ANESTHETIC MANAGEMENT OF THE PATIENT WHO REFUSES BLOOD

TRANSFUSION

PREPARED BY:AHMAD SHAFWAN BIN ABDULLAH

SUPERVISOR:DR ROHANI RAMLIY

Article by Jacques F. Dupuis; DY Tien Nguyen, Department of Anesthesiology and Critical Care, The University of Texas M.D, Anderson Cancer Center, Houston, Texas

2 MAJOR REASONS:

1. FEAR OF DISEASE TRANSMISSION-agree for autologous blood tranfusion

2. RELIGIOUS BELIEFS

MEDICAL CHALLENGES• LIMITATION IN MAINTAINANCE OF OXYGEN TRANSPORT, HEMOSTASIS AND

COAGULATION UNDER CONDITION WHICH ELEMENTS PROGRESSIVE DEPLETED, HOWEVER UNABLE TO REPLACE

OXYGEN DELIVERYIT IS NECESSARY TO MATCH OXYGEN CONSUMPTIONCRITICAL OXYGEN DELIVERY DEFINES AS POINT AT WHICH OXYGEN DELIVERY IS INSUFFICIENT TO OXYGEN CONSUMPTIONDELIVERY OXYGEN LIMITED > LIMITED IN TISSUE OXYGENATION > ORGAN DAMAGE > DEATH

HEMOSTASIS, COAGULATIONDEPENDS ON PERIPHERAL VASCULATURE INTEGRITY, PLATELET NUMBER & FUNCTION, COAGULATION FACTORS

Ott & Cooley report – 542 patient who underwent cardiovascular surgery with 12 deaths related to blood loss.

PHYSIOLOGY AND LIMITS OF OXYGEN TRANSPORT

1. HYPOVOLEMIA > ANEMIA > INADEQUATE OXYGEN DELIVERY BY REDUCTION OF CARDIAC OUTPUT

2. MAINTAIN NORMAVOLAEMIA > COMPENSATORY INCREASE IN CARDIAC OUTPUT UP TO LIMIT ALLOWABLE HB REDUCTION

3. HEMODILUTION > REDUCED BLOOD VISCOCITY > DECREASE IN PERIPHERAL VASCULAR RESISTANCE > TRIGGER SYMPATHETIC PATHYWAY TO INCREASE CARDIAC OUTPUT

BALANCE BETWEEN OXYGN DELIVERY & CONSUMPTION EXPRESSED BY OXYGEN EXTRACTION RATIO

O2 EXTRACTION RATIO = O2 CONSUMPTION/ O2 DELIVERY

ADEQUATE COMPENSATION OCCURS UNTIL RATIO IS 0,5. IF RATIO > 0.5 – METABOLIC & HEMODYNAMIC DISTURBANCE ENSUES

MECHANISM FOR COMPENSATION1. INCREASE IN CARDIAC OUTPUT & ORGAN

BLOOD FLOW2. INCREASE IN O2 EXTRACTION from THE

BLOOD3. DECREASE IN HEMOGLOBIN AFFINITY FOR

OXYGEN

INCREASE IN CARDIAC OUTPUT & ORGAN BLOOD FLOW

1. DECREASE IN BLOOD VISCOCITY > DECREASE IN SYSTEMIC VASCULAR RESISTANCE > INCREASE IN VENOUS RETURN

2. INCREASE IN PLASMA LEVEL OF CATECHOLAMINES

INCREASE IN O2 EXTRACTION FROM THE BLOOD

MYOCARDIUM HAS THE HIGHEST EXTRACTION RATIO (0.5-0.7) >> AEROBIC GLYCOLYSIS & LIMITED METABOLIC RESERVE

DECREASE IN HEMOGLOBIN AFFINITY FOR OXYGEN

Van Woerkens report-case of acutely anemic Jehovah’s witness-position of oxygen dissociation, corrected for pH & pCO2 shifted to the right, not before HCT reach at 8%

Wilkerson et al

Anemia was tolerated to hematocrit of 15%, severe deterioration in cardiac output occurs <10%

Arterial lactate start rising at HCT 10%

Left ventricular extraction ratio (0.5-0.6) does not change from HCT 20% to 4%.

Gerd report • Evidence in clinical setting of chronic anemia

in 7 children (aged 7months – 11 years)• Average Hb: 3.3 , with the lowest 1.9g/dL• All patients had elevated cardiac index, heart

rate and stroke volume and decreased systemic vascular resistance that reverted to normal after blood tranfusion

Van Woerkens report

In a fully monitored Jehovah’s witness under anesthesia – acute hemodilution from 31% hematocrit (10.1g/dL) to Hct :20% (Hb 6.1) induced a decrease in systemic vascular resistance of 53% & increase in cardiac output of 54%

Critical oxygen delivery after which oxygen consumption gradually decreased at 184mL/m2/min or 4.9ml/kg/min at Hb 4. Oxygen extraction was 0.44 (mixed venous PaO2 34mm Hg, mixed venous saturation 56%)Death postoperatively at Hb 1.6g/dL.

