anaemia evaluation
TRANSCRIPT
In the name of God, Most Gracious, Most Merciful
- Dr. Mohammed Sadiq Azam
PG M:1 (Dr. Siraj’s Unit)
DCMS @ PEH
EVALUATION OF A CASE OF ANAEMIA
CASE HISTORIES:
• 22/F presented with complaints of shortness of breath (NYHA GR IV),
orthopnoea+, chest discomfort and palpitations on exertion which gradually
increased over the last 6 months to attain present severity. H/s/o Pica+, H/o
passing worms in stools+. No h/o rash, photosensitivity or seizures. O/E: Pallor+,
BPPE+, JVP , s3 gallop+, b/l basal creps (fine)+, no organomegaly, no FF.
• 45/F presented with c/o shortness of breath (NYHA GR II-III), no orthopnoea, no
PND. Past h/o jaundice+. H/o blood transfusion in past +. O/E: Pallor++, Icterus++
+, Hepatomegaly~2 cm below C/m, Splenomegaly~15cm, no FF.
• 75/F presented with c/o fatigability and lethargy over last 8 month, initially mild
now increased in intensity. H/o sob on exertion (NYHA GR I-II). No H/o
orthopnoea/PND. No H/o chest discomfort. Not a known diabetic. H/s/o malena+.
H/o loss of appetitie, loss of weight+ over last 5 months. O/E: Pallor++, anicteric
no PE, CVS/RS – NAD, P/A- NAD.
EVALUATION – HISTORY:
• Age/Sex
• Rate of onset – Rapid/Slow
• Blood loss – Haematemesis / malena / bleeding piles / menorrhagia /
metorrhagia / epistaxis / hematuria / haemoptysis
• Abdomen – Appetitie / weight loss / dysphagia / regurgitation / dyspepsia / abd
pain / diarrhoea / constipation / jaundice / soreness of tongue / previous abd
surgeries
• Reproductive – Menstrual history in detail / number & interval between
pregnancies / miscarriages
• Urinary system – Nocturnal polyuria
• CNS – Parasthesiae / difficulty in walking
EVALUATION – HISTORY:
• Bleeding tendency – Easy bruising / prolonged bleeding after trivial injuries /
bleeding from more than one site
• Skeletal system – Bone pain / Arthritis / Arthralgia
• Temperature – Fever / Night sweats
• Drug ingestion – Previuos / current
• Occupation – Metal dusts / solvent fumes / lead
• Diet
• Social history – Alcoholism
• Past H/o – Previous anaemia: diag & Rx, response to Rx
• Family H/o – Anaemia / recurrent jaundice / IUD & childhood deaths
EVALUATION – EXAMINATION:
• Skin – Colour, texture, petechiae, ecchymoses, scratch marks.
• Nails – Brittleness, longitudinal ridging, koilonychia
• Conjunctiva/Sclera – Pallor, icterus, haemorrhages
• Retina – Haemorrhages, s/o HTN/renal failure, other changes
• Mouth – Mucous membrane: Pallor, petechiae
• Gums: Bleeding, hypertrophy
• Tongue: Redness, atrophy of papillae
• Abdomen – HSM, either HM or SM, tenderness, mass, ascites
• CVS – BP, valvular, vascular prosthesis
• CNS – Peripheral neuritis, s/s/o SADSC
EVALUATION – EXAMINATION:
• Supf LN – Enlargement of cervical, axillary, inguinal, epitrochlear nodes
• Bones – Tenderness (esp. of sternum), tumour
• Legs – Ulcers / scars of healed ulcers
• P/R – Haemorrhoids / CA Rectum
• Pelvic – Menorrhagia, metorrhagia, uterus, cervix
• Torniquet test
• Urine – Protein, urobilinogen, BS/BP
THE APPROACH …
Provisional Diagnosis: Anaemia for evaluation
Is anemia associated with other haematological abnormalities?
Yes No
BM Examination
LeukemiasAplastic anaemiasMDS / MFMyelophthisisMegaloblastic anaemia
Is there an appropriate reticulocyte response to anaemia?
Yes No
Evidence of haemolysis?
