ER-Surg FR

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)

-Disorder of DM 1 and characterized by hyperglycemia, ketonemia, and acidosis · Precipitated by: lack of insulin (forgot or reduced amount), infx or injury, pregnancy, major illnesses (CVA, AMI, GI bleeding, MI, PE), ETOH/Drug use (cocaine) Pathophysiology - relative or absolute def of insulin + increased stress level hormones · Insulin acts on liver · Lipolysis produces ketone bodies resulting in acidosis · Hyperglycemia causes profound osmotic diuresis (volume depletion, electrolyte loss) · Ketonemia: high anion gap metabolic acidosis · Dehydration w numerous electrolyte abnormalities S/S - · Rapid onset N, V, abdominal pain · Vital Signs Abnormal: tachycardia, deep tachypnea (Kussmaul respiration) · Fruity breath (acetone excretion) · Dehydration - dry mucous membranes/skin, orthostasis · Mental status changes +/- evidence of infx DX - · ADA Guidelines Require: o Glucose > 250 o Acidemia Ph < 7.3 o Ketonemia or ketonuria o Serum bicarb < 18 mEq/L · Accucheck reading may not be accurate if BG is "too high", need serum levels TX - · CLOSE THE GAP! · Correct hypovolemia, address electrolyte abnl, tx underlying, get pt to ICU and out of ED · Fluids: o 1 L/hr of NS x 2 hrs then 500 mL/hr à consider restraint in CHF/ESRD pt o Later titrate fluid to pts clinical picture o Switch to D5 ½ NS when glucose < 250 mg/dL & continue until insulin stopped · Insulin: bolus IV à change to SQ when improving · Potassium: usually severely depleted, but may have elevated K+ o K+ will decreased w Tx d/t renal loss and intracellular shift o K+ given IV or PO · Bicarb: given w pH < 6.9 or when hyperkalemia is severe · Monitor serum glucose, anion gap, K+, bicarb hourly until recover Disposition - admit to ICU Complication - cerebral edema à reduce fluids + give Mannitol THEN order CT Correct potassium slowly?

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

-Local soft tissue inflammatory response 2^ to bacterial invasion of skin -RF: elderly, immunocompromised, peripheral vascular ds S/S - -Localized tenderness, erythema, and induration -Lymphangitis & lymphadenitis = more severe infx -+/- fever, chills (not bacteremic) DX - Clinical presentation --> WBC count but doesn't change management -LE cellulitis may be complicated by DVT + require venogram or Doppler -If systemic toxicity (fever and leukocytosis) - culture puss, bullae, blood ED Care & Disposition - -Simple (No MRSA): Outpatient Cephalexin, Dicloxacillin, or Clindamycin -Highly Suspect MRSA: Clindamycin, Bactrim, Doxycycline, +/- Cephalexin -All discharged follow up in 2-3 days, skin marker for spreading -Systemic Toxicity or Bacteremia: admit + IV ABX (Clindamycin, Vancomycin, Linezolid) **DM, ETOH, other immunosuppressive disorders

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 -Contra-indications : Cerebral edema, neuro surgical procedures , Acute ischemic stroke, Hypovolemic shock, Hyponatremia , water intoxication, Same iv line blood transfusion - hemolysis: clumping occurs, Uncontrolled DM , severe hyperglycemia -Maintenance Rate of infusion (ie pre-operative patients)-: 0.5 gm/kgBW/hr 0.9% NS (Isotonic Saline) -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 -Contra-indications : Avoid in pre-eclamptic patients, CHF, renal disease and cirrhosis, Dehydration with severe hypokalemia - deficit of ICF potassium, Large volume may lead to hyperchloremic acidosis. -Rate of infusion depends upon calculating the fluid/electrolyte deficit for the patient Ringer's Lactate -Most physiologic fluid, rapidly expands IV volume -Composition Each 1 litre of fluid contains: sodium = 130meQ Potassium = 4mEq Calcium = 3 mEq Chloride = 109 mEq Bicarbonate = 28 mEq -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 -Contraindications: Liver disease, severe hypoxia and shock, Severe CHF , lactic acidosis takes place, Addison's disease, Vomiting or NGT induced alkalosis, Simultaneous infusion of RL and blood, Certain drugs - amphotericin, thiopental, ampicillin doxycycline D5 with ½ 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, Treatment of hypernatremia, Compatible with blood transfusion -Contra indications : hyponatremia Severe dehydration Colloids -Large molecular wt substances that largely remain in the intravascular compartment thereby generating oncotic pressure -3 times more potent -1 ml blood loss = 1ml colloid = 3ml crystalloids -Example: Albumin: Maintain plasma oncotic pressure - 75-80 -Indications : Plasma volume expansion in acute hypovolemic shock, burns, severe hypoalbuminemia, Hypo proteinemia - liver disease, nephrotic syndrome, Oligourea, In therapeutic plasmapheresis , as an exchange fluid -Contra-indications : Severe anemia, cardiac failure Hypersensitive reaction

Necessary pre-surgical work-up

Complete patient history when available -In emergent situation: AMPLE **Allergies **Medications **Past Medical History **Last Meal **Events preceding Surgery Allergies: -Food, meds, anesthesia problems or issues with anesthetic agents, difficulty with intubation, malignant hyperthermia or previous reaction to anesthetic agent Medications -Bleeding tendencies: ASA, Warfarin, alcohol, NSAIDS, chemo, antibiotics Medical Conditions: -Significant cardiopulmonary risk, endocrine disorders, cirrhosis, renal disease, immunosuppression and previous surgical procedures -Preoperative surgical risk in elective populations may require ancillary tests such as stress testing, coronary angiography, carotid artery duplex and pulmonary function tests Events leading up to presentation should be documented. -Determine if complaint is acute, subacute or chronic -Seven cardinal signs of the symptom: Location of the complaint Quality of the symptom Quantity or severity Timing Setting Alleviating or aggravating factors Any associated complaints Laboratory assessment -EKG in ALL pts > 40 yo -H and P is the MOST important evaluation -CBC **s/s compatible with anemia **Hemoglobin in those patient > 65 years of age -Serum Electrolytes **Not indicated in the absence of medical problems **Considered in patients on certain meds-Warfarin: associated with K+ abnormalities and toxicity -Serum Creatinine **Inexpensive marker for renal function; decrease with age and decreased muscle mass **ALL patients older than 40 years. -Blood Glucose -Hepatic Enzymes **Not indicated routinely **Order if clinical s/s indicate hepatic disease -Coagulation Studies **Should be documented in patients taking anticoagulants. -Urinalysis **Concern whenever prosthetic device is used **Transient bacteremia during vascular procedures can infect the pseudo intimal layer of the bladder and seed to orthopedic prosthetic devices -Arterial Blood Gas **Perform if indication of severe underlying cardiopulmonary disease or to confirm acid-base disturbance **Carries risk of bleed from the site in postoperative period **Pulse ox should be considered first -ECG **Consider in all patients older than 40 years of age **Used to identify preoperative MI or arrhythmias that are associated with higher mortality and morbidity **Reasonable in patients undergoing vascular or intermediate risk surgery with at least one risk factor **AHA also recommends ECG in all severely obese patients with at least one other risk factor (BMI > or = to 40 kg/m2) -Chest Radiography **Indicated in patients over 60 years and all patients regardless of age, who have a history of significant pulmonary or cardiac disease **AHA recommends in those with BMI > or = to 40 kg/m2 to assess for heart failure and chamber enlargement -Spirometry **Indicated in abdominal surgery if pulmonary disease is poorly controlled or if extent of disease is not clear -A1C for DM pts

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

Corneal injuries 1. Corneal Abrasion: sensation of foreign body, light sensitivity, tearing -Topical anesthetic drops -Fluorescein staining with cobalt blue light -Treat with abx ointment (erythromycin) 2. Corneal Foreign Body : same presentation as Abrasion -Evert upper lid in exam -Dirt/glass/metal (rust ring) -Removal: 25G needle, lateral approach using slit lamp, Rust Ring removal not recommended 3. Corneal Ulcer: pain, redness, photophobia -Timing of eye pain > 2-3 days Infections of the corneal stroma caused by extreme dryness, trauma, contact lenses -Slit lap reveals the ulcer - opacity without staining.. also stains -TX: fluoroquinolone abx drops -Referral to ophtho within 12-24 hours -Do not patch 4. Herpes Simplex Keratitis -Infection of Cornea by VZV -Similar to Corneal ulcer presentation -Abnormal ulcer - Branching/ "dendritic" -Can Cause corneal scarring -TX with topical Acyclovir and Oral Acyclovir -Refer to Ophtho 5. Chemical Burns to Eye -Acids: toilet/pool cleaner, battery fluid, Exploded E-cig (!!) -Alkalis (more harmful): lime, mortar/plaster, drain cleaner, oven cleaner, ammonia -Immediate copious irrigation, check pH -Degree of vascular blanching (esp at limbus) proportional to severity of burn -Cycloplegic, narcotic pain medication -Emergent ophtho referral 6. Blunt trauma to eye -Subconjunctival Hemorrhage **Non-painful, does not cause vision issues usually benign. **Can Coags if no trauma history **Will resolve without treatment within 2 weeks -Hyphema: blood in anterior chamber **If >1/3 = damage to drainage angle, risk glaucoma **Re-bleeding can occur semirecumbent/rest **no NSAIDs **Emergent ophtho referral 7. Acute Anterior Uveitis (Iritis) -Trauma common cause. autoimmune causes, infectious causes and can be idiopathic -Unilateral, painful red eye, blurred vision, reactive photophobia, tearing -Signs: **Peri-limbal injection, worse closer to limbus: (conjunctivitis= worse further from limbus) **Visual acuity may be decreased **Increase in protein content of aqueous causes an effect known as "flare", looks "smoky" **White or red blood cells may be observed in the anterior chamber **Severe cases - Hypopyon -Treatment - topical steroids, cycloplegics, ophtho referral 8. Ruptured globe -May be from blunt or penetrating trauma -Signs: **Pupil : peaked, tear drop shaped, or otherwise irregular **Enophthalmos (recession of the globe within the orbit) **Exophthalmos from retrobulbar hemorrhage -Evaluate with orbital CT -ED care involves placing patient in upright position, eye shield for protection, IV broad spectrum abx, analgesia -Emergent ophtho consult

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

Examples -Cataract (most common) -Angle Closure Glaucoma (#2) -Central Retinal Artery Occlusion -Central Retinal Vein Occlusion -Optic Neuritis -Giant Cell Arteritis -Retinal Detachment Acute angle closure glaucoma -Acute ocular pain, nausea/vomiting, intermittent blurred vision with halos, conjunctiva injection, hazy cornea, mid-dilated non-reactive pupil -OP >21 mmHg can be >60 mmHg -Treatment : **Ophtho consultation **Acetazolamide 500mg IV **Topical beta-blocker **Analgesics/Anti-emetics/Supine **Once pressure-induced ischemic paralysis of the iris resolves around 1 hour post initial Rx then: Pilocarpine: a miotic (constricts pupil) - opens angle, should be administered every 5 mins for 30 mins **Laser peripheral iridotomy performed 24-48 hours after IOP is controlled is definitive treatment Central Retinal Artery Occlusion -Sudden, painless vision loss of one eye. -Amaurosis Fugax : transient loss of vision lasting seconds to minutes, can precede -Associated with embolus in retinal artery -Pale fundus with narrowed arterioles with segmented flow (boxcars) and bright red "cherry" macula TX -Ophtho consult -Decrease intra-ocular pressure with Acetazolamide , anti-coagulate, revascularize Central Retinal Vein Occlusion -Sudden painless, unilateral vision loss -Associated with 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 with eye movements, central scotoma -Usually unilateral, F 18-45yo -May be 1st presentation of demyelinating disease-MS -Swollen optic disc -May have other neurologic S/S -Ophtho referral, neurology work-up -IVIG, steroids Giant Cell Arteritis -Inflammatory condition occurs in elderly -Profound unilateral visual loss -Jaw claudication -Headache -Scalp tenderness -Polymyalgia Rheumatica in 50% -ESR >60mm/hr -CTA gold standard of diagnosis -Rx Ophtho referral, steroids Retinal Detachment -Result of retinal hole or tear with seepage of fluid between retina and choroid -Risk factors **age, Trauma, Myopia, Cataract surgery -Signs: flashing lights, floaters, vision loss: filmy, cloudy, irregular, or curtain-like visual field defects -Treatment: Ophtho referral

Potential complications of using lidocaine or epinephrine when repairing local lacerations

Never give lidocaine w Epi in fingers, toes, nose bc can get gangrene because of small vessels in these areas

Etiology, ED care and disposition of distal finger tip injuries

Subungal Hematoma: -Very painful to pt --> lots of pressure on that nail -Trephination (making burr hole) w 18 gauge needle or electrical Bovey cautery -Use ABX if trephination & have underlying fx -No need to remove nail -Nail growth extremely long process Skier's Thumb (Game Keeper's): -Injury involving ulnar collateral ligament -May have assoc avulsion fx -Mechanism of Injury: usually fell directly onto thumb or overuse of thumb -Compare to normal side -Laxity & focal pain -TX: thumb spica splint or cast initially Some need operative care Ganglion Cyst: -Encapsulated, mobile mass found near joint or tendon sheath -Typically cause no clinical problem unless impinge adjacent structures -Tx: can be aspirated or surgical excision, but recurrence common -Pt into "cosmesis" generally want it removed

DDX of lower GI bleeding that may present to the ER

-50% of acute lower GI bleeding from diverticulitis -Perforated diverticula -diverticulosis is MC cause of painless bleeding -AV Malformations -Polyps -IBD -Anorectal disease -COLON CA -Ischemic colitis -ulcerative colitis -hemorrhoids Clinical Features - -Hematochezia (bright red blood) -Hypotension and tachycardia - if severe -Angina, syncope, weakness, confusion ED Workup - -Rectal exam w GUIAC stool testing -Labs (type and scree, CBC w diff - include hematocrit, BMP, PT/PTT, BUN, CR, LFT) **Hgb & Hematocrit will be low -CT: Controversial -Colonoscopy: study of choice for diagnosed, but would not be performed in ED TX - Emergency stabilization of ABCs O2 + Cardiac monitor + IV fluids w large bore IV + admit for colonoscopy +/- blood transfusion (based on clinical picture)

Clinical features, necessary ED diagnostic work-up, ED treatment for junctional arrhythmias

-Clinical features: Junctional escape beats may occur in pts with sinus bradycardia, SA node exit block, or AV block, usually at a rate between 40 and 60 beats/min, depending on the level of the rescue pacemaker within the conduction system. Junctional escape beats may conduct retro-gradely into the atria, but the QRS complex usually will mask any retrograde P wave. -Alternating rhythmically with the SA node, junctional escape beats may cause bigeminal or trigeminal rhythms. ED Treatment 1. Isolated, infrequent junctional escape beats usually do not require specific treatment. 2. If sustained junctional escape rhythms are producing symptoms, treat the underlying cause. 3. Unstable patients: atropine IV = accelerate the SA node discharge rate and enhance AV nodal conduction. 4. Use transcutaneous or tranvenous pacing in unstable patients not responsive to atropine. 5. Manage patients with digoxin toxicity as discussed for SVT.

DDX of headache pain in the ED

-Meningitis -Brain tumor -Cerebral venous thrombosis - HA, vomiting, seizures, rare -Temporal arteritis - age >50, new onset localized HA, temporal artery tenderness, ESR > 50, +biopsy. Treat with high 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 -NO OPIATES IN HA

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

-Most common cause of in hospital mortality from AMI -Approximately 5-7% of patients with AMI will develop cardiogenic shock -Early in the course of AMI; median time 8 hours Clinical Features -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 -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 Diagnosis -H and P -ECG consistent with AMI -CXR for evidence of CHF, abnormal mediastinum and evaluation of cardiac silhouette -2D transthoracic echocardiography (TEE) at bedside : Regional hypokinesis; akinesis; dyskinesis Lab studies -Cardiac enzymes; coagulation parameters; serum lactate; chemistries -BNP to predict for development of heart failure after AMI: Normal serum levels < 100 pg/mL ED care and disposition -Stabilize patient **Endotracheal intubation, IV access, High flow Oxygen, Cardiac monitor, Pulse oximeter, ECG and rhythm strip -ASA: Bite and chew 160 to 325 mg unless allergy -IV nitroglygerin and/or Morphine-to 100 ug/min IV) or Nitroprusside (0.5 to 10 ug/kg/min IV) respectively -Dobutamine and/or dopamine!! (both dosed at 2 to 20 ug/kg/min IV) for hypotension despite adequate fluid resuscitation -Norepinephrine (0.5 to 12 ug/min IV)if inadequate response to dopamine. -Milrinone (phosphodiesterase inhibitor) **Increased inotropism and cardiac output and decreased peripheral vasoconstriction -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

Etiology, ED care and disposition of aspirated foreign body

-90% of pts are under 4yo with 1/3 aspirations not witnessed. 3000 deaths per year with increased incidence over the holidays. -Most common aspirations are latex balloons, food, and toys. 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. -asymmetric breath sounds -Medical Emergency due to respiratory arrest. -Chest Xray: Uncommonly radiopaque -Tracheal: sagital plane: anterior-posterior -Esophageal: coronal plane: left-right -Can see secondary findings: segmental atelectasis, pneumonia, hyperinflation, pneumothroax Diagnosis: Bronchoscopy, nasolaryngoscopy CXR Tmt: O2, calm pt, no back blows or finger sweeps, conscious sedation -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 **Repeat until FB expelled or pt is unconscious **If unconscious straddle pt's thighs and repeat as above, ventilate.

