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Neurologic Emergencies PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Neurologic Emergencies” by Joseph D. Burns, MD.

This medical PowerPoint presentation is about neurological emergencies, medical conditions that require immediate attention from medical professionals. They can be caused by a wide range of factors, including trauma, infections, strokes, tumors, and other medical conditions. Here are some examples of neurological emergencies:

Stroke: A stroke occurs when blood flow to the brain is disrupted, causing brain cells to die. This can lead to permanent brain damage or death. Symptoms of a stroke include sudden weakness or numbness in the face, arm, or leg, trouble speaking, loss of vision, dizziness, and severe headache.
Traumatic brain injury: A traumatic brain injury (TBI) occurs when the brain is injured by a blow or jolt to the head. This can cause swelling, bleeding, or damage to the brain tissue. Symptoms of a TBI include headache, nausea, confusion, memory loss, and loss of consciousness.
Seizures: A seizure is a sudden and uncontrolled electrical disturbance in the brain that can cause a wide range of symptoms, including convulsions, loss of consciousness, and confusion.
Meningitis: Meningitis is an infection of the membranes that surround the brain and spinal cord. Symptoms of meningitis include headache, fever, neck stiffness, and sensitivity to light.
Intracranial hemorrhage: Intracranial hemorrhage is bleeding inside the skull, which can be caused by trauma, aneurysms, or other medical conditions. Symptoms of intracranial hemorrhage include severe headache, nausea and vomiting, seizures, and loss of consciousness.

If you or someone you know is experiencing any of these symptoms, it is important to seek medical attention immediately. Delaying treatment can lead to further damage or even death.

Tags : neurological emergencies, Stroke, Traumatic brain injury, Seizures, Meningitis, Intracranial hemorrhage, Neurology, Neurology PowerPoint presentation

Published on : Jun 20, 2023 | Views : 824 | Downloads : 0

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Neurologic Emergencies Joseph D. Burns, M.D. Attending Neurointensivist Assistant Professor of Neurology and Neurosurgery
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Learning Objectives Gain an appreciation for the significant public health burden created by neurologic emergencies Understand the diagnostic and treatment considerations unique to emergencies involving diseases of the nervous system Be familiar with the differential diagnosis and diagnostic and therapeutic approach to common neurologic emergencies
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Why does this matter?
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Clinical and Economic Relevance of Neurologic Emergencies Stroke Incidence 795,000 new strokes each year in the US 1 stroke every 40 seconds Prevalence 2.5% of American adults Mortality Third leading cause of death in US Someone dies of stroke every 3-4 minutes Disability 15-30% permanently disabled 20% require institutional care at 3 months post-stroke Cost $68.9 billion in the US in 2009 Acute care, long-term care, lost productivity Lloyd-Jones, Circulation, 2009
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Clinical and Economic Relevance of Neurologic Emergencies Emergency care burden 5-15% of all ED visits involve non-traumatic neurologic problems 20% of non-surgical admissions are for neurologic problems Nawar EW, Advance Data, 2007
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What’s different about neurologic emergencies?
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Goal 1: Don’t let the patient die Not unique ACLS, ATLS, other strategies common to all emergency medical care Not complicated
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Goal 2: preserve as much nervous system tissue as possible (complicated)
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Neurologic Emergencies are Complex CNS exquisitely vulnerable to ischemia and hypoxia Normal CBF: 50-100 mL/100g/min Ischemia (loss of function): 20 mL/100g/min Infarction: 10 mL/100g/min
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Neurologic Emergencies are Complex CNS heals poorly Tissue that dies is not replaced Function never returns to normal
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Neurologic Emergencies are Complex Treatment depends on a rapid, accurate neurologic diagnosis Requires (unfortunately) unique training and experience Attention to detail As many as 1/3 of patients with Neurology consultation in ED are misdiagnosed by the requesting physician Moeller JJ, Can J Neurol Sci, 2008
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General Approach ABCs MORE – not less – important Hypotension and hypoxemia exacerbate CNS injury Hypercapnia elevates intracranial pressure
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General Approach History ALWAYS the key to diagnosis Key elements Time of symptom onset Last time seen normal Temporal profile of symptom onset Paroxysmal? Minutes? Hours? Days?
