Search

For severe lithium intoxication haemodialysis is recommended to lower serum lithium levels rapidly. Frequently, serum lithium levels rebound after dialysis and repeated dialysis is needed. This is the first report of an adult patient with severe lithium intoxication who underwent haemodialysis (HD) followed by continuous veno-venous haemodiafiltration (CVVHDF). Mean lithium clearances with HD and CVVHDF were 173 and 61 ml/min, respectively. Serum lithium levels were rapidly lowered and did not rebound. Two compartment simulations illustrate that HD followed by CVVHDF is the most effective strategy for removing lithium from the intracellular compartment.

Imported falciparum malaria is increasing in Western countries. In patients with severe disease, exchange transfusion has been added to antimalarial and conventional supportive therapy to increase removal of parasitized erythrocytes, but hemodynamic compromise limits its use; automated erythrocytapheresis may be advantageous. We review published reports of patients with severe falciparum malaria treated by automated erythrocytapheresis combined with standard therapy and add three more cases to the literature. No studies have been conducted to evaluate its clinical efficacy, and this adjunct therapy should therefore be considered as salvage therapy. Apheresis of red cells appears feasible, safe and effective in rapidly reducing parasite count.

Venomous snakebites are a rarity in the Netherlands. In this report we describe the case of a 26-year-old male amateur snakekeeper who was bitten in his left index finger by a Western bush viper (Atheris chlorechis). His clinical condition deteriorated rapidly with acute renal failure and considerable blood loss due to coagulopathy. Antidote was not readily available and was finally supplied by a zoo in Antwerp, Belgium. One day after admission the blood loss diminished.

Objective: To find out if there is an association between hyperglycaemia and mortality in mixed ICU patients., Design and Setting: Retrospective cohort study over a 2-year period at the medical ICU of a university hospital., Measurements: Admission glucose, maximum and mean glucose, length of stay, mortality, insulin therapy and Apache-II score., Results: In 1085 consecutive patients, ICU- and hospital mortality were 20 and 25%, respectively. The total number of blood glucose measurements was 10.012. Admission glucose was 7.9 +/- 4.5 mmol/l (mean +/- SD), mean glucose 7.5 +/- 2.9 and maximum glucose 10.0 +/- 5.4 mmol/l. Median ICU length of stay (LOS) was 3.0 days (range 2.0-6.0 days, IQR), and hospital LOS was 16 days (range 7-32 days). In 28% of patients insulin treatment was started. Median Apache-II score was 13. 68% of patients were mechanically ventilated. Univariate analysis showed an association with ICU mortality for mean glucose (non-survivors 8.6 +/- 4.3 vs 7.2 +/- 2.4 survivors), maximum glucose (11.7 +/- 5.9 vs 9.6 +/- 5.2, non-survivors vs survivors, respectively), use of insulin (mortality 29 vs 17% in patients not using insulin) and age (61 vs 55.7 years). Gender and a history of diabetes mellitus were not associated with mortality. In a multivariate model, the Apache-II score was the only variable associated with mortality independent of other variables, including mean blood glucose., Conclusion: In this retrospective study mean glucose level was not an independent risk factor for mortality in mixed ICU patients.

Introduction: The aim of transferring a critically ill patient to the intensive care unit (ICU) of a tertiary referral centre is to improve prognosis. The transport itself must be as safe as possible and should not pose additional risks. We performed a prospective audit of the quality of interhospital transports to our university hospital-based medical ICU., Methods: Transfers were undertaken using standard ambulances. On departure and immediately after arrival, the following data were collected: blood pressure, heart rate, body temperature, oxygen saturation, arterial blood gas analysis, serum lactic acid, plasma haemoglobin concentration, blood glucose, mechanical ventilation settings, use of vasopressor/inotropic drugs, and presence of venous and arterial catheters. Ambulance personnel completed forms describing haemodynamic and ventilatory data during transport. Data were collected by our research nurse and analyzed., Results: A total of 100 consecutive transfers of ICU patients over a 14-month period were evaluated. Sixty-five per cent of patients were mechanically ventilated; 38% were on vasoactive drugs. Thirty-seven per cent exhibited an increased number of vital variables beyond predefined thresholds after transport compared with before transport; 34% had an equal number; and 29% had a lower number of vital variables beyond thresholds after transport. The distance of transport did not correlate with the condition on arrival. Six patients died within 24 hours after arrival; vital variables in these patients were not significantly different from those in patients who survived the first 24 hours. ICU mortality was 27%. Adverse events occurred in 34% of transfers; in 50% of these transports, pretransport recommendations given by the intensivist of our ICU were ignored. Approximately 30% of events may be attributed to technical problems., Conclusion: On aggregate, the quality of transport in our catchment area carried out using standard ambulances appeared to be satisfactory. However, examination of the data in greater detail revealed a number of preventable events. Further improvement must be achieved by better communication between referring and receiving hospitals, and by strict adherence to checklists and to published protocols. Patients transported between ICUs are still critically ill and should be treated as such.

