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문제

A nurse is caring for a 45-year-old client diagnosed with vitamin B12 deficiency anemia who reports fatigue, weakness, and tingling in hands and feet. Which nursing intervention should the nurse prioritize?

A 65-year-old client has been diagnosed with vitamin B12 deficiency anemia and reports fatigue, weakness, and tingling in hands and feet.
해설
Vitamin B12 injections are the priority intervention as they directly treat the deficiency, especially when absorption is impaired. Other options do not address the underlying cause.
같은 주제 다음 문제A nurse is assessing a client with suspected vitamin B12 deficiency anemia. Which assessme…

심화 해설

Understanding the Priority Intervention for Vitamin B12 Deficiency Anemia

The correct answer is to administer vitamin B12 injections as prescribed. This is the priority because the client's neurological symptoms—specifically the tingling in hands and feet (peripheral neuropathy)—indicate that the deficiency has progressed beyond a simple hematologic issue and requires immediate and direct repletion to prevent potentially irreversible nerve damage.

Why Not the Other Options?


  • 1. Encourage the client to increase iron-rich foods in their diet: This intervention is appropriate for iron deficiency anemia, not vitamin B12 deficiency. The two conditions have different underlying causes, diagnostic findings, and treatments. Increasing iron intake will not correct the neurological or hematological abnormalities caused by a lack of B12.



  • 2. Administer folic acid supplements as prescribed: While folic acid can partially correct the megaloblastic anemia caused by B12 deficiency, it does nothing to halt or reverse the neurological damage. In fact, administering folic acid without B12 can mask the hematologic signs of B12 deficiency while allowing the peripheral neuropathy to silently progress, a dangerous clinical pitfall.



  • 3. Provide education about increasing dietary fiber intake: This is unrelated to the core problem of B12 deficiency. While general health promotion is important, it does not address the client's immediate symptoms or the underlying pathophysiological process.



Deep Dive into the Pathophysiology and Clinical Reasoning

The client’s presentation of fatigue, weakness, and paresthesia is a classic triad for vitamin B12 deficiency. To understand why parenteral (injection) replacement is the priority, you must connect the symptoms to the underlying biochemical roles of vitamin B12.

Vitamin B12 is a critical cofactor for two essential enzymatic reactions in human cells:

  1. Methylmalonyl-CoA mutase reaction: B12 is required to convert methylmalonyl-CoA to succinyl-CoA. Without B12, methylmalonic acid (MMA) accumulates. Elevated MMA is directly neurotoxic, causing demyelination of the spinal cord and peripheral nerves. This is the mechanism behind the client’s tingling in hands and feet [1].

  2. Methionine synthase reaction: B12 is required to convert homocysteine to methionine. Methionine is essential for DNA synthesis and the formation of myelin sheaths. A deficiency traps folate in an unusable form, disrupting DNA synthesis in rapidly dividing cells, such as the hematopoietic precursors in the bone marrow. This leads to megaloblastic anemia, which explains the client's fatigue and weakness [1].



The presence of neurological symptoms is a critical clinical differentiator. It signals that the deficiency is severe and has bypassed the body's stores. In many cases, especially in adults, the root cause is not a dietary lack but a malabsorptive condition, such as pernicious anemia, where the stomach lacks intrinsic factor [1]. A 65-year-old client is at higher risk for such conditions. If the client cannot absorb B12 through the gastrointestinal tract, oral supplements will be ineffective. Therefore, the definitive and most reliable treatment to halt neurological progression and reverse anemia is parenteral administration, typically intramuscular injections of cyanocobalamin or hydroxocobalamin.

The second provided source reinforces the importance of recognizing the systemic nature of B12 deficiency. It highlights that dermatological signs like skin hyperpigmentation can be an early, overlooked clue, particularly in individuals with long-term inadequate dietary intake [2]. This underscores that B12 deficiency is a multisystem disorder. The priority for a nurse is to address the most threatening systemic effect, which is the neurological injury signaled by paresthesia, by ensuring the client receives the prescribed B12 injections without delay. Monitoring for a positive response, such as a gradual resolution of paresthesia and improved energy levels, is a key subsequent nursing action.
References (research sources)
  • [1]
    Vitamin B12 deficiency: testing and treatment.Research articleBedz D, Forsyth C. (2026) · DOI: 10.18773/austprescr.2026.012
  • [2]
    Skin Hyperpigmentation: An Under-Recognized Dermatological Clue to Vitamin B12 Deficiency.Research articleMathur M, Paudel S, Karki S, Regmi S, Maharjan S, Bhattarai N. (2026) · DOI: 10.1002/ccr3.72634

임상 시나리오

Managing Vitamin B12 Deficiency with Neurological SymptomsPrioritizing Parenteral Replacement to Prevent Irreversible Nerve Damage

For clients with peripheral neuropathy (tingling, numbness), the priority is immediate vitamin B12 replacement, typically via intramuscular injection. Oral supplements are insufficient for severe deficiency or pernicious anemia due to lack of intrinsic factor.

Initial therapy often involves 1000 mcg of cyanocobalamin intramuscularly, administered daily or weekly until hematologic parameters normalize, then transitioned to monthly maintenance injections for life if the cause is irreversible.

Caution

Never administer folic acid alone before confirming B12 status. It can resolve megaloblastic anemia but allows neurological damage to progress silently. Monitor serum potassium levels during initial therapy, as rapid cell production can cause hypokalemia.

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