In subjects with restricted coronary flow , some studies indicate that cardiac function is maintained or improved with moderate hemodilution due to flow & increase in oxygen extraction. However, few factors eg degree of stenosis, metabolic demands of myocardium, myocardial dysfunction affects in oxygen extraction.

Singbarti et al reportASA I : patient who undergoing hip arthroplasty showed evidence of ischemia based online ST segment at Hb 4.5ASA II-III : Hb 6.6

In term of age, elderly patient shows similar compensatory increase in cardiac output younger patient.

THERAPEUTIC OPTIONS

• Preservation for oxygen transport & reduction of oxygen consumption

• Reduction of oxygen consumption• Preservation of hemostasis and coagulation

A. Hemodilution (normovolemia/hypervolemia) – nonoxygen- carrying solutions, colloids, crystalloids, oxygen-carrying solutions, fluorocarbon emulsion, Hb solutions

B. Reduction of blood loss due to invasive monitoring & instrumentation- Controlled hypotension, pharmacologic interventions,

coagulation factor stimulation, topical hemostatics, intraoperative positioning, surgical techniques, non surgical approach, radiologic techniques (embolization), avoidance of iatrogenic blood loss, avoidance of negative interference with hemostasis & coagulation (dextrans, starch

C. Autologous transfusion - Preoperative storage(liquid/ frozen)- Intraoperative/ postoperative blood salvage – passive

systems (unprocessed blood) & active systems (cell separator/ saver, cardiopulmonary bypass machine)

D. Increase in erythopoeisisE. Increase in oxygen-carrying capacity of Hb – increase FiO2, avoidance of agents that limit FiO2 such as Desflurane or limitation of concentration, avoidance of negative interferencewith O2 carrying capacity of blood, control of factors responsible for Hb affinity for O2 (pH, pCO2, temperature)

F. Increase in oxygen-carrying capacity of plasma – hyperbaric O2, hypothermia

G. Increase cardiac output (inotrope eg, dobutamine) & avoidance of negative interference with tissue oxygen uptake (cyanide ion toxicity)

REDUCTION OF OXYGEN CONSUMPTIONHypothermia, Artificial ventilation, Sedation

PRESERVATION OF HEMOSTASIS AND COAGULATIONPlateletpharesis/ plasmapharesisReduction of blood loss

ANESTHETIC IMPLICATIONSMONITORING

• COMMON PARAMETERSOXYGEN SATURATION, HB LEVEL, ARTERIAL AND MIXED VENOUS BLOOD GASES, CARDIAC OUTPUT – CALCULATION OF OXYGEN DELIVERY AND OXYGEN CONSUMPTION & OPTIMAL TIMING OF REINFUSION OF PREOPERATIVELY HARVESTING RBC

• ARTERIAL LINE & PUMONARY ARTERY CATHETER• MONITORING OF HEMOSTASIS & COAGLATION - ALLOW

FOR CORRECT TIMING OF PLASMA AND PLATELET TRANFUSION

SPECIAL REQUIREMENTS FOR INTRAOPERATIVE BLOOD HARVESTING

• A CIRCUIT, WHICH H INFLOW TO RESERVOIR FROM ARTERIAL/ VENOUS AND OUTFLOW FROM RESERVOIR IS VENOUS. SIMPLEST METHOD IS BLOOD WITHDRAWAL BY GRAVITY INTO COLLECTION BG WITH ANTICOAGULANT

• CELL PROCESSOR – ALLOWS FOR TEMPORARY SEPARATION & REINFUSION OF PLATELETS/ PLASMA – USUALLY FOR OPERATION WHICH INVOLVED EBL >25% FROM BLOOD VOLUME

