Monthly Archives: July 2017

ABCD2 Score

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TIA Prognosis and Key Mx Considerations by National Stroke Association

 

Reference:

Stroke.org. (2017). [online] Available at: http://www.stroke.org/sites/default/files/resources/tia-abcd2-tool.pdf?docID [Accessed 31 Jul. 2017].

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Heads up Maneuver

Clinical scenario:  Patient with stroke comes in with large vessel occlusion and neuro deficits; he was placed supine for CT scan and NIHSS improved.  Vascular imaging still shows clot, but deficits are now nondisabling and NIHSS is low.  Should you proceed with thrombectomy?

Small study from UCLA used the Heads Up maneuver to select patients who should proceed to thrombectomy.

 

Patients included:

  1. stroke within 7.5h onset
  2. disabling neuro deficit on presentation
  3. improved while on CT to nondisabling deficit
  4. evidence (in MRA) of persisting large vessel occlusion

 

Heads up Maneuver: (performed in angio suite)

  1. position 90 degrees upright x 30 minutes, monitor BP/HR q5-10mins
  2. if worsened –> lower to supine, proceed with angio
  3. if remained stable –> lower to supine or 30 deg HOB; transfer to stroke unit

 

Pathophysiology of Delayed Collateral Failure:

STROKE –> increased CO / SVR –> improved flow to peri-infarct regions –> MI / CHF / dysrhythmias / sepsis / dysautonomia / drugs –> reduced CPP –> delayed collateral failure –> expansion of core infarct

 

Heads Up:

Head position influences collateral flow by increasing flow velocity in affected MCA. Impaired autoregulation allows perfusion to collateral channels to become passive-pressure dependent.  Head flat position increases CPP by 20%, improves neurologic function in 15% of patients.  Risk of aspiration PNA with head flat position is <5%.

 

Outcome:

The study found that heads up maneuver can be used to stress collateral systems and identify those patients who are vulnerable to hemodynamic failure.

  1. Only 5 patients included in the series – all had high NIHSS on arrival, improved during MRI scanning.
  2. Two patients tolerated 30 minutes, no thrombectomy performed, had excellent outcome with just medical therapy.
    1. *Spontaneous recanalization occurred within 72h (assumed that vigorous collaterals promoted recanalization).
  3. Three patients worsened with manuever and had successful recanalization and excellent outcomes as well.

 

Reference:

Ali, L., Weng, J., Starkman, S., Saver, J., Kim, D., Ovbiagele, B., Buck, B., Sanossian, N., Vespa, P., Bang, O., Jahan, R., Duckwiler, G., Viñuela, F. and Liebeskind, D. (2016). Heads Up! A Novel Provocative Maneuver to Guide Acute Ischemic Stroke Management. Interventional Neurology, 6(1-2), pp.8-15.

Mt. Fuji Sign

The Mt. Fuji sign is a radiologic finding seen in tension pneumocephalus.  Bilateral hypoattenuating collections are seen in the frontal subdural space, which causes compression and separation of the frontal lobes.

 

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Notice the widening of the interhemispheric space between the tips of the frontal lobes which resembles the silhouette of Mt. Fuji.  

 

In tension pneumocephalus, air enters into the cranial vault through disruption of the skull or skull base.  Air pressure increases within the subdural space due to a ball-valve mechanism, where air enters into subdural space but egress of air is blocked by an obstruction.

Tension pneumocephalus may occur after surgical evacuation of SDH (2.5-16%), skull base surgery, paranasal sinus surgery, posterior fossa surgery in sitting position, or head trauma.

To diagnose tension pneumocehpalus, CT findings should correlate with clinical signs of deterioration.

Peaking sign” (compression of frontal lobes without separation of frontal lobes) has also been linked to tension pneumocephalus.

Treatment includes:

  1. emergent decompression to alleviate pressure
    1. drilling burr holes
    2. craniotomy
    3. needle aspiration
    4. EVD placement
  2. administration of 100% oxygen
  3. closure of dural defects
  4. careful monitoring for clinical signs of deterioration
  5. serial CT scanning of brain

This is Mt. Fuji in Japan

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Reference

Michel, Steven J. “The Mount Fuji Sign.” Radiology 232.2 (2004): 449-450.

 

Upper Extremity Veins

Deep Veins:

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1. paired ulnar, radial and interosseous veins in forearm
2. paired brachial veins of upper arm
3. axillary vein (continues as subclavian vein)

 

Superficial Veins:

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  1. cephalic vein
  2. basilic vein

 

References

“Deep Veins Of The Upper Extremity.” Uptodate.com. Web. 27 July 2017.

“Primary (Spontaneous) Upper Extremity Deep Vein Thrombosis.” Uptodate.com. 27 July 2017.

Vocera Stuff

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Diabetes Insipidus

Production of arginine vasopressin – by magnocellular neurons in the supraoptic and paraventricular nuclei of the hypothalamus.  Transported to the neurohypophysis via hypothalamo-hypophyseal tract.  Injury to these structures leads to DI.

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Triphasic response in DI:

  1. First phase – DI caused by “stunning” of the magnocellular neurons, no AVP secretion.
  2. Second phase – injured hypothalamic cells degenerate and release their stored AVP
  3. Third phase – if majority of these neurons are destroyed, permanent phase of DI begins

 

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Reference:

Schreckinger, Matthew, Nicholas Szerlip, and Sandeep Mittal. “Diabetes Insipidus Following Resection Of Pituitary Tumors”. Clinical Neurology and Neurosurgery 115.2 (2013): 121-126.

Classification and Severity of Diabetes Insipidus

Interesting classification of DI, taken from Neurology India, groups DI into mild and severe based on some clinical and lab findings.

 

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This was their protocol for diagnosis and management of DI in patients who underwent craniopharyngioma surgery.

 

Protocol for diabetes insipidus

  • Diagnosis:  UO > 4ml/kg/h over 6 h perior OR Na >145 mEq/L with USG <1.005
  • Monitoring
    • if drowsy, unable to drink – measure Is and Os hourly, sum every 6 hours
    • Foley until UO reasonably controlled
    • intraop Na if surgery >6h determines type of IV fluids and if pitressin required in OR
    • measure Na q6h day 1
    • measure Na q12h day 2 until stable x 3 days
    • measure Na daily x 1 week
  • Treatment
    • Fluids until patient is awake and demonstrates intact thirst mechanism
      • 0.45% saline when UO 4-6 ml/Kg/h
      • D5W when UO >6ml/kg/h
    • DDAVP
      • day 1 – 5 unit IV boluses of pitressin
      • started as early as possible, usually on 2nd day, oral DDAVP 100 ug tablets of fractions of tablets
  • Adequacy of control
    • based on serum Na rather than Is and Os
      • check frequency >150 or <130 or inc/dec by >10mEg/L in 1 day

 

Other pearls:

  • Adipsia may be complication of hypothalamic damage
    • diminished thirst sensation
    • higher risk of developing hpyernatremia
    • require round the clock DDAVP
    • need to be trained to drink 2-3L water per day
    • gradually resolves with partial or complete thirst recovery by 9 months
  • Polydipsic with high UO
    • patient compensating with increased PO intake, normal or low Na
    • at risk for water intoxication or hyponatremia
    • use oral rehydration solution rather than plain water

 

Reference:

Chacko, AriG et al. “Evaluation Of A Protocol-Based Treatment Strategy For Postoperative Diabetes Insipidus In Craniopharyngioma”. Neurology India 63.5 (2015): 712.