Thoracic Duct Flow Research Articles

Diagnostic imaging, therapeutic interventions and suggestions for thoracic duct congestion in postoperative hepatic lymphorrhea: a retrospective analysis of 20 cases

ObjectiveTo retrospectively evaluate thoracic duct (TD) congestion in hepatic lymphorrhea (HL) and propose treatment suggestions.MethodsRetrospectively analyze cases of postoperative HL admitted from August 2007 to November 2023. Twenty cases were enrolled and followed up. The medical history, ascites characteristics, lymphoscintigraphy, direct lymphangiography, and other clinical data were reviewed.ResultsTwenty patients with ascites after cholecystectomy or radical gastrectomy were included. There were 15 patients with cirrhosis and 5 patients with hepatitis. Ascites were light yellow even if the patients had a non-low-fat diet. Triglyceride level mean of ascites was 0.61 ± 0.20 mmol/L. There were 94.1% (16/17) of patients whose ascitic cholesterol ≥ 45 mg/dL or SAAG < 11.0 g/L. Mild abdominal radioactivity was shown in 89.5% (17/19) patients. Left subclavian-jugular venous angle radioactivity was observed in 84.2% (16/19) patients. In 10% (2/20) cases, lipiodol presenting as oil droplets traveled upwards quickly and flowed into the vein rapidly. In 90% (18/20) cases, tortuous and dilated thoracic duct, stagnant lipiodol, and poor flow into the vein were demonstrated. One patient refused treatment and died soon. By thoracic duct outlet reconstruction combined with other treatments, 16 patients were cured and the ascites of another 3 patients were controlled.ConclusionsTD congestion and elevated lymphatic pressure could be caused by increased lymph flow and TD outlet stenosis. TD decompression by outlet reconstruction may be an alternative approach to HL.

Ascites in Animals With Right Heart Failure: Correlation With Lymphatic Dysfunction.

Background Congestive heart failure is a leading cause of morbidity and mortality worldwide. One of the signs of congestive heart failure is fluid overload including pulmonary edema, peripheral edema, and ascites. The cause of fluid overload remains incompletely understood, and management of these patients continues to be a challenge. The role of lymphatic circulation abnormalities in the cause and pathophysiology of fluid overload also remains unclear. Here we report on a study in a large animal model of right heart failure caused by severe tricuspid regurgitation comparing cardiovascular and lymphatic findings in a group of animals that did not develop ascites with a group of animals that developed ascites. Methods and Results Thirteen Yorkshire pigs were included in this study divided into 2 groups. Group 1 included 6 animals that did not develop ascites, and Group 2 included 7 animals that had developed ascites. The groups were compared on hemodynamic parameters as well as comparison of the animal's lymphatic anatomy and function. There was no difference between the groups in degree of tricuspid regurgitation and central venous pressure, with inferior vena cava pressure measuring 11.6±1.6 versus 13.2±3.7 (P=0.534) and superior vena cava pressure measuring 12.0±2.3 versus 13.7±3.2 (P=0.366). There was also no difference between the groups in all measured hemodynamic parameters, including right ventricular pressure, pulmonary artery pressure, and left ventricular function. The weighted liver size in the ascites group was significantly larger than in the nonascites group (30.3±12.4 versus 63.3±14.0 mL/kg, respectively; P=0.001). The 2 groups also differed in the number of animals with regurgitant thoracic duct flow (Group 1: 1/6,17% versus Group 2: 6/7, 86%; P=0.029) and the minimal thoracic duct diameter (Group 1: 2.3±0.3 versus Group 2: 4.2±2.2; P=0.035). Conclusions In animals with right heart failure caused by severe tricuspid regurgitation, fluid overload did not correlate with hemodynamic parameters but rather with changes in the lymphatic system, including regurgitant lymphatic flow, minimal thoracic duct diameter, and liver size. This study is consistent with lymphatic dysfunction and not cardiovascular function playing a significant role in the cause of fluid overload. Further studies are needed to confirm these findings.

