LAST MINUTE EMERGENCY MEDICINE - PART 4 ppt

180 CHAPTER 7 / HEAD, EAR, EYE, NOSE AND THROAT DISORDERST A B L E 7 - 1 INNER EAR DISEASES notably the cochleaMost commonly from viralinfection most common viralinfection is mumps Posit

VENOMOUS BITES AND STINGS 173

T A B L E 6 - 1 4 VENOMOUS BITES AND STINGS—NORTH AMERICA PIT VIPERS

CLASSIFICATION AND VENOM DELIVERY AND CLINICAL

rFacial pits (between

nostril and eye)

Infrared sensing

rTerminal bud or rattles

(rattlesnakes only)

rRetractable, anterior,paired fangs

rMixture of enzymes,peptides, polypeptides,proteins

rCauses local necrosis,vascular endothelialcell lysis with increasedpermeability

coagulopathy andneuromusculardysfunction

rVenom characteristicsvary between genusand species

rApproximately 25% ofbites are

nonenvenomations(dry bites)Local:

rOne or more puncturewounds, nonclotting

rPersistent burning,sharp pain

rEdema progressingbeyond puncture site

rLocal paraesthesias

rMay see ecchymosisand blister formationSystemic:

rAnxiety

rNausea and vomiting

rPerioral and extremityparesthesias

rWeakness

rAlteration in taste(metallic)

rSpontaneous bleeding(i.e., hematuria, GIbleed)

rCoagulopathy(decreased platelets,fibrinogen) (Increased

rABCs and IV x 2

rLocal wound care and tetanusprophylaxis

rLaboratory evaluation—CBC,platelets, coagulation studiesincluding fibrinogen and fibrindegradation products,electrolytes, BUN, creatinine,type and screen

rInitial dose 4–6 vials IV over 1 h

rRepeat dose of 6 vials if initialcontrol not obtained

rIf initial control is obtained(progression of edemastopped, systemic toxicity andcoagulopathy reversed) thantreat with additional 2 vials IV at

6, 12, 18 h post initial control

rContraindicated in patients withallergy to papain or otherpapaya extracts

174 CHAPTER 6 / ENVIRONMENTAL EMERGENCIES

T A B L E 6 - 1 5 VENOMOUS BITES AND STINGS—CORAL SNAKE

CLASSIFICATION AND VENOM DELIVERY AND CLINICAL

Classification:

rElapid

Common names:

rEastern coral snake

rTexas coral snake

rSonoran coral snake

Identification:

rVertically arranged

yellow, black, and

red colored banding

rRed on black,

venom lack; red on

yellow, kill a fellow

rShort fixed fangs

rBites then chews invenom

rVenom is significantneurotoxin withminimal localmanifestations ortoxicity

Local:

rSmall puncture wounds

rMinimal pain at bite siteSystemic: (can have adelayed onset)

Prehospital:

rElastic pressure wrap tobitten extremityHospital:

rABGs

rMonitor PFTs (tidal volumeand vital capacity)Antivenom:

rImmediate treatment of allknown bites (exceptSonoran coral snake) withMicrurus fulvius antivenom

5 vials IV

rRepeat dose forcontinuous progression ofsymptoms

rAntivenom iscontraindicated in patientwith an allergy to horseserum

rAsymptomatic suspectedbites can be observed for

12 h and discharged

VENOMOUS BITES AND STINGS 175

T A B L E 6 - 1 6 MARINE ENVENOMATIONS—INVERTEBRATES

CLASSIFICATION AND VENOM DELIVERY AND CLINICAL

rIndo-Pacific BoxJellyfish has world’smost potent marinevenom

rWeakness

rMuscle spasms

rParesthesiasIrukandji syndrome:

rCarukia Barnesi-BoxJellyfish

rLocalized pain anderythema followed bysevere generalized bodypain

rRemove tentacles withtweezers

rRemove remainingnematocysts by applyingshaving cream or talc thenshaving with razor

rIntense burning pain

rErythema and localedema

rBleeding from puncturesites

rSystemic effectsuncommon

rImmersion in hot water(45◦C) for 30–90 min

rIrrigate wounds withdebridement ofembedded spines

Mollusks:

rBlue ringed

Octopus

rTetrodotoxins deliveredvia bite

rSmall puncture wounds

rSupportive care

rEarly intubation andmechanical ventilation

rAntivenom notcommercially available

176 CHAPTER 6 / ENVIRONMENTAL EMERGENCIES

T A B L E 6 - 1 7 MARINE ENVENOMATIONS—VERTEBRATES

CLASSIFICATION AND VENOM DELIVERY AND CLINICAL

rStingrays rVenom delivery via tail

with distal barbed spine

rPuncture wound or laceration

rImmediate severe pain

rErythema and cyanosis ofwound

rSystemic effects uncommon

rImmersion in hot (45◦C)water for 30–90 min

rOral or pararenal opioidfor analgesia

rIrrigation and exploration

of wound for retainedsheath or spines

rProphylactic antibioticsfor contaminatedwounds

rScorpion, Lion, or

Stonefish

rDorsal and pelvicspines with venomglands

rCyanotic puncture wound

rImmediate intense pain

rErythema and edema

rSystemic effects rare

rSame as above

FURTHER READING

Becker GD, Parell GJ Barotrauma of the Ears and Sinuses after Scuba Diving Euro Arch Otorhinolaryngol 2001;258:159.

Clark RF, Werthern-Kestner S, Vance MV, Gerkin R Clinical Presentation and Treatment of Black Widow Spider

Envenomation: A Review of 163 Cases Ann Emerg Med 1992;21:782.

Dart RC, McNally J Efficacy, Safety, and Use of Snake Antivenoms in the United States Ann Emerg Med 2001;37:181 Freeman T Hypersensitivity to Hymenoptera Stings N Eng J Med 2004;351:1978–1984.

Gold BS, Barish RA, Dart RC North American Snake Envenomation: Diagnosis, Treatment, and Management Emerg

Med Clinics N Amer 2004;22:423–443.

