Hypothermia is an entity that can be due to environmental as well as physiologic issues. Various levels of hypothermia exist and are categorized as the following: mild (32-35 C), moderate (28-32 C) and severe (>28 C). Each classification requires varying levels of attention to resuscitation as each has varying levels of pathophysiologic consequence.
Let’s first consider presentation and pathophysiologic issues that result from hypothermia. Vigorous shivering that creates a large amount of heat for the patient as the body is trying to rewarm itself marks mild hypothermia. Other presenting symptoms include cold diuresis and cool blanched skin. Moderate hypothermia may have some cardiac instability, slurred speech, depressed shivering response, altered mental status and loss fine motor skills. In severe hypothermia, patients will no longer be shivering, cold edematous skin, hypotension, hypoventilation, severe altered mental status or coma, fixed dilated pupils (which is not a function of brainstem death) and some cases death.
Cardiovascular instability in moderate to severe hypothermic patients is important to identify and address. Hypothermia slows depolarization and repolarization, therefore, it manifests as prolonged PR, QRS and QT intervals. The classic EKG finding (found in ~80% of hypothermic patients) is the Osborn wave (J-wave) pictured below:
These manifestations are related to temperature and disappear with rewarming. Other rhythm abnormalities may also occur including atrial fibrillation (supraventricular arrhythmias), AV blocks, ventricular tachycardia and ventricular fibrillation. Vtach/Vfib may be a precipitated by acidosis, hypocapnia, physical manipulation or hyperkalemia. Of note, patients are typically hypokalemic in mild hypothermia and progress to hyperkalemia in severe hypothermia. Vtach/Vfib is rare presenting symptom as asystole/PEA are more common findings.
Other organ systems are also affected by hypothermia. Many patients have resultant renal failure. The resultant acidosis associated with hypothermia as well as enzymatic dysfunction strongly distort the coagulation cascade. Therefore patients will have prolonged coagulation times. In addition, hypothermia may cause for bone marrow suppression, thrombocytopenia and splenic sequestration.
When treating a hypothermic patient, the medical team should start with a primary survey, resultantly exposing the patient and begin rewarming efforts. In situations where patients have been immersed in cold water, the removal of wet clothes is imperative. Accurate temperature monitoring for rewarming is also very important. It is also important to mention that sources of trauma or other causes of hypothermia including medication intoxication and infection need to be pursued during evaluation of the patient. Patients should have core temperature monitored because core temperature may drop with active rewarming as cold blood from the periphery is circulated to the core. Probes may be placed in the bladder, rectum or endotracheal tube to accurately assess core temperature. As per a review article by Aslam et al., (2006) no large trials exist distinguishing the benefit of slow rewarming versus rapid rewarming. Anecdotal evidence does exist that slow rewarming is preferred. Using external rewarming techniques including bear hugger, warmed IV fluids, warm blankets as well as warm water bottles in the axillae and groin are recommended as patient is being transported. Goheen et al (1997) suggested forced hot air for radiant rewarming was effective in a model where shivering was blunted and reduced drop in core temperature by 30-40%. The same study also suggested that inhalation rewarming was as effective as external rewarming (blankets etc.) and provided no advantage in their model (note: small sample sizes).
Mild and Moderate hypothermic patients who are hemodynamically stable (perfusing rhythm) should be treated with external rewarming alone. Care should be taken when placing IV lines and moving the patient as any aggressive movement may precipitate ventricular dysrhythmia. Of note, certain medications including some opiates and cardiac medications may impair the shiver response. As per the AHA, the regular ACLS pulseless arrest algorithm can treat patients who are in cardiac arrest and have a core temperature above 30 C. Those patients that are severely hypothermic have a slight modification to the algorithm when Ventricular tachycardia or fibrillation is being addressed. In these patients, an initial shock and medication bolus should be given. If the rhythm is not immediately converted, further defibrillation attempts and medication boluses should be delayed until the patient is rewarmed to >30 C. Invasive techniques including chest tube irrigation, bladder and gastric irrigation with warm saline, intubation and even peritoneal lavage should be considered. Cardiac bypass is considered the most effective means of rewarming. Dialsysis and ECMO can also be considered. An asystolic patient that goes into PEA is likely achieving a reperfusion rhythm.
“A patient is dead until they are warm and dead.” This has been then typical clinic mantra we have followed in resuscitation. When a patient has arrested and arrives at the hospital it may be unclear if the hypothermia is primary or secondary. Clinic judgment should trump this mantra when deciding to withhold resuscitative efforts.
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9) Image attained from Wikipedia at the following site: http://en.wikipedia.org/wiki/Osborn_wave