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Sufentanil, fentanyl, and alfentanil in head trauma patients: A study on cerebral hemodynamics
Abstract
To determine the effects of bolus injection and infusion of sufentanil, alfentanil, and fentanyl on cerebral hemodynamics and electroencephalogram activity in patients with increased intracranial pressure (ICP) after severe head trauma.
Randomized, unblended, crossover study.
Intensive care unit and trauma center in a university hospital.
Six patients with head trauma and ICP monitoring, sedated at the time of the study with propofol infusion and full neuromuscular blockade.
Following a randomized order, in an unblended and crossover fashion, the level of sedation was deepened with a 6-min injection of either sufentanil (1 microg/kg), alfentanil (100 microg/kg), or fentanyl (10 microg/kg) followed by an infusion of 0.005, 0.7, and 0.075 microg/kg/min, respectively, for 1 hr. The three opioids were given to each patient at 24-hr intervals.
Mean arterial pressure (MAP), ICP, cerebral perfusion pressure (CPP), and jugular vein bulb oxygen saturation (Svjo2) were continuously measured and recorded at 1-min intervals throughout the 60-min study period. Sufentanil, fentanyl, and alfentanil infusions were associated with a significant but transient increase in ICP (9+/-2 mm Hg [SD], 8+/-2 mm Hg, and 5.5+/-1 mm Hg, respectively; p<.05). The increase in ICP peaked at 5, 6, and 3 mins, respectively, then gradually decreased and returned to baseline values after 15 mins. This result was accompanied by a significant decrease in MAP (21+/-2 mm Hg, 24+/-2 mm Hg, and 26+/-2 mm Hg, respectively; p<.05) and, thus, in CPP (30+/-3 mm Hg, 31+/-3 mm Hg, and 34+/-3 mm Hg, respectively; p<.05). After 5 mins, MAP and CPP gradually increased, although they remained significantly decreased throughout the study period. No changes in lactate-oxygen index, used as an ischemia index, were observed. Changes in electroencephalogram tracings were characterized by a switch from a fast to a decreased activity, together with an improvement in the background activity.
The results of the present study show that alfentanil, sufentanil, and fentanyl produce similar transient increases in ICP when administered by bolus injection in patients with increased ICP. No evidence of cerebral ischemia was observed in the study patients.
... Nine studies (13,15,16,20,23,24,27,30,33) were RCTs, of which four (13,20,30,33) utilized a crossover design. Three RCTs (15,20,30) were good quality (PEDro = 6-8) and six RCTs (13,16,23,24,27,33) were fair quality (PEDro = 4-5). ...
... Nine studies (13,15,16,20,23,24,27,30,33) were RCTs, of which four (13,20,30,33) utilized a crossover design. Three RCTs (15,20,30) were good quality (PEDro = 6-8) and six RCTs (13,16,23,24,27,33) were fair quality (PEDro = 4-5). Three studies (22,26,31) were prospective controlled trials. ...
... All included studies were conducted in intensive care units, such that all patients were receiving mechanical ventilation. Sedation was administered prior to intervention in the majority of studies: midazolam in 12 studies (15,16,19,20,23,(26)(27)(28)(29)(30)(31)(32), propofol in 6 studies (12,13,17,18,21,23), etomidate in 1 study (14), and diazepam in 1 study (33). Four studies (22)(23)(24)(25) reported that no sedatives were administered before at least one of the interventions. ...
Background:
Following traumatic brain injury (TBI), optimization of cerebral physiology is recommended to promote more favourable patient outcomes. Accompanying pain and agitation are commonly treated with sedative and analgesic agents, such as opioids. However, the impact of opioids on certain aspects of cerebral physiology is not well established.
Objective:
To conduct a systematic review of the evidence on the effect of opioids on cerebral physiology in TBI during acute care.
Methods:
A comprehensive literature search was conducted in five electronic databases for articles published in English up to November 2017. Studies were included if: (1) the study sample was human subjects with TBI; (2) the sample size was ≥3; (3) subjects were given an opioid during acute care; and (4) any measure of cerebral physiology was evaluated. Cerebral physiology measures were intracranial pressure (ICP), cerebral perfusion pressure (CPP), and mean arterial pressure (MAP). Subject and study characteristics, treatment protocol, and results were extracted from included studies. Randomized controlled trials were evaluated for methodological quality using the Physiotherapy Evidence Database tool. Levels of evidence were assigned using a modified Sackett scale.
