Case Based Learning for May 2025

Following is the presentation a patient I recently had in the ED, where I felt I could have done better, especially with documentation. I think it brings up a number of good issues for possible learning/discussion, several of which I’ll mention below. I welcome any thoughts people have. – Gordan Luther, M.D. 

HPI:
70 y.o. male, presented for evaluation of a possible stroke. He stated that the prior evening at about 8:00, almost 17 hours prior to his presentation, he had sudden onset of weakness of his left arm and leg. The weakness was severe enough that he had a hard time walking and he feels he had a couple light falls that did not result in injury. He denies any speech or visual change. The same areas have decreased sensation. He had no other complaints. He denied any palpitations, chest pain or SOB. He stated he did not have a history of diabetes despite the blood sugar in the 400s we found on arrival. There was almost no history in the EMR, and he stated he hadn’t seen a doctor for many years.

PMH: None other than minor orthopedic injuries

No allergies or meds. Lives alone. A friend talked him into coming in for evaluation.

VS:
BP 202/116 Pulse 102 Temp 36.7 °C Resp 20 SpO2 96%

Physical Examination.
General: No distress. Cooperative. Appears pale, although nontoxic.
Head: Normocephalic. Atraumatic.
Eyes: EOMI. PERRL.
ENT: No nasal congestion. No pharyngeal erythema or exudate. Mucous membrane moist.
Neck: Nontender. Supple.
Lungs: Clear bilaterally. No rales, rhonchi, or wheezing.
Heart: Regular rate and rhythm.
Abdomen: Bowel sounds normal. Soft. Nontender. No rebound or guarding. No palpable masses.
Neuro: Alert. Oriented x3. Speech fluent. Cranial nerves 2-12 intact. He has 4 out of 5 muscle strength on the left compared with 5 out of 5 on the right. Some paresthesia in the same distribution. He has a left-side drift.

ED Course
Clinically I felt he showed likely signs of an acute CVA, and although not within the time window for thrombolysis, it seemed possible he might represent and LVO and potentially be an interventional candidate. He therefore was sent quickly to CT. EKG showed sinus rhythm with V2-V3 showing what looked most like J-point elevation, potentially with some peaked T waves in those leads only, and no reciprocal changes. CT returned as follows:

CT HEAD:
1. Findings worrisome for acute ischemia most notably involving the
right PCA territory.
2. Nonspecific hypoattenuation within the left insular cortex and
putamen may also represent acute/subacute ischemia.
3. Slightly increased attenuation within the region of the right
occipital lobe may represent petechial hemorrhage.
4. No significant mass effect, midline shift, or herniation.

CTA HEAD AND NECK:
1. Significantly limited evaluation of the neck arteries due to bolus
timing.
2. Within this limitation, there is suggestion of diminished
intraluminal contrast within the right vertebral artery. Evaluation
for potential high-grade stenosis/occlusion proximally limited.
3. Likely occlusion of the right PCA at the P2 segment.
4. Diminished opacification of the right SCA.
5. Poorly opacified right PICA.
6. Likely 50% narrowing of the proximal left ICA.

ED Course (cont): I reached out at this point to the receiving stroke center, and spoke with the neurologist. Labs began to return. The neurologist accepted the patient, thinking intervention was unlikely, but she wasn’t sure. When I mentioned the troponin, she stated “we see that all the time”. She recommended aspirin and a plavix load. I then spoke with the accepting hospitalist, calling her back once to specifically discuss the trop and EKG. She felt she would likely just get a cardiology consult, but wasn’t acutely worried. Thankfully the patient was quickly picked up by the chopper and arrived expeditiously at the referral center.

Pertinent Labs:
WBC 26.1
H/H and Plt normal

Na 136
K 5.1
CO2 17
Gluc 416
Anion Gap 19 (not flagged as abnormal at this hospital, no normal range given)
Remainder of CMP negative

PT/PTT neg
HS Trop 1968
Acetone neg (beta-hydroxybuterate not available at this facility)
Ven pH 7.55
pCO2 21

At the referral center the hospitalist evaluated the patient, and got some additional labs. The anion gap was again 19, which was elevated at that facility. Beta-hydroxybuterate returned high and the patient was deemed to be in DKA. This unfortunately necessitated a move to the ICU which had not been anticipated. In the ICU a cardiology consult was requested, as the troponin continued to rise. The cardiologist felt this was a Type 2 MI, or what we used to call “demand ischemia”. He was cathed a couple of days later and multi-vessel disease was found. He was felt not to be a candidate for stents or CABG, considering the location of disease. There were worries of sepsis with his WBC count high, and a lactate of 3.4 was found. Nothing ever grew on cultures. Ultimately he was discharged to a rehab facility.

Thoughts:
We all work in rural settings, where it is sometimes questionable how much we should attempt to do at the initial evaluation. This most classically applies to trauma imaging. In this case, the patient’s care was in the context of potential neurologic intervention, and we tried to proceed quickly. I’ve wondered if I should have added a lactate, cultures and abx, considering the white count.
Unfortunately with 20/20 hindsight I also feel this issue affected the quality of my documentation, trying to have my full note for the receiving MD. As I reviewed the case, I’ve wished that I documented a few other pertinent negatives which I usually do, as well as the comments from my consulting docs. ** Take home lesson – never rush your documentation.

I did not appreciate that the patient was in DKA. I quickly looked at the nonacidotic pH and negative acetone, as well as thought the AG of 19 must be normal at that institution, since it was not flagged. UpToDate reminds me that dx of DKA is based on a metabolic acidosis (can be compensated), hyperglycemia and ketosis.
** Take home lesson — I cannot simply assume DKA is not present with a nonacidotic pH. Also, we know that beta-hydroxybuterate is the most reliable ketone to measure for ketosis.

https://www.uptodate.com/contents/diabetic-ketoacidosis-and-hyperosmolar-hyperglycemic-state-in-adults-clinical-features-evaluation-and-diagnosis?search=dka%20diagnostic%20criteria&sectionRank=2&usage_type=default&anchor=H5509770&source=machineLearning&selectedTitle=1~150&display_rank=1#H5509770

Having practiced many years, it is only relatively recently that I’ve been hearing cardiologists refer to MI’s as Type 1 or Type 2. As a review, Type 1 is the acute occlusion process that often results in a STEMI. Type 2 is more of a demand ischemia. What is sometimes unclear in my opinion is the difference between Type 2 MI and “myocardial injury”. I think the most straight forward explanation of this that I’ve found is in the demand ischemia section here:

https://www.uptodate.com/contents/elevated-cardiac-troponin-concentration-in-the-absence-of-an-acute-coronary-syndrome?search=type%202%20mi&source=search_result&selectedTitle=2~9&usage_type=default&display_rank=2

Unfortunately I’ve found varying recommendations from cardiologists on the management of Type 2 MI and myocardial ischemia.
** Take home lesson –I need to consult cardiology each time in such situations.

https://www.emrap.org/corependium/chapter/rec8tYnfjz2FpdGrE/Acute-Coronary-Syndromes

Written by Gordon Luther, MD, Site Director, ERx Group

**

This is for informational purposes only. For medical advice or diagnosis, consult a physician.

**