• Aspirin Toxicity (Harmon)
  • Sources of salicylates
    • Aspirin
    • Oil of Wintergreen
    • Pepto-Bismol
    • Bengay
    • Alka-Seltzer
    • Skincare products
  • Mechanism of toxicity
    • Fatal dose 10-30 g in adults
    • Dose dependent
    • Acute vs chronic
    • Increases respiratory center sensitivity, uncouples oxidative phosphorylation, inhibits TCA cycle/amino acid metabolism, stimulates chemoreceptor/trigger zone
  • signs/symptoms
    • Tinnitus, nausea, vomiting, dizziness, fever
    • Ataxia, anxiety, lethargy, AMS, seizure, arrhythmias, seizure
  • Evaluation in ED
    • Serum salicylate concentration and trend
    • ABG
    • CBC, CMP, coags, EKG, UA, tox
  • Management
    • Gastric decontamination (ingestion w/in past 1-2 hours)
    • Sodium bicarb (consider if level >40)
    • Avoid intubation as long as possible
    • Fluids
    • HD
    • Poison Control
• Acetaminophen Toxicity (Cook)
  • Signs/Symptoms
    • Stage I: anorexia, n/v, elevated transaminases
    • Stage II: RUQ pain, elevated transaminases
    • Stage III: hepatic failure, acidosis, renal failure, pancreatitis, peak transaminase levels
    • Stage IV: multi-organ failure vs resolution
  • Lab Assessment
    • APAP levels
      • Within 1-4 hrs of ingestion, used to exclude ingestion
      • Obtain 4 hour level to get estimated peak absorption
    • CBC, CMP, ABG
  • Rumack Matthew Nomogram
    • Treatment line 
      • begins at 4 hr mark
      • If above line, treat
  • Treatment
    • Activated charcoal
    • N-Acetyl Cysteine
      • Replenishes glutathione stores to conjugate NAPQI to limit hepatocyte injury and promote renal excretion
• TCAs (Weeman)
  • MOA
    • SSRI/SNRI, antihistamine, alpha antagonist, anti-muscarinic 
  • Symptoms
    • Early: anticholinergic effects, HTN, AMS
    • Late: myocardial suppression, QRS widening, seizures, ventricular dysrhythmia, hypotension
  • Mimics: diphenhydramine, carbamazepine, sympathomimetic toxicity, serotonin syndrome
  • Assessment
    • EKG, UDS, TCA level (does not correlate with severity)
  • Management
    • Activated charcoal if within 1 hour of ingestion
    • Do not treat early HTN as patients will likely develop hypotension as they progress, treat hypotension with normal saline
    • Sodium bicarbonate
      • IV push if QRS exceeds 100 msec
      • Infusion to maintain pH 7.5-7.55
    • If seizing, use IV benzos or phenobarbital if refractory
• Clinical Pathway Opioid Overdose (Leavitt, Sizemore)
  • Duration:
    • Heroin half life: 3-8 min, metabolites ~3hrs
    • Fentanyl half life: 2-4 hrs
    • Oral opioid half life: 3 or more hours
  • Narcan
    • Opioid antagonist
    • In general, don’t exceed ~5-10 mg, but can titrate to effect
    • Route
      • IN/IM/SC: slower onset, longer duration
      • Intranasal can last ~3hrs
      • IV
      • Infusion: 
        • Mix 4mg naloxone in 100 mL D5W
        • Infusion rate at ⅔ of effective dose that initially reversed the patient
    • Can repeat dosing every 3 minutes 
  • St. Paul’s Early Discharge Rule
  • HOUR Study
  • Clinical Pathway to be posted soon
• Envenomation (Giddings)
  • Ciguatera
    • Heat stable toxin
    • Barracuda, red snapper, mostly reef/tropical fish
    • GI symptoms, paresthesias, hot/cold reversal, bradycardia
    • Treatment: antiemetics, atropine, mannitol
    • Mechanism: increases permeability of sodium channels inducing membrane depolarization
  • Scombroid
    • Caused by improperly stored fish, heat stable toxin
    • Symptoms: flushing, warmth, urticarial rash, palpitations, itching
    • Causes histamine release
    • Tx: antihistamine
  • Coral Snake (Elapidae)
    • Presentation: minimal local symptoms, severe systemic symptoms, respiratory paralysis, AMS, CN palsies
    • Complications: hypovolemic shock, DIC
    • Work up: CBC, CMP, coags, fibrinogen, d-dimer
    • Treatment: anti-venom, aggressive supportive care
    • Dispo: Admit, concern for neurotoxic effects including respiratory failure, can have delayed presentation
    • Mechanism: cholinergic
  • Crotaline (Pit Vipers)
    • Presentation: Local pain/tissue damage, fang marks, coagulopathy, weakness, n/v
    • Complications: swelling, compartment syndrome, DIC, hypotension
    • Treatment: CroFab (give if bad systemic symptoms, abnormal labs, AMS, significant swelling)
  • Black Widow
    • Presentation: Pinprick bite, pain to whole extremity, muscle cramps, tachycardia, hypertensive, can mimic appendicitis
    • Management: supportive care, antivenin for severe symptoms
  • Tarantula
    • Barbed hair, can penetrate cornea, may need ophthalmology consult
    • Supportive care
  • Brown Recluse
    • Painless bite, local tissue necrosis
    • Systemic effects are rare
    • Treatment: supportive
• High Altitude Medicine (Thurman)
  • Physiology
    • High Altitude: 1500m, Very High: 3500m, Extreme: 5500m
    • Begin to see altitude illness at around 2500m/8000ft
    • As altitude increases, percentage of oxygen available decreases
  • Acclimatization
    • Respiratory compensation by increasing minute ventilation, which decreases PaCO2
    • Renal compensation by increasing excretion of bicarbonate
      • Associated diuresis can exacerbate altitude illness and increase dehydration
  • Acute Mountain Sickness
    • Headache, GI symptoms, fatigue/weakness, dizziness/light-headedness
    • Prevention (ideally start 1 day before trip, continue 1-2 days after patient is at highest altitude)
      • Acetazolamide 125 mg q12hr
      • Dexamethasone 2mg q6hr or 4mg q12hr
      • Gradual ascent
      • Ibuprofen 600 mg q8hr
    • Treatment
      • Halt ascent until symptom free
      • Only need to descend for severe symptoms
      • Supplemental oxygen, dexamethasone, acetazolamide
  • High Altitude Cerebral Edema
    • Acute mountain sickness + mental status change, ataxia
    • Treatment
      • Immediate descent/evacuation
      • Supplemental oxygen
      • Dexamethasone
      • Portable hyperbaric chamber
      • Acetazolamide 
  • High Altitude Pulmonary Edema
    • Non-cardiogenic pulmonary edema
    • Symptoms (need at least 2)
      • Dyspnea at rest
      • Cough
      • Chest tightness/congestion
      • Weakness/decreased exercise tolerance
    • Signs (need at least 2)
      • Crackles or wheeze
      • Central cyanosis
      • Tachypnea
      • Tachycardia
    • Prevention
      • Gradual ascent
      • Nifedipine 30 mg q12hr or 20 mg q8hr
      • Tadalafil/Sildenafil
    • Treatment:
      • Immediate descent
      • Supplemental oxygen
      • Nifedipine
      • Portable hyperbaric chamber
      • tadalafil/sildenafil
      • CPAP
• COVID (Brown)
  • Symptoms
    • Typical of most viral syndromes
  • Lab abnormalities
    • Elevated WBC, LDH, d dimer, ferritin, ESR/CRP, procal, ALT/AST, t bili, troponin, CK
    • Low lymphocyte count, albumin, platelet count, hemoglobin
  • Imaging
    • Normal vs bilateral pulmonary opacities
  • Airway management
    • Pre-oxygenate with NRB or HFNC
    • Consider supraglottic airway with viral filter
    • Video laryngoscopy
    • Trial HFNC or non-invasive ventilation prior to taking airway
    • Low tidal volumes, permissive hypercapnia, ARDSNet protocol
    • Consider proning
  • Treatment
    • Supportive treatment
    • Bamlanibimab
    • Dexamethasone
    • Remdesivir
    • DVT ppx if hospitalized
  • Disposition
    • Walking O2 test
    • 4C mortality score
• Pacemakers (D. Thomas)
  • Prevent HR from falling below set limit
    • Pacing
    • Sensing
  • Malfunction
    • Failure to capture
      • Low battery
      • Inflammation
      • Loose or displaced lead
    • Sensing issues
      • Undersensing
      • Oversensing 
  • Management
    • Typical bradycardia management
    • Atropine, epinephrine, transcutaneous pacing, transvenous pacing
  • Magnet placement
    • Opens Reed switch with breaches sensing circuit and will pace regardless of intrinsic cardiac activity 

2020 AHA Guidelines (Dr. Price)

• Confirmation
  • CPR depth 2 to 2.4
  • CPR Rate 100 to 120
• New changes
  • Recommend lay rescuers initiate CPR for presumed cardiac arrest
  • Double sequential defibrillation for nonresponsive vfib/vtach not recommended anymore
  • Reasonable to attempt IV access prior to IO access first
  • Recommending epinephrine in non-shockable rhythms as soon as possible
  • Give epinephrine for shockable rhythm after defibrillation fails
  • Recommends against use of POCUS for prognostication, can be used to detect ROSC. 
  • Delay neuro-prognostication in coma for 72 hours
  • Should avoid excessive ventilation during cpr- causes harm
  • Amiodarone or lidocaine may be considered for CF/pVT unresponsive to defibrillation
  • Routine administration of Ca, NA bicarbinate, Magnesium not recommend in cardiac arrest
• Pediatric changes
  • 1 breath every 2-3 seconds (20-30 breaths per minute)
  • Reasonable to use Cuffed- ET tubes
  • Epinephrine may increase survival to discharge rates (unlike adults)
• Field termination rule
  • If patient had arrest not witnessed, no bystander CPR, No ROSC, No shock was delivered can consider stopping. 

Sickle cell disease in pediatrics (Amar Singh)

1. Vasocclusive pain crisis
   • Causes- sickling leads to occlusion leading to ischemia and pain. 
   • Dactylitis- sickling and infarction of hands. Usually first presentation in kids 6months to 2 years of age
   • Mgt: Fluids and pain control with NSAIDS/narcotics
2. Stroke- 300 fold increase risk . 
   • Tx is exchange transfusion and hydration. TPA not recommended. 
3. Acute chest syndrome
   • Pulmonary infiltrate and any respiratory symptom. Indicative of infection and or infiltrate. 
   • Mgt: 02, hydration, antibiotics, blood transfusion or exchange transfusion. 
4. Splenic sequestration
   • See acute hemoglobin drop at least 2 points with LUQ pain, splenomegaly
   • Tx: IVF with blood transfusion, find underling cause (Likely infection)
5. Sepsis
   • Streptococcus pneumonia- most common cause of sepsis in asplenic patient. 
   • Other encapsulated Strep, H.Flu, salmonella, ecoli.
   • Increased risk for salmonella osteomyelitis 
6. Aplastic Crisis 
   • Commonly caused by parvovirus b-19 with marked severe anemia with decreased reticulocyte count. 
   • Mgt- transfusion and IVIG to help clear parvovirus infection. 

Hyperglycemic emergencies (Dr. Mcgee)

1. DKA
   • Hyperglycemia >250mg/dl
   • Ketonemia- produced by excessive breakdown of fatty acids (includes acetoacetate, acetone, BHOB)
   • Acidosis pH <7.3
     • Can be normal 2/2 to compensation and contraction alkalosis, elevated anion gap may be only clues
   • Other types of ketoacidosis    
     • Alcoholic ketoacidosis, starvation ketoacidosis, isopropyl alcohol ingestion (ketonemia)
   • Mgt: focus should be on closing the gap. 
     • 1. Volume repletion most patients 3-6L down. When sugars < 250 include dextrose containing fluids. 
     • 2. Electrolyte repletion K<3.5 consider stopping insulin, K3.5 to 5.5, consider adding K to fluids 20-30meq/L. <5.5 no need to add potassium. Check Mg, Phos levels as well. 
     • Insulin drip >1units/kg dose. Switch to subQ after gap normalized and bicarbonate normalized. 
2. Hyperosmolar hyperglycemic state
   • Triad
     • Severe hyperglycemia (> 600 usually)
     • Elevated serum osmolality (>320 osm/kg)
     • Altered mental status 
   • Treat similarly to DKA, usually require more fluids as patients more dehydrated.  

Resuscitative Hysterotomy (Ben Turner and Harrison Brown)

1. Indications to do
   • Maternal cardiac arrest without ROSC within 4 minutes
   • Estimated gestational age of infant >20 weeks (fundus > 20 cm)
   • Not necessary to document FHT prior to procedure.      
2. Contraindications 
   • Known age < 20 weeks
   • ROSC within 4 minutes of arrest
3. Procedure
   • https://www.youtube.com/watch?v=IwDWv2iyAos

• Secrete meeting of the minds.

