Neurological Emergencies

Neurological Emergencies - Neurological Emergencies...

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Unformatted text preview: Neurological Emergencies Neurological Emergencies Patrick M. O’Shaughnessy, D.O. Attending Physician Department of Emergency Medicine Beth Israel Medical Center Neurologic Emergency Outline Neurologic Emergency Outline • • • • • • • Change in Mental Status / Coma Stroke/TIA Syndromes Seizure & Status Epilepticus Head Trauma / C­Spine Injury Infectious Vertigo/Headaches Peripheral Neuropathies The Neurologic Exam • KEY!! Must do a complete thorough neuro exam to • properly identify and diagnose any neurologic abnormality. Exam should include 5 parts always!: – – – – – – Mental status, level of alertness (AAO, GCS) Cranial nerve exam Motor / Sensory exam Reflexes Cerebellar Consider ; MMSE if Psych / AMS components Change in Mental Status / COMA Change in Mental Status / COMA • Potential Causes – “AEIOU TIPS” • • • • • • • • • A = Alcohol ( Drugs & Toxins) E = Endocrine, Exocrine, Electrolyte I = Insulin O = Opiates, OD U = Uremia T = Trauma, Temperature I = Infection P = Psychiatric disorder S = Seizure , Stroke, Shock, Space occupying lesion Change in Mental Status/Coma Change in Mental Status/Coma • Trauma Stroke / Space Occupying Lesions Stroke / Space Occupying Lesions Space Occupying Lesion Space Occupying Lesion Change in Mental Status/Coma Change in Mental Status/Coma • Temperature – – Hypothermia: causes coma when Temp<32.0 C Hyperthermia: causes coma when Temp>42.0C • Infection – Meningitis, Encephalitis, Sepsis • Endo/Exocrine, Electrolyte – – – – Hypo/Hyperglycemia Hypo/hyperthyroidism Hypo/hypernatremia Hepatic encephalopathy • Opiods/ OD / Alcohol – Heroin, Psych Meds (TCA’s, SSRI’s) AMS / COMA Physical Exam AMS / COMA Physical Exam Pearls • Always attempt to get a complete history!! • LOOK at your patient! – – – Smell the breath (ketones,alcohol,fetid,uremia) Observe respiratory rate & patterns (Cheyne­Stokes) Look for abnormal posturing. • Decorticate (Flexion of UE with Extension of LE) • Decerebrate (Extension of all Ext.) – Look for needle marks, cyanosis, signs of trauma • Obtain GCS Score! E4 V5 M 6 – If less than 8, IMMEDIATE airway stabilization FIRST priority!! Glasgow COMA Scale Glasgow COMA Scale • • • Scores range from 3 (Worst) – 15 (Best) Important for classifying degree of alteration. (Head Trauma) GCS < 8 = INTUBATE!! • EYE Opening Response – – – – 4 = Spontaneous 3 = To Voice 2 = To Pain 1 = None • Remember as “4 eyes” Glasgow COMA Scale Glasgow COMA Scale • Verbal Response – 5 = Oriented and converses – 4 = Confused but converses – 3 = Inappropriate words – 2 = Inappropriate sounds – 1= None • Remember as “Jackson 5 – sing/voice” Glasgow COMA Scale Glasgow COMA Scale • Motor – – – – – – 6 = Obeys commands 5 = Localizes pain 4 = Withdraws to pain 3 = Decorticate (flexes to pain) 2 = Decerebrate (extends to pain) 1 = None • Remember as “ 6 Cylinder engine – motor” AMS / COMA Essential AMS / COMA Essential Stabilization & Assessment Measures • Always assess & stabilize ABC’s first – Special attention to airway with C­Spine control/ protection. Oxygenate! – IV line , fluids, Thiamine 100mg IV, 1 amp D 50, & Narcan(if needed) 0.4mg increments until response. • Complete history and physical exam after • • stabilization Radiographic clearance of C­Spine Labs / CT as indicated Stroke / TIA Syndromes Stroke / TIA Syndromes • Anatomy of Cerebral Blood Flow – Anterior Circulation: 80% of cerebral blood flow originates from the carotids which supplies the • Frontoparietal lobes • Anterior temporal lobes • Optic nerve and retina – Posterior Circulation: 20 % of cerebral blood flow which originates from the vertebrobasilar arteries • Thalamus & Brainstem • Occipital cortex and Cerebellum • Upper Spinal cord & Auditory and Vestibular functions