Is Fasting Required for Serum Creatinine Test
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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. -
Laboratory Testing for Chronic Kidney Disease Diagnosis and Management
Test Guide Laboratory Testing for Chronic Kidney Disease Diagnosis and Management Chronic kidney disease is defined as abnormalities of kidney prone to error due to inaccurate timing of blood sampling, structure or function, present for greater than 3 months, incomplete urine collection over 24-hours, or over collection with implications for health.1 Diagnostic criteria include of urine beyond 24-hours.2,3 a decreased glomerular filtration rate (GFR) or presence Given that direct measurement of GFR may be problematic, of 1 or more other markers of kidney damage.1 Markers of eGFR, using either creatinine- or cystatin C-based kidney damage include a histologic abnormality, structural measurements, is most commonly used to diagnose CKD in abnormality, history of kidney transplantation, abnormal urine clinical practice. sediment, tubular disorder-caused electrolyte abnormality, or an increased urinary albumin level (albuminuria). Creatinine-Based eGFR This Test Guide discusses the use of laboratory tests that GFR is typically estimated using the Chronic Kidney Disease 4 may aid in identifying chronic kidney disease and monitoring Epidemiology Collaboration (CKD-EPI) equation. The CKD-EPI and managing disease progression, comorbidities, and equation uses serum-creatinine measurements and the complications. The tests discussed include measurement patient’s age (≥18 years old), sex, and race (African American and estimation of GFR as well as markers of kidney damage. vs non−African American). Creatinine-based eGFR is A list of applicable tests is provided in the Appendix. The recommended by the Kidney Disease Improving Global information is provided for informational purposes only and Outcomes (KDIGO) 2012 international guideline for initial is not intended as medical advice. -
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. -
Wellness Labs Explanation of Results
WELLNESS LABS EXPLANATION OF RESULTS BASIC METABOLIC PANEL BUN – Blood Urea Nitrogen (BUN) is a waste product of protein breakdown and is produced when excess protein in your body is broken down and used for energy. BUN levels greater than 50 mg/dL generally means that the kidneys are not functioning normally. Abnormally low BUN levels can be seen with malnutrition and liver failure. Creatinine – a waste product of normal muscle activity. High creatinine levels are most commonly seen in kidney failure and can also been seen with hyperthyroidism, conditions of overgrowth of the body, rhabdomyolysis, and early muscular dystrophy. Low creatinine levels can indicate low muscle mass associated with malnutrition and late-stage muscular dystrophy. Glucose – a simple sugar that serves as the main source of energy in the body. High glucose levels (hyperglycemia) is usually associated with prediabetes and can also occur with severe stress on the body such as surgery or events like stroke or trauma. High levels can also be seen with overactive thyroid, pancreatitis, or pancreatic cancer. Low glucose levels can occur with underactive thyroid and rare insulin- secreting tumors. Electrolytes – Sodium, Calcium, Potassium, Chloride, and Carbon Dioxide are all included in this category. Sodium – high levels of sodium can be seen with dehydration, excessive thirst, and urination due to abnormally low levels of antidiuretic hormone (diabetes insipidus) as well as with excessive levels of cortisol in the body (Cushing syndrome). Low levels of sodium can be seen with congestive heart failure, cirrhosis of the liver, kidney failure, and the syndrome of inappropriate antidiuretic hormone (SIADH). -
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. -
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. -
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 ................................................................................................................................................... -
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. -
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). -
Tests…But Maybe You Transports Don’T 2
