Asian Cardiovasc Thorac Ann 2004;12:81-82
© 2004 Asia Publishing EXchange Ltd
Retrograde Cerebral Perfusion for Treatment of Air Embolism After Valve Surgery
Vitthal Gadhinglajkar Shrinivas, MD,
R Sankarkumar, MCh,
Sreedhar Rupa, MD
Sree Chitra Tirunal Institute for Medical Sciences and Technology, Kerala, India
For reprint information contact: Vitthal Gadhinglajkar Shrinivas, MD Tel: 91 0471 244 3152 Fax: 91 0471 244 6433 Email: shri{at}sctimst.ker.nic.in Department of Anesthesia, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum – 695011, Kerala, India.
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ABSTRACT
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Air embolism occurred after termination of cardiopulmonary bypass in a 22-year-old man undergoing aortic valve replacement for rheumatic aortic insufficiency. Normothermic retrograde cerebral perfusion was instituted for 5 min at a flow rate of 300–500 mL·min-1, maintaining internal jugular vein pressure < 25 mmHg. The aortic cannula was declamped intermittently for 5–10 seconds. Mean arterial pressure was kept at 60–70 mmHg. The patient recovered without any neurological deficit.
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INTRODUCTION
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Retrograde cerebral perfusion (RCP) during hypothermia has traditionally been used for treatment of air embolism on cardiopulmonary bypass (CPB). In this case, air embolism occurred after weaning from CPB.
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CASE STUDY
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A 22-year-old man with severe rheumatic aortic insufficiency underwent surgery under CPB with bicaval cannulation. The aortic crossclamp was removed after aortic valve replacement and a standard deairing protocol. The patient was rewarmed and weaned off CPB. Numerous air bubbles were noticed rising from the aortic root into the clamped aortic cannula. The bubbles continued to rise in spite of 5 attempts to remove them by bloodletting from the aortic cannula after disconnecting it from the arterial return line. The pupillary reaction to light was bilaterally sluggish. The arterial return line was connected to the superior vena caval cannula, and RCP was delivered for 5 minutes at a flow rate of 300–500 mL·min-1, maintaining internal jugular vein pressure < 25 mmHg. The aortic cannula was decamped for 5–10 seconds intermittently. Mean arterial pressure was maintained at 60–70 mmHg. The patient was placed in the Trendelenburg position, and both carotid arteries were compressed intermittently. At the end of RCP, papillary reaction became rapid. Pharmacological cerebral protection after RCP included dexamethasone 16 mg, sodium pentothal 15 mg·kg-1, and mannitol 1 g·kg-1. Mean arterial pressure was maintained > 100 mmHg using dobutamine support after protamine administration. Cerebral protective strategies included ventilation with 100% oxygen, maintenance of normoglycemia, normal serum electrolytes, slight hypocapnia, and supranormal blood pressure. The patient awoke 4 hours after transfer to the intensive care unit. He had no gross neurological deficit but remained drowsy over the next 2 hours. Detailed neurological and neuropsychological examinations a week later revealed no abnormality. There was no renal or hepatic dysfunction postoperatively.
