Ms. D, age 38 years, presented to the critical care area with severe muscle spasms. She reported severe muscle knots in her legs, which she said felt like “golf balls moving from one spot to another.” She also noted jaw stiffness and difficulty chewing. Ms. D reported no dyspnea but told the clinicians that she “couldn’t take a deep enough breath.” After several days of low-grade fever, she was evaluated in an outpatient clinic and received steroids; she continued to feel poorly and returned to the clinic. Ms. D was then transferred to our facility for further evaluation.
Medical history was unremarkable. Ms. D reported no previous similar episodes. The patient had a 30 pack-year smoking history and was unemployed. There was no history of recent travel. She reported no pet, animal, inhalation, or pesticide exposure. There was no history of neuroleptic medications. Ms. D reported stepping on a nail, which penetrated her sandal, approximately 10 days prior to admission. Her most recent tetanus booster had been administered two years earlier. The patient’s physical exam was unremarkable other than increased reflexes throughout all muscle groups and trace nystagmus; the sole of the left foot revealed a healing puncture wound without erythema or exudate. Laboratory data (complete blood count, comprehensive metabolic profile, urinalysis, partial thromboplastin time, and international normalized ratio) were within normal limits. X-ray of the chest and left foot were normal. ECG was normal. Strychnine levels (which arrived after her discharge) were undetectable. Vital capacity measurements were within normal limits. Ms. D was diagnosed with tetanus.
1. Incidence and risk factors
Tetanus was recognized more than 2,500 years ago and described by Hippocrates. An antitoxin was developed in the late 1800s, and passive tetanus immunization was used by the U.S. military during World War I, with active immunization development during World War II. The success of these immunizations within the military paved the way for similar programs within the general population.1
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Thanks to immunization, tetanus is essentially a preventable disease. Five vaccines are recommended for children younger than age 7 years, with tetanus booster recommendations every 10 years for adolescents and adults. All 50 states require children to be immunized prior to entering school.2
Tetanus incidence worldwide is estimated at one million annually.1 Incidence in the United States from 1998 to 2000 was 43 annually; adults older than age 60 years are at greatest risk, with mortality rates around 10%.3 In 2007, 28 cases of tetanus were reported by the CDC.4
2. Pathogenesis
Tetanus is caused by the gram-positive bacillus Clostridium tetani (Figure 1). Spores are dormant in the soil and feces of mammals and can enter via broken skin (especially through deep puncture wounds).5 Other at-risk abrasions or lacerations may include burns, simple splinters or corneal abrasions, tattoos or body piercings, injection drug usage, dental work,6 or surgical procedures;7 diabetic insufficiency vascular ulcers are also susceptible to tetanus.6 Germination can occur under anaerobic conditions, especially in necrotic and/or poorly vascularized tissues, and produce potent neurotoxins.5 The neurotoxins inhibit neurotransmitters, causing spasms, rigidity, and unopposed muscular contractions.8 The neurotoxin tetanospasmin attacks the nervous system, accelerating the motor neurons and leading to uncontrolled muscle contractions and rigidity.9
The three types of tetanus infections are local, generalized (the most common), and cephalic. Local tetanus causes symptoms at the point of entry with muscle rigidity (which can resolve without any systemic signs or symptoms).10 Local tetanus, including symptoms of jaw stiffness and muscle rigidity, can precede generalized tetanus. Cephalic tetanus, while rare, is associated with a previous head injury or otitis media. Symptoms begin with cranial nerve abnormalities and may progress to generalized tetanus.8
Tetanus incubation is 3-21 days.2 Shorter incubation periods correlate with poorer prognosis and higher risk for death. Short nerve pathways of facial muscles are usually affected first.9 Difficulty chewing, dysphasia, neck pain, and spasms may be the earliest symptoms.8 Risus sardonicus, facial muscle spasms resulting in a fixed smile and raised eyebrows, is a classic sign of tetanus.2 Duration and severity of spasms may result in fractures of long bones or spinal vertebrae.6 As the autonomic nervous system becomes involved, catecholamines can produce BP fluctuation, fever, arrhythmias, and diaphoresis.8 Most patients remain awake and alert throughout the illness.9