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Excess Anion Gap

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81. Citrate metabolism in blood transfusions and its relationship due to metabolic alkalosis and respiratory acidosis Full Text available with Trip Pro

Citrate metabolism in blood transfusions and its relationship due to metabolic alkalosis and respiratory acidosis Metabolic alkalosis commonly results from excessive hydrochloric acid (HCl), potassium (K(+)) and water (H2O) loss from the stomach or through the urine. The plasma anion gap increases in non-hypoproteinemic metabolic alkalosis due to an increased negative charge equivalent on albumin and the free ionized calcium (Ca(++)) content of plasma decreases. The mean citrate load in all

2015 International journal of clinical and experimental medicine

82. Renal Tubular Acidosis is Highly Prevalent in Critically Ill Patients

subset calculation based on a physical-chemical approach on the first seven days after ICU admission was used to compare the effects of free water, chloride, albumin, and unmeasured anions on the standard base excess. Calculation of the urine osmolal gap (UOG) − as an approximate measure of the unmeasured urine cation ammonium − served as determinate between renal and extra-renal bicarbonate loss in the state of hyperchloremic acidosis. Study Design Go to Layout table for study information Study Type (...) of RTA has never been studied in critically ill patients. Therefore, we aimed to investigate the prevalence, type, and possible risk factors of RTA in critically ill patients using a physical-chemical approach. This prospective, observational trial was conducted in a medical ICU of a university hospital. 100 consecutive critically ill patients at the age ≥18, expected to stay in the ICU for ≥24h, with the clinical necessity for a urinary catheter and the absence of anuria were included. Base excess

2015 Clinical Trials

83. Evaluation of the efficacy of simplified Fencl-Stewart equation in analyzing the changes in acid base status following resuscitation with two different fluids. Full Text available with Trip Pro

Evaluation of the efficacy of simplified Fencl-Stewart equation in analyzing the changes in acid base status following resuscitation with two different fluids. Metabolic acid-base disorders in critically ill patients may not be identified by base excess (BE) approach. Anion gap method can detect approximately 1/3 hidden "gap acidosis". In such conditions, when adjusted for hypoalbuminemia, Fencl-Stewart's approach can reliably detect the hidden abnormal anions.Evaluate the efficacy (...) effect on BE significantly increased in both the groups. Unmeasured ion effect on BE did not significantly change in both the groups. Measured standard BE level was significantly less as compared to unmeasured anion effect on BE, in both the groups.Simplified Fencl-Stewart equation is effective in identifying a mixed acid-base disorder, which otherwise would remain undetected.

2014 International journal of critical illness and injury science Controlled trial quality: uncertain

84. Effects of a dexmedetomidine constant rate infusion and atropine on changes in global perfusion variables induced by hemorrhage followed by volume replacement in isoflurane-anesthetized dogs. (Abstract)

VR than they did when anesthetized with isoflurane alone. Plasma lactate concentration, mixed venous-to-arterial carbon dioxide difference, base excess, and anion gap were unaltered by hemorrhage and VR and did not differ between anesthetic sessions.Results indicated that the use of a dexmedetomidine CRI combined with atropine in isoflurane-anesthetized dogs that underwent volume-controlled hemorrhage followed by VR did not compromise global perfusion sufficiently to result in anaerobic

2014 American journal of veterinary research Controlled trial quality: uncertain

85. Evaluation of acid-base status in patients admitted to ED-physicochemical vs traditional approaches. (Abstract)

measured and used to derive [HCO3(-)], BE, anion gap (AG), AG adjusted for albumin (AGadj), strong ion difference, strong ion gap (SIG) and SIG corrected for water excess/deficit (SIGcor). In each patient the acid-base status was evaluated using the BE, [HCO3(-)], and physicochemical approaches.A total of 365 patients were studied. Compared with BE (n = 202) and [HCO3(-)] (n = 151), physicochemical approach (n = 279) identified significantly more patients with metabolic acid-base disturbances (P (...) Evaluation of acid-base status in patients admitted to ED-physicochemical vs traditional approaches. The aim of this study is to evaluate the value of physicochemical, base excess (BE), and plasma bicarbonate concentration ([HCO3(-)]) approaches on the assessment of acid-base status in patients presented to the emergency department (ED).Upon presentation at ED, patients whose arterial blood was deemed in need of analysis were studied. Arterial blood gases, serum electrolytes, and proteins were

2014 American Journal of Emergency Medicine

86. Hyporeninemic Hypoaldosteronism (Overview)

. 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


87. Lactic Acidosis (Overview)

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


88. Hyperuricemia (Overview)

. 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


89. Hypermagnesemia (Overview)

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


90. Hypokalemia (Overview)

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


91. Isoniazid Hepatotoxicity (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


92. Metabolic Disease &amp (Overview)

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


93. Metabolic Alkalosis (Overview)

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


94. Metabolic Acidosis (Overview)

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


95. Hyperchloremic Acidosis (Overview)

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 (...) 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 the calculator). The AG


96. Azotemia (Treatment)

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


97. 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


98. 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

99. 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

100. 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

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