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Wednesday, May 2, 2018

Drownings among Older Swimmers on the Rise

BY TOM GRIFFITHS, EdD, RACHEL GRIFFITHS, & JUSTIN SEMPSROTT, MD

Odds are, when you picture a drowning victim, you visualize a child or other inexperienced swimmer. But the remarkable fact is that drownings have decreased in all age groups except for one—those aged 45 to 84.

That figure from the National Center of Health Statistics is startling, especially because the rate rose by a whopping 9.7 percent. (NCHS Data Brief No. 149, April 2014; http://bit.ly/2qIngWR.) Of course, some of these drowning deaths were precipitated by major medical events while others occurred in bathtubs and in the open water. But one study found that 17 percent of drownings in Australia between July 1, 2002, and June 30, 2012, were adults over 65. (BMJ Open 2017;7[12]:e019407; http://bit.ly/2qGCbRl.) And a case series about triathlon competitors from 1985 to 2016 concluded that deaths and cardiac arrests during the events are not rare, most occurring during the swimming portion and among men primarily middle-aged and older. (Ann Intern Med 2017;167[8]:529.)

Special Report elderly.jpg
 Photo by Juanmonino/iStockphoto.com

It's no surprise that the older population is growing significantly, in large part because of increasing life spans and aging of the baby boomers. (Centers for Disease Control and Prevention and the Merck Company Foundation. The State of Aging and Health in America 2007; http://bit.ly/2HcEnaf.) In fact, the population over 65 is expected to double, and will account for approximately 20 percent of the population by 2030 in the United States; that's 71 million Americans.

Of course, most older adults aren't participating in triathalons, but swimming often tops the list as exercise for them. It is also a safe choice because swimming does not place undue stress on the joints. By the numbers alone, this equates to more individuals recreating and exercising in the water.

Older adults, however, are more likely to have medical conditions and chronic diseases and are more likely to be on medications. The CDC reported, for example, that 63 percent of men and 64 percent of women ages 65-74 and 72 percent of men and 64 percent of women ages 75 and older have high blood pressure or take antihypertensive medicine. ("Older Persons' Health,"CDC, May 3, 2017; http://bit.ly/2qJZ463.)

Many older lap swimmers attempting to increase their longevity and quality of life choose to swim laps in the safe confines of a swimming pool with certified and qualified lifeguards on duty, meaning that older swimmers and lifeguards must maintain a high degree of vigilance.

Take the case of Penn State Professor Michael Rothkopf, who was in his mid-70s. He had a ritual of swimming a mile for time every morning, but he died in 2008 while swimming at McCoy Natatorium in State College, PA. Less than two years later, State College School Board President Rick Madore died of an apparent heart attack while swimming laps at the State College YMCA. He was 51. A third case occurred in 2011 when Pierre Henri Robert Lallement, 48, died of natural causes while swimming laps in the McCoy Natatorium at Penn State. Lap swimmer Gerard Brault suffered a major cardiac event in the Welch swimming pool in State College in 2013, but this time, the lifeguard on duty was able to respond immediately and successfully resuscitate him. Perhaps not coincidentally, Lifeguard Luc Lallement, the son of the third victim who died, was the first lifeguard to respond.

It is important to emphasize that none of the four lap swimmers suffered a drowning event but each experienced a major medical malady in the swimming pool. The lifeguards in each case responded so quickly that water did not enter the lungs, and the men did not die from drowning. The rapid recognition and response by lifeguards on duty is an important aspect in decreasing swimming deaths. Water safety experts have seen an alarming increase in actual drownings of older lap swimmers because lifeguards were too slow, leaving victims submerged for minutes before responding.

Emergency physicians can help by recommending to any older lap swimmers they see to consult with their physician to be certain that exercise, particularly swimming, is advised considering their medical history. Also recommend that they swim with a buddy who is aware of their medical background, that they know when to say when so they don't place themselves in harm's way by swimming too long or too hard, and that they do not attempt hypoxic training or extreme breath-holding, which can activate underlying medical conditions. Older swimmers should also consider informing the lifeguards on duty of their condition and ask him to keep an eye out.

