Week 9: Intracranial Pressure & Acute Head Injury

What are the 3 essential components of the skull?
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What are the 3 essential components of the skull?
-brain tissue
-blood
-cerebrospinal fluid (CSF)
Image: What are the 3 essential components of the skull?
What is the function of CSF in the skull and how much is normal?
cushions and protects the brain
normal= 80-200 mL
Name the function of these brain components:
1. Cerebrum
2. Corpus Collosum
3. Ventricles
4. Thalamus
5. Midbrain
6. Cerebellum
7. Brain Stem
8. Hypothalamus
9. Pituitary Gland
10. Pons
11. Medulla

Need to know?
1. Cerebrum: controls senses, thoughts, movements (occipital, temporal, frontal, parietal lobes)
2. Corpus Collosum: integrates motor, sensory, cognitive performances between cerebral cortex on one side of the brain to the other side
3. Ventricles: network of cavities filled with CSF
4. Thalamus: gray matter; relays sensory and motor signals to the cerebral cortex; regulates consciousness, sleep, and alertness
5. Midbrain: movements of the eye and in auditory and visual processing
6. Cerebellum: receives information from the sensory systems, the spinal cord, and other parts of the brain and then regulates motor movements; coordinates voluntary movements such as posture, balance, coordination, and speech, resulting in smooth and balanced muscular activity
7. Brain Stem: controls messages between brain and rest of body; controls breathing/swallowing/HR/BP/consciousness/ wakefullness
8. Hypothalamus: links nervous system to the endocrine system; temperature regulation; thirst; hunger; sleep; mood; sex drive; release of hormones
9. Pituitary Gland: produces and releases adrenocorticotropic hormones which stimulates the adrenal glands to secrete steroid hormones, principally cortisol. growth hormone, which regulates growth, metabolism and body composition.
10. Pons: sleep; respiration; swallowing; bladder control; hearing; equilibrium; taste; eye movement; facial expression/sensation; posture
11. Medulla: automatic functions (breathing/BP/circulation/heart functions/digestion; reflexes)
Image: Name the function of these brain components: 1. Cerebrum 2. Corpus Collosum 3. Ventricles 4. Thalamus 5. Midbrain 6. Cerebellum 7. Brain Stem 8. Hypothalamus 9. Pituitary Gland 10. Pons 11. Medulla Need to know?
What are factors that influence ICP (6)?
-arterial pressure (high BP= high ICP)
-venous pressure
-intraabdominal and intrathoracic pressure
-posture (trendelenburg=high ICP)
-temperature
-blood gases (high CO2=dilation of vasculature)
What is the first clinical manifestation of problems with ICP?
level of consciousness (LOC)
The _________________ doctrine states that the three components must remain at a relatively constant volume within the closed skull structure. If the volume of any one of the three components increases within the cranial vault and the volume from another component is displaced, the total intracranial volume will not change.
Monro-Kellie
Image: The _________________ doctrine states that the three components must remain at a relatively constant volume within the closed skull structure. If the volume of any one of the three components increases within the cranial vault and the volume from another component is displaced, the total intracranial volume will not change.
In what circumstances is the monro-kellie doctrine hypothesis not applicable?
-if there is a drain in the brain
-if a person has a displaced skull fracture or hemicranectomy

*This hypothesis is only applicable in situations in which the skull is closed.
Where can ICP be measured in the brain?
ventricles, subarachnoid space, subdural space, epidural space, or brain tissue using a pressure transducer.
What is normal ICP?
5-15 mmHg

*sustained pressure >20 mmHg is considered abnormal and must be treated
What are normal compensatory mechanisms for IICP?
First, compensatory mechanisms can include changes in the CSF volume. The CSF volume can be changed by altering CSF absorption or production and by displacement of CSF into the spinal subarachnoid space.

Second, changes in intracranial blood volume can occur through the collapse of cerebral veins and dural sinuses, regional cerebral vasoconstriction or dilation, and changes in venous outflow.

Third, tissue brain volume compensates through distention of the dura or compression of brain tissue.
True or False: The ability to compensate for IICP becomes limited if volume increase continues and ICP rises.true *Initially an increase in volume produces no increase in ICP as a result of these compensatory mechanisms. However, the ability to compensate for changes in volume is limited. As the volume increase continues, the ICP rises, and decompensation ultimately occurs, resulting in compression and ischemia. *Changes that occur slowly produce less of an effect on ICP than those that are rapid. These can be recognized clinically in some patients who present, for instance with large meningiomas and minimally elevated or normal ICP.What is the definition of cerebral blood flow?the amount of blood (in mL) that passes through 100g of brain tissue in 1 minuteWhat is normal cerebral blood flow?50mL/min per 100g of brain tissueWhy is the maintenance of blood flow to the brain critical?The maintenance of blood flow to the brain is critical because the brain requires a constant supply of oxygen and glucose. *The brain uses 20% of the body's oxygen and 25% of its glucose.A lack of blood flow to the brain results in _____________.anoxia (lack of oxygen and hypoglycemia)What must the MAP be for effective autoregulation of cerebral blood flow?70-150 mmHg Below 70mmHg, CBF decreases, and symptoms of cerebral ischemia, such as syncope and blurred vision, occur. When 150mmHg is exceeded, the vessels are maximally constricted, and further vasoconstrictor response is lostThe brain autoregulates cerebral blood flow. What does this mean?-adjusts the diameter of blood vessels -ensures consistent cerebral blood flow -The brain has the ability to regulate its own blood flow in response to its metabolic needs despite wide fluctuations in systemic arterial pressure. -is the automatic adjustment in the diameter of the cerebral blood vessels by the brain to maintain a constant blood flow during changes in arterial blood pressure (BP).If high SBP, the cerebral arterioles will _____________.constrictsIf low SBP, the cerebral arterioles will _____________.dilate *to get more blood flowWhat is the purpose of autoregulation of cerebral blood flow?The purpose of autoregulation is to ensure a consistent CBF to provide for the metabolic needs of brain tissue and to maintain cerebral perfusion pressure within normal limits. *Normally, autoregulation maintains an adequate CBF and perfusion pressure primarily by adjusting the diameter of cerebral blood vessels and metabolic factors that affect ICP. It is critical to maintain MAP when ICP is elevated.How is cerebral perfusion pressure (CPP) calculated?CPP = MAP - ICP *This formula is clinically useful, although it does not consider the effect of cerebral vascular resistance. Cerebral vascular resistance, generated by the arterioles within the cranium, links CPP and blood flow as follows: CPP = Flow x Resistance.What is a normal range for cerebral perfusion pressure (CPP)? normal range if in treatment?Normal: 60-100 mmHg Rx Goal: 70-80 mmHg *the pressure needed to ensure blood flow to the brain.What is a cerebral perfusion pressure of <50 indicative of? <30?