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Acid dialysate correction of metabolic alkalosis in renal failure
Acid Dialysate Correction of Metabolic Alkalosis in Renal Failure Robert E. Gerhardt,
MD, John D. Koethe, MD, Joel D. Glickman, MD, K. Adu Ntoso, MD, Joseph P. Hugo, BA, and Charles J. Wolf, MD
0 Severe metabolic acidosis may occur during hemodialysis when the incorrect acid dialysis a two-part bicarbonate dialysis system is used in an acetate dialysis machine. We deliberately nique to correct severe metabolic alkalosis in a patient with chronic renal failure. Rapid correction alkalosis was achieved and the procedure was well tolerated. 0 1995 by the National Kidney Foundation, Inc. INDEX
WORDS:
Metabolic
alkalosis;
hemodialysis;
conductivity;
0
VER THE YEARS, two alkalinizing dialysate concentrates have come into common usage in dialysis. The first system uses an acetate concentrate that is diluted with water to provide the final concentration of glucose and electrolytes for dialysis. The second system (bicarbonate dialysis) uses a two-part concentrate, one consisting of acetic acid and electrolytes and the other essentially containing sodium bicarbonate. Both of these concentrates are then diluted and, when mixed, provide the proper concentration of electrolytes, bicarbonate, and glucose for dialysis. In both systems, the electrical conductivity of the final dialysate mix is continually monitored and automatically blended to provide a safe dialysis solution. It is known that on certain acetate equipment, the acid concentrate (from the two-part bicarbonate system) can be inadvertently used, drawn up, and diluted so that its electrical conductivity will pass scrutiny of the monitor.’ This bath is highly acidic and contains essentially no bicarbonate and minuscule amounts of acetate. A patient recently presented to us with chronic renal failure and severe metabolic alkalosis due to gastrointestinal losses. The metabolic alkalosis was successfully treated by deliberately using the acid concentrate from a two-part bicarbonate mix as the only dialysis concentrate in a one-part acetate system. This technique may be used in selected cases as another modality of therapy in the treatment armamentarium for severe metabolic alkalosis.
acid
concentrate from applied this techof the metabolic
dialysis.
intraperitoneally after peritoneal fluid samples were obtained. Studies revealed a peritoneal fluid white blood cell count of 2,460 cells/m&, and both the exit site and peritoneal dialysis fluid subsequently grew Pseudomonas aeruginosa sensitive to aminoglycosides. The patient reported nausea and vomiting the day prior to admission with only mild abdominal pain. He continued to have nausea and vomiting with some distention. An obstructive series demonstrated obstruction at the level of the jejunum; a nasogastric tube was passed. Three days after presentation, the white blood cell count in the peritoneal fluid was 2,200 cells/mm3. Despite continued treatment with antibiotics, there was no improvement in the patient’s overall condition, and the peritoneal dialysis catheter was removed on the fourth hospital day. Abdominal pain, which had increased on the second and third days, rapidly improved after removal of the catheter. However, the patient continued to have an ileus and to have large outputs via the nasogastric tube. Nasogastric tube drainage averaged 2,000 to 2,500 mL/d. Despite intravenous ranitidine and intravenous fluid replacement with saline-containing solutions and total parenteral nutrition (the solutions containing low acetate and high chloride), the patient’s studies continually demonstrated a metabolic alkalosis (Table 1). Six days after admission the patient was noted to be severely obtunded with occasional apneic spells and was transferred for close monitoring to the intensive care unit. On transfer, the patient was noted to be obtunded with spontaneous myoclonus and asterixis, and appeared to be volume depleted. Therapy was initiated via venous access using a Gambro AK10 acetate dialysis machine (Gambro, Lund, Sweden) with the dialysis bath concentrate being the acid component of a two-part bicarbonate dialysis system. This bath has no bicarbonate and, when properly diluted, has 4 nunol/L acetic acid. The acetate Gambro AK10 machine rapidly came into acceptable conductivity range, clearly by adjusting the mixing of concentrate and water by its servo-
man with chronic renal failure secondary who had been receiving chronic ambulatory peritoneal dialysis for 3 years presented with cloudy peritoneal fluid but no chills or fever. There was some purulence noted at the exit site. The patient was treated at that time with vancomycin 2 g intraperitoneally and gentamicin 80 mg
From the Section on Renal Diseases and Hypertension, Department of Medicine, Pennsylvania Hospital, Philadelphia, PA. Received April 28, 1994; accepted in revised form September 13, 1994. Address reprint requests to Robert E. Gerhardt, MD, Section on Renal Diseases and Hypertension, Pennsylvania Hospital, 800 Spruce St, Philadelphia, PA 19107. 0 1995 by the National Kidney Foundation, Inc. 0272~6386/95/2502-0019$3.00/O
American
1995:
CASE
REPORT
A 60-year-old
to hypertension
Journal
of Kidney
Diseases,
Vol 25,
No 2 (February),
pp 343-345
343
344
GERHARDT Table
1. Laboratory Metabolic
Data in a Patient Alkalosis
Day
Day
3
6
7
Day 11
143 3.4 94 37 9.8 4.9 3.4
148 2.7 72 59 8.4 9.8 2.0
140 3.2 85 49 9.6 6.1 2.7
144 3.8 93 39
133 5.4 101 23
was given
between
Na+ (mEq/L) K+ (mEq/L) Cl- (mEq/L) TCOp (mmol/L) Ca (mg/dL) Pod (mg/dL) Albumin (g/dL) NOTE.