Lifeguards have to be alert when protecting older lap swimmers. They should walk along with the lap swimmers, which will keep them more alert and closer to the victim for rapid response. A lap swimmer should be checked whenever he stops swimming, and the lifeguard should respond immediately especially when the swimmer is face down on the water's surface or on the bottom of the pool. Remember, "When in doubt, pull them out," and "More than 10 (seconds), get them!" Lifeguards must also be rescue-ready with their rescue and emergency resuscitation equipment at hand, knowing and practicing their Emergency Action Plan. Swimmers do die in the water.

Dr. Griffiths is the president and founder of the Aquatic Safety Research Group, and has spent 38 years teaching, coaching, and managing aquatics at three major universities, producing videos, textbooks, articles, and presentations about aquatic safety. He and Ms. Griffiths are authors of the third edition of The Complete Swimming Pool Reference. Follow them on Twitter at @AquaticSafetyGr. Ms. Griffiths is the communication director of the Aquatic Safety Research Group and the president of Note and Float Life Jacket Fund, which donates life jackets to aquatic facilities. She recently received a Power 10 Advocate award from Aquatics International for her work with NFLJF. Dr. Sempsrott is an emergency physician who started out as a beach lifeguard in 1996, and was a founder of the nonprofit Lifeguards Without Borders, now serving as its executive director. He also serves as the medical director for the International Surf Lifesaving Association, Starfish Aquatics Institute, and Innovative Attraction Management Starguard Elite. He is a founding member of the International Drowning Research Alliance and a frequent author and lecturer on drowning prevention, rescue, and treatment. Follow him on Twitter at @LifeguardsWB. (Clockwise from top left.)


Read the original article, "'Drowning' in a Sea of Misinformation" at http://bit.ly/EMN-Drowning.


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Wednesday, May 2, 2018

The Myth of Dry Drowning Remains at Large

BY ANDREW SCHMIDT, DO, MPH; JUSTIN SEMPSROTT, MD; & SETH COLLINGS HAWKINS, MD

Frankie Delgado was on vacation with his family a week before he died. The 4-year-old had been playing in shallow water when a wave crashed over him, and his parents reported that he seemed fine at the time. The next night, however, he developed diarrhea and started to vomit, and he later complained of shoulder pain. Then, a week later, he stopped breathing. (CNN. June 9, 2017; http://cnn.it/2rECrOV.)

Initial reports blamed his death on "dry drowning," which started a media frenzy that sent panicked parents to EDs to have their children checked after inhaling water. As we suspected, Frankie Deglado did not die from drowning, dry or otherwise, but by that time, stopping the misinformation was like trying to dam a tidal wave.

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Photo by Daviles/iStockphoto.com

We wrote about this case in EMN last year, trying to shed light on the common use of outdated and confusing drowning-related terminology. (2017;39[8]:1; http://bit.ly/EMN-Drowning.) Most news outlets called what happened to Frankie "dry drowning," but we also saw reports using the terms "secondary drowning" and "near-drowning." As we said then, and have said many times since, these are not accepted medical terms.

Even today, searching online for Frankie Delgado's name yields myriad news reports of his "dry drowning," followed by articles about how to prevent it. As it turns out, and as we expected, the results of the autopsy revealed Frankie's cause of death was recurrent myocarditis. Few mainstream media outlets reported that, which stresses how important it is to continue the discussion and understand ED treatment and disposition for drowning. Some downplay the need for precise terminology, but words matter when describing something like drowning. Without a universal understanding of current terminology and nomenclature, we cannot work efficiently toward decreasing the global burden of drowning morbidity and mortality.

As expected with a disease like drowning where randomized controlled trials aren't ethically possible, the evidence surrounding much of these treatments is scarce and based on expert opinion.

