Other Systemic Complications Associated with Acute Pancreatitis
Hypocalcemia
Serum calcium comprises ionized (free) calcium and nonionized calcium bound to albumin. Hypocalcemia with normal free calcium due to a decrease in plasma albumin is frequent in moderate‐to‐severe disease, given the catabolic distress of such a disease and the binding of calcium to necrotic adipose tissue [44]. This “false” hypocalcemia should not be treated but it is a classic marker of severe disease [45]. In the case of hypocalcemia, therefore, calcium should be corrected by albumin or proteins or ionized calcium should be measured. In the case of low free calcium levels, plasma magnesium should be measured to rule out hypomagnesemia as the cause of hypocalcemia. Hypocalcemia has been defined as an ionized calcium below 1.12 mmol/l and severe hypocalcemia as an ionized calcium below 0.8 mmol/l (3 mg/dl) [46]. Hypocalcemia may result in neuromuscular irritability, spasms, paresthesia, numbness, hyperreflexia, seizures, hallucinations, bradycardia, and hypotension [46]. The classic Trousseau (carpopedal spasm) and Chvostek (facial muscle hyperreflexia) signs and QT prolongation are typical of hypocalcemia. Patients with symptoms, a prolonged QT interval, or severe hypocalcemia should be treated.
Disseminated Intravascular Coagulation
Disseminated intravascular coagulation (DIC) is the consequence of systemic activation of coagulation pathways resulting in the generation of fibrin clots that may cause organ failure with consumption of platelets and coagulation factors, predisposing to bleeding [47].The treatment of DIC involves the management of AP, and transfusion of platelets or plasma in the case of bleeding [48]. Patients with AP and DIC at admission have increased mortality (16% according to retrospective data) [49].
Gastrointestinal Bleeding
Severe AP predisposes to upper gastrointestinal bleeding, as seen in other critical illnesses. According to a retrospective study, severe AP is associated with an 18% incidence of upper gastrointestinal bleeding, mostly due to acute gastric mucosal lesions and peptic ulcers [50]. Mortality was higher when this complication was present (44 vs. 11%). A population‐based study concluded that, in the presence of organ failure, gastrointestinal bleeding increases the risk of death only slightly [51]. Proton pump inhibitors or histamine H2 receptor antagonists have been recommended in guidelines that address other acute critical illnesses like sepsis, to prevent gastrointestinal bleeding [52].
Pancreatic Encephalopathy and Posterior Reversible Encephalopathy Syndrome
Pancreatic encephalopathy comprises a wide spectrum of neuropsychiatric symptoms found mainly in severe AP that include disorientation, restlessness, delusions, unconsciousness or slowed reaction, apathy, and depression [53]. Pathogenesis is multifactorial [53], but in patients with chronic alcoholism, vitamin B1 deficit leading to Wernicke encephalopathy must be excluded. Pancreatic encephalopathy has no specific treatment. Posterior reversible encephalopathy syndrome is characterized by symptoms such as headache, altered mental status, visual changes, seizures, and occasionally other focal neurological signs, associated with typical radiological findings that include symmetrical white matter edema in the posterior cerebral hemispheres, particularly the parieto‐occipital regions, most often visualized on magnetic resonance imaging [54,55]. The treatment is symptomatic and the prognosis is usually good, with complete reversal of symptoms [54].
Abdominal Compartment Syndrome
The pressure in the abdominal cavity (IAP, usually 5–7 mmHg) can be measured via an indwelling urinary catheter (trans‐bladder technique) [56]. AP is associated with several conditions and complications that may raise IAP, such as retroperitoneal collections, paralytic ileus, visceral edema, ascites, and bleeding. A significant increase in IAP may be associated with damage to organs of the abdomen due to ischemia, with restriction to lung expansion and finally to organ failure, so IAP must be monitored in all patients with AP and organ failure. Abdominal compartment syndrome has been defined as a sustained IAP above 20 mmHg that is associated with new organ dysfunction or failure [56].
In the case of abdominal compartment syndrome in a patient with AP, several conservative measures should be attempted to decrease IAP, aiming to improve organ failure. Nasogastric and/or colonic decompression and neuromuscular blockade with mechanical ventilation may be the first steps [57]. If organ failure/dysfunction persists and IAP is still high, percutaneous drainage of collections may be helpful [58]. In case of sustained increased IAP and organ failure, abdominal decompression surgery (e.g. midline laparostomy) can be attempted [57], but there is a lack of randomized controlled studies comparing such an aggressive strategy with a more conservative one.
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