ER/SURG

Normal values for CBC, basic metabolic panel, ABGs

*CBC* RBC #: 4.2-6.1 WBC #: 4.5-10.5 hemoglobin: 12-17 MCV: 80-100 RDW: 11.6-14.8 Retic: 50-100 (.5-1.5%) platelets: 150-450 neutrophils: 2500-8000 or 55-70% lymph: 1000-4000 or 20-40% mono: 100-700 or 2-8% eos: 50-500 or 1-3% baso: 25-100 or 0-1% bands: 150-400 or 3-5% *BMP*/Chem 7 Na: 135-145 K: 3.7-5.2 Cl: 96-106 Bicarb: 23-29 BUN: 6-20 Cr: .6-1.2 Glu: 70-100 *ABG* pH: 7.35-7.45 PaCO2: 35-45 PaO2: 80-100 Bicarb: 21-27 Base excess: +/-2 SaO2: >95%

Clinical features, necessary ED diagnostic work-up, ED treatment for acute eye pain

*AACG* Acute ocular pain, N/V, intermittent blurred vision w/ halos, conjunctiva injection, hazy cornea, mid-dilated non-reactive pupil IOP >21 mmHg; can be >60 mmHg Tx w/ opth consult, acetazolamide 500mg IV, topical BB, analgesics, anti-emetics. one hour later, pilocarpine q5min x30 min to open the angle. laser peripheral iridotomy 24-48hrs after IOP is controlled. *optic neuritis* vision loss (esp. color) over hours-days, pain w/ eye movements, central scotoma. usually UL, F, 18-45 y/o (may be 1st sign of MS). swollen optic disc. may have other neurologic S/S opth referral, neurology work up. Tx w/ IVIG, steroids. *Corneal injuries* abrasion-- foreign body sensation, light sensitivity, tearing. topical anesthetic drops. fluorescein staining w/ cobalt blue light. treat with abx ointment (erythromycin) foreign body- some present as abrasion. evert upper lid in exam. dirt/glass/metal (rust ring?). remove w/ 25G needle, lateral approach, using slit lamp, rust ring removal not recommended. ulcer- pain, redness, photophobia. timing of eye pain >2-3d. infections of corneal stroma caused by extreme dryness, trauma, contacts. slit lamp reveals the ulcer (opacity w/o staining), also stains. Tx with fluoroquinolone abx drops; refer to optho w/in 12-24 hours. do not patch. *HSV keratitis* infection of cornea by VZV; similar to corneal ulcer presentation but dendritic/branching. can cause corneal scarring. tx with topical acyclovir and oral acyclovir, refer to optho. *acute anterior uveitis* trauma MCC but could be AA, infectious, idiopathic. UL painful red eye, blurred vision, reactive photophobia, tearing. Sx: perilimbal injection, worse closer to limbus (conjunctivitis is the opposite). decreased visual acuity. increase in protein content of aqueous causes an effect known as "flare"; looks smoky. white or red BC in anterior chamber. if severe, hypopyon.

Complication of transfusion therapy and how to manage

*Acute hemolytic transfusion reaction:* d/t transfusion of incompatible donor red cells. S/S: EARLY- fever, chills, back pain, pruritus, burning sensation @ site of transfusion & centrally along the vein and chest pain. In an unconscious pt, more severe features like hypotension, shock, hemoglobinuria, oliguria and XS bleeding d/t DIC develop Tx: Stop transfusion immediately if a transfusion rxn is suspected. Change the blood transfusion set & maintain the venous access using NS. Perform PE w/ spl attention to BP, urine output, and evidence of bleeding. Withdraw blood samples from the opposite arm. Get a coagulation screen to exclude DIC. If hypotension develops, administer fluids and if required vasopressors. Administer furosemide to maintain urine output. In rare cases patients can have a delayed autoimmune transfusion rxn that occurs 3-21 days after receiving blood products *Febrile non hemolytic rxn* Generally occur d/t anti leukocyte abys in a pt who has been pregnant or has been previously transfused, reacting against leukocytes in the transfused blood. Can also occur d/t cytokines in stored platelet concentrates. Generally occurs towards the end of infusion or within hrs of completing the transfusion Management is symptomatic w/ antipyretics. Incidence can be reduced by leukoreduction in which WBCs are reduced in no. through centrifugation or filtration. *Urticaria* Abys in the recipient's blood to infused plasma proteins or infusion of allergens that react w/ IgE abys in the pt *Anaphylaxis* Occurs in pts who have abys against IgA and are often deficient in IgA. The antibodies react with IgA present in the donor blood *Transfusion realted acute lung injury (TRALI)* Pt develops an acute resp rxn w/ fever, cough, SOB typical appearance on chest X-ray. The rxn occurs during or soon after transfusion and may be life threatening *Non immune rxns* -Transfusion associated circulatory overload[TACO], especially in pts with renal and cardiac failure - blood components are excellent volume expanders. -Hyperkalemia -occurs due to RBC leakage during storage -Citrate toxicity - due to commonly used anti coagulants -Iron overload - symptoms appear after 100 units of RBCs have been transfused. -HYPOTENSIVE REACTIONS- in pts taking ACE inhibitors -Air and fat embolism -Thrombophlebitis

Clinical features, necessary ED diagnostic work-up, ED treatment for SDH

Bleeding b/w dura & arachnoid membranes HA after remote trauma d/t tearing of bridging of the veins of surface of the brain Elderly, alcoholics, on thinners - people w/ cerebral atrophy S/S: Classically lucid interval then coma Dx: Rapidly non-con head CT, then MRI more sensitive *Crescent shape*. Tx: Burr holes, craniotomy, non operative management

Etiology, ED care and disposition carbon monoxide poisoning

Carbon monoxide poisoning must be suspected in those with smoke inhalation injury w/ HA, vomiting, confusion, lethargy, coma (esp. if "slow fire" like burning trash). labs: Carboxyhemoglobin levels if CO poisoning is suspected Tx: (*5 minute consult*) Prompt removal from the CO source Supportive care as necessary Intubation and mechanical ventilation may be necessary for severe intoxication, particularly if the patient is unable to protect their airway or if there are signs of respiratory failure. 100% oxygen via nonrebreathing reservoir facemask until COHb is normal (<3%) and patient is asymptomatic, regardless of oxygen saturation or PO2

Classification of shock

Classified into four categories by *ETIOLOGY*: *Hypovolemic* (Blood VOLUME problem) *Cardiogenic* (Blood PUMP problem) *Distributive* (neurogenic, anaphylaxis, septic) (Blood DISTRIBUTION problem) *Obstructive* (extra cardiac obstruction to blood flow) BY *SEVERITY*: mild, moderate, severe (depends on amount of blood loss, duration of shock) *see screenshot* by *STAGE* initial, compensated, decompensated, refractory

Description of fistula, s/sxs, treatment

Connection b/w 2 cavities with epithelial linings that doesn't normally exist: Enterocutaneous Colovesical Colovaginal Enteroenteral Mgt: depends on which cavities are connected Often requires reoperation or NPO status for up to 6 months with nutritional support There are sometimes options for stents or plugs

Clinical features, necessary ED diagnostic work-up, ED treatment for hypothermia

Demographics: >700 ppl/year die of hypothermia (1/2 >65 y/o). People at extremes of age are at risk. EtOH/drug intox patients, psych patients most commonly. Pathophys: body temp falls d/t heat loss (conduction, convection, radiation, evaporation). Heat conservation normally controlled by hypothalamus -> shivering, peripheral vasoconstriction, behavioral responses (dress appropriately, seek shelter). Initial response is rise in HR, BP, CO, vasoconstriction. Impairs platelet function. Leftward shift of oxyhemoglobin dissociation curve impairs oxygen release to tissues Causes: exposure to cold, depressed metabolic rate (severe hypothyroid), CNS dysfunction, sepsis, dermal disease, drug use. S/S: increased blood viscosity, extracellular ice crystal formation, *intracellular dehydration*, lysis. If mild (32-35 degrees/ 89.6-95 degrees), shivering, tachycardia, elevated BP. If below 32/89.6 degrees, mentation slows. Loss of cough and gag reflex -> aspiration. Impairs renal concentrating ability, leading to cold diuresis (leads to dehydration). Lethargy, comatose. Prolonged immobility increases risk, leads to rhabdomyolysis and ARF. Hemoconcentration and volume depletion leads to *intravascular thrombosis, DIC*. Hyperglycemia is common, so is hypoglycemia. Acid-base disturbances (variable). ECG shows PR, QRS, QT interval prolongations. HR goes from tachycardia to bradycardia to a fib w/ slow ventricular rate to v fib and then asystole *Osborn J waves* Tx: ABCs and initial resuscitation. Evaluate for cardiac stability. If in V fib, refractory to defibrillation until 30 degrees Celsius or 86 degrees Fahrenheit; attempt 3 countershocks. Rewarming can be passive (removal from cold environment, insulation) or active (warm water immersion RARE, heating blankets at 40 degrees Celsius COMMON, radiant heat, forced air). Mild hypothermia can be treated with passive, severe active. CORE rewarming at 40 degrees via inhalation, IVF, GI tract lavage, bladder lavage, peritoneal lavage, pleural lavage, extracorporeal rewarming, mediastinal lavage via thoracotomy. If CV stable, radiant heat/warmed blankets/immersion/objects/IVF/humidified air. If unstable, do the lavage. For frost bite, rapid rewarming with circulating water at 42 degrees C (107 F) x10-30 min thawing of frostbite. Dry air rewarming may cause FURTHER tissue injury and should be avoided. Treat pain with narcotics, ibuprofen, aloe vera (or some kind of skin protectant), Penicillin G 500K units q6hours x48-72 hours if weeping (controversial). If blisters are clear, debride or aspirate as rich in PG and thromboxane (IRL we usually leave alone tho); hemorrhagic definitely leave intact. Suspected thiamine depletion and alcoholism treat with thiamine 100mg IV bag, 50% glucose if rapid glucose testing is not available or if glucose low. If suspected hypothyroid or adrenal insufficiency—Tx with IV thyroxine and hydrocortisone 100mg. All patients with more than isolated superficial frostbite or mild hypothermia, admit to hospital, do not d/c unless they can return to a warm environment.

Prophylactic antibiotics prior to surgery (when to use, when to administer?)

Factors that increase infection risk in surgical patients: Malnutrition Advanced age Immunosuppressive drugs Prolonged hospitalization Recent antibiotic use Anergy to skin test Severity of underlying disease Obesity Indwelling catheters Poor tissue perfusion Glucocorticoid medications Radiation therapy Shower w/ *Chlorhexidine* Gluconate soap for MRSA + MSSA Decolonization for joint replacements, spinal surgeries, or other implantation of foreign material *Prophylactic ABX* Choice of ABX should be an agent that is active against the most likely pathogens to contaminate the surgical site. Not given for prophylaxis of infection associated with indwelling catheters (urinary or intravascular), intubation, or open wounds but RATHER for prevention of *surgical wound infection* Not more than 24 hours before operation; IV Recommendation is to give within *1-2 hour* of surgical incision

Necessary pre-surgical work-up

HP, HX CBC Lytes (esp. if on certain meds) serum Cr (all pts >40) blood glucose if Hx DM, A1C lIVer enzymes if hepatic dz coag studies (bleeding issue) UA ABG if cardio pulm issue or acid base disturbance ECG for MI, arrythmias, >60 CXR spirometry If pt have Hx of smoking, SOB, thoracic Sx

Patient related risk factors that may contribute to cardiac complications post-operatively, and how to optimize these factors prior to surgery.

Emergency surgery in pt with cardiac dz is 4x more likely to be fatal than elective. All cardiac dz must be stabilized pre-op, electrolyte problems corrected, and anesthesia is well informed. pre-op eval: H&P. Consider EKG on patients >45, patients who have significant cardiac history, patients who are symptomatic (CP, dyspnea, palpitations, etc.) or anyone who has significant underlying medical conditions. Echo may be ordered for suspicion of CHF or valvular disease. At times, cardiac cath may be performed prior to elective procedures. *ischemic heart dz:* Stable angina—not a huuuge risk Unstable angina or a MI in past 30 days—MAJOR risk factor! intense management and possible delay of surgery. Management: nitrates (don't stop pre-op) to protect coronary arteries, reduce preload and afterload; try a patch instead of orals. Continue BB UNLESSS patient goes into severe heart failure. *arrhythmias* A-fib *PPP 24,25*—if ventricular rate is CONTROLLED (<90bpm), minimal risk but does increase risk of embolism from any left atrial thrombus. If uncontrolled, can cause peri-op CHF. Management: Balance risk of clotting w/ bleeding risk. Control ventricular rate pre-operatively w/ meds (BBs, CCBs verapamil, digoxin, or amiodarone). Post-op tachycardia—can b d/t hypotension, sepsis. CHF, fluid overload, anxiety, sometimes hyperthyroidism. Think about cardiac problems first. Post-op bradycardia—complete heart block? (check EKG...) If so, emergent transvenous pacing (unless d/t MI). if this occurs along with RBBB, consider PE. Another cause could be too much digoxin or beta blockers; if <60bpm, omit today's dose and review prescribed dose. If patient has a pacemaker, could be electromagnetic interference (EMI) in the surgical field leads to ventricular oversensing (MCC= electrosurgery unit). Risk is greater in monopolar electrosurgery > bipolar. Devices programmed to unipolar sensing are more susceptible to EMI than those programmed to be bipolar. Modern day devices can be programmed to either. Occurring DURING operation—can be caused by hypoxia, hypercapnia and hypo or hyperkalemia. Inadequately treated CHF. Make sure you check pre-op EKG, CBC, lytes, digoxin level (if needed). *HTN* *PPP 60* As long as systolic <180 and diastolic <110, minimal risk of cardiac complications. Can be d/t anxiety about operation and drops post-op. Management: in diuretics, check for fluid and electrolyte abnormalities and correct. Most HTN meds should NOT be stopped before general anesthesia (at U of M, d/c ACEi 18 hours before d/t risk of hypotension): BB, CCBs, ACEi, nitrates, methyldopa. Monitor for post-op orthostasis. Still give normal dose of meds with small amount of water, just no closer than 2 hours before op. withdrawal can lead to rebound HTN. Severe HTN—higher risk of periop CHF or stroke (esp. with labile BP). Cannot put them under general anesthesia until they are stabilized. Surgery may get cancelled the day of. *cerebrovascular dz* Cerebral atherosclerosis - BF to brain impaired. Hi risk of stroke in periop period from hypotension or high blood viscosity secondary to dehydration. Suspect if Hx of stroke or TIA. Ischemic heart disease or PVD—ASSUME cerebrovascular dz. Auscultate carotids for bruits. High risk patients --> carotid duplex doppler. If >70% occluded, consider carotid endarterectomy if possible. Asymptomatic carotid bruit, prophylactic surgery reduced risk of stroke from 11 to 5%, judgement call. Post-stroke: avoid Sx for at least 3 months after a stroke (some prefer to wait 6-9 months). Prescribe low dose ASA for anti-coagulation. Consult with surgeon regarding bleeding risks, talk to anesthesiologist regarding carotid dz. (keep on ASA usually unless CNS surgery). *valvular heart dz* Stenotic lesions (esp. aortic stenosis) more serious than regurg. During surgery may cause MI, hypotension, CHF, arrhythmia, or thromboembolism. Predisposes to infective endocarditis so use prophylactic antibiotics. Aortic stenosis *PPP 83*—most serious valvular disorder in surgical patient, limits cardiac output, patients often don't have much reserve. Mechanical valves *PPP 76*—abx prophylactically. Anticoagulation reduced before surgery often safe to continue INRs at 1.5-2.0. if a lot of bleeding is anticipated, some surgeons stop warfarin 2 days before operation and sub IV heparin. Stop heparin 6-12 hours before operation and restart when danger of bleeding over. Can reverse hep quickly with protamine if needed. Follow protocols for abx.

Clinical features, necessary ED diagnostic work-up, ED treatment for hyperthermia, heat stroke

Heat stroke is life threatening injury involving *hyperthermia + CNS dysfunction* as result of thermoregulatory response failure, exaggerated acute phase response, altered HSP response. Results in endothelial injury, coagulation disorder, microcirculatory failure, ultimate multi-organ failure. RF: very young, very old. Predisposing conditions (HF, psych, EtOH abuse, dehydration, poverty, social isolation). Meds (anticholinergics, BB, CCBs). Lack access to air conditioning, poor physical conditions, poorly acclimatized to hot weather. S/S: Hx of heat exposure. AMS w/ CNS abnormalities (ataxia, confusion, bizarre behavior, agitation, seizures, obtundation, coma). Core temp 40 - 47 degrees C or 104-116 F. Anhidrosis is not invariably present. Dx: time dependent medical emergency; consider in the context of heat stress, hyperthermia, AMS. Tachycardic, hyperventilating, respiratory alkalosis (exertional heat stroke may have both respiratory alkalosis and lactic acidosis). 20% hypotensive. Exertional heat stroke leads to rhabdo, hyperkalemia, hyperphosphatemia, hypocalcemia. Work up can be individualized as clinically indicated (including neuroimaging studies). Differential: infection (sepsis, meningitis, encephalitis, malaria, typhoid), toxins (serotonin syndrome, anticholinergics, phenothiazine, salicylate, PCP, sympathomimetic abuse, alcohol withdrawal), metabolic/endocrine emergencies (thyrotoxicosis, DKA), CNS disorders (status epilepticus, stroke), neuroleptic malignant syndrome, malignant hyperthermia. Treatment: *ABCs, cardiac monitoring, IV line.* High flow supplemental O2 (ET intubation if significant AMS, diminished gag reflex, hypoxia). Core temp should immediately be obtained via rectal or bladder probe. Continuous monitoring, bring to 40 degrees C. Rehydrate w/ IV NS or lactated Ringer's. Maintain MAP >60mmHg. Central venous line or pulm artery catheter may be required to guide fluid therapy. Care to not volume overload the patient. Inotropic support and pressors may be required. *Evaporative cooling* is most efficient/practical cooling (fans, disrobe, spray with tepid water). For XS shivering or seizures, give *benzos* midazolam 2mg IV. Other methods of cooling (immersive w/ cold water gastric, urinary bladder, thoracostomy, cardiopulmonary lavage). Tx rhabdo with IV hydration, diuretics (furosemide 40mg IV), sodium bicarb (3 amps in 1 liter of D5W at 250 ml/H). Hyperkalemia treat with protocol. Monitor lytes per hour. Admit to ICU for further observation and monitoring.

