Succinylcholine: indications and contraindications

Why examiners ask this

Succinylcholine is the drug examiners love to put in your hand and then take away: the burn patient, the paraplegic, the boy with an undiagnosed myopathy, the patient with a potassium of 5.8. It tests whether you understand receptor upregulation and the hyperkalemic mechanism rather than a memorized list, and whether you have a fallback when you cannot use it. It stresses application of knowledge and judgment.

The 60-second answer

Decision points and the "why"

• Hyperkalemia mechanism — normally potassium rises up to about 0.5 mEq/L.¹ In denervation, burns or immobility, immature and alpha-7 acetylcholine receptors spread across the whole muscle membrane, each staying open longer, so the potassium rise can exceed 5 mEq/L and cause arrest. Risk is minimal in the first 24–48 hours, peaks at 7–10 days after the injury, and upregulation can last up to 2 years;³ the label states that the exact onset and duration are undetermined.²
• Pre-existing hyperkalemia — in renal failure, the rise is the usual 0.5 mEq/L; I use it if the potassium is below about 5.5 and the patient is not acidotic, because the problem is the starting value, not the response.
• Children and undiagnosed myopathy — the FDA boxed warning describes acute rhabdomyolysis with hyperkalemia, ventricular dysrhythmias and death in apparently healthy children, often boys with unrecognized Duchenne.² I avoid routine use in children and reserve it for emergencies: laryngospasm or the full stomach.
• Pseudocholinesterase deficiency — patients homozygous for the atypical gene (about 1 in 2,500) are extremely sensitive and can stay paralyzed for hours;² I keep the patient sedated and ventilated until a train-of-four shows full recovery, then send dibucaine number and refer the family.
• Rising intragastric, intraocular and intracranial pressure — the rise is small and transient; the label advises avoiding it in a penetrating eye injury unless the benefit outweighs the risk,² so in the open-globe full-stomach case I accept succinylcholine only if rocuronium is not an option, because aspiration is the larger threat and a smooth induction matters more.
• Bradycardia — muscarinic stimulation, common in children after a first dose and worst with a second dose given within minutes;³ anticholinergic pretreatment reduces it,² so I give atropine 0.02 mg/kg before a repeat dose.
• Masseter spasm — I abort elective surgery, check CK and urine myoglobin, and monitor for MH.

The complication they will inject

A 34-year-old who fell from a roof four days ago, now paraplegic at T6, comes for a spinal fixation; the resident has drawn up succinylcholine. I stop it, because four days after cord injury the receptors have proliferated below the lesion and the potassium could jump to lethal levels. I explain this to the resident and use rocuronium 1.2 mg/kg. If the examiner says the succinylcholine was already given and the ECG shows peaked T waves then a wide-complex rhythm, I call for help, give calcium chloride 1 g IV, insulin 10 units with 25 g dextrose, hyperventilate, start CPR if there is no pulse, and continue ACLS for a prolonged period, because hyperkalemic arrest responds to sustained resuscitation.

Pitfalls that cost points

• Listing contraindications without the mechanism or the time window.
• Saying renal failure is an absolute contraindication.
• Forgetting the MH link and the obligatory MHAUS-style workup after masseter rigidity.
• Giving a second dose to a child without atropine.
• No backup plan: always state the rocuronium and sugammadex alternative.

Rapid-why

Q: Why the fasciculations? A: Depolarization causes disorganized contraction before the end plate becomes inexcitable; it produces myalgia and a small potassium rise.

Q: What is a phase II block? A: After large or repeated doses (the label describes the transition after accumulated doses of 2–4 mg/kg) the block takes on non-depolarizing characteristics, with fade and post-tetanic potentiation.²

Q: Why does a myasthenic need more succinylcholine? A: Fewer functional receptors resist depolarization; they need about 2 mg/kg, and they are very sensitive to non-depolarizers.

Q: Why is a burn patient safe in the first 24 hours? A: Upregulation takes time; risk is minimal in the first two days, then rises to a peak at 7–10 days and persists while the receptors remain upregulated.³

Numbers to know

Links

• Rapid sequence induction and full stomach, hyperkalemia, Malignant hyperthermia, Muscular dystrophies and myotonias (coming), burns, Spinal cord injury and autonomic hyperreflexia
• MHAUS guidance on masseter muscle rigidity