Neurological Emergencies. Neurologic Emergency Outline Change in Mental Status / Coma Change in...

Neurological EmergenciesNeurological Emergencies

Neurologic Emergency Neurologic Emergency OutlineOutline

• Change in Mental Status / ComaChange in Mental Status / Coma

• Stroke/TIA SyndromesStroke/TIA Syndromes

• Seizure & Status EpilepticusSeizure & Status Epilepticus

• Head Trauma Head Trauma

• InfectiousInfectious

• Vertigo/HeadachesVertigo/Headaches

• Peripheral NeuropathiesPeripheral Neuropathies

The Neurologic ExamThe Neurologic Exam

• KEY!! Must do a complete thorough neuro exam KEY!! Must do a complete thorough neuro exam to properly identify and diagnose any neurologic to properly identify and diagnose any neurologic abnormality.abnormality.

• Exam should include 5 parts:Exam should include 5 parts:– Mental status, level of alertness (GCS)Mental status, level of alertness (GCS)– Cranial nerve examCranial nerve exam– Motor / Sensory examMotor / Sensory exam– ReflexesReflexes– CerebellarCerebellar– Consider ; MMSE if Psych componentsConsider ; MMSE if Psych components

Change in Mental Status / Change in Mental Status / COMACOMA

• Potential Causes – “AEIOU TIPS”Potential Causes – “AEIOU TIPS”• A = Alcohol ( Drugs & Toxins)A = Alcohol ( Drugs & Toxins)• E = Endocrine, Exocrine, ElectrolyteE = Endocrine, Exocrine, Electrolyte• I = InsulinI = Insulin• O = Opiates, ODO = Opiates, OD• U = UremiaU = Uremia• T = Trauma, TemperatureT = Trauma, Temperature• I = InfectionI = Infection• P = Psychiatric disorderP = Psychiatric disorder• S = Seizure , Stroke, Shock, Space occupying lesionS = Seizure , Stroke, Shock, Space occupying lesion

Change in Mental Change in Mental Status/ComaStatus/Coma• TemperatureTemperature

– Hypothermia: causes coma when Temp<32.0 CHypothermia: causes coma when Temp<32.0 C– Hyperthermia: causes coma when Temp>42.0CHyperthermia: causes coma when Temp>42.0C

• InfectionInfection– Meningitis, Encephalitis, SepsisMeningitis, Encephalitis, Sepsis

• Endo/Exocrine, ElectrolyteEndo/Exocrine, Electrolyte– Hypo/HyperglycemiaHypo/Hyperglycemia– Hypo/hyperthyroidismHypo/hyperthyroidism– Hypo/hypernatremiaHypo/hypernatremia– Hepatic encephalopathyHepatic encephalopathy

• Opiods/ OD / AlcoholOpiods/ OD / Alcohol– Heroin, Psych Meds (TCA’s, SSRI’s)Heroin, Psych Meds (TCA’s, SSRI’s)

Change in Mental Change in Mental Status/ComaStatus/Coma• T for TraumaT for Trauma

-S for Stroke / Space -S for Stroke / Space Occupying LesionsOccupying Lesions

Space Occupying LesionSpace Occupying Lesion

AMS / COMA Physical Exam AMS / COMA Physical Exam PearlsPearls

• Always attempt to get a complete history!!Always attempt to get a complete history!!

• LOOK at your patient!LOOK at your patient!– Smell the breath (ketones,alcohol,fetid)Smell the breath (ketones,alcohol,fetid)– Observe respiratory rate & patterns (Cheyne-Stokes)Observe respiratory rate & patterns (Cheyne-Stokes)– Look for abnormal posturing.Look for abnormal posturing.

• Decorticate (Flexion of UE with Extension of LE)Decorticate (Flexion of UE with Extension of LE)

• Decerebrate (Extension of all Ext.)Decerebrate (Extension of all Ext.)

– Look for needle marks, cyanosis, signs of traumaLook for needle marks, cyanosis, signs of trauma

• Obtain GCS Score! E4 V5 M 6Obtain GCS Score! E4 V5 M 6– If less than 8, IMMEDIATE airway stabilization FIRST If less than 8, IMMEDIATE airway stabilization FIRST

priority!!priority!!

Glasgow COMA ScaleGlasgow COMA Scale

• Scores range from 3 (Worst) – 15 (Best)Scores range from 3 (Worst) – 15 (Best)• Important for classifying degree of alteration. Important for classifying degree of alteration.

(Head Trauma)(Head Trauma)• GCS < 8 = INTUBATE!!GCS < 8 = INTUBATE!!

• EYE Opening ResponseEYE Opening Response– 4 = Spontaneous4 = Spontaneous– 3 = To Voice3 = To Voice– 2 = To Pain2 = To Pain– 1 = None1 = None

• Remember as “4 eyes”Remember as “4 eyes”


• Verbal ResponseVerbal Response– 5 = Oriented and converses5 = Oriented and converses– 4 = Confused but converses4 = Confused but converses– 3 = Inappropriate words3 = Inappropriate words– 2 = Inappropriate sounds2 = Inappropriate sounds– 1= None1= None

• Remember as “Jackson 5 – Remember as “Jackson 5 – sing/voice”sing/voice”


• MotorMotor– 6 = Obeys commands6 = Obeys commands– 5 = Localizes pain5 = Localizes pain– 4 = Withdraws to pain4 = Withdraws to pain– 3 = Decorticate (flexes to pain)3 = Decorticate (flexes to pain)– 2 = Decerebrate (extends to pain)2 = Decerebrate (extends to pain)– 1 = None1 = None

• Remember as “ 6 Cylinder engine – motor”Remember as “ 6 Cylinder engine – motor”

AMS / COMA Essential AMS / COMA Essential Stabilization & Assessment Stabilization & Assessment MeasuresMeasures• Always assess & stabilize ABC’s firstAlways assess & stabilize ABC’s first

– special attention to airway with C-Spine special attention to airway with C-Spine immobilization / protection. Oxygenate!immobilization / protection. Oxygenate!

– IV line , fluids, Thiamine 100mg IV, 1 amp D IV line , fluids, Thiamine 100mg IV, 1 amp D 50, & Narcan(if needed) 0.4mg increments 50, & Narcan(if needed) 0.4mg increments until response.until response.

