SVC Thrombosis Research Articles

In-hospital outcomes of patients with lung cancer with and without superior vena cava thrombosis: A nationwide analysis.

e23322 Background: Malignant superior vena cava syndrome (SVCS) is a clinical problem that results from the obstruction of blood flow in the superior vena cava by an underlying malignancy. It may be caused by external compression or internal obstruction due to a thrombus or direct invasion by tumor cells. Though lung malignancy is the most common cause of SVCS, there is a lack of data on in-hospital outcomes in these patients. Methods: We queried the National Inpatient Sample 2018-2020 to identify hospitalizations with lung cancer including both small cell and non small cell lung cancer. Hospitalizations with diagnosis of acute SVC thrombosis were determined by using ICD-10 codes.Demographics and mortality rates were compared between two groups using chi square for categorical variables and t test for continuous variables. Multivariate regression analysis was further performed to study the impact of SVC thrombosis on mortality, LOS and total hospitalization cost. Results: A total of 2011620 hospitalizations with lung cancer were identified. Of these, 2855 (0.0014%) had acute SVC thrombosis. These patients were younger with a mean age of 63 years. African-Americans and Hispanics were in a higher proportion in the cohort of hospitalizations with SVC thrombus as compared to those without. (Table 1). Multivariate regression analysis revealed higher odds of mortality (OR-1.94; C.I: 1.53-2.47; P < 0.001), LOS (OR 1.66; C.I:1.20- 2.31; P < 0.005) and total hospitalization cost (26211.15; C.I:22183.56- 30238.74; P < 0.001) in lung cancer hospitalizations. Conclusions: Our study shows that SVCT, has higher odds of mortality, length of stay and total hospital cost. Though the general recommendation is to continue anticoagulation, sometimes patients may require endovascular stent placement with/without thrombectomy. Though rare, SCVT can be life threatening and requires prompt attention.[Table: see text]

S2784 Unveiling the Link: SVC Thrombosis and the Emergence of Esophageal Varices

S2784 Unveiling the Link: SVC Thrombosis and the Emergence of Esophageal Varices

RARE CASE OF SVC THROMBOSIS LEADING TO CHYLOTHORAX

RARE CASE OF SVC THROMBOSIS LEADING TO CHYLOTHORAX

Assessing inpatient outcomes for patients with small cell lung cancer presenting with superior vena cava thrombosis.

8589 Background: Superior Vena Cava Syndrome (SVCS) is a condition characterized by obstruction of the SVC that can commonly be caused by thrombus formation in the SVC. Small cell lung cancer (SCLC) frequently results in obstruction of the SVC. When severe enough, SVCS can present as a life-threatening oncological emergency. In this study we aim to explore baseline characteristics of SVC thrombosis (SVCT) in patients with SCLC, the prevalence of US hospitalizations, and disparities with regards to race and socioeconomic status. Methods: National Inpatient Sample was utilized to obtain pertinent data. Total hospitalizations with coexistent comorbidities of SCLC were extracted from the 2016 to 2019 database. Adult patients with a secondary diagnosis of SVC thrombosis were determined by using ICD-10 codes. We studied the racial and socioeconomic differences as well as length of stay (LOS), total hospital charges (THC), and all-cause mortality outcomes in cancer patients with and without SVC thrombosis. Statistical analysis was performed on STATA, with logistic regression analyses and chi-square tests. Results: A total of 480,750 patients were hospitalized for SCLC. 720 of these patients had SVC thrombosis (0.15% of SCLC patients). The mean age of those with thrombi was significantly lower compared to those without thrombi (64 vs. 69, p < 0.001). The SCLC with SVCT cohort had statistically higher proportion of black patients than the other cohort. Charlson index was significantly higher in SCLC with SVCT cohort (5.8 vs. 5, p < 0.001). Average income between the two cohort groups were similar. Medicaid and private insurance utilization were more common in SCLC with SVCT admissions compared to without SVCT. Patients presenting with SVC thrombosis had an increased hospital LOS (10 vs. 6 days, p < 0.001) and cost compared to other cohorts ($117,320 vs. $80,806, p < 0.005). All-cause mortality in patients with SCLC was 7.7% and the presence of SVC thrombosis significantly increased the odds of inpatient mortality (18.0%). Non-White races were associated with higher odds of mortality in SCLC admissions. In addition, patients with SVC thrombus also had greater odds of having a concomitant pulmonary embolism during hospitalization. Conclusions: In this study we found that race, insurance type, and comorbidities impacted the likelihood of developing thrombosis in the superior vena cava in patients with SCLC. Though the incidence is rare, SVC thrombosis indicates a poor prognostic factor for patients with SCLC. Further studies to evaluate these disparities in race and socioeconomic factors are warranted. The development of thrombosis and subsequent SVC syndrome is a potentially life-threatening condition; addressing potential reversible risk factors could improve mortality in a large subgroup of hospitalizations related to SCLC.