​Systemic Hypoxia
Drowning is the process of experiencing respiratory impairment from submersion or immersion in liquid. The primary cause of morbidity and mortality, and the focus of treatment, is systemic hypoxia. No matter the factors involved in the drowning event or the current condition of the presenting patient, the primary goal in the provider's mind must be optimizing systemic oxygenation. As with most medical and traumatic derangements, this all starts with a rapid evaluation of the airway and breathing status of the patient.

One physiologic process that may be apparent and that should immediately alert the physician to an airway compromise is fluid coming from the patient's mouth. This can have numerous causes, including emesis from reflexive swallowing while underwater or air gulping and noncardiogenic pulmonary edema from direct airway and alveolar injury from water aspiration and surfactant disruption. Whatever the cause, this is common in severe drowning patients and can greatly complicate the patient's ability to breathe and the physician's ability to establish a definitive airway. During the initial resuscitation, this is not a process that will quickly cease, so spending time attempting to clear the airway without attempting oxygenation could be detrimental to the critical or crashing patient.

Recommended oxygenation strategies are:
Awake and alert, protecting airway, no fluid material from airway:
  - Oxygenation via nasal cannula or nonrebreather mask to maintain SaO2 > 95%

Awake and alert, respiratory distress, minimal fluid material from airway:
  - Oxygenation via nasal cannula or nonrebreather mask to maintain SaO2 > 95%
  - Noninvasive positive pressure ventilation (NIPPV) if the patient is a candidate based on mentation
  - Proceed to intubation if the patient does not improve on NIPPV within 10 minutes.
  - Endotracheal intubation (ETI) for refractory hypoxemia or worsening respiratory distress

Altered mental status, large amount of fluid material from airway, or respiratory failure:
  - Rapid setup for endotracheal intubation
  - If necessary, bag-valve-mask ventilation attempted though fluid material to pre-oxygenate

The disposition of drowning patients, primarily those who appear clinically well, is a poorly studied subject that tends to cause a great deal of anxiety among providers. Only a few small, retrospective studies provide the basis for disposition recommendations:

- Discharge home from the ED:
  - Normal mentation and oxygenation and no continued dyspnea or tachycardia when off supplemental oxygen for more than four to eight hours
  - Adequate social support or family structure to observe for worsening symptoms

- Admit to inpatient floor bed
  - Continued dyspnea, tachycardia, altered mental status, hypothermia, or hypoxia that is improving or stabilized with ED treatment and mild-moderate in nature
  - Not requiring NIPPV, ETI, or vasoactive medication

- Admit to Intensive Care Unit:
  - Continued dyspnea, tachycardia, altered mental status, hypothermia, or hypoxemia refractory to ED treatment or severe in nature
  - NIPPV, ETI, or vasoactive medication

Drowning continues to be a leading cause of injury death worldwide, especially among children. Hypoxemia and subsequent cerebral hypoxia are the primary causes of morbidity and mortality, and their immediate reversal should be the goal of any initial intervention. Following these recommendations will give your next patient the best chance of walking out of the hospital with minimal morbidity.

Dr. Schmidt, top, is an assistant professor with the University of Florida-Jacksonville Department of Emergency Medicine, where he also serves as deputy medical director for the TraumaOne Flight Program. His specific areas of research and teaching are drowning resuscitation and prehospital medicine. Other positions held include the medical director for Jacksonville Beach Ocean Rescue and a director of Lifeguards Without Borders. Follow him on Twitter @904Schmidt. Dr. Sempsrott, center, is an emergency physician who started out as a beach lifeguard in 1996, and was a founder of the nonprofit Lifeguards Without Borders, now serving as its executive director. He also serves as the medical director for the International Surf Lifesaving Association, Starfish Aquatics Institute, and Innovative Attraction Management Starguard Elite. He is a founding member of the International Drowning Research Alliance and a frequent author and lecturer on drowning prevention, rescue, and treatment. Follow him on Twitter at @LifeguardsWB. Dr. Hawkins, bottom, is an emergency physician in active clinical practice, an assistant professor at Wake Forest University School of Medicine, and a lifelong competitive swimmer. He is the medical director of Starfish Aquatics Institute, Landmark Learning, the Burke County EMS Special Operations Team, and the North Carolina State Parks system. He is an author of numerous medical textbook chapters about drowning and the Wilderness Medical Society's evidence-based drowning practice guidelines. He serves as a board member of Lifeguards Without Borders, and is a certified wilderness lifeguard instructor. Follow him on Twitter @hawkvox.

