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
• 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
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
History cont.:
• PSHx:
– Inguinal hernia repair – Umbilical hernia repair
• Past Anesthesia Hx:
– GA – No complications with GA
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
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.
Ultrasound done in Oberlin hospital:
Ascending Thoracic Aorta
45 mm
Intimal flap
Ultrasound done in Oberlin hospital:
Blood in dissection
Aorta
Type A ascending aortic aneurysm
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
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
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
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
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
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
Cold agglutinins antibody (CAA)
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
Cold agglutinins antibody - CAA:
• Thermal amplitude - blood temperature below CAA
• • • • • •
react Higher thermal amplitude = more malignant CAA (35 C o) Routine screen by blood banks for CAA @ 37C o 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)
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)
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
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
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
Thanks for the attention
The End