Metabolic response to the stress of critical illness.

The metabolic response to stress is part of the adaptive response to survive critical illness. Several mechanisms are well preserved during evolution, including the stimulation of the sympathetic nervous system, the release of pituitary hormones, a peripheral resistance to the effects of these and other anabolic factors, triggered to increase the provision of energy substrates to the vital tissues. The pathways of energy production are altered and alternative substrates are used as a result of the loss of control of energy substrate utilization by their availability. The clinical consequences of the metabolic response to stress include sequential changes in energy expenditure, stress hyperglycaemia, changes in body composition, and psychological and behavioural problems. The loss of muscle proteins and function is a major long-term consequence of stress metabolism. Specific therapeutic interventions, including hormone supplementation, enhanced protein intake, and early mobilization, are investigated. This review aims to summarize the pathophysiological mechanisms, the clinical consequences, and therapeutic implications of the metabolic response to stress.

Prevalence of hypophosphatemia in the ICU - Results of an international one-day point prevalence survey.

BACKGROUND & AIMS: Hypophosphatemia (HypoP) is associated with organ dysfunction and mortality. Despite its potential severe consequences, HypoP remains poorly characterized in terms of real prevalence and timing of onset. The primary objective was to determine the prevalence of HypoP defined as blood phosphate <0.8 and < 0.65 mmol/l on one particular day at international level. METHODS: One-day point prevalence survey conducted by the Section of Metabolism, Endocrinology and Nutrition (MEN) of the European Society of Intensive Care Medicine (ESICM) during week 11-2020. RESULTS: In total, 56 adult and 4 paediatric ICUs, from 22 countries participated: 41 ICUs were mixed medico surgical, the 19 others being cardiac, medical or surgical. Phosphate measurements were performed daily in 21 ICUs, and 1-3 times per week in 39 ICUs. On D-Day 909 patients (883 adults) were present and 668/883 (75.7%) had serum/plasma phosphate determined, revealing a HypoP in 103 (15.4%) patients aged 62 [18 to 85] years. Of those, 49 patients presented phosphate <0.65 mmol/l: cases of hypophosphatemia were detected at any time of patient's ICU stay. No HypoP was observed in children. A treatment protocol existed only in 41.1% of adult ICUs, independently of ICU type, or size. Only 41/98 of the HypoP patients (29/41 of patients with phosphate <0.65 mmol/l) were receiving phosphate. CONCLUSION: HypoP is present at least in 15.4% of ICU patients, and may occur at any time during the ICU stay. The absence of phosphate repletion protocols in 60% of participating ICUs is an unexpected finding, and confirms the necessity for the development of ICU phosphate protocols and guidelines. CLINICALTRIALS IDENTIFIER: NCT04201899.

Management of liver failure in general intensive care unit.

