Advertisement

Physiopathology of Intraoperative Visceral Ischemia and Anesthesiological Management of Supravisceral Aortic Clamping

  • Fabrizio MonacoEmail author
  • Barucco Gaia
  • Mattioli Cristina
  • De Luca Monica
Chapter
  • 486 Downloads

Abstract

Vascular surgery, in which a supraceliac aortic clamp is required, is at highest risk of visceral ischemia and postoperative complications. The interruption of the blood flow to the organs, secondary to the artic cross-clamp, triggers cellular and molecular alterations with local and systemic effects. In particular, the tissues distal to the clamp become ischemic with a shift from aerobic to anaerobic metabolism. Since the reperfusion, following aortic clamp removal, may further increase the organ damage of the ischemic tissues, an ischemia/reperfusion (I/R) injury is usually observed during aortic surgery. The I/R injury is responsible for an extensive systemic inflammatory response which may trigger postoperative multi-organ failure. Polymorphonuclear neutrophils, oxygen radicals, nitric oxide, complement system, and cytokines are mainly involved in this double pathophysiological phenomenon.

In light of this, any technique, strategy, or drug able to mitigate the I/R injury may significantly affect the outcome. Although several perioperative medications have been proposed, the results remain elusive. On the contrary, left heart bypass, CFS drainage, and avoidance of nephrotoxic drugs, together with a maintenance of a mean arterial pressure above 80 mmHg, have shown to be the only measures effective in reducing perioperative morbidity and mortality.

14.1 Introduction

In patients undergoing aortic surgery, visceral ischemia is the leading cause of visceral dysfunction and injury [1, 2]. In fact, acute kidney injury (AKI), spinal cord ischemia (SPCI), and bowel ischemia are catastrophic complications which may occur during surgical procedures involving the supra- and juxta-renal aorta cross-clamping [2, 3]. Because of the fact that the higher the extent of the surgical aortic repair, the greater the risk of organ dysfunction, thoracoabdominal aortic aneurysm open repair (TAAAr) is more prone to developing visceral ischemia than infrarenal abdominal aortic aneurysm [1, 3]. The application of the aortic clamp, decreasing the blood supply to the organs, is associated with extensive physiological changes which may affect patient outcomes. Therefore, it is important for surgeons and anesthesiologists to understand the pathophysiologic changes occurring during aortic cross-clamping in order to mitigate the deleterious effect of ischemia-reperfusion injuries.

14.2 Physiopathology of Intraoperative Visceral Ischemia

Vascular surgery, in which the aorta is clamped proximally to the celiac artery, is one of the few surgical procedures producing ischemia of the liver, bowel, kidneys, spinal cord, and inferior limbs contemporarily. Aortic cross-clamping produces rapid hemodynamic changes and induces ischemic insults. Following the aortic clamp removal, the reperfusion itself may lead to a sudden drop in blood pressure and cellular damage. Therefore, aortic surgery shows double physiological phenomena named ischemia/reperfusion (I/R) injury which is the major determinant of an extensive systemic inflammatory response and the trigger for postoperative multi-organ dysfunction (MODS) [4, 5]. In particular, after aortic clamping in the district distal to the aortic clamp, visceral tissues suffer a sudden decrease of the blood flow with an acute hypoxic insult, shift from an aerobic to an anaerobic metabolism, production of lactate, and development of acidosis [6]. At the same time, cellular membranes increase their permeability, leading to cellular swelling [4, 7, 8]. Following aortic clamp removal, the reperfusion of tissue is responsible for additional injuries on the top of ischemia [4, 5, 6, 7, 8]. In some instances, the reperfusion damage may exceed the original ischemic injury; in fact, the restoration of the blood flow account for the activation of several inflammatory pathways and biochemical changes [4]. In the I/R syndrome, polymorphonuclear neutrophils, oxygen radicals (ROS), nitric oxide (NO), complement system, and various cytokines play a pivotal role, showing their effects in both re-perfused tissues and distal organs [9, 10]. The re-oxygenation enhances ROS production, which are associated with lipid peroxidation, complement activation, platelet aggregation, white cell activation, suppression of adenosine triphosphate synthesis, and inactivation of metabolic enzymes [10, 11]. Moreover, the ROS leading to the depletion of antioxidant reserves, disruption of cellular and mitochondrial membrane, derangement of intracellular electrolytes boost the phenomenon of apoptosis [12, 13].

A growing body of literature suggests that polymorphonuclear neutrophils play a central role in the pathophysiology of I/R [10]. In fact, the upregulation of adhesion molecules, chemoattractants, chemokines, and integrins due to I/R stimulates the migration of polymorphonuclear neutrophils from the postcapillary venules to the area of inflammation. Polymorphonuclear neutrophils, then, may disrupt the contiguous tissues by the secretion of proteolytic enzymes, production of free radicals, and microcirculation disarrangement [11]. Of note, the oxidative stress and ROS formation reach their peak during the ischemic attack (15–60 min of clamping), while PMN infiltration is at a maximum during reperfusion [10, 11, 12].

Notably, the NO has both cytotoxic and cytoprotective effects. In fact, it is an oxygen-free radical scavenger, maintains normal vascular permeability, inhibits the proliferation of smooth muscle, reduces PMN adherence, and decreases platelet aggregation [13]. However the release of large amounts of NO may account for tissue injury, bacterial translocation, mucosal apoptosis, and pulmonary injury [14, 15, 16].

The complement, acting together with ROS, NOS, and PNM, increases vascular permeability and tissue edema [17, 18, 19, 20]. It elicits a cascade of pro-inflammatory events with release of high concentration of TNF-α and interleukin (IL)-1 [18, 21]. Finally, the occurrence of edema in the interstitium of the injured organ further decreases the oxygen diffusion gradient from the microcirculation to the cells [9].

14.3 Postoperative Effects of Ischemia/Reperfusion Injury

Interestingly, the I/R injury has an effect on both the organs directly affected by the ischemia and the organs not involved in the ischemic insult, by a systemic release of inflammatory mediators [22]. Therefore, it is not surprising that during aortic surgery, along with the bowel and kidney, even the heart, lungs, and spinal cord may suffer I/R damage [4]. When the damage is extensive, multi-organ failure may occur [22, 23]. Each organ and apparatus has a specific sensitivity to I/R insult and deserves specific considerations.

14.3.1 Bowel

Since labile cells are settled at the tips of the villi and supplied by the end of the distribution of a central arteriole, they are much more vulnerable to the ischemia when compared to cells located within the crypts [24]. The various acute-phase proteins, hydrogen peroxide, hormones, and cytokines produced by intestinal mucosa during I/R injury have deleterious effects onto the intestinal microvasculature and may lead to bowel infarction, short-bowel syndrome, systemic inflammatory response syndrome, acute respiratory distress syndrome, and MOF [25]. Moreover, the impairment of the mucosal barrier allows the release in the systemic circulation of the endotoxin which induces the systemic activation of PMN, complement, and clotting pathways and further increase of the mucosal permeability [26].