in ear – Circle of Willis: connects the Anterior and Posterior circulations Pathophysiology of Stroke / TIA Pathophysiology of Stroke / TIA • Ischemic Strokes: (thrombi or emboli) – Cerebral Thrombi may result from: • Atherosclerosis (#1 cause) • Infective arteritis • Vasculitis • Hypercoaguable states • Post traumatic carotid or vertebral artery dissections – Cerebral emboli may result from: • Mural thrombus from heart (#1 cause) • Aortic plaques • Endocarditis • Long bone or Dysbaric injuries (fat / air emboli) Pathophysiology of Stroke/TIA Pathophysiology of Stroke/TIA • Hemorrhagic Strokes result from – Spontaneous rupture of berry aneurysm or AV malformation (Subarachnoid hemorrhage) – Rupture of arteriolar aneurysms secondary to: • Hypertension • Congenital abnormality • Blood dyscrasia / Anticoagulant usage • Infection • Neoplasm – Trauma (Epidural / Subdural Hematomas) – Hemorrhagic transformation of embolic stroke Stroke /TIA Syndromes Stroke /TIA Syndromes • Type of Stroke (rule of 2/3’s) – 2/3 of ALL Strokes will be ISCHEMIC • 2/3 of these will be thrombotic • Therefore thrombotic ischemic strokes most common. – Incidence of Stroke • Biggest Risk Factors – – – – – – Prior TIA ( 30 % will have stroke in 5 years) HTN Atherosclerosis DM Hyperlipidemia Smoking Ischemic Stroke Syndromes Ischemic Stroke Syndromes • Thrombotic Syndromes – Usually slow, progressive onset – Sx develop shortly after awakening and are progressive • Embolic Syndromes – Usually abrupt onset with maximal deficit that tends to improve over time as the embolus breaks up. Occlusive Stroke Syndromes Occlusive Stroke Syndromes • Middle Cerebral Artery Occlusion (MCA) – # 1 type – Contralateral hemiplegia, hemianesthesia, and homonymous hemianopsia – Upper extremity deficit >> Lower extremity – Aphasia (if dominant hemisphere involved) – Conjugate gaze impaired in the direction of the lesion Occlusive Stroke Syndromes Occlusive Stroke Syndromes • Anterior Cerebral Artery Occlusion (ACA) – – – Contralateral leg, arm, paralysis Lower Extremity deficit >> Upper extremity Loss of frontal lobe control • Incontinence • Primitive grasp and suck reflexes enacted • Posterior Cerebral Artery Occlusion (PCA) – Ipsilateral CN III palsy, visual loss – Contralateral hemiparesis and hemisensory loss – Memory loss Occlusive Stroke Syndromes Occlusive Stroke Syndromes • Vertebrobasilar Artery Occlusion (VBA) Keys: CN AND Cerebellar deficits that affect BOTH sides of the body, with contralateral pain and temperature deficits. ­ Contralateral hemiplegia ­ Ipsilateral CN III palsy with Cerebellar findings. ­ Nausea/Vomiting ­ Vertigo, Nystagmus, ­ Ataxia, Dysarthia ­ Tinnitus, deafness Hemorrhagic Syndromes Hemorrhagic Syndromes (SAH, & Intracerebral) • Subarachnoid Hemorrhage Highest incidence in 35­65 year old. Usually from the rupture of a berry aneurysm Clinically: • abrupt onset of “worst headache of life” • Nuchal rigidity, photophobia, vomiting, retinal hemorrhages. – Diagnosis : CT + LP!!!! • CT only 92% sensitive within 24 hours of event, loses – – – sensitivity >24 hours out from headache. 72 hours out CANNOT r/o without LP! • – Management: (See Stroke Mgmt) • Consider adding Nimodipine 60 mg Q6 to reduce vasospasm TIA’s (Transient Ischemic Attacks) TIA’s (Transient Ischemic Attacks) • Definition: A temporary loss of neurologic function, that resolves • completely <24 hours. Clinically; – Arm numbness, weakness, HA – Facial droop, slurred speech – Sx resolved, or improve over time • Main point: These patients at high risk for stroke if: • • • – – – >50 HTN, DM, Smoker, Prior TIA in last month Any prior CVA…… ADMISSION IS THE RULE!! Treat as CVA : Head CT (CVA protocol) ASA 165­325mg po Consider Heparin, after Head CT and Neuro consultation and ONLY if cardiac arrhythymia present. Subarachnoid Hemorrhage Subarachnoid Hemorrhage Hemorrhagic Stroke