Death from cerebral hypoperfusion during nitroprusside treatment of acute angiotensin-dependent hypertension.

A 37-year-old woman, while being treated with nitroprusside for acute hypertension due to an intramural renal artery hemorrhage, became blind on the fourth hospital day, comatose on the fifth, and brain dead on the seventh. Postmortem examination of her brain revealed border-zone infarcts in the parietal-occipital regions and cerebrellum of the sort associated with cerebral hypoperfusion due to hypotension. Yet her blood pressure had been lowered judiciously to a mean pressure in the vicinity of 110 to 120 mm Hg, and episodes of hypotension had been avoided. As possible explanations for this unusual complication, the roles of acute hyperangiotensinemia and nitroprusside administration are discussed.

Use of sodium nitroprusside in post-coronary bypass surgery. A plea for conservatism.

In 292 patients who underwent coronary artery bypass graft (CABG) surgery, seven patients developed sodium nitroprusside (SNP) toxicity in the postoperative period. Duration of infusion varied between 26 to 160 hrs and total SNP dose ranged from 1.8 to 12 mg/kg body weight. All patients were critically ill and required ventilatory support in the postoperative period. Tachyphylaxis to SNP requiring increase of SNP dose for control of hypertension, and loss of consciousness were the major signs of toxicity. Other commonly described signs of SNP toxicity were absent in those patients. Discontinuation of SNP therapy and treatment with sodium thiosulfate was followed by improvement in four patients. Three patients who failed to regain consciousness later died because of hemodynamic, pulmonary and/or renal complications. Our observation suggests that recommended doses of SNP may be toxic in unstable post-CABG patients. We recommend that the dose and duration of SNP infusion be minimized in critically ill patients.

Variable hemodynamic response to sodium nitroprusside in hypertensive crisis.

Five patients, three males and two females, admitted with severe hypertensive crisis underwent hemodynamic investigations before and during vasodilator therapy with sodium nitroprusside. In three hypervolemic patients with congestive heart failure and/or renal insufficiency, the drug induced a rapid fall in systemic arterial pressure and a beneficial effect on cardiac performance, as shown by a shift of the ventricular function curves to the left. In two hypovolemic patients, the hemodynamic response was quite different; vasodilator therapy induced a confusing clinical picture characterized by significant fluctuations in blood pressure, a severe fall in cardiac output and clinical signs of shock in spite of normal blood pressure. Hemodynamic response to vasodilator therapy with sodium nitroprusside in hypertensive crisis appears to be directly related to the circulating blood volume. The syndrome of hypertension associated with hypovolemia needs to be recognized promptly in order to avoid inappropriate therapy; in such cases volume expansion under precise hemodynamic monitoring appears to be an effective means of stabilizing the cardiocirculatory conditions.

Transient leucopenia and thrombocytopenia associated with sodium nitroprusside infusion.

The case history of a 42 year old male on CAPD who was receiving sodium nitroprusside (SNP) for hypertensive encephalopathy is described. Leucopenia and thrombocytopenia developed but were resolved by hydroxocobalamin infusion during administration.

Delayed postoperative neurological deterioration from prolonged sodium nitroprusside administration. Case report.

Sodium nitroprusside is commonly used for the induction of hypotension during neurosurgical procedures. Its toxicity stems from hemodynamic compromise as well as from its metabolites, especially the formation of cyanide. A patient is described who underwent craniotomy for hypertensive intracerebral hemorrhage. He gradually recovered following the operation, but needed continued administration of sodium nitroprusside for control of hypertension. On the 7th postoperative day, he deteriorated into coma with evidence of severe edema and herniation on the computerized tomography scan. Cessation of sodium nitroprusside and treatment for cyanide poisoning resulted in resolution of his symptoms within hours. The potential toxicity of sodium nitroprusside, measures to prevent toxicity, and therapeutic steps are discussed.

Adverse effect of sodium nitroprusside 48 hours after myocardial infarction.

We present a patient with acute myocardial infarction in whom the use of nitroprusside 48 hours after the first symptom, was accompanied by a rise in the ST segment representative of the ischemic area. Our experience suggests that precaution is needed in the use of nitroprusside even several days after an acute myocardial infarction.

Cyanide encephalopathy following therapy with sodium nitroprusside: report of a case.

