emergency medicine pocketbook

• M:F, 2:1; Caucasian > Hispanic > Asian > African; peak incidence 40–60 y/o
• Renal colic (acute, spasmodic, unilateral flank pain radiating to groin/testes/labium)

& visceral sxs (N/V/diaphoresis)
• Distal stones may cause lower abdominal pain & lower urinary tract sxs (dysuria,

frequency, hematuria)
• PMH: FH nephrolithiasis, hyperparathyroidism, sarcoidosis, RTA, malignancy,

Crohn’s, jejunoileal bypass, recurrent UTI, gout, DM2, HTN, structural urologic
abnormalities
• Meds: Indinavir, loop/thiazide diuretics, laxatives, carbonic anhydrase inhibitors,
ciprofloxacin, sulfonamides have been a/w drug-induced calculi

Physical Exam

• Fever? Tachycardic? Generally uncomfortable appearing, diaphoretic, cool/clammy
skin

• CVA tenderness; lower abdominal/pelvic tenderness (if stone has migrated)
• Assess for midline spinal TTP, acute abdomen, etc. which suggest alterative dx

Evaluation

• UA (may show +RBCs, though sens 84% spec 48% for stone; proteinuria,
crystalluria), Ucx

• Consider BUN/Cr; CBC usually nonspecific & not helpful
• Imaging:
Renal U/S (sens 96%, spec 100% for stone >5 mm; sens 78%, spec 31% for all

locations):
• May be initial radiographic exam w/ high pretest probability or if CT not possible

(pregnancy); esp useful for detection of hydronephrosis or ureteral dilatation; not
sens stones <5 mm; can be done point-of-care
Nonenhanced helical CT (sens 94–100%, spec 92–100%)
• Useful as initial radiographic exam, particularly w/ 1st presentation of suspected
stone or low-moderate probability; able to make alternative diagnoses; modality of
choice when available
*Note: Indinavir stones not visible on CT

Treatment

• Data suggests IVFs likely not useful for acute renal colic from urolithiasis
• Pain control: NSAIDs (ibuprofen 600 mg PO TID or ketorolac 15–30 mg IV if unable to

take PO [caution in renal insufficiency]) & morphine 0.1 mg/kg × 1 then titrated for
further relief
• Medical expulsive therapy: Tamsulosin 0.4 mg PO QD × 14 d or until stone passage
(effective for distal ureteral stone >4 mm w/ respect to stone expulsion rate & time to
expulsion); other alpha-antagonists (doxazosin, terazosin, alfuzosin) & nifedipine may
also be effective
• Urology consult: For concomitant infection, renal insufficiency, or low likelihood of
stone passage (>10 mm)

Disposition

• Home: Adequate pain control in ED, nl Cr; f/u w/ urology in 24–48 h if stone >5 mm
(see below)

• Admit: Intractable pain, unable to tolerate POs, renal failure, infection, renal
transplant, single kidney, comorbid conditions (DM, baseline CRI), infected stone w/
obstruction

Pearls

• Presence or absence of hematuria alone cannot be used to diagnose or exclude
nephrolithiasis

• Stones <5 mm 46–86% chance of passage, b/w 5 & 8 mm have a 30–50% chance, >8
mm have <20% chance

• Send pts home w/ strainer, esp 1st-time stone formers for stone analysis
• Cx: Obstructed infected kidney (urologic emergency requiring urgent decompression),

renal insufficiency, failed expulsion

HEMATURIA

Approach to the Patient

Definition

• Hematuria defined as >5 RBCs/hpf in urine sediment, although variably defined in
the literature

• Hematuria must be distinguished from pigmenturia (discoloration of urine).
Pigmenturia can be caused endogenously by melanin, porphyrins, bilirubin,
myoglobin, or hemoglobin or exogenously by medications (ie, warfarin, rifampin,
phenazopyridine, phenytoin, etc.)

History

• Onset (sudden vs. chronic)? Dysuria/urinary frequency/renal colic? During entire or
part of urine stream? (hematuria at beginning of urination → urethral; throughout
urination → upper urinary tract or proximal bladder; end of urination → bladder neck
or prostatic urethra)

• Painless hematuria should raise suspicion for genitourinary malignancy
• ROS (fever, weight loss, night sweats, rash, sore throat, abdominal pain, N/V, recent

viral infection or UTI; trauma; excessive exercises; pelvic radiation)
• PMH (kidney stones, HTN, cancer, congenital kidney dz, vascular dz, bleeding

diathesis, SCD, hereditary spherocytosis)
• MEDS:

• Drug that cause pigmenturia: Warfarin, rifampin, phenazopyridine, phenytoin,
azathioprine, deferoxamine, doxorubicin, riboflavin

• Drugs that cause myoglobinuria: Amphotericin B, barbiturates, cocaine, diazepam,
ethanol, heroin, methadone, statins

• Drugs that cause hematuria: NSAIDs, anticoagulations, busulfan, cyclophosphamide,
OCPs, quinine, vincristine

• Social (smoking, benzene or aromatic amine exposure)

Physical

• Evaluate for HTN, petechiae, arthritis, rash
• Assess for suprapubic & CVA tenderness; thorough GU exam including prostate exam
• Postvoid residual if concern for urinary retention

Evaluation

Key question: Is this truly hematuria?
• Urine dipstick + blood (can be seen w/ hematuria, hemoglobinuria, myoglobinuria,

or other pigmenturias); urine sediment necessary to confirm >5 RBCs/hpf as well as
identify protein, RBC casts (suggests glomerulonephritis), & crystalluria (suggests
urolithiasis)
• Other urine studies: Urine cytology
• CBC, BUN/Cr, coags (if isolated hematuria—erythrocytes in sediment, but no protein
—suggests bleeding diathesis)
• Consider renal U/S, contrast-enhanced CT, CT urography; cystoscopy

Disposition

• Large, gross hematuria may warrant continuous monitoring of HCT & urology eval. If
microscopic, can obtain further outpt eval by nephrology or urology.

ACUTE RENAL FAILURE

Approach to the Patient
Definition & Staging

• AKI is defined as any of the following:
• Increase in serum Cr by ≥0.3 mg/dL (≥26.5 μmol/l) w/i 48 h; or
• Increase in serum Cr by ≥1.5 times baseline, which is known or presumed to have

occurred w/i prior 7 d; or
• Urine volume <0.5 mL/kg/h for 6 h
• AKI is staged for severity according to the following criteria:

• AKD is defined as any of the following:
• AKI
• GFR 60 mL/min/1.73 m2 for <3 mo
• Decrease in GFR by ≥35% or increase in serum Cr >50% for <3 mo

• CKD is defined as GFR <60 mL/min/1.73m2 for >3 mo
• CKD is classified by Cause, GFR & Albuminuria (CGA) staging

• Cause: Is based on the presence or absence of systemic dz & location w/i the kidney
of observed or presumed pathologic-anatomic finding

• GFR: GFR categories are assigned as follows

• Albuminuria: Based on albumin excretion rate & not practical to calculate in ED, but
may be referenced as part of pt’s problem list

• Equations for estimation of GFR:
• Modification of Diet in Renal Disease (MDRD)

• Estimated GFR (mL/min/1.73 m2) = 1.86 × (PlasmaCr)1.54 × (age)0.203

• Multiply by 0.742 for women
• Multiply by 1.21 for African American
• Cockcroft–Gault equation
• Estimated Cr clearance (mL/min) = [(140 – age) × (weight, kg)]/(72 ×
PlasmaCr)

• Multiply by 0.85 for women

History

• ARF is usually asymptomatic & diagnosed when labs reveal renal abnormalities
• Sxs may include decreased urine output, weight gain, fluid retention (peripheral

edema, anasarca, ascites), fatigue, anorexia, N/V, pruritus, altered sensorium,
thirst/orthostasis (prerenal)
• ROS (fever, rash, flank pain, hematuria)
• PMH: Baseline renal impairment, CHF, liver dz, SLE, multiple myeloma
• MEDS (ACEI/ARB, NSAIDs, aminoglycosides, other abx, cisplatin, amphotericin B,
diuretics)

Physical

• Assess volume status; myoclonus, pericardial or pl rub, rash, mental status, edema
• Stigmata of CHF, liver dz, collagen vascular dzs

Evaluation

• CBC, Chem 10 (BUN/Cr ratio), serum osmolality; consider VBG w/ STAT potassium
• Urinalysis/sediment, urine lytes (urine Na, urine K, urine Cr, urine osmolality)

• FENa% = (Urine Na × Plasma Cr)/(Plasma Na × Urine Cr) × 100
• Consider LFTs, BNP if indicated
• EKG for cardiac electrical instability from potential electrolyte abx
• Consider point-of-care cardiac, IVC, renal U/S
• Imaging: Renal U/S (r/o obstruction, assess flow); consider CT abdomen if c/f pelvic

mass, Doppler U/S of renal vasculature
• Other studies: Renal biopsy

Treatment

• Prerenal: Correct volume status/perfusion pressure (IVFs, pressors, PRBCs if indicated,
diuresis/inotropes if cardiorenal)

• Intrinsic: Eliminate nephrotoxins, treat underlying cause, consider glucocorticoids
• Postrenal: Transurethral or suprapubic catheter placement; may require ureteric stents

or percutaneous nephrostomy tube placement
• Consider sodium bicarbonate if pH <7.2 or HCO3 <15 mmol/L as bridge to dialysis

Indications for Emergent Dialysis and Renal Replacement Therapy “A, E,
I, O, U”

• Acidosis (pH < 7.1)
• Electrolyte imbalance (hyperkalemia, hypocalcemia, hyperphosphatemia)
• Intoxication (lithium, salicylates, ethylene glycol, methanol, among others)
• Overload (volume overload)
• Uremia (pericarditis, encephalopathy, neuropathy, bleeding)

Disposition

• Home: Mild prerenal azotemia may be adequately treated w/ hydration; pts w/
postobstructive ARF can be sent home if obstruction is relieved (ie, w/ bladder
catheter) & no significant comorbidities

• Admit: Pts w/ uremia, significant electrolyte abnormalities, volume overload, severe
metabolic acidosis, unexplained ARF

Pearl

• Cx: Intravascular volume overload, hyponatremia, hyperkalemia, hyperphosphatemia,
hypocalcemia, hypermagnesemia, metabolic acidosis, uremia, anemia, arrhythmias

Guideline: Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury
Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int
Suppl. 2012;2:1–138.