Behçet's Disease: A Radiological Review of Vascular and Parenchymal Pulmonary Involvement.

Behcet's disease (BD) is a chronic systemic inflammatory disorder characterized by underlying chronic vasculitis of both large- and small-caliber vessels. Thoracic involvement in BD can occur with various types of manifestations, which can be detected with contrast-enhanced MSCT scanning. In addition, MR can be useful in diagnosis. Characteristic features are aneurysms of the pulmonary arteries that can cause severe hemoptysis and SVC thrombosis that manifests as SVC syndrome. Other manifestations are aortic and bronchial artery aneurysms, alveolar hemorrhage, pulmonary infarction, and rarely pleural effusion. Achieving the right diagnosis of these manifestations is important for setting the correct therapy and improving the patient's outcome.

Superior vena cava syndrome management in limited source setting: a case report

Superior vena cava syndrome (SVCS) is syndrome caused by mass compression, tumor invasion, and/or thrombosis of SVC. In the past, SVCS was mostly linked to infection. Nowadays, SVCS is mostly linked to malignant tumor and medical procedures. Most common malignant cause of SVCS is non small cell lung cancer. A 69-year-old man was presented with breathing difficulty. Symptom began 4 months before admission, with worsening of symptom since 2 weeks before admission. Symptom improved with sitting position, and worsened with supine position. Patient had been sleeping with 2 pillows. Patient had productive cough and hoarseness. Swelling of face and neck were present. Collateral vein distention was visible in the area of head, neck, and chest. Physical examination of lung revealed decreased vesicular breath sound at right side. Non pitting edema was found at both sides of upper extremity. SVCS in this case can be categorized into grade 2, chronic SVCS case. CT showed center right lung mass, although malignant cells were not obtained from pleural puncture and CT guided needle biopsy. Staging of mass was T4N3M1a. Mass finding at the center of right lung is in accordance with the previous findings that SVCS generally arise from lung (not mediastinum), and that right sided masses are generally more likely to cause SVCS. Management in this case was done by giving corticosteroid and diuretic. Surgery, radiotherapy, and immunotherapy were not done since malignancy diagnosis hadn’t been able to be concluded.