14.3.2 Kidney

Acute renal failure (AKI) during aortic surgery is multifactorial and it may occur as a result of I/R damage, hemodynamic changes, bleeding, acute heart failure, and cytotoxic agents [27, 28, 29, 30, 31, 32, 33, 34, 35, 36]. The level at which the aortic clamp is applied affects the renal perfusion [37]. In fact, it decreases by 80% in the event of the suprarenal aortic cross-clamping, while it decreases by 45% when the aortic clamp is infrarenal [38]. To counteract the decrease of the renal blood flow, an increase of the renal vascular resistance is mediated by the hormone angiotensin II which redistributes the blood flow away from renal medulla and cortex, significantly decreasing renal perfusion [28, 39]. This effect persists after aortic clamp removal, despite a normal mean perfusion pressure [40]. Similarly, the glomerular filtration rate and renal blood flow may remain impaired for a long period of time after the surgery [31]. Besides this, ROS, complement, IL-1, IL 6, and IL8 released by the damaged mesangial cells increase the local inflammation worsening the renal function [41].

14.3.3 Heart

Aortic surgery is associated with the highest risk of myocardial infarction and cardiovascular complications compared to other noncardiac-related surgeries [42, 43]. The reasons for that include the increase of afterload and preload associated with the aortic cross-clamp, massive bleeding with consequent volume shift, and inflammatory response following I/R injury of abdominal organs [22]. Several authors have proposed that IL-2, IL-1β, IL-6, IFN-γ, and TNF-α may affect the cardiac function [44]. In I/R injury of the heart, the NO is probably involved in the decrease of ventricular compliance [4]. The activation of the NO synthesis leads to higher NO concentration which significantly affects the cardiac adrenergic and cholinergic stimulation [4]. A ventricle with low compliance is “difficult to fill,” and it is associated with lower cardiac output and impairment of the coronary blood flow due to a decrease in the aortocoronary pressure gradient. Moreover, the ROS released from the injured myocytes and endothelial cells promotes membrane damage, endothelial injury, and vessel permeability [45, 46]. The treatment of the diastolic dysfunction is challenging: in fact, the administration of exogenous inotropes/vasopressors may further decrease a microcirculation already impaired by the endothelial swelling, exacerbating the ischemic damage [46]. In addition, activation of the coagulation cascade, formation of microthrombi, platelet aggregation stimulated by the use of vasopressors, and accumulation of reactive neutrophils act together impairing the microcirculation and decreasing the myocardial perfusion [47].

14.3.4 Lungs

The respiratory function after aortic surgery is commonly impaired. While in the vast majority of cases, damage is moderate with nonsignificant clinical manifestations; in several circumstances, it may be part of MOF [22]. Since in a physiological state the pulmonary vasculature is a neutrophil reserve, the respiratory system is at the highest risk of developing an inflammatory response during aortic surgery [11]. In fact, it is particularly sensitive to the circulating cytokines released from several organs during the postoperative period [48]. The I/R damage releases “per se” cytokines, which activate the pulmonary endothelium, stimulate the leucocytes migration into the interstitial and alveolar space, and promote inflammation [22]. Similarly, the anaphylatoxins C3a and C5a play a role in increasing the pulmonary vascular tone, favoring capillary leakage, and activating the mast cells which release histamine [49, 50]. The most severe clinical respiratory manifestation of this “vicious circle” is the acute respiratory distress syndrome which is associated with refractory hypoxia and death in a high percentage of patients [51].

14.3.5 Spinal Cord

Spinal cord ischemia is one of the most dreadful complications in aortic surgery [1, 2, 3]. The abrupt interruption of the blood flow to the spinal cord leads to ischemic injury [5256]. Even when the thoracic aorta is not involved (abdominal aorta aneurysm open repair), a profound shock may impair the medulla perfusion pressure causing SCI [53]. The pathogenesis includes oxygen-free radical-induced lipid peroxidation, intracellular calcium overload, leukocyte activation, inflammatory response, and neuronal apoptosis. All these factors acting together cause the disruption of the blood-spinal cord barrier, which in turn exacerbates the spinal cord edema, increases the leukocyte infiltration, and amplifies inflammation and oxidative stress [57].

14.4 Anesthesiological Management of Supravisceral Aortic Clamping

Given the complexity of the physiopathology of the visceral ischemia in procedures involving supravisceral aortic clamping, the aim of the anesthesiological management is to avoid the hemodynamic fluctuations which may induce irreversible damage to organs and apparatus.

14.5 Hemodynamic Response to Cross-Clamping

Generally speaking, the higher the location of the aortic clamp, the greater the increase of the afterload against which the heart has to work [58]. The immediate effect of aortic clamping is a rapid increase of blood pressure due to an increase in systemic vascular resistance (SVR) [58, 59] (Fig. 14.1). Reasons for that are higher impedance to aortic flow, increased venous return (preload) from the viscera, and release of catecholamines and angiotensin [6, 58, 59, 60, 61, 62]. In particular, in the event of supraceliac aortic clamping, a rapid decrease of venous capacity in the splanchnic district is associated with a blood volume shift proximal to the clamp site [63]. When the aortic clamp is infra-celiac, the increase of preload is directly related to the splanchnic venous tone: with a lower preload when the venous tone is low and higher preload if the venous tone is higher [38, 63]. The consequence of the increase of afterload and preload is the improvement in contractility [59]. The increase of the left ventricular end-diastolic pressure, following the increase in arterial blood pressure, leads to a transitory subendocardial ischemia which triggers the augmentation of the coronary blood flow toward the endocardia (Anrep effects) [64]. The effect is an increase of contractility and then of cardiac output [65]. On the contrary, patients with low coronary reserve, due to coronary artery disease, fail to respond to the subendocardial ischemia with an increase of the coronary flow leading to subendocardial ischemia and low cardiac output. In this case, vasodilators may improve the Anrep effect, increasing coronary blood flow and reducing, at the same time, pre- and afterload [66]. When a distal perfusion technique is not provided and an aortic clamp is present, the perfusion of the vital tissues distal to the aortic clamp is provided by collateral vessels and depends upon the proximal perfusion pressure [62]. Thus, hypotension should be avoided as much as possible [62, 66, 67].
Fig. 14.1

Hemodynamic response to aortic cross-clamping

When the aortic clamp is released, the rapid decrease in vascular resistance produces hypotension. Reperfusion of previous ischemic tissues which are vasodilated for the effect of hypercapnia, acidosis, and high concentration of adenosine and lactate [58] leads to central hypovolemia. Furthermore, the washout into the systemic circulation of myocardial depressant metabolites from ischemic area is associated with further vasodilation and decrease in cardiac output [59] (Fig. 14.2).
Fig. 14.2

Hemodynamic response to aortic unclamping

Following aortic clamp removal, a transient increase in CO2 is commonly observed due to both CO2 washout from the ischemic tissues into the systemic circulation and increased CO2 production secondary to increased oxygen consumption of the re-perfused tissues [58, 59]. Carbon dioxide causes further vasodilation [68].

Hypotension after aortic cross-clamp release can be prevented and treated with volume loading, infusion of vasoactive medications, prompt treatment of metabolic abnormalities, and gradual release of aortic cross-clamp. In this dynamic setting, the anesthesiologist has to continuously assess the patient’s global hemodynamic status, integrating cardiac function, intravascular volumes (estimated from transesophageal echocardiography, filling pressures, or both), blood loss, and the total amount of fluid administered [59, 60]. Moreover, adequate tissue perfusion is based on the availability of oxygen delivered. In situations where the blood flow is suboptimal, an arterial oxygen saturation as high as possible and a hemoglobin concentration above 10 g/dL are mandatory [69].

