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Induced hypothermia in neurocritical care: a review.


Induced hypothermia (IH) continues to become a more prevalent treatment modality in neurocritical care. Reducing core temperature has been shown to protect brain tissue during injury and disease. IH has been particularly beneficial in the medical management of refractory intracranial hypertension and malignant cerebral edema. These pathologies are often the result of diffuse cerebral edema after traumatic brain injury, malignant ischemic stroke, or intracerebral hemorrhage. Although there are many benefits to IH, it is not without complications. Chief among these is shivering, which decreases oxygen delivery to brain tissue, increases metabolic demands, and consequently reduces nutrient delivery. This article will review indications for IH administration, methods of providing IH, nursing responsibilities, and identifying and/or managing complications.

Keywords: cerebral edema, hypothermia, intracranial pressure, neurocritical care, therapeutic hypothermia


Induced hypothermia (IH) has been used in postcardiac-arrest patient populations for decades because of its cardioprotective properties (Peberdy et al., 2010). It continues to become more prevalent in neurological aggregates as IH has been associated with decreased damage to the brain and improved patient outcomes. This is due, in part, to reduced core body temperature delaying the development of cerebral ischemia. IH is also known as therapeutic hypothermia or temperature targeted management and is defined as the intentional reduction of core body temperature to 32[degrees]C-35[degrees]C (Urbano & Oddo, 2012). This is a reduction of at least 2[degrees]C from homeostasis because normal core body temperature (or normothermia) is defined as 37[degrees]C. IH in neurocritical care has the potential to offer new opportunities for reducing morbidity and mortality. The purpose of this article is to review the pathophysiology of common brain injuries, indications for administering IH, benefits and complications of IH, nursing implications for accurately assessing and treating shivering, and a brief review of administering IH via the Arctic Sun machine (see Supplemental Digital Content 1 at

Traditional Management of Cerebral Edema and Intracranial Hypertension

After a neurological insult, the body has two innate compensatory mechanisms that have a temporizing effect to accommodate swelling and intracranial pressure (ICP) changes. The primary mechanism involves shunting cerebral spinal fluid from the cranial subarachnoid spaces into the spinal subarachnoid space (Ropper, 2012). The other mechanism involves the shunting of blood out of the cranial vault via the jugular veins or through the emissary and scalp veins (Morton & Ellenbogen, 2012). Once these anatomic compensatory methods are exhausted, hyperosmolar therapy is often implemented (Ennis & Brophy, 2011). Because the brain parenchyma is predominately composed of water (nearly 80%), the brain tissue is extremely responsive to osmotic gradient shifts (Ropper, 2012). Hyperosmolar therapy works by shifting the osmolar gradient and pulling free water from the brain (cranial vault) into the serum. Several medications may be deployed including mannitol (Osmitrol) and hypertonic saline solutions (1.5%, 3%, 7.5%, and 23.4% NaCI). Additional management strategies include hyperventilation, opiate medication administration, and deep sedation via propofol (Diprivan) or pentobarbital (Nembutal). Surgical intervention may include decompressive hemicraniectomy to allow for space additional swelling to reduce the risk of cerebral herniation. Once these options have been optimized, hypothermia is emerging as the next intervention along the treatment spectrum.


Traditionally, IH has been used for patients after cardiac arrest. The American Heart Association highlights that IH, in conjunction with treatment of the underlying cause of cardiac arrest, has been shown to influence survival and neurological outcomes (Peberdy et al., 2010). This is recommended for cardiac arrest patients with ventricular tachycardia or fibrillation who fail to regain consciousness after return of spontaneous circulation (ROSC; Nunnally et al., 2011).

