Who’da thunk: hospital mortality down during Joint Commission visits

From JAMA Internal Medicine.

The article talks about unannounced JC visits. True, they are unannounced, but not unexpected. Hospital administrators seem to be able to predict their arrival with a margin of error of a few days and prepare months in advance. More than anything else it is probably the heightened vigilance around the visits that is of benefit.

Why are docs the only ones who can’t use jargon?

Via Kevin MD.

IVIG for severe refractory HIT

Preliminary results are encouraging.

A complication of IVC filters

From JAMA Internal Medicine:

A woman in her 20s with ulcerative colitis presented with acute-onset left-sided pleuritic chest pain for 3 days. She had a medical history of unprovoked deep vein thromboses (DVT) and pulmonary embolism (PE) and had been taking coumadin without any issues. Ten years before, she had had a retrievable inferior vena cava filter (RIVCF) placed for intraoperative PE prophylaxis for total colectomy for ulcerative colitis. She denied being off anticoagulation medication ever or any medical history of bleeding or new thromboses while on warfarin, or during the perioperative period. The RIVCF was never removed. A computed tomographic (CT) angiography ruled out any new PE, but showed IVCF fragments in the pulmonary vasculature. Two of the 3 pieces (Figure, A) and the RIVCF (Figure, B) were removed and her pain improved. The third piece was irretrievable owing to location deep in the pulmonary vasculature. She continued to have intermittent chest pain over the next 6 months and CT showed another IVCF fragment in right atrial musculature (Figure, C) which was obscured by contrast on prior CT angiograms. The risks involved with open-heart surgery for retrieval of this fragment were discussed with the patient and she decided against any intervention. Her chest pain resolved spontaneously over the next 2 months. She continues to take coumadin without any issues.

To top it off it was done for a weak indication and could have been removed early.

Parenteral angiotensin II: will it have a role in the treatment of shock?

Here’s a systematic review on the safety:

Objective: Angiotensin II is an endogenous hormone with vasopressor and endocrine activities. This is a systematic review of the safety of IV angiotensin II.

Data Sources: PubMed, Medline, Scopus, and Cochrane.

Study Selection: Studies in which human subjects received IV angiotensin II were selected whether or not safety was discussed.

Data Extraction: In total, 18,468 studies were screened by two reviewers and one arbiter. One thousand one hundred twenty-four studies, in which 31,281 participants received angiotensin II (0.5–3,780 ng/kg/min), were selected. Data recorded included number of subjects, comorbidities, angiotensin II dose and duration, pressor effects, other physiologic and side effects, and adverse events.

Data Synthesis: The most common nonpressor effects included changes in plasma aldosterone, renal function, cardiac variables, and electrolytes. Adverse events were infrequent and included headache, chest pressure, and orthostatic symptoms. The most serious side effects were exacerbation of left ventricular failure in patients with congestive heart failure and bronchoconstriction. One patient with congestive heart failure died from refractory left ventricular failure. Refractory hypotensive shock was fatal in 55 of 115 patients treated with angiotensin II in case studies, cohort studies, and one placebo-controlled study. One healthy subject died after a pressor dose of angiotensin II was infused continuously for 6 days. No other serious adverse events attributable to angiotensin II were reported. Heterogeneity in study design prevented meta-analysis.

Conclusion: Adverse events associated with angiotensin II were infrequent; however, exacerbation of asthma and congestive heart failure and one fatal cerebral hemorrhage were reported. This systematic review supports the notion that angiotensin II has an acceptable safety profile for use in humans.

SGLT2 inhibitors for DM 2 reduce blood pressure

A systemic review and meta-analysis.

Machine learning in medicine

This JAMA Viewpoint article highlights the weakness of reliance of computer decision support for diagnostics.

Patterns of interstitial lung disease in the elderly

From a recent paper in Chest:

Background

Despite the relationship between idiopathic pulmonary fibrosis (IPF) and advancing age, little is known about the epidemiology of interstitial lung disease (ILD) in the elderly. We describe the diagnoses, clinical characteristics, and outcomes of patients who were elderly at the time of ILD diagnosis.

Methods

Among subjects from a prospective cohort study of ILD, elderly was defined as age ≥ 70 years. Diagnoses were derived from a multidisciplinary review. Differences between elderly and nonelderly groups were determined using the χ2 test and analysis of variance.