<50: ischemia and neuronal death <30: ischemia and incompatible with life *as CPP decreases, autoregulation fails and cerebral blood flow decreasesWhat is the effect of cerebral vascular resistance?CPP = flow x resistance *When cerebral vascular resistance is high, blood flow to brain tissue is impaired.What is compliance in the brain? What does compliance impact?-the expandability of the brain -impacts the effect of volume change on pressure -compliance = volume/pressureExplain the pressure-volume curve of cerebral blood flow as it relates to brain compliance-Compliance is represented as the volume increase for each unit increase in pressure. -With low compliance, small changes in volume result in greater increases in pressure. Stage 1: -high compliance; increase in volume does not increase ICP Stage 2: -compliance decreases; increases in volume places patient at risk of increased ICP and secondary injury Stage 3: -significant reduction in compliance; any addition of volume causes a great increase in ICP Stage 4: -ICP rises to lethal levels with little increase in volumeWhat are the stages of increased ICP?Stage 1: total compensation; autoregulation intact Stage 2: decreased compensation; risk for IICP Stage 3: failing compensation; loss of autoregulation; clinical manifestations of IICP (cushing triad; HA; chx in LOC; increased SBP) Stage 4: herniation imminent (shift of brain tissue from compartment of greater pressure to lesser pressure; pressure on brainstem) --> deathWhat are factors that affect cerebral blood vessel tone?CO2 (high=dilation, decreased cerebrovascular resistance, increased cerebral blood flow; goal is 35-45) O2 (low <50mmHg=dilation, decreased cerebrovascular resistance, increased cerebral blood flow, increased O2 tension) H+ concentration (increased concentration = vasodilation in attempt to increase blood flow) * if O2 tension is not increased, anaerobic metabolism begins, resulting in an accumulation of lactic acid.True or False The combination of a severely low partial pressure of oxygen in arterial blood (PaO2) and an elevated hydrogen ion concentration (acidosis), which are both potent cerebral vasodilators, may produce a state where autoregulation is lost and compensatory mechanisms fail to meet tissue metabolic demands.trueWhat is increased ICP caused by?increase in any component--brain tissue, CSF, blood volume-- due to a mass like a hematoma/contusion/abscess/tumor or cerebral edema associated with tumors/hydrocephalus/head injury/brain inflammation *life threatening *diminishes cerebral perfusion pressure *may result in hypercapnia, cerebral acidosis, impaired autoregulation, systemic HTN *increased cerebral edema and risk of brain ischemia/infarctionPathophysiology of increased intracranial pressure?1- insult to brain 2- tissue edema 3- increased ICP 4- compression of ventricles and blood vessels 5-decreased cerebral blood flow 6- decreased O2 with death of brain cells 7-edema around necrotic tissues 8- accumulation of CO2 9- vasodilation 10- increased ICP due to increased blood volume 11- death *Cerebral edema distorts brain tissue, further increasing the ICP, and leads to even more tissue hypoxia and acidosis. *It is critical to maintain CBF to preserve tissue and thus minimize secondary injury. Sustained increases in ICP result in brainstem compression and herniation of the brain from one compartment to another. *Displacement and herniation of brain tissue can cause a potentially reversible process to become irreversible. Ischemia and edema are further increased, compounding the preexisting problem.What is brain herniation?shift of brain tissue from a compartment of high pressure to a compartment of lower pressure which potentially causes: -compression of the brainstem and cranial nerves -forces cerebellum and brainstem downward thru the foramen magnum *if compression of brainstem is unrelieved, respiratory arrest will occur b/c of compression of the respiratory control center in the medullaWhat is cerebral edema?increased accumulation of fluid in the extravascular spaces of brain tissueThere are a variety of causes of cerebral edema (such as mass lesions, head injuries, cerebral infection, vascular insult, and toxic or metabolic encephalopathy). Regardless of the cause, what does cerebral edema result in?-increase in tissue volume that can increase ICP *The extent and severity of the original insult are factors that determine the degree of cerebral edema.What are the clinical manifestations of increasing ICP?#1: change in level of consciousness (flattening of affect --> coma) #2: change in vital signs (cushing's triad; change in body temp) #3: ocular signs Other: decreased motor functioning, headache, vomitingTrue or False Level of consciousness is the most sensitive and reliable indicator of the patient's neurologic status.True *Changes in LOC are a result of impaired CBF, which deprives the cells of the cerebral cortex and the reticular activating system of oxygen.What is cushing's triad?widening pulse pressure bradycardia bounding pulses irregular respirations (cheyne-stokes breathing) *a neurologic emergency; manifestations like Cushing's triad may be present but often do not appear until ICP has been increased for some time or is suddenly markedly increased (e.g., head trauma). *Always recognize Cushing's triad as a medical emergency as this is a sign of brainstem compression and impending death.What are possible treatment options for cushing's triad?-administration of mannitol -hyperventilation -elevation of HOB (reverse trendelenburg; HOB at 30) -decrease stimulationWhat is cushing's reflex (different from cushing's triad)?-hypothalamic response to brain ischemia where the SNS is activated causing: 1) increased peripheral vascular resistance and 2) increased BP; 3) activation of the parasympathetic nervous system via carotid artery baroceptors; 4) vagal-induced bradycardia -brain ischemia usually caused by poor perfusion resulting from IICP due to head bleeds or mass lesions -Cushing reflex leads to clinical manifestations of cushings triadWhy is there a change in body temperature in IICP?-usually increased body temp due to compression of the hypothalamusWhat causes ocular changes in IICP?-Compression of cranial nerve (CN) III, the oculomotor nerve. -Results in: 1) dilation of the pupil on the same side as or ipsilateral to the mass lesion 2) sluggish or no response to light 3) inability to move the eye upward 4) ptosis of the eyelid. *These signs can be the result of a shifting of the brain from the midline, compressing the trunk of CN III and paralyzing the muscles controlling pupillary size and shape. In this situation, a fixed, unilateral, dilated pupil is considered a neurologic emergency that indicates herniation of the brain.What other cranial nerves may be affected with IICP?The optic (CN II), trochlear (CN IV), and abducens (CN VI) nerves. Signs of dysfunction of these cranial nerves include blurred vision, diplopia (double vision), and changes in extraocular eye movements. Papilledema (an edematous optic disc seen on retinal examination) is also noted and is a nonspecific sign associated with persistent increases in ICP. *Central herniation may initially manifest as sluggish but equal pupil response. Uncal herniation may cause a dilated unilateral pupil.What decreases in motor functioning are clinical manifestations of IICP?-hemiparesis/hemiplegia -decorticate posturing (flexor; less serious) -deceberate posturing (extensor; more serious)What is decorticate posturing?