14.6 The Distal Perfusion Technique as a Strategy to Prevent Visceral Ischemia

Cross-clamping of the descending thoracic aorta produces visceral, spinal cord, kidney, bowel, and limb ischemia and is also challenging for the heart due to an abrupt increase of the pre- and afterload. In order to prevent and mitigate the consequences of visceral ischemia, several pharmacological and mechanical strategies have been proposed [70]. To date, distal organ perfusion is universally recognized as the best technique to limit ischemic injury in the organs distal to the clamp site, to support the heart, and to control proximal hypertension during thoracoabdominal aneurysm open repair [71, 72]. Distal perfusion may be performed by partial cardiopulmonary bypass (CPBP), left bypass (LBP), or left heart bypass (LHBP). Among these, LHBP is associated with a low risk of bleeding due to a mild heparinization [73]. Briefly, the basic circuit for LHBP is composed by an inflow cannula, a centrifugal pump, and an outflow cannula. In the left heart bypass (LHBP), the inflow cannula is placed in the pulmonary vein or left atrial appendage (Fig. 14.3), while the outflow cannula is positioned in the distal aorta or the femoral artery [74]. During the surgical anastomosis of the visceral vessels, perfusion of the abdominal organs is usually guaranteed by a selective catheterization of individual arteries [75, 76]. A flow of 200–300 mL/min of normothermic oxygenated blood for each catheter maintains a visceral perfusion pressure around 70 mmHg. The kidneys are perfused by cold crystalloids or cold Custodiol. Several studies have reported that a cold Ringer lactate solution is superior to normothermic oxygenated blood in terms of prevention of renal dysfunction during selective renal artery perfusion and supraceliac aortic cross-clamp [77, 78, 79]. Moreover, Tshomba et al. observed that in patients undergoing TAAA open repair, a selective renal perfusion with histidine-tryptophan-ketoglutarate solution (Custodiol; Dr. Franz-Kohler Chemie GmbH, Bensheim, Germany) significantly decreases the incidence of postoperative renal failure when compared with cold Ringer lactate [80].
Fig. 14.3

Transesophageal echocardiography. Off-axis view of the outflow cannula joining the left atrium by the inferior left pulmonary vein

There is no agreement on which is an adequate distal perfusion pressure when the LHBP is used. Some authors, for instance, suggest that a flow as high as 40 mL/kg/min is adequate to guarantee an optimal distal perfusion. On the contrary, others report that a flow ranging between 1.5 and 3 L/min with a mean femoral artery pressure of 70 mmHg can be considered sufficient for organ perfusion [81]. As practical rule, during aortic cross-clamping, a distal aortic pressure above 70 mmHg and a proximal perfusion pressure above 90 mmHg can be considered optimal for organ and spinal cord perfusion. Further indices of optimal organs perfusion are renal output above 1 mL/kg/h without diuretics and no lactate production [61].

14.7 Strategy to Prevent Postoperative Organ Dysfunction in Visceral Ischemia

Although the distal perfusion technique mitigates the effects of visceral ischemia, postoperative complications due to organ hypoperfusion remain relatively high [1, 2, 3, 4]. Several strategies have shown to be effective in mitigating organ ischemia following aortic clamp.

14.7.1 Renal Protection

Postoperative acute kidney injury (AKI) after vascular surgery is a major cause of morbidity and mortality [33, 82]. The etiology of renal failure in the setting of vascular surgery is multifactorial [83]. Ischemic injury (clamp time), nephrotoxic agents (antibiotics, anesthetic agent, contrast media, diuretics, myoglobin), and pre-existing renal failure are major factors related to the development of acute renal failure after aortic surgery [31, 34, 83, 84, 85]. In light of this, the avoidance of nephrotoxic insult, prevention of renal hypoperfusion by adequate cardiac output, and MAP have recently been reported as the only measures effective in decreasing the incidence of AKI [86, 87, 88]. On the contrary, the use of drugs such as dopamine and fenoldopam is not able to prevent perioperative renal dysfunction [89, 90, 91]. Since methylprednisolone, at a dosage of 30 mg/kg, may be a scavenger of free radicals with immunomodulatory proprieties, some authors have postulated that its administration may prevent renal ischemia/reperfusion injury [92, 93, 94, 95]. Unfortunately, the results are elusive [96]. Even mannitol (0.5 g/kg), which theoretically has a favorable profile in terms of renal failure prevention due to the induction of osmotic diuresis, the prevention of tubular obstruction, the decrease of epithelial and endothelial cell swelling, the action of free radical scavenger, and the stimulation of the synthesis of intrarenal prostaglandin with a renal vasodilation effect, has shown to be ineffective in preventing AKI [86, 97]. Moreover side effects such as volume depletion and an increased medullary consumption of O2 are very well known and may have a detrimental impact on renal function [98].

14.7.2 Spinal Cord Protection

Paraplegia caused by ischemic spinal cord injury is a devastating potential complication of aortic surgery [1, 99, 100]. Patients with SCI have poorer long-term survival compared to those who do not [1]. The position of aortic cross-clamping may affect the spinal cord perfusion, with the highest risk during extent II repair (7–10%) and the lowest risk in extent IV (1%) [1, 54, 55]. During surgery, the maintenance of a spinal cord perfusion pressure (SCPP) above 80 mmHG may prevent the development of paraplegia [101, 102]. Notably, the SCPP is the difference between the MAP and the cerebrospinal fluid (CSF) pressure. Interestingly, CSF pressure is influenced by the central venous pressure (CVP). After surgical occlusion of the spinal arteries, the perfusion of the spinal cord depends on the collateral network fed by hypogastric arteries, internal thoracic arteries, and branches from the subclavian arteries. The SCPP is a balance between the driving pressure affected by MAP, cardiac output, and blood volume and outflow pressure which depends on CSF and venous pressure. An increased CVP is associated with higher pressure in the extensive vertebral venous and impairment of spinal cord outflow. For the reasons mentioned above, the use of LHB, inotropes, and vasopressor, acting on the MAP and CVP, prevents paraplegia. The use of CSF drainage has been shown to decrease the risk of paraplegia reducing the CSFP [103]. In a large randomized controlled clinical trial the CSF drainage strategy in patients undergoing TAAA open surgery has shown an 80% decrease of postoperative paraplegia rate [104]. Recently Tshomba et al. observed that the use of the LiquoGuard automated device (Möller Medical GmbH, Fulda, Germany) during TAAA open repair is safe and effective in maintaining the desired CSF pressure values with a significant reduction in complication rates when compared with a standard catheter connected to a dripping chamber [105].

Somatosensory-evoked potentials are used to monitor the integrity of the posterior (sensory) spinal cord, and motor-evoked potentials (MEPs) are used to monitor dysfunction of the anterior (motor) spinal cord, detecting the spinal cord ischemia during the surgery [106, 107, 108]. Hypothermia has protective effects on the spinal cord and central nervous system by reducing both metabolic rate and oxygen requirement [109, 110].

