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POTASSIUM THERAPY A BREAK WITH TRADITION
175 well. We felt that if we could relieve our patient of his heartfailure and enable him to lead a restricted life in the future we should have achieved something worth while. This objective has been reached, and he is now able to get about without discomfort and to manage without the help of diuretics. The ultimate prognosis is of course unknown, but it may be no worse than that of any male of his age who has had a first coronary thrombosis with extensive myocardial infarction. As far
as
operative technique is concerned, myocardial
anoxia in patients with coronary-artery and myocardial disease is likely to be badly tolerated. For this reason we believe that hypothermia should be used, and that periods
cross-clamping should be strictly limited to 5 minutes, and alternated with periods of coronary-artery flushing " for at least 1 minute. The timing of operation may be of great importance in these patients. There seems little point in advising operation on a desperately ill patient immediately after extensive myocardial infarction, because the infarcted tissue surrounding the perforation may be too soft and friable to hold sutures (Romanoff and Cooley 1960). For this reason, if the patient can be supported through the early phase with intensive medical treatment, it may be wise to delay operation for at least a month, by which time firm edges to the defect will have had a chance to form. One month after his perforation our patient was considered too ill to have a chance of surviving operation, but at 3 months of aortic
"
the tissue around the defect was firm and held sutures without trouble. The site of the ventriculotomy must also be of considerable importance. Any incision must interfere further with the coronary blood-supply. The least possible damage will be done by incising through an infarcted area, but this may not always be visible. When it is not, there is a natural tendency to make the conventional anterior right ventriculotomy. We think this is unsuitable and suggest that the approach for such cases is through the inferior surface of the right ventricle, near to the apex. This site is away from major vessels and also more directly over the defect which, unlike the congenital variety, is always in the muscular septum and near the apex of the heart. In our patient the obvious entry was through the large aneurysm of the left ventricle, and excision of the aneurysmal tissue gave perfect exposure of the septum.
Summary The first successful closure of an interventricular septal perforation, after myocardial infarction, is described. A left ventricular aneurysm was excised in the same
patient.
A BREAK WITH TRADITION
HANS
JØRGEN CLEMENTSEN
Cand. Med.
Copenhagen
From the Department
of Anœsthesia, Bispebjerg Hospital, Copenhagen, Denmark
TRADITIONALLY, in the management of potassium deficiency, there are certain doses of parenteral potassium which must not be exceeded. Le Quesne (1957) has put these at 20 mEq. per hour and 100 mEq. per 24 hours. Others have suggested 80 mEq. per 24 hours (Bland 1956, Wilkinson 1960), adding, however, that greater doses may sometimes have to be given. But it is my impression that too much attention is paid to these upper limits, so that intravenous potassium is often given with too much hesitation and in inadequate dosage, especially in cases where really intensive parenteral potassium therapy is indicated. A major acute loss of potassium quickly leads to depletion of intracellular potassium. Potassium ions, moving outward from the cells, will be replaced in the intracellular phase by sodium and hydrogen ions in the ratio 2:1. The result is extracellular alkalosis combined with intracellular acidosis (Cooke et al. 1952). The body tries to compensate for the extracellular alkalosis by respiratory adjustment; retention of CO2 leads to an increase in the extracellular concentrations of H-’ and HCOg’. On the other hand, the renal response is " paradoxical ", because the increased intracellular H concentration in the tubular cells causes a greater urinary output of HT which aggravates the extracellular alkalosis. Hypokalaemic alkalosis can be effectively treated only by supplying sufficient potassium. The most characteristic signs of the condition are apathy, reduced muscular power, intestinal paresis leading on to paralytic ileus, muscular fibrillations and tetanic twitchings, mental confusion, and a tendency to oedema. This last is particularly outstanding in patients who have been wrongly treated with large quantities of saline solution. Electrocardiographic changes, in the form of flattened T waves, may be observed as a result of a reduced concentration of extracellular potassium. The case-histories which follow illustrate how hypokalaemic extracellular alkalosis may prove refractory to " potassium given in traditional " doses, while a dose many times higher may quickly restore conditions to normal. Case-records
Case 1 REFERENCES
Bailey, C. P., Bolton, H. E., Nichols, H., Gilman, R. A. (1958) J. thorac. Surg. 35, 37. Bond, V. F., Welfare, C. R., Lide, T. N., McMillan, R. L. (1953) Ann. intern. Med. 38, 706.
