Week 3 Review PDF

Week 3: Increased intracranial pressure, TBI & stroke Increased intracranial pressure There are 3 components of the cranium o Brain tissue (makes up most of the content) o Blood o Cerebrospinal fluid (CSF) Normally, the volume of these 3 components is...

Week 3: Increased intracranial pressure, TBI & stroke Increased intracranial pressure There are 3 components of the cranium o Brain tissue (makes up most of the content) o Blood o Cerebrospinal fluid (CSF) Normally, the volume of these 3 components is stable and intracranial pressure is within normal limits If there is any change to the volume of any of the 3 components, this will change the intracranial pressure Regulating and maintaining ICP Normal ICP: under usual conditions, the balance among brain tissue, blood and CSF maintain the ICP (normal range 3-15 mmHg) Modified monro-kellie doctrine o Describes a dynamic equilibrium in the skull o If the volume of one component increases, another must decrease to maintain total intracranial volume o If one component’s volume increases without a corresponding dec in another, ICP rises Anything above 20 = increased pressure Kids are more resistant to higher pressure bc of sutures, skulls are not as rigid, and have different soft parts Factors that can affect ICP Changes in: o Blood pressure o Cardiac function —> increase venous pressure —> can cause changes o Intra-abdominal and intra-thoracic pressure o Body position – lying flat can inc pressure, upright can reduce o Temperature (hyperthermic —> inc cerebral blood flow —> inc ICP) o Blood gases, particularly CO2 (inc CO2 = inc ICP) Degree to which these factors increase or decrease ICP depends on the ability of the brain to accommodate to the changes Regulating and maintaining ICP Compliance – the ability of the brain to adapt to increases in ICP Normal compensatory mechanisms o Displacement of CSF into the spinal canal o Reduction of blood volume – this alters brain metabolism and eventually leads to hypoxia and ischemia o Brain tissue can shift or compress (but has limited ability to do this) If compensatory mechanisms fail, this leads to: o Increased ICP o Neuronal compression (displacement and herniation of brain tissue) o Ischemia (sustained ICP —> neurocompression —> herniation —> ischemia) ▪ Herniation = medical emergency Herniation occurs really late in ICP inc This is last thing that may happen and is potentially fatal Cerebral blood flow The brain uses 25% of body’s oxygen and 25% of body’s glucose o Doesn’t have the ability to store O2 and glucose so we have to have adequate blood flow to ensure functioning o If we have any disruption in cerebral blood flow it can lead to significant neuro deficits Autoregulation Ability of the brain to maintain cerebral blood flow to meet metabolic needs Cerebral blood vessels can dilate or constrict to ensure the brain received enough blood Does not work in cases of severe hypotension or severe hypertension o If mean arterial pressure is less than 50 mmHg or greater than 150 mmHg Other factors affecting cerebral blood flow CO2 – important one o Increasing levels of CO2 will cause increasing vasodilation bc body will attempt to increase cerebral blood flow o Decreased levels –> vasoconstriction Low levels of oxygen – body will cause cerebrodilation form ore blood flow into brain o If oxygen levels are really high – cerebrovascular vasoconstriction Acidosis: high level of hydrogen ion = dilation. Low levels = constriction Regulation to ensure we have adequate perfusion But what if it doesn’t work? Switch to anaerobic metabolism —> producing lactic acid —> H+ —> increase vasodilation —> loss of autoregulation Cerebral hemodynamics Cerebral perfusion pressure (CPP): amount of blood flow from the systemic circulation needed to maintain adequate blood flow to brain tissue o Normal CPP is 70-100 mmHg o Minimum CPP of 50-60 mmHg is needed for adequate perfusion o CPP < 50 mmHg —> cerebral ischemia Mean arterial pressure (MAP): the avg pressure during the cardiac cycle o MAP = DBP + 1/3 (SBP-DBP) or SBP + 2(DBP) (no questions on calculating MAP) 3 o 70-110 mmHg o CPP = MAP – ICP ▪ Understand that diastolic pressure is longer in terms of length of cardiac cycle ▪ MAP has to balance ICP out – if ICP is stable but MAP decreases = problems with perfusion —> dec perfusion to brain Pressure-volume curve (not asked to draw on test) Intracranial compliance is the change in volume per unit change in pressure Compliance refers to the ability of the volume of brain tissue, blood and CSF to accommodate change in volume Curve has 4 stages from high compliance to