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Excess Anion Gap

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141. Acidosis, Metabolic (Diagnosis)

Ethanol, ethylene glycol Salicylates A normal anion gap metabolic acidosis occurs when loss of bicarbonate from the GI tract or kidneys is excessive or when hydrogen ions cannot be secreted because of renal failure. The causes can be represented by the mnemonic USEDCARP: Ureterostomy Small bowel fistula Extra chloride Diarrhea Carbonic anhydrase inhibitors (eg, acetazolamide) Adrenal insufficiency (RTA) Pancreatic fistula Infants are more likely to develop a normal anion gap metabolic acidosis (...) an increased acid load generally begins 12-24 hours after the compensatory hyperventilation begins and continues for 1-3 days. Over time, the kidneys attempt to increase reabsorption of HCO 3 - to compensate for the acidosis. The severity of the acidosis depends on the rapidity of bicarbonate loss and the ability of the kidney to replenish bicarbonate. Anion gap To achieve electrochemical balance, ionic elements in the extracellular fluid must equal a net charge of zero. Therefore, the number of negatively

2014 eMedicine Pediatrics

142. Alcoholic Ketoacidosis (Diagnosis)

> Emergent Treatment of Alcoholic Ketoacidosis Updated: Nov 02, 2016 Author: Adam Blumenberg, MD, MA; Chief Editor: Erik D Schraga, MD Share Email Print Feedback Close Sections Sections Emergent Treatment of Alcoholic Ketoacidosis Overview Overview Alcoholic ketoacidosis (AKA) is an acute seen in persons with a recent history of binge drinking and little or no nutritional intake. is characterized by high serum ketone levels and an elevated anion gap (see the calculator). A concomitant is also common (...) . [ ] If the patient's mental status is diminished, consider administration of and . Note information about the patient's social situation and the presence of intoxicating agents besides alcohol. Previous Next: Emergency Department Care Diagnostic Considerations Suspect alcoholic ketoacidosis in any patient with recent binge drinking and an elevated anion gap. A history of alcoholism is not necessary for the development of alcoholic ketoacidosis. One episode of heavy alcohol intake combined with inadequate

2014 eMedicine Emergency Medicine

143. Lactic Acidosis (Diagnosis)

. Chronically, renal compensation occurs by means of reabsorption of HCO 3 . [ , ] Acidosis arises from an increased production of acids, a loss of alkali, or a decreased renal excretion of acids. The underlying etiology of metabolic acidosis is classically categorized into those that cause an elevated anion gap (AG) (see the calculator) and those that do not. Lactic acidosis, identified by a state of acidosis and an elevated plasma lactate concentration is one type of anion gap metabolic acidosis and may (...) assists ongoing medical management. When findings of systemic hypoperfusion are not present, consider possible toxin-induced or bowel-associated impairment of cellular metabolism causing a lactic acidosis, such as biguanide therapy (metformin), malignancy (lymphoma, leukemia, solid malignancies), alcoholism, HIV medications (reverse transcriptase inhibitors), or short gut (malabsorptive) syndromes. A study by Xu et al indicated that in the emergency department, anion gap screening is a poor modality

2014 eMedicine Emergency Medicine

144. Metabolic Acidosis (Diagnosis)

an appropriate respiratory response for a metabolic acidosis has been established, the workup for the presence of unmeasured anions can progress by using the traditional anion gap, the delta-delta approach, or the strong ion gap. This allows the differential of metabolic acidosis to be narrowed and the appropriate therapy applied. To differentiate between the causes of metabolic acidosis, one traditionally calculates the anion gap (AG), corresponding the presence of unmeasured anions. [ ] AG = (Na + ) - ([Cl (...) - ] + [HCO 3 - ]) The anion gap allows for the differentiation of 2 groups of metabolic acidosis. Metabolic acidosis with a high AG is associated with the addition of endogenously or exogenously generated acids. Metabolic acidosis with a normal AG is associated with the loss of HCO 3 from the kidney or GI tract, or the failure of the kidney to excrete H + . The delta/delta concept allows for the partitioning of metabolic acidosis into an anion gap and a non-anion gap component, which can occur