-"towards the core"; flexor; less serious -flexion of arms, wrists and fingers -adduction of upper extremities -extension, internal rotation, and plantar flexion in lower extremities Decorticate posture consists of internal rotation and adduction of the arms with flexion of the elbows, wrists, and fingers as a result of interruption of voluntary motor tracts in the cerebral cortex. Extension of the legs may also be seen.What is deceberate posturing?-all 4 extremities in rigid extension; extensor -more serious -hyperpronation of forearms and plantar flexion of feet A decerebrate posture may indicate more serious damage and results from disruption of motor fibers in the midbrain and brainstem. In this position, the arms are stiffly extended, adducted, and hyperpronated. There is also hyperextension of the legs with plantar flexion of the feet.Why are headache and vomiting signs of IICP?Although the brain itself is insensitive to pain, compression of other intracranial structures, such as the walls of arteries and veins and the cranial nerves, can produce headache. -The headache is often continuous but worse in the morning. -Straining, agitation, or movement may accentuate the pain. Vomiting, usually not preceded by nausea, is often a nonspecific sign of increased ICP. -This is called unexpected vomiting and is related to pressure changes in the cranium. -Projectile vomiting may also occur and is related to increased ICP.What are the major complications of uncontrolled increased ICP?-inadequate cerebral perfusion -cerebral herniationWhat are the types of cerebral herniation?-tentorial herniation (upward/downward; not survivable) -uncal/tonsillar herniation (upward/downward; not survivable) -cingulate herniation (lateral; survivable) *To better understand cerebral herniation, two important structures in the brain must be described. The falx cerebri is a thin wall of dura that folds down between the cortex, separating the two cerebral hemispheres. The tentorium cerebelli is a rigid fold of dura that separates the cerebral hemispheres from the cerebellum. It is called the tentorium (meaning tent) because it forms a tentlike cover over the cerebellum.What is tentorial herniation?-central herniation -occurs when a mass lesion in the cerebrum forces the brain to herniate downward thru the opening created by the brainstem -usually not survivableWhat is uncal/tonsillar herniation?lateral and downward herniation -usually not survivable -Uncal: compresses CN II at base of midbrain -Tonsillar: damages respiratory control centers in lower medulla; herniates into brainstem thru foramen magnumWhat is cingulate herniation?lateral displacement of brain tissue beneath the falx cerebri -survivable -compresses anterior cerebral artery (cingulate gyrus under falx cerebri)brain herniation pictureWhat are diagnostic studies done for someone with IICP?CT Scan MRI PET Scan EEG (look for seizure and brain activity) Cerebral Angiography (if related to vasculature; hemorrhagic stroke or brain aneurysm dx) ICP and brain tissue oxygenation measurement (LICOX) Doppler and evoked potential studiesWhy should you not perform a lumbar puncture on a person with IICP?-risk for herniation due to even further increased pressureTrue or False The measurement of ICP guides clinical care.trueWhat are indications for ICP measurement?-Glasgow Coma Scale of </= 8 -Abnormal CT scans or MRI -Patients with evidence of altered cerebral tissue perfusion, have a normal CT, but have 2 of the following: over 40; unilateral or bilateral motor posturing; SBP <90 mmHgWhat are the 3 categories in the glasgow coma scale and what are the ratings within the categories?1) Eye Opening Response (4-spontaneously; 3-to speech; 2- to pain; 1- no response) 2) Best Verbal Response (5- oriented to time/place/person; 4- confused; 3- inappropriate words; 2-incomprehensible sounds; 1-no response) 3) Best Motor Response (6-obeys commands; 5-moves to localized pain; 4-flexion withdrawal from pain; 3-abnormal flexion, decorticate; 2-abnormal extension, decebrate; 1-no response) 15: best response <8: comatose client 3: totally unresponsive; not compatible with lifeGlasgow coma scale chartWhat are potential placements of ICP monitoring devices? (picture)-ventricular device (gold standard): monitor CSF & you can drain CSF if neededWhat is a ventriculostomy type of measurement of ICP?-catheter placed into lateral ventricle -coupled with an external transducer and drainage system (intermittent or continuous drainage; careful monitoring of volume of CSF drained is essential) -gold standard for monitoring ICP -This technique directly measures the pressure within the ventricles, facilitates removal and/or sampling of CSF, and allows for intraventricular drug administration. -CSF can be drained via a ventriculostomy when ICP exceeds the upper pressure parameter set by the physician. Intermittent drainage involves opening the three-way stopcock to allow CSF to flow into the drainage bag for brief periods (30 to 120 seconds) until the pressure is below the upper pressure parameters. ICP, Intracranial pressure. -risk for infection, leakage, etc.How do you level a ventriculostomy?-level the ventriculostomy to the level of the tragus (the foramen magnum) -keep a bit above the tragus -if device dropped- a lot of CSF would leak out and pressures would dropWhat are other ways you can measure ICP: fiberoptic catheter? subarachnoid bolt/screw?Fiberoptic Catheter: sensory transducer located within the catheter tip Subarachnoid Bolt/Screw: between arachnoid membrane and cerebral cortexWhat are important considerations when measuring ICP?-prevent and monitor for infection -measure as mean pressure -waveform should be recorded (normal, elevated, and plateau waves) -evaluate changes with the patient's condition -aseptic technique with dressing changes of ICP measurement devices or sampling of CSFWhat are inaccurate ICP readings potentially caused by?-CSF leaks -Obstruction in catheter/kinks in tubing -Differences in height of bolt/transducer -Incorrect height of drainage system -Bubbles/air in tubingComplications of ventricular catheter ICP measurement/monitoring?ventricular collapse, infection, and herniation or subdural hematoma formation from rapid decompression.What does a LICOX cathether and Jugular venous bulb catheter measure?measures brain oxygenation (PbtO2), temperature & intracranial pressureWhat is done in the collaborative care of a person with IICP?-treat the underlying cause (usually an increase in blood due to hemorrhage, brain tissue expansion due to a tumor or edema, or extra CSF from hydrocephalus in the brain) -early identification and treatment -adequate oxygenation (PaO2 >100mmHg; PaCo2 35-45mmHg; intubation; mechanical ventilation; possible sedation) (ABGs guide oxygenation therapy)True or False: If increased ICP is caused by a mass lesion (e.g., tumor, hematoma), surgical removal of the mass is the best treatment (see the sections on brain tumors and cranial surgery later in this chapter). In aggressive situations, a craniectomy (removal of part of skull) may be performed to reduce ICP and prevent herniation.trueWhat are (8) potential drug therapies that could be used in the treatment of IICP?-mannitol (osmitrol) -hypertonic saline -corticosteroids -antiseizure medications (not needed if no seizure activity after 1st week) -antipyretics (Rx temperature dysregulation; fever increases metabolic demands) -sedatives (propofol; presedex; drug holiday to assess neuro status) -analgesics (pain) -barbiturates (coma induction)How does mannitol work to treat IICP? expected effects? nurse monitoring?-diuretic; causes plasma expansion; osmotic effect -expected effects: increased UOP -monitor: fluid and electrolyte statusHow does hypertonic saline work to treat IICP? nurse monitoring?