systemic or peripheral vascular resistance the heart is pumping againstafterloaddecreased perfusion causes a shift to anaerobic metabolism which results in what?formation of lactic acid and the development of metabolic acidosisHR / SBPshcok index SIwhat is the normal shock index? what shows severe shock?N= < 0.7 > 1 is severethis pt population may NOT exhibit tachy bc of their limited cardiac response to catecholamine stimulation or concurrent use of bb and/or presence of pacemakerelderlythis suggests significant blood lossnarrowed pulse pressurewhat is the most common form of shock in trauma? - defined when the circulatory volume is depleted from blood or fluid losseshemorrhagic shockin normal adults, tachycardia after blood loss indicates what?at least a 15% loss of blood volume (>750mls)this is obstructive and not cardiogenic?cardiac tamponadewhat are the 5 spaces where you find hemorrhages in hypovolemic shock?chest, abd, pelvis, long-bones, streetsepsis, anaphylaxis, drug reactions, endocrine, and neurogenic abnormalities. - occurs due to inappropriate vasodilatation of the peripheral blood vessels fromdistributive shockInjury to the spinal cord at the level of the cervical spine or above the level of the 6th thoracic vertebra may lead to a form of vasogenic shock. This is estimated to occur in up to 20% of cervical spine injuries. The damage to the spinal cord, in effect, leads to a sympathectomy. Bradyarrhythmias, inappropriate vasodilation, and resultant hypotension and temperature dysregulation result. *Note: narrow pulse pressure is not seen and it presents classically as hypotension without tachycardia.* Isolated intracranial injuries do not cause shock.neurogenic shockas the name implies, is associated with obstruction of the heart or the great vessels. Tension pneumo/hemothorax and cardiac tamponade, leads to high pressure in the chest; either in the hemithorax or pericardial sac, respectively. This effectively obstructs venous return and diminishes cardiac output leading to inadequate perfusion. Massive pulmonary embolism may impede outflow of the right heart and lead to ventilation and perfusion mismatchobstructive shockfailure of the "pump." Classical cardiogenic shock is most often thought of as myocardial infarct; however, valvular insufficiency, and arrhythmias may also lead to diminished cardiac output and thiscardiogenic shock- 1500 cc blood - 1/3 blood volume in child - blunt trauma - rib fx, intercostal artery, lung lac - penetrating trauma, systemic or hilar vesselsmassive hemothorax- penetrating - most common dx: - becks triad - uncommon (low arterial blood pressure, distended neck veins, and distant, muffled heart sounds.) - cvp line - us tx: - pericardiocentesiscardiac tamponadeconsider mechanism - xrays if penetrating FAST is often diagnostic DPA if pt remains unstable, FAST emergent ORmassive hemoperitoneumexam PLUS hypotension R/O associated injuries "sheet" the pelvis if transfusing blood consider intervention: IR vs ORunstable pelvic fractureusually in non-acclimatized individuals (elderly) may have swelling of feet and ankles with heat exposure generally associated with periods of prolonged sitting or standing caused by muscular and cutaneous vasodilation combined w/ venous stasis - interstitail fluid subsequently accumulates in LE tx: - self limited - support hose and elevation of lower limbs *diuretics are not indicated*heat edemaTransient LOC or collapse that occurs suddenly after exertion in the heat - Cutaneous and muscular vasodilation redistributes intravascular volume to the periphery of the body - Volume loss and prolonged standing cause pooling in the lower extremities - Both lead to inadequate central venous return and insufficient cerebral perfusion signs: - cool/moist skin, weak pulse, transient HoTN, core temp normal to mildly elevated r/o hypoglycemia, arrhythmias, and fixed myocardial or cerebrovascular lesions tx: - rest in recumbent position - cooling - oral rehydrationheat syncoped/t sodium depletion painful spasms of the voluntary muscles of the abdomen and extremities - primary after cooling signs: - muscle fasciculations my be present; core temp is normal to only slightly elevated tx: - oral fluid and sodium replacement if severe, IV normal saline also give oral potassium and replace glucose if needed be in cool place and massage and stretch muscles but avoid intense physical exertion for 1-3 daysheat cramps*systemic reaction* d/t sodium depletion, dehydration, accumulation of metabolites may rapidly evolve to heat stroke BUT *CNS symptoms are not present* core body temp < 40C (104F) signs; - HA, N/V, malaise, muscle cramps, dizzy, dehydration(tahcy, hotn, diaphoresis) dx: measure electrolyte and renal function - serum sodium may be markedly low; myoglobinuria indicates subclinical rhabdomyolysis tx: cool place and give adequate oral hydration and electrolyte replacement if severe, IV NS or lactated ringer if severe hyponatremia: IV hypertonic saline but avoid rapid fluid shiftsheat exhaustionwhen someone in a hot environment lacks appropriate hydrationhypernatremic (primary water loss)when someone sweats excessive amounts and replaces fluid losses with only plain waterhyponatremic (primary sodium loss)AMS from confusion to coma core body temp >40 (104F) can cause sig rhabdomyolysis and multiorgan dysfunction - has the highest mortality of all heat-related illness prompt cooling!!! 2 categories - classic and exertional signs: - HA, dizzy, N/D, visual, seizures, delirium, ataxia, and coma, skin is hot, flushed, and dryheath strokeassociated with heat exposure from strenuous physical activity or occupation and develops rapidlyexertional heat strokewhat is standard of care for heat stroke?water immersion therapyCore body temperature <35°C (<95°F) May be due to exposure to prolonged extremely low temperature (primary), or due to thermoregulatory dysfunction (secondary). Must be considered in any patient with prolonged exposure to an ambient cold environment. Laboratory values inaccurate if warmed for testing signs: - decreased: respiratory drive, oxygen consumption, central/peripheral nerve conduction, gi motility, myocardial repolarization, activity of coagulation cascadeaccidental systemic hypothermiaShivering & possibly poor judgment/coordination Hemodynamic stability and a normal level of consciousness tx: treat with external rewarming Remove & replace wet clothes with dry ones Apply warm bedding, blankets or packs Immersion into a 40°C (104°F) bathstage I hypothermia (core body tempBradycardia Dilated pupils Slowed reflexes Cold diuresis Confusion & lethargy J wave/Osborn wave on ECG Skin may appear blue or puffy when body temp <28°C 32-25) tx: Requires close monitoring of vital signs and cardiac rhythm Warm IV fluids (38-42°C)stage II hypothermia (body temp 28-32)LOC vital signs present tx: Requires close monitoring of vital signs and cardiac rhythm Warm IV fluids (38-42°C)stage III hypothermia (body temp 24-28)loss of vital signs coma loss of reflexes asystole v fib tx: -High-quality CPR must be continued until the patient's core body temperature is at least 32°C Extracorporeal membrane oxygenation (ECMO) is a treatment that uses a pump to circulate blood to bypass heart & lungstage IV hypothermia (body temp < 24)when does cyanosis develop?tissue temp of 25when does tissue damage occur?15Cwhen does freezing (frostbite) occur-4 to -10 CMild & temporary Local paresthesias of the involved area Completely resolves with passive external rewarming Cold fingers in axilla Removing cold footwear & drying feetfrostnipInflammatory skin changes caused by exposure to cold No actual freezing of the tissues Red or purple papular lesions Painful or pruritic (burning or paresthesias) Edema or blisteringerythema perinoAggravated by warmth This may resemble vasculitis or peripheral thromboemboli Differentiate chilblains from other conditions to avoid unnecessary diagnostic testing Treatment consists of elevating and passively externally rewarming the affected part.chilblainCaused by prolonged immersion in cold water or mud, usually <10°C Early symptoms of cold are anesthesia of the affected area (prehyperemic) Hot sensation, intense burning, and shooting pains (hyperemic) Affected part becomes pale or cyanotic with diminished pulses (posthyperemic) May result in blistering, swelling, redness, ecchymoses, hemorrhage, necrosis, peripheral nerve injury, or gangreneimmersion foot (trench foot)Injury from formation of ice crystals in the tissue Most tissue destruction follows reperfusion When confined to only the skin and subcutaneous tissues: Numbness, Prickling, Itching, Pallor when deeper involved: skin appears white/yellow, loses elasticity and becomes immobile, edema, blisters, necrosis, gangrene, paresthesias tx: systemic analgesics for nonfrozen injuries and monitor fluid/electrolytes and hydrate warm water bath, check tetanus staus, protect skin blebs, keep wound open/dry, watch for compartment syndromefrostbiteSigns & symptoms include dyspnea, cough, wheezing, trismus, chest pain, dysrhythmia, hypotension, cyanosis, and apnea. HA, neurologic deficits, and altered level of consciousness A pink froth from the mouth and nose indicates pulmonary edema. +/- N/VD metabolic acidosis PaO2 & pH usually dec blood sugar must be checked rapidly Urinalysis shows proteinuria, hemoglobinuria, and acetonuria Leukocytosis usually present Treatment: The first requirement of rescue is immediate basic life support treatment & CPR + OXYGEN +/- cPAP or PEEP if needed ECMO for ARDSdrowning - aspiration, laryngospasm, hypoxemia, and acidemia*phagocytic* Vasodilatation - leaking of exudates, white cells move in to cleanse wound (macrophages and neutrophils) Triggers healing cascade Vasoconstriction - platelets release and deposit fibrin for homeostasis (more chronic wounds)inflammatory phase of wound managementfibroblastic Granulation tissue: • fibroblasts begin collagen synthesis • Angiogenesis: new blood vessels form Wound contraction occurs Epithelial cells migrate in from edges of woundproliferative phase of wound managementCollagen realigns in the wound, organizes into bundles and creates scar tissue Tensile strength of scar tissue is permanently only 75% of normal (variable timeframe when that strength level is reached - months)maturation or remodeling phase (day 9 to 2 years) of wound managmentwhat is the MC reason why a wound won't heal?mechanical insultLocation: Medial lower leg and ankle Cause: poor blood return due to failure of valves (incompetence) and hydrostasis or fluid leaking into surrounding tissue Appearance and characteristics: Irregular edges, large and shallow Ruddy colored base Hemosiderin deposits - brown staining of skin Heavy exudates (drainage)venous stasis ulcersLocation: Dorsal toes and feet, distal lateral 1/3rd of leg Cause: poor blood supply Appearance and characteristics Well defined borders (punched out or cookie cutter) Dry, pale base Gangrene and necrosis common Painful at rest, increases with elevation or walking Absent or decreased pulses in lower legarterial insufficiency ulcersLocation: plantar surface of foot Cause: combination of arterial and vascular problems, poor glucose control, and insensate foot with trauma Appearance: Small and deep Dry base with periwound callousdiabetic ulcersLocation: over any bony prominence Cause: Pressure: most common Shear: skin moves over bone Friction: surface moves over skin Maceration: excessive moisture (URINE)pressure ulcers decubitiSpecific and safe Vacuum from suction can promote granulation and epithelialization (theory behind VAC treatment).pulsed lavage with suctionWhirlpool-good for when wound is desiccated, for very "dirty" wounds, or widespread areas (burns)whirlpoolWet to dry dressing: apply wet gauze to wound, let it dry, and then manually rip it off woundmechanical debridementMost common are papain-urea such as accuzyme or gladase - Specific and safe, but often slowerchemical or enzymatic debridementuse of gauze to rub wound base or edges to remove non-adherent necrotic tissue or to remove epithelial cells to retard premature closure (when wound edge has rolled - healed under edge)abrasionclassically characterized by cheilosis, glossitis, seborrheic