Abnormal vital signs are always something to keep an eye on. Always important to explain it in documentation, but keep an eye on the trend throughout your shift as it’s one piece of information that might tip you off that something else may going on. Try to resolve the vital signs prior to discharge, looks better from a chart buffing standpoint, but also an indication that you have corrected the original problem. And if you can’t, again explain it, or just don’t discharge the patient. You will never be 100% in this job, and your initial impression could be flat out wrong, so putting in little safeguards to protect yourself, from well yourself, can help you not miss things.

Quick case…..47 y/o M, history of 75% TBSA burns, active c-diff, PNA presents to the ED for low Hgb. Had Hgb of 7 at NH, 6.4 when checked here. Was just discharged recently from our ER (by myself, VSS at d/c) with new blisters on L scalp, Hgb was 7.3 at that time, 7-7.8 on prior visits. Wbc count: 11.8. Chronic indwelling foley. Urine dip: blood/wbcs/bacteria, neg leuk esterase/nitrite, already on levaquin for known PNA as well. Sinus tach to 120s. Received transfusion x2 units and initial plan was d/c back to nursing home per initial resident. Checked out to 2nd resident (myself) HR remained tachy to 120. Medicine consulted for admission. He was Afebrile. Blood cultures/urine cultures/ sputum cultured ordered as he did have an elevated WBC. Broad spectrum abx ordered. Rectal temp ordered x2, which were both normal. Medicine consulted for low hgb, sinus tach, and they cancelled cultures and abx, felt it was due to anemia although it did not improve with 2 unit transfusion (they are not always right). Planned for anemia work up and obs.

The patient admitted to the hospital and transfused. Hgb trended down again and patient required transfusion again on 9/26. Neg hemoccult/GI bleeding. Anemia work up not completed, but appeared to likely be of chronic disease vs iron deficiency. Patient became febrile on 9/23, BP dropped (that’s 3 days later…..) Started on broad spectrum abx, pan cultured. Urine grew acinetobacter. Blood cultures neg/c-diff negative. Hypotension was not responsive to fluids. Palliative consulted, patient and family elected to be comfort care. Made DNR. Comfort measures in place, was to be discharged to hospice. Patient subsequently expired prior to discharge on 10/4, etiology believed to be sepsis.

This patient had obviously a lot going on. Sinus tach could’ve been from anemia, pain, sepsis, stress, anxiety, etc. The initial thought it was due to anemia. but if this was true, it should come down with fluids and/or blood? Or at least partially respond? But it didn’t budge. He’s obviously had a long in-house history with the history of the burns so he was set up for a resistant bug, odd presentation. And honestly when we start seeing PNA + UTI we should start leaning towards sepsis from 1 agent with seeding, rather than a PNA and a UTI as two different infections going on. But in the end when he was checked out to me and the HR hadn’t budged, that was the tip off that something else was going on.

To expand on this as you can see things weren’t handled as they should’ve been initially. I see some people use the medicine service as a consultant. Which I thoroughly don’t believe in. They practice essentially the same thing as us, except less broad, more in depth, and a hell of a lot more boring (yes offense). When we talk to NES or neurology, or OB, or any of the other sub-specialties we are generally looking for guidance and information about a practice that is beyond our skills, beyond just basic medicine. And they have texts/papers/experience/OR time that allows them to function as a consultant and specialist in their area (especially the surgical services!).

But the medicine service is not all that different from what we do. When we call them, it shouldn’t be, “come see if this guy is ok for discharge.” We know which ones are and aren’t. And if you don’t, read more, use 5-minute EM consult, follow up on the patients you admit, so you can get a better understanding of what happens beyond the ED. You might not know the entire algorithm for hyponatremia and what work up they exactly do, but you should know when to admit one and how to emergently treat it. Or when to transition from insulin gtt to metformin, but you know when the glucose is too high to dispo home. Etc etc……. In their defense, sometimes we call them with patients that can theoretically be managed at home to begin with, but don’t fool yourself into thinking they know exactly what can go home and what can stay, and that they are the almighty, all-knowing doctor (case in point above.) They are residents too, and they don’t have an attending looking into them real time like you do (they have uptodate, which I can only assume why it takes 6 hours to admit asthma or whatever.)

Anyways to get back to my points.
1.Keep a close and scrutinizing eye on those VS.
2.And don’t let medicine pretend to be smarter than you.

A middle age male with history of HTN, smoking, and seizures presenting with “mini seizures” since last night. History of a TBI and subsequent seizure disorder back in 1998. Takes phenytoin for it, used to be on phenobarb as well but was taken off of it 1.5 months prior. His seizures have been of the generalized, tonic/clonic variety in the past. Since last night he has had L sided numbness on his face/arm. They have been episodic, coming every 10 min, and they last 2 min. He feels some “clumsiness” in that arm during these episodes but no reported weakness. No difficulty in speech/vision/swallowing. No fevers/chills/LOC/convulsive activity noted.

