A review of external lumbar drainage for the management of intracranial hypertension in traumatic brain injury.

BACKGROUND: The Brain Trauma Foundation (BTF) published evidence-based guidelines with a detailed approach to the management of intracranial hypertension (ICH) in traumatic brain injury (TBI) patients. However, management with cerebrospinal fluid (CSF) drainage in TBI patients remains a controversial topic and is a recent addition to the 4th Edition of the BTF guidelines. External lumbar drainage (ELD) has been proposed for the management of patients with refractory ICH despite aggressive measures. ELD has been described in the literature with possible benefits in outcomes; still, many questions remain unanswered. METHODS: A systematic search on MEDLINE was conducted for articles that studied lumbar CSF drainage in adult TBI patients with ICH. RESULTS: Eleven studies met the inclusion criteria, which included 5 prospective and 6 retrospective studies. Several studies showed that CSF drainage via lumbar drain resulted in significant reduction of ICP compared to before ELD placement and had a low complication rate. However, the data reporting mortality and functional outcomes are varied across studies. CONCLUSION: The literature suggests that ELD may play a role in the management of refractory ICH in TBI patients when first and second-tier measures fail and may be a safe, effective, and minimally invasive method to significantly lower ICP. Additional research and standardized treatment protocols are necessary.

Vena cava filter placement using a cutdown of the superficial epigastric vein.

Percutaneous placement of vena cava filters through the femoral vein has been associated with insertion site venous thrombosis. Reported incidence varies from 2% to 41%. In the majority of placements, sequential dilators are used to create the venotomy and subcutaneous tract. This technique disrupts all layers of the vein wall. The injured area may extend as far proximal as the dilator or sheath is placed. The authors present their experience with placement of vena cava filters using a cutdown of the superficial epigastric vein. During a 5-year period, 27 patients underwent placement of the LGM-Vena Tech vena cava filter via a femoral approach. A cutdown of the superficial epigastric vein was performed. The guidewire, dilator, and introducer sheath were inserted under direct fluoroscopic examination. After removal of the dilator, the LGM-Vena Tech filter was placed through the introducer. There were no wound infections and no clinical signs of insertion site venous thrombosis in the postoperative period. Insertion site venous thrombosis is a well-documented complication of percutaneous filter placement. Superficial epigastric vein cutdown is a reasonable alternative technique, which allows gentle atraumatic manipulation of the femoral vein. It is a simple, safe procedure that can be performed without any significant increase in operative time and no additional morbidity.

Double-layer everted saphenous vein patch angioplasty for carotid endarterectomy.

Saphenous vein patch angioplasty is the preferred method of closure of the arteriotomy site during carotid endarterectomies. A major early complication of the saphenous vein patch is rupture of the patch which can occur within the first few postoperative days. The reported incidence varies from 0.5% to 4%. Patch rupture can result in stroke or death. From May 1992 to April 1999, autogenous everted double-layer saphenous vein patch was used in 192 carotid endarterectomies performed on 168 patients; 96 males and 72 females. The age range was from 54 to 94 years with a mean age of 73 years. The saphenous vein is harvested from the ankle. It is everted and then used as a double-layer patch. The follow-up period was from 3 to 74 months, with a mean of 24 months. Postoperatively, there were no patch ruptures or late aneurysm formation. There was no perioperative mortality. Everted double-layer saphenous vein patch eliminates the risk of patch rupture and at the same time retains the benefits of an autologous nonprosthetic graft. Saphenous vein from the ankle can be safely used for carotid angioplasty as a double layer patch.

Use of a Fogarty catheter to open an incompletely expanded Vena Tech-LGM vena cava filter--a case report.

A Vena Tech-LGM 30D/U filter (B. Braun/Vena Tech; Evanston, IL) opened incompletely after transjugular placement in the infrarenal vena cava. The cephalic points of the stabilizing side rails were open and had engaged the caval wall. The base of the filter failed to open. The filter would not successfully inhibit the clots and could possibly migrate. The filter base was not placed in a clot as shown with intraoperative venography before and after the placement. The balloon of a 6F Fogarty catheter was used successfully to dilate the distal legs of the filter, and fully expand the base.

