Head Trauma Nursing Case Study

A 71-year-old man is brought to the emergency department by his family after he tripped and fell in his backyard 30 minutes before presentation. He hit the side of his head against a brick wall in the garden, but he had no loss of consciousness and felt fine prior to tripping. He has a mild headache but no other injuries. He has a history of hypertension and atrial fibrillation and takes metoprolol and warfarin.

His examination is normal except for a small contusion just above his right ear. His neurologic examination, including memory, is normal as well.

Blood work is done, and his labs are normal except for an international normalized ratio (INR) of 2.4. His head CT is shown below. He feels fine and wants to go home.

What does the CT scan show? What should you recommend?

Click to the next page for the answer.

 

RN/DREXEL Home Study Program
CE CENTER

CE credit is no longer available for this article. Expired July 2005


Originally posted April 2004

SANDRA J. BRETTLER, RN, MSN, CCRN, CNRN

SANDRA BRETTLER is a clinical nurse educator in surgical intensive care and postanesthesia care at Pennsylvania State University Milton S. Hershey Medical Center in Hershey, Pa.

KEY WORDS: traumatic brain injury (TBI), intracranial pressure (ICP), Glasgow Coma Scale (GCS), cerebral blood flow (CBF), cerebral perfusion pressure (CPP), ventriculostomy

Traumatic brain injury is a leading cause of death and long-term disability in the United States. Knowing how to properly assess and care for patients with this type of injury can save their lives.

Kevin Campbell, 22, and his fiancée were on their way to a celebratory dinner when a deer jumped out in front of their car. Mr. Campbell swerved to miss the deer, ran off the road into an embankment, and hit a tree head on. His fiancée was wearing her seat belt and had only minor cuts and scratches, but Mr. Campbell wasn't, and his head hit the windshield. He lost consciousness, sustained several large cuts to his forehead, and was bleeding from his nose and mouth. His fiancée used her cell phone to dial 911.

When emergency medical service personnel arrive, Mr. Campbell is unconscious but breathing. The paramedics stabilize his spine using a rigid cervical collar, and place him on a long board for transport. While en route to the nearby trauma center, they monitor his airway, insert two large-bore intravenous lines, and begin infusing normal saline.

The EMS staff report Mr. Campbell's vital signs to the receiving emergency department as stable: heart rate is 95, respiratory rate is 18, and blood pressure is 115/74. Oxygen saturation is 96% and the cardiac monitor shows sinus rhythm without ectopy.

Mr. Campbell's pupils are equal and reactive and he withdraws his extremities to a stimulus of deep pain but doesn't open his eyes or speak. Based on these findings, the EMS crew and ED staff suspect a traumatic brain injury (TBI).

TBI often results in long-term disability

TBI occurs when a blow or jolt to the head disrupts the normal function of the brain.1 Its effects range from a brief change in consciousness to long-term coma, permanent disability, or death.

Each year, approximately 1.5 million people in the United States sustain a TBI; 50,000 of them die from the injury and as many as 90,000 experience long-term disability.2 In this country, there are currently about 5.3 million people living with disabilities resulting from a TBI.2

The main causes of TBI are motor vehicle crashes, violence, and falls.3 Motor vehicle crashes account for approximately 50% of all TBIs.3 Shootings are responsible for less than 10% but are the leading cause of death from TBI; about two-thirds of firearm-related TBIs are suicides or suicide attempts.3 Falls account for slightly more than a quarter of all TBIs and are the leading cause of TBI among elderly patients.3

Males are twice as likely as females to suffer a TBI. At highest risk are people in the 15 – 24 age group and those over 75.1

There are several ways to classify TBIs. They can be classified as penetrating (open) or non-penetrating (closed) head injuries.4 A penetrating injury is one in which there is a break in the skull—say, from a bullet piercing the brain. Non-penetrating brain injuries are caused by rapid back-and-forth movement of the brain inside the skull. These movements result in bruised and torn brain tissue and blood vessels. Non-penetrating head injuries are usually the result of a fall or a motor vehicle crash.4

TBI can also be classified as primary or secondary. Primary brain injury refers to the mechanical disruption of axons, cell bodies, and cell membranes that occurs at the time of the initial impact.5 Secondary injury occurs in response to the primary injury and leads to cerebral edema, ischemia, increased intracranial pressure (ICP), and other changes within the brain tissue. ICP is discussed in more detail in the "A quick review of intracranial pressure" box. Causes of secondary injury include hypoxia, hypercapnia, and hypertension.

