A PEM adventure
It’s time for another PEM adventure. Join us on another journey (with an inbuilt time travel machine) as we manage Elsa, a 2-year-old girl who is a huge fan of the Disney movie Frozen.
Elsa was found face down in the family pool 20 minutes after the last visual contact and was picked up without resuscitation. Emergency Medical Services found her apneic and pulseless.
She was intubated at the scene and transported to your ED, with cardiopulmonary resuscitation (CPR) performed en route.
Upon arrival in resus, she had a core temperature of 27.3⁰C and remained pulseless.
She received three rounds of adrenaline, and her pulse returned approximately 30 minutes after retrieval from the pool.
She’s intubated and ventilated on 100% FiO2.
The PICU team is with you in resus, stabilising Elsa for transfer to the unit. Her GCS is 3, and her pupils are sluggish but reactive.
You look at her monitor and an arterial blood gas performed moments ago.
Your eye catches an unusual rhythm on the monitor.
You request a 12 lead ECG and repeat a blood gas, asking for it to be run on the PICU analyser.
Your trusted nurse hands you the ECG:
Paediatric ECG interpretation has never been your strong suit. You convince yourself that you can see widespread ST depression and T-wave inversion.
But the PICU is a few corridors and a flight of stairs away, and you don’t have those electrolytes yet. You try to think from the first principles – what electrolyte shifts happen in severe acidosis? Does the temperature play a role? “Oh,” you say out loud, “I wish I paid more attention in physiology class.”
What is the likely cause of Elsa’s ECG changes?
a) Hyperkalaemia?
As you ponder these options, the matron hands you the repeat gas.
Oh, blimey, it’s hypokalaemia! The K+ is 1.7.
You can now convince yourself that you can also see a U-wave!
Hindsight is a beautiful thing. You recall that severe acidosis causes K+ to shift from the intracellular to the extracellular space. Still, after a quick Google search, you realise that hypothermia potently affects potassium shift from the extracellular to the intracellular and extravascular spaces.
b) Hypokalaemia?
As you ponder these options, the matron hands you the repeat gas.
Oh, blimey, it’s hypokalaemia! The K+ is 1.7.
You can now convince yourself that you can also see a U-wave!
Hindsight is a beautiful thing. You recall that severe acidosis causes K+ to shift from the intracellular to the extracellular space. Still, after a quick Google search, you realise that hypothermia potently affects potassium shift from the extracellular to the intracellular and extravascular spaces.
c) Hypocalcaemia
As you ponder these options, the matron hands you the repeat gas.
Oh, blimey, it’s hypokalaemia! The K+ is 1.7.
You can now convince yourself that you can also see a U-wave!
Hindsight is a beautiful thing. You recall that severe acidosis causes K+ to shift from the intracellular to the extracellular space. Still, after a quick Google search, you realise that hypothermia potently affects potassium shift from the extracellular to the intracellular and extravascular spaces.
d) Hypothermia
As you ponder these options, the matron hands you the repeat gas.
Oh, blimey, it’s hypokalaemia! The K+ is 1.7.
You can now convince yourself that you can also see a U-wave!
Hindsight is a beautiful thing. You recall that severe acidosis causes K+ to shift from the intracellular to the extracellular space. Still, after a quick Google search, you realise that hypothermia potently affects potassium shift from the extracellular to the intracellular and extravascular spaces.
e) Metabolic acidosis
As you ponder these options, the matron hands you the repeat gas.
Oh, blimey, it’s hypokalaemia! The K+ is 1.7.
You can now convince yourself that you can also see a U-wave!
Hindsight is a beautiful thing. You recall that severe acidosis causes K+ to shift from the intracellular to the extracellular space. Still, after a quick Google search, you realise that hypothermia potently affects potassium shift from the extracellular to the intracellular and extravascular spaces.
Knowing Elsa’s blood gas, what are you going to do next?
a) Give IV K+?
As the infusion is put up, Elsa goes into a VF rhythm due to a rapid shift in potassium and arrests soon after.
Despite good quality CPR, there is no ROSC. Maybe we shouldn’t have given that potassium after all.
If only I had a time machine, you think to yourself…
Oh, we do! Let’s hop in.
Close the tab and choose another option.
Zydlewski, A. W., & Hasbargen, J. A. (1998). Hypothermia-induced hypokalemia. Military medicine, 163(10), 719-721.
b) Rewarm
Correct.
