Chapter 17, 18, 19: Acute Stroke Injury, Traumatic Brain Injury, Acute Spinal Injury Flashcards
(137 cards)
1
Q
What are medical, modifiable, and non-modifiable risk factors of stroke?
A
Medical: High cholesterol, high blood pressure, heart disease, atrial fibrillation, carotid artery disease, diabetes, coagulopathies.
Modifiable: smoking, obesity, excessive ETOH intake, drug abuse, sedentary lifestyles, poor diet habits.
Non-modifiable: age, gender, race, family history, prior stroke or TIA.
2
Q
What is the pathophysiology behind stroke?
A
Atherosclerosis can lead to thrombus or embolus which cut off circulation. Global ischemia is complete lack of blood flow and irreversible damage. Focal ischemia some blood flow, some neurons survive, fix it quick. SAVE THE PENUMBRA. TPA.
3
Q
What are the signs and symptoms of stroke?
A
Sudden: severe headache, trouble walking, dizziness, loss of balance, lack of coordination, confusion, trouble seeing (in one or both eyes), trouble speaking or understanding speech, numbness, weakness especially on one side of the body.
4
Q
What medications can you give to someone who is having a stroke? What is the management of the medications?
A
TPA: infused over one hour. Give 10% IV push over 1 min. Total dose 0.9 mg/kg or max of 90 mg. Can give within 3 hrs but NOT recommended after 4 1/2 hrs. Perform frequent neurological assessments during and after the infusion including BP. If pt develops N/V, severe headache, or acute HTN stop infusion and notify physician immediately (these are adverse drug effects that can be life threatening). Pt w/ acute ischemic stroke d/t occlusion of proximal cerebral artery can administer TPA within 6 hrs.
5
Q
Describe the nursing management of stroke in terms of initial priorities.
A
Initial priorities: Assess ABCs. Hemiplegia, dysphagia, a weak cough reflex, and immobility have a high risk for hypoxemia, pneumonia, and aspiration. Continuously monitor breath sounds, breathing patterns, oxygen saturation, skin color, arterial blood gases (ABGs, ability to handle secretions). Pt who is comatose and has evidence of increased ICP then intubate and mechanical ventilate. Prevent hypercapnia by monitoring rate and rhythm of breathing, ABGs, and LOC. HR and BP monitoring. Assess heart rhythm for dysrhythmias by continuous telemetry. Palpate peripheral and carotid pulses.
6
Q
What factors lead up to traumatic brain injury?
A
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7
Q
What is the pathophysiology behind traumatic brain injury?
A
f
8
Q
What are the signs and symptoms of traumatic brain injury?
A
f
9
Q
What medications can you give to someone who has a traumatic brain injury?
A
f
10
Q
Describe the nursing management of traumatic brain injury.
A
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11
Q
What are the signs and symptoms of a UMN injury?
A
Weakness or paralysis, spasticity, increased tendon reflexes, + Babinski, loss of abdominal reflexes, little to NO muscle atrophy.
12
Q
What are the signs and symptoms of a LMN injury?
A
Motor weakness, flaccidity, muscle wasting, loss of tendon reflexes if those neurons are involved, normal abdominal and plantar reflexes if neuron is preserved.
13
Q
What are the signs and symptoms of spinal shock?
A
There is absence of all reflexes so pt is very flaccid and loses sensation below lvl of injury. Tachycardia, cold and moist, no deep tendon reflexes, no bladder tone, paralytic ileus, anhidrosis, loss of piloerection, no sweating, loss of vasomotor tone, prone to dependent edema.
14
Q
How do you treat spinal shock?
A
Symptomatic tx. Self limiting, usually lasts 24 hours but can last up to 7-20 days.
15
Q
How do you spinal shock patient is getting better?
A
Pt is getting better when DTRs return, is spastic, and increased muscle tone.
16
Q
What causes spinal shock?
A
Due to acute cervical and upper thoracic spinal cord transections
17
Q
What causes neurogenic shock?
A
Injuries above T6 which leads to loss of sympathetic vascular tone from hypothalamus
18
Q
What are the signs and symptoms of neurogenic shock?
