Anemia

Anemia is a common issue encountered in the family medicine. By definition it is a deficit of red blood cells or hemoglobin. It is important to identify the underlying etiology to further manage this issue.

History

 * fatigue, weakness, dyspnea, CP, palpitations, decreased exercise tolerance, pre-syncope, syncope
 * Symptoms of infection/recurrent, malignancy, blood loss, ongoing bleeding
 * PMHx: mechanical valves
 * Medications: anticoagulants, anti-platelets, new medications
 * SHx: Diet, ETOH

Physical

 * Vitals + volume status (red flags, tachycardia/hypotension/fluctuation in LOC)
 * Skin/LN: angular chelosis, pallor, jaundice, lymphadenopathy, petechiae, glossitis, nail changes (brittle)
 * Chest: orthostatic hypotension, systolic flow murmur, wide pulse pressure, signs of CHF
 * Abdo: HSM, masses, DRE
 * Neuro: proprioception (if suspecting B12 deficiency)

Differential

 * T - thalassemia
 * A- Anemia of chronic disease
 * I - Iron deficiency anemia (IDA)
 * L- Lead poisoning
 * S - Sideroblastic anemia

Work-up

 * CBC (microcytic anemia, RDW), Ferritin, TIBC, serum iron
 * +/- lead level, HbG electrophoresis, blood smear

Iron deficiency

 * Etiology:
 * increase demand (e.g. pregnancy, lactation, growing child)
 * decrease supply (diet, malabsorption)
 * increase loses (hemorrhage, intravascular hemolysis)
 * Screening: immigrants, refugees, pregnancy
 * high risk pediatric patients (well baby care): preterm or low birth weight, infants introduced to cows milk < 12 months of age, breast fed infants without adeqate iron in diet after 6 months, children who consume >24 oz daily of cow's milk, special health concerns (chronic disease, trauma, surgery, medications, diets),
 * also consider screening: children in poverty, poor weight gain, or poor diet
 * Work-up:
 * Attempt to identify a source of bleeding
 * Initial investigation of microcytic anemia --> ferritin 
 * If male of any age or non-menstuating female --> Evaluate for GI source (endoscopy/colonoscopy)
 * If neither male/non-menstruating female a trial of iron is acceptable x 1 month (should see increase in HbG by 10-20). If not evaluate for GI source/malabsorption. If see improvement continue iron x3-6 months to be replenish stores then r/a
 * In anemic patients with menorrhagia, determine the need to look for other causes of the anemia
 * Treatment:
 * If clinical status is compromised by moderate to severe anemia consider admission to acute care facility and blood transfusion
 * Prevention: encourage full balanced diet
 * Oral preparations preferred over IV form
 * Oral: Target 100mg of elemental iron 3x/day
 * Best absorption on empty stomach with addition of  Vitamin C. Absorption may be decreased by antacids, supplemetation (aluminum, magnesium, zinc, calcium). Recommend 2 hours between taking Rx.
 * Iron can decrease absorption of bisphosphonate, tetracycline, fluroquinolones, levodopa, thyroid rx
 * S/E: nausea, vomit, dyspepsia, constipation dark stool, bloating (can trial smaller dose)
 * After HbG returns to normal should be continued for 3-6 months to restore iron stores

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  Anemia of Chronic Disease


 * Etiology: underproduction and impaired iron utilization
 * Diagnosis: of exclusion, often co-exists with iron deficiency
 * Treatment: manage underlying, may consider transfusion/erythropoietin PRN

Lead Poisoning

 * LEAD: lead lines (epiphysis of long bones, gingivae), encephalopathy, abdominal pain colicky/anemia (basophilic stippling), Drops (wrist, foot)
 * Diagnosis: lead level
 * Treatment: remove source, chelation therapy, EDTA (adults)

Sideroblastic Anemia

 * Etiology: defect in heme biosynthesis in RBC precursors (hereditary x-linked, reversible, and idiopathic forms)
 * Diagnosis: smear (ringed sideroblasts), bone marrow biopsy
 * Treatment: heriditary (high dose B6), acquired (Epo and G-CSF), reversible (remove precipitating)

Thalassemia

 * Etiology: defect in production of alpha or beta chains of HbG (4alpha, 2 beta)
 * Beta-thalassemia: common in Mediterranean, Asian
 * Alpha- thalassemia: Asians and Africans
 * Diagnosis: HbG electrophoresis

