Life threatening skin conditions Flashcards
fever and skin rash after new medication. CBC with eosinophilia.
DRESS syndrome
DRESS is a
when does it start?
potentially life threatening drug reaction that happens 2-8 weeks after initial exposure
which drugs cause DRESS?
anticonvulsants (phenytoin or carbamazepine), allopurinol and sulfonamides (sulfasalazine) and abx (minocycline and vancomycin)
acabavir (HIV NRTI)
fever, generalized LAD, facial edema and diffuse morbilliform rash that can progress to confluent erythema and follicular accentuation
DRESS presentation
DRESS rash
morbilliform rash that can progress to confluent erythema and follicular accentuation
can involve the mucosa (mouth and pharynx) and doesn’t cause erosions
what other organ systems are affected in DRESS?
can see liver (hepatomegaly and jaundice)
Can see kidney (acute interstitial nephritis)
Can see lung (cough and dypsnea)
labs of DRESS
see eosinophilia and atypical lymphocytes and elevated hepatic transaminases
treatment of DRESS
stop offending drug and this resolution can take up to 6-9 weeks
hypersensitivity vasculitis clinical presentation
fever, palpable purpura and petechiae, arthralgias, LAD and elevated ESR. Seen with anticonvulsants. NO esosinophilia
Hypereosinophilic syndrome HES) is defined by
profound eosinophilia >1500 and multi system involvement (Heart, GI, lungs, brain, skin, kidneys) without a identifiable cause.
what is serum sickness like syndrome
seen after exposure to new drugs (antiseizure drugs, antibiotics, and infections (hep B or strep)
Can cause systemic symptoms arthralgias, and urticarial or serpiginous macular rash. This happens within 1-2 weeks after drug exposure and NO eosinophilia
Steven Johnson syndrome
triggered by new medications and seen with sudden onset of mucocutaneous lesions with subsequent necrosis and sloughing of of skin. NO eosinophilia or elevation in LFTs.
Staph toxic shock syndrome risk factors are:
tampon use,
nasal packing,
surgical/post partum wound infection
what causes staph toxic shock syndrome?
staph aureus
exotoxin release acting as superantigens
what are clinical features of staph toxic shock syndrome?
fever >102 or 38.9
hypotension
diffuse macular rash involving the palms and soles
desquamation 1-3 weeks after disease onset
vomiting and diarrhea
altered mental status without focal neurological signs
treatment of Staph toxic shock syndrome?
supportive care (IVF replacement) removal of foreign body (Tampon or nasal packing) antibody therapy (clindamycin and vancomycin
pt has progressive lethargy and confusion and has shaking chills and diarrhea. Had nasal packing for a nose fracture. Has fever and hypotension and tachycardia and ill. Has diffuse erythema of mucous membranes and skin and palms and soles and pitting edema of both legs
staph toxic shock syndrome
treat with clindamycin and vacomycin
remove nasal packing.
desquamating rash, multiorgan failure and hypotension and diffuse erythroderma and encephalopathy
staph toxic shock syndrome
encephalopathy occurs due to cerebral edema.
are there positive blood cultures in toxic shock syndrome?
no but should still get them if someone is septic shock
generally can culture at the infection source.
why do we use clindamycin and vancomycin for staph toxic shock syndrome?
because clindamycin - helps stop /inhibits toxin production
after recovery what is long term management for toxic shock syndrome from nasal packing?
eradication of S aureus with mupirocin
what staph bacteria causes toxic shock syndrome?
group A strep.
when to use vancomycin and cefepime to treat someone after a fight?
only use this if there’s a basal skull fracture during the fight and they develop meningitis.
Side effects of bactrim
skin - Steven Johnson syndrome, TEN (toxic epidermal necrolysis) exfoliative dermatitis- seen up to 15% in HIV positive pts
Hematological: megaloblastic pancytopenia (folate deficiency)
Renal: hyperkalemia, impairs tubular secretion of Cr without affecting GFR
see crystalluria
interstitial nephritis
difference between SJS and TEN?
<10% body surface area: Steven johnson syndrome
10-30% of BSA: SJS/TEN overlap
>30% of BSA: TEN
clinical features of Steven Johnson syndrome:
4-28 days after exposure to trigger (2 days after repeat exposure)
acute influenzae like prodrome
rapid onset of erythematous macules, vesicles, bullae
necrosis and sloughing of epidermis
mucosal involvement
Common triggers for Steven Johnson syndrome and TEN
drugs: allopurinol antibiotics like bactrim or sulfonamides anticonvulsants: carbamazepine, lamotrigene, phenytoin NSAIDS: piroxicam sulfasalazine
what other common triggers can cause Steven Johnson and TEN?
mycoplasma pneumoniae
vaccination
Graft vs host dx
which population of people is most vulnerable to developing Steven Johnson syndrome from antibiotics or common triggers?
HIV positive pts
3X more common
initial prodrome of fever and influenza symptoms with new onset of painful red or purple macules. Skin lesions then progress to bullae formation and necrosis and sloughing
presentation of SJS
Can see mucosal lesions - ocular, oral, genital and respiratory surfaces
What kills most people with SJS and TEN
secondary infection
management of SJS?
need to be managed in hospital setting in ICU burn unit
all suspected or unnecessary medications should be immediately discontinued as prognosis of SJS or TEN improves with early removal of causative medications
Tx is supportive and wound care. Consider steroids nad IVIG in severe cases.
pt takes bactrim for sinusitis. 5 days later states she has improved but has redness and “blisters” on her arms?
send to the hospital and stop bactrim immediately.
Concern for SJS
fever, rash, LAD, and eosinophilia and elevated LFTs after starting a medication like phenytoin, carbamazepine or phenobarbital
anticonvulsant hypersensitivity reaction
subtype of DRESS but has a mortality rate of 10%
anticonvulsant hypersensitivity reaction presents how long after starting a new drug?
seen up to 2 months after starting and see fever, rash, pharyngitis and LAD, and facial edema and can have hepatitis or nephritis
anticonvulsant hypersensitivity reaction labs:
eosinophilia and anemia
can have megaloblastic anemia, hepatitis, and rhabdomyolysis
anticonvulsant hypersensitivity reaction can be caused by
phenytoin, lamotrigene, allopurinol carbamazepine phenobarbital, ACEi, antidepressants, and beta blockers.
Medications that need genetic testing prior to starting:
allopurinol in asians
oxcarbamazepine in asians
acabavir in HIV pts
Rule of Nine’s for Total body surface area:
each lower extremity represents 18% TBSA
each upper extremity represents 9% TBSA
anterior and posterior trunk each represent 18% TBSA
head represents 9% TBSA
necrotizing dermatitis differential
zinc deficiency on TPN
allopurinol toxicity
glucagonoma
