Brain ischemia Notes


Osmosis High-Yield Notes

This Osmosis High-Yield Note provides an overview of Brain ischemia essentials. All Osmosis Notes are clearly laid-out and contain striking images, tables, and diagrams to help visual learners understand complex topics quickly and efficiently. Find more information about Brain ischemia:

Saccular aneurysm

Subarachnoid hemorrhage

Subdural hematoma

Transient ischemic attack

Epidural hematoma

Intracerebral hemorrhage

Ischemic stroke

NOTES NOTES BRAIN ISCHEMIA GENERALLY, WHAT IS IT? PATHOLOGY & CAUSES DIAGNOSIS ▪ Impaired brain function due to lack of blood DIAGNOSTIC IMAGING TYPES CT scan ▪ Visualize trauma, bleeding, skull fracture Focal ischemia ▪ Occlusion of blood vessel → ↓ perfusion → affected regions damaged ▪ ↓ oxygen → ischemic stroke ▪ Blood vessel rupture → hemorrhagic stroke; bleeding inside parenchyma/between brain membranes Global ischemia ▪ Cardiac arrest → whole brain hypoperfusion → brain damage CAUSES Atherosclerotic plaque/thrombosis/emboli Hypertension Blood vessel malformation Cardiac arrest, tachycardia, congenital heart problems ▪ Tumors ▪ ▪ ▪ ▪ SIGNS & SYMPTOMS ▪ Altered consciousness; weakness; problems with vision, hearing, swallowing; dizziness, vertigo ▪ See mnemonic for common symptoms MRI ▪ Visualize hypointense, hyperintense blood clot MR/CT angiography ▪ Visualize occlusions, aneurysms TREATMENT MEDICATIONS ▪ Antiplatelet medications (e.g. aspirin/ clopidogrel) ▪ IV tissue plasminogen activator (tPA) ▪ Mannitol, other osmotic diuretics ▫ ↑ intracranial pressure treatment SURGERY ▪ Evacuation of blood clot ▪ ↑ intracranial pressure treatment OTHER INTERVENTIONS ▪ Manage conditions that worsen prognosis (e.g. hyperglycemia, fever) MNEMONIC: FAST Common stroke symptoms Facial drooping Arm weakness Speech difficulties Time: reminder to call emergency services 482 OSMOSIS.ORG
Chapter 64 Brain Ischemia EPIDURAL HEMATOMA PATHOLOGY & CAUSES ▪ Nervous tissue compression due to accumulation of blood in epidural space ▪ Head trauma → skull fracture → damage of blood vessels through dura mater → extradural blood accumulation → rapid, limited expansion of hematoma due to tight dura adherence at cranial sutures → brain tissue compression → neurological decline TYPES Intracranial ▪ Frontal injuries ▫ Anterior ethmoidal artery ▪ Temporoparietal (most common) ▫ Middle meningeal artery ▪ Occipital ▫ Transverse, sigmoid sinus ▪ Vertex ▫ Superior sagittal sinus Spinal ▪ Venous plexus of lumbar, thoracic regions CAUSES ▪ Neurosurgical procedures complication ▪ Trauma Intracranial epidural hematoma ▪ Head trauma → pterion skull fracture (most common) ▪ Blood vessel malformations Spinal epidural hematoma ▪ Trauma (e.g. lumbar puncture/epidural anesthesia) RISK FACTORS ▪ More common in individuals who are biologically male, between 2–60 years ▪ Pregnancy ▫ Spontaneous spinal hematoma (very rare) ▪ Systemic lupus erythematosus ▫ Vasculitis, associated with immune system reaction ▪ Coagulopathies, bleeding diathesis, sickle cell anemia COMPLICATIONS ▪ ↑ intracranial pressure ▪ Supratentorial herniation → compression of arteries → ischemic stroke ▪ Infratentorial herniation → brainstem compression → heart, respiratory arrest ▪ Paralysis/sensory loss ▪ Seizures SIGNS & SYMPTOMS ▪ Initial loss of consciousness, lucid state if blood slowly accumulating; delayed neurological deterioration consequence of enlarging hematoma compression ▪ Intracranial epidural hematoma ▫ Broken skull with hematoma ▫ Otorrhea/rhinorrhea ▫ Altered consciousness ▪ ↑ intracranial pressure ▫ Headache ▫ Nausea with vomiting ▫ Cushing reflex (↑ blood pressure, ↓ heart rate, irregular breathing) ▫ Focal signs (weakness of extremities on opposite side; dilated pupil on injured side due to compression of CN III) ▪ Spinal epidural hematoma ▫ Radicular back pain (resembles pain from herniated discus) ▫ Sensory defects ▫ Urinary, fecal incontinence OSMOSIS.ORG 483