Either primary or secondary brain injury can result in cell death. Minimizing or preventing secondary injury greatly increases a patient's chances of preserving or recovering function.6

Secondary injury prevention starts in the ED

Managing a patient with severe TBI requires a well-defined plan, plenty of resources, and an organized team to prevent secondary injuries, such as cerebral edema and ischemia, from occurring.

If you work in the ED, begin your assessment with the ABCDs: airway, breathing, circulation, and disability. As always, establishing and maintaining an airway is top priority. Deliver supplemental oxygen using a bag-valve-mask device until a definitive airway is placed.

Intubation and mechanical ventilation are necessary if the patient can't maintain or protect his airway because his level of consciousness (LOC) is depressed. Intubation and ventilation are also necessary if the patient is in danger of losing his airway because of swelling from a neck or pharyngeal injury or if he is expected to deteriorate neurologically.

Ensure that the patient has two large-bore IVs and that they're still intact and patent. If volume resuscitation becomes necessary, use warmed isotonic saline (0.9% NaCl); it's the fluid of choice for head injury patients because it won't aggravate cerebral edema.7 Hypertonic saline has also been used for volume resuscitation in TBI patients and has been shown to reduce ICP.8 Dextrose 5% in water (D5W) should be avoided because it tends to leave the vascular space rather quickly, therefore promoting swelling. Fluids given to trauma patients, especially those to be given in large volumes, should be placed on a fluid warmer to prevent hypothermia.

Maintain a systolic blood pressure above 90 mm Hg.7 In general, if blood loss is greater than 30% of total blood volume, blood products should be used as part of volume resuscitation.

Once the patient is hemodynamically stable and his airway is secure, the most important part of your assessment will be his neurological assessment, including LOC and pupillary reaction. As the "The Glasgow Coma Scale at a glance" box explains, the Glasgow Coma Scale (GCS) is the most frequently used tool for determining LOC following a TBI.

Scores range from 3 to 15; the lower the score, the greater the impairment in LOC. A score of 8 or less may indicate a severe head injury and a high probability of permanent or long-term damage. Because Mr. Campbell's GCS score was 8, he was intubated and placed on a ventilator.

In addition to LOC, assess the patient's pupil size and reactivity. Pupils are normally round, approximately 3 – 5 mm in diameter, equal in size, and briskly reactive to light.9 Although oval pupils indicate increased ICP, pupils may be round even if ICP is elevated. Dilated and bilaterally fixed pupils indicate massive elevations in ICP, which can result in brain death.9 If the patient's pupils are not the same size, or if he experiences any changes in pupil size, shape, and reactivity, notify the physician immediately.9

Also assess the patient's brainstem responses, including the cough, gag, corneal (blink), and oculocephalic (doll's eyes) reflexes.9 If a patient has these reflexes, the integrity of his brainstem has not been disrupted; if he doesn't, his prognosis is poor.

Palpate the patient's scalp to detect signs of fracture, and gently probe any scalp lacerations to check for depressed fractures or foreign bodies.6 Look for signs of basal skull fracture, including hemotympanum, which is a collection of blood in the middle ear space; leakage of cerebrospinal fluid from the ears or nose; mastoid ecchymosis, also known as Battle's sign; and periorbital ecchymosis, or raccoon eyes.6

If you suspect a basal skull fracture, don't place a nasogastric tube; you may inadvertently insert it into the brain through the fracture.7 An orogastric tube is recommended instead because the tube does not come into contact with the paranasal sinuses. If possible, an orogastric tube should be placed before intubation to prevent aspiration.

If your patient is posturing, has unequal or nonreactive pupils, or other assessment findings suggestive of increased ICP, you may need to administer mannitol (Osmitrol) 0.25 – 1 gm/kg IV as ordered.8 Best given as a bolus, this potent hyperosmolar diuretic can decrease ICP and reduce blood viscosity. Because high doses of mannitol significantly increase a patient's risk of acute renal failure, particularly if his serum osmolality exceeds 320 mOsm/kg, maintain the patient's serum osmolality at <320 mOsm/kg.8 Make sure your patient is well hydrated and not hypovolemic before administering mannitol.

Send specimens for routine laboratory tests, including complete blood counts, electrolytes, type and cross match, coagulation profiles, and toxicology screens for alcohol and illicit drugs. Also consider tetanus prophylaxis for these patients.7

Imaging studies are useful diagnostic tools

After the patient has been stabilized, a computed tomography scan is typically done to determine whether the injury is hemorrhagic or non-hemorrhagic. If arterial bleeding is suspected, a neurosurgical consultation and surgery is usually required, and may be initiated early in the ED visit. If the bleeding is from a venous source, treatment will depend on several factors, including the patient's age, prognosis, the size and location of the blood clot, and the presence of other injuries.

