INJURIES OF THE HEAD (4 periods) 
COURSE PRESENTED TO:011-18D30, Special Operations Medical Sergeant 
PLACE: Classroom 
REFERENCES: Mills, Ho and Trunkey. Current Emergency Diagnosis and Treatment. 
Lange Medical Publications, 1985. 
Committee on Trauma, American College of Surgeons. Early Care of the Injured 
Patient. Philadelphia: W. B. Saunders Company, 1983-1984. 
Weiner and Barrett. Trauma Management. 
W. B. Saunders Company, 1986. 
RELATED SOLDIER'S MANUAL MQS/TASKS: See Annex C. 
STUDY ASSIGNMENT: None 
STUDENT UNIFORM AND EQUIPMENT: Duty uniform. 
TOOLS, EQUIPMENT, AND MATERIALS: M 27XAXB-04/K issued at the beginning of class. 

PERSONNEL: One instructor (MC or PA). 
INSTRUCTIONAL AIDS: Colored chalk, chalkboard, eraser, slides (see Annex B), 
slide projector. 
TROOP REQUIREMENTS: None. 
TRANSPORTATION REQUIREMENTS: None. 
METHOD OF INSTRUCTION: Conference. 
RISK ASSESSMENT LEVEL: Low. 
SAFETY REQUIREMENTS: None. 
* This Lesson Plan supersedes LP 27XAXB-01/K, 020. 
I. INTRODUCTION (5 min) 
A. Opening Statement: Head injury causes more deaths and disability than any 
other neurologic cause in victims under age 50. Mortality in severe injury 
approaches 50 percent and is only little reduced by treatment. Damage results 
from penetration of the skull or from rapid acceleration or deceleration of 
brain, which injures tissue at the point of impact, at its opposite pole 
(contrecoup), and also diffusely along the frontal and temporal lobes. Nerve 
tissue, blood vessels, and meninges are sheared, torn, and ruptured, resulting 
in neural disruption, intra- and extracerebral ischemia or hemorrhage, and 
cerebral edema. Hemorrhage or edema acts as an expanding intracranial lesion, 
causing increased intracranial pressure that can lead to fatal herniation of 
brain tissue through the tentorial opening. Skull fractures may lacerate 
meningeal arteries or large venous sinuses, producing epidural or subdural 
hematoma. Infectious organisms may reach the meninges even when a fracture is 
not clearly evident. Few head injuries occur in isolation, and most cases 
require simultaneous attention to other seriously traumatized parts of the body. 

NOTE: Show S 27XAXB-OY/K-01 thru -05 to support Objectives. 
B. Objectives 
1. Terminal Learning Objective 
Given a trauma scenario, describe emergency management for head injuries IAW 
cited references. 
2. Enabling Learning Objectives 
a. Select from a list, two mechanisms of injury to the head IAW Mills, Ho and 
Trunkey, Current Emergency Diagnosis and Treatment, 1985. 
b. Select from a list, characteristics of a scalp laceration and management 
techniques IAW Mills, Ho and Trunkey, Current Emergency Diagnosis and Treatment, 
1985. 
c. Select from a list, types of skull fractures according to physical 
characteristics and locations IAW Weiner and Barrett, Trauma Management, 1986. 
d. Select from a list, intracranial hematoma locations IAW Mills, Ho and 
Trunkey, Current Emergency Diagnosis and Treatment, 1985. 
e. Select from a list, three types of brain injuries IAW Weiner and Barrett, 
Trauma Management, 1986. 
f. Describe evaluation procedures/ techniques for a patient with a head injury 
IAW Early Care of the Injured Patient, American College of Surgeons, 1983-1984. 
g. Describe emergency management procedures of head injury IAW Weiner and 
Barrett, Trauma Management, 1986. 
C. Class Procedure and Lesson Tie-in: This lesson is directly related to anatomy 
and physiology of HEENT, physical examination of HEENT, and emergency care of 
the injured patient. 
FIRST PERIOD 
II. EXPLANATION (170 min) 
NOTE: Show S 27XAXB-0Y/K-06 to support Main Point II A. 
A. General. 
1. Head injuries occur in 70% of MVAs or falls. 
2. About 70% of total killed accidentally die as a result of head injuries. 
3. Most will have significant damage to rest of body--face, chest, abdomen, 
pelvis, extremities. 
