A 70-year-old white male presents to the emergency department with sudden onset of severe back pain. The pain is described as severe and constant without alleviating or aggravating symptoms. He has never had pain like this before. He denies chest pain, shortness of breath, or loss of consciousness. He denies any history of an abdominal aortic aneurysm. His past medical history is significant for hypertension, and chronic obstructive pulmonary disease that requires home oxygen therapy. He had bilateral inguinal herniorrhaphy some years ago, but has never had a laparotomy.
His vital signs yielded a pulse at 90 bpm and a blood pressure of 110/60 mmHg. He is appropriately conversant and appears older than his stated age. He was without abdominal tenderness or masses and no bruits were heard; however, his belly was slightly obese and the examination was difficult. He has bilaterally palpable lower extremity pulses.
Abdominal/back pain, shortness of breath, and a pulsatile mass.
Abdominal/back pain, syncope, and a pulsatile mass.
Abdominal/back pain, nausea, and syncope.
Abdominal/back pain, chest pain, and hematochezia.
The patient remained stable while the emergency department staff obtained laboratory results and cross-matched blood, and performed an electrocardiogram (ECG).
Serum creatinine = 1.8 mg/dL
Age = 75 years
Preoperative blood pressure = 80 mmHg (systolic)
Patients with unknown AAA history and symptoms should undergo further diagnostic imaging if they are hemodynamically stable.
Symptomatic AAA should undergo emergency repair to prevent possible rupture.
Patients with an unknown AAA history must have diagnostic imaging confirmation of an AAA before proceeding to the operating theatre.
An ECG demonstrating ischemic changes in a patient with epigastric pain, hypotension and tachycardia is the sine qua non for a myocardial infarction and any operation should be postponed.
CT scans are reserved for elective evaluation of AAA and have no place in the work-up of a symptomatic AAA.
Ultrasound is more reliable than CT scan for the diagnosis of ruptured AAA.
The location of the rupture is typical for most ruptured AAAs.
Ultrasound can be performed quickly at the bedside.
Ultrasound can be used to provide endograft measurements.
Ultrasound is best used in unstable patients to confirm the presence of a known AAA.
After the confirmation of ruptured AAA by radiology, the patient is taken immediately to the operating room.
Surgical preparation and drape before induction.
Preoperative resuscitation to normal blood pressure.
Passive cooling of the patient.
Heparinization before cross-clamping.
Blood recuperation and autotransfusion devices.
The patient is prepared and draped, the anesthetic administered, and operation commenced. The medical student asks if this could be done via an endovascular approach.
Infrarenal neck diameter > 30 mm.
Infrarenal neck length < 10 mm.
Systolic blood pressure < 100 mmHg.
Endograft or “endograft team” not available.
Thrombus present at infrarenal neck.
The patient was determined to have too large a neck diameter for an endovascular stent, so you decide to proceed with an open repair. After induction, the patient’s blood pressure falls to a systolic of 60 mmHg. A supraceliac clamp is quickly placed and the aneurysm exposed. The rupture was contained to the retroperitoneum, but is rather large. The supraceliac clamp is moved to an infrarenal position after about 10 min. Anesthesia quickly catches up and his systolic blood pressure rises to 100 mmHg. The inferior mesenteric artery was not patent and the iliac arteries were without aneurysms, allowing a Dacron tube graft to be placed. The clamp is slowly removed and he remains hemodynamically stable. The bowel appears well perfused and distal pulses are palpable before closure. Postoperatively, the patient recovers in the surgical intensive care unit.
Acute renal failure.
He is noted to have a creatinine that rises to 4.7 mg/dL 2 days after operation and his urine output falls to less than 100 mL/day. He is eventually placed on intermittent hemodialysis because of volume overload. Over the next 2 weeks he is weaned off the ventilator, his urine output slowly increases, and his creatinine levels stabilizes at 2.0 mg/dL. He is discharged to a convalescence facility 19 days after operation.
The optimal treatment of rAAA is prevention; unfortunately close to 70% of presenting patients have no prior diagnosis . The overall mortality rates for rAAA are 80–90% with operative mortality around 50% [2, 3, 4]. Although more than three-quarters of patients with an rAAA report either abdominal or back pain, they can present with a myriad of symptoms and signs that are both broad and inconsistently present . The triad of hypotension, abdominal pain, and a pulsatile mass [Q1: B] are found together in only half of cases . A great deal of effort has been applied to identifying perioperative risk factors for patients who have a decreased survival advantage. Preoperative risk factors include: age < 75–76 years, hypotension = 80–95 mmHg, creatinine = 1.8–1.9 mg/dL, loss of consciousness, ECG ischemia or dysrhythmia, CHF congestive heart failure, hemoglobin <9 g/dL, base deficit >8, and free rupture [7, 8, 9, 10]. [Q2: A] Intraoperative risk factors include: blood loss >2–3.5 L, duration of surgery >200 min, aortic cross-clamp time > 47 min, lack of autotransfusion devices, bifurcated grafts, and technical complications (i.e., left renal vein injury) [11, 12, 13]. Postoperative risk factors include renal failure, coagulopathy, and cardiac complications. Hardman et al.  found that possession of three or more preoperative risk factors correlated with 100% mortality. Currently, no recommendation exists to withhold surgery for patients with any or all of these risk factors; this decision is made on a case-by-case basis, making risk factor analysis useful mostly from the standpoint of guiding patient decisions on surgery and family discussions on prognosis.
