pathopharm 3: exam 2: intracranial regulation: spinal cord disorders and emergencies

what is the blood brain barrier

§ Specialized endothelium present in brain capillaries

§ Permits selective entry of substances

· Tight junctions between endothelial cells

· Few pinocytotic vesicles

· No fenestra

· Active transport

substances that can cross the blood brain barrier

· Highly lipophilic substances cross directly

· Water crosses membrane by simple diffusion

· Most nutrients cross barrier by facilitated diffusion

what is cerebral autoregulation

autoregulatory mechanisms fail; loss of match between O2 supply and demand of tissues

what is intracranial pressure

pressure exerted by brain tissue, blood, and CSF (contents of the cranium)

what is monro-kellie hypothesis

If the volume of one component of intracranial pressure increases slightly, it is offset by reduction in volume of the other two

-a brain tumor increases volume of brain tissue

-blood and CSF volume reduced in response

causes of intracranial pressure

-brain volume

-CSF

-blood volume

-other causes

how does brain volume cause ICP

brain edema, hemorrhage, tumor, abscess, infart

how does CSF cause ICP

increased production, choroid plexus tumor, hydrocephalus, meningeal inflammation

how does blood volume cause ICP

increased cerebral blood flow, venous stasis, elevated central venous pressure

what are the other causes of ICP

idiopathic intracranial HTN, skull deformities, tetracycline use

hx assessment for spinal cord injury

§ How injury occurred

§ Mechanism of injury

§ Pre-hospital care

physical assessment/S/S for SCI

-priority is ABCs

-spinal shock

what is spinal shock

complete but temporary loss of motor, sensation, reflex, and autonomic function that often lasts less than 48 hours but may continue for several weeks

what is the first priority after an SCI

respiratory status

respiratory status for SCI

§ involuntary respirations can be affected d/t a lesion at or above the phrenic nerve or swelling from a lesion immediately below C4; lesions in cervical or upper thoracic area will also impair voluntary movement of muscles used in respiration (increase in depth or rate)

§ Provide O2 and suction PRN

§ Assist with intubation and mechanical ventilation if necessary

§ Assist the pt to cough by applying abd pressure when attempting to cough

§ Teach pt about incentive spirometer use and encourage the pt to perform coughing and deep breathing regularly

neurogenic shock from SCI

· Complication of spinal trauma, causes a sudden loss of communication within the sympathetic nervous system that maintains muscle tone in blood vessel walls

· Neurogenic shock can occur within 24 hours of a SCI, resulting in peripheral vasodilation that leads to venous pooling in the extremities, a drop in cardiac output and heart rate, and a life-threatening decrease in BP

· Can last several days to weeks

interventions for neurogenic shock

o Ensure proper positioning of the pt by stabilizing the spinal cord following an injury

o Monitor for hypotension, bradycardia, dependent edema, loss of temp regulation (abrupt onset of fever)- common s/s

o Pts who experience neurogenic shock are at greater risk for development of venous thromboembolism (VTE)

§ Monitor for manifestations fo VTE (swelling of extremity, absent/decreased pulses, and areas of warmth/tenderness)

§ Pt may be on anticoagulants to prevent development of lower extremity emboli

muscle tone for pts with upper motor neuron injuries (above L1 and L2)

convert to a spastic muscle tone after neurogenic shock

muscle tone for pts with lower motor neuron injuries (below L1 and L2)

convert to a flaccid type of paralysis

interventions for muscle strength and tone after SCI

§ Encourage active ROM when possible and assist with passive ROM if pt lacks all motor function

§ Muscle spasticity can be so severe that pts develop pressure injuries- can make sitting in a wheelchair very difficult

