Direct Sac Research Articles

Dyna CT Scanning, Image Fusion, and Virtual Guidance Systems for Direct Sac Access in Therapy of Persistent Type II Endoleaks after EVAR

Dyna CT Scanning, Image Fusion, and Virtual Guidance Systems for Direct Sac Access in Therapy of Persistent Type II Endoleaks after EVAR

Intra-aneurysm Sac Pressure in Patients with Unchanged AAA Diameter after EVAR

Objective: To study intra-aneurysm sac pressure and subsequent abdominal aortic aneurysm (AAA) diameter changes in patients without endoleaks that remain unchanged in AAA diameter more than 1 year after endovascular aneurysm repair (EVAR). Methods: A total of 23 patients underwent direct intra-aneurysm sac pressure (DISP) measurements 16 months (IQR: 14–35 months) after EVAR. Tip-pressure sensors were used through translumbar AAA puncture. Mean pressure index (MPI) was calculated as the percentage of mean intra-aneurysm pressure relative to the simultaneous mean intra-aortic pressure. Aneurysm expansion or shrinkage was assumed whenever the diameter change was ≥ 5 mm. Values are presented as median and interquartile range. Results: In 18 patients, no fluid was obtained upon AAA puncture (group A). In five patients, fluid was obtained (group B). In group A, follow-up continued for 29 months (IQR: 15–35 months) after DISP; five AAAs shrank, 10 remained unchanged and three expanded (MPIs of 26% (IQR: 18–42%), 28% (IQR: 20–48%) and 63% (IQR: 47–83%) and intra-sac pulse pressures of 3 mmHg (IQR: 0–5 mmHg), 4 mmHg (IQR: 2–8 mm Hg) and 12 mmHg (IQR: 6–20 mmHg), respectively, for the three subgroups). MPI and intra-sac pulse pressures were higher in AAAs that subsequently expanded (P = 0.073 and 0.017, respectively). MPI and pulse pressure correlated with total diameter change (r = 0.49, P = 0.039 and r = 0.39, P = 0.109, respectively). Pulse pressure had a greater influence than MPI on diameter change (R2 = 0.346, P = 0.041, beta standardised coefficient of 0.121 for MPI and 0.502 for pulse pressure). Similar results with stronger, and significant correlation to pulse pressure were obtained when relative diameter changes were used (r = 0.55, P = 0.017). In group B, MPI and AAA pulse pressure were 32% (IQR: 18–37%) and 1 mmHg (IQR: 0–6 mmHg), respectively. After 36 months (IQR: 21–38 months), one AAA shrank, three continued unchanged while one expanded. Conclusions: AAAs without endoleak and unchanged diameter more than 1 year after EVAR will often continue unchanged. Expansion can eventually occur in the absence of intra-sac fluid accumulation and is associated with higher and more pulsatile intra-sac pressure. However, in patients with intra-sac fluid, expansion can occur with low intra-sac pressures.

