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Toxic Acidosis

Toxic Alcohol Ingestion

Toxic Alcohol Ingestion

This month, EBMedicines Emergency Medicine Practice series tackles toxic alchol ingestion: Patil N, Becker MWL, Ganetsky M (2010). Toxic Alcohols: Not Always A Clear-Cut Diagnosis. Emergency Medicine Practice, 12 (11). [ Abstract and subscription link ] The article begins with a clinical scenario and then moves rapidly into an in-depth discussion of the relevant aetiology, pathophysiology and clinical features of toxic alcohol poisoning, focusing on the three most common toxic alcohol ingestions: methanol , ethylene glycol and isopropanol . This is followed by detailed sections on diagnosis, treatment and disposition including evidence-based treatment algorithms for toxic alcohol ingestion (these are gold!) and a step-by-step approach to calculating the osmolar gap, anion gap and estimating toxic alcohol concentrations. The review concludes with a discussion of toxic alcohol poisoning in special circumstances (paediatric patients and pregnancy), recent controversies/new developments, some common pitfalls in risk management and finally a CME quiz to assess your learning. It is a huge review, so I have chosen to focus on the following topics: Aetiology, pathophysiology and clinical features Aetiology, Pathophysiology and Clinical Features Methanol is commonly found in windshield-wiper fluid and de-icing products, and may also be found in gas-line antifreeze, paint removers, shoe dyes and embalming fluid. Methanol is metabolised by alcohol dehydrogenase (ADH) to formaldehyde, which is further metabolised by aldehyde dehydrogenase (ALDH) to formic acid. Formic acid is the main toxic metabolite responsible for the retinal, ophthalmic and neural toxicity seen with methanol ingestion. Ocular effects include blurry vision, reduced visual acuity, photophobia and the classic sno Continue reading >>

Salicylate Poisoning

Salicylate Poisoning

Child-resistant packaging , low number of pills per package [1] Salicylate poisoning, also known as aspirin poisoning, is the acute or chronic poisoning with a salicylate such as aspirin . [1] The classic symptoms are ringing in the ears , nausea , abdominal pain , and a fast breathing rate . [1] Early on these may be subtle while larger doses may result in fever . [1] [4] Complications can include swelling of the brain or lungs , seizures , low blood sugar , or cardiac arrest . [1] While usually due to aspirin, other possible causes include oil of wintergreen and bismuth subsalicylate . [2] Excess doses can be either on purpose or accidental. [1] Small amounts of oil of wintergreen can be toxic. [2] Diagnosis is generally based on repeated blood tests measuring aspirin levels and blood gases . [1] While a type of graph has been created to try to assist with diagnosis, its general use is not recommended. [1] In overdose maximum blood levels may not occur for more than 12 hours. [2] Efforts to prevent poisoning include child-resistant packaging and a lower number of pills per package. [1] Treatment may include activated charcoal , intravenous sodium bicarbonate with dextrose and potassium chloride , and dialysis . [2] Giving dextrose may be useful even if the blood sugar is normal. [2] Dialysis is recommended in those with kidney failure , decreased level of consciousness , blood pH less than 7.2, or high blood salicylate levels. [2] If a person requires intubation a fast respiratory rate may be required. [1] The toxic effects of salicylates have been described since at least 1877. [5] In 2004 more than 20,000 cases with 43 deaths were reported in the United States. [1] About 1% of those with an acute overdose die while chronic overdoses may have worse outcomes. [3] Old Continue reading >>

Metabolic Acidosis Due To Paracetamol (acetaminophen)

Metabolic Acidosis Due To Paracetamol (acetaminophen)

