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Tetanus – the silent killer: how safe are you?
ABSTRACT:. While The tetanus toxoid is one of the most potent poisons h. of contracting immmisable diseases. Tetanus &en leads to pro vention and management. This case study iUustrates a number of important points concerning the recognition, treatment, management and preuention of tetanus poisoning, and highlights the importance of considering the immunisation status of our elderly patients. Fry M , Edwards G B Taylor A. Tetanus - the siknt kilkr: how safe are you? Australian Critical Care 1998; 1I (3):82-85.
INTRODUCTION Despite the fact that tetanus is entirely preventable, mortality and morbidity as a result of this disease, even in the Western world, remain significant. Immunisation programs are a major preventive and cost-reducing strategy, but such programs focus primarily on children, overshadowing the need to develop and monitor similar programs for the elderly. While the tetanus vaccine is readily available, elderly people in most industrialised countries have a poor level of tetanus immunity l. In Australia, there is a paucity of literature examining the immunity status of the elderly population.
spores are found in soil and as part of normal human enteric flora, with the human carrier rate varying from 0 to 25 per cent '.', These terminal spores may enter the body through an open wound such as a laceration, puncture, bum, compound fracture, surgical incision, abortion or even during childbirth 3.4*9.They are also a real threat to users of illicit drugs who inject with contaminated needles. C. tetani spores remain localised at the site of entry, living in the anaerobic environment of the necrotic tissue. Spores lysed by the body's normal immune response release a deadly neurotoxin called tetan~spasmin'*~* lo, 11, which is also produced when the spores germinate or cells reproduce. The neurotoxin reaches the central nervous system (CNS) by travelling along the axons located near the site of infection ".
The tetanus toxoid is one of the most potent poisons known. Indeed, the literature suggests that, even with appropriate treatment, mortality may be higher than 50 per cent and death usually occurs within 2 days of the onset of the infection1-'. In NSW, tetanus is a Time from infection to onset of symptoms is usually 2-60 days notifiable disease and, while its incidence is uncommon, there are In most cases, signs and symptoms develop within a fortnight. A indications that it may be increasing in the elderly p o p ~ l a t i o n ~ ~ ' ~ ~ -shorter ~ . ~ . incubation period is associated with higher mortality and The following case study illustrates a number of important points morbidity9. The neurotoxin travels at a rate of 75-250 mm per day; concerning the recognition, treatment, management and cost of prehence the delay in presentation after exposure '. ventable diseases. Once in the CNS, tetanospasmin prevents the inhibition of acetylcholine at the neuromuscular junction, so normal relaxation of OF the skeletal muscles does not occur. This results in muscular spasm. CLOSTRIDIUM TETANI Tetanospasmin blocks the release of inhibitory neurotransmitters at inhibitory neurones, allowing excitory neurones to remain conWhile tetanus is uncommon, when it does appear it requires the tinuously stimulated, and this produces the spastic paralysis acute services of both the emergency and intensive care departments. The disease is caused by a Gram-positive, spore-forming characteristic of the disease. The signs and symptoms of C . tetani anaerobic bacillus known as Clostridium tetani ( C . tetani). C . tetani are trismus, dysphagia, 'risus sardonicus' (facial muscle rigidity with
PATHOPHYSIOLOGY
d
AUSTRALIAN CRITICAL CARE
the appearance of a grimace) and severe, seizure-like muscular spasms 4. 9- lo. Other signs and symptoms include autonomic dysfunction and cardiac dysrhythmias 5- ", 135 Is. Unfortunately, tetanus can develop in a neglected or forgotten wound; indeed, in some patients no entry wound for the organism can be discovered 2. 4- lo.
CASE STUDY A 76-year-old man presented to the emergency department on two consecutive occasions. On the first he had pain in hi jaw, weakness, diaphoresis and hypertension and was discharged with a primary diagnosis of left ventricular failure and upper respiratory tract infection. Two days later he arrived by ambulance with trismus and complaining of pain on jaw movement plus inability to open his mouth. He was extremely anxious and diaphoretic and also complained of back pain, leg-muscle spasm and poor mobility. There was no history of recent trauma; nor were there any visible wounds, although the patient did report that 2 weeks previously he had cut his foot in the garden. On examination, he was in atrial fibrillation at a rate of 105 beats per minute, was afebrile, had a blood pressure of 160190 mmHg, a Glasgow Coma Score of 15, a respiratory rate of 18 perlmin, an oxygen saturation of 96 per cent on room air and widespread urticaria. Routine blood samples were collected and a chest X-ray performed. Power and reflexes tested normal in both his upper limbs, with decreased patellar reflexes in the lower limbs.
