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Intravascular temperature modulation as an adjunct to secondary brain injury prevention in a patient with an epidural hematoma.

Abstract: Epidural hematomas (EDHs) account for 1 0% of fatal injuries in patients with head trauma. Up to 35% of patients suffering EDHs develop secondary brain injury within days after the initial trauma. Secondary brain injury can profoundly affect a patient's subsequent neurologic recovery and functional status. This case study presents a patient who developed an EDH following severe head trauma with signs and symptoms of secondary brain injury; intravascular temperature modulation was used to treat the secondary injury for a prolonged period of 13 days. The patient showed a complete neurologic recovery with return to work 6 months after her injury.


Epidural hematomas (EDHs) are caused by trauma, usually associated with a skull fracture of the temporoparietal region that causes a tear in the middle meningeal artery. While EDHs are seen in only 1%-4% of patients with head trauma, they account for a disproportionate 10% of fatalities.

With rare exceptions, EDHs are unilateral and supratentorial and are usually found in the temporoparietal area. Reported mortality rates range from 5% to 43%, with poor outcomes most often related to a delay in surgical intervention. Higher mortality rates are also associated with lower Glasgow Coma Scale (GCS) scores, additional intradural lesions, temporal location, larger hematoma volumes, rapid clinical progression, pupil abnormalities, and increased intracranial pressure. Advanced age is also associated with higher mortality, but EDH is uncommon in elderly patients because the dura usually adheres to the inner table of the skull. The following case study describes the course of care, and subsequent recovery, of a patient with a severe EDH with many of the risk factors associated with high mortality rates.

Secondary Brain Injury

After surviving the initial trauma, patients with EDH are also at risk for secondary brain injury. In fact, up to 35% of patients develop secondary brain injury within days after the initial trauma (Wright, 2005). Prevention of secondary brain injury is imperative, as it results in cell necrosis, leading to unfavorable neurological outcomes, even death, in the patient with an EDH. Mechanisms of secondary brain injury include impairment of cerebral autoregulatory mechanisms, accumulation of toxic levels of free radicals and excitatory amino acids, cellular inflammatory response, and regional hyperthermia (Marion, 1997).

A recent study has shown that elevated body temperature, controlled for severity of illness, diagnosis, age, and complications, is independently associated with a longer intensive care unit (ICU) and hospital stay, higher mortality rates, and worse neurological outcomes (Diringer, Reaven, Funk, & Uman, 2004). Maintaining normothermia, or mild hypothermia, is crucial in modifying cerebral metabolic processes that contribute to secondary brain injury. Every degree that a fever is reduced also reduces the metabolic rate of brain cells up to 10% (Schaller & Graf, 2003). Lowering core temperature acts to reduce secondary brain injury by suppressing excitotoxins and free-radical reactions, stabilizing cell membranes, reducing intracellular acidosis, and reducing abnormal electrical activity (Kabon, Bacher, & Spiss, 2003).

Mechanisms for Lowering Body Temperature

Maintaining normothermia, or mild hypothermia, is common practice in neurological ICUs. Several methods have been employed to achieve this goal. Cooling blankets and external applications of ice have been, and still are, being used. Such measures have the untoward effect of causing the patient to shiver, thereby increasing cerebral metabolic rate. In addition to being unreliable, external applications of cold can contribute to skin breakdown and patient discomfort. Antipyretics, such as acetaminophen and ibuprofen, are also used but are often ineffective and can lead to complications such as liver and renal involvement, respectively.

In the past 5 years, intravascular cooling catheters have been used increasingly in our institution, largely due to their efficacy. Cooling catheters can be inserted via femoral or subclavian veins. The subclavian vein is the preferred access in patients who are active because it avoids the risk of more serious [cent] complications from dislodgement of a femoral catheter. Intravascular temperature modulation (IVTM) rapidly lowers core temperature by up to 3-4[degrees]C per hour to a target temperature determined by the physician or institution protocol (Lasater, 2006). The IVTM system used in the case study below consists of a multilumen catheter with inflow and outflow lumens and three central infusion lines. The catheter is powered by a console that provides continuous temperature monitoring and feedback via a bladder thermistor component of a Foley catheter. The clinician sets the desired patient temperature, and the system circulates cooled saline via the inflow and outflow lumens, providing effective heat exchange until the goal temperature is reached.