High reticulocytes

 * Blood loss - reticulocyte count can be normal at initial onset of bleeding
 * Hemolysis - peripheral smear, LDH (increased), haptoglobin (decreased), indirect bilirubin (increased)
 * Inherited:
 * Hemoglobinopathies - thalassemia, sickle cell. W/U HbG electrophoresis
 * Abnormal membrane (hereditary spherocytosis) - W/U: osmotic fragility test. Rx: vaccinations, splenectomy
 * Abnormal enzymes (G6PDeficiency, pyruvate kinase deficiency)- W/U: enzyme assays
 * Acquired
 * Autoimmune (cold/warm) W/U: direct Coomb's testing
 * Infection (e.g. malaria)
 * Microangiopathic hemolytic anemia (MAHA) (intravascular hemolytic anemia)
 * TTP, DIC, HEELP, malignant hypertension, vasculitis
 * W/U: peripheral smear (schistocytes), hemolytic w/u, urine hemoglobinuria
 * Drug related

Low reticulocytes

 * Pancytopenia: aplastic anemia, MDS, myelofibrosis, leukemia, TB, amyloidosis, sarcoidosis, drugs
 * Investigation: bone marrow aspiration
 * Non-pancytopenia: anemia of chronic disease, liver disease, renal disease

Sickle Cell Anemia

 * Etiology: mutation B-globin chain Glu-->Val
 * Higher incidence in African and Mediterranean
 * Sickle cell disease = two HbS (HbSS) - sickling occurs at pO2 80mmHg. Sickle cell trait HbAS - sickling occurs at pO2 40mmHg
 * Clinical: hemolytic anemia, jaundice, growth retardation, spenomegaly (functional asplenism), aplastic crisis, splenic sequestration crisis, vaso-occlusive crisis (pain, chest), priapism
 * Diagnosis: Peripheral smear, HbG electrophoresis
 * Treatment:
 * folic acid
 * Hydroxyurea (promotes HbF (fetal))
 * Manage vaso-occlusive events: hydration, analgesics, Abx, magnesium, exchange transfusion
 * Avoid conditions that promote sickling (acidosis, hypoxia, dehyration, fever)
 * Vaccination

Macrocytic Anemia

 * Megaloblastic: B12 deficiency, folate deficiency, drug related (e.g. MTX)
 * Non-megaloblastic: alcohol, hypothyroidism, MDS, liver disease, reticulocytosis
 * Investigations can include: b12 level, folate level, TSH, peripheral smear, LFTs, reticulocyte count, +/- bone marrow aspiration
 * B12 deficiency: confusion, ataxia, symmetric peripheral neuropathy (propioception/vibration - dorsal columns), memory loss, dementia, personality changes
 * Etiology:  pernicious anemia (antibodies to intrinsic factor), diet (vegetarian), post-gastrectomy, intestinal malabsorption (crohn's, celeiac, tapeworm, drugs, pancreatic insufficiency)
 * If intestinal absorption okay --> 1200mcg PO daily
 * If intestinal absorption impaired (e.g. pernicious anemia - lacking intrinsic factor)--> Intramuscular
 * Investion for pernicious anemia versus other causes use to be schilling test

Iron deficiency in pediatrics

 * risk of irreversible motor and cognitive deficits
 * Introduce iron rich food at 6 months
 * Treatment: look for source, ferrous sulphate 3-6mg of elemental iron/kg/day in divided dosing. Monitor for toxicity

Iron deficiency in Pregnancy

 * Recommend increase in iron consumption by 15-30mg elemental iron/day for pregnancy/breastfeeding in non-anemic women
 * Anemia is pregnancy T1 HbG < 110, T2 HbG < 104, T3 HbG < 110

Anemia in elderly

 * Often multifactorial
 * Recommend investigations if > 1 year of life or symptomatic

Transfusion

 * If symptomatic - transfuse
 * Cut-off (these are general cut-offs)
 * stable but critically ill with no active bleed --> Transfuse HbG < 70
 * patientw with ischemic heart disease wtth no active bleed --> Transfuse HbG 90-100

Resources
http://www.aafp.org/afp/2013/0115/p98.html

uptodate- anemia

http://www2.gov.bc.ca/gov/content/health/practitioner-professional-resources/bc-guidelines/iron-deficiency

dietary aspects of iron

Toronto Notes 2012

