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Acetazolamide Metabolic Acidosis Anion Gap

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 >>

Metabolic Alkalosis

Metabolic Alkalosis

Metabolic alkalosis is common—half of all acid-base disorders as described in one study (1). This observation should not be surprising since vomiting, the use of chloruretic diuretics, and nasogastric suction are common among hospitalized patients. The mortality associated with severe metabolic alkalosis is substantial; a mortality rate of 45% in patients with an arterial blood pH of 7.55 and 80% when the pH was greater than 7.65 has been reported (2). Although this relationship is not necessarily causal, severe alkalosis should be viewed with concern, and correction by the appropriate intervention should be undertaken with dispatch when the arterial blood pH exceeds 7.55. Metabolic alkalosis occurs when a primary pathophysiologic process leads to the net accumulation of base within or the net loss of acid from the extracellular fluid (ECF); typically, the intracellular compartment becomes more acidic in potassium-depletion alkalosis (3). Unopposed by other primary acid-base disorders, metabolic alkalosis is recognized by increases in both arterial blood pH—alkalemia—and plasma bicarbonate concentration. The increase in arterial blood pH promptly, normally, and predictably depresses ventilation resulting in increased PaCO2 and the buffering of the alkalemia. The PaCO2 increases about 0.5 to 0.7 mmHg for every 1.0 mM increase in plasma HCO3 concentration (4). Although a PaCO2 greater than 55 mmHg is uncommon, compensatory increases to 60 mmHg have been documented in severe metabolic alkalosis. Failure of an appropriate compensatory increase in PaCO2 should be interpreted as a mixed acid-base disturbance in which a stimulus to hyperventilation—primary respiratory alkalosis—accompanies primary metabolic alkalosis. Classification and Definitions Metabolic alkalosi Continue reading >>

Hyperchloremic Acidosis

Hyperchloremic Acidosis

Author: Sai-Ching Jim Yeung, MD, PhD, FACP; Chief Editor: Romesh Khardori, MD, PhD, FACP more... This article covers the pathophysiology and causes of hyperchloremic metabolic acidoses , in particular the renal tubular acidoses (RTAs). [ 1 , 2 ] It also addresses approaches to the diagnosis and management of these disorders. A low plasma bicarbonate (HCO3-) concentration represents, by definition, metabolic acidosis, which may be primary or secondary to a respiratory alkalosis. Loss of bicarbonate stores through diarrhea or renal tubular wasting leads to a metabolic acidosis state characterized by increased plasma chloride concentration and decreased plasma bicarbonate concentration. Primary metabolic acidoses that occur as a result of a marked increase in endogenous acid production (eg, lactic or keto acids) or progressive accumulation of endogenous acids when excretion is impaired by renal 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+) - [(HCO3- + Cl-)], in which Na+ is plasma sodium concentration, HCO3- is bicarbonate concentration, and Cl- is chloride concentration; all concentrations in this formula are in mmol/L (mM or mEq/L) (see also the Anion Gap calculator). The AG value represents the difference between unmeasured cations and anions, ie, the presence of anions in the plasma that are not routinely measured. An increased AG is associated with renal failure, ketoacidosis, lactic acidosis, and ingestion of certain toxins. It can usually be easily identified by evaluating routine plasma chemistry results and from the clinical picture. A normal AG Continue reading >>

Metabolic Acidosis And Hyperventilation Induced By Acetazolamide In Patients With Central Nervous System Pathology

Metabolic Acidosis And Hyperventilation Induced By Acetazolamide In Patients With Central Nervous System Pathology

