TRAUMATIC CLOSED HEAD INJURIES
Robert W. Stein, III, RN, MSHA, CHE, LNC
Trauma is the leading cause of death in young people in the United States. Two thirds of
these deaths are a direct result of a head injury. Approximately ten million head injuries are treated each year
at an enormous annual cost.5 The impact
of head trauma is far reaching and warrants its study. The focus of this paper will be on the mechanisms of injury,
the types of head injuries, their diagnosis and treatment, and the implications for the practice of nursing.
When the skull is struck by a blunt object there is a molding of the skull that occurs. Lesions
beneath this point are referred to as coupe lesions. A corresponding out bending of the skull occurs on the opposite
side. Lesions in this area are referred to as contra-coupe lesions. Lesions at locations in between are known as
intermediate coupe lesions. The brain, being relatively incompressible, responds to this force by shifting, sliding,
and rotating within the skull. This motion results in a shear stress on the brain and dura. Motion is greatest
in the parietal and occipital areas where the skull is smooth. A lessor amount of motion occurs in the frontal
and temporal regions where the irregular and sharp edges retard motion, but result in lacerations of the brain.4 The brainstem is relatively secured by its anatomic location,
but remains susceptible to injury as a result of the rotational movement of the brain on impact. Brain injury,
in the form of laceration, contusion, or disruption of the cerebral vasculature is a result of this force and motion.7
There are four specific groups of closed head injuries: hematomas, hemorrhages, concussions,
and contusions. Each group may be further subdivided according to their anatomic location. A hematoma may be epidural,
subdural, or intracerebal. Hemorrhages may occur anywhere, but the most common is the subarachnoid hemorrhage.
A contusion is a localized coupe and/or contra coupe brain surface injury. A concussion is a clinical diagnosis
without evidence of gross neurological damage.4 Each
of these injuries will be addressed individually.
Concussion is defined as a neurological deficit without grossly visible brain damage. Currently
there are two prominent theories as to how this occurs. Groat found histological changes in the neurons of the
reticular formation following rotational motion of the brain as seen in blunt head trauma.4 The reticular formation, the center of consciousness in the brain,
is rendered temporarily inactive as a result of the damaged neurons. The second theory, proposed by Holburn suggests
the neurological deficit seen in concussion is a result of shearing stress produced by the motion and rotation
of the brain on blunt impact.4 Shearing
stress, by producing a tearing of the nerve fibers, would functionally disconnect the temporal lobes from the diencephalon
resulting in amnesia. A functional disconnection of the reticular formation from the cerebral cortex would produce
a loss of consciousness. Both hypotheses remain on a theoretical and experimental level.4
Concussion is a clinical diagnosis made by the history of transient neurological deficit
or loss of consciousness following blunt head trauma. The deficit should clear within an hour of the injury and
may be accompanied by a period of amnesia or disorientation.7 The physical examination will be normal as well as any laboratory or radiologic studies.1
The treatment of concussion is limited to a period of observation long enough to determine
that the patient is improving, and to symptomatic treatment such as non-narcotic analgesics for headache. Upon
discharge from the Emergency Department, head injury precautions (see figure 1) should be given to a responsible
party that will be able to continue observation for the first twelve hours post-injury.8
Nursing care for the patient with a concussion will include: taking an accurate history,
performing a complete physical assessment and serial neurological evaluations, monitoring of vital signs, and explaining
the Head Injury Discharge Instructions to the responsible party.8
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HEAD INJURY INSTRUCTIONS
1. Eyes: pupils should be equal in size and react equally to light. Eyes should
move together. If pupils are not equal or eyes act independently, notify your doctor.
2. Headaches are not unusual after a head injury. Aspirin or similar medications
are good to use. CHILDREN UNDER 12 YEARS OF AGE SHOULD BE GIVEN TYLENOL (or Tylenol substitute) NOT ASPIRIN. DO
NOT ask your doctor for, and do not take strong medicines since they might hide or cover important symptoms.
3. Observe patient for changes in behavior, eating or walking habits.
4. Nausea or vomiting is not uncommon after head injury however if you have more
than 2 episodes of vomiting call your doctor. Drowsiness or slight dizziness is not unusual. Notify your doctor
immediately if any of the following symptoms occur:
a. Vomiting that comes out like a bullet and that is NOT preceded by "feeling sick".
b. If you are unable to walk patient or if patient has excessive, unusual drowsiness.
c. Any bleeding or fluid discharge from ears or nose.
d. High Fever, especially in a small child.
Call Dr. ____________________ at ______________ for follow-up care or for any questions
or difficulty.