a rebreathing mask. Overnight his PaCOz continued to rise and he was intubated following worsening bronchospasm and the onset of stridor. The intubation was difficult because of laryngospasm and tracheal deviation due to right lower lobe collapse. On day 10, a tracheostomy tube was inserted for long-term ventilation. Diazepam had been reduced and the baclofen ceased, as muscular spasm had markedly reduced. On day 15 the patient had a short run of self-limiting ventricular tachycardia, which was felt to be due to autonomic dysfunction. By day 21, however, he was alert, obeying commands and breathing spontaneously. By day 25, after a prolonged period of ventilation, he was weaned from the ventilator and had a mini-trache inserted to facilitate sputum removal due to muscle weakness. This patient spent another month in hospital, receiving physiotherapy and occupational therapy. His recovery was complicated by pneumonia and bilateral deep-vein thrombosis ( D W ) and, having spent a total of 26 days in ICU, he was another 30 days in the rehabilitation unit before being discharged. On discharge he had no neurological deficits and required follow-up for D W only.
DISCUSSION With tetanus, deaths are often the result of complications arising from impaired or absent ventilation caused by laryngospasm and spasms of the diaphragm and intercostal muscles 5-16. The advent of intensive care units, sophisticated drugs and advanced nursing care has significantly reduced mortality and morbidity, along with the complications associated with the disease '.I7 "'p
Given the presenting signs and symptoms, tetanus was the most likely diagnosis. In the emergency department the patient was treated with tetanus immunoglobulin 750mcg MI, tetanus toxoid 0.5 mg SC and penicillin 2 million units IV, Diazepam 2.5 mg IV incrementallywas used to control muscular spasm On being transferred to the intensive care unit (ICU) for airway monitoring and physiotherapy he was able to cough effectively, maintain his airway and ventilate adequately. Bibasal crepitations were present and an abdominal examination revealed a tender lower abdomen, hepatomegaly and normal bowel sounds. He was distressed, diaphoretic, alert and orientated on arrival at the ICU. Over the next 24 hours the patient's muscular spasms increased and intensified with noise, touch and movement. A strychnine test was performed, to exclude strychnine poisoning as a diagnosis. Meanwhile, the patient became increasingly diaphoretic, agitated and anxious. Copious amounts of purulent sputum were suctioned from his nasopharyngeal airway and he developed an expiratory wheeze. Increased oral sucrioning was required, to remove saliva and secretions. Since he was unable to void, an indwelling catheter was inserted. A nasogasuic tube was also inserted and nasogastric feeding commenced without incident.
To date, the medical focus appears to be on drug resistance and new infections, at the expense of pre-existing, 'controlled' diseases. Despite immunisation programs, all diseases preventable by way of immunisation (except diphtheria) have been reported in Australia. While children, primarily, are targeted by such irnmunisation programs, it is becoming evident that the elderly population remains at significant risk. Research suggests that tetanus antibody coverage is reduced to 50 per cent by the sixth decade of life and to 30 per cent One study demonstrated by the seventh and eighth decades that 45 per cent of its geriatricpopulation had reduced tetanus antibody titres6. In 1997 the Australian Institute of Health and Welfare reported seven cases of tetanus, with a steady increase in cases and tetanus-related deaths reported 18. ,4a'.'
A diagnosis of tetanus is based substantially on clinical criteria. Thus, an early presentation of the disease can easily be overlooked, as in this case study. A patient may complain simply of a sore throat with dysphagial, and many other differential diagnoses need to be eliminated (see Table 1).
Table 1.
Differential diagnoses of tetanus.
By day 3, the patient was becoming increasingly agitated due to worsening spasms in his abdomen and thighs. While the trismus had decreased the spasms continued. He was febrile at 38.3" C and experiencing hallucinations. By day 8, with the patient still on diazepam 10 mg QID via a nasogastric tube (NGT) and prn IV morphine, it was decided to commence baclofen 5mg via NGT for greater muscle spasm control. Splints were made, to prevent footdrop, and regular aperients given to prevent constipation. Over the next 3 days the patient's condition deteriorated and by day 8 his SaOz was 91 per cent and he was peripherally shut down. g Since his arterial blood gases were poor, with a PaOz of 40 d and a PaCOz of 60 l ~ m H on g room air, oxygen was administered via VOLUME 1 1
NUMBER 3
I SEPTEMBER 1998
*-
AUSTRALIAN CRITICAL CARE
Of the many other differential diagnoses listed, strychnine poisoning most closely mimics the clinical picture of tetanus. It can be caused by rodenticides and certain street drugs which have been mixed with strychnine. Absorption occurs mainly via the gastrointestinal tract and nasal mucosa. Strychnine, like tetanus, excites all levels of motor neurones, resulting in a lack of normal inhibitory neurone activation1'. Onset of signs and symptoms is usually rapid and similar to the case reviewed. Victims often present with muscle twitching, hyperreflexia, anxiety and seizures. The seizures and twitching usually appear before trismus, making strychnine poisoning distinguishable from tetanus. Further, there seem to be episodes of relaxation between spasms and muscle pain usually remains for 3-7 day^^^*'^.
