I’m gonna pump you up…..with heparin

Another weird one for you all.  42yo wm presents with 2 weeks of intermittent right arm swelling and pain.    Worse with exertion.  Some numbness of the fingertips.    Seen 1 week prior.  No labs done.   US negative.  So I walk into the room and stop in my tracks.    Dude looks like he should be jumping off a turnbuckle in a pro wrestling match.   Absolutely huge.  Second thing I notice is despite being ripped bilaterally,  I can see from 20 feet away, his right arm is almost twice the size of his left.  Third,  I immediately decide this cat gets whatever he wants for pain because there are peanuts in his stool bigger than me.

Start my exam.   Guy states he works out 5-6 hours a day.  Swelling went down with rest and immobilization/elevation .  Started training for a bodybuilding show 3 days ago and it came back with avengence.  Swelling is diffuse and symmetric, extends all the way to the distal pectoral muscle on the lateral chest wall.   Subjective numbness to the digits, non focal.  Cap refill < 2 seconds.  5/5 strength  (more like 9/5) full range of motion.  Lung exam normal.  No neck or supraclavicular masses. Prominent superficial veins of neck and pectoral area.  Bilaterally but right noticeably greater than left. Only other important note, does add he had a history of Non-Hodgkins lymphoma when he was a teenager.

So…….what now?  I decide I am worried about venous outflow or lymphatic obstruction from a mass amongst other things.  Talk to our radiologist about best imaging.  He recommends CTA of chest and ‘I’ll tell them to get the neck too’ .     Lab him up- cbc, bmp, ck.  All normal.  Radiologist calls me with this report ‘i see some schmutz in the axillary region, consistent with superficial thrombophlebitis’.

Go back and check on him.   Looks miserable, states arm feels even tighter.  I decide this seems extreme for superficial thrombophlebitis.  Order a repeat US.    Field the inevitable ‘he just had one a week ago ‘ call.  Lo and behold,  axillary DVT that extends through all the distal venous circulation.

This is called Paget-Schroetter syndrome.  Effort induced thrombosis of the upper extremity.   The axillary vein sits right in between the clavicle and first rib.  Can get a ‘nutcracker’ compression of it.

Then repeated shear force causes fixed intrinsic damage and extrinsic scar tissue formation.   Making the vessel extremely prone to clot formation .    So patients with a tight squeeze on the axillary vein at baseline who are active in exercises that increase shear are prone.  Classic examples are bodybuilders like this guy and baseball pitchers .    For you gunners (nerds) the distention of the chest wall superficial veins association with this condition is called Urschel’s sign.  Treatment consist of anticoagulation and consideration of thrombolysis as most of these patients are young, healthy,  and active .    Surgical first rib resection is an option for refractory cases.

I started him on heparin in case vascular or IR was interested in lysing him.  They weren’t,  and he was discharged home on xarelto in good condition after an obs admission for n/v checks.  Thought about following up by looking him up on Facebook, but that would entail entirely too many pics of him flexing with a spray tan and a Speedo.

Couple of learning points I think .

#1 if you have an index of suspicion for a dvt or a positive d dimer,  repeat ultrasound at 1 week.  Hold your ground if you get pushback.   The data is behind  you and I catch one about 2 times a year.  Initial US too early at times and it propagates later.

#2 if you have a weird case, talk to your radiologist early.  Give them background and get them invested in the test.  You will get a 1000x better read and likely way more timely of a read.  Good rule of thumb in general- better reason for the test, better read.    I see this all the time, we piss and moan about radiology hedging,  then we look back at the indication given and it’s something generic like ‘abdominal pain’

CO Poisoning

HPI:      57 yo M w/ PMHx of HTN, HLD presents with concern for carbon monoxide poisoning. Pt reports he was using a gas-powered saw in an enclosed bathroom to cut concrete. After some time, he began to feel hot and dizzy. When he stood up to walk out of the bathroom, he reported being unable to walk straight. He then began to feel lightheaded and developed a headache. He has also developed photophobia since. He reports no other problems. Smokes approximately 1ppd.

 

Exam: Vital Signs WNL

GEN: Alert, with no distress

CV: RRR, S1S2 present, No M/R/G

Pulm: CTAB, Non-labored

Neuro: CN II-XII intact, Strength 5/5 in all extremities, Normal Sensation/Coordination

 

Labs:    CarboxyHb lvl 19.3%

ABG showed normal pH, pCO2, pO2, Bicarb

CBC, CMP, Troponin, EKG, and CXR negative for acute process

 

Dispo:  He was placed on a NRB and symptoms began improving. After discussion with Poison Control and Jewish, pt was transferred to Jewish to receive a hyperbaric O2 treatment. He felt much improved after the treatment and was discharged in good condition.