MRI ▪ T2-WI: acutely ▫ Hypointense blood clot due to deoxyhemoglobin ▪ T1, T2-WI: in following weeks ▫ Deoxy → methemoglobin; hyperintense blood clot ▪ T1-WI: months later ▫ Methemoglobin → hemosiderin; hypointense mass TREATMENT MEDICATIONS Figure 64.1 A CT scan of the head in the axial plane demonstrating a large epidural hematoma with a classical biconvex shape. DIAGNOSIS DIAGNOSTIC IMAGING X-ray ▪ Skull fracture CT scan ▪ Hematoma: typically presents as a biconvex, relatively heterogeneous, high density mass in the space between skull, brain; does not cross sutures ▪ Swirl sign: bleeding into blood clot, diverse hypoattenuated foci ▪ Assess hematoma volume ▪ Skull fracture 484 OSMOSIS.ORG ▪ Mannitol, other osmotic diuretics ▫ ↑ urine excretion, ↓ intracranial pressure ▪ Anticoagulation reversal ▫ Individuals undergoing surgery, on anticoagulation therapy SURGERY ▪ Craniotomy ▫ Evacuation of blood mass ▪ Embolization/ligation of damaged blood vessel ▪ Trephination (burr-hole) ▫ In acute EDH, if neurosurgical procedure delayed ▪ Laminectomy ▫ ↓ blood in spinal epidural hematoma OTHER INTERVENTIONS ▪ Observation, nonoperative management ▫ Awake, conscious individuals ▫ If hematoma volume < 30cm3, thickness < 15mm, midline shift < 5mm
Chapter 64 Brain Ischemia INTRACEREBRAL HEMORRHAGE PATHOLOGY & CAUSES ▪ Condition characterized by blood vessels rupture → intraparenchymal blood accumulation ▪ Blood vessel trauma, rupture → creates pool of blood → tissue, surrounding blood vessel compression → hypoxia in downstream tissue → damage due to compression, oxygen lack CAUSES Hypertension ▪ Most common ▪ Leads to ▫ Atherosclerosis in large arteries ▫ Hyaline arteriolosclerosis → focal arterioles necrosis → small wall ruptures → subclinical microbleeds ▫ Charcot–Bouchard aneurysms (microaneurysms) ▪ Basal ganglia; thalamus; midbrain; pons; cerebellum primarily affected Vascular abnormalities ▪ Cerebral amyloid angiopathy ▫ Deposition of amyloid in blood vessel walls → vessels more prone to rupture ▫ Lobar localization: parietal, occipital lobes ▫ Blood vessels: leptomeningeal, cerebral cortical arterioles ▪ Arteriovenous malformations ▫ Usually affect children ▪ Aneurysm, vasculitis, vascular tumours (e.g. hemangioma) Other causes ▪ Secondary to ischemic stroke ▫ Blood flow blockage → reperfusion → ↑ chance of blood vessel rupture → bleeding into dead tissue (hemorrhagic conversion) ▪ Posttraumatic ▪ Coagulopathies ▪ Sickle cell disease RISK FACTORS ▪ Individuals who are biologically male of Asian descent ▪ Black individuals who are biologically male of African descent ▪ Heavy alcohol use; amphetamines, cocaine abuse, antithrombotic medications; ↓ LDL, cholesterol, triglycerides; previous cerebrovascular insult COMPLICATIONS ▪ Hemorrhage enlargement ▫ In hemorrhage border ▫ Poor prognosis ▪ Intraventricular, subarachnoid expansion ▪ Hydrocephalus SIGNS & SYMPTOMS ▪ Begin slowly, worsen gradually ▪ Enlargement of hematoma within few hours, ↑ intracranial pressure ▫ Altered consciousness, headache, nausea, vomiting, unequal pupil size ▪ Fever Area of brain affected ▪ Anterior/middle cerebral artery: numbness, sudden muscle weakness ▪ Posterior cerebral artery: impaired vision ▪ Broca’s area: slurred speech ▪ Wernicke’s area: difficulty understanding speech Focal neurological signs ▪ Basal ganglia manifestation: loss of contralateral sensory, motor functions; homonymous hemianopsia ▪ Thalamus: contralateral loss of OSMOSIS.ORG 485
sensory, motor functions; homonymous hemianopsia; aphasia if dominant/neglect if nondominant; narrowed pupils unreactive to light ▪ Lobar manifestation: homonymous hemianopsia; if frontal region, contralateral leg plegia/paresis; seizures ▪ Pons: coma within few minutes of hemorrhage; quadriplegia, miosis/deafness; speaking difficulties when awake ▪ Cerebellum: ataxia; same side face weakness; loss of face, body sensory function; occipital headache, neck stiffness DIAGNOSIS DIAGNOSTIC IMAGING CT scan ▪ Hyperdense blood mass acutely; isodense, ring enhancement appearance in subsequent weeks; hypodense chronically ▪ Trauma ▫ Multifocal bleedings ▪ Coagulum retracts, edema develops ▫ Confused with hemorrhagic infarction CT angiography ▪ Spot sign: unifocal/multifocal enhancement of contrast; ↑ risk of hematoma expansion MRI (T2-WI) ▪ Hyperacute (first 24 hours) ▫ Hyperintense center of mass ▫ Hypointense