LAB. INTERPRETATION CBC,ELECTROLYTES,LFT

VBG /ABG

DR TAZEEM HUSSAIN . MBBS,MCPS,FCPS

ED.KSMC

.

Common haematology valuesHaemoglobin men: 13–18g/dL women: 11.5–16g/dL Mean cell volume, mcv76–96fL ↓; ↑Platelets 150–400 × 109/L White cells (total) 4–11 × 109/L Neutrophils 40–75% lymphocytes 20–45% Eosinophils 1–6%If outside this range, consult:

.

. Microcytic Hypochromic Anemia (MCV < 83; MCHC < 31)

Condition Serum IronTotal Iron-Binding

Capacity (TIBC)Bone Marrow Iron Comment

Iron deficiency ↓ ↑ 0 Responsive to iron therapy

Chronic inflammation

↓ ↓ ++ Unresponsive to iron therapy

Thalassemia major ↑ N ++++ Reticulocytosis and indirect bilirubinemia

Thalassemia minor N N - ↓ ++ Elevation of fetal hemoglobin and Hb A2, target cells, and poikilocytosis

Lead poisoning N N ++ Basophilic stippling of RBCs

Sideroblastic ↑ N ++++ Ring sideroblasts in marrow

Hemoglobin N N ++ Hemoglobin electrophoresis

↓ = decreased; ↑ = increased; 0 = absent; +'s indicate the amount of stainable iron in bone marrow specimens, on a scale of 0-4; N = normal.

Macrocytic Anemia (MCV >95)Megaloblastic bone marrow Deficiency of vitamin B-12

Deficiency of folic acid

Drugs affecting deoxyribonucleic acid (DNA) synthesis

Inherited disorders of DNA synthesis

Nonmegaloblastic bone marrow Liver disease

Hypothyroidism and hypopituitarism

Accelerated erythropoiesis (reticulocytes)

Hypoplastic and aplastic anemia

Infiltrated bone marrow

Macrocyte Larger than normal (>8.5 µm diameter).

Microcyte Smaller than normal (< 7 µm diameter).

Hypochromic Less hemoglobin in cell. Enlarged area of central pallor.

Spherocyte Loss of central pallor, stains more densely, often microcytic. Hereditary spherocytosis and certain acquired hemolytic anemias

Target cell Hypochromic with central "target" of hemoglobin. Liver disease, thalassemia, hemoglobin D, and postsplenectomy

Leptocyte Hypochromic cell with a normal diameter and decreased MCV. Thalassemia

Elliptocyte Oval to cigar shaped. Hereditary elliptocytosis, certain anemias (particularly vitamin B-12 and folate deficiency)

Schistocyte Fragmented helmet- or triangular-shaped RBCs. Microangiopathic anemia, artificial heart valves, uremia, and malignant hypertension

Stomatocyte Slitlike area of central pallor in erythrocyte. Liver disease, acute alcoholism, malignancies, hereditary stomatocytosis, and artifact

Various Forms of RBCs

.Tear-shaped RBCs Drop-shaped erythrocyte, often microcytic. Myelofibrosis and infiltration of marrow with tumor. Thalassemia

Acanthocyte Five to 10 spicules of various lengths and at irregular intervals on surface of RBCs

Echinocyte Evenly distributed spicules on surface of RBCs, usually 10-30. Uremia, peptic ulcer, gastric carcinoma, pyruvic kinase deficiency, and preparative artifact

Sickle cell Elongated cell with pointed ends. Hemoglobin S and certain types of hemoglobin C and l

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Classification of the Hemolytic Disorders

Hereditary Acquired

Intracorpuscular defect

Hereditary spherocytosis Hereditary elliptocytosis Hemoglobinopathies Thalassemias Congenital dyserythropoietic anemias Hereditary RBC enzymatic deficiencies Rarer hereditary abnormalities

Vitamin B-12 and folic acid deficiency Paroxysmal nocturnal hemoglobinuria Severe iron deficiency

