[Clinical case of the month. Acute methanol intoxication].
We report a fatal methanol intoxication and discuss its physiopathology, diagnosis and treatment.
Acute Disease↗
Biomedical subjects
B Lambermont
Publications and source records attributed to B Lambermont.
[Venous and arterial thromboembolism in a patient with factor V R506Q Leiden mutation and heparin-induced immuno-allergic reaction].
A forty-six-year old in-patient was treated with heparin for massive pulmonary embolism. During the hospitalization, the clinical evolution was unusual and characterised as follows: a) the extent of pulmonary embolism justified a thrombolysis by streptokinase; b) an acute thrombocytopenia occurred a few days later, preceded by a slower, but significant decrease of platelet count; c) a non-occlusive aortic thrombosis developed, distal to renal arteries, causing distal embolisation, successfully treated by local fibrinolysis. The prompt correction of platelet count after interruption of heparin therapy confirmed the diagnosis, before the detection of antibodies against heparin-PF4 complexes. Heparin was immediately replaced by another direct anticoagulant, recombinant hirudin (lépirudine-Refludan), initially given alone and progressively replaced by an antivitamin K (Sintrom). The occurrence of distal embolism from aortic thrombosis, developed during the critical period, characterizes this syndrome, which appears rare but whose incidence is probably underestimated. A subsequent investigation for risk factors for venous thromboembolism in this patient revealed a heterozygous mutation of the Leiden type factor V in our patient, and also in others family members.
Anticoagulants↗
[Clinical case of the month. Porto-pulmonary hypertension syndrome associated with severe hypoxemia].
We report the case of a patient with liver cirrhosis who was admitted to the emergency room for rapid occurrence of dyspnea and severe hypoxemia at rest. Lung CT-scan and echocardiography did not disclose any right-to-left shunt and right-sided heart catheterization evidenced major precapillary pulmonary hypertension. The present feature supports the hypothesis that the pulmonary complications of cirrhosis, the hepatopulmonary syndrome and the portopulmonary hypertension, which are usually considered as mutually exclusive, may coexist. In such circumstances, the right failing heart is the major determinant to the immediate prognosis.
Female↗
Effects of cold and warm ischemia on the mitochondrial oxidative phosphorylation of swine lung.
BACKGROUND: The aim of the study was to investigate the consequence of warm and cold ischemia on lung mitochondria in order to define bioenergetic limits within lung could be suitable for pulmonary transplantation. METHODS: Twenty-two pigs underwent lung harvesting after lung flush with Euro-Collins solution. Mitochondria were isolated from fresh lungs, from lungs submitted to 24 or 48 hr of cold ischemia, to 30 or 45 min of warm ischemia, and to 30 min of warm ischemia followed by 24 or 48 hr of cold ischemia. Mitochondrial oxidative phosphorylation parameters were determined in isolated mitochondria by in vitro measurement of oxygen consumption. RESULTS: Relative to controls, mitochondria submitted to cold ischemia showed an alteration in the oxidoreductase activities of the respiratory chain but no membrane permeability alteration. After 48 hr of cold ischemia, there was a decrease in the yield of the oxidative phosphorylation. Thirty minutes of warm ischemia did not alter the mitochondrial respiratory parameters. However, lung submitted to 45 min of warm ischemia showed mitochondrial damage as a decrease in the oxidative phosphorylation efficiency and ADP availability but no change in the oxidoreductase activities. Relative to cold ischemia alone, 30 min of warm ischemia preceding cold ischemia promoted no significant change in the respiratory parameters. CONCLUSIONS: On bioenergetic basis, lung submitted to warm ischemia could be suitable for transplantation if the warm ischemia duration does not exceed 30 min. This could be a major concern in lung procurement from non-heart beating donors.
Animals↗
Antioxidant status after cold ischemia of rabbit lung.
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Animals↗
[Application of the Simplified Acute Physiology Score II (SAPS II) in a medical intensive care unit].
