Ruptured aneurysm presenting with a subdural hematoma.
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Biomedical subjects
Publications and source records attributed to J K Smith.
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The CT and MR findings of a nasopharyngeal nonossifying variant of an ossifying fibromyxoid tumor are presented. The findings are radiographically indistinguishable from more common malignant neoplasms encountered in this region. The tumor was isointense with muscle on T1-weighted images. On proton density- and T2-weighted images, the mass was mostly isointense with gray matter but contained some areas of lower intensity that might reflect the fibrous tissue component. The tumor eroded through the floor of the middle cranial fossa.
CT and MR revealed a case of nasopharyngeal atresia, a malformation in which the soft palate is not formed, and the hard palate extends posteriorly to fuse with the anterior surface of the clivus, resulting in complete isolation of the nasal and oral cavities and the absence of a nasopharynx. We believe this rare anomaly results from abnormal persistence of the embryologic bucconasal plate and/or anomalous migration of the nasoseptal elements.
Many plasmapheresis techniques cause greater activation of platelets, complement and coagulation than does simple whole blood collection. Activation of the coagulation cascade has been particularly evident in tests for potential thrombogenicity in prothrombin complex concentrates made from apheresed plasma. Attempts to improve the factor VIII content and fractionation yield of source plasma have centred on rapid freezing, increased concentration of anticoagulants and the exploitation of anticoagulants optimal for the preservation of coagulant, rather than cellular, activities. The cumulative advantage is of the order of 10% over recovered plasma. There are potential pitfalls in applying low-citrate anticoagulation strategies to plasmapheresis. Recalcification of citrated plasma, under cover of an optimal concentration of heparin, might be explored more vigorously.
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Calcium channel antagonists can be quite toxic. In the management of poisoning, early recognition is critical. Calcium channel antagonists are frequently prescribed, and the potential for serious morbidity and mortality with overdosage is significant. Ingestion of these agents should be suspected in any patient who presents in an overdose situation with unexplained hypotension and conduction abnormalities. The potential for toxicity should be noted in patients with underlying hepatic or renal dysfunction who are receiving therapeutic doses. Because there is no specific antidote, decontamination of the gastrointestinal tract is crucial. Intravenous calcium should be administered to symptomatic patients because it is relatively innocuous and may be beneficial. Volume expansion should be the initial approach to hypotension unrelated to bradycardia. Patients who have had a verapamil overdose should be observed in intensive care units where Swan-Ganz catheterization and ventricular pacing are routinely available. The choice of sympathomimetic agents for treatment remains controversial. According to the published literature, isoproterenol, epinephrine, and norepinephrine may be more effective in improving bradycardia and the resultant hypotension than dopamine. However, none of these agents is universally effective. A more logical approach may be to improve cardiac output with agents like amrinone. Bay K 8644 and 4-aminopyridine show promise as potential antidotes but at present are still experimental.
We have described the case of a 65-year-old man who had a right hemothorax from rupture of an aneurysm of the ascending thoracic aorta and survived. This type of subacute presentation with survival of the patient has not been documented previously in contemporary medical literature.
We describe a case of fever of unknown origin (FUO) of 9 months' duration in which the finding of regularly spaced multiple Beau's lines (the "ladder nail" sign) pointed to the possibility of a relapsing fever of the Pel-Ebstein variety and an underlying lymphoma. Subsequent investigation confirmed the association of the Beau's lines and fever, as well as the diagnosis of Hodgkin's disease as the cause of the FUO. In this setting, Beau's lines may provide an important diagnostic clue and should be carefully looked for on physical examination.
Acetolactate synthase (ALS) catalyzes the first common step in the biosynthesis of isoleucine, leucine, and valine. The previous cloning of two tobacco (Nicotiana tabacum) ALS genes (SurA and SurB) has allowed transcript accumulation from these genes to be monitored. mRNA blot analysis of ALS transcripts showed a message size of 2.2 kb. Quantitation of the levels of ALS messages in tobacco organs indicated that there was 3- to 4-fold variation in the levels of expression of the ALS genes in different organs. This variability correlated with the developmental stage of the samples, with the highest levels of expression found in developing organs. In situ hybridizations of anti-mRNA probes to plant sections established that ALS messages are most prevalent in metabolically active and dividing cells of roots, stems, and floral tissue. Using RNase protection assays, the transcriptional start sites of the ALS genes were determined, and the expression levels of the two tobacco ALS genes were then followed separately. Both tobacco ALS genes are expressed in a coordinated manner in all tobacco organs examined, with the SurB gene being consistently expressed at higher levels than the SurA gene.
