Characteristics of Cerebrospinal Fluid in Tuberculous Meningitis Patients with Hydrocephalus Astrid Tamara Maajid Budiman,1 Nida Suraya,2 Ahmad Faried,3 Ida Parwati2

Total Page:16

File Type:pdf, Size:1020Kb

Characteristics of Cerebrospinal Fluid in Tuberculous Meningitis Patients with Hydrocephalus Astrid Tamara Maajid Budiman,1 Nida Suraya,2 Ahmad Faried,3 Ida Parwati2 Original Article Characteristics of Cerebrospinal Fluid in Tuberculous Meningitis Patients with Hydrocephalus Astrid Tamara Maajid Budiman,1 Nida Suraya,2 Ahmad Faried,3 Ida Parwati2 1Faculty of Medicine, Universitas Padjadjaran 2Department of Clinical Pathology, Faculty of Medicine, Universitas Padjadjaran-Dr. Hasan Sadikin General Hospital, Bandung 3Department of Neurosurgery, Faculty of Medicine, Universitas Padjadjaran-Dr. Hasan Sadikin General Hospital, Bandung Abstract Objective: meningitis (TBM) with hydrocephalus patients as diagnostic criteria of TBM. To describe cerebrospinal fluid (CSF) characteristics in tuberculous Methods: A cross-sectional using retrospective method was applied in this study by obtaining medical records of TBM with hydrocephalus patients that were treated at Department of Neurosurgery Dr. Hasan Sadikin General Hospital, Bandung from January 2014–September 2016. Results: Sixty one records were included in the study. Patient characteristics and differential count, protein, and glucose were recorded and descriptively such as age, gender, and CSF laboratory features such as color and clarity, cells 3 with analyzed.lymphocyte The predominance majority of CSF (median: macroscopic 76%). appearance Increased protein was seen from to benormal clear (88%) and colorless (88%). Median for CSF cell count was 25 cells/mm value range was seen in CSF (median: 50 mg/dL) while the mean for CSF glucose in this study remained in its normal value range (mean: 58.9±26.68 mg/dL)Conclusions: with lower CSF to blood glucose ratio (mean: 0.41±0.27). Received: November 2, 2017 Clear CSF with colorless appearance, lymphocyte pleocytosis, highNeurosurgery, protein level, Dr. Hasanand low Sadikin CSF glucose General as Hospital, well as blood Bandung. glucose ratio remain Revised: typical CSF characteristics of TBM patients found at the Department of Keywords: MayAccepted: 15, 2018 pISSN: 2302-1381; eISSN: 2338-4506; http://doi.org/10.15850/ijihs.v6n2.1129 IJIHS. 2018;6(2):57–62Cerebrospinal fluid, hydrocephalus, tuberculous meningitis September 5, 2018 Introduction Early diagnosis and proper management Tuberculosis (TB) currently remains a major global health issue. Indonesia is currently in of TBM is an important factor that influences the top three in terms of TB cases where 10% mortality and morbidity. Cerebrospinal fluid of the total TB population in the world is found includes macroscopic, microscopic, chemical, 1 (CSF) examination is an important parameter in this country. One of extrapulmonary TB inand the microbiological diagnosis of TBM examinations. This CSF examinations Bacterial with high mortality and morbidity, esepcially in children, is tuberculosis meningitis (TBM).2 Hydrocephalus is the most frequently found culturediagnosis. or2,3 acid-fast A previous bacilli study (AFB) has observation reported complication of TB and one of the predictors inthat CSF the are ratio used of positiveto establish culture TBM results definitive were of mortality and morbidity.2 13% among TBM patients.4 In several cases, Correspondence: Astrid Tamara Maajid Budiman Universitas Padjadjaran lowobserve results the ofmacroscopic, bacterial culture microscopic, and AFB and on Jl. Raya Bandung-Sumedang KM, Faculty21 Jatinangor, of Medicine, Indonesia CSFchemical may characteristicbe seen. Hence as ait referenceis important for the to e-mail: [email protected] laboratory-based diagnosis of TBM.4 International Journal of Integrated Health Sciences. 