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Search Results: 1 - 10 of 108 matches for " Albertus Beishuizen "
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Interfacing the ICU with the general practitioner
Armand RJ Girbes, Albertus Beishuizen
Critical Care , 2010, DOI: 10.1186/cc9066
Abstract: Admission to the intensive care unit (ICU) is only part of the course that a patient makes during their illness. Intensive care is not a gatekeeper speciality and patients therefore generally have their first contact in a hospital with emergency physicians, surgeons, internists, cardiologists, and so forth.After discharge from the ICU, most patients will return to the gatekeeper speciality - surgery, internal medicine, or the like. Following discharge from the hospital, patients will return to their homes and therefore the contact with their lifetime physician from their home situation, the general practitioner (GP), is of utmost impor tance. This is even more relevant when coordination of care from different specialists is required. The GP is also expected to have longstanding knowledge of the home situation of the patient. Whenever decisions in terms of end-of-life decisions have to be taken during ICU admission, the intensivist should be well informed. Not only is medical professional judgement important, but also the will and wishes of the patient. To gather all this information, the intensivist should contact doctors who have been involved in the treatment of the patient so far, including the GP, as well as the patient and relatives if possible. It should therefore be stressed as crucial that treating intensivists have (regular) contact with GPs.Etesse and colleagues report in the present issue of Critical Care about the relationship between GPs and intensivists in a part of southeastern France [1]. The authors mailed an anonymous questionnaire to over 7,000 GPs in their region. The response rate was very low (20%) and this will influence the results and conclusion. However, the results were devastating. Only one-half of the GPs rated their contact with the intensivist (on a scale from 1 to 100) at >57, and only 25% rated as >77. The conclusion that GPs are not very satisfied by communication with intensivists is therefore an under statement. To which extent th
Hypothalamo-pituitary-adrenal axis activity after intracranial catastrophies: what is enough?
AB Johan Groeneveld, Albertus Beishuizen, Nienke Molenaar
Critical Care , 2009, DOI: 10.1186/cc7131
Abstract: The expression 'enough is enough' refers to the idea that we can unambiguously decide on what is sufficient in life. The question is whether this also applies to medicine and science, where uncertainties may outweigh certainties. In the previous issue of Critical Care, the sufficiency of hypothalamo-pituitary-adrenal (HPA) function over time following subarachnoid hemorrhage (SAH) is addressed [1]. We interpret the findings by the authors on the basis of increases in circulating adrenocorticotropic hormone (ACTH), but not of circulating cortisol, with increasing clinical severity of SAH, and that some (relative) adrenal insufficiency is present in severely afflicted patients in the acute phase, compared to controls, even though the study does not allow one to determine whether controls (after aneurysm surgery) were equally stressed. In any case, lower cortisol levels than in acute SAH patients suggest lower stress levels. A comparison with the literature is hard, since there are very few data on acute HPA axis activity after SAH [2].Indeed, expected responses to stress – caused, for instance, by intracranial catastrophes such as traumatic brain injury and SAH – would include increases in endogenous ACTH and, thereby, in cortisol secretion relative to normal, unstressed levels, with a concomitant elevation of circulating (total and free) cortisol levels [2-5]. Sufficient adaptation to the stress response would be suggested by parallel increases in ACTH and cortisol levels acording to the degree of stress associated with the severity of disease (assessed by scoring systems) [2,6,7]. The ratio between ACTH levels and free cortisol levels, which is expected to be maintained because of feedback activity, could provide an index of adrenal sensitivity to ACTH [5]. Adrenal sensitivity can increase with prolonged stress-induced ACTH stimulation or release of stimulating factors other than ACTH, which cause the ratio to decrease; on the other hand, an increase in the ratio wo
Insulin: a wonder drug in the critically ill?
