Choosing Wisely Campaign - Part I

I am on outpatient this month. The questions I find myself asking on most of the patients are focused on the type of health maintenance that the patient needs. I understand that medical care is ever evolving and changing but I find that preventative medicine, in my very limited experience, seems to change faster, more often. I came across the AAFP's recent release of the Choosing Wisely Campaign. It was released just last week and I thought it would be good to summarize a few (the table is 89 pages long) recommendations on topics I know I will deal with frequently in the clinical setting. 

Allergy/Immunology 

• Don’t perform screening panels, IgE panels, for food allergies without previous consideration of medical history -It is important to use clinical correlation when considering allergen testing. For example, only consider testing a patient specifically for peanut allergy if the patient endorses symptoms after ingestion of peanuts. Studies have shown that about 8% of the population tests positive to peanuts but only approximately 1% are truly allergic and exhibit symptoms upon ingestion. When symptoms suggest a food allergy, tests should be selected based on a careful medical history. 

Cardiovascular

• Don't order annual electrocardiography or any other cardiac screening for asymptomatic, low-risk patients - Who is considered low risk? Risk factors can be combined in many ways to allow classification of a person's risk for a CHD event as low, intermediate, or high. Several calculators and models are available to quantify a person's 10-year risk for CHD events. The Framingham Adult Treatment Panel III calculator (http://hp2010.nhlbihin.net/atpiii/calculator.asp) performs well for the U.S. population. Persons with a 10-year risk greater than 20% are generally considered high-risk, those with a 10-year risk less than 10% are considered low-risk, and those in the 10% to 20% range are considered intermediate-risk.
• Don’t perform stress cardiac imaging or advanced noninvasive imaging in the initial evaluation of patients without cardiac symptoms unless high risk markers are present - Asymptomatic, low-risk patients account for up to 45% of unnecessary “screening.” Testing should be performed only when the following findings are present: diabetes in patients older than 40 years; peripheral arterial disease; or greater than 2% yearly risk of coronary heart disease events.
• Avoid using stress echocardiograms on asymptomatic patients who meet "low-risk" scoring criteria for coronary disease -Stress echocardiography is mostly used in symptomatic patients to assist in the diagnosis of obstructive CAD. There is very little information on using stress echocardiography in asymptomatic individuals for the purposes of cardiovascular risk assessment, as a stand-alone test or in addition to conventional risk factors. 
• Don't repeat echocardiograms in stable, asymptomatic patients with a murmur or click when no pathology has been previously found and there has been no clinical change in the patient’s condition - Trace mitral, tricuspid, and pulmonic regurgitation can be detected in 70% to 90% of normal individuals and has no adverse clinical implications. Aortic stenosis is an exception. The 2014 American Heart Association/American College of Cardiology valvular guideline recommends serial echocardiography in patients with aortic stenosis. In patients with Stage B mild AS (transvalvular velocity 2 to 2.9 m/s), echocardiography is recommended every three to five years. In patients with Stage B moderate AS (transvalvular velocity 3 to 3.9 m/s), echocardiography is recommended every one to two years. In patients with asymptomatic Stage C1 severe AS (transvalvular velocity 4 m/s or higher), echocardiography is recommended every 6 to 12 months. Echocardiography is indicated earlier if there is a change in symptoms or signs suggestive of worsening cardiac status. 
• Don't perform routine annual stress testing after coronary artery revascularization - Routine annual stress testing in patients without symptoms does not usually change management. This practice may lead to unnecessary testing without any proven impact on patient management

Asthma

Definition - A common chronic disorder of the airways that is complex and characterized by variable and recurring symptoms, airflow obstruction, bronchial hyperresponsiveness, and an underlying inflammation. The latter definition of asthma has features that overlap with the description of COPD. Besides historic features (such as the onset of disease in middle age/older, history of cigarette smoking), the characteristic that best distinguishes COPD from asthma is the degree of reversibility of airflow obstruction.

Clinical Features

•  Asthma is diagnosed before the age of seven years in approximately 75 percent of cases and may resolve when the patient begins puberty. Asthma may reoccur later in adulthood. 
• A pattern of respiratory symptoms that occur with exposure to triggers (such as a allergen, exercise, viral infection) and resolve with trigger avoidance or asthma medication is typical of asthma. 
• Patients often report 2 out of 3 of the following symptoms
• Wheezing
• Coughing (often worse at night)
• Shortness of Breath or difficulty breathing

Diagnosis - A history of intermittent symptoms typical of asthma plus the finding on physical examination of characteristic musical wheezing, when patient is symptomatic, strongly point to a diagnosis of asthma. Diagnosis is confirmed by evaluating the following...

