The pain scale shares the blame for the opioid crisis

Of course it does.

Pain is not a vital sign

Something we dared not say aloud 15 years ago.

Continuing our look back at the pain dogma of years past.

Nontuberculous mycobacteria: clinical profiles and mortality

Study here.

Pain management reversal

Safe use of opiates, from SHM 2017.

Here’s more on this topic. Diametrically opposed to what they were preaching at hospitalist meetings a decade ago.

Pain dogma reversal at SHM

Medscape reported on the pain management sessions at SHM 2017 in an article titled Rethinking Pain Can Help Hospitalists Fight Opioid Crisis. I did not attend that year but from the sound of the article it was more like a complete reversal than a rethinking, and a reversal is what is needed.

Starting in about 1999, when this movement was launched, uncontrolled pain was the big public health crisis. Now it’s the opioid crisis. How interesting.

From the beginning of the “fifth vital sign” movement SHM (then known as NAIP, the National Association of Inpatient Physicians) was in lockstep and served up its share of the prevailing dogma. It’s particularly interesting that this occurred when evidence based medicine was the hot new thing, just 7 years following its launch. Near the top of everyone’s mind was the notion that science was here to replace dogma. Except, apparently, when the discussion was about pain. As I read the Medscape piece numerous then and now contrasts started swirling through my mind. I wish I still had my notes from NAIP and SHM sessions of past years but I don’t so I’ll have to do this from memory. I’ll cite a couple of comments from the article followed by my recollections of meetings past:

From the 2017 sessions:

"The message to patients should not be that the goal is to become pain free," she explained. "We should not be expecting opioids to decrease pain by more than 20% to 30%."

Old dogma: nearly all pain can be eliminated and no hospitalized patient should have to endure pain.

"The pattern of reflexively prescribing opioids when a patient in the hospital reports a high pain score needs to be broken, she said."

Old dogma: opioids are just fine. Concerns about addiction are  largely driven by myth. Take patients’ reports of their pain at face value.

Did anyone at SHM stand up and say “we were wrong”?

Nucleated red cells on the peripheral smear in critically ill patients

In those who survive they predict adverse post hospital events and readmission.

Pacemaker troubleshooting: commonly encountered situations

Free full text.

Experience in outpatient treatment of PE

Form a recent study:

Highlights

More patients with confirmed PE were managed as outpatients over 10 years.

Outpatients with confirmed PE had unchanged mortality.

Readmission rates for outpatients with confirmed PE were stable.

Major bleeding rates among outpatients were very low.

Abstract

Introduction

In clinical trial settings, outpatient management of pulmonary embolism (PE) is feasible and safe, but less is known on its use in routine care. We determined trends in outpatient management of PE and associated mortality in a large non-select patient population.

Methods

All residents of Quebec, Canada with a first-ever work-up for suspected PE in the emergency department (ED) over 10 years were included. Patients could transition to outpatient management and from unconfirmed to confirmed PE in a time-varying fashion. Comparing the years 2005–9 with 2000–4, we assessed the odds ratio (OR) for outpatient management, and relative risk (RR) for all-cause mortality, readmissions for PE, and major bleeding in 30 days. We adjusted the RR for a mortality risk score.

Results

Of 15,217 patients included, 7583 were outpatients (7.5% confirmed PE) and 7634 were inpatients (60.6% confirmed PE). In all, 10.9% of patients with confirmed PE were outpatients, but outpatient management of confirmed PE was more likely in the latter study period (OR 1.73, 95%CI 1.44–2.09). Among outpatients with confirmed PE, mortality (RR 0.84, 95%CI 0.15–4.61) and readmission (RR 1.25, 95%CI 0.45–3.48) rates were stable, and only 3 major bleeding events were noted. Inpatients with confirmed PE had stable mortality rates (RR 0.95, 95%CI 0.72–1.24).

Conclusion

Outpatient PE management increased over 10 years while remaining fairly uncommon. Nevertheless, stable mortality and readmission rates indicate this practice is safe in routine care, and add to the growing evidence in support of outpatient PE management.

