Therapeutic Hypothermia in the Emergency Department
Therapeutic Hypothermia in the Emergency Department
Remember the principle of homeostasis from first-year physiology the idea that the human body has self-regulating processes to maintain a desirable internal state? What were we taught to do when disease disrupted the self-regulating processes, and physiologic parameters were abnormal? Use medical treatments to restore them to normal values. Well, now we know that this may not be the best way to enhance survival.
So, now we allow the severe asthma patient to remain hypercarbic if placed on a ventilator. We allow the patient with traumatic shock due to a gunshot wound to the abdomen to remain hypotensive until surgery is started. And, as in this article, we purposely should lower the body temperature away from normal in a patient who is successfully resuscitated from cardiac arrest and who does not quickly recover consciousness.
The principle that restoration of normal physiology is desirable following an acute severe insult should not be dogma. And, in many conditions, it is being proven wrong.
J. Stephan Stapczynski, MD, FACEP, FAAEM, Editor
A 51-year-old male with a history of hypertension is brought into your emergency department (ED) by paramedics after collapsing while doing yard work. After three rounds of chest compressions, defibrillation, and epinephrine, the patient has a pulse of 135 and BP of 100/60. On arrival, he is intubated and unresponsive with intermittent decorticate posturing.
What can we do in the ED to improve the patient's chance of survival and good neurologic outcome?
Epidemiology The Role of Therapeutic Hypothermia
Every year there are more than 290,000 victims of sudden cardiac death in the United States.1 For out-of-hospital cardiac arrest, the mortality remains a staggering 65-95%. Of the few survivors, on average only 10-20% are discharged with a good neurologic outcome.2 Until recently, few therapies have been shown to significantly improve outcomes for survivors of cardiac arrest. Today, therapeutic hypothermia (TH) provides a relatively straightforward and inexpensive technique demonstrated in multiple studies to improve both survival and neurologic outcomes.3 In fact, recent meta-analyses conclude that only seven patients need to be treated to save one life, while only five need to be treated to prevent one poor neurologic outcome.4,5
The use of TH has slowly been gaining public acceptance throughout the United States. A 2006 USA Today article described the story of a cardiac arrest victim who survived neurologically intact after being treated with TH. The article described early adoption of TH protocols, including initiation of cooling by EMS in Washington, Virginia, and North Carolina.6 More recently, New York City announced in December 2008 that ambulances would be instructed to bypass the closest hospital and instead go to the nearest resuscitation center hospital with a therapeutic hypothermia protocol for cardiac arrest patients.7
The History of Hypothermia Not a Novel Concept
Hypothermia has been investigated since the 1940s. Early studies using deep hypothermia (< 30ºC) were complicated by difficult-to-control side effects and a lack of modern intensive care support. In the 1950s, studies of moderate hypothermia (26-32ºC) for the treatment of comatose survivors of cardiac arrest were again inconclusive.2 Animal studies and small clinical studies in the 1980s and early 1990s renewed interest in mild hypothermia (32-35ºC).
Two landmark randomized, controlled trials independently demonstrated in 2002 that mild therapeutic hypothermia (32-34ºC) improved survival and neurologic outcome in comatose survivors of cardiac arrest with a presenting rhythm of pulseless ventricular tachycardia or ventricular fibrillation.8,9 Both trials had similar patient populations and produced similar outcomes despite differences in protocols. From Europe, the Hypothermia After Cardiac Arrest Study cooled patients with an external air cooling mattress device at presentation in the emergency department to a temperature between 32-34ºC as measured by a bladder probe. After 24 hours, patients were passively rewarmed over 8 hours.8 In the Bernard study from Australia, cooling was initiated by paramedics with ice packs applied to the head and torso. In the ED, patients were cooled using ice packs only to 33ºC with temperatures measured with a bladder or tympanic probe.9 Patients were maintained for 12 hours, passively rewarmed for 6 hours, and then actively rewarmed as required.9 Both studies maintained sedation and paralysis throughout the cooling period.