periphery, border ▪ Subacute ▫ Hypointense in > three days: intracellular methemoglobin ▫ Hyperintense in > seven days: lysis of red blood cells; extracellular methemoglobin ▫ Chronic: hypointense; after two weeks 486 OSMOSIS.ORG MR angiography ▪ Vasculitis, arteriovenous malformations, other blood vessel pathology LAB RESULTS ▪ Prothrombin time (PT), activated partial thromboplastin time (aPTT), platelet count ▫ If cause for bleeding diathesis unclear TREATMENT MEDICATIONS ▪ Vitamin K, unactivated prothrombin ▫ With anticoagulant usage ▪ Protamine sulfate ▫ For heparin users ▪ Antipyretics ▫ Fever reduction ▪ Osmotic diuretics (e.g. mannitol) ▫ Regulation of ↑ ICP ▪ Saline ▫ Fluid replacement ▪ Nicardipine/nitroprusside/enalapril/ nitroglycerin ▫ Hypertension ▪ Phenytoin/levetiracetam ▫ Seizures SURGERY ▪ Ventriculostomy ▫ Regulation of ↑ intracranial pressure ▪ If hemorrhage > 3cm/1.2in/lobar of young persons/brainstem compression ▫ Craniotomy with clot removal ▫ Stereotactic aspiration ▫ Endoscopic evacuation
Chapter 64 Brain Ischemia Figure 64.2 A CT scan of the head in the axial plane demonstrating a right-sided, periventricular, intracerebral hemorrhage. ISCHEMIC STROKE PATHOLOGY & CAUSES ▪ Decreased blood supply in specific brain area due to blood vessel obstruction → hypoperfusion, tissue hypoxia, infarction ▪ ↓ blood flow → lack of oxygen, glucose in brain → ↓ adenosine triphosphate (ATP) production, electrochemical gradient → cell death Two mechanisms of cell death ▪ Sodium buildup: water follows sodium → cell swelling, death ▪ Calcium buildup: creates oxygen radicals → damages mitochondrial, lysosomal lipid membrane → seeping of degradative enzymes, apoptosis-inducing factors → cell death Two zones ▪ Ischemic core ▫ Brain tissue dies from ischemia within few minutes of stroke ▫ Blood flow < 10ml/100g tissue/minute ▪ Ischemic penumbra ▫ Periphery of affected region preserved due to collateral circulation; chance of survival if blood restored quickly ▫ Blood flow < 25ml/100g tissue/minute ▫ Infarction zone spreads if blood supply not restored quickly TYPES Five subtypes (TOAST classification) ▪ Large artery atherosclerosis ▪ Small artery strokes ▪ Cardioembolic infarction ▫ Formation of emboli in heart → lodging in brain arteries ▪ Other determined pathology ▪ Undetermined pathology OSMOSIS.ORG 487
CAUSES Thrombosis ▪ May lead to obstruction inside blood vessel ▪ Narrowing of blood vessel due to atherosclerotic plaque → gradual ↓ blood flow ▪ Damage to atherosclerotic fibrous cap → platelet, clotting cascade activation → thrombus formation with sudden stop of blood flow Embolism ▪ Four classes based on emboli origin ▫ Cardiac emboli: atrial fibrillation, rheumatic valve disease, infective endocarditis, dilated cardiomyopathies, left atrial myxoma ▫ Possible cardiac/aortic emboli: calcification of mitral valve annulus, patent foramen ovale, atheroma in ascending/arch of aorta, atrial septal aneurysm ▫ Arterial emboli: detachment of blood clot (e.g. atherosclerotic plaque in bigger upstream artery) → emboli travels through blood → lodges in smaller downstream artery ▫ Cryptogenic: unknown origin of emboli Lacunar infarct ▪ Affects small blood vessels of distal vertebral, basilar artery, middle cerebral artery, circle of Willis ▫ Lipohyalinosis: buildup of hyaline in arterioles wall → hypertrophy of tunica media → progressive narrowing of arterioles until blood flow stops ▫ Microatheromatoma: narrowing of blood vessel due to debris accumulation within wall Hypoperfusion ▪ Lack of blood reaching brain due heart failure, ↓ cardiac output ▪ Most vulnerable ▫ Spaces between supply of two arteries (watershed regions) Inflammation of blood vessel wall ▪ E.g. Takayasu/giant cell arteritis 488 OSMOSIS.ORG Moyamoya disease ▪ Progressive stenosis of cerebral arteries → ischemia Dissection of artery wall RISK FACTORS ▪ Age (esp. > 55) ▪ More common in individuals who are biologically male ▪ More common in black individuals of African descent ▪ Migraine headaches with aura ▪ Genetics; specific gene loci associated with stroke subtypes ▫ ABO loci: all subtypes ▫ HDAC9: large vessel stroke ▫ PITX2, ZFHX3: cardioembolic