Which nursing action may cause an after drop in a patient with moderate hypothermia?

10 What stabilizing measures should prehospital care providers undertake?

The patient should be handled as gently and carefully as possible because ventricular fibrillation has been ascribed to excessive mechanical stimulation. In cases of immersion, wet clothing should be removed. Further heat loss should be limited by provision of a dry and insulated environment. Blankets, sleeping bags, or aluminum-coated foils can be used for this purpose. Ethanol should not be given because it suppresses shivering thermogenesis, promotes peripheral vasodilatation, and can prompt hypoglycemia in these typically glycogen-depleted patients. Massage of the extremities provides unnecessary physical stimulation and, like ethanol, can mitigate both shivering and appropriate peripheral vasoconstriction. If venous access can be acquired, 50 mL of 50% dextrose, 2 mg of naloxone, and 100 mg of thiamine are appropriate. A fluid challenge of 50%-dextrose normal saline, 250–500 mL (preferably heated to 43°C), is indicated because the majority of patients with moderate to severe hypothermia have sustained cold-induced diuresis. Lactated Ringer's solution is a less preferred crystalloid because the hypothermic liver is less able to metabolize lactate.

AER measures are safe in minimally hypothermic patients, but unnecessary. In a patient with moderate to profound hypothermia, only truncal AER should be considered. The only method of ACR appropriate in the field is heated, humidified oxygen. Several portable devices are available for this purpose.

Hypothermia: Guidelines 2000 for CPR and ECC. 102:1–229, 2000.

Key Points: Hypothermia

Endotracheal intubation is a safe and appropriate procedure in patients with hypothermia.

Rigor mortis, lividity, and fixed pupils do not necessarily portend death in severe hypothermia.

Doppler devices and ultrasound can be used to ascertain the presence of pulse and cardiac activity, respectively.

Cardioversion of hypothermia-induced ventricular fibrillation is unlikely to be successful at core temperatures below 28–30°C.

External core rewarming is indicated in severe hypothermia when there is little or no cardiac activity.

Introduction and Background

Hypothermia is defined as a core temperature of less than 35° C (95° F).1 Primary (“accidental”) hypothermia is a result of environmental exposure, while secondary hypothermia is a result of underlying disease. Hypothermia is more frequently seen in cold environments and in winter months,2,3 but children may become hypothermic in any location or climate. While the role of therapeutically induced hypothermia is an area of ongoing investigation for a number of different medical conditions,4–12 this discussion focuses on accidental hypothermia.

Classification

Hypothermia can be classified as accidental, primary, and secondary. Cases of idiopathic hypothermia, sometimes spontaneous and episodic, have been reported. These are usually not severe or protracted, however. Hypothermia is also classified by severity as mild (32–35°C), moderate (28–32°C), and severe (<28°C). Hypothermia may also be acute (minutes), subacute (hours), or chronic (days) depending on the time of development.

Hypothermia may also be thought of in terms of excessive heat loss (cold weather or immersion in cold water), abnormal heat conservation and reduced heat production [hypothyroidism, hypoglycemia (substrate depletion), hypopituitarism, hypoadrenalism, uremia, spinal cord transection above T1, peripheral neuropathy, autonomic neuropathy, and certain drugs (alcohol, barbiturates, and neuroleptics)], and defective heat regulation [hypothalamic lesions including Wernicke's encephalopathy, strokes, tumors, head trauma, and congenital abnormalities (e.g., Shapiro's syndrome)].

Abstract

Hypothermia most often results from inadequate heat production, usually because of prolonged exposure to a cold environment (accidental hypothermia), but sometimes because of endocrinopathy, abnormal glucose metabolism, or drugs. Hypothermia can also be caused by excessive heat dissipation, malfunction of the thermoregulatory system, or interruption of effector pathways. Hypothermia has profound effects both on nervous system function and on the physiology of numerous other organ systems, especially the cardiovascular system. It is treated by rewarming, which can be external (either passive or active) or central (active). When possible, the underlying cause should also be identified and treated.

17 What are the important side effects of therapeutic hypothermia?

Hypothermia affects nearly every organ system and so has myriad side effects of variable clinical significance. Electrolyte abnormalities and infectious complications are most likely to concern the clinician. Electrolyte abnormalities commonly require management and must be actively monitored. During cooling, hypomagnesemia and hyperglycemia are common, whereas, during rewarming, hypoglycemia and hyperkalemia are dangers. Most centers check electrolyte panels every 30 to 60 minutes during cooling and every 4 to 6 hours during the maintenance of hypothermia. Hypothermia may be immunosuppressive via a number of mechanisms and masks the normal febrile response to infection. Many centers draw routine daily blood cultures during induced hypothermia to monitor for infection. An aggressive stance toward investigation and empiric treatment of other potential infectious sources is appropriate, though routine antibiotic prophylaxis is not justified.

Key Points

Hypothermia

Rigor mortis, dependent lividity, and fixed pupils do not reliably indicate death in severe hypothermia.

Endotracheal intubation is safe and has the same indications as in normothermia.

VF should be treated with standard ACLS in conjunction with rewarming, but multiple rounds of cardioversion and amiodarone should be avoided when the temperature is < 30° C.

CPR should be performed in patients with hypothermia without spontaneous circulation.

CPB should be initiated in patients with severe hypothermia without return of spontaneous circulation.

Therapeutic hypothermia (temperature = 30° C-34° C) is recommended for comatose survivors of cardiac arrest and is likely to be used for more conditions in the future.

