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Hyperchloremic Metabolic Acidosis Treatment

Treatment Of Acute Non-anion Gap Metabolic Acidosis

Treatment Of Acute Non-anion Gap Metabolic Acidosis

Treatment of acute non-anion gap metabolic acidosis Medical and Research Services VHAGLA Healthcare System, Division of Nephrology, VHAGLA Healthcare System Correspondence to: Jeffrey A. Kraut; E-mail: [email protected] Search for other works by this author on: Clinical Kidney Journal, Volume 8, Issue 1, 1 February 2015, Pages 9399, Jeffrey A. Kraut, Ira Kurtz; Treatment of acute non-anion gap metabolic acidosis, Clinical Kidney Journal, Volume 8, Issue 1, 1 February 2015, Pages 9399, Acute non-anion gap metabolic acidosis, also termed hyperchloremic acidosis, is frequently detected in seriously ill patients. The most common mechanisms leading to this acidbase disorder include loss of large quantities of base secondary to diarrhea and administration of large quantities of chloride-containing solutions in the treatment of hypovolemia and various shock states. The resultant acidic milieu can cause cellular dysfunction and contribute to poor clinical outcomes. The associated change in the chloride concentration in the distal tubule lumen might also play a role in reducing the glomerular filtration rate. Administration of base is often recommended for the treatment of acute non-anion gap acidosis. Importantly, the blood pH and/or serum bicarbonate concentration to guide the initiation of treatment has not been established for this type of metabolic acidosis; and most clinicians use guidelines derived from studies of high anion gap metabolic acidosis. Therapeutic complications resulting from base administration such as volume overload, exacerbation of hypertension and reduction in ionized calcium are likely to be as common as with high anion gap metabolic acidosis. On the other hand, exacerbation of intracellular acidosis due to the excessive generation of carbon dioxide migh Continue reading >>

Approach To The Adult With Metabolic Acidosis

Approach To The Adult With Metabolic Acidosis

INTRODUCTION On a typical Western diet, approximately 15,000 mmol of carbon dioxide (which can generate carbonic acid as it combines with water) and 50 to 100 mEq of nonvolatile acid (mostly sulfuric acid derived from the metabolism of sulfur-containing amino acids) are produced each day. Acid-base balance is maintained by pulmonary and renal excretion of carbon dioxide and nonvolatile acid, respectively. Renal excretion of acid involves the combination of hydrogen ions with urinary titratable acids, particularly phosphate (HPO42- + H+ —> H2PO4-), and ammonia to form ammonium (NH3 + H+ —> NH4+) [1]. The latter is the primary adaptive response since ammonia production from the metabolism of glutamine can be appropriately increased in response to an acid load [2]. Acid-base balance is usually assessed in terms of the bicarbonate-carbon dioxide buffer system: Dissolved CO2 + H2O <—> H2CO3 <—> HCO3- + H+ The ratio between these reactants can be expressed by the Henderson-Hasselbalch equation. By convention, the pKa of 6.10 is used when the dominator is the concentration of dissolved CO2, and this is proportional to the pCO2 (the actual concentration of the acid H2CO3 is very low): TI AU Garibotto G, Sofia A, Robaudo C, Saffioti S, Sala MR, Verzola D, Vettore M, Russo R, Procopio V, Deferrari G, Tessari P To evaluate the effects of chronic metabolic acidosis on protein dynamics and amino acid oxidation in the human kidney, a combination of organ isotopic ((14)C-leucine) and mass-balance techniques in 11 subjects with normal renal function undergoing venous catheterizations was used. Five of 11 studies were performed in the presence of metabolic acidosis. In subjects with normal acid-base balance, kidney protein degradation was 35% to 130% higher than protein synthesi Continue reading >>

Is Correcting Hyperchloremic Acidosis Beneficial?

Is Correcting Hyperchloremic Acidosis Beneficial?

