Reconstruction of Complex Abdominal Wall Defects

Introduction

Reconstruction of large abdominal wall defects not amenable to primary closure remains a challenging problem. These defects result from trauma, previous surgery, infection and tumour resection. The primary objectives of abdominal wall reconstructions are to protect abdominal contents and provide functional support. The abdominal wall reconstruction aims at providing basic component parts, i.e. skin, soft tissue and fascia. For large soft tissue defects, pedicled or free flap closure can be used. In clean wounds, fascial replacement is accomplished with synthetic mesh provided there is adequate soft tissue coverage.

Methods

We treated a total of 20 consecutive patients with complex abdominal wall defects utilizing various reconstructive procedures. There were 15 males (75%) and 5 females (25%). The aetiology included dehiscence of laparotomy wounds in eight (40%), following ablative surgery for malignant tumours in seven (35%), trauma in three (15%) and congenital defects in two (10%) cases. The reconstructive procedures consisted of onlay prolene mesh in seven (35%), Gore-Tex (PTFE) dual mesh both as inlay and onlay in five (25%), facial partition release technique in three (15%), inlay prolene mesh covered with omentum and split skin graft in two (10%), inlay prolene mesh covered with expanded skin in two (10%), and Gore-Tex dual mesh covered with latissimus dorsi myocutaneous flap in one (5%) case. Postoperatively none developed mesh infection or extrusion. Three patients with malignant aetiology received postoperative radiotherapy. During follow up, one patient developed ventral hernia cephalad to the repair and one died due to recurrence of abdominal wall malignancy.

Conclusion

The reconstruction of an abdominal wall defect requires a comprehensive plan of preoperative and post operative care of the patient and aims toward restoration of abdominal structural integrity by a variety of procedures. The use of new biomaterials and tissue expanders provides reliable and durable abdominal wall closure along with good aesthetic results.Key Words: Abdominal wall defect, Mesh repair, Abdominal wall reconstruction     

The Role of anti-HBc IgM in Screening of Blood Donors

Background

Transfusion transmitted hepatitis B has always been a dreaded disease, with incidence of increased transmission through donated blood. The screening test for hepatitis B infection is detection of HBsAg that does not rule out the risk of transmission of hepatitis B as the donor may be in the ‘window period’. During this period, detection of the antibody to the hepatitis B core antigen (anti-HBc) IgM type serves as a useful serological marker. The aim of this study was to screen blood donors for anti-HBc type IgM and anti - HBc Ag total for detection and to find their incidence amongst blood donors.

Methods

2552 voluntary blood donors were screened by the ELISA method for HBsAg and anti - HBc IgM and other mandatory screening markers. 704 of the test blood samples were also screened for anti-HBc total.

Result

Of the 2552 donor, 47 (1.84 %) cases were HBsAg positive. A total of 11 (0.43 %) blood units were reactive for HBcAg IgM and of these, 10 (0.39 %) were HBsAg negative and reactive for anti-HBcAg IgM. Of the 704 samples tested for anti - HBcAg total, 112 (15.9%) samples were reactive.

Conclusion

Screening of blood for anti-HBc total is practical in the western world as the incidence of HBsAg and anti-HBc is low in these countries and these positive blood units for anti - HBcAg total can be discarded. This may not be practical in India as the incidence of anti- HBcAg total is high in our population. It is recommended that all blood units should be tested for anti - HBc IgM for infectivity status of the blood donors in the window period and to discard blood if positive.Key Words: Window period, Hepatitis B surface antigen, Anti hepatitis B core antigen     

Enhanced allostimulatory activity of host antigen-presenting cells in old mice intensifies acute graft-versus-host disease

Older bone marrow transplantation (BMT) recipients are at heightened risk for acute graft-versus-host disease (GVHD) after allogeneic BMT, but the causes of this association are poorly understood. Using well-characterized murine BMT models we have explored the mechanisms of increased GVHD in older mice. GVHD mortality, morbidity, and pathologic and biochemical indices were all worse in old recipients. Donor T cell responses were significantly increased in old recipients both in vivo and in vitro when stimulated by antigen-presenting cells (APCs) from old mice, which also secreted more TNF-alpha and IL-12 after LPS stimulation. In a B6 --> B6D2F1 model, CD4(+) donor T cells but not CD8(+) T cells mediated more severe GVHD in old mice. We confirmed the role of aged APCs in GVHD using B6D2F1 BM chimeras created with either old or young BM. Four months after chimera creation, allogeneic BMT from B6 donors caused significantly worse GVHD in old BM chimeras. APCs from these mice also stimulated greater responses from allogeneic cells in vitro. These data demonstrate a hitherto unsuspected mechanism of amplified donor T cell responses by aged allogeneic host APCs that increases acute GVHD in aged recipients in this BMT model.     