dermatitis, and stomatitis. Severe dietary deficiency can lead to altered mental status and seizures. Dietary deficiency in infants can result in seizures (as a consequence of a reduced synthesis of γ-aminobutyric acid), anemia (caused by impaired synthesis of heme), and homocystinuria (because of impaired formation of cystathionine).dietary deficiency of pyridoxineinvolves breathing pure oxygen in a pressurized room or tube. The air pressure is increased to three times higher than normal air pressure. Under these conditions, your lungs can gather more oxygen than would be possible breathing pure oxygen at normal air pressure. - helps fight bacteria and stimulates release of growth factors and stem cells potential risks include: - temporary myopia - middle ear injuries - lung collapse - seizureshyperbaric oxygen treatmentUsed for relief of pressure from a full circumferential burn injury - *if vascular compromise is evident* The eschar is incised with a scalpel to the level of the fat on the mid-lateral portion of the limb, using care to avoid incising the fascia (i.e., fasciotomy). The incision may be extended to the hand and fingersescharotomyUsed for relief of pressure in extremities *Compartment syndrome most common pathology* Long incisions are necessary to release pressure in the affected compartment and simultaneously incise adjacent compartments. To treat the resulting loss of circulation to an area of tissue or muscle The wounds should be initially left open and a second look procedure for debridement and possible closure scheduled for 48 to 72 hours after the initial intervention.fasciotomyDuring this operation, a clinician will completely remove the necrotic material using a scalpel and forceps, resulting in a bleeding wound bedsurgical debridementThis is similar to surgical debridement, except that it involves the use of surgical scissors.sharp debridementMaggots or their larvae are placed on the wound site and eat away at the dead skin, leaving the healthy tissue behindlarval therapymore effective for liquid poisons or small pill fragments than for intact tablets or pieces of mushroom. It is most useful when started within 60 minutes after ingestion. sometimes used after very large ingestions (eg, massive aspirin overdose), for collection and examination of gastric contents for identification of the poison, and its use makes it easier to administer charcoal and oral antidotes. CI: - stuporous or comatose pts with *depressed airway protective reflexes* - caustic materialgastric lavageRule of 9's adultHead = 9% arm = 9% leg = 18% ant trunk = 18% post trunk = 18% genitals = 1%dead tissuezone of coagulationtissue that is sick but potentially able to be saved requires inc in perfusion to remain viablezone of stasiszone of viable tissue w/ inc blood flow can die if perfusion dropszone of hyperemia*only epidermis and dermis are involved* - injury to the superficial capillaries leads to dilation which causes redness that blanches w/ pressuresuperficial burn*involved epidermis and part of the dermis* - blister formation healing occurs from stem cells that reside in basal layer of epidermis and hair folliclespartial-thickness burns*all layers of epidermis and dermis destroyed and subcutaneous tissues often injured* dead and denatured dermis forms, eschar that is usually intact heals by epithelialization from the edges, with scarring and contracturefull thickness burnWhich of the following is an example of appropriate reduction of VTE risk in a patient during a long flight? - Wearing restrictive clothing - Drinking a lot of water - Drinking a lot of carbonated beverages - Avoiding stretching and walkingdrinking alot of waterA 45 YOM presents to the ED with abrupt onset of headache, nausea, and lethargy. He states he began hiking in the mountains for the first time 24 hours ago and has never experienced symptoms like these before. Based on your suspected diagnosis and his mild symptoms, what is the medication indicated for his condition? - Dexamethasone - Nifedipine - Furosemide (Lasix) - AcetazolamideacetazolamideA