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

Oral Boards:
Have a system/flow/approach, use the grid layout if that helps
Remember to go through AMPLEFRIENDS
Make sure to let the patient know what you’re doing/why.

Cardiac Tamponade:
200-400cc of fluid usually necessary to cause tamponade, faster accumulation more likely to cause tamponade.
Cardiac path (CA, trauma, etc) -> pericardiac filling -> cycle of heart failure to pump against building pressure
Signs: SOA, CP, fatigue, dizziness, elevated JVD, hypotension, narrow pulse pressure, possible cardiomegaly
-Beck’s triad only 10% of the time
EKG: sinus tach or alternans
Dx: clinically, can use US +/- CXR, EKG
Tx: 1L IVF, pericardiocentesis, window

AAA:
50% increase in normal diameter (normal ~3cm)
Infrarenal is most common location (classified by where it starts/location of most superior aspect)
Smoking and Age are biggest RFs, also fluorquinolones (don’t use em)
Asymptomatic Signs: pulsatile abdominal mass
Symptomatic non-rupture: abd pain, back pain, flank pain, limb ischemia
Symptomatic ruptured: pain, hypotension, pulsatile mass. Pain radiating to back.
Dx: Stable gets CTA (non-con CT for those who can’t do contrast). Unstable gets OR (CT surg or vascular) if known AAA, if unknown then US.
Tx: crossmatch 6U, pain control, esmalol/labetalol/nitroprusside (permissive hypotension 80-100 SBP if conscious), get them to OR
Complications: aortoenteric fistula, aortocaval fistula, limb ischemia, graft infection, inflammatory AAA, endoleak
Beware of thrombolytics since it can break up mural thrombus and send emboli

Aortic Dissection:
Tear in aortic intima. Type A involves ascending aorta, Type B doesn’t
Hypertension is #1 RF, also some sort of prior cardiac path, connective tissue disorders, inflammatory vasculitities
Hx: sudden onset chest pain most common, look for pulse deficit
Paraplegia if it involves the vertebral arteries
Mitral valve complications if involvement of aortic root
Horner’s syndrome if dissection compresses superior cervical ganglion
Dx: BP in both arms, CTA chest
Tx: control HR and BP, as well as pain
-Esmolol (quick on/quick off, good for HR control, titrate to HR 60-70), add cardene if BP still too high once HR controlled (SBP goal 100-110)
-Fentanyl for pain
Surgery for Type A, Type B can be medically managed
Complications: MI, Tamponade, rupture

Air embolism:
Iatrogenic is common, occurs due to pressure gradient (low pressure in venous system allows air from central line to easily enter system)
Central line air embolism 1 in 772
RFs: patient sitting upright, hypovolemic, negative intrathoracic pressure
Lethal dose thought to be 200-300cc of air (3ml/kg)
Signs and symptoms: sudden CNS/Resp/cardiac symptoms with central line placement
-looks like PE with CP, SOB, cough, tachy, syncope, anxiety, possible cardiac arrest, mental status change
Tx: prevent further air, reduce air volume, 100%FiO2, fluids, ionotropic support, hyperbaric oxygen (less so with CVC related), ECMO, L lateral decub positioning (takes embolus out of RV outflow track), and trandelenburg (unless arterial then avoid for cerebral complications)
Prevention: flush lumens and cap hubs prior to placement, adequately hydrate patient, keep insertion site below the heart

SHOCK:
Hypotension doesn’t mean hypoperfusion
Stressor->body compensates->decompensates->end-organ dysfunction->Death
-goal is to treat the stressor
diastolic is good indicator for PVR, systolic is good indicator for the strength of the heart
Shock index: HR/SBP, normal is 0.5-0.7 (HR goes up before BP)
Lactate up in times of lack of blood flow/oxygenation, but also depends on sympathetic nervous system and B-blockade can lead to lower lactate despite how sick patient is
Shock types: Obstructive, cardiogenic, hypovolemic, distributive
Obstructive: decreased CO, increased CVP, increased SVP (trying to shunt blood to heart), cool extremities (from shunting)
-PE, tension pneumo, tamponade, restrictive pericarditis, abdominal compartment syndrome, dissection
Cardiogenic: decreased CO, increased CVP, increased SVR, cool extremities
-MI, arrhythmia, cardiomyopathy, valve disease
-Ionotropes: dobutamine, milrinone, dopamine, epi (below 5-10mcg/kg/min)
-Milrinone solely renal clearance and better in chronic B-blockade, dobutamine is fast on/fast off. Make sure properly fluid resuscitated prior to starting these meds
Hypovolemic: CO normal or decreased, decreased CVP, increased SVR (trying to get blood back to heart), cool extremities (elderly might be a little warm due to slowed response)
-Fluid loss (GI/kidney/skin/DKA/3^rd space) or hemorrhage
-Permissive hypotension (MAP 65-70) has mortality benefit in trauma
-Balanced resuscitation (whole blood, keeping prbcs:ffp:plts 1:1:1)
-Calcium will be low because all the product are in citrate which will bind Ca so make sure to replete
Distributive: Septic, anaphylactic, neurogenic
Anaphylactic: consider delayed sequence intubation, need IM epinephrine (slowly diffuses over hours), consider glucagon if chronically B-Blockade
Neurogenic: Dx of exclusion, MAP>85

Narcan 1hr rule
-Safe to discharge patient 1hr after Narcan administration if provider feels comfortable and if has not needed further Narcan in the department and meets 6 criteria:
1. Able to walk
2. Temp >36C and <38C
3. RR 10-20
4. Sats 95%
5. HR 60-100
6. GCS 15

