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Excess Anion Gap

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141. Acidosis, Metabolic (Overview)

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. Alzheimer Disease in Individuals With Down Syndrome (Diagnosis)

development of AD pathology is due to a third copy of the APP gene. Nonetheless, many steps in the amyloid cascade hypothesis remain unproven. The Abeta peptide has been found in the brains of children with DS as young as 8 years, and the deposits increase with age. Interestingly, despite the extensive deposits in the brain, there is no linear correlation with AD. There is a gap between the presence of abnormal brain pathology and the early signs of AD, suggesting that other factors (genetic (...) in the development of neuropathology and dementia in DS. Several genes that might play a role in the development of AD are found in chromosome 21. Among them are the APP and cytoplasmic enzyme superoxide dismutase ( SOD-1 ) genes, both of which are important in the regulation of potential toxic metabolites, the reactive oxygen species (ROSs), which are the result of the normal metabolism of O 2 . These ROSs include free radicals (superoxide anions, nitric oxide, hydroxyl radical) and other non radical


143. Alcoholic Ketoacidosis (Diagnosis)

07, 2018 Author: George Ansstas, MD; Chief Editor: Romesh Khardori, MD, PhD, FACP Share Email Print Feedback Close Sections Sections Alcoholic Ketoacidosis Overview Background In 1940, Dillon and colleagues first described alcoholic ketoacidosis (AKA) as a distinct syndrome. AKA is characterized by metabolic acidosis with an elevated anion gap, elevated serum ketone levels, and a normal or low glucose concentration. [ , ] Although AKA most commonly occurs in adults with alcoholism, it has been (...) ) to nicotinamide adenine dinucleotide (NAD + ) This goal can usually be achieved through the administration of dextrose and saline solutions (see Treatment). Next: Pathophysiology The pathogenesis of AKA is complex. [ ] Although the general physiological factors and mechanisms leading to AKA are understood, the precise factors have not been fully elucidated. The following are the 3 main predisposing events: Delay and decrease in insulin secretion and excess glucagon secretion, induced by starvation and counter


144. 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


145. Hypermagnesemia (Diagnosis)

to the existence of hypermagnesemia would be the disease context (preeclampsia, renal failure), the presence of magnesium-containing preparations, or a decreased anion gap. Previous Next: Prevention and Treatment of Hypermagnesemia Prevention of hypermagnesemia is usually possible. Anticipate hypermagnesemia in patients who are receiving magnesium treatment, especially those with reduced renal function. Initially, withdraw magnesium therapy, which often is enough to correct mild to moderate hypermagnesemia (...) : Tibor Fulop, MD, PhD, FACP, FASN; Chief Editor: Vecihi Batuman, MD, FASN Share Email Print Feedback Close Sections Sections Hypermagnesemia Overview Overview Hypermagnesemia is an uncommon laboratory finding and symptomatic hypermagnesemia is even less common. This disorder has a low incidence of occurrence, because the kidney is able to eliminate excess magnesium by rapidly reducing its tubular reabsorption to almost negligible amounts. In healthy adults, plasma magnesium ranges from 1.7-2.3 mg/dL


146. Hyperchloremic Acidosis (Diagnosis)

A study by Toyonaga and Kikura of 206 patients indicated that hyperchloremic acidosis is a precursor to the development of acute kidney injury (AKI) following abdominal surgery. The study found that a postoperative base excess-chloride level of less than -7 mEq/L was an independent risk factor for AKI and suggested that the AKI risk being can be reduced by decreasing the intraoperative chloride ion load in fluids. [ ] Previous References Kraut JA, Kurtz I. Treatment of acute non-anion gap metabolic (...) by renal insufficiency are characterized by decreased plasma bicarbonate concentration and increased anion gap without hyperchloremia. The initial differentiation of metabolic acidosis should involve a determination of the anion gap (AG). This is usually defined as AG = (Na + ) - [(HCO 3 - + Cl - )], in which Na + is plasma sodium concentration, HCO 3 - is bicarbonate concentration, and Cl - is chloride concentration; all concentrations in this formula are in mmol/L (mM or mEq/L) (see also


147. 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

148. Uremia (Diagnosis)

compensation is accomplished in the lungs. Failure to secrete hydrogen ions and impaired excretion of ammonium may initially contribute to metabolic acidosis. As kidney disease continues to progress, accumulation of phosphate and other organic acids, such as sulfuric acid, hippuric acid, and lactic acid, creates an increased anion-gap metabolic acidosis. In uremia, metabolic acidemia may contribute to other clinical abnormalities, such as hyperventilation, anorexia, stupor, decreased cardiac response (...) a normal potassium load, which can lead to hyperkalemia if dietary intake remains constant. In addition, other metabolic abnormalities, such as acidemia or type IV renal tubular acidosis, may contribute to decreased potassium excretion and lead to hyperkalemia. (Most cases of hyperkalemia are multifactorial in etiology.) Hyperkalemia can occur in several instances, including the following: Excessive potassium intake in patients with a creatinine clearance of less than 20 mL/min Hyporeninemic