Intra-aneurysm Sac Pressure in Patients with Unchanged AAA Diameter after EVAR

To study intra-aneurysm sac pressure and subsequent abdominal aortic aneurysm (AAA) diameter changes in patients without endoleaks that remain unchanged in AAA diameter more than 1 year after endovascular aneurysm repair (EVAR). A total of 23 patients underwent direct intra-aneurysm sac pressure (DISP) measurements 16 months (IQR: 14-35 months) after EVAR. Tip-pressure sensors were used through translumbar AAA puncture. Mean pressure index (MPI) was calculated as the percentage of mean intra-aneurysm pressure relative to the simultaneous mean intra-aortic pressure. Aneurysm expansion or shrinkage was assumed whenever the diameter change was > or =5mm. Values are presented as median and interquartile range. In 18 patients, no fluid was obtained upon AAA puncture (group A). In five patients, fluid was obtained (group B). In group A, follow-up continued for 29 months (IQR: 15-35 months) after DISP; five AAAs shrank, 10 remained unchanged and three expanded (MPIs of 26% (IQR: 18-42%), 28% (IQR: 20-48%) and 63% (IQR: 47-83%) and intra-sac pulse pressures of 3 mmHg (IQR: 0-5 mmHg), 4 mmHg (IQR: 2-8mm Hg) and 12 mmHg (IQR: 6-20 mmHg), respectively, for the three subgroups). MPI and intra-sac pulse pressures were higher in AAAs that subsequently expanded (P=0.073 and 0.017, respectively). MPI and pulse pressure correlated with total diameter change (r=0.49, P=0.039 and r =0.39, P=0.109, respectively). Pulse pressure had a greater influence than MPI on diameter change (R(2)=0.346, P=0.041, beta standardised coefficient of 0.121 for MPI and 0.502 for pulse pressure). Similar results with stronger, and significant correlation to pulse pressure were obtained when relative diameter changes were used (r=0.55, P=0.017). In group B, MPI and AAA pulse pressure were 32% (IQR: 18-37%) and 1 mmHg (IQR: 0-6 mmHg), respectively. After 36 months (IQR: 21-38 months), one AAA shrank, three continued unchanged while one expanded. AAAs without endoleak and unchanged diameter more than 1 year after EVAR will often continue unchanged. Expansion can eventually occur in the absence of intra-sac fluid accumulation and is associated with higher and more pulsatile intra-sac pressure. However, in patients with intra-sac fluid, expansion can occur with low intra-sac pressures.

Orchiectomy as a result of ischemic orchitis after laparoscopic inguinal hernia repair: case report of a rare complication

BackgroundIschemic orchitis is an established complication after open inguinal hernia repair, but ischemic orchitis resulting in orchiectomy after the laparoscopic approach has not been reported.Case presentationThe patient was a thirty-three year-old man who presented with bilateral direct inguinal hernias, right larger than left. He was a thin, muscular male with a narrow pelvis who underwent bilateral extraperitoneal mesh laparoscopic inguinal hernia repair. The case was complicated by pneumoperitoneum which limited the visibility of the pelvic anatomy; however, the mesh was successfully deployed bilaterally. Cautery was used to resect the direct sac on the right. The patient was discharged the same day and doing well with minimal pain and swelling until the fourth day after surgery. That night he presented with sudden-onset pain and swelling of his right testicle and denied both trauma to the area and any sexual activity. Ultrasound of the testicle revealed no blood flow to the testicle which required exploration and subsequent orchiectomy.ConclusionIschemic orchitis typically presents 2–3 days after inguinal hernia surgery and can progress to infarction. This ischemic injury is likely due to thrombosis of the venous plexus, rather than iatrogenic arterial injury or inappropriate closure of the inguinal canal. Ultrasound/duplex scanning of the postoperative acute scrotum can help differentiate ischemic orchitis from infarction. Unfortunately, testicular torsion cannot be ruled out and scrotal exploration may be necessary. Although ischemic orchitis, atrophy, and orhiectomy are uncommon complications, all patients should be warned of these potential complications and operative consent should include these risks irrespective of the type of hernia or the surgical approach.

Endoleaks after endovascular aneurysm repair lead to nonuniform intra-aneurysm sac pressure

This was a study of intra-aneurysm sac pressures in patients who presented with endoleaks after endovascular repair (EVAR) of abdominal aortic aneurysms (AAA). Twenty-five patients (18 men, 7 women) with endoleaks, age (IQR 68 to 80), underwent 31 direct intra-aneurysm sac pressure measurements, DISP at 16 months after EVAR (IQR, 14 to 26 months). Diameter of AAA was 59 mm (IQR, 52 to 67 mm). Six patients underwent DISP twice. Tip-pressure sensors were used through direct translumbar puncture of the AAA except in three patients (transabdominal puncture in 2; endoluminal in 1). Mean pressure index (MPI) was calculated between simultaneously registered intra-aneurysm sac and systemic pressures. Values presented are medians with interquartile range (IQR). Type I endoleaks (n = 1) showed MPI of 93% in the nidus and 62% in the thrombus. Type II endoleaks were associated with lower MPIs in the thrombus (35%; IQR 24% to 38%) when AAAs shrank (n = 4) compared with when the AAAs remained unchanged (n = 11; MPI, 78%; IQR, 47% to 85%) or expanded (n = 6; MPI, 74%; IQR, 58% to 87%; P = .019). The nidus of type II endoleaks (MPI, 79%; IQR, 70% to 90%) had higher pressure than the thrombus (45%, IQR, 34% to 85%; P = .047; n = 7). Successful embolization of type II endoleaks led to AAA shrinkage (n = 3; MPI reduction, 13% to 31%) or diameter stability (n = 3; unchanged MPIs, 37% to 44%). Type III endoleaks (n = 3) had MPIs in the thrombus of 33% to 70%. Endoleaks after EVAR pressurize the AAA sac nonuniformly, with higher, near-systemic, pressure in the endoleak nidus compared with the thrombus. Nevertheless, type II endoleaks in shrinking AAAs have lower intra-sac pressure than expanding or stable aneurysms, and successful endoleak embolization reduces pressure.