2014 eMedicine Emergency Medicine

145. Diabetic Ketoacidosis (Diagnosis)

, another consequence of insulin resistance/insulin deficiency. The excess acetyl coenzyme A is therefore rerouted to ketogenesis. Progressive rise of blood concentration of these acidic organic substances initially leads to a state of ketonemia, although extracellular and intracellular body buffers can limit ketonemia in its early stages, as reflected by a normal arterial pH associated with a base deficit and a mild anion gap. When the accumulated ketones exceed the body's capacity to extract them (...) mEq/L or less (less than 5 mEq/L is indicative of severe DKA). These biochemical changes are frequently associated with increased anion gap, increased serum osmolarity and increased serum uric acid. (See Clinical Presentation.) Herrington et al collected simultaneous arterial and venous samples from 206 critically ill patients and analyzed in duplicate. [ ] They calculated coefficients of variation and 95% limits of agreement for arterial and venous samples and constructed statistical plots

2014 eMedicine Emergency Medicine

146. Tumor Lysis Syndrome (Overview)

and a high anion gap acidosis (see the calculator). Acidemic states can worsen the many electrolyte imbalances already present in tumor lysis syndrome; intracellular uptake of potassium is hindered, uric acid solubility is decreased, and extracellular shift of phosphate is promoted. Calcium phosphate solubility, however, improves in acidic conditions. The myriad of metabolic disorders must be assessed and treated rapidly. Proper fluid management, alkalinization of the urine, correction of acidosis (...) and hypocalcemia, predispose patients to cardiac arrhythmia and seizures. Iatrogenic complications, such as pulmonary edema from overly vigorous hydration or metabolic alkalosis from excess exogenous administration of bicarbonate, can also occur and are life threatening if not immediately addressed. Acute kidney injury Renal tubule precipitation of uric acid, calcium phosphate, or hypoxanthine causes acute kidney injury. This is often oliguric (< 400 mL daily) in nature, leading to volume overload

2014 eMedicine Pediatrics

147. Toxicity, Iron (Overview)

cardiac output, and increased pulmonary vascular resistance. The decrease in cardiac output may be related to a decrease in myocardial contractility exacerbated by the acidosis and hypovolemia. Free radicals from the iron absorption may induce damage and play a role in the impaired cardiac function. The systemic iron poisoning in phase 3 is associated with a positive anion gap metabolic acidosis. The following explanations for the acidosis have been proposed: Conversion of free plasma iron to ferric (...) mucosa and can affect the heart, lungs, and liver. Excess free iron is a mitochondrial toxin that leads to derangements in energy metabolism. Although iron poisoning is a clinical diagnosis, serum iron levels are useful in predicting the clinical course of the patient. In treatment of iron poisoning, consider both bowel decontamination with whole bowel irrigation and chelation using intravenous deferoxamine. In addition, chronic iron overload may develop in pediatric cancer patients who receive

2014 eMedicine Pediatrics

148. Toxicity, Isoniazid (Overview)

toxicity Acute INH overdose predominantly involves the brain and may cause prolonged seizures, anion gap metabolic acidosis, and coma. Note the following: Patients who are affected may present with active tonic-clonic seizures and thus may be unable to give a history of INH use; this often makes rapid identification of acute INH toxicity difficult without third-party input. The amount ingested is also often difficult to ascertain, making accurate antidote (pyridoxine) dosing challenging. Clinical (...) in the central nervous system (CNS), as well as a relative increase in the amounts of glutamate, the primary excitatory neurotransmitter. INH metabolites directly inhibit pyridoxine phosphokinase. This enzyme converts pyridoxine (vitamin B-6) to its active form, pyridoxal-5'-phosphate, a key cofactor in the production of GABA. This functional depletion of pyridoxine causes a disruption of glutamate and GABA homeostasis and leads to an excessive excitatory milieu in the brain. Chronic toxicity Chronic INH

