Skepticism about accountable care organizations

Here is a JAMA Viewpoint piece expressing a negative opinion about ACOs. (A companion article in the same issue was favorable). Key points:

The authors point out that any cost savings attributable to the ACOs appear to be nominal. Moreover they tend to be offset by the bonuses paid out to the participants. These bonuses cannot be considered optional because they are inherent to the core notion of the ACO: that “quality” will be rewarded.

The model creates incentives to integrate services. Thus smaller hospitals close or are merged, resulting in monopolies among health care delivery systems. This reduces competition and tends to drive costs up, not down.

Accountable care organizations: how are they working?

The authors of this JAMA Viewpoint article say the model has been a success, but the arguments are unconvincing. Here are some caveats:

The experiment is in its infancy.

Overall the results are mixed.

Cost savings have been modest and in some cases are diminishing and may prove to be transient. That's what we saw in the managed care experiment of a couple of decades ago.

Statements about quality improvement are suspect because real quality cannot be measured. Outcome data are very soft.

Multiple clinical manifestations of IgG4 related disease (IgG4-RD)

Here are some key issues addressed in a recent review.

What are some of the IgG4 related diseases?

These may coexist in the same patient:

Autoimmune pancreatitis type 1

Mikulicz disease (salivary gland infiltration)

Constrictive pericarditis

Coronary artery aneurysm

Inflammatory abdominal aortic aneurysm (and the related condition retroperitoneal fibrosis)

Sclerosing mediastinitis

Riedel's thyroiditis (and other forms of thyroid involvement)

Sclerosing mastitis

Pulmonary mass or interstitial disease

Hypophysitis

Prostatitis

Lymphadenopathy (Castleman like and other forms)

Tubulointerstitial nephritis

Sclerosing cholangitis (which differs in some features from primary sclerosing cholangitis)

How is IgG4-RD diagnosed?

This has been in a state of some controversy and flux. From the article:

According to an international symposium held in 2011, the diagnosis of IgG4-RD requires both an appropriate histological appearance and increased numbers of IgG4-positive plasma cells (or an elevated IgG4:IgG ratio) in tissue...

In 2011, an “All Japan IgG4 Team,” with the aim to draft comprehensive diagnostic criteria for IgG4-RD 51 ( Table 3 ), proposed three major items 51 69 (1) single or multiple organs involved with diffuse or localized swelling, masses, nodules, and/or hypertrophic lesions; (2) elevated serum IgG4 levels (greater than or equal to 135 mg/dL); and (3) histopathologic features that include marked lymphocytic and plasma cell infiltration and fibrosis, with IgG4-positive plasma cell infiltration (IgG4/IgG-positive cell ratio of greater than or equal to 40% and IgG4-positive plasma cells exceeding 10/HPF). Based on these criteria, patients can be classified into the categories of definite, probable, or possible IgG4-RD.

How do autoimmune pancreatitis (AP) types 1 and 2 differ?

Age: older onset (6^th decade) typical of type 1

Gender: male predominance in type 1, not 2

Relationship to IgG4: present in type 1, not clearly present in 2

Histology: lymphoplasmacytic sclerosing pancreatitis in type 1, idiopathic duct centric pancreatitis in 2

Abdominal pain: common in type 2, not in 1

Other organ involvement common in 1, not 2

Steroid responsiveness characterizes both types but type 1 is more prone to relapse.

IgG-4 related disease overview

Here is an overview from Disease of the Month. IgG-4 diseases include one of the two types of autoimmune pancreatitis and several other conditions:

Immunoglobulin G4-related disease is a rare but increasingly recognized multisystem entity characterized by lymphoplasmacytic tissue infiltration...Related manifestations of this disease include Reidel’s thyroiditis, chronic sclerosing dacryoadenitis, autoimmune pancreatitis (type 1 AIP), retroperitoneal fibrosis, and tubulointerstitial nephritis. Usually occurring in older men, the diagnosis is primarily based upon finding of histopahtologic changes..

High flow nasal cannula vs NIPPV post extubation

From a recent report in JAMA:

Question Is high-flow nasal cannula noninferior to noninvasive ventilation for preventing reintubation and postextubation respiratory failure?

Findings In this multicenter randomized noninferiority clinical trial that included 604 adults, the proportion requiring reintubation was 22.8% with high-flow therapy vs 19.1% with noninvasive ventilation, and postextubation respiratory failure was observed in 26.9% with high-flow therapy vs 39.8% with noninvasive ventilation, reaching the noninferiority threshold.

