Cases reported "Necrosis"

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1/20. Polyester fibre prosthetic anterior cruciate ligament implant rupture: necrosis of ingrown connective tissue.

    AIMS: To describe the histopathological and microanalytical features in seven cases of ruptured Apex(R) polyester (Terylene(R)) fibre anterior cruciate ligament prosthesis. methods AND RESULTS: Transmitted and polarized light microscopy was performed in all cases; one case was investigated by immunohistochemistry, transmission electron microscopy and scanning electron microscopy, with backscatter and X-ray detectors for elemental microanalysis. For comparison we also studied synovial biopsy material and unused polyester fibres. In the excised ligaments there was much ingrowth of fibrous tissue accompanying a florid giant cell reaction to the individual intact polyester fibres throughout the ligaments. phagocytosis of particles of prosthesis-derived material was demonstrated and a striking finding was of necrosis of the ingrown connective tissue in the central portions of the ligaments. Hyalinized areas and 'neoligament growth' were less striking. A consistent finding in the polyester fibres was of small particles containing antimony, used as a catalyst in the manufacturing process. CONCLUSIONS: The pattern of reaction to the prosthetic material and the presence of necrosis differ from previous descriptions in animal and human explants of this and other prosthesis types. The mechanical effect of the necrosis is unlikely to be of significance with this ligament, which is load-bearing ab initio.
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2/20. In utero development of hypertensive necrotizing pulmonary arterial lesions: report of a case associated with premature closure of the ductus arteriosus and pulmonary hypoplasia.

    Premature closure of the ductus arteriosus (PCDA) is an uncommon defect in which pulmonary hypertension (PH) has been documented by echocardiography in patients and by direct measurement after experimental PCDA in animals. The pulmonary vascular histology in human cases has received little attention but in the few recorded observations the vessels were either normal or showed increased muscularity. We report the case of a 31 week hydropic female stillborn monozygotic twin in whom postmortem examination disclosed PCDA and hypoplasia of the lungs. Atypical plexiform lesions with necrotizing pulmonary arteritis were present. These lesions represent vascular consequences of severe pulmonary hypertension produced by greatly enhanced blood flow through a restricted vascular bed resulting from the combined effects of these two abnormalities. The findings in this case of PCDA with presumed severe PH indicate that severe pulmonary vascular changes can develop in utero and that the interval of time needed for development of such chances in secondary PH is relatively short.
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3/20. spinal cord infarction following vertebral angiography: clinical and pathological findings.

    spinal cord damage from radiographic contrast material has been known to occur in both spinal and nonspinal angiographic procedures. Reported here is cervical spinal cord injury (SCI) during vertebral angiography. During the procedure, the patient displayed signs of acute cervical spinal cord irritation that should have been taken as a warning of impending injury. autopsy 9 years later showed evidence of central cervical spinal cord necrosis. The pathological findings are similar to those seen in animal models of contrast media-induced SCI; and the pathophysiological mechanisms of such injury are discussed.
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4/20. Microvascular submandibular gland transfer for severe cases of keratoconjunctivitis sicca.

    Free submandibular salivary gland transfer was investigated as a surgical method for the treatment of severe keratoconjunctivitis sicca. In an animal model, we examined the tolerance of warm ischemia of the submandibular gland. After temporary interruption of the blood supply (1 to 6 hours), the morphologic changes in the submandibular gland were analyzed histologically and immunohistochemically in 41 rabbits. From 1.5 hours ischemia onward, an increasing structural damage of the parenchyma with emphasis on the secretory cells was seen. Six hours of ischemia caused total necrosis of the salivary gland. Our clinical experience includes 24 highly selected patients suffering from keratoconjunctivitis sicca, in whom we transferred 31 autologous submandibular glands to the temple for permanent autologous tear substitution within the past 4 years. The glands were implanted into a pocket prepared in the temporalis muscle, and the nourishing vessels were anastomosed to the superficial temporal artery and vein. The submandibular duct was implanted into the upper lateral conjunctival fornix. The transferred glands were left denervated. In addition to the clinical examination, scintigraphy with Tc 99m pertechnetate was used to document the graft's viability after the transfer. Viable incorporation with longstanding secretory function occurred in 26 of the 30 transplanted denervated salivary glands. The resulting lubrication of the treated eyes was irregular for up to 3 months in almost even case. One year after surgery, all patients with a viable transplant developed at least occasional epiphora, which was surgically managed by reducing the size of the graft in 10 patients. No severe side effects were seen in this series. The ophthalmologic evaluation of the method included the assessment of dry eye symptoms and of the volume and quality of ocular lubrication (Schirmer test, fluorescein break-up time), the pathology of the ocular surface (rose bengal staining), and the need for pharmaceutical tear substitutes. One year after surgery, 18 of 27 cases assessed were judged as significantly improved by these tests.
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5/20. The cutaneous cellular infiltrate to stingray envenomization contains increased TIA cells.