2014 eMedicine Pediatrics

149. Tumor Lysis Syndrome (Diagnosis)

and a high anion gap acidosis (see the calculator). Acidemic states can worsen the many electrolyte imbalances already present in tumor lysis syndrome; intracellular uptake of potassium is hindered, uric acid solubility is decreased, and extracellular shift of phosphate is promoted. Calcium phosphate solubility, however, improves in acidic conditions. The myriad of metabolic disorders must be assessed and treated rapidly. Proper fluid management, alkalinization of the urine, correction of acidosis (...) and hypocalcemia, predispose patients to cardiac arrhythmia and seizures. Iatrogenic complications, such as pulmonary edema from overly vigorous hydration or metabolic alkalosis from excess exogenous administration of bicarbonate, can also occur and are life threatening if not immediately addressed. Acute kidney injury Renal tubule precipitation of uric acid, calcium phosphate, or hypoxanthine causes acute kidney injury. This is often oliguric (< 400 mL daily) in nature, leading to volume overload

2014 eMedicine Pediatrics

150. Toxicity, Iron (Diagnosis)

cardiac output, and increased pulmonary vascular resistance. The decrease in cardiac output may be related to a decrease in myocardial contractility exacerbated by the acidosis and hypovolemia. Free radicals from the iron absorption may induce damage and play a role in the impaired cardiac function. The systemic iron poisoning in phase 3 is associated with a positive anion gap metabolic acidosis. The following explanations for the acidosis have been proposed: Conversion of free plasma iron to ferric (...) mucosa and can affect the heart, lungs, and liver. Excess free iron is a mitochondrial toxin that leads to derangements in energy metabolism. Although iron poisoning is a clinical diagnosis, serum iron levels are useful in predicting the clinical course of the patient. In treatment of iron poisoning, consider both bowel decontamination with whole bowel irrigation and chelation using intravenous deferoxamine. In addition, chronic iron overload may develop in pediatric cancer patients who receive

2014 eMedicine Pediatrics

151. Toxicity, Isoniazid (Diagnosis)

toxicity Acute INH overdose predominantly involves the brain and may cause prolonged seizures, anion gap metabolic acidosis, and coma. Note the following: Patients who are affected may present with active tonic-clonic seizures and thus may be unable to give a history of INH use; this often makes rapid identification of acute INH toxicity difficult without third-party input. The amount ingested is also often difficult to ascertain, making accurate antidote (pyridoxine) dosing challenging. Clinical (...) in the central nervous system (CNS), as well as a relative increase in the amounts of glutamate, the primary excitatory neurotransmitter. INH metabolites directly inhibit pyridoxine phosphokinase. This enzyme converts pyridoxine (vitamin B-6) to its active form, pyridoxal-5'-phosphate, a key cofactor in the production of GABA. This functional depletion of pyridoxine causes a disruption of glutamate and GABA homeostasis and leads to an excessive excitatory milieu in the brain. Chronic toxicity Chronic INH

2014 eMedicine Pediatrics

152. Glycogen-Storage Disease Type I (Overview)

the substrate for glycolysis and produces lactate. Lactate exits the hepatocyte, causing clinically significant lactic acidemia in proportion to the degree of stimulus for glycogen breakdown. The accumulation of lactic acid in blood can cause true acidosis with a large anion gap, a characteristic of glycogen-storage disease type I. The immense increase in the intracellular phosphorylated intermediate compounds of glycolysis concurrently inhibits rephosphorylation of adenine nucleotides, activating (...) =aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvOTQ5OTM3LW92ZXJ2aWV3 processing > Genetics of von Gierke Disease (Glycogen-Storage Disease Type 1) Updated: Aug 10, 2017 Author: Karl S Roth, MD; Chief Editor: Maria Descartes, MD Share Email Print Feedback Close Sections Sections Genetics of von Gierke Disease (Glycogen-Storage Disease Type 1) Overview Background In 1929, von Gierke provided the initial description of glycogen-storage disease type I (GSD I) from autopsy reports of 2 children whose large livers contained excessive glycogen. He also reported