Syndromes Hemorrhagic Stroke Syndromes • Intracerebral – Hypertensive intracerebral hemorrhage MOST common cause. – Traumatic, contusion, coup/contracoup – Rupture of small blood vessels with bleeding inside the brain parenchyma • Putamen • Cerebellar • Thalamic • Pontine ( 3 P’s – pinpoint pontine pupils) Intracerebral Hemorrhage Intracerebral Hemorrhage Treatment of Stroke Treatment of Stroke • AS ALWAYS – ABC’s FIRST with C­Spine Precautions • What’s the FS?? – Consider Thiamine 100mg IV, D 50 bolus if hypoglycemic. – Treat Hyperglycemia if FS > 300mg/dl • Protect the “Penumbra” – Keep SBP >90mm ( CPP = MAP – ICP) • Goal keep CPP > 60mm Hg – Treat Fever ( Mild Hypothermia beneficial) – – • Acetaminophen 650mg po or pr, cooling blanket Oxygenate (Keep Sao2 >95%) Elevate head of bed 30 deg. (Clear c­spine) • Frequent repeat Neuro checks!! Reassess GCS! Treatment of Stroke Treatment of Stroke • What type of stroke is Present?? – Bleed vs Ischemic • Any signs of shift herniation? • Neurosurgery evaluation or transfer necessary? • Other management adjuncts: • Ischemic strokes – ASA 75­325mg – Patients with Systolic BP >220 , Diastolic>130 need BP control with Nitroprusside or Labetolol. – DO NOT OVERTREAT BP or risk extending the infarct. – Consider Heparin if area of infarct small and neurologist agrees. • No bolus, just infusion. • Risk of hemorrhagic transformation. Treatment of Strokes Treatment of Strokes • Strokes with Edema, Mass Effect or Shift – Load with Dilantin 1 g @ rate no faster than 50mg/min. Acute seizure prophylaxis still of benefit. – Mannitol, Decadron?? • Recently shown to be of NO benefit, some Neurosurgeons still advocate, so consult first. – Hyperventilation?? • NOT beneficial and perhaps harmful, don’t do it! • Thrombolytics??? – – – – Ischemic strokes ONLY with large deficit NOT improving. Time from symptom onset <3 hours No ABSOLUTE Contraindications!! Benefit Questionable Thrombolytic Therapy for Acute Thrombolytic Therapy for Acute Stroke Checklist • Answer to ALL must be YES: – Age 18 or older – Clinical diagnosis of Acute Ischemic Stroke causing a measurable NON improving neurologic deficit. – NO high clinical suspicion for SAH – Time of onset to treatment is <180 minutes. Thrombolytic Therapy for Acute Thrombolytic Therapy for Acute Ischemic Stroke Checklist • Answer to ALL MUST be NO: – – – – – – – – Evidence of hemorrhage on CT Active internal bleeding (GI/GU) within last 21 days. Known bleeding diasthesis: • Platelets<100,000 • Heparin within last 48 hours with elevated PTT • Warfarin use with PT > 15 seconds Within 3 months of IC injury, prior surgery or prior ischemic stroke. Within 14 days of serious trauma, major surgery Recent AMI, arterial puncture/LP within 7 days History of prior ICH, AVM, tumor,or aneurysm or seizure at stroke Systolic BP >185mmHg, or Diastolic BP >110Hg Seizures & Status Epilepticus Seizures & Status Epilepticus • Background: – 1 – 2% of the general population has seizures – Primary • Idiopathic epilepsy: onset ages 10­20 – Secondary • Precipitated by one of the following: • Intracranial pathology – Trauma, Mass, Abscess, Infarct • Extracranial Pathology – Toxic, metabolic, hypertensive, eclampsia Seizure Types Seizure Types • Generalized Convulsive Seizures (Grand Mal): – Tonic , clonic movements, (+) LOC, apnea, incontinence and a post ictal state • Non Convulsive Seizures (Petit Mal) – – Absence seizures – “blank staring spells” Myoclonic – brief contractions of selected muscle groups • Partial Seizures – – – Characterized by presence of hallucinations Simple = somatic complaints + no LOC Complex = somatic complaints + AMS or LOC Approach for 1st Seizure, New Approach for 1 Seizure, or Substance/ Trauma Induced Seizure • • As always ABC’s First with C­ Spine precautions IV, O2, Monitor. – – – Send blood for CBC, Chem 20, Tox screen as appropriate Anticonvulsant