Should you get immunoglobulin levels on patients admitted with community acquired pneumonia?

From a recent study:

BACKGROUND: Immunodeficiency is an underrecognized risk factor for infections, such as community-acquired pneumonia (CAP).

OBJECTIVE: We evaluated patients admitted with CAP for humoral immunodeficiency.

DESIGN: Prospective cohort study.

SETTING: Inpatients

PATIENTS, INTERVENTION, AND MEASUREMENTS: We enrolled 100 consecutive patients admitted with a diagnosis of CAP from February 2017 to April 2017. Serum IgG, IgM, IgA, and IgE levels were obtained within the first 24 hours of admission. CURB-65 score and length of hospital stay were calculated. The Wilcoxon rank-sum test, Kruskal-Wallis test, and simple linear regression analysis were used in data analysis.

RESULTS: The prevalence of hypogammaglobinemia in patients with CAP was 38% (95% CI: 28.47% to 48.25%). Twenty-seven of 100 patients had IgG hypogammaglobinemia (median: 598 mg/dL, IQ range: 459-654), 23 of 100 had IgM hypogammaglobinemia (median: 38 mg/dL, IQ range: 25-43), and 6 of 100 had IgA hypogammaglobinemia (median: 36 mg/dL, IQ range: 18-50). The median hospital length of stay for patients with IgG hypogammaglobinemia was significantly higher when compared to patients with normal IgG levels (five days, IQ range [3-10] vs three days, IQ range [2-5], P = .0085). Fourteen patients underwent further immune evaluation, resulting in one diagnosis of multiple myeloma, three patients diagnosed with specific antibody deficiency, and one patient diagnosed with selective IgA deficiency.

CONCLUSION: There is a high prevalence of hypogammaglobinemia in patients hospitalized with CAP, with IgG and IgM being the most commonly affected classes. IgG hypogammaglobinemia was associated with an increased length of hospitalization. Screening immunoglobulin levels in CAP patients may also uncover underlying humoral immunodeficiency or immuno-proliferative disorders.

Should docusate be removed from your hospital’s formulary?

According to this article it should.

Prealbumin testing is not useful in the assessment for malnutrition

Prealbumin (aka transthyretin) is, like albumin, an acute phase reactant. It is, also like albumin, a negative acute phase reactant because it goes down during illness. It was originally proposed as better nutritional marker than albumin because of its shorter half life, giving more of a “right now” nutritional assessment. Nowadays, neither test is considered useful for nutritional assessment. Instead one should use a clinical instrument based on a nutrition focused H&P.

From the Journal of Hospital Medicine’s Things We Do for No Reason series.

What’s the value in diagnosing malnutrition in the first place? Well, it identifies you and your hospital as having a population of patients with a markedly higher mortality. That’s good for reimbursement and severity adjustment, as the linked article points out. Does it help patients? The evidence that it leads to interventions that improve outcome is scant to none as far as I know.  What I am prompted to do, at least, is give thiamine.

Very low utilization of advance care planning (ACP) CPT codes among hospitalists

From a recent study:

We analyzed advance care planning (ACP) billing for adults aged 65 years or above and who were managed by a large national physician practice that employs acute care providers in hospital medicine, emergency medicine and critical care between January 1, 2017 and March 31, 2017. Prompting hospitalists to answer the validated “surprise question” (SQ; “Would you be surprised if the patient died in the next year?”) for inpatient admissions served to prime hospitalists and triggered an icon next to the patient’s name. Among 113,621 hospital-based encounters, only 6,146 (5.4%) involved a billed ACP conversation: 8.3% among SQ-prompted who answered “no” and 4.1% SQ-prompted who answered “yes” (for non-SQ prompted cases, the fraction was 3.5%; P less than .0001). ACP conversations were associated with a comfort-focused care trajectory. Low ACP rates among even those with high hospitalist-predicted mortality risk underscore the need for quality improvement interventions to increase hospital-based ACP.