Larger clots usually require evacuation, provided the patient is a candidate for surgery; smaller clots may be managed medically. Mr. Campbell's CT scan showed bilateral frontal contusions and a small subdural bleed. Since subdural blood is usually from a venous source, and the patient's clot was small, the neurosurgeons ordered close observation in the ICU to monitor Mr. Campbell rather than operate on him.

Some trauma centers have the capability to do computed tomographic angiography (CTA), a procedure that evaluates the intracranial and extracranial vessels.7 Cerebral angiography may be performed if a vascular injury, such as carotid or vertebral artery dissection, a traumatic pseudoaneurysm, or an arteriovenous fistula, is suspected.7

Magnetic resonance imaging scanning is useful when a patient's CT scan doesn't provide a clear picture of the injury. MRIs can provide valuable information on posterior fossa structures and allow for better definition of mass lesions than CT; however, because MRI requires more time than CT, it's usually not done on acute or unstable patients.9 Magnetic resonance angiography (MRA) and magnetic resonance venograms (MRV) are useful if vascular or sinus injuries are suspected.7

Monitoring the brain is the key to treatment

Once the patient has been transferred to the ICU, his neurological care focuses on close observation and monitoring to prevent secondary brain injury. To achieve this goal, closely monitor ICP, cerebral blood flow (CBF), cerebral perfusion pressure (CPP), and vital signs, along with neuro status.9

Over the last few decades, technological advances have been developed to help prevent or minimize secondary injury following TBI. One such advance is ICP monitoring.

A variety of ICP monitoring devices are available. Ventriculostomy devices are placed in the ventricles of the brain. Other types of ICP monitoring devices are placed in the cerebral parenchyma or in the subdural or subarachnoid space.

Typically, ICP monitors are placed in all patients with a GCS score of 8 or lower.6 Because Mr. Campbell had a score of 8, he had a ventriculostomy catheter inserted before being transported to ICU.

Ventriculostomy devices are preferred over other types of devices because they're highly accurate and they allow you to lower ICP by draining CSF.6 The goal is to maintain ICP below 20 mm Hg or as otherwise ordered by the physician.

Nursing interventions to prevent increased ICP include keeping the patient's head and neck properly aligned and the head of the bed elevated a minimum of 30 degrees or as ordered; both of these interventions promote cerebral venous drainage and, in doing so, help keep ICP down.

Although hyperventilation can rapidly lower ICP in some patients, it can also result in markedly reduced cerebral blood flow; therefore, limiting its use may help improve neurologic recovery.8 Prophylactic hyperventilation to keep PaCO2 ¾35 mm Hg should be avoided during the first 24 hours following severe TBI.8 Hyperventilation may be necessary for brief periods in patients with severe neurologic deterioration whose ICP cannot be lowered by other methods, such as sedation.8

CPP should be monitored in addition to ICP. CPP is the pressure it takes for the heart to get blood to the brain. It's calculated by subtracting ICP from mean arterial pressure (MAP).10 Normal CPP is 70 – 95 mm Hg, so the goal in severe TBI is to maintain a CPP of at least 70 mm Hg.8 This can be achieved by supporting MAP and reducing ICP.

Cerebral blood flow is also used to guide treatment in severe TBI. Normal CBF is approximately 15% of the cardiac output—or about 750 – 800 ml/min.11

Transcranial Doppler (TCD) studies are used to determine the adequacy of CBF. This noninvasive test measures the velocity of blood flow in the cerebral vessels. As vessels narrow due to vasospasm, blood flow velocity increases. Generally, a velocity greater than 140 cm/sec indicates arterial narrowing; greater than 200 cm/sec indicates severe vasospasm.

Studies suggest that measuring the oxygen levels of the brain tissue may be clinically important in the assessment of TBI patients.5 Both global and regional measuring devices are available.

A jugular bulb oxygen saturation (SjO2) monitor is a global measuring device that can be used to diagnose and monitor cerebral ischemia. A small fiberoptic catheter is placed in the jugular vein to monitor the amount of oxygen in the blood returning from the brain. A normal value for SjO2 is 50 – 75%.12 A drop in SjO2 indicates an imbalance between oxygen consumption and delivery.12

Brain tissue oxygenation monitoring can also be done with a regional-type monitor. Most studies to date have been performed with the LICOX system. This system includes a monitor that displays oxygen and temperature values and a variety of probes for use in the brain, cardiac muscle, and peripheral muscles. It measures oxygen status and brain temperature within the brain tissue itself, providing more reliable data than jugular catheters.