Adenocarcinoma Lung Presenting with Bilateral Chylothorax and SVC Thrombosis

Adenocarcinoma Lung Presenting with Bilateral Chylothorax and SVC Thrombosis

A Case of Malignant Superior Vena Cava Syndrome Presenting as Syncope

SESSION TITLE: Student/Resident Case Report Poster - Disorders of the Mediastinum SESSION TYPE: Student/Resident Case Report Poster PRESENTED ON: Tuesday, October 25, 2016 at 01:30 PM - 02:30 PM INTRODUCTION: Superior Vena Cava Syndrome (SVCS) is a constellation of clinical symptoms and signs caused by either extrinsic compression or SVC thrombosis. Lung Cancer is the most common cause of SVCS. We present an uncommon case of malignant SVCS presenting with syncope. CASE PRESENTATION: A 55-year-old male presented to the emergency department after passing out in his niece’s parked car. He had lightheadedness and blurred vision before the witnessed, one minute, syncopal episode. He denied any previous history of syncope, heart disease or seizure. He endorsed having progressive neck pain and swelling over the past six months, a twenty-two pounds weight loss over the past year and a forty year pack history of tobacco smoking. Physical examination revealed normal vital signs except for heart rate of 105 bpm. Multiple solid, non-mobile masses were noted on the neck and the chest wall (Figure 1). Distended superficial veins were observed on the diffusely swollen right upper extremity. Significant clubbing was noted in all extremities. Routine syncope workup was unremarkable. CT scan of the neck and chest with intravenous contrast showed the presence of a speculated nodule in the right upper lobe, a large right neck mass, evidence of venous collaterals and soft tissue edema, and extensive upper mediastinal lymphadenopathy significantly narrowing the SVC (Figure 2). Surgical incisional biopsy of a chest wall mass was performed. Histology and immunohistochemistry studies (Figure 2) along with the clinical and radiographic findings confirmed the diagnosis of malignant SVCS secondary to stage IV (T4 N3 M1) poorly differentiated adenocarcinoma of lung origin. Imaging of the brain revealed no evidence of metastases. The patient was hemodynamically stable and with no significant cardiorespiratory compromise. Combined palliative treatment with radiation and chemotherapy was elected. Two years later, the patient continues to maintain good functional capacity. DISCUSSION: This is a case of malignant SVCS presenting uncommonly as syncope. Proper diagnosis, grading, and staging of malignant SVCS are key to its management. Worrisome signs like laryngeal or cerebral edema might warrant an emergent placement of an endovascular stent. Our patient’s SVCS was secondary to stage IV lung adenocarcinoma and was severe based on proposed grading system by Yu et al. Patient has responded well to palliative radiation and chemotherapy. CONCLUSIONS: Accurate diagnosis and staging of SVCS are necessary and help determine the modality and goal of therapy. Reference #1: Wilson, L. D. (2007, 05). Superior Vena Cava Syndrome with Malignant Causes. NEJM, 356(18), 1862-1869. Reference #2: Yu, J. B. (2008, 08). Superior Vena Cava Syndrome—A Proposed Classification System and Algorithm for Management. Journal of Thoracic Oncology, 3(8), 811-814. DISCLOSURE: The following authors have nothing to disclose: Mahrous Abo Hassan, Yahya Kurdi, Xiaoyi Yu, Eric Speakman, Rupesh Raina, Harish Kakarala, Osei-Tutu Owusu No Product/Research Disclosure Information