AB Johan Groeneveld, Albertus Beishuizen, Frans C Visser
Critical Care , 2002, DOI: 10.1186/cc1463
Abstract: Intensive care unit patients often have complex disorders. For instance, bouts of inflammation, trauma and ischaemia/reperfusion may occur sequentially or synchronously in patients following surgery, sepsis or shock, thereby upregulating inflammatory and metabolic responses, including cytokine release, protein breakdown and insulin resistance [1,2,3,4]. In spite of elevated insulin levels, insulin resistance at the receptor and postreceptor levels may contribute to hyperglycaemia, even in non-diabetic persons, particularly when stress hormones that promote glycogenolysis are released, including catecholamines and cortisol [2,3,5]. 'Stress' hyperglycaemia can be reproduced after administration of minute amounts of endotoxin to healthy volunteers or by injecting several stress hormones at the same time [5]. Stress hyperglycaemia may occur during the acute phase of illness in 5–30% of patients with stroke, myocardial infarction, sepsis, burns, trauma, surgery and other conditions.Recent evidence suggests that even mild hyperglycaemia is harmful in animals and humans, and aggravates ischaemia/reperfusion damage to heart and brain. Myocardial infact size in humans, with or without diabetes, is greater in the presence of hyperglycaemia [6]. That the former results from the latter (i.e. more severe stress hyperglycaemia causes greater infarct size) rather than vice versa is supported by animal studies [7]. Similarly, hyperglycaemia is associated with poor neurological outcome after traumatic brain injury and stroke [8]. In rodents hyperglycaemia aggravates endotoxin shock, and insulin treatment may decrease mortality [9,10]. Hyperglycaemia may contribute to morbidity and mortality after burns or surgery in humans [3,11]. Therefore, during the course of diabetes mellitus but also during the course of stress hyperglycaemia, untreated or insufficiently controlled hyperglycaemia may adversely impact on organ function after inflammation, trauma or ischaemia/reperfusion, and con
Acute transient thyroid swelling after catheterization of the subclavian vein
R Arthur Bouwman, Martijn R Meijerink, Albertus Beishuizen
Critical Care , 2009, DOI: 10.1186/cc8032
Abstract: A 69-year-old male was admitted to our ICU for epileptic seizure activity and was treated for status epilepticus. Hemodynamic instability prompted us to insert a central venous catheter. The subclavian vein was the preferred site because the enlarged thyroid gland was clinically judged to interfere with the internal jugular vein approach. Fifteen minutes after multiple unsuccessful attempts, progressive diffuse swelling of the neck was noticed. Auscultation revealed bilateral vesicular breathing sounds and chest X-ray revealed clear lung fields without evidence of pneumo- or hematothorax. Palpation revealed a diffuse swollen thyroid gland without evidence of bleeding or crepitations, which was confirmed by ultrasound (Figure 1a). Thyroid hormone levels remained in the normal range and the swelling spontaneously resolved within 4 hours (Figure 1b).Acute swelling of the thyroid gland is very rare, but a 1.5- to 3-fold increase in volume has been reported to occur after diagnostic fine-needle aspiration [2-4]. In these reports, the episode started with acute thyroid swelling within minutes after puncture and completely resolved after a few hours, similar to our case. We highly suspect that the thyroid gland had been inadvertently punctured during the attempted catheterization. In the case of normal anatomy, it is unlikely that the thyroid gland can be reached during subclavian vein puncture [5]. However, the thyroid gland of our patient was enlarged, demonstrated by computed tomography imaging of the neck (Figure 2), which in combination with a too cephalad needle direction may have contributed to an advertent needle pass into the thyroid gland. The mechanism of acute thyroid gland swelling remains speculative, but Bruel and colleagues suggested that acute release of vaso-active substances, such as calcitonin gene-related peptide, leads to acute edema formation through vasodilation and capillary leak [4]. Previous reports have described thyroid swelling as being terrif
Decreased levels of dehydroepiandrosterone sulphate in severe critical illness: a sign of exhausted adrenal reserve?
Albertus Beishuizen, Lambertus G Thijs, István Vermes
Critical Care , 2002, DOI: 10.1186/cc1530
Abstract: This was a prospective observational clinical and laboratory study, including 30 patients with septic shock, eight patients with multiple trauma, and 40 age- and sex-matched control patients. We took serial measurements of blood concentrations of DHEAS, cortisol, tumour necrosis factor-α and IL-6, and of adrenocorticotrophic hormone immunoreactivity over 14 days or until discharge/death.On admission, DHEAS was extremely low in septic shock (1.2 ± 0.8 mol/l) in comparison with multiple trauma patients (2.4 ± 0.5 μmol/l; P < 0.05) and control patients (4.2 ± 1.8; P < 0.01). DHEAS had a significant (P < 0.01) negative correlation with age, IL-6 and Acute Physiology and Chronic Health Evaluation II scores in both patient groups. Only during the acute phase did DHEAS negatively correlate with dopamine. Nonsurvivors of septic shock (n = 11) had lower DHEAS levels (0.4 ± 0.3 μmol/l) than did survivors (1.7 ± 1.1 μmol/l; P < 0.01). The time course of DHEAS exhibited a persistent depletion during follow up, whereas cortisol levels were increased at all time points.We identified extremely low DHEAS levels in septic shock and, to a lesser degree, in multiple trauma patients as compared with those of age- and sex-matched control patients. There appeared to be a dissociation between DHEAS (decreased) and cortisol (increased) levels, which changed only slightly over time. Nonsurvivors of sepsis and patients with relative adrenal insufficiency had the lowest DHEAS values, suggesting that DHEAS might be a prognostic marker and a sign of exhausted adrenal reserve in critical illness.Dehydroepiandrosterone (DHEA) and its sulphate (DHEAS) are the most abundant steroids secreted by the adrenal cortex [1]. The concentration of DHEA in the blood oscillates in parallel with cortisol, in response to levels of adrenocorticotrophic hormone (ACTH), but without feedback control at the hypothalamic–pituitary level.The physiological role and biological actions of DHEA(S) are not well known but s
Unstandardized Treatment of Electroencephalographic Status Epilepticus Does Not Improve Outcome of Comatose Patients after Cardiac Arrest
Jeannette Hofmeijer,Michiel J. Blans,Albertus Beishuizen,Michel J. A. M. van Putten
Frontiers in Neurology , 2014, DOI: 10.3389/fneur.2014.00039
Abstract: Objective: Electroencephalographic status epilepticus occurs in 9–35% of comatose patients after cardiac arrest. Mortality is 90–100%. It is unclear whether (some) seizure patterns represent a condition in which anti-epileptic treatment may improve outcome, or severe ischemic damage, in which treatment is futile. We explored current treatment practice and its effect on patients’ outcome.