stroke ▪ Hematologic disorders ▫ Multiple myeloma, sickle cell disease, polycythemia vera; esp. in younger individuals ▪ Hypertension, diabetes mellitus, heart diseases, dyslipidemia, hyperhomocysteinemia, smoking, physical inactivity, cocaine abuse COMPLICATIONS ▪ Blood reaches infarcted regions through collateral blood vessel/dissolution of occlusive embolus/thrombus; first week Hemorrhagic transformation ▪ Ischemia → impaired cellular, metabolic functions of affected region; ↑ permeability of damaged blood vessels → resolved cause of ischemia → restored blood flow → blood extravasation ▪ Gray matter more commonly affected; large number of collateral vessels worsen reperfusion injury ▪ Massive cerebral infarction; hyperglycemia; ↓ cholesterol, LDL, IV recombinant tissue plasminogen activator (rtPA): higher risk of hemorrhagic transformation Cerebral edema ▪ ↑ intracranial pressure with possible herniation ▫ Cytotoxic: defective ATP pump, swelling of brain cellular elements due to water
Chapter 64 Brain Ischemia accumulation ▫ Vasogenic: ↑ permeability of blood-brain barrier → ↑ extracellular fluid volume due to ↑ passing of proteins, other macromolecules Liquefactive necrosis ▪ First 48 hours: edema, paleness of affected region ▪ 2–10 days: affected area gelatinous; noticeable border between healthy, damaged tissue ▪ 3–21 days: liquefaction of tissue; fluid-filled cavity Seizures ▪ Brain injury → ↑ irritability of nervous tissue with neuronal discharges Deep vein thrombosis ▪ Esp. immobilized individuals Pneumonia ▪ Swallowing mechanism impairment → aspiration pneumonia ▪ Intubation/ventilatory support → ↑ risk for pneumonia Dysphagia ▪ Due to damage of cortex, subcortical structures responsible for swallowing Dementia ▪ Altered memory, cognition, behavior due to brain damage SIGNS & SYMPTOMS Thrombosis ▪ Neurological defects Embolism ▪ Sudden start of symptoms; maximum defects Lacunar stroke ▪ Contralateral, mostly motor/sensory defects; four syndromes ▫ Pure motor stroke: internal capsule lesion ▫ Pure sensory stroke: thalamus lesion ▫ Ataxic hemiparesis ▫ Dysarthria: speech, swallowing difficulties; facial weakness; hand weakness, clumsiness (clumsy hand syndrome) Anterior cerebral artery ▪ Contralateral hemiparesis (esp. leg, face), sensory deficit; inability to understand, produce speech (left hemisphere); impaired judgment; incontinency Middle cerebral artery ▪ Contralateral paresis (esp. face, arm), sensory deficit; inability to understand, produce speech (left hemisphere); hemispatial neglect (right hemisphere); homonymous hemianopsia; deviation of eye to damaged side Posterior cerebellar artery ▪ Homonymous hemianopsia ▪ Cortical blindness (bilateral lesion) ▪ Midbrain ▫ Oculomotor, trochlear palsy → dilated pupil ▪ Thalamus ▫ Sensory loss, impaired memory, altered consciousness ▪ Posterior cerebellar artery syndrome (PICA) ▫ AKA “Wallenberg” syndrome ▫ Dizziness, nystagmus; speech, swallowing difficulties ▫ Ipsilateral: facial sensory loss, Horner’s sign, ataxia ▫ Contralateral: loss of pain, temperature sensation in limbs Basilar, vertebral arteries ▪ Dizziness; gait, vision disorders; dysarthria, dysphagia ▪ Locked-in syndrome ▫ Thrombosis/embolism of basilar artery ▫ Plegia of head, body muscles, except eye; only blinking, vertical eye movement possible DIAGNOSIS DIAGNOSTIC IMAGING ▪ If applicable Noncontrast CT scan ▪ First few hours OSMOSIS.ORG 489
▫ Affected tissue appears normal ▪ Later ▫ Loss of differentiation between white, grey matter ▫ Hypodense parenchyma with sulcal effacement ▫ Loss of insular ribbon sign CT perfusion ▪ Detection of core, ischemic penumbra CT angiography ▪ Find thrombus, embolus in blood vessel/ intra-arterial thrombolysis MRI ▪ T1, T2 weighted imaging (see table) ▪ Diffusion-weighted imaging ▫ Shows ischemic stroke early; differentiation from acute, chronic ▪ Fluid-attenuated inversion recovery (FLAIR) sequence ▫ Hyperintense signal within 12 hours Transcranial Doppler ultrasound ▪ Visualization of occlusion in middle cerebral artery/intracranial carotid/vertebrobasilar artery Conventional angiography ▪ Visualize occlusion; for confirmation of CTA, MRA