Therapeutic hypothermia recently has been studied for numerous other indications, including traumatic brain injury, stroke, subarachnoid hemorrhage, myocardial infarction, ARDS, and perinatal hypoxic encephalopathy. However, current data are either conflicting or limited. Small studies of ischemic stroke have suggested promise, but a controlled trial of both ischemic stroke and subarachnoid hemorrhage is needed.10 The use of hypothermia in acute myocardial infarctions has not been shown to decrease infarct size or limit the number of adverse events despite the promise of earlier animal studies.11 The use of TH in the treatment of traumatic brain injury also has produced conflicting results.3 Other areas of ongoing study include spinal cord injury,12 multi-system trauma,13 and acute liver failure.14 Until better evidence exists, there is no current recommendation to induce therapeutic hypothermia for these indications.2 The one exception is perinatal hypoxic encephalopathy, for which TH again dramatically improved outcomes.15
Despite the evidence and inclusion within the 2005 ACLS guidelines, a recent survey of U.S. physicians reported that only 26% of physicians have implemented TH. The remaining 74% reported not using TH for several reasons, including the belief that TH was not part of ACLS protocols, it was too technically difficult, it simply was not considered, or that there were not yet enough data.16 A clear gap exists between current literature and actual practice. Since victims of sudden cardiac death present first to the emergency departments, emergency physicians must be at the forefront of creating and implementing effective institution-specific protocols in collaboration with specialists from intensive care, cardiology, and neurology.
Pathophysiology How Cooling Limits Injury
The post-cardiac arrest syndrome is a complex pathophysiologic process consisting of brain injury, myocardial dysfunction, systemic ischemia, and reperfusion response, and the precipitating pathology.3 Brain injury is the reported cause of death in two-thirds of patients after out-of-hospital arrests and one quarter of patients after in-hospital arrest. Cerebral ischemia and impaired vascular autoregulation result in neuronal apoptosis, necrosis, and ultimately degeneration. The immediate post-injury period provides a window of opportunity to interrupt these mechanisms, limit injury, and improve neurologic outcomes.17
A myriad of cellular mechanisms contributes to neuronal apoptosis and necrosis, including free radical formation, disruption of calcium homeostasis, altered gene expression, protease activation, mitochondrial dysfunction, and generalized inflammation from cytokine activity.3,18 The influx of free radicals during reperfusion further exacerbates the cellular injury and impairs cerebral aerobic energy.19
Rather than infarction, cardiac arrest actually results in only a temporary myocardial stunning.3,20 Although not permanent, this reduction in ejection fraction results in reduced end organ oxygen delivery that initiates a vicious downward spiral of systemic injury. Accumulating oxygen debt activates an inflammatory endothelial response.21 Reactive oxygen intermediates exacerbate the systemic inflammatory and reperfusion response. Continuing organ injury results in further changes in vasoregulation, intravascular volume depletion, and an increased susceptibility to infection.3 Ultimately, cellular apoptosis and necrosis occurs, leading to end organ damage.
The initial systemic ischemic insult results in global tissue hypoxia, a switch to anaerobic metabolism, and subsequent acidosis. Within the cell, there is an increase in calcium and a decrease in adenosine triphosphate. However, returning blood flow to ischemic areas does not end the downward spiral. Instead, restoring blood flow actually increases intracellular calcium and activates phospholipases, resulting in further production of inflammatory cytokines and reactive oxygen intermediates, continuing the cycle of mitochondrial and cellular death.3 Limiting this reperfusion injury provides yet another opportunity for intervention.