girl scout was hiking and started to experience shortness of breath, chest tightness and dyspnea disproportionate to her exertion. Being a well trained Girl Scout she knew that the first line of treatment for the most common cause of death from altitude sickness is - Nifedipine - Descent - Lying down until symptoms improve - Rehydrate/nutritional supportdescentA 60 year old male relocated to a mountain range 2 months ago. For the past month, he has had a chronic headache, muddled thinking, and chest congestion. He is also drowsy during the day. What is the best diagnostic tool for his condition? a) WBC > 15K b) Hgb > 20-22 c) LFT > 40 d) K+ > 6hgb > 20-22A 26 year old female begins experiencing dyspnea and cough while ascending mount Kilimanjaro. This is her first attempt at reaching the peak of a mountain. She has no headache, dizziness, confusion, edema, tachycardia, or palpitations. What is she most likely suffering from? Subacute mountain sickness Decompression illness High altitude cerebral edema Dysbarismsubactue mountain sicknessA 36 year old male presents after hiking up Mount Valparaiso (10,000 ft). His friends state that he developed confusion and was disoriented upon reaching the summit. After 10 minutes, he developed a seizure and had to be airlifted off the mountain. On physical exam he has papilledema and retinal hemorrhage. What is your leading diagnosis? - Acute Mountain Sickness - High Altitude Cerebral Edema - High Altitude Pulmonary Edema - Phobia of Heights - Rocky Mountain Spotted Feverhigh altitude cerebral edemaJohn Smith is doing his first scuba diving class, when he panicked 40 feet underwater. Pt ascended to the surface in a high rate of speed. Within the hour, John started to have pain in his joints, his skin was pruritic and burning, and he had room-spinning dizziness. What's the next best step? - Acetazolamide 250 mg BID, then lay supine for 1 hour - Meclizine 25 mg PO divided bid - 100% oxygen via nasal cannula until able to administer hyperbaric oxygen tx - Hydrocodone 2.5 mg PO q 4 hours or prn with 100% oxygen therapy for 48 hours100% oxygen via nasal cannula until able to administer hyperbaric oxygen txAn obese alcoholic with a hx of DM2 presents to the ED with complaints of pain, redness and swelling to the dorsal aspect of his left foot. Pain has been present for the past 2 days, but worsened this morning after accidentally clipping his toenails too short. You exam the pt and suspect cellulitis. What findings would make you suspect necrotizing fasciitis instead? Elevated serum CK or AST Leukocytosis with left shift Fever of 103F Erythema and warmthElevated serum CK or ASTWhat should you do if you suspect a patient may have necrotizing fasciitis? Initiate broad-spectrum antibiotics and discharge with plan for follow-up in 2 days Consult surgery for surgical exploration Apply Sulfasalazine and administer IV fentanyl for pain Incision and drainage of the blistersConsult surgery for surgical explorationWhere does necrotizing fasciitis most commonly present? Upper extremities Trunk Lower extremities PerineumLower extremities4. What is the difference between SJS and TEN? - SJS affects >10% of the body whereas TEN affects <30% - SJS affects <10% of the body whereas TEN affects >30% - SJS affects <50% of the body whereas TEN affects >50% - SJS affects <75% of the body whereas TEN affects >75%SJS affects <10% of the body whereas TEN affects >30%5. Which class of drugs is strongly associated with SJS? Sulfonamides Penicillins Beta2-adrenergic blockers AntihistaminesSulfonamides6. What would be the most appropriate differential diagnosis for Steven Johnson Syndrome? Contact dermatitis, cellulitis, neurodermatitis Genital herpes, scabies, warts Urticaria, pemphigoid, erythema multiforme Vasculitis, atopic dermatitis, Lyme diseaseUrticaria, pemphigoid, erythema multiformeWhat is the most common etiology of erythema multiforme? Hypersensitivity reaction to a medication Exposure to environmental toxin resulting in a rash Autoimmune response Immune complex deposition following an infectionImmune