Tetanus

Tetanus is a neurologic disorder caused by a toxin (tetanospasmin) elaborated by Clostridium tetani. The point is, the bacteria itself is not the direct cause of the disease, that's why it is useless to do a blood culture because most of the time, you wont find any of the bacteria. Moreover, the toxin (along with botulism) is one of the most powerful and potent toxins in existence. Hence, just a little amount could cause intense disease. Tetanus is different from Tetany. Both have the same root word, "tetanos" which in greek means "to stretch" or to put "tension" (i find etymology of words to be very helful, you should try to generate interest in this boring field. :) However, tetanus is a specific disease caused by a specific etiological agent, C. tetani. Tetany, is non-specific as it is a clinical syndrome characterized not caused by a specific agent, but usually caused by hypocalcemia. Hypocalcemia in turn, can be caused bby many other pathologies and imbalances. EPIDEMIOLOGY: Tetanus almost always affects people who do not have a protective serum anti-toxin level (> .15 U/ml). Which is brought about either because they did not get their primary immunization, or the needed boosters. For instance, tetanus occurs predominantly in neonates and young children, but the risk of development is highest among the elderly. Risk is high in the elderly because most have already low effective serum levels of anti-tetanus immunoglobulins. Key points: tetanus is entirely preventable through immunity, and maintaining an effective serum level is important. Occurrence is probably high in the neonatal and childhood age group because most cases of tetanus follow an acute injury: kids love to injure themselves. Neonates usually get it from inadequately immunized mothers after unsterile treatment of the umbilical cord. PATHOGENESIS CORRELATED WITH CLINICAL MANIFESTATIONS: Most cases of tetanus happen after an acute injury because the C. tetani only germinates and produces

toxins in conditions of low redox potential (no oxygen), examples of which are necrotic tissue, foreign bodies or acute infection (anaerobic nga kasi e). Remember, it is the toxin that is responsible for the pathology and not the bacteria itself. The toxin released binds to peripheral motor neuron terminals and travels up the axon in retrograde fashion to reach the presynaptic terminals in the spinal cord and brainstem. Netter says that it can also disseminate hematogenously, which is plausible, to reach the CNS. But the toxin cannot go into the cortex through the BBB. Subsequently, the toxin then migrates across the pre-synaptic terminal where it blocks the release of inhibitory neurotransmiters: Glycine (spinal cord) and GABA (CNS). Tetany in contrast, is caused by a decreased firing threshold (tetany: easier to fire... tetanus: over firing). The point is, there is diminished inhibition of all that needs to be inhibited. First of all, the resting firing rate of the alpha motor neuron increases. Therefore, instead of the normal resting "tone", it becomes a resting "rigidity", as it were. Secondly, because reflexes that limit the polysynaptic spread of impulses (for instance renshaw cells in the spinal cord secreting glycine as inhibition in agonist-antagonist recruitment), agonists and antagonists can be recruited simultaneously. Spasms occur. At this point, i must mention that the speed of retrograde transport is the same in all nerves, but remember that not all nerves are of the same length. Therefore, shorter nerves, such as those in the axial muscles are affected first. As such, there is a sequential involvement: head, trunk and then proximal extremities. In the head, the patient usually first notices that there is increased tone and spasms in the masseter, which leads to a forcefull apposition of the jaws (open the mouth and you will see the jaws strongly opposed. This is called lock-jaw or Trismus and is usually, but not exclusively associated with tetanus. Rigidity of the proximal muscles (neck, facial muscles, shoulder and back muscles) follow shortly. Sustained contraction of the facial muscles results in