14.7.3 Heart

Aortic surgery is a deeming procedure for the heart due to aortic clamp and large volume shift. Since the driving pressure for organs and apparatus depends on the native cardiac performance, it is crucial to optimize preload, afterload, and contractility. In light of this, TEE is an invaluable tool allowing for quick diagnosis and guiding the use of inotropes/vasopressors [111, 112]. Markers of right ventricle dysfunction are CVP over 12 mmHg, tricuspid annular plane systolic excursion below 16 mm, tissue Doppler index below 10 cm/s, right mid-cavity diameter above 42 mm, and longitudinal diameter longer than 9.2 mm (Figs. 14.414.6). With pressure or volume overload, the septum becomes flat and the LV assumes a D shape at the end of the systole or diastole, respectively (Videos 14.1 and 14.2). The RV is particularly sensitive to the increase of the pulmonary vascular resistance secondary to hypercapnia, hypoxia, acidosis, protamine and blood transfusion, and reduction of the pulmonary vascular bed, commonly observed during single-lung ventilation. Therefore, the first-line treatment of the right ventricular dysfunction is gas exchange optimization with high FiO2, moderate hyperventilation, and alkalization (pH > 7.40). Central venous pressure above 15 mmHg affecting SCPP should be treated with aggressive diuretic therapy. For moderate RV dysfunction, dobutamine is the drug of choice, while epinephrine is indicated in the event of poor RV contractility with hypotension associated (or not) to left ventricular failure. When RV failure coexists with low systemic vascular resistance, norepinephrine is effective in maintaining coronary perfusion pressure.
Fig. 14.4

Tissue Doppler index of the right ventricle. A value above 10 cm/s is normal under general anesthesia

Fig. 14.5

Tricuspid annular plane systolic excursion. A value above 16 mm is normal under general anesthesia

Fig. 14.6

Transesophageal echocardiography. In the midesophageal four-chamber view, the diameters of the right ventricle are best assessed

Markers of left ventricle dysfunction are wedge pressure above 15 mmHg, ejection fraction below 50%, and left ventricular outflow tract velocity time integral below 20 cm/s with good RV function. In transgastric midpapillary short-axis view, the TEE allow to identify whether the hypotension depends on low preload (papillary kissing) or poor contractility (increase end-diastolic diameter) (Videos 14.3 and 14.4). Poor contractility is managed with epinephrine or dobutamine. Mean arterial pressure is a critical factor, and it is not unusual to observe a significantly altered ST segment and regional wall motion abnormalities with low MAP that become almost normal with adequate systemic perfusion pressure. When the increased afterload is associated with a systolic ventricular dysfunction, “inodilators” are suggested, while with an almost normal systolic contraction brief, acting vasodilator drugs (nitroglycerine) are recommended. As proximal aortic hypotension compromises the perfusion to collateral-dependent tissue beds distal to the aortic clamp, the use of short-term drugs are recommended. Short-acting beta-blockers are preferred agents when a hypertensive episode is associated with tachycardia.

14.7.4 Abdominal Viscera

Surgical occlusion by aortic clamp of the celiac axis and superior and inferior mesenteric leads to hypoxia of the abdominal viscera. The clamping time plays a pivotal role in the development of visceral ischemia, and the adoption of the selective perfusions of the visceral arteries with warm blood mitigates this phenomenon [78]. Even a transitory period of bowel ischemia, affecting the mucosal integrity, promotes the translocation of intestinal bacteria into the circulation promoting systemic infection and sepsis.

With the aortic clamp release, the washout of both the endotoxins produced by intestinal bacteria and the cardio-depressant metabolites from the ischemic area contributes to the systemic vasodilation and hemodynamic instability observed after visceral reperfusion [16]. Therefore, acid-base alterations occurring throughout the surgery should be promptly treated even by the administration of sodium bicarbonate.

In addition, visceral ischemia may be associated with systemic coagulopathy due to increased intestinal permeability, bacterial translocation, hepatic ischemia, and primary fibrinolysis. Therefore, the use of antifibrinolytic such as tranexamic acid or aminocaproic acid is strongly suggested [18].

14.7.5 Lungs

Postoperative pulmonary complications are common after aortic surgery [1, 3]. In addition to surgical trauma, diaphragm incision, and need of the one-lung ventilation (OLA), lung manipulation, blood transfusion, and fluid overload are very well-recognized risk factors. Furthermore, preoperative risk factors, such as COPD and history of smoking, significantly increase the chance of postoperative lung dysfunction. With this in mind, the adoption of a “protective ventilation” with low tidal volume, higher levels of positive end-expiratory pressure, and low plateau pressure is able to decrease the occurrence of acute lung injury [113]. However during the OLV, the priority is to guarantee oxygen saturation above 90%. A drop in oxygen saturation may lead to a significant decrease in the delivery oxygen with relative tissue hypoxia. A parsimoniously administration of blood products contributes to decreasing the risk of transfusion-related acute lung injury and transfusion-related immune modulation. To avoid large-volume transfusion, a ROTEM-guided protocol may be useful. Further studies are needed to confirm this data.

14.8 Conclusion

Visceral ischemia during supraceliac aortic cross-clamp is a multifactorial complex syndrome associated with an increased risk of developing severe postoperative organ dysfunction, requiring therefore an extensive and detailed anesthesiological and surgical workup. Often, visceral ischemia is devious, and only a prompt treatment may avoid severe postoperative complications. For all these reasons, adequate preoperative assessment and risk stratification, a skillful anesthetic technique, a meticulous intraoperative monitoring, and an appropriate postoperative course are all necessary measures to guarantee an uneventful procedure and avoid potentially fatal complications.

Supplementary material

Video 14.1

Midesophageal four-chamber view. Severe right ventricle dysfunction (WMV 1325 kb)

Video 14.2

Midpapillary transgastric view. Severe right ventricle dysfunction with left ventricle D-shape (WMV 1568 kb)

Video 14.3

Midpapillary transgastric view. Severe left ventricle dilation and systolic dysfunction (AVI 1916 kb)

Video 14.4

Mid-transgastric short-axis view. Empty left ventricle with papillary muscles “kissing” (AVI 14042 kb)

