Circulatory Arrest with Deep Hypothermia

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CHAPTER 346 Circulatory Arrest with Deep Hypothermia

Paul Gigante, Robert A. Solomon, E. Sander Connolly, Jr.

Most aneurysms are amenable to endovascular or traditional microsurgical treatment with general neurovascular anesthesia. However, there is a small subset of aneurysms that present the surgeon with an unusually complex technical challenge, and pose a higher risk of surgical morbidity and mortality when traditional techniques are employed.¹ Large size, calcified, or atherosclerotic walls, intimacy with critical perforator branches, and the incorporation of afferent or efferent arteries in the dome, are characteristics that often preclude safe clipping while the aneurysm remains tense with high-pressure flow. Circumferential dissection or freeing of adhesions may be impossible with a full, tense dome. Further, calcified or thrombosed aneurysms may be impossible to occlude with a clip without first removing thrombus or calcified components from inside of the aneurysm.

To more safely manipulate such complicated aneurysms, three main strategies have evolved to reduce pressure within the aneurysm dome: systemic hypotension, temporary clipping of major arterial branches, and complete or low-flow circulatory arrest. Systemic hypotension is largely avoided because of the risks associated with hypoperfusion to other organ systems and normal cerebral tissue. Focal hypotension with temporary clipping is used for proximal control in most aneurysms, yet is subject to significant limitations related to time of tolerance and inadequate cessation of flow. Therefore, in conjunction with highly skilled cardiothoracic surgeons and anesthesiologists, neurosurgeons have developed techniques to approach complicated aneurysms under total circulatory arrest or low-flow cardiopulmonary bypass with hypothermic cerebral protection. Complete circulatory arrest converts a tense, large aneurysm into a soft, collapsed sac whose adjacent perforating arteries and total anatomy may be more easily visualized and manipulated.

Deep hypothermic circulatory arrest for aneurysm clipping was first employed more than 50 years ago. Initially, the technique carried an unacceptably high incidence of systemic complications, limiting its application to neurosurgery.² Over time, however, the refinement of bypass techniques via evolving cardiac procedures has allowed for safer employment of circulatory arrest for aneurysm surgery. Coupled with a better understanding of cerebral physiology under hypothermic conditions, these techniques have enabled neurosurgeons to approach otherwise untreatable complex cerebral aneurysms with acceptable morbidity and mortality. Deep hypothermic circulatory arrest is still a relatively high-risk procedure, however, and must performed for appropriate indications at centers able to provide sophisticated neurosurgical and cardiothoracic care. The morbidity and mortality must be weighed against the surgical risks of treating complicated intracerebral aneurysms with traditional techniques.

Temporary Clipping: Limitations of Focal Circulatory Arrest

The utility and complications of temporary clipping for focal circulatory arrest have been explored extensively since its inception in 1961.³^–¹³ Though all cerebral arteries can withstand temporary occlusion for a brief duration, vascular territories vary in the length of occlusion time they may tolerate before ischemia and/or permanent infarction ensue.⁶ In some cases, the proximal internal carotid artery can be occluded for an hour or more, whereas the perforator-bearing segments of the proximal middle cerebral artery or the basilar apex may tolerate occlusion for only 5 to 15 minutes.^8,¹² In one recent series, increasing duration of temporary occlusion was shown to correlate significantly with the development of radiographic or clinical infarction.¹² Permanent vessel damage and consequent infarction can result from injury to individual perforators captured in the temporary clip because these vessels are not strong enough to withstand the closing force of the clip itself. Additionally, temporarily trapped arterial segments may be subject to intravascular thromboembolism. Finally, a steal phenomenon may occur if a hole is created in the aneurysm while the vessel is temporarily proximally occluded, further exacerbating ischemic intolerance.

Cerebral Ischemia: Pathophysiology and Protection

Cerebral arterial occlusion, either by design or a pathologic event, is known to produce two distinct zones of tissue immediately after occlusion: (1) a central core of densely ischemic tissue, and (2) a penumbra that receives collateral circulation and thus possesses prolonged viability compared to the core. The ischemic core undergoes anaerobic glycolysis, acidosis, adenosine triphosphate (ATP) depletion, and ultimately dysregulated ion homeostasis. The potassium-sodium pump loses function in the absence of ATP, intracellular sodium accumulates, and eventually chloride and toxic calcium accumulate intracellularly causing acidosis, edema, and cell death. If the penumbral zone continues without perfusion, it too is progressively recruited into the ischemic core. Over time the penumbra is exposed to increasing concentrations of toxic neurotransmitters, such as glutamate and nitric oxide released from the actively infarcting ischemic core, which lead to cellular depolarization and spreading neuronal death.^14,¹⁵