The underlying precipitating pathology resulting in cardiac arrest must be addressed. Acute coronary syndrome is the cause of up to 50% of out-of-hospital cardiac arrests.22 Elevations of troponin T are present in up to 40% of patients at the time of cardiac arrest, suggesting an ongoing cardiac ischemia or injury hours prior to the event.23 Other etiologies to consider include pulmonary embolism, sepsis, drug toxidromes, primary pulmonary disease (asthma, chronic obstructive pulmonary disease, pneumonia), and severe hemorrhagic shock.3
TH limits neurologic injury and improves outcomes by interrupting multiple processes in this complex downward spiral of pathology. Hypothermia decreases epileptic activity and slows metabolic rate with a 5-8% decrease in cellular oxygen and glucose requirements per degree Celsius reduction in core body temperature.17 The systemic inflammatory response, including neutrophils, macrophages, and pro-inflammatory cytokines, is inhibited. Cooling stabilizes cell membranes, limiting the permeability of the blood-brain barrier and blood vessel walls and decreasing edema formation. Reduced calcium influx results in less activation of the cellular cascades that lead to apoptosis and necrosis. Reperfusion injury is suppressed by a reduction in mitochondrial dysfunction and free radical production.24 Mild anticoagulant effects may result in protection from microthrombus formation that otherwise can worsen brain injury.17
Current Indications and Evidence for TH
The American Heart Association (AHA) recommends cooling to 32-34ºC for 12-24 hours for unconscious adult patients with spontaneous circulation after out-of-hospital cardiac arrest when the initial rhythm was ventricular fibrillation or ventricular tachycardia. Furthermore, the AHA recommends considering TH in patients with other rhythms as well as for inpatient cardiac arrest survivors.25
The two landmark studies published in 2002 utilized strict inclusion criteria. TH was performed only on comatose patients with a return of spontaneous circulation after out-of-hospital cardiac arrest with an initial rhythm of ventricular fibrillation or ventricular tachycardia.8,9 The commonly accepted definition of coma is a complete failure of the arousal system with no spontaneous eye opening and corresponds to a Glasgow Coma Score (GCS) of 8 or less. One study excluded any patients with longer than 15 minutes until EMS arrival, patients with greater than 60 minutes until return of spontaneous circulation, and patients with a pre-existing coagulopathy.8 Furthermore, patients needed to be between the ages of 18 and 75, not pregnant, and not in cardiogenic shock after starting pressors.8,9
These strict inclusion criteria led to only 10% of screened patients being eligible for treatment.2 Follow-up studies have demonstrated a benefit in other types of patients, including patients with other initial rhythms on presentation,22,26,27 patients in cardiogenic shock,28,29 and in-hospital arrest patients.30
Exclusion criteria also must be considered. Patients who are hypothermic (< 30°C), comatose prior to the cardiac arrest, terminally ill, or have a do-not-resuscitate order should not be cooled. If the cause of the arrest is not cardiac in origin, or if the coma is not due to the arrest itself, as in cases of head trauma or stroke, TH currently is not indicated.8,9 A primary coagulopathy and uncontrolled arrhythmias also are contraindications. The time frame for instituting hypothermia is not clear. Consider excluding patients with more than 60 minutes from arrest to return of spontaneous circulation8 and those who are greater than 6 hours post-arrest.5 (See Table 1.)
Pregnant and pediatric patients have been excluded from most studies. A single case report of therapeutic hypothermia in a pregnant patient reports favorable outcomes for both the mother and the infant.31 Until there is further information or studies, pregnancy should be considered a relative contraindication.
For pediatric patients, international resuscitation guidelines published in 2006 recommend that physicians consider the induction of TH for 12-24 hours in children who remain comatose after resuscitation from cardiac arrest.32,33 Neonates with hypoxic-ischemic encephalopathy have been successfully cooled for 72 hours.15 However, there is only a single inconclusive retrospective study on TH for cardiac arrest patients younger than age 18.34 Based on limited available data, cooling appears safe and should be considered in pediatric cardiac arrest cases.
Multiple ongoing studies are currently seeking to clarify specific indications and contraindications. Specifically, investigators are attempting to determine optimal timing, duration, target temperature, cooling technique, and other clinical roles.