• Pulmonary function test - will tell you if the lung disease is a obstructive pattern (FEV1/FVC < 0.7) and what the response after bronchodilator therapy
• Response to bronchodilator - The presence of a bronchodilator response, in isolation, is not enough to diagnose asthma. Asthma is typically distinguished from these other conditions (COPD, bronchiectasis, cystic fibrosis, and bronchiolitis) by the large response as at least 15 to 20 percent. 

Treatment - Once you have diagnosed Asthma, what are the goals of management and treatment options? The goals of chronic asthma management may be divided into two domains...

•  Reduction in impairment - Specific goals for reducing impairment include..
• Freedom from frequent or troublesome symptoms of asthma
• Minimal need (≤2 days per week) of inhaled short acting beta agonists to relieve symptoms
• Few night-time awakenings (<2 nights per month) due to asthma
• Oral glucocorticoid courses and/or urgent care visits should be needed no more than once per year
• Maintenance of normal daily activities, including work or school attendance and participation in athletics and exercise
• Satisfaction with asthma care on the part of patients and families
• Reduction in risk 
• Prevention of recurrent exacerbations and need for emergency department or hospital care
• Prevention of reduced lung growth in children, and loss of lung function in adults
• Optimization of pharmacotherapy with minimal or no adverse effects

Treatment - First, you want to categorize the patient's report of symptoms into a category (See figure below)

Once you have the patient's symptom categorized, you can chose a treatment plan. 

• Mild Intermittent - Patients with mild intermittent asthma are best treated with a quick-acting inhaled beta-2-selective adrenergic agonist, taken PRN for relief of symptoms.
• Mild Persistent - distinction between intermittent and mild persistent asthma is important, because current guidelines for mild persistent asthma call for initiation of daily long-term controller medication, a low dose inhaled glucocorticoid.
• Moderate Persistent - the preferred therapies are either low-doses of an inhaled glucocorticoid plus a long-acting inhaled beta agonist, or medium doses of an inhaled glucocorticoid
• Severe Persistent - medium or high doses of an inhaled glucocorticoid, in combination with a long-acting inhaled beta-agonist

Management of Diabetic Ketoacidosis (DKA) and Hyperosmolar Hyperglycemic State (HHS) in Adults

This is the common internal medicine problem that will keep me quite busy if it rolls in on night float...or anytime of the day, I suppose.

Definitions 

• DKA - metabolic acidosis, secondary to ketones, is often the major finding, while the serum glucose concentration is generally below 800 mg/dL. 
• In HHS, there is little or no ketoacid accumulation, the serum glucose concentration frequently exceeds 1000 mg/dL, the serum osmolality may reach 380 mosmol/kg.

Initial Evaluation

• Take care of your ABCs first! (Airway,Breathing and Circulation)
• Establish a diagnosis with CBC, BMP, UA for ketones, ABG, plasma osmolality
• Try to find the underlying etiology of the DKA or HHS and treat that. Most are secondary to infection (pneumonia and UTI) so obtain blood cultures, chest xray and EKG

Monitoring

Once you have established the diagnosis, how should you monitor?

•  Serum glucose should initially be measured every hour until stable, while serum electrolytes, blood urea nitrogen, creatinine, osmolality, and venous pH, which is about 0.03 units lower than arterial blood gas, should be measured every two to four hours, depending upon disease severity and the clinical response. 
• Monitor the acidosis by either directly measuring beta-hydroxybutyrate or the anion gap.

Treatment

• FLUIDS!! - Fluids should be given first as it increases the effectiveness of the insulin therapy to come. Initial fluid therapy in DKA and HHS is directed toward expansion of the intravascular volume and restoration of renal perfusion. The average fluid loss is 3 to 6 L in DKA and up to 8 to 10 L in HHS, due largely to the glucose osmotic diuresis . Start with NS and switch over to D5NS when the serum glucose is <250. As mentioned below, if the patient is hemodynamically stable, then you will want to switch to 1/2NS when adding potassium to the fluid.
• Replenish the Potassium - To prevent hypokalemia, potassium chloride (20 to 30 meq/L) is generally added to the replacement fluid once the serum potassium concentration falls below 5.3 meq/L. If the patient is hemodynamically stable, one-half isotonic saline is preferred since the addition of potassium to isotonic saline will result in a hypertonic solution that will delay correction of the hyperosmolality.
• Insulin of course!! - After you have given fluids and serum potassium is > 3.5, you may give insulin. A continuous IV administration of regular insulin is the treatment of choice. DKA and HHS can be treated either with an IV bolus (0.1 U/kg body weight), followed by a continuous infusion of regular insulin at a dose of 0.1 U/kg per hour or with an intravenous infusion alone at a rate of at least 0.14 U/kg per hour.
• Sodium Bicarbonate - We recommend administering bicarbonate if the arterial pH is less than 6.90. UptoDate recommends giving 100 meq of sodium bicarbonate in 400 mL sterile water with 20 meq of potassium chloride, if the serum potassium is less than 5.3 meq/L, administered over two hours. 

