Triple-H Therapy for Cerebral Vasospasm following Aneurysmal Subarachnoid Hemorrhage
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The document discusses the relevance and effectiveness of Triple H therapy in preventing and treating vasospasm, highlighting that its mainstay protocols—hypervolemia, hypertension, and hemodilution—have raised concerns due to associated risks and complications. Current evidence suggests that hypervolemia does not improve outcomes and may worsen cerebral oxygenation, while the use of induced hypertension lacks proven benefits and carries high complication rates. Recent guideline recommendations have shifted towards maintaining normovolemia and induced hypertension only for specific cases, reflecting an evolution in clinical practice driven by emerging research findings.
![Hemodilution [Hematocrit 30]
• 40%–50% of patients with SAH develop anemia during in ICU
• Age, sex, surgery, and blood drawing for investigations
• Anemia has been associated with increased morbidity
because of infarction, disability, and eventually death
• Low brain tissue oxygen because of anemia, leading to
neuronal injury in patients with acute brain injury
• Optimal Hb concentration is still a matter of debate
• Target Hb >10 g% is a reasonable option
Chugh C, et al. Neurol India 2019.](https://image.slidesharecdn.com/triplehtherayp-190721020307/85/Triple-H-Therapy-for-Cerebral-Vasospasm-following-Aneurysmal-Subarachnoid-Hemorrhage-8-320.jpg)
Triple-H Therapy for Cerebral Vasospasm following Aneurysmal Subarachnoid Hemorrhage
- 1. Is Triple H Therapy still relevant in preventing & treating vasospasm? current status Dhaval Shukla NIMHANS, Bangalore
- 2. J. Neurosurg. / Volume 45 / August, 1976 Kosnik AJ, et al. JNS 1976
- 3. 3-H Original Protocol • Elevate the SBP 40 to 60 points upto 250 mm Hg • As much as 3 L transfusion with colloid and/or blood is necessary (regardless of normal hematocrit) in the first 24 h in addition to daily maintenance fluid • Autoregulation is poor or absent in these patients, and that CBF therefore follows the MAP • Increasing CPP is the most effective available treatment, provided it is instituted before vascular membranes are extensively damaged • Caution in the use of this technique is advised, since the regimen is not without risk Kosnik AJ, et al. JNS 1976
- 4. 3-H Therapy • 3-H became the mainstay in the prevention and treatment of cerebral vasospasm • Hypervolemia • Hypertension • Hemodilution
- 5. Hypervolemia - RCT Lennihan L, et al. Stroke 2000. There was no difference in symptomatic vasospasm
- 6. Hypervolemia Increased risk of complications • Pulmonary edema • Cardiac • Arrhythmia • Congestive heart failure • Cerebral edema • Sepsis
- 7. Hypervolemia • No difference in designated clinical endpoints between the two therapies • Hypervolemia does not improve and might even worsen cerebral oxygenation • Hypervolemia is associated with complications Careful fluid management to avoid hypovolemia may reduce risk of DCI after SAH Prophylactic hypervolemic therapy is unlikely to confer an additional benefit
- 8. Hemodilution [Hematocrit 30] • 40%–50% of patients with SAH develop anemia during in ICU • Age, sex, surgery, and blood drawing for investigations • Anemia has been associated with increased morbidity because of infarction, disability, and eventually death • Low brain tissue oxygen because of anemia, leading to neuronal injury in patients with acute brain injury • Optimal Hb concentration is still a matter of debate • Target Hb >10 g% is a reasonable option Chugh C, et al. Neurol India 2019.
- 9. Induced Hypertension iHT - RCT Gathier, et al. Stroke 2018. •Poor outcome at 3 months (mRS>3) •30-day case-fatality •Barthel Index •Stroke Specific Quality of Life Scale •Hospital Anxiety and Depression Scale •Cognitive Failures Questionaire
- 10. Induced Hypertension Complications • Cardiac arrhythmia • Pulmonary edema • Hemorrhagic transformation • Intracranial bleeding iHT is a labor-intensive treatment There is still no evidence that iHT improves outcome in patients with DCI High rate of serious complications associated with iHT Widespread use of iHT in aSAH patients with DCI and the pertinent guideline recommendations may require reconsideration
- 11. 3H Therapy RCT Intervention • 1000 to 1500 ml of colloids • dopamine, 5–15 microg/kg/min Target • CVP 8 -12 cm H2O • Hematocrit 30 -35% • MAP >20 mm Hg Outcome –No Difference • Cerebral vasospasm – Clinically/ TCD • CBF • GOS at 1 year • Neuropsychological Cost and Complication Egge A, et al. Neurosurgery 2001.
- 12. Current Practices of 3-H Prophylaxis and Therapy in Patients with SAH • Members of the Neurocritical Care Society • 167 (45%) respondents Meyer, et al. Neurocritical Care 2011.
- 13. International Survey • 626 respondants • Variablity America Vs. Europe • High volume Vs. Low volume Center Stevens RD, et al. Intensive Care Medicine 2009.
- 14. International Survey Stevens RD, et al. Intensive Care Medicine 2009.
- 15. International Survey Stevens RD, et al. Intensive Care Medicine 2009.
- 16. Survey 19 35 45 39 10 4 0 5 10 15 20 25 30 35 40 45 50 1987 1996 2005 2009 2011 2015 Year %
- 17. Guidelines for 3-H 1994 -2011 • Preventive treatment in 1994 (level of evidence III to V, grade C) • Reasonable approach in symptomatic vasospasm treatment in 2005 to 2009 (class IIa, level of evidence B) • Finally abandoned in 2011 (moderate-quality evidence; strong recommendation) • Increasing evidence of harm (high-quality evidence; strong recommendation) • Maintain euvolemia, rather than hypervolemia (moderate-quality evidence; strong recommendation) • Induced hypertension remains a recommendation for the treatment of patients clinically suspected of cerebral vasospasm and cerebral delayed ischemia (CDI) (moderate-quality evidence; strong recommendation)
- 18. What we follow in our unit • Normovolemia • Normotension • Early mobilization • Post op lab including hemoglobin and electorlytes • CT scan if neurological deterioration • DCI – Normalize blood pressure if low – Intraarterial nimodipine
- 19. Current Practices of 3-H Prophylaxis and Therapy in Patients with SAH • No consensus on how to administer therapy • No agreement on clinical endpoints to guide therapy • No clear patterns or trends for initiating prophylactic therapy • Variability in the administration of prophylactic 3-H derives from the lack of evidence and guidelines
- 20. Acknowledgement