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. • Post-renal • In this case, the BUN/creatinine ratio was – Obstruction: stone, tumor, enlarged prostate 34.8. • Pre-renal • Do you want to stick with the same – Dehydration, shock, heart failure treatment? 2 11/12/15 Creatinine Clearance Creatinine Clearance • About 50% of the nephrons must be • Calculated from the 24-hr urine creatinine, destroyed before the serum creatinine rises urine volume, and the serum creatinine above the reference range • Should be corrected for body surface area • Creatinine Clearance is a more accurate test • Decreases naturally with age of renal function • Reference Ranges: • Clearance is defined as the mL of plasma – Males >85 mL/min/1.73 m2 cleared of a substance per minute – Females >75 mL/min/1.73 m2 Creatinine Clearance Anion Gap • Problems in collecting 24-hr urine • The purpose of the anion gap is to • Various calculations used to estimate Creatinine determine the etiology of a metabolic Clearance acidosis. • Current is the MDRD equation: • The anion gap is a measurement of – http://www.niddk.nih.gov/health-information/health- communication-programs/nkdep/lab-evaluation/gfr- unmeasured anions. These unmeasured calculators/Pages/gfr-calculators.aspx anions are the conjugate bases of organic – Corrected for African-American race & sex acids. – Normals are reported as "≥60 mL/min/1.73 m2" – Lactate, ketone bodies from DKA, salicylate… Anion Gap CASE #1 • Based on the principle of electroneutrality A 72 year-old woman is admitted after being found unwell + - - in her home by family members. She has a decreased • Anion Gap = [Na ] – [Cl ] – [HCO3 ] level of consciousness and cannot give any history, but • Normal range = 12 ± 4 mmol/L her daughter states that the dosage of one of her diabetes medications was increased 2 weeks ago, and earlier in the – Normal range varies with methodology. week she seemed to be suffering from a “stomach flu.” On examination, she is hypotensive, tachycardic, and tachypneic. She responds only to painful stimuli but has no other remarkable findings. You order basic laboratory studies and find a [high] anion gap metabolic acidosis. 3 11/12/15 MUDPILES Anion Gap Toxin Organic acid that accumulates High Anion Gap Metabolic Normal Anion Gap (Unmeasured anion) Acidosis Metabolic Acidosis Methanol Formic acid Lactic acidosis (metformin) Diarrhea (most common) Uremia Uremic toxins Ketoacidosis (diabetic, alcoholic, starvation) Diabetic ketoacidosis Acetoacetate, End-stage renal failure β-hydroxybutyrate Methanol intoxication Paraldehyde Ethylene glycol intoxication Iron or isoniazid Lactic acid from iron toxicity Salicylate intoxication Ethylene glycol Oxalic acid (binds calcium) Lactic acidosis Lactic acid Salicylates (aspirin) Salicylic acid CASE STUDY 2 HYPERKALEMIA • Na 129, Cl 78, tCO2 12 • Is the sample hemolyzed? • Anion Gap = 129 – (78 + 12) = 39 – Hemolysis raises potassium • Blood glucose = 1,890 mg/dL • How old is the sample? • Diagnosis is diabetic ketoacidosis HEMOGLOBIN A CALCIUM 1c Glycosylated Hemoglobin Chemical form Percentage Free (ionized) 47% • Glucose reacts non-enzymatically with Protein-bound (mostly albumin) 43% hemoglobin to form HbA Complexed (phosphate, carbonate, citrate, etc.) 10% 1c • The extent of glycosylation increases with pH incr.-> increasing glucose concentration Ca2+ + albumin-H Ca-albumin complex + H+ <-pH decr. • The HbA1c level is an indication of the • If the albumin is significantly decreased (malnutrition, average glucose level for the past 3 months liver disease), the total calcium will be low but the • Reference Range: 4-6% ionized calcium may be normal. 