Common ED psychiatric emergencies and steps to stabilize patient

-Admission for any child with threatening conditions, or at serious risk for continued and worsening abuse; report to social work, to CPS; child psych eval Common ED psychiatric Emergencies -Suicidality -Violent behavior -Abuse of child or adult -Akathisia, dystonia, catatonia w/d from psych meds or caused by meds -Conversion disorder -Alcohol/drug intoxication or withdrawal -Acute decompensation (bipolar, schizophrenia) -Neuroleptic malignant syndrome -Serotonin Syndrome -Delirium, dementia Emergency Psychiatric Assessment Steps 1) Safety and Stabilization -Contain violent and dangerously psychotic persons to provide a safe environment for staff, patients, family, and visitors while simultaneously attending to airway, breathing, and circulation -Address initial survey, ABCs 2) Identification of homicidal, suicidal, or other dangerous behaviors -Determine if the patient needs to be forcibly detained for emergency evaluation (committed involuntarily) -Utilize screening tools, address risk factors (Suicidal, homicidal or violent patients should be disrobed, gowned and searched for potentially dangerous items. Approach the violent patient with a non threatening voice, avoid excessive eye contact, keep the exit from the room accessible, and enforce acceptable limits of behavior. Determine if the patient needs to be detained for emergency evaluation.) 3) Medical Evaluation -Determine the presence of any serious organic medical conditions that might cause or contribute to abnormal behavior or thought processes (eg, hypoglycemia, meningitis (other infections or CNS infections), drug withdrawal/intoxication, or other causes of delirium) 4) Psychiatric Evaluation - targeted psychiatric H&P May need psychiatric consult, especially if the patient needs psychiatric admission Admit to hospital? 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

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

-As common or more common than cardiac complications -Most common form of postoperative morbidity in patients who undergo abdominal procedures and thoracotomy **Pneumonia, Massive lobar collapse due to mucus plugging, Pneumonitis, atelectasis Patient related risk factors -Smoking: Cessation of smoking 8 weeks before surgery to decrease risk -Poor general health status -Older age -Obesity -COPD -asthma Pre and Post operative management PULM -Defer surgery with exacerbation of COPD -Aggressive treatment for patients without optimal reduction in symptoms or optimal exercise capacity **bronchodilators, PT, abx, smoking cessation, corticosteroids **Preoperative education in lung expansion maneuvers **Deep breathing **Incentive spirometry-lung expansion **Chest physiotherapy -In kids more dangerous - cancel if there is "wet cough" w wheeze and fever -Resp Infx: cancel elective operations

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

-Assess risk, correction of predisposing factors, precise timing of operaition, judicious use of ABX and containment of contamination (anytime someone is at risk then they will get one) -The duration of contamination must be limited to brief periods, usually within the operative procedure -The anticipated degree of contamination should be sufficiently great to result in an expected incidence of infection greater than 2% -Where significant bacterial contamination is expected -Not given for prophylaxis of infection associated with indwelling catheters (urinary or intravascular) intubation and open wounds -Prevention of surgical wound infection **Before operation; IV; not more than 48-72 hours **Recommendation is to give within 1 hour of surgical procedure -people with mechanical valves or endocarditis are at very high risk -use on immunocompromised patients -if the pt is at risk of Cdiff (age) then you might not want to give antibiotics

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

-Between dura and the skull -Mostly adolescents and young adults, due to significant trauma. -Lens shape on head CT -May initially lose consciousness right away, then lucid, then coma CT: convex -Craniotomy with hematoma evacuation

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

-Bleeding between dura and arachnoid membranes -Headache after remote trauma -Due to tearing of bridging of the veins of surface of the brain -Elderly, alcoholics, on thinners - people with cerebral atrophy -gradual onset of neuro issies, slower bleed -Classically lucid interval then coma -Rapidly non-con head CT, then MRI more sensitive -Crescent shape -Burr holes, craniotomy, non operative management

Classification of burns

-Categorized by size and depth -Burn size is calculated as the percentage of total BSA (body surface area) involved. -Size **Most common method to estimate the percentage of BSA is "rule of nines" **More accurate especially in infants and children is the Lund and Browder burn diagram **Smaller burns: patient's hand can be used as "ruler" to estimate percentage BSA. Represents 1% of the patient's BSA -Depth **Historically described as first, second, third and fourth **More clinically relevant classification used to determine the need for surgical intervention A. Superficial partial-thickness B. Deep partial-thickness C. Full-thickness Superficial partial-thickness burns -Exposed dermis is red and moist -Intact capillary refill!!!! -Healing occurs in 14 to 21 days -Little or no scar formation Deep partial-thickness burns -White to yellow in color -Pressure applied to the skin can be felt -Two 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 and painless -Do not heal spontaneously -All dermal elements are destroyed -Surgical repair and skin grafting is needed Discontinue blood thinners before surgery & start LMWH or Unfractionated SQ Heparin

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

-Common problem in general surgical patients -Fluid and electrolyte imbalances are seen, and increased BUN/Cr -Divide pts into mild CRF and severe CRF -Risk of complications increases with severity of renal failure MILD Chronic Renal Failure -Common in elderly -Might be caused by HTN -Impaired excretion of drugs (titrate doses downward) -Fluid and lyte abnormalities -Monitor carefully: BUN, Cr, lytes (especially if you are giving diuretics) -Reduction in renal reserve: may cause them to go into ARF SEVERE Chronic Renal Failure -Might be receiving dialysis -Surgery is usually for renal transplant -Periop problems: **Fluid overload (poor GFR): correct with diuretics, fluid restriction and hemofiltration if needed -Monitor I&O in an ICU postop: **Check lytes; BUN, Cr **Vitals, PE **Serum osmolality (esp hypo/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) **Hyper: cardiac standstill; stabilize preop potassium to < 5.0 mmol/L **Chronic anemia (normocytic, normochromic) low EPO from kidney **Compensation disrupted by general anesthesia and from more acidosis secondary to tissue ischemia or hypoxia **Metabolic acidosis; usually compensated respiratory alkalosis Pre-Op: look for hydration or JVD, check CBC, lytes, BUN:CR, Bicarb

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

-Compression of heart by fluid in pericardial sac -Gradual accumulation up to 250mL -Rapid accumulation -Prevents diastolic relaxation of ventricles -RV filling pressure equals left **Loss of normal pressure differentials prevents filling Causes of Pericardial Tamponade -Same causes of effusion -Idiopathic is most common: like autoimmune/viral -Viral: Coxsackis, influenza, parovirus B19, etc. -Bacterial: Staph, Strep, TB, etc. -Fungal: Candida -Trauma -Malignancy (Breast/Lung mets) -Autoimmune: SLE, RA, Sarcoid -Meds: procainamide, isoniazid, etc. S/S Cardiac Tamponade -SOB/dyspnea -Fatigue, tachycardia -CP -syncope -JVD, friction rub -Pulsus Paradoxus: decrease pulse with inspiration, pathopneumonic <10mmHg in systolic BP -Beck's Triad: Muffled heart sounds, Narrow Pulse pressure, Hypotension Evaluation -Echo: **FAST Exam **Large effusion present, Chamber collapse -CXR: Enlarged Cardiac Silhouette in slow CT, normal in acute -EKG: **Sinus tach **Low voltage QRS **Electrical alterns:beat-to-beat alterations in QRS Tmt for Tamponade -Drainage of pericardial effusion -Immediate Pericardialcentesis under U/S or Surgical Drainage **Sub-xiphoid approach, angulated shoulder **Send for cytology if non-traumatic **Catheter left in until <25mL/day -Emergency Thoracotomy **Used in trauma if refractory to PC -IV Fluids/Positive Pressure Ventilation post PC **Due to negative intrathoracic pressure

ED assessment of suicidality

-Eval included detailed HPI, PMH/psych hx, med hx, social hx, PE -Important Components of MSE: physical appearance, affect, orient, speech pattern, bx, LOC, attention, language, memory, judgment, thought content, perpetual abnl -3rd party accounts of pt's bx as compares to pt's baseline & level of functioning -Suicidal ideation, hx of attempts (repeated, realistic plan w access to means, lethal), relationship w health professional, social support S-sex: male higher risk A-Age: extremes of age higher risk <18, >55 D-Depression or other psych comorbidity higher risk P-Previous attemp higher risk E-Ethanol/alcohol use higher risk R-Rational thinking loss (hallucinations) S-Social support; no support higher risk O-Organized plan N-No spouse S-Sickness: medical or psych illness may confer higher risk 0-2 points: pt can go home but one needs to ensure follow up in future 3-4 points: close follow up needs to be ensured and hospitalization considered 5-6 points: hospitalization strongly considered 7-10 points: ensure hospitalization and consider involuntary admission if necessary

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

-Feels better when they lean forward. Worse laying flat. -Sharp, sudden pain in chest, shoulders, back -Diffuse ST segment elevation on EKG, all leads -Can have depression of PR segments -echo shows fluid in area -Pericardial friction rub / muffled on auscultation -Depending on etiology - NSAIDS / antibiotics/ intervention

Indications for undergoing a classic stress test prior to hospital discharge

-For post-MI pts not undergoing cardiac cath, stress testing should be done > 48 hrs but before discharge or max 3-6 wks after discharge -Should be used in MI pts who received thromboembolytic therapy as means of selecting appropriate candidates for CABH -Done to confirm angina/inducible ischemia, assess prognosis of CAD or MI recovery, eval therapy response, ID low vs high risk, and screen for silent ischemia **exercise stress test for low risk pt's without baseline ST abnormality** -DO NOT do MPI on pt's w severe asthma d/t risk of bronchospasm ---> perform 2D Stress echo w IV Dobutamine instead You do this on a stable person, no active symptoms, you ruled out active MI, normal ECG

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

-Ischemia: OPQRST Onset: Gradual intensity Provocation: Provoked with activity, non-pleuritic, Nitro Quality: Discomfort, difficult to describe, squeezing, tightness, pressure, etc. Radiation: abdomen, jaw, shoulder, arms, etc. Site: Diffuse Time Course: Angina vs ACS S/S -Besides CP/Discomfort (substernal/epigastric) -SOB -N/V/D, Indigestion -Diaphoresis -Dizziness/Lightheadedness -Fatigue/Pale Appearance -Atypical Symptoms: Elderly and Females Work up -Vitals **HR: Variable **Usually Sinus brady due to inferior wall MI **Arrhythmias/Dysarrythmias **BP: HTN usually prior to MI **Hypotension: indicates large infract, indicator for poor outcome **Resp: Tachy usually due to pain or anxiety **Temp: low grade fever or normal Physical Exam **Usually Unremarkable **Diaphoresis, pale cool skin, sinus tach, 3rd or 4th heart sounds, crackles or other pulmonary findings, hypotension **Heart Failure: JVD, new murmur or worsening, hypotension, tachycardia, S3 gallop, crackles **Focused Neuro exam: Assess for focal lesions for safe use of thrombolytic therapy EKG: Infraction Patterns **T-wave inversion, flat, depressed or inverted, usually symmetrical **ST segment elevation: >2mm elevated in consecutive chest leads, depression can also occur **Elevated cardiac marker but NO ST elevation = NSTEMI **Clinical dx, subtle changes in EKG, & non-dx changes in cardiac biomarkers = unstable angina **Q-waves: Significant/Pathological >25%-30% of QRS, >0.04 sec or 1mm width STEMI -Both ST elevation and depression, look at leads with elevation for anatomical location, even if depression is pronounced Immediate Tmt of ACS-MONAH (initial tx for all except stable) -ASA: prevent platelet aggregation **324mg non-enteric coasted chewed **Use with caution in h/o of UD, bleeding diathesis, ASA allergy -Oxygen: Limit ischemic injury **4L/min then titrated -NTG **IV: 12.5-25ug bolus followed by 10ug/min infusion titrated Q5 min maximum dose of 200ug/min **Use in pts with persistent sxs, pulmonary congestion or HTN **Contraindicated in Hypotension (<90mmHg systolic), severely brady (<50bpm), recent use of PDE5 inhibitors. -Morphine Sulfate: Dilates arteries and veins **Anxiolytic and analgesia **Use in pts with persistent symptoms after **NTG or with pulm congestion **Contraindicated in hypotension -Statin: 80mg Atorvastatin early as possible if pt is not on a statin, switch if low or moderate -Beta Blocker: Lowers BP, reduces workload by slowing heart, reducing muscle contraction STEMI Tmt 1. Fibrinolysis (thrombolysis) within 30 min ****Alteplase (tPA), Reteplase (rPA), Tenceteplase (TNK-tPA) **Absolute CI to thrombolysis- prior intracranial hemorrhage, structural cerebral vascular neoplasms, ischemic stroke within 3 mo except stroke within 3 hrs, aortic dissection, active bleeding, or bleeding diathesis (except menses), sig closed head or facial trauma wn 3 hrs **Relative CI- recent 2-4 wk internal bleeding, non-compressible vascular punctures, pregnancy, active peptic ulcer, current use anticoag (higher the INR, higher risk of bleed) -Persistent sxs >12 hours, fibrinolytic tmt is not indicated, emergent PCI can be considered if non-going ischemia or high risk of death 2. Primary PCI for STEMI **PCI of infarct artery within 12 hours of symptom onset **Balloon inflation within 90 minutes of presentation **First medical contact-to-balloon or door-to-balloon shoulder be within 90 minutes, fibrinolysis within 30 minutes NSTEMI Tmt -NO THROMBOLYSIS, PCI For High Risk Pts -Antiplatelet therapy in addition to ASA **Ticagrelor **Very high risk: consider adding GP Iib/IIIA inhibitor (etifibatide or triofban) -Anticoagulant therapy in all pts -Urgent Cath or invasive strategy (angiography within 4-48 hours) use UFH **Non-invasive: Fondaparinux of enoxaparin -Very High Risk: Cardiogenic shock, overt HF or severe L vent dysfunction, recent or persistent rest angina despite intensive med tx, hemodynamic instability, unstable ventricular arrhythmias Standard Cardiac Workup CBC/BMP - cell counts and electrolytes. Troponin, serial if symptoms just started EKG CXR All chest pain patients or suspects are considered an acute emergency until proven otherwise!!! Cardiac Monitor IV access Full Dose Aspirin Oxygen Pain control, morphine, nitro or nitropaste If the patients BP is elevated nitropaste helps with pain and pressure Add-Ons for Other Considerations Consideration of PE work-up (D-dimer, spiral CT) BNP GI cocktail CK-MB - not very specific

Etiology, ED care and disposition of cervical sprain/strain (whiplash)

-Ligament/tendonous/paraspinous muscle strain injuries. -Diagnosis of exclusion of imaging negative. -NSAIDS, +/- Narcotics, +/- steroids. -Soft collars are neck warmers, no proof they help. -Seatbelt sign of neck- is there underlying damage to anterior chest wall, carotids, laryngeal injuries. Do good examination!