Preparation. Perform a rapid yet thorough neurological examination, including Glasgow Coma Scale, pupillary light reflex, corneal reflex, facial movements, eye movements, gag, cough, and motor response to painful stimuli. Note that any preservation of these reflexes suggests a good prognosis, but absence does not predict a poor outcome.3 Intubate and sedate the patient with the mechanical ventilator humidified air turned off. Perform an electrocardiogram (ECG) and check basic laboratory tests, including CBC, serum chemistry, phosphorous, calcium, magnesium, coagulation profile, cardiac markers, urinalysis (UA), urinary pregnancy, and arterial blood gas (ABG). Insert a Foley catheter to monitor urine output with goal greater than 0.5 mL/kg/hr. (See Table 2.)
Insert a continuous core temperature monitor. A pulmonary artery catheter temperature probe is considered the gold standard, but other sites have a high level of accuracy, including the esophagus, bladder, nasopharynx, and rectum. These secondary sites have the advantage of being easier to place in the ED, with the disadvantages of a time lag in temperature reading and a risk of displacement.17 Esophageal probes have the shortest lag time and most accurately reflect the gold standard.17
Sedatives and analgesics are given to facilitate mechanical ventilation. Animal studies of global anoxia show that neurological improvement is lost without adequate sedation.17 Commonly used sedatives and analgesics include lorazepam, midazolam, propofol, fentanyl, and morphine. For control of shivering, paralytics remain the first-line treatment after adequate sedation and analgesia in the emergency department.17 Commonly used paralytics include pancuronium and vecuronium. Shivering during TH should first be treated with opioids (meperidine, fentanyl, or morphine), buspirone, or benzodiazepines.35,36
Treatment of suspected underlying acute coronary syndromes with thrombolytics or percutaneous coronary intervention (PCI) should occur simultaneously with the therapeutic hypothermia when clinically indicated.37,38 The initial 2002 studies included patients treated with thrombolytics or PCI. In 2007, two other groups published studies confirming the safety of therapeutic hypothermia in those receiving PCI.39,40 Additionally, a recent study confirmed that the use of therapeutic hypothermia does not affect door-to-balloon time while showing the same improvement in neurological outcomes and a lower mortality.38
Phases: Induction, Maintenance, Rewarming. Therapeutic hypothermia is most commonly described in three distinct phases. Multiple different methods can be used in each phase with the same goals of rapidly cooling, maintaining stable core temperature, and then slowly rewarming.
Induction. The goal of the induction phase is to rapidly induce hypothermia to reach a desired core temperature of 32-34ºC. Since the patient is more stable at this temperature, reach 33.5ºC as quickly as possible.17 Animal studies suggest that a delay in implementation decreases the effectiveness.41 Furthermore, the induction phase has the greatest instability, so cooling the patient quickly results in the best possible outcome.17 The induction of hypothermia is assisted by the typical decrease in temperature seen in survivors of cardiac arrest.3
Cooling is achieved through increasing convection and conductive heat loss. (See Table 3.) The simplest method is the application of ice packs and cool wet towels to the head, neck, torso, and groin regions.42 Another easy and rapid induction method is the infusion of cold intravenous fluid through a peripheral vein. A 1.5 to 2 liter (30 mL/kg) fluid bolus of 4ºC normal saline or lactated Ringers will lower a patient's temperature by 1.5-2.3ºC.43-45 After the initial infusion, a repeat bolus of 500 mL can be repeated every 10 minutes until a target temperature of 33.5°C is reached.46 Continuously monitor the patient for signs of fluid overload and stop infusions when clinically indicated. Patients requiring PCI can be transported to the catheterization laboratory with these cooling measures in place without affecting door-to-balloon time.38
The placement of ice packs or bolus of cold fluids has been shown to be safe even in the prehospital setting.9,43-45 However, the application of cooling measures must never distract the healthcare provider from the primary goal of CPR: the return of spontaneous circulation.
