clin med er/sx pt 1

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Last updated 5:16 PM on 8/2/26
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147 Terms

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resp distress ED workup

pulse oximetry

ABGs

CXR

EKG

CBC

lytes

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goal o2 saturation for dyspnea

at least 94%

unless chronic dz such as COPD where they may rest at 91%

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nasal cannula

4-6L/minute

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high flow nasal cannula

up to 60L/minute

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oxygen face mask

under 6L/minute

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non-rebreather

6-15L/min

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acute respiratory distress syndrome (ARDS)

diffuse inflammatory lung injury, increased alveolar-capillary permeability, noncardiogenic pulmonary edema leading severe hypoxemia refractory to O2

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ARDS causes

trauma, sepsis, severe pneumonia, influenza, aspiration

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ARDS components on dx testing

bilateral infiltrates on CXR

PaO2: FIO2 under 200

pulmonary wedge pressure under 18mmHg or no clinical sign of evaluated left atrial pressure

ABG: respiratory alkalosis

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ARDS tx

prone position can be helpful

treat underlying cause and give high dose steroids

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management of asthma exacerbation

oxygen

albuterol/ipratropium bromide nebulizer relaxes smooth muscle: can repeat 3x

steroids PO, IM, IV started ASAP

CPAP, BIPAP or intubation if signs of impending respiratory arrest or failure

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COPD complications

respiratory infections

pulmonary hypertension

cor pulmonale

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sxs COPD exacerbation

change in sputum

hypercapnia: confusion, tremor, plethora, stupor

increased dyspnea

wheezing

prolonged expiration

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COPD exacerbation tx

oxygen

ipratropium bromide/albuterol nebulizer

corticosteroids

broad spectrum abx pending work-up: azithromycin (macrolide), doxycycline

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pts presenting to the ED with pneumonia most likely have

community acquired pneumonia

unless presenting from nursing home or other LTC facility (healthcare setting)

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what can be done to test for pathogen in pneumonia

urine testing for strep or legionella

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CAP management

MC organisms: strep pneumo, mycoplasma

emperic abx: azithromycin, if admission respiratory FQ

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what can be used to eval whether pneumonia cases need admission

pneumonia severity index (PSI)

CURB-65 (confusion, uremia, resp rate over 30, BP (hypotension), age over 65) with 2+ admit

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factors associated with increased risk of poor outcomes

RR over 30

HR over 140

BP under 90 systolic

temp over 101

change in mental status

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aspiration pneumonia

sxs: fever, cough, dyspnea, hx suggesting risk for aspiration, dysphagia, intoxication, stroke/AMS

tx: ampicillin-sulbactam IV or augmentin PO with extended coverage of anaerobes (clindamycin or metronidazole)

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pneumothorax classification flow

spontaneous: primary vs secondary

traumatic: iatrogenic (interventional procedures or positive pressure ventilation) or traumatic (penetrating trauma or blunt trauma)

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sxs and dx of pneumothorax

sxs: sudden pleuritic CP, dyspnea, decreased breath sounds in area of PTX, hyperresonance

dx: CXR ± bedside US (trauma) or CT

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spontaneous pneumothorax

primary: occurs in absence of an underlying lung dz

secondary: complication of preexisting pulmonary dz

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traumatic PTX

results from penetrating or blunt trauma

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Iatrogenic PTX

may follow procedures such as thoracentesis, biopsy, etc.

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tension PTX

pressure of air in the pleural space exceeds ambient pressure throughout respiratory cycle

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primary spontaneous ptx

affect mainly tall, thin boys and men 10-30y/o

thought to occur from rupture of subpleural apical blebs

fam hx and cigarette smoking may also be important factors

sxs usually begin during rest and resolve within 24 hours even if ptx persists

if under 15% may only have tachycardia

imaging may be normal or CXR may show visceral pleural line

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tension pneumo

tx involves needle decompression followed by chest tube

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foreign body aspiration

MC aspirations are latex balloons, food, and toys

tracheal: sagittal plane, AP

esophageal: coronal plane, left-right

can see: segmental atelectasis, pneumonia, hyperinflation, pneumothorax

add expiratory view on XR

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hemoptysis

MCC: bronchitis, pneumonia, TB

CXR 1st line then CT

small-volume: O2 if needed, tx underlying cause

massive: ABCs, O2, intubation, CT, consult

initial workup: CBC, PT, INR, PTT, type and cross, sputum gram stain and culture, ABG, renal fxn

death is usually due to asphyxiation

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rib fracture

multiple fractures should raise suspicion for underlying parenchymal damage (pneumo, flail chest, esp fractures of 1st and 2nd rib)

