Hematology and Oncology
ITE Review




Bleeding disorders
o Hemostasis is a balance between excessive bleeding and thrombosis
o Four components of hemostasis
 Vascular integrity
 Platelet function
 Coagulation factors
 Fibrinolysis
Coagulation studies
o Prothrombin time
 Affected by extrinsic (and common) pathways
 PT >2 seconds more than control is abnormal
 Increased PT: Vitamin K deficiency, warfarin use, liver disease
o International normalized ratio (INR)
 PT ratio that would be obtained if WHO’s thromboplastin has been used
 INR of 1 is normal; 2-3 therapeutic; 2.5-3.5 for valves
o Partial thromboplastin time (PTT)
 Affected by intrinsic (and common) pathways
 PTT >8-10 seconds above normal is significant
 Increased PTT: Factor VIII, IX, XI, XII deficiency, heparin therapy
o Increased PT and PTT
 Heparin overdose, warfarin overdose, Vitamin K deficiency and severe liver
disease, DIC, massive transfusion, thrombolytic therapy
o Vitamin K dependent factors
 II, VII, IX, I
Platelet vs coagulation disorders
o Platelet disorders
 Petechiae, purpura (don’t blanch), epistaxis, gum/mucosal bleeding, GIB,
menorrhagia
 Women; often acquired
o Coagulation disorders
 Deep muscle or joint bleeding (rarely epistaxis, menorrhagia, GIB)
 Men; congenital
Platelet disorders
o Thrombocytopenia
 Normal 150-400K
 Decreased production- marrow disease (malignant infiltration, myelofibrosis,
aplastic anemia), drugs (chemo, alcohol, thiazides), vitamin B12 or folate
deficiency

o
o
o
o
Increased destruction- ITP, TTP, HUS, HELLP, sepsis, viral (HIV, mumps, varicella,
EBV), SLE, drugs (PCN, sulfa, quinine, Lasix, heparin, ASA)
 Splenic sequestration- hypersplenism, cirrhosis, heme malignancy
 Dilution- massive transfusion
Platelet transfusion
 Six pack increases platelet count approx. 50K
 Indications- platelet count <10-20K, life threatening bleeding
Idiopathic thrombocytopenic purpura (ITP)
 Acute ITP
 Antiplatelet antibody IgG (both acute and chronic)
 Kids 2-6 yrs
 Follows viral infection
 Self limited; resolves spontaneously
 Tx supportive unless severe bleeding (plt <50K) or plt <20K
 Prednisone 1 mg/kg
 IVIG
 Platelet transfusion only for life-threatening hemorrhage
 Chronic ITP
 Women 20-50 yrs
 Remission rare
 Underlying autoimmune, collagen vascular, or malignant disease
 Steroids
 IVIG, immunosuppressives, splenectomy
 Platelet transfusion only for life-threatening hemorrhage
Thrombotic thrombocytopenic purpura (TTP)
 Subset of thrombotic microangiopathies
 Subendothelial and intraluminal deposits of fibrin and platelet aggregation
 Females; 80% mortality if untreated
 Infection, autoimmune disease, immunosuppressives, chemo
 Treatment- steroids, plasmapheresis, dialysis, FFP
 Avoid platelet transfusions
 FAT RN
 Fever
 Anemia- MAHA; schistocytes on peripheral smear
 Thrombocytopenia
 Renal
 Neurologic
Hemolytic uremic syndrome (HUS)
 Thrombotic microangiopathy
 Thrombocytopenia, hemolytic anemia, fever, neurologic, renal
 Less mental status change and more renal dysfunction than TTP
 Often kids
 Bacterial gastroenteritis (E coli O157:H7, Shigella)
o
o
o
o
ASA/NSAIDs block cyclooxygenase, which decreases thromboxane formation
decreased platelet aggregation
 ASA effect irreversible
 NSAID effect reversible
Disseminated intravascular coagulation (DIC)
 Platelet, coagulation, fibrinolytic disorder
 Diffuse bleeding from multiple sites
 Acrocyanosis, thrombosis, pregangrenous changes of fingers, toes, genitalia,
nsoe (purpura fulminans)
 Trauma, burns, pregnancy, sepsis, transfusion, carcinoma, acute leukemia, liver
disease, snake bites, heat stroke
 Treat underlying cause
 If hemorrhageblood products
 If thrombosis low dose heparin
 More commonly seen with Gram (-) sepsis in pregnancy, retained fetus,
chronic DIC, purpura fulminans
 Findings
 Increased PT/INR
 Increased PTT
 Decreased platelets
 Decreased fibrinogen
 Increased FSP (fibrin split products)
 Increased D-dimer
 Schistocytes
Heparin induced thrombocytopenia (HIT)
 Antibodies to heparin/platelet factor 4 complex platelet activation and clot
formation
 Occurs 5-10 days after exposure
 Heparin > LMWH
 Thrombocytopenia <150K or drop of 50% from baseline
 Arterial or venous thrombosis
 Stop the heparin!
 Avoid platelet transfusions, lower limb dopplers (high incidence of DVT), test for
HIT antibodies
Von Willebrand’s disease
 Most common genetic bleeding disorder
 Von Willebrand factor functions
 Facilitates platelet adhesion
 Links platelet to endothelium
 Plasma carrier for factor VIII
 Autosomal dominant
 Deficiency or dysfunction of vWF and mild factor VIII defect
 Type I- decreased vWF (most common)
 Type II- abnormal or dysfunctional vWF



 Type III- no vWF
Mucocutaneous bleeding (epistaxis, menorrhagia, GIB)
Abnormal platelet function studies, increased bleeding time, normal platelet
count, normal PT/PTT
Treatment- DDAVP (desmopressin), factor VIII concentrates, cryoprecipitate

