State of Illinois Trauma Nurse Specialist Program

HEAD TRAUMA
Connie J. Mattera M.S., R.N., TNS Time allotment: 2 hours

OBJECTIVES: Upon completion the participant will 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. state the incidence, morbidity, and mortality often associated with head trauma. apply knowledge of anatomy and physiology of the CNS to anticipate the pathophysiology existent in traumatic brain injuries. predict nervous system trauma based on mechanism of injury. distinguish between head injury and brain injury. differentiate primary from secondary injuries. distinguish between focal and diffuse injuries. list five immediate complications of head injury that will worsen the prognosis. explain the dynamics of cerebral blood flow and cerebral perfusion pressure. sequence the evolution of increased intracranial pressure. differentiate early from late signs of ↑ ICP including herniation syndromes. explain the primary assessments to be performed on a head injured patient state the resuscitative priorities based on the BTF guidelines which focus on methods to establish airway control, provide ventilatory assistance and perfusion support. sequence the steps in performing a neurological exam on a head injured patient with an emphasis on the mental status assessment including GCS, cranial nerve exam, motor, sensory and reflex exams. interpret assessment data to formulate appropriate nursing diagnoses associated with head and brain injured patients. classify head injuries as mild, moderate, or severe according to assessment findings. describe appropriate nursing interventions for the management of head injured patients. describe methods by which nurses can appropriately participate in, and assist with, medical management of head injured patients. state the radiological and laboratory tests that physicians typically order for head injured patients. explain the pathophysiology, patient presentation, and management priorities for the following vault fractures: linear, comminuted, depressed, basilar. explain the pathophysiology, patient presentation, and management priorities for the following focal injuries: epidural, subdural, and subarachnoid hemorrhages; cerebral contusion; intracranial hemorrhage. explain the pathophysiology, patient presentation, and management priorities for the following diffuse injuries: concussion and diffuse axonal injury. evaluate the effectiveness of emergency interventions and amend the care plan as indicated by patient responses.

CJM: 6/07

State of Illinois Trauma Nurse Specialist Program

HEAD TRAUMA
Connie J. Mattera M.S., R.N., TNS

I.

Epidemiology of head trauma
A.

Definitions
1. 2.

A head injury is defined as external influences causing traumatic insult to the head that may result in injury to soft tissue, bony structures and/or brain. Traumatic brain injury (TBI), as defined by the National Head Injury Foundation, is "a traumatic insult to the brain capable of producing physical, intellectual, emotional, social, and vocational changes." It is classified as direct (primary) or indirect (secondary) injury to the tissue of the cerebrum, cerebellum, or brainstem. Brain injury affects who we are, the way we think, act, feel and move. It can change everything about us in a matter of seconds (Brain Injury Association of America, 2004).

B.

Incidence: Estimated at 200/100,000 population which translates to one every 21 seconds or 1.6 million/year with 230,000-270,000 hospitalized. Of these, about 50,000 – 52,000 die and another 70,000 – 90,000 survive with disabilities (BTF, 2004, CDC, 2001). TBI is more than twice as likely in males as in females; with the highest incidence in people 15-24 years of age and 75 years and older. Children ages 5 and younger are also a high-risk group. An estimated 5.3 million Americans live with disabilities resulting from traumatic brain injury (Brain Injury Association (2004), NIH, 2002). Common etiologies
1.

C.

Motor vehicle crashes (MVCs) are the most common cause of closed head injury followed by falls, which are seen more frequently in children and the elderly. Other etiologies: intentional battery, use of firearms, water or recreational or sport-related injuries, pedestrian impacts, or domestic violence. Children: 10% of TBI are due to MVCs, falls, recreational (bicycling-related), home or birth injuries. Behaviors that increase the risk of sustaining head trauma
a. b. c. d. e.

2. 3.

Alcohol ingestion Use of mild-altering drugs Incorrect use or nonuse of restraint systems Nonuse of helmets Participating in team sports without protective equipment

D.

General categories of injury
1.

Head injuries can be classified according to
a. b. c. d.

Severity of the injury Anatomical classification Pathological classification Primary and secondary brain injury

2.

Blunt (closed) trauma: The person receives an impact to the head from an outside force, but the skull and dura remain intact and brain tissue is not exposed to the environment. More common than penetrating. The structures of the head and face generally protect well against most blunt trauma. However, when the magnitude of forces exceeds the tensile strength of the structures, severe injury can occur. For example, the sinus cavities of the face are frequently injured with blunt facial trauma. The air-filled spaces collapse upon impact and help to dissipate energy forces. A person may have a closed head injury with mild to severe traumatic brain injury.

State of Illinois TNS Program Head Trauma - page 2
3.

Penetrating (open) trauma: A penetrating injury produces an opening through the skull into cranial contents exposing them to the environment, creating a risk for infection and other injuries. Often caused by missiles such as rifles, hand guns, or shotguns and less commonly by other penetrating implements like knives, ice picks, exes, etc. While not as common as blunt trauma, they are very disruptive due to energy forces that can project hair, skin, bone and debris into the brain and contaminate the region. If the projectile is traveling at a low rate of speed through the skull, it can ricochet within the skull and widen the area of damage. High velocity projectiles can produce significant trauma from shock waves. Sharp projectiles may be superficial because of the protection afforded by the skull, but may pierce through bone and meninges into the brain. A “through and through” injury occurs if an object goes through the skull, brain, and exits the skull. These will produce the effects of penetration injuries, plus additional shearing, stretching, and rupture of brain tissue (Brain Injury Assoc. of America, 2004). Acceleration: Stationary head is hit by a moving object as in car vs. pedestrian, abuse or sports injury. Deceleration injury: Moving head hits a stationary object as in falls, abuse, sports injuries and MVCs. Sudden deceleration may produce bony deformity or cause the brain to slide back and forth by ½ inch at 38 mph collision. The brain can move in a straight linear acceleration with no loss of consciousness but can be injured as it moves across the rough base of the skull. The initial impact and pressure wave may tear tissue and result in injury on the side of the impact (coup) and the side opposite the point of impact (contrecoup). When these forces are applied, shearing, tensile and compressive stresses may lead to fractures, hemorrhage, hematomas, and contusions. Acceleration/deceleration injury: Moving head hits a moving object Distraction injuries: Ex. hanging. If the head is suspended in a drop 18" taller than the person; it causes a fatal blow to the CNS. Penetrating trauma 0%: Mild head injury 7%: Moderate head injury 25%: Severe head injury (BTF, 2007) 90%: GSW to head: Nearly 2/3 are classified as suicides. Firearms are the single largest cause of death from traumatic brain injury, causing 44% of TBI deaths (CDC, August 22, 2002). In the last 12 years, more people have died of traumatic brain injury (TBI) than in all the wars combined. It contributes significantly to the outcome in 40%-50% of all trauma deaths (Feliciano, 267). TBI is the leading single-organ cause of death related to trauma. Fifty percent of deaths due to MVC involve head trauma (Bourg, 2007). The challenge of improving outcome rests on advances in prehospital management, critical care and rehabilitation.

E.

Mechanisms of injury: Brain injury is usually due to a combination of forces
1. 2.

3. 4. 5. F.

Mortality rates
1. 2. 3. 4.

5.

6. 7. G.

Morbidity: Brain injury can result in memory loss, rapid mood swings, fatigue, intellectual dullness, mental rigidity, personality changes, and physical disabilities. The terms mild moderate and severe traumatic brain injury are used to describe the level of initial injury in relation to the neurological severity caused to the brain. There may be no correlation between the initial Glasgow Coma Score and the initial level of brain injury and a person’s short or long-term recovery or functional abilities (Brain Injury Assoc. of Am, 2003).

State of Illinois TNS Program Head Trauma - page 3
1.

Mild brain injury (MBI) or concussion: Up to 75% of all diagnosed head injuries (Bazarian et al, 2005) results in brief amnesia or loss of consciousness for a few seconds up to 30 minutes without major complications such as hematomas. The person may not lose consciousness, but be dazed and confused. Only 3% should deteriorate. Five percent with GCS 14-15 and 10% with GCS of 13 will require surgery (ATLS, 2005). Symptoms include temporary headaches, memory disturbance, dizziness, irritability, fatigue, mild mental slowing with decreased concentration and attention span, impaired perception or mood, sleep disturbances, sensitivity to noise or light, and balance problems. They and almost always improve over one to three months. Infants and young children may have observed signs of irritability, lethargy or vomiting following MBI. Moderate brain injury results in a loss of consciousness usually lasting minutes to a few hours. It is followed by a few days or weeks of confusion, and may be accompanied by brain contusions or hematomas. Although people usually have physical, cognitive and psychosocial or behavioral impairments that may last several months, treatment will often allow them to recover fully. However, some symptoms may be permanent. Severe brain injury is defined as an abbreviated injury score (AIS) for the head of 4, 5, or 6. Severe injury almost always results in prolonged unconsciousness or coma lasting days, weeks, or longer. Complications include brain contusions, hematomas, or damage to the nerve fibers, and some may have suffered from anoxia. It is sometimes possible to make significant improvements in the first year after injury that can continue to improve slowly for many years with excellent rehabilitation. However, these patients will often be left with some permanent physical, behavioral, and/or cognitive impairments (Brain Injury Association, NIH, 2002). Severe brain injury is further categorized into subgroups with separate features:
a. b. c. d. e. f.

2.

3.

Coma Vegetative state Persistent vegetative state Minimally responsive state Akinetic mutism Locked-in syndrome 30% - injuries limited to one body area 70% - involve two or more body areas

4.

Head injury often does not occur alone; 75% are associated with multiple trauma
a. b.

H. I.

Cost: TBI carries a greater cost than CV disease and stroke combined; $40 billion/year in U.S. Three databases provide information about severe head injuries
1.

International Data Bank: (Central and Eastern European Traumatic Brain Injury program. Established first; population - GCS 8 or less, 6 hours after injury. Participants: Centers in Glasgow (Scotland), Rotterdam, Groningen (Holland), and Los Angeles. NIH Traumatic Coma Data Bank: Population - GCS 8 or less after resuscitation. Participants: six centers in U.S. TBI-trac: Interactive database designed as a Q/A program to track prehospital and in-hospital care and outcome for trauma centers treating patients with severe traumatic brain injury through the Brain Trauma Foundation.

2. 3.

II.

Patient destination and trauma team composition for optimal outcomes
A.

Need 5 R's for optimal outcomes
1.

Right patient, to the

State of Illinois TNS Program Head Trauma - page 4
2. 3. 4. 5.

Right hospital, in the Right amount of time, to be cared for by the Right physician (neurosurgeon) and trauma team and receive good Rehabilitation.

Right hospital note: Patients with severe traumatic brain injury should be transported directly to a Level I or Level II trauma center that offers CT scanning, neurosurgical care, ICP monitoring, and treatment capabilities (BTF Prehospital Guidelines for the Management of Severe Traumatic Brain Injury, 2000) even if this center may not be the closest hospital. Transport decisions in the field are among the most important decision affecting outcome in patients with severe TBI. When an integrated EMS and trauma system is in place and EMS agencies transport a patient directly from the scene of the incident to an appropriate receiving facility (trauma center) the patient is entered into a system of care that has been shown to improve overall patient outcome. Härtl et al (2006) found that indirect transport to a trauma center (all but two hospitals in their study were Level I) was associated with an almost 50% increase in mortality. Inter-hospital transfers of these patients are known to delay the time until neurosurgical consultation and intervention occur at a time of great risk for secondary insult to the brain (BTF, 2007).
B.

Traumatic brain injury care team should include the following:
1. 2. 3.

4. 5. 6. III.

EMS providers: ground and/or air transport Physicians specializing in emergency medicine, trauma, neurosurgery, neurology, radiology, and anesthesiology Nursing professionals from the ED, Neuro/Trauma ICU and/or trauma service, Neuro Med-Surg Units, OR and PACU (some facilities would also include case management, discharge planners) Ancillary departments that include CT, radiology, lab, pharmacy, physical medicine and rehabilitation, speech therapy and dietary Social services Pastoral care

How the brain is injured: There are two distinct phases of injury that produce neurological dysfunction to the tissues of the cerebrum, cerebellum, or brainstem.
A.

Primary (direct) injury: Mechanical injury that occurs at the moment of energy transfer and is associated with a variety of mechanisms, i.e., acceleration/deceleration, penetration. The impact or forces may cause bony deformity and injury to cranial contents. Pressure waves travel across the brain and dissipate causing physical transection, shearing, bruising, bleeding, or damage of cranial contents that cannot be reversed (Bourg, 2007). Disrupted blood flow to the injured area may cause ischemia and compromise of the blood/brain barrier or death of neurons. Irritation of nervous system tissue may create electrical instability. Treatment is prevention. Secondary (indirect) injury: All brain damage does not occur at the moment of initial trauma. Secondary injury occurs as a direct result of the primary injury and evolves over minutes, hours and days. Patient outcomes improve when these delayed insults are prevented or respond to treatment (BTF, 2007). Secondary injury is due to a variety of metabolic and physiologic processes initiated by regional ischemia.
1.

B.

Ischemia: Cerebral ischemia may be the single most important secondary event affecting outcome following severe traumatic brain injury (BTF, 2003). Cerebral blood flow during the first day after injury is less than half that of normal individuals even though levels may subsequently increase to normal or supranormal levels. The initial hypoperfusion may cause irreversible damage (See section on CPP). Systemic causes
a.

2.

Hypoxia: Hypoxia, defined as apnea/cyanosis or PaO2 <60 (SpO2 < 90%) and hypotension are among the five most powerful predictors of poor outcome, independent of other major predictors such as age, admission GCS, intracranial diagnosis, and pupillary status (BTF, 2007). There is

State of Illinois TNS Program Head Trauma - page 5 intense cerebral vasodilation in the presence of hypoxia that adds to an increase in ICP. The temporal lobe is particularly sensitive to oxygen deprivation that results in memory losses due to decreased protein synthesis. The combination of hypoxia and hypotension increases mortality to 75% (ATLS, 2005).
b.

Hypotension: Almost 1/3 of head injured patients present in shock with hypotension. In the early stages, shock may be more important than hypoxia to treat due to its threat to cerebral perfusion (Chesnut, 1997). The injured brain is more susceptible to shock. It has been shown that even one prehospital BP < 90, doubles the patient's mortality (BTF Field Guidelines, 2000). This observation was reaffirmed in a recent study by Henzler et al (2007) that found lower blood pressures in the first four hours after admission were associated with mortality and may have increased the rate of secondary brain injury. A MAP <=65 mmHg during the first four hours after trauma was associated with a four-fold increase in the odds of non-survival. They also found that intracranial pressure monitoring and ICU admission tended to be initiated later in non-survivors, possibly delaying recognition and management of inadequate cerebral perfusion pressure. In addition, hypothermia did not normalize during the first 24 hours after injury in non-survivors. Electrolyte imbalances (Na, K, Ca) Anemia Hyperthermia Hypercarbia (respiratory acidosis): also vasodilation adding to intracranial pressure. Hypoglycemia causes intense cerebral

c. d. e. f. g. 3.

Intracranial causes: Intracranial hypertension, delayed intracerebral hematoma evacuation, edema, hyperemia, carotid dissection, seizures, vasospasm, and infection. Large mass lesions result in shifts and displacement of IC contents that result in vascular occlusion, edema, and increased ICP (Feliciano, 268). Secondary injury causes breakdown of the blood brain barrier, disruption of cerebral autoregulation, accumulation of toxic extracellular levels of excitatory amino acids and free radicals, and initiates cellular inflammatory responses and regional hyperthermia. It diminishes the effectiveness of autoregulatory and compensatory mechanisms of the brain, thus compromising perfusion and producing ischemia. The tissue surrounding the initial injury is known as the ischemia penumbra and is at highest risk. Secondary injury is often preventable. The "secondary" brain damage opens a window of opportunity where injury and loss of nerve function may be minimized by proper medical treatment (Brain Trauma Foundation, 2000).

4.

5.

IV.

Pathophysiology of traumatic brain injury
A.

The initial trauma sets in motion a series of molecular events which activate endogenous substances, i.e., oxygen free radicals, monoamines, neuropeptides, arachidonic acid metabolites, and alter calcium metabolism (Wagner, p.2). Oxygen free radicals: Superoxides and lactic acid are released as a result of mitochondrial dysfunction in the absence of obvious ischemia. These oxygen radicals cause lipid peroxidation of polyunsaturated fatty acids disrupting cell membranes and possibly resulting in the breakdown of the blood-brain barrier and progressive axonal degeneration (Wagner, p.2). Either through overt damage or by some other mechanism, voltage gates burst open releasing bradykinin, kallikrein, excitatory amino acids (particularly glutamate which is the most excitatory neurotransmitter), and arachidonic acid and its metabolites.

B.

C.

State of Illinois TNS Program Head Trauma - page 6
D.

Current research is exploring the causal relationship between these substances and the development of brain edema and secondary brain damage. Glutamate is stored inside of cells or is shuttled discretely between them. The temporal lobe is filled with glutamate. When trauma occurs, this major neurotransmitter spills freely. There are mechanisms responsible for glutamate uptake by neurons, but these mechanisms quickly become overwhelmed when there is an excess of glutamate and a drop in ATP needed to pump it across the membrane. When the flood of glutamate pours into synaptic clefts, it triggers the opening of key ion channels in the neuron that receives the glutamate signal and over stimulates the neurotransmitter's receptors with a subsequent rush of ions across the cell membrane wall, particularly passage of calcium through N-Methyl-D-Aspartate [NMDA]-receptor mediated channels. Potassium is flushed out of the cell. Calcium is considered essential in normal neuronal activity and is normally activated in small amounts. It reshapes parts of the cell wall membrane under controlled conditions. The drop in energy availability after injury triggers uncontrolled calcium activity late in the cascade of events. One of the first effects of this Ca flux is that glycolysis is stepped up to provide more energy to pump ions across the cell membrane. The Ca blockers used in CV disease are not very effective in blocking the Ca channels in the brain. Brain ion channels have very unique properties. Bruce Bean, professor of neurobiology at Harvard Medical School in Boston and his associates have identified a toxin produced by the funnel web spider of the Southwestern U.S. Through study of this toxin, they have identified a type of Ca blocker that appears to occur only in certain kinds of brain cells [Neuron (1992) 9; 85-89]. The spider venom toxin selectively binds to and blocks a newly recognized Ca channel (P-type), named after the Purkinje neurons where it was first discovered in rat brains. P-type channels occur in central and peripheral neurons, but there is no evidence that they occur in cardiac muscle. They also appear to be used in synaptic transmission and may play a major role in normal as well as diseased neuronal activity. If this evidence can be supported, it suggests that the spider toxin may be a good model for a synthetic compound that could prevent the effects of stroke, trauma and some epilepsy.

E.

F.

G.

H.

Protein synthesis that is needed for normal membrane permeability is slowed. The inhibition of protein synthesis (especially in the temporal lobe) may be one cause of postconcussive amnesia. Glycolysis may initially protect the cell by helping to correct the ion imbalance, but it steadily increases the amount of lactic acid in the cell through anaerobic metabolism. Studies have shown that immediately following injury, glucose metabolism increases, but that this trend is followed by a prolonged decrease that lasts several days. Treating animals with excitatory amino acid antagonists greatly decreased the brain's demand for glucose. The resulting acidosis leads to a breakdown of the cell membrane with bloating of the cell. This causes self-destruction and eventual death. A similar progression can be charted in both contusion and stroke, although the timing and topography of the events are different. Within seconds of trauma, the release of fatty acids from the cell membrane is initiated. The entry of calcium ions into the cell is followed by lipolysis, then proteolysis, and finally protein phosphorylation, which may ultimately be what kills the cell. Stimulation of lipases and phospholipases can be prevented by glutamate antagonists like MK-801. It's a receptormediated process. Cerebral metabolism: The brain is small but greedy. It is only three pounds of tissue (2% of body weight), but is the most metabolically active and perfusion-sensitive organ. It metabolizes 25% of the body’s glucose, burning 60 mg/min. It consumes 20% of the cardiac output and 20% of the total body oxygen (49 mL/min). It has no storage mechanism for oxygen or glucose so brain tissue is dependent on an on-going source of both fuels via a constant source of cerebral blood flow (CBF) via the internal carotid and

I.

J.

V.

Dynamics of cerebral blood flow (CBF) and cerebral perfusion pressure (CPP)
A.

State of Illinois TNS Program Head Trauma - page 7 vertebral arteries and will demonstrate altered mental status within moments of a reduction in either.
B.