You are here: Home / PULMCrit / Is correcting hyperchloremic acidosis beneficial? Is correcting hyperchloremic acidosis beneficial? An elderly woman presents with renal failure due to severe dehydration from diarrhea. She has a hyperchloremic acidosis from diarrhea with a chloride of 115 mEq/L, bicarbonate of 15 mEq/L, and a normal anion gap. During her volume resuscitation, should isotonic bicarbonate be used to correct her hyperchloremic acidosis? Does correcting her hyperchloremic acidosis actually help her, or does this just make her numbers better? The use of bicarbonate for treatment of metabolic acidosis is controversial. However, this controversy centers primarily around use of bicarbonate for management of lactic acidosis or ketoacidosis.Treatment of these disorders requires reversing the underlying disease process, with bicarbonate offering little if any benefit.Hyperchloremic metabolic acidosis is different.Whether due to bicarbonate loss or volume repletion with normal saline, the primary problems is a bicarbonate deficiency.Treating this with bicarbonate is a logical and accepted approach: Giving bicarbonate to a patient with a true bicarbonate deficit is not controversial. Controversy arises when the decrease in bicarbonate concentration is the result of its conversion to another base, which, given time, can be converted back to bicarbonate However, clinicians are often reluctant to treat hyperchloremic metabolic acidosis with bicarbonate, since the benefits of treatment are unclear.This post will attempt to clarify the rationale for treatment. Resuscitation with balanced crystalloids improves renal function There is growing evidence that resuscitation with normal saline impairs renal blood flow and function ( Young 2014 ).For example, Chowdhury 2012 inve Continue reading >>

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

Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Causes 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 >>

Sid Hyperchloremic Acidosis

Sid Hyperchloremic Acidosis

Strong ions are cations and anions that exist as charged particles dissociated from their partner ions at physiologic pH. The SID (Strong Ion Difference) is the difference between the positively- and negatively-charged strong ions in plasma. This method of evaluating acid-base disorders was developed to help determine the mechanism of the disorder rather than simply categorizing them into metabolic vs. respiratory acidosis/alkalosis as with the Henderson-Hasselbalch equation. Strong cations predominate in the plasma at physiologic pH leading to a net positive plasma charge of approximately +40: SID = [strong cations] [strong anions] = [Na+ + K+ + Ca2+ + Mg2+] [Cl- + lactate- + SO42-] Disturbances that increase the SID increase the blood pH while disorders that decrease the SID lower the plasma pH. According to the law of electroneutrality the sum of positive charges is equal to the sum of negative charges. Therefore the SID must be equal to the sum of weak anions in the body (such as bicarbonate, albumin, and phosphate). Hyperchloremic acidosis may result from chloride replacing lost bicarbonate. Such bicarbonate-wasting conditions may be seen in the kidneys (renal tubular acidosis) or the GI tract (diarrhea). This may also occur with aggressive volume resuscitation with normal saline (>30cc/kg/hr) due to excessive chloride administration impairing bicarbonate resorption in the kidneys. The strong ion difference of normal saline is 0 (Na+ = 154mEq/L and Cl- = 154mEq/L SID = 154 154 = 0). Therefore, aggressive administration of NS will decrease the plasma SID causing an acidosis. Administering a solution with a high SID such as sodium bicarbonate should be expected to treat this strong ion acidosis. Continue reading >>

Hyperchloremia (high Chloride Levels)

Hyperchloremia (high Chloride Levels)

Hyperchloremia is an electrolyte imbalance that occurs when theres too much chloride in the blood. Chloride is an important electrolyte that is responsible for maintaining the acid-base (pH) balance in your body, regulating fluids, and transmitting nerve impulses. The normal range for chloride in adults is roughly between 98 and 107 milliequivalents of chloride per liter of blood (mEq/L). Your kidneys play an important role in the regulation of chloride in your body, so an imbalance in this electrolyte may be related to a problem with these organs. It may also be caused by other conditions, like diabetes or severe dehydration , which can affect the ability of your kidneys to maintain chloride balance. The symptoms that may indicate hyperchloremia are usually those linked to the underlying cause of the high chloride level. Often this is acidosis , in which the blood is overly acidic. These symptoms may include: Like sodium, potassium, and other electrolytes, the concentration of chloride in your body is carefully regulated by your kidneys. The kidneys are two bean-shaped organs located just below your rib cage on both sides of your spine. They are responsible for filtering your blood and keeping its composition stable, which allows your body to function properly. Hyperchloremia occurs when the levels of chloride in the blood become too high. There are several ways that hyperchloremia can occur. These include: intake of too much saline solution while in the hospital, such as during a surgery Hyperchloremic acidosis, or hyperchloremic metabolic acidosis, occurs when a loss of bicarbonate (alkali) tips the pH balance in your blood toward becoming too acidic (metabolic acidosis). In response, your body holds onto chloride, causing hyperchloremia. In hyperchloremic acidosis, Continue reading >>

