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Chest Imaging and Pathology for Clinicians |

A Rare Cause of Postoperative HypotensionPostoperative Hypotension FREE TO VIEW

Pedro D. Salinas, MD; Laura N. Toth, MD; Harold L. Manning, MD, FCCP
Author and Funding Information

From the Departments of Medicine (Drs Salinas and Manning) and Pathology (Dr Toth), Dartmouth-Hitchcock, Lebanon, NH.

CORRESPONDENCE TO: Pedro D. Salinas, MD, Critical Care Medicine, Dartmouth-Hitchcock, One Medical Center Dr, Lebanon, NH 03756; e-mail: Pedro.D.Salinas@hitchcock.org


Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2015;147(5):e175-e180. doi:10.1378/chest.14-2245
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A 62-year-old woman presented with a 3-month history of abdominal distension and decreased exercise tolerance. A chest radiograph showed a probable left pleural effusion (Fig 1). A CT scan of the abdomen revealed a solid ovarian mass with omental caking and a large volume of ascites; there was also confirmation of a left pleural effusion. Three days before surgery a CT pulmonary angiogram (CTPA) showed no evidence of pulmonary thromboembolism (PTE). The patient had some improvement in her symptoms after paracentesis and thoracentesis with drainage of 2,000 mL and 250 mL of fluid, respectively. She underwent total abdominal hysterectomy, bilateral oophorectomy, and partial sigmoid resection with an estimated blood loss of 850 mL. During the operation, she received 5 L of crystalloid and required phenylephrine at 40 to 80 μg/min to maintain a mean arterial pressure > 65 mm Hg. She was extubated after surgery, but immediately after extubation, she became markedly hypotensive and hypoxemic with a BP of 50/20 mm Hg and an oxygen saturation of 70%. An ECG showed T-wave inversions from V1 to V5 and an S1Q3T3 pattern (Fig 2). A bedside echocardiogram showed an enlarged right ventricle (RV), septal dyskinesia, and obliteration of the left ventricle, all consistent with systolic and diastolic RV overload (Fig 3).

Figures in this Article

A massive pulmonary thromboembolism (PTE) was suspected, and a pulmonary angiogram was performed, which demonstrated no intravascular filling defects (Fig 4). The pulmonary artery pressure was significantly increased at 60/34 mm Hg.

Figure Jump LinkFigure 1 –  A posteroanterior chest radiograph shows a probable left pleural effusion.Grahic Jump Location

Figure Jump LinkFigure 2 –  ECG showing T-wave inversions from V1 to V5 and an S1Q3T3 pattern, consistent with right ventricular “strain.”Grahic Jump Location

Figure Jump LinkFigure 3 –  Echocardiographic image from the parasternal short-axis view showing an enlarged, “D-shaped” right ventricle (arrows) consistent with right ventricular overload.Grahic Jump Location

Figure Jump LinkFigure 4 –  Anteroposterior view from the pulmonary arteriogram showing no evidence of intravascular filling defects.Grahic Jump Location

The patient remained hypotensive despite treatment with norepinephrine, vasopressin, and epinephrine. Inhaled epoprostenol was added as a pulmonary vasodilator. On an Fio2 of 0.3 and positive end-expiratory pressure of 5 cm H2O, her oxygen saturation was 98%. Despite all medical efforts, she remained in shock with severe lactic acidosis and a central venous saturation of only 37%. A repeat echocardiogram (Fig 5) revealed a massively dilated right ventricle (RV) with a totally obliterated left ventricular cavity. After discussion with the patient’s family, the patient was placed on comfort measures only, and she died a short while later. Her death occurred 15 h after the completion of her surgery.

Figure Jump LinkFigure 5 –  A still echocardiographic image from the parasternal long-axis view. The left ventricular cavity is totally obliterated (arrow), with endocardial walls “kissing.”Grahic Jump Location

At autopsy, the RV was enlarged, but there was no evidence of right ventricular hypertrophy. The lung sections revealed fibrin microthrombi in > 50% of the vessels. Figure 6 shows tumor emboli with some of the vessels showing fibrin deposits. Immunohistochemistry was positive for vascular endothelial growth factor (VEGF) (Fig 7).