2018;6(2) 57 :57–62 Characteristics of Cerebrospinal Fluid in Tuberculous Meningitis with Hydrocephalus Patients This study aimed to observe the chemical, macroscopic, and microscopic characteristics color, clarity, leukocyte cell numbers, cell countVariables percentage, used inprotein this study level, were and age,glucose CSF the Department of Neurosurgery Dr. Hasan level. Data were then analyzed descriptively by ofSadikin CSF in General TBM patients Hospital, with Bandung. hydrocephalus at counting the number and percentage for the results of macroscopic examination while for microscopic and chemical examination results, Methods mean and standard deviations or median and range were used based on the distribution of This design used in this study was retrospective the data. cross-sectional descriptive study. TBM patients with hydrocephalus treated at the Department of Neurosurgery, Dr. Hasan Sadikin General Results Hospital, Bandung who met the inclusion and exclusion criteria were included. The inclusion There were 477 patients with TBM in Dr. Hasan criteria in this study were inpatients during Sadikin General Hospital Bandung from 2014 the period of January 2014–September 2016, treated at the Department of Neurosurgery results that suggested hydrocephalus who toDr. 2016. Hasan A Sadikintotal of 170General (35.6%) Hospital, patients Bandung were with a computerized tomography (CT) scan TBM with hydrocephalus. Sixty six cases had undergo CSF examination with specimens with 149 cases (31.2%) were diagnosed as derivedGeneral fromHospital, ventricular Bandung, drainage with macroscopic,at the Clinical them must be excluded, resulting a total of Pathologymicroscopic, Laboratory and chemical of characteristicDr. Hasan Sadikin result, (44.3) met the inclusion criteria but five of including protein and glucose levels. Exclusion criteria included congenital hydrocephalus, 61patients (40.9%) were cases. taken Allfrom were ventricular included drainage in the meningitis caused by organisms other than study. All CSF samples collected from these 61 Mycobacterium tuberculosis, positive Human suchThe as numberextra ventricular of male patients drainage was (EVD) higher or incomplete medical record. Samples were ventriculoperitonealthan the number of female (VP) shunt. patients (Table 1). Immunodeficiencyselected using the total Virus sampling (HIV) method.status, and Age categorization of children and adults in this study referred to the existing consensus in Dr. Hasan Sadikin General Hospital, Bandung Approval from the Ethics Committee of the with 0–14 years categorized as children, and Faculty of Medicine, Universitas Padjadjaran underwas conducted the ethical from clearanceAugust to DecemberNo. 102/UN6. 2016 pediatric patients was higher when compared C1.3.2/KEPK/PN/2016by collecting data from thewas medical gained. Thisrecords study of >14to adults years patients. classified Median as adults. age wasThe 6number years old of TBM inpatients with hydrocephalus i who were treated at the Department of Neurosurgery, Dr. Hasan Sadikin General Hospital, Bandung. withpatients a range with of hydrocephalus 6 months–58 years. and the results wereExamination compared ofto CSF normal was performedvalues and on criteria TBM from Marais et al.3 CSFhospital. of these patients were examined at the Laboratory of Clinical Pathology of the same (Table 2). Cerebrospinal fluid color in TBM patients with hydrocephalus Table 1 Distribution of Tuberculous Meningitis with Hydrocephalus Patients Based on Age and Gender Gender Children Adults Total (%) Male 20 7 27 (44) 15 34 (56) Total 22 61 (100) Female 19 39 58 International Journal of Integrated Health Sciences. 2018;6(2) :57–62 Astrid Tamara Maajid Budiman, Nida Suraya, et al. in this study was generally colorless. Similarly, could only be calculated in 11 patients (mean: showed a clear result. the clarity level of CSF in this study generally 0.41±0.27). 