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General Approach Physical examination: Is there evidence of brainstem dysfunction? Mental status: level of arousal Cranial nerves: pupillary responses Motor: Hemiparesis? Pathologic reflexes? Pathologic posturing
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General Approach Imaging: non-contrast CT Fast Widely available Labs ALWAYS look for hypoglycemia CBC, electrolytes, aPTT, PT/INR, LFTs, BUN, Cr CSF Lumbar puncture CNS infections, subarachnoid hemorrhage, Guillain-Barre Syndrome
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Pearls Time is brain Successful treatment depends on accurate diagnosis Use only normal saline for IV fluids Time is brain
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Common Neurologic Emergencies
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Vignette #1 55yo woman with a history of rheumatic heart disease suddenly falls while walking and is unable to move her left limbs She has a mechanical mitral valve replacement and stopped warfarin one week ago in preparation for unrelated surgery
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Sudden-onset hemiparesis Differential diagnosis Ischemic stroke Intracerebral hemorrhage Post-ictal paresis (Todd’s paralysis)
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Sudden-onset hemiparesis Rapid diagnosis History Time of onset or time last seen normal Cerebrovascular risk factors Anticoagulant use History of seizures Exam Large deficit with preserved arousal: ischemic stroke Decreased arousal or vomiting: ICH or posterior circulation Delirium, visual problems, dizziness, cranial nerve dysfunction: posterior circulation
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Sudden-onset hemiparesis Rapid diagnosis Imaging: CT head, CTA head and neck Labs: serum glucose, CBC, aPTT, PT/INR
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Time is Brain Saver JL. Stroke. 2006
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Time is Brain Lees KR. Lancet. 2010
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Ischemic Stroke Emergent Treatment Goal: maximize perfusion to limit infarction Earlier reperfusion = more salvaged brain = better functional outcome Allow hypertension, give IV normal saline, lay head of bed < 30 degrees Do NOT treat hypertension unless >220/110 mmHg or end-organ dysfunction IV tissue plasminogen activator (tPA) Within 4.5h of symptom onset Exclusion criteria extensive (bleeding) Endovascular therapy Contraindications to or failure of IV tPA Mechanical thrombectomy Intra-arterial tPA Within 6h in anterior circulation (ACA, MCA) Within 12h in posterior circulation (vertebral, basilar)
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ICH Emergent Treatment Goal Prevent hematoma expansion Occurs in 70% of patients, mostly in 1st 6h 10% volume increase = 5% mortality increase 16% increase in chance of worsening by 1 point on the modified Rankin scale Treat hypertension Goal SBP 130-150 mmHg IV Drugs!!! Prns: labetalol, hydralazine Nicardipine gtt Correct coagulopathy FAST! Goal INR < 1.4, platelets > 100k PCC, Vitamin K, fresh frozen plasma
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Acute hypertension and ICH Occurs in 50-75% of patients Mechanism Destruction/interruption of autonomic centers Prefrontal cortex, insula, hypothalamus Increased ICP Associated with increased risk of hematoma expansion and poor outcome in a number of retrospective studies Chicken or Egg? Quereshi AI. Circulation. 2008
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Acute hypertension and ICH Retrospective, single center study from Japan Patients 76 consecutive adult hypertensive ICH Outcome Hematoma growth by ≥ 40% Ohwaki K et al. Stroke. 2004
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Acute hypertension and ICH Post-hoc analysis of prospectively collected data on 98 ICH patients Normal INR Within 3h of symptom onset No relationship between hematoma SBP DBP MAP Pulse pressure (PP) PP x HR MAP x HR Jauch EC et al. Stroke. 2006
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Lower the Blood Pressure INERACT (Intensive Blood Pressure Reduction in Acute Cerebral Haemorrhage Trial) Open-label, blinded outcome, randomized, controlled trial of antihypertensive treatment initiated within 6 hours of ICH onset Exclusion criteria <18yo SBP <150 or >220 Clear indications for or contraindications against lowering BP Anderson CS et al. Lancet Neurology. 2008
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Lower the Blood Pressure Treatment strategies Two groups AHA/ASA guidelines (target SBP = 180 mmHg) Intensive treatment (target SBP = 140 mmHg) Achieve target w/in 1h of randomization Maintain target BP for 7 days Any antihypertensive(s) routinely available at the treating hospital could be used
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Lower the Blood Pressure Outcomes Proportional change in hematoma volume in the 1st 24h Secondary Substantial hematoma growth (>33% or >12.5 mL) in 1st 24h Death or dependency (mRS 3-6) at 90d Complications
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Lower the Blood Pressure Results 404 patients total Most commonly used drugs Urapidil (primarily a peripheral α-1 antagonist) Furosemide BP goal achievement in Intensive group 42% at 1h, 66% at 6h