Refractory intracranial hypertension may be caused by any of the aforementioned disease processes once conventional medical treatment has failed (e.g., hypertonic saline administration, hyperventilation, etc.). IH is implemented immediately after failure of traditional therapies because a delay in management of intracranial hypertension may be life threatening. For instance, if a patient has intracranial hypertension despite receiving a hypertonic saline infusion and fails to respond to additional hypertonic boluses, hyperventilation, and so forth, with a reduction in ICP to <20 mmHg, then IH will be initiated. IH is indicated for refractory intracranial hypertension, which is defined as an ICP > 20 mmHg (Perez-Barcena et al., 2008). The clinical significance of intracranial hypertension is that it can disrupt blood flow to the brain tissue and compress vital structures leading to cerebral herniation and death.

Performing IH

IH is typically achieved using one of two methods. Each addresses one of the heat capacitances or storage units in the body. The first capacitance is the core; the second capacitance is the skin (Riggs, 1970). The first cooling method involves the placement of an endovascular catheter in the femoral vein, which is then advanced to the inferior vena cava. Cooled intravenous fluids may be administered via the endovascular catheter (Geocadin & Carhuapoma, 2005). This method achieves the goal temperature by cooling the core. This method is typically used for post-cardiac-arrest patients. This method tends to be avoided in IH for refractory intracranial hypertension because the duration of therapy is longer than post cardiac arrest (24 hours) and the risk of infection is greater in the setting of a femoral catheter. These catheters are magnetic resonance imaging compatible (Zoll Medical Corporation, 2011). The second cooling method involves using external pads that are placed along the patient's trunk and thighs. These pads connect directly to a machine through tubing. The machine circulates cooled water through the pads, ultimately reducing the patient's core temperature. Both methods require a continuous temperature probe so that cooled infusions and/or the machine can regulate the water temperature in response to the patient's core temperature until the goal IH temperature is achieved (Geocadin & Carhuapoma, 2005). Continuous temperature measurements are commonly achieved via foley catheter or esophageal temperature probes.


To understand the physiologic significance of cerebral edema and intracranial hypertension, it is helpful to review the Monro-Kellie hypothesis. This concept describes the skull, or cranial vault, as a rigid box with a finite volume. Within the cranial vault, the sum of intracranial volumes of blood, brain matter, and cerebral spinal fluid remains constant. Therefore, any increase in one of these compartments must be met with a proportional decrease in another compartment or the ICP will increase (Rangel-Castilla, Gopinath, & Robertson, 2008). The equation below shows this tenet:

[V.sub.cranium] = [V.sub.Blood] + [V.sub.brain matter] + [V.sub.CSF] + [V.sub.tumor]

An additional category accounts for a tumor or mass lesion, which would also increase the cranial contents, and ultimately, the ICP.


There are several pathologies that can cause cerebral edema and intracranial hypertension. Below are three examples of common pathologies:

1. Traumatic brain injury (TBI) is characterized by stages. The first stage is the initial insult that causes direct tissue damage. The injury altered cerebral blood flow (CBF) and cellular metabolism. The insult triggers a response that closely mimics that of an ischemic injury. Ultimately, the metabolic pathways shift to anaerobic because there is insufficient oxygen. This leads to lactic acid production, increased membrane permeability, and edema (Wemer & Engelhard, 2007). The second stage involves the opening of ion channels secondary to inadequate adenosine triphosphate supply. This favors membrane depolarization with an exaggerated neurotransmitter response (glutamate and aspartate). Calcium moves intracellularly and activates lipid peroxidases, proteases, and phospholipases. Additional enzymes are released, which change the structural integrity of the cellular membrane and ultimately cause apoptosis (Wemer & Engelhard, 2007). These inflammatory responses result in cerebral edema.

2. Ischemic stroke may be caused by (a) thrombus or (b) embolus, which occludes a cerebral artery impeding blood flow. The ischemia that ensues causes the release of destructive vasoactive enzymes by the endothelium, leukocytes, platelets, and other neuronal cells (Shah, n.d.). The ischemic injury at the molecular level is the result of an exaggerated release of neurotransmitters (glutamate and aspartate). Again, these substances cause the calcium channels to open, leading to membrane depolarization. The influx of calcium into the cell triggers destructive enzymes (proteases, lipases, and endonucleases) to discharge cytokines, disrupting the continuity of the cellular membranes (Shah, n.d.). The inflammatory response involves tumor necrosis factor as well as leukocytes and cytokines. The leukocytes arrive to the damaged tissue, contribute to obstruction of the microcirculation, and stimulate vasoactive substances to be released (including cytokines), which increase permeability, platelet aggregation, and leukocyte attachment to the endothelial wall. These changes lead to inflammation and swelling (i.e., cerebral edema).

