- Email: [email protected]
TERMINAL DEHYDRATION
306
embolism.6,7 In non-valvular heart disease, atrial fibrillation is associated with a five-fold increased risk of stroke.8,9 Sinoatrial disorder, characterised by the tachycardia/ bradycardia syndrome and paroxysmal atrial fibrillation and flutter, is also associated with a substantially increased risk of thromboembolism (16%) compared with that of patients with chronic atrioventricular block and normal atrial rhythm
The new Framingham data suggest that all patients with atrial fibrillation, irrespective of any underlying cardiac disease, are at risk of stroke; this adds more weight to the argument for long-term anticoagulation in the absence of contraindications.
(1-3%).
TERMINAL DEHYDRATION
There of atrial
-
little doubt, therefore, that the mere presence fibrillation, from whatever cause, predisposes to thromboembolism, and especially to stroke. A retrospective study of patients with stroke and atrial fibrillation in association with non-valvular heart diseasellillustrates the seriousness of this complication. 53 (38%) of 140 patients died of the initial stroke. Of the 59 patients available for follow-up, further strokes occurred at a rate of 20% per year over nine years. In all, a further stroke occurred in 22/59, causing death in 7. None of these patients was anticoagulated. Can this serious complication of atrial fibrillation be prevented? Szekelyl2 showed that embolism in rheumatic heart disease was virtually abolished by anticoagulation, although the numbers studied were small. He and others9,13,14 also showed that patients with rheumatic heart disease were at greatest risk of embolism within the first year after onset of fibrillation. These results, and the fact that embolism also occurs in patients with mitral valve disease in sinus rhythm,12 suggest that all patients with mitral valve disease should be given anticoagulants prophylactically. There are no published trials of anticoagulation in patients with atrial fibrillation in the absence of rheumatic heart disease, but the available data imply that embolic stroke is preventable in such cases. But is long-term anticoagulation safe? In the Dutch reinfarction study1S in which patients over 60 were randomly allocated to receive full anticoagulation or placebo following acute myocardial infarction, overall mortality and recurrent infarction were significantly reduced by active treatment over two years. Stroke was also less frequent in the treated group, although when it did occur it was more commonly haemorrhagic. However, major non-fatal extracranial haemorrhage was significantly higher in the anticoagulated population, occurring in 6%. Anticoagulation at the time of presentation with embolic stroke of cardiac origin has also been shown to be safe and to reduce the risk of recurrence. 16,17 In general, long-term anticoagulant therapy would appear to be safer than the effects of embolic stroke. seems
6. Coulshed
N, Epstein EJ, McKendrick CS, Galloway RW, Walker E. Systemic in mitral valve disease. Br Heart J 1970; 32: 26-34. Fleming HA, Bailey SM. Mitral valve disease, systemic embolism and anticoagulants. embolism
7.
Postgrad Med J 1971; 47: 599-604. PA, Kannel WB, McGee DL, Meeks SL, Bharacha NE, McNamara PM. Duration of atrial fibrillation and imminence of stroke. The Framingham study. Stroke 1983; 14: 664-67. 9. Hmton RC, Kistler JP, Fallon JT, Freidlich AL, Fisher CM. Influence of etiology of atrial fibrillation on incidence of systemic embolism. Am J Cardiol 1977; 40: 509-13. 10. Fairfax AJ, Lambert CD, Leatham A. Systemic embolism in chronic sino-atrial disorder. N Engl J Med 1976; 295: 190-92. 11. Sage JI, van Uitert RL. Risk of recurrent stroke in patients with atrial fibrillation and non-valvular heart disease. Stroke 1983; 14: 537-40. 12. Szekely P. Systemic embolism and anticoagulant prophylaxis in rheumatic heart disease. Br Med J 1964; i: 1209-12 13. Fisher CM. Reducing risks of cerebral embolism. Geriatrics 1979; 34: 59-66. 14. Aberg H. Atrial fibrillation. Acta Med Scand 1969; 185: 373-79. 15. Sixty Plus Reinfarction Study Research Group. A double-blind trial to assess long-term oral anticoagulant therapy in elderly patients after myocardial infarction. Lancet 1980; ii 989-94. 16. Furlan AJ, Cavalier SJ, Hobbs RE, Weinstein MA, Modic MT. Hemorrhage and anticoagulation after non-septic embolic brain infarction. Neurology 1982; 32: 280-82. 17. Koller RL. Recurrent embolic cerebral infarction and anticoagulation. Neurology 1982; 32: 283-85. 8. Wolf
As a patient with terminal illness approaches death, eating and drinking may become troublesome and intravenous fluids may then be given to relieve the distress of dehydration. This decision is open to challenge.I Experimentally, dehydration has been shown to cause many symptoms
including thirst, dry mouth, weakness, lethargy, confusion, and coma.i In terminal illness, however, the symptoms associated with dehydration seem to be much milder-usually only thirst and a dry mouth2-and can be relieved easily by provision of regular small sips of fluid, ice cubes to suck, and good mouth care.22 Why, then, are intravenous fluids used in these circumstances ? The provision offood and water is symbolically very important for the patient, the family, and the medical attendants.3The cessation of this "feedirig" may be seen as a resignation to the inevitability of death, and the continuation of intravenous fluids may be part of the denial of death by the family and doctor.4 Some doctors also feel the need to keep5 the blood chemistry as near to normal as possible until death; but even for this purpose an infusion may not be necessary. Oliver6 reported that, of twenty-two patients dying peacefully without an intravenous infusion or a nasogastric tube within 48 h of a blood test, twelve had essentially normal electrolytes, the only consistent abnormality being a mildly raised urea. In a US survey of physicians’ attitudes to the care of the dying patient, a hypothetical case of a comatose dying patient was presented.4 Three-quarters of the physicians would have used intravenous fluids at a sufficient rate to maintain