When Esophageal Varices Go Downhill

Patient Presentation: A 32 year old female with ESRD secondary to mesangial proliferative glomerulonephritis, recurrent SVC catheters due to failed AVG's, Mixed Connective Tissue Disorder and a failed renal transplant, presented with 2 days of melena and 2 episodes of hematemesis. There was no history of alcoholism, hepatitis, abdominal pain, NSAID or anticoagulant use. Physical examination was significant for tachycardia to 128 BPM, dilated superficial veins on the anterior chest wall, and melenic stool. There was no scleral icterus, abdominal distention, or hepatomegaly. The patient was transferred to the MICU. Work Up/Interventions: Laboratory studies were as follows: Hb 6.0 g/dL, Bilirubin 0.7, μmol/L, AST 7 U/L, ALT 6 U/L, INR 1.06 and Albumin 3.3 g/dL. The patient received transfusion of PRBC. EGD demonstrated F3 esophageal varices in the upper and mid-esophagus and presence of red wale signs and oozing blood. Endoscopic band ligation was performed. The melena resolved and the hemoglobin remained stable. Abdominal ultrasound demonstrated a normal liver. The portal veins were patent with normal direction of flow. The IVC and hepatic veins were patent. CT angiography of the abdomen demonstrated numerous abdominal wall collateral vessels. CT angiography of the chest revealed occlusion of the SVC along with numerous right-sided chest wall collaterals. The occlusion was at the junction of the SVC and the R brachiocephalic vein. A prominent azygous vein was seen. Diagnosis: Downhill esophageal varices secondary to SVC thrombosis due to multiple prior central venous catheters. Therapy: Balloon angioplasty of the SVC successfully improved flow. Subsequent EGD showed improvement of the esophageal varices. Definitive therapy consisted of right axillary vein to right atrium bypass graft.Figure 1Figure 2Figure 3Discussion: Downhill esophageal varices cause less than 0.1% of all variceal bleeds. Occlusion of the SVC results in increased pressure to the azygous and hemiazygous systems responsible for drainage of the venous plexuses of the upper two thirds of the esophagus. If the occlusion does not interfere with azygous drainage to the SVC, only the upper two thirds of the esophagus will be involved, as in the present case. Occlusion of the azygous drainage into the SVC results in varices throughout the esophagus. Treatment of downhill varices focuses on restoring venous drainage. Options include balloon angioplasty, SVC stenting and open surgical therapies. Endoscopic options include proximal banding. Sclerotherapy is avoided due to concerns over embolization.

Superior vena cava syndrome – changing etiology in the third millennium

Superior vena cava syndrome (SVCS), is diagnosed following different degrees of central venous system obstruction, which traditionally was caused by infections, tumors or fibrosing mediastinitis. Recently the role of SVC thrombosis secondary to indwelling central venous devices or pacemaker leads as well as different hypercoagulable states have drawn much attention. In the current review we present a 58-year-old female patient who underwent recurrent pacemaker replacements due to recurrent infections. The patient was hospitalized with superior vena cava syndrome and multiple thrombi in the upper body circulation. Additionally the evaluation was conducted for thrombophilia, which revealed the presence of high titers of antiphospholipid antibodies, suggesting the concurrent diagnosis of the antiphospholipid syndrome (APS). This case reflects the changes in the etiology of SVCS, and the need for a comprehensive evaluation of patients, in the search for additional factors that may complicate a pacemaker insertion, such as the presence of antiphospholipid antibodies. We review the relevant literature and highlight the importance for an interdisciplinary approach in the treatment of SVCS nowadays.

Phase II study of topotecan and bevacizumab in advanced refractory non-small cell lung cancer (NSCLC).

7563 Background: Bevacizumab in combination with carboplatin and paclitaxel improves survival of patients with NSCLC in a first-line setting. We hypothesized that non-cross-resistant, second-line salvage therapy with the topoisomerase 1 inhibitor, topotecan, in combination with bevacizumab would have activity in NSCLC. Methods: Forty-two patients were enrolled between 10/2006-9/2010. Patients received topotecan 4.0 mg/m2 on days 1, 8 and 15 and bevacizumab 10 mg/kg on days 1 and 15 as IV infusions. Treatment was repeated every 28 days in the absence of disease progression or unacceptable toxicity. Eligibility criteria included age older than 18 years, ECOG PS of 0-1, and adequate organ function. Patients with treated brain metastases were permitted to enter this study. Response assessment (using RECIST) was performed every two cycles. Primary endpoint of this study was progression-free survival (PFS). Results: Forty-two patients were enrolled in the study. Median age was 60.6 years (range = 36-81). Patients had a median of 3 prior treatment regimens (range 1-7), and 93% had prior platinum therapy. The primary objective of PFS was 238 days (95% CI, 117-332 days). Overall survival (OS) was 345 days (95% CI, 213-464 days). Response rates were as follows: 14.3% partial response (PR), 54.8% stable disease (SD), 28.6% progressive disease (PD). Grade 3 hematologic toxicities seen in participants included thrombocytopenia (16.7%), neutropenia (9.5 %), and anemia (4.8%). There was no grade 4 or higher hematologic toxicities. Only one toxic death, due to pulmonary hemorrhage, occurred during the study. The only grade 4 toxicity was a pulmonary embolism in one patient. Grade 3 non-hematologic adverse events were minimal (<8%) and included: hyperglycemia, bone pain, gastroesophageal reflux, diarrhea, infection, shortness of breath, bowel obstruction, DVT, abdominal pain, pseudogout, and SVC thrombosis. Conclusions: The combination of bevacizumab and topotecan as a salvage therapy for metastatic NSCLC appears to be well tolerated and provides significant progression-free survival. A randomized trial should be performed to compare this combination with other NSCLC regimens.