References

  1. 1.
    Coselli JS, LeMaire SA, Preventza O, de la Cruz KI, Cooley DA, Price MD, Stolz AP, Green SY, Arredondo CN, Rosengart TK. Outcomes of 3309 thoracoabdominal aortic aneurysm repairs. J Thorac Cardiovasc Surg. 2016;151(5):1323–37.Google Scholar
  2. 2.
    Crawford ES. Thoraco-abdominal and abdominal aortic aneurysms involving renal, superior mesenteric, celiac arteries. Ann Surg. 1974;179:763–72.PubMedPubMedCentralGoogle Scholar
  3. 3.
    Deery S, Lancaster R, Baril D, Indes J, Bertges D, Conrad M, Cambria R, Patel V. Contemporary outcomes of open complex abdominal aortic aneurysm repair. J Vasc Surg. 2016;63(5):1195–200.PubMedPubMedCentralGoogle Scholar
  4. 4.
    Katseni K, Chalkias A, Kotsis T, Dafnios N, Arapoglou V, Kaparos G, Logothetis E, Iacovidou N, Karvouni E, Katsenis K. The effect of perioperative ischemia and reperfusion on multiorgan dysfunction following abdominal aortic aneurysm repair. Biomed Res Int. 2015;2015:598980.PubMedPubMedCentralGoogle Scholar
  5. 5.
    Welborn MB, Oldenburg HS, Hess PJ, Huber TS, Martin TD, Rauwerda JA, Wesdorp RI, Espat NJ, Copeland EM 3rd, Moldawer LL, Seeger JM. The relationship between visceral ischemia, proinflammatory cytokines, and organ injury in patients undergoing thoracoabdominal aortic aneurysm repair. Crit Care Med. 2000;28(9):3191–7.PubMedGoogle Scholar
  6. 6.
    Eide TO, Aasland J, Romundstad P, Stenseth R, Saether OD, Aadahl P, Myhre HO. Changes in hemodynamics and acid-base balance during cross-clamping of the descending thoracic aorta: a study in patients operated on for thoracic and thoracoabdominal aortic aneurysm. Eur Surg Res. 2005;37(6):330–4.PubMedGoogle Scholar
  7. 7.
    Norwood MGA, Bown MJ, Sayers RD. Ischaemia/reperfusion injury and regional inflammatory responses in abdominal aortic aneurysm repair. Eur J Vasc Endovasc Surg. 2004;28(3):234–45.PubMedGoogle Scholar
  8. 8.
    Lindsay TF, Luo XP, Lehotay DC, et al. Ruptured abdominal aortic aneurysm, a ‘two-hit’ ischemia/reperfusion injury: evidence from an analysis of oxidative products. J Vasc Surg. 1999;30(2):219–28.PubMedGoogle Scholar
  9. 9.
    Carden DL, Granger DN. Pathophysiology of ischaemia–reperfusion injury. J Pathol. 2000;190:255–66.PubMedGoogle Scholar
  10. 10.
    Aivatidi C, Vourliotakis G, Georgopoulos S, Sigala F, Bastounis E, Papalambros E. Oxidative stress during abdominal aortic aneurysm repair—biomarkers and antioxidant’s protective effect: a review. Eur Rev Med Pharmacol Sci. 2011;15(3):245–52.PubMedGoogle Scholar
  11. 11.
    Barry MC, Kelly C, Burke P, Sheehan S, Redmond HP, Bouchier-Hayes D. Immunological and physiological responses to aortic surgery: effect of reperfusion on neutrophil and monocyte activation and pulmonary function. Br J Surg. 1997;84(4):513–9.PubMedGoogle Scholar
  12. 12.
    Galle C, De Maertelaer V, Motte S, et al. Early inflammatory response after elective abdominal aortic aneurysm repair: a comparison between endovascular procedure and conventional surgery. J Vasc Surg. 2000;32(2):234–46.PubMedGoogle Scholar
  13. 13.
    Thompson MM, Nasim A, Sayers RD, Thompson J, Smith G, Lunec J, Bell PR. Oxygen free radical and cytokine generation during endovascular and conventional aneurysm repair. Eur J Vasc Endovasc Surg. 1996;12(1):70–5.PubMedGoogle Scholar
  14. 14.
    Lefer AM, Lefer DJ. The role of nitric oxide and cell adhesion molecules on the microcirculation in ischaemia-reperfusion. Cardiovasc Res. 1996;32(4):743–51.PubMedGoogle Scholar
  15. 15.
    Kubes P, McCafferty DM. Nitric oxide and intestinal inflammation. Am J Med. 2000;109(2):150–8.PubMedGoogle Scholar
  16. 16.
    Suzuki Y, Deitch EA, Mishima S, Lu Q, Xu DZ. Inducible nitric oxide synthase gene knockout mice have increased resistance to gut injury and bacterial translocation after an intestinal ischemia-reperfusion injury. Crit Care Med. 2000;28:3692–6.PubMedGoogle Scholar
  17. 17.
    Ziegenfuß T, Wanner GA, Grass C, et al. Mixed agonistic-antagonistic cytokine response in whole blood from patients undergoing abdominal aortic aneurysm repair. Intensive Care Med. 1999;25(3):279–87.PubMedGoogle Scholar
  18. 18.
    Holzheimer RG, Gross J, Schein M. Pro- and anti-inflammatory cytokine-response in abdominal aortic aneurysm repair: a clinical model of ischemia-reperfusion. Shock. 1999;11(5):305–10.PubMedGoogle Scholar
  19. 19.
    Heller T, Hennecke M, Baumann U, et al. Selection of a C5a receptor antagonist from phage libraries attenuating the inflammatory response in immune complex disease and ischemia/reperfusion injury. J Immunol. 1999;163(2):985–94.PubMedGoogle Scholar
  20. 20.
    Kimura T, Andoh A, Fujiyama Y, Saotome T, Bamba T. A blockade of complement activation prevents rapid intestinal ischaemia-reperfusion injury by modulating mucosal mast cell degranulation in rats. Clin Exp Immunol. 1998;111(3):484–90.PubMedPubMedCentralGoogle Scholar
  21. 21.
    Wada K, Montalto MC, Stahl GL. Inhibition of complement C5 reduces local and remote organ injury after intestinal ischemia/reperfusion in the rat. Gastroenterology. 2001;120(1):126–33.PubMedGoogle Scholar
  22. 22.
    Bown MJ, Nicholson ML, Bell PRF, Sayers RD. Cytokines and inflammatory pathways in the pathogenesis of multiple organ failure following abdominal aortic aneurysm repair. Eur J Vasc Endovasc Surg. 2001;22(6):485–95.PubMedGoogle Scholar
  23. 23.
    Maziak DE, et al. The impact of multiple organ dysfunction on mortality following ruptured abdominal aortic aneurysm repair. Ann Vasc Surg. 1998;12(2):93–100.PubMedGoogle Scholar
  24. 24.
    Mallick IH, Yang W, Winslet MC, Seifalian AM. Ischemia-reperfusion injury of the intestine and protective strategies against injury. Dig Dis Sci. 2004;49(9):1359–77.PubMedGoogle Scholar
  25. 25.
    Molmenti EP, Ziambaras T, Perlmutter DH. Evidence for an acute phase response in human intestinal epithelial cells. J Biol Chem. 1993;268(19):14116–24.PubMedGoogle Scholar
  26. 26.
    Soong CV, Blair PH, Halliday MI, McCaigue MD, Campbell GR, Hood JM, Rowlands BJ, Barros D’Sa AA. Endotoxaemia, the generation of the cytokines and their relationship to intramucosal acidosis of the sigmoid colon in elective abdominal aortic aneurysm repair. Eur J Vasc Surg. 1993;7(5):534–9.PubMedGoogle Scholar
  27. 27.
    Black SA, Brooks MJ, Naidoo MN, Wolfe JHN. Assessing the impact of renal impairment on outcome after arterial intervention: a prospective review of 1559 patients. Eur J Vasc Endovasc Surg. 2007;32:300–4.Google Scholar