Bilateral necrosis of the globus pallidus was observed in a 43-year-old man who had received treatment for malignant hypertension with sodium nitroprusside. Cyanide released from sodium nitroprusside may have caused the pallidal lesions in the presence of deranged liver function and episodes of hypoxia.

[Microcirculation in the brain during controlled arterial hypotension. Experimental study of the effect of nipruton]. / Mikrotsirkuliatsiia v golovnom mozge pri upravliaemoi arterial'noi gipotonii. Eksperimental'noe issledovanie vozdeistviia niprutona.

The effect of nipruton (sodium nitroprusside)-induced controlled arterial hypotension on the intracerebral microcirculatory channel was studied on 4 rabbits with transplanted induced tumors (anaplastic astrocytomas) and 7 intact rabbits under general anesthesia. It was found that nipruton injected in doses necessary for marked reduction of arterial pressure (35-45 mm Hg) for a sufficient duration (30-55 minutes) causes no circulatory disorders in the brain. In animals with tachyphylaxis to nitropruton, in which the amount of the injected agent must be increased to 9-10 mg/kg, controlled arterial hypotension even of lesser depth (60-65 mm Hg) and lesser duration (20-25 minutes) can lead to partial obstruction of the intracerebral microcirculatory channel. i. e. to the no-reflow phenomenon.

Nitroprusside-induced cyanide poisoning: antidotal effect of hydroxocobalamin.

Sodium nitroprusside was investigated as a potential source of cyanide poisoning, Whole-blood cyanide determinations were performed on arterial samples from baboons receiving nitroprusside while anesthetized. There was a statistically significant increase in cyanide levels, as well as development of tachyphylaxis and severe metabolic acidosis. Hydroxocobalamin (vitamin B12a) infused simultaneously with nitroprusside significantly lessened the increase in cyanide levels and eliminated the development of metabolic acidosis. Nitroprusside can cause cyanide intoxication in the baboon, and hydroxocobalamin appears to be an effective antidote.

Cerebrospinal fluid cyanide after nitroprusside infusion in man.

Sodium nitroprusside (SNP) is frequently used as an hypotensive agent for clipping of intracranial aneurysms, repair of arteriovenous malformations and resection of vascular tumours. Cyanide (CN), which is its main metabolic product, has been recovered from the cerebrospinal fluid (CSF) of the rat after intravenous administration of CN, but recovery of CN from CSF after SNP has not been reported in man. Seven consenting adults were studied. Adequate premedication was provided with pentobarbitone 2 mg x kg-1 and atropine 0.4 mg one hour before operation. Anaesthesia was induced with thiopentone 8 mg x kg-1 and maintained with nitrous oxide 60 per cent with oxygen and supplemental fentanyl 0.05 mg and pancuronium 0.5-1 mg as needed. Lumbar subarachnoid, radial artery, central venous, and Foley urinary catheters were inserted. Arterial carbon dioxide tension (PaCO2) was maintained between 4.6-5.32 kPa (35-40 torr) with an Air Shields ventilator. Red cell, plasma and CSF cyanide were measured using a digital ionanalyzer before and at 30 minutes interval after infusing SNP at a rate sufficient to maintain the blood pressure at two thirds of the pre-operative level. Average total dose of SNP was 0.51 mg x kg-1. CN concentration in the red blood cells increased from 9.5 +/- 2.05 to 75.12 +/- 17.12. Plasma CN increased from 0.54 +/- 0.05 to 1.09 +/- 0.14 micrograms per cent. CSF CN increased from 0.11 +/- 0.04 to 0.72 +/- 0.07 micrograms per cent. Significant increase in red cell, plasma and CSF CN occurred five minutes after the start of SNP and returned to the preoperative level 19 hours later. Conclusion CN crosses the blood-brain barrier. Large doses of SNP in patients with neurovascular brain disorders warrants caution because cytotoxic cerebral oedema and CN encephalopathy have been described in rats after intravenous injection of sodium cyanide or exposure to hydrogen cyanide.

Suspected sodium nitroprusside-induced cyanide intoxication.

Sodium nitroprusside-induced cyanide intoxication has been demonstrated in the laboratory animal and has been experienced clinically during induced hypotensive anesthesia. This is a care report of a successful resuscitation of a severe cardiovascular collapse secondary to suspected sodium nitroprusside-induced cyanide intoxication.