Fluid Comparison
-Across multiple studies Balanced Fluids (example LR) is non-inferior to NS and Odds Ratio would suggest possible superiority in terms of decreasing rate of AKI and reducing mortality.
-NS also associated with hyperchloremic metabolic acidosis, with balanced fluids leading to higher pH, lower chloride, and higher bicarb levels
-Balanced fluids more costly than NS (LR ~25% more expensive than NS)

NightShift Pro-Tips
-Phase delay scheduling is better than Phase advance (better to go morning shift then evening shift then night shift then morning shift, etc)
-Nap prior to shift, and nap on shift if possible (short 20min nap is best)
-Use Bright Lights (prior to 4am) to help keep you awake
-Caffeine early in shift and avoid big meals. Aim for snacks high in protein and fat and low in carbs (avoid big sugar swings)
-Minimize bright lights after shift and on drive home (sunglasses can help)
-Consider Melatonin 30min prior to sleep (shown to help fall asleep faster and stay asleep longer)
-Sleep in dark, cool room (blackout curtains and/or facemasks can help, and body needs cool temps to aid in sleep
-Try to avoid >3 night shifts in a row, but avoid 1 solo night shift (messes up your rhythm)

Neurogenic shock v spinal shock/stun

Spinal stun/shock: After spinal cord injury can have transient loss of function below the injury (loss of continence, anesthesia, paralysis). Can last hours to weeks.
-Can see priapism in males. (especially C-spine injury)
-Thought to be due to loss of K and thus reduced axonal transmission, with return of some if not all movement once K re-equilibrates
-Do Bulbocarvenosus Reflex checks to determine when distal spinal function has returned and gives idea of prognosis

Neurogenic shock: true shock from TBI/spinal cord injury. Interruption of autonomic pathways –> decreased SVR and alters vagal tone.            
-MAP goal 85, need to resuscitate with fluids in case there’s hypovolemic/hemorrhagic component to the trauma, otherwise need pressors (NE first line)

Lyme Disease Review

Lyme rarely transmitted in first 48hrs, ~25% chance in first 72hrs
Prophylactic ABx only if they meet all criteria:
-36hrs or more with tick attached, PPx started within 72hrs of removal, no contraindication to doxy (<8yrs old, pregnant, lactating), only if ixodes, inf disease society of America doesn’t recommend PPx unless in state with >20% lyme rate in ticks (which doesn’t count Kentucky, TN, IN, IL. Only surrounding state is WV)

-After removal (tweezers/foreceps, don’t crush or twist, just steady straight pull), clean and then have patient observe x30days for EM
-Observing for EM better plan of action than PPX ABx, serologic testing not recommended (don’t develop markers early in course)

If you believe they have early stage 1 lyme then doxy 100mg BID x10-14days
Stage 2/early disseminated (carditis/meningitis/bells): Doxy 100mg x14-28 days (14 days appropriate, will need ID f/u anyway) (Ceftriaxone if need IV)
Stage 3: severe arthritis 14-28days of doxy 100mg BID PO (again 14days shown to be appropriate, will need ID f/u), encephalitis x14-28days of ceftriaxone IV initially and Doxy PO when able
If contraindication to doxy then amox is second line

Serotonin Syndrome
autonomic hyperactivity, mental status changes, neuromuscular abnormalities

Mental status change (anxiety/restless/agitated delirium), autonomic (tachy, hyperthermic, diaphoretic, htn, vom, diarrhea), NM (clonus, rigidity, hyper-reflexive, tremor)
Fentanyl can cause serotonin release because 5-HT1A receptor agonist
Tx: stop offending agent, support, sedate with benzos PRN, cyproheptidine (12mg initial dose)

SCAPE

Increased afterload –> to pulm edema –> stress response with epi/NE/etc –> vasoconstriction –> afterload increase and the cycle continues

Workup: basic labs (including BNP), ekg, cxr, can do US/echo (can be normal or reduced EF)
-Concern if BNP >500
Treatment: BIPAP/CPAP for PPV, nitro drip (start at 100mcg/min and titrate from there, can give sublingual in the meantime while setting up drip)
-most are fluid down so don’t diurese (i.e. no Lasix right away, confirm fluid status first)
-Can wean BIPAP/CPAP once pt’s BP is at their normal and nitro <50mcg/min. Wean PEEP by 2 q10min, if patient doesn’t tolerate then turn back up. Once below PEEP 5 then can attempt switch to NC
-Can start ACE-I (enalapril/captopril) as patient improves
-Morphine can make some more comfortable but poor support for it overall

WPW and SVT

SVT: AVNRT and AVRT
AVNRT: abnormal circuit going round and round in the AV node, goes down septum so narrow
AVRT: doesn’t use AV node but rather accessory pathway (WPW), so often wide

WPW: 2 conduction pathways (AV node and accessory pathway), accessory pathway doesn’t have the pause that AV node provides thus PR is shortened and QRS broadens (can be wide, usuall 110s) and sloping upstroke (delta wave).
-Orthodromic and Antidromic
-Orthodromic has the impulse come back up the accessory pathway and going back into AV node. Antidromic is the opposite.
-Orthodromic is narrow because conducting through the AV node and bundle of His (looks like normal AVNRT)
-Antidromic is wide because it conducts through the ventricle, looks like VTach
-WPW+AFib: accessory pathway allows a lot of the atrial impulses to go down that are normally blocked by AV node. Looks like AFib with aberrancy but rate between some beats can be up to 300bpm. Also get some variation beat to beat in QRS structure, some will be narrow and some will be wide, overall different QRS morphologies of the different beats.

Adenosine blocks AV node, CCB and amiodarone slow AV node conduction. So Adenosine will return orthodromic WPW tachycardia to normal WPW ekg/rhythm. If antidromic then shock if unstable or procainamide because procainamide blocks the accessory pathway. Also, use procainamide or shock if WPW and AFib.