The last sentence is a non sequitur. The codes are an unreliable measure because many, I would wager most, ACP discussions are not billed with these particular codes. Many hospitalists don’t even know they exist. The codes, 99497 and 99498, were not even included in the fee schedule until 2016 so they were brand new at the time of the study.

Ten years ago similar codes were proposed under the Affordable Care Act but spurred fierce debate around “death panel” fears. Those provisions were dropped before final passage of the law. What’s interesting is how these provisions were slipped in out of most people’s awareness, with no public debate to speak of, seven years later. Political winds change and people are easily distracted.

Only the American Association of Physicians and Surgeons, (AAPS), a relatively minor player in the larger physician community, seemed to mind. They argued that the codes, which pay more than ordinary CPT codes, would incentivize doctors to talk patients out of life prolonging treatments. That’s an oversimplification, of course, because some ACP conversations produce decisions for more care, not less.  That said, the intent of the measure is to reward doctors for giving less care toward the end of life.  It creates the perception of a conflict of interest though based on the data above the measure has had minimal impact.

The public debate about the proposal in 2009 was confused. The idea of the “death panel” (merely an inflammatory term for an advance care discussion) was nothing new. We had been having those discussions for decades. Moreover, the pre-existing ordinary CPT codes already rewarded doctors for long discussions through the provision that a higher level of service could be coded if greater than half the encounter time was spent in counseling or care coordination. Nobody on either side of the debate seemed aware of those facts.

Survey data on the state of research in hospital medicine

From a recent paper in the Journal of Hospital Medicine:

BACKGROUND: Little is known about the state of research in academic hospital medicine (HM) despite the substantial growth of this specialty.

METHODS: We used the Society of Hospital Medicine (SHM) membership database to identify research programs and their leadership. In addition, the members of the SHM Research Committee identified individuals who lead research programs in HM. A convenience sample of programs and individuals was thus created. A survey instrument containing questions regarding institutional information, research activities, training opportunities, and funding sources was pilot tested and refined for electronic dissemination. Data were summarized using descriptive statistics.

RESULTS: A total of 100 eligible programs and corresponding individuals were identified. Among these programs, 28 completed the survey in its entirety (response rate 28%). Among the 1,586 faculty members represented in the 28 programs, 192 (12%) were identified as engaging in or having obtained extramural funding for research, and 656 (41%) were identified as engaging in quality improvement efforts. Most programs (61%) indicated that they received $500,000 or less in research funding, whereas 29% indicated that they received greater than $1 million in funding. Major sources of grant support included the Agency for Healthcare Research and Quality, National Institutes of Health, and the Veterans Health Administration. Only five programs indicated that they currently have a research fellowship program in HM. These programs cited lack of funding as a major barrier to establishing fellowships. Almost half of respondents (48%) indicated that their faculty published between 11-50 peer-reviewed manuscripts each year.

CONCLUSION: This survey provides the first national summary of research activities in HM. Future waves of the survey can help determine whether the research footprint of the field is growing.

Are residents getting enough training in managing crashing patients in the hospital?

From a recent study in the Journal of Hospital Medicine:

BACKGROUND: Internal Medicine (IM) residency graduates should be able to manage hospital emergencies, but the rare and critical nature of such events poses an educational challenge. IM residents’ exposure to inpatient acute clinical events is currently unknown.

OBJECTIVE: We developed an instrument to assess IM residents’ exposure to and confidence in managing hospital acute clinical events.

METHODS: We administered a survey to all IM residents at our institution assessing their exposure to and confidence in managing 50 inpatient acute clinical events. Exposures assessed included mannequin-based simulation or management of hospital-based events as a part of a team or independently in a leadership role. Confidence was rated on a five-point scale and dichotomized to “confident” versus “not confident.” Results were analyzed by multivariable logistic regression to assess the relationship between exposure and confidence accounting for year in training.