Direct sac puncture and N‐butyl cyanoacrylate embolization of medial canthal arteriovenous malformation supplied by the external carotid artery and the internal carotid artery branches

We report a periorbital arteriovenous fistula that was treated with direct sac puncture N-butyl cyanoacrylate embolization under controlled inflow and outflow. The efficacy of this technique in a periorbital lesion is discussed.

Direct intra-aneurysm sac pressure measurement using tip-pressure sensors: In vivo and in vitro evaluation

Direct intra-aneurysm sac pressure measurement with percutaneous translumbar puncture is a new method for follow-up after endovascular aneurysm repair. The purpose of this study was to evaluate a tip-pressure sensor system for intra-aneurysm pressure measurement in an in vitro aneurysm model and in vivo in patients by studying intraobserver variability. We used 0.014-inch guide wire-mounted tip-pressure sensors. For the in vitro aneurysm model, saccular aneurysms filled with thrombus were inserted in a left-heart-driven aneurysm model. Pressure was measured simultaneously with guide wire pressure sensors in the lumen of the model and within the aneurysm thrombus. In vivo, intraobserver variability was evaluated with double percutaneous translumbar puncture of the abdominal aortic aneurysm (AAA) with pressure measurement in 15 patients (14 men, 1 woman; median age, 75 years [63-80 years]; median AAA diameter, 55 mm [47-80 mm]) at a median of 32 months (2-100 months) after endovascular aneurysm repair. Mean pressure index was calculated as the percentage of mean intraaneurysm pressure relative to simultaneous mean systemic pressure. In vitro, the difference in pressure between the tip-sensor measurements and the pressure output of the aneurysm model was 2 mm Hg (1-4 mm Hg) when the output varied between 150/50 and 200/100 mm Hg (n = 90). Mean pressure in the lumen of the model and within the aneurysm thrombus differed by 1 mm Hg (-5-15 mm Hg (n = 10). In vivo, intraobserver variability of mean pressure index (Bland-Altman plot) was 0% (-7%-17%; n = 15%). Direct intra-aneurysm sac pressure measurement with tip-pressure sensors mounted on 0.014-inch guide wires is a reliable and reproducible technique for measuring intra-AAA pressure both in vitro and in vivo.

Intra-aneurysm sac pressure measurements after endovascular aneurysm repair: differences between shrinking, unchanged, and expanding aneurysms with and without endoleaks