Chronic Obstructive Pulmonary Disease (COPD) Exacerbation 

Introduction - The Global Initiative for Chronic Obstructive Lung Disease (GOLD), a report produced by the National Heart, Lung, and Blood Institute and the World Health Organization defines a Chronic Obstructive Pulmonary Disease Exacerbation as an acute increase in symptoms beyond normal day-to-day variation [1]. This generally includes an acute increase in one or more of the following cardinal symptoms...

• Cough increases in frequency and severity
• Sputum increases in volume or changes in character
• Dyspnea increases from baseline (using inhalers/breathing treatments more often, increase in O2 use at home)

Etiology - Most precipitants of COPD exacerbations are secondary to viral and bacterial respiratory infections (estimated as 70-80% of the time). The other 20% is secondary to environmental pollution or unknown etiology. 

Risk of Exacerbations - The GOLD guidelines suggest using a combination of an individual’s FEV1 and history of exacerbations to assess the exacerbation risk. The severity of lung function impairment is stratified based on the postbronchodilator FEV1, using the GOLD classification of airflow limitation (see table below). These components are combined into the following risk stratification...

• Low risk: Typically GOLD 1 or 2 (mild to moderate airflow limitation) and/or 0 to 1 exacerbation per year. 
• High risk: Typically GOLD 3 or 4 (severe or very severe airflow limitation) and/or ≥2 exacerbations per year

Initial Evaluation - Initial evaluation of a patient with a suspected exacerbation of COPD includes a medical history, physical examination, chest xray, sputum culture and routine laboratory studies. Arterial blood gas analysis should be performed in most patients to assess the severity of the exacerbation and to establish a baseline from which improvement or deterioration can be measured. Patients with COPD who present to the hospital with acute worsening of dyspnea should be evaluated for potential alternative diagnoses, such as heart failure, pulmonary thromboembolism, and pneumonia.

Treatment - Supplemental oxygen is a critical component of acute therapy. It should target an O2 saturation of 90 to 94 percent. The major pharmacologic components of managing an acute exacerbation of COPD include inhaled short-acting bronchodilators (beta adrenergic agonists and anticholinergic agents), glucocorticoids, and antibiotics. 

• Beta adrenergic agonists - Inhaled short-acting beta adrenergic agonists (albuterol) are the mainstay of therapy for an acute exacerbation of COPD because of their rapid onset of action and efficacy in producing bronchodilation.
• Anticholinergics - Inhaled short-acting anticholinergic agents (ipratropium) may be used in combination with inhaled short-acting beta adrenergic agonists. 
• Glucocorticoids - Systemic glucocorticoids, when added to the bronchodilator therapies described above, improve symptoms and lung function, and decrease the length of hospital stay. The route used depends on the stability of the patient. Oral glucocorticoids are rapidly absorbed and appear equally efficacious as intravenous glucocorticoids. In fact, a randomized trial assigned 210 patients hospitalized with a COPD exacerbation to receive oral or IV steroids for five days and found no difference between the two groups in the rate of treatment failure, length of hospital stay, improvement in spirometry, or improvement in quality of life. However, intravenous glucocorticoids are typically administered to patients who present with a severe exacerbation, who respond poorly to oral glucocorticoids or who are unable to take oral medication. 
• Antibiotics - The optimal antibiotic regimen for the treatment of exacerbations of COPD has not been determined. UpToDate recommends a "risk stratification" approach when selecting initial antibiotic therapy (see algorithim below). Specifically, they recommend prescribing a broader antibiotic regimen for patients who have risk factors for a poor outcome.

Hypertensive Urgency and Emergency

My last post was on defining hypertension and secondary causes of hypertension. Continuing with the theme, I wanted to refresh myself on this common inpatient problem.

