Tetanus is caused by a neurotoxin produced by Clostridium tetani, an anaerobic Gram-positive bacillus that contaminates wounds.12–3 General anesthesia is frequently indicated for wound debridement to eradicate the bacteria. However, the neck rigidity, trismus, and chest wall immobility caused by severe muscle spasms produce potential airway and ventilation difficulties.
After a scalp laceration and degloving hand injury suffered during the 2010 Haitian earthquake, an 80-year-old man developed dysphagia, truncal rigidity, and generalized muscle spasm. He was transferred to our hospital, the USNS Comfort, a United States Navy hospital ship sent to provide humanitarian assistance after the earthquake. The patient was alert, with no localizing neurological signs. No intracranial hematoma was detected by computerized tomography. Generalized tetanus was diagnosed clinically. He was treated with tetanus immune globulin, clindamycin, penicillin, diazepam, and IV rehydration. A wound debridement under general anesthesia was planned the same day.
On examination, he was noted to have generalized muscle rigidity. The severe muscle spasm inhibited chest wall movement, with limited respiratory tidal volumes achieved predominantly by diaphragmatic movement. The neck was fixed in the neutral position by muscle spasm. Mouth opening was limited to approximately 2 cm, with a resultant Mallampati class 4 view.
Standard monitors were applied. He received labetalol 10 mg IV before induction of anesthesia to treat arterial blood pressure of 200/100 mm Hg. After administration of oxygen, anesthesia was induced by incrementally increasing concentrations of inhaled sevoflurane in 100% oxygen. After induction, the muscle tetany resolved rapidly, with immediate improvement in chest wall excursion and tidal volumes. His mouth opening improved, and oral and nasal airways were inserted with ease. Anesthesia was maintained by spontaneous ventilation with 1.5% sevoflurane in oxygen via facemask. The hemoglobin peripheral oxygen saturations were 99% to 100%, end-tidal carbon dioxide was 33 to 34 mm Hg, and arterial blood pressure and heart rate decreased to 110–150/60–80 mm Hg and 80 to 90 bpm, respectively. The surgery lasted 70 minutes, during which time the patient received 50 μg fentanyl and 1 mg morphine. Upon transfer to the intensive care unit after an uneventful anesthetic, the nasal airway was left in place as a precaution against return of the trismus.
Three days later, the patient was anesthetized for a skin grafting procedure. Preoperative airway and ventilation findings were similar to the previous examination. Anesthesia was induced with 40 mg of IV propofol and maintained by spontaneous ventilation of 1% to 2% sevoflurane in a 50% oxygen/nitrous oxide mix through an oropharyngeal airway and facemask. As before, ventilation and airway access improved after induction of anesthesia. His blood pressure and heart rate were stable in the 120–140/50–60 mm Hg and 65 to 90 beats per minute range, respectively. Ventilation was uncomplicated. Thirty milligrams ketorolac and 1 mg morphine were administered IV during a 75-minute procedure. The anesthetic course was again uneventful, and the oral airway was removed at the end of the procedure.
Over the following days, the patient developed retention of pulmonary secretions due to chest wall rigidity, subsequent pneumonia, and progressive respiratory failure. The patient had been suffering from longstanding malnutrition, and because of his extremely frail preexisting baseline condition, it was thought he would not survive prolonged mechanical ventilation. Palliative care was initiated, and he died 14 days after admission to hospital.
A 29-year-old man suffered right-sided scalp lacerations, metatarsal fractures, and a comminuted distal radial fracture when his house collapsed. Over the following days, he developed progressive right-sided facial numbness and weakness, jaw pain, limited mouth opening, and difficulty swallowing. At a field hospital, a percutaneous gastric tube was inserted for nutrition, and he was referred to our hospital. Computerized tomography showed no jaw fracture, intracranial lesion, or local abscess. Cerebrospinal fluid obtained by lumbar puncture was normal. Cephalic tetanus was diagnosed on the basis of dysphagia, masseter spasm, and a right seventh cranial nerve palsy after an ipsilateral head laceration. Tetanus toxoid, tetanus immune globulin, and metronidazole were given. He was scheduled to undergo debridement for his foot wounds later that day.
On examination, the patient had a right seventh cranial nerve palsy, mouth opening was limited to 2 cm by masseter spasm, and neck extension was normal. After 2.5 mg IV Versed for sedation, he received a femoral-sciatic block with 50 mL of 0.5% ropivacaine, using ultrasound and peripheral nerve stimulator location. He was lightly sedated during a 17-minute procedure with 25 μg IV fentanyl and 10 mg IV ketamine.
Two days later, a general anesthetic was administered for a scalp debridement. The patient was premedicated with 0.5 mg IV midazolam. On induction of anesthesia with a 200-mg IV propofol bolus, his masseter spasm resolved and a laryngeal mask airway was inserted with ease. He breathed 2% to 3% sevoflurane in oxygen during a 28-minute debridement, and received 100 μg IV fentanyl and 4 mg IV ondansetron. The laryngeal mask was removed under deep anesthesia and he retained good mandibular mobility.
The patient was scheduled for a repeat wound washout 2 days later. He received 4 mg IV midazolam as premedication, followed by induction of anesthesia with a 200-mg IV propofol bolus. The masseter spasm again resolved sufficiently for laryngeal mask insertion. The masseter muscle remained relaxed during spontaneous ventilation of 0.8% sevoflurane in a 50% oxygen/nitrous mix for a 29-minute procedure.