findings LAB RESULTS ▪ Blood tests ▫ ↑ cardiac markers in heart disease ▫ ↑ erythrocytes in polycythemia vera ▫ Toxicology screening (individual suspected of sympathomimetics abuse) ▫ ↑ blood glucose level OTHER DIAGNOSTICS ▪ Symptoms, neurological changes scoring ▪ Based on National Institute of Health stroke scale (NIHSS) ECG ▪ Detection of myocardial ischemia/atrial fibrillation 490 OSMOSIS.ORG Figure 64.3 A CT scan of the head in the axial plane demonstrating a large ischemic stroke in territory of the middle cerebral artery. The scan was performed three days after the onset of symptoms. TREATMENT MEDICATIONS ▪ Establishment of blood flow in ischemic penumbra ▫ Thrombolytic enzymes: rtPA; alteplase given within 4.5 hours; after hemorrhagic stroke ruled out ▫ Antiplatelet therapy: aspirin (325mg orally within 48 hours); other drugs (e.g. clopidogrel/aggrenox) ▪ Hypertension treatment ▫ IV labetalol/nicardipine: only if systolic pressure > 220, diastolic > 120 mmHg; except in individuals with vital indications for lowering blood pressure (acute myocardial infarction, kidney failure, dissection of aorta) ▪ Cerebral edema management ▫ Antipyretic: if temperature ≥ 40°C/ 100.4ºF ▫ IV insulin: hyperglycemia; keep glucose between 140–180 mg/dl (7.8–10 mmol/L)
Chapter 64 Brain Ischemia ▪ Prevention ▫ Anticoagulant medications: emboli prevention (e.g. warfarin, aspirin) SURGERY ▪ Establishment of blood flow in ischemic penumbra ▫ Mechanical embolus removal in cerebral ischemia (MERCI) retriever ▫ Penumbra system (aspiration, extraction) ▫ Solitaire revascularization device, Trevo (stent-retriever systems) ▪ Cerebral edema management ▫ Craniectomy OTHER INTERVENTIONS ▪ Cerebral edema management ▫ Hyperbaric oxygen therapy: ↑ pure oxygen supply in damaged regions ▫ Fluid management: isotonic saline without dextrose ▪ Protection of airwaves, prevention of aspiration ▫ Head elevation by 30%, nothing by mouth/nil per os (NPO) status ▪ Prevention ▫ Control risk factors (for atherosclerosis): e.g. smoking, hypertension, diabetes, aspirin use; carotid endarterectomy ▫ Lifestyle alteration: exercising, appropriate diet PSYCHOTHERAPY ▪ If applicable ▪ Type of psychotherapy (e.g. group therapy, exposure therapy) with goal of psychotherapy OSMOSIS.ORG 491
SACCULAR ANEURYSM PATHOLOGY & CAUSES ▪ Asymmetrical ballooning of blood vessel wall ▪ Bifurcation of arteries common place esp. on circle of Willis due to weakness of wall, turbulent blood flow ▫ Anterior communicating (most common); posterior communicating; middle cerebral; internal carotid; basilar artery tip TYPES Type A ▪ Blood vessel wall with endothelium, linear smooth muscle Type B ▪ Disorganization of smooth muscle, thickening of wall Type C ▪ Hypocellular wall with thickening of intima/ luminal thrombosis Type D ▪ Hypocellular wall coated with thin thrombosis layer CAUSES ▪ Inborn defect of arteries, lack of external lamina, tunica media → hemodynamic stress over years → gradual ballooning of blood vessel wall, thickening of intima, adventitia RISK FACTORS ▪ More common in individuals who are biologically female, > 50 years (due to estrogen deficiency) ▪ Diseases associated with aneurysm ▫ Ehler–Danlos syndrome, pseudoxanthoma elasticum, lupus, autosomal dominant polycystic kidney 492 OSMOSIS.ORG disease (ADPKD), bacterial endocarditis, fibromuscular dysplasia ▪ Familial predisposition; smoking; alcohol, cocaine use; hypertension; trauma COMPLICATIONS ▪ Warning leaks ▫ May precede aneurysm rupture; strong headaches, photophobia, nausea/ vomiting ▪ Rupture → subarachnoid hemorrhage ▫ Apex of aneurysm/atheromatous plaque edge ▫ ↑ risk in smokers, individuals with migraines, elderly, affection of posterior circulation, larger size ▪ Ischemia ▫ Thrombus forms within aneurysm → detachment of small particles (emboli) → emboli lodges → ischemia of downstream tissue ▪ Multiple aneurysms SIGNS & SYMPTOMS ▪ May be asymptomatic if small ▪ Mass effect symptoms due to size ▫ Anterior communicating artery: both leg weakness with positive Babinski sign ▫ Posterior communicating, internal carotid artery: headaches with palsy of oculomotor nerve ▫ Left middle cerebral artery: inability to understand, produce speech ▫ Right middle cerebral artery: contralateral field vision loss
Chapter 64 Brain Ischemia DIAGNOSIS DIAGNOSTIC IMAGING CT/MR angiography ▪ Detect aneurysms > 2mm TREATMENT SURGERY ▪ Endovascular management ▫ Aneurysmal coiling with thrombosis → endothelialization across aneurysm neck → prevents rebleeding, regrowth ▫ In development: stent-assisted, balloonassisted coiling; disruptors, flow diverters ▪ Surgical clipping OTHER INTERVENTIONS ▪ Regular monitoring with CTA/MRA ▪ Avoid smoking, alcohol, drugs, excessive strain SUBARACHNOID HEMORRHAGE (SAH) ▪ Bleeding into space between pia mater, arachnoid membrane ▪ Injury/spontaneous event → rupture of blood vessel in subarachnoid space → release of blood into cerebrospinal fluid (CSF) → rapid ↑ intracranial pressure ▪ Smoking; hypertension; alcohol, cocaine abuse ▪ Diseases associated with saccular aneurysm (e.g. blood vessel disorders, Ehlers–Danlos syndrome, Marfan syndrome, polycystic kidney disease) ▪ Sickle cell disease ▪ Coagulopathies CAUSES COMPLICATIONS PATHOLOGY & CAUSES ▪ Traumatic: head injury (e.g. bridging vein tear) ▪ Spontaneous: arterial origin (more common) ▫ Rupture of saccular “berry” aneurysms (e.g. anterior half of circle of Willis) ▫ Arteriovenous blood vessel malformations RISK FACTORS ▪ More common in individuals who are biologically female, elderly ▪ Vasospasm ▫ Delayed ischemia; 4–11 days after SAH ▫ Blood clot lysis → release of spasmogenic substances (e.g. endothelin), ↓ production of nitric oxide → vasospasm due to smooth muscle contraction → brain ischemia ▪ Hydrocephalus ▫ Clogging of CSF drainage ▪ Rebleeding ▫ May occur two weeks after SAH ▫ ↑ tendency in individuals with OSMOSIS.ORG 493
▪ ▪ ▪ ▪ ▪ ▪ hypertension, anxiety, seizures postSAH ▫ Associated with ↑ mortality, neurological damage Sympathetic hyperactivity due to ↑ intracranial pressure, SAH (“sympathetic surge”) → sudden, life-threatening ↑ of blood pressure due to vasoconstriction ↑ plasma adrenaline levels due to sympathetic hyperactivity → arrhythmias Over-action of sympathetic nervous system → pulmonary vasoconstriction → ↑ capillary permeability, pressure → neurogenic pulmonary edema Hyponatremia Meningitis (irritation from presence of blood) Seizures SIGNS & SYMPTOMS ▪ Area of brain ▫ Anterior/middle cerebral artery: numbness, sudden muscle weakness ▫ Broca’s area: slurred speech ▫ Wernicke’s area: difficulty understanding speech ▪ ↑ intracranial pressure ▫ Thunderclap headache: “worst ever” headache; may be only symptom ▫ Nausea, vomiting ▪ Altered consciousness; coma, confusion, seizures ▪ Meningeal irritation: bleeding into subarachnoid space filled with CSF → blood degradation → irritation of meninges, development of aseptic meningitis ▫ Neck pain, stiffness ▫ Positive meningeal signs: Kernig’s (pain generated by knee extension from 90º); Brudzinski’s (forced neck flexion → spontaneous knee, hip flexion) ▫ Photophobia ▪ Focal neurological signs ▫ Posterior communicating artery aneurysm rupture/brain herniation due to ↑ intracranial pressure → oculomotor nerve paralysis → ipsilateral ptosis; eye pointed down, out; mydriasis, loss of pupillary light reflex 494 OSMOSIS.ORG ▫ ↑ intracranial pressure → abducens nerve paralysis → eye pointing out → diplopia DIAGNOSIS DIAGNOSTIC IMAGING Noncontrast CT scan ▪ Fisher scale grading ▫ Group 1: no hemorrhage ▫ Group 2: blood depositions < 1mm, without blood clots ▫ Group 3: blood depositions > 1mm, with localized clots ▫ Group 4: diffuse/lack of subarachnoid hemorrhage with extension to ventricles, brain parenchyma ▪ Hydrocephalus ▫ “Mickey Mouse” ventricular system appearance MRI ▪ Visualize arteriovenous malformations (not detected by angiography) Digital-subtraction cerebral/CT/MR angiography ▪ Visualize aneurysm LAB RESULTS ▪ Identify hematologic abnormalities ▪ PT, aPTT: identify coagulopathies ▪ ↑ troponin, if heart abnormalities present OTHER DIAGNOSTICS ▪ Lumbar puncture ▫ ↑ erythrocytes in all three samples ▫ CSF centrifugation: yellow coloration due to erythrocytes breakage, release of heme (“xanthochromia”); positive 3–4 weeks after SAH ▪ Physical examination ▫ Characteristic neurological presentation; fever; tachycardia; fundoscopy (optic disc swelling, retinal hemorrhages) ECG ▪ ↑ QRS, QT intervals; ↓ PR intervals; U waves; dysrhythmias