sympathetic hyperactivity. In recent studies clonidiine, an alpha receptor agonist, has also proved successful in controlling sympathetic hyperactivity1'. Magnesium sulphate, which prevents the release of catecholamine, is also considered useful in treating sympathetic hyperactivity 13.
Biochemical testing is of dubious benefit in diagnosing tetanus, since the absence of C. tetani does not exclude the diagnosis. Urine and blood samples are required, to rule out heavy metal and strychnine poisoning. Heavy metal testing usually includes both blood and urine samples and searching for arsenic, cadmium, iron, lead, mercury and thallium. However, little has been published on the therapeutic levels of strychnine, so clinical management bears little relationship to laboratory testing for it l9. Clinical assessment is therefore vital, as the effects of the tetanus toxin can present with varying degrees of severity and symptoms. Assessment of airways and breathing is also vital, as spasm of the diaphragm may be life-threatening. If intubation is required the use of intravenous muscle relaxants is essential, since laryngospasm may be induced lo. For ongoing neuromuscular blockade, the literature suggests vecuronium is the best choice, due to the minimal cardiovascular side-effects". A rectal temperature is required, to monitor for hyperthermia in the presence of persistent seizures. Complications from prolonged muscular spasm include hypoxaemia and biochemical disruption, which may lead to rhabdomyolis, hyperthermia, lactic acidosis, myoglobinuria and renal failure l.' With systemic tetanus drug therapy is essential, to neutralise the circulating tetanospasmin. Drugs such as human tetanus immunoglobulin (HTI) prevent the uptake of tetanospasmin by the motor neurones, thereby reducing muscular spasm. Antibiotic therapy using high-dose penicillin destroys the bacillus and its spores. Unfortunately, the wound is usually devitalised and this may reduce the efficacy of the penicillin. Some recent studies have shown metronidazole to be more effective than penicillin1~l'. Urgent IV relaxants must be used in the event of life-threatening muscular spasm. Diazepam or phenobarbitone is usually necessary to control such seizures and spasmss*19, which may intensify with noise, touch and movement; therefore, all nursing care must be attended to concurrently, to keep handling to a minimum. Control of muscular spasm is essential, to prevent potential complications. Human tetanus immunoglobulin (HTI), which prevents the uptake of neurotoxin by the motor neurones, is administered in a single IM dose of 3000-5000 units (300 mcq/kg) as soon as the diagnosis is made. No further dosage is needed, since the half-life of HTI is 25 days. Tetanus toxoid ( M I ) should also be given, using a separate site. Completion of the tetanus course program is essential, because the disease does not give its host immunity from subsequent infections4''. Autonomic disturbances often occur late in the disease process of systemic tetanus. The clinical manifestations are tachycardia and hypertension, usually alternating with hypotension and bradycardial. Alpha and beta adrenergic blocking agents are used to control VOLUME 11
NUMBER 3
Wound management is vital with tetanus. However, given the delay in onset of signs and symptoms, the wound site may be difficult to identify, as in this case study. Nevertheless, any break in the skin barrier can be a potential exposure risk6. Surgical wound management may prove necessary, with surgical debridement and cleansing extending to unaffected tissue around the wound margins. Debridement extending to normal tissue will stop further production of the toxin at the wound site. It appears from the literature that the elderly are at risk of decreased immunity to infectious diseases preventable through vaccinations; in particular, tetanus and diphtheria. Possibly, after obtaining an appropriate immunisation history, all our elderly patients should be considered for tetanus vaccination, especially where skin integrity is impaired1,6.11,23. Health-care providers must be mindful that contracting the disease does not provide immunity, as even a large dose of tetanospamin does not elicit an antibody response". Further, they must not become complacent and forget that preventable diseases remain a threat to the community. Prevention is the key. If a person has a potentially serious wound, then a booster of tetanus toxoid should be administered L,2,". More importantly, any presentation by an elderly patient may be an appropriate time to give a tetanus booster, even if there is no wound. Patient education must include the need for follow-up, to receive the second and third tetanus toxoid injections from their local doctor. The National Health and Medical Research Council has now begun incorporating adult vaccination programs into its schedule.
