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Metabolic Acidosis: Differentiating the Causes in the Poisoned Patient Bryan S

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Metabolic Acidosis: Differentiating the Causes in the Poisoned Patient Bryan S Med Clin N Am 89 (2005) 1107–1124 Metabolic Acidosis: Differentiating the Causes in the Poisoned Patient Bryan S. Judge, MDa,b,* aDeVos Children’s Hospital Regional Poison Center, Grand Rapids, MI, USA bGrand Rapids MERC/Michigan State University Program in Emergency Medicine, Grand Rapids, MI, USA Metabolic acidosis may be a significant consequence of a vast array of toxins. Hence, determining which drugs or toxins might be responsible for metabolic acidosis in a patient with an unknown ingestion, accidental exposure, or exposure from therapeutic drug use can present daunting diagnostic and therapeutic challenges. More importantly, vital cellular functions and metabolic processes become impaired with increasing acidosis [1,2]. Therefore, it is paramount that clinicians recognize the substances that can result in metabolic acidosis so that timely and appropriate therapy may be instituted. Metabolic acidosis is defined as a process that lowers serum bicarbonate ÿ þ (HCO3 ) and occurs when H ion production exceeds the body’s ability to compensate adequately through buffering or increased minute ventilation. Acidemia should not be confused with acidosis. Acidemia refers to a blood pH less than 7.40. Comprehensive discussion of acid-base disturbances is beyond the scope of this article, and the reader is referred elsewhere for further information [1,3,4]. Approach to the poisoned patient who has metabolic acidosis Evaluating a poisoned patient may pose numerous challenges to the treating physician. First, patients may present with altered mental status, substantially limiting the ability to take an adequate history. Second, significant clues at the scene suggestive of the nature of the poisoning may * DeVos Children’s Hospital Regional Poison Center, 1300 Michigan NE, Suite 203, Grand Rapids, MI 49503. E-mail address: [email protected] 0025-7125/05/$ - see front matter Ó 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.mcna.2005.06.011 medical.theclinics.com 1108 JUDGE be absent, may be overlooked by personnel at the scene, or may be inadequately conveyed to health care providers. Third, family members or friends, who are often able to provide critical information, may not immediately accompany the patient to the hospital. The exposure history can be enhanced by specific findings on the physical examination. The patient may have a characteristic toxidrome (eg, anticholinergic, cholinergic, opioid, or sympathomimetic), odor, track marks, or other physical ex- amination clues. Because many poisoned patients are unable or unwilling to provide an accurate history, laboratory evaluation is essential. Specific diagnostic tests, such as a comprehensive metabolic panel and 12-lead ECG, should be considered. They provide invaluable information regarding end-organ toxicity and may assist with diagnosis and treatment, gauge the gravity of the toxicologic process, and provide insight into potential deterioration in a patient’s condition [5]. A quantitative test for acetaminophen, aspirin, carboxyhemoglobin, ethylene glycol, iron, methanol, or theophylline may delineate the cause of an elevated anion gap metabolic acidosis. An arterial blood gas serves as a useful adjunct in differentiating acid-base disturbances; ÿ however, serum HCO3 remains an important initial diagnostic test, because a depressed level is an early indicator of many metabolic toxins. The routine use of serum and urine drug screens in the acutely poisoned patient is rarely beneficial. Standard urine drug screens test for a limited number of common drugs, and a negative screen does not exclude toxins as the cause of illness. A positive result on the urine drug screen may confirm exposure to a particular substance, but that substance may not be the cause of the patient’s clinical condition. Few institutions have readily available com- prehensive toxicology laboratory services, a situation which delays turn- around time for comprehensive drug testing [6]. Furthermore, the results of comprehensive drug screens rarely affect either treatment or outcomes, and often medical decision making is best accomplished through routine diagnostic testing and thoroughly assessing and reassessing the patient’s clinical condition [7–9]. Once the comprehensive metabolic panel has been obtained, an anion gap (AG) should be determined using the following equation: AG ¼ [Naþ] ÿ ÿ ÿ ([Cl ] þ [HCO3 ]). Historically, a normal AG has been defined as 12 G 4 mEq/L. However, a study by Winter and colleagues [10] suggests that a normal AG should be 7 G 4 mEq/L, because of an increase in measured chloride from improved instrumentation [11]. Therefore, it is important to recognize that the