David K. Chew

Extrahepatic portal vein aneurysm: a case report and review of the literature

Portal vein aneurysm is a rare clinical entity with only 42 published cases in the English literature. We present a 30-yr old woman who was incidentally diagnosed with an extrahepatic portal vein aneurysm during the investigation for dyspepsia. Expectant management with regular follow-up and surveillance imaging was adopted. This pathology is increasingly encountered with the frequent use of radiological imaging modalities in the work-up of abdominal disorders. Etiology, clinical significance and management strategies for extrahepatic portal vein aneurysms are discussed.

Transaortc Endarterectomy for Primary Mesenteric Revascularization

The optimal approach to revascularization for chronic mesenteric ischemia has not been firmly established during the past three decades. The present study was undertaken to evaluate the safety and results of primary mesenteric revascularization for chronic mesenteric ischemia by transaortic endarterectomy. A descriptive retrospective analysis of 14 patients who underwent trap-door transaortic endarterectomy for primary mesenteric revascularization was performed. Clinical presentations of the patients included abdominal pain (n = 13) and weight loss (n = 7). All patients underwent preoperative aortography and subsequent elective reconstruction. Demographic features, perioperative, and long-term outcomes were analyzed. The study population consisted of 12 females and two males with a mean age of 67 years. The mean operative duration was 3 hours with an ischemic time of 33 minutes. The initial success rate of mesenteric revascularization was 93%. One early graft failure was salvaged with urgent embolectomy without bowel resection. There was no hospital mortality, but the overall postoperative morbidity rate was 50% (n = 7). Thirteen patients (93%) were discharged within 2 weeks. Late recurrent ischemia and intestinal infarction developed in one patient, requiring emergency bowel resection. Sustained relief of symptoms was achieved in 13 of 14 patients (93%). The overall survival rates were 85% ± 10.0% and 77% ± 11.7% at 1 and 3 years, respectively. Transaortic endarterectomy is a safe and effective technique for elective primary mesenteric revascularization for patients with chronic mesenteric ischemia. This approach allows simultaneous revascularization of multiple visceral arteries and achieves durable relief of symptoms.

Elastase promotes aortic dilation by inhibiting Ca2+ influx into vascular smooth muscle.

Abstract: Abdominal aortic aneurysm (AAA) is a common vascular disease with, as of yet, unclear mechanism. Increased elastase activity and elastin degradation in the aorta are consistent findings in human AAA. Also, elastase perfusion of the aorta promotes aortic dilation in animal models of AAA. Although elastase-induced degradation of extracellular matrix proteins and the ensuing inflammation of the aortic wall have been implicated as possible causes of the aortic dilation in AAA, little is known regarding the effects of elastase on the mechanisms of aortic smooth muscle contraction. The purpose of this study was to test the hypothesis that elastase promotes aortic dilation by inhibiting the Ca2+ mobilization mechanisms of smooth muscle contraction. Isometric contraction and 45Ca2+ influx were measured in aortic strips isolated from male Sprague-Dawley rats non-treated or treated with elastase. Initial experiments suggested that elastase alone caused matrix degradation. To avoid potential degradation of the extracellular matrix proteins by elastase, the same experiments were repeated in the presence of saturating concentrations of elastin (10 mg/ml). In normal Krebs (2.5 mM Ca2+), phenylephrine (Phe, 10−5 M) caused contraction of the aortic strips that was significantly inhibited by elastase. The elastase-induced inhibition of Phe contraction was concentration- and time-dependent. At 5 U/ml elastase, the inhibition of Phe contraction was rapid in onset (2.4 ± 0.3 minutes) and complete in 32 ± 4 minutes. The inhibitory effects of elastase on Phe contraction were partially reversible. In Ca2+-free (2 mM EGTA) Krebs, Phe caused a small contraction that was not inhibited by elastase, suggesting that elastase does not inhibit Ca2+ release from the intracellular stores. Membrane depolarization by 96 mM KCl, which stimulates Ca2+ entry from the extracellular space, caused a contraction that was inhibited by elastase in a time-dependent and reversible fashion. The reversible inhibitory effects of elastase, particularly in the presence of saturating concentrations of elastin, suggest that they are not due to dissolution of the extracellular matrix or permanent damage to the smooth muscle contractile proteins. Elastase also caused significant inhibition of Phe- and KCl-induced 45Ca2+ influx. These data suggest that elastase promotes aortic relaxation by inhibiting the Ca2+ entry mechanism of vascular smooth muscle contraction, and thus further explain the role of increased elastase activity during the early development of AAA.

