Dermatology Flashcards
Associated with asthma and allergic rhinitis
Erythema, crusts, fissures, pruritis, excoriations, lichenification
Chronic pruritic skin condition
Infants: Blisters, crusts, exfoliation (face, scalp, extremities),1st few months. Resolves by age 2
Adults: Dryness and thickening in antecubital and popliteal fossae, neck
Positive family history, worse in winter (dry weather)
Eczema (Atopic Dermatitis)
Delayed type hypersensitivity Poison ivy, poison oak, poison sumac (linear extension) Contact with metal jewelry (nickel) Hair dyes, detergents Erythema, pruritus, vesicles, bullae Blister fluid contains no antigen Corticosteroids for severe cases
Allergic Contact Dermatitis
Generalized dermatitis, diffuse, scaly, warm, erythematous, non-tender, pruritic
Leads to exfoliation
Most are secondary to underlying disease
Involves most or all of skin
Flares of pre-existing skin disease (psoriasis, atopic dermatitis etc.)
Differential: SSSS, EM, TEN ,TSS
Exfoliative Dermatitis
Response to drugs, chemicals, systemic disease or malignancy (lymphoma, leukemia)
May be acute, subacute or chronic
Typically males over 40
Complications are 2° to disruption of epidermis
Hypothermia, volume loss, electrolyte abnormalities, 2° skin infection
Important to diagnose underlying cause
Admit, IV, steroids for severe cases
Exfoliative Dermatitis
Chronic papulosquamous eruption
Due to more rapid cell cycle
Erythematous plaques with white (silver) scales
Extensor surfaces of elbows, knees, scalp, palms, soles
Pitting of the nails
May be accompanied by psoriatic arthritis
Treatment: steroids, tar, UV light, methotrexate
Psoriasis
White, yellow, waxy scales with erythema
Localized to hairy skin areas
Scalp, eyebrow, ear, axilla, groin (wherever
there are sebaceous glands)
Malassezia (a fungus) is associated
Not contagious
Frequent recurrences, worse in cold weather
May be severe or generalized in HIV positive patients
Treatment: Rotating antidandruff shampoos,
ketoconazole shampoo or cream; steroids are discouraged
Seborrheic Dermatitis (Dandruff)
Children, young adults, spring and fall
Etiology unknown
No epidemics, not contagious
Rash evolves over weeks
Herald patch: Single salmon-colored lesion with raised boarder on trunk, 1–5 cm
1-2 weeks after herald patch: Widespread eruption, pink maculopapular oval patches that follow the ribs (“Christmas tree” pattern)
Rule out syphilis (if clinically indicated), drug reaction
Treatment: Symptomatic, antihistamines
Resolution in 2-10 weeks
Pityriasis Rosea
Deposits of blood under skin Non-blanching Petechiae <3 mm, purpura >3 mm Non-palpable: Platelet disorder, thrombocytopenia Palpable purpura = Vasculitis Treatment: Antibiotics, steroids, plasmapheresis (depends on etiology)
Petechiae / Purpura
Diffuse pruritus, wheals, hives (superficial dermis)
Lesions move around within 24 hours
Etiology is unknown most of time
IgE → mast cells → histamine release
Usually self-limited
Treatment: Antihistamines, steroids, antipruritics, H2 blockers, epinephrine
Urticaria
Bradykinin-mediated ↑ Vasodilation ↑ Vascular permeability Edema of the deeper dermis Common cause: ACE inhibitors ACE inhibitors decrease metabolism of bradykinins Can occur early or late 2/3 occur in hours 1/3 in months to years
Angioedema (1)
Familial - associated with C1 esterase inhibitor deficiency
C1 esterase inhibitor inhibits complement cascade
Deficiency leads to increased bradykinin
Edema of face, extremities, bowel wall
Responds to fresh frozen plasma and C1 esterase inhibitor concentrate
Autosomal dominant (positive family history)
Angioedema
Infants, toddlers, elderly
Usually Group A Strep, occasionally Staph
Superficial cellulitis, lymphangitis
Localized (face, legs, ear)
Butterfly facial rash (warm and tender)
Raised, well demarcated border
Treatment: PCN, dicloxacillin, erythromycin
Erysipelas
Painful, non-ulcerative, violaceous nodules (localized vasculitis) on anterior tibia, arms, trunk
