DOCSLIB.ORG

It Is Chloride Depletion Alkalosis, Not Contraction Alkalosis

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
It Is Chloride Depletion Alkalosis, Not Contraction Alkalosis SCIENCE IN RENAL MEDICINE www.jasn.org It Is Chloride Depletion Alkalosis, Not Contraction Alkalosis Robert G. Luke and John H. Galla Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio ABSTRACT Maintenance of metabolic alkalosis generated by chloride depletion is often attributed aspiration, chloruretic diuretics, NaNO3 to volume contraction. In balance and clearance studies in rats and humans, we infusion (an effect of un-reabsorbable showed that chloride repletion in the face of persisting alkali loading, volume anions), and prior hypercapnia (post- contraction, and potassium and sodium depletion completely corrects alkalosis hypercapnic CDA) were all used to gen- by a renal mechanism. Nephron segment studies strongly suggest the corrective erate CDA. These studies establish that 2 response is orchestrated in the collecting duct, which has several transporters Cl repletion by NaCl or KCl—but not integral to acid-base regulation, the most important of which is pendrin, a luminal replacement of Na+ and K+ losses without 2 2 Cl/HCO3 exchanger. Chloride depletion alkalosis should replace the notion of Cl —fully corrects CDA in the mainte- contraction alkalosis. nance phase. The issue of the specific role of ECF volume depletion was not re- J Am Soc Nephrol 23: 204–207, 2012. doi: 10.1681/ASN.2011070720 solved at this time. To separate chloride from volume re- pletion, we first studied rats with selective Chloridedepletionisthecommonestofthe identical to that in the plasma of the dogs CDA produced by peritoneal dialysis 3 three major causes of metabolic alkalosis; with stable alkalemia. These isometric in- against NaHCO3 and a normal serum po- theothersrelatetopotassiumdepletion/ fusions completely corrected alkalosis by tassium concentration. In rats given a 70 2 mineralocorticoid excess and to very low 24 hours without an increase in GFR, de- mEq/L Cl drink with either Na+ or cho- or absent glomerular filtration with base spite increasing potassium depletion; chlo- line, CDAwas completely corrected de- loading and are not further discussed in ride repletion was acknowledged. On the spite negative Na+ and K+ balances, detail. Metabolic alkalosis has generation, basis of the known characteristics of fluid decreased body weight, and obligatory maintenance, and recovery phases.1 This and electrolyte handling in the various sodium or choline bicarbonate loading.6 article focuses on the factors that affect nephronsegmentsatthattime,thevolume Acid-base status in choline-receiving con- the latter two phases. hypothesis in which the intranephronal re- trols was not altered. Rats treated in like In a seminal paper published in 1965, distribution of fluid reabsorption plays the manner with CDA maintained for 7–10 contraction alkalosis produced by etha- central role was expounded. ECF volume days responded in the same manner.7 crynic acid was described in humans that depletion accompanying alkalosis aug- The corrective response occurs by a renal gave rise to the hypothesis that extracel- ments fluidreabsorptionintheproximal mechanism.8 lular fluid (ECF) volume contraction pro- tubule where bicarbonate is preferentially To more rigorously exclude a role for duces alkalosis.2 The authors concluded reabsorbed compared with chloride; the volume expansion, CDA rats were infused that abrupt change in ECF volume was increased bicarbonate reabsorption in with 5% dextrose with either 6% albumin 2 the primary event, while acknowledging this segment thus maintains the alkalosis. or an isometric Cl solution. CDA that chloride depletion might influence During correction, volume expansion de- renal bicarbonate retention. creases proximal tubule fluid reabsorp- Published online ahead of print. Publication date In an effort to separate the correction tion, thereby delivering more bicarbonate available at www.jasn.org. of volume depletion from that of chloride to the distal nephron, which has a limited depletion, Cohen maintained alkalosis for capacity to reabsorb bicarbonate; bicarbon- Correspondence: Dr. Robert G. Luke, University of Cincinnati Medical Center, 231 Albert Sabin Way, 4 5 days in dogs treated with ethacrynic acid aturia ensues and the alkalosis corrects. PO Box 670556, Cincinnati OH 45267-0557. Email: and a NaCl-deficient diet, and then ex- Schwartz et al. studied the pathogen- [email protected] fl pandedECFvolumewitha