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RECOVERY AFTER RELIEF OF RENAL OBSTRUCTION
1429
requiring
ventilation
after
cardiorespiratory
resuscitation (cardiac arrest) do badly, with 90% mortality at 1 year.2,3 Patients with respiratory failure due to acute neurological disease were found to "do well" in one study! but in the other two fared no better3 or worse than average.2 Numbers in these categories were small. Patients with chronic obstructive lung disease, in the two reports carrying results in this group,2,3 show good survival from intensive care (82 and 70%) but poor long-term survival (36 and 30%). Postoperative cases requiring ventilation are a large and very heterogeneous group. Results in this group are about average-74% survival in the ITU and 43% alive at one year. Searle points out the prognostic significance of the number of complications. For survival in the ITU this varied from 94% in patients with no complications to 20% in patients with three or four and 0% with six or more. On the matter of cost, Witek et al2 make the point that the ITU charges were similar for survivors and for those who died (US$2200 in 1980). The average duration of stay in the ITU was about 6 days for both survivors and non-survivors. However, the total hospital charges were greater in survivors, owing to their longer stay in hospital. The ITU charges represented 16 and 25%, respectively, of the total hospital bill in these two categories of patient. The cost of intensive therapy in a British district general hospital in 1985 is roughly 350-450 a day. The high cost is very largely due to the high staff/patient ratio. So, when a patient is admitted to the ITU an average stay of 6 days consumes about z2400 of National Health Service resources compared with about 600 for a similar period in an acute ward. Of course, admission to the ITU may be life-saving, in which case it is obviously the correct course, but where hope of recovery is nil or where recovery can be expected in the general ward, intensive therapy is a waste of resources. More than that, inappropriate referral of hopeless cases is also bad medicine. It is unfair on ITU staff and may cause unnecessary suffering to the patient and relatives. Decisions as to whether to admit to the ITU are difficult and except in obvious cases should not be left to junior hospital staff. A knowledge of the likely outcome, both short and long term, provided by these studies may help in these decisions though the results need to be applied with caution in the individual case. The hardest decision is what to do in the case where inappropriate intensive therapy has already been started or when a patient in the ITU passes from the hopeful to the hopeless. A common situation mentioned by Searlel is the postoperative patient in whom surgeons have invested hours of effort-for instance, attempting to deal with a leaking abdominal aneurysm in an elderly man. It is difficult in such a case to refuse continued intensive care. In these circumstances one must avoid "the Vietnam mentality". Many people felt that the United States could not pull out of Vietnam because that would have let down all the American soldiers who had laid down
their lives there. Somehow one must focus on what is happening now and assess the appropriateness of continuing intensive care from this point on. Figures from the type of audit in these papers may help in these very difficult decisions. RECOVERY AFTER RELIEF OF RENAL OBSTRUCTION THE effect of bladder outflow obstruction on renal function on the intravesical pressure that develops. When intrinsic bladder pressure is high, the features tend to be those of glomerular dysfunction-uraemia, hypertension, and salt and water retention. 1,2 When intravesical pressure is low, renal tubular damage predominates with failure of sodium reabsorption and countercurrent mechanisms,3
depends partly
inability to concentrate or dilute the urine,4and impairment of acidificationa the result can be a profound saline diuresis and acidosis. When obstruction is relieved, there may be a further saline diuresis resulting in hypovolaemia.6,7 At least three mechanisms contribute to this potentially hazardous effect-clearance of retained solutes such as urea;clearance of excess fluid and electrolytes; and tubular dysfunction, with excretion of urine of osmolality similar to that of plasma.’,9 (Matters may be made worse by infection in an already damaged and catheterised urinary tract.) Long ago, Chisholm9,10 and Beck" warned of the dangers of giving too much fluid in these circumstances and lately Bishop has delivered the same message.12 However, it is not helpful to generalise about patients "rarely" needing intravenous fluids after relief of urinary obstruction. Of Bishop’s 55 patients, 12 did become hyponatraemic and 10 needed intravenous fluids. To avoid saline depletion, with its considerable dangers, two things are important. The first is to remember that saline depletion can be difficult to detect clinically without measurement of central venous pressure, and so to be alert to this potential hazard especially in patients who have already experienced a prolonged diuresis due to partial obstruction; 13 fluid replacement can then be guided by simple measurements of blood pressure, fluid balance, and body weight, and by central venous pressure monitoring when necessary. The second is not to replace saline losses with water in the form of 5% dextrose, which can often cause severe hyponatraemia, but to use physiological saline, supplemented to correct any hypokalaemia and acidosis. 1 Mitchell
JP. Principles of transurethral resection and haemostasis. Bristol: John Wright, 1972: chap 18. 2. George NJR, O’Reilly PH, Barnard RJ, Blacklock NJ High pressure chronic retention Br Med J 1983, 286: 1780-83 3. Suki WN, Guthrie AG, Martinez-Maldonado M, Eknoyan G Effects of ureteral pressure elevation on renal hemodynamics and urine concentration. Am J Physiol 1971, 220: 38-43. 4. Olesen S, Madsen PO. Renal function during experimental hydronephrosis: function during partial obstruction following contralateral nephrectomy in the dog. J Urol 99: 692-99 GM. Distal tubular function in chronic hydronephrosis. Quart J Med 1961, 30: 339-55. 6. Wilson B, Reisman DD, Moyer CA Fluid balance in the urological patient. J Urol
1968,
5.
