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Metabolic Acidosis Ppt

Toxin-induced Metabolic Acidosis

Toxin-induced Metabolic Acidosis

Acid-base disorders, poisoning, toxic, toxins, overdose, metabolic acidosis, acidosis, anion gap metabolic acidosis, strong ion gap acidosis Metabolic acidosis is a common and serious presentation of several toxins. Toxin-induced metabolic acidosis can be due to multiple diverse pathways and can become become evident at various stages and time-frames of the poisoning. These include organic acid production through metabolic pathways, exogenous acid addition, tissue hypoperfusion, renal impairment and cytopathic pathways. These variable pathways and presentations make the diagnosis and treatment challenging, and when a poisoning is suspected, consultation with a regional poison center and toxicologist is hightly recommended. There are numerous toxins that produce acid-base disturbances; however, we will only discuss the most common and serious toxins that result in a metabolic acidosis. The clinical features of metabolic acidosis are similar regardless of the etiology. Depending on the toxin, type and amount of exposure, there may be other specific clinical features. These may include respiratory compensatory signs such as tachypnea and Kussmaul respirations. Hyperventilation (rapid shallow or Kussmaul respirations). Chest pain, cardiac dysrhythmias, palpations. Many poisoned patients are unable to provide a reliable history; therefore, laboratory and other ancillary testing is essential. Some patients will present with classic toxidromes (e.g. opioid, anticholinergic, cholinergic or sympathomimetic), others will have family or friends relay important information regarding recent activity and possible exposure. To adequately assess these patients, it is essential to use a systematic approach, as many different poisons will have subtle overlapping signs and symptoms. Mana Continue reading >>

Metabolic Acidosis & Metabolic Alkalosis

Metabolic Acidosis & Metabolic Alkalosis

Published by Lambert Morgan Modified over 2 years ago Presentation on theme: "Metabolic acidosis & Metabolic alkalosis" Presentation transcript: 1 Metabolic acidosis & Metabolic alkalosis 3 Primary Change Secondary change Net effect Hco3 Pco2 pH ( H+) Pco2 should by 1.2 mmHg for each mEq plasma Hco3 Inability to excrete dietary acid load Renal failure Renal tubular acidosis type 1 &4 Increased H+ load Lactic acidosis Ketoacidosis Toxin ingestions Increased HCO3 loss diarrhoea 5 Normal anion gap or hyper chloremic acidosis AG = Na+ (Hco3 + Cl ) Normal = 12 4 ( 8 16 ) Measure of unmeasured anion (protiens) Normal anion gap or hyper chloremic acidosis High anion gap 6 Metabolic acidosis Lactic acidosis Ketoacidosis Diarrhoea High anion gap Normal anion gap Lactic acidosis Ketoacidosis Renal failure Toxin ingestions Salicylate Methanol Ethylene glycol Diarrhoea Renal tubular acidosis 7 Clinical features Kussmals respiration (increased depth than rate) Neurologic symptoms: lethargy to coma In severe acidosis (pH< 7.1): Cardiac arrhythmia Reduced cardiac contractility Decreased inotropic response to catecholamines. Chronic acidosis Impaired growth in children Osteomalacia/osteopenia 8 Treatment Treat the underlying cause NaHCO3 therapy: Severe metabolic acidosis (pH<7.1) Chronic acidosis (sodium or potassium citrate) To alkalanise urine in salicylate poisoning 9 NaHCO3 therapy in severe acidosis: pH <7.1 Always treat the pH and not the HCO3 Only one half of bicarbonate deficit to be corrected in initial 12 hrs NaHCO3 dose= desired HCO3 observed HCO3 * 50%of body wt desired HCO3 =12 meq/L in HAG acidosis and meq/L in NAG 10 Example A 24 yr old type 1 diabetic male, weighing aroud 50 Kg presenting with fever, tachypnoea and abd pain to the EMU pH HCO pCo Urine ketones + BP 100 Continue reading >>