uidcontaining esis of alkalosis produced by chloride de- Copyright © 2012 by the American Society of chloride and bicarbonate in concentrations pletion (CDA) in men and dogs.5 Gastric Nephrology 204 ISSN : 1046-6673/2302-204 J Am Soc Nephrol 23: 204–207, 2012 www.jasn.org SCIENCE IN RENAL MEDICINE persisted in rats infused with albumin de- secreting protons or bicarbonate and of CDA, pendrin is stimulated both by spite 15% ECF volume expansion, but was chloride bicarbonate exchange indepen- low chloride distal delivery22 and by corrected by the Cl--containing solu- dent of sodium was yet to come. metabolic alkalosis,20 including intra- tion despite persistent volume depletion The site at which this renal mainte- cellular alkalosis. In potassium deple- and decreased GFR.9 Delivery of chloride nance and correction of CDA occurs was tion metabolic alkalosis, a high serum to the collecting duct was not statistically addressed in micropuncture and micro- bicarbonate is maintained by intracellu- different between the groups but was ab- perfusion studies in our peritoneal di- lar acidosis in the renal tubular cells with solutely greater in rats that corrected. alysis rat model. First, GFR was inversely resulting increased bicarbonate reab- Urinary bicarbonate excretion increased correlated with the degree of CDA by sorption at several sites along the neph- as chloride was infused, whereas it de- tubuloglomerular feedback.12 Although ron. Pendrin is reduced in potassium creased further in the volume-expanded intact function of the proximal tubule depletion24; this suggests that the signal rats. The magnitude of bicarbonaturia and the loop of Henle are essential to the for increased activity for the luminal anion approximated the estimated amount of renal response, these segments have no exchanger is related to changes in intracel- chloride delivered to the collecting ducts. identifiable adaptive role in the corrective lular pH, rather than extracellular pH or Renal chloride conservation persisted response to chloride repletion in that glo- urine pH. Pendrin has been studied in until plasma chloride concentration re- merulotubular balance is maintained mice, rats, rabbits, and the gills of rays22 turned to normal.10 whether CDA is being corrected.8,9 Delivery (where it responds to changes in acid-base In normal human participants, we of chloride and bicarbonate out of the loop status on moving from sea to fresh water). turned to diuretic-induced CDA. Furose- of Henle was not different whether rats In renal pendrin null mice, serum + + 9,13 2 mide, Na ,K citrate supplementation, were maintaining or correcting CDA. HCO3 concentration is higher and 2 and dietary Cl restriction produced sta- In the distal convoluted tubule, alkalosis urine is less acidic than in controls.25 bly maintained CDA for 5 days that was can induce HCO3 secretion, which is in- Humans with Pendred syndrome (hypo- completely corrected thereafter by oral hibited by the removal of luminal chlo- thyroid goiter and deafness) seem to KCl, despite the presence of maintained ride; it is likely that such effects emanate have normal acid-base status. However, negative Na+ balance and plasma volume from the connecting tubule.14 two recent descriptions of a severe met- contraction (measured by the 131I albu- In perfused cortical collecting ducts, abolic alkalosis in a child, given thiazide 2 26 min space and plasma albumin concen- HCO3 is secreted in tubules from CDA for excess endolymph and severe alka- trations) and persistently lowered GFR rats and is dependent on luminal chlo- losis and potassium depletion in re- and estimated renal plasma flow.11 During ride, whereas it is reabsorbed in normal sponse to vomiting,27 suggest that an correction, net acid excretion decreased rats.15 The magnitude and direction of intact functioning of B-type intercalated 2 2 with HCO3 diuresis. In contrast, neutral HCO3 transport is dependent upon the cells are important for defense against sodium phosphate given in lieu of KCl degree of alkalosis and chloride repletion chloride depletion. was associated with increased serum in vivo at the time of tubule harvesting.16 The role of aldosterone, if any, in 2 HCO3 concentration despite increased Thus, our studies in rats and humans regulating pendrin’s response to changes plasma volume. In control participants, suggest that the single and necessary in dietary chloride and to acid-base 2 furosemide administration without Cl correction effect for CDA is an increase changes is not clear. We showed that an- restriction did not cause CDA and serum in distal nephron chloride; the B-type giotensin II was not regulatory in main- electrolyte concentrations and net acid ex- intercalated cells along the cortical collect- tenance or correction of CDA.28 High cretion did not change with the same ingductwerepoisedtosecretebicarbonate aldosterone levels are also not necessary amount of KCl administration. Thus, in in exchange for administered chloride for maintenance of CDA29 and correction both rats and humans, chloride repletion (Figure 1). H+-ATPase activity was in- by chloride occurs despite rising levels.10 in the face of