Pelvic inflammatory disease (Alaina Royalty)

• Pelvic Inflammatory Disease (PID) comprises spectrum of infections of the upper reproductive tract:
  • Salpingitis, endometritis, myo/parametritis, and oophoritis
  • Perihepatitis (Fitz-Hugh-Curtis) is caused by lymphatic spread
  • Tubo-ovarian abscess is caused by direct extension
• Physical with pelvic with possible cervical motion tenderness Lower abdominal tendernes, Uterine and or adnexal tenderness, Mucopurulent discharge, Fever 
• DX: Sexually active women with lower abdominal pain without other cause found with PE with CMT, Adnexal tenderness, or uterine tenderness
• Tubo-ovarian Abscess
  • Dx via ct or US
  • Needs admission for IV antibiotics and OB/GYN Consult. Can have IR drainage. 
  • Predictors of failure of antibiotic treatment: WBC 16k or abscess > 5.2 cm 
• Outpatient management
  • Rocephin 250mg IM + Doxycyclin 100mg Po BID x 14 days with Metronidazole 500mg Po BID x 14 days
• Dispo
  • Admit of they have TOA, pregnant, cannot tolerate po, septic, failed outpatient antibiotics

Ovarian Torsion (Tyler Bayers)

• Ovary can rotate around suspensory ligaments or utero-ovarian ligament, compression of ovarian vein with leads to obstructed venous outflow leading to ischemia and necrosis
  • Risk factors mass >5cm, hx of cyst, ovarian malignancy, TOA, pregnancy
  • Presentation
    • 90% with pelvic pain, Adnexam mass, nausea and vomiting
    • Pearl- Right sided torsion more common due to presence of sigmoid colon on left  
  • Ultrasound- Evaluate for decreased venous/arterial flow
    • 2/3^rd might have normal flow
    • Can see enlarged unilateral ovarian volume
    • Lpelvic free fluid
    • Loss of echogenicitiy 
    • Whirlpool sign
  • CT
    • Can be used for evaluation of suspected torsoin, 
    • Sensitive for secondary findings in torsion
    • Can find ovarian enlargement, ovarian mass, distended pedical, lack of enhancement
  • Management
    • Pain and nausea control, transabdominal/transvaginal US, Emergent OBGYN consult
    • Definitive diagnosis by direct visualization

Bartholin Gland Cyst/Abscess (Dan Fischer)

• Ducts of the glands drain into posterior vestibule at 4 oclock and 8oclock positions. See mass near the posterior introitus medial to labia minora
• Usually sterile initially but can become infected
• Abscess- erythema, fluctuance, severely painful
• Dx- Clinical consider sti testing
• Tx: Word catheter placement 
  • Make small incision so that word catheter will not fall out
  • Drain abscess, explore wound
  • Place word catheter and inflate balloon with 2-4cc of water with blunt kneedle 
  • Keep in place for 4-6 weeks
  • Fllow up with gyn

HTN emergencies in Pregnancy (Joshua Sennets)

• Can occur from 20 weeks gestation to 6 weeks post partum
• Definition- new onset htn and proteinuria
• With severe features- new onset htn and signs of end organ dysnfucntion after 20 weeks gestation and up to 6 weeks gestation
  • Platlet <100,000, S CR >1.1, LFT >2X ULN, Palm edema, persistant headache, visual disturbance
• Labs: CBC, type and screen, Coags, Fibrinogen, CMP, LDH, Urine protein/creatine ratio, serum and urine tox
• Eclampsia- convulsive manifations of HTN in pregnancy
  • 60% antepartum, 20percent intrapartum, 20 percent post partum
• Manegement- ABCS, IV Magnesium, IV antihypertensvies, Fetal monitorinfg, 
• Magnesium
  • 4-6 gram in 15=20 min, repeat 2-4 gm LD PRN then 1-2/hr
  • Goal mag of 5-9 mg/dL
  • Monitor respiratory status and evaluate for decreased patellar reflexes
• BP control
  • Hydralzine, labetalol, nifedipine can all be used
  • 20mg IV labetalol, 10mg IV hydralazine, 10mg PO Nifedipine
  • Initiate for BP > 160mmhg

Cold Related Illness (MJ)

• Nonfreezing injury
  • Temp >32, wet exposure
  • Cold urticaicaria
    • Hypersensitivity to cold air/water
    • Treat like allergic reaction 
  • Paniculitis
    • Mild necrosis of subqutations fat
    • Seen more in kids, supportive care
  • Chilblains/pernio
    • Vasculitis causing tingling and numbness 12-24 hours post exposure with localized edema. After rewarming can see tender blue nodules. 
    • Supportive care, can use nifedipine for topical vasodilation, corticosteroids
  • Trenchfoot/Immersion Injury
    • Direct injury to the soft tissue from prolonged cold exposure
    • Stage 1 cold exposure-white
    • Stage 2 rewarming- mottled pale blue, pain and edema, can last  a few hours. 
    • Stage 3 hyperemia- severe burning pain, can last days to months. 
    • Rewarm slowely, can use vasodilators, cool if severe pain in hyperremia. 

Clinical Features

Classification

Visual determination of tissue viability is difficult in first few weeks; classify early injuries as superficial or deep

Degree	First (frostnip)	Second	Third	Fourth
Pathophys	Partial-skin freezing	Full-thickness skin freezing	Tissue loss involving entire thickness of skin	Extension into subcutaneous tissues, muscle, bone, and tendon; little edema
Symptoms	Stinging and burning, followed by throbbing	Numbness followed by aching and throbbing	Extremity feels like a “block of wood” followed by burning, throbbing, shooting pains	Deep, aching joint pain
Course	Numbness, erythema, swelling, dysesthesia, desquamation (days later)	Substantial edema over 4-6 hours; skin blisters form within 6-24 hours; Desquamate and form hard black eschars over several days	Hemorrhagic blisters form and are associated with skin necrosis and blue-gray discoloration	Skin is mottled with nonblanching cyanosis and formation of deep, dry, black eschar
Pain with rewarming	Minimal	Mild to moderate	Severe	None
Prognosis	Excellent	Good	Often poor	Extremely poor

Biliary US (Dr. Baker)

• Tips
  • • Get sagittal view and transverse view 
    • X-7 technique- used phased aray probe and go 7 cm lateral to xiphiod process 
    • Have patient inspire, have them lay left lateral decubitus, can tilt feat down
  • Portal triad with common duct (normal <7cm you can have 1mm enlargement per decade of life), portal vein, hepatic artery
  • Cholelithiasis
    • See hyperechoic with posterior shadowing
    • Diagnosis cholecystitis: Gallstones, sonographic Murphy’s, Wall thickening >3mm, pericholecystic fluid

Emergency Delivery Small group (Aaron Kuzel)

A 26-year-old G1P0 38 weeks and 4 days female presents as a Code Green to the ambulance circle. The patient brought back to Room 9 for assessment. The patient states her “water broke” and it soaked through her pants. She is feeling contractions. Vitals are HR 120 BP 128/78 RR 24 SPO2 100% and T 97.6 F. On external vaginal exam you palpate a pulsating vessel in the vaginal canal and fetal head at 0 station.

●       What is the diagnosis? Umbilical cord prolapse

●       What is the most important next step in the management of this patient? Elevate presenting part to reduce compression and transport to OR for emergent c-section

●       What positions can you place the patient in to alleviate pressure on the protruding part? Knee to chest position, no pushing or Valsalva

A 27-year-old G1P0 at 37 weeks and 4 days is presenting in active labor to the emergency department. She is endorsing painful contractions that began within the last hour. Contractions are occurring every 2 minutes. Vitals are HR 106  BP 136/68 RR 18 SPO2 98% and T 98.8 F. Physical exam reveals fetal head crowning and bloody show. During delivery, you are able to advance the posterior shoulder, however as you attempt to advance the posterior shoulder the fetal head retracts. An episiotomy is made; however, you are still unable to advance the anterior shoulder.

●               What is the diagnosis? Shoulder dystocia

●               What is the most appropriate next course of action?HELPERR pneumonic. Chall for Help, Evaluate for episiotomy, Legs flex (Mcroberts maneuver), Pressure (suprapubic pressure), Entry maneuvers (Wood’s corkscrew or Rubin II maneuver, Remove posterior arm by sweaping it across chest, R Roll on all fours

●               What are some risk factors for this condition?Preterm labor, macrosomia, small materanal pelvis, prolonged labor

●               Failure to recognize this condition and correct it can have what damaging results? Fetal demise

●               Which of these three maneuvers is the most effective in relieving this condition? Roll on all four 

Case 3:

A 21 year-old G4P3 woman presents to your Rural Emergency Department in Ashland, KY in active labor and has a spontaneous vaginal delivery in the emergency department. Prenatal care was appropriate and the patient’s blood type is O-positive. The infant is full-term and well. An intact placenta passes shortly thereafter, followed by vaginal bleeding. There are no obvious lacerations to repair, and the bleeding appears to be originating from the cervical os. Vital signs are within normal limits. The patient continues to have oozing of blood from the vagina several minutes after birth.

What is the diagnosis? Post partum hemorrage

What is the most common cause of this diagnosis? Uterine atony

What is your next step in management? Bimanual massage,

What medications (and in what order) would you use to stop the bleeding? Pitocine 80units bolus IV or 10units IM, Misoprostol 600mcg SL or 1000mcg rectally

What is a rare complication of this diagnosis that results in high fetal and maternal death?Uterine rupture

Journal Club

Review of the Basics of Cognitive Error in Emergency Medicine and Updates: Still No Easy
Answers by Hartigan et al, 2020.

• Despite research, Cognitive Error remains a source of frustration
• Rapid decision making in the ED relies on a combination of intuition and analytic reasoning, both based on experience and training.
• Reviews studies on Cognitive Error interventions and assesses applicability in ED. Not much statistical data to support that these interventions translate into productive changes in clinical practice, but studies are limited and further research is needed.

Contrast-Associated Acute Kidney Injury by Mehran et al, 2019.

• Proposes change of nomenclature from “Contrast-Induced” AKI to “Contrast-Associated” AKI
• Historical significance of Contrast-Associated Acute Kidney Injury may be overstated
• Reviewed historical interventions for preventing CAAKI
• Recommend fluids and follow-up for patients at high risk of renal injury (those with known renal dysfunction)

Deaths in ED and 72 Hour Returns

• Excellent work last month, Team.
• Reviewed palliative care in ED, post-traumatic growth, and toolkits for dealing with trauma.
• https://www.psychologytoday.com/us/basics/post-traumatic-growth
• https://healthcaretoolbox.org/self-care-for-providers.html

Morbidity and Mortality Case

• Unexpected decompensation in ED with subsequent PEA arrest
• Reviewed traditional ACLS algorithm as well as updated literature discussing potential for treating PEA based on its morphology (i.e., wide complex vs narrow complex)

Ethical Considerations in Pre-Hospital Care with Dr. Selk

• Autonomy, beneficence, nonmaleficence, justice
• Capacity: ability to understand medical situation and make an informed decision about care after being advised of the risks and benefits of a particular course of action
• Competence: a legal determination.  If you are concerned that a patient is not competent, then you can refer for 
• Refusal of EMS care:  Patient must articulate reasoning for refusing and articulate ramifications regarding their decision.  This conversation should be documented and witnessed as well. 
• Death on Scene: non-traumatic cardiac arrest, unresponsive/apneic/pulseless/F&D pupils/ALS EKG with asystole in at least two leads.  Lividity, rigor mortis, presence of venous  pooling, destruction of body incompatible with life
• Law enforcement information gathering activities should not interfere with patient care.  Law enforcement video or audio recording should only be used with permission from all parties

Management of Variceal Bleeds with Dr. D. Thomas and Dr. D. Grace

• ABCs:  HOB up, preoxygenate, RSI with cardiostable sedative and high dose paralytic, have video and 2 suctions available.  Place tamponade tube PRN and call GI.
• Tamponade tube depends on the institution.  No matter what, inflate gastric tube and apply proximal traction. Start by placing 50cc air into balloon and shoot a CXR to confirm placement in stomach.  Once placement is confirmed, fully inflate balloon.  Gastric balloons can potentially migrate into the esophagus and will compress the trachea, causing high peak pressures.  If you see increased peak pressures, repeat CXR to check placement. 
  • Blakemore tube:  Gastric balloon (250mL) + esophageal balloon + gastric suction
  • Minnesota tube: Gastric balloon (500mL) + esophageal balloon + gastric suction + esophageal suction
  • Linton tube: Gastric balloon (750mL) 

Mushroom Toxicity with Dr. Webb

• Orellenine:  symptom onset 36hrs-17days, severe renal failure, frequently no other symptoms with insidious onset
• Amatoxin:  gradual onset over several days.  Initially emesis and diarrhea → elevated LFTs → GI bleeding, hepatic encephalopathy, renal failure → death.  Can treat early ingestion with charcoal and gastric decontamination.  Silbinin, NAC, benzathine penicillin have been proposed as potential treatments. 
• Ibotenic acid and mucimol:  Increases GABA And serotonin. Onset minutes but up to 3 hours → visual distortions and hallucinations.  Can see N/V, ataxia, and hypotension.  Very rarely cause coma, convulsions, and death.  Symptoms typically resolve within 24 hours. 
• Monomethylhydrazine:  Inhibits pyridoxine function in CNX. Most common presentation is N/V/D.  Can rarely cause jaundice, liver failure, and seizure. Treatment is typically symptomatic, but should give pyridoxine if patient develops seizures
• Muscarine: Sweating, salivation, lacrimation, miosis, bradycardia, wheezing.  Treatment typically symptomatic, but if severe, can use atropine. 
• Coprine: causes disulfiram-like reaction.  Don’t mix with alcohol.
• Chlorophyllum: most common mushroom poisoning in the US.  N/V/D.  Supportive treatment.  