Management of Common Oncologic Emergencies

The common oncologic emergencies include Superior Vena Cava Syndrome (SVCS) and Superior Mediastinal Syndrome (SMS), Tumor Lysis Syndrome (TLS), Hyperleukocytosis and Febrile Neutropenia. SVCS denotes compression, obstruction or thrombosis of SVC and SMS denotes SVCS and tracheal compression. The diagnosis should be established early with minimum invasive techniques. Steroids should be administered immediately. Sedatives are contraindicated. TLS describes the metabolic derangements in various combinations that include hyperuricemia, hyperphosphatemia, hyperkalemia hypocalcemia and uremia which arise from death of and release of contents from tumor cells. Early recognition of patients at risk and initiation of preventive therapy for TLS is essential. Treatment is directed at adequate hydration, use of allopurinol and alkalinization of urine. Hyperluekocytosis is defined as peripheral leukocyte count exceeding 100,000 per microlitre and therapy is tailored at reduction of blood viscosity with hydration, alkalinization of urine allopurinol; chemotherapy should be started once the child is metabolically stable. Febrile neutropenia is a common oncologic emergency directly related to the immune suppression related to cancer treatment. Successful outcome depends on careful evaluation, identification of cause and prompt treatment with antimicrobials (empirical/directed to a specific focus).

Clinical review and analysis of complications of totally implantable venous access devices for chemotherapy

Since the first implant of totally implantable venous access device (TIVAD), performed by Niederhuber and colleague in 1982, the systems have increasingly been used in the field of oncology. We analyzed the clinical reviews and complications of TIVAD in an effort to achieve optimal management. We retrospectively studied 442 cases with TIVAD device at our hospital and we report the results. Four hundred and forty-two TIVAD were placed in the right subclavian vein in 345 cases, the left subclavian vein in 93 cases, the right jugular vein in 2 cases, the left jugular vein in 1 case, and the right femoral vein in 1 case. The immediate complications were 28 cases in malposition of the catheter, 10 cases of arterial puncture, and 2 cases of pneumothorax. The late complications were 3 cases of pocket infection, 2 cases of catheter related to sepsis, 3 cases of catheter obstruction, 2 cases of SVC thrombosis, and 1 case of catheter fracture (pinch-off syndrome: Hinke grade 3). There were no other early or late complications. The low rate of complications in the study confirms the safety and convenience of using TIVAD in patients undergoing prolonged chemotherapy. Yet because infection, thrombosis and catheter fracture are the most common long-term complications of TIVAD, early diagnosis and management of these problems can prevent severe complications.

Endovascular Treatment of Superior Vena Cava Syndrome by Percutaneous Venoplasty

Thrombosis of the superior vena cava leads to obstruction of venous outflow of the head and upper extremities and causes severe clinical symptoms. The management of SVC syndrome depends on aetiology and acuity at clinical presentation and ranges from conservative medical treatment to bypass surgery. Endovascular treatment can provide rapid relief of symptoms and substantial clinical improvement independent of aetiology. We report a case of successful interventional treatment in a patient with catheter-induced SVC thrombosis and present a review of the literature.

