Diabetes insipidus as the presenting symptom of Wegener's granulomatosis.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to E F van Bommel.
Explore the source record for details and available documents.
A detailed description is presented of the hemodialysis treatment for 6 weeks of a patient strongly positive for hepatitis B virus ([HBV], hepatitis B surface antigen, hepatitis B e antigen, HBV DNA), which was performed without any special precautions. All 59 patients potentially exposed to the HBV-positive patient, of whom 29 appeared fully unprotected by antibody, were followed for at least 9 months but remained negative. This illustrates the feasibility of following Universal Precautions instead of using exceptional procedures for one single agent.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Despite impressive advances in the field of general intensive care and in the techniques available for the treatment of acute renal failure (ARF), particularly the development of continuous renal replacement therapies (CRRT), it is suggested that outcome of ARF patients has remained similar to that observed 2 or more decades ago. This article focuses on the impact of several factors, including the dialysis regimen, on outcome in ARF patients in a recent time period compared with an earlier period to assess whether a change has occurred in the patient population, dialysis regimen, or renal and patient outcome. Critical differences between intermittent hemodialysis (IHD) and CRRT and the authors' preference for continuous venovenous hemofiltration (CWH) are explained. However, using the APACHE II score and more specifically use of the ratio between this score at 2 different time points (ICU admission v time of start of dialysis), the need for an easy-to-use and reliable severity-of-illness score to allow adequate comparison of patient groups or treatment strategies is emphasized. Using data from a recent survey, attention is also given to the implementation of acute dialytic support, particularly CRRT, in the Netherlands.
Mannitol is widely used because of its osmotic diuretic action and its presumed antioxidant properties. In pre-existent renal dysfunction, however, mannitol may accumulate leading to potentially deleterious effects. We describe a 71-year-old woman with moderate chronic renal failure due to diabetic nephropathy who developed acute anuric renal failure after mannitol administration for post-traumatic reflex sympathetic dystrophy. After haemodialysis symptoms of acute renal failure rapidly disappeared with recovery of pre-existent renal function. Daily measurement of the osmolal gap as a simple and accurate way of monitoring patients receiving mannitol infusion is emphasized. A rapid increase in the osmolar gap should prompt adjustment of the dose or even discontinuation of mannitol, especially in the case of pre-existent risk factors.
The case history of a patient with pulmonary embolism 4 months following a kidney transplantation is presented. Ultrasonography of the abdomen suggested a large ovarian tumour for which she had a laparotomy. Histological examination after resection of the tumour revealed a benign multicystic mesothelioma of the peritoneum. During the course of 1 year the tumour recurred 5 times and different attempts to aspirate and obliterate the cyst were ineffective. Eventually, cure was achieved by permanent transvaginal catheter drainage, which resulted in infection and obliteration of the cyst.
Accumulating experience with the use of continuous renal replacement therapy (CRRT) in critically ill patients with acute renal failure suggests that these treatment modalities have distinct advantages relative to conventional dialysis in terms of solute clearances, fluid removal and hemodynamics, which may translate in improved renal and patient outcome. Recent data point to a possible beneficial effect of CRRT on the clinical course, independent from an impact on fluid balance, in critically ill patients with shock which is attributed to the continuous elimination of inflammatory mediators from the circulation. This has raised the question as to whether CRRT might be used for 'non-renal' indications such as the systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS). In some animal models of experimental septic and non-septic shock, (short-term) hemodialysis and hemofiltration were found to improve hemodynamics and/or gas exchange. However, data were inconsistent and the clinical relevance questionable. Observations from both uncontrolled and controlled clinical studies (comprising only a small number of patients) support the hypothesis that CRRT may exert beneficial effects on the clinical course in critically ill patients with SIRS and MODS, independent from volume removal. Although several mediators known to play a role in the development of SIRS/MODS may pass hemofiltration membranes, quantitative data on the extent of its extracorporeal clearance relative to the production rate and endogenous clearance is often lacking. In addition, this aspecific elimination with CRRT may also effect levels of anti-mediators, which may be harmful. Ultrafiltrate properties include depression of cardiac performance, induction of proteolysis and immunosuppressive activity suggesting that water-soluble factors responsible for these deleterious effects are removed from the circulation by convection. However, no significant survival advantage has yet been shown for critically ill patients with SIRS/MODS when treated with CRRT as an adjunct to conventional therapy. Only prospective controlled studies of appropriate sample size, which requires a multicenter approach, might answer the question whether use of CRRT may alter the clinical course and outcome in critically ill patients with SIRS and MODS. Until such studies are performed, the rationale for the use of CRRT in the absence of conventional indications for dialytic support remains unproven.