Peds GI Emergencies with Dr. Stevenson

• Obstruction– atresia (esophageal, jejunoileal, anorectal), meconium ileus, webs/stenoses/duplication.  Typically present within early weeks of life.  Can see double bubble sign with duodenal atresia.  Call surgery. 
• Malrotation– First week or so of life, bilious emesis.  Call surgery. 
• Pyloric stenosis– First month of life.  Child appears hungry and fussy, but non-toxic.  Olive-shaped mass.  Diagnostic test of choice is ultrasound.  Call surgery. 
• Incarceration– hernia or torsion.  Associated with prematurity.  Reduce and call surgery.
• Intussusception– paroxysmal abd pain, vomiting, lethargy.  Can have positive hemoccult.   

Implicit Bias in ED with the Office of Diversity and Inclusion

• Implicit bias is an unconscious cognitive shortcut between previous experiences and current data input
• IAT as a tool to evaluate your implicit bias
• Snap judgements, elitist behaviors, negative stereotypes, positive stereotypes, cloning, wishful thinking
• Can impact our ability to effectively interact with patients and colleagues
• Can unintentionally reinforce historical social inequalities 
• How to mitigate individual biases:  develop the capacity to self-reflect, get feedback, practice “constructive uncertainty,” engage “others,” and explore awkwardness

discomfort.  

Anorectal Disorders with Dr. Harmon

Rectal prolapse–typically painless presentation, requires reduction. If edematous, can use sugar to improve swelling prior to reduction. 

Anal fissures–painful rectal pain with small bright red blood with BMs. Symptomatic management. 

Hemorrhoids–external can be painful, internal can be painless. Symptomatic management.  Referral to CRS.

Abscesses–Beware the anorectal abscess. Requires DRE looking for any disproportionate tenderness or fluctuance.  If exam concerning for deeper abscess, obtain CT. Treatment of choice is I&D.  If simple perianal, can do bedside I&D.  Any other abscess should be operatively managed.    

Cirrhosis with Dr. Cook:

Path: Progresssive hepatic fibrosis and subsequent liver dysfunction 2/2 hep C and/or alcohol.

Clinical presentation: Encephalopathy, asterixis, hepatorenal syndrome, jaundice, ascites, varices (+/- bleed), +/- SBP, HCC

Work up: Basic labs, +/- sepsis evaluation, +/- CT head, ammonia level if no history 

Treatment: Airway management and BP management PRN, beta blockers, lactulose, +/- antibiotics if concern for SBP or GI bleed.

Gallbladder Pathology with Dr. Carter:

Most gallbladder pathology related to stone–cholesterol vs pigment–formation.  Ultrasound continues to be imaging of choice.

Cholelithiasis: relenting RUQ pain after eating without systemic signs.  Should see normal labs.   Typically managed outpatient.  Can refer for outpatient HIDA. 

Cholecystitis (cal vs acalc):  Elevated WBC, +/- elevated AST/ALT, less likely to have bili elevation, + Murphy’s Sign.  Requires surgical consult. 

Ascending Cholangitis: SICK. WBC, AST/ALT and bili elevation, alk phos elevation. Charcoat’s Triad and Reynold’s Pentad aren’t present in most patients.  Focus on resuscitation, antibiotics, and surgery consult. 

Start with ultrasound (evaluating for GB wall thickening, sonographic Murphy’s, pericholecystic fluid). If ultrasound is non-diagnostic, alternative imaging includes CT w contrast (Fast) or MRI (does not require contrast, safer in pregnancy)

Room 9 Follow-up with Dr. Davenport:

Elderly female presents to resus bay with concern for fall vs ?anaphylactic reaction, per EMS.  Intubated prior to arrival for airway protection.  Given epi, benadryl, steroids PTA.

Arrives HDS.

Initial physical exam with concern for profound facial edema and upper body subcutaneous emphysema. 

Access obtained, labs drawn, CXR not super helpful given subQ air and habitus.  FAST limited 2/2 subQ emphysema. 

BP progressively starts dropping and Radiology calls with concern for tension pneumothorax.  Chest tube subsequently placed with clinical improvement. Panscan obtained with multiple rib fractures, lung contusions, pneumomediastinum, chest tube in place with small residual pneumothorax. 

Family arrives and states patient had significant fall.  No history of anaphylaxis or angioedema. EMS concern for anaphylaxis was likely related to traumatic facial swelling.  This report led to some early diagnostic anchoring, which could have caused a harm event.

Patient was admitted to trauma service, had improvement over hospital course, eventually discharged to SAR.

Learning Points:

* Epi elevates BP, which can make a hypotensive patient look falsely HDS.

* Resus bay CXRs can be difficult to read in resus bay 2/2 body habitus, as well as small screen and bright lights.

* Pneumomediastinum: typically treated with symptomatic support and observation unless injury to great vessels.

* Pulm contusions: hypoxia and hypercarbia–>respiratory acidosis.  High risk for developing ARDS. 

* Cognitive bias: beware anchoring and overconfidence.  These can be natural digressions into energy-sparing cognitive shortcuts in our high acuity in our work environment.  It is easy to develop cognitive biases.  Recognition, mindfulness, and discussion can help prevent cognitive bias.

IR PE Management with Dr. Glaenzer:

Tool for IR-directed treatment of major pulmonary embolism via aspiration of clot.  Presents an alternative to traditional EKOS (directed lytic therapy)

PE–>RV dilatation–>Increased RV wall tension–>Myocardial Tension and Inflammation–>Increased myocardial demand–>Decreased RV output–>Decreased LA preload–>Hypotension–>Death

Inari can be considered in patients with both intermediate and high mortality PE

Upper GI Bleed with Dr. Shah:

Causes:  PUD, H pylori, anticoagulation, hepatic pathology

Physical exam:   DRE, look for signs of cirrhosis (Ascites, jaundice, angioma, hepatosplenomegaly), abdominal scars? (consider aortic enteric fistula), cardiac murmurs? (consider anticoagulation status)

Workup:  CBC, CMP, PT/PTT/INR, type and cross, lactic, trop (in elderly), ammonia (if AMS)

Scoring systems:  Glasgow Blatchford Score (most useful in ED), Clinical Rockall SCore, AIMS65

MGMT:  Blood for Hbg<7.  Platelets for active bleeding and plt<50k.  PCC for INR>2 and life-threatening bleeds on warfarin.  TXA for severe upper GI bleed.  Pantoprazole 80mg IV bolus. Octreotide 25-50mcg IV bolus.  Antibiotics–typically Ceftriaxone 1g IV if concern for variceal bleed. Blakemore tube as last line for unstable patients. Endoscopy>IR>Surgery.

Taking the Risk: Anticoagulation and Low Risk PE in the ED 

Pauline Thiemann, Pharm D

-50% of patients with PE can be safely treated at home-Recommend outpatient management for patients with low risk PE 

-Low risk: hemodynamically stable, low Risk Scores (HESTIA Criteria, PESI score, S-PESI), no RV dysfunction and negative troponin 

-then see if the patient has any contraindications to Anticoagulation

                  – HAS-BLED score

-IV therapy: Unfractionated heparin

                  -immediate onset and half-life is 1-2 hours. Easy turn on and off 

                  -dosing: VET Protocol 80 u/kg bolus 16 u/kg/hr 

                  -Severe renal dysfunction

                  -Reversable

                  -Cons: Hx of HITT, not for outpatient, not fast time to therapeutic PTT 

-Subq: Lovenox 

                  – onset: 3-5 hours and ½ life 4-7 hours

                  -eliminated by renal

                  -Dosing: 1mg/kg q12h (preferred), Renal dysfunction 1 mg/kg daily 

                  -Reversible with protamine

                  -Cons: HIT, Subq injection (need patient education), not studied in dialysis patients 

-Oral Agents

                  -Warfarin: 

                                    -5mg a daily or 2.5 mg daily in HF, elderly, liver failure, malnourishment 

                                    -INR based dosing (goal is 2-3) 

                                    – Keep Vitamin K intake consistent week to week 

                                    – patient needs INR checks (think if patient can do that and has access to care) 

                                    – tell physician/pharmacist anytime a change in medication. 

                                    -Reversable: PCC or FFP (+vitamin K)

                                    -Bridge: VTE/PE ALWAYS BRIDGE 

                  -Pradaxa: Direct thrombin inhibitor

                                    -requires 5 days of initial therapy before starting

                                    -Caution with liver disease

                                    -cannot send home directly

                                    -Reversible: Praxibind 

                  -Savaysa (Edoxaban)

                                    -Same as pradaxa: need to be on 5 days of parenteral anticoagulation 

                                    -watch in creatinine also (very specific) 

                                    -good for cancer patients 

                                    -reversible: PCC

                  -Xarelto: Factor Xa inhibitor

                                    – Reversal: PCC 

-Dosing: 3 week loading dose (15 mg BID x 21 days) and then 20mg daily with a meal

-Avoid in kidney and liver dysfunction

                                    – patients cannot miss doses 

                  -Eliquis: Factor Xa inhibitor

                                    -10mg BID x 7 days and then 5mg BID after 

                                    – no renal dose adjustments needed 

                                    – can be taken with or without meals, less rates of major and minor bleeding

                                    – Reversible with PCC

                                    – patients cannot miss doses 

-Writing the Script: 

-Apixaban 5mg tablets, directions: take 2 tablets twice daily for 7 days and then take 1 tablet BID after.  Qty: 74 tablets 

                  –DOACS are contraindicated with Phenytoin

Small Group PE

Becca Leavitt, MD PGY-2

CASE 1 

Patient is a 16 YOF with PMH of seasonal allergies who presents to your ER with a 1 day history of intermittent shortness of air at rest.  She denies cough and fever or recent known COVID contacts, but adds that she just came back from a week-long cross-country road trip with her boyfriend. She takes an OCP every day, which she just started after having a Nexplanon removed 3 months prior.  She does not smoke cigarettes, but does endorse occasional marijuana use.  Her physical examination and vitals are grossly normal barring a heartrate of 120 BPM. 

• What are the components of the PERC score and what are some exclusion criteria?
  • Components: Age <50, pulse <100, O2 >or = 95%, hemoptysis, hormone use, surgery/trauma in 4 wees, prior VTE, unilateral leg swelling, cancer 
  • Inclusion Criteria: Tachycardia, Hormone Use:
  • Exclusion: age, no leg swelling, trauma, history of blood clots 
• What are common abnormalities seen on CXR in acute PE?
  • Hamptons Hump(wedge infarct) Westermarks Sign, ATX, Pleural Effusion, elevation of hemidiaphragm 
  • Cardiomegaly in 35%
  • Pallas sign: enlargement of descending pulmonary artery 
• Other than CT, what are other modalities that can be used in the diagnosis of acute PE and how useful are they
  • US (McConnel’s Sign-ECHO) Bilateral lower extremity US, VQ, CXR, EKG (d dimer) 
  • Dimer: if pretest probability for PE is low.  False negative rate is <1%. Dimer levels naturally increase with age (age adjusted age x 10).  If it comes back positive then further testing should be undertaken. 
  • VQ scan: only if there is an absolute contraindication to CT, if there is an abnormal CXR the VQ scan is going to be abnormal. Normal means the patient does not have a PE. 
  • ECHO: New right heart strain or thrombus in PA
  • CTA PE:  gold standard for diagnosis of PE 

CASE 2 

Patient 63-year-old African American man, with a background of poorly controlled diabetes mellitus type 2 and hypertension presented with 1-week history of dyspnoea on exertion.  A week before he was hospitalised at another facility with severe hyperglycaemia after running out of his oral diabetes medications. During that hospitalisation, he developed a new-onset breathing difficulty.  Ventilation/perfusion lung scan done at that time was indeterminate probability for PE and no further work up was pursued. After hospital discharge, his shortness of breath progressively got worse along with increasing fatigue. He denies leg swelling or pain, chest pain, palpitations, haemoptysis, light-headedness or syncope. Physical examination reveals an anxious man who is dyspnoeic with minimal exertion.   He is afebrile, heart rate was 82 beats/min, blood pressure 129/89 mm Hg and respiratory rate 24 breaths/min. The patient was hypoxaemic on room air (oxygen sats 84%) requiring high-flow oxygen through a non-rebreather mask.

