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Here is a nice summary of what we have learned about ED crowding over the past 10 years. There exists quite a bit in the literature for those interested enough to read further. Of course at UL we don’t know much about ED crowding.
I’ve seen about 3 cases now that presented with intractable pain. One was leg pain, put him in Room 9 much to the dismay of nursing, dude ended up having an acute arterial clot and received an amputation. One was acute on chronic back pain (history of chronic norco use, no change in quality) that ended up with an infected ulcer on his aorta (died later). And now this case….
67 y/o M presents with hip pain. Reports he was riding on a mower, hit a bump, had mild pain afterwards in his hip, but overall did well. He ambulated inside, took a shower, and after he sat down to do his business on the toilet he started to worsen. Especially when he stood up. No numbness/tingling/weakness/nausea/vomiting/fevers/chills/bowel or bladder incontinence. VSS. He has pin point tenderness behind his R hip. Worse with palpation. NO pain with axial load, internal/external rotation of leg. Pain with movement of torso. Pain isn’t nearly as bad when he’s just laying there. Appears in pain though at all times. Like TOO much pain.
Skip the XR knowing it won’t satisfy me, go straight to CT pelvis w/o contrast. It is normal. Decide to check labs at this point because I forsee an admission. He has a WBC count of 12. Cr of 1.8 (which is old) I admit him to the hospital for pain control as the idea of ambulation wasn’t happening, let alone just sitting up in the bed.
He is discharged the next day after MRIs of the L spine and hip are showing degenerative changes and lumbar stenosis and he is walking now (with the assistance of PT)
He presents again today and sees one of my partners. Again appears in pain, uncomfortable. Now has abdominal pain in the LLQ as well CT shows DIFFUSE pneumoperitoneum. He’s in the operating room at this moment…..
Sorting out theatrics/drama from reality can be a fine line we walk. Opiate abuse complicates things, and we often meet plenty of actors. But keep in mind pain out or proportion is almost always bad and delineating that can be difficult!
Always have your radar up, don’t be afraid to work up patients (regardless of what your ancillary staff and colleagues say)….. and don’t be afraid to be patient advocates and put them in the hospital to allow things to develop…..Remember One EKG, one CT, one lab draw, they are all stand still pictures of one moment in time and don’t always tell the whole truth. Certainly didn’t here in this case…..
Hey guys here is an interesting article with actual patient oriented outcomes related to admission for chest pain.
Several take home points:
1. From highest quintile of admission rate to lowest (81% to 38%) the rate of MI and death went up by 3.6 per 1000 and 2.8 per thousand. This correlation implies that when you admit more patients you save lives.
2. It is VERY IMPORTANT to note the patient population. These are Medicare patients with average age of 71 years. So we ARE NOT talking about low risk chest pain ED patients.
3. Even though it looks impressive to save these lives, the NNT or number needed to admit to prevent one MI is 250 and to prevent one death is 333. Thats a lot of admissions. And admitting geriatric patients is often not a good thing for them. May be why the decrease in deaths is less than the decrease in MIs. They were dying because of a hospital acquired infection or deconditioning or something else.
4. It is striking to see how different the practice patterns are at different hospitals regarding admission of a fairly homogenous cohort of patients.
Appreciate any further comments.
I have had a couple of good EKG’s in the setting of hyperkalemia that I thought I would share.
The first case is a 68 y/o female with ESRD on dialysis presenting with “back pain”. Turns out that her back pain was actually chronic and at baseline, but she had missed her last two dialysis appointments. She denied any chest pain or SOA. I ended up getting an EKG while waiting on labs.
Initial EKG:
Previous EKG (~6 months ago)
What says you? New onset LBBB? After seeing this we gave Calcium Gluconate and asked one of our wonderful techs to grab a quick iStat as labs were taking forever to result. Potassium was 6.8. Gave insulin + D50 and bicarb. EKG was repeated after Hyperkalemia treatment:
Renal consulted for emergent dialysis and medicine admitted.
Here’s another EKG that I had recently from a DKA patient who had an initial potassium of 7.8:
Here’s a couple of good hyperkalemia resources:
In patients with some suspicion for PE, even with a negative d dimer, I have often ordered a walking O2 sat and HR. This was not really evidence based, but maybe now could be. Below is the abstract for a prospective cohort study of patients known to be with and without PE. Interesting data even if only 114 patients. Cannot get full text yet.
Take home point. Combined sensitivity of HR increase of 10 BPM AND Sat decreased of >/= 2% was 100%.
ie if HR does not go up by 10 or more AND sat does not drop by 2 or more they are very unlikely, based on this small study, to have a PE.
Diagnosing pulmonary embolism can be difficult given its highly variable clinical presentation. Our objective was to determine whether a decrease in oxygen saturation or an increase in heart rate while ambulating could be used as an objective tool in the diagnosis of pulmonaryembolism.
This was a two-site tertiary-care-centre prospective cohort study that enrolled adult emergency department or thrombosis clinic patients with suspected or newly confirmed pulmonary embolism. Patients were asked to participate in a standardized 3-minute walk test, which assessedambulatory heart rate and ambulatory oxygen saturation. The primary outcome was pulmonary embolism.
We enrolled 114 patients, including 30 with pulmonary embolism (26.3%). A ≥2% absolute decrease in ambulatory oxygen saturation and an ambulatory change in heart rate >10 beats per minute (BPM) were significantly associated with pulmonary embolism. An ambulatory heart rate change of >10 BPM had a sensitivity of 96.6% (95% confidence interval [CI] 83.3 to 99.4) and a specificity of 31.0% (95% CI 22.1 to 45.0) forpulmonary embolism. A ≥2% absolute decrease ambulatory oxygen saturation had a sensitivity of 80.2% (95% CI 62.7 to 90.5) and a specificity of 39.3% (95% CI 29.5 to 50.0) for pulmonary embolism. The combination of both variables yielded a sensitivity of 100.0% (95% CI 87.0 to 100.0) and a specificity of 11.0% (95% CI 6.6 to 21.0).
In summary, our study found that an ambulatory heart rate change of >10 BPM or a ≥2% absolute decrease in ambulatory oxygen saturation from baseline during a standardized 3-minute walk test are highly correlated with pulmonary embolism. Although the findings appear promising, neither of these variables can currently be recommended as a screening tool for pulmonary embolism until larger prospective studies examine their performance either alone or with pre-existing rules.
Here are some highlights of Dr. Smock’s Forensic lecture. This will help remind me what to document in my next GSW pt. Here is a pfd version. Forensic GSW Documentation
Forensic GSW Documentation:
| Bullet causes… | Abrasion collar |
| Unburned gunpowder causes… | Tattooing aka. stippling (this lasts a few days, seen as punctate abrasions, DO NOT CALL THIS “GUN POWDER”) |
| Burned gunpowder causes… | Soot |
| Flame causes… | Seared skin |
| Injected gas causes… | Triangular tears |
| Muzzle causes… | Muzzle contusion |
Distance from Weapon:
| Indeterminate | abrasion collar present |
| Intermediate < 40 in | Tattooing & abrasion collar present |
| Close < 6 in | Soot & abrasion collar present |
| Contact | Seared skin, triangular shaped tears, & soot present |