2024 FSA Podium and Poster Abstracts
P082: USE OF KETAMINE IN THE MANAGEMENT OF SEVERE TETANUS IN THE INTENSIVE CARE UNIT
Ryan M Lynn, BS1; Collin VanGordon, BS1; Michael W West, MD2; 1New York Institute of Technology College of Osteopathic Medicine; 2Good Samaritan University Hospital
Introduction: Tetanus is an acute condition triggered by tetanospasmin, a potent exotoxin produced by Clostridium tetani. This toxin primarily acts by inhibiting the release of inhibitory neurotransmitters gamma-aminobutyric acid (GABA) and glycine at the spinal cord and brainstem. This mechanism leads to the hallmark symptoms of trismus (lockjaw), laryngeal spasms, opisthotonic posturing, alongside autonomic instability symptoms like tachycardia and profuse secretions. Tetanus is exceedingly rare in the United States with on average 30 cases per year. The management of severe tetanus involves prompt wound debridement, administration of metronidazole, tetanus immunoglobulins, and controlling muscle spasms with benzodiazepines. In cases where spasms are a cause of airway compromise, neuromuscular blockers in conjunction with mechanical ventilation are employed for supportive care.
Methods/Case Presentation: A 49 year old male with no significant past medical history presented to the ED with complaints of a stiff neck and trismus following a severe laceration to his lower leg from a motorcycle accident while in Haiti eight days prior to admission. He reports never receiving the tetanus vaccine or immunoglobulins. Upon his return to the United States, he reported stiffness spreading to his back and jaw; which prompted him to seek medical attention. On presentation, neck stiffness and trismus were provoked with movement. The patient was administered Tdap and tetanus immune globulin, and empirically treated with piperacillin-tazobactam, vancomycin, metronidazole under suspicion of tetanus and meeting sepsis criteria. Two hours later, an episode of trismus caused the patient’s oxygen saturation to decline to 75%. IV Lorazepam did not arrest the trismus and a decision was made to intubate the patient due to airway compromise.
The patient was initially sedated with midazolam and fentanyl infusion with the goal of achieving Richmond Agitation & Sedation scale (RASS) -4 to -5. However, the addition of dexmedetomidine and propofol were required for successful sedation. Diazepam was administered to manage breakthrough spasms. On Day 5 of admission, the patient experienced a diffuse spam with an oxygen saturation declining to the mid 70’s and a ketamine infusion at 20mg/hr was started. On Day 9, a tracheostomy and feeding access was performed.
Results: Use of ketamine as an adjunct treatment helped decrease spasms and allowed the patient to recover and meet RASS goals during ICU stay. On Day 22, the patient tolerated being tapered off ketamine infusion. On Day 37, the patient’s status improved to the point of tolerating weaning off of the ventilator and all other sedatives were discontinued. On day 49, the tracheostomy collar was removed prior to discharge.
Discussion: While benzodiazepines and neuromuscular blockers are the cornerstone of therapy for controlling spasms, this case illustrates the necessity of adjunctive treatments, such as ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist that reduces glutamate binding and can mitigate the excessive neuronal excitation driving spasms. The successful use, despite concerns about its potential to exacerbate autonomic symptoms, suggests its utility in managing refractory tetanus spasms. This experience advocates for further exploration into the role of ketamine, especially given the disease's significant mortality risk.