Meaning High-flow nasal cannula immediately after scheduled extubation was not inferior to noninvasive mechanical ventilation for risk of reintubation and postextubation respiratory failure in patients at high risk of reintubation.

Epilepsy driving laws by state

Here is the database from the epilepsy foundation.

Cystic lung disease as a manifestation of Sjogren Syndrome

From a recent paper in Chest:

Methods Eighty-four patients with primary or secondary SS and chest imaging, chest radiograph, or CT scan were retrospectively evaluated for CLD. Thirteen patients with cysts were found. Baseline characteristics of all patients were collected. A multivariate logistic regression model was used to look for predictors of CLD in patients with CT scan. Additional imaging, SS activity, and complications from CLD and SS were collected for the patients with cysts.

Results CLD had a frequency of 15.4% for all patients with chest imaging. Not all cysts were evident on radiography, and CLD frequency was 30.9% for the patients with chest CT scan. Six patients had cysts without other radiographic findings. CLD was associated with older age (OR, 1.1; 95% CI, 1.0-1.16), a diagnosis of secondary SS (OR, 12.1; 95% CI, 1.12-130.4), and seropositivity for anti-SS-related antigen A/Ro autoantibodies (OR, 26.9; 95% CI, 1.44-93.61). There was no radiologic progression of CLD for 12 patients after a 4-year median follow-up. Lung function did not exhibit temporal worsening. CLD did not correlate with a specific pattern in pulmonary function testing. Two patients had secondary infectious complications of the cysts.

And here is a nice general review of cystic lung disease and its various associations.

Cardiac imaging in pulmonary hypertension

Review here.

Viral infection in community acquired pneumonia

From a recent systematic review and meta-analysis:

Abstract:
The advent of PCR has improved the identification of viruses in patients with community-acquired pneumonia (CAP). Several studies have used PCR to establish the importance of viruses in the aetiology of CAP.



We performed a systematic review and meta-analysis of the studies that reported the proportion of viral infection detected via PCR in patients with CAP. We excluded studies with paediatric populations. The primary outcome was the proportion of patients with viral infection. The secondary outcome was short-term mortality.



Our review included 31 studies. Most obtained PCR via nasopharyngeal or oropharyngeal swab. The pooled proportion of patients with viral infection was 24.5% (95% CI 21.5–27.5%). In studies that obtained lower respiratory samples in greater than 50% of patients, the proportion was 44.2% (95% CI 35.1–53.3%). The odds of death were higher in patients with dual bacterial and viral infection (OR 2.1, 95% CI 1.32–3.31).



Viral infection is present in a high proportion of patients with CAP. The true proportion of viral infection is probably underestimated because of negative test results from nasopharyngeal or oropharyngeal swab PCR. There is increased mortality in patients with dual bacterial and viral infection.

PE may be hiding out in patients with COPD exacerbation

From a recent systematic review and meta-analysis:

Background COPD patients encounter episodes of increased inflammation, so-called acute exacerbations of COPD (AE-COPD). In 30% of AE-COPD no clear etiology is found. Since there is a well-known crosstalk between inflammation and thrombosis, the objectives of this study were to determine the prevalence, embolus localization and clinical relevance, and clinical markers of pulmonary embolism (PE) in unexplained AE-COPD.
Methods A systematic search was performed using MEDLINE and EMBASE platforms from 1974 – October 2015. Prospective- and cross-sectional studies that included patients with an AE-COPD and used pulmonary CT-angiography for diagnosis of PE were included.
Results The systematic search resulted in 1650 records. Main reports of 22 articles were reviewed and 7 studies were included. The pooled prevalence of PE in unexplained AE-COPD was 16.1% (95% confidence-interval 8.3%-25.8%) in a total of 880 patients. Sixty-eight percent of the emboli found were located in the main pulmonary arteries, lobar arteries or inter-lobar arteries. Mortality and length of hospital admission seem to be increased in patients with unexplained AE-COPD and PE. Pleuritic chest pain and cardiac failure were more frequently reported in patients with unexplained AE-COPD and PE. In contrast, signs of respiratory tract infection was less frequently related to PE.
Conclusions PE is frequently seen in unexplained AE-COPD. Two-thirds of emboli are found at localizations that have a clear indication for anticoagulant treatment. These findings merit clinical attention. PE should receive increased awareness in patients with unexplained AE-COPD, especially when pleuritic chest pain and signs of cardiac failure are present and no clear infectious origin can be identified.

The mechanism of the association, as pointed out in the abstract above, may be the association between inflammation and thrombosis.