CONCLUSION We have presented this case study to demonstrate the difficulty in diagnosing a disease generally considered eradicated. The episode of tetanus described resulted in a total hospital stay of 56 days, of which 26 were spent in intensive care. This paper, then, highlights the importance of updating vaccinations or boosters to prevent tetanus. Health-care staff need to identify patients with a high risk of exposure to tetanus and instigate appropriate prophylactic management, especially among the very young and the elderly. In emergency and intensive care units, aggressive treatment of elderly patients with severe tetanus is necessary if those people are to resume the same quality of life they enjoyed before their illness'. All nursing and medical staff should monitor the immunisation status of their patients and take every opportunity to extend immunisation coverage in the community, remembering that the incidence of this disease has been reduced not through eradication of the organism but by way of effective immunisation programs.
REFERENCES 1.
Sanford J. Tetanus - forgotten but not gone. The New England Journal of Medicine 1995; 3:812-13.
2.
Conn H & Conn R. Current Diagnosis (6th ed). WB Saunders Company, Philadelphia, 1980.
3.
JoUiet P, Magnenat J, Kobe1 T & Chevrolet J. Aggressive intensive care treatment of very elderly patients with tetanus is justified. Chest 1990; 3:702-04. SEPTEMBER 1998
A%
f.44
AUSTRALIAN CRITICAL CARE
4.
Shreve S & Spivack B. Tetanus in a 74-year-old woman. Journal of the American Geriatric Society 1994; 42:424-25.
15. Knight A &Richardson J. The management of tetanus in the elderly. Journal of American Board of Family Practice 1992; 5(1):43-49.
5.
Tmjillo M, Castill0 A, Espana J, Manzo A & Zerpa R. Impact of intensive care management on the prognosis of tetanus. Chest 1987; 1:63-65.
16. The Centre for Disease Control and Prevention. Tetanus Kansas. JAMA 1994; 27(2):1732.
6.
7.
Gareau A, McLellan B & Williams D. Tetanus immunisation status and immunologic response to a booster in an emergency department geriatric population. Annals of Emergency Medicine 1990; 19(2):1377-82. Gergen P, McQuillian G, Kiely ,'F Ezzatti-Rice T, Sutter R & Virella G. A population-based serologic survey of immunity to tetanus in the United States. The New England Journal of Medicine 1995; 332(12): 766-61.
".
Olgilvie C (ed). Birches Emergencies in Medical Practice (11th ed). Churchill Livingstone, New York, 1981.
9.
Oh T (ed). lntensive Care Manual (4th ed). Butterworth Heinemann, Sydney, 1997.
17. Udwadia F, La11 A, Udwadia 2, Sekhar M & Vora A. Tetanus and its complications: intensive care and management experience in 150 Indian patients. Epidemiology & Infection 1987; 99(3):675-84.
,
18. The Australian Institute of Health and Welfare. Communicable Diseases (serial online) 1997 (cited 1997 May). 19. Ellenhorn M & Barceloux D. Medical toxicology diagnosis and neatment of human poisonings. Elsevier, New York, 1988. 20. Dudley Hmt F (ed). French's Index of Differential Diagnosis ( I lth ed). John Wright & Sons Ltd, Bristol, 1979. 21. Fassoulaki A & Forakopoulou EM. Vecuronium in the management of tetanus: is it the muscle relaxant of choice? Acta Anaesthesiologica Belgica 1988; 39(2):75-78.
10. Pousada L & Osborne H. Emergency Medicine for the House Officer. William & Wilkins, Baltimore, 1986. 11. Todar K. Tetanus and Botulism. University of Wisconsin Department of Bacteriology (serial online) 1997 (cited 1997 May).
22. Sutton D, Tremlett M, Woodcock T & Nielsen M. The management of autonomic dysfunction in scvere tetanus: the use of magnesium sulphate and clonodine. Intensive Care Medicine Journal 1990; 16 (2):75-80. 23. Lichtenhan J, Kellennan R & Richards J. Tetanus: a threat to elderly patients. Postgraduate Medicine 1992; 92(7):59-72.
12. Richardson J & Knight A. The management and prevention of tetanus. Journal of Emergency Medicine 1993; 11(6):757-58.
24. Stewart K. Tetanus: protecting the airway and preventing toxin spread. Nursing Journal 1994; 551.
13. Titinalli J, Ruiz E & Korne R (eds). Emergency Medicine: A Comprehensive Study Guide (4th ed). American College of Emergency Physicians. McGraw Hill, New York, 1996 p667.
FURTHER READING
14. Wright D. Autonomic nervous system dysfunction in severe tetanus: current perspectives. Critical Care Medicine 1989; 17(4):371-75.
