scholarly journals Oesophageal Variceal-Pulmonary Venous Fistula - A Rare Cause of a Right-to-Left Shunt

2020 ◽  
Author(s):  
Neeraja Swaminathan ◽  
Siddique Chaudhary
Keyword(s):  
Transplant Patient ◽  
Venous Pressure ◽  
Systemic Circulation ◽  
Portal System ◽  
Oesophageal Varices ◽  
Rectal Varices ◽  
Paradoxical Emboli ◽  
Left Pulmonary Vein ◽  
Venous Fistula ◽  
Main Complication

Oesophageal varices are a dilated submucosal venous plexus in the lower third of the oesophagus which result from increased pressure in the portal venous system. The portal system is connected to the systemic circulation in specific locations referred to as sites of portosystemic anastomosis. An increase in portal venous pressure is therefore reflected at these anastomotic sites, causing manifestations such as oesophageal varices, rectal varices, caput medusae and splenorenal shunts. Varices do not cause symptoms until they leak or rupture and this is the main complication which requires prompt treatment. Here, we present a post-liver transplant patient with metastatic hepatocellular carcinoma who had oesophageal varices that fistularized with a left pulmonary vein, thus creating a right-to-left shunt. Right-to-left shunts are usually intracardiac or intrapulmonary in location. The complications of a right-to-left shunt include predominantly hypoxia, cyanosis and, sometimes, paradoxical emboli in the case of intracardiac shunts. This patient had a very uncommon cause of such a shunt caused by a direct fistulous connection.

Non-invasive methods in the assessment of portal hypertension severity

2021 ◽  
Vol 75 (2) ◽  
pp. 125-133
Author(s):  
Soňa Franková ◽  
Jan Šperl
Keyword(s):  
Portal Hypertension ◽  
Liver Fibrosis ◽  
Shear Wave ◽  
Transient Elastography ◽  
Venous Pressure ◽  
Liver Stiffness ◽  
Invasive Technique ◽  
Hepatic Veins ◽  
Oesophageal Varices ◽  
Non Invasive

Portal hypertension represents a wide spectrum of complications of chronic liver diseases and may present by ascites, oesophageal varices, splenomegaly, hypersplenism, hepatorenal and hepatopulmonary syndrome or portopulmonary hypertension. Portal hypertension and its severity predicts the patient‘s prognosis: as an invasive technique, the portosystemic gradient (HPVG – hepatic venous pressure gradient) measurement by hepatic veins catheterisation has remained the gold standard of its assessment. A reliable, non-invasive method to assess the severity of portal hypertension is of paramount importance; the patients with clinically significant portal hypertension have a high risk of variceal bleeding and higher mortality. Recently, non-invasive methods enabling the assessment of liver stiffness have been introduced into clinical practice in hepatology. Not only may these methods substitute for liver biopsy, but they may also be used to assess the degree of liver fibrosis and predict the severity of portal hypertension. Nowadays, we can use the quantitative elastography (transient elastography, point shear-wave elastrography, 2D-shear-wave elastography) or magnetic resonance imaging. We may also assess the severity of portal hypertension based on the non-invasive markers of liver fibrosis (i.e. ELF test) or estimate clinically signifi cant portal hypertension using composite scores (LSPS – liver spleen stiff ness score), based on liver stiffness value, spleen diameter and platelet count. Spleen stiffness measurement is a new method that needs further prospective studies. The review describes current possibilities of the non-invasive assessment of portal hypertension and its severity.

The Generation of Kinins in the Blood of Dogs during Hypotension Due to Haemorrhage

1970 ◽  
Vol 39 (3) ◽  
pp. 349-365 ◽  
Author(s):  
H. E. Berry ◽  
J. G. Collier ◽  
J. R. Vane
Keyword(s):  
Blood Pressure ◽  
Time Course ◽  
Venous Pressure ◽  
Venous Blood ◽  
Systemic Circulation ◽  
Substantial Effect ◽  
Mixed Venous Blood ◽  
Shed Blood ◽  
Arterial Blood ◽  
Organ Technique

