Organisation and planning of anaesthesia for emergency surgery.

Patients presenting for emergency surgery represent a category at high risk of complications, with substantial morbidity and mortality, whose management may be extremely challenging. In this first of two articles we consider the identification and evaluation of high risk emergency patients, the provision of critical care support, the management of sepsis, common postoperative complications and in-theatre death.

The principles and conduct of anaesthesia for emergency surgery.

In this second article we examine the principles underlying delivery of the components of anaesthesia. Topics considered include anaesthetic technique, management of the airway and lung ventilation, induction and maintenance of anaesthesia, patient monitoring including the place of cardiac output devices. We summarise recent research on the management of shock and sepsis syndromes including goal directed therapy and examine some controversies around intravenous fluid therapy. Finally, we discuss intra-operative awareness and challenges during emergence including peri-operative cognitive dysfunction.

Interleukin-1-mediated release of interleukin-8 by asbestos-stimulated human pleural mesothelial cells.

The pleuropulmonary response to inhaled asbestos frequently involves inflammation and release of various cytokines from lung cells. Among these, interleukin-8 (IL-8) released from the mesothelium could augment inflammation of the pleura by attracting neutrophils to the pleural space. We used cultures of human pleural mesothelial cells (HPMC) to examine the mechanism of IL-8 production by asbestos and cytokines. Suspensions of amosite, chrysotile, or crocidolite asbestos in concentrations as low as 5 micrograms/ml enhanced release of IL-8 from HPMC during 6 h of incubation at 37 degrees C. Electron microscopy of asbestos-treated HPMC showed that the cells avidly engulfed each of the different types of asbestos fibers. Two proinflammatory cytokines, interleukin-1 alpha (IL-1 alpha) and tumor necrosis factor-alpha, enhanced IL-8 release within 2 h and had an even greater effect after 6 h. Release of IL-8 was measured by an enzyme-linked immunosorbent assay, and functional activity of the cytokine was assessed by chemotaxis of human neutrophils. Identity of IL-8 in HPMC supernatants was established by absorption with an antibody to IL-8. Preincubation of HPMC with IL-1 receptor antagonist (IL-1ra) significantly decreased release of IL-8 after stimulation with amosite or crocidolite asbestos. We conclude that HPMC release IL-8 in response to asbestos stimulation and that the response is, in part, mediated by IL-1, mainly in the form of IL-1 alpha.

Laboratory diagnosis of bacterial meningitis.

Bacterial meningitis is relatively common, can progress rapidly, and can result in death or permanent debilitation. This infection justifiably elicits strong emotional reactions and, hopefully, immediate medical intervention. This review is a brief presentation of the pathogenesis of bacterial meningitis and a review of current knowledge, literature, and recommendations on the subject of laboratory diagnosis of bacterial meningitis. Those who work in clinical microbiology laboratories should be familiar with the tests used in detecting bacteria and bacterial antigens in cerebrospinal fluid (CSF) and should always have the utmost appreciation for the fact that results of such tests must always be reported immediately. Academic and practical aspects of the laboratory diagnosis of bacterial meningitis presented in this review include the following: anatomy of the meninges; pathogenesis; changes in the composition of CSF; etiological agents; processing CSF; microscopic examination of CSF; culturing CSF; methods of detecting bacterial antigens and bacterial components in CSF (counter-immunoelectrophoresis, coagglutination, latex agglutination, enzyme-linked immunosorbent assay, Limulus amebocyte lysate assay, and gas-liquid chromatography); use of the polymerase chain reaction; and practical considerations for testing CSF for bacterial antigens.

Neutral endopeptidase from nuchal ligament of fetal calves.

The nuchal ligament of unborn calves contains a neutral endopeptidase that is biochemically and immunologically similar to the neutral endopeptidase (NEP), or enkephalinase, from human kidney. Enzymatic activity was inhibited more than 90% by phosphoramidon (1 microM). The specific activity in membrane fractions, as determined by hydrolysis of the dansylated substrate, DAPGN, was similar in tissue from fetuses of gestational ages ranging from 100 to 280 days. NEP activity in adult ligament tissue, however, was less than 10% of that in fetal tissue. Fibroblasts dissociated from ligament tissue by collagenase displayed less NEP activity than did preparations of intact ligament, and activity was even lower in cultured cells. By contrast, fibroblasts cultured from fetal calf lungs had NEP activity comparable to that in the ligament tissue. When ligament fibroblasts were cultured on subcellular matrices derived from fetal lung fibroblasts the NEP activity increased relative to those cultured on plastic alone. These studies confirm the presence of neutral endopeptidase (NEP) in the nuchal ligament of the fetal calf. The consistent activity through a range of gestational ages and the influence of the subcellular matrix suggest that this enzyme might be involved in growth of the ligament during fetal life.