low compliance o Small changes in volume —> high compliance = no change in ICP o At 4, any increase in volume can lead to extreme changes in pressure (increase) Causes of Increased ICP Brain tissue o Brain tumour —> growth in brain tissue o Contusion —> leads to swelling o Abscess —> can increase tissue volume o Edema  Blood o Hemorrhages —> accumulation of blood in spaces o Hematoma —> pool of mostly clotted blood in an organ, tissue, or body space o Metabolic and physiological factors – hypoxia, hyper cap is, lying flat CSF o Hydrocephalus – excess CSF within brain ventricle o Brain tumour that affects CSF —> tumour can obstruct flow or stimulate production of CSF or disrupt areas in brain where CSF is being absorbed Cerebral Edema Contributes to increased ICP, as fluid accumulates in the extra vascular spaces of brain tissue Many causes (e.g. lesions, tumours, hemorrhages, infections) Three types of cerebral edema o Vasogenic (most common): blood-brain barrier is disrupted, causing fluid to leak from blood vessels into the surrounding brain tissue; primarily affects the white matter o the brain o Cytotoxic: brain cells swell d/t the accumulation of fluid inside the cells —> inc risk for stroke o Interstitial: CSF leaks from the ventricles into the surrounding brain tissue ▪ Associated with conditions like hydrocephalus or meningitis Clinical manifestations of increased ICP Earliest indicator is change of LOC Changes in VS are caused by pressure on the thalamus, hypothalamus, pons and medulla Cushing’s triad is associated with increased ICP o Abnormal resp patterns o Bradycardia with full bounding pulse o Increased SBP with widening pulse pressure ▪ Seeing all 3 signs in cushing’s triad = not good Early signs – compensatory Late Signs – compensatory Terminal signs – decompensation mechanisms intact mechanisms failing Altered LOC (confusion, dec LOC (stupor) Coma restlessness) Unilateral or bilateral pupillary Bilaterally fixed and dilated Unilateral pupil change in size, changes: size, equality and/or pupils equality, and/or reactivity reactivity Respiratory arrest Altered resp pattern Ineffective breathing pattern Absence of motor response (bradypnea, or irregular) (Cheyne-Stokes respirations) (flaccid) Unilateral hemiparesis (one- Abnormal motor response sided muscle weakness) (decorticate or decerebrate posturing) Variable signs Variable signs Focal findings (e.g. speech HTN with widened pulse pressure difficulty, visual disturbances) Bradycardia Papilledema (swollen optic Hyperthermia nerve) Vomiting Headache Seizures Cerebral herniation Life threatening complication Brain tissue can shift downwards from the skull into the brainstem, and pressure can force the cerebellum and brain stem downward through the foramen magnum (hole in the base of the skull where brain connects to spinal cord) Signs: unilateral, fixed dilated pupil; Cushing’s triad Diagnostic tests Goal is to identify the underlying cause CT scan – x-rays to see brain injury, bleeding, tumours etc. MRI – takes very long, not good for emergencies o Provides good picture, good for brain tumour identification, stroke, etc. CTA/MRA – computed tomography angiography & magnetic resonance angiography o Non-invasive imaging that provides detailed info about blood vessels  Measurement of intracranial pressure (neuro-monitoring in ICU) Management Monitoring (vitals, electrolytes, ICP, brain tissue oxygenation) Decrease environmental stimuli (can inc ICP) Positioning can help to reduce ICP include by improving venous drainage: o Elevation of HOB at 30 degrees o Maintaining the head and neck in alignment o Avoiding flexion at the hip Surgical intervention if required – decompressive craniotomy, evacuating hematomas Medications (e.g. sedatives, mannitol) o Mannitol is an osmotic diuretic that moves fluid from the extravascular space into the blood (intravascular space) ▪ Given via IV o Need to monitor fluids and electrolytes o Sedatives: dec metabolic need, vasodilator, dec agitation of pt Nutritional therapy o Early nutrition after TBI can improve pt outcomes o Ideally started within 5 days of injury o Can use tube feeds or TPN Glasgow Coma Scale (GCS) GCS is standardized way to assess pt’s LOC 3 areas corresponded to the definition of coma as: o Inability to speak o Inability to obey commands o Inability to open eyes to verbal/painful stimuli 3 indicators o Eye opening o Best verbal response o Best motor response Conditions that render GCS invalid o Nonverbal pt (may be dementia) o Baby o If condition doesn’t allow us to assess them using the parameters o Language barrier o Trauma – eyes swollen