 

Read the original article, "'Drowning' in a Sea of Misinformation" at http://bit.ly/EMN-Drowning.


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Wednesday, May 2, 2018

Do All Drowning Victims Drown?

BY PADDY J. MORGAN, MD, & MICHAEL J. TIPTON, PHD

It may be that many immersion deaths attributed to drowning are actually caused by cardiac problems, casting a different light on how to diagnose and treat these conditions. Deaths from immersion represent the third leading cause of unintentional injury death worldwide, according to the World Health Organization (http://bit.ly/2qHUdm2), and drowning is a common but not the only cause of these deaths.

Instead, cardiac problems are the likely cause of some immersion deaths, but these are underestimated because the incapacitation caused by cardiac conditions often results in agonal gasping and the aspiration of water, which leads to a drowning diagnosis. That is complicated further because the fatal cardiac arrhythmias experienced in immersion are not detectable post-mortem.

Special Report 3.JPG
Triathlete swimmers in Chicago's Monroe Harbor, Lake Michigan. Photo by Kelly Martin.

The incidence of cardiac arrhythmias in the initial minute of immersion is one to three percent, but that number rises to 81 percent if the face is immersed and maximum breath-holding is involved. (J Appl Physiol 2006;100[6]:2057.) An accidental immersion is, in fact, likely to involve face immersion and breath-holding, but these also occur even in some non-accidental scenarios, like the somewhat chaotic mass start of a triathlon. A case series of U.S. Triathlon participant deaths found that 67 percent occurred in the swim phase, and these were thought to be cardiac-related. (USA Triathlon Fatality Incidents Study. 2012. https://go.teamusa.org/2EXzMqr.)

Complex interplay between the two arms of the autonomic nervous system occurs in these situations, with multiple combinations of variables (relative magnitudes of sympathetic and parasympathetic stimuli, constant or pulsatile in nature) being applied to myocardial tissue that has a variable response according to an individual's genetics, medications that induce changes to repolarization, and metabolic status at a cellular level (acidosis, hypoxia, hypercapnia). The result may be a fatal arrhythmia or a simple ectopic beat. This has been termed autonomic conflict (AC), defined as the strong and coincidental activation of the two limbs of the autonomic nervous system via the cold shock response or the exercise (sympathetic stimuli) and the diving response (parasympathetic stimuli). (J Physiol 2012;590[14]:3219.)

The cold shock response occurs when cold thermoreceptors are rapidly stimulated during immersion, and that triggers profound sympathetic activation. (Clin Sci [Lond] 1989;77[6]:581.) It is characterized by a rapid and large respiratory gasp, uncontrollable hyperventilation, peripheral vasoconstriction, hypertension, and tachycardia. The parasympathetic component is activated by stimulation of receptors in the distribution of the ophthalmic and maxillary divisions of the trigeminal nerve during submersion (head under) or wave splash resulting in the dive reflex.

This features a profound sinus bradycardia, breath-hold, and peripheral vasoconstriction. (J Physiol 2012;590[14]:3219.) During the breath-hold, stretch receptors of the lungs will contribute an additional neural component to the bradycardia. (Acta Physiol Scand 1968;73[1]:139.) The bradycardia will also have mechanical contributions from the cephalic redistribution of blood volume due to the hydrostatic pressure of water on the body and intrathoracic pressure changes at the break of breath-hold. (Pflugers Arch 1978;374[2]:115.)