OBJECTIVE: To produce French guidelines on Management of Liver failure in general Intensive Care Unit (ICU). DESIGN: A consensus committee of 23 experts from the French Society of Anesthesiology and Critical Care Medicine (Société française d'anesthésie et de réanimation, SFAR) and the French Association for the Study of the Liver (Association française pour l'étude du foie, AFEF) was convened. A formal conflict-of-interest (COI) policy was developed at the start of the process and enforced throughout. The entire guideline process was conducted independently of any industrial funding. The authors were advised to follow the principles of the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system to guide their assessment of the quality of evidence. The potential drawbacks of making strong recommendations in the presence of low-quality evidence were emphasised. Some recommendations were ungraded. METHODS: Two fields were defined: acute liver failure (ALF) and cirrhotic patients in general ICU. The panel focused on three questions with respect to ALF: (1) Which etiological examinations should be performed to reduce morbidity and mortality? (2) Which specific treatments should be initiated rapidly to reduce morbidity and mortality? (3) Which symptomatic treatment should be initiated rapidly to reduce morbidity and mortality? Seven questions concerning cirrhotic patients were addressed: (1) Which criteria should be used to guide ICU admission of cirrhotic patients in order to improve their prognosis? (2) Which specific management of kidney injury should be implemented to reduce morbidity and mortality in cirrhotic ICU patients? (3) Which specific measures to manage sepsis in order to reduce morbidity and mortality in cirrhotic ICU patients? (4) In which circumstances, human serum albumin should be administered to reduce morbidity and mortality in cirrhotic ICU patients? (5) How should digestive haemorrhage be treated in order to reduce morbidity and mortality in cirrhotic ICU patients? (6) How should haemostasis be managed in order to reduce morbidity and mortality in cirrhotic ICU patients? And (7) When should advice be obtained from an expert centre in order to reduce morbidity and mortality in cirrhotic ICU patients? Population, intervention, comparison and outcome (PICO) issues were reviewed and updated as required, and evidence profiles were generated. An analysis of the literature and recommendations was then performed in accordance with the GRADE® methodology. RESULTS: The SFAR/AFEF Guidelines panel produced 18 statements on liver failure in general ICU. After two rounds of debate and various amendments, a strong agreement was reached on 100% of the recommendations: six had a high level of evidence (Grade 1 ±), seven had a low level of evidence (Grade 2 ±) and six were expert judgments. Finally, no recommendation was provided with respect to one question. CONCLUSIONS: Substantial agreement exists among experts regarding numerous strong recommendations on the optimum care of patients with liver failure in general ICU.

Botulism and hot-smoked whitefish: a family cluster of type E botulism in France, September 2009.

A family cluster of three cases of type E botulism were identified in south-east France in September 2009. The suspected food source of infection was a vacuum packed hot-smoked whitefish of Canadian origin purchased by the family during a visit to Finland and consumed several weeks later in France on the day prior to symptom onset. No leftover fish was available to confirm this hypothesis. Vacuum packed hot-smoked whitefish has previously been associated with cases of type E botulism in multiple countries, including Finland, Germany, the United States and Israel.

Terrorist attack in Nice - The experience of general surgeons.

INTRODUCTION: After the attacks in Paris, France was again struck by terrorism in the city of Nice during the night of July 14, 2016. At 22:33 in the evening, a 19-ton truck drove into the crowd of holiday celebrators. The attack resulted in 458 wounded and 86 deaths. The purpose of this study was to describe the management of patients with abdominal trauma admitted alive in our institution, in the context of a massive influx of victims. MATERIAL AND METHODS: We performed a retrospective analysis of the management of adults with abdominal trauma arising from the terrorist attack in Nice. RESULTS: Among the 182 victims admitted to our trauma center, eleven patients presented with abdominal trauma. The median age was 44 years [14-63] and the median Injury Severity Score (ISS) was 34 [9-59]. Eight patients underwent urgent surgical treatment in the operating room including six for abdominal trauma. These patients were treated according to the principles of surgical damage control, albeit without the need for temporary abdominal closure or packing. Three patients could have had their lesions managed non-operatively had they been admitted outside this surge episode, which saturated the technical means of the receiving hospital. CONCLUSION: The terrorist attack that victimized the citizens of Nice resulted in the second largest number of dead of any attack on French soil. A large number of patients were admitted to the city's only center for adult trauma care. The management of these patients posed diagnostic, therapeutic and logistical problems. Increased use of pre-hospital pelvic restraint belts may help to reduce vehicular trauma. We do not feel that non-operative management of abdominal lesions can be envisaged in the context of a mass influx of victims. We recommend surgical hemostasis for patients with secondary hemorrhagic risk from visceral trauma in the context of a massive influx of victims.

Correction to: Serum sodium and intracranial pressure changes after desmopressin therapy in severe traumatic brain injury patients: a multi-centre cohort study.

Following publication of the original article [1], we were notified that the collaborators' names part of the "The TBI Collaborative" group has not been indexed in Pubmed. Below the collaborators names full list.