Figure Jump LinkFigure 6 –  Photomicrograph of lung sections. A, C, Tumor thromboemboli immunohistochemically express CKAE1/3 (black arrows). The adjacent type 2 pneumocytes were also CKAE1/3 positive (yellow arrow). B, D, H&E stain showing tumor emboli (arrows) and fibrin thromboemboli (stars). CKAE1/3 = cytokeratin AE1/3; H&E = hematoxylin and eosin.Grahic Jump Location

Figure Jump LinkFigure 7 –  Photomicrographs of lung sections. A, B, Tumor thromboemboli immunohistochemically express VEGF (black arrows). VEGF = vascular endothelial growth factor.Grahic Jump Location
What is the diagnosis?
Diagnosis: Pulmonary tumor thrombotic microangiopathy
Clinical Discussion

In the perioperative setting, hypotension is commonly associated with hypovolemia secondary to hemorrhage, anesthesia-induced vasodilation, or myocardial ischemia.1 Bedside echocardiography is often used to diagnose and manage shock.2 The etiologies of RV failure may be pathophysiologically conceptualized as either decreased or increased preload, increased afterload, or decreased contractility.3 The lack of ST changes on left-sided and right-sided ECG (not shown) and modest troponin elevation (troponin T, 0.08 ng/mL) were evidence against RV infarction, and the elevated pulmonary artery, right ventricular, and right atrial pressures were all consistent with increased RV afterload. The underfilled left ventricle excluded this as the cause of the elevated right-sided pressures (Fig 5).

Current management of RV failure centers on quickly defining the etiology and implementing specific treatment, such as pharmacologic or mechanical thrombolysis, when possible. Other important steps include limiting IV fluid administration if severe RV dilatation is present and correction of hypotension to maintain adequate coronary artery perfusion pressure.3 When vasopressors are required, norepinephrine and vasopressin are recommended as first-line and second-line agents, respectively.4 A short-acting pulmonary vasodilator, such as nitric oxide or inhaled epoprostenol, is also recommended, and inodilators, such as milrinone or dobutamine, can be used, if tolerated. When the resources are available, consideration may also be given to circulatory support devices, such as venoarterial extracorporeal membrane oxygenation.3-5

Radiologic Discussion

Basic echocardiographic assessment generally includes evaluation of left and right ventricular size and function, assessment for the presence or absence of pericardial effusion or gross valvular insufficiency, and measurement of inferior vena cava diameter and associated respirophasic changes.2 Our case highlights the importance of the bedside echocardiogram in quickly establishing right ventricular failure as the cause of shock.

Even though a basic echocardiographic examination was sufficient to establish the diagnosis of acute RV failure in this patient, advanced echocardiographic measurements provide additional data that may sometimes help to establish a specific diagnosis and determine the primary pathophysiologic process.6,7 For example, evidence of RV systolic dysfunction in the absence of an elevated pulmonary artery pressure will exclude elevated afterload as the etiology of RV failure.6 Advanced measurements for the intensivist include semiquantitative measurements of right ventricular size (right ventricular end-diastolic area to left ventricular end-diastolic area ratio), right ventricular systolic function by tricuspid annular plane systolic excursion, stroke volume at the right ventricular outflow tract or main pulmonary artery, M-mode interrogation of septal kinetics, and evidence of left ventricular underfilling by pulse-wave Doppler interrogation of the mitral valve inflow.6,7

Despite the reported high specificity of echocardiography in diagnosing PTE, our case illustrates that other rare causes of RV failure can mimic the echocardiographic findings of PTE.8 CT pulmonary angiogram (CTPA) has emerged as the gold standard for diagnosing PTE,9 but this patient was hemodynamically unstable with a significantly increased risk for bleeding complications with systemic administration of thrombolytics. Therefore, a conventional pulmonary angiogram was chosen as a diagnostic and potential therapeutic modality (ie, catheter-directed pharmacologic or mechanical thrombolysis). In some cases of tumor emboli or pulmonary tumor thrombotic microangiopathy (PTTM), a CTPA can reveal “dilated and beaded” peripheral pulmonary vessels,10 but those findings were not present in this patient. 18F-Fluorodeoxyglucose PET/CT scanning can help distinguish PTE from pulmonary tumor embolism or pulmonary artery sarcoma, but its role in patients with acute right ventricular failure who have a negative CTPA or pulmonary angiogram remains to be determined.11,12