  28. 28.
    Wahlberg E, Dimuzio PJ, Stoney RJ. Aortic clamping during elective operations for infrarenal disease: the influence of clamping time on renal function. J Vasc Surg. 2002;36:13–8.PubMedGoogle Scholar
  29. 29.
    Kudo FA, Nishibe T, Miyazaki K, et al. Postoperative renal function after elective abdominal aortic aneurysm repair requiring suprarenal aortic cross-clamping. Surg Today. 2004;34:1010–3.PubMedGoogle Scholar
  30. 30.
    Powell RJ, Roddy SP, Meier GH, et al. Effect of renal insufficiency on outcome following infrarenal aortic surgery. Am J Surg. 1997;174:126–30.PubMedGoogle Scholar
  31. 31.
    Dariane C, Coscas R, Boulitrop C, Javerliat I, Vilaine E, Goeau-Brissonniere O, et al. Acute kidney injury after open repair of intact abdominal aortic aneurysms. Ann Vasc Surg. 2017;39:294–300.PubMedGoogle Scholar
  32. 32.
    Drews JD, Patel HJ, Williams DM, Dasika NL, Deeb GM. The impact of acute renal failure on early and late outcomes after thoracic aortic endovascular repair. Ann Thorac Surg. 2014;97(6):2027–33.PubMedGoogle Scholar
  33. 33.
    Jalalzadeh H, Indrakusuma R, Vogt L, van Beek SC, Vahl AC, Wisselink W, et al. Long-term survival after acute kidney injury following ruptured abdominal aortic aneurysm repair. J Vasc Surg. 2017;66(6):1712–8.PubMedGoogle Scholar
  34. 34.
    Kopolovic I, Simmonds K, Duggan S, Ewanchuk M, Stollery DE, Bagshaw SM, et al. Risk factors and outcomes associated with acute kidney injury following ruptured abdominal aortic aneurysm. BMC Nephrol. 2013;14(1):99.PubMedPubMedCentralGoogle Scholar
  35. 35.
    Safi HJ, Harlin SA, Miller CC, et al. Predictive factors for acute renal failure in thoracic and thoracoabdominal aortic aneurysm surgery. J Vasc Surg. 1996;24:338–44.PubMedGoogle Scholar
  36. 36.
    Breckwoldt WL, Mackey WC, Belkin M, O’Donnell TF Jr. The effect of suprarenal cross-clamping on abdominal aortic aneurysm repair. Arch Surg. 1992;127(5):520–4.PubMedGoogle Scholar
  37. 37.
    Chong T, Nguyen L, Owens CD, Conte MS, Belkin M. Suprarenal aortic cross-clamp position: a reappraisal of its effects on outcomes for open abdominal aortic aneurysm repair. J Vasc Surg. 2009;49:873–80.PubMedGoogle Scholar
  38. 38.
    Giulini SM, Bonardelli S, Portolani N, Giovanetti M, Galvani G, Maffeis R, Coniglio A, Tiberio GA, Nodari F, De Lucia M, Lussardi L, Regina P, Scolari F, Tomasoni GSM. Suprarenal aortic cross-clamping in elective abdominal aortic aneurysm surgery. Eur J Vasc Endovasc Surg. 2000;20:286–9.PubMedGoogle Scholar
  39. 39.
    Rothenbach P, Turnage RH, Iglesias J, Riva A, Bartula L, Myers SI. Downstream effects of splanchnic ischemia-reperfusion injury on renal function and eicosanoid release. J Appl Physiol. 1997;82:530–6.Google Scholar
  40. 40.
    Myers SI, Wang L, Liu F, Bartula LL. Suprarenal aortic clamping and reperfusion decreases medullary and cortical blood flow by decreased endogenous renal nitric oxide and PGE2 synthesis. J Vasc Surg. 2005;42(3):524–31.PubMedGoogle Scholar
  41. 41.
    Laufer J, Oren R, Farzam N, Goldberg I, Passwell J. Differential cytokine regulation of complement proteins in human glomerular epithelial cells. Nephron. 1997;76(3):276–83.PubMedGoogle Scholar
  42. 42.
    Schouten O, Sillesen H, Poldermans D. New guidelines from the European society of cardiology for perioperative cardiac care: a summary of implications for elective vascular surgery patients. Eur J Vasc Endovasc Surg. 2010;39:1–4.PubMedGoogle Scholar
  43. 43.
    Abraham N, Lemech L, Sandroussi C, et al. A prospective study of subclinical myocardial damage in endovascular versus open repair of infrarenal abdominal aortic aneurysms. J Vasc Surg. 2005;41:377–80.PubMedGoogle Scholar
  44. 44.
    Kelly RA, Smith TW. Cytokines and cardiac contractile function. Circulation. 1997;95:778–81.PubMedGoogle Scholar
  45. 45.
    Garcia-Dorado D, Oliveras J. Myocardial oedema: a preventable cause of reperfusion injury? Cardiovasc Res. 1993;27:1555–63.PubMedGoogle Scholar
  46. 46.
    Park JL, Lucchesi BR. Mechanisms of myocardial reperfusion injury. Ann Thorac Surg. 1999;68(5):1905–12.PubMedGoogle Scholar
  47. 47.
    Böttiger BW, Motsch J, Böhrer H, Böker T, Aulmann M, Nawroth PP, Martin E. Activation of blood coagulation after cardiac arrest is not balanced adequately by activation of endogenous fibrinolysis. Circulation. 1995;92:2572–8.PubMedGoogle Scholar
  48. 48.
    Paterson IS, Smith FC, Tsang GM, Hamer JD, Shearman CP. Reperfusion plasma contains a neutrophil activator. Ann Vasc Surg. 1993;7(1):68–75.PubMedGoogle Scholar
  49. 49.
    Koyama S, Sato E, Nomura H, Kubo K, Miura M, Yamashita T, Nagai S, Izumi T. Bradykinin stimulates type II alveolar cells to release neutrophil and monocyte chemotactic activity and inflammatory cytokines. Am J Pathol. 1998;153(6):1885–93.PubMedPubMedCentralGoogle Scholar
  50. 50.
    Grommes J, Soehnlein O. Contribution of neutrophils to acute lung injury. Mol Med. 2011;17(3–4):293–307.PubMedGoogle Scholar
  51. 51.
    Fanelli V, Vlachou A, Ghannadian S, Simonetti U, Slutsky AS, Zhang H. Acute respiratory distress syndrome: new definition, current and future therapeutic options. J Thorac Dis. 2013;5(3):326–34.PubMedPubMedCentralGoogle Scholar
  52. 52.
    Panthee N, Ono M. Spinal cord injury following thoracic and thoracoabdominal aortic repairs. Asian Cardiovasc Thorac Ann. 2015;23(2):235–46.PubMedGoogle Scholar
  53. 53.
    David Rosenthal MD, et al. Spinal cord ischemia after abdominal aortic operation: is it preventable? J Vasc Surg. 1999;30(3):391–7.Google Scholar
  54. 54.
    Etz DC, Luehr M, Aspern KV, et al. Spinal cord ischemia in open and endovascular thoracoabdominal aortic aneurysm repair: new concepts. J Cardiovasc Surg. 2014;55(2 Suppl 1):159–68.Google Scholar
  55. 55.
    Melissano G, Bertoglio L, Rinaldi E, Leopardi M, Chiesa R. An anatomical review of spinal cord blood supply. J Cardiovasc Surg. 2015;56:699–706.Google Scholar
  56. 56.
    Melissano G, Bertoglio L, Mascia D, Rinaldi E, Del Carro U, Nardelli P, Chiesa R. Spinal cord ischemia is multifactorial: what is the best protocol? J Cardiovasc Surg. 2016;57(2):191–201.Google Scholar
  57. 57.
    Yu Q, Huang J, Hu J, Zhu H. Advance in spinal cord ischemia reperfusion injury: blood-spinal cord barrier and remote ischemic preconditioning. Life Sci. 2016;154:34–8.PubMedGoogle Scholar
