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Excess Anion Gap

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121. 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

122. Hypermagnesemia (Treatment)

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

123. Chronic Renal Failure (Overview)

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

124. Alzheimer Disease in Individuals With Down Syndrome (Overview)

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

125. 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

126. 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

127. 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

128. 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

129. 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

130. Uremia (Overview)

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

2014 eMedicine.com

131. Seizures and Epilepsy: Overview and Classification (Overview)

, 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

2014 eMedicine.com

132. 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.com

133. Azotemia (Follow-up)

of decrease in serum sodium should be no more than 0.7 mEq/h (17 mEq/24 h). Volume depletion due to blood loss requires IV saline and transfusion to maintain pressure (as well as interventions to halt further loss). Diarrhea often causes isotonic volume loss that necessitates replacement with normal saline. Normal–anion gap metabolic acidosis occurring with diarrhea warrants infusion of bicarbonate in 0.5% normal saline. Diuretic-induced volume depletion, especially in the elderly, manifests (...) of nephrotoxicity. In both scenarios, early initiation of renal replacement therapy if azotemia sets in has a better prognosis than late initiation. Albumin can be administered in combination with high-dose furosemide to enhance the diuretic effect of furosemide. The use of albumin in this context is not for volume expansion; rather, it allows more furosemide to be bound to albumin for delivery to the organic anion transporter in the kidney, thereby enabling more furosemide to enter the tubule than would

2014 eMedicine.com

134. 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

135. 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

136. Multisystem Organ Failure of Sepsis (Treatment)

. 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

137. Alzheimer Disease in Individuals With Down Syndrome (Treatment)

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

138. Metabolic Disease &amp (Treatment)

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

139. Metabolic Alkalosis (Treatment)

):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

140. Metabolic Acidosis (Treatment)

. 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

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