Once the decision to operate has been made, several preoperative measures should be undertaken. A natural instinct is to bolus intravenous (IV) fluid in an attempt to normalize the blood pressure; this should be avoided. Instead, adopting a permissive hypotensive strategy will allow the patient’s own physiologic response to minimize blood loss . Although there are times when fluids are necessary, this strategy can be effective in preventing accelerated blood loss until the aorta is clamped or occluded. Every effort should be made to keep the patient warm with blankets, raising the operating room temperature, and utilizing warmed IV fluids and blood products . The patient should be prepared and draped before induction as the loss of sympathetic tone with anesthesia may cause a marginally compensated patient to collapse.
A midline laparotomy provides the quickest route of entry and best exposure in most cases. A low threshold to obtain supraceliac control will prevent inadvertent venous injury, especially in cases with large retroperitoneal hematomas. This control is obtained by incising the gastrohepatic ligament and diaphragmatic crura, and then bluntly dissecting the periaortic tissue; a preoperative nasogastric tube can aid in identification of the laterally positioned esophagus. A clamp or manual pressure is applied to the supraceliac aorta. The transverse colon is reflected cephalad and the small bowel eviscerated. The supraceliac control can then be moved to the infrarenal neck after it is carefully dissected out. Systemic heparinization is avoided and heparinized saline (10 units/mL) is used locally down both iliacs before balloon occlusion. The use of intraoperative blood recuperation and autotransfusion devices is crucial in minimizing postoperative mortality by limiting homologous blood transfusions . The use of a tube graft, typically knitted Dacron or PTFE polytetrafluoroethylene, will shorten operative times and restore flow sooner than a bifurcated graft; this may necessitate leaving aneurysmal iliac arteries alone . [Q5: B, C, D] After completion of grafting, bowel and lower extremity perfusion are assessed, usually by inspection and Doppler probe. The aneurysm sac is closed around the graft in an attempt to prevent later aortoenteric fistulas. Depending on the size of retroperitoneal hematoma and degree of resuscitation, the abdomen may not close easily. In these cases, it is best to perform a temporary closure with plans to return to the operating room for washout and definitive closure at a later, more stable time.
The dismal mortality following open repair of rAAA and the expansion of endovascular techniques has prompted recent exploration into application of stent grafts for primary therapy. Patient candidacy for an endovascular repair of AAA (EVAR) is the first hurdle when considering this approach. Measurements to determine this are typically done by CT angiography, although the Montefiore group have been successful utilizing digital subtraction angiography in two views . The concern of sending a potentially unstable patient with known or suspected ruptured AAA to the CT scanner was recently addressed by Lloyd et al.  from Leicester; they found that 87.5% of patients survived longer than 2 h after admission, with 92% of these patients having systolic blood pressures greater than 80 mmHg. Ruptured or symptomatic AAAs are found to have larger infrarenal neck diameters and smaller neck lengths . Despite these morphological differences, several reports have found amazingly high feasibility rates for EVAR, ranging from 46% to 80% [22, 23]. Dimensional requirements for endografts are constantly shifting as new devices improve the field, but currently an infrarenal neck = 10 mm and a diameter = 30 mm are needed . [Q6: A, B, D] The next hurdle is availability of an endograft team and the graft itself. The importance of a knowledgeable and experienced team cannot be overstated as any program without this is destined for failure. A variety of grafts are being utilized, with favor towards a modular aorto-uniiliac device; this set-up decreases the need for large inventories [23, 24]. The Montefiore group have developed an aorto-unifemoral graft which they use in conjunction with a crossover femoral-femoral graft . Surprisingly few patients are rejected for EVAR secondary to unfavorable hemodynamics. Supraceliac balloon occlusion via a brachial or femoral route under fluoroscopic guidance can allow proximal aortic control under local anesthesia; a technique being utilized by some for control prior to laparotomy in open cases . The prospective randomized IMPROVE trial demonstrate a true survival benefit and a better quality of life in patients with ruptured AAA treated by EVAR compared to the open approach .
The most common complication of rAAA repair is renal failure, followed by ileus, sepsis, myocardial infarction, respiratory failure, bleeding, and bowel ischemia [1, 11]. [Q7: E] Postoperative renal failure has been found by several authors to correlate with mortality [1, 11]. Minimizing suprarenal clamp time and use of mannitol before cross-clamping the aorta to initiate brisk diuresis may limit renal damage. The inflammatory mediators and cytokines released from the shock state, visceral hypoperfusion, and massive transfusions associated with open repair can lead to multi-organ system failure; the avoidance of supraceliac clamping and lower blood loss are some of the potential advantages of the EVAR approach. But EVAR has its own unique complications which include endoleaks, graft malfunction, and groin wound issues.
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