• ATRIOVENOUS LOOP – FOR INCIRCULATION & REINFUSION

MANAGEMENT OF ANESTHESIA

• MODE OF ANESTHESIA – ALONE OR COMBINED REGIONAL / GENERAL ANESTHESIA

• INDUCED HYPOTENSION• HEMODILUTION WITH MINIMAL DEPRESSION OF

CARDIAC FUNCTION• INHALATIONAL AGENT – DESFLURANE LIMITS FIO2• FIO2 1.0 – MAXIMIZE HB SATURATION & DISSOLVED

OXYGEN IN PLASMA• MODERATE HYPOTHERMIA• REDUCE O2 CONSUMPTION – AVOID SHIVERING &

RESTLESSNESS POSTOPERATIVELY, THUS ARTIFICIAL VENTILATION, SEDATION, & MUSCLE RELAXANT CAN BE USED

CASE REPORT39 YEARS OLD WHITE WOMA (170CM, 89KG) WITH DIAGNOSIS OF HUGE OSTEOSARCOMA OF RIGHT FEMUR WITH LUNG METASTASIS FOR 3 YEARSBACKGROUND OF: CHILDHOOD RHEUMATIC FEVER & ANEMIASOCIAL HX: JEHOVAH’S WITNESS REFUSED TRANSFUSION OF BLOOD, BUT AGREED FOR BLOOD HARVEST INTRAOPERATIVELY

PATIENT WAS GIVEN HEMATINICS AND ERYTHROPEITIN 8 WEEKS PRIOR OPERATION

PRIOR HEMATINICS & E-PO : HB 9.7, HCT 27.6A DAY PRIOR SURGERY: HB 10.5, HCT 33.4ON DAY OF SURGERY: HB 9.7, HCT 31

ECG: SINUS TACHYCARDIA, HR: 118/MIN, LV HYPERTROPHYCXR: POORLY AERATED LUNG AT RIGHT LUNG BASECT PELVIS: “GIGANTIC OSTEOSARCOMA” OF RIGHT FEMUR, EITHER DIRECTLY EXTENDING OR METASTASIZING TO RIGT ACETABULUM WITH MARKED ENLARGEMENT OF RIGHT ILIC VEIN & VENA CAVA

ECHO:MILD DILATED CARDIOMYOPATHY WITH MILD DIFFUSE HYPOKINESIS, EF 0.59, MILD MITRAL REGURGITATION, LA AND LV ENLARGEMENT, SMALL PERICARDIAL EFFUSION

MONITORING: PULMONARY ARTERY CATHETER, CONTINOUS MIXED VENOUS OXYMETRY

PATIENT ANESTHESIZED WITH NARCOTIC AND ISOFLURNE TECHNIQUE. PATIENT THEN HEMODILUTED WITH CRYSTALLOIDS IN TOTAL VOLUME OF 3L, THEN BLOOD RESTORED IN BLOOD CELL PROCESSOR. POSTHEMODILUTION – HB 6.6, HCT 21.4%.

HB 4.5 – RAPID REINFUSION OF HARVESTED BLOOD INTIATED DUE TO DETERIORATING HAEMODYNAMICS (INCREASE PULM CAPILLARY WEDGE PRESSURE & HYPOTENSION) & WORSENING TISSUE OXYGENATION (DECREASED MIXED VENOUS OXYGENATION

OPERATIVE TIME: 14H, 10MINSOPERATIVE SPECIMEN: 29.4KG (1/3 PATIENT WEIGHT)

COAGULATION TEST: PT 15.6, PTT 39.3, PLT 245.000/MM3OXYGEN DELIVERY 551ml O2/min at Hb 4.8 compared to prehemodiluton 1067 ml O2/min OXYGEN CONSUMPTION at Hb 4.8 110 ml O2/min VS 108.5 at Hb 9.7

LOWEST MICES VENOUS O2 SATURATION – 52% AT HB 4.5 AND HIGHEST LACTATE 3.1 AT HB 6.0

FLUID BALANCE*INTAKE AUTOLOGOUS BLOOD – 2875MLCRYSTALLOID – 30,600ML

*OUTPUTEBL: 3600MLS URINE OUTPUT: 20,600ML

MONITORING:LOWEST HB 4.8, HCT 14.6AT COMPLETION OF SURGERY HB 6.9, HCT 21%

POSTOP ADMITTED TO SURGICAL ICU & EXTUBATED POD1. POST OP XRAY: BILATERAL PLEURAL EFFUSION, INCREASED PULMONARY VASCULAR CONGESTION, POSSIBL CONSOLIDATION IN RIGHT AND LEFT LUNG BASES. REPEATED X RAY – CLEARING PULMONARY EDEMA

PATIENT THEN DISCHARGED ON 38TH POSTPERATIVE DAY WITH HB 11.1, HCT 32.6

TIME INTAKE OUTPUT HB/ HCTOR DAY 34, 930 ML 27, 040 ML 6.9/ 21.0POD1 2, 146 ML 5, 988 ML 8.2/ 25.3POD2 1, 609 ML 6, 390 ML 8.1/ 25.2POD3 2, 185 ML 4, 640 ML 8,2/25.7