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Satisfactory Outcome After Severe Ethanol-Induced Lactic Acidosis and Hypoglycemia
The Journal of Emergency Medicine, Vol. 34, No. 3, pp. 337–339, 2008 Copyright © 2008 Elsevier Inc. Printed in the USA. All rights reserved 0736-4679/08 $–see front matter
Letters to the Editor e SATISFACTORY OUTCOME AFTER SEVERE ETHANOL-INDUCED LACTIC ACIDOSIS AND HYPOGLYCEMIA
Table 1. Hematological and Biochemical Results on Admission
e To the Editor:
Hematology RBC (Mio/L) Hemoglobin (g/dL) MCV (fl) WBC (1/L) Neutrophils (%) Lymphocytes (%) Platelet (103/L) Arterial blood gas pH PaO2 (mm Hg) PaCO2 (mm Hg) HCO3⫺ (mmol/L) Base excess (mmol/L) Blood chemistry Na⫹ (mmol/L) K⫹ (mmol/L) Cl⫺ (mmol/L) Anion gap Glucose (mg/dL) Lactate (mmol/L) Creatinine (mg/dL) Urea (mg/dL) SGOT/AST (U/L) SGPT/ALT (U/L) LDH (U/L) AP (U/L) GGT (U/L) Total bilirubin (mg/dL) Lipase (U/L) Ethanol in plasma (g/L) Urinary ketone bodies
We have read with interest the article of Lien and Mader reporting on a patient presenting with a profound alcohol-related lactic acidosis (1). Cases of severe lactic acidosis after alcohol ingestion are rare; however, they require clinical attention. Therefore, we wish to contribute a case of a male patient who experienced severe lactic acidosis and hypoglycemia due to acute and chronic ingestion of alcohol.
CASE PRESENTATION
A 38-year-old man was brought to the Emergency Department for evaluation of symptomatic hypoglycemia (initial blood glucose 35 mg/dL). His past medical history revealed chronic alcohol misuse with an alcohol binge (160 g of ethanol) and fasting the day before admission. The patient was not receiving any medication and denied surreptitious administration of antidiabetic medication. Physical examination revealed a slightly overweight adult man (178 cm, 82 kg, body mass index 26 kg/m2) in good general health. Vital signs were as follows: blood pressure 120/70 mm Hg, pulse rate 137 beats/min, and respiratory rate 27 breaths/min. The physical examination was otherwise unremarkable. Laboratory findings on admission are summarized in Table 1. Arterial blood gas analysis showed severe metabolic acidosis with inadequate respiratory compensation and markedly increased lactic acid concentration. A urine toxicology screen was negative for all drugs of abuse. The patient received 100 mg thiamine intravenously and a continuous intravenous infusion with 5% glucose solution followed by physiological saline. An abdominal computed tomography scan was performed that was not consistent with intestinal ischemia. Blood lactate and pH returned to normal levels within 20 h after admission
Patient’s Value
Normal Range
4.74 16.2 106.4 27,420 89.0 3.7 304
4.2–6.2 14.0–18.0 80–93 4000–9500 40.0–80.0 20.0–45.0 150–450
7.08 106 19 9.0 ⫺21.5
7.35–7.45 65–100 35–45 22.0–26.0 ⫺3.0–3.0
145 4.1 105 32.2 59 17.3 1.4 36 229 127 445 57 616 0.7 31 0.3 ⫹⫹
136–148 3.5–4.8 96–110 7–16 70–110 0.5–2.2 0–1.3 12–46 ⬍50 ⬍50 ⬍250 40–130 ⬍60 ⬍1.1 ⬍60 ⬍0.1 Negative
RBC ⫽ red blood cells; MCV ⫽ mean corpuscular volume; WBC ⫽ white blood cells; SGOT/AST ⫽ aspartate aminotransferase; SGPT/ALT ⫽ alanine aminotransferase; LDH ⫽ lactate dehydrogenase; AP ⫽ alkaline phosphate; GGT ⫽ gamma glutamyltransferase.
(Figure 1). The subsequent course was uneventful and the patient was discharged home refusing outpatient alcohol rehabilitation and counseling.
