UNDERSTANDING TETANUS

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INTRODUCTION
Tetanus is a non contagious and preventable medical condition characterized by prolonged contraction of skeletal muscles. The name was actually derived from 2 Greek words: ‘tetanos‘ and ‘teinien‘ meaning ‘taut’ and ‘stretch’ respectively. It has been dated as far back as the ancient days when people started to recognise that there was a relashionship between wounds and deadly muscle spasms, and continue to live in fear of this condition whenever a person sustains injuries/wounds especially deep cuts and puncture wounds.
It occurs when a wound is contaminated with the spores of a bacteria called Clostridium tetani (C.tetani).
Tetanus affects all the skeletal (striated) muscles used in voluntary movement of the body except the heart muscles. Though it is striated alright, but it can not be tetanized because it has its own (intrinsic) electrical properties and is capable of producing its own contactions without nerve stimulations.
The breakthrough finally came in 1924 when Descombey developed the tetanus toxoid vaccine that was widely used during the 2nd world war, to prevent the disease through battle wounds.

tet1 Adult tetanus with facial spasms

INCIDENCE
WHO estimated that 59000 newborns worldwide (more in developing world) died in 2008 from neonatal tetanus! Oh yes, it is true. Neonates who do not acquire a passive immunity from their mothers are particularly at risk.
Because of the ubiquitous (widely distributed) nature of the spores of C.tetani, tetanus is a worldwide problem but most prevalent in hot damp/humid climate with soil rich in organic matter, especially with manure (from human and animal faeces) treated soils. This is because spores are present in the intestine as well as the skin surfaces of humans and animals!
Farmers are at risk!
Drug (especially heroin) abusers who inject the drugs are at high risk of contracting tetanus.

CAUSE (AETIOLOGY)
Tetanus is caused by 2 toxins of Clostridium tetani, a rod shaped, spore forming, obligate, gram negative anaerobe.
The infective stage is the spore, which transforms into the rod shaped bacterium following entry into the tissues, and produce the toxins.
The toxins are tetanospasmin and tetanolysin.

TYPES
1. Generalized tetanus ~ the most common type of tetanus seen in about 80% of the cases and shows the typical clinical features (symptoms and signs) of tetanus.
2. Localized tetanus ~ this type is seen in newborn babies who have not acquired passive immunity from their unimmunized mothers. Highest in this group are those found in rural communities who practise unhealthy cultural/traditional treatments such as cutting the umbilicus with dirty/unsterilised sharps or covering the unhealed umbilical stump with animal (cow) dungs.
3. Neonatal tetanus ~ an uncommon form of tatanus where the patient experiences a persistent contraction of musckes in the same anatomical area where the injury is located. It may persist for many weeks before subsiding gradually. Fatal in about 1% of the cases and may precede the onset of generalized tetanus.
4. Cephalic tetanus ~ a rare form of tetanus occasionally following infection of the middle ear (otitis media). This is possible because C.tetani is present in the flora of the middle ear but can also be introduced through piercing injuries or wounds. There is invokvement of the cranial nerves especially in the facial area.

MECHANISM

tet3Involuntary smiles of tetanus (risus sardonicus)
Following the introduction of C.tetani spores into damaged tissues, the spores transform into rod shaped bacteria which produce the neurotoxin responsible for the manifestation of tetanus. Inside the bacteria, the toxin is inactive but when they die, the released toxins are activated by enzymes (proteases) and then enter the nervous system, through the spinal cord to the brain. Active tetanospasmin enters the nerve cells (neurons) and are carried through backward axonal transport to the spinal cord. There, it binds irreversibly to a neurotransmitter (Gamma aminobutyric acid ~ GABA) in the upper neurons and blocks nerve transmission. This also damages the nerve cell and makes it impossible for the upper neurons to inhibit or control reflex responses to afferent sensory stimuli. This in turn, produces muscle rigidity and spasms ~ the hallmark of the disease!
In the same vein, those that enter the nerves of the adrenal gland, also damage them and produce loss of neuronal control of the gland. This leads to uncontrolled release of the catecholamines (adrenaline and noradrenaline) and the resultant hypersympathetic state that is also seen in tetanus.
The function of tetanolysin is unclear but some authorities postulated that it is responsible for cell breakdown (lysis) especially the polymorphonuclear cells and release of cytokines (unverified).
Incubation period is between 8 days and several months but the farther away the site of the injury is from the central nervious system, the longer the incubation period. The shorter the incubation period, the more severe the disease.
In neonates, symptoms usually appear between 4 and 14 days with an average of 7 days, after birth.