• Complete history and physical exam after Complete history and physical exam after stabilizationstabilization

• Radiographic clearance of C-Spine Radiographic clearance of C-Spine

• Labs / CT as indicatedLabs / CT as indicated

Stroke / TIA SyndromesStroke / TIA Syndromes

• Anatomy of Cerebral Blood FlowAnatomy of Cerebral Blood Flow– Anterior Circulation: 80% of cerebral blood flow Anterior Circulation: 80% of cerebral blood flow

originates from the carotids which supplies theoriginates from the carotids which supplies the• Frontoparietal lobesFrontoparietal lobes• Anterior temporal lobesAnterior temporal lobes• Optic nerve and retinaOptic nerve and retina

– Posterior Circulation: 20 % of cerebral blood flow which Posterior Circulation: 20 % of cerebral blood flow which originates from the vertebrobasilar arteriesoriginates from the vertebrobasilar arteries• Thalamus & BrainstemThalamus & Brainstem• Occipital cortex and CerebellumOccipital cortex and Cerebellum• Upper Spinal cord & Auditory and Vestibular functions in earUpper Spinal cord & Auditory and Vestibular functions in ear

– Circle of Willis: connects the Anterior and Posterior Circle of Willis: connects the Anterior and Posterior circulationscirculations

Pathophysiology of Stroke / Pathophysiology of Stroke / TIATIA• Ischemic Strokes: (thrombi or emboli)Ischemic Strokes: (thrombi or emboli)

– Cerebral Thrombi may result from:Cerebral Thrombi may result from:• Atherosclerosis (#1 cause)Atherosclerosis (#1 cause)• Infective arteritisInfective arteritis• VasculitisVasculitis• Hypercoagulable statesHypercoagulable states• Post traumatic carotid or vertebral artery dissectionsPost traumatic carotid or vertebral artery dissections

– Cerebral emboli may result from:Cerebral emboli may result from:• Mural thrombus from heart (#1 cause)Mural thrombus from heart (#1 cause)• Aortic plaquesAortic plaques• EndocarditisEndocarditis• Long bone or Dysbaric injuries (fat / air emboliLong bone or Dysbaric injuries (fat / air emboli))

Pathophysiology of Pathophysiology of Stroke/TIAStroke/TIA• Hemorrhagic Strokes result fromHemorrhagic Strokes result from

– Spontaneous rupture of berry aneurysm or AV Spontaneous rupture of berry aneurysm or AV malformation (Subarachnoid hemorrhage)malformation (Subarachnoid hemorrhage)

– Rupture of arteriolar aneurysms secondary to:Rupture of arteriolar aneurysms secondary to:• HypertensionHypertension• Congenital abnormalityCongenital abnormality• Blood dyscrasia / Anticoagulant usageBlood dyscrasia / Anticoagulant usage• InfectionInfection• NeoplasmNeoplasm

– Trauma (Epidural / Subdural Hematomas)Trauma (Epidural / Subdural Hematomas)– Hemorrhagic transformation of embolic strokeHemorrhagic transformation of embolic stroke

Stroke /TIA SyndromesStroke /TIA Syndromes

• Type of Stroke (rule of 2/3’s)Type of Stroke (rule of 2/3’s)– 2/3 of ALL Strokes are ISCHEMIC2/3 of ALL Strokes are ISCHEMIC

• 2/3 of these are thrombotic2/3 of these are thrombotic• Therefore thrombotic, ischemic strokes most Therefore thrombotic, ischemic strokes most

common.common.

– Incidence of StrokeIncidence of Stroke• Biggest Risk FactorsBiggest Risk Factors

– Prior TIA ( 30 % will have stroke in 5 years)Prior TIA ( 30 % will have stroke in 5 years)– HTNHTN– AtherosclerosisAtherosclerosis– DMDM– HyperlipidemiaHyperlipidemia– SmokingSmoking

Ischemic Stroke Syndromes:Ischemic Stroke Syndromes: Thrombotic vs. Embolic Thrombotic vs. Embolic

• Thrombotic SyndromesThrombotic Syndromes– Usually slow, progressive onsetUsually slow, progressive onset– Sx develop shortly after awakening and Sx develop shortly after awakening and

are progressiveare progressive

• Embolic SyndromesEmbolic Syndromes– Usually abrupt onset with maximal Usually abrupt onset with maximal

deficit that tends to improve over time deficit that tends to improve over time as the embolus breaks up.as the embolus breaks up.

Ischemic Stroke SyndromesIschemic Stroke Syndromes

• Middle Cerebral Artery Occlusion (MCA)Middle Cerebral Artery Occlusion (MCA)– # 1 type# 1 type– Contralateral hemiplegia, hemianesthesia, Contralateral hemiplegia, hemianesthesia,

and homonymous hemianopsiaand homonymous hemianopsia– Upper extremity deficit >> Lower extremityUpper extremity deficit >> Lower extremity– Aphasia (if dominant hemisphere involved)Aphasia (if dominant hemisphere involved)– Conjugate gaze impaired in the direction of Conjugate gaze impaired in the direction of

the lesionthe lesion


• Anterior Cerebral Artery Occlusion (ACA)Anterior Cerebral Artery Occlusion (ACA)– Contralateral leg, arm, paralysisContralateral leg, arm, paralysis– Lower Extremity deficit >> Upper extremityLower Extremity deficit >> Upper extremity– Loss of frontal lobe controlLoss of frontal lobe control

• IncontinenceIncontinence• Primitive grasp and suck reflexes enactedPrimitive grasp and suck reflexes enacted

• Posterior Cerebral Artery Occlusion (PCA)Posterior Cerebral Artery Occlusion (PCA)– Ipsilateral CN III palsy, visual lossIpsilateral CN III palsy, visual loss– Contralateral hemiparesis and hemisensory lossContralateral hemiparesis and hemisensory loss– Memory loss Memory loss


• Vertebrobasilar Artery Occlusion (VBA)Vertebrobasilar Artery Occlusion (VBA) Hallmark: Crossed Neurological DeficitsHallmark: Crossed Neurological Deficits CN AND Cerebellar deficits that affect BOTH CN AND Cerebellar deficits that affect BOTH

sides of the body, with contralateral pain and sides of the body, with contralateral pain and temperature deficits.temperature deficits.

- - Contralateral hemiplegiaContralateral hemiplegia- Ipsilateral CN III palsy with Cerebellar findings.Ipsilateral CN III palsy with Cerebellar findings.

- Nausea/VomitingNausea/Vomiting- Vertigo, Nystagmus, Vertigo, Nystagmus, - Ataxia, DysarthiaAtaxia, Dysarthia- Tinnitus, deafnessTinnitus, deafness

TIA’s (Transient Ischemic TIA’s (Transient Ischemic Attacks)Attacks)• Definition: A temporary loss of neurologic function, that resolves Definition: A temporary loss of neurologic function, that resolves

completely <24 hours.completely <24 hours.• Clinically;Clinically;

– Arm numbness, weakness, HAArm numbness, weakness, HA– Facial droop, slurred speechFacial droop, slurred speech– Sx resolved, or improve over timeSx resolved, or improve over time

• Main point: These patients at high risk for stroke if:Main point: These patients at high risk for stroke if:– >50>50– HTN, DM, Smoker, Prior TIA in last monthHTN, DM, Smoker, Prior TIA in last month– Any prior CVA…… ADMISSION IS THE RULE!!Any prior CVA…… ADMISSION IS THE RULE!!

• Treat as CVA : Head CT (CVA protocol)Treat as CVA : Head CT (CVA protocol)• ASA 81-325mg poASA 81-325mg po• Oxygen, 2L NCOxygen, 2L NC• If cardiac arrythmia (atrial filbrillation) present, consider Heparin If cardiac arrythmia (atrial filbrillation) present, consider Heparin

ONLY after Head CT and Neuro consultation.ONLY after Head CT and Neuro consultation.

