## Clinical Context This patient presents with **megaloblastic anemia** with neurological manifestations (paresthesias, positive Romberg sign) consistent with **B12 deficiency with subacute combined degeneration (SCD)**. The low serum B12 (180 pg/mL) and characteristic blood findings confirm the diagnosis. ## Why Parenteral B12 is Essential **Key Point:** Neurological complications of B12 deficiency require **immediate parenteral replacement** — oral therapy is insufficient because: - Neurological damage can be **irreversible** if delayed - Parenteral route bypasses intestinal absorption defects (suspected pernicious anemia given glossitis and positive Romberg) - Parenteral B12 achieves rapid, high-dose tissue saturation ## Investigation Strategy **High-Yield:** Once B12 replacement is initiated, investigation for the **cause** (parietal cell antibodies, intrinsic factor antibodies, Schilling test if available) should proceed in parallel: - Suspected pernicious anemia (autoimmune gastritis) is the most common cause in this age group - Identifying the etiology guides long-term management (lifelong B12 supplementation) **Clinical Pearl:** Neurological signs (paresthesias, ataxia, positive Romberg) indicate **urgent need for treatment** — do not delay with additional confirmatory testing before starting parenteral B12. ## Why Not the Other Options? | Option | Reason | | --- | --- | | Oral cyanocobalamin | Ineffective in pernicious anemia (intrinsic factor deficiency); neurological complications demand parenteral route | | Antibody testing first | Diagnostic confirmation should not delay treatment in a symptomatic patient with neurological signs | | Metabolite levels before treatment | Methylmalonic acid and homocysteine are elevated in B12 deficiency but are **confirmatory, not therapeutic**; starting treatment immediately is the priority | [cite:Harrison 21e Ch 102]
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