Lateral leads of EKG

I, aVL, V5, V6

Inferior leads of EKG

II, III, aVF

Patient education for post-surgical wounds. Right after surgery, prior to discharge, how do they care for it when they go home?

If there is great tension (tendon or abdominal fascia) protect the wound from stress for 6 weeks No lifting/pushing/pulling more than 10 pounds Carrying groceries, laundry basket, vacuuming, mowing lawn/shoveling snow, lifting small children/pets Avoid constipation If primary intention closure was done, *wound can get wet in 24 hours* (epithelialization complete) Remove blood and exudate when washing: promotes good result Good scars are from good approximation If tension is inherent in the area, use nonabsorbable dermal sutures Use steri-strips (or silicone gel sheeting) to reduce inflammation and eventual scarring topical agents-- *Silver sulfadiazene cream* best Slowly release ionic silver into the wound Has broad-spectrum antimicrobial activity and some anti-inflammatory benefit Applied once or twice a day

DDX of headache pain in the ED

Migraine intracranial bleeding (SAH, ICH, SH, EH) Meningitis Brain tumor Cerebral venous thrombosis - HA, vomiting, seizures, (rare) Temporal arteritis - age >50, new onset localized HA, temporal artery tenderness, ESR > 50, +biopsy. Tx w/ hi dose steroids Hypertensive HA Sinusitis Pseudotumor cerebri (benign intracranial HTN) - young fertile women. NV, visual changes. Papilledema w/o AMS Post LP headache - treat with caffeine or blood patch Cluster HA - treat with oxygen IMPROVEMENT WITH TXT DOES NOT RULE OUT SECONADRY CAUSES

S/sxs, treatment of atelectasis

One of those most common causes of post-op fever in the first *24-48*hrs Affects 25% of patients with abdominal surgery Partial lung collapse caused by shallow breathing post-operatively Patients w/ copious secretions can --> bronchial plugging, lobar collapse S/s: fever, tachypnea, tachycardia (low-grade) Tx: supportive; encourage coughing, deep breathing, incentive spirometry, ambulation, mobility out of bed Can give Tylenol for pt. comfort during fever Have patients stop smoking prior to surgery

Causes of/treatment (prophylaxis) for stress ulcers

PUD *PPP 188*—surgical admission can exacerbate ulcer w/ serious illness/trauma, operations, drugs (NSAIDs, steroids). Stressors can sudden hemorrhage (hematemesis or melena) or a perf. Stress ulcer= bleeding in a seriously ill patient caused by splanchnic perfusion impairment and increase in acid-pepsin. Management: perioperatively Tx with sucralfate (protects gastric mucosa) plus and H2 blocker or PPI.

Patient related risk factors that may contribute to pulmonary complications post-operatively, and how to optimize these factors prior to surgery.

RF: duration of anesthesia. Pre-existing respiratory dz (COPD, asthma, bronchiectasis). Higher risk w/ smoking (5x risk of post op issues so stop at least 4-8weeks prior; if stop just before surgery, increases mucus production), cardiac failure, obesity, old age, debility. abd Sx COPD *PPP 102*— predisposes to pneumonia, lobar collapse, pneumothorax. specific management= prior to surgery, measure peak expiratory flow before and after treatment with a bronchodilator. Asthma *PPP 110*—problems include bronchoconstriction, bronchial wall edema, XS mucus, airway plugging. All predispose to atelectasis, infection, hypoxia. specific management= Continue usual meds in perioperative period if possible. Use nebulizer treatments for 1st 24 hours. Postpone Sx during acute exacerbations. Previous PE *PPP 145*: increased risk of subsequent PE. specific management= Follow anticoagulation or prophylactic guidelines. *MANAGEMENT* (general): preop physiotherapy. Drug therapy includes nebulizer bronchodilators. Adequate hydration to thin secretions. Encourage smokers to quit (when you book for elective surgery). Alternative methods of anesthesia (local, regional, spinal). Postop physiotherapy includes enhance deep breathing, coughing, general mobility, and incentive spirometry.

S/Sxs, treatments of patient with acute heroin overdose

S/S: constricted pupils, seizure, hypothermia, slow, deep respirations, hypotension, bradycardia, skin changes - flushed, urticaria Tx: Institute measures to prevent patient and staff injury. ABC's. Give *naloxone* until the drug's CNS depressant effects are reversed (2mg q3minutes for a total of 10mg). Replace fluids, IV to raise circulating volume. Correct hypothermia, reorient the patient often. Auscultate the lungs often for crackles, possibly indicating pulmonary edema. Administer oxygen to correct hypoxemia from hypoventilation. Monitor cardiac rate and rhythm. Be alert for signs of withdrawal such as piloerection, diaphoresis, hyperactive bowels *Catapres and clonidine* are often used to reduce GI effects of withdrawal. SW consult for possible long-term treatment program

Managing anticoagulation prior to surgery

Small extra risk of operative hemorrhage. Most people need to have SOME sort of anticoag continued. If on oral coumadin, consider tapering off and bridging with lovenox, heparin. ASA—irreversible inhibitory effect on platelet aggregation x10 days; effect isn't reversed until affected platelets have been replaced. NSAIDs effect platelets the same way. Causes oozing during and after operation so d/c 7-10 days pre op. Anticoagulation reduced before surgery often safe to continue INRs at 1.5-2.0. if a lot of bleeding is anticipated, some surgeons stop warfarin 2 days before operation and sub IV heparin. Stop heparin 6-12 hours before operation and restart when danger of bleeding over *spinal surgery delay at least 96 hr after surgery.*

ED assessment of suicidality

Some patients may present after a clear suicide attempt, but more commonly present with self-injurious thoughts and behaviors (SITB). clearest RF for suicide is a *prior suicide attempt*; every patient for whom there is a concern of current suicidality should be asked about prior attempts. Other high-risk factors include *lethality and intent*(home alone), hopelessness, access to high lethality means* (especially firearms), *recent stressors* (breakup with partner), and *poor social support* (living alone). There are several standardized tools developed to assist w/ SITB screening, the Suicide Assessment and Five-Step Evaluation and Triage (*SAFE-T*) tool > and the modified *SAD PERSONS* score. These tools have been used in the ED setting and could be helpful for the ED provider. The SAFE-T tool is based on practice parameters from the American Psychiatric Association and the American Academy of Child and Adolescent Psychiatry. admit if pt is a danger to self or others.

S/sxs risk factors of wound dehiscence

Surgical emergency Risk factors: poor nutrition, steroid use, infection, diabetes, older age Affects 5% of patients over 60 yo having laparotomy Often occurs suddenly when coughing/pt. feels/hears a 'pop' Treatment: return to operating room for surgical repair

Evaluation of a patient's tetanus status, when/what to administer for tetanus prophylaxis

clean minor wounds need tetanus proph if >10 years since last doze. all other wounds--> tetanus proph .5 mL IM if >5 years since last dose. if they've never gotten it, give tetanus IMIG in a series of 3 immunizations ???? Tetanus occurs most frequently from a *puncture wound* Wound infected with *Clostridium tetani* produces an exotoxin → causes generalized muscle rigidity and muscular contractions → frequently fatal RF: Dirty wounds (Wounds > 6 hr old, contaminated with soil, saliva, feces or dirt) Puncture or crush wounds Avulsions, wounds from missiles, burns, frostbite *Unknown tetanus status*: give Td 0.5 mL IM PLUS TIG 250 U IM *3+ Tetanus toxoid doses* by history: give Td 0.5 mL IM if > 5 years since last dose; NO TIG necessary (give if >10 years since last dose in clean/minor wounds)

Reversal agents for common anti-coagulants (heparin, Coumadin)

coumadin-- vitamin K, FFP INR heparin-- protamine sulfate aPTT

Clinical features, necessary ED diagnostic work-up, ED treatment for acute CVA

etiology: 87% ischemic stroke, 10% intracerebral hemorrhage, 3% subarachnoid hemorrhage. 10-25% of stroke in young and middle aged people d/t cervical artery dissection (*TIA* is stroke Sx/transient neuro deficits <24hours) Sx: based on anatomical distribution of the ischemia (lacunar, ACA, MCA, PCA, posterior circulation, etc). Hx: last seen normal? meds? Workup: CXR, EKG, labs (PT/INR, CBC, BMP, trop, glucose) *noncontrast head CT*-- if + for bleed, treat it, consult neuro surgery, BP control. if -, NIHSS stroke scale, ASA, talk to stroke neuro and decide on tPA and other imaging or treatment. if tPA or thrombectomy-> admit to ICU, SICU. order *MRI/MRA brain and neck* must give 325 ASA w in 24-48hrs if no tPa *permissive HTN*- no attempts to lower BP unless systolic >220 or diastolic >120. lower or no more than 15% on 24 hours. need systolic BP <180 to give tPA.

Septal leads of EKG

V1, V2

Anterior leads of EKG

V3, V4

Etiology, ED care and disposition of aspirated foreign body

demographic: 90% of pts are under < 4y/o w/ 1/3 not witnessed. 3000 deaths/year w/ increased incidence over the holidays. Most common aspirations are latex balloons, food, and toys. S/S: Pt is often chocking, wheezing, or coughing after eating or playing. Stridor. Keep in mind when one foreign body present there might be another. Also, keep in DDX with prolonged cough. Medical Emergency d/t respiratory arrest. Dx: CXR tho object is uncommonly radiopaque Tracheal: sagittal plane: anterior-posterior Esophageal: coronal plane: left-right Can see secondary findings: segmental atelectasis, pneumonia, hyperinflation, pneumothorax Diagnosis officially made by Bronchoscopy, nasolaryngoscopy. Tmt: O2, calm pt, no back blows or finger sweeps. *heimlich maneuver*-- Only preform if pt cannot talk or speak. NO FINGER SWEEPS. Age <1: cycles of 5 back blows and 5 chest thrusts Age>1: abdominal thrusts Stand behind pt wrap hands around waist Make fist with thumb against abdomen and place midline over naval Grasp with other hand and pressure with quick upward thrust HARD. Repeat until FB expelled or pt is unconscious If unconscious straddle pt's thighs and repeat as above, ventilate.

Rule of nines calculation for burns

each arm is 9 full head is 9 ant leg is 9 post leg is 9 GU area is 1 chest is 9 abdomen is 9 upper back is 9 lower back is 9

Etiology, ED care and disposition of chemical burns

etiology: 5-10 % of burn center admissions. Household chemical burns (lye/drain cleaner, halogenated hydrocarbons/paint removers, phenols/deodorizers/disinfectants, sodium hypochlorite, sulfuric acid/toilet bowl cleaner). Body sites include face, eyes, extremities. Smaller than thermal burns w/ lower mortality rate but healing and hospital stays are longer. Patho: skin damage similar to thermal injury; superficial erythema --> full thickness loss. May appear initially deceptively mild then progress to more extensive skin damage and systemic toxicity. Majority caused by acids or alkalis (alkalis more damaging to tissue). *Acid burns*: *coagulation necrosis*. Protein precipitation and formation of leathery eschar. Eschar forms barrier which helps limit the penetration of the acid. *Alkali*: lye, lime, Portland cement. Combine w/ protein and fat in skin tissue to form soluble protein complexes and soaps. The resulting *liquefaction necrosis* permits the passage of hydroxyl ions into deep tissues. S/S: depends on type of agent, concentration, volume, duration of exposure. *HCl & HS*- if not decontaminated early -> coagulation necrosis -> dark brown or black skin discoloration. *Eye burns*- chemical burns of the eye are ocular emergencies that cause redness, pain, tearing. Acidic quickly precipitates proteins in the superficial eye structures resulting in "ground glass" appearance. Alkali are more severe cuz they go deeper w/ liquefaction necrosis. Severe chemosis, blanched conjunctiva, opacified cornea that can obscure view of iris and lens. Tx: terminate the burning process by removal of garments, copious irrigation. Dry chemicals should be manually removed before irrigation. *Eye exposure*: irrigation w/ 1-2L of NS x 1 hour min. is needed. W/ alkali or acid exposure, return of pH -> neutral (7.4) measurable end point. Visual acuity check should FOLLOW *not precede* ocular irrigation. After initial measures, treatment similar to that of thermal burns (*IVF, analgesia, tetanus immunoprophylaxis*).

Patient factors increasing risk of wound infection.

Where the wound is *located*: Most of body surface - bacteria density low (Trunk, Upper arms, Legs) Heavily contaminated with bacteria are Moist areas (*Head, face, hands, feet*) clay and high organic soil have high infection rates as opposed to sand, black highway dirt. diabetes, emergency procedures, smoking, severe obesity, altered immune function, malnutrition, low body temperature, and long operation times. trauma, shock, blood transfusion, hypothermia, hypoxia, and hyperglycemia

Clinical features, necessary ED diagnostic work-up, ED treatment for aortic aneurysms

aortic aneurysms (AAA) are defined as a focal aortic dilation >3.0cm (but 5 is rly when u gotta worry). infrarenal most common RF: smokers, HTN, >60y/o, white males, HLD, atherosclerosis, CT disorder (marphan), syphilis. S/S: usually asymptomatic but can be IDd by abdominal bruit/mass, imaging. if its symptomatic but UNRUPTURED may present with abdominal, flank, back pain. pulsatile abdominal mass, bruit. if symptomatic but RUPTURED, tearing knife abdominal/flank/back pain w/ pulsatile mass/bruit, hypotension, syncope, CVA. flank ecchymosis (grey-turner). Dx: EKG (ischemic changes). CXR (widened aortic silhouette). CT scan w/ contrast if hemodynamically stable but bedside USN if unstable. If known AAA, str8 to operating room. Tx: if symptomatic or ruptured, immediate surgical repair (endovascular stent graft or open repair) and BB (esmolol, labetolol) or nicardipine, nitroprusside to reduce shearing forces and HTN. want BP <120/80, HR <60. screening: male >65 who has ever smoked, do abdominal USN. if <3cm, whatever. if >5cm, operate. if grows >0.5 cm per year, operate.