Broadly, the concept of protection from ischemic injury has evolved to include traditional, well-described measures employed during the ischemic insult, and more recently in experimental models, measures implemented before the ischemic insult that provide endogenously mediated protection, known as “ischemic preconditioning.” Preconditioning is a method by which a noxious stimulus near to but below the threshold of damage is applied to cerebral tissue, and shortly thereafter the tissue develops tolerance or resistance. So when the same noxious stimulus is applied at or above the threshold of damage, the tissue is resistant to or protected from injury. Preconditioning has been studied in ischemic stroke, carotid endarterectomy, and myocardial infarction, but has yet to find evidence-supported therapeutic application in these diseases or the ischemia induced in aneurysm surgery.¹⁶

Neurosurgeons therefore employ traditional methods of ischemic protection in aneurysm surgery, which are based largely on basic oxygen supply and demand. Neurons consume oxygen (cerebral metabolic rate of oxygen consumption, or CMRO₂) for two general purposes: (1) to maintain basic cellular structure and (2) to transmit electrical impulses. Interventions that decrease or eliminate the electrical activity of neurons reduce the CMRO₂ of the brain and enhance membrane viability.

Barbiturates are the best studied agent for decreasing brain electrical activity and have been shown to reduce CMRO₂ by as much as 50%.¹⁷ However, other CMRO₂-reducing agents have been used because barbiturates are associated with adverse effects pertinent to hypothermic cardiac arrest. Propofol and isoflurane, for example, are shorter acting and produce less myocardial depression than barbiturates.¹⁸ Whichever combination of agents the anesthesiologist uses, one must be mindful that CMRO₂ is reduced by only about 50% once electrical activity is eliminated, therefore adding other agents does not effectively lower CMRO₂ any further.

Several groups have examined drugs that act by interfering with the toxic events that follow ischemia and deranged ion flux, including free radical scavengers, calcium channel blockers, and glutamate receptor blockers.¹⁹^–²¹ Others have examined the beneficial effects of adhesion molecule blockers (anti-ICAM-1 antibody), nonspecific anti-inflammatories (steroids), and rheologic enhancers (mannitol) in preventing progressive microvascular failure and in stabilizing plasma membranes.⁸ Though these agents tend to be useful for protecting the penumbral zone, they provide little benefit for the already damaged ischemic core.

Hypothermia is one of the few interventions that has proven capable of sufficiently reducing CMRO₂ and protecting ionic gradients and structural homeostasis in the setting of prolonged ischemia. Even mild hypothermia down to 33°C has been shown to have demonstrable protective effects, but deep hypothermia to 18°C allows the brain to be totally deprived of blood flow for up to 1 hour without noticeable damage.¹⁷

Hypothermia: Cerebroprotective Effects

Hypothermia as a cerebroprotective agent has been used extensively in neurotrauma, cardiac arrest, neurovascular surgery, and cardiac surgery. Deep hypothermia with circulatory arrest has been routinely used in the correction of pediatric cardiac malformations and aortic arch reconstruction.^22,²³ Ischemic protection provided by hypothermia is attributed primarily to a decrease in metabolic demand (CMRO₂), and more recently hypothermia has been shown to reduce proteolysis and excitotoxic damage caused by glutamate toxicity and neuronal calcium influx.^17,^24,²⁵ Hypothermia has also been suggested to reduce free radical production and eliminate spreading depression in ischemic tissue.^26,²⁷ Hypothermia tends to affect the at-risk penumbral tissue but has a minimal effect on the core of infarcted tissue.

Hypothermic tolerance is directly related to the degree of temperature reduction and occurs in the presence of proportional reductions in cerebral blood flow (CBF).²⁸ In cell culture, oxygen consumption has been shown to decrease 50% for every 10°C drop in temperature. However, in vivo reductions in metabolism are even greater (approximately 7% for each 1°C drop in temperature), likely related to hypothermia’s combined effect on basal metabolic rate, electrical activity, and excitatory neurotransmitter and inflammatory cytokine release.²⁹^–³⁵ Temporal limitations still exist, however, as humans cannot tolerate deep hypothermia for much longer than 90 minutes. Extended hypothermia results in IQ reduction and neuropsychological deficits as membrane stability becomes threatened.^35,³⁶ Therefore, surgeons recommend temporary reperfusion for periods of arrest longer than this.

