1. When do you use NIPPV in status asthmaticus?
The use of NIPPV (non-invasive positive pressure ventilation) for respiratory failure has been proven to be beneficial and widely accepted in practice for multiple indications including COPD exacerbations and pulmonary edema from CHF. As it has been shown to work in these disease processes, there is naturally interest in determining whether NIPPV would be useful as a treatment modality for severe asthma exacerbations or status asthmaticus. By providing external PEEP, NIPPV is proposed to offset the intrinsic PEEP of bronchospasm, which results in alveolar recruitment, improved ventilation-perfusion mismatch, and decreased work of breathing (Lim, 2012). According to the Global Initiative for Asthma (GINA, 2015), a severe asthma exacerbation is clinically defined as a patient who talks in words only (rather than in full sentences), sits hunched forward, agitated, RR >30 breaths/min, accessory muscle usage, pulse rate >120, SpO2 <90% on room air or PEFR </= 50% of predicted. Additionally, after one hour of therapy if PEFR or FEV1 remains <60% of predicted, then the patient is considered as having a severe asthma exacerbation. These patients are the ones in whom we are interested in knowing if NIPPV has any benefit.
There have been several randomized, controlled trials that directly compare NIPPV to standard medical therapy in severe asthma. Brandao, et al. (2009), randomized 36 patients with an FEV1 <60% of predicted to receive standard therapy, bi-level NIPPV (Inspiratory positive airway pressure = 15cm H2O, Expiratory positive airway pressure = 10cm H2O) or bi-level NIPPV (IPAP= 15 cm H2O, EPAP = 5cm H2O). When they analyzed FVC, FEV1, PEF and FEV25-75% at 30 minutes after initiation of therapy, the low EPAP NIPPV group showed statistically greater improvement in FVC, FEV1, PEF and FEV25-75% when compared to the standard therapy group. Interestingly, the high EPAP group only showed significant difference in improvement in peak-expiratory flow.
Two additional studies, Soroksky, et al. (2003) and Gupta, et al. (2010), reported rates of endotracheal intubation as well as mortality, in addition to objective respiratory parameters. Soroksky, et al. randomized 30 patients with severe asthma (defined by FEV1 <60% of predicted) to receive either nasal bi-level NIPPV or placebo with a sham device providing a pressure of 1cm H2O. This study showed a greater improvement in FEV1 in the NIPPV group compared to the placebo group at both 3 and 4 hours. Additionally, they reported greater improvement from baseline in PEFR, FVC and respiratory rate at both 3 and 4 hours in the NIPPV group. No patients in either group died or were intubated. Finally, in Gupta, et al. 53 patients with severe asthma who were admitted to a pulmonary ICU were randomized to NIPPV or standard asthma therapy. This study showed a trend toward improvement in a number of patients with FEV1>50% improvement from baseline in the NIPPV group, though this trend did not reach statistical significance. Interestingly, there was a statistical advantage in both ICU length of stay and hospital length of stay in the NPPV group with the NIPPV group requiring almost half the amount of time in the ICU (10hr versus 24 hr; p=0.01) and a shorter total hospital stay (38hr versus 54 hr; p= 0.01). There were two patients in the NPPV group who went on to intubation, though the difference was not statistically significant.
There was also a 2012 Cochrane Review, which performed a meta-analysis on these and several other studies on the use of NIPPV in acute asthma (Lim, 2012). This analysis also showed no benefit for NIPPV with respect to intubation or mortality, but did show that NIPPV may improve both ICU length of stay as well as total hospital length of stay in the asthmatic patient. The meta-analysis also confirms the difference in respiratory parameters noted in Soroksky and Gupta, namely that patients in a ward setting were more likely to show improvement in pulmonary function parameters with NIPPV than their ICU counterparts indicating that asthma severity requiring admission to an ICU may predict failure of NIPPV.
With respect to pediatrics, several studies have shown a potential benefit in the setting of both moderate and severe asthma. Though multiple observational studies and case reports exist (Akingbola, 2002; Carroll, 2006; Beers, 2010; Williams, 2010) which all support the safety and potential efficacy of NIPPV in pediatrics patients. Basnet, et al. (2012) represents the largest prospective, randomized-controlled trial specifically looking at NIPPV in the setting of pediatric status asthmaticus. Though this study suffers from low numbers with only 20 patients randomized, it does show a statistical benefit in the NIPPV group with regards to clinical asthma scores, respiratory rate, and supplemental oxygen need. In this study, one patient was discontinued from NIPPV for persistent cough.
Bottom Line: NIPPV has not been shown to be superior to standard therapy with respect to mortality or need for intubation, though it does appear to potentially show a benefit with respect for hospital length of stay and other respiratory effort parameters. NIPPV has also been shown to be safe for use in pediatrics with severe asthma.
2. Do you start inhaled corticosteroids on asthma patients who are going to be discharged from the ED?
Inhaled corticosteroids (ICS) are the mainstay of therapy for long-term control of mild to severe-persistent asthma. In its 2015 report on a global strategy for asthma management, the National Heart, Lung and Blood Institute recommends initiation of ICS therapy at ED discharge for patients with an acute asthma exacerbation, citing a known reduction in mortality with daily ICS use in asthmatics (GINA, 2015; Suissa, 2000). This recommendation is specifically for long-term use of ICS, though there has also been some study into the efficacy of ICS use for a shorter period for patients discharged from the emergency department both for the treatment of acute asthma exacerbations as well as for the purpose of chronic asthma management.
Inhaled corticosteroids work by directly targeting the inflamed airways and have the benefit of minimal systemic absorption and, therefore, minimal systemic side-effects. For long term asthma care, this greatly decreases the need for chronic use of systemic corticosteroids.
As initiation of systemic corticosteroids in the setting of an acute asthma exacerbation is recommended by multiple professional societies and is considered standard of care, we won’t go into significant depth into the evidence for ICS use alone for the treatment of asthma in the emergency department and at discharge. It is, however, worthwhile to note that there are multiple studies that support the initiation of ICS in the emergency department. Some research comparing ICS directly to systemic corticosteroids, both IV and PO, has demonstrated shortened time to improvement in respiratory parameters (usually FEV1 as percent of predicted) as well as decreased time to discharge (Scarfone, 1995; Devidayal, 1999; Rodrigo, 2005; Starobin, 2008). When ICS therapy was added to corticosteroid therapy in the ED, multiple studies and a systematic review indicate that ICS therapy decreased rate of admissions, though the reviewers caution that the newest evidence trended toward no difference (Edmonds, 2012).