hydration, only a quarter opting for small amounts of fluid or no infusion.4 Moreover, of the physicians who favoured the use of intravenous fluids at the higher rate, 40% would have been prepared to insert a central line or perform a cut-down to restart the infusion, and only 2107o would have considered stopping the infusion after three days without improvement in the patient’s condition. Half of all the physicians mentioned intravenous fluids as part of the standard care of the terminally ill patient. Thus the use of an intravenous infusion is often seen as "normal" in the dying patient, rather than as an extraordinary procedure for the treatment of a specific abnormality such as hypercalcaemia, hyperglycaemia, or hypoglycaemia. The infusion is not without side-effects. It may cause discomfort and distress to the patient, and acts as a barrier between the patient and his or her family-it is much more difficult to embrace a spouse who is attached to a plastic tube. Moreover, the medical and nursing staff may find their attention diverted from the care of patient and family to the control of electrolytes and fluid balance. 1. 2. 3.
4. 5. 6.
Comfort measures for the terminally ill: is dehydration painful? J Am Geriatr Soc 1985; 33: 808-10. Baines MJ. Control of other symptoms. In: Saunders C, ed. The management of terminal malignant disease, 2nd ed. London: Edward Arnold, 1984: 101 Wanzer SH, Adelstein SJ, Cranford RE, et al. The physician’s responsibility toward hopelessly ill patients. N Engl J Med 1984; 310: 955-59. Micetich KC, Steinecker PH, Thomasma DC. Are intravenous fluids morally required for a dying patient? Arch Intern Med 1983; 143: 975-78. Simpson MA. The facts of death. Englewood Cliffs, NJ: Prentice Hall, 1979. Oliver DJ. Terminal dehydration. Lancet 1984; ii: 631.
Billings JA.
embolism.6,7 In non-valvular heart disease, atrial fibrillation is associated with a five-fold increased risk of stroke.8,9 Sinoatrial disorder, characterised by the tachycardia/ bradycardia syndrome and paroxysmal atrial fibrillation and flutter, is also associated with a substantially increased risk of thromboembolism (16%) compared with that of patients with chronic atrioventricular block and normal atrial rhythm
The new Framingham data suggest that all patients with atrial fibrillation, irrespective of any underlying cardiac disease, are at risk of stroke; this adds more weight to the argument for long-term anticoagulation in the absence of contraindications.
(1-3%).
TERMINAL DEHYDRATION
There of atrial
-
little doubt, therefore, that the mere presence fibrillation, from whatever cause, predisposes to thromboembolism, and especially to stroke. A retrospective study of patients with stroke and atrial fibrillation in association with non-valvular heart diseasellillustrates the seriousness of this complication. 53 (38%) of 140 patients died of the initial stroke. Of the 59 patients available for follow-up, further strokes occurred at a rate of 20% per year over nine years. In all, a further stroke occurred in 22/59, causing death in 7. None of these patients was anticoagulated. Can this serious complication of atrial fibrillation be prevented? Szekelyl2 showed that embolism in rheumatic heart disease was virtually abolished by anticoagulation, although the numbers studied were small. He and others9,13,14 also showed that patients with rheumatic heart disease were at greatest risk of embolism within the first year after onset of fibrillation. These results, and the fact that embolism also occurs in patients with mitral valve disease in sinus rhythm,12 suggest that all patients with mitral valve disease should be given anticoagulants prophylactically. There are no published trials of anticoagulation in patients with atrial fibrillation in the absence of rheumatic heart disease, but the available data imply that embolic stroke is preventable in such cases. But is long-term anticoagulation safe? In the Dutch reinfarction study1S in which patients over 60 were randomly allocated to receive full anticoagulation or placebo following acute myocardial infarction, overall mortality and recurrent infarction were significantly reduced by active treatment over two years. Stroke was also less frequent in the treated group, although when it did occur it was more commonly haemorrhagic. However, major non-fatal extracranial haemorrhage was significantly higher in the anticoagulated population, occurring in 6%. Anticoagulation at the time of presentation with embolic stroke of cardiac origin has also been shown to be safe and to reduce the risk of recurrence. 16,17 In general, long-term anticoagulant therapy would appear to be safer than the effects of embolic stroke. seems
6. Coulshed
N, Epstein EJ, McKendrick CS, Galloway RW, Walker E. Systemic in mitral valve disease. Br Heart J 1970; 32: 26-34. Fleming HA, Bailey SM. Mitral valve disease, systemic embolism and anticoagulants. embolism
7.