Summarized from McGregor A, Laight N, Nolan S. Paracetamol and high anion gap metabolic acidosis. J Intensive Care Society 2012; 13: 54-56 Armenian P, Gerona R, Blanc P et al. 5-oxoprolinemia causing elevated anion gap metabolic acidosis in the setting of acetaminophen use. J Emerg Med 2012; 43: 54-57 Metabolic acidosis is a common metabolic disturbance among the acutely/critically ill that has many possible causes. The condition is diagnosed by arterial blood gas analysis which reveals primary reduction in pH and bicarbonate, followed by secondary (compensatory) reduction in pCO2. Abnormal accumulation of endogenous organic acids is one broad mechanism that gives rise to metabolic acidosis, which is differentiated from other mechanisms by being associated with high anion gap. The most common endogenous organic acid metabolic acidosis are: lactic acidosis (accumulation of lactic acid) and ketoacidosis (accumulation of ketoacids). Rarer causes of high anion gap metabolic acidosis due to organic acid accumulation are those that result from ingestion of a toxic substance whose metabolism involves production of an organic acid. For example, the toxicity of ethylene glycol is due in part to its metabolism to oxalic acid and the metabolic acidosis that results from accumulating oxalic acid. In recent years there has been increasing recognition that regular/frequent paracetamol use at recommended dosage is a risk factor for high anion gap metabolic acidosis because it can be associated with accumulation in blood of the organic acid, 5-oxoproline (alternative name pyroglutamic acid). Two recently published papers contain three illustrative case histories. The first paper focuses on two similar case histories including that of a 63-year-old woman with mild chronic kidney disease Continue reading >>

Toxic Alcohol Ingestions: Clinical Features, Diagnosis, And Management

Toxic Alcohol Ingestions: Clinical Features, Diagnosis, And Management

Abstract Alcohol-related intoxications, including methanol, ethylene glycol, diethylene glycol, and propylene glycol, and alcoholic ketoacidosis can present with a high anion gap metabolic acidosis and increased serum osmolal gap, whereas isopropanol intoxication presents with hyperosmolality alone. The effects of these substances, except for isopropanol and possibly alcoholic ketoacidosis, are due to their metabolites, which can cause metabolic acidosis and cellular dysfunction. Accumulation of the alcohols in the blood can cause an increment in the osmolality, and accumulation of their metabolites can cause an increase in the anion gap and a decrease in serum bicarbonate concentration. The presence of both laboratory abnormalities concurrently is an important diagnostic clue, although either can be absent, depending on the time after exposure when blood is sampled. In addition to metabolic acidosis, acute renal failure and neurologic disease can occur in some of the intoxications. Dialysis to remove the unmetabolized alcohol and possibly the organic acid anion can be helpful in treatment of several of the alcohol-related intoxications. Administration of fomepizole or ethanol to inhibit alcohol dehydrogenase, a critical enzyme in metabolism of the alcohols, is beneficial in treatment of ethylene glycol and methanol intoxication and possibly diethylene glycol and propylene glycol intoxication. Given the potentially high morbidity and mortality of these intoxications, it is important for the clinician to have a high degree of suspicion for these disorders in cases of high anion gap metabolic acidosis, acute renal failure, or unexplained neurologic disease so that treatment can be initiated early. Effect of Alcohols on Serum Osmolality and the Osmolal Gap The normal serum Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis is the most common acid–base disorder and can be life threatening. It results from excessive cellular acid production, reduced acid secretion, or loss of body alkali. The body has two buffering mechanisms to counteract an increase in acid. The initial response is to increase carbon dioxide excretion by increasing ventilation. The second response is increased renal excretion of acids and renal regeneration of bicarbonate. The adequacy of compensation can be assessed by the quick check method or the Winter formula (Table 2). Metabolic acidosis can be classified into two categories using the anion gap. Each category has a distinct differential diagnosis. Anion gap = [Sodium] – ([Chloride] + [Bicarbonate]) Normally, the anion gap is approximately 12 ± 2 meq/L (12 ± 2 mmol/L). Most unmeasured anions consist of albumin. Therefore, the presence of either a low albumin level or an unmeasured cationic light chain, which occurs in multiple myeloma, results in a low anion gap. Increased hydrogen ion concentration or decreased bicarbonate concentration will increase the gap. When the primary disturbance is a metabolic acidosis, the anion gap helps to narrow the diagnostic possibilities to an increased anion gap acidosis or a normal anion gap acidosis. Increased Anion Gap Metabolic Acidosis Common causes include ketoacidosis (diabetes mellitus, alcohol abuse, starvation), lactic acidosis, chronic kidney disease, salicylate toxicity, and ethylene glycol and methanol poisoning. Diabetic ketoacidosis is the most common cause of an increased anion gap acidosis, but a normal anion gap acidosis may be present early in the disease course when the extracellular fluid (ECF) volume is nearly normal. Ketoacidosis also may develop in patients with a histor Continue reading >>