1. Circulating kinins were detected and continuously assayed during hypotension due to haemorrhage in dogs, using the blood-bathed organ technique and isolated strips of cat jejunum as the assay tissue. 2. In arterial blood kinin concentrations of 1–5 ng/ml were attained after a hypotension of 35–65 mmHg had been maintained for 10–190 min. When portal venous blood was simultaneously assayed kinins appeared earlier and in concentrations 1–2 ng/ml higher than in arterial blood. No differences in time course of kinin generation or in concentration were found when mixed venous blood and arterial blood were compared. In those instances in which the blood pressure was restored to normal by returning the shed blood, kinin formation stopped. 3. Kinin generation was due to the presence in the circulation of a kinin-forming enzyme, such as kallikrein. When kallikrein was infused into the portal vein, it was partially inactivated by the liver. 4. Prolonged intravenous infusions of kallikrein (20–60 mu kg−1 min−1) generated kinins in the circulation in concentrations (1–5 ng/ml) which were well maintained throughout the infusion, demonstrating that kinin generation is not limited by depletion of the precursor kininogen; nevertheless, the effects of kallikrein infusions on the blood pressure and central venous pressure waned. 5. It is concluded that in hypotension due to haemorrhage, an active kallikrein appears in the portal circulation. Delay in the appearance of kallikrein in the systemic circulation may be due to the kallikrein inactivating mechanism of the liver. This inactivating mechanism may fail during shock. Kinins are generated in amounts sufficient to have a substantial effect on the circulation and an influence on the course of events in shock.

Ultrasound Guided Noninvasive Measurement of Central Venous Pressure

2008 ◽  
pp. 1331-1337
Author(s):  
Vikram Aggarwal ◽  
Yoonju Cho ◽  
Aniruddha Chatterjee ◽  
Dickson Cheung
Keyword(s):  
Heart Failure ◽  
Central Venous Pressure ◽  
Venous Pressure ◽  
Vena Cava ◽  
Heart Association ◽  
Systemic Circulation ◽  
The Body ◽  
Physiological Parameter ◽  
Central Venous ◽  
Mean Pressure

Central venous pressure (CVP) is a measure of the mean pressure within the thoracic vena cava, which is the largest vein in the body and responsible for returning blood from the systemic circulation to the heart. CVP is a major determinant of the filling pressure and cardiac preload, and like any fluid pump, the heart depends on an adequate preload to function effectively. Low venous return translates into a lower preload and a drop in overall cardiac output, a relationship described by the Frank-Starling Mechanism. CVP is an important physiological parameter, the correct measure of which is a clinically relevant diagnostic tool for heart failure patients. In addition to other vitals such as heart rate and mean arterial pressure, accurate measures of central venous pressure through simple diagnostic instrumentation would provide physicians with a clear picture of cardiac functionality, and allow for more targeted treatment. Recent literature has also shown that measuring CVP can be an important hemodynamic indicator for the early identification and treatment of more widespread conditions, such as sepsis (Rivers, Nguyen, Havstad, & Ressler, 2001). With over five million patients (American Heart Association, http://www.americanheart.org/presenter. jhtml) in the U.S. presenting with heart failure-like symptoms annually, a current challenge for physicians is to obtain a quick and accurate measure of a patient’s central venous pressure in a manner that poses minimum discomfort.

Pulmonary and systemic blood pressure response to serotonin: role of chemoreceptors

1961 ◽  
Vol 201 (2) ◽  
pp. 369-374 ◽  
Author(s):  
K. Braun ◽  
S. Stern
Keyword(s):  
Pulmonary Artery ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Femoral Vein ◽  
Venous Pressure ◽  
Systemic Blood Pressure ◽  
Systemic Circulation ◽  
Ascending Aorta ◽  
Pulmonary Arterial

Large doses of serotonin (200 µg/ kg) in the anesthetized open-chest dog, administered into the femoral vein, right heart, pulmonary artery, left heart, ascending aorta or common carotid arteries, caused a marked pressor response in the systemic circulation. The latent period became shorter with the shift of the site of the injection toward the ascending aorta. After injection into the descending aorta a "double peak" pressor response was obtained. These observations, together with the demonstration of a much less pronounced pressor effect after elimination of the aortic and carotid chemoreceptors, indicate participation of chemoreceptor stimulation in the systemic pressor response. In the pulmonary artery the pressure rose markedly and consistently. A rise in the pulmonary venous pressure without any significant change in the left atrial pressure was observed, indicating pulmonary venous constriction. Chemoreceptor stimulation was shown to play a part also in the rise of both the pulmonary arterial and pulmonary venous pressures.