The management of ultrasound equipment at Sheffield Teaching Hospitals NHS Foundation Trust

Management of ultrasound equipment at Sheffield Teaching Hospitals NHS Foundation Trust is described. The organisation and input of various stakeholders and their involvement with ultrasound equipment management and scientific ultrasound is discussed. Two important stakeholders are the Medical Equipment Management Group and the Radiation Safety Steering Committee. The Medical Equipment Management Group has a specific sub-group, the Ultrasound sub-group, and its role is to coordinate the purchase, replacement and quality assurance of ultrasound equipment in the Trust. The Radiation Safety Steering Committee has a non-ionising radiation representative and the role of this committee is to provide corporate assurance that any health and safety issues arising from the use of radiation to either patients, members of the public or staff within the Trust are being effectively managed. The Ultrasound sub-group of the Medical Equipment Management Group has successfully brought together management of all ultrasound equipment within the Trust and is in the process of fulfilling the quality assurance and training milestones set out by the Medical Equipment Management Group. Advice from the Radiation Safety Steering Committee has helped to increase awareness of ultrasound safety and good scanning practice, especially in the case of neonatal ultrasound imaging, within the Trust. In addition, the RSSC has given advice on clinical pathways for patients undergoing ionising radiation imaging while being treated by extra-corporeal shockwave lithotripsy.     

Recurrent B-cell non-Hodgkin's lymphoma in two brothers with X-linked lymphoproliferative disease without evidence for Epstein-Barr virus infection

We present two male siblings suffering from recurrent manifestations of B-cell non-Hodgkin's lymphoma (NHL) and recurrent infections of the lower respiratory tract associated with bronchiectasis. Immunodeficiency could not be demonstrated by any laboratory investigation. In both patients, lymphomas developed without evidence for Epstein-Barr virus (EBV) infection, i.e. no antibody response to EBV-specific antigens, negative EBV-PCR (polymerase chain reaction) in peripheral blood cells, and absence of latent membrane protein (LMP) and EBV-encoded RNA (EBER) in lymphoma cells. Molecular analysis of the SH2D1A, the gene for X-linked lymphoproliferative disease (XLP) led to the identification of a deletion in the first exon in both patients. Therefore, we postulate that the genetic defect and the following dysregulation of the B-/T-cell interaction rendered these patients susceptible to the early onset of B-cell NHL and that EBV infection is not an obligate prerequisite.     

Effect of surfaces on fluid-phase prekallikrein activation

The activation of prekallikrein by factor XII fragments (XIIf), during incubation in plastic tubes was previously noted to be increased by high molecular weight (HMW) kininogen as well as other plasma proteins. In this report, we investigated the mechanism responsible for this increase. Although we confirmed that HMW kininogen, bovine serum albumin, fibrinogen, cold insoluble globulin, and mixed phospholipids apparently increased prekallikrein activation, we found that the product of prekallikrein activation (kallikrein) lost substantial activity in less than 0.5 min after exposure to a variety of fresh surfaces. This loss was partially prevented by the presence of various proteins and phospholipids. Similar protection against inactivation of XIIf, the enzyme in this reaction, was also found. In contrast, no loss of the substrate, prekallikrein, was observed during incubation. The loss of kallikrein activity was found to be proportional to the surface area of the incubation vessel as well as the concentration of kallikrein. Further loss of kallikrein activity could also be prevented by pretreating the vessel with kallikrein. We therefore conclude that various substances apparently affect prekallikrein activation in a purified system by preventing the enzyme and product in the reaction mixture from losing activity due to adsorption to a surface.     

A human antibody binds to alpha-galactose receptors and mimics the effects of Clostridium difficile toxin A in rat colon

BACKGROUND & AIMS: Nearly all human sera contain an immunoglobulin G antibody (antigalactose) that binds the trisaccharide Gal alpha 1-3Gal beta 1-4GlcNAc expressed on cells from most mammals but not humans. Because the Clostridium difficile toxin A receptor in rodents contains this trisaccharide, the aim of this study was to examine whether antigalactose could mimic the enterotoxic effects of toxin A and bind to receptors containing this trisaccharide. METHODS: Fluid secretion, [3H]-mannitol permeability, and release of rat mast cell protease II and prostaglandin E2 were measured after luminal exposure of rat colon to either purified human anti-galactose, control immunoglobulin G, toxin A, or buffer. RESULTS: Toxin A (5 micrograms) and antigalactose (250 micrograms) but not control immunoglobulin (250 micrograms) stimulated colonic fluid secretion and caused increased mannitol permeability and rat mast cell protease II release. Antigalactose and toxin A and, to a lesser degree, control immunoglobulin G also stimulated release of prostaglandin E2, but only toxin A produced acute inflammation of rat colonic mucosa. Antigalactose and toxin A bound specifically to a single class of colonic brush border receptors with dissociation constants of 10(-6) mol/L and 5.4 x 10(-8) mol/L, respectively. CONCLUSIONS: Fluid secretion, increased permeability, and mast cell activation occur in rat colon when toxin A or human antigalactose immunoglobulin G bind to receptors bearing the trisaccharide Gal alpha 1-3Gal beta 1-4GlcNAc. (Gastroenterology 1996 Jun;110(6):1704-12)     

