Vitamin [B.sub.12] deficiency: issues in nursing care.
Vitamin [B.sub.12] deficiency is a relatively common occurrence, affecting 3% to 40% of the general population (Dharmarajan & Norkus, 2001). Among older adults, the incidence is as high as 15% (Groff & Gropper, 2000), with an additional 15% undiagnosed over the age of 60 (Andres et al., 2001). In the Framingham Heart Study, 18% of participants aged 22 to 63 and 40% of those aged 65 to 99 had decreased vitamin [B.sub.12] levels (Brown, 2002). Specific groups at risk for developing vitamin [B.sub.12] deficiency include elders, alcoholics, and patients who have undergone surgeries of the gastrointestinal tract (Groff & Gropper, 2000).
Absorption, Metabolism, and Function
Vitamin [B.sub.12] also known as cyanocobalamin, is only available from exogenous dietary or synthetic origins. It is synthesized by bacteria and found in all animal sources. Generally, vitamin [B.sub.12] is bound to food proteins when ingested. In the stomach, gastric acid and pepsin split the vitamin from the food proteins. It then combines with carrier glycoproteins (R proteins) found in saliva, bile, and gastric and intestinal secretions. Pancreatic enzymes in the small intestine assist in freeing the vitamin from the R proteins. The vitamin then forms a complex with intrinsic factor, a specific glycoprotein that is secreted postprandially by parietal cells in the gastric lining, and moves toward the ileum to attach to receptors on the terminal ileum membrane. The vitamin is absorbed via phagocytosis (macrophages and monocyte cells engulf and ingest bacterial microorganisms) into the bloodstream for binding with proteins known as transcobalamin I, II, or III. Transcobafamin II mediates the majority of vitamin [B.sub.12] uptake at the cellular level (Baik & Russell, 1999; Dharmarajan & Norkus, 2001; Groff & Gropper, 1999). A small amount (approximately 1% to 3%) of vitamin [B.sub.12] that is ingested may be absorbed by passive diffusion, a process not requiring the presence of intrinsic factor (Dharmarajan & Norkus, 2001; Groff, & Gropper 1999). For every 10 micrograms of vitamin [B.sub.12] lost in bile, 90% is reabsorbed via the enterohepatic circulation (Kastin & Buchman, 2002). Unlike many other water-soluble vitamins, vitamin [B.sub.12] can be stored in the body for periods of 5 to 7 years. The liver, the main storage site, is capable of warehousing 2,000 to 5,000 micrograms (Kastin & Buchman, 2002; Mahan & EscottStump, 2000).
Vitamin [B.sub.12] has many important uses in the body, including fat and carbohydrate metabolism and protein synthesis. Adequate levels are essential for producing nucleic acids, forming neurotransmitters, and manufacturing myelin sheath. Vitamin [B.sub.12], vitamin [B.sub.6], and folate share common metabolic pathways involving homocysteine. A deficiency in vitamin levels is associated with an increased synthesis of homocysteine. Elevated homocysteine levels have been linked to arterial vascular disease and may pose an independent risk for cardiovascular disease (Gemmati et al., 1999; Hankey & Eikelboom, 2001; Malinow, Bostom, & Krauss, 1999).
In the United States, vitamin [B.sub.12] deficiency more frequently is related to problems with absorption rather than inadequate intake (Groff & Gropper, 1999). One common cause, particularly in older adults, is chronic atrophic gastritis, which affects as many as 30% of elders (Brown, 2002). The condition results in degeneration and thinning of the stomach wall, leading to gastric cell atrophy and a decrease in the production of stomach acids. This contributes to a decreased ability to split vitamin [B.sub.12] from food proteins (Huether & McCance, 2000). Helicobactor pylori is often associated with atrophic gastritis, which leads to gastric inflammation and a further decrease in gastric acid production (Brown, 2002). H. pylori represents one of the most common types of gastric infections, estimated to affect 90% of the adult population in developing countries and more than 50% of the population in developed countries (Kaptan et al., 2000).
