Tetanus

INTRODUCTION AND EPIDEMIOLOGY

Tetanus is uncommon in the United States but continues to have a substantial health impact in developing countries. The worldwide incidence of tetanus is approximately 1 million cases per year, with a mortality rate of 20% to 30%.¹

The Centers for Disease Control and Prevention defines tetanus as a syndrome of acute onset of hypertonia and/or painful muscular contractions (usually of the muscles of the jaw and neck) and generalized muscle spasms without other apparent medical cause as reported by a health professional.² In the United States, tetanus is a reporTable disease, aggregated through the National Notifiable Diseases Surveillance System.

Improved childbirth practices, widespread immunization programs for children, decennial tetanus boosters for adults, mechanization of agriculture, and use of chemical fertilizers rather than animal manure have resulted in a >95% decline in the annual incidence of tetanus in the United States since 1947.² From 2001 to 2008, 233 tetanus cases were reported in the United States from 45 states, with the majority of cases reported from five states: California (n = 60), Florida (n = 25), Texas (n = 12), New York (n = 12), and Pennsylvania (n = 11).² Most patients who develop tetanus have inadequate immunity to the disease. Due to waning immunity and failure to receive routine boosters, only 31% of Americans >70 years old have adequate tetanus immunity.³ As a result, the average annual incidence of tetanus among those ≥65 years of age is higher (0.23 cases per 1 million population) than among those age 5 to 64 years (0.08 cases per 1 million population). Tetanus among children and neonatal tetanus are uncommon in the United States as well as in other developed countries. The case fatality rate is approximately 13%, with the elderly accounting for the majority of deaths.²

Most cases of tetanus in the United States are associated with an acute wound. Puncture, contaminated, infected, or devitalized wounds account for approximately 70% of tetanus cases. Although less common, chronic wounds, ulcers and other wounds in diabetics, and dental abscesses are also associated with the disease. Diabetics and injection drug users have an increased risk of contracting tetanus.^2,4

Most patients who develop tetanus do not seek medical care for their initial wound. In those who do seek initial treatment and later develop tetanus, up to 95% do not receive appropriate therapy.²

PATHOPHYSIOLOGY

Clostridium tetani is a motile, nonencapsulated, anaerobic gram-positive rod, and its toxins cause tetanus. C. tetani exists in either a vegetative or a spore-forming state. The spores are ubiquitous in soil and in animal feces and are resistant to destruction, surviving on environmental surfaces for years. In agricultural areas, adults may harbor the organism, and spores have been found on skin or in contaminated heroin.^4,5 C. tetani is usually introduced into a wound in the spore-forming, noninvasive state but can germinate into a toxin-producing, vegetative form if tissue oxygen tension is reduced. Crushed or devitalized tissue, a foreign body, or the development of infection favors the growth of the toxin-producing form of C. tetani.^5,6

C. tetani produces two exotoxins: tetanolysin, which appears to favor the expansion of the bacterial population, and tetanospasmin, a powerful neurotoxin responsible for all of the clinical manifestations of tetanus. Tetanospasmin reaches the nervous system by hematogenous spread of the exotoxin to peripheral nerves and by retrograde intraneuronal transport. Tetanospasmin does not cross the blood–brain barrier, but retrograde intraneuronal transport of the exotoxin enables tetanospasmin to gain access to the CNS.⁶

Tetanospasmin prevents the release of the inhibitory neurotransmitters glycine and γ-aminobutyric acid from presynaptic nerve terminals, releasing the nervous system from its normal inhibitory control. Loss of inhibition may also affect the preganglionic sympathetic neurons, resulting in sympathetic overactivity and high circulating catecholamine levels.^5,6,7,8

CLINICAL FEATURES

Tetanus results in generalized muscular rigidity, violent muscular contractions, and autonomic nervous system instability.⁶ Wounds that become contaminated with toxin-producing C. tetani are often puncture wounds, but contaminated wounds range from deep lacerations to minor abrasions.² No wound is identified in up to 10% of patients with tetanus. Tetanus can also develop after surgical procedures, otitis media, or abortion and can develop in injection drug users from contaminated heroin and in neonates through infection of the umbilical stump.^4,9

The incubation period for tetanus ranges from <24 hours to >1 month. Short incubation periods are associated with severe disease and a poor prognosis for recovery. Clinical tetanus can be categorized into three forms: generalized, cephalic, and local. Generalized tetanus accounts for about 80% of cases. The most frequent presenting complaints of patients with generalized tetanus are pain and stiffness in the masseter muscles (lockjaw). Nerves with short axons are affected initially, so symptoms appear first in the facial muscles, with descending progression to the muscles of the neck, trunk, and extremities. The transition from muscle stiffness to rigidity leads to the development of trismus and the characteristic facial expression: risus sardonicus (sardonic smile). Reflex convulsive spasms and tonic muscle contractions are responsible for the development of dysphagia, opisthotonos flexing of the arms, clenching of the fists, and extension of the lower extremities. Spasms can last for 3 to 4 weeks, and recovery depends on regrowth of axonal nerve terminals and may take months.⁶ Complications of tetanus include rhabdomyolysis and long-bone fractures secondary to violent muscle contractions. The mental status is normal, an important consideration in differentiating tetanus from other disorders (Table 156-1). Patients remain conscious and alert unless laryngospasm or contraction of respiratory muscles results in respiratory compromise. Other complications of prolonged hospitalization include pulmonary embolus, pneumonia, and sepsis. Aspiration pneumonia is present in 50% to 70% of autopsied cases.^5,6

TABLE 156-1 Differential Diagnosis of Tetanus

Disorder	Comments
Strychnine poisoning	See chapter 201, “Pesticides.”
Dystonic reaction (phenothiazines, metoclopramide)	See chapter 180, “Antipsychotics.”
Hypocalcemic tetany	See chapter 17, “Fluids and Electrolytes.”
Malignant neuroleptic syndrome	See chapter 180, “Antipsychotics.”
Serotonin syndrome	See chapter 178, “Atypical and Serotonergic Antidepressants”
Stiff man syndrome	Centrally mediated motor hyperexcitability with persistent and intense spasms, particularly of the proximal lower limbs and lumbar paraspinal muscles.
Peritonsillar abscess	See chapter 246, “Neck and Upper Airway.”
Peritonitis	See chapter 71, “Acute Abdominal Pain.”
Meningeal irritation (bacterial meningitis, subarachnoid hemorrhage)	See chapters 174, “Central Nervous System and Spinal Infections” and 166, “Spontaneous Subarachnoid and Intracerebral Hemorrhage.”
Rabies	See chapter 157, “Rabies.”
Temporomandibular joint disease	See chapter 243, “Face and Jaw Emergencies.”

Autonomic changes are generally a hypersympathetic state, occurring during the second week of clinical tetanus and including tachycardia, labile hypertension, profuse sweating, hyperpyrexia, and increased urinary excretion of catecholamines.^6,7,8 Neonatal tetanus

Only gold members can continue reading. Log In or Register to continue