ACETAZOLAMIDE, a carbonic anhydrase inhibitor, is used in patients with meningeal inflammation, mild intracranial hypertension, and basal skull fractures to decrease the formation of cerebrospinal fluid (CSF). It causes mild metabolic acidosis by inhibiting the reabsorption of bicarbonate (HCO−3) ions from renal tubules. This effect has been used successfully in the treatment of patients with chronic respiratory acidosis with superimposed metabolic alkalosis 1 and central sleep apnea syndrome. 2 Life-threatening metabolic acidosis during acetazolamide therapy has been observed only in patients with renal impairment or 3 diabetes 4 and in elderly patients. 5 Severe metabolic acidosis, associated with acetazolamide, in the absence of other predisposing factors has not been reported in patients with central nervous system disease. We report three cases of severe metabolic acidosis and hyperventilation during acetazolamide therapy in normal doses in adult patients without renal impairment. A 35-yr-old man with a head injury underwent craniotomy for evacuation of a traumatic left temporal extradural hematoma. Postoperatively, the patient underwent mechanical ventilation to maintain a partial pressure of arterial carbon dioxide (Paco2) of 30–35 mmHg. On the third postoperative day, 250 mg acetazolamide administered every 8 h through a nasogastric tube was started to treat a CSF leak from the operative wound. A T-piece trial of weaning was started on the fourth postoperative day. On the fifth postoperative day, patient respiratory rate increased to 40–44 breaths/min. Arterial blood gas analysis showed metabolic acidosis resulting in compensatory hypocapnia and a normal pH (table 1). The patient was sedated and underwent artificial ventilation for the next 6 days. Attempt Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Increases 0.3-0.7 mEq/l [0.3-0.7 mmol/L] per 0.1 decr pH Difference between measured plasma cation (ie, Na+) and anions (ie, chloride (Cl-), HCO3-) concentrations Lactic acidosis (mild LA may have normal AG) Also called hyperchloremic acidosis (decreased HCO3, increased Cl) Renal tubular acidosis: impairment in renal acidification Type III (term no longer used) Formerly used to define distal RTA with bicarbonate wasting in children Bicarbonaturia resolves with age and is not truly part of a pathologic process Type IV: common in obstructive nephropathy, DM, hyporenin/hypoaldosteronehyper K+, acidosis Intestinal loss of bicarbonate (diarrhea, pancreatic fistula) Carbonic anhydrase inhibitors (e.g. acetazolamide) Dilutional acidosis (due to rapid infusion of bicarbonate-free isotonic saline) Ingestion of exogenous acids (ammonium chloride, methionine, cystine, calcium chloride) Drugs: amiloride, triamterine, Bactrim, chemotherapy, pentamidines As diagnostic aid, is not absolute "Delta gap" = calculated anion gap:nl anion gap In anion gap acidosis, "delta gap" should equal "delta HCO3" If HCO3 higher than predictedsuperimposed metabolic alkalosis If HCO3 lower than predictedsuperimposed non-anion gap metabolic acidosis Allows diagnosisof mixed metabolic disturbance Mixed metabolic disturbance plus respiratory disturbance Check urine pH before initializing therapy NaHCO3 therapy for pH < 7.1 - 7.2 Only used emergently to raise pH to > 7.1 or 7.2 Controversial, depends on disorder and symptoms i.e. NaHCO3 not beneficial in DKA treatment with pH under 7.0) DO NOT give this entire amount 2 ampulesof 8.4% NaHCO3 in 1 Liter of 1/4 NS OR 3-4 ampulesof 8.4% NaHCO3 in 1 Liter D5W Overaggressive NaHCO3"overshoot alkalosis" Bicarbonate level should be corrected only to 15 mEq/L [15 m Continue reading >>

Metabolic Acidosis; Non-gap

Metabolic Acidosis; Non-gap

Non-gap metabolic acidosis, or hyperchloremic metabolic acidosis, are a group of disorders characterized by a low bicarbonate, hyperchloremia and a normal anion gap (10-12). A non-gapped metabolic acidosis fall into three categories: 1) loss of base (bicarbonate) from the gastrointestinal (GI) tract or 2) loss of base (bicarbonate) from the kidneys, 3) intravenous administration of sodium chloride solution. Bicarbonate can be lost from the GI tract (diarrhea) or from the kidneys (renal tubular acidosis) or displaced by chloride. A. What is the differential diagnosis for this problem? Proximal renal tubular acidosis: (low K+) Distal renal tubular acidosis: (low or high K+) Prostaglandin Inhibitors, (aspirin, nonsteroidal anti-inflammatory drugs, cyclooxygenase 2 inhibitors) Adrenal insufficiency (primary or secondary) (high K+) Pseudoaldosteronism, type 2 (Gordon's syndrome) B. Describe a diagnostic approach/method to the patient with this problem. Metabolic acidosis can be divided into two groups based on anion gap. If an anion gap is elevated (usually greater than 12), see gapped metabolic acidosis. Diagnosis of the cause of non-gapped metabolic acidosis is usually clinically evident - as it can be attributed to diarrhea, intravenous saline or by default, renal tubular acidosis. Occasionally, it may not be clear whether loss of base occurs due to the kidney or bowel. In such a case, one should calculate the urinary anion gap. The urinary anion gap (UAG) = sodium (Na+)+K+- chloride (Cl-). Caution if ketonuria or drug anions are in the urine as it would invalidate the calculation. As an aid, UAG is neGUTive when associated with bowel causes. Non-gapped metabolic acidosis can further be divided into two categories: 1. Historical information important in the diagnosis of Continue reading >>