Hemorrhagic Stroke Hemorrhagic Stroke SyndromesSyndromes (SAH, & Intracerebral) (SAH, & Intracerebral)• Subarachnoid HemorrhageSubarachnoid Hemorrhage

– Highest incidence in 35-65 year old.Highest incidence in 35-65 year old.– Usually from the rupture of a berry aneurysmUsually from the rupture of a berry aneurysm– Clinically:Clinically:

• abrupt onset of “worst headache of life”abrupt onset of “worst headache of life”• Nuchal rigidity, photophobia, vomiting, retinal Nuchal rigidity, photophobia, vomiting, retinal

hemorrhages.hemorrhages.– Diagnosis : CT + LP!!!!Diagnosis : CT + LP!!!!

• CT only 92% sensitive within 24 hours of event, loses CT only 92% sensitive within 24 hours of event, loses sensitivity >24 hours out from headache.sensitivity >24 hours out from headache.

• 72 hours out CANNOT r/o without LP!72 hours out CANNOT r/o without LP!– Management: Management:

• Consider adding Nimodipine 60 mg Q6 to reduce Consider adding Nimodipine 60 mg Q6 to reduce vasospasmvasospasm

Hemorrhagic Stroke Hemorrhagic Stroke SyndromesSyndromes• IntracerebralIntracerebral

– Hypertensive intracerebral hemorrhage MOST Hypertensive intracerebral hemorrhage MOST common cause.common cause.

– Traumatic, contusion, coup/contracoupTraumatic, contusion, coup/contracoup– Rupture of small blood vessels with bleeding Rupture of small blood vessels with bleeding

inside the brain parenchymainside the brain parenchyma• PutamenPutamen

• CerebellarCerebellar

• ThalamusThalamus

• Pontine ( 3 P’s – pinpoint pontine pupils)Pontine ( 3 P’s – pinpoint pontine pupils)

Intracerebral HemorrhageIntracerebral Hemorrhage

Treatment of StrokeTreatment of Stroke

• AS ALWAYS – ABC’s FIRST AS ALWAYS – ABC’s FIRST • What’s the Serum Glucose??What’s the Serum Glucose??

– Consider Thiamine 100mg IV, D 50 bolus if Consider Thiamine 100mg IV, D 50 bolus if hypoglycemic.hypoglycemic.

– Treat Hyperglycemia if Serum Glucose > 300mg/dlTreat Hyperglycemia if Serum Glucose > 300mg/dl• Protect the “Penumbra”Protect the “Penumbra”

– Keep SBP >90mm HgKeep SBP >90mm Hg– Goal keep CPP > 60mm Hg (CPP=MAP-ICP)Goal keep CPP > 60mm Hg (CPP=MAP-ICP)– Treat Fever ( Mild Hypothermia beneficial)Treat Fever ( Mild Hypothermia beneficial)

• Acetaminophen 650mg po or pr, cooling blanketAcetaminophen 650mg po or pr, cooling blanket– Oxygenate (Keep Sao2 >95%)Oxygenate (Keep Sao2 >95%)– Elevate head of bed 30 deg. (Clear c-spine)Elevate head of bed 30 deg. (Clear c-spine)

• Frequent repeat Neuro checks!! Reassess GCS!Frequent repeat Neuro checks!! Reassess GCS!

Treatment of StrokeTreatment of Stroke

• What type of stroke is Present??What type of stroke is Present??– Hemorrhagic vs IschemicHemorrhagic vs Ischemic

• Any signs of shift herniation?Any signs of shift herniation?• Neurosurgery evaluation or transfer necessary?Neurosurgery evaluation or transfer necessary?

• Other management adjuncts:Other management adjuncts:• IschemicIschemic strokes strokes

– ASA 81-325mg ASA 81-325mg – Patients with Systolic BP >220 , Diastolic>120 need BP control Patients with Systolic BP >220 , Diastolic>120 need BP control

with Nitroprusside or Labetolol.with Nitroprusside or Labetolol.– DO NOT OVERTREAT BP or risk extending the infarct.DO NOT OVERTREAT BP or risk extending the infarct.– Heparin not shown to be of benefit in recent studies, however, Heparin not shown to be of benefit in recent studies, however,

still still frequently used.frequently used.

• Consult Neurologist before useConsult Neurologist before use• If used, No bolus, just infusion.If used, No bolus, just infusion.• Risk of hemorrhagic transformation.Risk of hemorrhagic transformation.

Treatment of StrokesTreatment of Strokes

• Strokes with Edema, Mass Effect or ShiftStrokes with Edema, Mass Effect or Shift– Load with Phosphenytoin 1000mg for seizure prophylaxis Load with Phosphenytoin 1000mg for seizure prophylaxis – Acute seizure prophylaxis still of benefit.Acute seizure prophylaxis still of benefit.– Mannitol, Decadron??Mannitol, Decadron??

• Recently shown to be of NO benefit, some Neurosurgeons still Recently shown to be of NO benefit, some Neurosurgeons still advocate, so consult first.advocate, so consult first.

– Hyperventilation??Hyperventilation??• NOT beneficial and perhaps harmful, don’t do it!NOT beneficial and perhaps harmful, don’t do it!

• Thrombolytics???Thrombolytics???– Ischemic strokes ONLY with large deficit NOT improving.Ischemic strokes ONLY with large deficit NOT improving.– Time from symptom onset <3 hoursTime from symptom onset <3 hours– No ABSOLUTE Contraindications!!No ABSOLUTE Contraindications!!– Inclusion and Exclusion CriteriaInclusion and Exclusion Criteria– Benefit QuestionableBenefit Questionable

Thrombolytic Therapy for Thrombolytic Therapy for Acute Stroke ChecklistAcute Stroke Checklist

• Answer to ALL must be Answer to ALL must be YESYES::– Age 18 or olderAge 18 or older– Clinical diagnosis of Acute Ischemic Clinical diagnosis of Acute Ischemic

Stroke causing a measurable NON Stroke causing a measurable NON improving neurologic deficit.improving neurologic deficit.

– NO high clinical suspicion for SAHNO high clinical suspicion for SAH– Time of onset to treatment is <180 Time of onset to treatment is <180

minutes.minutes.

Thrombolytic Therapy for Thrombolytic Therapy for Acute Ischemic Stroke Acute Ischemic Stroke

ChecklistChecklist• Answer to ALL MUST be Answer to ALL MUST be NONO::

– Evidence of hemorrhage on CTEvidence of hemorrhage on CT– Active internal bleeding (GI/GU) within last 21 days.Active internal bleeding (GI/GU) within last 21 days.– Known bleeding diasthesis:Known bleeding diasthesis:

• Platelets<100,000Platelets<100,000• Heparin within last 48 hours with elevated PTTHeparin within last 48 hours with elevated PTT• Warfarin use with PT > 15 secondsWarfarin use with PT > 15 seconds

– Within 3 months of IC injury, prior surgery or prior ischemic Within 3 months of IC injury, prior surgery or prior ischemic stroke.stroke.