Definitions

• Hypertensive Emergency - Severe hypertension in adults (systolic blood pressure ≥180 mmHg and/or diastolic blood pressure ≥120 mmHg) associated with symptoms that signal end-organ damage (hypertensive encephalopathy, subarachnoid or intracerebral hemorrhage, retinal hemmorrhage, kidney injury, acute pulmonary edema, aortic dissection, and rebound after withdrawal of antihypertensive medications).
• Hypertensive Urgency - Severe hypertension in adults (systolic blood pressure ≥180 mmHg and/or diastolic blood pressure ≥120 mmHg) associated with none or mild symptoms, often a mild headache, but no signs of acute end-organ damage.

Etiology - often occurs in patients who have been non adherent with either their antihypertensive drug regimen or their low-sodium diet. Severe hypertension can also develop in patients who are adherent to their medications and following ingestion of large quantities of salt and can be controlled by resuming a low-salt diet.

Treatment

Hypertensive Urgency - The blood pressure should be reduced over a period of hours to days. The blood pressure should usually be lowered to <160/<100 mmHg. However, the mean arterial pressure should not be lowered by more than 25 to 30 percent over this relatively short period of time. This means that patient's who have very elevated blood pressures, the goal may be a little higher than 160/100. The choice of therapy depends on the timeline. If the blood pressure needs to be lowered over a period of hours (Patients judged to be at high risk for imminent cardiovascular events due to severe hypertension, including those with known aortic or intracranial aneurysms), UptoDate recommends oral furosemide, oral clonidine, or oral captopril. If the blood pressure needs to be lowered over a period of days, resumption of antihypertensive therapy, initiation of antihypertensive therapy, or the addition of another antihypertensive drug is adequate.

Hypertensive Emergency - Nitroprusside dilates both arterioles and veins and is generally considered to be the most effective parenteral drug for most hypertensive emergencies. Nitroprusside acts in less than one minute and its effects disappear within 1 to 10 minutes, thereby minimizing the risk of hypotension. Nitroprusside's major limitation is its metabolism to cyanide which could lead to the development of cyanide or rarely thiocyanate toxicity. Nitroglycerine, CCB, Labetalol (a combined beta-adrenergic and alpha-adrenergic blocker with a rapid onset of action, 5 min, makes it useful in the treatment of hypertensive emergencies), Esmolol, Hydralazine and Phentolamine (good in catecholamine excess). On my ward rotations, the most common drugs I see used in Hypertensive Emergencies are Nitro drips and Labetolol.

Hypertension

First, some definitions...

• Normal blood pressure: systolic <120 mmHg and diastolic <80 mmHg
• Prehypertension: systolic 120 to 139 mmHg or diastolic 80 to 89 mmHg
• Hypertension:
• Stage 1: systolic 140 to 159 mmHg or diastolic 90 to 99 mmHg
• Stage 2: systolic ≥160 or diastolic ≥100 mmHg

Primary (Essential) Hypertension 

Pathogenesis - poorly understood for but the following have been implicated in primary HTN

• Increased sympathetic neural activity
• Increased Ang II and mineralcorticoid activity
• Genetic predisposition
• Reduced nephron mass

Risk Factors 

• Excess Na or ETOH intake
• Obesity and weight gain
• Physical inactivity
• dyslipidemia
• Depression
• Vitamin D deficiency

Secondary causes of HTN

• Medications - chronic NSAIDs, oral contraceptives and antidepressants. 
• Primary renal disease - vascular and glomerular
• Hyperaldosteronism - the presence of primary mineralocorticoid excess, primarily aldosterone, should be suspected in any patient with the triad of hypertension, unexplained hypokalemia, and metabolic alkalosis.
• Cushing's syndrome
• Hyper/Hypothyroidism and Hyperparathyroidism
• Obstructive sleep apnea
• Coarctation of the aorta

When should you start working up secondary causes of HTN?

It is not cost effective to perform a complete evaluation for secondary hypertension in every hypertensive patient. Thus, it is important to be aware of the clinical clues that suggest secondary hypertension. Clinical clues include...

• Severe or resistant hypertension. Resistant hypertension is defined as the persistence of hypertension despite concurrent use of adequate doses of three antihypertensive agents from different classes, including a diuretic.
• An acute rise in blood pressure developing in a patient with previously stable values.
• Age < 30 years of age in non-obese, non-black patients with a negative family history of and no other risk factors (obesity, HLD) for hypertension.
• Malignant or accelerated hypertension (patients with severe hypertension and signs of end-organ damage such as retinal hemorrhages or papilledema, heart failure, neurologic disturbance, or acute kidney injury). 
• Proven age of onset before puberty.