A
Massive vasodilation leading to systemic hypotension and pooling of blood in the lower extremities. Loss of SNS control. Loss of venous return to heart. Pt very hypotensive, bradycardic, decreased CO, inability to sweat below lvl of lesion, warm.
19
Q
How do you treat neurogenic shock?
A
Fluid resuscitation
Vasopressor medications
20
Q
What causes autonomic dysreflexia?
A
Distended bladder, fecal impaction, skin lesions: pressure ulcer, ingrown toenail, blisters. UTI, pain.
21
Q
What are the signs and symptoms of autonomic dysreflexia?
A
Severe HTN (240/140), tachycardia, severe pounding bilateral HA, redness of the face, neck and trunk. Sweating, anxiety, blurred vision, SOB.
22
Q
What are complications of autonomic dysreflexia?
A
If left untreated it can lead to retinal hemorrhage, hemorrhagic stroke, SAH, seizures, pulmonary edema, MI.
23
Q
Describe nursing interventions of autonomic dysreflexia.
A
Find the cause and fix it to lower the BP. Nitro S/L to decrease BP. Palpate bladder to see if distended, if blocked irrigate through cath. Check tubing to see if it’s messed up. Do a bladder scan. Check for bowel impaction. Palpate and auscultate the abdomen. Loosen any constrictive clothing. Inspect skin. Educate regarding prevention.
24
Q
Define stroke.
A
Occurs when the brain is not getting enough blood which injures brain tissue.
25
What is ischemic stroke? What three components make up ischemic stroke? Explain.
Ischemic stroke occurs when blood supply to a part of the brain is topped. There are three different types: Thrombotic and Embolic, and TIA. Thrombotic strokes are caused by a blood clot that blocks flow to a part of the brain due to narrowing of the artery. Happens when person is asleep. Emoblic strokes are caused by a blood clot that travels and gets stuck in an artery which blocks off blood flow to the brain. Happens when person is awake. Transient ischemic attack is like stroke but doesn't leave damage and goes awak
26
What is hemorrhagic stroke? What two components make up hemorrhagic stroke?
Hemorrhagic stroke occurs when a blood vessel in the brain ruptures. There are one of two places the bleed can occur. Either in the brain (interacerebral hemorrhage) or the subarachnoid space (subarachnoid hemorrhage).
27
How does intracerebral hemorrhage occur, what happens as a result, and where is the most common place it happens.
Occurs suddenly without warning causing blood to accumulate in the brain (most common site is basal ganglia).
28
What causes intracerebral hemorrhage?
HTN (is the most common cause), anticoagulant therapy, AV malformations, aneurysms, trauma, and erosion of blood vessels by tumors.
29
How do you treat intracerebral hemorrhage?
Control BP, close observation, anticoagulation reversal of agent.
30
What causes subarahnoid hemorrhage?
HTN is the number one cause, weakening and dilatation of blood vessel walls, artherosclerosis
31
Where does subarachnoid hemorrhage occur?
The circle of willis
32
How do you diagnose subarachnoid hemorrhage?
CT scan (THE CHICKEN). Hunt and hess grading scale for SAH.
33
What are the signs and symptoms of subarachnoid hemorrhage?
Sudden severe HA on side of bleed described as "the worse HA of my life", nuchal rigidity, photophobia, N/V, syncope, lethargy, 3rd and 4th CN palsy, hemiparesis, hemiplagia, aphasia, low back pain.
34
What is the treatment of subarachnoid hemorrhage?
Clipping or coiling
35
What is transient ischemic attack?
Brief episodes of focal neuro deficit that resolves in a few minutes or within 24 hours.
Does not cause permanent brain injury but is a warning sign of an impending stroke.
36
What causes transient ischemic attack?
Emboli from heart (atrial fibrillation)
| or emboli from unstable plaque in a vessel.
37
What are signs and symptoms of transient ischemic attack?
Sudden: severe headache, trouble walking, dizziness, loss of balance, lack of coordination, confusion, trouble seeing (in one or both eyes), trouble speaking or understanding speech, numbness, weakness especially on one side of the body.