Hazinski MF, Chameides L, Elling B, Hemphill R (eds) Electric Shock and Lightning Strikes Circulation

2005;112:154–155

Kitchens CS, Van Mierop LHS Envenonmation by the Eastern Coral Snake (Micrurus Fulvius): A Study of 39 Victims.

JAMA 1987;258:1615.

Neuman TS Arterial Gas Embolism and Decompression Sickness News Physiol Sci 2001;17:77.

Wasserman G, Anderson P Loxoscelism and Necrotic Arachnidism J Toxicol Clin Toxicol 1983–1984;21:451–472 Whitcomb D, Martinez JA, Daberkow D Lightning Injuries South Med J 2002;95:1331.

CHAPTER 7

HEAD, EAR, EYE, NOSE

AND THROAT DISORDERS

EAR

External Ear

F O R E I G N B O D Y

Etiology: Foreign bodies (FBs) in the external ear canal are most commonly found in patients less than

8 years old or the mentally disabled These FBs include beans, pebbles, toys, candies, or insects For adults,the FBs are usually cotton-tipped swabs or earplugs

Clinical Presentation: Patients usually complain of a FB A retained FB should also be considered inpediatric patients with a persistent purulent, foul-smelling ear discharge

Diagnosis: The diagnosis is made by direct visualization of the FB

Treatment: Direct removal of the FB can be accomplished by an alligator forcep, suction catheter for rigid

objects, right-angle blunt hook, or ear curette Indirect removal can be accomplished by gentle irrigation of

the canal with room temperature saline For live insects, first instill 2–4% viscous lidocaine or mineral oilbefore irrigation to kill the insect For impacted cerumen, over-the-counter solutions, such as carbamideperoxide (Debrox) or colace, soften the cerumen prior to irrigation Unsuccessful FB removal is common,because of patient discomfort or FB depth These patients should be referred for ENT follow-up within12–24 hours for removal, likely under general anesthesia or procedural sedation in the operating room.Prescribe topical antibiotics, such as a mixture of neomycin, polymyxin, and hydrocortisone (corticosporinotic) or a fluoroquinolone such as ciprofloxacin or ofloxacin for external canal damage In the setting of aperforated tympanic membrane (TM), topical ofloxacin is recommended and is safe for infants and children

If administering corticosporin, use a suspension formulation because of its higher viscosity; this reduces theincidence of middle and inner ear toxicity

Complications: Iatrogenic complications include external ear canal abrasions and lacerations, a perforated

TM, or a retained FB that was missed on examination In the setting of a retained FB, other complicationsinclude external otitis, perforated TM, and cervical adenitis

Comments: Meticulously examine the contralateral ear and both nostrils for additional FBs Reexaminethe TM after removal of the FB to check for perforation Immediate ENT consultation is necessary forretained button batteries, because of the risk of caustic battery leakage

177

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178 CHAPTER 7 / HEAD, EAR, EYE, NOSE AND THROAT DISORDERS

P E R I C H O N D R I T I S

Definition: Perichondritis is an infection of the tissue surrounding the ear cartilage

Etiology: Perichondritis is usually caused by trauma and is most commonly associated with ear piercing

The most common bacterial pathogen is Pseudomonas aeruginosa.

Clinical Presentation: Perichondritis presents with nodular inflammation and erythema of the ear pinna

Diagnosis: The diagnosis is made by physical examination

Treatment: Administer oral or parenteral antipseudomonal antibiotics

Complications: Chondritis and ear deformity may result from perichondritis

O T I T I S E X T E R N A ( O E )

Definition: OE is an inflammation or infection of the external auditory canal and auricle OE mostcommonly occurs during the summer months and is most commonly seen in the tropics

Etiology: The two most common bacterial pathogens are P aeruginosa and Staphylococcus aureus.

Clinical Presentation: OE presents with otalgia, pain with auricular movement, and edema of theexternal auditory canal

Diagnosis: The diagnosis is made by physical examination

Treatment: The treatment for OE includes ear cleansing and topical antibiotics Apply a wick if there issignificant external canal edema

Fungal otitis externa—Fungal OE, usually from Aspergillus, accounts for 10% of all OE cases Risk factors

include diabetes mellitus, HIV, and previous antibiotic treatment The external auditory canal appearsblack or blue-green in discoloration

Necrotizing (malignant) otitis externa—This aggressive form of OE primarily affects adults with diabetes

mellitus and is most commonly caused by P aeruginosa Patients complain of severe ear pain, otorrhea,

headache, and periauricular swelling The pathogen erodes the ear canal floor into the temporal bone skullbase, causing an osteomyelitis Complications include a cranial nerve palsy (most commonly the facialnerve), sigmoid sinus thrombosis, and meningitis Treatment requires at least antipseudomonal coveragewith parenteral penicillin plus aminoglycoside, or the single-agent ciprofloxacin Be sure to check theblood glucose level in patients with severe OE

Middle Ear

O T I T I S M E D I A ( O M )

Background: Acute OM is an inflammation of the middle ear cavity, which most commonly occurs inpatients 6 months to 3 years old An upper respiratory infection usually precedes this disease Those at higherrisk for OM include children attending daycare, those being bottle fed, those in families where cigarette issmoked, and those in families where there is a history of OM

Treatment: Amoxicillin is the first-line antibiotic treatment for OM (90 mg/kg/day for children) Alternativeagents include cefdinir, cefuroxime, cefpodoxime, ceftriaxone, an advanced macrolide (azithromycin orclarithromycin), and amoxicillin-clavulanate A follow-up visit should be arranged to detect treatment failure.

