S2E4: Hypothermia and Drowning - Winter Special
It’s that fuzzy time of year again. Wrap up warm… it’s our winter special.
Mohammed is joined by Jimmy, Callum and Peter for a case that had their teeth chattering.
Thankfully, our Adult in the Room this month Dr Michael Dunphy was there to check their work!
Mohammed sat down with Prof. Conor Deasy then to chat about getting the department ready for the winter.
Right, let’s get to it!
How cold… is cold?
There are various levels of hypothermia. The general rule of thumb is “mild” is between 32-35C, “moderate” is 28-32C and severe is <28C. However, establishing a reliable core temperature can sometimes be challenging in the prehospital setting. This is especially noted when thermometers such as tympanic or axillary ones are usually calibrated to read only between 34 and 42C.
So, in comes the Swiss Staging System.
Usually stage I correlates to mild, stage II to “moderate” and stages III and IV cover “severe”.
What does cold look like?
Let’s pop back to our old A, B, C approach.
A- Laryngospasm/bronchospasm
B- Diaphragmatic fatigue, increased dead space, metabolic acidosis caused by ventilation* and decreased hepatic metabolism
C- Bradycardia, widened QRS, increased PR and QT (all increasing risk of VF- usually <28C), vasoconstriction, increased viscosity (both increasing myocardial work).
D- Fixed dilated pupils <30°C, neuroprotective
E- Impaired coagulation with increased bleeding time, but ALSO increased VTE risk
Nerdy Sideboard… Metabolic Acidosis?
So when a patient becomes hypothermic, their metabolic rate drops. This means their tissues consume less O2, but also produce less CO2. Pretty clear up to that point.
So, less CO2 production means lower pCO2, and so any bit of ventilation that happens will blow off pretty much all the remaining pCO2.
The low pCO2, and the low temperature, both push the oxygen dissociation curve to the left, meaning the haemoglobin has a higher affinity to the circulating O2, and it greedily latches onto it… making it less available to the tissues, which become anoxic and produce buckets of lactic acid.
All the while, the liver is similarly reducing its metabolic rate due to the hypothermia, so there’s less hepatic clearance of the circulating lactate.
So there you go, a respiratory cause (sort of) for a metabolic acidosis.
What should we Prioritise at the Roadside?
JEMS has some great content on the retrieval of accidental hypothermic patients in the pre-hospital setting.
First and foremost… move the patient. Change the environment even if that’s just getting them out of any cold water and into the back of an ambulance. Most importantly, handle with care. These patients are particularly vulnerable to developing cardiac arrhythmias and even rough movement and transport of patients can be the trigger factor. Passive rewarming with blankets and the heated ambulance is usually sufficient for mild hypothermia but further measures may be required.
External rewarming can be an option in some cases depending on resources but caution in patients may develop burns. Usually, this comes in the form of in-hospital bair huggers.
Now, active internal rewarming in-hospital
Overall, there are mixed reports in the literature for different methods of internal active rewarming. Procedures such as humidified air, warmed IV fluids and bladder lavage are actually not currently recommended in evidence-based clinical practice. However, here are some highlights.
Humidified Air
Ideal temperature required is 45C
Usually, the limit on humidifiers is 41C
Warmed IV Fluids
Pretty weak effect
Bladder Lavage
Small surface area for heat exchange
These are usually only of most benefit when used in association with…
Pleural Lavage
Of benefit in patients with severe hypothermia
250ml boluses of warmed crystalloid to 40-42C
Insert 2x 36F Chest Drains
First- slightly anterior and superior to normal drain position
Second- more posterior and basal for drainage
Alternatively, can use a single one for insertion and then drain after 2 minutes
What’s Changed in ACLS?
Overall, it’s key to remember that the rate of chest compressions and ventilations is the same as in normothermic patients. Mechanical devices such as the LUCAS are still of benefit as well. However, if you have a patient with persistent ventricular fibrillation despite three shocks, it’s now advised to delay further attempts until it’s possible to raise the core temperature to >30°C. This is a key number becuase we also do not give adrenaline in patients at a temperature <30°C. As the temperature rises to between 30-34°C, increase your adrenaline administration intervals to 6-10 minutes.
The new ACLS guidelines also discuss the use of extra-corporeal life support (ECLS) and suggest that where possible, the use of ECMO is largely recommended over cardiopulmonary bypass (CPB). However, if access to these services isn’t available within about 6 hours, non-ECLS rewarming should be started in a peripheral hospital.
Drowning
Drowning is the process of experiencing respiratory impairment from submersion/immersion in liquid.
Respiratory impairment is the key thing here. As Jimmy said, the d-word has no business being there without that. I mean, otherwise you just got wet…
There are some older terms that you may hear still floating around to discuss different variations, but they’re neither commonly used nor useful these days, so we’ll leave them out of the discussion here.
Only meaningful distinction is really fatal or non-fatal.
What about salt or fresh water?
Doesn’t really matter as much as you might think. The salt means there’s a different osmotic gradient, but that doesn’t seem to have any greater effect on the degree of lung injury or electrolyte abnormalities.
Fresh water is a more hospitable environment, so you do get a greater microbial burden with fresh water.
So how the damage is done is determined by how much rather than what kind of water.
More water means more surfactant washout, more damage to the alveolar-capillary membrane, more frothy pink stuff in the tube from the bloodstained pulmonary oedema, more atelectasis, V/Q mismatch, bronchospasm and decreased lung compliance
ARDS is an obvious complication considering all this, but you may also see arrhythmias, ischaemic cardiomyopathies, laryngospasm, pulmonary oedema, hypoxic ischaemic encephalopathy, aspiration pneumonitis and… hypothermia.
Resources & References
Modifications in life support for hypothermia:
https://www.ahajournals.org/doi/full/10.1161/circ.102.suppl_1.I-229Comparison of temperature measurement devices vs gold standard
https://link.springer.com/article/10.1007%2Fs00134-002-1619-5
Metabolic acidosis during profound hypothermia
Hypothermia Outcome Prediction after Extracorporeal Life Support for Hypothermic Cardiac Arrest Patients. Estimation of the survival probability using HOPE.
https://www.hypothermiascore.org/