General Information

Hypothermia is a decrease in body temperature to a level that is below normal. The normal metabolism and exercise of the human body produce heat. The body tries to save or lose this heat to keep the body's temperature within a narrow range.

The vascular system is the prime regulator of body temperature. Because of aging changes, it is possible for elderly patients to lose heat or to fail to conserve heat faster than at a younger age. Elderly patients are particularly susceptible to hypothermia.

Besides vascular changes, a number of other factors can contribute to hypothermia. Malnutrition, which can be thought of as lack of fuel, is one important factor. Changes in the central nervous system or the brain, such as those that occur in dementia, can impair one's ability to feel cold so that one does not take the protective actions necessary to warm up. Loss of the usual insulating layer of fat below the skin may be another factor.

Drugs, particularly sedatives and tranquilizers that can impair perception of cold, can lead to hypothermia. Any disease that decreases the ability to feel cold, impairs the response of the heart and the circulation, causes inactivity, or causes a decrease in exercise can also promote the development of hypothermia.

Normally, when a person chills, the response includes shivering, which is a kind of exercise of the muscles that promotes warming. Shivering is often absent in elderly patients with hypothermia. These patients feel cold not just in the extremities, which can be normal, but also in the trunk. They appear pale. As the cold progresses, it depresses bodily functions. Finally, coma may occur.

Risk Assessment and Implications

Hypothermia may benefit the patient by providing organ protection against ischemia. Oxygen utilization is halved for each 10°C decrease in normal body temperature. Mild hypothermia (33°C to 36°C) provides important central nervous system protection. There is increasing evidence that it may play a protective role after stroke and cardiac arrest due to ventricular fibrillation.

Even mild hypothermia induces platelet dysfunction and may increase intraoperative bleeding. Platelet thromboxane generation, required for platelet aggregation and local hemostatic vasoconstriction, is impaired by cold. Quantitative laboratory assessment is misleading because blood samples are warmed to 37°C. Massive transfusion of cold blood can induce severe hypothermic coagulopathy with irreversible bleeding. There is now evidence that even mild intraoperative hypothermia may increase the risk for postoperative wound infection, possibly due to vasoconstriction with low tissue oxygen tension. This impairs chemotaxis and facilitates bacterial growth.

Severe hypothermia (<33°C) has adverse effects on almost every organ system (Table 100-3; Fig. 100-2).

Emergence from anesthesia may be delayed by a number of cold-induced factors, including impairment of central nervous system function (e.g., obtundation, confusion, somnolence), slowed hepatic or renal clearance of anesthetic drugs and neuromuscular blocking agents, and impaired ventilatory response to hypoxemia and hypercarbia.

Cold-induced vasoconstriction and increased systemic vascular resistance may exacerbate postoperative hypertension (blood pressure of 160/90 mm Hg in the patient in the case synopsis is characteristic). Together with high norepinephrine concentrations, both may produce myocardial ischemia in susceptible patients.

The consequences of rewarming from hypothermia may outweigh the implications of hypothermia itself. Postoperative shivering greatly increases oxygen demand and carbon dioxide production, leading to increased minute ventilation, work of breathing, and oxygen consumption. If minute ventilation is fixed (mechanical ventilation) or suppressed (by anesthetic agents or opioids), hypercarbia and acute respiratory acidosis may result. When oxygen consumption is increased but cardiac output cannot compensate, oxygen extraction increases, setting the stage for hypoxemia and its sequelae. Shivering can also cause patient discomfort and other adverse sequelae, such as wound disruption and increased bleeding or intracranial and intraocular pressures.

Subsequently, rewarming vasodilatation may unmask hypovolemia, resulting in even more dangerous hypotension and tachycardia.

4. Hypothermia

Hypothermia is a neuroprotective approach that antagonizes multiple injury mechanisms in all cells. In a review of hypothermia in stroke treatment and the description of a new approach and experimental studies with local hypothermia, we have cited many current references in both clinical and animal model studies [18]. The efficacy of hypothermia in reducing ischemia-induced brain injury is very well described. However, the challenges for hypothermia-induced neuroprotection in the clinical setting include the best route of delivery (surface cooling or endovascular), the difficulties in patient management, and the potential secondary adverse events [18]. In this previous report, we also reviewed findings from combined studies of drug therapies with hypothermia including work by Aronowski and Grotta and colleagues on the robust effects of caffeinol and other agents, including free radical scavengers, magnesium, and growth factors [18]. Overall, the preclinical findings of hypothermia alone and hypothermia plus adjunctive drugs have been quite remarkable.

Hypothermia

Hypothermia has been shown to provide protection against the devastating effects of prolonged ischemia. In animal models, hypothermia profoundly decreases the release of glutamate, free radical activity, and enzymes responsible for transducing intracellular Ca2+ signals. Hypothermia is currently employed in many centers for comatose patients after transient global cerebral ischemia associated with cardiac arrest as well as in neonatal hypoxic injury, but its utility in stroke is less clear. Animal studies of postischemic hypothermia provide conflicting data, with some suggesting that cooling applied after an ischemic period delays rather than prevents ischemic injury. It is clear that the degree of neuronal protection varies with the length of delay to administration and the duration of hypothermia. The well-known risks of hypothermia, such as ventricular fibrillation, acidosis, and pneumonia, need to be considered when contemplating its use as a therapeutic modality.