Recorded vital signs and anesthetic and surgical courses on all 3 occasions were unremarkable. The patient was discharged the next day to an intermediate-care facility and received metronidazole 500 mg 6 hourly to complete eradication of the infection; sertraline 50 mg daily for posttraumatic stress disorder; gabapentin 300 mg 6 hourly for neuralgia; and oxycodone, ibuprofen, and acetaminophen for additional analgesia, all administered via the gastric tube.
Tetanus is endemic to economically underdeveloped countries,12–3 where advanced anesthetic training, endotracheal intubation, and mechanical ventilation are often scarce or unavailable resources. The disease also occurs in epidemics after natural disasters,1–3 when the acute strain on medical facilities during a mass surge of casualties can result in a similar shortage of resources. Consequently, simple anesthetic techniques are preferable.
Tetanus is typically diagnosed clinically. The presence of C tetani does not establish a diagnosis, nor does the presence or absence of antibodies. Differential diagnoses include strychnine poisoning, meningitis, status epilepticus, hypocalcemia, dystonic drug reaction, orofacial infection, rabies, and psychiatric disorders.1–3 However, these diagnoses can usually be excluded by history and physical examination.
The tetanus neurotoxin tetanospasmin is a zinc metalloprotease that blocks the release of neurotransmitters. It selectively prevents fusion of the synaptic vesicle to the presynaptic cell membrane by degradation of synaptobrevin, a vesicle-specific protein needed for membrane fusion.4,5 Clinical effects are dependent on which neurotransmitters are blocked and the location of the toxin within the nervous system.
After release by C tetani, tetanospasmin is taken up by local nerve terminals.1–3 Inhibition of acetylcholine exocytosis into the neuromuscular cleft produces local muscle weakness. Retrograde intraaxonal transport of the toxin up the neuron is followed by subsequent spread to adjacent neurons in the spinal cord, brainstem, and midbrain. The toxin predominantly affects inhibitory neurons, blocking release of glycine and γ-aminobutyric acid. Dysfunction of the spinal interneurons that inhibit α motor neurons causes disinhibited efferent discharge and intense muscle rigidity.6
Generalized tetany, seen in the first patient, was caused by toxin uptake from the hand laceration and extensive spread in the spinal cord. In the second patient, the peripheral uptake of the toxin into the seventh cranial nerve from the scalp laceration produced peripheral blockade of excitatory neurotransmitter release and facial palsy. Although the precise locations of central disinhibition of cephalic tetanus are ill-defined,3 the trismus and dysphagia presumably result from disinhibition of the trigeminal innervations of the ipsilateral muscles of mastication.
Although the first published report of the discovery of anesthesia in 1846 prompted immediate consideration of using ether to treat tetanus, an editorial suggested this would “assuredly end in disappointment; (tetanus being a disease) of motion, not of sensation, and remaining with an intensity as perfect during insensibility as in complete consciousness.”7 However, clinicians soon reported that ether and chloroform relieved the muscle spasms.8
Volatile anesthetics enhance the activity of inhibitory postsynaptic receptors (γ-aminobutyric acid and glycine), while inhibiting excitatory synaptic channel activity (nicotinic acetylcholine, serotonin, and glutamate). In addition to “insensibility”7 (hypnosis, amnesia, and analgesia), these drugs inhibit motion, predominantly by acting at the level of the spinal cord.9 The presynaptic impairment of inhibitory neurotransmitter release by tetanospasmin may therefore be countered, in part, by the enhancement of postsynaptic inhibitory receptor activity at the spinal cord by volatile anesthetics.
The limited access to the airway and the impairment of chest movement may suggest the need for neuromuscular blockade and positive pressure ventilation. However, because volatile anesthetics or propofol relieve the tetany, airway maintenance and ventilation may easily be achieved without endotracheal intubation. A nasal airway can facilitate airway access, even in the presence of masseter spasm. Spontaneous ventilation is a simple technique that is suitable in situations with limited anesthetic equipment or personnel.
Hyperreactive laryngeal reflexes can trigger fatal or life-threatening laryngospasm.1–3 Although dysphagia and hypersalivation are common clinical features of tetanus, a laryngeal mask will protect the vocal cords from secretions and consequent laryngospasm. This airway management also avoids the potential difficulties of an irritant tracheal tube on emergence from anesthesia.
Mechanisms of death include obstruction of airways by secretions and progressive respiratory failure, autonomic instability and cardiac arrest, laryngospasm, and renal failure.1–3 Long-term management often requires prolonged tracheal intubation and ventilation. Although neuromuscular blockade is usually required, the central action of sedatives such as propofol and benzodiazepines may lower the high doses of peripheral neuromuscular blocking drugs needed to achieve adequate muscle relaxation.
In summary, general anesthetics such as propofol and sevoflurane relieve the muscle spasm induced by the neurotoxin tetanospasmin. Consequently, a basic anesthetic technique that avoids neuromuscular blockade, tracheal intubation, and positive pressure ventilation, may be sufficient to manage a patient with severe tetanic muscle spasm. This approach is particularly suitable for the settings of limited resources in which tetanus usually presents.