DR TAZEEM HUSSAIN. MBBS,MCPS,FCPS ED.KSMC

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Common haematology values Haemoglobin men: 13–18g/dL women: 11.5–16g/dL Mean cell volume, mcv 76–96fL ↓ ; ↑ 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:

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. Microcytic Hypochromic Anemia (MCV < 83; MCHC < 31) ConditionSerum Iron Total Iron-Binding Capacity (TIBC) Bone Marrow IronComment Iron deficiency ↓↑ 0Responsive to iron therapy Chronic inflammation ↓↓ ++ Unresponsive to iron therapy Thalassemia major ↑ N++++ Reticulocytosis and indirect bilirubinemia Thalassemia minorN N - ↓ ++ Elevation of fetal hemoglobin and Hb A2, target cells, and poikilocytosis Lead poisoningNN++ Basophilic stippling of RBCs Sideroblastic ↑ N++++ Ring sideroblasts in marrow HemoglobinNN++ 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 marrowDeficiency of vitamin B-12 Deficiency of folic acid Drugs affecting deoxyribonucleic acid (DNA) synthesis Inherited disorders of DNA synthesis Nonmegaloblastic bone marrowLiver disease Hypothyroidism and hypopituitarism Accelerated erythropoiesis (reticulocytes) Hypoplastic and aplastic anemia Infiltrated bone marrow

MacrocyteLarger than normal (>8.5 µm diameter). MicrocyteSmaller than normal (< 7 µm diameter). HypochromicLess 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 StomatocyteSlitlike 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 Uremia, peptic ulcer, gastric carcinoma, pyruvic kinase deficiency, and preparative artifact Sickle cellElongated cell with pointed ends. Hemoglobin S and certain types of hemoglobin C and l

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College of Physicians & Surgeons Pakistan

urea and electrolytes Sodium 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:

LFT Bilirubin 3–17 μmol/L Alanine aminotransferase, alt 5–35iu/L Aspartate transaminase, ast 5–35iu/L Alkaline phosphatase, alp 30–150iu/L

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

Acid–base balance Arterial 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 method 1 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 respiratory problem. 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 gap estimates 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 acidosis pH ↓, 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 anions associated 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 alkalosis pH ↑, 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 alkalosis pH ↑, 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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