Hemodilution, Hypervolemic, Hypertension Therapy for Vasospasm patient

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Presentation transcript:

Hemodilution, Hypervolemic, Hypertension Therapy for Vasospasm patient Intern 陳凱峰

Outline Vasospasm in SAH Rational of HHH therapy Pulmonary edema

Vasospasm in SAH SAH Vasospasm hydrocephalus, meningeal irritation, fluid and e disturbances, cerebral vasospasm Vasospasm True vasospasm after clipping / coiling Limitation of CBF More due to remodeling of blood vessel Peak: 7~10 days after bleeding

Best Practice & Research Clinical Anaesthesiology Vol. 18, No. 4, pp

Neuro-protective Hyperoxygenation Hypothermia Avoid hyperthermia Avoid hyperglycemia Triple H ( hypertension, hemodilution, hypervolemia) CBF and prevent ischemia Best Practice & Research Clinical Anaesthesiology Vol. 18, No. 4, pp. 595–630, 2004

Pharmacology Calcium channel blocker Mannitol Magnesium Antifibrinolytic Corticosteroid

HHH therapy First in 1976 For Reduced blood volume, plasma volume, erythrocyte mass 1. CVP ( hypervolemic) 2. Hct ( Hemodilution) 3. BP ( Hypertension)

Hypervolemia Hypovolemia ( cerebral salt-wasting) Reduced delayed cerebral ischemia IVF Complicated with pulmonary edema, brain edema Hard to monitor and target Best Practice & Research Clinical Anaesthesiology Vol. 18, No. 4, pp. 595–630, 2004

Hemodilution Hct to 30%~35% Cerebral oxygen transport and cerebral O2 metabolism Crystalloid, plasma volume expander Dextran, albumin CMRO2 = CBF x OEF x SaO2 Best Practice & Research Clinical Anaesthesiology Vol. 18, No. 4, pp. 595–630, 2004

Hypertension 30~40% more than baseline SBP Ischemic Symptom resolve  regional CBF in ischaemic brain areas Vasopressor delayed global brain edema Phenylephrine, Dopamine preferred Best Practice & Research Clinical Anaesthesiology Vol. 18, No. 4, pp. 595–630, 2004

Journal of Clinical Neuroscience Volume 1, Issue 2 , April 1994, Pages 78-92

Prophylactic post-op fluid therapy How Hypervolemic? Prophylactic post-op fluid therapy

Norway study Normovolemic GrA(16): Hypervolemic GrB(16): 1000ml D5W + 1000ml N/S Until POD12 Keep I/O balance Hypervolemic GrB(16): 2000ml D5W + 2000 ml N/S + 1000~1500 ml colloids Colloid: 500 ml of 4% albumin solution and/or 500–1000 ml of Rheomacrodex (Dextran 40) Until POD 12 CVP: 8~12 MAP: 20%> baseline with Dopamine 5–15 g/kg/min 32 patients received continuous intravenous nimodipine infusions (0.2 mg/ml, 10 ml/h) for the entire study period (Days 1 to 12), followed by oral administration (360 mg/d) for 10 to 14 days norway Mannitol Nimodipine TCD for vasospasm: flow MCA/ICA>3 >6 TCD vasospasm GCS Albumin, Dextran, Glycerol Neurosurgery, Vol. 49, No. 3, September 2001

Neurosurgery, Vol. 49, No. 3, September 2001

Follow up with TCD and SPECT Neurosurgery, Vol. 49, No. 3, September 2001

Normal life independent Conscious BY GCS withini 1 year 5 Good Recovery Resumption of normal life despite minor deficits  4 Moderate Disability Disabled but independent. Can work in sheltered setting  3 Severe Disability Conscious but disabled. Dependent for daily support  2 Persistent vegetative Minimal responsiveness  1 Death Non survival Conscious Neurosurgery, Vol. 49, No. 3, September 2001

Complication

CPMC, NY June 1991 and October 1994 Aneurysmal SAH 2000;31;383-391 Stroke

CPMC HV: PADP>14mmHg CVP>8mmHg NV: PADP 7mmHg CVP: 5 mmHg Fluid HV & NV: D5W 80ml/h 0.9% saline 80ml/h HV: 250ml 5% alb q2h 2000;31;383-391 Stroke

CBF 2000;31;383-391 Stroke

Complication NV HV Cerebral edema 7 (17%) 6 (15%) CHF 1 (3%) 1 (3%) Hyponatremia (<135) 2(5%)

Universal protocol? No double blind randomized clinical trial with exact dosage of fluid Collect three trials CPMC, Presbyterian Medical Center, New York 1999 2 quasi-randomised P Cochrane Database Syst Rev. 2004 Oct 18;(4):CD000483

Others even more complication Only the Philadelphia trial ->reduce the frequency of preoperative secondary ischemia (1984) Others even more complication insufficient data on the effect of volume expansion Thirty hypertensive patients with subarachnoid hemorrhage were divided randomly into two groups. The treated group was begun on preliminary volume expansion, and control of hypertension was carried out using vasodilators and centrally acting drugs. The control group was treated in the classical manner for hypertension, with a diuretic as the foundation for therapy. The incidence of clinical vasospasm was compared to that of angiographic spasm. The incidence of preoperative vasospasm in the treated group was 20%, as compared to 60% in the untreated group (P less than 0.01). Of the treated group, 87% survived to operation, whereas only 53% of the control group survived to operation (P less than 0.01). Cochrane Database Syst Rev. 2004 Oct 18;(4):CD000483

How to reduce pulmonary edema rate? Reduction of Pulmonary Edema After SAH With a Pulmonary Artery Catheter-Guided Hemodynamic Management Difficult to monitor

How to reduce pulmonary edema rate? Sample: 453 spontaneous SAH Group I: 174 (July 1998 – Jan 2000 ) Group II: 279 ( Feb 2002 - Jun 2002) identical Average age , Co-morbidity, hemorrhage severity, incidence of vasospasm Neurocritical Care August 2005, Volume 3, Issue 1, pps. 011-015

Method – PA catheter guide Group I: 174 (July 1998 – Jan 2000 ) Hypervolemia : CVP > 8mmHg Hypertension: MAP: 110-130 mmHg Group II: 279 ( Feb 2002 - Jun 2002) normovolemia :wedge pressure: 10–14 mmHg Cardiac index: >4.5 L/minute/m2 Moderated HTN: mean pressure: >100 mmHg Neurocritical Care August 2005, Volume 3, Issue 1, pps. 011-015

Complication Group I Group II P value Pulmonary edema 14% 6% <0.03 Sepsis rate Mortality 34% 29% <0.04 Neurocritical Care August 2005, Volume 3, Issue 1, pps. 011-015

Summary 3 H therapy No randomize trial proved Monitor directed therapy is important

Thanks !