Clostridia
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, Fig. 7.18). 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
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).
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
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.
Treatment
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 (Chapter 43).
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 it
has 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.
Gas
gangrene
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 (Chapter 19).
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.
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.
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.