– Within 14 days of serious trauma, major surgeryWithin 14 days of serious trauma, major surgery– Recent AMI, arterial puncture/LP within 7 daysRecent AMI, arterial puncture/LP within 7 days– History of prior ICH, AVM, tumor,or aneurysm or seizure at History of prior ICH, AVM, tumor,or aneurysm or seizure at

strokestroke– Systolic BP >185mmHg, or Diastolic BP >110HgSystolic BP >185mmHg, or Diastolic BP >110Hg

Seizures & Status Seizures & Status EpilepticusEpilepticus• Background:Background:

– 1 – 2% of the general population has seizures1 – 2% of the general population has seizures– PrimaryPrimary

• Idiopathic epilepsy: onset ages 10-20Idiopathic epilepsy: onset ages 10-20

– SecondarySecondary• Precipitated by one of the following:Precipitated by one of the following:

• Intracranial pathologyIntracranial pathology– Trauma, Mass, Abscess, InfarctTrauma, Mass, Abscess, Infarct

• Extracranial PathologyExtracranial Pathology– Toxic, metabolic, hypertensive, eclampsiaToxic, metabolic, hypertensive, eclampsia

Seizure TypesSeizure Types

• Generalized Convulsive Seizures (Grand Mal):Generalized Convulsive Seizures (Grand Mal):– Tonic , clonic movements, (+) LOC, apnea, incontinence Tonic , clonic movements, (+) LOC, apnea, incontinence

and a post-ictal stateand a post-ictal state

• Non Convulsive Seizures (Petit Mal)Non Convulsive Seizures (Petit Mal)– Absence seizures – “blank staring spells”Absence seizures – “blank staring spells”– Myoclonic – brief contractions of selected muscle groupsMyoclonic – brief contractions of selected muscle groups

• Partial SeizuresPartial Seizures– Characterized by presence of auditory or visual Characterized by presence of auditory or visual

hallucinationshallucinations– Simple = somatic complaints + no LOCSimple = somatic complaints + no LOC– Complex = somatic complaints + AMS or LOCComplex = somatic complaints + AMS or LOC

Approach for 1Approach for 1stst Seizure, New Seizure, New Seizure, or Substance/ Trauma Seizure, or Substance/ Trauma Induced Seizure Induced Seizure • As always ABC’s First As always ABC’s First • IV, O2, Monitor.IV, O2, Monitor.

– Send blood for CBC, Chem 20, Tox screen as appropriateSend blood for CBC, Chem 20, Tox screen as appropriate– Anticonvulsant levelsAnticonvulsant levels– Prolactin levels / Lactate levelProlactin levels / Lactate level

• CXR / UA/ Head CTCXR / UA/ Head CT• Is patient actively seizing? Post ictal? Is patient actively seizing? Post ictal?

Pseudoseizure?Pseudoseizure?– Consider treatment optionsConsider treatment options

• Complete History and Physical ExamComplete History and Physical Exam– Including detailed Neuro ExamIncluding detailed Neuro Exam– Repeat Neuro evaluations a must!Repeat Neuro evaluations a must!

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

Approach to Breakthrough Approach to Breakthrough SeizureSeizure

• As Before, But History, History, History!!As Before, But History, History, History!!

• Main causes of Breakthrough Seizure:Main causes of Breakthrough Seizure:– Noncompliance with anticonvulsant regimenNoncompliance with anticonvulsant regimen– Start of new medication (level alteration)Start of new medication (level alteration)

• Antibiotics, OCP’sAntibiotics, OCP’s

– InfectionInfection• FeverFever

– Changes in body habitus, eating patternsChanges in body habitus, eating patterns– Supratherapeutic levelSupratherapeutic level

Status EpilepticusStatus Epilepticus

• DefinitionDefinition: operationally defined as seizure lasting : operationally defined as seizure lasting greater than 5 minutes OR two seizures between greater than 5 minutes OR two seizures between which there is incomplete recovery of which there is incomplete recovery of consciousness.consciousness.

• Treatment algorhythmTreatment algorhythm::– As before ABC’sAs before ABC’s– IV, O2, MonitorIV, O2, Monitor– Consider ALL potential causesConsider ALL potential causes

• INH (pyridoxime/B-6 deficiency)INH (pyridoxime/B-6 deficiency)• EclampsiaEclampsia• Alcoholic (thiamine/B-1 deficiency)Alcoholic (thiamine/B-1 deficiency)• Other Tox ingestion (TCA’s, sulfonylurea OD)Other Tox ingestion (TCA’s, sulfonylurea OD)• TraumaTrauma

Status Epilepticus Status Epilepticus TreatmentTreatment• FIRST LINE TREATMENTFIRST LINE TREATMENT

– Lorazepam (Ativan) 2mg/min IV up to 10 mg Lorazepam (Ativan) 2mg/min IV up to 10 mg max. OR Diazepam(Valium) 5mg/min IV or PR up max. OR Diazepam(Valium) 5mg/min IV or PR up to 20mgto 20mg

• SECOND LINE TREATMENTSECOND LINE TREATMENT– Phenytoin or Fosphenytoin (Cerebyx):Phenytoin or Fosphenytoin (Cerebyx):

• 20mg/kg IV at rate of 50mg/min20mg/kg IV at rate of 50mg/min

• THIRD LINE TREATMENTTHIRD LINE TREATMENT– Get Ready to intubate at this point!!Get Ready to intubate at this point!!– Phenobarbitol 10-20mg/kg @ 60 mg/minPhenobarbitol 10-20mg/kg @ 60 mg/min

Status Epilepticus Status Epilepticus TreatmentTreatment• FINAL TREATMENTFINAL TREATMENT

– Barbiturate ComaBarbiturate Coma• Pentobarbitol 5mg/kg @ 25 mg/minPentobarbitol 5mg/kg @ 25 mg/min• Stat Neurology consult for evaluation and EEGStat Neurology consult for evaluation and EEG• Pentobarbitol titrated to EEG response.Pentobarbitol titrated to EEG response.

• Always get a through HISTORYAlways get a through HISTORY– Possible traumaPossible trauma– Medications in houseMedications in house– Others sick, symptomaticOthers sick, symptomatic– Overall appearance of patientOverall appearance of patient

Status Epilepticus Adjunctive Status Epilepticus Adjunctive Treatment by HistoryTreatment by History

• Thiamine 100mg IV, 1-2 amps D 50Thiamine 100mg IV, 1-2 amps D 50– If suspect alcoholic, malnourished, If suspect alcoholic, malnourished,

hypoglycemiahypoglycemia

• Magnesium Sulfate 20cc of 10% Magnesium Sulfate 20cc of 10% solutionsolution– As above of if eclampsia (BP does NOT As above of if eclampsia (BP does NOT

have to be 200/120!!)have to be 200/120!!)

• Pyridoxine 5 gms IVPyridoxine 5 gms IV– INH or B-6 deficiencyINH or B-6 deficiency

Closed Head InjuryClosed Head Injury

• Definitions :Definitions :– Concussion:Concussion: refers to a transient LOC refers to a transient LOC

following head injury. Often associated with following head injury. Often associated with retrograde amnesia that also improves.retrograde amnesia that also improves.