Pre-operative risk assessment of hemostatic ability. What increases a patient's bleeding risk? What questions do you ask to assess bleeding risk? When to order labs? What labs to order?

ask for a *history* of: Easy bruising Nose bleeds Prolonged bleeding after cuts Bleeding >3 min. after brushing teeth Prolonged/excessive menstrual cycles Severe bleeding after tooth extraction / surgery Liver disease, renal failure or hypersplenism Family history of bleeding disorders Current or recent use of drugs that may interfere with hemostasis Warfarin, heparin, ASA (including many OTC preparations), NSAIDS, CCBs, steroids *physical exam* Look for signs of liver disease, platelet dysfunction, hematomas, splenomegaly Bleeding tendencies increase with *medications*: ASA, Plavix, Warfarin, alcohol, NSAIDS, chemo, antibiotics *congenital* Defects of hemostasis: Hemophilia A (factor VIII deficiency) Hemophilia B (factor IX deficiency) Von Willebrand's disease *Acquired* Liver disease Vitamin K deficiency Disseminated intravascular coagulation Massive blood transfusion Platelet disorders At particular risk are those undergoing CNS procedures or spinal anesthesia and risk should be re-evaluated in the presence of these agents. labs: *Coagulation Studies* Best determinant of bleeding tendencies is an accurate history detailing response to minor traumas Bleeding time, aPtt, PT do NOT reveal risk of perioperative bleed in healthy patients Should be documented in patients taking anticoagulants. *Hepatic Enzymes* •Not indicated routinely •Order if clinical s/s indicate hepatic disease *CBC* if s/s compatible with anemia, loss of blood during procedure is thought to be significant Hemoglobin in patients > 65 years of age undergoing major surgery *from other PPT*: •Bleeding time - may not be clinically useful, studies show it does not accurately address risk of surgical bleeding •Prothrombin time/INR - measures fibrinogen (I), prothrombin (II), V, VII, X. Used to follow patients on Warfarin •Partial thromboplastin test (PTT) - measures above and VIII thru XII •Platelet count •Risk of bleeding increases with platelet counts < 100,000/µL •Accelerates w/ counts <50,000 Extremely high with <5,000 •LFTs •fibrinogen •BUN/Cr •Other testing as indicated (blood smear, bone marrow biopsy etc)

Clinical features, necessary ED diagnostic work-up, ED treatment for hypertensive urgency/emergency

check BP guidelines cuz syed, PPT say diff things *Hypertensive urgencies*-- BP must be reduced w/in *few hours*. examples include *asymptomatic* severe hypertension (systolic >220, or diastolic >125 that persists after a period of observation) & those w/ optic disk edema, progressive target-organ complications, and severe perioperative hypertension. Elevated BP levels w/o symptoms of new or progressive target-organ damage rarely require emergency therapy. Parenteral drug therapy is *not* usually required; partial reduction of BP w/ relief of symptoms is the goal. Effective oral agents are *clonidine, captopril*, and slow-release *nifedipine*. *hypertensive emergencies*-- BP must be reduced within *1 hour* to avoid morbidity/death. BP usually strikingly elevated (diastolic >130), the correlation between pressure and end-organ damage is often poor. the presence of critical multiple end organ injury determines the seriousness of the emergency & the approach to treatment. Emergencies include *hypertensive encephalopathy* (headache, irritability, confusion, and altered mental status due to cerebrovascular spasm), *hypertensive nephropathy* (hematuria, proteinuria, and acute kidney injury due to arteriolar necrosis and intimal hyperplasia of the interlobular arteries), *intracranial hemorrhage, aortic dissection, preeclampsia-eclampsia, pulmonary edema, unstable angina, or MI*. Encephalopathy or nephropathy accompanying hypertensive retinopathy has historically been termed "malignant hypertension", but the therapeutic approach is identical to that used in other hypertensive emergencies. *Parenteral therapy* is indicated in most hypertensive emergencies, esp. if encephalopathy present. initial goal is to reduce the pressure by *no more than 25% w/in minutes to 1-2 hours* and then toward a level of *160/100 w/in 2-6 hours*. XS reductions in pressure may -->coronary, cerebral, or renal *ischemia*. To avoid such declines, the use of agents that have a predictable, dose-dependent, transient, and progressive antihypertensive effect is preferable. In that regard, the *use of sublingual or oral fast-acting nifedipine preparations is avoided*. *specific emergency Tx* *Acute ischemic stroke* often associated w/ marked elevation of BP, which will usually fall spontaneously. In such cases, antihypertensives should only be used *if systolic >180-200* & BP should be reduced cautiously by *10-15%*. If thrombolytics are to be given, BP should be maintained at <185/110 mm Hg during treatment and for 24 hours following treatment. In *intracerebral hemorrhage*, the aim is to minimize bleeding by reducing systolic BP in most patients to *130-140 mm Hg* within the *first 6 hours*. In *acute subarachnoid hemorrhage*, as long as the bleeding source remains uncorrected, a compromise must be struck b/w preventing further bleeding and maintaining cerebral perfusion in the face of cerebral vasospasm. In this situation, BP goals depend on the patient's usual blood pressure. In *previously normotensive patients*, the target should be a systolic 110-120. in *hypertensive patients*, BP should be treated to 20% below baseline pressure. In the treatment of hypertensive emergencies complicated by (or precipitated by) CNS injury, *labetalol or nicardipine* are good choices, since they are nonsedating and do not appear to cause significant increases in cerebral blood flow or intracranial pressure. Patients w/ subarachnoid hemorrhage should receive *nimodipine x3 weeks* following presentation to minimize cerebral vasospasm. In hypertensive emergencies arising from catecholaminergic mechanisms, such as *pheochromocytoma or cocaine use*, BB can worsen the HTN bc of unopposed peripheral vasoconstriction; *nicardipine, clevidipine, or phentolamine* is preferred. Labetalol is useful in these patients if the heart rate must be controlled. *ACE inhibitors* are specifically indicated for hypertensive crisis from scleroderma.

Brief description of types of replacement fluids

*5% dextrose D5W* Composition : Glucose 50 gms Pharmacological basis : Corrects dehydration and supplies energy( 170Kcal/L) Indications : -Prevention and treatment of dehydration -Pre and post op fluid replacement -IV administration of various drugs -Prevention of ketosis in starvation, vomiting, diarrhea -Adequate glucose infusion protects liver against toxic substances -Correction of hypernatremia *.9% NS* Composition : Na+ 154 mEq, Cl- 154 meq Pharmacological basis : provide major ECF electrolytes, corrects both water and electrolyte deficit. ›Indications -Water and salt depletion - diarrhea, vomiting, excessive diuresis -Hypovolemic shock -Alkalosis with dehydration -Severe salt depletion and hyponatremia -Initial fluid therapy in DKA -Hypercalcemia -Fluid challenge in pre-renal ARF -Irrigation - washing of body fluids Vehicle for certain drugs *Ringer's lactate* most physiologic fluid; rapidly expands IV volume. each 1L of fluid contains 130 Na, 4 K, Cl 109, Ca 3, bicarb 28. indications -Correction in severe hypovolemia -Replacing fluid in post op patients -Burns - (Parkland formula) -Diarrhea induced hypokalemic metabolic acidosis -Fluid of choice in diarrhea induced dehydration in pediatrics -DKA , provides water, correct metabolic acidosis and supplies potassium -Maintaining normal ECF fluid and electrolyte balance *D5 w/ 1/2 NS* Pharmacological basis : -Supply major EC electrolytes, energy and fluid to correct dehydration -more water with less salt -Can add K+ (generally 20 mEq/L) ›Indications : -pediatric & very elderly -Maintenance fluid in early post operative periods ›Often see 100-125 ml/hr D5 ½ NS with 20 mEq K+/L ›Some surgeons use only ½ NS -Treatment of hypernatremia -Compatible with blood transfusion

Clinical features, necessary ED diagnostic work-up, ED treatment for spider bites

*Brown recluse bites* *PPP 615* Mildly erythematous("*redhalo*") lesion that is firm, heals over several days to weeks. CAN be a severe rxn w/ immediate pain, blistering, bluish discoloration --> *necrotic* over next 3-4 d and form eschar from 1-30cm in diameter. *Loxoscelism* is systemic rxn that may occur *1-2d after* envenomation. S/S—fever, chills, vomiting, arthralgia, myalgia, petechiae and hemolysis. Severe cases progress to seizure, renal failure, DIC, death. Diagnosis may need to be made on clinical grounds since the bite is often unwitnessed. Tx: supportive measures; *no antivenom available*. Tetanus prophylaxis, analgesics, abx may be offered when appropriate. Surgery is reserved for *lesions >2cm* in size and is deferred for 2-3 w following the bite. *Dapsone 50-100mg/d* (abx) & *hyperbaric O2* may prevent some ongoing local necrosis. Pts w/ severe systemic rxns & hemolysis must be hospitalized for consideration of blood transfusion and hemodialysis. *Black widow bite* Immediate pin prick sensation --> 1hr later, pt may experience erythematous skin lesion that are often *target shaped*, swelling, and diffuse *large muscle cramps* (abdominal wall cramps that mimics peritonitis). Severe pain x3 days, muscle weakness xWeeks to months. Serious acute complications include HTN, respiratory failure, shock, coma. Tx: local wound Tx and supportive care w/ *analgesics, benzodiazepines*. Hospitalization required for severe envenomation including parenteral pain meds and *horse antivenom* therapy (rapidly effective; IV dose 1-2 diluted vials over 30 minutes)

Clinical features, necessary ED diagnostic work-up, ED treatment for acute vision loss

*Cataract*; MCC *Angle Closure Glaucoma* (#2) Acute ocular pain, N/V, intermittent blurred vision w/ halos, conjunctiva injection, hazy cornea, mid-dilated non-reactive pupil IOP >21 mmHg; can be >60 mmHg Tx w/ opth consult, acetazolamide 500mg IV, topical BB, analgesics, anti-emetics. one hour later, pilocarpine q5min x30 min to open the angle. laser peripheral iridotomy 24-48hrs after IOP is controlled. *Central Retinal Artery Occlusion* Sudden, painless vision loss of one eye. Amaurosis Fugax- transient loss of vision lasting seconds to minutes, can precede. Associated w/ embolus in retinal artery. Pale fundus w/ narrowed arterioles with segmented flow (boxcars) and bright red "cherry" macula TX- ophtho consult. Decrease IOP w/ acetazolamide, anti-coagulate, revascularize. *Central Retinal Vein Occlusion* Sudden painless, unilateral vision loss associated w/ DM, HTN, CAD. Decreased visual acuity, Relative Afferent pupillary Defect, abnormal red reflex. Fundoscopy reveals retinal hemorrhages, cotton wool spots, optic disc edema (blood and thunder) Ophtho referral *Optic Neuritis* vision loss (esp. color) over hours-days, pain w/ eye movements, central scotoma. usually UL, F, 18-45 y/o (may be 1st sign of MS). swollen optic disc. may have other neurologic S/S opth referral, neurology work up. Tx w/ IVIG, steroids. *Giant Cell Arteritis* Inflammatory condition in elderly. profound UL visual loss. jaw claudication. HA, scalp tenderness, polymyalgia rheumatica in 50%. ESR >60mm/hr; CTA gold standard of Dx. Tx w/ ophtho referral, steroids *Retinal Detachment* Result of retinal hole or tear w/ seepage of fluid b/w retina & choroid. RF=age, trauma, myopia, cataract surgery. S/s: flashing lights, floaters, vision loss: filmy, cloudy, irregular, or curtain-like. visual field defects Tx ophtho referral

Common UE fractures and their ED management

*Colles & Smith Fx* MOI: FOOSH but smith (drunk) fracture is falling on flexed wrist. *Colles*--transverse fx of distal radial metaphysis w/ dorsal displacement of distal fragment. Classic "dinner fork deformity." *Smiths*--transverse fx of the distal radial metaphysis w/ volar displacement of distal fragment. Also known as reverse Colles fx. Tx: Sugar tong splint with wrist in flexion. *Skier's thumb* (gamekeepers) Injury involving the ulnar collateral ligament. May have associated avulsion fracture MOI-usually fell directly onto thumb or overuse of thumb •Compare to normal side •Laxity and focal pain Tx: Some need operative care. Thumb spica splint or cast for both initially *scaphoid fracture* This fracture cannot be missed because AVN and nonunion d/t to unique retrograde blood supply. Most frequently fractured carpal bone; generally FOOSH injury S/s: "snuff box tenderness". Pain with axial loading. Tenderness of scaphoid loading. Dx: Xray non diagnostic. Tx: Long arm thumb spica with repeat Xray in 7-10 days. Radial shaft fracture / *Galeazzi fracture* PPP 300 Patho/etiology: usually occurs with ulnar shaft fractures/dislocation. Occur from direct blow to forearm or FOOSH.Treatment: orthopedic referral; generally surgical.

Risk factors, work-up, brief treatment of PE

*PPP 145* obstruction of pulm artery or branch from somewhere else (usually DVT) RF: post-op (esp. abd and ortho Sx) d/t VIrchow's triad (venous stasis, hypercoaguability, vessel wall injury), OCPs, malignancy, chemo, prior DVTs. S/S: fever, asymmetric edema, calf pain, SOB, chest pain, tachycardia, sense of impending doom. Sx of DVT. syed said easiest way to rule IN a PE= hypoxic, CXR is normal. labs: CBC, CXR, EKG, *helical CT chest*, PE protocol, DVT scan (USN). EKG shows S1Q3T3. CXR shows Westermark's sign (focal oligemia, focal peripheral hyperlucency distal to large vessel occluded by PE), Hampton's hump (wedge-shaped pleural consolidation usually peripheral; represents infarction). d-dimer-- not 1st line; only do it if low suspicion for PE. Tx: anticoagulation, O2 supp, IVC filter if not candidate for anticoagulation if unstable-- thrombolytic/embolectomy C/I for thrombolysis- stroke in recent past, AVM, CNS Sx, stuff like that

Etiology, ED care and disposition of swallowed foreign body

*PPP 156* kinda etiology: 75% peds. kids are usually inorganic objects whereas adults are food impaction at sites of underlying esophageal pathology. 80% spontaneously resolve but at 4 areas of narrowing (UES/cricopharyngeous muscle at C6, aortic arch at T4, left main stem bronchus, and LES at T10-11). S/S: history. dysphagia, chest pain, neck pain. drooling, choking. odynophagia may indicate esophageal spasm, laceration, or perf. inability to swallow secretions indicates complete obstruction. peds may only have decreased PO intake, vomiting, or stridor. *concerning ingestants* include disk/button batteries (can cause liq necrosis of esophagus), magnets (obstruction, entrapment, necrosis), and sharp objects (obvi). imaging: XR of neck, chest, abd to diff between airway and GI foreign bodies. button batteries show double density to ddx from coin. CT scan if suspicion for perf. Tx: *conscious w/ severe choking* BLS removal procedure (heimlich). may need immediate airway management w/ surveillance. *emergent endoscopy* if esophageal button batteries, sharp objects, and suspected complete obstruction. urgent if incomplete esophageal food bolus, sharp objects in stomach or duodenum, objects longer than 6cm, suspected drug packets, magnets, or anything in there >24 hr. *upper esophagus* direct visualization and FB removal using kelly clamp or magill forceps. doesnt work? foley balloon extraction. doesnt work? bougienage to advance coins and smooth them from the esophagus to stomach using esophageal dilator. otherwise, consult GI/SURGERY.

Clinical features, necessary ED diagnostic work-up, ED treatment for cholecystitis

*PPP 158* inflammation of gallbladder usually d/t *gallstone obstruction* of the *cystic duct*, though could be acalculous. RF-- fat female forty fair complications: gangrenous cholecystitis (elderly, DM), gallbladder perforation results from this gangrene. can lead to cholecystenteric distulas. if gallstones obstruc this fistula, can lead to gallstone ileus. emphysematous cholecystitis (elderly, DM). S/S: RUQ pain that refers to right shoulder (+Boas sign) similar to biliary colic but duration is longer and more severe. precipitated by fatty foods. fever, N/V, + Murphy sign. if peritonitis--> perf. labs: WBC can be normal or elevated, same w/ liver transferases. Dx: *from current ER* USN preferred; can show gallstones, dilatation of the intra or extrahepatic bile ducts or thickening of the gallbladder wall > 3mm, pericholecystic fluid, and murphy sign. *From PPT* USN (>90% sensitivity, specificity) will show stones in dilated gallbladder, gallbladder wall thickening, trace pericholecystic fluid. If elevated WBC + elevated bilirubin, alk phos, transaminases, suspect cholangitis. CT can incidentally find gallbladder dz during abd pain workup but inferior to US. Superior in defining course and status of extrahepatic biliary tree and adjacent structures (test of choice in malignancy). HIDA scan is 95% sensitivity and specify for acute cholecystitis. Tx: *From current ER* NPO. IV crystalloid resuscitation. antiemetics and analgesics (NSAIDs, opioids) as needed. antibiotics are indicated for complicated cholecystitis as well as for preoperative surgical prophylaxis in uncomplicated cholecystitis. parenteral abx options include monotherapy w/ piperacillin/tazobactam or meropenem, or combo therapy with metronidazole + ceftriaxone. Surgical consultation is advised for admission and treatment guidance with options to include surgical removal, percutaneous cholecystostomy, or endoscopy. Select patients with uncomplicated cholecystitis may be candidates for outpatient treatment and close surgical follow-up, as per the surgeon's recommendations. Outpatient antibiotic options include levofloxacin plus metronidazole. *from PPT* IVF; consider NG tube if emesis. Abx to cover gram - and anaerobes. Analgesia, VTE prophylaxis. Laparoscopic cholecystectomy. Early cholecystectomy performed within 72 hours of acute cholecystitis is preferred > delayed surgery performed 6-10 weeks later. Laparoscopic > open (<5% rate of conversion to open). When patient is medically unfit for OR, abx and cholecystostomy tube for biliary decompression. Intraoperative cholangiography and CBD exploration can be performed at same time if there is difficulty identifying the critical view of safety. Dissect out Calot's triangle (bordered by cystic duct, common hepatic duct, and base of liver). ID the cystic duct and cystic artery PRIOR to proceeding with surgery. Postop—clear liquids, then advance as tolerated. Patients can have referred shoulder or neck pain from the CO2 insufflation causing diaphragmatic irritation. Analgesia. Abx usually stopped postop. Consider lifting restrictions for a couple of weeks. F/u clinic 2-4weeks post op.

Clinical features, necessary ED diagnostic work-up, ED treatment for pancreatitis

*PPP 224* S/S: acute severe *epigastric pain* often *radiating to back*. N/V. Hx of GB dz, EtOH, ERCP, hypertriglyceridemia. VS show tachycardia, tachypnea, fever, hypotension. if cullen/grey-turner signs, think necrotizing. Dx: CBC, CMP, amylase<lipase, lactic acid, LDH, T&S. Leukocytosis, lipase 3x normal, ALT >150. *Ranson's criteria* 1 pt for >55, WBC >16, glucose >200, LDH >350, AST >250 if score is >3, pancreatitis likely. mortality of 1% for score under 3, and 40% for score greater than 5. Imaging: abdominal series to assess for free air. USN abdomen to ID gallstone. CT scan if acute and severe to ID necrotizing pancreatitis, abscess, pseudocyst or hemorrhage. Treatment: *if mild,* treat with analgesia, NPO, IVF, no abx. admit general. *if severe (Ranson >3),* admit to ICU for shock, ARDS, RF, GI bleed, multisystem failure. abx for abscess or necrotizing. surgery consults for necrotizing, abscess drainage, or hemorrhagic. if gallstone, cholecystectomy prior to d/c is usual.