38
What is the treatment of transient ischemic attack?
Diagnostic workup to find root cause
39
Describe the nursing management of stroke in terms of nutrition.
Dietary consult. Evaluate ability to swallow. Nutrition provided through enteral route until pt is safe to swallow or percutaneous endoscopic gastrostomy is placed for long-term tube feedings.
40
Describe the nursing management of stroke in terms of preventing infections.
In pts with acute ischemic stroke or TIA give aspirin therapy at dose of 160-325 mg. In pts with acute ischemic stroke and restricted mobility give anticoagulant meds, LMWH or heparin between days 2 and 4 following administration of thrombolytic agents. Increased risk of bleeding; contraindicated in first 24 hrs after tPA treatment. If stroke was caused by embolism give chronic anticoagulation with warfarin (to maintain an INR of 2–3) or aspirin (325 mg/day) is indicated to decrease the risk for recurrent stroke. Don’t give these drugs together b/c increases risk of intracranial hemorrhage. Non-cardiac related embolic strokes give long-term antiplatelet regimen with aspirin (81–325/per day) within 48 hours of stroke onset. Young pts w/o discernable risk factors for stroke hypercoagulation work up is warranted. Manage seizures with benzos and anticonvulsant meds. Cerebral edema can occur which leads to neurologic deterioration & respiratory failure.
41
Define focal brain injuries.
Occur in a defined area of brain.
42
What are the different types of focal brain injuries?
Contusions and hematomas.
43
Describe contusions in terms of definition, level of injury, uncs, prognosis, and signs and symptoms.
A bruising of soft tissue. Level of injury is moderate to severe and detected on MRI. Longer periods of uncs. Guarded prognosis (watching for deterioration). Signs and symptoms include macroscopic tissue and vessel damage, focal deficits become more diffuse over time.
44
What are hematomas?
An accumulation of blood.
45
Describe epidural hematoma in terms of definition, what happens as a result, signs and symptoms, and treatment.
Arterial bleed
that happens between the middle meningeal artery that results in bleeding between dura mater and skull. As a result there is rapid bleeding with decreased o2 to tissues. Signs and symptoms include rapid neurologic deterioration (brief loss of consciousness immediately following the injury from the initial traumatic impact, followed by an episode of being alert and oriented, and then a loss of consciousness again as the growing hematoma exerts excessive pressure on the brain). Treatment is neurosurgery.
46
Describe subdural hematoma in terms of definition, what happens as a result, subtypes, signs and symptoms, and treatment.
Slow venous bleeding under the skull but outside the brain in the subdural space. As a result blood accumulates and increases ICP.
Acute (within 48 hrs), subacute (48hrs-2 wks), chronic (>2 wks).
Signs and symptoms include large hematoma, pupillary dilation on side of hematoma, altered LOC, seizures, vision field alterations, hemiparesis. Treatment ranges from watchful waiting to brain surgery for evacuation.
47
Describe intracerebral hematoma in terms of definition, causes, signs and symptoms, and treatment.
The accumulation of blood in the parenchyma of the brain rather than between the meningeal layers. Results from uncontrolled HTN, ruptured aneurysm, trauma. Signs and symptoms include HA w/ decreased LOC, dilation of one pupil, hemiplegia.
48
What are different types of diffuse brain injuries?
Concussions, diffuse axonal injuries, subarachnoid hemorrhage.
49
Describe concussion in terms of definition, level of injury, uncs, and signs and symptoms.
Blunt trauma to the lead (injury is microscopic). Mild traumatic injury not detectable on imaging. Transient period of uncs (
50
Describe coup and countracroup in terms of definition, causes, and symptoms.
Coup: the direct impact that caused the brain to hit the skull. Contracroup: the skull bouncing off the other side of the skull. Causes for both are the same: car accidents, assault, shake baby syndrome, falls, sports and athletic injuries. Symptoms are the same: impaired concentration,
impaired memory, difficulty swallowing, problems with balance and coordination, muscle weakness or paralysis, sensory changes.
