Portal Vein Aneurysms

* Esophageal Varices Bleeding: scarring of liver causes blood flow through the liver to decrease. With the decrease in liver blood flow, more blood pumps through veins causing them to balloon outward. The increased amount of blood in the veins results in a vein bursting and leads to bleeding. This condition is secondary to portal hypertension because of the alternate routes the blood takes due to the scarred liver, causing the veins to work harder and accumulate more blood within a certain span of time, not being able to drain in a timely matter.

Hemorrhoids are veins that are swollen or enlarged in the rectum or anus. The can be either external or internal. The causes for hemorrhoids are pregnancy, pushing too hard when releasing stool, and obesity. Treatment may include special cream to reduce swelling (external), change of diet, ice pack and also surgery to get them removed.

The upper GI series shows a dilated first and second portion of the duodenum with an abrupt and vertical obstruction of the third portion. (Gebhart 2015). CT scan may also be used to provide images of both the abdominal tissue in cross-sections allowing to see the superior mesenteric artery and the abdominal aorta including the internal organs (Brunner's and Suddarths 2014). An Endoscopic ultrasound can also be used to visualize the aorta mesenteric angle with accuracy. The use of an upper endoscopy can rule out other pathologies such as mechanical lumen structure and duodenal ulcerations that can mimic superior mesenteric artery syndrome (Gebhart

Deep vein thrombosis (also known as “DVT”) occurs when a blood clot (thrombus) forms in one or more of the deep veins in the body, however usually it often occurs in the legs. The most common symptom is leg pain or swelling, but it can also occur without any symptoms. Sometimes certain medical conditions can affect the development of DVT, especially if the condition has to do with how the blood clots. Another way DVT can come about is if someone does not move for a long time, such as a patient who is be confined to a hospital bed. Deep vein thrombosis is very serious because blood clots in the veins can break loose, travel through the blood stream, and possibly lodge into the lungs, which in turn blocks the blood flow causing a possible pulmonary embolism.

Invasion or external compression can cause an SVC blockage. One way external compression can occur is by the involvement of lymph nodes. When cancer is present in the body, there is a chance that it can spread to surrounding lymph nodes. If this occurs, the lymph nodes can enlarge and compress the SVC and cause an obstruction. Other ways external compression can occur are by the right lung, other mediastinal structures, or by thrombosis of blood within the vein itself. As blood flow becomes blocked, the blood from the upper body is unable to drain back into the heart correctly. These collaterals provide an alternate pathway so the blood can ultimately reach the right atrium. Collateral veins can originate from the azygos vein, lateral thoracic, inter mammary, and esophageal venous systems.

Before those subjects it is necessary to understand what an abdominal aortic aneurysm is. An abdominal aortic aneurysm is an augmented area of the lower aorta, most commonly occurring in the portion of the aorta below the renal artery origin and iliac bifurcation.

An abdominal aortic aneurysm (AAA) is defined by Gordon and Toursarkissian as, “A dilation of the vessel diameter of more than 150% of the diameter just proximal to it” (Gordon & Toursarkissian, 2014). It is stated that in general, a diagnosis of an AAA is made if the aortic diameter is three centimeters or larger (Gordon & Toursarkissian, 2014). The etiology of an AAA is largely complex in which both environmental and genetic factors play vital roles, the most important being smoking (Björck & Wanhainen, 2013). Abdominal aortic aneurysms may be secondary to atherosclerotic changes, inflammatory conditions, infectious diseases, trauma or genetic collagen disorders (Gordon & Toursarkissian, 2014).