Looks like erythema, feels like nodes
EN is often a marker for systemic disease
Drug reaction (oral contraceptives, sulfa, PCN)
Systemic infection (TB, fungal)
Sarcoid
Inflammatory bowel disease (ulcerative colitis)
Malignancy (leukemia, lymphoma)
Most common in women 30-50
Resolves in 3-6 weeks
Treatment is directed at underlying disease
Erythema Nodosum (EN)
Consider in any acute, symmetrical eruption
Common: PCN, cephalosporins, sulfa
Usually disappears within 1-2 weeks
Immediate hypersensitivity: IgE (urticaria)
Delayed hypersensitivity: IgM (serum sickness)
Urticaria, morbilliform rash (discreet red-brown papules coalesce to erythema), erythema multiforme
Treatment: Discontinue drug, antihistamines, steroids
Complications: Stevens-Johnson syndrome (mucosal and cutaneous), Severe bullous (form can be fatal)
Drug Eruption
Minor (erythema multiforme) EM major (Stevens-Johnson) EM maximum (TEN)
Hypersensitivity reaction
Infection (Mycoplasma, Herpes), malignancy, drugs
Sulfa, oral hypoglycemics, anticonvulsants, PCN (memory aid: “SOAP”)
Palms, soles, extensor surfaces
“Bull’s eye” or “target” lesions
Treatment: Remove offending agents; symptomatic for minor forms; major forms may need resuscitation, ICU admission
Erythema Multiforme
Severe bullous form of EM, 10-30% of BSA, mucosal involvement, can be fatal
Bullous cutaneous lesions, mucositis, stomatitis, conjunctivitis, crusted nares
Children, adolescents, males
Serious, potentially fatal form of E. multiforme
Hypersensitivity reaction
Severe reaction to medication: Sulfonamides PCN, barbiturates, phenytoin, tetracycline, thiazides
Stevens-Johnson Syndrome
Erythema multiforme, Stevens-Johnson syndrome and TEN
Probably variants of the same disease process. The difference is in severity and body surface area affected
TEN affects >30% of BSA
Exposure to drugs, chemical agents, infections
Sulfa, PCN, barbiturates, phenytoin, allopurinol, NSAIDs
Mycoplasma, HSV
Toxic patient, large bullae, mucous membranes, widespread systemic manifestations
Toxic Epidermal Necrolysis (TEN) 1
Separation of dermal-epidermal junction
Nikolsky’s sign: Skin peels off with light pressure
Older age group has high mortality
Increased mortality from dehydration and 2° infection
Primary causes of death: Sepsis, pneumonia
Treatment: Admit to ICU
Toxic Epidermal Necrolysis (TEN)
Usually children <2 years old
Staph aureus exotoxin
Fever, scarlatiniform rash followed by exfoliation
Nikolsky’s sign: Skin peels off with light pressure
Antibiotics (vancomycin) indicated, but do not alter cutaneous disease
More favorable prognosis than TEN
Steroids are contraindicated
Staphylococcal Scalded Skin Syndrome
Painful intradermal bullae, 40-60 years old, possible autoimmune etiology
Associated with penicillamine, captopril, phenobarbital
Bullae on normal skin, often start in mouth
Mucus membranes are frequently involved
Blisters are fragile, break easily, leave red or crusted erosions
Small flaccid bullae erosions, ulcerations
Nikolsky sign positive (like TEN)
Can be lethal: Mortality due to secondary infection, dehydration
Treatment: Steroids, admission, biopsy
Pemphigus Vulgaris
Chronic benign bullous eruption. Autoimmune disease
Risk factors: Age > 60, female, malignancy, furosemide (Lasix)
Begins with urticarial lesions, then tense blisters up to 10 cm
Large bullae (2-5 cm) arise from erythematous skin
Mucus membranes infrequently involved
Nikolsky sign negative
IgE deposited on basement membrane
Course is usually benign. Mortality much less than in pemphigus
Bullous Pemphigoid
Most common skin malignancy Pearly, rolled border with central ulceration Not a metastasizing tumor Slow growing, usually head and neck Seen only where hair follicles exist Cure rate 100% if found early
Basal Cell Carcinoma
Increasing incidence
Ages 30-50
Risk factors: Adulthood, dysplastic nevi, family history of melanoma, fair skin, UV exposure, congenital nevi
Account for majority of skin cancer deaths