3 3). Discussion TheThe differential median ofcell the count CSF ofleukocyte the cerebrospinal cells was 25 cells/mm (range was 1-613 cells/mm This study reveals that the prevalence of TBM of mononuclear (MN) and polymorphonuclear with hydrocephalus is predominated by males. fluidcells (PMN).was presented Mononuclear in the cellsform were of percentage shown to of previous studies.4–6 A study found that the percentage for both PMN and MN was 0% to Thisprevalence finding of is pediatric in agreement patient with with the TBM results with be100%. the dominantThere were cell two in thecases CSF. which The scopeshowed of hydrocephalus as complication is 71% while the same prevalence for adults is 12%.7 This 3 in both. study also shows that more children has TBM the percentage of PMN of 100%, with a CSF with hydrocephalus compared to adult. leukocytethe normal cell value count but of not 1 cell/mm as high as the one in Macroscopic examination on the color and MaraisThe etmedian al.3 CSF protein was higher than criteria. The mean CSF glucose clarityclear and of CSF colorless. was performed. This is Thein line macroscopic with the was 58.9±26.68 mg/dL which was still in the appearance of CSF in this study was generally normal limit. The CSF to blood glucose ratio Table 2 Cerebrospinal Fluid Examination in Tuberculous Meningitis Patients with Hydrocephalus Marais et al.3 Variable Normal value Criteria for TBM Result Macroscopic appearance CSF color* Colorless Yellowish, n(%) 4 (7) Colorless, n(%) 54 (88 Yellow, n(%) 3 (5) Clarity Clear Clear 6 (10) Clear, n(%) 54 (88) Turbid, n(%) 1 (2) Cloudy, n(%) Microscopic examination 3 3 3 25 (1–613) Differential count, median (range) CSF cells, median (range) <5 cells/mm 10-500 cells/mm cells/mm 24 (0–100) MN (%)# 76 (0-100) PMN (%)** <50% Chemistry >50% >50% Protein, median (range) deviation 10–40 mg/dL >100 mg/dL 50 (5–977) mg/dL Absolute CSF glucose, mean±std 50–800.6 mg/dL <40 mg/dL 58.9±26.68 mg/dL CSF to blood glucose ratio##, <0.5 0.41±0.27 mean±std deviation Note: *CSF = Cerebrospinal fluid; **PMN = polymorphonuclear; #MN = mononuclear; ##Could only be done in 11 patients
Recommended publications
  • Cerebrospinal Fluid in Critical Illness
    Cerebrospinal Fluid in Critical Illness B. VENKATESH, P. SCOTT, M. ZIEGENFUSS Intensive Care Facility, Division of Anaesthesiology and Intensive Care, Royal Brisbane Hospital, Brisbane, QUEENSLAND ABSTRACT Objective: To detail the physiology, pathophysiology and recent advances in diagnostic analysis of cerebrospinal fluid (CSF) in critical illness, and briefly review the pharmacokinetics and pharmaco- dynamics of drugs in the CSF when administered by the intravenous and intrathecal route. Data Sources: A review of articles published in peer reviewed journals from 1966 to 1999 and identified through a MEDLINE search on the cerebrospinal fluid. Summary of review: The examination of the CSF has become an integral part of the assessment of the critically ill neurological or neurosurgical patient. Its greatest value lies in the evaluation of meningitis. Recent publications describe the availability of new laboratory tests on the CSF in addition to the conventional cell count, protein sugar and microbiology studies. Whilst these additional tests have improved our understanding of the pathophysiology of the critically ill neurological/neurosurgical patient, they have a limited role in providing diagnostic or prognostic information. The literature pertaining to the use of these tests is reviewed together with a description of the alterations in CSF in critical illness. The pharmacokinetics and pharmacodynamics of drugs in the CSF, when administered by the intravenous and the intrathecal route, are also reviewed. Conclusions: The diagnostic utility of CSF investigation in critical illness is currently limited to the diagnosis of an infectious process. Studies that have demonstrated some usefulness of CSF analysis in predicting outcome in critical illness have not been able to show their superiority to conventional clinical examination.