Alpha- and beta-adrenergic mechanisms in the control of vascular capacitance by the carotid sinus baroreflex system

1994 ◽  
Vol 267 (1) ◽  
pp. H201-H210 ◽  
Author(s):  
K. Shigemi ◽  
M. J. Brunner ◽  
A. A. Shoukas
Keyword(s):  
Adrenergic Receptor ◽  
Carotid Sinus ◽  
Venous Pressure ◽  
Systemic Circulation ◽  
Adrenergic System ◽  
Beta Adrenergic ◽  
Vascular Volume ◽  
Adrenergic Mechanisms ◽  
Vascular Capacitance ◽  
Carotid Sinus Baroreflex

We examined the active and passive contributions of the alpha- and beta-adrenergic receptor mechanisms to the changes in systemic vascular capacitance caused by the carotid sinus baroreflex system in anesthetized, vagotomized dogs. The carotid sinuses were isolated from the systemic circulation and perfused with controlled pressures. To determine the changes in vascular capacitance, a constant flow, constant venous pressure cardiopulmonary bypass was used. The changes in unstressed vascular volume were calculated when carotid sinus pressure was reduced from 200 to 50 mmHg without any adrenergic receptor antagonist, with either an alpha- (phentolamine) or a beta- (propranolol) antagonist and then with both. The reflex change in unstressed vascular volume in the systemic circulation (22.6 +/- 9.0 ml/kg without any antagonist) was reduced by 72% with phentolamine, by 35% with propranolol, and by 73% with both antagonists. Our results suggest that the alpha-adrenergic mechanisms contribute significantly to active changes in systemic venous capacity. In addition, the beta-adrenergic system has very little effect on active changes in venous vessels but does contribute to the overall capacity changes by dilating the hepatic outflow resistance when the carotid sinus baroreflex system is activated.

scholarly journals Anaesthesia for Neurosurgery in the Sitting Position: A Practical Approach

2005 ◽  
Vol 33 (3) ◽  
pp. 323-331 ◽  
Author(s):  
C. M. Domaingue
Keyword(s):  
Superior Vena ◽  
Venous Pressure ◽  
Vena Cava ◽  
Air Embolism ◽  
Transoesophageal Echocardiography ◽  
Systemic Circulation ◽  
Right Atrial ◽  
Sitting Position ◽  
Volume Loading ◽  
Venous Air Embolism

Neurosurgery in the sitting position offers advantages for certain operations. However, the approach is associated with potential complications, in particular venous air embolism. As the venous pressure at wound level is usually negative, air can be entrained. This air may follow any of four pathways. Most commonly it passes through the right heart into the pulmonary circulation, diffuses through the alveolar-capillary membrane and appears in expelled gas. It may pass through a pulmonary-systemic shunt such as a probe patent foramen ovale (paradoxical air embolism); it may collect at the superior vena cava-right atrial junction. Rarely it may traverse through lung capillaries into the systemic circulation. Many monitors, such as the precordial Doppler, capnography, pulmonary artery catheter, transoesophageal echocardiography are useful for venous air embolism detection, with transoesophageal echocardiography being today's gold standard. Various manoeuvres, including neck compression and volume loading, are also useful in reducing the incidence of venous air embolism. Volume loading, in particular, is very helpful as it reduces the risk of hypotension. Other particular concerns to the anaesthetist are airway management, avoidance of pressure injuries, and the risk of pneumocephalus, oral trauma, and quadriplegia. Newer anaesthetic agents have made the choice of anaesthetic technique easier. An appreciation of the implications of neurosurgery in the sitting position can make the procedure safer.

scholarly journals Etiology of Portal Hypertension in Children-An Experience in a Tertiary Centre of Bangladesh

2016 ◽  
Vol 39 (1) ◽  
pp. 14-17
Author(s):  
Salahuddin Mahmud ◽  
Syed Shafi Ahmed ◽  
Jahida Gulshan ◽  
Farhana Tasneem
Keyword(s):  
Portal Hypertension ◽  
Venous Pressure ◽  
Tertiary Care ◽  
Splenic Vein ◽  
Portal System ◽  
Biliary Cirrhosis ◽  
Vein Thrombosis ◽  
Hepatic Diseases ◽  
Chronic Hepatitis B Virus ◽  
Hypertension In Children