Pathologic Discussion

The autopsy confirmed the findings of the previous debulking surgery, with residual metastatic high-grade serous carcinoma of the ovary involving the left dome of the diaphragm, the mesenteric and serosal surfaces of the large bowel, the pericardial fat, and the serosal surface of bladder. Microscopic examination revealed numerous fibrin and tumor thromboemboli in vessels throughout the lungs. The vessels showed evidence of prior chronic, organizing thromboemboli in the form of luminal recanalization but luminal-occlusive fibrocellular intimal proliferation was not identified. The atypical thromboemboli cells, intermingled with fibrin, were positive for pan-cytokeratin marker Cytokeratin AE1/3 (CKAE1/3), but negative for the ovarian marker Paired box gene 8 (PAX-8). PAX-8—a crucial transcription factor for organogenesis of the thyroid gland, kidney, and Müllerian system, and a regulator of the Wilms’ tumor suppressor gene (WT1)—is a useful marker for the differential diagnosis of ovarian and breast carcinomas, particularly nonmucinous ovarian carcinomas.13 Interestingly, the metastatic ovarian carcinoma diagnosed in the premortem pleural fluid was weakly immunoreactive for PAX-8 (Fig 8).

Figure Jump LinkFigure 8 –  A-D, Photomicrographs of pleural fluid cytology. A, H&E stain shows clusters of malignant cells (black arrow), consistent with an ovarian primary. B, C, D, The tumor cells show negative immunohistochemical expression for CK20, TTF-1, and PR, but positive immunohistochemical expression of CK7 and PAX-8. Photomicrographs of lung sections. E, Tumor thromboemboli in the lung are negative for PAX-8. CK = cytokeratin; PAX-8 = paired box gene 8; PR = progesterone receptor; TTF = thyroid transcription factor. See Figure 6 legend for expansion of other abbreviation.Grahic Jump Location

Tumor emboli and PTTM are overlapping clinical entities and can only be differentiated by histology and immunohistochemistry. The pathophysiology has not been completely elucidated, but in simple tumor emboli, the tumor emboli occlude small vessels, whereas in PTTM, the tumor cells embolize and cause only partial occlusion of small vessels, which in turn leads to activation of the coagulation cascade and deposition of fibrin thrombi in the vessel. Another feature of PTTM is intimal proliferation. The presence of VEGF and tissue factor (TF) is the main distinguishing feature between the two entities.14-16 In this case, the tumor cells in the tumor thromboemboli did show positive immunoreactivity for VEGF (Fig 7). Endothelial cells were also VEGF positive but were CKAE1/3 negative. The fibrocellular and fibromuscular intimal proliferation changes with associated luminal occlusion were not seen in our case. Given the rarity of the documented cases of PTTM, it may be that these vascular morphologic changes are not always consistently present and that the prevalence, clinical significance, and pathologic features of PTTM have yet to be fully clarified.

PTTM is most commonly associated with gastric adenocarcinoma, and regardless of the site of the primary tumor, > 90% are histologically adenocarcinomas.14-17 The largest series of 30 PTTM cases confirmed with VEGF and TF is shown in Table 1, which was derived from 2,215 consecutive autopsies performed over a 25-year period.17 In contrast to PTTM, tumor emboli are most commonly associated with cancer of the breast, stomach, lung, and liver.10 It is possible that some cases classified as tumor emboli were, in fact, PTTM, as intimal proliferation was described in many cases, and no VEGF and TF stains were reported.10 There are case reports in the literature of PTTM associated with ovarian cancer, one of which had a fulminant postoperative course similar to that occurring in this patient.14,18 In the majority of patients, PTTM remains a postmortem diagnosis. Very few antemortem reports exist in the literature; two patients are described who had subacute presentations.19,20 Case series indicate that the interval between onset of dyspnea and death ranges from 3 to 74 days, with a median of 9½ days.17

Table Graphic Jump Location
TABLE 1 ]  PTTM in 30 Patients

PTTM = pulmonary tumor thrombotic microangiopathy.