Novel antidotes for calcium blocker and beta blocker overdoses: lipid rescue and high dose insulin

Nice review here.

The 2011 norepi shortage was associated with increased mortality in septic shock

From JAMA.

Non MI troponin elevations in patients 50 yo or younger

From an abstract presentation at AHA:

Abstract

Background: While increased serum troponin levels are often due to myocardial infarction (MI), increased levels may also be found in a variety of other clinical scenarios. Although these causes of troponin elevation have been characterized in several studies in older adults, they have not been well characterized in younger individuals.

Methods: We conducted a retrospective review of patients 50 years of age or younger who presented to two large tertiary care centers between January 2000 and April 2016 with elevated serum troponin levels. Patients with prior known coronary artery disease (CAD) were excluded. The cause of troponin elevation was adjudicated via review of electronic medical records. All-cause death was determined using the Social Security Administration’s death master file.

Results: Of the 6081 cases meeting inclusion criteria, 3574 (58.8%) patients had an MI, while 2507 (41.2%) had a non-MI cause of troponin elevation. Over a median follow-up of 8.7 years, all-cause mortality was higher in patients with non-MI causes of troponin elevation compared with those with MI (adjusted HR: 1.32, 95% CI: 1.17-1.49, p less than 0.001). Specifically, mortality was higher in those with CNS pathologies (adjusted HR: 2.21, 95% CI: 1.86-2.62, p less than 0.001), non-ischemic cardiomyopathies (adjusted HR: 1.70, 95% CI: 1.40-2.06, p less than 0.001), and ESRD (adjusted HR: 1.36, 95% CI: 1.07-1.73, p=0.012). However, mortality was lower in patients with myocarditis compared with those with an acute MI (adjusted HR: 0.43, 95% CI: 0.31-0.60, p less than 0.001).

Conclusion: There is a broad differential for troponin elevation in young patients, which differs based on demographic features. Most non-MI causes of troponin elevation are associated with higher all-cause mortality compared with acute MI.

Non-gastrointestinal presentations of celiac disease

From a recent paper in the American Journal of Medicine:

Abstract

Purpose

The purpose of our study is to investigate the delay in diagnosis of patients with biopsy-proven celiac disease in those who present with gastrointestinal complaints vs nongastrointestinal complaints at our tertiary care center. Celiac disease is an autoimmune disorder that affects approximately 1% of the population worldwide. Celiac disease can have variable clinical presentations; it can be characterized by predominately gastrointestinal symptoms, or it may present without any gastrointestinal symptoms.

Methods

We retrospectively reviewed the charts of 687 adult patients who carried the diagnosis of celiac disease. Patients included had biopsy-proven celiac disease and were categorized based on presence or absence of gastrointestinal symptoms prior to their diagnosis.

Results

There were 101 patients with biopsy-proven celiac disease that met inclusion criteria. Fifty-two patients presented with gastrointestinal symptoms and 49 had nongastrointestinal complaints. Results from Mann-Whitney statistical analysis showed a median delay in diagnosis of 2.3 months for the gastrointestinal symptoms group and 42 months for the nongastrointestinal group (P less than .001); 43.2% of patients with nongastrointestinal symptoms had abnormal thyroid-stimulating hormone, as opposed to 15.5% in the gastrointestinal symptom group (P = .004). Of patients with nongastrointestinal symptoms, 69.4% had anemia, compared with 11.5% of the gastrointestinal symptom group (P less than .001). The majority of patients in the nongastrointestinal symptom group, 68%, were noted to have abnormal bone density scans, compared with 41% in the gastrointestinal symptom group. No sex differences were noted on chi-squared analysis between the 2 groups (P = .997).

Conclusions

Although there is growing awareness of celiac disease, the delay in diagnosis for patients without gastrointestinal symptoms remains prolonged, with an average delay of 3.5 years.

Clinical Significance

There is a mean delay in the diagnosis of celiac disease of 3.5 years in patients who present with nongastrointestinal symptoms.

Specifically, patients with thyroid abnormalities, anemia, or bone mineral density loss should be screened for celiac disease.