– ““Coup” = injury beneath the site of traumaCoup” = injury beneath the site of trauma– ““Countrecoup” = injury to the side polar Countrecoup” = injury to the side polar

opposite to the traumatized area.opposite to the traumatized area.– Diffuse Axonal InjuryDiffuse Axonal Injury : tearing and shearing : tearing and shearing

of nerve fibers at the time of impact secondary of nerve fibers at the time of impact secondary to rapid acceleration/deceleration forces. to rapid acceleration/deceleration forces. Causes prolonged coma, injury, with normal Causes prolonged coma, injury, with normal initial head CT and poor outcome.initial head CT and poor outcome.

Closed head Injury FactsClosed head Injury Facts

• The single most important factor in the neurologic The single most important factor in the neurologic assessment of the head injured patient is level of assessment of the head injured patient is level of consciousness. (LOC)consciousness. (LOC)

• Always assume multiple injuries with serious Always assume multiple injuries with serious mechanism.mechanism.– ESPECIALLY C - SPINE!!!!ESPECIALLY C - SPINE!!!!– Unless hypotensive WITH bradycardia and WARM Unless hypotensive WITH bradycardia and WARM

extremities (spinal cord injury); hypotension is ALWAYS extremities (spinal cord injury); hypotension is ALWAYS secondary to hypovolemia from blood loss in the trauma secondary to hypovolemia from blood loss in the trauma patient!patient!

• The most common intracranial bleed in CHI is The most common intracranial bleed in CHI is subarachnoid hemorrhage.subarachnoid hemorrhage.

Closed Head Injuries with Closed Head Injuries with HemorrhageHemorrhage

• Cerebral ContusionCerebral Contusion– Focal hemorrhage and edema under the site of Focal hemorrhage and edema under the site of

impact.impact.– Susceptible areas are those in which the gyri Susceptible areas are those in which the gyri

are in close contact with the skullare in close contact with the skull• Frontal lobeFrontal lobe• Temporal lobesTemporal lobes

– Diagnostic Test of Choice: NC Head CTDiagnostic Test of Choice: NC Head CT– Treatment: Supportive with measures to keep Treatment: Supportive with measures to keep

ICP normal. Repeat Neuro checks. Repeat Head ICP normal. Repeat Neuro checks. Repeat Head Ct in 24 hours. Good prognosis.Ct in 24 hours. Good prognosis.

Cerebral ContusionCerebral Contusion

Subdural HematomaSubdural Hematoma

• Occurs secondary to acceleration/decelleration Occurs secondary to acceleration/decelleration injury with resultant tearing of the bridging veins injury with resultant tearing of the bridging veins that extend from the subarachnoid space to the that extend from the subarachnoid space to the dural sinuses. dural sinuses.

• Blood dissects over the cerebral cortex and Blood dissects over the cerebral cortex and collects under the dura overlying the brain.collects under the dura overlying the brain.

• Patients at risk:Patients at risk:– AlcoholicsAlcoholics– ElderlyElderly– Anticoagulant usersAnticoagulant users

• Appears as “sickle shape” and does not Appears as “sickle shape” and does not extend across the midlineextend across the midline

Subdural HematomaSubdural Hematoma

Epidural HematomaEpidural Hematoma

• Occurs from blunt trauma to head especially over Occurs from blunt trauma to head especially over the parietal/temporal area.the parietal/temporal area.

• Presents as LOC which then patient has lucid Presents as LOC which then patient has lucid interval then progressive deterioration, coma , interval then progressive deterioration, coma , death. ( Patient talks to you & dies!) death. ( Patient talks to you & dies!)

• Commonly associated with linear skull fractureCommonly associated with linear skull fracture• Mechanism of bleed is due to tear of artery, Mechanism of bleed is due to tear of artery,

usually middle meningeal.usually middle meningeal.• PE reveals ipsilateral pupillary dilitation with PE reveals ipsilateral pupillary dilitation with

contralateral hemiparesis.contralateral hemiparesis.• CT Scan : a BICONVEX (lens) density which can CT Scan : a BICONVEX (lens) density which can

extend across the midlineextend across the midline

Epidural HematomaEpidural Hematoma

Management of Closed Head Management of Closed Head InjuriesInjuries• As always ABC’s with C-Spine precautionsAs always ABC’s with C-Spine precautions• IV, O2, Monitor.IV, O2, Monitor.• Stabilize and resuscitateStabilize and resuscitate

– Sao2>95%Sao2>95%– SBP>90SBP>90– Treat FeverTreat Fever

• Head of Bed 30% (once C-Spine cleared)Head of Bed 30% (once C-Spine cleared)• Stat Head CT with Stat Neurosurgical Stat Head CT with Stat Neurosurgical

evaluation for surgical lesions.evaluation for surgical lesions.• Repeat Exams, looking for signs of Repeat Exams, looking for signs of

herniation.herniation.

Signs of Herniation / Increased Signs of Herniation / Increased ICPICP• Headache, nausea, vomitingHeadache, nausea, vomiting• Decreasing LOCDecreasing LOC• Sixth nerve paresis (one or both eyes adducted)Sixth nerve paresis (one or both eyes adducted)• Decreased respiratory rateDecreased respiratory rate• Cushing reflex Cushing reflex

(hypertension/bradycardia/bradynpea)(hypertension/bradycardia/bradynpea)• PapilledemaPapilledema• Development of signs of herniationDevelopment of signs of herniation

– Fixed and dilated pupilFixed and dilated pupil– Contralateral hemiparesisContralateral hemiparesis– PosturingPosturing

Herniation SyndromesHerniation Syndromes

• CPP = MAP – ICP: Must keep CPP >60 mm CPP = MAP – ICP: Must keep CPP >60 mm HgHg

• Uncal Herniation:Uncal Herniation:– Occurs when unilateral mass pushes the uncus Occurs when unilateral mass pushes the uncus

(temporal lobe) through the tentorial incisa, (temporal lobe) through the tentorial incisa, presenting as:presenting as:• Ipsilateral pupil dilatationIpsilateral pupil dilatation

• Contralateral hemiparesisContralateral hemiparesis

• Deepening comaDeepening coma

• Decorticate posturingDecorticate posturing

• Apnea and deathApnea and death

Herniation SyndromesHerniation Syndromes

• Cerebellar HerniationCerebellar Herniation– Downward displacement of cerebellar Downward displacement of cerebellar

tonsils through the foramen magnum.tonsils through the foramen magnum.– Presents as :Presents as :

•Medullary compressionMedullary compression

•Pinpoint pupilsPinpoint pupils

•Flaccid quadriplegiaFlaccid quadriplegia

•Apnea and circulatory collapseApnea and circulatory collapse

Infectious EmergenciesInfectious Emergencies

MeningococcemiaMeningococcemia

Infectious Neurologic Infectious Neurologic EmergenciesEmergencies

• Meningitis: inflammation of the meningesMeningitis: inflammation of the meninges• History:History:

– Acute Bacterial Meningitis:Acute Bacterial Meningitis:• Rapid onset of symptoms <24 hoursRapid onset of symptoms <24 hours

– Fever, Headache, PhotophobiaFever, Headache, Photophobia– Stiff neck, ConfusionStiff neck, Confusion

