Tetanus is a serious, life threatening infection caused by the bacterium, Clostridium tetani. Due to almost widespread vaccination against tetanus toxoid the incidence in the developed world is extremely low. Vaccination in childhood does not result in lifelong immunity and requires “booster” doses of the vaccination every ten years. In the United States, the Centre for Disease Control and Prevention 1 reported between 18 and 37 cases of tetanus occurring annually between the years of 2009 and 2012 with almost all of these cases being the result of no primary immunization or a failure to obtain a booster in the preceding ten years. We report the diagnosis and management of a case of tetanus in a 60-year-old male who’s only known injury was an oral laceration. It is imperative that practitioners remember to enquire about the tetanus immunization status of all trauma patients and that they are aware of this rare, but known source of tetanus.
A 60-year-old male presented to the Department of Oral and Maxillofacial Surgery (OMS), Queen Elizabeth II Health Sciences Centre, with a chief complaint of lower jaw pain. History revealed that the patient had bitten his tongue following a fall from heavy machinery four days earlier. No other soft-tissue injuries were noticed by the patient. He presented to a walk-in medical clinic three days after the fall with a suspected dental infection and was prescribed oral Amoxicillin 500mg, three times daily for seven days. Little improvement in his symptoms occurred and he presented 24 hours later to the emergency department. The OMS service was consulted due to a suspected odontogenic infection.
The patient was afebrile and had vital signs within normal limits. Maxillofacial examination noted no facial edema but the patient’s maximum inter-incisal opening was limited to 20 mm. Intra-oral exam noted a healing laceration of approximately 9 mm in length on the right lateral aspect of the tongue adjacent to the lower right second premolar. The patient’s dental status was extremely poor as evident on the orthopantomograph (Fig. 1). There was no evidence of swelling in the floor-of-mouth, submandibular, or lateral pharyngeal spaces. The patient’s past medical history was significant for hypertension and dyslipidemia for which he was taking atenolol and rosuvastatin. He had no known drug allergies. The patient had a 40 pack-year history of smoking, and minimal alcohol intake.
Clinical photograph: Patient upon attempted straight gaze. Note eyes fixed to right.
The patient’s trismus was initially believed to be secondary to odontogenic pain and/or infection even though no evidence of an odontogenic infection involving a facial-space could be detected. He was scheduled for extraction of all remaining teeth in the OMS clinic and was told to continue his previously prescribed amoxicillin. In addition, he was prescribed oral metronidazole 500 mg twice daily for seven days.
The patient presented for the extraction of his teeth three days following his initial consult and reported no improvement of his pain or limited mouth opening. Intravenous sedation was initiated using a combination of midazolam and fentanyl. Local anesthesia consisting of 2% lidocaine with 1:100,000 epinephrine was administered and the patient’s remaining maxillary teeth were extracted uneventfully. Hypertensive urgency occurred during the extraction of the patient’s mandibular teeth and the procedure was terminated, which led to normalization of the blood pressure. It was later elicited that the patient had not taken his daily dose of atenolol. The patient was rebooked for extraction of his mandibular teeth the following week.
The following day, the patient presented back to the OMS clinic complaining of being “unable to swallow”. Urgent computed tomography (CT) with contrast was ordered. Neither clinical exam nor CT of the head and neck could identify any appreciable swelling or mass and the airway was deemed normal. Examination of the oral cavity proved difficult as the patient seemed to be experiencing intense, involuntary, bilateral masseteric spasms. Nasopharyngoscopy revealed a decreased gag reflex and failure to protect the airway at the level of the vocal cords. No neoplastic process was visualized. The patient was admitted to hospital and started on intravenous antibiotics, namely penicillin G four million units every four hours and metroniadazole 500 mg every twelve hours. Due to the concern that the patient was at risk of aspiration, the patient’s oral intake was restricted and a nasogastric tube was placed. A modified barium swallow was planned to further investigate the dysphagia.
The day following admission, the patient began to complain of foot cramping and spasms, which seemed to be exacerbated by touch. The patient was unable to open his mouth without eliciting a jaw spasm. Tetanus was suspected and the Infectious Disease (ID) service was consulted. Initially, ID did not believe the cause of the spasms was tetanus due to a lack of soft-tissue injury apart from the tongue laceration. Over the next twelve hours the patient developed further neurological signs consistent with a diagnosis of tetanus. He developed a left eye lateral gaze and a right eye medial gaze paralysis. He was unable to protrude his tongue due to intense bilateral masseter muscle spasms whenever he attempted to open his mouth. Neurological examination revealed normal strength bilaterally. Babinski sign was not present but hyper-reflexive knee and ankle jerk reflexes were noted. Neurosurgery was consulted to rule out a brain stem lesion or brain abscess. An urgent MRI was performed and was unremarkable with no intracranial mass, hydrocephalus, hemorrhage or infarct being noted. No abnormal cranial nerve enhancement was seen. Neurology performed a lumbar puncture to rule out leptomeningeal disease, and a 1 mg IV benzotropine challenge was performed to rule out oculogyric crisis. Neither test detected any abnormalities.