3. Intracerebral hemorrhage consists of three phases: (a) initial hemorrhage, (b) hematoma expansion, and (c) edema. Once the initial hemorrhage has occurred, the management focuses primarily on controlling the extent of the subsequent phases. Hematoma expansion can lead to intracranial hypertension as the volume of blood in the cranial vault increases. This may lead to impaired venous outflow, which stimulates the release of thromboplastin, which leads to coagulopathy (Magistris, Bazak, & Martin, 2013). Edema occurs because of inflammation and disruption of the integrity of the blood-brain barrier (Magistris et al., 2013).

Although the precise physiology of the therapeutic benefits of IH is not completely understood, there are certain aspects that have been identified. Neuronal injury often includes increased levels of neurotransmitters, specifically glutamate and aspartate, which activate receptors along the cell surface leading to an influx of calcium and sodium (Dash, 2012). The increase in intracellular calcium leads to apoptosis, or cellular death, as the presence of calcium activates proteases, lipases, and free radical release and alters mitochondrial function. The proteases and lipases break down proteins and lipid membranes compromising cellular stability and structure. Similarly, the increased sodium leads to cellular damage by causing swelling of the neuronal cells (Dash, 2012). The principal physiological effect of IH focuses on delaying the cascade of events from the initial injury to the secondary injury. It is the secondary injury that clinicians attempt to manage medically and pharmacologically. For example, if a patient experienced a hemorrhagic stroke, the initial area of bleeding would be the primary injury. As a clinician, once a hemorrhagic stroke has occurred, the event cannot be reversed. Therefore, the aim focuses on preventing the secondary injury that ensues. In this example, the secondary injury includes hematoma expansion, which may result in increased ICP and/or damage to a larger territory of the brain tissue (Broessner, Fischer, Schuber, Metzler, & Schmutzhard, 2012). IH is emerging as a therapeutic intervention to control the extent of secondary injury.


IH offers several benefits. Chief among these is a reduced metabolic rate. This is important because it decreases oxygen and glucose consumption in the brain tissue. The brain is a unique organ because, unlike the other organs of the body that can temporarily survive in an anaerobic state, the brain cannot. The brain only uses glucose as an energy source except during periods of severe starvation (Berg, Tymoczko, & Stryer, 2002). Because the brain lacks energy storage units, it requires a constant supply of glucose. To put this in perspective, during periods of rest, the brain will consume approximately 60% of the entire body's glucose supply (Berg et al., 2002). These metabolic effects are thought to be the basis for the neuroprotective qualities associated with IH.

Second, hypothermia allows brain tissue to tolerate lower thresholds of oxygen delivery (Sakoh & Gjedde, 2003). This aids in adapting to a lower blood flow rate while continuing to provide the necessary amount of oxygen for brain tissue viability. In animal studies, the CBF and oxygen consumption decline to 50% of the baseline in the 3- and 5-hour marks after IH was implemented (Sakoh & Gjedde, 2003). There are limited data regarding outcomes to date.

Third, IH shifts the oxyhemoglobin curve to the left. Because the metabolic rate is reduced, oxygen consumption and carbon dioxide production are also decreased (Hooley, 2015). Carbon dioxide dilates cerebral blood vessels, which can increase the volume within the cranial vault (skull) and exacerbate intracranial hypertension. Historically, hyperventilation was used as a temporary means to reduce intracranial hypertension; however, due to its transient effects, it is rarely used (Rangel-Castilla et al., 2008).

