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