Changes of thoracic duct flow and morphology in an animal model of elevated central venous pressure

Objective: Investigation of lymph fluid dynamics in thoracic duct during central venous pressure elevation. Background: Lymphatic flow is affected by elevated central venous pressure (CVP) in congestive heart failure. The changes of thoracic duct (TD) lymph flow have not been studied chronically in the setting of elevated CVP. This study is to investigate fluid dynamics and remodeling of the TD in the elevated CVP animal model. Methods: A flow probe was implanted on the swine TD (n = 6) and tricuspid regurgitation (TR) was created by cutting tricuspid chordae percutaneously. Six swine were used as control group animals. The TD flow was measured for 2 weeks (baseline) before TR and 4 weeks postop-TR surgery. Arterial pressure and CVP were measured. The pressure and flow in the TD were measured percutaneously. Histological and morphological analyses were performed. Results: TR resulted in an increase in CVP from 4.2 ± 2.6 to 10.1 ± 4.3 mmHg (p < 0.05). The lymph flow in the TD increased from 0.78 ± 1.06 before TR to 8.8 ± 4.8 ml/min (p < 0.05) 2 days post-TR and remained plateau for 4 weeks, i.e., the TD flow remained approximately 8–11 fold its baseline. Compared to the 8.1 ± 3.2 mmHg control group, the TD average pressures at the lymphovenous junction increased to 14.6 ± 5.7 mmHg in the TR group (p < 0.05). The TD diameter and wall thickness increased from 3.35 ± 0.37 mm and 0.06 ± 0.01 mm in control to 4.32 ± 0.57 mm and 0.26 ± 0.02 mm (p < 0.05) in the TR group, respectively. Conclusion: The elevated CVP results in a significant increase in TD flow and pressure which causes the TD’s outward remodeling and thickening. Our study implicates that the outward remodeling may result in the TD valve incompetence due to failure coaptation of leaflets.

THORACIC DUCT STENT-GRAFT DECOMPRESSION WITH 3-MONTH PATENCY: REVISITING A HISTORICAL TREATMENT OPTION FOR PORTAL HYPERTENSION

This report introduces the rationale for thoracic duct stent-graft decompression in cirrhotic patients with portal hypertension and provides a case example with 3-month stentgraft patency. Thoracic duct flow and pressure are elevated in cirrhosis. Historically, complications of portal hypertension have been successfully treated with external drainage of the thoracic duct or surgical lymphovenous bypass. A 45-year-old woman with cirrhosis, chronic portosplenomesenteric thrombosis, and acute variceal hemorrhage underwent percutaneous thoracic duct stent-graft placement across the lymphovenous junction. The hemorrhage subsequently resolved and follow up endoscopy demonstrated decompression of the bleeding varices. Venography 40 days later demonstrated a partially patent stent-graft with fibrin sheath formation distally. The stent-graft was extended distally to the right atrium and was fully patent on venography 3 months later. The patient had no further episodes of hemorrhage.

Video‐assisted thoracoscopic thoracic duct sealing is inconsistent when performed with a bipolar vessel‐sealing device in healthy cats

To describe a technique for video-assisted thoracoscopic (VATS) thoracic duct ligation (TDL) in normal cats with a bipolar vessel-sealing device and to assess durability of the seal. Prospective case series. Six healthy research cats. Cats were placed under anesthesia for computed tomography lymphangiography (CTLA) to identify thoracic duct anatomy. On the basis of CTLA findings, cats were positioned in either right or left lateral recumbency for a 3-port VATS TDL. Thoracic duct branches were dissected from the aorta after subcutaneous indirect near-infrared fluorescence (NIRF) lymphography with indocyanine green was performed to optimize detection. A vessel-sealing device was used to seal each thoracic duct in 1 or more locations. Postattenuation, indirect NIRF lymphography was repeated to confirm complete occlusion of thoracic duct flow. CTLA was repeated in all cats 3 months postoperatively. The thoracic duct was surgically approached from the right in 3 cats and from the left in 3 cats. A median of 2.5 (range 1-6) TDL seal sites were applied. In 2 cats, leakage of chyle was detected during dissection. At 3 months postoperatively, CTLA confirmed reestablished chylous flow in 5 of 6 cats, appearing to occur through recanalization of previously sealed sites rather than through development of de novo lymphatic vessels. VATS TDL is feasible in cats, although the variable and delicate nature of feline thoracic duct anatomy should be considered preoperatively. Bipolar vessel-sealing devices are not a durable modality for thoracic duct sealing in healthy cats in a seal only fashion.