Phenytoin Level: 14.7
Labwork unremarkable
CT head: negative for acute pathology

Stroke or seizure? I wasn’t sure and I had the attending meet the patient as well. Both of us felt like these were probably seizures. Now I very rarely call neurology about seizures but you can make the argument that this is status so I called them. However, they informed me that isolated sensory symptoms for a seizure is VERY rare and that you are dealing with a possible stroke until proven otherwise. That was news to me, but to his point this was the first case I’ve seen. Anyways, we got the MRI/MRA and they were negative. His EEG showed multiple R sided epileptiform discharges. Loaded him with keppra in the ER, and a repeat EEG improved the seizure activity noted symptomatically and on the EEG. So yay, no stroke!

Main reason I point this out there is to avoid the pitfall of missing a stroke, as Neurology themselves were highly suspicious. Our initial thought process ended up being right, but in order to get there, the point here is to rule out stroke first! Same thing with a Todd’s paralysis BTW. Rule out stroke before you start making that assumption!

Great case I had in December. Overall good month, but this case was especially interesting, and humbling. It combines the excitement of chest pain, the enigma that is leg weakness, and humbling realization of a life threatening diagnosis.

Working in the ED one day and the psychiatry intern goes to see a patient. Routine patient, who had presented with right leg tingling and weakness that made it all the way to the back of the ED. Bed 15. Basic labs pre-ordered as well as a chest X-ray for a brief episode of chest pain that the patient told triage. Of course, the sixth vital sign, an ekg. Intern is with the patient for about 5 minutes and returns. He tells me that he is concerned that the patient is sick and wants me to see the patient sooner than later. He is concerned for possible stroke due to right leg weakness and pain. I tell him of course and I go see the patient.

HPI: 58 y/o AAM with hx of seizures on Dilantin but no other medications or PMH presents with chief complaint of right lower leg pain and tingling. Patient states that while at work today, he was lifting boxes and felt a sharp chest pain that started in the middle of his chest and radiated to between his shoulder blades. It then shot to his pelvis and went away. He went back to work for about 10 minutes then started to have right leg pain. He tried to drive to the hospital, but had to stop and call an ambulance due to sever RLE pain. All other symptoms had resolved at this point. No n/v, diaphoresis, dizziness, loss of bowel or bladder.

Pertinent Hx: NKDA, 30yr pack hx of smoking, dilantin.

Vitals: BP: 148/62, HR 66, RR 18, O2 100% T 98.5

Significant Physical Exam –

RRR, no m/r/g, CTAB, abd soft, nt, nd, no bruit, no pulsating mass

RLE strength 4/5, LLE 5/5.

No DP, PT, popliteal, or femoral pulse in the right leg.

At this point I was concerned. I excused myself and got the bedside ultrasound. In my head I wondered was this just a arterial occlusion, or was this something greater?

Well this is when I started to sweat. I tell the patient what I think my diagnosis is, and head back to my desk to get orders going. At this time I review the labs and chest X-ray.

CBC – WNL, CMP – K 3.3, UA WNL, Troponin Neg, Tox Screen Neg, Coags neg.

Chest Xray –

Any more concern? At this point I ordered a CTA of the Chest/Abdomen/Pelvis as well as called the surgery team. I wanted to get them involved early in the case that the patient deteriorates. I assessed the patients blood pressure at at the time was 130/60 and HR 58. I got the nurse to get the patient to the CT scanner as well as discussed with the trauma team. At this time patient had stable vital signs and pain controlled with morphine. Trauma evaluated and the CT resulted.

We now have our diagnosis. When patient got back from CT scanner, his blood pressure was increasing and now 150/80 and HR 68 with increasing pain.

Esmolol gtt was started, arterial line place, and the patient was transferred to another local hospital to undergo cardio-thoracic surgery for repair.

Diagnosis – Aortic Dissection from the level of the aortic valve down through the bifurcation of the iliac arteries. From the one slice, you can see he had no flow to the right leg. CTA demonstrated some collateral from the gastrics, but overall no flow.

Patient outcome – survived surgery. Otherwise have not been able to follow-up past that time. I shared this case because I feel it is a good representation of a case where easy bedside diagnostics can give you the diagnosis early and lead to your diagnosis. With the chest X-ray as well as the bedside ultrasound, we knew what the patient had. The CTA was just icing on the cake. Never be afraid to use the ultrasound. If it had been negative, this could have gone a completely different direction. Credit to the psychiatry resident for getting me involved early.

Use the ultrasound. Use it early. Diagnose early.

Aorta ultrasound.x