Serum sodium and intracranial pressure changes after desmopressin therapy in severe traumatic brain injury patients: a multi-centre cohort study.

BACKGROUND: In traumatic brain injury (TBI) patients desmopressin administration may induce rapid decreases in serum sodium and increase intracranial pressure (ICP). AIM: In an international multi-centre study, we aimed to report changes in serum sodium and ICP after desmopressin administration in TBI patients. METHODS: We obtained data from 14 neurotrauma ICUs in Europe, Australia and UK for severe TBI patients (GCS ≤ 8) requiring ICP monitoring. We identified patients who received any desmopressin and recorded daily dose, 6-hourly serum sodium, and 6-hourly ICP. RESULTS: We studied 262 severe TBI patients. Of these, 39 patients (14.9%) received desmopressin. Median length of treatment with desmopressin was 1 [1-3] day and daily intravenous dose varied between centres from 0.125 to 10 mcg. The median hourly rate of decrease in serum sodium was low (- 0.1 [- 0.2 to 0.0] mmol/L/h) with a median period of decrease of 36 h. The proportion of 6-h periods in which the rate of natremia correction exceeded 0.5 mmol/L/h or 1 mmol/L/h was low, at 8% and 3%, respectively, and ICPs remained stable. After adjusting for IMPACT score and injury severity score, desmopressin administration was independently associated with increased 60-day mortality [HR of 1.83 (1.05-3.24) (p = 0.03)]. CONCLUSIONS: In severe TBI, desmopressin administration, potentially representing instances of diabetes insipidus is common and is independently associated with increased mortality. Desmopressin doses vary markedly among ICUs; however, the associated decrease in natremia rarely exceeds recommended rates and median ICP values remain unchanged. These findings support the notion that desmopressin therapy is safe.

[Septic shock: blood glucose regulation]. / Sepsis sévère: le contrôle glycémique.

Blood glucose regulation is controlled by several hormones, neurological mechanisms and the hepatic autoregulation. Glucose uptake necessitates glucose transporters which are called GLUT. In physiological situation, 80% of glucose uptake of the whole body is produced by the non-insulin dependant tissues, via the GLUT 1 to 3 transporters. Glucose uptake by insulin dependant tissues is mediated by insuline, which activates GLUT-4 transporters. Because of the production of pro-inflammatory mediators (TNF-alpha), sepsis induces hyperglycemia, which results essentially from an hepatic insulinoresistance. This phenomenon leads to an acute load and uptake of glucose by the non-insulin dependant tissues. Hyperglycemia modifies inflammatory and immune reactions and enhances the production of reactive oxygen species. Thus, sepsis has an impact on blood glucose control and conversely. Blood glucose control has been found to decrease mortality and morbidity in critically ill patients. The exact mechanism, by which these beneficial effects are produced, remains controversial, due to euglycemia or to insulin infusion. Probably both mechanisms are implicated. In all cases the beneficial effects seem to be multifactorial: a decrease in oxydative stress, a protective effect in front of the burst suppression, multiple anti-inflammatory effects. The optimum level of blood glucose is still discussed and must be evaluated in further studies. In all cases, blood glucose level must be under or equal to 1,4 g/l. Even no clinical study evaluates precisely the impact of hyperglycemia during sepsis, a lot of arguments supports that blood glucose level must be a therapeutic goal in these situations.

[Metformin-associated lactic acidosis]. / Acidose lactique et metformine.

