Hyponatremia

Written by: Jim O’Brien, MD (NUEM ‘23) Edited by: David Kaltman, MD (NUEM ‘20)
Expert Commentary by: Sarah Dhake, MD (NUEM ‘19) & Josh Waitzman, MD, PhD

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Expert Commentary

Thanks for a great review on hyponatremia by Drs. O’Brien & Kaltman. I’ve recruited the expert insight from one of my favorite colleagues and fellow Northwestern University Feinberg School of Medicine graduate Joshua Waitzman, MD PhD, Instructor of Nephrology at Beth Israel Deaconess Medical Center in Boston, MA. 

I’ll highlight a few points from an emergency medicine point of view with Dr. Waitzman’s additional commentary from the nephrology perspective. 

• I’d argue the primary question you need to answer in the ED for hyponatremia patients is whether or not hypertonic saline is indicated. For those well-appearing neurologically intact hyponatremia patients w/ sodium levels > 120, further work-up & analysis of the underlying etiology can be deferred to the inpatient side. It’s always appreciated to send the hyponatremia labs (eg urine lytes, osms, TSH, etc) for the admitting team, however differentiating SIADH from cerebral salt-wasting should not be at the top of your priority list. Especially as the etiology of hyponatremia is commonly multifold. 

  • Dr. Waitzman: additionally, a key reminder is to STOP AND THINK before giving isotonic fluids (0.9% NS, LR, bicarb gtt, etc). For most patients with moderate-to-severe hyponatremia, giving a liter of normal saline is normally the wrong answer.

    • If your patient has SIADH, heart failure, or cirrhosis (common causes of hyponatremia), additional IV fluids will end up worsening the hyponatremia. 

    • If your patient is volume depleted, isotonic fluids will fix the volume problem and shut off ADH, leading to rapid increases in urine output and rises in sodium. The worst thing we can do to patients with bad hyponatremia is overcorrect them too quickly. 

• If you are considering hypertonic saline, make sure to get your nephrologist on board early. Nephrology is the primary team that will be following your patient from arrival in the ED through discharge so if you’re debating whether the patient requires 3% NaCl, please consult your nephrology team ASAP.  Though w/ that said, if your patient is seizing due to hyponatremia, push the hypertonic then get nephrology on board afterwards.

  • Dr. Waitzman: 100%. If you’re debating on hypertonic saline, call nephrology at any time. However, for the sake of your friendly overworked nephrology fellow, please wait until the AM before calling about patients who appear well and have sodium > 125. When consulting nephrology for hyponatremia, please have a urine sodium, potassium, and creatinine at the ready.

• Hypertonic saline is not only indicated for seizures, coma, suspected cerebral herniation or focal neurological deficits as noted above. Keep in mind the indication for 3% also extends to altered mental status and can present w/ simple confusion or even “just acting off” from baseline. Do keep in mind the acuteness of the neurologic status is also imperative to determining the need of hypertonic. More acute symptoms = higher likelihood of needing 3%. It’s essential to get background information from family/friends if the patient is unable to provide any additional history regarding their own baseline level of functioning. 

  • Dr. Waitzman: In my mind, using hypertonic saline should be based on three things.

    • First, how bad is the sodium level? It’s normally not worth it for most patients above 120. 

    • Second, how acute is the hyponatremia? Hypertonic can be risky for those with chronic hyponatremia but curative for those with hyperacute hyponatremia like marathon runners.

    • Third, how severe are the symptoms? Seizures attributed to hyponatremia need treatment ASAP. 

  • Because I’m a nephrologist, I approach the use of hypertonic saline like an equation, combining the acuteness of the hyponatremia with the severity of symptoms. For example, the more recent the sodium drop w/ more severe symptoms = more comfortable w/ hypertonic. The more chronic the hyponatremia and the less severe symptoms = hypertonic may have more risk than benefit. 

• Of note, you do NOT need a central line for hypertonic saline administration. Though this is dictated by your own hospital protocols, hypertonic saline has been shown to be safe when pushed in small doses through a large-bore peripheral (proximally placed) IV [1,2]. Though if your administration says differently, do not waste time putting in a triple lumen catheter if hypertonic is truly indicated in your hyponatremia patient. Drill an IO and push the 100-150cc 3% NaCl as soon as possible. 

  • Dr. Waitzman: PREACH.