B. Anatomy of Scalp and Skull. 
NOTE: S 27XAXB-OY/K-07 thru -17 to support Main Point II B-C. 
1. Scalp--extends from eyebrows to external occipital protuberance and from 
right to left zygomatic arches. 
a. S--skin.
b. C--connective tissue. 
(1) Composed of dense, fibrous bands that run through subcutaneous tissue 
connecting skin to the next layer. 
(2) These bands split subcutaneous tissue into numerous fat-filled pockets. 
(3) Blood vessels and nerves of scalp lie in these pockets. 
c. A--aponeurotica galea--tendon that unites the bellies of the frontal and 
occipital muscles.
d. L--loose connective tissue. 
(1) Allows scalp to slide freely over cranium. 
(2) Since this is relatively avascular and porous in nature, this layer is a 
"danger area" for fluids to collect and infection or abscesses to develop. 
e. P--periosteum--soft tissue covering of cranial bones. 
2. Cranium. 
a. "Brain box" for protection of the semisolid brain. 
b. Composed of an inner and outer table of bone separated by cancellous bone 
(diploe). 
3. Intracranial (only outermost contents). 
a. Meninges--membrane coverings of both brain and spinal cord. 
(1) D--dura mater. 
(a) Thick, double-layered, fibrous, vascular membrane. 
(b) Has double duty of periosteum for the inner cranium and supporting the brain 
within the cranium. 
(c) Vascular supply is via middle meningeal artery.

(2) A--arachnoid. 
(a) Thin, delicate, transparent, avascular membrane that has many fine little 
strands (trabeculae) in subarachnoid space connecting it to pia mater 
(b) Cerebral spinal fluid (CSF) is found in subarachnoid space--functions as a 
fluid-filled, sponge-like, protective cushion for brain. 
(3) P--pia mater. 
(a) Very thin, vascular membrane covering all the "hills and valleys" of brain's 
cortex (Gyri and Sulci). 
(b) Vascular supply is via cerebral blood vessels which lie on brain's outer 
surface (these vessels then send branches into brain). 
b. Cerebral cortex. 
(1) Outermost portion of brain. 
(2) Composed of six layers, each about 50-100 cells thick. 
NOTE: Emphasize the use of the mnemonics S.C.A.L.P. and D.A.P. to remember the 
appropriate structures. 
C. Mechanisms of Head Injury. 
1. Blunt trauma. 
a. Direct--injury produced directly beneath impact point. 
(1) Laceration. 
(2) Contusion--coup injury. 
(3) Epidural hematoma. 
(4) Subarachnoid hematoma. 
(5) Fracture. 
b. Indirect--brain rotates or slides linearally slightly out of phase relative 
to the movement of the skull at time of impact. 
(1) Concussion. 
(2) Contusion--contrecoup injury. 
(3) Subdural hematoma. 
(4) Subarachnoid hematoma. 
2. Penetrating or perforating trauma--any foreign body like knife, stake, 
shrapnel, or bullet is a more serious fracture injury. 
NOTE: Show S 27XAXB-OY/K-18 thru -25 to support Main Point II D. 
D. Scalp Laceration--least serious head injury, but must rule out a more serious 
underlying fracture and other injuries. 
1. Characteristics. 
a. Differs from other skin lacerations. 
(1) Scalp has a far greater vascularity. 
(2) Vessels are interspersed both vertically and horizontally in a dense network 
of fibrous, connective support tissue that doesn't allow vessel retraction when 
cut. 
(3) Most cuts also involve the galea; it is a tendon, and it will retract when 
cut. 
(4) This retraction pulls overlying cut blood vessels apart. 
b. May be minimal, yet appear to bleed excessively. 
(1) Severe lacerations can cause hypotension. 
(2) Hemostasis can usually be achieved with simple pressure dressing. 
(a) Hemostat clamps don't work well due to the density of the thick, fibrous, 
connective support tissue. 
(b) Only way to definitively achieve hemostasis is to suture your way out 
(suture in layers); pressure of wound edge abutment is sufficient to tamponade 
vessels. 
2. Management. 
a. General. 
(1) Every laceration, no matter how innocent appearing, should be considered a 
potential penetrating wound of the brain. 
(2) If X-ray capability is available, then use it. 
