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Anesth Analg 2004;99:1032-1034
© 2004 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000131725.40714.9F


CARDIOVASCULAR ANESTHESIA

Fatal Acute Pulmonary Embolism in a Patient with Pelvic Lipomatosis After Surgery Performed After Transatlantic Airplane Travel

Ognjen Gajic, MD*, Juraj Sprung, MD PhD{dagger}, Brian A. Hall, MD{dagger}, and Deborah J. Lightner, MD{ddagger}

*Division of Pulmonary and Critical Care Medicine, {dagger}Department of Anesthesiology, and {ddagger}Department of Urology, Mayo Clinic College of Medicine, Mayo Clinic, Rochester, Minnesota

Address correspondence and reprint requests to Juraj Sprung, MD, PhD, Department of Anesthesiology, Mayo Clinic College of Medicine, 200 First St. S.W., Rochester, MN 55905. Address e-mail to Sprung.juraj{at}mayo.edu


    Abstract
 Top
 Abstract
 Introduction
 Case Report
 Discussion
 References
 
We describe a case of a 37-yr-old patient who traveled from Europe to the United States and succumbed to a massive pulmonary embolism 6 days after elective pelvic surgery despite routine postoperative thrombotic prophylaxis. In retrospect, he was likely to have developed a deep venous thrombosis during the transatlantic trip to our hospital. Anesthesiologists and other physicians involved in perioperative management need to be aware of the prevalence of venous thromboembolism in patients with a history of recent prolonged air travel. This is particularly true in tertiary referral centers, where patients with rare diseases may have a major surgical intervention within days of prolonged air travel.

IMPLICATIONS: Anesthesiologists and other perioperative physicians need to be aware of the prevalence of venous thromboembolism in patients with a history of recent long-haul air travel.


    Introduction
 Top
 Abstract
 Introduction
 Case Report
 Discussion
 References
 
Venous thromboembolism (VTE) associated with air travel is a recognized clinical entity (1–3). Most travelers who develop VTE have additional risk factors, such as advanced age, obesity, estrogen use, recent surgery, malignancy, or familial thrombophilic disorder (4). Pelvic lipomatosis is a rare disease that develops as a result of an excessive proliferation of benign fat tissue within the perivesical and perirectal spaces (5). In addition to urinary and intestinal symptoms, compression of pelvic vascular structures can lead to venous stasis, lower extremity swelling, and deep venous thrombosis (DVT) (6). We describe a case of a young patient with pelvic lipomatosis who developed leg swelling during his transatlantic trip and who succumbed to a massive pulmonary embolism 6 days after elective pelvic surgery, despite routine postoperative thrombotic prophylaxis.


    Case Report
 Top
 Abstract
 Introduction
 Case Report
 Discussion
 References
 
A 37-yr-old patient (188 cm; 114 kg; body mass index, 32 kg/m2) with pelvic lipomatosis and secondary bladder outlet obstruction with hydronephrosis traveled from Europe to the United States in economy class and was scheduled for an elective ileal conduit urinary diversion. In 1995 he had been diagnosed with pelvic lipomatosis on the basis of bilateral ureteral obstruction, azotemia, and symptomatic constipation. Sigmoidoscopy revealed a diminished intestinal lumen consistent with extrinsic compression, and he was treated with operative debulking of the benign fat and bilateral ureteral reimplantation. Despite improvement in his bowel symptoms, his urinary symptoms continued, and he was treated with bilateral percutaneous nephrostomies for worsening azotemia. He was offered elective ileal conduit urinary diversion. His predominant complaint after arrival from Europe (October 2003) was "cramping and swelling in his legs after disembarking from the plane." His preoperative physical examination was unremarkable except for the bilateral tibial edema. There was no evidence clinically or radiographically (computed tomography scan) for caval occlusive disease, and pedal edema was attributed to his renal disease. In addition, the patient stated that he occasionally had lower extremity swelling, especially after long hours of work in the standing position. The patient’s preoperative medications were amlodipine, calcitriol, and norfloxacin. The patient had smoked one pack of cigarettes per day for 15 yr.

The patient underwent a 3-day bowel preparation. During the bowel preparation, the patient felt well and had no new complaints relating to his lower extremity swelling, but he had symptoms of intermittent nausea and had a single episode, 2 days before the operation, described as a severe "anxiety attack" manifested by hyperpnea and shortness of breath associated with nausea that lasted approximately 30 min. The patient attributed his sudden nausea to the "hospital smell." At that time, he did not complain of chest pain, and auscultation of his lungs was normal. In addition to the patient’s described respiratory symptoms, the surgeon believed that his bowel preparation was incomplete, and the surgery was postponed for 48 h. During this time, the patient continued bowel preparation, and he was ordered not to take any solid foods. Two days later, he tolerated surgery well. A routine thrombotic prophylaxis with unfractionated heparin, 5000 U subcutaneously 3 times daily, was initiated after surgery and was continued until his discharge from the hospital.