Pharmacy Pressor Lecture (A=alpha, B=Beta, doses in mcg/kg/min unless specified)

Vasopressors: vasopressin and phenylephrine (increase SVR)
Ionotropines: dobutamin, milrinone, isoproterenol (increase CO)
Inopressors: NE, epi, dopa (SVR and CO increase)
Beta-1 increases myocardial contractility and chronicity
Alpha-1 is arterial smooth muscle contracture

Vasopressin acts on V1 (vasoconstrict) and V2 (fluid resorption in kidney, slower) receptors
Dose is 0.3U/min, no more, no less. NE sparing effect. Can cause tissue ischemia and other ischemia at higher doses.

Dopamine: 0.5-5mcg/kg/min primarily hits dopamine receptors, but as you increase it hits B-1 (5-10mcg), and at 10-20 you hit A receptors. More arrhythmia than NE. Usually start around 5mcg/kg/min, max 20mcg/kg/min.

NE: strong A with some B. Start at 0.02mcg/kg/min (can start 0.1 or 0.2 if really needing it) and max 0.8mcg/kg/min. Too high can cause peripheral and GI ischemia.
-Safe to give up to 24hrs peripherally

Epi: mainly B activity below 0.05, then above you get more A activity. Starting dose 0.02, max 0.8

Phenylephrine: strong A only, start 0.5mcg/kg/min, max at 3. Reflex bradycardia and tachyphlaxis are possible adverse reaction.

Dobutamine (Do-beta-mine): Almost all Beta (1>2), start 2.5, max 20, used for HF and symptomatic brady, does increase myocardial demand

Milrinone: PDE-3 inhibitor, Start 0.125, max 0.75. Increases contractility and improves relaxation. Vasodilation leading to hypotension is adverse effect

Weight-based dosing: ideal BW for the morbid obesity. Can always titrate.
If extravasation: Stop infusion, aspirate as much fluid as possible, warm compresses for 30mn q4hrs for 24hrs, give phentolamin (5-10mg diluated in 10ml NS) injected in affected site

Cardiogenic shock: first line is NE, if low output can consider adding Epi
Hypovolemic shock: Stop the bleed and replace volume, pressors not recommended, adequately resuscitate before any pressor
Neurogenic shock: MAP goal >85, NE phenylephrine or dopa (>10mcg) but NE #1
Septic shock: NE then add vaso if needed. If refractory to pressors -> hydrocortisone 50 q6hrs

Push-dose pressors: Phenylephrine and epi
-Phenylephrine: concentration 100mcg/ml, giving 0.5-2ml q2-5min, onset 1min, lasts 10-20min. Good for patients who are hypotensive and tachy
Our code phenylephrine sticks are 1mg/10ml which are the correct concentration
-Epi: 10mcg/ml, dose 0.5-2ml every 2-5min.
Our code epi sticks are 1mg/ml, to make the push dose concentration mix 1ml from code epi into 9ml of NS and you get appropriate concentration.

Arrhythmias:
Think IV, O2, monitor, then look at rhythm strip: fast or slow, narrow or wide, regular or irregular, P waves present? Is patient stable?
Fast and unstable gets shocked, Slow and unstable gets paced

Bradycardia: wide is less responsive to meds and block is below AV node, narrow is normally faster and more responsive to Atropine

Sinus(narrow) Brady DDx think “DIE”
Drugs: BB/CCB OD, med SE
Ischemia: RCA supplies SA node, sick sinus syndrome
Electrolyte abnormality: Hyperkalemia causes no response to pacer or meds due to inability to repolarize

Wide, Fast, Regular: VTach, WPW antidromic, SVT with aberrancy
Tx: Amio, Procainamide, synchronized cardioversion

Wide, Fast, Irregular: AFib w/BBB, polymorphic VTach, AFib with WPW, Torsades
Tx: Cardioversion or Block AV node depending on stability, (Torsades gets Magnesium)

Fast, Narrow, Regular: SVT, orthodromic WPW, AFlutter, Narrow complex VTach
Tx: unstable gets cardioverted, stable gets adenosine, dilt, verapamil, or metoprolol depending on rhythm

Nursing Update:
-Broselow tape in the top drawer of the Peds code carts
-2+ SIRS with suspected infection -> within 3hrs needs lactate, blood culuture, broad spectrum ABx, 30cc/kg if lactate >4.
-Monotherapy ABx in sepsis that meet bundle criteria: Ceftriaxone for PNA or urinary (Cefepime if pseudomonas concern), Zosyn, Unasyn. (Just Vanc doesn’t cut it)

(Pediatric emergency medicine playbook is good podcast for Peds EM education)
Peds congenital heart disease (CHD):
Normal baby caloric intake is 100kcal/kg/day, CHD babies can need closer to 150
QTc cutoff in peds 460
Most common CHD in bicuspid aortic valve, most common cyanotic lesion is Tetrology.
CHD is leading cause of death in babies
Risk Factors: prematurity, 1st degree relative with CHD, genetic syndrome, maternal DM, HTN, obesity, thyroid d/o, epilepsy, in-utero infection (TORCH)

Ductal Dependent Lesions:
-Ductus Arteriosus closes around 42wks gestation (~2wks old)
-Left->Right shunting seen around 6-8weeks with sweating with feeds, tachypnea/cardia, FTT
-If reliant on duct for pulmonary flow: severe cyanosis and shock when it closes (critical pulm stenosis or pulm atresia, tetralogy)
-If reliant on duct for systemic flow: tachypnea, cardiogenic shock, lactic acidosis (hypoplastic L heart, critical aortic stenosis)

