Yet another study on rapid response systems

The evidence in support of RRS is mixed. The RRS is favored in some before and after studies but not RCTs. This study, published in Resuscitation, is another before and after study but it does have some strengths compared to the older ones. From the paper:

Methods

For the period 2002–2009, we compared a teaching hospital with a mature RRS, with three similar teaching hospitals without a RRS. Two non-RRS hospitals began implementing the system in 2009 and a third in January 2010. We compared the rates of in-hospital cardiopulmonary arrest (IHCA), IHCA-related mortality, overall hospital mortality and 1-year post discharge mortality after IHCA between the RRS hospital and the non-RRS hospitals based on three separate analyses: (1) pooled analysis during 2002–2008; (2) before–after difference between 2008 and 2009; (3) after implementation in 2009.

Results

During the 2002–2008 period, the mature RRS hospital had a greater than 50% lower IHCA rate, a 40% lower IHCA-related mortality, and 6% lower overall hospital mortality. Compared to 2008, in their first year of RRS (2009) two hospitals achieved a 22% reduction in IHCA rate, a 22% reduction in IHCA-related mortality and an 11% reduction in overall hospital mortality. During the same time, the mature RRS hospital showed no significant change in those outcomes but, in 2009, it still achieved a crude 20% lower IHCA rate, and a 14% lower overall hospital mortality rate. There was no significant difference in 1-year post-discharge mortality for survivors of IHCA over the study period.

A related editorial makes some important points. First, the rationale and plausibility for the RRS are strong. In hospital arrests are often preceded by hours or even days of deterioration, presenting opportunities for intervention. Why can't the RRS be proven in high level studies? For one thing, says the editorial writer, the RRS is not a “clean intervention.” How it's used depends on the staffing and culture of the institution. It is one thing to say your hospital has a rapid response system but quite another to use it for all it's worth. What's most important is to recognize the signs of deterioration, then “have the big discussion” or pull out all the stops early. That, of course, is nothing more than a principle of clinical vigilance we've known for decades: when you smell a rat, get aggressive early.

Bottom line? A rapid response system can be beneficial in many ways depending on the needs and resources of the institution. However, general claims that these systems save lives cannot be justified.

Will this or that technology revolutionize education?

Throughout the history of education one innovation after another has failed to live up to the hype. Electronic media developed in recent years are no exceptions. It's really all about what happens in the mind of the learner and the social interaction with the teacher as explained in this video. (HT to Life in the Fast Lane). Individual learners have different styles. One size does not fit all.

NASH as an emerging indication for liver transplant

A study form an organ transplant database:

We queried 2,356 patients with nonalcoholic steatohepatitis, alcoholic cirrhosis (ETOH), and hepatitis C cirrhosis from the Ohio Solid Organ Transplantation Consortium who were listed for and/or received an orthotopic liver transplant from 2000 to 2012.

Results

The proportion of listed patients with nonalcoholic steatohepatitis increased from 0% to 26% and the proportion of transplanted patients increased from 0% to 23.4%.

Via Hospital Medicine VirtualJournal Club.

Point of care ultrasound for hospitalists

From a review:

We review the literature on diagnostic point-of-care ultrasound applications most relevant to hospital medicine and highlight gaps in the evidence base. Diagnostic point-of-care applications most relevant to hospitalists include cardiac ultrasound for left ventricular systolic function, pericardial effusion, and severe mitral regurgitation; lung ultrasound for pneumonia, pleural effusion, pneumothorax, and pulmonary edema; abdominal ultrasound for ascites, aortic aneurysm, and hydronephrosis; and venous ultrasound for central venous volume assessment and lower extremity deep venous thrombosis. Hospitalists and other frontline providers, as well as physician trainees at various levels of training, have moderate to excellent diagnostic accuracy after brief training programs for most of these applications. Despite the evidence supporting the diagnostic accuracy of point-of-care ultrasound, experimental evidence supporting its clinical use by hospitalists is limited to cardiac ultrasound.