Hypothermia: Physiologic Considerations

The entire multidisciplinary team, including the neurosurgeon, must understand the widespread systemic effects of profound hypothermia to optimally manage the patient’s intraoperative and postoperative course. Of concern to the anesthesia team is hypothermia’s ability to increase both oxygen and CO₂ solubility, which has created controversy among anesthesiologists with regards to temperature-correction of blood gases by adding CO₂. Recent evidence suggests it may unnecessarily increase cerebral blood volume, swelling, and intracranial pressure that may be successfully avoided by titrating ventilation to uncorrected gases.^37,³⁸ Another major physiologic effect of hypothermia is its role in increasing blood viscosity. Plasma viscosity increases approximately 3% for every 1°C reduction in temperature. The anesthesiologist must therefore counteract the changing viscosity by aggressive isovolemic hemodilution to preserve the integrity of the microcirculatory bed, with the final hematocrit titrated approximately to temperature (i.e., 18°C = HCT of 18).³⁹ Hypothermia may also induce a metabolic acidosis as tissues become relatively underperfused. Metabolic acidosis can then lead to dilation of cerebral vasculature and increased cerebral blood flow, which may be important in the setting of cerebral edema.^40,⁴¹

Careful glucose monitoring and avoidance of glucose-containing solutions should be maintained during profound hypothermia because hypoinsulinemia and resultant cerebrotoxic hyperglycemia can occur. Endogenous corticosteroid production may be diminished after prolonged hypothermia, necessitating perioperative replacement and continued hypothalamic-adrenal axis surveillance for up to a year. Profound hypothermia can occasionally cause a complement-mediated pneumonitis, which may necessitate prolonged postoperative intubation. Though frank hepatic dysfunction is extraordinarily rare, hypothermia can lead to mild hepatic dysfunction with decreased dilantin metabolism and resultant supratherapeutic levels. Rarely, postoperative renal failure occurs because of transient decreases in glomerular filtration rate, hemolysis, and blood product reactions.⁴¹^–⁴⁴ Hemoglobinuria may be managed with osmotic alkalinization of the urine.^45,⁴⁶ Hypothermia may also have profound effects on myocardial contractility and conduction, which persist into the postoperative period. Widening of the PR interval, QRS complex changes, systolic and diastolic dysfunction, sinus bradycardia, and sensitization to pharmacologic challenge have all been reported.⁴⁷^–⁴⁹

Of greater concern than these rare complications is the more common coagulopathy caused by circulatory arrest techniques and deep hypothermia. The surgeon encounters difficulty with hemostasis because of both platelet dysfunction and slowing of the enzymatic coagulation cascade.⁵⁰ Fortunately, platelet dysfunction is mostly due to sequestration that resolves within an hour of rewarming, and major clotting factors are mostly unaffected. Heparinization and extracorporeal circuitry account for the remainder of the coagulopathy, and while hypothermia may prolong the anticoagulant effects of the former, its half-life generally is less than 2 hours. As for the latter, removal of the circuits results in an immediate reduction in turbulence and shear-induced red blood cell and platelet destruction. Progressive hemoconcentration during warming also helps to correct the coagulopathy, and warming causes a decrease in plasmin-dependent fibrinolysis.⁵¹^–⁵³

Although hypothermia is intended to be neuroprotective, neurologic dysfunction can still occur after prolonged, profound hypothermia.⁵⁴^–⁵⁷ Global hypoperfusion and macroembolization and microembolization may all contribute to the development of neurological injury. Age and preexisting cerebrovascular disease are major risk factors for neurological complications.⁵⁸ Some recent improvement in neurological complication rates can be found with the use of barbiturate alternatives, which more effectively reduce cerebral metabolism and have fewer cardiovascular effects.^38,^52,⁵⁹^–⁶¹

Deep Hypothermic Circulatory Arrest: Indications

Careful consideration of the limitations of focal arrest and conventional microsurgical techniques may lead the surgeon to choose total circulatory arrest with deep hypothermia to most safely treat a complicated aneurysm. In general the major considerations involved in selecting cases include factors related to the: (1) aneurysm, (2) anatomic parent artery, and (3) patient.

Aneurysm Characteristics

Anatomic Location: Parent Artery

Aneurysms of the posterior circulation have predominated in previously published series of aneurysms treated with hypothermic circulatory arrest.⁶²^–⁶⁴ Some argue that advances in surgical approaches, particularly the orbitozygomatic craniotomy and drilling of the anterior clinoid, provide improved access to the internal carotid artery and give the aneurysm surgeon total proximal control,⁶² negating the need for circulatory arrest. In fact, before our recently published series of 66 patients outlined below, in which 50% of aneurysms treated with circulatory arrest resided in the anterior circulation, the largest series previously published reported only 4 of 58 aneurysms treated were in the anterior circulation.⁶² We maintain, however, that particularly risky aneurysms of the anterior circulation may be best treated with hypothermic circulatory arrest.