OBJECTIVE: Our study was to assess the validity of SAPS II (New Simplified Acute Physiology Score) to predict the probability of in hospital mortality, in a cohort of patient admitted to a medical intensive care unit. STUDY DESIGN: Prospective study. PATIENTS AND METHODS: Out of 467 the 525 patients admitted were included. SAPS score and in hospital mortality prediction were calculated for each of them. RESULTS: In this group, SAPS II offered a satisfactory discrimination power with an area under the curve of 0.843. However, calibration showed a lack of fit (chi 2 = 28.5, P < 0.001), with an overall under prediction of mortality (observed versus expected ratio of 1.12). CONCLUSION: This SAPS II lower predicting accuracy in a specific population and for individual outcome prediction may reduce its interest in clinical decision-making.
Area Under Curve↗
Increased aortic compliance maintains left ventricular performance at lower energetic cost.
OBJECTIVE: The aim of this study was to investigate left ventricular contractility and energetic cost of cardiac ejection under conditions of acute increase in aortic compliance. METHODS: In six anaesthetized pigs, ascending aortic compliance was increased by adding a volume chamber in parallel to the ascending aorta. Systemic vascular parameters, including characteristic impedance, peripheral resistance, total vascular compliance, and inertance, were estimated with a four-element windkessel model. Arterial elastance was derived from these parameters. Left ventricular systolic function was assessed by end-systolic pressure-volume relationship (end-systolic elastance), and stroke work. Pressure-volume area was used as a measure of myocardial oxygen consumption. Heart rate remained constant during the experimentation. RESULTS: Adding the aortic volume chamber significantly increased vascular compliance from 0. 95+/-0.08 to 1.17+/-0.06 ml/mmHg (P<0.01), while inductance, characteristic impedance, peripheral resistance, and arterial elastance remained statistically at basal values, respectively 0. 0020+/-0.0003 mmHg.s(2)/ml, 0.105+/-0.009 mmHg.s/ml, 1.27+/-0.12 mmHg.s/ml, and 2.43+/-0.21 mmHg/ml. During the same interval, stroke work and pressure-volume area decreased respectively from 2700+/-242 to 2256+/-75 mmHg.ml (P<0.01), and from 3806+/-427 to 3179+/-167 mmHg.ml (P<0.01). Stroke work and pressure-volume area decreased at matched end-diastolic volumes. In contrast, end-systolic elastance, ejection fraction, and stroke volume remained statistically unchanged, respectively at 2.29+/-0.14 mmHg/ml, 48.1+/-2.1 %, and 32. 4+/-1.7 ml. CONCLUSIONS: These data suggest that, when facing an increased aortic compliance, the left ventricle displays unchanged contractility, but the energetic cost of cardiac ejection is significantly decreased. These data may be of clinical importance when choosing an artificial prosthesis for ascending aortic replacement.
Animals↗
Auditory processing in the vegetative state.
H(2)(15)O-PET was used to investigate changes in regional cerebral blood flow in response to auditory stimulation in patients in the vegetative state. Five patients in a vegetative state of hypoxic origin were compared with 18 age-matched controls. In addition, the cerebral metabolism of these patients and 53 age-matched controls was studied using [(18)F]fluorodeoxyglucose. In control subjects, auditory click stimuli activated bilateral auditory cortices [Brodmann areas (BA) 41 and 42] and the contralateral auditory association cortices (BA 22). In the patients, although resting metabolism was decreased to 61% of normal values, bilateral auditory areas 41 and 42 showed activation as seen in the controls, but the temporoparietal junction cortex (BA 22) failed to be activated. Moreover, the auditory association cortex was functionally disconnected from the posterior parietal association area (BA 40), the anterior cingulate cortex (BA 24) and the hippocampus, as revealed by psychophysiological interaction analysis. Thus, despite altered resting metabolism, the auditory primary cortices were still activated during external stimulation, whereas hierarchically higher-order multi- modal association areas were not. Such a cascade of functional disconnections along the auditory cortical pathways, from the primary auditory areas to multimodal and limbic areas, suggests that the residual cortical processing observed in the vegetative state cannot lead to the integrative processes that are thought to be necessary for the attainment of the normal level of awareness.