(3) Consider old injury (hematoma, brain contusion, etc.). 
b. Copiously irrigate with normal saline and prep the wound with Betadine. 
(1) Irrigate especially well an accessible "danger area" or an open flap of 
scalp, even up to point of manually cleaning. 
(2) Must avoid missing dirt, hair, or gravel that can later produce massive 
facial gangrene. 
c. Shave around laceration--2" in circumference and preprep. 
d. Anesthetize with local injections of 1% lidocaine with epinephrine. 
e. Drape wound, palpate gently with gloved fingers for fracture; if found, close 
with temporary sutures and immediately evac. 
f. If no fracture found, minimally debride. 
g. If aponeurotica galea, occipital, or frontalis muscle is involved, close in 2 
layers; otherwise, close with 1 layer. 
(1) Galea or muscle--use 3-0 chromic sutures. 
(2) Skin--use 3-0 silk or synthetic sutures. 
h. Remove skin sutures in 6-7 days; if evidence of pus or hematoma buildup, then 
remove sutures earlier, 
NOTE: Show S 27XAXB-OY/K-26 thru -51 to support Main Point II E. 
E. Skull Fracture. 
1. General. 
a. If associated with a laceration, it is then a compound fracture by 
definition. 
(1) Risk of infection or meningitis is great. 
(2) Usually is accompanied by a tear in dura that can extend into the arachnoid 
through which CSF can potentially leak out. 
b. Diffuse or localized scalp edema without a laceration suggests an underlying 
fracture. 
2. Types of fractures by physical characteristics. 
a. Linear--fractures through cranium with no displacement of bone fragments. 
(1) If fracture crossed an artery; i.e., middle meningeal or a venous sinus, may 
result in formation of epidural hematoma. 
(2) No specific management for fracture other than close observation for 24-48 
hours and periodic neuro exams to exclude a developing epidural hematoma. 
b. Depressed. 
(1) Cranial bones broken, comminuted, and depressed or pushed into brain; 
severity of cerebral injury and neuro deficits depend on extent and location of 
the damage. 
(2) Refer/evac--requires surgical intervention with elevation of the fracture 
fragment. 
c. Penetrating--foreign object fractures the skull; enters the cranial vault. 
(1) Stabilize foreign object if still in place to limit further brain damage. 
(2) Antibiotics--war wound therapy. 
(3) Refer/evac for definitive surgery and long-term management of complications 
(abscesses, meningitis, etc.). 
d. Perforating--foreign object, like a bullet, fractures the skull, enters the 
cranial vault, then fractures the skull again by exiting the cranial vault. 
Treat as in penetrating injury. 
3. Types of fractures by locations. 
a. Vault--any part of the skull other than base. 
(1) Prominence of parietal bone makes it most common site of fractures; followed 
by temporal, frontal, and least often the occipital bone. 
(2) Critical when fracture crosses artery or venous sinus since an epidural 
hematoma can be easily produced. 
(3) If cortex of brain is injured, cranial nerves III-VI may cause eyes to turn 
toward side of injury. 
b. Basilar. 
(1) Difficult to assess due to location. 
(2) Possible signs of basilar skull fracture depending on location. 
(a) Basilar fracture of anterior fossa. 
1. Can fracture the frontal sinuses. 
2. Blood and/or CSF can leak from nose (rhinorrhea) in 2% - 9% of injuries. 
3. Bilateral bleeding into medial eyelids (Raccoon's eyes sign) in absence of 
direct trauma 24-36 hours postinjury when a frontal fracture extends into roof 
of eye orbit. 
(b) Basilar fracture of middle fossa. 
1. Frequently fractures through petrous portion of temporal bone and extends to 
sella turcica or foramen magnum. 
2. Blood and/or CSF can leak from ear or build up behind tympanic membrane 
(otorrhea, hema-tympanum). 
3. Blood and/or CSF can leak into pharynx or cause mastoid discoloration 
(Battle's sign). 
4. Deficits of affected cranial nerves. 
a. I--olfactory disturbances. 
b. II--visual disturbances. 
c. III, IV, VI--eyes turn away from side of injury (injury then causes a brain 
stem squeeze). 
d. VII--ipsilateral facial paralysis. 
e. VIII--hearing and balance disturbance. 
f. XI--trapezius muscle weakness. 