§ Muscle spasms can be painful for some pts while others do not feel pain

can pts with complete injuries regain mobility

no

can pts with incomplete injuries regain mobility

can regain some function that will allow mobility with various types of braces

-functional mobility can still be best attained through the use of a wheelchair

what needs to be stabilized to prevent further injury in SCI's

head and neck

-cervical collars

-use log roll technique when transferring

-maintain traction if prescriped

common traction for SCI's

skeletal and halo

what may pts with high levels of SCI experience when in an upright position

postural hypotension

prevention of postural hypotension in high levels of SCI

o Raise HOB and be ready to lower the angle if the pt reports dizziness

o Transfer the pt into a reclining wheelchair with the back of the wheelchair reclined

o Be ready to lock and lean wheelchair back onto knee to a fully-reclined position if the pt reports dizziness after the transfer

o Do not attempt to return the pt to the bed

how to prevent secondary SCI

reduce and immobilize fracture

how to reduce and immobilize fracture to prevent secondary SCI

· External fixation

· Surgical intervention

· Hard collar

· Halo crown

· Med management

o PPI

o Muscle relaxants

o Celecoxib

· Surgical management

what is a TBI

head trauma

components of mild head trauma

· Loss of consciousness seconds to minutes

· Amnesia or loss of memory of event

· Change in mental status at time of event

· Persistent or transient focal neurologic deficit

· Sensitivity to light

· N/V

· GCS score 13-15

components of moderate/severe head trauma

· GCS score 9-12 (mod), less than 9 (severe)

· LOC for minutes to hours

· Seizures

· Extremity weakness and coordination challenges

· Aggression, depression

· Difficulty understanding, communicating, or concentrating

· Mortality rates very low

· Long-term disabilities as high as 50%

· Occur 1-2 days after TBI : ^^^^

signs of severe head trauma

what is a TIA

temporary episode of neurologic dysfunction --> caused by focal brain, spinal cord, or retinal ischemia without acute infarction --> resolves in 1-24 hours

etiology/pathogenesis of TIA

-same as ischemic stroke

-clot blocking blood supply to region of brain

-atherosclerosis

TIA

what is the most common type of stroke

ischemic stroke

what is a stroke

interruption in blood supply to region of brain/bleeding of vessel resulting in brain tissue damage or infarction

hemorrhagic stroke

embolic stroke

nonmodifiable risk factors for stroke

§ Age

§ Family hx

§ Prior TIA/stroke

§ Race

§ Sex

§ Sickle cell disease

modifiable risk factors for stroke

§ CVD

§ CAD

§ Diabetes

§ Excess weight

§ HTN

§ High cholesterol

§ Cigarette smoking

§ Heavy drinking

§ Physical inactivity

§ Poor nutrition

§ Use of birth control pills

s/s of right cerebral hemisphere stroke

-visual and spatial awareness and proprioception

-disoriented

-impulsivity and poor judgement

-depression, anger, and quick to become frustrated

-ataxia

-loss of depth perception

-left sided weakness/paresthesia

what is ataxia

decreased coordination/loss of balance

s/s of left cerebral hemisphere stroke

-speech, language, mathematic skills, analytic thinking

-alexia

-agraphia

-agnosia

-expressive and receptive aphasia

-right-sided weakness and paresthesia

what is alexia

reading difficulty

what is agraphia

writing difficulty

what is agnosia

unable to recognize familiar objects

etiology/pathogenesis of ischemic stroke

partial or complete occlusion of cerebral blood flow d/t thrombus or embolus

where do most embolisms come from

cardiac origin

-atherosclerosis

-Afib

-breakage of atherosclerotic plaque from carotid artery

most common cause of ischemic stroke

emboli that pass through carotid arteries typically occlude the middle cerebral artery

less common cause of ischemic stroke

emboli that pass through vertebral or basilar arteries lodge at the apex of the basilar artery or posterior cerebral arteries

etiology/pathogenesis of hemorrhagic stroke

· Bleeding into brain from burst blood vessel

o Intracerebral

o Intraventricular

o Extracerebral

· Subarachnoid hemorrhage

· Cerebral aneurysm

· Arteriovenous malformations (AVMs)

· Hematologic conditions that increase stroke risk:

o Thrombocytosis

o Hypercoagulable states- meds

non-surgical tx for hemorrhagic stroke

-priority of care depends on adequate ventilation and management of BP (reverse meds)

