Pancreatitis, acute hypocalcemia

Causes of hypocalcemia include hypoparathyroidism, hypomagnesemia, alcoholism, hyperphosphatemia, blood product infusion (due to chelation by the citrate buffers), chronic renal failure, vitamin D deficiency, acute pancreatitis, alkalosis, and hypoalbuminemia. Medications that cause hypocalcemia include phosphate replacement products, loop diuretics, phenytoin (Dilantin, available as generic), pheno-barbital (available as generic), corticosteroids, aminoglycoside antibiotics, and acetazolamide (available as generic).34,39,42... 

Pancreatic toxicity is common. Hypoglycemia due to inappropriate insulin release often appears 5-7 days after onset of treatment, can persist for days to several weeks, and may be followed by hyperglycemia. Reversible renal insufficiency is also common. Other adverse effects include rash, metallic taste, fever, gastrointestinal symptoms, abnormal liver function tests, acute pancreatitis, hypocalcemia, thrombocytopenia, hallucinations, and cardiac arrhythmias. Inhaled pentamidine is generally well-tolerated but may cause cough, dyspnea, and bronchospasm. 

Acute symptomatic hypocalcemia may be seen in hospitalized patients for various reasons. Rapid remineralization of bone after surgery for primary hyperparathyroidism (hungry bone syndrome), treatment for hyperthyroidism, or treatment for hematological malignancy may result in hypocalcemia. Acute hemorrhagic or edematous pancreatitis is frequently complicated by hypocalcemia. Vitamin D deficiency may also be associated with hypocalcemia because of impaired intestinal absorption of calcium and skeletal resistance to PTH. Osteomalacia and rickets are discussed in a later section of this chapter. 

Hypotension hypoglycemia often followed by diabetes melhtus vomiting blood dyscrasias renal damage pain at injection site GI disturbances may aggravate diabetes shock hypocalcemia liver damage cardiotoxicity delirium rash Herxheimer-type reaction anaphylaxis acute pancreatitis hyperkalemia Permethrin... 

Key findings that have been reported include significant hypoxia, acidosis, and carbon dioxide retention (Sofer et al., 1989). Also, hyperglycemia, hypokalemia, and leukocytosis were observed in a case series of OP exposures (Levy-Khademi et al., 2007). A study done on 17 children with typical OP or carbamate poisoning looked at laboratory abnormalities that are associated with acute pancreatitis. Five of the patients (30%) had laboratory values consistent with pancreatitis with elevated immunoreac-tive trypsin, amylase, and serum glucose. None of the patients had hypocalcemia, renal dysfunction, or acidosis, and all experienced complete recovery of pancreatic function. The authors concluded that acute pancreatihs, due to anticholinesterase (anti-AChE) intoxication, is not xmcommon in the pediatric population (Weizman and Sofer, 1992). Pancreatitis has been described in adult exposures, and the association has been investigated in animal studies (Weizman and Sofer, 1992). 

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