2024 NUR 730 Study Guide: Brain Trauma, Tumors, & Aneurysms PDF

**2024 NUR 730 Content Review for Brain Trauma (TBI), Brain Tumors, & Brain Aneurysms** **Brain Tumors & Aneurysms** - **Review Slides 6-8 What is the Windkessel Effect? Be able to describe this in detail**. - The **Windkessel effect** is a phenomenon in the cardiovascular sys...

**2024 NUR 730 Content Review for Brain Trauma (TBI), Brain Tumors, & Brain Aneurysms** **Brain Tumors & Aneurysms** - **Review Slides 6-8 What is the Windkessel Effect? Be able to describe this in detail**. - The **Windkessel effect** is a phenomenon in the cardiovascular system that describes how large, elastic arteries (like the aorta) help dampen the pulsatile nature of blood flow from the heart. It allows for a smoother, continuous flow of blood in smaller vessels, even between heartbeats. - Passive contraction after vessel expansion helps maintain relatively constant pressure in the arteries - If a vessel wall is weakened (as in an aneurysm), the increased pulsatile pressure from the heart may not be properly absorbed or smoothed out. - The excessive stress caused by these pulsatile forces can contribute to the growth and potential rupture of the aneurysm. - **What is arterial elasticity?** also called arterial compliance. The ability of arteries to expand/contract with each heartbeat - Cerebral aneurysms are caused by a loss of elasticity in brain's arterial walls - **How does the Windkessel effect help in cerebral aneursyms?** - Dampens pulsatile flow and aids perfusion by keeping pressure inside the vessel constant which helps prevent hemorrhage in the distal circulation - In larger aneurysms, the aneurysmal pouch serves as a reservoir in systole and releases blood in diastole - **What conditions increase arterial oscillations?** dehydration, hemorrhage, upright posture - **Review Slides 9-24- Subarachnoid hemorrhage-** - What is it? What is the incidence of SAH? - Arterial bleeding from the SA space between the arachnoid and pia maters of the brain usually the result of a ruptured cerebral aneurysm - How will patients with SAH present? Worst headache of my life with signs and symptoms of increased ICP - What are the risk factors associated with SAH? Risk factors = smoking, HTN, birth control pill use+ smoking, Marfan syndrome, primordial dwarfism, Ehlers Danlos syndrome - What happens in the body when a SAH occurs? - Mass effect due to blood pouring into the SA space - Acute global ischemia caused by increased ICP and resulting decreased CBF - Cellular changes = increased inflammatory mediators, platelet and thrombin activation, disrupted BBB - Systemic complications associated with SAH - Decreased intravascular volume - Electrolyte abnormalities = hyponatremia, hypokalemia, hypocalcemia - Cardiac changes such as ST elevation/depression, t wave abnormalities, U and Q waves - Peak symptoms appear at 2-3 days - Etiology = injury to the posterior hypothalamus resulting in NE release - Respiratory - Cardiogenic and neurogenic pulmonary edema - ARDS, pneumonia, sepsis - Hepatic dysfunction in 25% of pts - Renal dysfunction appears mostly in septic pts - Thrombocytopenia associated with sepsis, antibiotic use - GI bleeding suspected with sudden ST changes and hypotension Name the types of cerebral aneurysms? - Saccular are \2.5 cm - Fusiform severe atherosclerotic or childhood degenerative processes - Dissecting caused by tear between endothelium and media of vessel - Traumatic - Mycotic caused by infection - Dolichoectatic are chronic and progressive -- cause brainstem ischemia - Serpentine consist of partially thrombosed giant aneurysm transversed by a patent twisting intraneurysmal vascular channel with an entry and an exit point - Where are they located? - 90% in anterior circulation, 10% in posterior circulation - Females usually have aneurysm in internal carotid - Male usually located in anterior communicating artery - Children usually located in internal carotid bifurcation - What is the treatment for these? - How should these be managed? - How are they graded? - Higher scores are associated with worse outcomes - Hunt and Hess based on clinical signs and symptoms - World federation of Neurological surgeons scale based on GCS - What are the associated complications -- - Rebleeding - Highest risk in first 24 hours - Risk decreases 1-2% per day for the next 13 days - Sx = decreased LOC and focal neurologic