Objective Our objective was to study intra-aneurysm pressure after endovascular aneurysm repair (EVAR) in shrinking, unchanged, and expanding abdominal aortic aneurysms (AAAs) with and without endoleaks. Methods Direct intra-aneurysm sac pressure measurement (DISP) by percutaneous translumbar puncture of the AAA under fluoroscopic guidance was performed 46 times during the follow-up of 37 patients (30 men; median age, 73 years [range, 58-82 years]; AAA diameter: median, 60 mm [range, 48-84 mm]). Three patients were included in two different groups because DISP was performed more than once with different indications. Tip-pressure sensors mounted on 0.014-inch guidewires were used for simultaneous measurement of systemic and AAA sac pressures. Mean pressure index (MPI) was calculated as the percentage of mean intra-aneurysm pressure relative to the simultaneous mean intra-aortic pressure. Results Median MPI was 19% in shrinking (11 patients), 30% in unchanged (10 patients), and 59% in expanding (9 patients) aneurysms without endoleaks. Pulse pressure was also higher in expanding (10 mm Hg) compared with shrinking (2 mm Hg; P < .0001) AAAs. Four of the nine patients with expanding AAAs underwent five repeated DISPs later in the follow-up, and MPIs were consistently elevated. Seven of the 10 patients with unchanged AAAs without endoleaks underwent further computed tomography follow-up after DISP; 2 expanded (MPI, 47%-63%), 4 shrank (MPI, 21%-30%), and 1 remained unchanged (MPI, 14%). Type II endoleaks (6 patients, 7 DISPs) were associated with wide range of MPI (22%-92%). Successful endoleak embolization (n = 4) resulted in pressure reduction. Conclusions Intra-aneurysm sac pressure measurement is an important adjunctive for EVAR evaluation, possibly allowing early detection of failures. High pressure is associated with AAA expansion and low pressure with shrinkage. Type II endoleaks can be responsible for AAA pressurization, and successful embolization appears to result in pressure reduction.

Direct yolk sac volume manipulation of zebrafish embryos and the relationship between offspring size and yolk sac volume

Through direct manipulation of yolk sac volume (Vy), in the zebrafish Danio rerio, Vy and offspring size was positively correlated and the relationship was independent of geographical location, parental size or age and, most importantly, parental genetic factors. Larval survivorship, under a non‐feeding regime and up until hatch, was not significantly affected by the manipulation. Decreased Vy significantly decreased maximum standard length (LS), maximum body surface area (AB), time to yolk sac absorption, LS and AB at yolk sac absorption, and the LS and AB at starvation. The methodology of Vy adjustment will be useful for the studies of the interaction between early life‐history traits and offspring size, egg quality variables and early vertebrate development.

Translumbar Embolization of Type 2 Endoleaks after Endovascular Repair of Abdominal Aortic Aneurysms

ENDOVASCULAR repair of abdominal aortic aneurysms is a rapidly proliferating technique. Unlike conventional “open” aneurysm repairs, patients may develop immediate or delayed “endoleaks” requiring remediation either by catheter-based or surgical intervention. Endoleaks are classified into one of four categories (1,2). A leak at an attachment site (proximal, middle, or distal) is classified as type 1. In collateral endoleaks (type 2), blood travels from a branch vessel in the nonstented portion of the aorta or iliac arteries. Blood flow then takes a circuitous route, emptying into the aneurysm sac via retrograde flow through a lumbar artery, inferior mesenteric artery, or other vessel originating from the aneurysm. This type of leak is the most common and is unrelated to the type or configuration of stent-graft used. Endoleaks that are a result of a defect in, or failure of, the graft material are defined as type 3, whereas those resulting from stent-graft wall porosity are called type 4. Most controversial is the fate of branch vessel (type 2) endoleaks, usually arising from inferior mesenteric artery or lumbar artery retrograde flow into the excluded abdominal aortic aneurysm sac. While some of these leaks have been demonstrated to thrombose with the passage of time, distressing reports of continued abdominal aortic aneurysm enlargement from untreated branch endoleaks are accumulating (3–5). One of the barriers to catheterbased remediation of type 2 endoleaks has been access to the offending vessel supplying the excluded abdominal aortic aneurysm sac. Access to the inferior mesenteric artery can be gained by catheterization of the superior mesenteric artery and selecting the inferior mesenteric artery through collaterals. This approach is tedious, time-consuming, and not always successful, particularly if there is an incomplete arc connecting the SMA-IMA axis (6– 10). Patent lumbar arteries are even less easily accessed. Translumbar access to the abdominal aorta was first introduced more than 70 years ago (11,12). Modifications made this technique of clinical value in the 1960s (13). Even though the long history and safety of this procedure is well documented, at the present time, translumbar angiography is usually reserved for patients with poor peripheral vascular access. The purpose of our investigation was to access the feasibility of direct aneurysm sac puncture and endoleak embolization via a translumbar approach. MATERIALS AND METHODS

