From the Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota.
Accepted for publication April 10, 2013
Funding: Not funded.
The authors declare no conflicts of interest.
Address correspondence to Sher-Lu Pai, MD, Department of Anesthesiology, Mayo Clinic, 4500 San Pablo Rd, Jacksonville, FL 32224. Address e-mail to email@example.com.
Acute aortic occlusion (AAO) is an uncommon vascular emergency that can present with predominantly neurologic symptoms due to spinal cord ischemia. It frequently causes mortality unless urgent and appropriate diagnosis is followed immediately by proper management.1 We report a case demonstrating the difficulty of arriving at an early accurate diagnosis because of the numerous etiologies that may present with similar symptoms.
We did not intend to publish the outcome at the time we were providing treatment for the patient. The patient’s death was unexpected, so no consent was obtained when treatment was provided. The Mayo Clinic IRB stated that patient consent was not required to publish the case report because the information had been adequately deidentified in accordance with institutional policy and the Health Insurance Portability and Accountability Act.
A 72-year-old woman with a body mass index of 24.8 kg/m2 presented for elective laparoscopic cholecystectomy to treat symptomatic cholelithiasis. The patient’s medical history included osteopenia and hyperlipidemia, which were both well controlled with medications. No recurrence was found of her T2N1 breast cancer that was treated with partial mastectomy, chemotherapy, and radiation therapy 7 years previously. The patient had no history of vascular or neurologic disease, nor did she have any history of chronic hypertension or hypercoagulable conditions. Preoperative laboratory studies showed that all plasma electrolyte levels, complete blood cell count, creatinine and blood urea nitrogen levels, and urinalysis findings were within normal limits. Complete history taking and physical examination showed an older woman in fair health with an active lifestyle whose symptoms were limited to biliary colic caused by cholelithiasis.
After the preoperative work-up, a decision to operate was made. The patient was taken to the operating room with standard ASA monitors applied. After adequate oxygen administration, general anesthesia was induced with 60 mg lidocaine, 100 mcg fentanyl, 180 mg propofol, and 30 mg rocuronium, all administered IV. After tracheal intubation, anesthesia was maintained with sevoflurane. Her arterial blood pressure ranged from 80/61 mm Hg to 83/60 mm Hg, accompanied by decreased end-tidal CO2 for approximately 5 minutes at the time of insufflation for pneumoperitoneum. The hypotensive episode resolved immediately after discontinuing insufflation and IV administration of 15 mg ephedrine. The laparoscopic surgical procedure was then performed without any apparent decrease in blood pressure after a pneumoperitoneum was again achieved for an adequate surgical view. The procedure lasted 105 minutes from tracheal intubation to extubation.
Immediately after transfer to the recovery room, the patient complained of intense lower back pain, with numbness and severe weakness in both legs. Physical examination revealed a patient in moderate distress with severe paraplegia. However, she had no discrete dermatome level of sensory deficit and no point tenderness on the thoracic or lumbar spine. The lower extremities had intact dorsalis pedis pulses bilaterally and slightly diminished popliteal and posterior tibialis pulses. The patient also had no signs of upper extremity motor or sensory deficit. She was otherwise awake, alert, and oriented to person, place, time, and situation.
Magnetic resonance imaging without IV contrast enhancement of the thoracic and lumbar spine showed a widely patent spinal canal with no cord compression or intrinsic abnormality of the cauda equina. A computed tomographic arteriogram of the abdomen, pelvis, and lower extremities revealed generalized thrombus within the infrarenal aorta, with a segment of marked narrowing (Fig. 1). This thrombus formation extended to bilateral popliteal arterial occlusions without collateral flow or runoff to either foot. The arteriogram was performed approximately 2 hours after the end of the laparoscopic cholecystectomy. The thrombus occlusion must have been incomplete during the patient’s stay in the recovery room as the dorsalis pedis pulses did not disappear until she was reexamined after she returned from having the computed tomographic arteriogram. The image also showed near-occlusive thrombus in the right renal artery, with associated infarction of a large portion of the right kidney. Nonocclusive thrombi also existed within the left common iliac artery, right hypogastric artery, and proximal right common femoral artery and at the bifurcation of the right common femoral artery extending into the deep femoral artery.
An emergent interventional radiology procedure was initiated for catheter-directed alteplase infusion therapy to the thrombosed vessels. Twelve hours later, angiography still demonstrated both popliteal arteries with persistent thrombosis, and alteplase infusion was continued.