OBJECTIVE: The aims of this review are to precise the pathophysiological mechanisms leading to biguanide-associated lactic acidosis, to give elements of diagnosis, and to underline the precautionary conditions for prescribing these drugs by an improvement in physicians and patient's education. DATA SOURCES: A PubMed database research in English and French language reports published until December 2005. The keywords were: lactic acidosis, metformin, biguanide, diabetes mellitus. DATA EXTRACTION: Data in selected articles were reviewed, clinical and basic science research relevant informations were extracted. DATA SYNTHESIS: Metformin, which is an oral antidiabetic agent, is the only one biguanide available in France. It acts by enhancing the sensitivity to insulin by a decrease in the hepatic glucose production and an increase in its peripheral use. In term of glycemic control, it has the same efficiency than the other hypoglycemic agents. It represents the treatment of choice for overweight type 2 diabetic patients because of its beneficial effects on the weight loss and on the cardiovascular complications. The incidence of metformin-associated lactic acidosis is very low when contra-indications and appropriate rules for prescribing this drug are respected. The relationship between metformin and lactic acidosis remains largely controversial. In practical, we can distinguish three situations which have different prognosis. In the first case, metformin seems to be responsible for lactic acidosis because of self-poisoning or accidental overdose, and prognosis is good. In the second case, the association between metformin and lactic acidosis is coincidental rather than causal, and may be induced by an underlying organ failure. In the last case there is a cause of lactic acidosis which is worsened by a precipitating factor leading to metformin accumulation. The 2 latter situations are very severe as mortality rate is about 50%. Symptomatic treatments and renal replacement therapy which allows metformin removal are the curative treatment. Prevention is essential. It requires the respect of metformin contraindications and a better education of physicians and patients for a safe prescription. CONCLUSION: Due to its beneficial effects, metformin is the gold standard treatment for overweight type 2 diabetic patients. The essential precautionary conditions for prescribing metformin as well as the respect of its contra-indications permit largely to prevent lactic acidosis. This complication is serious when it is associated with intercurrent illnesses and metformin accumulation. The curative treatment is based on renal replacement therapy. Prevention only rests on the respect of the contra-indications. Education of physicians and patients concerning the rules of prescription remains essential.

[Pasteurella multocida meningo-encephalitis with aphasia in a young adult]. / Méningoencéphalite à Pasteurella multocida avec aphasie chez une adulte jeune.

We report the first case of Pasteurella multocida meningo-encephalitis with aphasia in a 28 year-old-patient. The investigations confirmed the diagnosis of bacterial meningitis. But the delay in identification of the organism involved iterative changes of antibiotherapy. The evolution was finally favourable with appropriate antibiotic treatment. The epidemiologic investigation highlighted the responsibility of a patient's cat carrying the same bacterial strain. Finally we discuss the epidemiologic, clinical and therapeutic features of this unusual meningitis.

Reliability of anion gap as an indicator of blood lactate in critically ill patients.

OBJECTIVE: To evaluate the sensitivity, specificity, and predictive values of an elevated anion gap as an indicator of hyperlactatemia and to assess the contribution of blood lactate to the serum anion gap in critically ill patients. DESIGN: Prospective study. SETTING: General intensive care unit of a university hospital. PATIENTS: 498 patients, none with ketonuria, severe renal failure or aspirin, glycol, or methanol intoxication. MEASUREMENTS AND RESULTS: The anion gap was calculated as [Na+]-[Cl-]-[TCO2]. Hyperlactatemia was defined as a blood lactate concentration above 2.5 mmol/l. The mean blood lactate concentration was 3.7 +/- 3.2 mmol/l and the mean serum anion gap was 14.3 +/- 4.2 mEq/l. The sensitivity of an elevated anion gap to reveal hyperlactatemia was only 44% [95% confidence interval (CI) 38 to 50], whereas specificity was 91% (CI 87 to 94 and the positive predictive value was 86% (CI 79 to 90). As expected, the poor sensitivity of the anion gap increased with the lactate threshold value, whereas the specificity decreased [for a blood lactate cut-off of 5 mmol/l: sensitivity = 67% (CI 58 to 75) and specificity = 83% (CI 79 to 87)]. The correlation between the serum anion gap and blood lactate was broad (r2 = 0.41, p < 0.001) and the slope of this relationship (0.48 +/- 0.026) was less than 1 (p < 0.001). The serum chloride concentration in patients with a normal anion gap (99.1 +/- 6.9 mmol/l) was comparable to that in patients with an elevated anion gap (98.8 +/- 7.1 mmol/l). CONCLUSIONS: An elevated anion gap is not a sensitive indicator of moderate hyperlactatemia, but it is quite specific, provided the other main causes of the elevated anion gap have been eliminated. Changes in blood lactate only account for about half of the changes in anion gap, and serum chloride does not seem to be an important factor in the determination of the serum anion gap.

