This document summarizes key points about IV fluid management in neurosurgery patients. It discusses how monitoring volume status is important but fluid therapy should be individualized. Restrictive fluid therapy was found to reduce hypoxemic episodes in SAH patients with comparable outcomes to liberal fluid management. Fluid responsiveness can be assessed dynamically. Sodium levels need to be monitored in SAH, ICH, and TBI patients as dysnatremia impacts outcomes. Fluid therapy should target euvolemia using isotonic fluids to avoid complications in brain injured patients.

1. IV Fluids in Neurosurgery
Department of Neurosurgery
JOURNAL CLUB
Dr RE Anto

2. Articles

4. Key Points
• A fluid management strategy is essential for patients with critical
neurological illness.
• Monitoring of volume status is recommended.
• Fluid therapy should be individualized rather than standardized.
One relatively straightforward goal: avoid brain ischemia!

5. Volume status
• Central venous pressure – poor predictor of preload
• Arterial Pulse pressure variation
• Mechanically ventilated (TV atleast 8ml/kg)
• Sinus rhythm
• Closed chest
• Observational study by Drevet et al. on SAH patients
• Restrictive fluid therapy vs. weight based liberal fluid management
• Fewer hypoxemic episodes
• Had comparable outcomes (Kidney injury; Incidence of vasospasm; Mortality)

6. Fluid responsiveness
• Dynamic measure.
• Frank Starling curve (1920)
• 250-500ml fluid blous
• Limitations:
• Right atrial filling pressure increase
in parallel with the infused volume?
• Less than 5% of infused volume
remains intravascular
• Decreased Afterload by Fluid-
Induced Hemodilution
• Measurement of Hb

7. Sodium homeostasis - SAH
• Hyponatremia – increased morbidity and mortality
• Longer hospital stays
• 1 day prior to vasospasm
• ? Identifying patients at risk of vasospasm
• Location of aneurysm has no relationship
• No optimal management strategy in dysnatremia
• First 4 days: hypernatremia
• 6-12 days: hyponatremia
• Fludrocortisone – does not improve outcomes

8. • ICH
• 15% of patients are hyponatremic
• Worse NIHSS scores on admission and during hospitalization
• Higher mortality rates.
• Mechanism – osmotic changes – cerebral oedema
• TBI
• Dysnatremia in 40%
• Hyponatremia – increased mortality rates
• Worsening GCS
• Cerebral edema
• Hypernatremia
• hyperosmolar therapy; hypovolemia; central DI; SIADH; CSW

9. Targeting fluid therapy
• Amount of fluid vs. how it is guided
• SAH
• CO- guided therapy, esp high risl of cardiopulmonary complications
• Improved neurological outcomes
• Delayed cerebral ischemia
• Vasospasm (TCD)
• Trial by Egge et al.
• Normovolemia (3 l/day)
• Triple H (hypertension hypervolemic haemodilution – 4-5 l/day
• More complications in HHH group

11. • TBI-Triggered vasospasm
• Vasogenic and cytotoxic edema
• Impaired autoregulation
• BBB Breakdown
• CPP 60-70mmHg
• Adjusted MAP to keep ICP < 20mmHg
• Individualizing therapy
• Prospective analysis (Czosnyka et al)
• CPP optimization strategy vs Fixed range BTF
• Pressure reactivity index (ABP and ICP)
TBI

12. Fluid selection
• Which fluid?
• Avoid hypotonic and glucose containing solutions
• Worse outcomes
• SAFE trial (2004)
• Saline vs Albumin Fluid evaluation
• 2007 subgroup of TBI patients
• Strong preference of crystalloid over albumin
• Normal saline vs Balanced crystalloid (eg Ringers Lactate)
• No high quality data
• Recent large prospective cluster-randomized trial
• Potentially slightly more favourable outcomes with balanced solution
• More stable electrolytes, Less fluid intake, Less stress hormones

14. Conclusion
• May influence outcomes in brain injured patients
• Hypervolemia is detrimental
• Avoid hypovolemia
• Euvolemia using isotonic fluids
• More or less our current practice in SBAH

15. THANK YOU