Results

Of the 327 subjects enrolled, 80 (24%) were elderly. The majority of elderly subjects were white men. The most common diagnoses were unclassifiable ILD (45%), IPF (34%), connective tissue disease (CTD)-ILD (11%), and hypersensitivity pneumonitis (8%). Most elderly subjects (74%) with unclassifiable ILD had an imaging pattern inconsistent with usual interstitial pneumonia (UIP). There were no significant differences in pulmonary function or 3-year mortality between nonelderly and elderly subjects combined or in a subgroup analysis of those with IPF.

Conclusions

Although IPF was the single most common diagnosis, the majority of elderly subjects had non-IPF ILD. Our findings highlight the need for every patient with new-onset ILD, regardless of age, to be surveyed for exposures and findings of CTD. Unclassifiable ILD was common among the elderly, but for most, the radiographic pattern was inconsistent with UIP. Although the effect of ILD may be more pronounced in the elderly due to reduced global functionality, ILD was not more severe or aggressive in this group.

Appealing to patients’ altruism to reduce low value care: surprise surprise, it doesn’t work

Not only that, it results in lower physician ratings.  From a recent paper in JGIM:

Objective

To determine whether altruistic appeals reduce hypothetical requests for overused services and affect physician ratings.

Design

Experimental survey using hypothetical vignettes describing three overused health services (antibiotics for acute sinusitis, imaging for acute low back pain, and annual exams for healthy adults).

Participants

U.S. adults recruited from Research Now, an online panel of individuals compensated for performing academic and marketing research surveys.

Interventions

In the control version of the vignettes, the physician’s rationale for recommending against the service was the minimal benefit and potential for harm. In the altruism version, the rationale additionally included potential benefit to others by forgoing that service.

Main Measures

Differences in requests for overused services and physician ratings between participants randomized to the control and altruism versions of the vignettes.

Key Results

A total of 1001 participants were included in the final analyses. There were no significant differences in requests for overused services for any of the clinical scenarios (P values ranged from 0.183 to 0.547). Physician ratings were lower in the altruism version for the acute sinusitis (6.68 vs. 7.03, P = 0.012) and back pain scenarios (6.14 vs. 6.83, P less than 0.001), and marginally lower for the healthy adult scenario (5.27 vs. 5.57, P = 0.084).

Conclusions

In this experimental survey, altruistic appeals delivered by physicians did not reduce requests for overused services, and resulted in more negative physician ratings. Further studies are warranted to determine whether alternative methods of appealing to patient altruism can reduce overuse.

Though this study is not very “real world” it makes sense, especially the finding of lower physician ratings.

An argument against low value care based on ineffectiveness is fine and patients ought to be able to respect it.  But an appeal to altruism sends a message that you can’t whole heartedly advocate for them as individuals. Imagine you are accused of a crime and your attorney says “I’ll work hard to represent you but please keep in mind the interests of ‘the people’ in these proceedings.”

Choosing ever so slightly more wisely?

From the Journal of Hospital Medicine:

As part of the Choosing Wisely® campaign, the Society of Hospital Medicine recommends against performing “repetitive complete blood count chemistry testing in the face of clinical and lab stability.” With this recommendation as a framework, we targeted 2 hospitalist-run inpatient medicine units that employed bedside, scripted, interdisciplinary rounds. Our multifaceted intervention included prompting the hospitalist to identify clinically stable patients for next-day discharge and to discontinue labs when appropriate. It was coupled with the education of the clinicians and a regular data review for the hospitalists and unit staff. Among 2877 discharges included in a 1-year period, there was a significantly decreasing trend after the intervention in the percentage of patients getting labs in the 24, 48, and 72 hours before discharge (−1.87%, −1.47%, and −0.74% decrease per month, respectively; P less than 0.05). Our structured, multifaceted approach effectively reduced daily lab testing in the 24 to 48 hours prior to discharge.

Though statistically significant the magnitude of success was not what I would call robust.

H pylori diagnosis: FAQs

Here are some key points from a recent review.

Who should be tested?

Any one with PUD, past or active.

Any patient with MALT lymphoma.

Here are some additional recommendations from the ACG guidelines:

All patients with active peptic ulcer disease (PUD), a past history of PUD (unless previous cure of H. pylori infection has been documented), low-grade gastric mucosa-associated lymphoid tissue (MALT) lymphoma, or a history of endoscopic resection of early gastric cancer (EGC) should be tested for H. pylori infection…

Patients initiating chronic treatment with a non-steroidal anti-inflammatory drug (NSAID) should be tested for H. pylori infection (strong recommendation, moderate quality of evidence)...

When upper endoscopy is undertaken in patients with dyspepsia, gastric biopsies should be taken to evaluate for H. pylori infection…

Patients with unexplained iron deficiency (ID) anemia despite an appropriate evaluation should be tested for H. pylori infection.