Brum, F. (1923) Wien. Arch. inn. Med. 6, 533. Cooley, D. A., Belmonte, B. A., Zeis, L. B., Schnur,
S. (1957) Surgery, 41, 930. — Henley, W. S., Amad, K. H., Chapman, D. W. (1959) Ann. Surg. 150, 595. Diaz-Rivera, R. S., Miller, A. J. (1948) Amer. Heart J. 35, 126. Edmondson, H. A., Hoxie, H. J. (1942) ibid. 24, 719. Goetz, A. A., Gropper, A. N. (1954) ibid. 48, 130. Gottsegen, G., Szám, I., Romoda, T., Matheides, P. (1957) Acta med. scand.
158, 157.
Harrison, R. J., Shillingford, J. P., Allen, G. T., Teare, D. (1961) J. i, 1066. Hudson, W. A. (1958) Proc. R. Soc. Med. 51, 591. Latham,
Brit. med.
P. M. (1846) Lectures on Clinical Medicine, comprising Diseases of the Heart; vol. 2, p. 168. London. Long, D. M., Sanchez, L., Varco, R. L., Lillehei, C. W. (1961) Surgery, 50. 12. Maher, J. F., Mallory, G. K., Laurenzi, G. A. (1956) New Engl. J. Med.
255, 1. Malone, R. G. S., Parkes,
POTASSIUM THERAPY
W. E. (1955) Brit. Heart J.
17,
448.
46-year-old man, weighing 100 kg. (15 st. 5 lb.), had a pancreatitis and cholecystitis; he was admitted on May 30, 1961, after a few days’ abdominal pain and occasional vomiting. He had previously been in good health except for a brief mild attack of acute pancreatitis diagnosed during a stay A
recurrent
MR. COLLIS AND OTHERS:
REFERENCES—continued
Muller, O., Humerfelt, S., Rasmussen, H., Storstein, O. (1950) Acta cardiol., Brux. 5, 633. Oblath, R. W., Levinson, D. C., Griffith, G. C. (1952) J. Amer. med. Ass. 149, 1276. Romanoff, H., Cooley, D. A. (1960) Israel med. J. 19, 103. Sager, R. V. (1934) Arch. intern. Med. 53, 140. Sanders, R. J., Kern, W. H., Blount, S. G. (1956) Amer. Heart J. 51, 736. Shickman, M. D., Fields, J., Pearce, M. L. (1959) Arch. intern. Med. 103, 140.
Schlappi, J. C., Landale, D. G. (1954) Amer. Heart J. 47, 432. Telling, M., Wooler, G. H. (1961) Lancet, ii, 181. Wood, F. C., Livezey, M. M. (1942) Amer. Heart J. 24, 807. Wood, P. (1956) Diseases of the Heart and Circulation. London. Zucker, R., Leibowitz, S., Brody, H., Sussman, R. M. (1952) Arch. intern. Med. 89, 899.
176 in hospital a year earlier. The urine had then been free of sugar. On admission the temperature, pulse-rate, electrocardiogram (E.c..), and serum-electrolytes were normal (fig. 1). 3 days later the rectal temperature rose to 107°F and the pulse-rate to 144 per minute. Treatment with a cooling mattress was begun, and pethidine and chlorpromazine were given. The temperature and pulse-rate returned to normal in a few hours and remained normal throughout the rest of the illness. Gastric suction yielded increasing quantities of gastric juice-from 500 to 1000 ml. per 24 hours. The patient was treated with penicillin and propantheline bromide; blood and plasma were transfused, and 5% glucose solution and 0-9% sodium-chloride solution were given intravenously; 2-4 g. potassium chloride was given parenterally, in each 24 hours. Moreover, 12 l.u. long-acting insulin was given daily for the mild diabetes which had developed during his stay in hospital. In spite of this treatment, the patient’s condition steadily worsened. The abdomen became even more distended, and was dull to percussion all over. Moderate alkalosis remained unchanged. On June 7, for example, the following results were obtained: total CO2-combining power 34-2 mEq. per litre;
Fig. 2-Case 1 : electrocardiographic changes (leads infusion of 25 g. potassium chloride.
