Unexpected tracheal compression detected after immediate extubation failure.
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Biomedical subjects
Publications and source records attributed to H J van Leeuwen.
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Neutrophils can be primed by bacterial lipopolysaccharide (LPS) for an enhanced oxidative burst, which is a key element in the pathogenesis of Gram-negative sepsis. Some serum proteins (e.g. lipopolysaccharide-binding protein) avidly bind LPS and markedly enhance receptor binding and cellular activation while other serum factors (lipoproteins, bactericidal/permeability-increasing protein) neutralize LPS and prevent neutrophil activation. In this paper we examined the kinetics of this priming reaction in whole blood. To study the balance between neutrophil activation and LPS neutralization a sensitive chemiluminescence assay was used in a whole blood system. LPS was able to prime neutrophils for enhanced oxidative burst in whole blood with an optimum incubation time of 25 min. However, LPS was neutralized very rapidly with a t(1/2) of 10 min. After 20 min a second priming factor was already generated, which was shown to be monocyte-derived tumour necrosis factor (TNF).
Two female patients, aged 39 and 52 years, developed severe pneumococcal meningitis. Both patients had undergone splenectomy in the past (one after trauma and one for idiopathic thrombocytopenic purpura) and pneumococcal vaccination was only given immediately after the splenectomy. After antibiotic treatment and intensive care one patient remained disabled and the other patient died. There is a higher risk of developing severe sepsis after splenectomy, with Streptococcus pneumoniae being the causative micro-organism in more than 50% of cases. Vaccination after splenectomy in order to prevent a severe sepsis syndrome is very important. Indications for the 7 valent pneumococcal conjugate vaccine and the 23 valent polysaccharide vaccine are given.
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Procalcitonin is a calcitonin prohormone. During systemic inflammatory response it has the characteristics of an acute-phase protein. However, plasma levels rise more rapidly than those of the parameter (i.e. C-reactive protein) currently used in clinical practice to assess an acute-phase response. The procalcitonin assay is easy to perform and results can be available within a short period of time. This makes procalcitonin a valuable addition to the current diagnostic work-up for acutely ill patients. Procalcitonin can be used as a marker of inflammation, to differentiate serious bacterial infections from other generalised inflammatory diseases, to differentiate bacterial from viral infections, to differentiate infection from disease activity in patients with autoimmune diseases, to differentiate infection from rejection in transplant patients, and as a prognostic marker in critically ill patients. Procalcitonin may prove to be a valuable adjunct in diagnosing and treating patients with a variety of inflammatory disorders.
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OBJECTIVE: To describe the underlying pathophysiologic mechanisms of the effect of corticosteroids in a patient with late septic shock. DESIGN: Case report. SETTING: The medical intensive care unit at University Medical Center Utrecht. PATIENT: An 86-yr-old female patient with late septic shock requiring mechanical ventilation and vasopressive agents. INTERVENTIONS: Administration of hydrocortisone, 300 mg daily. MEASUREMENTS AND MAIN RESULTS: Within 3 days of corticosteroid treatment, the patient could be weaned of vasopressive agents and mechanical ventilation. Serum C-reactive protein levels normalized. Nuclear factor-kappaB activation in unstimulated and in vitro lipopolysaccharide-stimulated peripheral blood mononuclear cells decreased to background level within 5 days. Repeated functional tests of the hypothalamic-pituitary-adrenal axis were normal. CONCLUSION: Our data suggest that the pathophysiologic mechanism behind the clinical effects of supraphysiologic doses of corticosteroids in late septic shock is directly related to the inhibition of nuclear factor-kappaB in peripheral blood mononuclear cells.
Lipopolysaccharide (LPS)-binding components in serum play an important role in modifying LPS toxicity. We analyzed the binding characteristics of LPS in the presence of serum using gel filtration of FITC-labeled LPS (FITC-LPS) with on line detection of optical density and fluorescence. FITC-LPS separately behaves as an aggregate resulting in a low, dequenched, fluorescence. Binding of single LPS molecules, segregated from the aggregate, to serum components results in an increase in the fluorescence due to dequenching, and a comigration of fluorescence and optical density signals using gel filtration. This method, in combination with the use of specific antibodies inducing additional shifts, demonstrated that in serum high-density lipoproteins (HDL), albumin and low-density lipoproteins (LDL) were able to monomerize LPS. An ELISA on collected fractions of the gel filtration revealed binding of the recently identified LPS-binding protein, serum amyloid P component (SAP), to the high molecular weight LPS aggregate. In serum, binding of soluble CD14 (sCD14) and LPS-binding protein (LBP) to LPS could not be detected. However, this was probably due to an overshadowing effect of albumin, as an extra addition of recombinant sCD14 to serum clearly monomerized FITC-LPS. Biosensor technology revealed that, of all LPS-binding components tested, only SAP clearly bound to the LPS-coated sensor chip. These results show that gel filtration of FITC-LPS is a quick and reliable method to study the binding characteristics of LPS-binding components.
BACKGROUND: Despite improved treatment modalities, the mortality of HIV infected patients admitted to the intensive care unit with respiratory failure remains high. To help ICU physicians in advising HIV infected patients whether to undergo mechanical ventilation, we retrospectively investigated prognostic factors predicting hospital outcome for HIV-infected patients, admitted to a medical intensive care unit with respiratory failure before the era of highly-active anti-retroviral therapy. METHODS: A retrospective chart review was carried out of all HIV-infected patients with respiratory failure admitted to the medical ICU of a Dutch University Hospital between 1991 and 1997. RESULTS: In the six year period, 29 HIV-infected patients were admitted to the ICU for respiratory failure. Mechanical ventilation, CD4 cell count, APACHE II score, APACHE III score, ARDS and length of ICU stay all differed significantly between survivors and non-survivors. However, a multivariate analysis only showed the need for mechanical ventilation as an independent risk factor for mortality. The only combination of factors able to accurately predict mortality for the individual patient was the development of ARDS and the requirement of mechanical ventilation. CONCLUSIONS: The combination of mechanical ventilation and ARDS accurately predicts hospital outcome in HIV-infected patients presenting with respiratory failure before the HAART era.
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A 36-year-old white male suffering from auto-immune granulocytopenia with recurrent infections and subsequent systemic AA-amyloidosis developed ischemic necrosis of bone (INB) in several joints following long-term corticosteroid treatment. Early signs of INB in one joint were detected by Magnetic Resonance Imaging and joint damage could be prevented by core decompression. The importance of early detection of INB Magnetic Resonance Imaging is stressed. According to the present theory regarding the pathogenesis of INB, amyloidosis might contribute to intra- as well as extra-osseous factors. However, no relation was found between amyloidosis and INB.
In 25 patients with bullous pemphigoid, the presence of IgE on the epidermal basement membrane (BM) and the cell membrane of mast cells was investigated by immunofluorescence microscopy. In four cases, a linear staining of the BM was found. Strongly positive fluorescence of the mast cells was found in seven cases; in seven others there was weakly positive staining. The positive staining of mast cells seemed to be related to the serum IgE level. The IgE levels in the serum samples of 30 patients were determined by the immunoradiometric assay. In 11 cases, elevated levels (greater than 400 IU/mL) were found. Circulating IgE anti-BM antibodies could be demonstrated in one of 15 serum samples by indirect immunofluorescence. Our results do not indicate that IgE-mediated mechanisms play an important role in the pathogenesis of bullous pemphigoid.
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