Problem-Based Review: a Patient with Metabolic Acidosis

Total Page:16

File Type:pdf, Size:1020Kb

Problem-Based Review: a Patient with Metabolic Acidosis Acute Medicine 2012 11(4): 251-256 251 Trainee Section Problem-Based Review: A patient 251 with metabolic acidosis saf R Allan & C Foster Abstract Metabolic acidosis is a common metabolic derangement present in the acute medical patient. A thorough and structured investigative approach is required as there are many causes and management is reliant on identifying these. In particular calculation of the anion gap with correction for albumin level and use of the delta ratio can be helpful in complex cases especially in patients where a combination of metabolic derangements may be present. Keywords metabolic acidosis, anion gap, delta ratio, renal tubular acidosis, bicarbonate Key points • Calculation of the anion gap is crucial in identifying the cause of metabolic acidosis. • Metabolic acidosis is often multi-factorial and the delta ratio calculation can be useful in identifying situations where a normal gap acidosis coexists with a raised anion gap cause. • Identification of the specific cause(s) of metabolic acidosis is vital as this will usually guide treatment. • Bicarbonate treatment has a role in some cases but adverse effects should be considered. Case Vignette Although the anion gap calculation will narrow A 37 year old male with no past medical history presents our differential (Table 2), many possible explanations to the acute medical unit (AMU) with a history of general for the acidosis remain, especially when the gap is deterioration in health over the last 8 months. He has lost 10 high. The mnemonic MUDPILERS (Methanol, kg of weight and has severe fatigue. More recently he describes a Uraemia, Diabetic Ketoacidosis or other causes Table 1. arterial blood gas of patient in case vignette Table 2. Causes of Metabolic Acidosis according to Anion Gap1,2,3,4,5 pH 7.2 Raised anion gap Normal anion gap pCO 2.6kPa 2 - Renal failure HCO3 loss HCO3 8mmol/l Ketoacidosis GI – diarrhoea, ileus, pO 15kPa (on room air) 2 (DKA,sarvation,alcohol) pancreato- or uretero fistula feeling of breathlessness. A blood gas is performed (see Table 1). Paraldyhyde, Toluene, Type 2 – Renal Tubular Iron,Tricyclics, Isoniazid Acidosis (RTA) What are the potential causes of this acidosis and how can these be further classified? Ethylene Glycol, Ethanol, Acetazolamide Methanol The low bicarbonate and low carbon dioxide is consistent with a metabolic acidosis with an attempt Lactate (type A or B), D Addition of chloride at respiratory compensation. The differential for lactate (short bowel) (e.g. 0.9% saline use) Russell Allan ST5 Acute Medicine, a diagnosis that explains this finding remains large Rhabdomyolysis Failure to secrete H+ Western Infirmary, but can be narrowed significantly by calculating the Type 1 RTA Glasgow anion gap using the following equation: Email: russellallan@doctors. Type 4 RTA org.uk + + - - Type 3 RTA Anion gap (AG) = (Na + K ) – (HCO3 + Cl ) Hypoaldosteronism Christopher Foster [Normal range – 10-20 (on old colorimetry (1o/2o), Consultant Acute Medicine, Royal Alexandra Hospital, measurements); 3-11 (on modern ion-selection electrode Tubulo-interstital renal Paisley. measurements)] disease Email: cjfoster@doctors. org.uk © 2012 Rila Publications Ltd. 252 Acute Medicine 2012; 11(4): 251-256 Problem-Based Review: A patient with metabolic acidosis of ketoacidosis, Paraldyhyde, Iron/Isoniazid, expressed by the delta gap and delta ratio, calculated Lactate, Ethylene glycol/Ethanol, Rhabdomyolysis, using the following formulae: Salicylate) may be helpful. What else can influence the anion gap? Delta gap (ΔAG) = (Calculated AG – 12) – The anion gap can also be expressed as: (24 – measured HCO3) Delta ratio = (Calculated AG – 12) / (24 – Unmeasured anions – Unmeasured cations measured HCO3) This demonstrates how an anion gap can be high The delta ratio should be approximately balanced if or low in the absence of an acidosis. The major a pure raised anion gap (AG) acidosis exists (ratio of anion that can act in this way is albumin. A low or between 1-2) high anion gap will result, depending on whether A delta gap > 6 (or ratio > 2) suggests a concurrent the albumin level is lower or higher than normal, metabolic alkalosis (or chronic respiratory acidosis), respectively. When calculating an anion gap we A delta gap < -6 (or ratio <1) suggests there is also can adjust for an abnormal albumin by using the a concurrent normal AG metabolic acidosis4,5 following equation:6 His corrected anion gap is calculated at 20 and the cause Corrected anion gap = 0.25 x (40 – albumin (g/l)) of this elevation is found to be due to ketones identified in + anion gap (AG) his urine. His blood glucose is elevated at 28mmol/l and as a result, a diagnosis of type 1 diabetes is made with a Any other ion not represented in the AG equation first presentation of DKA. His delta ratio is calculated at can influence the gap but this is usually to a lesser 0.5 suggesting the co-existing presence of a normal anion degree than that seen with albumin. As well as gap acidosis. The treating physicians are aware that there the anion, phosphate, and cations, magnesium is a potential connection between diabetes and renal tubular and calcium, we must consider the presence of acidosis and plan to explore this possibility. other charged particles not present in normal What is meant by the term renal tubular acidosis circumstances. Paraproteins seen in myeloma and (RTA)? other gammopathies can be positively or negatively RTAs by definition are a group of disorders with charged and lithium has a positive charge resulting dysfunction of renal tubule acidification mechanisms in a low AG when taken in excess. Rarely the AG but well preserved glomerular filtration rate. Table 3 can even become negative, a phenomenon that is describes the RTA types and the differential causes most likely to be seen with lab errors – for example, for a normal anion gap acidosis,highlighting any chloride level can be over-estimated in the presence differences which will aid diagnosis. of bromide containing drugs, hyperlipidaemia or In type 2 RTA, it is the proximal tubule HCO – salicylate poisoning. 3 reabsorption that malfunctions. Clearly this results in - How will we know if there is more than one disorder a high loss of HCO3 in the urine. However, distal present? tubular reabsorption does still occur, resulting in a – When a raised AG cause is found we should continue serum acidosis with a [HCO3 ] that rarely falls below – to explore for other metabolic derangements. This 12. When the serum [HCO3 ] falls it means less is will involve testing for other anions that may have filtered and, as a result, less is present in the tubular accompanied an acid (e.g. lactate, ketones etc.) and lumen. For this reason, the high urinary pH and high – also calculating the delta ratio. [HCO3 ] in the urine may not be obvious until the – serum [HCO3 ] is normalised. In fact, the urine pH What is the Delta ratio and how can it be calculated? can be <5.3 when an equilibrium has been established. It should be appreciated that where the AG is The proximal tubular reabsorption defect may not – increased, the degree of change from a normal gap be unique to HCO3 and often is accompanied by reflects the quantity of non-chloride anion added. that of glucose, phosphate, urate, potassium and This anion will have an accompanying H+, each of others. The obvious treatment for this should be to which will be buffered by a bicarbonate ion. It follows replace the deficit using high doses of bicarbonate. that the change in the anion gap (ΔAG) from that The correction of the acidosis can be problematic as - individual’s normal and the change in the HCO3 it will cause the already hypokalaemic state to worsen - concentration (ΔHCO3 ) from that individual’s further. Potassium must therefore always be replaced normal should be approximately the same. Where along with alkalinization therapy. In adults, the most the ΔAG is significantly less than the measured common cause of type 2 RTA is myeloma and this - 