Sodium Nitroprusside
Sodium
nitroprusside (sodium nitroferricyanide) exerts its vasodilatory effects after
being metabolised in the RBC, and releasing nitric oxide. It also releases five
atoms of cyanide which can cause significant toxicity in the presence of renal
insufficiency or low thiosulfate stores (infants, malnourished individuals,
critically ill patients).
Sodium
nitroprusside* is used intravenously mainly for the treatment of hypertensive
emergencies, and also to induce controlled hypotension during anaesthesia in
order to reduce bleeding in surgical procedures. It is also used to control
acute congestive heart failure (CHF). Sodium nitroprusside reacts with
haemoglobin and is then nonenzymatically decomposed to cyanide in the blood.
Following IV administration, nitro-prusside is rapidly metabolised to cyanogen
(cyanide radical). Like cyanide, it inhibits electron transport in
mitochondrial cytochrome oxidase, thus inhibiting cellular respiration. The
mitochondrial enzyme, rhodanase, located primarily in the liver, converts
cyanide to thiocyanate, which is then cleared renally.
Acute
onset of anxiety, restlessness, muscle twitching, and diaphoresis has been
observed following excessive nitroprus-side infusion rates. Toxic accumulation
of cyanide with severe lactic acidosis can also occur if sodium nitroprusside
is infused at a rate greater than 5 mcg/kg/min. This can be prevented by
concomitant administration of sodium thiosulfate. The overall incidence of
cyanide toxicity associated with nitroprusside appears to be infrequent. Risk
factors for development of nitroprusside-induced cyanide toxicity include
hypoalbumi-naemia, cardiopulmonary bypass procedures, renal impairment, or the
administration of moderate to high doses of nitroprusside.
·
Blood cyanide concentrations may be
the most useful parameter to monitor nitroprusside toxicity, especially for
those infusions less than 7 days in duration, at normal rates. Thiocyanate
levels may be appropriate to monitor during prolonged nitroprusside use or at unusually
high infusion rates. Generally, blood cyanide and serum thiocy-anate
concentrations are toxic if they are greater than 500 mcg/L and greater than
100 mg/L, respectively; however, patients do not consistently display signs or
symptoms at these levels.
·
Acute toxicity following therapeutic
use is characterised by vasodilation and hypotension, possibly complicated by
nausea, vomiting, sweating, headache, palpitations, and substernal distress.
·
Development of severe acidosis has
been reported with increasing blood cyanide levels.
·
Thiocyanate may cause a neurotoxic
syndrome manifested by toxic psychosis, hyperreflexia, confusion, weakness,
tinnitus, seizures and coma.
· Administer 100% oxygen to maintain
an elevated PO2. Oxygen may reverse the cyanide-cytochrome oxidase
complex and facilitate the conversion to thiocyanate following thiosulfate
administration.
· Patients exhibiting dyspnoea,
headache, and impaired mental status should be treated with sodium nitrite and
sodium thiosulfate.
· Hypotension secondary to excessive
infusion rates of nitro-prusside typically responds to discontinuation of
infusion (within minutes). Fluid replacement and pressors may be necessary if
hypotension persists.
· Administer sodium bicarbonate, 1
mEq/kg IV to acidotic patients. Base further sodium bicarbonate administration
on serial arterial blood gas determinations.
·
Haemodialysis may be an effective adjunct by correcting
resistant acidaemia, and by increasing thiocyanate clear-ance, thereby
favouring thiosulfate-cyanide reaction to thiocyanate.
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