Anemia With Hemodynamic Compromise or Complications

The No Nonsense Teds Fat Melting

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1. If patient is hemodynamically unstable, transfuse immediately.

2. If evidence of acute bleeding, stop bleeding and obtain adequate IV access (anticipating need for transfusion).

B. Anemia Without Hemodynamic Compromise or Complications. Proceed with workup in an orderly fashion. Laboratory testing is not always diagnostic, and bone marrow biopsy may be indicated.

C. Iron Deficiency Anemia. Alter patient's diet as indicated to prevent recurrence or persistence. Sample stools for occult blood, especially in children older than 2-3 years of age; if positive, source of blood loss must be found. Heavy menstrual losses are most common cause of iron deficiency in young women. Iron stores are replenished with 6 mg/kg/day of elemental iron divided into 2 or 3 doses. Treatment is continued for at least 3 months after normalization of CBC to ensure adequate stores.

D. Folate Deficiency. Usually due to dietary insufficiency. Supplement 1 mg folate PO daily. Folate, 1 mg daily, is also given for chronic hemolytic anemias to meet increased needs in replacing RBCs.

E. Vitamin B12 Deficiency. Inadequate dietary intake and true pernicious anemia occur rarely in children. More likely causes of vitamin B12 deficiency in children and adolescents include bacterial overgrowth, ileal disease, postsurgical gastrectomy, and ileal resection.Vitamin B12 is replaced by administration of 100 mcg IM daily for 2 weeks, then 60-100 mcg IM every 4 weeks.

F. Hemolytic Anemia. With elevated reticulocyte count and no obvious source of blood loss, consider a destructive process. Brisk ongoing hemolysis results in elevation of total and indirect bilirubin and increased LDH without concomitant increase in AST or ALT. Immune-mediated processes are diagnosed using Coombs test. Ill patients with a microangiopathic smear may have hemolytic anemia associated with hemolytic uremic syndrome or thrombotic thrombocytopenic purpura, or disseminated intravascular coagulation (DIC). Low platelets and fibrinogen, elevated PT and PTT, and fibrin degradation products indicate DIC. Inherited disorders (thalassemia, sickle cell anemia, or an enzymopathy) must be ruled out. The possibility of paroxysmal nocturnal hemoglobinuria and Wilson disease should be considered in cases with unclear etiology.

G. Anemia of Chronic Disease. Usually a diagnosis of exclusion. There is no specific diagnostic test for this disorder; treatment is that of underlying disease.

VI. Problem Case Diagnosis. Review of systems and past medical, social, dietary, and family history for the 18-month-old boy were benign. Physical exam findings were normal except for pallor, decrease in visible scleral vessels, and lack of pink color in palmar creases. CBC showed normal WBC count and differential, elevated platelet count, normal MCV and RDW, and normal RBC morphology. Reticulocyte count was 0.1%. Results of bone marrow biopsy demonstrated absence of all erythroid precursors except the most primitive line. Patient was transfused expectantly when the hemoglobin level dropped to 5 g/dL and reticulocyte count remained at 0.1%. Seven weeks later, after a second transfusion, the reticulocyte count was 8%. The CBC normalized without recurrence of anemia. Patient was diagnosed with transient erythroblastopenia of childhood.

VII. Teaching Pearl: Question. What bedside trick can help in the diagnosis of cold agglutinin hemolytic anemia?

VIII. Teaching Pearl: Answer. In a patient with pallor and dark urine, rotate a tube of the patient's anticoagulated blood at room temperature and after chilling to look for large RBC aggregates termed bedside cold agglutinins. This form of hemolytic anemia is most

■ commonly associated with Mycoplasma pneumoniae or Epstein-Barr virus infection. If transfusion is indicated, keep all skin surfaces of patient very warm (and warm blood as it is transfused) to prevent pathologic IgM antibody from binding to the RBC surface, with resultant complement fixation and hemolysis.

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