Complications

Complications include the following:

Recurrent OM—Acute OM in an infant’s first year of life places him or her at increased risk for recurrent

OM in the future

TM perforation—When the middle ear cavity builds with positive pressure from fluid accumulation in OM,the TM may perforate These perforations usually spontaneously heal

Labryinthitis—Hearing loss Although 90% of middle ear effusions from OM spontaneously resolve in

3 months in OM, persistent middle ear effusions can lead to deafness and speech delay in children

Mastoiditis—Intracranial infection and thrombosis, such as meningitis and lateral sinus thrombosis, are rare

M A S T O I D I T I S

Definition: This disease is a serious complication of acute otitis media when the infection spreads to theadjacent mastoid air cells via the aditus ad antrum

Etiology: The most common organism is S pneumoniae.

Clinical Presentation: Patients may present with fever and headache in addition to pain, swelling, anderythema in the posterior auricular region

Diagnosis: The diagnosis can usually be established by physical examination, but computerized phy (CT) may be useful for delineating the extent of mastoid bony involvement

tomogra-Treatment: Because of the risk of local periosteal infection and meningitis, patients should be admitted andtreated with a parenteral third generation cephalosporin Concurrent surgical drainage is often necessary

180 CHAPTER 7 / HEAD, EAR, EYE, NOSE AND THROAT DISORDERS

T A B L E 7 - 1 INNER EAR DISEASES

notably the cochleaMost commonly from viralinfection (most common viralinfection is mumps)

Positional or nonpositionalvertigo, peaking in severity in2–4 h and lasting 3–10 daysHearing loss

Diagnosis: The diagnosis is made by physical examination

Treatment: A well-tolerated FB-removal technique maneuver involves having the caregiver attemptpositive-pressure dislodgement of the nasal FB The caregiver “kisses,” or blows air into the patient’s mouth,while occluding the unaffected nostril Alternatively, an insufflation bag can be used Other techniquesinvolve direct manipulation with alligator forceps, a small suction catheter, or a blunt right-angle probe

Complications: Iatrogenic complications include aspiration, which may occur if the FB is pushed deeper,and epistaxis, which may be induced when removing the FB In the setting of a prolonged retained FB, the

FB may erode into or be forced into a sinus cavity, causing sinusitis

NOSE 181

T A B L E 7 - 2 TYPES OF EPISTAXIS

Anterior Kiesselbach plexus Direct nasal pressure,

cautery, and/or anteriornasal packing

Oral antibiotics shouldprophylactically cover fornasal packing-inducedsinusitis (cephalexin oramoxicillin-clavulanate)

Accounts for 90% of all epistaxiscases

Silver nitrate cautery should not bedone bilaterally in order to avoidseptal necrosis

Complications of nasal packing:sinusitis, otitis media, toxic shocksyndrome

Posterior Sphenopalatine artery Posterior, then anterior,

nasal packingOral antibiotics shouldprophylactically cover fornasal packing-inducedsinusitis (cephalexin oramoxicillin-clavulanate)

Suspect in patients with persistentepistaxis despite anterior nasalpacking

Hospital admission necessary,because of nasopulmonary reflexrisk (hypoxia, bradycardia, apnea,dysrhythmias) with posterior nasalpacking

Other complications of nasalpacking: sinusitis, otitis media,toxic shock syndrome

Comments: A retained nasal FB should be suspected in pediatric patients with persistent purulent nasaldischarge despite empiric antibiotic treatment for sinusitis or persistent unilateral epistaxis A button battery

FB requires immediate removal from the nostril, because of the risk of caustic damage and liquefactionnecrosis

R H I N I T I S

Definition: Rhinitis is an inflammation of the nasal mucosal lining

Etiology: Rhinitis is typically caused by a viral respiratory infection or allergen

Clinical Presentation: Patients present with nasal mucosal edema and copious, watery nasal discharge.Because of ostiomeatal obstruction, this may progress to sinusitis

Diagnosis: The diagnosis is made by physical examination

Treatment: Treatment includes nasal or oral decongestants and removal of the trigger, if allergic in etiology

Comments: To avoid “rhinitis medicamentosa,” which is the undesired, rebound vasodilation from overuse

of nasal vasoconstrictors, topical decongestants such as phenylephrine should only be used for 3–5 days

182 CHAPTER 7 / HEAD, EAR, EYE, NOSE AND THROAT DISORDERS

Diagnosis: Patients with frontal, maxillary, and ethmoid sinusitis exhibit focal percussion tenderness overthe affected areas There is no role for plain radiographs in acute sinusitis management CT imaging should

be reserved for patients with clinical findings suspicious for complicated sinusitis and sphenoid sinusitis

Treatment: For uncomplicated sinusitis, outpatient topical decongestants should be administered for3–5 days, but not longer to avoid “rhinitis medicamentosa” (see Rhinitis section) Antibiotics (amoxicillin,amoxicillin-clavulanate, trimethoprim-sulfamethoxasole, a cephalosporin, or an advanced macrolide) should

be given, if suspicious for bacterial sinusitis For cystic fibrosis and HIV patients, antipseudomonal coverageshould be added

Complications: Complications arise from direct extension of the infection beyond the sinus cavity andinclude the following: facial and orbital soft tissue infection, intracranial infection, meningitis, and cavernoussinus thrombosis (CST) Specifically in frontal sinusitis, erosion into the anterior sinus wall can lead toforehead swelling (Potts puffy tumor) For ethmoid sinusitis, direct extension can lead to periorbital andorbital cellulitis And for sphenoid sinusitis, local erosion can lead to optic neuritis, blindness, meningitis,CST, or an intracranial abscess

Comment: Be aware of mucormycosis, which can cause an invasive sinusitis presenting with a black char on the nasal mucosa This fungal infection predominantly occurs in patients with diabetes mellitus

es-or HIV

C A V E R N O U S S I N U S T H R O M B O S I S

Definition: CST is a venous thrombosis of the cavernous sinus This sinus is contiguous with cranialnerves III, IV, V1, V2, and VI, the carotid artery, and the optic nerve, and drains the ophthalmic veins of theface

Etiology: CST usually develops as a late complication of sinusitis or a central facial infection by direct

extension The most common organism is Staph aureus.

