Intractable Pain

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…..

Sinus tach Part II

This is a case that ended up being a 72 hour return. Another good example that sinus tach should have a good explanation. Another good reason to know discharge vitals!

Middle aged M, history of TBI, PE, MRSA bacteremia, s/p trach/g-tube/IVC filter, presents with displaced g-tube and increased agitation. Trauma consulted, g-tube replaced. Fluro shows good placement. Exam otherwise unremarkable. No labs performed. Documentation of to be non-verbal/not following commands and this was baseline. VS prior to discharge. Normal BP, HR trend: 68->70->115->111 (at discharge)

Patient returns for changed mental status. Not documented in what way he was changed from baseline. But found to have BUN: 115., Cr: 2.96. BP 90’s systolic, HR wnl. Head CT negative. Hgb: 12, INR: 1.6 (on coumadin) Na: 154, Cl: 112. Otherwise labwork unremarkable.

Patient admitted to medicine service. Hgb trended down 12.4->9.8->8.4. Patient receiving IV fluids during this time. Mild improvements in BUN/Cr. Patient was a STAT response 5 days later. Hypotensive/tachy. Hgb: 5.3 Dark stools noted. Transferred to MICU. GI scoped, found to have erosion of IVC filter into duodenum. Vascular consulted. Patient transfused/stabilized. IVC filter removed, transferred to floor. BUN/Cr normalized during stay.

Two things here, the HR as mentioned, should always have a good explanation. In a patient like this, the history is limited, more information is probably useful than less. Granted a patient like this is very difficult to evaluate at baseline, I’d lean towards shotgun labs/imaging etc. Not sure if it would’ve made a difference in the end but nonetheless.

On the 2nd visit though, a BUN of 115 should raise an eyebrow That’s a BUN/Cr ratio greater than 20. This patient could be just a simple AKI due to hypovolumia. But a BUN that high should also raise the suspicion of a GI bleed. A hemoccult probably is indicated at this point (for somebody that can’t relay much information at baseline). I don’t think anybody would’ve predicted the cause, but nonetheless, neither any of us, nor IM really interpreted that BUN as it should’ve. Just a few notes on Bun/Cr below taken from life in the fast lane. Not definitive, but just something to do a double take on.

Urea:Creatinine Ratio (in the setting of renal failure / elevated creatinine)

20:1 – normal or post renal cause of AKI
>20:1 – pre-renal cause (urea absorption increased compared to creatinine)
<20:1 – intrinsic renal damage (urea unable to be absorbed -> become like creatinine -> ratio gets closer to 1)

Sinus Tach Part 1

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.

Stroke or seizure?

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!

Wellens’ Or Not?

A middle aged male presented for evaluation of AMS; he had agitation, confusion, and tremors. He has a history of Bipolar disease and schizophrenia as well as HTN.  Vital signs were all stable on presentation and within normal limits.  On exam he was oriented only to name, but not place or time. Neurological exam was normal, with the exception of tremors.  Med list includes Haldol Injection, Lithium, Benztropine, Olanzapine, and Propranolol.  At this point, I was not quite sure what is going on with him, so I had a bit of a shotgun approach.  Initial EKG revealed the EKG below.

20140325_223727

It appears to be similar to Wellens’ syndrome but not consistent with my gentlemen’s symptoms.

A quick literature search revealed a case report showing lithium induced EKG changes, similar to his EKG above.  Further supporting his lithium induced changes in this scenario is no clinical findings to suggest ACS, and a negative troponin 3x.  He was ultimately admitted and treated for lithium toxicity, without any cardiac complications.

EKG changes seen in lithium toxicity:
– ST elevations (1 other single case report)
– QT prolongation
– non-specific ST segment changes/T-wave abnormalities

The Trauma-Stroke Eval

Middle age male brought into Room 9 s/p crush injury. The patient was reportedly crushed against a box truck and a wall for a short period, but no prolonged extrication.

He complains of LUQ chest pain, pleuritic in nature, and denies abdominal pain. He was ambulatory after the event. PMH only significant for HTN, otherwise no PSH, no allergies, and takes lisinopril and hydrochlorothiazide.

He is AOx3, moving all extremities, well appearing in Room 9, and acting appropriate. He goes for man scan as he did strike his head and although can give me all the details of the accident he reports LOC.

Upon return from the CT scanner his VS are stable, and is placed in a regular ED bed.  Image review revealed multiple rib fractures, and suspicious appearing spleen.  Radiologist confirms grade 1 spleen laceration, but no active extravasation, as well as bilateral rib fractures.

While evaluating another Room 9 patient, the nurse came to update me that the patient was now unresponsive and foaming at the mouth.  I told her to give Narcan, thinking it could be iatrogenic analgesia toxicity, and I would be right there.

I arrive in the room, and he does NOT look right. He is foaming at the mouth, the narcan certainly changed his pupil size when she gave it, but did nothing to his mental status. Sternal rub, nipple pinch, and ammonia capsule all failed to appropriately arouse him.  The trauma resident is now at the bedside as well and just as perplexed as this isn’t what I described on the phone. I call radiology ask them to re-check his CT head but they said no, they see nothing. I again re evaluate him and now he will move only his L side, and follow commands on the L side of his body.

Well…..crap, this is dysarthria R sided hemiplegia. Stroke paged, obtained stat CTA head and neck, and then straight to Room 9 to intubate him. See the CTA imaging below:

CTA

Carotid artery dissection…

He obviously is not a tPA candidate, but he did go for an intervention procedure with the stroke service.  He did have a clot retrieved, but I have visited him on the floor a few days later and he had no improvement.

He went on to develop cerebral edema as well and had a large hemicraniectomy. He also had an ex-lap for an increase in abdominal distension, and found to have pancreatic ascites (3L removed from the abdomen). The spleen did fine.

Looking back, his mechanism did not support a reason for him to dissect a carotid. He had no external signs of injury, he had no neck pain, my guess is he did have a whiplash type injury but again, not something I expected. In addition, this man had a normal neuro exam upon presentation, full strength, no numbness/tingling with the exception of reporting headache, which I thought was from him striking his head.

After a lit review, there are a few teaching points I want to highlight from this case.

Traumatic Dissection (carotid, vertebral, spinal arteries)

– consider it with hangings, significant head/neck trauma, hyper-extension injuries, lateral rotation injuries of the head, base of the skull fx, c-spine fractures(especially those with displacement or involvement of the transverse foramen,vertebral body), lefort fractures (types II and III), or seat-belt sign over the neck
– Sign/Symptoms vary greatly. Stroke like symptoms are concerning but can be as generalized as headache/migraine, neck pain, neck hematoma, blindness, aphasia, weakness/sensory loss, Horner’s syndrome, tinnitus, CN deficits, diplopia, locked in syndrome, ataxia, vertigo, dizziness