Clinical features, necessary ED diagnostic work-up, ED treatment for small bowel obstruction

*PPP 229* S/S: *CAVO*= cramps, abdominal distention, vomiting, obstipation (obst. usually late finding). Generalized colicky abdominal pain, nausea, distention, decreased flatus. Tachycardia, fever, hypotension. Prior abdominal surgical adhesions in 60%. Generalized tenderness, +/- guarding/rebound. High pitched tinkling, hyperactive, quiet, absent bowel sounds. Abdominal/inguinal/femoral masses. Dx: CBC, CMP, lactic acid, UA, blood cultures (if septic). Imaging: Abdominal series will show free air, dilated loops of small bowel, airfluid levels. CT scan abd + pelvis will show dialted bowel w/ transition zones, hernia, mass, ischemia. bowel wall thickening, pneumatosis, portal gas --> early strangulation. Tx: all receive fluid resuscitation, analgesics, antiemetics. *abx* if peritoneal signs, fever. surgery consult. cover for gram negative and anaerobes. *nonoperative tx* includes NPO, IVF, NG tube decompression (if simple or partial obstruction, most resolve over 72 hrs) and reduce any incarcerated hernia. *operative* for complete obstructions or nonresolved partial that worsens MOSTLY strangulated hernias, malrotations, masses.

Etiology, signs and symptoms, treatment of paralytic ileus. (focus mainly on surgical patients)

*PPP 230* clinical diagnosis of a "sleepy bowel" --> decreased peristalsis in absence of structural obstruction; very common after abdominal surgery; XS narcotic use. S/S: similar to SBO; abdominal pain, N/V, obstipation, distention, flatus, inability to tolerate PO diet. Decreased or absent bowel sounds (differentiates from SBO high pitched tinkling) Dx: plain radiographs show dilated loops of bowel w/o transition zone. CT if further testing required. Tx: supportive. NPO--> clear fluids --> liquid diet --> regular. encourage pt to ambulate. gum chewing may help. +/- pharm therapy (metoclopramide, alvimopam). NG suction if moderate persistent N/V.

Clinical features, necessary ED diagnostic work-up, ED treatment for appendicitis

*PPP 233* S/S: vague periumbilical pain, followed by anorexia, nausea, and vomiting. Over the next 4 to 48 hours, pain migrates to the RLQ. pain before vomiting, anorexia. fever, tachycardia. Rovsing sign (referred LLQ pain), psoas sign (for retrocecal appendix, extending right thigh), obturator sign (pain with internal rotation of flexed right thigh). McBurney point tenderness. Labs—CBC w/ diff, CRP, bilirubin, IL-6, procalcitonin, urine pregnancy, UA to r/o pyelo, stone. Imaging-- CT with contrast; USN in pregnancy, children, and women with suspected gynecologic pathology Dx—maximal outer diameter >6mm, wall thickening >2mm, periappendiceal fat stranding, appendicolith Tx: laparoscopic appendectomy, but pre-op we are gonna start abx (cover for negative, *cefoxitin or Unasyn* alone AKA ampicillin/Sulbactam. Otherwise, *cefazolin + metronidazole*), lytes/IVF, NPO, treat pain. Post-op—ADC VANDALISM (admit, Dx, condition, vitals, allergies, nursing orders, diet, activity, labs, IVF, special studies, meds) +/- VTE prophylaxis. IV abx x48 hours, NPO d/t ileus, cardiac monitor. If perfed: NONseptic, Indication for operation is fail treatment, free air. Otherwise try conservative. If SEPTIC: indication for surgery although further risk for complications.

Clinical features, necessary ED diagnostic work-up, ED treatment for epistaxis

*PPP 343* 1. figure out if its anterior vs posterior bleed: *Anterior* - visualized on exam. Kiesselbach's plexus *Posterior* - bleeding occurs from both nares, blood is draining into posterior pharynx, blood source cannot be visualized Tx: *Anterior* - stepwise 1. Ice packs/ pressure 2. Drug therapy - *oxymetazoline* (vasoconstricts) 3. If anterior source of bleed is visible, can try chemical cautery 4. If still bleeding, anterior nasal packing. *Posterior* packing may require ENT consult, hospital admission. Patients w/ nasal packing require abx prophylaxis w/ *augmentin* to prevent TSS

Clinical features, necessary ED diagnostic work-up, ED treatment for ectopic pregnancy

*PPP 385* S/S: *unilateral* abdominal/pelvic pain, N/V, vaginal bleeding. beware if diarrhea if rupture, sudden worsening of pain, syncope. normal vitals or tachycardia, hypotension, orthostatic. abdominal tenderness focally +/- peritoneal signs, adnexal tenderness, fullness, CMT, vaginal bleeding. Dx: hcg (quant and qual), Uhcg, CBC, type Rh. Hcg *wont double* over 48 hours like regular pregnancies. Imaging: pelvic/transvaginal USN if hcg >1500 cuz u should be able to see IUP on USN by then. if no IUP at discriminatory zone, gestational sac outside uterus, adnexal mass without IUP, hemosalpinx, free pelvic fluid/cul de sac w/o IUP. Tx: in the ED, IV access (2 large), IVF, blood products. analgesia, antiemetics. surgery.. salpingostomy vs salpingectomy. *methotrexate* in a reliable patient who is stable w/ no signs of rupture. it is C/I if HCG 115,000+, fetal cardiac activity, or free fluid in the cul de sac.

Clinical features, necessary ED diagnostic work-up, ED treatment for PID

*PPP 405* S/S: Low abd/pelvic pain, dull, achy or crampy. mucopurulent vaginal discharge in 75% VS usually stable. PE: lower abdominal tenderness, CMT (chandelier sign), adnexal tenderness or fullness Dx: HCG, Gyn consult, UA....may be all you need after pelvic exam. CBC, CMP, ESR, blood cultures Imaging: *USN* if concern for other cause or complication i.e. fever, peritonitis, failed out pt. may show thickened (>5 mm), fluid-filled fallopian tubes = pyosaplinx, tubo-ovarian abscess, complication of PID *CT* if diagnostic dilemma to R/O appendicitis or other lower abdominal infection/inflammation Dx criteria: Criteria for diagnosis and empiric treatment is low cuz it can be super bad: Pelvic/lower abdominal pain, no cause for the illness other than PID can be identified, and 1+ of the following minimum criteria are present on pelvic examination: cervical motion tenderness, uterine tenderness, adnexal tenderness. Tx against C. trachomatis, N. gonorrhea, anaerobes (Bacteroides fragilis), BV also implicated *Oral Doxy 100 mg BID x14 d* plus *Rocephin* 250 mg IM once OR plus *Ofloxacin* 400 mg PO once OR plus *Levaquin* 500 mg PO once Consider adding *Flagyl 500 mg BID* x14 d *Admit if* failed outpatient, fever, peritonitis, signs of sepsis, comorbidities TOA Tx w/ parenteral Doxy 100 mg IV/PO BID + Cefoxitin 2 gm IV BID *OR +* Cefotetan 2 gm IV BID *OR* Unasyn 3 gm IV QID Add *Flagyl or clinda* for TOA OR if not doxy, Clindamycin 900 mg IV TID + Gentamycin 2 mg/kg IV one, then 1.5 mg/kg VI TID

Clinical features, necessary ED diagnostic work-up, ED treatment for diabetic hyperosmolar syndromes

*PPP 439* Distingushed from DKA by no significant ketosis, usually T2DM, *relative* deficiency of insulin. Same precipitating factors as DKA (infections, major illness like CVA, AMI, GI bleed, noncompliance w meds, new onset) *Dx*: Severe hyperglycemia (>600) often > 1000mg/dL Hyperosmolality (serum osmolality >315) Lack of significant acidosis (pH >7.3) or ketosis Serum bicarbonate > 15 mEq/L S/S: develops gradually over days to weeks. hyperglycemia --> profound osmotic diuresis. dehydration and electrolyte abnormalities *more* significant than DKA--> orthostasis. *more severe AMS*. seizures. ARF. *DDx*: other causes of AMS changes, DKA, OD, CNS infection, uremia. *workup* CBC, BMP, Mg, Phos, ABG or venous pH, serum ketones (beta hydroxybutyrate), UA, urine hcg, EKG, troponins, CXR, FOBT. identify the precipitating cause w/ CXR, CT brain, blood cultures, urine cultures, EKG, troponin. average *labs*: glucose 1000, serum osmolality 365 (normal 275-295), BUN:Cr 65:3, *no anion gap*. sodium deficit, potassium deficit, free water deficit. *Tx*: *gluids* 1-2L bolus NS x2hr then 250-1000mL/hour (look for CHF, ESRD tho). switch to 1/2NS after initial bolus if BP stable and corrected NA >140. switch to D5 1/2NS when glucose is less than or equal to 300 then continue until insulin stopped. *insulin* bolus .1-.15 units/kgIV and then at rate of .1units/kg/hr if K+ not too low. change from IV insulin to subQ typically when glucose <300. *potassium* if <3.3, aggressive IV replacement. if 3.3-3.5, IV replacement. >5.3, just monitor. treat precipitating problems. *admit to MICU*- the sooner out of the ED, the better bc they can decompensate.

Clinical features, necessary ED diagnostic work-up, ED treatment for acute CHF

*PPP 54-58* can present acutely d/t ischemic injury or acute valvular decompensation OR can be an exacerbation of known CHF Hx: cardiac dz, current meds, change/noncompliance w/ meds, diet changes, recent weight gain (how much, how quick), Sxs (chest pain, dyspnea, orthopnea, edema) S/S: *right sided* presents with dependent edema, JVD, hepatomegaly, ascites. *left sided* presents with acute pulmonary edema (respiratory distress, frothy sputum, rales, S3/S4) and complaints of dyspnea on exertion, paroxysmal nocturnal dyspnea, orthopnea, nocturia, weakness. *either* dysrhythmias, HTN. workup: basic labs, echo for VF and EF; PCWP via swan catheter. BNP (often markedly elevated), CXR (Kerley B lines, butterfly/batwing pattern with increased PCWP) Tx: if acute, LMNOP; lasix, morphine, nitrates, oxygen, postion (sit them up) and positive pressure ventilation. once stable, loop diuretics, ACEi, BB. monitor serum electrolytes (esp. potassium). treat existing BP issues.

Etiology, ED care and disposition of thermal burns

*PPP 640* Pediatric burns, 70% d/t scalds but 20% from child abuse. Working age adults, flame injuries more common. RF: highest risk is 18-35. Death rate much higher in >65 y/o. risk of death associated with increased burn size, age, concomitant inhalation injury, and female sex. patho: Local effects= direct tissue coagulation & microvascular rxns --> release of vasoactive substances (histamine, serotonin, arachidonic acid metabolites, free O2 radicals) which increase capillary permeability --> egress of fluid from the intravascular space to interstitial areas adjacent to the burn wound. In larger burns, the fluid shift is coupled w/ evaporative water loss --> hypovolemic shock. In burns *>20% of body surface area, systemic response*. Interstitial edema in distant organs and soft tissues 2ndary to wound release of vasoactive mediators and hypoproteinemia. Intensity of response is proportional to the size of the burn. After fluid resuscitation--> hypermetabolic. Near doubling of the CO & BMR. Full thickness burns are in 3 concentric zones of tissue injury: zone of coagulation (tissue is irreversibly destroyed by thrombosis of BV), zone of stasis (tissue viable but there is stagnation of the microcirculation, and zone of hyperemia (tissue is viable and there is an increased BF). Transformation to the zone of stasis to coagulation is attributed to the degree of dermal ischemia and reflects inadequate resuscitation. S/S *Superficial partial-thickness burns*: exposed dermis is red & moist. Intact capillary refill. Healing occurs in 14-21 days. Little or no scar formation. *Deep partial-thickness burns*: white to yellow in color. Pressure applied to the skin can be felt. 2-point discrimination is diminished. Capillary refill & pain sensation are absent. Difficult to differentiate from full thickness burns. Healing occurs in 3 weeks to 3 months. Scarring is common. *Full thickness burns*—charred, pale, leathery, painless. Do not heal spontaneously. All dermal elements are destroyed. Surgical repair, skin grafting needed. Tx: *ABCs*, hi flow O2. ET intubation if signs of compromise or airway burn (oral/perioral burns, circumferential neck burns, stridor, depressed mental status, respiratory distress). Establish at least *2 IV lines* over unburned areas and initiate fluid resuscitation by the *Parkland formula* (2-4mL/kg x %BSA burns per 24 hours). 24-hour time period begins from when patient sustained the burn injuries, NOT the time of resuscitation. BSA should only include 2nd and 3rd degree burns. ½ given first 8 hours post-injury, ½ given over the next 16 hours. Lactated ringer's recommended. Foley catheter to ensure output is maintained at .5-1ml/kg/h. eval mental status, capillary refill, BP, pulse rate, base deficit. Cooling of burns immediately by immersion in cold water (rare af), *application of cool compress* (common). In small wounds, helps limit burn depth and decrease release of damaging inflammatory mediators. *Prolonged cooling of larger BSA burns for >30 minutes can result in hypothermia*. Ice should *NOT *be directly applied (frostbite). For pain, IV narcotics, anxiolytic agents adjuvant. Minor burns Tx outpatient. *blisters*: Large blisters >2cm or those involving large joints; drain and debride. Small blisters in nonmobile areas may be left intact. Antibiotics and dressings—*topical abx* (silver sulfadiazine; low systemic toxicity, broad spectrum, painless application) to prevent wound infection and sepsis. Bacitracin alternate. Synthetic occlusive dressings instead of topical abx for partial-thickness, outpatient wounds. *Admission if moderate and major burns; refer to hospital with a burn center.* After eval and resuscitation, sterile drapes over burns. Topical abxs not used until admitting service evaluates. Circumferential burns on limbs may develop compromise of distal circulation. On chest and neck, may cause mechanical ventilatory restriction; escharotomy may be need. Tetanus—patients with clean minor wounds require *tetanus proph* if it has been >10 years since last dose. Tetanus prophylaxis of .5mL IM is indicted for all other wounded patients if it has been more than 5 years since the last dose. Tetanus IMIG administered to those without a history of a primary series of 3 tetanus immunizations. 2nd dose is required in 1-2 months and a 3rd dose in 6-12 months.

Etiology, ED care and disposition smoke inhalation

*PPP 646* occurs most frequently in closed space fires but also patients with decreased cognition d/t EtOH intox, drug abuse, head injury, dementia. Injury can occur to both upper and lower airways d/t exposure to heat, particulate matter, toxic gases. Upper airway edema 2ndary to thermal injury. Can result in acute airway compromise. S/S: signs of pulm smoke inhalation injury, often delayed 12-24 hours. Cough, wheezing, respiratory distress. Facial burns, signed nasal hair, soot in nose or mouth, hoarseness, carbonaceous sputum, wheezing. Carbon monoxide poisoning must be suspected in those with smoke inhalation injury w/ HA, vomiting, confusion, lethargy, coma (esp. if "slow fire" like burning trash). Dx: clinical history. Exam findings (burns, singed nasal hairs, carbonaceous sputum, soot, wheezing). CXR may be normal initially. Flexible fiberoptic bronchoscopy can confirm Dx. Carboxyhemoglobin levels if CO poisoning is suspected. Tx: humidified oxygen, ET intubation/mechanical ventilation, bronchodilators, pulmonary toilet. Hyperbaric oxygen therapy for severe CO poisoning.