(c) Posterior fossa fracture--mastoid discoloration from bleeding (Battle's 
sign) in absence of direct trauma to mastoid area when temporal or occipital 
bone is fractured. 
(d) Any cranial nerve damage may occur 
NOTE: You must carefully observe for any CSF drainage from nose, ear, or 
posterior pharynx. Test via ring test or use glucose urine dipstix (since CSF 
glucose is two-thrids that of blood); CSF may not initially be present if 
fracture line is very fine due to slow leakage. Similarly, Raccoon's eyes sign 
and Battle's sign may not appear immediately, as they depend on the rate of 
blood diffusion under the scalp to these areas of thin, transparent skin. 
BREAK: (10 min) 
SECOND PERIOD 
F. Intracranial Injury--may involve hematoma formation between any of the 
meningeal layers, or alternatively, may involve injury to the brain tissue 
itself as in a penetrating missile or a depressed skull fracture. 
NOTE: Show S 27XAXB-OY/K -52 thru -60 to support Main Point II F1. 
1. Hematoma--(based on location). 
a. Epidural (extradural). 
(1) Etiology. 
(a) Significant head injury with a vault skull fracture--most common cause (91% 
in adults). 
1. Typically in the parietal-temporal region. 
2. Fracture line tears across an artery, typically the middle meningeal. 
3. Leaking blood under arterial pressure collects between dura and inner table 
of skull. 
4. Expanding hematoma puts pressure on brain that results in OICP. 
5. Depending on bleeding rate, it can take minutes-hours for enough pressure to 
be put on brain to cause characteristic signs. 
(b) Insignificant head injury without skull fracture. 
1. Relatively minor blow to any part of head, but usually to side of head. 
2. Blow produces a transient local inbowing deformation of the skull, stripping 
the dura from inner table over a small area and shearing or rupturing arteries. 
3. Bleeding with pressure may build up as above. 
4. Common in children, who have greater skull elasticity and ease of dural 
detachment; less common in adolescents and young adults who were "just knocked 
out for a minute." 
(2) Signs and symptoms--classical clinical presentation (Epidural = Express). 
(a) Transient period of unconsciousness followed by apparent improvement, 
sometimes to normal (lucid interval). 
(b) Lucid interval--long considered a hallmark; lasts minutes-hours depending on 
rate of bleeding and subsequent pressure on brain. 
(c) Increasing headache, N&V--typically accompany lucid intervals. 
(d) Increasing brain compression (OICP)--finally results in decreasing level of 
consciousness with pupil dilation on same side, positive Babinski, 
hemiparesis/hemiplegia, coma, abnormal extension, hyperreflexia, and death. 
(e) May not have this typical time progression sequence in every case since a 
wide clinical spectrum exists due to force of original blow and resultant 
bleeding rate; the most dependable sign is decreasing LOC due to OICP. 
(3) Management--requires immediate surgical decompression to prevent certain 
death. 
b. Subdural. 
(1) Etiology. 
(a) May result from trivial injury, particularly in the alcoholic and elderly 
that is often forgotten; in only 25% of cases is the trauma sufficient enough to 
produce unconsciousness. 
(b) The force of injury can be from a blow to side of head, jaw, or forehead; or 
force can be from an acceleration-deceleration event. 
(c) Previously explained out-of-synch brain-skull movement component results. 
(d) Cerebral veins, which are located on surface of pia mater, traverse the 
subdural space to venous sinuses. 
(e) Rotating or sliding brain shears vein in subdural space since it has no 
structural support. 
(f) Blood oozes out into subdural space which has no absorbing capability. 
(g) Unlike an epidural hemorrhage, where the bleeding is confined to a specific 
area by the strong retention of the dura tightly attached to inner skull, 
subdural bleeding is free to spread thinly and widely throughout the subdural 
space. 
(2) Signs and symptoms (Subdural = Slow) 
(a) Similar to epidural hematoma, but due to a slower venous bleed into a larger 
space. This causes a slower increase of ICP, resulting in a slower development 
of the clinical cause (days to weeks) without a lucid interval. 
(b) In elderly, only symptom may be personality change--age atrophied brain 
allows for more subdural space to be filled, so there is minimal brain squeeze 
with the resultant neuro deficits occurring; atrophied brain also stretches 
veins more tightly making them very easy to rip. 
(3) Management--requires surgical decompression. 
c. Subarachnoid. 
