Advanced cardiac life support update: the new ILCOR cardiovascular resuscitation guidelines. International Liaison Committee on Resuscitation.
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Biomedical subjects
Publications and source records attributed to L Huyghens.
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STUDY OBJECTIVE: we studied the long-term effect of a combined treatment with resuscitative mild hypothermia and induced hypertension on survival rate and neurological outcome after asphyxial cardiac arrest (CA) in rats. METHODS: 36 male Wistar rats, were randomised into three groups: Group I (n=10): anaesthetised with halothane and N(2)O/O(2) (70/30%) had vessel cannulation but no asphyxial CA; mechanical ventilation was continued to 1 h. Group II (n=13): under the same anaesthetic conditions and vessel cannulation, was subjected to asphyxial CA of 8 min, reversed by brief external heart massage and followed by mechanical ventilation to 1 h post restoration of spontaneous circulation (ROSC). Group III (n=13): received the same insult and resuscitation as described in group II, but in contrast to the previous group, a combination treatment of hypothermia (34 degrees C) and induced hypertension was started immediately after ROSC and maintained for 60 min ROSC. Survival rate and neurological deficit (ND) scores were determined before arrest, at 2 and 24 h, and each 24-h up to 4 weeks after ROSC. RESULTS: Baseline variables were the same in the three groups. Comparison of the asphyxial CA groups (groups II and III), showed an increased, although not statistically significant, survival rate at 72 h after ROSC in group III, and it became highly significant at 4 weeks after ROSC. The ND scores were the same in both asphyxial CA groups (groups II and III). CONCLUSIONS: Resuscitative mild hypothermia and induced hypertension after asphyxial CA in rats is associated with a better survival rate. This beneficial effect persisted for 4 weeks after ROSC.
STUDY OBJECTIVE: To test the feasibility and the speed of a helmet device to achieve the target temperature of 34 degrees C in unconscious after out of hospital cardiac arrest (CA). METHODS: Patients with cardiac arrest due to asystole or pulseless electrical activity (PEA) who remained unconscious after restoration of spontaneous circulation (ROSC) were enrolled in the study and randomised into two groups: a normothermic group (NG) and a hypothermic group (HG). Bladder and tympanic temperature were monitored every 15 min. A helmet device was used to induce mild hypothermia in the HG. Later on, the effect of mild hypothermia on the haemodynamics, electrolytes, lactate, arterial pH, CaO2, CvO2 and O2 extraction ratio were analysed and compared to the values obtained from the NG. RESULTS: Thirty patients were eligible for the study, 16 were randomised into the HG and 14 were randomised into the NG. The median tympanic temperature at admission in both groups was 35.5 degrees C (range: 33.3-38.5 degrees C) and the median tympanic temperature after haemodynamic stabilisation was 35.7 degrees C (range: 33.6-38.2 degrees C). In the HG, the core and the central target temperature of 34 degrees C were achieved after a median time of 180 and 60 min, respectively after ROSC. At the start of the study, no significant differences between the NG and HG were seen. At the end of the study, lactate concentration and O2 extraction ratio were significantly lower in the HG; however the CvO2 was significantly lower in the NG. CONCLUSIONS: Mild hypothermia induced by a helmet device was feasible, easy to perform, inexpensive and effective, with no increase in complications.
BACKGROUND AND AIMS: Attempts to control enteral nutrition associated diarrhea in the critically ill tube-fed patient by implementing feeding formulas enriched with fiber were mostly unsuccessful. Recently, it was shown that enteral feeding containing soluble partially hydrolyzed guar decreased the incidence of diarrhea in a cohort of non-critically ill medicosurgical patients. We investigated whether this type of enteral feed could also influence stool production in patients with severe sepsis, a population at risk for developing diarrhea. METHODS: The study was double-blind. Patients with severe sepsis and septic shock were consecutively enrolled and at random received either an enteral formula supplemented with 22 g/l partially hydrolyzed guar or an isocaloric isonitrogenous control feed without fiber. All patients were mechanically ventilated and treated with catecholamines and antibiotics. Enteral feeding was provided through a nasogastric tube for a minimum of 6 days. A semiquantitative score based on stool volume and consistency was used for daily assessment of diarrhea. RESULTS: 25 patients fulfilled the criteria for data analysis. Soluble fiber was administered in 13 of them. The two groups were well-matched for gender, age, disease severity, cause of sepsis, laboratory parameters, total feeding days and time to reach nutritional goals. The mean frequency of diarrhea days was significantly lower in patients receiving fiber than in those on standard alimentation (8.8+/-10.0 % vs 32.0+/-15.3 %; P=0.001). The whole group of fiber-fed patients had less days with diarrhea per total feeding days (16/148 days (10.8%) vs 46/146 days (31.5%); P<0.001) and a lower mean diarrhea score (4.8+/-6.4 vs 9.4+/-10.2; P<0.001). The type of enteral diet did not influence sepsis-related mortality and duration of stay in the intensive care unit. CONCLUSION: Total enteral nutrition supplemented with soluble fiber is beneficial in reducing the incidence of diarrhea in tube-fed full-resuscitated and mechanically ventilated septic patients.