• What differentiates massive from sub-massive PE?
  • Massive: Right heart strain, and HD instability, pulselessness, arrhythmia, LV dysfunction
  • Submassive: without hypotension but with RV strain.  Elevation of BNP >90 or ProBNP>500
• What are common EKG changes associated with pulmonary embolism?
  • Tachycardia (44%) , Peaked P waves, RBBB (associated with increased mortality if new), Inverted T waves in V1-V4, S1Q3T3, nonspecific ST/T wave changes, RAD
• What are the absolute and relative contraindications for TPA?
  • Absolute, previous headache bleed, surgery encroaching the spine, Ischemic stroke in 3 months, intracranial neoplasm, known AVM, concern for aortic dissection, active or bleeding diathesis, recent closed head/facial fracture
  • Relative: 75 years, current anticoagulation/ PE in pregnancy, noncompressible vascular punctures, Recent CPR lasting >10 minutes, recent internal bleeding 2-4 Weekes ago, poorly controlled HTN, uncontrolled HTN on presentation, major surgery in 3 weeks, dementia

CASE 3 

Patient is a 35 YO Amish male with no significant past medical history who presented to a community ED following collapse.  Per his wife, patient was working in the yard, when one of her sons came to alert her that her husband had collapsed while he was lifting logs onto a cart.   On presentation, patient is hypotensive, tachycardic, diaphoretic and appears anxious.  He relays that he is having difficulty breathing.  Fluids are initiated; however, patient remains persistently hypotensive despite 30ml/kg fluid bolus.  Lab work is remarkable to for troponin of .12ng/ml, lactic acid 4 mg/dl, WCC elevated to 17, CMP is unremarkable.

• What echocardiographic findings are seen in acute pulmonary embolism?
  • McConnel’s Sign (RV free wall hypokinesis), RV dilation, D sign (bowing of the septum), right hear thrombus
• What is the indication for medical thrombolysis in the management of acute PE?
  • HD instability, arrest, massive PE, 
  • Relative: stable PE with evidence of new RV dysfunction, morbid clot burden, new or worsening pulmonary HTN, Presence of extensive DVT 
  • 50mg/2hr for submassive PE
  • 100mg/2hr for massive PE
  • Cardiac Arrest: 50mg/1 minute with CPR continued for 30-60 min after push 

PE in Pregnancy

-Start with compressive US in bilateral lower extremities 

– obtain CXR: if abnormal discuss with the patient about CT Scanning 

-Adjusted D Dimers for pregnancy

-Pregnant patients were excluded in PERC rule 

Cerner Fun

Dr. Shoff 

Helpful tips:

-November 13-14: Jewish hospitals will change to ULH Cerner – you will be able to see their records (whole system by January)

-make about 80% and you can see more patients and most of the patients

-labs will turn red: if they should have been back but is not (but if solid red then critical lab)

-Radiology: when finalized readings and you read it a paper shows up (once you have read then then the paper goes away) 

-now shows MEWS scores 

Orders:

-Quick orders: click the lab button and without going into tabs you can order

-Set up Favorites folder (name the folder LP Lab, LP Rad, LP Med) and then add to favorites then you will be able to order labs using the quick orders. 

Outside records (in the patient’s chart)

-you can see EPIC and CERNER documents from outside hospitals

-Norton, Baptist, or ULH hospitals

PNED : Equivalent 

Check out button (top right next to search bar)

Pick the hours (12 hours)

You can click custom: you can see a week at a time. 

Patients without a dispo will not appear in check out 

Can also go to Message center and look under saved documents (you must open a note, and take over scribed notes) 

Monthly Review

Dr. Shaw 

FB esophagus: foreword facing coin 

Epiglottitis: thumb print sign, unvaccinated, OR an emergent ENT consult

Septic emboli: admit for endocarditis

Massive PE: Deep Inverted T waves (acute right heart strain) will have HD instability.  tPA systemic (boards answer) 

Small left Pneumothorax with HDS: observation O2 stable is <20% <3cm apex), Observation for 6 hours

Pulmonary Edema: B lines > or equal to 3

Pneumomediastinum: “crunch” causes: asthma exacerbations, choking/coughing, vomiting and drug use.  Conservative treatment that is self-limited. Avoid increase in pulmonary pressure (Valsalva) Can discharge if HDS or signs of tension

Legionella: Hyponatremia, diarrhea, associated with fresh water, HVAC repair, NH, can transmit through ventilation systems 

Contraindication to BIPAP in acute severe asthma: AMS (weight risk vs benefit), significant secretions, inability to form a seal

                  Asthma treatment: Albuterol/Ipratropium/steroidsMagnesiumEPI/NIPPVintubation 

Tension Pneumothorax: Needle Decompression (due to tracheal deviation, JVD, and HD unstable) 

                  Midclavicular: average depth of 4.28 cm (too long for 16 g IV) 

                  Anterior Axillary: 3.42 cm

Most common cause of death in massive hemoptysis: Hypoxia/Asphyxiation. >100-600 cc/24 hr.  Early intubation, mainstem good lung if possible, bad lung down, and IR or bronchoscopy. You can use a Boogie to mainstem the left or right lung 

Croup: racemic Epi (stridor at rest) decadone PO if no strider at rest

EM Doc: *Cringes before picking up the phone*
“Hey…it’s Dr. SaltySweet from the ED. I have a placement patient for you…”
Admitting Doc: *Cringes. Sighs. Shakes head.* (This is all one smooth motion, typically.)

I know you dislike calling your (usually) friendly neighborhood hospitalist for the “placement patient” about as much as the receiving hospitalist dislikes receiving that call. However, I would argue that you should never be making that call in the first place. Let me explain.

One of the most dangerous cognitive errors we can make as physicians is premature closure. This is the concept that when the “diagnosis” and disposition are decided, the thinking stops and one disengages from the diagnostic reasoning process. As a hospitalist, I see this happen all too often to patients who are characterized as “placement patients” in the ED. Once the premature closure occurs, the work up frequently comes to a grinding halt. When the patient is labelled as a “placement” in the ED, the admitting physician may be deleteriously biased about the patient before even seeing him or her. As a result, the admitting physician is at higher risk for glossing over important details about the case due to anchoring bias and diagnosis momentum. As you might imagine, this does not promote optimal patient care. On occasion, it can even be dangerous.

As a former EM fanatic myself, one of the reasons I ultimately did not pursue emergency medicine was because I enjoyed continuity of care. I (usually) like knowing what happens to my patients and following them through their hospital courses. As a hospitalist, I have watched the hospitalizations of innumerable “placement” patients play out which is a perspective that EM physicians do not have by nature of their jobs. Sometimes these “placement” hospitalizations are very boring, but that often is not the case. Unfortunately, I have seen “placement” patients unintentionally misdiagnosed and/or misrepresented as more stable than they actually were due to premature closure. I have witnessed these patients become quite ill during their hospital courses through no one’s fault; they were just sick. On a side note, I contend that you should chart check your admitted patients at least once to see if you were correct or incorrect in your initial clinical reasoning and treatment approach; being wrong often feels just the same as being right when you do not see the effects of your actions.

In my career, I have cared for “placement patients” with missed spinal cord injuries, infections, fractures, and intracranial bleeding to name a few diagnoses. I have seen “placement patients” go into respiratory failure and/or shock. I have seen “placement patients” die. I am not saying any of this to place blame, but rather, to contend that physicians should consider looking at the “placement patient” a little more closely before admitting them upstairs. Ask yourself if you might be missing something. Keep your eyes, ears, and “Spidey sense” open. Roll them over and look at their backs and bums; you might be surprised by how many wounds and ulcers you find. You might even find Fournier’s gangrene!

All of this is why I want to educate young EM physicians on why you are doing patients a disservice when you label them as “placement patients” at the very beginning of their hospitalizations. These days, I cringe when I am called about a “placement patient” because I know there is likely more to the story than meets the eye. These patients have illnesses and social situations that are decompensated enough to land them in an emergency department and warrant admission to the hospital. They are not healthy people. They often are (unintentionally) very good at hiding occult illness that later becomes, well, not so occult. Lastly (and this is the superstitious, non-evidence-based part of me speaking), I swear calling someone a “placement patient” brings bad juju into the equation.

In closing, please remember that these so-called “placements” are human beings who are spouses, significant others, parents, brothers, sisters, aunts, uncles, friends, etc. to someone. I would not want my mom or dad labelled as a “placement” if they were admitted to the hospital, and I suspect most of you would feel the same way about your own loved ones. I challenge you to reframe how you evaluate and treat these “placement patients.” Keep an open mind and do not anchor on the idea that the only thing wrong is that they need “placement.” It is almost never just that. Ask yourself questions like: My patient is debilitated and can’t walk, but WHY is that? WHY is it that they laid on the ground for 3 days and could not get up? WHY is their potassium 2.8? WHY do they have altered mental status? Is there something reversible that I can diagnose and treat? In the end, you will do yourself and your patients a favor by reframing how you think and talk about them. Even if your patient truly just needs “placement,” find a more creative and fact-based way to present the patient to your admitting doc. Everyone will be happier, and arguably, safer!

EMS: Mass Casualty Triage

Phil Giddings PGY-2 

Mass Casualty: Resources are overloaded

-Type 1-3 -based on how many patients 

-Triage: to sort and select

                   – MUCCC: model Uniform Core Criteria-

Green: minimal injury- self-limited injury can tolerate extended delays in treatment without increased mortality risk

Yellow: Delayed-deep lacerations with hemostasis, open fractures, abdominal injuries with stable vitals, head injuries with intact airway 

Red: IMMEDIATE– unresponsive, AMS, Respiratory distress. Uncontrolled hemorrhage, amputation, proximal to elbow or knee, pneumothorax, cyanosis, weak pulses

Black: Deceased- no respirations following basic airway maneuvers 

 SALT TRIAGE 

Sort: 3 categories: Walk (assess 3), Wave/purposeful movements (assess 2^nd), Still Obvious life threaten assess 1^st) 

Assess:  individual assessment 

Life-saving interventions

• Control hemorrhage, open airway (consider rescue breaths in children), chest decompression, and auto injector antidotes
  • Minimal
  • Delayed
  • Immediate
  • Expectant
  • Dead

Treatment/transport 

START TRIAGE

-based off of respirations

                   Tachypneaperfusioncontrol bleedingcare 

Pediatrics- JUMP START for triage 

Respiratory Emergencies 

PEM-Dr. Said  

Croup: acute subglottic inflammatory process 

-6months to 3 years (morbidity is greatest in first year of life)

-etiology: Parainfluenza 1 and 3 most common (Influenza, human metapneumovirus, RSV) and COVID

– Presentation: 1-3 days URI sx and seal like cough, +/- stridor, clinical diagnosis 

       – if you cannot r/p epiglottitis or foreign body get a lateral neck x-ray (steeple sign) 

– Severity: Severe (barky cough and stridor at rest) 

             Moderate (stridor with agitation and barky cough)

             Mild barky cough no stridor 

-Treatment: Give Decadron 0.6 mg/kg

                 Racemic epi: stridor at restthen watch for 2-3 hours for rebound swelling

                 Other Therapies:  Heliox, if you need to intubate (use tube that is 1-1.5 smaller)

Foreign Body Aspiration

                   -Small children are at higher risk

                   -Anatomic immature: High epiglottis and immature swallowing coordination 

                   -Acute: lead to respiratory distress, immediate episode of coughing, gagging, choking or cyanosis  

                   -Delayed: younger kids (not verbal)

-may lead to: persistent febrile illness, chronic cough, recurrent pneumonia, recurrent croup, lung abscess, hemoptysis

-location: Larynx: obstruction, Trachea: biphasic stridor or dry cough, Bronchus (80-95%): cough wheeze and decreased breath sounds, Esophagus: can impinge the trachea in small children 

                   -CXR:

                                      50% will have negative CXR

• If high enough suspicion should be bronched, most sensitive indicator is witnessed aspiration
• Xray: hyperinflated lung, ATX, pneumonia (if delayed) 

Choking

-Infants <12 months: 5 back blows followed by 5 chest compressions using 2 fingers, baby’s head should be tilted

-Children >1 year: Heimlich maneuvers

Partially occluded airway

– Place child in sniffing position, provide supplemental oxygen, do not perform maneuvers that may dislodge the FB and move it to the central airway, Rigid Bronchoscopy needed 

Bronchiolitis: acute inflammation of lower airways, increased mucous production, edema of small airways, bronchospasm and V/Q mismatch 

-Most common respiratory wheezing under 2 years.  Occurs in winter

-Etiology: RSV

-Severe: 

respiratory rate depends on age (50 as a general number)

retractions: intercostal, sub costal, supraclavicular 

PO intake: Decreased 

Other: apnea, cyanosis

                   -Management:

-examine patient from waist up.  Evaluate signs of respiratory distress of heart disease

                                      – supportive care: O2 vs HFNC prn, IV, Suctioning

Asthma

-Clinical Presentation: Dyspnea wheezing and cough, can have retractions due to obstruction, AMS in those with impending ventilatory failure

-Complications: pneumothorax and pneumomediastinum 

-Management: CXR not routine

                   -albuterol

                   -ipratropium both nebulized

                   -magnesium 50-75mg/kg bolus 

-Ventilation: Intubation

                   -incidence is 0.55% associated with higher mortality

-Complications: can cause cardiac arrest, hypotension occurs as a result of hyperinflation leading to decreased cardiac preload 