Because the system can detect only what's happening in the area around the monitoring probe, the best location for the probe has not been determined. When placed in the injured area of brain, the probe provides information about oxygenation and swelling in that region of the brain, but no data on what's happening in the rest of the brain. Placing the probe in unaffected brain tissue limits your ability to see the subtle changes in hypoxia in the injured area. Normal values for brain tissue oxygenation (PbtO2) range from 20 – 35 mm Hg.13

Data on brain temperature provided by the LICOX system is helpful in the management of TBI. Temperature within the brain is significantly higher than core body temperature after TBI.14

For years, many clinicians believed that rectal temperature was fairly close to brain temperature, but studies show that cerebral temperature is actually about 2° F (1.1 °C) higher than the rectal temperature.14 Increases in body temperature by one degree can increase the cerebral metabolic rate by about 7%, leading to problems with cerebral ischemia. The question, though, is what to do about such increases in temperature. The efficacy of hypothermia in TBI patients remains controversial. Some studies, though, show that moderate hypothermia may improve outcomes.7

While in the ICU, nurses assess Mr. Campbell every hour, noting his cardiovascular parameters, neurologic status, ICP, CPP, and temperature. They maintain his body temperature within normal range and keep him hydrated, enough to maintain a urine output of 0.5 – 1 ml/kg/hr. After several days, he begins to wake up and becomes agitated. He's still unable to follow commands, but he opens his eyes to the sound of his fiancée's voice. Over the next few days, he continues to improve, but slowly.

Recovery can be lengthy and unpredictable

A structured discharge and follow-up plan is essential. Once a TBI patient no longer needs acute care, he can be transferred to a subacute care unit, and then to acute rehab. Following rehab, he may be discharged home and referred to community-based rehab and outpatient services.

A long-term treatment plan may include speech and language therapy, cognitive rehabilitation, and psychological, physical, and occupational therapy, some of which may start while the patient is in the ICU.15 Some patients will have no long-term deficits, while others will have multiple cognitive and physical disabilities.15

The potential for improvement after TBI can be unpredictable. Progress can be painfully slow and the patient may never be the same as he was before the injury. As the brain heals, personality and behavior may change and the patient may face new issues and challenges. For example, Mr. Campbell will need to relearn many of the simple, basic tasks he had mastered over the last 22 years.

A TBI greatly affects the patient's family as well. Family members will need education regarding traumatic brain injury, rehabilitation, and caregiving. They will also need referrals to appropriate community resources and support groups. (For information on caring for the family of a TBI patient, see "Traumatic brain injury: Help for the family" in the November 2002 issue of RN.)

Advances in emergency and critical care have considerably reduced the death rate from TBI.16 Over the past 30 years, the mortality rate for severe TBI has decreased from 50% to 25%.16 Providing prompt, state-of-the-art care may help improve the odds that your TBI patient will survive and, perhaps, spare him a lifetime of severe disability.

REFERENCES

1. Centers for Disease Control and Prevention. "Traumatic brain injury." 2003. www.cdc.gov/ncipc/factsheets/tbi.htm (13 Jan. 2004).

2. Thurman, D. J., Alverson, C., et al. (1999). Traumatic brain injury in the United States: A public health perspective. J Head Trauma Rehabil, 14(6), 602.

3. Centers for Disease Control and Prevention, National Center for Injury Prevention and Control. "Traumatic brain injury in the United States—A report to Congress." 1999. www.cdc.gov/doc.do?id=0900f3ec8001011c (13 Jan. 2004).

4. University of Utah Health Sciences Center. "Physical medicine and rehabilitation: Acquired brain injury." 2002. www.med.utah.edu/healthinfo/adult/Rehab/braininj.htm (13 Jan. 2004).

5. Littlejohns, L. R., Bader, M. K., & March, K. (2003). Brain tissue oxygen monitoring in severe brain injury I: Research and usefulness in critical care. Crit Care Nurse, 23(4), 17.

6. Bergsneider, M., & Kelly, D. F. (2003). Brain injury. In G. P. Naude, F. S. Bongard, & D. Demetriades (Eds.), Trauma secrets (2nd ed.), (pp. 51 – 59). Philadelphia: Hanley & Belfus.

7. Vinas, F., & Pilitsis, J. "Penetrating head trauma." 2003. www.emedicine.com/med/topic2888.htm (13 Jan. 2004).

8. Brain trauma foundation. "Management and prognosis of severe traumatic brain injury." 2000. www2.braintrauma.org/guidelines/downloads/btf_ guidelines_management.pdf (13 Jan. 2004).

