Caring for Patients with Acute
By PHYLLIS DUBENDORF, MSN, RN, CS, ACNP, CNRN
Head injury refers to a continuum of neurological injury with sequelae that vary from mild headache to persistent vegetative state. Head injury claims as many as 30 per 100,000 population per year in the United States. It is estimated that nonfatal head injury affects 200 per 100,000-population yearly in the country. However this statistic may not reflect actual incidence due to potential under-reporting of head injury occurrences.1
Overall, approximately 500,000 head injuries occurring in the United States are serious enough to require hospitalization.2 Severity of head injuries is based on post-resuscitative Glasgow coma scores (GCS); a score of three to eight denotes severe injury, nine to 12 denotes moderate injury and a GCS of 13-15 indicates mild or minimal injury.1 Although severe head injury is statistically uncommon, it comes with significant consequences such as long term disability or delayed mortality. "Mild" head injury can be a misnomer, resulting in a post-concussive syndrome that includes serious neuropsychological deficits and physical disabilities.2 (See Table)
The GCS and its variations are the most widely utilized scales to classify extent of head injury, although there are other scales used to categorize severity of injury. These classification systems focus on evaluation of specific populations, such as pediatrics or minor head injury, or include scoring based on results of neurodiagnostic studies, such as size and location of lesion based on computed tomography.
One scale, the Injury Severity Scale (ISS), is used to objectively quantify injury related to multiple trauma, head injury being one component of the score.
The Glasgow Outcome Scale (GOS) is a five point scale that identifies outcomes from head injury as ranging from "good" to "death," very broad and somewhat subjective categories. The Rancho Los Amigos Scale identifies levels of post-injury behavior and is very helpful at focusing therapies at appropriate times in the post-acute head injury phase.
The advantage of scaling or scoring injury is the ability to objectively assess and compare serial clinical evaluations, evaluate treatment strategies and apply statistical methods to scores in order to determine significance.
The highest risk age group for head injury in the United States is between 15 and 24 years of age, so in addition to the cost of injury in direct dollars of care provided to the patient and family, there is also a financial burden incurred in lost wages and productivity.3
Other high risk groups are children under the age of 10 and adults 60-65 years of age.
Men are at a higher risk for head injury than women.2 High risk has also been connected to substance abuse. Kraus found that more than 50 percent of those sustaining head injury tested positive for blood alcohol.4
Etiology & Mechanisms of Head Injury
High velocity impacts resulting from motor vehicle crashes, violence and falls are all recognized as significant etiologies of head injury. Sports and recreation are also recognized as significant factors. These types of injuries result most often in deformation of the skull, acceleration-deceleration of the intracranial contents and rotation of the brain tissue over supportive bony elements.3 Focal (or localized) brain injury occurring beneath deformation impact is known as a coup injury. Injuries occurring at the opposite pole of impact are named contracoup, and result from acceleration-deceleration.
Symptoms of head injury reflect the area and severity of damage to the brain; treatment of head injury is determined by understanding the relationship between injury and cerebral dynamics. In order to understand brain injuries and treatments aimed at preserving neurological function, it is necessary to review several basic tenets of neurological physiology and physiopathology:
The brain and its constituents (blood and cerebrospinal fluid) function within the constraints of a constant pressure environment (intracranial pressure) which is maintained in a closed box system (the skull). Movement within this box is further restricted by folds of the dura separating and supporting the delicate neural tissue.
Blood supply to the brain is governed by autoregulatory processes which, under normal parameters, are not dependent on systemic blood pressure. Once injury occurs, cerebral autoregulation is impaired (either focally or globally) and cerebral blood flow becomes dependent on systolic blood pressure (SBP).
The measurement of intracranial pressure (ICP) reflects swelling within the cranial vault; measurement of cerebral perfusion pressure (CPP) is calculated by subtracting the ICP from the mean arterial blood pressure (MAP) and indirectly reflects and trends occurrences of cerebral ischemia.
Primary vs. Secondary Injury
Primary damage to the brain and its constituents is reflected as cranial fracture, contusion, laceration, intracerebral hematomas, intraparenchymal hemorrhage and diffuse axonal injury. Primary damage is generally associated with mechanical impact to the cranium.
