VA morning report 1.16 – Stroke and clotting on anticoagulation

Case Summary

Thanks to Arielle for presenting a fascinating case of a 65M with multiple prior stokes who presented with AMS, hypernatremia and then found to have new multifocal strokes.

Top pearls

  1. Head imaging [CT non-contrast] is not necessary in patients presenting with altered mental status [without trauma] after an obvious cause [e.g. hypernatremia] is uncovered on routine labs.
  2. Multiple trials have previously shown that PFO closure does not reduce the incidence of recurrent stroke(CLOSURE-I, PC, and RESPECT). However, two recent meta-analyses showed potential benefit in patients with recurrent cryptogenic strokes at the cost of an increases risk of Afib/flutter . Link 1      Link 2
  3. While a thrombosis on anti-coagulation raises concern for a number of hypercoaguable conditions [see below] the first step is to clarify whether the patient was receiving adequate anticoagulation [e.g. under-dosing].

Stroke

Initial evaluation of a stoke
  • Is this a stoke? [DDx: Seizure, hypoglycemia, syncope, other]
    • If so, what kind?
      • Ischemic
      • Hemorrhagic
        • Where in the skull?
  • Last known normal?
  • NIH stroke scale?
  • contraindications to tPA?
    •  Benefits
      • <90 min —> NNT for functional independence = 3.6
      • <180 min —> NNT = 4.3
    •  Risk
      • 6% of any bleed
      • 1-2% of significant bleed
  • Embolectomy?
    • More evidence to suggest benefit up to 24h
    • NNT 2-3
Work up
ink-image
Initial treatment
  • Aspirin 325 x1 —> 81
    • Give in ED if no tPA
    • Give 24h later if tPA given
  • Statin
    • Atorvastatin 80
  • BP management
    • Permissive HTN up to 220, usually < 1 week
  • See above for tPA or embolectomy

Clotting on anticoagulation

  • An important part of the management of  VTE is the reversal of any underlying trigger.
    • Easier when the DVT is provoked [e.g. surgery]
  • In cases with unprovoked VTE either:
    • provoking factor was not recognized OR
    • There is a genetic disruption [e.g anti-thrombin 3] in the control of the coagulation cascade.
      • These disruptions are usually related to a protein deficiency in the regulation of the cascade [e.g., protein C deficiency]
      • The urge to uncover this disorder is tempered by the fact that it rarely changes management [life long anticoagulation]
      • Down-regulation of the pro-coagulant factors [e.g. Factor 2] with lifelong anticoagulation is usually sufficient for these conditions.
  • In some acquired causes, the driver for the hypercoaguability exists outside the coagulation cascade  [e.g. heparin-induced thrombocytopenia].
    • Syndrome specific features may offer clues to the Dx [e.g. recent receipt of heparin –> thrombocytopenia], but other features include
      • Clotting in atypical locations – e.g. Budd Chiari/venous sinus thrombosis
      • Multiple simultaneous thrombi
      • Clotting while on full dose anticoagulation.

Here’s one approach to this scenario

Step 1: Is the patient taking/on the right dose of anticoagulation?
Step 2:  Consider embolic disease
emboli.png
Step 3:  Consider thrombotic disease
Thrombotic.png

VA Ambulatory Report 1.10.18 – Aches and Pains all over – PMR and RA

Thank you Monica for presenting the case of an elderly gentleman presenting with chronic fatigue, muscle aches, wrist and hand joint pain, and weight loss found to have PMR and RA.

Learning Peals  Screen Shot 2017-10-11 at 12.58.11 PM

  1. LT’s pearl: Many patients with PMR present with acute onset of symptoms
  2. Other lab findings that may be present in patients with PMR: mild normocytic anemia, elevated alk phos (although more common in patients with GCA)
  3. Patients with PMR only need temporal artery biopsy if they have symptoms of arteritis. About 5-30% of patients with PMR will have GCA

 