Don't Treat The Poison

Don't Treat The Poison

Treat the patient, not the poison. If you remember just one thing about overdoses, that should be it, said Kennon Heard, MD, during a session on toxicology at the Society of Hospital Medicine's annual meeting in April. There are a lot of poisons but really only a few significant symptoms we have to worry about, said Dr. Heard, an associate professor of medicine and emergency medicine and section chief of medical toxicology at the University of Colorado School of Medicine in Denver. Probably the most important advice I've ever gotten is to treat the patient regardless of what [he] took. Kennon Heard, MD. Photo courtesy of the Society of Hospital Medicine. Supportive care is key, he added: If you can keep the patient breathing and his blood pressure stable, he will usually be fine. The symptoms to worry about in the first few hours of a patient's hospital visit are deactivation or activation of the central nervous system (CNS), with the latter manifesting as agitation or seizures; cardiac dysrhythmias; depressed cardiac function; and anion gap acidosis. Deactivation of the CNS is the most common clinical effect of drug overdose and the most common reason people die, Dr. Heard said. And the reason patients die is because they lose their airway, he added. Common deactivating drugs include benzodiazepines, most seizure medications, opioids, muscle relaxants, ethanol, newer antidepressants, clonidine and antipsychotics, he said. Most of these drugs don't cause respiratory depression other than the opioids, so if you can manage the patient's airway, he is going to survive, Dr. Heard said. People die from things like hypoxia: If the airway closes off they hypoventilate, or they aspirate. Intubation is the usual solution to managing the airway, he said. It's best to use a short Continue reading >>

Mala: Metformin-associated Lactic Acidosis

Mala: Metformin-associated Lactic Acidosis

By Charles W. O’Connell, MD Introduction Metformin is a first-line agent for type 2 diabetes mellitus often used as monotherapy or in combination with oral diabetic medications. It is a member of the biguanide class and its main intended effect is expressed by the inhibition of hepatic gluconeogenesis. In addition, metformin increases insulin sensitivity, enhances peripheral glucose utilization and decreases glucose uptake in the gastrointestinal tract. Phenformin, a previously used biguanide, as withdrawn from the market in the 1970’s due its association with numerous cases of lactic acidosis. Metformin is currently used extensively in the management of diabetes and is the most commonly prescribed biguanide worldwide. The therapeutic dosage of metformin ranges from 850 mg to a maximum of 3000 mg daily and is typically divided into twice daily dosing. It is primarily used in the treatment of diabetes but has been used in other conditions associated with insulin resistance such as polycystic ovarian syndrome. MALA is a rare but well reported event that occurs with both therapeutic use and overdose states. Case presentation A 22-year-old female presents to the Emergency Department after being found alongside a suicide note by her family. She was thought to have taken an unknown, but large amount of her husband’s metformin. She arrives at the ED nearly 10 hours after ingestion. She was agitated, but conversant. She reports having nausea and vague feelings of being unwell and is very distraught over the state of her critically ill husband. She has some self-inflicted superficial lacerations over her left anterior forearm. Her vital assigns upon arrival were: T 98.9 degrees Fahrenheit, HR initially 140 bpm which improved to 110 bpm soon after arrival, BP 100/50, RR 22, Continue reading >>

Ethylene Glycol Poisoning: A Rare But Life-threatening Cause Of Metabolic Acidosisa Single-centre Experience

Ethylene Glycol Poisoning: A Rare But Life-threatening Cause Of Metabolic Acidosisa Single-centre Experience