Sonography is the primary imaging technique for evaluating the scrotal contents. In this pictorial essay, we illustrate a range of normal and abnormal sonographic findings in patients after orchiectomy, including the appearances of the normal postorchiectomy space, acute and subacute hematomas, recurrent neoplasm, second primary tumor in the remaining testis, and testicular prostheses.
Factor XI deficiency is an uncommon bleeding disorder usually manifested by excessive bleeding after surgery or trauma. Until recently the only effective therapy has been fresh-frozen plasma (FFP) infusion. We describe the efficacy and safety of a new factor XI concentrate produced from human donor plasma by a modification of the method used for antithrombin III concentrate. The mean recovery of factor XI in the circulation measured on 62 occasions was approximately 91% of the injected dose, and the mean half-disappearance-time was 52 h. The concentrate was used for 31 invasive procedures in 30 patients, including 16 patients who had a definite bleeding tendency on previous occasions, with normal haemostasis being achieved in all but 1. Only 1 patient (previously experiencing allergy to FFP) experienced adverse effects during infusion. Monitoring of liver function tests and viral antibody status in suitable patients has shown no evidence of transmission of hepatitis viruses, HIV-1 or parvovirus B19. We conclude that this concentrate provides effective treatment for patients with factor XI deficiency. Preliminary results suggest safety from virus transmission, but this needs to be established in further studies of previously untreated patients.
OBJECTIVE: Some of the genomic instability that is observed in solid tumors may be due to the loss of telomeric sequences. These experiments were designed to compare the number of telomeric repeat sequences in endometrial adenocarcinoma with that found in adjacent normal tissue. STUDY DESIGN: Deoxyribonucleic acid was extracted from normal and malignant uterine tissue of 11 patients undergoing hysterectomy for treatment of endometrial adenocarcinoma and also from five endometrial carcinoma cell lines. The relative number of telomeric repeat sequences in each sample was measured by hybridization of these deoxyribonucleic acids to a probe specific for the human telomeric repeat. Hybridization signals were quantified by autoradiography and a beta-particle detection system. RESULTS: A reduction of telomeric repeat sequences in tumor versus normal tissue was found in 10 of 11 cases. Telomere reduction was also seen in endometrial carcinoma cell lines. CONCLUSIONS: Telomere reduction is a genetic characteristic of many endometrial tumors. Telomere reduction may contribute to the genesis and progression of endometrial carcinoma, or it may be a secondary effect of the tumorigenesis process.
A transparent polyurethane dressing (Omiderm) for free flaps is presented. Considering the importance of reliable flap monitoring postoperatively, this synthetic membrane allows for constant ability to observe the flap, assess the capillary filling, and detect the blood flow with an ultrasound Doppler device.
A 63-year-old woman presented with extensive bruising. An inhibitor to factor XIII was detected. Subsequent subcutaneous bruising and soft tissue haemorrhage into the left foot were treated with infusions of pasteurized factor XIII concentrate with good effect. Immunosuppression with cyclophosphamide was attempted but in spite of this she suffered a right cerebral haemorrhage necessitating further intensive therapy with factor XIII concentrate. This overcame the inhibitor, adequate post-infusion factor XIII levels were achieved and she made an excellent recovery. Factor XIII concentrate was well tolerated with no evidence of transmission of hepatitis or HIV infection. The inhibitor appeared to interfere with haemostasis by hindering the fibrin binding site of factor XIII, resulting in interference in clot-solubility tests. Subsequently the inhibitor resolved.