Chapter 64 Brain Ischemia TREATMENT MEDICATIONS ▪ Antihypertensive therapy: beta-blockers; hydralazine, calcium channel blockers; ACE inhibitors ▪ Intracranial pressure treatment: osmotic, loop diuretics ▪ Prior all procedures: IV midazolam (initial treatment) ▪ Vasoconstriction treatment: calcium channel blocker (e.g. nimodipine), recombinant tissue plasminogen activator ▪ Seizure treatment: phenytoin/phenobarbital ▪ Pulmonary edema treatment: diuretics, dobutamine SURGERY Figure 64.4 A CT scan of thea head in the sagittal plane demonstrating high signal in the sulci of the frontal lobe, consistent with a subarachnoid hemorrhage. ▪ Aneurysm treatment: endovascular coiling (with aneurysm obliteration), craniotomy (with aneurysm neck clipping, coiling) ▪ Vasoconstriction: aspiration/irrigation of blood clot during clipping process, CSF drainage, transluminal balloon angioplasty ▪ Hydrocephalus: temporary/serial lumbar puncture for CSF drainage, permanent ventricular shunt, ventriculostomy OTHER INTERVENTIONS ▪ Vital sign stabilization ▪ Intubation if comatose, heart monitoring (initial treatment) ▪ Keep blood pressure < 140mmHg to avoid rebleeding OSMOSIS.ORG 495
SUBDURAL HEMATOMA (SDH) PATHOLOGY & CAUSES ▪ Intracranial bleeding with blood accumulation between dura mater, arachnoid membrane ▪ Head trauma → tearing of venous blood vessels/small cortical arteries → blood accumulation → limited blood mass expansion due to adherent dural attachments → brain tissue compression TYPES Acute ▪ Slow blood outflow into subdural space due to low pressure in bridging veins Subacute ▪ Combination of fluid, clotted blood Chronic ▪ Caused by minor trauma/inflammation ▪ More common in elderly ▪ Head trauma with small bleeding, dural border cell damage → inflammation, unsuccessful attempt to repair border cells with formation of granulation tissue → encapsulation; development of blood vessels within new membrane → erythrocytes, plasma exudation from leaky capillaries to encapsulated space → recurrent bleeding with expansion CAUSES ▪ Head trauma (most common) ▪ Acceleration-deceleration (coupcontrecoup injury) ▪ cceleration of body → sudden stop with forwarding momentum carrying brain → impacts front of skull → backward brain movement → impacts back of skull → bridging veins tear ▪ Intracranial hypotension ▫ ↓ CSF due to lumbar puncture/ lumboperitoneal shunt → ↑ traction 496 OSMOSIS.ORG of brain on surrounding structures → bridging veins tear ▪ Shaken baby syndrome ▪ Spontaneous ▫ Vascular malformations ▪ Neurosurgical procedure complication RISK FACTORS ▪ Brain atrophy elderly ▫ ↑ bridging veins stretch ▪ Infants, alcohol abusers ▫ Thinner wall of bridging veins ▪ Epilepsy, anticoagulant drugs, thrombocytopenia COMPLICATIONS ▪ Liquefaction of granulation tissue in chronic subdural hematoma (subdural hygroma) → ↑ protein → expansion of mass due to water drawn by osmotic pressure → mass effect brain injuries ▪ ↑ intracranial pressure → supratentorial, infratentorial herniation of brain ▪ Progressive dementia in chronic subdural hematoma SIGNS & SYMPTOMS ▪ Loss of consciousness after trauma/in ensuing days due to hematoma expansion ▪ Bleeding characteristics ▫ Hemispheric: most common ▫ Interhemispheric: altered consciousness, headache, hemiparesis ▪ Physical examination ▫ Broken basilar skull: periorbital ecchymosis (raccoon eyes), retroauricular ecchymosis (Battle’s sign) ▫ CSF rhinorrhea/otorrhea ▪ Acute subdural hematoma ▫ Neurological presentation in 48–72 hours