    [Show full text]
  • CSF Xanthochromia
    CSF Xanthochromia Pseudonyms – CSF bilirubin For investigation of suspected subarachnoid haemorrhage (SAH) in CT negative patients Xanthochromia is the yellow discoloration indicating the presence of bilirubin in CSF which appears as oxyhaemoglobin released from the breakdown of red blood cells following haemorrhage into the CSF is converted in vivo into bilirubin in a time‐dependent manner. A subarachnoid haemorrhage (SAH) is a spontaneous arterial bleeding into the subarachnoid space, usually from a cerebral aneurysm, and characterised by a severe sudden‐onset headache. The majority of positive cases are detected by computed tomography (CT) scanning but for those CT‐ negative patients presenting with a history suggestive of SAH the measurement of xanthochromia in CSF is advocated to detect those patients who actually have sustained a SAH and require treatment and to eliminate the possibility of SAH in the remainder without the need of confirmatory angiography. The CSF is collected by means of lumbar puncture (LP). For full interpretation of the result other CSF and blood tests must be collected at the same time – CSF protein and glucose; plasma glucose; and serum protein and bilirubin. General information CSF Xanthochromia sample collection kits are provided in the ACU (ORC) and AMU (Trafford) and also available from the Specimen Receptions at the laboratories at both sites. Concurrent samples should be requested for CSF protein and glucose, plasma glucose and serum LFTS (for protein and bilirubin) using the sample containers supplied. Collection container: CSF xanthochromia: White topped Universal container (In addition the following samples should be collected:‐ CSF glucose & protein: 1.2 mL fluoride‐EDTA glucose (Sarstedt yellow top) Serum protein & bilirubin: 4.9 mL SST (Sarstedt brown top) Plasma glucose: 2.7 mL fluoride‐EDTA glucose (Sarstedt yellow top) Type and volume of sample: 1 mL CSF requested, minimum 400 µL required for analysis Specimen transport/special precautions: A CSF Xanthochromia sample collection kit should be used.
    [Show full text]
  • BVH Reference Ranges LTR 35106 Chemistry Reference Ranges
    BVH Reference Ranges LTR 35106 Last Reviewed: (Revised 05.08.2018) Chemistry Reference Ranges: DXC 600 Reference Ranges: Test Method Sex Criteria Reference Range Units Critical Range Acetaminophen DXC 600 Therapeutic 10 - 30 ug/mL > 150 Hepatotoxic 4 hrs Post Ingestion > 150 ug/ml 8 hrs Post Ingestion > 75 ug/ml 12 hrs Post Ingestion > 40 ug/ml A/G Ratio Calculation 1.1 - 2.2 Albumin BCG DXC 600 0 Day - 30 Days 2.6 - 4.3 gm/dL 1 Month - 5 Months 2.8 - 4.6 gm/dL 6 Months - 1Year 2.8 - 4.8 gm/dL 2+ Years 3.2 - 4.9 gm/dL Alcohol (ETOH) DXC 600 <0.005 (none detected) gm/dL > 0.300 Alkaline Phosphatase DXC 600 Both 0 - 4 Years 80 - 350 IU/L Both 5 Years - 9 Years 60 - 385 IU/L Both 10 Years - 13 Years 60 - 485 IU/L Male 14 Years - 18 Years 50 - 350 IU/L Female 14 Years - 18 Years 40 - 195 IU/L Both 19+ Years 32 - 91 IU/L ALT (SGPT) DXC 600 Male 17 - 63 IU/L Female 14 - 54 IU/L Ammonia DXC 600 9 - 35 uMOL/L > 100 Amylase DXC 600 28 - 100 U/L Anion Gap DXC 600 7 - 17 mmol/L AST (SGOT) DXC 600 0 Years - 4 Years 10 - 60 IU/L 5 Years - 9 Years 5 - 50 IU/L 10+ Years 15 - 41 IU/L Beta Hydroxybutyrate DXC 600 0.0 - 0.3 mmol/L BUN DXC 600 8 - 26 mg/dL > 100 BUN/Creatinine Ratio Calculation 15 - 25 Ratio Calcium DXC 600 0-2 days 6.2 - 11.0 mg/dL < 5.8, > 13.3 > 2 days 8.5 - 10.3 mg/dl < 6.3, > 13.3 Cardiac Risk Factor Calculation Male 1/2 Average 3.43 Average 4.97 2X Average 9.55 3X Average 23.99 Female 1/2 Average 3.27 Average 4.44 2X Average 7.05 3X Average 11.04 5/8/2018 pg.