A 52-year-old man developed fever, headache, tinnitus, and painful joints. He reported a tick bite contracted during a summer holiday in the Netherlands, followed by erythema on his left arm three weeks earlier. Initial treatment with doxycycline had failed and he had now developed signs of meningoencephalitis. Laboratory tests showed an increased white cell count (16.1 x 10(9)/1), and elevated ESR (51/1h).

Background: To evaluate the possibility of preventing endotoxin induced renal damage by p38-MAPK inhibition in a human model., Design and Methods: Twenty-one healthy young male volunteers received 4 ng/kg Escherichia coli endotoxin as a single dose. Four groups of volunteers received an oral dose of placebo or 350, 700 or 1400 mg RWJ-67657, a p38-MAPK inhibitor, 20 min before endotoxin infusion. Urine samples were collected at set time intervals. The urinary excretion rate of beta(2)-microglobulin and N-acetyl-beta-D-glucosaminidase, as indicators of tubular dysfunction was determined., Results: There was a significant increase of beta(2)-microglobulin and N-acetyl-beta-D-glucosaminidase urine excretion rate after endotoxin infusion in the placebo group. p38-MAPK inhibition prevented the increase of markers for tubulopathy., Conclusions: Endotoxin infusion induces measurable tubular damage. Blocking the p38-MAPK may prevent this damage. The mechanism is unclear, but blocking TNF-alpha release is a possible explanation.

Objective: To study the relationship between cytokine levels and cardiac troponin I (cTnI)., Design: Prospective experimental study., Setting: Intensive care unit of a university hospital., Participants: Six healthy male volunteers. INTERVENTIONS. Endotoxin, 4 ng/kg, was given as a 1-min intravenous infusion., Measurements and Results: Circulating cardiac troponin I levels and proinflammatory cytokines tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-8 (IL-8) were analysed at various time points during a 24-h period. TNF-alpha appeared in the circulation 30 min after injection (T=0.5 h), reaching peak levels (5,665+/-1,910 pg/ml) 2 h after infusion. At T=24 h TNF-alpha was still elevated in the circulation compared to T=0. None of the six volunteers had a cTnI value higher than 0.1 microg/l at T=0, 6 h or 24 h., Conclusion: The presence of significant amounts of TNF-alpha, IL-6 and IL-8 in the systemic circulation does not lead to increased levels of cTnI in experimental human endotoxaemia.

Objective: We studied the activity of a single oral dose of RWJ-67657, a synthetic p38 mitogen-activated protein kinase inhibitor, in preventing dual leukocyte/endothelial activation after endotoxin infusion in healthy volunteers., Design: Prospective placebo-controlled study., Setting: Intensive care unit at a university medical center., Subjects: Twenty-one healthy male volunteers., Interventions: Endotoxin (4 ng/kg) as a 1-min infusion. According to randomization, the volunteers received placebo (n = 6) or 1400 mg (n = 4), 700 mg (n = 6), or 350 mg (n = 5) of RWJ-67657., Measurements and Main Results: Neutrophil activation was investigated by analyzing the extent of membrane expression of adhesion markers by calibrated flow cytometry. Circulating intercellular adhesion molecule-1 and E-selectin were measured by enzyme-linked immunosorbent assays. The endotoxin-induced shedding of L-selectin was diminished in a dose-dependent manner (p <.0001). High-dose RWJ-67657 prevented up-regulation of the integrins CD11b (p <.01) and CD 66b (p <.01) on neutrophils. The endotoxin-induced increase in circulating intercellular adhesion molecule-1 and circulation E-selectin was almost completely prevented by high-dose RWJ-67657., Conclusion: A single oral dose of RWJ-67657 prevented neutrophil and endothelial activation after endotoxin infusion.

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.

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.