I and
II) during
serum-chloride 90 mEq. per litre; serum-potassium 3-2 mEq. per litre; serum-calcium 9-5 mg. per 100 mI.; and serumcreatinine 1-5 mg. per 100 ml. The clinical picture, however, had become far more serious than these results suggest. The patient was hallucinated, and had constant muscular fibrillations and tetanic twitchings. The electrolyte and fluid balance revealed a moderate retention of water and sodium, as well as an apparently small negative potassium balance. The condition was therefore thought to be the result of severe intracellular electrolyte disturbances due to the loss of large amounts of potassium into fluid in the distended paralytic intestine. Intravenous administration had become increasingly difficult because veins had had to be pierced several times and phlebitis set in. On the evening of June 7, however, a suitable vein was found, and it was decided to give a large dose of potassium in a small quantity of fluid. Earlier in the day the patient had received an intravenous infusion of 4 g. potassium chloride; he was given an additional 25 g. dissolved in 2000 ml. 5% glucose solution with 48 l.u. of soluble insulin. This dose of potassium, which corresponds to 335 mEq. potassium, was infused over 5 hours 20 minutes without any untoward side-effects. No alarming E.C.G. changes occurred; on the contrary, the previous hypokalxmic abnormalities of the T waves disappeared (fig. 2). There was an almost dramatic improvement in the alarming clinical signs during the intensive potassium therapy and the subsequent few hours. Blood samples were taken .F/2 hours after the potassium infusion was completed; analyses showed that the alkalosis had been abolished without the potassium level having been pushed above the normal. The blood-sugar level was 101 mg. per 100 ml. The paralytic ileus resolved within the next few days, and the patient was discharged in good health on June 22.
Fig. 1-Case 1: serum concentrations of potassium, carbon dioxide, and chloride, with potassium and sodium balances, before and after treatment of hypokalsemic alkalosis with large doses of potassium chloride.
Case 2 A 61-year-old woman, weighing 55 kg. (8 st. 1 Ib.), had mild diabetes mellitus which did not necessitate insulin. She was admitted after a short period of vomiting which had led to hypokalaemic alkalosis (fig. 3) and paralytic ileus, which was confirmed by X-ray examination. Her general condition was affected surprisingly little. Gastric juice was not aspirated. After my experience with case 1, I decided to treat her
177 "
according to the same principle. After 24 hours’ traditional " chloride potassium therapy, she was given 28 g. potassium solution with of mi. 5% 2000 glucose (375 mEq. potassium) in 40 LU. soluble insulin. This amount of potassium was given intravenously in 5 hours 45 minutes. The serum-potassium, serum-bicarbonate, and pH were controlled hourly during the infusion. The estimations of bicarbonate and pH were made on samples of capillary blood (Siggard Anderson et al. 1960). The serum-potassium level rose gradually from 1.5 mEq. per litre before the treatment to 4-3 mEq. immediately after the infusion had been completed. But the E.C.G., which had shown flat T waves before the
potassium infusion, was unchanged. During the next few days "traditional potassium therapy was continued. The hypokalaemic alkalosis and the paralytic ileus resolved a few days after the large dose of potassium had been given. This patient excreted only 20 mEq. potassium during the 24 hours in which she received a total of 425 mEq. "
Discussion
When the content of potassium and sodium in the transfused blood-plasma and electrolyte solutions is compared with the corresponding loss in the urine and
gastric juice, it appears that, on June 7, the first patient received 392 mEq. potassium ; 335 mEq. of this was given
intravenously in5 hours 20 minutes, and 333 mEq. was retained. The of part greater this potassium must have replaced sodium and hydrogen ions in the cells. The extracellular alkalosis was abolished by these emigrating
hydrogen ions, and the urinary output of sodium increased. Over the 6 days after the large dose of potassium there was a
negative
so-
dium balance of 817 mEq. and a negative fluid balance of 6000 ml. Each litre of water was therefore excreted with 136 mEq. of sodium, and this corresFig. 3-Case
2: data
as
in fig, 1.
(bicarbonate = standard bicarbonate)
ponds to
the
closely actual
concentration. After the large potassium infusion, an increasing dose of potassium chloride did not lead to potassium retention, showing that the intracellular potassium depots were then filled. extracellular
sodium
In case 2 there was also distinct retention of potassium after the intravenous infusion of 375 mEq.; only 20 mEq. was excreted in the urine. By the next day the serumpotassium level had already dropped to 2-2 mEq. per litre. A normal serum level was apparently not attained until the intracellular potassium concentration had returned to normal.