Clinical Presentation: Because the venous drainage of the infraorbital face is by the valveless ophthalmicveins, periorbital or orbital cellulitis can progress to CST Ocular palsies are common but may be subtle.Contralateral eye findings, such as periorbital cellulitis or ocular palsies, are pathognomonic for CST, becausecommunicating veins connect the right and left cavernous sinuses

OROPHARYNX AND THROAT 183

Diagnosis: CT imaging with intravenous contrast, showing a filling defect in the cavernous sinus, confirmsthe diagnosis

Treatment: The treatment for CST is early broad-spectrum antibiotics, covering positive, negative, and anaerobic organisms

gram-Complications: Patients can develop cranial nerve palsies and elevated intraocular pressure from increasedretrobulbar pressure, in addition to meningitis, altered mental status, sepsis, and coma

OROPHARYNX AND THROAT

D E N T A L G I A

Definition: Dentalgia or tooth pain can arise from both dental and non-dental origins

Etiology and Clinical Presentation:

P E R I O D O N T A L D I S E A S E S

T A B L E 7 - 4 PERIODONTAL DISEASES

O R A L D I S E A S E S

T A B L E 7 - 5 ORAL DISEASES

184 CHAPTER 7 / HEAD, EAR, EYE, NOSE AND THROAT DISORDERS

Tenderness to tooth percussionPlaque on tooth enamel

Pain control Most common cause for

dentalgiaSuspect periapical abscess ifsevere tooth pain withpercussion

Pericoronitis Inflammation of occlusal gingival

surface, directly overlying an eruptingpermanent tooth (usually the thirdmolar tooth)

Oral antibioticsHydrogen peroxidemouth rinsesPain controlAcute

alveolar

osteitis

A localized bone infection from apostextraction dry socket, caused bydislodgement of a healing blood clot

Pain controlOral antibioticsDental packing toprevent bonycontact with air

Avoid disrupting currentblood clot, which mayworsen osteomyelitisOccurs 3–5 dayspost-extraction (unlike simpleperiosteitis, which occurs1–2 days postextraction)Maxillary

sinusitis

Tenderness over maxillary sinusPurulent nasal drainageClassically, the maxillary teeth will bemore painful with lying supine

Antibiotics ifsuspicious forbacterial etiology

Tic

douloureux

This trigeminal neuralgia may have

“electric shocks” which radiate to theteeth

Carbamazepine Most common cranial

Oral corticosteroids

to preventblindness fromischemic opticneuropathyAcute

OROPHARYNX AND THROAT 185

T A B L E 7 - 4 PERIODONTAL DISEASES

Gingivitis Noninvasive, inflammation of

gingival liningPainlessGingival swelling and/or bleedingwith minimal trauma (brushingteeth)

Improved oralhygiene

Can progress toperiodontitis

Periodontitis Progression of gingivitis, now

involving alveolar boneCauses destruction of periodontalattachments to teeth, leading totooth mobility

Usually painlessGingival swelling, bleeding, and/ortenderness

Oral antibioticsHydrogen peroxidemouth rinses

Most common cause

Incision and drainageOral antibioticsHydrogen peroxidemouth rinsesAcute

Oral antibioticsPain controlHydrogen peroxidemouth rinses

Risk factors:

Immunocompromisedstatus, emotionalstress, local trauma,smoking

186 CHAPTER 7 / HEAD, EAR, EYE, NOSE AND THROAT DISORDERS

T A B L E 7 - 5 ORAL DISEASES

Ludwig’s angina Bilateral soft tissue infection of

submandibular, submental, andsublingual spaces

Dysphagia and odynophagiaTrismus

Tongue elevationBrown, woody induration ofoverlying skin

Parenteral antibiotics(penicillin plusmetronidazole for

better Bacteroides

coverage)Surgical drainage

Caused by mixed flora of

Streptococcus, Staphylococcus,and

BacteroidesorganismsUsually caused by trauma ordental infection

Complications: Airwayobstruction, mediastinitis

Herpes

gingivo-stomatitis

Small painful ulcers often involvingbuccal mucosa, gingiva, and palateProdromal fever, lymphadenopathy,oral burning or tingling

Supportive Etiology: Herpes simplex

type IRecurrent with stressors

Aphthous

stomatitis

Painful ulcers with centralfibropurulent centerLocated usually on the labial andbuccal mucosa, sparing keratinizedsurfaces (hard palate, dorsum oftongue)

Supportive+/−

topical corticosteroid

Most common oral mucosadisease in North AmericaOccurs in

immunocompetent patientsRecurrent with stressors

Herpangina High fever, sore throat, malaise

Painful ulcers isolated to the softpalate, uvula, posterior pharynx,and tonsillar pillars

Spares gingival and buccal mucosa

Supportive Caused by coxsackie viruses

Occurs usually in thesummer and autumn

Hand-Foot-Mouth

disease

Painful intraoral ulcers (gingiva,buccal mucosa, tongue, soft palate)Concurrent vesicles/ulcers on thepalms and soles

Supportive Caused by coxsackie viruses

Oral antifungalagent (nystatin)

Risk factors: Extremes ofage, antibiotic use,immunocompromisedstatus

Leukoplakia White plaque, which can NOT be

scraped offUsually affects the buccal mucosa

Treat underlyingcause

Most common oralprecancer

Most common risk factor istobacco use

OROPHARYNX AND THROAT 187

C A U S E S O F P H A R Y N G I T I S

T A B L E 7 - 6 CAUSES OF PHARYNGITIS

Viral Mild-moderate tonsillar

erythemaAssociated viral syndromesymptoms (cough, coryza,myalgias)

Supportive Most common cause for

pharyngitisEpstein-Barr virus can causepharyngitis, fevers, posteriorcervical lymphadenopathy, andsplenomegaly (infectiousmononucleosis)Group A

beta-hemolytic

Streptococcus

(GABHS)

FeverAnterior cervicallymphadenopathyExudative tonsillitisLack of viral symptoms(coryza, cough)Scarlet fever rash(scarlatiniform)