Load more

Recommended publications
  • Body Fluid Compartments Dr Sunita Mittal
    Body fluid compartments Dr Sunita Mittal Learning Objectives To learn: ▪ Composition of body fluid compartments. ▪ Differences of various body fluid compartments. ▪Molarity, Equivalence,Osmolarity-Osmolality, Osmotic pressure and Tonicity of substances ▪ Effect of dehydration and overhydration on body fluids Why is this knowledge important? ▪To understand various changes in body fluid compartments, we should understand normal configuration of body fluids. Total Body Water (TBW) Water is 60% by body weight (42 L in an adult of 70 kg - a major part of body). Water content varies in different body organs & tissues, Distribution of TBW in various fluid compartments Total Body Water (TBW) Volume (60% bw) ________________________________________________________________ Intracellular Fluid Compartment Extracellular Fluid Compartment (40%) (20%) _______________________________________ Extra Vascular Comp Intra Vascular Comp (15%) (Plasma ) (05%) Electrolytes distribution in body fluid compartments Intracellular fluid comp.mEq/L Extracellular fluid comp.mEq/L Major Anions Major Cation Major Anions + HPO4- - Major Cation K Cl- Proteins - Na+ HCO3- A set ‘Terminology’ is required to understand change of volume &/or ionic conc of various body fluid compartments. Molarity Definition Example Equivalence Osmolarity Osmolarity is total no. of osmotically active solute particles (the particles which attract water to it) per 1 L of solvent - Osm/L. Example- Osmolarity and Osmolality? Osmolarity is total no. of osmotically active solute particles per 1 L of solvent - Osm/L Osmolality is total no. of osmotically active solute particles per 1 Kg of solvent - Osm/Kg Osmosis Tendency of water to move passively, across a semi-permeable membrane, separating two fluids of different osmolarity is referred to as ‘Osmosis’. Osmotic Pressure Osmotic pressure is the pressure, applied to stop the flow of solvent molecules from low osmolarity to a compartment of high osmolarity, separated through a semi-permeable membrane.
    [Show full text]
  • Mechanical Ventilation Bronchodilators
    A Neurosurgeon’s Guide to Pulmonary Critical Care for COVID-19 Alan Hoffer, M.D. Chair, Critical Care Committee AANS/CNS Joint Section on Neurotrauma and Critical Care Co-Director, Neurocritical Care Center Associate Professor of Neurosurgery and Neurology Rana Hejal, M.D. Medical Director, Medical Intensive Care Unit Associate Professor of Medicine University Hospitals of Cleveland Case Western Reserve University To learn more, visit our website at: www.neurotraumasection.org Introduction As the number of people infected with the novel coronavirus rapidly increases, some neurosurgeons are being asked to participate in the care of critically ill patients, even those without neurological involvement. This presentation is meant to be a basic guide to help neurosurgeons achieve this mission. Disclaimer • The protocols discussed in this presentation are from the Mission: Possible program at University Hospitals of Cleveland, based on guidelines and recommendations from several medical societies and the Centers for Disease Control (CDC). • Please check with your own hospital or institution to see if there is any variation from these protocols before implementing them in your own practice. Disclaimer The content provided on the AANS, CNS website, including any affiliated AANS/CNS section website (collectively, the “AANS/CNS Sites”), regarding or in any way related to COVID-19 is offered as an educational service. Any educational content published on the AANS/CNS Sites regarding COVID-19 does not constitute or imply its approval, endorsement, sponsorship or recommendation by the AANS/CNS. The content should not be considered inclusive of all proper treatments, methods of care, or as statements of the standard of care and is not continually updated and may not reflect the most current evidence.
