EPAP
expiratory positive airway pressure
CPAP
continuous positive airway pressure
a treatment for apnea involving keeping a patient’s airways open using air pressure delivered via a face mask
IPAP=EPAP
ABCDE
asymmetry, border, color, diameter >6mm, evolving
skin eruptions or exanthema 3 groups
1. Macular and maculopapular lesions
2. vesicular or bullous lesions
3. pustular, petechial, or purpuric lesions
secondary changes of skin lesions
comedones, crusting, excoriation, lichenification, scales, scarring, telangiectasia
acne
inflammatory disease of the skin involving the sebaceous glands and hair follicles
causes: corticosteriods, isoniazid
bullous lesions
Caused by exfoliative toxins A and B
Have the appearance of wrinkled tissue paper
Lead to widespread desquamation of the skin
Patients are left vulnerable to secondary bacterial infections
causes: barbiturate overdose, penicillamine, sulfonamides
eczematous dermatitis
most common inflammatory skin disorder, several forms including irritant contact dermatitis allergic contact dermatitis and atopic dermatitis
causes: abx, methyldopa, phenylbutazone, sulfonamides
erythemia multiforme
Hypersensitivity reaction characterized by targetoid rash and bullae; *HSV and mycoplasma infections; EM with oral mucosa and fever is steven-johnson syndrome
causes: barbiturates, hydantois, penicillin, salicylates, sulfonamides, sulfonylureas
erythema nodosum
inflammation of subcutaneous tissues resulting in tender, erythematous nodules; may be an abnormal immune response to a systemic disease, an infection, or a drug
causes: contraceptives, sulfonamides
exfoliative dermatitis
a condition in which there is widespread scaling of the skin, often with pruritus, erythroderma, and hair loss
causes: allopurinal, gold, indomethacin, phenylbutazone
lichenoid eruption
violaceous to purple, polygonal lesions that resemble those seen in lichen planus
Causes: cholorquine, chlorpropamide, mepacrine, quinidine, quinine, thiazides
photosensitivity
increased reaction of the skin to exposure to sunlight
causes: amiodarone, nalidixic acid, sulfonamides, tetracycline
pigmentation
coloration caused by deposit, or lack, of colored material in the tissues
causes: chloroquine, heavy metals, mepacrine
Psoriasiform rash
causes: gold, methyldopa
purpura
multiple pinpoint hemorrhages and accumulation of blood under the skin
causes: cytotoxic drugs, meprobamate, quinidine, quinine
systemic lupus erythematosus (SLE)
chronic autoimmune inflammatory disease of collagen in skin, joints, and internal organs
causes: hydralazine, isoniazid, penicillamine, procainamide
urticaria
allergic reaction of the skin characterized by the eruption of pale red, elevated patches called wheals or hives
causes: aspirin, imipramine, penicillin, serum, toxoid, vaccines
Bulla
a large blister that is usually more than 0.5 cm in diameter
Comedones
plug of keratin and sebum wedged in a dilated pilosebaceous
crust
accumulated dried exudate
Excoriation
a superficial loss of skin, e.g., by scratching
lichenification
area of increased epidermal thickening with exaggerated skin markings, caused by constant rubbing (atopic eczema)
keloid
a sharply elevated, irregularly shaped, progressively enlarging scar due to excessive collagen formation in the dermis during connective tissue
macule
flat, colored spot on the skin
nodule
circumscribed, palpable area of the skin that is >0.5 cm in diameter and appears in part or wholly within the dermis
papule
A circumscribed, solid elevation of skin < 1cm in diameter, with no visible fluid
patch
large macule, >2cm in diameter
plaque
circumscribed, disk-shaped elevated area of the skin >1cm diameter
purpura
multiple pinpoint hemorrhages and accumulation of blood under the skin
pustule
raised spot on the skin containing pus
scales
flakes or dry patches made up of excess dead epidermal cells
scar
area of fibrous tissue that replaces the lost epidermis
stria
streak-like, linear, atrophic, pink, purple, or white lesion caused by stretching of the skin
Telangiectasia
skin lesion due to permanently enlarged and dilated blood vessels that are visible
ulcer
loss of epidermis and part or whole of the dermis
vesicle
visible accumulation of fluid beneath the epidermis (<0.5 cm in diameter)
weal
circumscribed, elevated area of cutaneous edema
Dermatitis Medicamentosa
Hypersensitivity reaction to a drug.