The
of insulin and glucose during the intensive potassium therapy was based on the well-known treatment of alarming acute hyperkalmmia with glucose and insulin, which promote the intracellular deposition of potassium that was desired in this particular case. use
Conclusion
Potassium, given intravenously with glucose and insulin, proved to be retained in large quantities within a surprisingly short time when the dose did not exceed the intracellular potassium deficit. In the management of potassium deficiency the amount of potassium given should exceed the measured and estimated losses, even though this means exceeding the traditional upper limits of dosage. If possible, the potassium should be administered by mouth. Where it is given intravenously in excess of the traditional quantities, the patient should be under close supervision which includes electrocardiographic control and measurement of the potassium and sodium balance. Summary Two cases are described in which hypokalaemic alkalosis was treated with 25-28 g. potassium chloride (335-375 mEq. potassium), combined with glucose and insulin, and infused intravenously over some 5 hours.
In both cases, after this massive dose of potassium, the condition promptly returned to normal without any untoward side-effects. The greater part of the potassium was
retained.
Severe potassium deficiency may best be treated by the rapid intravenous administration of potassium chloride in doses whose upper limit should be determined exclusively by the potassium deficit at the time. To accelerate the transfer of potassium to the intracellular phase, such a massive dose should be given in combination with glucose and insulin. During the infusion of potassium the patient must be under close supervision, which includes electrocardiographic control and measurement of the potassium and
sodium balance. I wish
Hospital
to thank the staff of the central for their kind assistance.
laboratory
of
Bispebjurg
REFERENCES
Bland, J.
H.
London.
(1956) Disturbances of Body Fluids; p. 497. Philadelphia and
Cooke, R. E., Segar, W. E., Cheek, D. B., Coville, F. E., Darrow, D. C. (1952) J. clin. Invest. 31, 798. Le Quesne, L. P. (1957) Fluid Balance in Surgical Practice; p. 85. London.
Siggard Andersen, O., Engel, K., Jorgensen, K., Astrup, P. (1960) Scand. J.
clin. Lab. Invest. 12, 172. Wilkinson, A. W. (1960) Body Fluids in Surgery; p. 64. Edinburgh and
London.
as
operative technique is concerned, myocardial
anoxia in patients with coronary-artery and myocardial disease is likely to be badly tolerated. For this reason we believe that hypothermia should be used, and that periods
cross-clamping should be strictly limited to 5 minutes, and alternated with periods of coronary-artery flushing " for at least 1 minute. The timing of operation may be of great importance in these patients. There seems little point in advising operation on a desperately ill patient immediately after extensive myocardial infarction, because the infarcted tissue surrounding the perforation may be too soft and friable to hold sutures (Romanoff and Cooley 1960). For this reason, if the patient can be supported through the early phase with intensive medical treatment, it may be wise to delay operation for at least a month, by which time firm edges to the defect will have had a chance to form. One month after his perforation our patient was considered too ill to have a chance of surviving operation, but at 3 months of aortic
"
the tissue around the defect was firm and held sutures without trouble. The site of the ventriculotomy must also be of considerable importance. Any incision must interfere further with the coronary blood-supply. The least possible damage will be done by incising through an infarcted area, but this may not always be visible. When it is not, there is a natural tendency to make the conventional anterior right ventriculotomy. We think this is unsuitable and suggest that the approach for such cases is through the inferior surface of the right ventricle, near to the apex. This site is away from major vessels and also more directly over the defect which, unlike the congenital variety, is always in the muscular septum and near the apex of the heart. In our patient the obvious entry was through the large aneurysm of the left ventricle, and excision of the aneurysmal tissue gave perfect exposure of the septum.
Summary The first successful closure of an interventricular septal perforation, after myocardial infarction, is described. A left ventricular aneurysm was excised in the same
patient.
A BREAK WITH TRADITION
HANS
JØRGEN CLEMENTSEN
Cand. Med.
