Noncardiogenic pulmonary edema after abdominal aortic aneurysm surgery

I. S. Paterson, J. M. Klausner, R. Pugath, P. Allen, J. A. Mannick, D. Shepro, H. B. Hechtman

Research output: Contribution to journalArticle

102 Citations (Scopus)

Abstract

Limb ischemia in experimental animals leads to white blood cell (WBC) and thromboxane (Tx)A2 dependent pulmonary dysfunction. This study examines the pulmonary sequelae of lower torso ischemia in 20 consecutive patients aged 63 ± 5 years (mean ± SEM) who underwent elective abdominal aortic aneurysm surgery. After 30 minutes of aortic cross-clamping, plasma TxB2 levels had risen from 77 ± 26 pg/ml to 359 ± 165 pg/ml (p < 0.01) and was temporally related to increases in mean pulmonary artery pressure (MPAP) from 18 ± 1 to 23 ± 3 mmHg (p < 0.01), as well as to increases in pulmonary vascular resistance (PVR) from 0.07 ± 0.02 to 0.12 ± 0.02 mmHg sec/ml (p < 0.01). Each time that the aortic clamp was repositioned and with final declamping, after 83 ± 10 minutes, there were further increases in MPAP to a peak of 32 ± 2 mmHg (p < 0.01) and in PVR to 0.26 ± 0.030 mmHg sec/ml (p < 0.01), corresponding to a plasma TxB2 level of 406 ± 177 pg/ml (p < 0.01). MPAP and PVR returned to baseline values within 30 minutes of declamping. Ten minutes after removal of the aortic clamp, platelet levels had fallen from 180 ± 41 to 97 ± 17 x 103/mm3 (p < 0.01) and WBC levels from 8900 ± 1100 to 4700 ± 400/mm3 (p < 0.01). Both platelets and WBC returned towards normal levels, but at 24 hours, while WBC was elevated at 13000 ± 900/mm3 (p < 0.01), platelets were 44% of baseline at 135 ± 14 x 103/mm3 (p < 0.01). Four to 8 hours after surgery, pulmonary dysfunction was manifest by increases in physiologic shunt from 9 ± 2% to 16 ± 2% (p < 0.01), and peak inspiratory pressure (PIP) from 23 ± 2 to 33 ± 2 cmH2O (p < 0.01). Chest radiography demonstrated interstitial pulmonary edema in all patients, whereas pulmonary artery wedge pressure was 12 ± 2 mmHg, excluding the possibility of left ventricular failure. After 24 hours, pulmonary edema had resolved, and the PIP and PaO2 had both returned to baseline. These data indicate that reperfusion of the ischemic lower torso leads to the synthesis of TxA2, an event temporally related to pulmonary hypertension and transient leukopenia with subsequent pulmonary microvascular injury manifest by interstitial edema.

Original languageEnglish (US)
Pages (from-to)231-236
Number of pages6
JournalAnnals of Surgery
Volume209
Issue number2
StatePublished - 1989
Externally publishedYes

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Abdominal Aortic Aneurysm
Pulmonary Edema
Pressure
Leukocytes
Vascular Resistance
Pulmonary Artery
Torso
Blood Platelets
Lung
Ischemia
Thromboxane A2
Pulmonary Wedge Pressure
Leukopenia
Lung Injury
Pulmonary Hypertension
Constriction
Radiography
Reperfusion
Edema
Thorax

ASJC Scopus subject areas

  • Surgery

Cite this

Paterson, I. S., Klausner, J. M., Pugath, R., Allen, P., Mannick, J. A., Shepro, D., & Hechtman, H. B. (1989). Noncardiogenic pulmonary edema after abdominal aortic aneurysm surgery. Annals of Surgery, 209(2), 231-236.

Noncardiogenic pulmonary edema after abdominal aortic aneurysm surgery. / Paterson, I. S.; Klausner, J. M.; Pugath, R.; Allen, P.; Mannick, J. A.; Shepro, D.; Hechtman, H. B.

In: Annals of Surgery, Vol. 209, No. 2, 1989, p. 231-236.