Coagulation disorders
o Hemophilias
 Delayed/protracted bleeding after mild trauma or dental extraction
 Spontaneous hematuria
 Hemarthrosis and muscle hematomas
 Most common in ankle in kids; knee in adults
 Intracranial hemorrhage
 Proloned PTT; normal PT and platelets
 Hemophilia A
 X-linked recessive deficiency of Factor VIII
 Mild (hematuria, deep lac)- 20 U/kg
 Moderate (oral lac, dental, minor surgery, late hemarthrosis)- 25 U/kg
 Severe (CNS/GI/abd, major trauma)- 50 U/kg
 1 U/kg increases activity level by 2%
 Cryoprecipitate, DDAVP, FFP
 Hemophilia B
 Aka Christmas Disease
 X-linked recessive deficiency of Factor IX
 Factor IX concentrate
 Prothrombin Complex Concentrates (PCC), FFP, NOT Cryo
o Hypercoagulability
 Factor V Leiden (most common inherited hyercoagulability disorder)
 Prothrombin mutation
 Hyperhomocysteinemia
 Protein C deficiency
 Protein S deficiency

Red blood cell disorders
o RBC incides
 Mean corpuscular hemoglobin (MCH)- measure of hemoglobin content within
RBC
 Mean corpuscular hemoglobin concentration (MCHC)- measure of
concentration of hemoglobin within RBC
 Mean corpuscular volume (MCV)- measure of RBC size
 RBC distribution width- measure of deviation in volume of RBCs
o Microcytic anemias
 Iron deficiency anemia

o
o
o
Hypochromic (decreased MCHC), decreased retics, decreased iron,
increased TIBC, increased RDW
 Lead poisoning
 Hypochromic, basophilic stippling
 Lead lines- hyperdense lines at metaphyses (knee and wrist)
 Thalassemia
 Mediterranean, African, Asian
 Hypochromic
 Spherocytosis
 Hyperchromic (increased MCHC)
Macrocytic anemias
 Vitamin B12 deficiency (pernicious anemia), folate deficiency (alcoholism)large, oval RBCs, hypersegmented neutrophils
 Liver disease, hypothyroidism
Hemolytic anemias
 Findings in hemolysis- decreased hemoglobin, decreased haptoglobin, increased
LDH, increased unconjugated bilirubin, schistocytes on peripheral smear
 G6PD deficiency
 X-linked nonimmune hemolytic anemia
 Coombs test negative
 Protects against malaria
 Stressors- infection, fava beans, medications (sulfa, nitrofurantoin,
pyridium, antimalarials, dapsone)
 Heinz bodies on peripheral smear
Sickle cell disease
 Autosomal recessive abnormal hemoglobin resulting from single amino acid
substitution
 Deoxygenated HbS results in sickle-shaped, nondeformable rbc that cannot
traverse small capillaries
 Sickle cell trait
 Spontaneous bleeding (hematuria, hyphema)
 Hyposthenuria (impaired ability to concentrate urine)
 Vaso-occlusive crises (rare, only extreme hypoxia)
 Presentation in kids
 Unexplained gnawing bone pain
 LUQ pain (splenic infarction)
 RUQ pain (gallstones)
 Severe hemolytic anemia
 Jaundice
 Painful swelling of hands and/or feet (dactylitis)
 Increased susceptibility to infection
o Encapsulated organisms (S pneumoniae, H influenzae)
o Salmonella osteomyelitis







Stressors
 Global/local hypoxia
 High altitude
 Low temperature
 Acidosis
 Radiographic contrast dye
Diagnostic studies
 Decreased hemoglobin, increased WBC, increased platelets
 Sickled RBCs on peripheral smear
 Increased retic count
 Increased alkaline phosphatase, increased bilirubin, increased LDH
Vaso-occlusive (thrombotic) crisis
 Most common
 CBC to exclude aplastic/sequestration; retic count to exclude aplastic
crisis
 Treatment- analgesics, hydration, supportive
Hemolytic crisis
 Usually from infection or drugs
 Jaundice, pallor, increased retic count, decreased hemoglobin
Sequestration crisis
 Kids 6 mo-6 yrs
 Abdominal pain, distention, splenomegaly, shock, pallor, hemoglobin
very low, high retic count
 Treatment includes splenectomy
Aplastic crisis
 Precipitated by infection (parvovirus B19)
 Hemoglobin very low, retic count very low (pathognomonic)
Complications
 Infections
o Due to functional asplenia, poorly migrating neutrophils
o Encapsulated organisms
o Broad spectrum antibiotics if suspected
 Acute chest syndrome
o Pulmonary infiltrate on CXR with fever, chest pain, cough,
wheezing, tachypnea
o Can be from infection, fat embolism, rib infarction,
thromboemboli, reactive airway disease, fluid overload,
atelectasis
o Broad spectrum antibiotics, ICU, exchange transfusion
 Priapism- 10-40%
 Cerebrovascular accident- thrombotic or hemorrhagic
o Immediate exchange transfusion
 Renal papillary necrosis






Congestive heart failure
Pulmonary hypertension
Leg ulcers
Retinal infarction/detachment
Avascular necrosis (digits in children, femoral head in young adults)
Pigmented gallstones

Proliferative disorders
o Polycythemia vera
 Markedly increased hemoglobin
 Abnormal proliferation of all 3 cell lines
 JAK2 mutation
 Hypertension, plethora, headache, hepatosplenomegaly, epistaxis, engorged
retinal veins, erythromelalgia
 Sludging, thrombosis, infarction in peripheral circulation
 Itching after hot showers- histamine release from increased basophil and mast
cell production
 Treatment- phlebotomy
o Hyperviscosity syndrome
 Blurred vision, headache, fatigue, somnolence, stroke, mesenteric ischemia
 Causes
 Waldenstrom macroglobulinemia (IgM)- most common
 Multiple myeloma (IgG or IgA)
 Leukemia with blast formation
 Polycythemia vera
 Management
 Phlebotomy for polycythemia
 Plasmapheresis for dysproteinemias
 Leukapheresis for blast transformations
 Multiple myeloma
 Proliferation of plasma cells causing a monoclonal immunoglobulin
 Extensive skeletal destruction and osteolytic lesions on imaging
 “punched out”
 Bone pain, anemia, hypercalcemia, renal insufficiency, hyperviscosity
 Rouleaux on peripheral smear
 Bence Jones protein on urine protein electrophoresis
 M spike on serum protein electrophoresis

