Some amount of pancreatic fat necrosis occurs due to exposure to:

Ans. b (Extremely low temperature). (Ref. Parikh's Textbook of FMT, 6th ed., 3.65, 3.79, 10.3)Temperature ExtremesHypothermic injuryHyperthermic injury# Slows cellular metabolic processes# Heat cramps# Ice crystal formation and frostbite# Heat exhaustion # Heatstroke # Protein denaturationPostmortem findings in adults exposed to hypothermiaEXTERNALLY: The appearance depends on how rapidly the cooling took place and its duration. When it is slow, the gross appearance of the skin resembles myxedema because of the edematous condition of the face and limbs. Particularly striking are bright red erythematous areas rather than the dark postmortem lividity blotches usually noted. Bullae may occur over areas of chronic pressure or contact. When death follows rapid cooling, the lack of cyanosis in the skin in hypostatic areas is the significant external sign.INTERNALLY: Even with rapid cooling, and minimal external signs, internal examination demonstrated conclusive features. In order of frequency, gastrointestinal lesions are noted in about 90% of cases and about 80% in the pancreas. In the gastrointestinal tract, order of frequency of involvement is the stomach, the duodenum, and occasionally the esophagus. Seen early, the lesions consist of many small submucosal hemorrhages (black in color). Later, lesions present as small shallow ulcers. Gross pancreatic changes vary from focal fat necrosis to severe hemorrhage of the pancreas and nearby tissue. Microscopically, there were micro-infarcts in all organs except the liver due to hemoconcentrated packed RBCs in capillaries. Fat is noted in liver, adrenals, and kidney. Some cases show myocardial changes.