Herpes simplex virus type 1 and normal protein permeability in the lungs of critically ill patients: a case for low pathogenicity?
Joanne Verheij, AB Johan Groeneveld, Albertus Beishuizen, Arthur van Lingen, Alberdina M Simoons-Smit, Rob Strack van Schijndel
Critical Care , 2004, DOI: 10.1186/cc2850
Abstract: In four critically ill patients with persistent pulmonary infiltrates of unknown origin and isolation of HSV-1 from tracheal aspirate or bronchoalveolar lavage fluid, at 7 (1–11) days after start of mechanical ventilatory support, a pulmonary leak index (PLI) for 67Gallium (67Ga)-transferrin (upper limit of normal 14.1 × 10-3/min) was measured.The PLI ranged between 7.5 and 14.0 × 10-3/min in the study patients. Two patients received a course of acyclovir and all survived.The normal capillary permeability observed in the lungs argues against pathogenicity of HSV-1 in the critically ill, and favors that isolation of the virus reflects reactivation in the course of serious illness and immunodepresssion, rather than primary or superimposed infection in the lungs.In some critically ill patients, herpes simplex virus type 1 (HSV-1) is isolated from the upper or lower respiratory tract [1-15]. On the one hand, immunodepressed patients may be susceptible for transmission and acquisition of viral diseases, but on the other hand viral reactivation may occur and may contribute relatively little to morbidity and mortality. Indeed, reactivation of human herpes virus-6 is common in the critically ill and does not worsen outcome [16,17]. In immunocompetent patients, however, isolation of HSV-1 may be associated with viral pneumonia, even if reactivation rather than primary infection is likely [6,8,18]. Although HSV-1 has been associated with acute respiratory distress syndrome (ARDS) or ventilator-associated pneumonia in the critically ill [1-14], either as primary or superimposed infection, there are only few reports that the virus has elicited an infectious host response, as demonstrated by a rise of serum antibodies, by bronchoscopic airway disease, by "typical" findings on computer tomography of the lungs, or by the presence of giant cells or nuclear inclusion bodies on cytology or biopsy of the lower respiratory tract [3,5,9,10,18]. Indeed, Tuxen et al. observed that prophyl
Optimal nutrition during the period of mechanical ventilation decreases mortality in critically ill, long-term acute female patients: a prospective observational cohort study
Rob JM Strack van Schijndel, Peter JM Weijs, Rixt H Koopmans, Hans P Sauerwein, Albertus Beishuizen, Armand RJ Girbes
Critical Care , 2009, DOI: 10.1186/cc7993
Abstract: This was a prospective observational cohort study in a mixed medical-surgical, 28-bed ICU in an academic hospital. 243 sequential mixed medical-surgical patients were enrolled on day 3–5 after admission if they had an expected stay of at least another 5–7 days. They underwent indirect calorimetry as part of routine care. Nutrition was guided by the result of indirect calorimetry and we aimed to provide at least 1.2 g of protein/kg/day. Cumulative balances were calculated for the period of mechanical ventilation. Outcome parameters were ICU, 28-day and hospital mortality.In women, when corrected for weight, height, Apache II score, diagnosis category, and hyperglycaemic index, patients who reached their nutritional goals compared to those who did not, showed a hazard ratio (HR) of 0.199 for ICU mortality (CI 0.048–0.831; P = 0.027), a HR of 0.079 for 28 day mortality (CI 0.013–0.467; P = 0.005) and a HR of 0.328 for hospital mortality (CI 0.113–0.952; P = 0.04). Achievement of energy goals whilst not reaching protein goals, did not affect ICU mortality; the HR for 28 day mortality was 0.120 (CI 0.027–0.528; P = 0.005) and 0.318 for hospital mortality (CI 0.107–0.945; P = 0.039). No difference in outcome related to optimal feeding was found for men.Optimal nutritional therapy improves ICU, 28-day and hospital survival in female ICU patients. Female patients reaching both energy and protein goals have better outcomes than those reaching only the energy goal. In the present study men did not benefit from optimal nutrition.Nutrition is an integral and important part of therapy in the ICU. Nutritional therapy aims at conservation or restoration of the body protein mass and of provision of adequate amounts of energy. On a hypothetical basis, surrogate markers for optimal nutrition with regard to energy and protein provision have proposed to be the delivery of energy as measured by indirect calorimetry, and provision of 1.2 to 1.5 g of protein per kg of pre-admission weight
