in life.
Treatment, as in the present case, consists of excision of the accessory peritoneal sac with lysis of the inter-loop adhesions. Bowel resection is unnecessary unless a nonviable segment is found.