Clinical features, necessary ED diagnostic work-up, ED treatment for cardiogenic shock

*PPP 68* patho/etiology: *MCC* of cause in hospital mortality from AMI. most commonly occurs *2ndary to LV infarct* involving approx 40% of LV mass. Early in the course of AMI; median time 8 hours. mortality high even with medical treatment (70-90%). Poor myocardial contractility so there is back up and venous pressure -> fluid extravasation and edema. Despite normal or high BP, organs are poorly perfused due to a reduction in blood flow. sympathetic over activity leads to vasoconstriction in order to maintain BP. *decreased CO, increased SVR and PCWP* RF: advanced age, female gender, large MI, anterior wall MI, previous MI, previous CHF, multivessel disease, proximal LAD artery occlusion, DM. S/S: reduction in CO --> oliguria, hepatic failure, anaerobic metabolism, lactic acidosis, hypoxia. further impair myocardial function. Almost always presents with hypotension Systolic < 90 mm Hg; >90mm Hg if pre-existing hypertension or compensatory increases in systemic vascular resistance Tachycardia or bradycardia If excessive should be treated appropriately Cool, clammy skin and become oliguric Diminished cerebral perfusion leads to altered mentation LV failure ◦Tachypnea, rales and frothy sputum Valvular dysfunction and septal defects ◦Discernible by auscultating a murmur JVD and abdominal jugular reflex Usually present Dx: H&P, ECG consistent w/ AMI. CXR for evidence of CHF, abnormal mediastinum and evaluation of cardiac silhouette. 2D *transthoracic echocardiography (TEE)* at bedside to ID regional hypokinesis; akinesis; dyskinesis. *Lab studies*: cardiac enzymes; coagulation parameters; serum lactate; chemistries BNP to predict for development of heart failure after AMI (normal < 100 pg/mL) *DDx*: aortic dissection, pulm embolism, pericardial tamponade, acute valvular insufficiency, hemorrhage, sepsis. *Tx*: stabilize pt (ET intubation, IV access, high flow oxygen, cardiac monitor, pulse oximeter, ECG and rhythm strip). *ASA* bite and chew 160-325mg unless allergy. *IV NTG* and/or morphine should be titrated for CP as well as hemodynamic parameters. preload and afterload reduction. *dobutamine/dopamine* dosed at 2-20ug/kg/min IV for hypotension despite adequate fluid resuscitation. *norepinephrine* .5-12ug/min IV if inadequate response to dopamine. *milrinone* is a PDE inhibitor -->increased inotropism and cardiac output and decreased peripheral vasoconstriction. Close support as may cause hypotension requiring pressor support Identify rhythm disturbances, hypovolemia, hypoxemia and electrolyte abnormalities early and treat accordingly Reperfusion modalities significantly decrease mortality (thrombolytics, intra-aortic balloon, counterpulsation, early revascularization) Cardiology and/or thoracic surgery should be consulted early Almost all require admission to ICU

Clinical features, necessary ED diagnostic work-up, ED treatment for septic shock

*PPP 69* *Pathophys*: Infection by gram-negative (most common), gram positive bacteria. Or viruses, fungi Endotoxins release inflammatory mediators which cause vasodilation and increase capillary permeability Shock results from massive dilation and alteration in peripheral circulation (type of distributive shock) *RF*: age, malnutrition, general debilitation, use of invasive lines, catheters, devices. traumatic or dirty wounds. drug therapies. S/S: *early* presentation is the "warm phase" where there is a hyperdynamic response --> massive vasodilation. skin is warm, flushed. tachycardia, tachypnea, increased CO. may have crackles. *later* presentation is the "cold phase" when pt is decompensating. body is vasoconstricting and skin is pale, cool. tachycardia, decreased BP, mental status changes, decreased urine output, acidosis with hypoxemia. *Tx*: begin broad spectrum abx. attempt to ID source of infection (CBC, lytes, CXR, UA, blood cultures, lactic acid). maximize oxygen delivery. fluid replacement as tolerated can actually make pulmonary edema worse. vasoconstrictors, ionotropic drugs. patient may need supportive therapy even after starting abx bc endotoxins can persist.

Clinical features, necessary ED diagnostic work-up, ED treatment for distributive shock

*PPP 69* AKA vasogenic; septic shock is most common form but there's also anaphylactic and neurogenic and endocrine XS vasodilation and altered distribution of BF leads to shunting of BF from vital organs to nonvital tissues decreased CO, decreased SVR, decreased PCWP. see card for *Septic shock* *anaphylactic shock* IgE mediated w/ Hx of allergen exposure within at least 60min. pruritis, hives, angioedema, respiratory distress, stridor, "lump in throat", hoarseness. Tx w/ epinephrine IM q5-10min. if CV collapse, epi 1mgIV. antihistamines, IVF. observe x6 hours. *neurogenic shock* d/t acute spinal cord injury or regional anesthesia. autonomic blockade --> increased vagal tone--> bradycardia, hypotension! warm, dry skin. wide pulse pressure. Tx w/ fluids, pressors +/- corticosteroids. *endocrine shock* usually d/t adrenal insufficiency (addisonian crisis) so treat with hydrocortisone 100mg IV (wont respond to fluids, pressors)>

Clinical features, necessary ED diagnostic work-up, ED treatment for anaphylaxis

*PPP 69-70* Epidemiology: range from mild cutaneous symptoms to life threatening anaphylaxis. Prevalence ranges from 5/1000 to 2/10,000 ED visits. 4 fatalities per 10 million people annually. Faster the onset, more severe the reaction; *50% of fatalities in first hour.* Type I HS (allergen induced IgE cross linking on basophil -> release of inflammation). Additional mechanisms through complement activation, direct stimulation of the mast cell or unknown reaction (anaphylactoid reactions) Common causes: PCN, ASA/NSAIDs, ACEi, TMP/SMX, radiocontrast, bee stings, peanuts, shellfish, milk, eggs, MSG, nitrites, dyes. Idiopathic anaphylaxis is by definition unknown cause. Anaphylaxis is not automatic on repeat exposure. Recurrence rates are 40-60% for insect stings; 20-40% for radiocontrast media; 10-20% for PCN. Concurrent use of BB increases risk for severe prolonged anaphylaxis S/S: Rxns may occur in seconds or may be delayed 1+ hrs after allergen exposure. Up to 20% are "biphasic" w/ further mediator release 4-8 hours later. *Anaphylaxis includes either respiratory compromise or cardiovascular collapse*. *Pruritus & urticaria* are most common initial symptoms. Urticaria is cutaneous IgE mediated reaction itchy red wheals of varying sizes which promptly disappear. *Angioedema* is similar w/ edema in the dermis usually of the face and neck. *Respiratory* stridor, dyspnea, and wheeze. *GI features* are nausea, cramps, diarrhea, and vomiting. Dx: Clinical. Hx of exposure to an agent followed by above-described symptoms. No diagnostic tests. Work up may focus on excluding other diagnoses or stabilization of cardiorespiratory symptoms DDX: vasovagal rxn, asthma, Acute coronary ischemic syndromes or dysrhythmias, epiglottitis or foreign body, carcinoid, mastocytosis or hereditary angioedema Tx: *A-G!* *A*irway: Anticipate intubation esp. in pts who are hoarse or describe a "lump in the throat". Edema may necessitate ET tube 1-2 x smaller than expected. Cricothyrotomy kit should be open and ready before starting intubation. *B*reathing. Administer high flow O2 as necessary. TX bronchospasm with nebulized albuterol .5ml of 5% soln in 3 mL saline. *C*irculation: Most patients (especially hypotensive) need large volumes of crystalloid. If hypotension persists after 1-2 L of fluid, IV epinephrine is needed. *D*iscontinue: the antigen exposure. Remove Bee stinger. *E*pinephrine: Severe respiratory distress, laryngeal edema, or shock. 0.1ml of 1:1000 epi in 10 ml saline and infuse over 5-10 minutes. If no response start Epi infusion of 1mg (1ml of 1:1000) in 500 ml saline at .5 to 2ml/min and titrate to effect. Less severe signs, IM Epi 0.3-0.5 ml of 1:1000 every 5-10 minutes. If no response, change to IV. *F*urther treatments: Antihistamines (H1 blockers such as diphenhydramine 25-50 mg IV, H2 blockers such as ranitidine 50 mg). Steroids (Only help control persistent or delayed allergic reactions; Methylprednisolone 125 mg IV, Oral Prednisone 60 mg in less severe cases). *G*lucagon: in patients on Beta blockers (1-2 mg every 5 mins for hypotension refractory to EPI and fluids) *General measures*: Observe patients with mild reactions for 1 hour. Observe those receiving Epinephrine for 6 hours. Severe reactions admit to ICU. ACEI angioedema patients are often refractory to conventional therapy, moderate to severe need admission and close observation. Epi-pen script and instructions on use at D/C. D/C patients with scripts for antihistamine and prednisone for 4 days. Referral to allergist for follow up

S/Sxs, treatments of patients with OD of acetaminophen, ASA

*PPP 98-99* *acetaminophen* metabolized in liver; small portion is metabolized via the cytochrome P450 oxidase system to a toxic metabolite that is detoxified by glutathione and then excreted in the urine. In OD, glutathione is depleted and the toxic metabolite accumulates in the liver causing hepatic necrosis *Stages of toxicity* *Phase I* ◦0 - 24 hours ◦Anorexia ◦N/V *Phase 2* ◦24 - 72 hours ◦Abdominal pain *Phase 3* ◦3 - 5 days ◦Jaundice ◦Hypoglycemia ◦Coagulopathy ◦Encephalopathy *Phase 4* ◦1 week Resolution of hepatic dysfunction (if phase 3 is not lethal) *Hx*: Nausea, vomiting, abdominal pain, diaphoresis, malaise, jaundice, sometimes asymptomatic *Physical Exam*: Acute mental status change, Icteral sclera, hepatomegaly, RUQ tenderness pallor, diaphoresis, jaundice. *labs:* CBC, SMA-7, PT/PTT/INR, LFTS, toxicity screen, serum acetaminophen level at baseline and at four hours, CXR *treatment* ◦Airway, IVF's, oxygen, monitoring ◦Naloxone, thiamine, glucose if indicated for decreased mental status change ◦Charcoal ◦Gastric lavage ◦*>150 microg/mL at 4 hours requires administration of glutathione substitute NAC (acetylcysteine)* ◦Standard loading dose 140 mg/kg with soda or juice then 70 mg/kg every four hours for 17 dosed ◦Increase loading dose if administering charcoal to 235 mg/kg PO ◦Admit to hospital The Rumack-Matthew nomogram *ASA* *◦increased anion gap metabolic acidosis, metabolic alkalosis (due to volume contraction) and respiratory alkalosis* patho: Absorption may be delayed or erratic. Peak serum levels may be significantly delayed. Toxic levels usually apparent within 6 hours. Peak levels from enteric coated or sustained released have been reported up to 60 hrs after ingestion. Forms a gelatinous mass; large amounts remain in stomach long after ingestion-->inhibitory effect on gastric emptying. *After absorption*: Hydrolyzed to salicylate. Toxicity depends on cellular salicylate concentration @ physiologic pH (7.0), all salicylate molecules are ionized. decrease in pH increases the proportion of nonionized salicylate-->cross cell membranes, the BBB-->increases intracellular salicylate concentration At urinary pH or 8.0-->Ionizes salicylate enhances urinary elimination toxicity--> inhibition of the Krebs cycle enzymes-->increased catabolism-->elevated CO2-->increased heat production, increased glycolysis and demand for glucose Increased production of organic acids contributing to acidosis of salicylate poisoning (Lactate, pyruvate, ketoacids). leads to alterations of central and peripheral glucose metabolism; Normoglycemia, hyperglycemia or hypoglycemia may be seen. Hypoglycemia in brain cells despite normal serum glucose levels Tx: ABCs, ECG, IV line. activated charcoal. IV NS if volume depletion then 5% dextrose (If neuro Sx or hypoglycemia--> 10% dextrose). potassium 40meq/L. IV bicarb bolus then with D5W to alkalize urine and increase excretion. early intubation and controlled ventilation. hemodialysis if renal insufficiency/failure, severe acid base disorder, AMS, ARDS.

Etiology, ED care and disposition of flail chest

*PPT* Definition: Segmental fracture of 3+ adjacent ribs in 2 separate isolated areas of greater than three rib fracture areas. Paradoxical inward movement of chest wall with inspiration and outward with expiration. Pt has gross trauma with respiratory distress Dx: Must R/O Pulmonary contusion. CXR. Tx: Do not stabilize segment. CPAP, BiPAP, O2, pain meds/nerve block, intubation if RF. *tintanillis* etiology: Segmental fractures of *3+ adjacent ribs* anteriorly or laterally often result in an unstable chest wall physiology known as flail chest. S/S: paradoxical inward movement of the involved chest wall segment during spontaneous inspiration and outward movement during expiration. Although paradoxical motion can greatly increase the work of breathing, the primary cause of the hypoxemia is contusion to the underlying lung. These patients may fatigue rapidly as a vicious cycle of decreasing ventilation, increased work of breathing, and hypoxemia may develop, resulting ultimately in sudden respiratory arrest. Absent or abnormal breath sounds may indicate flail chest, Tx: *mild to moderate flail chest w/ little or no underlying pulmonary contusion* or associated injury can often be managed w/o a ventilator. pain relief by analgesics or nerve blocks allowing good ventilation and pulmonary toilet are important adjuncts. *Indications for early ventilatory support* include shock, severe head injury, comorbid pulmonary disease, fracture of 8+ ribs, other associated injuries, age >65, or arterial PO2 <80 mm Hg despite supplemental oxygen. Increased age and global injury severity are poor prognostic signs in flail chest. Early intubation and ventilatory assistance in patients w/ flail chest reduce mortality compared with delaying intubation until the onset of respiratory failure.

Classification of surgical wounds (clean, clean contaminated, contaminated, dirty (infected))

*PPT*: dirty= Wounds > 6 hr old, contaminated with soil, saliva, feces or dirt *CDC*: *Class 1 wounds = clean*. uninfected, no inflammation, primarily closed. If draining of these wounds is necessary, a closed draining method is necessary. these wounds do not enter respiratory, alimentary, genital, or urinary tracts. I.e. wound made and sewed up by surgeon under sterile conditions. *Class 2 wounds = clean-contaminated*. These wounds lack unusual contamination. Class 2 wounds DO enter the respiratory, alimentary, genital, or urinary tracts. However, these wounds have entered these tracts under controlled conditions. *Class 3 wounds = contaminated*. fresh, open wounds that can result from insult to sterile techniques or leakage from the GI tract into the wound. incisions made that result in acute or lack of purulent inflammation are considered class 3 wounds. *Class 4 wounds = dirty-infected*. typically result from improperly cared for traumatic wounds. Class 4 wounds demonstrate devitalized tissue. most commonly result from microorganisms present in perforated viscera or the operative field.

Clinical features, necessary ED diagnostic work-up, ED treatment for pneumothorax

*Primary spontaneous pneumothorax* occurs in absence of an underlying lung disease. *Secondary spontaneous pneumothorax* is a complication of preexisting pulmonary disease *Traumatic pneumothorax* results from penetrating or blunt trauma *Iatrogenic* pneumothorax may follow procedures such as thoracentesis, biopsy or PEEP. *Tension pneumothorax* the pressure of air in the pleural space exceeds ambient pressure throughout the respiratory cycle *Primary pneumothorax* affects mainly *tall, thin boys* and men between the ages of 10 and 30 years. Thought to occur from rupture of subpleural apical blebs in response to high negative intrapleural pressures. Family hx and smoking may also be important factors. *S/S*: Chest pain ranging from minimal to severe on the affected side occur in nearly all patients, dyspnea. Sx usually begin during rest and usually resolve w/in 24hrs even if the pneumothorax persists *Clinical findings* may be minimal in a small pneumothorax If < 15% of hemithorax, might only have tachycardia. If larger, can have diminished breath sounds, decreased tactile fremitus, & unilateral lag. *Testing*: Generally (especially in smaller pneumothorax) lab findings will be normal. CXR will demonstrate the visceral pleural line. *Treatment* stable patient w/ a small (<15%) pneumothorax, observation alone may be appropriate. Supplemental O2 can facilitate reabsorption of air. W/ larger pneumothorax, need aspiration of air (can use catheter or small bore chest tube) *tension pneumothorax* occurs most commonly w/ penetrating trauma, severe lung infection, or positive-pressure ventilation. A check-valve mechanism allows air to enter the space on inspiration, but does not allow it to exit on expiration. Increases the intrathoracic pressure. Patients develop tachycardia, hypotension, mediastinal shift. CXR will show large amount of air on affected side, contralateral shift of mediastinum. Needs immediate decompression either w/ large bore needle, or if available immediate chest tube placement!

