Ascending thoracic aneurysm repair with CPB

and circulatory arrest (case presentation)

Darko J. Vodopich MDAntonio Cooper MD

MetroHealth Medical Center - CWRU Department of Anesthesiology

Presented Aug 2002

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:

AscendingThoracic

Aorta

Intimal flap

45 mm

Ultrasound done in Oberlin hospital:

Aorta

Blood in dissection

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 02:40Off 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 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)

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

• 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:.

Thanks for the attention

The End