complex deposition following an infectionWhich underlying disorder puts a patient at increased risk for Erythema Multiforme? Rheumatoid Arthritis Diabetes Herpes Simplex Virus HTNHerpes Simplex VirusA 55 YOM presents to the ED with a 4 day history of a viral illness. His symptoms began to improve, but 2 days ago he noticed lesions inside his mouth. Today, he noticed lesions on his hands that contain 3 concentric components, resulting in a "target" appearance. What is the likely diagnosis? SJS/TEN Bullous pemphigoid Maculopapular drug eruption Erythema MultiformeErythema MultiformeA pt presented to the ED one day ago for a painful mass in her axilla. She was Dx with an abscess, had an I&D procedure, and was sent home with a prescription for Bactrim. One hour after taking her second dose of Bactrim she develops a painful erythematous mass which has progressed to blisters and diffuse exfoliation of her skin. Physical exam findings show detachment of 45% of skin. What is the most important next step? Begin IVIG and prednisone Start cyclosporine Stop use of sulfa drug Perform an ocular examination with fluoresceinStop use of sulfa drugWhat percentage of body surface area affected is necessary to make a diagnosis of TEN? <10% 10-30% >30% >50%> 30%Which class of antibiotics are commonly associated with SJS/TENS? Aminoglycosides Fluoroquinolones Sulfa drugs MacrolidesSulfa drugsa life-threatening condition caused by a dysregulated host response to infection +/- organ dysfunctionsepsisstandards of care that reduce complications and lead to better pt outcomes. pt and families can use this to objectively compare hospitals locally or nationally.core measureswhat are some predisposing factors for sepsis?- ICUE admission (nosocomial infection) - bacteremia - immunosuppression - advanced age and too young age - DM and CA - CAP - previous hospitalization - genetic defectsTemp > 38°C (100.4°F) or < 36°C (96.8°F) HR > 90 beats/min RR > 20 breaths/min or PaCO2 <32 mm Hg WBC > 12,000, < 4000 or > 10% bandsmedicare/medicaid SEP-1 2+Altered mental (GCS <15) RR > 22 breaths/ min SBP < 100 mmHginternation consensus sepsis - 3 2 +systolic bp estimation: >80 mmHgcarotid, femoral, and radialsystolic bp estimation: 70-80 mmHGcarotid and femoral pulsesystolic bp estimation: 60-70 mmHgcarotid pulsewidespread inflammatory response two or more of the following: - temp >38 or <46 - hr > 90 - tachypnea, RR>20 or - hyperventilation paCO2 <32 mmHg - WBC >12K or < 4K or presence of >10% bands, immature neutrophilsSIRSSIRS + definitive source of infectionSepsissepsis + organ dysfunction, hypoperfusion or hypotensionsevere sepsissepsis + hypotension despite fluids perfusion abnormalities - lactic acidosis - oliguriaseptic shock1. respiratory rate 22+ 2. mental status 3. systolic BP 100 mmHg or lessqSOFA1. PaO2/Fio2 ration 2. GCS score 3. MAP 4. vasopressors w/ type and dose rate 5. serum Cr or urine input 6. bilirubin 7. platelet countSOFAsubset of sepsis in which underlying circulatory, cellular and metabolic abnormalities are associated w/ a greater risk of mortality than sepsis alone includes pt who fulfill criteria for sepsis despite adequate fluid resuscitation, pt remains w/ persistent HotN requiring vasopressor to maintain a MAP of > 65 and a lactate level of > 2septic shockanterior uveitis is synonymous with? no foreign body sensation, pain when light is shinned in affected and uninvolved eye, photophobia is present *ciliary flush* r/o corneal abrasion and glaucoma should see ophthalmologist withina few daysiritisfinding of WBC layered out in the anterior chamber. associated with infectious keratitis or endophthalmitits; same day referral to ophthalmologistHypopyonsame day ophthalmologist *foreign body sensation* difficulty opening eye pathogens: s. aureus, pseudomona, coag-neg staph, strep pneumonia *MC RF is contact wear* stains with fluorescein mucopurulent discharge is common abx dropsbacterial keratitisHSV - red eye, photophoia, foreign body sensation and waterery discharge branching opacity on fluorcein stain topical or oral antiviral but