Alagappan K, Rennie W, Kwiatkowski T, Falck J, Silverstone F & Silverman R. Seroprevalence of tetanus antibodies among adults older than 65 years. Annals of Emergency Medicine 1996; 28(1):18-21.
A
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dvanced Standing may be granted on the basis of previously co ertiary qualifications and specialtylprofessional certificates. Critical Care) upon completion
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VOLUME 1 1
NUMBER 3
SEPTEMBER4 998
INTRODUCTION Despite the fact that tetanus is entirely preventable, mortality and morbidity as a result of this disease, even in the Western world, remain significant. Immunisation programs are a major preventive and cost-reducing strategy, but such programs focus primarily on children, overshadowing the need to develop and monitor similar programs for the elderly. While the tetanus vaccine is readily available, elderly people in most industrialised countries have a poor level of tetanus immunity l. In Australia, there is a paucity of literature examining the immunity status of the elderly population.
spores are found in soil and as part of normal human enteric flora, with the human carrier rate varying from 0 to 25 per cent '.', These terminal spores may enter the body through an open wound such as a laceration, puncture, bum, compound fracture, surgical incision, abortion or even during childbirth 3.4*9.They are also a real threat to users of illicit drugs who inject with contaminated needles. C. tetani spores remain localised at the site of entry, living in the anaerobic environment of the necrotic tissue. Spores lysed by the body's normal immune response release a deadly neurotoxin called tetan~spasmin'*~* lo, 11, which is also produced when the spores germinate or cells reproduce. The neurotoxin reaches the central nervous system (CNS) by travelling along the axons located near the site of infection ".
The tetanus toxoid is one of the most potent poisons known. Indeed, the literature suggests that, even with appropriate treatment, mortality may be higher than 50 per cent and death usually occurs within 2 days of the onset of the infection1-'. In NSW, tetanus is a Time from infection to onset of symptoms is usually 2-60 days notifiable disease and, while its incidence is uncommon, there are In most cases, signs and symptoms develop within a fortnight. A indications that it may be increasing in the elderly p o p ~ l a t i o n ~ ~ ' ~ ~ -shorter ~ . ~ . incubation period is associated with higher mortality and The following case study illustrates a number of important points morbidity9. The neurotoxin travels at a rate of 75-250 mm per day; concerning the recognition, treatment, management and cost of prehence the delay in presentation after exposure '. ventable diseases. Once in the CNS, tetanospasmin prevents the inhibition of acetylcholine at the neuromuscular junction, so normal relaxation of OF the skeletal muscles does not occur. This results in muscular spasm. CLOSTRIDIUM TETANI Tetanospasmin blocks the release of inhibitory neurotransmitters at inhibitory neurones, allowing excitory neurones to remain conWhile tetanus is uncommon, when it does appear it requires the tinuously stimulated, and this produces the spastic paralysis acute services of both the emergency and intensive care departments. The disease is caused by a Gram-positive, spore-forming characteristic of the disease. The signs and symptoms of C . tetani anaerobic bacillus known as Clostridium tetani ( C . tetani). C . tetani are trismus, dysphagia, 'risus sardonicus' (facial muscle rigidity with
PATHOPHYSIOLOGY
d
AUSTRALIAN CRITICAL CARE
the appearance of a grimace) and severe, seizure-like muscular spasms 4. 9- lo. Other signs and symptoms include autonomic dysfunction and cardiac dysrhythmias 5- ", 135 Is. Unfortunately, tetanus can develop in a neglected or forgotten wound; indeed, in some patients no entry wound for the organism can be discovered 2. 4- lo.
CASE STUDY A 76-year-old man presented to the emergency department on two consecutive occasions. On the first he had pain in hi jaw, weakness, diaphoresis and hypertension and was discharged with a primary diagnosis of left ventricular failure and upper respiratory tract infection. Two days later he arrived by ambulance with trismus and complaining of pain on jaw movement plus inability to open his mouth. He was extremely anxious and diaphoretic and also complained of back pain, leg-muscle spasm and poor mobility. There was no history of recent trauma; nor were there any visible wounds, although the patient did report that 2 weeks previously he had cut his foot in the garden. On examination, he was in atrial fibrillation at a rate of 105 beats per minute, was afebrile, had a blood pressure of 160190 mmHg, a Glasgow Coma Score of 15, a respiratory rate of 18 perlmin, an oxygen saturation of 96 per cent on room air and widespread urticaria. Routine blood samples were collected and a chest X-ray performed. Power and reflexes tested normal in both his upper limbs, with decreased patellar reflexes in the lower limbs.