Drug-induced Metabolic Acidosis

Drug-induced Metabolic Acidosis

Go to: Introduction Metabolic acidosis is defined as an excessive accumulation of non-volatile acid manifested as a primary reduction in serum bicarbonate concentration in the body associated with low plasma pH. Certain conditions may exist with other acid-base disorders such as metabolic alkalosis and respiratory acidosis/alkalosis 1. Humans possess homeostatic mechanisms that maintain acid-base balance ( Figure 1). One utilizes both bicarbonate and non-bicarbonate buffers in both the intracellular and the extracellular milieu in the immediate defense against volatile (mainly CO 2) and non-volatile (organic and inorganic) acids before excretion by the lungs and kidneys, respectively. Renal excretion of non-volatile acid is the definitive solution after temporary buffering. This is an intricate and highly efficient homeostatic system. Derangements in over-production, under-excretion, or both can potentially lead to accumulation of excess acid resulting in metabolic acidosis ( Figure 1). Drug-induced metabolic acidosis is often mild, but in rare cases it can be severe or even fatal. Not only should physicians be keenly aware of this potential iatrogenic complication but they should also be fully engaged in understanding the pathophysiological mechanisms. Metabolic acidosis resulting from drugs and/or ingestion of toxic chemicals can be grouped into four general categories ( Figure 2): Some medications cannot be placed into one single category, as they possess multiple mechanisms that can cause metabolic acidosis. In suspected drug-induced metabolic acidosis, clinicians should establish the biochemical diagnosis of metabolic acidosis along with the evaluation of respiratory compensation and whether there is presence of mixed acid-based disorders 2, then convert the bioche Continue reading >>

Diamox Sequels (acetazolamide) Dose, Indications, Adverse Effects, Interactions... From Pdr.net

Diamox Sequels (acetazolamide) Dose, Indications, Adverse Effects, Interactions... From Pdr.net

Acetazolamide/Acetazolamide Sodium/Diamox Intravenous Inj Pwd F/Sol: 500mg Acetazolamide/Diamox Oral Tab: 125mg, 250mg Acetazolamide/Diamox/Diamox Sequels Oral Cap ER: 500mg For the adjunctive treatment of open-angle glaucoma. 250 mg PO given 1 to 4 times daily. Maintenance dosage should be titrated to response. The maximum dosage is 1 g/day. Consider dosage reduction. An elderly patient is more likely to develop hyperchloremic metabolic acidosis in addition to an age-related renal impairment. 8 to 30 mg/kg/day PO or 300 to 900 mg/m2/day, given in divided doses every 8 hours. 5 to 10 mg/kg IV every 6 hours for acute glaucoma. Maximum dosage is 1 g/day. For use as an alternative agent in the treatment of absence seizures. NOTE: The extended release preparation is not recommended for use as an anticonvulsant. Oral dosage (regular-release tablets only) 8 to 30 mg/kg/day PO, given in up to 4 divided doses. The usual maintenance dosage is 375 to 1,000 mg/day. Consider dosage reduction. An elderly patient is more likely to develop hyperchloremic metabolic acidosis in addition to an age-related renal impairment. 8 to 30 mg/kg/day IV, given in up to 4 divided doses. The usual maintenance dosage is 375 to 1,000 mg/day. Consider dosage reduction. An elderly patient is more likely to develop hyperchloremic metabolic acidosis in addition to an age-related renal impairment. For the treatment of acute altitude sickness. 250 mg PO twice daily is recommended by clinical practice guidelines. Descent is the preferred initial treatment. When descent is not possible or effective, symptomatic treatment (e.g., analgesics and antiemetics), oxygen, and other treatments, including acetazolamide, should be considered. The FDA-approved dosage is 500 to 1,000 mg PO daily, in divided doses, for 48 Continue reading >>