DISCUSSION The differential diagnosis of lactic acidosis is classified into two general categories: Type A, due to impaired tissue oxygenation; and Type B, due to other 337
338
The Journal of Emergency Medicine
Karsten Müssig, MD Erwin D. Schleicher, PHD Hans-Ulrich Häring, MD Department of Endocrinology, Diabetology, Angiology, Nephrology, and Clinical Chemistry University Hospital of Internal Medicine University of Tübingen Tübingen, Germany
Figure 1. Clinical course of our patient after thiamine repletion, intravenous administration of glucose, and extracellular volume repletion.
Reimer Riessen, MD Interdisciplinary Intensive Care Unit University Hospital of Internal Medicine University of Tübingen Tübingen, Germany doi:10.1016/j.jemermed.2007.04.028
disorders, including alcohol ingestion (2). Ethanol is mainly metabolized in the liver by alcohol dehydrogenase, the rate-limiting enzyme in alcohol metabolism. The acetaldehyde is further oxidized to acetic acid by aldehyde dehydrogenase, both enzymatic steps resulting in the generation of NADH. The increase of the NADH/NAD⫹ ratio favors the production of lactate from pyruvate by lactate dehydrogenase and, thus, decreases the amount of pyruvate entering the gluconeogenesis system. In fasted subjects with depleted glycogen stores, hypoglycemia may occur after ethanol ingestion. In addition to the acute effects, chronic alcoholism may also decrease lactate utilization due to inadequate intake of biotin and thiamine. These watersoluble vitamins are important cofactors of enzymes catalyzing the conversion of pyruvate to acetyl CoA and gluconeogenesis, on which elimination of lactate mainly depends (3). The degree of hyperlactatemia in our patient was similar to that in the patient described by Lien and Mader (17.3 vs. 16.1 mmol/L, respectively) (1). Blood lactate levels are closely related to prognosis, with an increased mortality rate of up to 80% in patients with levels exceeding 5 mmol/L (4). Identification of the underlying disorder and directed therapy, including extracellular fluid administration and pharmacological correction of acidosis, are of significant importance in the treatment of lactic acidosis. In patients at high risk for thiamine deficiency, for example, in malnourished patients or alcoholics presenting with life-threatening metabolic acidosis, immediate empiric thiamine administration has been shown to be beneficial (5). In conclusion, rapid diagnosis and appropriate therapy of severe ethanol-dependent lactic acidosis resulted in a satisfactory outcome in our patient. Our purpose in presenting this case is to further raise awareness of alcoholinduced hyperlactatemia in the differential diagnosis of severe lactic acidosis.
REFERENCES 1. Lien D, Mader TJ. Survival from profound alcohol-related lactic acidosis. J Emerg Med 1999;17:841– 6. 2. Stacpoole PW. Lactic acidosis. Endocrinol Metab Clin North Am 1993;22:221– 45. 3. Lieber CS. Biochemical and molecular basis of alcohol-induced injury to liver and other tissues. N Engl J Med 1988;319:1639 –50. 4. Stacpoole PW, Wright EC, Baumgartner TG, et al. Natural history and course of acquired lactic acidosis in adults. DCA-Lactic Acidosis Study Group. Am J Med 1994;97:47–54. 5. Klein M, Weksler N, Gurman GM. Fatal metabolic acidosis caused by thiamine deficiency. J Emerg Med 2004;26:301–3.
