DR (MRS) M.B. FETUGA1 TETANUS. 2 Tetanus is an acute, often fatal, disease caused by an exotoxin...

DR (MRS) M.B. FETUGA 1

TETANUS


• Tetanus is an acute, often fatal, disease caused by an exotoxin produced by Clostridium tetani.

• It is a disease from which no age is immune. Mortality is typically highest at the extremes of life.

• Natural immunity to tetanus is not known.


CLOSTRIDIUM TETANI

• Clostridium tetani is a slender, gram-positive, anaerobic rod that may develop a terminal spore, giving it a drumstick appearance.

• Sensitive to heat and cannot survive in the presence of oxygen while the spores, in contrast, are very resistant to heat and the usual antiseptics.

• Spores are widely distributed in soil, intestine and feces of horses, sheep, cattle, dogs, cats, rats, guinea pigs, and chickens. Manure-treated soil may contain large numbers of spores.


• Clostridium tetani produces two exotoxins, tetanolysin and tetanospasmin. The function of tetanolysin is not known with certainty in man. Tetanospasmin is a neurotoxin and causes the clinical manifestations of tetanus.

• Tetanospasmin is one of the most potent toxins known on a weight basis. The estimated minimum human lethal dose is 2.5 nanograms per kilogram of body weight which is far smaller than the dose required to stimulate immunity. This is why tetanus does not confer immunity.


OCCURRENCE

• Occurrence is worldwide, but it is most prevalent in the developing world: densely populated, hot, damp climates with soil rich in organic matter.

• Transmission is via contaminated penetrating wounds (apparent and in-apparent).

• Tetanus may follow elective surgery, burns, ear piercing, crush wounds, otitis media especially with profuse discharges, dental infection, animal bites, abortion, and pregnancy deep penetrating wounds.

• In the NB- umbilical cord- cutting , tying, dressing


OCCURRENCE

• Tetanus is not contagious - it is the only vaccine-preventable disease that is infectious, but not contagious.


PATHOGENESIS 1• C. tetani usually enters the body through a wound.

Toxins are produced and disseminated via blood and lymphatics.

• Sometimes, the vegetative forms of the microbe are destroyed but the spores are left behind in the wound.

• In the presence of anaerobic (low oxygen) conditions, the spores germinate into the vegetative forms which in turn produce the toxins.

• Tetanospasmin, a zinc metalloprotease, is released in the wound and binds to the peripheral motor neuron terminal, enters the axon, and via retrograde intraneuronal transport, reaches the nerve cell body in the brainstem and spinal cord.


PATHOGENESIS 2

• The toxin migrates across the synapse to presynaptic terminals where it blocks the release of the inhibitory neurotransmitters glycine and gamma-aminobutyric acid (GABA). This diminished inhibition results in an increase in the resting firing rate of the motor neuron, and this is responsible for the observed muscle rigidity and unopposed muscle contraction and spasm.


PATHOGENESIS 3

• Localized tetanus occurs when only the nerves supplying the affected muscle are involved.

• Generalized tetanus occurs when the toxin released at the wound spreads through the lymphatics and blood to multiple nerve terminals. The blood-brain barrier prevents direct entry of toxin to the central nervous system (CNS).


CLINICAL FEATURES

• IP varies from 3 to 21 days, usually about 8 days.

• Period of onset refers to the interval between the first symptom and the first spasm.

• The further the injury site is from the central nervous system, the longer the incubation period.

• Consciousness is usually preserved in tetanus.


CLINICAL TYPES OF TETANUS

Local tetanus is an uncommon form of the disease, in which patients have persistent contraction of muscles in the same anatomic area as the injury.

Cephalic tetanus is a rare form of the disease, occasionally occurring with otitis media or following injuries to the head. There is involvement of the cranial nerves, especially in the facial area.


CLINICAL TYPES OF TETANUS

Generalized tetanus is the most common type (about 80%) of the disease. The disease usually presents with a descending pattern. The hallmark is generalized spasms. Spasms may occur frequently and last for several minutes. Spasms continue for 3–4 weeks and rigidity may persist for up to 6 weeks. Complete recovery may take months.