Estrogen mediates the sex difference in post-burn immunosuppression

Previous studies in our laboratory have demonstrated that cell-mediated immune function was suppressed in female, but not male, mice at 10 days after burn injury and was mediated, in part, by increased production of interleukin-6 (IL-6). Because 17beta-estradiol (E(2)) influences immune function after trauma and the hormone is known to regulate IL-6 production, the effect of E(2) on immune function after thermal injury was examined. Increased circulating concentrations of E(2) corresponded with suppressed delayed-type hypersensitivity (DTH) and splenocyte-proliferative responses, and increased circulating concentrations of IL-6 in female mice after burn. Ovariectomy restored the suppressed DTH response and decreased IL-6 concentrations, and administration of exogenous E(2) to both ovariectomized females and intact male mice resulted in a suppressed DTH response. In addition, in vitro treatment with E(2) suppressed splenocyte proliferation in a macrophage-dependent manner and enhanced macrophage production of IL-6. These results strongly suggest that the sex difference in cell-mediated immunity 10 days after burn injury is mediated by altered concentrations of E(2), which in turn modulate key macrophage-derived immunoregulatory cytokines.     

Fibrinogen biosynthesis in isolated guinea pig megakaryocytes

Fibrinogen synthesis was investigated in guinea pig megakaryocytes. Purified megakaryocytes were incubated with 35S-methionine in methionine-free incubation medium for 18 hours. Newly synthesized fibrinogen in megakaryocyte lysates enriched with purified carrier guinea pig fibrinogen was immunoprecipitated with a specific anti- guinea pig fibrinogen antiserum produced in rabbits. Proteins in the immunoprecipitates were analyzed with a 3.5% to 10.0% gradient polyacrylamide slab gel electrophoresis and auto-radiography. Radioactivity was detected in a protein band of 340,000 daltons. In order to verify fibrinogen synthesis, immunoprecipitate was analyzed by two-dimensional slab gel electrophoresis: (1) the first dimension separated unreduced fibrinogen using a 3.5% to 10.0% gradient gel; (2) following reduction by 2-beta-mercaptoethanol, fibrinogen chains were separated in the second dimension using a 10% gel. Alpha, beta, and gamma fibrinogen chains, which represented carrier guinea pig plasma fibrinogen, were visualized by Coomassie brilliant blue. Autoradiography identified the incorporation of radioactivity into the three fibrinogen chains. In control experiments, immunoprecipitates, produced by exposing megakaryocyte lysates to preimmune rabbit serum and goat anti-rabbit IgG, were also analyzed by the two-dimensional gel system. Radioactivity was not detected in sites corresponding to the migration of fibrinogen subunits. The study demonstrates that isolated guinea pig megakaryocytes can synthesize fibrinogen. The electrophoretic mobility of newly synthesized fibrinogen and subunits is similar to that of guinea pig plasma fibrinogen.     

Correlation of drug sensitivity in vitro with clinical responses in childhood acute myeloid leukemia

Clonogenic cells from 41 children with newly diagnosed acute myeloid leukemia (AML) were tested in vitro for their sensitivity to cytarabine (Ara-C) and daunorubicin (DNR). The findings were then compared with the patients' responses to induction chemotherapy that uniformly included Ara-C and DNR. Light-density marrow cells were incubated with either or both drugs for one hour and cultured over leukocyte feeder layers; clusters and colonies were scored on days 7, 10, and 14. Only the percentage of cell kill in the presence of 1.8 mumol/L DNR was significantly associated with responses to induction therapy: median of 45% (range, 0% to 98%) for patients achieving complete remission v 16% (range, 4% to 23%) for nonresponders (P = .007). The relationship between clonogenic cell kill less than or equal to 23% and clinical responses was striking. Of the 11 evaluable patients with in vitro findings in this category, ten either failed induction therapy or relapsed within 1 year after attaining remission. Kaplan-Meier analysis of relapse-free survival times indicated longer durations of remission for patients whose blast cells showed increased sensitivity in vitro to Ara-C alone, DNR alone, or a combination of the two agents. Seven of 11 patients with cell kills of greater than or equal to 49% in the presence of 1.25 mumol/L Ara-C remain free of leukemia, compared with only one of 12 whose cells were less sensitive to the drug (P = .006). We conclude that the in vitro sensitivity of clonogenic leukemic progenitors to DNR and Ara-C correlates with treatment outcome in children with newly diagnosed AML.