The anxiety and stress associated with an unexpected immersion or the mass start or congested turns of a triathlon are, along with anger, profound sympathetic stimulants. Equally, the enforced, potentially prolonged breath-hold associated with unexpected immersions or the submersion of the head and water entering the nasopharynx during the congested periods of a triathlon swim will produce profound parasympathetic stimulation. These conditions do not occur in training, making the problems more profound in competition because the swimmers have never experienced them before. (Br J Sports Med 2014;48[15]:1134.)

Strong associations exist between fatal cardiac arrhythmias and the stress of a "drowning" event. The inherited long QT syndrome (LQTS) type 1 has been described as a trigger for torsades de pointes associated with swimming, and sudden death has been described in LQTS type 2 when a sudden surge of sympathetic activity occurs on a background of high parasympathetic tone. (Mayo Clin Proc 1999;74[11]:1088; Circulation 2001;103[1]:89.) Recent work demonstrates that AC is a pro-arrhythmic stimulus in LQTS. (J Mol Cell Cardiol 2018;116:145.) Combined adrenergic and parasympathetic stimulation has a complex relationship with arrhythmogenicity, with differences in the effects of steady-state adrenergic activation vs. sudden adrenergic stress. Specifically, sudden adrenergic stress appears to be the more arrhythmogenic.

Understanding AC is important for prevention, diagnosis, and treatment. Knowledge of AC enables those at risk to be screened for long QT syndrome; open water swims can have intelligent courses and rescue provision at high-risk points. (J Mol Cell Cardiol 2018;116:145.) AC also explains some deaths associated with immersion that are not explained by drowning-induced hypoxic cardiac arrest. It is possible that an immersion victim may be in cardiac arrest as a result of arrhythmia and that the arrhythmia may be torsade de pointes.

Appropriate treatment and the prognosis may be better based on cardiac arrest of cardiogenic origin, with near-immediate cessation of cerebral blood flow, rather than the progressive hypoxia leading to hypoxic cardiac arrest seen in drowning, where the hypoxemia occurring before cessation of cerebral blood flow exacerbates the neuronal injury post-return of spontaneous circulation. (Resuscitation 1997;35[1]:41.) Theory and increasing evidence suggest that AC is not confined to immersion, and may act as an arrhythmogenic factor in other situations. (High Alt Med Biol 2014;15[3]:356.)

Dr. Morgan is a post-graduate student in the Extreme Environments Laboratory in the Department of Sport and Exercise Science at the University of Portsmouth in the United Kingdom and an anesthetist in Southmead Hospital, North Bristol NHS Trust, Bristol, UK. Follow him on Twitter @drpaddymorgan. Dr. Tipton is a professor of human and applied physiology,also in the Extreme Environments Laboratory. Follow him on Twitter @ProfMikeTipton.

Read the original article, "'Drowning' in a Sea of Misinformation" at http://bit.ly/EMN-Drowning.


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Wednesday, April 25, 2018

Is Paracentesis for All Admitted Patients Overkill?
Maybe, but You Should Do It Anyway

BY RICHARD PESCATORE, DO

Patients presenting with peritoneal ascites represent a common therapeutic and diagnostic challenge for emergency physicians. By the very nature of their systemic disease, these patients often present with a multitude of symptoms that are just as likely caused by underlying illnesses as they are by an ascitic infection.

what to do.jpg
 

We all have no trouble recognizing the classic triad of spontaneous bacterial peritonitis (SBP)—fever, abdominal pain, and worsening ascites—but less than a quarter of patients presenting with SBP will manifest such symptoms. (Dig Liver Dis 2001;33[1]:41.) Some older data sets suggested that up to 12 percent of cirrhotic patients presenting for admission harbor peritonitis, prompting the revision of the American Association for the Study of Liver Diseases (AASLD) Practice Guideline dictating that all patients undergo diagnostic paracentesis prior to hospitalization. (Hepatology 2013;57[4]:1651.)

This recommendation lacks important nuance, however; it would seem silly, for example, to tap a trauma patient just because he walked through our doors, but it does underline the low threshold we should have for peritoneal fluid analysis in patients with ascites who are presenting with the classic triad, GI symptoms, vital sign abnormalities, or any other concerning clinical findings.

