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Thoracic Aortic Aneurysm Repair PowerPoint Presentation

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  • Slide 1 - 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 Presented Aug 2002
  • Slide 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
  • Slide 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
  • Slide 4 - History cont.: PSHx: Inguinal hernia repair Umbilical hernia repair Past Anesthesia Hx: GA No complications with GA
  • Slide 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
  • Slide 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.
  • Slide 7 - Ultrasound done in Oberlin hospital: Ascending Thoracic Aorta Intimal flap 45 mm
  • Slide 8 - Ultrasound done in Oberlin hospital: Aorta Blood in dissection Type A ascending aortic aneurysm
  • Slide 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
  • Slide 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
  • Slide 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
  • Slide 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
  • Slide 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
  • Slide 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
  • Slide 15 - Cold agglutinins antibody (CAA)
  • Slide 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
  • Slide 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)
  • Slide 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)
  • Slide 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
  • Slide 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
  • Slide 21 - 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 Management of CAA and CPB:.
  • Slide 22 - Thanks for the attentionThe End

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