Liberation of a neutrophil enzyme-releasing peptide from the surface of human alveolar macrophages.

The human alveolar macrophage product, enzyme-releasing peptide (ERP), has a molecular mass of 8,000 Da, and releases azurophilic and specific granule constituents from neutrophils. A murine monoclonal anti-ERP antibody (12E10H), previously used to show a lack of antigenic identity between ERP and C5a, interleukin 1, tumor necrosis factor, and gamma-interferon, showed no cross-reactivity with interleukin 8. 12E10H and a fluorescein-labeled second antibody were used to visualize ERP on the macrophage surface. ERP was removed from alveolar macrophages by a 3-min incubation with 5 X 10(-7) M bovine pancreatic trypsin at 37 degrees C. The washed trypsinized cells could readhere to plastic and exclude trypan blue. Dilution of the trypsin-derived ERP released myeloperoxidase from cytochalasin-B-treated neutrophils dose dependently. The enzyme-releasing ability of the trypsin-derived material was removed by immunoprecipitation using antibody 12E10H bound to Staphylococcal protein A Sepharose 4B. The estimated molecular mass of the trypsin-derived ERP (by molecular sieve chromatography on HPLC) was approximately 8,500 Da. Other proteases (plasmin, thrombin, and cathepsin G) also released ERP from the cell surface, but the ERP was not an active secretagogue for neutrophils. However, macrophages cultured with protease inhibitors did not show decreased ERP accumulation in the medium. Our data indicate that ERP exists on the surface of human alveolar macrophages and can be released by proteases found within the lung environment in some disease states.

A modified bronchoalveolar lavage procedure that allows measurement of lung epithelial lining fluid volume.

We replaced the standard serial bronchoalveolar lavage technique with a new "rewash" lavage procedure to allow estimation of the volume and protein concentration of the epithelial lining fluid (ELF) in anesthetized sheep. A bronchoscope 6.0 mm in diameter wedged in an airway was used to lavage a segment of lung with four cycles of instillation and aspiration of the lavage solution containing a radioactive tracer (technetium pertechnetate, 99mTcO4-). Errors caused by the fall in concentration of the tracer during the lavage were minimized by extrapolating the tracer concentration back to time zero when the lavage solution had mixed with the ELF, but had not had time to be affected by loss of the tracer or influx of fluid from the interstitium. In control sheep, the ELF of these lavaged segments had a mean volume of 1.6 +/- 1.0 ml and a mean protein concentration that was 26 +/- 19% of the protein concentration measured in the plasma. Increasing the left atrial pressure 19 +/- 5 cm H2O to cause "cardiac lung edema" had no significant effect on the ELF volume, but it increased the mean protein concentration to 57 +/- 30% of the plasma value (p less than 0.01). Lung injury caused by intravenous oleic acid caused lung edema, increased the mean ELF volume to 6.8 +/- 2.2 ml, and increased the mean ELF protein concentration to 86 +/- 26% of the plasma value (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Wound infection caused by Branhamella catarrhalis.

Branhamella catarrhalis was isolated from sputum, tracheal secretions, and a nonhealing and infected thoracic surgical wound in a 59-year-old woman who had a history of a chronic, interstitial fibrosis and who had undergone an open lung biopsy procedure. The patient's upper respiratory tract was the likely source of the organism. To our knowledge, this is the first report of a wound infection caused by B. catarrhalis.

Laboratory diagnosis of systemic fungal diseases.

The increase in the number of fungal infections seen in debilitated and immunocompromised patients in the last several years makes it necessary to consider all fungi as potential pathogens. Clinical microbiology laboratories are playing increasingly important roles in the recovery, isolation, and identification of these fungi. This article contains specific recommendations and references concerning a practical approach to the laboratory identification of systemic fungi. The proper and timely selection, collection, and transport of specimens is imperative, and clinicians are responsible for appropriate specimen selection to ensure optimal chances of recovery of pathogens. Respiratory tract secretions and blood are excellent sources for detection of disseminated fungal infection. Specimens should be placed into transport media if the sample size is small or if only a small number of organisms are thought to be present. Direct microscopic examination of specimens can provide valuable information, often allowing a clinician to initiate immediate therapy. Specimens that are more likely than others to contain systemic fungi and that should be examined routinely include the following: pulmonary biopsy material, bronchial washes and lavages, specimens from immunocompromised patients, purulent specimens, and specimens suspected of containing a specific fungus. Valuable methods of examining specimens directly include treatment with KOH and calcofluor white. Use of media to recover fungi is the basis of making a laboratory diagnosis of a fungal disease, and the use of proper recovery and subculture media is imperative. Noninhibitory media allow contaminants to grow readily and should be used only to recover fungi from normally sterile body sites or for subculture. Blood-enriched media allow almost all pathogenic and saprophytic fungi to flourish. Therefore, such media, unless they contain antibiotics, should not be used as primary recovery media. Media that contain antibiotics should be used as primary recovery media to prevent overgrowth of pathogenic fungi by contaminants. Yeasts recovered from clinical specimens can be identified by a combination of tests, which include direct microscopic examination, germ tube formation, microscopic morphology of growth on corn meal agar, and ability to utilize certain carbohydrates. Molds recovered from clinical specimens are identified by a combination of growth rate, colonial characteristics, size and shape of hyphae, and microscopic examination of reproductive structures and other fungal elements.(ABSTRACT TRUNCATED AT 400 WORDS)

