Avoiding laparotomy in nonsurgical pneumoperitoneum.

Patients with free intraperitoneal air collections usually undergo emergency surgery, and the majority will have a gastrointestinal tract perforation. However, there is a subset of patients in whom no identifiable perforation is found at surgery. This entity of noniatrogenic, nonsurgical spontaneous pneumoperitoneum is being diagnosed more frequently at present and is commonly associated with other disease processes that, together, may suggest a benign process. Therefore, a diagnostic algorithm that would preclude operative intervention in this cohort of patients would be of paramount clinical importance. In this report, we present representative cases of the most common types of nonsurgical pneumoperitoneum, review the pathogenesis of this disorder, and discuss its relationship with pneumatosis cystoides intestinalis, pulmonary disorders, scleroderma, and gynecologic processes. Finally, we outline a diagnostic algorithm that may identify patients who can safely be observed, thereby reducing the incidence of negative laparotomies and, secondarily, the aggregate cost of health care.

Proliferative pancreatic cysts: pathogenesis and treatment options.

Proliferative pancreatic cysts are subdivided into microcystic and mucinous cystadenomas. These rare, slow-growing, multilocular lesions usually remain localized for long periods of time, therefore frequently becoming rather sizeable before becoming symptomatic. Patients present with intermittent abdominal or back pain, nausea and vomiting, early satiety, and a palpable mass without a history of trauma or alcoholism. Computed tomographic scanning is the most useful laboratory test. The lesions are more often found in women, with the microcystic adenomas usually located in the head of the pancreas and the mucinous lesions in the pancreatic body or tail. At surgery, if it is at all possible, the lesions should be completely removed, even if it means performance of a Whipple procedure. This is particularly important for mucinous cysts because of their potential for malignant degeneration. Internal drainage or marsupialization procedures should not be done in these patients. The long-term results are excellent if the entire lesion is removed.

L-alpha-phosphatidylcholine-induced stimulation of PGI2 production in canine gallbladders following hypovolemic shock and Escherichia coli sepsis.

In vitro production of PGI2 in canine gallbladders subjected to hypovolemic shock and Escherichia coli sepsis was studied to determine whether a precursor above arachidonic acid in the cyclooxyenase cascade might be operative in the production of prostacyclin, which, in turn, may play a role in the pathogenesis of acute acalculous cholecystitis (AC). L-alpha-phosphatidylcholine (LaP), an arachidonic acid precursor, was used as the test agent. LaP did not stimulate PGI2 production from either gallbladder surface in the hypovelimic animals or the mucosa of the septic shock group. However, it did stimulate PGI2 production from the SS serosa compared with controls, 1375 +/- 432 versus 633 +/- 198 pg/cm2/min (P less than .05). In conclusion, lack of stimulation of PGI2 in the hypovolemic model suggests that PGI2 does not play a role in AC. Alternatively, it may play a role in preventing this disease process in septic shock. This study demonstrates the use of precursors of arachidonic acid and the cyclooxygenase pathway as active participants in the production of PGI2, although it is unclear whether the prostacyclin produced helps prevent AC in septic shock.

The effects of dimethyl sulfoxide on aortic prostacyclin production and serum thromboxane and plasma fibrinogen levels in rabbits fed a normal versus a cholesterol-enriched diet.

Through an unknown mechanism, dimethyl sulfoxide (DMSO) retards atherogenesis in cholesterol-fed rabbits (CFR). We studied the effects on the development of lesions and prostacyclin (PGI2) production in the thoracic aorta and total serum lipid and cholesterol content of the abdominal aortic serum thromboxane (TXB2) and plasma fibrinogen levels in rabbits fed control versus atherogenic diets, with and without DMSO. Without DMSO, PGI2 production was significantly higher in CFR versus control animals (8.65 +/- 1.0 vs 6.38 +/- 0.3 ng/15 min [p less than 0.02]). DMSO did not influence PGI2 production in any of the groups but significantly reduced the number of atheromatous lesions in CFR (78% +/- 9% vs 8% +/- 4% [p less than 0.001]). With DMSO, CFR had a significant reduction in total lipid levels (422 +/- 5 vs 300 +/- 21 mg/gm dry wt [p less than 0.01]) and cholesterol levels (74 +/- 12.8 vs 31.8 +/- 6.4 mg/gm dry wt [p less than 0.01]) compared with control animals. Fibrinogen levels were significantly lower in CFR versus control animals (0.83 +/- 0.07 vs 2.42 +/- 0.13 mg/ml [p less than 0.01]). TXB2 was lower in DMSO plus control versus control animals alone. In conclusion, DMSO does not appear to act through changes in PGI2 or fibrinogen activity. Its effect in lowering TXB2 in CFR suggests an action on platelet function.