The patient’s serum creatinine increased from 0.9 to 2.9 mg/dL within 36 hours of the surgery. Severe lactic acidosis and respiratory failure necessitated tracheal intubation. She then received continuous renal replacement therapy to manage her hyperkalemia and severe myoglobinemia. The patient’s condition continued to deteriorate; she had 2 episodes of cardiac arrest secondary to uncontrolled hyperkalemia, metabolic acidosis, and hypotension and died 44 hours after surgery after the family changed the level of care to comfort only. A request for autopsy was refused by the family.
Paraplegia, discovered in the postanesthesia care unit, requires immediate investigation. The differential diagnosis is vast and includes both neurologic and vascular etiologies, such as an acute epidural hematoma, anterior spinal artery embolism, or direct cord compression from a herniated disk, that can be associated with considerable morbidity and mortality if they are not treated as soon as they are recognized. Among the possible causes, AAO is a rare but catastrophic occurrence, with high mortality even after revascularization.2,3 This syndrome can be mistaken for a neurologic complication.4 As with our patient, incomplete occlusion can leave the distal pulses intact, which further obscures the diagnosis.
Despite the different causes of the occlusion, AAO usually presents with acute onset of ischemia to the bilateral lower extremities. The classic presenting symptoms of ischemia are commonly referred to as the 5 Ps: pain, pulselessness, pallor, paresthesias, and paralysis. The symptoms of severe ischemia, including pallor and loss of distal pulses, can have a delayed onset of >6 hours.4 The subtle and delayed presentation of these classic symptoms of AAO may be mistaken initially for a neurologic or spinal pathology, thus delaying a correct diagnosis. Paraplegia is first caused by occlusion of the aorta above the level of the spinal radicular arterial supply, namely, the great radicular artery of Adamkiewicz, leading to serious cord ischemia and infarction. Then, ischemia of the peripheral nerves and musculature distal to the occlusion further worsens the paraplegia in the lower extremities.
AAO is such a rare entity that most of the available literature are case presentations of nonsurgical patients. AAO is primarily caused by either an in situ thrombosis of an atherosclerotic abdominal aorta or, less frequently, embolization from a cardiac source. Hypercoagulability, a low flow state, and endothelial damage such as ruptured atherosclerotic plaque or vessel trauma are the 3 broad categories of factors thought to contribute to thrombus formation. Most patients with AAO from thrombosis have a known history of aortoiliac occlusive disease with previous intervention or had an abdominal aortic aneurysm. As for embolic occlusion, the most commonly associated disease is atherosclerotic cardiac disease, followed by atrial fibrillation.5
Although the patient had no formal history for thrombophilia, she did have a history of breast cancer in the remote past that was treated with mastectomy and chemotherapy. Arterial thrombosis has long been recognized as a rare cause of morbidity in advanced-stage cancer.6 Precipitating mechanisms of thrombosis in cancer include increased levels of coagulation factors, such as cancer procoagulant and tissue factors. With possible concurrent diseases or surgery and the use of cytotoxic chemotherapy, the hypercoagulable state may be further worsened in cancer patients.7 Other possible sources of hypercoagulability include inherited hypercoagulable states such as mutations of genes encoding for factor V Leiden, prothrombin, protein C, and protein S. Autoimmune diseases like the phospholipid syndrome may also be a possible culprit as an acquired cause of a hypercoagulable state. These causes were not investigated in our patient but may have contributed to her complication.
Although unlikely, a low flow state induced by insufflation of the abdomen may predispose a patient to acute thrombus formation and may have been a potential source of our patient’s complication. With the introduction of a pneumoperitoneum, the cardiac index can be reduced by as much as 50% while the systemic vascular resistance may increase by 65%.8–10 Some studies have shown decreased cardiac output and decreased flow in the splanchnic and portal venous system with introduction of a pneumoperitoneum.11,12 Sternberg et al.13 described a patient who underwent a laparoscopic cholecystectomy in whom a mesenteric arterial thrombosis subsequently developed, resulting in a fatal outcome.
A disruption of an aortic atherosclerotic plaque is another possible explanation for the patient’s complication. The computed tomographic arteriogram did show the patient to have an atherosclerotic and ectatic infrarenal aorta. Beless et al.14 described a patient with an atherosclerotic plaque in whom an acute aortoiliac occlusion developed after a fall. Trauma to the aorta by surgical manipulation or a pneumoperitoneum may have contributed to plaque disruption and precipitated the occlusive thrombus formation. An autopsy may have provided more information about the actual cause of the patient’s AAO, but the request for autopsy was refused by the patient’s family.
The onset of paraplegia in the postanesthesia care unit requires immediate investigation. AAO is a vascular emergency with a high mortality rate, requiring rapid diagnosis and management. Its clinical presentation can be misinterpreted as a neurologic disorder. AAO should be considered a possible diagnosis in all postsurgical patients with acute paraplegia.
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