RESULTS: A total of 140 of 170 IM residents (82%) responded. Postgraduate year 1 (PGY-1) residents had managed 31.3% of acute events independently vs 71.7% of events for PGY-3/4 residents (P less than .0001). In multivariable analysis, residents’ confidence increased with level of training (PGY-1 residents were confident to manage 24.9% of events vs 72.5% of events for PGY-3/4 residents, P less than .0001) and level of exposure, independent of training year (P = .001). Events with the lowest levels of exposure and confidence for graduating residents were identified.

CONCLUSIONS: IM residents’ confidence in managing inpatient acute events correlated with level of training and clinical exposure. We identified events with low levels of resident exposure and confidence that can serve as targets for future curriculum development.

Atul Gawande on the electronic medical record

Atul Gawande has a piece in the New Yorker titled Why Doctors Hate their Computers. The title is deceptive. In the first place doctors don’t hate computers (I’ve never met one who did, have you?). In the body of the paper Gawande doesn’t even seem to attempt to make that case. He does point out how doctors hated the way in which they were forced to adopt health information technology and the culture that went alongside. But, though he talks around it (and he talks a lot around it) he fails to answer the question of why. Is there something wrong with computers themselves in the current state of development? Is it the way policymakers and administrators have forced the implementation? Or is it that docs just need an attitude adjustment? He implies a little of each. Overall the article is incoherent.

Gawande has thrown together a mishmash of anecdotes, unreferenced claims and quotes from supposed experts. And the qualifications of these experts? Well, consider this one:

Gregg Meyer sympathizes, but he isn’t sorry. As the chief clinical officer at Partners HealthCare, Meyer supervised the software upgrade. An internist in his fifties, he has the commanding air, upright posture, and crewcut one might expect from a man who spent half his career as a military officer.

Hmmm. A commanding air, an upright posture and a crewcut. I think I’m afraid of this guy. He seems to think doctors have too much autonomy and a bad attitude to boot. He says:

“But we think of this as a system for us and it’s not,” he said. “It is for the patients.” 

Emphasis his.

Meyer just gave himself away. He’s operating on the idea that the interests of doctors are opposed to the interests of patients. It’s an ethical question worth pondering but not a great starting premise. Gawande seems to accept it uncritically. A little further on Gawande says of Meyer, also uncritically:

Gregg Meyer is understandably delighted to have the electronic levers to influence the tens of thousands of clinicians under his purview. He had spent much of his career seeing his hospitals blighted by unsafe practices that, in the paper-based world, he could do little about.

Evidence based medicine, particularly its third pillar (the importance of the expertise of the individual clinician) opposes such a top down approach. Does Gawande see anything wrong with Meyer’s line of thinking? If he does he doesn’t say so.

It’s style over substance:

Jessica Jacobs, a longtime office assistant in my practice—mid-forties, dedicated, with a smoker’s raspy voice—

As if that’s supposed to be a convincer in some way. But what does it mean, exactly? That she’s got savvy? That her dedication to her work has taken its toll? It’s left to our imagination.

Gawande fails to even come close to making the case that doctors hate computers, let alone answer the question of why, but he does point out some of the negative consequences of the EMR. Maybe this is progress, because it would have been nearly forbidden speech about a decade ago.

The EMR mess and its horrible consequences

What practicing docs knew all along.

Extended infusion protocols for piperacillin-tazobactam (PTZ): do they mitigate nephrotoxicity?

Not in this study. From the paper:

Our findings suggest a similar rate of nephrotoxicity between patients who received vancomycin in combination with PTZ EI versus PTZ SI. These results need to be further validated in a prospective randomized controlled study.