Results:
In total, 22 studies met inclusion criteria, from which six different opioids were identified: morphine, fentanyl, sufentanil, remifentanil, alfentanil, and phenoperidine. The evidence for individual opioids demonstrated equally either: (1) no effect on ICP, CPP, or MAP; or (2) an increase in ICP with associated decreases in CPP and MAP. In general, opioids administered by infusion resulted in the former outcome, whereas those given in bolus form resulted in the latter. There were no significant differences when comparing different opioids, with the exception of one study that found fentanyl was associated with lower ICP and CPP than morphine and sufentanil. There were no consistent results when comparing opioids to other non-opioid medications.
Conclusion:
Several studies have assessed the effect of opioids on cerebral physiology during the acute management of TBI, but there is considerable heterogeneity in terms of study methodology and findings. Opioids are beneficial in terms of analgesia and sedation, but bolus administration should be avoided to prevent additional or prolonged unfavourable alterations in cerebral physiology. Future studies should better elucidate the effects of different opioids as well as varying dosages in order to develop improved understanding as well as allow for tighter control of cerebral physiology.
Abbreviations:
CPP: Cerebral Perfusion Pressure, GCS: Glasgow Coma Scale, ICP: Intracranial Pressure, MAP: Mean Arterial Pressure, PEDro: Physiotherapy Evidence Database, RCT: Randomized Controlled Trial, TBI: Traumatic Brain Injury.
... This can lead or worsen the secondary brain insult (ischemia/hypoxia) [34,35]. If autoregulation is intact, this reduction on MAP will produce reflex cerebral vasodilation and may lead to an increase in intracranial pressure [36]. The hemodynamic effects are usually dose dependent, so it is important to assess the preload status of the patient in order to predict the hemodynamic response to the sedative agent, particularly in those with previous cardiac dysfunction. ...
... Sedation is a first-line therapy that should be integrated with other specific interventions as hyperventilation, osmotic agents and head-of-bed elevation. Bolus of opioids needs caution for the transient decrease in mean arterial pressure and increase in ICP due to autoregulatory cerebral vasodilation [36]. When compared with opioids, propofol showed an association with a lower ICP and less ICP treatments in patients with severe traumatic brain injury (TBI) [6]. ...
Sedation is an important topic in neurocritical patients. When compared with general intensive care unit and traumatic brain-injured patients, sedation has its therapeutic indications, such as management of intracranial pressure, treatment of status epilepticus, sedation for targeted temperature management patients and paroxysmal sympathetic activity. Nowadays, the assessment of sedation is done by neurological evaluation and new monitors based on electroencephalography signals that help the physician titrate the sedative agents. Therefore, the aim of this chapter is to discuss the main pharmacological properties of sedatives and analgesics, their proper indications related to pathophysiological issues and their titrations based on the abovementioned new technologies.
... This procedure is applied in head injury, cerebral infarction and removes the clots or tumour. (Albanese et al., 1999). ...
Normal intracranial pressure is exerted by the cerebrospinal fluid on the cerebral tissue which produces a pressure in the cranium. This is maintained in the range of 7-15 mm Hg. The cranium is formed as a protecting framework to the brain tissues through eight bones 2 temporal, 2 parietal, frontal, occipital, sphenoid, and ethmoid bones. The neurocranium contains three components the brain Tissues 80%, Blood 10 % and CSF 10%. These are responsible for ICP, if any one of these increases in volume, then other of one or two compresses and adjusts a limited time to avoid increasing ICP but after some instant, brain is exhausted and increase ICP, So that one increased ?Volume increased ? ICP increased ? Brain shrank ? Brain Injury. There are elastance and compliance mechanism which stable the ICP in some instant, because the brain 100–150 ml CSF additionally absorb without changes in the ICP. In adult, normally CSF volume is 150 ml, the 125ml within subarachnoid spaces and 25ml in the ventricles. Whenever CSF volume increases then the compensatory mechanism is started so, low pressure of vein is collapsed and CSF egress into the lumbar subarachnoid space, when the compensatory mechanism is exhausted then increased of additional volume cause sudden ICP rise. The cerebrospinal fluid is circulating through the neuroaxis from the site of secretion to the site of absorption due to rhythmic systolic pulse wave in choroid arteries. The CSF circulation is depending on frequency of respiration, jugular venous pressure, postures and the individual physical activity. The mechanism of compliance is changing the ICV and ICP. It means, the ICP is elevated, then ICV becomes low, when ICP is normal, the ICV is become high. So, small changes in the ICV that changes in the ICP.