Asbestos-induced endothelial cell activation and injury. Demonstration of fiber phagocytosis and oxidant-dependent toxicity.

Vascular endothelial cell injury is important in the development of a variety of chronic interstitial lung disorders. However, the involvement of such injury in the inflammatory response associated with the inhalation of asbestos fibers is unclear and the mechanism of asbestos fiber cytotoxicity remains unknown. In the present study, human umbilical vein endothelial cells were challenged with amosite asbestos and several parameters of cellular function were examined. Electron microscopic examination revealed that endothelial cell exposure to asbestos resulted in active phagocytosis of these particulates. Biochemical evidence of dose-dependent asbestos-mediated endothelial cell activation was indicated by increased metabolism of arachidonic acid. For example, amosite asbestos (500 micrograms/ml) produced a ninefold increase in prostacyclin (PGI2) levels over those levels in non-exposed cells. Incubation of human endothelial cells with asbestos fibers induced specific 51Cr release in both a dose- and time-dependent fashion indicative of cellular injury. Injury induced by amosite asbestos was not significantly attenuated by treatment of the endothelial cell monolayer with either the iron chelator deferoxamine, which prevents hydroxyl radical (.OH) formation, or by the superoxide anion (O2-) scavenger, superoxide dismutase. However, significant dose-dependent protection was observed with the hydrogen peroxide (H2O2) scavenger, catalase. Chelation of elemental iron present within amosite asbestos fibers by deferoxamine produced a 33% reduction in asbestos cytotoxicity, suggesting a potential role for hydroxyl radical-mediated injury via the iron-catalyzed Haber-Weiss reaction.(ABSTRACT TRUNCATED AT 250 WORDS)

Isolated levator myositis.

A 54-year-old woman presented with a 1-day history of ptosis of the left upper lid. On examination, the patient exhibited a moderate ptosis, poor levator function, lid lag on down-gaze, and no limitation of ocular motility. A computed tomography (CT) scan with contrast demonstrated enhancement of the levator muscle and levator aponeurosis on the involved side. Treatment consisted of systemic steroid administration and led to complete resolution of the ptosis in 2 weeks. The combined clinical and CT scan findings give a characteristic pattern of an isolated levator myositis.

Pulmonary lymphatic clearance of 99mTc-DTPA from air spaces during lung inflation and lung injury.

A total of 22 sheep with lymphatic cannulas were used to determine if 99mTc-labeled diethylenetriaminepentaacetic acid (DTPA) clears directly from the air spaces of the lungs into the lymph vessels. Each sheep was anesthetized and ventilated with an aerosol of the DTPA for 2-5 min, and the DTPA activities in the lymph and plasma were measured every 15 min for 2 h. After the first 45 min, the average ratio of the DTPA in the lymph to that in the plasma (L/P) was 1.03 +/- 0.06 (SD) in the six control experiments and 1.11 +/- 0.05 in the six experiments in which the lungs were inflated with a positive end-expired pressure of 10 cmH2O throughout the study. Direct movement of the DTPA from the air spaces into the lymph was not necessary to account for the DTPA clearance in these experiments because the L/P ratio was not significantly different from 1.0. Eight additional sheep received intravenous infusions of air at 0.2 ml.kg-1.min-1 for 2 h to induce lung injury before depositing the DTPA. In these sheep L/P was 1.53 +/- 0.28, which was significantly higher than the value measured in the control group (P less than 0.01). We considered the possibility that the increased L/P ratio in these sheep could be due to alterations in the distribution of the blood flow to the tissue, but the L/P ratio in four sheep whose distribution of blood flow was altered by inflation of a balloon in the right pulmonary artery was 1.05 +/- 0.10, the same as the control value.(ABSTRACT TRUNCATED AT 250 WORDS)