| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Guest Access | Sign In via User Name/Password
|
|
|
|||||||
Guest Access | Sign In via User Name/Password |
|||||||||
* From the Department of Medicine, New York University Medical Center, New York, NY.
Correspondence to: Nidhi Kumar, MD, Department of Medicine, New York University Medical Center, 550 1st Ave, NBV 16N 26, New York, NY 10016; e-mail: kumarn01{at}med.nyu.edu.
Key Words: percutaneous mechanical thrombectomy • pulmonary embolism • shock
 |
Introduction |
|---|
 TOP Introduction Case ReportsDiscussionReferences |
|---|
Percutaneous mechanical thrombectomy (PMT) performed by interventional radiologists is a novel approach to reduce pulmonary arterial clot burden and reverse acute cor pulmonale when pharmacologic thrombolysis is contraindicated or ineffective. PMT use in major PE has been favorably described in the literature,56789 and its use in venous thromboembolic disease will likely continue to emerge secondary to improvements in technology and availability. The ability to simultaneously image and treat clot locally as well as document improved perfusion is appealing.
We report the use of rheolytic thrombectomy in a postpartum patient with obstructive shock due to acute PE. Although the angiographic result was excellent and the patient hemodynamically improved and fully recovered in the days following the procedure, she experienced a paradoxical worsening of hemodynamics immediately following the intervention. We suspect that significant intravascular hemolysis related to the thrombectomy device contributed to the transient decompensation. While some interventional radiologists know the indications and potential complications of PMT, its increasing use will require that the broader group of physicians become familiar with this treatment modality.
|
Case Reports |
|---|
|
TOPIntroductionCase ReportsDiscussionReferences |
|---|
Due to the immediate postoperative status, systemic thrombolysis was contraindicated. Thoracic surgery was notified, and preparations were made for "rescue" open embolectomy if necessary. The patient was sent to the interventional radiology suite for angiography and attempted therapy. Selective angiography revealed a large nonocclusive thrombus in the right main pulmonary artery and clots occluding flow to the middle and lower lobes. Rheolytic thrombectomy (AngioJet System; Possis Medical; Minneapolis, MN) was performed. A local thrombolytic was not administered. Repeat arteriography after thrombectomy showed a patent right main pulmonary artery and restoration of flow to the right lung segments. Immediately after the procedure, on arrival to the medical ICU, the patient was found to be more hypotensive and tachycardic, with cyanotic distal extremities, a central venous pressure of 20 mm Hg, and clear lungs. Both norepinephrine and dobutamine drips were increased. The patient was noted to have gross hematuria. A hemogram revealed a drop in hemoglobin from 12.7 to 9.7 g/dL and a stable platelet count of 160,000/µL. Postprocedure serum chemistry analysis was significant for an increase in potassium from 3.5 to 5.8 mmol/L; total bilirubin, 5.9 mg/dL (normal range, 0.1 to 1.1 mg/dL); direct bilirubin, 0.5 mg/dL; and lactate dehydrogenase, 6,679 U/L. Serial blood samples sent for prothrombin time, partial thromboplastin time, d-dimer level, and fibrinogen were reported as "hemolyzed."
The patient did not receive any blood products prior to the onset of hematuria, and the groin catheter insertion site did not reveal a hematoma. The patient was treated supportively with packed RBC, fresh frozen plasma, and cryoprecipitate for possible disseminated intravascular coagulation with significant hematuria. The heparin infusion was discontinued. Hematology studies performed 2 h after PMT revealed a prothrombin time of 14.8 (normal range, 9.1 to 11.5 s), partial thromboplastin time of 37 s (normal range, 24 to 35 s), a hemoglobin level of 10.6 g/dL, and platelet count of 136,000/µL. Schistocytes present on the peripheral blood smear and red supernatant on a centrifuged plasma sample consistent with free plasma hemoglobin suggested the development of fragmentation hemolysis secondary to mechanical thrombectomy. An atypical presentation of HELLP (hemolysis, elevated liver, low platelet) syndrome, an early consideration, was believed unlikely due to the time course and the minor platelet drop. Hematuria was attributed to hemoglobinuria, and the unfractionated heparin infusion was resumed. The hemolysis, resulting hemoglobinuria, and shock resolved within 24 h, allowing for extubation and transfer from the ICU. The remaining hospital course was uneventful, and the patient was discharged home on hospital day 7. An outpatient echocardiogram obtained shortly after discharge revealed normal biventricular function and pulmonary artery pressure.
|
Discussion |
|---|
|
TOPIntroductionCase ReportsDiscussionReferences |
|---|
In the setting of major PE, severe obstruction of right ventricular outflow results from the intravascular thrombi directly as well as pulmonary arterial vasoconstriction secondary to hypoxemia, acidemia, and local release of vasoactive mediators. Our patient presented with hypoxia, hypotension, and hypoperfusion consistent with acute cor pulmonale secondary to PE. Despite initial stabilization with vasopressor and inotropic support as well as unfractionated heparin, persistent shock led to an attempt to reduce right ventricular afterload.