Intravenous nicardipine does not alter hepatic blood flow after orthotopic liver transplant.

OBJECTIVE: To evaluate the effects of nicardipine on hepatic blood flow in patients with recent liver transplants. Secondly, to evaluate the liver extraction of nicardipine in order to determine the influence of liver transplantation on its disposition. DESIGN: Prospective self-controlled clinical study. SETTING: University hospital intensive care unit. PATIENTS: Eight patients in the early postoperative period of orthotopic liver transplantation. MEASUREMENTS AND RESULTS: Patients were given 5 mg of i.v. nicardipine. Systemic and splanchnic haemodynamic and metabolic parameters were measured before nicardipine administration (T0) and at 5 min (T1), 30 min (T2), and 120 min (T3) after administration. A catheter was inserted into a hepatic vein to determine the total hepatic blood flow (HBF) and the hepatic extraction coefficient of nicardipine. Nicardipine caused no significant changes in HBF, oxygen delivery, oxygen uptake, hepatic venous oxygen saturation, or the hepatic venous partial pressure of oxygen. Likewise, neither blood lactate concentrations nor arterial and hepatic venous lactate-pyruvate ratios were modified by nicardipine. The hepatic extraction coefficient of nicardipine was approximately 0.70 in the first 3 min after complete infusion, then decreased and remained stable at approximately 0.50, showing a non-linear first-pass metabolism pattern. CONCLUSIONS: Nicardipine administration after liver transplantation appears to have no deleterious effects on HBF. Nicardipine can be classified as a drug of intermediate hepatic extraction coefficient, whose elimination partly depends on hepatic enzyme activity.

The increase in CO2 production induced by NaHCO3 depends on blood albumin and hemoglobin concentrations.

OBJECTIVE: To evaluate the origin of H+ ions participating in the generation of CO2 coming from sodium bicarbonate infusion during metabolic acidosis. We hypothesized that these H+ ions come from a back-titration of the main non-bicarbonate buffers present in the blood, i. e. the hemoglobin and the albumin, and thus postulated that the rate of CO2 release from a bicarbonate load is dependent on the concentration of these buffers. DESIGN: Prospective clinical and experimental study. SETTING: Surgical intensive care unit of a university hospital. PATIENTS AND MATERIAL: (1) Sixteen stable sedated and artificially ventilated critically ill patients with a mild base deficit. (2) Acidotic human blood (bicarbonate 5 mM, pH 7.0) of hematocrit 5, 10, 20 and 40% regenerated from a mixture of frozen fresh plasma and packed red blood cells. PATIENTS: infusion of 1.5 mmol/kg sodium bicarbonate over 5 min. Regenerated blood: 25 mM sodium bicarbonate load. PATIENTS: continuous measurement of CO2 production (VCO2) on the expired gas using a metabolic monitor and arterial blood gas analysis before (T0), at the end (T5) and at 10, 30 and 60 min after the beginning of the bicarbonate infusion. The increase in VCO2 was 18 +/- 7% leading to a rise in PaCO2 from 39.6 +/- 2.3 at T0 to 46.2 +/- 2.7 mmHg at T5. The increases in VCO2 and in PaCO2 were significantly correlated to the albumin (r = 0.73, p < 0.005 and r = 0.70, p < 0.005, respectively) and to the hemoglobin (r = 0.51, p < 0.05 and r = 0.65, p < 0.01, respectively) concentrations. Regenerated blood: gas analysis 1 min after the bicarbonate load. The increase in PCO2 was closely related to the hematocrit (Ht) of the blood as it was 15.9 +/- 7.5 mmHg for Ht 5%, 29.0 +/- 9.6 for Ht 10%, 44.2 +/- 5.9 for Ht 20% and 71.0 +/- 3.5 for Ht 40% (n = 5 for each, p < 0.001). CONCLUSIONS: The importance of the release of CO2 from a bicarbonate load is dependent on the concentration of the blood non-bicarbonate buffers. It is therefore likely that the adverse effects of bicarbonate therapy linked to the CO2 generation are more important in patients with high blood albumin and hemoglobin concentrations.