-moves water out of cells and into blood/vasculature -monitor: BP; serum sodium levelsHow do corticosteroids help in the treatment of IICP? monitoring?-treats vasogenic/cerebral edema -monitor: fluid intake, serum sodium, glucose levels -concurrent antacids. H2 receptor blockers, PPIsWhat nutritional therapy is suggested for those with IICP?-hypermetabolic and hypercatabolic state increases needs for glucose -enteral or parenteral nutrition -early feeding (within 3 days of injury) -keep patient normovolemic -IV 0.9% NaCl preferred (to D5W or 0.45% NaCl)What is the nursing assessment done for a person with IICP? (subjective data)-LOC (use glasgow coma scale) -Pupillary check (for size, movement, reactivity, shape, response) -Cranial Nerve Assessment (eye movements, corneal reflex, oculocephalic reflex, oculovestibular) -Vital Signs (cushing's triad) -Motor strength (squeeze hands, palmar drift test, raise foot off bed or bend knees) -Motor response (spontaneous or to pain)Discuss pupil reactivity/dilation and what injury that may indicate: -dilated pupil on one side -bilaterally dilated pupils -pinpoint pupilscompressed cranial nerve III-dilated pupil on one side ominous sign-bilaterally dilated pupils pons damage or drugs-pinpoint pupilsTrue or False If the oculomotor nerve [CN III] is compressed, the pupil on the affected side (ipsilateral) becomes larger until it fully dilates. If ICP continues to increase, both pupils dilate.true *Test pupillary reaction with a penlight. The normal reaction is brisk constriction when the light is shone directly into the eye. Also note a consensual response (a slight constriction in the opposite pupil) at the same time. A sluggish reaction can indicate early pressure on CN III (oculomotor nerve). *A fixed pupil unresponsive to light stimulus usually indicates increased ICP. However, it is important to note that there are other causes of a fixed pupil, including direct injury to CN III, previous eye surgery, administration of atropine, and use of mydriatic eyedrops.)--What eye cranial nerves are assessed for a patient with IICP?1) Eye movements controlled by cranial nerves III, IV, and VI can be examined in the patient who is awake and able to follow commands and can be used to assess the function of the brainstem. 2) Testing the corneal reflex gives information about the functioning of cranial nerves V and VII. If this reflex is absent, initiate routine eye care to prevent corneal abrasion. 3) Eye movements of the uncooperative or unconscious patient can be elicited by reflex with the use of head movements (oculocephalic/doll's eye reflex) and caloric stimulation (oculovestibular/caloric stimulation).How do you test the oculocephalic reflex?To test the oculocephalic reflex (doll's-eye reflex), turn the patient's head briskly to the left or right while holding the eyelids open. A normal response is movement of the eyes across the midline in the direction opposite that of the turning. Next, quickly flex and then extend the neck. Eye movement should be opposite to the direction of head movement—up when the neck is flexed and down when it is extended. Abnormal responses can help locate the intracranial lesion. This test should not be attempted if a cervical spine problem is suspected.How can you test motor strength in a person with IICP?-Test motor strength by asking the awake and cooperative patient to squeeze your hands to compare strength in the hands. -The palmar drift test is an excellent measure of strength in the upper extremities. The patient raises the arms in front of the body with the palmar surface facing upward. If there is any weakness in the upper extremity, the palmar surface turns downward, and the arm drifts downward. -Asking the patient to raise the foot from the bed or to bend the knees up in bed is a good assessment of lower extremity strength. Test all four extremities for strength and evaluate for any asymmetry in strength or movement. -Assess the motor response of the unconscious or uncooperative patient by observation of spontaneous movement. If no spontaneous movement is possible, apply a pain stimulus to the patient and note the response. -Resistance to movement during passive range-of-motion exercises is another measure of strength. Do not include hand squeezing as part of the assessment of motor movement in the unconscious or uncooperative patient, as this is a reflex action and can provide a misrepresentation of the patient's status.What are abnormal respiratory patterns of coma?Nursing diagnoses for a patient with IICP?-Decreased intracranial adaptive capacity related to decreased cerebral perfusion or increased ICP -Risk for ineffective cerebral tissue perfusion related to reduction of venous and/or arterial blood flow and cerebral edema -Risk for disuse syndrome related to altered level of consciousness, immobility, and altered nutritional intakeWhat are nursing goals for a patient with IICP?-maintain a patent airway -maintain CPP and ICP within normal limits -normal fluid and electrolyte balance -prevent complications secondary to immobility and decreased LOCWhat are nursing interventions in respiratory functioning for a patient with IICP?-maintain patent airway -elevate HOB 30 degrees -suctioning needs -minimize abdominal distention -monitor ABGs -maintain ventilatory supportWhat are nursing interventions in pain and anxiety management for a patient with IICP?-opioids (morphine sulfate and fentanyl have minimal effect on CBF or oxygen metabolism) -propofol (treatment of anxiety and agitation; rapid onset and short half-life; An accurate neurologic assessment can be performed very soon after turning off the infusion of propofol. A side effect of this drug is hypotension.) -dexmedetomidine (precedex) (alpha 2 adrenergic agonist; continuous IV sedation for the intubated and mechanically ventilated patients for up to 24 hours; easy to obtain a neuro assessment without altering dose due to anxiolytic properties; side effects=hypotension; lower CPP) -neuromuscular blocking agents (ex: vecuronium, cisatracurium besylate) (must combine with sedation or benzos) (complete ventilatory control in the treatment of refractory intracranial HTN) -benzodiazepines (sedation; usually avoided in IICP treatment due to hypotensive effect and long half-life) *Pain, anxiety, and fear from the primary injury, therapeutic procedures, or noxious stimuli can increase ICP and BP, thus complicating the management and recovery of the brain-injured patient. *It may be necessary to temporarily suspend drug therapy to appropriately assess neurologic status.What are nursing interventions in fluid and electrolyte balance management for a patient with IICP?1) monitor IV fluids 2) monitor I&Os 3) daily electrolytes (glucose, Na, K, Mg, osmolality) 4) monitor for DI or SIADH (measure specific gravity of urine to see if too much or not enough UOP, based on increased ADH or decreased ADH) (Diabetes insipidus is caused by a decrease in antidiuretic hormone (ADH). It results in increased urinary output and hypernatremia. The usual treatment of diabetes insipidus is fluid replacement, vasopressin (Pitressin), or desmopressin acetate (DDAVP) (see Chapter 50). If not treated, severe dehydration will occur. SIADH is caused by an excess secretion of ADH. SIADH results in decreased urinary output and dilutional hyponatremia. It may result in cerebral edema, changes in LOC, seizures, and coma.) 5) monitor and minimize increases in ICPTrue or False Valsalva maneuver, coughing, sneezing, suctioning, hypoxemia, and arousal from sleep are factors that can increase ICP. Be alert to these factors and attempt to minimize them.trueWhat are nursing interventions to optimize ICP and CCP?