CHD signs and symptoms: HR >160, ASD causes fixed S2 splitting, extra heart sounds, pathologic murmur, decreased pulses, cyanosis/pallor, sweating with feeds, tachypnic, decreased activity, increased irritability, weight loss/FTT, hepatomegaly

Workup: PE (want BP and pulse ox in all 4 extrem), CXR, EKG, CBC, CMP, iCal, Mg, vbg, consider hyperoxia test to r/o pulm cause (100%, PaO2 should be >150 if pulm path), Echo stat
Tx: Control airway PRN (likely needed), Cyanotic 75-85% is okay (over oxygenating causes vasodilation and that can cause issues and more R-side shunting) (goal is 85% if you don’t know what’s going on), ABx for r/o sepsis, PGE-1 0.05-0.1mcg/kg/min (start high and wean down, titrate to palpable femoral pulses and SpO2 improves. This can cause apnea so make sure to be ready for airway)

CXR findings: Boot-shaped heart in tetrology, Eggs on a string in Transposition (see below)

Tet Spell: AMS, LOC, and death from cyanosis
Tx: knees to chest (increase SVR to push blood to R-side of heart), 100% O2 (vasodilate pulm to push blood to R-side), Morphine .1mg/kg IM or IV (helps relax the kid), 5-10cc/kg NS bolus, phenylephrine.5-5mcg/kg/min (same effect as knees to chest), propranolol (if needed, decrease HR and increase ventricle filling), RSI with ketamine 1-2mg/kg (if needed)

Hypoplastic L Heart Emergency: Needs fluids (clot if dehydrated), heparin (break up and prevent clotting), consider pressors, Call CV-surg ASAP, ECMO

Infective Endocarditis:
Dx with Duke Criteria: diagnostic if 2 major, 1 major and 3 minor, or all 5 minor
-Major criteria: Both BCx’s positive, Endocardial involvement (vegetation, abscess, prosthetic valve dehiscence, new valve regurg)
-Minor criteria: Fever, predisposing heart condition or IVDU, Vascular Phenomena (Major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway’s lesions), Immunologic Phenomena (Glomerulonephritis, Osler’s nodes, Roth’s spots, and rheumatoid factor), Blood culture + but not meeting major criteria

Growing more common in elderly with increase in valves and stents (higher risk of subacute). L-sided more common since mitral and aortic valve issues more common in older individuals.

Acute decompensated Heart failure is #1 COD (think valve rupture, need CV surg ASAP, can consider nitroprusside or dobutamine in the interim)

Valve Ring Abscess: needs CV surg repair or will recur and destroy heart. Also surgery for recurrent septic emboli or metastatic infection.

Increased risk in first 3months post-surgery because that’s how long endothelialization takes

STEMI Mimics:
Read “Dr Smith’s ECG blog”!!!!!! and OMI manifesto
STEMI mimics: hyperacute T waves, posterior MI, LCMA occlusion, DeWinters, wellens, sgarbossa and smith
Hyperacute T waves: occur early in MI
Posterior MI: look for ST depression in V1-V4
LMCA occlusion: aVR ST elevation predicts left main involvements
DeWinter: hyperacute T wave with broad base and low J-point/ST depression
Sgarbossa: use with BBB or paced rhythm or PVCs
Wellens: biphasic T wave (up and then down), not stemi equivalent, it represents reperfusion T waves, can be spontaneous or after cath. Has poor R wave progression

A FAQ by many in the department, whether it be out loud or kept silently in our hearts, is “How much pain meds can I/should I give the patient?” I came across this question frequently last month on my teaching elective. Whether from an intern who doesn’t understand their MD powers yet, from an upper level second-guessing or verifying their decision, or from myself second-guessing my own decisions, how much pain meds to give is a common question. Hydrocodone/Norco and Oxycodone/Percocet come in 5, 7.5, and 10mg (+/- the 325mg acetaminophen). But how much should one give? And when can one give dilaudid? Or Morphine? And how much? The simple answer is: it depends. It depends on what they normally take at home. It depends on the injury and your assessment of the patient’s pain. It depends on their allergies. It depends on so many factors. Can they take PO or do they need IV? With all these questions and variables, it’s good to break it down into levels or treatment.

Basic non-narcotics (these are your simple household names everyone knows and loves): Ibuprofen 400-600mg, Tylenol 500-625mg (Chronic liver disease patients can take tylenol, Max 3g per day. Just don’t give it in acute liver failure). Can also give tylenol IV and rectal. IV gets bad rap for being “super expensive.” While it is expensive compared to PO, it is not the >$1K some med schools generally teach people (closer to $40, expensive compared to PO which is <<$1). Thus totally okay for a dose if needed.

Next Level non-narcotics and adjuncts: Toradol 15-30mg IV or IM (studies suggest 10-15mg is plenty and above that doesn’t add much more than side effects. No need for the 60mg order in Cerner), Cyclobenzaprine 10mg (don’t order 5mg, nurses will hunt you down and make you split the pills yourself because they only come in 10mg tabs), other muscle relaxers (there’s plenty to choose from, great in those car accident patients with sore neck/back/muscles). There’s also Gabapentin as well as other less common options, but for now let’s stick to more of the basics.

Narcotics: PO you have a few options but staples are Oxycodone/Percocet and Hydrocodone/Norco. There is MS contin but just give that to people already on it (Onc patients). When deciding how much to give, if patient is taking it at home it is appropriate to give their home dose. You can always give more later, looks bad if you have to give Narcan because you gave too much. Just watch out for the amount of Acetaminophen given. It’s more than appropriate to give someone 2 Norco 5mg tablets to get 10mg hydrocodone and full dose of 650mg Acetaminophen, just dont give more Norco if they need further meds, consider Oxycodone or hydrocodone alone. If they aren’t on narcotic meds at home, always appropriate to start low and increase from there. Again, can always give more, harder to take it away.