Secondary damage to the brain is based in a cycle of cerebral swelling and ischemia resulting in a biochemical cascade of injury. Secondary injury occurs within minutes, hours and even days after the initial injury. Numerous neurotransmitters, metabolites and pathological processes have been implicated in this process, such as endorphin release; increased glutamate, aspartate and acetylcholine activity; calcium flow disturbances; lactate production; electrolyte imbalances; free radicals production and lipid peroxidation of the cellular membrane.3
Treatment of Head Injury
Treatment of the head injured patient is focused on preserving the brain and preventing further injury, multisystem support strategies and preventing common complications. Optimizing neurological outcome is the single most important goal of any management strategy. Aggressive medical/surgical management continues to stress maintenance of normothermia, optimizing hemodynamic function, treatment of hypoxia, cerebral ischemia and intracranial hypertension.2
Current recommendations for the treatment of severe head injury have recently undergone several notable changes based on the 1995 report from the Brain Trauma Foundation, a meta-analysis of treatment variables aimed at managing severe head injury and increased intracranial pressure.5 Key recommendations are as follows:
* Hypoxia has been identified as a significant predictor of unfavorable outcome in severe head injury and therefore must be scrupulously avoided or rapidly corrected. The goal of oxygenation is to maintain or correct PaO2 values to at least 60 mm Hg.
Severely head injured patients will require intubation for therapeutic management. Consider also that head injured patients arising from multisystem trauma frequently have co-existing morbidities such as flail chest, hemo/pneumothorax and cervical spinal cord injury, impairing pulmonary function.2
* Hypotension is associated in approximately one-third of all severely head-injured patients, and is an even more ominous predictor of poor outcome than hypoxia.2 Systolic blood pressure should be maintained or corrected to at least 90 mm Hg or greater.5 If the patient is hypotensive, the source of hypotension must be identified and addressed.
The traumatically head-injured patient may have also sustained abdominal or vascular derangements resulting in hypovolemia. Volume correction may be achieved by administration of blood, crystalloids or colloids, or the addition of vasopressor agents when appropriate. Recent study of hypertonic saline and colloid infusions used as volume expanders for the head-injured patient have not revealed any distinct advantage over isotonic saline.2
* Hyperventilation, a mainstay of intracranial pressure management, has been linked with potentiating cerebral ischemia, and as such, cautious use is now recommended. The basis for the use of hyperventilation is vasoconstriction, limiting the amount of blood to the brain, thereby diminishing pressure within the cranium. Although limiting blood flow facilitates intracranial pressure requirements, it can result in significant cerebral ischemic events. Hyperventilation (PCO2<35 mm Hg) should be avoided if possible within the first 24 hours post injury, when cerebral blood flow is at its lowest. Moderate hyperventilation (PCO2 30-35 mm Hg) may be advocated if intracranial hypertension remains problematic.5
If hyperventilation is chosen as a therapeutic measure, efforts must be taken to further evaluate and assess blood flow to the brain. One mechanism to achieve this is by monitoring venous jugular bulb saturation to determine cerebral oxygen delivery and usage.2
* Mannitol continues to be the diuretic of choice for treating increased ICP. However, bolus doses of 1 gr/kg are recommended over continuous infusion.
* Barbiturates play a role in managing cerebral hypertension refractory to standard treatment. Barbiturates affect intracranial pressure in several ways: decreasing vascular tone, diminishing cerebral metabolic demands and inhibiting free radical mediated lipid peroxidation. However, barbiturates will depress cerebral responsiveness, therefore, other measures of ensuring and monitoring cerebral activity will be necessary if barbiturate therapy is instituted.
* Intracranial pressure monitoring is an integral aspect of head-injury evaluation. Strategies to reduce ICP should be initiated when ICP reaches 20-25 mm Hg.5 Methods to monitor include ventriculostomy, subarachnoid screw and fiberoptic monitoring.
* Cerebral perfusion pressure (CPP) must also be calculated in order to monitor and trend the relationship between systemic blood pressure and ICP. The Brain Trauma Foundation recommends that CPP be maintained or manipulated to a minimum of 70 mm Hg.
* Steroids, although beneficial in managing cerebral edema resulting from intracranial tumors, have not been statistically helpful in reducing cerebral edema related to trauma and trauma-related ischemia. Steroid administration in the head-injured patient is therefore not recommended.
