Page 10 - Acute Pancreatitis (Viêm tụy cấp)

CHAPTER 58 Acute Pancreatitis 901

systematic review of 31 studies comprising 1340 patients with for developing severe disease, such as obesity and underlying
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hypertriglyceridemic AP reported that this condition accounts comorbidities. 58
for 9% of all cases of AP, and that 14% of patients with signifi-
cant hypertriglyceridemia will develop AP. Hypertriglyceridemia Hypercalcemia
is also implicated in more than half of cases of gestational pan-
creatitis. Serum TG concentrations above 1000 mg/dL (11 Hypercalcemia of any cause is rarely associated with AP. Proposed
mmol/L) may precipitate attacks of AP. However, more recent mechanisms include deposition of calcium salts in the PD lumen
studies suggest that the serum TGs may have to be even higher and calcium activation of trypsinogen to trypsin within the
to precipitate AP, perhaps above 2000 mg/dL, and with obvious pancreatic parenchyma. 119 The low incidence of AP in chronic
lactescent (milky) serum due to increased concentrations of chy- hypercalcemia suggests that mechanisms other than the serum
lomicrons. 110 calcium level per se responsible for pancreatitis (e.g., acute eleva-
The pathogenesis of hypertriglyceridemic pancreatitis is tions of serum calcium). Acute calcium infusion into rats leads
unclear, but the local release of free fatty acids by pancreatic to conversion of trypsinogen to trypsin, hyperamylasemia, and
lipase may damage pancreatic acinar cells or endothelial cells. dose-dependent morphologic changes of AP.
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Release of free fatty acids that induce free radical damage can Primary hyperparathyroidism causes less than 0.5% of all cases
directly injure cell membranes. 92 of AP, and the incidence of AP in patients with hyperparathyroid-
Most adults with hyperchylomicronemia have a mild form ism varies from 0.4% to 1.5% (Chapter 37). 120 Interestingly, in a
of genetically inherited type I or type V hyperlipoprotein- community-based study there was no increased occurrence of AP
emia and an additional acquired condition known to raise in patients with hyperparathyroidism and there was no cause and
serum lipids (e.g., alcohol abuse, obesity, diabetes mellitus, effect association. 121 Rarely, pancreatitis occurs with other causes
hypothyroidism, Cushing syndrome, pregnancy, nephrotic of hypercalcemia, including metastatic bone disease, TPN, sar-
syndrome, and drug therapy [estrogen 111 or tamoxifen, gluco- coidosis, vitamin D toxicity, and infusion of calcium in high doses
corticoids, thiazides, or beta adrenergic blockers]). Typically, during cardiopulmonary bypass.
3 types of patients develop hypertriglyceridemia-induced
pancreatitis. The first is a poorly controlled diabetic patient Infections
with a history of hypertriglyceridemia. The second is an alco-
holic patient with hypertriglyceridemia detected on hospital Although many infectious agents have been proposed as caus-
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admission. The third (15% to 20%) is a nondiabetic, non- ing AP, these published reports often do not clearly establish
alcoholic, nonobese person who has drug- or diet-induced a causal relationship. The diagnosis of AP caused by an infection
hypertriglyceridemia. Drug-induced disease is more likely to requires evidence of AP, evidence of an active infection, and the
occur if there is a background of hypertriglyceridemia prior absence of a more likely cause of AP. AP has been associated with
to drug exposure. viruses (mumps, coxsackievirus, hepatitis A, B, and C, and several
Most persons who abuse alcohol have moderate but transient herpesviruses, including cytomegalovirus, varicella-zoster, herpes
elevations of the serum TG level. This condition is likely an epi- simplex, and EBV); the vaccine that contains attenuated measles,
phenomenon and not the cause of their pancreatitis, 112 because mumps, and rubella viruses; bacteria (Mycoplasma, Legionella,
alcohol itself not only damages the pancreas (see earlier) but Leptospira, Salmonella, TB, and brucellosis); fungi (Aspergillus,
also increases serum TG concentrations in a dose-dependent Candida); and parasites (Toxoplasma, Cryptosporidia, Ascaris lum-
manner. Alcoholic patients with severe hypertriglyceridemia bricoides, Clonorchis sinensis). C. sinensis and A. lumbricoides cause
often have a coexisting primary genetic disorder of lipoprotein pancreatitis by blocking the main PD. In patients with AIDS (see
metabolism. Chapter 35), infectious agents causing AP include cytomegalo-
Whether hyperlipidemic AP results in more severe disease virus, Candida species, Cryptococcus neoformans, Toxoplasma gondii,
compared with the other causes of AP is not clear. 113 On the other and possibly Mycobacterium avium complex.
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hand, a meta-analysis of 15 studies (1564 patients) found a worse
prognosis compared with non-hypertriglyceridemia causes. 114 Vascular Disease
The serum amylase and/or lipase level may not be substantially
elevated at presentation in patients with hypertriglyceridemic Rarely, pancreatic ischemia causes AP. In most cases it is mild,
pancreatitis (see later). but fatal necrotizing pancreatitis may occur. Ischemia may result
from vasculitis (e.g., SLE, 122 polyarteritis nodosa), 123 athero-
Diabetes Mellitus matous embolization of cholesterol plaques after transabdomi-
nal aortography, 124 intraoperative hypotension, 125 hemorrhagic
Diabetics are at an increased risk for developing AP (see shock, 127 ergotamine overdose, and transcatheter arterial cath-
Chapter 37). 108 The risk may be due to the increased prevalence eter embolization for hepatocellular carcinoma. Also, ischemia
of gallstones and hypertriglyceridemia in this population. In a is 1 possible explanation for pancreatitis after cardiopulmonary
large study of type 2 diabetic patients (LEADER, Liraglutide bypass. In pigs, cardiogenic shock induced by pericardial tam-
Effect and Action in Diabetes: Evaluation of Cardiovascular ponade causes vasospasm and selective pancreatic ischemia due
Outcome Results), nearly 25% had elevated serum lipase or to activation of the renin-angiotensin system. 127 AP has occurred
amylase levels without symptoms of AP. The clinician must in long-distance runners, which may be on an ischemic basis. 128
take these data into account when evaluating abdominal symp-
toms in type 2 diabetic patients. 115 Patients with diabetes tend Trauma
to develop gallstones due to a combination of concurrent dys-
lipidemia, leading to cholesterol-supersaturated bile resulting Either penetrating trauma (gunshot or stab wounds) or blunt
in precipitation of cholesterol crystals (see Chapter 65). Also, trauma can damage the pancreas. 129 Blunt trauma results from
patients with long-standing diabetes often develop bile stasis compression of the pancreas by the spine, such as in an automo-
in the gallbladder, leading to the precipitation of cholesterol bile accident with compression by the steering wheel. In blunt
crystals and to gallstones. Epidemiologic studies have confirmed trauma, it is important to determine preoperatively whether there
the increased risk of AP in the diabetic population. 116-118 The is injury to the pancreas because, depending on the severity of
diabetic population is also at greater risk for developing severe pancreatic injury, it will be necessary to include the pancreas in
AP because they often have many of the known risk factors the surgical plan. Secondly, even in the absence of serious injury