Topiramate-induced Metabolic Acidosis: A Case Study

Topiramate-induced Metabolic Acidosis: A Case Study

Nefrologia (English Version) 2012;32:403-4 | doi: 10.3265/Nefrologia.pre2011.Dec.11308 Topiramate-induced metabolic acidosis: a case study Acidosis metablica inducida por topiramato: a propsito de un caso. We present the case of a 75 year-old male with hypertension and chronic obstructive pulmonary disease who was diagnosed with chronic delusional disorder and mixed personality disorder, along with partial epilepsy due to a left parietal haematoma from several years prior. The patient was under treatment with topiramate, levetiracetam, quetiapine, sertraline, clobazam, and bronchodilators. He sought treatment for a respiratory infection and functional deterioration consisting of apathy, drowsiness, and periods of aggressive behaviour. A physical examination revealed that the patient had no fever, although he did suffer from disorientation and slurred speech, and would drift off to sleep, but with no apparent focal loss of motor function. The patient also had shallow tachypnoea, widespread rhonchi, and crackles in the left base, with radiological images indicative of superinfection of the abnormally widened bronchial tubes. We performed a laboratory analysis, revealing mildly elevated chlorine (114mEq/l), with normal renal function and all other ion parameters (sodium: 138mEq/l; potassium: 4.2mEq/l), and baseline arterial gasses compatible with a diagnosis of metabolic acidosis (pH: 7.24; pCO2: 33mm Hg; pO2: 67mm Hg; bicarbonate: 17mmol/l; base excess [BE]: -9.1mmol/l). The anion GAP value (difference between serum sodium and the sum of chlorine and bicarbonate) was 7mEq/l. The patient received treatment with systemic steroids and quinolones, with rapid clinical improvement until reaching a normal baseline levels. However, later controls revealed persistent hyperchlorem Continue reading >>

Attending Rounds: Patient With Hypokalemia And Metabolic Acidosis

Attending Rounds: Patient With Hypokalemia And Metabolic Acidosis

Attending Rounds: Patient with Hypokalemia and Metabolic Acidosis Department of Medicine, Yale School of Medicine, New Haven, Connecticut Dr. Asghar Rastegar, Department of Medicine, Yale School of Medicine, 333 Cedar Street, 1074 LMP, P.O. Box 208030, New Haven, CT 06520-8030; Phone: 203-737-2078, Fax: 203-785-7030; E-mail: . Summary Hypokalemic paralysis represents a medical emergency requiring both rapid diagnosis and treatment. In this Attending Rounds a patient with hypokalemia and metabolic acidosis is presented to emphasize the role of routine laboratory studies in the assessment of such patients so that a correct diagnosis can be made and appropriate treatment can be initiated promptly. A 39-year-old woman who had been in excellent health presented with a chief complaint of weakness in her lower extremities. She gave a history of intermittent vomiting for the past 2 months that was worse over the past 3 days. Two weeks before admission she was found to be positive for Helicobacter pylori antigen and was treated with amoxicillin, clarithromycin, and lansoperazole. One day before admission she was seen in the emergency department complaining of 3 days of vomiting. The serum lipase was mildly elevated, and she was diagnosed with mild pancreatitis. The serum potassium concentration was 3.1 mEq/L. She was treated with intravenous fluids and prochlorperazine and sent home. On the day of admission, she noted onset of bilateral lower extremity weakness, inability to walk without a cane, and profound fatigue. She also stated that she had been having intermittent leg cramps and that she recalled having been told previously that she had a low serum potassium level on several occasions. Her past medical history was unremarkable aside from migraine headaches during her mens Continue reading >>

Transient Perioperative Metabolic Acidosis In A Patient With Ileal Bladder Augmentation | Anesthesiology | Asa Publications

Transient Perioperative Metabolic Acidosis In A Patient With Ileal Bladder Augmentation | Anesthesiology | Asa Publications

