| Abstract|| |
We present the case of a 36-year-old man with type-1 diabetes who was hospitalized with diabetic ketoacidosis (DKA). On admission, he had hypothermia, hypokalemia and combined metabolic and respiratory alkalosis, in addition to hyperglycemia. Hypothermia, hypokalemia and metabolic alkalosis, with a concurrent respiratory alkalosis, are not commonly seen in DKA. After admission, intravenous infusion of 0.45% saline was administered, which resulted in the development of pure metabolic acidosis. After starting insulin infusion, hypokalemia and hypophosphatemia became evident and finally resulted in massive rhabdomyolysis. Hyperkalemia accompanying oliguric acute kidney injury (AKI) warranted initiation of hemodialysis (HD) on Day-five. On the 45th hospital day, his urine output started to increase and a total of 22 HD sessions were required. We believe that in this case severe dehydration, hypothermia and hypokalemia might have contributed to the initial symptoms of DKA as well as the prolongation of AKI.
|How to cite this article:|
Saito O, Saito T, Sugase T, Kusano E, Nagata D. Hypothermia and hypokalemia in a patient with diabetic ketoacidosis. Saudi J Kidney Dis Transpl 2015;26:580-3
|How to cite this URL:|
Saito O, Saito T, Sugase T, Kusano E, Nagata D. Hypothermia and hypokalemia in a patient with diabetic ketoacidosis. Saudi J Kidney Dis Transpl [serial online] 2015 [cited 2021 Jan 20];26:580-3. Available from: https://www.sjkdt.org/text.asp?2015/26/3/580/157387
| Introduction|| |
Diabetic ketoacidosis (DKA) is a combination of the biochemical triad of hyperglycemia, ketonemia and metabolic acidosis.  Initial hypokalemia in DKA is a rare finding, with an incidence of 4-10%.  Hypothermia is rarely seen in patients with DKA, and the prognosis of this association is poor, with a mortality of 60% in the Western countries.  Also, combined metabolic and respiratory alkalosis is rarely seen in DKA, with an incidence of 7.5%. 
We herewith report the case of a 36-year-old man with type-1 diabetes who was admitted to the hospital with DKA in association with hypothermia, hypokalemia and combined metabolic and respiratory alkalosis.
| Case Report|| |
A 36-year-old man was brought to the emergency department of our hospital with hypothermia and disturbance of consciousness. His body weight had decreased by 10 kg over the previous two months due to severe nausea, which had stopped him from eating. He had been drinking two liters of soft drinks for thirst every day. On admission, his height was 186 cm, body weight was 70 kg, blood pressure was 50 mm Hg, pulse was 130 beats/min and body temperature was 32.4°C. Laboratory data at admission are shown in [Table 1]. In addition to renal dysfunction, hypernatremia, hypokalemia, hyperglycemia and moderate elevation of creatine kinase (CK) were seen. Initial arterial blood gas analysis showed metabolic alkalosis with a concurrent respiratory alkalosis. The initial diagnosis suspected was hyperosmolar hyperglycemic state (HHS) because of the absence of metabolic acidosis. The patient was treated with infusion of 0.45% saline; eight liters was administered over the first 24 h along with potassium, 80 mmol/day, without insulin therapy because of hypokalemia. The following day, blood gas analysis showed a pH of 7.322, partial pressure of carbon dioxide PaCO 2 ) of 33.1 mm Hg, bicarbonate (HCO 3 - ) of 16.7 mmol/L and base excess of -8.2, with 3+ urinary ketones. The serum creatinine was 587.8 μmol/L, creatine phosphokinase (CK) was 13148 U/L, potassium (K) was 2.0 mmol/L and glucose was 69.3 mmol/L. The serum Cpeptide and anti-Glutamic acid decarboxylase (GAD) antibody levels were 0.033 nmol/L and 85.2 U/mL, respectively. A final diagnosis of DKA due to type-1 diabetes was made as his laboratory data showed the typical findings of DKA following correction of hypothermia and dehydration. Continuous insulin infusion (10-20 U/h) was started in addition to the infusion of 20-30 mmol/h of potassium. After six hours of these infusions, his respiratory effort weakened possibly due to hypokalemia and hypophosphatemia; potassium was 4 mmol/L and phosphate was 0.28 mmol/L. He was mechanically ventilated and continued to receive potassium and phosphate replacement. After the insulin infusion, the plasma glucose was reduced to 16.6-27.7 mmol/L; however, blood pressure remained low at 80 mm Hg and the urinary volume decreased with a progressive rise in serum creatinine levels. On the fifth hospital day, he developed bradycardia due to hyperkalemia (K: 8.9 mmol/L), which warranted initiation of hemodialysis (HD) for acute kidney injury (AKI).
