Monday, January 22, 2018

Your patient wants to leave AMA. Now what?

There’s an interesting article in the Journal of Hospital Medicine on what to do when a patient wants to leave the hospital against medical advice. After reading and rereading it I had to disagree with the conclusion but it took me a bit to get there because the article, with its confusing use of terms, is a masterpiece of obfuscation. The most obvious example is the oxymoronic use of the term “AMA discharge” in the title and throughout the article. If a patient leaves AMA it's not your decision. How is that a discharge? Put another way, if you discharge the patient you are making a statement that the patient is medically ready to leave the hospital. A discharge order can only mean the patient is leaving in accordance with, not against, your advice. Why, after all, would you enter an order for something that is against your own judgment?

Another example of language confusion is the authors’ statement that leaving the hospital AMA can be a process of informed consent. Quoting directly from the article:

Because all competent patients have the right to decline recommended inpatient treatment, the ethical and legal standard is that the physician obtain the patient’s informed consent to leave…

Consent to leave? That’s an inappropriate use of the word. Consent leads to adherence with the physician’s recommendation, which in this case would be to remain in the hospital. In the AMA situation the patient’s decision to leave is a demand, not a consent.

Getting past all the confusion, there were a few good points. When the patient leaves against your advice you don’t have to destroy the rapport. It doesn’t have to be an adversarial transaction. But the authors go beyond that principle by stating that when the patient leaves AMA not only should it be handled as a regular discharge but that you should not even document that the departure is against your advice. Again, form the article:

The solution to improve quality is straightforward—avoid designating discharges as AMA…

Treat all discharges similarly. Avoid designating an inpatient discharge as AMA.

That is where I have to disagree.

There's more to unpack. The authors make frequent mention of shared decision-making. Indeed shared decision-making is a is a core principle of evidence-based medicine but it is just one component. The AMA departure sometimes pushes shared decision making to the level of absurdity. How does it apply, for example, if the patient with an actively evolving myocardial infarction wants to leave the emergency room? What if the patient just swallowed antifreeze because he ran out of his beverage of choice? Where does shared decision making come in when the patient’s choice means almost certain harm? Some patient preferences and choices are simply wrong.

Finally there's the matter of legal protection. The authors make this statement:

Although clinicians may presume that the AMA designation provides protection from liability, the claim is not supported by the available literature.14,15 In these studies, which reviewed relevant case law, defendants prevailed not because of the physician’s AMA designation, but because the plaintiff was not able to prove negligence.

That’s a misrepresentation of the cited articles. Both articles (see here and here) contain statements to the effect that the AMA designation may indeed afford some legal protection.

So what should we do? Why not consider each case on its individual merits? If the patient wants to leave prematurely but the risk is low it may be reasonable to capitulate and enter a discharge order. In other situations where the patient's choice is clearly ill-advised and the risk is high a discharge order may be inappropriate and the departure should be documented as being against medical advice. Even in such cases try to work with the patient to help formulate a follow-up plan and, if appropriate, provide medication prescriptions. Assure the patient that you are not angry, respectfully ask that they reconsider and assure them that they are welcome to return. Clearly advise them about the danger of leaving but don’t threaten them or imply adverse insurance consequences.

Hepatocellular carcinoma (HCC) with a focus on diagnosis and screening

Recommendations are that all patients with cirrhosis be screened as well as certain hepatitis B patients regardless of cirrhosis if certain risk factors are present. Some guidelines make similar recommendations for hepatitis C. The screening modality of choice is ultrasound. Imaging is favored over tumor markers.

Sunday, January 21, 2018

Calcium pyrophosphate crystal deposition disease

Below are some key points from a couple of free full text reviews [1] [2].