Transient Perioperative Metabolic Acidosis in a Patient with Ileal Bladder Augmentation (Azzam) Associate Professor of Anesthesiology and Pediatrics. (Steinhardt) Associate Professor of Surgery and Pediatrics. (Tracy, Gabriel) Associate Professor of Orthopedics. Received from the Cardinal Glennon Children's Hospital, St. Louis University, St. Louis, Missouri. Submitted for publication October 27, 1994. Accepted for publication February 17, 1995. Address reprint requests to Dr. Azzam: St. Louis University Hospital, 3635 Vista Avenue, St. Louis, Missouri 63110. Transient Perioperative Metabolic Acidosis in a Patient with Ileal Bladder Augmentation Anesthesiology 7 1995, Vol.83, 198-200.. doi: Anesthesiology 7 1995, Vol.83, 198-200.. doi: Farid J. Azzam, George F. Steinhardt, Thomas F. Jr. Tracy, Keith R. Gabriel; Transient Perioperative Metabolic Acidosis in a Patient with Ileal Bladder Augmentation. Anesthesiology 1995;83(1):198-200.. 2018 American Society of Anesthesiologists Transient Perioperative Metabolic Acidosis in a Patient with Ileal Bladder Augmentation You will receive an email whenever this article is corrected, updated, or cited in the literature. You can manage this and all other alerts in My Account Key words: Acid-base equilibrium, acidosis: metabolic, Bladder. A poorly compliant, small-capacity bladder sometimes is seen in pediatric patients with myelomeningocele and other clinical entities. [1] Bladder augmentation with an intestinal segment provides the low-pressure reservoir required to preserve renal function and allow for urinary continence. [2] Metabolic complications of this procedure are well described [3] and include hyperchloremic acidosis, decrease in serum bicarbonate, and increase in serum phosphate and sulfate levels, leading to osteomalac Continue reading >>

Hyperchloremic Acidosis

Hyperchloremic Acidosis

Hyperchloremic acidosis is a known complication of intestinal bypass, due to both intestinal bicarbonate loss and renal tubular acidosis (RTA). Julian L. Seifter, in Goldman's Cecil Medicine (Twenty Fourth Edition) , 2012 Hyperchloremic Metabolic Acidosis of Nonrenal Origin Associated with Hypokalemia Hypokalemic, hyperchloremic acidosis may result from loss of a body fluid that is low in Cl relative to Na+ and K+ when compared with the ratio of Cl to Na+ in extracellular fluid. For example, stool losses of Na+, K+, and HCO3 in small bowel diarrhea or organic acid anions of bacterial origin in colonic diarrhea lead to hyperchloremic acidosis (Chapter 142). Pancreatic secretions (Chapter 201) or heavy losses from ileostomy sites may lead to loss of bicarbonate-containing fluids. Secretagogues such as vasoactive intestinal peptide (VIP), which is associated with neoplasms of the pancreas or sympathetic chain (Chapter 201), cause large losses of HCO3 in stool, with a resulting hypokalemic, hyperchloremic metabolic acidosis. Concomitant gastric achlorhydria is part of the syndrome known as watery diarrhea, hypokalemic, hypochlorhydric acidosis. Urinary diversions, such as ureterosigmoidostomies and ileal loops, may increase chloride absorption in exchange for bicarbonate in the intestinal segment and lead to hyperchloremic acidosis. Thomas D. DuBose, in Therapy in Nephrology & Hypertension (Third Edition) , 2008 Both uremic acidosis and hyperchloremic acidosis of renal insufficiency require oral alkali replacement to maintain [HCO3] between 20 and 24 mEq/L. This can usually be accomplished with relatively modest amounts of alkali (1-1.5 mEq/kg/day). Sodium citrate (Shohl's Solution or Bicitra) has been shown to enhance the absorption of aluminum from the gastrointestinal t 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 >>

Mechanism Of Normochloremic And Hyperchloremic Acidosis In Diabetic Ketoacidosis

Mechanism Of Normochloremic And Hyperchloremic Acidosis In Diabetic Ketoacidosis

Oh M.S. · Carroll H.J. · Uribarri J. Man S. Oh, MD, Department of Medicine, State University of New York, Health Science Center at Brooklyn, Brooklyn, NY 11203 (USA) Continue reading >>