• Do remember that pseudo-hyponatremia is a thing. Most commonly seen in our ED patients w/ hyperglycemia, other solutes which can lead to pseudo-hyponatremia are mannitol, glycol, or maltose (all three most commonly encountered on the inpatient side or post-outpatient urologic procedures). If you appreciate an elevated glucose on your chemistry panel, you can use the following equation 

Corrected Na = Measured Na + [(1.6 * (glucose-100)/100)] [3]

or this helpful link via MDCalc (https://www.mdcalc.com/sodium-correction-hyperglycemia) to determine the appropriate corrected sodium. 

• Dr. Waitzman: If you hate math, consider a blood gas sodium. There is no pseudohyponatremia on a blood gas sodium and it results faster than your normal chemistry panel sodium level.

• MDMA/ecstasy use is an uncommon cause of hyponatremia that should not be forgotten [4]. Keep that in mind in your presumed “intoxicated” young party-goers, especially those where these drugs are prevalent (eg raves, music-festivals, etc). MDMA leads to hyponatremia by activation of arginine vasopressin which increases kidney free water absorption [5]. 

• Vaptans have not been established as standard of care for hyponatremia in emergency medicine. If these are to be utilized in an ED patient, it is essential that there is a nephrologist on board who is actively involved in the patient’s management.  

  • Dr. Waitzman: wholeheartedly agree. Vaptans don’t have a place in the acute settings (like the ED) and have a huge risk of over-correcting the sodium. If you need to acutely correct hyponatremia, hypertonic is the answer, not vaptans. 

• With boarding being a nation-wide issue, one final piece of commentary from both the emergency medicine & nephrology perspective: if you’re sending your patient to the ICU for hyponatremia, it’s because they require q2hr sodium levels. Please continue those q2hr sodium levels while they remain under your care in the ED while waiting for an ICU bed. Blood gas sodiums are a great way to trend sodium levels as they’re accurate & result quickly (and avoid the potential for pseudohyponatremia as described above). 

I’d like to extend an incredibly huge thank you & sincere gratitude to Dr. Waitzman for his assistance & expertise on this expert commentary. We’re all exceptionally lucky to work with such fantastic nephrology colleagues and are eternally appreciative for all their help, insight, and expertise. 

References:

1. Alenazi AO, Alhalimi ZM, Almatar MH, Alhajji TA. Safety of Peripheral Administration of 3% Hypertonic Saline in Critically Ill Patients: A Literature Review. Crit Care Nurse. 2021 Feb 1;41(1):25-30. doi: 10.4037/ccn2021400. PMID: 33560431.

2. Mesghali E, Fitter S, Bahjri K, Moussavi K. Safety of Peripheral Line Administration of 3% Hypertonic Saline and Mannitol in the Emergency Department. J Emerg Med. 2019 Apr;56(4):431-436. doi: 10.1016/j.jemermed.2018.12.046. Epub 2019 Feb 8. PMID: 30745195.

3. Katz MA. Hyperglycemia-induced hyponatremia--calculation of expected serum sodium depression. N Engl J Med. 1973 Oct 18;289(16):843-4. doi: 10.1056/NEJM197310182891607. PMID: 4763428.

4. Petrino R, Marino R. Fluids and Electrolytes. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw Hill; Accessed July 21, 2021.

5. Campbell GA, Rosner MH. The agony of ecstasy: MDMA (3,4-methylenedioxymethamphetamine) and the kidney. Clin J Am Soc Nephrol. 2008 Nov;3(6):1852-60. doi: 10.2215/CJN.02080508. Epub 2008 Aug 6. PMID: 18684895.

Sarah Dhake, MD

Division of Emergency Medicine, NorthShore University HealthSystem

Clinical Assistant Professor, University of Chicago - Pritzker School of Medicine

Twitter: @ssandersEM

sdhake@northshore.org

Joshua Waitzman, MD PhD

Instructor in Medicine, Harvard Medical School
Division of Nephrology, Department of Medicine
Beth Israel Deaconess Medical Center

Twitter: @Jwaitz
jswaitzm@bidmc.harvard.edu

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How To Cite This Post:

[Peer-Reviewed, Web Publication] O’Brien, J. Kaltman, D. (2022, Jan 10). Hyponatremia. [NUEM Blog. Expert Commentary by Dhake, S and Waitzman, J]. Retrieved from http://www.nuemblog.com/blog/hyponatremia

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Management of Environmental Heat Injury in the ED

Written by: Sean Watts, MD (NUEM PGY-3) Edited by: Phil Jackson, MD (NUEM ‘20) Expert Commentary by: George Chiampas, DO, CAQSM, FACEP

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Heat related illness has become an increasing source of morbidity and mortality due to environmental injuries from rising global temperatures and increased interest in outdoor activities. The National Oceanic and Atmospheric Administration reported that 2016 was the hottest year on record, and that temperatures were on average 3.2 F° higher than the 20th century averages.[1] Increasing temperatures have manifested in fatal heat waves such as one claiming the lives of 70,000 individuals living in Europe during 2003.[1] The population most subject to these heat waves include the extremes of age and athletes.

