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PAEDIATRIC PERFUSION: ANTEGRADE CEREBRAL PERFUSION IN NEONATES - OUR EXPERIENCE WITH THE NORWOOD PROCEDURE. |
Various methods of cerebral protection have been used during aortic arch operations, such as the Norwood procedure and operations on the interrupted aortic arch, in neonates and infants. Deep hypothermia with circulatory arrest is the most common technique, but it has a limited safe period for circulatory arrest. Antegrade cerebral perfusion has been introduced to prolong this safe period. We reviewed our experience with antegrade cerebral perfusion during surgical repair, in patient with hypoplastic left heart syndrome in the stage 1 palliation.
Key words: Antegrade cerebral perfusion, neonates, cerebral protection
Aortic arch reconstruction such as in the Norwood procedure has commonly required deep hypothermic circulatory arrest. Although it is a useful technique, potential risks of complications such as neurological damage cannot be ignored [1]. We introduced a cardiopulmonary bypass technique using a double arterial cannulation of the pulmonary trunk and the Blalock-Taussig shunt (BT-Shunt) through a median sternotomy combined with antegrade cerebral perfusion, through the right subclavian artery (via BT-Shunt) to avoid circulatory arrest.
SURGICAL TECHNIQUE
After median sternotomy and full heparinization, the ascending aorta, pulmonary trunk, the brachiocephalic trunk, and the right subclavian artery were mobilizied. A BT-Shunt (Goretex) was constructed, end-to-side to the right subclavian artery. After this, the main pulmonary artery and the BT-Shunt were cannulate with a 8 F polyurethane cannulae (Stöckert Inst.,Munich). The right atrium was cannulated with a 16 F single venous cannula (Bard, Mass.)
Before we start the perfusion, the right and the left pulmonary artery were clamped to improve hemodynamic stability, by decreasing pulmonary artery run-off, while maintaining adequate oxygen saturation. Pump flow rates were maintained at 2,8 l/m2 /min. Rectal temperature was lowered to 22°C, the hematocrit and the protein were adjusted to 22% and 2,6 g/dl, the colloid osmotic pressure to 14 mmHg, and for the blood gas management we used the alpha-stat strategie. At a rectal temperature of 22°C the pulmonary trunk cannula was clamped, the ductus arteriosus was ligated, the pulmonary trunk was transacted and the distal end was closed. After clamping all the arch vessels and the descending aorta, the pump flow rate was reduced, and the antegrade cerebral perfusion was started with a flow of 25 ml/kg/min and a cerebral perfusion pressure of about 40–80 mmHg.
Frist et al and Kazui et al [2,3,4] reported a technique that uses partial brachiocephalic selective cerebral perfusion, like this one in adults. Perfusion of both carotids may be necessary only in patients with a compromised circle of Willis or severe carotid artery stenosis. Frist`s use of moderate systemic hypothermia may reduce the risk of excessive bleeding and decrease the complications associated with long CPB times, such as the capillary leak syndrome, by avoiding low temperatures and prolonged cooling and rewarming periods associated with deep hypothermic circulatory arrest.
The normal principles of cerebral autoregulation that are present during normothermia are maintained during moderate hypothermic CPB. Cerebral blood flow depends on brain metabolism. If metabolism is high, the cerebral vascular resistance falls and cerebral blood flow increases. This is known as flow/metabolism coupling and it remains intact during moderate hypothermic CPB. Pressure/flow autoregulation or the ability to maintain a constant CBF despite wide ranges in mean arterial pressure also remains intact during moderate hypothermic CPB. The cerebral vasculature remains capable of dilating during low perfusion pressure and constricts when perfusion pressure is high. At temperatures under 22°C and/or ph-stat managment this benefit were lost [5].