Two cases of chylopericardium after aortic valve surgery

Chylopericardium is a rare clinical condition. It is largely idiopathic but could be iatrogenic from breached thoracic duct collaterals or secondary to thoracic duct flow obstruction. We describe 2 patients seen in a single cardiothoracic center within 6 weeks, and detail the clinicopathologic correlation of an unusual complication of cardiac surgery, as well as provide an algorithm for the diagnosis and management of postcardiotomy pericardial chylous effusion.

Near-infrared fluorescence imaging of thoracic duct anatomy and function in open surgery and video-assisted thoracic surgery

Chylothorax resulting from thoracic duct damage is often difficult to identify and repair. We hypothesized that near-infrared fluorescent light could provide sensitive, real-time, high-resolution intraoperative imaging of thoracic duct anatomy and function. In 16 rats, 4 potential near-infrared fluorescent lymphatic tracers were compared in terms of signal strength and imaging time: indocyanine green, the carboxylic acid of IRDye 800CW (LI-COR, Lincoln, Neb), indocyanine green adsorbed to human serum albumin, and IRDye 800CW conjugated covalently to human serum albumin. Optimal agent was validated in 8 pigs approaching human size (n = 6 by open surgery with FLARE imaging system [Beth Israel Deaconess Medical Center, Boston, Mass] and n = 2 by video-assisted thoracoscopic surgery minimally invasive [m-FLARE] imaging system [Beth Israel Deaconess Medical Center]). Lymphatic tracer injection site, dose, and timing were optimized. For signal strength, sustained imaging time, and clinical translatability, the best lymphatic tracer was indocyanine green, which is already Food and Drug Administration approved for other indications. In pigs, a simple subcutaneous injection of indocyanine green into lower leg (≥ 36 μg/kg), provided thoracic duct imaging with onset of about 5 minutes after injection, sustained imaging for at least 60 minutes after injection, and signal-to-background ratio of at least 2. With this technology, normal thoracic duct flow, collateral flow, injury models, and repair models could all be observed under direct visualization. Near-infrared fluorescent light could provide sensitive, sustained, real-time imaging of thoracic duct anatomy and function during both open and video-assisted thoracoscopic surgery in animal models.

Gut emptying affects dietary fat contribution to postprandial lipemia following sequential meals in healthy subjects

Objective The present study examined the kinetic of plasma triacylglycerol (TAG) and gut emptying after sequential ingestion of breakfast and lunch, and the contribution of dietary fat ingested at breakfast to subsequent TAG after lunch. Methods Nine subjects ingested a breakfast (0730 h) and a lunch (1200 h) containing 25 and 44 g of fat, respectively. [1- 13C] palmitate was added in breakfast only. Plasma TAG and chylomicron-TAG (CM-TAG) concentrations and [1- 13C] palmitate enrichment were sequentially measured. On a consecutive day, an identical breakfast labeled with 123I-Lipiodol was ingested, followed by a lunch for three controls. 123I-Lipiodol dynamics was followed in vivo by scintigraphic imaging focused on the stomach, small bowel, and thoracic duct arch. Results An early rise in plasma and CM-TAG was observed after lunch ingestion. After breakfast, [1- 13C] palmitate enrichment was maximal 150 and 210 min in plasma TAG and CM-TAG, respectively, decreased thereafter, and increased rapidly (50 min for plasma TAG and 30 min for CM-TAG) after lunch ingestion. Scintigraphic imaging appeared to show that fat ingested at breakfast was retained in part within the gut at lunch time. For the three subjects who ingested a lunch, a decrease of activity in the stomach and small bowel and a tendency for increased activity in the thoracic arch were observed. Conclusion Contribution of fat ingested at breakfast to lipemia after lunch is confirmed. Fat ingested at breakfast was partly retained within the gut and was mobilized after lunch ingestion, as assessed by acceleration of gut emptying and thoracic duct flow after lunch.

