Hypotension phosphates

The adverse reactions associated witii die administration of chloroquine (Aralen HC1 and phosphate) and hydroxychloroquine include hypotension, electrocardiographic changes, visual disturbances, headache, nausea, vomiting, anorexia, diarrhea, and abdominal cramps. 

Shackney S, Hasson J. Precipitious fall in serum calcium hypotension and acute renal failure after IY phosphate treatment of hypercalcemia. Arch Intern Med 1968 122 150. 

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 (pamidronate, calcitonin, saline diuresis with furosemide, and plicamycin) 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 hypotension. Oral phosphate can also lead to ectopic calcification and renal failure if serum calcium and phosphate levels are not carefully monitored, but the risk is less and the time of onset much longer. Phosphate is available in oral and intravenous forms as the sodium or potassium salt. Amounts required to provide 1 g of elemental phosphorus are as follows ... 

Shackney S, Hasson J. Preciptious Fall In Serum Calcium, Hypotension, and Acute Renal Failure After Intravenous Phosphate Therapy for Hypercalcemia. Ann of Intern Med 1967 5 906-16. 

Finally, intravenous phosphate may rapidly reduce ionized calcium concentrations through the formation of insoluble calcium-phosphate salts. However, intravenous phosphate is extremely hazardous because extraskeletal precipitation of calcium-phosphate may result in metastatic calcification, hypotension, acute renal failure, or death. Therefore intravenous phosphates should be reserved for the extraordinary patient with severe hypercalcemia and concomitant hypophosphatemia. Oral phosphorus is not used chronically for the treatment of hypercalcemia because calcium-phosphate crystals may precipitate in the kidneys or other major organs when the calcium-phosphorus product is > 50 to 60 mg /dL . Serum calcium, phosphorus, and creatinine should be monitored closely. Oral phosphorus treatment is only indicated when there is concomitant hypophosphatemia (<2 mg/dL). 

Myelosuppression mucositis worse with continuous infusion moderately emetogenic may cause acute and delayed (by 24 8 hours) emesis vesicant severe extravasation injury cardiotoxicity (similar to other anthracyclines) may be less cardiotoxic than doxorubicin controversy about equ ivalent doses cardiac toxicity associated with cumulative doses >900 mg/m Myelosuppression moderately emetogenic may be worse with oral and high-dose regimens alopecia mucositis hypotension infusion rate-related etoposide phosphate can be given IV push without hypotension risk hypersensitivity reactions especially common in children... 

Extremely toxic phosphate ester however, snsceptible to hydrolyze in acid or alkali cholinesterase inhibitor toxic properties are similar to those of dicrotophos, symptoms inclnde headache, dizziness, pinpoint pnpils, blnrred vision, weakness, mnscle spasms, vomiting, diarrhea, abdominal cramp, shortness of breath, and hypotension high expo-snre may canse seizure, coma, and respiratory paralysis. 

Williams JV, Colbert SD, Revington PJ. Sudden hypotensive syncope and significant iatrogenic maxillofacial trauma following administration of oral sodium phosphate purgative solution. J Perioper Pract 2010 20 181-2. 

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