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Atrial fibrillation occurs frequently in medical intensive care unit patients. Most intensivists tend to treat this rhythm disorder because they believe it is detrimental. Whether atrial fibrillation contributes to morbidity and/or mortality and whether atrial fibrillation is an epiphenomenon of severe disease, however, are not clear. As a consequence, it is unknown whether treatment of the arrhythmia affects the outcome. Furthermore, if treatment is deemed necessary, it is not known what the best treatment is. We developed a treatment protocol by searching for the best evidence. Because studies in medical intensive care unit patients are scarce, the evidence comes mainly from extrapolation of data derived from other patient groups. We propose a treatment strategy with magnesium infusion followed by amiodarone in case of failure. Although this strategy seems to be effective in both rhythm control and rate control, the mortality remained high. A randomised controlled trial in medical intensive care unit patients with placebo treatment in the control arm is therefore still defendable.

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.

A 47-year-old man from Armenia presented at the emergency department with abdominal pain. He had had a kidney transplant 2 years earlier for renal failure caused by amyloidosis that was secondary to familial Mediterranean fever. He was also known to have chronic hepatitis B with persistent viraemia. He had not received any prophylactic anti-tuberculosis treatment due to impaired liver function, but an extensive work-up was performed prior to transplant, including chest radiography, a Mantoux tuberculin skin test and cultures from 3 consecutive fasting gastric lavage samples, which were all negative for active or latent tuberculosis infection. The patient had presented at the emergency department repeatedly with abdominal pain that was attributed to the familial Mediterranean fever. During his last visit his complaints were accompanied by vomiting, coughing, night sweats and weight loss. He was diagnosed with an intestinal perforation with faecal peritonitis and underwent several laparotomies to treat the faecal peritonitis. Histopathological examination of resected bowel tissue revealed granulomatous inflammation, and acid-fast bacilli were seen with appropriate staining. Later, cultures appeared to be positive for normally sensitive Mycobacterium tuberculosis. The patient died as a result of the disseminated tuberculosis. In immunocompromised patients, tuberculosis often has an atypical course and an increased chance of dissemination that may be difficult to recognize.

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.

We describe the cases of two patients discharged home directly from the ICU. Both patients had the strong wish to die at home after being told that there were no therapeutic options. Sometimes discharge is feasible and can mean very much for patients and their family. Taking measures to ensure a "good deathbed" is an obligation for doctors and nursing staff. However, due to the focus on cure this palliative goal is not always pursued.

A ventilator-dependent child had been in the paediatric intensive care unit (PICU) ever since birth. As a result, she had fallen behind considerably in her development. After 18 months, continuous positive airway pressure was successfully administered via a tracheostomy tube with a novel lightweight device. This enabled her to walk in the PICU. With this device, the child was discharged home where she could walk with an action range of 10 m. Subsequently, her psychomotor development improved remarkably. To the authors' knowledge, this is the first case report of a patient, adult or paediatric, who could actually walk with a sufficient radius of action while receiving long-term respiratory support.

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.

In 1952, Copenhagen was confronted with a poliomyelitis epidemic that involved the respiratory musculature in large numbers of patients. The anaesthetist B. Ibsen, who established carbon dioxide intoxication due to severe hypoventilation as the cause of death, proposed that the patients be treated by tracheostomy and positive pressure respiration in order to achieve better ventilation than with an iron lung. In the Netherlands, it was decided to organise the control ofthe epidemics on a nationwide basis. Various hospitals were asked to set up artificial respiration centres. In addition, the Beatrix Fund was set up in order to collect money for combating poliomyelitis. The epidemic reached the Netherlands in 1956. In Groningen University Medical Centre, 74 patients were admitted, of whom 36 had to be ventilated. In two cases, the mechanical ventilation could not be stopped and one of these was ultimately discharged home with chronic ventilation in 1960, thus becoming the first patient in the Netherlands to be given mechanical ventilation at home. The mechanical ventilation centres developed into the intensive care units as we know them today. Most of the forms of treatment now in use are based on the techniques thought up and elaborated by the pioneers working in the mechanical ventilation centres. The latest development in this series is the development of centres for home mechanical ventilation.