Polymyalgia Rheumatica Refresher

  • Clinical Manifestations
    • Proximal pain and morning stiffness
      • Shoulder pain is the most common symptom
      • LT’s pearl: Many patients report acute onset of symptoms
      • Distal symptoms occur in ~50% of patients including peripheral arthritis, carpal tunnel, pitting edema of hands and feet)
    • Systemic symptoms (fever, weight loss, malaise) are present in ~1/3 of patients
    • Laboratory Findings
      • Elevated inflammatory markers
      • Non specific findings (not present in all patients)
        • Mild normocytic anemia
        • Elevated Alk Phos – although more common in patients with GCA
  • Diagnosis
    • No other systemic disease to explain symptoms
    • Onset of symptoms after age 50
    • Proximal aching and morning stiffness lasting >30 minutes for at least 2 weeks
      • LT’s pearl: Many patients report acute onset of symptoms
      • Shoulder pain is the most common presenting symptom
    • ESR > 40
    • Rapid resolution of symptoms with prednisone
      • Lack of response strongly suggests another diagnosis
    • There are no set diagnostic criteria, but the ACR/EULAR have proposed criteria to be used in research studies but do not recommend use for diagnosis in individual patients
    • Atypical PMR
      • Asymmetric symptoms
      • Low ESR
        • Some patients have normal or mildly elevated ESR (7-20% at time of diagnosis)
          • Check CRP
          • If both ESR and CRP are normal, much less likely to be PMR
  • Does my patient with PMR have GCA?
    • 50% of patients with GCA have PMR. Of those with PMR, 5-30% get GCA
    • Clinical manifestations of GCA
    • Only need to get temporal artery biopsy if the patient is having symptoms of temporal arteritis
  • Treatment
    • Goal of therapy: Improve symptoms
    • Starting dose: 15-20 mg prednisone per day
    • After a period of quiescence (2-4 weeks) then start a slow taper by 10-20% every 2-4 weeks
    • 50% of patients will have recrudesce of their symptoms and need re-treatment with steroids or increase in their steroids

Evernote Link: https://www.evernote.com/l/AMr2DzbkfG9K56vgSepfENvXq9AhGchMp04

VA Morning report pearls: Struvite stones and LBBB

Here are some round-up pearls from 2 great cases this week!


Case summary 1: On Monday, Jill presented the case of an elderly man with a history of obstructive struvite stones and Proteus bacteremia s/p nephroureterostomy tube, who presented with septic shock from recurrent/persistent struvite stones.

  • Interestingly, Proteus contributes to recurrent stone formation in 2 ways:
    • Urease splitting bacteria generate high urinary pH levels
    • The body can’t clear the urinary tract of the bacteria because they are embedded in the stones.
  • Other reasons to have alkaline urine: 
    • (1) urinary tract infection (Proteus and others)
    • (2) metabolic or respiratory alkalosis
    • (3) failure of acidification (renal tubular acidosis)
    • (4) ingestion (alkaline diet [a fad diet right now!], medications like sodium bicarbonate).
  • This is important, as alkaline urine can precipitate struvite and calcium phosphate stone formation
    • Acidify urine with cranberry juice or betaine
    • In contrast uric acid, cystine and calcium oxalate [most common in adults] stones precipitate in acidic urine (prevent with alkalinzation of urine via dietary changes or calcium citrate/K citrate

Here’s a great review on nephrolithiasis:  https://www.aafp.org/afp/2011/1201/p1234.html#afp20111201p1234-c1

  • A nephroureterostomy tube has both internal (via ureter) and external (via nephrostomy tube) drainage, so lack of external drainage does not necessarily indicate tube dysfunction.

Here’s a diagram for the visual-minded:

nephrostomy_catheter-fig_5-en


Case summary 2: At intern report, we discussed a patient who was post-op day #1 s/p an ankle fusion who developed chest pain and was found to have diffuse ST depressions and STE in aVR. This got us to talking more broadly about ACS and “STEMI equivalents.”

  • Moral of the story: new or presumed new LBBB may not predict ACS.
  • 2 retrospective studies looked at ~900 and ~300 patients with new or presumed new LBBB and concluded
    • Those patients with new or presumably new LBBB are a high-risk group (older, higher TIMI scores, more cardiomyopathy).
    • However only ~1/3 had acute MI, while the remaining patients had other cardiac or non-cardiac diagnoses

Here’s a Medscape article summarizing the literature on LBBB as a STEMI equivalent: https://www.medscape.com/viewarticle/753695_1