Why EPs?
Why is this incumbent upon us? Our waiting rooms overflow with patients requesting flu swabs and with victims of asymptomatic hypertension, and the time investment in performing paracentesis, much less waiting for lab analysis of the collected fluid, seems almost wasteful when the patient is headed for a room upstairs anyway. Isn't this something that can be referred for hospitalist disposition or to the inpatient proceduralist? With or without a dose of antibiotics to cover our bases, the arguments against ED paracentesis are not without merit. After all, a slim possibility of simmering infection lacks the emergency moniker we often use as a barometer of necessity.

Nonetheless, I firmly believe that performing paracentesis and diagnosing SBP should ride high on our list of priorities. A diagnostic tap takes all of a few minutes, no more than an ultrasound-guided IV, for which we're called on at an alarmingly increasing rate. Early diagnosis of SBP matters not only because of the high mortality associated with it (nearly 40% in most cohorts) but also because early ED intervention makes a difference. (Hepatology 2013;57[4]:1651.) Albumin infusion, an often-forgotten but critical therapy when delivered quickly after diagnosis, can save lives.

The benefit of albumin infusion in SBP is not entirely known, although multiple possible mechanisms have been identified. Albumin has been demonstrated to alleviate endotoxemia, block lipopolysaccharide-stimulated neutrophil activity, and modulate nitric oxide activity, mitigating systemic vasodilation and capillary leak. Most saliently, however, two randomized clinical trials have demonstrated a consistent reduction in renal failure and mortality when albumin is infused after diagnosis of SBP. (N Engl J Med 1999;341[6]:403; J Dig Dis 2002;3[1]:32.) Importantly, this mortality benefit came when albumin was administered within six hours of diagnosis, placing the onus of therapy and the opportunity of intervention squarely in the lap of emergency physicians.

The 2012 AASLD guideline, based largely on the trial by Sort, et al., recommended that patients with SBP who also have concomitant azotemia or bilirubin elevation receive IV albumin (1.5 g/kg) within six hours of detection as well as 1.0 g/kg on day three. (Hepatology 2013;57[4]:1651.) It's a large volume of colloid, and it typically requires an impetus of purpose that seems rare outside of the ED. When so much of our daily practice makes little impact in comparison, however, the chance to prevent renal failure or save a life is an opportunity and an obligation we shouldn't pass up.

Dr. Pescatore is the director of emergency medicine research for the Crozer-Keystone Health System in Chester, PA. He is also the host with Martha Roberts, ACNP, of the podcast EMN Live, which previews each issue of EMN ahead of print: Follow him on Twitter @Rick_Pescatore, and read his past columns at http://bit.ly/EMN-Pescatore.


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Wednesday, April 18, 2018

​Inconsistencies in Hydrocortisone Trial
for Septic Shock Make Findings Suspect

BY RORY SPIEGEL, MD

We have existed in a state of ambiguity, torn between two contradictory randomized, controlled trials, when it comes to glucocorticoid therapy for septic shock. The Annane trial suggested a mortality benefit in giving corticosteroids to patients found to have relative adrenal insufficiency. (JAMA 2002;288[7]:862.) The larger CORTICUS study, however, found no benefit in using corticosteroids compared with placebo. (N Engl J Med 2008;358[2]:111.)

myths.jpg

Those in favor of administering corticosteroids have argued that patients in the Annane, et al., trial were much sicker, isolating the subset of patients who truly benefit from steroid supplementation. They contended that the negative results in the CORTICUS trial were the consequence of enrolling a much healthier population, washing out any chance of identifying the underlying signal. The contrary opinion is simple: Those against corticosterioids say the results of the Annane trial were due to statistical noise and a small sample size and CORTICUS was nothing more than the expected regression to the mean.

Now there is a third study that could liberate us from this limbo—the ADRENAL trial, a pragmatic, double-blind, parallel-group RCT comparing hydrocortisone with placebo in patients with septic shock. This trial's impressive sample size and methodological rigor overshadow those of the Annane and CORTICUS cohorts, but I fear its results will deliver far less certitude than we had hoped.