6 ΔHCO3 , a coexistent normal AG acidosis should should therefore always be considered . be considered. Where the ΔAG is significantly more In type 1 RTA, the deficient mechanism is at - + than the measured ΔHCO3 , the coexisting presence the terminal tubule involving the excretion of H . – of a metabolic alkalosis may be present. This can be In comparison to type 2 RTA, the serum [HCO3 ] © 2012 Rila Publications Ltd. Acute Medicine 2012; 11(4): 251-256 253 Problem-Based Review: A patient with metabolic acidosis Table 3.1,7Classification and causes of Renal Tubular Acidosis Type 1 RTA Type 2 RTA GI HCO3 loss Tubulo- RTA T4 interstital disease Mechanism Defect exists at Defect exists Gastrointestinal In renal Aldosterone the distal tubule in the proximal loss of failure, failure resistance/ + preventing H tubule preventing bicarbonate ions to filter deficiency - secretion. reabsorption of HCO3 sulphuric acid (+/-glucose, amino is the main acids,phosphate,K+etc) mechanism for acidosis (high AG). When glomerulus intact but tubules affected only H+ secretion fails (i.e. normal AG) Causes Autoimmune Usually Myeloma in Gastroenteritis, Multiple Hypoadrenalism disease (esp. adults IBD, causes (1oor2oto Sjögrens (Fanconi syndrome in Ureteric or hyporeninaemia), syndrome), children) pancreatic fistula, CKD (esp. Renal transplant, Endocrinecasues Diabetic obstructive nephropathy), uropathy, Sickle Congenital cell disease, resistance cirrhosis Serum [K+] Low and Low and worsens as Low Often low High improves as acidosis is corrected acidosis does (can be high) Serum Very low ~12-20 Mild decrease Mild decrease [HCO3] (Often <10) only (usually > 17) Urinary pH Always > 5.5. Often < 5.5. Increases to < 5.3 Variable < 5.5 Can’t acidify >7.5 when bicarbonate urine infused Associations Nephrocalcinosis, Rickets/ osteomalacia Features of calcium stones cause Renal Usually normal Usually normal Can be Often Normal unless function deranged if also deranged cause is hypovolaemic CKD causing aldosterone resistance can fall significantly and be less than 10.
Recommended publications
  • Severe Metabolic Acidosis in a Patient with an Extreme Hyperglycaemic Hyperosmolar State: How to Manage? Marloes B
    Clinical Case Reports and Reviews Case Study ISSN: 2059-0393 Severe metabolic acidosis in a patient with an extreme hyperglycaemic hyperosmolar state: how to manage? Marloes B. Haak, Susanne van Santen and Johannes G. van der Hoeven* Department of Intensive Care Medicine, Radboud University Medical Center, Nijmegen, the Netherlands Abstract Hyperglycaemic hyperosmolar state (HHS) and diabetic ketoacidosis (DKA) are often accompanied by severe metabolic and electrolyte disorders. Analysis and treatment of these disorders can be challenging for clinicians. In this paper, we aimed to discuss the most important steps and pitfalls in analyzing and treating a case with extreme metabolic disarrangements as a consequence of an HHS. Electrolyte disturbances due to fluid shifts and water deficits may result in potentially dangerous hypernatriema and hyperosmolality. In addition, acid-base disorders often co-occur and several approaches have been advocated to assess the acid-base disorder by integration of the principles of mass balance and electroneutrality. Based on the case vignette, four explanatory methods are discussed: the traditional bicarbonate-centered method of Henderson-Hasselbalch, the strong ion model of Stewart, and its modifications ‘Stewart at the bedside’ by Magder and the simplified Fencl-Stewart approach. The four methods were compared and tested for their bedside usefulness. All approaches gave good insight in the metabolic disarrangements of the presented case. However, we found the traditional method of Henderson-Hasselbalch and ‘Stewart at the bedside’ by Magder most explanatory and practical to guide treatment of the electrolyte disturbances and in exploring the acid-base disorder of the presented case. Introduction This is accompanied by changes in pCO2 and bicarbonate (HCO₃ ) levels, depending on the cause of the acid-base disorder.
