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Unilateral Absence of Pulmonary Artery Perfusion

Krishna Kandarpa, MD, PhD
David E Drum, MD, PhD
J Stevan Nagel, MD
Barbara J McNeil, MD, PhD

March 29, 1983

Presentation

A 33-year-old white woman was diagnosed with chronic myelogenous leukemia on routine blood examination in 1976. Untreated, she remained asymptomatic until 1981 when she was noted to have a rising white blood cell count. Chemotherapy was started and she subsequently suffered its complications (immunosuppression, thrombocytopenia). In July 1982 she developed blast crisis and neurological deterioration (attributed to brain abscess).

Six days prior to her death in December 1982, she was admitted to the hospital because of shortness of breath and pleuritic chest pain following a fall and a 30 second loss of consciousness. She was hypotensive and tachycardic. Her temperature was 97 degrees F and arterial pO2 was 36 mmHg.

Imaging Findings

Chest Radiograph
Perfusion Lung Scintigraphy
Pulmonary Angiogram
Second Perfusion Scan

A chest radiograph showed a faint infiltrate in the right middle lobe.

A perfusion scan showed no perfusion to the entire right lung. She was not ventilated.

A pulmonary angiogram revealed a massive right pulmonary artery embolus (arrow) extending into the main pulmonary artery (PA). Her Hickman line was free of thrombi.

A second perfusion scan a few days later showed fragmentation of the thrombus with new defects (arrow) on the left.

A CT scan of the thorax (not shown) revealed that the right PA was not visible on pre- or post-contrast studies. Multiple patchy parenchymal densities could be seen in the right lung.

A CT of the head (not shown) showed a low density lesion in the left frontal lobe.

Diagnosis

Unilateral abscence of pulmonary artery perfusion due to organizing saddle fungal (Aspergillus) thrombus.

Discussion

Autopsy showed an organizing saddle fungal (Aspergillus) thrombus involving 90% of the main PA, 90% of the left PA, and 100% of the right PA. Propagation of the thrombus into secondary and tertiary arterial branches was noted. On microscopic view, the right PA wall had inflammatory changes with destruction and evidence of fungal invasion. Since there was no evidence of deep venous, pelvic vein or Hickman line thrombosis, the pathologists hypothesized that the saddle thrombosis was primary (ie, due to direct fungal infection of the vessel wall with subsequent vasculitis and injury) rather than embolic. Death was attributed to progressive right ventricle failure. The primary Aspergillus infection was most likely pulmonary parenchymal which later spread hematogenously.

Unilateral pulmonary artery nonperfusion on a radionuclide scan is uncommon. Unilateral nonperfusion with a normally perfused ontralateral lung is even less common. In a study conducted by White et al, 607 ventilation perfusion (VQ) scans done during a one year (1969) period were reviewed. They found 2% (13/607) to have unilateral nonperfusion.

In a study conducted by McNeil, 1 out of 67 with pulmonary embolism had a single defect involving the one lung only and 3 out of 67 with pulmonary embolism and multiple defects had the largest defect involving a whole lung. The urokinase pulmonary embolism trials did not break down defect size in a manner which allows comparison.

On a percentage basis, bronchogenic carcinoma, congenital heart disease (CHD), and hyperlucent lung syndrome are most commonly associated with unilateral nonperfusion on a lung scan. The incidence of unilateral nonperfusion in bronchogenic carcinoma varies from 7 to 50%. In these patients bronchial obstruction may be a mechanism by which arterial perfusion is eventually lowered. Emphysema and cardiac anatomy/surgery may play a role in nonperfusion associated with hyperlucent lung and CHD, respectively. Less common causes of unilateral nonperfusion include foreign bodies in major airways in children and rare primary and secondary neoplasms in adults.

References

1. White RI, James AE Jr, Wagner HN. The significance of unilateral absence of pulmonary artery perfusion by lung scanning. Am J Roentgenol 1971;111:501-9.

2. McNeil BJ. Ventilation-perfusion studies and the diagnosis of pulmonary embolism: Concise communication. J Nucl Med 1980;21:319-23.

3. Tow DE, Simon AL. Comparison of lung scanning and pulmonary angiography in the detection and follow-up of pulmonary embolism: The urokinase-pulmonary embolism trial experience. Progr Cardiovasc Dis 1975;17:239-245.

4. Apau RL, Saenz R, Siemsen JK. Bloodless lung due to bronchial obstruction. J Nucl Med 1972;13:561-2.

5. Olsson HE, Spitzer RM, Erston WF. Primary and secondary pulmonary artery neoplasia mimicking acute pulmonary embolism. Radiology 1976;118:49-53.

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