Clinical pharmacology of nicardipine in liver transplant patients.

Slow calcium channel antagonists are widely used among transplanted patients suffering from hypertension, although some of them tend to reduce hepatic blood flow. The aim of our study was to determine the pharmacological properties of nicardipine in transplanted patients with hypertension. Ten hours after liver transplantation, six patients (three men, three women) received 5 mg of intravenous nicardipine to prevent high blood pressure during intensive care. Prior to the administration and during the study (at the completion of the infusion, 3, 5, 10, 15, 20, 30, 45, and 60 min after infusion), the systemic and splanchnic parameters were measured (Swan Ganz catheter). Blood samples were drawn simultaneously from radial artery and free hepatic veins, in order to obtain the hepatic extraction of nicardipine. The hepatic extraction ratio was around 70% for the first 3 min, then decreased and remained stable thereafter, around 45%, showing a non linear first-pass metabolism pattern. Plasma hepatic clearance of nicardipine (699-850 ml/min) was close to total plasma clearance throughout the study (978 +/- 222 ml/min, from 71 to 87%) and half of the estimated hepatic plasma flow values at the same times (1467-1770 ml/min, from 44 to 51%). No statistically significant changes were observed in cardiac output and hepatic blood flow during the study, although there was a decrease in mean arterial blood pressure from 87 +/- 6 mmHg baseline level to 76 +/- 3 mmHg, 60 min after administration. Nicardipine chlorhydrate seems to be appropriate in post operative liver transplant patients when blood pressure must be decreased. Nicardipine safely lowers peripheral resistance, and does not induce changes in hepatic blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

[Osmolality and brain]. / Osmolalité et cerveau.

A modification of serum osmolarity induces always movements of water across cell membranes and therefore variations of cell volume of all tissues, including brain. To avoid a severe cell dehydration or hyperhydration, the organism has several regulation means called osmoregulation. Cerebral osmoregulation is essential as the brain is contained in a unexpandable box. In comparison with other organs, this phenomenon is complex and particular as: 1) cerebral volume consists of 3 sub spaces (intracellular, extracellular and cerebrospinal fluid [CSF]); 2) exists a blood-brain barrier (BBB) which behaves functionally as a semi-permeable membrane, essentially sensitive to osmolar disturbances. This brain volume regulation mechanism is working whatever the nature of the solutes initiating the osmotic deviation (sodium, glucose, mannitol...). Cerebral osmoregulation results from intracerebral osmolar modifications. Thus, every variation of plasma osmolarity elicits a similar variation of intracerebral osmolarity. This phenomenon results from modifications of the brain cell "protective" osmoles content. When the osmolar disturbance occurs quickly (in a few hours), cerebral osmoregulation is not complete. It results essentially from modifications of brain cell inorganic solutes content, i.e. electrolytes (Na, K, Cl) which originate from plasma, CSF and extracellular brain spaces uptake. When the osmolar disturbance is more progressive, cerebral osmoregulation is complete. The brain volume returns then to its initial value, by increasing its brain cell electrolytes, but above all organic "idiogenic" osmoles content. These idiogenic osmoles are identified as amino acids, polyols and trimethylamines. During treatment, the delayed normalization of brain osmolarity compared with plasma osmolarity prescribes a slow correction of the osmolar disturbance, as much as it is a chronic one.