previously accepted range for the AG may not be suitable with newer laboratory technology. If the ingestion of a toxic alcohol (ie, ethylene glycol, isopropanol, methanol) is suspected, osmo- larity should be estimated by the following equation: osmolarity ¼ 2 Â [Naþ] þ [glucose]/18 þ [blood urea nitrogen {BUN}]/2.8 [12]. An osmol gap (OG) may then be determined by subtracting calculated osmolarity from measured osmolality (OG ¼ measured osmolality ÿ calculated METABOLIC ACIDOSIS 1109 osmolarity). Note that osmolarity refers to the number of particles in 1 L of solution (osmoles/L of solution), and osmolality refers to the number of particles per kilograms of solution (osmoles/kg of solution), but the terms are often used interchangeably because they are almost equivalent for body fluids [13]. Classification of toxicants associated with metabolic acidosis Although there is no ideal way to classify poisons that cause metabolic acidosis, a clinically useful and systematic approach is to differentiate toxins based on whether they are associated with an elevated AG (Boxes 1 and 2) or a normal AG (Box 3). Many medical conditions are also associated with an increased or normal AG metabolic acidosis and should be included in the differential diagnosis. An elevated AG metabolic acidosis occurs when an acid is paired with an unmeasured anion (eg, lactate), whereas a normal AG metabolic acidosis results from a gain of both Hþ and Clÿ ions or a loss of ÿ ÿ HCO3 and retention of Cl , preserving electroneutrality. This classification method has several limitations. The AG may be affected by inherent errors in calculation, laboratory anomalies, and numerous non–acid-base disor- ders and disease states that may disguise an elevated AG or augment a normal AG (Box 4) [14]. Also, a normal AG acidosis may occur with several of the toxins that produce an AG; therefore, a normal AG should not be used to exclude a possible cause of metabolic acidosis [15]. Many common toxicologic and illness-related causes of an increased AG metabolic acidosis may be remembered with the mnemonic MUDPILES (see Box 1). There are however, several other causes (see Box 2) for an elevated AG metabolic acidosis that should not be overlooked. In this author’s experience, acetaminophen, amphetamines, carbon monoxide, cocaine, toluene, and valproic acid are toxins commonly encountered in the clinical setting that might contribute to an increased AG metabolic Box 1. Toxins and disease states associated with an elevated anion gap metabolic acidosis Methanol Uremia Diabetic ketoacidosis, alcoholic ketoacidosis, starvation ketoacidosis Paraldehyde, phenformin Iron, isoniazid Lactic acidosis Ethylene glycol Salicylates 1110 JUDGE Box 2. Drugs and medical conditions not listed in MUDPILES mnemonic associated with an elevated anion gap metabolic acidosis Acetaminophen Aminocaproic acid Amphetamines Benzene Carbon monoxide Catecholamines Citric acid Cocaine Cyanide Didanosine Diethylene glycol Ephedrine Fluoride Formaldehyde Hydrogen sulfide Ibuprofen Inborn errors of metabolism Nalidixic acid Metformin Niacin Nitroprusside Nonsteroidal anti-inflammatory drugs Polyethylene glycol Propofol Propylene glycol Pseudoephedrine Streptozotocin Sulfur Theophylline Thiamine deficiency Toluene Triethylene glycol Valproate Zidovudine From Seifert SA. Unexplained acid base and anion gap disorders. In: Dart RC, editor. Medical toxicology. 3rd edition. Philadelphia: Lippincott Williams & Wilkins; 2004. p. 1914; with permission. METABOLIC ACIDOSIS 1111 Box 3. Drugs and medical conditions associated with a normal anion gap metabolic acidosis Acetazolamide Acids (ammonium chloride, calcium chloride, hydrochloric acid) Cholestyramine Diarrhea Hyperalimentation Magnesium chloride Pancreatic fistula Posthypocapnia Rapid intravenous fluid administration Renal tubular acidosis Sulfamylon Topiramate Ureteroenterostomy acidosis but are not listed in the MUDPILES mnemonic. Recognizing the many toxins associated with an increased AG metabolic acidosis is imperative, because the presence of a profoundly elevated AG may help identify specific causes of the acidosis and have prognostic value [16–18]. The osmol gap may provide additional information in a patient with an elevated AG acidosis who has ingested a toxic alcohol. Although the OG may be increased in the presence of toxic alcohols, several other medical conditions, such as ketoacidosis, renal failure, and shock states, may also increase the measured serum osmolality [19–21]. Toxins that elevate the OG can be memorized with the mnemonic MADGAS (Box 5) [13]. For simplicity, a ‘‘normal’’ OG is considered to be less than 10 G 6 mOsm/L [22]. However, the use of the ‘‘normal’’ range for the OG has inherent limitations, owing to wide variability of the OG in the population [19,20,23] and potential errors in calculation and laboratory methodology (eg, freezing
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