 

The suspicion for carbon monoxide poisoning is based primarily on history. Most symptoms are non-specific. Mild to moderate CO poisoning presents with headache (most common), nausea, dizziness. Don’t forget to ask about LOC. Severe CO toxicity can produce neurologic symptoms (seizures, syncope, or coma) and/or end organ damage. If CO toxicity is suspected based on history, a careful and detailed neurologic exam should be performed.

 

If sufficient concern after history and physical, the diagnosis is made by an elevated carboxyhemoglobin level measured off an arterial blood gas sample. Nonsmokers should have baseline level of less than 3% carboxyhemoglobin. Smokers may have baseline levels of 10-15%. Once the diagnosis of CO poisoning is confirmed, an EKG should also be performed. CMP should also be considered to evaluate for electrolyte abnormalities and to assess renal function. Troponin should be obtained in patients with EKG abnormalities, cardiac comorbidities, and older patients.

 

CO binds hemoglobin with greater affinity than oxygen. This results in impaired oxygen transport. CO can also precipitate an inflammatory cascade that results in CNS lipid peroxidation and delayed neurologic sequelae. The half-life of CO can be changed by manipulating O2 delivery to the patient. CO half-life is approximately:

·      250 to 320 minutes on room air

·      90 minutes on high-flow oxygen via a NRB face mask

·      30 minutes with 100 percent hyperbaric oxygen

 

Some evidence suggest that HBO treatment can decrease the chance of delayed neurologic sequelae. Patients can often be discharged soon after HBO treatment is completed.

 

Recommendations for Hyperbaric Oxygen from Rosen’s 9E:

·      Carboxyhemoglobin (COHb) independent of clinical findings

o   >25% with no clinical findings

o   >15% in pregnancy or fetal distress

 

·      Or an elevated COHb with one or more of the following findings:

o   Syncope

o   Coma

o   Seizure

o   Altered mental status (GCS <15) or confusion

o   Abnormal cerebellar function

o   Prolonged CO exposure with minor clinical findings

 

Suggested treatment algorithm from UpToDate:

 

 

 

 

References:

 

Walls, Ron M., et al. “Inhaled Toxins.” Rosen’s Emergency Medicine: Concepts and Clinical Practice, Elsevier, 2018.

 

Clardy, Peter F, et al. “Carbon Monoxide Poisoning.” UpToDate, 28 Feb. 2017, www.uptodate.com/.

Conference Follow Up Info

Great Blog Posts reviewing LVAD & its complications/management.

Left Ventricular Assist Device


https://lifeinthefastlane.com/ccc/ventricular-assist-device/

Blog Post on REBOA from Life in the Fast Lane:
https://lifeinthefastlane.com/ccc/resuscitative-endovascular-balloon-occlusion-aorta-reboa/

Attached is Dr. Steve Smith’s article for his Equation for Subtle LAD STEMI.

Subtle Stemi- Stephen Smith 2010

IV Metronidazole Currently on Shortage

Currently, we are using approximately 20 bags/day and at this rate, we have estimated a 14-17 day supply. At this time, please follow the recommendations listed below. We would like to avoid restricting this medication while on shortage. However, a restriction to dedicate remaining supply may be necessary and released as early as mid-next week. The Pharmacy Team is looking at all purchasing options each day. We are buying allocations when they are available and avoiding loaning our current supply.

Please work with your team to facilitate the below options. Please also be aware that, at this time, there is no automatic medication switches or discontinuations. All actions need to be approved with team, except for automatic IV to PO conversions meeting criteria.
PLAN:
Share shortage news with your teams
Be extra diligent with IV to PO/per tube conversions (po metronidazole is available at this time) – Please make this a high priority!
Discontinue unnecessary IV metronidazole and/or duplicate anaerobic coverage
Consider alternative IV anaerobic coverage agents, if needed (examples below – some helpful suggestions)
Anaerobic coverage (non-CNS): IV clindamycin **Reminder: Clindamycin does not penetrate CNS like metronidazole
Hospital acquired infection needing anaerobic coverage (non-CNS): Piperacillin/tazobactam, cefepime + clindamycin
Non-Pseudomonas risk infection needing anaerobic coverage (non-CNS): Ampicillin/sulbactam, cefoxitin, ceftriaxone + clindamycin, fluoroquinolone + clindamycin
Clostridium difficile: PO vancomycin
Please try to reserve IV metronidazole to those with:
CNS abscess
Clostridium difficile treatment in patients with high risk/no gut absorption requiring IV
We would like to avoid using carbapenems, but they are alternatives if the shortage worsens
Contact the ID Pharmacist or ID Team with any questions on substitution or alternatives

Details known on shortage:
Reason for the shortage: Manufacturer delays
Estimated resupply dates: BBraun and Claris are unable to estimate a release date; Pfizer estimates some additional allocation mid-September (not guaranteed)