Etiology, ED care and disposition smoke inhalation

-Occurs most frequently in closed space fires -Patients with decreased cognition: Alcohol intoxication, Drug abuse, Head injury, dementia -Injury can occur to both upper and lower airways -Due to exposure: Heat, Particulate matter, Toxic gases -Upper airway edema **Secondary to thermal injury **Can result in acute airway compromise Signs of pulmonary smoke inhalation injury -Often delayed 12-24 hours **Cough, Wheezing, Respiratory distress -Clinical indicators of smoke inhalation injury **Facial burns, Singed nasal hair, Soot in the nose or mouth, Hoarseness, Carbonaceous sputum, wheezing Diagnosis of Smoke inhalation -Primarily made on clinical history of enclosed space fire -Labs: ABG, lactic acid (HCN), carboxyhemoglobin, CBC, trop -Eval: EKG, CXR, PFT, bronchoscopy -Exam findings: **Facial burns, Singed nasal hairs , Carbonaceous sputum, Soot in mouth and nose, Wheezing -Flexible fiberoptic bronchoscopy: Can confirm diagnosis -Carboxyhemoglobin levels: If carbon monoxide poisoning is suspected Treatment may include: -Humidified oxygen **Endotracheal intubation and mechanical ventilation **Bronchodilators **Pulmonary toilet -Hyperbaric oxygen therapy **Used for severe carbon monoxide poisoning

Etiology, ED care and disposition of esophageal rupture

-Linear (longitudinal) tear of lower esophagus -Only mediastinal pleura contains contents -Contents leak into mediastinum -Mediastinitis -Empyema Causes of E.R. -MC cause is intraluminal procedures -Esophageal Cancer -Foreign body -Severe Retching/Vomiting -Trauma -Penetrating Chest Trauma -Blunt force to sternum, epigastrium S/S of E.R. -Depends on location: Cervical, intrathoracic, intrabdominal. -Excruciating retrosternal CP -History of N/V: 25-45% no history -Crepitus to palpation/auscultation -Hamman's sign-mediastinal crackling w each heart beat -Dyspnea, sepsis, odynophagia -Cyanosis -Tachypnea and tachycardia -Hypotension -Syncope -acute pain, severe, diffuse -can radiate to back and shoulders -pain with swallowing Diagnosis -Usually incidentally found on C-XR when pt evaluated for CP. -Suspect in severe chest, neck upper abdominal pain after vomiting/retching with Subq emphysema -Thoracic/Cervical X-ray **Subsequent emphysema/mediastinal or peritoneal air, pleural effusion, mediastinal widening, usually abnl but non-specific takes hrs to develop -Contrast Esophagogram -CT **use if unacceptable esophagram Esophageal wall edema & thickening periesophageal fluid **Mediastinal widening, air & fluid in pleural space, cannot localize exact size Imaging -Xray **Subq emphasema/mediastinal or peritoneal air **Pleural Effusions **Mediastinal Widening **Takes hours to develop -Contrast Esophagram **Establishes diagnosis and extent/location **Gastrografin and Barium -CT **Chest and abdomen if needed **Use if unacceptable esophagram **Esophageal wall edema and thickening periesophageal fluid **Mediastinal widening **Air and fluid in pleural spaces **Cannot localize exact site Treatment -Emergent Surgical Intervention! -Surgery: Primary closure/resection if <24hrs -Medical Tmt: **NPO **Parenteral nutritional support/NG suction **IV ABX **IV PPI

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

-MC distributive shock -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 Presentation -Early presentation is the "warm phase" - hyperdynamic response. Massive vasodilation. Skin is warm, flushed. Tachycardia, tachypnea, increased cardiac output. May have crackles. -"Cold shock" is the later, decompensated phase - body starts to vasoconstrict, skin becomes pale and cool. Tachycardia, decreased BP, mental status changes, decreased urine output, acidosis with hypoxemia. DX -elevated wbc's -CBC, Platelet count, DIC panel, lytes, LFTs, ABGs, lactic acid, UA, CXR -2 separate blood cultures -CRP elevated in sepsis, prolactin has greater sensitivity Treatment -Begin broad spectrum abx therapy -Attempt to identify the 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 because endotoxins can persist

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

-MC occur from obstruction of the gallbladder or biliary duct by gallstones S/S: Fertile, female, fat, fourty -unexplained fever or right upper quadrant pain: consider acalculus cholecystitis (NO STONES) unexplained fever or RUQ pain within 2-4 weeks critically ill patient who has had no oral intake for a prolonged period -steady, severe pain, and tenderness in the right hypochondrium or epigastrium -pain radiates around to the right shoulder -may begin after eating but usually has no association to meals characterized by sudden appearance of steady pain localized to the epigastrium or right hypochondrium -usually associated with muscle guarding and rebound tenderness -Murphy sign or inhibition of inspiration by pain on palpation of the RUQ palpable gallbladder -N/V Labs: US right away! -High WBC -Total serum bilirubin values of 1-4mg/dL, even in the absence of bile obstruction -serum aminotransferase and alkaline phosphatase levels are usually elevated serum amylase may be moderately elevated Imaging: -plain films of the abdomen may show radiopaque gallstones -HIDA scan-demonstrates obstructive cystic duct, usual cause of acute cholecystitis reliable if the bilirubin is under 5mg/dL -RUQ ultrasonography: initial study of choice -CT may show complications such as perforation and gangrene Treatment: -NPO -IV alimentation: fluids -analgesics -antiemetics -morphine or meperidine -NG tube if distended or actively vomiting -IV antibiotics **third generation cephalosporin such as Cefoxitime or Ceftriaxone PLUS Addition of Metronidazole 500mg IV q 6 hours -may need to add third like ampicillin, gentamicin, or clindamycin if obvious peritonitis -surgery consult

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

-MCC of R sided HF is L sided HF -Preload, afterload, and contractility determine ventricular stroke volume. Couple w HR, stroke volume, determines CO Clinical Features - -Left Sided: Acute pulm edema or congestion cardinal, pt usually present w severe resp distress, frothy pink or white sputum, moist pulm rales, S3 or S4 **Dyspnea on exertion, paroxysmal nocturnal dyspnea, orthopnea, nocturia, fatigue, weakness **Tachycardia, cardiac dysrhythmias (AFib or PVC), HTN -Right Sided: dependent edema of extremities, JVD, hepatic enlargement, hepatojugular reflex DX - -CXR: vascular resdistribution to upper lung fields, cardiomegaly, interstitial edema, enlarged pulm artery, pleural effusions, alveolar edema, prominent SVC, Kerley B lines (short linear markings in periphery of lower lung fields) -BNP: markedly elevated (>500) or N-terminal pro-BNP (>1000) - if low, can exlcude CHF TX - admit** LMNOP: lasix, morphine, nitrates, oxygen, position (sit them up) -100% O2 by non-rebreather --> achieve 95% pulse ox -BiPAP or CPAP --> if in any resp distress -Immediate intubation --> if visibly tiring, uncooperative w non-invasive vent, unconscious, unstable -Nitroglycerin IV Drip--> If BP >150/100 --> Nitroprusside if not working **Then IV Furosemide after Nitro ---> monitor electrolytes (esp K+) -Morphine --> pain control -Dopamine or Dobutamine --> hypOtension Long Term Management: -Dietary salt reduction, preload reduction through chronic use diuretics (Furosemide), afterload reduction via BB (Metoprolol), ACE-I (Captopril), and Digoxin

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

-Majority due to blunt trauma and penetrating trauma (10 to 15% of cases: GSW/stab wounds) **MVC **Falls **Sports-related Pathophysiology -Acute spinal cord injury disrupts sympathetic flow resulting in hypotension and bradycardia Clinical Features -Within 2 to 3 mins: **Hypertension **Widened pulse pressure **tachycardia -As sympathetic tone is lost **Hypotensive **Warm, dry skin -Any injury above T1 **Disrupt entire sympathetic chain -Between T1 and L3 **Partial sympathetic disruption **Symptoms last from 1 to 3 weeks Dx-clinical ED Care and Disposition -ABCD's addressed -Diagnosis of neurogenic shock is made -Therapy aimed at mitigating hypotension and bradycardia **Crystalloid should be infused with goal of MAP of 70 mm Hg **Dobutamine or dopamine (2 to 20 ug/kg/min) if inotropic support is necessary **Symptomatic bradycardia use atropine **Asystole or heart block develops, a pacemaker may be necessary **Steroids for spinal cord injury

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

-Status Epilepticus: continuous seizure >5 min without recovery of consciousness -Non-convulsive Status Epilepticus: assoc w minimal or imperceptible convulsive activity + confirmed by EEG HX and Workup - -Hx from pt & witnesses -Onset, aura? Type of movement, incontinence? Drugs, ETOH, meds, pregnancy? -Look for injuries --> tongue, dislocated shoulder -CBC, b-hCG, BMP, Ca, Mg, Glucose -Prolactin - elevated 15-60 mins after -Non-contrast CT -MRI, lumbar puncture, EEGS TX - -During Seizure: protect from injury, prevent aspiration, Benzos during prolonged seizure -Afterward: check antiepileptic levels if they are on any -IV Benzos!! -Load w Keppra or Phenytoin --> if not on any meds -Consider admission if any abnl labs or persistent mental status changes -No driving for 6 months -Status Epilepticus: seizure > 5 in --> give IV Ativan or Diazepam*** -can be refractory if > 30 mins, continue Benzos + load w antiepileptics, always treat ABCs

Etiology, ED care and disposition carbon monoxide poisoning

-Suspected in those with smoke inhalation injury Clinical signs -Headache -Vomiting -Confusion -Lethargy -coma ED Care -Hyperbaric oxygen therapy -Used for severe carbon monoxide poisoning

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

-Temporary paralysis of intestinal function d/t surgery, med illness, trauma surgery of abd or retroperitoneum likely to stop normal motility -Neurogenic failure or loss of peristalsis in intestine without mechanical obstruction -Clinical diagnosis -Very common after abdominal surgery Dx: clinical radigraphs show it too Causes -Appendicitis -Botulism (poisoning with botulinum, a neurotoxin) -Certain medications, such as opiates and sedatives -Diabetic ketoacidosis (life-threatening complication of diabetes) -Electrolyte imbalance -Gastroenteritis (inflammation or infection of the stomach or intestines) -Neonatal necrotizing enterocolitis (disease that causes death of intestinal tissue in newborns) -Obstruction of the mesenteric artery, which supplies blood to the abdomen -Pancreatitis -Porphyria (metabolic disorder) -Surgical complications S/S: sleepy bowel Abdominal swelling, distension or bloating Constipation Diarrhea Foul-smelling breath Gas Lack of bowel sounds Nausea with or without vomiting Stomach pain and spasms Decreased bowel sounds Treatment: mainly supportive -NPO -NG suction if NV -encourage pt. to ambulate, some data to suggest gum chewing may help, ?role for pharmacologic therapy

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

-common in anterior communicating artery -"worst headache of my life", severe & sudden onset -20% occur during exertion ie sex, heavy lifting -Can be due to berry aneurysm or AVM -May also have nausea, vomiting, photophobia, stroke symptoms. But headache may be the only symptom -Symptoms may improve so don't be fooled -CT, MRI is no better -Lumbar puncture is the next modality if high suspicion and CT neg -Consult Neurosurgery, Keep MAP <130 mmhg with IV Lopressor

Clinical features, necessary ED diagnostic work-up, ED treatment for ankle injuries (sprains)

-very flexible joint w lots of ligamentous structures esp on lateral aspect -all radiographs of the region must be AP, lateral, mortise -deltoid ligament injuries: medial ankle ligament is very thick & sturdy, MOI is eversion. Not as common as lateral ankle sprains. Look for fx of medial malleolus. PRICER -Ottawa ankle rules **Ankle x-ray -Required if pain in malleolar zone and -Bone tenderness at posterior edge or tip of lateral malleolus -Bone tenderness at posterior edge of tip of medial malleolus OR -Inability to bear weight at time of injury/in ER **Foot X-ray: -Required if pain in midfoot zone and -Bone tenderness base or 5th metatarsal OR -Bone tenderness in navicular OR -Inability to bear weight at time of injury/in ER Usually inversion>eversion Lateral ligaments. -almost all sprains involve the anterior talofibular ligament, more severe will affect calcaneofibular ligament. PRICER. Ace wrap Ankle stirrup Posterior OCL (ortho casting lab)

Rule of nines calculation for burns

Burn size is calculated as the percentage of total BSA (body surface area) involved. Most common method to estimate the percentage of BSA is "rule of nines" -HEAD IS 9% ON FRONT AND BACK TOTAL -CHEST IS A TOTAL OF 18%-9 ON BACK 9 ON FRONT -ABDOMEN IS TOTAL OF 18%-9 ON FRONT 9 ON BACK -ARMS ARE 9 PERCENT TOTAL EACH -LEGS ARE 18% TOTAL EACH -GENITALIA IS 1%

Patient education for post-surgical wounds.

1. Dressings -topical antibiotics may be used to provide a warm, moist environment. Topical antibiotics may reduce the rate of wound infection and also may prevent scab formation. Wounds closed with tissue adhesives should not be treated with topical antibiotic ointment because it will loosen the adhesive. 2. Positioning -The injured site should be elevated, -Splints are useful for extremity injuries because they decrease motion and edema and increase attention paid to the body part -Pressure dressings minimize the accumulation of fluid and are most useful for ear and scalp lacerations 3. PROPHYLACTIC ANTIBIOTICS -Prophylactic antibiotics are recommended for human bites, dog or cat bites on the extremities, intraoral lacerations, open fractures, and wounds with exposed joints or tendons. Patients with wounds in areas with lymphedema will likely benefit from prophylactic antibiotics as well. 4. Tetanus prophylaxis -The need for tetanus prophylaxis should be considered for every wounded patient -The only contraindication to tetanus toxoid is a history of neurologic or severe systemic reaction after a previous dose -LOOK AT CHART IN OUTLINE 5. WOUND CLEANSING: no peroxide or alcohol -Sutured or stapled wounds may be cleansed as early as 8 hours after closure w -Wounds should be gently cleansed with soap and water and examined for signs of infection daily. -Application of topical antibiotics for the first 3 to 5 days decreases scab formation and prevents edge separation. -Patients with wounds closed with tissue adhesives may shower, but should not immerse the wound or apply topical antibiotics, as this will loosen the adhesive bond and cause earlier sloughing of the adhesive 6. WOUND DRAINS Advise patients to change packing daily until the wound stops producing exudate. 7. PAIN CONTROL -Inform patients about the expected degree of pain and measures that might reduce pain. -Splints help reduce pain and swelling in extremity lacerations. -Analgesics may be needed although narcotic analgesia is rarely necessary after the first 48 hours. 8. HEALTH CARE PROVIDER FOLLOW-UP -Patients with high risk wounds or conditions or those unable to identify signs of infection should be instructed to return for re-exam, usually in 48 hours. -Facial sutures should be removed in 3 to 5 days. -Most other sutures can be removed in 7 to 10 days, except for sutures in the hands or over joints, which should remain for 10 to 14 days. -Tissue adhesives will slough off within 5 to 10 days of application. 9. Long term cosmetic outcome -inform pts that there may be scarring and that short term cosmetic appearance is not highly predictive of ultimate cosmetic outcome avoid sun while wound heals bc of hyperpigmentation -wear sunblock for at least 6-12 mos after surgery

Stages of wound healing

1. Inflammatory Phase- this is within the first 3 days -Vasoconstriction **Lasts 5-10 minutes **Reduces blood loss -Vasodilation **Increases blood supply to wound **Causes erythema -Coagulation **Clot made of fibrin and platelets that traps RBCs **Biologically active proteins are released **Complement system activated **In 24 hours, PMNs enter the wound through leaky capillaries **They phagocytose the clot by releasing proteases **Kill bacteria by releasing free radicals **48-72 hours: monocytes come into the picture through capillaries and become activated macrophages **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 **VEGF and other growth factors stimulate angiogenesis **At surface of the wound, exposed collagen causes keratinocyte migration up from the basal layer: epitheliazation complete at 24 hours (if edges are well approximated) **Creates a water barrier **Over a few days, it becomes multilayered OVERALL: -Initial response w hemostasis by fibrin platelet clot entrapping RBCs. Platelets degranulate & release derived growth factor. Complement is activated, fibrinectin & fibrin create matrix -In 1st 24 hrs ---> PMNs adhere to capillary endothelium & phagocytose the clot w proteases & kill bacteria by releasing free radical, epithelization complete & there is not a water barrier. -In next 48-72 hrs ---> monocytes migrate across capillary bed, become macrophages & release growth factors, these help matrix deposition Can take days-months for keratinization in open wound 2. Proliferative Phase -72 hours after wound created til day 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 -Then wound contracts and enters final stage of wound healing 3. Remodeling Phase -3 weeks after wound creation -Inflammatory cells and angiogenesis slows down and stops -The total collagen content in the wound increases for 2-3 weeks -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 70% of normal -Scars are visible because of residual disorganized collagen OVERALL -2-3 wks after wounding begun increased density of inflammatory cells & capillaries resolves/apoptosis, collagen buildup continues along w breakdown, months to yrs, collagen bcomes progressively more organized and scared are less noticeable, scar appearance directly related to how well wound was cleaned at first 4. Next Several Months -Wound contraction (changes cosmetic appearance) -Need to repair lacerations with everted edges because of this -Scar remodeling continuesx

Clinical features, necessary ED diagnostic work-up, ED treatment for ventricular arrhythmias

1. Premature Ventricular Contractions - -Clinical Features: Impulses originating from single or multiple areas in the ventricles. If three or more PVCs occur in a row, patients are considered to have non sustained VT -EKG: (a) a premature and wide QRS complex (b) no preceding P wave (c) the ST segment and T wave of the PVC are directed opposite the preceding major QRS deflection (d) most PVCs do not affect the sinus node, so there is usually a fully compensatory post- ectopic pause, or the PVC may be interpolated between two sinus beats (e) many PVCs have a fixed coupling interval (within 0.04 second) from the preceding sinus beat (f) many PVCs are conducted into the atria, thus producing a retrograde P wave -ED Treatment 1. Stable pts require no treatment. 2. Pts with 3 or more PVCs occurring in a row should be managed as VT. 3. For hemodynamically unstable pts with PVCs, lidocaine IV 2. Accelerated Idioventricular Rhythm - -Clinical features: Condition MC found with an acute MI or in the setting of reperfusion after successful thrombolysis -EKG: (a) wide and regular QRS complexes (b) rate between 40 and 100 beats/min, often close to the preceding sinus rate (c) most runs of short duration (3-30 beats/min) (d) often beginning with a fusion beat. -ED Treatment: Treatment is not necessary. AIVR may be the only functioning pacemaker, and suppression with lidocaine can lead to cardiac asystole. 3. Ventricular Tachycardia - -Clinical features: Occurrence of 3 or more successive beats from a ventricular ectopic pacemaker at a rate faster than 100 beats/min EKG: (a) a wide QRS complex (b) a rate faster than 100 beats/min (most commonly 150-200 beats/min) (c) a regular rhythm, although there may be some initial beat-to-beat variation (d) a constant QRS axis [Atypical VT (torsade de pointes, or twisting of the points) occurs when the QRS axis swings from a positive to a negative direction in a single lead at a rate of 200-240 beats/min. Drugs that further prolong repolarization—quinidine, disopyramide, procainamide, phenothiazines, and tricyclic antidepressants—exacerbate this arrhythmia.] -ED Treatment **Defibrillate pulseless VT with unsynchronized cardioversion starting at 100 J. **Unstable pts who are not pulseless: synchronized cardioversion **Hemodynamically stable pts: amiodarone IV; Second-line agents procainamide and lidocaine. **Torsades de pointes pts: Try overdrive pacing set at 90-120 beats/min to terminate torsades de pointes. Magnesium sulfate IV **Isoproterenol IV in refractory torsades but carries a risk of increased myocardial oxygen demand. Ventricular Tachycardia versus SVT w Aberrancy -Pts with wide-complex tachycardia should be approached as having VT until proven otherwise. Age over 35 years, a history of MI, CHF, or coronary artery bypass grafting strongly favor VT. EKG signs favoring VT include AV dissociation, fusion beats, precordial lead QRS concordance, and a QRS duration longer than 0.14 second. Ventricular Fibrillation - -Clinical features: Totally disorganized depolarization and contraction of small areas of ventricular myocardium during which there is no effective ventricular pumping activity. Primary VF occurs suddenly, without preceding hemodynamic deterioration, and usually is due to acute ischemia or peri-infarct scar reentry. Secondary VF occurs after a prolonged period of hemodynamic deterioration due to LV failure or circulatory shock. -EKG: a fine-to-coarse zigzag pattern without discernible P waves or QRS complexes -EMERGENCY DEPARTMENT CARE AND DISPOSITION **Immediate electrical defibrillation (unsynchronized); If VF persists, do five cycles of CPR, check pulse, and defibrillate again if no pulse is present. **If the initial 2 cycles of CPR and defibrillation are unsuccessful, amiodarone IV push. Lidocaine is second-line. Repeat the CPR-defibrillation cycle. If no pulse is present after the third CPR-defibrillation cycle, give epinephrine IV push, or vasopressin IV push and immediate resumption of the CPR-defibrillation cycle. **In refractory VF, administer magnesium sulfate IV

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 with damaged muscle cells deposit into the bloodstream and build up. -Patient says they feel weak and tired, fatigued, N/V, confusion. Dark cola colored urine. May have gross soft tissue abnls on PE, but may have nothing. -Get CPK>20,000-100,000 units and U/A-increased protein levels. -TMT of choice-IVF (lots and lots of fluids!)-6-12 Liters within 24 hours. Close lyte monitoring.

