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Ascending thoracic aneurysm repair with CPB and circulatory arrest (case presentation) Darko J. Vodopich MD Antonio Coop

Presented Aug 2002. Ascending thoracic aneurysm repair with CPB and circulatory arrest (case presentation) Darko J. Vodopich MD Antonio Cooper MD MetroHealth Medical Center - CWRU Department of Anesthesiology. History.

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Ascending thoracic aneurysm repair with CPB and circulatory arrest (case presentation) Darko J. Vodopich MD Antonio Coop

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  1. Presented Aug 2002 Ascending thoracic aneurysm repair with CPB and circulatory arrest (case presentation) Darko J. Vodopich MD Antonio Cooper MD MetroHealth Medical Center - CWRU Department of Anesthesiology

  2. History • CC: 81 y.o. white male coming to ED after found in the bathroom. + LOC, no amnesia. Responsive on arrival. • C/o stroke like symptoms: • headache, • confusion, • left sided weakness, • unable to turn the head to the left side

  3. History cont.: • Allergy: Ciprofloxacin, Levaquin • PMHx: • HTN well controlled on Lisinopril and HCTZ • Type 2 DM well controlled by diet/exercise • Prostate cancer (on Megestrol) • Occasional CP (no AMI in the past) • COPD • PVD

  4. History cont.: • PSHx: • Inguinal hernia repair • Umbilical hernia repair • Past Anesthesia Hx: • GA • No complications with GA

  5. Physical: • HEENT: PEERL, EOMI • MP class 1, TMD 5 cm, Mouth opening 4 FB, good neck mobility, own dentition in a good shape • Cor: RRR, S1S2, no murmurs, no thrill, tones silent, distant on auscultation • Pulmo: decreased sounds bilaterally, no crackles or wheezing • Extremities: no gross abnormalities, left sided weakness • Neurological: AOx3, left sided focal signs • ASA 5, Case type: Emergency

  6. Laboratory and studies report: • CBC: WBC=8.4, Hb=11, Hct=35, Plt=207 • Na=128, K=3.6, HCO3-=19, Cl=98, BUN=11, Creat=0.6, Glu=131 • Pt=12.0, PTINR=1.02, PTT=42.9 • ECG: NSR~100 BPM, nonspecific S-T changes, no signs of acute ischaemia • ECHO: 19 July 2002: EF 74%, no ischaemic changes • Adenosine myocardial perfusion test: 19 July 2002: NSR, left axis anterior hemiblock, mild S-T changes. No evidence of ischaemia. Normal test.

  7. Ultrasound done in Oberlin hospital: Ascending Thoracic Aorta 45 mm Intimal flap

  8. Ultrasound done in Oberlin hospital: Blood in dissection Type A ascending aortic aneurysm Aorta

  9. Chronology: • Pt taken to OR 15. • Difficulty cross matching the blood • Anesthesia start time @ 20:28 with a-line and 2 large bore 16 G i.v. lines in place • Smooth i.v. induction: Fentanyl 100+150+200+250 mcg; Midazolam 5mg, Vecuronium 10 mg. • Easy ventilation and intubation; ET 8, Grade 1 view, atraumatic, secured @ 23 cm. • Left IJ 9 F introducer placed, PAC introduced, good waves and wedge detected, secured @ 54 cm. Patient tolerated procedure well. No complications. • Initial CI=2.4, SVO2=75%, CVP=14, PAP=24/14 mmHg

  10. Intraoperative facts: • Maintenance of anesthesia before bypass: • Isoflurane 1.0%, O2 =2L, Air = 2L. • Fentanyl: 0.05 mcg/kg/min • Vecuronium: 3mg/h • Other drips: • Amicar • Sodium nitroprusside • NTG • Neosynephrine • BIS: ~ mid 40’s • BP titrated to a mean of 80’s • ABG @ the beginning surgery: pH=7.43, CO2=31.8, O2=207, HCO3=21.1, BE=-2.0, HCT=30, Na=123, K=3.4, Glu=160

  11. Intraoperative during bypass: 1st time 2nd time 3rd time On pump 22:12 00:05 02:40 Off pump 22:56 01:48 04:05 • Circulatory arrest @ 22:35 = BIS 00 • Temperature during arrest: 18 C • MAP 15-20’s during circulatory arrest • ABG on the pump: pH=7.40, CO2=35, O2=336, HCO3=22, BE=-2.1, HCT=22, Na=123, K=3.8, Glu=167