The impact of continuous hemofiltration (CHF) using a polyacrylonitrile membrane on the kinetics of tumor necrosis factor alpha (TNF alpha), interleukin-1 beta (IL-1 beta), and their inhibitors (soluble TNF receptors [sTNFrI, sTNFrII], interleukin-1 receptor antagonist [IL-1Ra]) was assessed in nine oliguric patients suffering from systemic inflammatory response syndrome. Blood and plasma flow (Qb, Qp), sieving coefficient (SC), plasma and ultrafiltrate clearances (Kp, Kuf), and plasma extraction rates (ERp) were calculated at different time points using standard formulas. No significant improvement of hemodynamics or gas exchange was noted following HF but a significant increase in serum bicarbonate occurred after 24 h (P < 0.05). TNF alpha was detected in plasma from all patients (153 +/- 2.3 pg/mL [mean +/- SEM]). None of the patients had detectable IL-1 beta levels. High levels of the TNF receptors (sTNFrI 20.338 +/- 2.431 pg/mL; sTNFrII 17.839 +/- 2.630 pg/mL) and IL-1Ra (19.775 +/- 3.943 pg/mL) were found in all patients. Upon initiation of hemofiltration (HF), the mean individual sTNFrI/TNF alpha ratio amounted to 269 +/- 84.6 and the sTNFrII/TNF alpha ratio to 249 +/- 91.8. Mean ultrafiltrate volume (Vuf) was 11.8 +/- 0.4 L/day. Appreciable sieving of IL-1Ra (SC 0.45 +/- 0.10), but not of the other cytokines, was noted (SC TNF alpha, sTNFrI, sTNFrII < 0.09). Despite minimal Kuf of TNF alpha, sTNFrI, and STNFrII (Kuf < 0.8 mL/min), appreciable Kp was noted, suggesting that membrane adsorption occurs (Kp approximately 8 mL/min). There was a nonsignificant increase of the ratios between both TNF receptors and TNF alpha across the filter (sTNFrI/TNF alpha ratio [pre] 231 +/- 37.9 versus [post] 312 +/- 75.3); sTNFrII/TNF alpha ratio [pre] 211 +/- 42.1 versus [post] 291 +/- 79.3). Appreciable Kp of IL-1Ra was noted (Kp 17.3 +/- 1.61 mL/min), which was only in part due to Kuf (4.0 +/- 0.86 mL/min). There was a significant decrease of IL-1Ra levels across the membrane, both overall ([pre] 20.223 +/- 2.282 versus [post] 16.637 +/- 2.039 pg/mL; P < 0.01) and at different time points (P < 0.01). Only for IL-1Ra was significant extraction from plasma noted (ERp 26 +/- 6.0%). Plasma levels of TNF alpha, sTNFrI, sTNFrII, and IL-1Ra were not altered by 24 h of CHF. In conclusion, both cytokines and cytokine inhibitors can be removed from the circulation, either by convective transport or by membrane adsorption. Using low-volume HF (Vuf approximately 12 L/day), no impact on cytokine plasma levels nor the patients hemodynamics or gas exchange was noted. The appreciable SC of IL-1Ra (0.45), however, suggests that HF with high(er) UF volumes (> 50 L/day) may be able to achieve reductions in plasma levels of some peptide (anti)mediators. However, whether this aspecific elimination of both mediators and antimediators may alter the clinical course in critically ill patients remains to be investigated.
BACKGROUND: Chronic haemodialysis causes blood loss and iron-deficiency. This can be corrected with intravenous preparations, e.g. sodium ferric-gluconate (FeGl). In two patents complaints of hypotension and malaise during FeGl infusion coincided with high levels of serum iron and a calculated transferrin iron saturation above 100%. Iron toxicity could be the cause of these complaints. Free iron is known to aggravate the toxicity of free radicals and other reactive oxygen products that are constantly formed in the body. We compared four rates of FeGl infusion with regard to iron parameters. METHODS: 20 dialysis patients received a total of 26 infusions of FeGl. A rapid infusion of 135 mg (Protocol A (n=10)) or 62.5 mg (Protocol B (n=7)) of FeGl was given during the last 30 min of dialysis. A slow infusion of 125 mg (Protocol C (n=9)) or 62.5 mg (Protocol D (n=10)) was given during 4 or 4.5 h of dialysis. Blood was taken at regular intervals, before, during, and after dialysis for determination of serum iron, transferrin, ferritin, haematocrit, total protein, albumin, and lactate dehydrogenase (LDH). Transferrin saturation was calculated from transferrin and serum iron. RESULTS: With rapid infusion A (125 mg) the highest levels of serum iron (median 120 (range 40-159) micromol/l) and transferrin saturation (207 (84-331)%) were seen at the end of the infusion. These were significantly higher than the peak levels with B, C, and D (P</=0.03). With rapid infusion B (62.5 mg), peak levels were intermediately high (serum iron 61 (50-96) micromol/l; transferrin saturation 118 (91-174)%). With slow infusion C (125 mg) similar peak levels were seen (serum iron 83 (43-106) micromol/l; transferrin saturation 141 (88-172)%). With slow infusion D (62.5 mg), the lowest peak levels were seen (serum iron 38 (31-55) micromol/l; transferrin saturation 78 (43-92)%). These levels were significantly lower than those with A, B and C (P<=0.002). Only with D all patients showed a transferrin saturation lower than 100%. Ferritin was increased before the next dialysis in all patients. LDH was not significantly elevated during any infusion. CONCLUSIONS: The commonly used rapid infusion rate (A) of FeGl causes 'oversaturation' of transferrin. This is compatible with iron toxicity due to free iron which may explain our patients' complaints. Free iron cannot be measured directly. LDH as a crude measure of cell damage was not elevated. Better measurements to prove free iron toxicity, like lipid peroxides, are not yet readily available. Infusion during a longer period at a lower dose (D) is effective and eliminates 'Oversaturation' of transferrin and probably the danger of iron toxicity.