After surgery, the patient experienced a low-grade fever and nausea, and needed supplemental oxygen to maintain his oxyhemoglobin saturation above 90%. He required repeated verbal stimulation to take a deep breath, which would promptly correct his oxyhemoglobin desaturation. The nausea and oxyhemoglobin desaturations were therefore attributed to morphine administered via patient-controlled analgesia. On postoperative Day 6, he was discharged from the hospital. Five hours after discharge, he reported acute shortness of breath after bending over to connect his urostomy tube, and he became visibly distressed, tachypneic, and pale (witnessed by J.S.; the patient was a guest in his home). Arterial blood pressure could not be measured, nor could the brachial pulse be palpated. Paramedics arrived 7 min later, during which time the dyspnea rapidly progressed, and the patient became unconscious. In the ambulance, his trachea was intubated, and advanced cardiac life support protocols were initiated. Cardiac rhythm on arrival to the emergency department, 27 min after paramedics arrived at the scene, was asystole. Resuscitation efforts were continued for 10 more minutes, but without a rhythm change from asystole, and the patient was pronounced dead. Autopsy confirmed acute massive pulmonary embolism with large thrombi lodged in the main pulmonary artery (Fig. 1), in the left and right pulmonary artery branches, in all lobar and segmental arteries, and in the right ventricle. Other significant findings were deep lower extremity venous thrombosis and advanced pelvic lipomatosis partially compressing pelvic structures. There was no evidence of caval venous thrombus or occlusion.


Figure 1
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Figure 1. Section through the pulmonary artery shows occlusion of the entire lumen of the vessel by the clot.

 

    Discussion
 Top
 Abstract
 Introduction
 Case Report
 Discussion
 References
 
In retrospect, our patient probably developed DVT during the transatlantic air travel and became symptomatic after surgery. The presence of symptoms (tachypnea and "anxiety attacks") and signs (pretibial edema, perioperative oxyhemoglobin desaturation, and low-grade fever) are strongly suggestive of the development of sentinel VTE before the terminal embolic event. In addition to possible venous compression caused by pelvic lipomatosis (6,7), several other VTE risk factors were present before operation: the patient was 1) overweight (8), 2) a heavy smoker (9,10), and 3) spent >10 hours in the airplane during the transatlantic flight (1,4). Dehydration secondary to bowel preparation could have been a contributing factor as well. Routine postoperative prophylaxis with subcutaneous unfractionated heparin, although usually effective in the prevention of postoperative VTE (11), was clearly insufficient in the setting of our patient’s multiple risk factors. In fact, our patient developed fatal pulmonary embolism eight hours after the last heparin dose and after increased mobility after discharge.

In retrospect, the lower extremity swelling in our patient, primarily attributed to the venous stasis during the prolonged flight and to the patient’s renal insufficiency, could have been a sign of DVT, possibly facilitated by vascular compression caused by pelvic lipomatosis. Similarly, the "anxiety attack" was likely to be the first symptom of a pulmonary embolic event. In a young patient without underlying malignancy, however, these warning signs escaped the attention of the caregivers, who were unaware of the antecedent air travel as a risk factor for thromboembolic complications.

Although transoceanic flights pose a risk of immobility, which may result in DVT (1,4,12–14), it is rarely an isolated risk factor. McQuillan et al. (4) found at least one additional clinical or laboratory risk factor to be present before travel in more than 80% of patients who developed clinically recognized VTE within 30 days of travel. The common patient-related risk factors are obesity, use of estrogen contraceptives, a previous VTE episode, heavy smoking, and familial thrombophilic disorder, including the presence of factor V Leiden deficiency (1,4). Cabin-related factors include immobility ("economy class syndrome" and excessive alcohol consumption-induced sleep), hemoconcentration secondary to mild dehydration, and hypoxia-induced hypercoagulability and venous stasis (2,15–17). Travelers who develop symptoms usually do so within the first 24 hours after takeoff (1). Although clinically recognized VTE in the setting of prolonged air travel appears to be rare (<5 per 1 million prolonged flights) (1,18), most VTE episodes associated with prolonged air travel are silent (3,19). Indeed, several recent studies have shown that asymptomatic DVT may be present in up to 10% of passengers during prolonged (>10 hours) air travel (3,19–22). Importantly, these randomized studies suggest that the risk of DVT can be greatly reduced by simple interventions, including elastic stockings in low- to medium-risk subjects and a single dose of subcutaneous low-molecular-weight heparin or a single dose of PinokinaseTM (Baywood International), an oral profibrinolytic drug, in high-risk subjects (3,19–22). Many of the unresolved aspects of VTE in the setting of air travel are expected to be answered by a comprehensive study launched by the World Health Organization in 2001, with expected completion by the year 2006 (23).

Because patients with clinically recognized VTE in the setting of prolonged air travel usually have additional risk factors (1,4), the cumulative effect of multiple risk factors may be the most important consideration (22). In addition to the usual surgical factors, during the perioperative period physicians need to consider multiple patient-related VTE risk factors, including length of air travel. Routine preoperative testing or more aggressive thromboprophylaxis in high-risk patients may be intuitive but still needs to be formally studied.

In conclusion, anesthesiologists and other physicians involved in perioperative management need to be aware of the prevalence of DVT and VTE in patients with a history of recent prolonged air travel. This is particularly true in tertiary referral centers, where patients with rare diseases have a major surgical intervention within days of prolonged air travel. Long-haul airplane passengers, especially those who, like our patient, have additional DVT/VTE risk factors, need to be informed about simple and effective measures for DVT/VTE prevention during prolonged air travel.


    References
 Top
 Abstract
 Introduction
 Case Report
 Discussion
 References
 

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Accepted for publication April 23, 2004.




This article has been cited by other articles:


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O. Gajic, D. O. Warner, P. A. Decker, R. Rana, D. L. Bourke, and J. Sprung
Long-Haul Air Travel Before Major Surgery: A Prescription for Thromboembolism?
Mayo Clin. Proc., June 1, 2005; 80(6): 728 - 731.
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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2004 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press