Sunday, January 15, 2017

Your syncope admission: could it be PE?


The prevalence of pulmonary embolism among patients hospitalized for syncope is not well documented, and current guidelines pay little attention to a diagnostic workup for pulmonary embolism in these patients.


We performed a systematic workup for pulmonary embolism in patients admitted to 11 hospitals in Italy for a first episode of syncope, regardless of whether there were alternative explanations for the syncope. The diagnosis of pulmonary embolism was ruled out in patients who had a low pretest clinical probability, which was defined according to the Wells score, in combination with a negative d-dimer assay. In all other patients, computed tomographic pulmonary angiography or ventilation–perfusion lung scanning was performed. Results

A total of 560 patients (mean age, 76 years) were included in the study. A diagnosis of pulmonary embolism was ruled out in 330 of the 560 patients (58.9%) on the basis of the combination of a low pretest clinical probability of pulmonary embolism and negative d-dimer assay. Among the remaining 230 patients, pulmonary embolism was identified in 97 (42.2%). In the entire cohort, the prevalence of pulmonary embolism was 17.3% (95% confidence interval, 14.2 to 20.5). Evidence of an embolus in a main pulmonary or lobar artery or evidence of perfusion defects larger than 25% of the total area of both lungs was found in 61 patients. Pulmonary embolism was identified in 45 of the 355 patients (12.7%) who had an alternative explanation for syncope and in 52 of the 205 patients (25.4%) who did not.


Pulmonary embolism was identified in nearly one of every six patients hospitalized for a first episode of syncope

But, as pointed out by the blogger at Emergency Medicine Literature of Note, this should not be as shocking as it sounds (and will be spun by the popular media). As pointed out there:

The primary issue here is the almost certain inappropriate generalization of these results to dissimilar clinical settings. During the study period, there were 2,584 patients presenting to the Emergency Department with a final diagnosis of syncope. Of these, 1,867 were deemed to have an obvious or non-serious alternative cause of syncope and were discharged home. Thus, less than a third of ED visits for syncope were admitted, and the admission cohort is quite old – with a median age for admitted patients of 80 (IQR 72-85). There is incomplete descriptive data given regarding their comorbidities, but the authors state admission criteria included “severe coexisting conditions” and “a high probability of cardiac syncope on the basis of the Evaluation of Guidelines in Syncope Study score.” In short, their admission cohort is almost certainly older and more chronically ill than many practice settings.

Then, there are some befuddling features presented that would serve to inflate their overall prevalence estimate. A full 40.2% of those diagnosed with pulmonary embolism had “Clinical signs of deep-vein thrombosis” in their lower extremities, while 45.4% were tachypneic and 33.0% were tachycardic. These clinical features raise important questions regarding the adequacy of the Emergency Department evaluation; if many of these patients with syncope had symptoms suggestive of PE, why wasn’t the diagnosis made in ED? If even only the patients with clinical signs of DVT were evaluated prior to admission, those imaging studies would have had a yield for PE of 65%, and the prevalence number seen in this study would drop from 17.3% to 10.3%. Further evaluation of either patients with tachypnea or tachycardia might have been similarly high-yield, and further reduced the prevalence of PE in admitted patients.

Put another way, it is likely that many of these patients with PE had all the red flags. It has long been known that PE can present with syncope. When it does it tends (in my subjective experience) to be massive or submassive and would likely yield electrocardiographic or echocardiographic clues. Selective use of imaging based on clinical assessment would likely find these patients. So, I tend to agree with the blogger that while this study should not change practice all that much it in all likelihood will.

Saturday, January 14, 2017

Non invasive ventilation for respiratory failure following abdominal surgery

From a recent JAMA paper:

Importance It has not been established whether noninvasive ventilation (NIV) reduces the need for invasive mechanical ventilation in patients who develop hypoxemic acute respiratory failure after abdominal surgery.

Objective To evaluate whether noninvasive ventilation improves outcomes among patients developing hypoxemic acute respiratory failure after abdominal surgery.

Design, Setting, and Participants Multicenter, randomized, parallel-group clinical trial conducted between May 2013 and September 2014 in 20 French intensive care units among 293 patients who had undergone abdominal surgery and developed hypoxemic respiratory failure (partial oxygen pressure less than 60 mm Hg or oxygen saturation [Spo2] less than or equal to 90% when breathing room air or less than 80 mm Hg when breathing 15 L/min of oxygen, plus either [1] a respiratory rate above 30/min or [2] clinical signs suggestive of intense respiratory muscle work and/or labored breathing) if it occurred within 7 days after surgical procedure.

Interventions Patients were randomly assigned to receive standard oxygen therapy (up to 15 L/min to maintain Spo2 of 94% or higher) (n = 145) or NIV delivered via facial mask (inspiratory pressure support level, 5-15 cm H2O; positive end-expiratory pressure, 5-10 cm H2O; fraction of inspired oxygen titrated to maintain Spo2 greater than or equal to 94%) (n = 148).

Main Outcomes and Measures The primary outcome was tracheal reintubation for any cause within 7 days of randomization. Secondary outcomes were gas exchange, invasive ventilation–free days at day 30, health care–associated infections, and 90-day mortality.

