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Acid-Base and Electrolyte Disorders in Alcohol Abuse

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Electrolyte Disorders in Chronic Alcohol Use Disorder: A Case Based Approach Biff F. Palmer, M.D. Professor of Internal Medicine University of Texas Southwestern Medical Center, Dallas Texas Case • A 52-year-old homeless man presents to the emergency room complaining of weakness. He typically drinks one pint of whisky daily. He noted the onset of epigastric pain 3 days ago but continued to drink until 1 day prior to presentation, when he developed the onset of nausea and persistent vomiting. He reports having had no food intake over the last 24 hours. • PE: BP 138/90 mm Hg supine, 110/74 mm Hg standing, pulse 105 beats/minute. There is tenderness to palpation in the epigastrium but no rebound tenderness. Laboratory Data Creatinine 1.2 mg/dl Arterial blood gas: BUN 22 mg/dl – pH 7.47 Serum electrolytes –PCO2 28 (mEq/l): – Na + 142 –K+ 3.8 – Cl - 92 - – HCO 3 22 Glucose 110 mg/dl Which of the following best describes the acid- base disturbance in this patient? 1. Chronic respiratory alkalosis 2. Anion gap metabolic acidosis 3. Respiratory alkalosis and metabolic acidosis 4. Anion gap metabolic acidosis, respiratory alkalosis, and metabolic alkalosis Case • Arterial pH = 7.47 142 92 22 • pCO 2 = 28 mmHg 3.8 22 1.2 Anion gap 28 • Anion gap metabolic acidosis • Metabolic alkalosis • Respiratory alkalosis Case • A man with chronic alcohol use disorder is found lying semiconscious at the bottom of a stairwell with a broken arm by his landlady, who called an ambulance to take him to the ED. + + - - • Labs (mEq/l): Na 137, K 3.6, Cl 90, HCO 3 15 (anion gap 32), ethanol level 150 mg/dl, glucose 38 mg/dl Which of the following best accounts for the hypoglycemia and increased anion gap? 1. Increased insulin release 2. Glycosuria secondary to ethanol-induced proximal tubular dysfunction 3. Increased cellular NADH/NAD + 4. Decreased secretion of glucagon Alcohol-Induced Hypoglycemia • Occurs in chronic malnourished or weekend binge drinker, children or adolescents particularly susceptible • Variable period of fasting present (liver glycogen depleted in 14-24 hours) • Onset 5-20 hours after last ingestion • Transition from alcoholic stupor to hypoglycemia coma can be imperceptible Metabolism of Alcohol Increases the NADH/NAD + Ratio Alcohol Acetaldehyde Ethanoldehydrogenase Acetaldehydedehydrogenase Acetate + NAD NADH 2 + NAD NADH 2 Increases in the NADH/NAD + Ratio Leads to Shunting of Gluconeogenic Precursors Away From Gluconeogenic Pathways Tricarboxylic acid cycle, (Krebs cycle) Citrate Isocitrate Oxaloacetate + NADH + H + NAD + NAD + NADH + H Malate α-Ketoglutarate NAD + + Fumarate NADH + H Succinyly-CoA Succinate Alcohol-Induced Hypoglycemia • Oxalacetate is reduced to malate • α-ketoglutarate is converted to glutamate Citrate Isocitrate ↓ Oxaloacetate Glutamate NADH + H + NAD + NAD + NADH + H + NADH + H + NAD + Malate ↓ α-Ketoglutarate NAD + + Fumarate NADH + H Succinyly-CoA Succinate ↓ Glucose Glucose The Increased ADH/AD + Ratio Shunts Gluconeogenic Precursors Away From Gluconeogenic Pathways ↓ Phosphoenolpyruvate PEPCK Pyruvate ↓ Oxaloacetate Citrate Acetyl CoA Isocitrate ↓ Oxaloacetate Glutamate NADH + H + NAD + NAD + ↓ Pyruvate NADH + H + NADH + H + NAD + NADH + Malate ↓ α-Ketoglutarate NAD + NAD + + Lactate Fumarate NADH + H Succinyly-CoA NADH Favors reduction of pyruvate to lactate Succinate NAD + reducing availability of OAA Alcohol-Induced Hypoglycemia and Ketoacidosis • Alcohol can be associated with both hypoglycemia and ketoacidosis • In patients with alcohol -induced hypoglycemia (n=101)* - – plasma HCO 3 <15 mEq/L in one third - – plasma HCO 3 <9 mEq/L in 17% – urinary ketones frequently positive Madison L. Advances in Metabolic Disorders, 1968 Alcoholic Ketoacidosis • Chronic alcoholics with recent debauch, often with no alcohol in past 24-48 hours • Poor dietary intake in preceding 1-2 days • Ketoacidosis predominates, lactic acid also present • Mechanism related to increases in the NADH/NAD + ratio along with augmented free fatty acid mobilization ↓ Glucose ↑↑ Fatty acid Mobilization VLDL Glucose Fatty acid VLDL Cytosol Fatty Acyl CoA Pyruvate ↓ OAA Mitochondria ↓ Pyruvate Citrate NADH + Acetyl CoA Isocitrate Glutamate Oxaloacetate NAD + NAD + NAD + NADH + H + + NADH + H + NADH + H + ↑ Lactate Malate NAD α-Ketoglutarate NAD + NADH + H + Fumarate Succinyly-CoA Succinate ↓ Glucose ↑↑ Fatty acid Mobilization VLDL Glucose Fatty acid VLDL Cytosol Fatty Acyl CoA Malonyl CoA ACC (inhibited by glucagon, epinephrine stimulated by insulin Acetyl CoA Pyruvate ↓OAA ↓ Citrate ↓ OAA Mitochondria ↓ Pyruvate Citrate NADH + Acetyl CoA Isocitrate Glutamate Oxaloacetate NAD + NAD + NAD + NADH + H + + NADH + H + NADH + H + ↑ Lactate Malate NAD α-Ketoglutarate NAD + NADH + H + Fumarate Succinyly-CoA Succinate ↓ Glucose ↑↑ Fatty acid VLDL Glucose Fatty acid VLDL Cytosol Fatty Acyl CoA Malonyl CoA ACC (inhibited by glucagon, epinephrine stimulated by insulin Acetyl CoA Pyruvate Fatty Acyl Carnitine ↓OAA ↓ Citrate ↓ OAA Fatty Acyl Carnitine Mitochondria Fatty Acyl CoA ↓ Pyruvate Citrate NADH + Acetyl CoA Isocitrate Glutamate PDH Oxaloacetate NAD + NAD + NAD + NADH + H + + NADH + H + NADH + H + ↑ Lactate Malate NAD α-Ketoglutarate ↑ Acetoacetate NAD + NADH + NADH + H + Fumarate NAD + Succinyly-CoA ↑↑ β-Hydroxybutyrate Succinate Alcohol withdrawal ↓ Glycogen stores Starvation Volume depletion Sympathetic nerve activation Lipolysis ↓ Insulin ↑ Glucagon Fatty acids ↓ Gluconeogenesis Ketogenic State Ethanol NAD NADH NADH β-hydroxybutyric acid + NaHCO 3 Acetaldehyde NAD NAD NaBOH H2CO 3 NADH Acetate CO 2 and H 2O Loss through the lungs Palmer BF, Clegg DJ. New Engl J Med. 2017;377:1368-1377 Indirect Loss of NaHCO 3 Which of the following best accounts for the hypoglycemia and increased anion gap? 1. Increased insulin release 2. Glycosuria secondary to ethanol-induced proximal tubular dysfunction 3. Increased cellular ADH/AD + 4. Decreased secretion of glucagon Therapy • Initial therapy is 5% dextrose in 0.9% normal saline – Restore ECF volume and stabilize hemodynamics – Provides Cl - for correction of metabolic alkalosis • Volume resuscitation decreases sympathetic nerve activity • Dextrose decreases ketogenesis by stimulating insulin release and suppressing glucagon • Supplemental thiamine (100 mg intravenous or intramuscular) prior to glucose containing solutions to minimize risk of precipitating Wernicke encephalopathy or Korsakoff syndrome • Benzodiazepines to treat alcohol withdrawal. • Monitor for development of hypomagnesemia, hypophosphatemia, and hypokalemia Case • A 