-HOB elevated appropriately -Prevent extreme neck flexion -Turn slowly -Avoid coughing, straining, Valsalva (give stool softener) -Avoid hip flexion -space out nursing interventions to allow for restWhat are nursing interventions to prevent further injury from IICP?-minimize complications of immobility -protection from self-injury (judicious use of restraints; sedatives; seizure precautions; quiet/non-stimulating environment) -psychologic considerationsA patient with a head injury has an arterial BP of 92/50 mm Hg and ICP of 18 mm Hg. The nurse uses the assessments to calculate the cerebral perfusion pressure (CPP). How should the nurse interpret the results? The CPP is so low that brain death is imminent. The CPP is low, and the BP should be increased. The CPP is high, and the ICP should be reduced. The CPP is adequate for normal cerebral blood flow.The CPP is low, and the BP should be increased. (Goal on treatment CPP= 70-80 CPP= low)A patient with increased ICP is positioned in a lateral position with the head of the bed elevated 30 degrees. The nurse evaluates a need for lowering the head of the bed when the patient experiences ptosis of the eyelid. unexpected vomiting. a decrease in motor functions. decreasing level of consciousness.decreasing level of consciousness. (for more blood flow to the brain)What are causes of head injury?-any trauma to the: skull, scalp, brain -traumatic brain injury -high incidence of TBI and SCI -MVCs -falls -firearm related injuries -assaults -sports related injuries -recreational accidents -war related injuriesTrue or False: With a head injury, there is a high potential for poor outcomes.trueDeaths occur at three points in time after a head injury. What are they?Immediately after the injury Within 2 hours after the injury 3 weeks after the injury.What are the types of head injuries?1) Scalp Lacerations (external head trauma; scalp is highly vascular and leads to profuse bleeding; major complications are blood loss and infection) 2) Scalp Fractures (linear or depressed; simple/comminuted/compound; closed or open; location determines manifestation; major complications are infection, hematoma, and tissue damage) 3) Diffuse (large insult; anoxic) 4) Focal (localized) 5) Minor (GCS 13-15) 6) Moderate (GCS 9-12) 7) Severe (GCS 3-8; ICP measurement and mechanical ventilation needed for patient)What are the types of skull fractures?Linear fracture occurs when there is a break in continuity of bone without alteration of relationship of parts. It is associated with low-velocity injuries. A depressed skull fracture is an inward indentation of skull and is associated with a powerful blow. A simple linear or depressed skull fracture is without fragmentation or communicating lacerations. It is caused by low to moderate impact. A comminuted fracture occurs when there are multiple linear fractures with fragmentation of bone into many pieces. It is associated with direct, high-momentum impact. An example of a compound fracture is a depressed skull fracture and scalp laceration with communicating pathway to intracranial cavity. This is associated with severe head injury. Fractures may be closed or open, depending on the presence of a scalp laceration or extension of the fracture into the air sinuses or dura.What is a basilar skull fracture?a specialized type of linear fracture that occurs when the fracture involves the base of the skull. Manifestations can evolve over the course of several hours, vary with the location and severity of fracture, and may include cranial nerve deficits, Battle's sign (postauricular ecchymosis), and periorbital ecchymosis (raccoon eyes). -This fracture generally is associated with a tear in the dura and subsequent leakage of CSF. -Rhinorrhea (CSF leakage from the nose) or otorrhea (CSF leakage from the ear) generally confirms that the fracture has traversed the dura. Rhinorrhea may also manifest as postnasal sinus drainage. The significance of rhinorrhea may be overlooked unless the patient is specifically assessed for this finding. The risk of meningitis is high with a CSF leak, and antibiotics should be administered to prevent the development of meningitis. -Two methods of testing can be used to determine whether the fluid leaking from the nose or ear is CSF. The first method is to test the leaking fluid with a Dextrostix or Tes-Tape strip to determine whether glucose is present. CSF gives a positive reading for glucose. -If blood is present in the fluid, testing for the presence of glucose is unreliable because blood also contains glucose. In this event, look for the halo or ring sign. To perform this test, allow the leaking fluid to drip onto a white gauze pad (4 × 4) or towel, and then observe the drainage. Within a few minutes, the blood coalesces into the center, and a yellowish ring encircles the blood if CSF is present. -Note the color, appearance, and amount of leaking fluid because both tests can give false-positive results. -Classic injury; survivable -Causes issues with their sinuses causing rhinorrhea and otorrea (drainage of CSF from nose or ear) -If we know there is a break between brain and sinus; at high risk for infection -Would not want to put an NG tube in (would probably put in an OG tube insteadWhat is a common cause of a diffuse injury?Concussion (sudden, transient, mechanical injury with a brief disruption of neural activity and LOC; retrograde amnesia; headache; short duration; may result in post-concussion syndrome) -a sudden transient mechanical head injury with disruption of neural activity and a change in the LOC) is considered a minor diffuse head injury. The patient may or may not lose total consciousness with this injury. -Typical signs of concussion include a brief disruption in LOC, amnesia regarding the event (retrograde amnesia), and headache. The manifestations are generally of short duration. -If the patient has not lost consciousness, or if the loss of consciousness lasts less than 5 minutes, the patient is usually discharged from the care facility with instructions to notify the health care provider if symptoms persist or if behavioral changes are noted.What is post-concussion syndrome? s/sx?-persistent headache -lethargy -personality and behavior changes -shortened attention span, decreased short-term memory -changes in intellectual ability *can develop in some patients anywhere from 2 weeks-2months after the initial injury **At the time of discharge, it is important to give the patient and the caregiver instructions for observation and accurate reporting of symptoms or changes in neurologic status.What is a diffuse axonal injury, a type of head injury?-widespread axonal damage that causes: decreased LOC, IICP, decortication --> decerebration, global cerebral edema *90% fatal **The damage occurs primarily around axons in the subcortical white matter of the cerebral hemispheres, basal ganglia, thalamus, and brainstem. ***There is increasing evidence that axonal damage is not preceded by an immediate tearing of the axon from the traumatic impact, but rather the trauma changes the function of the axon, resulting in axon swelling and disconnection. ****This process takes approximately 12 to 24 hours to develop and may persist longer.What is a focal injury, a type of head injury?-laceration -contusion -hematoma -cranial nerve injuries *can be minor to severe and can be localized to an area of injuryWhat are lacerations, a type of focal head injury?