DDX of central versus peripheral vertigo

*central vertigo* •Brainstem & cerebellum •Sudden or slow onset, less intense sx •Constant sx, *vertical nystagmus* •*Cannot fatigue* symptoms •*No* hearing loss/tinnitus *peripheral* •Vestibular apparatus & 8th cranial nerve •Sudden onset and intense symptoms •Paroxysmal sx, worse with movement •Nausea, vomiting, nystagmus (*horizontal*, rotary -vertical) •*Can* fatigue symptoms •*May* have auditory symptoms •No CNS sx

Responsibility of provider when treating victims of abuse/assault

*child abuse*: PAs are mandatory reporters of child maltreatment to child protective services. Admission for any child with threatening conditions, or at serious risk for continued and worsening abuse Report to social work, to CPS Child needs psychological evaluation *elder abuse*: Use an appropriate screening tool Caregiver may give conflicting report of injury or illness, or may seems overly concerned with possible costs of treatment Patient may seem withdrawn or fearful Patient's medical and psychosocial issues may be best addressed with hospital admission Report to Adult Protective Services, SW referral Caregivers may need support, education, resources if abuse is unintentional *sexual assault*: A complete history should be documented see Screen for suicidal or homicidal ideation A PE should be performed looking for any signs of trauma If the assault has occurred within 72 hours of presentation, a rape kit to collect and document evidence should be performed by trained individuals A rape kit examination requires informed consent Obtain a pregnancy test Offer emergency contraception with 1.5 mg PO levonorgesterol Offer prophylactic treatment for Gonorrhea, Chlamydia, Trich, BV, Syphillis, HIV, hepatitis Assess the immediate risk to the patient of further violence/assault Refer patient to SW, psychological services

Common ED psychiatric emergencies and steps to stabilize patient

*common ones* suicidality, violent behavior, child or adult abuse, akathesia, dystonia, catatonia, conversion disorder, EtOH/drug intoxication or withdrawal, acute decompensation (bipolar, schizophrenia), neuroleptic malignant syndrome, delirium, dementia. *overall*: Quickly analyze the situation, assessing for possible risks (both to patient, the provider, and others) Make the decision to commit, admit, or discharge the patient with appropriate follow-up *step 1*: contain violent and dangerous, psychotic individuals to a safe area and employ chemical sedation PRN. keep visitors/family away. address initial survey, ABCs *Step 2*: identify suicidal, homicidal, or other dangerous behaviors. determine if pt will need to be committed even involuntarily. use screening tools (SADPERSON, SAFE-T), address RF. *step 3*: medical eval. determine if there is an underlying medical condition causing or contributing to the abnormal thoughts/behaviors. ex: hypoglycemia, infections (CNS, others), drug intox/withdrawal. psych eval, targeted psych H&P. may need psychiatric consult, esp. if the patient needs psychiatric admission. *admit IF* : a medical condition that needs further treatment is causing the symptoms If the disorder is not readily reversible If the symptoms are likely to reoccur or get progressively worse If the patient is an imminent danger to self or others

Clinical features, necessary ED diagnostic work-up, ED treatment for status epilepticus

*definition* - Continuous seizure >5 minutes. *Tx*: Give IV ativan or diazepam Can be refractory; if >30 minutes, continue benzos plus load with antiepileptics(phenobarbitol), always treat ABCs ? current says give antiepilpetics with it idk

Clinical features, necessary ED diagnostic work-up, ED treatment for diabetic hypoglycemia

*definition*: low serum glucose associated with typical Sx that resolve on administration of carbs *patho* glucose homeostasis balancing act bw food intake, insulin, glucagon, other hormones (epi, norepi, cortisol, etc). brain very sensitive to drops in glucose and focal neuro deficits rapidly develop; main energy source for brain. if severe--> brain damage, death. causes most commonly insulin, sulfonylureas (-ides, glyburide). elderly, young more susceptible. other causes include EtOH, sepsis, adrenal insufficiency, malnutrition, insulinomas. *S/S*: rapid onset of tremor, palpitations, anxiety, sweating, hunger, N/V, paresthesias, cognitive impairment, behavioral changes, psychomotor abnls, seizure, coma. *DDx*: CVA, OD, CNS infection, psych problem, other causes of AMS changes. *labs*: usually <50-55mg/dL (lower level of normal is 70 mg/dL). can be higher in diabetics used to higher glucose levels. if ur gonna admit, do *cbc* and *BMP*. *Tx*: usually initiated by EMS; *D50IV* (short lived and may be repeated). continuous infusion of 10% dextrose may be required. *feed pt* ASAP. in alcoholics/malnutrition, *thiamine 100mg IV* prior to glucose ot prevent Wernicke's encephalopathy. if sulfonylurea OD, *octreotide* 50-100mcg SQ (somatostatin analogue) that prevents rebound hypoglycemia q6hrs. *glucagon* .5-2mg IM or SQ if IV access not available but response is SLOWER than D50. *observe* x2-3hours in ED or admit to observation unit. *disposition* can d/c home if Sx improve, they are eating, and no further problems while observed. prolonged observation for alcoholics, others with precarious social situations. give diabetic education to pt. if related to sulfonylurea use, they need admission d/t prolonged t1/2. consider admission in those on long acting insulin.

DDX of patient presenting with delirium, dementia, psychiatric disease with psychosis

*delirium* Depression (disturbance of mood, normal level of consciousness, fluctuates weeks to months) Acute stress disorder (disturbance of mood, normal level of consciousness, precipitated by traumatic event) Bipolar disorder, manic episode (pressured speech, impulsivity, fluctuates weeks to months, rarely sudden onset in older adults) Dementia (insidious onset, memory problems, normal level of consciousness, fluctuates days to weeks) Psychosis (rarely sudden onset in older adults) Seizure disorders (i.e., nonconvulsive status epilepticus) *Dementia* Major depression Medication side effect Chronic alcohol use Delirium Subdural hematoma Normal pressure hydrocephalus Brain tumor Thyroid disease Parkinson disease Vitamin B12 deficiency Toxins (aromatic hydrocarbons, solvents, heavy metals, marijuana, opiates, sedative-hypnotics) *psychosis* Schizophrenia: positive symptoms (psychosis) and negative symptoms (flat affect), prodrome of social withdrawal, cognitive impairment; schizophreniform disorder: psychotic/prodromal symptoms in <6 months; schizoaffective disorder: manic/depressive mood disorder with psychosis that persists even when euthymic; schizotypal personality disorder: no true psychosis but distance in relationships and odd beliefs; delusional disorder: nonbizarre delusion (e.g., erotomanic, grandiose, jealous, persecutory, somatic), no negative/mood symptoms Mood disorder with psychotic features: can occur in mania or depression. Delusions often mood congruent; psychosis remits when mood improves. Substance-induced psychosis: alcohol and benzodiazepine withdrawal, intoxication with cocaine, bath salts, PCP, cannabis, synthetic cannabinoids, MDMA, amphetamines, hallucinogens, and alcohol; may persist beyond acute intoxication Borderline personality disorder: During extreme stress, patients often experience auditory/visual hallucinations (psychosis NOS). Posttraumatic stress disorder: psychosis associated with traumatic recollections; often visual hallucinations (vs. more auditory in schizophrenia) Psychosis due to general medical condition: delirium, stroke, infection, collagen vascular disease, head injury, tumor, interictal, porphyria, syphilis, and so forth Medication-induced psychosis: common causes: steroids, l-dopa, anticholinergics, antidepressants in bipolar patients, interferon, digoxin, stimulants

Clinical features, necessary ED diagnostic work-up, ED treatment for diverticulosis/diverticulitis

*diverticulosis* is outpouchings d/t herniation of mucosa into colon wall along natural openings at the vasa recta of the colon (left colon most common but right colon bleeds more). RF are low fiber diet, constipation, obesity. associated with painless bleeding (#1 cause of painless hematochezia) and if these get microscopically perforated, can lead to *diverticulitis*, the inflammation and focal necrosis. *S/S* of diverticulitis (bc diverticulosis is asymptomatic aside from painless bleeding sometimes which stops spontaenously): Mean age of 60 w/ lower abdominal (R/L/Suprapubic; predominantly LLQ) pain worse after eating. low Grade fever, N/V, anorexia, constipation or diarrhea. *Diagnostics*: Moderate WBC elevation w/ left shift Chemistries, urine usually normal Imaging CT abdomen/pelvis with Contrast shows pericolonic fat stranding, thickened bowel wall, colonic diverticula, microperforation, abscess. *dont do colonoscopy, barium enema d/t perf risk* Tx: abx to cover gram - and anaerobes. rocephin+flagyl, cipro+flagyl, Unasyn, cefotetan. *if no fever, vomiting, abscess, or perf and pain is controlled*, send home on orals and follow up with PCP in 1-2d. *admit on IV abx if any of the above or if immunocompromised*. surgery should be *Acute* if large perf w/ feculent peritonitis, ruptured abscess, obstruction, uncontrolled sepsis. *elective* if recurrent disease, often after the second (tho new studies question this approach) 6-12w post event.

DDX of upper GI bleeding that may present to the ER

*duodenal > gastric ulcers* epigastric, LUQ burning pain worse or better w/ food. Hx of dyspeptic Sx. duodenal better w/ food, gastric worse w/ food. *gastritis* rarely causes bleeding but can occur in presence of portal HTN and coagulopathies. do an endoscopy. associated with EtOH or ASA, NSAIDs, caffeine. anorexia, nausea, pain, dyspepsia, immediate postprandial emesis. *esophagitis* *esophageal varices* underlying liver dz, portal HTN. alcohol induced and viral cirrhosis main causes. but could be parasitic in 3rd world. endoscopic verification. *mallory-weiss tear* Hx of forceful retching -> tear in esophageal mucosa/submucosa. hematemesis. EtOH major RF. Do EGD. *esophageal rupture* excruciation retrosternal chest pain worse w/ deep breathing, swallowing. N/V, crepitus to palpation/auscultation. Hamman's sign. dyspnea, odynophagia, cyanosis, tachypnea, tachycardia, hypotension, syncope.

Peri-op management of patients (especially, but not limited to med management) of patients with epilepsy, diabetes, HTN

*epilepsy*: Do not make changes to meds; they will do fine. General anesthesia depresses epilepsy. *diabetes*: Major risk from general anesthesia and surgery d/t predisposition to ischemic heart dz (esp. silent MI). Increased danger of cardiac arrest (autonomic neuropathy). Diabetic nephropathy. PVD (more strokes and lower limb ischemia). Heel pressure sores. High postop infection (wound, chest, or UTIs). Obesity (increased operative morbidity). Stress of surgery increases catabolic hormones, opposing action of insulin. Serum glucose control becomes more difficult. Surgery, anesthesia, NPO, and postop vomiting mess up the therapeutic insulin. Preop assessment: maintain *glucose <130*. Arrange for operation as *early* in the day as possible. Insulin 50-70% the usual dose AM of surgery. Give infusion of dextrose (glucose) throughout operative period: 5 or 10% glucose infusion at 125ml/hour. Add potassium to dextrose. Insulin drip for tight glucose control perioperatively. Monitor blood glucose and lytes often throughout operative and early postop period. Postop: check serum glucose q2-4hours and lytes q shift and adjust infusions PRN. Continue infusion until oral diet then move back to subq insulin. *Oral hypoglycemic drugs: d/c night before surgery* EXCEPT 1st gen sulfonylureas (diabinese); stop that *2-3d prior*. Metformin stop 48 hours prior to admission d/t contrast. SGLT-2 inhibitors (Invokana, Farxiga, Jardiance); stop 2 days before surgery. Use sliding scale insulin post-surgery if necessary, otherwise resume orals when tolerated. *HTN* >25% of patients presenting for surgery are hypertensive or being Tx for HTN. As long as systolic <180 and diastolic <110, minimal risk of cardiac complications. Can be caused by anxiety about operation and drops post-op. Management: in diuretics, check for fluid and electrolyte abnormalities and correct. Most HTN meds should NOT be stopped before general anesthesia (at U of M, d/c ACEi 18 hours before d/t risk of hypotension): BB, CCBs, ACEi, nitrates, methyldopa. Monitor for post-op orthostasis. Still give normal dose of meds with small amount of water, just no closer than 2 hours before op. withdrawal can lead to rebound HTN. Severe HTN—higher risk of periop CHF or stroke (esp. with labile BP). Cannot put them under general anesthesia until they are stabilized. Surgery may get cancelled the day of.

Common post-op complications (see powerpoint, focus on signs/symptoms and timing). How do you DDX between these complications?

*fever*: "5 W's of post-op fever" WIND = atelectasis or pneumonia WATER = urinary tract infections WALK = deep vein thrombosis WOUND = surgical site infection WONDER DRUGS = drug induced fever *atelectasis* One of those most common causes of post-op fever in the first 24-48hrs Affects 25% of patients with abdominal surgery Partial lung collapse caused by shallow breathing post-operatively Patients with copious secretions can lead to bronchial plugging and lobar collapse S/s: fever, tachypnea, tachycardia (low-grade) Tx: supportive; encourage coughing, deep breathing, incentive spirometry, ambulation, mobility out of bed Can give Tylenol for pt. comfort during fever Have patients stop smoking prior to surgery *pneumonia* carries up to 20-40% mortality. Often related to aspiration or ventilator-associated S/S: fever, shortness of breath, cough, chest pain Labs/studies: CBC (leukocytosis), CXR, sputum culture Mgt: Antibiotics, Bronchodilators (if wheezing) Prevention: Aspiration Precautions in vulnerable patients; supervised PO intake, HOB>30 degrees Oral chlorhexidine for ventilated patients Epidural analgesia decreases risk as it improves pulmonary toilet and early return of bowel function *UTI* Very common in patients that had indwelling catheters Generally occurs 48-72 hours after surgery S/S: urinary retention, dysuria, fever/chills, malaise, altered mental status (older patients) Labs: bacteruria, +leuk esterase, +nitrites, +/- hematuria, leukocytosis (WBC>10K) Mgt: discontinuation of catheter, urine culture, empiric Abx (keep in mind concern for resistant organisms in hospital setting) Prevention: clean technique w/ insertion of catheters. Early discontinuation of indwelling catheters *VTE* Includes DVT and PE Post-op patients at high risk d/t Virchow's Triad: (Venous stasis, Hypercoaguability, Vessel wall injury) S/S: fever, asymmetric edema, calf pain, shortness of breath, chest pain, tachycardia, sense of 'impending doom' Labs/studies: CBC, CXR, EKG, CT chest PE protocol, DVT scan (ultrasound) Mgt: anticoagulation, O2 supplementation, IVC filter if not a candidate for anticoagulation EKG finding= S1Q3T3 XR: Westermark's sign (Focal oligemia; only seen in 2% of patients with PE but highly specific finding. Focal peripheral hyperlucency distal to a large vessel that is occluded by the PE) Hampton's hump (Wedge-shaped pleural consolidation. Usually peripheral. Represents infarction) *surgical site infection* S/S: blanchable erythema at site, pain, warmth, drainage from the site, fever/chills, malaise Labs: leukocystosis (WBC>10K), +/- wound culture Treatment: Abx targeted at GPCs (cephalosporins vs. Bactrim if concern for MRSA) +/- opening wound and allowing to heal by secondary intention Wound Vac Drain placement *catheter site infection* Particularly central lines S/S: redness/irritation at insertion site, fever Labs: CBC, blood culture (from line and a 2nd site) Mgt: removal of line (send tip for Cx), Abx (usually IV) Nearly 15% of hospitalized patients will acquire central venous line sepsis 12-25% mortality when central venous line infection becomes systemic Prevention: Sterile technique with line insertion and maintenance/access. Close monitoring of catheters. Avoidance of unnecessary lines. Rotation of peripheral line sites *wonder drugs* Anesthetics, sulfa-containing antibiotics & others. Often implicated in drug fever that develops 1 week postop Dx of exclusion and should be considered when faced w/ a negative sepsis workup in a postop patient w/ fever

Patient education regarding smoking cessation prior to surgery

*from PPT* Higher risk of post op respiratory issues with smoking (5x risk of post op issues so stop at least 4-8weeks prior). if stop just before surgery, increases mucus production messes with wound healing *from american society of anesthesiologists* If you smoke, your heart and lungs don't work as well as they should. You may have breathing problems during or after surgery, and you are at greater risk of developing pneumonia. You are also much more likely to need a ventilator, a machine that breathes for you, after surgery. In addition, smoking reduces blood flow, which slows healing, so your surgical incision is more likely to become infected. Because smoking is a major cause of heart disease, your chances of suffering a heart attack during or after surgery increase.

DDX frostbite, trenchfoot, chillblains

*frostbite*-- first and second degree -> superficial injuries (edema, burning, erythema, blistering in 2nd degree). Third degree--> freezing damage to the deeper subdermal plexus. Hemorrhagic blisters (black looking), necrosis, blue-gray discoloration of the involved extremity). Fourth degree--> deep injuries involving the subQ tissue, muscle, tendon, bone. Little edema (dry, mummified). Cyanotic insensate tissue (may have hemorrhagic blisters, skin necrosis that later appears mummified). *Trench foot*—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. *Chilblains/pernio*—painful and inflamed skin lesions caused by chronic, intermittent exposure to damp, nonfreezing ambient temperatures (confused with cellulitis). Associated with rheumatology conditions too. Once affected by chilblains, frost nip or bite, involved body part more susceptible to reinjury. TREATMENT for *chilblains and trench foot*, elevation, warming, bandaging of affected tissues. Nifedipine 20 mg PO TID. Topical corticosteroids, prednisone and PGE1 (limaprost 20mcg PO TID) may be helpful. for *frost bite*, For frost bite, rapid rewarming with circulating water at 42 degrees C (107 F) x10-30 min thawing of frostbite. Dry air rewarming may cause FURTHER tissue injury and should be avoided. Treat pain with narcotics, ibuprofen, aloe vera (or some kind of skin protectant), Penicillin G 500K units q6hours x48-72 hours if weeping (controversial). If blisters are clear, debride or aspirate as rich in PG and thromboxane (IRL we usually leave alone tho); hemorrhagic definitely leave intact.

