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Alcoholic Ketoacidosis Associated with Multiple Complications: Report of 3 Cases

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Alcoholic Ketoacidosis Associated with Multiple Complications: Report of 3 Cases □ CASE REPORT □ Alcoholic Ketoacidosis Associated with Multiple Complications: Report of 3 Cases Masami TANAKA,Yasushi MIYAZAKI, Shinsuke ISHIKAWA and Kimihiko MATSUYAMA Abstract abroad (2, 7–9), there is little Japanese literature on AKA (10–12). Considering that AKA is the causative factor in We report 3 patients with alcoholic ketoacidosis 20% of patients presenting with ketoacidosis (4, 13), AKA (AKA). All had a history of excessive intake and abrupt might be overlooked or confused with DKA and not uncom- termination of alcohol. They showed tachypnea, mon in Japan. Here, we report these three cases of AKA with tachycardia, abdominal tenderness, and epigastralgia. a review of the literature. Metabolic acidosis with an increased anion gap, de- creased PaCO2 and ketonemia were present. One patient Case Report whose ratio of 3-hydroxybutyric acid to acetoacetic acid was 4.0 was associated with diabetic ketoacidosis. All pa- Case 1 tients were successfully hydrated with electrolyte, glucose The patient was a 50-year old woman. She had been a se- and thiamine. Complications such as liver dysfunction, vere alcoholic for the previous 10 years. She had been diag- lactic acidosis, acute pancreatitis, Wernicke’s encephalo- nosed with chronic alcoholic hepatitis. Nausea and vomiting pathy, rhabdomyolysis and heart failure were present. occurred on July 3, 2002. She kept vomiting overnight. The Attention should be paid to multiple complications in the following morning, she was admitted to Misato Kenwa treatment of AKA. Hospital. She was 151 cm tall and weighed 41 kg. Vital signs (Internal Medicine 43: 955–959, 2004) were body temperature of 37.3°C, blood pressure of 104/70 mmHg, respiratory rate of 24/min, and regular pulse of Key words: metabolic acidosis, anion gap, 3-hydroxybutyric 130/min with clear consciousness. Her palms were erythe- acid matous, and she had vascular spider. She complained of epigastralgia. Laboratory data on admission are summarized in Table 1. Urinalysis showed proteinuria (+), hematuria (+) and ketonuria (3+) without glycosuria. The white blood cell Introduction count (WBC) was 11,000/l, hemoglobin; 9.74 g/dl. Total bilirubin was 1.41 mg/dl, aspartate aminotransferase (AST); The entity of alcoholic ketoacidosis (AKA) was first de- 319 IU/l, alanine aminotransferase (ALT); 109 IU/l, - scribed by Dillon et al in 1940 (1). AKA affects only chronic glutamyltransferase (-GTP); 911 IU/l, and plasma glucose; alcoholics. It is characterized by a metabolic acidosis with an 73 mg/dl. The serum concentration of acetoacetic acid increased anion gap. The typical patient with AKA has a his- (AcAc) and 3-hydroxybutyric acid (3-OHB) were 1,400 tory of chronic alcohol abuse, and recent binge drinking fol- mol/l (normal range [NR]: <70) and 10,900 mol/l (NR: lowed by the abrupt cessation of alcohol consumption. The <70), respectively. The serum concentration of lactic acid clinical findings of AKA are very similar to those of diabetic and pyruvic acid were 98.6 mg/dl (NR: 3.3–15.6) and 1.5 ketoacidosis (DKA), but hyperglycemia and glycosuria are mg/dl (NR: 0.4–1.2), respectively. Arterial blood gas analy- usually absent. AKA has been rarely described in patients sis in room air showed pH 7.140, PaCO2 25.6 mmHg, PaO2 – with diabetes mellitus (DM), and there is no documented 117.7 mmHg, HCO3 8.5 mmol/l. She was diagnosed with connection between AKA and DKA (2–6). AKA and lactic acidosis. Endoscopic examination of the Recently we encountered 3 cases of AKA, 2 of which pre- upper digestive tract revealed esophagitis, erosive gastritis sented with DM. While there are several reviews of AKA and duodenitis. After hydration with 5% glucose solution From the Department of Internal Medicine, Misato Kenwa Hospital, Misato Received for publication July 25, 2003; Accepted for publication May 14, 2004 Reprint requests should be addressed to Dr. Masami Tanaka, the Department of Internal Medicine, Misato Kenwa Hospital, 4-494-1 Takano, Misato, Saitama 341-8555 Internal Medicine Vol. 43, No. 10 (October 2004) 955 TANAKA et al Table 1. Laboratory Data (Case 1, July 2002) Urinalysis Blood chemistry Arterial blood gas analysis (room air/rest) Glucose (–) Total bilirubin 1.41 mg/dl pH 7.140 Protein (+) AST 319 IU/l PaCO2 25.6 mmol/l Occult blood (+) ALT 109 IU/l PaO2 117.7 mmol/l – Ketone (3+) LDH 427 IU/l HCO3 8.5 mmol/l -GTP 911 IU/l Anion gap 33.5 mEq/l Hematology CPK 215 IU/l Ketone body WBC 11,000/l Amylase 168 IU/l AcAc 1,400 mol/l Hb 9.74 g/dl BUN/Cr 18/0.8 mg/dl 3-OHB 10,900 mol/l Plt 27.7×104/l Na/K/Cl 131/4.4/89 mEq/l Lactic acid 98.6 mg/dl Plasma glucose 