    [Show full text]
  • ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic Ketoacidosis and the Hyperglycem
    Received: 11 April 2018 Accepted: 31 May 2018 DOI: 10.1111/pedi.12701 ISPAD CLINICAL PRACTICE CONSENSUS GUIDELINES ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic ketoacidosis and the hyperglycemic hyperosmolar state Joseph I. Wolfsdorf1 | Nicole Glaser2 | Michael Agus1,3 | Maria Fritsch4 | Ragnar Hanas5 | Arleta Rewers6 | Mark A. Sperling7 | Ethel Codner8 1Division of Endocrinology, Boston Children's Hospital, Boston, Massachusetts 2Department of Pediatrics, Section of Endocrinology, University of California, Davis School of Medicine, Sacramento, California 3Division of Critical Care Medicine, Boston Children's Hospital, Boston, Massachusetts 4Department of Pediatric and Adolescent Medicine, Medical University of Vienna, Vienna, Austria 5Department of Pediatrics, NU Hospital Group, Uddevalla and Sahlgrenska Academy, Gothenburg University, Uddevalla, Sweden 6Department of Pediatrics, School of Medicine, University of Colorado, Aurora, Colorado 7Division of Endocrinology, Diabetes and Metabolism, Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, New York 8Institute of Maternal and Child Research, School of Medicine, University of Chile, Santiago, Chile Correspondence Joseph I. Wolfsdorf, Division of Endocrinology, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA. Email: [email protected] 1 | SUMMARY OF WHAT IS Risk factors for DKA in newly diagnosed patients include younger NEW/DIFFERENT age, delayed diagnosis, lower socioeconomic status, and residence in a country with a low prevalence of type 1 diabetes mellitus (T1DM). Recommendations concerning fluid management have been modified Risk factors for DKA in patients with known diabetes include to reflect recent findings from a randomized controlled clinical trial omission of insulin for various reasons, limited access to medical ser- showing no difference in cerebral injury in patients rehydrated at dif- vices, and unrecognized interruption of insulin delivery in patients ferent rates with either 0.45% or 0.9% saline.
    [Show full text]
  • A Case-Based Approach to Acid-Base Disorders
    A Case-Based Approach to Acid-Base Disorders Justin Muir, PharmD Clinical Pharmacy Manager, Medical ICU NewYork-Presbyterian Hospital Columbia University Irving Medical Center [email protected] Disclosures None Objectives At the completion of this activity, pharmacists will be able to: 1. Describe acid-base physiology and disease states that lead to acid-base disorders. 2. Demonstrate a step-wise approach to interpretation of acid-base disorders and compensatory states. 3. Analyze contemporary literature regarding the use of sodium bicarbonate in metabolic acidosis. At the completion of this activity, pharmacy technicians will be able to: 1. Explain the importance of acid-base balance. 2. List the acid-base disorders seen in clinical practice. 3. Identify potential therapies used to treat acid-base disorders. Case A 51 year old man with history of erosive esophagitis, diabetes mellitus, chronic pancreatitis, and bipolar disorder is admitted with several days of severe nausea, vomiting, and abdominal pain. 135 87 31 pH 7.46 / pCO 29 / pO 81 861 2 2 BE -3.8 / HCO - 18 / SaO 96 5.6 20 0.9 3 2 • What additional data should be obtained? • What acid base disturbance(s) is/are present? Introduction • Acid base status is tightly regulated to maintain normal biochemical reactions and organ function • Body uses multiple mechanisms to maintain homeostasis • Abnormalities are extremely common in hospitalized patients with a higher incidence in critically ill with more complex pictures • A standard approach to analysis can help guide diagnosis and treatment Important acid-base determinants Blood gas generally includes at least: Normal range Measurement Description (arterial blood) pH -log [H+] 7.35-7.45 pCO2 partial pressure of dissolved CO2 35-45 mmHg pO2 partial pressure of dissolved O2 80-100 mmHg Base excess calculated measure of metabolic acid/base deviation from normal -3 to +3 SO2 calculated measure of Hgb O2 saturation based on pO2 95-100% - HCO3 calculated measure based on relationship of pH and pCO2 22-26 mEq/L Haber RJ.