The guideline makes these additional statements regarding patients who should be considered for testing (softer recommendation):

In patients with uninvestigated dyspepsia who are under the age of 60 years and without alarm features, non-endoscopic testing for H. pylori infection is a consideration…

In patients taking long-term low-dose aspirin, testing for H. pylori infection could be considered to reduce the risk of ulcer bleeding…

Adults with idiopathic thrombocytopenic purpura (ITP) should be tested for H. pylori infection. Those who test positive should be offered eradication therapy (conditional recommendation, very low quality of evidence).

How should testing be carried out?

If an EGD is not being done, from the review:

Helicobacter pylori infection can be diagnosed using noninvasive and invasive methods. In general, both noninvasive and invasive tests are equally accurate.13 Noninvasive tests include the urea breath test, fecal antigen test, and serologic test. The preferred noninvasive tests in the outpatient setting are the urea breath test and fecal antigen test given their excellent accuracy and ability to diagnose active infection. The fecal antigen test relies on identifying H pylori antigens in the stool using an enzymatic immunoassay.13 In the urea breath test, urea labeled with 13C or 14C is given to patients. Urease, if present, converts urea into ammonia and labeled CO2 that is exhaled, indicating a positive result.13 Before testing, proton pump inhibitors (PPIs) and antibiotics should be discontinued at least 2 and 4 weeks, respectively, as these can interfere with the urea test.10 Pretreatment sensitivity and specificity of both these tests are approximately 95%.13 Although the cost of testing varies by location and laboratory, the estimated cost of the urea breath test and fecal antigen test is $102.80 and $19.70, respectively.14 Serologic testing is not recommended to detect active infection, as it cannot distinguish between active disease and previous exposure. Antibodies to H pylori can remain elevated for a long time even after treatment, potentially increasing the number of false-positive results.13 The 1 positive aspect of serologic testing is that it is the only test for H pylori that is not affected by PPI therapy, antibiotics, or by the presence of blood in the stomach.

If EDG done, again from the review:

Invasive testing strategies require upper endoscopy and include the biopsy urease (campylobacter-like organism) test, histologic assessment, and culture. The biopsy urease test is a good first-line test, as it is accurate, rapid, and inexpensive. This test relies on H pylori urease to convert urea into ammonia, increase the pH, and change the color of the pH indicator.15 Although the specificity is excellent with this test (greater than 95%), the sensitivity can vary from 75% to 98%.15 The urease test is preferred in patients without recent use of PPIs and antibiotics, as outlined above.10 However, in patients with recent PPI or antibiotic use, histologic assessment of biopsy samples is the better choice, although these medications can interfere with bacterial density.

Jump into the political fray or you’ve made the wrong moral choice and are guilty of harm

And be sure you line up on the correct side. Berwick.

Hypertrophic cardiomyopathy (HCM) FAQs

Unless stated otherwise the information below is based on a review in Circulation. It’s a little dated but good, and available as free full text.

What are the differences between HCM as it classically presents in younger patients and HCM of the elderly? Is there such a thing as acquired HCM of the elderly?

Genetic HCM can have its presentation delayed until old age but genetic testing, as opposed to young patients, has a low yield in HCM of the elderly lacking a positive family history.

Certain mutations are known to predispose to later onset disease.

Later onset disease is associated with milder hypertrophy and a more benign course attributable to the disease itself.

Upper septal hypertrophy (USH), aka disproportionate upper septal thickening (DUST) (overlapping with the concept of sigmoid septum) is characteristic though not exclusively seen in the elderly. Its relationship to genetic HCM is unclear but when seen in isolation it is not associated with a bad prognosis.

It is currently believed that an acquired form of HCM, including “IHSS physiology”, can be seen in the elderly, arising from LVH secondary to hypertension or valvular aortic stenosis. The exception is that these patients generally don’t have asymmetric septal hypertrophy (ASH) but rather concentric LVH.

What about the genetics?

A genetic abnormality can be found in most younger patients with HCM and a positive family history.

Up to Date says many mutations have been found in 11 genes.

According to the ACC/AHA guidelines genetic screening has a class IIa recommendation for an index case. Screening of first degree relatives can be clinical (phenotypic) or genetic. Genetic screening to assess the risk of SCD carries only a IIb recommendation. Cost considerations apply in the real world.

What are the anatomic and physiologic variants?

HCM does not always present with the classic “IHSS” phenotype. From my reading of Up to Date, other variants include DUST (which may occur in isolation and not represent HCM, see above), mid septum and free wall hypertrophy resulting in an intracavitay gradient, free wall greater then septal hypertrophy (rare), varying degrees of concentric LVH, and apical HCM (Yamaguchi syndrome).