can resolve on ownviral keratitissudden acute PAINLESS loss of monocular vision - form of stroke - tx the acute event, find the source of vascular occlusion to prevent further branch of internal carotid Rare in 60-65 RF: HTN, smoking, and DM carotid artery atherosclerosis is most common etiology if under 40 - cardiogenic embolism if over 70 - giant cell arteritis (get ESR and CRP) OCCULAR EMERGENCY tx: revascularization, ocular massage, IV acetazolamide, vasodilater meds: pentoxifylline, nitroglyceren, isosorbid dinatrateretinal artery occlusioninfection involving the content of the orbit (fat and ocular muscles) but NOT the globe itself may cause loss of vision AND life pain with eye movement and proptosis more common in children than adults MC route of infection is ethmoid sinuses BACTERIAL : s. aureus and streptococci dx: confirmed with CT tx: vancomycin + cefriazone or cefotaxime if tooth origin - add metronidazoleorbital cellulitisoccurs when the multilayer neurosensory retina separates from the underlying retinal pigment epithelium and choroid. this separation can occur passively d/t accumulation of fluid btwn the 2 layers or it may occur activly d/t vitreous traction on the retina (in diabetcs) myopia is major risk factor complication of cataract surgery use of fluoroquinolones inc number of floaters in one eye dx: sudden onset of floaters, test visual acuity and visual field.retinal detachmentwhat chemical substance causes more severe damage in the eye ?alkaline over acids - continue irrigation until pH of eye normalizes (usually 30-60 min)true ocular emergency inc pressure is transmitted to the eye and optic nerve causing ischemia and this findings: markedly dec visual activity, afferent pupillary defect, proptosis, diffuse subconjunctival hemorrhage, evidence of inc intraorbital pressure, restricted EOM, periorbital ecchymosisorbital compartment syndromemay indicate a retinal tear of detachment and is also associated with abusive head trauma in infants and young children as well as subarachoindor subdrual hemorrhage >>>*****retinal hemorrhagewhat the #1 complication of cataract surgery (or trauma)?bacterial endophthalmitisrefers to bacterial or fungal infection within the eye, including involement of vitreous and/or aqueous humors. NOT caused by viruses or parasites most cases are exogenous if acute AND bacterial it is considered vision-threatening and must be managed as an emergencyendophthalmitiswhat is the second MC cause of of vision loss from retinal vascular disease (second to diabetic retinopathy) ?retinal vein occlusioncomplication of AOM often seen on CT (which should always be obtained if this is suspected) severely symptomataic is rare; occurs more commonly in children than adults, but incidence has dec clinically: fever, posterior ear pain and local erythema over mastoid bone, edema of the pinna or posteriorly and downward displaced auricle tx: - acute should be admiitted for iv abx - if dont respond may need mastoidectomy and myringotomy +/- typanomastoidectomy (if cholesteatoma present)mastoiditisinvasive infection of the external auditory canal and skull base typically occurs in the elderly with DM, but now on the in in HIV pts pseudomonas aeruginosa is almost always the organism involved exquitis otaliga and otorrhea which are not response to topical measures - more sever, nocturnal and can extend into TMJ causing pain with chewing on exam: granulation tissue visual in the inferior portion of the external auditory canal at the bone cartilage junction can progress to osteomyelitis w/ cranial nerve palsies elevated ESR and CRP CT/MRI to dx tx: cipro IV q 8 hours then pomalignant (necrotizing) otitis externainflammation of the tympanic membrane that occurs in association with AOM in which bullaous are present in the TMbullous Myringitiscollection of blood within the cartilaginous auricle which is usually a result of blunt trauma during sports; prompt drainage and measures to prevent reaccumulation of the blood if not, then permanent deformity caused by fibrocartilage overgrowthauricular hematomarelatively uncommon - inc w/ age inc intraocular pressure appear in distress, slumped over, covering an eye, HA, malaise, N/V dull pain described as HA, rather than eye pain red eye w/ ciliary flush - no discharge pupil is fixed mid-dialation and anterior chamber is shallow RF: >60, femald, hyperopia, meds, inuit, and asian *halos around lights*acute angle glaucomawhat is empiric tx if intraocular pressure is ? 