TESTICULAR TORSION/TORSION OF TESTICULAR APPENDIX

History

Testicular Torsion

• Sudden onset pain (± swelling) in scrotum w/ radiation into abdomen; pain may be
intermittent; N/V; most commonly in puberty

Torsion of Appendix

• Similar presentation to testicular torsion but pain can be localized to superior pole of
testicle; benign condition

Physical Exam

Testicular Torsion

• Ill appearing, very tender/swollen/elevated testicle that may lie horizontally or
anteriorly rotated; no relief w/ elevation of testicle (negative Prehn sign); ipsilateral
loss of cremasteric reflex

Torsion of Appendix

• Normal-appearing testes; tenderness localized to superior pole of testicle; may have
nodular “blue dot” at superior pole of testicle

Evaluation

• Labs: Preop labs if surgery anticipated
• Imaging: Scrotal duplex U/S to assess flow to testicle, but imaging should not delay

time to OR; HRUS if duplex equivocal

Treatment

• Consult urology immediately if concern for testicular torsion as time to OR is critical
for survival of testicle; if delay to OR, may attempt manual detorsion in medial to
lateral direction (‘open book” technique)

• Analgesia
• Antiemetics

Pearls

• 100% salvage rate if detorsion occurs <6 h
• Continuous pain >24 h is a/w an infarcted testicle

PHIMOSIS AND PARAPHIMOSIS

History

Phimosis

• Inability to retract the distal foreskin over the glans penis; “ballooning” of the
prepuce during urination; painful erection, preputial pain, weak urinary stream

Paraphimosis

• Pain, swelling of glans w/ entrapment of a retracted foreskin behind the coronal
sulcus; a/w vigorous sexual activity & chronic balanoposthitis

• Occurs exclusively in uncircumcised males & is a urologic emergency
• Pediatric: Often seen w/ forceful retraction or forgetting to reduce foreskin after

bathing/voiding; irritability may be the only sign in nonverbal children

Physical Exam

Phimosis

• Inability to retract foreskin proximally over glans penis

Paraphimosis

• Foreskin retracted behind the glans & cannot be replaced to nl position; proximal
shaft is soft (unless there is accompanying infection) w/ glans appearing
erythematous/edematous & eventually blue/black & firm

Treatment

• If significant manipulation is expected, you may perform a penile block. On the dorsal
aspect of the penis in the 2- & 10-o’clock positions, deposit 1% lidocaine; subsequently
complete a ring block by depositing anesthetic circumferentially around the proximal
shaft.

Phimosis

• No acute intervention needed unless infection suspected. Consider topical steroids
(0.05–0.1% betamethasone) × 4–6 wk for mild–moderate cases.

Paraphimosis

• Compress the foreskin & glans by snugly grasping it w/ the palm of the hand & apply
pressure for several minutes. Other methods to reduce edema include:
• Dundee micropuncture technique: Make ∼20 puncture holes in edematous foreskin
tissue w/ a small needle (27 gauge) & express the fluid
• Hyaluronidase technique: Inject 1 cc of hyaluronidase (150 U/mL) using a tuberculin
syringe into the site of edematous foreskin
• Sugar technique: Soak a swab of 50 mL of 50% dextrose solution & leave it wrapped
around the foreskin for 1 h

• Attempt manual reduction by placing index fingers on dorsal border of glans behind
retracted prepuce & thumbs on glans; may facilitate w/ ice, elastic bandage over glans
or spreading hyperosmolar agents (such as sugar/dextrose) over glans to reduce
swelling

• Consult urology if manual reduction unsuccessful

Disposition

• Home: Phimosis ± abx for accompanying infection; paraphimosis if skin is in the nl
position. Urology f/u for all paraphimoses.

• Admit: Paraphimosis not reduced by conservative methods

Pearls

• Educate parents/caretakers of children on importance of avoiding forcible retractions
& of gentle reduction of foreskin after bathing & voiding

• Paraphimoses that are not immediately treated are at risk for necrosis &
autoamputation

PRIAPISM

Definitions

• Priapism is defined as a prolonged erection lasting generally >4 h in the absence of
sexual stimulation

• Ischemic (low-flow) priapism is the most common subtype & is due to painful
engorgement of the corpora cavernosa. This can lead to intracavernosal acidosis,
sludging of blood, thrombosis of cavernal arteries, & impotence

• Nonischemia (high-flow) priapism is rare, painless, & is caused by increased arterial
inflow to the penis as a result of traumatic arterial–cavernosal fistulas

History

• Painful, persistent erection lasting >4 h, not relieved by ejaculation
• RFs: SCD, leukemia, urogenital malignancies (prostate, bladder), CVA, spinal cord

injury antihypertensives (hydralazine, prazosin, doxazosin), antidepressants
(trazodone, fluoxetine, sertraline), antipsychotics (phenothiazines & atypicals),
phosphodiesterase inhibitors, cocaine, toxins (scorpion, black widow, CO)

Physical Exam

• Obvious erection, generally involving only the corporal cavernosa & flaccid corpora
spongiosum

Evaluation

• Labs: Preoperative labs if contemplating OR
• May send a blood gas from penile aspirate

Treatment

• Pain control
• To reduce flow/vasoconstriction:

• Oral/IM: Terbutaline 5 mg PO × 1; terbutaline 0.25–0.5 mg IM × 1 (unclear
benefit)

• Intracavernosal phenylephrine injection: Using a 25- or 27-gauge needle (or
tuberculin syringe), inject 0.2–0.5 mg of phenylephrine into corporus q10–15min
(maximum 4–5 doses) 2 cm distal to origin of shaft on dorsal penis at 2- or 10-o’clock
position

Note: Must dilute phenylephrine solution. Take phenylephrine 1% solution (10 mg/mL) &
extract 1 mL (10 mg) from solution. Add this 1 mL to 9 mL of saline, which will give you 1
mg/mL of phenylephrine solution. You can then extract 0.2–0.5 mL (0.2–0.5 mg) of this for
intracavernosal injection.

• If unsuccessful, aspiration/irrigation technique:

• Perform penile nerve block: On the dorsal aspect of the penis in the 2- & 10- o’clock
positions, deposit 1% lidocaine; subsequently complete a ring block by depositing
anesthetic circumferentially around the proximal shaft

• Prep & drape penis in sterile fashion
• At 2- or 10-o’clock position insert a 16–18 g needle (also consider 18-gauge dialysis

butterfly access needle), & using a 10–30 mL syringe, slowly aspirate while milking
corporus w/ other hand until return if bright red blood & detumescence occurs
• If this fails, you can attempt to irrigate by injecting 20–30 mL of phenylephrine &
NS solution (10 mg phenylephrine in 500 mL NS) as exchange for 20–30 mL aspirate
• W/ sickle cell crisis: IVFs, O2, pain control, consider exchange transfusion

• Consult urology for refractory priapism (may necessitate surgical decompression)

Disposition

• Recommended to observe for at least 2 h to assess for recurrence
• Home: Once detumescence achieved. Recommended to d/c w/ 3-d course of oral α-

adrenergic agent (pseudoephedrine)
• Admit: If priapism not responsive to ED tx

Pearls

• >12 h of priapism a/w onset of tissue demise w/ >24 h a/w permanent impotence
• Cx: Hematoma, infection, systemic absorption of vasoactive agents (severe HTN),

recurrence, impotence (this risk should be discussed w/ pt & is a possibility despite
efforts & timeliness of therapy)

EMERGENCIES IN DIALYSIS PATIENTS

Definition

• Any complication involving dialysis catheters or fistulas as well as infection,
electrolyte imbalances, cardiac complaints, or signs of fluid overload among others

• Common complaints & special considerations include:

Approach to the Patient

History

• Should focus on assessing for common causes of respective chief complaints, w/
attention to special considerations unique to ESRD pt

Physical

• Attention to abnl vital signs
• Pulmonary & cardiac exam including assessment of friction rub, rhonchi, & rales
• Abdominal exam, esp in pts w/ PD catheters
• Extremity exam & JVP for signs of fluid overload
• Skin exam for e/o calciphylaxis
• Assess graft site for thrill & signs of bleeding, infection, edema, & bruising; assess

tunneled catheter site for e/o cellulitis or underlying abscess formation

Diagnostics

• CBC, Chem 10; consider ABG w/ STAT potassium & to assess acid–base status
• Consider LFTs, BNP, cardiac markers if indicated
• Consider contacting PD access nurse for sample of PD dialysate fluid (cell count [WBC

>50–100 cell/mm3 suggest peritonitis], gram stain, culture)
• EKG for cardiac electrical instability from potential electrolyte abx, ischemia
• Consider point-of-care cardiac & lung US & FAST exam to assess for effusion & ascites,

respectively
• Imaging: Appropriate imaging for respective complaints; Doppler imaging of AF

fistula site if concern for thrombosis

Treatment

• Refer to appropriate sections for tx of conditions noted above
• Special considerations:

• Peritonitis: Vancomycin 2 g AND cefepime/ceftazidime 1 g each added to 1 bag of
dialysate infused into & allowed to dwell in the peritoneal cavity for 6 h

• Dialysis disequilibrium syndrome: Reduce ICP (HOB elevation >30°, hyperosmolar
therapy [mannitol, hypertonic saline], euglycemia, euthermia, eunatremia, MAP >
65, CO2 40 mmHg, CPP 50–70 mmHg); renal consult

• Clotted AV graft/fistula: Immediate vascular surgery consultation for consideration
of catheter-directed thrombolysis, pharmacomechanical thrombolysis, surgical
thrombectomy

• Clotted Vascular Access Catheters: Consult institutional policies; if feasible,
attempt catheter-directed tPA via infusion of 2 mg tPA into occluded lumen & fill
remainder w/ saline. After 15 min, inject 0.3 mL saline to move the active enzyme
toward the tip of the catheter. After another 15 min, inject another 0.3 mL to move
the active enzyme toward the tip of the catheter. After another 15 min, try to
aspirate catheter. If unsuccessful, send pt for catheter exchange.

• Vascular Access Hemorrhage: Apply direct pressure for 10–15 min; if occurs w/
hours of dialysis, consider protamine 1 mg per 100 U heparin received (or 10–20 mg
if dose unknown) to reverse heparin anticoagulation; consider application of
gelfoam, surgical, or other hemostatic agent; immediate vascular surgery
consultation for uncontrolled hemorrhage

Disposition depends upon presenting complaint, but most will invariably require
admission

Pearls

• BP measurement over & use of AV fistula sites for blood draw/administering therapy
is contraindicated

• BNP levels are not reliable in diagnosing fluid overload/HF in dialysis pts as basal
BNP levels are typically elevated & increased BNP levels from baseline may not
correlate w/ clinical HF

• Chronically elevated troponin common & a/w increased mortality; makes assessment
of ACS challenging; however, the National Academy of Clinical Biochemistry (NACB)
recommends a 20% change in troponin concentration from baseline for Dx of AMI

VAGINAL BLEEDING

Approach to the Patient
History

• Onset? Painful? Quality (dark vs. clots vs. bright red)? Quantity (number of pads/h)?
Pregnant or postpartum? LMP? Last intercourse? Use of protection? Gravida and
parity? Trauma? ROS: Dizziness or lightheadedness? Presyncopal? Other bleeding?
Fever? PMH (clotting disorder, hypo- or hyperthyroid, liver dz) MEDS (anticoagulants
or antiplatelet tx, contraceptives, hormonal therapy), SOCIAL (domestic violence)

Diagnostics

• CBC, type and screen (Rh), urine hCG; quantitative hCG if pt is pregnant; crossmatch
(if heavily bleeding); consider pelvic U/S

Pearls

• Average pad holds 5–15 cc of blood
• Average tampon holds 5 cc of blood

Miscarriage
History

• Vaginal bleeding ± passage of clots or tissue at <20 wk; abdominal pain/cramps

Physical Exam

• Speculum and bimanual inspection to assess for passage of blood/POC and whether os
is open or closed. (If copious bleeding, remove POC w/ gentle traction to allow uterus
to clamp.)