Hyperchloremia Why And How - Sciencedirect

Hyperchloremia Why And How - Sciencedirect

Volume 36, Issue 4 , JulyAugust 2016, Pages 347-353 Hyperchloremia Why and howHipercloremia: por qu y cmo Author links open overlay panel Glenn T.Nagami Open Access funded by Sociedad Espaola de Nefrologa Hyperchloremia is a common electrolyte disorder that is associated with a diverse group of clinical conditions. The kidney plays an important role in the regulation of chloride concentration through a variety of transporters that are present along the nephron. Nevertheless, hyperchloremia can occur when water losses exceed sodium and chloride losses, when the capacity to handle excessive chloride is overwhelmed, or when the serum bicarbonate is low with a concomitant rise in chloride as occurs with a normal anion gap metabolic acidosis or respiratory alkalosis. The varied nature of the underlying causes of the hyperchloremia will, to a large extent, determine how to treat this electrolyte disturbance. La hipercloremia es una alteracin electroltica frecuente que se asocia a una serie de distintos trastornos clnicos. El rin desempea una funcin importante en la regulacin de la concentracin de cloruro a travs de diversos transportadores que se encuentran a lo largo de la nefrona. Sin embargo, puede aparecer hipercloremia cuando la prdida hdrica sea mayor que la de sodio y cloruro; cuando se sobrepase la capacidad de excretar el cloruro en exceso; o cuando la concentracin srica de bicarbonato sea baja y al mismo tiempo haya un aumento de cloruro, como sucede en la acidosis metablica con brecha aninica normal o en la alcalosis respiratoria. La heterognea naturaleza de las causas subyacentes de la hipercloremia determinar, en gran medida, el modo de tratar esta alteracin electroltica. Continue reading >>

Normal Anion Gap Acidosis

Normal Anion Gap Acidosis

In renal physiology , normal anion gap acidosis, and less precisely non-anion gap acidosis, is an acidosis that is not accompanied by an abnormally increased anion gap . The most common cause of normal anion gap acidosis is diarrhea with a renal tubular acidosis being a distant second. The differential diagnosis of normal anion gap acidosis is relatively short (when compared to the differential diagnosis of acidosis): Diarrhea : due to a loss of bicarbonate. This is compensated by an increase in chloride concentration, thus leading to a normal anion gap, or hyperchloremic, metabolic acidosis. The pathophysiology of increased chloride concentration is the following: fluid secreted into the gut lumen contains higher amounts of Na+ than Cl; large losses of these fluids, particularly if volume is replaced with fluids containing equal amounts of Na+ and Cl, results in a decrease in the plasma Na+ concentration relative to the Clconcentration. This scenario can be avoided if formulations such as lactated Ringers solution are used instead of normal saline to replace GI losses. [2] Continue reading >>