Acoustic Stimulation↗
Unusual complication after percutaneous dilatational tracheostomy: pneumoperitoneum with abdominal compartment syndrome.
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Abdomen↗
Analysis of endotoxin effects on the intact pulmonary circulation.
OBJECTIVE: The mechanism of sustained alterations in pulmonary hemodynamics during endotoxin shock remains unclear. To gain more detailed knowledge we used the four-element windkessel model as a descriptor of the pulmonary circuit. METHODS: Consecutive changes in characteristic resistance (R1), vascular compliance (C), input resistance (R2) and inductance (L) were continuously assessed following injection of endotoxin in 6 anaesthetised pigs, and were compared with the corresponding values measured in a similar group of sham-operated animals. RESULTS: Endotoxin challenge resulted in a biphasic pulmonary artery pressure response. Blood flow decreased progressively from 2.8 +/- 0.2 l/min to 2 +/- 0.2 l/min. Ohmic pulmonary vascular resistance (PVR) increased gradually from 0.2 +/- 0.04 to 0.76 +/- 0.1 mm Hg s ml-1. The early increase in PAP (from 14 +/- 2 to 27 +/- 4 mm Hg) was mediated by changes in both R1 (from 0.04 +/- 0.01 to 0.06 +/- 0.01 mm Hg s ml-1) and R2 (from 0.16 +/- 0.04 to 0.61 +/- 0.2 mm Hg s ml-1). These responses, in turn, altered the proximal vascular compliance. A subsequent increase in PAP (from 27 +/- 2 to 32 +/- 3 mm Hg) paralleled the specific decline in distal pulmonary vasculature compliance from 0.84 +/- 0.1 to 0.65 +/- 0.1 ml/mmHg. Analysis of the time course of PVR did not allow us to distinguish between vasoconstriction and stiffening of the vascular tree as mechanisms accounting for PAP changes. CONCLUSIONS: Endotoxemia leads to pulmonary hypertension, which is a result of constriction of proximal pulmonary arteries during the early phase, whereas the late phase is characterised by a decline in distal pulmonary vasculature compliance.
Animals↗
Effects of inhaled nitric oxide on pulmonary hemodynamics in a porcine model of endotoxin shock.
OBJECTIVE: To evaluate the effects of inhaled nitric oxide (NO) on pulmonary circulation in a porcine endotoxin shock model. DESIGN: Prospective, randomized trial. SETTING: Laboratory at a large university medical center. SUBJECTS: Twelve pathogen-free pigs weighing 15 to 31 kg. INTERVENTIONS: After surgical preparation, all pigs received a 0.5 mg/kg endotoxin infusion over 30 mins. One hour after the start of endotoxin, NO inhalation (40 ppm) was initiated in six pigs, whereas the six remaining pigs served to control the progression of shock in this model. Consecutive changes in systemic and pulmonary hemodynamics, including characteristic resistance, vascular compliance, peripheral vascular resistance, and inductance, were continuously assessed during the experimental protocol using a four-element Windkessel model of the pulmonary circulation. MEASUREMENTS AND MAIN RESULTS: Endotoxin insult resulted in a biphasic pulmonary artery pressure increase from 14 +/- 2 to 32 +/- 4 mm Hg. Inhaled NO reversed the resistance to blood flow in small pulmonary arteries from 596 +/- 69 to 424 +/- 36 dyne-sec/ cm5. In contrast, the vascular capacitance of the entire pulmonary circuit, which decreased from 2.4 +/- 0.2 to 0.8 +/- 0.1 mL/mm Hg throughout endotoxin challenge, remained insensitive to NO administration. CONCLUSION: In endotoxin-induced pulmonary hypertension, inhaled NO may function as a modulator of distal pulmonary arterial tone but fails to act as a regulator of larger capacitance pulmonary vessels.
Administration, Inhalation↗
Comparative effects of University of Wisconsin and Euro-Collins solutions on pulmonary mitochondrial function after ischemia and reperfusion.
