Conference Notes 11-20-2012
Chandra Thoracic Aortic Dissection
Tupak Shakur is still alive! (Urban myth)
Stanford Type A involves ascending aorta. Type B Stanford is only descending aorta.
Two different anatomic systems, the DeBakey and Daily (Stanford) systems, have been used to classify aortic dissection [2,23-25]. The Stanford system is more widely used. It classifies dissections that involve the ascending aorta as type A, regardless of the site of the primary intimal tear, and all other dissections as type B. In comparison, the DeBakey system is based upon the site of origin with type 1 originating in the ascending aorta and propagating to at least the aortic arch, type 2 originating in and confined to the ascending aorta, and type 3 originating in the descending aorta and extending distally or proximally.
Ascending aortic dissections are almost twice as common as descending dissections. The right lateral wall of the ascending aorta is the most common site of aortic dissection [1]. In patients with an ascending aortic
6.4% of patients have been found to have painless aortic dissection. Most of the time these are ascending dissections that present with stroke or syncope.
In patients with shock in the setting of suspected aortic dissection, think pericardial tamponade. The dissection can bleed into the pericardial sac.
Diagnosis: Ekg is mostly non-specific but can have ami in 5% of patients with dissection. CXR can show wide mediastinum. CT angio has sens/spec in the mid to high 90%’s. MRI has the highest sens/spec 98%! Aortography has sensitivity of 88% and specificity 94% so it is no longer used. TEE has a sens/spec of about 98%. This is probably the way to go for the unstable patient or the patient with high risk for aortic dissection who can’t take contrast. Harwood comment: If you aren’t sure if the patient has a PE or dissection, get the CT PE protocol because it is harder to identify PE than dissection. Harwood and Elise both agreed that if you suspect one diagnosis over the other, get the test specific for that diagnosis. The timing of the dye load is different for both tests and if you get the CT PE study it decreases your sensitivity for dissection. The CT test for dissection lowers your sensitivity for pe.
Management: BP control start with esmolol and follow with nitroprusside. You want to decrease shear stress on the aortic wall. Labetalol is another good single angent choice. Maletich comment: How bout esmolol and nicardipine? Paarul/Harwood/Elise al felt this was reasonable as well. Type A dissections are managed surgically. Type B dissections are managed medically unless they have signs of ischemia, progressive dissection, intractable pain,impending rupture, or uncontrolled hypertension. Harwood comment: You have to advocate for the patient and get them to the OR with descending dissections when they have one of the above complications.
Poor prognosis: advanced age, hypotension, renal failure, pulse deficit, need for massive transfusion, many others.
Girzadas comment: Some respected authorities say It is the standard of care to miss aortic dissection. Harwood comment: Aortic dissection is the hardest diagnosis in the world. Harwood’s own decision rule for dissections is classic aortic pain get ct angio. If pain is not classic but you still have suspicion: check bp’s in both arms if abnormal get a CT angio, if chest pain and abnormal cxr get CT angio, if chest pain and abnormal d-dimer get a ct angio. Coghlan comment: remember this diagnosis in pregnant patients and patients who had a recent coronary angio. Gupta comment: this diagnosis is rare and difficult. It should be considered ok to miss this diagnosis. Work up for dissection delays diagnosis of other more common diagnoses and these patients generally do poorly. Chastain comment: gotta look at your own CXR’s because you have a different perspective on the mediastinum than the radiologist.
Putman Neck Trauma
Harwood comment: Intubate early to avoid losing the airway. The risk of losing airway due to expanding hematoma is much greater than an early intubation. Doing a cric in a patient with neck trauma is very difficult. Lovell comment: You have one shot to get this airway. Go right to most reliable device which may be glidescope.
Prior to RSI, check for neuro deficits especially cranial nerves. You only need to immobilize cspine in patients with blunt trauma and/or neuro deficit. Isolated penetrating neck injury does not require cspine immobilization.
Penetrating Trauma Hard signs: hypotension, arterial bleed, decreased carotid pulse, expanding hematoma, thrill or bruit, lateralizing signs, air bubbles in wound, hemoptysis/hemetemesis, tracheal deviation. These all go to the OR.
Penetrating Trauma Soft signs: hypotension in field, history of arterial bleed, bradycardia, large hematoma, apical cap on CXR, stridor, hoarse voice, subQ air, CN7 deficit. These patients all require further evaluation.
Zone 3 injuries need CT head.
Helical CTA is the work horse study for neck injuries. It shows vascular structures as well as cspine and aerodigestive tract. Harwood comment: Selective angiography is very rarely done. CTA is the way to go all the time, unless there is metallic FB’s or hardware obscuring the CTA image.
If CTA is neg then patients should get CXR, EGD and contrast esophogram. Also they get laryngoscopy/broncoscopy. Zone 3 injury gets catheter angiography.
Blunt Trauma
Wallenberg syndrome: Can get from vertebral artery injury
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E Kulstad CV Study Guide
Asa has 4% absolute mortality benefit from 13% to 9% in AMI (25% relative risk reduction). ACMC’s overall AMI mortality is 15.2% which is lower than the national norm.
Bening Early Repol: widespread ST elevation (precordial greater than limb leads), J point elevation, concave up st segment, notching of J point, prominent concordant t waves. Girzadas comment: BER should not have reciprocal st depression
Electrical alternans is a sign of pericardial effusion. Low sensitivity/high specificity.