a rebreathing mask. Overnight his PaCOz continued to rise and he was intubated following worsening bronchospasm and the onset of stridor. The intubation was difficult because of laryngospasm and tracheal deviation due to right lower lobe collapse. On day 10, a tracheostomy tube was inserted for long-term ventilation. Diazepam had been reduced and the baclofen ceased, as muscular spasm had markedly reduced. On day 15 the patient had a short run of self-limiting ventricular tachycardia, which was felt to be due to autonomic dysfunction. By day 21, however, he was alert, obeying commands and breathing spontaneously. By day 25, after a prolonged period of ventilation, he was weaned from the ventilator and had a mini-trache inserted to facilitate sputum removal due to muscle weakness. This patient spent another month in hospital, receiving physiotherapy and occupational therapy. His recovery was complicated by pneumonia and bilateral deep-vein thrombosis ( D W ) and, having spent a total of 26 days in ICU, he was another 30 days in the rehabilitation unit before being discharged. On discharge he had no neurological deficits and required follow-up for D W only.
DISCUSSION With tetanus, deaths are often the result of complications arising from impaired or absent ventilation caused by laryngospasm and spasms of the diaphragm and intercostal muscles 5-16. The advent of intensive care units, sophisticated drugs and advanced nursing care has significantly reduced mortality and morbidity, along with the complications associated with the disease '.I7 "'p
Given the presenting signs and symptoms, tetanus was the most likely diagnosis. In the emergency department the patient was treated with tetanus immunoglobulin 750mcg MI, tetanus toxoid 0.5 mg SC and penicillin 2 million units IV, Diazepam 2.5 mg IV incrementallywas used to control muscular spasm On being transferred to the intensive care unit (ICU) for airway monitoring and physiotherapy he was able to cough effectively, maintain his airway and ventilate adequately. Bibasal crepitations were present and an abdominal examination revealed a tender lower abdomen, hepatomegaly and normal bowel sounds. He was distressed, diaphoretic, alert and orientated on arrival at the ICU. Over the next 24 hours the patient's muscular spasms increased and intensified with noise, touch and movement. A strychnine test was performed, to exclude strychnine poisoning as a diagnosis. Meanwhile, the patient became increasingly diaphoretic, agitated and anxious. Copious amounts of purulent sputum were suctioned from his nasopharyngeal airway and he developed an expiratory wheeze. Increased oral sucrioning was required, to remove saliva and secretions. Since he was unable to void, an indwelling catheter was inserted. A nasogasuic tube was also inserted and nasogastric feeding commenced without incident.
To date, the medical focus appears to be on drug resistance and new infections, at the expense of pre-existing, 'controlled' diseases. Despite immunisation programs, all diseases preventable by way of immunisation (except diphtheria) have been reported in Australia. While children, primarily, are targeted by such irnmunisation programs, it is becoming evident that the elderly population remains at significant risk. Research suggests that tetanus antibody coverage is reduced to 50 per cent by the sixth decade of life and to 30 per cent One study demonstrated by the seventh and eighth decades that 45 per cent of its geriatricpopulation had reduced tetanus antibody titres6. In 1997 the Australian Institute of Health and Welfare reported seven cases of tetanus, with a steady increase in cases and tetanus-related deaths reported 18. ,4a'.'
A diagnosis of tetanus is based substantially on clinical criteria. Thus, an early presentation of the disease can easily be overlooked, as in this case study. A patient may complain simply of a sore throat with dysphagial, and many other differential diagnoses need to be eliminated (see Table 1).
Table 1.
Differential diagnoses of tetanus.
By day 3, the patient was becoming increasingly agitated due to worsening spasms in his abdomen and thighs. While the trismus had decreased the spasms continued. He was febrile at 38.3" C and experiencing hallucinations. By day 8, with the patient still on diazepam 10 mg QID via a nasogastric tube (NGT) and prn IV morphine, it was decided to commence baclofen 5mg via NGT for greater muscle spasm control. Splints were made, to prevent footdrop, and regular aperients given to prevent constipation. Over the next 3 days the patient's condition deteriorated and by day 8 his SaOz was 91 per cent and he was peripherally shut down. g Since his arterial blood gases were poor, with a PaOz of 40 d and a PaCOz of 60 l ~ m H on g room air, oxygen was administered via VOLUME 1 1
NUMBER 3
I SEPTEMBER 1998
*-
AUSTRALIAN CRITICAL CARE
Of the many other differential diagnoses listed, strychnine poisoning most closely mimics the clinical picture of tetanus. It can be caused by rodenticides and certain street drugs which have been mixed with strychnine. Absorption occurs mainly via the gastrointestinal tract and nasal mucosa. Strychnine, like tetanus, excites all levels of motor neurones, resulting in a lack of normal inhibitory neurone activation1'. Onset of signs and symptoms is usually rapid and similar to the case reviewed. Victims often present with muscle twitching, hyperreflexia, anxiety and seizures. The seizures and twitching usually appear before trismus, making strychnine poisoning distinguishable from tetanus. Further, there seem to be episodes of relaxation between spasms and muscle pain usually remains for 3-7 day^^^*'^.
sympathetic hyperactivity. In recent studies clonidiine, an alpha receptor agonist, has also proved successful in controlling sympathetic hyperactivity1'. Magnesium sulphate, which prevents the release of catecholamine, is also considered useful in treating sympathetic hyperactivity 13.