BACKGROUND: The aim of this study was to compare the effects of Euro-Collins and University of Wisconsin solutions on pulmonary mitochondrial function after cold ischemia and subsequent warm reperfusion. METHODS: Seventeen pigs underwent lung harvesting after classical lung flush with either University of Wisconsin or Euro-Collins solutions. The mitochondria were isolated from fresh swine lungs, from swine lungs subjected to 24 hr of cold ischemia, and from swine lungs subjected to 24 hr of ischemia followed by 30 min of subsequent ex vivo reperfusion at 37 degrees C with Krebs-Henseleit buffer solution and air ventilation. Mitochondrial oxidative phosphorylation parameters were determined in isolated mitochondria by in vitro measurement of oxygen consumption rates. During reperfusion, the lung function was assessed by the pulmonary aerodynamic parameters and the pulmonary vascular resistance. RESULTS: Relative to controls, mitochondria submitted to cold ischemia showed an alteration in the oxidoreductase activities of the respiratory chain. However, the yield of oxidative phosphorylation was conserved. After reperfusion, pulmonary mitochondria underwent a significant worsening in the oxidoreductase activities of the respiratory chain, and a decrease in the respiratory control and the efficiency of oxidative phosphorylation. Meanwhile, the reperfused lungs showed evidence of early dysfunction, assessed by the aerodynamic parameters and pulmonary vascular resistance. In this model, there was no advantage of University of Wisconsin solution over Euro-Collins solution. CONCLUSIONS: The mild mitochondrial alterations after cold ischemia were not sufficient to explain the limited tolerance of lung to ischemia. After reperfusion, the mitochondrial damage was more severe and could be involved in the posttransplant lung dysfunction.
Adenosine↗
Near fatal respiratory distress following massive ether intravenous injection.
To the best of our knowledge, no case of ether-induced acute respiratory distress syndrome (ARDS) has been published as yet. A 36-year-old female developed pneumonitis which showed all the characteristics of a chemical-associated ARDS due to intravenous self-administration of ether: the hemodynamic investigation demonstrated a normal blood flow pattern with low left-heart filling pressure while the anteroposterior roentgenogram evidenced disseminated bilateral lung edema. Advanced symptomatic respiratory support including inhaled nitric oxide and steroidal anti-inflammatory use was the treatment of choice.
Adult↗
Pulmonary impedance and right ventricular-vascular coupling in endotoxin shock.
OBJECTIVE: We tested the hypothesis that right heart failure during endotoxin shock may result from altered ventriculovascular coupling responsible for impeding power transfer to the pulmonary circulation. METHODS: The changes in vascular pulmonary input impedance and right ventricular contractility produced by low-dose endotoxin infusion were studied in 6 intact anesthetized dogs. RESULTS: Endotoxin insult resulted in pulmonary hypertension (from 22 +/- 2 to 33 +/- 3 mmHg) associated with significant decreases in stroke volume (from 26.9 +/- 4 to 20.2 +/- 3 ml) and right ventricular ejection fraction (from 41 +/- 3 to 32 +/- 2%). The first minimum of input impedance spectrum and zero phase were shifted towards higher frequencies. Input resistance and characteristic resistance were dramatically increased. The latter change contributed to a significant increase in the pulsatile component of total right ventricular power output from 13 to 21%, indicating a reduction in the hydraulic right ventricle power output delivered into the main pulmonary artery. Overall changes in input pulmonary impedance were indicative of increased afterload facing the right ventricle leading to depressed performance. In contrast, right ventricular systolic elastance was simultaneously increased from 0.56 to 0.93 mmHg/ml indicating an increase in right heart contractility. CONCLUSION: These data suggest that pulmonary hypertension in the setting of experimental endotoxin shock is accompanied by deleterious changes in the pulmonary impedance spectrum, which are responsible for a mismatch of increased contractile state of the right ventricle to the varying hydraulic load ultimately leading to ventricular-vascular uncoupling.
Analysis of Variance↗
Effects of PEEP on systemic venous capacitance.
