Accidental hypothermia is an environmental condition with basic principles of classification and resuscitation, and is associated with significant morbidity and mortality [1]. Mortality rates are high despite aggressive treatment [2]. Hypothermia is defined as a decrease in core body temperature (CBT) below 35°C. Hypothermia can be staged in to mild (32°C-35°C), moderate (30°C-32°C), and deep (< 30°C) [3]. The latter group is associated with significant risk of circulatory arrest.

The considerations regarding acute illness and complicating hypothermia presents some challenges concerning stabilization and treatment.

We report a case of an elderly woman found comatose outside on a cold winter morning. The patient had developed severe hypothermia was hypo ventilating and had sinus bradycardia. As a result of the severe hypothermia we expected the patient to develop life-threatening complications during her hospital stay. We want to describe the course of a patient undergoing rewarming without any complications despite high age and comorbidity.

On a cold winter morning with an outside temperature of 1°C, an 88 year-old woman was found lying in her garden in front of her house. The patient was of normal stature, dependent on daily care for medication, but lived alone in a house with a medical history of severe dementia, first-degree atrioventricular block and stroke. The ambulance call center dispatched paramedics and an emergency doctor to the site within 10-15 minutes. The patient was unresponsive, with a GCS (Glasgow Coma Score) of 4, only providing unintelligible sounds. She was breathing slowly and had a heart rate of 25-30 and a sinus rhythm. The patient was moved carefully to the ambulance, and an initial temperature reading showed 19°C. A large caliber peripheral intravenous line was provided for rewarming with heated isotonic crystalloid and a warm blanket. An uncomplicated, rapid sequence induction and subsequent intubation was performed using alfentanil 1 mg, propofol 50 mg and suxamethonium 50 mg iv. She was admitted to the emergency room one hour after being found, without any complications during transport. Core temperature in the bladder was not immediately measurable, but two hours later it was registered to 21.1°C, despite on-going treatment with external warming using a Bairhugger^® blanket and almost 2 liters heated crystalloid. The patient was subsequently admitted to the intensive care unit (ICU).

She was normoventilated using the PRVC mode, FiO₂ 0.5 and PEEP 5 cm H₂O). She was severely hypotensive (non-invasive blood pressure, 60/20 mmHg) and bardycardic (30 beats/minute). An ECG showed no sign of ischemia. A feeding tube was placed to avoid aspiration.

An arterial blood gas analysis showed pH 7.29, base excess-10.3 mmol/L, plasma-glucose 9.7 mmol/L. Further laboratory data revealed hemoglobin 7.7 mmol/L and lactate 3.5 mmol/L, INR 1,1 and thrombocyte count 235 mmol/l.

At the ICU we continued internal and external rewarming according to Danish Guidelines [3] by heated crystalloid infusion and warmed humidified oxygen via a Bairhugger®. No epinephrine was used on the premise that drug responses could be unpredictable due to hypothermia until core temperature had reached 30°C.

Physical manipulations were kept at a minimum due to the risk of cardiac arrhythmias.

During rewarming at the ICU, the patient was circulatory stable and gradually reached 35°C the next day. Approximately 3.5 liter of warmed crystalloid was administered intravenously during her stay at the ICU. Urine production began as the core temperature reached 30°C, and the patient transiently exhibited atrial fibrillation at 34°C, which self-converted to normal sinus rhythm without any medication. A small amount of propofol for sedation and tube acceptance was administered during the first night.

The day after, the patient was extubated; she was fully awake and mentally inconspicuous. She was discharged from the ICU the next day, and two days later she was discharged to home in her habitual condition.

Due to a decreased physiologic reserve, social isolation, chronic diseases and medications that impair compensatory responses, the elderly are at increased risk of developing hypothermia and accompanying complications, and should therefore be urgently assessed [4].

Hypothermia is related to a variety of physiological changes affecting most organ systems [5,6]. Some of these changes occur at critical points in the development of hypothermia, but in the bird’s eye view, some general temperature dependent effects may be observed: consciousness, cerebral and total body metabolic rate, oxygen consumption, CO₂ production, cardiac output, renal blood flow and respiratory function are all progressively reduced by depth of hypothermia.

Core body temperature is normally tightly regulated by an effective thermoregulatory system, and even during different stages of illness the regulatory system maintains a stable core body temperature.

Normal body temperature is controlled by effective thermoregulatory defences [7]. Thermal information from skin, peripheral tissues and core organs are integrated and processed prior to arriving at the hypothalamus, which is the dominating thermal control center. A balance between heat production (thermogenesis) and heat elimination (thermolysis) is maintained. This active equilibrium keeps the normal core body temperature (CBT) on an average 37°C [8]. The effectiveness of the thermoregulation decreases with age due to a decrease in sensitivity to small temperature changes, a lower rate of metabolism, a less effective vascular response and change in body mass composition [9]. The initial response of the body to cold exposure is to maintain a normal CBT by means of active movements, peripheral vasoconstriction and involuntary shivering. The risk of clinically significant arrhythmias including cardiac arrest increases as the CBT drops below 32°C, and increases substantially if the temperature becomes less than 28°C [1].