-Expiratory time: 4-5 second I:E ratio should be 1:4

-Ketamine for sedation

Lightening Lectures

Pleural Effusions: Alaina Royalty, MD PGY1 

-Abnormal collection of fluid within the pleural space between parietal and visceral pleura

-Transudative: increased hydrostatic pressure or low oncotic pressure: CHF, Cirrhosis, Nephrotic, PE, Hypoalbuminemia, myxedema, peritoneal dialysis, SVC obstruction

-Exudative: occurs due to inflammation and increased capillary permeability: Pneumonia, Cancer, Tb, viral infection, PE, autoimmune, GI disorders, Chylothorax, medications 

-CXR: at least 200ml required to be seen on upright AP/PA 

– blunting of costophrenic angel 

-US thoracic: detects as little as 5-50cc’s best to have the patient is sitting up

-Thoracentesis: 

– New effusions with unknown cause likely need diagnostic thoracentesis: however, does not typically need to be done emergently 

–Therapeutic: should be done for massive effusions mediastinal shift, hemodynamic instability if you suspect empyema, or esophageal rupture this will be done in THE EMERGENCY DEPARTMENT

                   –Test: cell count differential, pH, protein, LDH, Glucose 

                                      – REMEMBER LIGHTS CRITERA via protein, LDH 

Acute Respiratory Distress Syndrome (ARDS):  Craig Schutzman PGY1

-Non cardiogenic pulmonary edema

-Clinical: worsening dyspnea, hypoxemia and bilateral diffuse crackles

-Many common cause: sepsis, pancreatitis, TRALI, trauma

-Pathophysiology:

-Exudative phase proliferative phase Fibrotic phase (bad prognosis)

– Berlin Criteria 

– Labs: are non specific But get proBNP/BNP

-ABG: elevated pH, low PaO2, Low PaCO2, low-normal HCO3 (acute hypercapnic respiratory acidosis indicated severe disease, impending respiratory arrest)  

-Imaging: CXR: diffuse ground glass opacities, CT chest: bilateral opacities widespread 

-Management: 

-treat underlying cause

-Supplemental oxygen

-Analgesia, sedation and paralysis

       – Sedation improves tolerance to ventilation and decrease oxygen consumption

-Lung protective Ventilation

       -Ventilator Mode: Volume AC

       – tidal Volume: low per Ideal body weight -6 cc/kg

       – Inspiratory flow rate 60-80 lpm

       -respiratory rate: 16-18

       -FIO/PEEP: titrate to spO2 goal 88-95% (can have permissive hypercapnia)

       -maintain plateau pressure <30 mmHg to prevent barotrauma 

–GO TO ARDS NET FOR ALL YOUR ARDS FRIENDLY INFORMATION!

-PRONING ventilation: V/Q mismatch improves as depending lung receives majority of blood flow as alveoli open 

-Steroids: only give if severe, look at the Meduri Protocol 

-ECMO:  early application <1 week is crucial for success 

COPD Exacerbation: Mitchell Weeman PGY1

-Persistent air flow limitation that is progress and assisted with enhanced chronic inflammatory response in the lungs to noxious particle or gas 

-Clinical: dyspnea, productive cough, decreased physical activities, +/-wheezing.  End stage: cor pulmonale, muscle wasting, chronic ventilatory failure

-Diagnosis: via PFT

-Management: 

                   – ABC: IV, telemetry, O2 saturation, vitals

                   – O2 correct to baseline if unknown 90-94%

                   -EKG, trop, BNP, CXR, CBC, CMP, ABG for accurate PaO2 

                   – Mild: DuoNeb or single agent +/-steroids and abx

-Moderate: same as mild plus Prednisone 60mg or Solumedrol 125mg IV and abx, /-Magnesium, BIPAP

-Severe: same as above: plus BIPAP (10/5 is a good setting) , IV steroids. 

       – +/- intubation use ketamine or etomidate (FIO2100%, TV 6-8 cc/kg, RR: 8-10, PEEP 5-8) 

       -Magnesium

-Disposition:

-Uncomplicated: can go home- they have no comorbidities, <65 y/o <3 exacerbations per year, FEV >50% 

       -Give steroid 3-5 days, abx refill nebs and follow up with PCP 

-Complications: new or increased o2 requirements or needing BIPAP, AMS due to hypercapnia, inability for self care or risk of poor follow up 

Room 9 follow up

MB Hatch PGY3 

-for Boards do not take a hypotensive patient to the CT scanner 

-resuscitation is key 

Cognitive dispositions to respond

-Anchoring and diagnosis momentum

-Base rate bias, multiple alternative bias, and confirmation bias

-Commission and Omission Bias: feeling bias that you have to intervene 

-Feedback sanction: we don’t see the long-term consequences 

-Gamblers Fallacy thinking that everything is going to be fine because everything else has been fine 

-Overconfidence and sunk cost

-Vertical Line failure: patterns of thinking, and not straying from the regular thinking. You need to lateral think as well

-Visceral bias: doing things by anticipating what people want from you 

What can we do?

-Practice mindfulness, ask yourself “what else might this be?”, create metacognitive processes, contribute to a supportive culture, participate in institutional review 

Ventilator Management: 

Dr. Richie 

-Indications: Acute failure, airway protection, respiratory arrest, upper airway trauma, relive work of breathing operative procedures 

-Oxygenation improved with increased FIo2 and increase PEEP

-Ventilation: respiratory rate and tidal volume 

-PIP : Peek Inspiratory pressure

                   -pressure at the end of inspiration

                   -high peak pressures are not good >30 or 40

-Compliance: change in volume/change in pressure 

-most people >50, intubated about 30

-ARDS is 15 or less 

-decreased compliance: pulmonary edema, pneumonia, ARDS, pneumothorax, obesity, burns, ascites, abdominal compartment syndrome.

-Increased: COPD 

Modes of Ventilation: 

-Pressure: push in a constant pressure (flow will vary)

-Volume: push in a constant flow (pressure will vary) 

Types of breaths

-Mandatory: machine initiated, machine does the work  

-Assisted: patient initiates breath, patient does some work and ventilator assists 

Assist control Ventilation (AC) 

-set rate and set volume or pressure

-If patients breathe over set rate it will assist at the same preset volume or pressure

• If a patient wants to take a breath at 10 sec they will get 500cc regardless of whether he wants 300cc or 700cc

SIMV: similar to assist control but patient initiates breaths can be different set support

Pressure Control: set pressure. Variable flow, set rate, Cycle time: 

• You set I time 

Volume Assist control: set volume, variable pressure, set rate Cycle time 

• If patient wants more volume because they feel air hunger it wont let them get more flow, it can be very distressing
• COPD, increased dead space, may need larger volume, and patient can feel distress because they need a much larger flow and

Pressure Support: set pressure, variable flow, patient determined RR, cycle flow

• There is no back up rate 
• Most tolerable and most like natural breathing 
• Good for COPD, but you need to think about I:E Ratio 

PRVC: pressure give can change breath to breath 

• Best of both worlds 
• Need to give I time (set to 1 second) 

Trouble shooting: 

Peak inspiratory pressure vs Plateau Pressure 

High plateau: alveolar level problems

-inspiratory pause and they are very different: something wrong with large airways, or ventilator problem

                   – easy to bag vent problem, hard to bag large airway vs ET tube problem

-not very different think alveolar 

Air trapping: responds to increased PEEP, bronchodilators,

-Ineffective trigger: if patient is spontaneous breathing are they triggering the ventilator 

Ventilator induced lung injury

Conference 10/7/2020

CCU follow up

-John Cook, PGY1 

45 y/o male with syncope vs seizure. Patient had a syncopal episode en route and was pulseless during this episode. Did resolve upon arrival to the ED.  With concerning rhythm strip.

EKG: NSR, rate 65,1^st degree AV block, LBBB, no ischemia 

Continued to have syncope with pulselessness of 5-10 seconds. Patient had 2^nd degree type II and 3^rd degree AV block.

-placed on dopamine gtt and push does epi, and placed on epi gtt

-Cardiology placed transvenous pacemaker 

Acquired Complete Heart block:

-ischemia/infarction

-Neuromuscular disorders

-Infectious: Chaga, Lyme’s 

-Metabolic

-Cardiomyopathy

-Iatrogenic causes: medications 

Patient also traveled to places endemic to Lyme’s disease 

Lyme disease: treatment Doxycycline

Disseminated Lyme disease: IV Ceftriaxone 2g daily 

MICU follow up

Blaine Jordan, PGY1 

75 y/o transferred from OSH (Jewish) presented with Digoxin toxicity with hyperkalemia and bradycardia, and Warfarin toxicity.  Along with lactic acidosis and sepsis positive

Labs: WBC 18.3, Trop 0.0, Potassium 4.9 (was higher), INR: 7.2 Digoxin level >9 (normal high is >2) 

Digoxin Toxicity

-Digoxin causes increased inotropy, increases vagal tone and decreased conduction through SA and AV node 

-Toxicity: 

Cardiac: arrythmias basically any arrhythmia. 

GI: vague

Neurological: AMS 

Metabolic: hypo/hyperkalemia 

       Hyperkalemia: acute toxicity

EKG: Digoxin effect: Salvador Dali – ST Depressions in lateral leads 

U waves prominent, flattened inverted or biphasic T waves, shorten QT 

Treatment: Digoxin Antibody Fragments (FAB)

-indications: life threatening/ hemodynamically unstable arrythmia, Hyperkalemia >5.5, evidence of end organ damage

-10 vials adult and 5 vials for children 

-Calcium not recommended for HyperK, and treating hyperK does not decrease mortality 

CALL POISON CONTROL! 

Capstone

Cal Staben, PGY3 

Hypothermia: Core Temp <35oC

-Potassium: >7 mortality outcomes increase 

-Cardiovascular: 

EKG Changes: Osborn Wave-J Wave (32oC and below), prolonged PRQRSQTc prolongation, bradycardia (50% <28oC), Hypotension and decreased CO (50% at <25oC) 

Arrythmia: VF and asystole 

Vasoactive and electricity is not going to help need to warm >30oC 

-CNS

                   Losing Shivering <31, loss of corneal reflexes 23-25oC and flat EEG <19oC 

-Respiratory

Bradypnea, decreased compliance, respiratory acidosis, change in airway anatomy (Trismus), drug physiology (decrease doses) 

-Coagulopathy: Thrombocytopenia, PTT Prolongation and DIC 

Rewarming

-passive rewarming, Warm IVF, Invasive rewarming (bladder/gastric/peritoneal/thoracic), Dialysis/ECMO

Frost bite

1^st degree: mild edema

2^nd degree: superficial vesiculation, erythema, edema (bulky warm dressing, lance blisters) 

3^rd degree, hemorrhagic blisters (lance blisters and pharmacologic treatment) 

4^th: complete extension through dermis into muscle and bone (most likely amputation)

Treatment: 

-Field Management -prevention-socks, pain control (ibuprofen 12 mg/kg/day), rewarming

-Hospital: consider thrombolytics if deep <24 hours after thaw, Iloprost (vasodilate and platelet aggregation) within 48 hrs after thaw, source control (amputation) 

Clinical Pathway-Management of Pneumonia

Zach Heppner, Michael Carter PGY2 

Pneumonia -new lung infiltrate plus clinical evidence that the infiltrate is of an infectious origin, with new onset fever, purulent sputum leukocytosis and increase O2 demand

                   Viral Pneumonia, Fungal Pneumonia, Mycobacterium (Tb), Bacterial 

CAP

-Strep pneumo, H flu, Moraxella, 

-Atypical: mycoplasma, Legionella, Chlamydia pneumoniae 

-Aspiration: Klebsiella, anaerobes

-high macrolide resistance don’t use as monotherapy (especially in Kentucky) 

HAP/VAP (multi-drug resistant) 

-Staph aureus, Pseudomonas, ESBL-GNB, VRE 

-HCAP is no longer a thing  since 2016 

Risk Stratification scores 

PSI/PORT Score-See MD calc (score >90 patient should come in to the hospital)

CURB-65

-BUN >19, RR >30, SBP<90 or DBP <60, Age >65. Score >3 admission

MDRO Risk factures: MRSA, pseudomonas, ESBL, VRE

-risk factors: BIGGEST RISK FACTOR prior IV abx in 90 days

Outpatient Abx therapy for CAP

-no comorbidities: Amoxicillin or Doxycycline or Macrolide (remember in Kentucky macrolide as monotherapy is a no no)

-Comorbidities: Augmentin or Cephalosporin AND macrolide or doxycycline.  OR monotherapy with respiratory Fluoroquinolone (Moxifloxacin, gemifloxacin and Levofloxicin) 

Inpatient treatment CAP

-non severe: Beta-lactam _Macrolide OR respiratory fluoroquinolone (if prior MRSA add coverage)

-Severe: Beta lactam + Macrolide or Beta-lactam +Respiratory fluroquinolone (add coverage if MRSA previously).

                   Remember add coverage if IV abx in the past 90 days

COVID pneumonia

-RECOVER TRIAL

                   Effect of dexamethasone on 28-day mortality in COVID- mortality benefit based on severity

                   Intubated group: more benefit 

-Dexamethasone use

                   IDSA does not recommend

                   In severe pneumonia may cause more benefit 

-Airway Isolation Precautions 

Pathway- Please see Room 9er 

Radiology-Chest CT

Dr. Van Bogaert

Protocols: 

-CT chest with contrast: looking for confirmatory for pneumonia.  You get okay visualizations of aorta, soft tissues and lungs. 

