Acute hypocalcemia

Tetany is the hallmark sign of acute hypocalcemia, which manifests as paresthesias around the mouth and in the extremities muscle spasms and cramps carpopedal spasms and, rarely, laryngospasm and bronchospasm. 

After acute hypocalcemia is corrected, the underlying cause and other electrolyte problems should be corrected. 

Hypocalcemia may manifest as neuromuscular, CNS, dermatologic, and cardiac sequelae. Acute hypocalcemia is more likely to manifest as neuromuscular (paresthesias, muscle cramps, tetany, and laryngeal spasm) and cardiovascular symptoms, whereas chronic hypocalcemia often presents as CNS (depression, anxiety, memory loss, confusion, hallucinations, and tonic-clonic seizures) and dermatologic symptoms (hair loss, grooved and brittle nails, and eczema). The hallmark sign of acute hypocalcemia is tetany caused by enhanced peripheral neuromuscular irritability. Tetany manifests as paresthesias around the mouth and in the extremities, muscle spasms and cramps, carpopedal (hands and feet) spasms, and rarely as... 

Neurologic Chvostek s and/or Trousseau s signs can be elicited during physical examination. The hallmark of acute hypocalcemia is tetany, which is characterized by neuromuscular irritability including seizure potential. Ex-trapyramidal disorders, mainly parkinsonism but also dystonia, hemiballismus, choreoathetosis, and oculogyric crises, occur in 5% to 10% of patients with idiopathic hypoparathyroidism. 

A. Oxalic acid solutions are highly irritating and corrosive. Ingestion and absorption of oxalate cause acute hypocalcemia resulting from precipitation of the insoluble calcium oxalate salt. Calcium oxalate crystals may then deposit in the brain, heart, kidneys, and other sites, causing serious systemic damage. 

C. Group 2b plants contain soluble oxalate salts (sodium or potassium) that can produce acute hypocalcemia, renal injury, and other organ damage secondary to precipitation of calcium oxalate crystals in various organs (see p 295). Mucous membrane irritation is rare, allowing patients to ingest sufficient quantities to cause systemic toxicity. Gastroenteritis may also occur. 

C. Group 2b. Soluble oxalates may be absorbed into the circulation, where they precipitate with calcium. Acute hypocalcemia and multiple-organ injury, including renal tubular necrosis, may result (see Oxalates, p295). 

Acute hypocalcemia and acidosis may precede renal damage damage occurs only after a latent pe, when caldum oxalale precipitates form in die kidney... 

Magnesium ion is essential for normal Ca " and K" metaboHsm. In acute experimental magnesium deficiency in humans, hypocalcemia occurs despite adequate calcium intake and absorption and despite normal renal and parathyroid functions. Negative K" balance is also observed. AH biochemical and clinical abnormaHties disappear upon restoration of adequate amounts of magnesium to the diet (64). 

When acute overuse or chronic misuse of saline or stimulant laxatives is suspected, it may be necessary to check for electrolyte disturbances (e.g., hypokalemia, hypernatremia, hyperphosphatemia, or 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... 

For acute symptomatic hypocalcemia, 200 to 300 mg of elemental calcium is administered IV and repeated until symptoms are fully controlled. This is achieved by infusing 1 g of calcium chloride or 2 to 3 grams of calcium at a rate no faster than 30 to 60 mg of elemental calcium per minute. More rapid administration is associated with hypotension, bradycardia, or cardiac asystole. Total calcium concentration is commonly monitored in critically ill patients. Under normal circumstances, about half of calcium is loosely bound to serum proteins while the other half is free. Total calcium concentration measures bound and free calcium. Ionized calcium measures free calcium only. Under usual circumstances, a normal calcium level implies a normal free ionized calcium level. Ionized calcium should be obtained in patients with comorbid conditions that would lead to inconsistency between total calcium and free serum calcium (abnormal albumin, protein, or immunoglobulin concentrations). For chronic asymptomatic hypocalcemia, oral calcium supplements are given at doses of 2 to 4 g/day of elemental calcium. Many patients with calcium deficiency have concurrent vitamin D deficiency that must also be corrected in order to restore calcium homeostasis.2,37,38... 

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. 