Cerebral blood flow is a function of cerebral perfusion pressure and the brain’s ability to autoregulate cerebral blood vessels. Any injury that affects CBF (perfusion) has a rapid and devastating effect on the brain and its control of body systems (Bledsoe, 2006). Cerebral blood flow (CBF) following injury may be disrupted by compression of cerebral blood vessels from mass lesions, reduced cerebral metabolism, or to posttraumatic vasospasm as has been documented in as many as 40% of these patients (BTF, 2003). It can also be reduced due to increased ICP or low systemic BP (hypotension). Autoregulation
1. 2.

C.

The capacity of the brain to regulate its own cerebral blood flow to meet the needes of the brain despite variations in systemic arterial pressures. The fluctuating tone of cerebral arterioles depending on the brain’s changing metabolic needs, normally maintains a constant blood flow to the brain over a wide range of perfusion pressures. Normal cerebral blood flow is 50 mL/100 Gm/min. Autoregulation functions maximally at a MAP of 60 - 180 mmHg. Metabolic or chemical influences: A change in metabolic rate will lead to a change in CBF.
a.

3.

pO2
(1) (2) (3)

(4) b.

Little effect on CBF when in physiologic ranges Hyperbaric levels result in vasoconstriction Hypoxia increases the severity of any head injury. A pO2 < 50 mmHg (SpO2 < 90) causes cerebral vasodilation, increased CBF, and increased cerebral blood volume. This contributes to increased ICP. PaO2 < 30 doubles the CBF 1 mmHg change = 2%-3% change in CBF between 20-80 mmHg A pCO2 > 45 (hypercarbia) causes cerebral blood vessels to dilate with corresponding increases in CBF and cerebral blood volume. In the presence of an already high ICP, this extra dilation can have devastating effects. Conversely, low levels of CO2 cause pronounced vasoconstriction that can almost stop perfusion through the brain. This effect will decrease after 6 to 10 hours. Impaired CO2 reactivity impairs O2 reactivity.

pCO2
(1) (2)

(3)

(4) 4.

Impaired autoregulation in TBI
a.

Autoregulation is often compromised in the TBI patient. There is a flow/metabolism uncoupling. Stimulation of the brain (increased metabolic demand) does not increase cerebral blood flow. Increased ICP with pressure on the brain stem leads to increased MAP (Cushing’s response) with no compensatory cerebral blood flow control, which further increases ICP. The brain now becomes dependent on BP for perfusion. If arterial pressure is ≥ 160 torr, cerebral blood volume increases. Low flow states may lead to blood brain barrier breakdown, an increase in cerebral edema, and predisposes patients to secondary brain injury from ischemia (ATLS, 2005). In states of ischemia, CBF drops to 18-20 mL/100 Gm/min. At 8-10 mL/100 Gm/min, the brain will infarct.

b.

c. d.

State of Illinois TNS Program Head Trauma - page 8
D.

Intracranial pressure: The intracranial volume is fixed in an adult (1200-1500 mL) and does not vary
1.

Three intracranial components
a. b.

c. 2.

80%: Cerebral tissue: Brain is 75% H2O; constant blood brain barrier from intact cell wall membranes 12%: Cerebral blood volume: Result of cerebral blood flow – 750 mL constant. 80% of brain blood is venous. Head position is critical to maintain venous outflow and to prevent venous congestion. 8%: Cerebral spinal fluid (CSF): 125-150 mL is constant.

Any increase in volume in one compartment must be matched by a similar reduction in another compartment or ICP will rise (Monroe-Kellie hypothesis or "No room in the inn theory"). Intracranial pressure values
a.

3.

Normal
(1) (2)

Child: 0-5 mmHg Adult: 5-12 mmHg

b. c.

Intracranial hypertension: 15-20 mmHg Malignant intracranial hypertension
(1) (2) (3)

≥ 20 mmHg sustained for 30 minutes ≥ 30 mmHg sustained for more than 15 minutes ≥ 40 mmHg sustained for more than 2 minutes

E.

Volume pressure relationship:
1.

CBF is dependent on cardiac output (CO) and is independent of systemic arterial resistance (TPR). If arterial pressure is > 160 torr, cerebral blood volume increases. Initially, as volume increases, there is little or no increase in pressure due to compensation, but as compliance is lost, small additions of volume result in large increases in pressure. There is significant post-traumatic vasospasm as well as changes in pressure and metabolic autoregulation. Cerebral vascular resistance is altered (often increased) by trauma. There is increasing evidence that CBF is typically very low following TBI and, in many cases, may be near the ischemic threshold. A low CPP may jeopardize regions of the brain with preexisting ischemia. CBF in the vicinity of posttraumatic contusions and subdural hematomas is reduced even further than global CBF (BTF, 2003). To compensate for an elevated ICP, one of the following must happen:
a. b. c.

2.

3.

Blood volume to brain must diminish, The body must increase CSF resorption, decrease production, displace fluid down the spinal cord, or Brain tissue is displaced (herniation)/

F.

Evolution of pathology causing ↑ ICP: pressure + time are big killers!
1.

Increase in brain volume
a. b.

Mass: Brain tumor, abscess, blood clot, AV malformation; CSF, blood and/or tissue Edema
(1) (2) (3)

Cytotoxic – intracellular Vasogenic – extracellular edema (tumors) Hydrostatic – tissues surrounding ventricles

State of Illinois TNS Program Head Trauma - page 9
2.

Increase in CSF volume (hydrocephalus)
a. b. c.

CSF is produced in the ventricles by the choroid plexus (20 mL/hr) It is reabsorbed in the arachnoid space by the arachnoid villi Communicating (1) Overproduction of CSF (2) Under reabsorption (blood in subarachnoid space) Non-communicating (1) Also called obstructive hydrocephalus (2) An obstruction causing the inability of CSF to circulate to the arachnoid villi to be reabsorbed Influx pressures (systole) Efflux pressure (venous pressure) Vascular radius Blood viscosity

d.

3.

Increase in blood volume: Cerebral blood flow is a function of
a. b. c. d.

4. 5.

6. 7. 8. G.

↑ ICP leads to compression of arteries → cell ischemia → edema In the presence of ischemia/compression of medulla; the body will attempt to fix itself (maintain cerebral perfusion) producing a CNS response called the Cushing response (systolic hypertension, widened pulse pressure and reflex bradycardia) Respiratory insufficiency; hypercapnia Vasodilation/hyperemia; increased CBF Rapid clinical deterioration and death Cerebral perfusion pressure is the physiologic variable that defines the pressure gradient driving cerebral blood flow (CBF) and metabolic delivery and is, therefore, closely related to ischemia (BTF, 2003). Factors that influence CPP
a. b.

Cerebral perfusion pressure (CPP)
1.

2.

MAP = mean arterial pressure (MAP = Diastolic BP + 1/3 pulse pressure) ICP = intracranial pressure

3.

CPP = MAP – ICP a. Normal MAP = 90-100 mmHg b. Normal ICP in adults: 5-12 mmHg c. CPP = 100 – 10 d. Normal CPP = > 60 mmHg but should be patient specific (1) Infants > 50 (2) Children > 60 As the ICP rises near the MAP, the gradient for CBF decreases and perfusion is restricted. In a hypotensive patient, even a marginally elevated ICP can be harmful. The body usually compensa tes for increased ICP by elevating the arterial BP to maintain CPP. Ultimately, the adequacy of CPP is more important than increased ICP. A decrease in CPP results in a reduction in cerebral blood flow. Decreased CPP = altered level of consciousness. Need a minimum CPP gradient of 60 mmHg to be conscious. Never lower the BP in a head trauma patient!
a. b. c. d. e.

4.

5.

6.

CPP < 60 = Impaired blood flow to brain CPP < 50 = Critical reduction in brain tissue oxygen CPP < 40 = CBF down 25% CPP ≤ 30 = Irreversible brain ischemia If ICP ≥ MAP: The patient is dead

State of Illinois TNS Program Head Trauma - page 10
7.

Enhancing intravascular hydrostatic pressure by increasing the BP and CPP can help to improve cerebral perfusion. In most cases, CPP is amendable to clinical manipulation, and enhancement of CPP may help to avoid both global and regional ischemia (BTF, 2003). There is no direct relationship between CBF and ICP. Studies have shown that ICP changes very little when BP is increased by as much as 30 mmHg in head-injured patients, and this is true regardless of the status of autoregulation. Thus moderate increases in BP, as might be needed to maintain an adequate CPP should not be expected to cause an increase in ICP in most patients (BTF, 2003). BTF Guideline for CPP (2003): CPP should be maintained at a minimum of 60 mmHg. In the absence of cerebral ischemia, aggressive attempts to maintain CPP above 70 mmHg with fluid and pressor should be avoided because of the risk of adult respiratory distress syndrome (ARDS).

8.

9.

H.

Clinical signs of ↑ ICP
1.

Early to progressive signs
a.

b. c. 2.

Pressure is exerted downward. Cerebral cortices and/or reticular activating system and cranial nerves are affected producing the following: (1) Altered mental status: progressive restlessness, confusion, disorientation and lethargy or combativeness; changes in speech or loss of judgment (2) Amnesia of events before or after the injury (3) Increased severity of headaches (4) Visual abnormalities: Diplopia, blurred vision, visual field deficits (lose sight in part of field) (5) Conjugate deviation of eyes or gaze palsies (6) Deterioration in motor function: Monoplegia, hemiplegia. First part of boy to show an increase in ICP is the wrist that will over pronate or supinate; pronator drift (7) Sensory loss (8) Oval pupils with hippus (pupil rapidly dilates and constricts when stimulated with light so it looks like it is jiggling up and down) Pressure on the hypothalamus: Vomiting (often without nausea); temp changes Nuchal (neck) rigidity Further alteration in mental status; decreased responsiveness and level of consciousness (coma) Pressure on brainstem
(1)

Later signs – game over
a. b.

Cushing's triad (brainstem pressure):
(a) (b) (c)

Systolic hypertension w/ widening pulse pressure Bradycardia (Vagal nerve pressure) Bradypnea or irregular respirations: pressure respiratory centers

on

(2) (3) (4) c.

Pupillary changes (unilateral to bilateral dilation) and decreased reactivity to light (CN III paralysis) Further deterioration in motor function: flexor-extensor posturing (non-purposeful movement that is a brain stem reflex) Absent or decreased brainstem reflexes: cough, gag, corneal, Doll's eyes and calorics

Wide fluctuations in core temperature

State of Illinois TNS Program Head Trauma - page 11
d. e. 3.

Papilledema Seizures

Levels of intracranial pressure with corresponding S&S
a.

Cerebral cortex and upper brain stem involved
(1) (2) (3) (4) (5)

BP rising and pulse rate begins to slow Pupils still midsize and reactive Cheyne-Stokes ventilations Initially tries to localize and remove painful stimuli, eventually withdraws then abnormal flexion occurs All S&S should be reversible at this stage Wide pulse pressure and bradycardia Pupils pinpoint to mid-size, sluggish or non-reactive (CN III) Central neurogenic hyperventilation Abnormal extensor posturing Few patients function normally from this level Pupils both dilated and non-reactive Respirations ataxic or absent Flaccid, does not react to pain Irregular pulse rate QRS, ST, and T wave changes Decreased BP Not considered survivable

b.

Middle brain stem (pons) involved
(1) (2) (3) (4) (5)

c.

Lower portion of brain stem (medulla) involved
(1) (2) (3) (4) (5) (6) (7)

I.

Herniation syndromes; life threatening
1.

The brain tissue will treat itself if the pressure is not relieved. Folds of dura compartmentalize the brain. Herniation occurs when increased volume, pressure and/or decreased compliance causes a part of the brain to shift from one compartment into another, causing compression of other structures. If the compression results from a building mass along the central region of the cerebrum (epidural or subdural hematoma), pressure is first directed to the midbrain, then the pons, and finally, to the medulla. The S&S of this progressive pressure and structural displacement are known as the central syndrome (Bledsoe, 2006). It is often a life-threatening event. Types of herniation
a.

2.

Supratentorial herniation
(1) (2)

Cingulate herniation: Cingulate gyrus herniated into the falx Uncal herniation: Medial edge of the temporal lobe herniates down through the tentorial notch into the posterior fossa. Ipsilateral pupil dilates and fixes. Contralateral motor weakness or paralysis. Transtentorial (central) herniation: Downward displacement of the cerebral hemispheres, diencephalon, and midbrain through the elongated tentorial notch. Both pupils are fixed and dilated; bilateral motor posturing.

(3)

b.

Infratentorial herniation: Cerebellar (tonsilar) herniation – Cerebellar tonsils herniate into the foramen magnum. Causes almost immediate death.

State of Illinois TNS Program Head Trauma - page 12
3.

Signs of herniation
a. b. c. d. e.

f. g. 4.

Deterioration in the level of consciousness. GCS decreases by 2 or more points BP and ICP shoot up HR drops to 30-40 Respiratory pattern changes Pupillary changes (unilateral to bilateral dilation and non-reactive to light). Pupil first dilates on same side as the clot (ipsilateral dilation) then both may dilate and become nonreactive Motor abnormality (contralateral deficits) to extensor motor posturing Brainstem dysfunction Have two minutes to act after herniation. If medulla brainstem function is altered, the BP will drop to 40-20. HR will increase to 140-150. The brain will not go back to its normal alignment. This is an indication for temporary hyperventilation. Generally poor outcomes in the presence of hypoxia, hypotension, hypercarbia, hyperglycemia (which usually means a clot), or increased Ca levels. Check Mg; Mg runs with Ca.

Outcomes
a.

b.

VI.

Guidelines for assessing and managing patients with TBI The American Association of Neurological Surgeons and the Brain Trauma Foundation (BTF) published patient care guidelines for the management of severe head injury in 1995 with widespread distribution in 1996. These were updated in 2000 and again in 2007. EMS Guidelines were published by the BTF in 2000 under a grant from the U.S. DOT and NHTSA. The guidelines address care of traumatic brain injury (TBI) patients with a GCS of 8 or less. Penetrating head trauma guidelines were published in 2001. Pediatric guidelines came out in 2002, and Spinal Cord injury guidelines were issued in 2001-2002. The BTF also maintains Guidelines for the Surgical Management of Traumatic Brain Injury and Prognosis of Severe Traumatic Brain Injury. A full text of the guidelines can be obtained from the BTF website: www.braintrauma.org.
A.

Classifications of evidence (BTF, 2007)
1. 2. 3.

When assessing the value of therapies or interventions, the available data is classified into one of three categories according to the following criteria: Class I evidence: Data from good quality, prospective randomized controlled trials (RCT). The gold standard of clinical trials. . Class II evidence: Moderate quality RCT, Clinical studies that violated one or more of the criteria for a good quality random controlled trial. Types of studies so classified: good quality case-controlled or good quality cohort studies. Class III evidence: Poor quality RCT with major violations of the criteria for a good or moderate quality RCT. Also included were moderate or poor quality cohort and case-controlled studies, and case series, databases or registry data. Level I Represent the strongest evidence for effectiveness based on accepted principles of patient management that reflect a high degree of clinical certainty usually based on Class I evidence. Level II: Represent a particular strategy or range of management strategies that reflect a moderate clinical certainty based on class II evidence. Level III (opinions): Remaining strategies for patient management for which there is unclear clinical certainty based on class III evidence.

4.

B.

Level of recommendation (BTF, 2007)
1.

2. 3.

State of Illinois TNS Program Head Trauma - page 13
VII.

Initial assessment and resuscitative interventions
A.

The first two hours post-injury are characterized by ischemia and a 3% decrease in CBF that must be corrected. The first priority is rapid physiologic resuscitation and prevention of secondary injury. No specific treatment should be directed at intracranial hypertension in the absence of transtentorial herniation or progressive neurological deterioration not attributable to extracranial explanations (BTF, 1995). Assess, establish and control a patent airway
1.

B.

Maintain spine motion restriction, if indicated, while establishing airway access
a. b.

Check spine motion restriction devices applied in the field; maintain until spine is cleared clinically or radiographically. If the airway is impaired from the tongue, secretion, trauma and/or edema, use positioning, suction, and manual maneuvers to clear the airway of obstructions. If repositioning opens the airway, secure with a NPA or OPA depending on the presence or absence of a gag reflex. Vomiting precautions Airway tissues are extremely vascular, bleed profusely and swell rapidly. Blood is a great gastric irritant that frequently induces vomiting. If the patient is not paralyzed, anticipate vomiting from the head injury or increased ICP with pressure on the medulla, although uncommon in adults. May or may not have associated nausea.
(1)

c.

Projectile vomiting is due to direct pressure on the medulla or vagus nerve roots (CN X), which aborts normal sensory pathways and results in violent contractions of abdominal and thoracic muscles (Wooten, 1996). Seen more often in children. Vomiting is especially dangerous in patients with head trauma who have an altered gag reflex as they cannot protect their airways and frequently aspirate. Gastric contents are extremely acidic and will rapidly damage pulmonary tissues leading to a high patient mortality.

(2)

d.

Have large bore suction equipment available at all times. Suction as necessary. Limit deep tracheal suctioning to 10-15 seconds to avoid hypoxia. Oxygenate prior to and after suctioning. The high incidence of hypoxia and risk of aspiration in patients with traumatic brain injury have been used to justify an aggressive approach to airway management, including intubation by EMS personnel (Davis et al, 2006). The Prehospital Guidelines recommend that patients with severe TBI, who demonstrate hypoxia not corrected by supplemental oxygen and those who lack the ability to maintain their own airway have advanced airway management. Of concern, Wang et al (2004) found threefold increased odds of mortality in those that were intubated in the field after adjustment for injury severity and other cofounders. The high incidence of hyperventilation following intubation, desaturation and bradycardia during tube placement, and undetected esophageal intubation may be important contributors to increased mortality in intubated patients. Laryngoscopy without benefit of neuroprotective drugs may be harmful in this subset of patients. Positive intrathoracic pressure caused by over ventilation may decrease venous return and impair cardiac output in hypovolemic patients. High intrathoracic pressures can also cause an increase in ICP. Hyperventilation results in hypocapneic cerebral vasoconstriction and brain ischemia. Permissive hypercapnia results in an increase in cerebral blood

2.

Airway adjuncts
a.

b.

c.

State of Illinois TNS Program Head Trauma - page 14 flow and may prevent cerebral ischemia, but no studies have yet shown improved outcomes.
d.

Davis et al (2006) report improved survival rates for intubated patients with pCO2 values ranging between 30 and 49 mmHg with a rapid decrease in survival for results less than 30 or over 49 mmHg. Non-intubated patients did not show the same outcome differentials. In their study, most intubated patients arrived with pCO2 values outside the optimal range especially with use of manual ventilation. This underscores the potential dangers of prehospital intubation associated with positive pressure ventilation and hyperventilation. This data is important in the ED setting. The use of ventilators or capnometry-guided ventilations for patients with moderate to severe TBI is important. If intubated in the field, check pCO2, tube placement and patency. If not intubated and procedure is indicated: Prepare equipment for patients with a GCS ≤ 8 as many have a pO2 < 60 torr and are hypercarbic.
(1) (2) (3)

e. f.

If awake or responsive to pain and/or gag reflex present: Drugassisted intubation with in-line stabilization. If unresponsive and/or apneic: Orotracheal intubation with in-line stabilization. Directed intubation: In some patients, facial and upper airway trauma is such that airway landmarks are all but impossible to see. Airway access in these patients may be very difficult. Patients may need to be log rolled onto their side to keep tissues out of the way. Copious suction is needed. A laryngoscope is used to attempt glottic visualization, but if not immediately apparent, look for bubbling air escaping from the trachea with expiration. Have an assistant compress the chest to create bubbling if necessary. Attempt to pass the tube through the bubbling source into the trachea.

g.

If intubation attempts fail and the patient cannot be adequately ventilated with a BVM, anticipate the need for a rescue airway or salvage airway (needle or surgical cricothyrotomy). Gold standard in children may be NO intubation. Insert an oral airway and attempt ventilations with a BVM. Monitor patient's hemodynamic baselines and responses during procedure (BP; HR and rhythm; RR and depth; SpO2; skin color, temperature) Premedicate hypopharynx with topical anesthetic prior to intubation. Apply in-line stabilization, lip retraction, Sellick's maneuver, thyroid cartilage pressure and/or assist with intubation per local protocols. Observe patient for allergic reaction during and just after drug injection Document the following:
(1) (2) (3)

h. 3.

Nursing participation in the procedure
a. b.

c. d.

Name, dose, route, and time of all medications administered Patient's responses to medications Pertinent monitoring data: BP, HR, ECG, SpO2 pre & postintubation

C.

Ineffective breathing pattern; potential or actual
1.

Assess general respiratory rate (very fast or slow), depth, pattern and effort.

State of Illinois TNS Program Head Trauma - page 15
2.

Assist ventilations as needed with a BVM at 10-12 breaths/minute for adults; 15-20 BPM for children; and 30 BPM for infants (BTF, 2007). If long-term ventilatory assist is necessary, prepare the patient for intubation and place on mechanical ventilator. Current BTF indications for hyperventilation: In the absence of herniation, routine prophylactic hyperventilation should be avoided during the first 24 hours as it can compromise cerebral perfusion during a time when cerebral blood flow is reduced by up to 2/3rds (BTF, 2007) causing cerebral ischemia.
a.

3.

Hyperventilation produces a rapid decrease in the pCO2 that causes vasoconstriction, decreased cerebral blood flow, and lowers the intracranial pressure. For each 1 torr drop in pCO2, there is a corresponding decrease in CBF of 3%. Hyperventilation may be necessary for brief periods when there is an ICP ≥ 25, signs of cerebral herniation such as unilateral or bilateral pupillary dilatation, asymmetric pupillary reactivity, motor posturing, or neurologic deterioration (decrease in GCS of more than 2 points when initial GCS was < 9) after correction of hypotension or hypoxemia (BTF, 1995). Hyperventilation may be indicated for longer periods if there is ↑ ICP refractory to sedation, paralysis, CSF drainage, and osmotic diuretics. If hyperventilation is used, ventilate at 12-15 mL VT/kg augmented by 15 L O2 to maintain pCO2 between 30-35 torr for as short a time as possible. Allow time for exhalation. If patient fails this regimen, anticipate a poor outcome. Excessive vasoconstriction can worsen cerebral ischemia. A PaCO2 of ≤ 25 should be avoided. Aggressive hyperventilation may cause loss of autoregulation. Slight hyperemia is probably preferable. Hyperventilation rates
(1) (2) (3)

b.

c.

d.

Adolescents and adults: Elementary school children Infants and toddlers

16-20 breaths/min 30 breaths/min 35-40 breaths/min (BTF, 2007)

e.

Jugular venous O2 concentration (SvO2), arterial-jugular oxygen content difference (AVdO2), and CBF monitoring may identify cerebral ischemia if hyperventilation resulting in pCO2 values < 30 mm Hg is necessary. Don't hyperventilate or give PEEP in shock as it will increase intrathoracic pressure and decrease venous return and cardiac output.

f. D.

Inadequate gas exchange; potential or actual
1. 2.

Level III recommendation: Oxygenation should be monitored and hypoxia (PaO2 < 60 mmHg or O2 saturation < 90% avoided (BTF, 2007). Clinically assess patient for signs of hypoxemia/hypoxia and hyper/hypocapnia. Hypoxia (PaO2 <60) generates free radicals and must be corrected immediately. Most hypoxia resistant cells: pupils; most hypoxia susceptible cells: temporal lobe. Hypoxemia (apnea, cyanosis, or arterial hemoglobin oxygen saturation < 90%) must be avoided, if possible, or corrected immediately. Oxygen saturation should be monitored on all patients with severe traumatic brain injury as frequently as possible or continuously. Hypoxemia should be corrected by administering supplemental oxygen to achieve an SpO2 of 90% or greater. Monitor capnography/end tidal CO2 (normal = 35). EtCO2 increases before ICP goes up. Use as a monitor of pulmonary blood flow, correct placement of an ET tube, and adequacy of ventilations and/or chest compressions. Anticipate 100% FiO2 to achieve a PaO2 > 100 mmHg and SpO2 > 95%

3.

4.

State of Illinois TNS Program Head Trauma - page 16
5.

Monitor ABG results: pH, PaCO2; HCO3; BE; PaO2; O2 sat. Maintain normocarbia or controlled hypercarbia in the absence of clinical signs of herniation (pupillary dilation or asymmetric reactivity, motor posturing, coma).

E. F.

Assess for tension pneumothorax, open pneumothorax, or flail chest; resuscitate per Chest Trauma outline if found. Alteration in vascular volume, cardiac output, cardiac rhythm, or cerebral perfusion
1.

Assess general rate (fast, normal, slow); presence and quality of peripheral pulses, and skin condition. Assume hypotension if radial pulse is absent. Hypotension must be avoided or corrected immediately to maintain CPP > 60 mmHg. Cold, moist skin suggests hypovolemic shock. Patients cannot loose enough blood due to intracranial bleeding to cause hypotension except in infants. If pulses are weak, thready, tachycardic, or absent at the radials and present at the carotids, attempt to determine the reason. Look for large scalp hematomas or hemorrhage, tension pneumothorax, hemothorax, pericardial tamponade, hemoperitoneum, pelvic fracture, loss into an extremity, and retroperitoneal bleeding. While undressing the patient, quickly look for obvious wounds or deformities. If patient as altered mental status, maintain supine position to enhance CPP as autoregulation may be lost. Do not elevate the head of the backboard. Control external hemorrhage with direct pressure and pressure dressings or topical hemostatic agents. These are particularly effective for scalp injuries. Wrap pressure dressings circumferentially above the ears over a vascular pressure point. Do not apply pressure over a possible depressed skull fracture. Cover open scalp/skull wounds as needed. Stabilize impaled objects. Cardiac monitor: 90% have dysrhythmias which are brainstem mediated due to release of catecholamines Maintain euvolemia/mean arterial pressure. The prevention of shock and/or prompt treatment of hypotension are important considerations in the patient with TBI (BTF, 2007).
a.

2.

3. 4. 5.

6. 7.

Level I: There are insufficient data to support any treatment standard given that it would be unethical to conduct prospective randomized trails concerning the effects of hypotension and hypoxia on patients with TBI. Level II: Blood pressure should be monitored and hypotension (systolic blood pressure in adults < 90 mmHg avoided. In children, hypotension can be defined as systolic BP < the fifth percentile for age. Fluid resuscitation in patients with TBI should be administered to avoid hypotension and/or limit hypotension to the shortest duration possible. Fluid therapy is used to augment cardiac preload, support cardiac output, blood pressure and peripheral oxygen delivery in an effort to maintain adequate cerebral perfusion pressure limiting secondary brain injury. The most commonly used resuscitation fluid is an isotonic crystalloid solution. This is administered in quantities necessary to support blood pressure in the normal range, though there are little data to support a specific target blood pressure. Inadequate volume resuscitation can precipitate sudden hypotension and should be avoided. Fluid resuscitation should be done in such as way that does not cause secondary blood loss or hemodilution. Hyperosmolar resuscitation, generally using hypertonic saline with or without Dextran, significantly increased BP and decreased overall fluid requirements (BTF, 2007). Avoid dextrose containing solutions unless hypoglycemia is confirmed due to their potential risk of worsening CNS lactic acidosis and cerebral edema

b.

c.

d.

e.

State of Illinois TNS Program Head Trauma - page 17
f. g. G.

Administer volume expanders and blood products as prescribed. If a hypotensive trauma patient does not respond to fluids, the brain becomes a secondary consideration (ATLS, 2005).

D = Disability: Mini-neurological exam: GCS, pupil size and response, gross motor function, and possible glucose check. Coma is defined as a GCS ≤ 8 (ATLS, 2005). Repeated assessments are crucial to monitor for presence of increased ICP.
1.

Glasgow coma score
a.

The GCS was published in 1974 and revised in 1977 by Drs. Graham Teasdale and Bryan Jennett to serve as a rapid, objective, quantifiable and reproducible tool to assess the depth and duration of impaired consciousness and coma at the bedside 24-hours or so after brain injury or brain surgery. Both Teasdale and Jennett were affiliated with the University of Glasgow in Scotland, thus the city’s name was incorporated into the title of the scale (Fischer & Mathieson, 2001). It was not originally conceived to evaluate all trauma patients. However, subsequent research has shown that severely traumatized patients who are in a shock-like state will experience deterioration in the GCS as it really measures brain function rather than brain injury and brain function can be affected by many things, including shock. Originally known as the Coma Index, it reported three independent subscores of motor, verbal, and eye. It evolved into the Glasgow Coma Scale as the minimum score for each variable was changed to 1 and the sum of the three components was reported as a single score. One huge advantage of this scoring system is its simplicity. With a little practice, all caregivers can learn to accurately obtain and document this aspect of the neuro assessment. Scale is used to
(1) (2) (3) (4)

b.

c.

d.

e.

decide whether injury severity is sufficient to require or justify certain types of treatment; compare different series of injuries; and predict the degree of the ultimate recovery to be expected (Norwood et al, 2002). Examples:
(a)

BTF Guideline: Class II data indicate that the prehospital measurement of the GCS score is a significant and reliable indicator of the severity of head injury, particularly in association with repeated scoring and improvement or deterioration of the score over time. A single measurement of GCS does not predict outcome, however, a decrease of 2 or more points with a GCS of 9 or lower suggests serious injury. Studies indicate that a GCS of 3-5, as well as lack of improvement or deterioration of GCS score by 2 points or more from the field to the ED have at least a 70% positive predictive value for a poor outcome. Liberman et al (2003) reported that trauma patients presenting with a GCS of 3 as well as fixed and dilated pupils in the absence of paralysis, sedation, substance abuse or the use of atropine have no reasonable chance of functional recovery.

(b)

State of Illinois TNS Program Head Trauma - page 18
(c)

American College of Surgeons (ATLS, 2005) recommends intubation or a surgical airway for any trauma patients with a GCS of 8 or less.

f.

Scoring systems that incorporate GCS into their calculations:
(1) (2) (3) (4) (5) (6)

Revised Trauma Score (RTS) Trauma and Injury Severity Score (TRISS) Severity Characteristic of Trauma score Acute Physiology and Chronic Health Evaluation (APACHE) II and III scores Circulation, Respiration, Abdomen, Motor, Speech Scale Simplified Acute Physiology Score II Limitations
■ ■ ■ ■ ■ ■ ■ ■ ■ ■ ■ ■ ■ ■ Variation in inter-rater reliability Inconsistent use by caregivers in prehospital and hospital settings Decreased BP (if SBP < 80, can’t assess GCS with respect to possible outcomes) Hypoxia Hypothermia Hypoglycemia Sedating or paralyzing drugs Intubated patients Patients with facial/ocular trauma Hearing impairments Language barrier Children younger than 3 years Alcohol/drug intoxication Patients that speak a foreign language or have immature language skills GCS relationship to mortality differs considerably between blunt and penetrating head trauma

Strengths
■ ■ Simplicity Provides a common language to report neurologic findings based on bedside observations Ability to trend over time

g.

Obtaining the GCS: GCS should be assessed through interaction with the patient (i.e., by giving verbal directions or for patients unable to follow commands, by application of a noxious or painful stimulus).
(1)

Ideally, GCS scoring should occur after a clear airway is established, and after hypoxemia and hypotension have been corrected, the patient has been resuscitated and before administration of sedative or paralytic agents or after these drugs have been metabolized (Livingston, 2000; BTF, 2007). Components: Unconsciousness can be simplistically defined as failure to respond appropriately to environmental stimuli. Coma is defined as a state of unconsciousness from which the individual cannot be awakened, in which the individual responds minimally or not at all to stimuli, and initiates no voluntary activities (BIAA, 2004). The GCS is the sum of three independent coded values that measure a patient’s eye opening, verbal, and motor responses either spontaneously or in response to verbal or painful stimuli (Healey et al, 2003). Always report the patient’s BEST response, even if different on one side of the body from the other.

(2)

h.

Best eye opening: Assesses both wakefulness, arousal mechanisms in the brainstem, and content of behavioral response. Ask the patient, “What happened to you?” If the patient opens his eyes, then ask the questions in the verbal and motor section of the GCS to determine the total score.

State of Illinois TNS Program Head Trauma - page 19
(1)

If the patient does not open his or her eyes, apply a central pain stimulus. Pinch the earlobe or apply pressure over the supraorbital ridge. If the patient is spontaneously moving all four extremities, apply blunt pressure to the nailbed or pinch the anterior axillary skin. Alternative method of appropriate pain stimulus: pinch muscles to top of shoulder. Eye opening to command or speech is a higher level of stimulus recognition and one can assume that the cerebral cortex is processing information..

(2)

4 3 2 1 Confrounding variables

Spontaneous: Eyes are open or open spontaneously when a person approaches the bedside or is observed while caring for the patient. Indicates an intact arousal mechanism. To voice: Eyes open to either spoken or shouted verbal stimulation. To pain: Eyes open to a painful stimulus. Use only when patient does not open eyes to verbal stimulus. Opening to pain only represents a lower brain functioning. No eye opening: despite painful stimuli Chemically sedated or paralyzed/or eyes swollen shut/orbital trauma; cranial nerve injury.

i.

Best verbal response: Assesses the eloquent cortex (where we speak) by evaluating the content and context of speech. While this evaluates a high level of cognitive function, its absence does not imply a total loss of function. This is a difficult area to score with consistency, especially between the options of 4 and 5.

5 4 3 2 1 Confounding variables

Converses and is oriented to person, where he or she is located (place), time (approximate date - at least month, season or year), and situation. Converses but is confused or disoriented. Should have a good attention span, but responses may be inaccurate. Inappropriate words, poor attention span; does not converse. The patient may repeat random, repetitive words, numbers, or profanity. Incomprehensible sounds, moans, or cries No sounds even after painful stimuli Intubated, paralyzed, sedated, intoxicated or chemically impaired, maxillofacial trauma, grossly swollen tongue, cricothyrotomy, tracheotomy, mutism, aphasia, hearing loss, language barrier, dementia, and/or psychiatric disorders.

j.

Best motor response: Assesses both arousal and content of behavioral response. This element is the least affected by trauma. It allows evaluation of interface between sensing a stimulus, interpreting the information and reacting to it. Note best response, even if seen only unilaterally.

6

Obeys commands: Ask a conscious patient to move his fingers or toes. Ideally, would obey a motor command to move an extremity. If limbs are paralyzed due to high spine trauma, have the patient blink eyes in response to a command. Localizes (Protective response); Localizes pain stimulus and attempts to remove it or move away from it with purposeful movement. This is best assessed by pinching the trapezius muscle or the ear lobe and observing if the patient tries to move your hand away or to pull away from the pain source. The hands should move across midline or above the nipples to confirm purposeful movement. Behaviors that indicate this response: pt. tries to remove a c-collar or oxygen mask; moves the arm in which a pain stimulus like an IV start or blood draw is being applied. This response indicates that the parietal lobe is functioning to to interpret and localize the stimulus and that it can communicate with the motor cortex in the frontal lobe for purposeful movement..

5

State of Illinois TNS Program Head Trauma - page 20
4
Withdraws: Generalized purposeful movements pulling both arms in toward the torso. Pt. knows he is in pain, but cannot localize the stimulus. This response indicates that pain pathways to the thalamus are intact, but the parietal lobe is not interpreting or localizing the pain source. Abnormal flexion (old decorticate posturing): Adduction of upper extremities with flexion or the wrist or elbows and extension of the legs in non-purposeful, reflexive movement. Indicates lesions in the cerebral hemispheres or internal capsule (Fischer & Mathieson, 2001). Abnormal extension (old decerebrate posturing): Adduction, hyperpronation and extension of upper extremities, internal rotation of shoulders, extension and plantar flexion of the legs in nonpurposeful movement. May progress to arching of the back (opisthotonos). Reflects midbrain to upper pontine damage. Posturing is a brain stem reflex. No response (movement) to pain Chemically or traumatically paralyzed, peripheral nerve injury, extremity trauma with immobilization, pain, inability to comprehend commands, dementia, psychiatric disorders, alcohol/drug intoxication.

3

2

1 Confounding variables

k.

There is currently debate over the sensitivity and specificity of GCS scoring with evolving consensus that the motor component alone can predict neurological outcomes (Gill et al, 2005). Recommended scoring for intubated, sedated, or paralyzed patients from the National Trauma Data Bank:
(1)

l.

Record the score exactly as it is measured (Legitimate, unaltered value). In a separate field, add any of the following codes that apply:
(a) (b) (c) (d)

T: TP: S: U:

Intubated Intubated and paralyzed Sedated Untestable

(2)

The legitimate score is accurate if one is describing the results at the moment, but it is highly skewed if using the score to determine the seriousness of a head injury or if trying to predict prognosis. When patients are sedated, using the GCS recorded before sedation is preferable to the assumption of normalcy (Livingston et al, 2000).

m.

Young children: Champion et al described a better method to describe the verbal responses of children younger than three years:
(1) (2) (3) (4) (5)

5: 4: 3: 2: 1:

Appropriate for age Consolable cries Persistent irritation Restlessness and agitation No verbal response

n.

Interpreting the results: GCS severity distinctions can be debated depending on full physical exam but management of brain injury is often still determined by GCS (ATLS, 2005).
(1)

GCS 13-15 - Mild head injury: Should be awake with no significant focal deficits. Increasingly, a GCS of 15 is considered a mild head injury. Risk levels for those with a GCS of 15 can be stratified as follows:
(a) (b)

Low risk: No symptoms or previous symptoms of dizziness, headache or vomiting. Intermediate risk: Loss of consciousness or posttraumatic amnesia.

State of Illinois TNS Program Head Trauma - page 21
(c) (2)

High risk: Severe headache, persistent nausea or more than one vomit (Batchelor & McGuiness, 2002).

GCS 9-12 - Moderate head injury: Patient presents with altered sensorium and/or focal deficits but is still able to follow simple commands. Scores within this range represent 10% of all head injuries. Up to 20% deteriorate to coma; 40% have abnormal CT scans, and 8% require surgery (ATLS, 2005). Should be admitted for observation, even if the CT is normal. GCS 3-8 - Severe head injury: Patients within this range do not follow simple commands after resuscitation and stabilization. They are at risk for secondary brain injury from hypoxia, hypotension, and anemia.

(3)

o.

Accurate Glasgow Scoring is essential in determining the need for resuscitative interventions, selecting the appropriate receiving hospital, trending a patient over time, and calculating a RTS.

2.

Treating the causes of altered mental status (AMS): Hypoglycemia and drug toxicity have been reported as the cause of traumatic events. As with brain injury, hypoglycemia and drug intoxication may present with AMS with or without focal neurologic deficits. It is recommended that patients with AMS of undetermined etiology have a rapid glucose determination (BTF, 2007). Evidence exists that patients with ischemic brain injury with hyperglycemia (>200) have worse outcomes than those with normal serum glucose levels. An injured brain is hypermetabolic and glucose intolerant. If glucose levels or available, do not give dextrose unless they are hypoglycemic. Use clinical assessments when making treatment decisions. Consider the presence of drug toxidromes that may be reversible.

H. I.

Expose to examine and recover to maintain warmth Adjuncts to primary survey
1. 2.

Place urinary catheter as ordered; carefully monitor and record intake and output. Insert an NG or OG tube depending on the nature of the trauma to prevent gastric distention and to decrease the risk of vomiting and aspiration.

VIII.

Secondary survey
A.

Chief complaint and SAMPLE history: What are the patient’s current symptoms?
1.

Nursing diagnosis: Pain. Headache may be due to cerebral edema, vascular dilation, traction on bridging veins, or stretching of the arteries at the base of the brain.
a.

Ask the patient about the onset, provocation/palliation efforts, quality (throbbing, constant/intermittent etc.) region/radiation/recurrence, severity (0-10), and time (how long has this lasted?) Ask about associated S&S such as visual disturbances, nausea, vomiting, sinus congestion, photophobia, etc. If the patient has a known hematoma, contusion, cerebral edema, aneurysm, or AV malformation, worsening headache may signal an increase in the size of the lesion, additional bleeding, or brain tissue swelling. Notify a physician immediately. If the patient is conscious, ask if they lost consciousness (or remember waking up) Did the patient vomit?

b. c.

2.

SAMPLE history
a. b.

State of Illinois TNS Program Head Trauma - page 22
c. d. e.

Allergies Has the patient ingested any drugs or alcohol? Medications: Patients on warfarin (Coumadin) who sustain a traumatic intracranial hemorrhage have a mortality rate that is 5 times that of patients not anticoagulated and is a common cause of preventable death (Ivascu et al, 2006). These authors recommended a very aggressive approach to anticoagulated patients: immediate triage; rapid ED physician evaluation; head CT with immediate reading; and 2 units of fresh frozen plasma (FFP) thawed while patient is in CT. If CT is positive, give FFP and vitamin K, and then an additional 2 units of FFP two hours later. Admit to ICU or take to surgery if required. If CT is negative, admit for 24 hours of observation (Sutphen, 2006). Significant underlying illnesses Last oral intake Ask about mechanism of injury and events surrounding the trauma

f. g. h. B.

Vital signs: The vital signs may provide very valuable information about the patient’s underlying injuries. Obtain a full set of manual vital signs before hooking the patient up to automated devices. Repeat at least every 15 minutes while unstable or as indicated by local protocols.
1.

Respiratory rate, patterns, and depth. Provides more clues as to the location of pathology than any other vital sign. Be particularly alert for sudden apnea and be prepared to assist ventilations. Look for diaphragmatic breathing, an indication of intercostal muscle paralysis.
a. b. c.

Eupnea: Normal pattern of ventilations. Bradypnea: Decreased rate. Respiratory rate may slow initially after an acute increase in ICP. Cheyne-Stokes: Crescendo/decrescendo respirations (waxing and waning depth and rate) with periods of apnea up to 20 seconds; seen with increased ICP. Due to increased sensitivity to CO2 that results in a change in depth and rate and decreased stimulation from respiratory centers that results in apnea. Lesions are most often located bilaterally deep within the cerebral hemispheres, diencephalon (thalamus and/or hypothalamus) or basal ganglia. Central neurogenic hyperventilation: Regular, sustained, increased rate and depth of respirations with forced inspiration and expiration. Thought to be due to release of the reflex mechanisms for respiratory control in the lower brainstem and results in decreased CO2 and alkaline pH. Giving oxygen does not change the pattern. Lesion location unclear, often in the midbrain and upper pons. Apneustic: A pause of 2-3 seconds noted after a full or prolonged gasping inspiration followed by an inefficient, brief expiration. May alternate with an expiratory pause. Lesion located in the lower pons, usually due to a basilar artery occlusion. Cluster: Clusters of slow irregular breaths with periods of apnea at irregular intervals (gasping breathing has features similar to cluster breathing). Lesion in the lower pons or upper medulla. Ataxic (Biot's) breathing: Complete irregular, unpredictable pattern with deep and shallow random breaths and pauses. Lesion in the medulla.

d.

e.

f.

g. 2.

Pulse: Count rate, evaluate rhythmicity, quality, location; compare equality.

State of Illinois TNS Program Head Trauma - page 23
3.

BP
a.

Blood pressure should be measured using the most accurate system available under the circumstances. It should be obtained as often as possible and, if possible, continuously by trained medical personnel. Hypotension (SBP < 90) must be avoided or corrected immediately to maintain a CPP > 60 (BTF, 2007). A single prehospital BP < 90 was associated with a doubling of mortality as compared with a matched group of patients without hypotension (Traumatic Coma Data bank). A combination of hypoxia and hypotension increases mortality to 75% (ATLS, 2005). It is possible that SBP needs to be significantly higher than 90 to maintain CPP but no studies have been performed to determine an ideal number. Once ICP monitoring has been established, manipulation of BP should be guided by CPP management (BTF, 2007). In children, the following SBPs have been linked to poor outcomes:
(1) (2) (3) (4)

b. c.

d.

e.

0-1 years: 1-5 years: 5-12 years: 12-16 years:

65 mmHg 70-75 mmHg 75-80 mmHg 80-90 mmHg

f.

Compensatory alterations in vital signs: Cushing's triad
(1) (2) (3)

↑ SBP, widened pulse pressure ↓P ↓ RR Hypotension (Chesnut et al, 1998) Tachycardia (grave sign) ECG changes: (a) Q wave with ST depression (b) Prolonged QT interval (c) Dysrhythmias: atrial: PACs, biphasic Ps, A-Fib

g.

Decompensatory alterations
(1) (2) (3)

4.

Evaluate core temperature for hyper or hypothermia. Note: The anterior hypothalamus keeps us from getting too hot (radiator). It sits right next to the pituitary stalk and is directly stimulated at 42° C. The posterior hypothalamus is the heater. It sets the hypothalamic set point and raises the body temp. The patient will change temps without sweating or gooseflesh. Each degree increase in temp. = 6% increase in CBF.

C.

Review of systems - See Patient Assessment module Focused exam of head should include inspection for deformities, asymmetry, contusions, abrasions, puncture wounds, bruising, lacerations, swelling/edema, bleeding, and drainage of CSF from eyes, nose (rhinorrhea), mouth or ears (otorrhea). Inspect eyes, nose, mouth, and ears for signs of injury.

D.

Focused neuro exam: Extent of exam depends on the patient's level of consciousness and acuity. If awake, alert and cooperative, can perform detailed assessment. If comatose, the nursing exam is usually limited to GCS, pupillary check, and pain responses.
1.

Level of consciousness: Most sensitive indicator of neurological status. In a conscious patient, altered mental status (AMS) is the first sign of deterioration. To provide consistency, describe patient's response in specific behavioral terms.
a.

Arousal
(1)

Alert: Awake, responds immediately to commands

State of Illinois TNS Program Head Trauma - page 24
(2) (3) (4) b.

Lethargic: Response to commands may be incomplete or slow. Needs stimuli, but obeys. Returns to sleep. Stuporous: Decreased awareness. Does not obey commands. Spontaneous or purposeful movements may be noted. Comatose: Unable to arouse. Abnormal flexion or extension to stimuli. May be flaccid (Wooten, 27).

Awareness: Orientation to person (himself and/or loved ones), place and time. Determine if changes are new or if they pre-date the trauma (e.g., dementia) Assess for short-term memory (amnesia); shortened attention span; difficulty following simple/complex commands. Determine if affect and behavior reveal restlessness, agitation, irritability or combativeness. Evaluate cognition by determining if the patient's responses to questions are appropriate or inappropriate. Ask a conscious patient if they are experiencing audio or visual hallucinations. Evaluate cognition and their ability to process information: A study by de Kruijk et al (2002) found that the most prevalent symptoms reported in those admitted to an ED with mild TBI are forgetfulness, drowsiness, headache, dizziness, trouble concentrating and lightheadedness and will need cognitive retraining. Determine if the patient’s responses to questions are appropriate or inappropriate. Anticipate slowing of thought processing speed. Attempt to orient patient to person, place, time and situation. Restrain patient only as necessary to provide safety. I: Olfactory (smell detection and interpretation): Probably the least tested and least helpful in neurological testing because of changes that occur from a wide rage of influences, i.e., rhinitis, craniofacial trauma, smoking. Evaluate in patients with suspected anterior basilar skull fractures, those who complain of taste disturbances, seizures, or headaches. Do not use ammonia capsules as they trigger pain receptors of the trigeminal nerve.
(1)

2.

Mental status exam
a. b.

c. d.

3.

Nursing diagnosis: Alteration in cognitive function
a. b.

4.

Cranial nerve exam: see Neuro A&P study guide
a.

Ask patient to close eyes. Testing one nostril at a time, put a freshly opened alcohol wipe or a bar of soap near their nose and ask them to tell you what they smell.
Results: Lost entirely - anosmia. Lost some - hyposmia.

(2) b.

II: Optic Transmits visual information to occipital lobe for processing (visual acuity; visual fields):
(1)

Visual acuity: Ability of the eyes to perceive visual detail (near and/or far). Ask patient if they wear corrective lenses or contacts. Testing one eye at a time, have them read your name badge or a near car, count fingers at 6 inches, detect the movement of your hand, or detect the projection of light in descending order of visual acuity. Worst visual acuity is an NLP (no light perception) eye. Assess for double vision, visual deficits. Visual fields: peripheral vision

(2)

State of Illinois TNS Program Head Trauma - page 25
(a)

Exam: Have the patient cover one eye and sit facing you. Extend your arm out perpendicularly and wiggle a finger in each of the visual quadrants. Ask patient to identify what quadrant the movement is in. Results: Visual fields can be impaired in head injury/stroke. With one hemisphere disease, neither eye sees the contra-lateral environment (hemianopsia). Evaluate appearance of optic disk Assess for venous pulsations Look for retinal hemorrhages

(b)

(3)

Funduscopic exam
(a) (b) (c)

c.

III: Oculomotor (regulates pupil size; constriction and reactivity; eye movement up, down and in to the nose; lifts eye lid). There are insufficient data to draw conclusions on the diagnostic and prognostic value of findings on the pupillary exam. Conditions that affect pupil size and reactivity besides brain stem or CN III trauma: hypoxia, orbital trauma, drugs diabetes mellitus (affects blood supply to the nerve); alcohol; aneurysms; and hypothermia. Pupils should be assessed and documented for each eye after the patient has been resuscitated and stabilized. The duration of pupillary dilation and fixation should also be documented (BTF, 2007).
(1)

Size - Normal range: 3-4 mm. Unilaterally or bilaterally dilated pupils unresponsive to light in an unconscious patient may indicate transtentorial uncal herniation due to ipsilateral compression of CN III. This patient is in need of emergent interventions to lower the intracranial pressure. A unilaterally fixed and dilated pupil may also reflect direct injury to the orbit or globe.
(a) (b) (c) (d) Midrange bilaterally reactive Midrange, bilaterally non-reactive Pin point bilaterally non-reactive Dilated, bilaterally non-reactive = midbrain OK = midbrain lesion = pontine lesion = medullary lesion

Drugs and toxins that affect pupil size/reactions Constriction
■ ■ Sympathetic blockade: beta blockers, MAO inhibitors Parasympathetic stimulant: acetylcholine, narcotics, methadone, neostigmine, nicotine, physostigmine, pilocarpine, tetraethyl ammonium Narcotics ■ ■

Dilation
Sympathetic stimulants: Cocaine, epinephrine, phenylephrine, tyramine ephedrine,

Parasympathetic blockers: Alpha-methyldopa, atropine, botulinus toxin, chlorpheniramine maleate, clonidine, curare, dopamine, doxepin hydrochloride, ibopamine, imipramine hydrochloride, jimson weed, methantheline bromide, scopolamine, toadstool toxin, wild sage. Early and late barbiturate intoxication High blood alcohol levels over 300 mg/dl

■ ■

(2)

Shape – Pupils are generally round. Assess and report changes immediately.
(a)

Ipsilateral oval pupil frequently heralds the early stages of transtentorial herniation with compression of CN III. If unreversed, the pupil will continue to dilate and become nonresponsive to light.
Tear drop: often means ruptured globe Key hole: old iridectomy during cataract surgery

(b) (c)

State of Illinois TNS Program Head Trauma - page 26
(3)

Equality – Inspect simultaneously before checking the light reflex. Some people have naturally unequal pupils with less than a 20% difference (1 mm) (anisocoria) with no pathologic significance.
Others show unequal pupils due to an earlier injury or neck surgery. If comatose, attempt to find their picture from a driver's license or ask significant others to determine if pupils were always unequal or whether it is a new development. If condition is physiologic, the pupils should maintain their relative sizes in both bright and dim light.

Greater than a 1 mm difference in a patient with AMS is significant.
If a disparity is accentuated in dim light, suspect Horner's Syndrome (CN III deficit). If > 3 years of age with a dilated pupil after trauma oxygenate and assume brain shift. (4)

Reactivity (CN II & III): The light reflex depends on an intact afferent system that carries the light impulse on the Optic nerve (CN II) to the occipital lobe to be interpreted as too much light and parasympathetic fibers on the outside of CN III from the midbrain to the pupil. A bright light shined into one eye should result in brisk constriction of at least 1 mm of both the ipsilateral eye (direct response) and the contralateral eye (consensual response). The Oculomotor nerve has its nuclei adjacent to the midbrain areas controlling consciousness. Assessing pupils is essential in all patients with altered mental status. The nerve exits the midbrain under the medial portion of the temporal lobe called the uncus. It is susceptible to compression from edema, intracerebral hemorrhage, and epidural or subdural hematomas. Unilateral CN III compression compromises the efferent pathway, thus blocking the direct light response, while preserving the consensual response (swinging light test) (BTF, 2007). See note under size for significance of non-reactivity.
(a) (b) (c)

(d)

(e) (f)

Have patient look straight ahead in as dim a light as possible Bring light in from the side (out of the visual axis) and shine into one eye. Observe that pupil for its response (direct response). Note as brisk, sluggish, or non-reactive. Should briskly constrict at least 1 mm. Bring light in again from the side and shine into the same eye. Observe the opposite pupil for its response (consensual response). Repeat the procedure on the other eye. If a dilated, non-reactive pupil is due to injury inside or outside of the brainstem, it is likely that this will be accompanied by other prominent neurologic symptoms, like diplopia or altered consciousness (Goldberg, 31).

(5)

Accommodation: Pupil should constrict when the focus changes from a distant object to a nearby object. Argyll-Robertson's or "prostitute's pupil" - accommodates, but does not respond. Hippus: Pupil spontaneously dilates and constricts after a light stimulus. Indicates ↑ ICP. Seen in pre/postictal patients. Both eyes = herniation. Observe eye lid for ptosis.

(6)

(7) d.

Gaze palsies: CN III, IV, VI Control lateral and vertical gaze. Examine together as they collectively control ocular motility. When stimulated, these muscles shorten.

State of Illinois TNS Program Head Trauma - page 27
(1) Exam: Extra ocular movements (EOM's) - Have patient follow a finger in all six directions of gaze. Eyes should move together. Assess conjugate or dysconjugate gaze. (a) IV (Trochlear) innervates superior oblique muscles that depress the adducted eye and help move the eye in other positions. VI (Abducens) innervates lateral rectus muscle and normally pulls eye towards ear; most sensitive nerve (first to become dysfunctional) in the presence of ↑ ICP. III (Oculomotor) supplies all the other ocular muscles (superior rectus, medial rectus, inferior rectus, inferior oblique and levator palpebrae).

(b)

(c)

(2)

Results: May have traumatic III, IV, and VI nerve palsies
(a)

If large pupil, ptosis and eye pulled to ear: assess for complete 3rd nerve loss. Eyes look towards a lesion as neither can move to the contralateral side. Sign generally first seen just before herniation. If eyes deviate toward the nose, anticipate loss of CN VI and ↑ ICP. Pupils fixed in the midline indicate compression of CN III or the brain stem. Tested in unconscious patient (see Dolls-Eyes maneuver). Roving eyes = frontal lobe dysfunction
(Pearl: before 6 or 7 months old, nerves are unmyelinated, that is why infants often look cross-eyed Nystagmus may be horizontal or vertical. Slight nystagmus at the extreme lateral position is normal. Marked nystagmus on extreme lateral gaze or forward gaze is abnormal. Jerk nystagmus with a fast and slow component suggests CNS or PNS lesion. Vertical nystagmus suggests brain stem lesion. Diplopia or double vision should disappear when one eye is covered. Exception: dislocated lens, retinal detachment.

(b) (c)

(d) (e) (f)

(g) e.

V: Trigeminal: Sensation to facial skin, cornea, and various mucous
membranes (ocular, nasal, and oral) by way of three branches: ophthalmic, maxillary, and mandibular. Mandibular branch also supplies motor ability to muscles of mastication. (1) Sensory component: Test by whisping cotton swab across midline of forehead, upper lip/cheeks and chin. Alternate with broken tip of cotton swab to distinguish sharp from dull. Blink reflex: With eyes closed, gently stroke lashes or tap forehead between the eyebrows (glabellar tap) to check for a blink reflex. Motor component: Have patient bite down and clench teeth to test occlusion and strength of temporalis and masseter muscles. Results: Cerebral lesion results in full loss of sensation on opposite side of the face. Peripheral nerve damage will result in deficit on one branch. Unilateral weakness or the inability to contract the jaw muscles suggests a trigeminal nerve lesion. Bilateral dysfunction suggests motor neuron involvement.

(2) (3)

f.

VII: Facial: : Motor to muscles of facial expression; closes eye lids

State of Illinois TNS Program Head Trauma - page 28
(1) Exam: Inspect face during conversation for any asymmetry, tics, or abnormal movements. Have patient smile, frown, open and close eyelids against resistance, puff out cheeks, whistle - observe for asymmetry or weakness on one side or flattening of the nasolabial fold. When lids are tightly closed, assess if one side shows more lashes than the other. If so, motor deficit on that side. Taste from the anterior 2/3rd of the tongue (salt, sour, sweet) and sensory from the soft palate and salivary glands. Not usually tested. Results: Lesions generally result in contralateral paralysis of the lower face (below the eye) due to bilateral connections to the forehead and eyelids from each hemisphere. Typical stroke results in weakness in elevating the corner of the mouth, but no significant weakness in wrinkling the forehead. Bell's palsy or peripheral nerve damage results in total ipsilateral hemi-facial paralysis.

(2) (3)

g.

VIII: Vestibulocochlear: Two separate nerves purely sensory: vestibular function and cochlear (auditory) function.
(1) Exam: Check auditory reception/equality through whispered speech. Softly whisper a phrase, word or number in each ear and ask the patient to repeat it. Have patient hum. If a conductive defect, the poorly hearing ear hears the hum louder. Can test on self by occluding one ear and humming. Results: Auditory information is processed bilaterally, so may not be affected. If CN VII has dysfunction, check CN VIII very carefully as they run together.

(2)

h.

IX & X: Glossopharyngeal & Vagus: Examine together; lifts palate, provides gag reflex (1) (2) Exam: Have patient say, "Ah" or repeat "Ha, ha, ha". Look for elevation of the palate (normal) or deviation of uvula (abnormal). Results: Vagal dysfunction will result in hoarseness or vocal cord paralysis. Not significantly affected by unilateral cerebral lesions.

i.

XI: Spinal accessory: Supplies sternocleidomastoid muscles and the upper portion of the trapezius muscles. Sternocleidomastoids on each side of the neck turn the face to the opposite side. An isolated XI nerve does not exist (Henry, 2004) (1) Exam: Have patient turn head against your hand and shrug shoulders with and without resistance. Assess equality of strength, bulk of muscle. If patient is

j.

XII: Hypoglossal: Supplies most of extrinsic lingual muscles. speaking normally, do not test XII separately. (1)

Exam: Have patient stick out tongue. Observe any asymmetry, deviation or atrophy. Tongue usually points to side of a lesion. Have patient push tongue into cheek against resistance, assess for strength. Result: Weakness on one side of the tone will cause the tongue to deviate to that side. Rare for this nerve to be affected.

(2) 5.

Motor exam
a.

Assess spontaneous, purposeful movement, muscle tone & strength to gravity and against resistance. Have patient extend arms in front of them with palms up and eyes closed. Watch for pronator drift to indicate unilateral weakness.

State of Illinois TNS Program Head Trauma - page 29
b.

Conscious patient: Assess ability to shrug shoulders, flex and extend elbows and wrists, hold fingers spread open against resistance and to open fingers against resistance; flex and extend knees, plantar and dorsiflex feet; wiggle toes. If unconscious: Observe spontaneous or purposeful movements and then begin applying stimuli from least noxious to pain. Assess for weakness by holding up both upper extremities and releasing them simultaneously. A weak extremity will fall more quickly. To check lower extremities, bend the knees and place feet together flat on the cart. Hold the knees together and release at the same time. A weak or paralyzed limb will fall immediately. Grading function
(1) (2) (3) (4) (5) (6)

c.

d.

5 = normal muscle strength 4 = normal range of motion against some resistance 3 = normal range of motion against gravity only 2 = weak contraction; unable to overcome gravity 1 = slight muscle contraction; no joint movement 0 = complete paralysis Paresis (weakness) Paralysis (inability to move at all) Posturing: Abnormal flexion or extension Clonus: Spasm in which contraction and relaxation alternate in rapid succession Decreased: flaccid/atonic Increased: spasticity, rigidity

e.

Movement/strength abnormalities
(1) (2) (3) (4)

f.

Muscle tone abnormalities
(1) (2)

6.

Sensory exam
a. b. c. d. e.

Superficial touch Superficial and deep pressure/pain Sensitivity to heat and cold Sensitivity to vibration Proprioception: joint position sense Have patient rapidly turn their hands palm up and palm down (rapid alternating movements), rotate their hands in concentric circles (posting), touch their finger to your finger (light on an object), and run the heel of one foot down the shin of the opposite leg. An inability to smoothly start and stop or coordinate motion is called ataxia and may indicate cerebellar dysfunction DTRs, anal wink Babinski: upper motor neuron (UMN) lesion Brainstem
(1)

7.

Cerebellar exam
a.

b. 8.

Reflex exam
a. b. c.

Doll's eyes (oculocephalic reflex): Done only after C-spine is cleared in a comatose patient
(a)

Lift both eyelids. Rapidly turn the head from midline to one side.

State of Illinois TNS Program Head Trauma - page 30
(b)

Normally, the eyes continue to look upward at the ceiling, so they appear to move in a direction opposite to the way the head is turned, i.e., when head is rapidly turned to right, eyes appear to move left. Record as normal response, abnormal response (dysconjugate or asymmetrical eye movement), or pathologic response (no movement of either eye so they move in the direction the head is turned - like eyes painted on a doll). Performed when the oculocephalic test is equivocal or contraindicated Verify integrity of the tympanic membrane Irrigate the tympanic membrane with ice water Normal response: slow deviation of eyes toward the side of the stimulus followed by rapid override by the cortical centers to direct eyes back toward the midline. Creates impression of nystagmus away from cold. Abnormal response: eye does not move

(c)

(2)

Calorics; oculovestibular reflex
(a) (b) (c) (d)

(e) IX.

Definitive interventions
A.

Currently, there is no treatment that can prevent nerve damage or promote nerve healing. After ABCs are addressed, management is aimed at early CT scanning, immediate evacuation of intracranial mass lesions, followed by aggressive management in an ICU that includes ICP monitoring. This is done to maintain cerebral perfusion and oxygenation and to control and prevent complications of secondary injury including increased intracranial pressure. Monitor/maintain cerebral perfusion
1. 2. 3. 4.

B.

ICP monitoring: The only way to reliably determine CPP and cerebral hypoperfusion is to continuously monitor ICP and BP (BTF, 2007). Transcranial Doppler Jugular venous oxygen extraction Direct or indirect cerebral blood flow monitors Recommendations: (BTF, 2007)
a. b.

C.

Intracranial pressure (ICP) monitoring
1.

Level I: There are insufficient data to support a treatment standard for this topic. Level II: Intracranial pressure (ICP) should be monitored in all salvageable patients with severe traumatic brain injury (TBI); Glasgow Coma Scale (GCS) score of 3-8 after resuscitation) and an abnormal computed tomography (CT) scan. An abnormal CT scan of the head is one that reveals hematomas, contusions, swelling, herniation, or compressed basal cisterns. Level III: ICP monitoring is indicated in patients with severe TBI with a normal CT scan if two or more of the following features are noted at admission:
(1) (2) (3)

c.

Age over 40 years Unilateral or bilateral motor posturing Systolic BP < 90 mmHg

d.

Post-op w/ significant brain swelling

State of Illinois TNS Program Head Trauma - page 31
e.

Routine ICP monitoring is not indicated in patients with mild or moderate head injury. However, it may be undertaken in certain conscious patients with traumatic mass lesions at the discretion of the treating physician. Of note, 78% of trauma centers now comply with the BTF guidelines and monitor ICP (BTF, 2007). It is questionable as to whether one can prognosticate from the readings. For example, one can only speculate that if the pressure is greater than 25 for 24 hours, the patient can't be normal upon recovery. ICP data can be used to predict outcome and worsening intracranial pathology, calculate and manage CPP, allow therapeutic CSF drainage with ventricular ICP monitoring and restrict potentially deleterious ICP reduction therapies (BTF, 2007). Can be the first indicator of worsening status and evolving mass lesions requiring surgery. Treatment of ICP without ICP monitoring carries risk
(1) (2) (3) (4)

f.

2.

ICP data use
a.

b. c.

Prolonged hyperventilation significantly reduces CBF. Prophylactic paralysis increases pneumonia and ICU stay. Barbiturates have a significant risk prophylactic use is not recommended. of hypotension and

Mannitol has a variable ICP response in extent and duration of ICP reduction.

3.

Types of ICP monitoring systems (BTF, 2007)
a.

The Association for Advancement of Medical Instrumentation (AAMI) has developed the American National Standard for Intracranial Pressure Monitoring Devices in association with a Neurosurgery committee. According to the AAMI, an ICP device should have the following specifications:
(1) (2) (3)

Pressure range 0-100 mmHg Accuracy: ±2 mm Hg in range of 0-20 mmHg Maximum error 10% in range of 20-100 mmHg

b.

Intraventricular fluid-coupled catheter with an external strain gauge transducer or catheter tip pressure transducer is the most accurate, low cost, and reliable monitor and is the established reference standard. The monitor is set to a prescribed maximum pressure and an alarm sounds when that pressure is reached. It can be recalibrated in situ. ICU nurses are authorized to drain CSF for about 10 seconds to relieve the pressure. An external transducer must be consistently maintained at a fixed reference point relative to the patient’s head to avoid measurement error (BTF, 2007). ICP transduction via fiberoptic or micro strain gauge devices placed in ventricular catheters provide similar benefits but at a higher cost. Parenchymal: Camino catheter: Closed fiberoptic system placed using micro strain pressure transducers through 18 gauge needles, read tissue pressures and provides results similar to ventricular ICP. Monitoring at 30° is best. No head turning! Have the potential for measurement differences and drift due to the inability to recalibrate. Less accurate

c. d.

e.

State of Illinois TNS Program Head Trauma - page 32
(1) (2) (3) 4.

Subdural devices: Catheter tip pressure transducer of fluidcoupled catheter with an external strain gauge. Subarachnoid: Fluid-coupled device with an external strain gauge Epidural devices

Normal ICP = 5-12 torr. Initiate ICP interventions at an upper threshold of 20-25 mm Hg. Manage patient care according to ICP readings, frequent clinical exams, and CPP data. May treat ↑ ICP by draining CSF through monitoring system Nursing responsibilities for patients with ventriculostomy and ICP monitors
a. b. c. d. e. f. g. h. i. j. k. l.

5. 6.

Explain need for monitor to patient and family. Gather and assemble equipment. Flush the lines and calibrate equipment. Perform neurological assessment. Administer sedation/analgesia as prescribed. Place head of bed at 30 degrees if prescribed in a hemodynamically stable patient. Prepare operative site, establish sterile field, assist physician as needed. Connect monitoring catheter to transducer or monitor. Observe the numeric reading and wave patterns; adjust characteristics to obtain visual reading. Cover site with sterile dressing. Adjust alarm system to unit parameters. Obtain frequent checks of neuro status and patency of system. Irrigate system using sterile technique to maintain patency according to unit policy (Bourg, 2007). If left in place for longer than 4-5 days, infected is a risk - give antibiotics as ordered. Hemorrhage: Rare in ventriculostomy catheters. Malfunction or obstruction: In fluid coupled ventricular catheters, subarachnoid bolts, or subdural catheters has been reported in up to 16% of patients (BTF, 2007). No publications on the complication rate of fiberoptic transducer in populations studied since 1999. Malfunctions of microstrain gauge devices are reported as 0%. Malposition

7.

Risk/complications:
a. b. c.

d. D.

Transcranial dopplers: Common carotid branches into the external carotid that perfuses the face and the internal carotid that perfuses scalp and brain. The velocity of the middle carotid artery (MCA)/ext. carotid = 1.7; > 3 = vasospasm. Systemic jugular venous oxygen saturation (SjVO2 or SjO2), arterial-jugular venous oxygen content differences (AVdO2) (extraction ratios), and CBF monitoring may help to identify cerebral ischemia if hyperventilation values < 30 mmHg are necessary.
1. 2. 3. 4. 5. 6.

E.

Monitor patients with TBI, SAH in vasospasm, and post-op patients with suspicious pathology of significant brain swelling or intracranial hemorrhage. Tests are less expensive Assess oxygen availability to brain Depend on CBF and HbO2 content Normal SjO2 = 65-75%; goal: keep above 55% SjO2 decreases with
a.

decreased CBF which increases O2 extraction;

State of Illinois TNS Program Head Trauma - page 33
b. c. d. 7.

anemia; and a decrease in arterial oxygen extraction. If SjO2 is < pO2 27 - look for above increased ICP and decreased CPP; excess hyperventilation; cerebral spasm; and systemic hypotension.

Cerebral blood flow decreases with
a. b. c. d.

F.

Anti-cerebral edema measures
1.

Hyperosmolar therapy: Mannitol and hypertonic saline
a.

Recommendations (BTF, 2007)
(1) (2)

Level I: There are insufficient data to support a Level I recommendation for this topic. Level II: Mannitol is effective for control of raised intracranial pressure (ICP) at doses of 0.25 gm/kg to 1 gm/kg body weight. Arterial hypotension (systolic blood pressure < 90 mmHg) should be avoided. Level III: Restrict mannitol use prior to ICP monitoring to patients with signs of transtentorial herniation or progressive neurological deterioration not attributable to extracranial causes.

(3)

b.

Mannitol is a hypertonic simple sugar - super oxide (free radical) scavenger. It creates an osmotic gradient that pulls fluid from the intracellular and parenchymal spaces into the vascular space thereby decreasing cerebral edema, lowering blood viscosity to increase cerebral blood flow, and increasing oxygen delivery to the cells. Mannitol reduces ICP within 15-30 minutes of its administration while osmotic gradients are established between plasma and cells. Effects last from 90 minutes to six hours or more depending on the patient’s clinical condition (BTF, 2007). Indications for use (BTF, 2007)
(1) (2)

c.

d.

Management of TBI with suspected or actual raised intracranial pressure. Single administration for short-term benefits while further diagnostic procedures (CT scan) and interventions (surgical evacuation of an intracranial mass) can be accomplished. Prolonged therapy for increased ICP.

(3) e.

Mannitol should not to be used prophylactically. Caution in CHF. Mannitol may be used prior to ICP monitoring in the presence of transtentorial herniation or progressive neuro deterioration not attributable to systemic pathology, but only under conditions of adequate volume resuscitation (BTF, 2007). Don't dehydrate the brain! Avoid hypovolemia by providing fluid replacement. If you decrease blood volume you decrease cerebral blood flow.
(1) (2)

f.

There may be a lot of cerebral swelling, but not a lot of free water. An indwelling urinary catheter is essential in these patients. Maintain serum sodium levels at 145 to 150.

State of Illinois TNS Program Head Trauma - page 34
(3)

Osmoles normally = 2 X Na (143) = 286. Keep serum osmoles ≤ 320 mOsml if concerned about renal failure. Serum sodium and serum osmoles are good tests to follow, as a 10 mOsml gradient (296) is needed to get fluid out of brain. Arterial hypotension, sepsis, nephrotoxic drugs, or preexisting renal disease place patients at risk for renal failure with hyperosmolar therapy (BTF, 2007). Effect on ICP is due to the osmotic gradient that moves water across an intact blood-brain barrier reducing the cerebral water content of mainly non-traumatized brain tissue. HS also dehydrates endothelial cells producing vessel dilation and shrinks RBCs that increases their deformability (ability to perfuse through capillaries) leading to plasma volume expansion and improved blood flow. It also reduces WBC adhesion in traumatized brain (BTF, 2007). Side effects: Risk of central pontine myelinolysis when given to patients with preexisting chronic hyponatremia. Risk of inducing or aggravating pulmonary edema in patients with underlying cardiac or pulmonary problems (BTF, 2007). Current evidence is not strong enough to make recommendations on the use, concentration and method of administration of hypertonic saline for the treatment of traumatic intracranial hypertension (BTF, 2007).

(4)

g.

Hypertonic saline (HS)
(1)

(2)

(3)

2.

Prophylactic hypothermia
a. b. c.

Level I: There are insufficient data to support a Level I recommendation for this topic. Level II: There are insufficient data to support a Level II recommendation for this topic. Level III: Pooled data indicate that prophylactic hypothermia is not significantly associated with decreased mortality when compared with normothermic controls. However, preliminary findings suggest that a greater decrease in mortality risk is observed when target temperatures are maintained for more than 48 h. Prophylactic hypothermia is associated with significantly higher Glasgow Outcomes Scale (GOS) scores (46% better chance of a good outcome) when compared to scores for normothermic controls (BTF, 2007). Target temperatures with best outcomes: 32-33°C and 33-35°C. Patients with TBI often require sedation for agitation, restlessness, mechanical ventilation, or pain (Bourg, 2007) to decrease metabolic requirements, decrease ICP, facilitate effective ventilations, and provide comfort. IV narcotics (morphine, fentanyl), benzodiazepines, e.g., lorazepam (Ativan) or midazolam (Versed), or short-acting anesthetic agents (propofol) can facilitate management of patients who are agitated, thus helping to keep their ICPs down. Benzodiazepines minimally affect ICP, cerebral oxygen demand or cerebral blood flow (Bourg, 2007). Propofol can markedly reduce BP and may not be the best choice until hemodynamic stability is assured to prevent a drop in CPP. Sedation does not provide pain management. Need to treat both if necessary.

d. 3.

Sedation & pain management
a.

b.

State of Illinois TNS Program Head Trauma - page 35
c.

Barbiturates induce an anesthesia-like state to provide cerebral protection if ICP cannot be reduced. High dose barbiturate therapy may be considered in hemodynamically stable salvageable severe head injury patients with increased ICP refractory to maximal medical and surgical ICP lowering therapy (Origitano, 1996). Barbs may also be beneficial for near drowning but are contraindicated in hypotensive patients (ATLS, 2005). Attempt to rule out other causes of agitation including hypoxia or electrolyte imbalance. Use extreme caution in monitoring ventilatory status.

d.

Neuromuscular blockade may be employed when sedation alone proves inadequate and short-acting agents should be used when possible (BTF, 1995). Unfortunately, pharmacologic relaxation has the undesirable effect of limiting the neurologic examination to the pupils and CT scan. Therefore, its use in the absence of evidence of herniation should be limited to situations where sedation alone is not sufficient to optimize safe and efficient patient transport and resuscitation. Maintain patient's head and neck in neutral alignment to facilitate venous drainage. Assess airway securing and spine motion restriction devices for JV constriction.

4.

Maintain venous outflow from cranium
a. b.

5. 6. 7.

Reduce environmental stimuli: Dim lights and decrease noise as much as possible Evaluate patient's response to pain and consider need for analgesics. Avoid increased intrathoracic or intra-abdominal pressure
a. b. c. d.

Minimize time in Trendelenburg position during central line placement. Attempt to prevent the elicitation of a Valsalva maneuver, cough, gag, vomiting or sneezing. Avoid hip flexion and isometric muscular activity. Minimize activities that stimulate posturing. Beware of sudden decreases in BP - notify physician immediately. Titrate medications slowly. Space nursing procedures that ↑ ICP such as suctioning. Limit environmental stimuli as indicated.

8.

Avoid rapid and wide fluctuations in BP
a. b. c. d.

G.

Anticonvulsant medications
1.

In the acute period, seizures may precipitate adverse events in the injured brain due to elevations in intracranial pressure, BP changes, changes in oxygen delivery, and also excess neurotransmitter release (BTF, 1995). Give only to prevent early post-traumatic seizures in high risk patients
a. b. c. d. e. f. g. h.

2.

GCS < 10 Cortical contusion Depressed skull fracture Subdural hematoma Epidural hematoma Intracerebral hematoma Penetrating head wound Seizure within 24 hours of injury

State of Illinois TNS Program Head Trauma - page 36
3.

Ativan (lorazepam) 0.1 mg/kg or Versed (midazolam). Versed can be given intranasally using a mucosal atomizer device (MAD) at 0.2 mg/kg up to 1 mL/nostril or 10 mg total single dose. Fosphenytoin (Cerebyx) 10-20 mg PE (phenytoin sodium equivalents)/kg IVPB not faster than 150 PE/min. If patient is in status, the loading dose of fosphenytoin is 15-20 mg PE/kg infused at 100-150 mg PE/min. Side effects of fosphenytoin: nystagmus, pruritus, paresthesia, dizziness, somnolence, ataxia, tinnitus, nausea, vomiting, and headache. Incidence and severity of side effects are dose and rate dependent. After termination of initial seizure activity, Dilantin (phenytoin) can be used to prevent further tonic-clonic and temporal lobe seizures. Dose: No more than 50 mg per min IVP through a filter up to 18 mg/kg. Monitor ECG during infusion (Bourg, 2007). Prophylactic use of fosphenytoin, carbamazepine, or phenobarbital is not recommended for preventing late (occurring after 7 days following injury) posttraumatic seizures.

4.

5.

6.

H. I.

Narcotic antagonists if suspected overdose: Naloxone 0.4 to 2 mg IVP Infection prophylaxis (BTF, 2007)
1. 2.

Level I: There are insufficient data to support a Level I recommendation for this topic. Level II: Periprocedural antibiotics for intubation should be administered to reduce the incidence of pneumonia. However, it does not change length of stay or mortality. Early tracheostomy should be performed to reduce mechanical ventilation days. However, it does not alter mortality or the rate of nosocomial pneumonia. Level III: Routine ventricular catheter exchange or prophylactic antibiotic use for ventricular catheter placement is not recommended to reduce infection. Risks of infection and aspects of care
a.

3. 4.

As many as 70% of mechanically ventilated patients can develop pneumonia and ICP monitor infection rates can be as high as 27% (BTF, 2007). Risk of infection is affected by the duration of external ventricular drainage, use of prophylactic parenteral antibiotics, presence of concurrent other systemic infections, presence of intraventricular or subarachnoid hemorrhage, open skull fracture, including basilar skull fractures with CSF leak leakage around the ventriculostomy catheter, and flushing of the ventriculostomy tubing (BTF, 2007). Ventriculostomies and other ICP monitors should be placed under sterile conditions to closed drainage systems, minimizing manipulation and flushing. There is no support for routine catheter exchanges as a means of preventing CSF infections. There is also no support for use of prolonged antibiotics for systemic prophylaxis in intubated TBI patients, given the risk of selecting for resistant organisms. Early tracheostomy or Extubation in severe TBI patients have not been sown to alter the rates of pneumonia, but may reduce the duration of mechanical ventilation (BTF, 2007). If suspected basilar skull fracture, prophylactic administration of Pneumovax is sometimes recommended.

b.

c.

d. J.

Deep vein thrombosis (DVT) prophylaxis (BTF, 2007)
1.

Level I: There are insufficient data to support a Level I recommendation for this topic.

State of Illinois TNS Program Head Trauma - page 37
2. 3.

Level II: There are insufficient data to support a recommendation for this topic. Level III:
a.

Graduated compression stockings or intermittent pneumatic compression (IPC) stockings are recommended, unless lower extremity injuries prevent their use. Use should be continued until patients are ambulatory. Low molecular weight heparin (LMWH) or low dose unfractionated heparin should be used in combination with mechanical prophylaxis. However, there is an increased risk for expansion of intracranial hemorrhage. There is insufficient evidence to support recommendations regarding the preferred agent, dose, or timing of pharmacologic prophylaxis for DVT.

b.

c. 4. 5. 6. 7.

In the absence of prophylaxis, patients with severe TBI are at high risk for developing DVT with embolic events. Methods used for detection: clinical evidence; or Duplex scanning, venography, radiolabeled fibrinogen scans in asymptomatic patients. Treatment in neurosurgical patients is complicated by the uncertainty of the safety of anticoagulant therapy (BTF, 2007).Prevention is critical. Mechanical agents: Graduated compression stockings, intermittent pneumatic compression stockings. Do not increase BP, ICP or CVP. Lower extremity injuries may limit their use or application may limit ambulation and physical therapy. Pharmacological agents
a. b. c.

8.

Low-dose heparin Low-molecular weight heparin Risks associated with both include intracranial and systemic bleeding that may lead to morbidity and death.

K. L. M.

The use of glucocorticoids is not recommended for improving outcome or reducing intracranial pressure in patients with severe head injury (BTF, 1995) Impaired verbal communication: Create alternative methods to communicate for those who need intubation and are awake Alteration in thermoregulation
1. 2. 3. 4.

Adjust room temperature as needed Adjust patient covering as needed Monitor for fluctuations in temp and alert physician if either occurs Administer hypothalamic depressants as ordered Prepare patient for craniotomy if they have an extracererbral hematoma > 1 cm thickness. Neurosurgeon will consider acute removal of intracerebral hematomas causing substantial mass effect. Unstable comatose patients who are taken to surgery for thoracic or abdominal injury may be candidates for diagnostic bur holes or insertion of ICP monitoring if there is a significant scalp injury or signs of herniation. Temporal Bur Hole: Only to be used in situations where immediate neurosurgical care is not available by a surgeon properly trained in the procedure. Indications: hemiplegia, dilated pupil; 85% dilate on side of mass; 15% dilate contralateral to mass (Kernohan's Phenomenon). Need to remember that 1) most head injured patients do not have hematomas, 2) a burr hole may fail to locate the hematoma, 3) only a small portion of the hematoma can be evacuated through a burr hole, 4) the procedure may produce brain damage, 5) the procedure may not be life-saving, and 6) the time involved in performing the procedure may equal the time to get the

N.

Surgical management: Operative considerations
1.

2.

3.

State of Illinois TNS Program Head Trauma - page 38 patient to a neurosurgeon (ATLS, 2005). Should only be done with the advice and consent of a neurosurgeon.
4.

In extreme cases of cerebral edema, surgeons may remove a portion of the skull to allow for brain swelling to prevent herniation and death. Patients may be fitted with a protective helmet until the skull defect can be reconstructed or repaired.

X.

Lab profiles
A. B.

C. D. E. F. G. H. I. J. K.

H&H or CBC Glucose (injured brain is hypermetabolic and glucose intolerant; levels increase in intracranial hemorrhage and decrease in secondary ischemia. If glucose > 200 = poor outcome) Serum lactate Electrolytes Drug/tox screen ABG, SpO2, AVdO2, SjO2. Creatinine, blood urea nitrogen (BUN) International normalized ratio (INR) Prothrombin time (PT) and partial thromboplastin time (PTT) Urine electrolytes, urea and glycerol q. 6 hours. Monitor Na levels for SIADH. Serum osmolarity: diagnoses injury to hypothalamus which may result in diabetes insipidus as indicated by serum osmolarity > 295 mOsm/kg, or syndrome of inappropriate ADH secretion (SIADH) with serum osmolarity less than 280 mOsm/kg. A normal PE, normal CT, and a normal MRI DO NOT mean a normal patient X-Rays: Lateral C-Spine must show all 7 cervical vertebrae to presumptively clear neck for emergency procedures. Need AP, bilateral obliques and open-mouth odontoid views ASAP when patient is stabilized and all emergency procedures are completed; portable chest if prepping for OR. Skull films are not needed if CT is planned. Note: Pencil lead doesn't show up on X-ray. C-T scan: Probably the most important diagnostic tool in the emergent treatment period. Shows neurons or gray matter (not axons), hematomas, contusions, fluid-filled ventricles, mass lesions of localized injury, and associated bony structures. They do not detect diffuse injury. ICP cannot be reliably predicted by CT alone.
1.

XI.

Neuro diagnostic radiography
A. B.

C.

High-yield criteria for identifying adult patients at risk for significant intracranial injuries after blunt head trauma (defined as any injury that led to neurosurgical intervention, rapid clinical deterioration, or had the potential for long-term neurologic impairment) and need for CT– BEAN BASH (Mower et al, 2005):
a. b. c. d. e. f. g. h.

B Behavior abnormal E Emesis intractable A Age > 65 N Neurological deficit B Bleeding disorder A Altered mental status S Skull fracture H Hematoma scalp Loss of consciousness > 5 minutes Combativeness Facial injury Penetrating skull injury Acute pupillary inequality Skull films reveal IC air or shift of the pineal gland from midline

2.

Other criteria that suggest the need for CT
a. b. c. d. e. f.

State of Illinois TNS Program Head Trauma - page 39
g. h. i. 3.

Alcohol or other drug intoxication is a confounding factor Anticoagulant use Amnesia, particularly antegrade

A meta-analysis done by the World Health Organization Centre Task Force (Borg et al, 2004) studied the diagnostic tools available to detect mild brain injury and found that CT could reveal unsuspected lesions in patients with MBI. Only 8% of those with GCS scores of 15 had an abnormal CT, but 30% of patients with a GCS of 13 had abnormal CT results. NO CONTRAST in most cases. If basal cistern is absent anticipate 88% mortality in 24 hours Need iron in blood to see it on CT. There are some isodense subdurals. If there is anemia from trauma with a ↓ Hct, won't see the clot on CT.

4. 5. D.

Air ventriculography: If CT not possible due to multiple injuries and need for immediate operative intervention, the neurosurgeon may perform a ventriculostomy while other surgeons stabilize the patient (ATLS, 1997). Ten ml of CSF are drained and replaced with air. A portable AP skull film is taken to look for the presence of midline shift. Shift indicates a possible mass lesion requiring immediate evacuation. Rarely used. MRI/MRA: Forty-one percent of TBI patients with a normal CT will have an abnormal MRI. Increased sensitivity reveals small or subtle lesions. More useful in subacute and chronic phases of head injury. More time consuming than other imaging studies. Magnetic field may make it incompatible with monitoring and resuscitative equipment; access to patient limited during study. SPEC scan: Single Photon Emission Scan: measures metabolism of the brain. They can see if the brain is "idling" and try to determine if it is a biochemical or electrical event. PET scan Cerebral angiography: used if CT unavailable and vascular injury is suspected. Transfemoral approach preferred. Other studies
1. 2. 3. 4.

E.

F. G. H. I.

Lumbar puncture EEG Evoked potentials; visual, brain stem auditory, and somatosensory Xenon blood flow studies

XII.

Ongoing patient monitoring
A. B. C. D. E. F.

A patient is considered in coma until they can obey commands and localize pain. VS as ordered. Mentation, orientation, responses and GCS Neuro signs including pupils, motor strength and sensory response to stimuli Report any change from previous assessments A patient is deteriorating if:
1. 2. 3.

GCS drops by 2-3 points; there is a unilateral pupil change; or there is lateralized extremity weakness.

XIII.

Sequelae of head trauma
A.

Glasgow Outcome Scale 1. Good recovery 2. Moderate disability 3. Severe disability: never return to work 4. Persistent vegetative state (very costly care) - awake but unaware 5. Death

State of Illinois TNS Program Head Trauma - page 40
B. C. D.

Mild head injury: May have prolonged problems with memory, dizziness, headaches, attention deficits and other CNS dysfunctions. Initial GCS 13-15 = 4% morbidity. Moderate and severe injuries may have significant cognitive deficits requiring an aggressive approach to PT, occupational and speech therapy. Poor outcomes can be anticipated in the presence of 1. hypoxia; 2. shock (hypotension) with ↑ ICP; 3. hypercarbia; 4. hyper (Michaud et al, 1991) or hypoglycemia; 5. hypercalcemia; 6. hypermagnesemia; 7. drop in cerebral blood flow; 8. CPP < 50 and ischemic brain injury; 9. 40% mass lesions; 10. GCS that drops 2-3 points; 11. pupil asymmetry; and/or 12. unilateral extremity weakness and drift leg lag. MPX Scores (Mamelak et al, 1996) 1. Age, best motor score and pupillary reactivity at admission and 24 hours are significant predictors of outcome 2. Extraocular motility predictive at 24 hours only 3. Age most important independent predictor with an inverse relationship between age and survival. There is an approximate 10% decrease in survival each decade after the 20's. 4. 24 hour MPX data is generally a better predictor of six-month outcomes and more specific in predicting negative outcomes than admission findings. Rehabilitation: Comprehensive neuropsychological rehabilitation involves combination therapies for persons with cognitive, emotional, interpersonal and motivational deficits associated with TBI and is beneficial for symptom management, community reintegration, and return to work.

E.

F.

XIV.

Specific traumatic brain injuries (TBI)
A.

Morphology of injury (ATLS, 1997)
1. 2.

Skull fractures: Involve the cranial vault or basilar skull bones. Classified as linear, stellate, open/closed; vertex/basilar Intracranial lesions
a.

Focal injuries: Specific, grossly observable lesions, e.g., structural or expanding mass lesions with local brain damage. Brain shifting causes coma from brain stem compression. Twenty seven to 60% of patients with severe head injury (unable to speak or follow commands) have focal injury (mass lesions) requiring operative intervention (Wagner, 1996). They cause 50% of all admits and 66% of all deaths. Produced by contact or non-movement forces and/or accelerationdeceleration forces.

b.

Diffuse injuries: There is no macroscopic brain injury that can be seen on skull film or CT scan. There is wide-spread microscopic disruption of both structure and function due to shearing, stretching, or tearing forces applied to nerve fibers. Coma is due to direct damage of brainstem or cortex, but no brainstem compression. Examples are cerebral concussions and diffuse axonal injuries.

State of Illinois TNS Program Head Trauma - page 41
B.

Extracranial scalp injuries: There are five layers to the scalp and it is well vascularized. The blood vessels do not constrict as well as in other areas of the body, so are at risk for bleeding profusely when injured. Common injuries:
1.

Lacerations: Due to blunt trauma that can tear skin and underlying connective tissue causing it to separate. This can leave elevated borders surrounding a depression that mimics a depressed skull fracture (Bledsoe, 2006). Incisions: Smooth wound margins as if cut with a knife Hematomas: Closed injury causing blood to accumulate within the layers of the scalp. May bleed enough over a depressed skull fracture to fill the depression and conceal the injury. Abrasions, contusion, burns Avulsions: Scalp tissue is only loosely attached to the skull. Shearing forces may tear a flap of tissue, exposing a portion of the skull. This can create serious contamination and bleeding. A scalp hematoma or laceration may suggest deeper injury beneath. Always have a high index of suspicion for skull fracture. Danger: blood loss that can put the patient into shock. Must be controlled as soon as possible.

2. 3.

4. 5.

6.

C.

Skull fractures
1.

Epidemiology
a. b.

There are approximately 111,000 skull fractures/year in the U.S. The frontal and occipital are the thickest bones. The temporal bone is the thinnest; 50% of fractures occur here. Keystones of the skull base are the sphenoid bones and petrous processes of the parietal bone, which bear lateral forces when the head is hit. They, and the cribriform plate, are often the bones that are injured in a basilar skull fracture. Only 5% of people who hit their heads sustain a skull fracture, but 20% of patients with skull fractures had a major head injury. Skull fractures make the brain more susceptible to trauma. A compound fracture with neuro impairment > 4 hours has a 25 times greater chance of deterioration. Skull fracture with obtundation = major head injury. 25% will develop a surgically significant lesion. Little growth of new skull bone occurs after two years of age and places patients at risk for post-injury infections. They must have all openings covered with sterile dressings followed later by split thickness grafts.

c.

d.

e.

2.

Vertex fractures
a.

Linear
(1)

Definition: An inbending of the skull at the point of injury with simultaneous outbending around the region of impact which dissects both tables of bone causing a crack. Etiology: Low-velocity, blunt or compression trauma Incidence: 80% of all skull fractures. Occur most frequently in children and elderly. Pathogenesis: 50% involve temporal and parietal bones Morbidity/mortality
(a) (b)

(2) (3) (4) (5)

Most are essentially benign A diastatic (sprung suture) is the biggest predictor of who will deteriorate from a linear fracture

State of Illinois TNS Program Head Trauma - page 42
(c) (6) (7) (8)

A fracture over the temporal/parietal bones should cause suspicion for an epidural hematoma

Clinical presentation: External soft tissue trauma, subgaleal hematoma, and pain Diagnostic radiography: standard skull film or CT Emergency intervention: Usually requires no treatment. If fracture extends into orbit, paranasal sinus or crosses a major vascular channel, admit to observe. Fracture line usually disappears in 6 months (children) and 3-4 years in adults. Definition: Skull fractures into multiple fragments that may penetrate the meninges and damage structures beneath Etiology: Moderate-velocity blunt or compression trauma Definition: Combination of a depressed skull fracture and a scalp laceration. The dura may be torn. Pathogenesis (a) Blunt and/or penetrating trauma (b) AK 47 with Teflon bullet produces 2100 lbs/in2 of force that explodes the inside of the head Morbidity/mortality: High Clinical presentation: Depends on site Diagnostic radiography: Standard skull films; CT Emergency intervention: OR Definition: Fracture with inward displacement of a bony segment Etiology: High velocity contact over a small surface area results in compression trauma Pathogenesis: Results from direct applied forces. Frequently seen in MVCs and violence. Ex: Hammer creates 1600 lb/in2. Classifications
(a) (b) (c)

b.

Stellate/comminuted
(1) (2)

c.

Open: See penetrating injuries
(1) (2)

(3) (4) (5) (6) d.

Depressed
(1) (2) (3) (4)

Closed with scalp intact Compound with scalp open but dura intact Complex with scalp and dura lacerated by bone fragments = cortical laceration and hemorrhage

(5) (6)

Morbidity/mortality: Causes intracranial damage like contusion and laceration; infections and seizures Clinical presentation: Can usually see or feel depression unless covered by a scalp hematoma. May present with focal brain injuries. Diagnostic radiography: standard skull films, CT Emergency intervention: If open, greater than 1 cm depressed, or associated with neurological deficit: surgical debridement, evacuation of clots and bone fragments, and elevation of depressed bone and repair of lacerated dura. Prophylactic anticonvulsants and antibiotics.

(7) (8)

State of Illinois TNS Program Head Trauma - page 43
e.

Growing fracture
(1) (2)

Unique to pediatric population Brain under 5 torr pressure; will pulsate through linear fracture

3.

Basilar skull fractures
a. b.

Definition: A fracture that involves the base of the skull Location: Anterior, middle or posterior fossa bones, cribriform plate, sphenoid wings, and/or petrous bones. This area is rough and ridged and has many foramina (openings) for the spinal cord (foramen magnum), cranial nerves, ear (auditory canal), and blood vessels. It forms the roof of the orbits and nasal sinuses. These spaces weaken the skull and make it vulnerable to fracture. Pathogenesis: Caused by blunt trauma to the head, especially to the mandible, or when the vertebral column is driven against the occipital condyles, e.g., fall on the buttocks. Morbidity/mortality: Risk for meningitis/encephalitis or a cerebral abscess. Clinical presentation: Varies by location. However, if the patient has been supine and develops a headache when they sit up, suspect basilar skull fracture.
(1)

c.

d. e.

Anterior fossa (Cribriform plate, fovea ethmoidalish, sphenoid sinus)
(a)

Telecanthus - Medial eyelids spread out towards ear causing the bridge of the nose to appear widened and flattened. This is the first sign EMS personnel are likely to see. CSF Rhinorrhea: 25% of these injuries tear the dura and arachnoid, allowing CSF to leak out through the fracture site into the nasal cavity. Because CSF is high in sodium (159 mEq in CSF compared to 142 in blood), patients may c/o a salty taste in the back of their mouth. Epistaxis Raccoon eyes: Classic triangular bruising of the lower eye lids. Appears later. May be associated with facial fractures and bleeding into the orbit causing subconjunctival hemorrhages of lateral sclera giving it a blood red appearance w/o evidence of direct trauma (ocular Battle Sign). Anosmia: CN I (Olfactory nerve) deficit. One third of patients with an anterior basilar skull fracture will permanently lose their ability to smell, and therefore the ability to "taste" most foods. Visual field deficits: CN II (Optic) Pneumocephalus Sinus air-fluid levels CSF otorrhea: Glucose oxide reaction to glucose test tape or check for B2 transferin Hemotympanum or ear drum perforation

(b)

(c) (d) (e)

(f)

(g) (h) (i) (2)

Clinical presentation: Middle fossa also involves middle ear
(a) (b)

State of Illinois TNS Program Head Trauma - page 44
(c) (d) (e)

Conductive hearing deficit: (Vestibulocochlear) involvement Dizziness; look for nystagmus

8th

nerve

Facial weakness/paralysis on the affected side: Facial nerve (CN VII) runs right next to CN VIII as they exit through the base of the skull to surface structures. They are often both injured in a middle fossa fracture. Battle sign: Mastoid ecchymosis that presents 24-36 hrs after injury

(f) f. g.

Diagnostic radiography: May not see on skull films Emergency interventions
(1) (2) (3)

Semi-Fowler's position. Avoid nose blowing, straining, and sneezing. Avoid iatrogenic contamination. Usual cause for persistent bleeding from ear is canal laceration CSF leak may be helping to blunt a rise in ICP and limit brain damage. Do not try to stop it. Place nothing in the nose or ear. Collect drainage from nose on a rolled 4 X 4 (moustache dressing) taped over the upper lip. Place a loose dressing over the ear to collect drainage. If mixed with blood, look for the characteristic "halo" sign as blood cells are heavier and will stay in the middle while CSF wicks out to the perimeter causing a larger strawcolored ring. This sign is most reliable if fluid is leaking from the ear (Bledsoe, 2006). Don't always start on prophylactic antibiotics. Eighty percent of CSF leaks self-seal. If it persists longer than 7-14 days, may need dura repair. Starting to see prophylaxis with Pneumovax.

(4)

D.

Focal intracranial injuries Anatomy review: All central nervous system tissue is surrounded by three layers of meninges: dura (outer layer attached to the inner table of skull bone and inner layer folding to surrounding all CNS structures); arachnoid; and pia (attached to brain surface). There are potential spaces between these layers into which bleeding may occur, creating a hematoma or hemorrhage.
1.

Epidural hematomas
a. b. c.

Definition/incidence: Blood clot between skull and dura that doesn't involve the brain. Etiology: Falls, direct blows to the head, MVC, sports injuries Pathogenesis: Classically, epidurals are associated with a linear fracture in the temporal area that can tear the middle meningeal artery (which is encased in a groove o the skull bone after the age of 3). They can occur in other sites due to brisk oozing of blood from diploic vessels (those contained in the spongy middle layer of skull bone) injured by skull fractures. They may be venous in origin if fracture crosses a dural sinus (usually under a skull suture line). The arterial bleeding must "peel" the dura away from the inner table of skull in order to form the hematoma. This creates a contained clot. However, there is no room for extra bleeding inside the skull, so intracranial pressure rises rapidly. The clot will compress cerebral structures (shutting them down) and may eventually shift the brain onto midline structures (brainstem and cranial nerves).

State of Illinois TNS Program Head Trauma - page 45
d.

Morbidity/mortality data: Five to 28% overall mortality. Mortality of 3-4% if caught before coma. Needs to get to OR before coma evolves, otherwise mortality starts doubling. Peds considerations: Clots not common in children but they experience epidurals more frequently than subdurals except in infant child abuse. Intracranial blood loss may precipitate shock in young children < 3 years. More common bilaterally in children. May tend to watch longer before operative intervention.

e.

f.

Clinical presentation: Depends on the source and rapidity of bleeding
(1) (2) (3) (4) (5) (6) (7)

Palpate temple for boggy hematoma indicating trauma to the vessels that spread out to the temporalis muscle. Unequal pupils: Ipsilateral (same side) dilated pupil that becomes fixed due to pressure on CN III. Change in consciousness: GCS drops by 2-3 points. May have a lucid interval (9%-33%). Headache of increasing severity Possible seizures, vomiting Localized contralateral extremity weakness. Very important sign. Look for pronator drift. Beware posterior fossa epidural hematoma
(a) (b) (c) (d) (e) (f) (g) (h)

Occipital skull fracture Cranial nerve dysfunction Cerebellar signs Abnormal extraocular movements Motor dysfunction Nausea/vomiting ↓ VS and respiratory arrest May be delayed in appearance

g. h. 2.

Diagnostic radiography: Looks like a lens or is C-shaped on CT. Brain is 70% water, cannot be compressed so shift compresses ventricles. Emergency interventions: Surgical evacuation if S&S of brain shift. Don't operate on all, may resolve in a couple of days if small. Definition/incidence: Blood accumulation in the potential space between the dura and arachnoid meningeal layers. Incidence: 17-29% of head injuries. Most common traumatic mass lesion (51%-68%). Three times more common than an epidural with the worst prognosis. Two times more common in adults than children due to increased violence. Etiology: MVCs, falls, assaults, industrial and sports injuries. Occur from frontal or occipital impacts more often than from lateral impact. Populations at risk: Elderly, alcoholics, and infants as their brains are chronically dehydrated, smaller due to degeneration of cortical tissue, or smaller due to immature development. This places tension on the veins that bridge the cerebral cortex with the dural sinuses (venous outflow tracts) attached to the skull and makes them vulnerable to injury. Pathogenesis
(1)

Acute subdural hematomas
a.

b. c.

d.

Classified as acute (within 48 hrs), subacute (2-14 days), and chronic (>14 days) depending on symptoms onset after injury

State of Illinois TNS Program Head Trauma - page 46
(2) (3) (4) (5) e.

Bridging veins which traverse the space between the cerebral cortex and venous sinuses shear and tear. Rare arterial cause. Beneath the clot, the cortex may be damaged by contusion, ruptured veins and arteries Bilateral in 8%-21% of cases If less than 72 hours old, may be liquid or clotted blood

Morbidity/mortality: 28%-73% die as clot is under dura and almost directly against brain. Represents 33%-75% of mass lesion mortality.
(1)

Attributed to primary brain damage underlying the clot, vascular injury, hyperemic response leading to increased intracranial volume, ipsilateral hemispheric or total brain swelling, and ↑ ICP. Factors predictive of functional recovery
(a) (b) (c) (d)

(2)

Evaluation within 4 hours of injury Post-op ICP < 20 mmHg Normal post-op evoked potentials GCS > 5

f.

Clinical presentation
(1)

Acute: Headache, drowsiness, agitation, slow cerebration, confusion. If brain is shifting: ipsilateral dilated and fixed pupil, contralateral hemiparesis. Lucid interval in 13%. Subacute: Similar to acute with failure to regain consciousness Chronic: Headache that progresses in severity, slow cerebration, confusion, drowsiness, giddiness, possible seizure, papilledema, and contralateral hemiparesis. Hematoma may reaccumulate or calcify.

(2) (3)

g. h.

Diagnostic radiography: Looks like a smudge covering the brain surface on CT Emergency interventions: Surgical evacuation of clot if 3 mm or more thick, hemorrhage control, or need for resection of the contused, nonviable brain. Definition: Blood in the subarachnoid space Pathogenesis: Most common cause is trauma. Traumatic SAH is usually diffuse, does not form a definite hematoma and does not create a mass effect. Bleeding occurs from superficial cortical vessels, an AV malformation, or leaking congenital intracranial aneurysm and is often associated with subdural hematoma. Causes swelling around the brain stem (not good). Twelve percent of females and 7% of males have unsuspected cerebral aneurysms. Morbidity/mortality data: If system is filled with blood, outcome is poor Clinical presentation
(1)

3.

Subarachnoid hemorrhage (SAH)
a. b.

c. d.

(2) (3)

Severe headache – Intense pain (worst headache of their life) becoming occipital, aggravated by any movement worse lying down. Can mimic migraine and tension headaches. A majority of non-traumatic SAH patients have a premonitory leak and headache days to weeks before major rupture with neuro damage. Optic fundi have pre-retinal hemorrhages; visual disturbances Ipsilateral dilated pupil

State of Illinois TNS Program Head Trauma - page 47
(4) (5) (6) (7) e.

Meningeal irritation signs: nuchal rigidity requires 12-24 hours to develop and is not a reliable early sign Deterioration of mental status Hemiparesis; R/O c-spine injury Seizures

Diagnostic radiography: CT; arteriography. CT changes may not appear for up to 4 hours (longer with a minimal bleed). Appear as high-density fluid collections within the cerebrospinal fluid spaces. Emergency interventions
(1) (2) (3) (4)

f.

Blood in CSF causes intense vasoconstriction leading to extensive infarction - therefore no hyperventilation ICP monitoring may be indicated If CT scan is negative, but clinical suspicion is strong physician will do an LP Surgical evacuation, nimodipine (60 mg q. 4 hours PO or per NG tube) for vasospasm, and standard treatment for cerebral edema

g. 4.

Complications: Extensive SAH puts patient at risk for communicating hydrocephalus Definition: A deep contusion or tear in blood vessels that result in hemorrhage in the brain parenchyma Pathogenesis: Single or multiple hemorrhages may occur from blows to the skull, rotational acceleration, missile-type injuries, and coup-contrecoup lesions. Sixty percent are associated with skull fractures, especially depressed fractures, and 60% appear under contusions. The majority (85%) are located in the frontal and anterior temporal lobes at the anterior base of the brain. They may take some time to develop. Sudden deceleration or head rotation causes these regions to impact the rough surface of the basilar skull. Morbidity/mortality: Depends on size. Mortality 65% if at a point around a contusion or complicated by progressive focal edema and mass effect. Majority of deterioration occurs within first 48-72 hours. Delayed hemorrhage is a risk. Clinical presentation: Similar to contusions; depends on location. Will often share S&S of a stroke. (1) Headache (2) Deteriorating consciousness to deep coma (3) Contralateral hemiplegia (4) Ipsilateral dilated pupil (5) Speech deficits Diagnostic radiography
(1) (2)

Intracerebral hemorrhage
a. b.

c.

d.

e.

CT can determine the volume of blood. If≥ 35-40 cc or if they are located in the posterior temporal lobe → OR Cerebral arteriography Size > 30 ml, temporoparietal clot, or

f. 5.

Surgical indications: coup/contrecoup lesion

Cerebral contusions
a.

Definition: Actual bruising of, or cortical bleeding into, cortical tissue, generally without puncture of the pial covering. Classified as coup (found at

State of Illinois TNS Program Head Trauma - page 48 the site of impact), contrecoup (in a line directly opposite the point of impact which is the worse of the two impacts), gliding, and petechial. May involve laceration of vessels and brain tissue with tissue necrosis, pulping and infarction. With most contusions, there is any area of brain cells that are destroyed and will not regenerate. But the surrounding tissue (penumbra) that is being affected by the swelling can be saved with appropriate management.
b.

Pathogenesis: Temporal and frontal lobes are the primary sites of coup lesions. The frontal lobes bang on the frontal bone. Temporal lobes hit the middle cranial fossa (sphenoid wings) and start to bruise and swell. After the initial impact, the brain "sloshes" backward, again impacting the internal skull structures. If hit on the forehead, the contrecoup lesion is often in the occipital lobes producing visual disturbances (seeing stars). Often multiple and occur in combination with other lesions. The blood-brain barrier in the area of the contusion may lose its integrity, which can lead to the development of an intracerebral hematoma. Contusions and hematomas that are initially small may increase in size causing rapid worsening of a previously stable patient's condition.

c. d.

Morbidity: Worsens with ICP ≥ 20-25 mmHg. Goal: ICP ≤ 10 mm Hg. Significant due to associated hemorrhage, edema, and brain swelling. Clinical presentation: Depends on involved structures but often presents with localizing personality, behavior, motor, speech. memory, or visual deficits. Temporal lobe contusions especially severe due to close proximity of the midbrain. Diagnostic radiography: CT Emergency interventions: Monitor patient with small lesion (<5-7 mm of brain shift on CT) for ↑ ICP. Extensive contusion with hemorrhage and mass effect require surgery. Definition: Open head injuries due to a projectile Pathogenesis
(1)

e. f.

6.

Impalement/penetrating injuries
a. b.

Bullets and other projectiles destroy a path of brain tissue along their trajectory (primary injury). Trauma to cerebral vessels may cause large hematomas. Bone fragments, imploded debris, and the breach in cranial integrity may result in the development of infections and cerebral abscesses. Large fragments that lodge in the ventricles or on the brain surface may migrate with catastrophic results. High velocity injuries: Large shock waves and zones of negative pressure result in significant cavitation. Swelling of adjacent tissue may result in fatal ↑ICP.

(2)

c. d. e.

Morbidity/mortality: High (50%) due to structural damage, massive brain swelling and uncontrolled ↑ ICP Clinical presentation: Depends on sites of injury Impaled objects: Patient presentation depends on the structures involved. Some patients are awake and aware with rather large objects impaled into their skull. Do not move or remove. Diagnostic radiography: skull film, CT

f.

State of Illinois TNS Program Head Trauma - page 49
g. 7.

Emergency interventions: Stabilize impaled objects in place pending removal in OR. Prophylactic antibiotics; anticonvulsants may be ordered. Definition: Bleeding into the midbrain, pons, or medulla Pathogenesis
(1) (2)

Brain stem hemorrhage
a. b.

Primary: Direct impact or torsion injuries of the brain stem Secondary: Compression from ↑ ICP, cerebral edema, or laceration of temporal lobes Midbrain: Deep coma, midpoint fixed pupils, ophthalmoplegia, abnormal extension response to pain Pons: Coma, pin-point pupils, extension response to pain ophthalmoplegia, abnormal

c.

Clinical presentation
(1) (2) (3)

Medulla: Pupils bilaterally dilated and fixed; death

d. e. E.

Morbidity/mortality: Almost 100% if comatose Diagnostic radiography: CT; MRI

Diffuse injuries: 50% of all admits; 1/3 of all TBI deaths
1.

Concussion
a. b.

Incidence: 2-4 million/yr - most common head injury Definition: Traumatic, microscopic damage to cells deep in the white matter of the brain causes reversible physiologic disturbance of neurological function that occurs at the instant of trauma. Pathogenesis
(1)

c.

Linear motion of the brain "stuns" the affected cells and puts them on "idle". While in this state, the cells are not dead, but they do not function as they should. Traumatic forces cause transient ischemia, neural depolarization following sudden acetylcholine release, or microscopic axonal disruption of fibers in upper brain stem (ascending reticular activating system) and temporal lobe producing the classic S&S. Patients don't have to hit their head or lose consciousness They may report seeing stars or flashes of light. (Note: seeing stars is K related. Linear motion causes K to run out of cells and short circuits the occipital lobe.) Most neurons stain blue. Neurons in temporal lobe following a concussion stain red from damage.

(2)

(3) (4)

(5) d.

Clinical presentations
(1)

Grade I
(a) (b) (c)

Short-lived confusion No loss of consciousness Post-traumatic amnesia less than 30 minutes

(2)

Grade II (a) Loss of consciousness less than 5 minutes (b) Post-traumatic amnesia greater than 30 minutes (c) Retrograde amnesia 5-10 minutes after impact

State of Illinois TNS Program Head Trauma - page 50
(3)

Grade III (a) Loss of consciousness greater than 5 minutes but < 6 hours (b) Post-traumatic amnesia greater than 24 hours (c) Retrograde amnesia Emotional lability; may be crying and weeping May be associated with more severe structural lesions, most common is cerebral contusion. Alert; no initial loss of consciousness Minutes to hours later, child becomes sleepy, somnolent, irritable, pale, tachycardic and clammy Vomits then shows rapid improvement in 24 hours Between 20% and 80% of people with mild head injury continue to experience S&S six months after the injury (de Kruijk et al, 2002). Concussions are cumulative. Memory cells in temporal lobe are most subject to damage. Repetitive concussions will cause recent memory loss. The American Psychological Association defines PCS as quantifiable deficits in memory or attention and the onset or worsening of any three of the following symptoms: tiring easily, disordered sleep, headaches, vertigo/dizziness, irritability, anxiety/depression/affective lability, changes in personality, or apathy. Neuropsychological deficits detectable after resolution of neuro symptoms . Recovery may take 6-12 mos. Patients may also have problems with sunlight, coffee, nervousness, irritability, negative energy syndrome, difficulty with abstract thinking and judgment, loss of inhibition and libido, and avoidance of crowds. Preinjury factors (age, education, emotional adjustment) and postinjury factors (pain, family support, stress) interact with cognitive functioning and significantly affect recovery from TBI (McCauley et al, 2001). Reorient patient to time and place Analgesia for headache Prophylactic anticonvulsants controversial - not generally used

(4) (5) e.

Post concussive syndrome in peds patients - observe carefully
(1) (2) (3)

f.

Post concussive syndrome (PCS) in adults
(1)

(2)

(3)

(4)

g.

Emergency interventions
(1) (2) (3)

2.

Diffuse axonal injuries (DAI)
a.

Definition: Shearing, tearing, or stretching force on nerve fibers causing widespread disruption of neurologic function without any focal lesions noted. Characterized by white matter degeneration as the axon is disrupted close to the cell body resulting in progressive focal axonal abnormalities in the cerebral hemispheres, brainstem, and less frequently in the cerebellum over 12 - 24 hours (Wagner, 1996).

b.

Pathogenesis: During rotation, mechanical forces act on the long axonal fibers and cause certain axons to experience structural failure as they are physically separated (stretched, sheared) into distal and proximal

State of Illinois TNS Program Head Trauma - page 51 segments. The distal segment degenerates resulting in profound deficits. Frequent targets: temporal lobe and brainstem. See reactive astrocytes 4-6 hours after the injury. Dead neurons stain red and can never recover.
c.

Morbidity/mortality: Results in global neurologic dysfunction and diffuse swelling. Coma is due to brain stem dysfunction. Accounts for ½ of all admissions and 2/3 of all TBI deaths. May have residual neurologic deficits. Recovery dependent on amount and location of neuronal damage. Currently no effective treatment for severed axons. Clinical presentation
(1)

d.

Mild DAI (Grade 1): Widespread axonal damage in the parasagittal white matter of the cerebral hemispheres and is found in those who have a brief loss of consciousness and do not experience come or those with milder injuries. Mortality 15%. Moderate DAI (Grade 2): Tissue tear hemorrhages and axonal abnormalities in the cerebral hemispheres and corpus callosum. Coma ≥ 24 hours, may have abnormal posturing. Mortality 20%24%. Severe DAI (Grade 3): Grade II findings plus abnormalities in the upper brain stem, and an increased degree of axonal hemispheric abnormalities. Point of maximum stress where tissues of different density interface (between gray and white matter). Coma is immediate, lasting longer than 24 hours with positive brain stem signs (posturing) and incomplete recovery. Mortality 60% due to direct hemorrhage in brain stem. Classic picture: For patients with milder injuries, the clinical presentation can be unclear (Bay & McLean, 2007). In more severe injuries, immediate, deep, prolonged coma may last weeks to months, accompanied by ↑ ICP, persistent brain stem reflexive posturing (flexion or extension), hypertension, ↑ temperature (104°-105° F), and hyperhidrosis indicating diencephalon involvement. No mass lesions or S&S on CT; no brain stem compression - so no pupil signs. May be associated with a persistent vegetative state. Interventions: Support ABCs. At present, there is no effective curative treatment for DAI. If an axon is injured but not severed, providing an optimum environment for healing may enable it to recover. If secondary injury occurs the loss will be permanent (Feliciano, 269). CT may show characteristic small hemorrhagic lesions in the corpus callosum, superior cerebellar peduncles, or periventricular region Visualized better on MRI with contrast.

(2)

(3)

(4)

(5)

e.

Diagnostic radiography
(1)

(2)

State of Illinois TNS Program Head Trauma - page 52

Centers for Disease Control and Prevention Screening Instrument for Detection of MBI Question 1.
2. 3. 4. At the time of your trauma, did you experience any period of transient confusion, disorientation, or impaired consciousness?* At the time of your trauma, did you experience any dysfunction of memory (amnesia)?* Did you experience any of the following in relation to your trauma: seizures, headache, dizziness, irritability, fatigue, or poor concentration?** At the time of your trauma, did you experience any loss of consciousness lasting 30 minutes or less?* YES YES YES YES No No No No

* Answer of yes on any of these items indicates mild traumatic brain injury ** If yes, must answer yes on one other item.
Source: J Neurosci Nurs © 2007 American Association of Neuroscience Nurses

Sample discharge instructions for patients with mild head injury 1. No serious brain or skull injuries have been found on your initial examination. However, it is possible for more serious signs or symptoms to develop later. If possible, have a responsible adult stay with you for 24 hours after the injury. This person should wake you every 4 hours to look for the symptoms listed below. You may take acetaminophen (Tylenol) every 4 hours to relieve pain. DO NOT take aspirin or ibuprofen until approved by a physician. Take only your normal medications and those prescribed for you at this time. If you are on any blood thinners, follow the physician’s instructions about taking them. NO alcoholic beverages for 24 hours. It is better to avoid alcoholic beverages until all symptoms from the injury resolve. Rest for the next 24 hours and resume normal activities as tolerated. Fatigue following mild head injury is normal. Do not drive, operate machinery, or make important legal decisions until symptoms resolve. Contact your physician if you experience any of the following symptoms within the next few weeks: ■ Inability to answer simple questions, such as “What day is it?” or “What happened to you?” ■ Increased headache or the inability to wake up completely ■ Nausea and vomiting three or more times ■ Problems with walking or stumbling or difficulty with coordination ■ Slurred speech ■ Seizures or convulsions ■ Weakness or the arms or legs ■ Vision changes NORMAL signs and symptoms following mild head injury may be experienced for some time (up to six months to one year). If they increase in severity or persist to the extent that your daily activities are disrupted, contact your physician. ■ Trouble remembering things ■ Difficulty with concentration, sequencing tasks, making decisions ■ Headache ■ Mood changes: irritability ■ Fatigue ■ Difficulty sleeping or a noticeable change in the number of hours you are sleeping Adapted from Bourg, 2007

2.

3. 4. 5. 6.

7.

CJM: 8/97; Rev. 1/03; 6/07

State of Illinois TNS Program Head Trauma - page 53 References American Association of Neurological Surgeons and the Brain Trauma Foundation (1996). Guidelines for the management of severe head injury (in press). ACS Committee on Trauma. (2005). Advanced Trauma Life Support Course. ACS: (in press). Batchelor, J. & McGuiness, A. (2002). A meta-analysis of GCS 15 head-injured patients with loss of consciousness or post-traumatic amnesia. Em Med J, 19, 515-519. Bay, E. & McClean, S.A. (2007). Mild traumatic brain injury: an update for advanced practice nurses. J Neurosci Nurs, 39(1), 43-51. Bazarian, J., McClung, J., Shah, M.l, Cheng, Y., Flesher, W., & Kraus, J. (2005). Mild traumatic brain injury in the United States 1998-2000. Brain Injury, 19(2), 85-91. Bledsoe, B.E., Porter, R.S., & Cherry, R.A. (2001). Head, facial and neck trauma. In Paramedic Care: Principles & Practice Trauma Emergencies (pp. 263-315). Upper Saddle River: Brady. Borg, J., Holm, L., Cassidy, D., Peloso, P.;, Carroll, L., Holst, H., et al. (2004). Diagnostic procedures in mild traumatic brain injury: Results of the WHO Collaborating Centre Task Force on mild traumatic brain injury. J of Rehabilitation Medicine, 43, 61-75. Bourg, P. (2007). Head and face trauma. In Oman, K.S. & Koziol-McLain, J. (Eds), Emergency Nursing nd Secrets (2 ed) (288-297). St. Louis: Mosby. Brain Trauma Foundation (2007). Guidelines for the management of severe traumatic brain injury. J of Neurotrauma, 24(suppl), S-1-106. Brain Trauma Foundation (2003). Update notice: Guidelines for the management of severe traumatic brain injury: cerebral perfusion pressure. Jointly published by The Brain Trauma Foundation, The American Association of Neurological Surgeons, The Congress of Neurological Surgeons, and The Joint Section on Neurotrauma and Critical Care. Chesnut, R.M., Gautille, T., Blunt, B.A. et al. (1998). Neurogenic hypotension in patients with severe head injuries. J of Trauma, 44, 958-964. Chesnut, R.M. (1997). Avoidance of hypotension: condition sine qua non of successful severe head-injury management. J of Trauma: Injury, Infection, and Crit Care, 42(5), S5-S9. Davis, D.P., Idris, A.H., Sise, M.J., Kennedy, F., Eastman, A.B., Velky, T., Vilke, G.M., & Hoyt, D.B. (2006). Early ventilation and outcome in patients with moderate to severe traumatic brain injury. Crit Care Med, 34(4), 1202-1208. De Kruijk, J., Leffers, P., Menheere, P., Meerhoff, S., Rutten, J., & Twijnstra, A. (2002). Prediction of posttraumatic complications after mild traumatic brain injury: Early symptoms and biochemical markers. J of Neurology, Neurosurgery and Psychiatry, 73, 727-732. Dries, D.J. (1995). Permissive hypercapnia. J of Trauma: Injury, Infection, and Crit Care, 39, 984-989. Gill, M., Windemuth, R., Steele, R., & Green, S. (2005). A comparison of the Glasgow Coma Scale score to simplified scores for the prediction of traumatic brain injury outcomes. Annals of Em Med, 45(1), 2742. Harders, A., Kakarieka, A., Braakman, R. et al. (1996). Traumatic subarachnoid hemorrhage and its treatment with nimodipine. J of Neurosurgery, 85, 82-89.

State of Illinois TNS Program Head Trauma - page 54 Harrahill, M. (1996). Glasgow coma scale: A quick review. JEN, 22(1), 81-83. Härtl, R., Gerer, L.M., Iacono, L., Quanhong, N., Lyons, K., & Ghajar, J. (2006). Direct transport within an organized state trauma system reduces mortality in patients with severe traumatic brain injury. J of Trauma, 60(6), 1250-1256. Henzler, D., Cooper, D.J., Tremayne, A.B., Rossaint, R., & Higgins, A. (2007). Early modifiable factors associated with fatal outcome in patients with severe traumatic brain injury: A case control study. Crit Care Med, 35(4), 1027-1031. Ivascu, F.A., Janczyk, R.J., Junn, F.S., Bair, H.A., Bendick, P.J., & Howells, G.A. (2006). Treatment of traumatic patients with intracranial hemorrhage on preinjury warfarin. J of Trauma, 61, 318-321. Kibby, M.Y. & Long, C.J. (1996). Minor head injury: attempts at clarifying the confusion. Brain Injury, 10(3), 159-186. Lehmkuhl, L.D. (1996). Brain injury glossary. The Traumatic Brain Injury Model System Research Program of The Institute for Rehabilitation and Research. Maddocks, D. & Saling, M. (1996). Neuropsychological deficits following concussion. Brain Injury, 10(2), 99103. Mamelak, A.N., Pitts, L.H. & Damron, S. (1996). Predicting survival from head trauma 24 hours after injury: a practical method with therapeutic implications. Journal of Trauma, 41(1), 91-99. Michaud, L.J., Rivara, F.P., Longstreth, W.T. et al. (1991). Elevated initial blood glucose levels and poor outcome following severe brain injuries in children. J of Trauma, 31, 1356-1362. Newell, D.W., Weber, J.P., Watson R. et al. (1996). Effect of transient moderate hyperventilation on dynamic cerebral autoregulation after severe head injury. Neurosurgery, 39, 35-44.
Sutphen, S.K. (2006). Trauma update from the 2006 annual scientific assembly of the American college of emergency physicians. Available on line: www.medscape.com/viewarticle/547419. Accessed 12/297/06.

Valadka, A.B. & Narayan R.K. (1996). Injury to the cranium. In Feliciano, D.V., Moore, E.E., & Mattox, K.L. (Eds.) Trauma (3rd ed.) (pp. 267-278). Stamford: Appleton & Lange. Wang, H.E., Beitzman, A.B., Cassidy, L.D., Adelson, P.D., & Yealy, D.M. (2004). Out-of-hospital endotracheal intubation and outcome after traumatic brain injury. Annals of Em Med, 44(5), 439450. Wooten, C. (1996). The top ten ways to detect deteriorating central neurological status. J Trauma Nursing, 3(1), 25-27. Resources: TBI-trac.ed: An internet-based distance learning program designed to provide healthcare professionals with the most current evidence-based treatment strategies for TBI care. Brain Trauma Foundation: www.braintrauma.org Brain Injury Association of America: www.BIAUSA.org National Institute of Neurological Disorders and Stroke (NINDS) Traumatic Brain Injury information: www.ninds.nih.gov/health_and_medical/disorders/TBI_doc.htm

State of Illinois TNS Program Head Trauma - page 55 Brain & Spine Trauma Glossary A Accident An event causing loss, which takes place without being expected. In most cases, the accident can be characterized with regard to time and place of occurrence. The public commonly associates this term with an unavoidable event. Therefore, when referring to injuries caused by motor vehicles, the preferred term is motor vehicle "crash" rather than accident as virtually all crashes are preventable. Sharpness or quality of a sensation. Sharp, severe, having sudden onset, sharp rise and short course; lasting a short time; seriously demanding urgent attention. The observable emotional condition of an individual at any given time. State of being watchful or ready. Lack of memory about events occurring during a particular period of time. A balloon-like deformity in the wall of a blood vessel. The wall weakens as the balloon grows larger, and may eventually burst, causing a hemorrhage. Loss of the sense of smell. Loss of the ability to express oneself and/or to understand language. Caused by damage to brain cells rather than deficits in speech or hearing organs. Inability to carry out a complex or skilled movement; not due to paralysis, sensory changes, or deficiencies in understanding. Being awake. Primitive state of alertness managed by the reticular activating system (extending from medulla to the thalamus in the core of the brain stem) activating the cortex. Cognition is not possible without some degree of arousal. A problem of muscle coordination not due to apraxia, weakness, rigidity, spasticity, or sensory loss. Caused by lesion of the cerebellum or basal ganglia. Can interfere with a person's ability to walk, talk, eat, and to perform other self care tasks. Conscious of stimulation, arising from within or from outside the person. The total collection of actions and reactions exhibited by a person. Pertaining to both right and left sides. A more specific term than head injury. Damage to the brain that results in impairments in one or more functions, including: arousal, attention, language, memory, reasoning, abstract thinking, judgment, problem-solving, sensory abilities, perceptual abilities, motor abilities, psychosocial behavior, information processing and speech. The damage may be caused by external physical force, insufficient blood supply, toxic substances, malignancy, disease-producing organisms, congenital disorders, birth trauma, or degenerative processes. Occurs when the head accelerates and then rapidly decelerates or collides with another object (for example the windshield of a car) and brain tissue is damaged, not by the presence of a foreign object within the brain, but by violent smashing, stretching, and twisting, of brain tissue. Closed brain injuries typically cause diffuse tissue damage that results in disabilities which are generalized and highly variable. A patient who has had a traumatically-induced physiological disruption of brain function, as manifested by at least one of the following: 1) any loss of consciousness, 2) any amnesia for events immediately before or after the incident, 3) any alteration in mental state at the time of the incident (e.g., feeling dazed, disoriented, or confused, 4) focal neurological deficit(s) which may or may not be transient; but where the severity of the injury does not exceed the following: a) loss of consciousness 30 minutes or less; b) after 30 minutes, an initial GCS score of 13-15 (now under debate to only include a GCS of 15); and c) post-traumatic amnesia not greater than 24 hours.

Acuity Acute Affect Alert Amnesia Aneurysm Anosmia Aphasia Apraxia Arousal

Ataxia

Awareness B Behavior Bilateral Brain injury

Brain injury, closed

Brain injury, mild

State of Illinois TNS Program Head Trauma - page 56 Brain injury, moderate A GCS of 9-12 during the first 24 hours Brain injury, severe Brain stem Produces at least 6 hours of coma; GCS of 8 or less during the first 24 hours The lower extension of the brain where it connects to the spinal cord. Neurological functions located here include those necessary for survival (breathing, heart rate) and for arousal (being awake and alert). The portion of the brain (located inferior and posterior to the cerebrum) which helps coordinate movement. Damage may result in ataxia. Marked by long duration or frequent recurrence. The conscious process of knowing or being aware of thoughts or perceptions, including understanding, and reasoning.

C Cerebellum Chronic Cognition

Cognitive impairment Difficulty with one or more of the basic functions of the brain: perception, memory, attentional abilities, and reasoning skills. Coma A state of unconsciousness from which the patient cannot be awakened or aroused, even by powerful stimulation; lack of any response to one's environment. Defined clinically as an inability to follow a one-step command consistently; GCS of 8 or less. Used to describe an absence of sensory and motor function in the lowest sacral segment. Understanding of spoken, written or gestural communication. The common result of a blow to the head or sudden deceleration usually causing an altered mental state, either temporary or prolonged. Physiologic and/or anatomic disruption of connections between some nerve cells in the brain may occur. A state in which a person if bewildered, perplexed, or unable to self-orient.

Complete injury Comprehension Concussion

Confusion

Conjugate movement Both eyes move simultaneously in the same direction. Convergence or the eyes toward the midline (crossed eyes) is a dysconjugate movement. Consciousness Contralateral Cortical blindness Contrecoup Coup damage D Dermatome Diffuse axonal injury (DAI) Diplopia Disinhibition Disorientation F Flaccid Frontal lobe Lacking normal muscle tone; limp Front part of the brain; involved in planning, organizing, problem solving, selective attention, personality, and a variety of "higher" cognitive functions. Refers to the area of the skin innervated by the sensory axons within each segmental nerve (root). There are 28 dermatomes on each side of the body. A shearing injury of large nerve fibers (axons covered with myelin) in many areas of the brain. It appears to be one of the two primary lesions of brain injury, the other being stretching or shearing of blood vessels from the same forces, producing hemorrhage. Seeing two visual images of a single object; double vision. Inability to suppress (inhibit) impulsive behavior and emotions. Not knowing where you area, who you are, or the current date. The state of awareness of the self and the environment. Opposite side Loss of vision resulting from a lesion of the primary visual areas of the occipital lobe. Light reflex is preserved. Bruising of brain tissue on the side opposite where the blow was struck. Damage to the brain at the point of impact.

State of Illinois TNS Program Head Trauma - page 57 G Glasgow Coma Scale A standardized system used to assess the degree of brain impairment and to identify the seriousness of injury in relation to outcome. The system involves the patient's BEST responses involving: eye opening, verbal ability, and motor activity all of which are evaluated independently according to a numerical value that indicates the level of consciousness and degree of dysfunction. Score run from a high of 15 to a low of 3. H Hematoma Hemianopsia Hemiplegia Hemiparesis Hydrocephalus Hypertonicity The collection of blood is tissues or a space following the rupture of a blood vessel. May refer to an epidural, subdural, subarachnoid or intracerebral collection of blood. Visual field cut. Blindness for one half of the visual field in each eye. Paralysis of one side of the body as a result of injury to neurons carrying signals to muscles from the motor areas of the brain. Weakness of one side of the body. Enlargement of fluid-filled cavities in the brain, not due to brain atrophy. The ability of a hyperosmolar solution to redistribute fluid from the intra- to the extracellular compartment. Urea, for example, may be hyperosmotic but since it equilibrates rapidly across membranes, it is not hypertonic. Loss and/or abnormality of cognitive, emotional, physiological, or anatomical structure of function; including all losses or abnormalities, not just those attributable to the initial pathophysiology. Partial preservation of sensory and/or motor function found below the neurological level including the lowest sacral segment. Sacral sensation includes sensation at the anal mucocutaneous junction as well as deep anal sensation. The test of motor function is the presence of voluntary contraction of the external anal sphincter upon digital examination. A problem with coordination of movement of parts of the body, resulting from dysfunction of the nervous system rather than weakness of muscles. Cerebrospinal fluid (CSF) pressure measured from a needle or bolt introduced into the CSF space surrounding the brain. It reflects the pressure inside the skull. Same side of the body. A severe reduction in the supply of blood to body tissues.

I Impairment Incomplete injury

Incoordination Intracranial pressure Ipsilateral Ischemia J Judgment

Process of forming an opinion, based upon an evaluation of the situation at hand in comparison with personal values, preferences, and insights regarding expected consequences. The ability to make appropriate decisions. The sensory awareness of body parts as they move. See proprioception.

K Kinesthesia L Leg bag Lethargic Lucid interval M Memory The process of organizing and storing representations of events and recalling these representations to consciousness at a late time. A small, thick plastic bag that can be tied to the leg and collects urine. It is connected by tubing to a catheter inserted into the urinary bladder. Awakens with stimulation; drowsy but awake. A period shortly after injury when the patient was reported to have talked.

State of Illinois TNS Program Head Trauma - page 58 Memory, long term Memory, remote In neuropsychological testing, this refers to recall 30 minutes or longer after presentation. requires storage and retrieval of information that exceeds the limit of short-term memory. Information an individual correctly recalls from the past, stored before the onset of brain injury. There is no specific requirement for the amount of elapsed time, but it is typically more than six months to a year. Preserved information from delayed memory becomes part of remote memory. Primary or "working" memory; its contents are in conscious awareness. A limited capacity system that holds up to seven chunks of information over a period of 30 seconds to several minutes, depending upon the person's attention to the task. The quality or state of being competent; having adequate mental abilities; legally qualified or adequate to manage one's personal affairs. An individual found by a court to be mentally incompetent has a guardian appointed to make personal and/or economic decisions on their behalf. Paralysis of one arm or one leg. Used in clinical practice to describe the resistance of a muscle to being stretched. When the peripheral nerve to a muscle is severed, the muscle becomes flaccid (limp). When nerve fibers in the brain or spinal cord are damaged, the balance between facilitation and inhibition of muscle tone is disturbed. The tone of some muscle may become increased and they resist being stretched - a condition called hypertonicity or spasticity. Refers to the collection of muscle fibers innervated by the motor axons within each segmental nerve (root). There are 10 myotomes on each side of the body. The first of these terms refers to the most caudal segment of the spinal cord with normal sensory and motor function on both sides of the body. In fact, the segments at which normal function is found often differ by side of the body and in terms of sensory vs. motor testing. Up to four different segments may be identified in determining the neurological level: R-sensory; L-sensory; R-motor; Lmotor. It is strongly recommended to separately record each segment rather than a single level as this can be misleading. When the term sensory level is used, it refers to the most caudal segment of the spinal cord wit normal sensory function on both sides of the body. The motor level is similarly defined with respect to motor function. Movement that a person may make which has no apparent goal. Ex. Flexor or extensor posturing. Involuntary horizontal, vertical, or rotary movement of the eyeballs.

Memory, short term

Mental competence

Monoplegia Muscle tone

Myotome N Neurological level, sensory level, and motor level:

Non-purposeful movement Nystagmus O Occipital lobe Oncotic pressure Osmolality Osmolarity Osmotic pressure

Region in the back of the cerebrum which processes visual information. Damage to this lobe can cause visual deficits. A small portion of the total osmotic pressure that is due to the presence of large protein molecules. The osmotic concentration of a solution expressed as osmoles of solute per kg of solution The osmotic concentration of a solution expressed as osmoles of solute per L of solution. The pressure exerted by a solution necessary to prevent osmosis into that solution when it is separated from the pure solvent by a semipermeable membrane. Osmotic pressure (mmHg) = 19.3 X osmolality (mOsm/kg). Awareness of one's environment and/or situation, along with the ability to use this information appropriately in a functional setting. See disorientation. Weakness of a muscle Refers to impairment or loss of motor and/or sensory function in the thoracic, lumbar or sacral (but not cervical) segments of the spinal cord, secondary to damage of neural elements within the spinal canal. With paraplegia, arm functioning is spared, but, depending on the level of injury, the trunk,

Orientation P Paresis Paraplegia:

State of Illinois TNS Program Head Trauma - page 59 legs and pelvic organs may be involved. The term is used in referring to cauda equina and conus medullaris injuries but not to lumbosacral plexus lesions or injury to peripheral nerves outside the neural canal. Parietal lobe One of the two paired lobes of the brain located behind the frontal lobe at the top of the brain. Interprets and localizes sensory stimuli. Damage to the right parietal lobe can cause visual-spatial deficits causing the person to have difficulty finding their way around new or even familiar places. Damage to the left parietal lobe may disrupt a person's ability to understand spoken and/or written language. Pathology Perception Post traumatic amnesia Interruption or interference of normal bodily processes or structures. The ability to make sense of what one sees, hears, feels, tastes, or smells. Perceptual losses are often very subtle and the patient and/or family may be unaware of them. A period of hours, weeks, days, or months after the injury when the patient exhibits a loss of day-to-day memory. The patients is unable to store new information and therefore has a decreased ability to learn. Memory of the PTA period is never stored, therefore things that happened during that period cannot be recalled. May also be called antegrade amnesia. Ability of the individual to bring cognitive processes to the consideration of how to accomplish a task. Ability to consider the probable factors that can influence the outcome of each of various solutions to a problem, and to select the most advantageous solution. Individuals with deficits in this skill may become "immobilized" when faced with a problem. By being unable to think of possible solutions, they may respond by doing nothing. The sensory awareness of the position of body parts with or without movement. Combination of kinesthesia and position sense. Drooping of a body part, such as the upper eyelid, from paralysis or drooping of visceral organs from weakness of the abdominal muscles.

Problem solving

Problem solving skill

Proprioception Ptosis

Purposeful movement Motor activity with an apparent goal Q Quadriplegia R Retrograde amnesia S Skeletal level: Somatic Stimulus Refers to the level at which, by radiographic examination, the greatest vertebral damage is found. Relating to, or affecting the body. That which causes sensation (i.e., light for vision, sound for hearing). When a patient begins to emerge from coma, an organized program of controlled stimulation is sometimes used to begin "exercising" the brain. However, when a patient becomes agitated, the amount an intensity of simulation should be limited (only one task for one sense at a time). Deep sleep; unresponsive but can be awakened with repeated, noxious stimulation. Awareness is depressed but present. Two paired lobes located about the level of the ears. They allow one to tell the difference between one smell from another and one sound from another. They also help in sorting new information and are responsible for short-term memory. The right lobe is primarily involved with visual memory (pictures and faces). The left lobe is involved in verbal memory (words and names). Inability to recall events that occurred prior to the accident; may be a specific span of time or type of information. Paralysis of all four limbs (from the neck down). Now more commonly referred to as tetraplegia, meaning four.

Stupor T Temporal lobes

State of Illinois TNS Program Head Trauma - page 60 Preferred to quadriplegia: Refers to impairment or loss of motor and/or sensory function in the cervical segments of the spinal cord due to damage of neural elements within the spinal canal. Tetraplegia results in impairment of function in the arms as well as in the trunk, legs, and pelvic organs. it does not include brachial plexus lesions or injury to peripheral nerves outside the neural canal.

Tetraplegia

State of Illinois TNS Program Head Trauma - page 61 STUDY QUESTIONS 1. List four major initial complication of TBI that should be anticipated and prevented if at all possible:

2.

If a patient presents with a MAP of 70 and an ICP of 30; what is the cerebral perfusion pressure?

Would this indicate adequate perfusion or cerebral ischemia?

3.

If a patient presents with oval pupils and hippus, what should a TNS suspect?

4.

List the three findings of the Cushing's triad:

5.

List two defining signs and symptoms of brain shift or herniation:

6.

All patients with a severe traumatic brain injury and a Glasgow Coma Score of ≤ 8 should have their airway secured via:

7. 8.

True or False: The BTF Guidelines state that normocarbia or controlled hypercarbia should be maintained in the absence of clinical signs of herniation. Why must all uncontrolled bleeding and hypotension be avoided or corrected immediately in a patient with TBI? What abnormal ventilations are described as crescendo/decrescendo with periods of apnea? A. B. C. D. Central Neurogenic Hyperventilation. Apneustic. Cheyne Stokes. Cluster.

9.

10.

A patient’s only verbal utterances are random, repetitive words or profanity. How should this verbal response be scored? A. B. C. D. Converses Confused speech Inappropriate words Incomprehensible sounds

State of Illinois TNS Program Head Trauma - page 62 11. An adult cannot localize pain and generally pulls up or withdraws both arms in purposeful movement when a pain stimulus is applied. How should the GCS motor response be rated? A. B. C. D. 12. 5 4 3 2 Protective response Withdrawal response Abnormal flexion Abnormal extension

When assessing a comatose adult, you note that the patient flexes their right arm and extends left arm extends when a pain stimulus is applied. When scoring the motor aspects of the Glasgow Coma Score, which number would you select? A. B. C. D. 5 4 3 2 Protective response Withdrawal response Abnormal flexion Abnormal extension

13.

What is the most sensitive test of unilateral motor weakness in a head injured patient who can cooperate with your motor commands?

14.

Name two brainstem reflexes a physician may evaluate to determine presence of absence of brainstem function:

15.

Why is hyperventilation to be avoided during the first 24 hours after TBI?

16.

Under what three circumstances may brief periods of hyperventilation be indicated?

17.

Which osmotic diuretic serves as a free radical scavenger and is given to patients with head trauma to control ↑ ICP w/ signs of neurological deterioration?

18.

Under what circumstances are barbiturates considered for TBI patients?

19.

Under what circumstances should anticonvulsant medications be administered?

20.

List two TBI patients who should be prepared for emergent surgery:

State of Illinois TNS Program Head Trauma - page 63 21. Why is serum glucose at the time of injury or in the ED an important consideration for the patient's morbidity?

22.

List three TBI patients who need cranial CT scanning to r/o significant injury:

23.

List three cardinal signs of neurological deterioration in a TBI patient:

24.

How do basilar skull fractures damage cranial nerves or cause leaks of cerebral spinal fluid?

25.

What is one of the earliest, specific or defining signs that a patient has sustained an anterior basilar skull fracture that you can assess while inspecting the face?

26.

Why is insertion of a nasopharyngeal airway or an NG tube contraindicated if a patient has midface or above fractures?

27.

What two cranial nerves frequently present with dysfunction in a middle fossa basilar skull fracture?

28.

A patient who sustains a linear fracture to the temporal or parietal bones from blunt trauma and experiences disruption of the middle meningeal artery, a rapidly deteriorating level of consciousness, and clinical signs of brain shift should be suspected of having a(n):

29. 30.

Name the type of hematoma associated with venous bleeding, commonly encountered in the elderly or alcoholic population: Which hematoma has the greater morbidity and mortality: epidural or subdural? Why???

State of Illinois TNS Program Head Trauma - page 64 31. List three specific signs and symptoms of subarachnoid hemorrhage:

32.

A blow to the head causing actual bruising of cortical tissue is called a

33.

What clinical signs could suggest that a comatose patient had a brain stem hemorrhage at the level of the pons?

34.

A diffuse injury causing transient loss of cerebral function following a deceleration injury to the brain where loss of consciousness (if one occurs) does not exceed 6 hours is called a/n:

35.

Why is the hallmark of this injury amnesia?

36.

Any patient who remains comatose over six hours after TBI with no demonstrable lesion evident on C-T should be suspected of having a/n:

37. 38.

In what range would you expect the physician to maintain a head-injured patient's pCO2 who has an increase in intracranial pressure? _________________________________________________ A 72-year-old male was cleaning the gutters on his house when he became dizzy and fell to the ground. On assessment, you note he withdraws to deep, painful stimuli, does not open his eyes, and is silent. RR: 10 and shallow with periods of apnea. There is thin, bloody fluid draining from his nose. Which is contraindicated in this situation? A. B. C. D. Transilluminated intubation with sedation An oropharyngeal airway prior to BVM ventilation Nasotracheal intubation Drug-assisted intubation

39

An adult has severely elevated intracranial pressure from an acute TBI. VS: BP 210/100; P 50; R 12 and irregular. Which of these is contraindicated? A. B. C. D. Administer IV fluids to ensure brain perfusion. Administer Nipride to reduce the blood pressure. Control seizure activity quickly with Valium/Ativan. Oxygenate well before suctioning the patient.

40.

Patients with cerebral hematomas are more likely to dilate a pupil on the (same/opposite) side as the lesion and lose motor function on the (same/opposite) side when the brain begins to shift.

State of Illinois TNS Program Head Trauma - page 65 Notes:

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