onset is abrupt, widespread, and symmetric erythematous eruption
type 1: immediate-type immunologic reaction
IgE mediated
manifested by urticaria and angioedema of skin or mucosa, edema of other organ, and fall in BP (anaphylatic shock)
Type 2: Cytotoxic reaction
drug or causative agent causes lysis of cells, such as platelets or leukocytes, or may, by combo with another drug, produce antibodies (immune complexes) that causes lysis or phagocytosis
type 3: serum sickness, drug-induced vasculitis
IgG and IgM antibodies are formed against a drug
manifested by vasculitis, urticaria-like lesions, arthritis, nephritis, alveolitis, hemolytic anemia, thrombocytopenia, and agranulocytosis
type 4: morbilliform (exanthematous) reaction
cell-mediated immune reaction
sensitized lymphocytes react with the drug, releasing cytokines, resulting in cutaneous inflammatory response
Drug rash with eosinophilia syndrome (DRESS)
– present as hepatits, eosinophilia, pneumonia, lymphadenopathy, and nephritis
-symptoms may last 2-6 weeks after beginning the medication, most commonly associated with anticonvulsants, sulfonamines, beta blockers, antimicrobials, antidepressants, and allopurinal medication
m/c cause of urticaria and maculopapular allergic skin reaction
penicillin-based medicaiton and trimethoprim-sulfamethoxazole
penicillin-sensitive patients
cephalosporins are assocaited with reaction in 5-15%
carbapenems 15-30%
red man syndrome
not an allergic reaction, associated with vanc often responds to slowing of infusion rate and administration of antihistamine
ACE-I
chronic cough and angioedema
Beta Blockers
precipitate asthma and should not be given to patients at high risk of anaphylaxis, BB may block the action of epi
anticonvulsants and sulfonamines
m/c cause of toxic epidermal necrolysis (TEN) and Stevens-Johnson syndrome (SJS)
radiocontrast media and opiois
stimulate mast cell histamine release through a non-IgE-mediated mechanism
lab and diagnostic for drug eruption
LFT as a baseline
skin bx
allergy skin test
patch and photo test
challenge dosing
Management of drug eruption
withdrawal of drug
epi
antihistamines
when does SJS or TEN usually occur
during first 8 weeks of starting a new medicaiton
m/c medications to cause SJS or TEN
allopurinol, lamotrigine, sulfonamines, sulfasalazine, nevirapine, and oxicams
SCORTEN score
prognosis of SJS/TEN
seven variables with max score of 7
age 40 or greater = 1 pt
malignancy = 1 pt
body surface area detached greater than or equal to 10% = 1 pt
tachycardia greater or equal to 120 = 1 pt
serum urea >10 = 1 pt
serum glucose >14 = 1 pt
serum bicarb <20 = 1 pt
Treatment of SJS/TEN
discontinue agent asap
treat them as a burn patient – thermoregulation and electrolyte management
immunomodulation: cyclosporine, ATN agent, IVIG, plasmapheresis
long term affects of SJS/TEN
eye disorders
vulvovaginal and urinary sequelae
causative agent of cellulitis
gram + cocci
group A B-hemolytic streptococci and staphylcococcus aureus
risk factors for cellulitis
prior trauma, underlying skin lesion, DM, pedal edema, venous and lymphatic compromise, IV drug use
cellulitis of the L.E. of the elderly is often complicated by?
DVT
Gram negative rods causing cellulitis
e. coli
gram negative bacilli causing cellulitis in neutropenic and immunosuppressed patient
serratia, proteus, enterobacter, and fungi (cryptococcus neoformans)
Facial or upper extremity cellulitis
H. influenzae
patient with DM, cellulitis pathogens
streptococci and staphylococci
Erysipelothrix rhusiopathiae
A cause of disease in swine, turkeys, and marine mammals, including diamond skin disease.
