Grand Rounds Recap 7.25.18


Case 1: Posterior STEMI

75-80% of people have a right dominant circulation with the posterior descending artery supplied by the RCA. 5-10% of people have a left dominant circulation. 5-10% are co-dominant.(1) This will affect how a posterior STEMI may present.

EKG Characteristics of Posterior STEMI:

  1. ST depression in the anterior leads. This is because the anterior leads are looking at the opposite side of the heart of the actual STEMI. Therefore, these are essentially reciprocal changes. This is only seen in 61% of cases of posterior STEMI though. It unfortunately does not have great specificity because sub-endocardial ischemia can do the same thing, but it should increase suspicion in the right clinical scenario. 
  2. Large R wave in V2-V3. This usually disrupts the normal R-wave progression. If this is seen, consider posterior MI. Only seen in 44% of patients, however. 
  3. Upright T waves in the anterior leads in combination with ST depression in the same leads. 
  4. Often co-exists with an inferior or lateral STEMI because of the extension of the ischemia. It can be a posteroinferior STEMI if the patient has a right dominant circulation. It can be a posterolateral STEMI if a left dominant circulation. 
  5. ST elevation in the posterior leads. If concerned for posterior STEMI, move V4-V6 to the back and look at a posterior EKG (V7-V9). 

Case 2: Midbrain Stroke Presenting as Diplopia

Diplopia represents 0.1% of all ED visits. Nonetheless, ED providers should have a general approach to this complaint because of the wide variety of potentially dangerous etiologies. The following is a proposed approach that can be used in the ED.(2)

  1. Is the diplopia monocular or binocular? Have the patient close one eye and see if the symptoms resolve. If it is monocular, it is nearly always due to an intraocular cause. Therefore, the patient can likely be discharged with ophthalmology follow-up. 
  2. If a patient has binocular diplopia, find out if they have any other neurologic symptoms. Specifically, do they have brainstem symptoms such as dizziness, speech changes, or crossed signs such as contralateral face and extremity weakness. This would suggest brainstem stroke and should prompt stroke work-up with CT and CTA. 
  3. Is there an obvious abnormality of ocular motility? Most commonly, this will be an isolated 6th nerve palsy (inability of eye to abduct). This is often related to microischemia of the 6th cranial nerve. A 3rd nerve palsy will cause ptosis, mydriasis, and a "down and out" eye. This is generally idiopathic but can also be due to microvascular ischemia. CT and CTA are indicated in this scenario, however, to evaluate for a posterior communicating artery aneurysm that can cause this. A 4th nerve palsy will result in diplopia that is worse with downgaze. This is frequently due to trauma or can be congenital. 
  4. Are there any other ocular motility abnormalities that are not explained by a single cranial nerve? Think about where multiple nerves are in a close anatomic area.
    1. Orbital Apex Syndrome: this is the most posterior part of the orbit. It contains sympathetic fibers, cranial nerves 3, 4, 6, V1, V2, and the optic nerve. If the patient presents with diplopia and involvement of any of these nerves, assessment of the orbital apex should be considered. This can be diagnosed with a CT of the orbits.
    2. Cavernous Sinus: contains sympathetic fibers, cranial nerves 3, 4, 6, V1, V2, and the internal carotid artery. Work-up of this should include a CT and CTV to assess for signs of infection, thrombosis, or compression. 
  5. Are there any signs of other systemic disease processes? For example, signs of myasthenia gravis (fatigability and variability of symptoms), MS (due to involvement of the median longitudinal fasciculus), or temporal arteritis. Work-up of these should be pursued if clinical signs and symptoms are present.  

Case 3: Aortic Dissection

The classic presentation of aortic dissection is tearing chest and back pain associated with hypotension. In reality, chest and back pain are not always present, making the diagnosis exceptionally difficult. Neurologic complaints are not uncommon in dissection, and some cases can even be painless. 

In one study, 86% of patients with aortic dissection had either chest or back pain.(3) 25% of patients with type A aortic dissections had neurologic complaints. In fact, such cases were more likely to be painless if some sort of neurologic complaint was reported. Even more frighteningly, 50% of patients reporting neurologic complaints will have transient symptoms, making this diagnosis even more difficult. 

Neurologic Symptoms in Type A Aortic Dissection:

  1. Ischemic stroke (15%): This is most often from the carotid circulation, and they are predominantly right sided. Interestingly, there is not always direct dissection of the involved vessel, highlighting that there can be an embolic component to this as well.
  2. Spinal cord ischemia (1%): This is related to occlusion of the spinal arteries from extension of the dissection. 
  3. Ischemic neuropathy (11%): Patients may report symptoms consistent with limb ischemia, paresthesias, pulse deficit, etc. 
  4. Hypoxic encephalopathy (2%): This is thought to be related to profound hypotension from the dissection.
  5. Seizures (3%): All reported seizures were tonic-clonic in nature. This was commonly a single seizure at the onset of the dissection with no additional episodes thereafter.
  6. Syncope (6%): This can occur at onset of the dissection.
  7. Transient global amnesia was also reported but quite rare.

In summary, neurologic symptoms are not uncommon with aortic dissection. Suspicion for this diagnosis should be heightened if a patient reports chest or back pain plus another complaint such as syncope, seizure, etc. 

Case 4: NSAIDs

NSAIDs are commonly prescribed from the ED, but providers need to be well-versed in their potential side-effects. Recall that NSAIDs block the COX enzymes, all to varying degrees. This leads to inhibition of prostaglandins and thromboxane A2. This results in a variety of potential adverse effects. 

