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Excess Anion Gap

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121. Alcoholic Ketoacidosis (Overview)

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

2014 eMedicine.com

122. Multisystem Organ Failure of Sepsis (Follow-up)

. Lactic acidosis of septic shock usually causes anion gap metabolic acidosis. Administration of bicarbonate has the potential to worsen intracellular acidosis. Correction of acidemia with sodium bicarbonate has not been proved to improve hemodynamics in critically ill patients with increased blood lactate levels. Nevertheless, bicarbonate therapy has been used in cases where the pH is less than 7.20 or the bicarbonate level is lower than 9 mmol/L, though no data to support this practice exist (...) low-dose dopamine administration in patients who are critically ill. Administering low-dose dopamine does not protect the patient from developing acute renal failure, and there is no evidence that it preserves mesenteric profusion. Consequently, routine use of this practice is not recommended. Aggressively resuscitating patients with septic shock, maintaining adequate perfusion pressure, and avoiding excessive vasoconstriction are effective measures for protecting the kidneys. Phenylephrine

2014 eMedicine.com

123. Metabolic Acidosis (Follow-up)

. This is especially true in certain forms of metabolic acidosis. For example, in high anion gap acidosis secondary to accumulation of organic acids, lactate, and ketones, these anions are eventually metabolized to HCO 3 - . When the underlying disorder is treated, the serum pH corrects; thus, caution should be exercised in these patients when providing alkali to raise the pH much higher than 7.20, because an overshoot alkalosis may occur. To minimize the risk of hypernatremia and hyperosmolality, two 50-mL (...) ampules of 8.4% NaHCO 3 (containing 50 mEq each) are added to 1 L of 0.25 normal saline or three ampules are added to 1 L of 5% dextrose in water. Volume overload can be a consequence of alkali therapy. Loop diuretics can be used in these circumstances. Another consequence of treatment with NaHCO 3 is a rise in PaCO 2 . This can become a very important factor in patients who have reduced ventilatory reserve. In high anion gap acidosis secondary to accumulation of organic acids, lactate, and ketones

2014 eMedicine.com

124. Metabolic Disease &amp (Follow-up)

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

2014 eMedicine.com

125. Metabolic Alkalosis (Follow-up)

):1861-8. . Weise WJ, Serrano FA, Fought J, Gennari FJ. Acute electrolyte and acid-base disorders in patients with ileostomies: a case series. Am J Kidney Dis . 2008 Sep. 52(3):494-500. . Kraut JA, Madias NE. Serum anion gap: its uses and limitations in clinical medicine. Clin J Am Soc Nephrol . 2007 Jan. 2(1):162-74. . . Stewart PA. How to understand acid-base: a quantitative acid-base primer for biology and medicine. [AcidBase.org]. Available at . Accessed: Aug 10, 2009. Kaplan LJ, Cheung NH, Maerz (...) , metabolic alkalosis and hypertension are responsive to dexamethasone. Cushing syndrome Potassium-sparing diuretics should correct the alkalosis until surgical therapy is performed. Definitive therapy includes transsphenoidal microresection of adrenocorticotropic hormone (ACTH)–producing pituitary adenomas and adrenalectomy for adrenal tumors. Syndrome of apparent mineralocorticoid excess Metabolic alkalosis in the syndrome of AME may be treated with potassium-sparing diuretics. On the other hand

2014 eMedicine.com

126. Hypermagnesemia (Follow-up)

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

2014 eMedicine.com

127. Toxicity, Ethylene Glycol (Treatment)

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

128. Critical Care Considerations in Trauma

of thought have merit, and the optimal strategy is a combination of both. Major management techniques used in the ICU are described below. PO 2 of greater than 100 Torr to avoid cerebral tissue hypoxia PCO 2 of 35-40 Torr to avoid cerebral hyperemia or excessive vasoconstriction and induction of cerebral ischemia Maintenance of a neutral cervical spine position to avoid impairment of cerebral venous drainage Avoidance of jugular venous lines on the ipsilateral side of a brain injury Drainage of CSF (...) of hypovolemia from excessive intravascular volume loss. The use of craniectomy is controversial in the management of cerebral edema. Interrogate for intra-abdominal hypertension in the patient with intractably elevated ICP, as there are reports of successful management with abdominal decompression. ICP can be measured by various routes and devices; however, the criterion standard is considered to be a fluid-coupled ventriculostomy catheter inserted into a lateral ventricle (normal ICP < 15 mm Hg). Other

2014 eMedicine Surgery

129. Burns, Thermal

period, glomerular filtration rate and renal blood flow are reduced in proportion to the reduction in intravascular volume. GI dysfunction also appears to be proportional to the magnitude of thermal injury. In patients with burned areas in excess of 25% TBSA, gastroparesis is commonly noted until the third to fifth postburn day. Burn shock may be complicated by an acute erythrocyte hemolysis caused by both direct heat damage and by a decreased half-life of damaged red blood cells (RBCs). In major

2014 eMedicine Surgery

130. Alzheimer Disease in Individuals With Down Syndrome (Follow-up)

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

2014 eMedicine.com

131. Lactic Acidosis (Treatment)

. 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

132. Lactic Acidosis (Follow-up)

. 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

133. 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

2014 eMedicine.com

134. 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

2014 eMedicine.com

135. 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

2014 eMedicine.com

136. 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.com

137. 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

138. 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

139. Chronic Kidney Disease (Follow-up)

), 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

140. 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

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