Laparoscopic pyloroplasty in idiopathic hypertrophic pyloric stenosis in an adult.

BACKGROUND AND OBJECTIVES: Idiopathic hypertrophic pyloric stenosis, in adults, is a rare disease. Partial gastrectomy, gastroenterostomy, pyloromyotomy, pyloroplasty and endoscopic dilatation have all been recommended with variable results. A 54-year-old white female is presented with the onset of symptoms of idiopathic hypertrophic pyloric stenosis one year prior to operation. Two endoscopic pyloric sphincter balloon dilatations provided only temporary relief. METHOD: A laparoscopic pyloroplasty was performed. RESULT: The patient tolerated a solid diet on postoperative day three. The patient was symptom-free at a 13 month follow-up. CONCLUSIONS: Idiopathic hypertrophic pyloric stenosis in adults can be treated with laparoscopic pyloroplasty, offering a minimally invasive alternative to open repair.

Phospholipase A2 enzymes regulate alpha IIb beta3-mediated, but not Fc gammaRII receptor-mediated, pp125FAK phosphorylation in platelets.

The alphaII(b)beta3 integrin and FcgammaRII receptors mediate, respectively, platelet adhesion and spreading on fibrinogen and immunoglobulin (IgG) coated surfaces. Platelet adhesion to fibrinogen resulted in a partial conversion of the faster to the slower migrating (phosphorylated) form of Ca(+2)-sensitive cytosolic phospholipase A2(cPLA2) but failed to trigger arachidonic acid (AA) release. Full mobility shift of cPLA2 and a massive release of AA release were stimulated by platelet adhesion to IgG or addition of thrombin to the fibrinogen adherent platelets. IgG and thrombin induced AA production were blocked by methyl arachidonyl fluorophosphonate (MAFP), an irreversible inhibitor of cPLA2 and the Ca(+2)-independent phospholipase A2 (iPLA2). In contrast, bromoenol lactone (BEL), a specific inhibitor of iPLA2 had no effect on the release of AA. MAFP and BEL prevented pp125FAK phosphorylation and platelet spreading on fibrinogen having no effect on pp125FAK phosphorylation or platelet spreading on immobilized IgG. We conclude that alpha(IIb)beta3-mediated pp125FAK phosphorylation and platelet spreading on fibrinogen are regulated by PLA2 enzymes.

The FcgammaRII receptor triggers pp125FAK phosphorylation in platelets.

Platelets express a single low affinity receptor for immunoglobulin, FcgammaRII, that triggers multiple cellular responses upon interaction with multivalent immune complexes. In this study we show that immobilized IgG is also a potent stimulant of platelet activation triggering adhesion, aggregation, massive dense granule secretion, and thromboxane production. Platelet adhesion to IgG was blocked by the FcgammaRII receptor-specific monoclonal antibody, IV. 3. Pretreatment of the platelets with cytochalasin D to inhibit actin polymerization similarly prevented cell binding to IgG having no effect on platelet binding to fibrinogen. Platelet adhesion to IgG also led to the induction of tyrosine phosphorylation of multiple proteins including pp125(FAK) and p72(SYK). These proteins were also tyrosine-phosphorylated in alphaIIbbeta3-deficient IgG-adherent platelets from patients with Glanzmann's thrombasthenia. These data demonstrate that FcgammaRII mediates pp125(FAK) phosphorylation and platelet adhesion to IgG independent of the integrin alphaIIbbeta3. Treatment of the platelets with bisindolylmaleimide to inhibit protein kinase C prevented phosphorylation of pp125(FAK) as well as several other proteins, but not p72(SYK) phosphorylation. This study establishes that the FcgammaRII receptor mediates pp125(FAK) phosphorylation via protein kinase C.