In terms of IV, go-to options are morphine, dilaudid, and Fentanyl. Morphine 2mg or 4mg are generally safe starting dose, 2mg better for the older and narcotic-naive patients needing something a little extra. Dilaudid 0.5mg is generally lowest dose but can do 0.25mg if you really want to. If patient appears in a lot of pain (broken bone, appendicitis, diverticulitis, etc) then 1-2mg is appropriate. This is all at the physician’s discretion, but again, can always give more, so safer to start with 0.5-1mg and can give more from there. Fentanyl dosage is generally 50-100mcg, it is fast on, fast off, great for room 9 when you want something fast to help with pain. Can always then give something like dilaudid that lasts longer but takes a little longer to kick in.

Other Option: Ketamine 0.3mg/kg (generally 20-30mg) IV is a great pain dose, just don’t give too much and sedate em.

When considering how much to give of each and/or when switching between drugs, it is important to remember their strengths compared to one another. Refer to the tables below. But in general, 0.5mg dialudid IV is about 4-5mg of morphine IV. Oxy PO is 1.5x the strength of hydrocodone PO (only in 2nd chart). 5mg of Oxy PO is about 3.75mg morphine IV (assuming their gut is working…). One common thing people do is they give 2-4mg morphine IV and it doesn’t do enough for the pain so they give 1mg dilaudid next. That’s basically giving the patient greater than or equal to 2x the original dose, would be better to simply repeat first dose or switch to equivalent dilaudid dose (4mg morphine -> 0.5mg dilaudid). Lastly, remember Fentanyl is in micrograms, it is generally the only pain med we deal with that isn’t described as in milligrams.

Earlier this month, our ED pharmacist gave a detailed lecture on procedural sedation. One of the drugs discussed was ketamine, a dissociative anesthetic that is often the drug of choice among emergency medicine doctors for joint reductions, chest tubes, and other short, painful procedures. One of the reasons ketamine has become so commonly used is because of its limited effects on respiratory mechanics.  Given this advantageous property, ketamine has been utilized for “procedural sedation” for the purpose pre-oxygenation during resuscitations. This term as term has been coined Delayed Sequence Intubation (DSI).

Imagine you are walking into room 9 after receiving an EMS report about a delirious elderly male with suspected pneumonia who has been hypoxic en route by despite supplemental oxygen. Patient rolls in and looks sick with O2 sats in 70s on nasal cannula. Vitals are as follows: BP 104/72, HR 95, RR 26. As you try to place a nonrebreather, he swats it away. You have decided this patient needs intubation and consider rapid sequence intubation (RSI) with bag valve mask ventilation during the paralysis period with hopes of obtaining first pass success prior to patient critically desaturating and becoming hemodynamic unstable leading to cardiac arrest. You also realize that BVM alone without PEEP valve will unlikely raise O2 sats in this shunted patient and BVM during apneic period during RSI increases risk for gastric insufflation and aspiration. Then, you remember reading this blog on DSI. You ask the pharmacist to draw up a dose of 1mg/kg of ketamine, which is then administered by slow IV push(to avoid apnea) which subsequently results in a calmed patient in about 30 seconds. You place the patient on 15L NC as well as non-invasive mask CPAP with sats now 96% on the monitor and continue this method for 3 minutes to allow for adequate denitrogenation. Succinylcholine is then administered and then after a 45 second period of apneic oxygenation with nasal cannula still in place, patient was intubated without complication.

This method of separating the induction agent from the paralytic to allow for adequate pre-intubation preparation was described by Weingart and colleagues in a prospective observational study published in Annals of Emergency Medicine. The authors reported clinically and statistically significant increases in 02 sats using DSI with ketamine. Again, ketamine was used due to its ability to allow for the continuation of spontaneous breathing after administration. Below, I have listed take home points but highly recommend reading the article to gain a better understanding of this concept as well as the limitations with this study. (link to article and podcast at bottom of post, possible future journal club selection?)

Take home points:

• Start ketamine dosing at 1mg/kg, with 0.5mg/kg aliquots thereafter until dissociation occurs (Typically achieved by 1.5mg/kg)
• In patients with high blood pressure and tachycardia, may want to add small dose of a benzo, labetalol, or avoid ketamine altogether and use an agent like dexmedetomidine
• Recommend against etomidate or propofol or sedation agents such as midazolam because the non apnea-inducing dosages of these agents may be very different among these patients
• Two choices for pre-oxygenation: 1) 15L Nasal cannula plus 15L non-rebreather. If sats do not improve to greater than 95%, then shunt physiology present. Switch to option 2) 15L Nasal cannula with non-invasive CPAP settings 5cm to 15cm or BVM with PEEP valve
• DSI also applicable for the agitated, trauma with suspected head injury who is disrupting the resuscitation (especially now that the increased intracranial pressure phenomenon from ketamine is in question). One could argue this patient is dangerous to immediately paralyze, and therefore, DSI can be utilized to decrease 02 consumption while simultaneously calming the room and allowing for proper positioning of patient for intubation.
• It is possible to avoid intubating some patients (COPD, asthmatics) as evidenced by the study, although not currently a recommended aspect of DSI

In conclusion, I would advocate adding DSI to your toolbox for those uncooperative patients requiring intubation who have failed initial attempts at preoxygenation by placing a mask on their face. Additionally, as the COVID-19 pandemic continues, it will be interesting to see if evidence supports using this method in those patients with agitation from significant hypoxemia and perhaps already low functional residual capacity at baseline. At the time we take our oral boards, RSI will likely still be the correct pathway for these scenarios, however, this concept seems to gaining traction in EM literature and is worth considering in room 9 under certain circumstances