Extracorpuscular defect

Physical agents: Burns, cold exposure Traumatic: Prosthetic heart valves, march hemoglobinuria, disseminated intravascular coagulation (DIC), graft rejection Chemicals: Drugs and venoms

College of Physicians & Surgeons Pakistan

urea and electrolytesSodium 135–145 mmol/L Potassium 3.5–5 mmol/L Creatinine 70–150 μ mol/L Urea 2.5–6.7 mmol/L If outside this range, consult:

LFTBilirubin 3–17 μmol/L Alanine aminotransferase, alt 5–35iu/L

Aspartate transaminase, ast 5–35iu/L

Alkaline phosphatase, alp 30–150iu/L

.Blood gasespH 7.35–7.45 P aO2 >10.6kPa (75–100mmHg) P aCO2 4.7–6kPa (35–45mmHg) Base excess ±2mmol/L

Acid–base balanceArterial blood pH is closely regulated in

health to 7.40 ± 0.05 by various mechanisms including bicarbonate, other plasma buffers such as deoxygenated hemoglobin, and the kidney.

a few simple rules are applied, then interpretation and diagnosis are easy. The key principle is that primary changes in

H CO–3 metabolic CO2 respiratory

A simple method1 Look at the pH: is there an acidosis or alkalosis?CO2 is an acidic gas—is CO2 raised with an

acidosis, lowered with an alkalosis? If so, it is in keeping with the

pH and thus caused by a respiratoryproblem. If there is no change, or an

opposite one, then the change is compensatory.

.3 Is the HCO 3 abnormal? (Normal

concentration 22–28mmol/L)If so, is the change in keeping with the pH? is alkaline—HCO3 is raised with an alkalosis, lowered with an acidosis? If so, the problem is metabolic

.Your patient’s blood gas shows: pH 7.05, CO2

2.0kPa, HCO 3 8.0mmol/L.There is an acidosis. The CO2 is low, and thus

it is a compensatory change. TheHCO3is low and is thus the primary change, ie a metabolic acidosis.

.The anion gapestimates unmeasured plasma anions (‘fixed’

or organic acids such as phosphate, ketones, and lactate, which are hard to

measure directly). It is calculated as the difference between plasma cations (Na & K ) and anions (Cl &HCO3 ).

Normal range: 10–18mmol/L. It is helpful in determining the cause of a metabolic acidosis.

.Metabolic acidosispH↓, HCO3↓Causes of metabolic acidosis and an increased anion gap:Due to increased production, or reduced excretion, of

fixed/organic acids. HCO 3 falls and unmeasured anionsassociated with the acids accumulate.• Lactic acid (shock, infection, tissue ischaemia)• Urate (renal failure)• Ketones (diabetes mellitus, alcohol)• Drugs/toxins (salicylates, biguanides, ethylene glycol,

methanol)

Causes of metabolic acidosis and a normal anion gap:

Due to loss of bicarbonate or ingestion of H ions (Cl is retained).

• Renal tubular acidosis• Diarrhoea• Drugs (acetazolamide)• Addison’s disease• Pancreatic fistula• Ammonium chloride ingestion

.Metabolic alkalosispH↑, HCO 3 ↑• Vomiting• K depletion (diuretics)• Burns• Ingestion of base

Respiratory acidosis

pH↓, CO ↑• Type 2 respiratory failure due to any lung,

neuromuscular, or physical cause • Most commonly chronic obstructive

pulmonary disease (COPD). Look at the P O2 . It will probably be low.

Is oxygentherapy required? Use controlled O2 (Venturi connector) if COPD is the underlying cause, as too much oxygen may make matters worse

.Respiratory alkalosispH↑, CO ↓A result of hyperventilation of any cause.CNS causes:Stroke; subarachnoid bleed; meningitis.

SEE.in VBG.Step 1. PH.Step 2. BICARBONATE.Step 3. CARBON DI OXIDE.Step 4. compensation ?

IF ABG.See oxygen /carbon di oxide.

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