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The outcome and metabolic control was studied in 60 critically ill patients with acute renal failure (ARF) treated by continuous arteriovenous hemodiafiltration (CAVHD) in a single surgical intensive care unit. Mean age (+/- SEM) was 60 +/- 2 years with a male predominance (80%). The majority of patients required mechanical ventilation (83%) and/or vasopressor support (70%) and suffered from multiorgan failure [mean number of organ system failures 3.3 +/- 0.3 (range 1-6)]. CAVHD resulted in a rapid decline of serum urea and creatinine levels during the first 72 h (urea 47.4 +/- 2.3 to 30.3 +/- 1.4 mmol/l, p < 0.05, and creatinine 572 +/- 27 to 361 +/- 23 mumol/l, p < 0.05); thereafter, controlled steady-state levels were achieved with serum urea levels kept below 30 mmol/l with full protein alimentation and often despite hypotension, surgery and septicemia. Significant electrolyte derangements could be easily corrected and maintained within normal limits. Bicarbonate homeostasis could be restored within 48 h in patients with severe metabolic acidosis (HCO3- < 20 mmol/l) with use of bicarbonate as a buffering anion (17 +/- 0.5 to 23.2 +/- 0.6, p < 0.05). CAVHD allowed rapid removal of excess body and lung water (up to 5 liters/day) without hemodynamic instability. Despite a mean pretreatment APACHE II score of 26.5, 26 patients (43%) survived until discharge from the intensive care unit, of whom 23 (38%) survived to leave hospital. Requirement of mechanical ventilation or vasopressor support, higher APACHE II scores and septicemia were all associated with a poor prognosis.(ABSTRACT TRUNCATED AT 250 WORDS)
Explore the source record for details and available documents.
The study objective was to determine the applicability of the acute physiology and chronic health evaluation (APACHE) II score in surgical patients with acute renal failure (ARF) requiring dialytic support, and to assess its utility in evaluating data from this specific disease group. This was a retrospective, partly prospective follow-up study of patients who developed ARF during their course of stay on the surgical intensive care unit (ICU) of a Dutch university hospital from January 1, 1986, to January 31, 1994. A total of 111 patients were identified, of whom 104 patients were considered eligible for this study. Data for the individual APACHE II scores were calculated from the most deranged values during the initial 24 h of ICU admission (APACHE II1) and on the day dialytic support was instituted (APACHE II2). The ratio between the two APACHE II scores was also calculated for each patient (AP2/AP1 ratio). Receiver operating characteristic curves (ROC) were constructed. Other variables evaluated included age, sex, serum creatinine, diagnostic category, time from ICU admission to start of dialytic support, and the type of dialytic support. Of these 104 patients (median age 64; range 23-85 years), 51 (50%) survived to leave the ICU, of whom 47 (46%) survived to leave hospital. The APACHE II2 score (27.0 +/- 4.4 vs. 22.4 +/- 3.5; p < 0.001) and AP2/AP1 ratio (1.12 +/- 0.09 vs. 0.97 +/- 0.06; p < 0.001) were significantly higher for nonsurvivors as compared to survivors. The ROC curve was most discriminative for the AP2/AP1 ratio (area under the curve 0.92) and to a lesser extent for the APACHE II2 score (area under the curve 0.78). Estimated risk of death with the APACHE II equation did not improve predictive power. Multivariate analysis of various variables revealed the AP2/AP1 ratio as the single most important factor predicting death (odds ratio 13.8, p < 0.001). Adjusting for the AP2/AP1 ratio, no impact on outcome was observed for age, diagnostic category, time from ICU admission to start of dialytic support, and the type of dialytic support. Above a value of 1.0 of the AP2/AP1 ratio, logistic regression revealed a sharp increase in death probability with increasing AP2/AP1 ratio. APACHE II, when used at the time of initiation of dialytic support, proved to be a valid way in our surgical ICU to stratify ARF patients by the severity of their illness. Moreover, use of the AP2/AP1 ratio further improved the usefulness of this severity index and may help to identify patients who have little chance of survival. Predicting death with the APACHE II equation did not improve predictive power.
Explore the source record for details and available documents.
A rare case is described of coexistent idiopathic retroperitoneal and mediastinal fibrosis presenting with portal hypertension. Portal hypertension was caused by fibrotic entrapment of the portal venous system. The present case provides further evidence for the concept of systemic idiopathic fibrosis and underlines the variable manifestations of the disorder.