Giant Basilar Aneurysms

Giant basilar apex aneurysms often obscure visualization of the contralateral posterior cerebral artery. Further, critical perforators emanate from the top of the basilar artery, usually immediately behind the aneurysm dome. Even if the apex can be totally trapped, there will be no supply to the perforators that emanate from the top of the basilar artery, usually located immediately behind the aneurysm dome. The territory supplied by these vessels cannot withstand more than a few minutes of loss of blood flow at normothermia. Although arrest is usually reserved for truly giant lesions in this location, somewhat smaller lesions may benefit from this technique when the aneurysm is oriented posteriorly into the interpeduncular cistern.

Ophthalmic/Paraclinoid Giant Aneurysms

The surgeon may be unable to achieve proximal clipping of the internal carotid artery feeding an ophthalmic aneurysm because the proximal internal carotid artery (ICA) may be located entirely within the cavernous sinus. Alternatively, proximal cervical occlusion of the carotid via neck dissection may still leave intracavernous branches and the ophthalmic artery supplying the aneurysm.

Other Aneurysms

Any other giant aneurysm of the anterior or posterior circulation may be an appropriate candidate for circulatory arrest because the aneurysm may obstruct important afferent or efferent branches, or may be adherent to critical structures.

Patient Specific Factors

Despite possessing an aneurysm with preoperative studies suggesting candidacy for hypothermic circulatory arrest, the patient’s medical status may preclude performing circulatory arrest with an acceptable risk of morbidity and mortality. Preexisting cardiopulmonary disease and/or age may contraindicate arrest surgery. Internal medicine or cardiology consultation should be obtained for preoperative testing and clearance. An echocardiogram is always obtained to define cardiac function and valvular competency. Ultimately the decision to proceed is made after a multidisciplinary evaluation by the neurosurgical, medical, and anesthesiology teams.

Clinical Techniques

Technical Preparations

Before performing an institution’s first arrest case a multispecialty team needs to be assembled, with all members having ideally been trained in this technique at specialized centers. Once this team is assembled an operative protocol should be designed. Next, an appropriate operating suite should be identified. The size of this suite must accommodate two surgical teams and a significant amount of extra equipment (including neurophysiologic monitors, transesophageal ultrasound, heat-exchange pumps, perfusion pump and oxygenator, and the cardiovascular surgery equipment trays. The electrical demands placed by this amount of equipment should not be underestimated and coordination with hospital electricians is critical.

Preoperative Medical Evaluation

Once a patient is deemed an appropriate arrest candidate from a neurosurgical point of view it is imperative that coronary/valvular heart disease, pulmonary disease, and systemic blood pressure abnormalities be addressed fully. In particular, aortic valve function should be carefully evaluated with transthoracic echocardiography. If insufficiency is detected central cannulation and left ventricular venting through a median sternotomy may be required. In addition, the status of the patient’s peripheral arterial disease should be assessed because it also might complicate peripheral cannulation. General medical examination with attention to renal and hepatic function, as well as to the competence of the coagulation cascade is also a prerequisite.

Choice of Cannulation Sites

Cannulation for cardiopulmonary bypass can be done peripherally through an inguinal incision (femoral-femoral), or centrally through a sternotomy (aortic-right atrial). With peripheral cannulation, the two surgical fields are comfortably separate, but neurosurgical instrumentation must still allow access to the sternal notch in the event central access suddenly becomes necessary. Cross-contamination, blood loss, and the risk of sternal osteomyelitis are reduced with this peripheral technique. In return, one accepts a 10% risk of more minor wound and vascular complications.

Advocates of central cannulation point out that direct exposure of the heart assures rapid response to distention or fibrillation, and they claim that cooling and warming times are reduced. We, however, prefer peripheral cannulation in the nonatherosclerotic individual, and in our experience, cooling and warming are not significantly different from those obtainable with central cannulation. With aortic valve competence, and continuous transesophageal echo, ventricular fibrillation for lengthy periods is well tolerated in a decompressed, perfused heart, and parallel circuit venting systems replace a cardiotomy reservoir. Occasionally, if flow cannot be improved once bypass is begun, then central cannulation may be required.

Patient Preparation

In addition to the usual equipment necessary for aneurysm surgery, cardiac arrest procedures require a Swan-Ganz catheter, a transesophageal echocardiography probe, scalp and cortical EEG electrodes, a brain temperature needle probe, a cooling/warming blanket, and the placement of specialized grounding plates for defibrillation. These take some time to attach or insert and therefore a full day should be committed to this effort and an early start planned.

