Chapter 94. Tetanus and Rabies

Tetanus is an acute, frequently fatal spasmodic disease resulting from a wound infected with the organism Clostridium tetani. The disease is exotoxin mediated. In the United States, 69% of Americans > 70 years old not have adequate immunity. The incidence has increased in the 20 to 59 years old.

Clinical Features

As a result of an injury, C. tetani and its spores are introduced into the wound. Devitalized tissue, if any, favors toxin formation. The incubation varies from 24 hours to more than 30 days. The spores can germinate and release the toxin. Most injuries are unrecognized, and vary from puncture wounds, surgical procedures, abortions, or in neonates because of inadequate umbilical cord care. Clinically, tetanus is categorized into 4 forms: local, generalized, cephalic, and neonatal.

Local tetanus presents with rigidity of muscles in proximity to the injury site and usually resolves without sequelae. Generalized tetanus is the most common and presents with pain and stiffness in the jaw. Later, the rigidity leads to the development of trismus and the characteristic facial expression, risus sardonicus, “sarcastic grimace.” Violent spasms and tonic contractions of muscle groups are responsible for the symptoms of the disease including dysphagia, opisthotonos, flexing of the arms, fist clenching, and extension of the lower extremities. Importantly, mentation remains normal, unless laryngospasm and chest rigidity cause respiratory compromise.

In the second week of the illness, a hypersympathetic state develops and manifests as tachycardia, hypertension, sweating, and hyperpyrexia, this difficult to manage hyperactivity contributes to the morbidity and mortality.

Cephalic tetanus follows injuries to the head and neck, can result in dysfunction of cranial nerves, most often the seventh nerve, it has a poor prognosis.

Neonatal tetanus carries an extremely high mortality rate and results from inadequate maternal immunization and poor umbilical cord care.

Diagnosis and Differential

Tetanus is diagnosed clinically. Prior immunization does not eliminate tetanus as a diagnostic possibility. There are not any confirmatory laboratory tests. The differential diagnosis includes strychnine poisoning, dystonic reactions to phenothiazine, hypocalcemic tetany, rabies, peritonsillar abscess, peritonitis, meningitis, SAH and TMJ disease.

Emergency Department Care and Disposition

Patients with tetanus are best managed in an intensive care unit due to the potential for respiratory compromise. Environmental stimuli must be minimized to prevent precipitation of convulsive spasms. Identification and debridement of the inciting wound and devitalized tissue, after immune globulin administration, is necessary to minimize further toxin production.

1. Tetanus immune globulin 3000 to 6000 units IM in a single injection should be given, in the opposite site of the toxoid administration. It should be given before any wound debridement because more exotoxin may be released during wound manipulation.

2. Tetanus toxoid (DTap or Td depending on age), 0.5 mL IM at presentation, and 6 weeks and 6 months after presentation (see Chapter 16).

3. Antibiotics are of questionable value in the treatment of tetanus. If warranted, parenteral metronidazole 500 milligrams IV every 6 hours is the antibiotic of choice. Penicillin is contraindicated because it may potentiate the effects of tetanospasmin.

4. Midazolam, 0.05 to 0.15 milligram/kilogram/h IV given as a continuous drip to effect. Often, large quantities of sedatives are needed and, the Glycol vehicle found in diazepam and lorazepam may cause a metabolic acidosis. Midazolam lacks the Glycol, making it the drug of choice. Lorazepam 2 milligrams IV to effect, may be used in small quantities.

5. Neuromuscular blockade may be required to control ventilation and muscular spasm and to prevent fractures and rhabdomyolysis. In such cases, vecuronium initial bolus of 0.1 milligram/kilogram IV followed infusion at 1 microgram/kilogram/min is the agent of choice. Sedation during neuromuscular blockade is mandatory.

6. The combined α- and β-adrenergic blocking agent, labetalol 0.25 to 1 milligram/min continuous IV infusion (0.3 to 1 milligram/kilogram/h in children), has been used to treat the manifestation of sympathetic hyperactivity. Magnesium sulfate 70 milligrams/kilogram loading, then 1 to 4 grams/h IV has been advocated as a treatment for this condition. Morphine sulfate 0.5 to 1 milligram/kilogram/h is also useful and provides sympathetic control without compromising cardiac output. Clonidine 300 micrograms every 8 hours nasogastrically, an α-receptor agonist, may be helpful in the management of cardiovascular instability.

7. Patients who recover from clinical tetanus must undergo active immunization (see Chapter 16 for immunization schedule).

Rabies, a form of encephalitis, is commonly fatal and is transmitted by a viral inoculation from infected animal saliva. Most emergency physicians never encounter clinical rabies, yet must decide on the need for post exposure prophylaxis on a regular basis.

In the United States, dog and cat bites, and exposure to bats are the most common reason for postexposure prophylaxis. The most important source of active rabies is wildlife transmission. Animal bites contracted outside the United States should be considered at high risk for rabies transmission.

High risk rabid wildlife species include bats, skunks, raccoons, cows, dogs, foxes, and cats. Rodents (squirrels, chipmunks, rats, mice, etc) and lagomorphs (rabbits, hares, hamsters etc.) are at very low risk for rabies transmission. Most rabid animals are agitated and cause unprovocued attacks. In the United States, one-third cases are diagnosed postmortem since, the exposure is not often reported.