levels Prolactin levels / Lactate levels • CXR / UA/ Head CT • Is patient still seizing? Post ictal? Pseudoseizure? – More later • Complete History and Physical Exam – Including detailed Neuro Exam – Repeat Neuro evaluations a must! ACEP Guidelines for Postictal ACEP Guidelines for Postictal Head CT Scans in the ED • • • • • • • • • Status Epilepticus ( a true emergency) Abnormal Neuro findings No return to GCS 15 Prolonged HA History of malignancy CHI HIV infection of high risk for HIV Anticoagulant use Age > 40 Approach to Breakthrough Seizure Approach to Breakthrough Seizure • As Before, But History, History, History!! • Main causes of Breakthrough Seizure: – Noncompliance with anticonvulsant regimen – Start of new medication (level alteration) • Antibiotics, OCP’s – Infection • Fever – Changes in body habitus, eating patterns – Supratherapeutic level Status Epilepticus Status Epilepticus • Definition: operationally defined as seizure lasting • greater than 5 minutes OR two seizures between which there is incomplete recovery of consciousness. Treatment algorhythm: – As before ABC’s – IV, O2, Monitor – Consider ALL potential causes • INH • Eclampsia • Alcoholic B­6 deficiency • Other Tox ingestion (TCA’s, sulfonylurea OD) • Trauma Status Epilepticus Treatment Status Epilepticus Treatment • FIRST LINE TREATMENT – Lorazepam (Ativan) 2mg/min IV up to 10 mg max. OR Diazepam(Valium) 5mg/min IV or PR up to 20mg • SECOND LINE TREATMENT – Phenytoin or Fosphenytoin: • 20mg/kg IV at rate of 50mg/min • THIRD LINE TREATMENT – Get Ready to intubate at this point!! – Phenobarbitol 10­20mg/kg @ 60 mg/min Status Epilepticus Treatment Status Epilepticus Treatment • FINAL TREATMENT – Barbiturate Coma • Pentobarbitol 5mg/kg @ 25 mg/min • Stat Neurology consult for evaluation and EEG • Pentobarbitol titrated to EEG response. • Always get a through HISTORY – – – – Possible trauma Medications in house Others sick, symptomatic Overall appearance of patient Status Epilepticus Adjunctive Status Epilepticus Adjunctive Treatment by History • Thiamine 100mg IV, 1­2 amps D 50 – If suspect alcoholic, malnourished, hypoglycemia • Magnesium Sulfate 20cc of 10% solution – As above of if eclampsia (BP does NOT have to be 200/120!!) • Pyridoxine 5 gms IV – INH or B­6 deficiency Head & C­ Spine Injury Head & C­ Spine Injury Head & C­Spine Injury Head & C­Spine Injury Head & C­ Spine Injury Head & C­ Spine Injury • Closed Head Injury – – – – 3 sub classifications based on initial GCS Major Head Injury (GCS <8) Moderate Head Injury (GCS 9­12) Minor Head Injury (GCS 13­15) • Pathophysiology – Trauma to the head causes distortion of the brainstem and decreased activity in the RAS leading many times to a transient LOC. Closed Head Injury Closed Head Injury • Definitions : – Concussion: refers to a transient LOC following head injury. Often associated with retrograde amnesia that also improves. – “Coup” = injury beneath the site of trauma – “Countrecoup” = injury to the side polar opposite to the traumatized area. – Diffuse Axonal Injury : tearing and shearing of nerve fibers at the time of impact secondary to rapid acceleration/deceleration forces. Causes prolonged coma, injury, with normal initial head CT and poor outcome. Closed head Injury Facts Closed head Injury Facts • The single most important factor in the • neurologic assessment of the head injured patient is level of consciousness. (LOC) Always assume multiple injuries with serious mechanism. – ESPECIALLY C ­ SPINE!!!! – Unless hypotensive WITH bradycardia and WARM extremities; hypotension is ALWAYS secondary to hypovolemia from blood loss in the trauma patient! • The most common intracranial bleed in CHI is subarachnoid hemorrhage. Closed Head Injuries with Closed Head Injuries with Hemorrhage • Cerebral Contusion – Focal hemorrhage and edema under the site of impact. – Susceptible areas