51
What's the difference between a secondary and primary injury?
Primary: the reason for the injury. Secondary: complications resulting from the primary injury.
52
What are the different types of skull fractures?
Linear, depressed, open, and basilar.
53
Describe linear skull fracture.
Straight line fracture in skull, no fragmentation. These are typically minor and not obvious. Usually discovered through CT. Not life threatening and heal on their own.
54
Describe depressed skull fracture.
There is fragmentation of bone. These occur with higher forces of impact. May be visible and papable, open or closed. Surgery to fix and drainage of hematoma if indicated.
55
Describe open skull fracture.
Tearing of scalp which causes risk for infection. Surgery is required and debridement of wound. Antibiotics administered.
56
Describe basilar skull fracture.
Fracture of one or more skull bones due to high impact. Signs include: bruise behind ear (battle sign), ottorrhea, rhinorrhea, facial paralysis, raccoon eyes, brain can herniate through nose in severe cases. Leaking CSF fluid. Test for halo sign: drop of blood on gauze, if CSF present yellow ring around outside of blood. Allow fluid to drain, if injury doesn't heal within 1-2 wks, surgery.
57
What is the nursing management of patient with skull fracture?
Pain management, frequent neurological assessment to look for signs of deterioration, monitor for s/s of infection, change dressing aseptically.
58
Name some key physical assessment findings of stroke?
Assess extremity position and handgrips, arm drifts, and leg pushes for strength, tone (flaccidity or spasticity). Assess speech for coherency, content, and fluency. Assess orientation and ability to follow commands. Assess sensitivity to cognitive and perceptual-visual-spatial deficits. Assess pt behavior manifesting as neglect or poor judgement choices. Hemispheric stroke (anterior or carotid). Posterior (vertebrobasilar) stroke characterised by ptosis of eyelid and cranial nerve III, LOC, cranial nerve abnormalities (III to XII). Bilateral hemispheric stroke. Brainstem involvement.
59
What are some diagnostic tests and procedures for stroke?
Rapid diagnosis to determine whether pt can receive thrombolytic therapy. Goal – save damaged brain tissue and minimize permanent deficits. 3 hour window for administration of thrombolytic therapy. Perform variety of tests and procedures upon arrival to determine exact nature of stroke. Imaging studies – determine type, extent and location. Lumbar puncture – detects blood in CSF if SAH is suspected but not confirmed by CT scan. Transesophageal echocardiography – detects cardiac and aortic causes of embolism. 12-lead ECG – cardiac abnormalities are prevalent among patients with stroke. CBC including platelets, PT, PTT, INR, fibrinogen – detect coagulopathies and establish baselines for therapy. Serum electrolytes and BGLs – rule out other conditions that may mimic stroke, including hypoglycemia and severe electrolyte imbalances, which are a potential source of cardiac dysrhythmias. ABGs, drug screens, serum alcohol level – detect possible causes .
60
Describe interventions necessary when oxygenating a patient with stroke.
Maintain o2 at 92%. Elevate HOB to 30 degrees which decreases risk of aspiration and cerebral edema. Evaluate ability to swallow before offering oral nutrition or liquids b/c aspiration contributes to hypoxia.
61
Describe serum glucose management in a patient with stroke.
Manage stress hyperglycemia with rapid-acting insulin to decrease serum glucose levels if >140 mg/dL. >155 mg/dL this leads to higher mortality and worse outcomes. IV insulin infusion can be used to maintain acceptable level.
62
Describe blood pressure management in a patient with stroke.
Usually pts are hypertensive. Permissive hypertension – higher than normal blood pressures are allowed for maintaining optimal cerebral blood flow (don’t want penumbra to get worse). Severe HTN treatments – labetalol, nicardipine, and nitroprusside. Goal in days – weeks following stroke = pt have normal BP to reduce risk for recurrent stroke. Prevent hypotension following stroke to avoid inadequate cerebral blood flow which leads to ischemia in penumbra. Correct with fluid administration or IV vasopressor. Goal – administer enough to achieve normal BP and euvolemia (normal fluid volume). Avoid hemodilution and fluid volume overload which increase risk of cerebral edema.