-tearing of brain tissue -occurs with: depressed and open fractures and penetraing injuries; intracerebral hemorrhage; subarachnoid/intraventricular hemorrhage (secondary to head trauma) *tissue damage is severe and surgical repair of laceration is impossible due to nature of brain tissue **medical management consists of: abx (until meningitis is r/o) & preventing secondary injury related to IICP ***s/sx of intracerebral hemorrhage are unconsciousness, hemiplegia on contralateral side, dilated pupil on ipsilateral sideWhat is a contusion, a type of focal head injury?-bruising of the brain tissue; associated with a closed head injury -can cause hemorrhage, infarction, necrosis, and edema -can re-bleed (worsens neurological outcome) -focal and generalized manifestations -monitor for seizures -potential for increased hemorrhage if on anticoagulants (especially in the older population)What is the difference in a concussion and a contusion?Concussion -temporary loss of neuro function with NO structural damage lasting for a few seconds to a few minutes Contusion -more severe injury in which the brain is bruised, with possible surface hemorrhage -Unconscious for more than a few seconds or minutes -Similar to shockWhat is a coup-countrecoup injury?Damage from this injury occurs when the brain moves inside the skull due to a high-energy or high-impact injury mechanism Contusions or lacerations occur BOTH at the site of the direct impact of the brain on the skull (coup) and at a secondary area of damage on the opposite side away from the injury (contrecoup); leading to multiple contused areas Contrecoup injuries tend to be more severeWhat is an epidural hematoma, a type of focal head injury? s/sx?-bleeding between the dura and the inner surface of the skull -2 possible origins: venous origin slow; arterial origin rapid -S/sx: initial period of unconsciousness followed by a brief lucid interval followed by decreased LOC; HA; n/v; focal findings -Rx: requires rapid evacuation (surgery to evacuate the hematoma and prevent cerebral herniation); management fo IICP *neurologic emergency (usually associated with a linear fracture crossing a major artery in the dura, causing a tear)What is a subdural hematoma, a type of focal head injury?-bleeding between the dura mater and the arachnoid layer of the meninges -most common source are the veins that drain the brain surface into the sagittal sinus (can be arterial though)What is an acute subdural hematoma?-develops within 24-48 hours after the injury -s/sx: similar to those associated with brain tissue compression in IICP and include decreasing LOC; HA; ipsilateral pupil dilated and fixed if ICP is significantly elevated (size of hematoma determine clinical presentation and prognosis) *Blunt force injuries that produce acute subdural hematomas also may cause significant underlying brain injury, resulting in cerebral edema. The resulting increase in ICP from the cerebral edema can cause increased morbidity and mortality risk despite surgical intervention to evacuate the hematoma.What is a subacute subdural hematoma?-develops within 2-14 days of the injury -may appear to enlarge over time, after the initial bleeding, as the breakdown of products of the blood draw fluid into the subdural spaceWhat is a chronic subdural hematoma?-develops weeks-months after the injury -more common in older adults (due to potentially larger subdural space as a result of brain atrophy; brain tension increased and subject to tearing) -presents with focal symptoms (due to larger size of the subdural space) -high risk for misdiagnosis (due to symptoms that mimic other health problems in this age group such as confusion, lethargy, and memory loss, or stroke symptoms)What is an intracerebral hematoma, a type of focal head injury?-bleeding within the brain tissue itself (usually within the frontal and temporal lobes) -size and location of hematoma determine patient outcomes -s/sx: no inhibitionsLocation of hematomas: pictureWhat diagnostic studies are done when head trauma/injury is suspected?-CT scan (best diagnostic test to determine craniocerebral trauma b/c it allows rapid diagnosis and intervention in acute care settings) -MRI, PET, evoked potential studies (used in diagnosis and differentiation of head injuries; MRI more sensitive than CT in detecting small lesions) -transcranial doppler studies (measures CBF velocity) -cervical spine x-ray (impt in acute head injury) -glasgow coma scaleWhat is the collaborative care and emergency treatment of a patient with a head injury?1) patent airway 2) stabilize cervical spine 3) oxygen (via non-rebreather mask) 4) IV access (2 large bore catheters for NS or LR) 5) intubate if GCS <8, or otherwise indicated 6) control external bleeding 7) remove patient's clothing Other: -ongoing monitoring (of vitals, LOC, O2 sat, cardiac rhythm, GCS, pupil size/reactivity, rhinorrhea, otorrhea, scalp wounds) -maintain patient warmth (with blankets, warm IV fluids, overhead warmers, warm humidified O2) -anticipate need for intubation if gag reflex impaired -assume neck injury with head injury administer fluids cautiously to prevent fluid overload and IICPWhat are the treatment principles for someone with a head injury?-prevent secondary injury (by treating cerebral edema and managing IICP) -timely diagnosis -surgery if necessaryWhat is done in the collaborative care of concussions and contusions?observation and management of ICPWhat is done in the collaborative care of skull fractures?conservative treatment; surgery if depressed *For depressed fractures and fractures with loose fragments, a craniotomy is necessary to elevate the depressed bone and remove the free fragments. If large amounts of bone are destroyed, the bone may be removed (craniectomy), and a cranioplasty will be needed at a later time.What is done in the collaborative care of subdural and epidural hematomas?surgical evacuation: -craniotomy (generally performed to visualize and allow control of the bleeding vessels) -burr-holes (may be used in an extreme emergency for a more rapid decompression, followed by a craniotomy; A drain may be placed postoperatively for several days to prevent reaccumulation of blood.) -craniectomy if there is extreme swelling (piece of skull is removed to reduce pressure inside cranial vault, reducing risk of herniation)What is done in the nursing assessment for a patient with a head injury: Subjective Data?-PMH (mechanism of injury) -Medications (anticoagulants?) -Health perception/management: Alcohol/drug use; Risk taking behaviors -Cognitive-perceptual: Headache; Mood or behavioral changes; mentation changes; impaired judgment; Aphasia or dysphagia -Coping-stress tolerance: Fear, denial, anger, aggression, depressionWhat is done in the nursing assessment for a patient with a head injury: Objective Data?-Altered mental status -Integumentary: lacerations, contusions, abrasions, hematoma, battle's sign, periorbital edema, ecchymosis, otorrhea, exposed brain -Respiratory: rhinorrhea (if fluid + for glucose, then it is CSF), impaired gag reflex, inability to maintain a patent airway; impending herniation, altered/irregular RR and pattern -Cardiovascular: impending herniation, cushing's triad -GI/GU: vomiting, bowel/bladder incontinence -Reproductive: uninhibited sexual expression -Neurologic: altered LOC, seizures, pupil dysfunction, cranial nerve deficits -Musculoskeletal: motor deficit/impairment, weakness, palmar drift, paralysis, spasticity, decorticate/deceberate posturing, muscular rigidity, increased tone, flaccidity, ataxia -Possible diagnostic findings: location and type of hematoma, edema, skull fracture, and/or foreign body on CT scan and/or MRI; abnormal EEG; positive toxicology screen or alcohol level, ↓ or ↑ blood glucose level; IICPWhat are nursing diagnosis for the patient with a head injury?