Multiple external and internal cooling devices are available to provide the advantage of continuous cooling with feedback control. (See Table 4.) External systems consist of a cooling pad or blanket applied directly to the skin. (See Figure 1.) The external devices allow for easy application and work through circulation of cooled water or air. Internal devices consist of an intravascular catheter that directly cools the blood. There are no studies comparing internal and external cooling devices in cardiac arrest patients.42 A manufacturer study conducted in neurosurgical patients showed that an internal device cooled faster and maintained a tighter temperature control with no increase in complications.47
Maintenance. Cooling is stopped at 33.5ºC to prevent unintentional overcooling.2 The goal of the maintenance phase is to maintain core temperature between 32-34ºC with minimal fluctuations. Shivering, fluid shifts, and hemodynamic and electrolyte instability all decrease once core temperature drops below 33.5ºC. Overcooling should be avoided as the risk of arrhythmias increases at 30ºC.24 (See Table 5.)
Ideally, maintain the core temperature with a commercially available internal endovascular or external surface cooling device with a temperature control feedback system. (See Figure 2.) Other methods include the use of ice packs or cool wet blankets placed around the head, neck, torso, and extremities.48 Although cheap and easy to apply, the ice and blankets are more time consuming and less accurate than a continuous feedback system. Fluid boluses alone do not allow the maintenance of hypothermia.49
General supportive ICU care and monitoring must continue. Maintain a mean arterial pressure of 65-100 mmHg and a central venous pressure of 8-12 mmHg.3 Due to cold diuresis, laboratory tests and urine output need to be monitored and corrected. Glucose control improves survival and neurologic outcomes. Sedation and analgesia are maintained at lower doses due to decreased drug clearance with hypothermia. Since shivering decreases and may cease below 33.5°C, paralytics often are no longer required.17 Neurology should be consulted for continuous EEG to monitor for seizures, especially when paralytics are continued.
Rewarming. Rewarming typically begins 24 hours after initiating hypothermia. In contrast to the induction phase, rewarming is a slow process. Fast rewarming is associated with adverse outcomes in animal studies and post-surgical patients.50 Rewarm at 0.2-0.5ºC per hour over 6-8 hours.17 This slow rewarming process helps to prevent rapid fluctuations in hemodynamics, electrolytes, and metabolic rate. Many cooling devices allow a controlled rate of rewarming through the temperature control mechanisms. Other options include passive rewarming or the addition of warm blankets. (See Table 6.)
For patients who still are paralyzed, stop the neuromuscular blockade at core temperatures between 35.5 and 36.5ºC.22 Avoid hyperthermia greater than 37.5ºC for 72 hours post cardiac arrest. Although the incidence after rewarming is unknown,51 hyperthermia is associated with brain death and increased risk of unfavorable neurologic recovery.52,53 If necessary, use cooling blankets and acetaminophen to avoid rebound hyperthermia.3 Shivering during rewarming can be treated with warm blankets and opioids (meperidine, fentanyl, or morphine), buspirone, or benzodiazepines.
Since TH affects every organ system in the body, many benign and serious complications can occur. Knowing whether problems are a result of therapeutic hypothermia or the underlying post-arrest state and how to treat common complications is essential to ensuring the best outcome. (See Table 7.)
Frequently encountered during the induction phase, shivering has been directly linked to an increased risk of cardiac events and adverse outcomes in postoperative patients.17 This seemingly benign protective response results in increased heat production, metabolic rate, work of breathing, heart rate, and stress response, all of which can increase oxygen consumption from 40% to as much as 100%.3,30
Many medications may be used to prevent shivering. Buspirone and meperidine have been shown to lower the shivering threshold in awake patients.35,36 Other options include propofol, benzodiazepines, fentanyl, morphine, clonidine, dexmedetomidine, and neostigmine.54 Magnesium sulfate 2-3 grams has been shown to decrease shivering, have anti-arrhythmic and neuroprotective effects, and increase cooling rates through vasodilatation.55,56 Adequate sedation and analgesia are essential to ensuring the best outcomes and preventing side effects from neuromuscular blockade. Patients with adequate sedation and analgesia often will not require paralytics for shivering.
