Mysterious Encephalopathy (Manjuck, 3/27/2024)

 A link to this presentation is available HERE.

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Thanks to Dr. Janice Manjuck, our amazing ICU director, for an entertaining and information-packed Grand Rounds this week on Evaluation of Encephalopathy in Medical Patients. I learned so much, and cannot wait to have Dr. Manjuck back. She is funnier as a presenter than I am a writer, so please do listen to her talk if you have time! If you do not, here are my brief notes.

Key points:

• When evaluating an altered patients, make sure you know their baseline
• Don't forget to look at vitals: BP (normal for them?), temperature (core) and oxygen saturation
• Labs can be helpful to determine etiology
• Labs include glucose, LFTs, ammonia (increase in mortality regardless of cause), calcium, sodium, thyroid function tests (+/- cortisol), VBG/ABG, carbon monoxide, tox screen, alcohol and drug levels.
• Ask yourself if there is a primary neurological process
• CT (non-con) vs. CTA, vs CTV (if you are concerned about hypercoagulable state), MRI (if CT normal)
• Sometimes medication administration can be diagnostic: D50, naloxone (don't ever give naloxone without suction nearby), thiamine

Altered level of consciousness (ALOC) is a spectrum. Every time you evaluate and examine a patient, you should document their baseline level of consciousness. 

• Alert
• Lethargic ("patient looks like they are just waking up from a heavy sleep")
• Obtunded ("patient looks like they took a sleeping pill)
• Stupor ("patient not waking to shaking"
• Coma

Dr. Manjuck, used a this acronym (a model by a neuro-intensivist) to explain most common reasons for encephalopathies: DOTSS: Drugs, Osmotic demyelination, Thiamine, Structural disease, Seizures)

Drugs

50% of patients with AMS are altered due to a "drug problem" -- either a drug taken by the patient, rx'd to the patient, or not given to the patient. This makes MEDICATION RECONCILIATION a very very very important tool in understanding why a patient is altered. Common meds that are associated with AMS in hospitalized patients and are not immediately recognized include: levodopa, antidepressants, and baclofen. 

Don't forget the half-life and a patient's renal function!

Anti-depressant discontinuation syndrome: FINISH (flu-like syndromes, insomnia, nausea, imbalance, and sensory disturbances including hyperarousal).

Also don't forget meth detox in altered patients

So,  as per Dr. Manjuck's pearl of the talk: "Look at the med list every single day like flossing"

Osmotic demyelination syndrome 

This is a rare but serious cause of AMS in patients with hyponatremia that is corrected too quickly.  Unlike what you may think, this actually happens much LATER than I realized -- 4-7 days AFTER correction. Clinical manifestations include: short term memory loss, dysarthrias and ataxia, flaccid quardiparesis, locked-in syndromes, seizures, and coma. 

Neuroimaging can confirm the diagnosis: "snout" and "trident" sign

ODS occurs really when initial sodium is <120 and MORE likely when it was <110, and it can occur EVEN if it was corrected slowly. 

Goal is to correct 6-8mg max per 24 hours

Thiamine Deficiency

Patients with chronic alcohol use are at high risk for Wernicke's encephalopathy, which presents as change in mental status, oculomotor dysfunction and cerebella dysfunction. 

Structural Abnormalities

10-15% of patients in the ICU with AMS have an abnormal head CT, but that doesn't mean that the abnormal head CT explains the AMS. In order for a structural lesion to cause AMS, you need to have broad disruption of the reticular activating system! This must occur in the dorsolateral upper midpons, upper mid pons, bilateral thalamus, or diffuse bi-hemispheric.

That being said, some structural abnormalities DO cause AMS. These include:

• Posterior reversible encephalopathy syndrome (PRES
• Hydrocephalus
• Diffuse cerebral edema
• Subdural hematoma
• Subarachnoid hematoma
• Diffuse cardioembolic stroke

Seizures

Non-convulsive status epilepticus (NCSE) is largely unrecognized. 

Seizures are not a "binary" thing -- that is, it is not 

The longer it takes to control them, the longer it takes to get rid of them. 