Specifically looking at the original question, there are two published studies that report the addition of ICS therapy to systemic steroids at ED discharge for the treatment of acute asthma exacerbations. Rowe, et al. (1999) performed a placebo-controlled, double-blind, randomized trial where they randomized 188 patients to be discharged with a prednisone burst for seven days with placebo or with inhaled budesonide for 21 days. Their primary outcome was relapse after discharge. They report a statistically significant reduction in relapse in 21 days among the budesonide group (12.8% versus 24.5%; P= 0.049) which resulted in a NNT = 9 for the prevention of relapse. The other published study, Brenner, et al. (2000), compared a prednisone burst for 5 days plus placebo or inhaled flunisolide for 24 days Their primary metric was PEFR at 3, 7, 12, 21, and 24 days. They had a fairly high lost to follow-up rate at 28% but were unable to demonstrate any difference in PEFR improvement in the flunisolide group compared to placebo (87% versus 83% at 24 days). While it was not the primary outcome, they reported similar relapse numbers in the groups.
Though these studies represent mixed data with regard to actual treatment of acute exacerbations, there is more robust data to support starting ICS therapy out of the emergency department for the prevention of future exacerbations. In Sin, et al. (2002), they followed 1295 patients who presented to an ED with an acute asthma exacerbation. They determined that if the patients used an ICS medication after discharge from this index visit, they were 45% less likely to have a relapse ED visit within two years (RR, 0.55; 95% CI, 0.44-0.69). Though it was not entirely clear from the study if the ICS medications had been started by the ED providers or by the patient’s PCP, there is also good evidence that PCP’s do not routinely start ICS medications after an ED visit. In a study by Cydulka, et al. (2005), fewer than half of patients who presented to the ED with acute asthma exacerbations were started on ICS therapy as an outpatient by their PCP.
With this in mind, both GINA (2015), and the NIH/National Asthma Education and Prevention Program recommend initiation of long-term (2-month supply) ICS medications at the time of ED discharge. Though long-term ICS use is only recommended for patients with persistent asthma, multiple studies have shown that between 67-85% of patients who present to the ED with an asthma exacerbation have symptoms consistent with persistent asthma (Self, 2009).
Bottom Line: Long-term use of ICS is the standard of care for patients with persistent asthma for the prevention of exacerbations and improvement in mortality. As there is a high rate of patients with persistent asthma among those who present to the ED with an acute asthma exacerbation, and there is inconsistent follow-up initiation of ICS therapy by PCP’s, the ED physician should strongly consider starting long-term ICS therapy on any patient with symptoms of persistent asthma prior to discharge.
3. When, if ever, do you use ketamine for induction or for treatment without intubation?
Ketamine (ketamine hydrochloride) is a dissociative anesthetic that has been used both for primary treatment of bronchospasm and as adjunctive therapy for bronchospasm in the form of an induction agent when intubating a patient with severe asthma. First described in a case report in 1971 (Betts, 1971), ketamine has long been studied in pediatric patients for direct reversal of bronchospasm. The mechanism of action, studied by Gateau, et al. (1989) in human bronchial preparations, is felt to not involve the beta receptor or prostaglandins, but this basic science research did show a direct bronchodilatory effect.
Unfortunately, since these potential effects were first described, there has been a paucity of good studies to support the clinical benefit of ketamine in the asthmatic patient. There are many case reports which describe the observed efficacy of ketamine in the refractory asthmatic patient, particularly among pediatric patients, though only a few observational studies or RCT’s. Petrillo, et al. (2001) performed a prospective, observational study looking at ten pediatric patients who had been unresponsive to standard therapy but had not yet been intubated. In this bolus and continuous infusion therapy model, the authors report an improvement in clinical asthma score as well as improvement in oxygen saturations. Allen, et al. (2005) went further by performing a double-blinded RCT comparing bolus and continuous infusion dose ketamine to placebo for pediatric patients with an acute asthma exacerbation. They did not demonstrate a benefit of ketamine over placebo when using the Pulmonary Index score as their primary outcome.
In adult patients, Howton, et al. (1996) peformed a double-blinded RCT with a bolus and continuous infusion in adult patients, similar to Allen, et al. (2005) In this study, the authors did not find any benefit of ketamine to placebo, however they did have to decrease the bolus dose from 0.2mg/kg to 0.1mg/kg during the study due to a significant number of dysphoric reactions. The dissociative effect of ketamine has also made it of interest to investigators looking at sedation to enable implementation of NPPV therapy for patients who otherwise are not tolerating it. The use of a sedative like ketamine for the purpose of pre-oxygenation (with NPPV or NRB mask) is termed Delayed Sequence Intubation or DSI (Weingart, 2015). As described in the observational prospective study by Weingart, et al. (2015), ketamine was used to sedate agitated patients with respiratory failure requiring intubation in the peri-intubation period for the purpose of better pre-oxygenation.
In contrast, Kiureghian, et al. (2015) describes a case report where ketamine was used for the sole purpose of applying NPPV in a patient with a severe asthma exacerbation. Recognizing the limited evidence to support NPPV for acute asthma exacerbations, it’s not clear how useful this method would be for primary treatment of these patients. DSI for better pre-oxygenation using ketamine may have applications for a certain subset of severe asthmatic patients requiring intubation.
Finally, utilization of ketamine as an induction agent for rapid-sequence intubation in the severely asthmatic patient has also been of interest given the described bronchodilatory properties. L’Hommedieu, et al. (1987) presented a small case-series of five pediatric patients who were intubated using ketamine as the induction agent, with succinylcholine as the paralytic. All patients who had an initial pCO2 measured (one was in respiratory arrest) were noted to be hypercarbic prior to intubation and had improvement in pCO2 values after intubation. Whether this is an effect of the ketamine or of positive pressure ventilation is not clear, as there is no control or standard therapy group to compare the ketamine group to in this tiny case-series. There do not appear to be any additional studies looking at ketamine as an induction agent in severe asthma.