-PE protocol: inject contrast looking at the pulmonary artery, and once it reaches a threshold then scan the patient and the contrast will be in the pulmonary arteries 

-MAN, scan CT Chest abdomen and pelvis (a CTA chest essentially) – similar to PE protocol however shows aorta and its branches between  

-CT non-Contrast: confirming pneumothorax, pleural effusion, pneumonia. You don’t need to look at solid organs

Start on the inside and work your way out

-looking at vessels: window level abdominal angio

-looking on sagittal view can help you see pseudoaneurysm and confirm dissections 

-always look at pulmonary arteries: incidental PE’s can be found.  Also looking at the sagittal view can help you view smaller PE’s 

Pulmonary vein is not as opacified as the pulmonary artery, so make sure you are looking at the artery for PE. Follow the filling defect back and the pulmonary vein will go into the atrium 

Lung window

• Good for pneumothorax, pulmonary nodules show up well 
• Look for bronchial injuries
• Pneumonias 
• Pulmonary contusions 

Bone Window

• Especially look in trauma patients
• Sagittal images are good for chest trauma- sternal fractures and first rib fractures, scapular fractures 

Best way to approach- step by step look at individual structures

Vessels heart, mediastinum,airwaylungs bones 

Toxic Gases

Dr. Bosse

Nerve Agents: potent organophosphates

• Usually a liquid 
• Depends on temperature and pressure: can be a fine line between gas and a liquid/solid 
• Toxic Gas Classification
  • Irritants
    • High water and lower water solubility
      • High: rapid onset and upper airway
      • Poor: delayed onsent and lower lung injury 
  • Simple asphyxiants
  • Systemic (formerly chemical) asphyxiants 

Anhydrous ammonia:

• Fertilizer, pesticide, pharmaceuticals, refridgerater gas, disinfectant 
• Highly water solubleammonia hydroxide and you get chemical burns
• Sx: nasal and throat eye irritation 
• Tx: remove from source, symptomatic and supportive care 

Chlorine

• Manufacturing non agricultural chemicals, paper industry, household bleach, water purification
• DON’T MIX HOUSEHOLD BLEACH and ACIDIC DRAIN CLEANER
• Intermediate water solubility, heavier than air and reactive and explosive
• Tx: remove from source control and supportive care
  • Neutralization with nebulized sodium bicarb 

Phosgene

• Low water solubility, colorless gas and 3.4x heavier than air 
• Can smell like “musty hay” 
• Can cause latent development of lung injury 
• Tx: removal from source and symptomatic and supportive care
• Admission for observation of delayed signs and symptoms

 Asphyxiants 

Simple asphyxiants displace oxygen from environment (Helium, CO2, Nitrogen, methane. Ethane, CO)

• Signs and s related to hypoxemia 
• Treatment: remove form source, supplemental oxygen, supportive care 

Systemic

• Inhibit binding of O2 to the cells. 
• Carbon monoxide, cyanide and hydrogen sulfide
• CO
  • Fires, engine exhaust, heating equipment, methylene chloride, cigarettes, endogenous production
  • Bind to Hbg and forms Carboxyhemoglobin 
  • Clinical effects: cardiac (tachycardia, arrhythmias) and neurologic (AMS, seizures, HA Very common) 
    • Delayed neurological effects: Parkinsonism, peripheral neuropathy, behavioral disturbances, incontinence, dementia 
  • Lab Dx: Carboxyhemoglobin, can be determined on a VBG 
  • Tx: oxygen, and hyperbaric oxygen (does it work)
    • HBO indications: syncope, coma, seizure, AMS, COHbg >25% and pregnancy >15% 

• Cyanide
  • Plants, labs, industry, nitroprusside, laetrile (Cancer tx), acetonitrile, combustion/smoke inhalation 
  • Clinical manifestations: involvement of oxygen sensitive organs:  CV and neurologic manifestations.  May have a brady arrhythmia prior to demise 
    • Bitter almond odor
  • Labs: CN levels, metabolic acidosis, lactic acid
  • Tx remove from source and decon with protective gear for liquid or solid exposures. Then symptomatic and supportive care
  • Antidotes: nitrites, Thiosulfate and hydroxocobalamin
    • Indications for hydroxocobalamin- Per Bosse hemodynamic instability, metabolic acidosis with elevated LA, AMS 
• Hydrogen Sulfide
  • Bacterial decomposition of protein, sewer gas, industry, inhibition of Cytochrome oxidase
  • Antidote: amyl nitrite and sodium nitrite 

Dr Bernadoni Right Heart Failure

PULMONARY HTN +  RV SPIRAL OF DEATH-

Definition is mean pulmonary artery pressure >20mmHg (on R heart cath). This can be estimated based on PA pressure >35 on echo

• In patients with acute PE or with chronic pHTN and an acute VQ mismatch (eg pneumonia)

• This is translated as an increased afterload on the RV, which does not tolerate this well. Pt becomes hypotensive, shocky.

• Of note the LV will appear underfilled and hypokinetic on XR- this does not represent hypovolemia and the heart will not respond well to fluid administration.

• RV vs LV perfusion- LV gets perfused only during diastole, whereas under normal circumstances the RV gets perfusion throughout the cardiac cycle. When pHTN is present (and right heart pressures are subsequently high) the transmural pressure across the RV only allows perfusion during diastole, causing ischemia and reduced contractility. It can also leads to relative or bradycardia through hypoperfusion of the SA/AV node

This group of events is known as the RV spiral of death.

HOW TO AVOID IT-

Fluids-

These pts are rarely volume responsive in a good way. Fluid administration pushes them further into above spiral

(In the setting of PE or chronic RHF/pHTN) when patients have evidence of R heart failure on echo (dilated RV, Mcconell’s sign, low TAPSE) they will not respond well to further fluid administration.

If their RV looks small/empty too, may consider a very small fluid bolus and evaluate for effect.

Most patients will benefit from diuresis, even when they are hypotensive and have LV underfilling (diuresis improves RV function and allows the pt to better fill their LV and increase their CO

PRESSORS

Instead, aggressively support MAP with pressors-

Aim is to raised MAP without raising pulmonary blood pressure

• Norepinephrine is go to- increases contractility, gives peripheral vasoconstriction and at low doses should increased pulmonary vascular constriction much
• Vaso is next line- gives peripheral vasoconstriction but actually reduces pulmonary pressures- this is exactly what is wanted
• Can consider dobutamine as third line- start at 5mcg/kg/min

AIRWAY MANAGEMENT (+INHALED MEDS)

• Intubation should be avoided if at all possible.
• Consider use of nitric oxide prior to intubation (via BIPAP/HFNC)- see below
• Paralysis causes hypoxia and hypercarbia- leading to hypoxic vasoconstriction and worsened pulm HTN and RV afterload
• PPV increases RV afterload and reduces output

SO:

• Have push dose pressors ready and strongly consider placing an arterial line prior to intubation
• Have atropine at bedside
• Use etomidate for sedative (ketamine may increase pulmonary vascular resistance)
• Do not use straight RSI- continue ventilation (bagging or BIPAP)
• Can break from ARDS net protocols and consider high FiO2 without raising PEEP as much as normal. Keep plateau AND PEAK pressures low

If pt remains hypotensive/hypoxic use inhaled nitric oxide- start at 40ppm

Or consider inhaled epoprostenol

In the absence of the above nebulize 5mg of nitroglycerin

SYSTEMIC VASODILATORS

Many chronic pHTN pts have continuous vasodilator pumps running

If pt has pump failure/otherwise their systemic meds are stopped restart them at the same dose immediately. They can be given peripherally if necessary

MASSIVE PE

SBP <90 for 15mins (submassive PE is with RV strain based on trop, BNP, echo etc)

• Thrombolysis if bleeding risk is acceptable (this is a case by case decision taking into account a large number of factors). Note that is unclear how much thrombolysis actually causes bleeding in acute PE (studies show similar rates of bleeding with heparin alone cf heparin and tpa)
• In patients with a pulse typical is 100mg IV tPA over 2h. Can give 10mg as a push and the other 90 as an infusion over the 2 hours
• In cardiac arrest 50mg IV push
• Note above doses have minimal evidence base.
• Run heparin concurrently

INTERVENTIONAL THERAPY + ECMO

Catheter directed therapy recommended in patients with high bleeding risk, tPA contraindicated. This should initially be percutaneous embolectomy, can use catheter directed thrombolysis (tPA) if unsuccessful.

ECMO- Extra-corporeal membrane oxygenation

In PE ECMO is run Venousà Arterial (VA ECMO).

This allows circulation to bypass the heart and lungs, bypassing the failing right heart and the elevated pulmonary pressures. Helpful with the R heart failure of PE (or the reduced CO in STEMI, myocarditis, low+slow poisoning etc)

In patients with pure lung pathology (ARDS, asthma, pulmonary contusion) it can be run Venous-Venous (VàV), which bypasses the lungs but still requires good cardiac function

Consider ECMO if non ECMO mortality is >50%, even more so if >80% (and has ECMO responsive pathology)

Reserve for pts likely to have benefit (reversable cause of current illness, no major life limiting comorbidities or advanced age) and less likely to have harm (pts require heavy anticoagulation so those with high bleeding risk are likely to be harmed)

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Josh Senn- GU abx

• Don’t treat asymptomatic bacteria (>10⁵ CFU) without symptoms unless pregnant or a guy pending a urological procedure

• Use nitro 100 bid (if CrCl >30) or cephalexin qid for 5 days for uncomplicated UTI in a male or female

• Chlamydia- use 1g azithromycin PO one time. Use doxy 100mg BID for 7 days if PID. Second line levofloxacin, erythromycin, ofloxacin.

• Gonorrhea- Ceftriaxone 250mg IM x1 (+azithro or doxy). Alternatives are cefixime or gentamicin + azithro

• Trichomoniasis- metronidazole 500mg PO BID x7 days has higher cure rate than 2g one time. Topical gel does not have good cure rate. Alternative is tinidazole

• BV- 500mg BID x 7 days, can use vaginal gel BID x 7 days. Alternatives are clinda or tinidazole

• Benzathine penicillin 2M units for primary or early latent. More complex with neurosyphilis

Avery- phimosis and paraphimosis

Conditions presenting in uncircumcised or partially circumcised males.

Phimosis-

Inability to retract the foreskin

This is not an emergency. It is present physiologically at birth but most males can retract by age 5-7.

Becomes pathological when a constricting band forms between glans and foreskin.

Do not retract forcefully- treat with topical steroids and gentle daily traction, admit to urology if there is urinary obstruction

Paraphimosis-

Inability to protract the foreskin

Can cause necrosis within hours to days

Tx is manual reduction-

• Pretreat with ice/mannitol/sugar
• Dorsal penile nerve block
• Hold foreskin between index and middle finger of both hands, use both thumbs to push the glans whilst pulling the foreskin
• If this fails can consider protraction using forceps, multiple need punctures to foreskin to allow improvement edema, or aspirate glans
• As a last resort, to be performed if the above techniques fail AND urology is not available, incise a dorsal slit using scalpel, protract foreskin and then suture the inflicted wound

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Dan- Testicular torsion-

Usually caused by an abnormal fixation of the testicle within the tunica vaginalis (when present this is usually bilateral)- most commonly the bell-clapper deformity

Bimodal distribution- perinatal and at puberty. Can occur at any age but is less common over 40.

HPI/Exam

• Unilateral testicular/flank/lower abdominal pain. This is not usually positional. May be atypical or colicky pain
• In children commonly presents only as vomiting or abdominal pain
• Testicle is usually firm, elevated and in transverse lie
• Unilateral loss of cremasteric lie may increase suspicion but is not specific and is not always present/easy to identify

Differential-

• Appendiceal torsion- isolated torsion of the testicular appendix- presents with more focal pain on the posterior portion of the testicle- ‘blue dot sign’ may be seen
• Epididymitis/epididymo-orchitis- inflammation, most commonly infectious of the epididymis and/or testicle. Most commonly cause by STI in those <35, UTI in those >35 (though this is not a hard/fast rule). Look for isolated tenderness over the epididymis, symptoms of infection, prehn’s sign

Mx-

• If the diagnosis is clear contact urology immediately
• In the meantime provide supportive care
• If urologist is delayed or not available can attempt manual detorsion- manually rotate the affected testicle externally- ‘open the book’. Most testicles torse internally (internal rotational) and so the opposite motion is used to detorse. However, not all testicles torse internally, so this could worsen the patient’s condition. When effective, 540 degrees of external rotation is usually required

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Austin- Hernias-

Abnormal exit of tissue or an organ through the wall of a cavity within which it normally resides

Most common-

• Inguinal hernia- presents as groin mass. Direct inguinal hernias pass through the transversalis fascia in the Hesselbach triangle (triangle formed by inguinal ligament, rectus abdominis and the inferior epigastric vessels). Indirect inguinal hernias pass through the internal and external inguinal rings
• Ventral hernias- bowel passes through a defect in the anterior abdominal wall- can be umbilical, epigastric, incisional
• Femoral- bowel protrudes through the femoral canal. These are much more prone to strangulation and incarceration, and require urgent f/u, even if not currently incarcerated/obstructed/strangulated
•     Protrusion of the stomach through the diaphragm and into the thorax- often presents as ‘heartburn’/epigastric discomfort

Hernias should be soft, non-tender and reducible.