... Therefore, appropriate analgesia and sedation should be given. [56] In the process of adjuvant treatment, the treatment of primary disease is also extremely important. Anticoagulation therapy, such as heparin or warfarin, thrombolysis therapy such as urokinase or alteplase, and interventional thrombolysis are the treatment measures. ...
Rationale:
Immune thrombocytopenia (ITP) is an autoimmune disease with an increased risk of bleeding. However, in recent years, it has been reported that patients with this hemorrhagic disease have the risk of thrombosis and embolism.
Patient concerns and diagnosis:
The patient, in this case, was a young female who was diagnosed with ITP. When the platelet count was low, she had skin, mucosa, internal organs, and intracranial hemorrhage. In the process of ITP and hemostatic treatment, superior sagittal sinus thrombosis occurred when she was still bleeding.
Interventions:
She was given treatments for reducing intracranial pressure and controlling epilepsy.
Outcomes:
And then the embolectomy operation failed. It was suggested in this case that ITP patients with severe thrombocytopenia and bleeding tendency also have a risk of having thrombotic disease. We reviewed literatures regarding the mechanism of the simultaneous occurrence of 2 antinomy diseases and cerebral venous thrombosis.
Lessons:
There are many factors for ITP patients to have thrombosis involving ITP itself, its treatment and the patients' constitution, medical history, and former medication. ITP is not only a hemorrhagic disease but also a thrombotic disease. Clinicians should be alert to the risk of thrombotic diseases in ITP treatment. Therefore thrombus monitoring and screening should be carried out, and early prevention or appropriate anticoagulant treatment should be selected, especially for patients with high risk.
... Reviews крови, применение их для терапии болевого синдрома избегают, считая их небезопасными для пациентов. Кроме того, у опиоидов есть ряд других нежелательных побочных эффектов, таких как тошнота, рвота, динамическая непроходимость кишечника, задержка мочи, острая опиоидная абстиненция, галлюцинации и гипотензия [21,[25][26][27][28][29][30][31]. Опасения по поводу безопасности опиоидов были подтверждены лабораторными данными, при исследовании влияния морфина на ауторегуляцию мозгового кровотока у крыс в условиях экспериментального субарахноидального кровоизлияния. ...
This review of the literature is devoted to the current state of the problem of management of headache in patients with non-traumatic subarachnoid hemorrhage (NSAH). This pathology is associated with severe and prolonged headache. Despite the huge amount of references on subarachnoid hemorrhage, a little attention is paid to headache in this pathology, so it remains largely unexplored. The article presents data on the epidemiology of the syndrome, possible mechanisms of occurrence, diagnostic methods. Details of the advantages and disadvantages of drugs for anesthesia, available in the arsenal of the clinician at the moment. The results of many previously published studies are diametrically opposed, which does not facilitate the choice of tactics for effective treatment and prevention of complications. The article also identifies the problems, the solution of which, possibly, will lead to an improvement in the results of treatment of SAH and further the quality of life of the patients. The lack of evidance data on the subject suggests that the research is relevant.
... Second, a decrease in CPP after fentanyl was seen in these TBI studies 24,25 ; this has been commented on in past review articles. 2,38 Along with this, there was a limited response in CBF in the three TBI studies with PCO 2 being constant through the studies, indicating that fentanyl has little influence on CBF in the setting of ventilatory and cardiovascular support/control seen during treatment in an intensive care unit (ICU). ...
Intravenous propofol, fentanyl, and midazolam are utilized commonly in critical care for metabolic suppression and anesthesia. The impact of propofol, fentanyl, and midazolam on cerebrovasculature and cerebral blood flow (CBF) is unclear in traumatic brain injury (TBI) and may carry important implications, as care is shifting to focus on cerebrovascular reactivity monitoring/directed therapies. The aim of this study was to perform a scoping review of the literature on the cerebrovascular/CBF effects of propofol, fentanyl, and midazolam in human patients with moderate/severe TBI and animal models with TBI. A search of MEDLINE, BIOSIS, EMBASE, Global Health, SCOPUS, and the Cochrane Library from inception to May 2020 was performed. All articles were included pertaining to the administration of propofol, fentanyl, and midazolam, in which the impact on CBF/cerebral vasculature was recorded. We identified 14 studies: 8 that evaluated propofol, 5 that evaluated fentanyl, and 2 that evaluated midazolam. All studies suffered from significant limitations, including: small sample size, and heterogeneous design and measurement techniques. In general, there was no significant change seen in CBF/cerebrovascular response to administration of propofol, fentanyl, or midazolam during experiments where PCO2 and mean arterial pressure (MAP) were controlled. This review highlights the current knowledge gap surrounding the impact of commonly utilized sedative drugs in TBI care. This work supports the need for dedicated studies, both experimental and human-based, evaluating the impact of these drugs on CBF and cerebrovascular reactivity/response in TBI.