Transfusion reactions

o
o
o

TRALI (transfusion related acute lung injury)
 Presents acutely within 4-6 hours
 Noncardiogenic pulmonary edema
 Hypotension
 Looks like ARDS
 Stop transfusion immediately
TACO (transfusion associated circulatory overload)
 Presents within several hours of transfusion
 Cardiogenic pulmonary edema
 Hypertension
Massive transfusion
 Transfusion of volume of blood equivalent to patient’s entire blood volume
within 24 hour period OR
 Transfusion of the equivalent of one-half of patient’s blood volume at one time
 Coagulopathy- dilution of clotting factors, platelet destruction, DIC
 Hypothermia
 Microembolization- degeneration products of platelets, leukocytes,
fibrinARDS
 Micropore filtration decreases
 Hypocalcemia- citrate toxicity
Cyanosis and methemoglobinemia
o Cyanosis
 >5 g/dL reduced unsaturated hgb, 0.5 g/dL sulfhemoglobin, 1.5 g/dL
methemoglobin
 Central- decreased arterial oxygen saturation





Decreased atmospheric pressure (high altitude)
Impaired pulmonary function- hypoventilation, V/Q mismatch, impaired
O2 diffusion
 Anatomic shunts- congenital heart disease, pulmonary AV fistulas,
multiple small intrapulmonary shunts
 Hgb abnormalities- methemoglobinemia, sulfhemoglobinemia
Peripheral- normally saturated arterial blood with increased O2 extraction
 CHF, cold exposure, shock states, peripheral vascular disease
Methemoglobinemia
 Cyanosis when concentration >15%
 Pulse ox 85% regardless of O2 sat
 Blood is dark brown-purple
 Precipitated by meds- nipride, nitroglycerin, local anesthetics (lidocaine,
benzocaine), quinolones
 Treatment is methylene blue
Oncologic emergencies
o Cardiac tamponade
 Carcinoma of lung and breast, lymphoma (Hodgkin’s and NHL), leukemia,
malignant melanoma
o SVC syndrome
 Carcinoma of lung, lymphoma
 Slow, progressive tumor development
 Symptoms occur in early morning
 Edema/venous distention of face and upper extremities, SOB, headache, feeling
of fullness in head, facial plethora, telangiestasia, papilledema
 Treatment- radiation, chemo, elevate HOB; steroids or diuresis if laryngeal or
cerebral edema
o Infections
 Neutropenia- absolute neutrophil count (ANC) <500
 Nadir occurs 5-10 days after chemo
 Bacterial, viral, or fungal
 Most common Gram negative in neutropenic fever- Pseudomonas
 Isolate, broad spectrum antibiotics
o Spinal cord compression
 Lung (most common), breast, prostate, multiple myeloma, lymphoma
 Back pain, motor loss, paresthesias, incontinence
 Treatment- steroids, radiation, surgery
o Hypercalcemia
 Stones- kidney stones
 Bones- pain, pathological fx, osteoporosis, osteomalacia, arthritis
 Groans- constipation, indigestion, N/V, PUD, pancreatitis
 Moans- lethargy, fatigue, depression, memory loss, psychosis, delirium, coma

o
Carcinoma of lung, breast prostate; multiple myeloma; parathyroid hormone
like substance (SCC lung); osteoclast activating factor (NHL, Adult T-cell
lymphoma-leukemia)
 Check ionized calcium level
 Shortened QT interval
 Treatment- IV hydration, Lasix diuresis, bisphosphonates
Acute tumor lysis syndrome
 1-5 days after chemo for hematologic malignancy (leukemia, lymphoma)
 Also with SCLC, high tumor burden, highly chemosensitive tumors
 More likely if underlying renal dysfunction
 Hyperuricemia (DNA breakdown)
 Hyperkalemia (cytosol breakdown)
 Hyperphosphatemia (protein breakdown)
 Hypocalcemia (secondary to hyperphosphatemia)
 AKI, dysrhythmias (K, Ca), neuromuscular instability (Ca)
 Treatment- Hydration, allopurinol
 Dialysis if
 K >6
 Uric acid >10
 Cr >10
 Phos >10
 Volume overload
 Symptomatic hypocalcemia
ENT ITE Review
EAR
Sudden hearing loss



Conductive loss: lesions of external auditory canal, TM, middle ear, ossicles
o Cerumen impaction (most common)
o Canal obstruction (FB)
o Otitis externa
o Middle ear effusion
o TM perforation
o Sclerosis of TM or ossicles
Sensorineural loss: lesions of cochlea, auditory nerve, brainstem auditory pathways
o Bilateral
 ototoxic drugs (antibiotics-AG, emycin, vanco, antimalarials, NSAIDs, loops,
antineoplastics-cisplatin, nitrogen mustard)
 exposure to loud noise
o Unilateral
 viral neuritis (cochlear branch of CN VIII)
 Acoustic neuroma
 Meniere’s disease
 Temporal bone fracture
Hearing loss tests
o Rinne test (rinne rings right next to the ear)
 Tuning fork on mastoid, then next to ear
 Normal: air conduction better than bone (still hear vibrations next to ear)
 Conductive loss: bone > air conduction (vibration not heard next to ear)
 Sensorineural loss: test is normal
o Weber (Weber wrinkles forehead)
 Tuning fork on forehead (normally sounds equally loud in both ears)
 Conductive loss: heard better in affected ear
 Sensorineural loss: heard better in unaffected ear
o With bilateral sensorineural hearing loss, both tests are normal but there is decrease in
hearing acuity
Vertigo


A sensation of movement of oneself (subjective vertigo) or the environment (objective vertigo)
Peripheral (85-90%) vs central (10-15%) vertigo
PERIPHERAL
CENTRAL
Onset
Severity
Pattern
Worse on movement
Nausea/sweating
Nystagmus
Fatigues
Hearing loss/tinnitus
Abnormal TM
CNS symptoms