A little background on thalidomide

From a recent review article:

Thalidomide is a drug with interesting therapeutic properties but also with severe side effects which require a careful and monitored use. Potential immunomodulatory, antiinflammatory, anti-angiogenic and sedative properties make thalidomide a good candidate for the treatment of several diseases such as multiple myeloma. Through an increase in the degradation of TNFα-mRNA, thalidomide reduces the production of TNFα by monocytes and macrophages stimulated by lipopolysaccharide or by T lymphocytes induced by mitogenic stimuli. The decreased level of TNFα alters the mechanisms of intracellular transduction by preventing the activation of NF-kB and by decreasing the synthesis of proteins, in particular IL-6, involved in cell proliferation, inflammation, angiogenesis and protection from apoptosis. Furthermore, thalidomide affects VEGF levels by down-regulating its expression. Nowadays, new safer and less toxic drugs, analogs of thalidomide, are emerging as beneficial for a more targeted treatment of multiple myeloma and several other diseases such as Crohn';s disease, rheumatoid arthritis, sarcoidosis, erythema nodosum leprosum, graft-versus-host disease.

Syncope guidelines

Unbelievably long for what should be a simple topic, but everything you’re likely to want or need to know is here.

Visceral fat: an inflammatory engine driving worse outcomes in sepsis?

Recent study findings here.

Strength training improved cognition in older patients

---in this study.

What explains strokes in young people (ages 18-55)?

Traditional, modifiable risk factors in almost 80% in this study.

Do you really need a TSH receptor antibody test to distinguish Grave’s disease from other forms of hyperthyroidism?

In this study clinical assessment alone was poor.

Low vitamin D levels associated with increased mortality

From a recent study published in Mayo Clinic Proceedings:

Objective

To determine the relationship between 25-hydroxyvitamin D (25[OH]D) values and all-cause and cause-specific mortality.

Patients and Methods

We identified all serum 25(OH)D measurements in adults residing in Olmsted County, Minnesota, between January 1, 2005, and December 31, 2011, through the Rochester Epidemiology Project. All-cause mortality was the primary outcome. Patients were followed up until their last clinical visit as an Olmsted County resident, December 31, 2014, or death. Multivariate analyses were adjusted for age, sex, race/ethnicity, month of measurement, and Charlson comorbidity index score.

Results

A total of 11,022 individuals had a 25(OH)D measurement between January 1, 2005, and December 31, 2011, with a mean ± SD value of 30.0±12.9 ng/mL. Mean age was 54.3±17.2 years, and most were female (77.1%) and white (87.6%). There were 723 deaths after a median follow-up of 4.8 years (interquartile range, 3.4-6.2 years). Unadjusted all-cause mortality hazard ratios (HRs) and 95% CIs for 25(OH)D values of less than 12, 12 to 19, and more than 50 ng/mL were 2.6 (95% CI, 2.0-3.2), 1.3 (95% CI, 1.0-1.6), and 1.0 (95% CI, 0.72-1.5), respectively, compared with the reference value of 20 to 50 ng/mL. In a multivariate model, the interaction between the effect of 25(OH)D and race/ethnicity on mortality was significant (P<.001). In white patients, adjusted HRs for 25(OH)D values of less than 12, 12 to 19, 20 to 50, and greater than 50 ng/mL were 2.5 (95% CI, 2.2-2.9), 1.4 (95% CI, 1.2-1.6), 1.0 (referent), and 1.0 (95% CI, 0.81-1.3), respectively. In patients of other race/ethnicity, adjusted HRs were 1.9 (95% CI, 1.5-2.3), 1.7 (95% CI, 1.1-2.6), 1.5 (95% CI, 1.0-2.0), and 2.1 (95% CI, 0.77-5.5).

Conclusion

White patients with 25(OH)D values of less than 20 ng/mL had greater all-cause mortality than those with values of 20 to 50 ng/mL, and white patients had greater mortality associated with low 25(OH)D values than patients of other race/ethnicity. Values of 25(OH)D greater than 50 ng/mL were not associated with all-cause mortality.

Testosterone replacement associated with better cardiovascular outcomes

Will a randomized controlled trial some day blow this out of the water like we saw in the case of ERT?

Troponin elevation in stroke may point to a cardioembolic etiology

From a recent paper:

Abstract

Background Our aim was to determine whether patients with embolic strokes of undetermined source (ESUS) have higher rates of elevated troponin than patients with noncardioembolic strokes.