(1) Etiology--blood in CSF is common in head injuries. 
(2) Signs and symptoms--typically, sudden onset of "worst headache in my life" 
occurs with signs of meningeal irritation (stiff neck). 
(3) Management--spinal fluid drainage by LP in hospital will lessen symptoms and 
speed convalescence. 
NOTE: Show S 27XAXB-OY/K-61 thru -72 to support Main Point II F2. 
2. Brain injuries. 
a. Concussion. 
(1) Etiology. 
(a) Force of an injury causes brain to move out of synch with skull movement. 
(b) Brain minimally impacts on bony shelves in skull without anatomic damage. 
(c) Since brain is "shaken up," neurons are incapable of functioning properly 
for very short time periods, but quickly return to normal (seconds-minutes). 
(2) Signs and symptoms--assessment is made clinically since there are no 
available tests. 
(a) Transient unconsciousness, less than 5-10 minutes--very important to 
determine this time period. 
(b) Amnesia--either retrograde, antegrade, or both is a constant feature. 
(c) Possible loss of equilibrium. 
(d) Possible visual disturbances--diplopia, decreased acuity. 
(e) Vomiting in children is common. 
(3) Management. 
(a) Observe for at least 24 hours. 
(b) If patient's symptoms are minimal and the neuro exam is still normal, send 
patient home in the care of a responsible adult issued following home after-care 
instructions. These instructions will assist in monitoring for signs and 
symptoms that indicate a more serious injury! 
1. Eat and drink minimally during the next 24 hours--NO alcoholic beverages. 
2. Place cool cloth an patient's head for mild headache and/or give ASA. 
3. Check the patient q2h for the following. 
a. If asleep--ease of awakening. 
b. Ability to talk clearly. 
c. Size of each pupil. 
d. Strength of arms and legs. 
e. Pulse rate for 1 minute 
4. Return with patient if any of the following occur: 
a. Progressive difficulty to awaken. 
b. Slurred speech. 
c. One pupil becomes larger. 
d. Pulse below 60 in adult; below 80 in a child. 
e. Weakness of arm or leg. 
f. Severe headaches. 
g. Vomiting more than twice. 
b. Contusion. 
(1) Etiology. 
(a) Same as in concussion but the movement component of brain-skull interface 
causes injury to brain tissue. Alternatively, direct impact of force can cause 
the injury. 
(b) Force was great enough to cause anatomic damage, as well as functional 
damage. 
(c) Anatomic damage is a bruise-like superficial bleeding of brain plus neural 
destruction. 
1. Coup--damage directly beneath impact point. 
2. Contrecoup--damage occurring on side opposite impact point. 
(d) If force was still greater, bony shelves can lacerate cortex in addition to 
the contusion and/or fracture that can also accompany injuries. 
(2) Signs and symptoms. 
(a) Severity depends on location and extent of damage. 
(b) Range from mild, which is similar to concussion except unconsciousness is 
greater than 5-10 minutes, to severe with devastating neuro impairment or coma. 
(c) Special diagnostic studies are available in the hospital to confirm and 
pinpoint damage. 
(3) Management--refer/evac for definitive evaluation and management. 
c. Intracerebral hemorrhage (subpial)--symptoms are those of a stroke. 
NOTE: Show S 27XAXB-OY/K-73 thru -80 to support Main Point II F3. 
3. Evaluation of the head injury patient. 
a. History--most important aspect of the evaluation. 
(1) Mechanism of injury. 
(a) Meticulously seek out details of accident. 
(b) If patient is unable to clearly delineate events, then question witnesses. 
(c) Awareness of the magnitude of energy involved will help in management 
decisions as well as assessment. 
(2) Associated medical problems. 
(a) Epilepsy, CA, MI, alcoholism, or drugs could have been the precipitating 
cause of a fall and subsequent head injury. 
(b) Lack of knowledge of these conditions will interfere with the assessment by 
masking or changing signs or affecting the subsequent clinical course. 
b. Symptoms--question patient about these. 
(1) Loss of consciousness and duration. 
(2) Loss of function (motor or sensory). 
(3) Occurrence of seizures. 
(4) Extent of any amnesia. 
(5) Headache. 
(6) Extent of any blood loss. 
