It has been estimated that, every year, between 300 000 and 500 000 cases of tetanus occur world-wide with an overall mortality of 40—45 per cent. In the UK, 200 cases occur annually, and the condition is also relatively uncommon elsewhere in Europe, in the former Soviet Union and in North America. The burden of this agonising infection falls on those in the other countries of the world, particularly on the children, the neonates (tetanus neonatorum) and the elderly. An education programme to have universal active immunisation can and will lead to a reduction in the number of cases and, significantly, the mortality. Tetanus toxoid (now known as tetanus vaccine) practically eliminated tetanus in the armies during World War II. Today, if active immunity is properly initiated and maintained in an individual, death is unlikely even in the presence of clinical tetanus.
Clostridium tetani, the causal organism, is a Gram-positive anaerobic rod with terminal spores (drumstick appearance, ). Found in manure and soil (notably in market garden areas), it will invade any wound. It multiplies and produces a powerful toxin in any deep, contused wound in the presence of dead tissue, foreign bodies and other bacteria. Penetrating injury from the hoof of an animal can be associated with this infection, while the prick from a rose thorn in a well-manured rose garden can be the sting of death to an elderly assiduous horticulturalist. The exotoxin produced in the inoculation site inhibits the cholinesterase at the motor endplates, resulting in an excess of acetylcholine locally and, therefore, a sustained state of tonic muscle spasm. The exotoxin also travels along the nerves to the central nervous system and causes extreme hyperexcitability of motor neurons in the anterior horn cells, thereby evoking explosive and widespread reflex spasms of muscle in response to sensory stimuli. Once fixed in the nerve tissue, the toxin can no longer be neutralised by antitoxin.
Period of onset
The shorter the interval between the first symptom and the first reflex spasm the poorer is the prognosis. (Hippocrates, circa 46—77 BC, is believed to have been the first to recognise this fact.) If the interval is less than 48 hours, death is likely. It should be remembered that wounds containing tetanus organisms may have healed and been forgotten for months or years before some (unknown) change produces the right conditions for the organism to multiply and produce toxin (latent tetanus).
Symptoms and signs
Dysphagia, jaw stiffness and severe pains in the neck, back and abdomen precede the tonic muscle spasms. The sardonic smile of tetanus (risus sardonicus) is evidence of the onset of tonic muscle spasm. Respiration and swallowing become progressively more difficult, and reflex convulsions occur affecting all muscles and causing great pain, opisthotonus (spasm of the extensors of the neck, back and legs to form a backward curvature) and even muscle rupture. The spasms are spontaneous, but can be induced by trivial stimuli such as noise or movement and, when severe, will prevent respiration and produce cyanosis. Between the reflex convulsions, the tonic muscular spasm remains, thus distinguishing tetanus from strychnine poisoning. The temperature is elevated, the pulse is rapid, and respiratory failure and death during a cyanotic attack will usually follow if treatment is not initiated.
At an early stage, the symptoms and signs of tetanus might be mistaken for tonsillitis, flu, backstrain or an acute upper abdominal condition. Therefore, careful examination of the patient for a wound is of paramount importance.
Isolation, quietness and comfort, drainage of pus and wound toilet will be needed. Human anti-tetanus globulin (e.g. Humotet) is given intramuscularly (i.m.) to limit the effects of free toxins and should be used in doses of 25—500 units to give cover throughout the period of establishing active immunity by giving toxoid (tetanus vaccine, adsorbed) i.m. Equine tetanus antiserum has been used but about 20 per cent of patients develop serum sickness and occasional anaphylactic reactions occur. Antibiotics, including penicillin and metronidazole, are indicated along with measures to protect the lungs.
Stage 1. A mild case, where there is tonic rigidity alone, will require initial sedation, relaxation by drugs such as promazine up to 200 mg i.m. and a barbiturate or diazepam [—50 mg intravenously (i.v.)]. These drugs will be needed approximately four times during any 24-hour period.
Stage 2. A seriously ill patient, with dysphagia and reflex spasm, will need to have a nasogastric tube passed and sedation continued. The diet, the need for intravenous nutrition, the maintenance of balanced protein intake, and of renal function and cardiac function will be priorities. A tracheostomy should be considered if the patient has any difficulty in breathing. The meticulous care of the tracheostomy tube includes suction and humidification .
Stage 3. In dangerously ill patients, a major cyanotic convulsion will require curarisation, e.g. up to 40 mg tubocurarine i.v. initially and afterwards i.m. to maintain relaxation. It should be remembered that the curarised patient, although unresponsive, is conscious and sensitive and can hear everything that is being said. Intermittent positive-pressure respiration should be provided, and intensive nursing care with increasing sedation would be needed because ithas been estimated that a patient at this stage will require at least 350 individual acts of nursing each day. The objective is to reduce the risk of death from spasms or pneumonia wherever possible, while realising that a lethal amount of toxin has already caused severe damage to the motor neurons and the brain with concomitant myocarditis and vascular failure. If recovery takes place, the patient can be weaned from the ventilator (after about 14 days as long as convulsions do not recur when the effects of the relaxants wear off).
