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PROLONGED PARESIS FOLLOWING GALLAMINE
CORRESPONDENCE PROLONGED PARESIS FOLLOWING GALLAM1NE
Sir,—Dr. Feldman's reply to my letter (Brit. J. Anaesth., 36, 323) has provided some of the information I was hoping for. Barry and Malloy (1962) have suggested that acute renal failure is preceded by a reversible functional failure in most patients. Their results have shown that intravenous mannitol given at the right moment will produce a diuresis and prevent the organic renal failure. My personal experience has confirmed this. This means that acute renal failure occurring in hospital is a preventable disease. In this case a simple peritonitis was allowed to develop into a lethal condition. Why? I believe thai failure to recognize unsuspected dehydration was what led to renal shutdown and eventually to irreversible renal damage. According to Campbell, Dickinson and Slater (1963), "if the signs of fluid depletion are obvious (this woman was described as 'clinically dehydrated') then the deficit amounts to about 6 per cent of the body weight". Assuming she was a small woman of 8 stone (45 kg), 6 per cent of this is 2.7 kg, which is equivalent to 2.7 1. She was given 4 pints of blood. In each pint of blood there are only the 120 ml of citrate fluid available for use outside the bloodstream; the rest is kept inside the vascular system by the plasma proteins in the donor's blood. So this woman had 2,480 ml of usable fluid in the 12 hours following operation. She would have lost at least 300 ml of water through her skin and her lungs in that time, making a minimum deficit of 620 ml. To which must be added an unspecified amount aspirated from the peritoneal cavity during the operation, from her stomach while the Ryle's tube was in place before and after operation, and there must have been further loss of fluid into the bowel and into the peritoneum as a result of her general peritonitis. Dr. Feldman states that in England it is customary to operate on patients with peritonitis following bowel perforation as an emergency. The same is true in Australia. However, we are still old-fashioned enough to believe that it is wiser, and better for the patient, to restore the patient's fluid and electrolyte levels to near normal before operation. The 3 hours between admission and operation would give plenty of time to rehydrate the patient without risking heart failure, as the electrolyte solutions given intravenously pass out of the vascular system very rapidly in the dehydrated patient In Dr. Feldman's letter there is no mention of pre-operative resuscitation. Dr. Feldman is "at a loss to know what 'attention to detail in the pre-operative, operative and early postoperative phases' that was not given to this patient either at Kingston Hospital or . . . ". Putting myself in the position of the anaesthetist I would give the following answers to the question "Where might I have made a mistake in my treatment?"
(1) Under-estimate of fluid deficit. (2) No pre-operative resuscitation. (3) Replacement of electrolytes in the wrong proportions. Our hospital laboratory can tell us the serum electrolyte levels 20 minutes after the blood has been taken. Perhaps Dr. Feldman is not so lucky. (4) Operation was performed before the electrolyte and water levels had been restored to normal. (5) The amount of fluid sucked out of the peritoneum and the stomach seems to have been left out of the calculation of water requirements. (6) Assuming that, because the patient's fluid intake exceeded her output, the patient had a positive water balance. (7) Assuming that oliguria was due to irreversible renal damage without using mannitol to see if a diuresis could be produced. From the closing paragraph of Dr. Feldman's letter it would seem that his second case of prolonged paresis after gallamine also had poor renal function. Perhaps the answer to the final paragraph of my letter is "Keep the kidneys secreting and your won't have this trouble". R. J. KNIGHT
Victoria REFERENCES
Barry, K. G., and Malloy, J. P. (1962). Oliguric renal failure, evaluation and therapy by the intravenous infusion of mannitol. /. Amer. med. Ass., 179, 510. Campbell, B. J. M., Dickinson, C. J., and Slater, J. D. H. (1963). Clinical Physiology, 2nd ed., p. 31. Oxford: Blackwell.
The following reply was sent by Drs. Feldman and Levi. Sir,—Dr. Knight's letter reveals a continued failure to grasp the point of interest of this case. It was implicit in the title of our article and reiterated in our letter. The patient described developed paresis lasting five days following a modest dose of gallamine. This cannot be explained as a simple failure of renal excretion of the drug as the paresis was not reversed by neostigmine. Muscle power did, however, return to normal during haemodialysis. This unusual event was considered important enough to record briefly. It is not our intention to discuss the treatment of renal disease or tubular necrosis as this has no bearing whatsoever on these observations. We can see no useful purpose that would be served by commenting on Dr. Knight's irrelevant and highly speculative hypothesis.