The initial landmark studies used midazolam, fentanyl, and pancuronium or vecuronium. Paralytics are highly effective at controlling shivering and have the advantage of not causing hypotension. However, paralytics in the short term mask seizure activity and insufficient sedation while in the long term increase the risk of the critical illness polyneuromyopathy. When using continuous neuromuscular blockade, continuous EEG monitoring is necessary to detect seizure activity.17,57
Induction of hypothermia induces a cold diuresis and worsening hypovolemia and leads to electrolyte abnormalities, including hypokalemia, hypophosphatemia, hypomagnesemia, and hypocalcemia.3,58 These electrolyte abnormalities can exacerbate neurologic injury or arrhythmias. Hypotension and hyperkalemia commonly occur during rewarming but can be corrected with a slower rise in temperature.3,26,27 Hypothermia also inhibits insulin secretion and decreases insulin sensitivity, leading to hyperglycemia. Hyperglycemia in critically ill patients is associated with negative outcomes and may increase brain injury.59 However, overly tight glucose control to a level of 80-110 mg/dL leads to an increase in hypoglycemic episodes. Pending the results of current studies, a glucose level of between 145-180 mg/dL provides the best improvement in mortality.60
Reported cardiovascular side effects include vasoconstriction resulting in an increase in systemic vascular resistance and blood pressure, and subsequent decrease in cardiac output. However, the decrease in metabolic rate is greater than this decrease in cardiac output.61,3 The vasoconstriction further leads to an increase in venous return and central venous pressure. A sinus bradycardia at 40-45 beats/min range commonly develops as the core temperature decreases. Electrocardiographic changes are common, including prolonged PR, QRS, and QT intervals, and T wave inversion. Osborn J waves generally occur only with severe hypothermia.62 Incidental arrhythmias occur more frequently with the use of endovascular cooling technique.27 However, clinically significant arrhythmias including atrial fibrillation, ventricular tachycardia, and ventricular fibrillation generally occur only with core temperatures less than 30°C.27
Hypothermia carries an increased risk of infections through suppression of inflammatory response and immune function. Pneumonia and sepsis are observed in up to 50% of hypothermic post-cardiac arrest patients.8,22,26,63 Prophylactic antibiotics may be considered for this reason. Due to immobilization and skin peripheral vasoconstriction, the risk of wound infections also increases. External cooling devices may lead to skin breakdown and tissue necrosis.42 Close attention must be paid to existing wounds and frequent repositioning of the patient. Internal cooling devices require large central catheters and thus carry the risk of local infection and catheter-related thrombosis.47
The coagulopathy associated with TH is rarely clinically significant.17,64 A decrease in platelet number and function results in an increased bleeding time. Prothrombin and partial thromboplastin times are prolonged due to slowing of enzymatic reactions and impairment of the coagulation cascade and fibrinolytic activity.63 These side effects may remain hidden since standard coagulation profiles occur at room temperature and will not show the abnormality unless performed at the patient's core temperature.65 Control active bleeding prior to initiating a TH protocol. Although an increased risk of bleeding exists, fibrinolytics and percutaneous coronary intervention have been demonstrated in multiple studies to be safe and effective when performed simultaneously with TH.37,38
Other laboratory abnormalities include increases in renal markers, liver function tests, lactate, and amylase as well as a decrease in the leukocyte count.17 Acute renal failure may occur. Hypothermia alters drug clearance and metabolism, resulting in increased drug levels and effects.63,66 In the maintenance and rewarming phases, repeat neurological assessments are necessary due to the prolonged effects of benzodiazepines, neuromuscular inhibitors, and opiates with hypothermia.