or trauma to face o Blind pts o Prior paralysis A: abnormal flexion of extremities – damage to both sides of cerebral hemisphere o Brain injury above level of brain stem o Better prognosis than B B: abnormal extension of extremities – more severe damage to brainstem o Poorer prognosis Traumatic brain injury Scalp lacerations – bleeding, watch for infection and extent of injury  Skull fractures – simple, basilar, depressed, etc. Head trauma – general term for any head injuries (e.g. bruising, hematoma, concussion) o Leading cause is car accidents, driving under influence o Males, young adults under 30 are most likely to be affected Basilar Skull Fracture Key signs and symptoms o Periorbital edema and ecchymosis – raccoon eyes, bleeding under skin deep down o Postauricular ecchymosis – battle’s sign – bruising ver the mastoid process o Rhinorrhea – CSF comes out of nose o Otorrhea – CSF out of ear o Serious head trauma Testing fluid for CSF Use gauze and apply to liquid – see clear yellowish ring around spot of blood = halo sign o Suggests leak of CSF Traumatic brain injury Categorized as diffuse (generalized) or focal (localized) Mild: GCS 13-15 Moderate: GCS 9-12 Severe: GCS 3-8 (lowest GCS score is 3 – can have score lower than 3 if unable to assess) Diffuse brain injury Involves multiple areas of the brain Major cause: sports Concussion o Mild concussion o Post-concussion syndrome o Chronic traumatic encephalopathy Diffuse axonal injury – rapid acceleration/severe force causing injury o Some damage along the axons o Very serious implications Concussion Jarring injury of the brain – results in a disturbance of cerebral function; aka mild traumatic brain injury (mTBI) Only one symptom (e.g. dizzy, nausea, H/A) following a head injury is needed for diagnosis Sport concussion assessment tool: SCAT-5 Signs and symptoms include: H/A, weakness, dizziness, vomiting, nausea, lack of coordination, difficulty balancing Treatment = bed rest (physical and mental), followed by a slow transition to light activity Red flags (indicate severe concussion): neck pain or tenderness, double vision, weakness or tingling/burning in arms or legs + severe or increasing headache, seizure or convulsion, loss of consciousness, deteriorating conscious state, vomiting, increasingly restless, agitated or combative Post-concussion syndrome Chronic traumatic encephalopathy Can occur 2 weeks to 2 moths post From repeated concussions concussion H/A, lethargy, personality changes, Progressive brain disease, behaviour changes, changes to development of dementia attention, dec short-term memory Diffuse axonal injury (DAI) With DAI, there is shearing, tearing or stretching of axons Can occur w mild, mod, or severe brain injury Develops 12-24 hours post-brain injury Signs: decreased LOC, inc ICP, cerebral edema Focal brain injury Mild to severe, localized to the injured area Lacerations involve tearing of brain tissue – occurs with skull fractures & penetrating injuries Contusion is a bruising of brain tissue o Associated with skull fractures o May develop with hemorrhage, infarction, and edema Coup & contrecoup injury Review of Brain Anatomy Brain is protected by the skull, CSF, and 3 membranes called the meninges Dura mater = outermost layer of protection o Tough, fibrous, and leather-like tissue Arachnoid mater = middle protective layer o Thin, delicate, fibrous membrane Pia mater = innermost protective layer of connective tissue Epidural hematoma Results from bleeding between the dura mater and the skull (epidural space) Most caused by arterial bleeding and are an emergency o Venous epidural hematomas are less common and develop slowly Typically, person becomes unconscious, has moment of lucidity, and then dec LOC Pt will need rapid surgical intervention to remove hematoma to relieve pressure on the brain Subdural hematoma Results from bleeding between dura mater and arachnoid mater Usually caused by brain and brain blood vessel injury Typically venous bleeding Can be acute, subacute, or chronic Symptoms: dec LOC, confusion, lethargy o Symptoms can take weeks to develop Intracerebral hematoma & subarachnoid hemorrhage Intracerebral hematoma Subarachnoid hemorrhage Bleeding within the brain tissue itself Bleeding between arachnoid mater and pia mater Can be a result of trauma, ruptured Can be result of trauma, ruptured cerebral aneurysm, arteriovenous cerebral aneurysm, or an arteriovenous malformation, or hypertensive injury to malformation blood vessel walls Cerebral hemorrhage: clinical manifestations Depend on type of hemorrhage Common manifestations include: changes in LOC, H/A, N&V