Effects of Surgery
Abdominal surgery may impair greatly the absorption of vitamin [B.sub.12]. Total gastrectomy is associated with a loss of cells that secrete pepsin or intrinsic factor and hydrochloric acid. This results in an inability to absorb vitamin [B.sub.12]. Partial gastrectomy leads to decreased vitamin absorption due to the eventual development of atrophic gastritis. Following Bilroth II surgery, patients frequently develop gastric bacterial overgrowth. The bacterial uptake of vitamin [B.sub.12] limits the total amount available for gastrointestinal absorption (Mahan & Escott-Stump, 2000; McNally, 2001).
Small bowel surgery can lead to complications such as dumping syndrome, postprandial hypoglycemia, and bile reflux gastritis (Kastin & Buchman, 2002). As soon as possible after surgery, patient teaching should begin. The medical-surgical nurse can begin with the acute needs in the hospital while also introducing discharge instructions. Immediate needs related to discomfort and wound care are followed by lifestyle modifications as necessary (see Table 1).
Disorders of the pancreas or bowel also may affect vitamin [B.sub.12] absorption. A decrease in pancreatic enzymes affects the ability to split vitamin [B.sub.12] away from the R proteins so that it may complex with intrinsic factor. Thus, any pancreatic insufficiency can lead to decreased vitamin [B.sub.12] absorption (Mahan & Escott-Stump, 2000; Shils, Olson, Shike, & Ross, 1999). Crohn's disease, which is associated with multiple vitamin deficiencies, can occur anywhere along the gastrointestinal tract and commonly occurs in the ileum. Absorption of vitamin [B.sub.12] may be limited severely due to ongoing bowel inflammation and/or surgical resection (Kastin & Buchman, 2002). Other conditions resulting in decreased vitamin [B.sub.12] absorption include Whipple's disease and sprue. These disorders affect gastrointestinal mucosal function in the small intestine, thus impairing vitamin absorption (Montoya, Wink, & Sole, 2002).
Pernicious anemia is the absolute deficiency of intrinsic factor. Without intrinsic factor, vitamin [B.sub.12] absorption is limited to a minute amount through passive diffusion. The absence of intrinsic factor may be congenital or acquired, as with atrophic gastritis. Nearly 90% of those with pernicious anemia have serum autoantibodies to gastric parietal ceils or to intrinsic factor itself. The percentage of those with parietal cell autoantibodies increases with age, rising from 2.5% in the 3rd decade to 9.6% in the 8th decade of life (Balk & Russell, 1999). The average person with pernicious anemia is 50 to 60 years of age; occurrences in older women are slightly more than men (Montoya et al., 2002).
Congenital transcobalamin deficiency is an autosomal recessive disorder. As previously noted, transcobalamin is important in vitamin [B.sub.12] transport and cellular uptake (McNally, 2001).
Intestinal parasites, such as the broad fish tapeworm (Diphyllobothrium latum), may be identified occasionally as the source of vitamin [B.sub.12] deficiency. The parasites, ingested in raw or undercooked fish (often pike or salmon), attach to the wall of the small intestine. Absorption ultimately is impaired due to vitamin uptake by the worms (Tierney, McPhee, & Papadakis, 2000).
Finally, several medications impair vitamin [B.sub.12] absorption (see Table 2). Vitamin C in doses of 500 mg or more may impair or destroy the bioavailability of vitamin [B.sub.12] if taken with meals or within 1 hour after meals (Groff & Gropper, 1999). Chemotherapeutic medications are diverse, but some can interfere with the cobalaminfolate-dependent metabolic pathway. The oncologist can determine the type of chemotherapy interaction if any, and direct the treatment for vitamin [B.sub.12] deficiencies (Montoya et al., 2002).
Signs and Symptoms
Of Vitamin [B.sub.12] Deficiency The patient with vitamin [B.sub.12] deficiency may be asymptomatic or may present with acute or subtle symptoms. Proper diagnostic testing and treatment require careful consideration of the patient's history and presenting symptoms. The patient may complain of weakness, fatigue, depression, difficulty concentrating, and memory loss. Vitamin [B.sub.12] deficiency is more common after the age of 50. Because older patients may attribute these symptoms to aging (Dharmarajan & Norkus, 2001), they may delay reporting to the health care provider. Additionally, older adults with vitamin [B.sub.12] deficiency may present with conditions or symptoms that have worsened in the past few days or weeks, such as congestive heart failure, dyspnea, cognitive impairment, dizziness, or apathy (Smith, 2000).