Ethylene glycol poisoning: a rare but life-threatening cause of metabolic acidosisa single-centre experience Department of Internal Medicine, Division of Nephrology, Robert-Bosch Hospital, Stuttgart, Germany Search for other works by this author on: Department of Internal Medicine, Division of Nephrology, Robert-Bosch Hospital, Stuttgart, Germany Search for other works by this author on: Department of Internal Medicine, Division of Nephrology, Robert-Bosch Hospital, Stuttgart, Germany Search for other works by this author on: Department of Internal Medicine, Division of Nephrology, Robert-Bosch Hospital, Stuttgart, Germany Search for other works by this author on: Clinical Kidney Journal, Volume 5, Issue 2, 1 April 2012, Pages 120123, Joerg Latus, Martin Kimmel, Mark Dominik Alscher, Niko Braun; Ethylene glycol poisoning: a rare but life-threatening cause of metabolic acidosisa single-centre experience, Clinical Kidney Journal, Volume 5, Issue 2, 1 April 2012, Pages 120123, Intoxication with ethylene glycol happen all around the world and without rapid recognition and early treatment, mortality from this is high. In our study, we retrospectively analysed six cases of ethylene glycol intoxication in our department. We measured ethylene glycol or glycolate levels, lactate levels and calculated the osmolal and anion gap. Data from six patients admitted to the nephrology department between 1999 and 2011 with ethylene glycol poisoning are reported. All patients were men. The mean pH on admission was 7.15 0.20 and the anion and osmolal gap were elevated in five of six patients. Four patients had an acute kidney injury and one patient had an acute-on-chronic kidney injury. All patients survived and after being discharged, two patients required chronic intermittent haemodialys Continue reading >>

Toxin-induced Metabolic Acidosis

Toxin-induced Metabolic Acidosis

Acid-base disorders, poisoning, toxic, toxins, overdose, metabolic acidosis, acidosis, anion gap metabolic acidosis, strong ion gap acidosis Metabolic acidosis is a common and serious presentation of several toxins. Toxin-induced metabolic acidosis can be due to multiple diverse pathways and can become become evident at various stages and time-frames of the poisoning. These include organic acid production through metabolic pathways, exogenous acid addition, tissue hypoperfusion, renal impairment and cytopathic pathways. These variable pathways and presentations make the diagnosis and treatment challenging, and when a poisoning is suspected, consultation with a regional poison center and toxicologist is hightly recommended. There are numerous toxins that produce acid-base disturbances; however, we will only discuss the most common and serious toxins that result in a metabolic acidosis. The clinical features of metabolic acidosis are similar regardless of the etiology. Depending on the toxin, type and amount of exposure, there may be other specific clinical features. These may include respiratory compensatory signs such as tachypnea and Kussmaul respirations. Hyperventilation (rapid shallow or Kussmaul respirations). Chest pain, cardiac dysrhythmias, palpations. Many poisoned patients are unable to provide a reliable history; therefore, laboratory and other ancillary testing is essential. Some patients will present with classic toxidromes (e.g. opioid, anticholinergic, cholinergic or sympathomimetic), others will have family or friends relay important information regarding recent activity and possible exposure. To adequately assess these patients, it is essential to use a systematic approach, as many different poisons will have subtle overlapping signs and symptoms. Mana Continue reading >>

Metabolic Acidosis Due To Drugs And Toxins

Metabolic Acidosis Due To Drugs And Toxins

3.1.4.7.Metabolic Acidosis due to Drugs and Toxins Metabolic Acidosis due to Drugs and Toxins Several drugs and toxins have been implicated as direct or indirect causes of a high-anion gap metabolic acidosis (HAGMA). A consideration of these drugs needs to be included in an differential diagnosis of a HAGMA. The three most common ones to consider are methanol, ethylene glycol and salicylates. Other toxins which can cause acidosis are isopropyl alcohol and butoxyethanol. Toluene also causes an acidosis and the anion gap may be normal or elevated. * Initially no acid-base disorder due to long latent period while methanol is metabolised * Later, typically develop a high anion gap metabolic acidosis -due to formic acid * May also develop a respiratory acidosis secondary to CNS depression (with depression of respiratory centre and/or airway obstruction) * May occasionally present with normal anion gap acidosis if smaller ingestion * If patient is an alcoholic, there may other types of acidosis present as well (eg alcoholic ketoacidosis, starvation ketoacidosis, lactic acidosis, respiratory acidosis due aspiration, respiratory alkalosis due chronic liver disease.) Principles of Treatment of Methanol Poisoning Resuscitation: Airway, Breathing, Circulation. Obtunded patients require intubation for airway protection and ventilation. Haemodialysis is the most effective technique; it also removes ethanol so ethanol infusion rate must be increased during periods of dialysis This involves competitive inhibition of alcohol dehydrogenase (ADH). The aim is to delay the production of the toxic metabolites and limit the peak concentrations achieved. Two agents are currently in use: * Ethanol: "Ethanol blocking" treatment is the traditional treatment but has the disadvantage of causing i Continue reading >>