Late arterial erosion of a Crutchfield vascular clamp presenting with transient ischemic attacks: review of treatment options.

Crutchfield clamps were once widely used for proximal carotid artery ligation in the treatment of intracranial aneurysms and cavernous sinus fistulae. Consequently, there are a number of patients being followed who were treated with this device 10 to 15 years ago. The most important complication of this treatment modality in both the early and late postoperative period is thromboembolic phenomenon presenting as transient ischemic attacks, or a frank stroke. Because of the residual patient population with this device still in place, interval reports regarding the occurrence and treatment of late complications are important. We report a patient who underwent Crutchfield clamp application for control of a cavernous sinus fistula and had done well for 20 years when he developed transient ischemic attacks (TIA). Arteriography revealed a severe stenotic lesion (greater than 90%) in the common carotid artery with a patent internal carotid artery and no evidence of the previous fistula and an ulcerated plaque. At surgery, the pressure plate of the clamp had achieved an intraluminal position. The stenotic area was resected and an end to end anastomosis performed with complete resolution of symptoms after 18 months of follow-up. In this report we review the literature for complications of this device and discuss treatment options.

Jejunal angiodysplasia presenting as acute lower gastrointestinal bleeding.

Vascular malformations of the bowel are uncommon sources of gastrointestinal (GI) tract bleeding with the majority of cases occurring in the right colon in elderly patients. Angiodysplasia can be difficult to diagnose, thereby complicating management as well. In the past, the diagnosis of angiodysplasia was rarely made early and rested upon a high index of suspicion in patients with lower GI bleeding and multiple negative diagnostic evaluations. Consequently, surgery was often performed late with increased morbidity and high recurrence rates. With the advent of pre- and intraoperative selective angiography, these vascular malformations are readily demonstrated in most cases and will often respond to conservative interventional radiologic procedures. Failing this, angiographic localization has made segmental resection both safe and quite accurate, thus obviating extensive, blind excision.

Decrease in cyclosporin-mediated prostacyclin production in renal versus carotid arteries: a mechanism for cyclosporin-induced hypertension.

Although the mechanism of cyclosporin (CsA)-induced hypertension is unknown, it has been shown to inhibit prostacyclin (PGI2) production directly, which may be a factor. We determined whether CsA had a differential effect on PGI2 production from the carotid artery (CA) and internal jugular vein (JV) compared to that from the renal artery (RA) and vein (RV) as a possible contributing factor to renovascular hypertension based upon the ability of organs to regulate their own blood flow according to local circumstances. The neck and renal vessels were removed from anesthetized adult female dogs (N = 8) and placed in a stimulation chamber, with Cell I being control (Hepes buffer), Cell II containing 0.3 mg/ml CsA, and Cell III containing CsA and 25 microM arachidonic acid (AA). Following serial stimulation periods, the supernatant was evaluated for PGI2 production by radioimmunoassay. PGI2 production from CA was significantly higher than that from RA following control and AA stimulation, 1474 +/- 382 pg/cm2-min vs 733 +/- 173 pg/cm2-min (P less than 0.05) and 2236 +/- 347 vs 1090 +/- 217 (P less than 0.01), respectively. CsA-induced PGI2 production from the carotid arteries was significantly greater than that from the renal arteries, 2944 +/- 586 vs 1003 +/- 235 (P less than 0.005). However, stimulation with AA following CsA resulted in sustained PGI2 production in both arteries that was similar to stimulation with CsA alone, 3014 +/- 600 vs 2944 +/- 586 for the carotids and 1278 +/- 280 vs 1003 +/- 235 for the renal arteries.(ABSTRACT TRUNCATED AT 250 WORDS)