    [Show full text]
  • Basic Skills in Interpreting Laboratory Data, 5Th Edition
    CHAPTER 1 DEFINITIONS AND CONCEPTS KAREN J. TIETZE This chapter is based, in part, on the second edition chapter titled “Definitions and Concepts,” which was written by Scott L. Traub. Objectives aboratory testing is used to detect disease, guide treatment, monitor response Lto treatment, and monitor disease progression. However, it is an imperfect sci­ ence. Laboratory testing may fail to identify abnormalities that are present (false After completing this chapter, negatives [FNs]) or identify abnormalities that are not present (false positives, the reader should be able to [FPs]). This chapter defines terms used to describe and differentiate laboratory • Differentiate between accuracy tests and describes factors that must be considered when assessing and applying and precision laboratory test results. • Distinguish between quantitative, qualitative, and semiqualitative DEFINITIONS laboratory tests Many terms are used to describe and differentiate laboratory test characteristics and • Define reference range and identify results. The clinician should recognize and understand these terms before assessing factors that affect a reference range and applying test results to individual patients. • Differentiate between sensitivity and Accuracy and Precision specificity, and calculate and assess Accuracy and precision are important laboratory quality control measures. Labora­ these parameters tories are expected to test analytes with accuracy and precision and to document the • Identify potential sources of quality control procedures. Accuracy of a quantitative assay is usually measured in laboratory errors and state the terms of an analytical performance, which includes accuracy and precision. Accuracy impact of these errors in the is defined as the extent to which the mean measurement is close to the true value.
    [Show full text]
  • Ascites and Related Disorders
    AscitesAscites andand RelatedRelated DisordersDisorders LuisLuis S.S. Marsano,Marsano, MDMD ProfessorProfessor ofof MedicineMedicine DirectorDirector ofof HepatologyHepatology UniversityUniversity ofof LouisvilleLouisville CausesCauses ofof AscitesAscites Malignant Neoplasia 10% Cardiac Insufficiency 3% Tuberculous Peritonitis Chronic hepatic 2% disease Nephrogenic 81% a scite s (dia lysis) 1% Pancreatic ascites 1% Biliary ascites 1% Others 1% PathophysiologyPathophysiology ofof CirrhoticCirrhotic AscitesAscites Hepatic sinusoidal pressure Activation of hepatic baroreceptors Compensated Peripheral arterial vasodilation with hypervolemia, (normal renin, aldosterone, vasopressin, or norepinephrine) Peripheral arterial vasodilation (“underfilling”) Decompensated Neurally mediated Na+ retention, (with elevated renin, aldosterone, vasopressin, or norepinephrine) ClassificationClassification ofof AscitesAscites SerumSerum--ascitesascites albuminalbumin gradientgradient (SAAG)(SAAG) SAAGSAAG (g/dl)(g/dl) == albuminalbumins –– albuminalbumina GradientGradient >>1.11.1 g/dlg/dl == portalportal hypertensionhypertension Serum globulin > 5 g/dl:: – SAAG correction = (SAAG mean)(0.21+0.208 serum globulin g/dl) AscitesAscites withwith HighHigh SAAGSAAG >>1.11.1 g/dlg/dl == portalportal hypertensionhypertension Cirrhosis Alcoholic Hepatitis Cardiac ascites Massive hepatic metastasis Fulminant hepatic failure Budd-Chiari syndrome Portal vein thrombosis Veno-occlusive disease Acute fatty liver of pregnancy Myxedema Mixed ascites LowLow SAAGSAAG <1.1<1.1
    [Show full text]
  • Hyperchloremia – Why and How
    Document downloaded from http://www.elsevier.es, day 23/05/2017. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited. n e f r o l o g i a 2 0 1 6;3 6(4):347–353 Revista de la Sociedad Española de Nefrología www.revistanefrologia.com Brief review Hyperchloremia – Why and how Glenn T. Nagami Nephrology Section, Department of Medicine, VA Greater Los Angeles Healthcare System and David Geffen School of Medicine at UCLA, United States a r t i c l e i n f o a b s t r a c t Article history: Hyperchloremia is a common electrolyte disorder that is associated with a diverse group of Received 5 April 2016 clinical conditions. The kidney plays an important role in the regulation of chloride concen- Accepted 11 April 2016 tration through a variety of transporters that are present along the nephron. Nevertheless, Available online 3 June 2016 hyperchloremia can occur when water losses exceed sodium and chloride losses, when the capacity to handle excessive chloride is overwhelmed, or when the serum bicarbonate is low Keywords: with a concomitant rise in chloride as occurs with a normal anion gap metabolic acidosis Hyperchloremia or respiratory alkalosis. The varied nature of the underlying causes of the hyperchloremia Electrolyte disorder will, to a large extent, determine how to treat this electrolyte disturbance. Serum bicarbonate Published by Elsevier Espana,˜ S.L.U. on behalf of Sociedad Espanola˜ de Nefrologıa.´ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/ licenses/by-nc-nd/4.0/).