The pharmacologic spectrum of furosemide

AbstractObjective: To review the clinical spectrum and mechanisms of action of furosemide in human and small animal veterinary patients.Data sources: Review of human and veterinary literature.Data synthesis: Furosemide is used primarily for its properties as a loop diuretic; however, it has many other actions that may be clinically applicable. Furosemide has a vasodilatory effect that precedes diuresis that may confer its immediate benefit in patients with volume overload. Furosemide can be inhaled to relieve dyspnea in patients with bronchospasm. Furosemide also shows promise as an adjunct to antiseizure therapy to help control epilepsy, status epilepticus, and acute ischemic damage related to seizures. It has activity as an antioxidant, iodine depletive, and may increase thoracic lymph duct flow. Reported furosemide side effects include altered drug metabolism, electrolyte depletion, ototoxicity, mucociliary impairment, endocrine and exocrine pancreatic effects, delayed wound healing, sulfonamide toxicity, and thyroid binding interference. It is worthwhile to consider the implications of these effects when using furosemide either alone or in combination with other drugs.Conclusions: Despite the research in animal models that demonstrates a wide spectrum of pharmacologic activity, furosemide has not been widely recognized or used clinically in veterinary medicine except as a loop diuretic.

Unusual cause of dyspnea after pneumonectomy

The patient was readmitted to the hospital 2 weeks after surgery because of increasing shortness of breath. He had not experienced paroxysmal nocturnal dyspnea, orthopnea, angina, or symptoms of acute cardiac decompensation. The patient’s oxygen saturation was 90% while breathing room air, his pulse was regular at 80 beats/min, and his blood pressure was 130/70 mmHg. There were no signs of heart failure. The trachea was central to the suprasternal notch on palpation. Chest examination revealed dullness to percussion and auscultation on the left side and good aeration on the right side. An electrocardiogram revealed no changes in a right bundlebranch block that was seen preoperatively. Levels of cardiac enzymes (troponin-I and creatine kinase-MB) were normal. Computed tomography and computed tomography angiography of the chest showed no evidence of pulmonary embolism or pulmonary infection. Positive findings included a small rightsided pleural effusion, mild emphysematous changes in the right lung, and near-complete filling with fluid of the pleural space within the left hemithorax. A portable chest radiograph was also obtained, and the image is shown in Fig 1. What was the diagnosis?

Lymph Flow Pattern in the Intact Thoracic Duct in Sheep

1. To study the lymph flow dynamics in the intact thoracic duct, we applied an ultrasound transit-time flow probe in seven anaesthetized and four unanaesthetized adult sheep (approximately 60 kg). In unanaesthetized non-fasting animals we found that lymph flow in the thoracic duct was always regular pulsatile (pulsation frequency, 5.2 +/- 0.8 min-1) with no relation to heart or respiratory activity. At baseline the peak level of the thoracic duct pulse flow was 11.6-20.7 ml min-1 with a nadir of 0-3.6 ml min-1. Mean lymph flow was 5.4 +/- 3.1 ml min-1. The flow pattern of lymph in the thoracic duct was essentially the same in the anaesthetized animals. 2. In both the anaesthetized and unanaesthetized animals, the lymph flow response to a stepwise increase in the outflow venous pressure showed interindividual variation. Some were sensitive to any increase in outflow venous pressure, but others were resistant in that lymph flow did not decrease until outflow venous pressure was increased to higher levels. This resistance was also observed in the high lymph flow condition produced by fluid infusion in the anaesthetized animal and mechanical constriction of the caudal vena cava in the unaesthetized animals. Pulsation frequency of the thoracic duct flow initially increased and then decreased with a stepwise increase in the outflow venous pressure. This initial increase might be a compensatory response to maintain lymph flow against elevated outflow venous pressure. 3. To test the effect of long-term outflow venous pressure elevation in unanaesthetized sheep, outflow venous pressure was increased by inflation of a cuff around the cranial vena cava for 1, 5 or 25 h. The cuff was inflated to a level where lymph flow was reduced. Lymph flow remained low or decreased further during the entire cuff-inflation period. We calculated the lymph debt caused by the outflow venous pressure elevation and the amount 'repaid' when venous pressure returned to normal. Lymph debt for 25 h was 6400 ml but only 200 ml was repaid. Since we observed no visible oedema formation in the lower body of the sheep, the non-colloidal components of the lymph must have been reabsorbed into the bloodstream, most likely in the lymph nodes.