Sudden
Intense spinning
Intermittent
Yes
Frequent
Horizontal, rotatory (NEVER
vertical
Yes
May occur
May occur
Absent
Slow
Less intense, ill-defined
Constant
No
Infrequent
Multi-directional, horizontal,
rotatory, or vertical
No
No
No
Usually present (headache,
diplopia, dysarthria,
dysphagia, ataxia, facial
numbness, hemiparesis)
Peripheral vertigo causes
o Benign paroxysmal positional vertigo (BPPV): most common cause
 Caused by canalolithiasis; delayed unilateral activation of posterior semicircular
canal because of impaired endolymph flow caused by clumped otoliths
 Dix-Hallpike to help dx
 No hearing problems or tinnitus
 Tx: particle repositioning, sedative, antihistamines
o Vestibular neuronitis
 Acute onset, viral etiology??; lasts days to weeks
 Symptoms limited to vestibular system (balance)
o Laybrinthitis
 Infection of labyrinth (concurrent/recent URI) or result of ototoxic drugs
 Usually viral, rarely bacterial; look for OM/mastoiditis as cause
 Vestibular and hearing symptoms
o Meniere’s disease
 Unilateral or bilateral excess production of endolymph
 Triad: tinnitus, vertigo, sensorineural hearing loss; also N/V
 Ages 40-60; spells last hours but can have long symptom free intervals b/t
attacks
o Ototoxicity
 AG, emycin, minocycline, quinolones, NSAIDs (ASA), loops, cytostatic drugs,
antimalarials
 Vertigo is uncommon with these because the damage they cause is bilateral and
vertigo requires an imbalance of sensory input between the vestibular
mechanisms
o VIII nerve lesions
 Involving VIII directly: meningioma, acoustic schwannoma; gradual onset of
mild vertigo and unsteadiness
 Tumors of cerebellopontine angle: neuromas, meningiomas, dermoids;
deafness, ataxia, ipsilateral facial weakness, cerebellar signs
 Herpes zoster oticus (Ramsay Hunt syndrome): deafness, vertigo, facial palsy;
grouped vesicles on erythematous base inside the ear canal

Central vertigo causes
o Cerebellar or brainstem hemorrhage, infarction or tumor
o Vertebrobasilar insufficiency
o Multiple sclerosis: due to demyelination; look for other signs of MS
o Migraine related dizziness and vertigo: basilar migraine aura—vertigo, decreased
hearing, visual disturbances, dysarthria, diplopia, decreased LOC
Otitis externa





Pruritis, pain, tenderness of external canal, sense of ear fullness, white/cheesy/green discharge,
pulling on ear or pressing tragus causes pain, erythema/edema of external canal
Precipitated by excessive moisture (swimmer’s ear) or trauma
Causes: Pseudomonas aeruginosa, Staph aureus (also Proteus, Enterobacteriaceae, strep)
Treatment
o Mild, nonpurulent: 2% acetic acid solution with hydrocortisone 1%
o Edema and discharge: polymyxin B, neomycin, hydrocortisone (Cortisporin) suspension
or solution; use suspension if TM perforation present b/c less toxic to middle ear
o Avoid water for 2-3 weeks
Malignant otitis externa
o Extension of otitis externa into the mastoid or temporal bone
o Seen in adult diabetics and debilitated and immunocompromised
o Caused by Pseudomonas aeruginosa
o Mortality up to 50%
o Fever, excruciating pain, friable granulation tissue in external canal, edema/erythema of
pinna and periauricular tissue; +/- CN palsies and trismus
o Admit, IV abx, ENT consult
Acute otitis media (AOM)








Epidemiology: kids 6-36 months; winter and spring; often with viral URI; viral > bacterial
Eustachian tube dysfunctionretention of secretionscolonization
Pathogens: S. pneumo (most common), H. flu, M. catarrhalis, S. pyogenes; S. aureus, group B
strep and gram-negative enterics may be seen in neonatal period
Hx: irritability, poor feeding ear-pulling, otalgia hearing loss, URI sx
Exam: TM red/opaque and may be bulging, otorrhea, loss of light reflex, decreased mobility of
TM on pneumatic otoscopy (most reliable)
Tx: WASP (Wait and see prescription): ask parents not to fill rx for 48 hours and only if kid is
worse or no better
o Amoxicillin (high dose): 80-90 mg/kg/day
o Others: augmentin, clindamycin, cefuroxime, macrolides, erythromycin
Beware of infants less than 2 months, especially if fever or toxic; need septic workup and broad
spectrum coverage b/c more likely to be infected by coliforms, GBS, S. aureus
Complications: TM perforation, hearing loss, mastoiditis, labyrinthitis, meningitis, brain abscess,
cavernous sinus thrombosis, facial nerve palsy
Bullous myringitis

AOM with clear or hemorrhagic blisters within the layers of TM; ear pain and mild hearing loss

Etiology: viral or bacterial (same organisms as AOM); not really Mycoplasma pneumonia as
previously thought
Mastoiditis






Complication of untreated or inadequately treated AOM; also complication of leukemia, mono,
sarcoma of temporal bone, Kawasaki disease
S. pneumo (most frequent), H. flu, S. pyogenes, S. aureus
Otalgia, otorrhea, fever, headache, hearing loss, outward and downward displacement of pinna,
posterior auricular (mastoid) tenderness, abnormal TM
Complications: osteitis, labyrinthitis, meningitis, encephalitis, brain abscess, damage to CN VII
Dx with CT temporal bone
Admit, IV abx (ceftriaxone, unasyn), ENT consult, +/- myringotomy with tubes or mastoidectomy
TM perforation






Penetrating object, loud noise, infection (AOM, myringitis), blast injury (explosion, slap,
lightning), rapid pressure change (airplane, scuba), cerumen irrigation complication
Sudden hearing loss, severe otalgia, vertigo
If acute, see irregular borders with blood on edges or in canal; if chronic, smooth margins and
no blood
Most common area to perforate is pars tensa because most anterior and thinnest
If complete hearing loss, nausea, vomiting, vertigo, facial palsyimmediate ENT because might
have concurrent injury to ossicles, labyrinth or temporal bone
Tx: no water in ear, reassurance, analgesia, ENT referral; consider abx if due to infection or
forceful water entry (water skiing) or polluted water; if coexisting otitis externa, topical
antibiotic suspension (not solution) should be used
Ear FB: if live bug in ear, instill lidocaine to kill it prior to removal
Auricular hematoma


Must I&D and place protective pressure dressing to prevent formation of “cauliflower ear”
Reassess in 24 hours for blood reaccumulation; may require repeat drainage
NOSE
Epistaxis