Other factors were mentioned as possible mechanisms for the association, as pointed out in a review of the paper by ACP Hospitalist Weekly.

This is not the first time such an association has been mentioned, and I have blogged about it several times in the past including here.

STEMI versus ventricular aneurysm: two ECG prediction tools

Report here.

Pulmonary manifestations of Sjogren's syndrome

This free full text review focuses on the pulmonary manifestations but also covers the disease in general.

Stress ulcer prophylaxis: an example of a non evidence based “standard of care”

Stress ulcer prophylaxis, generally with a PPI, has long been an in house performance measure in many institutions, but the practice was never evidence based. According to this review there is equipoise for a clinical trial.

The emerging link between community acquired pneumonia and cardiac disease

This is a growing concern and was recently reviewed here. From the review:

Recent findings: Recent evidence suggests that a large proportion of deaths from CAP are attributable to cardiovascular disease, including sudden cardiac death, acute myocardial infarction (MI), arrhythmias and cardiac failure. Up to one-third of patients with CAP may experience cardiovascular complications within 30 days of hospital admission, while data also suggest that CAP managed in the community is associated with increased risk of acute MI. The risk is maximal within a few days of hospitalization with CAP and reduces over time. Most studies suggest that risk is still increased at 1 year, and some suggest risk continues to be increased at 10 years post-CAP. This clearly contributes to the well-recognized increased long-term mortality associated with CAP. The mechanism is not entirely clear, but recent published data have better defined the impact of the host response, including systemic inflammation and platelet activation. The contribution of Streptococcus pneumoniae has also been recently investigated, with animal studies suggesting a direct effect of S. pneumoniae on the myocardium, forming microlesions that heal with resulting myocardial fibrosis. Several studies suggest a key role for the pore-forming toxin pneumolysin in S. pneumoniae-induced cardiac toxicity.

Summary: Several therapies have been shown to improve the outcomes in cardiovascular disease, but whether these would be effective in improving outcomes in CAP is unknown. In this review, we argue that cardioprotective treatments may hold the greatest promise in terms of reducing long-term mortality in patients with CAP.

By way of background I have posted extensively about this before [1] [2] [3] [4].

Thrombocytopenia as a prognostic marker in septic shock

This paper was highlighted in ACP Hospitalist Weekly as an important study and although it is the first time thrombocytopenia has been looked at in this way in my view it is not fundamentally new or practice changing. From the paper:

Design: Prospective, multicenter, observational cohort study.

Setting: Fourteen ICUs from 10 French university teaching and nonacademic hospitals.

Patients: Consecutive adult patients with septic shock admitted between November 2009 and September 2011 were eligible.

Intervention: None.

Measurements and Main Results: Of the 1,495 eligible patients, 1,486 (99.4%) were included. Simplified Acute Physiology Score II score of greater than or equal to 56, immunosuppression, age of more than 65 years, cirrhosis, bacteremia (p less than or equal to 0.001 for each), and urinary sepsis (p = 0.005) were globally associated with an increased risk of thrombocytopenia within the first 24 hours following the onset of septic shock. Survival at day 28 estimated by the Kaplan-Meier method was lower in patients with thrombocytopenia and decreased with thrombocytopenia severity. By multivariate Cox regression, a platelet count of less than or equal to 100,000/mm3 was independently associated with a significantly increased risk of death within the 28 days following septic shock onset. The risk of death increased with the severity of thrombocytopenia (hazard ratio, 1.65; 95% CI, 1.31-2.08 for a platelet count below 50,000/mm3 vs greater than 150,000/mm3; p less than 0.0001).

Conclusions: This is the first study to investigate thrombocytopenia within the first 24 hours of septic shock onset as a prognostic marker of survival at day 28 in a large cohort of ICU patients. Measuring platelet count is inexpensive and easily feasible for the physician in routine practice, and thus, it could represent an easy "alert system" among patients in septic shock.

The last statement is not practice changing and almost sounds silly given that all patients with sepsis get at least an automated CBC which routinely includes a platelet count.

TIMI and GRACE perform poorly in the evaluation of patients presenting with chest pain to the ER

From a recent prospective cohort study:

Purpose

The Thrombolysis in Myocardial Infarction (TIMI) and the Global Registry in Acute Coronary Events (GRACE) scores were largely evaluated and validated in stratifying risk of cardiovascular events in patients with chest pain and acute coronary syndrome. Our objective was to compare these 2 scores in predicting outcome in emergency department (ED) patients with undifferentiated chest pain.