Evaluation

• Labs: UA, quant hCG, HCT, type and screen (crossmatch if HD unstable). If products
expelled, send to pathology.

• Imaging: Pelvic U/S to determine location of pregnancy

Classification of Miscarriage

• Threatened: Os closed, no passage of POC, viable fetus w/ heart tones, mild
cramping/bleeding (∼20% will eventually abort)

• Inevitable: Os dilated and effaced; POC not passed; cramps, moderate bleeding

• Complete: POC expelled, cervical os closed; little cramping or bleeding
• Incomplete: Clots and tissue in cervical os w/ os open; severe cramps and bleeding
• Missed: Uterus fails to expel fetus for >2 mo, os closed, no heart tones, pregnancy

test negative

Treatment

• ED:
• Supportive management: IVFs, O2, monitoring, position on L side

• Blood products: Transfuse if HD unstable
• Medication therapy:

• Oxytocin: 20 U in 1 L NS for incomplete or inevitable abortion
• Rh immunoglobulin: 300 mcg if Rh-negative
• Consult: Gyn service if HD unstable or if need for D&C anticipated (inevitable,

incomplete or missed abortion)
• Home management:

• Hormonal therapy: Methotrexate may be indicated under guidance of OB/Gyn
• Abx: Consider prophylaxis w/ doxycycline or testing for STD if discharging home w/

open os

Disposition

• Home: Stable pts w/ complete or threatened abortion; f/u w/ OB/Gyn w/i 72 h to
monitor hCG levels

• Admit: Uncontrolled bleeding or pts requiring immediate D&C

Pearl

• Threatened and missed abortions can only be distinguished by pelvic U/S

Ectopic Pregnancy

History

• Abdominal pain, vaginal bleeding. Most often presenting 6–10 wk after LMP.
• RFs: H/o PID, IUD, fertility tx, recent abortion or prior ectopic

Physical Exam

• Assess for HD stability. Signs of peritonitis if rupture has occurred. Speculum and
bimanual exam may reveal pelvic tenderness and/or adnexal mass.

Evaluation

• Labs: Quant hCG, HCT, Rh screen, PT/PTT and type and crossmatch 4 U (if HD
unstable)

• Imaging: Pelvic U/S; if HD unstable, FAST exam to assess for free fluid

Treatment

• Supportive: 2 large-bore IVs, IVF resuscitation, monitor
• Transfusion: If HD unstable

• Medications: Rh immunoglobulin 300 mcg if Rh-negative
• Consult: Urgent Gyn eval for consideration of medical (MTX) vs. surgical

(laparoscopy/laparotomy) tx options

Placenta Previa and Abruptio Placentae

History

• Placenta previa: Painless, bright red, vaginal bleeding usually after 28 wk (from
placental implantation in adjacent to or over os). RFs: Multiple gestation, multiparity,
advanced maternal age, previous placenta previa/C-section, maternal smoking or
cocaine

• Abruptio placentae: Painful, dark red bleeding (80%); may also present w/ signs/sxs
of DIC. RFs: Eclampsia, DM, renal dz, HTN, abdominal trauma

Physical Exam

• Check fundal height, contractions, and uterine tenderness:
• Firm/tender uterus = placental abruption until proven o/w

• AVOID SPECULUM AND VAGINAL EXAM

Evaluation

• Labs: CBC, Chem 7, LFTs, PT/PTT, fibrinogen (r/o DIC), UA, type/crossmatch 2 U
• Imaging: Doppler U/S (fetal heart tones); bedside abdominal U/S to assess placenta

and signs of fetal movement, though may not always detect abruption

Treatment

• Supportive: Place on L side, 2 large-bore IVs, IVF resuscitation, monitor pt and fetus
• Transfusion: Blood products ± FFP (HD unstable or signs of DIC)
• Medications: Rh immunoglobulin 300 mcg if Rh-negative, magnesium for fetal

neuroprotection if emergent delivery under 32 wk
• Consult: Urgent Gyn eval for possible STAT C-section

Disposition

• Admit: All pts to the OB service even if HD stable for close monitoring

Retained Products of Conception and Postabortion Sepsis

History

• Retained POC: Cramping, heavy bleeding
• Postabortion sepsis: Cramping, bloody or purulent d/c, fever

Physical Exam

• Fever, vaginal bleeding or purulent/bloody d/c, uterine tenderness

Evaluation

• Labs: Quant hCG, type/crossmatch/preop labs

• Imaging: Pelvic U/S

Treatment

• Supportive: Stabilize (see Sepsis chapter), correct coagulopathy/anemia
• Abx: If suspected infection, (Clindamycin 900 mg IV q8h PLUS gentamicin 2 mg/kg IV

× 1 then 1.5 mg/kg q8h) OR (cefoxitin 2 g IV q8h PLUS doxycycline 100 mg IV q12h)
• Consult: Gyn service for D&C

Disposition

• Admit: All pts to OB/Gyn for D&C

Postcoital Bleeding

History

• Trauma during intercourse? Vaginal d/c, assess domestic violence or abuse.
• RFs: Cervical abnormalities, STDs, postmenopausal

Physical Exam

• Ongoing bleeding; vaginal lacerations, abrasions

Evaluation

• Labs: Urine hCG, GC/Chlamydia testing; HCT

Treatment

• ED:
• Abx: Treat STI appropriately (see STD section in Renal/GU)
• Consult: Gyn service for laceration requiring extensive repair; social services if
concern for domestic violence

PREECLAMPSIA AND ECLAMPSIA

Definition

• Preeclampsia: BP >140/90 after 20 wk gestation, w/ associated edema and
proteinuria, can be classified as mild to severe based on end-organ damage

• Eclampsia: Preeclampsia w/ szs or coma; generally 3rd trimester or postpartum
• Atypical preeclampsia/eclampsia can present postpartum or <20 wk

Approach to the Patient

History

• HA, visual disturbances, mental status changes, abdominal pain, edema. ROS plural
gestation? PMH (prior preeclampsia, nulliparity, extremes of age, HTN, obesity,
antiphospholipid antibody syndrome, DM, chronic renal dz, connective tissue disorder)

Physical Exam

• HTN, abdominal tenderness, hyperreflexia/clonus, peripheral edema, papilledema,
altered sensorium

Evaluation

• UA, CBC, Chem 7, LFTs, uric acid, coags, type and crossmatch, fetal/maternal
monitoring

Treatment

• BP: Hydralazine, labetalol, or nitroprusside (goal BP <140/90)
• Sz prophylaxis: Magnesium 2–6 g IV load + 1–2 g/h
• Szs: Magnesium (2–4 g IV q5–10min); refractory szs: Diazepam (5 mg IV q5min up to

20 mg) OR phenobarbital (200 mg IV)
• Consult: Gyn for all pts; delivery = only definitive tx for eclampsia

Disposition

• Home: Mild preeclampsia; schedule OB f/u in 24 h
• Admit: Eclamptic and most severe preeclamptic pts need urgent delivery (pending BP

and sz control) and ICU admission

HYPEREMESIS GRAVIDARUM

Approach to the Patient

History

• Persistent vomiting? Poor urine output? Weight loss?

Physical Exam

• Orthostatic hypotension, tachycardia, decreased skin turgor

Diagnostics

• Chem 7, UA (for spec gravity and ketones)

Treatment

• Supportive: IVF resuscitation w/ substrate (dextrose)
• Antiemetics: Ondansetron (Class B, 1st line) or Compazine (Class C, 2nd line)

Disposition

• Admit: Severe dehydration, unable to tolerate POs, acidosis or ketosis

EMERGENCY DELIVERY

Definition

• True labor: Regular uterine contractions of increasing intensity at decreasing intervals
• 1st stage: Cervical dilatation and effacement (up to 12 h)
• 2nd stage: Complete cervical dilatation, culminating in delivery (up to 2 h)

Approach to the Patient

History

• Frequency and intensity of contractions, rupture of membranes, fetal movement, has
pt had prenatal care for eval of cx of pregnancy, screening tests, etc.

Physical Exam

• External exam: Assess for crowning or active bleeding (if so, defer speculum/bimanual
exam)

• Sterile speculum exam: Confirm ROM by checking for ferning and/or Nitrazine test
• Bimanual exam: Assess cervical effacement and dilatation (10 cm = complete),

position, presentation (fetal part in canal), lie (relation of long axis to mother →
longitudinal or transverse), and station (–3 to +3; 0 is at level of ischial spines); cord
prolapse?

Diagnostics

• Abdominal U/S if placenta previa of concern

Treatment

• ED:
• Cord prolapse: Manually place hand in vaginal vault, lift presenting part away from
cord; place pt in knee–chest position or deep Trendelenburg. Administer tocolytics
(magnesium 4–6 g IV, terbutaline 0.25 mg SQ).
• Vaginal delivery: Place mother in lithotomy position; cleanse/drape perineum if
possible; w/ contractions, ask mother to “bear down”
• Head: One hand on occipital area and other on perineum, maintain fetal head in
flexed position; if cord wrapped at neck loosen or cut cord
• Shoulders: Rotate head and exert gentle pressure until anterior shoulder delivered;
lift head upward to deliver posterior shoulders, attempt to guide posterior shoulder
over perineum. If shoulders will not deliver, perform episiotomy by anesthetizing
perineum; make sure to avoid anal sphincter.
• Body: Support head and catch body w/ the other hand. Suction mouth and nose.
• Cord: Clamp cord twice and cut, send cord blood for serology and Rh. Clamp cord
1–3 cm distal to navel and place child in heated isolette. Obtain Apgar scores at 1
and 5 min.
• Placenta: Apply pressure above symphysis w/ minimal traction on cord (too much
traction will cause uterine inversion); sudden gush of blood and lengthening cord
will signify imminent placental delivery.
• Aftercare: Massage uterus ± oxytocin 20 U IV (can be given as 10 U IM if no IV
access for ongoing hemorrhage); inspect and repair lacerations of cervix, vagina

• Perimortem delivery: >23 wk gestational age, should initiate w/i 4 min of maternal
arrest, potential benefit up to 20 min post arrest
• Vertical incision from 2–3 cm above pubic symphysis to 1 cm below the umbilicus
and extend through subcutaneous fat to rectus sheath

• Grasp rectus sheath w/ forceps and make incision w/ Mayo scissors to expose the
uterus

• Make midline vertical incision through uterus w/ scalpel/scissors and deliver fetus

FEMALE PELVIC PAIN

Approach to the Patient

History

• Dyspareunia, vaginal bleeding or d/c? Urinary sxs, ROS PMH (STDs, recent
procedure) MEDS (contraceptive devices, hormonal therapy), social (domestic
violence)

Physical Exam

• Abdominal exam; Gyn exam (d/c or bleeding, masses or tenderness)

Diagnostics

• Labs: UA, GC/Chlamydia, Wet mount
• Imaging: Pelvic U/S (assess flow, torsion, mass, fluid)

Ovarian Cyst

History

• Dull, vague, unilateral sensation of pelvic pain or dyspareunia
• Rupture: Sudden, unilateral, sharp pelvic pain; can also present as diffuse peritonitis

Physical Exam

• Lower quadrant abdominal tenderness, adnexal tenderness/mass, vaginal bleeding

Evaluation

• Labs: CBC, type and screen (crossmatch if HD unstable)
• Imaging: Pelvic U/S to assess for size, complexity, torsion, presence of free fluid.