73 mg/dl Pyruvic acid 1.5 mg/dl CRP 0.6 mg/dl Table 2. Treatment within 24 Hours after Arrival at Our Hospital for Our 3 Cases Case 1 Case 2 Case 3 Volume of intravenous drip (ml) 2,500 3,500 3,500 Sodium (mEq) 135.5 314.5 166 Potassium (mEq) 42 38 24 Glucose (g) 86 64.5 43 Thiamine (mg) 100 50 100 Insulin (units) – 24 – containing electrolyte and thiamine (Table 2), her metabolic blood gas analysis in room air showed pH 7.179, PaCO2 12.2 – acidosis was improved quickly. Subsequently, she had 2 re- mmHg, PaO2 119.4 mmHg, HCO3 5.8 mmol/l. The anion – current episodes of AKA. gap (Na-[Cl+HCO3 ]) was 35.2 mEq/l. Abdominal CT re- vealed swelling of the pancreas. He was diagnosed with Case 2 DKA because of hyperglycemia, acidemia, decreased bicar- The patient was a 62-year-old man. He had been diag- bonate, positive urinary ketones, increased serum ketones nosed with type 2 DM when he was 48 years old. Insulin and increased anion gap. In addition, acute pancreatitis was therapy had been introduced using biphasic isophane insulin present. Initial treatment consisted of intravenous infusion of (10 units in the morning and 6 units in the evening). Diabetic regular insulin (8 units injection followed by 8 units/hour) retinopathy was absent, but intermittent proteinuria and dia- and a large volume of saline (mainly 0.9% NaCl 1 l/first 2 betic neuropathic pain in his legs were present. He had been hours) containing thiamine (Table 2). Two hours later, his consuming excessive alcohol for years. Gastric pain occurred plasma glucose became as low as 91 mg/dl. Therefore, insu- and worsened after binge drinking. He could not drink alco- lin infusion was reduced and 0.9% NaCl was replaced by 5% hol because of severe epigastralgia for 3 days and was admit- glucose solution. At that time, we diagnosed him as having ted to our hospital on July 3, 2002. He was 165 cm tall and AKA concomitantly. Acute pancreatitis was treated simulta- weighed 40 kg. Vital signs were body temperature of 35.3 neously with gabexate mesilate and antibiotics (cefmetazole °C, blood pressure of 166/90 mmHg, respiratory rate of sodium). His metabolic acidosis and pancreatitis were cured. 28/min, and regular pulse of 105/min. His consciousness was However, his drowsiness persisted. Brain computed tomo- drowsy and palms were erythematous. Abdominal examina- graphy revealed slight brain atrophy. Although vitamin B1 tions revealed tenderness in the epigastrium. Laboratory data was not measured, the cause of his consciousness distur- on admission are summarized in Table 3. Urinalysis showed bance might be Wernicke’s encephalopathy considering the glycosuria (4+), proteinuria (2+), hematuria (2+) and clinical course. ketonuria (2+). The platelet count was 3.9×104 /l. Total bilirubin was 2.09 mg/dl, AST; 244 IU/l, ALT; 134 IU/l, lac- Case 3 tate dehydrogenase (LDH); 497 IU/l, -GTP; 3,246 IU/l, The patient was a 53-year-old man. He was admitted to a amylase; 1,308 IU/l and plasma glucose; 428 mg/dl. His he- hospital due to alcoholic hepatitis and had never been diag- moglobin A1c was 7.3 %. The serum concentration of AcAc nosed with DM. He had been consuming excessive alcohol. and 3-OHB were 3,100 mol/l and 10,900 mol/l, respec- Vomiting because of gastric irritation occurred and worsened tively. The serum concentration of lactic acid and pyruvic on November 18, 2001. He kept vomiting frequently for 2 acid were 29.1 mg/dl and 1.6 mg/dl, respectively. Arterial days, and then, was transferred to our hospital on November 956 Internal Medicine Vol. 43, No. 10 (October 2004) 3 Cases of Alcoholic Ketoacidosis Table 3. Laboratory Data (Case 2, July 2002) Urinalysis Blood chemistry Arterial blood gas analysis (room air/rest) Glucose (4+) Total bilirubin 2.09 mg/dl pH 7.179 Protein (2+) AST 244 IU/l PaCO2 12.2 mmol/l Occult blood (2+) ALT 134 IU/l PaO2 119.4 mmol/l – Ketone (2+) LDH 497 IU/l HCO3 5.8 mmol/l -GTP 3,246 IU/l Anion gap 35.2 mEq/l Hematology CPK 43 IU/l Ketone body WBC 8,600/l Amylase 1,308 IU/l AcAc 3,100 mol/l Hb 11.6 g/dl BUN/Cr 15.1/1.1 mg/dl 3-OHB 12,400 mol/l Plt 3.9×104/l Na/K/Cl 131/4.7/90 mEq/l Lactic acid 29.1 mg/dl Plasma glucose 428 mg/dl Pyruvic acid 1.6 mg/dl CRP 0.3 mg/dl Hemoglobin A1c 7.3% Table 4. Laboratory Data (Case 3, November 2001) Urinalysis Blood chemistry Arterial blood gas analysis (room air/rest) Glucose (3+) Total bilirubin 2.74 mg/dl pH 6.934 Protein (2+) AST 98 IU/l PaCO2 12.6 mmol/l Occult blood (3+) ALT 29 IU/l PaO2 157.6 mmol/l – Ketone (3+) LDH 785 IU/l HCO3 2.6 mmol/l -GTP 506 IU/l Anion gap 48.4 mEq/l Hematology CPK 1,046 IU/l Ketone body WBC 20,400/l Amylase 93 IU/l AcAc 360 mol/l Hb 12.8 g/dl BUN/Cr 12.1/2.4 mg/dl 3-OHB 4,400 mol/l Plt 9.8×104/l Na/K/Cl 129/4.8/78 mEq/l Lipase 92 U/l Plasma glucose 286 mg/dl Elastase-1 545 ng/dl CRP 0.3 mg/dl Hemoglobin A1c 7.0% 20.
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