Venkatesh, et al., enrolled adults 18 and older with septic shock who had two or more SIRS criteria, who had been on vasoactive agents for at least four hours, and who required mechanical ventilation. (
N Engl J Med 2018;378[9)]:797.) Patients were randomized to receive an intravenous infusion of hydrocortisone at a dose of 200 mg per day or matching placebo for seven days. The authors enrolled 3,800 patients in 64 ICUs over four years and across five countries, and 1,898 were assigned to hydrocortisone and 1,902 to placebo.

The authors found no difference in the primary outcome—90-day mortality—between the hydrocortisone and placebo groups (27.9% v. 28.8%; CI 0.82 to 1.10; p=0.5). Nor did they find a difference in 28-day mortality (22.3% v. 24.3%; CI 0.76 to 1.03; p=0.13). The authors noted that patients in the hydrocortisone group had a faster time to resolution of shock (three v. four days), a shorter time to discharge from the ICU (10 v. 12 days), and a shorter duration of initial mechanical ventilation (six v. seven days). These results were statistically significant, but it is important to remember that these are secondary endpoints and are acutely vulnerable to the whimsies of statistical chance.

Time to ICU discharge was statistically shorter in patients randomized to receive hydrocortisone, for example, but the authors found no difference in the number of days alive and outside the ICU or days alive and outside the hospital. And duration of initial mechanical ventilation was shorter in the hydrocortisone group, but no difference was seen in days alive and free of mechanical ventilation nor in the rate of recurrent mechanical ventilation. Such inconsistencies make one wonder if these findings were simply due to multiple measurements and statistical chance.

A Nominal Effect
Even the improvement in time to resolution of shock seems to be of questionable clinical relevance. It did not translate into a mortality benefit, the mean difference in mean arterial pressure between the two groups was only 5.39 mm Hg, and no difference in the daily dose of norepinephrine existed. The authors also observed a 4.7 percent absolute increase in the need for blood transfusion in patients in the placebo group (37% v. 41.7%). Given the secondary nature of this finding and the unclear mechanistic underpinning, it is hypothesis at best.

The authors also noted a statistically significant increase in the rate of adverse events in the hydrocortisone group (1.1% v. 0.3%, p=0.009). Most of these were clinically inconsequential (hyperglycemia, hypernatremia, etc.), but it is important to remember that RCTs are notoriously poor at identifying rare harms and will underestimate the harm of the treatment in question.

I am sure some will find minute chinks in the scientific armor of the ADRENAL trial to discount its findings despite its methodological rigor. Most notably, no minimum dose of vasopressors was required before enrollment. The argument is, like the CORTICUS trial, this cohort represents a group of patients that is unlikely to benefit from hydrocortisone supplementation. But when the authors examined patients with elevated pressor requirements (both >15 mcg/min and >25 mcg/min) and elevated APACHE scores (>25) who met the Sepsis-3 criteria for septic shock, they were unable to identify a signal of benefit in any of these sicker subsets of patients, all of whom represent a far larger sample size than the Annane cohort.

It is difficult to view these results as anything but negative. Some potential signals of benefit are seen in patients who received hydrocortisone, but they were fleeting and ultimately had minimal influence on patient-centered outcomes. Any true benefit, if it exists, is small and would require an impossibly large trial to demonstrate empirically.

In the end, the ADRENAL trial will have a nominal effect on practice. The desire to act in the face of critical illness is strong enough that we will reason away this lack of benefit simply because we have so little else to offer. Many of us faced with a patient in refractory shock will continue to give corticosteroids in the hope that they may help the individual patient before us. We will just do so with an added degree of hand-wringing, knowing that we have read the literature refuting our practice and simply want nothing to do with its conclusions.

Dr. Spiegel is a clinical instructor in emergency medicine at the University of Maryland Medical Center. Visit his blog at http://emnerd.com, follow him on Twitter @emnerd_, and read his past articles at http://bit.ly/EMN-MythsinEM.

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