[The internal environment and intracranial hypertension]. / Milieu intérieur et hypertension intracrânienne.

Intracranial pressure depends on cerebral tissue volume, cerebrospinal fluid volume (CSFV) and cerebral blood volume (CBV). Physiologically, their sum is constant (Monro-Kelly equation) and ICP remains stable. When the blood brain barrier (BBB) is intact, the volume of cerebral tissue depends on the osmotic pressure gradient. When it is injured, water movements across the BBB depend on the hydrostatic pressure gradient. CBV depends essentially on cerebral blood flow (CBF), which is strongly regulated by cerebral vascular resistances. In experimental studies, a decrease in oncotic pressure does not increase cerebral oedema and intracranial hypertension (ICHT). On the other hand, plasma hypoosmolarity increases cerebral water content and therefore ICP, if the BBB is intact. If it is injured, neither hypoosmolarity nor hypooncotic pressure modify cerebral oedema. Therefore, all hypotonic solutes may aggravate cerebral oedema and are contra-indicated in case of ICHT. On the other hand, hypooncotic solutes do not modify ICP. The osmotic therapy is one of the most important therapeutic tools for acute ICHT. Mannitol remains the treatment of choice. It acts very quickly. An i.v. perfusion of 0.25 g.kg-1 is administered over 20 minutes when ICP increases. Hypertonic saline solutes act in the same way, however they are not more efficient than mannitol. CO2 is the strongest modulating factor of CBF. Hypocapnia, by inducing cerebral vasoconstriction, decreases CBF and CBV. Hyperventilation is an efficient and rapid means for decreasing ICP. However, it cannot be used systematically without an adapted monitoring, as hypocapnia may aggravate cerebral ischaemia. Hyperthermia is an aggravating factor for ICHT, whereas moderate hypothermia seems to be beneficial both for ICP and cerebral metabolism. Hyperglycaemia has no direct effect on cerebral volume, but it may aggravate ICHT by inducing cerebral lactic acidosis and cytotoxic oedemia. Therefore, infusion of glucose solutes is contra-indicated in the first 24 hours following head trauma and blood glucose concentration must be closely monitored and controlled during ICHT episodes.

[Energy substrates in parenteral nutrition]. / Apports énergétiques en nutrition parentérale.

The most appropriate nutriment for total parenteral feeding (TPF) must be nutritionally efficient, safe and easy to use. Glucose is the most used carbohydrate as it has most of these qualities, as well as a high rate of metabolism by all tissues. It has not been clearly demonstrated that the administration of exogenous insulin with glucose improves nitrogen retention. Substitutes for glucose, such as fructose, maltose, galactose or polyols (xylitol, surbitol, glycerol) are not really superior to glucose itself. On the other hand, they have major side-effects. Therefore, they are not much used as energy substrates for TPF, at least not for long term TPF. Intravenous fat emulsions have taken an important place as a source of energy during TPF. Fat emulsions containing long chain triglycerides (LCT) supply essential fatty acids (EFA) (linolenic and linoleic acids), thus preventing EFA deficiency. The metabolism of fat emulsions is influenced by various factors: age, metabolic and nutritional status, the amount of glucose intake, insulin deficiency, sepsis, heparin therapy. Recently, medium chain triglycerides (MCT) have been proposed as an alternative energy source. The latter are cleared more rapidly from the blood, and are therefore less liable to be deposited in the liver and adipose tissue; they are also oxidized more quickly and more completely. MCT are safe to use at a rate of less than 0.12 g.kg-1.h-1 and with a MCT/LCT ratio less than 3 to 1. The simultaneous administration of glucose prevents an acceleration of ketogenesis. MCT/LCT emulsions are a safe and effective source of calories. It is important that those patients for whom such nutriment may be of particular interest should be identified. Fat emulsions associated with glucose seem to be more efficient in terms of nitrogen sparing effect than glucose alone. They also avoid the problems due to the infusion of large amounts of glucose (excessive carbon dioxide production, fatty infiltration of the liver), while there is no EFA deficiency. If the infusion of TPF nutriment must be continuous in intensive care patients, or during the postoperative period, cyclic nocturnal parenteral nutrition over a 12 or 16 hour period may be used in patients who are not in a catabolic state, or only mildly so. This is a safe and efficient method of nutritional support, which reduces the incidence rate of TPF-induced cholestasis.