Bedside FAST if HD unstable.

Treatment

• Supportive: IVFs, transfuse if HD unstable
• Analgesia: NSAIDs, Narcotics prn
• Consult: Gyn Service for persistent pain, large-volume hemorrhage

Disposition

• Home: Stable, pain well controlled; f/u w/ Gyn or PCP in 1–2 mo for repeat U/S to
reassess size

• Admit: HD unstable

Ovarian Torsion

History

• Acutely worsening unilateral lower abdominal/pelvic pain, N/V
• Can present as intermittent torsion w/ intermittent sxs
• RFs: Ovarian cysts, dermoid and other tumors, pregnancy

Physical Exam

• Nonspecific and variable; Gyn exam reveals unilateral, adnexal mass in majority of
cases ± tenderness (though tenderness absent ∼30% of the time)

Evaluation

• Labs: Urine hCG
• Imaging: Pelvic U/S to assess for ovarian edema, cyst/mass, blood flow

Treatment

• Analgesia/antiemetics
• Consult: Gyn service for urgent laparoscopy

VAGINAL DISCHARGE (SEXUALLY TRANSMITTED INFECTION)

History

• Purulent or malodorous d/c? Dyspareunia? Pruritus? Postcoital bleeding? Dysuria,
urinary frequency or urgency

• RFs: Multiple sexual partners and unprotected intercourse

Physical Exam

• External: Inspect for lesions, ulcerations; adenopathy
• Speculum: Vaginal wall inflammation/d/c; cervical inflammation/d/c
• Bimanual: If cervical motion tenderness or adnexal tenderness, think PID (see below)

Evaluation

• Labs: GC/Chlamydia testing; wet mount

Treatment

• N. gonorrhoeae: Ceftriaxone 125 mg IM × 1
• C. trachomatis: Azithromycin 1 g PO × 1 OR doxycycline 100 mg PO BID × 7 d OR

levofloxacin 500 mg PO QD × 7 d
• T. vaginalis: Metronidazole 2 g PO ×1 OR 500 mg PO BID × 7 d
• Bacterial vaginosis metronidazole 500 mg PO BID × 7 d OR metronidazole 0.75% gel

intravaginally × 5 d × 1 OR clindamycin 2% cream intravaginally × 7 d
• Candidiasis: Topical azoles (over the counter) × 7 d OR fluconazole 150 mg PO × 1

Pearls

• Educate all pts on safe sex practices
• Advise pts to tell their partners to get tested/treated

PELVIC INFLAMMATORY DISEASE AND TUBO-OVARIAN ABSCESS

History

• As above, plus abdominal/back pain, fever/systemic sxs

Physical Exam

• Abdominal exam: Abdominal tenderness; RUQ tenderness (Fitz-Hugh–Curtis
syndrome)

• Speculum: Cervical inflammation/d/c
• Bimanual: Cervical motion tenderness, adnexal mass/tenderness

Evaluation

• Labs: GC/Chlamydia testing, CBC, blood cultures if suspected sepsis
• Imaging: Pelvic U/S ± CT if concern for TOA

Treatment

• Abx: Ceftriaxone 250 mg IM × 1 AND (doxycycline 100 mg PO BID OR azithromycin 1
g qwk × 14 d) OR cefoxitin 2 g IV q6h OR cefotetan 2 g IV q12h AND doxycycline 100
mg PO/IV q12h OR clindamycin 900 mg IV q8h AND gentamicin 2 mg/kg IV × 1 then
1.5 mg/kg q8h

• Consult: Gyn service if concern for TOA

Disposition

• Home: Reliable pts w/ simple PID
• Admit: Tubo-ovarian abscess, pregnant, unable to tolerate POs

RASH

Definition

• Skin lesions that display a spec distribution & pattern

Approach

• Nature of rash: D-I-M-P-L-E-S mnemonic

• ROS, PMH, h/o skin lesions, travel, exposures (pets or hobbies), sick contacts,
immunizations, sexual hx, menstrual hx, new medication hx (including OTC)

• Physical exam: Assess for fever, hypotension, tachycardia, AMS; Nikolsky sign?
• Distribution of rash: Central/peripheral, flexor/extensor surface, dermatomal,

intertriginous, follicular, acral, localized/grouped/regional/generalized, sun-exposed,
mucosal
• Shape or configuration: Annular (ring-shaped), round/nummular/discoid (coin-
shaped), targetoid, arcuate (arc-shaped), linear, serpiginous, reticular (net-like/lacey),
whorled (marble-like), polycyclic (coalescing circular/ring-shaped lesions)
• Characterize rash based on morphology (see table)

VIRAL EXANTHEMS

Measles (Rubeola; “First Disease”)

Definition

• Highly contagious dz caused by the measles virus, spread by droplet contact
• Failure rate of vaccine estimated to be <0.2%; typically seen in nonimmunized

History

• Assess vaccination status, as this guides serologic interpretation
• Typically occurs in winter & spring months. Incubation period of 8–12 d.
• Viral prodrome (fever, cough, coryza, conjunctivitis, but also HA, photophobia, sore

throat not uncommon), lasting 3 d, typically 3rd decade of life

Physical Findings

• Fever; adenopathy
• Koplik spots: Small, irregular spots on buccal mucosa w/ bluish coloration during

prodromal period (pathognomonic); usually fades w/i 3 d of rash
• Rash starts behind ears, on the face, & neck beginning as discrete purple-red

maculopapular lesions & patches. Over 2–3 d spreads to trunk/extremities & becomes
confluent; rash may extend to palms; typically lasts 3–7 d & fades.

Diagnostics

• Routine labs rarely indicated, but CBC may show leukopenia
• Lab confirmation: Measles serologies (enzyme immunoassay for measles IgG & IgM),

throat or nasopharyngeal swab for viral isolation/RT-PCR. Contact lab specialist.

Treatment

• Supportive, treat cx (see below)

Disposition

• Home if absence if cx
• ID consultation should be considered
• Measles is designated as notifiable infectious dz at national level by CDC; requires

notification w/i 24 h

Pearl

• Highly contagious, thus contacts should be aware

• Milder forms can occur in children & adults w/ partial immunity
• Cx: OM (most common), pneumonia (most common severe complication) mastoiditis,

croup, febrile szs, postinfectious encephalitis, keratitis, corneal ulcerations, blindness,
TTP, myocarditis, pericarditis, myositis

Rubella (German Measles; Three-day Measles; “Third Disease”)

Definition

• Dz of childhood caused by rubella virus, spread by droplet contact
• Causes 2 distinct syndromes: A mild self-limited postnatal infection occurring in early

childhood as well as a severe, disseminated congenital infection (represents the “R” in
“TORCH” congenital infections). Only postnatal infection will be discussed.

History

• Assess vaccination status
• Typically occurs in winter & spring months. Incubation period of 2–3 wk.
• Viral prodrome (malaise cough, sore throat, low-grade fever, HA); arthralgias also

common

Physical Findings

• Low-grade fever, suboccipital & posterior auricular/cervical adenopathy may be
present

• Pink maculopapular rash that begin on face/forehead w/ caudal progression to
trunk/extremities, may coalesce; typically lasts 3 d & fades

Diagnostics

• Routine labs rarely indicated, but CBC may show leukopenia &/or TCP
• Lab confirmation: Rubella serologies (enzyme immunoassay, latex agglutination, IFA),

throat or nasopharyngeal swab for viral isolation/RT-PCR. Contact lab specialist.

Treatment

• Supportive, treat cx (encephalitis, arthritis, TCP)
• Avoid contact w/ pregnant women (severe congenital defects)

Disposition

• Home
• Rubella is designated as notifiable infectious dz at national level by CDC; requires

notification w/i 24 h

Erythema Infectiosum (“Fifth Disease”)

Definition

• Viral exanthem caused by Parvovirus B19
• Spread by respiratory droplets & secondary infectious rates by household contacts are

high. Transmission via blood products has also been described.

History

• Affects mainly school-age children (2–14 y/o) in late winter/spring months
• Incubation period of 1–2 wk w/ a prodrome of low-grade fever, malaise, HA
• Arthropathy is a common manifestation in adults w/ arthralgias or inflammatory

arthritis

Physical Findings

• Intensely red face (“slapped cheek”) w/ circumoral pallor lasting 1–4 d followed by a
generalized rash that has a reticular/lacey pattern, particularly on extensor surfaces of
the extremities w/ progression to trunk/buttocks/thighs; spares palms & soles; can wax
& wane for weeks

Diagnostics

• Routine labs rarely indicated; consider CBC, reticulocyte count, & haptoglobin in pts
w/ known hemolytic anemia (ie, hereditary spherocytosis) or hemoglobinopathies (ie,
SCD)

• Lab confirmation: Serologic testing, DNA assays (direct hybridization)

Treatment

• Symptomatic
• If complicated (see below), can consider course of IVIG in consultation w/ hematology

Disposition

• Home

Pearl

• Cx: Arthritis (most common), transient aplastic crisis (pts w/ hemolytic anemias &
hemoglobinopathies [ie, SCD]), persistent anemia (pure red cell aplasia), fetal hydrops
& spontaneous miscarriage

Roseola Infantum (Exanthema Subitum; “Sixth Disease”)

Definition

• Dz of children 3–36 mo (95%) caused by HHV-6 & HHV-7
• It is the most common exanthema in children <3 y/o
• Mechanism of transmission unclear, but presumed to be via salivary secretions
• 3 basic stages of infection: Acute infection in infants/young children, latent infection

in adults w/ possible excretion in saliva, & reactivation/reinfection, particularly in
immunocompromised
• Although rare, primary infection in adulthood may cause a heterophile-negative
mononucleosis-like illness

History

• No seasonal variation is observed & incubation period is 1–2 wk
• High fevers, occasional febrile sz, rash begins after defervescence