Human body temperature is normally set at 37 ° C, and is maintained via the preoptic nucleus of the anterior hypothalamus.[1,2] Hyperthermia results from exposure to an exogenous heat source without altering the hypothalamic set point. As core temperatures elevate during exertion and with exposure to heat, the posterior hypothalamic nucleus signals sympathetic pathways that result in vasodilation of peripheral vascular beds and shunting blood away from gastrointestinal vasculature in order to maximize heat dissipation. Additionally, eccrine sweat glands are cholinergically activated resulting in an evaporative cooling effect. When the duration and magnitude of heat exposure outpace these physiologic mechanisms, the symptoms of heat-related illness become evident and vary from mild heat cramps to severe heat stroke and death.[2]

Heat cramps result from both potassium wasting from persistent utilization of aldosterone in order to maintain a euvolemic state and sodium loss through sweat. Edema can result from increased hydrostatic pressure of the peripheral vasculature. Additionally, syncope and hypotension can manifest due to dehydration, orthostatic pooling of blood, peripheral vasodilation, and a subsequent decrease in cardiac output. Without appropriate treatment, heat exhaustion and the more extreme heat stroke can present.

Heat exhaustion is defined as a core temperature between 37 ° C and 40 ° C with signs and symptoms including intense thirst, weakness, discomfort, anxiety and dizziness.[1,2,6,8] Heat stroke, on the other hand, is defined as a core temperature greater than 40 C° with signs of central nervous system dysfunction. Heat stroke can be further categorized into exertional and non-exertional.[4] The demographic of exertional heat stroke includes athletes, military personal, or young individuals participating in prolonged exercise.[4,8] Non-exertional heat stroke includes the elderly, young children, or individuals with metabolic or cardiac comorbidities that engage in brisk to minor activity at elevated temperatures.[1,4] When the body reaches 40 C° denaturation of proteins, release of pro-inflammatory mediators, and direct activation of the coagulation cascade occurs.[1,2] This can ultimately result in disseminated intravascular coagulation, which is a common complication of heat stroke.[1,4,5] Disruption of the liver and the cerebellum from tissue ischemia, hypoxia, vascular dysfunction, secondary cascade inflammation manifest with elevated liver function tests and ataxia dysmetria, and coma.[1,6]

Summary of the Pathophysiology of Heat Stroke [1]

Treatment of heat related illness in the emergency department rests on appropriate recognition of the severity of disease. For heat syncope and heat cramps, isotonic or hypotonic electrolyte solutions may be administered in addition to actively flexing leg muscles to prevent peripheral pooling of blood.[7,8] Ice packs or cold towels around the neck, axillae and groin can also be used for comfort measures 6. In general, these heat illnesses are self-limiting.

For heat exhaustion and heat stroke, treatments become more aggressive and should be initiated within 30 minutes of recognition of the signs/symptoms.[1,4] These patients often present critically ill and rapid assessment of the patient’s airway, breathing, and circulation is paramount. Caregivers should obtain good IV access, as well as intubate the patient if they are obtunded or in danger of loss of airway protection.[1,6] Broad spectrum critical care labs should be obtained, as well as a CK to assess for evidence of rhabdomyolysis.[5]  Additionally, obtaining an accurate core body temperature is a crucial first step to determine the severity of illness.[1,2,4,5,6] This is best performed through continuous rectal probe monitoring. Rehydration should then be performed, preferably with 1 to 2 L of isotonic fluids.[1,4] Care should be taken to not over-correct hypovolemia as the aforementioned pathophysiology makes this population vulnerable to pulmonary edema.[1] Additionally, care should be taken not to over bolus hypotonic or isotonic solutions as this population, especially those involved in long distance endurance sports like triathlons or marathons, are particularly prone to hyponatremia.[9] If these patients are given too much of these solutions, this can actually exacerbate the hyponatremia. Patients with profound hyponatremia will actually require IV hypertonic solutions or salt tabs.[9]