  58. 58.
    Zammert M, Gelman S. The pathophysiology of aortic cross-clamping. Best Pract Res Clin Anaesthesiol. 2016;30(3):257–69.PubMedGoogle Scholar
  59. 59.
    Gelman S. The pathophysiology of aortic cross-clamping and unclamping. Anesthesiology. 1995;82(4):1026–60.PubMedGoogle Scholar
  60. 60.
    Cuzick LM, Lopez AR, Cooper JR Jr. Pathophysiology of aortic cross-clamping. In: Chiesa R, Melissano G, Zangrillo A, Coselli JS, editors. Thoraco-abdominal aorta: surgical and anesthetic management. Milan: Springer; 2011. p. 65–72.Google Scholar
  61. 61.
    O’Connor CJ, Rothenberg DM. Anesthetic considerations for descending thoracic aortic surgery: part II. J Cardiothorac Vasc Anesth. 1995;9:734–47.PubMedGoogle Scholar
  62. 62.
    Subramaniam K, Caldwell JC. Anesthesia for descending aortic surgery. In: Subramaniam K, Park K, Subramaniam B, editors. Anesthesia and perioperative care for aortic surgery. New York, NY: Springer; 2011.Google Scholar
  63. 63.
    El-Sabrout RA, Reul GJ. Suprarenal or supraceliac aortic clamping during repair of infrarenal abdominal aortic aneurysms. Tex Heart Inst J. 2001;28(4):254–64.PubMedPubMedCentralGoogle Scholar
  64. 64.
    Cingolani HE, Pérez NG, Cingolani OH, Ennis IL. The Anrep effect: 100 years later. Am J Physiol Heart Circ Physiol. 2013;304(2):H175–82.PubMedGoogle Scholar
  65. 65.
    Nichols CG, Hanck DA, Jewell BR. The Anrep effect: an intrinsic myocardial mechanism. Can J Physiol Pharmacol. 1988;66(7):924–9.PubMedGoogle Scholar
  66. 66.
    Kahn RA, Stone ME, Moskowitz DM. Anesthetic consideration for descending thoracic aortic aneurysm repair. Semin Cardiothorac Vasc Anesth. 2007;11(3):205–23.PubMedGoogle Scholar
  67. 67.
    Puchakayala MR, Lau WC. Descending thoracic aortic aneurysms. Contin Educ Anaesth Crit Care Pain. 2006;6(2):54–9.Google Scholar
  68. 68.
    Cullen DJ, Eger EI. Cardiovascular effects of carbon dioxide in man. Anesthesiology. 1974;41(4):345–8.PubMedGoogle Scholar
  69. 69.
    McLellan SA, Walsh TS. Oxygen delivery and haemoglobin. Contin Educ Anaesth Crit Care Pain. 2004;4(4):123–6.Google Scholar
  70. 70.
    Di Luozzo G. Visceral and spinal cord protection during thoracoabdominal aortic aneurysm repair: clinical and laboratory update. J Thorac Cardiovasc Surg. 2013;145(3 Suppl):S135–8.PubMedGoogle Scholar
  71. 71.
    Coselli JS, Lemaire SA. Descending and thoracoabdominal aortic aneurysms. In: Cohn LH, editor. Cardiac surgery in the adult., 3rd edn. New York: McGraw-Hill Medical; 2008. p. 1277–98.Google Scholar
  72. 72.
    Crawford ES, Walker HS 3rd. Graft replacement of aneurysm in descending thoracic aorta: results without bypass or shunting. Surgery. 1981;89:73–85.PubMedGoogle Scholar
  73. 73.
    Coselli JS. The use of left heart in the repair of thoracoabdominal aortic aneurysms: current techniques and results. Semin Thorac Cardiovasc Surg. 2003;15:326–32.PubMedGoogle Scholar
  74. 74.
    Hessel EA. Circuitry and cannulation techniques. In: Gravlee GP, Davis RD, Stammers RD, et al., editors. Cardiopulmonary. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2008. p. 63–144.Google Scholar
  75. 75.
    Aftab M, Coselli JS. Reprint of: renal and visceral protection in thoracoabdominal aortic surgery. J Thorac Cardiovasc Surg. 2015;149(2 Suppl):S130–3.PubMedGoogle Scholar
  76. 76.
    Aftab M, Coselli JS. Renal and visceral protection in thoracoabdominal aortic surgery. J Thorac Cardiovasc Surg. 2014;148(6):2963–6.PubMedGoogle Scholar
  77. 77.
    Jacobs MJ, Eijsman L. Reduced renal failure following thoracoabdominal aortic aneurysm repair by selective perfusion. Eur J CardiothoracSurg. 1998;14:201–5.Google Scholar
  78. 78.
    Kuniyoshi Y, Koja K, Miyagi K, et al. Selective visceral perfusion during thoracoabdominal aortic aneurysm repair. Ann Thorac Cardiovasc Surg. 2004;10:367–72.PubMedGoogle Scholar
  79. 79.
    Lemaire SA. Randomized comparison of cold blood and cold crystalloid renal perfusion for renal protection during thoracoabdominal aortic aneurysm repair. J Vasc Surg. 2009;49:11–9.PubMedGoogle Scholar
  80. 80.
    Tshomba Y, Kahlberg A, Melissano G, Coppi G, Marone E, Ferrari D, Lembo R, Chiesa R. Comparison of renal perfusion solutions during thoracoabdominal aortic aneurysm repair. J Vasc Surg. 2014;59(3):623–33.PubMedGoogle Scholar
  81. 81.
    De Luca M, De Simone F. Left heart bypass. In: Chiesa R, Melissano G, Zangrillo A, editors. Thoraco-abdominal aorta. Milano: Springer; 2011.Google Scholar
  82. 82.
    Grams ME, Sang Y, Coresh J, Ballew S, Matsushita K, Molnar MZ, et al. Acute kidney injury after major surgery: a retrospective analysis of veterans health administration data. Am J Kidney Dis. 2016;67(6):872–80.PubMedGoogle Scholar
  83. 83.
    Roh GU, Lee JW, Nam SB, Lee J, Choi JR, Shim YH. Incidence and risk factors of acute kidney injury after thoracic aortic surgery for acute dissection. Ann Thorac Surg. 2012;94(3):766–71.PubMedGoogle Scholar
  84. 84.
    Marrocco-Trischitta MM, Melissano G, Kahlberg A, Vezzoli G, Calori G, Chiesa R. The impact of aortic clamping site on glomerular filtration rate after juxtarenal aneurysm repair. Ann Vasc Surg. 2009;23(6):770–7.PubMedGoogle Scholar
  85. 85.
    Wong GT, Lee EY, Irwin MG. Contrast induced nephropathy in vascular surgery. Br J Anaesth. 2016;117 Suppl 2:ii63–73.PubMedGoogle Scholar
  86. 86.
    Kellum JA, Lameire N, KDIGO AKI Guideline Work Group. Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (part 1). Crit Care. 2013;17(1):204.PubMedPubMedCentralGoogle Scholar
  87. 87.
    Sasabuchi Y, Kimura N, Shiotsuka J, Komuro T, Mouri H, Ohnuma T, et al. Long-term survival in patients with acute kidney injury after acute type a aortic dissection repair. Ann Thorac Surg. 2016;102(6):2003–9.PubMedGoogle Scholar
  88. 88.
    Landoni G, Bove T, Székely A, Comis M, Rodseth RN, Pasero D, et al. Reducing mortality in acute kidney injury patients: systematic review and international web-based survey. J Cardiothorac Vasc Anesth. 2013;27(6):1384–98.PubMedGoogle Scholar
  89. 89.
    Joannidis M, Druml W, Forni LG, Groeneveld ABJ, Honore PM, Hoste E, Ostermann M, Oudemans-van Straaten HM, Schetz M. Prevention of acute kidney injury and protection of renal function in the intensive care unit: update 2017: expert opinion of the working group on prevention, AKI section, European society of intensive care medicine. Intensive Care Med. 2017;43(6):730–49.PubMedPubMedCentralGoogle Scholar