Neuroanesthetic Management

Once these special monitoring devices have been arranged, the case may begin, and the neurosurgeon may concentrate on the superficial dissection as per routine. Nevertheless it is critical that the neurosurgeon understands the routine in order to help solve problems. All patients are given perioperative antibiotics, steroids, and anticonvulsants. Steroids purportedly stabilize membranes, prevent vasogenic edema, and minimize complement generation.⁶⁵ Antibiotics are especially important as hypothermia increases the risk of infection (both independently and in association with prolonged operative exposure). Anticonvulsants are employed only in the immediate perioperative period, and while their use has little scientific merit, Dilantin (phenytoin) especially may be mildly cerebroprotective. Anesthesia is induced with intravenous midazolam, fentanyl, and thiopental. Vecuronium, lidocaine, and esmolol are used immediately before intubation and maintenance anesthesia consists of a balanced technique of narcotics, oxygen, and isoflurane. Ventilation is controlled to maintain a normal PaCO_2, and the concentration of isoflurane is minimized (less than 0.75%) to facilitate electrophysiologic monitoring. In general, aneurysm patients should have their fluids conservatively managed; however, hypothermic circulatory arrest often makes this difficult. The vasodilatory effects of warming, together with third space losses because of membrane dysfunction, often renders the patient relatively hypovolemic. Euvolemic correction is guided by both central pressures and urine output, and maintained primarily with glucose-free isotonic crystalloids. However, colloid, both as packed cells and albumin, is occasionally necessary.

A critical adjunct in optimizing fluids and, by extension, cardiopulmonary function is the use of a 5-MHz phased-array ultrasonic esophageal transducer, positioned so that left ventricular short axis images can be continuously obtained at the level of the papillary muscles. Adjunctive intraoperative monitoring also includes compressed spectral array EEG analysis, which facilitates titration of anesthetics to burst suppression. Unlike other groups, we have not found either somatosensory evoked potentials (SSEPs) or brainstem auditory evoked potentials (BAEPs) to be useful adjuncts, and they require an extra level of sophistication to interpret. EEG burst suppression for cerebral protection is induced just before cardiopulmonary bypass with a loading dose of propofol followed by a constant infusion. Although considerably more literature exists regarding the use of barbiturates for this purpose, we have found the level of protection to be adequate with propofol and emergence times are significantly shorter, leading to quicker extubations and potentially reducing pulmonary complications. Propofol also appears to have less cardiosuppressive qualities than barbiturates, perhaps shortening overall bypass times. This propofol infusion is continued until the EEG becomes isoelectric secondary to cooling (around 25°C), at which time it is discontinued. It is resumed at the same constant infusion rate on rewarming and continued until the patient is safely in the ICU.

Unlike routine aneurysm surgery in which mild hypothermia is induced with surface cooling blankets, deep hypothermic circulatory arrest requires the use of both surface cooling and extracorporeal circulatory cooling. The latter requires the use of both chilled IV solutions and a refrigerated water bath heat exchanger set at 8°C. Using these, cooling is more uniform than with a blanket alone and ensures better protection of all organ systems. Despite this greater degree of protection, two caveats exist. First, it should be realized that cooling does not proceed in a uniform fashion, and second that the temperature should not be allowed to drift below 16°C. To avoid problems, vasodilators are employed as are multiple temperature monitors to verify that equilibration has in fact occurred. In our center we employ esophageal, tympanic, pulmonary artery, and cortical brain temperature probes. The latter can be placed safely into the frontal lobe after cauterizing the pia. We find this less variable than epidural monitors and less bulky as well. Despite others’ suggestions that the rectal temperature approximates brain temperature, we consistently observe brain cooling to lag behind esophageal cooling. Sole reliance on the latter could lead to premature initiation of arrest. In our institution, surface cooling is generally employed preferentially from the beginning of the case and over 1 to 2 hours; mild hypothermia to 33°C can be achieved. Only when the surgeon has finished the dissection, and realizes that arrest is a certainty, does final cooling begin. Surgeons should expect this to take 30 to 45 minutes.

Thus if circulatory arrest is determined to be necessary, operative times can be minimized by calling the cardiac surgeon 45 minutes before the need for arrest so that the cutdowns for cannula placement may be initiated. At this point, anticoagulation with heparin is titrated to an activated clotting time of 450 to 500 seconds. An initial bolus of 300 IU/kg is generally adequate followed by an infusion. A 19 French femoral artery cannula and a long 21 French femoral venous right atrial cannula are used in conjunction with centrifugal bypass pumps and a membrane oxygenator. The pump is primed bloodlessly with saline or a colloid such as mannitol. Although the appropriate flow rate and perfusion pressure are controversial, we have found that a rate of 2.5 L/min/m² works quite well. Ventricular fibrillation occurs during cooling (approximately 27°C), and KCl can be given to induce diastolic arrest. The echo is critical to ensure that the heart does not distend at this point. When the brain temperature finally reaches 18°C, the circulation is arrested and the patient is allowed to exsanguinate through the venous cannula until the neurovasculature is adequately decompressed. Too much exsanguination carries the risk of air embolism and a no reflow phenomenon in small blood vessels, but arterial pressure is generally almost zero. Although others have used as many as 72 minutes of circulatory arrest without adverse sequelae, we generally aim for no more than 45 to 60 minutes. In our recent series, if it appears that more time is needed then recirculation is generally performed for a period of 20 minutes or so, somewhere around the 40-minute mark.

