Grand Rounds Recap 2.9.22
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R4 SIMULATION WITH DRS. CONNELLY, HASSANI, HUNT AND IRANKUNDA
Aortic Dissection
Epidemiology
Occurs in ~3/100,000 patients per year
Males >>> females
Median age is 63
In those <40, more than half of cases are associated with either Marfan syndrome or bicuspid aorta
- Risk factors
HTN (76%)
Atherosclerosis (27%)
Aortic aneurysm (16%)
Previous cardiac surgery (16%)
Marfan syndrome (5%)
Iatrogenic injury (4%)
Cocaine use (2%)
Pathophysiology
Normal aorta wall is made up of three layers: tunica intima (innermost), tunica media, and tunica adventitia (outermost)
Aortic dissection occurs when the integrity of the tunica intima is disrupted, allowing pulsatile blood to dissect through the tunica media leading to the creation of a false lumen
Normal aging leads to medial degeneration of the aorta, with hypertension accelerating this process.
Classification
Stanford system: classified by the proximal site of the dissection
Type A (67%): involves the ascending aorta
Type B (33%): involves the descending aorta (distal to the left subclavian)
DeBakey system – classified by both the proximal site as well as the distal extent of the dissection
Type I: starts in the ascending aorta, through the aortic arch, continuing into the descending or abdominal aorta
Type II: starts in the ascending aorta and does NOT extend into the descending aorta
Type IIIa: starts in the descending aorta and does NOT extend into the abdomen
Type IIIb: starts in the descending aorta and extends into the abdominal aorta
Clinical Presentation
Notoriously difficult to diagnose and is missed in as many as 1/3 of patients on their initial presentation.
Often mistaken for ACS
Most common symptom is pain (usually sudden and severe)
Increased probability of aortic dissection with:
Tearing or ripping pain
Migrating pain
Sudden onset chest pain
Focal neuro deficit
Pulse deficit
Physical exam
Usually normal upon initial presentation
Exam findings associated with aortic dissection are only present in <1/3 of all cases and can include:
Aortic regurgitation murmur
Pulse deficit
Focal neurological deficits (hemiplegia, paraplegia, etc)
Diagnostic evaluation
Labs: nonspecific. May see evidence of malperfusion (ex: AKI) if flap is propagating.
Note: cannot safely exclude dissection with D-dimer
EKG: nonspecific. May see evidence of ischemia if flap propagates towards the coronaries
Imaging
o CXR: not sensitive nor specific but may see the following findings
Widening of the mediastinum (62%)
Widening or abnormal contour of the aortic knob (50%)
Pleural effusions (19%)
The calcium sign (14%) – separation of the intimal calcification from the outer border of the aortic knob by 1 cm or more
CT angiogram: imaging of choice
TTE: sensitivity of 73-100% and specificity of 71-91% based on cardiology performed echos
TEE: sensitivity of 86-100% and specificity of 90-100%
MRA: not ideal
Management
Mortality increases by 1-2%/hr following symptom onset
Even worse prognosis if any of the following complications are present:
Cardiac tamponade
Mortality 54% with vs 25% without tamponade
Aortic insufficiency
Aortic free wall rupture
End-organ ischemia
Pharmacological interventions:
BP control
goal HR<60 + SBP <100-120 (as low as tolerable)
Clevidipine: start at 1-2 mg/hr and double the dose every 90 seconds until you are close to your BP goal then make smaller adjustments over longer period of time (5-10 minutes) until at goal. Max dose 32 mg/hr.
Rapid onset and offset. The esmolol equivalent of CCB
Nicardipine: 5-15 mg/hr. No bolus.
Sodium nitroprusside: 0.3-10 mcg/kg/min. No bolus.
Nitroglycerin: 5 mcg/min – 200 mcg/min (can theoretically go over this)
Hydralazine: pushes of 10-40 mg
Fenoldopam: 0.01-0.03 mcg/kg/min to make dose of 1.6
Dopamine agonist
HR control
Esmolol (preferred): 500 mcg/kg bolus followed by 50 mcg/kg/min gtt. Titrate up by 25-50 mcg/kg/min with a max dose of 300 mcg/kg/min. Have to bolus with each titration.
Labetalol: bolus of 10-80 mg followed by infusion of 0.5-10 mg/min. May theoretically be used as a single agent for both HR and BP control. Don’t use if concerned about cardiogenic shock.
Diltiazem: 0.25 mg/kg bolus followed by 5-15 mg/hr gtt. Don’t use if concerned about cardiogenic shock.
Analgesia: intermittent bolus of opioids (fentanyl preferred) when pain is present
SVC Syndrome
Caused by partial or complete obstruction of blood flow through the SVC
Epidemiology & Pathophysiology
Most commonly a result of thrombus formation or tumor infiltration of the vessel wall
Mediastinal Malignancies, especially small cell bronchogenic carcinoma
Increasing rates from iatrogenic thrombus formation or stenosis as a sequelae from pacemaker wires or indwelling central lines
Incidence 1/650 to 1/3100 patients
Signs/Symptoms
Face and/or Neck Swelling
Upper Extremity Swelling
Dyspnea
Cough
Dilated Chest Vein Collaterals
Can rarely include dyspnea, facial plethora, headache, lightheadedness, obstructive respiratory distress
Diagnosis
History and physical exam are key to diagnosis
Symptoms develop over days to week due to compensation from collateral flow
CT chest w/ IV contrast has sensitivity of 96%, specificity of 92%.
