Controversies in the Management of Aneurysmal Subarachnoid Hemorrhage*

Total Page:16

File Type:pdf, Size:1020Kb

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. challenge to the clinician. Surgical man- Recent years have seen a considerable rebral salt wasting and to cardiac dys- agement has traditionally emphasized the expansion in the use of image-guided en- function after aSAH. For each prevention of renewed intracranial bleed- dovascular therapies for aSAH, including controversy, a critical evaluation of the ing by clipping or wrapping the respon- coiling of aneurysms and balloon angio- available evidence is coupled with recom- sible aneurysm. Medical management is plasty or intraarterial drug delivery for mendations for further clinical investiga- based on the detection and treatment of cerebral vasospasm (1–4). These ad- tion. The review is selective, focusing on cerebral and extracerebral complications vances have occurred in a general setting the principal debates at the expense of of aneurysmal subarachnoid hemorrhage of increasing knowledge of aSAH epide- other equally important but arguably less (aSAH). Cerebral complications of aSAH miology, pathophysiology, diagnosis, and controversial issues (e.g., post-aSAH hy- include recurrent intracranial hemor- prevention and of significant refinements drocephalus and ventricular drainage). rhage, vasospasm, cerebral infarction, hy- in microsurgical technique and in medi- drocephalus, cerebral edema, and intra- cal therapy. There is a widespread percep- cranial hypertension; extracerebral Controversy 1: Surgical vs. tion that this broader understanding and Endovascular Aneurysm Repair complications include respiratory failure, expertise is yielding benefits in the form derangements of water and electrolyte of improved outcome after aSAH. Indeed, Endovascular coiling emerged as an homeostasis, myocardial dysfunction, a progressive increase in aSAH survival alternative to surgery in patients with over the past three decades has been re- intracranial aneurysms who were deemed ported in several studies (5–7). However, poor surgical candidates due to signifi- *See also p. 571. evidence of a direct relationship between cant neurologic injury, the presence of From the Division of Neurosciences Critical Care, aSAH outcomes and a specific strategy or severe medical co-morbidities, or difficult Departments of Neurology, Anesthesiology/Critical Care Medicine, and Neurological Surgery, Johns Hop- intervention is limited (2, 3, 8, 9). In surgical access to the aneurysm (1). More kins University School of Medicine, Baltimore, MD. several key areas of management, sup- recent work has sought to extend the Supported, in part, by U.S. Public Health Service porting data are lacking or equivocal in indications of endovascular coiling to National Institutes of Health NS NS046379 and by an nature, generating uncertainty and con- other patient categories. In a small ran- Established Investigator Grant (A. Bhardwaj) from the troversy among clinicians. American Heart Association. domized trial of 109 patients with aSAH, The authors have no financial interests to disclose. This review focuses on controversies 3- and 12-month clinical and neuropsy- Copyright © 2006 by the Society of Critical Care that are central to the acute management chological outcomes were the same be- Medicine and Lippincott Williams & Wilkins of aSAH. These include surgical vs. endo- tween the surgical group and the endo- DOI: 10.1097/01.CCM.0000198331.45998.85 vascular aneurysm repair, the diagnosis vascular group (10). This was followed by Crit Care Med 2006 Vol. 34, No. 2 511 the International Subarachnoid Aneu- after the first year for the endovascular spasm was either not significantly differ- rysm Trial (ISAT), a multiple-center, ran- group and 3,107 patient years of fol- ent (19–21) or slightly higher (22, 23) domized study of endovascular coiling vs. low-up for the neurosurgical group, with among surgically treated patients. An surgical clipping conducted in 2,143 pa- a mean follow-up of 4 yrs, risk of recur- early nonrandomized study of 156 pa- tients with aSAH who were deemed suit- rent aSAH was higher in patients ran- tients had suggested a higher rate of ce- able for either therapy. Posterior circula- domized to coiling (seven patients) com- rebral infarction in patients receiving en- tion aneurysms accounted for only 58 of pared with clipping (two patients), but dovascular vs. surgical therapy; however, 2,143 patients (as many of these patients mortality related to recurrent aSAH was the proportion of patients with poor ini- were not enrolled because coiling was equal in both groups. A higher risk for tial neurologic presentation was higher considered the preferred modality of seizures and poor cognitive outcomes in the endovascular group (24). treatment). At 1 yr, endovascular coiling was seen in the surgical group, and cu- Comment. The available data indicate was associated with dependency or death mulative 7-yr mortality curves showed that in patients with good neurologic in 23.5% of patients compared with more deaths in the surgical group com- grade aSAH who undergo treatment for 30.9% in the surgical group, a relative pared with coiling. The increased risk of aneurysms in the anterior circulation, risk reduction of 22.6% (p Ͻ .001). Of re-bleeding in the coiling group did not 1-yr outcomes are clearly superior after concern, however, nonprocedural re- seem to reverse the early benefit seen endovascular coiling when compared bleeding within 1 yr was higher in pa- with this modality. Notwithstanding its with surgical clipping. Follow-up of pa- tients randomized to endovascular treat- limitations, ISAT represents level I evi- tients receiving endovascular treatment ment (40 recurrent aSAHs, with 22 dence that in this patient population, en- in some studies suggests that despite deaths) compared with patients allocated dovascular coiling is associated with bet- good clinical results, a significant propor- to neurosurgical treatment (33 patients ter 1-yr outcomes, with trends toward tion of patients may require repeat endo- with aSAHs, 30-day mortality in 21 pa- superior long-term outcomes, when vascular or surgical therapy for residual tients) (2, 3). compared with surgical clipping. or recurrent aneurysmal lesions. How- Although widely regarded as a land- Apart from the recently published in- ever, long-term (Ͼ1 yr) clinical trends in mark trial, the ISAT has been criticized formation stemming from the ISAT trial, patients enrolled in ISAT do seem to sug- with regard to biases in patient selection, randomized trials comparing long-term gest that endovascular coiling is likely to low rates of randomization of eligible pa- outcomes after coiling vs. clipping of rup- retain its advantage over clipping as a tients, the definition of clinical equipoise, tured aneurysms are not available. How- superior procedure, and further fol- expertise of the neurosurgeons and inter- ever, in an analysis of patients who un- low-up of these patients is likely to add ventionists, the failure to use an opera- derwent coiling of unruptured aneurysms insight to this debate. Preliminary results tive microscope, the higher than ex- and were followed for a median of 22.3 from various studies have failed to con- pected morbidity in the surgically treated months, annual re-bleeding rates were sistently show an association between group, the absence of angiographic data 0.8% in the first year, 0.6% in the second treatment modality and the rate of de- after the initial treatment, the lack of year, and 2.4% in the third year after layed cerebral ischemia. For posterior long-term (Ͼ1 yr) follow-up, and the ap-
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]
  • 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.
    [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]
  • 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]