Download Free Medical Neurological Emergencies PowerPoint Presentation

Neurological Emergencies PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Neurological Emergencies".

This medical PowerPoint presentation talks about neurological emergencies.

Neurological emergencies refer to conditions that affect the nervous system and require immediate medical attention.

Neurological emergencies can include Stroke, Traumatic Brain Injury (TBI), Seizures, Meningitis, and Spinal cord injury etc.

Tags : Neurological Emergencies, nervous system, Stroke, Traumatic Brain Injury, Seizures, Meningitis, Spinal cord injury, critical care medicine, critical care medicine PowerPoint presentation

Published on : Mar 28, 2023 | Views : 1070 | Downloads : 2

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Neurological Emergencies
Slide 2-

Neurologic Emergency Outline Change in Mental Status / Coma Stroke/TIA Syndromes Seizure & Status Epilepticus Head Trauma Infectious Vertigo/Headaches Peripheral Neuropathies
Slide 3-

The Neurologic Exam KEY!! Must do a complete thorough neuro exam to properly identify and diagnose any neurologic abnormality. Exam should include 5 parts: Mental status, level of alertness (GCS) Cranial nerve exam Motor / Sensory exam Reflexes Cerebellar Consider ; MMSE if Psych components
Slide 4-

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
Slide 5-

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)
Slide 6-

Change in Mental Status/Coma T for Trauma
Slide 7-

-S for Stroke / Space Occupying Lesions
Slide 8-

Space Occupying Lesion
Slide 9-

AMS / COMA Physical Exam Pearls Always attempt to get a complete history!! LOOK at your patient! Smell the breath (ketones,alcohol,fetid) Observe respiratory rate & patterns (Cheyne-Stokes) 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!!
Slide 10-

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”
Slide 11-

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”
Slide 12-

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”
Slide 13-

AMS / COMA Essential Stabilization & Assessment Measures Always assess & stabilize ABC’s first special attention to airway with C-Spine immobilization / 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 C-Spine Labs / CT as indicated
Slide 14-

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
Slide 15-

Pathophysiology of Stroke / TIA Ischemic Strokes: (thrombi or emboli) Cerebral Thrombi may result from: Atherosclerosis (#1 cause) Infective arteritis Vasculitis Hypercoagulable 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)
Slide 16-

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
Slide 17-

Stroke /TIA Syndromes Type of Stroke (rule of 2/3’s) 2/3 of ALL Strokes are ISCHEMIC 2/3 of these are 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
Slide 18-

Ischemic Stroke Syndromes: Thrombotic vs. Embolic 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.
Slide 19-

Ischemic 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
Slide 20-

Ischemic 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
Slide 21-

Ischemic Stroke Syndromes Vertebrobasilar Artery Occlusion (VBA) Hallmark: Crossed Neurological Deficits 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
Slide 22-

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 81-325mg po Oxygen, 2L NC If cardiac arrythmia (atrial filbrillation) present, consider Heparin ONLY after Head CT and Neuro consultation.
Slide 23-

Hemorrhagic Stroke Syndromes (SAH, & Intracerebral) Subarachnoid Hemorrhage Highest incidence in 35-65 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: Consider adding Nimodipine 60 mg Q6 to reduce vasospasm
Slide 24-

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 Thalamus Pontine ( 3 P’s – pinpoint pontine pupils)
Slide 25-

Intracerebral Hemorrhage
Slide 26-

Treatment of Stroke AS ALWAYS – ABC’s FIRST What’s the Serum Glucose?? Consider Thiamine 100mg IV, D 50 bolus if hypoglycemic. Treat Hyperglycemia if Serum Glucose > 300mg/dl Protect the “Penumbra” Keep SBP >90mm Hg Goal keep CPP > 60mm Hg (CPP=MAP-ICP) Treat Fever ( Mild Hypothermia beneficial) Acetaminophen 650mg po or pr, cooling blanket Oxygenate (Keep Sao2 >95%) Elevate head of bed 30 deg. (Clear c-spine) Frequent repeat Neuro checks!! Reassess GCS!
Slide 27-