    [Show full text]
  • Metabolic Alkalosis in Adults with Stable Cystic Fibrosis Fahad Al-Ghimlas*,1, Marie E
    The Open Respiratory Medicine Journal, 2012, 6, 59-62 59 Open Access Metabolic Alkalosis in Adults with Stable Cystic Fibrosis Fahad Al-Ghimlas*,1, Marie E. Faughnan1,2 and Elizabeth Tullis1,2 1Department of Medicine, University of Toronto, Canada 2St. Michael’s Hospital, Li Ka Shing Knowledge Institute, Canada Abstract: Background: The frequency of metabolic alkalosis among adults with stable severe CF-lung disease is unknown. Methods: Retrospective chart review. Results: Fourteen CF and 6 COPD (controls) patients were included. FEV1 was similar between the two groups. PaO2 was significantly higher in the COPD (mean ± 2 SD is 72.0 ± 6.8 mmHg,) than in the CF group (56.1 ± 4.1 mmHg). The frequency of metabolic alkalosis in CF patients (12/14, 86%) was significantly greater (p=0.04) than in the COPD group (2/6, 33%). Mixed respiratory acidosis and metabolic alkalosis was evident in 4 CF and 1 COPD patients. Primary metabolic alkalosis was observed in 8 CF and none of the COPD patients. One COPD patient had respiratory and metabolic alkalosis. Conclusions: Metabolic alkalosis is more frequent in stable patients with CF lung disease than in COPD patients. This might be due to defective CFTR function with abnormal electrolyte transport within the kidney and/ or gastrointestinal tract. Keywords: Cystic fibrosis, metabolic alkalosis. BACKGROUND METHODS Cystic fibrosis (CF) is a multi-system disease that is After obtaining ethics approval, a retrospective chart and caused by mutations in a 230 kb gene on chromosome 7 database review was performed on clinically stable CF encoding 1480 aminoacid polypeptide, named cystic fibrosis patients (Toronto CF Database) and COPD patients (Chest transmembrane regulator (CFTR) [1].
    [Show full text]
  • Acid-Base Balance
    Intensive Care Nursery House Staff Manual Acid-Base Balance INTRODUCTION: The newborn infant is subject to numerous conditions that may disturb acid-base homeostasis. Management of ventilation, which controls the respiratory component of acid-base balance, is discussed in the section on Respiratory Support (P. 10). This section is a brief discussion of the metabolic aspects of acid-base balance. METABOLIC ACIDOSIS, defined as a base deficit >5 mEq/L on the first day and >4 mEq/L thereafter, occurs from: •Loss of buffer (mainly bicarbonate) or •Excess production of acid or decreased excretion of acid The anion gap is a useful calculation in assessing metabolic acidosis. + - - Anion gap = [Na ] – ([Cl ] + [HCO3 ]) Loss of buffer has no effect on anion gap. Accumulation of organic acid (e.g., lactic acid) causes an increase in anion gap. Normal anion gap: <15 mEq/L Increased anion gap: >15 mEq/L in LBW infants (<2,500 g) >18 mEq/L in ELBW infants (<1,000 g) Newborn infants normally have a base deficit of 1 to 3 mEq/L. Common causes of metabolic acidosis: •Bicarbonate loss, especially via immature kidney or from GI tract •Lactic acidosis from inadequate tissue perfusion and oxygenation (e.g., from asphyxia, shock, severe anemia, hypoxemia, PDA, NEC, excessive ventilator pressures with ↓ cardiac output) •Hypothermia •Organic acidemia due to an inborn error of metabolism (see P. 155) •Excessive Cl in IV fluids •Renal failure •Excessive acid load from high protein formula in preterm (late metabolic acidosis of prematurity ) - •Excretion of HCO3 as metabolic compensation for respiratory alkalosis Dilution acidosis is caused by excessive volume expansion (with saline, Ringer’s lactate or dextrose solutions).