Clinical features, necessary ED diagnostic work-up, ED treatment for human or animal bites

*human bites* crushing or tearing of tissue w/ potential for injury to underlying structures and inoculation of tissues with oral flora. Most often reported on hands and UE. Infection most serious sequela. S/S: *clenched fist injury* (CFI) occurs in the MCP region as fist strikes the mouth, teeth of another individual. Increased risk for serious infection so any questionable injury in that area of the hand should be considered a CFI until proven otherwise. Assessment: direct injury and ALL of the underlying structures (tendons, vessels, nerves, deep spaces, joints, bone). Use local anesthesia for wound exploration. CFI, examine wound thru full range of motion to MCP joint to detect extensor tendon involvement and assess for joint space violation. Radiographs for factures or foreign bodies. Compilations: cellulitis, lymphangitis, abscess, tenosynovitis, septic arthritis, osteomyelitis. Polymicrobial w/ staph and strep common isolates. Viral diseases like HSV, herpetic whitlow, hep B. Tx: *irrigation* of wound w/ NS and judicious limited *debridement* of devitalized tissue are critical to management. Other places than hand can undergo primary closure unless there is a high degree of suspicion for infection. *Prophylactic abx* (Augmentin 500-875mg PO BID) considered in all by the most trivial of human bites. In uncomplicated hand wound, leave open w/ appropriate dressing. Immobilize and elevated for 24 hours. Prophylactic abx then re eval in 1-2 days. If there is a laceration to the extensor tendon or joint capsule or radiographic findings, *consult hand surgeon* for possible exploration & IV abx. Wounds that are infected at presentation require systemic abx after cultures are obtained. Local cellulitis may be managed on an outpatient basis in a reliable patient with abx, immobilization, and close follow up. Moderate to severe infections require admission for surgical consultation and parenteral abx.... *ampicillin-sulbactam* 3g q6hours IV or *cefoxitin* 2g q8hours IV. Penicillin allergic patients may be treated with clindamycin and cipro. All patients should receive *tetanus* according to guidelines. *animal bites* *dog* Account for 80-90% of bites, infections 5% of cases mostly in patients >50, hand wounds, deep puncture wounds, delay treatment x24 hours. Dx: thorough Hx and exam. XR if evidence of infection, suspicion of a foreign body, bony involvement, or intracranial penetration bites to the heads of small children. Tx: copious *irrigation and debridement* of devitalized tissue. *Primary closure* of wounds to the scalp, face, torso, extremities *other than hands and feet*. Lacerations of hands and feet need to be left open initially. Large, extensive lacerations (esp. in kids) are best explored and repaired *in OR*. For puncture wounds, wounds to the hands and face, and high-risk patients, Tx with *Augmentin* 500-875 PO BID x3-5 days or clinda plus cipro. In kids, clinda plus Bactrim. *Penicillin 500mg QID D.O.C. for capnocytiphaga canimorsus* and should be used prophylactically for high-risk immunocompromised patients (EtOH, asplenia, chronic lung dz). Cephalosporins, tetra, erythromycin all reasonable alternatives. Culture infected wounds. Tetanus prophylaxis. *cat* 5-18% of reported animal bites, up to 80% become infected. P. multocida major pathogen, Pasturella Rapidly developing intense inflammatory response with pain, swelling. May cause serious bone and joint infections and bacteremia. Septic arthritis also possible in patients with altered host defenses d/t glucocorticoids or alcoholism. Dx: XR if evidence of infection, foreign body, or bony involvement. Tx: same as dog bites; local wound care with copious irrigation and debridement. Primary wound closure except in puncture wounds or lacerations smaller than 1-2cm. delayed closure in cosmetically important areas. Prophylactic abx in high-risk patients (prosthetic joints, arthritis, immunocompromised, hand punctures) w/ Augmentin 500-875mg BID or cefuroxime or doxy. Tetanus prophylaxis.

Clinical features, necessary ED diagnostic work-up, ED treatment for DKA (make sure to pay attention to what happens to the patient's potassium before, during, after treatment)

*ppp 438* *patho*: disorder of T1 DM characterized by hyperglycemia, ketonemia, acidosis. relative or absolute deficiency of insulin and increased levels of stress hormones is the cause. insulin acts on the lvier by promiting glucose sotrage as glycogen, causes adipose tissue to store triglycerides, and causes skeletal muscle to create protein. lipolysis produces ketone bodies --> acidosis. hyperglycemia causes profound osmotic diuresis (Volume depletion, electrolyte loss). high anion gap metabolic acidosis resulting from ketonemia. dehydration with electrolyte abnormalities. *causes* lack of insulin (33%) d/t forgot or reduced amount. infection, injury, pregnancy, major illness (CVA, AMI, GI bleed, MI, PE). EtOH, drug use (Cocaine). *S/S*: rapid onset of N/V, abdominal pain. tachycardia, deep tachypnea (Kussmauls). fruity breath (acetones), dehydration (dry MM and skin, orthostasis). metnal status changes not uncommon, may have evidence of infection on exam. *DDx*: HHS, hypoglycemia, EtOH ketoacidosis, starvation ketoacidosis, MUDPILERs. *diagnosis*: glucose >250, acidemia so pH <7.3, ketonemia or ketonuria, sodium bicarb <18. accucheck may no tbe accurate if BG is too high; will need serum levels. If DKA--> determine cause. *workup*: CXR, EKG, CBC, BMP (pseudohyponatremia common), *total body potassium low but blood may read as high*, Ca, Mg, Phos are often low. ABG or venous pH. serum ketones beta-hydroxybutyrate. UA, urine Hcg, blood culture if suspected infectious etiology. *treatment*: close the gap; correct hypovolemia. address electrolyte abnormalities. treat underlying cause. get patient to ICU and out of the ED. often institutions have algorithms *fluids* 1L/hr NS x2 hours and then 500mL/hr. consider restraint in CHF/ESRD patients. later, titrate fluid to the clinical picture. *switch to D51/2 NS* when glucose is less than or equal to 250 then continue til insulin stopped. *insulin* bolus at .1-.15 units/kgIV then at rate of .1 units/kg/hr. change to subQ when improving. *potassium* will decrease with Tx d/t renal loss and intracellular shift so give it IV or PO. *bicarb* given w/ pH <6.9 or when hyperkalemia is severe. *monitor* serum glucose, anion, gap, K, HCO3 hourly until recovered. *cerebral edema* may occur esp. in pediatric 4-12hrs into treatment. deterioration in neuro status will occur. reduce fluids, give mannitol 1g/kg, THEN order CT. *disposition* most often admitted to MICU.

DDX of serotonin syndrome versus neuroleptic malignant syndrome versus anticholinergic toxicity

*serotonin syndrome*: S/S altered mental status, confusion, agitation, hallucinations, hypomania. hyperthermia, tachycardia, diaphoresis, BP changes. N/V, increased bowel sounds, diarrhea. Spontaneous or inducible clonus, hypertonia, restlessness, mydriasis (dilated pupils), dry mucous membranes, flushed skin. Causes: occurs w/in 6-24 hours of initiation or change in serotonergic drugs. *neuroleptic malignant syndrome*: S/S: FEVER + ALTERED MENTAL STATUS, lead-pipe muscle rigidity, diaphoresis, autonomic instability, incontinence, leukocytosis, rhabdomyolysis (increased CPK, WBC, LDH, LFTs), tremor. *REGULAR SIZED PUPILS whereas serotonin syndrome will have dilated pupils*. Causes of / risk factors caused by antipsychotic drug use (especially haloperidol and droperidol, 1st gen). Young males early in Tx. *anticholinergic toxicity*: mad as a hatter (AMS), blind as a bat (pupillary dilation w/ loss of acuity, similar to serotonin syndrome), red as a beed (vasodilation), hot as a hare (anhydrosis), dry as a bone, full as a flask (urinary retention), stuffed as a pepper (constipation).

Lab markers for MI

*troponin* and *CK-MB* indicate muscle death but troponin more specific for cardiac muscle. elevates 3-4h after onset so do serial; takes 1+ weeks to normalize. can be increased in moderate to large PE if right ventricle affected; associated with worse prognosis. CK-MB could indicate MSK injury so less specific but normalizes faster (48h) so if u wanna see if there is a NEW MI different from another recent one, this will be better. *normals* troponin- between 0 and 0.4 ng/mL. CK-MB- 3 to 5% (percentage of total CK) or 5 to 25 IU/L.

Clinical features, necessary ED diagnostic work-up, ED treatment for drowning victims (wet drowning, "dry drowning", drowning in cold water)

*wet drowning*-- aspiration of fluid leads to asphyxia *dry drowning*-- laryngeal spasm caused by victim gasping under water leads to asphyxia (airway obstruction). S/S: appearance may vary from asymptomatic to marked distress w/ abnl VS. respiratory difficulty (dyspnea, cough, wheezing, apnea), trismus, chest pain, dysrhythmia, hypotension, cyanosis, and hypothermia (from cold water or prolonged submersion). A pink froth from the mouth and nose indicates pulmonary edema. Diarrhea and vomiting may be present. The patient may experience headache, neurologic deficits, and altered level of consciousness. labs: *Metabolic acidosis* is common & ABG results may be helpful in determining the degree of injury since initial clinical findings may appear benign. *PaO2 is usually decreased*; PaCO2 may be increased or decreased; pH is decreased. Bedside blood sugar must be checked rapidly. Other testing is based on clinical scenario. and may include serum electrolytes, creatinine, eGFR, lactate, troponin, complete blood count, prothrombin time and INR, urinalysis, and serum alcohol level and drug screen. UA shows proteinuria, hemoglobinuria, and acetonuria. Leukocytosis is usually present. Tx: BLS, CPR. airway management. assess for hypothermia, hypoglycemia, concurrent medical conditions and associated trauma, esp brain and c spine injury. do not do heimlich. continue BLS until body temp 32 degrees C. maintain O2 90%+. CPAP, PEEP, intubation/ventilation. ECMO for ARDS has shown to be effective. CXR. pneumonitis, atelectasis, and pulmonary edema. Bronchodilators to treat wheezing, bronchospasm d/t aspiration.

Indications for transfusion therapies and what type of blood product(s) to use

*whole blood* A unit of whole blood consists of 450ml +/- 10% of blood from a suitable donor plus 63ml of anticoagulant which is then leukocyte depleted. --Indicated for patients who have sustained acute hemorrhage of >25% total blood volume loss. --Stored @ 4ºC; has a shelf life of 5 weeks --Whole blood is now rarely used for transfusion *RBCs/PRBCs* --Used when primary aim is to increase the oxygen carrying capacity of blood --Can improve platelet function particularly in uremic pts --1 unit of RBC can be expected to result in raise of Hb of 1gm/dl in an adult. Indications: --Symptomatic anemia (fatigue, tachycardia, hypotension, disorientation, SOB) --Hgb < 7 g/dL --Patients w/ vascular disease, or other critical risk factors Hgb between 7-9 *platelet* indications: --Microvascular bleeding d/t thrombocytopenia & platelet dysfunction --Prophylactic platelet transfusion may be indicated if platelet count is <10,000 --For Sx patients w/ thrombocytopenia *Not* indicated for patients w/ HIT or autoimmune thrombocytopenia. One random donor unit generally raises platelet count by 20-50 x 109 *plasma/FFP* Used in pts w/ a factor deficiency (not platelet issue) --Contains all coagulation factors including von willebrand factor --Plasma contains antiA and antiB antibodies depending upon blood groups; Pt should only receive plasma which doesn't contain an antibody which would attack their own red cells --Rh Compatibility is not required --FFP is not concentrated plasma, volume overload may occur if requirements are high. --A dose of 10ml/kg will typically provide sufficient coagulation factors to achieve hemostasis. *cryoprecipitate* --Derived from plasma that has been frozen and thawed --Administered to patients w/ fibrinogen deficiency --Doesn't require crossmatching before transfusion

Classification of burns

1st degree *Superficial partial-thickness burns*: exposed dermis is red, moist. Intact capillary refill. Healing occurs in 14-21 days. Little or no scar formation. *Deep partial-thickness burns*: white to yellow in color. Pressure applied to the skin can be felt. 2-point discrimination is diminished. Capillary refill and pain sensation are absent. Difficult to differentiate from full thickness burns. Healing occurs in 3 weeks to 3 months. Scarring is common. *Full thickness burns*: charred, pale, leathery, painless. Do not heal spontaneously. All dermal elements are destroyed. Surgical repair, skin grafting needed.

Clinical features, etiology, necessary ED diagnostic work-up, ED treatment for rhabdomyolysis

3 classic presentations: •1. I have fallen and I cannot get up. •2. I work out! But, I drink no water! •3. My body was crushed! Patho: breakdown of skeletal muscle w/ damaged muscle cells deposit into bloodstream & build up. Pt says they feel weak & tired, fatigued, N/V, confusion. Dark cola colored urine. May have gross soft tissue abnls on PE, but may have nothing. Labs: Get *CPK*>20,000-100,000 units & UA-*increased protein levels*. Tx: of choice-IVF (lots and lots of fluids!)-6-12 Liters w/in 24 hours. Close lyte monitoring.

Stages of wound healing

3 phases Hemostasis and inflammation Proliferation Maturation and remodeling *hemostasis and inflammation* 1. Vasoconstriction -Lasts 5-10 minutes -Reduces blood loss 2. Vasodilation -Increases blood supply to wound -Causes erythema 3. Coagulation -Clot made of fibrin and platelets that traps RBCs -Biologically active proteins are released Complement system activated In 24 hours, polymorphonuclear leukocytes (PMNs, neutrophils) enter the wound through leaky capillaries -Phagocytosis of bacteria and tissue debris by releasing proteases Kill bacteria by releasing free radicals 48-96 hours: monocytes come into the picture through capillaries and become activated macrophages -Participate in phagocytosis -They release growth factors Macrophages cause the wound to become highly proliferative and very cellular by 7 days The growth factors stimulate cell migration, cell proliferation and deposition of matrix At surface of wound, exposed collagen causes keratinocyte migration up from the basal layer: epithelialization complete in <48 hours (if edges are well approximated) Creates a water barrier Over a few days, it becomes multilayered *proliferative phase* ~*Days 3 through 21* Provisional matrix made of fibrin and fibronectin allow fibroblasts to migrate along its structure They give structure by providing collagen (mostly Type I) New vascular tissue that forms has a granular appearance and is called granulation tissue Fills in the gaps of missing damaged tissue Angiogenesis: new capillaries form Then wound contracts and enters final stage of wound healing *maturation & remodeling phase* *3 weeks after wound creation* Inflammatory cells and angiogenesis slows down and stops The total collagen content in the wound increases x2-3 weeks, tho simultaneous collagen breakdown occurs Remodeling phase lasts from many months-2 years Collagen fibrils are more organized and cross-linked Strength of wound is increased to 75-80% of normal Scars are visible because of residual disorganized collagen over the next couple of months... -Wound contraction (changes cosmetic appearance) -When repairing lacerations, evert the edges to allow the final wound to lay flat rather than become depressed at the center after contraction occurs -Scar remodeling continues

Clinical features, necessary ED diagnostic work-up, ED treatment for cardiac tamponade

E.O.D: compression of heart by fluid in pericardial sac. gradual accumulation up to 250mL. rapid accumulation. prevents *diastolic relaxation* of ventricles bc the RV filling pressure equals that of the left. loss of normal pressure differentials prevents filling. causes: same as effusion. idiopathic/viral most common. autoimmune (SLE, RA, sarcoidosis), viral (coxsackie, flu, parvovirus B19), bacterial (staph, strep, TB), fungal (candida), trauma, malignancy (Breast/lung), meds (procainamide, isoniazid). S/S: SOB/dyspnea, fatigue, tachycardia, CP, syncope, JVD, friction rub, *pulsus paradoxus* (decrease pulse w/ inspiration; fall in BP of 10mmHg+), *Beck's triad* (muffled heart sounds, narrow pulse pressure, hypotension). eval: *echo* FAST exam; large effusion present and diastolic collapse. *CXR* shows enlarged cardiac silhouette in slow tamponade, normal in acute. *EKG* shows sinus tach low voltage, *electrical alterns* (beat to beat alterations in QRS) Tx: *drain effusion*: immediate pericardialcentesis under USN OR surgical drainage (subxiphoid approach, angulated shoulder). send for cytology if non-traumatic. catheter left in until <25mL/d. *emergency thoracotomy* in trauma if refractory to PC. *IVF* and *positive pressure ventilation* post PC d/t negative intrathoracic pressure.

Clinical features, necessary ED diagnostic work-up, ED treatment for cellulitis

PPP 618 patho: diffuse spreading infection of dermis and subQ tissue. Lower leg frequently involved. gram + cocci, most common entry point is tinea pedis of toe web with fissuring (*group A B-hemolytic strep & staph aureus*) RF: IV drug use, chronic LE edema, chronic vascular disease, open ulcerations, diabetic foot.S/S: starts as small, tender patch. Swelling, erythema, pain. Lesion expands over hours (onset to presentation 6-36h). Patient becomes sicker as lesion grows (chills, fever, malaise). If septicemic, hypotension + shock. Labs: leukocytosis or neutrophilia early. +blood cultures if bacteremia, septicemia. aspirate a pustule or abscess, not advancing edge. DDx: DVT, necrotizing fasciitis (toxic, bullae, crepitus/anesthesia of involved skin, overlying skin necrosis, high CPK, rapid debridement required). Treatment: IV abx for first 24-72 hours (nafcillin, cefazolin, clindamycin). Then, dicloxacillin or cephalexin (Keflex) x5-10d. Bacterial strains are usually susceptible to clinda, genta, rifampin, Bactrim, and vanco (IV).

S/Sx, work-up, and BASIC surgical management of colon cancer

etiology: MCC adenomateous polyps RF: AA, >50, Hx UC, poor diet S/S: IDA (fatigue, weakness), rectal bleeding, abdominal pain, change in bowel habits (most common cause of *LBO* in adults). if advanced, ascites, abd masses, hepatomegaly. if *right sided* (proximal), chronic occult bleeding (IDA, + guaiac) and diarrhea. if *left sided* (distal) lesions tend to cause bowel obstruction, present later, cause changes in stool diameter. may develop strep bovis endocarditis. Dx/workup: colonoscopy w/ Bx test of choice but if cannot tolerate oral contrast, barium enema that shows *apple core lesion* then follow up with colonoscopy or CT colonography. labs reveal IDA, CEA is the tumor marker but not specific. Tx: Stage 4: operation (left colectomy) and chemo (only really op for stage 4). Post-op: foley out POD #1. VTE prophylaxis. Colostomy care (refer to ostomy nurse educator). Fluids. Consider TPN. Labs. Continue NG until output drops. Hem onc consult. Await pathology. screening-- 45+ w/o RF. If RF, 40 or 10 years prior to when family member got it.

Etiology, ED care and disposition of mastoiditis

etiology: complication of OM; infection spreads to adjacent mastoid air cells. *strep pneumo* usually. Dx: CT diagnostic Tx: IV abx, ENT consult for I&D, mastoidectomy.