PenicillinAntibiotics reducerisk for rheumatic

fever, but not

Neisseria

gonorrhoeae

FeverLymphadenopathyMild-moderate erythematoustonsillitis

Ceftriaxone and(azithromycin ordoxycycline)

Sexually transmitted disease fromorogenital intercourse

Consider child abuse ifdiagnosed in young childrenAzithromycin or doxycycline isrecommended for presumptive

concurrent Chlamydial infection

Corynebacterium

diphtheriae

Toxic appearanceFever

DysphagiaGreen–graypseudomembranouspharyngitis

Penicillin andhorse-serumantitoxinHospital admissionwith respiratoryisolation

Consider in nonimmunizedpediatric patients

Complications: Airwayobstruction, myocarditis,polyneuritis (especially bulbarneuropathy causing ptosis,strabismus, dysphonia)

D I S E A S E S O F T H E P H A R Y N X , L A R Y N X , A N D T R A C H E A

T A B L E 7 - 7. DISEASES OF THE PHARYNX, LARYNX, AND TRACHEA

T A B L E 7 - 7 DISEASES OF THE PHARYNX LARYNX, AND TRACHEA

Retropharyngeal

abscess

Group Aβ

hemolyticstreptococci(mostcommon)Polymicrobial

Age predominance: 6 months–4years old (rare after 4 years of age,because of retropharyngeal lymphnode atrophy)

Symptoms: Fever, sore throat,muffled voice, decreased intake, lack

of coughOnset: Insidious progression of upperrespiratory symptoms for 2–3 days(unlike epiglottitis, which is rapidwithin hours)

Exam: Toxic appearance, dysphagia,hyperextended neck, inspiratorystridor, retropharyngeal massSimilar presentation to epiglottitis,except for age predominance andsymptom onset

Parenteral broad-spectrumantibiotics includingclindamycinPossible endotrachealintubation for airwaycontrol

Children: Caused by infection ofretropharyngeal lymph nodesAdults: Caused by local extension

of infection (parotitis, otitis media,nasopharyngitis)

Imaging: Lateral neck radiograph:Retropharyngeal soft tissue spacewidening (end-inspiratory, mildneck extension is best qualityradiograph to prevent falsepositive result)

Definitive imaging: CTComplications: Airway obstruction,mediastinitis, aspiration

pneumonia, sepsis

Bacterial

tracheitis

S aureus(mostcommon)

Age predominance: 3 months–13years old, but usually<5 years old

Symptoms: Fever, barky cough(unlike epiglottitis andretropharyngeal abscess), sore throat,minimal voice change, no dysphagiaOnset: 2–7 days of upper respiratorysymptoms

Exam: Toxic appearance, inspiratoryand expiratory stridor

Parenteral antibiotics(third generationcephalosporin pluspenicillinase resistantpenicillin or clindamycin)Consider vancomycin forMRSA

Endotracheal intubation

Also known as membranouslaryngotracheobronchitisPathophysiology: Bacterialsuperinfection of the trachealepithelium with thickmucopurulent secretionsGenerally more toxic-appearingthan patients with croup infectionLateral neck radiograph: Normalexcept for shaggy tracheal aircolumn

Complication: Airway obstruction

Onset: Abrupt within hoursExam: Anxious and toxic appearance,sitting upright in “sniffing” position,drooling, inspiratory stridor

Parenteral antibiotics(second or thirdgeneration cephalospori)Nebulized racemicepinephrine (for airwayedema)

Endotracheal intubation,ideally with fiberopticlaryngoscopy for airwaycontrol

Imaging: Lateral neck radiograph:

“Thumbprint” sign with swollenepiglottis

Avoid manipulation (e.g., tongueblade insertion to visualizeepiglottis), because this mayworsen airway occlusionAllow patient to remain in mostcomfortable position (usuallyupright in caregiver’s lap)Peritonsillar

abscess

Polymicrobialwith the mostcommonbacterialorganism being

S pyogenes

Age predominance: 20–30sSymptoms: Fever, odynophagia,dysphagia, drooling, “hot potato”

voiceExam: Exudative tonsillitis, unilateralperitonsillar erythema and swelling,trismus, uvular deviation

Aspiration or incision anddrainage of abscessAntibiotics (penicillin,cephalosporin orclindamycin)

Most common deep spaceinfection of the head and neck inadults

Suppurative complication ofpharyngitis

Complication: Airway obstruction

190 CHAPTER 7 / HEAD, EAR, EYE, NOSE AND THROAT DISORDERS

D I S E A S E S O F T H E S A L I V A R Y G L A N D S

T A B L E 7 - 8 DISEASES OF THE SALIVARY GLANDS

Sialolithiasis Age predominance: 30–50

years oldUnilateral painful salivary gland,usually the submandibulargland

Classic history: worse witheating foods

May express intraoral pus fromWharton’s (submandibular) orStenson’s duct (parotid gland)

SialogoguesDigital massage ofduct

Warm compresses

A clinical diagnosis

Parotitis Fever

TrismusPain and swelling over parotidgland, obliterating angle ofmandible

Purulent drainage fromStenson’s duct

Antibiotics(amoxicillin/

clavulanate orampicillin/

sulbactam)SialogoguesSurgical drainage iffluctuant abscesspresent

A clinical diagnosis, caused byinfection, sialolithiasis,granulomatous disease, neoplasmMost common viral pathogen:Mumps (should check for orchitis

or oophoritis)Most common bacterial

pathogens: Staph aureus,

Strep pneumoniae and Strep.

viridans , H influenzae

T E M P O R O M A N D I B U L A R J O I N T D I S O R D E R S

Etiology: Temporomandibular joint (TMJ) pain can be caused by myofascial disorders from periarticularmuscle spasm or inflammation from articular meniscal trauma Meniscal trauma can occur from eithermajor blunt injury or repeated microtrauma, such as from bruxism (teeth grinding)