Sun exposed areas (head, neck, trunk)
The greater the depth, the worse the prognosis
Metastases are common
Malignant Melanoma
Second most common cutaneous malignancy
Common in elderly males, fair skin, sun
exposure
Face, lips, ears, tongue, hands
Rapid growth, central ulcer, raised and indurated border
Metastases occur early
Treatment: Excisional surgery, radiationSquamous Cell Carcinoma
Tinea capitis (scalp) and tinea barbae (beard)
Bald, broken hair
Scaly patch
Edematous nodules and pustules (kerion)
Tinea corporis (ringworm)
Non-hairy parts of the body, outward spreading, annular lesion, clear center
Tinea pedis (athlete’s foot)
Tinea cruris (jock itch)
Groin and inner thigh (sharp demarcation)
Scrotum not involved
Causes: Trichophyton, Microsporum, Epidermophyton
Treatment: Antifungal (topical or oral)
Tinea (Dermatophytosis
Hypopigmented or hyperpigmented circular, scaly patches
Poor hygiene, moisture
Malassezia fungus
Treatment: Selenium shampoo, ketoconazole shampoo or cream
Pityriasis (Tinea) Versicolor
Pathogenic spirochete
Reservoirs: Rats, cattle, pigs, dogs
Skin contact with urine of infected animal
Contaminated water
Hepatitis, nephritis, meningitis, coagulopathy
Weil’s disease (severe form): Jaundice, subconjunctival hemorrhage, hepatitis, DIC
Risk of death from hepatorenal failure
Diagnosis by serology
Treatment: Pen G, tetracycline, doxycycline
Leptospirosis
Borrelia burgdorferi (spirochete) Transmitted by bites of Ixodes ticks Tick reservoirs: Rodents, rabbits, deer Most do not recall tick bite Fever, myalgias, arthralgias, headache 3 stages Localized (rash) Disseminated (neurologic and cardiac) Persistent (arthritis)
Lyme Disease
Erythema migrans: Annular, expanding erythematous lesion with central clearing (spares palms, soles)
Neuro: CN VII palsy, meningitis, peripheral neuropathy
Cardiac: Myocarditis, pericarditis, heart block
Diagnosis: ELISA (screening); Western blot
Treatment: Doxycycline, amoxicillin, cefuroxime; macrolides if others not tolerated
Probable risk = Test
Probable disease = Treat
Lyme Disease
N. meningitidis (encapsulated Gram negative diplococcus)
Broad spectrum of disease
Bacteremia, sepsis, meningitis
Fever, myalgias, headache, rash
1-2 mm petechiae purpura
Poor prognosis if petechiae, hypotension, T> 40 °C, decreased platelets, no meningismus or leukocytosis
Meningococcemia
Prophylaxis: Close contacts, nursing home, dormitory, family
Prophylaxis is not indicated for brief hospital encounter (ER patient, no close contact)
Rifampin, Cipro for prophylaxis
Diagnosis: CSF and blood serology, cultures
Treatment: PCN, chloramphenicol, isolation
Meningococcemia
shock, petechiae, adrenal infarction
Waterhouse-Friderichsen syndrome
associated with meningococcemia
Virulent, toxin-producing bacteria
Often seen with IVDU
Widespread fascial and muscle necrosis, sparing of skin
Crepitant anaerobic cellulitis (necrotic soft tissues, subcutaneous gas)
Myonecrosis (clostridial, non-clostridial)
Necrotizing fasciitis (rapid dissection and necrosis in superficial and deep fascial planes)
Necrotizing Soft Tissue Infections
Flesh-eating” bacteria Strep, clostridia, polymicrobial “Pain out of proportion” is hallmark Surgical emergency Pen G + imipenem, or amp + gent + clinda Fournier's gangrene: Necrotizing fasciitis involving scrotum, vulvar or perianal skin
Necrotizing fasciitis
Hospital acquired MRSA
Hospitalized, dialysis, IVDU, nursing home
Community acquired MRSA
Skin and soft tissue infections
High prevalence in many areas
Resistant to beta-lactam antibiotics
Milder infections: clindamycin, doxycycline or trimethoprim/sulfamethoxazole
Serious infections: vancomycin or linezolid
Methicillin ResistantStaph aureus (MRSA)
Staph aureus exotoxin
Prolonged tampon use, packed surgical wounds, nasal packing
Menstruating females, postpartum, also in males
Fever, hypotension
Rash: Diffuse, erythematous, nonpruritic, macular
Involvement of at least three systems