-risk for ineffective cerebral tissue perfusion r/t interruption of CBF associated with cerebral hemorrhage, hematoma, and edema -hyperthermia r/t to increased metabolism, infection, and hypothalamic injury -impaired physical mobility r/t decreased LOC -anxiety r/t abrupt changes in health status, hospital environment, and uncertain future -potential complication of IICP r/t cerebral edema and hemorrhageWhat are overall nursing goals for the patient with a head injury?-maintain adequate cerebral oxygenation and perfusion -remain normothermic -achieve control of pain and discomfort -be free of injection -have adequate nutrition -attain maximal cognitive, motor, and sensory functionWhat are some nursing interventions for the patient with a head injury: Health Promotion?-prevent care and motorcycle accidents by promoting the use of helmets, seat belts, car seats -be active in campaigns that promote driving safety and speak to drive education classes regarding the dangers of unsafe driving and driving under the influence -home safety evaluation for those who are at risk for fallsWhat are some acute nursing interventions for the patient with a head injury: general? eye problems? hyperthermia?-maintain cerebral perfusion/oxygenation -prevent secondary cerebral ischemia -monitor for changes is neurologic status (GCS) -patient and family teaching (about changes in neuro status) -major focus of care relates to IICP -eye problems (loss of corneal reflex may necessitate administering lubricating eye drops or taping the eyes shut to prevent abrasion; periorbital ecchymosis and edema decrease with time but cold and warm compressions provide comfort and hasten the process; diplopia can be relieved by using an eye patch) -hyperthermia (due to injury of hypothalamus; avoid hyperthermia with goal of 36-37 degrees C; reduce temp with sedation as needed to prevent shivering)What are the dangers of hyperthermia in a patient with a head injury?Hyperthermia may occur from injury to or inflammation of the hypothalamus. Elevations in body temperature can result in increased CBF, cerebral blood volume, and ICP. Increased metabolism secondary to hyperthermia increases metabolic waste, which in turn produces further cerebral vasodilation.What are some acute nursing interventions for the patient with a head injury: measures for patients leaking CSF?-HOB elevated (to decreased CSF pressure so the tear can seal) -loose collection pad (under nose or ear) -no sneezing or blowing nose -no NG tube or nasotracheal suctioning (due to high risk of meningitis)What are some acute nursing interventions for the patient with a head injury: measures for immobilized patients?-Nursing measures specific to the care of the immobilized patient, such as those related to bladder and bowel function, skin care, and infection, are also indicated.What are some acute nursing interventions for the patient with a head injury: measures for nausea and vomiting? pain? surgery?-N/v: administer antiemetics -HA: administer acetaminophen or codeine -pain: analgesics -surgery: help prep with surgeon, witness consent (usually from family)What are some nursing interventions for the patient with a head injury: ambulatory and home care- acute rehabilitation?-May be chronic problems related to: motor and sensory deficits; communication issues; memory and intellectual functioning; nutrition; bowel and bladder management; spasticity; dysphagia; DVT; hydrocephalus -Monitor for seizures (anti-seizure prophylaxis for 1 week) -Mental and emotional difficulties -Progressive recovery may continue for 6 months or more before a plateau is reached, and a prognosis for recovery can be made. Specific nursing management in the posttraumatic phase depends on specific residual deficits. -Family teaching, education, guidance, and participationWhat are the expected outcomes of nursing interventions?-maintain normal cerebral perfusion pressure -achieve maximal cognitive, motor, and sensory function -experience no infection or hyperthermia -achieve pain controlThe nurse is caring for a patient after a head injury. How should the nurse position the patient in bed? Prone with the head turned to the right side High-Fowlers position with the legs elevated Supine position with the head on two pillows Side-lying with the head elevated 30 degreesSide-lying with the head elevated 30 degreesSPINAL CORD INJURY (SCI)What are the causes of a spinal cord injury?1) MVCs 2) Falls 3) Violence 4) Sports accidentsWhat are the priorities for a patient with a SCI (what do you monitor for in acute SCI)?1) pulmonary status: airway 2) neurogenic shock 3) spine precautions: aspen collar; log rollingWhat is the goal MAP for a patient with an acute SCI?MAP of 85-90 mmHgTrue or False: A spinal cord injury can be complete or incomplete.trueWhat are the dermatomes of SCI? (picture)Dermatomes for cervical injury?C2: face, upper portion of skull C3: neck, upper portion of back of neck C4: collar bone area; back of neck C5: upper chest; back of neck; part of nerves in arms C6: upper back; arms; thumbs C7: upper back; arms; fingers C8: upper back; arms; fingersDermatomes for thoracic injury?T1: upper portion of chest and back; arms T2: chest/back/abdomen T3:chest/back/abdomen T4:chest/back/abdomen T5:chest/back/abdomen T6:chest/back/abdomen T7:chest/back/abdomen T8:chest/back/abdomen T9:chest/back/abdomen T10:chest/back/abdomen T11:chest/back/abdomen T12:chest/back/abdomen (in descending fashion) *The spinal roots form the intercostal nerves that run along the inferior rib margin and innervate the associated dermatomes **Contains sympathetic nerves that innervate the heart and abdominal organsDermatomes for lumbar injury?L1: waist and back of waist L2: upper thigh and back of waist L3: middle thigh and back of waist L4: thigh around knee; front of knee/shin; back of waist; big toe L5: lateral shin; back of waist; toes/footDermatomes for sacral injury?S1: lateral side of feet/ankles; genitalia; buttocks S2: medial side of feet/ankles; genitalia; buttocks S3: buttocks S4:buttocks S5:buttocksWhat is paralyzed in a injury to: C4? C6? T6? L1?C4: tetraplegia; complete paralysis below neck C6: partial paralysis of hands/arms/lower body T6: paraplegia; paralysis below the chest L1: paraplegia; paralysis below waistWhat is the ASIA scale?-American Spinal Injury Association impairment scale for SCI A: complete: no motor or sensory function preserved in sacral segments S4-S5 B: incomplete: sensory but not motor function is preserved below the neurological level and includes the sacral segments S4-S5 C: incomplete: motor fxn is preserved below the neurological level and more than half of the key muscles below the neurological level have a muscle grade less than 3 D: incomplete: motor function is preserved below the neurological level and at least half of the key muscles below the neurological level have a muscle grade of 3 or more E: normal: motor and sensory function are normalWhat areas are innervated by the cervical spine: C3-C5? C4-C7? C6-C8? C8-T1?C3-C5? diaphragm (the chief muscle of inspiration) thru the phrenic nerve C4-C7? shoulder and arm musculature (no need for ventilator) C6-C8? forearm extensors and flexors C8-T1? hand musculatureNerve roots and peripheral nerves corresponding to the principal movements of the upper extremity (picture)What do these innervate for the lumbar spine and sacral spine: L2-L3? L3-L4? L4-L5? L5-S1? S1-S2?L2-L3? hip flexion L3-L4? knee extension L4-L5? ankle dorsiflexion and hip extension L5-S1? knee flexion S1-S2? ankle plantar flexionA young adult is hospitalized after an accident that resulted in a complete transection of the spinal cord at the level of C7. The nurse informs the patient that after rehabilitation, the level of function that is most likely to occur is the ability to breathe with respiratory support. drive a vehicle with hand controls. ambulate with long-leg braces and crutches. use a powered device to handle eating utensils.drive a vehicle with hand controls.What is central cord syndrome?