40 and ophthalmologist is not availble within an hour?one drop 1 min apart in this order! - 0.5% timolol maleate - 1% apraclonidine - 2% pilocarpine - IV acetazolamide REPEAT if pressure still over 40RBC layered out in the anterior chamber common complication of blunt or penetrating injury to the eye and can result in permanent vision loss tx: eye shield, bed rest w/ dim lighting, elevated head of bed, control pain, tx N/v, dilating eye drops, and correct any coagulopathyhyphemainflammation of the uvea, the middle portion of the eye, the anterior portion including the iris and ciliary body, and posterior portion of the choroid frequently occurs with other systemic medical conditions VIRAL, systematic (autoimmune), drugsuveitisif traumatic may indicate retinal tear/detachment also associated w/ abusive head trauma in infants and young children dec or hazy vision, black spots, or cob webs if large, red reflex may be absent need CTvitreous hemorrhagesevere eye pain, photophobia, reluctance to open eye, *foreign body sensation*. normal visual activity after pain control (usually tetracaine) normal pupil response *uptake w/ fluorescein* tx: abx drops and follow up with ophthalmologycorneal abrasioninfection of the nasolacrimal system characterized by erythema, swelling, warmth, tenderness of the lacrimal sac +/- purulent discharge can be complicated by orbital cellulitis, sepsis, or meningitis and should be tx promptly w/ systemic abxacute dacryocysitis*aka vincent dz or trench mouth* localized ulceration of the gingiva to necrosis spread to the adjacent tissues of the cheeks, lips, and underlying facial bones secondary signs: fetid breath, pseudomembrane formation "wooden teeth" feeling, foul metallic taste, tooth mobility, lymphadenopathy, fever, and malaiseacute necrotizing ulcerative gingivitiswhat is the diagnostic triad for acute necrotizing ulcerative gingivitis ?*triad: 1. pain, 2. ulcerated "punched out" interdental papillae, 3. gingival bleedingfascia lined areas that can be eroded or distended by purulent exudate. these are potential spaces that do not exist in healthy people, but become filled during infectionsfascial spaceswhat fascial spaces are concerning?submental, submandibular, sublingual, caninelies btwn the muscle and overlying skin and the superficial fascia. this potential space may become involved via upper jaw or lower jaw molarsbuccal spacethis space btwn the mylohyoid muscle and skin and superficial fascia. primarily 2nd and 3rd molars infect itsubmandibular spacea form of firm, acute, toxic, and severe diffuse cellulitis that spreads rapidly, bilaterally, affecting the submanidbular, sublingual, and submental spaces and resulting in a woody feel, hard, non fluctuating swelling is rapid onset dyspnea, odynophagia, restricted/elevated tongue, salivation, muffled voice (hot potato voice)ludwing anginachemistry, immunology, and serology panels; blood bankred topchemitry, immunology, and serology panelsgold toprequires a full draw of sample; uses include coagulation tests, such as thrombin and prothrombin timeslight blue toprequires a full draw and inverting slowly at least 8 times to prevent clotting and platelet clumping; uses include hematology, blood bankgreen or lavender toprequires a full draw to prevent hemolysis; uses include lithium, sodium heparin, and glucose levelsgray topwhat is the order of drawing tubes?red - gold- light blue - green or lavender- graywhat angle should you insert the needle in a venipuncture?15-30 degreewhat angle should you insert the needle in an abg?45what angle should you insert the needle in for an IV line?15

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