(7) Extent of any vomiting-aspiration 
(8) Right- or left-handed to establish cerebral dominance in order to compare 
later abnormal lateralization neuro findings. 
c. Signs in head injury--must be especially concerned with assessment of 
increased ICP as this is manageable if handled promptly; if not promptly 
corrected, after a certain point, it is irreversible and death will follow. 
(1) General. 
(a) Baseline evaluation. 
1. It is critically important to establish a baseline neuro eval starting on 
first contact with patient; use following as a minimum: 
a. LOC. 
b. Pupillary response. 
c. Motor response. 
d. Reflexes. 
e. Vital signs. 
2. Key words in determining a worsening patient from this baseline. 
a. Progression--deteriorating LOC with worsening pupil, motor, and reflex 
parameters. 
b. Lateralization--worsening parameters confine themselves to opposite half of 
body from head injury (except pupils). 
3. Failure to appreciate deterioration in the unconscious patient results from 
insufficient and infrequent patient observation; even a patient in alcoholic 
stupor can be followed adequately by his reaction to painful stimuli (see GCS). 
4. Observation means repeated careful examination of the patient; the key to 
head injury management is careful and repetitive neuro exams with timely 
intervention; i.e., q 15 min. 
5. Progressive deterioration in LOC is the guidon bearer of increased ICP!! 
a. Expanding hematoma. 
b. Cerebral edema--brain swells when injured, just like any other tissue. 
c. Pressure builds up in hard, unyielding cranial cavity resulting in squeezing 
the soft brain tissue. 
(b) Status of consciousness. 
1. If unconsciousness is immediate and continuous, contusion or laceration 
should be considered. 
NOTE: ICP can be acute or delayed. 
2. An improving LOC after unconsciousness is associated with concussion, while 
one that is deteriorating, either while still unconscious or after return to 
consciousness, indicates OICP causing brain compression or focal injury 
(epidural hematoma). 
3. A patient can have two pre- sentations of injury. 
a. Initial, transient un- consciousness, then improve-ment--concussion. 
b. Or second episode of unconsciousness minutes-hours after the initial 
state--due to OICP from an expanding hematoma. 
4. Guiding principle is follow the patient closely with repeated neuro exams and 
expect a change from the baseline. 
(c) Shock. 
1. Rarely associated with head injury alone without severe lacerations. 
2. If no obvious blood loss is present with shock and head injury, internal 
bleeding is the cause until proven otherwise. 
a. Head injuries don't cause a silent or rigid abdomen. 
b. Failure to look beyond the obvious head injury in assessing the patient 
precludes recognition of associated trauma. 
3. If shock and OICP coexist in the same patient. 
a. Vital sign changes will be those of shock. 
b. Vital sign changes of OICP will appear only after volume deficit has been 
corrected!!! 
4. Vital signs, LOC, and pupils should be monitored q 15 min, as a minimum, 
during the acute phase. 
(2) Level of consciousness--assess using the Glasgow Coma Scale (GCS). 
(a) Eyes. 
1. Open. 
a. Spontaneously--4. 
b. To command--3. 
c. To pain--2. 
2. Closed (no response)--1. 
(b) Best motor response. 
1. To verbal command (obeys)--6. 
2. To painful stimuli-- 
a. Localizes pain--5. 
b. Flexion (withdrawal)--4. 
c. Abnormal flexion--3. 
d. Abnormal extension--2 (more common than flexion). 
e. No movement--1. 
NOTE: The occurrence of abnormal flexion or extension on one or both sides, 
either spontaneously or in response to noxious stimulus, is an ominous finding 
that indicates injury to upper brain stem or midbrain. 
(c) Best verbal response--arouse patient with painful stimuli if necessary. 
1. Oriented and converses--5. 
2. Disoriented and converses--4. 
3. Inappropriate words--3. 
4. Incomprehensible sounds--2. 
5. No response--2. 
(d) Score--the greater the number, the lesser the probability for death or 
vegetation. 
1. Less than 4--80% death or vegetative state probability. 
2. 5 to 7--54% death or vegetative state probability. 
3. 8 to 10--27% death or vegetative state probability. 
4. Greater than 10--6% death or vegetative state probability. 
(3) Vital sign changes in increased ICP. 
(a) Blood pressure increases, particularly the systolic pressure (widening pulse 
pressure) to overcome OICP in order to perfuse brain with oxygenated blood. 