  90. 90.
    Bove T, Zangrillo A, Guarracino F, Alvaro G, Persi B, Maglioni E, Galdieri N, Comis M, Caramelli F, Pasero DC, Pala G, Renzini M, Conte M, Paternoster G, Martinez B, Pinelli F, Frontini M, Zucchetti MC, Pappalardo F, Amantea B, Camata A, Pisano A, Verdecchia C, Dal Checco E, Cariello C, Faita L, Baldassarri R, Scandroglio AM, Saleh O, Lembo R, Calabrò MG, Bellomo R, Landoni G. Effect of fenoldopam on use of renal replacement therapy among patients with acute kidney injury after cardiac surgery: a randomized clinical trial. JAMA. 2014;312(21):2244–53.PubMedGoogle Scholar
  91. 91.
    Zangrillo A, Biondi-Zoccai GG, Frati E, Covello RD, Cabrini L, Guarracino F, Ruggeri L, Bove T, Bignami E, Landoni G. Fenoldopam and acute renal failure in cardiac surgery: a meta-analysis of randomized placebo-controlled trials. J Cardiothorac Vasc Anesth. 2012;26(3):407–13.PubMedGoogle Scholar
  92. 92.
    Jongkind V, Yeung KK, Akkersdijk GJM, et al. Juxtarenal aortic aneurysm repair. J Vasc Surg. 2010;52(3):760–7.PubMedGoogle Scholar
  93. 93.
    Chiesa R, Marone EM, Brioschi C, et al. Open repair of pararenal aortic aneurysms: operative management, early results, and risk factor analysis. Ann Vasc Surg. 2006;20(6):739–46.PubMedGoogle Scholar
  94. 94.
    Sasaki T, Ohsawa S, Ogawa M, et al. Postoperative renal function after an abdominal aortic aneurysm repair requiring a suprarenal aortic cross-clamp. Surg Today. 2000;30(1):33–6.PubMedGoogle Scholar
  95. 95.
    Allen BT, Anderson CB, Rubin BG, et al. Preservation of renal function in juxtarenal and suprarenal abdominal aortic aneurysm repair. J Vasc Surg. 1993;17(5):948–59.PubMedGoogle Scholar
  96. 96.
    Girbes AR. Prevention of acute renal failure: role of vaso-active drugs, mannitol and diuretics. Int J Artif Organs. 2004;27(12):1049–53.PubMedGoogle Scholar
  97. 97.
    Yallop KG, Sheppard SV, Smith DC. The effect of mannitol on renal function following cardio-pulmonary bypass in patients with normal pre-operative creatinine. Anaesthesia. 2008;63:576–82.PubMedGoogle Scholar
  98. 98.
    Solomon R, Werner C, Mann D, et al. Effects of saline, mannitol, and furosemide to prevent acute decreases in renal function induced by radiocontrast agents. N Engl J Med. 1994;331:1416–20.PubMedGoogle Scholar
  99. 99.
    Coselli JS, LeMaire SA, Miller CC III, et al. Mortality and paraplegia after thoracoabdominal aortic aneurysm repair: a risk factor analysis. Ann Thorac Surg. 2000;69:409–14.PubMedGoogle Scholar
  100. 100.
    Acher C, Wynn M. Paraplegia after thoracoabdominal aortic surgery: not just assisted circulation, hypothermic arrest, clamp and sew, or TEVAR. Ann Cardiothorac Surg. 2012;1(3):365–72.PubMedPubMedCentralGoogle Scholar
  101. 101.
    McGarvey ML, Mullen MT, Woo EY, et al. The treatment of spinal cord ischemia following thoracic endovascular aortic repair. Neurocrit Care. 2007;6:35–9.PubMedGoogle Scholar
  102. 102.
    Cheung AT, Weiss SJ, McGarvey ML, et al. Interventions for reversing delayed-onset postoperative paraplegia after thoracic aortic reconstruction. Ann Thorac Surg. 2002;74(2):413–9.PubMedGoogle Scholar
  103. 103.
    Erbel R, Aboyans V, Boileau C, et al. 2014 ESC guidelines on the diagnosis and treatment of aortic diseases. Eur Heart J. 2014;35:2873–926.PubMedGoogle Scholar
  104. 104.
    Coselli JS, LeMaire SA, Köksoy C, Schmittling ZC, Curling PE. Cerebrospinal fluid drainage reduces paraplegia after thoracoabdominal aortic aneurysm repair: results of a randomized clinical trial. J Vasc Surg. 2002;35:631–9.PubMedGoogle Scholar
  105. 105.
    Tshomba Y, Leopardi M, Mascia D, Kahlberg A, Carozzo A, Magrin S, Melissano G, Chiesa R. Automated pressure-controlled cerebrospinal fluid drainage during open thoracoabdominal aortic aneurysm repair. J Vasc Surg. 2017;66(1):37–44.PubMedGoogle Scholar
  106. 106.
    Liu LY, Callahan B, Peterss S, Dumfarth J, Tranquilli M, Ziganshin BA, Elefteriades JA. Neuromonitoring using motor and somatosensory evoked potentials in aortic surgery. J Card Surg. 2016;31(6):383–9.PubMedGoogle Scholar
  107. 107.
    Keeling B, Chen EP. Reaching the full potential of MEP monitoring during surgery of the thoracoabdominal aorta. J Thorac Cardiovasc Surg. 2016;151(2):518–9.PubMedGoogle Scholar
  108. 108.
    Estrera AL, Sheinbaum R, Miller CC 3rd, Harrison R, Safi HJ. Neuromonitor-guided repair of thoracoabdominal aortic aneurysms. J Thorac Cardiovasc Surg. 2010;140(6 Suppl):S131–5.PubMedGoogle Scholar
  109. 109.
    Martirosyan NL, Patel AA, Carotenuto A, Kalani MY, Bohl MA, Preul MC, Theodore N. The role of therapeutic hypothermia in the management of acute spinal cord injury. Clin Neurol Neurosurg. 2017;154:79–88.PubMedGoogle Scholar
  110. 110.
    Kang J, Albadawi H, Casey PJ, Abbruzzese TA, Patel VI, Yoo HJ, Cambria RP, Watkins MT. The effects of systemic hypothermia on a murine model of thoracic aortic ischemia reperfusion. J Vasc Surg. 2010;52(2):435–43.PubMedGoogle Scholar
  111. 111.
    Fayad A, Shillcutt SK. Perioperative transesophageal echocardiography for non-cardiac surgery. Can J Anaesth. 2018;65(4):381–98.PubMedGoogle Scholar
  112. 112.
    Kristensen SD, Knuuti J, Saraste A, Anker S, Bøtker HE, De Hert S, Ford I, Gonzalez Juanatey JR, Gorenek B, Heyndrickx GR, Hoeft A, Huber K, Iung B, Kjeldsen KP, Longrois D, Luescher TF, Pierard L, Pocock S, Price S, Roffi M, Sirnes PA, Uva MS, Voudris V, Funck-Brentano C, Authors/Task Force Members. 2014 ESC/ESA guidelines on non-cardiac surgery: cardiovascular assessment and management: the joint task force on non-cardiac surgery: cardiovascular assessment and management of the European Society of Cardiology (ESC) and the European Society of Anaesthesiology (ESA). Eur J Anaesthesiol. 2014;31(10):517–73.PubMedGoogle Scholar
  113. 113.
    Şentürk M, Slinger P, Cohen E. Intraoperative mechanical ventilation strategies for one-lung ventilation. Best Pract Res Clin Anaesthesiol. 2015;29(3):357–69.PubMedGoogle Scholar

Copyright information

© Springer Nature Switzerland AG 2019

Authors and Affiliations

  • Fabrizio Monaco
    • 1
    Email author
  • Barucco Gaia
    • 1
  • Mattioli Cristina
    • 1
  • De Luca Monica
    • 1
  1. 1.Department of Cardiothoracic and Vascular Anesthesia and Intensive CareIRCCS San Raffaele Scientific InstituteMilanItaly

Personalised recommendations