Link to Article : https://emcrit.org/wp-content/uploads/2014/07/dsi-article.pdf

Head and Neck Trauma – Dr. Sizemore

• signs of basilar skull fracture: hemotympanum, raccoon eyes (intra-orbital bruising], battle sign(retroauricular bruising) or cerebrospinal fluid leak (oto- or rhinorrhea, halo/ring)
• patients with LeFort II fractures and LeFort III fractures should have a CTA to screen for BCVI
• penetrating neck trauma
  • Know anatomy associated with zones of neck (I,II,II)
  • Early airway control should be considered in patients with hard signs
  • Hard Signs > OR
  • Soft Signs > CTA
  • Zone I injuries can result in pneumothorax
• do not probe wounds with active bleeding as may dislodge clot
• if direct pressure cannot control bleeding, consider placement of a foley catheter and balloon inflation

Intro to Research: An Overview – Alyssa Thomas and Dr. Huecker

• interns, start thinking about project ideas now. Pick something that interests you
• remember, there are different type of “research” projects
• human subjects
• quality improvement
• program evaluation
• All members of the research team must have a valid CITI Human subjects and HIPPA research training
• Great resource when time for writing paper : https://www.strobe-stamenent.org

Delivering Bad News – Dr. Coleman

• These conversations are nuanced, demanding, personally impacting
• Dr. Hueckers ABCs
• Awareness: focus on this one thing, they know if you are distracted
• Blueprint: have a blueprint based on studies and based on experience, then modify based on circumstances
• Compassion: Stay composed and expect tough responses
• SPIKES, a six step protocol/mnemonic for delivering bad news mnemonic
• Set up (Structure)
  • mental rehearsal
  • sit down
  • control the situation
  • maintain eye contact
• Perception/Professionalism
  • before you tell, ask
• Invitation
  • break it down, a little at a time
• Knowledge
  • be direct, avoid “passed away”
  •  use plain language, avoid medical jargon
• Emotions
  • Keep your cool, safety first
• Summary
  • Explain what happens next
  • Ask to be excused and how to reconnect

Social Media – Dr. Capocaccia       

• Please follow us on twitter: @UofLEM and Instagram:uoflem
• Will be posting “white board talks” and conference pearls on twitter
• Please send Dr. Capocaccia any images pertaining to wellness that we can share on social media with applicants

How Emergency Doctors Think – Dr. O’Brien

• classic thinking “what does the patient have?” (obtain history, perform physical exam, differential diagnosis, testing, final diagnosis)
• in the ED, the classic model breaks down for a variety of reasons
  • chaotic environment, “anyone, anything, anytime, anywhere”
  • can average 4000 clicks over ten hour shift using EMR
  • Constant interruptions/task switching
  • Frequently responsible for ten or more patients
  • Patients are unknown
• instead, we should ask “what does the patient need?” and whether or not any immediate action is required
• pearls
  • Be the nicest, calmest person in the resuscitation room
  • Rule-out first: diagnose second
  • Focus on smaller list of smaller list of life threatening diseases related to chief complaint
  • If you can, sit at the bedside to collect history
  • Perform an uninterrupted physical exam
  • Avoid diagnostic testing when able using rule-use tool
  • Only order tests that will affect disposition/exclude life threatening/most likely
  • Allow 2-3 minutes of interrupted time to mentally process each patient
  • Mentally process one patient at a time to process disposition
  • You can carry many patients but try to carry a max of 5 “undecided” patients
  • Listen to nurses
  • Avoid the biggest obstacle to the correct diagnosis, the previous diagnosis
  • Avoid inheriting someone else’s thinking on a patient
  • High risk times – sign out, hand offs, high volume, fatigue
  • High risk patients – hostile, violent psych, drug abuse

Dr. Baker – The Lecture Lecture (Tips for Giving Presentations)

• If using powerpoint:
  • avoid wordy slides, rather use simple slides that are visually appealing that supplement content
  • when importing images, utilize websites such as Pixabay to access free high quality images
  • if using videos, do not paste link onto slide. Instead, use software such as capto to put videos directly onto slide.
  • Try creating a story board before making slides
• Prior to presenting, record yourself
• Stand up, move around
• Plan to end early to allow for questions
• See Dr. Baker’s post below for more resources

Dr. Dan Grace – Post-Intubation Desaturation (Room 9 Follow up)

• Differential for the alarming vent/deterioration after intubation: think DOPE
• Displacement/dislodgement –see if tube has migrated, check EtC02, obtain chest xray, video scope verification
• Obstruction – think mucous plug, vent tube kink, make sure patient not biting down, try passing a suction catheter through tube
• Pneumothorax – auscultation, US, chest xray
• Equipment failure – disconnect from vent and bag, If it is “too easy” to ventilate, suggests air leak or dislodgement, if too difficult, think obstruction.
• Other things to consider: chest wall rigidity from fentanyl → give Narcan and breath stacking →disconnect vent and apply pressure to chest

Cordis and Subclavian Central Line Sim– Dr. Webb and Davenport

• Cordis: aka sheath introducer, preferred catheter in hemorrhagic shock resuscitation, provides faster flow rate given large diameter and short length
• Also used for transvenous pacing in unstable bradycardia
• The steps differ from those of a triple-lumen central line, in that the dilator and catheter are inserted together into the vessel.
• Subclavian Central Venous Access – Ideal for trauma patients with pelvic and intra-abdominal injuries and c-collar
• Contraindications -significant trauma or injury to the clavicle or first rib. And If there is concern for coagulopathy or thrombocytopenia, arterial injury is dangerous, as this site is non-compressible
•  Locate a spot 1-2cm below the clavicle where the proximal 1/3 and distal 2/3 of the clavicle meet. The needle should travel parallel to the floor towards the suprasternal notch. Use the contralateral hand to provide downward traction on the needle tip to facilitate clearance of the inferior edge of the clavicle.