Treatment of Stroke What type of stroke is Present?? Hemorrhagic vs Ischemic Any signs of shift herniation? Neurosurgery evaluation or transfer necessary? Other management adjuncts: Ischemic strokes ASA 81-325mg Patients with Systolic BP >220 , Diastolic>120 need BP control with Nitroprusside or Labetolol. DO NOT OVERTREAT BP or risk extending the infarct. Heparin not shown to be of benefit in recent studies, however, still frequently used. Consult Neurologist before use If used, No bolus, just infusion. Risk of hemorrhagic transformation.
Slide 28-

Treatment of Strokes Strokes with Edema, Mass Effect or Shift Load with Phosphenytoin 1000mg for seizure prophylaxis 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!! Inclusion and Exclusion Criteria Benefit Questionable
Slide 29-

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.
Slide 30-

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
Slide 31-

Seizures & Status Epilepticus Background: 1 – 2% of the general population has seizures Primary Idiopathic epilepsy: onset ages 10-20 Secondary Precipitated by one of the following: Intracranial pathology Trauma, Mass, Abscess, Infarct Extracranial Pathology Toxic, metabolic, hypertensive, eclampsia
Slide 32-

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 auditory or visual hallucinations Simple = somatic complaints + no LOC Complex = somatic complaints + AMS or LOC
Slide 33-

Approach for 1st Seizure, New Seizure, or Substance/ Trauma Induced Seizure As always ABC’s First IV, O2, Monitor. Send blood for CBC, Chem 20, Tox screen as appropriate Anticonvulsant levels Prolactin levels / Lactate level CXR / UA/ Head CT Is patient actively seizing? Post ictal? Pseudoseizure? Consider treatment options Complete History and Physical Exam Including detailed Neuro Exam Repeat Neuro evaluations a must!
Slide 34-

Guidelines for Postictal Head CT Scans Status Epilepticus ( a true emergency) Abnormal Neuro findings No return to GCS 15 Prolonged HA History of malignancy CHI (Closed Head Injury) HIV infection or high risk for HIV Anticoagulant use Age > 40
Slide 35-

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
Slide 36-

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 (pyridoxime/B-6 deficiency) Eclampsia Alcoholic (thiamine/B-1 deficiency) Other Tox ingestion (TCA’s, sulfonylurea OD) Trauma
Slide 37-

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 (Cerebyx): 20mg/kg IV at rate of 50mg/min THIRD LINE TREATMENT Get Ready to intubate at this point!! Phenobarbitol 10-20mg/kg @ 60 mg/min
Slide 38-

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
Slide 39-

Status Epilepticus Adjunctive Treatment by History Thiamine 100mg IV, 1-2 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 B-6 deficiency
Slide 40-

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.
Slide 41-

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 (spinal cord injury); hypotension is ALWAYS secondary to hypovolemia from blood loss in the trauma patient! The most common intracranial bleed in CHI is subarachnoid hemorrhage.
Slide 42-

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.
Slide 43-

Cerebral Contusion
Slide 44-

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
Slide 45-

Subdural Hematoma
Slide 46-

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
Slide 47-

Epidural Hematoma
Slide 48-

Management of Closed Head Injuries As always ABC’s with C-Spine precautions IV, O2, Monitor. Stabilize and resuscitate Sao2>95% SBP>90 Treat Fever Head of Bed 30% (once C-Spine cleared) Stat Head CT with Stat Neurosurgical evaluation for surgical lesions. Repeat Exams, looking for signs of herniation.
Slide 49-

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
Slide 50-

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, presenting as: Ipsilateral pupil dilatation Contralateral hemiparesis Deepening coma Decorticate posturing Apnea and death
Slide 51-

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
Slide 52-

Infectious Emergencies Meningococcemia
Slide 53-

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: 0-4 weeks: E. Coli, Group B Strep, Listeria 4-12 weeks: neotatal pathogens, S. pneumo, N. meningitides, H. flu 3mos – 18 years: S.pneumo, N. menin.,H. flu >50/ alcholics: S. pneumo, Listeria, N. menin., Gram(-) bacilli
Slide 54-

Meningitis Lymphocytic Meningitis (Aseptic/Viral) Gradual onset of symptoms as previously listed over 1-7 days. Etiology: Viral Atypical Meningitis History (medical/social/environmental) crucial Insidious onset of symptoms over 1-2 weeks Etiology: TB(#1) Coccidiomycosis, crytococcus
Slide 55-