Epidural hematoma Subdural hematoma Subarachnoid hematoma Intracerebral hematoma -may present w initial LOC, a -acute presentation is -sudden onset severe h/a -h/a, vomiting, dec LOC lucid interval, followed by similar to epidural “worst ever”; associated -neuro signs vary w location rapid deterioration (H/A, hematoma symptoms incl: brief LOC, of hemorrhage vomiting, drowsiness, -chronic – more insidious vomiting, neck pain or (h/a, light-headed, cognitive stiffness  confusion, aphasia, seizure, impairment, apathy, -signs of meninges hemiparesis) somnolence, occasional irritation/inflammation -signs of inc ICP seizures); symptoms may (nuchal rigidity, not appear till wks later photophobia, blurred vision, irritability, restlessness, low- grade fever); positive kermit sign, positive Brudzinski sign Management Specific to cause; focus on cessation of bleeding and controlling ICP Diagnostic tests similar to those for pts with inc ICP Always do neck x-ray to assess for assoc C-spine injury (head injury can cause C-spine injury) Often requires ICU or specialized care Large subdural and epidural hematomas may req surgery Stroke Referred to as cerebral vascular accident (CVA) Stroke is the leading cause of disability and 3rd leading cause of death in Canada Risk factors include: o HTN and type 2 diabetes o CVD o A fib o Valvular disease o Oral contraceptive use in certain conditions ▪ Hypertensive and smokers ▪ Use with migraines inc risk for stroke Transient ischemic attacks Episodes where neurological deficits occur for up to one hour Considered to be a warning sign of an ischemic stroke Signs and symptoms depend on the location of the affected artery o Include unilateral weakness or numbness, diplopia (double vision), sudden confusion, loss of balance, and speech deficits (slurring words) Ischemic stroke Occurs when there is an obstruction to arterial blood flow to the brain which causes ischemia and can lead to death of brain tissue (infarction) Thrombotic stroke o Usually due to atherosclerosis and inflammatory processes that damage the walls of blood vessels in the brain o Plts and fibrin stick to the damaged blood vessel wall and forms a clot o Risk factors: HTN and diabetes Embolic stroke o Occurs when embolus lodges in and occludes cerebral artery o Sources of emboli include blood clot or other debris (i.e. fat, tumour) o Risk factors: A fib, endocarditis, valvular heart disease Hemorrhagic strokes Primary cause of an intracerebral hemorrhage is chronic HTN o Weaken blood vessels OT – can lead to rupture and bleeding Intracerebral hemorrhages are also caused by trauma, coagulation disorders and cocaine use (cocaine use assoc. w severe HTN)  Subarachnoid hemorrhages are caused by ruptured cerebral aneurysms or arteriovenous malformations Clinical manifestations of stroke Similar between ischemic and hemorrhagic stroke S&s will depend on the location of the stroke Clinical manifestations include o Hemiparesis – weakness on one side of body o Hemiplegia – paralysis on one side of body o Dysphagia – difficulty swallowing o Dizziness o Ataxia – lack of muscle coordination —> inc falls risk o Sensory deficits Inc ICP and development of cerebral edema more common w hemorrhagic stroke, but can occur w ischemic stroke Left-brain damage Right-brain damage Paralyzed right side: hemiplegia Paralyzed left side: hemiplegia Impaired speech-language (aphasias) Left-sided neglect Impaired right-left discrimination Spatial-perceptual deficits Slow performance, cautious Tends to deny or minimize problems Aware of deficits: depression, anxiety Rapid performance, short attention span Impaired comprehension related to language, Impulsive; safety problems math Impaired judgment Impaired time concepts Evaluation of stroke CT or MRI of head used for diagnosis o CT scan = easier to access and faster o Either can indicate the size & location of stroke and differentiate b/w ischemic and hemorrhagic CTA – allows for visualization of cerebral blood vessels o Identify blockages, aneurysms, or arterial malformations Cerebral angiography – more detailed images of blood vessels Stroke: prevention Control of HTN, DM, and treatment of underlying cardiac issues (i.e. AF) Lifestyle mods (i.e. quit smoking, exercise, limit alchol, etc) Med therapy (in patients with previous transient ischemic attacks (TIA)) Antiplatelets o Aspirin (ASA): antiplatelet drug ▪ Inhibits cycle-oxygenate, the enzyme req to help plts create thromboxane ▪ Thromboxane plays key role in pat aggregation o Clopidogrel (placid) ▪ Inhibits plt aggregation ▪ Works by inhibiting P2Y12 receptor on plts which prevents pat