Elastase-Induced Suppression of Endothelin-Mediated Ca2+ Entry Mechanisms of Vascular Contraction

Abstract—Abdominal aortic aneurysm (AAA) is associated with increased endothelin (ET-1), both systemically and locally in the aorta. Also, elastase activity is increased in human AAA, and elastase perfusion of the aorta induces aneurysm formation in animal models of AAA. However, whether elastase directly affects the ET-1-induced mechanisms of aortic smooth muscle contraction is unclear. Isometric contraction and 45Ca2+ influx were measured in aortic strips isolated from male Sprague-Dawley rats and treated with elastase (5 U/mL). To avoid degradation of the extracellular matrix proteins by elastase, experiments were performed in the presence of elastin (10 mg/mL). In normal Krebs solution (2.5 mmol/L Ca2+), ET-1 (10−7 mol/L) caused contraction of aortic strips that was inhibited by elastase (5 U/mL). The elastase-induced inhibition of ET-1 contraction was slow in onset (4.6±0.4 minutes), time-dependent, complete in 34±3 minutes, and reversible. In Ca2+-free Krebs solution, caffeine (25 mmol/L) caused a small contraction that was not inhibited by elastase, suggesting that elastase does not inhibit Ca2+ release from the intracellular stores. Membrane depolarization by 96 mmol/L KCl, which stimulates Ca2+ entry from the extracellular space, caused a contraction that was inhibited by elastase in a concentration-dependent, time-dependent, and reversible fashion. The reversible inhibitory effects of elastase, particularly in the presence of elastin, suggest that they are not due to dissolution of the extracellular matrix or smooth muscle contractile proteins. Elastase also inhibited ET-1 and KCl-induced 45Ca2+ influx. Thus, elastase directly inhibits ET-1-induced Ca2+ entry mechanisms of vascular smooth muscle contraction, which may explain the role of elastase and ET-1 during the development of AAA.

Mycotic aneurysm of the superior mesenteric artery: a delayed complication from a neglected septic embolus-a case report.

Mycotic aneurysm formation in a visceral artery carries a significant risk of mortality and morbidity. The authors present a case of a symptomatic superior mesenteric artery aneurysm secondary to a septic embolus in a patient who had undergone aortic valve replacement. The patient initially presented with evidence of acute intestinal ischemia from a presumed embolic source. Although an extensive bowel resection was performed, an adequate search for the embolus was not carried out. Prompt diagnosis and removal of suspected septic emboli must be performed to avoid the formation of delayed mycotic aneurysms.

Mycotic Aneurysm of the Superior Mesenteric Artery: A Delayed Complication from a Neglected Septic Embolus

Mycotic aneurysm formation in a visceral artery carries a significant risk of mortality and morbidity. The authors present a case of a symptomatic superior mesenteric artery aneurysm secondary to a septic embolus in a patient who had undergone aortic valve replacement. The patient initially presented with evidence of acute intestinal ischemia from a presumed embolic source. Although an extensive bowel resection was performed, an adequate search for the embolus was not carried out. Prompt diagnosis and removal of suspected septic emboli must be performed to avoid the formation of delayed mycotic aneurysms.

Role of the Inferior Mesenteric Artery in Predicting Secondary Intervention for Type II Endoleak After Endovascular Aneurysm Repair

Objective: The objective of this study was to determine whether flow velocities measured on Doppler ultrasound after endovascular aneurysm repair can predict whether a type II endoleak can resolve without intervention. In addition, we assessed the relationship of flow velocities to sac growth and the need for an intervention. We hypothesized that hemodynamic properties suggesting low flow velocity would predict resolution of type II endoleaks. Methods: Patients with type II endoleaks after endovascular aneurysm repair identified on Doppler ultrasound between January 2014 and December 2017 were retrospectively analyzed. Twenty patients were found to have type II endoleaks, and they were split into two groups. Group 1 consisted of 10 patients with resolved endoleaks or shrinking sac size; group 2 consisted of 10 patients with increasing sac size or those who required intervention to seal the endoleak because of an increased sac size. An analysis of the velocities of the endoleak nidus was conducted. Results: Doppler ultrasound velocities were significantly lower in patients with resolved type II endoleaks and in those with shrinking aneurysm sac size compared with those requiring intervention or demonstrating an increase in aneurysm sac size (43.6 6 20.5 cm/s vs 147.30 6 103.45 cm/s; P < .01). Nine of 10 patients in group 2 underwent intervention with either translumbar embolization or transarterial embolization, with only 1 having complete resolution of the type II endoleak despite intervention. All patients in group 2 had at least one duplex ultrasound examination with endoleak nidus velocities >100 cm/s, whereas there was no patient in group 1 who had any duplex ultrasound examination with endoleak nidus velocities >100 cm/s. Average follow-up time was similar in both groups, with group 1 at 581 days and group 2 at 547 days postoperatively. Conclusions: Doppler ultrasound velocities of type II endoleaks can be used to predict whether type II endoleaks will spontaneously seal or lead to sac growth. Type II endoleaks on Doppler ultrasound with endoleak nidus flow velocities >100 cm/s remain persistent, even with attempted treatment.

Portasystemic Venous Shunt Surgery for Portal Hypertension

Portal hypertension, defined as sustained elevation of the portal pressure above 12 mmHg, can arise from a myriad of causes. In Western countries, the most common cause is alcoholic liver cirrhosis, whereas in Asia, and developing countries, it is postnecrotic cirrhosis (from viral hepatitis) and schistosomiasis. The adverse effects of chronic portal hypertension include the formation of esophageal, and extraesophageal varices, ascites, splenomegaly with hypersplenism, hepatorenal syndrome, and hepatic encephalopathy. Hemorrhage from gastroesophageal varices is the most lethal of these complications. Thus, its prevention and treatment has assumed paramount importance in the management of these patients.