    [Show full text]
  • PHAR 503 Exam 2
    PHAR 503 Exam 2 Rho Chi Acid-Base Disorders Which medication would most likely NOT lead to a metabolic alkalosis? A. Loop Diuretic B. Thiazide Diuretic C. Desmopressin D. Citrate Which medication would most likely NOT lead to a metabolic alkalosis? A. Loop Diuretic B. Thiazide Diuretic C. Desmopressin D. Citrate Diuretics increase loss of H+, vomiting, hypokalemia, citrate is metabolized to HCO3- A patient suffering from an acute panic attack might be at risk for developing: A. Respiratory alkalosis B. Metabolic alkalosis C. Respiratory Acidosis D. Metabolic Acidosis A patient suffering from an acute panic attack might be at risk for developing: A. Respiratory alkalosis B. Metabolic alkalosis C. Respiratory Acidosis D. Metabolic Acidosis Hyperventilating -> blowing off CO2 (acid) If you have a patient who is experiencing a respiratory acidosis, which of the following sets of labs would most likely match the patient? A. pH: 7.41, HCO3-: 20 B. pH: 7.35, CO2: 52 C. pH: 7.35, HCO3-: 20 D. pH: 7.45, CO2: 32 If you have a patient who is experiencing a respiratory acidosis, which of the following sets of labs would most likely match the patient? A. pH: 7.41, HCO3-: 20 B. pH: 7.35, CO2: 52 C. pH: 7.35, HCO3-: 20 D. pH: 7.45, CO2: 32 Metabolic: HCO3- abnormalities, respiratory: PaCO2 What is the normal range for PaCO2? What is the normal range for HCO3-? What is the normal range for PaCO2? 35-45 (40!) What is the normal range for HCO3-? 22-26 (24!) ROME Respiratory Opposite: PaCo2 and pH go in opposite directions Metabolic Equal: HCO3- and pH go in the same direction Which of the following would NOT cause a metabolic acidosis? A.
    [Show full text]
  • Diabetic Ketoalkalosis in Children and Adults
    Original Article Diabetic Ketoalkalosis in Children and Adults Emily A. Huggins, MD, Shawn A. Chillag, MD, Ali A. Rizvi, MD, Robert R. Moran, PhD, and Martin W. Durkin, MD, MPH and DR are calculated because the pH and bicarbonate may be near Objectives: Diabetic ketoacidosis (DKA) with metabolic alkalosis normal or even elevated. In addition to having interesting biochemical (diabetic ketoalkalosis [DKALK]) in adults has been described in the features as a complex acid-base disorder, DKALK can pose diagnostic literature, but not in the pediatric population. The discordance in the and/or therapeutic challenges. change in the anion gap (AG) and the bicarbonate is depicted by an Key Words: delta ratio, diabetic ketoacidosis, diabetic ketoalkalosis, elevated delta ratio (DR; rise in AG/drop in bicarbonate), which is metabolic alkalosis normally approximately 1. The primary aim of this study was to de- termine whether DKALK occurs in the pediatric population, as has been seen previously in the adult population. The secondary aim was iabetic ketoacidosis (DKA), a common and serious dis- to determine the factors that may be associated with DKALK. Dorder that almost always results in hospitalization, is de- Methods: A retrospective analysis of adult and pediatric cases with a fined by the presence of hyperglycemia, reduced pH, metabolic 1 primary or secondary discharge diagnosis of DKA between May 2008 and acidosis, elevated anion gap (AG), and serum or urine ketones. August 2010 at a large urban hospital was performed. DKALK was as- In some situations, a metabolic alkalosis coexists with DKA sumedtobepresentiftheDRwas91.2 or in cases of elevated bicarbonate.