Anterior (Kiesselbach’s plexus on anteroinferior nasal septum)-90%; posterior (sphenopalatine
artery)-10%
Posterior bleeds usually in elderly, hypertensive pts with atherosclerosis
Causes
o Trauma (look for septal hematoma)
o Foreign body
o Nose picking (most common)
o Dry nasal mucosa (winter)
o Allergies
o Nasal irritants (cocaine, nasal sprays)



o Anticoagulants
o Pregnancy
o Change in atmospheric pressure
o Infection (rhinitis, sinusitis)
o Osler-Weber-Rendu (telangiectasias, visceral lesions, family hx)
Jury is out on whether hypertension causes nosebleeds
Treatment
o Direct pressure for 10 minutes
o Blow nose to clear clots
o Couple squirts of neosynephrine
o Control focal anterior epistaxis with silver nitrate (only helpful when bleeding minimal;
hold for 5-10 sec and on one side of septum-cauterizing both sides of septum can
perforate)
o Hemostatic materials-Surgicel, Gelfoam
o Anterior nasal packing
 Leave in place 1-3 days
 Discharge on antistaph abx (Keflex) to prevent sinusitis, toxic shock syndrome
o If posterior bleed, needs posterior packing, admission, ENT consult, supplemental O2
Complications
o Rebleeding/severe bleeding (may require transfusion)
o Sinusitis, otitis media-due to obstruction of sinus ostia and Eustachian tubes by packing
o Toxic shock syndrome
o Pressure necrosis of septum
o Nasopulmonary reflex-with posterior packs; promotes bronchoconstriction and
increases vascular resistancehypoxia, hypercarbia
o Fatal airway obstruction with dislodgement of posterior packing
o Bradycardia, dysrhythmias, coronary ischemia with posterior packing
Nasal fractures






Most commonly fractured facial bone
Diagnose on exam; imaging not required unless other facial fractures suspected
If no deformity, need only analgesia and nasal decongestant
Refer to ENT in 2-7 days (when swelling has subsided) for reduction
Gross angulation can be reduced in ED
If fracture associated with laceration of nasal mucosa or skin, anti-staph abx needed
Nasal septal hematoma



Bluish-purple, grapelike swelling of nasal septum
Need to vertically incise and drain, pack nasal cavity, anti-staph abx, ENT in 24-48 hrs
Failure to drainavascular necrosis of nasal septum-“saddle nose” deformity
CSF rhinorrhea




Fracture of cribriform plate of ethmoid bone
May not develop for days to weeks
Clear nasal discharge following trauma; may have hyposmia/anosmia and headache
Usually unilateral and increased by leaning forward or compression of jugular vein


Dx: CT (most reliable); ring sign (filter paper on bed sheet—2 rings=CSF); dipstick CSF glucose
>30 mg/dl
Tx: place patient in upright position, neurosurgery consult, avoid
coughing/sneezing/blowing/nasal packing
Nasal FB



Most common in kids 2-3 years
May present only with unilateral foul smelling nasal discharge, persistent unilateral epistaxis,
foul body odor
Removal: topical vasoconstrictor and anesthetic facilitates exam and therapy; positive pressure
techniques (have parent blow puff of air into child’s mouth while occluding uninvolved nostril),
suction catheter, forceps, etc
FACE
Sinusitis









Infection of paranasal sinuses (ethmoid, maxillary, frontal, sphenoid); maxillary most common
Results from occlusion of sinus ostia, most commonly caused by local mucosal swelling
secondary to viral URI (also allergic rhinitis, trauma, mechanical obstruction from
tumors/FB/abnormal anatomy)
Less than 3 weeks-acute; greater than 3 months-chronic
Purulent nasal discharge, upper tooth/facial pain, maxillary sinus tenderness, headache,
percussion tenderness, swollen nasal mucosa, opacification on transillumination, nasal
congestion
Acute: same bugs as AOM (S. pneumo, H. flu, S. pyogenes, M. catarrhalis, S. aureus)
Chronic: anaerobes
Usually doesn’t require imaging for initial dx
o Water’s view—sinus opacification, air-fluid levels, >6mm mucosal thickening
o CT—most sensitive/gold standard—sinus opacification, air-fluid levels, >4mm mucosal
thickening, sinus wall displacement
o CT not specific—40% asx and 87% pts with recent URI have abnormal findings
Tx: most resolve spontaneously
o Decongestants –topical and oral
o Consider abx if sx >7 days—amoxicillin, Bactrim, augmentin, doxy, azithromycin for 1014 days
Complications
o Orbital cellulitis (ethmoid)
o Skull osteomyelitis-Pott’s puffy tumor (frontal)—doughy-feeling tender mass
o Meningitis, epidural abscess, subdural empyema, brain abscess (frontal)
o Cavernous sinus thrombosis (sphenoid or ethmoid)
 Also caused by central face infection
 Veins of face, oral cavity, middle ear, mastoid drain to cavernous sinus
 High fever, toxic, eyelid edema, proptosis, chemosis, facial edema, altered
mental status, headache, cranial nerve palsies (III, IV, V1, V2, VI); VI most
commonly affected-lateral gaze palsy
Parotitis/sialolithiasis




Paramyxovirus (mumps)
o Kids 5-15; winter
o Tender bilateral parotid swelling, low grade fever, headache, malaise, clear saliva from
Stensen’s duct
o Can affect gonads (epididymitis, orchitis), meninges (meningoencephalitis), pancreas
(pancreatitis)
o Other complications—transverse myelitis, Guillain-Barre, myocarditis, deafness
Suppurative
o Elderly, debilitated, postop, decreased salivary flow (dehydration, drugs, irradiation)
o S. aureus
o Unilateral parotid swelling, trismus, purulent discharge from Stensen’s duct, fever
o Tx: heat, massage, abx, sialogogues
Sialolithiasis
o Usually submandibular
o Dry mouth, pain, worse at meal times
o 90% seen on xrays
o Can get secondary staph infections
o Tx-massage, analgesics, sialogogues, warm compresses, milking, sometimes surgery
Parotid duct/facial nerve proximity
o A vertically oriented laceration posterior to the corner of the eye and bisecting a line
drawn from the tragus of the ear to the center of the upper lip and involve both the
facial nerve and the parotid ductENT should repair these
Facial fractures



