Emergency Medicine

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Dr. Donald Sefcik

Donald J. Sefcik is the Associate Dean at the Chicago College ofOsteopathic Medicine (CCOM), Midwestern University (N[WU), inDowners Grove, IL. He is a tenured professor and board certified in bothEmergency Medicine and Family Medicine. From June 1997 through May2000, Dr. Sefcik served as Medical Director for the Physician AssistantProgram, Coliege of Health Sciences (CHS), at MWU. Dr. Sefcik's lecturesare based upon his experiences as a clinician and preceptor, tenure as amedical school faculty member, and his student assessrnent research.

Dr. Sefcik has practiced with physician assistants since 1988 and beeninvolved in the clinical training of physician assistants since 1990. Prior tojoining Midwestem University's faculty, Dr. Sefcik was a faculty member inthe Pharmacology Department at Butler University and in the NursingDepartment at Marian College, both in Indianapolis, Indiana. Dr. Sefcik hasa Bachelor of Science in Pharmacy (1981), a Master of Science inPharmacology (1994), both from Butler University, ffid an MBA (May2004) from Purdue University.

CME ResourcesCertification & Recertification Exam Review

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Cerffication & RecertiJication Exam ReviewCME Resources

2004

Emergency Medicine TopicsDonald J. Sefoik, D.O., FACOEP

Learning Objectives

Upon completion of flris portion of the review course, the participant should be able to:

1. Discuss the basic principles of toxicolory.2. Describe colnmon toxidromes and their management.3. Differentiate the three common causes of primary headaches.4. Discuss cofirmon secondary headaches.5. Describe the evaluation/management of common ophthahnologic fraumatic injuries.6. Discuss hyperkalemia - its presentation and management.7. Discuss cerebrovascular accidents and traumatic brain injuries.8. List and describe corrmon abnormal findings in urine specimens.9. List and describe common physical examination "signs" and findings.

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Overdose Sfafes

ldentifu the Druq

A, History

Who was there ?

What did they find out ?

Are there any bottles ?

Abiliiy to 'quantity'the ingestion ?Pafient's medical history ?' Time since ingestion ?

B. Physical Data

S - SalivaiionL. LacrimaiionU - UrinationD - DefecationG - Gl DistressE - Emesis

Flo'ir:; , sG'rr'r'u-u

opiates (- ftr'\.rxo^e-\IVliosis - Iin;.t\ p.ry',r(BradycardiaHypotensionHypoveniilationReduced LOC

?d^pt(

Heart Rate 1Respiratory Rate-----r ,Z-.1 gz Signs-Biood Pressure / Toxidrome \Temperature -1 \- / (-symptoms.

* Level of consciousness, Pupil size, Breath..,.etc.

Toxidromes

Signs

..Nff)-. VI- Chssic Toxidromes

LhS''- q)9..d\.WL Cholinergic Aqents

Nomoqrams

Acute, One-time lnqestions

y *Acetarninophen - Rumack-Matthew

,-+ AnTih"sIr rer,AGS\

nnticno[nerqic AHyperemia (Red as a Beet)Dry Skin (Dry as a Bone)Dilated Pupils (Blind as a Bat)Delirium (Mad as a Hatter)Tachycardia

+

L

I

Y1I* Aspirin - Done ( b e".,e \

ncr\v:.ig-^ )

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(G eneralizations - Common F eatures)

CIIARACTERISTICS

Age of Onset

Frequenelt

Duratiott

Description

Site

Time of Onsa

Associated Featura

Anu&x"cr--ff\C^u\C4 tt'O''ASl

Aggravatkg Factors(Precipitdingfaaors)

Clinical Appestance

Tredtments

MIGRAINE

Childhood-< 3OyoF>M

l-4 /.month

+-tzLrs

"Throbbiag"

Unilateral (65%)

Variable (often AIv!

AA{A/ (75o/o)

Phono/photophobia70% Fam.IIxC/assic - auraCommon - no aura

Multiple

Withdrawal fromactivify

Prescription RxAbortiveProphylactic

TENSION

Eariy Adulthood

Variable

30 min - weelcs

"Vise-like'l

Biiateral

Later in day

AnorexiaMuscle tendemess

Stess/Fatigue

Mild disability

MildAaalgesics

CLUSTER LIt".u" Lln s)20-40 yo \M>>F (,f .. t 1Cyclic,(Muitipie/day)

10-120 mi:r

t'Boring"

Peri-orbital

Uniiateral

Bed time

IpsilateralAI,IS Dvsfxn

LacrimationRhinorrhea

Ptosis/miosis

Aicohol

PaceAgitated

02Many Rxs

* hsgrp"d','.\ h nls*-:t<;;Ae rale,

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S elect S econdarv Ileadaches

SUBARACHNOI D HEMORRHAGE

Sudden Onset & SeverityUsually innamanial areurysm (beny) rupture

50%(+; with Altered LOCAverage age = 50yq,..: .