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DISCUSSION
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Air embolism can occur after weaning from CPB in patients undergoing valve surgery.1 Air may be retained in lung veins or the left atrium despite cardiac deairing. The left atrium and left ventricle were enlarged in this patient. Trovar and colleagues2 encountered a similar event with the patient suffering seizures postoperatively. Linden and colleagues3 detected cerebral air embolism in 100% of patients during open heart surgery, and found that cerebral emboli were most likely to occur during return of blood from the heart-lung machine when the heart is beginning to eject actively. Quigley and colleagues4 used RCP after weaning from CPB and demonstrated blood flow reversal in the middle cerebral artery by transcranial Doppler ultrasonography; the stroke rate was 0% compared to 2.4% without RCP. We followed Quigley’s method for RCP but also released the aortic clamp intermittently.4 During clamp release, mean radial artery pressure was reduced by 20–30 mmHg, reflecting the fall in pressure inside the aortic arch. This might reverse the flow across the carotid arteries and wash out air bubbles. The major risk in RCP is cerebral edema, which can be minimized by maintaining superior vena caval pressure < 25 mmHg.5
In previous reports, the patients were in a hypothermic condition as CPB was in progress. They were subjected to deep hypothermia after completion of RCP. However, normothermia was maintained in our patient during and after RCP. Deep hypothermia reduces the size of the gas bubbles, but to establish it in our patient would have delayed other strategies for cerebral protection. Palatial perfusion significantly increases cerebral blood flow,6 but a device to generate palatial flow was not available. Raising the arterial blood pressure forces bubbles through tissue beds to the venous side of the circulation, and also allows better perfusion of the microvasculature. Maintenance of physiological palatial flow, supranormal blood pressure and cardiac output, and hyperoxia, rather than inducing deep hypothermia on CPB is preferable in the post-CPB period. Hyperbaric oxygenation, a highly specific treatment for air embolism, was not available.7 Retrograde cerebral perfusion is an established treatment and it was justified as the CPB cannulae were in place. Dexter and colleagues8 using a mathematical model, estimated that absorption does not affect the disposition of air introduced into the arterial circulation because clinically relevant microbubbles have radii of 50–1500 microns and the maximum rate of absorption of microscopic air emboli in blood is 1.57 microns per second. Thus, it was unwise to apply only conservative cerebral protective strategies without RCP in this patient. The air bubbles were small in size and the volume of embolized air might not have been large enough to cause gross neurological deficit. However, changes in pupillary size and electroencephalography may not occur until embolized air causes significant cerebral damage. This experience shows that RCP is safe and effective and may be considered as a treatment strategy when air embolism is detected in the immediate post-bypass period.
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REFERENCES
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- Nussmeier NA. Adverse neurologic events: risks of intracardiac versus extracardiac surgery. J Cardiothorac Vasc Anesth
1996;10:31–7.[Medline]
- Tovar EA, Del Campo C, Borsari A, Webb RP, Dell JR, Weinstein PB. Postoperative management of cerebral air embolism: gas physiology for surgeons. Ann Thorac Surg
1995;60:138–42.
- van der Linden J, Casimir-Ahn H. When do cerebral emboli appear during open heart operations? A transcranial Doppler study. Ann Thorac Surg
1991;51:237–41.[Abstract]
- Quigley RL, Fuller BC, Sampson LN, Reitknecht FL. Passive retrograde cerebral perfusion during routine cardiac valve surgery reverses middle cerebral artery blood flow and reduces the risk of stroke. J Heart Valve Dis
1997;6:288–91.[Medline]
- Usui A, Oohara K, Liu TL, Murase M, Tanaka M, Takeuchi E, et al. Determination of optimum retrograde cerebral perfusion conditions. J Thorac Cardiovasc Surg
1994;107:300–8.[Abstract/Free Full Text]
- Murkin JM, Farrar K. The influence of pulsatile versus non-pulsatile cardiopulmonary bypass on cerebral blood flow and cerebral metabolism. Anesthesiology
1989;71:A41.
- Toscano M, Chiavarelli R, Ruvolo G, Macchiarelli A, Scibilia G, Marino B. Management of massive air embolism during open-heart surgery with retrograde perfusion of the cerebral vessels and hyperbaric oxygenation. Thorac Cardiovasc Surg
1983;31:183–4.[Medline]
- Dexter F, Hindman BJ, Marshall JS. Estimate of the maximum absorption rate of microscopic arterial air emboli after entry into the arterial circulation during cardiac surgery. Perfusion
1996;11:445–50.[Abstract/Free Full Text]
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Retrograde cerebral perfusion and delayed hyperbaric oxygen for massive air embolism during cardiac surgery
Interactive CardioVascular and Thoracic Surgery,
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382 - 383.
[Abstract]
[Full Text]
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