(b) Pulse rate decreases--to compensate for increased BP. 
(c) Temperature rises. 
(d) Respiratory rate falls--if increased, then look for thoracic trauma. 
(4) Neurological abnormalities. 
(a) General. 
1. The more severe an injury is, the more bleeding intracranially occurs. 
2. This bleeding puts pressure on specific parts of the brain. 
3. This causes pupil, Babinski reflex, motor, and DTR changes (in this order). 
(b) Pupils. 
1. Pupil dilates (and may be fixed) ipsilateral of injury 85% of the time; 15% 
is contralateral pupil dilatation. 
2. Opposite pupil is normal unless a general state of hypoxia exists, as in 
respiratory insufficiency--leads to dilation and slow response. 
NOTE: Anisocoria occurs in 20% of population--normal. 
3. An ipsilateral dilating pupil that is still reactive to light is often the 
first sign in an epidural hematoma of the middle fossa (temporal lobe). 
(c) Babinski reflex positive--one of the first signs to appear after pupillary 
changes. 
(d) Fundus. 
1. Potential papilledema from OCIP. 
2. Usually not initially present since it takes about 12 hours for optic nerve 
head to swell after an acute rise in ICP. 
(e) Motor--following abnormalities in order of severity occur on side of body 
opposite the head injury in a progressively worsening patient. 
1. Monoplegia--a localized paralysis occasionally seen in trauma. 
2. Hemiparesis--partial paralysis or muscle weakness on one side of body. 
3. Hemiplegia--paralysis of entire one side of body. 
4. Total body paralysis--develops in a progressively worsening or bilateral head 
injury patient. 
5. Abnormal extension--first on opposite side, then bilaterally. 
(f) Epilepsy. 
1. Occurs in 10% of head injuries. 
2. Incidence is much higher with depressed fracture or penetrating wounds of 
brain. 
(g) Sensory--deficit usually only present in spinal injuries; when present, 
follows the distribution of the motor nerves. 
(h) Deep tendon reflexes (DTRs). 
1. Hyperactive--side opposite injury. 
2. Develops in a progressively worsening patient. 
3. Coma with unobtainable reflexes is an ominous finding. 
(i) Cranial nerve damage. 
1. Any could be damaged. 
2. Most vulnerable are I-VIII. 
(j) Incontinence--only important in previously continent patient (damage to 
nerve X). 
(k) Restlessness in previously quiet patient. 
1. First ensure this isn't due to pain from uncomfortably tight bandages, wraps, 
straps, casts, I.V.s, dehydration, full bladder, fecal impaction, etc. 
2. In the absence of the above, may be the first sign of an expanding hematoma 
and thus OICP 
G. Emergency Management of Head Injury--standard ABCs; remember the patient may 
be multiply injured, so don't forget to manage the total patient 
BREAK: (10 min) 
THIRD PERIOD 
NOTE: Show S 27XAXB-OY/K-81 thru -90 to support Main Point II G. 
1. Airway management. 
a. General. 
(1) Neurons of brain are very dependent from minute to minute on an adequate 
supply of oxygen and glucose (lead a very "hand-to-mouth" existence). 
(2) Maintenance of an airway is the single most important emergency measure that 
can be done for an unconscious patient and has priority over all else in every 
phase of management!! 
(3) Cerebral swelling can be massively increased by even moderate degrees of 
underventilation. 
(a) Resultant hypercapnia and hypoxia cause cerebral vasodilation. 
(b) Vasodilation increases brain-blood volume which leads to further cerebral 
edema. 
(c) This edema causes further increased ICP to possibly lethal levels. 
(4) Adequate ventilation is especially important in patients with head injuries. 

b. Maintain C-spine control throughout by using chin lift or jaw thrust method, 
not head tilt, to open airway. 
c. Oropharyngeal airway if unconscious. 
d. Endotracheal tube or cricothyroidotomy, if necessary. 
(1) Hyperventilate at 30 per minute to maintain PaCO2 of about 26-28 mg Hg. 
(2) Maintaining this respiratory rate also achieves PaO2 greater than 100 mm Hg 
(decreases ICP). 
e. Oxygen--by mask at 8-10 liters per minute. 
f. Frequent suctioning of mouth and oropharynx. 
g. Position patient in head neutral position and transport.



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