Celiac disease is an autoimmune disorder that affects approximately 1% of the population worldwide.1 As many as 6 of 7 cases of celiac disease remain undiagnosed.2 This discrepancy falls in line with the widely accepted “celiac iceberg” concept and may be due to the fact that patients have variable presentations of celiac disease. Manifestations of celiac disease range from typical gastrointestinal complaints characterized by malabsorption and diarrhea, to more silent forms in patients without overt gastrointestinal complaints. Nongastrointestinal presentations may include anemia, thyroid dysfunction, osteoporosis, liver function test abnormalities, and skin manifestations such as dermatitis herpetiformis. The variable presentations create a clinical challenge to physicians in reaching an early diagnosis. As a result, delay in diagnosis is not uncommon and does not go without consequence. Undiagnosed celiac disease can lead to osteoporotic fractures, infertility, unnecessary surgical procedures including bowel resection, and malignancy.1 As the majority of cases of celiac disease can be treated with a strict gluten-free diet alone, adherence to this diet can reverse the risk for adverse clinical outcomes.

Neurogenic orthostatic hypotension

From a recent update:

Purpose of review

Orthostatic hypotension is a phenomenon commonly encountered in a cardiologist's clinical practice that has significant diagnostic and prognostic value for a cardiologist. Given the mounting evidence associating cardiovascular morbidity and mortality with orthostatic hypotension, cardiologists will play an increasing role in treating and managing patients with orthostatic hypotension.

Recent findings

The American College of Cardiology, American Heart Association, and Heart Rhythm Society recently published consensus guidelines on the diagnosis, treatment, and management of syncope and their instigators, including orthostatic hypotension. Additionally, consensus guidelines have also been recently updated, reinforcing the universal definition orthostatic hypotension and its closely associated pathologies. Finally, the United States Food and Drug Administration (FDA) recently approved droxidopa, a synthetic oral norepinephrine prodrug, in 2014 for the treatment of neurogenic orthostatic hypotension (nOH), and it represents a well tolerated, effective, and easy to use intervention for nOH. This represents only the second drug approved by the FDA for orthostatic hypotension, the first being midodrine in 1986. A handful of smaller head-to-head studies have pitted not only pharmacologic agents to one another but also nonpharmacologic interventions to pharmacologic agents. Additionally, recent studies have also reported on more convenient screening tools for orthostatic hypotension.

Summary

Though there have been many advances in the management of orthostatic hypotension, nOH remains a chronic, debilitating, and often progressively fatal condition. Cardiologists can play a very important role in optimizing hemodynamics in this patient population to improve quality of life and minimize cardiovascular risk.

Exhaled nitric oxide to guide management of asthma

The conclusion from a recent Cochrane review:

AUTHORS' CONCLUSIONS:

With new studies included since the last version of this review, which included adults and children, this updated meta-analysis in adults with asthma showed that tailoring asthma medications based on FeNO levels (compared with primarily on clinical symptoms) decreased the frequency of asthma exacerbations but did not impact on day-to-day clinical symptoms, end-of-study FeNO levels, or inhaled corticosteroid dose. Thus, the universal use of FeNO to help guide therapy in adults with asthma cannot be advocated. As the main benefit shown in the studies in this review was a reduction in asthma exacerbations, the intervention may be most useful in adults who have frequent exacerbations. Further RCTs encompassing different asthma severity, ethnic groups in less affluent settings, and taking into account different FeNO cutoffs are required.

Anticoagulant nephropathy: is it unique to warfarin?

Probably not but it is at least worse with warfarin. Here’s the latest comparative study. The reason? Although all anticoagulants have a common mechanism (intraglomerular and intratubular hemorrhage) warfarin has a second one. It promotes vascular calcification in the kidney. It does this by inhibiting the local carboxylation of certain vascular protective proteins. But there’s even more to it than that. NOACs, by their inhibition of factors II and X, may be vascular protective because these clotting factors are involved in vascular inflammation, according to the audio summary for the JACC article linked above.