Aeromonas
gram negative bacillus; freshwater exposure
vibrio
salt water exposure
confirm the diagnosis of cellulitis
lymph node enlargement and lymphatic streaking (lymphangitis)
differential diagnosis of cellulitis
DVT and necrotizing fasciitis
necrotizing fasciitis
very toxic appearing, bullae, crepitus, anesthesia of the involed skin, overlying skin necrosis, evidence of rhabdomyolysis (elevated creatinine phosphokinase), disseminated intravascular coagulation
management of cellulitis
abx coverage for both streptococci and staphylococci
outpatient duration 5 days
Mild cellulitis (nonpurulent)
– penicillin V-K
– cephalexin
– Dicloxacillin
– allergy to penicillin: clindamycin or doxy
CA-MRSA Cellulitis Treatment
Doxy
TMP-SMX
Clindamycin
linezolid
MSSA cellulitis treatment
Dicloxacillin
cephalexin
TMP-SMX DS
inpatient therapy for cellulitis
nafcillin or oxacillin
cefazolin
MRSA cellulitis inpatient therapy
Vanc
linezolid
deptomycin
ceftaroline
treat till afebrile then outpatient treatment
– linezolid
– clindamycin
– TMP-SMX DS
Immunocompromised Cellulitis treatment
hospitalization and empiric abx
Vanc + antipseidomonal abx
– cefepime
– zosyn
– imipenem-cilastatin
– meropenem
Erysipelothrix cellulitis treatment
penicillin, cephalexin, clindamycin
Vibrio species cellulitis treatment
doxy + ceftriaxone
aeromonas hydrophila cellulitis treatment
doxy + ceftriaxone or cipro
Tinea (skin infection) treatment
terbinafine hydrochloride 1%
butenafine 1%
recurrence cellulitis caused by MSSA treatment
long-term low dose Penicillin G
recurrence cellulitis caused by MRSA treatment
long-term low dose clindamycin
herpes zoster (shingles)
a disease that involves a painful, blistering rash accompanied by headache, fever, and a general feeling of unwellness
herpes zoster lab/diagnostics
polymerase chain reaction testing, Tzanck smear
ophthalmic zoster
5th cranial nerve involvement: tip of the nose (emergency)
50-50-50 rule
guide for antiviral therapy
< 50 hrs since onset of lesions
> 50 years
> 50 lesions
antiviral for herpes zoster treatment
acyclovir
valacyclovir
acyclovir-resistance varicella-zoster virus treatment
foscarnet
adjunct therapy for Herpes Zoster treatment
tylenol, cold compress, tramadol, opioids, oral corticosteriods, hydroxyzine (pruritus)
PHN treatment
Lidocaine or capsaicin skin patch
Gabapentin (Gralise, Horizant, Neurontin) and pregabalin (Lyrica)
Antidepressants — such as nortriptyline (Pamelor), amitriptyline, duloxetine (Cymbalta) and venlafaxine (Effexor XR) can be effective
Prevention of herpes zoster
Zoster vaccine indicated in all patients above 60
-Zoster vaccine live
-recombinant zoster vaccine
should not be administered to immunocompromised patient or pregnant women
m/c type of Skin cancer in the US
basal cell carcinoma
basal cell carcinoma (BCC)
malignant tumor of the basal layer of the epidermis;
papule or nodule with a central scab or eroded area. Nodule has a waxy “pearly” appearance
squamous cell carcinoma
nonhealing ulcer or wart-like nodule
found on skin-exposed areas in fair-skin people
may develop from actinic keratosis
malignant tumor or epithelial keratinocytes
– capacity to metastize
– usually the result of exogenous carcinogens
BCC predisposing factors
sun exposure
arsenic exposure
m/c on face and neck
SCC predisposing factors
M-F ration 2:1
SCC of lip, temple, ear, oral cavity, tongue, and genitalia have a higher rate of metastasis
smokers have increased risk for lip involvement
legs of females
HPV
BCC characteristics
noldules, papules, non-healing ulcers, or scabbed lesions
waxy, pearly nodules with telangiectatic vessels, or as visual or scaly plaques
borders are translucent, elevated, and shiny with fine telangiectasia
SCC characteristics
scaly, red, hard nodular, crusty, does not heal
usually asymptomatic
firm, skin-colored to reddish-brown nodules on damaged skin
may arise out of actinic keratosis
central ulceration
scaling and crusting
heaped-up edges of lesions appear fleshy rather than clear
lesion on the lower lip appear as firm, whitish macules