63
Describe angioplasty and stent placement.
Cerebral angioplasty – reverse neurological deficits caused by atherosclerotic lesions. Balloon catheter mechanically dilates vessels introduced through the femoral artery and directed to major arteries at base of brain. After- assess for neurologic and vital sign changes frequently until neurologically stable. Vascular stenting. Both have risks- intracerebral hemorrhage, injury to the vessel wall, and distal embolization.
64
Describe craniotomy.
Emergency surgery for cerebellar infarction or hemorrhage with clinical evidence of brainstem compression and increased ICP. Evidence – decreasing LOC, restlessness, cranial nerve palsies. Hemorrhage into area of ischemic infarct is complication of stroke. Use of thrombolytic and antithrombotic agents and inc BP which inc risk of hemorrhagic complications that are life threatening and compromise brainstem. Large hemorrhages more likely to cause brainstem compression and an urgent need for surgery.
65
Describe aneurysm clipping.
Bleeding into subarachnoid space (aneurysm) requires immediate attention. No neurological deficit then cerebral arteriography and early surgery. Aneurysm clipping – performed within 72 hrs of the bleed; opening the cranium (craniotomy) and inserting a metal clip around the aneurysm to prevent rebleeding. Postoperative complication – cerebral vasospasm which leads to decreased perfusion to brain tissue. Vasospasm treated with “triple H” therapy: hypervolemia, hypertension, and hemodilution leads to augment cerebral perfusion pressure (CPP) by raising systolic blood pressure, cardiac output, and intravascular volume to increase cerebral blood flow and minimize cerebral ischemia. Maintain or first 2-3 days. CCBs (nimodipine) can be ordered to treat and prevent cerebral vasospasm.
66
Describe carotid endarterectomy.
Surgery to prevent recurring cerebral infarcts and TIAs. Removes source of occlusion (plaque) and increases cerebral blood flow to ischemic area.
67
What are the nursing interventions of the patient after carotid endarterectomy?
Position patient on the nonoperative side; with HOB elevated 30 degrees. Maintain head and neck alignment; avoid rotating, flexing, or hyperextending head. Support the head during position change (teach pt to do the same). Watch for complications: hemorrhage, respiratory distress, cranial nerve impairment, and alterations in blood pressure.
68
Damage to wernicke's area leads to what?
Patient is not able to understand speech but can talk.
69
Damage to broca's area leads to what?
Patient is able to understand speech but can't talk.
70
How does diffuse axonal injury occur? What does it lead to? How is the patient going to present and what are the CT findings? What characterizes mild and severe coma?
Results from high-speed acceleration, deceleration or rotational injury that occurs with motor vehicle crashes. This leads to shearing of neurons and nearby blood vessels. The patient is going to present comatose but the CT scan is going to look normal. Damage is microscopic, punctate hemorrhages. If patient is mildly comatose: coma is going to last hrs-days, patient is going to have persistent dizziness, HA, and confusion, recovery is possible with minimal residual neuro damage. If patient is severely comatose: coma is going to last wks-mons, poor prognosis, frequent cause of persistent vegetative state.
71
What is thalmic storming?
It is a stress response characterised by sympathetic surge of hormones which leads to an increase in corticoids and cathecholamines.
72
Describe the pathophysiology of thalmic storming.
It is an exaggerated sympathetic response.
73
What are some of the signs and symptoms of thalmic storming?
HTN, hyperthermia, tachycardia, tachypnea, profuse diaphoresis, extreme agitation, increased posturing, increased muscle tone.
74
What is the treatment of thalmic storming?
Control the duration and severity, prevent additional brain injury, meds: morphine sulfate, versed, beta blockers, thorazine (suppresses hypothalamic activity).
75
What is prognosis of thalmic storming?
Eventually storming episodes stabilize with time.
76
Define subarachnoid hemorrhage.
The accumulation of blood between the meningeal archnoid layer and the brain.
77
What causes subarachnoid hemorrhage?