In deep hypothermia, a relatively high blood flow is distributed to the brain. Hypothermia registered in the hypothalamus and the fourth ventricle is partly responsible for shivering and cognitive and respiratory dysfunction. Hypothermia affects cerebral functioning, with initial impairment of cerebral cortex, followed by subcortical structures. Finally, respiratory arrest occurs when medullary cellular activity is suppressed; at 20°C, a flat EEG and no respiratory response by CO₂ increase or hypoxia may be observed. Although the coldest core temperature a person has been revived from is 13.7°C [7]. Asystole often occurs at 18°C. The oxyhaemoglobin dissociation curve initially shifts to the left, causing impaired oxygen delivery and tissue hypoxia, which in turn causes anaerobic metabolism, lactate acidosis and an eventual right shift of the dissociation curve. Fluid shifts predispose to noncardiogenic pulmonary oedema, and the functions of respiratory muscles are gradually impaired. Heart rate becomes bradycardic and unresponsive to atropine, a variety of ECG changes occurs due to temperature sensitive purkinje fibers, and catecholamine release is gradually blunted. Finally, an increased risk of arrhythmias become resistant to cardio version attempts, reduced chest wall elasticity makes chest compressions difficult, and most antiarrhythmic agents (perhaps except for bretylium) are largely rendered ineffective. Because the pacemaker cells are extremely sensitive at this point, non-life threatening arrhythmias seen below 34°C should not be treated with defibrillation or drugs. Changes in ADH secretion, tubular reabsorption and renal blood flow cause cold-induced diuresis with the risk of hypovolemia. Hypokalemia may occur due to the influx of potassium into cells. However, it is generally accepted that natriuresis and pH changes should not be actively corrected, since they may lead to ventricular fibrillation as well.

Several complex events occur in the coagulation system during hypothermia, most of which lead to increased bleeding tendency. The activity of coagulation factors for the clotting cascade is progressively reduced with decreasing temperature, bone marrow function is suppressed, vascular permeability is increased, and thrombocytopenia occurs due to sequestration in the liver and the spleen. Fibrinogen levels and fibrinolysis increase, with impaired endothelial synthesis of prostacyclin promoting platelet aggregation. In spite of this hypocoagulable state, microinfarcts and even DIC syndrome may appear. Immune function is inhibited by leukocyte depletion and impaired neutrophil migration and phagocytosis ability. Local vasoconstriction decreases oxygen partial pressure in tissues, macrophages become less responsive to interferone, and increased corticosteroid levels enhance immunosuppression [6]. Insulin levels may vary and glucagon levels increase, but blood glucose depends primarily on the metabolic state rather than the degree of hypothermia. Mitochondrial dysfunction may lead to apoptosis.

The effects of hypothermia on drug disposition are not fully understood due to the complex interaction between pharmacokinetics including metabolism and drug response [7]. Drug metabolism during hypothermia may be more complex than simply increasing the concentrations of active metabolites. The speed of enzyme-mediated reactions is temperature-dependent, and the speed of various reactions is significantly influenced by hypothermia. Decreased splanchnic blood flow and failure to utilize glucose suppresses hepatic detoxification and conjugation processes, prolonging the elimination half-lives of many drugs [8]. Having said this little is actually known about pharmacokinetics and dynamics during hypothermia; blood/gas solubility of gas anesthetics is increased, causing longer emergence time. When CBT is below 30°C, adrenalin and other vasoactive drugs should be administered with great caution. Reduction in vasoactive drug metabolism may cause potentially toxic concentrations [8].

In retrospect, we reflect on the various procedures done to support vital organ functions, and some of the concurred conditions. In this particular case report, the following benefits and disadvantages may be addressed: The advantages of sufficient oxygenation and prevention of aspiration outweigh the risk of triggering ventricular fibrillation by performing a tracheal intubation [9]. We rapidly infused warm fluids consisting of crystalloids as part of an internal rewarming regimen. This was combined with external rewarming. ECMO (extra corporal membrane oxygenation) was not considered because of advanced age and comorbidity. Epinephrine was actively withheld to maintain a sufficient circulation. The body responds poorly to vasoactive drugs at low temperatures, and the reduction in metabolism may give rise to potentially toxic concentrations when administered on a repeated basis. Hypothermia may decrease insulin sensitivity and the amount of insulin secreted by the pancreas, leading to hyperglycaemia. Doses of insulin required to maintain normoglycaemia are likely to decrease when the patient is rewarmed, meaning that hypoglycaemia may easily develop in the rewarming phase [10].

In conclusion, the actions during treatment of a severe hypothermic patient should always cause the practitioner to reflect on the physiological and pharmacological changes that depart from normal resuscitative practice, and a less aggressive treatment approach. Especially concerning insertion of central lines due to the risk of triggering cardiac arrhythmias, and the administration of virtually all kinds of drugs due to the changes in drug metabolism and effect. Although we did not encounter a plethora of physiological complications in this case story, we want to highlight that simple measures may be a successful strategy even in fragile, elderly patients with severe accidental hypothermia.

MV conceived of the case, did the clinical research and drafted the manuscript. KJ did the pharmacological research and assisted in writing the manuscript. VLL did research and assisted in drafting the manuscript.

All authors have read and approved the final manuscript.

This manuscript is not previously published or under consideration by another journal

None

The authors have no conflicts of interest to disclose.