Evidence based medicine

1) Analyze both cases (2 pages per case)

2) verify that conclusion matches with the case study answers provided here.

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3) Use evidence based medicine resources.

Case 1: A 25-year-old woman who has been on a strict vegan diet for the past 2 years presents with increasing numbness and paresthesias in her extremities, generalized weakness, a sore tongue, and gastrointestinal discomfort. Physical examination reveals a pale woman with diminished vibration sensation, diminished spinal reflexes, and extensor plantar reflexes (Babinski sign). Examination of her oral cavity reveals atrophic glossitis, in which the tongue appears deep red in color and abnormally smooth and shiny due to atrophy of the lingual papillae. Laboratory testing reveals a macrocytic anemia based on a hematocrit of 30% (normal for women, 37–48%), a hemoglobin concentration of 9.4 g/dL, an erythrocyte mean cell volume (MCV) of 123 fL (normal, 84–99 fL), an erythrocyte mean cell hemoglobin concentration (MCHC) of 34% (normal, 31–36%), and a low reticulocyte count. Further laboratory testing reveals a normal serum folate concentration and a serum vitamin B12 (cobalamin) concentration of 98 pg/mL (normal, 250–1100 pg/mL). Once megaloblastic anemia was identified, why was it important to measure serum concentrations of both folic acid and cobalamin? Should this patient be treated with oral or parenteral vitamin B12?



This patient’s megaloblastic anemia appears to be due to vitamin B12 (cobalamin) deficiency secondary to inadequate dietary B12. It is important to measure serum concentrations of both folic acid and cobalamin because megaloblastic anemia can result from deficiency of either nutrient. It is especially important to diagnose vitamin B12 deficiency because this deficiency, if untreated, can lead to irreversible neurologic damage. Folate supplementation, which can compensate for vitamin B12–derived anemia, does not prevent B12-deficiency neurologic damage. To correct this patient’s vitamin B12 deficiency, she would probably be treated parenterally with cobalamin because of her neurologic symptoms, followed by oral supplementation to maintain her body stores of vitamin B12



Case 2: A 14-year-old girl with a history of asthma requiring daily inhaled corticosteroid therapy and allergies to house dust mites, cats, grasses, and ragweed presents to the emergency department in mid-September, reporting a recent “cold” complicated by worsening shortness of breath and audible inspiratory and expiratory wheezing. She appears frightened and refuses to lie down but is not cyanotic. Her pulse is 120 bpm, and respirations are 32/min. Her mother states that she has used her albuterol inhaler several times a day for the past 3 days and twice during the previous night. She took an additional two puffs on her way to the emergency department, but her mother states that “the inhaler didn’t seem to be helping so I told her not to take any more.” What emergency measures are indicated? How should her long-term management be altered?



This patient demonstrates the destabilizing effects of a respiratory infection on asthma, and her mother’s comments demonstrate the common (and dangerous) phobia about “overuse” of bronchodilator or steroid inhalers. The patient has signs of imminent respiratory failure, including her refusal to lie down, her fear, and her tachycardia, which cannot be attributed to her minimal treatment with albuterol. Critically important immediate steps are to administer high-flow oxygen and to start albuterol by nebulization. Adding ipratropium (Atrovent) to the nebulized solution is recommended. A corticosteroid (0.5–1.0 mg/kg of methylprednisolone) should be administered intravenously. It is also advisable to alert the intensive care unit, because a patient with severe bronchospasm who tires can slip into respiratory failure quickly, and intubation can be difficult.


Fortunately, most patients treated in hospital emergency departments do well. Asthma mortality is rare (fewer than 4000 deaths per year among a population of more than 20 million asthmatics in the USA), and when it occurs, it is often out of hospital. Presuming this patient recovers, she needs adjustments to her therapy before discharge. The strongest predictor of severe attacks of asthma is their occurrence in the past. Thus, this patient’s therapy needs to be stepped up to a higher level, like a high-dose inhaled corticosteroid in combination with a long-acting β agonist. Both the patient and her parents need instruction on the importance of regular adherence to therapy, with reassurance that it can be “stepped down” to a lower dose of inhaled corticosteroid (although still in combination with a long-acting β agonist) once her condition stabilizes. They also need instruction on an action plan for managing severe symptoms. This can be as simple as advising that if the patient has a severe, frightening attack, she can take up to four puffs of albuterol every 15 minutes, but if the first treatment does not bring significant relief, she should take the next four puffs while on her way to an emergency department or urgent care clinic. She should also be given a prescription for prednisone, with instructions to take 40–60 mg orally for severe attacks, but not to wait for it to take effect if she remains severely short of breath even after albuterol inhalations. Asthma is a chronic disease, and good care requires close follow-up and creation of a provider-patient partnership for optimal management. If she has had several previous exacerbations, she should be considered a candidate for monoclonal anti-IgE antibody therapy with omalizumab, which effectively reduces the rate of asthma exacerbations—even those associated with viral respiratory infection—in patients with allergic asthma. Alternatively, if the patient is found to have blood eosinophilia, treatment with an anti-IL-5 monoclonal antibody (eg, mepolizumab) should be considered as well.

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