    [Show full text]
  • 1 Molecular Physiology and Pathophysiology of Bilirubin Handling by the Blood, Liver
    1 1 MOLECULAR PHYSIOLOGY AND PATHOPHYSIOLOGY OF BILIRUBIN HANDLING BY THE BLOOD, LIVER, 2 INTESTINE, AND BRAIN IN THE NEWBORN 3 THOR W.R. HANSEN1, RONALD J. WONG2, DAVID K. STEVENSON2 4 1Division of Paediatric and Adolescent Medicine, Institute of Clinical Medicine, Faculty of Medicine, 5 University of Oslo, Norway 6 2Department of Pediatrics, Stanford University School of Medicine, Stanford CA, USA 7 __________________________________________________________________________________ 8 2 9 I. Introduction 10 II. Bilirubin in the Body 11 A. Bilirubin Chemistry 12 1. Bilirubin structure 13 2. Bilirubin solubility 14 3. Bilirubin isomers 15 4. Heme degradation 16 5. Biliverdin and biliverdin reductase (BVR) 17 B. Bilirubin as an Antioxidant 18 C. Bilirubin as a Toxin 19 1. Bilirubin effects on enzyme activity 20 2. Toxicity of bilirubin conjugates and isomers 21 D. Other Functions/Roles 22 1. Drug displacement by bilirubin 23 2. Bilirubin interactions with the immune system and 24 inflammatory/infectious mechanisms 25 III. The Production of Bilirubin in the Body 26 A. Heme Catabolism and Its Regulation 27 1. Genetic variants in bilirubin production 28 B. The Effect of Hemolysis 29 1. Disorders associated with increased bilirubin production 30 IV. Bilirubin Binding and Transport in Blood 31 V. Bilirubin in the Liver 32 A. Hepatocellular Uptake and Intracellular Processing 33 B. Bilirubin Conjugation 34 1. Genetic variants in bilirubin conjugation 3 35 a. Crigler-Najjar syndrome type I 36 b. Crigler-Najjar syndrome type II 37 c. Gilbert syndrome 38 2. Genetic variants in transporter proteins 39 C. Bilirubin Excretion 40 VI. Bilirubin in the Intestines 41 A.
    [Show full text]
  • Routine Cerebrospinal Fluid (CSF) Analysis
    CHAPTER4 Routine cerebrospinal fluid (CSF) analysis a b a ) F. Deisenhammer, A. Bartos, R. Egg, Albumin CSF/serum ratio (Qalb should be pre- N. E. Gilhus,c G. Giovannoni,d S. Rauer,e ferred to total protein measurement and normal F. Sellebjergf upper limits should be related to patients’ age. Elevated Qalb is a non-specific finding but occurs mainly in bacterial, cryptococcal, and tubercu- Background A great variety of neurological diseases lous meningitis, leptomingeal metastases as well require investigation of the cerebrospinal fluid as acute and chronic demyelinating polyneu- (CSF) to prove the diagnosis or to rule out relevant ropathies. differential diagnoses. Pathological decrease of the CSF/serum glu- cose ratio or an increase in lactate concentration Objectives To evaluate the theoretical background indicates bacterial or fungal meningitis or lep- and provide guidelines for clinical use in rou- tomeningeal metastases. tine CSF analysis including total protein, albumin, Intrathecal immunoglobulin G synthesis is best immunoglobulins, glucose, lactate, cell count, demonstrated by isoelectric focusing followed by cytological staining, and investigation of infec- specific staining. tious CSF. Cellular morphology (cytological staining) should be evaluated whenever pleocytosis is found or Methods Systematic Medline search for the above leptomeningeal metastases or pathological bleed- mentioned variables. Review of appropriate publi- ing is suspected. Computed tomography-negative cations by one or more of the task force members. intrathecal bleeding should be investigated by Grading of evidence and recommendations was bilirubin detection. based on consensus by all task force members. Introduction CSF should be analysed immediately after collec- tion. If storage is needed 12 ml of CSF should The cerebrospinal fluid (CSF) is a dynamic, be partitioned into three to four sterile tubes.