lab/diagnostics for BCC and SCC
bx, shaved or punch bx
BCC and SCC management
dermatologist referral
bx
curettage and electrodesiccation of BCC lesion <1cm in diameter and in nonfacial area
BCC follow up – annually for 5 years
SCC – every 3 months with close exam of lymph nodes for 1 year then twice a year after that
Melanoma
dark, pigmentation; may be flat or raised irregular borders; may be red, black, or bluish in color; size >6 mm
develop from benign melanocytic cells
Melanoma predisposing factors
leading cause of death from skin cancer
preventative measure – avoidance of blistering solar radiation and use of sunscreen
fair skin, freckles, blonde, blue eyes
melanoma characterisics
bleeding and ulceration are ominous signs
scaling
texture change and irregular border
size change >6mm
development of inflammation
color change
itching
Six Signs of Malignant Melanoma (ABCDEEF
Assymetry, Border, Color, Diameter, Elevation, Enlargement, Friend
primary malignant melanomas
superficial spreading – m/c, caucasians
lentigo maligna
nodular malignant
acral lentiginous – palms, soles, and nail beds, more common in darkly pigmented people
malignant melanoma on mucous membrane
amelanotic (nonpigmented)
arising from blue nevi
congenital and giant nevocytic nevi
labs/diagnostics for melanoma
surgical bx
should never be curetted, electrodesiccated, or shaved
sentinel lymph node bx for staging
Staging of melanoma
Stage I-II = Tumor (depth)
Stage III = Node involvement
Stage IV = Metastases
management of melanomas
dermatologist referral
follow up 3-6 months with skin exam
self exam skin weekly
FAST
face drooping, arm weakness, speech difficulty, Time to call 911
LAPSS
Los Angeles Prehospital Stroke Screen
VAN assessment
Vision, aphasia, neglect
RACE
Rapid arterial oCclusion Evaluation
Lacunar stroke
small subcortical infarcts <15mm diameter
basal ganglia, internal capsule, thalamus, corona radiata, and pons
sxs of lacunar stroke
hemiparesis or heiplegia
dysarthria and dysphagia
Ataxic hemiparesis
lacunar stroke of the anterior limb of internal capsule or PONS base
weakness and ataxia on ipsi side of body, usually leg weakness more than arm
Stoke BP control
lowering BP initially by 15% during first 24 hr
tPA BP limits
prior SBP <185 DBP <110
during and after <180 and DBP <105
Cryptogenic stroke
an ischemic stroke whose cause cannot be attributed to a specific source of embolism, thrombosis, or small artery disease even with extensive medical testing
hemorrhagic stroke
occurs when a blood vessel in the brain leaks or ruptures; also known as a bleed
hemorrhagic stroke symptoms
Impaired LOC, headache, nausea/vomiting, mobility, speech patterns, one sided weakness, blood pressure, respiratory status, pulse rate
risk factors for hemorrhagic stroke
HTN, cerebral amyloid angiopathy, anticoag or thrombolytic use, street drugs, heavy alcohol use, hematologic disorders, OTC stimulants/energy drinks
leading cause of ICH in >60 y.o.
cerebral amyloid angiopathy
subarachnoid hemorrhage
“Worst headache of my life”
Hunt and Hess Scale
predictor of mortality presenting with subarachnoid hemorrhage
1- no symptoms
2- CN palsy, HA, nuchal rigidity
3- mild focal deficit, lethargy, confusion
4- stupor, moderate/severe hemiparesis
5- deep coma
Fisher Grade
Predicts vasospasm risk d/t SAH based on CT scan
1 – no hemorrhage
4 – SAH with IPH and IVH
intracerebral hemorrhage
AIS and ICH
basal ganglia hemorrhage
Contralateral hemiparesis and hemisensory loss
ipsilateral Homonymous hemianopsia
ipsilateral Gaze palsy
decreased LOC
Thalamic hemorrhage
downward deviation of the eyes
pupils pinpoint with positive reaction
coma
flaccid quadriplegia
Cerebellar hemorrhage
NO HEMIPARESIS
facial weakness, ataxia, nystagmus, occipital headache, neck stiffness
ipsilateral horizontal conjugate gaze paresis
pupils PERRLA
inability to walk
vertigo and dysarthria
formula for estimating ICH hematoma volume
ABC/2
(AxBxC)/2
A=longest axis
B=longest axis perpendicular to A
C=# of slices x slice thickness
management of ICH/SAH
