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Interdisciplinary Geriatric Assessment:
Mrs. Curtis

Action Plan

The diagnostic information leads to the conclusion of vit B₁₂ deficiency resulting in the diagnosis of anemia and peripheral neuropathy. Anemia is a complex disease and is a diagnostic challenge to correct the underlying disease.

Diagnostically, the anemia is represented by the low hematocrit and hemoglobin. Other parameters, such as the mean corpuscular volume (MC) and the red blood cell distribution width (RDW) are used to categorize the type of anemia. Reticulocyte count can also help, but this was not available in this case. Examination of the peripheral blood is also critical in the diagnostic evaluation, and in this case, the macrocytes and increased lobulation are consistent with macrocytic anemia. The absence of certain blood cell abnormalities is just as crucial to the differential diagnosis of the type of anemia.

Macrocytic anemia is likely the result of vit B₁₂ deficiency, or folic acid deficiency. These can be differentiated by measurement of both levels in the blood, and in this case, the results indicated a deficiency in vit B₁₂, but not red cell folic acid. The clinical setting is consistent with vit B₁₂ deficiency since the patient presented with signs of neurological dysfunction. In this case, there was confounding clinical evidence for signs of folic acid deficiency, which accompanies a history of poor diet (also alcoholism or pregnancy, not apparent issues in this case.)

The most common cause of vit B₁₂ deficiency is pernicious anemia, caused by the absence of gastric intrinsic factor production, which aids absorption of vit B₁₂ from the intestine.

Neurologic symptoms may appear in the early stage of the disease. Symptoms may include paresthesia, numbness, and weakness, usually due to peripheral neuropathy, but eventually the deficiency (if not treated) may affect the spinal tracts in the CNS. Weakness and ataxia follow the sensory symptoms. There are diminished extensor plantar responses and ankle reflexes. In some cases, encephalopathy can occur and appear as somnolence and irritability in late stages. Other symptoms may include glossitis, anorexia and weight loss.

The anemia and neuropathy in this case will respond rapidly to vitamin administration. Improvement of the anemia can be expected after a single injection of vit B₁₂, resulting in a rapid improvement of blood cell formation, and a feeling of well-being. To sustain this progress vit B₁₂ supplementation should continue until liver stores are replenished. The hemoglobin level will rise within a week. With continued treatment, a normal blood cell profile should occur within 8 weeks. The completeness of the neurologic response is not as rapid and may not be as complete as the hematological response. In this case, sensory and motor changes of a few weeks may be fully reversible. Dysfunction for a period of several months has a worse prognosis.

In treating the deficiency, the goals are to reverse the abnormalities produced by the deficiency, prevent a relapse, and replenish tissue stores with vitamin B₁₂. Since the deficiency may be related to malabsorption, therapy may be parenteral with lifelong maintenance when the disease is irreversible. Usual doses are 100 to 1000 µg, beginning daily IM for about a week and tapering in frequency to monthly maintenance injections.

Mrs. Curtis is scheduled for discharge from the hospital tomorrow. She will need skilled nursing, occupational therapy, and physical therapy services. What other services might be indicated for her to return to her prior level of function?

The interdisciplinary team, including the patient's family, has been called together to develop a plan of action for Mrs. Curtis. Print your IGA form. Acting as the team leader, develop a plan of action for Mrs. Curtis. When you have completed your IGA form, compare it to the form completed by the CIGAP team.

Reference:
Kelley WN. Textbook of internal medicine. 4^th ed. Philadelphia: JB Lippincott, 2000.