A longitudinal incision of the aortic arch was made. The neoaorta was constructed with a homograft, direct anastomosis of the pulmonary trunk to the ascending aorta and the aortic arch. The perfusion to the BT-Shunt was stopped and the whole body was perfused with 2,8 l/m2/min by the arterial cannula in the neoaorta. After reperfusion, the perfusion was arrested for a few minutes to enlarge the atrial septal defect through the right atriotomy. Modified BT- Shunt was completed by anastomosing the distal end of the graft to the right pulmonary artery. At a temperature of about 30°C we corrected the pH (7,4), calcium (1,5 mmol/l), potassium (4,5 mmol/l), colloid osmotic pressure (20 mmHg) and hematocrit (34 %). We rewarmed and hemofiltrated the patients to 36°C rectal. Weaning from CPB should be slow and careful, because the Qp/Qs must be balanced. Patients with a low pulmonary vascular resistance to systemic vascular resistance ratio are likely to have luxuriant pulmonary blood flow. We ventilate them with a reduced FiO2 and increased PaCO2. Those with a high pulmonary vascular resistance to systemic vascular resistance ratio should be hyperventilated with a higher FiO2.
PERFUSION MANAGEMENT
Currently, there are no established guidelines for the site of cerebral perfusion, flows, temperatures, or perfusion pressure. Further studies and physiological parameters will help to answer some of this questions.
CEREBRAL METABOLISM
In order for cerebral ischemia to occur, CBF must be reduced below CMRO2 either globally or locally; therefore, an understanding of the effect of CPB on CMRO2 is necessary. During CPB, hypothermia usually constitutes the dominant factor on CMRO2, although CPB per se has also an effect on CMRO2 which is independent of temperature. In clinical [6] and experimental [7] studies, brain metabolism is reduced by 35% to 50% during normothermic CPB. Why CMRO2 decreases on CPB is unknown, but the phenomenon may represent depressed neural activity [ 8] or inadequate capillary perfusion as an consequence of cerebral microembolization [7].
TEMPERATURE
Temperature is a major factor directly affecting metabolism by reducing CMRO2 by approximately 7%/°C reduction in temperature [9,10]. Hypothermia reduces both the electrophysiologic (60%) and cellular homeostatic (40%) components of brain energy expenditure. Hypothermia protects the brain during ischemia by diminishing high-energy phosphate depletion [11] and inhibiting excitatory neurotransmitter release [12], thereby limiting the extent of ischemic damage. With a temperature from 18°C to 22°C cerebral vascular resistance increases greatly and pressure-flow autoregulation is impaired, which may be secondary to cold-impaired cerebrovascular relaxation [6,13,14].
CARBON DIOXIDE MANAGEMENT
Cerebral vascular resistance is markedly affected by PaCO2. Carbon dioxide diffuses rapidly across the blood brain barrier, reducing extracellular fluid pH and causing cerebral vasodilatation. Elevating PaCO2 levels may cause sufficient vasodilatation with a 4% increase in CBF per mmHg, to abate the normal autoregulatory response to changes in perfusion pressure [15]. Blood temperature can profoundly alter carbon dioxide solubility, causing a reciprocal change in PaCO2 of approximately 4,5%/°C. The use of hypothermia during antegrade cerebral perfusion, therefore, influences PaCO2 and consequently the cerebral blood flow. The PaCO2 level during hypothermic antegrade cerebral perfusion is controlled using one of two techniques. The pH-stat and the alpha-stat modes differ in terms of whether PaCO2 and pH are maintained at normal values at the actual temperature of the patient or at 37°C (of the blood gas analyzer). When the two techniques are compared during hypothermic CPB at 28°C, a difference in PaCO2 levels exists between patients managed with the alpha-stat and pH-stat technique. This gradient is sufficient to significantly alter CBF since cerebrovascular carbon dioxid responsiveness is maintained during nonpulsatile CPB [16]. Under hypothermic conditions (22°C – 28°C) pH-stat management results in pressure-depent CBF with impaired cerebral autoregulation [6,17] and flow-metabolism coupling . In contrast, alpha-stat management maintains pressure autoregulation as well as metabolic coupling during hypothermic CPB with greater carbon dioxid responsiveness [5,6]. Using alpha-stat management, cerebral autoregulation and PaCO2 responsiveness have been shown to be preserved 3 to 8 hours into the post bypass period [18].
HEMODILUTION
Blood viscosity normally increases with hypothermia, causing reduced microcirculatory flow at a constant perfusion pressure. This effect may promote sludging of red cells and could cause of cerebral ischemia, from the no-reflow phenomen.