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


150. Metabolic Disease &amp (Diagnosis)

Cardioembolic stroke Disorders of carbohydrate metabolism Fabry Disease Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke (MELAS) syndrome Posterior cerebral artery stroke Previous Next: Laboratory and Imaging Studies Laboratory studies Initial laboratory studies may reveal metabolic acidosis with anion gap, hypoglycemia, hyperammonia, and ketonuria. One should eliminate the common causes of ketoacidosis and first. Seizures, diabetes, , liver disease, shock, and anoxic and/or ischemic (...) , was spared. An alternative hypothesis implicates direct basal ganglia damage due to dysfunction of cytochrome-c oxidase. Accumulation of propionic acid apparently results in an abnormal cytochrome-c oxidase. Another competing hypothesis states that hyperammonemia, which is often associated with propionic acidemia, leads to an accumulation of glutamine and/or glutamate in astrocytes. This excess glutamate may be excitotoxic to neuronal cells in the basal ganglia. A mouse model lacking the PCCA gene has


151. Metabolic Alkalosis (Diagnosis)

is almost always caused by metabolic alkalosis. Metabolic alkalosis is diagnosed by measuring serum electrolytes and . If the etiology of metabolic alkalosis is not clear from the clinical history and physical examination, including drug use and the presence of hypertension, then a urine chloride ion concentration can be obtained. Calculation of the serum anion gap may also help to differentiate between primary metabolic alkalosis and metabolic compensation for respiratory acidosis. (See (...) hydroxide or carbonate, the hydroxide anion buffers hydrogen ions in the stomach. The cation binds to bicarbonate secreted by the pancreas, leading to loss of bicarbonate with stools. In this process, both hydrogen ions and bicarbonate are lost, and, usually, no acid-base disturbance occurs. Sometimes, however, not all the bicarbonate binds to the ingested cation, which means that some bicarbonate is reabsorbed in excess of the lost hydrogen ions. This occurs primarily when antacids are administered


152. Metabolic Acidosis (Diagnosis)

cations are Na + and K + , and the major measured urinary anion is Cl - . Urine AG = ([Na + ] + [K + ]) - [Cl - ] The major unmeasured urinary anions and cations are HCO 3 - and NH 4 + , respectively. HCO 3 - excretion in healthy subjects is usually negligible, and average daily excretion of NH 4 + is approximately 40 mEq/L, which results in a positive or near-zero gap. In the face of metabolic acidosis, the kidneys increase the amount of NH 3 synthesized to buffer the excess H + and NH 4 Cl excretion (...) . This bone buffering can lead to significant loss of bone calcium, with resulting osteopenia and osteomalacia. Anion gap Plasma, like any other body fluid compartment, is neutral; total anions match total cations. The major plasma cation is Na + , and major plasma anions are Cl - and HCO 3 - . Extracellular anions present in lower concentrations include phosphate, sulfate, and some organic anions, while other cations present include K + , Mg 2+ , and Ca 2+ . The anion gap (AG) is the difference between


153. Seizures and Epilepsy: Overview and Classification (Diagnosis)

, including those of China, Egypt, and India. An ancient Egyptian papyrus described a seizure in a man who had previous head trauma. Hippocrates wrote the first book about epilepsy almost 2500 years ago. He rejected ideas regarding the divine etiology of epilepsy and concluded that the cause was excessive phlegm leading to abnormal brain consistency. Hippocratic teachings were forgotten, and divine etiologies again dominated beliefs about epileptic seizures during medieval times. Even at the turn (...) of the 19th century, excessive masturbation was considered a cause of epilepsy. This hypothesis is credited as leading to the use of the first effective anticonvulsant (ie, bromides). Modern investigation of the etiology of epilepsy began with the work of Fritsch, Hitzig, Ferrier, and Caton in the 1870s. These researchers recorded and evoked epileptic seizures in the cerebral cortex of animals. In 1929, Berger discovered that electrical brain signals could be recorded from the human head by using scalp


154. Isoniazid Hepatotoxicity (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


155. Lactic Acidosis (Diagnosis)

that cause an elevated anion gap 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 result from numerous conditions. [ ] Severe metabolic acidosis with arterial pH of less than 7.2 is associated with impaired cardiac contractility and suboptimal response to exogenous catecholamines. Elevation of serum lactate concentration may have negative inotropic effects independent of serum pH. Go (...) lactate levels of greater than 2.5 mmol/L have been associated with an increase in mortality rate. Antiretroviral-associated hyperlactemia rarely causes death, but generally, the outcome for patients has been favorable after antiretroviral therapy has been stopped and supportive treatment with vitamins and antioxidants has been initiated. Early diagnosis, vigilance, and routine measurements of the anion gap are crucial. The clinical significance of mild hyperlactatemia greater than 3 mmol/L but less


