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Elevated b12 level icd 10:
Definition Field Listing
Aetna considers measurement of serum homocysteine medically necessary in persons with borderline vitamin B-12 deficiency, where the results will impact the member's management (See CPB 0763 - Homocysteine Testing ). Neuropathies associated with pernicious anemia (Addisonian anemia, Biermer's anemia); or. Intramuscular or subcutaneous administration of vitamin B-12 injections for more than 2 to 3 months is subject to review to ascertain if deficiency/abnormalities have improved and to decide whether continued treatment is medically necessary. Footnotes * Documentation of B-12 deficiency is not required in these circumstances. In a systematic review of randomized trials on vitamin B-6, B-12, and folic acid supplementation and cognitive function, Balk and colleagues (2007) stated that despite their important role in cognitive function, the value of B vitamin supplementation is unknown. A total of 14 trials met selection criteria; most were of low quality and limited applicability. Approximately 50 different cognitive function tests were assessed. Three trials of vitamin B-6 and 6 of vitamin B-12 found no effect overall in a variety of doses, routes of administration, and populations. One of 3 trials of folic acid found a benefit in cognitive function in people with cognitive impairment and low baseline serum folate levels. Six trials of combinations of the B vitamins all concluded that the interventions had no effect on cognitive function. Among 3 trials, those in the placebo arm had greater improvements in a small number of cognitive tests than participants receiving either folic acid or combination B-vitamin supplements. The evidence was limited by a sparsity of studies, small sample size, heterogeneity in outcomes, and a lack of studies that evaluated symptoms or clinical outcomes. The authors concluded that there is insufficient evidence of an effect of vitamin B-6, B-12, or folic acid supplementation, alone or in combination, on cognitive function testing in people with either normal or impaired cognitive function. This is in agreement with Clarke et al (2007) who stated that randomized trials are needed to ascertain the relevance of vitamin B-12 supplementation for the prevention of dementia. Cobalamin deficiency is more common in the elderly primarily because of the increasing prevalence with age of Cbl malabsorption due to autoimmune atrophic gastritis. Aetna considers intramuscular or subcutaneous vitamin B-12 injections medically necessary only for members with current or previously documented B-12 deficiency and any of the following diagnoses and conditions:. Tobacco Amblyopia Retrobulbar neuritis associated with heavy smoking, also known as tobacco amblyopia. In a randomized, double-blind, placebo-controlled trial, Albert et al (2008) examined if a combination of folic acid, vitamin B-6, and vitamin B-12 lowers risk of cardiovascular disease (CVD) among high-risk women with and without CVD. A total of 5,442 women aged 42 years or older, with either a history of CVD or 3 or more coronary risk factors, were enrolled in this study. Subjects received a combination pill containing 2.5 mg folic acid, 50 mg vitamin B-6, and 1 mg vitamin B-12 or a matching placebo, and were treated for 7.3 years. Main outcome measures were a composite outcome of myocardial infarction, stroke, coronary re-vascularization, or CVD mortality. Compared with placebo, a total of 796 women experienced a confirmed CVD event (406 in the active group and 390 in the placebo group). Patients receiving active vitamin treatment had similar risk for the composite CVD primary end point (226.9/10,000 person-years versus 219.2/10,000 person-years for the active versus placebo group; relative risk [RR], 1.03; 95 % confidence interval [CI]: 0.90 to 1.19; p = 0.65), as well as for the secondary outcomes including myocardial infarction (34.5/10,000 person-years versus 39.5/10,000 person-years; RR, 0.87; 95 % CI: 0.63 to 1.22; p = 0.42), stroke (41.9/10,000 person-years versus 36.8/10,000 person-years; RR, 1.14; 95 % CI: 0.82 to 1.57; p = 0.44), and CVD mortality (50.3/10,000 person-years versus 49.6/10,000 person-years; RR, 1.01; 95 % CI: 0.76 to 1.35; p = 0.93). In a blood substudy, geometric mean plasma homocysteine level was decreased by 18.5 % (95 % CI: 12.5% to 24.1%; p. Aetna considers vitamin B-12 injections experimental and investigational for all other indications, including use for treatment of age-related cataract, autism, chronic fatigue syndrome (myalgic encephalomyelitis), delayed sleep-wake phase disorder, non-24-hour sleep-wake rhythm disorder, depression, diabetic peripheral neuropathy, elevated homocysteine in persons not diagnosed with homocysteinuria, fibromyalgia, impaired cognitive function (except for dementia secondary to vitamin B-12 deficiency), peripheral entrapment neuropathies (e.g., carpal tunnel syndrome), and tinnitus; for the prevention of osteoporotic fracture, for the reduction of cardiovascular risks, for the prevention of stroke, and as adjunctive therapy for weight loss because there is insufficient evidence in the peer-reviewed literature to support the use of B-12 injections for these indications. Metformin Members with vitamin B-12 deficiency due to use of metformin that is not corrected by oral vitamin B-12. Acute phase or acute exacerbation of a neuropathy due to malnutrition or alcoholism Footnotes for neuropathy *; or. Aetna considers measurements of holotranscobalamin (a biologically active vitamin B-12 fraction) for the diagnosis of vitamin B-12 deficiency experimental and investigational because its clinical value has not been established. Malabsorption syndromes (e.g.,sprue, idiopathic steatorrhea, and other malabsorption syndromes); or. Vitamin B-12 belongs to the family of cobalamins. It is available in all animal-derived foods, and is absorbed at a rate of 5 mcg per day. After being ingested, vitamin B-12 becomes bound to intrinsic factor, a protein secreted by gastric parietal cells. The vitamin B-12/intrinsic factor complex is absorbed in the terminal ileum by cells with specific receptors for the complex. The absorbed complex is then transported via plasma and stored in the liver. Since the liver stores 2,000 to 5,000 mcg vitamin B-12 (adequate for up to 5 years), dietary deficiency of cobalamin (Cbl) is rare. In most cases, vitamin B-12 deficiency is due to an inability of the intestine to absorb the vitamin, which may result from an autoimmune disease that reduces the production or blocks the action of intrinsic factor, or from other diseases that result in intestinal malabsorption. The most frequent underlying cause of vitamin B-12 deficiency is pernicious anemia, which is associated with decreased production of intrinsic factor. Abdominal surgery may cause Cbl deficiency in several ways: gastrectomy eliminates the site of intrinsic factor production; blind loop syndrome results in competition for vitamin B-12 by bacterial overgrowth in the lumen of the small intestine; and surgical resection of the ileum eliminates the site of vitamin B-12 absorption. Rare causes of vitamin Cbl deficiency include pancreatic insufficiency; fish tapeworm infection, in which the parasite uses luminal vitamin B-12; and severe Crohn's disease, resulting in reduced ileal absorption of vitamin B-12. Members receiving methotrexate or pralatrexate (Folotyn) Footnotes for pralatrexate *. Most patients with overt Cbl deficiency report serum vitamin B-12 levels of less than 100 pg/ml. The hallmark of vitamin B-12 deficiency is megaloblastic anemia. Vitamin B-12 deficiency also leads to neurological deficits including paresthesias, sensory loss, ataxia, disequilibrium, diminished or hyperactive reflexes, and spasticity. In more advanced cases, cerebral function may also be affected resulting in disturbances of mood, psychoses, and dementia. Physician administration of intramuscular or subcutaneous vitamin B-12 injections is considered medically necessary for the diagnoses and conditions listed above. Surgical or mechanical disorders (e.g., gastrectomy (subtotal or total), blind loop syndrome, intestinal anastomosis, intestinal strictures, and resection of the small intestine). Conditions associated with decreased production of intrinsic factor; or. Note: Most Aetna plans exclude coverage of nutritional supplements. Under these plans, Aetna does not cover charges for oral vitamins that can be purchased without a prescription, or for oral vitamins that are prescribed solely as a dietary supplement even if a physician's prescription is needed for purchase. Please check benefit plan descriptions. This is the American ICD-10-CM version of D51.8 - other international versions of ICD-10 D51.8 may differ. Diseases of the blood and blood-forming organs and certain disorders involving the immune mechanism. 2016 (effective 10/1/2015): New code (first year of non-draft ICD-10-CM). Hydroxocobalamin injection usp(1000 mcg/ml) is a clear red liquid solution of hydroxocobalamin which is available in a 30-ml brown glass multidose vial packaged in a paper box. Shown is 500 mcg B-12 (as 1/2 cc) drawn up in a 0.5-cc U-100 27 gauge x 1/2" insulin syringe, as prepared for subcutaneous injection. The most common initial symptom is feeling tired. [4]. Impaired B 12 absorption can also occur following gastric removal ( gastrectomy ) or gastric bypass surgery. In these surgeries, either the parts of the stomach that produce gastric secretions are removed or they are bypassed. This means intrinsic factor, as well as other factors required for B 12 absorption, are not available. However, B 12 deficiency after gastric surgery does not usually become a clinical issue. This is probably because the body stores many years' worth of B 12 in the liver and gastric surgery patients are adequately supplemented with the vitamin. [30]. A buildup of certain metabolites occurs in B 12 deficiency due to its role in cellular physiology. Methylmalonic acid (MMA) can be measured in both the blood and urine, whereas homocysteine is only measured in the blood. An increase in both MMA and homocysteine can distinguish between B 12 deficiency and folate deficiency because only homocysteine increases in the latter. [40]. It more commonly affects people of northern European descent. [2]. abnormal findings on antenatal screening of mother ( O28.- ) abnormalities of lipids ( E78.- ) abnormalities of platelets and thrombocytes ( D69.