TetanusMuhammad Asim

Rana MBBS, MRCP, SF-CCM, EDIC,

FCCPDepartment of Critical Care

Medicine King Saud Medical City

Riyadh, KSA

INTRODUCTION Nervous system disorder

characterized by muscle spasms Caused by the toxin-producing

anaerobe, Clostridium tetani. Four clinical patterns

Generalized Local Cephalic Neonatal

EPIDEMIOLOGY

Developed countries 0.16 cases/million population Developing countries approximately 1,000,000 cases of

tetanus are estimated to occur worldwide each year with 200,000 to 300,000 deaths

Neonatal tetanus, accounted for 180,000 deaths in the year 2002

PATHOGENESIS  Spores of Clostridium tetani, an

obligate anaerobe After inoculation, C. tetani

transforms into a vegetative rod-shaped bacterium and produce the metalloprotease, tetanospasmin (also known as tetanus toxin).

After reaching the spinal cord and brain stem via retrograde axonal transport and binding tightly and irreversibly to receptors at these sites

tetanus toxin blocks neurotransmission by its cleaving action on membrane proteins involved in neuroexocytosis.

The net effect is disinhibition of neurons that modulate excitatory impulses from the motor cortex.

Disinhibition of anterior horn cells and autonomic neurons result in increased muscle tone, painful spasms, and widespread autonomic instability

Adrenal malfunction Lack of neural control of adrenal

release of catecholamines induced by tetanus toxin produces a hypersympathetic state that manifests as

sweating, tachycardia andhypertension.

Muscular rigidity increase in the resting firing rate of

disinhibited motor neurons and lack of inhibition of reflex motor responses to afferent sensory stimuli

Remember Tetanus toxin-induced effects on

anterior horns cells, the brain stem, and autonomic neurons last are long-lasting because recovery requires the growth of new axonal nerve terminals.

Tetanolysin is another toxin produced by C. tetani during its early growth phase. It has hemolytic properties and causes membrane damage in other cells, but its role in clinical tetanus is uncertain.

Predisposing factors (C. tetani will not grow in healthy tissues,

a convergence of factors must be present in order for tetanus toxin to be elaborated in the human host.)

A penetrating injury resulting in the inoculation of C. tetani spores

Co-infection with other bacteria Devitalized tissue A foreign body Localized ischemia

These predisposing factors can also explain why tetanus can develop in unusual clinical

settings such as in: Neonates (due to infection of the

umbilical stump) Obstetric patients (after septic abortions) Postsurgical patients (with necrotic

infections involving bowel flora) Patients with dental infections Diabetic patients with infected extremity

ulcers Patients who inject illicit and/or

contaminated drugs

CLINICAL FEATURES Incubation period The incubation period of tetanus can

be as short as one to three days or as long as several months, with a median of 7 to 8 days (range 0 to 112 days in one report) Inoculation of spores in body locations

distant from the central nervous system (eg, the hands or feet) results in a longer incubation period than inoculation close to the central nervous system (eg, the head or neck).

Generalized tetanus  Trismus (lockjaw) symptoms of autonomic overactivity

irritability restlessness sweating tachycardia cardiac arrhythmias labile hypertension hypotension, fever

Stiff neck Opisthotonus Risus sardonicus (sardonic smile) A board-like rigid abdomen Periods of apnea due to vise-like

contraction of the thoracic muscles and/or glottal or pharyngeal muscle contraction

Dysphagia

Cephalic tetanus  injuries to the head or neck involving initially only cranial nerves may manifest confusing clinical

findings including dysphagia, trismus and focal cranial neuropathies

facial nerve is most commonly in cephalic tetanus, but involvement of cranial nerves VI, III, IV, and XII may also occur either alone or in combination with others

Neonatal tetanus infants within 14 days following birth

Local tetanus tonic and spastic muscle contractions in one

extremity or body region  

Severity of illness the amount of tetanus toxin that

reaches the CNS to the incubation period of the illness the interval from the onset of symptoms

to the appearance of spasms the longer the interval, the milder the

clinical features of tetanus.

DIFFERENTIAL DIAGNOSIS  Drug-induced dystonias such as

those due to phenothiazines  Trismus due to dental infection Strychnine poisoning due to

ingestion of rat poison Malignant neuroleptic syndrome Stiff-man syndrome

TREATMENT The goals of treatment include:

Halting the toxin production Neutralization of the unbound toxin Control of muscle spasms Management of dysautonomia General supportive management

Halting toxin production

Wound management Antimicrobial therapy Penicillin G cefazolin, cefuroxime, or ceftriaxone Metronidazole

Neutralization of unbound toxin

Since tetanus toxin is irreversibly bound to tissues, only unbound toxin is available for neutralization.

Human tetanus immune globulin (HTIG) should be readily available and is the preparation of choice. A dose of 3000 to 6000 units intramuscularly should be given as soon as the diagnosis of tetanus is considered.

Intrathecal administration of tetanus immune globulin is of unproven benefit.

Where HTIG is not readily available, equine antitoxin is used in doses of 1500 to 3000 units intramuscularly or intravenously in order to achieve a serum concentration of 0.1 IU/mL

The use of pooled intravenous immune globulin (IVIG) has been proposed as a possible alternative to HTIG.

Active immunization does not confer immunity following

recovery from acute illness ALL patients with tetanus should

receive active immunization with a total of three doses of tetanus and diphtheria toxoid spaced at least two weeks apart, commencing immediately upon diagnosis

Subsequent tetanus doses, in the form of Td, should be given at 10-year intervals throughout adulthood.

Control of muscle spasms 

Generalized muscle spasms are life-threatening

respiratory failure lead to aspiration induce generalized exhaustion in the patient.

Drugs used to control spasm Sedatives Neuromuscular blocking agents  Propofol Intrathecal Baclofen

Management of autonomic dysfunction

Beta blockade Labetalol (0.25 to 1.0 mg/min) has frequently

been administered because of its dual alpha and beta blocking properties.  

Morphine sulphate (0.5 to 1.0 mg/kg per hour by continuous

intravenous infusion) is commonly used to control autonomic dysfunction as well as to induce sedation  

Magnesium sulfate acts as a presynaptic neuromuscular blocker, blocks

catecholamine release from nerves, and reduces receptor responsiveness to catecholamines

Other drugs — Other drugs for the treatment of various autonomic events, which have been reported to be useful, are: atropine, clonidine and epidural bupivacaine.

Supportive care  In patients with severe tetanus, prolonged

immobility in the intensive care unit is common

Such patients are predisposed to nosocomial infection decubitus ulcers tracheal stenosis gastrointestinal hemorrhage thromboembolic disease.

PROGNOSIS  Case-fatality rates for non-neonatal

tetanus in developing countries range from 8 to 50 percent, while the majority of patients with tetanus recover when modern supportive care is available.

Neonatal tetanus, once nearly always fatal, now has mortality rates of 10 to 60 percent

Thank you