Introduction: Tight glycaemic control is an important issue in the management of intensive care unit (ICU) patients. The glycaemic goals described by Van Den Berghe and colleagues in their landmark study of intensive insulin therapy appear difficult to achieve in a real life ICU setting. Most clinicians and nurses are concerned about a potentially increased frequency of severe hypoglycaemic episodes with more stringent glycaemic control. One of the steps we took before we implemented a glucose regulation protocol was to review published trials employing insulin/glucose algorithms in critically ill patients., Methods: We conducted a search of the PubMed, Embase and Cochrane databases using the following terms: 'glucose', 'insulin', 'protocol', 'algorithm', 'nomogram', 'scheme', 'critically ill' and 'intensive care'. Our search was limited to clinical trials conducted in humans. The aim of the papers selected was required to be glycaemic control in critically ill patients; the blood glucose target was required to be 10 mmol/l or under (or use of a protocol that resulted in a mean blood glucose = 10 mmol/l). The studies were categorized according to patient type, desired range of blood glucose values, method of insulin administration, frequency of blood glucose control, time taken to achieve the desired range for glucose, proportion of patients with glucose in the desired range, mean blood glucose and frequency of hypoglycaemic episodes., Results: A total of twenty-four reports satisfied our inclusion criteria. Most recent studies (nine) were conducted in an ICU; nine others were conducted in a perioperative setting and six were conducted in patients with acute myocardial infarction or stroke. Studies conducted before 2001 did not include normoglycaemia among their aims, which changed after publication of the study by Van Den Berghe and coworkers in 2001; glycaemic goals became tighter, with a target range between 4 and 8 mmol/l in most studies., Conclusion: Studies using a dynamic scale protocol combining a tight glucose target and the last two blood glucose values to determine the insulin infusion rate yielded the best results in terms of glycaemic control and reported low frequencies of hypoglycaemic episodes.

Objective: The Brugada syndrome is a clinical and electrocardiographic familial entity, which may lead to sudden cardiac death. A Brugada pattern ECG may occasionally be caused by conditions such as an overdose of tricyclic antidepressants (TCA). Toxicity of TCA frequently results in the need for critical care support. We retrospectively studied characteristics and electrocardiographic indicators of toxicity of all TCA poisoned patients., Setting: All patients admitted from 1/1/2000 to 1/11/2004 to our ICU after an act of deliberate self-poisoning were included. The ECG's were analysed retrospectively by a cardiologist. Patients with an overdose of TCA were divided in three groups; I. without ECG abnormalities, II. Presence of ECG abnormalities but without Brugada signs, III patients with a Brugada pattern ECG., Results: 134 patients were admitted. In 35 patients a TCA was the main toxic substance. In 12 (34%) TCA patients no ECG abnormalities were found. An increase in QRS duration (>100 ms) was seen in 13 (37%) cases. Six (17%) of them demonstrated a Brugada like pattern. The ECG abnormalities resolved quickly after administration of sodium bicarbonate. Length of stay did not differ between groups. APACHE II and the amount of sodium bicarbonate administered were the highest in the Brugada pattern group. Two patients died., Conclusions: in TCA poisoning the Brugada pattern ECG is a particular manifestation of the frequently occurring intraventricular conduction disturbances. In intoxicated patients in whom the substance is unknown early recognition of the conduction disturbances is important for suspecting a poisoning with TCA.

Acute hyperglycaemia has been associated with complications, prolonged intensive care unit and hospital stay, and increased mortality. We made an inventory of the prevalence and prognostic value of hyperglycaemia, and of the effects of glucose control in different groups of critically ill patients. The prevalence of hyperglycaemia in critically ill patients, using stringent criteria, approaches 100%. An unambiguous negative correlation between hyperglycaemia and mortality has been described in various groups of critically ill patients. Although the available evidence remains inconsistent, there appears to be a favourable effect of glucose regulation. This effect on morbidity and mortality depends on patient characteristics. To be able to compare results of future studies involving glucose regulation, better definitions of hyperglycaemia (and consequently of normoglycaemia) and patient populations are needed.