Low-flow cardiopulmonary bypass has been described as an alternative to complete circulatory arrest, providing a means to maintain continuous cerebral oxygenation while still reducing intravascular perfusion pressure and cerebral blood flow. Studies comparing low-flow bypass with complete circulatory arrest have suggested that low-flow bypass actually results in a lower likelihood of clinical and electroencephalogram (EEG) seizures, a shorter time to recovery of normal EEG activity, and a lesser release of BB isoenzyme in the immediate postoperative period.⁶⁶ For selected cases in which complete cessation of flow is not required for the entirety of the aneurysm dissection, the surgeon may choose to employ low-flow cardiopulmonary bypass for a period of time.

Once the neurosurgeon is satisfied with the clip placement, circulation is reestablished, and reperfusion is accompanied by rewarming. Due to the risk of hypoxia, acidosis, and air embolism, gradual rewarming is critical. In keeping with this, the perfusate temperature is gradually increased, never exceeding the venous temperature by more than 10°C (maximum of 40°C). At about 30°C, the heart may resume a sinus rhythm or develop ventricular fibrillation which requires cardioversion (200 to 400 J). Mild ischemia and hypothermia may cause some myocardial depression requiring the temporary use of inotropic agents. With the abandonment of barbiturates this has become rare. A final rewarming temperature of 37°C is targeted. Warming blankets, heated ventilation, and warmed IV solutions maintain the patient’s temperature, and protamine is carefully titrated (1.3 mg protamine/mg heparin) to reverse the heparin-induced coagulopathy. Despite this, a mild ooze is noted well into rewarming because platelet damage and dilution of the clotting factors take some time to stabilize. Unlike many groups who routinely infuse autologous whole blood, platelets and fresh frozen plasma, and even occasionally use a cryoprecipitate, we generally avoid these. Similarly we have not used desmopressin because complications have been reported. Instead we simply wait to leave the operative field until this ooze is entirely reversed and the patient is at least 34°C. This generally takes 1 to 2 hours. At the end of the procedure, the patient is taken to the intensive care unit by way of CT scan, having removed the electrophysiologic monitors and the transesophageal echo. The patient is left intubated and is ventilated if necessary, and the CT helps confirm intracranial hemostasis.

Surgical Management

Craniotomy and initial dissection of the aneurysm are done in a standard fashion, with extra attention to hemostasis. Any small ooze will develop into a major one once heparin is given. At the point where further dissection seems unduly hazardous without aneurysm softening or decompression, the anesthesiologist places the patient in burst suppression with a propofol drip and the cardiac surgeon institutes deep hypothermia. It is critical that the cardiac team is immediately available because a delay will lengthen the overall brain retraction time and may predispose to lobar hematoma formation. At this point the operating surgeon generally takes a short break to review the films while the assistant maintains close inspection of the field. With essentially no blood pressure and the brain at 18°C, aneurysm repair can proceed in an unencumbered environment. There is no mechanical intrusion of temporary clips, bleeding from opened arterial structures can be titrated to zero if required, and the ischemic tolerance of the brain shut off from blood flow does not even begin to be an issue for at least 60 minutes after the initiation of complete circulatory arrest. A more perfect clipping can generally be achieved than with other techniques. Clip placement is checked by reinstituting pump circulation. Adjustments can be made by turning off the pump. When repair is deemed secure, full flows and normal pressures are restored. Special care needs to be taken to preserve all perforating vessels. During the arrest these can appear to be bands of arachnoid rather than vessels. Once clipped or disrupted they may not refill, giving no signal to the surgeon that a major error has been committed. During heparinization retractors should not be moved if possible to decrease the shear on small vessels. This will also protect against lobar clot formation. All operative irrigation during the arrest period should be cooled so as to create no mismatch in brain temperature.