Berlyne
1951; 66: 805-15.
NS, Shwayri EI, Rearden JB, Kellog D, Merrill JP, Holmes JH. An abnormality in renal function resulting from urinary tract obstruction. Am J Med
7 Bricker
1957; 23: 554-64. 8 9
Maher JF, Schreiner GE, Waters TJ Osmotic diuresis due to retained urea after release of obstructive uropathy. N Engl J Med 1963; 268: 1099-104. Chisholm GD Bilateral renal clearance studies in experimental obstructive uropathy.
Proc R Soc Med 1964; 57: 571-73. 10 Chisholm GD Pathophysiology of obstructive uropathy. In: Chisholm GD, Innes Williams D, eds. Scientific foundations of urology, 2nd ed. London: Heinemann, 1982: 98-105 11. Beck AD. Benign prostatic hypertrophy and uraemia. Br J Surg 1970; 57: 561-65. 12 Bishop MC Diuresis and renal functional recovery in chronic retention. Br J Urol 1985, 57: 1-5. 13. Roussak NJ, Oleesky S. Water-losing nephritis: syndrome simulating diabetes insipidus Quart J Med 1954, 23: 147-64.
requiring
ventilation
after
cardiorespiratory
resuscitation (cardiac arrest) do badly, with 90% mortality at 1 year.2,3 Patients with respiratory failure due to acute neurological disease were found to "do well" in one study! but in the other two fared no better3 or worse than average.2 Numbers in these categories were small. Patients with chronic obstructive lung disease, in the two reports carrying results in this group,2,3 show good survival from intensive care (82 and 70%) but poor long-term survival (36 and 30%). Postoperative cases requiring ventilation are a large and very heterogeneous group. Results in this group are about average-74% survival in the ITU and 43% alive at one year. Searle points out the prognostic significance of the number of complications. For survival in the ITU this varied from 94% in patients with no complications to 20% in patients with three or four and 0% with six or more. On the matter of cost, Witek et al2 make the point that the ITU charges were similar for survivors and for those who died (US$2200 in 1980). The average duration of stay in the ITU was about 6 days for both survivors and non-survivors. However, the total hospital charges were greater in survivors, owing to their longer stay in hospital. The ITU charges represented 16 and 25%, respectively, of the total hospital bill in these two categories of patient. The cost of intensive therapy in a British district general hospital in 1985 is roughly 350-450 a day. The high cost is very largely due to the high staff/patient ratio. So, when a patient is admitted to the ITU an average stay of 6 days consumes about z2400 of National Health Service resources compared with about 600 for a similar period in an acute ward. Of course, admission to the ITU may be life-saving, in which case it is obviously the correct course, but where hope of recovery is nil or where recovery can be expected in the general ward, intensive therapy is a waste of resources. More than that, inappropriate referral of hopeless cases is also bad medicine. It is unfair on ITU staff and may cause unnecessary suffering to the patient and relatives. Decisions as to whether to admit to the ITU are difficult and except in obvious cases should not be left to junior hospital staff. A knowledge of the likely outcome, both short and long term, provided by these studies may help in these decisions though the results need to be applied with caution in the individual case. The hardest decision is what to do in the case where inappropriate intensive therapy has already been started or when a patient in the ITU passes from the hopeful to the hopeless. A common situation mentioned by Searlel is the postoperative patient in whom surgeons have invested hours of effort-for instance, attempting to deal with a leaking abdominal aneurysm in an elderly man. It is difficult in such a case to refuse continued intensive care. In these circumstances one must avoid "the Vietnam mentality". Many people felt that the United States could not pull out of Vietnam because that would have let down all the American soldiers who had laid down