A thorough history should include presence of other medical conditions (particularly gastrointestinal conditions), dietary patterns, use of prescriptive and non-prescriptive medications and supplements, alcohol use, and previous surgeries (Montoya et al., 2002). Any family history of pernicious anemia is important to ascertain. Approximately 20% of people who have relatives with pernicious anemia will go on to develop vitamin [B.sub.12] deficiency (Balk & Russell, 1999).
The deficiency of vitamin [B.sub.12] leads to a variety of symptoms related to impaired DNA synthesis at the cellular level. Rapidly dividing ceils such as those of the intestinal tract frequently are affected, resulting in a smooth, shiny, beefy red tongue; glossitis; and mucosal ulceration (Balk & Russell, 1999). The patient's skin may take on a yellow tint due to jaundice, concurrent anemia, and ineffective erythropoiesis. Conjunctival pallor may be noted (Mahan & Escort-Stump, 2000; Montoya et al., 2002). (See Table 3 for a list of common symptoms of vitamin [B.sub.12] deficiency.)
Neurologic symptoms occur as a result of demyelination of axons and related nerve tracts. Neural involvement first appears in peripheral nerves and cerebral white matter. If the patient is untreated, involvement will progress to both corticospinal tracts and posterior columns of the spinal cord. Symptoms may include central vision loss (indicating involvement of the optic nerve), clumsiness, gait disturbance, sensory disturbances in the extremities (especially paresthesias or numbness in the fingers), ataxia, altered deep tendon reflexes, impaired Romberg test (a neurologic test that identifies loss of position sense), loss of vibratory and fine touch, and altered proprioception. The patient may exhibit forgetfulness, lapses of memory, inability to concentrate, or poor judgment. Rarely, cognitive syndromes may be observed. These may include personality changes, dementia, hallucinations, violent behavior, paranoia, or frank psychosis, which is sometimes referred to as megaloblastic madness (Baik & Russell, 1999; Browning, 2002).
It may be helpful to separate diagnostic tests into two categories: tests that screen for vitamin [B.sub.12] deficiency, and tests that determine the cause of the problem. Patients who are at increased risk for the deficiency, either by history or presenting symptoms, should be screened immediately. Also, because the incidence of vitamin deficiency increases with age, routine screening should be considered in all patients over the age of 50 (Dharmarajan & Norkus, 2001). Often, the deficiency is suspected following a routine complete blood count. Impaired cell division in the bone marrow may lead to increased production of immature, abnormally large (macrocytic) red cells, as well as an elevated mean cell volume (MCV) and increased red cell distribution width (RCDW) (Balk & Russell, 1999; Mahan & Escott-Stump, 2000). Along with an overall reduction in hematocrit and hemoglobin levels, this may suggest vitamin [B.sub.12] deficiency. However, this test is not specific; other conditions such as folate deficiency may cause the same results (Ho, Kanwell, & Bailey, 1999).
The deficiency also may he detected if serum vitamin [B.sub.12] levels are less than 200 pg/mL. While the test is inexpensive, the results must be viewed cautiously because false negatives may occur even if the deficiency is significant. A false negative (elevated level in the presence of deficiency) may be noted in patients who have active liver disease, autoimmune disease, lymphoma, or myeloprofiferative disorders. Conversely, false positives can occur in pregnancy, folate deficiency, excessive vitamin C intake, and multiple myeloma (Dharmarajan & Norkus, 2001).
Serum or urine methylmalonic acid (MMA) levels are recommended if serum [B.sub.12] levels are between 100 and 400 pmol/mL (Dharmarajan & Norkus, 2001). The MMA is a more sensitive and specific test because vitamin [B.sub.12] is necessary in the conversion of L methylmalonic acid to succinyl coenzyme. Therefore, decreased vitamin levels result in increased levels of MMA. Elevated serum homocysteine levels also may be noted with vitamin [B.sub.12] deficiency. This test is less specific because the level also will be increased in folate deficiency (Ho et al., 1999).