are those in which the gyri are in close contact with the skull • Frontal lobe • Temporal lobes – Diagnostic Test of Choice: NC Head CT – Treatment: Supportive with measures to keep ICP normal. Repeat Neuro checks. Repeat Head Ct in 24 hours. Good prognosis. Cerebral Contusion Cerebral Contusion Subdural Hematoma Subdural Hematoma • Occurs secondary to acceleration/decelleration injury • with resultant tearing of the bridging veins that extend from the subarachnoid space to the dural sinuses. Blood dissects over the cerebral cortex and collects under the dura overlying the brain. • Patients at risk: – – – Alcoholics Elderly Anticoagulant users • Appears as “sickle shape” and does not extend across the midline Subdural Hematoma Subdural Hematoma Epidural hematoma Epidural hematoma • Occurs from blunt trauma to head especially over the • • • • • parietal/temporal area. Presents as LOC which then patient has lucid interval then progressive deterioration, coma , death. ( Patient talks to you & dies!) Commonly associated with linear skull fracture Mechanism of bleed is due to tear of artery, usually middle meningeal. PE reveals ipsilateral pupillary dilitation with contralateral hemiparesis. CT Scan : a BICONVEX (lens) density which can extend across the midline Epidural Hematoma Epidural Hematoma Management of Closed Head Management of Closed Head Injuries • • • As always ABC’s with C­Spine precautions IV, O2, Monitor. Stabilize and resuscitate – Sao2>95% – SBP>90 – Treat Fever • Head of Bed 30% (once C­Spine cleared) • Stat Head CT with Stat Neurosurgical evaluation • for surgical lesions. Repeat Exams, looking for signs of herniation. Signs of Herniation / Increased ICP Signs of Herniation / Increased ICP • • • • • • • Headache, nausea, vomiting Decreasing LOC Sixth nerve paresis (one or both eyes adducted) Decreased respiratory rate Cushing reflex (hypertension/bradycardia/bradynpea) Papilledema Development of signs of herniation – Fixed and dilated pupil – Contralateral hemiparesis – Posturing Herniation Syndromes Herniation Syndromes • CPP = MAP – ICP: Must keep CPP >60 mm Hg • Uncal Herniation: – Occurs when unilateral mass pushes the uncus (temporal lobe) through the tentorial incisa, prersenting as: • Ipsilateral pupil dilatation • Contralateral hemiparesis • Deepening coma • Decorticate posturing • Apnea and death Herniation Syndromes Herniation Syndromes • Cerebellar Herniation – Downward displacement of cerebellar tonsils through the foramen magnum. – Presents as : • Medullary compression • Pinpoint pupils • Flaccid quadriplegia • Apnea and circulatory collapse Cervical Spine Injury Cervical Spine Injury Normal Cervical Spine – 3 views Normal Cervical Spine – 3 views Cervical Spine Injuries Cervical Spine Injuries • • Injuries classified by mechanism of injury and stability. Unstable C­ Spine fractures: – Remember “ Jefferson bit off a hangmans thumb ” – Jefferson Fracture ( burst Fx of C1) – Bilateral facet dislocation – Odontoid fracture – Any fracture with sublux – Hangmans fracture – Teardrop fracture Jefferson Fx / Bilateral Facet Jefferson Fx / Bilateral Facet Odontoid Fx / Any Fx with Sublux Odontoid Fx / Any Fx with Sublux Hangmans Fx / Teardrop FX Hangmans Fx / Teardrop FX C – Spine Injury PE Pearls C – Spine Injury PE Pearls • Suspect Spinal Cord Injury in: – Patients with AMS • Secondary to trauma or toxin (ETOH) – Patients with unexplained hypotension and bradycardia – Elderly patients with OA or spondylosis – Children, especially <8 years old. • SCIWORA – Normal XR with Neuro abnormality Spinal Cord Injury PE Findings Spinal Cord Injury PE Findings • • • • • • Flaccid arreflexia Loss of sphincter tone Diaphragmatic abdominal breathing Priapism Hypotension + Bradycardia Facial reaction to painful stimulus above (but not below) the clavicle Spinal Cord Injury PE Findings Spinal Cord Injury PE