    [Show full text]
  • ACS/ASE Medical Student Core Curriculum Acid-Base Balance
    ACS/ASE Medical Student Core Curriculum Acid-Base Balance ACID-BASE BALANCE Epidemiology/Pathophysiology Understanding the physiology of acid-base homeostasis is important to the surgeon. The two acid-base buffer systems in the human body are the metabolic system (kidneys) and the respiratory system (lungs). The simultaneous equilibrium reactions that take place to maintain normal acid-base balance are: H" HCO* ↔ H CO ↔ H O l CO g To classify the type of disturbance, a blood gas (preferably arterial) and basic metabolic panel must be obtained. A basic understanding of normal acid-base buffer physiology is required to understand alterations in these labs. The normal pH of human blood is 7.40 (7.35-7.45). This number is tightly regulated by the two buffer systems mentioned above. The lungs contain carbonic anhydrase which is capable of converting carbonic acid to water and CO2. The respiratory response results in an alteration to ventilation which allows acid to be retained or expelled as CO2. Therefore, bradypnea will result in respiratory acidosis while tachypnea will result in respiratory alkalosis. The respiratory buffer system is fast acting, resulting in respiratory compensation within 30 minutes and taking approximately 12 to 24 hours to reach equilibrium. The renal metabolic response results in alterations in bicarbonate excretion. This system is more time consuming and can typically takes at least three to five days to reach equilibrium. Five primary classifications of acid-base imbalance: • Metabolic acidosis • Metabolic alkalosis • Respiratory acidosis • Respiratory alkalosis • Mixed acid-base disturbance It is important to remember that more than one of the above processes can be present in a patient at any given time.
    [Show full text]
  • The Basic Principles of Acid-Base Regulation*
    The Basic Principles of Acid-Base Regulation* ORHAN MUREN, M.D. Associate Professor of Medicine and Anesthesiology, Medical College of Virginia, Health Sciences Division of Virginia Commonwealth University, Richmond, Virginia Acid-base homeostasis refers to those chemical In normal people, the concentration of H• is and physiological processes which maintain the hy­ approximately 40 nanomoles ( n moles) per liter of drogen ion (H•) activity in body fluids at the levels plasma. One nanomole equals 10-9 moles. However, compatible with life and normal functioning. This is it would be more correct to indicate the thermo­ an enormous task due to the fact that reactions which dynamic activities rather than the concentrations, produce H• and reactions which consume H• are the two being related as follows: continously occurring in human beings. On one hand there is acid production (fixed activity ----.- = activity coefficient and volatile acid) and on the other hand acid elimi­ concentration nation (fixed and volatile acid). Normally in a given time, such as in a day, acid elimination is equal At infinite dilution the activity coefficient is to acid production. Whenever there is imbalance equal to one. However, in concentrations in body between input and output, acid-base disturbances fluids, it is much less than one. The pH meter will occur. electrode responds to hydrogen ion activity and not Many biochemical processes require optimum concentration. However, it is customary to work in H• ion concentration. Changes in H• concentration concentrations, and values for the different equilib­ markedly affect the catalytic activity of enzymes. rium constants are adjusted accordingly, as indicated Myocardial and muscular contraction, vascular tone, by a prime after a symbol such as K'.