[Effects of positive expiratory pressure on cardiac output and estimated hepatic blood flow during controlled ventilation in man]. / Effets de la pression expiratoire positive sur les débits cardiaque et hépatique plasmatique estimé au cours de la ventilation contrôlée chez l'homme.

This study aimed to discover the effects of artificial ventilation with positive end-expiratory pressure (PEEP) on cardiac output and hepatic blood flow in ten patients with chronic stable post-anoxic or post-traumatic coma, without any cerebral oedema or any other visceral pathology. This study was carried out at four levels of end-expiratory pressure (0, 5, 12 and 29 cmH2O) and after 24 h of artificial ventilation with a PEEP arbitrarily fixed at 12 cmH2O. Cardiac output was measured by thermodilution and hepatic blood flow by applying Fick's principle on a continuous infusion of indocyanine green with an analysis of suprahepatic venous samples. Hepatic blood flow is given by the amount of indocyanine green infused (0.5 mg.min-1) divided by the difference between arterial and suprahepatic venous indocyanine green concentration. For all levels of PEEP, mean arterial, right atrial, wedge and suprahepatic pressures and hepatosplanchnic resistances were measured. Artificial ventilation with PEEP induced a fall of cardiac output and hepatic blood flow proportional with the increase in PEEP level. The fall in hepatic blood flow began to be statistically significant for a PEEP level of 5 cmH2O (-17%; p less than 0.01) and was maximum for a PEEP of 20 cmH2O (-49.51%; p less than 0.001). There was no linear correlation between cardiac output and hepatic blood flow: the fall in hepatic blood flow was more important than the fall in cardiac output. These changes in hepatic blood flow were accompanied by a significant increase in hepatosplanchnic resistances (p less than 0.01 for PEEP = 12 cmH2O), without any changes in other haemodynamic parameters or biological signs of hepatic disturbance.(ABSTRACT TRUNCATED AT 250 WORDS)

[Metformin-associated lactic acidosis remains a serious complication of metformin therapy]. / L'acidose lactique reste une complication grave du traitement par metformine.

We report 4 cases of lactic acidosis in diabetic patients usually treated with metformin. For the first 3 patients, the clinical history was similar because lactic acidosis was precipitated by gastro-intestinal disorders whereas all of them were simultaneously treated with several nephrotoxic drugs. These 3 patients presented with acute renal failure on arrival at hospital. Their issue was fatal whereas any obvious cause of overproduction of lactate was found. The fourth case, which was due to a voluntary intoxication, was the only one presenting with a favourable evolution. The metformin plasma and red blood cell levels were performed for 2 of 4 patients and confirmed the overdose. These observations remind that metformin-associated lactic acidosis remains a serious complication, and that medical doctors must respect strictly contra-indications and guidelines for withdrawing metformin.

[Fatal acute liver failure: a rare complication of exertion-induced heat stroke]. / Insuffisance hépatique aiguë mortelle: une complication rare du coup de chaleur d'effort.

Liver injury is a well-known complication of exertional heat stroke. However severe acute irreversible liver dysfunction is rarely associated. Persistent centrolobular hepatocellular necrosis without any regeneration remains very uncommon. We report a case of fatal acute liver failure occurring after exertional heat stroke. Despite the conventional symptomatic treatment, especially active cooling, the patient experienced multiple organ failure with brain death 6 days after his admission. In this case, a chronic treatment with neuroleptic and anticholinergic agents may be considered as a predisposing factor.