• Incarceration is the inability to reduce the hernia back into the cavity within which it should reside. This term is used when blood flow to the herniated section of bowel is maintained. Symptomatic hernias should be reduced in the ed to avoid strangulation.

• Strangulation is when blood flow to the hernia is impaired- this causes ischemia, necrosis, perforation, sepsis. These should NOT be reduced as this makes the ischemic portion of bowel difficult to find and moves potentially necrotic tissue back into the abdomen, causing infection. Strangulation should be suspected in a pt with significant pain, tenderness, any skin change or findings of ischemia on ct/elevated lactic acid.

Reduction-

• Grasp and elongate the hernia neck with one hand whilst applying steady pressure to the proximal portion of the hernia at the neck of the fascial defect. Pushing on the most distal portion of the hernia simply causes the hernia to bulge more proximally, preventing reduction through the fascial defect

Complications of reduction-

• Risk of reducing strangulated bowel
• Reduction en masse- this is reduction of the majority of the hernia, often with improvement in symptoms. However small portions of bowel can remain incarcerated and remain at risk for strangulation. Watch hernia patients post reduction to ensure complete resolution of symptoms- consider ct/ultrasound/surgical review if any ongoing symptoms

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Dr McGee Renal Emergencies-

Indications for emergent hemodialysis-

A- Acidosis- dialyze for pH <7.1

E- Significant electrolyte abnormality- especially hyperkalemia

I- Intoxications

O- Overload/oxygenation

U- Symptomatic uremia

Consider rhabdomyolysis as a cause for renal failure, especially in pts unable to provide good history. Tip offs are hepatitic pattern LFTs and dipstick hematuria without blood on micro.

Hyperkalemia-

Weakness, symptoms of causative pathology, AMS.

EKG changes with peaked T waves, prolonged QRS à sine wave

EKG changes do not always progress smoothly through the above stages- pts can go from NSR with narrow qrs to asystole very quickly.

Mx-

• Stabilize the membrane- with calcium. Gluconate if stable, chloride if unstable or if pt has central access
• Move the potassium back into the cells- Insulin and glucose, fluids, albuterol, bicarb if acidotic
• Typically 10 units of insulin in 1 amp of d50 is use, but this depends on the pt. if they are normoglycemic consider 2 amps of d50. If they are very hyperglycemic may consider not giving glucose. REGARDLESS, IT IS IMPERATIVE THAT BLOOD GLUCOSE IS CHECKED REGULARLY TO MONITOR FOR HYPOGLYCEMIA
• Give fluids- LR does contain potassium but the amount is negligible and not clinically significant. LR is a better choice than normal saline as the NAGMA caused by NS will increase potassium more than the minimal potassium contained in LR
• If acidotic- can bolus bicarbonate and then use 2-3 amps of bicarbonate in d5w for fluid resuscitation/maintenance
• If the patient is volume overloaded use furosemide. If normovolemic give fluids and furosemide. Can discuss diuretic use with renal if pt is hypovolemic/dry.
• Dialysis if all else fails

Drug intoxications-

Many drugs can be dialyzed out of the blood stream-

• LEMS mnemonic
• Lithium
• Ethylene glycol
• Methanol
• Salicylates
• (and others- these are the most commonly encountered clinically)

Discuss with poison control

Uremia-

End organ damage-

• Pericarditis or uveitis
• Uremic encephalopathy
• Bleeding- uremia causes platelet dysfunction

Hemodialysis access-

• Short term dialysis access- shiley/trialysis catheter- a necessary skill for EM
• Medium term- Tunneled dialysis catheters
• AV fistulas- most commonly brachiocephalic
• Peritoneal dialysis catheters

Complications of AV fistulas-

• Acute bleeding- direct pressure with a finger may stop bleeding. TXA soaked gauze may help. Avoid tourniquet placement if possible. Figure of 8 sutures can be placed if necessary, though above options should be exhausted prior. Note that heparin is given during hemodialysis- if bleeding is hard to control can give protamine, though risk of allergic reaction is common. DDAVP can improve platelet function in pts with azotemia.

• Call vascular for any fistula or graft issues

• Infected HD catheters can cause sepsis. Look at the site. Metastatic infection from the catheter is also common and can cause septic arthritis, osteomyelitis etc

• PD patients should always have clear peritoneal fluid. Abdominal pain/fever in a PD pt can be a sign of peritonitis. Dx for PD related peritonitis is different than SBP when assessed with fluid microscopy. >100 PMNs or >50% PMNs is suggestive of infection

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SANE lecture

Sexual Assault Nurse Examiner

Purpose is to evaluate and treat victims of sexual assault, collect evidence and document injuries

See male and female victims of sexual assault age 12 or older

Injury terminology-

Contusions- These are bruises. Either term is acceptable. Do not attempt to date bruises, though it can be stated that bruises are in different stages of healing

Abrasions- Scrapes/grazes/road rashes are abrasions. Vaginally, these are most common at 5 and 7 o clock.

Petechiae- burst capillaries, appearance like paint splatter. Can be the result of direct pressure or of strangulation

Incised wounds are not lacerations and should not be documented as such. Incised wounds are inflicted by sharp objects such as a knife or a piece of glass. When these are described as lacerations it may cast doubt on the mechanism of injury/use of weapons. Simple puncture wounds should be described as such – ‘puncture wound’.

Pattern injuries are bruises/contusions whose shape is suggestive of a specific mechanism (eg a bat, a bite mark). Describe these injuries as pattern injuries and document the patient reported mechanism of injury. Photographs and forensic experts will determine mechanism

GSWs- Describe as GSW or penetrating injury. Do not document entry/exit wounds- photographs and expert review will determine this

Royalty- CCU Follow Up
CASE-
37yo M, GSW to chest
Awake, stable.
RUQ fluid, no pericardial effusion.
Bullet fragment in pelvis on xray, cxr unremarkable.

Ex-lap w extensive intra-abd injury
Trans diaphragmatic pericardial window performed

POD2 pt develops chest pain
EKG with anterior q waves. Upright T wave in V1.

LEARNING POINT – Assess precordial T wave balance when you see an upright T wave in V1. Typically T waves should be more upright in V6 than in V1. If they are more upright in V6 consider ischemia in the right clinical setting.
(exceptions include LVH, LBBB, others)
BACK TO THE CASE
Pt’s troponin returned elevated and went for cath- 90% LAD, LCx with total occlusion, RCA with 90%

Pt was diagnosed with T2 NSTEMI due to low flow state in the setting of chronic obstructive CAD without acute plaque rupture

TAKE HOME-
Beware upright T waves in V1- suggestive of underlying or acute ischemia
In this setting assess precordial t wave balance
Always follow serial EKGs when concerned for ischemia

Additional discussion-
Look for signs of prior MI, may act to increase suspicion/pre-test probability for acute MI

Type 1 MI- ischemia secondary to plaque rupture
Type 2 MI- ischemia secondary to reduced blood supply (often in the setting of chronic CAD

Weeman- MICU f/u

CASE
38yo F G6 P4 presents at 20W+1D. dyspneic, pleuritic chest pain.
PMH with protein S deficiency, prior TIA during a previous pregnancy
Uses enoxaparin, methadone. Hx of drug use and alcoholism
On exam pt is in resp distress, 92% on 14L NRB. B/L reduced breath sounds
No obvious DVT
Workup w bilateral CXR infiltrate- ARDS pattern, TTE with EF 69%.

– Pt was admitted to MICU, 45L, 100% on HFNC. On abx and steroids

– Gradually worsened, became uncooperative but was eventually intubated around 1 week into stay.

– All infectious cultures and covid swab were negative, abx were stopped

– Eventually weaned vent and extubated to 4.5L NC. Sent to floor, began to deteriorate but refused ICU. Overnight BIPAP on the floor, then to HFNC and moved to ICU

– On return to ICU was started on 40mg methylprednisolone 40mg q8 and improved, transferred to floor and now on 2L

Dr Hart Neonatal ED Presentations
INTRODUCTION
Normal neonates undergo significant stress + change-
Drop in pulmonary pressures causes increased pulmonary circulation
PDA closes

Most common ER attendances are jaundice, difficulty breathing, fussiness, feeding problems, stooling issues and irritability/lethargy

Fussiness
****Differential- IT CRIES****
– I- infection
– T- Trauma.tourniquets
– C- Cardiac disease
– R- Reflux/rectal fissure, reaction (to meds)
– I- intussusception
– E- Eyes (corneal abrasion, foreign body, glaucoma)
– S- strangulation, surgical process (hernia, torsion, volvulus)
**Do a FULL exam**- take special note of HEENT, HR/monitor, GU, extremities for tourniquet, fracture, septic joint
Hair tourniquet- Usually extremities. Also penis/clitoris. Can usually unwind w forceps. If required can incise through hair, skin.
Corneal abrasions- Look for conjunctival injection. Flurorescein stain

Jaundice-
Newborn jaundice is usually catabolism of hb  unconjugated
First thing is to send fractionated bili to assess
Unconjugated causes- Physiologic, breast milk jaundice, Hemolysis- ABO incompatiblity
Conj-

Jaundice in first 24 hours of life is ALWAYS pathologic

1- Send fractionated Bili
2- Compare this to the normogram to assess home vs inpatient, phototherapy vs exchange transfusion
3- other labs, eg type and screen if requires exchange transfusion

Conjunctivits-
12-24hours of life- Chemical
2-5 days- Gonorrhea
5-14 days- Chlamydia
Gonorrhea is typically more severe and more purulent
Send pus for drain/culture- for either chlamydia/gonorrhea admit for parenteral abx (topical treatment used only for prophylaxis against gonorrhea)

Feeding/stooling problems
Feeding-
Newborns feed on demand, may be small, frequent intake, not concerning unless gaps >4 hours or so
By 1 month usually take 2=4 hours every 2-4 hours
Spitting up often secondary to overfeeding

Stooling-
Rule of 7s- >7 times per day abnormal, 100.4) <4 weeks, or <60 days if they look unwell- full sepsis workup for SBI- CBC, CMP UA, CRP, Procal, LP, urine and blood culture. CXR if resp sx.
Above may change with new literature on use of procal. See protocols in peds ED
Most common pathogens at this age are GBS, E Coli, Listeria (also consider HSV, and if any suspicion at all test and treat early)
Ampicillin and cefotaxime / amp and gent as broad abx coverage (switch ampicillin for vancomycin if high concern for meningitis)
Sepsis mimics- pertussis, CHD, Inborn error of metabolism
Always look for omphalitis- assess the umbilical stump for cellulitis, swelling, drainage, crepitus. This can progress from mild appearance to fatal very quickly (hours) given proximity to central vasculature and peritoneum. Usually cause by staph

Seizure like activity-
Differential- Seizures, infantile spasms, hypoglycemia, benign myoclonus, uncoordinated sucking movements, disconjugate eye movements
Check glucose, check temperature, cbc, rfp, magnesium

Seizure aetiology-
– Perinatal asphyxia/hypoxia/cerebral ischemia
– Infection
– Hypoglycemia
– Hyponatremia How are they making formula (too much water hyponatremic seizures)
– Trauma (SDH)
Seizure neonate mx-
1st Line- Lorazepam 0.1mg/kg
2nd Line- Phenobarbital 20mg/kg (Or levetiracetam 60mg/kg)
If seizures aren’t controlled with above and electrolytes/glucose are normal give pyridoxine (as well as other third line seizure meds)

Congenital heart Disease
Will present with shock, cyanosis, heart failure- poor perfusion, difficulty feeding, respiratory distress, hypoxia, hypotension
Crashing neonate is statistically more likely CHD than sepsis
Get four extremity blood pressures
Note absence of response to O2 suggests cardiovascular abnormality, presence of response suggests pulm
Cyanotic –
– Truncus arteriosus
– TGA
– Tricuspid atresia
– ToF
– TAPVR
– HLHS
Non cyanotic-
– ASD
– VSD
– AV canal
– Coarctation
Have a VERY low threshold for starting prostaglandins in crashing/hypotensive neonate but watch out for respiratory depression.
Once on this pathway target SaO2 of 75-80%
If prostaglandins aren’t working, consider adding inotropes in discussion w pediatric center. Consider dx of persistent pulmonary hypertension. Prostaglandins don’t work- pt’s require hyperventilation, nitric oxide, ECMO

Dr O’Brien- introduction to ED Echocardiography
4 main views used in the ED-
– Parasternal long axis (often PSLAX)- for effusion, EPSS, LVOT diameter, visual assessment of LVEF
– Parasternal short axis (often PSAX)- for AV/MV assessment. For right heart strain, regional wall motion abnormality
– Apical four chamber (often A4C)- For TAPSE, other right heart strain measures, for MV/TV assessment.
– Sub-xiphoid- For pericardial effusion, assessing IVC,
Note that required probe positioning and orientation is variable and depends on the patient, the selected machine settings. Note that all probe positioning should be relative to the heart, not the patient, and so should be learned through repeated exams.
Vast array of skill levels/uses for echo- below is most basic most advanced-
– Most basic is assessing for the presence/absence of pericardial effusion and cardiac activity- easiest in the sub-xiphoid view or the parasternal long axis. In the PSLAX assess the position of the effusion relative to the descending aorta. Anterior to the DA is pericardial effusion, posterior is pleural effusion.