- ) abnormalities of white blood cells classified elsewhere ( D70 - D72 ) coagulation hemorrhagic disorders ( D65 - D68 ) diagnostic abnormal findings classified elsewhere - see Alphabetical Index hemorrhagic and hematological disorders of newborn ( P50-P61 ). When suspected, diagnosis is made by blood and, occasionally, bone marrow tests. [6]. Antibodies to intrinsic factor and parietal cells cause the destruction of the oxyntic gastric mucosa, in which the parietal cells are located, leading to the subsequent loss of intrinsic factor synthesis. Without intrinsic factor, the ileum can no longer absorb the B 12. [27]. The term "pernicious" means "deadly", and was used as before the availability of treatment the disease was often fatal. [5]. H. pylori is involved in the pathogenesis of the disease. A long-standing H. pylori infection may cause gastric autoimmunity by a mechanism known as molecular mimicry. Antibodies produced by the immune system can be cross-reactive and may bind to both H. pylori. Pernicious anemia refers to anemia that results from lack of intrinsic factor. [5]. With proper treatment, most people live normal lives. [5]. Although the healthy body stores three to five years' worth of B 12 in the liver, the usually undetected autoimmune activity in one's gut over a prolonged period of time leads to B 12 depletion and the resulting anemia. B 12 is required by enzymes for two reactions: the conversion of methylmalonyl CoA to succinyl CoA, and the conversion of homocysteine to methionine. In the latter reaction, the methyl group of 5-methyltetrahydrofolate is transferred to homocysteine to produce tetrahydrofolate and methionine. This reaction is catalyzed by the enzyme methionine synthase with B 12 as an essential cofactor. During B 12 deficiency, this reaction cannot proceed, which leads to the accumulation of 5-methyltetrahydrofolate. This accumulation depletes the other types of folate required for purine and thymidylate synthesis, which are required for the synthesis of DNA. Inhibition of DNA replication in red blood cells results in the formation of large, fragile megaloblastic erythrocytes. The neurological aspects of the disease are thought to arise from the accumulation of methylmalonyl CoA due to the requirement of B 12 as a cofactor to the enzyme methylmalonyl CoA mutase. [23]. Anemia (essential) (general) (hemoglobin deficiency) (infantile) (primary) (profound) D64.9. Because pernicious anemia is due to a lack of intrinsic factor, it is not preventable. [10]. Vitamin B 12 deficiency anemia, of which pernicious anemia is a type, [8]. The treatment of PA varies by country and area. Opinions vary over the efficacy of administration (parenteral/oral), the amount and time interval of the doses, or the forms of vitamin B 12 (e.g. cyanocobalamin/hydroxocobalamin). More comprehensive studies are still needed in order to validate the feasibility of a particular therapeutic method Abnormal findings on examination of blood, without diagnosis. ] including depressive mood, low-grade fevers, diarrhea, dyspepsia, weight loss, [17]. Posner JB, Saper CB, Schiff ND, Plum F (2007). Plum and Posner's Diagnosis of Stupor and Coma. Oxford University Press, USA. p. 41. ISBN. Clinical Methods: The History, Physical, and Laboratory Examinations. Butterworth Publishers. Retrieved 2008-07-04. Mass lesions within monkey coma by virtue of direct effects on the reticular formation of monkey. Once the level of consciousness is determined, clinicians seek clues for the cause of any alteration. [9]. Stroke and intracranial hemorrhage are other causes. [12]. person shows excessive drowsiness and responds to stimuli only with incoherent mumbles or disorganized movements. [8]. Tindall SC (1990). "Level of consciousness". In Walker HK, Hall WD, Hurst JW. The ascending reticular activating system is a postulated group of neural connections that receives sensory input and projects to the cerebral cortex through the midbrain and thalamus from the retucular formation. [9]. Usually the first tests in the ER are pulse oximetry to determine if there is hypoxia, serum glucose levels to rule out hypoglycemia. A urine drug screen may be sent. A CT head is very important to obtain to rule out bleed. In cases where meningitis is suspected, a lumbar puncture must be performed. A serum TSH is an important test to order. In select groups consider vitamin B12 levels. Checking serum ammonia is not advised. [. Some scales have "delirious" below this level, in which a person may be restless or agitated and exhibit a marked deficit in attention. [2]. Although the neural science behind alertness, wakefulness, and arousal are not fully known, the reticular formation is known to play a role in these. [9]. Comatose people do not even make this response to stimuli, have no corneal or gag reflex, and they may have no pupillary response to light. [8]. Mass lesions in the brain stem normally cause coma due to their effects on the reticular formation. [11]. This article is about the medical concept. For the psychological concept, see Altered state of consciousness. Responsiveness to pain is determined with a mild painful stimulus such as a pinch; moaning or withdrawal from the stimulus is considered a response to pain. [3]. A confused person may be bewildered, disoriented, and have difficulty following instructions. [9]. The AVPU scale is another means of measuring LOC: people are assessed to determine whether they are a lert, responsive to v erbal stimuli, responsive to p ainful stimuli, or u nresponsive. [3]. Using ACDU, a patient is assessed for a lertness, c onfusion, d rowsiness, and u nresponsiveness. [10]. Assessing LOC involves determining an individual's response to external stimuli. [12]. Text is available under the Creative Commons Attribution-ShareAlike License. A lowered level of consciousness indicate a deficit in brain function. [4]. Dunlosky, J. & Bjork, R. A. (Eds), Handbook of Metamemory and Memory. Psychology Press: New York.