Ameet G. Patel

Superselective microcoil embolization: treatment of choice in high-risk patients with extrahepatic pseudoaneurysms of the hepatic arteries.

BACKGROUNDnOnly a few isolated case reports of extrahepatic pseudoaneurysms of the hepatic arteries have been published. We present the first documented series of patients with extrahepatic pseudoaneurysms treated at a single institution, and discuss the etiology and management of this condition.nnnSTUDY DESIGNnA retrospective review of all cases of extrahepatic pseudoaneurysms of the hepatic arteries between 1989 and 1997.nnnRESULTSnA total of seven patients with extrahepatic pseudoaneurysms of the hepatic arteries all had upper abdominal pain; five patients were also in shock secondary to a gastrointestinal bleeding from ruptured pseudoaneurysms. The most common factor of the pseudoaneurysms was previous pancreatobiliary surgery in five patients with blunt truncal trauma and chronic pancreatitis in the remaining two patients. Initial endoscopy and ultrasonography were unrevealing, whereas dynamic computed tomography (CT) scan and angiography were diagnostic. The median size of the pseudoaneurysms was 3.6 cm (range 2.1-5.7). Treatment consisted of superselective transcatheter microcoil embolization in five hemodynamically unstable patients and surgical resection of the pseudoaneurysms with vascular reconstruction in the two stable patients. Mortality and morbidity were 0% and 43%, respectively. In a median followup of 35 months (range 2-96), no recurrence of pseudoaneurysm has been found.nnnCONCLUSIONSnA high index of suspicion combined with appropriate diagnostic modalities are required for the diagnosis of extrahepatic pseudoaneurysms. In high-risk patients, superselective transcatheter microcoil embolization should be considered the treatment of choice.

Role of nitric oxide in the relationship of pancreatic blood flow and exocrine secretion in cats

BACKGROUND/AIMSnRecent studies have suggested that, in the gastrointestinal tract, nitric oxide is an important mediator of alterations in blood flow and, in some organs, a second messenger involved in secretion. This study examined the role of NO in changes in pancreatic blood flow associated with basal and stimulated pancreatic exocrine secretion.nnnMETHODSnIn anesthetized cats, we determined the effects of the NO synthase inhibitor NG-monomethyl-L-arginine (10 mg/kg) and the NO donor sodium nitroprusside (10 micrograms.kg-1.min-1) on pancreatic secretion and blood flow (hydrogen gas clearance).nnnRESULTSnNG-monomethyl-L-arginine had no effect on the increase in blood flow associated with secretin stimulation (271 +/- 52 vs. 290 +/- 50 mL.min-1.100 g-1) but reduced that associated with cholecystokinin stimulation (189 +/- 17 vs. 53 +/- 15 mL.min-1.100 g-1; P < 0.001). In contrast, NG-monomethyl-L-arginine significantly reduced both secretin- and cholecystokinin-stimulated secretion. Sodium nitroprusside had no effect on basal blood flow but significantly increased secretion.nnnCONCLUSIONSnNO has a selective role in mediating changes in pancreatic perfusion and secretion. It seems to be important in stimulus-secretion coupling with both secretin and cholecystokinin but is only responsible for the accompanying increase in pancreatic blood flow with cholecystokinin.

Pancreatic interstitial pH in human and feline chronic pancreatitis.

BACKGROUND & AIMSnAdvanced chronic pancreatitis is associated with a reduction in pancreatic blood flow. To determine the physiological significance of this decrease, pancreatic interstitial pH was measured in a model of obstructive chronic pancreatitis in cats and in patients with chronic pancreatitis.nnnMETHODSnIn cats, pancreatic interstitial pH and blood flow were measured serially under basal conditions and after secretory stimulation as chronic pancreatitis evolved. Basal pancreatic interstitial pH was also measured in patients undergoing an operation for chronic pancreatitis or periampullary cancer (controls).nnnRESULTSnIn normal cats, pancreatic interstitial pH was 7.41 +/- 0.01 and blood flow was 124 mL.min-1.(100 g pancreas-1). With the evolution of chronic pancreatitis, interstitial pH and blood flow progressively decreased to 7.21 +/- 0.04 (P < 0.007) and 75 +/- 11 (P < 0.007), respectively. From 1 to 2 weeks, secretory stimulation reduced pancreatic interstitial pH and blood flow further, but as secretory function was lost, this effect disappeared. In patients with chronic pancreatitis, the interstitial pH was lower (7.02 +/- 0.06) than in controls (7.25 +/- 0.04; P < 0.05).nnnCONCLUSIONSnThese observations are consistent with the hypothesis that, in chronic pancreatitis, acidic metabolites associated with pancreatic secretion accumulate within the pancreas, probably because of impaired blood flow.