Therapy
day
alkalosis. The patient’s symptoms, including myoclonus and tetany, disappeared and his mental status improved to baseline over the next 4 to 6 hours. No significant changes in hemoglobin, hematocrit, or total white blood cell count were noted with the exposure to the acid bath.
With
Day Admission
6 and day
DISCUSSION
While the correction of severe metabolic alkalosis in patients with normally functioning kidneys usually is readily accomplished by the provision of chloride-containing solutions, the treatment of a severe metabolic alkalosis in patients with renal or hepatic failure is more difficult. Traditionally, the available therapies have included ammonium chloride,’ arginine monohydrochloride,3 or dilute hydrochloric acid4; all may have significant problems. Ammonium chloride obviously is to be avoided in hepatic failure, and arginine monochloride is not readily available and may cause hyperkalemia.3 Intravenous hydrochloric acid appears to be safe when properly diluted and does not appear to cause hemolysis; however, it requires administration via a catheter in a large central vein.4 A modification of the REDY dialysis system (Renal Intensive Care, Division of CGH Medical, Inc, Lakewood, CO) has been reported to be useful in the correction of metabolic alkalosi? and
7.
controlled, variable-speed dialysate pump. Analysis of several samples of the final dialysate revealed an average content of sodium 134 mEq/L, potassium 3.0 &q/L, chloride 125 mEq/L, and bicarbonate 0.2 mEq& and pH 5.6. RESULTS
The patient tolerated the treatment well with a rapid improvement of metabolic alkalosis within 2 hours, at which time he was changed over to a regular acetate dialysis bath. Table 2 shows the changes in serum bicarbonate and electrolytes in this patient treated with acid dialysate. As can be seen, there is a marked decrease in serum bicarbonate with a consequent decrease in systemic pH and correction of the metabolic
Table
2. Serum
Electrolytes
Time 0 min
Na+ (mEq/L) K+ (mEq/L) Cl- (mEq/L) Total COP (mmol/L) PH PO, (mm W Pco2 (mm Hg) K+ (mEq/L) HCO, (mEq/L) Ionized calcium (mmol/L) Abbreviations: specimen.
A Line
V Line
141 3.2 85
137 3.3 111
49
16
A Line, venous
and
Blood
Gases
Time 30 min
Art
A Line
V Line
140 2.6 106
131 3.5 116
in Patient
Treated
A Line
V Line
With
Art
A Line
V Line
139
7.47 111 66.9 3.2 49.4
7.39 70 64 3.3 38.8
<5 7.33 37 69 3.3 36.8
35 7.29 43 72 3.4 35
0.99
1.18
1.29
1.38
blood
to dialyzer;
blood
Dialysate
return
from
Art
Time 180 min A Line
V Line
Art
141 3.3 97
3.4 98
V Line, venous
Acid
Change to Acetate Dialysis: Time 120 min
Time 90 min
At-l
ET AL
35 7.36 106 56.5 32
dialyzer;
Art, peripheral
arterial
blood
ACID
DIALYSATE
CORRECTION
OF ALKALOSIS
hemodialysis using either a high chloride, low acetate dialysate or a low bicarbonate dialysate also have been reported, but these baths are not readily available.6V7 Recent reports have demonstrated clearly that the inadvertent use of an acid dialysis bath in an acetate machine may in fact produce severe metabolic acidosis.839 Hartmann et al have reported that acidosis can be provoked within the normal range of conductivity on the Gambro machine if the acid concentrate is used in place of acetate concentrate.’ Prevention of such inadvertent use of the incorrect bath can be performed by either a manual or an on-line pH determination of the bath.’ As demonstrated, we were able to rapidly correct a severe life-threatening metabolic alkalosis in a patient with renal failure using a dialysis bath containing no buffer bases in the form of acetate or bicarbonate. Close monitoring revealed no untoward effects and there appeared to be no cellular damage. While the inadvertent use of an incorrect dialysis bath may be clearly life-threatening and produce severe metabolic acidosis, its application in appropriately selected cases of severe metabolic alkalosis may be therapeutic. We caution that the described technique may rapidly and dangerously lower serum bicar-