    [Show full text]
  • D40. Cerebrospinal Fluid.Pdf
    CEREBROSPINAL FLUID D40 (1) Cerebrospinal Fluid (CSF) Last updated: June 3, 2019 PHYSIOLOGY ............................................................................................................................................ 1 CSF PRODUCTION .................................................................................................................................. 1 CSF REABSORPTION ............................................................................................................................... 1 PARAMETERS ........................................................................................................................................... 2 NORMAL ................................................................................................................................................ 2 OPENING PRESSURE ................................................................................................................................ 3 COLOR ................................................................................................................................................... 3 BLOODY CSF ......................................................................................................................................... 3 VISCOSITY & TURBIDITY ....................................................................................................................... 4 CELLS ...................................................................................................................................................
    [Show full text]
  • 2017 LAB GUIDE TEST MENU March 2017Edition
    2017 LAB GUIDE TEST MENU March 2017Edition Replaces: Sept 2015 Edition STAT TESTING MENU (2 Pages) 30 Minute In-Lab Turnaround Time (TAT) Unless Further Noted Below (In-Lab Time) MICROBIOLOGY 1. Spinal Fluid Culture set up and Gram Stain of sediment, India Ink prep 2. Gram Stain, other sites 3. Planting of cultures 4. Wet prep 5. Rapid Strep A Antigen Test (15 min. TAT) 6. Rapid Influenza A & B Antigen test 7. Rapid RSV Antigen test 8. Malaria Prep (60 min. TAT), Evening and Night shifts will only report “Parasites present or absent” 9. Screen, Gastric Urease, for Helicobacter Pylori (60 min. TAT) 10. Clostridium difficile DNA amplification (60 min. TAT) BLOOD BANK 1. Compatibility testing (leuko-reduced packed cells) 2. Type and Screen (60 min. TAT) 3. Cord Blood (2 hours) HEMATOLOGY 1. Complete Blood Count (CBC) SEE NOTE #1 2. Fibrinogen 3. Hemogram (ABC) 4. Monospot Test 5. Partial Thromboplastin Time (PTT) (60 min. TAT) 6. Prothrombin Time (PT) (60 min. TAT) 7. Fluid Cell Count (60 min. TAT) 8. Complete Urinalysis 9. D-dimer 10. Fluid pH CHEMISTRY 1. Arterial Blood Gases 2. Acetone 3. Ammonia 4. Amylase 5. Basic Metabolic Panel: Sodium, Potassium, Chloride, CO2, Creatinine, BUN, Glucose, and Calcium 6. Bilirubin (Total) 7. Blood Urea Nitrogen (BUN) 8. Calcium (Total and Ionized) 9. CPK (Total) (60 min. TAT for CPK total with MB fraction. CPKMB only run if CPK total > 113) UVM HEALTH NETWORK-CVPH 2 TEST MENU 10. Creatinine 11. CSF (Glucose and Protein) 12. Electrolytes: Sodium (Na), Potassium (K), Chloride (Cl), CO2 13.