Human rabies has decreased in the United States. In 60% of the cases in the 1980s, a source of infection was not identified. After inoculation, the virus remains in the wound vicinity for up to 90 days, then ascends to the CNS and spinal cord to replicate. The Incubation averages 35 to 64 days; periods as short as 12 days or as long as 700 days have been reported.

Clinical Features

The initial symptoms of human rabies are nonspecific and last 1 to 4 days: fever, malaise, headache, anorexia, nausea, sore throat, cough, and pain, or paresthesia at the bite site (80%). Subsequently, central nervous system involvement becomes apparent with restlessness and agitation, altered mental status, painful bulbar and peripheral muscular spasms, opisthotonos, and bulbar or focal motor paresis. Alternatively, in 20%, an ascending, symmetric, flaccid, and areflexic paralysis, comparable to the Landry-Guillain-Barré syndrome, may be seen. Hypersensitivity to sensory stimuli and hydrophobia may occur at this stage, with the latter resulting from the sight, sound, swallowing, or even mention of water. Progressively lucid and confused intervals may become interspersed, cholinergic abnormalities may manifest (hyperpyrexia, mydriasis, and increased lacrimation and salivation), and brainstem dysfunction (dysphagia, optic neuritis, and facial palsies) with hyperreflexia may occur. Extensor plantar responses may be positive. Common complications include adult respiratory distress syndrome, diabetes insipidus, syndrome of inappropriate secretion of antidiuretic hormone, hypovolemia, electrolyte abnormalities, pneumonia, and cardiogenic shock with hypotension and dysrhythmia from rabies myocarditis. Coma, convulsions, and apnea are the final manifestations of rabid death.

Diagnosis and Differential

The diagnosis of rabies in the emergency department is clinical. A final diagnosis is made by postmortem analysis of brain tissue. Cerebrospinal fluid and serum antibody titers should be sent to a laboratory skilled in rabies antibody analysis. Elevated cerebrospinal fluid protein and a mononuclear pleocytosis are also seen.

The differential diagnosis includes viral or other infectious encephalitis, polio, tetanus, viral encephalitis, meningitis, CVA, brain abscess, septic cavernous sinus thrombosis, cholinergic poisoning, and the Landry-Guillain-Barré syndrome. The diagnosis is especially difficult without history of exposure but should be considered for patients with a picture of progressive and unexplained encephalitis.

Emergency Department Care and Disposition

The treatment of rabies exposure consists of assessment of risk of rabies, public health and animal control notification, and, if warranted, the administration of specific immunobiological products to protect against rabies.

Remember to call public health officials for advice and guidance as needed.

1. Debridement of devitalized tissue, if any, is important in reducing the viral inoculum. Wounds of special concern should not be sutured because this promotes rabies virus replication.

2. Tetanus should always be considered and primary or reimmunization prophylaxis should be administered (see Chapter 16).

3. In cases of bites by bats, skunks, raccoons, foxes, and most other carnivores, administer Human Rabies Immune Globulin and start the rabies vaccine series (see below).

4. Bats are a special case. It is currently recommended to consider postexposure prophylaxis for persons who were in the same room as a bat and who might be unaware that a bite or direct contact had occurred (asleep or intoxicated). If the bat can be caught and tested by local/state animal control, prophylaxis can be stopped if tests are negative.

5. If the bite was due to domestic dogs, cats, or ferrets with normal behavior the animal should be quarantined for 10 days, which is sufficient for the disease to manifest if the animal is infected. If no signs become apparent, the animal can be considered nonrabid.

6. In cases of livestock, small rodents, lagomorphs (rabbits and hares) large rodents (wood chucks and beavers) and other mammals, consultation should be immediately obtained from local health department officials. If any cases of rabies have been reported or suspected in these animals locally, administer postexposure prophylaxis. If the animal can be captured, it should be sacrificed and tested. In many of these cases, postexposure prophylaxis is initiated and stopped if testing is negative.

7. Human rabies immune globulin (HRIG) is administered only once at the outset of therapy or even up to the seventh day. The dose is 20 IU/kg, with half of the dose or more (based on tissue volume constraints) infiltrated locally at the exposure site and the remainder administered intramuscularly. Do not administer the HRIG and vaccine in the same anatomic site.

8. Human diploid cell vaccine (HDCV) and Purified chick embryo cell culture vaccine (PCEV), both are for active immunization. The HDCV or PCEV can be administered intramuscularly in 41 mL doses on days 0, 3, 7, and 14 (the formerly recommended day 28 dose has been dropped). Serum sickness reactions have not been reported with PCEV.

9. In adults and children, HRIG and HDCV or PCEV should be administered in the deltoid muscle to avoid failure.

10. State or local officials should be consulted regarding the possibility of rabies in local animal populations before decisions on initiating rabies prophylaxis are made. This action may not be possible before the first treatment but may affect subsequent treatments. Animal bites should be reported to the local animal control unit or police department so that the animal can be quarantined for observation.

11. The Centers for Disease Control and state or county health departments can provide assistance in the management of complications. The most current information available on the rabies home page is produced and updated regularly by the Centers for Disease Control at www.cdc.gov/rabies/.