their lives there. Somehow one must focus on what is happening now and assess the appropriateness of continuing intensive care from this point on. Figures from the type of audit in these papers may help in these very difficult decisions. RECOVERY AFTER RELIEF OF RENAL OBSTRUCTION THE effect of bladder outflow obstruction on renal function on the intravesical pressure that develops. When intrinsic bladder pressure is high, the features tend to be those of glomerular dysfunction-uraemia, hypertension, and salt and water retention. 1,2 When intravesical pressure is low, renal tubular damage predominates with failure of sodium reabsorption and countercurrent mechanisms,3
depends partly
inability to concentrate or dilute the urine,4and impairment of acidificationa the result can be a profound saline diuresis and acidosis. When obstruction is relieved, there may be a further saline diuresis resulting in hypovolaemia.6,7 At least three mechanisms contribute to this potentially hazardous effect-clearance of retained solutes such as urea;clearance of excess fluid and electrolytes; and tubular dysfunction, with excretion of urine of osmolality similar to that of plasma.’,9 (Matters may be made worse by infection in an already damaged and catheterised urinary tract.) Long ago, Chisholm9,10 and Beck" warned of the dangers of giving too much fluid in these circumstances and lately Bishop has delivered the same message.12 However, it is not helpful to generalise about patients "rarely" needing intravenous fluids after relief of urinary obstruction. Of Bishop’s 55 patients, 12 did become hyponatraemic and 10 needed intravenous fluids. To avoid saline depletion, with its considerable dangers, two things are important. The first is to remember that saline depletion can be difficult to detect clinically without measurement of central venous pressure, and so to be alert to this potential hazard especially in patients who have already experienced a prolonged diuresis due to partial obstruction; 13 fluid replacement can then be guided by simple measurements of blood pressure, fluid balance, and body weight, and by central venous pressure monitoring when necessary. The second is not to replace saline losses with water in the form of 5% dextrose, which can often cause severe hyponatraemia, but to use physiological saline, supplemented to correct any hypokalaemia and acidosis. 1 Mitchell
JP. Principles of transurethral resection and haemostasis. Bristol: John Wright, 1972: chap 18. 2. George NJR, O’Reilly PH, Barnard RJ, Blacklock NJ High pressure chronic retention Br Med J 1983, 286: 1780-83 3. Suki WN, Guthrie AG, Martinez-Maldonado M, Eknoyan G Effects of ureteral pressure elevation on renal hemodynamics and urine concentration. Am J Physiol 1971, 220: 38-43. 4. Olesen S, Madsen PO. Renal function during experimental hydronephrosis: function during partial obstruction following contralateral nephrectomy in the dog. J Urol 99: 692-99 GM. Distal tubular function in chronic hydronephrosis. Quart J Med 1961, 30: 339-55. 6. Wilson B, Reisman DD, Moyer CA Fluid balance in the urological patient. J Urol
1968,
5.
Berlyne
1951; 66: 805-15.
NS, Shwayri EI, Rearden JB, Kellog D, Merrill JP, Holmes JH. An abnormality in renal function resulting from urinary tract obstruction. Am J Med
7 Bricker
1957; 23: 554-64. 8 9
Maher JF, Schreiner GE, Waters TJ Osmotic diuresis due to retained urea after release of obstructive uropathy. N Engl J Med 1963; 268: 1099-104. Chisholm GD Bilateral renal clearance studies in experimental obstructive uropathy.
Proc R Soc Med 1964; 57: 571-73. 10 Chisholm GD Pathophysiology of obstructive uropathy. In: Chisholm GD, Innes Williams D, eds. Scientific foundations of urology, 2nd ed. London: Heinemann, 1982: 98-105 11. Beck AD. Benign prostatic hypertrophy and uraemia. Br J Surg 1970; 57: 561-65. 12 Bishop MC Diuresis and renal functional recovery in chronic retention. Br J Urol 1985, 57: 1-5. 13. Roussak NJ, Oleesky S. Water-losing nephritis: syndrome simulating diabetes insipidus Quart J Med 1954, 23: 147-64.