Treat the cause, not the numbers.
Elsa is cardiovascularly stable, so there is no urgent reason to replace the potassium.
Rewarming in itself can cause rebound hyperkalaemia. Adding more potassium at this stage would only add to the risk. Avoid additional potassium unless the arrhythmia causes CVS instability, and check the potassium frequently.
Kattih, Z., J. Le, E. L. Altschul, and B. A. Mina. “Hypothermia, Rewarming, and Potassium Shifting: A Case of Accidental Hypothermia and Hyperkalemia.” In C44. CRITICAL CARE CASE REPORTS: METABOLIC, RENAL, AND ENDOCRINE, pp. A5175-A5175. American Thoracic Society, 2020
c) Rewarm and give IV K+
As the infusion is put up, Elsa goes into a VF rhythm due to a rapid shift in potassium and arrests soon after.
Despite good quality CPR, there is no ROSC. Maybe we shouldn’t have given that potassium after all.
If only I had a time machine, you think to yourself…
Oh, we do! Let’s hop in.
Close the tab and choose another option.
Zydlewski, A. W., & Hasbargen, J. A. (1998). Hypothermia-induced hypokalemia. Military medicine, 163(10), 719-721.
d) Just add 20mmol/L of K+ to the bag of IV fluids
A few hours later Elsa goes into a VF rhythm due to a rapid in potassium and arrests soon after.
Despite good quality CPR, there is no ROSC. Maybe we shouldn’t have given that potassium after all.
If only I had a time machine, you think to yourself…
Oh, we do! Let’s hop in.
Close the tab and choose another option.
Zydlewski, A. W., & Hasbargen, J. A. (1998). Hypothermia-induced hypokalemia. Military medicine, 163(10), 719-721.
A rectal thermometer is inserted to have a more accurate temperature reading.
It reads 30.1⁰C.
Hmmm, it feels like there’s a decision to make here.
How fast and to what target should you rewarm Elsa?
a) 5⁰C/hr to 36⁰C
Oh, good grief, that was not a good thing to do.
Elsa goes into VF arrest due to a rapid shift of potassium from the cells, and despite your best efforts, she dies.
Hop back in that time machine and make a different choice.
b) 3⁰C/ hr to 34⁰C
The PICU reg disagrees, explaining that rewarming too fast will risk a rapid potassium leak from the cells, causing hyperkalaemia and worsening secondary brain injury.
They continue to explain that aiming for a “low normal” temperature of 34⁰C, prolonging hypothermia, is of no benefit.
Close the toggle and choose another option.
c) 3⁰C/ hr to 36⁰C
The PICU reg disagrees, explaining that rewarming too fast will risks a rapid potassium leak from the cells, causing hyperkalaemia and worsening secondary brain injury.
Close the toggle and choose another option
d) 1⁰C/ hr to 36⁰C
The PICU reg agrees with this plan, weighing in with some advice.
The rate of rewarming depends on the starting point in the hypothermic patient that has arrested after drowning. Any temperature under 30⁰C needs rapid rewarming. The consensus is that patients (irrespective of age) should be rewarmed above the commonly accepted danger zone for ventricular fibrillation (28–30°C), as quickly as possible.
Mazur P, Kosinski S, Podsiadlo P, et al.: Extracorporeal membrane oxygenation for accidental deep hypothermia-current challenges and future perspectives. Ann Cardiothorac Surg 2019; 8:137–142
But Elsa’s temperature is 30.1⁰C. After the patient has reached 30⁰C, the key is to rewarm slowly. The “sweet spot” is between 0.5-2⁰C an hour, so aim for the median of 1.2⁰C/hr.
A rapid rewarming rate greater than 5°C/hr is associated with higher in-hospital mortality.
Saczkowski, R., Kuzak, N., Grunau, B. and Schulze, C., 2021. Extracorporeal life support rewarming rate is associated with survival with good neurological outcome in accidental hypothermia. European Journal of Cardio-Thoracic Surgery, 59(3), pp.593-600
Therapeutic hypothermia is no longer recommended in survivors of pediatric out-of-hospital cardiac arrest due to drowning. The THAPCA-OH trial found that hypothermia did not result in a statistically significant benefit for survival with good functional outcomes at one year compared to normothermia. Mortality risk at 28 days and 12 months also did not differ between treatment groups.