Bottom Line: Ketamine has been shown in laboratory models to have a bronchodilatory effect. The use of ketamine for improved oxygenation though delayed-sequence intubation appears safe and may improve pre-intubation hypoxia. Using ketamine as an induction agent in the severe asthmatic patient has some theoretical advantage and may be considered in a patient without contraindications to ketamine administration.
4. When do you use epinephrine in status asthmaticus and when do you avoid it?
First described in the medical literature by Melland (1910), the use of systemic epinephrine for the reversal of bronchoconstriction was a mainstay of asthma treatment for many years. Epinephrine can be administered through a variety of routes including subcutaneous, inhaled and intravenous administration. It has both alpha and nonselective beta receptor activity, which is in contrast to the beta2 selective agents we more commonly use today. It has been proposed that the alpha receptor stimulation may also have a benefit in acute asthma exacerbations by decreasing bronchial wall congestion and edema (Grandordy, 1995).
Perhaps the first study of epinephrine that demonstrated a measurable improvement in respiratory parameters was by Hurtado, et al. (1934). This small observational study of 5 patients demonstrated an improvement in the vital capacity after administration of subcutaneous epinephrine. In a later study, Rees, et al. (1967) administered subcutaneous epinephrine to nine asthmatic patients and measured FVC and PaO2 both before and after epinephrine administration. This study showed an improvement in both FVC and PaO2 after epinephrine was given. When looking at both dosing of subcutaneous epinephrine as well as timing of administration in reference to peak effect, Gotz, et al. (1988) demonstrated that patients after ephinephrine administration continued to show improvement in peak expiratory flow rates (PEFR) for up to 40 minutes, no matter what the initial dose given was (0.1mg, 0.3mg or 0.5mg). There was also no difference in degree of improvement in PEFR between the different doses.
In the 1970’s, more selective beta2-agonists such as terbutaline began to come into favor with the theory that they would have fewer adverse effects than epinephrine due to their more selective profile. Schwartz, et al. (1976) directly compared subcutaneously injected terbutaline to epinephrine and found that terbutaline improved both FVC and FEV1 by almost double that of epinephrine, indicating that terbutaline may be a superior bronchodilating agent. In Smith, et al. (1977) , 49 patients were randomized to receive 1mg of terbutaline versus 0.5mg of epinephrine. There was no statistical difference in improvement of respiratory parameters between the groups, though there was more tachycardia in the terbutaline group which called into question how selective this compound was for the beta2 receptor at increased doses. In Spiteri, et al. (1987), 20 patients with severe asthma exacerbations were randomized to either 0.5mg of terbutaline or 0.5mg epinephrine subcutaneously. When looking at the outcomes of peak expiratory flow (PEF) and FEV1, there was no statistical difference in the degree of improvement between the study groups.
In addition to its nonselective adrenergic properties, the need to inject epinephrine subcutaneously was felt to be invasive and contributing to increased pain and anxiety in patients, especially pediatric patients. This led to increased interest in both aerosolized/nebulized selective beta2-agonists as well as inhaled epinephrine. Becker, et al. (1983) examined nebulized albuterol with injected epinephrine in 40 pediatrics patients with acute asthma. Though they failed to show any benefit to one therapy over the other they did conclude that the noninvasive administration of albuterol was preferred over the more invasive subcutaneous epinephrine given the similar efficacy.
At this point in asthma treatment research, it had been demonstrated that nebulized administration of beta2-agonists was superior to IV administration in terms of side-effect profile. There was increased interest in determining whether nebulized administration of epinephrine might demonstrate a similar effect Kjellman, et al. (1980) compared nebulized racemic epinephrine to albuterol in a randomized crossover trial of ten children. Specifically, they compared the percent change in FEV1 as a response to the drug. Both racemic epinephrine and albuterol showed an improvement in FEV1 from baseline, and there was no statistical difference seen. Abroug, et al. (1995) compared nebulized albuterol and nebulized epinephrine in 22 adult patients presenting to an ED with an acute asthma exacerbation. Again, this study failed to show a statistically significant difference in the degree of bronchodilation, in this case by measuring PEFR. In probably the largest randomized study comparing nebulized albuterol to epinephrine, Plint, et al. (2000) randomized 120 pediatrics patients with pulmonary index score (PIS) as their primary outcome. The groups were well-balanced from a prognostic standpoint in regards to age, prior ED visits, inhaled beta agonist or steroid use, and each group had an average PIS of 8 on arrival. Neither group showed a statistically different improvement in PIS. There was also no statistical difference in SpO2 between the groups, though there was a greater decrease in heart rate by an average of 8bpm as well as increase in respiratory rate by 2 breaths/min in the albuterol group.
In a 2006 meta-analysis by Rodrigo, et al. (2006), the authors combined data from 6 trials, which reported FEV1 or PEFR when comparing nebulized albuterol to nebulized epinephrine. This pooled analysis showed no difference between the treatment modalities, however this analysis suffered from a high degree of heterogeneity as the different studies used different doses of epinephrine. When they dichotomized the data into a low dose epinephrine (1-2mg) and a high dose epinephrine (>2mg) group, they noted that albuterol was superior to low dose epinephrine with no difference compared to high dose epinephrine.
Though there is a paucity of evidence on the efficacy of intravenous epinephrine, there are two retrospective chart reviews describing the safety/adverse effects seen when it is administered to patients considered to have severe asthma. In Smith, et al. (2003), the authors searched for any patient admitted to the ICU from two separate ED’s who was given IV epinephrine over the course of 8 years. They identified 27 patients who met their study criteria. They looked for adverse events such as arrhythmia, cardiac ischemia, cerebral ischemia, hypotension or hypertension. They observed that 9 patients developed new tachycardia and 4 had new/worsening hypertension. They noted no incidents of arrhythmia or cardiac/cerebral ischemia in any patients. This led the authors to conclude that IV epinephrine was potentially safe for use in the severe asthmatic as an adjunct after failure of beta2-agonist therapy. On a similar safety note, Cydulka, et al., found subcutaneous epinephrine in anaphylaxis-style dosing caused no adverse events in ninety-five asthmatics aged 15 to 96 (Cydulka, 1988).