Endoscopic measurement of pancreatic tissue perfusion in patients with chronic pancreatitis and control patients

BACKGROUNDnPancreatic blood flow is diminished in experimental models of acute and chronic pancreatitis. We attempted to develop a safe and reliable technique for its measurement in patients and to examine blood flow in patients with chronic pancreatitis and in control subjects.nnnMETHODnPancreatic blood flow was measured using the hydrogen gas clearance technique and an endoscopically placed platinum ductal electrode. Pancreatic blood flow was measured in 12 patients with chronic pancreatitis diagnosed clinically and radiographically, and in 11 control patients undergoing endoscopic retrograde cholangiopancreatography (ERCP) for non-pancreatic pathology.nnnRESULTSnPatients with chronic pancreatitis had a significantly lower pancreatic blood flow compared with control patients (51.5 versus 91.7 mL/min/100 gm, p < 0.01). With secretin stimulation pancreatic blood flow increased in two control patients, whereas this notable rise was not seen in three patients with chronic pancreatitis.nnnCONCLUSIONSnMeasurement of pancreatic blood flow with an endoscopically placed electrode is relatively safe and simple to perform. The scarring and vascular fibrosis associated histologically with chronic pancreatitis is reflected in lower pancreatic blood flow.

Feline model of chronic obstructive pancreatitis : Effects of acute pancreatic duct decompression on blood flow and interstitial pH

BACKGROUNDnThe mechanism by which duct decompression (DD) relieves pain in patients with chronic pancreatitis (CP) is unknown. CP is associated with increased tissue pressure (IP), low pancreatic microvascular blood flow (PMBF), and interstitial pH (pH(I)). The aims of this study were to examine the effects of acute DD on PMBF, increased IP, and pH(I) in cats with CP.nnnMETHODSnThe main pancreatic duct was partially obstructed. At 6 weeks PMBF (ml/min/100g H2 gas clearance), IP (mmHg needle electrode), and pH(I) (microelectrode) were measured before and after secretin stimulation. The duct was then opened, and the studies were repeated.nnnRESULTSnPMBF normally increased with secretin stimulation (118 +/- 20 versus 271 +/- 52, P < 0.05). IP was unaltered, and pH(I) decreased as hydrogen ions produced during bicarbonate secretion were dissipated (7.41 +/- 0.01 versus 7.38 +/- 0.01, P < 0.05). In CP, basal PMBF was lower than normal (51 +/- 6 versus 118 +/- 20, P < 0.05) and decreased with stimulation (51 +/- 3.5 versus 31 +/- 3.5, P < 0.05). Basal pancreatic IP was increased (3.47 +/- 0.7 versus 0.05 +/- 0.3, P < 0.05) and increased further with secretory stimulation (3.47 +/- 0.7 versus 4.41 +/- 0.7, P < 0.05) (a compartment syndrome). The low basal pancreatic pH(I) (7.23 +/- 0.02) did not change with secretin stimulation, since bicarbonate secretion was minimal. DD decreased IP (3.66 +/- 0.5 versus 2.81 +/- 0.5, P < 0.05) and increased PMBF (50 +/- 6 versus 79 +/- 6, P < 0.05) and pH(I) (7.24 +/- 0.02 versus 7.34 +/- 0.02, P < 0.05). The normal increase in PMBF after stimulation was restored (79 +/- 6 versus 218 +/- 54, P < 0.05). pH(I) now increased with stimulation (7.34 +/- 0.002 versus 7.37 +/- 0.002, P < 0.05), perhaps due to the marked hyperaemic response.nnnCONCLUSIONSnDD acutely restored basal and stimulated PMBF and IP towards normal. Basal pancreatic pH(I) also improved and reflects the underlying ischaemia.

Stenting does not decompress the pancreatic duct as effectively as surgery in experimental chronic pancreatitis