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Lower the Blood Pressure Results (adjusted for baseline hematoma volume and time to randomization) Proportional increase in hematoma size at 24h Guideline: 36% Intensive: 14% (p=0.06) Substantial (>33%) hematoma growth at 24h Guideline: 23% Intensive: 15% (p=0.05) No differences in mortality, neurologic outcomes, or complications Phase 3 trial (INTERACT 2): hematomas smaller Lowering BP is safe no difference in neurologic outcome ATACH2
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Vignette #2 20yo male college student is found confused and drowsy by his friends on a Sunday morning He has a history of epilepsy, is known to be poorly compliant with medications, and was drinking the night before 5 minutes after arriving at the ED, he begins to convulse. 3 min into the convulsion, he is not slowing down
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Generalized Convulsive Status Epilepticus Status epilepticus Any single seizure lasting > 5min ≥ 2 seizures without clearing of mental status between them Differential diagnosis Underlying epilepsy with or without AED withdrawal Drug intoxication (many types) or withdrawal (esp. EtOH and benzodiazepines) Hypoglycemia Vascular disease (infarct, ICH, SAH, AVM) Electrolyte abnormalities (↓Na, Mg, Ca; ↑Na) CNS infection Tumor Psychogenic, non-epileptic seizure (conversion disorder)
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Generalized Convulsive Status Epilepticus Rapid diagnosis History: epilepsy, other neurologic disease, diabetes, drug ingestion/withdrawal, infectious symptoms, pre-seizure neurologic symptoms Exam: subtle signs of ongoing seizure (periorbital/perioral clonus, forced horizontal conjugate eye deviation, hippus)
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Generalized Convulsive Status Epilepticus Rapid diagnosis Imaging: CT for associated mass lesion Labs: glucose, electrolytes, urine and serum toxicology screens CSF Evidence of infection OR No other clear cause from history, exam, CT, and labs
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Generalized Convulsive Status Epilepticus Seizures beget seizures Early treatment = higher chance of success Balance this with side effects of treatment (need for intubation, hypotension) Excitotoxic neuronal death
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Lactic andrespiratoryacidosis Cardiacarrhythmias Rhabdomyolysis pH  pCO2  Lactate  Aspiration pneumonia Pulmonary edema Shoulderdislocation Ribfracture Myoglobinuria CP1142808-43 Figure courtesy of Dr. Eelco F.M. Wijdicks
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Emergency Treatment of Generalized Convulsive Status Epilepticus Abort the seizure Lorazepam 4-6mg IV push Repeat 5min later if seizure continues or returns Prevent future seizures Phenytoin load: 20mg/kg IV infusion DO NOT just give 1g  only enough for a small, 50kg person Alternatives: IV valproic acid 20-30mg/kg IV levetiracetam 25-30mg/kg
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Vignette #3 35yo woman with a history of migraine headaches was awakened by the worst headache of her life and severe nausea. A few minutes later, she vomited. ED: BP 170/90. Ill and uncomfortable. Holding an emesis basin, preferred to keep her eyes closed. Slightly drowsy. Resisted passive neck flexion.
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Sudden, Severe Headache Differential diagnosis Aneurysmal subarachnoid hemorrhage Aneurysmal subarachnoid hemorrhage Aneurysmal subarachnoid hemorrhage Aneurysmal subarachnoid hemorrhage Aneurysmal subarachnoid hemorrhage
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Sudden, Severe Headache Differential diagnosis Cervical artery dissection Cerebral venous sinus thrombosis Intracranial mass Pituitary apoplexy Meningitis Encephalitis Spontaneous intracranial hypotension
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Sudden, Severe Headache Rapid diagnosis History (features of aneurysmal SAH) Instantaneous onset of headache Decrease in arousal/loss of consciousness at onset Nausea, vomiting Family history of aneurysm, SAH Neck stiffness
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Sudden, Severe Headache Exam Meningismus Retinal subhyaloid hemorrhages (Terson syndrome) CN III palsy (ptosis; deviation “down and out”; pupil fixed and dilated)
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Sudden, Severe Headache Rapid diagnosis Imaging CT sensitivity declines with time after ictus Nearly 100% sensitive within 6h >95% sensitive for SAH within 12h CT angiogram: identifies aneurysm Treatment planning 20% will have multiple aneurysms CSF LP required if SAH diagnosis is considered and CT negative 90-95% sensitive for SAH when CT negative Findings Gross blood Xanthochromia
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Emergency Treatment of Aneurysmal SAH Notify neurosurgery and neurointerventional team immediately Prevent rebleeding Risk = 5-15% in 1st 24h; mortality 70-80% Treat hypertension: Keep SBP 110-150 mmHg IV Antihypertensives Prns: labetalol, hydralazine Nicradipine gtt Judicious analgesia Tylenol  Ultram  very low-dose IV fentanyl or hydromorphone Antifibrinolytics (tranexamic acid) if securing is expected to be delayed > 6h after arrival