Renal, hepatic, hematologic, GI, musculoskeletal, mucosal, CNS
Treatment: Fluids, remove source, antibiotics
Group A Strep variant (higher mortality)
Toxic Shock Syndrome
Rickettsia rickettsii (obligate intracellular bacterium)
Bite from infected tick
Most cases seen in April-September (tick season)
Commonly seen in children <15
Endemic in Southeastern US
Fever, headache, myalgias
Small pink macules petechiae, purpura (from a vasculitis) / (wrists, ankles)
Rocky Mountain Spotted Fever (RMSF)(
Rash begins on extremities, wrists, ankles, palms and soles
Spreads up trunk, spares face
Lab: WBC count normal, left shift, mild anemia, moderate thrombocytopenia, hyponatremia
Diagnosis: Clinical (don’t wait for serology tests)
Treatment: Doxycycline preferred, chloramphenicol
Complications (due to vasculitis)
DIC
Loss of limbs
CNS
Lungs
Kidneys
Rocky Mountain Spotted Fever (RMSF)(
Clinical presentation similar to rocky mountain spotted fever
Transmission through tick bite
Two types
HME: human monocytic
HGE: human granulocytic
Fever, headache, myalgias
Maculopapular rash
Leukopenia, thrombocytopenia, hyponatremia, anemia, LFTs
Diagnosis: Clinical suspicion
Treatment: Doxycycline, tetracycline, chloramphenicol
Complications: DIC, renal failure, coma, death
Ehrlichiosis
Tick-borne hemolytic disease, blood transfusions
Intra-erythrocyte protozoan parasite
Endemic to northeastern USA
Fever, chills, fatigue, malaise
Hepatosplenomegaly, jaundice
Peripheral blood smear – parasites in RBCs
Usually mild unless asplenic, elderly, or immunosuppressed
Treatment: Quinine plus clindamycin; Atovaquone plus azithromycin
Babesiosis
A member of the herpes virus group (dormant until reactivated)
The most common of the TORCH infections
Congenital: Chorioretinitis, jaundice, hepatosplenomegaly, deafness, rash
Acquired: Asymptomatic or mono-like illness
Immunocompromised: CMV retinitis, nephritis, pneumonitis, colitis. Carries high mortality
Diagnosis: Atypical lymphocytosis, ELISA
Treatment: IV ganciclovir or foscarnet
Cytomegalovirus
Toxoplasmosis, Other (Syphilis), Rubella, CMV, Herpes simplex
Organisms associated with congenital transmission
TORCH Infections
HSV-1: Stomatitis, fever, decreased fluid intake, oral lesions, corneal ulcers (steroids are contraindicated)
Herpetic whitlow: Vesicles grouped on digits, non-surgical treatment, often misdiagnosed
HSV-2: Painful vesicles of genitalia and anus
Diagnosis: Viral culture, PCR
Complications: Congenital transmission (TORCH), encephalitis
Treatment: Acyclovir and analogs, vidarabine
Herpes Simplex
Varicella-zoster virus reactivation
Painful vesicles in dermatome distribution
Cranial nerve involvement
HZ ophthalmicus: Opthalmic branch of CN V, lesion seen on tip of nose (Hutchinson’s sign), vision- threatening
Ramsay Hunt: CN VII, zoster presenting with facial nerve palsy, ear pain
Complications: Pneumonia, meningitis, post-herpetic neuralgia, 2° infection, dissemination
Treatment: Acyclovir and analogs, prednisone
Herpes Zoster (Shingles)
HIV types 1, 2 (RNA retroviruses)
Virus multiplication in CD4 lymphocytes
Acquired Immune Deficiency
Pneumocystis jiroveci pneumonia (PJP) is the most frequent infection CXR: bilateral infiltrates, hypoxemia Treatment: TMP/SMX, steroids Cryptococcal meningitis Most common CNS fungal infection Diagnosis: CSF (India ink, cryptococcal antigen) Treatment: amphotericin B Toxoplasmosis Most common cause of encephalitis Diagnosis: CT (ring-enhancing lesions) Treatment: pyrimethamine, sulfadiazine Oral candida is most common GI tract infection
Acquired Immune Deficiency
Second most common AIDS manifestation
Seen in men who have sex with men (MSM)
Not a cause of significant morbidity or mortality
Purple, painless, non-pruritic areas, flush with skin or raised strawberry-like plaques
Persist, enlarge, coalesce, may bleed
Extracutaneous involvement: GI tract, liver, spleen, lungs, CNS
Kaposi’s Sarcoma
Viral infection of skin (poxvirus)
2-5 mm umbilicated, pink, dome-shaped papules