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

3 types - -Primary Spontaneous: no underlying ds tall, thin male & young d/t blebs -Secondary Spontaneous: underlying lung ds -Tension: d/t blunt chest trauma from fx to rib air enters into pleural space & compress lung/mediastinum S/S - tension pneumothorax -Tachypnea, CP, hypotension, JVD, hypoxia, tracheal deviation to opposite side -Hyper-resonance to percussion, UL absent breath sounds, resp distress Imaging - -Tension Pneumo: clinical dx --> use imaging post-decompression/tx -Supine, CXR, upward AP --> repeat CXR in 6 hrs but 1st is (-) -US, CT: commonly in multi-trauma TX - Emergent Needle Decompression: do NOT wat for CXR, top 3rd rib mid-clavicular line Chest Tube: immediately after need decompression, top 5th rib mid-axillary line

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

A. Anterior Cerebral Artery: -CL leg weakness>arms + sensory changes -urinary incontinence B. Middle Cerebral Artery: -Hemiparesis (arm > leg), facial plegia, sensory loss -Weakness in lower half of face & IL gaze preference -If dominant hemisphere involved (usually L): Aphasia -Nondominant hemisphere: CL hemineglect C. Posterior Cerebral Artery (Cerebellar stroke presents similarly): -UL HA, visual field defects, diplopia, dizziness, vertigo, dysphagia, ataxia, CN deficits, BL limb weakness D. Basilar Artery: severe quadriplegia, coma, locked in syndrome E. Lacunar Stroke: pure motor or sensory s/s F. Inferior Cerebral: IL blindness Workup - -Emergent non-contrast CT to determine hemorrhage or stroke mimic is present (most ischemic strokes not visualized within first few hrs of stroke) -CBC, EKG, pulse ox, lyte & coag studies, cardiac enzyme levels, toxicology screen, blood ETOH level, Echocardiogram, carotid duplex scanning ED TX - -ABCs + keep O2 sat > 92% -Establish IV access + place pt on cardiac monitor; obtain blood glucose & normalize any hypoglycemia; keep pt NPO -Once stabilized, send for non-contrast head CT -HTN: If not candidate for thrombolysis, then HTN permissible unless systolic > 220, diastolic > 120 **If BP correction needed, use Labetalol to reduce MAP 10-25% -If candidate for thrombolysis, target BP is systolic < 195, diastolic < 110 **Labetalol or Nitro Paste or Nicardipine -If < 3 hrs since s/s onset --> rtPA used for ischemic stroke (exclusion/inclusion criteria) **No ASA or Heparin administered in initial 24 hrs after tx **24-48 hrs after rtPA, give pt PO ASA If evidence outside therapeutic range for rtPA, provide aggressive supportive care Aspiration, prevention, normalization of glucose, fall precaution, tx comorbidities -Evidence of increased ICP **Elevated HOB to 30 degrees + analgesics + sedation --> if fails to lower ICP Mannitol -Emergent neuro consult in difficult stroke cases (intracerebral hemorrhage w evidence of elevated ICP, cerebellar strokes) - often leads to rapid deterioration -Admit all pts w acute ischemic stroke or intracerebral hemorrhage (preferably to specialized stroke unit) Ischemia stroke: tpa keep BP under 220 Hemorrhagic: BP meds?

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

A. Brown Recluse -Bite produces a mildly erythematous lesion that may become firm and heal over several days to weeks. Occasionally, a severe reaction with immediate pain, blister formation and bluish coloration may occur -These lesions often become necrotic over the next 3-4 days and form an eschar from 1 to 30 cm in diameter -Loxoscelism is a systemic reaction that may occur 1 to 2 days after envenomation. S/S include fever, chills, vomiting, arthralgias, myalgias, petechiae and hemolysis. Severe cases progress to seizure, renal failure, disseminated intravascular coagulation (DIC) and death Diagnosis may need to be made on clinical grounds since the bite is often unwitnessed Emergency Department Care and Disposition -Supportive measures -No antivenin available -Tetanus prophylaxis, analgesics, and antibiotics may be offered when appropriate -Surgery is reserved for lesions greater than 2 cm in size and is deferred for 2-3 weeks following the bite -Dapsone (50 to 00 mg per day) and hyperbaric oxygen may prevent some ongoing local necrosis -Patients with severe systemic reactions and hemolysis must be hospitalized for consideration of blood transfusion and hemodialysis B. Black Widow Spider -Immediate pin prick sensation that often allows the victim to identify the offending agent -Within 1 hour patient may experience erythematous skin lesions that are often target shaped, swelling and diffuse muscle cramps -Large muscle groups are involved with abdominal wall cramps that mimics peritonitis. -Severe pain for 3 days, muscle weakness for weeks to months -Serious acute complications include hypertension, respiratory failure shock and coma Emergency Department Care and Disposition -Local wound treatment and supportive care of analgesics and benzodiazepines for pain and cramping -Hospitalization required for severe envenomations including parenteral pain meds and antivenom therapy -Antivenin from horses is rapidly effective and if patient tolerates cutaneous test dose, usual IV dose is 1 to 2 diluted vials over 30 minutes

Complication of transfusion therapy and how to manage

Acute hemolytic transfusion reaction: -Due to transfusion of incompatible donor red cells. -Clinical features: early features are fever, chills, back pain, pruritus, burning sensation at the site of transfusion and centrally along the vein and chest pain -In an unconscious pt, more severe features like hypotension, shock, hemoglobinuria, oliguria and excessive bleeding due to DIC develop -Stop the transfusion immediately if a transfusion reaction is suspected -Change the blood transfusion set and maintain the venous access using normal saline -Perform physical examination with spl attention to BP, urine output, and evidence of bleeding Withdraw blood samples from the opposite arm . -Get a coagulation screen including partial thromboplastin time , platelet count , fibrinogen level , fibrin degradation products to exclude DIC -If hypotension develops, administer fluids and if required vasopressors -Administer furosemide to maintain urine output FEBRILE NON HEMOLYTIC REACTION -Generally occur due to anti leukocyte antibodies in a pt who has been pregnant or has been previously transfused , reacting against leukocytes in the transfused blood. -Can also occur due to cytokines in stored platelet concentrates -Generally occurs towards the end of infusion or within hrs of completing the transfusion -Management is symptomatic with antipyretics -Incidence can be reduced by leukoreduction in which WBCs are reduced in no. through centrifugation or filtration. URTICARIA: -Antibodies in the recipient's blood to infused plasma proteins or infusion of allergens that react with IgE antibodies in the pt ANAPHYLAXIS: -Occurs in pts who have antibodies against IgA and are often deficient in IgA. The antibodies react with IgA present in the donor blood TRANSFUSION RELATED ACUTE LUNG INJURY [TRALI] -Pt develops an acute resp rxn with fever, cough, shortness of breath typical appearance on chest X-ray. The rxn occurs during or soon after transfusion and may be life threatening NON IMMUNE REACTIONS -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 epistaxis

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-Woodruffs plexus Anterior bleed treatment - stepwise -Ice packs/ pressure -Drug therapy - oxymetazoline If anterior source of bleed is visible, can try chemical cautery -If still bleeding >> anterior nasal packing. Posterior packing may require ENT consult, hospital admission -Patients with nasal packing require abx prophylaxis to prevent toxic shock syndrome -Augmentin

Managing anticoagulation prior to surgery

Anticoagulation Therapy -Small extra risk of operative hemorrhage -Most people need to have some sort of anticoag continued -INR needs to be around 1.5 for most surgeries to happen -Continue oral Coumadin: reduce prothrombin ratio during perioperative period -Usually change to heparin 4 days prior -Aspirin **Irreversible inhibitory effect on platelet aggregation which lasts for at least 10 days **Effect is reversed when affected platelets have been replaced **Causes oozing during and after operation **Major arterial surgery: stop aspirin 2 weeks before surgery Book- Bleeding Disorders - -Mostly d/t too much anticoagulation, liver ds, aspirin therapy -Need good H&P ---> If suspected, order Coags (PT, aPtt, INR, Platelet count) -Need to balance risk of bleeding w benefit of surgery Previous PE - Increased risk subsequent PE Follow anticoag or prophylactic guidelines Mechanical Valves - -Anticoagulation reduced before surgery; often safe to continue INRs at 1.5-2.0 -If a lot of bleeding anticipated, some surgeons stop Warfarin 2 days before operation & substitute IV Heparin -Stop heparin 12 hours before operation & restart when danger of bleeding over

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

Background -Distinguished from DKA by no significant ketosis -Occurs usually in poorly controlled Type 2 diabetics -Same precipitating factors as DKA To diagnose: -Severe hyperglycemia (>600) often > 1000mg/dL -Hyperosmolality (serum osmolality >315) -Lack of significant acidosis (pH >7.3) or ketosis -Serum bicarbonate > 15 mEq/L -BUN:Cr 65:3 -NO anion gap -Na, K, free water deficit -Differs from DKA in that there is a relative deficiency of insulin -Tends to develop gradually over days to weeks -Hyperglycemia causes profound osmotic diuresis -Dehydration and electrolyte abnormalities more significant than in DKA Precipitated by: Infections - common presentation Major illness: CVA, AMI, GI bleed Noncompliance with hypoglycemic therapy New onset diabetes Work up -CBC -BMP, Mg, Phos -ABG or Venous pH -Serum Ketones - Beta-hydroxybutyrate -UA, urine HCG -EKG, Troponin -CXR -FOBT -Identify precipitating cause: CXR, CT brain, blood cultures, urine cultures, EKG, troponin -Average labs: **glucose 1000 mg/dL **serum osmolality 365 **BUN/Creat 65/3.0 **no anion gap -Sodium deficit, potassium deficit, free water deficit HHS: Clinical Presentation -Similar to DKA, but with more severe mental status changes -Severely dehydrated with orthostasis -Seizures possible -ARF common ED Treatment -Fluids (Often more dry than DKA) **1-2 L bolus NS x 2 hours and then 250-1000 mL/hour (CHF ESRD?) **Switch to ½ NS after initial bolus if BP stable and corrected Na+ >140 **Switch to D5 ½ NS when glucose </= 300 mg/dL and continue until insulin drip stopped -Insulin **Bolus at 0.1-0.15 units/Kg IV and then at rate of 0.1units/Kg/hour if K+ not too low **Change from IV insulin to sub q **Typically when glucose <300 -Potassium **If < 3.3 aggressive IV replacement 3.3-5.3 - IV replacement **>5.3, monitor -Treat precipitating problems

S/Sxs, treatments of patients with OD of acetaminophen

Background -Mostly 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 acetaminophen overdose, glutathione is depleted and the toxic metabolite accumulates in the liver causing hepatic necrosis -Toxicity Stages 1. Phase I **0 - 24 hours **Anorexia **Nausea **Vomiting 2. Phase 2 **24 - 72 hours **Abdominal pain 3. Phase 3 **3 - 5 days **Jaundice **Hypoglycemia **Coagulopathy **Encephalopathy 4. Phase 4 **1 week **Resolution of hepatic dysfunction (if phase 3 is not lethal) -Nausea, vomiting, abdominal pain, diaphoresis, malaise, jaundice, sometimes asymptomatic -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 @ baseline and @ 4 hrs, CXR Treatment -Airway, IVF's, oxygen, monitoring and N-acetylcysteine? -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

Common UE fractures and their ED management

COLLES VS SMITH -Usually both have same mechanism of injury FOOSH -Colles: transverse fx of distal radial metaphysis w dorsal displacement of distal fragment. Classic **"dinner fork deformity" -Smith: transverse fx of distal radial metaphysis w volar displacement of distal fragment. Also known as reverse colles fx Tx: sugar tong splint w wrist in flexion Elbow Dislocation: -Posterior MC -Be very careful w these injuries bc there can be lots of damage to the capsule & underlying structures -FOOSH injuries MCC -TX: may require procedural sedation. Post-reduction film needed -Usually utilize traction on the distal forearm w external rotation & abduction 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 -"snuff box tenderness" -Pain with axial loading. -Tenderness of scaphoid loading. -Xray non diagnostic. -Long arm thumb spica with repeat Xray in 7-10 days.

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

Causes - Primary intracranial disease Systemic ds secondarily affecting CNS Exogenous toxins Drug withdrawal Delirium - -acute confusional state that often occurs in response to an identifiable trigger, such as drug or alcohol intoxication or withdrawal, medication side effects (benzodiazepines, sleeping aids, opioids, antihistamines, neuroleptics, corticosteroids, and other sedative or psychotropic agents) -UTI, metabolic disorders, sleep deprivation, hypo or hyperglycemia, etc. S/S: -fluctuating levels of arousal (drowsiness or agitation) Treatment: remove the cause Dementia: S/S: -insidious onset -followed by decline in multiple cognitive abilities over years -first symptom is inability to learn new material (rapid forgetting or loss of short term memory) additional cognitive problems follow -early sxs are under recognized -onset insidious as disease progresses slowly -progression varies from person to person DELIRIUM -ONSET: over days -Course over 24 hr: fluctuating -Consiousness: Reduced or hyperalert -Attention: Disordered -Cognition: Disordered -Orientation: Impaired -hallucinations: visual and/or auditory -Delusions: transient, poorly organized -Movements: asterixus, tremor may be present DEMENTIA: -Onset: insidious -Course over 24 hr: stable -Consciousness: Alert -Attention: Normal -Cognition: impaired -Orientation: often impaired -Hallucinations: often absent -Delusions: usually absent -Movements: often absent Psychosis: -Onset: sudden -Course over 24 hr: stable -Consciousness: alert -Attention: may be disordered -Cognition: may be impaired -Orientation: may be impaired -Hallucinations: usually auditory -Delusions: sustained -Movements: Absent

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?

