British Journal of Radiology 74 (2001),962-964 © 2001 The British Institute of Radiology
Reversed portal vein pulsatility on Doppler ultrasound secondary to an iatrogenic mediastinal haematoma
C Görg, MD,
B Wollenberg, MD and
J Beyer, MD
Department of Internal Medicine, Philipps University, Baldingerstraße, 35043 Marburg, Germany
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Abstract
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The Doppler ultrasound pattern of reversed pulsatile flow (RPF) of the portal vein (PV) is strongly associated with high atrial pressure. Tricuspid regurgitation is considered to be the main cause of RPF in patients with chronic heart disease, but the precise pathomechanism of this PV flow pattern has not yet been resolved. We descibe for the first time a RPF of the PV in a young patient with a mediastinal haematoma after inadvertent puncture of the subclavian artery. In this patient, transcutaneous echocardiography demonstrated normal valves without any tricuspid regurgitation as well as normal diameters of the cardiac cavities. The RPF of the PV in this patient resolved spontaneously within 7 days. An increased hepatic outflow resistance with transmission of hepatic artery pulsations across arterioportal communications seems the most likely pathomechanism to explain our finding.
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Introduction
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In healthy adults, portal venous flow is typically continuous hepatopetal with minimal variations related to cardiac or respiratory activity [1]. Using Doppler ultrasound, marked pulsatile flow has recently been demonstrated in healthy adults, especially in thin subjects [2]. In almost all other patients, reversed pulsatile flow (RPF) of the portal vein (PV) is pathological and has been attributed to the presence of tricuspid insufficiency [3], elevated right atrial pressure [4], liver diseases, for example cirrhosis or Budd–Chiari syndrome [5], and constrictive pericarditis [6].
To the best of our knowledge, this is the first report of transient pulsatile reversed portal flow in a patient with a mediastinal haematoma and a small haemopericardium, following inadvertent puncture of the right subclavian artery.
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Case report
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A 29-year-old female patient was admitted to hospital for an allogenic bone marrow transplant for severe aplastic anaemia. Physical examination and laboratory parameters were normal, except for severe pancytopenia.
Implantation of a tunneled Groshong® catheter (Bard Access System, Salt Lake City, UT) into the right subclavian vein was unsuccessful owing to inadvertent arterial puncture. The patient complained of thoracic pain, but no other symptoms, after the procedure. A chest radiograph on the same day as the procedure demonstrated enlargement of the mediastinum (Figure 1
). CT demonstrated a haematoma within the right upper mediastinum and a small haemopericardium around the right atrium (Figure 2). No haematothorax and no pneumothorax was demonstrated. Abdominal ultrasound examination was unremarkable except for mildly distended hepatic veins.
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Figure 2. CT demonstrating a mediastinal haematoma and a small haemopericardium around the right atrium.
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Despite normal ultrasound scans, Doppler tracing showed an increase of the retrograde phase of hepatic venous flow (Figure 3) as well as a RPF in the PV that was even transmitted into the hilar splenic vein. Subsequent transcutaneous echocardiography showed normal heart valves without any regurgitation and, particularly, no tricuspid regurgitation. The diameters of the heart cavities were also normal. The haemopericardium around the right atrium was considered to be too small to cause haemodynamic impairment. No further pericardial effusion was seen. Cardiac catheterization or drainage of the haemopericardium was not performed as the patient remained haemodynamically stable with minimal symptoms. A repeat Doppler ultrasound examination 6 days after the initial event showed a normal phasic wave form in the hepatic veins, and repeat spectral analysis showed regular, continuous hepatopetal flow patterns in the PV and the hilar splenic vein (Figure 4).
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Figure 3. Doppler wave form of the hepatic veins (left), the portal vein (middle) and the hilar splenic vein (right). The Doppler trace of the hepatic vein shows a regular triphasic flow pattern with a pronounced retrograde phase. A marked pulsatile pattern with temporarily reversed flow is seen in the portal vein and the splenic vein.
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Figure 4. On follow-up examination, the pathological flow pattern has resolved. The Doppler trace of the hepatic vein (left) now shows a regular phasic wave form. A regular continuous hepatopetal flow is seen in the portal vein (middle) and the splenic vein (right).
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Discussion
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Several pathophysiological mechanisms are involved in the modulation of portal venous flow. Principal determinants of PV pulsatility may include the retrograde trans-sinusoidal transmission of atrial pulsations [5], the respiratory cycle [2] and the transmission of vena caval, hepatic arterial or splanchnic arterial pulsations [2].
Two patterns of portal venous pulsatility have been described [2]. The continuous pulsatile pattern is characterized by a phasic hepatopetal flow with marked pulsatility. This has been interpreted as a sign of congestive heart failure [3] but may occur in the absence of any cardiovascular disease, particulary in thin subjects [2].
The RPF pattern is characterized by variation in flow velocity and direction related to the cardiac cycle. RPF is strongly correlated with high pressures (>20 mmHg) in the right atrium in patients with chronic heart failure [4] and can be explained by the presence of tricuspid regurgitation [3]. The suggested predominant pathomechanism of hepatofugal pulsatile venous flow in patients with cirrhosis and Budd–Chiari syndrome is the transmission of hepatic artery pulsations across arterioportal communications [5].
Most recently, Gorka et al [6] found no tricuspid regurgitation in a patient with constrictive pericarditis and a RPF pattern in the PV, but a right atrial pressure of only 17 mmHg. They assumed that pulmonary hypertension may have induced RPF irrespective of the degree of tricuspid regurgitation, concluding that increased hepatic venous outflow resistance with subsequent trans-sinusoidal shunting between the hepatic artery and the PV may have been responsible for the RPF in their patient [6]. This pathophysiological mechanism may be similar to the outflow obstruction that causes RPF in patients with liver cirrhosis and Budd–Chiari syndrome [3, 6].
Significant tricuspid regurgitation was excluded in our patient by Doppler and colour-coded Doppler echocardiography. Moreover, the cavities of the right heart were entirely normal and there was no relevant pericardial effusion. Because of the unremarkable echocardiographic examination and the absence of liver cirrhosis and Budd–Chiari syndrome, we assume that the mediastinal haematoma had been the main cause for an increased hepatic outflow resistance and consecutive RPF of the PV in this case.
Received for publication April 12, 2001.
Revision received June 15, 2001.
Accepted for publication June 22, 2001.
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References
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Abstract
Introduction