Niacin hasn’t lived up to its original promise in cardiovascular prevention

From a recent systematic review:

Results

Thirteen trials (N = 35,206) were selected for final analysis. The mean follow-up duration was 32.8 months. Overall, niacin led to significant increases in serum high-density lipoprotein cholesterol levels from baseline trial enrolment by 21.4%, 9.31 (95% confidence interval [CI] 5.11-13.51) mg/dL. However, we did not observe any differences in all-cause mortality rates (RR 0.99; 95% CI 0.88-1.12) between niacin and control arms. Further, niacin treatment was associated with a trend toward lower risk of cardiovascular mortality (RR 0.91; 95% CI 0.81-1.02), coronary death (RR 0.93; 95% CI 0.78-1.10), nonfatal myocardial infarction (RR 0.85; 95% CI 0.73-1.0), revascularization (coronary and noncoronary) (RR 0.83; 95% CI 0.65-1.06), and stroke (RR 0.89; 95% CI 0.72-1.10), compared with control.

Conclusion

Niacin therapy does not lead to significant reductions in total or cause-specific mortality or recurrent cardiovascular events among persons with or at risk of atherosclerotic cardiovascular disease.

The review also pointed out adverse effects including worsening of or increased risk of onset of diabetes.

Niacin showed promise in 15 year follow up of the coronary drug project (its use was associated with lowered all cause mortality) and is the only lipid regulating agent that has been associated with regression of atherosclerosis. [1] [2] Although the review cited an article on the 15 year follow up of the coronary drug project (CDP) the analysis of research findings only included the early report of the CDP, which did not show reduction in mortality.

The American College of Cardiology Fourth Universal Definition of Myocardial Infarction has been published

You can access the full text of the document here. Following are some key points:

Any cardiac troponin value above the upper range limit is considered myocardial injury. If the elevation is static it is considered chronic myocardial injury. If there's a rise or fall it is considered acute. For this to be considered myocardial infarction there must be some additional clinical indicator which might be based on symptoms, ECG changes or imaging. There needs to be at least one.

The above criteria for troponin elevation apply to MI types one through three. For types four and five, different troponin cut offs apply. For these types of infarction troponin elevations must be greater than 5 or greater than 10 times the upper range limit, respectively. Troponin elevations that do not meet these cutoffs denote injury rather than infarction. (Note that a peri-PCI MI is termed type 4a. There is also a 4b and 4c MI and these terms refer to the more distant downstream complications of stent thrombosis and stent restenosis, respetively).

And now for an overview of types one through five. These categories are essentially unchanged from the prior edition of the universal definition. Type one MI is an acute coronary syndrome with plaque instability and thrombus, either occlusive or nonocclusive as indicated by the surrogates STEMI and NSTEMI respectively. Type 2 MI is not an acute coronary syndrome. It may occur in the presence or the absence of coronary disease. If coronary disease is present there is no plaque instability. The infarction is caused by an unfavorable balance and oxygen supply and demand. A couple of additional points are of note regarding type 2 MI. First of all in general patients with type 2 MI have a worse prognosis than those with type 1. This is due to the presence of comorbidity and is not surprising. Among patients with type 2 MI, those with coronary disease have a worse prognosis then those without. Of interest, studies have shown that ST elevation in type 2 MI occurs in between 3% and 24% of cases. In part this may be because coronary embolism and spontaneous coronary artery dissection (SCAD) are classified as type 2 MI. Finally it is not always possible to differentiate between type 2 MI and non-ischemic myocardial injury. In fact the two conditions may overlap. Type III MI is sudden cardiac death in which acute myocardial infarction was suspected but there was no opportunity to draw troponin levels. Type 4a is peri-PCI MI. Types 4 b and c represent the downstream manifestations already discussed. Type 5 MI is peri-CABG MI. The differences in troponin criteria for types four and five as opposed to types one through three have already been discussed.

A few special points should be made concerning perioperative ischemic events surrounding non-cardiac surgery. The ACC/AHA guidelines on perioperative evaluation and management for patients undergoing noncardiac surgery, updated in 2014, give troponin testing in the perioperative period a class I recommendation only for patients who exhibit signs or symptoms of myocardial ischemia. Troponin testing as a means of surveillance for patients deemed to be at high risk but without said signs or symptoms carries only a IIb recommendation. However a recent report and accompanying editorial published in the March 20, 2018 issue of Circulation suggest a role for pre and post operative troponin surveillance in selected high risk patients. There is still no consensus regarding this.