Introduction: To obtain strict glucose regulation, an accurate and feasible bedside glucometry method is essential. We evaluated three different types of point-of-care glucometry in seriously ill intensive care unit (ICU) patients. The study was performed as a single-centre, prospective, observational study in a 12-bed medical ICU of a university hospital., Methods: Patients with an expected ICU stay of more than 48 hours were included. Because the reference laboratory delivers glucose values after approximately 30 to 60 minutes, which is too slow to use in a glucose regulation protocol and for calibration of the subcutaneous continuous glucose monitoring system (CGMS) (CGMS System Gold), we first validated the ICU-based blood gas/glucose analyser ABL715 (part 1 of the study). Subsequently, part 2 was performed: after inserting (and calibrating) the subcutaneous CGMS, heparinised arterial blood samples were drawn from an arterial line every 6 hours and analysed on both the Precision PCx point-of-care meter using test strips and on the blood gas/glucose analyser ABL715. CGMS glucose data were downloaded after 24 to 72 hours. The results of the paired measurements were analysed as a scatter plot by the method of Bland and Altman and were expressed as a correlation coefficient., Results: Part 1: Four hundred and twenty-four blood samples were drawn from 45 critically ill ICU patients. The ICU-based blood gas/glucose analyser ABL715 provided a good estimate of conventional laboratory glucose assessment: the correlation coefficient was 0.95. In the Clarke error grid, 96.8% of the paired measurements were in the clinically acceptable zones A and B. Part 2: One hundred sixty-five paired samples were drawn from 19 ICU patients. The Precision PCx point-of-care meter showed a correlation coefficient of 0.89. Ninety-eight point seven percent of measurements were within zones A and B. The correlation coefficient for the subcutaneous CGMS System Gold was 0.89. One hundred percent of measurements were within zones A and B., Conclusion: The ICU-based blood glucose analyser ABL715 is a rapid and accurate alternative for laboratory glucose determination and can serve as a standard for ICU blood glucose measurements. The Precision PCx is a good alternative, but feasibility may be limited because of the blood sample handling. The subcutaneous CGMS System Gold is promising, but real-time glucose level reporting is necessary before it can be of clinical use in the ICU. When implementing a glucose-insulin algorithm in patient care or research, one should realise that the absolute glucose level may differ systematically among various measuring methods, influencing targeted glucose levels.

A 61-year-old man with no significant medical history was referred by the general practitioner with progressive dyspnoea despite treatment with steroids and antibiotics. The patient had severe hyponatraemia. Eventually hypervolemic hyponatraemia due to ischemic cardiac failure was diagnosed. After recompensation by fluid restriction and lisdiuretics coronary bypass surgery was carried out. The patient was discharged free of symptoms. This case is a reminder that heart failure may not present itself in a classical manner but as hypervolemic hyponatraemia.

Newer, more selective, antidepressant agents are increasingly being used as first-line treatment. However, clinical experience in patients after a deliberate overdose is limited. We present a case of venlafaxine intoxication complicated by a late rise in creatine kinase, seizures and serotonin syndrome. Rhabdomyolysis prolonged the hospital stay in our patient but had no other serious consequences. Physicians should be aware of this late phenomenon in patients with venlafaxine poisoning.

Cardiac troponin I (cTnI) and cardiac troponin T (cTnT) are valuable heart markers in patients presenting with symptoms of ischaemic heart disease. A number of categories of patients frequently have raised concentrations of cardiac troponin (cTn) without having ischaemic heart disease. These include patients with heart diseases such as heart failure, myocarditis and valvular disease but also those with lung emboli, renal failure and sepsis. Possible underlying mechanisms are diffuse necrosis, cTn proteolysis or leakage of cytoplasmatic cTn with no irreversible damage to the contraction complex of heart-muscle cells. It is possible that cTn-measurement in patients with non-cardiac conditions is of prognostic value but so far this has only been demonstrated in dialysis patients and patients with pulmonary embolism.

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.