The second study, Putland, et al. (2006), was much larger and included 220 patients who were initiated on an epinephrine infusion for the treatment of severe asthma. The primary endpoints of this retrospective chart review were serious adverse events which they defined as death, non-sinus tachyarrhythmia, hyper- or hypo- tension with adverse outcome requiring treatment, EKG changes or biomarker elevation consistent with ischemia, non-transient neurologic sequelae, or an extensive area of local tissue necrosis. They also reported other adverse events such as sinus tachycardia, hypertension/hypotension not requiring intervention, chest pain without objective evidence of cardiac ischemia, and local tissue ischemia. Sixty-seven patients were noted to have at least one adverse event with an adverse event rate per episode of 3.6% with 2 non-sinus tachyarrhythmias (both SVT), 4 episodes of hypotension requiring intervention and 2 episodes of objective myocardial ischemia. There was a much higher rate of other adverse events (30.5%) with the majority of these being sinus tachycardia (23 patients) or hypertension (30 patients).
The problem with determining the usefulness of these studies is their small size, the lack of a standard therapy or control group, limited reporting of demographic data (only reported in Smith 2003 which was by far the smaller of the trials), a relatively young patient population in the ages reported (median age 25 with a range of 19-58 in Smith 2003) and no reporting of association of adverse events with age or other comorbidities. Additionally, there is minimal literature looking at the sickest subset of patients with asthma.
There is no good evidence that the use of epinephrine is superior to inhaled albuterol or other selective beta-agonists. There is the theoretical advantage that epinephrine appears to be largely safe to administer through an IV or IM route which may result in better drug delivery in patients with severely restricted air movement.
Author: Curry; Editors: Bryant, Berkowitz, Swaminathan
1. When do you use non-invasive positive pressure ventilation (NPPV) in status asthmaticus?
3. When, if ever, do you use ketamine for induction, or for treatment without intubation, in status asthmaticus?
4. When do you use epinephrine in status asthmaticus and when do you avoid it?
- In which patients with syncope do you get a NCHCT?
Syncope is defined as a transient loss of consciousness and postural tone. It has a rapid onset, short duration, spontaneous recovery and is due to transient global cerebral hypoperfusion. It may have a prodromal phase. In the Emergency Room, about 3% of patients present with a chief complaint of syncope. As part of the work-up, a non-contrast Head CT-scan (NCHCT) is often ordered. The question is whether such a test is necessary and who should get it?
A 2007 prospective observational study looked at 293 adult ED patients with syncope, of which 113 (39%) underwent head CT and of those, 5 patients (5%) had an abnormal head CT (Grossman 2007). These abnormal findings included 2 subarachnoid hemorrhages, 2 intracranial hemorrhages, and 1 stroke. Each of these patients either had a focal neurologic finding, headache, or signs of trauma. Of the patients who did not have a head CT, none were found to have a new neurologic disease during hospitalization or 30-day follow-up. The results from this study suggested that limiting head CT to patients with neurologic signs or symptoms, trauma above the clavicle, or use of warfarin would potentially reduce scans by over 50%.
Several other small retrospective studies have shown a low yield for obtaining a head CT in syncope patients. In a 2005 study in Emergency Radiology, 128 patients presented to a community hospital with syncope of which 44 received a head CT scan (Giglio 2005). Only 1 CT (2%) showed acute evidence of a posterior circulation infarction. In another retrospective review of patients who got a head CT for syncope alone, none of the 117 patients had CT findings that were clinically related to the syncopal event (Goyal 2006). The authors concluded that a head CT in the absence of focal neurologic findings may not be necessary. It is important to note that the reason for obtaining head CTs in these retrospective studies is unclear. Additionally, syncope patients who did not get a head CT were not analyzed.
A more recent prospective study looked at 254 head CT patients (out of 292 with syncope) and classified them into four groups: 1) normal CT / normal neuro exam; 2) abnormal CT / abnormal neuro exam; 3) abnormal CT not related to their syncope presentation; 4) abnormal CT / normal neuro exam. The last group (abnormal head CT with normal neuro exam) which we are interested in capturing in the ED only included 2 patients (0.7%) (Al-Nsoor 2010).
Bottom Line: For patients presenting to the Emergency Department with a chief complaint of syncope, a NCHCT is of low yield and should only be considered in patients with focal neurologic deficits, complaints of headache, or signs of head trauma. This is consistent with the ACEP clinical policy for syncope, which states that no test should be routinely used in the absence of specific findings on physical exam or history (ACEP 2007).
- In which patients with syncope do you get a troponin?
Cardiovascular etiologies are at the top of the differential for dangerous causes of syncope. Identifying those at risk for adverse cardiac outcome after syncope is challenging. Cardiac markers such as troponins are often sent on patients with syncope as part of a standard work up, presumably as a general screen for cardiac etiology such as acute myocardial infarction (AMI). As with any test, its results are only relevant if interpreted correctly. To that end, the diagnostic and prognostic utility of troponin in syncope patients is examined here.
AMI is a relatively rare cause of syncope, accounting for approximately 1.4-3.5% of cases (Link 2001, Grossman 2003, Hing 2005). The diagnosis of AMI in patients without EKG changes on presentation is even less common, likely due to the significant infarct required to induce either a non-perfusing dysrrhythmia or severely impaired cardiac output, which manifests in syncope. The utility of ED troponins for diagnosis of AMI is quite limited, especially in the patient without EKG changes. One prospective cohort study evaluating troponin-I at 12 hours post-syncope for diagnosis of AMI diagnosed four AMIs, 1.5% of their 289 patients (Reed 2010). Of these four patients, all had ischemic changes on their presenting EKG.
A larger prospective cohort study of 1474 patients found a 3.1% incidence of AMI within 30 days of a syncopal event (McDermott 2009). Of these patients, 80% had abnormal EKGs on presentation (any change from baseline or any abnormality-overtly ischemic or not- if no comparison). A normal EKG showed a negative predictive value of 99%. Of these AMI patients, only 50% had positive troponins obtained in the ED. Along with an abnormal EKG, being male gender, having history of coronary artery disease (CAD) were both significantly more sensitive than a positive troponin in detecting AMI.