Final take homes from Dr. Manjuck:

• Make sure you do a good neuro exam on Day #1 of admission and every day. And don't forget to document that!
• Your exam should include: level of arousal, speech content, orientation, eye opening, and gross motor exam
• Do a medication reconciliation every single day. Be aware of opiate creep (opiates you didn't even know the patient was taking)
• Toxic-metabolic encephalopathy is very much a diagnosis of EXCLUSION
• Be aware of taking patient OFF anti-coagulation (diffuse cardioembolic stroke is a definite risk)

Chest Pain Workup (Peng, 3/13/2024)

 A recording of this presentation is found HERE. 

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Thanks to Dr. Jonathan Peng for an excellent Grand Rounds this week on Chest Pain Workup. A recording of his presentation is above. My favorite favorite moment of the presentation was his last statement: "If it is important to the patient, it should be important to us." In other words, don't dismiss a patient's concerns. I love this mantra, and I so appreciate Dr. Peng's presentation -- he took us through a little history of medicine, some biostatistics, a bit of art history, and finally, the black box of cardiac stress testing.

Here are my notes:

Dr. Peng's  recipe for cardiac evaluation:

1. Evaluate the patient by their baseline characteristics (i.e. pretest probability).What are a patient's risks for CAAD? We should all be  aware that increasing age increases the likelihood.
2. Evaluate the patient with their symptoms (using risk scoring). How likely is it that the patient in front of me has chest pain that is ACS?
3. Evaluate the patient with testing (EKG, laboratories, stress testing, etc.)

Cardiologists love acronyms and scores!

There are two main calculators that help us predict cardiovascular risk using risk factors

1. ASCVD Risk Estimator (2019) predicts 10 year risk 
2. PREVENT Online Calculator (2024), new from AHA, predicts 10-30 year risk, in specific populations

There is additional score, called the HEART Score (2011) that helps to predict a patient's risk of ACS during an acute event. Factors include:

• History
• EKG
• Age
• Risk Factors
• Troponin

This HEART Score for Major Cardiac Events predicts a patient's 6-week MACE (Major Adverse Cardiac Event) risk. A score of 0-3 is low risk (1.7%), 4-6 is intermediate risk (16%) and 7-10 is high risk (50%). The authors suggested that a low HEART score excludes a short term MACE with a 98% certainty!

Once cardiologists have decided that a patient needs evaluation, they consider the following:

• indications: why am I ordering the test?
• contraindications: why should I NOT order the test?
• types of test: which one to choose?
• interpretation: what do the results mean?

Stress tests are ordered to rule out ischemia and to assess for cardiac viability, but also to assess functional capacity (eg. in valvular heart disease, hypertrophic cardiomyopathy, cardiac vs. lung dz and preop capacity if otherwise unclear), risk stratify specific patients after an acute MI (if cardiac cath not performed), and assess efficacy of medical therapy. 

Dr. Peng reminded us that many such tests are likely to be most  helpful for patients in the middle -- that is patients who have a low pretest probability will likely have normal tests, and patients with known severe CAD will have abnormal tests. 

Complications from stress tests are extremely rare, as are complications from pharmacological stress. Absolute contraindications include: severe AS, recent MI (within 2 days), unstable angina, decompensate heart failure, unstable arrhythmia, acute PE, suspected aortic dissection, inability to walk. Relative contraindications include: left main disease, moderate AS, HCM, electrolyte abnormalities, afib w/RVR, high degree AV block, and resting BP >200/110.

All stress tests involve a stress (either treadmill/exercise or pharmacologic) and follow-up imaging (EKG, echo, or nuclear med). See diagram below for the menu of stress tests:

What they are looking during the stress for something called the ischemic cascade; that is, as stress is put on the heart in the form of an exercise load, you can see a cascade of events that occur in the setting of decreasing coronary blood flow. I really LOVE this image Dr. Peng shared about how that manifests on perfusion scans, echocardiograms and EKGs, as well as symptoms. 

Exercise (i.e. treadmill testing) remains the stress test of choice -- it's cheap, you don't need special equipment, and it gives us an idea of a patient's functional capacity. It does have lower sensitivity/specificity than pharmacologic stress and there are some conditions that make a stress EKG uninterpretable (e.g. people with pacemakers, LBBB).