Le Fort fractures
o Rarely occur in pure form; usually in combination
o Beware of airway and concurrent C-spine injury!!!
o Avoid NG tube to avoid intracranial passage
o Check for CSF rhinorrhea
o Le Fort I: horizontal fracture of maxilla at level of nasal floor
 Upper dental arch mobile
o Le Fort II: fractures through maxilla, nasal bones, and infraorbital rim
 Upper dental arch and nose mobile
 Look for injury to infraorbital nerve
o Le Fort III: fractures through zygomaticofrontal suture or zygoma and frontal bone
above nose
 Entire face is mobile; “dish pan” face
Basilar skull fracture
o Skull base involves floor or anterior/middle/posterior cranial fossa
o Battle’s sign, raccoon eyes, hemotympanum, CSF rhinorrhea
o May take hours to develop signs
Mandible fracture
o Second most commonly fractured facial bone
o Ring structure—look for second fracture (>50%)
o Jaw deviates TO the side of fracture, difficulty with mouth opening, decreased ROM,
malocclusion (most sensitive)—tongue blade test
o
o
o



Badly fx mandible can result in airway compromise (tongue support is compromised)
Dx with panorex, CT
Any fracture in tooth-bearing region considered open because periodontal ligament
communicates with oral cavity—antibiotics
o Teeth that are angulated and sometimes avulsed—alveolar fractures
o Lateral crossbite—unilateral condylar fractures
o Displacement of lower incisors, interruption of arch continuity—symphysis fractures
o Ecchymosis or hematoma of floor of mouth—suspicious for mandibular fx
o Anesthesia of lower lip—injury of inferior alveolar or mental nerve secondary to fx
o Admit for airway compromise, excessive bleeding, severely displaced, grossly infected,
comorbid disease
Mandible dislocation
o Can result from trauma, yawning, laughing
o Jaw locked open (condyle locked anterior to articular eminence), difficulty
talking/swallowing
o Bilateral—anterior open bite
o Unilateral—jaw displaced AWAY from dislocation
o Manual reduction with downward pressure applied to posterior teeth to dislodge
condyle; chin then pressed posteriorly so condyle returns to fossa. Protect your
thumbs!!
Tripod fractures (zygomatic-maxillary complex)
o Blow to cheek results in fx of zygomatic arch, zygomaticofrontal suture, infraorbital
foramen. Also, fx of lateral wall of maxillary sinus and orbital floor
o Flattening of cheek, periorbital swelling/ecchymosis, diplopia, step-off deformity of
inferior orbital rim, anesthesia of cheek/upper teeth/lip/gum
Orbital floor fractures (“blowout” fx)
o Orbital fat, bone, extraocular muscles may protrude into maxillary sinus and become
entrapped
o Diplopia, enophthalmos, upward gaze palsy, hypesthesia of infraorbital nerve
o CT, abx if sinus involvement, surgery if persistent enophthalmos, visual changes, muscle
entrapment
MOUTH


Numbering the teeth
o Adults: start from upper right third molar (#1) and around to upper left third molar (#16).
Then down to lower left third molar (#17) and around to lower right third molar (#32)
o Kids: lettered starting on upper right second molar (A) and around to upper left second
molar (J). Then down to lower left second molar (K) and around to lower right second molar
(T)
Nerve blocks
o Supraorbital nerve block: forehead/scalp
o Posterior superior alveolar nerve block: maxillary molars (except portion of first molar)
o Infraorbital nerve block: midface, maxillary incisors, premolars, lower eyelid, upper lip, side
of nose, portion of first molar
o Inferior alveolar nerve block: mandibular teeth, lower lip, chin




Tooth emergencies
o Tooth fractures
 Ellis I: fracture of enamel only; no hot/cold sensitivity; tx elective
 Ellis II: fracture of enamel and dentin; hot/cold sensitivity; see yellow dentin on
exam; tx with calcium hydroxide paste and see a dentist w/in 24 hrs
 Ellis III: fracture of enamel, dentin, pulp; severe pain; see pink dot on exam; moist
cotton or calcium hydroxide paste and see dentist ASAP
o Alveolar osteitis “dry socket”
 Loss of clot with localized osteomyelitis
 2-5 days postextraction (most often 3rd molar)
 Tx: pain meds not that great, nerve block, irrigate socket, pack with iodoform gauze
dampened with eugenol, antibiotics, dentist ASAP
o Dental pain
 Reversible pulpitis with caries: sharp intermittent tooth pain subsides quickly,
worse with cold temps; tx with filling
 Irreversible pulpitis with caries: dull, continuous pain persists minutes to hours,
worse with hot temps; tx with PCN, pain meds, root canal
 Pericoronitis: gum inflammation due to food impaction around crowded,
malerupted or impacted third molars; tx with irrigation and abx if surrounding
cellulitis
 Periapical abscess: most common cause of severe tooth pain. Inflammation,
infection, necrosis of apical portion of tooth; can erode into abscess through cortical
bone. Suspect if tooth severely painful on percussion. Parulis: abscess draining
externally on gums. Tx=abx, extraction
 Periodontal abscess: gum disease is MCC of tooth loss; gum inflammation, calculus,
infection, abscess; tx with I&D, clinda, flagyl
o Avulsed teeth
 Do not reimplant primary teeth—risk of alveolar ankylosis
 Reimplant quickly--1% loss of survival per minute
 Rinse gently with saline; do not brush or will remove periodontal ligament
 Transport medium: saliva, milk, Hank’s solution (best)
 Prophylactic PCN, soft diet, Td
Electrical burns to lip
o Worry about delayed hemorrhage from labial artery 3-14 days later
Acute necrotizing ulcerative gingivostomatitis (“trench mouth”)
o Infection of gingiva precipitated by psychological stress, smoking, poor oral hygiene
o Only periodontal lesion in which bacterial actually invade nonnecrotic tissue
o Fusobacterium, spirochetes
o Pt c/o pain, metallic taste, foul breath, fever, malaise, lymphadenopathy
o Gingivae swollen, fiery red; interdental papillae swollen, ulcerated, “punched out” and
covered with grayish pseudomembrane
o Warm saline irrigation, hexadine rinse, abx (PCN, clinda, flagyl)
o Other conditions with gingival hyperplasia: phenytoin, diabetes, nifedipine, acute leukemia
Aphthous ulcer vs herpetic lesions
o Aphthous ulcers: single circular ulcer <1cm with central yellow area surrounded by
prominent band of erythema. Can occur anywhere in oral cavity EXCEPT lips, hard palate,
attached gingiva. Tx with abx, topical steroids, anesthetic rinses
o