Chylothorax and chylopericardium as the initial clinical manifestation of Behcet’s disease

Behcet's disease (BD) is a chronic relapsing systemic vasculitic disorder affecting the arteries, veins, and vessels of any size. Large vein thrombosis in BD is not commonly developed and most commonly observed in the veins in the lower extremities and inferior or superior vena cava. In this report, a 18-year-old male patient with large vein thrombosis involving superior vena cava was presented. He was treated due to chylothorax and chylopericardium with SVC syndrome before diagnosis of BD. SVC thrombosis complicated by chylothorax and chyolpericardium can be a rare presenting initial symptom of BD.

Gastroschisis: A plea for risk categorization

The incidence of gastroschisis has increased in the past decade. A differing clinical course between "complex" (those with atresias, perforation, or stenosis) and "simple" cases has prompted a review of risk assessment factors. A retrospective chart review was conducted of 103 infants with gastroschisis over 5 years (1992 to 1997). Of 103 infants, 52 were girls and 51 were boys. Seventy-one infants (69%) had a simple defect, and 32 (31%) were complex. The simple group had an average estimated gestational age of 37.5 weeks (range, 26 to 40), and a birth weight of 3.0 kg (range, 1.7 to 3.8). A total of 71% underwent primary repair, whereas 29% required a silo. Mechanical ventilation averaged 6.8 days (range, 1 to 19). Enteral feedings were initiated at 15 days (range, 3 to 27) with full enteral intake achieved by 22.4 days (range, 5 to 40). Three infants required home parenteral nutrition. The average length of stay (LOS) was 26.4 days (range, 10 to 57). Complications occurred in 26 infants (36%), including intravenous catheter sepsis (n = 15), pneumatosis (n = 2), pneumonia (n = 1), bowel obstruction (n = 7), wound infection (n = 5), and SVC thrombosis (n = 1). Survival rate was 100%. Thirty-two infants had complex defects; 27 patients had atresias, stenosis, or perforations; and 3 had volvulus. The average estimated gestational age was 34 weeks (range, 26 to 38), and birth weight was 2.0 kg (range, 0.9 to 4.0). Primary repair was performed in 65% and silo placement in 35%. Mechanical ventilation was required for 22.3 days (range, 2 to 14). Enteral feedings were initiated at 22.5 days (range, 6 to 56) with full feedings achieved at 50 days (range, 21 to 113). Fourteen infants required home total parenteral nutrition (TPN). The LOS was 85.4 days (range, 24 to 270). A total of 47 complications occurred in the complex group including catheter sepsis (n = 15), short bowel syndrome (n = 7), pneumatosis (n = 3), bowel obstruction (n = 4), pneumonia (n = 2), superior vena cava thrombosis (n = 1), enterocutaneous fistula (n = 1), and 9 deaths (28% mortality rate). These data indicate gastroschisis can be divided into low-risk (simple) and high-risk (complex) categories. These 2 groups have significant differences in clinical behavior, postsurgical complications, LOS, and mortality rate (0 v 28%). Although the overall survival rate was 91% (94 of 103), parents, referring physicians, and insurers must be made aware of the impact of risk categorization on the estimated cost, LOS, and outcomes.

Echographic detection of latent severe thrombotic stenosis of the superior vena cava and innominate vein in patients with a pacemaker: integrated diagnosis using sonography, pulse Doppler, and color flow.