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!!!!!
Slide 56-

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!!
Slide 57-

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
Slide 58-

Meningitis Management Antibiotics By Age Group Neonates(<1month) = Ampicillin + Gent. or Cefotaxime + Gent Infants (1-3mos) = Cefotaxime or Ceftriaxone + Ampicillin Children (3mos-18yrs) = Ceftriaxone Adults (18yr-up) = Ceftriaxone + Vancomycin Elderly/Immunocomp = Ceftriaxone +Ampicillin + Vancomycin
Slide 59-

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
Slide 60-

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
Slide 61-

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
Slide 62-

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.
Slide 63-

Headache & Vertigo Headache Types of Headache: Migraine With aura Without aura Cluster Headache Subarachnoid hemorrhage Temporal arteritis
Slide 64-

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
Slide 65-

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 exam
Slide 66-

Migraines Management Place patient in cool, quiet, dark environment IV fluids if dehydrated Abortive therapy: Phenothiazines (antimigraine and antiemetic) DHE (vaso/venoconstrictor) + antiemetic Sumatriptan (5-HT agonist) Opiods as LAST RESORT!!
Slide 67-

Headaches Cluster Headaches Classically as boring headache on one side of face behind the eye. May be associated with signs of facial flushing, tearing, nasal stuffiness TX: 100% O2 by N/C at 6-8 l/min - If no relief, Sumatriptan
Slide 68-

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
Slide 69-

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 (nimodipine) 60 mg Q6 h to prevent vasospasm, and rebleeding
Slide 70-

Headaches Temporal Arteritis Etiology: a granulomatous inflammation of one or more of the branches of the external 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.
Slide 71-

Headaches Temporal Arteritis DX: Clinically + ESR elevation, usually >50 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
Slide 72-

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
Slide 73-

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
Slide 74-

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
Slide 75-

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 nystagmus (any direction) Associated neurological abnormalities: Ptosis Facial palsy, dysarthria Cerebellar findings, ataxia
Slide 76-

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
Slide 77-

Emergent Peripheral Neuropathies 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.
Slide 78-

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 (failure to thrive) Raw honey contains C. botulinum Tx: Aggressive airway stabilization! Trivalent serum antitoxin Lastly, there have been some recently reported cases of hypersensitivity to “Bo-tox” So ……..
Slide 79-

LOOK OUT JOAN!!!
Slide 80-

Emergent Peripheral Neuropathies Tetanus Symptoms 4 “T”’s Trismus, Tetany, Twitching, Tightness Risus sardonicus / opisthotonus Signs of sympathetic overstimulation. Tachycardia, hyperpyrexia, diaphoresis. Management: Human Tetanus Immunoglobulin (HTIG) dT Toxoid Metronidazole
Slide 81-

Emergent Peripheral Neuropathies Guillain-Barre Syndrome Most common acute polyneuropathy. 2/3’s of patients will have preceeding URI or gastroenteritis 1-3 weeks prior to onset. Presents as: paresthesias followed by ascending paralysis starting in legs and moving upwards. Remember Miller-Fischer variant: has minimal weakness and presents with ataxia, arreflexia, and ophthalmoplegia. DX: LP will show cytochemical dissociation. Normal cells with HIGH protein. TX: Self limiting, Early and aggressive airway stabilization.
Slide 82-

Emergent Peripheral Neuropathies Myasthenia Gravis Most common disorder of neuromuscular transmission. An autoimmune disease that destroys acetylcholine receptors (AchR) which leads to poor neurotransmission and weakness. Proximal >> Distal muscle 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!
Slide 83-

Emergent Peripheral Neuropathies Myasthenia Gravis Myasthenic crisis = A true emergency!! Occurs in undiagnosed or untreated patients Due to relative Ach (acetylcholine) deficiency Patients present with profound weakness and impending respiratory failure TX: Stabilize and manage airway Consider edrophonium 1 -2 mg IV (AchE inhibitor)
Slide 84-

New Emerging Treatments Stroke/ TIA’s Hypothermia units with cooling devices and blankets Lasers, cerebral angioplasty and clot retrieval See articles: “Established Treatments of Acute Ischemic Stroke”, Lancet 2007 “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
Slide 85-

References: CNS Emergencies Lecture adapted from Dr. Patrick O’Shaughnessy EM Attending Beth Israel Medical Center
Slide 86-

THE END ANY QUESTIONS????