"Sentinel" Headache Hx in 30%75% Neck Stifiness - ,f s,315% New-onset Seizures

V.f e e-,),,n5

CT Scan Misses 10-20% (False Negative)If CT Scan is negative and suspicion is high, DO A LUMBAR PLINCTTIRE

a, Hemo6hagrt fup (False Positive) a i;t-) a;t $Rr-'! ,\ isl'\i.tr '' ltuf ii$e-b. Cerebral Aagiography is the "GOLD" standard for diagnosis/aneurysm location

RE FENNAL TO NE UROS URGE ON

L BRAIN TUMOR HEADACHES

Dull, deep aching, nondescript, progressiveOften worse on awakeningUsually worsened by valsalva maneuver or exerlionMay have nausea/vomiting or focal furdingsVomiting that precedes headache- think posterior fossa fimorcrscans$S+t,

3 MEI-.llNGtTlS HEADACHE

Usualiy involves entire headOften associated with feverivomitingOften associated with Nuchal signs

Kcrnig's SignBrudzinski's sign

Diagnosis requires high index of suspicion and a lumbar pulcture

q HYPERTENSIVE HEADACHE

Usually a throbbing, occipital headacheMost often a morning headache \4.Usually does not occur until the diqslolic biood pressure ir o:gi-]{mmHg'Often overdia€nosed cause of headachesTreafinent- Antihypertensives

Disease of patients over 50yo/ESR> 50Women with 4:1 predorninanceUnilaterai, jabbing pain/worse at night \iArtery tender/pulseless- Biopsy=DiagnosisHigh dose rry to prevent biindness

L TEMPORAL ARTERITIS + Pa1*-*^g.r,. Rh"o*.";!z^ Lfncrc\Infiln'ation of Temporal Artery with lymphocytes, plasma cells and multinucleate giant cells

t

LUI<a { c:hcui'}

\e154\?,0 pt7 sui''i'h i*Y '*?t'* 'r',

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Ophthalmologic Trauma

ORBIT & LID

L Contusion ("Black Eye")a, RIO Other Injury

2, Orb it al Wall' Fr hittn' e' 1;' bi o,w o ut Fr ac fiir e " )a. Flydraulic forces tbroughout the globe; rupture of medial wall and floor,

fapping faVmuscle and occasionally injuring nerve

b, Findings:

$ - Diplopia on upward gaze- Enophthalmos' Infraorbital anesthesia- Subcutaneous emphysema

)r ;'glsuding" of Maxillary Sinus

c. Treatrnent- Consult

CORNEA A CONJUNCTWA

-1.. Chemical Init;a:iest Do NOT Delay Treannent !!!

a. Alkali Bums- Liquefaction Nemosis- Irrigate (sometimes 24 hrs+)

Check pH with litnus paper-Refer/ConsultNOW !

b. Acid Burns- Coagulation Necrosis- hrigate & Consult

I'3. Radiation Butns (Iieratitis)($T Vrr,* beqn sK'rq\ 1 s*'b'<th'n1 *A

a.IJV radiation causes comeal epithelial sweliing; pain & blunedvision, hours afterthe exposure

,s ut4-b. Findings Jce r,vr k

Multiple Punctate a^reas on fluorescein staining \}) RiSn r

b, Trearnent ()- p*,{Jt {*TfD,.Ly. bdY

- Mydriatic agent \:2/ g(i\6b Lorrta

- Systemic Analgesic- Follow-up

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4. Corneal Abrasions

a. Complaint of foreign body "feeling"

b. Findings

- Foreign Body (+l)s Check Lid in eversion

- "Ice Rink Sign" with fluorescein

c. Treatnent

- Cycloplegic Agent- Antibiotic topically- Follow-up in 24-48 hrs

5 . Sub conj mctiv al Hemorchagea. Bright Red blood overlying scierab. Be sure no bleeding diathesis existsc. Blood Stops at limbusd. Should NOT affect visione. No specific therapy