Dr. Adam Ross – Percutaneous Pigtail Catheters for Spontaneous Pneumothorax

• essentially 14 Fr chest tubes with curved tip that is inserted using Seldinger technique and is less traumatic/painful to patient than traditional chest tubes
• important to secure the ipsilateral arm above the patient’s head using soft restraints
• two options for insertion: target at or above the 4th/5th intercostal space along the anterior axillary line as in traditional chest tubes or can use an anterior approach (2nd intercostal space, midclavicular line)
• can attach to either Heimlich valve or chest drainage system to suction post-instertion
• guidelines recommend against prophylactic antibiotics except in cases of trauma, where there are conflicting data.
• See Dr. Ross’s post below for resources

Here are the links to the videos/references from my Pigtail Lecture today:

•https://www.emrap.org/episode/pigtailchest/pigtailchest : This is EMRAP’s video that I showed in the lecture of Dr. Sachetti placing a pigtail in a patient.

https://vimeo.com/72761317 : This video is placement of the straight Cook catheter that we currently have.

https://emcrit.org/emcrit/pigtail-video/ : this is Dr. Weingart’s video of actual placement of a pigtail in a real patient

https://emcrit.org/emcrit/pigtails/ : this link is Dr. Weingart’s discussion of pigtails in general

Abdominal Trauma, Dr. McKinney

Penetrating trauma

• OR if unstable, peritonitis, evisceration, evidence of GI bleeding, GSW traversing peritoneum or retroperitoneum, or penetrating object still in place on arrival
• Local exploration of anterior stab wounds can identify peritoneal violation
• X-ray can screen for retained foreign bodies, free air under the diaphragm, or coexisting thoracic injury
• FAST uses peritoneal free fluid as a marker for injury and cannot specifically check for retroperitoneal, diaphragmatic, solid-organ, or hollow viscus injuries.
• DPL, although not done frequently, can be performed in patients who do not have indications for immediate laparotomy and who have an unreliable or equivocal exam.

Blunt trauma

• unstable with positive FAST/DPL > Massive transfusion protocol, OR
• stable with positive FAST/DPL > +/- blood products > CT
• injuries that may be missed on CT : pancreatic, bowel/mesentery, bladder rupture, and diaphragm rupture.
• diaphragm injury: rare, may be noted on CXR by the presence of bowel in the chest cavity, Left-sided injury more common than right because the liver is protective. Left-side injuries typically require operative intervention to prevent the herniation of abdominal contents.
• seatbelt sign think hollow viscous injury, CT has poor sensitivity for diagnosis. Discuss case with trauma, patient will likely receive admission for serial abdominal exams
• Splenic injury: most common injured organ in blunt trauma. Lower grades are typically nonoperative and are treated with observation
• ecchymosis over the flank (Grey Turner sign) or periumbilical region (Cullen sign) are suggestive of retroperitoneal hemorrhage

Genitourinary Trauma, Dr. Kuzel

• kidney: most common injured GU organ, often see gross hematuria, flank ecchymosis, and lower rib fractures. obtain CT Abd/pelvis W, GRADE I-III usually non op, discus with trauma
• ureteral: 90% penetrating, often does not present with hematuria. CT abd/pelvis W> consult urology > surgical repair
• bladder: associated with pelvic fractures, look for hematuria and lower abdominal/scrotal bruising.  Gold standard test: cystogram. Extraperitoneal injuries managed w/ bladder catheter drainage alone, intraperitoneal > surgical exploration/repair
• urethral injuries: Males>Females,straddle injury mechanism, and pelvic fractures. Look for blood at meatus, swollen penis. Single attempt at foley may be attempted. Diagnosis made with retrograde urethrogram. Injuries either posterior vs anterior. Consult urology, Suprapubic catheterization may be required initially, may need OR
• testes/scrotal – blunt: obtain Doppler US, if testicular rupture > OR. Penetrating: often undergo immediate exploration
• penile: fracture- cracking sound, pain, discoloration > US. Amputation -have 8-12 hours for reimplantation

Chest Trauma, Dr. Selk

• Blunt aorta injury : majoirty die in the field. Check for asymmetric pulses, diastolic murmur. CXR followed by CT chest W.  Tight HR and blood pressure control, esmolol often first choice .Surgical or endovascular repair ultimate treatment for a traumatic aortic injury
• pulmonary contusions – SOB, tachypnea, might see patchy infiltrate on CXR, better seen on CT, tx: pulm toilet, mech ventilation in those with severe respiratory compromise
• cardiac contusions – get EKG. if abnormal, get cardiac biomarkers. If isolated injury, okay to discharge
• clavicle fracture – if less than age 2, think NAT
• hemothorax – consider autotransfusion in shock

EMS Radio Communications, Dr. Orthober

• various type of EMS agencies (fire based, private, hospital based, third service, provider, community based) and levels of providers: first responder, EMT, EMT advanced, paramedic
• typical EMS ambulance staffing – BLS crew (EMT + EMT) or ALS crew (EMT + Paramedic)
• Things paramedics can’t do – Chest tube, surgical cric, perimortem c-sec, central lines
• a paramedic shall not terminate in hypothermia, cold water drowning, lightning/electrical injuries
• in arrests, ask for end–tidal C02, ROSC unlikely if less than 10
• for trauma patients,, ask about hypotension and achycardia, GCS?
• for medical patients, use vitals and mental status to help guide room 9 decision
• for stroke patients: LKN? anticoagulated? collateral riding in with them?
• general pediatric considerations – penetrating trauma > 13 years to ULH (or look like an adult), blunt trauma > 15 years to ULH,  although this is a moving target
• nasal intubation: remember phrase, “if in ain’t hubbed, it ain’t in”
• don’t discount mechanism on radio
• Kentucky EMS DNR- has to be original copy – obligated to transport to hospital without one of these