-disproportionately greater motor impairment in the UPPER extremities vs the lower extremities -sensory loss below level of injury -bladder dysfunctionWhat is anterior cord syndrome?-lesion affecting the anterior or ventral 2/3 of spinal cord -direct injury to anterior cord by disc or bone fragments (related to vascular insufficiency) -can feel position, vibration, and touch, but no movement -complete motor paralysis and sensory anesthesia, but sparing of dorsal column (deep pressure and proprioception are only retained sensibility of the trunk and lower extremities; Not light touch) -patient demonstrates greater motor loss in the legs than arms -worst prognosis of all cord syndromes; prognosis good if recovery evident in first 24 hoursWhat is brown-sequard syndrome?-weakness, loss of vibration, and loss of proprioception ipsilateral to the lesion -no bladder symptoms -most common mechanism: knife/bullet injuryWhat is posterior cord syndrome?-loss of deep touch sensation -preserved motor function (difficult to rehab secondary to loss of proprioception)What are the syndromes associated with incomplete spinal cord injury?central cord syndrome, anterior cord syndrome, Brown-Séquard syndrome, posterior cord syndrome, cauda equina syndrome, and conus medullaris syndromeWhat are clinical manifestations of spinal cord injury: Respiratory?Respiratory injury closely corresponds to the level of injury -Above level C4: total loss of respiratory muscle function (requiring mechanical ventilation) -Below level C4: diaphragmatic breathing leads to respiratory insufficiency; unable to clear airway lead to risk for infection, atelectasis, pneumonia -Cervical and thoracic injury: paralysis of abdominal and intercostal muscles causes an ineffective cough --> atelectasis and pneumonia *increased risk for infection *increased risk for neurogenic pulmonary edemaWhat are clinical manifestations of spinal cord injury: Cardiovascular?-Above level T6: decreased influence of SNS -Bradycardia -Peripheral vasodilation --> hypotension and neurogenic shock (decreased venous return of blood to heart; decreased CO) -Relative hypovolemia r/t increase in venous capacitanceCollaborative care for cardiovascular manifestations of SCI?-cardiac monitoring -atropine to increase hr -IV fluids or vasopressors to increased bPA patient is just admitted to the hospital following a spinal cord injury at the level of T4. A priority of nursing care for the patient is monitoring for return of reflexes. bradycardia with hypoxemia. effects of sensory deprivation. fluctuations in body temperature.bradycardia with hypoxemia.What is the difference between spinal shock and neurogenic shock?SPINAL SHOCK: -Caused by: acute spinal cord injury (not a true shock state) -Manifestations: absence of all voluntary and reflex neurologic activity below level of injury (decreased reflexes; loss of sensation; flaccid paralysis below injury) -Duration: days-months (transient; temporary) NEUROGENIC SHOCK -Caused by: hemodynamic phenomenon; loss of vasomotor tone and SNS tone causing impaired cellular metabolism; can be caused by drugs that effect vasomotor center of medulla like opioids/benzos -Manifestations: hypotension (due to massive vasodilation); bradycardia (due to unopposed parasympathetic stimulation); poikilothermia (unable to regulate temperature) -Durations: occurs within 30 minutes of spinal cord injury level T5 or above; lasts up to 6 weeks -Management: determine underlying cause, airway support, fluids as needed (NS); atropine for bradycardia; vasopressors (phenylephrine) for BP support *spinal shock and neurogenic shock can occur in the same patient, but they are not the same disordersWhat are clinical manifestations of spinal cord injury: Urinary system?Acute Phase: -urinary retention -bladder atonic and over-distended -indwelling catheter needed Post-Acute Phase: -bladder may be hyperirritable -loss of inhibition from brain -reflex emptyingWhat are clinical manifestations of spinal cord injury: Gastrointestinal system?Above T5: hypomotility -risk for paralytic ileus -risk for gastric distention -Rx: NG tube, metoclopramide -risk for stress ulcers -risk for intra-abdominal bleeding Neurogenic Bowel -injury at T12 or below (loss of voluntary neuro control over bowel) -bowel initially areflexic with decreased sphincter tone, but when reflexes return, the sphincter tone is enhanced and reflex emptying occurs -regular bowel program to coordinate with gastrocolic reflexWhat are clinical manifestations of spinal cord injury: Integumentary system?-potential for skin breakdown -poikilothermism: interruption of SNS; decreased ability to sweat or shiver; more common with high cervical injuryWhat are clinical manifestations of spinal cord injury: Metabolic Needs?-NG suctioning --> metabolic alkalosis -Decreased tissue perfusion--> acidosis -Electrolyte imbalances -Increased nutritional needs: high protein dietWhat are clinical manifestations of spinal cord injury: Peripheral Vascular Problems?-Deep vein thrombosis (DVT): difficult to detect; if a patient is immobile; anticoagulant prophylaxis -Pulmonary embolism: leading cause of deathWhat is autonomic dysreflexia?-condition where a patient may experience headache, warmth, high BP, rapid HR, sweating, and strange sensations, -medical emergency that requires immediate attention to the stimulus -usually caused by a noxious stimuli that triggers SNS activation (body knows it is there, but person does not feel it) -interventions: lower BP (monitor BP); raise HOB immediately; find underlying cause *At or above t6...after spinal shock resolves. **Unopposed SNS stimulation...usually parasympathetic feedback controls. But only works above level of injuryYou are the nurse: Patient with T3 SCI is going on an all-day outing. What is your PRIORITY to ask the PT/OT to monitor closely? -Respiratory status, as this patient is at risk of pulmonary compromise. -Fevers, as this patient is at risk for infection. -Seizures, as she is not on any seizure medication. -Urine output, as this patient is on a scheduled bladder program.During assessment of a patient with a spinal cord injury at the level of T2 at the rehabilitation center, which finding would concern the nurse the most? A heart rate of 92 A reddened area over the patient's coccyx Marked perspiration on the patient's face and arms A light inspiratory wheeze on auscultation of the lungsMarked perspiration on the patient's face and arms (sign of autonomic dysreflexia)What is a HALO device? what is a nursing priority?Metal ring attached to skull with screw pins Weight of head is diverted through the brace Reduces movement of neck Safety -PRIORITYIF not a halo device, then ______________.tractionWhat are important considerations in SCI rehabilitation?DVT prophylaxis with Lovenox Nexium Maintaining skin integrity Pain Control - Percocet Orthostatic Hypotension - Midodrine Skin care - weight shifts Bowel regimens SMOKING CESSATION: http://www.uab.edu/medicine/sci/uab-scims-information/smokings-effects-on-secondary-complications-of-sci-video-Review cranial nerves -tentorial herniation, etc?