a grimace (risus sardonicus: painfully grinning face secondary to muscle spasm). Neck muscles and probably throat muscles spasm and can cause dysphagia. The abdominal rigidity causes a very stiff and board-like abdomen and the back is arched (opisthonos). The distal extremities are usually spared and mentation is not affected because the toxin does not cross the BBB. Protection of the airway is vital as langrygospasm may occur which reduces ventilation. Thirdly, loss of inhibition may also affect sympathetic outflow from the spinal cord resulting in sympathetic hyperactivity and catecholamine levels. Fourthly, the toxin may also reach the NMJ, producing paralysis. CATEGORIZED CLINICAL MANIFESTATIONS Generalized Tetanus: Most common. 1.) increased muscle tone (rigidity) 2.) generalized spasms. Median onset of 7 days. Severity of illness can be classified as mild (rigidity and a few spasms), moderate (trismus, dysphagia, rigidity and more spasms) severe (frequent and explosive spasms, with I think, all the preceding s/s) Neonatal Tetanus: As mentioned. Onset: first 2 weeks of life. Local tetanus: uncommon, only muscle at local site of infection is affected. Excellent prognosis. Cephalic Tetanus: Rare, often follows cranial injury. Additionally manifesting with cranial nerve defects, often 7th. Mortality high. DIAGNOSIS: Clinical Grounds. DIFFERENTIAL DIAGNOSIS: Local condistions producing trismus such as alveolar abcess (teeth, not lungs), strychnine poisoning, dystonic drug reactions from phenothiazine or metoclopromide, and hypocalcemic tetany. TREATMENT GOALS AND MODALITIES:

1.) Eliminate the source of the toxin [antibiotic therapy]: the vegetative bacteria, c. tetani. C. tetani is a gram positive and anaerobic. Either target the gram positivene factor (penicillin) or the anerobic factor (metronidazole). Metronidazole 500mg is the drug of choice because of better survival rates and absence of atagonistic GABA activity (which penicillin has). The wound should be cleaned and debrided thoroughly, so the bacteria will not replicate further. 2.) Neutralize the unbound toxin: The bound toxin cannot be dealt with, but we must prevent the unbound toxins from causing further damage, thereby lowering mortality. Therefore, give the anti-toxin Tetanus immune globulin (TIB) immediately in 500 unit divided doses (total is 3000-6000), immediately before manipulating the wounds. Equine tetanus antitoxin (TAT) is less preferred because it can cause hypersensitivity and serum sickness. 3.) Control the muscle spasms: because they can cause the dreaded complications, like hypoventilation and apnea. Besides, the spasms are painful. But, we must be careful, because the drugs we may give may over sedate and cause paralysis of the thoracic muscles for ventilation (remember anes?) Give something that abolishes spasmodic activity, without causing oversedation and hypoventilation. Diazepam, is widely used. Lorazepam and Midazolam puwede rin. barbiturates and chlorpromazine 2nd line. Moreover, because the spams may be spontaneous or provoked by the slightest stimulation (even a breeze), the patient should be admitted to a quiet intensive care room, where monitoring can continue and stimulation minimized. 4.) Respiratory Care: Intubation or tracheostomy may be required. Need for paralysis and danger of hypoventilation must be monitored and assessed daily. Autonomic dysfunction when present must be addressed by sympathetic blockers such as labetalol, esmolol, clonidine and morphine. I don't know which is the drug of choice.

PREVENTION: Vaccination is essential because even if a person has already suffered from tetanus, the immunity induced is not enough. Passive immunization with Td has adjuvants and greater amount of antigenic substance than being infected with a potent toxin (small amount--big effect, but not necessarily immunogenic). Last statement is from my thinking, no reference. Primary series: 3 doses. 1st, 2nd: 4-8 weeks apart. 3rd: 6-12 months apart. Booster: Every 10 years. Formulation: is usually coupled with diptheria (Td) because diptheria anti-toxin levels also go down after some time, and it is better to be sure, so give it na rin (Nelson's pedia). Adsorbed vaccine is preferred because it produces more persistent antibody levels. WOUND MANAGEMENT: Table 124-1. memorize. No way around it. Almost sure na itatanong ito. PROGNOSIS: The more acute and fulminant, the worse. Oxygenation lowers mortality from complications. Pictures: neonatal tetanus: opisthonos, extended extremities because of proximal extremity rigidity. High Mortality. Netter Tetanus: The face is risus sardonicus (Sardonic Laughter). the point is the face, not the jaw. Etymology: The greeks believed that eating the plant they called sardonion (a plant from sardinia), caused convulsions in the face causing a grimace resembling those of sardonic laughter. A sardonic laughter is a scornful laughter, like the ones villains have when they're shooting someone to death: "hehehehe", parang marlon brando laugh. Anyway, just look at that face: brando. But mind you, it is painful. Trismus: opening the oral stoma reveals forcefully opposed jaws. These signs are not specific, but often associated with tetanus. Risus Sardonicus can occur in thalamic hemorrhage and the trismus in conditions i have just

mentioned.