e RESIDENT INVOLVEMENT IN TACTICAL MEDICINE e To the Editor: In recent years there has been a surge of interest in tactical medicine: the provision of medical support to law enforcement and military tactical teams (1– 6). Providers of tactical medicine include paramedics as well as physicians and other medical personnel. The most common image of tactical medicine involves “care under fire” or initiating treatment of a gunshot victim while a battle still continues. However, this image is misleading; tactical medicine is much more than standard prehospital trauma care adapted to a special circumstance or situation. In reality, it includes the comprehensive medical support of tactical teams during training and missions and incorporates elements of primary care, health maintenance, preventive medicine, sports medicine, and toxicology as well as prehospital emergency medical services (EMS). Many of these aspects are beyond the scope of paramedic training and necessitate the active involvement of physicians with expertise in tactical medicine. Additional
Letters to the Editor e SATISFACTORY OUTCOME AFTER SEVERE ETHANOL-INDUCED LACTIC ACIDOSIS AND HYPOGLYCEMIA
Table 1. Hematological and Biochemical Results on Admission
e To the Editor:
Hematology RBC (Mio/L) Hemoglobin (g/dL) MCV (fl) WBC (1/L) Neutrophils (%) Lymphocytes (%) Platelet (103/L) Arterial blood gas pH PaO2 (mm Hg) PaCO2 (mm Hg) HCO3⫺ (mmol/L) Base excess (mmol/L) Blood chemistry Na⫹ (mmol/L) K⫹ (mmol/L) Cl⫺ (mmol/L) Anion gap Glucose (mg/dL) Lactate (mmol/L) Creatinine (mg/dL) Urea (mg/dL) SGOT/AST (U/L) SGPT/ALT (U/L) LDH (U/L) AP (U/L) GGT (U/L) Total bilirubin (mg/dL) Lipase (U/L) Ethanol in plasma (g/L) Urinary ketone bodies
We have read with interest the article of Lien and Mader reporting on a patient presenting with a profound alcohol-related lactic acidosis (1). Cases of severe lactic acidosis after alcohol ingestion are rare; however, they require clinical attention. Therefore, we wish to contribute a case of a male patient who experienced severe lactic acidosis and hypoglycemia due to acute and chronic ingestion of alcohol.
CASE PRESENTATION
A 38-year-old man was brought to the Emergency Department for evaluation of symptomatic hypoglycemia (initial blood glucose 35 mg/dL). His past medical history revealed chronic alcohol misuse with an alcohol binge (160 g of ethanol) and fasting the day before admission. The patient was not receiving any medication and denied surreptitious administration of antidiabetic medication. Physical examination revealed a slightly overweight adult man (178 cm, 82 kg, body mass index 26 kg/m2) in good general health. Vital signs were as follows: blood pressure 120/70 mm Hg, pulse rate 137 beats/min, and respiratory rate 27 breaths/min. The physical examination was otherwise unremarkable. Laboratory findings on admission are summarized in Table 1. Arterial blood gas analysis showed severe metabolic acidosis with inadequate respiratory compensation and markedly increased lactic acid concentration. A urine toxicology screen was negative for all drugs of abuse. The patient received 100 mg thiamine intravenously and a continuous intravenous infusion with 5% glucose solution followed by physiological saline. An abdominal computed tomography scan was performed that was not consistent with intestinal ischemia. Blood lactate and pH returned to normal levels within 20 h after admission
Patient’s Value
Normal Range
4.74 16.2 106.4 27,420 89.0 3.7 304
4.2–6.2 14.0–18.0 80–93 4000–9500 40.0–80.0 20.0–45.0 150–450
7.08 106 19 9.0 ⫺21.5
7.35–7.45 65–100 35–45 22.0–26.0 ⫺3.0–3.0
145 4.1 105 32.2 59 17.3 1.4 36 229 127 445 57 616 0.7 31 0.3 ⫹⫹
136–148 3.5–4.8 96–110 7–16 70–110 0.5–2.2 0–1.3 12–46 ⬍50 ⬍50 ⬍250 40–130 ⬍60 ⬍1.1 ⬍60 ⬍0.1 Negative
RBC ⫽ red blood cells; MCV ⫽ mean corpuscular volume; WBC ⫽ white blood cells; SGOT/AST ⫽ aspartate aminotransferase; SGPT/ALT ⫽ alanine aminotransferase; LDH ⫽ lactate dehydrogenase; AP ⫽ alkaline phosphate; GGT ⫽ gamma glutamyltransferase.
(Figure 1). The subsequent course was uneventful and the patient was discharged home refusing outpatient alcohol rehabilitation and counseling.