Causes of Bleeding during the Peri-operative period -Inadequate hemostasis during surgical procedure -Defects of hemostasis -Congenital **Hemophilia A (factor VIII deficiency) **Hemophilia B (factor IX deficiency) **Von Willebrand's disease -Acquired **Liver disease **Vitamin K deficiency **Disseminated intravascular coagulation **Anticoagulants **Massive blood transfusion **Platelet disorders Pre-Op Evaluation of Bleeding Risks -History!! **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!! PE -Look for signs of liver disease, platelet dysfunction, hematomas, splenomegaly -get a H and P for evaluation of anemia -family hx of anemia/bleeding Lab testing -Bleeding time - may not be clinically useful, studies show it does not accurately address risk of surgical bleeding -reticulocyte count -Prothrombin time/INR-Used to follow patients on Warfarin -PTT -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) -Type and Cross

DDX of central versus peripheral vertigo

Central -Brainstem & cerebellum -Sudden or slow onset, less intense sx -Constant sx, vertical nystagmus -Cannot fatigue symptoms -No hearing loss/tinnitus Causes: -Cerebellar damage - moderate vertigo, abnl Romberg -Vertebral artery dissection - sudden rotation of head (MVC, chiropractor, sneezing). HA & central vertigo -MS, neoplasm Peripheral -Vestibular apparatus & 8th cranial nerve -Sudden onset and intense symptoms -Paroxysmal sx, worse with movement -Nasuea, vomiting, nystagmus (horizontal, rotatry -vertical) -Can fatigue symptoms -May have auditory symptoms -No CNS sx Causes: -Meniere disease - sudden onset unilateral tinnitus, decreased hearing. Needs multiple attacks -Perilymph fistula -Vestibular neuritis - sudden severe vertigo, sometimes unilateral tinnitus and hearing loss. Viral, does not reoccur. -Eight cranial nerve tumors -Post closed head injury -Ototoxicity

Patient education regarding smoking cessation prior to surgery

Cessation of smoking 8 (or even 4 weeks if they can) weeks before surgery to decrease risk -Selective Dx Tools: recommends spirometry for pts being evaluated for thoracic & upper abdominal surgery who have hx of smoking or dyspnea **Indicated in abd surgery if pulm ds poorly control or if extent of ds not clear -Don't stop just before surgery bc Increased risk of mucous production -worse vascularity when you smoke -healing time worse when smoking

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

Characterized by: irreversible airflow obstruction, esp in expiratory airflow 2^ to airway secretions, mucosal edema, bronchospasms, and bronchoconstriction d/t impaired lung elasticity Clinical Features -Dyspnea, chest tightness, wheezing, cough -Emphysema: characterized by abnl permanent enlargement & destruction of air spaces distal to terminal bronchioles-"pink puffers" exhalation through pursed lips) **barrel chest, excessory muscle use -Chronic Bronchitis: excess mucus secretion in bronchial tree w chronic productive cough occurring on most days for at least 3 months, in the year for 2 consecutive years **"Blue bloater" causing excess sputum production/cough **Hypercapnia: confusion, tremor, hx of intubation, stupor, hypopnea, apnea Respiratory failure from COPD assoc w severe dyspnea refractory to initial tx, worsening hypoxemia or hypercapnia, or resp acidosis DX - HX + PE -Spirometry: peak expiratory flow rate (PEFR) <40% predicted -Pulse Ox: assess + monitor O2 sat during tx -ABGs: assess hypercapnia and resp acidosis -CXR: if suspect pneumothorax or pneumomediastinum -ECG: assess for cardiac ischemia, MI, arrhythmias w multifocal atrial tachycardia **R ventricular strain, abnl P wave, nonspecific ST-T wave abnormalities ED Care & Disposition - Cardiac monitor + puls ox + noninvasive BP monitor +/- IV access · Empiric supplemental O2 · 1st line à B-Adrenergic agent for bronchospasm + steroids à in hospital + at discharge o +/- nebulized anticholinergic (Ipratropium) o +/- ABX (if change in sputum color) · 2nd line à Noninvasive partial pressure ventilation (NPPV) o Pt w resp muscle fatigue,

Most common organisms responsible for post-surgical infections

Class 1 Procedures: Staph aureus Abdominal: E. Coli, Klebsiella, Enterobacter, Bacteroids Fragilis, Staph Pseudomonas in DM Streptococcus The organisms responsible for causing a surgical site infx best ID'd by cx of involved region

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-Depends on the degree of volume loss and duration of shock -MILD, MODERATE, SEVERE A. Mild Shock **Collapse of subcutaneous veins **Extremities become pale and cool **Sweating of forehead, hands, feet **Urine output normal **Pulse/BP normal **Patient may feel thirsty, cold B. Moderate Shock **Can start to appear drowsy, confused, anxious **Oliguria **Pulse rate increased **BP initially wnl, then falls **Decreased CAP refill C. Severe Shock **Unconscious **Gasping respirations **Anuria **Rapid pulse **Profound hypotension By Stage -Initial, Compensated, Decompensated, Refractory A. Initial - cells become "leaky" and switch to anaerobic metabolism. Body still able to function. B. Compensated (non-progressive) - body attempts to correct the metabolic upset of the shock C. Decompensated (progressive) - Compensatory mechanisms begin to fail D. Refractory (permanent) - organs fail, shock can no longer be reversed. Patient will die or have permanent damage.

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

Clean: breast biopsy, inguinal hernia repair without break in technique Clean contaminated: GI, GU, Gyn organs entered. No gross contamination, minor break in technique Contaminated: perforated appendectomy, colectomy for diverticulitis, perforated ulcer or bowel, penetrating GI trauma Dirty: traumatic wounds, burns older than 72 hours, free colon perforation

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

Clinical Features -Mild hypothermia (32-35 degrees C or 89.6-95 degrees F) **Shivering **Tachycardia **Elevated blood pressure -Below 32 degrees C (89.6 degrees F) **Mentation slows **Loss of cough and gag reflexes **Aspiration is a common problem -Hypothermia **Impairs renal concentrating ability **"cold diuresis" **May result in dehydration -Progressively lower core temperatures: Lethargic and comatose -Prolonged immobility: increaes risk of rhabdo, ARF -Hemoconcentration and volume depletion **Intravascular thrombosis, DIC -Hyperglycemia-common -Hypoglycemia -Acid-base disturbances -frostbite -Frostnip **Less severe **Resolves with rewarming **Involves no tissue loss **Trench foot **Chilblains (pernio) -ECG: PR, QRS and QT-interval prolongations, Osborn J waves -Cardiac rhythm: Progresses from tachycardia to bradycardia to atrial fibrillation with a slow ventricular rate to ventricular fibrillation and finally to asystole as the core temperature falls Treatment -Attention should be placed on the ABC's and initial resuscitation -Evaluation for cardiac stability -Ventricular fibrillation-Refractory to defibrillation until temperature of 30 degrees C (86 degrees F) **Three countershocks should be attempted Emergency Department Care and Disposition -Chilbains and trench foot: Elevation, Warming, Bandaging of the affected tissue, Nifedipine 20mg PO tid, Topical corticosteroids, prednisone and prostaglandin E1 (limaprost 20 micrograms PO tid) may be helpful -Rewarming A. Passive rewarming: **Removal from cold environment **insulation B. Active External rewarming: (more severe) **Warm water immersion **Heating blankets set at 40 degrees C **Radiant Heat **Forced Air -Active core rewarming at 40 degrees C: Inhalation rewarming, Heated IV fluids, GI tract lavage, Bladder lavage, Peritoneal lavage, Pleural lavage , Extracorporeal rewarming, Mediastinal lavage via thoracotomy -Rapid rewarming with circulating water at 42 degrees C (107 F) for 10-30 minutes result in thawing of frostbitten extremities -Dry air rewarming may cause further tissue injury and should be avoided -Mild hypothermia **Passive warming **Remove from cold environment **Use of insulating blankets -More severe hypothermia **No cardiovascular instability (Active external warming-Radiant heat, Warmed blankets, Warm water immersion, Heated objects , Warmed IV fluids , Warmed humidified air) **Cardiovascular instability (Aggressive core rewarming is required, Heated lavage fluids at 42 degrees C (107 degrees F), Gastric, Bladder, Peritoneal, pleural) -Severe hypothermic patients **Extracorporeal circuit is method of choice **If not available: Resuscitative thoracotomy , Internal cardiac massage, Mediastinal lavage Patients should receive: **Narcotics, Ibuprofen, Aloe vera, Penicillin G 500,000 units every 6 hours for 48-72 hours -Blisters **Clear-Rich in prostaglandins and thromboxane (Debrided or aspirated) **Hemorrhagic-Left intact -Suspected thiamine depletion and alcoholism **Thiamine 100 mg IV or IM **50% glucose 50-100 mL VI -Suspected hypothyroidism or adrenal insufficiency **IV thyroxine and hydrocortisone (100 mg) -All patients with more than isolated superficial frostbite or mild hypothermia: **Admitted to the hospital **Should not be discharged unless they can return to a warm environment

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

Clinical Features -Reactions may occur in seconds or may be delayed 1 hour or more after allergen exposure -By definition, anaphylaxis includes either respiratory compromise or cardiovascular collapse **Pruritus and urticaria are the most common initial symptoms **Urticaria is cutaneous IgE mediated reaction itchy red wheals of varying sizes which promptly disappear -Angioedema is similar with edema in the dermis usually of the face and neck -Respiratory symptoms are stridor, dyspnea and wheeze -GI features are nausea, cramps, diarrhea and vomiting Diagnosis -Clinically -History 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 ED A-G -A: Airway: Anticipate intubation especially in patients who are hoarse or describe a "lump in the throat. Edema may necessitate endotracheal tube 1-2 times smaller than expected. Cricothyrotomy kit should be open and ready before starting intubation -B: Breathing. Administer high flow O2 as necessary. TX bronchospasm with nebulized albuterol .5ml of 5% soln in 3 mL saline. -C: Circulation: Most patients (especially hypotensive) need large volumes of crystalloid. If hypotension persists after 1-2 L of fluid, IV epinephrine is needed -D: Discontinue: the antigen exposure. Remove Bee stinger -E: Epinephrine: 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: Further treatments: 1. Antihistamines **H1 blockers such as diphenhydramine 25-50 mg IV **H2 blockers such as ranitidine 50 mg. 2. Steroids **Only help control persistent or delayed allergic reactions. **Methylprednisolone 125 mg IV **Oral Prednisone 60 mg in less severe cases -G: Glucagon: 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

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

Clinical predictors of significant cardiac risk include: Major predictors: -Recent MI (within 30 days) -unstable coronary syndromes -decompensated CHF -Unstable or severe angina -Active heart failure -High-grade AV block -Symptomatic Ventricular arrhythmias with underlying cardiac disease -Supraventricular arrhythmias with an uncontrolled rate -Severe valvular disease -Afib Intermediate predictors: -mild angina pectoris, compensated or prior CHF, DM Minor predictors: advanced age, abnormal EKG (LVH, LBBB, ST abnormalities), hx of stroke, uncontrolled systemic HTN Preoperative Treatment: -NPO, continue cardiac meds (except Coumadin or Warfarin if can stop) esp nitrates/BB, EKG all pts >60 and any w cardiac hx -CABG before an elective procedure has immediate and long term benefit -Intensive medical therapy for CAD is alternative -Beta blockers **Decreases risk of ST depression and MI **Has been recommended in the absence of contraindications to be given in therapeutic doses to patients with an intermediate or high risk of cardiac complications -Calcium channel blockers -Nitrates -Mechanical Valves: ABX Prophylaxis, anticoag reduced before surgery -AFib: control rate pre-op meds (Digoxin, Verapamil, Amiodarone, BB), anticoag w Coumadin (pre-op, during peri-op, post-op) -HTN: Continue meds, if severe HTN wait until stabilized - CXR, EKG, BUN prior to surgery

Etiology, ED care and disposition of flail chest

Definition: Segmental fracture of 3 or more adjacent ribs in two separate isolated areas of greater than three rib fracture areas. Paradoxical inward movement of chest wall with inspiration and outward with expiration. Must R/O Pulmonary contusion Pt has gross trauma with respiratory distress Do not stabilize segment. CPAP, BiPAP, O2, pain meds/nerve block, intubation if RF.

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

Diabetes Mellitus -Stress of surgery increases catabolic hormones: oppose action of insulin; serum glucose control becomes more difficult -Preop Assessment: **Maintain glucose below 130 **Arrange for operation as early in the day as possible **Insulin: give 1/3 to ½ the usual dose AM of surgery since patient has not eaten or drank **Give infusion of dextrose (glucose) throughout operative period: 5-10% glucose infusion at 125ml/hr **Add potassium to dextrose **Monitor blood glucose and lytes often throughout operative and early postop period **Stop all 1st generation Sulfonylureas 2-3 days before, otherwise all others discontinue night before!! -Oral Hypoglycemic Drugs **Discontinue the night before surgery except for 1st generation sulfonylureas (like Diabinese): stop that 2-3 days prior, and Metformin stop 48 hours prior to hospital admission!! **Use sliding scale insulin post surgery if necessary; otherwise resume orals when tolerate Hypertension -HTN before surgery **Still give normal dose of HTN drugs with small amount of H2O **Sudden withdrawal can cause rebound HTN -Severe HTN **High risk of periop CHF or stroke (esp. with labile BP) **Can't put them under general anesthesia until they are stabilized -Minimal risk if < 180/110 -If severe HTN, > 180 systolic = HIGH risk of periop CHF or CVA --> CANNOT put under general anesthesia -Check electrolytes if on diuretics, also check CXR and EKG -Do NOT stop HTN meds even if general anesthesia, sudden withdrawal causes rebound HTN -OK to take PO meds before surgery w little water Epilepsy- can check medication drug level prior to surgery -Don't make changes -They do fine -General anesthesia depresses epilepsy

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

Dog Bites -Infections occur in 5% of cases and is more common in patients over 50 years old, those with hand wounds or deep puncture wounds and those who delay seeking initial treatment for more than 24 hours -A thorough history and exam...see human bites -Infections are often polymicrobial and include both aerobic and anaerobic bacteria Diagnosis Radiographs if evidence of infection, suspicion of a foreign body, bony involvement or intracranial penetration bites to the heads of small children Emergency Department Care and Disposition -Copious irrigation and debridement of devitalized tissue -Primary closure of wounds to the scalp, face, torso, and extremities other than the hands and feet -Lacerations of the hands and feet need to be left open initially. -Large, extensive lacerations, especially in small children, are best explored and repaired in the OR -Puncture wounds, wounds to the hands and face, and high risk patients **Augmentin 500-875 PO bid x 3-5 days (amoxicillin/clavulanate) **Clindamycin plus Ciprofloxin **In children, clindamycin plus Bactrim (trimethoprim/sulfamethoxazole) **Penicillin (500mg qid) drug of choice for Capnocytophaga canimorsus and should be used prophylactically for high-risk immunocompromised patients...those with asplenia, alcoholism, or chronic lung disease **Cephalosporins, tetracyclines, erythromycin, are reasonable alternatives -Infected wounds need to be cultured and ABX started -Reliable low risk patients, with only local cellulitis, can be treated outpatient Infection developing within 24 hours after injury suggests Pasteurella Multocida and needs to be treated with PCN, Cipro, or Bactrim. -Wound infection after 24 hours implicates staph or strep and should be treated with dicloxacillin or a first generation cephalosporin (cephalexin...keflex) -Significant infections require admission and parenteral ABX (includes associated lymphangitis, lymphadenitis, tenosynovitis, septic arthritis, osteomyelitis, systemic signs, and injury to underlying structures such as tendons, bones and joints) -Cultures should be obtained from deep structures, preferably in the OR. IV ABX with ampicillin-sulbactam 3 g IV q 6 hours or clindamycin plus ciprofloxacin. If the gram stain reveals gram negative bacilli, a third or fourth generation cephalosporin or aminoglycoside should be added. -Tetanus prophylaxis Cat Bites -P multocida is the major pathogen in 53-80% of cat wounds -Pasturella causes a rapidly developing intense inflammatory response with pain and swelling. May cause serious bone and joint infections and bacteremia -Septic arthritis is also possible in patients with altered host defenses due to glucocorticoids or alcoholism Diagnosis Radiographs for evidence of infection, foreign body or bony involvement Emergency Department care and Disposition -Essentially the same as for dog bites -Appropriate local wound care with copious irrigation and debridement -Primary wound closure except in puncture wounds or lacerations smaller than 1 to 2 cm -Delayed closure in cosmetically important areas -Prophylactic ABX in high risk patients including those with punctures of the hand, immunocompromised patients, and patients with arthritis and prosthetic joints -Augmentin 500-875 bid (45 mg/kg/day divided bid in children), cefuroxime 500 mg bid (45 mg/kg/day divided bid in children) or doxycycline 100 mg po bid. All for 3-5 days -Tetanus Prophylaxis

Causes of/treatment (prophlyaxis) for stress ulcers

Epidemiology/Pathophysiology - Occurs in critically ill patients due to issue with blood flow- burn victims, ICU -Stressors can cause a sudden hemorrhage (hematemesis or melena) or a perforation -Stress Ulcer: bleeding in a seriously ill pt caused by splanchnic perfusion impairement & increase in acid-pepsin TX- Sucralfate Prophylactic PPI Therapy -- -Rabeprazole (Aciphex), Esomeprazole (Nexium), Omeprazole (Prilosec), Pantoprazole (Protonix) H2 Blocker - -Cimetidine (Tagamet), Ranitidine (Zantac), Famotidine (Pepcid), Nizatadine (Axid)

Etiology, ED care and disposition of thermal burns

Etiology: -Pediatric burns **70% due to scalds **20% result from child abuse -Working age adults **Flame injuries are more common -ED care and disposition: Moderate/severe burns **Emergent priorities: Airway, Breathing, Circulation -High Flow Oxygen should be administered -Airway **Endotracheal intubation: Signs of compromise or airway burn **Oral/perioral burns **Circumferential neck burns **Stridor **Depressed mental status **Respiratory distress -Fluids **At least two IV lines should be established over unburned areas A. ½ given in first 8 hours post injury B. ½ given in the next 16 hours C.Lactated Ringer's recommended -Foley catheter: Urine output should be maintained at 0.5-1 mL/kg/h -Cooling of burns **Immediately cooled **Immersion in cold water **Application of cool compress **Prolonged cooling of lager BSA burns for greater than 30 minutes **Can result in hypothermia **Ice should not be directly applied **Can cause tissue injury from frostbite -Pain **IV narcotic analgesia titrated to patient's pain **Anxiolytic agents should be adjuvant -Large blisters (>2 cm) or those involving large joints **Drained and debrided -Small blisters on non mobile areas: Left intact -Antibiotics and Dressings **Topical antibiotics **Most common agent is Silver sulfadiazine -Alternate **Bacitracin: Triple antibiotic ointment -Synthetic occlusive dressings **Instead of topical ABX **Can manage partial-thickness wounds as outpatient Admission -Moderate and major burns require inpatient admission -Generally referred to a hospital with a burn center -Topical ABX not used until admitting service evaluated the burn wound -Empiric IV antibiotics are not recommended Circumferential burns -Limbs-May develop compromise of distal circulation -Chest and neck: May cause mechanical ventilatory restriction **Escharotomy may be needed in these cases Routine Tetanus Toxoid prophylaxis