Autoinoculation: Common locations are face, trunk, extremities (children), groin and genitalia (adults). Usually self-limited
Transmission: Close personal contact, swimming pools. Sexual transmission is common in adults
HIV/AIDS: Not uncommon, lesions can be extensive and atypical
Molluscum Contagiosum
Epstein-Barr virus (EBV)
Common in adolescents. Usually asymptomatic in infants and children
Fever, exudative pharyngitis, splenomegaly, lymphadenopathy, atypical lymphocytosis
Complications: Splenic rupture, thrombocytopenia
Diagnosis: Monospot, serology
Amoxicillin almost always causes a maculopapular rash (may be diagnostic)
Treatment: Rest, supportive, no contact sports
Infectious Mononucleosis
A collection of congenital infections that can cause severe fetal abnormalities that are associated with a variety of dermatologic manifestations
T = Toxoplamosis
O = Other (syphilis, EBV, VZV, HBV, Parvo B19)
R = Rubella
C = Cytomegalovirus (most common)
H = Herpes simplex
TORCH Infections
Human Parvovirus B19
Fever, myalgias, diarrhea, URI symptoms, flu symptoms
Rash: Abrupt onset, bright red cheeks (slapped cheeks), tiny papules on erythematous base, eyelids and chin spared
“Lace-like” erythematous rash on limbs, trunk
Complications: Arthritis, aplastic crisis (especially in sicklers)
Can cause fetal anemia if acquired during pregnancy
Treatment: NSAIDs
Erythema Infectiosum (Fifth Disease)
Coxsackie virus (enterovirus)
Occurs in outbreak
Fecal-oral transmission
Fever, sore throat, malaise, URI
Oral lesions: Painful vesicles on anterior mouth (buccal mucosa, tongue, soft palate, gingiva)
Skin lesions: Red papules (change to gray vesicles) on palms, soles, buttocks
Vesicles on hands, feet, soles
Avoid viscous lidocaine in young children because of risk of seizures
Hand-Foot-Mouth Disease
Coxsackie virus
Fecal-oral transmission, preschool age, spreads to siblings
Fever, dysphagia, drooling, vomiting, headache
Ulcerative lesions (vesicles rupture, leaving painful ulcers on posterior pharynx, soft palate, uvula)
Complications are rare
Resolves in 1 week
Anterior mouth spared
Herpangina
Most common acute vasculitis affecting children
Preceding Strep or GI infection (Salmonella, Shigella)
Ages 2-10, abdominal pain, GI bleeding, hematuria
Palpable purpura (legs, buttocks)
Thrombocytopenia is absent
Complications: Arthritis, glomerulonephritis, hematuria, GI bleeding, intussusception
Renal consult
Usually resolves spontaneously
Henoch-Schönlein Purpura
Mucocutaneous lymph node syndrome
About 2,000 cases/yr in the U.S.
Acute, febrile, exanthematous disease of children (age 2-5, males, Asian)
Self-limited vasculitis with predilection for coronary arteries
Cause unknown
Possibly an immune response to bacterial infection, since it occurs in outbreaks
Kawasaki’s Disease
Major criteria: Fever >5 days PLUS 4 of the following
Conjunctival injection (bilateral)
Strawberry tongue, fissures, lips cracked
Desquamation or swelling of fingers and toes
Erythematous rash (starts on palms and soles)
Enlarged (15mm or greater) cervical lymph nodes
↑ WBC, ↑ ESR, ↑ platelets
Coronary artery aneurysms
Treatment: Aspirin, IV immunoglobulin
Kawasaki’s Disease
Staph. aureus, Strep. pyogenes
Superficial epidermis, no fever, highly contagious
Preschool, young adults, poor hygiene
Red, moist vesicles
Painless, honey-crusted lesions
Rarely causes glomerulonephritis (antibiotics do not prevent this)
Treatment: Dicloxacillin, cephalosporin,
erythromycin, mupirocin ointment
Bullous impetigo suggests Staph infection
Impetigo
Acute viral illness (fever, sore throat, headache)
“Three day measles”
Rash (pink macules spread from head to feet)
Complications
Arthritis (immune complex)
Encephalitis
1st trimester pregnancy (congenital defects)
Prominent lymphadenopathy:
posterior auricular, cervical, occipital
Rubella (German Measles)
Fever, cough, conjunctivitis, coryza (3 “C”s)
Koplik spots: Buccal mucosa (before rash), non-tender, tiny white spots (“grains of salt”)
