In either case, pain typically starts as a generalized abdominal pain (with involvement of poorly localizing visceral innervation of the visceral peritoneal layer), and may become localized later (with involvement of the somatic innervation of the parietal peritoneal layer). Peritonitis is an example of an acute abdomen. Other symptoms
Diffuse abdominal rigidity (abdominal guarding) is often present, especially in generalized peritonitis
Fever
Sinus tachycardia
Development of ileus paralyticus (i.e., intestinal paralysis), which also causes nausea, vomiting and bloating
Reduced or no passage of abdominal gas and bowel sound

Complications
Sequestration of fluid and electrolytes, as revealed by decreased central venous pressure, may cause electrolyte disturbances, as well as significant hypovolemia, possibly leading to shock and acute kidney failure. A peritoneal abscess may form (e.g., above or below the liver, or in the lesser omentum)
Sepsis may develop, so blood cultures should be obtained. Complicated peritonitis typically involves multiple organs. Causes
Infection
Perforation of part of the gastrointestinal tract is the most common cause of peritonitis. Examples include perforation of the distal esophagus (Boerhaave syndrome), of the stomach (peptic ulcer, gastric carcinoma), of the duodenum (peptic ulcer), of the remaining intestine (e.g., appendicitis, diverticulitis, Meckel diverticulum, inflammatory bowel disease (IBD), intestinal infarction, intestinal strangulation, colorectal carcinoma, meconium peritonitis), or of the gallbladder (cholecystitis). Other possible reasons for perforation include abdominal trauma, ingestion of a sharp foreign body (such as a fish bone, toothpick or glass shard), perforation by an endoscope or catheter, and anastomotic leakage.
Carnitine palmitoyltransferase I deficiency is a rare metabolic disorder that prevents the body from converting certain fats called long-chain fatty acids into energy, particularly during periods without food. It is caused by a mutation in CPT1A on chromosome 11.Carnitine, a natural substance acquired mostly through the diet, is used by cells to process fats and produce energy. People with this disorder have a faulty enzyme, carnitine palmitoyltransferase I, that prevents these long-chain fatty acids from being transported into the mitochondria to be broken down. Symptoms and signs
Signs and symptoms of this disorder include low levels of ketones (hypoketosis) and low blood sugar (hypoglycemia). Together these signs are called hypoketotic hypoglycemia. People with this disorder typically also have an enlarged liver (hepatomegaly), muscle weakness, and elevated levels of carnitine in the blood. Genetics
Mutations in the CPT1A gene cause carnitine palmitoyltransferase I deficiency by producing a defective version of an enzyme called carnitine palmitoyltransferase I. Without this enzyme, long-chain fatty acids from food and fats stored in the body cannot be transported into mitochondria to be broken down and processed. As a result, excessive levels of long-chain fatty acids may more rapidly build up in tissues, damaging the liver, heart and/or brain. This condition has an autosomal recessive inheritance pattern, which means the defective gene must be inherited from both parents.