Most commonly results from a ruptured cerebral aneurysm, with a major risk factor being HTN.
78
What are the signs and symptoms of subarachnoid hemorrhage?
Acute onset of severe HA, the worst I ever had bruh. Sometime called thunderclap HA :p May also present with altered LOC, diplopia, meningeal signs (nuchal rigidity, photophobia) or seizures.
79
What are the complications of subarachnoid hemorrhage? Why is there an increased risk for bleeding?
Re-bleeding, vasospasm, seizures, hydrocephalus, cerebral edema, hyponatremia, cardiac abnormalities. There is an increased risk of bleeding the first 24-48 hours due to HTN caused by SNS w/ adrenal release. Also there is an increased risk 7-14 days out. 70% of pts that re-bleed die.
80
What landmark is associated with C4?
* Shoulders, ask the patient if they can shrug their shoulders or if they can feel an object touching their face
* If this area is damaged the patient will possibly be quadriplegic and on ventillator support
81
What landmark is associated with T4, and what happens when this area is affected?
* T4 is at the nipple line
* If this is affected the pt. will be paraplegic and be possibly on respiratory compromise
* The pt. might need assisted quad coughing
82
What landmark is associated with T10, and what happens when this area is affected?
* The umbilicus
| * If this area is affected the patient may become quadriplegic below the waist and will not be able to rotate waist
83
What landmark is associated with L1 and happens when this area is affected?
* L1 is at the level of the groin
* If this area is affected the patient may become paraplegic from the abdomen and legs
* The patient will not be able to control his bowel movements or have bladder control
84
When does vasospasm happen after SAH?
Vasospasm begins post SAH day 4-14. It peaks day 7-10 and may continue post SAH day 21.
85
What landmark is associated with c7?
Middle finger
86
What land mark is associated with c8?
little finger
87
What landmark is associated with t6?
xiphoid
88
What landmark is associated with l3?
Just above the patella
89
what landmark is associated with L4
the medial malleolus
90
What landmark is associated with L5
The great toe
91
What land mark is associated with s1
lateral malleolus
92
What landmark is associated with s4-5?
peri-anal
93
What is a concussion?
Transient loss of spinal cord function
94
What is a contusion?
It involves intramedullary hemorrhage and associated edema
95
What is a laceration?
It is a cut of the spinal cord
96
What is a transection?
It is a complete cut through the spinal cord. If this occurs the patient can become quadra or paraplegic?
97
Define hemorrhage in reference to spinal cord injuries?
It is Blood in or around the spinal cord
98
Describe vascular damage in reference to spinal cord injuries
It is damage that can result in cord ischemia
99
What is Eshau?
A Nig :')
100
Describe a complete injury?
It is a injury that results in loss of all voluntary motor and sensory function below the level of the injury
101
Describe an incomplete injury
It is an injury that can be reversed. This injury allows for some neurotransmission
102
Describe central cord syndrome
* Hyperextension injury to the cervical spine
* Deficits > in arms vs. legs
* Sensory loss in arms, often spastic
103
Describe anterior cord syndrome
* Injury of the anterior 2/3 of spinal cord 2/2 disruption of arterial supply
* Deficits > in Legs vs. arms
* Paralysis and loss of touch, pain, and temperature below the injury.
104
Describe Cauda equina syndrome
* Compression of the lumbosacral nerve roots below the L1 vertebrae
* Low back pain, sciatica, saddle sensory deficit, bladder/bowel dysfunc.
* M/B surgical emergency
105
Describe posterior cord syndrome
* Loss of Proprioception
| * Motor, pain & light touch preserved
106
Describe horner's syndrome
* Associated with spinal cord lesion at or above T1
* Disrupt the cervical sympathetic chain
* Classic triad: miosis, ptosis, anhidrosis (not sweating on certain side)
107
Describe conus medullaris syndrome
* Damage to the lower lumbar area of the spinal cord
* Urinary retention/bowel incontinence
* Leg weakness, Paresthesia and numbness
* Tx: w/ surgery
108
Describe brown-sequard syndrome
* Hemi transection of the spinal cord 2/2 penetrating injury
* Ipsilateral loss of voluntary motor
* Contralateral loss of pain & temp
109
When does vasospasm happen after SAH? What are the signs and symptoms?