Treatment Of Acute Non-anion Gap Metabolic Acidosis

Treatment Of Acute Non-anion Gap Metabolic Acidosis

Go to: Introduction Acute metabolic acidosis (defined temporally as lasting minutes to a few days) has traditionally been divided into two major categories based on the level of the serum anion gap: non-anion gap and high anion gap metabolic acidosis [1]. As implied, with the former acid–base disorder, the anion gap is within normal limits, whereas with the latter disorder it is increased. This categorization is primarily used to facilitate the differential diagnosis of metabolic acidosis. However, it also has relevance for predicting the clinical outcome and determining indications for treatment. Although many clinicians presume that acute metabolic acidosis in seriously ill patients will be due to a high anion gap acidosis, recent studies indicate that a non-anion gap metabolic acidosis or combination of non-anion gap and high anion gap metabolic acidosis might be more frequent [2, 3]. Based on these observations, it appears important to more clearly define the potential effects of non-anion gap metabolic acidoses on organ function as a basis for generating evidence-based guidelines for therapy. In the present review, we summarize our current understanding of the pathophysiology of acute non-anion gap acidosis, its clinical characteristics, its adverse effects on cellular function, and also the benefits and complications of therapy. Go to: Definition In non-anion gap or hyperchloremic metabolic acidosis, a reduction in serum [HCO3−] is matched by an approximately equivalent increase in the serum chloride concentration resulting in hypobicarbonatemia and hyperchloremia in the absence of an increase in the serum anion gap [4, 5]. In fact, since a decrease in blood pH alters the protonation of albumin (which normally makes up the majority of the anion gap), a slight Continue reading >>

Metabolic Acidosis Treatment & Management: Approach Considerations, Type 1 Renal Tubular Acidosis, Type 2 Renal Tubular Acidosis

Metabolic Acidosis Treatment & Management: Approach Considerations, Type 1 Renal Tubular Acidosis, Type 2 Renal Tubular Acidosis

Metabolic AcidosisTreatment & Management Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FASN more... Treatment of acute metabolic acidosis by alkali therapy is usually indicated to raise and maintain the plasma pH to greater than 7.20. In the following two circumstances this is particularly important. When the serum pH is below 7.20, a continued fall in the serum HCO3- level may result in a significant drop in pH. This is especially true when the PCO2 is close to the lower limit of compensation, which in an otherwise healthy young individual is approximately 15 mm Hg. With increasing age and other complicating illnesses, the limit of compensation is likely to be less. A further small drop in HCO3- at this point thus is not matched by a corresponding fall in PaCO2, and rapid decompensation can occur. For example, in a patient with metabolic acidosis with a serum HCO3- level of 9 mEq/L and a maximally compensated PCO2 of 20 mm Hg, a drop in the serum HCO3- level to 7 mEq/L results in a change in pH from 7.28 to 7.16. A second situation in which HCO3- correction should be considered is in well-compensated metabolic acidosis with impending respiratory failure. As metabolic acidosis continues in some patients, the increased ventilatory drive to lower the PaCO2 may not be sustainable because of respiratory muscle fatigue. In this situation, a PaCO2 that starts to rise may change the plasma pH dramatically even without a significant further fall in HCO3-. For example, in a patient with metabolic acidosis with a serum HCO3- level of 15 and a compensated PaCO2 of 27 mm Hg, a rise in PaCO2 to 37 mm Hg results in a change in pH from 7.33 to 7.20. A further rise of the PaCO2 to 43 mm Hg drops the pH to 7.14. All of this would have occurred whi Continue reading >>