345
bonate and cause severe metabolic acidosis. Frequent monitoring of electrolytes must be performed and the duration of dialysis carefully monitored. REFERENCES 1. Brueggemeyer CD, Ramirez G: Dialysis concentrate: A potential source for lethal complications. Nephron 46:397398, 1987 2. Zintel HA, Rhoads JE, Ravdin IS: The use of intravenous ammonium chloride in the treatment of alkalosis. Surgery 14:728-731, 1943 3. Bushinsky DA, Gennari FJ: Life-threatening hyperkalemia induced by arginine. Ann Intern Med 89:632-634, 1978 4. Quintanilla A, Singer I: Metabolic alkalosis in the patient with uremia. Am J Kidney Dis 17591-595, 1991 5. Swartz RD, Jacobs JF: Modified dialysis for metabolic alkalosis. Ann Intern Med 88:432-433, 1978 6. Swartz RD, Rubin JE, Brown RS, Yager HM, Steinman TI, Frazier HS: Correction of postoperative metabolic alkalosis and renal failure by hemodialysis. Ann Intern Med 86:.5255, 1977 7. Ayus JC, Oliver0 JJ, Adrogue HJ: Alkalemia associated with renal failure; correction by hemodialysis with low-bicarbonate dialysate. Arch Intern Med 140:513-515, 1980 8. Malhotra D, Goldberg C, Contigulia R, Klein M, Mishell J, Berl T, Babcock S: Unanticipated metabolic acidosis in an outpatient dialysis center. ASAIO Abstracts 21:78,1992 (abstr) 9. Hartmann A, Reisaeter A, Holdaas H, Rolfsen B, Fauchald P: Accidental metabolic acidosis during hemodialysis. Artif Organs 18:214-217, 1994
MD, John D. Koethe, MD, Joel D. Glickman, MD, K. Adu Ntoso, MD, Joseph P. Hugo, BA, and Charles J. Wolf, MD
0 Severe metabolic acidosis may occur during hemodialysis when the incorrect acid dialysis a two-part bicarbonate dialysis system is used in an acetate dialysis machine. We deliberately nique to correct severe metabolic alkalosis in a patient with chronic renal failure. Rapid correction alkalosis was achieved and the procedure was well tolerated. 0 1995 by the National Kidney Foundation, Inc. INDEX
WORDS:
Metabolic
alkalosis;
hemodialysis;
conductivity;
0
VER THE YEARS, two alkalinizing dialysate concentrates have come into common usage in dialysis. The first system uses an acetate concentrate that is diluted with water to provide the final concentration of glucose and electrolytes for dialysis. The second system (bicarbonate dialysis) uses a two-part concentrate, one consisting of acetic acid and electrolytes and the other essentially containing sodium bicarbonate. Both of these concentrates are then diluted and, when mixed, provide the proper concentration of electrolytes, bicarbonate, and glucose for dialysis. In both systems, the electrical conductivity of the final dialysate mix is continually monitored and automatically blended to provide a safe dialysis solution. It is known that on certain acetate equipment, the acid concentrate (from the two-part bicarbonate system) can be inadvertently used, drawn up, and diluted so that its electrical conductivity will pass scrutiny of the monitor.’ This bath is highly acidic and contains essentially no bicarbonate and minuscule amounts of acetate. A patient recently presented to us with chronic renal failure and severe metabolic alkalosis due to gastrointestinal losses. The metabolic alkalosis was successfully treated by deliberately using the acid concentrate from a two-part bicarbonate mix as the only dialysis concentrate in a one-part acetate system. This technique may be used in selected cases as another modality of therapy in the treatment armamentarium for severe metabolic alkalosis.
acid
concentrate from applied this techof the metabolic
dialysis.