Sepsis is characterized by disturbances in liver perfusion and alterations in intrahepatic cellular functions and interactions. This provokes structural and functional liver damage as well as hepatocellular activation that is believed to perpetuate the immuno-inflammatory response. Changes in hepatic perfusion during sepsis are still poorly understood due to the heterogeneity of septic animal models and the difficult accessibility of the hepatic circulation in humans. Sinusoidal blood flow is severely compromised during sepsis due to a decline in perfused sinusoidal area in association with a decrease in sinusoidal flow velocity. Imbalances in the production of nitric oxide may account for these (micro) circulatory disorders. Interactions between liver macrophages, activated endothelial cells and hepatocytes determine the intensity of inflammation and contribute to initial liver damage. Hepatocellular injury is then enhanced by attracted and invading neutrophils. The management of hepatic dysfunction during sepsis is largely supportive and based on prevention and vigorous resuscitation including early nutritional support and adequate oxygenation. Interestingly, experimental studies suggest that pharmacological interventions with significant hemodynamic effects, such as dobutamine and nitric oxide synthase inhibitors, may adversely affect the liver during the septic process.
Septic encephalopathy and critical illness polyneuropathy are two syndromes, appearing at different stages in critically ill patients. Their aetiology is unclear, but many arguments seem to associate them with respiratory insufficiency in a context of systemic inflammatory response syndrome (S.I.R.S.) and multiple organ dysfunction syndrome (M.O.D.S.). Septic encephalopathy appears early in the course of sepsis, diagnosis is based on clinical picture and electro-encephalogram. The exact pathogenesis is unclear. Prognosis is related to the underlying pathology, and treatment is supportive. Critical illness polyneuropathy is a predominantly motor axonal dysfunction, occurring in a setting of respiratory insufficiency, S.I.R.S., and M.O.D.S. A weaning problem often indicates the presence of critical illness polyneuropathy. Diagnosis is made on history, clinical picture and electromyographic studies. Indeed, motor and sensory conduction studies show a reduction of the amplitude of action potentials. In a later stage fibrillations and positive sharp waves emerge, with a further reduction of action potentials. Follow-up examinations reveal signs of axonal regeneration. The exact aetiology is unknown, but may be related to sepsis and M.O.D.S. Sepsis and M.O.D.S. are associated with the release of "mediator" substances, and somewhere in this cascade, there might be a toxin, influencing the nerve. A differential diagnosis with myopathy and neuromuscular transmission defects has to be made. Specific treatment is absent, and prognosis is related to the underlying pathology.