Terminology has changed and can be confusing

The current official term is calcium pyrophosphate crystal deposition (CPPD). Pseudogout, a term which historically referred to the acute attacks of CPPD, has been replaced by “acute calcium pyrophosphate crystal arthritis.” The plain radiographic finding known as chondrocalcinosis is frequently replaced by the term “cartridge calcification.” CC is not universal in patients with attacks nor is it entirely specific for CPPD.

Crystal identification is important in diagnosis

As opposed to the needle like negatively birefringent crystals of gout, the crystals of CPPD are variable in shape, often rectangular, and if birefringent at all, only weakly positively birefringent.

There are some disease associations

Metabolic disease associations of CPPD include haemochromatosis (18), hyperparathyroidism (19, 20), hypomagnesemia (21) and hypophosphatasia (22). Other diseases such as diabetes mellitus and hypothyroidism do not associate with CPPD once adjusted for age (22, 23). Haemochromatosis is the only metabolic disease associated with CPPD that results in structural arthropathy, and this commonly affects the knees, wrists, hips, MCPJs, and ankles (18, 24).

There are some genetic determinants as well.

Saturday, January 20, 2018

The importance of nutrition in cystic fibrosis

From a recent review:

Recent findings

Evidence-based and expert-based guidelines emphasize the need for adequate nutritional intake to improve nutritional status. For infants and young children, the aim is to achieve the 50th percentile of weight and length for a healthy same-age population up to age 2 years. For older children and adolescents 2–18 years, the target is a BMI of at or above the 50th percentile for healthy children. For CF adults of at least 18 years, the target is a BMI of at or above 22 kg/m 2 for women and at or above 23 kg/m 2 for men. Recently, new drugs are developed with the aim to treat the malfunction of the cystic fibrosis transmembrane conductance regulator gene. This potentiator/corrector therapy improves lung function and nutritional status and decreases the number of infective exacerbations. As survival is improving and the CF population is aging, it is important to focus on micronutrient and macronutrient intake of CF patients in different age and disease stages.


Recent evidence-based nutritional guidelines and improved medical treatment support the nutritional monitoring and interventions in CF patients. Nutritional care should be personalized and provided by a specialized CF dietitian because patients’ care needs may change dramatically during their disease progress.

Friday, January 19, 2018

Insomnia as a cardiovascular disease risk factor

Insomnia is the most prevalent sleep disorder in the United States and has high comorbidity with a number of cardiovascular diseases (CVDs). In the past decade, a number of observational studies have demonstrated an association between insomnia and incident cardiovascular disease (CVD) morbidity and mortality, including hypertension (HTN), coronary heart disease (CHD), and heart failure (HF). Despite some inconsistencies in the literature, likely due to variations in how insomnia is defined and measured, the existing data suggest that insomnia, especially when accompanied by short sleep duration, is associated with increased risk for HTN, CHD and recurrent acute coronary syndrome, and HF. Purported mechanisms likely relate to dysregulation of the hypothalamic-pituitary axis, increased sympathetic nervous system activity, and increased inflammation. This paper reviews the most recent studies of insomnia and CVD and the potential pathophysiological mechanisms underlying this relationship and highlights the need for randomized trials to further elucidate the nature of the relationship between insomnia and CVD.

Thursday, January 18, 2018

Insulin in type 2 diabetes: are we pushing too hard?


There is no significant evidence of long term efficacy of insulin on any clinical outcome in T2D. However, there is a trend to clinically harmful adverse effects such as hypoglycaemia and weight gain. The only benefit could be limited to reducing short term hyperglycemia. This needs to be confirmed with further studies.

Wednesday, January 17, 2018

Inhaled steroid/beta agonist treatments improved oxygenation in patients at risk for ARDS

Objectives: Effective pharmacologic treatments directly targeting lung injury in patients with the acute respiratory distress syndrome are lacking. Early treatment with inhaled corticosteroids and beta agonists may reduce progression to acute respiratory distress syndrome by reducing lung inflammation and enhancing alveolar fluid clearance.

