Hypocalcemia clinical presentation

B. Specific drugs and antidotes. When clinically significant hypocalcemia is present, administer intravenous calcium gluconate (see p 424), 10-20 mL (children 0.2-0.3 mL/kg), and monitor ionized calcium levels and titrate further doses as needed. Treat hypomagnesemia with intravenous magnesium sulfate, 1-2 g given over 10-15 min (children 25-50 mg/kg diluted to less than 10 mg/mL). Treat hyperkalemia with intravenous calcium and other usual measures (p 37). 

II. Toxic dose. Inhalation or ingestion of as little as 1 mg of fluoroacetate is sufficient to cause serious toxicity. Death is likely after ingestion of mote than 5 mg/kg. Clinical presentation. After a delay of minutes to several hours (in one report coma was delayed 36 hours), manifestations of diffuse cellular poisoning become apparent nausea, vomiting, diarrhea, metabolic acidosis, renal failure, agitation, confusion, seizures, coma, respiratory arrest, pulmonary edema, and ventricular arrhythmias may occur. One case series reported a high incidence of hypocalcemia and hypokalemia. 

Because the severity of symptoms and the absolute serum concentration are poorly correlated in some patients, institution of therapy should be dictated by the clinical scenario. All patients with hypercalcemia should be treated with aggressive rehydration normal saline at 200 to 300 mL/hour is a routine initial fluid prescription. For patients with mild hypocalcemia, hydration alone may provide adequate therapy. The moderate and severe forms of hypercalcemia are more likely to have significant manifestations and require prompt initiation of additional therapy. These patients may present with anorexia, confusion, and/or cardiac manifestations (bradycardia and arrhythmias with ECG changes). Total calcium concentrations greater than 13 mg/dL (3.25 mmol/L) are particularly worrisome, as these levels can unexpectedly precipitate acute renal failure, ventricular arrhythmias, and sudden death. 

In patients with renal failure, the occurrence of conditioned zinc deficiency may be the result of a mixture of factors, which at present are ill defined. If 1,25-dihydroxycholecalciferol plays a role in the intestinal absorption of zinc, an impairment in its formation by the diseased kidney would be expected to result in malabsorption of zinc. It seems likely that plasma and soft tissue concentrations of zinc may be "protected in some individuals with renal failure by the dissolution of bone which occurs as a result of increased parathyroid activity in response to low serum calcium. In experimental animals, calcium deficiency has been shown to cause release of zinc from bone. In some patients who are successfully treated for hyperphosphatemia and hypocalcemia, the plama zinc concentration may be expected to decline because of the deposition of zinc along with calcium in bone. Thus, in the latter group in particular, a diet low in protein and high in refined cereal products and fat would be expected to contribute to a conditioned deficiency of zinc. Such a diet would be low in zinc. The patients reported by Mansouri et al. (37), who were treated with a diet containing 20-30 g of protein daily and who had low plasma concentrations of zinc, appear to represent such a clinical instance. Presumably the patients of Halsted and Smith (38) were similarly restricted in dietary protein. In other patients with renal failure whose dietary protein was not restricted, plasma zinc concentration were not decreased. Patients on dialysis had even higher levels, particularly... 

Clinically, hypocalcemia most commonly presents with neuromuscular hyperexcitability, such as tetany, paresthesia, and seizures. A rapid fall in the serum calcium also may be associated with hypotension and electrocardiographic abnormalities. 

The clinical manifestations of hypocalcemia are quite variable. The acuteness of the development of hypocalcemia plays a large role in whether or not symptoms will occur." The more acute the drop in ionized calcium concentration, the more likely the patient will develop symptoms. Thus acid-base balance plays a significant role in the hkeiihood of the development of hypocalcemic symptoms, with alkalosis predisposing to symptom development. Concomitant hypomagnesemia, hypokalemia, hyponatremia, and additive side effects from prescribed medications also increase the likelihood of symptomatic presentation. 

Celiac disease is the commonest cause of intestinal malabsorption in childhood. The etiology is an intolerance to the gliadin component of gluten. Most patients present early in childhood with failure to thrive, abdominal distension, diarrhea and stools that may be steatorrheic. Adolescents have delayed puberty, anorexia and clinical findings due to hypocalcemia and hypoproteinemia. It is distinctly unusual in people of Asian and African descent. 

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