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| Figure 1: Head Injury Discharge
Instruction Sheet. |
Cerebral contusions are caused by direct blows to the head and result in coupe and/or contra-coupe
bruising and petechial hemorrhages. The patient with a cerebral contusionpresents with a history of blunt head
trauma, neurological deficit persisting longer than twelve hours post-injury, and may show signs of increased intracranial
pressure if cerebral edema results.1
As with concussion, cerebral contusion is a clinical diagnosis made by history and physical
examination. Laboratory and radiologic studies will be within normal limits. Computed Axial Tomographic (CT) Scan
may reveal petechial hemorrhages or cerebral edema in severe contusions. On examination aphasia implies a frontal
or temporal lobe contusion. Hemiparesis may be present in frontal lobe contusions. Numbness of one side of the
body may result from a contusion of the parietal lobe, but more commonly is hysterical in origin. Contusions to
the frontal or temporal lobes may result in confusion or combativeness. These findings in the lethargic, stuporous
patient may indicate contusion, but need further evaluation for the possibility of a hematoma.9
Treatment of cerebral contusion is usually to admit the patient to the hospital for close
observation for signs of increased intracranial pressure and the administration of steroids at the discretion of
the attending physician. Steroids are administered to retard the development of cerebral edema in the first few
days following the injury.9
Nursing care for the patient with a cerebral contusion would include taking a complete history
including the mechanism of injury. The physical examination should include a baseline neurological assessment.
Frequent serial neurological assessments every 15-30 minutes should be performed observing for changes from the
baseline exam.8
An epidural hematoma is a serious head injury resulting from a low velocity blow to the head.
The blunt trauma results in movement of the skull relative to the dura beneath it. The shearing stress of this
movement results in an abnormal epidural space where ruptured blood vessels bleed into.3 The most common epidural hematoma occurs in the parietal-temporal
area following the laceration of the middle meningeal artery by a temporal skull fracture.2 As the lesion expands, cerebrospinal fluid is displaced from the
subarachnoid space and ventricles. When maximal displacement is exceeded, herniation of the temporal lobe through
the tentorial hiatus will result in brainstem compression.4 If the lesion continues to expand, increased pressure and herniation result in death within 24 hours
of the injury without surgical intervention.2
The patient with an epidural hematoma presents with a history of blunt head trauma. A loss
of consciousness may precede a period of lucidness in about 50% of cases, the remaining 50% remain unconscious
from the time of the injury. Progressive neurologic deterioration is the general course for an epidural hematoma.4
Increased intracranial pressure is responsible for the initial symptoms of an epidural hematoma,
including the classic triad of headache, vomiting, and papilla edema. A decrease in the level of consciousness,
visual disturbances, and seizure activity may also occur.1
Later symptoms are related to progressive herniation of the temporal lobe resulting in increased
pressure on the brainstem. A decrease in the level of consciousness will be caused by increased pressure on the
reticular formation. The oculomotor nerve (cranial nerve Ill) will also be compressed and result in an initial
constriction of and later dilation and fixation of the ipsilateral pupil. Eventual paralysis of the extraocular
muscles may occur.4 Increased pressure
on the hemisphere or cerebral peduncle may result in an ipsilateral hemiplegia, or more frequently, a contralateral
hemiparesis.4 Continued neurologic deterioration
will result in decerebrate posturing and irregular respiratory patterns.2
The diagnosis of epidural hematoma is made on the basis of history and physical. The typical
history is of blunt head trauma, with or without a brief period of unconsciousness followed by a period of lucidness
and then progressive neurological deterioration. The physical and neurologic examinations reveal the findings related
to the pathophysiology discussed above. Laboratory studies will not be of benefit in making the diagnosis of epidural
hematoma. Radiologic studies may reveal a skull fracture. Cranial CT Scan (see Figure 2) will demonstrate the lesion
and resultant midline shift. If CT Scan is not available, carotid arteriography may be used to demonstrate the
avascular lesion.6
The only treatment for an epidural hematoma is surgical evacuation of the lesion. Following
evacuation, it is suggested that the dura be opened to inspect for any concomitant subdural hematoma.6
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| Figure 2: Cranial CT Scan
of an epidural hematoma. |
Nursing care should include obtaining an accurate history, especially the mechanism of injury
and clinical course since that time. Physical examination should include a baseline neurological assessment. Cervical
fractures are often associated with head injuries and should be assumed present until ruled out by radiologic studies.
Close monitoring of the neurological status should be done, observing for signs of increased intracranial pressure.
Mild analgesics or codeine may be given to control pain. The nurse should provide seizure precautions including
the administration of prophylactic anticonvulsants.1
Subdural hematomas result from blunt head trauma causing a shifting and rotation of the brain.
The shearing stress created causes laceration of vessels, usually veins, and bleeding into the subdural space.