Yes No
Evaluate causeof haemolysis
Evaluate:haemorrhagic causes
RBC Indices
MCV >100 MCV 80-100 MCV <80
Evaluate:Macrocytic anemia
Evaluate:Normocytic anemia
Evaluate:Microcytic anemia
(Ref: Bertil Glader: Anaemia: General Considerations, Wintrobe’s Clinical Haematology 11/e, 2004: 951-978)
• Retic count = % reticulocytes in RBC population
• Retic count corrected for anaemia = % retculocytes x pt Hb/15 or pt Hct/45
• BUT, Retics released under intense EPO stimulation remain in circulation for approx 2x the usual 1 day survival of non stress retics, so:
• Corrected Retic index = Retic count corrected for anaemia x 0.5
• < 2.5 = inadequate response – hypoprolifertive / maturation disorder (marrow prod impaired)
• ≥ 2.5 = adequate response – haemolytic / haemorrahgic
• Absolute retic count = %retics x RBC count/l3
• Low retic count + active marrow erythropoiesis = ineffective erythropoiesis
• IDA
• Sideroblastic anaemia
• Thalassemias
• (Also associated with LDH)
RETICULOCYTOSIS: A WORD
(Ref: Bertil Glader: Anaemia: General Considerations, Wintrobe’s Clinical Haematology 11/e, 2004: 951-978)
Macrocytic anaemia
Does the P/S reveal hypersegmented neutrophils / macroovalocytes?
Yes No
Megaloblastic anaemia – BM to confirmTest for B12/Folate levels
B12 def No def Folate def
Schilling’s test:Corrects with IF
Yes No
Pernicious anaemia:Gastric resection
Ileal diseasePrevious ileal SxSmall bowel bac overgrowthFish tapewormDrug induced malabsorption
Inherited disorders of DNA synDrugs tht interfere with DNA syn
Poor dietDrug induced malabsJejuneal resectionTropical sprueGluten sensitivity Needs - Pregnancy - Chronic hemolysis
Nonmegaloblastic anaemia
Reticulocytosis
Haemolytic N /
Consider: - Alcohol - Hypothyroidism - Liver disease
If NO: BM exam
- MDS- Red cell aplasia- Acq siderobl anaemia- Herid dyserythropoietic anaemia (I& III)
(Ref: Bertil Glader: Anaemia: General Considerations, Wintrobe’s Clinical Haematology 11/e, 2004: 951-978)
Microcytic anaemia Appropriate age: Rule out malignancy
Reticulocytes
Low / N Increased
P/S: Abnorm morphologyLabs for RBC destrucHb studies
- Homozygous β thal- Haemolytic elliptocyt- Herid pyropoikilocytosis
Iron Profile
Fe TIBC Ferritin
FeN/ TIBCN/ Ferritin
N. FeN. TIBCN. Ferritin
FeN. TIBC Ferritin
Iron deficiency
ESR, CRP+or other studies s/o underlying Inflammatory disorder
AOCD
Hb electrophoresis
- α Thal trait- β Thal trait- Hb E syn- Hb C disorder
BM examination with Fe stains
Sideroblastic anaemia
(Ref: Bertil Glader: Anaemia: General Considerations, Wintrobe’s Clinical Haematology 11/e, 2004: 951-978)
Normocytic anaemia
Reticulocytes
RBC prod N./ RBC prod
H/o jaundice, splenomegalyPresence of P/S abnormalities Bilirubin / LDH
Yes
No
Haemolysis
Haemolytic anaemia
S.Fe
LowN. / High
AOCDEarly IDA
- S. Chemistries to screen for renal, hepatic, endocrine disease- Consider EPO levels, thyroid studies
Positive Negative
- Anaemia of renal disease- Anaemia of liver disease- Anaemia due to endocrine failure
BM aspirate & Bx
- Infiltrative disorder (Leuk, myeloma, MF, Mets)
- Red cell aplasia- MDS- Dyserythropoietic anaemia (Type II)
• Retic index ≥ 2.5. Polychromatophilic macrocytes ++ in P/S
• Marrow examination is rarely required if retic index is increased appropriately.