What are the risk factors for SCD and how should they be taken into account in deciding whether to recommend an AICD?

From the Circulation article:

Accepted risk factors for SCD are unexplained syncope; family history of SCD due to HCM or occurring with no other explanation before 50 years of age; extreme (greater than 30 mm) LVH; ventricular tachycardia, as detected by Holter monitoring; and an abnormal blood pressure response to exercise. Young and middle-aged patients at risk of SCD are usually offered an implantable cardioverter-defibrillator. The risk of SCD may be lower in elderly patients with HCM, but there is uncertainty with regard to how to adapt the conventional risk factors to this population.

These factors are taken together, and a clinical scoring tool is available. Genetic testing to decide on device implantation is not highly recommended.

What are the medical treatments? Where do surgical treatments and septal ablation fit in?

A nice algorithm from the Circulation article is here.

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

Here is a free full text review.

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.

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

From the second reference above:

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.

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.

Summary

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.

Insomnia as a cardiovascular disease risk factor

From a review in Chest:

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.

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

From a recent meta-analysis:

Conclusions

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.

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

From the report:

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 (ClinicalTrials.gov: 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.

Reperfused STEMI and intramyocardial hemorrhage

This is interesting:

Abstract

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.

What the hospitalist needs to know about interstitial lung disease

Here are some key points from a review in the Journal of Hospital Medicine:

What is the classification?

Categories are exposure related (eg hypersensitivity pneumonitis, drugs, occupational), connective tissue disease related, idiopathic and miscellaneous (including sarcoid, Langerhans cell histiocytosis, eosiniphilic pneumonia and vasculitis (including diffuse alveolar hemorrhage).

What labs should be ordered initially on a patient suspected for the first time to have ILD?

According to the review, ANA, RA, anti cyclic citrullinated peptide, CK and aldolase. (Aldolase may be elevated while the CK is normal in some cases of inflammatory myopathy). (I would wonder if synthetase antibody testing should be added to this list). After this round of testing, subsequent tests can be added based on initial results and the ensuing clinical course.

What imaging studies should initially be done?

CXR and HRCT according to the article, which also mentioned that if clinical conditions warrant, instead of just doing a HRCT, get a CT PA gram with simultaneous high resolution images of the lung parenchyma.

What about bronchoscopy?

This is not considered routine and what I get from the review is that the diagnostic confidence derived from HRCT and the anticipation of how the results might change treatment will influence this decision. Circumstances that might favor doing bronchoscopy include suspected acute eosinophilic pneumonia (AEP), suspected acute hypersensitivity pneumonitis, suspected sarcoid and suspected unusual infection.

When should antibiotics be given?

According to the review, onset or exacerbation of ILD can be difficult to distinguish from infection, so always at least consider them. (Given the all too often undifferentiated nature of the presentation in critically ill patients, I suspect the threshold would be low). The review did not comment on the specific type of coverage. However, many such patients are immunosuppressed, have had frequent hospitalizations, or are critically ill and those factors would guide antibiotic choices.

Should corticosteroids be used?

In cases of clinical deterioration or respiratory failure, which is the case with most patients who require hospitalization, yes. The etiology is often unknown, and it must be kept in mind that some etiologies are known to be highly steroid responsive, particularly AEP and COP. Recommendations also support the use of steroids for CTD related ILD, acute HP and drug induced ILD. IPF by comparison is poorly steroid responsive but current guidelines conditionally recommend their use.

Cautions that would apply include the ever present risk of unusual infection and the potential for steroids to increase the risk of renal crisis in patients with systemic sclerosis.

Lung transplantation is a consideration for certain non responding patients

Form the article:

In these cases, lung transplantation may be the only remaining treatment option. This is particularly true for patients presenting with IPF, and it is 1 of the most common indications for lung transplantation. Patients with respiratory failure and ILD should be evaluated early in the hospital course for transplantation or considered for transfer to a transplant center. General contraindications to transplant are age older than 70 years, underweight or elevated BMI (generally higher than 30), malignancy within the last 2 years (with the exception of cutaneous squamous and basal cell tumors), untreatable major organ dysfunction other than the lung, noncurable chronic extrapulmonary infection (chronic active viral hepatitis B, hepatitis C, human immunodeficiency virus), significant chest wall deformity, untreatable psychiatric or psychologic disease, substance addiction within the last 6 months, or lack of dependable social support.4

Another excellent review, free full text, is here. Though a couple of years old it is still relevant and has lots of pearls.