    [Show full text]
  • ABG Analysis in Clinical Setting
    CHAPTER ABG Analysis in Clinical Setting 117 Rajesh Mahajan, Suman Sethi INTRODUCTION defined by the ratio of PCO2 to HCO3 and not by absolute Acid-Base balance is an intricate concept which requires an value of either one alone.5,6 intimate and detailed knowledge of the body’s metabolic Overview of Fundamentals of Acid-Base Disorder pathways used to eliminate the H+ ion. Accurately Normal metabolism of proteins and nucleotides generates interpreting acid-base balance requires simultaneous about 100 mmol H+ per day in the form of sulphuric and measurements of arterial pH and plasma electrolytes, phosphoric acids. By comparison, hydration of CO2 to as well as knowledge of compensatory physiologic form H CO generates 12,500 mmol H+ per day. mechanisms. In this article, we’ll review normal acid-base 2 3 physiology, acid-base disturbances, and lab techniques Carbon dioxide transport and mathematical calculations used to identify the cause 1. Transport of carbon dioxide in the blood is of acid-base derangements. considerably more complex. A small portion of carbon dioxide, about 5 percent, remains BASIC PHYSIOLOGY unchanged and is transported dissolved in blood. Acid-base Chemistry 2. The remainder is found in reversible chemical pH combinations in red blood cells or plasma. Some The concept of pH was put forward by the Danish chemist, carbon dioxide binds to blood proteins, principally Soren Peter Sorensen in 1909 to refer to the negative hemoglobin, to form a compound known as logarithm of hydrogen ion (H+) concentration. An increase carbamate. in the pH indicates a proportionate decrease in the 3., About 88 percent of carbon dioxide in the blood is [H+] and a decrease in the pH indicates a proportionate in the form of bicarbonate ion.
    [Show full text]
  • Acid-Base Disorders in Patients with Chronic Obstructive Pulmonary Disease: a Pathophysiological Review
    Hindawi Publishing Corporation Journal of Biomedicine and Biotechnology Volume 2012, Article ID 915150, 8 pages doi:10.1155/2012/915150 Review Article Acid-Base Disorders in Patients with Chronic Obstructive Pulmonary Disease: A Pathophysiological Review Cosimo Marcello Bruno and Maria Valenti Department of Internal Medicine and Systemic Diseases, University of Catania, 95100 Catania, Italy Correspondence should be addressed to Cosimo Marcello Bruno, [email protected] Received 29 September 2011; Accepted 26 October 2011 Academic Editor: Saulius Butenas Copyright © 2012 C. M. Bruno and M. Valenti. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The authors describe the pathophysiological mechanisms leading to development of acidosis in patients with chronic obstructive pulmonary disease and its deleterious effects on outcome and mortality rate. Renal compensatory adjustments consequent to acidosis are also described in detail with emphasis on differences between acute and chronic respiratory acidosis. Mixed acid-base disturbances due to comorbidity and side effects of some drugs in these patients are also examined, and practical considerations for a correct diagnosis are provided. 1. Introduction However, an alteration in respiratory exchanges, as occurs in advanced phase of COPD, results in retention of CO2. Chronic obstructive pulmonary disease (COPD) is a major Carbon dioxide is then hydrated with the formation of public health problem. Its prevalence varies according to carbonic acid that subsequently dissociates with release of country, age, and sex. On the basis of epidemiologic data, hydrogen ions (H+) in the body fluids according to the fol- the projection for 2020 indicates that COPD will be the lowing equation: third leading cause of death worldwide and the fifth leading − + cause of disability [1].
    [Show full text]
  • PGE2 EP1 Receptor Inhibits Vasopressin-Dependent Water
    Laboratory Investigation (2018) 98, 360–370 © 2018 USCAP, Inc All rights reserved 0023-6837/18 PGE2 EP1 receptor inhibits vasopressin-dependent water reabsorption and sodium transport in mouse collecting duct Rania Nasrallah1, Joseph Zimpelmann1, David Eckert1, Jamie Ghossein1, Sean Geddes1, Jean-Claude Beique1, Jean-Francois Thibodeau1, Chris R J Kennedy1,2, Kevin D Burns1,2 and Richard L Hébert1 PGE2 regulates glomerular hemodynamics, renin secretion, and tubular transport. This study examined the contribution of PGE2 EP1 receptors to sodium and water homeostasis. Male EP1 − / − mice were bred with hypertensive TTRhRen mice (Htn) to evaluate blood pressure and kidney function at 8 weeks of age in four groups: wildtype (WT), EP1 − / − , Htn, HtnEP1 − / − . Blood pressure and water balance were unaffected by EP1 deletion. COX1 and mPGE2 synthase were increased and COX2 was decreased in mice lacking EP1, with increases in EP3 and reductions in EP2 and EP4 mRNA throughout the nephron. Microdissected proximal tubule sglt1, NHE3, and AQP1 were increased in HtnEP1 − / − , but sglt2 was increased in EP1 − / − mice. Thick ascending limb NKCC2 was reduced in the cortex but increased in the medulla. Inner medullary collecting duct (IMCD) AQP1 and ENaC were increased, but AVP V2 receptors and urea transporter-1 were reduced in all mice compared to WT. In WT and Htn mice, PGE2 inhibited AVP-water transport and increased calcium in the IMCD, and inhibited sodium transport in cortical collecting ducts, but not in EP1 − / − or HtnEP1 − / − mice. Amiloride (ENaC) and hydrochlorothiazide (pendrin inhibitor) equally attenuated the effect of PGE2 on sodium transport. Taken together, the data suggest that EP1 regulates renal aquaporins and sodium transporters, attenuates AVP-water transport and inhibits sodium transport in the mouse collecting duct, which is mediated by both ENaC and pendrin-dependent pathways.