Lactic Acidosis

Lactic Acidosis

Lactic acidosis is a medical condition characterized by the buildup of lactate (especially L-lactate) in the body, which results in an excessively low pH in the bloodstream. It is a form of metabolic acidosis, in which excessive acid accumulates due to a problem with the body's metabolism of lactic acid. Lactic acidosis is typically the result of an underlying acute or chronic medical condition, medication, or poisoning. The symptoms are generally attributable to these underlying causes, but may include nausea, vomiting, rapid deep breathing, and generalised weakness. The diagnosis is made on biochemical analysis of blood (often initially on arterial blood gas samples), and once confirmed, generally prompts an investigation to establish the underlying cause to treat the acidosis. In some situations, hemofiltration (purification of the blood) is temporarily required. In rare chronic forms of lactic acidosis caused by mitochondrial disease, a specific diet or dichloroacetate may be used. The prognosis of lactic acidosis depends largely on the underlying cause; in some situations (such as severe infections), it indicates an increased risk of death. Classification[edit] The Cohen-Woods classification categorizes causes of lactic acidosis as:[1] Type A: Decreased tissue oxygenation (e.g., from decreased blood flow) Type B B1: Underlying diseases (sometimes causing type A) B2: Medication or intoxication B3: Inborn error of metabolism Signs and symptoms[edit] Lactic acidosis is commonly found in people who are unwell, such as those with severe heart and/or lung disease, a severe infection with sepsis, the systemic inflammatory response syndrome due to another cause, severe physical trauma, or severe depletion of body fluids.[2] Symptoms in humans include all those of typical m Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. See also separate Lactic Acidosis and Arterial Blood Gases - Indications and Interpretations articles. Description Metabolic acidosis is defined as an arterial blood pH <7.35 with plasma bicarbonate <22 mmol/L. Respiratory compensation occurs normally immediately, unless there is respiratory pathology. Pure metabolic acidosis is a term used to describe when there is not another primary acid-base derangement - ie there is not a mixed acid-base disorder. Compensation may be partial (very early in time course, limited by other acid-base derangements, or the acidosis exceeds the maximum compensation possible) or full. The Winter formula can be helpful here - the formula allows calculation of the expected compensating pCO2: If the measured pCO2 is >expected pCO2 then additional respiratory acidosis may also be present. It is important to remember that metabolic acidosis is not a diagnosis; rather, it is a metabolic derangement that indicates underlying disease(s) as a cause. Determination of the underlying cause is the key to correcting the acidosis and administering appropriate therapy[1]. Epidemiology It is relatively common, particularly among acutely unwell/critical care patients. There are no reliable figures for its overall incidence or prevalence in the population at large. Causes of metabolic acidosis There are many causes. They can be classified according to their pathophysiological origin, as below. The table is not exhaustive but lists those that are most common or clinically important to detect. Increased acid Continue reading >>

Who | Basic Analytical Toxicology

Who | Basic Analytical Toxicology

General laboratory findings in clinical toxicology Marked hypoglycaemia often results from overdosage with insulin, sulfonylureas, such as tolbutamide, or other antidiabetic drugs. Hypoglycaemia may also complicate severe poisoning with a number of agents including iron salts and certain fungi, and may follow ingestion of acetylsalicylic acid, ethanol (especially in children or fasting adults) and paracetamol if liver failure ensues. Hypoglycin is a potent hypoglycaemic agent found in unripe ackee fruit (Blighia sapida) and is responsible for Jamaican vomiting sickness. Hyperglycaemia is a less common complication of poisoning than hypoglycaemia, but has been reported after overdosage with acetylsalicylic acid, salbutamol and theophylline. Coma resulting from overdosage with hypnotic, sedative, neuroleptic or opioid drugs is often characterized by hypoxia and respiratory acidosis. Unless appropriate treatment is instituted, however, a mixed acid-base disturbance with metabolic acidosis will supervene. In contrast, overdosage with salicylates such as acetylsalicylic acid initially causes hyperventilation and respiratory alkalosis, which may progress to the mixed metabolic acidosis and hypokalaemia characteristic of severe poisoning. Hypokalaemia and metabolic acidosis are also features of theophylline and salbutamol overdosage. Hypokalaemia occurs in acute barium poisoning, but severe acute overdosage with digoxin gives rise to hyperkalaemia. Toxic substances or their metabolites, which inhibit key steps in intermediary metabolism, are likely to cause metabolic acidosis owing to the accumulation of organic acids, notably lactate. In severe poisoning of this nature, the onset of metabolic acidosis can be rapid and prompt corrective treatment is vital. Measurement of the Continue reading >>