 Clinicians should next focus on cooling core body temperature. The best treatment for exertional heat stroke is cold-water immersion therapy—where the patient gets placed in a cold body of water.[5,7] This method takes advantage of the high thermal conductivity of water and is most effective when the patient’s clothing is removed. Studies have demonstrated that immersion in an ice-water slurry at 2°C generated cooling rates of 0.35°C/min.[4] Comparatively, allowing hyperthermic subjects to rest in air-conditioned or temperature-controlled rooms only resulted in cooling rates of only 0.03°–0.06°C/min.[4] Evidence regarding an optimal temperature to halt cooling is still under debate, but is thought to be somewhere between 38°C to 39°C, with the fear that overcooling may result in cardiac arrhythmias, especially in the elderly suffering from non-exertional heat stroke.[1,4]

Subject in a cold water-immersion bath after heat- stroke [4]

The use of cold-water immersion therapy in non-exertional heat stroke is still under debate, but the limited evidence shows that evaporative and convective cooling by a combination of cool water spray with continual airflow over the body may be superior, especially in the elderly suffering from non-exertional heat stroke.[4] In many emergency departments, complete cold water immersion therapy may not be readily  available and limited by the placement of cardiac leads, intubation, and IV access, so evaporative and convective cooling methods become first-line for both exertional and non-exertional heat stroke in the emergency department setting should cold water immersion be unavailable.[1,4,5] Should shivering become problematic, benzodiazepines are considered first line therapy.[1,6] In severe or refractory cases the patient may benefit from ECMO.[6]

Evaporative and conductive cooling methods--note the placement of ice packs in axilla, groin as well as the cooling fan overhead [4]

With the rapid increase in heat-related injuries, and projected increase in global warming, researchers are continually seeking new and efficacious treatments. For example, recombinant activated protein C is currently being explored to manage the disseminated intravascular coagulation that may result from heat stroke.[2] Additionally, application of cold packs versus other methods of rapid cooling has been explored. An experimental study published in the journal of Wilderness and Environmental Medicine found that the use of ice packs provided a significantly higher enthalpy change over cold packs—suggesting that ice packs are more efficacious than cold packs when managing heat-injury.[3] Additionally, the study found that application of cold packs or ice packs to locations high in AV anastomoses provided superior cooling rates.[3] Evaporative plus convective cooling units are also under study as an alternative means to cold water immersion for the treatment of non-exertional heat stroke.[5]

Key Points and Summary

• Heat Injury continues to be a major cause of environmental morbidity and mortality, and will likely increase due to rising global temperatures

• Heat Injury exists on a continuum, with heat cramps/syncope on one end and heat exhaustion/stroke on the other end

• Obtain a rectal temperature if you suspect heat exhaustion/stroke, assess ABC’s, get good IV access, and be careful not to over bolus isotonic/hypotonic solutions due to the risk of worsening hyponatremia in athletes

• If feasible, cold water immersion is superior for exertional heat stroke, in the ED setting evaporative and conductive cooling with ice packs can be used

• In severe or resistant cases cardiopulmonary bypass can be effective

table of cooling methods [6]

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Expert Commentary

A great review and reminders of what is a preventable death especially in exertional heatstroke. Unfortunately, still in the United States there are still approximately fifteen to twenty heat-related deaths in athletes annually, mostly seen in august. While there is a spectrum of illness, preventative measures, a high index of concern and management can all mitigate negative outcomes.

In non-exertional heat illness, removal from the environment, addressing the medical condition and or removing any contributing factors is key. Cooling methods and the aggressiveness of cooling are determined by the patient’s mental status and stability. As highlighted, Heat exhaustion presents with headaches, nausea, dizziness, and weakness. Using cooling blankets and cold packs to the groin axilla and circulating fans all are measures in passive cooling. One key element to address as typically a patient presents undifferentiated is to obtain a rectal temperature in a timely fashion as highlighted. Temperatures and glucose in altered mental status patients are critical for efficient management and positive outcomes. There are key studies that highlight that time and duration above 42C lead to higher morbidity including death. 

In athletics, the death of Minnesota football player Korey Stringer in August of 2001 shed greater light on the risks of exertional heatstroke. Since his death, more work and research has been done including best practices in sport to mitigate these outcomes. Across many sports, including Marathons, best practices as outlined in the blog are being implemented pre-hospital. These measures are comparable to the recent out of hospital cardiac arrest best practices of on-sight CPR and utilization of an AED and transport second mantra. In heatstroke “cooling” on sight with ice tub submersion is the current thread being communicated. This messaging is evidenced by a recent EMS consensus paper  that highlights to first-responders the importance of recognizing but also cooling on-sight prior to transport. The delay of cooling and transport times to delay of recognition and cooling in emergency departments may lead to not initiating life-saving rapid cooling beyond the thirty minutes highlighted in the blog.