STUDY OBJECTIVE: To assess the effects of adjunctive treatment with N-acetyl-L-cysteine (NAC) on hemodynamics, oxygen transport variables, and plasma levels of cytokines in patients with septic shock. DESIGN: Prospective, randomized, double-blind, placebo-controlled study. SETTING: A 24-bed medicosurgical ICU in a university hospital. PATIENTS: Twenty-two patients included within 4 h of diagnosis of septic shock. INTERVENTIONS: Patients were randomly allocated to receive either NAC (150 mg/kg bolus, followed by a continuous infusion of 50 mg/kg over 4 h; n= 12) or placebo (n=10) in addition to standard therapy. MEASUREMENTS: Plasma concentrations of tumor necrosis factor-alpha (TNF), interleukin (IL)-6, IL-8, IL-10, and soluble tumor necrosis factor-alpha receptor-p55 (sTNFR-p55) were measured by sensitive immunoassays at 0, 2, 4, 6 and 24 h. Pulmonary artery catheter-derived hemodynamics, blood gases, hemoglobin, and arterial lactate were measured at baseline, after infusion (4 h), and at 24 h. RESULTS: NAC improved oxygenation (PaO2/FIO2 ratio, 214+/-97 vs 123+/-86; p<0.05) and static lung compliance (44+/-11 vs 31+/-6 L/cm H2O; p<0.05) at 24 h. NAC had no significant effects on plasma TNF, IL-6, or IL-10 levels, but acutely decreased IL-8 and sTNFR-p55 levels. The administration of NAC had no significant effect on systemic and pulmonary hemodynamics, oxygen delivery, and oxygen consumption. Mortality was similar in both groups (control, 40%; NAC, 42%) but survivors who received NAC had shorter ventilator requirement (7+/-2 days vs 20+/-7 days; p<0.05) and were discharged earlier from the ICU (13+/-2 days vs 32+/-9 days; p<0.05). CONCLUSION: In this small cohort of patients with early septic shock, short-term IV infusion of NAC was well-tolerated, improved respiratory function, and shortened ICU stay in survivors. The attenuated production of IL-8, a potential mediator of septic lung injury, may have contributed to the lung-protective effects of NAC.
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Because closed chest cardiopulmonary resuscitation (CCCPR) achieve restoration of spontaneous circulation (ROSC) in less than 50% of cases, and because of the apparent physiological superiority of open-chest cardiopulmonary resuscitation (OCCPR), we evaluated OCCPR in out-of hospital cardiac arrest in cases who did not respond to standard external cardiopulmonary resuscitation with advanced life support. Over a period of 12 years, OCCPR was performed in 33 patients with out-of-hospital cardiac arrest arising from different causes, after unsuccessful attempts to achieve ROSC with CCCPR efforts over 7-121 min (median 25 min). With OCCPR, ROSC was achieved in 13/33 patients. Of these, two recovered to discharge (one with no neurological deficit and one with mild brain damage). The other 11 rearrested either in the emergency department after a median period of 70 min of resuscitation, or in the intensive care unit after a median period of 104 h. One case of iatrogenic cardiac injury was observed. The OCCPR attempts were well accepted by the public. Our data suggest that OCCPR is more effective than CCCPR in achieving ROSC outside hospital in patients with major cardiac disease and prolonged arrest. OCCPR is feasible in the out-of-hospital setting. Survival without neurological deficit cannot be expected when CCCPR with no-flow is continued beyond 25 min.
Three cases of community-acquired pneumonia (CAP), requiring intensive care admission, are presented. The clinical picture of a "typical" bacterial pneumonia in the three patients led to an initial empirical treatment with amoxicillin clavulanic acid or 2(nd) generation cephalosporins. The treatment had to be changed in all three because of clinical failure. Erythromycin was added to the therapy with good clinical evolution. Serology confirmed atypical organisms to be responsible. Only the chest X-ray might have suggested an "atypical" or a "viral-like" agent. A proposition is made for an empirical combination of antibiotics in severely ill patients with CAP with more than unilobar consolidation.
Chronic thromboembolic pulmonary hypertension (CTEPH) is a disease often not recognized until it is far advanced. Medical management does not reverse the effects of the disease, nor does it prevent its progression. Pulmonary thromboendarterectomy is the preferred treatment. We present the case of a patient in whom CTEPH was mistaken for an interstitial lung disease with mediastinal lymph node enlargement. The mediastinal lymph node enlargement was due to vascular transformation of the lymph node sinuses (VTS). This is an unusual case of chronic thromboembolic pulmonary hypertension with vascular transformation of the lymph node sinuses.
OBJECTIVE: Conventional intermittent hemodialysis in the critically ill patient can be associated with hemodynamic and respiratory instability. Intermittent hemodialysis induced arterial hypotension might be detrimental. We therefore studied the influence of intermittent hemodialysis on systemic and regional oxygen transport in critically ill patients. DESIGN: Prospective descriptive study. SETTING: Medical/surgical 24-bed intensive care unit in a university hospital. PATIENTS: Eleven critically ill patients admitted to the intensive care unit (APACHE III score: 82 +/- 12) and developing multiple organ dysfunction syndrome with acute renal failure. All patients were mechanically ventilated and hemodynamically stable with inotropic support. Systemic oxygen transport variables were calculated, and arterial blood lactate concentration was measured before, during, and after intermittent hemodialysis. Tonometer PCO2 was measured using a tonometer, and arterial-tonometer CO2 gap was used as an indicator of intestinal intramucosal acidosis. RESULTS: Intermittent hemodialysis induced an increase in calculated systemic oxygen consumption (P < 0.01). During intermittent hemodialysis there was a significantly higher need of inotropic support (P < 0.05) to maintain arterial blood pressure, cardiac index, and calculated systemic arterial oxygen delivery. The arterial-tonometer CO2 gap increased significantly during and after the procedure. CONCLUSION: In critically ill patients with multiple organ dysfunction syndrome intermittent hemodialysis induces an increase in oxygen consumption. Despite higher inotropic support to maintain systemic calculated oxygen delivery intestinal intramucosal acidosis occurs during intermittent hemodialysis and may even persist after the procedure is terminated.