Since most blood gas machines warm blood samples to 37ºC, PO2, PCO2, and pH must be adjusted by the physician to the actual core temperature of the patient for correct ventilator management. For blood gas analyzers without temperature correction (or blood warmed to typical body temperature), for every 1ºC decrease in core body temperature, subtract 5 mmHg from measured PO2 and 2 mmHg from measured PCO2, and then add 0.012 points to measured pH to estimate true physiologic measurements.67 This correction will allow for optimal ventilator management of the patient's ventilation and oxygenation status.17
No definitive data exist to predict which patients will have favorable outcomes when treated with hypothermia. Since the optimal timing and recovery period have not fully been defined, early prognostication of post-cardiac arrest patients must be modified when TH is applied.3 Current recommendations for determining brain death in post-cardiac arrest patients are to wait for 72 hours post CPR. Hypothermia slows drug metabolism, prolonging the effects of sedatives and paralytics. Therefore, perform prognostication tests at least 72 hours after completion of hypothermia, instead of CPR, before making the final determination of brain death.
Currently, the bedside neurologic exam as well as somatosensory-evoked potentials (SSEPs) remain the most reliable predictors of outcome. Other methodologies, including biochemical markers, neuroimaging, intracranial pressure monitoring, EEG testing, and circumstances surrounding the event, have been studied with inadequate data to support or refute prognostication of poor outcomes.68-70 The neurological examination consists of mental status, cranial nerve function, motor and sensory evaluation, pertinent reflexes, and is mostly quantified by a Glasgow Coma Scale and Brainstem Reflex Score (BRS). The BRS consists of papillary reflex, corneal reflex, oculocephalic reflex, cough/gag reflex, and spontaneous breathing.71 Seventy-two hours post CPR, a GCS motor score of less than or equal to 2T or absence of brainstem reflexes accurately predicts poor outcomes.68
Beginning an Institution-Specific Therapeutic Hypothermia Protocol
The benefits of TH have been reported in large academic centers as well as smaller community hospitals outside of clinical trials. A European Registry reported equivalent efficacy and safety between larger hospitals and smaller community hospitals.27 Regardless of an institution's size or affiliation, the creation and implementation of a successful TH protocol requires collaboration between the physician and nursing staff of all involved departments, including emergency medicine, cardiology, critical care, anesthesia, neurology, and neurosurgery.72 Each department must provide enthusiastic, influential, and dedicated leaders who work together at regularly scheduled meetings to create a detailed program.
The Aware, Agreement, Adoption, Adherence model provides an effective pathway for the committee to create a successful institution-specific protocol based on existing TH guidelines.73 To create awareness, initial meetings are dedicated to the discussion of the latest literature as well as protocols from similar institutions. Agreement is then reached as the committee creates a detailed protocol tailored to the institution's patient population and available resources. Adoption of the protocol requires the presentation of the committee's protocol to the staff of the individual departments, educational and training modules, and a trial period to test and improve the protocol. Adherence results when TH becomes the standard of care at the institution as demonstrated by ongoing quality improvement monitoring and education.
Many of the preconceived barriers to the initiation of new treatment protocols are easily overcome by the organized and collaborative efforts of the TH committee. Initially, TH protocols can be instituted with almost no cost by using ice, cool blankets, and cool fluid boluses. Based on institutional resources, the purchase and maintenance of external and internal cooling devices will be the largest cost. For the emergency medicine physician, the main focus will be on initiating the TH protocol, monitoring the induction phase, and contacting the appropriate specialists (cardiology, intensive care, neurology) for further care of the patient.
Detailed protocols for therapeutic hypothermia from several institutions are available through the University of Pennsylvania's Center for Resuscitation Science at http://www.med.upenn.edu/resuscitation/hypothermia/protocols.shtml.
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73. Brooks SC, Morrison LJ. Implementation of therapeutic hypothermia guidelines for post-cardiac arrest syndrome at a glacial pace: Seeking guidance from the knowledge translation literature. Resuscitation 2008; 77:286-292.Remember the principle of homeostasis from first-year physiology the idea that the human body has self-regulating processes to maintain a desirable internal state? What were we taught to do when disease disrupted the self-regulating processes, and physiologic parameters were abnormal? Use medical treatments to restore them to normal values. Well, now we know that this may not be the best way to enhance survival.
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