    [Show full text]
  • Acid–Base Problems in Diabetic Ketoacidosis Kamel S
    The new england journal of medicine Review Article Disorders of Fluids and Electrolytes Julie R. Ingelfinger, M.D., Editor Acid–Base Problems in Diabetic Ketoacidosis Kamel S. Kamel, M.D., and Mitchell L. Halperin, M.D. From the Renal Division, St. Michael’s his review focuses on three issues facing clinicians who care for Hospital and University of Toronto, and patients with diabetic ketoacidosis; all of the issues are related to acid–base Keenan Research Center, Li Ka Shing Knowledge Institute of St. Michael’s disorders. The first issue is the use of the plasma anion gap and the calculation Hospital, University of Toronto, Toronto. T of the ratio of the change in this gap to the change in the concentration of plasma Address reprint requests to Dr. Halperin bicarbonate in these patients; the second concerns the administration of sodium bi- at the Department of Medicine, Univer- sity of Toronto Keenan Research Center, carbonate; and the third is the possible contribution of intracellular acidosis to the Li Ka Shing Knowledge Institute of St. development of cerebral edema, particularly in children with diabetic ketoacidosis. In Michael’s Hospital, 30 Bond St., Rm. this article, we examine the available data and attempt to integrate the data with 408, Toronto, ON M5B 1W8, Canada, or at mitchell . halperin@ utoronto . ca. principles of physiology and metabolic regulation and provide clinical guidance. N Engl J Med 2015;372:546-54. DOI: 10.1056/NEJMra1207788 Plasma Bicarbonate and the Plasma Anion Gap Copyright © 2015 Massachusetts Medical Society. The accumulation of ketoacids in the extracellular fluid leads to a loss of bicarbonate anions and a gain of ketoacid anions.
    [Show full text]
  • Ketoalkalosis: Masked Presentation of Diabetic Ketoacidosis with Literature Review
    Case Report J Endocrinol Metab. 2017;7(6):194-196 Ketoalkalosis: Masked Presentation of Diabetic Ketoacidosis With Literature Review Vinod Kumara, Sushant M. Nanavatia, c, Fnu Komala, Luis Carlos Ortiza, Namrata Paula, Manhedar Kumarb, Patrick Michaela, Monisha Singhal Abstract sis would be masqueraded by alkalosis. We present a unique case of 25 years old female with DKA and alkalemia. Most dreaded complication in type 1 diabetes mellitus remains dia- betic ketoacidosis (DKA): plasma blood glucose > 250 mg/dL, serum Case Report bicarbonate < 18 mEq/L, anion gap metabolic acidosis and ketosis. Insulin deficiency with high levels of glucagon and stress hormones causing ketogenesis in liver, elevated lipolysis in peripheral tissues, and A 25-year-old female with type 1 diabetes mellitus presented increased free fatty acids contribute the formation of ketones leading with complaints of intractable vomiting, generalized weakness to metabolic acidosis. And hence DKA is also termed as ketoacidosis. and abdominal pain. Six hours prior to arrival to emergency Unusually, patients with diuretic use, alkali ingestion, intractable vom- department (ED), she started to experience diffuse abdominal iting, or hypercortisolism may present with alkalemia in DKA. Con- pain around periumbilical area and subsequently started in- traction (Metabolic) Alkalosis masquerades metabolic acidosis with tractable non-bilious vomiting. At home, she was prescribed anion gap and low to normal bicarbonate that uncovers on provision of to insulin detemir 25 units once a day along with insulin aspart intravenous fluids. We present a case of a 25-year-old female with DKA 6 units along with three meals. She stated of adherent to insu- presenting with intractable vomiting, alkalotic pH and high anion gap.