Via Hospital Medicine VirtualJournal Club.

ST elevation in aVR and left main coronary syndromes: addressing the confusion

Here are a case presentation and a follow up on a patient with diffuse ST depression and ST elevation in aVR from the EMS 12-Lead blog.

A few learning points from the post:

Multi-lead ST depression with ST elevation in aVR suggest global subendocardial ischemia due to left main artery stenosis or its equivalent (multi-vessel) but not occlusion.

Rather than an unstable coronary plaque, the syndrome often reflects myocardial oxygen supply-demand imbalance in which case the troponin elevation represents a type 2 MI.

Treatment often consists of mitigating those factors causing supply-demand imbalance.

When should these patients go to the cath lab? Not always immediately, depending on clinical circumstances. That question is addressed further in this post from Dr. Smith's blog, which also discusses the much less common presentation of left main occlusion.

American College of Physicians to practicing docs: we are your conscience

A post by Bob Doherty in the ACP Advocate Blog supports an increasingly popular narrative: the idea that the interests of the medical profession are necessarily opposed to those of patients and that some entity must advocate for patients against the profession. The ACP, as I read the post, would like to appoint itself as that entity by being the "conscience of medicine."

Can the conscience of medicine be collective? Conscience is naturally collective for certain general virtues such as being honest and being good to people. It's based on precepts that are innate and form what philosophers call the natural law. But as the collective conscience moves from general to specific, as defined by a community, government or an organization trouble may ensue as examples from history have shown. When it is defined by a particular side in political debate bad consequences can be taken for granted. But based on Doherty's remarks that's exactly how the ACP seems to be defining it.

In his post he traces the evolution of the ACP from an apolitical society that existed to represent the professional and educational interests of physicians to an activist organization involved in many facets of politics. Despite Doherty's empty disclaimer that it's only about the well being of patients the ACP has come down squarely in a partisan manner on a variety of issues. In order to support such a disclaimer you would have to stretch to absurdity the idea that the political process exists to serve people.

There's nothing new or shocking about a professional medical organization being involved in politics. It takes on a new dimension, though, when you articulate a partisan stand on multiple issues and imply in the same breath to physicians at large “we are your conscience.” It smacks of intolerance because it says in effect “if you disagree you're in the wrong and not putting patients first.”

But as long as we have this new conscience of medicine we should note that it is strangely selective given its silence on the ethical questions now swirling around the American Board of Internal Medicine. That's something the conscience should be screaming about.

HT to Retired Doc's Thoughts.

Medical decisions by central authority without appropriate expertise---potentially harmful to patients

A recent post from Dr Wes notes:

Today I learned that CMS has issued a National Coverage Decision (NCD) for pacemakers effective 6 July 2015 that would restrict pacemaker implants to patients with "non-reversible symptomatic bradycardia" and require a so-called "KX" modifier to be added to codes for patients needing pacemakers.

That's right, even patients with asymptomatic complete heart block would not be covered.  Patients with asymptomatic Mobitz Type II heart block wouldn't be covered either.  Even though every piece of medical literature has supported the benefits of pacemakers in these indications, it seems doctors will be left with no choice but to lie in their documentation about patient symptoms to assure Medicare payment, or risk the government refusing to pay for their patients' medically indicated care. 

To my reading the original source linked in the post is fuzzy concerning what will and won't be covered ultimately. However the requirement for the KX modifier forces the physician to attest that the patient has symptomatic bradycardia.  That implies that patients with asymptomatic type 2 AV block would be denied permanent pacing, thus exposing them to significant mortality risk. 

So this is either a case of regulatory obfuscation or a top-down medical decision which will place patients at risk. If the latter, it reflects junior medical student level of expertise or worse. Stupidity can be dangerous. 

Medication alerts generated by the EMR are rarely heeded

---according to this study.

Via Hospital Medicine Virtual Journal Club.

LVH is a risk factor for sudden cardiac death

See this recent study.

There were hints of this association in the MRFIT study from decades ago.

