Dilip R Karnad,
Intensive Care Management of Severe Tetanus
[Year:2021] [Month:May] [Volume:25] [Number:S2] [Pages:6] [Pages No:S155 - S160]
Autonomic dysfunction, Benzodiazepine, Immunization, Intensive care unit, Laryngospasm, Muscle spasm, Rhabdomyolysis, Severe tetanus,Tracheostomy, Tropical infections
DOI: 10.5005/jp-journals-10071-23829 |
Open Access |
• Tetanus is caused by an exotoxin, tetanospasmin, produced by Clostridium tetani, an anaerobic gram-positive bacillus.
• Tetanospasmin prevents the release of inhibitory neurotransmitter gamma-aminobutyric acid (GABA) in the spinal cord, brainstem motor nuclei, and the brain, producing muscle rigidity and tonic spasms.
• Trismus (lockjaw), dysphagia, laryngeal spasms, rigidity of limbs and paraspinal muscles, and opisthotonic posture are common.
• Frequent severe spasms triggered by touch, pain, bright light, or sounds may produce apnea and rhabdomyolysis.
• Autonomic overactivity occurs in severe tetanus causing labile hypertension, tachycardia, increased secretions, sweating, and urinary retention. Dysautonomia is difficult to manage and is a common cause of mortality; magnesium sulfate infusion is often used.
• Antibiotics (penicillin or metronidazole) and wound care reduce toxin production and human tetanus immune globulin neutralizes the circulating toxin.
• Nasogastric tube placement for feeding and medications is needed.
• Early elective tracheostomy is performed in moderate or severe tetanus to prevent aspiration and laryngeal stridor.
• Benzodiazepines help reduce rigidity, spasms, and autonomic dysfunction. Large doses of diazepam (0.2–1 mg/kg/h) are administered via nasogastric tube.
• Neuromuscular blocking agents and mechanical ventilation are used for refractory spasms.
• Mortality ranges from 5% to 50%.