Primed in Great Britain by John Shcrratt
S. A. FELDMAN J. LEVI
London
Sir,—Dr. Feldman's reply to my letter (Brit. J. Anaesth., 36, 323) has provided some of the information I was hoping for. Barry and Malloy (1962) have suggested that acute renal failure is preceded by a reversible functional failure in most patients. Their results have shown that intravenous mannitol given at the right moment will produce a diuresis and prevent the organic renal failure. My personal experience has confirmed this. This means that acute renal failure occurring in hospital is a preventable disease. In this case a simple peritonitis was allowed to develop into a lethal condition. Why? I believe thai failure to recognize unsuspected dehydration was what led to renal shutdown and eventually to irreversible renal damage. According to Campbell, Dickinson and Slater (1963), "if the signs of fluid depletion are obvious (this woman was described as 'clinically dehydrated') then the deficit amounts to about 6 per cent of the body weight". Assuming she was a small woman of 8 stone (45 kg), 6 per cent of this is 2.7 kg, which is equivalent to 2.7 1. She was given 4 pints of blood. In each pint of blood there are only the 120 ml of citrate fluid available for use outside the bloodstream; the rest is kept inside the vascular system by the plasma proteins in the donor's blood. So this woman had 2,480 ml of usable fluid in the 12 hours following operation. She would have lost at least 300 ml of water through her skin and her lungs in that time, making a minimum deficit of 620 ml. To which must be added an unspecified amount aspirated from the peritoneal cavity during the operation, from her stomach while the Ryle's tube was in place before and after operation, and there must have been further loss of fluid into the bowel and into the peritoneum as a result of her general peritonitis. Dr. Feldman states that in England it is customary to operate on patients with peritonitis following bowel perforation as an emergency. The same is true in Australia. However, we are still old-fashioned enough to believe that it is wiser, and better for the patient, to restore the patient's fluid and electrolyte levels to near normal before operation. The 3 hours between admission and operation would give plenty of time to rehydrate the patient without risking heart failure, as the electrolyte solutions given intravenously pass out of the vascular system very rapidly in the dehydrated patient In Dr. Feldman's letter there is no mention of pre-operative resuscitation. Dr. Feldman is "at a loss to know what 'attention to detail in the pre-operative, operative and early postoperative phases' that was not given to this patient either at Kingston Hospital or . . . ". Putting myself in the position of the anaesthetist I would give the following answers to the question "Where might I have made a mistake in my treatment?"
(1) Under-estimate of fluid deficit. (2) No pre-operative resuscitation. (3) Replacement of electrolytes in the wrong proportions. Our hospital laboratory can tell us the serum electrolyte levels 20 minutes after the blood has been taken. Perhaps Dr. Feldman is not so lucky. (4) Operation was performed before the electrolyte and water levels had been restored to normal. (5) The amount of fluid sucked out of the peritoneum and the stomach seems to have been left out of the calculation of water requirements. (6) Assuming that, because the patient's fluid intake exceeded her output, the patient had a positive water balance. (7) Assuming that oliguria was due to irreversible renal damage without using mannitol to see if a diuresis could be produced. From the closing paragraph of Dr. Feldman's letter it would seem that his second case of prolonged paresis after gallamine also had poor renal function. Perhaps the answer to the final paragraph of my letter is "Keep the kidneys secreting and your won't have this trouble". R. J. KNIGHT
Victoria REFERENCES
Barry, K. G., and Malloy, J. P. (1962). Oliguric renal failure, evaluation and therapy by the intravenous infusion of mannitol. /. Amer. med. Ass., 179, 510. Campbell, B. J. M., Dickinson, C. J., and Slater, J. D. H. (1963). Clinical Physiology, 2nd ed., p. 31. Oxford: Blackwell.
The following reply was sent by Drs. Feldman and Levi. Sir,—Dr. Knight's letter reveals a continued failure to grasp the point of interest of this case. It was implicit in the title of our article and reiterated in our letter. The patient described developed paresis lasting five days following a modest dose of gallamine. This cannot be explained as a simple failure of renal excretion of the drug as the paresis was not reversed by neostigmine. Muscle power did, however, return to normal during haemodialysis. This unusual event was considered important enough to record briefly. It is not our intention to discuss the treatment of renal disease or tubular necrosis as this has no bearing whatsoever on these observations. We can see no useful purpose that would be served by commenting on Dr. Knight's irrelevant and highly speculative hypothesis.
Primed in Great Britain by John Shcrratt
S. A. FELDMAN J. LEVI
London