Predicting outcome of rethoracotomy for suspected pericardial tamponade following cardio-thoracic surgery in the intensive care unit
Birkitt L ten Tusscher, Johan AB Groeneveld, Otto Kamp, Evert K Jansen, Albertus Beishuizen, Armand RJ Girbes
Journal of Cardiothoracic Surgery , 2011, DOI: 10.1186/1749-8090-6-79
Abstract: Twenty-one consecutive patients undergoing rethoracotomy for suspected pericardial tamponade in the ICU, admitted after primary cardio-thoracic surgery, were identified for this retrospective study. We compared patients with or without a decrease in severe haemodynamic compromise after rethoracotomy, according to the cardiovascular component of the sequential organ failure assessment (SOFA) score.A favourable haemodynamic response to rethoracotomy was observed in 11 (52%) of patients and characterized by an increase in cardiac output, and less fluid and norepinephrine requirements. Prior to surgery, the absence of treatment by heparin, a minimum cardiac index < 1.0 L/min/m2 and a positive fluid balance (> 4,683 mL) were predictive of a beneficial haemodynamic response. During surgery, the evacuation of clots and > 500 mL of pericardial fluid was associated with a beneficial haemodynamic response. Echocardiographic parameters were of limited help in predicting the postoperative course, even though 9 of 13 pericardial clots found at surgery were detected preoperatively.Clots and fluids in the pericardial space causing regional tamponade and responding to surgical evacuation after primary cardio-thoracic surgery, are difficult to diagnose preoperatively, by clinical, haemodynamic and even echocardiographic evaluation in the ICU. Only absence of heparin treatment, a large positive fluid balance and low cardiac index predicted a favourable haemodynamic response to rethoracotomy. These data might help in deciding and timing of reinterventions after primary cardio-thoracic surgery.Whereas pericardial effusion is relatively common and may not require drainage, pericardial tamponade is a rare but potentially life-threatening complication after cardio-thoracic surgery and opening of the pericardium [1-11]. Recognition is difficult or late because tamponade is often regional rather than circumferential, contributing to relatively non-classical and non-specific findings [3-5,9,
Malabsorption and nutritional balance in the ICU: fecal weight as a biomarker: a prospective observational pilot study
Nicolette J Wierdsma, Job HC Peters, Peter JM Weijs, Martjin B Keur, Armand RJ Girbes, Ad A van Bodegraven, Albertus Beishuizen
Critical Care , 2011, DOI: 10.1186/cc10530
Abstract: This was an observational pilot study in a tertiary mixed medical-surgical ICU in hemodynamically stable adult ICU patients, without clinically evident gastrointestinal malfunction. Fecal weight (grams/day), fecal energy (by bomb calorimetry in kcal/day), and macronutrient content (fat, protein, and carbohydrate in grams/day) were measured. Diagnostic accuracy expressed in terms of test sensitivity, specificity, positive (PPV) and negative predictive value (NPV), and receiver operator curves (ROCs) were calculated for fecal weight as a marker for energy malabsorption. Malabsorption was a priori defined as < 85% intestinal absorption capacity.Forty-eight patients (63 ± 15 years; 58% men) receiving full enteral feeding were included. A cut-off fecal production of > 350 g/day (that is, diarrhea) was linked to the optimal ROC (0.879), showing a sensitivity and PPV of 80%, respectively. Specificity and NPV were both 96%. Fecal weight (grams/day) and intestinal energy-absorption capacity were inversely correlated (r = -0.69; P < 0.001). Patients with > 350 g feces/day had a significantly more-negative energy balance compared with patients with < 350 g feces/day (loss of 627 kcal/day versus neutral balance; P = 0.012).A fecal weight > 350 g/day in ICU patients is a biomarker applicable in daily practice, which can act as a surrogate for fecal energy loss and intestinal energy absorption. Daily measurement of fecal weight is a feasible means of monitoring the nutritional status of critically ill patients and, in those identified as having malabsorption, can monitor responses to changes in dietary management.A persistent negative energy balance, known as protein-energy malnutrition (PEM), depletes lean tissue and adipose mass. In critically ill patients, PEM is strongly correlated with complications, especially infections [1]. In general, malnutrition in critically ill patients is associated with impaired immune function, an increased risk of infections, and an increased mor
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