Biomedical subjects
J J Ligtenberg
Publications and source records attributed to J J Ligtenberg.
[Percutaneous dilating tracheostomy in intensive-care patients: technique, indications and complications].
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[Optimalization of antibiotic policy in the Netherlands. VII. SWAB-guidelines for antimicrobial therapy in adult patients with infectious endocarditis].
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[Sinusitis as a major cause of fever in intubated patients].
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The influence of tumor necrosis factor-alpha and interleukin-10 gene promoter polymorphism on the inflammatory response in experimental human endotoxemia.
In this study, we show that there is no correlation between tumor necrosis factor-alpha gene promoter polymorphism at position -308, interleukin-10 gene promoter polymorphism at position -1082, and the cytokine levels they produce in the human endotoxemia model.
[Relative adrenocortical insufficiency with sepsis, diagnosed and treated with hydrocortisone supplementation].
An 82-year-old woman was admitted to the ICU with septic shock and multiple organ failure. Despite the lack of a persistent septic focus she continued to be dependent on large doses of norepinephrine whilst receiving adequate antimicrobial therapy. After a trial treatment with hydrocortisone the norepinephrine infusion could be withdrawn within a few days and she made a full recovery. In the case of seriously ill patients the diagnosis 'relative adrenocortical insufficiency' is predominantly made on the basis of the clinical picture. The remarkable clinical response to the administration of hydrocortisone (400 mg in the first 24 h) confirmed the diagnosis. The dosage of vasopressors can be reduced remarkably quickly. The stimulatory test for adrenocorticotropin hormone (ACTH) has no added value as reference values for critically ill patients are not available and because the results do not predict the response to the treatment.
[Sodium bicarbonate infusion for intoxication with tricyclic antidepressives: recommended inspite of lack of scientific evidence].
Sodium bicarbonate infusion is widely recommended in textbooks for patients who present with self-poisoning from tricyclic antidepressives. Cardiac conduction disorders could also be treated or prevented by means of such an infusion. The scientific basis for these recommendations was investigated by using Medline to search for publications about clinical studies that supported the use of sodium carbonate; 111 articles were scrutinized. Observational studies and case reports mention a rapid improvement in hypotension and cardiac arrhythmias following the administration of sodium bicarbonate. Results from animal experiments are contentious; it is not clear whether alkalinisation or the administration of extra sodium causes the effect. Randomized studies in patients have not been carried out. As the toxicity of sodium bicarbonate is low, and its potential benefit appears to be high, we recommend its use, despite the lack of scientific evidence. No recommendations concerning dosing, concentration and the length of the therapy can be provided on the basis of the literature.
Fulminant necrotizing fasciitis and nonsteroidal anti-inflammatory drugs.
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[Three patients with massive pulmonary embolism].
Three patients presenting with massive venous pulmonary thrombo-embolism are described, who have been selected from a series of 22 patients treated with thrombolysis during a 6-year period. A 23-year-old female presented with tachycardia and dyspnoea. She had pulmonary angiography following scintigraphy with a perfusion deficit of more than 60%. Thrombolysis resulted in open blood vessels and a disappearance of the complaints. A 51-year-old woman presented with profound hypoxemia, probably due to a patent foramen ovale, with shunting and tachycardia. Perfusion defects on scintigraphy combined with a normal chest radiograph in the absence of pre-existent pulmonary disease established the diagnosis. She responded favourably to intravenous streptokinase. The third patient was an 80-year-old woman with hypertension. She developed dyspnoea, tachycardia and shock following immobilisation due to a fractured hip. Despite an initial improvement on streptokinase, she deteriorated and died from right-sided heart failure. The diagnostic tests should be limited and aimed at ruling out left-sided heart failure and pericardial tamponade. Echocardiography is often diagnostic in these patients. Thrombolysis may be life saving but there are no randomised trials to prove that survival rate is indeed better compared to heparin therapy. Streptokinase is less expensive than alteplase and there is no evidence from trials to suggest that it is inferior to more expensive thrombolytics such as alteplase or urokinase.
[CBO guideline 'Bacterial meningitis'].
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Stridor and trismus: safe airway by oral awake emergency intubation.
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Hormones in the critically ill patient: to intervene or not to intervene?
Critically ill patients show a variety of hormonal changes that appear to differ considerably in acute and prolonged critical illness. Whether these endocrine alterations serve as physiological adaptation or contribute to further deterioration remains an intriguing question. We review the recent literature and discuss whether measuring circulating hormone concentrations, performing stimulation tests, and intervening with hormone substitution could contribute to the recovery of critically ill patients.
Suppression of the clinical and cytokine response to endotoxin by RWJ-67657, a p38 mitogen-activated protein-kinase inhibitor, in healthy human volunteers.