Etiology, ED care and disposition of chemical burns

Etiology: Body sites-Face, eyes and extremities -Common household chemical burns **Lye (drain cleaner **Halogenated hydrocarbons (paint removers) **Phenols (deodorizers, disinfectants) **Sodium hypochlorite (bleach) **Sulfuric acid (toilet bowl cleaner) -Terminate the burning process **Removal of garments **Copious irrigation **Dry chemicals should be manually removed before irrigation -Ocular exposure **Alkalis, acids or lacrimators-Eye irrigation with 1 to 2 L of normal saline for a minimum of 1 hour is needed **With alkali or acid exposure-Return of pH to neutral (pH 7.4) is a measurable end point for irrigation-Visual acuity check should follow not preceded ocular irrigation After initial measures -Treatment similar to that of thermal burns -IV fluid resuscitation -Analgesia -Tetanus immunoprophylaxis

Etiology, ED care and disposition of swallowed foreign body

Etiology: you swallow it and it goes down esophagus -children MC -coins, toys, crayons -adults: those with esophageal disease, prisoners, psych patients **MC distal obstruction S/S: -restrosternal pain, dysphagia, coughing, choking, vomiting, aspiration Diagnostics: -PE assessment of airway -Plain films for radiopaque objects -CT has replaced barium swallow test for nonradiopaque objects -Endoscopy: if clearly indicated, performing advanced imaging study delays definitive intervention/adds little value ED care: -ABCs -emergent endoscopy for complete distal obstruction with pooling secretions **Ingestion of sharp/elongated objects (toothpick, aluminum soda can tab), multiple FB, button batteries, perforation, coin at level of cricopharyngeus muscle in child, airway compromise, present of FB for >24hr -indirect or fiberoptic layngoscopy in stable patients -consult surgery for worrisome FB's that are more distal in GI tract

Clinical features, etiology, necessary ED diagnostic work-up, ED treatment for facial/skull fx

Facial fractures -Basilar Skull Fracture -Orbit fractures -Maxillary Fractures (Le Fort Fractures) -Mandible Fractures -Nasal Bone Fractures Imaging -Head CT w/o contrast imaging of choice -Maxillofacial CT depending on exam -Indications: A. Canadian Head CT rules **Excluded: age <16, on anti-coagulants, seizure **Rule: Head CT if one of the following present: **GCS<15 at 2 hrs **Suspected open or depressed skull fracture **Signs of basilar skull fracture **2 or more vomiting episodes **65 or older **Amnesia >30 minutes prior to injury **Dangerous mechanism (car vs pedestrian, ejected from vehicle or fall from >3 ft/ 5 steps) B. Bony tenderness C. Penetrating trauma Basilar skull fracture -Specific signs: Battle Sign, Raccoon Eyes, CSF leak (otorrhea/rhinorrhea), hemotympanum -Battle Sign, Raccoon Eyes @ 1-3 days "Halo Sign" to determine CSF leak Mandible -Signs: **Jaw malocclusion **Trismus **Cranial nerve palsies **Dental abnormalities **Most need referral for surgical fixation -ORIF or Closed reduction with fixation -Timing dependent on amount of swelling Maxilla -Evaluate Teeth -"Le Fort" Fracture **Graded I-III dependent on anatomy Signs: -Midface instability -Ecchymosis over cheek -Cranial nerve palsies -Need surgical fixation Nasal Bone Fractures -Common facial fracture -Present with tenderness/swelling/ bruising over nasal bone -Non-displaced without complications - do not need imaging -Displaced - can be reduced if <6 hrs from injury Treatment -Elevate head -Ice -ENT referral as outpatient -Possible Complication: Septal hematoma Septal Hematoma: -Complication of nasal bone fx -Blood collection within nasal septum -Non-Traumatic Causes: Surgery, anticoag use, intranasal drug use -S/S: Nasal congestion, painful swelling -TX: Drainage of hematoma -Complications: Development of septum, septal perforation, saddle nose deformity Orbital blow-out fracture -usually inferior wall or "orbital floor" S/S -Diplopia/ophthalmoplegia from muscle entrapment. This prohibits the inferior rectus muscle leading to loss of upward movement -Proptosis from swelling or retrobulbar hemorrhage -Infraorbital nerve entrapment - numb cheek/upper teeth -Epistaxis TX - Ophtho consult + ABX prophylaxis (Augmentin) Tooth Trauma: -Primary Tooth: no tx required -Secondary Tooth: **Concussion **Subluxation: mobility without evidence of dislodgement: Dentist referral **Luxation: partially avulsed: Reposition, brace w zinc oxide, dental referral **Avulsion: tooth removed from socket: Attempt to reimplant ASAP --> within 20 mins (Rinse tooth, brace w zinc oxide, prophylactic ABX, refer to dentist)

Clinical features, necessary ED diagnostic work-up, ED treatment for drowning victims

Facts: -Prognosis after submersion injuries depends on the degree of pulmonary and central nervous system injury and therefore is highly dependent on early rescue and resuscitation. -Prevention is the most important means to reduce associated morbidity and mortality. Clinical features -Up to 20% of patients who suffer submersion injuries do not aspirate water. -Patients who aspirate water into their lungs have washout of surfactant, resulting in diminished alveolar gas transfer, atelectasis, ventilation perfusion mismatch, and hypoxia. -Noncardiogenic pulmonary edema results from moderate to severe aspiration. Physical examination findings at presentation vary. -Lungs may be clear or have rales, rhonchi, or wheezes. -Mental status ranges from normal to comatose. -Patients are at risk for hypothermia even in "warm water" submersions. Diagnosis -Evaluate patients for associated injuries (spinal cord) and underlying precipitating disorders including syncope, seizures, hypoglycemia, and acute myocardial infarction or dysrhythmias. -Respiratory acidosis may be present early followed by metabolic acidosis later. -Early electrolyte disturbances are unusual. -A CXR is usually obtained but is frequently normal in patients who are otherwise asymptomatic. Emergency Dept. Care and Disposition -Treatment for submersion events is summarized in Fig. 124-1 -Measure core temperature. Treat hypothermia if present. -Data do not support routine antibiotic prophylaxis for pulmonary aspiration. -Efforts at "brain resuscitation," including the use of mannitol, loop diuretics, hypertonic saline, fluid restriction, mechanical hyperventilation, controlled hypothermia, barbiturate coma, and intracranial pressure monitoring, have not shown benefit. -Hypothermic victims of cold-water submersion with cardiac arrest should undergo prolonged and aggressive resuscitation maneuvers until they are normothermic or considered not viable. -Patients who arrive in the ED in asystole or cardiac arrest after warm water submersion and are normothermic have a poor prognosis for recovery without significant neurologic handicaps. FIGURE 124-1 1. Prehospital care: Rapid rescue, cervical spine precautions if injury suspected or unknown, CPR PRN, transport, oxygen 2. Emergency Department: ABC, determine GCS, treat any associated injury or condition (hypovolemia, hypothermia, seizure, myocardial infarction) A. GSC 13 or above- clear cervical spine, monitor O2 stats -observe 4-6 hours -if o2 and pulm exam are normal, pt can go home -if O2 is less than 95% or patient has abnormal PE (rhales, rhonchi, wheezing, retractions) approach as if GCS <13 B. GSC less than 13 02<95- -clear cervical spine, oxygen saturation (supplemental oxygen as needed to keep O2 95), endotracheal intubation and positive pressure ventilation as needed (CPAP or PEEP) -ancillary tests( CXR, CBC, electrolytes, glucose, Trop I, PT/PTT, UA, CK, urine myoglobin, urine drug screen -monitor: acid base status, temperature, volume status (urine output)

Typical timing of post surgical complications

First 48 hrs -Inflammation from surgery itself -Atelectasis 3-5 days -Urinary tract infection -Pneumonia -Wound infection -Line infection -DVT 7+ Days -Abscess -Leak -Hernia -Bowel obstruction

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

Heparin: Protamine Sulfate Coumadin: Vitamin K, FFP

Responsibility of provider when treating victims of abuse/assault

How do victims of abuse or assault present to the ED? Can come in directly w complaints of the event, or brought in by police OR can come in indirectly For tx of injuries For emergency contraception, STD screening With acute intoxication, memory loss For acute mental health complaints, self-harm, or suicidality Can Be Difficult to Obtain Disclosure in ED Setting - ED exam rooms may not have desired privacy from other pts Provider generally not known to pt - no hx, no established therapeutic relationship Questions may be uncomfortable to both pt & providers Abuser may be present with pt ER Disposition for Child Abuse -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 Management -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 ED Care -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

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

Human bites -produce a crushing or tearing of tissue, with potential for injury to underlying structures and inoculation of tissues with normal human oral flora -Human bites are most often reported on the hands and upper extremities -Infection is the major serious sequela Clinical features -Clenched Fist Injury (CFI): occurs in the metacarpophalangeal (MCP) region as the fist strikes the mouth and teeth of another individual -Increased risk for serious infection and any questionable injury in that area of the hand should be considered a CFI to proven otherwise -Assessment: direct injury and ALL of the underlying structures including tendons, vessels, nerves, deep spaces, joints and bone. **Use local anesthesia to do wound exploration -Radiographs for fractures or foreign bodies Complications Emergency Department Care and Disposition -Copious Irrigation of the wound with normal saline and judicious limited debridement of devitalized tissue are critical to management. -Hand....leave open. Other places can undergo primary closure unless there is a high degree of suspicion for infection -Prophylactic antibiotics should be considered in all by the most trivial of human bites **Augmentin (Amoxicillin-clavulanate) 500-875 mg po bid -Uncomplicated Hand Wound **Leave open with appropriate dressing **Immobilize and elevated for 24 hours **Prophylactic ABX **Re evaluate 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 and 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, immobolization and close follow up -Moderate to severe infections require admission for surgical consultation and parenteral antibiotics...ampicillin-sulbactam 3 g, every 6 hours IV or cefoxitin 2 g every 8 hours IV -Penicillin allergic patients may be treated with clindamycin and ciprofloxacin -All patients should receive tetanus immunization according to guidelines.

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

Hypertensive Emergency -increased BP associated with target organ dysfunction such as aortic dissection, acute pulmonary edema, acute coronary syndrome, intracranial hemorrhage, acute ischemic stroke, etc. -HTN encephalopathy, eclampsia, unstable angina, MI Hypertensive Urgency (asymptomatic) -severe elevations in BP without progressive target organ dysfunction -greater than or equal to 180/110 is indiction for treatment -optic disc edema, usually asymptomatic Clinical Features -history of HTN usually, non compliance with BP meds, cardiovascular dz, renal dz -papilledema, retinal exudates, neurologic deficits, seizures, encephalopathy: hypertensive emergency, HA, N/V -carotid bruits, heart murmurs, gallops, asymmetrical pulses Diagnosis: -UA: renal impairment may present as hematuria, proteinuria, red cell casts, elevations in BUN, creatinine, and potassium levels -EKG: ST and T wave changes consistent with coronary ischemia, electrolyte imbalances, or LVH possible -CXR: identify CHF -CT: in patients with neurologic compromise -Urine/serum drug screen -pregnancy test ED Treatment: -Hypertensive emergency: patients require oxygen, cardiac monitoring, IV access **Treatment Depends on cause for hypertensive emergency: Lower BP gradually (BB, CCB, diuretics, nitroglycerin) **reduce pressure by no more than 25% within minutes to an hour toward a level of 160/100 mmHg within 2-6 hours -asymptomatic patients/hypertensive urgency: Diuretics, BB, ACEI within 2 to 6 hours ORAL AGENT URGENCY: PO NICARDIPINE OR CLEVIDIPINE OR LABETALOL OR ESMOLOL within 2-6 hours EMERGENCY: IV NICARDIPINE OR CLEVIDIPINE PLUS LABETALOL OR ESMOLOL within minutes to an hour

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

Hypoglycemia: Clinical Presentation -Rapid onset ~24 hrs -Hyperadrenergic signs/sxs* **Anxiety/nervousness **Irritability/combativeness **Tremor **Palpitations **n/v **Sweating **Neuroglycopenic signs/symptoms: AMS/confusion, Lethargy, Seizure, Focal neurologic deficits less common -Usually < 50-55 mg/dL - lower level or normal 70 -Can be higher in diabetics "used to" higher glucose levels Hypoglycemia: ED Diagnosis -Dx often made by EMS* -Many pts. refuse transport and seem to do well -Early Dx important b/c it can reduce 'overworkup' -Further workup may be indicated if sxs persist, sepsis is a concern, or in the setting of injury -Diagnostic studies often limited to serial accuchecks -If going to admit pt, send CBC and Chem7 (basic metabolic panel) Treatment -Tx often initiated by EMS -D50 IV -Continuous infusion of 10% dextrose solution may be required -Feed pt. ASAP -IV glucagon Treatment considerations -Consider thiamine 100 mg IV prior to glucose in alcoholics/malnutrition to prevent Wernicke's encephalopathy -If sulfonylurea overdose: Octreotide 50-100 mcg SQ (somatostatin analogue) that prevents rebound hypoglycemia (give q 6h) -Glucagon 0.5-2 mg can be given IM or SQ if IV access not available, but response is slower than D50: Observe for 2-3 hours in ED or admit to Obs Hypoglycemia: Disposition -Most can be d/c'd home if sxs improve, eating, and no further problems while observed -Prolonged observation or admission needed for alcoholics or others with precarious social situations -Give diabetic education to patient -Hypoglycemia related to Sulfonylurea use requires admission due to prolonged half-life -Consider admission in those on long-acting insulin

Etiology, ED care and disposition of mastoiditis

Infection spreads to adjacent mastoid air cells Strep Pneumo CT diagnostic IV abx, ENT consult for I&D

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

S/S: Look ill, have different type of hx --> chest pain, productive cough, fever, pleuritic chest pain, dyspnea -Pneumococcal: abrupt fever, rigor, rusty brown sputum -Lobar: signs of consolidation - bronchial breath sounds, egophony, increased tactile/vocal fremitus, dullness to percussion Clinical Dx: in ER, dx confirmed w imaging PE: Tachycardia, tachypnea, low pulse ox, bronchial breath sounds, rhonchi -wheezing at times -sometimes WBC, serum electrolytes, BUN, CR, glucose, blood gases, sputum gram staining, and cultures of sputum and blood provide benefit TX - -Vital respiratory functions (oxygenation and ventilation) -ABX treatment started in all cases of suspected bacterial pneumonia, based on pts environment -Outpatient CAP: Azithromycin --> additional days or switch to Doxycycline Levofloxacin or Amoxicillin + Azithromycin if significant comorbidities -Inpatient CAP: **No ICU: Levofloxacin or Ceftriaxone + Azithromycin **Need ICU: admit to ICU + Ceftriaxone or Vanco (if MRSA suspected)

S/Sxs, treatments of patients with OD of ASA

S/S: hyperthermia, tachypnea, AMS -Depend on: **Dose, Acute or chronic , Patient's age -Acute ingestion: **< 150 mg/kg **Mild toxicity with nausea, vomiting, and gastrointestinal irritation -150 mg/kg-300 mg/kg **Moderate toxicity with vomiting, hyperventilation, sweating and tinnitus ◦ Salicylate levels above 30 mg/dl -> 300 mg/kg **Usually severe -Acid base disorder **Pathognomonic: increased anion gap metabolic acidosis, metabolic alkalosis (due to volume contraction) and respiratory alkalosis **Most common clinical picture is combined respiratory alkalosis and increased anion gap metabolic acidosis -Uncommon manifestations **Fever, Neurologic dysfunction , Renal failure, Pulmonary edema, ARDS, Rhabdomyolysis (rare), Gastric perforation (rare), GI hemorrhage (rare) -Chronic (long term therapeutic use) **Elderly patients with underlying medical problems **Hyperventilation, tremor, papilledema, agitation, paranoia, bizarre behavior, memory loss, confusion, stupor -Children **Few hours of ingestion **< 4 years develop metabolic acidosis (pH< 7.38) **> 4 years mixed acid-base disturbance as in adults -Chronic is more serious and more likely to be lethal -May take several days for symptoms to appear -Hyperventilation, volume depletion, acidosis, marked hypokalemia and CNS disturbances -Pulmonary edema is rare Dx made in conjunction w pt's acid-base status: resp acidosis w anion-gap metabolic acidosis, hypokalemia +/- hyper or hypoglycemia ED care and disposition -Emergent priorities **ABC's **Cardiac monitoring **IV line -Activated charcoal 1 g/kg to minimize absorption Multiple doses are not beneficial Whole bowel irrigation if sustained release or enteric coated -IV normal saline to patients with volume depletion **Except for initial saline resuscitation all fluids should be 5% dextrose **If hypoglycemia or neurologic symptoms are present then IV fluid with 10% dextrose -After adequate urine output established (1-2 mL/kg/h) **If not contraindicated by initial electrolyte and renal function tests-potassium 40 mEq/L -Alkalization **Bolus of 1 to 2 mEq/kg of sodium bicarbonate **Then 150mEq (3 ampules) added to a liter of D5W and infused at 1.5 to 2.0 times the patient's maintenance rate and adjusted to maintain urine pH above 7.5 -Early intubation and controlled ventilation to avoid drop in pH from impending respiratory failure -Hemodialysis for clinical deteriorations despite supportive care and alkalization **Renal insufficiency or failure , Severe acid-base disorder , Altered mental status, ARDS -Hemorrhage **Rare **Due to chronic salicylism **Elevated PT **Treated with fresh frozen plasma -Dysrhythmias **Treated by correcting the underlying metabolic abnormalities **Standard antiarrhythmics

Patient factors increasing risk of wound infection.