Metabolic Acidosis Nursing Management And Interventions - Nurseslabs

Metabolic Acidosis Nursing Management And Interventions - Nurseslabs

Metabolic Acidosisis an acid-base imbalance resulting from excessive absorption or retention of acid or excessive excretion of bicarbonate produced by an underlying pathologic disorder. Symptoms result from the bodys attempts to correct the acidotic condition through compensatory mechanisms in the lungs , kidneys and cells. Metabolic acidosis is characterized by normal or high anion gap situations. If the primary problem is direct loss of bicarbonate, gain of chloride, or decreased ammonia production, the anion gap is within normal limits. If the primary problem is the accumulation of organic anions (such as ketones or lactic acid), the condition is known as high anion gap acidosis. Compensatory mechanisms to correct this imbalance include an increase in respirations to blow off excess CO2, an increase in ammonia formation, and acid excretion (H+) by the kidneys, with retention of bicarbonate and sodium . High anion gap acidosis occurs in diabetic ketoacidosis ; severe malnutrition or starvation, alcoholic lactic acidosis; renal failure; high-fat, low-carbohydrate diets/lipid administration; poisoning, e.g., salicylate intoxication (after initial stage); paraldehyde intoxication; and drug therapy, e.g., acetazolamide (Diamox), NH4Cl. Normal anion gap acidosis is associated with loss of bicarbonate form the body, as may occur in renal tubular acidosis, hyperalimentation, vomiting/ diarrhea , small-bowel/pancreatic fistulas, and ileostomy and use of IV sodium chloride in presence of preexisting kidney dysfunction, acidifying drugs (e.g., ammonium chloride). This condition does not occur in isolation but rather is a complication of a broader problem that may require inpatient care in a medical-surgical or subacute unit. Use of carbonic anhydrase inhibitors or anion-exchan Continue reading >>

Normal Anion Gap Metabolic Acidosis

Normal Anion Gap Metabolic Acidosis

Home | Critical Care Compendium | Normal Anion Gap Metabolic Acidosis Normal Anion Gap Metabolic Acidosis (NAGMA) HCO3 loss and replaced with Cl- -> anion gap normal if hyponatraemia is present the plasma [Cl-] may be normal despite the presence of a normal anion gap acidosis -> this could be considered a ‘relative hyperchloraemia’. Extras – RTA, ingestion of oral acidifying salts, recovery phase of DKA loss of bicarbonate with chloride replacement -> hyperchloraemic acidosis secretions into the large and small bowel are mostly alkaline with a bicarbonate level higher than that in plasma. some typical at risk clinical situations are: external drainage of pancreatic or biliary secretions (eg fistulas) this should be easily established by history normally 85% of filtered bicarbonate is reabsorbed in the proximal tubule and the remaining 15% is reabsorbed in the rest of the tubule in patients receiving acetazolamide (or other carbonic anhydrase inhibitors), proximal reabsorption of bicarbonate is decreased resulting in increased distal delivery and HCO3- appears in urine this results in a hyperchloraemic metabolic acidosis and is essentially a form of proximal renal tubular acidosis but is usually not classified as such. hyperchloraemic metabolic acidosis commonly develops during therapy of diabetic ketoacidosis with normal saline oral administration of CaCl2 or NH4Cl is equivalent to giving an acid load both of these salts are used in acid loading tests for the diagnosis of renal tubular acidosis CaCl2 reacts with bicarbonate in the small bowel resulting in the production of insoluble CaCO3 and H+ the hepatic metabolism of NH4+ to urea results in an equivalent production of H+ REASONS WHY ANION GAP MAY BE NORMAL DESPITE A ‘HIGH ANION GAP METABOLIC ACIDOSIS’ 1. Continue reading >>

Increased Anion Gap Metabolic Acidosis As A Result Of 5-oxoproline (pyroglutamic Acid): A Role For Acetaminophen

Increased Anion Gap Metabolic Acidosis As A Result Of 5-oxoproline (pyroglutamic Acid): A Role For Acetaminophen