9. Blank-Reid, C., & Barker, E. (2002). Neurotrauma: Traumatic brain injury. In E. Barker, Neuroscience nursing: A spectrum of care (2nd ed.), (pp. 409 – 437). St. Louis: Mosby.

10. Barker, E. (2002). Intracranial pressure and monitoring. In E. Barker, Neuroscience nursing: A spectrum of care (2nd ed.), (pp. 379 – 408). St. Louis: Mosby.

11. Hickey, J. V. (2002). The clinical practice of neurological and neurosurgical nursing (5th ed.), (p. 287). Philadelphia: Lippincott, Williams & Wilkins.

12. Trauma.org. "Neuromonitoring for traumatic brain injury." 2000. www.trauma.org/neuro/neuromonitor.html (13 Jan. 2004).

13. Bader, M., Littlejohns, L., & March, K. (2003). Brain tissue oxygen monitoring in severe brain injury II: Implications for critical care teams and case study. Crit Care Nurse, 23(4), 29.

14. Rumana, C. S., Gopinath, S. P., et al. (1998). Brain temperature exceeds systemic temperature in head-injured patients. Crit Care Med, 26(3), 562.

15. Bond, C. (2002). Traumatic brain injury: Help for the family. RN, 65(11), 60.

16. Zink, B. J. (2001). Traumatic brain injury outcome: Concepts for emergency care. Ann Emerg Med, 37(3), 318.


A quick review of intracranial pressure

The cranium is an enclosed space that houses three components: brain tissue, blood, and cerebrospinal fluid. The pressure within the skull—intracranial pressure (ICP)—is determined by these three components. Normal ICP is 0 – 15 mm Hg.

When one of these three components increases in volume, one or both of the other components must compensate by decreasing. Regulatory mechanisms, such as autoregulation (the capacity of the brain to regulate cerebral blood flow), compliance (the ability of the brain to tolerate an increase in intracranial volume), and the shunting of CSF into the spinal sac, help maintain ICP within a normal range. When the limits of compensation have been reached, ICP increases, compromising brain perfusion.

Sources: 1. Littlejohns, L. R., Bader, M. K., March, K. (2003). Brain tissue oxygen monitoring in severe brain injury I: Research and usefulness in critical care. Crit Care Nurse, 23(4), 17. 2. Barker, E. (2002). Intracranial pressure and monitoring. In E. Barker, Neuroscience nursing: A spectrum of care (2nd ed.), (pp. 379 – 408). St. Louis: Mosby.


The Glasgow Coma Scale at a glance

The Glasgow Coma Scale (GCS) is the most widely used system for scoring the level of consciousness of a patient who has had a traumatic brain injury. It's based on the patient's best eye-opening, verbal, and motor responses. Each response is scored and then the three scores are totalled. The lowest possible score is 3 and the highest is 15. GCS scores are often documented as three individual component scores followed by a total, such as E3 V3 M5 = GCS 11. A total score of ¾8 indicates severe brain injury; 9 – 12, moderate injury; and >13, mild brain injury.

 

Eye opening (E)Verbal response (V)Motor response (M)
4=Spontaneous
3=To verbal stimuli
2=To pain
1=No response
5=Normal conversation
4=Confused conversation
3=Inappropriate words
2=Incomprehensible speech
1=No response
6=Obeys commands for movement
5=Purposeful movement to pain
4=Withdraws in response to pain
3=Flexion to pain (decorticate posturing)
2=Extension to pain (decerebrate posturing)
1=No response

 

Source: Teasdale, G., & Jennett, B. (1974). Assessment of coma and impaired consciousness. A practical scale. Lancet, 2(7872), 81.


For more information

Brain Injury Association of America
8201 Greensboro Dr., Suite 611
McLean, VA 22102
(703) 761-0750;
Family helpline: (800) 444-6443
www.biausa.org

Brain Trauma Foundation
523 East 72nd St., 8th Floor
New York, NY 10021
(212) 772-0608
www.braintrauma.org

North American Brain Injury Society
5909 Ashby Manor Place
Alexandria, VA 22310
(703) 683-8400
www.nabis.org

The Perspectives Network
P. O. Box 121012
W. Melbourne, FL 32912-1012
E-mail: [email protected]
www.tbi.org


 

Kathleen Moore, ed. Sandra Brettler. Trauma nursing: Traumatic brain injury. RN Apr. 1, 2004;67:32.

Published in RN Magazine.

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