Although the utility of troponins in patients with syncope and normal EKGs looking for AMI is limited, a troponin may be useful in risk stratification of patients with alternate causes of syncope. Pulmonary embolism, type A dissection, and intracranial hemorrhage can all cause syncope and can cause type II ischemia (e.g. supply/demand ischemia). Additionally, an elevated troponin in the setting of syncope has been associated with worse outcomes. In one study, 50% of patients with a positive troponin (at 12 hours post-syncope) had a serious outcome (not including AMI) or all-cause death at 1 month, as opposed to only 6% of patients without the positive biomarker (Reed 2010).
A similar study design performed by the same research group used a lower cutoff for a diagnostically positive troponin-I and examined the outcomes in patients with any detectable troponin level (Reed 2012). They found the majority of syncope patients (77%) to have detectable values and 20% to have troponin levels above the new diagnostic threshold (although only 2.9% diagnosed with AMI). At both one month and one year, patients with any detectable troponin level were at higher risk of adverse outcomes and mortality. This risk increased with higher troponin values.
Another prospective study similarly showed a positive troponin-T (taken at least 4 hours post-syncope) to strongly predict adverse cardiac outcome (Hing 2005). However, a positive troponin proved to have no added value in predicting adverse cardiac outcomes over the OESIL* score (Colivicci 2003). The study also reports troponin to have a sensitivity of only 13% and a low negative predictive value.
*The OESIL score is a risk stratification score to predict recurrent syncope or adverse outcome and includes the following risk factors:
- Age >65years old
- History of cardiovascular disease (CAD, CHF, cerebrovascular or peripheral vascular disease)
- Syncope without prodrome
- Abnormal EKG
The benefit of a troponin’s prognostic ability in syncope patients has not been clearly determined. A recent study reports on the significantly improved clinical outcomes associated with using troponin-I at a lower threshold to detect positive values in patients with suspected acute coronary syndrome (Mills 2011). While this is a different subset of patients with a clearly defined disease, the results raise the question of whether the test’s prognostic value may translate into improved outcomes in syncope patients.
As a diagnostic screening test for AMI in syncope patients without chest pain or EKG changes, a single troponin is inadequate and does not appear to be helpful in risk stratification. Admitting syncope patients for serial troponins, or ‘rule-out AMI,’ is also low-yield and should be considered only in conjunction with patients’ symptoms and significant risk factors such as known CAD or CHF, older age, syncope preceded by palpitations or without prodrome. However, the value of a positive troponin is not limited to diagnosis of AMI. The value of a troponin as a predictor of adverse outcome may have utility for an inpatient team and potentially in the ED as high sensitivity troponins become more ubiquitous. Whether obtaining this prognostic data significantly improves outcomes is not clear.
- Do you get orthostatic measurements in patients with syncope and how do you use them?
Volume depletion (i.e. dehydration) and blood loss are two of the myriad reasons for patients to present with syncope in the Emergency Department. While it isn’t difficult for us to determine whether the patient with an active upper gastrointestinal bleed has significant volume loss, this determination can be more challenging in other patients (i.e. the elderly patient with a urinary tract infection). Thus, clinicians would benefit from having an easy bedside test that assesses volume status, particularly, one that improves our ability to pick up patients with moderate volume depletion or blood loss.
Orthostatic blood pressure measurements have historically been taught to be useful in determination of volume status. It is defined as either:
- A drop in systolic blood pressure (SBP) > 20 mm Hg OR
- Increase in heart rate (HR) by > 30 beats per minute (bpm)
when a patient stands from a supine position (McGee 1999). It is unclear from the available literature how these numbers were originally derived, but they are likely based on consensus rather than empirical data. Even available consensus statements differentiate the entities of symptomatic and asymptomatic orthostatic hypotension, bringing the overall utility of the test in to question. (Kaufmann 1996).
Despite the traditional teaching, orthostatic measurements have little if any proven utility. There are two major criticisms:
- Many patients without signs or symptoms of intravascular volume depletion will demonstrate orthostatic vital signs when measured
- Many patients with clear evidence of intravascular volume depletion will not exhibit orthostatic vital signs.
How prevalent are orthostatic vital sign measurements among asymptomatic patients? A number of studies investigated elderly patients living in nursing facilities. Results of these studies are inconsistent. Mader et al and Aronow et al found relatively low prevalence (6.4% and 8% respectively) of orthostatic vital signs in absence of symptoms (Mader 1987, Aronow 1988). These studies, however, were small and excluded elderly patients on medications that may cause hypotension reducing generalizability to the general population of elderly patients. More recent larger studies on unselected elderly patients showed higher rates ranging from 28 – 50% (Raiha 1995, Ooi 1997). Studies in adolescents show similarly poor numbers with approximately 44% of patients exhibiting orthostatic changes (Stewart 2002).
Witting et al attempted to define vital sign thresholds that would decrease false positives. They performed tilt-table testing in healthy volunteers after blood donation (moderate blood loss). In patients < 65 years of age, a change in pulse > 20 bpm or a change in SBP > 20 mm Hg had a sensitivity/specificity of 47%/84% (Witting 1994). This yields a (+) LR = 2.94 and a (-) LR = 0.63. Sensitivity and specificity were similar in patients > 65 (41%/86%) with similarly poor (+) LR = 2.93 and (-) LR = 0.69. McGee et al performed a systematic review in 1999 showing similarly dismal sensitivity for moderate blood or fluid loss (McGee 1999)
|Blood Loss – Pulse Change (> 30 bpm)||22%||NA|
|Blood Loss – SBP Change (> 20 mm Hg)||7-27%||NA|
|Fluid Loss – Pulse Change (> 30 bpm)||43%||75%|
|Fluid Loss – SBP Change (> 20 mm Hg)||29%||81%|
Mendu et al performed a retrospective study that stands as one of the few studies supporting the use of orthostatic blood pressure management in patients with syncope (Mendu 2009). The researchers found that in 18% of patients, orthostatics affected the final diagnosis and affected management in 25% of patients. However, the study is deeply flawed. The utility of the measurements was determined by the clinician with no gold standard for diagnosis with which to compare. Additionally, 55% of patients in whom orthostatics were measured were found to have abnormal results but far less of these findings were thought to be relevant. Finally, the average age in this study was near 80 years of age, the exact population in which prior studies (previously discussed) have shown poor sensitivity and specificity of these measurements (Raiha 1995, Ooi 1997).