• May have prodromal coryza, HA, & periorbital edema

Physical Findings

• Despite fever, pts are nontoxic appearing; lymphadenopathy is common
• Pink macules 2–3 mm, start on trunk & spreads to extremities, clears in 1–2 d

Diagnostics

• Routine labs rarely indicated, but CBC may show leukopenia
• Primary infection w/ HHV-6 is difficult to confirm diagnostically

Treatment

• Supportive
• Complicated dz in immunosuppressed pts (see below) may be treated w/ ganciclovir

or foscarnet

Disposition

• Home

Pearls

• Most common complication is febrile szs
• Cx: Reactivation in adults & immunocompromised pts may be a/w encephalitis as well

as bone marrow suppression (particularly in transplant recipients) leading to
pneumonitis, hepatitis, transplant failure or GVHD

Herpes Simplex 1 and 2 (HHV-1 and HHV-2)

Definition

• HSV-1 mainly implicated in orofacial lesions & HSV-2 in genital infections; however,
crossover secondary to sexual practices & autoinnoculation can occur

• Primary herpetic gingivostomatitis: Result of initial exposure to HSV-1; virus then
migrates to trigeminal ganglion via sensory nerve; viral reactivation can occur in
>1/3 pts

• Herpes labialis/recurrent intraoral herpes (cold sore, fever blister): Affects
perioral skin & mucous membranes, respectively; represents reactivation w/ local
replication

• Herpes genitalis: Transmitted via sexual contact w/ infected partner. Subclinical
viral shedding is common thus infected pts may not report contact w/ active lesions.
Lesions appear on genitals & mucous membranes of genitalia as well as perineum,
thighs or perianal area.

• Both forms of HSV are highly transmissible through contact w/ active lesions,
respiratory droplets, contaminated inanimate objects (ie, sharing kitchen/bathroom
utensils for HSV-1) & infected exudates/secretions

• Reactivation can be triggered by fever, menstruation, sun exposure, URI, stress
(physiologic/emotional), immunosuppression, etc. Most often recurrences
spontaneous.

History

• Herpes gingivostomatitis: Usually affects young children, prodromal fever, malaise,
dysphagia, lymphadenopathy followed by oral/perioral vesicles, oral ulcers, &
gingivitis lasting 1–2 wk

• Herpes labialis: Prodromal pruritus, tingling, burning followed by rash typically at
mucocutaneous junction at lips lasting 1–2 wk; sore throat & lymphadenitis common

• Herpes genitalis: Prodrome of localized pain, tingling or burning in genital region. Pts
may also have constitutional sx w/ HA, fever, inguinal adenopathy, malaise → rash.
Can be primary or recurrent. Primary lesions last 2–6 wk & clinically worse. Primary
infection usually begins 6 d after sexual contact; median 4 recurrences/y.

• RF for genital herpes: Number of lifetime sex partners, multiple partners, h/o STI, HIV

Physical Findings

• Herpes genitalis/labialis: Grouped vesicles on erythematous base (“dewdrop on a rose
petal”) → crusted lesions

• Recurrent intraoral herpes: Unilateral crop of small vesicles → small round vesicles on
palate & gingiva. May be confused w/ aphthous stomatitis.

Diagnostics

• Tzanck smear, viral cultures, PCR, biopsy available but are rarely needed

Treatment

• Pain control, hydration
• Herpes labialis: Topical therapy (docosanol 10% cream, penciclovir 1% cream,

acyclovir 5% ointment, cidofovir 0.3 or 1% gel) & oral therapy (Acyclovir,
Famciclovir, Valacyclovir) may decrease sxs & time to healing; sunscreen may decrease
relapses.
• Herpes genitalis: Therapy differs for primary infection, recurrence & suppressive
therapy
• Acyclovir 400 mg TID for 7–10 d (primary) or 5 d (recurrent)
• Famciclovir 250 mg TID for 7–10 d (primary) or 125 mg BID for 5 d (recurrent)
• Valacyclovir 1 g BID for 7–10 d (primary) or 1 g daily for 5 d (recurrent)
• IV acyclovir 5–10 mg/kg q8h should be given for severe or disseminated dz

Disposition

• Home

Pearls

• Cx: Encephalitis, hepatitis, pneumonitis
• Pts should be counseled on safe sex practices & prevention of spreading dz
Guideline: Centers for Disease Control and Prevention. Sexually transmitted diseases
treatment guidelines, 2010. MMWR Morb Mortal Wkly Rep. 2010;59:1–110.

Varicella (“Chickenpox,” HHV-3)

Definition

• Highly contagious caused by primary infection w/ VZV. Varicella attack rates among
susceptible household contacts exposed to VZV are ∼90%; more limited exposure
result in transmission rates 10–35%.

• Common childhood illness a/w fever & generalized pruritic vesicular rash
• Affects children usually b/w 5 & 10 y/o
• Can cause disseminated infection (see Herpes Zoster)
• Transmitted via respiratory droplets or vesicular fluid from infected person. Virus then

inoculated at mucous membranes → spread to regional LNs →1° viremia w/
replication in liver & spleen → 2° viremia w/ mononuclear cell transport to skin &
mucous membranes.

History

• Peaks late winter/spring & incubation period about 14 d (range 10–21 d)
• Viral prodromal sxs (fever, malaise, HA, abdominal pain) usually lasting 24–48 h

before skin lesions. Rash & new lesion formation over 1–7-d period.
• RFs include household or other personal close contacts (ie, classmate)

Physical Findings

• Maculopapular → vesicular (“dewdrop on a rose petal”) → crusted lesions, often
involves the scalp, face, or trunk & may generalize. Rash is pruritic.

• Ulcerative, painful lesions may appear on mucous membranes

Diagnostics

• Routine labs rarely indicated, but CBC may show lymphopenia & transaminitis

Treatment

• Healthy children: Symptomatic/supportive (calamine lotion, colloidal oatmeal baths),
avoid salicylates (a/w Reye syndrome in children)

• Oral antiviral therapy should be considered for certain groups at high risk for
moderate to severe varicella (healthy persons >12 y/o, those w/ chronic cutaneous or
pulmonary disorders, on long-term salicylate therapy, those on short or aerosolized
courses of corticosteroids, & pregnant women w/ serious viral-mediated cx)

• IV antiviral therapy prevents progressive varicella & visceral dissemination in high-
risk groups. Indicated for those w/ malignancy, bone marrow or organ-transplant
recipients, high-dose corticosteroid therapy, congenital T-cell immunodeficiencies, HIV,
neonatal varicella, & complicated or disseminated varicella (see below).

Postexposure Prophylaxis

• Antivirals not recommended for prophylaxis
• Varicella vaccine (live attenuated) recommended for exposures in those eligible for

vaccine & who do not have e/o immunity, ideally w/i 3–5 d after exposure
• Varicella zoster immune globulin can prevent varicella from developing or lessen

severity in high-risk groups & should be given w/i 96 h after exposure in those not

eligible for vaccine (allergy, altered immunity, pregnancy, infants)

Preventing Nosocomial Spread

• Pts should be placed on airborne precautions (negative air-flow rooms) & contact
precautions until lesions crusted

• Pts should be managed only by providers w/ e/o immunity
• Pregnant ED staff w/o known e/o immunity should avoid contact

Disposition

• Home for uncomplicated cases
• Admission for high-risk groups or those who develop complicated VZV

Pearls

• More severe in adults than children
• Complication in o/w healthy children include bacterial superinfection of skin,

transient hepatitis, varicella pneumonia, encephalitis, cerebellar ataxia, myelitis TCP,
purpura fulminans, nephritis, arthritis, myocarditis, pericarditis, pancreatitis, etc.
• Can be disseminated in immunocompromised w/ higher risk of cx
• In rare cases, maternal varicella in early gestation can result in a congenital varicella
syndrome (microcephaly, mental retardation limb hypoplasias, cutaneous defects,
etc.); later in pregnancy, varicella can cause preterm delivery & neonatal varicella

Herpes Zoster (“Shingles,” HHV-3)

Definitions

• Reactivation of VZV in sensory ganglia
• Herpes zoster ophthalmicus: Herpes zoster involving the 1st division of the trigeminal

nerve (V1 distribution – forehead, periocular area, & nose)
• Herpes zoster oticus (Ramsay Hunt syndrome): Herpes zoster involving the geniculate

ganglion w/ rash including the ear, hard palate, or anterior two-thirds of the tongue in
conjunction w/ involvement of CN VII (ipsilateral facial nerve palsy) & variable other
CN findings (tinnitus, hearing loss, N/V, vertigo, nystagmus, etc.)
• Ramsay Hunt syndrome zoster sine herpete: Clinical features similar to RHS w/o rash.

History

• Previous varicella infection, localized abnl skin sensations (tingling, hot/cold
sensation, pruritus, burning pain) prior to rash

• Pts may experience prodromal HA, photophobia, malaise
• RFs: Increasing age, immunosuppressive meds (ie, corticosteroids), neoplastic dz (esp

lymphoproliferative cancers), & organ-transplant recipients, HIV

Physical Findings

• Grouped vesicles on erythematous base → crusted lesions, dermatomal distribution
(pathognomonic), doesn’t cross midline. Note, lesions overlap adjacent dermatomes in
up to 20% of cases.

Treatment

• Therapy should be started w/i 72 h of onset of lesions, but should still be considered if
new vesicles are still forming after this period

• Therapy should be initiated in ALL pts who have herpes zoster ophthalmicus, are
immunocompromised, or older in age regardless of timing of presentation

• Antivirals (valacyclovir, acyclovir, famciclovir) decreased course & neuralgic pain
• Acyclovir 800 mg PO q4h 5 times daily × 7–10 d
• Valacyclovir 1000 mg PO q8h × 7 d
• Famciclovir 500 mg PO q8h × 7 d

• Corticosteroids may accelerate rate of cutaneous healing & alleviate pain, but have no
effect on incidence of postherpetic neuralgia

• Symptomatic (pain control w/ NSAIDs or opiates)

Disposition

• Home
• Pts w/ herpes zoster ophthalmicus should have f/u w/ ophthalmology

Pearls

• Cx: Encephalitis, myelitis, cranial & peripheral nerve palsies, a syndrome of delayed
contralateral hemiparesis, pneumonitis, hepatitis, & acute retinal necrosis. In herpes
zoster ophthalmicus, up to 50% pts can have ocular cx (ie, iritis, episcleritis, or
keratopathy) if untreated.