Herpetic lesions: clusters of small vesicles that coalesce. Occurs exclusively on the lips, hard
palate, attached gingiva. Tx with topical acyclovir
Candidiasis vs hairy leukoplakia
o Candidiasis: painless, white, curd-like plaques on erythematous base that SCRAPE off with
tongue blade. Risk: extremes of age, abx, dentures, diabetes, steroids, HIV, chemotherapy
o Hairy leukoplakia: asymptomatic white patches with hair-like projections, often on lateral
tongue, that CANNOT be scraped off with tongue blade. Caused by EBV; 80% develop AIDS
within 3 years
Ludwig’s angina
o Progressive cellulitis of floor of mouth; submandibular, sublingual, submaxillary spaces
involved bilaterally
o Airway obstruction occurs in 33%
o Precipitated by abscess to posterior mandibular molars (most commonly 2nd)
o Anaerobes (Bacteroides) and aerobes (staph, strep)
o Dysphagia, odynophagia, dysphonia, trismus, drooling, neck/sublingual pain, massive
brawny edema of floor of mouth/anterior neck, fever, elevated tongue
o Tx—keep sitting up, airway/airway/airway, ENT, abx (PCN+flagyl, cefoxitin, clinda, unasyn),
ICU
o Complications—Airway compromise is #1; extension to deeper layers of neck or
chestmediastinitis, mediastinal abscess
Masticator space infection
o Bounded by muscles of mastication (masseter and internal pterygoid muscles)
o From extension of anterior space infection (buccal, sublingual, submandibular space) or
infection of third molar
o Strep and anaerobes
o Lateral facial swelling, pain, fever, trismus
o Tx—abx (PCN, clinda), ENT, admission
NECK/THROAT


Croup (laryngotracheobronchitis)
o Most common cause of upper respiratory obstruction in childhood
o Usually 6 mo-3yrs, male>female; caused by virus (parainfluenza); fall and winter
o Affects glottis and sublottic tissues
o Preceding viral URI for 2-3 days, gradually increasing cough; insidious onset, nontoxic
appearing
o Barking cough (worse at night), hoarse voice, respiratory distress (tachypnea, dyspnea,
retractions, stridor), nasal discharge, low-grade fever
o CXR—subglottic narrowing of tracheal air column-“steeple sign”
o Tx--cool mist, O2, hydration, racemic epi if stridor at rest (observe for rebound), steroids
(decadron 0.15-0.6 mg/kg IM), no antibiotics
o Admit—persistent stridor at rest, unable to tolerate po, unreliable social, incomplete
response to racemic epi, multiple doses of racemic epi, severe presentation
Epiglottitis
o Adults >children since Hib vaccine; peak incidence 20-40 yrs; nonseasonal
o S. pneumo (also GABHS, toxic fumes, superheated steam, gasoline ingestion, angioedema)
o




Affects supraglottic tissues (epiglottis, aryepiglottic folds, arytenoids in kids; can extend to
prevertebral soft tissues, valleculae, base of tongue, soft palate in adults)
o Usually no prodome in kids; adults have 1-2 day URI; progression is rapid (adults can be
insidious)
o Toxic appearance, tripod position, “hot potato” voice, sore throat, dysphagia, drooling,
respiratory distress (tachypnea, dyspnea, inspiratory stridor), restlessness, tachycardia out
of proportion to fever; can be less impressive in adults
o Unremarkable oropharynx exam (if it is done)
o Diagnosis ideally in OR—cherry red epiglottis; do not disturb a child for exam and
radiographs; notify ENT, anesthesia
o If less severe, lateral xrayenlarged “thumbprint” epiglottis
o Tx—ceftriaxone, ENT, ICU
Bacterial tracheitis (membranous laryngotracheobronchitis)
o Bacterial infection of subglottic region with copious tracheal secretions; superimposed upon
viral URI
o Has features of both croup and epiglottitis
o Ages 3 mo -10 yrs (usually <3 yrs); nonseasonal
o S. aureus (also H. flu, S. pyogenes, M. catarrhalis)
o Prodrome of URI or croup then rapid progression, toxic appearance, barking cough,
respiratory distress (stridor and retractions), high fever
o Direct visualization confirms dx; should be done by ENT in OR; see pseudomembranes and
purulent secretions
o Tx—O2, ENT/anesthesia, abx (-cillin plus ceftriaxone), ICU
Parapharyngeal abscess
o Space lateral to pharynx and medial to masticator space; extends from base of skull to hyoid
bone
o Precipitated by dental, pharyngeal, tonsillar infection
o Anaerobes and aerobes
o Neck pain, sore throat, dysphagia, odynophagia, unilateral swelling of neck/angle of
mandible, restricted neck movement, torticollis, pharyngitis, bulging of pharyngeal wall,
drooling, cervical adenopathy, fever
o Tx—airway, IV abx, ENT, steroids, ICU
o Complications—airway obstruction, spread (CN IX-XII neuropathies, carotid artery
extension, septic thrombosis of internal jugular vein)
Peritonsillar abscess
o Most common deep head/neck infection
o Between tonsillar capsule and superior constrictor muscle; complication of untreated or
partially treated suppurative tonsillitis, also mucosal trauma, odontogenic spread
o Teenagers/young adults; rare in kids <12; males>females
o Can occur after tonsillectomy
o Polymicrobial (GABHS, strep, H. flu, staph, bacteroides, fusobacterium)
o Unilateral sore throat, dysphagia, odynophagia, drooling, “hot potato” voice, inferior and
medial displacement of tonsil, deviation of uvula to opposite side, ear pain, trismus, fever,
tender cervical lymphadenopathy, foul breath
o Abx (PCN, unasyn, clinda, cefoxitin, emycin), decadron, needle aspiration (not deeper than 1
cm and stay medial to avoid laterally located carotid artery)
Retropharyngeal abscess
o Anterior to prevertebral fascia and posterior to pharynx
o
o
o