Copenhagen
From the Department
of Anœsthesia, Bispebjerg Hospital, Copenhagen, Denmark
TRADITIONALLY, in the management of potassium deficiency, there are certain doses of parenteral potassium which must not be exceeded. Le Quesne (1957) has put these at 20 mEq. per hour and 100 mEq. per 24 hours. Others have suggested 80 mEq. per 24 hours (Bland 1956, Wilkinson 1960), adding, however, that greater doses may sometimes have to be given. But it is my impression that too much attention is paid to these upper limits, so that intravenous potassium is often given with too much hesitation and in inadequate dosage, especially in cases where really intensive parenteral potassium therapy is indicated. A major acute loss of potassium quickly leads to depletion of intracellular potassium. Potassium ions, moving outward from the cells, will be replaced in the intracellular phase by sodium and hydrogen ions in the ratio 2:1. The result is extracellular alkalosis combined with intracellular acidosis (Cooke et al. 1952). The body tries to compensate for the extracellular alkalosis by respiratory adjustment; retention of CO2 leads to an increase in the extracellular concentrations of H-’ and HCOg’. On the other hand, the renal response is " paradoxical ", because the increased intracellular H concentration in the tubular cells causes a greater urinary output of HT which aggravates the extracellular alkalosis. Hypokalaemic alkalosis can be effectively treated only by supplying sufficient potassium. The most characteristic signs of the condition are apathy, reduced muscular power, intestinal paresis leading on to paralytic ileus, muscular fibrillations and tetanic twitchings, mental confusion, and a tendency to oedema. This last is particularly outstanding in patients who have been wrongly treated with large quantities of saline solution. Electrocardiographic changes, in the form of flattened T waves, may be observed as a result of a reduced concentration of extracellular potassium. The case-histories which follow illustrate how hypokalaemic extracellular alkalosis may prove refractory to " potassium given in traditional " doses, while a dose many times higher may quickly restore conditions to normal. Case-records
Case 1 REFERENCES
Bailey, C. P., Bolton, H. E., Nichols, H., Gilman, R. A. (1958) J. thorac. Surg. 35, 37. Bond, V. F., Welfare, C. R., Lide, T. N., McMillan, R. L. (1953) Ann. intern. Med. 38, 706.
Brum, F. (1923) Wien. Arch. inn. Med. 6, 533. Cooley, D. A., Belmonte, B. A., Zeis, L. B., Schnur,
S. (1957) Surgery, 41, 930. — Henley, W. S., Amad, K. H., Chapman, D. W. (1959) Ann. Surg. 150, 595. Diaz-Rivera, R. S., Miller, A. J. (1948) Amer. Heart J. 35, 126. Edmondson, H. A., Hoxie, H. J. (1942) ibid. 24, 719. Goetz, A. A., Gropper, A. N. (1954) ibid. 48, 130. Gottsegen, G., Szám, I., Romoda, T., Matheides, P. (1957) Acta med. scand.
158, 157.
Harrison, R. J., Shillingford, J. P., Allen, G. T., Teare, D. (1961) J. i, 1066. Hudson, W. A. (1958) Proc. R. Soc. Med. 51, 591. Latham,
Brit. med.
P. M. (1846) Lectures on Clinical Medicine, comprising Diseases of the Heart; vol. 2, p. 168. London. Long, D. M., Sanchez, L., Varco, R. L., Lillehei, C. W. (1961) Surgery, 50. 12. Maher, J. F., Mallory, G. K., Laurenzi, G. A. (1956) New Engl. J. Med.
255, 1. Malone, R. G. S., Parkes,
POTASSIUM THERAPY
W. E. (1955) Brit. Heart J.
17,
448.
46-year-old man, weighing 100 kg. (15 st. 5 lb.), had a pancreatitis and cholecystitis; he was admitted on May 30, 1961, after a few days’ abdominal pain and occasional vomiting. He had previously been in good health except for a brief mild attack of acute pancreatitis diagnosed during a stay A
recurrent
MR. COLLIS AND OTHERS:
REFERENCES—continued
Muller, O., Humerfelt, S., Rasmussen, H., Storstein, O. (1950) Acta cardiol., Brux. 5, 633. Oblath, R. W., Levinson, D. C., Griffith, G. C. (1952) J. Amer. med. Ass. 149, 1276. Romanoff, H., Cooley, D. A. (1960) Israel med. J. 19, 103. Sager, R. V. (1934) Arch. intern. Med. 53, 140. Sanders, R. J., Kern, W. H., Blount, S. G. (1956) Amer. Heart J. 51, 736. Shickman, M. D., Fields, J., Pearce, M. L. (1959) Arch. intern. Med. 103, 140.