Postgrad Med J 1971; 47: 599-604. PA, Kannel WB, McGee DL, Meeks SL, Bharacha NE, McNamara PM. Duration of atrial fibrillation and imminence of stroke. The Framingham study. Stroke 1983; 14: 664-67. 9. Hmton RC, Kistler JP, Fallon JT, Freidlich AL, Fisher CM. Influence of etiology of atrial fibrillation on incidence of systemic embolism. Am J Cardiol 1977; 40: 509-13. 10. Fairfax AJ, Lambert CD, Leatham A. Systemic embolism in chronic sino-atrial disorder. N Engl J Med 1976; 295: 190-92. 11. Sage JI, van Uitert RL. Risk of recurrent stroke in patients with atrial fibrillation and non-valvular heart disease. Stroke 1983; 14: 537-40. 12. Szekely P. Systemic embolism and anticoagulant prophylaxis in rheumatic heart disease. Br Med J 1964; i: 1209-12 13. Fisher CM. Reducing risks of cerebral embolism. Geriatrics 1979; 34: 59-66. 14. Aberg H. Atrial fibrillation. Acta Med Scand 1969; 185: 373-79. 15. Sixty Plus Reinfarction Study Research Group. A double-blind trial to assess long-term oral anticoagulant therapy in elderly patients after myocardial infarction. Lancet 1980; ii 989-94. 16. Furlan AJ, Cavalier SJ, Hobbs RE, Weinstein MA, Modic MT. Hemorrhage and anticoagulation after non-septic embolic brain infarction. Neurology 1982; 32: 280-82. 17. Koller RL. Recurrent embolic cerebral infarction and anticoagulation. Neurology 1982; 32: 283-85. 8. Wolf
As a patient with terminal illness approaches death, eating and drinking may become troublesome and intravenous fluids may then be given to relieve the distress of dehydration. This decision is open to challenge.I Experimentally, dehydration has been shown to cause many symptoms
including thirst, dry mouth, weakness, lethargy, confusion, and coma.i In terminal illness, however, the symptoms associated with dehydration seem to be much milder-usually only thirst and a dry mouth2-and can be relieved easily by provision of regular small sips of fluid, ice cubes to suck, and good mouth care.22 Why, then, are intravenous fluids used in these circumstances ? The provision offood and water is symbolically very important for the patient, the family, and the medical attendants.3The cessation of this "feedirig" may be seen as a resignation to the inevitability of death, and the continuation of intravenous fluids may be part of the denial of death by the family and doctor.4 Some doctors also feel the need to keep5 the blood chemistry as near to normal as possible until death; but even for this purpose an infusion may not be necessary. Oliver6 reported that, of twenty-two patients dying peacefully without an intravenous infusion or a nasogastric tube within 48 h of a blood test, twelve had essentially normal electrolytes, the only consistent abnormality being a mildly raised urea. In a US survey of physicians’ attitudes to the care of the dying patient, a hypothetical case of a comatose dying patient was presented.4 Three-quarters of the physicians would have used intravenous fluids at a sufficient rate to maintain
hydration, only a quarter opting for small amounts of fluid or no infusion.4 Moreover, of the physicians who favoured the use of intravenous fluids at the higher rate, 40% would have been prepared to insert a central line or perform a cut-down to restart the infusion, and only 2107o would have considered stopping the infusion after three days without improvement in the patient’s condition. Half of all the physicians mentioned intravenous fluids as part of the standard care of the terminally ill patient. Thus the use of an intravenous infusion is often seen as "normal" in the dying patient, rather than as an extraordinary procedure for the treatment of a specific abnormality such as hypercalcaemia, hyperglycaemia, or hypoglycaemia. The infusion is not without side-effects. It may cause discomfort and distress to the patient, and acts as a barrier between the patient and his or her family-it is much more difficult to embrace a spouse who is attached to a plastic tube. Moreover, the medical and nursing staff may find their attention diverted from the care of patient and family to the control of electrolytes and fluid balance. 1. 2. 3.
4. 5. 6.
Comfort measures for the terminally ill: is dehydration painful? J Am Geriatr Soc 1985; 33: 808-10. Baines MJ. Control of other symptoms. In: Saunders C, ed. The management of terminal malignant disease, 2nd ed. London: Edward Arnold, 1984: 101 Wanzer SH, Adelstein SJ, Cranford RE, et al. The physician’s responsibility toward hopelessly ill patients. N Engl J Med 1984; 310: 955-59. Micetich KC, Steinecker PH, Thomasma DC. Are intravenous fluids morally required for a dying patient? Arch Intern Med 1983; 143: 975-78. Simpson MA. The facts of death. Englewood Cliffs, NJ: Prentice Hall, 1979. Oliver DJ. Terminal dehydration. Lancet 1984; ii: 631.
Billings JA.