Acid-base Physiology

Acid-base Physiology

8.4.1 Is this the same as normal anion gap acidosis? In hyperchloraemic acidosis, the anion-gap is normal (in most cases). The anion that replaces the titrated bicarbonate is chloride and because this is accounted for in the anion gap formula, the anion gap is normal. There are TWO problems in the definition of this type of metabolic acidosis which can cause confusion. Consider the following: What is the difference between a "hyperchloraemic acidosis" and a "normal anion gap acidosis"? These terms are used here as though they were synonymous. This is mostly true, but 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'. However, you should be aware that in some cases of normal anion-gap acidosis, there will not be a hyperchloraemia if there is a significant hyponatraemia. In a disorder that typically causes a high anion gap disorder there may sometimes be a normal anion gap! The anion gap may still be within the reference range in lactic acidosis. Now this can be misleading to you when you are trying to diagnose the disorder. Once you note the presence of an anion gap within the reference range in a patient with a metabolic acidosis you naturally tend to concentrate on looking for a renal or GIT cause. 1. One possibility is the increase in anions may be too low to push the anion gap out of the reference range. In lactic acidosis, the clinical disorder can be severe but the lactate may not be grossly high (eg lactate of 6mmol/l) and the change in the anion gap may still leave it in the reference range. So the causes of high anion gap acidosis should be considered in patients with hyperchloraemic acidosis if the cause of the acidosis is otherwise not apparent. Continue reading >>

Hyperchloremic Metabolic Acidosis: Is It Clinically Relevant?

Hyperchloremic Metabolic Acidosis: Is It Clinically Relevant?

SUMMARYFirst, do no harm. These words have been the doctrine of medicine since its inception. The era of evidence-based medicine now compels us to provide scientific evidence that we indeed do no harm and that the treatments we prescribe have a beneficial effect. The colloid/crystalloid debate continues to evolve and is as hotly contested now as it was a decade ago. There may be some international differences in the use of colloids or crystalloids, but most of us continue to use both. Whatever our preferred choice of intravenous fluid for the treatment of hypovolemia, clinical outcome studies suggest that when? and how much? are probably more important questions than what?. There are now a wide variety of fluids available to the clinician and most differ markedly in their composition. Aside from the gross classification of IV fluids into colloids and crystalloids, they may be subclassified into balanced or unbalanced categories, i.e., those that contain concentrations of electrolytes similar to those in the plasma and those that do not (see Table 1).The very fact that normal saline is unphysiological was recognized many years ago. This fact led Alexis Hartmann to develop Hartmann's solution in an attempt to produce an isotonic alkalizing solution. He recognized the need for proportionately more sodium than chloride1, which led to a solution very similar to Ringer's original2. The existence of hyperchloremic acidosis has been recognized in many areas for some time, e.g., diabetic ketoacidosis and ammonium chloride poisoning, and is generally termed a low-anion gap acidosis. There is now mounting evidence that the administration of intravenous saline and saline-based fluids is the commonest avoidable cause of clinically relevant hyperchloremic acidosis. Do you want to re Continue reading >>

Hyperchloremic Acidosis

Hyperchloremic Acidosis

Normal albumin-corrected anion gap acidosis Hyperchloremic acidosis is a common acid-base disturbance in critical illness, often mild (standard base excess >-10 mEq/L). Definitions of hyperchloremic acidosis vary. The best are not based on chloride concentrations, but on the presence of metabolic acidosis plus the absence of significant concentrations of lactate or other unmeasured anions. 2. standard base excess less than -3 mEq/L or bicarbonate less than 22 mmol/L, 3. Albumin corrected anion gap normal (5-15 mEq/L). A normal strong ion gap is an alternative indicator of the absence of unmeasured anions, although rarely used clinically and offering little advantage over the albumin corrected anion gap. The degree of respiratory compensation is relevant. It is appropriate if PaCO2 approximates the two numbers after arterial pH decimal point (e.g. pH=7.25, PaCO2=25 mm Hg; this rule applies to any primary metabolic acidosis down to a pH of 7.1). Acidosis is severe if standard base excess is less than -10 mEq/L, or pH is less than 7.3, or bicarbonate is less than 15 mmol/L. Common causes in critical illness are large volume saline administration, large volume colloid infusions (e.g. unbalanced gelatine or starch preparations) following resolution of diabetic keto-acidosis or of other raised anion gap acidosis, and post hypocarbia. Hyperchloremic acidosis often occurs on a background of renal impairment/tubular dysfunction. It is usually well tolerated, especially with appropriate respiratory compensation. The prognosis is largely that of the underlying condition. If associated with hyperkalemia, think of hypo-aldosteronism (Type 4 RTA), especially if diabetic. With persistent hypokalemia, think of RTA Types 1 and 2. Hyperchloremic acidosis is usually well tolerated in the Continue reading >>

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