Clinical Presentation: Patients may present with unilateral headache, tenderness over the TMJ, andmasseter muscle Often mandibular movement is limited by pain and associated with local clicking orpopping noises

Diagnosis: The diagnosis is made by clinical examination, by palpating the TMJ during mandibular ing, closing, and lateral excursion Radiographs are not useful

open-Treatment: Care is generally supportive and includes pain control, muscle relaxants for spasm, heat presses, and a soft diet

com-EYE 191

EYE

For diseases involving the eye or surrounding soft tissue, topical ophthalmic anesthetics should never beprescribed as an outpatient because of the risk of delayed healing and corneal ulcer formation Further,topical corticosteroids should be prescribed with caution because of the risk of worsening occult viral andfungal infections Follow-up with an ophthalmologist is crucial within 24–48 hours for ocular diseasesbeyond uncomplicated conjunctivitis and benign soft tissue diseases (blepharitis, dacryocystitis, hordeolum,chalazion)

External Eye

T A B L E 7 - 9 DISEASES OF THE EXTERNAL EYE

Anterior Chamber Diseases

T A B L E 7 - 1 0 ANTERIOR CHAMBER DISEASES

Posterior Chamber Diseases

T A B L E 7 - 1 1 POSTERIOR CHAMBER DISEASES

Periorbital Versus Orbital Cellulitis

T A B L E 7 - 1 2 PERIORBITAL VERSUS ORBITAL CELLULITIS

Traumatic Eye Injuries

T A B L E 7 - 1 3 TRAUMATIC EYE INJURIES

T A B L E 7 - 9 DISEASES OF THE EXTERNAL EYE

Blepharitis Symptoms: Eye burning and

itching, eyelid crustingExam: Eyelid margin swellingand erythema with vascularcongestion

Mild shampoo along eyelashesWarm compresses

Artificial tearsTopical erythromycin antibioticointment for severe casesSelenium sulfide shampoo forseborrhea

Caused by bacteria (Staph aureus and Staph.

epidermidis) or seborrheic dermatitis

Chalazion,

hordeolum

Acute painful (hordeolum) orsubacute painless (chalazion)nodular inflammatory process

of eyelid margin

Warm compressesTopical antibiotics(erythromycin)Incision and drainage only forrefractory cases

Dacryocystitis Pain, tenderness, erythema over

lacrimal ductTearing or discharge

Oral and topicalanti-staphylococcal antibioticsWarm compresses

Digital massage

Caused by obstruction of nasolacrimal duct

Most common organism: S aureus

Conjunctivitis Symptoms: Eye redness, itching,

irritation, foreign bodysensation, eyelid crusting in themorning

Exam: Inflammation ofconjunctiva, discharge, normalvisual acuity

Gonococcal infection: Severechemosis, lid edema,mucopurulent discharge

For bacterial infection: Topicalantibiotic ointment

For viral or allergic infection:

Artificial tears and coolcompresses

For gonococcal or chlamydialinfection: Ceftriaxone,erythromycin (or doxycycline),and topical erythromycinointment

Viral etiology more common than bacterial, allergic,

or toxic causesMost common viral cause is adenovirusComplication of bacterial conjunctivitis: Keratitis,corneal ulcer, perforation

Consider N gonorrhoeae for severe cases;

concern for disseminated gonorrheal infectionFor gonococcal or chlamydial infection, treat forboth pathogens concurrently

Neonatal conjunctivitis: N gonorrhoeae usually occurs in 2–4 days of life and C trachomatis in

days 3–15

Keratitis Symptoms: Eye pain and

redness, photophobia, foreignbody sensation

Exam: Multiple punctate cornealepithelial defects

Dendritic lesions classic forherpes simplex keratitis

Artificial tearsTopical antibioticsCycloplegicFor herpes simplex keratitis:

Topical trifluridine antiviral agentand avoid topical steroidsFor herpes zoster keratitis: Oralantiviral agent

Contact lens user: Topicalantipseudomonalfluoroquinolone antibiotic

Etiologies: ultraviolet burns (welders),conjunctivitis, contact lens wear, chemical injury, ortrauma

Risk for herpes zoster keratitis if observe zosterrash along ophthalmic branch of trigeminal nerve,especially if observe vesicles on tip of nose(Hutchinson’s sign)

Contact lens wearer: High association of keratitis

with P aeruginosa infection

Corneal ulcer Symptoms: Eye pain and

redness, photophobia, foreignbody sensation

Exam: Corneal epithelial defectwith surrounding cornealinfiltrate, visual defect ifoverlying central cornea

Topical antibioticsContact lens user: Topicalantipseudomonalfluoroquinolone antibiotic

The most common etiology is bacterial, more sothan fungal and herpetic causes

Never apply eye patch, because of increased riskfor pseudomonal infection

Contact lens wearer: High association of corneal

ulcer with P aeruginosa infection

194 CHAPTER 7 / HEAD, EAR, EYE, NOSE AND THROAT DISORDERS

T A B L E 7 - 1 0 ANTERIOR CHAMBER DISEASES

Glaucoma Symptoms: Eye pain or

retro-orbital headache,

halos around lights,

blurred vision, nausea

Exam: Mid-dilated and

Topical beta blocker (decreasesaqueous humor production)Topical alpha-2 agonist such asapraclonidine (decreasesaqueous humor production)Intravenous mannitol or glycerol(decreases intraocular volume)Topical cholinergic agent(cycloplegic to increaseaqueous humor outflow)

High intraocular pressure can

be from excess production ofaqueous humor or lack ofsufficient aqueous humoroutflow

Acute closed-angle glaucoma(versus open-angle) causesrapid onset of painTriggers: Stress, trauma,entering a dark roomComplication: blindnessTopical agents may havesystemic effects For example,topical beta-blockers havecaused heart block, asthma,and acute heart failure.Iritis

Etiologies: Autoimmunediseases, viral, bacterial,fungal, malignancies, toxicexposures