Practical aspects of the lumbar puncture

Very nice summary from S.O.A.P.

The skinny on lipid rescue

Here's a nice overview from Academic Life in Emergency Medicine. In the opinion of the blog author it's under utilized. A downside is that the resulting lipemia interferes with lab determinations. But as one of the commenters pointed out, an easy work around is to use the blood gas machine or a similar point or care device which gives accurate results in the presence of lipemia.

Lifestyle modification is key to treating the metabolic syndrome

Recent paper from the green journal.

What's the best timing for laparoscopic cholecystectomy in acute cholecystitis?

From a recent paper:

Design, Setting, and Participants We performed a retrospective review of prospectively collected data from the Nationwide Inpatient Sample (NIS) for 2005 through 2009. The population-based sample included 95 523 adults (18 years and older) who underwent LC within 10 days of presentation for acute cholecystitis.

Interventions Patients were categorized and analyzed in 2 ways based on length of time from presentation to surgery. First, patients were categorized into 3 groups: 0 through 1 day, 2 through 5 days, and 6 through 10 days. Second, we compared outcomes for each incremental preoperative day (days 0-5).

Main Outcomes and Measures Outcomes of interest were mortality, length of stay, complications, and cost. Propensity score matching and generalized linear modeling were used...

Results A total of 95 523 patients were selected. After matching the 3 groups based on propensity scores, patients who underwent surgery during days 2 through 5 and days 6 through 10 had increasingly worse outcomes when compared with those undergoing surgery on days 0 through 1. The odds of mortality were 1.26 (95% CI, 1.00-1.58) and 1.93 (95% CI, 1.38-2.68), and the odds of postoperative infections were 0.88 (95% CI, 0.69-1.12) and 1.53 (95% CI, 1.05-2.23) for days 2 through 5 and days 6 through 10, respectively. Adjusted mean hospital cost increased from $8974 (days 0-1) to $17 745 (days 6-10). Analysis by each incremental day revealed the optimal time of surgery to be within the first 48 hours of presentation.

Conclusions and Relevance Laparoscopic cholecystectomy performed within 2 days of presentation of acute cholecystitis yielded the best outcomes and lowest costs. Although causality could not be established, delaying LC was associated with more complications, higher mortality, and higher costs.

Via Hospital Medicine Virtual Journal Club.

Left atrial abnormality and the risk of sudden cardiac death

Recent findings:

This analysis included 15 375 participants (54.1±5.8 years, 45% men, 73% whites) from the Atherosclerosis Risk in Communities (ARIC) study. DTNPV1 was defined from the resting 12‐lead ECG as presence of biphasic P wave (positive/negative) in V1 with the amplitude of the terminal negative phase greater than 100 μV, or one small box on ECG scale. After a median of 14 years of follow‐up, 311 cases of SCD occurred. In unadjusted Cox regression, DTNPV1 was associated with an 8‐fold increased risk of SCD (HR 8.21; [95%CI 5.27 to 12.79]).

Over nine years ago I pointed out that this same finding was associated with stroke risk.

Negative cost incentives for hospitals and mortality

From a study in Journal of General Internal Medicine:

Results

We examined 12,341 admissions among 79 physicians. After propensity score matching, admission groups were similar with respect to all demographic and clinical characteristics. Admissions of patients receiving care from short length-of-stay physicians were associated with significantly increased risk of 30-day mortality in adjusted (OR 1.43, 95 % CI: 1.11–1.85), propensity score-matched (OR 1.33, 95 % CI: 1.08–1.63), and matched and adjusted analyses (OR 1.36, 95 % CI: 0.98–1.90).

Conclusions

Policies that incentivize short length of stay may lead to worse patient outcomes. The financial benefits of shortening inpatient length of stay should be weighed against the potential harm to patients.

Hospital associated complications and the July effect

Studies on the July effect have yielded mixed results. This new study found an increase in hospital associated complications for July admissions.