2014 eMedicine Pediatrics

153. Glycogen-Storage Disease Type I (Diagnosis)

the substrate for glycolysis and produces lactate. Lactate exits the hepatocyte, causing clinically significant lactic acidemia in proportion to the degree of stimulus for glycogen breakdown. The accumulation of lactic acid in blood can cause true acidosis with a large anion gap, a characteristic of glycogen-storage disease type I. The immense increase in the intracellular phosphorylated intermediate compounds of glycolysis concurrently inhibits rephosphorylation of adenine nucleotides, activating (...) =aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvOTQ5OTM3LW92ZXJ2aWV3 processing > Genetics of von Gierke Disease (Glycogen-Storage Disease Type 1) Updated: Aug 10, 2017 Author: Karl S Roth, MD; Chief Editor: Maria Descartes, MD Share Email Print Feedback Close Sections Sections Genetics of von Gierke Disease (Glycogen-Storage Disease Type 1) Overview Background In 1929, von Gierke provided the initial description of glycogen-storage disease type I (GSD I) from autopsy reports of 2 children whose large livers contained excessive glycogen. He also reported

2014 eMedicine Pediatrics

154. Toxicity, Isoniazid (Diagnosis)

toxicity Acute INH overdose predominantly involves the brain and may cause prolonged seizures, anion gap metabolic acidosis, and coma. Note the following: Patients who are affected may present with active tonic-clonic seizures and thus may be unable to give a history of INH use; this often makes rapid identification of acute INH toxicity difficult without third-party input. The amount ingested is also often difficult to ascertain, making accurate antidote (pyridoxine) dosing challenging. Clinical (...) in the central nervous system (CNS), as well as a relative increase in the amounts of glutamate, the primary excitatory neurotransmitter. INH metabolites directly inhibit pyridoxine phosphokinase. This enzyme converts pyridoxine (vitamin B-6) to its active form, pyridoxal-5'-phosphate, a key cofactor in the production of GABA. This functional depletion of pyridoxine causes a disruption of glutamate and GABA homeostasis and leads to an excessive excitatory milieu in the brain. Chronic toxicity Chronic INH

2014 eMedicine Emergency Medicine

155. Toxicity, Ethylene Glycol (Follow-up)

Med . 2005 Feb. 31(2):189-95. . Sabeel AI, Kurkus J, Lindholm T. Intensified dialysis treatment of ethylene glycol intoxication. Scand J Urol Nephrol . 1995 Jun. 29(2):125-9. . Soghoian S, Sinert R, Wiener SW, Hoffman RS. Ethylene glycol toxicity presenting with non-anion gap metabolic acidosis. Basic Clin Pharmacol Toxicol . 2009 Jan. 104 (1):22-6. . . Media Gallery Oxalate crystals. Courtesy of John D Schaldenbrand, MD, Department of Pathology, St Joseph Mercy Health System, Ann Arbor, MI (...) the bottle or container that held the ingested substance. Interviewing persons present at the site of the ingestion may be helpful in this regard. Obtain intravenous access and administer crystalloid infusions. Monitor cardiac function and determine blood dextrose level. Airway management is a priority because of the risk of aspiration. Previous Next: Emergency Department Care Rapidly evaluate patients who present with signs, symptoms, or history of toxic alcohol ingestion; determine serum osmolal gap

2014 eMedicine Emergency Medicine

156. Toxicity, Isoniazid (Overview)

toxicity Acute INH overdose predominantly involves the brain and may cause prolonged seizures, anion gap metabolic acidosis, and coma. Note the following: Patients who are affected may present with active tonic-clonic seizures and thus may be unable to give a history of INH use; this often makes rapid identification of acute INH toxicity difficult without third-party input. The amount ingested is also often difficult to ascertain, making accurate antidote (pyridoxine) dosing challenging. Clinical (...) in the central nervous system (CNS), as well as a relative increase in the amounts of glutamate, the primary excitatory neurotransmitter. INH metabolites directly inhibit pyridoxine phosphokinase. This enzyme converts pyridoxine (vitamin B-6) to its active form, pyridoxal-5'-phosphate, a key cofactor in the production of GABA. This functional depletion of pyridoxine causes a disruption of glutamate and GABA homeostasis and leads to an excessive excitatory milieu in the brain. Chronic toxicity Chronic INH