• Can be disseminated in severe cases/immunocompromised
• Postherpetic neuralgia occurs when pain persists >30 d after onset of rash, &

prevalence increases w/ age

Pityriasis Rosea (associated HHV-6 and HHV-7)

Definition

• Acute, self-healing exanthema thought to be a/w HHV-6 & HHV-7
• Lasts about 45 d (range 2 wk–5 mo)
• A/w asthma, eczema, recent URIs

History

• May be more frequent in cold seasons & clustering of cases can also be seen
• May be a/w constitutional sxs: Malaise, nausea, HA, irritability, anorexia, joint pain,

URI/GI sxs, sore throat, low-grade fever
• Mild pruritus

Physical Findings

• May present only w/ “Herald patch” which is oval, pink/salmon color & elevated
patch w/ fine scaling borders & pale, depressed center. May remain isolated for 2 wk
prior to eruption. May precede initial rash in 50% cases.
• Check axillae, groin & perineum as it may be hidden.

• Multiple small pink/salmon, oval-shaped, patches similar in appearance to herald
patch on trunk & prox. extremities (“Christmas tree pattern”); spares face, scalp,
palms, & soles typically, but can be present in 15–20%.

Treatment

• Symptomatic (oatmeal baths & emollients may help, but unlikely to benefit)

Disposition

• Home

Molluscum Contagiosum (associated Poxvirus)

Definition

• Benign, self-limiting epidermal eruption caused by poxvirus that may last months to
years

• Can serve as marker or opportunistic infection in pts w/ HIV
• Transmitted through fomite, skin-to-skin contact, & sexual contact
• Autoinnoculation may occur

History

• Nonpainful, nonpruritic rash

Physical Findings

• Firm, smooth, dome-shaped papules (2–5 mm) w/ umbilicated center, most common
on face, trunk, & extremities, but can be found in axilla, antecubital/popliteal fossa,
genitals

Treatment

• Self-limited, no tx needed
• Lesion eradication can be performed to decrease risk of autoinoculation (cryotherapy,

laser, curettage, imiquimod cream, trichloroacetic acid, or tretinoin)

Disposition

• Home

BACTERIAL EXANTHEMS

Scarlet Fever (Scarlatina, “Second Disease”)

Definition

• Rash in children (3–12 y/o) caused by gram+, erythrogenic, toxin-producing strains
of group A β-hemolytic streptococci.

• Transmitted via airborne droplets from those w/ active dz or asymptomatic carriers as
well as via fomites

History

• More prevalent in temperate climates & in early winter/spring
• Incubation period 1–4 d followed by acute onset sore throat, fever, HA, vomiting, then

rash 1–2 d after sore throat. Abdominal pain may also be present & severe.

Physical Findings

• Red/scarlet colored macules on background of diffuse erythema w/ finely punctate
lesions of “goose-bump” appearance, “sandpaper” texture, starts on neck/axilla/groin
→ trunk/extremities/face (spares palms/soles)
• Distinctive features include circumoral pallor & increased intensity at skin folds;
there are often transverse red streaks in skin folds known as Pastia’s lines
• Rash resolves w/i 1 wk followed by brawny desquamation 7–10 d later

• “Strawberry” tongue, beefy red pharynx & tonsils w/ or w/o exudative effusion
palatal petechiae

Evaluation

• Rapid strep test (sens 60–90%, spec 90%), throat cultures
• CBC rarely indicated but usually leukocytosis w/ PMN predominance present

Treatment

• Penicillin VK QID × 10 d, benzathine penicillin 1.2 million U IM × 1, or
erythromycin in penicillin-allergic pts

Disposition

• Home

Impetigo

Definition

• Highly contagious superficial epidermal infection affecting mainly children (2–5 y/o),
& is the most common bacterial skin infection in children

• Caused by S. aureus & group A β-hemolytic streptococci
• 2 types: Nonbullous & bullous impetigo

• Nonbullous impetigo accounts for majority if cases & represents a host response to
infection

• Bullous impetigo is caused by bacterial toxins, particularly staphylococcal exfoliative
toxins

• Transmitted via direct contact, autoinnoculation, & fomites

History

• More prevalent in early summer months

Physical Findings

• Nonbullous impetigo: Begins as red macule or papule that becomes a vesicle. Vesicle
ruptures to form an erosion & its contents dry, forming honey-colored crusts; usually
on face (cheeks or under lips) or extremities; self-limited over 2 wk.

• Bullous impetigo: Begins as rapidly enlarging vesicles that form sharply demarcated
bullae w/ little to no surrounding erythema. These rupture, forming yellow oozing
crusts; usually moist intertriginous areas involved (neck fold, axilla, groin, perineum);
self-limited.

Evaluation

• Dx is clinical; gram stain & culture rarely indicated

Treatment

• Supportive care as most will resolve spontaneously
• Topical abx: Mupirocin 2% ointment to affected area TID for 3–5 d
• Oral abx may be indicated in those who cannot tolerate topical tx or w/ extensive dz:

Amoxicillin/clavulanate, dicloxacillin, cephalexin, erythromycin for pen-allergic pts.
• Cx: Poststrep glomerulonephritis, cellulitis, lymphangitis, TSS, SSSS, osteomyelitis,

arthritis, sepsis, endocarditis

Disposition

• Home
• Instruction to prevent spreading
(Refer to Chapter 4, “Soft Tissue Infections” for other bacterial exanthems: Erysipelas,
Cellulitis, Staphylococcal Scalded Skin Syndrome, Toxic Shock Syndrome, and Necrotizing
Fascitis)

FUNGAL EXATHEMS

Dermatophytoses

Definitions

• All denote superficial fungal infections (mycoses) involving the stratum corneum, hair,
or nails; more specifically termed dermatophytoses

• Tinea capitis describes dermatophyte infection of hair & scalp caused by Trichopyton &
Microsporum species

• Tinea corporis refers to any dermatophytosis of glabrous (smooth, hairless) skin
except palms, soles, & the groin region. Most commonly caused by T. rubrum.

• Tinea cruris is a dermatophytosis of the groin, genitals, pubic area, or perineum. Most
commonly caused by T. rubrum or E. floccosum.

• Tinea pedis describes dermatophytosis of the feet, while tinea manuum involves the
hand (commonly the palms or interdigital regions). Most commonly caused by T.
rubrum, T. interdigitale, or E. floccosum.

• Tinea unguium/Onychomycosis describe fungal infections of the nail. Most commonly
caused by T. rubrum, T. interdigitale, or E. floccosum.

Disposition

• Home w/ primary care or dermatology f/u

Pearls

• A dermatophytid, or Id, rxn may occur in pts w/ dermatophytoses & may represent a
delayed-type hypersensitivity rxn to fungal antigens. Clinically, pts present w/ a
primary dermatophytosis as well as papules or vesicles on the hands & feet that are
often pruritic.

Tinea (Pityriasis) Versicolor

Definition

• Cutaneous infection caused by Malassezia species, which is normally found on skin
surface thus, not considered contagious

History

• Subacute/chronic skin discoloration usually noticed by pt; mild pruritus

• RFs: Warm/humid environments, immunosuppression, OCP use, poor nutrition

Physical Findings

• Scaly oval-to-round macules or patches that are typically hypopigmented, but may
also be hyperpigmented/salmon-colored distributed over neck, upper trunk, back, or
arms

• Wood’s lamp exam may show yellow-orange fluorescence
• KOH prep w/ fungal spores & short hyphae; “spaghetti & meatballs” appearance

Treatment

• Topical: Selenium sulfide lotion 2.5% for 10 min before rinsing, 3–4 times weekly;
also, zinc pyrithione, azole shampoos (ketoconazole 2%), terbinafine topical,
ciclopirox

• Systemic (for extensive dz): Ketoconazole, itraconazole, fluconazole

Disposition

• Home

Pearls

• May be confused w/ vitiligo, pityriasis rosea, or dermatophytoses among others
• Regular maintenance application of above topical txs may prevent recurrence

Cutaneous Candidiasis and Intertrigo

Definition

• Fungal infection (mycosis) by any of the Candida species (C. albicans)
• C. albicans has a predilection for colonizing skin folds (intertriginous areas) where the

environment is warm & moist

History

• Itching, burning, or asymptomatic rash in intertriginous areas (groin, axilla, web
spaces, inflammatory areas, beneath the pannus, gluteal fold)

• RFs: Obesity, DM, occlusive clothing, immunosuppressive medications, poor hygiene

Physical Findings

• Moist, red, shiny macules/patches w/ scalloped borders, adjacent satellite pustules

Treatment

• Keep dry, topical antifungals (Various preparations: Creams, lotions, powders,
with/without mild steroid combinations; poor data to support 1 type over the other)

Disposition

• Home

ALLERGIC/INFLAMMATORY EXANTHEMS

Psoriasis

Definition

• Genetic, chronic, inflammatory multisystem disorder affecting primarily skin & joints
• Common, affecting 2% of population
• Majority of pts have mild to moderate dz, thus tx can be initiated if identified in the

ED
• May be a/w other inflammatory disorders such as psoriatic arthritis, IBD, & CAD,

diabetes, & lymphoma
• Marked by characteristic skin manifestations that wax & wane; environmental triggers

include medications, skin trauma, infection, physiologic/psychologic stress
• Phenotypic classifications include plaque (most common), inverse, erythrodermic,

pustular, guttate, nail dz (onychodystrophy) & arthritis

History

• Pruritus, pain over fissures
• Assess recent strep pharyngitis, viral URI, immunization, new meds, skin trauma

Physical Findings

• Plaque psoriasis: Well-defined round to oval-shaped scaling, silver papules & plaques
on erythematous base mainly on extensor surfaces of extremities (knees,
elbows)/scalp/trunk and buttocks; painful fissuring may develop; tends to be
symmetric

• Inverse psoriasis: Erythematous plaques w/ minimal scale w/i skin folds, predominant
in axilla, inframammary, groin, perineum, intergluteal

• Erythrodermic psoriasis: Generalized erythema covering nearly entire BSA w/ varied
scaling; may be a/w fever & malaise

• Pustular psoriasis: Marked by cutaneous pustules on erythematous base
• Guttate psoriasis: Dewdrop-like, 1–10 mm salmon colored papules w/ fine scaling;

may be preceded by URI w/ group A β-hemolytic streptococci
• Psoriatic onychodystrophy: Nail dz common in all subtypes; involves nail pitting,

onycholysis, & subungal hyperkeratosis

Treatment

• Nonmedications: Daily sun exposure, sea bathing, topical moisturizers
• Options include topical steroids, UVB, PUVA (psoralen plus UV-A),

immunosuppressives (methotrexate, CyA), acitretin, biologic agents (alefacept,
efalizumab, adalimumab, etanercept, infliximab)
• Topical therapies often can be initiated in ED either as primary therapy for mild dz or
adjunctive therapy for those w/ severe dz on other systemic therapy; txs:
• Corticosteroids (midhigh potency 1–2 times daily; optimal end point unknown)
• Vit D analogs (calcipotriene twice daily to affected area) w/ corticosteroid
• Topical emollients or Aloe vera 1–3 times daily
• Other: Tazarotene, salicylic acid, coal tar, anthralin, tacrolimus/pimecrolimus