UNLABELLED: Sepsis resulting in multiorgan failure and death is still a major problem in intensive care medicine, despite extensive attempts to interfere in the supposed underlying mechanism of a deranged immune system. This is not only due to the persistent lacunae in knowledge about the immune system in sepsis but also due to the lack of sufficient instruments for intervention. Inhibitors of the p38 mitogen-activated protein kinase (p38MAPK) have been used to study the signalling pathway of the immune response. In vitro and animal studies have demonstrated that blocking p38MAPK could mitigate the pro-inflammatory response and improve survival after endotoxaemia. Using an endotoxaemia model in healthy human volunteers we evaluated the attenuation of clinical and cytokine response to endotoxin after inhibition of p38MAPK by an oral dose of RWJ-67657, a pyrindinyl imidazole. We measured the clinical parameters temperature, blood pressure and heart rate. The proinflammatory cytokines tumour necrosis factor-alpha, interleukin-6 and interleukin-8 were measured by ELISA at various points during a 24-h period. Drug toxicity was evaluated by routine clinical and laboratory examinations. After a single dose dose of RWJ-67657 the temperature and blood pressure response remained at the basal level. The inhibition of TNF-alpha, IL-6 and IL-8 response was a dose dependent. With the maximum dosage, reduction in peak serum levels of the proinflammatory cytokines was greater than 90%. There was no drug-related toxicity. INTERPRETATION: We conclude that inhibition of p38MAPK by RWJ-67657 might be a tool to intervene in the deranged immune response in sepsis and other inflammatory diseases.
Gliclazide mainly affects insulin secretion in second phase of type 2 diabetes mellitus.
We studied the effect of the acute administration of gliclazide at 160 mg on insulin release during hyperglycaemic clamps in 12 type 2 diabetes patients, age 50 +/- 9.0 years, diabetes duration 5.5 +/- 4.8 years, fasting blood glucose 9.6 +/- 2.1 mmol/L (means +/- SD). After a 210 min of hyperinsulinaemic euglycaemic clamp (blood glucose 4.6 +/- 0.14mmol/L), gliclazide or placebo (randomised, double-blind, cross-over) was administered; 60 minutes later, a hyperglycaemic clamp (4hr) at 8mmol/L was started. Plasma C-peptide levels increased significantly after the administration of gliclazide (increment 0.17 +/- 0.15 vs. 0.04 +/- 0.07 nmol/L, p = 0.024) before the clamp. After the start of the hyperglycaemic clamp, the areas under the curve (AUC) for insulin and C-peptide did not differ from 0-10 min (first phase) with gliclazide. However, second-phase insulin release (30-240 min) was markedly enhanced by gliclazide. AUC plasma insulin (30 to 240 min) was statistically significantly higher after gliclazide (12.3 +/- 13.9 vs. -0.56 +/- 9.4 nmol/L x 210 min, p = 0.022); similarly, AUC plasma C-peptide (30 to 240 min) was also higher: 128 +/- 62 vs. 63 +/- 50 nmol/L x 210 min, p = 0.002). In conclusion, in long-standing type 2 diabetes the acute administration of gliclazide significantly enhances second phase insulin release at a moderately elevated blood glucose level. In contrast to previous findings in mildly diabetic subjects, these 12 type 2 diabetes patients who had an inconsiderable first phase insulin release on the placebo day, only showed an insignificant increase in first phase with gliclazide.
Soluble L-selectin levels in experimental human endotoxemia.
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Immunosuppressive treatment for vasculitis associated with Lyme borreliosis.
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[Influenza A pneumonia].
The majority of influenza cases are not associated with complications. Secondary bacterial pneumonia, commonly caused by Streptococcus pneumoniae or Staphylococcus aureus, is well known to most clinicians. Primary influenza viral pneumonia, characterized by rapidly progressive hypoxia and respiratory insufficiency together with non-consolidating pulmonary infiltrates, has a high mortality rate. In 3 patients, a man aged 74 years, and two neonates aged 11 months and 4 weeks respectively, primary influenza A pneumonia was diagnosed. In the latter two patients the virus was cultivated from sputum. Despite intensive supporting and drug treatment, the first and the last patients died. In view of evolving therapeutic possibilities, notably regarding neuraminidase inhibitors, it is important that clinicians recognize this complication of influenza at an early stage.
[Hemodynamic and ventilatory complications of mechanical ventilation with high intrinsic positive end-expiratory pressure].
In three mechanically ventilated patients ventilatory and circulatory complications resulted from high levels of intrinsic positive end-expiratory pressure (PEEPi): progressive pulmonary hyperinflation due to impairment of the expiration. PEEPi was initially not considered as the cause of shock and low tidal volumes and/or high inflation pressures. In a 74-year-old man the circulation deteriorated further when hand bagging was started in an attempt to improve his ventilatory condition; after reduction of the respiration rate, he recovered well. In a 40-year-old woman with relapsing polychondritis sedation helped to reduce the respiratory rate so as to restore sufficient expiratory time. A 59-year-old woman developed acute exacerbation of severe chronic obstructive pulmonary disease, and went into shock during interhospital ambulance transport; she was stabilized after recognition of PEEPi and adjustment of the setting of the ventilator. Detection of PEEPi (e.g. by the finding of a deep inflation level on physical examination) is more important than exact measurement of PEEPi. If PEEPi is detected, the ventilator should be set at PEEP at 80-90% of PEEPi, low frequency (e.g. 8/min) and a long expiratory time, and high inspiratory flow.