Laparoscopic splenopexy for wandering spleen, a video demonstration of technique by encircling the spleen with polyglactin 910 woven mesh.

BACKGROUND: Wandering spleen is a rare clinical entity caused by absence of the spleen's peritoneal attachments, allowing the spleen to move freely within the peritoneal cavity [1]. This disease is most commonly seen in children and young women [1, 2]. Affected individuals are predisposed to complications including splenic torsion, splenic infarction, and pancreatic necrosis [3, 4]. Patients may present with constipation, an abdominal mass, swelling, or acute abdominal pain if splenic torsion has occurred [4]. Wandering spleen is difficult to diagnose without imaging, as symptoms are non-specific or may be absent. Imaging studies to confirm the diagnosis may include computed tomography (CT) scan or duplex ultrasonography [5]. Definitive management of a wandering spleen is primarily surgical [2]. Splenectomy is the preferred treatment in patients who present with an acute splenic infarction [2, 6]. Splenopexy, however, is first line treatment for patients with a non-infarcted wandering spleen [2, 7, 8]. CASE PRESENTATION: In this video, we present a case of an 11 year old male with a symptomatic wandering spleen who was treated at our institution with laparoscopic splenopexy. The patient had a history of arthrogryposis multiplex congenita and presented with recurrent, episodic abdominal pain, nausea, and vomiting. The diagnosis was confirmed by CT scan which demonstrated the spleen in the right lower quadrant. We performed laparoscopic splenopexy by encircling the spleen with polyglactin 910 woven mesh and attaching the mesh to the left lateral abdominal wall with absorbable tacks. DISCUSSION: Our surgical technique for splenopexy was successful and the patient returned home on postoperative day four. No significant complications occurred. This video demonstrates this technique and highlights the key steps. Splenopexy by encircling the spleen with polyglactin 910 mesh is feasible, preserves splenic function, and can be performed with standard laparoscopic equipment. Tacks or transfascial sutures are a potential option for securing mesh.

Drosophila polypyrimidine tract-binding protein is necessary for spermatid individualization.

Although mammalian polypyrimidine tract-binding (PTB) protein functions in most or all cell types to regulate a wide spectrum of transcripts, Drosophila PTB encodes an abundant male germline-specific mRNA isoform (dmPTB) whose expression correlates with male fertility. The biological function of this isoform is unknown. Using selection-amplification, we show that mammalian and Drosophila PTB have similar RNA sequence preference, suggesting that cell-specific expression rather than unique RNA-binding properties account for the sex-specific function of dmPTB. We also show that the dmPTB protein isoform expressed in the male germline is by far the most abundant isoform, and reduction of its levels correlates with male sterility. Finally, we show that dmPTB expression is necessary for proper spermatid individualization, the terminal step necessary for production of motile sperm. Loss of dmPTB results in severe disruption of the actin cones of the spermatid individualization complex. This represents a cytological defect resulting from PTB loss. We discuss the basis for functional differences between mammalian and Drosophila PTB orthologs.

Crystalline bacterial biofilm formation on urinary catheters by urease-producing urinary tract pathogens: a simple method of control.

The problem of catheter encrustation stems from infection by urease-producing bacteria. These organisms generate ammonia from urea, elevate the pH of urine and cause crystals of calcium and magnesium phosphates to form in the urine and the biofilm that develops on the catheter. In this study, a laboratory model was used to compare the ability of 12 urease-positive species of urinary tract pathogens to encrust and block catheters. Proteus mirabilis, Proteus vulgaris and Providencia rettgeri were able to raise the urinary pH above 8.3 and produce catheter-blocking crystalline biofilms within 40 h. Morganella morganii and Staphylococcus aureus elevated the pH of urine to 7.4 and 6.9, respectively, and caused some crystal deposition in the biofilms but did not block catheters in the 96 h experimental period. Isolates of Klebsiella pneumoniae, Klebsiella oxytoca, Enterobacter cloacae, Serratia marcescens, Pseudomonas aeruginosa and Providencia stuartii were only capable of raising the pH of urine to a maximum of 6.4 and failed to cause crystal deposition in the biofilm. The most effective way to prevent catheter encrustation was shown to be diluting urine and increasing its citrate concentration. This strategy raises the nucleation pH (pH(n)) at which calcium and magnesium phosphates crystallize from urine. Increasing the fluid intake of a healthy volunteer with citrated drinks resulted in urine with a pH(n) of >8.0 in which catheter encrustation was inhibited. It is suggested that this dietary strategy will be an effective means of controlling catheter encrustation, whichever bacterial species is causing the problem.

A study of the structure of the crystalline bacterial biofilms that can encrust and block silver Foley catheters.

The aim of this study was to examine the structure of the crystalline bacterial biofilms that encrust and block silver/hydrogel-coated latex catheters. Scanning electron microscopy was used to examine the crystalline deposits that were found encrusting catheters obtained from six patients undergoing long-term catheterization in a community setting. Large populations of bacilli and cocci were seen on all catheters developing on a basal foundation layer of crystalline material. These observations show that in patients prone to catheter encrustation, crystalline material formed in the urine can cover the surfaces of silver catheters. Extensive bacterial biofilms then develop on the crystals, shielded from the underlying silver. It is suggested that if antimicrobials are to be incorporated into catheters to prevent encrustation, they must diffuse out from the catheter surface and reduce the viable cell populations of the urease producing bacteria that elevate the urinary pH and trigger crystal formation.

Modulation of crystalline Proteus mirabilis biofilm development on urinary catheters.

The crystalline biofilms formed by Proteus mirabilis can seriously complicate the care of patients undergoing long-term bladder catheterization. The generation of alkaline urine by the bacterial urease causes calcium and magnesium phosphates to precipitate from urine and accumulate in the catheter biofilm, blocking the flow of urine from the bladder. The pH at which these salts crystallize from a urine sample, the nucleation pH (pH(n)), can be elevated by diluting the urine and by increasing its citrate content. The aim of this study was to examine whether manipulation of pH(n) in these ways modulated the rate at which crystalline biofilm developed. Experiments in laboratory models of the catheterized bladder infected with P. mirabilis showed that when the bladder was supplied with a concentrated urine (pH(n) 6.7) at a low fluid output (720 ml per 24 h), catheters blocked at 19-31 h. Diluting this urine 1:4 increased the pH(n) to 7.5 and models supplied with this urine at 2880 ml per 24 h took 110-137 h to block. When models were supplied with urine containing citrate at 1.5 mg ml(-1) or above (pH(n) 8.3-9.1), the catheters drained freely for the full 7 day experimental period. Scanning electron microscopy revealed that the catheter biofilms that developed in urine with high pH(n) values were devoid of crystalline formations. These observations should encourage a clinical trial to examine the effect of increasing a patient's fluid intake with citrate-containing drinks on the encrustation and blockage of catheters.