Results. With the proper attention to nursing care,
prophylactic antibiotic therapy, active and passive smmumsation against tetanus and, where indicated, tracheostomy, curarisation and assisted respiration, the death rate can be reduced to approximately 15 per cent. The results in the very young and very old nevertheless are still poor. The tetanospasmin produced by the infection is insufficient to generate an immune response so a course of immunisation is recommended on recovery.
Wounds allowing the patient’s own faecal flora, or clostridial spores in the soil, to enter the tissues can give rise to anaerobic gas-producing infections. Surgery around the hip joint and leg amputations are at high risk from this postoperative complication, as are the wounds of warfare .Clostridium perfringens (welchii) is usually the cause in about 80 per cent, but other clostridia, including Clostridium novyi (Clostridium oedematiens), Clostridium histolyticum, Clostridiumbifermen tans and Clostridium septicum may be causal. Clestridium welchii is found in the stools and therefore is also found on the perineum and, occasionally, as normal flora in the vagina. The clostridia produce numerous toxins, including an ct-toxin believed to be important in the pathogenesis of gas gangrene.
Clostridial invasion of a traumatised muscle affects the whole of that muscle from origin to insertion, producing a foul-smelling necrosis of the bundles which lose contractibility and become dull red, green or black in appearance. If septicaemia occurs, gas is produced in many organs, notably the liver (which at necropsy drips with frothy blood — the ‘foaming liver’).
Subcutaneous tissues alone can be infected; the foul-smelling necrosis, often spreading extensively, can begin in the margin of an abdominal or a thoracic wound.
The wound is under tension and between the sutures the pouting edges exude a brownish and foul-smelling fluid. The skin becomes discoloured — a khaki colour — owing to associated haemolysis. Crepitus can usually be detected. (Crepitus, to the examining hand, feels like an old hair mattress.) A radiograph will show the gas in the muscles or under the skin. The patient, although toxic and pale, with raised pulse, misleadingly appears mentally clear.
Treatment, to be effective, requires immediate action:
1. maximum doses of penicillin (up to 2.4 g 4-hourly) —traditionally the treatment of choice, although recent work suggests a better outcome with clindamycin and metronidazole;
2. blood transfusion;
3. either exposure of all the affected muscle groups by long incisions or, in the subcutaneous infections, multiple subcutaneous drainage and slough extraction by incisions into the subcutaneous tissue;
4. hyperbaric oxygen where this is available. It is said to be helpful in the postoperative period.
The use of antiserum used to be recommended, but clinical experience was variable, stocks are now depleted and there has been little interest in resuming production.
Clostridial pseudomembranous colitis
This is an acute, profuse, antibiotic-associated diarrhoea which produces characteristic changes of the colon, recognisable sigmoidoscopically by a pseudomembrane and subsequently by sloughing of the colonic mucosa. The organism responsible, C. difficile, produces a toxin which cross-reacts with Clostridium sordellii antitoxin to produce a serious, sometimes fatal, colitis. The toxin can be demonstrated by its cytopathic effect in cell culture as well as by a number of commercial enzyme-linked immunosorbent assay (ELISA) kits. The organism can be cultured from stool but this does not necessarily indicate a pathogenic role. A spectrum of disease is recognised, ranging from antibiotic-associated diarrhoea (AAD) to antibiotic-associated colitis (AAC) to pseudomembranous colitis (PMC). The incidence is high among older patients, especially where broad-spectrum antibiotics (penicillins and cephalosporins) or clindamycin have been used, although almost every antibiotic has been implicated.
Treatment involves stopping antibiotic therapy where possible, general supportive measures and oral metronidazole or vancomycin. Relapse is well documented and further courses of therapy may be required. Being a sporing organism, it survives well in the hospital environment and in some centres is a considerable problem. It is readily transmitted by hand contact.
Salmonella typhi, paratyphi. These are enteric pathogens which cause enteric fevers with bacteraemia, usteomyelitis and sometimes perforation of ileal ulcers. Persistence of the bacteria in the gallbladder may lead to the carrier state and subsequently person-to-person spread in the community (see Chapter 54). The use of ciprofloxacin 500 mg twice daily •for 10 days is recommended for S. typhiinfections although resistance has now been demonstrated in the Indian subcontinent. It is useful as it prevents or cures long-term carriage, and resistance to the more commonly used drugs (ampicillin, chloramphenicol) has reached very high levels in some parts of the world. The other salmonellas are associated with food poisoning, diarrhoea and, therefore, dehydration. Control of the symptoms only is usually required, and the use of antimicrohials is not usually helpful for thereby resistant strains are encouraged, excretion can be prolonged, and in any case the intestinal symptoms are self-limiting. In the unusual event of systemic spread and bacteraemia, it will be necessary to use the antibiotics to which the isolate is sensitive. If treatment is started before the organism is isolated, a broad-spectrum penicillin combined with an aminoglycoside may then be required. The commonest nontyphoid salmonellas are S. typhimurium, S. enteritidis and S. virchow. They are found in cattle, calves, poultry, turkeys and domestic animals, and infection in humans is by direct spread from contaminated food. These organisms can spread within a hospital if patients (Or staff) with diarrhoea are not recognised as a risk; close contacts of excreta must be properly protected by apron and gloves to reduce the likelihood of the infection being spread by unwashed hands which have become contaminated with faeces.
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