156. Chronic Renal Failure (Diagnosis)

of acidemia or from lack of insulin. Hypokalemia Hypokalemia is uncommon but can develop in patients with very poor intake of potassium, gastrointestinal or urinary loss of potassium, or diarrhea or in patients who use diuretics. Metabolic acidosis Metabolic acidosis often is a mixture of normal anion gap and increased anion gap; the latter is observed generally with stage 5 CKD but with the anion gap generally not higher than 20 mEq/L. In CKD, the kidneys are unable to produce enough ammonia (...) in the proximal tubules to excrete the endogenous acid into the urine in the form of ammonium. In stage 5 CKD, accumulation of phosphates, sulfates, and other organic anions are the cause of the increase in anion gap. Metabolic acidosis has been shown to have deleterious effects on protein balance, leading to the following: Negative nitrogen balance Increased protein degradation Increased essential amino acid oxidation Reduced albumin synthesis Lack of adaptation to a low-protein diet Hence, metabolic


157. Hyperuricemia (Diagnosis)

. Next: Pathophysiology Uric acid in the blood is saturated at 6.4-6.8 mg/dL at ambient conditions, with the upper limit of solubility placed at 7 mg/dL. Urate is freely filtered at the glomerulus, reabsorbed, secreted, and then again reabsorbed in the proximal tubule. The recent cloning of certain urate transporters will facilitate the understanding of specific mechanisms by which urate is handled in the kidney and small intestines. A urate/anion exchanger (URAT1) has been identified in the brush (...) -border membrane of the kidneys and is inhibited by an angiotensin II receptor blocker, losartan. [ ] A human organic anion transporter (hOAT1) has been found to be inhibited by both uricosuric drugs and antiuricosuric drugs, [ ] while another urate transporter (UAT) has been found to facilitate urate efflux out of the cells. [ ] These transporters may account for the reabsorption, secretion, and reabsorption pattern of renal handling of urate. Urate secretion does appear to correlate with the serum


158. Hyporeninemic Hypoaldosteronism (Diagnosis)

. Acidosis generally is mild, with serum bicarbonate levels in the range of 18-22 mEq/L. The bicarbonate level is useful for guiding therapy (see Treatment). Because unusual accumulation of unmeasured anions (either of endogenous or exogenous origin) does not occur, the anion gap generally is in the reference range (which varies from one laboratory to another). If the patient is presenting for the first time, order a complete workup for the underlying renal disease. Serologic studies for systemic lupus (...) ). Pharmacologic treatments include the following: Diuretics: These are the first-line therapy for patients with signs of volume overload on examination Sodium bicarbonate: This adjunctive agent usually corrects acidosis and, by increasing distal delivery of bicarbonate anion, increases urinary potassium excretion Fludrocortisone: Fludrocortisone is the third-line agent for patients with RTA type IV; it is used as an aldosterone analogue Sodium polystyrene sulfonate: Sodium polystyrene sulfonate is an exchange


159. Hypokalemia (Diagnosis)

of suspicion for the disorder is high: Drug screen in urine and/or serum for diuretics, amphetamines, and other sympathomimetic stimulants Serum renin, aldosterone, and cortisol 24-hour urine aldosterone, cortisol, sodium, and potassium Pituitary imaging to evaluate for Cushing syndrome Adrenal imaging to evaluate for adenoma Evaluation for Enzyme assays for 17-beta hydroxylase deficiency Thyroid function studies in patients with tachycardia, especially Asians [ ] Serum anion gap (eg, to detect toluene (...) magnesium assay, and an electrocardiogram (ECG). Measurement of urine potassium is of vital importance because it establishes the pathophysiologic mechanism and, thus, is used in formulating the differential diagnosis. This, in turn, will guide the choice of further tests. If the urine potassium level is less than 20 mEq/L, consider the following: Diarrhea and use of laxatives Diet or total parenteral nutrition (TPN) contents The use of insulin, excessive bicarbonate supplements, and episodic weakness


160. Chronic Kidney Disease (Treatment)

), eventually leading to a progressive metabolic acidosis. In children, overt acidosis is characteristically present when the estimated glomerular filtration rate (eGFR) is less than 30 mL/min per 1.73 m 2 (stage IV). The acidosis in chronic kidney disease in children can be associated with an increased or normal anion gap. Guidelines recommend maintaining a serum bicarbonate level of 22 mmol/L. If necessary, the authors recommend supplementation with sodium bicarbonate, started at 1-2 mEq/kg/d in 2-3 (...) for the growth disruption, height age should be the basis for energy estimation. Supplementation can be used as per requirement (enteral or parenteral nutrition as needed). Protein Protein is required to maintain positive nitrogen balance for growth and maintain body protein turn over. The protein intake must be carefully controlled, avoiding protein malnutrition from an excessively restricted diet while avoiding toxicity from nitrogenous waste products from an excessively generous diet. The diet should

2014 eMedicine Pediatrics

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