Based on the available literature, orthostatic vital signs do not appear to be either sensitive for screening patients for moderate blood or fluid loss or specific.
Bottom Line: Many asymptomatic patients will have positive orthostatic vital signs and many patients with moderate volume loss won’t have orthostatic vital signs. This makes checking orthostatic vital signs of questionable utility. More important is to see what the patient’s symptoms are. If the patient feels lightheaded or dizzy when they go from lying supine to sitting or from sitting to standing, they are orthostatic and this should be addressed.
- Do you manage patients with near-syncope differently than those with syncope?
Pre-syncope is a chief complaint commonly evaluated in the Emergency Department (ED). Defined as the sense of impending loss of consciousness, its symptoms can include lightheadedness, weakness, visual disturbances, “feeling faint”, and other nonspecific complaints. While there have been several attempts to develop and derive clinical prediction tools for syncope, most have been unsuccessful due to poor sensitivity and specificity and large performance variability (Constantino 2014, Birnbaum 2008, Serrano 2010). As one can imagine, if validation of prediction rules for the objective finding of syncope is fraught with difficulty, prediction rules for the more subjective and vague symptoms of pre-syncope would be an arduous task. As such, there is a lack of guidance when it comes to management and disposition decisions for patients who present to the ED with pre-syncope.
Though classically pre-syncope was thought to be benign with many of these patients being discharged from the ED, this may not be the case. In a study of approximately 200 patients presenting to the ED with nonspecific complaints (including weakness, dizziness, and feeling unwell) and Emergency Severity Index (ESI) scores of 2 or 3 with normal vital signs, 59% had a serious condition diagnosed within 30 days, and 30-day mortality was 6% (Nemec 2010). The median age of the study’s cohort was 82 years, and most had co-morbidities. While this study did not specifically assess patients with pre-syncope, given the overlap of the included symptoms with the symptoms seen in pre-syncope, it suggests that pre-syncope may similarly be a harbinger of serious disease.
Early syncope studies often excluded pre-syncope since its definition is poorly defined. However, recent literature corroborates the potential severity of pre-syncope. Some experts purport that the pathophysiologic mechanism for pre-syncope is the same as that for syncope except that the global cerebral hypoperfusion is not significant enough to cause complete loss of consciousness (Quinn 2014). A prospective observational pilot study of 244 patients with pre-syncope and 293 patients with syncope found similar ED hospitalization and 30-day adverse outcome rates in the two groups- 23% and 20% respectively (Grossman 2012). One of the reasons that the rates were so high may have been the broad and inclusive definition of adverse outcome (which included, amongst other conditions, cortical stroke, carotid stenosis and endarterectomy, and alterations in antidysrhythmics medications).
A larger prospective cohort study in 2014 found a significant number of adverse outcomes in pre-syncope patients. Of 881 adult patients with pre-syncope (which constituted 0.5% of total ED visits), 5.1% had serious outcomes at 30-day follow-up (Thiruganasambandamoorthy 2014). Furthermore, physicians were not accurate in predicting which patients were high risk for serious outcomes after their ED visit, with an area under the receiver operating characteristic (ROC) curve of 0.58-slightly better than a coin flip.
Should we be managing patients with pre-syncope similarly to those with syncope? Despite the paucity of literature on outcomes for ED patients presenting with pre-syncope, it appears as though the potential severity of pre-syncope has been under-appreciated. Once thought to be low-risk, recent literature challenges this dogma and suggests that a significant proportion of patients with pre-syncope suffer adverse outcomes similar to those who present with syncope. Intuitively it makes sense that true pre-syncope, syncope, and cardiac arrest exist on the same spectrum, differentiated by severity and duration of hypoperfusion, and thus should be risk stratified and managed similarly. However, to date no evidence exists on whether managing pre-syncope patients the same as syncope patients improves outcomes. As such, future studies are needed to further explore which patients with pre-syncope are at higher risk for adverse outcomes, with the ultimate goal to derive and validate a clinical decision rule for this patient population.
Previously thought to be a benign diagnosis, recent literature suggests that, like syncope, a non-insignificant proportion of patients with pre-syncope suffer serious adverse outcomes. Further studies are needed to determine which patients with pre-syncope are at higher risk for adverse outcomes, as we currently do not have clinical decision rules to guide our management for this patient population.
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Answers Created By:
2. In which patients presenting with syncope do you get a troponin?
3. Do you get orthostatic vital sign measurements in patients presenting with syncope? How do you use them?
4. Do you manage patients presenting with near-syncope differently than those presenting with syncope?
1. What imaging do you use for patients with possible acute, traumatic spinal cord injury?
Patients who can be cleared using the Nexus or Canadian C-spine criteria should be cleared clinically. However, those with moderate to high risk of a cervical spine (C-spine) injury should have cross sectional imaging, based on substantial amounts of data. The Eastern Association for the Surgery of Trauma (EAST) referenced 52 articles to construct guidelines recommending against plain radiographs in the assessment of potential C-spine injuries (Como, 2009). Although the C-spine is actually only injured in approximately 3% of all major trauma patients, (Crim, 2001) these tend to be some of the most disabling injuries. There is less data regarding the type of imaging preferred for patients with possible thoracic and lumbar spine injuries.
In patients in whom you cannot clear their C-spine clinically and you suspect an acute, traumatic spinal cord injury, computerized tomography (CT) scanning is the most appropriate initial imaging. There is a growing body of literature stating that plain films miss many clinically significant injuries, and have little to no role in evaluating spinal fractures, particularly those of the C-spine.
