A1,
A2,
B,
C1,
C2,
D,
E,
F,
G-H,
I-K,
L,
M,
N,
O,
P1,
P2,
Q-R,
S,
T,
U-V,
W-Z
Nitropress Side Effects, and Drug Interactions - Nitroprusside Sodium
Nitropress Side Effects, and Drug Interactions - Nitroprusside Sodium
SIDE EFFECTS
The most important adverse reactions to sodium nitroprusside are the
avoidable ones of excessive hypotension and cyanide toxicity, described
under WARNINGS. The adverse
reactions described in this section develop less rapidly and, as it happens,
less commonly.
Methemoglobinemia
As described in CLINICAL PHARMACOLOGY,
sodium nitroprusside infusions can cause sequestration of hemoglobin as
methemoglobin. The back-conversion process is normally rapid, and clinically
significant methemoglobinemia (>10%) is seen only rarely in patients receiving
NITROPRESS. Even patients congenitally incapable of back-converting methemoglobin
should demonstrate 10% methemoglobinemia only after they have received
about 10 mg/kg of sodium nitroprusside, and a patient receiving sodium
nitroprusside at the maximum recommended rate (10 µg/kg/min) would take
over 16 hours to reach this total accumulated dose.
Methemoglobin levels can be measured by most clinical laboratories. The
diagnosis should be suspected in patients who have received >10 mg/kg
of sodium nitroprusside and who exhibit signs of impaired oxygen delivery
despite adequate cardiac output and adequate arterial pO2.
Classically, methemoglobinemic blood is described as chocolate brown,
without color change on exposure to air.
When methemoglobinemia is diagnosed, the treatment of choice is 1-2 mg/kg
of methylene blue, administered intravenously over several minutes. In
patients likely to have substantial amounts of cyanide bound to methemoglobin
as cyanmethemoglobin, treatment of methemoglobinemia with methylene blue
must be undertaken with extreme caution.
Thiocyanate Toxicity
As described in CLINICAL PHARMACOLOGY,
most of the cyanide produced during metabolism of sodium nitroprusside
is eliminated in the form of thiocyanate. When cyanide elimination is
accelerated by the co-infusion of thiosulfate, thiocyanate production
is increased.
Thiocyanate is mildly neurotoxic (tinnitus, miosis, hyperreflexia) at
serum levels of 1 mmol/L (60 mg/L). Thiocyanate toxicity is life-threatening
when levels are 3 or 4 times higher (200 mg/L).
The steady-state thiocyanate level after prolonged infusions of sodium
nitroprusside is increased with increased infusion rate, and the half-time
of accumulation is 3-4 days. To keep the steady-state thiocyanate level
below 1 mmol/L, a prolonged infusion of sodium nitroprusside should not
be more rapid than 3 µg/kg/min; in anuric patients, the corresponding
limit is just 1 µg/kg/min. When prolonged infusions are more rapid than
these, thiocyanate levels should be measured daily.
Physiologic maneuvers (e.g., those that alter the pH of the urine) are
not known to increase the elimination of thiocyanate. Thiocyanate clearance
rates during dialysis, on the other hand, can approach the blood wflow
rate of the dialyzer.
Thiocyanate interferes with iodine uptake by the thyroid. Abdominal pain,
apprehension, diaphoresis, “dizziness,” headache, muscle twitching, nausea,
palpitations, restlessness, retching, and retrosternal discomfort have
been noted when the blood pressure was too rapidly reduced. These symptoms
quickly disappeared when the infusion was slowed or discontinued, and
they did not reappear with a continued (or resumed) slower infusion.
Other adverse reactions reported are:
Cardiovascular: Bradycardia, electrocardiographic changes, tachycardia.
Dermatologic: Rash.
Endocrine: Hypothyroidism.
Gastrointestinal: Ileus.
Hematologic: Decreased platelet aggregation.
Neurologic: Increased intracranial pressure.
Miscellaneous: Flushing, venous streaking, irritation at
the infusion site.
DRUG INTERACTIONS
The hypotensive effect of sodium nitroprusside is augmented by that of
most other hypotensive drugs, including ganglionic blocking agents, negative
inotropic agents, and inhaled anesthetics.
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