Prophylactic embolization

Kim DE, Yoon HK, Ko GY, Kwon JS, Song HY, Sung KB (1999) Hepatic falciform artery is prophylactic embolization needed before short-term hepatic arterial chemoin-fusion AJR Am J Roentgenol 172 1597-1599... 

Supraduodenal artery - This vessel provides blood supply to the upper portion of the duodenum and pylorus [2]. The origin of this vessel is also variable, and it communicates with the pancreaticoduodenal arcade as well as right gastric branches [7]. If identified, this vessel should be prophylactically embolized. 

Unlike other loco-regional therapies, pre-procedure planning and meticulous mesenteric angiography are of paramount importance in order to determine the safest and most effective treatment strategy. Identifying anatomic variants, isolating the hepatic circulation and prophylactic embolization requires... 

At all times during °Y embolization the treating physician should balance the risks of (1) infusion proximal to the cystic artery with potential radiation cholecystitis (2) infusion distal to the cystic artery but with suboptimal microsphere distribution and (3) infusion proximal to the cystic artery following its prophylactic embolization, resulting in optimal microsphere distribution but with a risk of ischemic cholecystitis [24]. 

Lang EV, Picus D, Marx MV, et al. (1992) Massive upper gastrointestinal hemorrhage with normal findings on arteriography value of prophylactic embolization of the... 

Embolization of massively bleeding duodenal ulcers constituted 5% of endoscopically treated duodenal ulcers and as little as 0.6% of all cases with upper gastrointestinal bleeding who underwent emergency endoscopy in one large series. Contrast extravasation was demonstrated in only half of these cases. Embolization did however induce haemostasis in 90% of cases (Toyoda et al. 1995). Prophylactic embolization of the GDA is sometimes performed with success (as in this series) even when no angiographic abnormality is demonstrated despite a proven endoscopic source of haemorrhage. 

Venous stasis resulting from prolonged bed rest, cardiac failure, or pelvic, abdominal, or hip surgery may precipitate thrombus formation in the deep veins of the leg or calf and may lead to fatal pulmonary embolism. Heparin may also be used prophylactically following surgery. 

In present times, because of early mobilization and shorter stays in hospital, venous thrombosis in the legs and resulting pulmonary embolism has declined to a large degree. In persons with acute myocardial infarction, prophylactic low-dose heparin has reduced the incidence of venous thrombosis in the legs. It is considered as a reasonable alternative to warfarin in selected patients. Preventive anlicoagulalion may be indicated in some cases to prevent strokes due to left ventricular mitral thrombi embolizing in tire brain. 

When these patients are discharged from hospital, prophylactic treatment with an oral anticoagulant is recommended to prevent recurrence of the thrombosis. Warfarin sodium, which antagonizes the effects of vitamin K, is used in prophylaxis and treatment of DVT and pulmonary embolism. It is usual to start with an induction dose of 10 mg daily for two days the dose can then be reduced. Patients need to be monitored as there is a risk of haemorrhage with oral anticoagulant drugs. 

Of the many drugs used as prophylactic antithrombotic agents, heparin has a long history as therapy for both DVT and pulmonary embolism (PE). Many studies have shown that in moderate and high risk patients, heparin can prevent postoperative DVT and PE (4,19-21). Now, with the introduction of LMWHs, these benefits can be had together with easier dosing and potentially less risk of bleeding. 

Another possible area of investigation includes the prophylactic radioemboiization of remnant liver tissue in patients undergoing hepatic resection for HCC or colorectal metastases. Although initially attractive, this approach may hinder and limit the ability for future Y to the prophylactically radio-embolized lobe. Furthermore, the blood supply to small metastases is derived from the portal vein, not the hepatic artery, bringing into question whether prophylactic treatment would yield any radiation effect to microscopic metastases [59]. Therefore, if such a study is undertaken, since imaging of micro-metastases is not possible, improved survival or decreased time to disease recurrence would represent possible endpoints. It is clear that further research is needed to address possible treatment options for advanced stage HCC. Any studies in this patient population require careful consideration of the risk of therapy induced liver failure vs. the benefit of lesion stabilization. 

The major aims of interventional procedures for portal hypertension are prophylactic and emergent treatment of variceal bleeding, control of hepatic encephalopathy, and treatment of refractory ascites. Hypersplenism associated with hematological disorder is an additional clinical problem in patients with portal hypertension. At present, the main primary embolotherapies available for portal hypertension are balloon-occluded retrograde transvenous obliteration (BRTO) and partial splenic embolization (PSE). In Japan, BRTO has recently been applied for gastric varices instead of either endoscopic treatment or transhepatic intrahepatic portosystemic shunt (TIPS) procedure, and numerous studies have reported that this method has an excellent success rate. Its efficacy for control of hepatic encephalopathy has also been demonstrated. 

Our approach to patients with abnormal placentation is to selectively embolize bilateral uterine and internal iliac arteries as soon as possible after delivery. Using the embolization technique, we obtained results similar to that of the prophylactic in controlling PPH, but without the risk of radiation to the fetus. 

Aberrant °Y microparticle embolization will result in inadvertent actinic effects in inappropriate vascular territories. This may lead to radiation-induced gastritis and ulcerations, duodenitis, cholecystitis, and pancreatitis, even if prophylactic antacid drugs and mucosal coating are applied, as several authors recommend (Salem and Thurston 2006). Nevertheless, these drugs may help to pre-vent/reduce additional enhancement of the radiation-induced inflammation. In our experience of three cases of radiation-induced duodenal ulcers, the clinical course was significantly prolonged in com-... 

Depending on the organ being embolized and the level of embolization, some tissue ischemia or even necrosis may occur. Prophylactic antibiotics maybe indicated to prevent bacterial seeding of the infarcted tissue from developing into an abscess. This may be more of a concern when the embolized artery is in an infected organ such as a renal pseudoaneurysm that occurs after a nephrostomy done for pyonephrosis. Certainly if the patient has known bacteremia, antibiotic coverage should be started prior to the embolization. 

In order to decrease the risk of carcinoid crisis in those patients with symptomatically active tumors, 150-500 micrograms of somatostatin may be given the day before embolotherapy and continued for 3 to 5 days post-treatment [35]. Despite pre-medication, however, carcinoid crisis can occur during the procedure, often manifested by hemodynamic instability. For noncarcinoid or islet cell tumors, treatment of underlying endocrinopathy must be initiated before referral for embolotherapy. In our institution, prophylactic intravenous antibiotic coverage with cefazolin 1 g q8h and metronidazole 500 mg q8h is used routinely during the inpatient stay. In some centers, allopurinol and lactulose are also administered to prevent urate-induced renal failure and post-embolization hepatic encephalopathy. 

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