Acute exacerbation of heart failure is a special case. The article recommends troponin testing in all such patients. If troponin is elevated and it is dynamic, there should be a high index of suspicion for MI. A static elevation may represent chronic myocardial injury as part of the heart failure syndrome.

Takotsubo cardiomyopathy, nowadays more appropriately referred to as stress cardiomyopathy, is considered separately. It is distinguished from MI of any kind. The mechanism of myocardial injury is the subject of controversy but it's probably at least in part catecholamine mediated injury in which case it would be nonischemic myocardial injury. Another special situation is myocardial infarction with nonobstructive coronary arteries. This is known as MINOCA and may arise as a result of either type 1 or 2 MI.

What about patients with CKD? Many of these patients who have elevated troponins have chronic myocardial injury as a result of the CKD. Diagnosis of MI may be difficult in this setting. It is based on changes in troponin along with the other clinical criteria previously discussed.

Critical illness is commonly associated with troponin elevation. Either type 1 or type 2 MI may occur. Quite often patients with critical illness experience troponin elevation due to non-ischemic myocardial injury as an organ manifestation of the underlying critical illness. These cases may be difficult to distinguish from MI, especially type 2. In such patients, whether to evaluate for coronary disease, usually after recovery from critical illness, as a matter for clinical judgment.

The document contains some discussion of the ECG changes of myocardial infarction. The section makes several important points. First, when the initial tracing is nondiagnostic in a patient having active chest pain, serial tracings 15 to 30 minutes apart for the first couple of hours are recommended. ST segment elevation in lead aVR is mentioned as an important prognostic indicator and an indication of left main or multi vessel coronary artery disease. De Winter and Wellens T waves are described in that section, without calling them by name.

Bundle branch block gets a very superficial discussion. Scarbossa like changes are hinted at without using that eponym. New bundle branch block, either right or left, is mentioned. Mention is made of electrical remodeling (otherwise known as cardiac memory) in patients with pacemakers, in reference to non-paced complexes.

Section 31 has a nice discussion of normal versus pathologic Q waves and/ or QS complexes. Section 33 discusses ST segment and T wave negativity commonly seen in rapid atrial fibrillation and SVT. It states that the cause is poorly understood but that the phenomenon does not necessarily represent myocardial ischemia. It is mentioned that some degree of anomalous ventricular activation and or electrical remodeling may somehow explain these findings. In some cases it may represent a type 2 MI but this should not automatically be classified as such without additional clinical indicators.

New in the gram negative pipeline: Imipenem-Relebactam and Meropenem-Vaborbactam

Report here.

Methamphetamine and pulmonary hypertension

This review describes the recently discovered association.

Harmful effects of raised “low T” awareness

From a recent review:

Purpose of review

To summarize the research evidence on promotion of testosterone for ‘Low T’, or age-related hypogonadism.

Recent findings

Marketing of testosterone for ‘Low T’ has relied on strategies that are inadequately regulated to prevent off-label promotion, such as unbranded ‘disease-awareness’ advertising campaigns targeting the general public, sponsored continuing medical education (CME) and ghostwriting. A recent US analysis of television advertising exposure levels versus insurance claims found that both unbranded ‘disease-awareness’ advertising and branded ads were associated with increased rates of testosterone testing, treatment initiation, and treatment without prior testing. Exposés of sponsored CME and ghostwriting indicate misrepresentation of the research evidence on the sequelae of untreated low testosterone and on treatment efficacy. In the United States, advertising to the general public ceased in 2014 after the Food and Drug Administration changed product labeling to clarify that testosterone is only indicated for pathological hypogonadism. Unbranded ‘disease-awareness’ advertising to the general public and ‘Low T’ messages for health professionals have continued elsewhere.

Summary

The review of the experience of promotion of testosterone for ‘Low T’ and research evidence on effects of advertising targeting the public highlights the need for improved regulation of unbranded ‘disease awareness’ advertising to ensure adequate protection of public.