ANTERTOR CHAMBER & LENS

l. Traumatic Hyphemaa. Blood in anterior charrber due to ciliary body or iris vessel disruptionb. Best seen with patient sitting upright with slit lampc. Must R/O other iqiuriesd. Findings

- MaY be ary':nPtomatic- PainlPhotophobia.tslured Vision- May cause N & V

e. Consult OphthaLnologist- Place a FOX Eye shield- Keep patient quiet @ 30-45 degree angle- Risk of secondary glaucoma

2. Lens Dislocationa. Marked VA Decreaseb. May be seen in Marfan's Syndromec. Consult your OphthaLnologist

3 . Tr^aumatic Mydriasisa.lmpairrrent of PSNS functionb. Referffsualiy temporary

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F{I?ERLATEMLA q R /o L.,\rrnue\\u;\er .

1. Definition - An elevated plasma potassium level (usually > 5.0 mEq/I-)

2. Pathophysiology

Hod\4/hy does it happen ?

Etiology -

L lncreased Potassium Load

Hemolysis (of sp ecimen) ; Leuko cytosis ; Thromb o cyto sis ; Phiebotomy

a, Exogenous - Excess intake; Dietary; Suppiemental, .,t\,8

b, Endogenous -Xedun'ibution )ll .r \r'so"o*htq\rb'^Y. 1, . C'-t

Kt t 'T ufAcidosis: Hemolysis; lnsulin deirciency; Exercise

C .KAJ 6r G], \2. Decreased Excrerion - T Kr Lh.,ire kt" \

Renal Failure; Rx Effect: NSAIDs; ACE inhibitors; K-Sparing Diuretics

3. Factitious -

Sims/Symptoms

Cardiac - Peaked T-wavesFiat P-wavesWidened QRS

Y"

V entricuiar fi brillation

Neuromusc- Paresthesias. Weakness

Fiaccidity

3. Differential Diagnosis -

^jU-*.-.-llh-t

^ni\** /JWII.

HypocalcemiaNeuromuscular disorderEKG abnormalities from other cause

4. Treatment Plan -

a, Rx - Sodi'hpolystlrene s{Y:}G\GXALATE) orally or rectaiiy

More sevet'e cases (Cardiac arrhythnzias, etc) may require:Dextrose & Insulin fV - temporizing measure/shifts potassium intracellularS o dium B i carb onate - temp orizin g measure/shifts potas sium intraceilularCalcium Giuconate - cardioprotective/potassium antagonist*\u_le"ut "{X s.

c, Other - Hemodialysis

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Cerebrovascular Accidents (CVAs)

FACTS & FIGURES

A. lncidence @ 730,000 per year

B. Risk Factors

Uncontrollable

a. Advancing {ge- 2/3 occur in patients > 65 yo feach decade after 55 yo doubles the risk......]

b. Gender:Verr t Women

c. Family History: CVA or TIA

d. Diabetes mellitus: - 2 - 3 times the risk

Controllable

a. Hypertension: - 4- 6 tirnes the riskA contributing factor in up to 70 olo of all CVAs

b, Atrial Fibrillaiion: - up to 6 iimes the riskA contribuiing factor in up to 15 % of all CVAs

,c, Transient lschemic Attack (TlA)Risk of a CVA is - 35 % wiihin 5 years

d. Cigarette smoking: -2-3 times the risk

e. Prior CVAMales: 42 o/o risk of a second CVA within 5 yearsFemales: 24 % risk of a second CVA within S years

f, Others: Myocardial lnfarction, Hypercholesterolemia, Sleep apnea

STROKE SYNDROMES - Nofes

A. Transient lschemic Attack (TlA) + rF- transient neurologic deficii, ihat by definition, lasts less than 24 hours 't- - 90 % last less than 60 minutes (many < 15 minutes)- Amaurosis fugax - transient, partial or complete monocular blindness- Rule of 1/3sr' 1/3 will have a CVA in the future \f l4l ,,r.,.1*",.trJ ../ 1/3 will have a second TIA

\r,/ 1/3 will have no sequelae

B, Lacunar lnfarct (Deep Subcortical/"Whiie Matter" Area Changes; rD^ lz.i fr. ir,l{ -LC

- Contralateral PURE Motor Deficit (lnternal capsule) lj'T N) pt- Contralateral PURE Sensory Deficii (Thalamus)

- Clumsy Hand - Dysarthria (Pons or lnternal capsule)

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Intracranial l{emorrhagic Events Cerebral Ischemic Evenl.sIrrlr'acranial Hemorrhage Snbarachnoitl llemorrhage l'hrombotic CYAs Ernbolic CVAs