Type 2 Renal Tubular Acidosis And Acetazolamide - Deranged Physiology

Type 2 Renal Tubular Acidosis And Acetazolamide - Deranged Physiology

Type 2 Renal Tubular Acidosis and Acetazolamide This form of renal tubular acidosis decreases the strong ion difference by interfering with bicarbonate resorption in the proximal tubule; the mechanism is analogous to the action of acetazolamide. Bicarbonate handling in the proximal tubule Behold, the familiar activity of carbonic anhydrase in the proximal tubule. Carbonic anhydrase converts the filtered bicarbonate into easily resorbed CO2, and then traps it again inside the cell. The filtered bicarbonate is essentialy completely reabsorbed. The concentration of chloride in the tubule is therefore expected to increase- if the bicarbonate has been reabsorbed, more chloride must remain in the tubule to maintain electroneutrality. However, the failure of carbonic anhydrase results in bicarbonate remaining trapped in the urine. This, of course, means that electroneutrality of the tubule is maintained without the excretion of any further chloride. Thus, the chloride which would otherwise be excreted, is retained. There is an excellent article which discusses the mechanisms of chloride retention in acetazolamide-intoxicated patients with metabolic alkalosis. Particularly, it contains a graph of urinary strong ion diference over time, after the administration of 500mg of acetazolamide. It looks a little like this : Causes of proximal renal tubular acidosis Isolated congenital Type 2 RTA is very rare, and would likely form a part of of a syndrome , being associated with a series of other tubular defects, or forming a part of a whole-proximal-tubule problem like Fanconi syndrome. Anong the elderly, a new onset of Type 2 RTA without any new medication changes can be due to a monoclonal gammopathy , where ligh chains selectively damage the proximal tubule. Similarly, amyloidosis Continue reading >>

Metabolic Acidosis - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition

Metabolic Acidosis - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition

(Video) Overview of Acid-Base Maps and Compensatory Mechanisms By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincent’s Ascension Health, Birmingham Metabolic acidosis is primary reduction in bicarbonate (HCO3−), typically with compensatory reduction in carbon dioxide partial pressure (Pco2); pH may be markedly low or slightly subnormal. Metabolic acidoses are categorized as high or normal anion gap based on the presence or absence of unmeasured anions in serum. Causes include accumulation of ketones and lactic acid, renal failure, and drug or toxin ingestion (high anion gap) and GI or renal HCO3− loss (normal anion gap). Symptoms and signs in severe cases include nausea and vomiting, lethargy, and hyperpnea. Diagnosis is clinical and with ABG and serum electrolyte measurement. The cause is treated; IV sodium bicarbonate may be indicated when pH is very low. Metabolic acidosis is acid accumulation due to Increased acid production or acid ingestion Acidemia (arterial pH < 7.35) results when acid load overwhelms respiratory compensation. Causes are classified by their effect on the anion gap (see The Anion Gap and see Table: Causes of Metabolic Acidosis ). Lactic acidosis (due to physiologic processes) Lactic acidosis (due to exogenous toxins) Toluene (initially high gap; subsequent excretion of metabolites normalizes gap) HIV nucleoside reverse transcriptase inhibitors Biguanides (rare except with acute kidney injury) Normal anion gap (hyperchloremic acidosis) Renal tubular acidosis, types 1, 2, and 4 The most common causes of a high anion gap metabolic acidosis are Ketoacidosis is a common complication of type 1 diabetes mellitus (see diabetic ketoacidosis ), but it also occurs with chronic alcoholism (see alcoholic ketoacidos Continue reading >>

Acid/base Disorders: Metabolic Alkalosis

Acid/base Disorders: Metabolic Alkalosis

Does this patient have metabolic alkalosis? How does one make the diagnosis of metabolic alkalosis and differentiate simple from mixed disturbances? Metabolic alkalosis is due either to a gain in bicarbonate or a bicarbonate precursor (HCO3-), loss of hydrogen ion (H+) or the loss of fluid that contains Cl- in higher concentration and bicarbonate in lower concentration than serum. The brainstem is sensitive to interstitial and cellular H+changes and the decline in H+with metabolic alkalosis inhibits ventilation (respiratory compensation). In simple metabolic alkalosis the resultant compensatory alveolar hypoventilation leads to an increase in arterial carbon dioxide content (PaCO2). For each 1 mEq/L rise in HCO3-, PaCO2 rises about 0.7 mmHg (range 0.6-1.0 mmHg). Based on the history, one can assess whether an increase in HCO3-is due to oral or intravenous alkali administration vs. H+ loss that results in addition of HCO3- to the body. The kidney plays a crucial role in maintaining HCO3-. Most often, the kidneys can excrete excess HCO3- and bicarbonaturia occurs. Factors that facilitate bicarbonaturia are adequate extracellular fluid (ECF) volume, dietary salt intake, potassium balance and appropriate mineralocorticoid activity. In order for metabolic alkalosis to be maintained the kidneys ability to excrete excess bicarbonate must be impaired, most commonly as a result of ECF volume contraction. Patients can present with either simple or mixed acid-base disturbances. The evaluation of a patient with suspected metabolic alkalosis on a set of arterial blood gases involves four simple steps: Step 1: Assess the arterial pH and identify the primary disturbance. An elevated serum HCO3-could be the result of metabolic alkalosis or may represent compensation for respiratory ac Continue reading >>

