Myasthenia Gravis

A patient's ptosis worsens throughout the day but improves after rest — this pattern of fatigable weakness is the signature of myasthenia gravis and drives every nursing priority.

Myasthenia gravis (MG) is an autoimmune disorder where antibodies attack acetylcholine receptors at the neuromuscular junction, blocking nerve-to-muscle transmission. The hallmark is skeletal muscle weakness that worsens with activity and improves with rest — a fatigability pattern distinct from other neuromuscular diseases. Ocular muscles are affected first (ptosis, diplopia), progressing to bulbar muscles (dysphagia, dysarthria), and potentially respiratory muscles. Myasthenic crisis — severe respiratory muscle weakness triggered by infection, stress, or missed medications — is the life-threatening emergency. Respiratory status is the top nursing priority: monitor forced vital capacity and oxygen saturation closely. Anticholinesterase drugs like pyridostigmine (Mestinon) are the mainstay treatment, given exactly on time because even small delays worsen weakness. The Tensilon (edrophonium) test differentiates myasthenic crisis (weakness improves with Tensilon) from cholinergic crisis (weakness worsens — too much medication). Keep atropine at the bedside during a Tensilon test as the antidote for cholinergic effects.

Key Distinctions

Don't confuse myasthenic crisis (undermedication — give more anticholinesterase) with cholinergic crisis (overmedication — hold anticholinesterase). Both present with respiratory failure, but Tensilon distinguishes them. Unlike Guillain-Barré, MG weakness is fatigable and fluctuates — GBS is ascending, progressive, and doesn't improve with rest. Unlike ALS, MG is treatable and does not involve upper motor neuron signs.

Clinical Pearl

Worse at the end of the day, better after rest. If the patient's eyelids droop more by evening and recover by morning, think MG — and think airway first.