Unlikely iritis diagnosis iftopical anesthetic relieves eyepain

Consensual photophobia(eye pain caused by lightshined in unaffected eye) is aclassic finding

T A B L E 7 - 1 1 POSTERIOR CHAMBER DISEASES

Topical corticosteroids forvasculitis (in consultationwith ophthalmologist)Treat underlying etiology

Etiologies: Autoimmune, infectious,malignancy, idiopathic

In pediatric patients, common infectiouscauses are congenital toxoplasmosis andCMV infection

Complication: Blindness

Optic neuritis Vision loss from optic nerve demyelination

Symptoms: Usually painful visual lossExam: Visual deficit (usually central fielddeficit and sparing peripheral fields), afferentpupillary defect, swollen optic disk onfundoscopic exam

Color vision more affected than visual acuity

Questionable benefit of oralcorticosteroids

Is often the first symptom of multiplesclerosis (MS)

30% of optic neuritis patients will develop

MS in next 5 yearsDifferential diagnosis: Compressiveneuropathy, ischemic neuropathy (temporalarteritis), diabetic retinopathy, infection(Lyme’s disease)

Papilledema A sequelae of elevated intracranial pressure

Symptoms: Headache, nausea, and vomitingFundoscopic exam: Bilateral optic diskswelling and disk margin blurringVision loss is a late finding

Treat the underlying etiologyFor intracranial hypertension(pseudotumor cerebri):

Diuretic, periodic therapeuticlumbar puncture

Etiology: Any intracranial mass effect (tumor,abscess, hemorrhage), hypertensive crisis,idiopathic intracranial hypertension(pseudotumor cerebri), meningitis,encephalitis

Earliest fundoscopic finding of elevatedintracranial pressure is absence of venouspulsations (not papilledema)

Unilateral optic disk swelling is optic neuritis

(Continued )

T A B L E 7 - 1 1 POSTERIOR CHAMBER DISEASES (CONTINUED)

Exam: Afferent pupillary defect, pale retinalbackground and paucity of retinal arteries,cherry-red fovea

Digital globe massageTopical beta-blocker toreduce intraocular pressureAcetazolamide (oral orintravenous) to decreaseintraocular pressure andincrease retinal blood flowBreath into paper bag, orcarbogen (95% oxygen, 5%

carbon dioxide) to increasepCO2, causing retinal arteryvasodilation

Risk factors: Cardiovascular disease, atrialfibrillation

Time window: 60 minutes before irreversibledamage

After stabilization, search for an embolicsource (cardiac valvular vegetation,ventricular thrombus, carotid artery plaque)

Risk factors: Hypertension, vasculitis,hypercoagulable disorders

Temporal

arteritis

An ischemic optic neuropathy from asystemic vasculitis of medium-sized arteriesSymptom: Gradual, unilateral, painless visionloss (which often becomes bilateral),headache, jaw claudication, myalgias,temporal artery tenderness

Eye exam: Often normal initially, afferentpupillary defect (if optic nerve circulationcompromised)

Elevated ESR and C-reactive protein levels

Oral or intravenouscorticosteroids to preservevision

Patients should be referred for a temporalartery biopsy for definitive diagnosis Thebiopsy will still remain diagnostic, despitesteroid treatment for up to 1 week

EYE 197

T A B L E 7 - 1 2 PERIORBITAL VERSUS ORBITAL CELLULITIS

PERIORBITAL CELLULITIS ORBITAL CELLULITIS

Definition Cellulitis anterior to orbital septum Cellulitis deep to the orbital septumEtiology Most common organism: S aureus

Starts as localized cellulitis or skindisruption (most common source), orsinusitis (usually ethmoid sinusitis)

Most common organism: S aureus

Starts as sinusitis (most commonsource and especially from ethmoidsinusitis), dental abscess, orbital foreignbody, local cellulitis

Clinical presentation Eyelid swelling, erythema, and pain

Conjunctival injectionNormal vision and painless eyemovement

More severe eyelid swelling, erythemaand pain

More toxic appearanceFever

Visual deficitPain with eye movementDecreased ocular mobilityProptosis

Afferent pupillary defectTreatment Antibiotics: second or third generation

Complications: Cavernous sinusthrombosis, intracranial infection, visualloss, and bacteremia

CT imaging necessary to evaluate forintracranial and retroorbital involvement

198 CHAPTER 7 / HEAD, EAR, EYE, NOSE AND THROAT DISORDERS

T A B L E 7 - 1 3 TRAUMATIC EYE INJURIES

Ocular burn Symptoms: Eye pain,

blurred vision, photophobia,tearing

Exam: Conjunctivalinjection, fluorescein uptakewhere corneal epitheliumdamaged

Copious saline irrigationuntil neutral pHTopical antibioticCycloplegicTreat high intraocularpressures, if present (seeGlaucoma, Table 7-10)

Alkali burns(liquefactivenecrosis) produce more

damage than acid burns

(self-limited coagulationnecrosis)

Anhydrous ammonia is theworst of the alkali burnsComplications: Cornealperforation, corneal scarring,acute and chronic glaucoma,cataract

Eyelid

laceration

Higher-risk lacerationsinvolve the eyelid marginand lacrimal duct

Superficial, partial-thicknesslacerations, sparing the lidmargin and lacrimal duct,can be repaired in theEmergency Department

Lacerations requiringophthalmologic surgical repair:

1 Eyelid margins: to preservecorneal wetting

2 Lacrimal duct (canalicularsystem): to prevent chronictearing from ductalobstruction

At risk for deeper injury (globerupture)

Exam: Foreign bodyembedded on cornea,possible rust ring

Slit lamp-guided removal offoreign body, if superficialTopical antibioticCycloplegicUpdate tetanusimmunization status

Check for globe perforation withhigh-velocity projectiles(consider CT imaging)Can delay rust ring removal byophthalmologist in 24 h

Corneal

abrasion

Symptoms: Eye pain,tearing, photophobia,foreign-body sensationExam: Shallow fluoresceinuptake at corneal abrasionsites