Subdural hematomas may be sub-classified as either acute, subacute, or chronic depending upon the delay in clinical
symptoms following the trauma. Acute subdural hematomas become symptomatic within the first three days following
the injury. Subacute subdural hematomas become symptomatic within the first two weeks following an injury. Chronic
subdural hematomas do not become symptomatic for several weeks following an injury, and often, the trauma was so
trivial that it is not recalled as significant.4
The increased intracranial pressure caused by the mass lesion of the subdural hematoma result
in the same symptoms as the epidural hematoma. The onset and speed of deterioration will vary depending on the
acuteness of the hematoma.4
The diagnosis of subdural hematoma is made on the basis of history and physical, and made
conclusive by CT Scan (see Figure 3).2
In the absence of CT Scan, the diagnosis may be confirmed by bilateral arteriography.6
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| Figure 3: Cranial CT Scan of a subdural hematoma. |
Treatment of subdural hematomas is also the same for epidural hematoma - surgical evacuation
of the mass lesion. This may need to be done on an emergent basis for the acute subdural hematoma, or on an urgent
basis for the subacute subdural hematoma. Chronic subdural hematomas may require surgical evacuation, or small
hematomas may be left to resolve themselves.2
Measures to reduce the intracranial pressure may be used such as hyperventilation, diuresis, and the administration
of steroids.9
Nursing care for the patient with a subdural hematoma is the same as for the epidural hematoma.
Care is based on observation for signs of increased intracranial pressure and imploring methods. to reduce the
intracranial pressure: elevation of the head of the bed 300, administration of diuretics such as mannitol, and
administration of steroids such as dexamethasone.9
Intracerebral hematomas are formed by motion of the brain upon blunt impact creating a shearing
stress. The shearing stress disrupts cerebral vessels deep within the brain. Typically, intracerebral hematomas
are found in the frontal and temporal lobes.2
The symptoms of an intracerebral hematoma as with the other hematomas are a result of increased
intracranial pressure. Coma, neuromotor deficits, and decorticate I decerebrate posturing may occur.2
CT Scan (see figure 4) or cerebral arteriography identify the intracerebral Iiemtaoma, confirming
the diagnosis of suspicion obtained through history and physical examination. Laboratory studies will reveal bloody
or xanthochromic (yellow) cerebral spinal fluid.2
The treatment for intracerebral hematomas is surgical decompression by the use of burr holes
or removing a bone flap. Therapies used with the other hematomas to control the increased intracranial pressure
may
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| Figure 4: CT Scan of an intracerebral hematoma. |
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| Figure 5: CT Scan of a subarachnoid hemorrhage. |
be used in addition to or instead of surgical intervention.2 Nursing care remains the same as for the other hematomas.9
A traumatic subarachnoid hemorrhage results when blunt head trauma causes shearing stress
sufficient to disrupt surface arteries lying in the subarachnoid space. The bleed may be immediate or delayed depending
on the size, vasoconstriction, and retraction of the disrupted vessel. Blood flowing into the subarachnoid space
mixes with the circulating cerebra-spinal fluid causing central nervous system irritability.3
Symptoms of a subarachnoid hemorrhage include severe headache, visual disturbances, fever,
malaise, vomiting, nuchal rigidity, seizures, and coma.2
A diagnosis of suspicion of subarachnoid hemorrhage can be made from the history and physical
examination. Laboratory studies to confirm the diagnosis will be a spinal tap with bloody or xanthochromic cerebral
spinal fluid The cerebral spinal fluid will also have increased monocytes and protein. Radiologic studies to confirm
the diagnosis include CT Scan (see figure 5) and cerebral angiography.2
Patients with a subarachnoid hemorrhage may be treated either surgically or conservatively
depending on their condition. The obtunded, and those with significant cerebral vasospasm are not good surgical
risks. Conservative treatment is aimed at reducing any increase in intracranial pressure protecting vital neurologic
functions until the patient stabilizes.2 Hyperventilation,
osmotic diuretics, and steroids will help decrease the intracranial volume, lowering the intracranial pressure.9 Nursing care for the patient with a subarachnoid hemorrhage
remains the same as for the hematomas.9
The frequency and seriousness of traumatic closed head injuries warrants its study by the
health care team. Survivors of these injuries do so with sometimes severe physiologic and psychologic handicaps.
These handicaps result in a serious loss for the social and economic community, making it a major health problem.3
REFERENCES
- Borg, N. (Ed.) (1981). Core Curriculum for Critical Care Nursing. Philadelphia: W.B. Saunders Co.
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A. Prensky, and W. Harden (Eds.), Neurological Pathophysiology
pp.329-347. New York: Oxford University Press.
- Jennett, B., G. Teasdale & S. Galbaith. (1977). Severe Head Injuries in Three Countries.
Journal of Neurology, Neurosurgery, and Psychology 40,
291-294.
- McKhann, C. (1976). Trauma to the head and Neck. In A. Harvey, R. Johns, A. Owens, and R.
Ross (Eds.), The Principles and Practice of Medicine
19th Ed.; (pp.1560-1564). New York: App1eton~Century-Crdfts;
- Roberts, J. (1980). Pathophysiology, Diagnosis, and Treatment of Head Trauma. Topics in Emergency Medicine, 1(1), 41-62.
- Smith D. & C. Germain (Ed.) (1975). Care of the Adult Patient, Philadelphia: J.B. Lippincott
Co.
- Smith, R. (1983). "Head Injuries". In C. Warner (Ed.), Emergency
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