Factors leading to care withdrawal after resuscitation from cardiac arrest

From a recent study:

Methods

Data was collected from 189 survivors to hospital admission. Patients were classified by survival status upon hospital discharge, and those who died were categorized into withdrawal vs. no withdrawal of care. Those who had care withdrawn were further subdivided into early care withdrawal i.e. less then or equal to 72 h vs. late withdrawal greater than 72 h. Multivariable adjusted odds ratios were used to assess factors associated with early care withdrawal.

Results

Of 189 patients with cardiac arrest, only 36 had advanced directives (19%) and 99 (52%) had care withdrawn. Most patients whose care was withdrawn died in hospital (94/99, 95%), and the remainder died in hospice. Care was withdrawn early less than or equal to 72 h in the majority of patients (59/94, 63%). Median time to early care withdrawal was 2 days IQR (1–3). Factors associated with early care withdrawal were age greater than or equal to 75 years, poor initial neurologic exam, multiple co morbidities, multi-organ failure, lactic acid greater than or equal to10 mmol L−1, Caucasian race and absence of bystander CPR. Advance directives did not appear to determine early care withdrawal.

Conclusions

Although most cardiac arrest patients do not have advance directives, care is often withdrawn in more than 50% and in many before the accepted time for neurological awakening (72 h). The decision to withdraw care is influenced by older age, race, preexisting co morbidities, multi-organ failure, and a poor initial neurological exam. Further studies are needed to better understand this phenomenon and other sociological factors that guide such decisions.

These findings are concerning. Basing care withdrawal on neurological findings before 72 hours is against current resuscitation research evidence. If age and comorbidities were factors one wonders why the patients were resuscitated in the first place.

Things non surgeons need to know about small bowel obstruction

If the patient with bowel obstruction doesn't need surgery, he/she does need surgical expertise. Either way SBO is a surgical disease. Nevertheless such patients increasingly get admitted to hospitalists. Like it or not, it is what it is. For a great overview on SBO written in language we hospitalists can understand check out this post from EMBlog Mayo Clinic.

Determining irregularity if you don't have calipers handy

Fold the paper on itself, hold it up to light and see if you can align the complexes. Via EM Updates.

(Or you can use the Magic Eye method).

Urgent warfarin reversal

When warfarin reversal must be accomplished rapidly, such as in cases of active bleeding or in preparation for an invasive procedure, multiple options exist, chief among them being fresh frozen plasma (FFP) and four factor prothrombin complex concentrate (4-PCC). Between those two options, the ACCP guidelines suggest (soft recommendation) 4-PCC over FFP. This was based on low level data (very small studies) showing more rapid INR reversal using the former. This study, which came out after publication of the ACCP guidelines, added further weight in favor of 4-PCC in patients deemed appropriate for rapid warfarin reversal in the emergency setting. Though considered low level in that it was a retrospective study, it was larger (around 150 patients in both groups) than prior studies. Despite mounting evidence in favor of 4-PCC some experts (e.g. the authors of this review) remain skeptical as to whether 4-PCC is superior, awaiting information from randomized controlled trials. One such trial has been completed but, as far as I can tell, the results have not been announced. That study, however, enrolled only patients needing urgent warfarin reversal in preparation for an invasive procedure. Though it will shed further light it is unlikely to settle the controversy.

An appeal of 4-PCC is it's rapid acquisition and ease of administration. One of the concerns has been a possible risk of thrombotic complications compared to FFP. That concern was not realized in the retrospective study referenced above.

The QTc: unreliable in the estimation of risk for Torsade de Pointes (TdP)

This post from Emergency Medicine PharmD makes the point that heterogeneity of repolarization time within the myocardial mass is more important than the QT interval itself. The best example of this is amiodarone, notorious for prolonging the QT but with minimal risk of TdP. Reliance on the QT, even the corrected QT, is simplistic as I previously posted here.

Pneumocystis jiroveci in HIV negative patients

From the American Journal ofMedicine:

We retrospectively analyzed all cases of documented pneumocystosis in HIV-negative patients admitted in our institution, a referral center in the area, from January 1990 to June 2010, and extracted data on their underlying condition(s)...