Increased Anion Gap Metabolic Acidosis as a Result of 5-Oxoproline (Pyroglutamic Acid): A Role for Acetaminophen *Department of Internal Medicine; Metabolic Disease Center, BRI Baylor University Medical Center, Dallas, Texas Dr. Andrew Z. Fenves, Nephrology Division, Baylor University Medical Center, 3500 Gaston, Dallas, TX 75246. Phone: 214-820-2350; Fax: 214-820-7367; E-mail: fenvesa{at}dneph.com The endogenous organic acid metabolic acidoses that occur commonly in adults include lactic acidosis; ketoacidosis; acidosis that results from the ingestion of toxic substances such as methanol, ethylene glycol, or paraldehyde; and a component of the acidosis of kidney failure. Another rare but underdiagnosed cause of severe, high anion gap metabolic acidosis in adults is that due to accumulation of 5-oxoproline (pyroglutamic acid). Reported are four patients with this syndrome, and reviewed are 18 adult patients who were reported previously in the literature. Twenty-one patients had major exposure to acetaminophen (one only acute exposure). Eighteen (82%) of the 22 patients were women. Most of the patients were malnourished as a result of multiple medical comorbidities, and most had some degree of kidney dysfunction or overt failure. The chronic ingestion of acetaminophen, especially by malnourished women, may generate high anion gap metabolic acidosis. This undoubtedly is an underdiagnosed condition because measurements of serum and/or urinary 5-oxoproline levels are not readily available. The endogenous organic acid metabolic acidoses that occur most frequently in adults are lactic acidosis and ketoacidosis. Other organic acidoses that are encountered in adult patients are those that are caused by the metabolism of toxic substances such as methanol to formaldehyde or ethy Continue reading >>

Metabolic Acidosis Nclex Review Notes

Metabolic Acidosis Nclex Review Notes

Are you studying metabolic acidosis and need to know a mnemonic on how to remember the causes? This article will give you a clever mnemonic and simplify the signs and symptoms and nursing interventions on how to remember metabolic acidosis for nursing lecture exams and NCLEX. In addition, you will learn how to differentiate metabolic acidosis from metabolic alkalosis. Don’t forget to take the metabolic acidosis and metabolic alkalosis quiz. This article will cover: Metabolic acidosis simplified Lab values expected with metabolic acidosis Causes of metabolic acidosis Signs and symptoms of metabolic acidosis Nursing interventions for metabolic acidosis Lecture on Metabolic Acidosis Metabolic Acidosis Metabolic Acidosis in Simple Terms: a metabolic problem due to the buildup of acid in the body fluids which affects the bicarbonate (HCO3 levels) either from: increased acid production (ex: DKA where ketones (acids) increase in the body which decreases bicarbonate) decreased acid excretion (ex: renal failure where there is high amount of waste left in the body which causes the acids to increase and bicarb can’t control imbalance) loss of too much bicarb (diarrhea) When this acidic phenomena is taking place in the body other systems will try to compensate to increase the bicarb back to normal. One system that tries to compensate is the respiratory system. In order to compensate, the respiratory system will cause the body to hyperventilate by increasing breathing through Kussmaul’s respirations. Kussmaul respirations are deep, rapid breathes. The body hopes this will help expel CO2 (an acid) which will “hopefully” increase the pH back to normal. Lab values expected in Metabolic Acidosis: HCO3: decreased <22 Blood pH: decreased <7.35 CO2: <35 or normal (may be normal b Continue reading >>

Acid-base (anesthesia Text)

Acid-base (anesthesia Text)

There are four native buffer systems – bicarbonate, hemoglobin, protein, and phosphate systems. Bicarbonate has a pKa of 6.1, which is not ideal. Hemoglobin has histidine residues with a pKa of 6.8. Chemoreceptors in the carotid bodies, aortic arch, and ventral medulla respond to changes in pH/pCO2 in a matter of minutes. The renal response takes much longer. Arterial vs. Venous Gases Venous blood from the dorsum of the hand is moderately arterialized by general anesthesia, and can be used as a substitute for an ABG. pCO2 will only be off by ~ 5 mm Hg, and pH by 0.03 or 0.04 units [Williamson et. al. Anesth Analg 61: 950, 1982]. Confounding variables include air bubbles, heparin (which is acidic), and leukocytes (aka “leukocyte larceny”). VGB/ABG samples should be cooled to minimize leukocyte activity, however when blood is cooled, CO2 solubility increases (less volatile), and thus pCO2 drops. As an example – a sample taken at 37°C and at 7.4 will actually read as a pH of 7.6 if measured at 25°C. Most VBG/ABGs are actually measured at 37°C. A-aDO2 increases with age, as well as with increased FiO2 and vasodilators (which impair hypoxic pulmonary vasoconstriction). In the setting of a shunt, pulse oximetry can be misleading, thus the A-aDO2 should be calculated. If PaO2 is > 150 mm Hg (i.e., Hg saturation is essentially 100%), every 20 mm Hg of A-aDO2 represents 1% shunting of cardiac output. A/a is even better than A-aDO2 because it is independent of FiO2. PaO2/FiO2 is a reasonable alternative, with hypoxia defined as PaO2/FiO2 < 300 (a PaO2/FiO2 < 200 suggests a shunt fraction of 20% or more). Mixed venous blood should have a pO2 of ~ 40 mm Hg. Values < 30 mm Hg suggest hypoxemia, although one must always keep in mind that peripheral shunting and cyanide tox Continue reading >>

