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대한응급의학회지 제 26 권 제 5 호 � 증례� Volume 26, Number 5, October, 2015

Medical A Case of Diabetic with Refractory Metabolic Successfully Treated with Continuous Hemodiafiltration

Department of Internal Medicine, Presbyterian Medical Center, Jeonju, Korea Seong Hee Lee, M.D., Byeong Gwan Kim, M.D., A Young Cho, M.D., Sang Sun Kim, M.D., Hong Shik Shin, M.D., Jeong Gwan Kim, M.D., In O Sun, M.D., Kwang Young Lee, M.D., Hyun Ju Yoon, M.D.

Diabetic ketoacidosis (DKA) is a complex medical disorder ate administration in the treatment of patients with DKA characterized by abnormalities in electrolyte, -base, is controversial1). On rare occasions, may be and volume status. in mild and moderate required to treat acidosis associated with renal failure. DKA is corrected with insulin therapy. therapy Although CRRT was previously performed to treat DKA may be indicated in cases of severe metabolic acidosis, patients with refractory metabolic acidosis, there is few however the use of bicarbonate in severe DKA is controver- case report of CRRT used for DKA in Korea2). Here, we sial due to a lack of prospective randomized studies. Renal report a case of DKA with refractory metabolic acidosis replacement therapy can be used for correction of systemic that was successfully treated with CRRT. acidemia. Continuous renal replacement therapy (CRRT) is used in patients who are too hemodynamically unstable to tolerate conventional hemodialysis, but has also been used Case Report in treatment of patients with severe DKA. CRRT has never been used previously in DKA patients with A comatose 26-year-old Korean woman was admitted refractory metabolic acidosis in Korea. Here, we describe to our hospital with respiratory insufficiency. She had no the successful treatment of a DKA patient with refractory significant medical or surgical history, but had lost 20 metabolic acidosis with CRRT. kilograms of weight with diet and exercise in 3 years. She had a family history of type 2 mellitus. The Key Words: , Hemodiafiltration, Renal patient began to complain of nausea and abdominal dis- replacement therapy comfort two days prior to admission. On arrival, her level of consciousness was E1V2M3 on the Glasgow coma scale. She had a temperature of 36�C, Introduction pulse rate of 114 beat/min, blood pressure of 78/41 mmHg, and respiratory rate of 44/min. Initial arterial Diabetic ketoacidosis (DKA) is a serious, life-threaten- blood gas analysis showed severe metabolic acidosis (pH - ing complication of diabetes that occurs when large =6.800, pCO2=12.0 mmHg, pO2=145.0 mmHg, HCO3 = amount of ketones are released into the blood. Ketones 0.0 mmol/L, and =34 mEq/L). Her serum glu- are cleared within hours if insulin is given in sufficient cose and hemoglobin A1c levels were 667 mg/dL and doses, but clearance of ketones may lag because of con- 15.8%, respectively. Urinalysis showed glycosuria and version of β-hydroxybutyrate to acetoacetate as the aci- strong positivity for ketonuria. Other laboratory studies dosis resolves. The correction of acidosis with bicarbon- produced the following results: serum osmolality, 332 mOsm/kg; serum sodium, 136 mEq/L; serum potassium, 3.8 mEq/L; serum calcium, 7.6 mg/dL; serum phosphate, 책임저자: 윤 현 주 6.1 mg/dL; serum chloride, 101 mEq/L; 0.8 전라북도 전주시 완산구 서원로 365 mmol/L; ketone body, 9935.0 umol/L; serum myoglobin, 예수병원 내과 114.0 ng/mL; serum lactate dehydrogenase, 273 IU/L; Tel: 063) 230-1339, Fax: 063) 230-1333 E-mail: [email protected] serum creatine phosphokinase, 38 U/L; serum amylase, 접수일: 2015년 5월 21일, 1차 교정일: 2015년 5월 26일 207 U/L; serum lipase, 800 U/L. Blood nitrogen 게재승인일: 2015년 7월 7일 480 Seong Hee Lee et al.: A Case of DKA with Refractory Metabolic Acidosis Treated with Continuous HD / 481 was 31 mg/dL (normal: 8~20 mg/dL) and serum creati- mL/h. The total amounts of fluid were 7410 mL and nine 0.8 mg/dL (normal: 0.6~1.2 mg/dL). Urinary con- intravenous insulin were 50 IU just before CVVHDF. centrations of sodium, potassium, chloride were 20 The patient’s metabolic acidosis was corrected 90 hours mEq/L, 19.5 mEq/L, and 11 mEq/L, respectively. Urine after the initiation of CVVHDF (Fig. 1). osmolality was 429 mOsm/kg. Her chest radiography pH already increased above 7.3 and urine output and and brain computed tomography appeared normal. Anti- serum were maintained within the normal glutamic acid decarboxylase (GAD), antibody (Ab) titer, range. As soon as CVVHDF was stopped, however, anti-IA-2 Ab, and anti-insulin Ab were absent, but anti- arterial pH decreased rapidly despite insulin therapy and islet cell Ab was positive. high anion gap metabolic acidosis and low levels of Upon the diagnosis of DKA, insulin was infused at bicarbonate lasted for several days. Accordingly we con- 6~10 U/h and isotonic saline was given at 1000 mL/h for tinued CVVHDF. On the fourth day of dialysis, the two hours. Even though fluid replacement with half bicarbonate level was higher than 15 mmol/L with a saline was continued, the patient’s metabolic acidosis did gradual stabilization