The decision to move from curative treatment to palliative care in the intensive-care situation is less related to morals and ethics than it is to the assessment of medical issues, professionalism, communication and orchestration. Treatment should be considered medically pointless if, in the view of the treating physicians, it does not offer realistic chance to return to a meaningful life. Continuing futile care can be seen as disrespectful, both to the patient, his partner and the family, as well as to the members of the ICU team. Intensivists are responsible for withholding or withdrawing life support to patients in whom further life support is considered futile and who are unable to express their wishes due to critical illness and sedation. The intensivist typically makes this type of decision after a period in which medical and other information has been collected and after intensive discussions with other medical professionals as well as the partner and family. This is based on the trust that is built up through their skill, attitude and behaviour and that is perpetuated in a continuing process of intensive communication. Conflicts should be prevented, or at least recognised early and discussed. Ifa conflict is ongoing then it should be tackled by planning a number of consecutive consultations.

Legionella pneumophila is an intracellularly-growing microorganism and the causative agent of Legionnaires' disease; this disease owes its name to the epidemic among American war veterans in Philadelphia in 1976. The analysis ofthe epidemic in Philadelphia revealed--retrospectively--that unlike beta-lactam antibiotica, erythromycin and tetracyclines provided protection against an unfavourable outcome. Despite the absence of prospective, blinded, randomised clinical trials, a well-founded choice for the antibiotic treatment of patients with a Legionella infection can be made using the evidence from in-vitro and cell culture studies, as well as studies in animal models. Although erythromycin, either or not in combination with rifampicin, is still recommended, there is not enough scientific evidence to support this as a first choice drug treatment. The available evidence suggests that quinolones (the most researched are ciprofloxacin and levofloxacin) are the treatment of choice in the case of severe Legionella pneumonia. Newer macrolides (especially azithromycin) have been shown to have some additional beneficial effect. However, the lack of an intravenous formulation limits the use of newer macrolides in severely ill patients.

A 23-year-old woman presented with renal failure resulting from polycystic kidney disease (PKD) aggravated by tubulo-interstitial nephritis. Emergency haemodialysis was planned, and cannulation of the right subclavian vein was attempted, but failed. During this procedure, inadvertent arterial puncture occurred. Transient mild ischaemia of the right arm, and a transient Horner's syndrome were noted. Seven weeks later she presented with severe stridor with impending respiratory failure necessitating emergency intubation; the right-sided Horner's syndrome had recurred. CT imaging showed a large pseudo-aneurysm of the brachiocephalic artery resulting in severe compression of the trachea. Using a prosthetic graft, the operation for the pseudo-aneurysm was successful; there were mild neurological sequelae. Although her family history was negative, autosomal dominant PKD should be considered, and we discuss the possible role of a pre-existing PKD-associated aneurysm.

Purpose of Review: Several clinical studies have given rise to optimism about low-dose steroid treatment in patients with sepsis. It reduces time to shock reversal and may even have a positive effect on mortality. The pathophysiology of the relative adrenal insufficiency syndrome has not yet been determined, and the usefulness of basal and stimulated cortisol levels in diagnosing this syndrome is still uncertain. This review will examine recent evidence to elucidate these questions., Recent Findings: Studies performed in more than 1000 patients in intensive care show convincingly that in general serum cortisol levels are increased. Basal or stimulated cortisol levels are at best useful to predict mortality in patients in intensive care, not to decide which patients to treat or when to discontinue treatment. Measuring free cortisol concentrations rather than total cortisol concentrations in critically ill patients may lead to new research strategies to identify the mode of action of low-dose steroid treatment., Summary: It has been shown that low-dose corticosteroid administration to catecholamine-dependent patients in septic shock results in shock reversal. There seems to be a relative shortage of cortisol, because low-dose hydrocortisone administration resulting in cortisol levels as much as four times the already increased levels results in shock reversal. Strong evidence for a positive effect on mortality is still lacking, perhaps because of the relatively low number of patients investigated. A very important topic in interpreting studies is that total (free plus protein-bound) cortisol has been measured. Future studies should also measure free cortisol concentrations, which could add to our knowledge of the pathophysiology and treatment of the relative adrenal insufficiency syndrome. On the basis of current knowledge, there is no evidence to support a treatment strategy based on a random or stimulated cortisol level. At the moment, rapid hemodynamic improvement of catecholamine-dependent patients after the administration of low-dose corticosteroids still seems the best available clue to diagnosis.