-osmotic diuretics (mannitol) decrease intracranial pressure

-glucose is monitored and normoglycemia maintained

surgical tx for hemorrhagic stroke

· Surgical evacuation for supratentorial intracranial hemorrhage

· Craniotomy for lobar and cerebellar hemorrhages

· Craniotomy with aneurysm clipping for aneurysmal subarachnoid hemorrhage

s/s of hemorrhagic/ischemic stroke

FAST

-facial drooping

-arm weakness

-speech impairment

-time to call 911

how to assess facial drooping

ask pt to smile- look for unilateral facial drooping

how to assess for arm weakness

ask pt to raise both arms- look for downward drift

how to assess for speech impairment/difficulty speaking

ask pt to repeat a simple phase- listen for unexpected findings such as slurred speech

s/s of hemorrhagic and ischemic stroke

-FAST

-sudden confusion, trouble speaking or understanding others

-sudden numbness/weakness in face, arm, or leg

-sudden trouble seeing in one or both eyes

-sudden dizziness, trouble walking, or loss of balance/coordination

stroke dx

· Exclusion of conditions that mimic TIA

· Blood glucose

· CBC, coag panel

· Electrocardiography

· Non-contrast CT

· MRI with diffusion-weighted image

· CT angiography/ magnetic resonance angiography

· Carotid doppler

· Dysphagia screening

joint commission core measures for stroke

· VTE prophylaxis

· Thrombolytic therapy

· Reevaluation of antithrombotic therapy

· Provide and document stroke education

· Determine the need for rehab

what is aphasia

cerebral hemisphere damage resulting in speech or language problems

types of aphasia

expressive, receptive, mixed/global

what is expressive aphasia

broca/motor

-motor speech problem

-pt can understand what is being said but cannot speak

what is receptive aphasia

Wernicke/sensory

-pt cannot understand the spoken or written word

what is mixed/global aphasia

reading and writing are equally affected

what is proprioception

body position sense and/or peripheral sensation to be free from injury

what is unilateral neglect

· most common with right cerebral stroke

o Teach the pt to touch and use both sides of the body

o Remind pt to dress the affected side

o Turn head from side to side to expand the visual field

o Place objects within field of vision

o Support affected arm: subluxation can occur from weight of arm

tx of ischemic stroke

-restoration of blood flow and reducing area of infarction

-penumbra

-know when symptoms started

-supplemental O2 (maintain 94%)

-frequent VS

-glycemic control

what is penumbra

tissue surrounding infarction

med therapy for ischemic stroke

-fibrinolytic therapy

-anticoagulants

-anti-HTN therapy

-cholesterol lowering agents

components of fibrinolytic therapy

-tissue plasminogen activator (t-PA)

-give within 45 mins

-can be within 3-4.5 hours

components of anti-coagulants

o Warfarin

o Dabigatran, apixaban, ribaroxaban

o Aspirin, clopidogrel

anti-htn therapy for ischemic stroke

ACE inhibitors, diuretics, CCB

components of cholesterol lowering agents with ischemic stroke

o Hypothermia

o Elevate HOB to 30 degrees to reduce ICP

o Seizure precautions

o NIHSS scoring

surgical interventions for ischemic stroke

-thrombectomy

-carotid artery angioplasty with stenting

-extra-cranial bypass

-carotid endarterectomy

types of thrombectomy

mechanical, endovascular, intra-arterial

components of carotid artery angioplasty with stenting

o involves inserting a catheter in the femoral artery and placing a distal/embolic protection device to catch clot debris during the procedure while a stent is being placed in the carotid artery to open a blockage

§ CAS is less invasive, blood loss is decreased, and length of hospitalization is shorter

§ Post op care is same as carotid endarterectomy

components of extracranial-intracranial bypass

o craniotomy performed to improve cerebral perfusion following a stroke or for pts who have had a TIA that is likely to progress to a stroke