Tests to order and Physical Exam findings

• BMP to look at the BUN and CR and assess for primary renal disease
• US of the renal vasculature to search for RAS or Fibromuscular Dysplasia 
• On physical exam, carotid, abdominal, or femoral bruits suggest atherosclerotic disease and possible renal artery stenosis, diminished femoral pulses and/or a discrepancy between arm and thigh blood pressures suggest aortic coarctation or significant aortoiliac disease
• Screening for primary aldosteronism begins with a paired, morning measurement of the plasma aldosterone concentration (PAC) and plasma renin activity (PRA) to determine whether the patient has an elevated or high-normal PAC, suppressed PRA, and elevated PAC/PRA ratio
• If the patient is showing clinical clues for pheochromocytoma (episodic headache, sweating, and tachycardia) then measuring fractionated metanephrines and catecholamines in a 24-hour urine collection is the intial step. 
• For Cushing disease workup, UptoDate recommends two first-line tests should be abnormal to establish the diagnosis of Cushing's syndrome. First line tests include...late night salivary cortisol, urinary cortisol, and the low-dose dexamethasone suppression tests
• Sleep study for OSA
• TSH and PTH levels

Acute Pancreatitis

Introduction -The most common cause of pancreatitis is gallstones. The second most common cause if alcohol. Pancreatitis can be divided into two categories. 

1. Edematous acute pancreatitis, which is characterized by acute inflammation of the pancreatic parenchyma and peripancreatic tissues, but without recognizable tissue necrosis
2. Necrotizing acute pancreatitis, which is characterized by inflammation associated with pancreatic parenchymal necrosis and/or peripancreatic necrosis

Clinical Features - Most patients with acute pancreatitis have acute onset of persistent, severe epigastric abdominal pain. In approximately 50 percent of patients, the pain radiates to the back. Approximately 90 percent of patients have associated nausea and vomiting which may persist for several hours.

Diagnosis - The diagnosis of acute pancreatitis requires the presence of two of the following three criteria

1. Acute onset of persistent, severe, epigastric pain often radiating to the back
2. Elevation in serum lipase or amylase to three times or greater than the upper limit of normal
3. Characteristic findings of acute pancreatitis on imaging (focal or diffuse enlargement of the pancreas on contrast-enhanced abdominal CT or MRI is suggestive of acute pancreatitis. Check out the image below...P is for pancreas and it is quite large in that picture)

Management

• Fluid replacement - Up to Date recommends aggressive hydration at a rate of 5 to 10 mL/kg per hour of isotonic crystalloid solution (NS or LR) to all patients with acute pancreatitis. Fluid management needs to be reassessed frequently during the hospital stay. Monitor the vital signs, keep HR <120 and MAP between 65-89 and monitor the BUN as both the BUN at the time of admission and the change in 24 hours since admission can predict mortality. Watch the urine output (should be >0.5 to 1 cc/kg/hour) and try to achieve a reduction in hematocrit with a goal of 35 to 44 percent
• Pain control - Abdominal pain is often the predominant symptom in patients with acute pancreatitis and should be treated with analgesics. Hydromorphone and Fetanyl are recommended. I remember while studying for the boards that Merperidine was recommended over Morphine because it is believed that Morphine will cause contraction of the Sphincter of Oddi which would exacerbate the pancreatitis. However, Merperidine has a very short half life and can be cumbersome to manage the patient's pain adequately. 
• Nutrition - In mild pancreatitis, in the absence of nausea or vomiting, oral feeds can be initiated as soon as the pain is decreasing and inflammatory markers are improving (about 24-48 hours). A low fat, soft diet is recommended. In moderately severe to severe pancreatitis, oral feeding is frequently not tolerated. Patients usually require enteral or parenteral feeding.  Early enteral nutrition (within 24 to 48 hours) should be initiated when a patient is transferred to the ICU, or has the development of organ failure, or systemic inflammatory response syndrome (SIRS) persisting for 48 hours. Enteral feeding requires the placement of a jejunal feeding tube beyond the ligament of Treitz. The reason it needs to be beyond the ligament of Trietz is to avoid the duodenal release of cholecystokinin, the hormone that will activate the pancreas. A feed that is high protein and low fat is best to avoid little activation of the pancreas.