Electrical alternans Every other QRS complex has a reduced amplitude alternating with a higher amplitude
Stress testing: Sensitivity/specificity is relatively low for coronary stenosis. Post-test probability = pretest probability X LR. The LR for stress testing is 0.25. So if you have a patient with 10% risk of coronary stenosis and he has a negative stress test, you bring his risk down to 2.5%. It is debatable about whether this is low enough for feel comfortable with.
Anterior wall AMI with new LBBB and first degree AV block: Pt should get stand by prophylactic temporary pacemaker. (Zoll Pacer Pads)
Plavix has not been shown to significantly decrease mortality in ACS. We use it because the composite end point of death/stroke/non-fatal mi is lower than placebo. This outcome has been accepted by our cardiology colleagues as beneficial for patients.
Heparin has also not been shown to lower mortality in ACS compared to placebo in a Cochrane review. Heparin has been shown to lower the risk of subsequent AMI in ACS. Cochrane review showed no difference between heparin and LMWH. As of today amazingly, the Cochrane review has not been concluded on heparin for STEMI.
History of CHF is a marker for risk of sudden death following syncope.
Beta-blockers and ACE-I’s and spironolactone have been shown to reduce mortality in CHF. Lasix has not been shown to decrease mortality.
High dose IV NTG has been shown to improve outcomes in acute CHF exacerbations.
CHF mortality is 50% in 4 years.
Contraindications to TPA in AMI: Prior ICH/Intracranial malignant tumor/structural cerebral vascular lesion/ischemic stroke in last 3 months/significant closed head trauma in last 3 months/active bleeding or bleeding diathesis.
Smoking cessation has the best mortality benefit of any intervention in CHF.
Sgarbossa Criteria:
The three ECG criteria with an independent value in the diagnosis of acute infarction and the score for each were:
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A minimal score of 3 was required for a specificity of 90 percent. The first two criteria are similar to those described above since the ST segment is concordant rather than discordant with the QRS complex. However, the third finding requires further validation, since a high take-off of the ST segment in leads V1 to V3 has been described with uncomplicated LBBB, particularly if there is underlying left ventricular hypertrophy. In a substudy from the ASSENT 2 and 3 trials, the third criteria added little diagnostic or prognostic value [15]. Harwood comment: It is not helpful in the vast majority of patients with LBBB. But when you have it is pretty specific.
Modi LVADS
Who can receive LVAD: Class 4 heart failure on max medical therapy, people who can’t come off bypass, cardiogenic shock, bridge to transplant.
Only 24 heart transplants in Illinois this year. 112 patients on destination therapy LVADS. Longest living patient on LVAD at ACMC is 8 years.
LVAD patients do not have a pulse. The pump is not a pulsatile pump, it is continuous flow. Probably more directly a cause is that the aortic valve doesn’t open with this pump. The pump connects the LV to the aorta. There may be more intracranial hemorrhages due to continuous laminar flow. Newest pump has a magnetically levitated internal rotor device so there is no wear on the rotor internally.
Initial eval: check for fever. Patients are at risk for infection with drive tube in abdomen. Most patients will not have a pulse. No affect on respirations. Blood pressure is usually around systolic of 90-120. Ekg is unaffected by LVAD. Pt’s may have VT while on the LVAD but will still have the pump working. Patients will be alert and talking with VT. You don’t need to shock patient if they are alert and talking and not in shock. Treat the arrhythmia with meds until pt has altered mental status/dyspnea/low bp. When evaluating a patient, check the computer reading, it will likely tell you of any problems with the device. If pt is unresponsive and arrives in the ED with a disconnected drive line, hook it back up. You run the risk of throwing a clot from the heart but the alternative is death for the patient. Chest compressions are ok for unresponsive patients with LVADs. Check the LVAD and make sure it has power. Otherwise perform resuscitation as you normally would.
Lovell Population Health
Population health aims to improve the health of a population. Reduces healthcare inequities. Aims to improve the overall health environment of a population.
Accountable Care Organizations and similar models focus on quality, preventative medicine approaches and shared savings instead of trying to increase the volume of healthcare delivered. Avoid unnecessary care and avoiding complications. We are accountable for all the patients in our catchment area.
This will be a new paradigm that we will be part of moving forward in our careers.
Erickson Eye Emergencies
Find out if the patient uses glasses or contacts.
Get a visual acuity of the affected eye!! Vital sign of the eye.
Chemical injury: Irrigate the heck out of the eye. Use topical anesthetic prior to irrigation. Check ph pre and post irrigation.
Acid causes coagulation necrosis. Coagulation necrosis actually prevents deeper penetration of acid into tissue.
Alkali causes liquefaction necrosis which is more serious and can penetrate more deeply into tissue.
Acute angle closure glaucoma: Precipitated by papillary dilation. Eye pain and emesis/headache. Hazy cornea and fixed mid-dilated pupil. Tx with beta blocker, alpha agonist, pilocarpine and mannitol and acetazolamide. Mnemonic: E=m2c: save the eye=miotics (pilocarpine/alpha agonist/beta blocker) and mannitol, carbonic anhydrase inhibitor.
Ruptured globe: eye pain, decreased visual acuity, teardrop shaped pupil, positive sidel’s test. CT orbits can be helpful. CT may show flat tire sign.
Corneal abrasion: topical antibiotics, consider a cycloplegic agent. Don’t give them topical anesthetic for home. Update tetanus shot.
Linsey went through a number of pattern recognition slides of eye emergencies.