House On Fire: Inflammation And Toxic Acidosis

House On Fire: Inflammation And Toxic Acidosis

House On Fire: Inflammation and Toxic Acidosis Anti-Aging , Chronic Degenerative Diseases | 0 comments I have created a 3 part course on dealing with chronic pain. Those who have chronic pain, no matter what the cause suffer in silence and the prevailing medical community offers very little in the way of hope or relief. What I have discovered that most cases of chronic pain have two common denominators: Toxic Acidosis and Inflammation. We know from the simplicity of health video post that the body is made up of a myriad of bio-chemical processes. All these chemical reactions take place in only two predominant environments. This is refereed to as either acid or alkaline. Click the blue link text to see that video. For those of you unfamiliar with the term pH which is how we measure the intensity or strength of an acid or alkaline environment in chemistry, I employe you to take the Basic Human Physiology course. It will simplify this not matter what level of education you have. The body always function in a predominantly alkaline chemistry. That is to say the pH of blood (the fountain of life) is 7.365 or rounded off to 7.4 pH. Anything over 7.o is alkaline and below 7.0 is acid. The blood must be alkaline or you will die quickly. The body is nothing more than groups of specialized cells performing specific functions. During this process it must give off metabolic waste products. Just as when we eat food it will go into our mouthes, down the esophagus, into the stomach and intestines. Food is digested, broken down to it can be absorbed and brought to the cells to feed them. When we are through with the digestion of food as it moves throughout the GI tract or intestinal tract it eventually reaches the colon which does some more processing and eventually this material wast Continue reading >>

Salicylate Toxicity: Practice Essentials, Etiology And Pathophysiology, Epidemiology

Salicylate Toxicity: Practice Essentials, Etiology And Pathophysiology, Epidemiology

Salicylates are ubiquitous agents found in hundreds of over-the-counter (OTC) medications and in numerous prescription drugs, making salicylate toxicity an important cause of morbidity and mortality. [ 1 , 2 , 3 , 4 ] Salicylates are used as analgesic agents for the treatment of mild to moderate pain. Aspirin is used as an antipyretic and as an anti-inflammatory agent for the treatment of soft tissue and joint inflammation and vasculitides such as acute rheumatic fever and Kawasaki disease. Aspirin is also used to treat acute coronary syndrome. Low-dose aspirin helps to prevent thrombosis. Acetylsalicylic acid is colorless or white in crystalline, powder, or granular form. The chemical is odorless and is soluble in water. Salicylate is available for ingestion as tablets, capsules, and liquids. Salicylate is also available for topical application, in creams or lotions. Salicylate ingestion continues to be a common cause of poisoning in children and adolescents. The prevalence of aspirin-containing analgesic products makes these agents, found in virtually every household, common sources of unintentional and suicidal ingestion. However, the incidence of salicylate poisoning in children has declined because of reliance on alternative analgesics and the use of child-resistant containers. Repackaging has decreased children's accessibility to lethal amounts, and salicylate's association with Reye syndrome has significantly decreased its use. Still, more than 10,000 tons of aspirin are consumed in the United States each year. Aspirin or aspirin-equivalent preparations (in milligrams) include children's aspirin (80-mg tablets with 36 tablets per bottle), adult aspirin (325-mg tablets), methyl salicylate (eg, oil of wintergreen; 98% salicylate), and Pepto-Bismol (236 mg of non-a Continue reading >>

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