As you accurately highlighted patients can present differently, however, the key is altered mental status (AMS). Based on experience this can have the forms of patients collapse and obtunded, seizing, irritable and combative to just being confused. Rapid assessments in the right environment with excluding other AMS possibilities will allow the practitioner to respond and manage in a timely fashion. At Northwestern, both Dr. Malik and Dr. Chiampas have published the attached “collapse algorithm” (below) which allows for a quick assessment and possible differential diagnoses. Lastly obtaining a rectal temperature, which at times may be challenging with the combative patient, allows the staff in the Emergency room to objectively determine when to cease cooling. I will share that some of these patients based on their presentation would traditionally be intubated upon arrival. I would caution and remind the practitioner that if you have prepared in advance and can rapidly cool the symptoms are reversible within 10-15 minutes of ice submersion.

Lastly for emergency departments, where out-door events (sporting, festivals or concerts) with the possibility of stimulant use, preparedness is key. At Northwestern, we have secured 100-gallon ice tubs, implemented the collapse algorithm in our trauma bay and on when high-risk events take place to trigger necessary resources. For the Chicago Marathon, Triathlon or major concerts such as Lolla Palooza we order ice to the ER, towels, and prep the tub while educating our staff of the likelihood of these conditions. As we head towards the summer ahead with all of the environmental concerns of climate change and increased temperatures, this blog provides key reminders of the emergency department’s role.

George Chiampas DO CAQSM

Assistant Professor Northwestern University, Feinberg School of Medicine

Departments of Emergency and Orthopedic Surgery

Chief Medical Officer U.S. Soccer

Chief Medical and Safety Officer Bank of America Chicago Marathon

Team Physician Chicago Blackhawks

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How To Cite This Post

[Peer-Reviewed, Web Publication] Watts S, Jackson P. (2020, July 6). Management of Environmental Heat Injury in the ED [NUEM Blog. Expert Commentary by Chiampas G. Retrieved from http://www.nuemblog.com/blog/environmental-heat-injury

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References 

1. Heat-Related Illness. Walter F. Atha, MD. Emerg Med Clin N Am 31 (2013) 1097–1108. http://dx.doi.org/10.1016/j.emc.2013.07.012

2. Wilderness Medical Society Practice Guidelines for the Prevention and Treatment of Heat-Related Illness: 2014 Update. Grant S. Lipman, MD; Kurt P. Eifling, MD; Mark A. Ellis, MD; Flavio G. Gaudio, MD; Edward M. Otten, MD; Colin K. Grissom, MD. WILDERNESS & ENVIRONMENTAL MEDICINE, 25, S55–S65 (2014)

3. Chemical Cold Packs May Provide Insufficient Enthalpy Change for Treatment of Hyperthermia. Samson Phan, MS; John Lissoway, MD; Grant S. Lipman, MD. WILDERNESS & ENVIRONMENTAL MEDICINE, 24, 37–41 (2013)

4. Cooling Methods in Heat Stroke Flavio G.Gaudio MD∗Colin K.Grissom MD†The Journal of Emergency Medicine, Volume 50, Issue 4, April 2016, Pages 607-616

5. Heat Stroke. Alan N. Peiris, MD, PhD, FRCP(London); Sarah Jaroudi, BS; Rabiya Noor, BS. JAMA. 2017;318(24):2503. doi:10.1001/jama.2017.18780

6. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e. Judith E. Tintinalli, J. Stephan Stapczynski, O. John Ma, Donald M. Yealy, Garth D. Meckler, David M. Cline. Section 16, Chapter 210: Heat Emergencies. http://accessmedicine.mhmedical.com.ezproxy.galter.northwestern.edu/content.aspx?bookid=1658&sectionid=109384117. Accessed June 10, 2019.

7. Heat-Related Illness in Athletes Allyson S. Howe MD, Barry P. Boden, MD First Published August 1, 2007 https://doi-org.ezproxy.galter.northwestern.edu/10.1177/0363546507305013

8. Heat-Related Illnesses. ROBERT GAUER, MD, Womack Army Medical Center, Fort Bragg, North Carolina. BRYCE K. MEYERS, DO, MPH, 82nd Airborne Division, Fort Bragg, North Carolina. Am Fam Physician. 2019 Apr 15;99(8):482-489.

9. Hyponatremia among runners in the Boston Marathon. Almond CS, Shin AY, Fortescue EB, Mannix RC, Wypij D, Binstadt BA, Duncan CN, Olson DP, Salerno AE, Newburger JW, Greenes DS. N Engl J Med. 2005 Apr 14;352(15):1550-6.