With no focal neurological explanation for the patient’s condition a diagnosis of generalized tetanus was made. He was immediately administered Tdap booster (diphtheria and tetanus toxoids, and acellular pertussis) as well as tetanus immune globulin (TIG, HyperTET S/D) 3000 Units IM. The patient was transferred to a monitored bed, penicillin G was discontinued and ceftriaxone 2g IV q24h was begun.
Through the following days the patient showed increasing irritability and agitation, and his gaze became fixed to the right (Fig. 2). He forcefully removed his nasogastric tube (NG) and during attempted re-placement of the NG tube, the patient experienced laryngospasm, which was broken with bag-valve-mask ventilation. Due to declining respiratory function and an inability to protect his airway, a tracheostomy was performed under general anesthetic at which time his remaining teeth were also extracted.
Orthopantomograph: Generalized severe bone loss with multiple retained roots and multiple teeth exhibiting periapical radiolucencies.
The patient was transferred to the care of the Internal Medicine service where he underwent a period of further decline, eventually requiring intervals of ventilatory assistance in the Intensive Care Unit. He appropriately received his second dose of Tdap booster. He unfortunately required multiple courses of antibiotics for ventilator-associated pneumonia. At seven weeks post-admission his condition had improved sufficiently to have the tracheostomy reversed and he was transferred for rehabilitation.
Clostridium tetani, a spore-forming gram-positive obligate anaerobe, is a normal gut flora in many mammals and is commonly found in soil 1. When the spores of C. tetani inoculate a wound they transform into a rod-shaped bacterium. C. tetani produces two exotoxins, tetanolysin and tetanospasmin. Tetanospasmin, a neurotoxin, gains access to receptors in the spinal cord and brainstem via retrograde axonal transport. 1 The end effect of the toxin is the blockade of inhibitory impulses to the anterior horn cells and autonomic neurons. Preventing the release of inhibitory neurotransmitters leads to the commonly seen clinical manifestations of increased muscle tone, painful spasms and widespread autonomic instability.
Three clinical forms of tetanus are recognized. Local tetanus is uncommon and is limited to spasm of a single anatomic area. It may progress to a more severe form but is rarely fatal. Cephalic tetanus is defined by the involvement of cranial nerves only. It is rare and again not commonly fatal. The most common and severe form is generalized tetanus, which accounts for approximately 80% of reported cases. 1 The typical sequence of signs and symptoms is trismus, followed by dysphagia and neck stiffness, progressing to abdominal and respiratory muscle involvement. Laryngospasm and spasm of respiratory musculature leads to respiratory distress. Fractures of the spine and long bones have been reported from contractions. Commonly seen autonomic symptoms include hypertension, arrhythmias and occasionally, cardiac arrest. Initial treatment includes thorough debridement of the wound and administration of tetanus booster. Treatment of generalized tetanus typically includes administration of 3000-6000 units of tetanus immune globulin, intravenous penicillin G and metronidazole, deep sedation and neuromuscular blockade with ventilatory support as required. 2 Spasms can occur for 3-4 weeks, with complete recovery taking months. 1
Practitioners should inquire about a patient’s vaccination status if they have incurred a soft-tissue injury particularly if it has been contaminated with dirt, feces, soil, or saliva. Wounds caused by crushing, tears, burns, frostbite and punctures are also susceptible to tetanus. Rapid tetanus antibody testing or immunochromatographic dipstick test can help determine immunization status when one is unable to obtain a reliable history. 3,4 Following an oral or peri-oral soft-tissue injury, particularly in a patient with poor oral hygiene, it is advisable that the practitioner determine the patient’s immunization status and possible need for a tetanus booster (Table 1) or prophylactic TIG administration (250 units IM). Intra-oral wounds are inherently in contact with saliva and therefore considered a contaminated wound. Facial and oral wounds have been implicated as the main portal of entry for tetanus, and therefore should not be overlooked. 5–8 Tetanus immunoglobulin will inactivate unbound toxin, but once the toxin reaches the nerve endings the binding is irreversible. Administration Tdap booster should occur as soon as possible following inoculation, but late presenting injuries should not be overlooked as the incubation period ranges from one day to several months, with the average being eight days.
Tetanus status and appropriate tetanus vaccine and/or tetanus immunoglobulin should be universally reviewed and managed by all healthcare providers that encounter soft tissue injury. Timely administration of tetanus toxoid and/or immunoglobulin is imperative to prevent the onset of generalized tetanus as outlined in this case report. Oral wounds should not be overlooked as a potential source of inoculation, especially in those patients with pre-existing poor oral health. OH
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About the Authors
Dr. Brad Fisher, BMedSc, DDS, Resident, Oral & Maxillofacial Surgery, Dalhousie University, Halifax, Nova Scotia.
Ben Davis received his DDS from the University of Western Ontario in 1992 and his Diploma in Oral and Maxillofacial Surgery and Anesthesia from The University of Toronto in 1997. Following a surgical Fellowship in OMFS at the QE II HSC, he began his academic career at Dalhousie where he is currently Professor and Chair of the Department of Oral and Maxillofacial Sciences and its affiliated teaching hospitals. He is a past president of the Canadian Association of Oral and Maxillofacial Surgeons and is heavily involved with the Royal College of Dentists of Canada where he is presently the Examiner in Chief.