If screening tests reveal a deficiency in vitamin [B.sub.12], additional tests may determine the cause of the problem. These may include gastrin level measurements or assays for intrinsic factor or parietal cell antibodies, or transcobalamin assays. A Schilling test may be done if vitamin malabsorption is suspected. However, the test is complex, and results may not be reliable if 24-hour urine samples are not collected accurately or the patient has renal failure (Dharmarajan & Norkus, 2001).
Management of Vitamin [B.sub.12] Deficiency
High doses of oral vitamin [B.sub.12] treat the deficiency effectively, regardless of the cause (Smith, 2000). Vitamin [B.sub.12] is available in oral, intramuscular, and intranasal forms. Significant deficiencies often are treated initially with injections. Typically, 100 to 1,000 mcg injections are given daily for 1 week, then weekly for 1 month, and monthly thereafter (Montoya et al., 2002). Hematologic improvement may be noted in the first week, and improvement in neurologic symptoms within 6 months (Kastin & Buchman, 2002; Montoya et al., 2002). For patients who do not want to have injections of vitamin [B.sub.12], a daily oral dose of 1,000 mcg will result in 10 mcg of absorbed vitamin [B.sub.12] that should be adequate to meet daily needs (Kastin & Buchman, 2002).
Treatment is determined by the cause of the deficiency, follow-up diagnostic testing, and the primary care provider's preferences. An intranasal form of vitamin [B.sub.12], widely available in Europe for years, has been approved by the Food and Drug Administration for use in the United States by patients after initial stabilization by other routes. Treatment consists of cyanocobalamin (Nascobal[R]) 500 mcg sprayed in one nostril once weekly. The intranasal form is contraindicated in patients using other intranasal medications or those with nasal disorders (Dharmarajan & Norkus, 2001; Montoya et al., 2002). Patients should understand the chronic nature of vitamin [B.sub.12] treatment.
Replacement therapy may continue for months to years, or may be a lifelong treatment (Food and Nutrition Board, 2000).
Preventing Vitamin [B.sub.12] Deficiency
Vitamin [B.sub.12] is usually taken in adequate amounts in the diet. The recommended daily allowance is 2.4 mcg/day for adults; most adults take in 4 to 7 mcg/day (Food and Nutrition Board, 2000). The best food sources for the vitamin are beef, fish, milk, and shellfish (see Table 4). However, vitamin [B.sub.12] and folate are two vitamins that are better absorbed in synthetic form. Synthetic forms of the vitamin, which are found in fortified foods and vitamin supplements, are not bound to food proteins (Brown, 2002). This can be beneficial for any patient who has a protein-bound vitamin malabsorption condition. All patients over the age of 51 should take synthetic forms of vitamin [B.sub.12] because 10 to 30% of this age group experience protein-bound vitamin malabsorption (Ho et al., 1999).
Vitamin [B.sub.12] is not present in plants and does not occur in vegetables or fruit. The average nonvegetarian diet generally contains 3 to 9 mcg of vitamin [B.sub.12] per day (Montoya et al., 2002). Strict vegetarian diets may result in significant vitamin deficiency. Symptoms may not appear for 20 to 30 years after the initial beginning of a vegan diet (Groff & Gropper, 1999). For lactovegetarians, milk is a very important source of vitamin [B.sub.12] (Balk & Russell, 1999).
Following patient discharge from an acute care facility, the medical-surgical nurse should assess the patient's ongoing dietary intake and then recommend modifications when appropriate to maintain good nutrition. In some cases, referral to a nutritionist might be needed. The patient should be instructed in the correct administration of the replacement therapy for vitamin [B.sub.12]. An evaluation of any previously recommended lifestyle changes should be reviewed with the patient and corrections or support given as appropriate. It is also important to encourage follow-up with the primary care provider at appropriate intervals.