4 11/12/15 HEMOGLOBIN A1c Point-of-care Glucose Tests Usage Cutoff • Fasting whole blood glucose is 12-15% lower than Goal for diabetic control <7.0% plasma. Screening for diabetes >6.5% • Fasting capillary glucose is 2-5 mg/dL higher than venous. • But post-prandial capillary glucose averages 30 mg/dL higher than venous. • Capillary glucose may be depressed with poor perfusion: cold, hypotension or shock, Raynaud’s, vasopressors, dehydration. Liver Function Tests • Enzymes released from liver cells when injured LIVER FUNCTION TESTS – Aspartate Transaminase (AST) – Alanine Transaminase (ALT) – Alkaline Phosphatase – Gamma-glutamyl transferase (GGT) • Bilirubin, total and direct • Why are there so many LFTs? Classifying acute liver disease Carcinoma of Pancreas Acute hepatocellular necrosis Obstructive jaundice • Viral hepatitis • Gallstone Bile duct obstruction • Alcoholic hepatitis • Stricture • Wilson’s disease • Granuloma 15 • α-1 Anti-trypsin deficiency • Abscess 10 • Autoimmune hepatitis • Tumor or metastasis • Hemochromatosis • Drug-induced 5 • Infectious mononucleosis • Primary biliary cirrhosis TimesULN • Non-alcoholic fatty liver • Primary sclerosing 0 disease cholangitis AST ALT ALP GGT 5 11/12/15 Acute Hepatitis B Non-hepatic cause of jaundice Surgery resident with jaundice • Dispatched for an 11-year old male who is “not acting right” and has been vomiting. 120 • Arrived to find AA patient lying in bed, 100 80 eyes open and staring ahead but otherwise 60 unresponsive. 40 Time ULN Time 20 0 AST ALT ALP GGT Non-hepatic causes of jaundice Non-hepatic causes of jaundice • Mother states patient developed a headache • Despite dark complexion, patient appears 2 days ago and has been vomiting since jaundiced, especially on palms. yesterday night. • Skin warm, not excessively dry • Denies diarrhea, negative PMH • RR 24, HR 135, BP 100/60, SpO2 100% • Treating with Aleve and Pedialyte but no • Glucose 150 mg/dL aspirin. • ECG sinus rhythm • Mother Haitian, father African-American • Abdomen soft & non-tender, not distended Non-hepatic causes of jaundice Diagnosis • Hemolytic anemia • Autoimmune hemolytic anemia – Transfusion-related – Incidence 1:80,000 in children – Autoimmune – Many cases are idiopathic – DIC, hemolytic uremic syndrome – Some cases may be triggered by: – Hemoglobinopathies, e.g., sickle cell anemia • Drugs, e.g., penicillin, α-methyldopa – Glucose-6-phosphate dehydrogenase deficiency • Viral illness 6 11/12/15 Laboratory Studies Laboratory Studies • CBC • Chemistry tests – Hemoglobin = 2.4 g/dL – Bilirubin – MCV normal (normocytic) • Total bilirubin increased – MCHC normal (normochromic) • Indirect bilirubin increased, more than direct – Ammonia normal • Reticulocyte count increased • Enzyme tests • Direct anti-globulin (Coombs test) positive – AST & LDH increased – Sign that RBCs are coated with antibodies – Alkaline phosphatase & GGT WNL Laboratory Studies Bilirubin Metabolism • Urine tests – Urine bilirubin (bile) negative or weak pos. – Urine urobilinogen increased Diagnosing Acid-Base Disorders • Look at the pH first Acid-Base and Blood Gases – If pH<7.35 Acidosis – If pH>7.45 Alkalosis • Look at the CO2 and bicarbonate next to determine the primary cause. • Once you have determined the primary cause, determine if there is compensation by the other component. 7 11/12/15 ACIDOSIS ALKALOSIS ACIDOSIS ALKALOSIS EXAMPLE 1 EXAMPLE 2 • pH 7.28, pCO2 58, bicarbonate 33 • pH 7.28, pCO2 23, bicarbonate 10.8 • Diagnosis: Partially compensated • Blood glucose 1,890 mg/dL Respiratory Acidosis • Diagnosis: Partially compensated Metabolic • Note that we determined the primary Acidosis disorder is respiratory first, then we looked – DKA at the bicarbonate second to see if there was • Tip for ventilator management: The low carbon compensation. dioxide here is compensatory and should not be fixed. 8 11/12/15 What’s new with Troponin? • Original (conventional) troponin assays CARDIAC BIOMARKERS lacked sensitivity – Most normal patients were “Not detected” – Needed to monitor Tn levels for 6-9 hr until MI ruled out • Newer (high-sensitivity) troponin assays are more sensitive Troponin I Non –MI causes of elevated troponin • iSTAT cTnI at Chippenham • Defibrillation • Cardiac