Severe acute lung injury may result from many infectious and other insults. Although the initial insult may cause overwhelming tissue damage with subsequent gas exchange impairment and risk of death, several strategies of management may also add substantial toxicity. This review focuses on damage incurred by recently identified toxic ventilator settings e.g., high inflation pressures, too low settings of positive end-expiratory pressure, and too high tidal volumes. Liberal fluid management may be another important source of toxicity. The evidence from the literature for survival advantage of lung protective and other strategies is critically reviewed.

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.

We performed a retrospective inventory of the condition of transferred patients to our 11-bed medical ICU, aimed firstly to measure the quality of these transports and secondly to identify variables that may predict a high risk of deterioration during transferral. By a search in our hospital database, we identified 112 consecutive patients (47 women/65 men) transferred from other hospitals (distance 20-350 km) to our ICU over a period of 14 months. The following data were collected on departure (if available) and on arrival: blood pressure, heart rate, temperature, oxygen saturation, routine laboratory parameters, arterial blood gas analysis, lactic acid, settings of mechanical ventilation, use of vasopressor/inotropic medication, presence of venous and arterial catheters and Apache II score on arrival. No major worsening during transportation was found, looking at the whole group. However, individual data showed severe deterioration of some patients during transport. We were not able to point out parameters that could predict hemodynamic or respiratory instability during transport or condition on arrival. In conclusion, quality of transport seems fairly good; in individual cases, improvements are possible. Therefore, we plan to investigate whether or not a strict protocol, based on recommendations in the literature and on local feasibility can further improve condition on arrival and survival of transferred ICU patients in our adherence region.

Background: At present, it is unclear whether in experimental endotoxemia, the pro-inflammatory response observed in healthy volunteers is followed by an anti-inflammatory response, as observed in patients with sepsis. We studied the evolution of a number of inflammatory parameters during a prolonged period (24 h) after infusion of endotoxin in healthy subjects. Methods: Six healthy male subjects received an infusion of endotoxin (4 ng/kg body weight). Blood was drawn before, and at various intervals up to and including 24 h after, endotoxin infusion. Circulating cytokine levels, leukocyte activation surface markers, plasma lactoferrin, and neopterin levels were measured, and clinical signs and symptoms were noted during a 24-h period. Monocyte and neutrophil activation after endotoxin infusion is investigated in relation to the inflammatory response. The extent of neutrophil and monocyte activation was correlated to clinical markers and blood levels of inflammatory mediators and cytokines. Results: Tumor necrosis factor-alpha appeared 30 min after infusion in the circulation, peaking (5665+/-1910 pg/ml) at 2 h. Interleukin-10 appeared 60 min after infusion, peaking (427+/-348 pg/ml) at 3 h. The expression of leukocyte activation markers increased significantly after infusion. Expression of HLA-DR on monocytes decreased significantly after 3 h (P=0.03). There was a correlation between the TNF-alpha:IL-10 ratio and the CD11b:HLA-DR ratio (P=0.03). Conclusions: During experimental human endotoxemia, an initial pro-inflammatory response is successfully compensated by an anti-inflammatory response, leading to homeostasis. This is in contrast to what happens in septic patients with compensatory anti-inflammatory response syndrome. The inflammatory balance, expressed as the cytokine pro:anti-inflammatory ratio, is reflected at a cellular level.

The hemolytic uremic syndrome (HUS) is known to have several causes, including infectious diseases, drugs, pregnancy, and malignant disease. We report a patient who developed acute renal failure attributable to HUS in the course of Capnocytophaga canimorsus bacteremia. Acute tubular necrosis as well as HUS should be considered as a cause of acute renal failure in the setting of Capnocytophaga canimorsus bacteremia.

Epidemiologic analysis of submersion cases admitted to the intensive and respiratory care unit showed that several interrelated factors preceded submersion. Accidental submersion and traffic accidents represented one third of the causes of submersion. Other relevant causes were illness (29.9%), psychosocial causes (20.1%), alcohol (18.1%), and suicide (9.1%). Age distribution, gender, and mortality rate were different in each group. Young age, submersion during recreational activities, summer months, and normothermia were epidemiologic factors with a favorable prognosis. Our data were compared with national data. WHO-ICD code 994.1 (drowning and nonfatal submersion) is the best entrance for epidemiologic analysis. Five hundred twenty deaths and 690 hospital admissions due to submersion occur in The Netherlands each year. About 460 victims die before they reach a hospital.