Pharmacologic testing options include adenosine (a vasodilator), dobutamine (a beta agonist), and lexiscan (most commonly used, shown to be safer, okay in people with BOPD).

Nuclear isotopes used in the nuclear portion of the stress test expose patients to 48 hours of high dose radiation. These types of nuc med tests can last anywhere between 2-4 hours and 2 days. Patients with higher BMI (>32-35) will often require a higher tracer dose and a longer test. 

example of nuc med imaging protocols

Stress imaging can be either via echocardiogram or nuclear med studies. Echo tends to be more specific (i.e. better for "ruling in" ischemia), nuclear med imaging tends to be more sensitives (i.e. better for "ruling out" ischemia). Other differences are seen in the table below. 

The next slide is probably my favorite from his talk, I'll call it a "Dummy's guide to stress testing". It is a flowsheet that takes us through the patient's clinical scenario and leads us down a path of which stress test to choose. Dr. Peng stressed that having good echo techs (which we do!) is an important caveat to which tests you order. 

att: Dr. Jonathan Peng, 3/13/2024

A treadmill EKG is 68% sensitive and 77% specific. In comparison, a treadmill echocardiogram has slightly increased sensitivity and specificity at 81% and 88%, respectively. A treadmill myoview has sen/spec of 87% and 70%. This makes me conclude that if we had a good echo tech to do the study, I would prefer a treadmill echo for myself (to avoid the radiation!).

What does an adequate study mean?

The results of stress tests don't always seem obvious. And this is because, you must first understand if the test was adequate before being able to interpret the results. Adequacy is defined as 1) patient being able to reach target heart rate,  (max predicted heart rates is traditionally defined as 220-age in years; the target heart rate is 85% of the max heart rate). A stress test is only negative IF the patient reached the target heart rate. 

On a related note, should we hold a beta blocker before a stress test?

It depends: for diagnosing ischemia then YES because you need to reach the target heart rate. For evaluation of medication efficacy then NO because we want to know if the meds are working correctly

It is also important to understand why a stress test was stopped. Absolute reasons for stopping include: ST elevations, BP drop >10mm hg with evidence of ischemia, mod/severe angina, dizziness/syncope, cyanosis/pallor, and sustained VT. Relative reasons for stopping the test early include: asymptomatic drop in BP, ST depressions >2mm, increasing chest pain, multiple PVCs, BP>220/115, fatigue/SOB/leg pain. 

Exercise time is prognostic! >8-9 minutes on the treadmill is a good prognostic sign. 

Of course, since we are talking cardiology, there are different scales to assess the outcomes of a treadmill tests and to use that to predict CV morbidity and mortality. These include the Duke Treadmill Criteria and the Cleveland Clinic score. The Duke score takes into account how long you were able to exercise, how bad the EKG changes, and whether or not you had chest pain during the test. The higher the number, the higher the CV risk.

High risk stress tests involve people with short time to symptom (3 minutes or less), induced hypotension, and prolonged time to recovery. The notion that having your heartrate return to baseline with relative quickness predicts the severity of your cardiac disease. For more high risk stress test outcomes, see the image below.

Unsurprisingly, exercise ability predicts prognosis -- that is, the more you can exercise (i.e. the higher METS you  achieve), the better your prognosis, regardless of your comorbidities. This is a reminder to us all to move move move our bodies as much as we possibly can! Stay in shape. 

Dr. Peng spent just a few minutes at the end talking about CT coronary angiography, a relatively new imaging study for intermediate and low-risk patients, those who are younger, have a lower BMI. It exposes people to much less radiation than a nuclear med study and decreases a need for unnecessary cardiac catheterization in the lower risk population. 

And finally, Dr. Peng ended the way I began this blog --with a plea to listen to patients: "When I was a younger clinician, I used to ignore my patients, sometimes disregard their symptoms. They would complain of pain or shortness of breath, and I would think 'oh, that isn't cardiac'. With time, I have learned to listen to my patients. If it is important to them, it should be important to us."

Amen. Dr. Peng.

Go forth and listen to your patients. 

Class of 2024 QI Project: Colorectal Cancer Screening (Mayeda, 3/7/2024)

 A recording of this presentation is available HERE.

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A summary of this presentation is forthcoming.