Methods and Results CAESAR (The Cornell Acute Stroke Academic Registry) prospectively enrolled all adults with acute stroke from 2011 to 2014. Two neurologists used standard definitions to retrospectively ascertain the etiology of stroke, with a third resolving disagreements. In this analysis we included patients with ESUS and, as controls, patients with small‐ and large‐artery strokes; only patients with a troponin measured within 24 hours of stroke onset were included. A troponin elevation was defined as a value exceeding our laboratory's upper limit (0.04 ng/mL) without a clinically recognized acute ST‐segment elevation myocardial infarction. Multiple logistic regression was used to evaluate the association between troponin elevation and ESUS after adjustment for demographics, stroke severity, insular infarction, and vascular risk factors. In a sensitivity analysis we excluded patients diagnosed with atrial fibrillation after discharge. Among 512 patients, 243 (47.5%) had ESUS, and 269 (52.5%) had small‐ or large‐artery stroke. In multivariable analysis an elevated troponin was independently associated with ESUS (odds ratio 3.3; 95% confidence interval 1.2, 8.8). This result was unchanged after excluding patients diagnosed with atrial fibrillation after discharge (odds ratio 3.4; 95% confidence interval 1.3, 9.1), and the association remained significant when troponin was considered a continuous variable (odds ratio for log[troponin], 1.4; 95% confidence interval 1.1, 1.7).

Conclusions Elevations in cardiac troponin are more common in patients with ESUS than in those with noncardioembolic strokes.

Unfortunately the test characteristics for determining cardioembolic stroke are poor. Most patients with cardioembolic stroke do not have elevated troponins and some with other types of stroke have elevations.

Appropriateness of troponin ordering in the hospital

Form a recent study:

Troponin assays are integral to the diagnosis of acute myocardial infarction (AMI), but there is concern that testing is over utilized and may not conform to published guidelines. We reviewed all testing performed at 14 hospitals over 12 months and associated troponin values with the primary and secondary diagnoses for each visit. Troponin was determined to be negative, indeterminate or elevated based on reference ranges. The majority of troponin measurements were single, not serial (64%). The rate of AMI was low, with only 3.5% of tested patients having a primary or secondary diagnosis of AMI. Sensitivity, specificity and negative predictive value were excellent, exceeding 90%. However, positive predictive value was low, suggesting testing of populations with diseases known to be associated with elevated troponin levels in the absence of AMI. The majority (79%) of elevated troponin values were associated with primary diagnoses other than AMI. Only 28% of elevated troponins were associated with a primary or secondary diagnosis of AMI. These data suggest possible overuse of troponin testing in our healthcare system. Journal of Hospital Medicine 2017;12:329-331. © 2017 Society of Hospital Medicine

This conclusion is premised on the idea that the only reason to order a troponin is to diagnose or exclude MI.

Triple antibiotic therapy against carbapenemase producing bacteria

Here is a review on the topic. These regimens have been our go-to for a while now and are effective although the crude mortality for these infections remains high, in the 30+% range. Newer antibiotics either approved or in the pipeline have brightened the outlook. From the article:

A few emerging treatment options for CPKP infections appear promising. The most prominent new agent is ceftazidime–avibactam, a cephalosporin combined with a novel β-lactamase inhibitor approved by the US Food and Drug Administration (FDA) in February 2015 [60]. Ceftazidime–avibactam has shown potent in vitro activity against CRE isolates [61–63]. and there have also been reports that ceftazidime–avibactam is effective for CPKP infections after other combination regimens have failed [19, 64, 65]. Other β-lactam/β-lactamase inhibitor combinations are also being investigated including ceftolozane–tazobactam and aztreonam–avibactam [12, 66]. Plazomicin, a novel aminoglycoside that has shown in vitro activity against CRE, is currently undergoing a Phase 3 clinical trial (NCT01970371) as part of a combination therapy [67]. Another agent showing potential is eravacycline, a tetracycline derivative, which has shown in vitro efficacy against CRE as well as for complicated intra-abdominal infections and complicated urinary tract infections in clinical trials [68, 69].