Results Among the 293 patients (mean age, 63.4 [SD, 13.8] years; n=224 men) included in the intention-to-treat analysis, reintubation occurred in 49 of 148 (33.1%) in the NIV group and in 66 of 145 (45.5%) in the standard oxygen therapy group within+ 7 days after randomization (absolute difference, −12.4%; 95% CI, −23.5% to −1.3%; P = .03). Noninvasive ventilation was associated with significantly more invasive ventilation–free days compared with standard oxygen therapy (25.4 vs 23.2 days; absolute difference, −2.2 days; 95% CI, −0.1 to 4.6 days; P = .04), while fewer patients developed health care–associated infections (43/137 [31.4%] vs 63/128 [49.2%]; absolute difference, −17.8%; 95% CI, −30.2% to −5.4%; P = .003). At 90 days, 22 of 148 patients (14.9%) in the NIV group and 31 of 144 (21.5%) in the standard oxygen therapy group had died (absolute difference, −6.5%; 95% CI, −16.0% to 3.0%; P = .15). There were no significant differences in gas exchange.

Conclusions and Relevance Among patients with hypoxemic respiratory failure following abdominal surgery, use of NIV compared with standard oxygen therapy reduced the risk of tracheal reintubation within 7 days. These findings support use of NIV in this setting.

Friday, January 13, 2017

Noninvasive ventilation in neuromuscular respiratory failure

Surprisingly, it can be useful in neuromuscular respiratory failure of a variety of causes with the notable exception of GBS. From a recent review:

Recent findings: Myasthenic crisis represents the paradigmatic example of the neuromuscular condition that can be best treated with noninvasive ventilation. Timely use of noninvasive ventilation can substantially reduce the duration of ventilatory assistance in these patients. Noninvasive ventilation can also be very helpful after extubation in patients recovering from an acute cause of neuromuscular respiratory failure who have persistent weakness. Noninvasive ventilation can improve quality of survival in patients with advanced motor neuron disorder (such as amyotrophic lateral sclerosis) and muscular dystrophies, and can avoid intubation when these patients present to the hospital with acute respiratory failure. Attempting noninvasive ventilation is not only typically unsuccessful in patients with Guillain–Barre syndrome, but can also be dangerous in these cases.

Summary: Noninvasive ventilation can be very effective to treat acute respiratory failure caused by myasthenia gravis and to prevent reintubation in other neuromuscular patients, but should be used cautiously for other indications, particularly Guillain–Barre syndrome.

Thursday, January 12, 2017

Negative pressure pulmonary edema

Here is a review in Chest. From the review:

Negative-pressure pulmonary edema (NPPE) or postobstructive pulmonary edema is a well-described cause of acute respiratory failure that occurs after intense inspiratory effort against an obstructed airway, usually from upper airway infection, tumor, or laryngospasm. Patients with NPPE generate very negative airway pressures, which augment transvascular fluid filtration and precipitate interstitial and alveolar edema. Pulmonary edema fluid collected from most patients with NPPE has a low protein concentration, suggesting hydrostatic forces as the primary mechanism for the pathogenesis of NPPE. Supportive care should be directed at relieving the upper airway obstruction by endotracheal intubation or cricothyroidotomy, institution of lung-protective positive-pressure ventilation, and diuresis unless the patient is in shock. Resolution of the pulmonary edema is usually rapid, in part because alveolar fluid clearance mechanisms are intact.

Wednesday, January 11, 2017

Mitral valve prolapse and sudden cardiac death

Here is an interesting case report in the green journal in which a patient presenting in cardiac arrest was found to have mitral valve prolapse (with a flail leaflet) and a markedly prolonged QT. Genetic analysis revealed a novel repolarization prolonging sodium channel mutation as well as a desmoplakin gene mutation of uncertain significance. Of interest, this latter mutation is one of the ones associated with arrhythmogenic right ventricular cardiomyopathy.

During the surge of interest in MVPduring the 1980s there was a belief that it was associated with sudden cardiac death but the mechanism was unclear and the purported association has since been disputed. There has also long been suspected an association between MVP and long QT.

Tuesday, January 10, 2017

Monday, January 09, 2017

More data on the macrovascular benefit of pioglitazone: pioglitazone after stroke or TIA

In this multicenter, double-blind trial, we randomly assigned 3876 patients who had had a recent ischemic stroke or TIA to receive either pioglitazone (target dose, 45 mg daily) or placebo. Eligible patients did not have diabetes but were found to have insulin resistance on the basis of a score of more than 3.0 on the homeostasis model assessment of insulin resistance (HOMA-IR) index. The primary outcome was fatal or nonfatal stroke or myocardial infarction.

By 4.8 years, a primary outcome had occurred in 175 of 1939 patients (9.0%) in the pioglitazone group and in 228 of 1937 (11.8%) in the placebo group (hazard ratio in the pioglitazone group, 0.76; 95% confidence interval [CI], 0.62 to 0.93; P=0.007). Diabetes developed in 73 patients (3.8%) and 149 patients (7.7%), respectively (hazard ratio, 0.48; 95% CI, 0.33 to 0.69; P less than 0.001). There was no significant between-group difference in all-cause mortality (hazard ratio, 0.93; 95% CI, 0.73 to 1.17; P=0.52). Pioglitazone was associated with a greater frequency of weight gain exceeding 4.5 kg than was placebo (52.2% vs. 33.7%, P less than 0.001), edema (35.6% vs. 24.9%, P less than 0.001), and bone fracture requiring surgery or hospitalization (5.1% vs. 3.2%, P=0.003).

In this trial involving patients without diabetes who had insulin resistance along with a recent history of ischemic stroke or TIA, the risk of stroke or myocardial infarction was lower among patients who received pioglitazone than among those who received placebo. Pioglitazone was also associated with a lower risk of diabetes but with higher risks of weight gain, edema, and fracture.

Background on the possible macrovascular benefits of pioglitazone here.