– Then looking at valves (eg mitral regurgitation in a febrile IVDA – might suggest infectious endocarditis)- often via the apical apical 4 chamber

– IVC for respiratory variation in diameter- >2.1cm with <50% collapse with a sniff inhalation (in spontaneously breathing patient) suggests CVP 10 or greater, and poor fluid responsiveness. Find the IVC from the sub-xiphoid position. (note and think about/look for the many possible confounders- tricuspid valve pathology for example)

– Assess LV for systolic function. EPSS (end point septal separation) is the simplest way to do so. Follow the tip of the anterior leaflet of the mitral valve throughout the cardiac cycle on M mode. <6mm separation from the septal wall at the most anterior point suggests normal LVEF. Do this from the parasternal long axis

– Assess for HFpEF by comparing E + A waves just LV side of mitral valve on doppler mode (can do from parasternal short axis

– Assess for RV failure with views of RV for TAPSE, McConnel’s sign. Find the most rightward point of the tricuspid valve (farthest from the septum) and assess range of motion throughout the cardiac cycle on M mode. Distance moved is the TAPSE (<16mm suggests RV systolic dysfunction). Also look for RV-LV diameter >1:1 and apex of RV ‘trampolining’ on the barely moving RV free wall (McConnel’s sign). Directly calculating RV systolic pressure is more complicated.

1- Dhruv Case Presentation-

57yo M Presented with AMS- Tachycardic, hypertensive, and very febrile
Exam- LE and ocular clonus, GCS 10. PERRL size 5
Hx of BPD, Dementia, MDD
On trazodone, fluoxetine- Serotonin drugs
On memantine, olanzapine- neuroleptic
Compensated metabolic acidosis, renal failure and prolonged qtc
Normal CK

Tubed with roc + propofol then started high dose midazolam drip
Presumed dx of serotonin syndrome and started cyproheptadine
Eventually diagnosed with NMS and managed with ECT

Teaching points-
Malignant catatonia- Fever, rigidity, autonomic instability in setting of a previously diagnosed catatonic state

NMS- Dopamine deficiency presents with rigidity, AMS, autonomic instability, elevated CK, low iron, usually within a few days of medication change (note haloperidol, metoclopramide, prochlorperazine, or stopping PD drugs)

Tx for both of above is-
ABCs, stop offending agent, benzos, calls to ICU for further mx

Serotonin syndrome-

• Hyperthermia, HTN, tachycardia, clonus, GI sx
• caused by SSRIs, SNRIs, TCAs, trazodone, fentanyl, ecstasy, MDMA
• tx with cyproheptadine (first gen antihistamine with 5HT activity) and ICU

General-
Consider non infectious causes of seizure, especially withT greater than 104
A- Acidosis, alcohol, ammonia
E- Environmental, electrolytes
I-Infection, ingestion, insulin
O- OD, oxygen
U- Uraemia
T-Trauma, thyroid, thiamine
I-See above
P-Psychosis
S-Stroke, seizure, SOL, syncope

2- Jessica EMS lecture
EMS Models-
Anglo-American model- Brings pt to the healthcare, reduces pre-hospital interventions in the interest of rapid access to well facilitated care
This is more common where EM is a well developed specialty

Franco-German model- Brings healthcare to patient, attempts to reduce use of hospital, and facilitates direct admission to the ward for inpatient care where necessary
This is common in continental Europe

Minimal evidence of benefit from one vs the other

Pre-hospital physicians
In trauma may be some benefit of having pre-hospital physician, though this could be confounded by the higher likelihood of helicopter transport and rapid transport to OR in systems that have pre-hospital physicians
In STEMI physicians may delay transport and worsen outcomes
Physicians usually aren’t required on ambulances, though they may somewhat reduce need for hospital care
Pre-hospital physicians may improve outcomes of OOH arrest

General learning points-
Stroke, STEMI, trauma- pt needs to get to definitive care- MT, PCI, OR.
Highest benefit from rapid transport for definitive care

3- Harrison R9 follow up
21yo M with burns to face following an explosion, given 500 IM ketamine and 10 IM midazolam on scene
A- intact
B- sats 97% on 2L NC
C- normal HR and BP
D- GCS 10 (after meds)

Singed nasal hair
Partial thickness burns to face and hands
No signs of blast injury

CXR clear and FAST negative, COHb 3.6

Trauma, plastics consulted and pt admitted to the ICU

Learning points-
1- Blast injury-
Primary- Blast/pressure wave- affects air filled structures (ears, lungs, GI)
Secondary- Things blast throws at you- shrapnel etc
Tertiary- Blast throws you somewhere
Quarternary- other associated injury (burns, CO, cyanide etc)

2- Blast lung-
Pulmonary barotrauma
CXR- look for butterfly pattern
look for HTX, PTX
PPV may increase alveolar rupture and raise risk of air emobilism
If using MV look for lung protective strategies

3- Inhalation-
Can cause airway swelling or lower respiratory tract injury
Upper airway-
Assess upper airway, consider fibre optic view
Consider intubation for bad oropharyngeal swelling, respiratory distress, soot in the supra-glottic region.
BUT intubation and MV could cause ARDS so it’s a judgement call
If you do intubate use a 7.5 or greater if possible to help with bronchoscopy

4- Dispo-
Normal VS, normal CXR and normal exam without sx can go home
Blast lung goes to the ICU

McKinney Nephrolithiasis Lecture-
See handout for cases
https://drive.google.com/file/d/1yvrwa3Ge6q8WaCgjvug3PLZIn5T6JUJl/view
Most stones are calcium stones- these are radiopaque, recurring and more common in men. First stone is most commonly in 3rd/4th decade of life.
Uric acid stones form as large staghorn calculi, always in the presence of urease forming bacteria. They then form an infectious seed, often resulting in recurrent UTI. Radiolucent.
Cysteine stones in homocystinaemia- rare, radiolucent.
Most stones <5mm will pass spontaneously (but can take 7-30 days)

Differentials + early/POC Ix-
Classic misdiagnosis is AAA. First time kidney stone in middle aged or older patient is less common. Think Aortic emergency
Consider renal and aortic US as screening (but not definitive imaging) and consider CT w contrast / CTA especially in these patients
Females- torsion, PID, TOA
Females child bearing age- pregnancy, ectopic
BMP and lipase (consider pancreatitis), urinalysis (INFECTION, hematuria)

Imaging- Decision is complex
American Urological Society recommends CT if first time, US if recurrent

SGEM consensus statement-
http://thesgem.com/2019/12/sgem-xtra-come-together-right-now-over-renal-colic/
Younger Patients (~35 years old): Even without a history of stones, CT may be avoided as long as pain is controlled (perfect consensus).
Middle-Aged Patients (~55 years old): We recommend CT if there is no history of kidney stones.
Older Patients (~75 years old): We recommend CT regardless of history.
Pregnant and Pediatric Patients: With a typical presentation they should undergo ultrasonography and do not require initial CT if symptoms are relieved.
Radiation Dose: We recommend reduced-radiation-dose CT whenever CT is used for suspected renal colic.

ED Tx-
Simple stones-
Analgesia (NSAIDS best + fastest if patient isn’t pregnant)
Alpha blockers- usually Tamsulosin (these are pregnancy category C, calcium channel blockers such as nifedipine are used instead, though efficacy is questionable)
Fluids don’t expediate passage

ABSOLUTE INDICATIONS FOR ADMISSION-
Intractable pain/vomiting
Urosepsis requires urgent decompression surgery
AKI
Hypercalcemic crisis
Single or transplanted kidney with obstruction

RELATIVE INDICATIONS FOR ADMISSION-
Infection without sepsis or obstruction (may DC if good follow up)
Significant comorbidities
Stone >5mm and located above the pelvic brim
Urinary extravasation

Dr Shaw Cardiovascular Summary-
Pericarditis-
– Widespread ST elevation. CANNOT have ST depression ecept in aVR. Usually concave upwards. Look for PR depression (and PR elevation in aVR), downsloping TP segments. Tx with NSAIDs
Brugada-
-With syncope- cardiac monitoring, admit cards, AICD
– Type 1- wide QRS w RBBB, TWI, coved STE 2mm in V1-3
– Type 2 – saddle back
-Type 3- Either shape with less than 2mm of elevation
-risk of vfib with any type. discuss with cards, always admit if symptomatic

WPW-
-Short PR, delta wave, broad QRS
-Aberrant conduction through an accessory pathway which doesnt have the AVN’s refractory period
– Causes AV re-entry tachycardia.
-When conduction is down AVN and up accessory, this looks like a regular SVT (AKA AV nodal re-entry tachycardia) and can be treated as such
-When conduction is down accessory and up AV node it causes wide complex tachycardia. Looks like VT and could be treated as such but it can be easy to mistake for WPW with AFib so consider electricity or procainamide depending on stability
-Afib with WPW is irregular, with qrs morphology variation from beat to beat and areas of the ekg will have rates approaching 250. This should always be shocked or get procainamide (or ibutilide)
– Monitor, admit for EP, possible ablation

Torsades –
-Polymorphic VT with proven long QTc when in sinus
-Give magnesium
– Shock
– Overdrive pace (pacing at 120bpm) if refractory
Hyperkalaemia
– Causes peaked Ts, broad QRS
– treat with calcium, insulin/glucose, fluids if they can take it, furosemide if they cant. Bicarbonate if they are acidotic. Albuterol may shift intracellularly too. Dialysis may be required with anuria/renal failure. Don’t use kaexelate
– can look like VT but VT usually has rate >120 and hyperkalaemia can have very broad QRS (broader than VT)
– This is important to distinguish because hyperkalaemia is dangerous because the added potassium has similar effect to a sodium channel blocker. Giving amiodarone worsens this
Pericardial effusion / cardiac tamponade-
– Hypotension, muffled heart sounds and JVD
– EKG low voltage, electrical alternans (alternating high/low voltage)
-Alternans should lead you to POCUS assessment for effusion and tamponade

Digoxin-
-EKG- digitalis- Salvador Dali / moustache sign with characteristic st depression. This is normal for patients on digoin, not a sign of toxicity
-In OD cause atrial tachycardia with block, bidirectional VT, bradycardias
– Digibind for K >5.5, life threatening arrythmia, Dig level >10
– Calcium for hyperkalemia is controversial, dosing of digibind is complicated- talk to your tox centre

EKG territories-
-Inferior II, III, aVF- RCA/LCx
-Lateral- V5, V6, I, aVL- Distal LAD + branches (OM etc)
-Septal- V1, V2 – LAD
-Anterior- V2-6- LAD (+/- II, III if LAD wraps around the apex ‘wrap-around’/type III anatomy)
– For reciprocical changes think PAILS-
­Posterior – Anterior – Inferior – Lateral – Septal.
For reciprocal changes take the area of interest, and then go to the next one in the list. For example anterior MI will have reciprocal change in inferior leads

MI medical treatment-
Give thrombolytics if its going to be greater than two hours from first medical contact to PCI center
Treat MI with aspirin (aspirin and thrombolysis are only meds with proen mortality benefit), also nitro if its not R sided (inferior/posterior). Consider thrombolytics, heparin, other anti platelet drugs depending on local policy/case specifics

SVT (AVNRT)-
-With hypotension —> synchronised DC cardioversion
-Stable- Adenosine (6mg —>12mg—>12mg) or Diltiazem
VT-
-Stable- chemical cardioversion with amio, lido or procainamide
– Unstable- Synchronised DC cardioversion

Heart blocks-
-1st degree- prolonged but constant PR- No tx
-2nd degree- Type 1 (wenchebach)- Prolonging PR before a dropped QRS- No tx
– Type 2- Constant PR with intermittent dropped QRS- Tx bradycardia
– 3rd degree- Complete AV block with AV dissociation- Treat bradycardia
-Treat bradycardia (symptomatic) with atropine, epi, pacing,
Transvenous pacing-
-R IJV is preferrable, L SCV if not (but SCV is often used for PPM so dont mess it up)
– Will look like LBBB on an EKG, on monitor will look like STEMI

PPM complications-
– Most common cause of failure is ovr sensing
-Magnet turns off all sensing on a PPM causing PPM to take over entirely
– Magnet causes AICD to trun off
Cardiac arrest-
-Hs- Hypoxia, Hypovolaemia, H+, Hypothermia, Hyperkalaemia
-Ts- toxin, tamponade, thrombus, tension
Dissection-
– control BP nicardipine (to 100-120 systolic)
– Control HR with esmolol (to 50-60bpm)
– Type A (involving ascending aorta) are surgical