This patient had a particularly fulminant postoperative course with death ensuing 15 h after arrival to the ICU despite rapid identification of acute RV failure by bedside echocardiogram. Medical therapy with recommended vasopressors and pulmonary vasodilators was administered to improve RV contractility and decrease RV afterload. Salvage mechanical support with venoarterial extracorporeal membrane oxygenation was unavailable.

Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Other contributions: We thank Wendy Wells, MD, Department of Pathology at Dartmouth-Hitchcock, for assisting with the pathology discussion. CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met.

Singh A, Antognini JF. Perioperative hypotension and myocardial ischemia: diagnostic and therapeutic approaches. Ann Card Anaesth. 2011;14(2):127-132. [CrossRef] [PubMed]
 
Oren-Grinberg A, Talmor D, Brown SM. Focused critical care echocardiography. Crit Care Med. 2013;41(11):2618-2626. [CrossRef] [PubMed]
 
King C, May CW, Williams J, Shlobin OA. Management of right heart failure in the critically ill. Crit Care Clin. 2014;30(3):475-498. [CrossRef] [PubMed]
 
Price LC, Wort SJ, Finney SJ, Marino PS, Brett SJ. Pulmonary vascular and right ventricular dysfunction in adult critical care: current and emerging options for management: a systematic literature review. Crit Care. 2010;14(5):R169. [CrossRef] [PubMed]
 
Ventetuolo CE, Klinger JR. Management of acute right ventricular failure in the intensive care unit. Ann Am Thorac Soc. 2014;11(5):811-822. [CrossRef] [PubMed]
 
Kaplan A, Mayo PH. Echocardiographic diagnosis and monitoring of right ventricular function.. In:Levitov A, Mayo P, Slonim A., eds. Critical Care Ultrasonography.2 ed. New York, NY: McGraw-Hill Education; 2014.
 
Narasimhan M, Koenig SJ, Mayo PH. Advanced echocardiography for the critical care physician: part 2. Chest. 2014;145(1):135-142. [CrossRef] [PubMed]
 
De Gennaro L, Giannoccaro V, Lopriore V, et al. New onset right ventricular enlargement in recent dyspnea: Is echocardiography enough for a diagnosis of pulmonary thrombo-embolism? Heart Lung. 2014;43(4):328-330. [CrossRef] [PubMed]
 
Mayo J, Thakur Y. Acute pulmonary embolism: from morphology to function. Semin Respir Crit Care Med. 2014;35(1):41-49. [CrossRef] [PubMed]
 
Roberts KE, Hamele-Bena D, Saqi A, Stein CA, Cole RP. Pulmonary tumor embolism: a review of the literature. Am J Med. 2003;115(3):228-232. [CrossRef] [PubMed]
 
Lee EJ, Moon SH, Choi JY, et al. Usefulness of fluorodeoxyglucose positron emission tomography in malignancy of pulmonary artery mimicking pulmonary embolism. ANZ J Surg. 2013;83(5):342-347. [CrossRef] [PubMed]
 
Shin S, Pak K, Kim SJ, Kim H, Kim SJ. Pulmonary tumor embolism derived from stomach cancer observation with serial 18F-FDG PET/CT. Clin Nucl Med. 2015;40(3):270-272. [CrossRef] [PubMed]
 
Ordóñez NG. Value of PAX 8 immunostaining in tumor diagnosis: a review and update. Adv Anat Pathol. 2012;19(3):140-151. [CrossRef] [PubMed]
 
Chinen K, Fujino T, Horita A, Sakamoto A, Fujioka Y. Pulmonary tumor thrombotic microangiopathy caused by an ovarian cancer expressing tissue factor and vascular endothelial growth factor. Pathol Res Pract. 2009;205(1):63-68. [CrossRef] [PubMed]
 
Chinen K, Tokuda Y, Fujiwara M, Fujioka Y. Pulmonary tumor thrombotic microangiopathy in patients with gastric carcinoma: an analysis of 6 autopsy cases and review of the literature. Pathol Res Pract. 2010;206(10):682-689. [CrossRef] [PubMed]
 