Moler, Frank W., Faye S. Silverstein, Richard Holubkov, Beth S. Slomine, James R. Christensen, Vinay M. Nadkarni, Kathleen L. Meert et al. Therapeutic hypothermia after out-of-hospital cardiac arrest in children. New England Journal of Medicine 372, no. 20 (2015): 1898-1908
As the PICU reg finishes their teaching and prescribes some warm IV fluids, Elsa’s sats drop to 54%.
She is already on 100% FIO2, a PEEP of 10 and a Ti of 1.2.
The PICU reg has checked DOPE, and all is in order. The CXR shows evolving ARDs with pulmonary oedema but no pneumothoraces. Aggressive bagging and physio fail to have the desired outcome and only serve in further derecruitment with lots of bloody, frothy secretions.
25 minutes in, Elsa’s sats are 40%.
What is your plan? How are you going to improve Elsa’s ventilation?
a) Place her prone
With a coordinated team effort, you flip Elsa prone. Nothing changes. What now?
Close the toggle and choose another option
b) Inhaled nitrous oxide
iNO is a risky choice. There’s already blood in Elsa’s airway, and iNO will make her bleed more and cause vasodilation.
And this is what happens.
When Elsa’s put on iNO, a hypotensive event drops her blood pressure to 41/22. The anaesthetic reg desperately tries to suction the blood in the ETT, but Elsa arrests and dies.
But fear not; we have a time travel machine for this reason.
Hop in and choose another choice.
c) Call ECMO
Nice idea, but you don’t have ECMO on site. The closest is 3 hours away. What else can you do?
Close the toggle and select another choice.
d) Surfactant
Yes! The Hail Mary of treatments!
Drowning affects how surfactant interacts with the alveolar membrane. Whilst freshwater inactivates surfactant, salt water merely dilutes it, leading to alveolar collapse and pulmonary dysfunction. Both salt and fresh water damage the basement membrane, leading to fluid shifts, ARDS, and pulmonary oedema.
No high-level evidence supports its routine use, mainly due to the limitations of RCT design in this very difficult setting and the increasing availability of ECMO. There is ample lower-level evidence that it can work, and physiology supports it.
Certainly, it can act as an important bridge to ECMO. Your local NICU colleagues won’t thank you, though, as the 200mg/kg dose in a bigger child will likely deplete most of their stocks! Be cautious in using it in patients with a pneumothorax due to the rapid increase in lung compliance and already high transmural pressures.
The NICU team has a big batch close to its expiry date and is happy to share that with you. You give the surfactant, and you can finally see the sats rise to 88%. The ECMO team are on their way…
Elsa’s gases are better three hours later, her PEEP is down to 8, and she’s oxygenating well on 80% oxygen. The ECMO team finally arrived and decided that you’d done such a good job that she may not need ECMO after all. You get a congratulatory nod from the PICU consultant when you’re called to resus by the matron for the next patient…
This post is part of the PEM Adventure at NEPTUNE 2023, hosted by Dani, Kat, Costas and Sarah. NEPTUNE 2023 was the inaugural UK PEM trauma conference, hosted by Nottingham University Hospitals Trust, one of the largest major trauma centres in the UK.
Selected references
Zydlewski, A. W., & Hasbargen, J. A. (1998). Hypothermia-induced hypokalemia. Military medicine, 163(10), 719-721
Kattih, Z., J. Le, E. L. Altschul, and B. A. Mina. “Hypothermia, Rewarming, and Potassium Shifting: A Case of Accidental Hypothermia and Hyperkalemia.” In C44. CRITICAL CARE CASE REPORTS: METABOLIC, RENAL, AND ENDOCRINE, pp. A5175-A5175. American Thoracic Society, 2020
Mazur P, Kosinski S, Podsiadlo P, et al.: Extracorporeal membrane oxygenation for accidental deep hypothermia-current challenges and future perspectives. Ann Cardiothorac Surg 2019; 8:137–142
Saczkowski, R., Kuzak, N., Grunau, B. and Schulze, C., 2021. Extracorporeal life support rewarming rate is associated with survival with good neurological outcome in accidental hypothermia. European Journal of Cardio-Thoracic Surgery, 59(3), pp.593-600
Moler, Frank W., Faye S. Silverstein, Richard Holubkov, Beth S. Slomine, James R. Christensen, Vinay M. Nadkarni, Kathleen L. Meert et al. Therapeutic hypothermia after out-of-hospital cardiac arrest in children. New England Journal of Medicine 372, no. 20 (2015): 1898-1908