intraperitoneally after peritoneal fluid samples were obtained. Studies revealed a peritoneal fluid white blood cell count of 2,460 cells/m&, and both the exit site and peritoneal dialysis fluid subsequently grew Pseudomonas aeruginosa sensitive to aminoglycosides. The patient reported nausea and vomiting the day prior to admission with only mild abdominal pain. He continued to have nausea and vomiting with some distention. An obstructive series demonstrated obstruction at the level of the jejunum; a nasogastric tube was passed. Three days after presentation, the white blood cell count in the peritoneal fluid was 2,200 cells/mm3. Despite continued treatment with antibiotics, there was no improvement in the patient’s overall condition, and the peritoneal dialysis catheter was removed on the fourth hospital day. Abdominal pain, which had increased on the second and third days, rapidly improved after removal of the catheter. However, the patient continued to have an ileus and to have large outputs via the nasogastric tube. Nasogastric tube drainage averaged 2,000 to 2,500 mL/d. Despite intravenous ranitidine and intravenous fluid replacement with saline-containing solutions and total parenteral nutrition (the solutions containing low acetate and high chloride), the patient’s studies continually demonstrated a metabolic alkalosis (Table 1). Six days after admission the patient was noted to be severely obtunded with occasional apneic spells and was transferred for close monitoring to the intensive care unit. On transfer, the patient was noted to be obtunded with spontaneous myoclonus and asterixis, and appeared to be volume depleted. Therapy was initiated via venous access using a Gambro AK10 acetate dialysis machine (Gambro, Lund, Sweden) with the dialysis bath concentrate being the acid component of a two-part bicarbonate dialysis system. This bath has no bicarbonate and, when properly diluted, has 4 nunol/L acetic acid. The acetate Gambro AK10 machine rapidly came into acceptable conductivity range, clearly by adjusting the mixing of concentrate and water by its servo-
man with chronic renal failure secondary who had been receiving chronic ambulatory peritoneal dialysis for 3 years presented with cloudy peritoneal fluid but no chills or fever. There was some purulence noted at the exit site. The patient was treated at that time with vancomycin 2 g intraperitoneally and gentamicin 80 mg
From the Section on Renal Diseases and Hypertension, Department of Medicine, Pennsylvania Hospital, Philadelphia, PA. Received April 28, 1994; accepted in revised form September 13, 1994. Address reprint requests to Robert E. Gerhardt, MD, Section on Renal Diseases and Hypertension, Pennsylvania Hospital, 800 Spruce St, Philadelphia, PA 19107. 0 1995 by the National Kidney Foundation, Inc. 0272~6386/95/2502-0019$3.00/O
American
1995:
CASE
REPORT
A 60-year-old
to hypertension
Journal
of Kidney
Diseases,
Vol 25,
No 2 (February),
pp 343-345
343
344
GERHARDT Table
1. Laboratory Metabolic
Data in a Patient Alkalosis
Day
Day
3
6
7
Day 11
143 3.4 94 37 9.8 4.9 3.4
148 2.7 72 59 8.4 9.8 2.0
140 3.2 85 49 9.6 6.1 2.7
144 3.8 93 39
133 5.4 101 23
was given
between
Na+ (mEq/L) K+ (mEq/L) Cl- (mEq/L) TCOp (mmol/L) Ca (mg/dL) Pod (mg/dL) Albumin (g/dL) NOTE.
Therapy
day
alkalosis. The patient’s symptoms, including myoclonus and tetany, disappeared and his mental status improved to baseline over the next 4 to 6 hours. No significant changes in hemoglobin, hematocrit, or total white blood cell count were noted with the exposure to the acid bath.
With
Day Admission
6 and day
DISCUSSION
While the correction of severe metabolic alkalosis in patients with normally functioning kidneys usually is readily accomplished by the provision of chloride-containing solutions, the treatment of a severe metabolic alkalosis in patients with renal or hepatic failure is more difficult. Traditionally, the available therapies have included ammonium chloride,’ arginine monohydrochloride,3 or dilute hydrochloric acid4; all may have significant problems. Ammonium chloride obviously is to be avoided in hepatic failure, and arginine monochloride is not readily available and may cause hyperkalemia.3 Intravenous hydrochloric acid appears to be safe when properly diluted and does not appear to cause hemolysis; however, it requires administration via a catheter in a large central vein.4 A modification of the REDY dialysis system (Renal Intensive Care, Division of CGH Medical, Inc, Lakewood, CO) has been reported to be useful in the correction of metabolic alkalosi? and
7.