Vitamin [B.sub.12] deficiency is more commonly linked to the inability to absorb the vitamin due to lack of intrinsic factor than to insufficient dietary intake. It is also more common among older adults than in younger people. The risk for developing the deficiency increases with age. The onset of vitamin [B.sub.12] deficiency is often insidious, and serious hematologic or neurologic impairment may be present before a diagnosis is made. Untreated vitamin [B.sub.12] deficiency can lead to irreversible neurologic damage within a few months to years.
Fortunately, treatments are readily available in oral, intranasal, and intramuscular form. Patients require teaching regarding foods high in vitamin [B.sub.12], the potential lifelong nature of the problem, and need for compliance and regular followup. Nurses must be alert to the possibility of vitamin deficiency, particularly in patients over the age of 50, alcoholics, and those with a history of gastric conditions, surgeries, or a family history of pernicious anemia. All diagnostic testing should proceed from screening to tests aimed at determining the cause of the deficiency. This comprehensive approach can result in early detection and treatment, and help to avoid the devastating, irreversible consequences of persistent, untreated vitamin [B.sub.12] deficiency.
Table 1. Patient Teaching Following Small Bowel Surgery 1. Pain related to surgical incision and gastric secretions and irritants. a. Determine pain characteristics from verbal and physical assessment. b. Administer prescribed medications or treatments as appropriate. c. Document pain assessment, interventions, and outcomes. 2. Lifestyle alterations related to postoperative physiologic needs. a. Instruct patient to: i. Cease smoking. ii. Avoid ingesting spicy foods. iii. Avoid very hot or very cold foods/beverages. iv. Use relaxation techniques to reduce pain and gastric secretions. 3. Ineffective management of therapeutic regimen. a. Assess the patient's understanding of the disease process. b. Instruct the patient to: i. Verbalize plan to modify lifestyle issues. ii. Identify stressors that can cause an exacerbation. iii. State plan to avoid coffee, tea, cola, and alcohol. iv. Discuss nutritional considerations specific to disease process. v. Discuss the use, side effects, and adverse reactions of medications that will be taken at home. vi. Identify circumstances when patient needs to have contact with the health care provider. vii. Describe the methods for contacting the health care provider. Table 2. Medications that Impair Vitamin [B.sub.12] Absorption Cholestyramine (Questran[R]) Colchicine Histamine 2 receptor antagonists: Cimetidine (Tagamet[R]) Ranitidine (Zantac[R]) Nizatidine (Axid[R]) Famotidine (Pepcid[R]) Metformin hydrochloride (Glucophage[R]) Neomycin (Mycifradin[R]) p-amino salicylic acid Proton pump inhibitors: Lansoprazole (Prevacid[R]) Omeprazole (Prilosec[R]) Adapted from Clark, Queener, & Karb (1999). Table 3. Common Symptoms of Vitamin [B.sub.12] Deficiency Eyes: Central vision loss Conjunctiva: Pale in color Mouth: Glossitis; oral mucosal ulceration(s) Tongue: Smooth surface, shiny, beefy red in color Skin: Yellow tint over the natural skin color Circulatory: Anemia Neurological: Clumsiness; gait disturbance, numbness in extremities; ataxia; altered deep tendon reflexes; impaired Romberg test; loss of vibratory and fine touch sensations; altered proprioception Memory: Forgetfulness; lapses of memory; poor concentration and/or judgment Adapted from Montoya et al., 2002; Smith, 2000. Table 4. Leading Sources of Vitamin [B.sub.12] and Folate Vitamin [B.sub.12] Clams Oysters Crab Liver Beef Milk Kidney Folate Liver Dark green, leafy vegetables Dried beans Green vegetables Oranges Avacados Whole wheat products Adapted from Montoya et al., 2002 Smith, 2000.
Andres, E., Kurtz, J.E., Perrin, A.E., Maloisel, E, Demangeat, C., Goichot, B., et al. (2001). Oral cobalamin therapy for the treatment of patients with food-cobalamin malabsorption. The American Journal of Medicine, 111(2), 126-129.