Metabolic Acidosis In The Newborn | Neonatology: Clinical Practice And Procedures | Accesspediatrics | Mcgraw-hill Medical

Metabolic Acidosis In The Newborn | Neonatology: Clinical Practice And Procedures | Accesspediatrics | Mcgraw-hill Medical

Metabolic acidosis in the neonate can be caused by several reasons, including increased acid intake from exogenous sources; increased endogenous production of an acid, such as seen in an inborn error of metabolism (IEM); inadequate excretion of acid by the kidneys; or excessive loss of bicarbonate in urine or stool. Presence or absence of an anion gap (AG) can help to distinguish the underlying etiology. In general, with a pure or uncompensated metabolic acidosis, every 10 mEq/L fall in bicarbonate (HCO3) results in an average pH fall of 0.15. Neonates have an average arterial pH of 7.37 (range of 7.357.45). The average bicarbonate level in a neonate is 20 mEq/L. A diagnosis of metabolic acidosis can be made when the pH is less than 7.35 and a base deficit greater than 5 exists. 1 The AG is calculated by subtracting the serum concentrations of the measured anions (bicarbonate and chloride) from the cation sodium ( Figure 60-1 ). The AG equation can be written as AG = ([Na+]) ([Cl] + [HCO3]). A normal AG is typically less than 12 mEq/L. 1 If the AG is elevated (ie, > 15 mEq/L), then there are anions that have not been accounted for, and an investigation must be performed to search for the culprit. Common anions that result in an elevated AG include lactate and the ketone bodies -hydroxybutyrate and acetoacetate. Neonates with intoxication IEMs usually have elevated AGs from accumulation of the toxic organic acid, such as isovaleric acid in isovaleric acidemia (IVA), in addition to lactate and ketone bodies secondary to clinical decompensation. Anions are molecules that contain a negative charge. Cations are molecules that contain a positive charge. Generally, the total amount of anions and cations in plasma, serum, or urine are equivalent. The anion gap (AG) is the diff Continue reading >>

What Is Metabolic Acidosis?

What Is Metabolic Acidosis?

Metabolic acidosis happens when the chemical balance of acids and bases in your blood gets thrown off. Your body: Is making too much acid Isn't getting rid of enough acid Doesn't have enough base to offset a normal amount of acid When any of these happen, chemical reactions and processes in your body don't work right. Although severe episodes can be life-threatening, sometimes metabolic acidosis is a mild condition. You can treat it, but how depends on what's causing it. Causes of Metabolic Acidosis Different things can set up an acid-base imbalance in your blood. Ketoacidosis. When you have diabetes and don't get enough insulin and get dehydrated, your body burns fat instead of carbs as fuel, and that makes ketones. Lots of ketones in your blood turn it acidic. People who drink a lot of alcohol for a long time and don't eat enough also build up ketones. It can happen when you aren't eating at all, too. Lactic acidosis. The cells in your body make lactic acid when they don't have a lot of oxygen to use. This acid can build up, too. It might happen when you're exercising intensely. Big drops in blood pressure, heart failure, cardiac arrest, and an overwhelming infection can also cause it. Renal tubular acidosis. Healthy kidneys take acids out of your blood and get rid of them in your pee. Kidney diseases as well as some immune system and genetic disorders can damage kidneys so they leave too much acid in your blood. Hyperchloremic acidosis. Severe diarrhea, laxative abuse, and kidney problems can cause lower levels of bicarbonate, the base that helps neutralize acids in blood. Respiratory acidosis also results in blood that's too acidic. But it starts in a different way, when your body has too much carbon dioxide because of a problem with your lungs. Continue reading >>