Schlappi, J. C., Landale, D. G. (1954) Amer. Heart J. 47, 432. Telling, M., Wooler, G. H. (1961) Lancet, ii, 181. Wood, F. C., Livezey, M. M. (1942) Amer. Heart J. 24, 807. Wood, P. (1956) Diseases of the Heart and Circulation. London. Zucker, R., Leibowitz, S., Brody, H., Sussman, R. M. (1952) Arch. intern. Med. 89, 899.
176 in hospital a year earlier. The urine had then been free of sugar. On admission the temperature, pulse-rate, electrocardiogram (E.c..), and serum-electrolytes were normal (fig. 1). 3 days later the rectal temperature rose to 107°F and the pulse-rate to 144 per minute. Treatment with a cooling mattress was begun, and pethidine and chlorpromazine were given. The temperature and pulse-rate returned to normal in a few hours and remained normal throughout the rest of the illness. Gastric suction yielded increasing quantities of gastric juice-from 500 to 1000 ml. per 24 hours. The patient was treated with penicillin and propantheline bromide; blood and plasma were transfused, and 5% glucose solution and 0-9% sodium-chloride solution were given intravenously; 2-4 g. potassium chloride was given parenterally, in each 24 hours. Moreover, 12 l.u. long-acting insulin was given daily for the mild diabetes which had developed during his stay in hospital. In spite of this treatment, the patient’s condition steadily worsened. The abdomen became even more distended, and was dull to percussion all over. Moderate alkalosis remained unchanged. On June 7, for example, the following results were obtained: total CO2-combining power 34-2 mEq. per litre;
Fig. 2-Case 1 : electrocardiographic changes (leads infusion of 25 g. potassium chloride.
I and
II) during
serum-chloride 90 mEq. per litre; serum-potassium 3-2 mEq. per litre; serum-calcium 9-5 mg. per 100 mI.; and serumcreatinine 1-5 mg. per 100 ml. The clinical picture, however, had become far more serious than these results suggest. The patient was hallucinated, and had constant muscular fibrillations and tetanic twitchings. The electrolyte and fluid balance revealed a moderate retention of water and sodium, as well as an apparently small negative potassium balance. The condition was therefore thought to be the result of severe intracellular electrolyte disturbances due to the loss of large amounts of potassium into fluid in the distended paralytic intestine. Intravenous administration had become increasingly difficult because veins had had to be pierced several times and phlebitis set in. On the evening of June 7, however, a suitable vein was found, and it was decided to give a large dose of potassium in a small quantity of fluid. Earlier in the day the patient had received an intravenous infusion of 4 g. potassium chloride; he was given an additional 25 g. dissolved in 2000 ml. 5% glucose solution with 48 l.u. of soluble insulin. This dose of potassium, which corresponds to 335 mEq. potassium, was infused over 5 hours 20 minutes without any untoward side-effects. No alarming E.C.G. changes occurred; on the contrary, the previous hypokalxmic abnormalities of the T waves disappeared (fig. 2). There was an almost dramatic improvement in the alarming clinical signs during the intensive potassium therapy and the subsequent few hours. Blood samples were taken .F/2 hours after the potassium infusion was completed; analyses showed that the alkalosis had been abolished without the potassium level having been pushed above the normal. The blood-sugar level was 101 mg. per 100 ml. The paralytic ileus resolved within the next few days, and the patient was discharged in good health on June 22.
Fig. 1-Case 1: serum concentrations of potassium, carbon dioxide, and chloride, with potassium and sodium balances, before and after treatment of hypokalsemic alkalosis with large doses of potassium chloride.