Thrombosis of the innominate vein and SVC is a serious complication in patients with pacemakers, inducing pulmonary embolism or SVC syndrome. Venography is the definitive method for its diagnosis; however, it is too invasive for related studies. The purpose of this study was to validate sonography, pulse Doppler, and color flow in detecting noninvasively innominate vein or SVC thrombosis in patients with pacemakers. In 53 patients with pacemakers, the 1 severe SVC stenosis and 18 severe innominate vein stenoses due to thrombosis were diagnosed by digital subtraction angiography. Sonography accurately showed the severe SVC stenosis due to thrombosis, but had limitations on the innominate vein thrombosis. Color flow demonstrated mosaic flow, indicating poststenotic turbulence due to stenosis of the innominate vein and SVC caused by thrombosis in 15 of 16 patients, and pulse Doppler disclosed absence of flow due to complete occlusion of the innominate vein in 2 of 2 patients. Sensitivity and specificity for detecting severe innominate vein stenosis due to thrombosis using combined color flow and pulse Doppler was 94% and 100%, respectively. In conclusion, sonography, pulse Doppler, and color flow allow accurate detection of severe innominate vein or SVC stenosis due to thrombosis, and are therefore useful for the follow-up of patients with a pacemaker.

Successful thrombolysis of SVC thrombosis associated with Hickman lines and continuous infusion chemotherapy

In a pilot study of continuous infusion 5-fluorouracil and intermittent bolus doxorubicin and cyclophosphamide in women with breast cancer, four of 24 patients developed symptomatic superior vena cava or innominate vein thrombosis associated with the Hickman line, despite prophylactic treatment with very low dose warfarin (1–3 mg/day). In all four patients, local thrombolysis with streptokinase was successful and chemotherapy was continued through the Hickman line under anticoagulant cover, maintaining an international normalized ratio of 2.0–3.0. No patient developed recurrent thrombosis. Prophylactic anticoagulation should be considered in patients receiving continuous infusion chemotherapy through Hickman lines, as they are at risk of proximal vein thrombosis. A randomized study is needed to address the question of the optimum anticoagulant regimen to prevent such thromboses.

Mortality in Patients on Home Parenteral Nutrition

Fifty out of 228 patients recorded on the U.K. Home Parenteral Nutrition Register have died. The earliest to die was at 10 days following the commencement of home parenteral nutrition (HPN), and the longest to die was after 5 1/2 years. Half of the patients who died, did so within 6 months of commencing HPN. Sixty % died of their underlying disease. Most patients with scleroderma or an underlying malignancy are dead within a year of commencing HPN. In contrast, patients with Crohn's disease or the short bowel syndrome due to volvulus do well. In only 14 patients was death attributable to the administration of HPN. In this group the main causes were septicemia, SVC thrombosis, and hepatic failure. Our study suggests that HPN should be used in patients with malignancy and scleroderma only in exceptional circumstances and that further work is necessary for the prevention of SVC thrombosis.

118 NON-INVASIVE EVALUATION OF SUPERIOR VENA CAVA (SVC) AND RIGHT ARTERIAL (RA) THROMBOSIS COMPLICATING CENTRAL HYPERALIMENTATION (CHA) IN PREMATURE INFANTS

Within the last 6 mos., we have encountered 3 infants who presented with signs of SVC obstruction complicating CHA. Signs occurred a mean of 30 days after placement of the central line (range 21-42 days) and included deterioration of pulmonary status with pleural effusions and edema of the upper trunk. In each case 2-D echocardiography (2DE) at a frequency of 5 mHz revealed a large, mobile echodense mass in the RA, with extension through the tricuspid valve into the right ventricular outflow tract. Two infants had the diagnosis confirmed by angiography and were treated with intravenous heparin for 10 days. The other infant did not receive heparin. Serial 2DE in the treated infants showed a decrease in size of the RA thrombosis in one and complete resolution in the other. Contrast echocardiography in one of the treated infants demonstrated patency of the inferior vena cava while the SVC appeared totally occluded. These findings were confirmed at autopsy. In the untreated patient the RA thrombosis remained stable in size and was operatively removed at age 6 mos. This series indicates that 2DE is a helpful non-invasive means of diagnosing SVC and RA thrombosis complicating CHA when the clinical signs suggest its presence. Further, serial 2DE is helpful in evaluating the status of the RA thrombosis during heparin therapy and in aiding the decision concerning operative removal.