aggregation ▪ Effects are not reversible, meaning that effects lasts 7-10 days after last dose ▪ Can be given w aspirin o Surgical therapy (e.g. transluminal angioplasty) ▪ Treat narrow or blocked arteries of the brain – good for ppl w large areas of atherosclerosis which can lead to full blockage Stroke: Acute Care Manage ABCs, maintain cerebral oxygenation Manage fluid and electrolyte balance Restore cerebral blood flow (ischemic stroke) – thrombolytic therapy Present and manage complications (i.e. bleeding, cerebral edema, stroke recurrence, aspiration) Surgical therapy o Ischemic stroke: endovascular tx can be used to remove the clot o Hemorrhagic stroke: may need surgery to evacuate the hematoma o Aneurysms can be treated by clipping of the aneurysm in the operation room or coiling of the aneurysm in interventional radiology Rehabilitation Medication summary Drug Use/Nursing Considerations Thrombolytics (alteplase [tPA]) Used to dissolve blood clots during an acute ischemic stroke. Most effective when administered within 3-4.5 hours of onset Monitor closely for signs of bleeding Perform frequent neuro vitals Antiplatelets (ASA, clopidogrel) Helps prevent blood clots Pts should be taught to recognize signs of bleeding Meds should be taken exactly as prescribed Avoid taking with NSAIDs (inc risk of bleeding) Anticoagulants (warfarin [Coumadin], Prevent clots from forming Apizaban [Eliquis]) Patients should be taught to recognize signs of bleeding Meds should be taken exactly as prescribed Warfarin is a Vit K antagonists and requires regular blood monitoring (INR 2-3) Warfarin interacts w a wide range of meds, supplements and foods (which can inc/dec its anticoagulant effect) Apixaban is a DOAC (direct oral anticoagulant) and can also interact w various meds Other meds (e.g. statins, Used to manage risk factors nano prevent stroke (e.g. high cholesterol, high bp) antihypertensives) Review Questions 1. Which cranial nerve is responsible for pupil constriction? a. Cranial nerve II b. Cranial nerve III c. Cranial nerve IV d. Cranial nerve VI 2. Which layer of the meninges is the innermost and closely adheres to the surface of the brain? a. Dura mater b. Arachnoid mater c. Pia mater d. Epidural space 3. What is the primary effect of increased levels of CO2 on cerebral blood vessels? a. Vasoconstriction b. Vasodilation c. No effect d. Inc blood viscosity 4. What is the earliest indicator of increased ICP? a. Change in level of consciousness (LOC) b. Headache c. Vomiting d. Seizures 5. Which ocular change is considered an emergency and indicates potential brain herniation in a patient with increased ICP? a. Blurred vision b. Diplopia (double vision) c. Fixed, dilated pupil  d. Sluggish response to light 6. A nurse is assessing a pt using the GSC. The pt opens their eyes only in response to pain, makes incomprehensible sounds, and withdraws from pain. What is the pt’s GCS score? a. 6 b. 7 c. 8 d. 9 ▪ Note: 2(eyes) + 2 (verbal) + 4 (pain) = 8 = intubate (threshold for intubation) 7. A nurse is caring for a pt with post concussion syndrome (PCS). Which of the following are common symptoms associated with this condition? (SATA) a. Long-term memory loss b. Persistent headache c. Difficulty concentrating d. Sensitivity to light and noise 8. A patient presents with a head injury and a period of lucidity followed by a rapid decline in consciousness. Which type of hematoma is most likely? a. Subdural hematoma b. Epidural hematoma c. Intracerebral hematoma d. Subarachnoid hemorrhage 9. Which type of brain injury is characterized by widespread damage to the brain’s white matter, particularly the axons? a. Concussion b. Epidural hematoma c. Diffuse axonal injury (DAI) d. Subarachnoid hemorrhage 10. A nurse is caring for a patient w a suspected transient ischemic attack (TIA). Which of the following symptoms should the nurse expect to find? a. Persistent headache b. Unilateral weakness c. Hemiplegia d. Fixed and dilated pupils 11. A nurse is assessing a pt with right-brain damage following a stroke. Which of the following findings is most likely? a. Impaired speech and language b. Right-sided neglect c. Impulsive behaviour d. Slow and cautious performance 12. A pt is prescribed Clopidogrel (Plavix) for stroke prevention. Which statement by the pt indicates need for further teaching? a. “I will take this medication to prevent my platelets from clumping together” b. “the effects of this medication will last for about a week after I stop taking it” c. “I can take this medication with aspirin if my doctor advises” d. “I can stop taking this medication whenever I feel better”