    [Show full text]
  • Metabolic Alkalosis a Brief Pathophysiologic Review
    CJASN ePress. Published on June 25, 2020 as doi: 10.2215/CJN.16041219 Metabolic Alkalosis A Brief Pathophysiologic Review Michael Emmett Abstract Metabolic alkalosis is a very commonly encountered acid-base disorder that may be generated by a variety of exogenous and/or endogenous, pathophysiologic mechanisms. Multiple mechanisms are also responsible for Divisions of Internal the persistence, or maintenance, of metabolic alkalosis. Understanding these generation and maintenance Medicine and mechanisms helps direct appropriate intervention and correction of this disorder. The framework utilized in Nephrology, Department of this review is based on the ECF volume-centered approach popularized by Donald Seldin and Floyd Rector in Medicine, Baylor the 1970s. Although many subsequent scientific discoveries have advanced our understanding of the University Medical pathophysiology of metabolic alkalosis, that framework continues to be a valuable and relatively Center at Dallas, straightforward diagnostic and therapeutic model. Dallas, Texas CJASN 15: ccc–ccc, 2020. doi: https://doi.org/10.2215/CJN.16041219 Correspondence: Dr. Michael Emmett, Department of Medicine, Baylor Introduction profile, or Gamblegram (Figure 2), shows why the 2 University Medical Metabolic alkalosis is a primary acid-base disorder increased [HCO3 ] must be accompanied by a re- Center at Dallas, 3500 that increases the serum bicarbonate concentration duction of [Cl2](independentof[Na1]), a reduction Gaston Avenue, Room 2 [HCO3 ] (this is usually approximated by its surro- of the [AG2], or both (7,8). In fact, metabolic alkaloses H-102, Dallas, TX 2 75246-2096. Email: gate the venous total [CO2]) above 30 meq/L (1), reproducibly increase the [AG ] to a small degree, 1 Michael.Emmett@ causing the arterial blood [H ]tofall,i.e., the arterial mostly owing to increased negative charge density of BSWHealth.org blood pH increases into the alkaline range (.7.45).
    [Show full text]
  • Management of Critically Ill Patients David Tofovic 34 Y.O
    Management of Critically Ill Patients David Tofovic 34 y.o. M • Presents with to the ED via EMS. • Per Brother/Chart Review: • Unable to provide history. • PMHx: SLE, Type 1 Diabetes (well controlled) • PSHx: Tonsillectomy, Insulin Pump (recently • Last seen earlier that morning by neighbor. removed) • Sister states she found him down at home. • Allergies: NKDA • Home Meds • Started CPR, neighbor called 911. • Prednisone (unknown dose or duration) • Sister is a nurse, believed that she couldn’t • Cellcept (mycophenolate) feel a pulse • Glargine • Lispro • Complained of “cold and and a bad cough” • SHx: No tobacco, no EtOH, no illicits several days prior. • FHx: SLE, HTN, DLD, stroke • Initial rhythm: asystole • Epi x 1 • ROSC 34 y.o. M • Vitals: • Physical Exam: • T: 38.3°C • General: nonresponsive • HR: 130s • BP: 76/44 • CVS: RRR, no m/r/g/c • RR: 24 • Lung: tachypnea, coarse breathe • Pox: 88% on bag and mask sounds bilaterally • Per EMR: Wgt 88 kgs • Neuro: PERRL, GCS 7 • Per EMR: Hgt 184 cm • Extremities: Radial, DP and PT 2+, no lower extremity pitting edema • Skin: No rashes, no ulcers 34 y.o. M • CBC: 13>17&50.1<294 • RFP: 122/7.3/81/5/74/5.53/1369 • Ca/Mg/Phos: 7.8/2.24/3.3 • INR/PTT: 2.2/64 • LFT • AST ~2100 • ALT ~1800 • ALKPHOS >3000 • Tbili: 6.5 • Dbili:4.1 • Alb: 3.3 • Tp: 6.4 • ABG: 6.9/55/18/3.1 • Lactate: 4.8 • Beta-hydroxybutyrate: 6.3 What’s wrong? systems systems Systems Based • CVS • Infectious • Pulmonary • Heme • Neuro/Psych • Supportive (FASTHUGS BID) • GU • Lines • GI • CODE • Endo/Rheum • Dispo • Infectious • PT/OT • Heme Procotalized Medicine You don’t look so good.
    [Show full text]