Bleeding risk of terminally ill patients hospitalized in palliative care units: the RHESO study.

Essentials Bleeding incidence as hemorrhagic risk factors are unknown in palliative care inpatients. We conducted a multicenter observational study (22 Palliative Care Units, 1199 patients). At three months, the cumulative incidence of clinically relevant bleeding was 9.8%. Cancer, recent bleeding, thromboprophylaxis and antiplatelet therapy were independent risk factors. SUMMARY: Background The value of primary thromboprophylaxis in patients admitted to palliative care units is debatable. Moreover, the risk of bleeding in these patients is unknown. Objectives Our primary aim was to assess the bleeding risk of patients in a real-world practice setting of hospital palliative care. Our secondary aim was to determine the incidence of symptomatic deep vein thrombosis and to identify risk factors for bleeding. Patients/Methods In this prospective, observational study in 22 French palliative care units, 1199 patients (median age, 71 years; male, 45.5%), admitted for the first time to a palliative care unit for advanced cancer or pulmonary, cardiac or neurologic disease were included. The primary outcome was adjudicated clinically relevant bleeding (i.e. a composite of major and clinically relevant non-major bleeding) at 3 months. The secondary outcome was symptomatic deep vein thrombosis. Results The most common reason for palliative care was cancer (90.7%). By 3 months, 1087 patients (91.3%) had died and 116 patients had presented at least one episode of clinically relevant bleeding (fatal in 23 patients). Taking into account the competing risk of death, the cumulative incidence of clinically relevant bleeding was 9.8% (95% confidence interval [CI], 8.3-11.6). Deep vein thrombosis occurred in six patients (cumulative incidence, 0.5%; 95% CI, 0.2-1.1). Cancer, recent bleeding, antithrombotic prophylaxis and antiplatelet therapy were independently associated with clinically relevant bleeding at 3 months. Conclusions Decisions regarding the use of thromboprophylaxis in palliative care patients should take into account the high risk of bleeding in these patients.

[Questions concerning an endotracheal intubation or a tracheotomy in amyotrophic lateral sclerosis]. / Quelle est la problématique liée à la trachéotomie et l'intubation en urgence?

Amyotrophic lateral sclerosis (ALS) is an illness in which respiratory complications often determine the terminal prognosis. Emergency situations lead one to pose questions concerning an endotracheal intubation or a tracheotomy. A tracheotomy should not be performed during an emergency situation. A tracheotomy necessitates a stable condition and prior reflection. Orotrachael intubation is the method of choice during emergency situations requiring invasive ventilation or airway protection. Intubation during an emergency situation presents specific problems: the lack of knowledge concerning the person and their pre-established desires, the impossibility of evaluating the potential reversibility of an acute pathology, the risk of not being able to wean the patient off the ventilator and the lack of time to gather all the elements necessary for a well-thought out decision. It may be appropriate for emergency personnel to introduce mechanical ventilation and leave the reflection for a later moment, but this approach is not suitable for people in end of life situations in which the person and the family wish to avoid all unreasonable therapeutics. One solution may be to develop among emergency care teams the practice of using non-invasive ventilation and airway clearance techniques as well as developing palliative care knowledge. Orotracheal intubation in an emergency situation presents certain practical difficulties, notably regarding the choice of anesthetics. Preventings situations where emergency intubation may be necessary is probably best obtained by anticipating acute problems, by preparing the ill person, the family and the care givers, by coordinating the potential care providers and by educating emergency personnel in palliative care.

[Rapid sequence intubation in emergency: is there any place for fentanyl?]. / Induction à séquence rapide en urgence: quelle est la place du fentanyl?

OBJECTIVES: Rapid sequence intubation (RSI) with the association of etomidate and succinylcholine is the French "Gold standard" for urgent "full stomach" endotracheal intubations. The aim of this study is to assess the fentanyl as a co-induction agent to take over the sedation between the RSI and the keeping of sedation, which is a critical period in which harmful neuro-vegetatives events, and awakening signs are frequently seen. STUDY DESIGN: Randomized, double blind controlled prospective study, after acceptation by the local ethical committee. PATIENTS AND METHODS: Three groups of patients undergoing RSI in the intensive care unit and by the out-of-hospital medical team were compared: group A patients received fentanyl 3 micrograms kg-1 during RSI, before paralysis was induced. Group B patients received the same dose of fentanyl immediately after endotracheal intubation. Group C patients did not received fentanyl (control group). Outcome measures were awakening signs arrival (respiratory movements, eyes opening, spontaneous limb movements), Ramsay score assessment, and haemody namics. Attempt at intubation and vomiting incident were also measured. Discrete data were compared by chi-2 analysis, continuous data were compared with two-way analysis of variance. A p value < 0.05 was the significant threshold. RESULTS: Thirty-six patients were enrolled and completed the study. All the included patients presented awakening signs. The use of fentanyl did not prevent the recourse of other sedative medications. Ten minutes after endotracheal intubation, significant differences has been noticed for the awakening signs arrival between fentanyl groups (A: 42% and B: 36%) and control group (C: 77%). The Ramsay score evolution follows the same variation. All the patients were intubated on the first attempt, there was no vomiting incident noticed. CONCLUSION: The use of fentanyl, as a co-induction agent with etomidate and succinylcholine during RSI, allows a significant delay of the awakening signs arrival and attenuate the neurovegetative response during the minutes after endotracheal intubation after RSI, without deleterious haemodynamic effects.

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.

[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.

[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.