Metabolic Acidosis: Causes, Symptoms, And Treatment

Metabolic Acidosis: Causes, Symptoms, And Treatment

The Terrible Effects of Acid Acid corrosion is a well-known fact. Acid rain can peel the paint off of a car. Acidifying ocean water bleaches and destroys coral reefs. Acid can burn a giant hole through metal. It can also burn holes, called cavities, into your teeth. I think I've made my point. Acid, regardless of where it's at, is going to hurt. And when your body is full of acid, then it's going to destroy your fragile, soft, internal organs even more quickly than it can destroy your bony teeth and chunks of thick metal. What Is Metabolic Acidosis? The condition that fills your body with proportionately too much acid is known as metabolic acidosis. Metabolic acidosis refers to a physiological state characterized by an increase in the amount of acid produced or ingested by the body, the decreased renal excretion of acid, or bicarbonate loss from the body. Metabolism is a word that refers to a set of biochemical processes within your body that produce energy and sustain life. If these processes go haywire, due to disease, then they can cause an excess production of hydrogen (H+) ions. These ions are acidic, and therefore the level of acidity in your body increases, leading to acidemia, an abnormally low pH of the blood, <7.35. The pH of the blood mimics the overall physiological state in the body. In short, a metabolic process is like a power plant producing energy. If a nuclear power plant goes haywire for any reason, then we know what the consequences will be: uncontrolled and excessive nuclear energetic reactions leading to the leakage of large amounts of radioactive material out into the environment. In our body, this radioactive material is acid (or hydrogen ions). Acidemia can also occur if the kidneys are sick and they do not excrete enough hydrogen ions out of th Continue reading >>

Lactic Acidosis

Lactic Acidosis

Lactic acidosis is a medical condition characterized by the buildup of lactate (especially L-lactate) in the body, which results in an excessively low pH in the bloodstream. It is a form of metabolic acidosis, in which excessive acid accumulates due to a problem with the body's metabolism of lactic acid. Lactic acidosis is typically the result of an underlying acute or chronic medical condition, medication, or poisoning. The symptoms are generally attributable to these underlying causes, but may include nausea, vomiting, rapid deep breathing, and generalised weakness. The diagnosis is made on biochemical analysis of blood (often initially on arterial blood gas samples), and once confirmed, generally prompts an investigation to establish the underlying cause to treat the acidosis. In some situations, hemofiltration (purification of the blood) is temporarily required. In rare chronic forms of lactic acidosis caused by mitochondrial disease, a specific diet or dichloroacetate may be used. The prognosis of lactic acidosis depends largely on the underlying cause; in some situations (such as severe infections), it indicates an increased risk of death. Classification[edit] The Cohen-Woods classification categorizes causes of lactic acidosis as:[1] Type A: Decreased tissue oxygenation (e.g., from decreased blood flow) Type B B1: Underlying diseases (sometimes causing type A) B2: Medication or intoxication B3: Inborn error of metabolism Signs and symptoms[edit] Lactic acidosis is commonly found in people who are unwell, such as those with severe heart and/or lung disease, a severe infection with sepsis, the systemic inflammatory response syndrome due to another cause, severe physical trauma, or severe depletion of body fluids.[2] Symptoms in humans include all those of typical m Continue reading >>