Research output: Contribution to journalArticle

Paterson, IS, Klausner, JM, Pugath, R, Allen, P, Mannick, JA, Shepro, D & Hechtman, HB 1989, 'Noncardiogenic pulmonary edema after abdominal aortic aneurysm surgery', Annals of Surgery, vol. 209, no. 2, pp. 231-236.
Paterson IS, Klausner JM, Pugath R, Allen P, Mannick JA, Shepro D et al. Noncardiogenic pulmonary edema after abdominal aortic aneurysm surgery. Annals of Surgery. 1989;209(2):231-236.
Paterson, I. S. ; Klausner, J. M. ; Pugath, R. ; Allen, P. ; Mannick, J. A. ; Shepro, D. ; Hechtman, H. B. / Noncardiogenic pulmonary edema after abdominal aortic aneurysm surgery. In: Annals of Surgery. 1989 ; Vol. 209, No. 2. pp. 231-236.
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abstract = "Limb ischemia in experimental animals leads to white blood cell (WBC) and thromboxane (Tx)A2 dependent pulmonary dysfunction. This study examines the pulmonary sequelae of lower torso ischemia in 20 consecutive patients aged 63 ± 5 years (mean ± SEM) who underwent elective abdominal aortic aneurysm surgery. After 30 minutes of aortic cross-clamping, plasma TxB2 levels had risen from 77 ± 26 pg/ml to 359 ± 165 pg/ml (p < 0.01) and was temporally related to increases in mean pulmonary artery pressure (MPAP) from 18 ± 1 to 23 ± 3 mmHg (p < 0.01), as well as to increases in pulmonary vascular resistance (PVR) from 0.07 ± 0.02 to 0.12 ± 0.02 mmHg sec/ml (p < 0.01). Each time that the aortic clamp was repositioned and with final declamping, after 83 ± 10 minutes, there were further increases in MPAP to a peak of 32 ± 2 mmHg (p < 0.01) and in PVR to 0.26 ± 0.030 mmHg sec/ml (p < 0.01), corresponding to a plasma TxB2 level of 406 ± 177 pg/ml (p < 0.01). MPAP and PVR returned to baseline values within 30 minutes of declamping. Ten minutes after removal of the aortic clamp, platelet levels had fallen from 180 ± 41 to 97 ± 17 x 103/mm3 (p < 0.01) and WBC levels from 8900 ± 1100 to 4700 ± 400/mm3 (p < 0.01). Both platelets and WBC returned towards normal levels, but at 24 hours, while WBC was elevated at 13000 ± 900/mm3 (p < 0.01), platelets were 44{\%} of baseline at 135 ± 14 x 103/mm3 (p < 0.01). Four to 8 hours after surgery, pulmonary dysfunction was manifest by increases in physiologic shunt from 9 ± 2{\%} to 16 ± 2{\%} (p < 0.01), and peak inspiratory pressure (PIP) from 23 ± 2 to 33 ± 2 cmH2O (p < 0.01). Chest radiography demonstrated interstitial pulmonary edema in all patients, whereas pulmonary artery wedge pressure was 12 ± 2 mmHg, excluding the possibility of left ventricular failure. After 24 hours, pulmonary edema had resolved, and the PIP and PaO2 had both returned to baseline. These data indicate that reperfusion of the ischemic lower torso leads to the synthesis of TxA2, an event temporally related to pulmonary hypertension and transient leukopenia with subsequent pulmonary microvascular injury manifest by interstitial edema.",
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T1 - Noncardiogenic pulmonary edema after abdominal aortic aneurysm surgery

AU - Paterson, I. S.

AU - Klausner, J. M.

AU - Pugath, R.

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AU - Shepro, D.

AU - Hechtman, H. B.

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N2 - Limb ischemia in experimental animals leads to white blood cell (WBC) and thromboxane (Tx)A2 dependent pulmonary dysfunction. This study examines the pulmonary sequelae of lower torso ischemia in 20 consecutive patients aged 63 ± 5 years (mean ± SEM) who underwent elective abdominal aortic aneurysm surgery. After 30 minutes of aortic cross-clamping, plasma TxB2 levels had risen from 77 ± 26 pg/ml to 359 ± 165 pg/ml (p < 0.01) and was temporally related to increases in mean pulmonary artery pressure (MPAP) from 18 ± 1 to 23 ± 3 mmHg (p < 0.01), as well as to increases in pulmonary vascular resistance (PVR) from 0.07 ± 0.02 to 0.12 ± 0.02 mmHg sec/ml (p < 0.01). Each time that the aortic clamp was repositioned and with final declamping, after 83 ± 10 minutes, there were further increases in MPAP to a peak of 32 ± 2 mmHg (p < 0.01) and in PVR to 0.26 ± 0.030 mmHg sec/ml (p < 0.01), corresponding to a plasma TxB2 level of 406 ± 177 pg/ml (p < 0.01). MPAP and PVR returned to baseline values within 30 minutes of declamping. Ten minutes after removal of the aortic clamp, platelet levels had fallen from 180 ± 41 to 97 ± 17 x 103/mm3 (p < 0.01) and WBC levels from 8900 ± 1100 to 4700 ± 400/mm3 (p < 0.01). Both platelets and WBC returned towards normal levels, but at 24 hours, while WBC was elevated at 13000 ± 900/mm3 (p < 0.01), platelets were 44% of baseline at 135 ± 14 x 103/mm3 (p < 0.01). Four to 8 hours after surgery, pulmonary dysfunction was manifest by increases in physiologic shunt from 9 ± 2% to 16 ± 2% (p < 0.01), and peak inspiratory pressure (PIP) from 23 ± 2 to 33 ± 2 cmH2O (p < 0.01). Chest radiography demonstrated interstitial pulmonary edema in all patients, whereas pulmonary artery wedge pressure was 12 ± 2 mmHg, excluding the possibility of left ventricular failure. After 24 hours, pulmonary edema had resolved, and the PIP and PaO2 had both returned to baseline. These data indicate that reperfusion of the ischemic lower torso leads to the synthesis of TxA2, an event temporally related to pulmonary hypertension and transient leukopenia with subsequent pulmonary microvascular injury manifest by interstitial edema.

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