2024 FSA Podium and Poster Abstracts
P004: PERIOPERATIVE MANAGEMENT OF A PATIENT WITH GENERALIZED TETANUS
Kevin Bennett, MD1; Hala Baaj2; Lori Gilbert, MD3; 1Memorial Healthcare System; 2Herbert Wertheim College of Medicine; 3Envision Physician Services
Tetanus is caused by Clostridium tetani infection in soft tissue and subsequent production of the neurotoxin tetanospasmin. Incidence and mortality are more common in underdeveloped countries where routine TDaP vaccination is less common, but overall incidence has decreased in recent decades[1]. Tetanospasmin degrades synaptobrevin, a pre-synaptic protein involved in vesicle-membrane fusion, and targets inhibitory GABA and glycine vesicles, impairing release of these hyperpolarizing neurotransmitters to counter acetylcholine's depolarizing activity[2]. Insufficient inhibition of alpha-motor neurons leads to diffuse muscle spasms, chest wall rigidity, autonomic instability, laryngospasm, respiratory failure, and eventual cardiac arrest without treatment[2,3].
55-year-old male presented with painful trismus and difficulty swallowing oral secretions. He reports a puncture wound two weeks earlier after stepping on a tree branch. He was admitted, given tetanus immunoglobulin, cyclobenzaprine, and discharged the next day with antibiotics. He had worsening symptoms for the next day and returned with shortness-of-breath and back pain. After admission, patient had sudden back stiffening, became hypoxic, and went into cardiac arrest. Despite trismus, he was successfully induced with propofol and paralyzed with succinylcholine, intubated, and placed on mechanical ventilation. Patient was taken to the operating room by oralmaxillofacial surgery who opened and closed the jaw without difficulty after paralysis with rocuronium and anesthesia with sevofluorane. Tetanus diagnosis was officially decided, and tracheostomy was recommended to allow for prolonged medical treatment.
Tetanic muscle spasms can be treated with medications that bypass tetanospasmin's activity by potentiating post-synaptic GABA activity directly[4]. Benzodiazepines, propofol, and inhaled volatile anesthetics are the most common agents; however, other medications like baclofen, cyclobenzaprine, and dantrolene are used in conjunction to good effect[4-7]. For severe cases, vecuronium and rocuronium work effectively and safely[6]. While still effective for inducing paralysis, succinylcholine should be avoided in patients with possible rhabdomyolysis or acute kidney injury for concern of hyperkalemia[8].
Hypoxemia can occur due to atelectasis from chest wall rigidity[2,3]. Patients struggle to compensate for V/Q mismatch and can desaturate quickly during acute chest and back spasms. Respiratory distress, decreased oxygen saturation, and ABG analysis are useful early to determine need for intubation. Autonomic dysfunction can complicate hemodynamic compensation during respiratory distress, but can be treated with non-selective beta blockers, alpha-2 agonists, and magnesium[9]. Ultimately, spontaneous or oral secretion-induced laryngospasm can lead to immediate respiratory arrest and will require paralysis and intubation.
In a patient presenting with high-risk for tetanus, trismus, difficulty controlling secretions, chest wall rigidity, and frequent full-body muscle spasms, the bar for aggressive airway management is low. The potential for spontaneous or secretion-induced laryngospasm alone is enough to consider elective intubation in a patient with severe physical presentation. Medications to control spasm, autonomic dysfunction, and tetanus immunoglobulin should be given immediately along with urgent airway assessment. While there is little evidence for specific anesthetic management, the mechanism-of-action for tetansospasmin does not interfere with non-depolarizing paralytics and is mitigated by GABA-potentiating medications.
1. PMID:37086867
2. PMID:23299659
3. PMID:10710833
4. PMID:1796932
5. PMID:3518923
6. PMID:11517134
7. PMID:3922250
8. PMID:30157697
9. PMID:34345131
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