Clinical features, necessary ED diagnostic work-up, ED treatment for SAH

etiology: most occur during exertion ie sex, heavy lifting Can be d/t berry aneurysm or AVM S/S: "worst headache of my life", severe & sudden onset. May also have N/V, photophobia, stroke symptoms. HA may be the only symptom. Symptoms may improve so don't be fooled. Dx: CT 98% sensitive <12 hrs, only 80% >12 hrs. MRI is no better LP is the next modality if high suspicion and CT neg Consult Neurosurgery, Keep MAP <130 mmhg w/ IV lopressor

Etiology, ED care and disposition of esophageal rupture

etiology: multiple. effort rupture (forceful vomiting, coughing, straining, pushing- Boerhaave syndrome) for most but could be blunt/penetrating trauma, iatrogenic (endoscopy), foreign body ingestion, caustic substance ingestion, and esophageal cancer comp. S/S: saliva, gastric contents--> mediastinum leading to acid burns, inflammation, infection, rupture of pleura. chest pain that may extend into neck or abdomen, worse w/ swallowing. subQ emphysema in chest or neck. *Hammond sign* is crunch on chest auscultation d/t air movement in mediastinum. *meckler triad* subQ emphysema, chest pain, vomiting (uncommon) labs: not rly helpful might be leukocytosis or severe sepsis. imaging: CXR abnormal within hours; shows pneumomediastinum, pneumothorax, subQ air may be visualized. pleural effusions. contrast scan can ID the perforation. esophagram w/ water soluble contrast agent to assess for contrast extravasation. tx: definitive airway stabilization. IVF resuscitation, broad spectrum abx. NPO, NG tube. *nonsurgical* for perfs contained within mediastinum and visceral pleura, no infection, and perf drains back into esophagus. *surgery* primary defect repair, diversion, gastric drainage, or esophagectomy otherwise. endoscopic stent placement if extensive perf if poor surgical candidates.

Clinical features, necessary ED diagnostic work-up, ED treatment for acute COPD exacerbation

generally present to ED w/ *worsening of known disease*, or *complications* d/t their COPD Complications from COPD include more frequent and severe respiratory infections, pulmonary hypertension, cor pulmonale S/S: changes in dyspnea, changes in quantity or color of sputum. May have acute or worsening hypoxemia, hypercapnia (confusion, tremor, plethora, stupor), peripheral edema, or changes in mental status Work-up: targeted toward *finding the reason* for their acute decompensation (ABGs, CBC, lytes, CXR, EKG). When they are admitted, may have additional studies (ie cardiac echo) Treatment: Supplemental O2, Ipratropium bromide/Albuterol nebulizer (*DuoNeb*), cortico*steroids*, broad spectrum *antibiotics* pending work-up Hospital admission until condition is stabilized and underlying etiology for the exacerbation is determined.

Clinical features, necessary ED diagnostic work-up, ED treatment for epidural hematoma

hematoma *b/w dura & skull*. Mostly adolescents and young adults, due to significant *trauma*. S/S: May initially lose consciousness, then lucid, then coma Dx: *Lens shape* on head CT. Tx: Craniotomy with hematoma evacuation

Potential complications during the peri-operative period for patients with chronic kidney disease. How to monitor, potentially mitigate these complications.

look for fluid overload (d/t poor GFR); correct w. diuretics, fluid restriction, hemofiltration/dialysis prn. monitor Is and Os in ICU postop. check lytes, bUN, Cr, vitals, PE. hyperkalemia huge risk so stabilize to 5.0 Divide patients into *MILD CRF and severe CRF*. *MILD*—common in elderly, may be caused by HTN. Impaired excretion of drugs so must titrate doses downward. Fluid and electrolyte abnormalities so monitor BUN, Cr, lytes carefully (esp. if on diuretics). Reduction in renal reserve can cause them to go into ARF. *SEVERE*—might be receiving dialysis. Periop problems include fluid overload (poor GFR); correct w/ diuretics, fluid restriction, and hemofiltration if needed. Monitor Is and Os in an ICU postop, check lytes, BUN, Cr, vitals, PE. Serum osmolality (esp. hypo and hypernatremia) check sodium content of IVF. Hyperkalemia—big risk in advanced CRF from transfusion, tissue damage or hypoxia or changes in GFR from CHF or hypotension. Arrythmia risk—stabilize preop potassium to <.5 mmol/L. chronic anemia (normocytic normochromic) low EPO from kidney. Metabolic acidosis is USUALLY compensated by respiratory alkalosis, but compensation is disrupted by general anesthesia and from more acidosis 2ndary to tissue ischemia or hypoxia.

DDX of lower GI bleeding that may present to the ER

most commonly a result of *diverticular disease*, followed by *angiodysplasia*, *colonic ulcers*, and other miscellaneous causes. The most common cause depends on the patient's age. In the *adolescent or young adult*, Meckel diverticulum, IBD, and polyps are the most likely causes. In *adults up to 60 years*, diverticula, IBD, and neoplasms are the more common causes. In patients *older than 60 years*, angiodysplasia, diverticula, and neoplasms predominate. *diverticulosis* typically asymptomatic but can be lower abd pain, LLQ TTP. tenesmus, constipation, diarrhea. massive bleeding w/ or w/o Sx of diverticulitis. do colonoscopy. *angiodysplasia* painless bleeding can be mild or massive. usually >60 y/o; Hx of cardiac or renal dz. usually ceases on own. *hemorrhoids* Hx of straining on defecation. frank hematochezia mixed with well formed normal stools. can lead to marked anemia. proctoscopy to Dx. *colonic polyps* painless rectal bleeding. discovery of polyp on sigmoidoscopy, colonoscopy, barium enema. *colitis* abdominal cramps, diarrhea bloody and mucopurulent, fever, weight loss, anemia. sigmoidoscopy shows eroded, friable mucosa. r/o infectious causes (shigella, campylobacter, c diff, salmonella, e. histolytica). *crohn's* frank blood (not really massive bleeding), abdominal pain, anorexia, diarrhea, weigh loss, fatigue, +/- fever, sepsis. fistulas, fissures, hemorrhoids. *solitary rectal ulcer* unusual. associated with rectal prolapse. results from straining. pt passes blood and mucus. elderly w/ chronic constipation. *meckel diverticulum* usually kids rarely after age 10. sx can be similar to appendicitis. can hemorrhage. Dx with technetium pertechnetate scintigraphy or angiography.

Clinical features, necessary ED diagnostic work-up, ED treatment for neurogenic shock

patho/etiology: SC injuries. Majority due to blunt trauma and penetrating trauma (10 to 15% of cases: GSW/stab wounds) MVC, falls, sports-related. *disruption in sympathetic flow--> hypotension, bradycardia*. primary prob happens right away, secondary ensues over several days-weeks. S/S: *2-3min* hypertension, widened pulse pressure, tachycardia. *as sympathetic tone is lost further*, hypotension, warm dry skin. *injuries above T1* disrupt ENTIRE sympathetic chain. *injury between T1-L3*--> partial sympathetic disruption. symptoms last 1-3 weeks. Tx: address ABCDs. once diagnosis is made, mitigate hypotension and bradycardia. *crystalloid* infusion w/ goal of MAP of 70mmHg. *dobutamine or dopamine* if inotropic support Is necessary. if symptomatic bradycardia, use *atropine*. Asystole or heart block --> Tx w/ *pacemaker*. for the injury itself, *steroids*.

Clinical features, necessary ED diagnostic work-up, ED treatment for acute meningitis

patho/etiology: evidence of meningeal inflammation w/ normal cerebral function. encephalitis - evidence of abnormal brain function. *H. Flu, Staph Pneumoniae, Neisseria meningitidis* (military & dorms) Enterovirus, herpes, flu, fungal meningitis, lyme disease. Bacteria *enters through subarachnoid space* -> disseminate through blood -> over blood-brain barrier, brain becomes edematous S/s: Fever, HA, neck stiffness, photophobia, AMS. seizures in some. fever & confusion in elderly. *brudzinski's* - flexion of hip and knees in response to passive neck flexion *Kernig's* - hamstring contraction in response to knee extension while hip flexed. look for rash - meningococcemia. Focal neuro deficits Dx: Obtain a *CT prior to LP* if concern for intracranial mass lesions (papilledema, immunocompromised state, cancer, seizure). concern is that if there was increased pressure, LP could cause herniation. Never delay antibiotics for CT *lumbar puncture* Gram stain & culture, cell count, protein, glucose, viral panel testing, opening pressure: *Bacterial meningitis* shows high protein high WBC (PMNs) low glucose. *Viral meningitis* shows normal glucose, increased WBCs (lymphocytes). *Fungal or TB meningitis* shows decreased glucose, increased WBCs (Lymphocytes) treatment: *bacterial* abx is priority; can get LP up to 2 hrs after abx admin and still have accurate culture/detection *Age 18-50* - strep pneumoniae, Neisseria meningitidis Ceftriaxone and vancomycin *Age >50* - above plus listeria and gram-neg bacilli Ceftriaxone, vancomycin *and ampicillin* *viral* Supportive therapy. Some can be managed outpatient. Monitor lyte abnormalities. if increased ICP - mannitol

Clinical features, necessary ED diagnostic work-up, ED treatment for pericarditis

patho/etiology: inflammation of pericardium. fibrinous or serofibrinous if post MI, infectious. serous in autoimmunity (SLE, RA). 2 most common causes are idiopathic and viral (coxsackie, echovirus). *dressler syndrome* is post mI pericarditis+fever+pleural effusion. S/S: sudden onset of pleuritic (sharp, worse with inspiration), persistent, postural (worse when supine &* improved w/ sitting forward*), pain radiates to shoulder, back, neck, arm, or epigastric area. Dx: ECG shows *diffuse ST elevations* in precordial leads (V1-V6) and PR depressions in same leads. aVR will have opposite (PR elevations, ST depressions). cardiac enzymes may be +. echo to look for pericardial effusion and/or Sx of cardiac tamponade. Tx: NSAIDs or ASA x1-2 weeks first line; colchicine 2nd line. for dressler syndrome avoid NSAIDs do ASA or colchicine

Clinical features, necessary ED diagnostic work-up, ED treatment for acute asthma exacerbation

patho/etiology: may be pt w/ new Dx or existing asthma patient w/ asthma attack not controlled by chronic meds. Can be triggered by ongoing respiratory infection, environmental exposures, new meds, exercise, emotional stress etc S/S: Dyspnea/SOB, cough, wheezing, chest tightness, wheezing, prolonged expiration. if severe, tripoding, diaphoresis, accessory muscle use, tachycardia/tachypnea, AMS, retractions. Eval: Vitals; O2 sat (pulse ox, ABGs), EKG, CBC, BMP, CXR Tx: Reassessment is critical!!! Place patient on cardiac monitor, continuous vitals, pulse oximetry. Ensure IV access. Supplemental oxygen. *Duoneb*: Albuterol/Ipratroprium Bromide (relaxes smooth muscle) can repeat x 3. *Steroids* oral, IM, IV. START ASAP. *CPAP, BIPAP, Intubation* if impending respiratory arrest

Clinical features, necessary ED diagnostic work-up, ED treatment for acute coronary syndromes

pt presents with chest pain--> cardiac monitor, IV access, ASA 325 chewed, oxygen >90%, NTG then morphine if refractory, hi dose statin. *labs* consider PE as well (d-dimer, spiral CT). do a BNP, GI cocktail, troponins, CK-MB (not v. specific), myoglobin. CXR unstable angina is CP (vague w/ arm discomfort/pain that occurs w/ physical exertion or stress) at REST, prolonged, >20min. may be severe or new onset, acceleration. MI can be STEMI v. NSTEMI. *triggers*: coronary spasm, mechanical obstruction, increased myocardial O2 demand, decreased supply. usually >1 cause. *S/S* besides CP (substernal, epigastric) include SOB, N/V/D, indigestion, diaphoresis, dizziness/lightheadedness, fatigue/pallor, or atypical Sx (elderly, women). vitals-- HR is variable but usually sinus brady d/t inferior wall MI. arrythmias, dysarrythmias. may be HTN prior to MI. if hypotension, large infarct, poor outcome. tachypnea d/t pain, anxiety. lo grade fever or normal temp. *PE*: diaphoresis, pale cool skin, sinus tachy, 3rd or 4th heart sounds, crackles or other pulm findings, hypotension. in setting of HF, JVD, new murmur or worsening, hypotension, tachy, S3 gallop, crackles. do a focused neuro exam to assess for focal lesions for safe use of thrombolytic therapy. *EKG*: T wave inversion, flat, depressed, inverted, usually symmetrical. ST segment elevation (infarct) of >2mm in consecutive chest leads. depression (ischemia) may occur. Q waves are significant/pathological and are in >25-30% of QRS for >.04s or 1 mm width. look at leads w/ elevation for location of infarct. *post-workup* classify into: 1. non cardiac Dx 2. chronic stable angina 3. possible ACS 4. definite ACS. *immediate Tx of all ACS*: *ASA* 325 mg chewed *oxygen* >90% 4L then titrate PRN *NTG* IV 12.5-25ug bolus then 10ug/min infusion titrated q5min. max dose 200ug/min. *morphine* If refractory to NTG or pulm congestion. in STEMI, 2-4mg IV up to 2 repeats q5-15min. In UA/NSTEMI, 1-5mg IV. *statin* atorvastatin 80mg early as possible. *BB* metoprolol 25mg oral unless HF, hemodynamic compromise, brady, severe RAD. *STEMI specific* in addition to above mgmt, give *clopidogrel* loading dose 300-600mg then 75mg/d. *anti-thrombin* heparin or enoxaprin. *PCI* if not available transfer or consider fibrinolytic *glycoprotein IIb/IIIa* inhibitors given immediately before cath lab. *NSTEMI specific* in addition to above mgmt, *anti-thrombin*. may consider *PCI* if ongoing ischemia, hi risk patient for cardiac events. *hi risk pts* cardiogenic shock, overt HF/severe LV dysfunction, recurrent/persistent rest angina despite medical Tx, hemodynamic instability, unstable ventricular arrhythmias.

Most common organisms responsible for post-surgical infections

staph aureus, strep, pseudomonas abdominal surgeries, E. coli, klebsiella, enterobacter

Clinical features, necessary ED diagnostic work-up, ED treatment for pneumonia

types: pts presenting to ED w/ pneumonia most likely have *Community Acquired Pneumonia* (CAP) (MC pathogens are Strep pneumonia, H flu, C pneumonia, S aureus, M cat, Klebsiella, Legionella) unless they are presenting from a nursing home or other LTC facility Don't miss *aspiration pneumonia*; patients can decompensate quickly and develop ARDS, or have complications like lung abscess S/S: tachypnea, tachycardia, rales, dyspnea, chest pain, fever, cough, hemoptysis RF for worse outcomes: RR > 30, HR > 140, BP <90 systolic, Temp >101 Change in mental status. Dx generally can be made on the basis of history and CXR *CXR* -->lobar consolidation or patchy infiltrates *WBC elevated* Can do *urine antigen testing* for Strep or Legionella Sputum cultures often low yield in CAP Blood cultures should be done in anyone who meets criteria for *possible sepsis*, generally done in any patient being considered for admission Tx: Start *empiric antibiotics*: if *healthy pts w/ no RF for pseudomonas, MRSA*--> amoxicillin, doxy PO. can do macrolide too. *if comorbidities, immunosuppressed*--> macrolide or doxycycline (as above) plus an oral beta-lactam (amoxicillin/clavulanate 500 mg/125 mg three times daily. ORRR can do Monotherapy with an oral fluoroquinolone (moxifloxacin, 400 mg daily; gemifloxacin, 320 mg daily; levofloxacin, 750 mg daily). *Inpatient management of nonsevere pneumonia* A respiratory fluoroquinolone. Oral and intravenous doses equivalent: moxifloxacin, 400 mg daily or levofloxacin, 500-750 mg daily or A macrolide (see above for oral therapy) plus a beta-lactam (see above for oral beta-lactam therapy). For intravenous therapy: ampicillin/sulbactam, 1.5-3 g every 6 hours; cefotaxime, 1-2 g every 8 hours; ceftriaxone, 1-2 g every 12-24 hours; ceftaroline, 600 mg every 12 hours. *Inpatient management of severe pneumonia* (typically requiring intensive care). All agents administered IV, except as noted. Azithromycin (500 mg orally as a first dose and then 250 mg orally daily for 4 days, or 500 mg orally daily for 3 days) or a respiratory fluoroquinolone (as above) plus an intravenous anti-pneumococcal beta-lactam (as above). For patients allergic to beta-lactam antibiotics, a fluoroquinolone plus aztreonam (2 g every 8 hours). *For patients at risk for P aeruginosa*, add coverage for P aeruginosa and obtain cultures to confirm infection or to allow de-escalation of therapy: piperacillin-tazobactam, cefepime. *If they are being considered for admission, generally start w/ resp fluoroquinolone* In the ED, you need to assess the patient's risk and determine if admission is appropriate Can use the Pneumonia Severity Index *(PSI) or CURB-65*

aspiration pneumonia specifics

•Pathogens enter the lung through inhalation of aerosols, hematogenous spread, or aspiration of oropharyngeal contents •Risk for aspiration in individuals with swallowing disorders, intoxication, altered mental status •When treating aspiration pneumonia, need extended coverage - add clindamycin or metronidazole to cover anaerobes