The aim of the present study was to determine effects of positive end expiratory pressure (PEEP) application on peripheral venous capacitance and relate them to concomitant central hemodynamic disturbances. The venous volume-pressure (V/P) relationships were studied in 6 intact anesthetized pigs to describe the effects of PEEP on systemic venous compliance (computed as the slope of the V/P relationship) and unstressed volume (referred to as the extrapolated volume intercept). Cardiac volumes as well as partitioning of circulating blood volume between central (ITBV) and peripheral (PBV) compartments were assessed by thermo-dye dilution techniques. During a 15 cm H2O PEEP application, venous compliance was reduced by 48%, while unstressed volume was increased by 25% and peripheral blood pooling increased from 63 to 74%. As a result, left heart and right ventricular end diastolic volumes were decreased by 8% and by 44%, respectively. It is concluded that increased venous unstressed volume and reduced compliance depicted the distension of the venous tree secondary to PEEP which acted as an impediment to venous return. As a consequence, cardiac output was reduced because of decreased preload.
Animals↗
Time domain method to identify simultaneously parameters of the windkessel model applied to the pulmonary circulation.
Lumped models are frequently used to provide a satisfactory description of the hemodynamic properties of the pulmonary vasculature. The purpose of this study is to describe a method to identify simultaneously the parameters values of windkessel models components. The following equation was used to obtain R1 (characteristic resistance), R2 (peripheral resistance), C (total compliance) and L (inertance): [formula: see text] where ki are the following functions of L, R1, R2 and C: [formula: see text] To assess the accuracy of the method, estimates of R1, R2, and C were compared to characteristic impedance Rc, vascular resistance PVR and pulmonary arterial compliance Cd respectively computed from referenced methods. Comparison between R1 and Rc, PVR and R1 + R2, C and Cd were obtained in 5 anaesthetised pigs during basal conditions and after endotoxin-shock. The results indicate that in both conditions, comparisons evidenced highly significant correlations between values computed by the different approaches (p < 0.0001). Although our method yielded to consistently lower values than values provided by referenced methods, the results were concordant with respect to the expected response of pulmonary vasculature to endotoxin insult. We conclude that our method of identification is suitable for the assessment of lumped parameters windkessel model estimates. The main interest is that actual resistance and compliance values can be obtained easily and simultaneously by a global method approach.
Animals↗
Correction of pressure waveforms recorded by fluid-filled catheter recording systems: a new method using a transfer equation.
BACKGROUND: Pressure measuring systems using fluid-filled catheters can result in the recording of distorted pressure waveforms. It results in phase delay, overestimation of systolic and, to a lesser extent, of diastolic pressure. We designed and evaluated a method to correct this pressure waveform distortion using an appropriate transfer equation obtained from the dynamic response of the fluid-filled catheter. This transfer equation is based on the principle that a fluid-filled catheter recording system is considered as an underdamped dynamic system fully characterized by its natural frequency (omega n) and damping ratio (zeta). METHODS: Pressure waveforms, simultaneously recorded in vitro or in vivo by a fluid-filled catheter (Pc) and a micromanometer-tipped catheter (Pref), were used to validate the method. Dynamic response of the catheter used was obtained from a fastflush test. The corrected signal (Ppred) was obtained using omega n, zeta and the following transfer equation: d2Pc/dt2 + 2 omega n zeta dPc/dt + omega n 2Pc = C Ppred (t) After correction of Pc, Ppred was compared, using a linear regression, with Pref taken as reference. RESULTS: Our results showed that Ppred was fitted to Pref with excellent coefficient correlation (0.99). The mean error and the standard error of estimate were respectively -1.16 mmHg and 1.4 mmHg. CONCLUSION: This new method can convert the distorted pressure waveforms transmitted by any fluid-filled catheters into high-fidelity signals. It suppresses the phase delay and the over-estimation of systolic pressure induced by fluid-filled catheters.
Animals↗
An unconscious patient with an electrocardiogram mimicking an acute myocardial infarct.
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Aged↗