Case Presentation

The following scenario presents a case of a woman, Nancy, who suffered an EDH. IVTM was a valuable adjunct to her care, resulting in an impressive return of neurological function that allowed this patient to return to her previous position as a NICU nurse.

Nancy was leaving church on a Sunday morning when she was struck by a car while crossing the street. Witnesses described her being "thrown over the car onto her head--doing a 360." Nancy was brought by paramedics to a local emergency department (ED). After experiencing a loss of consciousness for 2 minutes, she was alert but agitated, with a GCS score of 11 upon admission to the ED. Her admitting GCS score deteriorated to 8 as she lost the ability to see the examiner, speak, open her eyes to anything other than painful stimuli, or follow commands. Her right pupil was 5 mm and briskly reactive to 2 mm, and her left pupil was 5 mm and nonreactive. An emergent computed tomography (CT) scan showed a large right parietal EDH, measuring 6.4 x 1.5 cm, that extended to the right temporal lobe, causing a 4 mm midline shift to the left (Fig 1). Comminuted fractures of the right temporal bone also were seen. The tentorium was layered with a bilateral hematoma, and bilateral subarachnoid hemorrhage over the parietal and temporal regions was found, which was consistent with a coup/contrecoup injury.

Nancy received 100 g of intravenous (IV) mannitol for acute cerebral swelling. She was sedated with IV propofol prior to endotracheal intubation. She was prepared for surgery to evacuate the hematoma via a right frontal temporal craniotomy and repair of the skull fracture. After surgery she was admitted to the neurological intensive care unit (NICU).

Course of Care

On admission to the NICU, Nancy was ventilated and had normal vital signs. The propofol was discontinued. She was able to move all extremities and had equal and reactive pupils. Her pupils were 3 mm bilaterally with less-than-brisk reaction, and her left eyelid was noted to be swollen and ecchymotic. At this time, her GCS score was 7. Blood was noted in her right ear canal.

On the 1st postoperative day, Nancy was agitated, did not follow commands, and attempted to pull herself up in bed. Tube feedings were initiated via nasogastric tube for nutritional support. Bilateral soft wrist restraints were applied to prevent dislodgement of the endotracheal or nasogastric tubes. At this time, her temperature was 37.8[degrees]C despite around-the-clock acetaminophen. To maintain normothermia, an IVTM catheter was inserted via the right subclavian vein. The decision was made to extubate Nancy in the afternoon because she was fully awake, attempting to sit up in bed, and no longer requiring ventilatory support. Nancy was perseverating, "Let's go!", but demonstrating receptive aphasia, as was evidenced by her disregard of the examiner's commands.

On the 3rd through 5th days of hospitalization, Nancy remained on cooling therapy with her temperature maintained at the goal range of 36.5[degrees]C. Her GCS score was 12; she was unable to follow commands or answer orientation questions. She continued to be very restless, requiring upper-extremity restraints. Her pupils were 7 mm bilaterally and reactive. Enteral tube feedings were continued. Starting on the 5th day of hospitalization, Nancy was seen by physical therapy and assisted out of bed daily to a chair. The IVTM console was placed on standby for transfer, and cooling therapy was reinitiated once the transfer was complete. She tolerated the activity well but continued to be intermittently agitated, was unable to follow instructions due to aphasia, and perseverated "Help her!" and "Let's go!"