Complication Avoidance and Management

Thrombophlebitis: Deep venous thrombosis with pulmonary embolization is a potential complication of femoral cannulation.^67,⁶⁸ Postoperative bed rest and the use of antifibrinolytic agents compound this problem. Some have suggested cannulation of the saphenous bulb with postoperative ligation as a potential solution, while others have advocated open chest cannulation. We simply advocate the use of alternating compression stockings and early ambulation. In our series, all of whom had femoral cannulation, we experienced no problem with thrombophlebitis.

Delayed awakening: The use of hypothermia, barbiturates, and narcotics contributes to a significant degree of postoperative somnolence. The degree of sedation varies on an individual basis, although the total dose of barbiturates is the major predictor of the length of postoperative sedation. Postoperative hepatic or renal dysfunction can further delay elimination and recovery.³⁶ We have nearly eliminated this problem by substituting propofol for barbiturates, and emergence times are now on the order of 3 hours.⁶⁹

Temperature instability: Temperature maintenance is mandatory in the early postoperative period to prevent cardiopulmonary instability and continued coagulopathy. Initially, core temperature is maintained by vasoconstrictive shunting, but as rewarming continues, vasodilation occurs, resulting in hypotension, tachycardia, and cardiac strain. Persistent hypothermia also increases sympathetic tone, shivering, and oxygen consumption.⁷⁰^–⁷² Aggressive management is required. Vasodilators together with meperidine and prolonged muscle relaxation reduce shivering and provide for a smooth anesthetic emergence.^70,^71,⁷³

Coagulopathies: Although most problems with hemostasis are managed in the operating suite, continued bleeding diathesis can occur. The most common causes are further dilution, inadequate clotting factor replacement, and rebound heparinization. Less common causes include fibrinolysis, disseminated intravascular coagulopathy, and pharmacologic impairment of platelets by antibiotics, antihypertensive agents, and diuretics.^74,⁷⁵ Management requires close clinical and laboratory monitoring, appropriate fluid, and temperature maintenance. Occasionally clotting factor replacement is necessary to treat dilutional coagulopathies and disseminated intravascular coagulopathy.

Increased fluid shifts: Perioperatively, large volumes of fluids are required to maintain adequate circulating volume. This, coupled with hypothermia-induced alterations of membrane permeability, leads to interstitial fluid sequestration.⁷⁶ Hypervolemic hemodilution for postoperative vasospasm compounds the situation. Most patients mobilize and eliminate these fluids, rarely requiring more than time and, occasionally, diuretics. However, such patients are typically in a precarious position on the Starling curve, and the use of a pulmonary artery catheter can greatly simplify decision making.

Clinical Results: 15-Year Experience

Patient Characteristics

Over 15 years (1989-2004), 66 cardiac arrest procedures were performed at Columbia Presbyterian Medical Center, and were recently published as one of the largest reported case series of aneurysms treated with hypothermic circulatory arrest. Patient age ranged from 15 to 73 with a mean of 49 years. All but 9 patients had giant aneurysms; 50% of the aneurysms were in the posterior circulation (52% at the basilar tip, 12% superior cerebellar artery, 24% midbasilar, 12% vertebral or vertebrobasilar junction) and 50% were anterior circulation aneurysms (46% proximal internal carotid artery, 21% middle cerebral artery (MCA) bifurcation or trifurcation, 18% anterior communicating artery, 15% internal carotid bifurcation). In approximately 42% of cases, the aneurysm demonstrated evidence of calcification or thrombosis. These aneurysms require a longer ischemic duration because opening of the aneurysm and atheroma evacuation require meticulous dissection before surgical clipping. Twenty-three percent of patients had subarachnoid hemorrhage (SAH), either remotely (5%) or acutely (18%); 77% of patients had unruptured aneurysms found incidentally or during the evaluation of a neurological complaint. Based on the neurological examination performed at the time of admission, 39% of these patients had cranial nerve abnormalities, 26% complained of headache, 12% suffered from hemiparesis or quadriparesis, 12% showed evidence of mental status changes, and 8% had an unspecified gait disorder. Four percent of patients had visual disturbances and 2% had focal motor seizures; 3% of patients had aneurysms found incidentally and had normal neurological examinations.

The pterional, sylvian fissure splitting approach was used in 91% of anterior circulation aneurysms and 64% of posterior circulation aneurysms. The orbitozygomatic approach was used in 6% of cases and 12% of aneurysms were approached via the suboccipital route. Three percent of aneurysms were exposed by the bifrontal approach and 2% by the intrahemispheric approach.

The average time on cardiopulmonary bypass was 132 minutes and average time in circulatory arrest was 26.2 minutes. A mean brain temperature of 17.6°C was achieved over an average duration of 28.5 minutes. All patients were placed on bypass via a femoral-femoral technique. Beginning in 1991, propofol was substituted for barbiturates with no increase in complications and with a 73% reduction in the average time of emergence from 11 to 3 hours.