Survivalist’s Guide to the Pediatric ED, Dr. Lund

• Add order sets to favorites, get HPI and discharge do phrases
• Admissions: bed slip > tigertext > talk to admit team > choose dispo > order “ready for dispo”
• asthma: avoid decadron first time wheezers, get xray first to evaluate for neck mass
• neonatal fever (familiarize age considerations for testing/mgmt)
• neutropenic fever- CBC, blood cultures, cefepime within 1 hour
• healthychildren.org – good resource for normal newborn habits
• toxic, lethargic, irritable – use the descriptions with caution
• Tylenol 10 to 15mg/kg/dose, ibuprofen 5-10mg/kg/dose (>6 months of age)
• high dose amoxicillin (90mg/kg/day, BID) for AOM, pneumonia
• know 4-2-1 rule for MF calculation, typically use D5NS or D51/2NS

SANE Services, Amanda Corzine

• male or female victims of sexual assault age 12 and older (as long as have menses)
• Rape kit collection within 96 hours (4 days) of assault
• currently have 100% SANE coverage by nursing staff, at all of UofL health facilities and all Norton ERs
• same exam whether reporting or not reporting to police, kits are kept for 1 year
• level of alertness required for exam/consent. Search warrant for unconscious patients if suspicion high
• can go on to EPS if waiting for sane exam and otherwise medically clear, do not delay transfer
• always collect patient underwear, external and internal vaginal swabs with vaginal assault
• unlikely will have 24/7 SANE coverage when leaving residency, try to observe and familiar with an exam process now!
• toulidine blue dye – adheres to injured tissue helps injury identification by as much as 60%
• HIV PEP regimen Truvada and isentress (pharmacy can help with prescriptions at discharge)
• do NOT accept a transfer of patient for sole purpose of SANE exam

Conference Introduction- Dr Shaw

• Expectations
  • Come prepared
  • Deliver as if you are giving it at a regional/national meeting
  • Stay within time frame given
• Changes to conference for this year ***Full details in e-mail***
  • Will be given 2 days a semester (6 month period) that you can attend via Zoom
    • recurring meeting ID and password in e-mail
    • Please keep camera on during conference
    • Allowed 2 conference days a semester that you can attend via Zoom
    • FOAMed on 3^rd Thursday of each month
    • Will continue journal club during conference
    • EMCAT (the Emergency Medicine Curriculum Assessment Tool)
      • Link in email
      • Eval_Session_ID is the date of the lecture, followed by the presentation title, followed by presenter
      • Evals are anonymous but please keep professional
      • Conference curriculum will be online, link in email (word document will still be sent each month via email)

Sedation in the ED – David Roy, PharmD

• Know dosing, adverse effects, and benefits of the following sedatives:
  • Benzodiazepines
    • Provide amnesia, anxiolysis, and sedation but no analgesia
    • Drawbacks: respiratory depression, apnea, hypotension, variable response
  • Propofol
    • Reduces ICP and has anticonvulsive properties
    • Drawbacks: hypotension, myocardial depression
  • Ketamine
    • Amnestic, analgesic, sympathomimetic properties
    • Utility in pts with asthma/COPD, hypotension, status epilepticus
    • Look for nystagmus as sign achieved dissociation
    • Drawbacks increased secretions, caution in CV disease (hypertension, tachycardia)
  • Etomidate
    • Remember 15 (onset 15 secs, duration 15 minutes)
    • Hemodynamically neutral
    • Drawbacks: adrenal suppression, myoclonus
• Practicing using different agents during residency to get comfortable with them
• If remember RSI dosing, procedural duration doses are typically half and duration typically half as well

How to: Room 9 – Dr. Turner

• Familiarize yourself where equipment and supplies are located
• Examples of types of patients needing room 9: unconscious patients, GSWs(examine head to toe for wounds if rolling out), stab wounds, open fractures, STEMIs, and strokes
• familiarize with level 1 criteria and understand it’s purpose
• Provider roles: as intern -primarily US/procedures, upper level – team leader
• have a system that works for you and do it the same every time
• review imaging as soon as possible on these patients, don’t wait for the radiologist
• if you roll out patient, it is your patient

Transfer of Care, Dr. Platt

• happens more than you think! A patient can have multiple transfers of care for during ED stay
• good TOCs are clear, brief, timely, and complete
• for sample verbal handoff structure, look up IPASS
• use transfer of care note in Cerner at during sign-outs
• watch your tone and bias when talking to consults
• lead/frame the consult the way you want patient care to go
• if consulting medicine, be direct that you are consulting them for “admission”

US Basics, Jessica Kotha

• US generally safe. However, in first trimester, use M mode (not doppler) when calculating fetal heart rate
• linear probe (high frequency ), good for veins, soft tissue, ocular exam
• curvilinear probe (lower frequency) sacrifice resolution for depth, RUSH Exam
• Basic modes: 2-D (B-mode), M-mode (motion), doppler (Color, power)
• types of artifacts (posterior acoustic shadowing, reverberation, mirroring, etc)
• troubleshooting images: try more gel or pressure, adjust depth/gain
• RUSH exam: Heart, Inferior vena cava (IVC), Morrison’s/FAST abdominal views, Aorta, and Pneumothorax (HI-MAP).
• subxiphoid view- most sensitive for pericardial effusion
• familiarize yourself with findings of tamponade (diastolic RV collapse) as well as R heart strain for PE (RV dilation, McConnell’s sign)
• Look for lung sliding AND lung point when looking for pneumothorax
• measure aorta from outer wall to outer wall when evaluating for AAA