Biochemical testing is of dubious benefit in diagnosing tetanus, since the absence of C. tetani does not exclude the diagnosis. Urine and blood samples are required, to rule out heavy metal and strychnine poisoning. Heavy metal testing usually includes both blood and urine samples and searching for arsenic, cadmium, iron, lead, mercury and thallium. However, little has been published on the therapeutic levels of strychnine, so clinical management bears little relationship to laboratory testing for it l9. Clinical assessment is therefore vital, as the effects of the tetanus toxin can present with varying degrees of severity and symptoms. Assessment of airways and breathing is also vital, as spasm of the diaphragm may be life-threatening. If intubation is required the use of intravenous muscle relaxants is essential, since laryngospasm may be induced lo. For ongoing neuromuscular blockade, the literature suggests vecuronium is the best choice, due to the minimal cardiovascular side-effects". A rectal temperature is required, to monitor for hyperthermia in the presence of persistent seizures. Complications from prolonged muscular spasm include hypoxaemia and biochemical disruption, which may lead to rhabdomyolis, hyperthermia, lactic acidosis, myoglobinuria and renal failure l.' With systemic tetanus drug therapy is essential, to neutralise the circulating tetanospasmin. Drugs such as human tetanus immunoglobulin (HTI) prevent the uptake of tetanospasmin by the motor neurones, thereby reducing muscular spasm. Antibiotic therapy using high-dose penicillin destroys the bacillus and its spores. Unfortunately, the wound is usually devitalised and this may reduce the efficacy of the penicillin. Some recent studies have shown metronidazole to be more effective than penicillin1~l'. Urgent IV relaxants must be used in the event of life-threatening muscular spasm. Diazepam or phenobarbitone is usually necessary to control such seizures and spasmss*19, which may intensify with noise, touch and movement; therefore, all nursing care must be attended to concurrently, to keep handling to a minimum. Control of muscular spasm is essential, to prevent potential complications. Human tetanus immunoglobulin (HTI), which prevents the uptake of neurotoxin by the motor neurones, is administered in a single IM dose of 3000-5000 units (300 mcq/kg) as soon as the diagnosis is made. No further dosage is needed, since the half-life of HTI is 25 days. Tetanus toxoid ( M I ) should also be given, using a separate site. Completion of the tetanus course program is essential, because the disease does not give its host immunity from subsequent infections4''. Autonomic disturbances often occur late in the disease process of systemic tetanus. The clinical manifestations are tachycardia and hypertension, usually alternating with hypotension and bradycardial. Alpha and beta adrenergic blocking agents are used to control VOLUME 11
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Wound management is vital with tetanus. However, given the delay in onset of signs and symptoms, the wound site may be difficult to identify, as in this case study. Nevertheless, any break in the skin barrier can be a potential exposure risk6. Surgical wound management may prove necessary, with surgical debridement and cleansing extending to unaffected tissue around the wound margins. Debridement extending to normal tissue will stop further production of the toxin at the wound site. It appears from the literature that the elderly are at risk of decreased immunity to infectious diseases preventable through vaccinations; in particular, tetanus and diphtheria. Possibly, after obtaining an appropriate immunisation history, all our elderly patients should be considered for tetanus vaccination, especially where skin integrity is impaired1,6.11,23. Health-care providers must be mindful that contracting the disease does not provide immunity, as even a large dose of tetanospamin does not elicit an antibody response". Further, they must not become complacent and forget that preventable diseases remain a threat to the community. Prevention is the key. If a person has a potentially serious wound, then a booster of tetanus toxoid should be administered L,2,". More importantly, any presentation by an elderly patient may be an appropriate time to give a tetanus booster, even if there is no wound. Patient education must include the need for follow-up, to receive the second and third tetanus toxoid injections from their local doctor. The National Health and Medical Research Council has now begun incorporating adult vaccination programs into its schedule.