Vasospasm begins post SAH day 4-14. It peaks day 7-10 and may continue post SAH day 21. Signs and symptoms are diffuse: include lethargy, confusion, HA. And focal: to specific vascular territory involved.
110
What is a hard cervical collar used for?
decrease the degree of flexion-extension and decreases rotation. Stabilization of the chin and mandible
111
What is cervical traction used for?
to reduce cervical fracture dislocations and restore cervical
112
What is a halo vest used for?
stabilizes the neck by attaching a thoracic vest to a ring that is secured to the skull via pins
113
What are cervicothoracic orthoses used for?
stabilize the lower cervical and/or upper thoracic region of the vertebral column – open vest and assess skin
114
What are Thoracolumbosacral orthoses (TLSO) (clam shell) devices used for?
immobilization of fractures located from T6-L3 that are unstable during flexion
115
What are some nursing considerations with hard cervical collars?
* Philadelphia collar Miami J Aspen
* Ensure good collar fit
* Meticulous skin care
116
What are some nursing considerations with soft Cervical collars?
* Whiplash
* Symptom management
* Avoid dependence of pt
* Nighttime use, riding in car
117
What are some nursing considerations with cervical traction devices?
* Gardner Wells tongs
* Bridge to OR for spine stabilization and alignment
* Pin site care and assessment
* Reposition Patient every 2 hrs. via Log Roll
* Weights hang free with ordered amt. of traction
118
What are some nursing considerations when using a halo vest?
* Pin site assessment, and care
* Skin care
* Wrench available to remove vest in Emergencies
119
What are some nursing considerations when a patient is using a thoracic or lumbar spine?
* Thoraco-Lumbar support orthotic
* Clam Shell
* Custom fit
* After spinal decompressive and stabilization surgery
* Hastens healing * Diminishes pain
* Skin care
120
In reference to spinal cord injuries what is methylprenisolone used for?
* It is used post SCI to prevent secondary injuries
* If started within 3 hrs. of injury—infused x 24 hrs.
* If started within 3 to 8 hrs. infuse x 48 hours
121
In reference to spinal cord injuries what are some risks associated with using methylprenisolone ?
* Pneumonia
* Sepsis
* GI complications
* Electrolyte imbalances
* Delayed wound healing
122
How would you initially manage a patient with a spinal cord injury?
1. Maintain Oxygenation
* Need intubation
* STABILIZE NECK
* Humidified Oxygen
* Incentive Spirometry
* Assisted Quad Coughing – muscles compromised, pt sitting down pt take deep breathe, cough, nurse presses in and up on abd
2. Hypotension/ Low cardiac output/ Bradycardia
* Monitor CVP pressure
* PRN Atropine
* Vasopressors
* Fluids to replace losses without over hydration
* SBP
123
What can you use to detect a vasospasm? How do you tx a vasospasm? What can vasodilation cause?
Transcranial doppler, tx vasospasm w/ repeated IR prcedures (verapamil), vasodilation may cause intracranial HTN
124
Describe the treatment of seizures in regards to SAH.
There is no prophylactic tx (it actually gets worse). You can detect on EEG. 1st line tx is BENZOs. Antiepileptic can be added to prevent reoccurances.
125
Define hydrocephalus, how do you tx, and what is the management around tx.
The accumulation of fluid (blood in case of SAH) leading to increased ICP which eventually causes brain damage. Manage with extra ventricular drain, make sure not to overdrain. This can lead to SDH, aneurysm re-bleed, epidural bleed, low ICP syndrome, herniation,
H/A, lethargy, obtundation, N/V, dizziness, diplopia, CN neuropathies.
126
Define vasogenic edema, tx, nursing considerations.
Edema that occurs as a result of decreased capillary permeability. Tx using mannitol or hypertonic NSS 3% or 24.5% (pulls dah fluid out). Nursing considerations include: close monitoring of VS, ICP, CPP, and neuro. Monitor labs: Na (145-155) and serum osmolality (
127
Define cytotoxic edema, tx.