  12. Intraoperative events: • Proximal aortic graft required resuturing • Episode of hypotension/clotted pump filter • Marked reduction in systolic function after weaning from bypass • Unresponsive to iv epi/norepinephrine, but responsive to intracardiac Epinephrine 1 mg • Blood gas revealed PaO2=45 mmHg • Delayed reinstitution of CPB/clotted oxygenator

  13. Intraoperative events (2): • Persistent lactic acidosis on bypass • Low urine output • Weaned from bypass, with persistent hypoxemia and lactic acidosis, and hematuria • Return to bypass for the 3rd time • Weaned from the bypass after 1 hour and 25 minutes • Blood clot removed from right atrium • Patient remained H/D unstable and expired @ 05:30

  14. Intraoperative facts: • Total surgery time 20:28-05:02= 514 min • Total bypass time: 44min+103min +85 min= 232 min • Total circulatory arrest time = 27 minutes • EBL ~ 2000 ml • PRBC’s= 6 units • Platelets = 6 packs • Fluids: 2200 ml • Urinary output = 120 ml (hemolyzed) • Blood clot removed from right atrium • Patient expired 05:30 AM • CAA identified in the blood

  15. Cold agglutinins antibody (CAA)

  16. Cold agglutinins antibody - CAA: • Common but usually unimportant - in serum of almost all healthy patients • AHA caused WAB = 1:85.000; caused CAA = 1:300,000 • Female/male = 1.5/1.0 • Associated with: • Infectious mononucleosis (60%) • Lymphoreticular neoplasms • Mycoplasma pnuemoniae • IgM autoantibodies against RBC I-antigen

  17. Cold agglutinins antibody - CAA: • Thermal amplitude - blood temperature below CAA react • Higher thermal amplitude = more malignant CAA (35 Co) • Routine screen by blood banks for CAA @ 37Co • Significance of CAA is determined by: • Agglutination of RBC in 20 Co saline • Agglutination of RBC in 30 Co albumin • If tests are negative significant hemolysis is unlikely (Leach AB, Van Hasselt GL, Edwards JC:Cold agglutinins and deep hypothermia. Anesthesia 38:140;1983)

  18. CAA - physical exam and distribution: • PE: may reveal • nothing unusual • pallor only, unless the patient is observed during or shortly after cold exposure. • purplish discoloration of the ears, forehead, tip of the nose, and digits may then be observed. • Distribution is provided by a study of 78 patients with persistent cold agglutinins: • 31 lymphoma (40%), • 24 chronic, idiopathic CAD (31%) • 13 Waldenström syndrome (16%) • 6 chronic lymphocytic leukemia (CLL) (8%) (Crisp, 1982)

  19. CAA - Ddx: • DDX: • Cryoglobulinemia • Warm AIHA (Warm antibody–mediated autoimmune hemolytic anemia ) • Neoplasms • Drug-induced immune hemolytic anemia • Heparin-induced thrombocytopenia/thrombosis syndrome (HITTS) • Drug-induced hemolytic anemia • Infections

  20. Management of CAA and CPB:. • Depends on : 1.titers, 2.thermal amplitude • 1) During the bypass RBC agglutination can be determined by mixing the blood with cold cardioplegia • 2) Dilute the blood sample to simulate the dilution with CPB and cool it down. (may not have the reaction) • Many institutions avoid hypothermic CPB if CAA present • Cold cardioplegia may produce agglutination in small heart blood vessels • If hypothermia required despite CAA • preoperative plasmapheresis to reduce titers • limit hypothermia to temperature exceeding thermal amplitude • use standard hemodilution techniques

  21. Management of CAA and CPB:. • Cold cardioplegia with normothermic bypass and no plasmapheresis • normothermic CPB • cardioplegia 37 Co to washout CAA • 4 C cold cardioplegia • Malignant cold CAA • Consider total washout technique - exchange patient’s blood with donor’s blood • Heat all anesthetic gases, IV Fluids, blood, and plasma • Keep room warm • Use washed RBC’s

  22. Thanks for the attentionThe End

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