The Race to the Bottom

The Race to the Bottom

The dangers of de-resuscitation

Jan De Waele


Not giving excess fluid in the initial stages is much better than having to remove it, even if you do it well


Why remove fluid? To prevent or treat the toxic effects of fluid therapy



  • Effective but metabolic side effects, exacerbation of AKI, toxicity
  • Advantage of continuous diuretic infusions with hourly target




  • Able to control rate effectively
  • Invasive support


Targeted therapy: compartmentalized fluid collections (pleural effusions, ascites, etc)


Invasive monitoring, biomarkers of fluid overload, vasopressor requirements

Method TBD by: extent of fluid overload, organ dysfunction attributable to fluid overload, organ function/hemodynamic instability


FACTT Trial: higher neurocognitive impairment with conservative fluid strategy?


“We don’t have a biomarker for euvolemia. What is euvolemia?”


Dry enough? When to stop CVVH? P.M. Honore


We are trying to determine how much fluid is interstitial/intravascular

Bioimpedance key to monitor body water composition


Current methods to assessing volume status?

  • Traditional examinations: physical findings, lab parameters, static measures (CVP, LVV, etc), dynamic measures (SVV/PPV, echocardiography, etc)
  • ECW/ICW > 0.9, EVLWI > 12 mL/kg IBW

How to bring fluid back into the intravascular space?

  • Reabsorption: Plasma oncotic pressure, high dose Albumin, hypertonic saline
  • CRRT: 50-300 mL/hr; might be too slow for extreme hypervolemia, might not tolerate faster due to vascular refilling
  • Albumin only contributes 17% of oncotic pressure


HTS infused over 30 min, 500 mL x 1 hr via CRRT then back to maintenance extraction rate

  • This can be done at least 2x daily per speaker
  • Neuro evaluation, q4h electrolytes, lactate, daily monitoring with PiCCO or echo


DARE RCT on fluid removal

  • TBD (use of HTS, Albumin, CRRT for volume removal)


(Too) permissive hypotension

Karim Brohi


National traumatic hemorrhage data:

Initial death

Early death (cardiovascular collapse)

Late death (with but not of MSOF...TBI?)


In actively bleeding patient, change from perfusion model to a hemostatic one


Essentially, it is useless to attempt to target a blood pressure in these resuscitations; generally hemodynamic targets ended up getting significantly more volume without ever achieving target


Permissive hypotension: too long or too permissive = BAD

Too long: every minute hypoperfused is too long

Too low: for the brain? NO

  • Low, high vs pressor resuscitation: low volume resuscitation better, all animals on pressors DIED
  • Pig model: early resuscitation had higher early CI but massively increased ICP and decreased cerebral O2 delivery
  • Problem is if it’s too low for the heart; early high cardiac biomarkers correlated with death by cardiovascular collapse in 24hrs; significant micro changes in cardiac myocytes, apoptosis  
  • Must maintain coronary perfusion pressure; MAP > 50 or palpable central pulse (prefer not with fluids if bleeding, but if no other option, maybe only option to maintain cardiac support)


“Blood is for bleeding, salt water is for cooking pasta.”

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