Pneumonia in ventilated head trauma patients: the role of thiopental therapy

Nadal, P; Jm, Nicolás; Font, Carme; Vilella, Anna; Nogué, Santiago

doi:10.1097/00063110-199503000-00004

Cited by 20 publications

(10 citation statements)

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“…Its use, however, can have serious side effects, such as an increase in the incidence of secondary pneumonia from 35% to 53% [2]. Thiopental is another intravenous anaesthetic used in intensive care patients, usually for the management of patients with refractory status epilepticus or intracranial hypertension [1], but again can impair immune function, for example by suppressing bone marrow haematopoiesis [3].…”

Section: Introductionmentioning

confidence: 99%

“…Recent work has shown that Cys-loop receptors are present on immune cells, but their physiological roles and the effects of drugs that modify their function in the innate immune system are currently unclear [2]. We are interested in how and why anaesthetics increase infections in intensive care patients; a serious problem as more than 50% of patients with severe sepsis will die [3]–[6].…”

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confidence: 99%

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Anaesthetic Impairment of Immune Function Is Mediated via GABAA Receptors

et al. 2011

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BackgroundGABAA receptors are members of the Cys-loop family of neurotransmitter receptors, proteins which are responsible for fast synaptic transmission, and are the site of action of wide range of drugs [1]. Recent work has shown that Cys-loop receptors are present on immune cells, but their physiological roles and the effects of drugs that modify their function in the innate immune system are currently unclear [2]. We are interested in how and why anaesthetics increase infections in intensive care patients; a serious problem as more than 50% of patients with severe sepsis will die [3]–[6]. As many anaesthetics act via GABAA receptors [7], the aim of this study was to determine if these receptors are present on immune cells, and could play a role in immunocompromising patients.Principal FindingsWe demonstrate, using RT-PCR, that monocytes express GABAA receptors constructed of α1, α4, β2, γ1 and/or δ subunits. Whole cell patch clamp electrophysiological studies show that GABA can activate these receptors, resulting in the opening of a chloride-selective channel; activation is inhibited by the GABAA receptor antagonists bicuculline and picrotoxin, but not enhanced by the positive modulator diazepam. The anaesthetic drugs propofol and thiopental, which can act via GABAA receptors, impaired monocyte function in classic immunological chemotaxis and phagocytosis assays, an effect reversed by bicuculline and picrotoxin.SignificanceOur results show that functional GABAA receptors are present on monocytes with properties similar to CNS GABAA receptors. The functional data provide a possible explanation as to why chronic propofol and thiopental administration can increase the risk of infection in critically ill patients: their action on GABAA receptors inhibits normal monocyte behaviour. The data also suggest a potential solution: monocyte GABAA receptors are insensitive to diazepam, thus the use of benzodiazepines as an alternative anesthetising agent may be advantageous where infection is a life threatening problem.

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Section: Introductionmentioning

confidence: 99%

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confidence: 99%

Anaesthetic Impairment of Immune Function Is Mediated via GABAA Receptors

et al. 2011

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“…A retrospective study compared the rate of pneumonia between ventilated head trauma patients who received thiopental therapy (n = 75) and those who did not receive thiopental (n = 76) [149]. The rate of noscomial pneumonia was higher in patients who received thiopental compared with those who did not receive thiopental (53 vs 35%; OR, 1.85; 95% CI, 0.97 to 3.51).…”

Section: Discussionmentioning

confidence: 99%

Intensive care unit-acquired infection as a side effect of sedation

et al. 2010

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IntroductionSedative and analgesic medications are routinely used in mechanically ventilated patients. The aim of this review is to discus epidemiologic data that suggest a relationship between infection and sedation, to review available data for the potential causes and pathophysiology of this relationship, and to identify potential preventive measures.MethodsData for this review were identified through searches of PubMed, and from bibliographies of relevant articles.ResultsSeveral epidemiologic studies suggested a link between sedation and ICU-acquired infection. Prolongation of exposure to risk factors for infection, microaspiration, gastrointestinal motility disturbances, microcirculatory effects are main mechanisms by which sedation may favour infection in critically ill patients. Furthermore, experimental evidence coming from studies both in humans and animals suggest that sedatives and analgesics present immunomodulatory properties that might alter the immunologic response to exogenous stimuli. Clinical studies comparing different sedative agents do not provide evidence to recommend the use of a particular agent to reduce ICU-acquired infection rate. However, sedation strategies aiming to reduce the duration of mechanical ventilation, such as daily interruption of sedatives or nursing-implementing sedation protocol, should be promoted. In addition, the use of short acting opioids, propofol, and dexmedetomidine is associated with shorter duration of mechanical ventilation and ICU stay, and might be helpful in reducing ICU-acquired infection rates.ConclusionsProlongation of exposure to risk factors for infection, microaspiration, gastrointestinal motility disturbances, microcirculatory effects, and immunomodulatory effects are main mechanisms by which sedation may favour infection in critically ill patients. Future studies should compare the effect of different sedative agents, and the impact of progressive opioid discontinuation compared with abrupt discontinuation on ICU-acquired infection rates.

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“…For example, high-dose barbiturates were administered more frequently to the pressure-monitoring group than to the imaging-clinical examination group, who received more hypertonic saline and hyperventilation, which may have had secondary effects on outcome. High-dose barbiturates are known to have severe adverse effects in terms of pulmonary, circulatory and renal complications, 9,10 which could have influenced the trial outcome. Hypertonic saline might also have adverse effects, causing electrolyte disturbances and an increase in ICP on its withdrawal, and vasopressors can trigger pneumonia and adult respiratory distress syndrome.…”

Section: News and Viewsmentioning

confidence: 99%