Findings • A COMPLETE HISTORY AND PE a MUST – INCLUDING a thorough NEURO EXAM!! • Sensory/Motor Dermatones ROOT MOTOR SENSORY C3 Diaphragm, Trap Lower neck C4 Diaphragm Clavicular area C5 Biceps, Deltoid Below clavicle C6 Biceps Thumb & Lat. Forearm C7 Triceps Index & Middle Fingers C8 Finger Flexors Little Finger T1 Hand Intrinsics Medial Arm C – Spine Injury Diagnosis C – Spine Injury Diagnosis • Assume Injury • 3 View C­ Spine Xray – ANY abnormality • Keep in C­ Collar • Xray entire spine • Consider CT scan • CT SCAN of C­ Spine – Indications: • Inadequate or suspicious plain films • “Normal” films in patient with abnormal neuro exam • Fracture/dislocation, Posterior arch Fx, Burst Fx C­ Spine Injury Management C­ Spine Injury Management • • • • As always ABC’s with C­Spine immobilization IV, O2, Monitor Neuorsurgical evaluation Steroid Protocol: – Indications: • High dose steroids beneficial in patients with blunt cord injury • who present <12hours. Methyprednisolone 30mg/kg bolus, then start infusion @ 5.4mg/kg/hr for 23 hours Infectious Emergencies Infectious Emergencies Meningococcemia Infectious Neurologic Emergencies Infectious Neurologic Emergencies • • Meningitis: inflammation of the meninges History: – Acute Bacterial Meningitis: • Rapid onset of symptoms <24 hours – – Fever, Headache, Photophobia Stiff neck, Confusion • Etiology By Age: – 0­4 weeks: E. Coli, Group B Strep, Listeria – 4­12 weeks: neotatal patoogens, S. pneumo, N. meningitides, H. flu – 3mos – 18 years: S.pneumo, N. menin.,H. flu – >50/ alcholics: S. pneumo, Listeria, N. menin., Gram(­) bacilli Meningitis Meningitis • Lymphocytic Meningitis (Aseptic/Viral) – Gradual onset of symptoms as previously listed over 1­7 days. – Etiology: • Viral • Atypical Meningitis – – – History (medical/social/environmental) crucial Insidious onset of symptoms over 1­2 weeks Etiology: • TB(#1) • Coccidiomycosis, crytococcus Meningitis Meningitis • Physical Exam Pearls – Infants and the elderly lack the usual signs and symptoms, only clue may be AMS. – Look for papilledema, focal neurologic signs, ophthalmoplegia and rashes – As always full exam • Checking for above • Brudzinski’s sign • Kernigs sign – KEY POINT: If you suspect meningococcemia do NOT delay antibiotic therapy, MUST start within 20 minutes of arrival!!!!! Meningitis Meningitis • Emergent CT Prior to LP – Those with profoundly depressed MS – Seizure – Head Injury – Focal Neurologic signs – Immunocompromised with CD4 count <500 • DO NOT DELAY ANTIBIOTIC THERAPY!! Meningitis Meningitis • Lumbar Puncture Results TEST NORMAL BACTERIAL VIRAL Pressure <170 >300 200 Protein <50 >200 <200 Glucose >40 <40 >40 WBC’s <5 >1000 <1000 Cell type Monos >50% PMN’s Monos Gram Stain Neg Pos Neg Meningitis Management Meningitis Management • Antibiotics By Age Group – Neonates(<1month) = Ampicillin + Gent. or Cefotaxime + Gent ­ Infants (1­3mos) = Cefotaxime or Ceftriaxone + Ampicillin ­ Children (3mos­18yrs) = Ceftriaxone ­ Adults (18yr­up) = Ceftriaxone + Vancomycin ­ Elderly/Immunocomp = Ceftriaxone +Ampicillin + Vancomycin Meningitis Management Meningitis Management • Steroids – In children, dexamethasone has been shown to be of benefit in reducing sensiorneural hearing loss, when given before the first dose of antibiotic. – Indications: • Children> 6 weeks with meningitis due to H. flu or S. pneumo. Adults with positive CSF gram stain • – Dose: 0.15mg/kg IV Encephalitis Encephalitis • Always think of in the young/elderly or • • immunocompromised with FEVER + AMS Common Etiologies: Viral – – – – West Nile Herpes Simplex Virus (HSV) Varicella Zoster Virus (VZV) Arboviruses • Eastern Equine viruses • St. Louis Encephalitis Encephalitis Encephalitis • Defined as: inflammation of the brain itself • Most cases are self limited, and unless virulent strain, or immunocompromised, will resolve. • The ONLY treatable forms