* Nutritional needs are important for the patient with head injury because head injury and multiple trauma are known to increase the metabolic demands of the patient. In order to avoid deleterious affects of this hypercatabolic state, it is recommended that nutrition such as jejunal feedings are initiated by day seven after injury. One hundred-forty percent of caloric requirements should be given to nonparalyzed patients, and 100 percent of estimated caloric needs should be given to paralyzed, sedated patients. It is also recommended that at least 15 percent of these calories be delivered as protein.5 Some authors recommend initiating tube feeds as early as 24-48 hours after injury.2
* Seizure prophylaxis is a management option to prevent early post-traumatic seizures. Phenytoin and carbamezepine are both effective agents for early seizure prophylaxis. There is no convincing evidence to support the use of the agents in the prevention of late post-traumatic seizures.5,6
Acute Management Strategies
Acute care management strategies must also include prevention of further injury from common multisystem complications of head injury. In addition to impaired cerebral perfusion, some other complications to assess for in the head injured patient are: Pulmonary--pulmonary embolus, pneumonia; Cardio/Peripheral Vascular--cardiac arrhythmias, impaired blood pressure and end-organ perfusion, stroke, coagulation defects, skin alterations; Gastrointestinal--hemorrhage; Genitourinary--infection; and Metabolic--electrolyte imbalances, impaired nutrition.
The most effective means of addressing central nervous system trauma is through prevention.2 The use of seat-belts is now mandatory in 46 of the 50 states; seat-belt use has increased from 11 percent-66 percent based on that requirement.7 All new cars manufactured in the United States are required to include automatic seat belts and/or driver's side air bag. Many automotive manufacturers also advertise other safety features such as anti-lock brake systems, reinforced zones, crumple zones and side and passenger air bags.
Motor cycle helmet laws, bicycle helmet laws, and infant restraint mandates have also helped to decrease mortality and disability related to head injury. Strict enforcement of and adherence to legal age for alcohol consumption drunk driving laws will also be beneficial in diminishing alcohol-related injures.2 Continued educational efforts must be made to further reduce the incidence and severity of head injury.
Post-acute management of the brain injured patient is as varied as head injury itself. The focus of post-acute care shifts from physical care to functional self-care involving both the patient and the patient's family.
Individuals sustaining minor head injury may require neuropsychological testing and higher level outpatient therapy. Those experiencing significant sequelae from neurologic injury may exhibit continued motor, sensory-perceptual, communication, swallowing, bowel, bladder and cognitive/behavioral dysfunction, (or any combination of these) and will require long-term physical, occupational and vocational rehabilitation.3
Post-acute goals related to motor and sensory-perceptual dysfunction are chiefly those of mobility and sensory integration. Mobility is addressed through positioning, muscle strengthening, monitoring tone, balancing and transferring. Sensory-perceptual deficits are addressed by assisting the patient to recognize body position and to integrate other sensory input (including visual, auditory and tactile stimuli) into meaningful information.
Communication and swallowing disorders go hand-in-hand with the head-injured patient. Receptive and expressive areas in the brain govern the patient's ability to receive information and expressively communicate with others. Cranial nerve impairments may affect both motor and sensory function of the tongue, lips and pharynx, making communication and swallowing more difficult. Ineffective, incomplete or delayed swallowing places the patient at high risk for aspiration.
Bowel and bladder retraining may be instituted to help the patient achieve continence. Methods of feeding the head-injured patient range from long-term enteral feeding plans to a solid diet, again depending on the extent of head injury and the patient's progression in the recovery phase.
Examples of cognitive deficits include learning, memory and attention impairments. Behavioral changes in the head injured patient are to be expected, and may include impulsivity, changes in personality and even short-tempered, episodic violent behaviors.3
Safety can be difficult to ensure in the head-injured patient, because although physical therapy can improve motor impairment, the patient requires cognitive skills and insight to identify safe situations. Continuous supervision is required for those who are mobile and exhibit impulsive behaviors without identifying their consequences.
Head injury is a significant and devastating event in the lives of those experiencing the injury and on those supporting the head-injured patient. It is important to help these people realize that they do not have to be alone in the struggle to survive and manage the effects of head injury. Local and national groups, such as the National Head Injury Foundation, are good contact points for patients and family members. Success in head-injury recovery is realized in small incremental steps. The overall goal of head-injury care is maximizing the purpose and function of head-injury survivors.