Baik, H.W., & Russell, R.M. (1999). Vitamin [B.sub.12] deficiency in the elderly. Annual Review of Nutrition, 19, 357-378.
Brown, J.E. (2002). Nutrition through the life cycle (pp. 422-47, 470-74). Belmont, CA: Wadsworth/Thomson Learning.
Browning, R.H. (2002). What's wrong with this patient? RN, 65(1), 47-49.
Clark, J.F., Queener, S.F., & Karb, V.B. (1999). Pharmacologic basis of nursing practice (6th ed.). St. Louis: Mosby.
Dharmarajan, T.S., & Norkus, E.P. (2001). Approaches to vitamin [B.sub.12] deficiency: Early treatment may prevent devastating complications. Postgraduate Medicine, 110, 99-105.
Food and Nutrition Board, Institute of Medicine. (2000). Dietary reference intakes for thiamin, riboflavin, niacin, vitamin [B.sub.12], folate, vitamin B6, pantothenic acid, biotin, and choline. Washington, DC: National Academy Press.
Gemmati, D., Previati, M., Serino, M.L., Moratelli, S., Guerra, S., Capitani, S., et al. (1999). Low folate levels and thermolabile methylenetetrahydrofolate reductase as primary determinate of mild hyperhomocystinemia in normal and thromboembolic subjects. Arteriosclerosis, Thrombosis, and Vascular Biology, 19(7), 1761-1767.
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Case Study for Advanced Practice Nurses
A 52-year-old woman is seen in the primary care clinic for complaints of fatigue and weakness for the past few weeks. Upon further questioning, she indicates that she is experiencing difficulty concentrating at her job as an executive legal secretary. She attributes this to her fatigue. She states that sometimes when she walks, she feels "like my legs are going to go out from underneath me." In the past few days, she has noticed that her hands "feel funny ... like they are asleep."
Past Medical History
Her past medical history is not contributory, except for Type 2 diabetes, well-controlled for 3 years on biquanide metformin (Glucophage[R]). She does not take any other medications, except an occasional aspirin for headaches. She admits to drinking 1 to 2 cocktails occasionally in the evening before supper. Otherwise, she follows an ADA diet and has even been able to lose 20 pounds in the past 2 years.
Vital signs are within normal limits. The physical exam is within normal limits with the following exceptions: Grade I-II systolic murmur not present 6 months ago Pale conjunctiva 3 + deep tendon reflexes (DTRs) Abnormal Romberg test
Blood glucose: 121 mg/dL Vitamin [B.sub.12]:198 pmol/mL RBC: 4.6 million/[mm.sup.3] WBC: 5.6 x [10.sup.9]/L HCT: 32% HgB: 9 g/100ml MCV: 106 [mm.sup.3] RCDW: 15% Segs: 63% Lympohcytes: 29% Monophils: 4% Eosinophils: 2% Basophils: 1% Bands: 1%
The patient is diagnosed with hematologic and neurologic effects of vitamin [B.sub.12] deficiency. Support for the diagnosis of vitamin [B.sub.12] deficiency includes her age, gender, long-term use of biquanide metformin, use of alcohol, and use of aspirin.
The patient is very opposed to intramuscular injections and prefers to take oral medicine only. She is started on 1,000 mcg of oral cyanocobalamin every day. Additionally, she is referred to a nutritionist to develop a plan to increase foods high in vitamin [B.sub.12]. Her use of alcohol is further discussed. She has indicated her desire to quit drinking completely. She does not believe this will be a problem and is agreeable to information on resources and support services.
Lori Candela, EdD, MS, RN, CCRN, is an Assistant Professor of Nursing, University of Nevada, Las Vegas, NV.
Sue E. Meiner, EdD, APRN,BC, GNP, is an Assistant Professor of Nursing, University of Nevada, Las Vegas, NV; and a Geriatric Nurse Practitioner, HealthEssentials Home Care, Las Vegas, NV.
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|Title Annotation:||Clinical Practice|
|Author:||Candela, Lori; Meiner, Sue E.|
|Date:||Aug 1, 2004|
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