• RBC indices are typically normocytic or slightly macrocytic (reflects retics)
HAEMORRHAGIC ANAEMIA:
Blood loss
AcuteSubacute Chronic
Missed
No reticulocytosis
Modest reticulocytosis
Presents ///ar to IDAObserve for 2-3 weeksSigns of recovery - Hb - Retic count
HAEMORRHAGIC ANAEMIA:
Volume of blood loss (ml)
Blood volume (%)
Symptoms
500-1000 10-20 Few if any symptoms
1000-1500 20-30 Asymptomatic while at rest in a recumbent position; light headedness and hypotension when upright; tachycardia
1500-2000 30-40 Symptoms present when recumbent; thirst, SOB, clouding or LOC; BP, CO, venous pressure decrease, pulse usually rapid; extremities become cold, clammy & pale
2000-2500 40-50 Lactic acidosis, shock; irreversible shock, death
• Least common form of anaemia
• High retic count: Reflects the ability of the erythroid marrow to compensate for haemolysis, and, in the case of extravascular haemolysis, the efficient recycling of iron from the destroyed RBC to support RBC production.
• Intravascular haemolysis – PNH – loss of Fe – limits marrow response
• Hence, the level of marrow response depends on:
• The severity of anaemia
• The nature of the underlying disease process
• Hemoglobinopathies – mixed picture. (Retic count is but with respect to degree of marrow erythroid hyperplasia).
HAEMOLYTIC ANAEMIA:
• Presentation varies:
• Acute self limiting illness (autoimmune/EM pathway/GR defects)
• Chronic process (Hb defects/ RBC defects) with a typical history
• HS: chronic course – present with complications such as bilirubin gallstones or splenomegaly and not anaemia per se.
• Chronic haemolysis also prone to aplastic anaemia if infections occur.
HAEMOLYTIC ANAEMIA:
• PNH
• Erythrocyte fragmentation disorders
• Transfusion reactions resulting from ABO incompatability
• Paroxysmal cold haemoglobinuria
• AIHA (occasionally)
• Infections:
• Blackwater fever in falciparum malaria
• Clostridial sps
• Chemical mediated:
• Arsine poisoning
• Snake & Spider venoms
• Acute drug reactions with G6PD def
• I.V. admin of distilled water
• Thermal injury
HAEMOLYTIC ANAEMIA: INTRAVASCULAR LYSIS
• Morphological abnormalities: Spherocytes, Elliptocytes, Stomatocytes, Acanthocytes, Echinocytes, Sickle cells, Target cells, Schistocytes
• Direct Antiglobulin test (Coomb’s test): +ve in IHA (2-5% false neg)
• Osmotic fragility test : HS (Osmotic gradient ektacytometry is more sensitve & specific, but not widely available)
• Tests for Heinz bodies (supravital staining): G6PD def, unstable Hb disease, thalassemias, chemicals. (Not seen when spleen is intact)
HAEMOLYTIC ANAEMIA: LABS
• Asso with anaemia & retculocytosis:
• Hemorrhage
• Recovery from iron, folate or vitamin B12 deficiency
• Recovery from marrow failure
• Asso with jaundice & anaemia:
• Ineffective erythropoiesis (intramedullary erythropoiesis)
• Bleeding into a body cavity or tissue
• Asso with jaundice without anaemia
• Defective bilirubin conjugation
• Crigler-Najjar syndrome
• Gilbert syndrome
• Marrow invasion
• Myoglobinuria
HAEMOLYTIC ANAEMIA: D/D
• Any case of anaemia requires a detailed work up starting with history.
• Stepwise approach is the golden rule.
• IDA in elderly – avoid being ‘Penny wise, Pound foolish’
• In tropical countries, tropical malabsorption syndromes are more rampant than we realize – LOOK OUT, it may be missed unless you look for it.
• Better not to start any IFA or B12 supplements until we diagnose the cause of anaemia.
• Bone marrow is not the answer to every anaemia – AVOID indiscriminate use.
• No cost is greater than the patient’s life. Investigate what’s mandatory.
• Delayed diagnosis is better than a wrong diagnosis – DO NOT hurry to treat.
CONCLUSION: