NUR 205 Ch 45 Nursing Management: Patients With Neurologic Trauma

Medical and Nursing Management: Monitoring Intracranial Pressure

- Nursing management focuses on detecting early signs of increasing ICP b/c medical interventions are usually ineffective once later signs develop. - Frequent neurologic assessments & documentation & analysis of trends will reveal the subtle changes that may indicate increasing ICP

Types of Brain Injury: Contusion

- A cerebral contusion is a more severe injury than concussion, involving bruising of the brain, w/ possible surface hemorrhage. - The pt is unconscious for more than a few secs or mins. Clinical s/s depend on the size of the contusion & amount of associated swelling of the brain (cerebral edema). - The pt may lie motionless, w/ a faint pulse, shallow respirations, & cool, pale skin. The pt may be aroused w/ effort but soon slips back into unconsciousness. - BP & temperature are subnormal, & the clinical picture is somewhat similar to that of shock. - Pts may recover consciousness but pass into a stage of cerebral irritability. In this stage, the pt is conscious & easily disturbed by any form of stimulation, such as noises, light, & voices; he/she may become hyperactive at times. - Gradually, the pulse, respirations, temperature, & other body functions return to normal, but full recovery can be delayed for months. - Residual HA & vertigo are common, & impaired mental function or seizures may occur as a result of irreparable cerebral damage.

Types of Brain Injury: Concussion (Box 45-4)

- A concussion (also referred to as a mild TBI) involves an alteration in mental status that results from trauma, & may or may not involve loss of consciousness. - Typically lasts no longer than 24 hrs & may include sx such as HA, nausea, vomiting, photophobia, amnesia, & blurry vision - Treatment involves observing pt for sx including HA, dizziness, lethargy, irritability, anxiety, photophobia, phonophobia, difficulty concentrating, & memory difficulties. The occurrence of these sx after the injury is referred to as postconcussive syndrome - Giving the pt info, explanations, & encouragement may reduce some of the problems a/w postconcussive syndrome. - Pt is advised to resume normal activities slowly; the exact recovery time is not known. Once the pt is discharged home, he/she should be closely observed for the next 24 hrs, & awakened every 2 hrs in order to detect any changes in mental status. - Neuroimaging (CT & MRI) is generally not indicated in concussion.

Assessment and Diagnostic Findings

- A detailed neurologic exam is performed. - Diagnostic X-rays (lateral cervical spine X-rays) & CT are usually performed initially. - An MRI may be ordered as further workup if a ligamentous injury is suspected, b/c significant spinal cord damage may exist even in the absence of bony injury. - An assessment is made for other injuries b/c spinal trauma often is accompanied by concomitant injuries, commonly to the head & chest. - Continuous cardiac monitoring may be indicated if an SCI is suspected, b/c bradycardia & asystole are common in pts w/ acute SCIs.

Nursing Interventions: Providing Comfort Measures

- A pt who has had pins, tongs, or calipers placed for cervical stabilization may have a HA or discomfort for several days after the insertion. Pts initially may be bothered by the appearance of these devices, but usually they readily adapt to it b/c the device provides comfort for the unstable neck. Pt may complain of being caged in & of noise created by any object coming in contact w/ the steel frame of a halo device, but he/she can be reassured that adaptation to this will occur. - The areas around the 4 pin sites of a halo device are cleaned daily & observed for redness, drainage, & pain. The pins are observed for loosening, which may contribute to infection. If 1 of the pins becomes detached, the head is stabilized in a neutral position by 1 person, while another notifies the neurosurgeon. A torque screwdriver should be readily available in case the screws on the frame need tightening. - Skin under the halo vest is inspected for excessive perspiration, redness, & skin blistering, esp on the bony prominences. The liner of the vest should not become wet, b/c dampness causes skin excoriation.

Head Injuries: Pathophysiology (Skull Fracture) [Fig. 45-1]

- A skull fx is a break in the continuity of the skull caused by forceful trauma. May occur w/ or w/o damage to the brain. - Classified as simple, comminuted, depressed, or basilar: - Simple (linear) fx is a break in the continuity of the bone. Comminuted fx refers to a splintered fx line. When bone fragments are embedded into brain tissue, the fx is depressed. Fx of the base of the skull is called a basilar or basal skull fx. - Fx may be open, indicating a scalp laceration or tear in the dura, or closed, in which case the dura is intact.

Intracranial Hemorrhage/Hematoma: Subdural Hematoma (Box 45-5)

- A subdural hematoma (SDH) is a collection of blood b/w the dura & the brain, a space normally occupied by a thin cushion of CSF. - Most common cause is trauma, but can also occur as a result of coagulopathies (bleeding disorders) or rupture of an aneurysm. - The elderly are at increased risk for subdural hemorrhage secondary to whole brain atrophy. - *Acute & Subacute Subdural Hematoma:* a/w major head injury involving contusion or laceration. Clinical sx develop over 24 to 48 hrs. S/s: changes in LOC, changes in the reactivity of the pupils, & hemiparesis. May be minor or even no sx, w/ small collections of blood. Coma, increasing BP, decreasing HR, & slowing RR are all signs of a rapidly expanding mass requiring immediate intervention. - Subacute SDHs are the result of less severe contusions & head trauma. Clinical manifestations usually appear b/w 48 hrs & 2 wks after injury. S/s similar to those of an acute SDH. - If pt can be transported rapidly to the hospital, an immediate surgery may be performed to open the dura, allowing the subdural clot to be evacuated. Successful outcome also depends on the control of ICP & careful monitoring of resp function. Mortality rate is high b/c of associated brain damage - *Chronic Subdural Hematoma:* can develop from seemingly minor head injuries & are seen most freq in the elderly. Time b/w injury & onset of sx can be lengthy, so the actual injury may be forgotten. - Treatment typically consists of surgical evacuation of the clot if the pt is symptomatic & the bleed is at least 1 cm in size. Smaller bleeds are monitored until the body has fully reabsorbed the blood

Monitoring and Managing Complications: Promoting Bowel Function

- Abdomen is assessed for distention by listening for bowel sounds & measuring the girth of the abdomen - There is a risk for diarrhea from infection, antibiotics, & hyperosmolar fluids. Immobility & lack of dietary fiber can cause constipation. - Nurse monitors the number & consistency of bowel movements & performs a rectal exam for signs of fecal impaction. - Stool softeners may be prescribed & can be admin w/ tube feedings. To facilitate bowel emptying, a glycerin suppository may be indicated. Pt may require an enema every other day to empty the lower colon

Monitoring Intracranial Pressure: Detecting Later Indications of Increasing ICP (Figure 45-5 & Box 45-7) Cont'd

- B/c clinical assessment is not always a reliable guide in recognizing increased ICP, esp in comatose pts, monitoring of ICP is an essential part of management. ICP is monitored closely for continuous elevation or significant increase over baseline. Vital signs are assessed when an increase in ICP is noted. - ICP monitored w/ the use of an intraventricular catheter (ventriculostomy) or a subarachnoid bolt or screw. - When a ventriculostomy is used for monitoring ICP, a fine-bore catheter is inserted into a lateral ventricle, preferably in the nondominant hemisphere of the brain. The catheter is connected by a fluid-filled sys to a transducer, which records the pressure in the form of an electrical impulse. - In addition to obtaining continuous ICP recordings, the ventricular catheter allows CSF to drain, particularly during acute increases in pressure. - Complications a/w its use: infection, meningitis, ventricular collapse, occlusion of the cath by brain tissue or blood, & problems w/ the monitoring sys. - CSF drainage is frequently performed b/c the removal of CSF w/ a ventriculostomy drain can dramatically reduce ICP & restore cerebral perfusion. Caution should be used in draining CSF, however, b/c excessive drainage may result in collapse of the ventricles & herniation. - The subarachnoid bolt or screw is a hollow device that is inserted through the skull & dura mater into the cranial subarachnoid space. Has the advantage of not requiring a ventricular puncture. The subarachnoid bolt is attached to a pressure transducer, & the output is recorded on an oscilloscope. - Also has the advantage of avoiding complications from brain shift & small ventricle size. One disadvantage is the inability to obtain CSF for analysis or drainage purposes. - Complications include infection & blockage of the bolt by clot or brain tissue, which leads to a loss of pressure tracing & a decrease in accuracy at high ICP readings

Intracranial Hemorrhage/Hematoma: Epidural Hematoma

- After a head injury, blood may collect in the epidural (extradural) space b/w the skull & the dura. - Can result from a skull fx that causes a rupture or laceration of the middle meningeal artery (artery that runs b/w the dura & skull) inferior to a thin portion of temporal bone. Hemorrhage from this artery causes a rapid increase in pressure on the brain - Sx are caused by the expanding hematoma. Usually a momentary loss of consciousness occurs at the time of injury, followed by an interval of apparent recovery (lucid interval). - Although lucid interval is considered a classic characteristic of an epidural hematoma, no lucid interval has been reported in many pts w/ this lesion, and, therefore, should not be considered a critical defining criterion. - During the lucid interval, compensation for the expanding hematoma takes place by rapid absorption of CSF & decreased intravascular volume, both of which help maintain a normal ICP. - When these mechanisms can no longer compensate, even a small increase in the volume of the hematoma produces a marked elevation in ICP. Then, often suddenly, signs of compression appear (usually deterioration of consciousness & signs of focal neurologic deficits, such as dilation & fixation of a pupil or paralysis of an extremity), & the pt's condition deteriorates rapidly. - An epidural hematoma is considered an EXTREME EMERGENCY; neurologic deficit & resp arrest can occur within mins. - Treatment consists of making openings through the skull (burr holes) to decrease ICP emergently, remove the clot, & control the bleeding. A craniotomy (surgical procedure that removes part of the skull to gain access to the brain) may be required to remove the clot & control the bleeding. A drain may be inserted after creation of burr holes or a craniotomy to prevent reaccumulation of blood.

Altered LOC and Increased Intracranial Pressure: Clinical Manifestations (Figure 45-2)

- Alterations in LOC occur along a continuum, & the clinical manifestations depend on where the pt is along this continuum. - As the pt's state of alertness & consciousness decreases, changes will ultimately occur in the pupillary response, eye opening response, verbal response, & motor response. However, initial alterations in LOC may be reflected by subtle behavioral changes, such as restlessness or increased anxiety. - The pupils become sluggish (response is slower); as the pt becomes comatose, the pupils become fixed (no response to light). The pt in a coma does not open the eyes, respond verbally, or move the extremities in response to a request to do so. - Important to be familiar w/ the pt's baseline status, as many early signs of increased ICP are subtle; they include sudden onset of restlessness (w/o apparent cause), confusion, & increasing drowsiness. - As ICP increases, the pt becomes stuporous, reacting only to loud or painful stimuli. At this stage, serious impairment of brain circulation is likely taking place, & immediate intervention is required. - As neurologic function deteriorates further, the pt becomes comatose & exhibits decorticate & decerebrate posturing or flaccidity. If the coma is profound, w/ fixed & dilated pupils & impaired or absent respiration, death is usually inevitable

Altered Level of Consciousness and Increased Intracranial Pressure

- An altered LOC is apparent in the pt who is not oriented, does not follow commands, or needs persistent stimuli to achieve a state of alertness. - LOC is gauged on a continuum, w/ a normal state of alertness & full cognition (consciousness) on one end & coma on the other end. - Coma is a clinical state of unarousable unresponsiveness in which there are no purposeful responses to internal or external stimuli, although nonpurposeful responses to painful stimuli & brainstem reflexes may be present. - The duration of coma is usually limited to 2-4 wks. LOC is the most important indicator of the pt's condition. - The volume of the rigid cranial vault is approx 1,700 mL, containing brain tissue (80%), intravascular blood (10%), & CSF (10%). The volume & pressure of these 3 components are usually in a state of equilibrium, & together they produce the ICP. An alteration in LOC may be the result of increased ICP. - Increased ICP is explained by the Monro-Kellie hypothesis. The hypothesis states that b/c of the limited space for expansion within the skull, an increase in any 1 of the components causes a change in the volume of the others. B/c brain tissue has limited space to expand, compensation typically is accomplished by increasing absorption or diminishing production of CSF or decreasing cerebral blood volume. W/o such changes, ICP will begin to rise. - ICP is usually measured in the lateral ventricles, w/ normal pressure being 5-15 mm Hg. Treatment of increased ICP is generally initiated at a pressure of 20 mm Hg

Management of Brain Injuries

- Assessment & dx of the extent of injury are accomplished by the initial physical & neurologic exams. - CT & MRI are the primary neuroimaging diagnostic tools of choice & are useful in evaluating the brain structure. - Cervical spine injuries occur in 5% to 10% of pts w/ TBI. Pts at highest risk for cervical spine injury are those involved in motorcycle accidents & those w/ lower GCS scores (≤8) - Pt is transported from the scene of the injury on a board w/ the head & neck maintained in alignment w/ the axis of the body. A hard cervical collar should be applied & maintained until cervical spine X-rays have been obtained & the absence of cervical spinal cord injury (SCI) is documented. *** Any pt w/ a head injury is presumed to have a cervical spine injury until ruled out; therefore, immobilization of the spine via cervical collar, spinal backboard, & avoidance of movement is essential. - All therapy is directed toward preserving brain homeostasis & preventing secondary brain injury. Common causes of secondary injury: cerebral edema, hypotension, & resp depression. - Treatments to prevent secondary injury include stabilization of cardiovascular & resp function to maintain adequate cerebral perfusion, control of hemorrhage & hypovolemia, & maintenance of optimal blood gas values.

Monitoring and Managing Acute Complications of Spinal Cord Injury: Autonomic Dysreflexia

- Autonomic dysreflexia (or hyperreflexia) is an acute emergency that occurs as a result of exaggerated autonomic responses to stimuli that are harmless in normal ppl. - Only occurs after spinal shock has resolved in pts w/ cord lesions above T6. - This syndrome is characterized by a severe, pounding HA w/ paroxysmal htn, profuse diaphoresis (most often of the forehead), nausea, nasal congestion, & bradycardia - The sudden increase in BP may cause a rupture of 1 or more cerebral blood vessels or lead to increased ICP. - Autonomic dysreflexia is more commonly seen in pts w/ complete SCIs & in the chronic stages of SCI - A # of stimuli may trigger this reflex: distended bladder (most common); distention or contraction of the visceral organs, esp the bowel (from constipation, impaction); or stimulation of the skin (tactile, pain, thermal stimuli, pressure ulcer). - B/c this is an emergency situation, the objectives are to remove the triggering stimulus & to avoid the potentially serious complications.

Nursing Interventions: Maintaing Skin Integrity

- B/c pts w/ SCI are immobilized & have loss of sensation below the lvl of the lesion, they have the highest prevalence of pressure ulcers in the U.S. - Most common sites for pressure ulcers are over the ischial tuberosity, the greater trochanter, the sacrum, the gluteal region, & the occiput (back of the head). Pts who wear cervical collars for prolonged periods may develop breakdown from the pressure of the collar under the chin, on the shoulders, & at the occiput. - Nurse follows institutional policy regarding collar care, which typically may require changing of pads every 24 hrs & inspecting & cleaning the skin every shift. - Pt is repositioned q2h, & careful inspection of the skin is made every time pt is turned. The skin over pressure points is assessed for redness or breakdown. Pt's skin should be kept clean by washing w/ mild soap, rinsing well, & blotting dry.

Altered LOC and Increased Intracranial Pressure: Pathophysiology

- Cause may be neurologic (head injury, stroke), toxicologic (drug overdose, alcohol intoxication), or metabolic (hepatic or renal failure, diabetic ketoacidosis). - Increased ICP may significantly reduce cerebral blood flow, resulting in ischemia & cell death. - In the early stages of cerebral ischemia, the vasomotor centers are stimulated & the systemic pressure rises to maintain cerebral blood flow. This is typically accompanied by a slow, bounding pulse & resp irregularities. - These changes in BP, pulse, & respiration are important clinically b/c they suggest increased ICP. - Cerebral edema is an abnormal accumulation of fluid in the intracellular space, extracellular space, or both, & is a/w an increase in the volume of brain tissue. - As brain tissue swells within the rigid skull, several mechanisms attempt to compensate for the increasing ICP. These compensatory mechanisms include autoregulation & decreased production & flow of CSF. - Autoregulation refers to the brain's ability to change the diameter of its blood vessels automatically to maintain a constant cerebral blood flow during alterations in systemic BP. This mechanism may be impaired in pts who are experiencing a pathologic & sustained increase in ICP. - A clinical phenomenon known as the Cushing's response (or Cushing's reflex) is seen when cerebral blood flow decreases significantly. When ischemic, the vasomotor center triggers an increase in arterial pressure in an effort to overcome the increased ICP. A sympathetically mediated response causes an increase in the systolic BP, w/ a widening of the pulse pressure & cardiac slowing. It is a late sign requiring immediate intervention; however, perfusion may be recoverable if the Cushing's response is treated rapidly. - At a certain point, the brain's ability to autoregulate becomes ineffective & decompensation (ischemia & infarction) begins. When this occurs, the pt exhibits significant changes in mental status & vital signs. Bradycardia, htn, & bradypnea a/w this deterioration are known as Cushing's triad, a grave sign. - At this point, herniation of the brainstem & occlusion of the cerebral blood flow occur if therapeutic intervention is not initiated immediately.

Monitoring and Managing Complications: Reducing Metabolic Demands

- Cellular metabolic demands may be reduced through the admin of high doses of barbiturates if the pt is unresponsive to conventional treatment. - Use of high-dose barbiturates should be reserved for pts w/ refractory increased ICP who do not respond to other medical or surgical treatments. Barbiturates should not be used as prophylaxis to prevent increased ICP - Another method of reducing cellular metabolic demand & improving oxygenation is the admin of pharmacologic paralyzing agents such as pancuronium, vecuronium, & cisatracurium. Pt who receives these agents cannot move; this decreases metabolic demands & results in a decrease in cerebral O2 demand. B/c pt cannot respond or report pain, sedation & analgesia must be provided, b/c paralyzing agents do not provide either. - Pts receiving high doses of barbiturates or paralyzing agents require continuous cardiac monitoring, endotracheal intubation, mechanical ventilation, ICP monitoring, & arterial pressure monitoring. - The ability to perform serial neurologic assessments is lost w/ the use of barbiturates or paralyzing agents. Therefore, other monitoring tools are needed to assess the pt's status & response to therapy. - Important parameters that must be assessed: ICP, BP, HR, RR, & response to ventilator therapy. Potential complications include hypotension due to decreased sympathetic tone & myocardial depression

Monitoring and Managing Complications: Decreasing Cerebral Edema

- Cerebral edema is the leading cause of secondary brain injury. Osmotic diuretics, such as mannitol, may be admin to dehydrate the brain tissue & reduce cerebral edema. - Osmotic diuretics work by creating a gradient that draws water across intact membranes, thereby reducing the volume of the swollen brain. Secondarily they reduce blood viscosity & hematocrit & enhance cerebral blood flow. If pt is receiving osmotic diuretics, serum osmolality should be determined to assess hydration status. - Hypertonic saline is another med that works to reduce cerebral edema. - Another method is fluid restriction. Limiting overall fluid intake leads to dehydration & hemoconcentration, which draws fluid across the osmotic gradient & decreases cerebral edema. Fluid needs are met initially by admin the required IV fluids - Researchers hypothesized that lowering body temp decreases cerebral edema by reducing the O2 & metabolic requirements of the brain, thus protecting the brain from continued ischemia. The effect of hypothermia on ICP requires more study; thus far, induced hypothermia has not consistently been shown to be beneficial for pts w/ brain injury.

Head Injuries: Pathophysiology (Box 45-2)

- Damage to the brain from traumatic injury takes 2 forms: primary injury & secondary injury. - Primary: initial damage to the brain that results from the traumatic event. This may include contusions, lacerations, & torn blood vessels due to impact, acceleration/deceleration, or foreign object penetration - Secondary: evolves over the ensuing hrs & days after the initial injury & can be due to cerebral edema, ischemia, seizures, infection, hyperthermia, hypovolemia, & hypoxia - When the brain is injured, there is no room for swelling within the skull. Any bleeding or swelling within the skull increases the volume of contents & therefore can cause increased ICP. - If the increased pressure is high enough, it can cause herniation of the brain through or against the rigid structures of the skull. This causes restriction of blood flow to the brain, w/ resultant ischemia, infarction, irreversible brain damage, &, eventually, brain death

Monitoring and Managing Acute Complications of Spinal Cord Injury: Orthostatic Hypotension

- For the first 2 wks following SCI, BP tends to be unstable & quite low. It gradually returns to preinjury lvls, but periodic episodes of severe orthostatic hypotension frequently interfere w/ efforts to mobilize the pt. - Defined as a drop in SBP of at least 20 mm Hg or a drop in diastolic pressure of at least 10 mm Hg - Pts w/ SCI are prone to orthostatic hypotension during position changes due to a loss of reflex vasoconstriction & pooling of blood in the lower extremities & abdominal viscera. This results in decreased venous return to the heart & decreased CO. - To compensate, pts develop reflex tachycardia, although this is rarely sufficient to raise BP enough to return to normal lvls. - Close monitoring of vital signs before/during position changes is essential. Vasopressor med can be used to treat the profound vasodilation. Elastic compression stockings should be applied to improve venous return from lower extremities. Abdominal binders may also be used to encourage venous return & provide diaphragmatic support when pt is upright. - Activity should be planned in advance, & adequate time should be allowed for a slow progression of position changes from recumbent to sitting & upright.

Medical and Nursing Management

- Goals of management are to prevent further SCI & to observe for sx of progressive neurologic deficits. - There remains a debate on whether high-dose methylprednisolone should be standard protocol. Despite current literature, many centers continue using protocols for high-dose methylprednisolone in pts w/ acute SCI - In a more recent review of available therapies for SCI, it was concluded that administration of high-dose methylprednisolone was justified in nondiabetic & nonimmunocomprised pts as there are no alternative therapies currently available

Head Injuries (Box 45-1)

- Head injury is a broad classification that includes injury to the scalp, skull, or brain. It is the most common cause of death from trauma in the U.S. - Traumatic brain injury (TBI) is the most serious form of head injury. The most common causes of TBI are falls (28%), motor vehicle accidents (20%), collisions w/ stationary or moving objects (17%), & assaults (11%) - Males b/w 15 & 24 yrs old are at highest risk for TBI. The very young (<5 yrs) & the very old (>75 yrs) are also at increased risk. - Despite advances in care, only 40% of pts w/ severe TBI have good outcomes. The best approach to head injury is an emphasis on prevention (Box 45-1)

Types of Brain Injury: Intracranial Hemorrhage/Hematoma (Figure 45-3)

- Hematomas (collections of blood) that develop within the cranial vault are the most serious type of brain injury - May be epidural (above the dura), subdural (below the dura), or intracerebral (within the brain). - Major sx are frequently delayed until hematoma is large enough to cause distortion of the brain & increased ICP. - S/s of cerebral ischemia resulting from compression by a hematoma are variable & depend on the speed w/ which vital areas are affected & the area that is injured

Monitoring and Managing Complications: Controlling Fever

- High fever in the unconscious pt may be caused by infection of the resp or urinary tract, drug reactions, or damage to the hypothalamic temperature-regulating center. - B/c of damage to the temperature center in the brain or severe intracranial infection, unconscious pts often develop very high temperatures. Such temperature elevations must be controlled, b/c the increased metabolic demands of the brain can exceed cerebral circulation & oxygenation, resulting in cerebral deterioration - Studies have shown that fever within the 1st week of injury is a/w poor outcomes & should be treated aggressively. Persistent hyperthermia w/ no identified clinical source of infection indicates brainstem damage & a poor prognosis. - Strategies for reducing fever include: (1) Removing all bedding over the pt; (2) Administering acetaminophen as prescribed; (3) Giving cool sponge baths & allowing a fan to blow over the pt to increase surface cooling; (4) Using a hypothermia blanket; (5) Freq temperature monitoring is indicated to assess pt's response to the therapy & to prevent an excessive decrease in temperature & shivering, which increases heat production.

Intracranial Hemorrhage/Hematoma: Intracerebral Hemorrhage and Hematoma

- ICH is bleeding into the parenchyma of the brain. Commonly seen in head injuries when force is exerted to the head over a small area (e.g., bullet wounds & stab injuries). - Hemorrhages within the brain may also result from: (1) Systemic htn, which causes degeneration & rupture of a vessel; (2) Rupture of a saccular aneurysm; (3) Vascular anomalies; (4) Intracranial tumors; (5) Bleeding disorders; (6) Complications of anticoagulant therapy - Onset may be insidious, beginning w/ the development of neurologic deficits followed by HA. - Management includes supportive care, control of ICP, & careful admin of fluids, electrolytes, & antihypertensive meds. - Surgical intervention by craniotomy permits removal of the blood clot & control of hemorrhage but may not be possible b/c of the inaccessible location of the bleeding or lack of a clearly circumscribed area of blood that can be removed. - Decompressive craniectomies that are performed up to 24 hrs after the initial injury have been shown to improve outcomes. Performed to allow for swelling of the brain, which decreases ICP. The earlier the craniectomy can be done, the greater benefit it can have for the pt

Monitoring and Managing Complications: Managing Nutritional Needs (Box 45-9)

- If pt does not recover quickly & sufficiently enough to take adequate fluids & calories by mouth, a NG tube or gastrostomy tube is inserted for the admin of enteral feedings. - A nutritionist should be involved in the care of the unconscious pt. Nutritionist will determine pt's caloric needs & will make recommendations for the amount & type of tube feeding that is appropriate. - Daily I&Os should be recorded, as well as daily weights to ensure the pt has adequate caloric intake

Nursing Interventions: Improving Bowel Function

- Immediately after SCI, a paralytic ileus may develop due to neurogenic paralysis of the bowel; therefore, a NG tube is often required to relieve distention & to prevent vomiting & aspiration. - Bowel activity usually returns within the 1st wk following the injury. As soon as bowel sounds are heard on auscultation, the pt is given a high-calorie, high-protein, high-fiber diet, w/ the amount of food gradually increased. - Nurse administers prescribed stool softeners to counteract the effects of immobility & analgesic agents. A bowel regimen is instituted asap.

Nursing Interventions: Maintaing Urinary Elimination

- Immediately after SCI, the urinary bladder may become atonic & is unable to contract by reflex activity. Urinary retention typically results. B/c the pt has no sensation of bladder distention, overstretching of the bladder & detrusor muscle may occur, delaying the return of bladder function. - Intermittent catheterization is carried out to avoid overdistention of the bladder & UTI. If this is not feasible, an indwelling cath is inserted temporarily - Pt is taught to record fluid intake, voiding pattern, characteristics of urine, & any unusual sensations that may occur.

Brain Injury (Box 45-3)

- Most important consideration in any head injury is whether or not the brain is injured. Even seemingly minor injury can cause significant brain damage secondary to obstructed blood flow & decreased tissue perfusion. - The brain cannot store O2 or glucose to any significant degree. B/c neurons need an uninterrupted blood supply to obtain these nutrients, irreversible brain damage & cell death occur if the blood supply is interrupted for even a few mins.

Nursing Interventions: Promoting Adaptation and Perceptual Alterations

- Nurse assists the pt to compensate for sensory & perceptual alterations that occur w/ SCI. The intact senses above the lvl of the injury are stimulated through touch, aromas, flavorful food & beverages, conversation, & music. - Additional strategies include the following: (1) Providing prism glasses to enable the pt to see from the supine position; (2) Encouraging use of hearing aids, if indicated, to enable the pt to hear conversations & environmental sounds; (3) Providing emotional support to the pt; (4) Teaching the pt strategies to compensate for or cope w/ these deficits

Nursing Interventions: Promoting Adequate Breathing & Airway Clearance

- O2 is administered to maintain a normal sat lvl b/c hypoxemia can create or worsen a neurologic deficit of the spinal cord. If endotracheal intubation is necessary, extreme care is taken to avoid flexing or extending the pt's neck, which can result in extension of a cervical injury. - Possible impending resp failure is detected by observing the pt, noting rate & depth of respirations, assessing lung sounds, accessory muscle use, monitoring O2 sat through pulse ox, & monitoring ABGs. Early & vigorous attn to clearing bronchial & pharyngeal secretions can prevent retention of secretions & atelectasis. Suctioning may be indicated, but caution must be used b/c this procedure can stimulate the vagus nerve, producing bradycardia, which can result in cardiac arrest. - If pt cannot cough effectively b/c of decreased inspiratory volume & inability to generate sufficient expiratory pressure, chest physical therapy & assisted coughing may be indicated.

Medical and Nursing Management: Monitoring and Managing Complications

- Potential complications for pt w/ altered LOC include resp failure, pneumonia, pressure ulcers, & aspiration. - Resp failure may develop shortly after the pt becomes unconscious. If pt cannot maintain effective respirations, insertion of an airway & mechanical ventilation is initiated to provide adequate ventilation & to protect the airway. - Pt w/ altered LOC is subject to all the complications a/w immobility, such as pressure ulcers, venous stasis, musculoskeletal deterioration, & disturbed GI functioning. - Aspiration of gastric contents or feedings may occur, precipitating the development of aspiration pneumonia or airway occlusion - Endocrine abnormalities, including diabetes insipidus & syndrome of inappropriate antidiuretic hormone (SIADH), are common complications of TBI. - Diabetes insipidus is the result of decreased secretion of antidiuretic hormone (ADH). Pt has excessive urine output, decreased urine osmolality, & serum hyperosmolarity. Therapy consists of admin of fluids, electrolyte replacement, & vasopressin therapy. - SIADH is the result of increased secretion of ADH. Pt becomes volume-overloaded, urine output diminishes, & serum sodium concentration becomes dilute (<134 mEq/L). Treatment includes fluid restriction (typically <1 L/day), which is usually sufficient to correct the hyponatremia. Severe cases call for judicious admin of a 3% hypertonic saline solution. - Aggressive management may be required to correct hyponatremia as delaying treatment may result in irreversible brain damage. However, overcorrection of sodium lvl predisposes pt to central pontine myelinolysis, a disorder in which the white matter of the pons loses myelin (protective sheath surrounding nerves); this results in tetraplegia w/ cranial nerve deficits. To prevent this complication, nurse monitors results of sodium lvls (initially, may be ordered hourly), & the pt's response to hypertonic saline treatment. As a general guideline, the plasma sodium concentration should probably be raised by no more than 12 mEq during the 1st 24 hrs - B/c the unconscious pt's protective reflexes are impaired, the quality of nursing care provided literally may mean the difference b/w life & death. Nurse must assume responsibility for the pt until the basic reflexes (coughing, blinking, & swallowing) return & pt becomes conscious & oriented. Therefore, the major nursing goal is to compensate for the absence of these protective reflexes. - Potential complications: cerebral edema, high fever, alterations in BP & oxygenation, increased metabolic demand, & seizures. - Nurse must maintain oral hygiene, monitor for presence of pressure ulcers, avoid any complications a/w the eyes, monitor urinary output & bowel function, & assess nutritional status. - Nurse must always remember to be the pt's advocate, as an unconscious pt cannot advocate for him- or herself.

Monitoring and Managing Complications: Preserving Skin integrity

- Preventing skin breakdown requires continuing nursing assessment & intervention. Special attn is given to unconscious pts b/c they cannot respond to external stimuli. - Assessment includes a regular schedule of turning to avoid pressure, which can cause breakdown & necrosis of the skin. Turning also provides kinesthetic (sensation of movement), proprioceptive (awareness of position), & vestibular (equilibrium) stimulation. After turning, the pt is carefully repositioned to prevent ischemic necrosis over pressure areas.

Nursing Interventions: Improving Mobility

- Proper body alignment is maintained at all times. Pt is repositioned freq & is assisted out of bed as soon as the spinal column is stabilized. The feet are prone to footdrop; therefore, various types of splints are used to prevent it. When used, the splints are removed & reapplied every 2 hrs. Trochanter rolls, applied from the crest of the ileum to the midthigh of both legs, help prevent external rotation of the hip joints. - Pts w/ lesions above the midthoracic lvl have loss of sympathetic control of peripheral vasoconstrictor activity, leading to hypotension. These pts may tolerate changes in position poorly & require monitoring of BP when positions are changed. Usually, the pt is turned every 2 hrs by log rolling. The pt should not be turned unless the spine is stable & the provider has indicated that it is safe to do so. - Contractures develop rapidly w/ immobility & muscle paralysis. A joint that is immobilized too long becomes fixed as a result of contractures of the tendon & joint capsule. Atrophy of the extremities results from disuse. Contractures & other complications may be prevented by ROM exercises that help preserve joint motion & stimulate circulation. Passive ROM exercises should be implemented asap after injury.

Assessment and Diagnostic Findings (Box 45-6; Table 45-1 & 45-2)

- Pt w/ an altered LOC is at risk for alterations in every body sys. A complete assessment is performed, w/ particular attn to the neurologic sys. - The neurologic exam includes an eval of mental status, cranial nerve function, cerebellar function (balance & coordination), reflexes, & motor/sensory function. - LOC, a sensitive indicator of neurologic function, can be assessed based on the criteria in the Glasgow Coma Scale, which include eye opening (E), verbal response (V), & motor response (M). - A score of 13-15 is classified as mild TBI, 9-12 is moderate TBI, & 3-8 is severe TBI. - A score of 3 indicates severe impairment of neurologic function, deep coma, brain death, or pharmacologic inhibition of the neurologic response; a score of 8 or less typically indicates an unconscious pt; a score of 15 indicates a fully alert & oriented pt. - The pt's orientation to person, place, & time assesses verbal response. - Alertness is measured by the pt's ability to open the eyes spontaneously or in response to a vocal or noxious stimulus (pressure or pain). Pts w/ severe neurologic dysfunction cannot do this. - Motor response includes spontaneous, purposeful movement, movement only in response to painful stimuli, or abnormal posturing. - In addition to LOC, nurse monitors resp status, pupillary response, & vital signs on an ongoing basis. Body functions (circulation, respiration, elimination, fluid & electrolyte balance) are examined in a systematic & ongoing manner. - If pt is comatose & has localized signs such as abnormal pupillary & motor responses, it is assumed that neurologic disease is present until proven otherwise - If pt is comatose but pupillary light reflexes are preserved, a toxic or metabolic disorder is suspected.

Monitoring and Managing Complications: Maintaining Blood Pressure, Oxygenation, and Hyperventilation

- Pts w/ TBI may sustain a secondary insult if they become hypotensive or hypoxic. - A growing body of evidence shows harmful effects if the pt experiences hypotension & hypoxia - Recommended that SBP be maintained at >90 mm Hg & O2 sat maintained at >90% - Hyperventilation, which results in vasoconstriction, was previously used in pts w/ increased ICP. Recent research has demonstrated that hyperventilation may not be as beneficial as once thought. The reduction in PaCO2 may result in hypoxia, ischemia, & an increase in cerebral lactate lvls - Hyperventilation is an option for pts w/ ICP who are unresponsive to conventional therapies, but it should be used cautiously & should be avoided for the 1st 24 hrs following the initial injury

Monitoring and Managing Complications: Seizure Prophylaxis (Box 45-8)

- Pts w/ severe TBI are at risk for developing seizures. Seizures that develop after head injury are known as posttraumatic seizures (PTS) & are classified according to when they occur. Occur within 7 days of injury: early PTS; after 7 days after the injury: late PTS - There is evidence to support the use of prophylactic anticonvulsants only for early PTS. Not recommended that pts be started on seizure prophylaxis more than 1 wk after the injury if they have not had any seizures. - If pt develops late PTS, the seizures should be managed in the same way as new-onset seizures

Spinal Cord Injury (Box 45-1)

- Spinal cord injury is a major health problem. - Males account for 80% of SCI in a reported national database. Young ppl b/w the ages of 16-30 yrs account for more than half of the new SCIs each yr. - Most common cause of SCI is motor vehicle accidents, which account for 42% of SCI. Violence-related injuries account for 15%, w/ falls causing 26.7%, & sports-related injuries causing 7.6% of SCIs - The frequency of associated injuries & medical complications in SCI is high. The frequency w/ which these risk factors are a/w SCI serves to emphasize the importance of primary prevention. - Manifestations of SCI depend on the type & lvl of injury (box 45-10) - Incomplete spinal cord lesion: condition where there is preservation of the sensory or motor fibers, or both, below the lesion in the spinal cord - Complete spinal cord lesion: condition that involves total loss of sensation & voluntary muscle control below the lesion in the spinal cord

Medical and Nursing Management

- The 1st priority of treatment for the pt w/ altered LOC is to obtain & maintain a patent airway. - Pt may be orally or nasally intubated (unless basilar skull fx or facial trauma is suspected), or a tracheostomy may be performed. - Until the ability of the pt to breathe on his/her own is determined, a mechanical ventilator is used to maintain adequate oxygenation & ventilation. - The circulatory status (BP, HR) is monitored to ensure adequate perfusion to the body & brain. - An IV catheter is inserted to provide access for IV fluids & meds. - Increased ICP is a true emergency & must be treated promptly. Invasive monitoring of ICP is an important component of management. - Immediate management to relieve increased ICP requires decreasing cerebral edema, lowering the volume of CSF, & decreasing cerebral blood volume while maintaining cerebral perfusion. - These goals are accomplished by administering osmotic diuretics, restricting fluids, draining CSF, controlling fever, maintaining systemic BP & oxygenation, & reducing cellular metabolic demands. - Corticosteroids are not recommended in cases of increased ICP resulting from TBI

Monitoring and Managing Complications: Preventing Urinary Retention

- The bladder is palpated or scanned at intervals to determine whether urinary retention is present - If pt is not voiding, an indwelling urinary cath is inserted. A catheter may also be inserted during the acute phase of illness to monitor urinary output. - The urinary catheter is usually removed if the pt has a stable cardiovascular sys & if no diuresis, sepsis, or voiding dysfunction existed before the onset of coma. - An intermittent catheterization program may be initiated to ensure complete emptying of the bladder at intervals, if indicated

Nursing Process: The Patient With Acute Spinal Cord Injury (Assessment)

- The breathing pattern is observed, the strength of the cough is assessed, & the lungs are auscultated b/c paralysis of abdominal & resp muscles diminishes coughing & makes clearing of bronchial & pharyngeal secretions difficult. - Pt is monitored closely for any changes in motor or sensory function & for sx of progressive neurologic damage. Motor & sensory functions are assessed through careful neurologic exam. - Pt is also assessed for spinal shock, urinary retention, overdistention of the bladder, & paralytic ileus.

Monitoring and Managing Acute Complications of Spinal Cord Injury: Spinal and Neurogenic Shock

- The spinal shock a/w SCI reflects a sudden depression of reflex activity in the spinal cord (areflexia) below the lvl of injury. - The muscles innervated by the part of the spinal cord segment below the lvl of the lesion are w/o sensation, paralyzed, & flaccid. In particular, the reflexes that initiate bladder & bowel function are affected. - Bowel distention & paralytic ileus can be caused by depression of the reflexes & are treated w/ intestinal decompression by insertion of a NG tube - Neurogenic shock develops due to the loss of ANS function below the lvl of the lesion. The vital organs are affected, causing the BP & HR to decrease. - This loss of sympathetic innervation causes a variety of other clinical manifestations, including a decrease in CO, venous pooling in the extremities, & peripheral vasodilation resulting in mild hypotension, bradycardia, & warm skin. - In addition, the pt does not perspire on the paralyzed portions of the body b/c sympathetic activity is blocked; therefore, close observation is required for early detection of an abrupt onset of fever.

Monitoring and Managing Acute Complications of Spinal Cord Injury: Deep Vein Thrombosis

- Thrombophlebitis, inflammation of a vein r/t DVT is a relatively common potential complication of immobility & is common in pts w/ SCI - DVT occurs in a high %age (67% to 100%) of SCI pts, placing them at risk for PE. Pt must be assessed for sx both of DVT & PE. A low-grade fever may be the first sign of DVT. - Manifestations of PE include pleuritic chest pain, anxiety, & SOB - Thigh & calf measurements should be made daily. Pt is evaluated for the presence of DVT if the circumference of 1 extremity increases significantly. - Diagnostic studies used to detect DVT & PE include Doppler ultrasound, radiocontrast venography, & ventilation/perfusion lung scans - Anticoagulation therapy to prevent DVT & PE is initiated once head injury & other systemic injuries have been ruled out & there is low risk for bleeding. This may be followed by LT oral anticoagulation w/ a vit K antagonist (i.e., warfarin) or subq fractionated heparin injections - For thromboembolism, low-molecular-weight heparin was shown to be more effective at preventing DVT & had fewer bleeding complications than fractionated heparin. However, both are equally effective at preventing PE - Anticoagulant therapy should be continued for at least 6-12 wks after injury. - Nonpharmacologic measures, including elastic compression stockings as well as ROM exercises, are important preventive measures that work to reduce venous pooling & promote venous return.

Monitoring and Managing Complications: Preserving Corneal Integrity

- Unconscious pts may have their eyes open & have inadequate or absent corneal reflexes. The cornea may become irritated, dried out, or scratched, leading to ulceration. The eyes may be cleansed w/ cotton balls moistened w/ sterile NS to remove debris & discharge. If artificial tears are prescribed, they may be instilled every 2 hrs. - Periorbital edema often occurs after cranial surgery. Cold compresses may be prescribed, & care must be exerted to avoid contact w/ the cornea. Eye patches should be used cautiously b/c of the potential for corneal abrasion from contact w/ the patch.

Monitoring Intracranial Pressure: Detecting Later Indications of Increasing ICP

As ICP increases, the pt's condition worsens & the following s/s may be observed: - LOC continues to deteriorate until the pt is comatose. - RR decreases or becomes erratic, BP & temp increase. Pulse pressure widens & the pulse fluctuates rapidly, varying from bradycardia to tachycardia. - Altered resp patterns develop, including Cheyne-Stokes breathing (rhythmic waxing & waning of rate & depth alternating w/ brief periods of apnea) & ataxic breathing (irregular breathing w/ a random sequence of deep & shallow breaths). - Projectile vomiting may occur w/ increased pressure on the reflex center in the medulla. - Hemiplegia or decorticate or decerebrate posturing may develop as pressure on the brainstem increases; bilateral flaccidity occurs before death. - Loss of brainstem reflexes, including pupillary, corneal, gag, & swallowing reflexes, which is an ominous sign of impending death.

Monitoring Intracranial Pressure: Detecting Early Indications of Increasing ICP

Nurse assesses for & immediately reports any of the following early s/s of increasing ICP: - Disorientation, restlessness, increased resp effort, purposeless movements, & mental confusion; these are early clinical indications of increasing ICP b/c the brain cells responsible for cognition are extremely sensitive to decreased oxygenation. - Pupillary changes & impaired EOMs; these occur as the increasing pressure displaces the brain against the optic & oculomotor nerves (cranial nerves II, III, IV, & VI), which arise from the midbrain & brainstem - Weakness in 1 extremity or on 1 side of the body; this occurs as increasing ICP compresses the pyramidal tracts, which control motor function. - HA that is constant, increasing in intensity, & aggravated by movement or straining; this occurs as increasing ICP causes pressure & stretching of venous & arterial vessels in the base of the brain. *** The earliest sign of increasing ICP is a changes in LOC. Any changes in LOC should be reported immediately

Monitoring and Managing Acute Complications of Spinal Cord Injury: Autonomic Dysreflexia Cont'd

The following measures are carried out: (1) HOB is raised, & pt is placed immediately in a sitting position to lower BP; (2) Rapid assessment is performed to identify & alleviate the cause; (3) The bladder is emptied immediately via a urinary cath; (4) Rectum is examined for a fecal mass. If present the mass is removed b/c visceral distention or contraction can worsen autonomic dysreflexia. Nurse observes for sx of flushing, sweating, nasal congestion, & HA while performing a digital exam & ceases procedure if sx appear & assesses BP; (5) Skin is examined for any areas of pressure, irritation, or broken skin; (6) Any other stimulus that could be the triggering event, such as an object next to the skin or a draft of cold air, must be removed; (7) If these measures do not relieve the htn & excruciating HA, a ganglionic blocking agent (hydralazine hydrochloride) is prescribed & admin slowly by the IV route; (8) Medical record or chart is labeled w/ a clearly visible note about the risk for autonomic dysreflexia; (9) Pt is instructed about prevention & management measures.