Disposition

• Home w/ dermatology f/u

Erythema Nodosum

Definition

• A cutaneous reactive process marked by panniculitis that may be triggered by a wide
variety of possible stimuli: Infection, sarcoid, rheumatologic dz, IBD, medications (esp
sulfa & OCPs), autoimmune disorders, pregnancy, & malignancy among others

• There is an association b/w GAS infection & erythema nodosum, usually w/ onset of
rash 2–3 wk after throat infection

• Pathogenesis thought to result from cutaneous rxn from immune complex deposition
in an around venules of connective tissue septa of subcutaneous fat leading to acute
inflammation of the connective tissue surrounding subcutaneous adipose tissue

History

• Can occur at any age, but usually 2nd & 3rd decades; >F:M
• H/o recent sore throat/URI, or PMH/FH of connective tissue, rheum, autoimmune, or

inflammatory bowel dz; review current & new meds
• Pts typically present w/ pain & erythema over anterior tibial region
• May be a/w fever, fatigue, malaise, arthralgia, HA, GI complaints, URI
• Usually lasts 3–6 wk & is self-limited; may recur

Physical Findings

• Erythematous tender, warm nodules & plaques located predominantly over the
extensor aspects of the lower extremities (knees, anterior tibial surface, ankles)

• Subacute lesions become flat, & deep red or purplish in color & may mimic ecchymosis

Evaluation

• If needed for underlying dz
• CBC, ESR/CRP, CXR (particularly for e/o Tb or hilar adenopathy)

Treatment

• Supportive: NSAIDs, oral corticosteroids in severe cases

Disposition

• Home with/without referral to dermatologist or rheumatologist

Urticaria

Definition

• Urticaria can be acute, chronic (>6 wk), or contact related, & may also occur
secondary to physical triggers (dermatographism, cholinergic, exercise induced,
pressure, aquagenic, cold, etc.). Special syndromes include urticarial vasculitis &

pruritic urticarial papules & plaques of pregnancy (PUPPP).
• Acute urticarial is most common in clinical practice & commonly idiopathic in nature.

Precipitants include food, meds (esp β-lactam abx), insect stings, contact w/ external
allergens (ie, latex), or parasites
• Mechanisms include IgE mediated (Type I hypersensitivity), direct mast cell
degranulation, complement mediated, metabolism of arachidonic acid (ie, ASA,
NSAIDs), autoantibodies to the IgE receptor on mast cells (FcΕRI)
• The key mediator of urticarial formation is histamine

History

• Pruritic rash, may have h/o new exposure
• Maximal intensity of pruritus typically occurs in the evening
• Acute urticarial lasts <6 wk & usually resolves w/i 24 h
• May be a/w h/o atopy

Physical Findings

• Pruritic, pink-erythematous edematous plaques often w/ central pallor, ranging in size
from a few millimeters to several centimeters in size. They may appear round or
irregular in shape & can occur anywhere on the skin.

Treatment

• Avoidance of precipitants if known; counsel that causes are often not found
• Antihistamines H1-blockers (diphenhydramine, hydroxyzine, cetirizine, loratadine,

fexofenadine), H2-blockers (cimetidine, ranitidine, famotidine), steroids (prednisone)
for refractory cases, TCAs (doxepin) if unresponsive to antihistamines, epinephrine for
severe associated rxn

Disposition

• Home

Eczema

Definition

• Eczema represents a group of skin dz marked by skin inflammation (dermatitis) as
well as similar phenotypic clinical manifestations: Erythema, pruritus, scaling, fissures,
varying degrees of lichenification, & blistering

• Several common types of dermatologic conditions fall under this umbrella term:
• Atopic dermatitis
• Contact dermatitis
• Seborrheic dermatitis
• Dyshidrotic eczema (Pompholyx)

Atopic Dermatitis

Definition

• Chronic, relapsing & remitting skin dz seen in pts w/ h/o or FH of atopy
(asthma/allergic rhinitis/food allergies), 60% begins in 1st year of life

• Affects 10–20% of children & 1–3% of adults
• A/w increased serum IgE levels
• Precipitating factors: Temperature, humidity, irritants, infection, foods, allergens,

stress

History

• Dry pruritic rash w/ pruritus & chronic or relapsing eczematous lesions w/ typical
morphology & distribution in a pt w/ a h/o atopy

Physical Findings

• Intensely pruritic, erythematous papulovesicular lesions a/w excoriations & serous
exudate; chronic lesions w/ lichenification, papules, & excoriations

• In infants & young children, characteristically involves face, neck, & extensor surfaces
• In adults, usually localized to flexural folds of extremities
• Nummular eczema: Round-to-oval erythematous plaques most commonly found on

the arms & legs. Lesions often start as papules, which then coalesce into plaques w/
scale. Early nummular dermatitis lesions may be studded w/ vesicles containing serous
exudate.

Treatment

• Principles of therapy include skin hydration, topical anti-inflammatory medications,
antipruritic therapy, antibacterial measures, & elimination of exacerbating factors:
• Skin hydration: Warm soaking baths for 10 min followed by moisturizer
application
• Topical corticosteroids: Low-potency corticosteroids for maintenance therapy,
intermediate- & high-potency corticosteroids for tx of clinical exacerbation for short
course (see table below)
• Topical calcineurin inhibitors: Topical tacrolimus, pimecrolimus
• Antihistamines: Oral antihistamines for relief of pruritus; topical antihistamines
not recommended due to potential for skin sensitization
• Prevention: Avoid irritants—soaps, wool, fragrances, chemicals, etc.; humidity
control

Disposition

• Home
Guideline: Schneider L, Tilles S, Lio P, et al. Atopic dermatitis: A practice parameter
update 2012. J Allergy Clin Immunol. 2013;131:295–9.e1–e27.

Contact Dermatitis

Definition

• Encompasses all adverse cutaneous rxns that result from the direct contact of an

exogenous agent to the surface of the skin
• Can be allergic or nonallergic, irritant in etiology
• Allergic forms result from antigens that become immunogenic after conjugation w/

proteins in skin, triggering an inflammatory cascade (ie, plant dermatitis)
• Irritant forms are multifactorial responses that involve contact w/ a substance that

chemically abrades, irritates, or damages the skin w/ subsequent inflammation
• Tissue rxns are attributed to cellular immune (Type IV, delayed hypersensitivity)

mechanisms
• Common precipitants: Latex, plant substances (Toxicodendron [formerly Rhus]), metals

(nickel), cosmetics/personal hygiene products, hair products, sunscreen, & topical
medications among others
• Variants: Photoallergic CD, allergic contact cheilitis, allergic systemic CD

History

• Thorough hx surrounding onset: Work hx, exposure to industrial chemicals, exposure
to plant substances, new lotions/perfumes/fragrance soaps/detergent/cosmetics/hair
products, new jewelry w/ type of metallic substance, etc.

• Pruritic rash often w/ burning or stinging in the area of contact

Physical Findings

• Papulovesicular erythematous rash which may involve varying degrees of
lichenification, fissuring, scaling, & excoriation at the site of contact, usually well
localized

• Commonly affected areas include eyelids, face, neck, hands/proximal arms, axilla,
waste area, anogenital region, & exposed areas of the lower extremities

Evaluation

• Patch testing is the gold standard for identification of a contact allergen, but not
performed in the ED, thus may refer to allergist or dermatologist

Treatment

• Identification & avoidance of offending agent
• Symptomatic relief w/ cold compresses, colloidal baths, & emollients
• Topical corticosteroids are 1st-line tx for localized forms. Tx begins w/ high-potency

steroids that may be switched to mid- or low-potency as sxs improve (see table below)
• Systemic corticosteroids may be used for extensive or severe cases
• Consider abx if appears superinfected
• Antihistamines are generally ineffective for CD

Disposition

• Home with/without referral to allergist or dermatologist for patch testing
Guideline: American Academy of Allergy, Asthma and Immunology; American College of
Allergy, Asthma and Immunology. Beltrani VS, Bernstein IL, Cohen DE, Fonacier L.
Contact dermatitis: A practice parameter. Ann Allergy Asthma Immunol. 2006;97:S1–S38.

Seborrheic Dermatitis

Definition

• Papulosquamous disorder on the sebum-rich areas (scalp/face/trunk), abnl immune
response to nl skin fungus (Malassezia) is proposed etiology

• Common in infants (cradle cap), during puberty & in elderly
• Incidence is high among pts w/ AIDS & Parkinson’s dz

History

• M > W, 20% have h/o dandruff, worse in winter
• May be concomitant w/ other skin dzs including rosacea, blepharitis, & acne

Physical Findings

• Pink-erythematous, oily, flaking patches of skin on scalp/nasolabial
folds/eyebrows/ears/chest/flexural areas

Treatment

• Frequent cleansing → reduce oil, keratolytic shampoos (selenium/sulfur/coal tar),
topical ketoconazole (reduce fungal load), low-potency corticosteroids

• Scalp lesions: Selenium sulfide 2.5% shampoo (Selsun) twice weekly for 4 wk, zinc
pyrithione 1% shampoo (Head&Shoulders) once daily then twice weekly as needed, or
ketoconazole 2% shampoo twice weekly for 4 wk. Instruct pts to leave in for 5–10 min
before rinsing; selenium & zinc shampoos can be used daily.

• Face & body lesions: Apply hydrocortisone 1% cream once daily for 4 wk;
ketoconazole 2% cream QD or BID for 1 mo may also be effective. This can be used in
conjunction w/ the shampoos noted above.