INTRACRANIAL PRESSURE
Intracranial pressure (ICP) can directly affect the level of cerebral perfusion pressure (CPP) and possibly (CBF) cerebral blood flow (mean aortic pressure – ICP = CCP). Intracranial pressure progressively increases in experimental animals during hypothermic and normothermic CPB. The cause of increased intracranial pressure is unknown but could represent the development of cerebral edema. Some studies have shown that the blood-brain barrier remains intact during hypothermic CPB, and rewarming and brain water content, and intracranial compliance after CPB are unaltered. Another mechanism of increased intracranial pressure could be dilation of cerebral venules secondary to loss of pulsatile flow. Experimental studies have found that increasing the tonicity of the pump priming solution significantly reduces the magnitude of intracranial pressure change.
CPB guidelines for antegrade cerebral perfusion in neonates [19]:
Perfusion flow rate --------------------- 25 ml/kg/min
Perfusion pressure --------------------- 40-80 mmHg
Blood temperature --------------------- 220C
Hematocrit ------------------------------ 22%
Colloid osmotic pressure -------------- 14 mmHg
Alpha-stat blood gas management
PATIENTS AND METHODS
From 1997 to 2001, 35 unselected consecutive patients underwent a Norwood procedure in our unit. Twenty eight (28) patients had an HLHS, 1 patient a Shone`s syndrome with critical mitral valve stenosis, 1 patient had a critical aortic valve stenosis with hypoplastic left ventricle and 5 patients a single ventricle with L-Transposition of the great arteries and systemic outflow tract stenosis. According to a change in our operative technique for systemic outflow tract reconstruction from DHCA towards antegrade cerebral perfusion in 1999, 2 group of patients resulted (table.1).
OPERATIVE TECHNIQUE
Group 1 - DHCA was used in all patients for systemic outflow tract reconstruction and excision of the arterial septum. DHCA period: 41-77 min (mean 62.05 +/- 9,9 min)
Group 2 - Hypothermic circulatory arrest was restricted to excision of the atrial septum. The systemic outflow tract reconstruction was done with antegrade cerebral perfusion via modified BT-Shunt at a flow rate of 25 ml/kg/min. HCA period: 0-9 min (mean 3,7+/- 2,7 min) Period of antegrade cerebral perfusion: 34-79 min (mean 53+/- 12,5 min)
RESULTS
Table 2. Results.
Postoperative examination – All patients got repeated echographic studies and were routinely examined by a pediatric neurologist during their hospital stay. Data analysis – unpaired t-test, study limitation: retrospective, non randomised study
COMMENTS:
Perfusion via a modified BT-shunt with exclusion of the aortic arch provides continuous oxygen supply to the supraaortic region and via collaterals, even to the lower part of the body. Flow studies showed a good amount of blood returning to the heart via the IVC. Being concerned about cerebral hyperperfusion we use pressure control and do not exceed a flow rate of 25 ml/kg/min. The observation that no neurologic abnormalities occurred in our small series confirms us in our aim to avoid DHCA. During antegrade cerebral perfusion the subaortic vessels and the descending aorta have to be occluded to avoid return of blood into the operative field. Nevertheless total bypass time under antegrade cerebral perfusion was not significantly different from bypass time under DHCA. The assumption that serum lactat levels should decrease significantly in group 2, due to continuous perfusion could not be proved. We partially ascribe the significant improvement of survival in group 2 to the minimization of DHCA. The longer ICU-period in group 2 can be explained by the extraordinary long stay of one patient with Shone´s syndrome, due to her pulmonary vascular disease.
Figure 1. Antegrade cerebral perfusion by an BT-Shunt via the circle of Willis.
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a)A.cerebri ant.dext/sin b)A.communicans ant. c)A.cerebri media dext/sin d)A.carotis interna dext/sin e)A.communicans ant. dext/sin f)A.cerebri post.dext/sin g)A.basilaris h)A.vertebralis dext/sin i)A.carotis com.dext/sin j)A.subclavia dext/sin k)Truncus brachiocephalicus |
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