The main underlying conditions were hematological malignancies (32.5%), solid tumors (18.2%), inflammatory diseases (14.9%), solid organ transplant (12.3%), and vasculitis (9.7%). Estimated incidence rates could be ranked in 3 categories: 1) high risk (incidence rates greater than 45 cases per 100,000 patient-year): polyarteritis nodosa, granulomatosis with polyangiitis, polymyositis/dermatopolymyositis, acute leukemia, chronic lymphocytic leukemia, and non-Hodgkin lymphoma; 2) intermediate risk (25-45 cases per 100,000 patient-year): Waldenström macroglobulinemia, multiple myeloma, and central nervous system cancer; and 3) low risk (less than 25 cases per 100,000 patient-year): other solid tumors, inflammatory diseases, and Hodgkin lymphoma.

Inflammatory bowel disease and hypercoagulability

The association is nicely outlined in this post from The Bottom Line.

Medicare reimbursement for PCI in acute coronary syndrome

A recently published report helps smack down a few common myths and misstatements concerning Medicare payments to hospitals. It is available as free full text here.

Myth # 1: Medicare is a fee-for-service system of reimbursement.

This is true only for part B Medicare. For part A, under which hospitals are reimbursed, the payment is a lump sum based on the diagnosis. Although that payment can be modified based on certain severity indicators there is no direct payment for services rendered. If Medicare paid hospitals for the services rendered it would be a retrospective, rather than a prospective payment.

Myth # 2: The wildly popular use of cardiac stents is driving health care costs out of control.

Not for acute coronary syndrome, which accounts for about two thirds of stents, according to the article. Following an uptick attributable to the shift from bare metal to drug eluting stents costs stabilized and, when adjusted for inflation, decreased slightly according to the report. To stretch the point a bit further just go back to the days before the reperfusion era of double digit mortality and two week lengths of stay. Scientific advancement, not external pressure, has driven the improvements in emergency cardiac care.

Myth # 3: The use of cardiac stents has been a big money maker for hospitals.

It's really quite the opposite. Cardiac stents have been a money loser. According to the report, Medicare payments fall short of estimated costs for patients hospitalized for ACS who receive emergency PCI.

Under appreciated risk factors for AKI

From a recent review:

Recent findings: The risk of AKI is determined by patient factors and nephrotoxic exposures. Hyperuricaemia, obesity, hypoalbuminaemia and certain genetic polymorphism have been found to be associated with an increased susceptibility to AKI, especially in surgical patients. However, there is no convincing evidence that albumin replacement or uric acid lowering ameliorates the risk. Genetic predisposition contributes to AKI in general and also drug-nephrotoxicity. The exact relationship between obesity and AKI has not been fully understood.

Patients exposed to starches, chloride-rich fluids or mechanical ventilation have an increased risk of AKI. Starches in particular should be avoided in high-risk patients. Although chloride-rich fluids are associated with AKI based on observational studies, direct proof of harm is lacking.

Summary: Novel risk factors for AKI have been identified but more work is necessary to investigate the nature of the association. There is no evidence that correction of hyperuricaemia or hypoalbuminaemia is beneficial but high-risk exposures should be avoided in patients at risk of AKI.

Don't forget chronic hypersensitivity pneumonitis in the differential for ILD

From a recent update:

Recent findings: Several recent publications show the potential pathologic patterns induced by chronic hypersensitivity pneumonitis are broader than the classic triad of bronchiolitis, interstitial infiltrates and granulomas. Other pathologic patterns include nonspecific interstitial pneumonia, usual interstitial pneumonia, organizing pneumonia, bronchiolitis and airway centric fibrosis. Detecting a causative antigen in fibrotic hypersensitivity pneumonitis is challenging but critically important both for accurate diagnosis and improved prognosis. The prognosis in hypersensitivity pneumonitis worsens in the presence of fibrosis, but it remains significantly better than idiopathic pulmonary fibrosis.