The argument against this is that some patients may actually be appropriate for plain film imaging of the C-spine. These are patients who are deemed low risk mechanism, younger, and in whom good views can be obtained. There will still be some fractures that are missed, but these have a low chance of being clinically significant, and in a patient with low pre-test probability, this may be appropriate utilization of plain film imaging. The most compelling argument for this comes from the original NEXUS study. Of 34,069 patients with blunt trauma, 1,496 had C-spine injuries. Plain films missed 564 injuries in 320 patients. However, for 436 of these injuries, 0.80% of all patients, the plain films were interpreted as abnormal (although non diagnostic) or abnormal. Only 23 (0.07%) of all patients in the studies had injuries that were not seen on plain films that were also read as negative. Three of these patients had unstable c-spine injuries (Mower, 2001). In a retrospective review of a trauma database of 3,018 patients, 116 (9.5%) had a C-spine fracture. The injury was only seen in 75 of these patients on plain film. In the remaining 41 patients (3.2%), the injury was detected on CT scan, and in all cases these injuries required treatment. It is important to recognize that the mean Glasgow coma score (GCS) of this patient population was 13, thus, they were likely a high acuity patient population overall. These authors concluded that there was no role for plain imaging in patients in whom a C-spine injury is suspected in the Emergency Department population (Griffen, 2003). Most recently, Mathen, et al. performed a prospective cohort study of 667 patients who required C-spine imaging. They found that plain radiography missed 15 of 27 (55.5%) clinically significant c-spine injuries (Mathen, 2007).
In a cost effectiveness analysis, CT was found to be the preferred modality for imaging in moderate to high risk patients, given that missed C spine fractures and resultant paralysis may be devastating to both the patient and society (Blackmore, 1999).
Unlike C-spine fractures, we have no clinical decision rules to help guide our care of patients with potential thoracolumbar fractures. There is considerably less data on thoracolumbar injuries. According to a literature review published in the Journal of the American College of Radiology, which looked at studies on TL spine imaging comprising several thousand patients, those who should be evaluated for thoracic or lumbar spine injuries are those with high force mechanism and any of the following findings: back pain or midline tenderness, local signs of thoracolumbar injury, abnormal neurologic signs, C-spine fracture, GCS < 15, major distracting injury, or drug or alcohol intoxication (Daffner, 2007).
There is evidence to suggest that many injuries may be missed by plain films of the thoracolumbar regions. One study of seventy intubated trauma patients found that thin slice CT discovered 100% of unstable fractures in comparison with 56-80% (depending on spinal level) seen by conventional radiographs (Herzog, 2004). A prospective evaluation of 1.915 trauma patients presenting to a Level I trauma center compared the sensitivity of CT versus plain film in the detection of the 78 thoracic or lumbar spine fractures sustained by the group. CT sensitivity was 97% and 95% for thoracic and lumbar injuries, respectively. For plain films those numbers were 62% and 82% (Sheridan, 2003). Yet another study in high acuity trauma patients found the sensitivity of CT to be 97% and that for plain films to be an abysmal 33.3% (Wintermark, 2003). In a retrospective review of 3,537 patients, the only fractures missed by CT scan were a cervical compression fracture identified on MRI, and a thoracic compression fracture identified by plain films. This study recommended that plain films of the spine are unnecessary in the evaluation of blunt trauma patients. Furthermore, after a panel reviewed all literature on the topic, the American College of Radiology Appropriateness Criteria recommended that patients with potential thoracic or lumbar spine injury undergo CT scan, as opposed to plain films (Daffner, 2007). The ACR grades on a scale of 1-9, with 1-3 being usually not appropriate, 4-6 may be appropriate, and 7-9 usually appropriate. Their level of recommendation in this indication is a 9.
Due to the data regarding imaging, most patients should undergo CT imaging for possible spinal trauma. Only the lowest risk patients who have adequate plain films should be cleared without CT imaging.
2. How do you treat neurogenic shock?
Neurogenic shock is a form of distributive shock unique to patients with spinal cord injuries. Fewer than 20% of patients with a cervical cord injury have the classic diagnosis of neurogenic shock upon arrival to the emergency department, and it is a relatively uncommon form of shock overall (Guly, 2008). Patients with injuries at T4 or higher are most likely to be affected by neurogenic shock (Wing, 2008). It is caused by the loss of sympathetic tone to the nervous system, ultimately leading to an unopposed vagal tone (Stein, 2012). Many times the terms “spinal shock” and “neurogenic shock” are used interchangeably, although they are two separate entities. Spinal shock consists of the loss of sensation and motor function immediately following a spinal cord injury (Nacimiento, 1999). During this period of spinal shock, reflexes are depressed or absent distal to the site of the injury. Spinal shock may last for several hours to several weeks post injury (Nacimiento, 1999).
Symptoms of neurogenic shock consist of bradycardia and hypotension (Grigorean, 2009). Bradycardia is typically not present in other forms of shock, and may provide a clue to clinicians that a patient has sustained a spinal cord injury. However, emergency physicians should recognize that hemorrhagic shock needs to be first ruled out, even in patients with bradycardia, many patients with hemorrhagic shock are not tachycardic (Stein, 2012). Cardiac dysfunction is another feature of neurogenic shock, and patients may present with dysrhythmias following injury to the spinal cord (Grigorean, 2009).
The American Spinal Injury Association (ASIA) has classified injuries based on motor and sensory findings at the time of injury. ASIA A and B injuries are the worst; with A being a complete motor and sensory loss with no preserved function in the sacral segments S4-S5. ASIA B includes patients who have sacral sparing, meaning that they have function of S4 and S5 (Marino, 2003). Neurogenic shock is rarely encountered in the emergency department, however, it is important to recognize that almost 100% of patients who sustain complete motor cervical ASIA A or ASIA B injuries develop bradycardia. Thirty five percent of these patients ultimately require vasopressors, so management of neurogenic shock is imperative for emergency physicians (McKinley, 2006). There is no conclusive data regarding the optimal time to start vasopressors, however, it is important to maintain appropriate hemodynamic goals in patients with spinal cord injuries.
Hemodynamic goals in patients with spinal cord injuries are unique. A systolic blood pressure <90 mmHg must be corrected immediately (Muzevich, 2009). The American Association of Neurological Surgeons and the Congress of Neurological Surgeons Guidelines for the Acute Management of Spinal Cord Injuries both recommend a MAP at 85 to 90 mm Hg for the first seven days following a spinal cord injury based on observational descriptions of the hemodynamics in spinal cord injured patients (Levi, 1993; Licina, 2005).
Patients who are suspected of being in neurogenic shock should receive adequate fluid resuscitation prior to initiating vasopressors (Wing, 2008). However, there are no current recommendations regarding the first line vasopressor for neurogenic shock (Stein, 2012). Depending on a patient’s hemodynamics, this vasopressor will likely be norepinephrine, phenylephrine, or dopamine.