CXR or CT (CT is more sensitive and recommended in pts 65+)

tx: supportive, pain control, incentive spirometry

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flail chest

segmental fracture of 3+ adjacent ribs in 2+ areas leading to a free floating chest wall segment and paradoxical inward movement of chest wall with inspiration and outward with expiration

pt typically has gross trauma with respiratory distress

dx is clinical and CXR ± CT (commonly performed)

do not stabilize segment, CPAP or BIPAP, O2, aggressive pain control with pain meds/nerve block, intubation if RF

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diaphragmatic injury

associated injury: large vessel injury, hemo-pneumothorax (MC), liver spleen injuries, pelvic fracture, head injury

trauma tears diaphragm leading to possible herniation of abdominal contents into the thorax more common on the left side

dx: CXR 1st line, CT is preferred

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hypothermia

RF: exposure to cold environments, depressed metabolic rate, CNS dysfxn, sepsis, dermal dz, substance abuse

initial physiologic response: increase in HR, BP, and CO; shivering

impairs platelet fxn

leftward shift of oxyhemoglobin dissociation curve impairing oxygen release to tissues

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local cold injury and frostbite occur when

freezing temps are reached

hypothermia causes: increased blood viscosity, extracellular ice crystal formation, intracellular dehydration, lysis

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mild hypothermia

32-35 degrees C or 89.6-95 degrees F: shivering, tachycardia, hypertension

below 32: mentation slows, loss of cough and gag reflexes (aspiration is a common problem)

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hypothermia clinical features

impairs concentrating ability: cold diuresis may result in dehydration

progressively lower core temps: lethargic and comatose

prolonged immobility: increases risk for rhabdo and acute renal failure

hemoconcentration and volume depletion: intravascular hemolysis, DIC

hyperglycemia: common early on

hypoglycemia: later in up to 40% of pts

ECG: PR, QRS, and QT-interval prolongations, osborn J waves

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dysrhythmias in frostbite and hypothermia

progresses from tachycardia to bradycardia to trial fibrillation with a slow ventricular rate to ventricular fibrillation and asystole

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1st and 2nd degree frostbite

superficial injuries: edema, burning, erythema

blistering is present in 2nd degree

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3rd degree frostbite

freezing damage to the deeper subdermal plexus

hemorrhagic blisters, necrosis, blue-gray discoloration of the involved extremity is common

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4th degree frostbite

deep injuries involving subcutaneous tissue, muscle, tendon, an bone

little edema

cyanotic insensate tissue: may have hemorrhagic blisters, skin necrosis that later appears mummified

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chilblains (pernio)

painful and inflamed skin lesions

caused by chronic, intermittent exposure to damp, nonfreezing ambient temperatures

once affected by chilblains or frostbite, the involved body part becomes more susceptible to reinjury

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trenchfoot

cooling of the tissue in a wet environment at above-freezing temperatures over several hours to days

long-term hyperhidrosis and cold insensitivity are common

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frostbite and hypothermia tx

attention placed on ABCs and initial resuscitation

evaluate for cardiac instability

v-fib may occur: initiate ACLS, refractory to defibrillation until temp of 30C, three counter-shocks should be attempted

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chilbains and trenchfoot care

elevation and warming

bandaging of affected tissues

nifedipine 20mg PO tid

topical corticosteroids and PGE1 may be helpful

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active core re-warming occurs at

40 degrees C

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rewarming of extremities

rapid rewarming with circulating water at 42 degrees C (107F) for 10-30 minutes

dry air rewarming may cause further tissue injury and should be avoided

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mild hypothermia rewarming

passive warming

remove from cold environment

use of insulating blankets

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severe hypothermia with no CV instability

active external warming

warmed IV fluids

warmed humidified air

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severe hypothermia with CV instability rewarming

aggressive core rewarming with heated lavage fluids at 42 degrees C

ECMO

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other tx for hypothermia

narcotics, ibuprofen, alo vera, PCN G every 6 hours for 48-72 hours (prevent clostridial infections and gas gangrene)