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Neisseria meningitidis, a ubiquitous Gram-negative diplococcus, is responsible for a spectrum of clinical manifestations. This is illustrated by the history of three patients recently admitted to our hospital. Because of the possibly rapid and dramatic evolution, awareness for meningococcal diseases remains obligatory. Adequate antibiotic treatment instituted as soon as the diagnosis is suspected and early application of aggressive supportive care can lead to more favourable outcome.
A 58-year-old patient suffered from persistent Candida glabrata fungaemia. Transoesophageal echocardiography detected a central venous catheter-related intracardiac thrombosis. Cardiotomy permitted the removal of the catheter and its adherent clot. Candida glabrata was cultured from the thrombus.
Nosocomial pansinusitis (N P) is most often described in nasotracheally intubated patients with craniocerebral or facial trauma. We retrospectively reviewed its occurrence and complications in the course of prolonged mechanical ventilation in orotracheally intubated patients without maxillofacial or cranial injuries. N P was deemed to be present when (1) CT scan showed opacification and/or air-fluid levels in the maxillary, ethmoid and sphenoid sinuses and (2) aspiration of both maxillary sinuses yielded pus, cultures of which revealed a high concentration of micro organisms. Nosocomial pneumonia and bacteremia were considered related to the N P if the organisms found in the sinus were identical to those recovered from the blood and/or the bronchi. During an 18-month study period, 38 cases of sinusitis were diagnosed. N P was present in 13 patients: 18 organisms (12 Gram-negative, 5 Gram-positive and 1 Candida albicans) were isolated. Pneumonia occurred in 8 patients, 6 with multi-resistant Pseudominas aeruginosa and 2 with methicillin resistant Staphylococcus aureus. Pseudomonas aeruginosa was isolated from the blood, lung and sinus in two patients. This study demonstrates that N P is relatively frequent in patients requiring long-term mechanical ventilation, even in the absence of predisposing factors. N P in these patients is mostly monomicrobial with multi-resistant Pseudomonas aeruginosa and Staphylococcus aureus as the main causative agents.
Cimetidine is commonly used for stress ulcer prophylaxis in intensive care patients. Cimetidine contains an imidazole structure. Similar drugs have been shown to inhibit steroid synthesis by blocking cytochrome P450-dependent reactions in the adrenal cortex. It is suggested that bolus injections of cimetidine suppress the normal corticosteroid production. This might be deleterious since a decreased cortisol response seems to be associated with increased mortality during chronic severe stress. We therefore performed a prospective, randomized, and controlled study to assess the effect of a short-term continuous infusion of either cimetidine or ranitidine, a non-imidazole H2-pantagonist, upon cortisol secretion in a cohort of hemodynamically stable intensive care patients. Twenty patients were consecutively enrolled following determined inclusion criteria and divided in three treatment groups: 6 controls, 7 cimetidine- and 7 ranitidinetreated subjects. Both cimetidine (1200 mg) and ranitidine (200 mg) were administered by infusion pump over 24 hrs. A short corticotropin test was done within 24 hrs after admission (d0) and repeated 7 days thereafter (d7). On both occasions, plasma cortisol was measured immediately before the test and 30 min afterwards. The three treatment groups presented a normal cortisol response at d0 and d7. Peak cortisol levels after stimulation did not show any significant difference for both the cimetidine and the ranitidine group, either at d0 or at d7. Moreover, this response at d0 and d7 was also not significantly different from the one observed in the controls. From this study we can conclude that one week treatment with conventional intravenous doses of cimetidine does not induce significant alterations of the cortisol response in hemodynamically stable ICU patients.