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. Diabetes Mellitus! Cardiac issues: vascular flow issue Immunocompromised patient Mental impairment

Etiology, ED care and disposition of otitis media

Painful ear, red TM, "fullness" viral or bacterial S. pneumo > H. flu> M. Cat Can diagnose via otoscopy Treatment with Amoxicillin Complications include TM rupture, labrynthitis, mastoiditis

Common post-op complications (see powerpoint, focus on signs/symptoms and timing)

The "w"s of post-op fever WATER = urinary tract infections WIND = atelectasis or pneumonia -Pneumonia: fever, SOB, cough, chest pain WALK = deep vein thrombosis WOUND = surgical wound infection WEIRD DRUGS = drug induced fever 1. Urinary Tract Infection -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) 2. 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 S/s: fever, tachypnea, tachycardia (low-grade) 3. Pneumonia -Postoperative 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 4. Venous Thromboembolism (VTE) -Includes DVT and PE -Post-op patients at high risk -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) 5. Pulmonary Embolism -EKG and CXR findings -S1Q3T3 -Westermark's sign -Focal oligemia; only seen in 2% of patients with PE but highly specific finding -Hampton's hump-Wedge-shaped pleural consolidation 6. Surgical site infection S/S: blanchable erythema at site, pain at site, warmth at site, drainage from site, fever/chills, malaise Labs: leukocystosis (WBC>10K), +/- wound culture 7. Catheter-Site Infection -Particularly central lines S/S: redness/irritation at insertion site, fever Labs: CBC, blood culture (from line and a 2nd site) 8. Weird or wonder drugs -Anesthetics, sulfa-containing antibiotics and others -Often implicated in drug fever that develops 1 week postoperatively -Diagnosis of exclusion and should be considered when faced with a negative sepsis workup in a postop patient with fever 9. Surgical site complications A. Hematoma -Collection of blood and clot in wound Pt's on aspirin or other blood thinners at higher risk S/s: swelling, discoloration of wound edges, discomfort, drainage from wound B. Seroma -Similar to hematoma but fluid in wound is serous, often lymphatic drainage S/s similar to hematoma C. Wound Dehiscence -Surgical emergency -Risk factors: poor nutrition, steroid use, infection, diabetes -Affects 5% of patients over 60yo having laparotomy -Often occurs suddenly when coughing/pt. feels/hears a 'pop' D. Abscess -Infection inside the abdominal cavity -Typically appears ~POD#7 S/S: fever, ileus, pain Labs/studies: CBC, CT scan E. Anastamotic Leak -Less common -Typically at site of intestinal anastamosis S/S: fever, abdominal pain, nausea Labs/studies: CBC, CT or contrast study (esophagram with small bowel follow through or contrast enema) F. Fistula -Connection between 2 cavities with epithelial linings that doesn't normally exist **Enterocutaneous **Colovesical **Colovaginal **Enteroenteral 10. Dysrhythmias -Often asymptomatic, sometimes palpitations, chest pain, shortness of breath -Most commonly supraventricular -A fib, A flutter, SVT -Related to stress, electroyte abnormalities (esp hypokalemia), hypoxemia 11. Post-operative MI -Can be precipitated by hypotension, hypoxemia S/s: chest pain, hypotension, dysrhythmias Sometimes asymptomatic Tests: EKG, cardiac enzymes (troponin, CK-MB) 12. Urinary retention Very common in men with BPH (previously undiagnosed or not) and in general with anesthesia Usually self limited/resolves within 48 hrs 13. Paralytic Ileus 'sleepy' bowel Very common after abdominal surgery

Lab markers for MI

Troponin vs. CK-MB -Troponins and CK-MB are cardiac markers that indicate muscle cell death 2/2 ischemia. -Troponin more sensitive & specific for cardiac muscle **Begin to elevate 3-4 hours after infarct onset. Definitely abnormal by 8 hours. Serial. Elevated troponin takes a week or more to normalize. -CK-MB is great if you know 100% there is no skeletal muscle injury...but you never really know. -CK-MB normalizes faster, about 48 hours later. -So if your patient comes back with CP and had a recent MI. Trop will not be reliable if there is concern of another MI. CK-MB will be most appropriate. -Everyone has troponin flowing -Many other things cause an increase in trops. Renal failure is probably the most common cause of elevated trop after ACS. Can also have a "troponin leak" from CHF. Trops take 7-10 days to go to baseline whereas CKMB returns to baseline 3-4 days!

Risk factors, work-up, brief treatment of PE

Risk Factors -Virchow's Triad: venous stasis, endothelial injury, hypercoagulable state -High Risk Factors **Hip or leg fx, total knee or hip **Major surgery/trauma, Hospitalization -Intermediate Risk Factors **Central Venous Caths, Chemo, Malignancy, Respiratory failure/CHF, Estrogen Increase, Prior VTE -Weak Risks **Bed Rest >3 days, Air or car travel >8 hours, Advanced age, Morbid Obesity Varicosities S/S: Classic Triad: **CP Usually pleuritic, Cough, Hemoptysis -Dyspnea, Anxiety or apprehension, Syncope, Diaphoresis, Tachypnea, Hypoxemia, Rales, Tachycardia Fever, usually low, Phlebitis, Edema, Murmur, Cyanosis Labs in PE -PT/PTT/INR -Low Risk PE Probability get D-Dimer -Helical CT if D-dimer is positive -BNP-Associated with benign course if low -Troponin **Increased in moderate to large PE if right *ventricle affected -ABG Can be low or normal Respiratory Alkalosis -EKG in PE **Abnormalities are non-specific **Most common finding is tachycardia **Other findings associated with a worse pattern: Atrial arrhythmias, Bradycardia, or tachycardia, New RBBB, Inferior Q waves, S1Q3T3 pattern -Chest X-ray in PE **non-specific changes in 80% **Atelectasis, effusion, elevated right hemidiaphragm **Westermark's sign-Sharp cut off of pulmonary vessels with distal hypoperfusion **Hamptom's Hump-Shallow hump-shaped opacity in the periphery of the lung, base against pleura, hump hilum Diagnostics -Helical CT Scan is first choice -Then V/Q Scan 1. Unstable PE -If Stability restored following resuscitation **High suspicion: Immediate anticoagulation with imaging co-currently **Low or Moderate suspicion: Same as Stable 2. Unstable despite resuscitation -Bedside LE ultrasound/Transesophageal echo -Check for DVT and RV heart strain **These lead to presumptive diagnosis of PE and thrombolysis can be given Tmt of PE: Tmt Is based on stability. 1. Unstable PE -Immediate Anticoagulation with UFH with concurrent imaging, Pressors, O2, IV Thrombolytic therapy or embolectomy 2. Stable PE -IV access w/w/o IV fluids -O2 supplementation -Empiric anticoagulation UFH -Pts discharged home if Stable PE on anticoagulants -UFH bridge to Warafin/Paradax and if first PE on tmt for 3 months if provoked, if unprovoked, possibly indefinite, search for malignancy -Some medications due not need a Heparin Bridge like Eliqus and Xeralto -If recurrent/unprovoked VTE pt's on anticoagulation indefinitely -Also consider thrombophilia work-up -IVC Filter if anticoagulation contraindicated

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

Routine Tetanus Toxoid prophylaxis based on immunization history: -Patients with clean minor wounds require tetanus prophylaxis if it has been greater than 10 years since the last dose -Tetanus prophylaxis of ONE 0.5 mL IM is indicted for all other wounded patients if it has been more -than 5 years since the last dose Tetanus immune globulin ONE (250 units IM) should be administered to those without a history of a primary series of three tetanus immunizations. A second dose is required in 1-2 months and a third dose in 6 to 12 months -need for tetanus prophylaxis considered for every wounded pt -the only CI to tetanus toxoid is hx of neurologic or severe systemic rx after previous dose LOOK AT CHART IN OUTLINE Chemical and thermal burns Human bites Dog or cat bites Brown recluse Snake bites

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

S/S Asthma Exacerbation -Dyspnea/SOB, cough, wheezing, chest tightness, wheezing, prolonged expiration. -Severe: Tripoding, diaphoresis, accessory muscle use, tachycardia/tachypnea, AMS, retractions. -History: Onset, Triggers, Current medications and response, last systemic steroid use, frequency of episodes requiring EM care? Tobacco. Evaluation of Asthma Exacerbation -Evaluation: Vitals? O2 sat? Respiratory status? EKG, CBC, BMP, ABG as indicated. -Peak expiratory flow -CXR: If indicated: No history: R/O and narrow differential. Pneumo? Pneumonia, effusion? Findings: Increased bronchial markings, flattening of diaphragm, hyperinflation, atelectasis Treatment -check PERF then give steroids and albuterol or ipratropium and check PERF again -Reassessment is critical!!! -IMMEDIATE STEROIDS: PO Prednisone or IV Methylprednisolone -1st line:B-Agonist (Nebulized Albuterol) SQ Terbutaline or Epi (not in pregnant or CVD pt) Adjunct: -Anticholinergic: nebulized Ipratropium -Mag Sulfate: bronchodilation only for severe FEV1 <25% -Heliox: to lower airway resistance (want O2 sat > 90%) -If pt hemodynamically unstable, resp arrest --> normal partial pressure ventilation (CPAP, BiPAP) **Intubation/ventilation PRN

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

S/S: -mental confusion -delirium -chills -dizziness -LOC -convulsions or coma -body temperature of 105F or higher -Hot, dry, skin that may be red, mottled or bluish -a strong fast pulse -Life-threatening injury -History of environmental or occupational heat exposure usually discerned -Alteration in mental status -Neurologic abnormalities: Ataxia, Confusion, Bizarre behavior, Agitation, Seizures, Obtundation, Coma -Elevated body temperature **Core temperatures from 40 degrees C (104 F) to 47 degrees C (116 F) **Anhidrosis is not invariably present Diagnosis -True time dependent medical emergency -Should be considered in the clinical context of: Heat stress, Hyperthermia, Altered mental status, Tachycardic, Hyperventilating, Respiratory alkalosis **Exertional heat stroke may have both respiratory alkalosis and lactic acidosis **20% are hypotensive -Exertional heat stroke: Rhabdomyolysis, hyperkalemia, hyperphosphatemia, hypocalcemia Work up can be individualized as clinically indicated Including neuroimaging studies Emergency Department Care and Disposition -Priorities: ABC's: airway, breathing and circulation, Cardiac monitoring , IV line -High flow supplemental oxygen **Endotracheal intubation ** Significantly altered mental status **Diminished gag reflex **hypoxia -Core temperature should immediately be obtained **Rectal or bladder probe **Continuous monitoring **Goal is to bring the core temperature to 40 degrees C -Volume depleted should be rehydrated **IV normal saline or lactated Ringer's solution **MAP (mean arterial pressure ) >60mm hg **Central venous line catheter or pulmonary 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 the most efficient and practical means of cooling **Fans positioned near the disrobed patient **Sprayed with tepid water **Do not spray with ice water; causes shivering and thermogenesis -Excessive shivering: Benzodiazepines (midozolam 2 mg IV) -Other methods of cooling: **Immersion cooling **Cold water gastric lavage **Urinary bladder lavage **Thoracostomy lavage **Cardiopulmonary bypass -Seizures: Treated with benzodiazepines -Rhabdomyolysis **IV hydration ***Diuretics (furosemide 40 mg IV) **Sodium bicarbonate (3 ampules in 1 liter of D5W at 250 mL/h) -Hyperkalemia **Standard regimens **Electrolytes monitored hourly -Admission: ICU for further observation and monitoring

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

S/S: -rectal bleeding, anemia, weight loss, obstruction, perforation, abdominal pain, general malaise, change in bowel habits or stool caliber PE typically normal -may be able to palpate mass in abdomen check for hepatomegaly (metastases) Tests: -screening detects asymptomatic early stage malignancy -CBC for anemia -colonoscopy -FOBT -elevated LFTs: metastases -Carcinoembryonic antigen (CEA): must be measured always in proven colorectal CA -colonoscopy diagnostic procedure of choice: can do biopsy -do chest CR: look for metastatic cancer in lungs -abdominal and pelvic CT scans for staging -intraoperative eval of liver by palpation and US more accurate for liver mets -anorectal US -CT for rectal cancer -barium enema: apple core lesion!! Staging TNM Staging Colon Cancer Treatment -Time to Operate? **Probably stage IV **Only operate on stage IV for palliation (ie: obstruction) **Needs chemo/radiation ASAP -Colectomy -complete surgical excision depending on the location -tumor involvement of the sphincter complex or involvement within 2 cm of it needs colostomy -Night Before Surgery: mechanical bowel prep (Go-Lytely, Fleet's Phophosoda) + PO ABX prep to decrease risk operative infx

DDX of serotonin syndrome versus neuroleptic malignant syndrome versus anticholinergic toxicity

Serotonin Syndrome: -Can occur in patients taking multiple drugs that increase serotonin levels (i.e. SSRI and MAOIs). Initially causes lethargy, restlessness, confusion, flushing, diaphoresis, tremor, myoclonus -Can progress to hyperthermia, hypertonicity, rhabdomyolysis, renal failure, seizures, coma, death -Tx: stop all suspected meds, serotonin antagonist (Cyropheptadine) -Wait 2 wks before switching pts from SSRI to MAOI (5-6 wks with Fluoxetine d/t long t1/2) Neuroleptic Malignant Syndrome -More common in 1st generation meds -Change in mental status, autonomic instability (high fever, labile BP, tachycardia, diaphoresis), lead-pipe rigidity, elevated CPK levels, leukocytosis, metabolic acidosis -Medical emergency, must STOP all psych meds -Other SE -Prolonged QTc interval -Hyperprolactinemia -Fatigue -Sexual Dysfunction -Rashes, photosensitivity Anticholinergic Toxicity -Encountered bc of common cause of phenothiazines, mydriatics, skeletal muscle relaxants, antihistamines (Diphenhydramine), antidepressants, antispasmodics, antiparkinsonian drugs S/S: mydriasis, hypoactive/absent bowel sounds, tachycardia, flushed skin, disorientation, urinary retention, hyperthermia, dry skin/MM, confusion, agitation, auditory/visual hallucinations -"Dry as a Bone, Red as a beet, hot as a hare, blind as a bat, mad as a hatter, stuffed as a pipe" -ECG: sinus tachycardia, wide-complex tachydysrhythmias, QT interval prolongation DX: clinical TX: supportive + cardiac monitor + IV access +/- GI decontamination (charcoal) +/- BZD (for agitation)

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

Signs and Symptoms -Acute severe epigstric pain often radiating into the back -Nausea and vomiting -Hx of GB dz, ETOH, ERCP, -Hypertriglyceridemia -VS: tachycardia, tachypnea, fever +/-, hypotension Diagnostics-order amylase and lipase asap -CBC, CMP, Amylase/Lipase, Lactic Acid, LDH, T&S **Leukocytosis, Lipase 3X normal, ALT >150 (GSP) -Ranson's Criteria: age >55, WBC >16, Glucose>200, LDH >350 and AST>250 Score >3 severe pancreatitis likely Imaging -AAS: assess for free air -US Abdomen: gallstone -CT scan **Recommended for acute severe **Necrotizing Pancreatitis, Abscess, Pseudocyst or Hemorrhage Treatment -Mild: Analgesia, NPO, IVF, No ABX, admit general -Severe (Ranson's >3): **ICU admit for Shock, ARDS, Renal Failure, GI bleed, Multisystem Failure **ABX: for abscess or necrotizing -Surgery consult for necrotizing, abscess drainage or hemorrhagic -Gallstone: Cholecystectomy prior to d/c is usual

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

Signs and Symptoms -Generalized abdominal pain (colicky), nausea, distention, decreased flatus. Tachycardia, fever, hypotension possible. **Prior abdominal surgical adhesions in 60%. -Generalized tenderness, +/- guarding/rebound -High pitched tinkling, hyperactive, quite, absent bowel sounds. -Abdominal/inguinal/femoral masses. Diagnostics -CBC, CMP, Lactic Acid, UA, Blood Cultures (if septic) -Imaging **AAS- Free Air. Dilated loops of small bowel, Airfluid Levels **CT Scan Abdomen and Pelvis-Dilated bowel with transition zones, hernia, mass, ischemia-Bowel wall thickening, pneumatosis, portal gas = early strangulation Treatment -All receive fluid resuscitation, analgesics, antiemetics -ABX: peritoneal signs, fever, surgeon consult: Gram Negative and Anaerobic Coverage -Nonoperative: **NG tube decompression!!!: Simple/Partial obstructions for up to 72 hrs; 65-80% resolve **Reduce any incarcerated hernia -Operative **Complete obstructions or nonresolved partial that worsens