In the early morning on the 6th day of hospitalization, Nancy was noted to have decreased strength in her right upper extremity (RUE), with an RUE strength of 3/5, and a left upper-extremity strength of 5/5. Her pupils were equal and reactive at 4 mm. Her temperature rose to 39.5[degrees]C. Blood and sputum cultures were obtained and found to be negative; around-the-clock ibuprofen was added. A stat head CT and cerebral angiograms, performed due to the acute decrease in RUE strength, showed no acute changes. On the 7th hospital day, Nancy's temperature once again spiked to 39.5[degrees]C, and she was recultured. Cultures were positive for coagulase-negative staphylococcus, and appropriate antibiotics were started. On the 8th hospital day, Nancy continued to be restless and perseverate; her right side remained weak. The IVTM catheter was replaced per our routine line-change protocol (central lines are to be changed every 7 days). The IVTM system remained off for several hours while waiting for verification of catheter placement. During this time, Nancy's temperature rose to 39.7[degrees]C. Her temperature promptly declined to 36.5[degrees]C when cooling therapy resumed. On the 9th through 11th hospital days, Nancy's right-sided weakness improved, and there were no further temperature spikes. She was moving from the bed to the chair and ambulating with assistance. She was perseverating less and following simple commands. By the 12th day of hospitalization, her right-sided weakness had completely resolved, and the IVTM catheter was discontinued on the following day. On the 14th day of hospitalization, Nancy was transferred from the NICU to the neurology floor. She was beginning to tolerate some oral food and fluids that were administered to augment tube feedings and was cooperating with care, so restraints were no longer required. She was transferred to rehabilitation 3 days later and continued to steadily improve. She was discharged home 3 weeks later, and she continued with outpatient speech, physical, and occupational therapies.


Three months after her injury, Nancy completed her rehabilitation and was home with her family. She visited her workplace, complained of being bored, and wanted to return to work. She readily remembered her former coworkers and showed no signs of neurological deficit, instantly recalling numbers and dates. Six months after her injury, Nancy returned to her former position in the NICU.


Although EDHs can result in long-term neurological deficits, prompt surgical intervention and prevention of secondary brain injury can enable a full recovery. Maintaining normothermia has been shown to be associated with improved neurological outcomes (Lasater, 2005). Despite two temperature spikes associated with coagulase-negative staphylococcus infection and one fever episode associated with temporary suspension of cooling therapy for a catheter change, a temperature of 36.5[degrees]C was maintained for 13 days during the acute phase of the case study patient's hospitalization. Neurological changes such as right-sided weakness, along with hyperthermia (defined in our institution as a temperature of >38.5[degrees]C), resolved within several days of thermoregulation. This is an anecdotal finding with implications for further studies to evaluate the role of thermoregulation in ameliorating neurological changes in patients with traumatic brain injuries.


Diringer, M., Reaven, N., Funk, S., & Uman, G. (2004). Elevated body temperature independently contributes to increased length of stay in neurologic intensive care patients. Critical Care Medicine, 32(7), 1489-1495.

Kabon, B., Bacher, A., & Spiss, C. K. (2003). Therapeutic hypothermia. Best Practice and Research. Clinical Anaesthesiology, 17(4), 551-568.

Lasater, M. (2005). The role of thermoregulation in cardiac resuscitation. Critical Care Nursing Clinics of North America, 17(1), 97-102.

Lasater, M. (2006). Intravascular temperature modulation in the neurosurgical critical care unit. Journal of Neuroscience Nursing, 38(5), 379-383.

Marion, D. (1997). Therapeutic moderate hypothermia for severe traumatic brain injury. Journal of Intensive Care Medicine, 12, 239-248.

Schaller, B., & Graf, R. (2003). Hypothermia and stroke: The pathophysiological background. Pathophysiology, 10(1), 7-35.

Wright, J. (2005). Therapeutic hypothermia in traumatic brain injury. Critical Care Nursing Quarterly, 28(2), 150-161.

Questions or comments about this article may be directed to Marie Lasater, MSN RN CCRN CNRN, at She is a clinical nurse in the neuroscience unit at Barnes-Jewish Hospital, St. Louis, MO.
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Article Details
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Author:Lasater, Marie
Publication:Journal of Neuroscience Nursing
Article Type:Case study
Geographic Code:1USA
Date:Aug 1, 2008
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