    [Show full text]
  • University of Huddersfield Repository
    University of Huddersfield Repository Aburas, Omaro A Emhmed Investigation of aldehyde oxidase and xanthine oxidoreductase in rainbow trout (Oncorhynchus mykiss) Original Citation Aburas, Omaro A Emhmed (2014) Investigation of aldehyde oxidase and xanthine oxidoreductase in rainbow trout (Oncorhynchus mykiss). Doctoral thesis, University of Huddersfield. This version is available at http://eprints.hud.ac.uk/23543/ The University Repository is a digital collection of the research output of the University, available on Open Access. Copyright and Moral Rights for the items on this site are retained by the individual author and/or other copyright owners. Users may access full items free of charge; copies of full text items generally can be reproduced, displayed or performed and given to third parties in any format or medium for personal research or study, educational or not-for-profit purposes without prior permission or charge, provided: • The authors, title and full bibliographic details is credited in any copy; • A hyperlink and/or URL is included for the original metadata page; and • The content is not changed in any way. For more information, including our policy and submission procedure, please contact the Repository Team at: [email protected]. http://eprints.hud.ac.uk/ Investigation of aldehyde oxidase and xanthine oxidoreductase in rainbow trout (Oncorhynchus mykiss) Omaro Aburas B.Sc., M.Sc. Department of Chemical and Biological Science University of Huddersfield United Kingdom Thesis submitted in partial fulfilment of the requirements for the Degree of Doctor of Philosophy July 2014 Abstract Molybdo-flavoenzymes (MFEs), aldehyde oxidase (AOX) and xanthine oxidoreductase (XOR) are involved in the oxidation of N-heterocyclic compounds and aldehydes, many of which are environmental pollutants, drugs and vitamins.
    [Show full text]
  • Acid Base Cover.Cdr
    Workshop on Electrolyteand Acid-BaseDisturbances Organisers AKAgarwal,RKSingal Editor PraveenAggarwal Governing Body of Association of Physicians of India PresidentElect President PastPresident AKAgarwal, NewDelhi(2009) SKBichile,(Mumbai 2009) RKSingal,(NewDelhi 2009) Vice Presidents BRBansode,(Mumbai 2009) PritamGupta,(NewDelhi 2010) AlakaDeshpande,(Mumbai 2011) Hon.General Secretary Sandhya Kamath,(Mumbai 2010) Hon.Treasurer Milind Y Nadkar,(Mumbai 2009) Members ShyamSundar,(Varanasi 2009) RohiniHanda,(NewDelhi 2010) NarinderPalSingh,(NewDelhi 2011) YSatyanarayanRaju,(Hyderabad 2009) AmalKumarBanerjee,(Howrah 2010) MadhukarRai,(Varanasi 2011) JMukhopadhyay,(Howrah 2009) RSajithkumar,(Kottayam 2010) SurendraDaga,(Kolkata 2011) NKSingh,(Dhanbad 2009) AbhayNRai,(Gaya 2010) SArulrhaj,(Tuticorin 2011) Zonal Members NorthZone–RajeshUpadhyay,(NewDelhi 2011) MidSouthZone–GNarsimulu,(Hyderabad 2011) NorthWestZone–GurpreetSWander,(Ludhiana 2011) SouthZone–AMuruganathan,(Tirupur 2011) CentralZone–SanjivMaheshwari,(Ajmer 2011) MidEastZone–KamleshTewary, Muzaffarpur( 2011) WestZone–AshitBhagwati,(Mumbai 2011) EastZone–SamarKumarBanerjee,(Kolkata 2011) Ex Officio Member Dean ICP AK Das, Pondicherry Invited Members Hon.Editor,JAPI APIHouseChairman Editor-in-chief,APITextBook ShashankRJoshi, Mumbai SiddharthNShah, Mumbai YPMunjal, NewDelhi Co-opted Members Jt.Secretary, President’sPlace ArmedForces, MedicalServices Jt.Secretary(HQ) JMPhadtare, Mumbai(2009) Lt.Gen.SRMehta,(NewDelhi 2007-2008) FalguniParikh, Mumbai OrganisingSecretary, APICON2008 OrganisingSecretary,
    [Show full text]
  • Controversies in the Management of Aneurysmal Subarachnoid Hemorrhage*