Pressure within the thoracic duct modulates lymph composition

The amount of lymph received by the thoracic duct depends on each contributing organ's ability to produce interstitial fluid and generate a pressure differential moving lymph into the central lymphatic circulation. It has been reported that varying the pressure within the thoracic duct could alter each organ's contribution to thoracic duct flow. The thoracic duct above the diaphragm was cannulated to obtain lymph from the liver, gut, and lower body. Pressure within the thoracic duct was elevated serially by increasing the lymphatic cannula outflow height. This caused lymph protein concentration to increase while chyle concentration (measured by absorbance) decreased. The data demonstrate that as thoracic duct pressure increases, the percentage contribution of gut lymph flow (as represented by chyle concentration) decreases while the contribution of lymph originating within the liver (as indicated by higher protein concentration) increases. We conclude that pressure variation within the central lymphatic system affects the amount of lymph or edema fluid leaving any given organ.

Angiotensin II infusion increases thoracic duct lymph flow in chronically catheterized sheep.

Both pregnancy and estrogen administration are associated with a decrease in the systemic vasculature pressor response to angiotensin II infusion; however, the lymphatic vessel system response is not clear. In the present study we infused angiotensin II to nine nonpregnant splenectomized ewes with 0.1, 10, or 1,000 ng X kg-1 X min-1 for a 5-min period at each dose. At the lowest dose the mean arterial pressure increased from 10 to 20% over base line. At the highest dose, the left thoracic duct flow rate peaked at 361% 10 min after the infusion was started, whereas arterial pressure peaked at 183% of the control value. Peak lymph flow occurred 4-6 min after the maximal increase in mean systemic arterial pressure. Neither hematocrit nor venous pressure were altered at any of the doses administered. This suggests that the interstitial fluid space pressure remained unchanged and that the increase in lymph flow was not secondary to fluid transfer from the intravascular system. We postulate, therefore, that the effect of angiotensin II in the increase of lymph flow rate is by direct action on the lymphatic vessels themselves.

CIRCUMAORTIC CYSTERNA CHYLI LIGATION

Abdominal and thoracic lymphangiograms were done on seven dogs by cannulation of a mesenteric lymphatic. Dissection and ligation of the cysterna chyli were attempted in two dogs with poor success. Obstruction of thoracic duct flow by circumaortic ligation of the cysterna chyli was attempted in the remaining five dogs. Repeated contrast studies were done immediately following ligation and again after one to seven weeks. The dogs were killed, and postmortem examinations were done immediately after the third lymphangiogram. The circumaortic ligation was effective in all cases as judged by the immediate follow‐up study, however, in three of the subsequent follow‐up studies, thoracic duct flow had returned through recanalization past the ligature.

The significance of respiration for thoracic duct flow in relation to other driving forces of lymph flow.

Experiments were performed to study the effect of respiratory intrathoracic pressure changes upon thoracic duct lymph propulsion as compared to other forces driving lymph flow in anaesthetized and artificially ventilated dogs. The effect of an open bilateral pneumothorax upon thoracic duct flow and protein composition was determined at rest, with passive limb movement and during saline infusion. The effect of hyperventilation was also tested.

Development of an ultrasonic device for the destruction of thoracic duct lymphocytes, in vivo

The elimination of circulating lymphocytes in patients exhibiting autoimmune disease symptoms (e.g., rheumatoid arthritis) results in marked improvement of the signs and symptoms of the disease. The authors investigate the feasibility of using a hollow cylindrical ultrasonic transducer implanted in the patient to destroy the thoracic duct lymphocytes. Cultures of human peripheral blood lymphocytes are exposed, in vitro, to ultrasound waves. Measurements of thoracic duct flow rate, heating of the cell medium, voltage and frequency applied to the ultrasonic transducer in a pulsed or continuous mode of operation are investigated along with the optimization of these parameters. The advantages of an ultrasound device over other radiative sources were reported.

Renal contribution to thoracic duct lymph in dogs.