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frostbite blisters care

clear: rich in PG and TXA, often debrided and aspirated

hemorrhagic: often left intact initially, aspiration associated with worse outcome

topical aloe vera every 6 hours

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other conditions with hypothermia

suspected thiamine depletion and alcoholism: thiamine and glucose

hypothyroidism or adrenal insufficiency: IV thyroxine and hydrocortisone

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primary means of heat loss in cold vs hot environments

cold: radiation

hot: evaporation

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what happens in response to heat stress

CO is increased and core blood is shifted to the periphery and vasodilation occurs

several inflammatory cytokines and heat shock proteins are released which improve tissue repair and protect against injury and protein denaturation

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end result of heat stroke

endothelial injury

coagulation disorder

microcirculatory failure

ultimately multi-organ failure

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key sxs of heat stroke

altered mental status

elevated tem: core temps from 104F-116F

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meds that increase risk for heat stroke

anticholinergics, BBs, CCBs

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mainstay heat stroke management

high flow supplemental oxygen with possible intubation

goal to bring core temp down to 40C

replenish volume with IV normal saline and inotropic support as indicated

evaporative cooling with fans and mist

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excessive shivering and seizures with heat stroke is treated with

benzodiazepines (midazolam)

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heat stroke associated rhabdomyolysis tx

IV hydration

diuretics (furosemide)

sodium bicarbonate

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heat exhaustion

clinical syndrome that results from heat exposure

nonspecific sxs but neuro exam should be normal

labs: hemoconcentration, check creatinine kinase levels to exclude rhabdomyelosis

core body temperature is frequently elevated but may be normal

tx: rest, evaporative cooling, IV NS or electrolyte solution

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heat syncope

results from: volume depletion, peripheral vasodilation, decreased vasomotor tone

occurs most commonly in:: elderly, poorly acclimated individuals

potentially serious causes of syncope should be investigated

tx: rest, oral or IV hydration

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heat cramps

painful muscle spasms: typically calves, thighs and/or shoulders

common during athletic events: dilutional hyponatremia from evaporative loses being replaced with water and no salt

core temperature may be normal or elevated

tx: oral electrolyte solution IV NS

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heat tetany

due to effects of respiratory alkalosis: hyperventilation in response to intense heat stress

sxs: paresthesias of upper extremities, circumoral paresthesia, carpopedal spasm

tx: remove heat stress, cool pt, self rebreathing through paper bag

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heat edema

self limited, mild swelling of dependent extremities

occurs in the first few days of exposure to new hot environment due to cutaneous vasodilation and pooling of interstitial fluid

tx: elevation of extremities and severe with compression stockings

administration of diuretics for edema may exacerbate volume depletion and should be avoided

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heat rash/miliaria

maculopapular eruption MC in clothed areas of the body

due to inflammation of sweat ducts

early tx: antihistamines and chlorhexidine cream or lotion

continued blockage/miliaria profunda: antistaphylococcal antibiotics and 1% salicylic acid

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what vasoactive substances are released with thermal burns

histamine

serotonin

arachidonic acid metabolites

free oxygen radicals

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what does the release of vasoactive substances do

increases capillary permeability leading to an egress of fluid from the intravascular space interstitial areas adjacent to the burn wound

in larger burns if the fluid shift is coupled with evaporative water loss it can cause hypovolemic shock

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burn size greater than 20% BSA

systemic response

interstitial edema develops in distant organs and soft tissues

occurs secondary to wound release of vasocative mediators and hypoproteinemia

intensity of response is proportional to the size of the burn

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what happens after successful fluid resuscitation in thermal burns

hypermetabolic state

near doubling of the cardiac output

near doubling of the basal metabolic rate

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full thickness burns zones

zone of coagulation: tissue irreversibly destroyed by thrombosis of blood vessels

zone of stasis: tissue is viable but there is stagnation of the microcirculation

zone of hyperemia: tissue is viable and there is an increased blood flow

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more accurate way to calculate size of thermal burns in infants and children