SYMPTOMS AND SIGNS
The first symptom/sign of tetanus is the lock jaw (trismus) and involuntary/uncontrolled smiles (risus sardonicus) due to spasms of the facial muscles, followed by neck stiffness, pain on swallowing (odynophagia) and rigidity of the chest (pectoral) and leg (calf) muscles. Spasms may occur frequently and last for several minutes with forward aching of the back while the head is thrown back and the heels extending towards the back, like the letter ‘C’ written in the opposite direction (opisthotonos).
Hypersympathetic state and autonomic instability produce ~ fever, sweating (diaphoresis), elevated blood pressure, intermittent racing of the heart beat (tachycardia), e.t.c.
Spasms may continue uoto 4 weeks and complete recovery may take upto months!

tet2A child with tetanus

DIAGNOSIS
There are currently no blood tests that can be used to diagnose tetanus, so it is based on the clinical presentation of tetanus symptoms.
Diagnosis also does not depend on isolating the organism which is only recovered in about 30% of the wounds and can be isolated in patients who do not have tetanus.
However on physical examination, the spatula test can be done where the posterior pharyngeal wall (the back end of the mouth you see when you open the mouth wide, just behind the uvula) is touched with a soft sterile teat instrument, and then watch the effect. The normal reaction is a gag reflex, but in tetanus patients, there is an involuntary contraction of the jaw and biting down on the spatula. This test has a high specificity and sensisitivity (upto 94% accurate).

TREATMENT
Patients with tetanus should be managed in the intensive care unit (icu) with:
1. Adequate hydration
2. Calorie (for energy)
3. Antibiotics and wound care is done cleaning and dead tissues removed by debridement, and then administering antibiotics e.g. metronidazole. The drug however, has no effect on the toxins already bound to the nerves.
4. Spasm control which is the hallmark of management, is done with: Diazepam infusion (upto 60mg in 1litre of normal saline depending on the frequency of the spasms) and alternating with 5% dextrose in water. This is highly effective not just because it deeply sedates the patient and reduce spasms, it also competes with the neurotoxins for its binding sites in the central nervous system.
Chlorpromazine (another muscle relaxant) can be used to alternate diazepam 3 hourly, in such a way that the patient recieves a muscle relaxant every 3 hours but same drug 6 hourly. Spasm chart is kept to monitor the progression of the disease.
Passive immunization with human anti tetanospasm immunoglobulin (HAIg) or antitetanus serum (ATS) at 20,000iu (10,000 intravenously in 500mls of normal saline and 10,000 intramuscularly) is very important. This helps neutralize and mop up the circulating toxins in the blood, but the ones already bound to the neurons die with the nerve cells. A test dose is first given to the patient to make sure they do not react to it.

TIGHuman tetanus immunoglobulin

Hypersympathetic state and autonomic reflexes may be difficult to manage. Antipyretics may be given for fever, while calcuim channel blockers are drugs of choice the treatment of associated elevated blood pressure. Patient should also be nursed in a cool, quiet room away from light and noises as these may trigger spasms.

PROGNOSIS
This depends on the maintenance of the airway and adequate nutrition during the illness.
Indices of prognosis include;
1. Incubation period, remember we said the shorter the worse.
2. Onset time/ onset interval between the appearance of the first symptom/sign (lock jaw) and development of spasms. Again, the shorter the worse.
3. Frequency of spasms ~ increased frequency of spasms is associated with a poor prognosis.
4. Patients age ~ extremes of age i.e. neonates and the elderly, have a high mortality rate.
5. Injury site ~ the closer to the central nervous system the injury site is, the worse the outcome.

Finally, it is important to note that the disease does not confer immunity to its survivors, therefore, adequate counselling and latient education after is illness is mandatory.
Tetanus can be prevented by proper immuniztion with tetanus toxoid and by post exposure prophylaxis.
For complete immunization, Intramuscular 0.5ml of the toxoid is given thus;
At first contact (time zero)… a month later…6 months later and one year after the last dose. Booster doses can also be given annually.

Written by Dr. JOY OKECHUKWU EBUSSON.

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