    [Show full text]
  • Effects of Hyperglycemia and Rapid Lowering of Plasma Glucose in Normal Rabbits
    MILESTONES IN NEPHROLOGY J Am Soc Nephrol 11: 1776–1788, 2000 Mark A. Knepper, Feature Editor Studies on Mechanisms of Cerebral Edema in Diabetic Comas EFFECTS OF HYPERGLYCEMIA AND RAPID LOWERING OF PLASMA GLUCOSE IN NORMAL RABBITS ALLEN I. ARIEFF AND CHARLES R. KLEEMAN WITH THE TECHNICAL ASSISTANCE OF ALICE KEUSHKERIAN AND HELEN BAGDOYAN From the Departments of Medicine, Wadsworth Veterans Administration Center and Cedars-Sinai Medical Center, and the Cedars-Sinai Medical Research Institute, and University of California Los Angeles Medical Center, Los Angeles, California 90048 with comments by ALLEN I. ARIEFF AND RICHARD STERNS Reprinted from J. Clin. Invest. 52:571–583, 1973 A BSTRACT To investigate the pathophysiology of cerebral edema occurring during treatment of diabetic coma, the effects of hyperglycemia and rapid lowering of plasma glucose were AUTHOR COMMENTARY evaluated in normal rabbits. During 2 h of hyperglycemia (plasma glucose = 61 mM), both brain (cerebral cortex) and Allen I. Arieff muscle initially lost about 10% of water content. After 4 h of hyperglycemia, skeletal muscle water content remained low University of California, but that of brain was normal. Brain osmolality (Osm) (343 San Francisco mosmol/kg H2O) was similar to that of cerebrospinal fluid Sausalito, California (CSF) (340 mosmol/kg), but increases in the concentration of Na+, K+, Cl–, glucose, sorbitol, lactate, urea, myoinositol, and amino acids accounted for only about half of this increase. n 1936, Dillon, Riggs, and Dyer described a syndrome The unidentified solute was designated “idiogenic osmoles”. Iwhereby individuals who were being treated for diabetic When plasma glucose was rapidly lowered to normal with coma and apparently recovering suddenly deteriorated, with insulin, there was gross brain edema, increases in brain content worsening of coma, respiratory insufficiency, hypotension, of water, Na+, K+, Cl– and idiogenic osmoles, and a signifi­ tachycardia, high fever, and death (1).
    [Show full text]
  • The Pathophysiology of 'Happy' Hypoxemia in COVID-19
    Dhont et al. Respiratory Research (2020) 21:198 https://doi.org/10.1186/s12931-020-01462-5 REVIEW Open Access The pathophysiology of ‘happy’ hypoxemia in COVID-19 Sebastiaan Dhont1* , Eric Derom1,2, Eva Van Braeckel1,2, Pieter Depuydt1,3 and Bart N. Lambrecht1,2,4 Abstract The novel coronavirus disease 2019 (COVID-19) pandemic is a global crisis, challenging healthcare systems worldwide. Many patients present with a remarkable disconnect in rest between profound hypoxemia yet without proportional signs of respiratory distress (i.e. happy hypoxemia) and rapid deterioration can occur. This particular clinical presentation in COVID-19 patients contrasts with the experience of physicians usually treating critically ill patients in respiratory failure and ensuring timely referral to the intensive care unit can, therefore, be challenging. A thorough understanding of the pathophysiological determinants of respiratory drive and hypoxemia may promote a more complete comprehension of a patient’sclinical presentation and management. Preserved oxygen saturation despite low partial pressure of oxygen in arterial blood samples occur, due to leftward shift of the oxyhemoglobin dissociation curve induced by hypoxemia-driven hyperventilation as well as possible direct viral interactions with hemoglobin. Ventilation-perfusion mismatch, ranging from shunts to alveolar dead space ventilation, is the central hallmark and offers various therapeutic targets. Keywords: COVID-19, SARS-CoV-2, Respiratory failure, Hypoxemia, Dyspnea, Gas exchange Take home message COVID-19, little is known about its impact on lung This review describes the pathophysiological abnormal- pathophysiology. COVID-19 has a wide spectrum of ities in COVID-19 that might explain the disconnect be- clinical severity, data classifies cases as mild (81%), se- tween the severity of hypoxemia and the relatively mild vere (14%), or critical (5%) [1–3].
    [Show full text]