The patient was regularly treated with 4-h of HD three times per week. A renal biopsy was performed on the 39 th hospital day, at which time the serum creatinine was 565.7 μmol/L and urine volume was 250 mL/day. There were no diabetic changes in the glomeruli, but myoglobin casts were present in a few tubules [Figure 1]. Some Bowman's capsules showed a shrunken appearance. There was no fibrinoid degeneration in the renal arteries. These findings indicated the presence of AKI due to rhabdomyolysis and ischemic change due to hypothermia. On the 45 th hospital day, his urine output started to increase and a total of 22 HD sessions were required for renal recovery. The clinical course of this patient is shown in [Figure 2].
|Figure 1: Light microscopic findings of the kidney biopsy sample. PAS staining x400. Myoglobin casts were present in the tubules (arrow). Bowman capsules had a shrunken appearance (arrow cap). There were no diabetic changes in the glomeruli.|
Click here to view
|Figure 2: Clinical course in the study case. The serum levels of creatinine, creatine kinase (CK), plasma glucose, sodium, potassium and urine volume are shown.|
Click here to view
| Discussion|| |
Metabolic acidosis is a typical finding in DKA due to the accumulation of ketoacids. However, our patient showed combined metabolic and respiratory alkalosis at admission. Initial serum sodium concentration was 154 mmol/L, the adjusted sodium concentration was 174.8 mmol/L and calculated plasma osmolality was 401 mmol/kg, indicating severe hypertonic dehydration. The dehydration would have been aggravated by hypokalemia, which induces marked diuresis due to altered renal concentrating function. A large reduction in the extra-cellular fluid volume enhances reabsorption of bicarbonate in the renal tubules;  this phenomenon is referred to as contraction alkalosis. The patient initially had hypothermia, and respiratory alkalosis might have been caused by tachypnea and hyperventilation, which are common signs in hypothermia.  The cause of hypothermia in DKA might be impaired peripheral thermal regulation due to vascular collapse.  Another cause might be the decreased ability to produce heat.  In this patient, metabolic acidosis was absent initially, probably due to severe hypothermia and dehydration.
Initial hypokalemia in DKA is a rare finding. In this patient, loss of appetite for one month and low urinary excretion of potassium suggested decreased potassium intake. Initial hypothermia may also have driven potassium into the cells and further lowered the serum potassium concentration.  Additionally, the initial metabolic and respiratory alkalosis might have promoted entry of potassium into the cells, resulting in hypokalemia. After insulin therapy, potassium enters the intracellular compartment and hypokalemia gets aggravated. In addtion to hypokalemia, very high glucose levels, high osmolality and hypothermia, which are all risk factors for rhabdomyolysis, were apparent in this case, and these disorders might have triggered the occurrence of rhabdomyolysis in our patient.
Generally, long-term survival among patients with rhabdomyolysis and AKI is reported to be close to 80%.  However, the prognosis is substantially worse if renal failure develops. In this case, a total of 22 HD sessions were required for renal recovery. It seems that his recovery was slightly delayed, which might be due to hypothermia at admission. Recently, it has been reported that AKI occurs in over 40% of patients with accidental hypothermia.  The cold-induced diuresis and transient pre-renal injury, especially caused by ischemia and hypovolemia, may be involved in hypothermiainduced AKI.  Renal biopsy was performed in the oliguric stage that showed some shrunken glomeruli, indicating transient ischemia,  in addition to a few myoglobin casts. The main cause of AKI was rhabdomyolysis in this case, although pre-renal injury due to hypothermia might be involved in the prolongation of AKI.
In summary, this case illustrates that rare complications such as hypothermia, hypokalemia and metabolic alkalosis with a concurrent respiratory alkalosis can occur in DKA, with development of rhabdomyolysis and AKI.
| References|| |
Kitabchi AE, Umpierrez GE, Murphy MB, Barrett EJ, Kreisberg RA, Malone JI,. Management of hyperglycemic crises in patients with diabetes. Diabetes Care 2001;24:131-53.
Abramson E, Arky R. Diabetic acidosis with initial hypokalemia: Therapeutic implications. JAMA 1966;196:401-3.
Guerin JM, Meyer P, Segrestaa JM. Hypothermia in diabetic ketoacidosis. Diabetes Care 1987;10: 801-2.
Elisaf MS, Tsatsoulis AA, Katopodis KP, Siamopoulos KC. Acid-base and electrolyte disturbances in patients with diabetic ketoacidosis. Diabetes Res Clin Pract 1996;34:23-7.
Garella S, Chang BS, Kahn SI. Dilution acidosis and contraction alkalosis: Review of a concept. Kidney Int 1975;8:279-83.
Giesbrecht GG. Cold stress, near drowning and accidental hypothermia: A review. Aviat Space Environ Med 2000;71:733-45.
Gale EA, Tattersall RB. Hypothermia: A complication of diabetic ketoacidosis. BMJ 1978;2: 1387-9.
Hanania NA, Zimmerman JL. Accidental hypothermia. Crit Care Clin 1999;15:235-41.
Woodrow G, Brownjohn AM, Turney JH. The clinical and biochemical features of acute renal failure due to rhabdomyolysis. Ren Fail 1995; 17:467-74.
Megarbane B, Axler O, Chary I, Pompier R, Brivet FG. Hypothermia with indoor occurrence is associated with a worse outcome. Intensive Care Med 2000;26:1843-9.
Mallet ML. Pathophysiology of accidental hypothermia. Q J Med 2002;95:775-85.
Saito O, Sugase T, Saito T, et al. Two cases of renal hypouricemia in which dopamine infusion produced a good recovery from exercise-induced acute kidney injury. Clin Nephrol 2011;76: 83-9.
Dr. Osamu Saito
Division of Nephrology, Jichi Medical University, 3311-1 Yakushiji, Simotsuke, Tochigi, 329-0498
[Figure 1], [Figure 2]