11/12/15 Some things you should When lab tests are useful know about laboratory 1. Managing patients during critical care tests…But maybe you transports don’t 2. While transporting patient to medical facilities for evaluation of laboratory Steve Faynor, CCEMT-P abnormalities HCA Chippenham Medical Center Richmond Ambulance Authority Objectives 1. Review some basic laboratory tests. Treat the patient, not the 2. Appreciate how patterns of laboratory test results can offer insight into etiology. laboratory values. 3. Learn how laboratory test calculations can add additional clinical information. 4. Review some limitations of laboratory tests. ELECTROLYTES & A case of “bad labs” RENAL FUNCTION TESTS 1 11/12/15 Hypernatremia & Renal Failure Hypernatremia • 89 year old white female • Hyperaldosteronism • Coming from nursing home due to • Cushing’s disease or syndrome abnormal labs • Diabetes insipidus (deficiency of ADH) • Sodium 172 mmol/L • Dehydration • Potassium 4.2 mmol/L • Chloride 137 mmol/L • Carbon dioxide 21 mmol/L • What are some causes of hypernatremia? • BP 122/66, SBP 99 later • BUN 212 mg N/dL • HR 64/min • Creatinine 6.10 mg/dL • RR 21/min • What do these values indicate? • SpCO2 98% on 4 L oxygen per min • Does this change your therapy? • Tongue dry, skin turgor poor • What is the cause of the hypernatremia in this patient? Treatment? Acute Renal Failure Use of the BUN/creatinine ratio • Intrinsic renal disease • In intrinsic causes of acute renal failure, the – Acute tubular necrosis: ischemia, toxins BUN/creatinine ratio is typically 10-15. – Acute glomerulonephritis • In pre-renal causes of acute renal failure, – CKD with missed dialysis the BUN/creatinine ratio is typically >20. -
Common Laboratory Tests
Common Laboratory Tests BMP (Basic Metabolic Panel): A BMP is a common blood chemistry test that measures your sugar level, electrolyte balance, and kidney function. CBC (Complete Blood Count): A common blood test that helps determine an individual’s general health status. It evaluates hemoglobin, hematocrit, white blood cells, red blood cells, red blood cell indices, and platelets. It can be used as a tool to help diagnose various conditions, such as anemia, infection, inflammation, bleeding disorder, or leukemia. CMP (Complete Metabolic Panel): A CMP is similar to a BMP, in that it measures your sugar level, electrolyte balance, kidney function, but it also measures liver function. ESR (Erythrocyte Sedimentation Rate): A non-specific blood test that is used to help detect inflammation. It is said to be non-specific because an elevated result often indicates inflammation but does not tell exactly where the inflammation is in the body or what is causing it. It is typically used in conjunction with other testing. Ferritin: A blood test that assesses a person’s iron stores in the body. The test is sometimes ordered with an iron test and a TIBC (Total Iron Binding Capacity) to detect the presence and severity of iron deficiency or iron overload. FT4 (Free Thyroxine): Free T4 is a blood test used to help evaluate thyroid function and diagnose thyroid diseases usually after discovering that the TSH level is abnormal. FT3 (Free Triiodothyronine): Free T3 is a blood test used to assess thyroid function. It is primarily used to help diagnose hyperthyroidism and may be ordered to help monitor treatment of a person with a known thyroid disorder. -
Pneumomediastinum in a Patient with Cannabinoid Hyperemesis Syndrome
IMAGES IN MEDICINE Pneumomediastinum in a Patient with Cannabinoid Hyperemesis Syndrome MARC J. VECCHIO, MD; WILLIAM D. BINDER, MD, FACEP 48 49 EN CASE PRESENTATION Figure 1. (A) Red arrows illustrating extensive pneumomediastinum and pneumo- A 23-year-old man with a past medical retroperitoneum; (B) illustrating air extending into the neck and spinal canal. history of cannabinoid hyperemesis syn- drome presented to the emergency depart- A B ment with 1 week of nausea, emesis and poor oral intake. Prior to presentation, the patient had been treated in the emer- gency department several times for intrac- table vomiting. The patient reported he was a daily long-term user of marijuana cigarettes. On presentation, the patient was afebrile with a pulse of 117 beats per minute, res- pirations of 20 per minute, blood pressure of 111/79 and oxygen saturation of 99% on room air. Physical examination revealed a thin man with eructation and subcutane- ous crepitation over the neck and thorax. Lung sounds were clear to auscultation bilaterally. Laboratory testing revealed a pH of 7.26, anion gap of 33, blood-urea nitrogen of 107 mg/dL and a newly ele- vated creatinine of 13.01 mg/dL. Nota- bly, the patient had normal labs with a creatinine of 0.84 mg/dL during a similar presentation for intractable vomiting one month prior to presentation. Chest X-ray showed evidence of subcutaneous gas and pneumomediastinum. Computed tomog- raphy (CT) of the chest and abdomen with intravenous contrast revealed pneu- momediastinum and pneumoretroperito- neum with extension into the spinal canal (Figure 1).