CONCLUSION We have presented this case study to demonstrate the difficulty in diagnosing a disease generally considered eradicated. The episode of tetanus described resulted in a total hospital stay of 56 days, of which 26 were spent in intensive care. This paper, then, highlights the importance of updating vaccinations or boosters to prevent tetanus. Health-care staff need to identify patients with a high risk of exposure to tetanus and instigate appropriate prophylactic management, especially among the very young and the elderly. In emergency and intensive care units, aggressive treatment of elderly patients with severe tetanus is necessary if those people are to resume the same quality of life they enjoyed before their illness'. All nursing and medical staff should monitor the immunisation status of their patients and take every opportunity to extend immunisation coverage in the community, remembering that the incidence of this disease has been reduced not through eradication of the organism but by way of effective immunisation programs.
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Sanford J. Tetanus - forgotten but not gone. The New England Journal of Medicine 1995; 3:812-13.
2.
Conn H & Conn R. Current Diagnosis (6th ed). WB Saunders Company, Philadelphia, 1980.
3.
JoUiet P, Magnenat J, Kobe1 T & Chevrolet J. Aggressive intensive care treatment of very elderly patients with tetanus is justified. Chest 1990; 3:702-04. SEPTEMBER 1998
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4.
Shreve S & Spivack B. Tetanus in a 74-year-old woman. Journal of the American Geriatric Society 1994; 42:424-25.
15. Knight A &Richardson J. The management of tetanus in the elderly. Journal of American Board of Family Practice 1992; 5(1):43-49.
5.
Tmjillo M, Castill0 A, Espana J, Manzo A & Zerpa R. Impact of intensive care management on the prognosis of tetanus. Chest 1987; 1:63-65.
16. The Centre for Disease Control and Prevention. Tetanus Kansas. JAMA 1994; 27(2):1732.
6.
7.
Gareau A, McLellan B & Williams D. Tetanus immunisation status and immunologic response to a booster in an emergency department geriatric population. Annals of Emergency Medicine 1990; 19(2):1377-82. Gergen P, McQuillian G, Kiely ,'F Ezzatti-Rice T, Sutter R & Virella G. A population-based serologic survey of immunity to tetanus in the United States. The New England Journal of Medicine 1995; 332(12): 766-61.
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Olgilvie C (ed). Birches Emergencies in Medical Practice (11th ed). Churchill Livingstone, New York, 1981.
9.
Oh T (ed). lntensive Care Manual (4th ed). Butterworth Heinemann, Sydney, 1997.
17. Udwadia F, La11 A, Udwadia 2, Sekhar M & Vora A. Tetanus and its complications: intensive care and management experience in 150 Indian patients. Epidemiology & Infection 1987; 99(3):675-84.
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18. The Australian Institute of Health and Welfare. Communicable Diseases (serial online) 1997 (cited 1997 May)
10. Pousada L & Osborne H. Emergency Medicine for the House Officer. William & Wilkins, Baltimore, 1986. 11. Todar K. Tetanus and Botulism. University of Wisconsin Department of Bacteriology (serial online) 1997 (cited 1997 May)
22. Sutton D, Tremlett M, Woodcock T & Nielsen M. The management of autonomic dysfunction in scvere tetanus: the use of magnesium sulphate and clonodine. Intensive Care Medicine Journal 1990; 16 (2):75-80. 23. Lichtenhan J, Kellennan R & Richards J. Tetanus: a threat to elderly patients. Postgraduate Medicine 1992; 92(7):59-72.
12. Richardson J & Knight A. The management and prevention of tetanus. Journal of Emergency Medicine 1993; 11(6):757-58.
24. Stewart K. Tetanus: protecting the airway and preventing toxin spread. Nursing Journal 1994; 551.
13. Titinalli J, Ruiz E & Korne R (eds). Emergency Medicine: A Comprehensive Study Guide (4th ed). American College of Emergency Physicians. McGraw Hill, New York, 1996 p667.
FURTHER READING
14. Wright D. Autonomic nervous system dysfunction in severe tetanus: current perspectives. Critical Care Medicine 1989; 17(4):371-75.
Alagappan K, Rennie W, Kwiatkowski T, Falck J, Silverstone F & Silverman R. Seroprevalence of tetanus antibodies among adults older than 65 years. Annals of Emergency Medicine 1996; 28(1):18-21.
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Faculty of Nursing
aster of Nursing (Criticai This course has been developed in collaboration with clinicians and the healthcare sector to focus on the development of clinical knowledge and expertise, evidence and research-based practice, professional skill development and scholarship in specialty practi Areas of specialisation within the course include:
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Nursing 'Ikauma & Emergency Nursing Intensive Care Nursing euroscience Nursing Neonatal Intensive Care Nursing 8jJxr,':p$
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r of Nursing (Critical Care) is normally offered by part-time study. The course consists of eight units of study, clinical experience and a supervised clinical project in the final year. The second year of
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