    Stingrays result in approximately 2000 stings annually in the U.S.A., and thus are one of the most important venomous marine animals. After envenomization, there is immediate, intense pain with subsequent oedema, cyanosis followed by local erythema and petechiae. Progressive local necrosis and ulceration is variable, sometimes leading to gangrene. To characterize the inflammatory infiltrate at the site of a stingray injury, we examined tissue obtained approximately 4 days after stingray envenomization. Routine histology and immunohistochemical stains for lymphoid markers, including CD3, CD4, CD8, CD20, KP-1 and TIA were performed, and demonstrated a central area of haemorrhagic necrosis with a surrounding infiltrate of lymphoid cells and eosinophils. Approximately one-third of the mononuclear cells were TIA , and these cells appeared mainly to correspond to the cells which were CD3 and CD4 . The inflammatory cells, including the lymphoid populations, suggest that an immunological reaction may contribute to the delayed healing of stingray injuries.
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6/20. A study on pathogenicity of hepatitis G virus.

    AIM: To study the pathogenicity of hepatitis G virus (HGV) and observe the genesis and pathological process of hepatitis G. methods: HGV-rna in serum was detected by RT-PCR assay. The immunohistochemical assays of liver tissue were performed with HGV monocoloned antibody (McAb) expressed from the region of HGV NS5 nucleic acid sequence. The clinical and pathological data of 52 patients with hepatitis G were discussed. In animal experiment, the Chinese Rhesus monkeys were infected with the serum of a patient with HGV infection. And the dynamic changes in serology and liver histology of animals were observed. RESULTS: One hundred and fifty-four patients with HGV-rna positive were selected from 1552 patients with various kinds of hepatitis. Of 154 patients with HGV infection, 52 were infected with HGV only, which accounted for 33.8 (52/154) and 102 with positive HGV-rna were super-infected with other hepatitis viruses, which accounted for 66.2 (102/154). The clinical and pathological observation showed that the acute and chronic hepatitis could be induced by HGV. The slight abnormality of transaminases ALT and AST in serum of monkeys lasted nearly 12 months and histological results showed a series of pathological changes. CONCLUSION: HGV is a hepatotropic virus and has pathogenicty.
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7/20. Severe monochlorobenzene-induced liver cell necrosis.

    benzene derivatives can induce severe liver cell necrosis in animals. A case of a 40-year-old man whose daily consumption of alcohol was 200 g and who had a severe monochlorobenzene-induced liver necrosis is described. liver biopsy specimen showed centrilobular and mediolobular necrosis, similar to that in mice after experimental bromobenzene administration. Monochlorobenzene serum concentration, assayed from day 3 to day 15 after poisoning, decreased monoexponentially with a half-life of 40.3 hours. Prostaglandin E1 was administered from day 3 to day 8. The patient ultimately recovered. The mechanism of monochlorobenzene-induced liver injury and the possible aggravating role of chronic alcohol consumption are discussed.
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8/20. cocaine-induced liver cell injury: comparison of morphological features in man and in experimental models.

    Although investigative research of animal models in cocaine metabolism and associated liver cell injury has been fairly extensive during the past 10 yr, little evidence of hepatotoxicity has been documented in man. We report a case of fulminant hepatic failure and acute rhabdomyolysis resulting from cocaine use. Coagulative-type perivenular and midzonal necrosis and periportal microvesicular fatty change were the predominant morphological features throughout all lobules of the liver, in contrast to periportal necrosis described in the only previous case report with biopsy. Differences in zonal necrosis caused by the same drug are not typically seen in man experiencing direct or indirect intrinsic hepatotoxicity. However, experimental models have shown cocaine to have this ability, dependent on enzyme induction or inhibition, sex and dose. Therapeutic approaches for prevention of possible liver cell injury by cocaine toxicity are discussed.
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9/20. Management of laryngeal radionecrosis: animal and clinical experience.

    radiation necrosis of the laryngeal cartilages is an uncommon complication of radiotherapy for laryngeal carcinoma. It is a devastating process for which there is no one acceptable treatment. Medical management offers only temporary, symptomatic relief, which further necessitates surgical treatment. Surgical management may start with a tracheotomy; however, it often ends with a total laryngectomy. Physiologically, the necrotic cartilages are the source of the problem. It is a general surgical principle that nonviable tissue must be excised to promote healing. Therefore, if the affected laryngeal cartilages were removed, the larynx should heal. Total or near total removal of the thyroid and cricoid cartilages with preservation of the endolaryngeal soft tissues has not been reported in the literature. Theoretically, if the entire cartilaginous framework is removed, there would be no structural support for the airway. We have found using animal models, that submucosal resection of the laryngeal cartilages, leaving the perichondrium and endolaryngeal soft tissues intact can result in a competent airway. Animal and clinical experience will be presented.
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10/20. Dysgonic fermenter type 2 septicemia with purpura fulminans. Dermatologic features of a zoonosis acquired from household pets.

    Dysgonic fermenter type 2, a gram-negative bacillus that is part of the normal oral flora of dogs and cats, is responsible for increasing numbers of cases of fulminant septicemia in humans. patients usually have preexisting medical illnesses, but infection also occurs in otherwise healthy individuals. Most infections are acquired through animal contact. Dermatologic eruptions occur in half of the patients with dysgonic fermenter type 2 infection, and include petechiae, purpura, cellulitis, and gangrene.
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