DISCUSSION The differential diagnosis of lactic acidosis is classified into two general categories: Type A, due to impaired tissue oxygenation; and Type B, due to other 337
338
The Journal of Emergency Medicine
Karsten Müssig, MD Erwin D. Schleicher, PHD Hans-Ulrich Häring, MD Department of Endocrinology, Diabetology, Angiology, Nephrology, and Clinical Chemistry University Hospital of Internal Medicine University of Tübingen Tübingen, Germany
Figure 1. Clinical course of our patient after thiamine repletion, intravenous administration of glucose, and extracellular volume repletion.
Reimer Riessen, MD Interdisciplinary Intensive Care Unit University Hospital of Internal Medicine University of Tübingen Tübingen, Germany doi:10.1016/j.jemermed.2007.04.028
disorders, including alcohol ingestion (2). Ethanol is mainly metabolized in the liver by alcohol dehydrogenase, the rate-limiting enzyme in alcohol metabolism. The acetaldehyde is further oxidized to acetic acid by aldehyde dehydrogenase, both enzymatic steps resulting in the generation of NADH. The increase of the NADH/NAD⫹ ratio favors the production of lactate from pyruvate by lactate dehydrogenase and, thus, decreases the amount of pyruvate entering the gluconeogenesis system. In fasted subjects with depleted glycogen stores, hypoglycemia may occur after ethanol ingestion. In addition to the acute effects, chronic alcoholism may also decrease lactate utilization due to inadequate intake of biotin and thiamine. These watersoluble vitamins are important cofactors of enzymes catalyzing the conversion of pyruvate to acetyl CoA and gluconeogenesis, on which elimination of lactate mainly depends (3). The degree of hyperlactatemia in our patient was similar to that in the patient described by Lien and Mader (17.3 vs. 16.1 mmol/L, respectively) (1). Blood lactate levels are closely related to prognosis, with an increased mortality rate of up to 80% in patients with levels exceeding 5 mmol/L (4). Identification of the underlying disorder and directed therapy, including extracellular fluid administration and pharmacological correction of acidosis, are of significant importance in the treatment of lactic acidosis. In patients at high risk for thiamine deficiency, for example, in malnourished patients or alcoholics presenting with life-threatening metabolic acidosis, immediate empiric thiamine administration has been shown to be beneficial (5). In conclusion, rapid diagnosis and appropriate therapy of severe ethanol-dependent lactic acidosis resulted in a satisfactory outcome in our patient. Our purpose in presenting this case is to further raise awareness of alcoholinduced hyperlactatemia in the differential diagnosis of severe lactic acidosis.
REFERENCES 1. Lien D, Mader TJ. Survival from profound alcohol-related lactic acidosis. J Emerg Med 1999;17:841– 6. 2. Stacpoole PW. Lactic acidosis. Endocrinol Metab Clin North Am 1993;22:221– 45. 3. Lieber CS. Biochemical and molecular basis of alcohol-induced injury to liver and other tissues. N Engl J Med 1988;319:1639 –50. 4. Stacpoole PW, Wright EC, Baumgartner TG, et al. Natural history and course of acquired lactic acidosis in adults. DCA-Lactic Acidosis Study Group. Am J Med 1994;97:47–54. 5. Klein M, Weksler N, Gurman GM. Fatal metabolic acidosis caused by thiamine deficiency. J Emerg Med 2004;26:301–3.
e RESIDENT INVOLVEMENT IN TACTICAL MEDICINE e To the Editor: In recent years there has been a surge of interest in tactical medicine: the provision of medical support to law enforcement and military tactical teams (1– 6). Providers of tactical medicine include paramedics as well as physicians and other medical personnel. The most common image of tactical medicine involves “care under fire” or initiating treatment of a gunshot victim while a battle still continues. However, this image is misleading; tactical medicine is much more than standard prehospital trauma care adapted to a special circumstance or situation. In reality, it includes the comprehensive medical support of tactical teams during training and missions and incorporates elements of primary care, health maintenance, preventive medicine, sports medicine, and toxicology as well as prehospital emergency medical services (EMS). Many of these aspects are beyond the scope of paramedic training and necessitate the active involvement of physicians with expertise in tactical medicine. Additional