Suggested Alternatives for Differential Diagnosis Salmonellosis, pasteurellosis, enterotox-emia due to . coli, rabies, pregnancy toxemia, polioencephalomalatia, acute rumen impaction, louping-ill hypocalcemia, hypomagnesemia, and acute lead poisoning. 

Suggested Alternatives for Differential Diagnosis Sheep Scrapie, pregnancy toxemia, hypocalcemia, tetanus, listeriosis, tick pyemia, hypocuprosis, rabies, hydatid disease, and various plant poisons. Cattle Malignant catarrhal fever, listeriosis, pseudorabies, bovine spongiform encephalopathy, rabies, hypomagnesemia, hypocalcemia, acute lead poisoning, and certain plant poisons. 

Acute, symptomatic hypocalcemia requires IV administration of soluble calcium salts (Fig. 78-3). 

Workers exposed to an airborne fluoride concentration of 5mg/m complained of eye and respiratory tract irritation and nausea. The lethal oral dose of sodium fluoride for humans has been estimated to be 32-65 mg F/kg of body weight. Effects from ingestion are diffuse abdominal pain, diarrhea, and vomiting excessive salivation, thirst, and perspiration painful spasms of the limbs and sometimes albuminuria." Gastrointestinal effects produced after the acute ingestion of toxic amounts of fluoride likely arise from the corrosive action of hydrofluoric acid, which is produced within the acidic environment of the stomach. Cardiac arrest after accidental exposure to high levels of fluoride has been attributed to the development of hypocalcemia and/or hyperkalemia. ... 

Hypomagnesemia - Magnesium sulfate is used as replacement therapy in magnesium deficiency especially in acute hypomagnesemia accompanied by signs of tetany similar to those observed in hypocalcemia. In such cases, the serum magnesium (Mg++) level is usually below the lower limit of normal (1.5 to 2.5 or 3 mEq/L) and the serum calcium (Ca++) level is normal (4.3 to 5.3 mEq/L) or elevated. 

Severe - Leukopenia (less than 1000/mm ) 2.8% hypoglycemia (less than 25 mg/dL) 2.4% thrombocytopenia (less than 20,000/mm ) 1.7% hypotension (less than 60 mm Hg systolic) 0.9% acute renal failure (serum creatinine greater than 6 mg/dL) 0.5% hypocalcemia (0.2%) Stevens-Johnson syndrome and ventricular tachycardia (0.2%) fatalities caused by severe hypotension, hypoglycemia, and cardiac arrhythmias. 

The antiseizure drugs described in this chapter are also used in patients with febrile seizures or with seizures occurring as part of an acute illness such as meningitis. The term "epilepsy" is not usually applied to such patients unless chronic seizures develop later. Seizures are occasionally caused by an acute underlying toxic or metabolic disorder, in which case appropriate therapy should be directed toward the specific abnormality, eg, hypocalcemia. In most cases of epilepsy, however, the choice of medication depends on the empiric seizure classification. 

Giving intravenous phosphate is probably the fastest and surest way to reduce serum calcium, but it is a hazardous procedure if not done properly. Intravenous phosphate should be used only after other methods of treatment (bisphosphonates, calcitonin, and saline diuresis) have failed to control symptomatic hypercalcemia. Phosphate must be given slowly (50 mmol or 1.5 g elemental phosphorus over 6-8 hours) and the patient switched to oral phosphate (1-2 g/d elemental phosphorus, as one of the salts indicated below) as soon as symptoms of hypercalcemia have cleared. The risks of intravenous phosphate therapy include sudden hypocalcemia, ectopic calcification, acute renal failure, and... 

Sodium phosphate is available as a nonprescription liquid formulation and by prescription as a tablet formulation. When taking these agents, it is very important that patients maintain adequate hydration by taking increased oral liquids to compensate for fecal fluid loss. Sodium phosphate frequently causes hyperphosphatemia, hypocalcemia, hypernatremia, and hypokalemia. Although these electrolyte abnormalities are clinically insignificant in most patients, they may lead to cardiac arrhythmias or acute renal failure due to tubular deposition of calcium phosphate (nephrocalcinosis). Sodium phosphate preparations should not be used in patients who are frail or elderly, have renal insufficiency, have significant cardiac disease, or are unable to maintain adequate hydration during bowel preparation. 

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