Duraplasty: Our Current Experience - 3 go / dental&marketing

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56 Surg Neurol Caroli et al 2004;61:55–9 period. Four of the 239 remaining patients presented complications suspected to be related to the dural implant. CASE 1 A 28-year-old man was operated on for arachnoid cyst in posterior cranial fossa, and a Tutoplast pericardium implantation was performed. Immediately after operation, the patient presented fever and meningismus. A computed tomography (CT) scan showed a cerebral spinal fluid (CSF) collection in the operative field. Multiple CSF cultures failed to reveal bacterial growth. The symptoms were abated by corticosteroid administration. CASE 2 A 47-year-old woman was operated on for a melanoma of the cavernous sinus, and a Tutoplast pericardium patch implantation was performed. On the 50 th postoperative day she presented rhinorrhea, headache, neck stiffness, and fever. Cultures of the CSF were positive for Enterococcus faecalis. The patient was treated with antibiotic therapy, and after 1 week the clinical picture regressed and 1 month later the cultures of the CSF were negative. In this case a second operation was not performed because rhinorrhea ceased spontaneously. CASE 3 A 42-year-old man operated on for cerebellar hemangioblastoma underwent a Tutoplast Dura patch implantation. Two weeks later, the patient presented fever and swelling of the surgical wound. Cultures of the purulent material taken from the swelling and CSF cultures revealed Staphilococcus aureus. The patient was reoperated; during the second operation we found subcutaneous and submuscular purulent material. Tutoplast Dura was reabsorbed and cerebellar surface was unaltered. The operative field was meticulously cleaned with hydrogen peroxide and local antibiotics. A second Tutoplast Dura patch was implanted. Daily wound medications were administered. The postoperative course was uneventful, and the patient was discharged on sixth postoperative day. CASE 4 A 70-year-old man treated for a ponto-cerebellar angle neurinoma underwent a Tutoplast pericardium patch implantation. One month later, he complained of headache, vomiting, SC pain, and swelling at surgical wound. Cultures of purulent material taken from swelling revealed Staphilococcus epidermidis. The patient was reoperated, and during the second operation we found a corpuscolar collection under the cutaneous and muscular planes. Dural implantation was reabsorbed, and the cerebellar surface presented a small cavity coated with necrotic tissue. The operative field was meticulously cleaned with hydrogen peroxide and local antibiotics. A new Tutoplast pericardium patch was implanted. Daily wound medications were administered. The postoperative course was uneventful, and the patient was discharged on 7 th postoperative day. Tutoplast dura and Tutoplast pericardium are homologous materials treated with dehydration by solvent and sterilization by � irradiation. These materials are immersed in a hydrogen peroxide and acetone solution to minimize the antigenic potential and the infection risk. The preservation temperature is 15–30°C. For use, it is recommended to rehydrate Tutoplast dura and Tutoplast pericardium in sterile physiologic saline or Ringer’s solution. The rehydration makes these materials even softer and improves their handling properties at surgery. These materials are a network of collagen fibers that act as a scaffold for the formation of vascularized, vital, connective tissue. Discussion Since 1890 when Beach suggested use of gold foil to prevent meningocerebral adhesions [5], many substances have been tried experimentally and used clinically as dural substitutes. However, the ideal solution still remains to be found. Watertight dural closure is necessary to prevent postoperative cerebrospinal fluid fistula, infection, and cortical scarring. The large number of materials used as dural graft include both biologic tissues (autologous, homologous, and heterologous) [2,9,26,36,40,43] and synthetic materials [2,6,20,23,28,32,38,44–46,48]. Autografts, such as pericranium or temporal fascia, have several and certain advantages. They are easy to handle, nontoxic, inexpensive, and have a favorable biologic behavior [8,11,22,24,30,37]. Unfortunately, it is not always possible to perform autograft with these tissues. Pericranium can be damaged, especially in trauma, and can be insufficient when the dural defect is large or unavailable because it must be used in another way (e.g., for the frontal sinus closure). The use of autologous fascia lata has never been popular because it requires an additional operation, probable additional operating time, and it can be related with complications at the donor site [46]. We believe that autologous tissue such as pericranium or temporal fascia should be implanted when-