controlled, variable-speed dialysate pump. Analysis of several samples of the final dialysate revealed an average content of sodium 134 mEq/L, potassium 3.0 &q/L, chloride 125 mEq/L, and bicarbonate 0.2 mEq& and pH 5.6. RESULTS
The patient tolerated the treatment well with a rapid improvement of metabolic alkalosis within 2 hours, at which time he was changed over to a regular acetate dialysis bath. Table 2 shows the changes in serum bicarbonate and electrolytes in this patient treated with acid dialysate. As can be seen, there is a marked decrease in serum bicarbonate with a consequent decrease in systemic pH and correction of the metabolic
Table
2. Serum
Electrolytes
Time 0 min
Na+ (mEq/L) K+ (mEq/L) Cl- (mEq/L) Total COP (mmol/L) PH PO, (mm W Pco2 (mm Hg) K+ (mEq/L) HCO, (mEq/L) Ionized calcium (mmol/L) Abbreviations: specimen.
A Line
V Line
141 3.2 85
137 3.3 111
49
16
A Line, venous
and
Blood
Gases
Time 30 min
Art
A Line
V Line
140 2.6 106
131 3.5 116
in Patient
Treated
A Line
V Line
With
Art
A Line
V Line
139
7.47 111 66.9 3.2 49.4
7.39 70 64 3.3 38.8
<5 7.33 37 69 3.3 36.8
35 7.29 43 72 3.4 35
0.99
1.18
1.29
1.38
blood
to dialyzer;
blood
Dialysate
return
from
Art
Time 180 min A Line
V Line
Art
141 3.3 97
3.4 98
V Line, venous
Acid
Change to Acetate Dialysis: Time 120 min
Time 90 min
At-l
ET AL
35 7.36 106 56.5 32
dialyzer;
Art, peripheral
arterial
blood
ACID
DIALYSATE
CORRECTION
OF ALKALOSIS
hemodialysis using either a high chloride, low acetate dialysate or a low bicarbonate dialysate also have been reported, but these baths are not readily available.6V7 Recent reports have demonstrated clearly that the inadvertent use of an acid dialysis bath in an acetate machine may in fact produce severe metabolic acidosis.839 Hartmann et al have reported that acidosis can be provoked within the normal range of conductivity on the Gambro machine if the acid concentrate is used in place of acetate concentrate.’ Prevention of such inadvertent use of the incorrect bath can be performed by either a manual or an on-line pH determination of the bath.’ As demonstrated, we were able to rapidly correct a severe life-threatening metabolic alkalosis in a patient with renal failure using a dialysis bath containing no buffer bases in the form of acetate or bicarbonate. Close monitoring revealed no untoward effects and there appeared to be no cellular damage. While the inadvertent use of an incorrect dialysis bath may be clearly life-threatening and produce severe metabolic acidosis, its application in appropriately selected cases of severe metabolic alkalosis may be therapeutic. We caution that the described technique may rapidly and dangerously lower serum bicar-
345
bonate and cause severe metabolic acidosis. Frequent monitoring of electrolytes must be performed and the duration of dialysis carefully monitored. REFERENCES 1. Brueggemeyer CD, Ramirez G: Dialysis concentrate: A potential source for lethal complications. Nephron 46:397398, 1987 2. Zintel HA, Rhoads JE, Ravdin IS: The use of intravenous ammonium chloride in the treatment of alkalosis. Surgery 14:728-731, 1943 3. Bushinsky DA, Gennari FJ: Life-threatening hyperkalemia induced by arginine. Ann Intern Med 89:632-634, 1978 4. Quintanilla A, Singer I: Metabolic alkalosis in the patient with uremia. Am J Kidney Dis 17591-595, 1991 5. Swartz RD, Jacobs JF: Modified dialysis for metabolic alkalosis. Ann Intern Med 88:432-433, 1978 6. Swartz RD, Rubin JE, Brown RS, Yager HM, Steinman TI, Frazier HS: Correction of postoperative metabolic alkalosis and renal failure by hemodialysis. Ann Intern Med 86:.5255, 1977 7. Ayus JC, Oliver0 JJ, Adrogue HJ: Alkalemia associated with renal failure; correction by hemodialysis with low-bicarbonate dialysate. Arch Intern Med 140:513-515, 1980 8. Malhotra D, Goldberg C, Contigulia R, Klein M, Mishell J, Berl T, Babcock S: Unanticipated metabolic acidosis in an outpatient dialysis center. ASAIO Abstracts 21:78,1992 (abstr) 9. Hartmann A, Reisaeter A, Holdaas H, Rolfsen B, Fauchald P: Accidental metabolic acidosis during hemodialysis. Artif Organs 18:214-217, 1994