• Etiology By Age:Etiology By Age:– 0-4 weeks: E. Coli, Group B Strep, Listeria0-4 weeks: E. Coli, Group B Strep, Listeria– 4-12 weeks: neotatal pathogens, S. pneumo, N. 4-12 weeks: neotatal pathogens, S. pneumo, N.

meningitides, H. flumeningitides, H. flu– 3mos – 18 years: S.pneumo, N. menin.,H. flu3mos – 18 years: S.pneumo, N. menin.,H. flu– >50/ alcholics: S. pneumo, Listeria, N. menin., Gram(-) >50/ alcholics: S. pneumo, Listeria, N. menin., Gram(-)

bacillibacilli

MeningitisMeningitis

• Lymphocytic Meningitis (Aseptic/Viral)Lymphocytic Meningitis (Aseptic/Viral)– Gradual onset of symptoms as previously listed Gradual onset of symptoms as previously listed

over 1-7 days.over 1-7 days.– Etiology:Etiology:

• ViralViral

• Atypical MeningitisAtypical Meningitis– History (medical/social/environmental) crucialHistory (medical/social/environmental) crucial– Insidious onset of symptoms over 1-2 weeksInsidious onset of symptoms over 1-2 weeks– Etiology:Etiology:

• TB(#1)TB(#1)• Coccidiomycosis, crytococcusCoccidiomycosis, crytococcus


• Physical Exam PearlsPhysical Exam Pearls– Infants and the elderly lack the usual signs and Infants and the elderly lack the usual signs and

symptoms, only clue may be AMS.symptoms, only clue may be AMS.– Look for papilledema, focal neurologic signs, Look for papilledema, focal neurologic signs,

ophthalmoplegia and rashesophthalmoplegia and rashes– As always full examAs always full exam

• Checking for aboveChecking for above• Brudzinski’s signBrudzinski’s sign• Kernigs signKernigs sign

– KEY POINT: If you suspect meningococcemia do KEY POINT: If you suspect meningococcemia do NOT delay antibiotic therapy, MUST start within NOT delay antibiotic therapy, MUST start within 20 minutes of arrival!!!!!20 minutes of arrival!!!!!


• Emergent CT Prior to LPEmergent CT Prior to LP– Those with profoundly depressed MSThose with profoundly depressed MS– SeizureSeizure– Head InjuryHead Injury– Focal Neurologic signsFocal Neurologic signs– Immunocompromised with CD4 count <500 Immunocompromised with CD4 count <500

• DO NOT DELAY ANTIBIOTIC THERAPY!!DO NOT DELAY ANTIBIOTIC THERAPY!!


• Lumbar Puncture ResultsLumbar Puncture ResultsTEST NORMAL BACTERIAL VIRALTEST NORMAL BACTERIAL VIRAL

Pressure <170 >300 200Pressure <170 >300 200

Protein <50 >200 <200Protein <50 >200 <200

Glucose >40 <40 >40Glucose >40 <40 >40

WBC’s <5 >1000 <1000WBC’s <5 >1000 <1000

Cell type Monos >50% PMN’s MonosCell type Monos >50% PMN’s Monos

Gram Stain Neg Pos NegGram Stain Neg Pos Neg

Meningitis ManagementMeningitis Management

• Antibiotics By Age GroupAntibiotics By Age Group– Neonates(<1month) = Ampicillin + Gent. orNeonates(<1month) = Ampicillin + Gent. or

Cefotaxime + GentCefotaxime + Gent- Infants (1-3mos) = Cefotaxime or CeftriaxoneInfants (1-3mos) = Cefotaxime or Ceftriaxone

+ Ampicillin+ Ampicillin- Children (3mos-18yrs) = CeftriaxoneChildren (3mos-18yrs) = Ceftriaxone- Adults (18yr-up) = Ceftriaxone + VancomycinAdults (18yr-up) = Ceftriaxone + Vancomycin- Elderly/Immunocomp = Ceftriaxone Elderly/Immunocomp = Ceftriaxone

+Ampicillin ++Ampicillin + Vancomycin Vancomycin

Meningitis ManagementMeningitis Management

• SteroidsSteroids– In children, dexamethasone has been shown to In children, dexamethasone has been shown to

be of benefit in reducing sensiorneural hearing be of benefit in reducing sensiorneural hearing loss, when given before the first dose of loss, when given before the first dose of antibiotic.antibiotic.

– Indications:Indications:• Children> 6 weeks with meningitis due to H. flu or S. Children> 6 weeks with meningitis due to H. flu or S.

pneumo.pneumo.

• Adults with positive CSF gram stainAdults with positive CSF gram stain

– Dose: 0.15mg/kg IVDose: 0.15mg/kg IV

EncephalitisEncephalitis

• Always think of in the young/elderly or Always think of in the young/elderly or immunocompromised with FEVER + AMSimmunocompromised with FEVER + AMS

• Common Etiologies:Common Etiologies:• ViralViral

– West NileWest Nile– Herpes Simplex Virus (HSV)Herpes Simplex Virus (HSV)– Varicella Zoster Virus (VZV)Varicella Zoster Virus (VZV)– ArbovirusesArboviruses

• Eastern Equine viruses Eastern Equine viruses • St. Louis EncephalitisSt. Louis Encephalitis


• Defined as: inflammation of the brain Defined as: inflammation of the brain itselfitself

• Most cases are self limited, and Most cases are self limited, and unless virulent strain, or unless virulent strain, or immunocompromised, will resolve.immunocompromised, will resolve.

• The ONLY treatable forms of The ONLY treatable forms of encephalitis are: encephalitis are: – HSVHSV– ZosterZoster


• Management:Management:– Emergent CT : As indicated for meningitisEmergent CT : As indicated for meningitis– ABC’s with supportive care.ABC’s with supportive care.– Lumbar puncture:Lumbar puncture:

•Send for ELISA and PCRSend for ELISA and PCR

– Acyclovir 10 mg/kg Q 8 hours IV for HSV Acyclovir 10 mg/kg Q 8 hours IV for HSV and Zosterand Zoster

– Steroids not shown to be of benefit.Steroids not shown to be of benefit.

Headache & VertigoHeadache & Vertigo

• HeadacheHeadache

• Types of Headache:Types of Headache:– MigraineMigraine

•With auraWith aura

•Without auraWithout aura

– Cluster HeadacheCluster Headache– Subarachnoid hemorrhageSubarachnoid hemorrhage– Temporal arteritisTemporal arteritis

HeadacheHeadache

• MigraineMigraine– Now thought to be due to neurogenic inflammation and Now thought to be due to neurogenic inflammation and

abnormalities of serotonergic transmission.abnormalities of serotonergic transmission.– Symptoms:Symptoms:– Severe headache either preceeded by a visual Severe headache either preceeded by a visual

“aura”(scintillating scotoma or VF cut) or motor “aura”(scintillating scotoma or VF cut) or motor disturbance.disturbance.

