Consider the familiar “dry stroke” presentation: an older, hypertensive patient with poor intake, tachycardia, a sticky tongue and an elevated BUN/creatinine ratio. These findings prompt assessment; they do not establish the fluid deficit or the right infusion rate.
Reduced circulating volume can lower cardiac output and cerebral perfusion. In ischemic tissue, impaired autoregulation makes blood flow more dependent on perfusion pressure. That physiology explains why hypovolemia matters; it does not prove that expanding an already adequate blood volume improves recovery.
What did they actually do?
A 2025 Heliyon before–after study compared 824 patients receiving regular hydration with 324 treated after a rapid-hydration protocol was introduced. The regimens were approximately 40–60 mL/h saline versus 300 mL over one hour followed by 80 mL/h for at least six hours. These are study regimens, not bedside orders.
The later period had less early neurological deterioration (END) and more favorable three-month outcomes. However, alteplase and early dual-antiplatelet use also increased. The study excluded important fluid-sensitive groups and severe large infarctions; the title describes presentation within 24 hours while eligibility specifies 48 hours. These limitations prevent a causal claim or reliable protocol transfer. Original cohort.
But… what does the rest of the evidence say?
IVIS: 120 patients without dehydration were randomized to saline at 100 mL/h for 72 hours or no IV fluid. The trial stopped early after more END in the no-IV-fluid group, but the primary efficacy outcome did not differ. This small, early-stopped trial does not establish a universal infusion prescription or safety in patients with fluid contraindications. IVIS trial.
REVIVE: 487 participants with BUN/creatinine ≥15 were randomized to enhanced or standard saline hydration. Enhanced treatment used 20 mL/kg, one-third as a bolus and the remainder over eight hours; standard treatment used 60 mL/h for eight hours. Both groups then received 40–80 mL/h for 64 hours. Major END occurred in 2.9% versus 2.0%; there was no demonstrated overall disability benefit.
Low event rates limited REVIVE’s power, and post-randomization exclusions complicate interpretation. Most strokes were minor; patients receiving or planned for thrombolysis or surgical intervention were excluded. Failure to demonstrate superiority does not prove equivalence, and exploratory subgroups cannot define treatment rules. REVIVE trial.
The 2026 AHA/ASA guideline supports correcting hypotension and hypovolemia, while rejecting hemodilution/volume expansion as routine stroke treatment. It provides no universal fluid volume or duration. AHA/ASA guideline.
Hydration assessment in the ED: evidence and local decisions
1. Assess perfusion, intake, losses and congestion
Assess intake, losses, medications, perfusion, blood pressure trend, urine output, respiratory/venous congestion and electrolyte/renal results. Heart failure or CKD increases overload risk but does not exclude hypovolemia. Fluid assessment guidance.
BUN/creatinine ≥15 is a nonspecific research marker, not a treatment trigger; a lower value does not establish euvolemia. The threshold refers to BUN and creatinine in mg/dL, not urea/creatinine or an unconverted SI ratio. Renal disease, gastrointestinal bleeding and catabolism can alter interpretation. Marker limitations.
2. Use POCUS as part of the assessment
A-lines describe an aerated lung surface, not intravascular dehydration. B-lines can reflect edema, inflammation or fibrosis. Lung-ultrasound consensus. IVC diameter or collapse alone cannot tell you whether another bolus will help. Integrate cardiac, lung and venous findings with serial perfusion assessment; use an appropriate dynamic test when feasible. ESICM hemodynamic guidance.
3. Individualize fluid, reassessment and escalation
For a clinically significant circulating-volume deficit, use an appropriate isotonic crystalloid and reassess its effect. 0.9% saline is a reasonable practical option. Avoid hypotonic solutions for routine acute brain-injury hydration: lowering extracellular tonicity favors water movement into brain cells. Dextrose-containing hypotonic fluids are not routine resuscitation fluids. This does not prohibit dextrose for hypoglycemia or another specific indication. Neurocritical-care fluid consensus.
“Balanced” does not mean interchangeable in brain injury; check the actual sodium concentration and tonicity. A 2026 pilot trial in 80 patients, including 64 with ischemic stroke, found lower chloride with sodium chloride–acetate mixtures. Its size, mixed population and specific formulations do not establish superior neurological outcomes or justify substituting any balanced product. Pilot randomized trial.
A retrospective thrombolysis cohort associated balanced-fluid exposure with greater disability, but confounding and incomplete follow-up prevent causal interpretation. Neither that study nor general ICU findings settles the best crystalloid for AIS. Comparative cohort.
Prescribe the amount and rate for the deficit, ongoing losses and tolerance; count medication infusions and enteral intake. In euvolemia, avoid a routine bolus. Reassess during and after each challenge: perfusion, breathing, oxygen requirement and congestion. Stop or slow fluid if respiratory or venous congestion develops. Persistent hypotension needs cause-directed escalation, not repeated empiric loading. Monitor electrolytes, renal function and, with ongoing saline, chloride and acid–base status. Prescribing and monitoring.
Screen swallowing before oral fluids. If swallowing is unsafe, provide an individualized hydration plan while arranging an appropriate enteral route; reassess IV needs as intake becomes adequate. AHA/ASA supportive care.
4. Keep reperfusion moving
Assess and correct volume problems in parallel with imaging and reperfusion decisions. Follow the stroke pathway’s blood-pressure limits; avoid hypotension and abrupt excessive BP reduction. New hypotension after treatment requires evaluation for hemorrhage, cardiac dysfunction and other causes. Fluid is not a substitute for reperfusion.
Neurological deterioration requires urgent reassessment for hemorrhage, edema, re-occlusion and metabolic causes. Suspected raised intracranial pressure needs stroke/neurocritical-care escalation. Hypertonic saline or mannitol may treat edema or elevated ICP; they are not routine hydration, and improved long-term neurological outcome from these agents remains unproven. Cerebral-edema guideline.
Hyperglycemia alone does not justify aggressive fluid loading. SHINE found no functional benefit from intensive glucose control and more severe hypoglycemia. SHINE trial. Suspected HHS or DKA is different: assess osmolality, ketones, acid–base status and electrolytes, then use the relevant crisis pathway with cardiac/renal adjustments and controlled osmotic correction. Hyperglycemic-crisis consensus.
5. Audit a locally approved pathway
Handover should specify fluid indication, response, balance and the oral/enteral plan. Local order sets require multidisciplinary approval, monitoring and escalation rules; audit complications and reperfusion delays.
Take-Home Messages
Aim for euvolemia. Correct a demonstrated deficit, reassess promptly and keep reperfusion moving. Neither a high BUN/creatinine ratio nor a plausible perfusion mechanism establishes a benefit from routine volume expansion.