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

Signs and Symptoms -Lower abdominal/pelvic pain, dull, achy or crampy -Mucopurulent vaginal discharge in 75% -Vital signs usually stable. **Fever: question other cause or complication of PID i.e. TOA -Exam: lower abdominal tenderness, CMT, adnexal tenderness or fullness Diagnostics -HCG, Gyn cx, UA....may be all you need after pelvic exam. -CBC, CMP, ESR, blood cultures? Imaging -US **Concern for other cause or complication i.e. fever, peritonitis, failed out pt. **Thickened (>5 mm), fluid-filled fallopian tubes = pyosaplinx **Tubo-ovarian abscess, complication of PID CT -Diagnostic dilemma: R/O Appendicitis or other lower abdominal infection/inflammation Treatment -Criteria for diagnosis and empiric treatment **Pelvic/lower abdominal pain, no cause for the illness other than PID can be identified, and one or more of the following minimum criteria are present on pelvic examination: **cervical motion tenderness **uterine tenderness **adnexal tenderness. -Treat against *C. trachomatis, N. gonorrhea **Anaerobes (Bacteroides fragilis), BV also implicated -Oral **Doxcycyline 100 mg BID for 14 days **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 for 14 days -Admit **Failed outpatient, fever, peritonitis, signs of sepsis, comorbidities TOA -Parenteral **Doxycycline 100 mg IV/PO BID **Plus Cefoxitin 2 gm IV BID OR **Plus Cefotetan 2 gm IV BID OR **Unasyn 3 gm IV QID **Add Flagyl or clinda for TOA -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 aortic aneurysms

Signs and Symptoms-risk for rupture -Abdominal pain, back pain (mid/low), groin pain, flank pain, syncope, lightheaded, nausea and vomiting. -Pulsatile mass in abdomen -Hypotension, tachycardia, altered mental status Diagnostics -Labs not helpful in diagnosis, but needed in management -type and screen -type and cross -CBC, CMP, Coags, T&C (8 units) -EKG -Imaging **Plain xray: low diagnostic yield, may see calcified aneurysm, unable to detect rupture, leak **US Abd: near 100% and 96% sens./spec. in detection Difficult in detecting suprarenal, leakage or rupture **CT scan: 100% sensitivity. Detect rupture, leak, branch involvement, supra/infrarenal Treatment-GET THEIR BP DOWN -Prehospital >50% mortality -IV Access imperative (IV DRIP) -Hypotension: fluids, blood products -Reduce "shear forces" **HTN: goal SBP 100-120 mmHg **HR: goal 60-80 bpm -Medication **Nitroprusside-easily titratable, give beta-blocker for reflex tachycardia -Esmolol: half life 9 minutes -Labetalol -Metoprolol Surgery 100% fatal if leak/rupture no repaired Open vs Endovascular

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

Signs and symptoms -Unilateral abdominal/pelvic pain, N/V, vaginal bleeding **Beware of the patient with DIARRHEA -Rupture: sudden worsening of pain, syncope -Normal vitals or tachycardia, hypotension, orthostatic -Abdominal tenderness focally, +/- peritoneal signs, adnexal tenderness, fullness, CMT, vaginal bleeding Diagnostics -Quant. HCG, Qual. HCG, UHCG; CBC, Type Rh **HCG usually doubles in 48 hours, ectopics typically do not. Imaging -Pelvic US/Transvaginal (TV) US **Discriminatory Zone: HCG level at which IUP should be seen on TV US; 1500 **No IUP @ DZ, Gestational Sac outside uterus, Adnexal mass w/o IUP, Hemosalpinx, free pelvic fluid/cul-de-sac w/o IUP Treatment ED: -IV access (2 large), IVF, Blood Products -Analgesia, Antiemetics Surgical -Salpingostomy vs Salpingectomy Medical -Methotrexate -Reliable, compliant patient and good follow-up -Hemodynamically stable with no signs of rupture -Contraindicated **HCG l15,000 **fetal cardiac activity **free fluid in the cul-de-sac

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

Signs/ Symptoms -Mean age of 60 -Lower abdominal pain R/L/Suprapubic **Predominantly Left lower often pain worse after eating -Low Grade fever -Nausea/vomiting, Anorexia, Constipation or diarrhea Diagnostics -Moderate WBC elevation, with left shift -Chemistries usually normal -Urine usually normal Imaging -CT abdomen/pelvis with Contrast!! **Pericolonic fat stranding, thickened bowel wall, colonic diverticula, microperforation, abscess Treatment-npo and fluids -ABX against gram negatives and anaerobes **Rocephin + Flagyl, Cirpo + Flagyl, Unasyn, Cefotetan -Home on orals if no fever, no vomiting, no abscess and no perforation. Pain controlled. -Admit on IV ABX for any of the above or if immunocompromised or concerned -Surgery **Acute: Larger perforation, w/feculent peritonitis, Ruptured abscess, Obstruction, Uncontrolled Sepsis **Elective : Recurrent disease, often after the second. New studies question this approach. -Surgery usually 6 weeks after episode has cleared.

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

Signs/Symptoms -Periumbilical pain with radiation to the RLQ (McBurney's Point) -Often feeling of constipation/bloated sensation -Anorexia, N/V, occasionally fever-"Hamburger test" Diagnostics -Moderate WBC elevation with left shift -Chemistries usually normal -Urine may show hematuria in 20-30% of patients -Pregnancy Test negative in women of childbearing age Imaging -CT Scan: Nearly 100% sensitive. Dilated, elongated appendix. Fat Stranding in RLQ. -US: helpful in thin children. Treatment: -Surgery -Antibiotics: active against Gram Negatives and Anaerobes. **Rocephin + Flagyl, Cirpo + Flagyl, Unasyn, Cefotetan

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

Snake Bites -Identified by two retractable fangs and heat sensitive depressions (pits) locat4d bilaterally between each eye and nostril Clinical Features -Hallmark is fang marks with local pain and swelling -Severity criteria -Degree of local injury (swelling, pain, ecchymosis) -Degree of systemic involvement (hypotension, tachycardia, parasthesia) -Evolving coagulopathy (thrombocytopenia, elevated prothrombin time, hypofibrinogenemia) -Swelling usually within 30 minutes but may take up to 12 hours -Minimal envenomation describes cases with local swelling no systemic signs and no lab abnormalities -Moderate envenomation causes increased swelling that spreads form the site. May also have systemic signs such as nausea, paresthesia, hypotension and tachycardia. -Severe envenomation causes extensive swelling, potentially life threatening systemic signs and marked abnormal coagulation parameters that may result in hemorrhage Emergency Department Care and Disposition -Go to medical facility; minimize physical activity, remain calm and immobilize any bitten extremity in neutral position below the level of the heart -Wound care and tetanus prophylaxis -Limb circumference at several sites above and below the wound should be checked every 30 minutes and advancing edema should be marked If swelling progressing, receive antivenin -Sheep derived antivenin has generally replaced equine antivenin. Initial dose is 4-6 vials IV -Dosing same for adults and children Re examine 1 hour after initial dose; if ineffective, second dose of 4-6 vials and is continued until there is complete control of the envenomation -If symptoms controlled, protocol is 2 vial doses every 6 hours for 18 hours -Compartment syndrome may develop. Antivenen, limb elevation, IV mannitol and surgical fasciotomy may be required -Blood transfusions as needed -Observation for at least 8 hours Coral Snakes -"Red on yellow, kill a fellow. Red on black, venom lack" -Only the bite of the eastern coral snake requires significant treatment -Potent neurotoxin that produces tremor, salivation, respiratory paralysis, seizures and bulbar palsies (dysarthria, diplopia and dysphagia) Emergency Department Care and Disposition -Hospitalization 24-48 hours -3 vials of antivenin -Additional doses and ICU prn -Toxic effects may be preventable but not easily reversed

Clinical features, necessary ED diagnostic work-up, ED treatment for supraventricular arrhythmias

Supraventricular Tachyarrhythmias: Sinus Tachycardia - Clinical features o (a) normal sinus P waves and PR intervals o (b) an atrial rate usually between 100 and 160 beats/min o It's an effort to increase cardiac output to match increased circulatory needs. ED treatment: Diagnose and treat the underlying condition Supraventricular Tachycardia - Clinical features: regular, rapid rhythm that arises from impulse reentry (MC) or an ectopic pacemaker above the bifurcation of the His bundle o Present with acute, symptomatic episodes termed paroxysmal supraventricular tachycardia (PSVT). All forms of preexcitation are caused by accessory tracts that bypass part or all of the normal conducting system, the MC form being Wolff-Parkinson-White (WPW) syndrome. The ventricles are activated by an impulse from the atria sooner than would be expected if the impulse were transmitted down the normal conducting pathway. This premature activation causes initial fusion beat morphology with slurring (narrowing?) of initial QRS complex, causing the pathognomonic delta wave ED Treatment o Cardioversion in any unstable patient (ex. hypotension, pulmonary edema, or severe chest pain). o Stable patients: the first intervention should be vagal maneuvers, including: a. Valsalva maneuver, lift legs to increase venous return, Diving reflex (immerse the face in cold water or bag of ice water to face - for infants), Carotid sinus massage o Adenosine rapid IV bolus, into a large vein followed by a 20-mL normal saline rapid flush. If no effect w/in 2 mins, give a second dose (this is first line for WPW) May induce bronchospasm in asthmatics requiring treatment with bronchodilators. o In patients with narrow-complex SVT and normal cardiac function, cardioversion with second-line agents: § a. Calcium-channel blockers: Diltiazem IV or verapamil IV § b. Beta-blockers: Esmolol IV bolus, or metoprolol IV, or propranolol § c. Digoxin IV o Stable pts w/ wide-complex SVT: Procainamide IV until 50% QRS widening is noted (contraindicated in patients with myasthenia gravis since it may increase weakness). Atrial Fibrillation - · Clinical features: Multiple, small areas of atrial myocardium continuously discharging in a disorganized fashion = loss of effective atrial contraction and decreases LV end-diastolic volume. Afib may be paroxysmal (lasting for less than 7 days), persistent (lasting for more than 7 days), or chronic (continuous). · EKG: o (a) Fibrillatory waves of atrial activity, best seen in leads V1 V2 , V3, and aVF o (b) Irregular ventricular response, usually between 170 and 180 beats/min in patients with a healthy AV node · ED Treatment: o Unstable pts: cardioversion (50-100 J) o Stable patients with Afib for longer than 48 hours: anticoagulated with heparin for 3 weeks before cardioversion; consider a transesophageal echocardiogram to r/o atrial thrombus before cardioversion o Control rate with Diltiazem or Verapamil IV, or Metoprolol and Digoxin, or tx pts w/ preexcitation syndromes (ex. WPW) with procainamide. In pts with impaired cardiac function (EF <40%), use amiodarone o Afib for shorter than 48 hours: chemically or electrically cardioverted in the emergency department. Use amiodarone, ibutilide (see comments for atrial flutter), procainamide, flecainide, or propafenone in Atrial Flutter - -Clinical features: Rhythm that originates from a small area within the atria. May be a transitional arrhythmia between sinus rhythm and atrial fibrillation. -EKG: (a) a regular atrial rate between 250 and 350 beats/min (b) "sawtooth" flutter waves directed superiorly and most visible in leads II, III, and aVF (c) AV block, usually 2:1, but occasionally greater or irregular. One-to-one conduction may occur if a bypass tract is present. Carotid sinus massage or Valsalva maneuvers are useful techniques to slow the ventricular response by increasing the degree of AV block, which can unmask flutter waves in uncertain cases. ED treatment -Treat same as atrial fibrillation above. Multifocal Atrial Tachycardia - Clinical features: At least three different sites of atrial ectopy. Rhythm is irregularly irregular (confused with a-fib and a-flutter). MC in elderly patients with decompensated COPD, but also CHF, sepsis, methylxan-thine toxicity, or digoxin toxicity. EKG (a) three or more differently shaped P waves (b) changing P-P, PR, and R-R intervals (c) atrial rhythm usually between 100 and 180 beats/min ED Treatment 1. Treat the underlying disorder. 2. Specific antiarrhythmic treatment is rarely indicated. Rate control may be achieved with verapamil IV or diltiazem IV in patients with acute COPD or CHF exacerbations. 3. Magnesium sulfate IV may decrease ectopy and convert MAT to sinus rhythm in some patients. 4. Replete potassium levels to >4 mEq/L to increase myocardial membrane stability.

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

Symptoms -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 Lumbar Puncture -Gram stain & culture, cell count, protein, glucose, viral panel testing, opening pressure Normal values Bacterial VIRAL OP(<170 mm hg) >300 mm <300 WBC <5 >1000 <1000 %polymorphiccells (0%) >80% 1-50% Glucose (>40 mg/dL) <40 >40 Protein (<50 mg/dL) >200 <200 Gram stain (neg) pos neg Appearance (clear) Cloudy Clear CT before LP -Obtain a CT head 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 Treatment -Concern for bacterial meningitis? Antibiotics is priority!!! -Can get LP up to 2 hours after Abx administration 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 electrolyte abnormalities Increased intracranial pressure - mannitol

S/Sxs, treatments of patient with acute heroin overdose

Toxicity Signs and Symptoms -Constricted pupils (miosis) -Depressed level of consciousness but responsive to stimuli -Seizure -Hypothermia -Slow, deep respirations -Hypotension -Bradycardia -Skin changes - flushed, urticaria Opiate/Opioid Interventions -Institute measures to prevent patient and staff injury -ABC's -Give naloxone until the drug's CNS depressant effects are reversed **2mg every 3 minutes 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

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

Transfusion Components - 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. Transfusion Components - RBCs (or 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 with vascular disease, or other critical risk factors Hgb between 7-9 Transfusion Components - Platelets -Indications **Microvascular bleeding due to thrombocytopenia and platelet dysfunction **Prophylactic platelet transfusion may be indicated if platelet count is <10,000 **For surgical patients with thrombocytopenia **Not indicated for patients with HIT or autoimmune thrombocytopenia Transfusion Components - Plasma (FFP) -Used in patients with 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. Transfusion Components - Cryoprecipitate -Derived from plasma that has been frozen and thawed -Administered to patients with fibrinogen deficiency -Doesn't require crossmatching before transfusion

DDX frostbite, trenchfoot, chillblains

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 -Once affected by chilblains, frostnip or frostbite, the involved body part becomes more susceptible to reinjury Frostbite: A. First -degree and Second-degree frostbite -Superficial injuries: Edema, Burning, Erythema, Blistering is present in second-degree frostbite B. Third-degree injury -Freezing damage to the deeper subdermal plexus: Hemorrhagic blisters, Necrosis, Blue-gray discoloration of the involved extremity is common C. Fourth-degree injury -Deep injuries involving the subcutaneous tissue, muscle, tendon and bone: Little edema, Cyanotic insensate tissue, May have hemorrhagic blisters, Skin necrosis that later appears mummified

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

Types 1. Septic Shock (most common) 2. Anaphylactic 3. Neurogenic Anaphylactic Shock: -Hypersensitivity to allergen -Antigen exposure stimulates body to produce IgE Ab, continuous or repeated exposures can cause anaphylactic reaction -Anaphylactic response causes vasodilation, increased vascular permeability, bronchoconstriction, increased mucous production, increased inflame med to sites of antigen interaction S/S - warm, dry skin +/- fever, hypotension -Cutaneous: urticaria, erythema, pruritus, angioedema -Respiratory: stridor, wheezing, bronchorrhea, resp distress -Circulatory: tachycardia, vasodilation, hypotension DX - Clinical, consider any acute multi-system involvement TX - -Early recognition + tx Immediate withdrawal of antigen (if possible) -Epi (opens airways), antihistamines, corticosteroids, airway support -Judicious use of fluids, crystalloid administration, Vasopressors, Ionotropes

DDX of upper GI bleeding that may present to the ER

Upper GI -PUD -portal HTN -Mallory Weiss tear -vascular anomalies -gastric neoplasms -erosive gastritis: more commonly chronic blood loss, caused by NSAIDs -erosive esophagitis: chronic GERD -hemophilia -pancreatic malignancy -cancer -varices Clinical Features - Hematemesis, melena (dark, tarry stool) Hypotension & tachycardia (if severe) Angina, syncope, weakness, confusion Vigorous V/retching followed by hematemesis = Mallory Weiss tear ED Workup - Rectal exam w GUIAC stool testing Labs (type and scree, CBC w diff - include hematocrit, BMP, PT/PTT, BUN, CR, LFT) **Hgb & Hematocrit will be low CT: Controversial Endoscopy: study of choice for diagnosed, but not performed in ED + therapeutic TX - -Emergency stabilization of ABCs -O2 + Cardiac monitor + IV fluids large bore needle + Admit pt for endoscopy in most cases -+/- blood infusion (based on clinical picture) -NG tube placement -IV PPIs if concern for bleeding ulcer -Ocreotide: for uncontrolled bleed -Balloon Tamponade: w Sengstaken-Blakemore tube can control documented variceal hemorrhage