Fourth, IH reduces cerebral edema (Jacob, Khan, Jacobs, Kandiah, & Nanchal, 2009). Brain edema peaks between 24 and 72 hours after injury. The inflammatory response often disrupts the blood-brain barrier and compromises vascular permeability. When this barrier is disturbed, it allows for the proinflammatory mediators that are released during brain injury to penetrate in the brain tissue, causing severe damage. Therefore, hypothermia helps to support and reestablish the weakened blood-brain barrier, which results in neuroprotection (Schmutzhard, Fischer, Dietmann, & Brossner, 2012).

Additional benefits of IH include the following: slowing the inflammatory response, reducing free radicals, stabilizing cellular membranes, raising the seizure threshold, and preserving the integrity of the bloodbrain barrier. Table 1, available as Supplemental Digital Content 2 at, provides an organized description of the common results of brain injury and the intended effects of IH on each.

Review of Literature

The cardiac literature supports improved neurologic outcome in post-cardiac-arrest patients who sustained an out-of-hospital ventricular fibrillation arrest and were cooled between 32[degrees]C and 34[degrees]C for 12 or 24 hours after ROSC (Belliard et al., 2007). Determining the precise optimal temperature to achieve all possible benefits while limiting complications of therapy has been challenging for clinicians. A recent study compared mild versus moderate hypothermia, which was defined as 33[degrees]C and 36[degrees]C, respectively. The study was specific to out-of-hospital cardiac arrest patients and concluded that there was no additional benefit at 33[degrees]C (Nielsen et al., 2013). This study offers evidence that moderate hypothermia may be equivalent compared with mild hypothermia in certain patient populations. This is encouraging because complications of therapy increase at lower temperatures. This isolated study prompts further research to definitively assess whether this conclusion is accurate. A larger study that was a collaboration of five professional societies provided the following recommendations: (a) the term "targeted temperature management" should replace therapeutic hypothermia, (2) the term "mild" needs to be replaced with specific temperature values, and (3) a target temperature of 32[degrees]C-34[degrees]C is preferred to treatment of out-of-hospital cardiac arrest patients with ventricular fibrillation or pulseless ventricular tachycardia who fail to regain consciousness despite ROSC (Nunnally et al., 2011).

Neurocritical care literature provides limited evidence to date regarding the efficacy of IH. The Brain Trauma Foundation evaluated six "moderate quality RCTs" or randomized controlled trials, which failed to show a statistically significant reduction in mortality in patients who received IH (Brain Trauma Foundation, 2007). However, IH receives a level III recommendation, and the foundation calls for further research because patients who received IH were more likely to have improved Glasgow Outcome Score of 4 or 5, which corresponds with moderate or mild disability, respectively (Brain Trauma Foundation, 2007).

IH has been shown to reduce the cerebral metabolic rate of oxygen levels, which is neuroprotective; however, more research is needed to fully evaluate the effects on CBF and to determine if the benefits truly outweigh the many risks of therapy. There is some variability in the recommendations based on diagnosis. For large hemispheric cerebral infarcts, the current recommendations include (a) hypothermia administration for patients who are not eligible for surgical intervention and (b) target temperature of 33[degrees]C-36[degrees]C for a duration of 24-72 hours (Torbey et al., 2015). In general, refractory intracranial hypertension is the common indication for IH across multiple neurological etiologies.

The Neurocritical Care Society notes a lack of prospective research trials to provide evidence to support IH. Currently, their recommendations include targeting a normal temperature (class IIa; level of evidence C) and note that the effectiveness of therapeutic hypothennia before the development of brain swelling (prophylactic IH) is not known (class lib; level of evidence C). Level C evidence is applied to reflect that limited populations have been studied (Wijdicks et al., 2014).

Nursing Implications: Preventing, Recognizing, and Managing Complications

Nurses play a pivotal role in the care of patients receiving IH. Among the necessary skills that are required, nurses must be proficient in the methods of performing IH. A common method, using surface cooling pads, requires the nurse to properly apply the pads, connect the tubing to the machine, and input the desired temperature and the time to reach that temperature. If a patient is cooled too slowly, the therapeutic effect is lost. If a patient is cooled to a temperature below 34[degrees]C, they can have life threatening consequences including arrhythmias. This brief example above indicates the importance of having a skilled nurse to deliver this complex therapy because failure to administer therapy in a timely manner can compromise the intended benefit or lead to potentially fatal complications.