§ Can decrease blood flow around a blocked artery and can help restore blood flow to affected areas of that brain

components of carotid endarterectomy

o opens the artery by removing atherosclerotic plaque

§ Performed when carotid artery is blocked or when pt is experiencing TIAs

§ Assess for increased HA, neck swelling, and hoarseness of voice

§ Have emergency airway equipment available for use

s/s of increased ICP

§ Change in LOC

§ Change in GCS- decreasing score

§ Change in motor and sensory function

§ Change in breathing pattern

§ Trends in VSagitation

§ Impending doom

early signs of ICP

-HA, N/V

-confusion

-blurred/double vision

late signs of ICP

-cushing's triad

-pupils fixed and dilated

-posturing (decorticate/decerebrate)

-coma

what. is cushing's triad

widening of pulse pressure, bradycardia, irregular breathing patterns

decorticate/decerebrate posturing

interventions for increased ICP

§ ABC

§ Keep CPP >60 mmHg

· HOB 30-45 degrees

§ Maintain shunt

§ Sedation and analgesic

§ Skin integrity

§ Adequate nutrition: parenteral or enteral feedings

§ Prevent secondary injury

meds for increased ICP

§ Diuretics, osmotic agents

§ Sedation

§ Pain control

§ Barbiturates

§ Neuromuscular blocking agents

surgical tx for increased ICP

§ Hemicraniectomy

§ Ventriculostomy

§ Subarachnoid bolt

etiology/pathogenesis of post-concussive syndrome

persistence of symptoms following injury; may occur after TBI of any severity

s/s of post-concussive syndrome

· Lightheadedness

· Vertigo

· HA

· N/V

· Photophobia

· Cognitive and memory dysfunction

· Tinnitus

· Blurred vision

· Difficulty concentrating

· Amnesia

· Fatigue

· Personality change

· Balance disturbance

tx for ICP and subarachnoid hemorrhage

§ Mannitol, hypertonic saline, and barbiturates

§ Sedation and pain management: fentanyl and propofol

§ Seizure prophylaxis: start within 7 days of injury

§ Fever control- acetaminophen

§ Other: PPI, DVT prophylaxis, and insulin

§ Surgical:

· External ventricular drains or cistern ostomy

· Decompressive craniectomy

what is a subarachnoid hemorrhage

-blood enters space (arachnoid and pia membrane)

-initiates signaling cascade

-initiate multiple damaging processes within the brain; including disruption of the blood-brain barrier and damage brain cells

s/s of subarachnoid hemorrhage

-early brain injury, such as transient cerebral ischemia occurs within minutes of injury

-ICP begins increasing rapidly, decreasing the CPP and leading to reduced cerebral blood flow

-cerebral vasospasm typically can occur within 3 days after SAH and can continue for three weeks

optimal care guidelines for SAH

-reduce 1 year mortality

-admin of anti-HTNS (SBP greater than 160)

-admin of nimodipine

-coiling or clipping of ruptured aneurysm

pharm tx for SAH

o Antifibrinolytic therapy: tranexamic acid (TXA)

o Anti-HTN: CCB (nicardipine)

o Managing Vasospasms: CCB (Nimodipine)

o Anticonvulsants levetiracetam (Keppra)

o Anti-pyretic (acetaminophen)

o Managing hypotension norepinephrine (levophed)

surgical tx for SAH

o Clipping the rupture aneurysm: clip is placed on the neck of an aneurysm to prevent further blood flow

o Endovascular coiling: an aneurysm entails inserting a microcatheter into the femoral artery with a coil attached to the tip

hyperbaric O2 therapy for SAH

· using increased amount of atmospheric pressure and breathing of increased O2 amounts

o HBOT can also help improve cognitive functions, such as memory, executive function, attention, and motor skills

SAH

goals for end of life care

-managing symptoms of distress

-pain

how to manage symptoms of distress during end of life care

-pain

-weakness

-breathlessness/dyspnea

-N/V

-agitation/delirium

-seizures