For a copy of references see our Web site at advanceweb.com or call 800-355-5627, ext. 354.
Phyllis Dubendorf is a clinical faculty member, Acute Care Nurse Practitioner Program, University of Pennsylvania, Philadelphia.
Table: Signs and Symptoms of Post-Concussive Syndrome8
* Visual impairments
* Personality changes
* Sleep Disturbances
* Concentration &
Attention Disorders * Vertigo
Objectives & Questions
After you have completed reading this article, you will be able to:
1. Discuss etiologies and high risk groups related to head injury.
2. Discuss and differentiate between primary and secondary injury.
3. Identify at least three strategies to improve outcomes related to head injury.
4. Identify preventive measures related to head injury.
Learner Feedback Questions
(Complete the following multiple choice questions using the answer sheet on the next page.)
1. Risk of head injury increases in all but the following populations:
a. ages 15 to 24
d. situations in which alcohol or substances are involved
2. Etiologies of head injury include all but which of the following:
a. motor vehicle accidents
b. gunshot wounds
d. bicycle accidents
3. Mechanisms of primary injury to the brain include all but the following:
d. cerebral swelling
4. Under normal physiologic circumstances and parameters, cerebral blood flow is:
a. dependent on mean arterial blood flow.
b. dependent on systolic blood flow.
d. dependent on serum carbon dioxide levels.
5. Cerebral perfusion pressure reflects cerebral blood flow and is calculated by:
a. subtracting the mean arterial pressure from the systolic blood pressure.
b. adding the mean arterial and intra- cranial pressures.
c. subtracting the intracranial pressure from the mean arterial pressure.
d. adding intracranial pressure to the diastolic blood pressure.
6. Secondary injury involves all but the following:
a. rotation and shearing of neurological tissue across the bony base of the brain. b. cerebral swelling
c. the release of free radicals and lipid peroxidation
d. abnormal flux of calcium across the
7. Hyperventilation, based on Brain Trauma Foundation recommendations, can be used:
a. within the first 24 hours of injury only.
b. prophylactically to prevent increases in intracranial pressure.
c. in cases of refractory intracranial hyper- tension as long as further monitoring is initiated to determine cerebral oxygen delivery and usage.
d. to achieve a PCO2 < 30 mm Hg.
8. All of the following are recommended in the treatment of the brain-injured patient except:
c. nutrition support
9. Anticonvulsants are useful in the management of the head-injured patient:
a. to prevent early and late seizure activity.
b. to prevent early post-traumatic seizures only.
c. to prevent late post-traumatic seizures only.
d. anticonvulsants are not useful.
10. Post-acute management of the head injured patient includes which of the following:
a. physical therapy for muscle #009;strengthening
b.occupational therapy to teach and reinforce self-care activities
c.speech therapy to assist with commu-nication and swallowing dysfunction
d.all of the above
This continuing education offering expires Aug. 23, 2001.
Caring for Patients with Acute Head Injury
1 Contact Hour
To earn continuing education credit, before August 23, 2001, 1) complete the form above, 2) record answers to the questions on this page, 3) mail this form (or a photocopy) and $7.50 to: ADVANCE for Nurses Learning Scope, 2900 Horizon Dr., King of Prussia, PA 19406; Or fax (available with credit card payment only) to: (610) 278-1422.
Make checks or money order payable to Merion Publications Learning Scope
Payment is due when the test is submitted
A certificate of credit will be awarded to participants who achieve a passing grade of 70 percent or better. Participants should allow 45 days for notification of scores and receipt of certificate.
Evaluation -- Caring for Patients
with Acute Head Injury
Rate statements 1-6 below on a scale of 1 (strongly disagree) to 5 (strongly agree). Fill in the information for questions 7-8.
1. I can discuss the etiologies and high-risk groups related to head injury. 1 2 3 4 5
2. I can discuss and differentiate between primary and secondary injury. 1 2 3 4 5
3. I can identify at least three strategies to improveoutcomes related to head injury. 1 2 3 4 5
4. I can identify preventive measures related to head injury.1 2 3 4 5
5. The objectives relate to the overall goal of the article. 1 2 3 4 5
6.The teaching/learning resources were effective. 1 2 3 4 5
7.The article was well written, terms defined, graphics helpful, easy to understand. 1 2 3 4 5
8. How much time did you need to complete this CE offering?
9. Why did you choose this offering?