Design: Double-blind, randomized clinical trial ( NCT01783821). The primary outcome was longitudinal change in oxygen saturation divided by the FIO2 (S/F) through day 5. We also analyzed categorical change in S/F by greater than 20%. Other outcomes included need for mechanical ventilation and development of acute respiratory distress syndrome.

Setting: Five academic centers in the United States.

Patients: Adult patients admitted through the emergency department at risk for acute respiratory distress syndrome.

Interventions: Aerosolized budesonide/formoterol versus placebo bid for up to 5 days.

Measurements and Main Results: Sixty-one patients were enrolled from September 3, 2013, to June 9, 2015. Median time from presentation to first study drug was less than 9 hours. More patients in the control group had shock at enrollment (14 vs 3 patients). The longitudinal increase in S/F was greater in the treatment group (p = 0.02) and independent of shock (p = 0.04). Categorical change in S/F improved (p = 0.01) but not after adjustment for shock (p = 0.15). More patients in the placebo group developed acute respiratory distress syndrome (7 vs 0) and required mechanical ventilation (53% vs 21%).

Conclusions: Early treatment with inhaled budesonide/formoterol in patients at risk for acute respiratory distress syndrome is feasible and improved oxygenation as assessed by S/F. These results support further study to test the efficacy of inhaled corticosteroids and beta agonists for prevention of acute respiratory distress syndrome.

Tuesday, January 16, 2018

Reperfused STEMI and intramyocardial hemorrhage


Background Findings from recent studies show that microvascular injury consists of microvascular destruction and intramyocardial hemorrhage (IMH). Patients with ST‐segment elevation myocardial infarction (STEMI) with IMH show poorer prognoses than patients without IMH. Knowledge on predictors for the occurrence of IMH after STEMI is lacking. The current study aimed to investigate the prevalence and extent of IMH in patients with STEMI and its relation with periprocedural and clinical variables.

Methods and Results A multicenter observational cohort study was performed in patients with successfully reperfused STEMI with cardiovascular magnetic resonance examination 5.5±1.8 days after percutaneous coronary intervention. Microvascular injury was visualized using late gadolinium enhancement and T2‐weighted cardiovascular magnetic resonance imaging for microvascular obstruction and IMH, respectively. The median was used as the cutoff value to divide the study population with presence of IMH into mild or extensive IMH. Clinical and periprocedural parameters were studied in relation to occurrence of IMH and extensive IMH, respectively. Of the 410 patients, 54% had IMH. The presence of IMH was independently associated with anterior infarction (odds ratio, 2.96; 95% CI, 1.73–5.06 [P less than 0.001]) and periprocedural glycoprotein IIb/IIIa inhibitor treatment (odds ratio, 2.67; 95% CI, 1.49–4.80 [P less than 0.001]). Extensive IMH was independently associated with anterior infarction (odds ratio, 3.76; 95% CI, 1.91–7.43 [P less than 0.001]). Presence and extent of IMH was associated with larger infarct size, greater extent of microvascular obstruction, larger left ventricular dimensions, and lower left ventricular ejection fraction (all P less than 0.001).

Conclusions Occurrence of IMH was associated with anterior infarction and glycoprotein IIb/IIIa inhibitor treatment. Extensive IMH was associated with anterior infarction. IMH was associated with more severe infarction and worse short‐term left ventricular function in patients with STEMI.

Clinical Perspective
What is New?

This is the first study to link periprocedural additional glycoprotein IIb/IIIa inhibitor treatment to higher occurrence of intramyocardial hemorrhage in patients with reperfused ST‐segment elevation myocardial infarction.

What are the Clinical Implications?

The optimal application of aggressive antithrombotic therapies in patients with ST‐segment elevation myocardial infarction undergoing percutaneous coronary intervention remains to be studied, especially in the era of adequate double antiplatelet preloading.

Anterior infarct location predicted presence and severity of intramyocardial hemorrhage and may prove useful in direct risk stratification.