Travis Smith, DO Profile picture
Sep 2, 2020 25 tweets 29 min read Read on X
First, let's start w/ an initial PR:

A 49 y/o F w/ a PMH of HTN, ETOH/THC abuse p/w bilateral leg weakness that started a week ago following during an admission for CAP that has since gotten worse along with urinary and fecal incontinence
is it true weakness or asthenia?

If weakness is present, is it ascending/descending, any back pain, incontinence, sensory deficits?

is the weakness proximal, distal, both?

Also think vascular and myopathy causes
weakness could be anywhere in neuraxis - neuromuscular junction, peripheral nerve, cord, brain. Bilateral concerning for cord

diabetic myopathy can present with leg pain (usually proximal), although it’s usually unilateral

mechanical “pinched” peripheral nerve think unilateral
I think a lot of us think of Guillain Barre any recent upper resp or GI infection?

details about onset and progression are super important

Disease progression can be rapid, and most patients with GBS reach their maximum disability within 2 weeks. ncbi.nlm.nih.gov/pmc/articles/P…
DTR would be important too.. GBS has areflexia

Some myositis can also have decreased DTR,

49% of SRP necrotizing myositis have decreased DTR in one case study

with the pts h/o PNA could consider antisynthetase syndrome
Anti-synthetase syndrome is a rare condition characterized by myositis associated with interstitial lung disease (ILD)

ILD occurs in anti-synthetase syndrome in up to 80–90% of cases.

ncbi.nlm.nih.gov/pmc/articles/P…
check for mechanic hands in anti-synthetase syndrome

Autoimmune- ANCA, SLE, possible antisynthetase syndrome, overlap syndrome

fluoroquinolones can cause neuropathy, ncbi.nlm.nih.gov/pmc/articles/P…

Just another reason to not use first line for cap idsociety.org/practice-guide…
Would be helpful to know if an infectious organism was isolated during the prior admission. If bacteremic could consider epidural abscess with incontinence.

“CAP” could be malignancy with Lambert-Eaton myasthenic syndrome (LEMS)
Time for some more information:

She is afebrile, tachy, crackles in her right upper lobe.
There is 3/5 strength in her bilateral LE proximally and distally with hyperreflexia in both LE. There is no sesnory changes

Na slightly low at 133, CO2 20. WBC 11, Hgb 11, Plts low at 123
What about transverse myelitis? It is acquired focal inflammatory disorder often p/w rapid onset weakness, sensory deficits, and bowel/bladder dysfunction.

At peak 50% are complete paraplegic w/ virtually all of the patients having a degree of bladder/bowel dysfunction
The MCC of TM is idiopathic, & there is no causative factor found. Infections leading to TM include enteroviruses, West Nile, herpes, HIV, human T-cell leukemia virus type 1 (HTLV-1), Zika virus, neuroborreliosis (Lyme), Mycoplasma, & Treponema pallidum. statpearls.com/kb/viewarticle…
Lets back up a bit. what’s the story/labs/imaging leading to the cap dx?

Wonder about Na level too although doubt that would cause isolated symptoms, maybe Wernickes?

Maybe Na overcorrected at OSH and now with ODS? hmm @ABRezMed
pantoprazole can cause B12 deficiency - would explain weakness, not incontinence

subacute combined degeneration from b12 deficiency

Could she have an epidural abscess? PNA causing bacteremia and seeding to the spine. Would likely have back pain though
Would be odd to have TM without sensory findings as most commonly, there is sensory involvement with symptoms, including pain, dysesthesia, and paresthesia at the level involved.

Now for some imaging...
MRI of T and L spine are unremarkable

CXR shows a RUL infiltrate

Just got some records from her last admission. She was tx aggressively for HypoNa while there as her Na was 103 upon admission
An MRI of the brain was obtained showing very bright signal of the bilateral pons and thalami

Final dx central pontine myelinolysis (CPM)

She unfortunatley did poorly as she was sent to palliative care and passed away
CPM is a misnomer, demyelination is not limited to the pons.

wernicke encephalopathy or Machiafava Bignami due to alcohol use affect thalami nuclei first

Beer potomania is very prone to overcorrection. You often have to give D5W or DDAVP to avoid overcorrection.
Those at highest risk for ODM, women, low BMI, Na<120, cirrhosis, underlying eating disorder.

often presents slightly delayed 2-6 days after overcorrection.

More on ODM: Hyponatremia & Central Pontine Myelinolysis as a Result of Beer Potomania:

ncbi.nlm.nih.gov/pmc/articles/P…

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