sodium-bicarbonate and Alcoholism

The information on burden of alcohol abuse in Iran is scarce. However, the available data show that mortality rates and frequency of its use have increased in the Iranian community. In particular, Iran occupies the 1st rank in the number of outbreak incidents and victims of toxic alcohols such as methanol in the Middle East. Mortality and morbidity of toxic alcohols are high if prompt diagnosis and treatment are not initiated rapidly. On-time diagnosis, proper case finding, and standard treatment have an essential role to reduce mortality and morbidity of toxic alcohols particularly blindness and other physical and psychological disabilities. This review focuses on intoxication with methanol, ethylene glycol, and isopropanol, and their treatment.

Topics: 2-Propanol; Acidosis; Alcoholism; Antidotes; Ethanol; Ethylene Glycol; Fomepizole; Humans; Iran; Methanol; Poisoning; Pyrazoles; Renal Dialysis; Sodium Bicarbonate; Solvents

Lactate can be viewed as a metabolic dead end in that it can only be produced or utilized via pyruvate. Lactate production is determined primarily by pyruvate concentration and to a lesser extend by the redox state. Increased lactate production may result from tissue hypoxia, alkalosis, catecholamine and alanine transamination to pyruvate. Hyperlactatemia is observed in many pathological conditions. Current diagnostic criteria for lactic acidosis are a pH less than 7.35 and lactate concentration greater than 5 to 6 mmol/l. In our study series, malignancy was the most common underlying disease accompanied by lactic acidosis. Organ failure, cardiovascular disease and diabetes mellitus were also common. The prognosis of patients with these diseases were grave. In cases of lactic acidosis associated with diabetes mellitus, alcoholic liver disease, rhabdomyolysis and diabetic comas were noticeable as complications. Alcohol abuse was the most common cause of lactic acidosis associated with diabetes mellitus. In these cases, laboratory data showed prominent hyperlactatemia, hyperglycemia and acidemia and elevated anion gap. The mortality rate in these cases was 36% and higher in cases with organ failure. Treatment of lactic acidosis consists of alkalization by sodium bicarbonate with carbicarb, insulin-glucose-infusion, dichloroacetate therapy, tham administration, bicarbonate-buffered peritoneal dialysis and high bicarbonate-containing dialysis.

Topics: Acidosis, Lactic; Alcoholism; Cardiovascular Diseases; Diabetes Complications; Dichloroacetic Acid; Female; Humans; Insulin; Lactates; Male; Neoplasms; Sodium Bicarbonate; Tromethamine

Mortality associated with methanol has been of great concern time and again. The concurrence of cases from a particular area raises doubts about methanol as the culprit. Knowledge of the patho-physiological changes that occur in the body after methanol consumption is essential for all practicing doctors. This article elucidates the clinical presentation and emergency management of these cases under the framework of basic physiological and biochemical phenomena after methanol exposure. Conversion of methanol to formaldehyde by hepatic enzyme alcohol dehydrogenase triggers the cascade of metabolic events. The manifestations begin as early as 30 minutes and progress to decompensated metabolic acidosis in about 12 hours, if left untreated. Seizures, hypoglycemia and blindness frequently complicate the picture. Acute kidney injury warrants urgent haemodialysis. Fundoscopic examination and arterial blood gas analysis are the key diagnostic elements. The management comprises of intravenous sodium bicarbonate, correction of dyselectrolytemia, ethanol, folic acid and haemodialysis, if necessary. The basic steps in approach must be carried out in the emergency department and followed-up with meticulous monitoring in the intensive care unit for salvage as well as prevention of long term sequelae.