of the blood pressure. not improve. Thus, we administered On day 4, the patient regained consciousness and on 250 mEq and continued the infusion of intravenous day 6, we stopped CVVHDF. After supportive care, the insulin. The patient’s central venous pressure was 11~13 patient was discharged from the ICU on day 7. mmH2O, urine output was 50~250 mL/h, and echocar- diography showed good left ventricular systolic function without pulmonary hypertension. After twelve hours of Discussion treatment, we started norepinephrine (80 mg, mixed with 5% dextrose 500 mL, 30 mL/hour) and dopamine (1600 DKA is one of the most common and serious acute mg, mixed with dextrose saline, 5 mL/hour) because her complications of diabetes, and is characterized by abnor- blood pressure had remained low (<80/60 mmHg). malities in electrolyte, acid-base, and volume status. In However, arterial blood pH remained as low as 6.9. Western countries, the annual incidence rate of DKA Therefore, we started continuous veno-venous hemodi- estimated from population-based studies ranges from afiltration (CVVHDF) using the Prismaflex� system 4.6-8.0 episodes per 1000 diabetic patients. The inci- (Gambro Lundia AB, Sweden) on the first day of admis- dence of DKA increased seven-fold in Korea between sion at the following settings: blood flow, 150 mL/min; 1982 and 20023,4). The mortality rate for diabetic emer- replacement volume, 700 mL/h; and dialysate, 1700 gencies associated with mixed states of ketoacidosis and hyperosmolality is considerably higher than that with DKA alone5). Therefore, our patient was at high risk of mortality because of refractory acidosis, higher levels of serum osmolality, and comatose consciousness. Insulin deficiencies and elevated levels of counter-reg- ulatory hormones stimulate and inhibit lipogen- esis, resulting in the conversion of abundant free fatty acid to ketone bodies6). Thus, insulin treatment is a cor- nerstone of the management of DKA. Bicarbonate thera- py in patients with DKA remains controversial, but may be considered for the treatment of patients who exhibit marked decreases in their levels of consciousness or advanced renal dysfunction1). In our case, the patient was comatose on arrival, and her plasma pH did not improve Fig. 1. Time course of metabolic acidosis during admission. The patient’s metabolic acidosis was corrected after despite insulin therapy. Severe acidemia may be associ- the initiation of continuous veno-venous hemodiafil- ated with decreased cardiac contractility7), diminished tration (CVVHDF). CVVHDF was withdrawn on responses to endogenous and administered cate- day 4. 482 / 대한응급의학회지: 제 26 권 제 5 호 2015 cholamines, and predisposition to cardiac arrhythmias8), all of which may contribute to hemodynamic instability. REFERENCES The observed in our case might have been caused by refractory acidosis. However, there is no stan- 01. Kamel KS, Halperin ML. Acid-base problems in diabetic dard treatment for DKA in patients with refractory meta- ketoacidosis. N Eng J Med. 2015;372:546-54. bolic acidosis. 02. Kawata H, Inui D, Ohto J, Miki T, Suzue A, Fukuta Y, et Renal replacement therapy can be used to correct sys- al. The use of continuous hemodiafiltration in a patient with diabetic ketoacidosis. J Anesth. 2006;20:129-31. temic acidemia. Continuous renal replacement therapy 03. Johnson DD, Palumbo P, Chu CP. Diabetic ketoacidosis in (CRRT) has been used to treat patients who are too a community-based population. Mayo Clin Proc. 1980;55: hemodynamically unstable to tolerate hemodialysis. 83-8. 2) Kawata et al reported that a DKA patient with refracto- 04. Ko SH, Lee WY, Lee JH, Kwon HS, Lee JM, Kim SR, et ry metabolic acidosis was treated successfully with al. Clinical characteristics of diabetic ketoacidosis in CRRT2). In our case, the patient had refractory metabolic Korea over the past two decades. Diabet Met. 2005;22: acidosis and hypotension, and the acidosis was reversed 466-9. after CRRT without any complications, such as cerebral 05. MacIsaac RJ, Lee LY, McNeil KJ, Tsalamandris C, edema or pulmonary edema. Therefore, CRRT was also Jerums G. Influence of age on the presentation and out- effective in treatment of the DKA patient with refractory come of acidotic and hyperosmolar diabetic emergencies. Intern Med J. 2002;32:379-85. metabolic acidosis. 06. Androgue HJ, Wilson H, Boyd AE 3rd, Suki WN, Eknoyan In summary, we report a case of refractory acidosis G. Plasma acid-base pattern in diabetic ketoacidosis. N associated with DKA and hyperosmolality. The patient Eng J Med. 1982;307:1603-10. improved following treatment with CVVHDF and appro- 07. Mitchell JH, Wildenthal K, Johnson RL Jr. The effects of priate supportive care. Renal replacement therapy is one acid-base disturbances on cardiovascular and pulmonary of the treatment options for patients with refractory aci- function. Int. 1972;1:375-89. dosis associated with DKA. 08. Davies AO. Rapid desensitization and uncoupling of human beta-adrenergic receptors in an in vitro model of . J Clin Endocrinol Metab. 1984;59:398- 405.