– Nausea, vomiting, light sensitivity, sound sensitivityNausea, vomiting, light sensitivity, sound sensitivity

• Factors that may provoke an attack include:Factors that may provoke an attack include:– Menstruation, Sleep/food deprivationMenstruation, Sleep/food deprivation– Physical activity or certain foods (chocolate)Physical activity or certain foods (chocolate)– Contraceptive estrogensContraceptive estrogens

MigrainesMigraines

• History & PEHistory & PE– CRUCIAL to obtain HA history from CRUCIAL to obtain HA history from

patientpatient• Is this HA similar to others or is it “worst HA Is this HA similar to others or is it “worst HA

of life”of life”•Prior workupsPrior workups•MedicationsMedications•FoodsFoods•MensesMenses

– FULL PE including Neuro examFULL PE including Neuro exam

MigrainesMigraines

• ManagementManagement– Place patient in cool, quiet, dark Place patient in cool, quiet, dark

environmentenvironment– IV fluids if dehydratedIV fluids if dehydrated– Abortive therapy:Abortive therapy:

•Phenothiazines (antimigraine and antiemetic)Phenothiazines (antimigraine and antiemetic)

•DHE (vaso/venoconstrictor) + antiemeticDHE (vaso/venoconstrictor) + antiemetic

•Sumatriptan (5-HT agonist)Sumatriptan (5-HT agonist)

•Opiods as LAST RESORT!!Opiods as LAST RESORT!!

HeadachesHeadaches

• Cluster HeadachesCluster Headaches– Classically as boring headache on one Classically as boring headache on one

side of face behind the eye.side of face behind the eye.– May be associated with signs of facial May be associated with signs of facial

flushing, tearing, nasal stuffinessflushing, tearing, nasal stuffiness

TX: 100% O2 by N/C at 6-8 l/minTX: 100% O2 by N/C at 6-8 l/min- If no relief, Sumatriptan- If no relief, Sumatriptan

HeadachesHeadaches

• Subarachnoid hemorrhageSubarachnoid hemorrhage– Clinically: Abrupt onset of severe thunderclap Clinically: Abrupt onset of severe thunderclap

“worst HA of life”.“worst HA of life”.– Usually associated nausea and vomitingUsually associated nausea and vomiting– Nonfocal neurologic exam (usually)Nonfocal neurologic exam (usually)

• Etiology: usually due to leaking berry Etiology: usually due to leaking berry aneurysm.aneurysm.

• DX: CT +LP A MUSTDX: CT +LP A MUST– If CT (-), MUST perform LPIf CT (-), MUST perform LP– LP (+) if (+) xanthrochromia OR failure of CSF to LP (+) if (+) xanthrochromia OR failure of CSF to

clear RBC’s by tube #4clear RBC’s by tube #4

HeadachesHeadaches

• Subarachnoid HemorrhageSubarachnoid Hemorrhage– ManagementManagement– ABC’s as alwaysABC’s as always– IV, O2, MonitorIV, O2, Monitor– Head of bed @ 30 degressHead of bed @ 30 degress– Prophylax patient for seizures with Dilantin Prophylax patient for seizures with Dilantin

load.load.– Ca Channel blocker (nimodipine) 60 mg Q6 h Ca Channel blocker (nimodipine) 60 mg Q6 h

to prevent vasospasm, and rebleedingto prevent vasospasm, and rebleeding

HeadachesHeadaches

• Temporal ArteritisTemporal Arteritis– Etiology: a granulomatous inflammation Etiology: a granulomatous inflammation

of one or more of the branches of the of one or more of the branches of the external carotid arteryexternal carotid artery

– Clinically presents as:Clinically presents as:•Severe unilateral HA over Temporal areaSevere unilateral HA over Temporal area•Usually in middle aged females.Usually in middle aged females.•PE reveals: a tender, warm, frequently PE reveals: a tender, warm, frequently

pulseless temporal artery, with decreased pulseless temporal artery, with decreased visual acuity on the affected side.visual acuity on the affected side.

HeadachesHeadaches

• Temporal ArteritisTemporal Arteritis– DX: Clinically + ESR elevation, usually >50DX: Clinically + ESR elevation, usually >50– Confirm with biopsy of arteryConfirm with biopsy of artery– TX: HIGH dose steroids are VISION SAVING!TX: HIGH dose steroids are VISION SAVING!

•Start on prednisone IMMEDIATELY once Start on prednisone IMMEDIATELY once suspectedsuspected

– Prednisone 60 – 80 mg Q dayPrednisone 60 – 80 mg Q day

– Stat Neurology ConsultStat Neurology Consult

VertigoVertigo

• History and PE exam again History and PE exam again CRUCIAL!!CRUCIAL!!– History:History:

•Truly a vertiginous complaint?Truly a vertiginous complaint?– r/o syncope / near syncope??r/o syncope / near syncope??

•Acute onset of severe symptoms or more Acute onset of severe symptoms or more gradual coursegradual course

– PE:PE:•Full exam paying particular attention to:Full exam paying particular attention to:

– HEENT : Eyes, TM’sHEENT : Eyes, TM’s– Neuro : Cerebellar functionNeuro : Cerebellar function

VertigoVertigo

• Peripheral VertigoPeripheral Vertigo• History:History:

– Acute onset of severe dizziness, nausea, vomiting.Acute onset of severe dizziness, nausea, vomiting.– May be a positional worsening of symptomsMay be a positional worsening of symptoms– Recent history of URI or similar episodes in past which Recent history of URI or similar episodes in past which

resolved.resolved.• PE Pearls:PE Pearls:• Horizontal nystagmus which fatiguesHorizontal nystagmus which fatigues• Possible TM abnormalityPossible TM abnormality• Normal Neuro exam with normal cerebellar Normal Neuro exam with normal cerebellar

function and gait.function and gait.• Reproduction of symptoms with Hallpike Reproduction of symptoms with Hallpike

maneuvermaneuver

VertigoVertigo

• PeripheralPeripheral– Common Causes:Common Causes:– LabrynthitisLabrynthitis– Cerumen ImpactionCerumen Impaction– OMOM– OEOE– URIURI– Menieres Disease (tinnitus,hearing loss, vertigo)Menieres Disease (tinnitus,hearing loss, vertigo)

• TX: Symptomatic and treat underlying cause:TX: Symptomatic and treat underlying cause:– Antivert 25 mg Q6hAntivert 25 mg Q6h– Neurology / ENT follow upNeurology / ENT follow up

VertigoVertigo

• Central VertigoCentral Vertigo• Due to lesions of brainstem or cerebellumDue to lesions of brainstem or cerebellum• 10 – 15% of cases10 – 15% of cases

• Signs & SymptomsSigns & Symptoms::– Gradual onset of mild disequilibriumGradual onset of mild disequilibrium– Mild nausea and vomitingMild nausea and vomiting– Nonfatigable nystagmus (any direction)Nonfatigable nystagmus (any direction)– Associated neurological abnormalities:Associated neurological abnormalities:

• PtosisPtosis• Facial palsy, dysarthriaFacial palsy, dysarthria• Cerebellar findings, ataxiaCerebellar findings, ataxia

VertigoVertigo

• CentralCentral– Causes:Causes:

• Brainstem ischemia or infarctionBrainstem ischemia or infarction• Cerebellar hemorrhageCerebellar hemorrhage• Vertebrobasilar insufficiencyVertebrobasilar insufficiency• MSMS

– Diagnosis: Diagnosis: • Thorough Neurologic examThorough Neurologic exam• Head CT with Posterior fossa thin cutsHead CT with Posterior fossa thin cuts

– Management:Management:• Neuro consultNeuro consult• Admit and workup depending on etiologyAdmit and workup depending on etiology

Emergent Peripheral Emergent Peripheral NeuropathiesNeuropathies

• Acute Toxic NeuropathiesAcute Toxic Neuropathies– Diptheria (Cornybacterium diptheriae)Diptheria (Cornybacterium diptheriae)

• Acutely ill patient with fever, in a dPT deficient patient.Acutely ill patient with fever, in a dPT deficient patient.