    Controversies in the management of aneurysmal subarachnoid hemorrhage* Neeraj S. Naval, MD; Robert D. Stevens, MD; Marek A. Mirski, MD, PhD; Anish Bhardwaj, MD, FCCM Background: The care of patients with aneurysmal subarach- Data Source: Search of MEDLINE and Cochrane databases and noid hemorrhage has evolved significantly with the advent of new manual review of article bibliographies. diagnostic and therapeutic modalities. Although it is believed that Data Synthesis and Conclusions: Many aspects of care in these advances have contributed to improved outcomes, consid- patients with aneurysmal subarachnoid hemorrhage remain erable uncertainty persists regarding key areas of management. highly controversial and warrant further resolution with hypoth- Objective: To review selected controversies in the manage- esis-driven clinical or translational research. It is anticipated that ment of aneurysmal subarachnoid hemorrhage, with a special the rigorous evaluation and implementation of such data will emphasis on endovascular vs. surgical techniques for securing provide a basis for improvements in short- and long-term out- aneurysms, the diagnosis and therapy of cerebral vasospasm, comes. (Crit Care Med 2006; 34:511–524) neuroprotection, antithrombotic and anticonvulsant agents, cere- KEY WORDS: aneurysm; subarachnoid; hemorrhage; vasospasm; bral salt wasting, and myocardial dysfunction, and to suggest ischemia venues for further clinical investigation. he rupture of an intracranial sepsis, and thromboembolism. As many and management of cerebral vasospasm, aneurysm may be associated of these complications are life-threaten- neuroprotective strategies, use of anti- with an array of severe distur- ing but reversible, it is widely believed thrombotic agents (thrombolytic agents, bances in intracranial and sys- that patients with aSAH can benefit from heparin, and platelet inhibitors), prophy- Ttemic physiology that represent a unique laxis of seizures, and the approach to ce- management in an intensive care setting.
    [Show full text]
  • 1. Regarding Targeted Temperature Management TTM After Cardiac Arrest A) TTM Should Be Implemented for at Least 72 Hours After
    1. Regarding targeted temperature management TTM after cardiac arrest a) TTM should be implemented for at least 72 hours after arrest b) Target temperature should be between 32 and 36 degrees c) Rapid infusion of 60ml/kg of IV iced normal saline should be used after ROSC d) Once TTM period is finished, there is no guide on what temperatures should be kept at if a patient remains comatosed 2. Which of the following is incorrect in describing renal handling of acid base balance a) Renal tubular acidosis type 1 distal inhibits H+ extrusion and serum bicarb decreases to a steady state level b) 15% of bicarbonate reclamation occurs in the distal tubule c) If serum is acidotic, formation of new bicarbonate in the distal tubule to may take up to 4 -5 days to reach equilibrium d) Ammonia has no effect on acid excretion 3. Regarding acid and base compensation which is correct a) Correlation between venous and arterial pH is poor especially in DKA b) Compensation in chronic respiratory alkalosis may be efficient enough to normalize pH c) A patient cannot have a normal pH if there is a disease process causing metabolic acidosis d) In an ABG with a high pH, acidosis can be excluded 4. When calculating the anion gap a) Measured values of K is always needed to accurately calculate anion gap b) Anion gap > 12 is always abnormal c) Most of the normal anion gap in healthy individuals consists of albumin d) Anion gap cannot be normal if there is an elevated lactate 5.