avoid ketamine
succinylcholine can cause transient ICP increase
rocuronium is a neuromuscular blocking agent
BP control SBP <140
Cerebral perfusion pressure (MAP-ICP)
correction of coagulopathy (if INR >4)
check INR q 3-6 hr for first 24 hr
External ventricular drain placement (GCS <9)
goal ICP <20 and a CPP >60
strict bed rest
cardiac monitoring
no straining
seizures
cerebral edema (mannitol)
check serum osmolality and Na+ q8hr
management of aneurysm
surgical clipping or endovascular coiling ASAP
cerebral vasospasm
can occur before or after aneurism clipping and coiling; administer calcium channel blocker nimodipine (Nimotop);
re-bleeding
occurs between 2-19 days after initial rupture
repeat CT scan and occasionally repeat LP is needed to confirm re-bleed
Cerebral salt wasting
hyponatremia, excessive secretion of natriuretic peptides
crystalloid fluid replacement
3% saline solution to correct hyponatremia 30-60 ml/hr
q8 hr serum osmolality and Na+
fludrocortisone
m/c medical complication in aneurysmal SAH
fever
blast injury
hippocampus and brain stem
prehospital/emergancy department treatment for TBI
ACLS
spinal immobilization
GCS <8 intubation
avoid hypoxemia o2 sat >90 PaO2 >60
avoid hyperventilation: goal ETCO2 or PaCO2 35-45
avoid hyperventilation in TBI unless:
herniation symptoms are present of if measured ICP is severely high
AVPU
Awake, responsive to voice, responsive to pain, unresponsive
Decorticate posturing
characterized by upper extremities flexed at the elbows and held closely to the body and lower extremities that are externally rotated and extended. occurs when the brainstem is not inhibited by the motor function of the cerebral cortex.
Decerebrate posturing
posturing in which the neck is extended with jaw clenched; arms are pronated, extended, and close to the sides; legs are extended straight out; more ominous sign of brain stem damage. Most Severe.
lab studies for TBI
toxicology drug and alcohol, CBC, chemistry, coagulation
primary head injury
involves features that occur at the time of trauma, including fractured skull, contusions, intracranial hematoma, and diffuse injury. Secondary complications include hypoxic brain damage, increased ICP, infection, cerebral edema, and posttraumatic syndromes.
basilar fracture signs
anterior or posterior skull base
Sx’s of basilar skull fracture
CN dysfunction
hemotympanum
battle sign – mastoid ecchymosis
raccoon eyes – periorbital ecchymosis
CSF leaking from ear or nose – + dextrostix, halo sign, salty taste in mouth, beta-2 transferrin
hearing loss
brain injury
concussion, contusion, hematoma, subdural hematoma, traumatic subarachnoid hemorrhage, diffuse axonal injury
concussion
coup-contrcoup injuries; m/c found in the temporal lobe
contusion
m/c seen lesions are in the orbitofrontal or anterior temporal regions
Hematoma
epidural: m/c in the temporal/parietal region
Subdural hematoma: m/c caused by tearing of the bridging veins
acute subdural hematoma sxs
drowsiness, agitation, and confusion
HA
unilateral or bilateral pupil dilatation
hemiparesis
noncontrast CT
sx indications: >10mm thickness with >5mm midline shift regardless of GCS
chronic subdural hematoma sxs
HA
memory loss
personality changes
incontinence
ataxia
obtain CT scan
sx usually required, burr holes or craniotomy
traumatic subarachnoid hemorrhage
HA
reduced LOC
nuchal rigidity
hemiplegia
ipsilateral pupillary abnormalities
delayed vasospasm
diffuse axonal injury
type of brain injury characterized by shearing, stretching, or tearing of nerve fibers with subsequent axonal damage.
penetrating head trauma abx
ceftriaxone, metronidazole, and vanc immediately for minimum of 6 weeks
management of TBI
limit secondary injury
cerebral/elevated ICP/herniation
herniation
indicated by pupillary dilation
cushing triad: HTN, decreased RR, bradycardia, late finding of elevated ICP
barbiturate coma
may be used to treat ICP after admit; Reduces Metabolic Demand
Pentobarbital
hyperosmolar therapy
mannitol
serum osmolarity: maintain <320
hypertonic saline (2%,3%, or 23% NaCl)