of encephalitis are: – HSV – Zoster Encephalitis Encephalitis • Management: Emergent CT : As indicated for meningitis – ABC’s with supportive care. – Lumbar puncture: • Send for ELISA and PCR – Acyclovir 10 mg/kg Q 8 hours IV for HSV and Zoster – Steroids not shown to be of benefit. Headache & Vertigo Headache & Vertigo • Headache • Types of Headache: – Migraine • With aura • Without aura – Cluster Headache – Subarachnoid hemorrhage – Temporal arteritis Headache Headache • Migraine – Now thought to be due to neurogenic inflammation and abnormalities of serotonergic transmission. – Symptoms: – Severe headache either preceeded by a visual “aura”(scintillating scotoma or VF cut) or motor disturbance. – Nausea, vomiting, light sensitivity, sound sensitivity • Factors that may provoke an attack include: – – – Menstruation, Sleep/food deprivation Physical activity or certain foods (chocolate) Contraceptive estrogens Migraines Migraines • History & PE – CRUCIAL to obtain HA history from patient • Is this HA similar to others or is it “worst HA of life” • Prior workups • Medications • Foods • Menses – FULL PE including Neuro and Skin Migraines Migraines • Management – Place patient in cool quiet, dark environment – IV fluids if dehydrated – Abortive therapy: • Proclorperazine(compazine) 10 mg IV • DHE + antiemetic • Sumatriptan • Opiods as LAST RESORT!! Headaches Headaches • Cluster Headaches – Classically as boring headache on one side of face behind the eye. – May be signs of facial flushing, tearing, nasal stuffiness TX: 100% O2 by N/C at 6­8 l/min ­ If no relief, Sumatriptan Headaches Headaches • Subarachnoid hemorrhage – Clinically: Abrupt onset of severe thunderclap “worst HA of life”. – Usually associated nausea and vomiting – Nonfocal neurologic exam (usually) • Etiology: usually due to leaking berry aneurysm. • DX: CT +LP A MUST – – If CT (­), MUST perform LP LP (+) if (+) xanthrochromia OR failure of CSF to clear RBC’s by tube #4 Headaches Headaches • Subarachnoid Hemorrhage – – – – – – Management ABC’s as always IV, O2, Monitor Head of bed @ 30 degress Prophylax patient for seizures with Dilantin load. Ca Channel blocker (nimlodipine) 60 mg Q6 h to prevent vasospasm, and rebleed. Headaches Headaches • Temporal Arteritis – Etiology: a granulomatous inflammation of one or more of the branches of the ext. carotid artery – Clinically presents as: • Severe unilateral HA over Temporal area • Usually in middle aged females. • PE reveals: a tender, warm, frequently pulseless temporal artery, with decreased visual acuity on the affected side. Headaches Headaches • Temporal Arteritis – DX: Clinically + ESR elevation, usually>50mm/hr – Confirm with biopsy of artery – TX: HIGH dose steroids are VISION SAVING! • Start on prednisone IMMEDIATELY once suspected – Prednisone 60 – 80 mg Q day – Stat Neurology Consult Vertigo Vertigo • History and PE exam again CRUCIAL!! – History: • Truly a vertiginous complaint? – r/o syncope / near syncope?? • Acute onset of severe symptoms or more gradual course – PE: • Full exam paying particular attention to: – HEENT : Eyes, TM’s – Neuro : Cerebellar function Vertigo Vertigo • Peripheral Vertigo • History: • • • • • – Acute onset of severe dizziness, nausea, vomiting. – May be a positional worsening of symptoms – Recent history of URI or similar episodes in past which resolved. PE Pearls: Horizontal nystagmus which fatigues Possible TM abnormality Normal Neuro exam with normal cerebellar function and gait. Reproduction of symptoms with Hallpike maneuver Vertigo Vertigo • Peripheral – – – – – – – Common Causes: Labrynthitis Cerumen Impaction OM OE URI Menieres Disease (tinnitus,hearing loss, vertigo) • TX: Symptomatic and treat underlying cause: – Antivert 25 mg Q6h – Neurology / ENT follow up Vertigo Vertigo • Central Vertigo • Due to lesions of brainstem or cerebellum • 10 – 15% of cases • Signs & Symptoms: – Gradual onset of mild disequilibrium – Mild nausea and vomiting – Nonfatigable any direction nystagmus – Associated neurological abnormalities: • Ptosis • Facial palsy, dysarthria • Cerebellar findings, ataxia Vertigo Vertigo • Central – Causes: • Brainstem ischemia or infarction • Cerebellar hemorrhage • Vertebrobasilar insufficiency • MS – Diagnosis: • Thorough Neurologic exam • Head CT with Posterior fossa thin cuts – Management: • Neuro consult • Admit and workup depending on etiology Emergent Peripheral Neuropathies Emergent • Acute Toxic Neuropathies – Diptheria (Cornybacterium diptheriae) • Acutely ill patient with fever, in a dPT deficient patient. • Membranous pharyngitis that bleeds • Powerful exotoxin produces widespread organ damage. – – – Myocarditis/AV Block,Nephritis, Hepatitis. Neuritis with bulbar and peripheral paralysis. (ptosis, strabismus, loss of DTR’s) • TX: Parenteral PCN or Erythromycin – Horse Serum antitoxin – Respiratory isolation and admission the rule. Emergent Peripheral Neuropathies Emergent Peripheral Neuropathies – Botulism (Clostridium botulinum toxin) • Earliest finding(90%)= Blurred vision, diplopia, • • • ophthalmoplegia, ptosis Neurologic abnormalities descend and will lastly involve the respiratory musculature and cause respiratory paralysis and death with 6 hours if not treated! Mentation and sensation are normal. Remember in infants with FTT – Raw honey contains C. botulinum • Tx: Aggressive airway stabilization! • Trivalent serum antitoxin • Lastly some reported cases of hypersensitivity from “Bo­tox” – So …….. LOOK OUT JOAN!!! LOOK OUT JOAN!!! Emergent Peripheral Neuropathies Emergent Peripheral Neuropathies • Tetanus – Symptoms 4 “T”’s • Trismus, Tetany, Twitching, Tightness • Risus sardonicus • Signs of sympathetic overstimulation. – Tachycardia, hyperpyrexia, diaphoresis. – Management: • Human Tetanus Immunoglobulin (HTIG) • dT Toxoid • Metronidazole Emergent Peripheral Neuropathies Emergent Peripheral Neuropathies • Guillain­Barre Syndrome – Most common acute polyneuropathy. – 2/3’s of patients will have preceeding URI or gastroenteritis 1­3 weeks prior to onset. – Presents as: paresthesias followed by ascending paralysis starting in legs and moving upwards. • Remember Miller­Fischer variant: has minimal weakness and presents with ataxia, arreflexia, and ophthalmoiplegia. – DX: LP will show cytochemical dissociation. • Normal cells with HIGH protein. – TX: Self limiting, Early and aggressive airway stabilization. Emergent Peripheral Neuropathies Emergent Peripheral Neuropathies • Myasthenia Gravis – Most common disorder of neuromuscular transmission. – An autoimmune disease that destroys acetylcholine receptors which leads to poor neurotransmission and weakness. – Commonly will present as: • Muscle weakness exacerbated by activity, and is relieved by rest – Clinically: ptosis, diplopia and blurred vision are the most common complaints. Pupil is spared! Emergent Peripheral Neuropathies Emergent Peripheral Neuropathies • Myasthenia Gravis – Myasthenic crisis = A true emergency!! – Occurs in undiagnosed or untreated patients • Due to Ach deficiency • Patients present with profound weakness and impending respiratory failure – TX: Stabilize and manage airway • Look for chloinergic signs”SLUDGE” – If cholinergic give atropine 1mg IV prn • Consider edrophonium 1 ­2 mg IV New Emerging Treatments New Emerging Treatments • Stroke/ TIA’s – Hypothermia units with cooling TLC’s and blankets – Lasers, cerebral angioplasty and clot retrieval – See articles: – “Beyond TPA: Mechanical intervention in Acute Stroke”, Annals of EM June 2003 – “Acute Ischemic Stroke : Emergent Evaluation and Management”, Emerg. Clinics of North Am. August 2002 – “TIA Management” NEJM November 2002 THE END THE END ANY QUESTIONS???? ...
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