    [Show full text]
  • Mechanisms of Vascular Smooth Muscle Contraction and the Basis for Pharmacologic Treatment of Smooth Muscle Disorders
    1521-0081/68/2/476–532$25.00 http://dx.doi.org/10.1124/pr.115.010652 PHARMACOLOGICAL REVIEWS Pharmacol Rev 68:476–532, April 2016 Copyright © 2016 The Author(s) This is an open access article distributed under the CC-BY Attribution 4.0 International license. ASSOCIATE EDITOR: STEPHANIE W. WATTS Mechanisms of Vascular Smooth Muscle Contraction and the Basis for Pharmacologic Treatment of Smooth Muscle Disorders F.V. Brozovich, C.J. Nicholson, C.V. Degen, Yuan Z. Gao, M. Aggarwal, and K.G. Morgan Department of Health Sciences, Boston University, Boston, Massachusetts (C.J.N., Y.Z.G., M.A., K.G.M.); Department of Medicine, Mayo Clinic, Rochester, Minnesota (F.V.B.); and Paracelsus Medical University Salzburg, Salzburg, Austria (C.V.D.) Abstract ...................................................................................478 I. Introduction . ..............................................................................478 A. Scope and Limitations..................................................................478 B. Overview of Regulation of Blood Pressure/Vascular Tone. ...............................478 1. Guyton View of Regulation Blood Pressure, Kidney Role, Volume Regulation. .......478 2. Recent Direct Confirmation of Changes in Vascular Tone/Resistance Related to Changes in Systemic Vascular Resistance and Blood Pressure and Downloaded from the Importance of Vascular Smooth Muscle Contraction in both Normal Physiology and Pathophysiology—Hypertension......................................479 3. Racial Differences/Personalized
    [Show full text]
  • Chloride and Its Clinical Implications in Today's Clinical Practice: Not an Orphan Electrolyte
    rology & h T ep h e Goel, J Nephrol Ther 2015, 5:6 N r f a o p l e a u DOI: 10.4172/2161-0959.1000223 n t r i c u s o J ISSN: 2161-0959 Journal of Nephrology & Therapeutics Review Article Open Access Chloride and its Clinical Implications in Today’s Clinical Practice: Not an Orphan Electrolyte Narender Goel* Middletown Medical PC, 111, Maltese Drive, Middletown NY, USA; Consultant at Orange Regional Medical Center, NY, USA; Adjunct Clinical Assistant Professor (Internal Medicine and Nephrology) at Touro College of Osteopathic Medicine, New York, USA Abstract Though chloride is the predominant extracellular anion, it is mostly seen just as an anion accompanying sodium and hardly receives attention in textbooks. But independent evaluation of serum chloride may unearth several clinical and acid-base disorders. It is used in formulas to estimate serum anion gap, urine anion gap, and strong ion difference (Stewart method). Several critical functions of a cell such as maintenance of cell volume, neutralization of H+ in lysosomal vesicles, epithelial fluid transport, change in cell membrane potential and ligand-gated transmission in the post-synaptic membrane utilize chloride channels. In addition, chloride forms an integral part of anion exchanger proteins coded by SLC26A gene family. Chloride is an essential component of intravenous fluids used in day-to-day clinical practice. The role and contribution of chloride rich fluids and resulting acidosis in causing inferior outcomes in sepsis, renal vasoconstriction, and acute kidney injury has been debated. Numerous genetic diseases are known to be related with chloride channels and proteins abnormalities.
    [Show full text]