Functional Outcome

Sixty-seven percent of patients had an excellent or good outcome (Glasgow Outcome Scale [GOS] 4 or 5) at 3-month follow-up; 20% were dependent and 12% died. Discharge and follow-up data were not available on one patient. Patient characteristics that correlated with clinical outcome were age and preoperative neurological function. Aneurysm size was the only pathoanatomic factor significantly associated with outcome. Increasing time of circulatory arrest correlated with poor early postoperative GOS score. Patients experiencing more than 30 minutes of circulatory arrest had worse outcomes than those experiencing less than 30 minutes of circulatory arrest. Factors not correlated with outcome included a recent history of subarachnoid hemorrhage, aneurysm location, presence of extensive thrombus or calcium, duration of cardiopulmonary bypass, and brain temperature.

Treatment Complications

The series had a 9% surgical mortality. Two deaths were secondary to the bypass procedure and three were neurologic complications. The two main categories of adverse outcomes were bypass-related complications and neurological complications. Two patients (3.6%) had complications of the cardiopulmonary bypass procedure resulting in intraoperative deaths. One patient suffered a ruptured aortic root, thought to represent the extension of an iliac artery dissection. The other patient developed cardiac tamponade. Both patients had an emergent sternotomy performed as part of an extensive resuscitative effort. Two patients developed middle cerebral artery infarctions postoperatively and died. A third patient experienced intraventricular hemorrhage after clipping of a giant ophthalmic aneurysm, developed occlusion of the fourth ventricle, and died on postoperative day 2. One patient had a giant basilar artery aneurysm that was not clippable even with the assistance of circulatory arrest. The patient recovered from the circulatory arrest procedure uneventfully, was discharged in his preoperative condition, and went to another center for coil embolization. Two weeks after that procedure the patient died from a subarachnoid hemorrhage. Two patients required hemicraniectomy secondary to large MCA territory strokes. One patient developed a temporal lobe hematoma on the side of surgery and required decompression on postoperative day 2. Another patient developed a temporal lobe hematoma that did not require surgical evacuation. Three patients required shunts. In total, five patients (11%) required operations within 30 days of the circulatory arrest procedure. Eight patients (14%) had medical complications in the perioperative period (cardiac arrhythmias, pulmonary embolism, seizures, pneumonia, syndrome of inappropriate antidiuretic hormone [SIADH]).

CASE 1

Giant Carotid Bifurcation Aneurysm

This is the case of a 34-year-old truck driver who had left focal motor seizures. MRI revealed a giant right carotid bifurcation aneurysm abutting the right basal ganglia, hypothalamus, and foramen of Monro with mild hydrocephalus (Fig. 346-1, A and B). After confirming a 3.5 cm giant aneurysm with DSA (Fig. 346-2), the decision was made to perform surgical clipping under deep hypothermic circulatory arrest because of the aneurysm size and involvement with eloquent structures. At surgery, the aneurysm was collapsed after complete circulatory arrest, and multiple clips were successfully placed (Fig. 346-3) with no residual filling on postoperative angiogram. Postoperatively he had transient, mild left-sided weakness that resolved within days, and thereafter remained deficit free.

FIGURE 346-1 Preoperative MRI showing a giant, partially-thrombosed right carotid bifurcation aneurysm abutting the basal ganglia and hypothalamus.

FIGURE 346-2 Preoperative angiogram revealing a 3.5 cm right ICA bifurcation aneurysm involving the A1 segment.

FIGURE 346-3 Intraoperative photograph showing clip placement across the M1 and A1 segments of the ICA bifurcation aneurysm.

CASE 2

Giant Midbasilar Aneurysm

This is the case of a 22-year-old woman who presented complaining of intermittent headaches, vomiting, and double vision. MRI and angiogram revealed a large, thrombosed 2.7 cm midbasilar aneurysm without evidence of hemorrhage (Fig. 346-4, A). The aneurysm was coiled at an outside institution with good result (Fig. 346-4, B). However, an 8-month follow-up angiogram demonstrated migration of the coils with refilling of the entire aneurysm dome and resultant brainstem compression (Fig. 346-5). Because of the aneurysm size and involvement with the brainstem, the decision was made to perform surgical clipping under complete circulatory arrest. At surgery, exposure was achieved via left temporal craniotomy and suboccipital craniectomy with a presigmoid approach. After inducing hypothermia and complete circulatory arrest, the aneurysm dome was collapsed, partially dissected away from the brainstem, and clipped using fenestrated and straight clips (Fig. 346-6). Postoperatively her symptoms resolved and she remained deficit free.