Topical antibioticContact lens wearer: Topicalanti-pseudomonal

fluoroquinolone antibioticUpdate tetanus

immunization statusAvoid patching eye

Usually will have complete (buttransient) resolution of painwith topical anesthetic, unlikeiritis and glaucoma

Contact lens wearers are at

increased risk for Pseudomonas

infectionCheck for occult foreign bodyunder upper eyelid

EYE 199

T A B L E 7 - 1 3 TRAUMATIC EYE INJURIES (CONTINUED)

Ruptured

globe injury

Symptoms: Eye pain,significantly blurred visionExam: Irregular pupil shape,positive Seidel test(aqueous humor tricklingout of anterior chamber onfluorescein exam), shallowanterior chamber, bloodychemosis

Metal eye shield to preventfurther mechanical oculardamage and extrusion ofaqueous humorUpdate tetanusimmunization statusIntravenous cephalosporinantibiotic

Measurement of intraocularpressure is contraindicatedbecause it may worsen globeinjury

Traumatic

iritis

Symptoms and examsimilar to nontraumatic iritis(see Table 7-10)

Topical antibioticCycloplegicTopical corticosteroid, inconsultation withophthalmologistHyphema Blood in the anterior

chamber

Head elevation to allowblood to settle inferiorly andnot obstruct trabecularmeshwork

Cycloplegic, because theciliary body is often the site

of bleedingGlaucoma treatment, ifnecessary (see Table 7-10)Avoid aspirin and otherantiplatelet agents, because

of risk of delayed rebleeding

Spontaneous hyphemas occur

in sickle cell diseaseComplications: Acute glaucomafrom outflow obstruction, bloodstaining of cornea, delayedrebleeding after 3–5 daysCarbonic anhydrase inhibitorsshould be avoided inhyphemas, caused by sickle celldisease, because it lowers pH.This promotes increasedsickling and worseningintraocular pressureLens

movements)

Observation or surgicalrepair

Most common cause formonocular diplopia is lensdislocation

High-risk population: Marfan’ssyndrome, rheumatoid arthritis,homocystinuria

(Continued )

200 CHAPTER 7 / HEAD, EAR, EYE, NOSE AND THROAT DISORDERS

T A B L E 7 - 1 3 TRAUMATIC EYE INJURIES (CONTINUED)

Retinal

detachment

Symptoms: Flashes of light,floaters, visual field defect,blurred “curtain-like” vision,usually painless

Fundoscopic exam:

“Floating” gray retina which

is out of focus atdetachment site

Acute detachments requiresurgical repair within 24 h

Endoph-thalmitis

Deep infection of theanterior, posterior, andvitreous chambers, usually adelayed complication frompenetrating trauma,retained foreign body, orocular surgery

Symptoms: Eye pain andvision loss

Exam: Visual impairment,conjunctival injection,opaque infected chambers

Intravenous broad-spectrumantibiotics

Most common organisms:

Staphylococcus , Streptococcus,

Bacillus

Damage to the endothelial lining of blood vessels from trauma or disease exposes blood to the

suben-dothelial connective tissue, initiating the body’s hemostatic process Primary hemostasis occurs when platelets bind to collagen in the exposed walls of the blood vessel to form a hemostatic clot Secondary hemostasis

is the cascade of coagulation factors resulting in the formation of a fibrin clot The coagulation cascade

consists of the intrinsic and extrinsic pathway (Figure 8-1) Both pathways share clotting factors I, II, V,

and X The extrinsic pathway is initiated when tissue factor activates factor VII, resulting in the tion of factor X The intrinsic pathway consists of the activation of factor XII by vessel damage resulting

activa-in XII→XI→IX→VIII Activated factor VIII activates the common factor X The result of both pathways

is factor I, fibrin, a protein that cross-links platelets forming a stronger clot Degradation of the clot byfibrinolysis, the function of the protein plasmin, completes the repair process of the vessel Vitamin K

is an essential cofactor of factors II, VII, IX, and X, as well as the anticoagulation factors Protein S andProtein C

201

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202 CHAPTER 8 / HEMATOLOGIC DISORDERS

INTRINSIC PATHWAY

EXTRINSIC PATHWAY

Factor IXFactor IXa

Factor XIIa

Factor VIIIaFactor VIII

ThrombinProthrombin

FibrinFibrinogen

Factor XIIIaFibrin Stabling Factor XIII

PlasminPlasminogen

Products

– F I G U R E 8 - 1 — Coagulation cascade

HEMOSTASIS 203

T A B L E 8 - 1 LABORATORY TESTS FOR EVALUATING HEMOSTASIS

Bleeding time

(BT)

2.5–10 min(template BT)

Platelet function,local tissue factor,and clotting factors

Increased: Thrombocytopenia (DIC,ITP, TTP), von Willebrand disease,aspirin therapy

Platelet count 150–450,000µL Number of platelets Increased: trauma, acute

hemorrhage, polycythemia vera,primary thrombocytosisDecreased: Risk of bleeding usually

< 50,000 µL High risk of

spontaneous CNS bleed

<10,000 µL Seen in DIC, TTP, ITP,

aplastic anemia, burns, viralinfections, drugs (aspirin, thiazidediuretics)

Prothrombin

time (PT)

10–12 s Extrinsic and

common pathway,factors VII, X, V,prothrombin, andfibrinogen

Increased PT: Warfarin therapy(inhibits Vitamin dependent factors II,VII, IX, X), Vitamin K deficiency, liverdisease, DIC

INR 2-3 for DVT, A-fib, PE, and TIAsINR 3-4.5 for recurrent DVTs andmechanical heart valves

X, V, prothrombin,and fibrinogen

Increased aPTT: Heparin therapy,factor deficiencies

D-Dimer <0.5µg/mL Amount of fibrin

broken down intofragments

Increased: DIC, PE, thromboticdisease

Increased: Heparin therapy, DIC,fibrinogen deficiency

Fibrinogen 200–400 mg/dL Useful for detecting