Materials and methods

This was a prospective cohort study including patients presenting to 4 EDs with chest pain with nondiagnostic or normal ECG. For all included patients (n = 3125), TIMI and GRACE scores were calculated. Follow-up was conducted at 30-day and 1-year post-ED index admission...

Results

We reported 285 (9.1%) major adverse events at 30 days and 436 (13.9%) at 1 year. In patients with low TIMI (less than or equal to 2) and GRACE (less than 109) scores, a significant proportion had major adverse events at 30 days (5% and 7.5%, respectively) and 1 year (7.9% and 12.9%, respectively). Area under ROC curve at 30 days was 0.66 (95% confidence interval [CI], 0.62-0.71) vs 0.57 (95% CI, 0.53-0.62), respectively, for TIMI and GRACE scores. At 1 year, the area under ROC was 0.67 (95% CI, 0.62-0.71) and 0.65 (95% CI, 0.60-0.70), respectively, for TIMI and GRACE scores.

Conclusions

The TIMI and GRACE scores are not valid in short- and long-term risk stratification in our chest pain patients.

TPA administration in patients with stroke mimic

In patients with stroke mimic one would expect a lower incidence of head bleed as compared to patients with actual stroke because their brain tissues are not as friable. Reported experience confirms that this is the case as pointed out in this review. The incidence of head bleed in stroke mimic is in fact much lower. Comforting as that may seem the perspective offered by the article warrants emphasis:

In summary, the rate of sICH in patients with stroke mimic who receive intravenous thrombolytics is low in published data, although this estimate may be lower than that observed in clinical practice.9 Patients with stroke mimics generally were younger, were women, and had lower NIHSS scores. Fully functional outcome was 3-fold more likely for patients with stroke mimic compared with that for AIS patients. However, the risk of causing harm to even 1 patient given intravenous thrombolytics in the setting of a stroke mimic is concerning,

In ordering troponins, consider the pretest probability

From a recent paper:

Background

In clinical practice, we progressively rely on biomarkers, without estimating the pretest probability. There is not enough support for the use of cardiac troponin (cTn) I in the management of noncardiac patients. We studied the rate at which this test was ordered, the prevalence of detection of a positive result in noncardiac patients, and the impact of this incidental finding on clinical management.

Methodology

Patients admitted from December 2011 to 2013 to our community hospital with diagnosis of noncardiac disease who had positive cTn were included. Data collected included final diagnosis, patient disposition, cardiac monitoring, cardiology consult, and cardiac biomarker testing.

Results

Cardiac troponin I was ordered for 1700 patients in our emergency department. Seven hundred fifty patients had a positive cTn. Of the 750 patients, 412 had a positive cTn without any clinical suspicion of an acute coronary syndrome. An incidental finding of a positive cTn leads to ordering of cTn on average 4 times during admission, cardiac monitoring of 379 (91.99%) patients for at least 1 day, and a cardiac consultation for 268 (63.65%) of these patients. None of these patients was candidates for an invasive cardiac intervention.

TTP presenting as complete heart block

Although we typically think of a pentad of manifestations of TTP and, in fact, have a treatment threshold consisting of microangiopathic hemolytic anemia and thrombocytopenia otherwise unexplained, the disease can cause manifestations in multiple organs. Here is a discussion of cardiac manifestations.

Medical and surgical treatment of primary aldosteronisn

From a recent review:

Treatments for primary aldosteronism (PA) aim to correct or prevent the deleterious consequences of hyperaldosteronism: hypertension, hypokalemia, and direct target organ damage. Patients with unilateral PA considered fit for surgery can undergo laparoscopic adrenalectomy, which significantly decreases blood pressure (BP) and medications in most cases and cures hypertension in about 40%. Mineralocorticoid receptor antagonists (MRA) are used to treat patients with bilateral PA and those with unilateral PA if surgery is not possible or not desired. Spironolactone is more potent than eplerenone, but high doses are poorly tolerated in men. MRA can be replaced or complemented with epithelial sodium channel blockers, such as amiloride. Thiazide diuretics and calcium channel blockers are used when the first-line drugs are insufficient to control BP. Dietary sodium restriction should be implemented in all cases because the deleterious consequences of hyperaldosteronism are dependent on salt loading. Several studies comparing the results of surgery and MRA have reported no differences in terms of BP, serum potassium concentration, or cardiovascular and kidney outcomes, although the benefits of treatment tend to be observed sooner with surgery. Patients with PA display relative glomerular hyperfiltration, which is reversed by specific treatment, revealing CKD in 30% of patients. However, further kidney damage is lessened by the treatment of PA.