Since this type of surgery often has extensive blood loss, transfusion and related risks must be discussed. Also, informed consent should also be obtained for the urinary catheter.

Mr. Berg is scheduled to be transferred to the ICU after surgery, possibly intubated and ventilated. Furthermore, perioperative cerebral dysfunction could develop (see Sect. 18.​1.​2) causing him to accidentally remove various catheters or drains. Restraining devices might be needed on the ICU in order to prevent self-harm. Restraints used in acute medical care need to be ordered by a physician or another licensed health-care provider (e.g., a physician’s assistant or a nurse practitioner, depending upon state law) and should be for the shortest time frame necessary. As part of informed consent, it is always best to forewarn the patient and family of this possibility.

>> Mr. Berg shook his head in agreement, had no further questions, and signed the informed consent form. “We’ll see each other tomorrow morning!” said Dr. Elen and then added as she departed, “Everything will go well; I’m sure of it!” Mr. Berg watched as she left; for the rest of the day, he watched TV without much interest.

Dr. Elen prepared the anesthesia preoperative evaluation and orders. She ordered 4 units of packed red blood cells to be held on standby in the blood bank. For the morning of the surgery, she ordered Mr. Berg’s standard medications, intentionally omitting the glimepiride. She ordered a glucose check in the morning and 1 mg of lorazepam 1 h before the scheduled surgery. After one last check, Dr. Elen was satisfied. She went to see two other patients before reporting back to her attending anesthesiologist Dr. Eldridge.

On the morning of surgery, Mr. Berg woke up at about 4 a.m. He became quite annoying to the floor nurses. Every half hour he rang the nurses to ask if he could finally receive his sedative and to ask how much longer he would have to wait to be taken to the OR. Shortly after 6:30 a.m., he was finally in the preoperative area. Dr. Elen greeted him with a warm “Good morning!” to which he replied without much enthusiasm. She checked the patient and the OR to make sure everything was prepared to her satisfaction. Finally she nodded and said “All right then, let’s get started.” She took him back to the OR. The monitor showed that Mr. Berg was a little nervous, despite his lorazepam: blood pressure 185/65 mmHg and heart rate 85 beats/min. “Have you already decided on a nice dream, Mr. Berg?”

The induction was performed with propofol, fentanyl, and atracurium. After placement of the central line, the arterial line, a nasogastric tube, and lastly a urine catheter, Mr. Berg was ready for prepping 25 min later. At the first skin incision, his blood pressure was about 120/50 mmHg and heart rate 55 beats/min. Anesthesia depth was maintained with a mixture of desflurane, oxygen, and air, as well as fentanyl and atracurium. Dr. Elen checked everything again. The warming mats were hooked up, a temperature probe had been placed, and the urine collection bag was within view. She was satisfied. Anesthesia tech Heather brought an arterial blood gas (ABG) before saying that she was going to take a breakfast break. The ABG showed:

There was no reason to be worried. The arterial oxygen partial pressure was probably still elevated from the anesthesia induction and would normalize soon. Dr. Elen glanced with interest at the surgical area, in between filling out the anesthetic record. The surgeons had quickly opened the abdomen and were exploring the cavity when the blood pressure suddenly dropped to 60/35 mmHg and heart rate 130 beats/min. Dr. Elen got nervous and thought, “I hope the aneurysm didn’t just burst!”

Dr. Elen’s fears are not totally unjustified (see Sect. 26.1.1). Especially with an undiagnosed perforated aortic aneurysm, reduction of intra-abdominal pressure, via muscle relaxants or laparotomy, can increase the chance of rupture. In this case, there is another more likely diagnosis: mesenteric traction syndrome. During the surgical exploration of the abdomen, mesenteric traction syndrome often appears. The cause is histamine release from the mesenteric cast cells and prostacyclin (PGI₂) release [2].

The symptoms are:

Untreated, the hypotension persists for about 30 min, gradually improving; only few patients show a pronounced, prolonged hemodynamic impairment [14]. Prophylactic administration of prostaglandin synthesis inhibitors like ibuprofen, indomethacin, or diclofenac can attenuate the response. One study showed that the preoperative administration of H₁ and H₂ blockers cannot prevent the occurrence of flush but helps to maintain a stable blood pressure with reduced reliance on vasoconstrictor therapy [2]. A study comparing both therapies has not yet been carried out.