Chapter 64 Brain Ischemia ▫ May be comatose/awake ▫ Sudden, severe headache with nausea, vomiting; unequal pupils; difficulties in speech, swallowing; palsies of cranial nerves ▪ Subacute ▫ Presents 2–14 days ▪ Chronic ▫ Present 14 days after injury ▫ Impaired cognitive skills, altered consciousness, headaches, contralateral/ ipsilateral hemiparesis (depends on hematoma location), hemianopsia, optic disc swelling DIAGNOSIS DIAGNOSTIC IMAGING CT scan ▪ Acute: crescent-shape hyperdense blood collection ▪ Subacute/chronic: isodense/hypodense crescentic mass MRI ▪ T2-WI (acutely): hypointense blood clot due to deoxyhemoglobin ▪ T1, T2-WI (in following weeks): bright appearance; deoxy → methemoglobin ▪ T1-WI (months later): hypointense clot due to hemosiderin remains MR/CT angiography ▪ Spontaneous SDH Figure 64.5 A CT scan in the axial plane demonstrating a large, right-sided, subdural hematoma. The hematoma has a classical crescentic shape. TREATMENT MEDICATIONS ▪ Diuretics ▫ ↓ intracranial pressure ▪ Vitamin K/factor VIII inhibitor activity bypassing agent (FEIBA)/frozen plasma ▫ Anticoagulation reverse; ↓ risk of hematoma enlargement; individuals undergoing surgery SURGERY ▪ If clot thickness > 10mm, midline shift > 5mm, intracranial pressure > 20mmHg ▫ Burr hole, craniotomy, decompressive craniectomy, blood vessel ligation OTHER INTERVENTIONS ▪ Nonsurgical treatment based on Glasgow coma score (GCS); clot thickness (< 10mm); neurological examination; stable/ deteriorated condition; comorbidities, associated injuries; age OSMOSIS.ORG 497
TRANSIENT ISCHEMIC ATTACK (TIA) PATHOLOGY & CAUSES ▪ Short-lasting neurological dysfunction due to transient focal ischemia, without infarction ▪ Blood vessel occlusion/stenosis → ↓ blood flow in affected region → neurological dysfunction CAUSES ▪ Adults: thrombosis, hypoperfusion, emboli ▪ Children: congenital heart defects with thrombosis, coagulopathies, idiopathic progressive arteriopathy of childhood (Moyamoya disease) RISK FACTORS ▪ More common in black individuals of African descent who are biologically male; ↑ risk with age ▪ Family history, hypertension, diabetes, obesity, obstructive sleep apnea, ↑ lowdensity lipoprotein (LDL), ↓ high-density lipoprotein (HDL), atherosclerosis, cocaine abuse, smoking COMPLICATIONS ▪ Recurrent TIA ▪ Ischemic stroke SIGNS & SYMPTOMS ▪ Duration: few minutes to one hour ↓ flow in large arteries (few minutes) ▪ Numbness/paresis ▫ Face, cheek, tongue, arm, hand, leg ▪ Aphasia ▫ If dominant hemisphere affected ▪ Hemispatial neglect 498 OSMOSIS.ORG ▫ If nondominant hemisphere affected ▪ Distal vertebral artery ▫ Dizziness, difficulty speaking, double vision ▪ Mid-basilar artery ▫ Dizziness, paresis affecting both legs/ arms Embolic TIA (> one hour) ▪ Anterior cerebral circulation ▫ Symptoms depend on blood vessel lodged ▫ Middle cerebral artery: contralateral hemiplegia; aphasia if dominant hemisphere; hemispatial neglect if nondominant ▫ Branches of middle cerebral artery: numbness/motor function loss; face, arm, leg ▫ Ophthalmic artery: amaurosis fugax; transient monocular/binocular vision loss ▪ Posterior cerebral circulation ▫ Dizziness, focal hearing loss, speech difficulties, double vision, hemi/ quadrantanopia, face/body numbness ▫ Basilar artery: thalamus, subthalamus, medial midbrain, reticular activating system → stupor/coma DIAGNOSIS DIAGNOSTIC IMAGING CT/MR/conventional catheter angiography ▪ Occlusion within blood vessel Diffusion-weighted MRI ▪ Ischemic regions corresponding to neurologic symptomatology ▪ Changes seen within first few hours of symptoms
Chapter 64 Brain Ischemia Perfusion-weighted MRI ▪ ↓ tissue blood flow Neck Doppler ultrasound ▪ Evaluate carotid stenosis LAB RESULTS ▪ Hypoglycemia, hyponatremia, thrombocytosis: rule out conditions that mimic TIA OTHER DIAGNOSTICS ▪ See mnemonic ▫ ABCD2 score: evaluate risk for possible ischemic stroke (can occur two days after TIA) MNEMONIC: ABCD2 Evaluating ischemic stroke risk Age Blood pressure Clinical features Duration of symptoms Diabetes TREATMENT MEDICATIONS ▪ Antiplatelet (noncardioembolic TIA) ▫ Aspirin/extended-release dipyridamole/ aspirin + clopidogrel ▪ Anticoagulation ▫ Atrial fibrillation: low-molecular-weight heparin ▫ Heart thrombus: in acute myocardial infarction/rheumatic mitral valve; warfarin + direct acting oral anticoagulants (e.g. apixaban) ▪ Diuretics, angiotensin-converting enzyme (ACE) inhibitors ▫ Blood pressure control ▪ Statins ▫ Cholesterol management SURGERY ▪ Same side carotid stenosis/TIA ▫ Carotid endarterectomy OTHER INTERVENTIONS ▪ Mediterranean diet OSMOSIS.ORG 499

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