Nurses must be educated regarding common side effects to monitor. Because nurses care for patients at the bedside, they are essential for providing direct patient care and promptly communicating concerns to the rest of the healthcare team.

First, one of the most deleterious complications is shivering. Although this may seem like an expected occurrence, shivering affects patient outcomes by increasing metabolic demands by up to 600% (Badjatia et al., 2008). Therefore, once shivering occurs, the intended benefits of IH begin to diminish because of increased oxygen consumption, carbon dioxide production, and metabolic stress (Badjatia et al., 2008). Shivering is commonly treated based on the Columbia Bedside Shivering Assessment Scale (BSAS; Badjatia et al., 2008) and the corresponding treatment algorithm.

For a shivering assessment score of 0 on the Columbia BSAS, which corresponds to no shivering, there are several recommended pharmacologic interventions for shivering prophylaxis (Badjatia et al., 2008). These include standing acetaminophen to lower the shivering threshold by augmenting the fever threshold given the antipyretic effects of this medication. Skin counterwarming via a warming blanket placed on the patients' skin is also recommended. Skin counterwarming works by convincing the temperature sensors in the skin that the body is not as cool as the actual core temperature would indicate. Additional medications recommended in the literature for shivering prophylaxis include buspirone (Buspar) and magnesium sulfate (Choi et al., 2011). Buspirone is an anxiolytic that functions by binding to serotonin and dopamine receptors in the brain. This increases norepinephrine metabolism in the brain, which reduces the shivering threshold (Liu-DeRyke & Rhoney, 2008). Magnesium sulfate is an N-methyl-Daspartate receptor agonist, which decreases the release of norepinephrine and serotonin, creating an environment that favors a thermoregulatory effect. The exact mechanism of action is not fully understood (LiuDeRyke & Rhoney, 2008). The nurse is essential in the accurate assessment of the severity of shivering because it drives the corresponding pharmacologic intervention prescribed.

Mild-to-moderate shivering is described by a BSAS score of 1 or 2. Mild (score of 1) is defined as shivering localized to the neck and/or thorax. Moderate (score of 2) is defined as shivering involving gross movement of the upper extremities (Badjatia et al., 2008). The pharmacologic regimen recommended includes dexmedetomidine (Precedex) or opioids (Choi et al., 2011). Dexmedetomidine is an A2-adrenergic agonist, which suppresses neuronal firing and limited neurotransmitter released by limiting calcium entry into the nerve cell (De Witte & Sessler, 2002). Opiates, or narcotic analgesics, act on K-opioid receptors. The exact mechanism of action is unclear; however, the result is a reduction of the shivering threshold by nearly twice that of the vasoconstriction threshold (De Witte & Sessler, 2002).

Severe shivering corresponds with a BSAS score of 3, which involves gross movements of the trunk and upper and lower extremities (Badjatia et al., 2008). The literature recommendations include deep sedation via propofol (Dipivan) or neuromuscular blockade, which can be achieved by vecuronium (Choi et al., 2011). Propofol reduces the shivering and vasoconstriction threshold; however, the precise mechanism of action is unknown. If a patient continues to have severe shivering despite propofol, neuromuscular blockade may be required. Vecuronium terminates the shivering response by pharmacologically paralyzing the muscles responsible for shivering (Liu-DeRyke & Rhoney, 2008).