Disposition

• Home

Dyshidrotic Eczema (Pompholyx)

Definition

• Vesicobullous disorder involving palmoplantar skin
• It is a subtype of eczema w/ accumulation of edematous fluid in regions w/ a thick

epidermis & even thicker overlying horny layer as in the skin of palms & soles
• 2 clinical presentations include vesicular & bullous types
• May be acute, recurrent, or chronic
• Dyshidrosis is a misnomer, as sweat glands are unaffected in this disorder

History

• Pts present w/ pruritus of the palms or soles a/w vesicular or bullous lesions
• Can be a/w atopic dermatitis, contact dermatitis (esp nickel & cobalt), adverse drug

rxns, emotional stress or an id rxn in pts w/ tinea pedis

Physical Finding

• Vesicles & bullae on nonerythematous palmoplantar skin, particularly over the lateral
aspects of the fingers, palms, & soles

Treatment

• High-potency topical corticosteroids, systemic corticosteroids for severe cases
• Topical calcineurin inhibitors (tacrolimus, pimecrolimus)

Disposition

• Home

NEOPLASTIC/OTHER EXANTHEMS

Mycosis Fungoides and Sézary Syndrome

Definition

• Constitutes 1 of the most frequent primary cutaneous T-cell lymphomas
• Sézary syndrome is an erythrodermic leukemic variant of MF, but is now classified as

a separate form of cutaneous lymphoma itself. Denotes combination of skin &
peripheral blood involvement (>20% tumor lymphocytes or 1000/mm3 absolute cells).
• Postulated etiologies include environmental/occupational exposures, viral (HTLV-1 &
CMV), histocompatibility antigen associations, & chromosomal abnormalities
• The tumor cells of MF infiltrate the epidermis & circulate in the blood, & these cells
express T-cell–associated antigens (CD2μ+μ, CD3μ+μ, *CD4μ+μ, CD5μ+μ, & CD7μ+μ)
• Extracutaneous involvement can occur, most commonly in lung, spleen, liver, GI tract

History

• Median age 55–60 y/o w/ M:F of 2:1
• Indolent evolving rash w/ intense pruritus

Physical Findings

• Often begins w/ an indolent, persistent cutaneous eruption of asymmetrical, irregular,
sun-protected erythematous scaly patches or plaques (often resembles atopic dermatitis
or psoriasis) → generalized plaques → ulcerated or exophytic tumors

• May also present w/ generalized erythroderma w/ intense pruritus
• There may be prominent skin atrophy w/ hyperpigmentation & telangiectasias
• Lymphadenitis

Evaluation

• Histopathologic Dx from skin biopsy, flow cytometry showing expanded pathologic T-
cell populations, DNA microarray techniques

Treatment

• Depends on staging & not initiated in ED

Disposition

• Referral to Hematologist/Oncologist when suspected
• Home or admission depending on pt stability, f/u, & local institutional practice

Kaposi’s Sarcoma

Definition

• Kaposi’s sarcoma is a spindle-cell tumor arising from lymphatic endothelium
surrounding hyperemic vascular slits giving the lesions their characteristic violaceous
appearance

• There are currently 4 recognized variants:
• Classic: Seen in elderly men of Eastern European or Mediterranean origin
• Endemic: Seen in African children & adults
• Immunosuppression/transplant associated: Seen in transplant recipients
• Epidemic, or AIDS associated: Seen in pts w/ HIV w/ AIDS progression &
represents an AIDS-defining illness

• HHV-8 (Kaposi’s sarcoma–associated herpesvirus [KSHV]) is central to its
pathogenesis; transmitted via sexual contact, mucous membranes, maternal–fetal
transmission

• RFs: Endemic country, transplant recipient or on immunosuppression therapy, AIDS,
high-risk sexual practices (multiple partners, unprotected sex, MSM, etc.)

History

• Pts typically have 1 or more of the above RFs & present w/ development of an
indolent, nonpruritic exanthem described below

• Extracutaneous manifestations may include N/V, dysphagia, UGIB, cough, SOB,
hemoptysis, among others

Physical Findings

• Multiple firm, purple-blue or reddish-brown (violaceous) patches & plaques →
nodules, typically on hands & feet & progress up the arms & legs

• May also involve oral mucosa, lymph nodes, & visceral organs (GI & pulmonary)

Evaluation

• Histopathologic Dx from skin biopsy/bronchoscopy/EGD depending on location, PCR,
& serologic assays to detect KSHV Abs

• Suspected cases should include HIV testing (CD4μ+μ count & viral load)
• CXR

Treatment

• Requires specialist eval, but may include excisional biopsy, XRT, chemotherapeutics,
HAART in HIV-AIDS pts

Disposition

• Referral to Hematologist/Oncologist when suspected
• Referral to infectious dz specialist when in the context of HIV
• Home or admission depending on pt stability, f/u, & local institutional practice

Cutaneous Graft versus Host Disease (GVHD)

Background

• Allogeneic hematopoietic stem cell transplant (HSCT) has become an important tx
modality for the tx of various hematologic malignancies as well as for nonmalignant
stem cell disorders (ie, aplastic anemia), genetic dzs (ie, SCID), & solid tumors (ie,
renal cell carcinoma).

• These transplanted stem cells are used from a pt’s own cells (autologous), cells of a
twin (syngeneic), or related/unrelated donor (allogeneic) & can be collected from
bone marrow, peripheral blood, or umbilical cord blood

• GVHD develops in ∼50% of all pts undergoing allogeneic HSCT

Definition

• GVHD is a common cause of morbidity & mortality in recipients of allogeneic HSCT
• Occurs when donor T cells are clonally expanded in an antigen-specific manner after

recognition of nonself human leukocyte antigen (HLA) expressed on the surface of cell
in a host that is immunocompromised. These cells primarily attach epithelia of rapidly
proliferating tissues such as skin, liver, & GI tract.
• Can be acute (<100 d) or chronic (>100 d) after allogeneic HSCT

History

• Acute cutaneous GVHD presents w/ a skin rash that usually occurs w/i 14–42 d after
transplantation

• The skin is usually the 1st target organ affected before the liver & GI tract
• Presentation may be a/w preventive therapy noncompliance

Physical Findings

• Symmetrical erythematous morbilliform or maculopapular eruption involving upper
back, lateral neck, palms, soles, & cheeks; occasionally becomes generalized

• Severe dz can progress to erythroderma, bullae formation, & desquamation
• Stage I: 25% TBSA
• Stage II: 25–50% TBSA
• Stage III: 50% TBSA up to erythroderma
• Stage IV: Erythroderma w/ bullae

• Chronic GVHD lesions: Skin dryness, ichthyosis, psoriasiform, pityriasis rosea like →

lichen planus like (violaceous lichenoid papules & plaques on dorsal hands/forearms
and trunk) & sclerodermoid (plaques of dermal sclerosis)
• Mucous membranes, conjunctiva, hair, & nails may be affected
• A/w high fever, cholestatic hepatitis & intestinal sxs

Evaluation

• CBC, Chem 7, LFTs (bilirubin used for grading)
• GVHD grading incorporates TBSA skin involvement, degree of cholestatic hepatitis, &

volume of diarrhea
• Histopathologic Dx from skin biopsy

Treatment

• Requires specialist eval & consultation
• Cyclosporine or tacrolimus used for the prevention w/ or w/o MTX, T-cell depletion,

& corticosteroids
• Acute Stage I–II, topical high-potency corticosteroids or tacrolimus
• Acute Stage III–IV, high doses of systemic corticosteroids (methylprednisolone)

Disposition

• Home or admission depending on stage/grade, pt stability, f/u, & local institutional
practice

DERMATOLOGIC EMERGENCIES

Erythema Multiforme

Definition

• Acute, immune-mediated, mucocutaneous condition commonly caused by HSV & the
use of certain medications. Often self-limiting, but may be recurrent or persistent.

• Erythema multiforme major denotes presence of mucosal involvement, where erythema
multiforme minor denotes absence of mucosal involvement

• Originally thought to be on a spectrum of disorders including erythema multiforme
major → SJS → TEN, but now classified distinctly

• Etiologies include idiopathic, infection (90%, esp HSV, M. pneumoniae, HCV, EBV),
medication (esp NSAIDs, sulfa, AEDs, abx), malignancy, autoimmunity, immunization,
etc.

History

• Pts w/ EM major may have prodromal malaise & fever days prior to rash
• Pts may experience itching/burning of skin & pain in mouth from oral lesions
• Hx should include signs & sxs of associated infection (HSV, mycoplasma) review of

current or new medications/immunizations, & personal or FH of autoimmunity or
malignancy
• Lesions typically appear acutely over 3–5 d & self-resolve over 1–2 wk

Physical Findings

• Can be macular/papular/vesicular, maculopapular eruption w/ peripheral clearing
(target lesion) most characteristic, greater on extremities/palms/soles, & may be
accompanied by oral, genital, or ocular mucosal erosions

• Commonly symmetric on extremities w/ predilection for extensor surfaces; palms &
soles may be involved (see chart above)

• Mucosal & genital lesions present w/ edema, erythema, & progress to superficial
erosions w/ pseudomembranous formation

Evaluation

• Clinical, but ultimate histopathologic Dx from skin biopsy

Treatment

• Discontinue inciting factors; recall that often self-limiting
• Supportive (pain control, oral antihistamines); oral lesions may benefit from oral

anesthetic solutions/gels, oral antiseptic rinses, & oral corticosteroids if severe
• HSV & other infectious processes should be treated if inciting cause

Disposition

• D/c w/ f/u

Pearl

• Distinguishing features from SJS include the lack of significant erythematous/purpuric
macules, truncal involvement, painful tender skin, & severe level of mucosal
involvement which are all often more characteristic of SJS

Stephens-Johnson Syndrome (SJS)/Toxic Epidermal Necrolysis (TEN) SJS

Definition

• No universally accepted definition of SJS. Often described as a potentially life-
threatening dermatologic condition characterized by an acute febrile illness w/ target
lesions, involvement of at least 2 mucous membranes, w/ <20% TBSA skin involved.

• Mucous membranes involved in 92–100% of pts. Visceral involvement (sloughing of
GI tract mucosa, endotracheal/bronchial erosions, hepatitis) not uncommon.

• Etiologies include infection, immunization, meds (NSAIDs, AEDs, abx, antigout, etc.),
systemic dz, physical agents, etc.

History

• Prodromal febrile illness (malaise, HA, cough) w/ prodromal purpuric/erythematous
target lesions, followed by rapid progression to skin detachment

• Pts may experience itching/burning/severe pain of skin & pain in mouth from oral
lesions

• Hx should include signs & sxs of associated infection (HSV, mycoplasma) review of
current or new medications/immunizations, & personal hx or FH of autoimmunity or

malignancy

Physical Findings

• VS: Variably febrile, tachycardic, may be hypotensive
• Prodromal macular target lesions (bright pink/erythematous inner, lighter pink outer

ring, & dark red/violaceous outermost ring). Often begins on the trunk where it is
severe & spreads to extremities; palms & soles may be involved (see chart above).
• Rapid progression to skin detachment & +Nikolsky sign
• Extensive mucosal involvement in 2 or more sites w/ edema, erythema, & progression
to superficial erosions w/ pseudomembranous formation
• <20% TBSA involvement characteristic of SJS

Evaluation

• Blood cx CBC, BMP, lactate, +Nikolsky sign (slight pressure w/ thumb → skin
wrinkling, slides laterally, separates from dermis)

• Histopathologic Dx is gold standard

Treatment

• No definitive therapy other than supportive care
• Removal of inciting agent
• IVFs (replete as burns: Parkland formula), pressors if needed; phosphate repletion
• Increase room temperature from 30–32°
• Wound care similar to burns (débridement, bacitracin)
• Note: Plasmapheresis, immunomodulatory therapy, systemic corticosteroids, & IVIG

have all been used w/ varied success; not usually initiated in ED
• Early Burn specialist consultation; ophthalmology consultation if ocular involvement

Complications

• Mucosal ulcerations may involve the trachea or bronchi, potentially leading to airway
compromise

• GI involvement may result in dysphagia, odynophagia, & GIB
• Ocular involvement
• Superinfection secondary to breakdown of protective skin barrier

Disposition

• Burn unit admission

Pearls

• Mortality: 1–5%
• Superinfection common & sepsis w/ MOSF is the most common cause of death, but

prophylactic abx not indicated

TEN

Definition