deficits, HTN, bradycardia, irregular respirations, hemorrhage on ophthalmic exam - Vasospasm = reactive narrowing of the larger vessels in the SA space surrounding the clot after SAH - Onset occurs in 3^rd^ day with peak 6-8 days - Resolves by 3 weeks - All pts have 50% chance of vasospasm - Impaired autoregulation leads to oxidative stress and release of free radicals - Decrease CBF - Decrease CMRO2 - Change smooth muscle tone - Damage endothelial cell function = inflammation and eventual apoptosis - Preserved response to changes in CO2 so that level of autoregulation is maintained - Intracranial HTN - Hydrocephalus occurs due to disruption of production and drainage of CSF - Seizures - Headache - Prevent and treat rebleeding and vasospasm - Timely surgical intervention with critical time of 24-48 hours after SAH - Embolization = clotting or closing off the vessel via coils or clipping - Transluminal angioplasty - Prevention is key so that's why pt's are placed on Nimodipine = calcium antagonist aka calcium channel blocker - Nimodipine needs to be started within 96 hours of SAH - Nimodipine is a lipophilic cerebral vasodilator that can cross the BBB and prevents vasospasm - Nimodipine preferentially acts on cerebral blood vessels due to its lipophilic properties and ability to cross the BBB - Triple H therapy = hypertension, hypervolemia, hemodilution - **Slides 25-53- Anesthetic Considerations, Surgical Management & Aneurysm Rupture, Induction, Maintenance, Emergence-** - Surgical interventions - Aneurysm clip ligation - Aneurysm is clipped and ligated - Needs to be done in first 24-48 hours - Aneurysm coiling - Alternative to clipping that is done under fluoroscopy via a femoral artery approach - Done under GA with routine monitors and a-line - Nipride and phenyl drips are standard - Cannot be done for smaller aneurysms or in difficult areas to access - Flow diverting stents - Instead of placing a device inside the aneurysm sac, a stent is placed to bypass flow around the aneurysm - Only can use this in unruptured aneurysms - Complications = thrombosis and stenosis of patent artery - Aneurysm rupture on induction - Symptoms = increased BP with or without bradycardia - Potential for increased ICP - Need rapid surgical control! - Immediately after identification need to reduce MAP to \~40-50mmHg (i.e. permissive hypotension) for clipping and increase after clipping, replace blood loss with blood - Treatment = maintain CPP, control ICP, reduce bleeding - Blood should be in your room prior to incision - Medications to have ready - Nitroglycerin, nipride, and Neo gtt - Need at least 4 IV pumps - Mannitol 5 g - Dilantin 1 g - Decadron - Positioning considerations - HOB will be turned to left or right 90 degrees - Head tongs or pins will be applied by the surgeon and are very stimulating - Intraoperative management considerations - Temporary proximal occlusion clamp - Reduce risks of rupture of aneurysm during surgery - Produces local hypotension and decreases transmural pressure without problems associated with systemic hypotension - Temporary occlusion for \20cm above heart - Air entrainment occurs very slowly so that's why we use precordial dopplers - What happens in VAE? - Dead space ventilation is increased which results in decreased ETCO2 and increased PaCO2 - Nitrogen appears in exhaled gas on analyzer - Hypotension and tachycardia appear - Hypoxemia - Right heart pressures increase - If untreated, cardiac output decreases due to right heart failure and/or reduced LV filling - Prevention - PEEP and volume loading can increase ICP but can minimize the pressure gradient that allows air to enter the venous system - Deliberate hypoventilation can increase ICP - PAE = paradoxic air embolism = air crosses into arterial circulation - Risks = PFO, sitting position - Use different position - TEE gold standard for PAE detection - **Remember that the first 2 immediate courses of action for a VAE usually. occur simultaneously and are:** 1. Alert the surgeon and ask him to flood the field. The CRNA does not flood the field so answering "Flood the field" is not a complete answer. 2. CRNA will aspirate blood/air from the CVP. There is no need to reposition the patient unless you are unable to aspirate blood/air well. - **Immediately after aspiration, follow steps 3 & 4. All of these steps are done very close together** - 3\. Increase FiO2 o 100% if not already on 100% - 4\. Turn off N2O