CLINICAL PRESENTATION• SYMPTOMS – Diagnosis is clinical Fever Excessive sweating Inability to open the mouth Involuntary muscular movements (Spasms)• SIGNS Trismus-lock jaw (rigidity of masseter muscles) Risus sardonicus (facial) Neck stiffness Spasms – painful with no loss of consciousness Opisthotonus- (rigidity of extensor muscles dominate) Board-like abdominal rigidity Hypertension Tachycardia


COMPLICATIONS

• Laryngospasm and spasm of respiratory muscles leads to difficulty with breathing. Hyperpyrexia.

• Fractures of the spine or long bones may result from sustained contractions.

• Hyperactivity of the autonomic nervous system may lead to hypertension and cardiac arrhythmia.

• Nosocomial infections particularly septicaemia. • Aspiration pneumonia. • Rhabdomyolysis with the risk of acute tubular necrosis.• Pulmonary emboli.• Gastric dilatation and paralytic ileus.


DIFFERENTIAL DIAGNOSIS

• Rabies.• Pharyngitis.• Encephalitis.• Meningitis.• Dystonic drug reactions.• Strychnine poisoning.


PROGNOSIS

• Worse with decreasing age, short IP,

short period of onset, increasing frequency & duration of spasms,presence of autonomic dysfunction.

• Worse if the portal of entry is not easily accessible eg. deep penetrating wound.

• Worse in the presence of other invasive diseases like pneumonia and septicaemia.

• Improves with quality of nursing care


MANAGEMENT 1

• The principle of management include the following: (1) Supportive management to ensure adequate fluid and caloric intake and stability of vital signs. (2) Neutralization of tetanospasmin (3) Eradication of C. tetani with antibiotics. (4) Control of spasms.

• All wounds should be thoroughly cleaned. Necrotic tissue and foreign material should be removed.

• Patient should be nursed in a dark, quiet place with minimal disturbances. Injections should be minimized. If tetanic spasms are occurring, maintenance of an adequate airway is critical. Tracheostomy may be life saving.


MANAGEMENT 2

• Anti-tetanus serum (5,000 – 10, 000 units intramuscularly) neutralizes the toxins in circulation. It should be given only after a non-reactive test dose. The human form of tetanus immune globulin (3,000 – 6,000units) is preferable but not available in most places in the developing world.

• Active immunization with tetanus toxoid (0.5mL) should begin or continue as soon as the person’s condition has stabilized.


MANAGEMENT 3

• Penicillin is the drug of choice in tetanus hence it can be given as 200, 000u/ kg of Penicillin G in 4 divided doses for 5 days. The macrolides (Erythromycin, Azithromycin etc) and metronidazole may also be used. When septicaemia is suspected, Gentamicin (5 mg/kg) should be added to Penicillin pending laboratory sensitivity report.

• Control of spasms with sedation is the mainstay of treatment. A combination of Phenobarbitone (1mg/kg/dose 6 hourly), Diazepam (0.2 – 0.5mg/kg/dose 6 hourly) and Chlorpromazine (1mg/kg/dose 6 hourly) are used for synergistic maximal effect.


MANAGEMENT 4

• With severe spasms, Curarization with mechanical ventilation can be done.

• Tetanus disease does not confer immunity because of the very small amount of toxin required to produce illness. Persons recovering from tetanus should begin or complete active immunization with tetanus toxoid (Td) during convalescence.


PREVENTION 1

• Three doses of the triple vaccine DPT is recommended within the first 14 weeks of life (6, 10 and 14 weeks).

• Five booster doses of 0.5mL tetanus toxoid are recommended for all women in the reproductive age group (at first contact, 4 weeks later, at least 6 months after the 2nd dose, at least 1 year after the 3rd dose and at least 1 year after the 4th dose).


PREVENTION 2• Booster doses are also recommended when injuries

are sustained under circumstances that may encourage infection with C. tetani.

• Persons with dirty wounds:1) those who had taken tetanus toxoid in the

preceding 5 years need no booster dose of tetanus toxoid;

2) those with history of tetanus toxoid administration between the last 5 and 10 years, a single booster dose of tetanus toxoid is recommended;

3) those who have not taken tetanus toxoid within the last 10 years, a combination of tetanus toxoid and Anti-tetanus Serum should be given (on different sites).

DR (MRS) M.B. FETUGA1 TETANUS. 2 Tetanus is an acute, often fatal, disease caused by an exotoxin...

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