Topics: Acidosis; Alcoholism; Ethanol; Humans; Methanol; Sodium Bicarbonate

Loperamide, a non-prescription anti-diarrheal agent, is a peripheral mu-opioid receptor agonist that is excluded from the blood-brain barrier by p-glycoprotein at therapeutic doses. Overdoses of loperamide penetrate the central nervous system (CNS), leading to abuse. We report cardiac conduction abnormalities and dysrhythmias after ingestion of a recreational supra-therapeutic dose of loperamide confirmed with an elevated blood loperamide concentration.. A 48-year-old woman with a history of alcohol and benzodiazepine abuse presented to the emergency department (ED) with somnolence, weakness and slurred speech. She was taking 20 to 40 tablets of 2 mg loperamide 1-2 times/day for weeks along with clonazepam and whiskey. Vital signs were: blood pressure (BP), 124/90 mmHg; heart rate (HR), 88/min; respiratory rate(RR), 20/min; T, 36.9 °C; O2 saturation 100% on room air (RA). Glucose was 6.4 mmol/L. Electrocardiogram (ECG) had a ventricular rate of 58/min, QRS 164 ms, QT 582 ms with no discernable p-waves. Lactate was 3.5 mmol/L and potassium was 6.2 mEq/L. Labs were notable for an anion gap of 20 mEq/L, ethanol of 3.9 mmol/L, creatinine of 2.3 mg/dL and loperamide concentration of 210 ng/mL (average therapeutic plasma concentration 1.2 ng/mL). She became hypotensive, but responded to fluids. Following treatment for hyperkalemia with calcium, insulin, dextrose, and hypertonic sodium bicarbonate a repeat ECG had a ventricular rate of 66/min, QRS 156 ms, and QT 576 ms. Magnesium was given and pacer pads were placed. During the infusion of magnesium, her BP fell to 92/58 mmHg with a HR of 54/min, RR 14/min, O2 saturation of 97% on RA so the infusion was stopped. The ECG after the magnesium infusion had a ventricular rate of 51/min, QRS of 134 ms, and QT 614 ms. In the ICU she had multiple runs of non-sustained ventricular tachycardia that did not require therapy. Over the next 48 h she improved and was transferred to a floor bed. On day four of hospitalization the patient left against medical advice. At that time, her ECG showed sinus tachycardia with a heart rate 114/min, QRS 82 ms, QT 334 ms.. Loperamide produces both QRS and QT prolongation at supra-therapeutic dosing. A blood loperamide concentration of 210 ng/mL is among the highest concentrations reported. Supra-therapeutic dosing of loperamide is promoted on multiple drug-use websites and online forums as a treatment for opioid withdrawal, as well as for euphoric effects. With the current epidemic of prescription opioid abuse, toxicity related to loperamide, an opioid agonist that is readily available without a prescription is occurring more frequently. It is important for clinicians to be aware of the potentially life-threatening toxicity related to loperamide abuse in order to provide proper diagnosis, management and patient education.

Topics: Alcoholism; Arrhythmias, Cardiac; Benzodiazepines; Blood Pressure; Calcium; Central Nervous System; Clonazepam; Dose-Response Relationship, Drug; Drug Overdose; Electrocardiography; Emergency Service, Hospital; Female; Glucose; Heart Rate; Humans; Hyperkalemia; Insulin; Loperamide; Magnesium; Middle Aged; Respiratory Rate; Sodium Bicarbonate; Substance-Related Disorders

Underlying causes of metabolic alkalosis may be evident from history, evaluation of effective circulatory volume, and measurement of urine chloride concentration. However, identification of causes may be difficult for certain conditions associated with clandestine behaviors, such as surreptitious vomiting, use of drugs or herbal supplements with mineralocorticoid activity, abuse of laxatives or diuretics, and long-term use of alkalis. In these circumstances, clinicians often are bewildered by unexplained metabolic alkalosis from an incomplete history or persistent deception by the patient, leading to misdiagnosis and poor outcome. We present a case of severe metabolic alkalosis and hypokalemia with a borderline urine chloride concentration in an alcoholic patient treated with a thiazide. The cause of the patient's metabolic alkalosis eventually was linked to surreptitious ingestion of baking soda. This case highlights the necessity of a high index of suspicion for the diverse clandestine behaviors that can cause metabolic alkalosis and the usefulness of urine pH and anion gap in its differential diagnosis.

Topics: Acid-Base Equilibrium; Aged; Alcoholism; Alkalosis; Chlorides; Comorbidity; Eating; Humans; Hydrogen-Ion Concentration; Hypokalemia; Male; Sodium Bicarbonate; Thiazides; Urine

To report a case of reversible blindness associated with severe alcoholic ketoacidosis.. Observational case report.. A 44-year-old male presented with gradual bilateral blindness that developed within a 24-hour period. He suffered from ethanol-induced severe ketoacidosis and shock and was resuscitated with epinephrine and sodium bicarbonate.. The treatment of acidosis led to a rapid resolution of the patient's blindness.. It is important to understand the role of severe acidosis as the sole causative factor of reversible bilateral blindness.

Topics: Adult; Alcoholism; Blindness; Cardiopulmonary Resuscitation; Drug Therapy, Combination; Epinephrine; Glucose; Humans; Infusions, Intravenous; Isotonic Solutions; Ketosis; Male; Ringer's Solution; Shock; Sodium Bicarbonate; Visual Acuity; Vitamin B Complex

Topics: Acidosis; Alcoholism; Coma; Ethylene Glycol; Ethylene Glycols; Female; Humans; Injections, Intravenous; Middle Aged; Renal Dialysis; Sodium Bicarbonate

Topics: Adult; Alcoholism; Antacids; Bicarbonates; Calcium Carbonate; Humans; Hypercalcemia; Magnesium; Male; Sodium; Sodium Bicarbonate

Topics: Acidosis; Alcoholism; Bicarbonates; Carbon Dioxide; Coma; Diagnostic Tests, Routine; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Sodium Bicarbonate