BACKGROUNDnIn humans with chronic pancreatitis (CP), pancreatic interstitial pressure (IP) is elevated and pancreatic blood flow (PBF) is reduced. The efficacy of surgical decompression (SD) of the pancreatic duct (ie, pancreaticojejunostomy) is believed to be due to its ability to decrease IP and pancreatic vascular resistance (Rp), which increases PBF. Pancreatic duct stenting (STE) also probably reduces IP and Rp, which may explain its efficacy. The purpose of this study was to compare the efficacy of SD with STE.nnnMETHODSnCP in cats was created by narrowing the main pancreatic duct. Six weeks later, CP and normal pancreata were isolated and perfused ex vivo under basal conditions and after secretin stimulation. In normal and CP glands, IP and perfusion pressure were measured and Rp (U) was calculated. In two additional groups, the pancreatic duct was decompressed, either by stenting or by complete transection of the duct with a longitudinal capsulotomy.nnnRESULTSnIn CP glands, IP and Rp were increased and secretory output was markedly reduced compared with the normal (0.65 +/- 0.30 mm Hg and 0.46 +/- 0.04 U vs 3.90 +/- 0.80 mm Hg and 1.68 +/- 0.05 U; P < .05). Secretin administration (2 units) increased IP and Rp in CP glands (6.60 +/- 1.10 mm Hg and 2.87 +/- 0.07 U; P < .05), but these values did not chang in normal glands (0.81 +/- 0.20 and 0.53 +/- 0.03 U; NS). STE and SD decreased IP and Rp in CP glands (2.20 +/- 0.20 to 1.0 +/- 0.40 mm Hg and 1.20 +/- 0.015 to 0.90 +/- 0.01 U, respectively; P < .05). Both methods prevented an increase of IP and Rp after secretin administration. IP and Rp decreased to a greater degree following SD, compared with STE (P < .05).nnnCONCLUSIONSnBoth STE and SD decreased IP and Rp in this experimental model of CP. However, SD was significantly more effective than STE.

Palliation for pancreatic cancer

AbstractBackground: Although laparoscopy reveals undetected metastases in many patients with pancreatic cancer, most surgeons have chosen to proceed directly with laparotomy in an attempt at resection or for palliation of biliary and gastric outlet obstruction. In an effort to overcome this limitation, this study attempted to determine the feasibility of laparoscopic cholecystojejunostomy and gastrojejunostomy.nMethods: Under general anesthesia, seven pigs underwent laparoscopic cholecystojejunostomy and gastrojejunostomy using either a hand-sutured or the stapled/sutured technique.nResults: Mean operating time was less with the stapled/sutured vs hand-sutured technique (150±21 vs 230±13 min, P<0.05). All animals recovered completely and there was no change in their weight or liver function tests as a result of the procedure. At sacrifice, all anastomoses were patent, although some were significantly narrowed in these unobstructed animals.nConclusions: These results suggest that simultaneous laparoscopic palliation of biliary and gastric outlet obstruction is feasible. We believe these results warrant further study in the clinical setting.

Crossover saphenous vein bypass (Palma) in phlegmasia caerulea dolens caused by total iliac outflow obstruction.

Phlegmasia caerulea dolens (PCD) is a rare condition that usually tends to occur in association with malignancy, after surgery or trauma, postpartum, in patients with a history of deep vein thrombosis, and in association with a variety of inflammatory conditions. In approximately 10% of patients no underlying cause is found. PCD is characterized by total or near-total occlusion of the venous drainage of the limb. Associated mortality and morbidity rates are high. Contemporary venous thrombectomy, including thrombus removal and arteriovenous fistula (AVF), may improve results. A crossover saphenous vein bypass offers distinct advantages when surgical clearance of the iliac vein is not feasible.

Ethanol-Mediated Neutrophil Extravasation in Feline Pancreas

Ethanol is a common cause of both acute andchronic pancreatitis. Studies in other organs suggestthat polymorphonuclear neutrophils activated by ethanolmay cause tissue injury in a variety of conditions. The aim of this study was to investigate theeffects of ethanol on neutrophil extravasation in thefeline pancreas. Pancreata were isolated and perfused atdifferent flow rates with varying concentrations of ethanol in either a physiological orneutrophil depleted perfusate. Neutrophil extravasationwas assessed by measuring pancreatic tissuemyeloperoxidase (MPO) activity. Ethanol at 2.5 (54.25mmol/liter) was the lowest concentration that still causedsignificant neutrophil extravasation (3.1 ± 0.8vs 1.9 ± 0.2 units, P < 0.05) and wasaccompanied by an increase in vascular resistance of15%. Reduction of pancreatic perfusion by 15% did notsignificantly increase neutrophil extravasation. (1.1± 0.3 vs 1.6 ± 0.2 units, NS) Perfusion ofthe pancreas with neutrophil-depleted blood containingeither ethanol or saline, followed by perfusion withan ethanol-free perfusate, showed an increase inneutrophil extravasation in the ethanol group comparedto the control group (3.2 ± 0.9 vs 1.9 ±0.2 units, P < 0.05). In conclusion, ethanol causesneutrophil extravasation in the feline pancreasindependent of blood flow changes and occurs despite theabsence of direct neutrophil exposure toethanol.