Maculopapular, red-brown “morbilliform” rash spreads from head to feet
Complications: Encephalitis, pneumonia,
otitis media, conjunctivitis
Rubeola (Measles)
Exanthem subitum Human herpes viruses (HHV) 6 Common at ages 6-18 months High fever (3-4 days), then rash with defervescence Febrile seizures are common Pink macules and papules on trunk May spread to neck, face, extremities
Roseola Infantum
Head lice
Scalp and neck (erythema, scaling)
Nits (eggs) attached to the hair shaft
Body lice
Linear excoriations, nits in seams of clothing
Pubic lice (crabs)
Sexually transmitted
Intense pruritus, papular urticaria on thighs and abdomen
Treatment: Extensive cleaning of clothing and bedding, pediculicide creams and shampoos (pyrethrin, permethrin, malathion)
Pediculosis (Lice)
Severe pruritus (due to hypersensitivity reaction to scabies mite)
Web spaces, elbow, axilla, groin (favors thin skin)
Red papules, vesicles, crusts, linear burrows
Treatment: Permethrin cream, ivermectin; lindane lotion (not first line, age >2 yrs)
“Norwegian scabies” (severe disease) seen in immunocompromised
Scabies
Group A beta hemolytic Strep toxin
Sore throat, fever, headache, vomiting
Sandpaper rash starts on flexor creases and moves to trunk and extremities; circumoral sparing
“Strawberry” tongue
Groin, axilla, antecubital areas (Pastia’s lines)
Skin peeling (palms and soles)
Diagnosis: Throat swab, increasing ASO titer
Treatment: Pen G
Scarlet Fever
Varicella zoster virus
Fever, malaise, URI
Macules, papules vesicles (“dewdrop on a rose petal”) that come in crops crusts
Complications (mostly adults): Pneumonia, encephalitis, otitis media, 2° infection
Treatment: Acyclovir or analogues
Avoid salicylates (Reye syndrome)
Prevention: Immune globulin if immunocompromised or pregnant, vaccine in kids and non-immune adults
Varicella (Chicken Pox)
Hepatitis B
HB Surface antigen = Infectious
HB Surface antibody = Protective
HB e antigen = Highly infectious
Per the CDC, a needle stick or cut exposure if not successfully vaccinated = 6-30%
Risk is at the high end of the range (25-30%) if source is HBeAg-positive
Hepatitis B vaccination Very safe vaccine Three-dose series (0, 1, 6 months) Test for seroconversion (desired antibody level >10 mIU/mL) Repeat series if non-responder No boosters if responder
Hepatitis B Immune Globulin (HBIG)
Passive immunization (pooled antibodies)
Effective within 1 week of exposure
Management of possible hepatitis B exposure
Test source for HB surface antigen
Test exposed patient for HB surface antibody
Exposure to HBsAg-positive source
If the healthcare worker is unvaccinated, give HBIG and start the vaccine series
If the healthcare worker has protective levels of antibody (>10 mIU/mL), no treatment is needed
Special circumstances (known non-responders, partially vaccinated) – look it up!
b
Percutaneous transmission is common
Sexual transmission is rare
Per the CDC, after a cut or needle stick exposure the seroconversion risk about 2%
Test source for anti-HCV
No effective post-exposure prophylaxis
If positive do serial tests of the healthcare worker for anti-HCV and liver enzymes
Hepatitis C
HIV exposure
Transmission by percutaneous exposure 0.3%
Risk of transmission is increased when
Contaminating device is visibly contaminated with blood
A needle is placed directly into a blood vessel
Injury is deep
Contamination is with a hollow bore needle
Source is likely to have a heavy viral load (as occurs in terminal HIV)
Post-exposure prophylaxis recommended for significant HIV exposures
HIV Post-Exposure Prophylaxis For HIV-positive exposures HIV test source and healthcare worker Start meds within 1-2 hours of exposure Multi-drug protocols are standard Reverse transcriptase inhibitors (e.g., tenofovir-emtricitabine) and integrase inhibitors (e.g., raltegravir) are used Side effects often limit treatment PEP is continued for 4 weeks Consult ID for most cases CDC PEP hotline: 888-HIV-4911