Acid-base Disorders

Acid-base Disorders

An acid is a substance that can release a hydrogen ion (H+) In water, an acid dissociates reversibly into a H+ and its conjugate base (written as A-): HA H+ + A- The more an acid is present in the dissociated form at equilibrium (H+ + A-), the stronger the acid A base is a substance that can accept a hydrogen ion (H+) In the formula HA H+ + A-, A- is a base because it can accept H+ A buffer is a chemical that minimizes the change in pH when an acid or base is added to a solution The main buffer in the human body is carbonic acid (H2CO3) Carbonic acid buffers blood through the following reaction: Anions are atoms or groups of atoms that carry a negative charge. The main anions in human blood are chloride (Cl-) and bicarbonate (HCO3-). Cations are atoms or groups of atoms that carry a positive charge. The main cation in human blood is sodium (Na+). In blood, the concentration of cations and anions must always balance in order to maintain electroneutrality pH is a measure of free hydrogen ions (H+) in a solution pH is calculated in the following manner: pH = log10(1/[H+]) Because pH is inversely related to H+, the pH decreases as the concentration of H+ increases The normal pH of arterial blood is 7.35 - 7.45 PaCO2 is the partial pressure of CO2 in arterial blood Partial pressure is defined as the amount of pressure an individual gas contributes to the overall pressure of a mixture of gases In arterial blood, CO2 normally exerts a partial pressure of 38 - 42 mmHg The PaCO2 in arterial blood is identical to the PaCO2 in alveolar air PaCO2 is measured by drawing an arterial blood gas The normal PaCO2 in arterial blood is 38 - 42 mmHg PaO2 is the partial pressure of oxygen in arterial blood Partial pressure is defined as the amount of pressure an individual gas contributes t Continue reading >>

Acute Renal Failure Secondary To Sodium And Water Depletion Due To Diarrhoea Plus Acetazolamide

Acute Renal Failure Secondary To Sodium And Water Depletion Due To Diarrhoea Plus Acetazolamide

Nefrologia (English Version) 2011;31:757-8 | doi: 10.3265/Nefrologia.pre2011.Aug.11033 Acute renal failure secondary to sodium and water depletion due to diarrhoea plus acetazolamide Fracaso renal agudo secundario a deplecin hidrosalina por diarrea ms acetazolamida Key words: Metabolic acidosis with normal anion gap Palabras Clave: NOTICE Undefined index: es (contenidos/item.php[133]) The use of acetazolamide for the treatment of Menieres syndrome1,2 is uncommon, since other drugs constitute the first line used in the treatment of this pathology. Here we present the case of a 70-year old woman whose most relevant background involved Menieres syndrome, currently treated with acetazolamide at 250mg/12h with oral potassium supplements. The patient was referred to us due to severe renal failure (urea: 194mg/dl; C-reactive protein: 8.1mg/dl), with extremely severe metabolic acidosis (venous gas: pH: 7.1, bicarbonate: 6.5mmol/l, PCO2: 18mm Hg, PO2: 69mm Hg) and anuria. Laboratory analyses from a few months prior indicated C-reactive protein of 1mg/dl. The patient had been admitted to the nearest reference hospital 24 hours before as a result of severe diarrhoea, and continued taking the normal treatment. Hydration treatment had been started without diuresis, and the patient was transferred for monitoring. Upon hospitalisation, dehydration signs were present, with a blood pressure of 80/50mm Hg, anuria, and no fever. At this point the patient did not have diarrhoea. Laboratory analysis revealed acidosis, hypokalaemia (K: 2.9mEq/l) and renal failure similar to that described. We continued to provide intense rehydration therapy, despite which the patient continued with anuria for 24 hours more, with C-reactive protein levels reaching 11mg/dl. Once the volume level was normalise Continue reading >>

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