Second, arrhythmias are a potential complication. These include bradycardia or ventricular arrhythmias. This is because of slowed cardiac conduction and prolonged refractory periods creating an ambient environment for reentrant arrhythmias (Marshall & Siegel, 2009). If core temperature falls below 30[degrees]C, atrial fibrillation and ventricular fibrillation become more prevalent. Unfortunately, at this temperature, the myocardium is less responsive to conventional therapies with antiarrhythmics (e.g., diltiazem [Cardizem], amiodarone [Cordarone]) and defibrillation (Badjatia, 2006). All patients receiving IH are placed on continuous telemetry to observe for arrhythmias, although the risk is relatively low unless core temperature falls below 30[degrees]C. Nurses at the bedside have the responsibility to meticulously monitor core temperature to decrease the risk of arrhythmia because early recognition and communication with the provider will allow for early intervention. If the core temperature falls below the critical threshold, conventional advanced cardiac life support algorithms would be followed and indicated for treatment, despite the concern for diminished myocardial response.

Third, IH leads to immunosuppression and inhibition of proinflammatory mediators; therefore, nurses must be vigilant in care and maintenance of central and arterial lines, foley catheters, and endotracheal tube care (Marshall & Siegel, 2009). Nurses can also play an important role in recognizing early signs and symptoms of infection including trends in water temperature from the cooling machine. Specifically, if the water temperature continues to decrease, this is suggestive of the patient having a higher core temperature that is requiring a cooler water temperature to achieve the desired therapeutic goal temperature. This may represent early infection. For instance, if a patient is set at a goal temperature of 35[degrees]C and his or her water temperature via the cooling machine has been between 25[degrees]C and 27[degrees]C during the nurse's shift and then declines to a temperature of 10[degrees]C, the nurse can extrapolate that the patient is mounting a fever and thus requiring a cooler water temperature to achieve the goal temperature. Additional indicators may include increases in heart rate and respiratory rate.

Fourth, IH can cause skin breakdown and impaired wound healing. It is essential for the nurse to be judicious in his or her turning and positioning of the patient to alleviate pressure points. In addition, skin assessments each shift are paramount to identify early signs of skin breakdown including stage I pressure ulcers so that early intervention can be applied.


IH offers an additional treatment modality for critically ill patients experiencing neurological injuries. Although it offers the potential to combat several aspects of the secondary injury, IH is not without its own complications. Current literature is limited and is largely representative of meta-analyses, systematic reviews, and case studies. One meta-analysis supported a decrease in mortality compared with normothermia but failed to show statistical significance (Li & Yang, 2014). A recent study that provided a systematic review was able to show a significant reduction in both mortality and poor outcome (Crossley et al., 2014). Experimental evidence also supports the benefit of mild hypothermia on neuroprotection after TBI (Urbano & Oddo, 2012). There are certainly potential benefits to IH in neurocritical care; however, the limitations of current findings highlight the need for further research to be conducted to provide clarity.

There is clearly a lack of research on IH, and it will be essential for more prospective trials to be conducted to conclusively determine whether IH offers a benefit to neurocritical care patient populations. Presently, there are no formal guidelines that dictate when IH should be implemented, the specific patient populations that may benefit, and precise temperature or duration. Use of IH is controversial and largely provider and institution dependent. Some of the data are anecdotal because clinicians have observed a reduction in refractory intracranial hypertension after implementation of IH. It is imperative for nurses to be educated regarding this treatment because much of the implementation is done autonomously and nurses are often the first to note changes in the patients' clinical course. Nurses may be expected to provide IH in the neuroscience intensive care unit for patients with refractory intracranial hypertension because of intracerebral hemorrhage, large territory ischemic stroke, TBI, and so forth. Nurses should be familiar with both surface and endovascular cooling methods and available resources and reference manuals for detailed application and safe administration of these therapies.

Questions or comments about this article may be directed to Courtney J. Cook, ACNP DNP, at She is an Assistant Professor of Nursing, Vanderbilt School of Nursing, Nashville, TN.

No funding or financial resources are associated with the content of this article. There is no financial relationship with the Arctic Sun Corporation.

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (

The author declares no conflicts of interest.

DOI: 10.1097/JNN.0000000000000215


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Title Annotation:Clinical Nursing Focus
Author:Cook, Courtney J.
Publication:Journal of Neuroscience Nursing
Article Type:Report
Date:Feb 1, 2017
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