2014 eMedicine Emergency Medicine

157. Lactic Acidosis (Overview)

. Chronically, renal compensation occurs by means of reabsorption of HCO 3 . [ , ] Acidosis arises from an increased production of acids, a loss of alkali, or a decreased renal excretion of acids. The underlying etiology of metabolic acidosis is classically categorized into those that cause an elevated anion gap (AG) (see the calculator) and those that do not. Lactic acidosis, identified by a state of acidosis and an elevated plasma lactate concentration is one type of anion gap metabolic acidosis and may (...) assists ongoing medical management. When findings of systemic hypoperfusion are not present, consider possible toxin-induced or bowel-associated impairment of cellular metabolism causing a lactic acidosis, such as biguanide therapy (metformin), malignancy (lymphoma, leukemia, solid malignancies), alcoholism, HIV medications (reverse transcriptase inhibitors), or short gut (malabsorptive) syndromes. A study by Xu et al indicated that in the emergency department, anion gap screening is a poor modality

2014 eMedicine Emergency Medicine

158. Metabolic Acidosis (Overview)

an appropriate respiratory response for a metabolic acidosis has been established, the workup for the presence of unmeasured anions can progress by using the traditional anion gap, the delta-delta approach, or the strong ion gap. This allows the differential of metabolic acidosis to be narrowed and the appropriate therapy applied. To differentiate between the causes of metabolic acidosis, one traditionally calculates the anion gap (AG), corresponding the presence of unmeasured anions. [ ] AG = (Na + ) - ([Cl (...) - ] + [HCO 3 - ]) The anion gap allows for the differentiation of 2 groups of metabolic acidosis. Metabolic acidosis with a high AG is associated with the addition of endogenously or exogenously generated acids. Metabolic acidosis with a normal AG is associated with the loss of HCO 3 from the kidney or GI tract, or the failure of the kidney to excrete H + . The delta/delta concept allows for the partitioning of metabolic acidosis into an anion gap and a non-anion gap component, which can occur

2014 eMedicine Emergency Medicine

159. Alcoholic Ketoacidosis (Overview)

> Emergent Treatment of Alcoholic Ketoacidosis Updated: Nov 02, 2016 Author: Adam Blumenberg, MD, MA; Chief Editor: Erik D Schraga, MD Share Email Print Feedback Close Sections Sections Emergent Treatment of Alcoholic Ketoacidosis Overview Overview Alcoholic ketoacidosis (AKA) is an acute seen in persons with a recent history of binge drinking and little or no nutritional intake. is characterized by high serum ketone levels and an elevated anion gap (see the calculator). A concomitant is also common (...) . [ ] If the patient's mental status is diminished, consider administration of and . Note information about the patient's social situation and the presence of intoxicating agents besides alcohol. Previous Next: Emergency Department Care Diagnostic Considerations Suspect alcoholic ketoacidosis in any patient with recent binge drinking and an elevated anion gap. A history of alcoholism is not necessary for the development of alcoholic ketoacidosis. One episode of heavy alcohol intake combined with inadequate

2014 eMedicine Emergency Medicine

160. Diabetic Ketoacidosis (Overview)

, another consequence of insulin resistance/insulin deficiency. The excess acetyl coenzyme A is therefore rerouted to ketogenesis. Progressive rise of blood concentration of these acidic organic substances initially leads to a state of ketonemia, although extracellular and intracellular body buffers can limit ketonemia in its early stages, as reflected by a normal arterial pH associated with a base deficit and a mild anion gap. When the accumulated ketones exceed the body's capacity to extract them (...) mEq/L or less (less than 5 mEq/L is indicative of severe DKA). These biochemical changes are frequently associated with increased anion gap, increased serum osmolarity and increased serum uric acid. (See Clinical Presentation.) Herrington et al collected simultaneous arterial and venous samples from 206 critically ill patients and analyzed in duplicate. [ ] They calculated coefficients of variation and 95% limits of agreement for arterial and venous samples and constructed statistical plots

2014 eMedicine Emergency Medicine

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