A 32-year-old man was presented with severe hypothermia and respiratory insufficiency after submersion in water. The ECG showed Osborn waves and a prolonged QRS and QT duration which normalized after correction of the hypothermia.

Massive haemoptysis is life-threatening because of asphyxiation from flooding of the central airways with blood. The first step in treatment includes airway protection, usually managed by intubation. Imaging may be inconclusive, and bronchoscopy--rigid or flexible--is essential to establish the site and cause of the bleeding. Bronchoscopy may be therapeutic in that a balloon catheter may be inserted in the bleeding airway in order to tamponade the source of bleeding. Embolisation of pathological bronchial arterial vessels is the treatment of choice in most cases; surgery is limited to causes that cannot be managed by the endovascular treatment modality, or to cases that fail to respond to embolisation.

Despite extensive knowledge about the mechanisms behind sepsis, this syndrome still caries a large morbidity and mortality rate. Dysregulated immune and coagulation systems are held responsible. However, additional pathophysiological mechanisms such as uncontrolled apoptosis induced by death receptor ligands might well play a role. P38 mitogen-activated protein (MAP) kinase inhibitors are considered as potential drugs in inflammatory diseases. Therefore, the effect of endotoxin administration on the response of soluble(s) tumor necrosis factor-related apoptosis-inducing ligand (sTRAIL), a death receptor ligand, and the role of p38 MAP kinase inhibition was studied in 21 human volunteers. The volunteers received 30 min before the endotoxin infusion a single oral dose of placebo or the selective p38 MAP kinase inhibitor drug, RWJ-67657. Plasma sTRAIL increased 10-fold to 6564 +/- 511 pg/mL after 2.5 h. This increase was blocked completely by the highest dose of RW-J6765. This is the first report showing that endotoxin increases sTRAIL where the p38 MAP kinase signaling pathway is involved.

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).

A 51-year-old man became jaundiced, after experiencing flu-like symptoms for a week. On admission anaemia, thrombocytopenia, and hepatic and renal function disorders were present. One month previously he had had sinusitis. Thrombotic thrombocytopenic purpura (TTP)/haemolitic-uraemic syndrome (HUS) was suspected, but the thrombocyte count rose spontaneously. The leukocytosis indicated an infectious cause of the symptoms and the jaundice appeared to originate from intrahepatic cholestasis. All symptoms could be traced to leptospirosis icterohaemorrhagica (known as 'Weil's disease'). The source was possibly the patient's fishpond. He recovered spontaneously and was also treated with antibiotics. Leptospirosis, a multi-organ disease is seen ever more infrequently as an occupational disease in stock farmers and increasingly frequently in people whose hobbies involved animals.

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.

Positron emission tomography (PET) was used for the study of regional cerebral perfusion and metabolism in eight patients with severe post-hypoxic encephalopathy, caused by cardiac arrest and resulting in a coma lasting for at least 24 h. Using this method, we aimed to identify regional vulnerability, which was hypothesized to provide (i) insight in pathogenic mechanisms and (ii) early prognostic parameters. On day 1 post-resuscitation, 18-Fluor deoxyglucose ([F18]-FDG) indicated a marked decrease of cerebral metabolic activity. Gray matter glucose consumption was 54% of normal values, whereas white matter uptake was 70% of normal. Regional differences followed a pattern of neuronal density rather than specific patterns of functionally or biochemically defined regions or of vascular territories. In contrast to [F18]-FDG, the distribution of 15-oxygen labeled water ([O-15]-water) showed a better demarcation between gray and white matter, whereas focal deficit was not observed. In some patients, hyperperfusion relative to regional glucose consumption was observed in the occipital poles and basal ganglia. This suggests loss of vascular tone, i.e. vascular paralysis, in the basilar artery territory. CT and MRI scanning did not show any major change with respect to the hypoxic injury. In the small group studied, all patients had a poor outcome. The comparison between survivors and nonsurvivors did not reveal obvious differences in PET data, suggesting that this technique does not provide major prognostic clues adding to the prognostic information derived from serial neurological assessment in the restricted patient group characterized by prolonged coma.

A 38-year-old man presented with respiratory insufficiency due to a pneumothorax on the left side and giant bullae on the right side.