Edema that occurs as a result of proton pump failure. Shift from aerobic to anaerobic. Tx using mannitol or hypertonic NSS 3% or 24.5% (pulls dah fluid out).
128
What are some cardiac abnormalities of SAH? Patho behind it?
50% of pts who have SAH have cardiac abnormalities such as ST segment depression, QT prolongation, T wave changes, and U waves. Hypothalamus is jacked up which causes lots of catecholamines to be released. Monitor EKG.
129
How would you initially manage a patient with a spinal cord injury?
1. Maintain Oxygenation
* Need intubation
* STABILIZE NECK
* Humidified Oxygen
* Incentive Spirometry
* Assisted Quad Coughing – muscles compromised, pt sitting down pt take deep breathe, cough, nurse presses in and up on abd
2. Hypotension/ Low cardiac output/ Bradycardia
* Monitor CVP pressure
* PRN Atropine
* Vasopressors
* Fluids to replace losses without over hydration
* SBP
130
What are some nursing interventions for autonomic dysreflexia?
* Elevate the HOB 90 degrees
* Nitroglycerine S/L to decrease BP
* Palpate bladder for distension
* Catheter patent
* If blocked---Irrigate
* Is tubing kinked
* Bladder scan
* Check for Impaction
* Palpate and auscultate the abdomen
* Loosen any constricting clothing
* Inspect skin
* All pressure points
* Feet
* Toenails
131
Describe the nursing management of increased ICP.
Close monitoring of patient for: ICP >20, CPP 320, HA, lethargy, restlessness, posturing, changes in verbal/motor responses.
132
Describe the nursing management to maintain normal ICP.
Euvolemia: IV therapy, vasopressors, diuretic therapy as needed, monitor I&O, pitting edema, and third spacing. Venous drainage: HOB up to 30 degrees, neutral body alignment. Seizure: assess for development, continous bedside EKG. Prevent overstimulation: assess for effect of ICP w/ interventions, quiet dark environment. Normothermia: high fevers indicate neuronal injury.
133
Describe the pharmacologic therapies of acute TBI and increased ICP.
Antipyretics: Tylenol or ASA. Diuretic therapy: mannitol to decrease ICP. Hypertonic solutions: to decrease ICP, 3% or 24.5% NSS. Sedation: to control ICP - precedex, propofol, versed, ativan. Neuromuscular blockades: to decrease ICP - Nimbex, Norcuron, Pavulon. Barbiturates: penobarbital induce coma to decrease cerebral metabolism. Anticonvulsants: Dilantin, Cerebyx, Ativan. Pain medication: Morphine, Fentanyl.
134
Describe the nursing management used in order to optimize ventilation and oxygenation.
Monitor for inadequate cerebral oxygenation by hourly monitoring of ICP, CPP, and neuro assessments. Respiratory rate: adding rate to vent settings, decrease rate, ABG values to monitor for impending hypoxia, monitor for Hgb & Hct (maybe don't have enough carriers), monitor for o2 saturation.
135
Describe the nursing management used in order to optimize cerebral oxygenation.
ETT tube or nasal cannula, blood transfusion, pulmonary toilet (to drain mucus).
136
Describe the nursing management used in order to prevent complications of immobility.
DVT/VTE: inspect extremities for swelling, redness, warmth. Anticoagulant therapy: Heparin, Lovenox. Sequential compression devices: SCD, ICD, PCD. Anti embolism stockings (TEDS). Contractures: passive ROM, PT, body positioning with splints/braces, sneakers to prevent foot drop.
137
Describe the nursing management used to manage constipation, paralytic ileus/stress ulcers, and pressure ulcers.
Constipation: bowel program - colace, senna. Paralytic ileus/stress ulcers: provide early nutrition through tube feeding, Reglan - GI motility, Protonix - PPI, Zantac or Pepcid- H2 blockers, antacids. Pressure ulcers: frequent turning and positioning, skin barriers, and off loading pressure points.