Norepinephrine is an excellent first line vasopressor in neurogenic shock due to its alpha and some beta activity, thus leading to its ability to improve blood pressure and heart rate (Stein, 2012). Phenylephrine is another common choice because it is easy to titrate and can be given through a peripheral line. A disadvantage of phenylephrine is the fact that it can lead to reflex bradycardia due to its lack of beta agonism. This drug may be most appropriate in patients who are not bradycardic (Wing, 2008). Dopamine is another option, however, it may lead to diuresis and ultimately worsened hypovolemia (Stein, 2012). It does have beta agonism, and in bradycardic patients may be favored over phenylephrine (Muzevich, 2009). Dopamine is unlikely to be tolerated in patients who are experiencing dysrhythmias.
3. What is your management and disposition for elderly patients with vertebral compression fractures?
Vertebral compression fractures of the thoracic and lumbar vertebrae are extremely common in the elderly population, with an annual incidence of 1.5 million vertebral compression fractures per year (Barr, 2000). They are most commonly seen in patients with osteoporosis, although may be seen in younger patients, particularly those with malignancy. The majority of patients are treated non-surgically, usually with bed rest and hyperextension bracing (Gardner, 2006). Pain is typically the presenting symptom, and neurologic deficits are rare unless there is retropulsion of bone into the vertebral canal. This presentation is rare in compression fractures, but it does constitute a surgical emergency (Kavanagh, 2013).
Although some patients may experience mild or minor symptoms related to a vertebral compression fractures, many patients will have a significant degree of pain and decreased quality of life associated with their fracture (Adachi, 2002). At a minimum, patients with very mild symptoms and a normal neurologic exam may be discharged home with adequate pain control and spine surgery follow up established.
Therapy should be tailored toward avoiding a prolonged period of bed rest as well as adequate pain control (Wong, 2013). Prolonged immobilization may lead to poor pulmonary toilet, venous thromboembolism, and deconditioning, especially in elderly patients. Non-steroidal anti-inflammatory drugs (NSAIDS) are first line therapy since they are non-sedating, but may be poorly tolerated in certain groups of patients such as the elderly or those with underlying peptic ulcer disease (Wong, 2013). Opiates and muscle relaxers may be necessary for pain control, but should be used with caution in the geriatric population, especially those at risk of falls.
Although admission of elderly patients with vertebral compression fractures may not result in surgical management, it may provide other avenues of therapy that are unavailable or difficult to arrange in the ED setting. One of these therapies includes physical therapy, which may help patients regain early mobility if introduced appropriately. Physical therapy is also helpful in training patients to strengthen other extra-axial muscles, particularly the spine extensors (Wong, 2013). Several trials have demonstrated effectiveness of physical therapy in patients with vertebral compression fractures. Malmros et al evaluated a 10-week physical therapy program in a placebo-controlled, randomized, single-blinded study that demonstrated improved quality of life and reduction in pain and analgesic use (Malmros, 1998). Papioannou, et al. conducted a randomized controlled trial consisting of a 6 month home exercise program and found that patients in the physical therapy arm had significant improvement of quality of life scores and improved balance at one year (Papaioannou, 2003).
The decision of when to use thoracolumbosacral orthosis (TLSO) brace in a patient with a vertebral compression fracture is somewhat controversial. Pfeifer, et al. demonstrated in a randomized trial that the use of a brace increased trunk muscle strength and was associated with an improved quality of life, decreased pain, and improved daily functioning in patients with compression fractures (Pfeifer, 2004). However, an electromyelography study demonstrated increased muscle spasming in patients with brace placement (Lantz, 1986). Furthermore, braces may contribute to skin breakdown, especially in geriatric patients. If a TLSO brace is given to patients, it should be done in consultation with a spine surgeon.
Surgical management options for vertebral compression fractures include kyphoplasty and vertebroplasty. Both procedures are minimally invasive, but are traditionally only performed if patients are in pain several weeks following diagnosis of a compression fracture (Wong, 2013).
Patients who are discharged from the ED with compression fractures need to be able to ambulate and perform activities of daily living prior to discharge. If pain control limits these activities, they will likely require admission for pain control, physical therapy, and potentially rehabilitation.
4. How do you clear a C-spine after a negative CT in a trauma patient who is awake, neuro intact, wearing a collar?
According to EAST guidelines, there are multiple appropriate options in patients who are awake, neurologically intact, and still have midline tenderness after a negative CT (Como, 2009). Although CT scans will pick up the majority of injuries, it is well documented that they specifically may miss ligamentous injuries, subluxations, and dislocations (Woodring, 1992).
The first option is to obtain an MRI within 72 hours post injury. Very little data exists in the literature regarding this option. Schuster, et al. evaluated prospectively collected registry data for 2854 blunt trauma patients, 93 of whom had a normal neurologic exam at admission, a negative CT result, and persistent C-spine pain. These patients all had an MRI. In all 93 of these patients, the MRI was negative for clinically significant injury. However, the argument could also be made that since no clinically significant injury was detected by MRI in this case, that there was no need for any further imaging (Schuster, 2005).
The second option is to continue the C-spine immobilization until there is no midline tenderness and the patient has been followed up as an outpatient. This is not ideal in centers where there is no trauma team to assist in outpatient management of these patients. Furthermore, the collar itself poses a risk of skin breakdown and decubitus ulcers when worn for a prolonged period of time. This option may work best for patients who can rapidly be seen in a trauma clinic.
The third option is to obtain flexion-extension films in patients with a negative CT of the C-spine. Although studies have evaluated the utility of flexion-extension films in patients with negative plain films of the C spine, no study has completely evaluated flexion-extension films following a negative CT of the C-spine. Insko et al reviewed 106 patients with negative plain films or negative CT imaging in areas that were not visualized by plain films. This study demonstrated a false negative rate of zero in diagnosing C spine fractures when flexion extension films were performed in patients who were persistently tender (Insko, 2002).
Ultimately, more information is needed to determine the best course of action to take in a patient with persistent pain following negative CT imaging of the C-spine (Como, 2009). However, at this time, there are three potential options in ruling out a C-spine injury in these patients. The decision may largely depend on local practice patterns, clinical suspicion for injury, as well as a patient’s ability to follow up.