Pinckard JK, Wick MR. Tumor-related thrombotic pulmonary microangiopathy: review of pathologic findings and pathophysiologic mechanisms. Ann Diagn Pathol. 2000;4(3):154-157. [CrossRef] [PubMed]
 
Uruga H, Fujii T, Kurosaki A, et al. Pulmonary tumor thrombotic microangiopathy: a clinical analysis of 30 autopsy cases. Intern Med. 2013;52(12):1317-1323. [CrossRef] [PubMed]
 
Gru AA, Pai RK, Roma AA. Pulmonary tumor thrombotic microangiopathy in patients with low-grade ovarian serous neoplasm: a clinicopathologic review of 2 cases of a previously unknown association. Int J Gynecol Pathol. 2012;31(5):438-442. [CrossRef] [PubMed]
 
Kayatani H, Matsuo K, Ueda Y, et al. Pulmonary tumor thrombotic microangiopathy diagnosed antemortem and treated with combination chemotherapy. Intern Med. 2012;51(19):2767-2770. [CrossRef] [PubMed]
 
Miyano S, Izumi S, Takeda Y, et al. Pulmonary tumor thrombotic microangiopathy. J Clin Oncol. 2007;25(5):597-599. [CrossRef] [PubMed]
 

Figures

Figure Jump LinkFigure 1 –  A posteroanterior chest radiograph shows a probable left pleural effusion.Grahic Jump Location
Figure Jump LinkFigure 2 –  ECG showing T-wave inversions from V1 to V5 and an S1Q3T3 pattern, consistent with right ventricular “strain.”Grahic Jump Location
Figure Jump LinkFigure 3 –  Echocardiographic image from the parasternal short-axis view showing an enlarged, “D-shaped” right ventricle (arrows) consistent with right ventricular overload.Grahic Jump Location
Figure Jump LinkFigure 4 –  Anteroposterior view from the pulmonary arteriogram showing no evidence of intravascular filling defects.Grahic Jump Location
Figure Jump LinkFigure 5 –  A still echocardiographic image from the parasternal long-axis view. The left ventricular cavity is totally obliterated (arrow), with endocardial walls “kissing.”Grahic Jump Location
Figure Jump LinkFigure 6 –  Photomicrograph of lung sections. A, C, Tumor thromboemboli immunohistochemically express CKAE1/3 (black arrows). The adjacent type 2 pneumocytes were also CKAE1/3 positive (yellow arrow). B, D, H&E stain showing tumor emboli (arrows) and fibrin thromboemboli (stars). CKAE1/3 = cytokeratin AE1/3; H&E = hematoxylin and eosin.Grahic Jump Location
Figure Jump LinkFigure 7 –  Photomicrographs of lung sections. A, B, Tumor thromboemboli immunohistochemically express VEGF (black arrows). VEGF = vascular endothelial growth factor.Grahic Jump Location
Figure Jump LinkFigure 8 –  A-D, Photomicrographs of pleural fluid cytology. A, H&E stain shows clusters of malignant cells (black arrow), consistent with an ovarian primary. B, C, D, The tumor cells show negative immunohistochemical expression for CK20, TTF-1, and PR, but positive immunohistochemical expression of CK7 and PAX-8. Photomicrographs of lung sections. E, Tumor thromboemboli in the lung are negative for PAX-8. CK = cytokeratin; PAX-8 = paired box gene 8; PR = progesterone receptor; TTF = thyroid transcription factor. See Figure 6 legend for expansion of other abbreviation.Grahic Jump Location

Tables

Table Graphic Jump Location
TABLE 1 ]  PTTM in 30 Patients

PTTM = pulmonary tumor thrombotic microangiopathy.

References

Singh A, Antognini JF. Perioperative hypotension and myocardial ischemia: diagnostic and therapeutic approaches. Ann Card Anaesth. 2011;14(2):127-132. [CrossRef] [PubMed]
 
Oren-Grinberg A, Talmor D, Brown SM. Focused critical care echocardiography. Crit Care Med. 2013;41(11):2618-2626. [CrossRef] [PubMed]
 
King C, May CW, Williams J, Shlobin OA. Management of right heart failure in the critically ill. Crit Care Clin. 2014;30(3):475-498. [CrossRef] [PubMed]
 
