Botulism physical examination

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Michael Maddaleni, B.S., Keanu Ngo[2]

Overview

The physical examination of botulism classically reveals an afebrile, alert patient with symmetric, descending flaccid paralysis beginning in the cranial nerves, with preserved sensation and mental status. The most useful examination findings are bilateral cranial-nerve deficits (ptosis, ophthalmoplegia, facial weakness, diminished gag), autonomic/cholinergic signs (dilated poorly reactive pupils, dry mucous membranes, ileus), symmetric descending weakness with diminished or absent reflexes, and signs of evolving neuromuscular respiratory failure. In infants, the hallmark is generalized hypotonia ("floppy baby") with bulbar findings.

General appearance and vital signs

• Appearance: alert and oriented despite marked weakness; may appear lethargic purely because of facial/bulbar weakness and ptosis. Sensorium is preserved (toxin does not cross the blood–brain barrier).
• Temperature: characteristically afebrile (no fever in 99% of a 332-case CDC series). Fever suggests a superimposed infection or a wound abscess in wound botulism.
• Autonomic instability: orthostatic hypotension and labile heart rate/blood pressure may be present in both adults and infants; bradycardia can occur.

HEENT and cranial-nerve examination

Bilateral, symmetric cranial-nerve deficits are the diagnostic core; at least one ocular weakness finding was present in 84% of the CDC series:

• Eyes: ptosis, ophthalmoplegia/extraocular movement limitation, sluggish or absent pupillary light reflex. Dilated, fixed or poorly reactive pupils are present in about half of patients and are a key autonomic sign. Nystagmus is not characteristic.
• Face: symmetric facial weakness, loss of facial expression.
• Mouth/throat: dry mucous membranes, dysarthria, dysphonia, diminished gag reflex, pooling of oropharyngeal secretions, tongue weakness.

Neuromuscular examination

• Motor: symmetric weakness in a descending pattern (cranial → neck → upper limbs → trunk → lower limbs), proximal ≥ distal.
• Reflexes: deep tendon reflexes are diminished or absent; they may be normal early and decline as paralysis progresses.
• Sensory: normal (no true sensory loss); paresthesias are uncommon.

Respiratory examination

Serial bedside respiratory assessment drives disposition. Watch for tachypnea, shallow breathing, weak cough, staccato/breathy speech, use of accessory muscles, and paradoxical abdominal movement (diaphragmatic weakness). Bulbar and facial weakness can mask typical distress signs (grimacing, nasal flaring). Hypoxemia and hypercarbia are late; the decision to intubate should be based on clinical trajectory and bedside measures, not blood gases alone. Serial measurement of vital capacity and negative inspiratory force at the bedside helps track respiratory decline.

Abdominal and skin examination

• Abdomen: distension with decreased/absent bowel sounds (ileus), reflecting autonomic cholinergic blockade.
• Skin (wound botulism): inspect for wounds, injection sites/track marks, subcutaneous granulomas ("skin popping"), cellulitis, or abscess; a wound may appear benign despite toxin production.

Infant examination

• General: hypotonic ("floppy"), expressionless facies, feeble/weak cry, poor head control.
• Cranial nerves: ptosis (against gravity), ocular palsies, sluggish pupils, diminished gag/suck/swallow reflexes.<ref name="Cox2002">{{cite journal |author=Cox N; Hinkle R |title