A 19-year-old woman, gravida 1 para 0, at 34 weeks gestation is admitted to the hospital for preeclampsia with severe features. She has no chronic medical conditions and takes no medications. On admission, temperature is 36.7 C (98.1 F), blood pressure is 170/110 mm Hg, pulse is 80/min, and respirations are 16/min. While administering the magnesium sulfate bolus, the fetal heart rate becomes persistently bradycardic to the 90s. The patient is rushed to the operating room for an emergency cesarean delivery and undergoes general anesthesia. Immediately after intubation, intraoperative temperature is 39.4 C (102.9 F), blood pressure is 180/110 mm Hg, pulse is 130/min, and respiratory rate is 30/min. The patient is markedly rigid and increasingly difficult to ventilate. Which of the following is the most likely cause of this patient's acute decompensation?
Malignant hyperthermia | |
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This patient with preeclampsia with severe features was being managed appropriately (eg, magnesium sulfate) but developed fetal bradycardia requiring emergency cesarean delivery. Her acute decompensation following anesthetic induction is most likely due to malignant hyperthermia (MH), a rare but life-threatening condition likely due to a skeletal muscle receptor anomaly that results in excessive intracellular calcium accumulation upon anesthesia exposure (eg, anesthesia induction).
As a result of the calcium accumulation, patients with MH develop sudden-onset muscle rigidity (ie, prolonged muscle contraction) and resultant muscle hypermetabolism (eg, fever, tachycardia). In addition, MH causes hypercarbia and tachypnea (due to increased cellular metabolism), difficulty ventilating, and rhabdomyolysis (eg, myoglobinuria). Management is immediate cessation of the anesthetic, administration of dantrolene (a skeletal muscle relaxant), and supportive care (in addition to completing the emergency delivery as quickly and as safely as possible in this patient).
(Choice A) Amniotic fluid embolism (AFE) typically presents postpartum as acute cardiac or respiratory collapse and disseminated intravascular coagulopathy, possibly due to anaphylaxis from amniotic fluid entering maternal circulation. In contrast to this patient, AFE causes profound hypotension (systolic <90 mm Hg).
(Choice B) Eclamptic seizures can occur in patients with preeclampsia with severe features. Although this patient has severe-range blood pressures (eg, systolic ≥160 mm Hg or diastolic ≥110 mm Hg), she has received magnesium sulfate for seizure prophylaxis. In addition, eclampsia does not cause fever or tachypnea, making this diagnosis less likely.
(Choice C) Magnesium sulfate is used for seizure prophylaxis in patients with preeclampsia, likely via membrane stabilization that raises the seizure threshold. Toxic doses can affect both skeletal muscle (decreased acetylcholine release) and cardiac muscle (prolonged conduction time); therefore, patients can develop marked muscle weakness, loss of deep tendon reflexes, respiratory depression (rather than tachypnea), and cardiac arrest.
(Choice E) Although neuroleptic malignant syndrome has a similar presentation to MH (eg, fever, muscle rigidity), it is triggered by neuroleptic agents (eg, haloperidol, promethazine) rather than anesthetics. In addition, neuroleptic malignant syndrome develops over the course of days, not minutes.
Educational objective:
Malignant hyperthermia is a rare, life-threatening condition that presents after anesthetic induction with sudden-onset fever, tachycardia, tachypnea (eg, difficulty ventilating), and muscle rigidity. Treatment is immediate cessation of the anesthetic and administration of dantrolene.