Duraplasty Surg Neurol 2004;61:55–9 ever possible, but when it is not possible, we prefer to use homologous implants. Despite the theoretical advantages of no risk of infection of the synthetic materials [2], most of these have been rejected because of local tissue reactions, excessive scar formation, meningitic symptoms, or hemorrhage risk [1,2,13,19,31,33,34,35,41,50]. For many years lyophilized homologous dura mater sterilized by � rays (Lyodura) has been widely used because it is easy to handle and widely available [9,10,24,39,50]. Unfortunately, the current sterilization methods do not guarantee them free from risk of latent virus infections [16,42,49], and some cases of probable Creutzfeldt-Jacob disease (CJD) after homologous dura mater implant have been reported [42]. However, these cases remain circumstantial because there are not other cases in patients treated with the same lot of dura. Moreover, the use of cadaveric dural grafts has not been prohibited by World Health Organization [50]. In our institution we have used Tutoplast dura as dural substitution for many years because it is a material widely available, waterproof, with tensile strength, easily suturable, biocompatible, and relatively inexpensive. Despite achieving good results in our patients with Tutoplast Dura implant (no complication in more than 99% of the cases), we think that the risk of transmission of prionic disease, even if minimal and never proven, should proscribe its use. Until now, iatrogenic transmission of CJD occurred by corneal implantation, intracranial electrodes, human growth hormone extracts from cadaveric pituitary gland, and cadaveric dura mater graft [42]. In experimental transmission, the CJD agent has been found in brain, spinal cord, lung, liver, and kidney [7,27,42]. In the last several years in our institute we use Tutoplast pericardium that is a homologous material with the same advantages of the Tutoplast dura but likely safer than homologous dura mater. In our series, we found postoperative complications in 4 (1.7%) of the 250 patients subjected to implant of dural homologous substitutes. However, the relationship between dural patch and the complications in these four cases remains debatable. In patients No. 1 and No. 2 a postoperative meningeal syndrome was documented by clinical picture and laboratory test. In patient No. 1 meningeal reaction was aseptic, and the operation was performed in posterior cranial fossa. In this case we can hypothesize either an inflammatory reaction of the host against the implanted material or a spread of blood breakdown products into subarachnoidal spaces, causing an irritative meningeal syndrome. The latter hypothe- 57 sis is sustained by the fact that aseptic meningitis syndrome has been described as a common complication of posterior cranial fossa surgery [12,15,17]. In the remaining patients there was an infection, and in those cases it can be hypothesized as both an infection arising from dural plasty and a contamination unrelated to the dural graft. The latter hypothesis is supported by the fact that the method of preparation of Tutoplast and �-irradiation ensures the sterility of the grafts [10] and because there were no other cases of infection in patients of our series treated with the same lot of dura. In patient No. 2 it could be reasonably assumed that the development of infection was because of a contamination from extracranial bacteria. This is supported by the presence of a connection between the endocranium and the airways. In patients No. 3 and No. 4 we found at the previous surgical wound an SC and submuscular purulent collection positive for St. Aureus and St. Epidemidis, respectively. At reintervention, Patient No. 3 presented SC and submuscular purulent collection, disappearance of the dural patch, and no signs of infection on the cerebellar surface. From these aspects we can presume that the infection started in the superficial tissues and destroyed the dural patch. In Patient No. 4 there was an extradural purulent collection, complete dural patch resorption, and signs of inflammatory reaction on cerebellar surface. Also, in this case we can suppose that infection is originated extradurally because the cultures of the purulent SC and submuscular collection were positive for an infective agent commonly present in the skin and easily destroyed by �-sterilization. Keener [21] stated that only fibroblast originating from soft tissues (muscle, fascia, SC space) regenerate the dura, and when dural defect is adjacent to bone, dural healing is inadequate. In our cases No. 3 and No. 4 dural patch was adjacent to soft tissue, but it is likely that the septic contamination and consequent inflammatory reaction destroyed the dural graft more rapidly than the time needed for fibrous infiltration and dural regeneration processes. Adherence to the cortex were not observed in the 4 patients who underwent an early reoperation or in the 9 patients reoperated on tardily. Macroscopically, dural patch was preserved and appeared as host dura. In 1 patient there was granulation tissue above the graft when this was exposed in a small area without bone. In 3 patients who had post-
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