Lund and Browder burn program

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rule of nines

anterior and posterior trunk are each 18%: each is divided into 9% top and bottom

each entire arm is 9%: front and back is each 4.5%

each entire leg 18%: front and back is each 9%

perineum is 1%

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how can you calculate smaller burns

patients hand can be used as a ruler to estimate percentage BSA, represents 1% of the patients BSA

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superficial burn

red, dry, painful

no blisters

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superficial partial-thickness burns

exposed dermis is red and moist, blanches, blisters

intact capillary refill

healing occurs in 14-21 days

little or no scar formation

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deep partial-thickness burns

pale, white to yellow in color, drier

pressure applied to skin can be felt but 2 point discrimination is diminished

capillary refill and pain sensation are absent

sluggish/absent blanching

healing occurs in 3 weeks to 3 months

scarring is common

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full thickness burns

white/brown/charred, pale, leathery and painless

do not heal spontaneously

all dermal elements are destroyed

surgical repair and skin grafting is needed

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signs of pulmonary smoke inhalation injury

often delayed 12-24 hours

cough, wheezing, respiratory distress

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____ should be suspected in those with smoke inhalation injury

carbon monoxide

HA, vomiting, confusion, lethargy, coma

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dx of smoke inhalation

chest XR may be normal initially

flexible fiberoptic bronchoscopy can confirm dx

draw carboxyhemoglobin levels if CO poisoning is suspected

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fluids for burns

at least 2 large bore IVs

initial fluid resuscitation guided by Parkland formula

50% given in 1st 48 hours post injury, 50% given in the next 16 hours

lactated ringers recommended

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urine output in burn tx

maintained at 0.5-1mL/kg/hr

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cooling of burns

immediately cooled with immersion in cold water and application of cool compress

prolonged cooling of larger BSA burns for greater than 30 minutes can result in hypothermia

ice should not be directly applied, can cause tissue injury from frostbite

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tx of blisters with thermal burns

large over 2cm or involving large joints should be drained and debrided

small on non-mobile areas should be left intact

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topical antibiotics for thermal burns

most common is silver sulfadiazine (do not give with sulfa allergy)

alternatives: bacitracin or triple antibiotic ointment

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circumferential burns

limbs: may develop compromise of distal circulation

chest and neck: may cause mechanical ventilatory restriction

escharotomy may be needed in these cases

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smoke inhalation tx

humidified oxygen

intubation and mech ventilation

bronchodilators

pulmonary toilet: chest physiotherapy, suctioning, breathing exercises

hyperbaric oxygen therapy: used for severe carbon monoxide poisoning

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tetanus prophylaxis for thermal burns

clean minor wounds: if it has been over 10 years since last dose

0.5 mL indicated for all other wounded patient if over 5 years since the last dose

tetanus immune globulin administered to those without a hx of primary series of three immunizations

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common household chemical burns

lye: drain cleaner

halogenated hydrocarbons: paint removers

phenols: deodorizers, disinfectants

sodium hypochlorite: bleach

sulfuric acid: toilet bowl cleaner

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acid burns

coagulation necrosis

protein precipitation and formation of leathery eschar

eschar forms a barrier which helps limit the penetration of the acid

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alkalis

lye, lime, portland cement

combine with protein and fat in skin tissue to form soluble protein complexes and soaps

resulting liquefication necrosis permits the passage of hydroxyl ions into deep tissues

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hydrochloric and sulfuric acid burns

if not decontaminated early, can produce a coagulation necrosis that results in dark brown or black skin discoloration

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acid eye burns

quickly precipitate proteins in the superficial eye structures

result in a ground glass appearance

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alkali acid burns

severe chemosis, blanched conjunctiva, opacified cornea that can obscure the view of the iris and lens

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ocular exposure tx with chemicals

eye irrigation with 1-2 L NS for a minimum of 1 hour

return of pH to neutral pH of 7.4 is a measurable end point for irrigation

visual acuity check should follow not preceded ocular irrigation

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clenched fist injury

occurs in the metacarpophalangeal (MCP) region as the fist strikes the mouth and teeth of another individual

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complications of human bites

cellulitis, septic arthritis, lymphangitis, abscess formation, tenosynovitis, osteomyelitis

polymicrobial infection with staph and strep common isolates

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viruses that can be transmitted by human bite

HSV, herpetic whitlow, hep B

HIV risk is negligible