A prospective, randomized, controlled trial to examine the effects of antithrombin supplementation on mortality, coagulation and renal function has been carried out on 132 intensive care patients. Antithrombin activity was measured in all patients on admission to the intensive care unit (ICU). Patients with an antithrombin activity of less than 70% were randomized to either receive antithrombin replacement or to act as controls. Antithrombin activity was maintained above 70% in the treated patients throughout their stay on ICU. Ninety-three patients had an antithrombin activity of less than 70% and 35 received replacement therapy. Patients with antithrombin activity below 70% remained on the ICU significantly longer and had a significantly higher mortality rate than patients with antithrombin activity above 70%. Antithrombin supplementation neither reduced mortality nor shortened the intensive care stay. Fifty patients with reduced antithrombin activity remained on the ICU for at least 4 days, 25 received antithrombin and 25 acted as controls; coagulation parameters and renal function have been monitored in these patients. Fibrinogen concentration and platelet count were unaffected by antithrombin replacement. Antithrombin supplementation did not appear to reduce the incidence of impaired renal function in sepsis, trauma and postoperative patients. The creatinine clearance fell below 20 ml/min in eight patients in the no-treatment arm while by comparison only three patients in the treatment arm developed impaired renal function. Our study does not demonstrate a clear role for the use of antithrombin supplementation in intensive care, however the finding that antithrombin reduced renal impairment is encouraging and a larger study to confirm this finding is at present underway.
To determine the mechanisms whereby complement-activated granulocytes induce microvascular dysfunction in skeletal muscle, we examined the effect of antineutrophil serum (ANS), IB4 (a monoclonal antibody that inhibits CD18-dependent neutrophil adherence), xanthine oxidase inhibition or inactivation, deferoxamine, and catalase on the increase in canine gracilis muscle microvascular permeability induced by intravascular administration of zymosan-activated plasma (ZAP). Changes in vascular permeability were assessed by measurement of the solvent drag reflection coefficient (sigma) for total plasma proteins, and the extent of neutrophil infiltration was estimated by assessing muscle myeloperoxidase activity. ZAP infusion was associated with a marked increase in vascular permeability compared with control muscles that received no treatment or to muscles treated with zymosan heat-inactivated plasma (ZIP) (sigma = 0.51 +/- 0.04, 0.89 +/- 0.02, and 0.90 +/- 0.01, respectively). Estimates of sigma in animals rendered neutropenic with ANS, or treated with IB4, deferoxamine, or catalase before ZAP infusion were not significantly different from values obtained in control or ZIP-treated muscles (sigma = 0.96 +/- 0.02, 0.88 +/- 0.03, 0.85 +/- 0.02, and 0.79 +/- 0.01, respectively). However, xanthine oxidase inactivation or inhibition provided no protection from this ZAP-induced microvascular dysfunction (sigma = 0.58 +/- 0.02 and 0.58 +/- 0.01, respectively). In addition, neutropenia and inhibition of neutrophil adherence also prevented ZAP-induced increases in vascular resistance and tissue neutrophil infiltration.(ABSTRACT TRUNCATED AT 250 WORDS)
To determine the role of xanthine oxidase in the microvascular dysfunction produced by activated granulocytes, we examined the effect of xanthine oxidase depletion or inhibition on the increase in microvascular permeability produced by infusion of the neutrophil activator phorbol myristate acetate (PMA). Changes in vascular permeability were assessed by measurement of the solvent drag reflection coefficient for total plasma proteins (sigma) in rat hindquarters subjected to PMA infusion in xanthine oxidase-replete and -depleted animals, in animals pretreated with the xanthine oxidase inhibitor oxypurinol, and in animals depleted of circulating neutrophils by pretreatment with antineutrophil serum (ANS). Xanthine oxidase depletion was accomplished by administration of a tungsten-supplemented (0.7 g/kg diet) molybdenum-deficient diet. In animals fed the tungsten diet, muscle total xanthine dehydrogenase plus xanthine oxidase activity was decreased to less than 10% of control values. Estimates of sigma averaged 0.84 +/- 0.04 in control hindquarters, whereas PMA infusion was associated with a marked increase in microvascular permeability (decrease in sigma to 0.68 +/- 0.03). PMA infusion also caused an increase in the amount of the radical-producing oxidase form of xanthine oxidase (from 3.9 +/- 0.05 to 5.6 +/- 0.4 mU/g wet wt). ANS pretreatment attenuated this permeability increase (sigma = 0.77 +/- 0.04) and diminished the rise in xanthine oxidase activity (4.9 +/- 0.5 mU/g wet wt). Xanthine oxidase depletion with the tungsten diet or pretreatment with oxypurinol had no effect on this neutrophil-mediated microvascular injury (sigma = 0.69 +/- 0.06 and 0.67 +/- 0.03, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)