• Membranous pharyngitis that bleedsMembranous pharyngitis that bleeds

• Powerful exotoxin produces widespread organ damage.Powerful exotoxin produces widespread organ damage.– Myocarditis/AV Block,Nephritis, Hepatitis.Myocarditis/AV Block,Nephritis, Hepatitis.– Neuritis with bulbar and peripheral paralysis.Neuritis with bulbar and peripheral paralysis.– (ptosis, strabismus, loss of DTR’s)(ptosis, strabismus, loss of DTR’s)

• TX: Parenteral PCN or ErythromycinTX: Parenteral PCN or Erythromycin– Horse Serum antitoxinHorse Serum antitoxin– Respiratory isolation and admission the rule.Respiratory isolation and admission the rule.


– Botulism (Clostridium botulinum toxin)Botulism (Clostridium botulinum toxin)• Earliest finding(90%)= Blurred vision, diplopia, Earliest finding(90%)= Blurred vision, diplopia,

ophthalmoplegia, ptosisophthalmoplegia, ptosis• Neurologic abnormalities descend and will lastly Neurologic abnormalities descend and will lastly

involve the respiratory musculature and cause involve the respiratory musculature and cause respiratory paralysis and death with 6 hours if not respiratory paralysis and death with 6 hours if not treated!treated!

• Mentation and sensation are normal.Mentation and sensation are normal.• Remember in infants with FTT (failure to thrive)Remember in infants with FTT (failure to thrive)

– Raw honey contains C. botulinumRaw honey contains C. botulinum• Tx: Aggressive airway stabilization!Tx: Aggressive airway stabilization!• Trivalent serum antitoxinTrivalent serum antitoxin• Lastly, there have been some recently reported cases Lastly, there have been some recently reported cases

of hypersensitivity to “Bo-tox”of hypersensitivity to “Bo-tox”– So ……..So ……..

LOOK OUT JOAN!!!LOOK OUT JOAN!!!


• TetanusTetanus– Symptoms 4 “T”’sSymptoms 4 “T”’s

• Trismus, Tetany, Twitching, TightnessTrismus, Tetany, Twitching, Tightness

• Risus sardonicus / opisthotonusRisus sardonicus / opisthotonus

• Signs of sympathetic overstimulation.Signs of sympathetic overstimulation.– Tachycardia, hyperpyrexia, diaphoresis.Tachycardia, hyperpyrexia, diaphoresis.

– Management:Management:• Human Tetanus Immunoglobulin (HTIG)Human Tetanus Immunoglobulin (HTIG)

• dT ToxoiddT Toxoid

• MetronidazoleMetronidazole

Emergent Peripheral Emergent Peripheral NeuropathiesNeuropathies• Guillain-Barre SyndromeGuillain-Barre Syndrome

– Most common acute polyneuropathy.Most common acute polyneuropathy.– 2/3’s of patients will have preceeding URI or 2/3’s of patients will have preceeding URI or

gastroenteritis 1-3 weeks prior to onset.gastroenteritis 1-3 weeks prior to onset.– Presents as: paresthesias followed by Presents as: paresthesias followed by

ascending paralysis starting in legs and moving ascending paralysis starting in legs and moving upwards.upwards.• Remember Miller-Fischer variant: has minimal Remember Miller-Fischer variant: has minimal

weakness and presents with ataxia, arreflexia, and weakness and presents with ataxia, arreflexia, and ophthalmoplegia.ophthalmoplegia.

– DX: LP will show cytochemical dissociation.DX: LP will show cytochemical dissociation.• Normal cells with HIGH protein.Normal cells with HIGH protein.

– TX: Self limiting, Early and aggressive airway TX: Self limiting, Early and aggressive airway stabilization.stabilization.


• Myasthenia GravisMyasthenia Gravis– Most common disorder of neuromuscular Most common disorder of neuromuscular

transmission.transmission.– An autoimmune disease that destroys An autoimmune disease that destroys

acetylcholine receptors (AchR) which leads to poor acetylcholine receptors (AchR) which leads to poor neurotransmission and weakness. neurotransmission and weakness.

– Proximal >> Distal muscle weaknessProximal >> Distal muscle weakness– Commonly will present as:Commonly will present as:

• Muscle weakness exacerbated by activity, and is relieved Muscle weakness exacerbated by activity, and is relieved by restby rest

– Clinically: ptosis, diplopia and blurred vision are Clinically: ptosis, diplopia and blurred vision are the most common complaints. Pupil is spared!the most common complaints. Pupil is spared!


• Myasthenia GravisMyasthenia Gravis– Myasthenic crisis = A true emergency!!Myasthenic crisis = A true emergency!!– Occurs in undiagnosed or untreated Occurs in undiagnosed or untreated

patientspatients•Due to relative Ach (acetylcholine) deficiencyDue to relative Ach (acetylcholine) deficiency•Patients present with profound weakness and Patients present with profound weakness and

impending respiratory failureimpending respiratory failure– TX: Stabilize and manage airwayTX: Stabilize and manage airway

•Consider edrophonium 1 -2 mg IVConsider edrophonium 1 -2 mg IV (AchE inhibitor)(AchE inhibitor)

New Emerging TreatmentsNew Emerging Treatments

• Stroke/ TIA’sStroke/ TIA’s– Hypothermia units with cooling devices and Hypothermia units with cooling devices and

blanketsblankets– Lasers, cerebral angioplasty and clot retrievalLasers, cerebral angioplasty and clot retrieval– See articles:See articles:– ““Established Treatments of Acute Ischemic Stroke”, Lancet Established Treatments of Acute Ischemic Stroke”, Lancet

20072007

– “ “Beyond TPA: Mechanical intervention in Acute Stroke”, Annals Beyond TPA: Mechanical intervention in Acute Stroke”, Annals of EM June 2003of EM June 2003

– ““Acute Ischemic Stroke : Emergent Evaluation and Acute Ischemic Stroke : Emergent Evaluation and Management”, Emerg. Clinics of North Am. August 2002Management”, Emerg. Clinics of North Am. August 2002

– ““TIA Management” NEJM November 2002TIA Management” NEJM November 2002

References:References:

CNS Emergencies Lecture CNS Emergencies Lecture

adapted from adapted from

Dr. Patrick O’ShaughnessyDr. Patrick O’Shaughnessy

EM AttendingEM Attending

Beth Israel Medical CenterBeth Israel Medical Center

THE ENDTHE END

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