Onset/Progressiou Ol-ten actiye at onsetRapid progression

May be active/nonactiveVariable course

? 50% comatose atpresentation)

Nonacl.ive at onset- 60 % during sleepGradual progl'ession

Active at onsetRapicl onset

Etiology Aneurysm (berry)

Itisk(s) IlypertensionBleeding Diathesis

Associated with polycystickidney disease aud aorticcoarctation

fuleriosclerosis[IypeftensiorrDiabetes Mellitus

I-Ieart (Valvular) Disease

furatomic Locatiott Middle cerebralartery(comnon)

History Severe Cephalgia Severe CephalgiaStiff neckMay be lristory of alteredlevel ofconsciousness

tlsually no CephalgiaOften history of TtAs

Usually no Cephalgia

Physical Exanr Focal Neurological Signs Nonfocal examNuchal rigidity

Focal Neurological Signshrteural Carotid Bruit(s)

Focal Neurological Signs

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Arteny'Site of Involvernent Character-istic Feature(s) of CYA

lnternal Carotid Artery Ipsilateml Monocular Blindness (Anaurosis Fugax)Contmlateral HerniparesisContralateral l{emianesthesia/Hemianalgesia

Auterior Cerebral Artery Contralateral Lower Extremity paresis; aneslhesia,./analgesiaMinirnal Contralateral Upper ExtremityNo Face Clnnges

Middle Cerebral Artery Contralateral Upper Extrcmities paresis; anesthesia/analgesiaContralateral Lower Face droop (Tongue cleviates to sicle opposite of lesion; no fasiculal.ions)Minimal/No Lower Extrernify ChangesAphasia (if dorninant hemisphere is involved)

Posterior Cerebral Artery Contralateral l{omonymous Hemianopsia (rvith macu|ar sparing)Ipsilateral Cranial Nerve III PalsyMemory deficits (if hippocarnpus is involved)

Vertebrobasilar Artely Diplopia (PPRF or CN ltr, fV, VDWatch for CN dysftrnctionAtaxia / Vertigo (cerebellar signs)Bilateral Motor/Sensory Changes

Lacunar CVA Purc Motor (basilar pons or internal capsule) conlralateral to lesionPure Sensory (thalalnus) contralateral to lesionClurnsy I-Iand-Dysaltlu ia

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Traumatic Brain Iniuries

FACTS & F/GURES

A. lncidence

a. - 2 million Americans with Head Trauma annuallyb, - 500,000 are admitted to the hospitalc, - 100,000 deaths per year (- 60 % occur before arrivalto the ED)d, Aicohol consumpiion is involved in - 25 - 50 % of cases

B. Classificaiions (arrival to ED)

a. Mild Head lniury

.ay GCS=14-15

n ^. erra$1^*J

- 80 % of rniuries

.. h{'-1 -( ' d9.n v-.<v"' b, Moderate Head lniurv

d'n*>Z ecs=9-13oof' -1o%oflnjuries\ -ze%die

c. Severe head lniury

GCS=Eorless- 10 % of lnjuries-40%die

C. Tvpes of Brain lniurv

Primary Injury

,R

RCE(-1

NeuralTissue lniuru

ContusionLacerationDifiuse Axonal lnjury

Secondary lnjuryHypotensionHypoxemiaHypovolemialncreased lntracranial Pressure

Cerebral V ascul ar I niury

lntraparenchymal HemorrhageEpidural HematomaSubdural HematomaSubarachnoid Hemorrhage

00 ms)

\.|FO

^/

GLASGOW COIvIA SCALE

EYE Ooeninq4 Spontaneous3 To soeech2 To Pain1 No response

VERBAL Response5 Alert & Oriented4 Disoriented3 Nonsensical soeakino2 Moans/Unintelliqible sounds1 No response

MOTOR Response6 Follows commands

Localizes pain

4 Withdrawals from oain5 Decorticate posturinqI Decerebrate posturinq1 No response

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SPECIFIC DIAGNOSTIC ENTITIES

cLosED " rec #hcrL,'.a'h

-l

{-Eng-aryAl Lesions i

- Epidurai Hematota * SKr\ Rnr\.nc, I me''"5 r'rdrrrS

,/ - 1 % of all traumatic brain injuries (- 12 % die)./ - 80 - 90 % associated wiih a skull fracture (often tears a meningeal artery)\/ Only - 20 % have classic: lnjury - LOC - Lucid lnterval - Deterioration