Summary: Hypersensitivity pneumonitis is increasingly recognized as an important cause of fibrotic interstitial lung disease. Hypersensitivity pneumonitis demonstrates a remarkable tendency to mimic other idiopathic interstitial pneumonias. A detailed exposure history remains a cornerstone of diagnosis and management.

Myths and facts about diastolic heart failure

The misconceptions cited in this article from the green journal aren't complete myths, but the article highlights some of the oversimplifications in our thinking on the subject.

My take home points after reading this article are: 1) heart failure, whether systolic or diastolic, is a clinical diagnosis and not one made by echo; 2) the pathophysiology and mechanisms of symptom production are complex and go beyond diastolic relaxation properties of the left ventricle; and the distinction between systolic and diastolic dysfunction is not as sharp is commonly perceived.

Elevated blood ammonia levels and encephalopathy due to valproic acid

Here is a review post in Academic Life in Emergency Medicine.

Points of interest:

As valproic acid (VA) is seeing expanded indications this is an increasingly appreciated entity.

A metabolite of VA can inhibit the urea cycle, leading to raised ammonia levels.

The problem can occur early in the course of treatment or after long periods of tolerance of the drug.

It can occur with VA levels in the therapeutic range.

In addition to altered mental status, increased seizure frequency and GI manifestations can be presenting symptoms.

In addition to withdrawal of VA, IV carnitine therapy may be indicated.

The ProMISe trial in perspective

I'm a little late with this. This is the third of the three new randomized trials of early goal directed therapy (EGDT) for septic shock. From the NEJM article:

Results

We enrolled 1260 patients, with 630 assigned to EGDT and 630 to usual care. By 90 days, 184 of 623 patients (29.5%) in the EGDT group and 181 of 620 patients (29.2%) in the usual-care group had died (relative risk in the EGDT group, 1.01; 95% confidence interval [CI], 0.85 to 1.20; P=0.90), for an absolute risk reduction in the EGDT group of −0.3 percentage points (95% CI, −5.4 to 4.7). Increased treatment intensity in the EGDT group was indicated by increased use of intravenous fluids, vasoactive drugs, and red-cell transfusions and reflected by significantly worse organ-failure scores, more days receiving advanced cardiovascular support, and longer stays in the intensive care unit. There were no significant differences in any other secondary outcomes, including health-related quality of life, or in rates of serious adverse events. On average, EGDT increased costs, and the probability that it was cost-effective was below 20%.

Conclusions

In patients with septic shock who were identified early and received intravenous antibiotics and adequate fluid resuscitation, hemodynamic management according to a strict EGDT protocol did not lead to an improvement in outcome.

These trials, the other two being ProCESS and ARISE, have stirred some over reaction. Instead of hyping the issue with statements like “EGDT is dead” a more nuanced approach might be more informative. As I pointed out in my recent reaction to the ARISE results:

What was actually being compared in this study? To me it was strictly protocolized EGDT versus EGDT minus the SVO2 monitor with more room for clinical judgment.

In perspective

What do the Rivers study, ProCESS and ARISE tell us? Here's my take:

Volume assessment remains important but the best way to do so is unknown. Do it via CVP, physical exam or other means, however you will.

Assessment of tissue perfusion is important but the best method is unknown, whether via SVO2, lactate monitoring or bedside clinical examination.

Lower transfusion targets can be applied to septic shock just as in other conditions.

Since publication of the Rivers study “usual care” has risen to the standard of EGDT due to uptake of the Surviving Sepsis guidelines.

Guidelines and pathways must leave room for clinical judgment if evidence is to be applied for all it's worth.

EGDT is not dead. The notion is sound. How best to set resuscitation goals and monitor their achievement is not as simple as some have thought.

Beta lactam monotherapy was non-inferior to regimens with atypical coverage

---in this study form NEJM.

Hurricane Sandy: another experiment of nature demonstrating the relationship between stress and cardiovascular events

Recent report here.