Kids 6 mo-3yrs (b/c large retropharyngeal nodes prone to infection; these involute w age)
S. aureus, GABHS, anaerobes
Usually follows URI, pharyngitis, OM, wound infection s/p penetrating injury to posterior
pharynx (popsicle)
o Sore throat, dysphagia, labored respirations, stridor, muffled voice, fever, unilateral bulging
of posterior pharyngeal wall, tender cervical adenopathy, toxic, sit with neck in extension
o Soft tissue neck xray done in sniffing position—neck in extension and during inspiration
 normal retropharyngeal space <1/2 width of adjacent vertebral body; RPA will be
thickened
o Tx—airway, abx (-cillin + flagyl, clinda, cefoxitin, unasyn), ENT, ICU
o Complications—airway obstruction, aspiration, spread (mediastinum, vessels), sepsis
Prevertebral infection
o Space between prevertebral fascia and cervical spine
o Usually from cervical osteomyelitis (staph, TB)
o Bilateral bulging of pharynx, tenderness of C-spine
o Xray—retropharyngeal swelling or osteo of spine
o Tx—abx, neurosurgery
Infectious mononucleosis
o Caused by Epstein-Barr virus (human herpes virus 4)
o 10-25 yrs
o Sore throat, fever, malaise, fatigue, exudative pharyngitis, tender POSTERIOR cervical
adenopathy, splenomegaly, Kehr’s sign (left shoulder pain), atypical lymphocytosis, elevated
transaminases
o Monospot helpful if positive
o If given ampicillin, 95% get EBV-induced antibodies to it and a rash
o Care regarding potential splenic rupture is appropriate
o Steroids if: airway obstruction, severe hemolytic anemia, thrombocytopenia, neurologic
(encephalitis, GBS)
Diphtheria
o Secondary to noncompliance with DPT immunization; spread by contact with respiratory
secretions; incubation one week
o Corynebacterium diphtheria=club-shaped Gram + bacillus
o Infectious invasiontissue necrosis produces pseudomembrane in posterior pharynx; can
lead to airway obstruction
o ToxinCV (myocarditis/AV block/endocarditis); nephritis; hepatitis; neuro (eyes-strabismus,
ptosis; palate-first muscles affected; limb paralysis; loss of DTRs)
o Sore throat, fever, malaise, toxic, tachycardia, hoarse/muffled/absent voice, exudative
pharyngitis, white/gray adherent pseudomembrane, marked cervical adenopathy (“bull
neck”), fetid breath (“dirty mouse”)
o Culture on Loeffler’s or tellurite media
o Tx—Abx (PCN, emycin), diphtheria antitoxin
o Asymptomatic, immunized contacts—Td booster
o Asymptomatic, partially immunized or unimmunized—one dose IM PCN and begin
immunization series
Group A beta-hemolytic strep (GABHS)
o Late winter, crowded conditions; <20 yrs; rare in <3 yrs
o Centor criteria: fever, tender cervical adenopathy, exudative tonsillitis, no cough
o Abdominal pain, vomiting, headache common in kids
o
o


Strep screen helpful if positive
Tx—10 days PCN or single IM benzathine PCN; cephalosporins and azithro usually reserved
for recurrent; steroids
o Complications
 Suppurative: PTA, OM, sinusitis, necrotizing, fasciitis, bacteremia, meningitis, brain
abscess; abx decrease incidence
 Nonsuppurative
 Strep toxic shock syndrome
 Glomerulonephritis-abx do not decrease incidence
 Rheumatic fever-abx within 9 days prevent this
o Jones criteria for diagnosis (need 2 major or 1 major and 2 minor
PLUS evidence of recent strep infection
o Major criteria
 J (Joints): migratory polyarthritis of large joints, usually
starting in legs and migrating up
 O-imagine a heart (carditis): CHF, pericarditis, new murmur
(mitral valve damage)
 N (nodules): subcutaneous-painless, firm collections on
back of wrist, outside elbow, front of knees
 E (erythema marginatum): begins on trunk or arms as
macules and spreads outward to form snakelike ring while
clearing in middle. Never starts on face; worse with heat
 S (Syndenham’s chorea): St. Vitus’ dance; rapid movements
of face and arms
o Minor criteria
 Fever
 Arthralgias
 Labs-ESR, CRP, leukocytosis
 EKG-prolonged PR interval
 Previous rheumatic fever or rheumatic heart disease
o Evidence of Group A Strep infection
 Positive throat culture, elevated or rising ASO or DNAase
titer, recent scarlet fever
Airway obstruction
o Labored respirations: tachypnea, retractions, nasal flaring
o Stridor
 Inspiratory: (supraglottic or glottic) indicates obstruction above or at the larynx, ex.
epiglottis
 Biphasic: (subglottic) indicates obstruction below the larynx, ex. croup
 Expiratory: indicates bronchial or lower tracheal obstruction
o Hoarseness, dysphagia, coughing, cyanosis
Foreign body aspiration
o Kids 1-4 yrs; males>females
o Peanuts most common agent; hot dogs most common cause of fatal aspiration
o Narrowest part of airway is where FB get lodged
 Adults—vocal cords
 Kids—cricoid cartilage
o Presenting signs
o
o
 Aphonia: complete upper airway obstruction
 Stridor: incomplete upper airway obstruction
 Wheezing: incomplete lower airway obstruction
 Coughing: incomplete obstruction at larynx or distal airways
Is the coin in the esophagus or airway???
 Esophageal FB: lies in frontal/coronal plane and will be round in PA view
 Tracheal FB: lies in sagittal plane and will be round in lateral view (on edge in PA
view)
Partially obstructing FB
 Seen best on expiratory films
 “ball valve” effect: hyperinflation of obstructed lung due to air trapping, shift of
mediastinum away from affected side