Routine prophylaxis with prostaglandin inhibitors does not seem justified since mesenteric traction syndrome does not occur in every intra-abdominal procedure and occurs in very different intensities. When the syndrome becomes evident intraoperatively, treatment with vasopressors and IV fluids to replace the relative volume deficiency should be started. If the symptoms persist, administration of prostaglandin synthesis inhibitors may be considered. But one needs to consider that administration of ibuprofen or indomethacin for this purpose is off-label use.

>> Dr. Elen noticed that Mr. Berg’s head had become bright red and then promptly returned to normal. She had seen enough mesenteric traction syndromes already. She gave Mr. Berg 1,000 ml of a crystalloid infusion and started an infusion of phenylephrine. After 10 min, the vital signs were back to normal.

Shortly before 9.00 AM, at the request of the surgeon, Dr. Tristan, she administered 4,000 U heparin IV. Two minutes later he announced that he was going to cross–clamp the aorta. She checked the blood pressure and noted 280 ml of urine on the anesthesia record. As the aorta was clamped, the blood pressure increased to 160/90 mmHg and heart rate was 50 beats/min. Dr. Elen gave 200 μg fentanyl IV, which unfortunately had no effect. The surgeon scolded, “Hey, anesthesia! It’s bleeding all over the place in here. I can’t see a thing – much less sew it shut! What are you doing over there? What’s the systolic?” In a state of panic, Dr. Elen didn’t know what she should do next. The suction container was practically overflowing with blood, and the surgeon cursed under his breath. Attending anesthesiologist Dr. Eldridge was busy in another room, anesthesia tech Heather was still away eating her breakfast, and Dr. Elen had no one in the OR to help her.

An important phase in aortic surgery is the clamping of the aorta. The closure of the aorta terminates the blood flow distal to the occlusion and increases the arterial blood pressure proximally. The resulting increase of systemic resistance leads to an increase in afterload of the left ventricle. This is usually well tolerated by a healthy heart. In the presence of heart failure, the increase in afterload can lead to a decrease in stroke volume, with a consecutive decrease in cardiac output. The increased afterload increases the wall pressure and the left ventricular load and can lead to left-sided heart failure. In addition, the myocardial oxygen requirement increases due to the increased wall stress. There is danger of myocardial ischemia and arrhythmias.

The extent of the hemodynamic changes depends on the site of cross-clamping, the left ventricular contractility, and the myocardial perfusion. In patients with a healthy heart, the left ventricular filling pressure after infrarenal clamping is usually unchanged or only slightly reduced. If insufficient coronary perfusion is present, signs of acute left heart failure may occur. With suprarenal aortic clamping, the symptoms occur much more often. The cause is the interruption of renal perfusion, which accounts for about 25 % of the cardiac output. A greater increase in left ventricular end-systolic and end-diastolic volume occurs, together with a reduced ejection fraction. Patients with severe aortoiliac occlusive disease have a less pronounced hemodynamic reaction.

In order to prevent or reduce the symptoms of aortic clamping, preventative measures must be taken. These measures include increasing the depth of anesthesia before the clamping (e.g., by increasing the volatile anesthetic) and administration of vasodilators. A suitable vasodilator is short-acting nitroglycerin given as an infusion (Case 3, Sects. 3.​1.​5 and 3.​1.​6). Other options include clevidipine, rapidly acting, short-duration calcium channel blockers [1], or, for more severe uncontrolled hypertension, sodium nitroprusside. Clevidipine is more effective than nitroglycerin in lowering blood pressure [1]. The administration should be done in advance of the clamping, to avoid blood pressure peaks. Many authors recommend nitroglycerin immediately before clamping to ease placement of the clamp on the relaxed vessel, therefore reducing slips [16]. At the very least, nitroglycerin is the first choice to reduce the afterload if signs of increased left ventricular load or myocardial ischemia appear.