Up to 60 % have no loss of consciousness'/ Underlying brain injury is generally not severe./ 60 % occur in patients < 20 yor' < 10 % occur in patients > 50 yo

Subdural Hematorna'/ - 35 % of severe traumatic brain injuries

'v\.{a. rrtsvln'r' a' '/ Most occur in patients > 60 yo-i*).,n *W"Y \ * Atrophic brains (elderly and alcoholics) are at greatest risk

qJ- \

. . ^. yd vn,,X i Hffiliil3.tffii$;,ti:1?H,ltiJlla...r.,"tion mechanisms

t i,",*.r '/ Underlying brain injury is generally more severe'v '- J * Simple (no associated parenchymal injury - - 20 % die)* Complicated (associated brain injury - - 50 % die)

- Subarachnoid Bleed (Hemorrhage)

b. lntra-axial Lesions

- Cerebral Coniusions & Lacerations* Concussions

- Diffuse Axonal lnjuries (Axonal Shearing)

lncreased lntracranial Pressure

- Herniation Syndromes

Cn^ it:ru'cr{t,t\

ill6$ff:l''}jr" l'F[6sc- - Ariem.,t

4t(:f1s(,^f/

cYc [c'-

t . Cushing Response (hyperiension; bradycardia; irregular respirations)

OPENa. Penetrating lnjuries

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/-'"'''tqtut ' t

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lmmobilize cervical spine(GCS < 6 = 14 % have C1 or C2 fracture)

E lev ated Inttucranial PressureHyperventiiationMannitolPentobarbiotai

Causes

A. CausesMotor Vehicle Accidents (MVA) - 45 o/o (cause - 60 % of deaths)Falls - 15 % (cause - 12 0/o of deaths)Assaulis - 14 o/o (Firearms - 14 o/o of deaths - approximately 75 o/o occur at the scene)OccupationalAccidents - 10 %RecreationalAccidents - 10 %

B. Preventiona. Safety (Seat) Belts and Air Bagsb. Helmetsc. Firearm Legislation

f ro.'lrrt )LFr"rl'+ttINITIAL EVALUATION & TREATMENT

A, Salvage brain tissue not already irreversibly injured

B. ldeniifyicorrect eniiiies that may cause secondary injury

Operative Lesion

Epidural HematomaSubdural hematomalntracranial Hemorrhage with shiftDepressed Skull Fracture

GCS>9

lVsMonitorsFrequent Serial Examinations (NEURO)Secondary SurveyMonitor for ETTiHyperventilaiion need

Non-Operative Lesion

Non-Depressed Skull FractureContusionSubarachnoid Hemorrhage

GCS<9

lntubate (ETT)HyperventilatelVsMonitorsResuscitateSedation/ParalysisSecondary Survey(Life Threats....,)

4--""'

NeurosureeonCT

,/,/

/Scan

----a

lnjury

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Considerations at Presentation:

a. Low-risk lniuries

- Not likely to deteriorate- Normal neurologic examination

* Asymptomatic; Subjective complaints: Headache, Dizzy... .,.

- Minor injury:* Scalp wound - Hematoma, Abrasion, Laceration....

*"* Approximately 0,3 - 3 % will deteriorate

b. Moderate -risk lniuries

- Difficult group to ass.ign a prognosis- Neurologic Signs & Symptoms of unclear significance

" Brief LOC; Vomiting; Post-traumatic amnesia.....* Progressive headache; Child age < 2 yo..

- lnjury (?):

" Arduous Assessment to make (Work-up ???)

*** Approximately 40 % will have an abnormal CT scan** Approximately I % will need a neurosurgical procedure*n Approximately 10 % will deteriorate

c. Hiqh-risk lniuries

- Criteria-defined neurosurgical emergencies- Neurolog ic Assessment dem onstrates si gnificant findings

* Depressed LOC (not explained by drugs, EIOH...)* Focal Neurologic signs" Decreasing LOC* Skull Penetration or Depressed Fracture

- lnjury: Suspect Primdry or Secondary Brain lnjury

*** Approximately 25 % will need a neurosurgical procedure

References

Manual of Neurology; McGraw-Hill 2002 (0-07-137351-9)

Handbook of Neurosurgery; Thieme New York; 2001 (0-865Z7-909-0)

Emergency Medicine ReporlsDecember 3, 2001: Head Trauma: Emergency Management and lmagingDecember 17,20Q1: Head Trauma: Severe, Moderate and Minor Head TraumaMay 11, 1998: Traumatic Brain lnjury: State-of-the-Art Proiocols

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