Infectious Disease · Bacterial Infections
The facts most likely to be tested
Tetanus is caused by the exotoxin tetanospasmin, which is produced by the anaerobic, gram-positive, spore-forming rod Clostridium tetani.
The mechanism of action involves the irreversible blockade of inhibitory neurotransmitters glycine and GABA at the presynaptic terminals.
Clinical presentation typically begins with trismus (lockjaw) followed by risus sardonicus and opisthotonos due to sustained muscle spasms.
Diagnosis is strictly clinical, based on the patient's history of a puncture wound or contaminated injury and the presence of characteristic muscle rigidity.
Initial management requires tetanus immune globulin (TIG) to neutralize unbound toxin and the tetanus toxoid vaccine to induce active immunity.
Wound management necessitates thorough debridement and the administration of metronidazole or penicillin to eliminate the source of toxin production.
Patients with a dirty or deep wound require a tetanus booster if their last dose was more than 5 years ago, whereas clean, minor wounds require a booster only if the last dose was more than 10 years ago.
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A 45-year-old male presents to the emergency department with a 2-day history of progressive jaw stiffness and difficulty swallowing. He reports stepping on a rusty nail in his garden 10 days ago, which he cleaned with soap and water. On physical examination, he exhibits trismus, a fixed facial expression described as risus sardonicus, and periodic opisthotonos triggered by tactile stimuli. His vaccination history is uncertain.
What is the most appropriate initial management for this patient?
Tetanus immune globulin (TIG) and the tetanus toxoid vaccine
The patient presents with classic signs of generalized tetanus; management requires passive immunization with TIG to neutralize circulating toxin and active immunization with the tetanus toxoid vaccine.
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Etiology / Epidemiology
Caused by Clostridium tetani spores entering via puncture wounds or contaminated soil. Primarily affects unvaccinated or inadequately immunized individuals.
Clinical Manifestations
Presents with lockjaw (trismus), risus sardonicus, and opisthotonos. Muscle spasms triggered by sensory stimuli.
Diagnosis
Diagnosis is clinical. No specific lab test confirms the disease; serum antibody levels are not useful in acute settings.
Treatment
Administer Tetanus Immune Globulin (TIG) and Metronidazole. Do not use penicillin due to GABA antagonism.
Prognosis
High mortality if untreated. Autonomic instability and respiratory failure are the leading causes of death.
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Epidemiology & Etiology
The pathogen is an anaerobic, gram-positive, spore-forming rod found in soil and animal feces. Infection occurs through breaks in the skin, particularly puncture wounds, burns, or contaminated surgical sites. In neonates, tetanus neonatorum occurs via umbilical cord contamination in non-sterile environments.
Pertinent Anatomy
The toxin travels via retrograde axonal transport from the peripheral nerves to the central nervous system. It specifically targets the inhibitory interneurons in the spinal cord and brainstem.
Pathophysiology
The toxin, tetanospasmin, irreversibly binds to presynaptic membranes, preventing the release of inhibitory neurotransmitters GABA and glycine. This loss of inhibition leads to unchecked motor neuron firing and muscle rigidity. The process is irreversible, requiring the growth of new nerve terminals for recovery.
Clinical Manifestations
Early signs include trismus (lockjaw) and stiffness of the neck. Progression leads to risus sardonicus (fixed grimace) and opisthotonos (arched back). Laryngospasm and respiratory failure are life-threatening emergencies. Spasms are often precipitated by minor sensory stimuli like light or noise.
Diagnosis
Diagnosis is strictly clinical based on history and physical exam. There is no gold standard laboratory test for acute infection. A history of incomplete or absent tetanus toxoid vaccination is the most critical diagnostic clue.
Treatment
Immediate management includes Tetanus Immune Globulin (TIG) to neutralize unbound toxin and Metronidazole to eradicate the source. Penicillin is contraindicated as it may worsen spasms by inhibiting GABA. Provide benzodiazepines for muscle spasms and ensure aggressive wound debridement.
Prognosis
Recovery is slow, often requiring weeks of intensive care. Autonomic dysfunction (labile hypertension/tachycardia) is a major cause of morbidity. Respiratory failure remains the primary cause of mortality.
Differential Diagnosis
Strychnine poisoning: lacks the characteristic trismus of tetanus
Dystonic reaction: history of recent neuroleptic/antiemetic use
Meningitis: presence of fever and nuchal rigidity without trismus
Rabies: history of animal bite and presence of hydrophobia
Tetany: associated with hypocalcemia and positive Chvostek sign