42-year-old woman is admitted to the hospital with a several week history of increasing weakness and fatigue followed by the onset of paresthesias in the lower extremities one week ago. She normally drinks up to one pint of vodka per day but has not ingested any alcohol over the last 24 hours. Vital signs on admission show a blood pressure of 134/82 mmHg and a pulse of 110 beats per minute with no orthostatic changes. The respiratory rate is 24 per minute and she is afebrile. Physical examination shows a disheveled woman who appears visibly agitated. Laboratory Data Creatinine 1.2 mg/dl, Mg 2+ 0.6 mg/dl BUN 35 mg/dl Ca 2+ 6.5 mg/dl Glucose 110 mg/dl - PO 4 1.5 mg/dl Serum electrolytes Albumin 3.8 gm/dl (mEq/l): – Na + 140 Arterial blood gas: –K+ 2.4 • pH 7.50 – Cl - 103 • P 28 - CO2 – HCO 3 21 • PO 2 110 Skeletal Muscle Ion Composition in Chronic Alcohol Use Disorder Compared to Normal Persons - 2+ + 2+ + - PO 4 Mg K Ca Na Cl Normal 28.7 8.1 42.8 1.8 9.9 7.5 subjects Alcohol use 20.4 5.7 35.8 6.2 25.1 12.0 disorder patients All values are mEq per 100 mg fat-free dry weight except for - PO 4 which is mmol per 100 mg fat-free dry weight (data extracted from 2) Miner Electrolyte Metab 1980;4:106-112 Malabsorption • Steatorrhea • Diarrhea • Antacids Ethanol-induced myopathy ↓K + - ↓PO 4 General malnutrition ↓Mg 2+ Vitamin ,deficiency Dietary insufficiency Ethanol-induced tubular dysfunction + - 2+ 2+ ↑K ↑PO 4 ↑Mg ↑Ca Palmer BF, Clegg DJ. New Engl J Med. 2017;377:1368-1377 2+ Mg and FE Mg in 61 Alcoholics During 4 Weeks of Abstinence Serum Mg 2+ (mEq/l) Fractional excretion of Mg 2+ 1,8 3,5 1,7∗ 1.8 3.5 1,6 1,57 3 3.0 2,5 1,4 ∗ 1,4 2.5 1.4 2 2.0 1,5 1.5 1 1.0 1.0 1 1 4 7 28 1 4 7 28 114 4 7 7 28 28 Days Days ∗ p<0.02 vs day 1 De Marchi et al., NEJM 329:1927,1993 Malabsorption • Steatorrhea • Diarrhea • Antacids Ethanol-induced myopathy 2+ ↓K + ↓Mg - ↓PO 4 ↓PO - 4 ↓K + General malnutrition ↓Mg 2+ Vitamin ,deficiency Dietary insufficiency Ethanol-induced tubular dysfunction + - 2+ 2+ ↑K ↑PO 4 ↑Mg ↑Ca Palmer BF, Clegg DJ. New Engl J Med. 2017;377:1368-1377 Intracellular Mg ++ Decreases K + Secretion via ROMK Channel in CCD Principal Cell Lumen Interstitium ENaC 3Na + 3Na + + + Na Na 2K + 2K + ROMK + K+ K Mg ++ J Am Soc Nephrol 18:2649, 2007 Parathyroid glands Malabsorption • Steatorrhea ↓Ca 2+ • Diarrhea + • Antacids ↓PTH release PTH resistance Ethanol-induced Functional myopathy hypoparathyroidism 2+ ↓K + ↓Mg ↓K + ↓PO - 4 - ↓PO 4 General malnutrition ↓Mg 2+ Vitamin ,deficiency Dietary insufficiency Ethanol-induced tubular dysfunction + - 2+ 2+ ↑K ↑PO 4 ↑Mg ↑Ca Palmer BF, Clegg DJ. New Engl J Med. 2017;377:1368-1377 PTH is Inappropriately Low in Hypocalcemic Hypomagnesemic Patients 900 800 • 700 600 • 500 • Normal 400 • • 300 • • • Serum iPTH pg/ml pg/ml iPTHiPTH Serum Serum 200 • 100 •• • • Undetectable 0 • 0 2 4 6 8 10 12 14 Serum calcium (mg/dl) Clin Endocrinol 5:200, 1976 Effect of IV Mg 2+ on Serum Mg +2 , Ca 2+ , and iPTH in a Hypocalcemic Magnesium Deficient Patient 8 Mg ++ 8 mEq IV 7 mg/dl 2+ Ca 6 0 1 2 5 3 2 mg/dl mg/dl 2+ Mg 1 0 1 2 5 1300 PTH pg/ml 900 500 100 0 1 2 5 Minutes J Clin Endo Metab 47:800,1978 Electrolyte Disturbances Often Become More Severe After Admission to the Hospital Ethanol and Hypomagnesemia • 47 year old man presents with new onset ascites.
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