1. The renal contribution to thoracic duct lymph was measured in seventeen anaesthetized fasting dogs by measurement of thoracic duct flow before and after renal arterial occlusion.2. In eight experiments it was shown that thoracic duct flow and glomerular filtration rate were not significantly affected by the operation to expose the renal artery.3. In three experiments occlusion of the renal vein, after release of arterial occlusion, resulted in a sudden increase in thoracic duct flow.4. In animals infused with isotonic saline or dextrose (approximately 1 ml./min) the average values obtained for control thoracic duct flow, left renal flow and right renal flow were approximately 2.0, 0.7 and 0.3 ml./hr/kg body wt.: in non-infused animals these values were 1.4, 0.4 and 0.35 ml./hr/kg body wt. respectively.5. Possible reasons for the apparently smaller lymph flow from the right than the left kidney, and the relationship between the renal contribution to thoracic duct flow and actual renal lymph flow are discussed.6. Close correlation was found between control thoracic duct flow and body weight and between renal lymph flow and control thoracic duct flow.

Pulmonary lymph flow and the uptake of liquid from the lungs of the lamb at the start of breathing

1. Lymph from the lungs of lambs and sheep was found to enter both the right lymph duct and the thoracic duct. Right lymph duct flow was collected by constructing a venous sac, the venous tributaries of which were ligated but which the right lymph duct entered; thoracic duct flow was collected by cannulating the duct. Lymph from sites other than the lungs was excluded from the collections.2. Measurements were made of the surface tension characteristics of lung extracts and of the liquid present in foetal lungs. These values were used together with gestational age and crown-rump length to designate the foetal lambs into mature and immature groups.3. Lymph flow from the lungs averaged 0.99 ml./kg body wt./hr in immature foetal lambs, and 1.81 ml./kg/hr in mature foetal lambs before the start of ventilation. Lymph flow from the lungs of spontaneously delivered new-born lambs (mean age 51 hr) averaged 0.86 ml./kg/hr. In adult ewes right lymph duct flow averaged 0.11 ml./kg/hr and total lung lymph flow was estimated indirectly to be 0.33 ml./kg/hr. Calculated rates of protein flow in lung lymph (flow x protein concentration) were greater in foetal lambs than in adult sheep.4. Total thoracic duct flow averaged 2.48 ml./kg/hr in immature foetal lambs, 5.30 ml./kg/hr in mature foetal lambs, 3.65 ml./kg/hr in new-born lambs, and 2.92 ml./kg/hr in adult ewes.5. At the start of ventilation there was an increase in lymph flow from the lungs, which at 15-30 min reached a mean of 6.4 ml./kg/hr in mature lambs and 2.6 ml./kg/hr in immature lambs. At the same time the protein concentration of lymph decreased but the calculated protein flow increased.6. The lungs of foetal lambs weighed more than the lungs of spontaneously delivered new-born lambs, and the difference could be accounted for by liquid which could be aspirated through the trachea of the foetal lamb. On ventilation of the lungs for 2 hr, without first allowing the escape of any lung liquid, lung weight measurements indicated that about 66% of the lung liquid had been taken up in mature lambs and about 50% in immature lambs.7. It was concluded that the rate at which lymph is formed in the lungs is greater per kilogram body weight in foetal than in new-born lambs and greater in them than in ewes. The increase in lymph flow at the start of ventilation could account for the removal of about 40% of the liquid present in the lungs of the mature foetus and about 25% of the liquid in the lungs of the immature foetus.

Effect of mannitol on the flow of thoracic duct lymph and its renal component.

1. Thoracic duct flow during mannitol diuresis was measured in 23 anaesthetised dogs. With continuous 5 per cent mannitol infusions at 1 ml./minute thoracic duct flow (average 2.1 ml./hr./kg.) did not differ significantly from that obtained previously in non-diuretic dogs (average 2.06 ml./hr./kg.) infused with saline or dextrose at a similar rate. Intravenous injections of 5 ml. of 20 per cent mannitol had little or no effect on thoracic duct flow. Injections of 10, 50 or 100 ml. of 20 per cent mannitol caused an increase in thoracic duct flow which was related to the rise in urine flow.

Effect of increased systemic venous pressure on lymph pressure and flow.

Effect of increased systemic venous pressure on lymph pressure and flow.