Price LC, Wort SJ, Finney SJ, Marino PS, Brett SJ. Pulmonary vascular and right ventricular dysfunction in adult critical care: current and emerging options for management: a systematic literature review. Crit Care. 2010;14(5):R169. [CrossRef] [PubMed]
 
Ventetuolo CE, Klinger JR. Management of acute right ventricular failure in the intensive care unit. Ann Am Thorac Soc. 2014;11(5):811-822. [CrossRef] [PubMed]
 
Kaplan A, Mayo PH. Echocardiographic diagnosis and monitoring of right ventricular function.. In:Levitov A, Mayo P, Slonim A., eds. Critical Care Ultrasonography.2 ed. New York, NY: McGraw-Hill Education; 2014.
 
Narasimhan M, Koenig SJ, Mayo PH. Advanced echocardiography for the critical care physician: part 2. Chest. 2014;145(1):135-142. [CrossRef] [PubMed]
 
De Gennaro L, Giannoccaro V, Lopriore V, et al. New onset right ventricular enlargement in recent dyspnea: Is echocardiography enough for a diagnosis of pulmonary thrombo-embolism? Heart Lung. 2014;43(4):328-330. [CrossRef] [PubMed]
 
Mayo J, Thakur Y. Acute pulmonary embolism: from morphology to function. Semin Respir Crit Care Med. 2014;35(1):41-49. [CrossRef] [PubMed]
 
Roberts KE, Hamele-Bena D, Saqi A, Stein CA, Cole RP. Pulmonary tumor embolism: a review of the literature. Am J Med. 2003;115(3):228-232. [CrossRef] [PubMed]
 
Lee EJ, Moon SH, Choi JY, et al. Usefulness of fluorodeoxyglucose positron emission tomography in malignancy of pulmonary artery mimicking pulmonary embolism. ANZ J Surg. 2013;83(5):342-347. [CrossRef] [PubMed]
 
Shin S, Pak K, Kim SJ, Kim H, Kim SJ. Pulmonary tumor embolism derived from stomach cancer observation with serial 18F-FDG PET/CT. Clin Nucl Med. 2015;40(3):270-272. [CrossRef] [PubMed]
 
Ordóñez NG. Value of PAX 8 immunostaining in tumor diagnosis: a review and update. Adv Anat Pathol. 2012;19(3):140-151. [CrossRef] [PubMed]
 
Chinen K, Fujino T, Horita A, Sakamoto A, Fujioka Y. Pulmonary tumor thrombotic microangiopathy caused by an ovarian cancer expressing tissue factor and vascular endothelial growth factor. Pathol Res Pract. 2009;205(1):63-68. [CrossRef] [PubMed]
 
Chinen K, Tokuda Y, Fujiwara M, Fujioka Y. Pulmonary tumor thrombotic microangiopathy in patients with gastric carcinoma: an analysis of 6 autopsy cases and review of the literature. Pathol Res Pract. 2010;206(10):682-689. [CrossRef] [PubMed]
 
Pinckard JK, Wick MR. Tumor-related thrombotic pulmonary microangiopathy: review of pathologic findings and pathophysiologic mechanisms. Ann Diagn Pathol. 2000;4(3):154-157. [CrossRef] [PubMed]
 
Uruga H, Fujii T, Kurosaki A, et al. Pulmonary tumor thrombotic microangiopathy: a clinical analysis of 30 autopsy cases. Intern Med. 2013;52(12):1317-1323. [CrossRef] [PubMed]
 
Gru AA, Pai RK, Roma AA. Pulmonary tumor thrombotic microangiopathy in patients with low-grade ovarian serous neoplasm: a clinicopathologic review of 2 cases of a previously unknown association. Int J Gynecol Pathol. 2012;31(5):438-442. [CrossRef] [PubMed]
 
Kayatani H, Matsuo K, Ueda Y, et al. Pulmonary tumor thrombotic microangiopathy diagnosed antemortem and treated with combination chemotherapy. Intern Med. 2012;51(19):2767-2770. [CrossRef] [PubMed]
 
Miyano S, Izumi S, Takeda Y, et al. Pulmonary tumor thrombotic microangiopathy. J Clin Oncol. 2007;25(5):597-599. [CrossRef] [PubMed]
 
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