The main source for pumping blood through every single artery in the human body is the aorta. The aorta arises from the left ventricle of the heart and extends through the entire abdomen where it then bifurcates into the common iliac arteries. Over time, the arterial walls become weak and widen. As the pressure of blood pumping continues through the aorta, the weakened area starts to have an outpouching known as an aneurysm. “An aneurysm is an abnormal widening of an artery with an increase of greater than 1.5 times the normal diameter” (Medifocus, 2014, p. 19). The normal size of an aneurysm ranges from 1.4 cm to 3.0 cm. A diameter greater than 3 cm is considered to be an abnormal

In 1963, Harjola3 described a case of chronic abdominal pain in a young woman that he attributed to mesenteric ischemia caused by extrinsic compression of the celiac artery. Since then, the topic has been the focus of numerous controversies regarding its pathophysiology, definitive diagnosis, and optimal treatment4. There is still considerable doubt about the real existence of the CACS. Asymptomatic compression or stenosis of the celiac artery is common, and compression of this artery by fibers of the median arcuate ligament has been demonstrated on arteriography in asymptomatic patients1. Similarly, autopsy studies have shown that the celiac artery is compressed by the median arcuate ligament in up to one-third of individuals5. The difficulty

According to Middleton, Teefey and Darcy,8 TIPS placement is successful in about 90% of patients, but does hold a complication rate of 10-16%. Research has shown that placement of TIPS as a secondary treatment for variceal bleeding has produced encouraging results. In 13 random clinical trials, including over 900 patients, recurrent variceal bleeding rates were 9-40%, which is superior to endoscopic treatments that have recurrent bleeding rates from 20-60%. This success rate has made TIPS procedures more utilized in the setting of variceal bleeding. Additionally, the same clinical trials indicate that ascites reduction after shunting ranges from 38-84%, which is favorable to large volume paracentesis that reported rates of 0-43%. “Compared with large-volume paracentesis, TIPS improved transplant-free survival and the incidence of recurrent ascites in cirrhotic patients with refractory ascites.”26 There is evidence of an increase in the development of HE in patients who undergo TIPS, whereas endoscopic treatment does not show an increase. Furthermore, HE is twice as likely to occur when paracentesis is performed. An important consideration is that the complication rate for hepatic encephalopathy does increase with TIPS usage whereas it doesn’t with endoscopic treatment and it is twice as likely to occur as when paracentesis is performed.28 Presently, TIPS is often used as a temporary solution for patients who are

Diverticular leeding is usually acute, without any prior symptoms, and is self-limited in about 70%–80% of cases [1]. In contrast to the acuity of diverticular bleeding, chronic, intermittent, minimal blood loss per rectum is unlikely to be caused by diverticular bleeding, because diverticular bleeding is arterial in

Spontaneous splenic hematoma is one of the rare and life threatening complication of uremic coagulopathy. The diagnosis of spontaneous splenic hematoma mostly made by imaging either ultrasound or computed tomography. The management of spontaneous splenic rupture or hematoma is not standardised till now due to rarity of this condition. Splenectomy is recommended for those who is hemodynamically unstable or presented with features of shock. This is a case report of spontaneous splenic hematoma due to uremic

In patients who presents with gastrointestinal (GI) haemorrhage, about 20-33% are cases of Lower gastrointestinal bleeding (LGIB). In Western countries the annual incidence of LGIB is about 20-27 cases per 100,000 population2. In a recent study that takes place at National University Hospital of Iceland the incidence of acute lower GI bleed (ALGIB) was 87/100000/year3. Statistically upper GI bleeding (UGIB) is

Unfortunately, at first presentation, only 10% of patients are candidates for curative surgery2. Even among those suitable for surgery, the anatomical complexity of the portobiliary hepatic system, the morbidity/mortality associated with liver resection, and the risks of tumoural spread second to

The pathophysiology of CVI remained moderately darken as of not long ago, however late advances relating hemodynamic disarranges to cell science have revealed insight into how its components interlink. CVI might be because of inherited anomalies of vessel walls or tissues, or give off an impression of being auxiliary to profound vein thrombosis. The reason for CVI is then identified with a hover of activities, including the movement of venous hypertension (VH), prompting aggravations of blood stream and venous stasis. These two elements follow up on the dividers of primary veins and cause varicosities, and on the microcirculation, where they cause edema and ulcers.