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Emergency Treatment of Aneurysmal SAH Secure aneurysm Goal: ASAP; within 18h of presentation Conventional angiogram from ED Operative planning Endovascular coils if possible Otherwise, surgical clipping
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Vignette #4 45yo man with a history of IV heroin abuse presented to the ED with 3 days of worsening headache, confusion, and lethargy Exam: Temp 102, BP 100/50, HR 110. Opened eyes to pain only. Uncomfortable, groaning unintelligibly. Meningismus. Systolic murmur CSF: RBC 6, WBC 1090 (85% PMNs), glucose 32 (serum 81), protein 234 (nl <70) Cultures of blood, urine and CSF all grew MRSA
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Fever and Confusion Differential diagnosis Meningitis (bacterial, viral) Encephalitis (viral) Cerebral abscess (bacterial, toxoplasma, fungal) Subdural empyema Endocarditis with septic embolic brain infarcts Non-CNS infection with secondary encephalopathy
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Fever and Confusion Rapid diagnosis History Headache, neck stiffness Oral/nasal infection Immunosuppression (HIV, chemotherapy, transplant, diabetes, sickle cell disease, poor nutrition) Alcohol abuse IV drug use Sick contacts Travel
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Fever and Confusion Rapid diagnosis Exam: meningismus, skin rash, embolic skin lesions, heart murmur Imaging: CT to look for a mass lesion CSF (bacterial meningitis) 10-10,000 WBC/mm3; ≥ 80% neutrophils Glucose – CSF:serum ratio ≤ 0.5 Elevated protein (> 45 mg/dL) Check Gram stain and bacterial culture Labs: Blood cultures (3 sets), urine culture
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Emergent Treatment of Acute Bacterial Meningitis Rapid administration of corticosteroids and antibiotics is the key. Within two hours: Blood culture Dexamethasone 10mg IV (20min before ABx) Antibiotics (all IV) Vancomycin 1.5mg/kg, ceftriaxone 2g If >50yo or immunosuppressed: add ampicillin 2g CT LP
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Vignette #6 45yo man presented to the ED complaining of back pain, generalized weakness, and shortness of breath Illness began 5d ago when he awoke with tingling in the feet. Later that day, his walking became clumsy. Cold 3 weeks ago Exam: Afebrile. RR 35, diaphoretic, anxious. Bifacial weakness and mild dysarthria. Symmetric weakness of proximal limbs. Muscle stretch reflexes diffusely absent.
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Vignette #6 (cont) Intubated in ED LP: Protein 100mg/dL (normal < 70); RBC, WBC, glucose normal.
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Weakness and Difficulty Breathing Differential diagnosis Guillain-Barre syndrome Myasthenic crisis Cervical cord lesion Severe myopathy Sepsis
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Weakness and Difficulty Breathing Rapid diagnosis History GBS: gait unsteadiness, distal limb paresthesias, proximal weakness, cramping, back pain Myasthenic crisis: history of MG, prominent CN involvement (diplopia, “nasal” voice, dysphagia, nasal regurgitation) fatigability Exam GBS: diffuse hyporeflexia or areflexia MG: prominent CN symptoms; fluctuation of symptoms
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Figure courtesy of Dr. Eelco F.M. Wijdicks
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Weakness and Difficulty Breathing Rapid diagnosis Imaging: consider MRI of cervical spine if CNs are spared CSF GBS: elevated protein with up to 10 WBC (“albuminocytologic dissociation”) Labs: arterial blood gas
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Emergency Treatment of GBS and Myasthenic Crisis Goal: Control breathing before catastrophe Intubation and mechanical ventilation Airway compromise from CN dysfunction Even if O2 and CO2 are OK Vital capacity < 15mL/kg Negative inspiratory force worse than -30 cm H2O Rapidly worsening respiratory function Do not wait for ABG results
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Emergency Treatment of GBS and Myasthenic Crisis GBS Intravenous pooled human immunoglobulin (IVIg) Plasma exchange Myasthenic Crisis Plasma exchange  more rapid improvement IVIg only if plasma exchange contraindicated
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Take-Home Messages Time is brain Rapid diagnosis and treatment are crucial ABCs are important in neurologic illness Ischemic stroke: don’t lower BP and open the vessel ICH: lower BP and correct coagulopathy SAH: lower BP (carefully) and secure aneurysm
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Take-Home Messages Meningitis: give steroids, then antibiotics, as soon as the diagnosis is considered… before the LP MG crisis/GBS: respiratory failure is sneaky – intubate before the ABG Never sedate a patient with critical neurologic illness unless the neurointensivist or neurosurgeon says it’s OK Never give any IV solution other than Normal Saline unless the neurointensivist or neurosurgeon says it’s OK Time is brain