PMT techniques, originally developed for thrombus removal from coronary arteries, peripheral vessels,11 and occluded hemodialysis grafts,12 have not been approved by the US Food and Drug Administration for treatment of PE. Fragmentation thrombectomy, aspiration thrombectomy, and rheolytic thrombectomy have been considered the most promising of the PMT options for treatment of acute PE.513 The AngioJet rheolytic thrombectomy catheter injects a high-velocity saline solution stream to fragment thrombus and simultaneously evacuate resulting debris using the Venturi effect. Complications of PMT include bradyarrythmias, target vessel injury, embolization, and hemolysis.14 We focus our discussion on intravascular hemolysis and the possible role it played in the paradoxical worsening of shock, observed in our patient, during the hours immediately after thrombectomy.
Laboratory and clinical evidence of hemolysis related to the use of PMT devices has been previously reported.1516 Nazarian et al16 studied rheolytic thrombectomy in nine patients and nine dogs. The device was activated in peripheral vasculature sites for 1 to 2 min in dogs and 1 to 4 min in humans. After the procedure, the level of haptoglobin decreased and free plasma hemoglobin increased in eight humans and all dogs. Hemoglobinuria was detected in one human and all dogs. The authors16 theorized that hemolysis was more severe in partially occluded vessels, as circulating cells in addition to the thrombus came into contact with the device. Prolonged procedure time also correlated with the degree of hemolysis. They cautioned against using PMT in patients who were anemic, hypoxemic, or had potentially reversible renal insufficiency. In addition, renal insufficiency may potentiate hyperkalemia.
Kasirajan et al11 reported a series of 17 patients with extensive extremity deep vein thrombosis treated with rheolytic thrombectomy, and found that 24% had venographic evidence of > 90% thrombus removal, 35% had 50 to 90% thrombus removal, and 41% had < 50% thrombus extraction.11 While the authors11 caution against the possibility of hemolysis and fluid overload as potential side effects of the AngioJet system, these complications were not observed in their patients.
Clinical data on the safety and efficacy of PMT devices used in setting of PE in humans are limited, consisting mainly of case reports.5689 Zeni et al9 reported the use of the AngioJet in a case series of 17 patients with massive PE and hemodynamic compromise. Treatment resulted in immediate angiographic and clinical improvement in 16 of 17 patients. Hemoglobinuria after PMT was observed; however, clinically significant hemolysis was not described.
In our patient, hemolysis due to PMT was not anticipated by the critical care team and confounded patient management for several hours. In addition, despite significant reduction in clot burden demonstrated on pulmonary angiogram after PMT, the expected hemodynamic improvement was not immediately realized. In fact, worsening cor pulmonale was evident. We believe this paradox may be explained by the intravascular hemolysis causing local nitric oxide deficiency. The acute and chronic vasoconstrictive effects associated with the presence of free hemoglobin in the circulation are well described in the literature.17
Nitric oxide (NO), produced by the endothelium, is an important regulator of vascular homeostasis, helping to match tissue perfusion with oxygen demand. NO activity results in vasodilation and antagonism of platelet aggregation and thrombosis. Hemoglobin binds NO rapidly, and essentially irreversibly, to produce nitrate and methemoglobin.1718 The avidity of ferrous heme for NO is so great that uncontrolled access of even small amounts of free hemoglobin to endothelial-derived NO serves as a substantial NO sink, leading to local vasoconstriction and platelet aggregation. Evolution of the RBC membrane and free-heme scavenging mechanisms for physiologic intravascular hemolysis prevent this toxic effect of hemoglobin while allowing its vital oxygen-carrying role.17 When stroma-free hemoglobin solutions are infused as investigational blood substitutes in animals and humans, both systemic and pulmonary hypertension are predictably found.18192021 Chronic intravascular hemolytic anemias, such as sickle-cell anemia and hereditary spherocytosis, are also associated with systemic and pulmonary hypertension. We hypothesize that the small but significant free hemoglobin released in the pulmonary circulation during PMT-induced hemolysis in our patient caused transient endothelial dysfunction and vasoconstriction. Additionally, it is possible that inhaled NO, a potent local pulmonary arterial vasodilator, could have been used to prevent or reverse this effect. Inhaled NO has previously been used to reduce right ventricular afterload in major PE and, in one report,22 was effective in reversing sluggish pulmonary vascular reperfusion after PMT using both suction and rheolytic thrombectomy. Hemolysis was not reported in this latter case.22
Hemolysis was self limited in our patient, and she subsequently did well. However, had the complication of PMT been anticipated by the critical care team, unnecessary testing and delay in diagnosis may have been avoided. Controlled studies of PMT in PE should be performed to better define its risks and potential role, if any, in the multidisciplinary approach to major PE.
|
Footnotes |
|---|
The authors have no conflicts of interest to disclose.
Received for publication April 22, 2006. Accepted for publication December 5, 2006.
|
References |
|---|
|
TOPIntroductionCase ReportsDiscussionReferences |
|---|
Related Article
Related Editorial
This article has been cited by other articles:
|
|
 |
|
  W. T. Kuo, D. Y. Sze, L. V. Hofmann, and S. Z. Goldhaber Catheter-Directed Intervention for Acute Pulmonary Embolism: A Shining Saber Chest, January 1, 2008; 133(1): 317 - 318. [Full Text] [PDF]
|
|
|
|
|
|
S. Z. Goldhaber Percutaneous Mechanical Thrombectomy for Acute Pulmonary Embolism: A Double-Edged Sword Chest, August 1, 2007; 132(2): 363 - 365. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