Management
Elevation of HOB
Treat underlying etiology
Remove device if warranted
Anticoagulation +/- catheter-directed thrombolysis or thrombectomy
Leaking/Ruptured AAA
Risk factors for development of AAA:
Age >60
Male sex
HTN, HLD, CAD, PAD
Family history of AAA
Tobacco use - major modifiable risk factor
Risk of rupture related to size:
For AAA <4 cm, risk is ~2% within 5 years of diagnosis
For AAA >5 cm, risk is >25% within 5 years of diagnosis
Indications for elective repair of asymptomatic AAA:
Size >5.5 cm (men), >5 cm (women)
Rapid expansion
Extension into renal or iliac arteries
Clinical presentations concerning for rupture:
Back, flank, abdominal pain in patient w/ risk factors or known AAA
Pulsatile abdominal mass
Ecchymosis - flank (Grey-Turner’s sign), abdominal (Cullen’s), proximal thigh (Fox’s), scrotal (Bryant’s)
Hematuria secondary to renal artery involvement
Massive GI bleed due to aortoenteric fistula
[Pain + known AAA] or [hypotension + known AAA] = rupture until proven otherwise
Diagnosis:
Ultrasonography has a nearly 100% sensitivity and specificity for the diagnosis of AAA but is extremely insensitive for diagnosis of rupture
POCUS is the preferred initial imaging modality in a hemodynamically unstable patient with a known AAA
Positive FAST + AAA is strongly suggestive of rupture, however negative FAST does not exclude rupture as bleeding is often retroperitoneal
CT angiography is preferred in hemodynamically stable patients
CT should not delay OR in an unstable patient
Management:
Emergent surgical consult for repair – mortality for ruptured AAA is ~80%
Anticipate need for aggressive resuscitation, activate MTP if patient is hypotensive
Pain control
Rapid (typically HEMS) transport to surgical center if no Vascular services on site
R4 CAPSTONE WITH DR. EDDIE IRANKUNDA
Lessons from R1 Year:
Find people you can look up to and emulate
Every person your work with has something to teach you
Lessons from R2 Year:
acknowledge and learn from your mistakes
accountability builds trust
teach others
Lessons from R3 Year:
Mantra: “you set the tone”
Pressure/Pain – growth mindset is critical
Progress
May be more visible to others before you see it or believe it
Authority Gradient
First identified in aviation
Errors can be minimized by smoothing the transitions between each piece of the gradient.
Lead by example
Lessons from R4 Year:
Be present, gain the perspective of the big picture
We are prone to have a limited scope or perspective and then claim them as truth/absolute
Listen to understand
Treat the patients who have diseases, not the disease
Step Ups or transitions in our career:
There will be misses and mistakes
Don’t let your fear rule you
PEM-EM COMBINED CONFERENCE: VOMITING IN PEDIATRICS WITH DR. NANCY CLEMENS
PEM Combined Conference: Vomiting in Pediatrics
Differential Diagnosis Considerations
0-2 weeks:
Anatomic abnormalities
NEC
Neurologic insult (kernicterus, mass, hydrocephalus)
Sepsis or meningitis
Inborn errors of metabolism
2 weeks - 12 months:
GERD
Rumination
Obstruction (pyloric stenosis, intussusception, malrotation, hernia)
Neurologic insult (mass, hydrocephalus)
Gastroenteritis
Renal obstruction or failure (uremia)
Infection (sepsis, meningitis, pertussis)
Ingestion (aspirin, theophylline, digoxin)
12months and older:
Anatomic abnormalities (appendicitis, PUD, intestinal obstruction)
Metabolic (DKA, Reye’s syndrome, adrenal insufficiency
Tox
Red Flag Symptoms
Bilious Emesis – intestinal obstruction
Headache, especially in the morning – increased ICP
Hematemesis – esophagitis, gastritis, or peptic ulcer disease
Hematochezia/melena – mucosal GI injury, IBD
Weight loss/ poor weight gain – chronic illness, celiac, IBD, or metabolic abnormalities
Losing weight or plateauing under the age of ~12 should be concerning
Constipation or GERD typically don’t cause weight changes or vomiting
Special Consideration: UTI
Very commonly presents with isolated nausea and vomiting
Patient history is often negative (no dysuria, frequency, urgency, etc)
Important to consider, especially in females <5yo
Kids 2-23mos → UTI Calc
Special Consideration: Non-Accidental Trauma
Most common diagnosis in missed cases of NAT is gastroenteritis
Full head-to-toe skin exam in all young children with vomiting is critical
TEN-4-FACES P tool for determining abnormal bruising patterns