Case 2 A 61-year-old woman, weighing 55 kg. (8 st. 1 Ib.), had mild diabetes mellitus which did not necessitate insulin. She was admitted after a short period of vomiting which had led to hypokalaemic alkalosis (fig. 3) and paralytic ileus, which was confirmed by X-ray examination. Her general condition was affected surprisingly little. Gastric juice was not aspirated. After my experience with case 1, I decided to treat her
177 "
according to the same principle. After 24 hours’ traditional " chloride potassium therapy, she was given 28 g. potassium solution with of mi. 5% 2000 glucose (375 mEq. potassium) in 40 LU. soluble insulin. This amount of potassium was given intravenously in 5 hours 45 minutes. The serum-potassium, serum-bicarbonate, and pH were controlled hourly during the infusion. The estimations of bicarbonate and pH were made on samples of capillary blood (Siggard Anderson et al. 1960). The serum-potassium level rose gradually from 1.5 mEq. per litre before the treatment to 4-3 mEq. immediately after the infusion had been completed. But the E.C.G., which had shown flat T waves before the
potassium infusion, was unchanged. During the next few days "traditional potassium therapy was continued. The hypokalaemic alkalosis and the paralytic ileus resolved a few days after the large dose of potassium had been given. This patient excreted only 20 mEq. potassium during the 24 hours in which she received a total of 425 mEq. "
Discussion
When the content of potassium and sodium in the transfused blood-plasma and electrolyte solutions is compared with the corresponding loss in the urine and
gastric juice, it appears that, on June 7, the first patient received 392 mEq. potassium ; 335 mEq. of this was given
intravenously in5 hours 20 minutes, and 333 mEq. was retained. The of part greater this potassium must have replaced sodium and hydrogen ions in the cells. The extracellular alkalosis was abolished by these emigrating
hydrogen ions, and the urinary output of sodium increased. Over the 6 days after the large dose of potassium there was a
negative
so-
dium balance of 817 mEq. and a negative fluid balance of 6000 ml. Each litre of water was therefore excreted with 136 mEq. of sodium, and this corresFig. 3-Case
2: data
as
in fig, 1.
(bicarbonate = standard bicarbonate)
ponds to
the
closely actual
concentration. After the large potassium infusion, an increasing dose of potassium chloride did not lead to potassium retention, showing that the intracellular potassium depots were then filled. extracellular
sodium
In case 2 there was also distinct retention of potassium after the intravenous infusion of 375 mEq.; only 20 mEq. was excreted in the urine. By the next day the serumpotassium level had already dropped to 2-2 mEq. per litre. A normal serum level was apparently not attained until the intracellular potassium concentration had returned to normal.
The
of insulin and glucose during the intensive potassium therapy was based on the well-known treatment of alarming acute hyperkalmmia with glucose and insulin, which promote the intracellular deposition of potassium that was desired in this particular case. use
Conclusion
Potassium, given intravenously with glucose and insulin, proved to be retained in large quantities within a surprisingly short time when the dose did not exceed the intracellular potassium deficit. In the management of potassium deficiency the amount of potassium given should exceed the measured and estimated losses, even though this means exceeding the traditional upper limits of dosage. If possible, the potassium should be administered by mouth. Where it is given intravenously in excess of the traditional quantities, the patient should be under close supervision which includes electrocardiographic control and measurement of the potassium and sodium balance. Summary Two cases are described in which hypokalaemic alkalosis was treated with 25-28 g. potassium chloride (335-375 mEq. potassium), combined with glucose and insulin, and infused intravenously over some 5 hours.
In both cases, after this massive dose of potassium, the condition promptly returned to normal without any untoward side-effects. The greater part of the potassium was
retained.
Severe potassium deficiency may best be treated by the rapid intravenous administration of potassium chloride in doses whose upper limit should be determined exclusively by the potassium deficit at the time. To accelerate the transfer of potassium to the intracellular phase, such a massive dose should be given in combination with glucose and insulin. During the infusion of potassium the patient must be under close supervision, which includes electrocardiographic control and measurement of the potassium and
sodium balance. I wish
Hospital
to thank the staff of the central for their kind assistance.
laboratory
of
Bispebjurg
REFERENCES
Bland, J.
H.
London.
(1956) Disturbances of Body Fluids; p. 497. Philadelphia and
Cooke, R. E., Segar, W. E., Cheek, D. B., Coville, F. E., Darrow, D. C. (1952) J. clin. Invest. 31, 798. Le Quesne, L. P. (1957) Fluid Balance in Surgical Practice; p. 85. London.
Siggard Andersen, O., Engel, K., Jorgensen, K., Astrup, P. (1960) Scand. J.
clin. Lab. Invest. 12, 172. Wilkinson, A. W. (1960) Body Fluids in Surgery; p. 64. Edinburgh and
London.