7.9: Skeletal Muscle Relaxants: Adverse Effects

Skeletal muscle relaxants are widely used for muscle paralysis and relieving pain following any muscle injury or stiffness. However, depending on the drug type, they can have adverse effects that range from mild to severe. Usually, nondepolarizing neuromuscular blockers have minimal side effects. For example, drugs like d-tubocurarine, cisatracurium, and rocuronium cause hypotension, whereas drugs like baclofen, when stopped abruptly, can lead to the recurrence of spastic conditions.

Unlike nondepolarizing blockers, succinylcholine, a depolarizing blocker, has more severe adverse effects, including hyperkalemia, arrhythmia, postoperative muscle pain, increased intraocular pressure, and regurgitation of gastric content due to increased gastric pressure.

Adverse effects of directly acting agents like botulinum toxin and dantrolene include general muscle weakness and hepatotoxicity. Additionally, botulinum toxin can cause respiratory tract infections and loss of bladder control.

Lastly, centrally acting muscle relaxants, which affect the central nervous system or CNS, induce various symptoms of CNS depression. For example, tizanidine causes drowsiness, hypotension, dizziness, dry mouth, and hepatotoxicity, whereas diazepam causes anxiety, tremors, insomnia, and hallucinations. Avoiding high drug doses from being given to at-risk patients such as epileptic patients or pregnant women may help reduce the severity of the side effects.

Skeletal muscle relaxants are administered at regulated doses to minimize adverse effects. The adverse effects and their severity depend on the type of relaxant used.

For example, nondepolarizing blockers have minimal side effects, but directly acting agents may cause general muscle weakness and hepatotoxicity.

In contrast, a depolarizing blocker like succinylcholine is associated with severe adverse effects, including cardiac arrhythmia, postoperative muscle pain, prolonged apnea and even respiratory arrest.

So, a correct dose of succinylcholine becomes essential, especially for patients with mutated cholinesterases.

Because these patients cannot metabolize and eliminate succinylcholine properly, they experience delayed recovery of muscles, such as the diaphragm. As the diaphragm remains paralyzed, it leads to apnea, where sedated patients stop breathing.

Additionally, succinylcholine facilitates the release of potassium from intracellular storage. So, it must be avoided in patients with burns, nerve damage or kidney failure who have already suffered rapid potassium loss to prevent cardiac arrest.