Background: Portal hypertension is defined by a pathological increase in portal venous pressure. Any condition that interfere with blood flow at any level within the portal system can lead to portal hypertension. For better management, it is important to determine the underlying cause.Objective: To evaluate the etiology of portal hypertension in children admitted in a tertiary care centre of Bangladesh.Materials & Methods: This cross sectional study was done in the Department of Pediatric Gastroenterology, Hepatology & Nutrition, Dhaka Shishu (Children) Hospital, Dhaka, Bangladesh on 40 consecutive cases of portal hypertension enrolled from April 2014 to March 2015. Results: Age of the children was 2-12 years with mean age of 7.2±4.3 years and male:female ratio was 1.5:1. Out of 40 children, 32 (80%) developed portal hypertension due to pre-hepatic causes and 8 (20%) hepatic causes. In pre-hepatic causes of portal hypertension, out of 32 children, portal vein thrombosis was found in 20 (62.5%) cases, splenic vein thrombosis in 4 (12.5%) & 8 (25%) were idiopathic. On the other hand hepatic causes of portal hypertension, out of 8 children, cryptogenic was found in 4 (50%) cases, wilson’s disease, chronic hepatitis B virus infection, biliary cirrhosis & autoimmune hepatitis each was found in 1 (12.5%) case. In pre-hepatic cases first variceal bleed much earlier than hepatic cases (4.4±3.6 Vs 7.6±4.6 years).Conclusion: Extra-hepatic diseases were the most common etiology of portal hypertension in studied children. Portal venous thrombosis in extra-hepatic cases & cryptogenic liver disease in intra-hepatic cases were the most common causesBangladesh J Child Health 2015; VOL 39 (1) :14-17

scholarly journals Transjugular Intrahepatic Portosystemic Shunt: A Literature Review

2017 ◽  
Vol 34 (2) ◽  
pp. 114-122 ◽  
Author(s):  
Vicki R. Franklin ◽  
Layla Q. Simmons ◽  
Anthony L. Baker
Keyword(s):  
Portal Hypertension ◽  
Transjugular Intrahepatic Portosystemic Shunt ◽  
Venous Pressure ◽  
Portosystemic Shunt ◽  
Portal System ◽  
Refractory Ascites ◽  
Hepatic Veins ◽  
Technological Advances ◽  
Intrahepatic Portosystemic Shunt ◽  
Diseased Liver

Transjugular intrahepatic portosystemic shunt, or TIPS, is a procedure used to decompress the portal system resulting from portal hypertension. The technique was inadvertently discovered during a transjugular cholangiography procedure around 1969. Technological advances in the 1980s and 1990s have resulted in more positive outcomes for the TIPS procedure since its inception. There are several indications for performing the procedure, including refractory ascites, variceal bleeding, and portal hypertension. Liver disease can lead to portal hypertension, and few treatments are available; however, with TIPS, many patients obtain favorable results. The goal of placing an intrahepatic portosystemic shunt is to bypass the vascular resistance in the cirrhotic liver by creating a channel between the portal and hepatic veins, thereby reducing portal venous pressure and portal hypertension. Normal and diseased liver function is explained as well as the TIPS procedure process, materials, complications, and long-term outcomes.

Portal venous infusions of L-glutamine in anaesthetized dogs do not influence renal function

1992 ◽  
Vol 70 (10) ◽  
pp. 1432-1435
Author(s):  
Mortimer Levy
Keyword(s):  
Wistar Rats ◽  
Femoral Vein ◽  
Venous Pressure ◽  
Renal Perfusion ◽  
Portal Venous Pressure ◽  
Portal System ◽  
Similar Data ◽  
Free Base ◽  
Hepatorenal Reflex ◽  
Intraportal Infusion

It has been reported that the intraportal infusion of glutamine in Munich–Wistar rats will cause depression of renal perfusion and the urinary excretion of salt and water. We have attempted to reproduce these findings in anaesthetized dogs. L-Glutamine was infused at doses between 120 and 150 μmol/min into the portal vein and femoral vein of anaesthetized dogs. No effect was observed on portal venous pressure, blood pressure, or kidney function. Similar data were obtained with D-glutamine. Liver biopsy revealed no abnormalities. When 1.5–3 μg histamine (free base) was infused into the portal system, portal venous pressure rose from 15.2 ± 0.33 to 24.8 ± 0.40 cmH2O (p < 0.05) (1 cmH2O = 98.1 Pa). Glutamine infusions do not appear to initiate hepatorenal reflexes in dogs as they have been reported to do in rats.Key words: liver, portal hypertension, hepatorenal reflex.

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