Potential Adverse Effects from NSAIDs:

  1. GI: Increased risk of GI bleeds due to inhibition of prostaglandins and resultant reduced gastric mucosal protection. Risk factors for development of this include age over 65, history of a prior GI bleed event, use of steroids, and concurrent use of aspirin. 
  2. Cardiovascular: NSAIDs compete with aspirin for COX-1 inhibition. Therefore, it is thought that NSAIDs can decrease the effectiveness of aspirin, although this is not entirely understood. There are reports of increased risk of heart failure with all NSAIDs. Myocardial infarction rates are higher in patients taking diclofenac, coxibs, and ibuprofen over the course of one year. The was not seen with naproxen. 
  3. Renal: Reduced renal vasodilation due to inhibition of prostacyclin. This results in an increased relative risk for development of AKI. 

This data suggests that providers should consider tailoring NSAID use to the patient's risk factors. For example, consider adding a PPI when giving a brief course of NSAIDs in patients with increased risk for GI bleed. Remember to utilize alternative options such as lidocaine patches, decreased doses, shorter durations, etc. to help minimize NSAID use when needed. 

Case 5: Hyperglycemia

We often see hyperglycemic patients in the ED, and practice patterns are quite variable when deciding on the appropriate treatment. Many providers strive to improve blood sugar in the ED with the idea of reducing the potential for return visits for the same complaint. One study looked at the risk factors for return ED visits for hyperglycemia and found that this was mostly likely related to poor compliance 35% of the time.(4) Other risk factors found were younger patients, a glucose of greater than 360 at presentation, being on insulin, and having previous visits for hyperglycemia. On the other hand, another study found that the discharge glucose level was not associated with return visits and has not been shown to be associated with adverse outcomes, although these data were retrospective.(5) This highlights the variability in practice patterns. Ultimately, appropriate follow-up should be arranged to help optimize glycemic control long-term.

Case 6: Fluids in Sickle Cell Disease

Many sickle cell patients have pulmonary hypertension which makes fluid management difficult. Unfortunately, there is not great data to guide management on this. It is a reasonable approach to be judicious with fluid resuscitation to avoid overloading these patients who often have fragile pulmonary and cardiac systems. 

D-DIMER IN AORTIC DISSECTION with Drs. Baxter and Hill

Aortic dissection is a disease with exceptionally high mortality rates. Yet, it can be a very difficult diagnosis to make due to the variability in clinical presentations. In general, diagnosis is made on CT of the chest with contrast, but this obviously is a significant test that confers expense and radiation to the patient. It would be great to have a screening tool that is relatively cheap and without harm to the patient. It has been proposed that the D-Dimer can assist in the diagnosis.

D-Dimer was found to be markedly elevated in cases of aortic dissection with a negative likelihood ratio of 0.07.(6) It is a relatively cheap and easy screening test with good sensitivity and no risk to the patient, making it a decent screening test. However, ACEP gives a level C recommendation to avoid use of D-Dimer alone in detection of aortic dissection. In one study, only 2.7% of patients sent for CTA were found to have aortic dissection.(7) Consequently, the concern with D-Dimer is that its false-positive rate will be too high, prompting too many extensive work-ups.(7)

A decision tool has been proposed to help risk stratify patients for dissection. The Aortic Dissection Detection Risk Score(ADD-RS): It looks at three different categories on history and exam combined with a D-Dimer to assess patients with concern for aortic dissection. It includes underlying risk factors (e.g. aortic disease, Marfans), presence of high-risk pain features (e.g. tearing, abrupt, severe), and presence of high-risk exam features (e.g. perfusion deficit, BP differential). The score missed 0.3% of dissections seen on CT.(8) On prospective validation, the failure rate remained 0.3%.(7) Providers should continue to listen to their clinical gestalt to make this diagnosis, but this tool in combination with D-Dimer may assist in the assessment of relatively low-risk patients.

R4 SIM with Drs. Bernardoni, Soria, and Whitford

The case was a patient who presented with melena and hemetemesis. She was initially stable but then decompensated and became hypotensive and hypoxic. She had evidence of liver disease, prompting concern for variceal bleeding. 

Management of GI Bleeding:

  1. PPI: Improves EGD visualization. In post-endoscopy patients, a PPI bolus was no different than drip. 
  2. Octreotide: Helpful for patients with known cirrhosis and variceal bleeding because it decreases rebleeding rates and does provide a small mortality benefit. If upper GI bleed of unclear etiology and not obviously variceal, there still may be a benefit although the data is not as clear. 
  3. Antibiotics: Should be given in patients with liver disease. Does confer a mortality benefit and should be given as soon as possible.
  4. Blood Products: Should be used as the resuscitation fluid of choice in GI bleeds. Do not forget to give calcium if giving multiple units. 
  5. TXA: Limited evidence in GI bleeding but is promising and should be considered. 

Minnesota Tube: This is indicated in patients with refractory shock from upper GI bleeding from a variceal source. The patient should be intubated prior to placement.


  1. Insert the Minnesota tube to 50 cm. 
  2. Inflate gastric balloon with 50 ccs of air. Obtain a portable CXR to visualize the gastric balloon in stomach and ensure balloon is not intra-esophageal. Once appropriate placement is confirmed, inflate the balloon to 500 ccs. 
  3. Pull gentle traction on tube until it hangs up against the GE junction, usually at about 35 cm. 
  4. Aspirate from the esophageal port. If blood is aspirated back, the esophageal balloon will also need to be inflated. 
  5. The esophageal balloon should be inflated to 30 cm H2O using a manometer. If ongoing hemorrhage, can inflate to 45 cm H20.