Urine Ammonium, Metabolic Acidosis And Progression Of Chronic Kidney Disease

Urine Ammonium, Metabolic Acidosis And Progression Of Chronic Kidney Disease

Urine Ammonium, Metabolic Acidosis and Progression of Chronic Kidney Disease Pourafshar N.a · Pourafshar S.a · Soleimani M.b,c aDepartment of Medicine at University of Virginia, Charlottesville, VA, USA bDepartment of Medicine, University of Cincinnati, Cincinnati, OH, USA cDepartment of Medicine Services, Veterans Medical Center, Cincinnati, OH, USA The metabolism of a typical Western diet generates 50–100 mEq of acid (H+) per day, which must be excreted in the urine for the systemic acid-base to remain in balance. The 2 major mechanisms that are responsible for the renal elimination of daily acid under normal conditions are ammonium (NH4+) excretion and titratable acidity. In the presence of systemic acidosis, ammonium excretion is intensified and becomes the crucial mechanism for the elimination of acid. The impairment in NH4+ excretion is therefore associated with reduced acid excretion, which causes excess accumulation of acid in the body and consequently results in metabolic acidosis. Chronic kidney disease (CKD) is associated with the impairment in acid excretion and precipitation of metabolic acidosis, which has an adverse effect on the progression of CKD. Recent studies suggest that the progressive decline in renal ammonium excretion in CKD is an important determinant of the ensuing systemic metabolic acidosis and is an independent factor for predicting the worsening of kidney function. While these studies have been primarily performed in hypertensive individuals with CKD, a closer look at renal NH4+ excretion in non-hypertensive individuals with CKD is warranted to ascertain its role in the progression of kidney disease. The elimination of acid (H+) by kidney is the most crucial step in the maintenance of systemic acid-base homeostasis [ 1 , 2 ]. The rena Continue reading >>

Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Management Of Metabolic Acidosis

Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Management Of Metabolic Acidosis

Recommendations for the treatment of acute metabolic acidosis Gunnerson, K. J., Saul, M., He, S. & Kellum, J. Lactate versus non-lactate metabolic acidosis: a retrospective outcome evaluation of critically ill patients. Crit. Care Med. 10, R22-R32 (2006). Eustace, J. A., Astor, B., Muntner, P M., Ikizler, T. A. & Coresh, J. Prevalence of acidosis and inflammation and their association with low serum albumin in chronic kidney disease. Kidney Int. 65, 1031-1040 (2004). Kraut, J. A. & Kurtz, I. Metabolic acidosis of CKD: diagnosis, clinical characteristics, and treatment. Am. J. Kidney Dis. 45, 978-993 (2005). Kalantar-Zadeh, K., Mehrotra, R., Fouque, D. & Kopple, J. D. Metabolic acidosis and malnutrition-inflammation complex syndrome in chronic renal failure. Semin. Dial. 17, 455-465 (2004). Kraut, J. A. & Kurtz, I. Controversies in the treatment of acute metabolic acidosis. NephSAP 5, 1-9 (2006). Cohen, R. M., Feldman, G. M. & Fernandez, P C. The balance of acid base and charge in health and disease. Kidney Int. 52, 287-293 (1997). Rodriguez-Soriano, J. & Vallo, A. Renal tubular acidosis. Pediatr. Nephrol. 4, 268-275 (1990). Wagner, C. A., Devuyst, O., Bourgeois, S. & Mohebbi, N. Regulated acid-base transport in the collecting duct. Pflugers Arch. 458, 137-156 (2009). Boron, W. F. Acid base transport by the renal proximal tubule. J. Am. Soc. Nephrol. 17, 2368-2382 (2006). Igarashi, T., Sekine, T. & Watanabe, H. Molecular basis of proximal renal tubular acidosis. J. Nephrol. 15, S135-S141 (2002). Sly, W. S., Sato, S. & Zhu, X. L. Evaluation of carbonic anhydrase isozymes in disorders involving osteopetrosis and/or renal tubular acidosis. Clin. Biochem. 24, 311-318 (1991). Dinour, D. et al. A novel missense mutation in the sodium bicarbonate cotransporter (NBCe1/ SLC4A4) Continue reading >>

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