Aneurysm sac pressure measurements after endovascular repair of abdominal aortic aneurysms

Objectives: The goal of endovascular grafting of abdominal aortic aneurysms (AAAs) is to exclude the aneurysm sac from systemic pressure and thereby decrease the risk of rupture. Unlike conventional open surgery, branch vessels in the sac (eg, lumbar artery and inferior mesenteric artery [IMA]) are not ligated and can potentially transmit pressure. The purpose of our investigation was to evaluate the feasibility of various interventional techniques for measuring pressure within the aneurysm sac in patients who had undergone endovascular repair of AAAs. Methods: Sac pressure measurements were performed in 21 patients who had undergone stent graft repair of AAAs. Seventeen of 21 patients had endoleaks demonstrated on 30-day computed tomographic (CT) scans. Access to the aneurysm sac in these patients was through direct translumbar sac puncture (5 patients), through a patent IMA accessed via the superior mesenteric artery (SMA) (9 patients), or by direct cannulation around attachment sites (3 patients). Four patients had perioperative pressure measurements obtained through catheters positioned along side of the endovascular graft at the time of its deployment. Two of these catheters were left in position for 30 hours during which time CT and conventional angiography were performed. Pressures were determined with standard arterial-line pressure transduction techniques and compared with systemic pressure in each patient. Results: Elevated sac pressure was found in all patients. The sac pressure in patients with endoleaks was found to be systemic (15 patients) or near systemic (2 patients) and all had pulsatile waveforms. Elevated sac pressures were also found in patients without CT or angiographic evidence of endoleak (2 patients). Injection of the sacs in two of these patients revealed a patent lumbar artery and an IMA. Conclusions: It is possible to measure pressures from within the aneurysm sac in patients with stent grafts with a variety of techniques. Patients may continue to have pressurized AAA sacs despite endovascular AAA repair. Endoleaks transmit pulsatile pressure into the aneurysm sac regardless of the type. It is possible to have systemic sac pressures without evidence of endoleaks on CT or angiography. (J Vasc Surg 2001;33:32-41.)

Direct inguinal hernia in infancy and childhood

In 16 years in a provincial paediatric surgical practice, 19 direct inguinal hernias in 14 patients have been encountered amongst over 1,600 inguinal hernia operations. Nearly one-half of these presented as recurrent hernias. Five types of direct hernia were recognized: direct hernia with distinct sac (1 patient); hernia en pantaloon with associated indirect sac (1 patient); sliding direct hernia (1 patient); direct weakness with no indirect sac and no distinct direct sac; and giant indirect hernia with such a huge sac that the whole of the posterior wall of the inguinal canal is encroached upon and weakened. Direct inguinal hernia can be suspected clinically, but positive diagnosis is difficult. It should be suspected at operation if no significant indirect sac is found. Repair of the transversalis fascia seems to be effective surgical treatment, with no known recurrence in this series.

The Direct Mammotrophic Action of Lactogenic Hormone

SummaryThirty oophorectornized, virgin rabbits, injected subcutaneously 5 days weekly for 4 weeks with 200 I.U. of estrone and 1 I.U. of progesterone showed prolactational mammary growth approximating that of a 3-weeks′ pregnant rabbit. Three days after the last of these injections, 5 different levels of lactogenic hormone were tested on groups of 6 rabbits. The hormone was given intraductally in such a way that an individual sector in each animal received a constant volume of fluid (1.0 cc). Of the different doses of hormone tested, 6 and 3 I.U. caused localized sector lactation in all 6 animals; 1.5 I.U. in 5 of 6; and 0.75 I.U. in 3 of 6 animals. None of the 6 animals injected with 0.37 I.U. lactated; nor did the uninjected or control-injected sectors in any animal lactate. This experiment demonstrates for the first time that the hypophysial lactogenic hormone has a direct mammotrophic effect just as it was previously shown to have a direct crop sac stimulating action. With all other factors essentiall...