... Cuando se administra en pacientes con trauma craneoencefálico, se ha observado un aumento transitorio de la PIC y una disminución de la presión arterial media, independiente del principio activo empleado (fentanilo, alfentanilo o sufentanilo) tanto en estudios experimentales [42] como en clínicos [43]; pero, a pesar de los cambios hemodinámicos descritos, la estimación del flujo sanguíneo cerebral permaneció sin cambios [44]. ...
La secuencia de intubación rápida (SIR) es un procedimiento diseñado para minimizar el tiempo necesario en el aseguramiento de la vía aérea mediante la colocación de un tubo endotraqueal en pacientes con alto riesgo de broncoaspiración, especialmente en situaciones de emergencia. Teniendo claro este panorama, es indiscutible la importancia de la educación y el entrenamiento relacionado con la secuencia de intubación rápida que debe hacerse a los médicos responsables de las salas de reanimación, los servicios de urgencias y los paramédicos responsables del manejo de campo en emergencias y desastres. Este documento es una revisión actualizada del tema, cuyo objetivo es servir de guía para todos quienes estén interesados.
... No evidence was found that one sedative or opioid agent provided more efficacy than another in TBI patients. Arterial hypotension can be observed with barbiturates [111], bolus of midazolam [112] or bolus of opioids [113]. Attention should be paid to the control of systemic haemodynamics in the choice of drugs and their modalities of administration. ...
The latest French Guidelines for the management in the first 24hours of patients with severe traumatic brain injury (TBI) were published in 1998. Due to recent changes (intracerebral monitoring, cerebral perfusion pressure management, treatment of raised intracranial pressure), an update was required. Our objective has been to specify the significant developments since 1998. These guidelines were conducted by a group of experts for the French Society of Anesthesia and Intensive Care Medicine (Société Francaise d'Anesthésie Réanimation (SFAR)) in partnership with the Association de Neuro-Anesthésie-Réanimation de Langue Française (ANARLF), the Société Française de Neurochirurgie (SFN), the Groupe Francophone de Réanimation et d'Urgences Pédiatriques (GFRUP) and the Association des Anesthésistes-Réanimateurs Pédiatriques d'Expression Française (ADARPEF). The method used to elaborate these guidelines was the GRADE® method. After two Delphi rounds, 32 recommendations were formally developed by the experts focusing on the evaluation the initial severity of traumatic brain injury, the modalities of prehospital management, imaging strategies, indications for neurosurgical interventions, sedation and analgesia, indications and modalities of cerebral monitoring, medical management of raised intracranial pressure, management of multiple trauma with severe traumatic brain injury, detection and prevention of post-traumatic epilepsia, biological homeostasis (osmolarity, glycaemia, adrenal axis) and paediatric specificities.
... Previous studies have shown that fentanyl may cause an increase in ICP and a reduction in cerebral perfusion pressure after TBI. [69][70][71] Other data suggest, however, that the use of fentanyl may cause a blunting of ICP elevation in response to pain or clinical interventions that would otherwise have increased ICP. 49,72 Sufentanil. ...
Objective:
In neurotrauma care, a better understanding of treatments following traumatic brain injury (TBI) has led to a significant decrease in morbidity and mortality in this population. TBI represents a significant medical problem, and complications following TBI are associated with the initial injury and post-event intracranial processes such as elevated intracranial pressure (ICP) and brain edema. Consequently, appropriate therapeutic interventions are required to reduce brain tissue damage and improve cerebral perfusion. We present a contemporary review of literature on the use of pharmacologic therapies to reduce intracranial pressure following TBI and a comparison of their efficacy.
Methods:
This review was conducted by PubMed query. Only studies discussing pharmacologic management of patients following TBI were included. This review includes prospective and retrospective studies and includes randomized controlled trials as well as cohort, case-control, observational and database studies. Systematic literature reviews, metanalyses, and studies that considered conditions other than TBI or pediatric populations were not included.
Results:
Review of the literature describing the current pharmacological treatment for intracranial hypertension following TBI most often discussed the use of hyperosmolar agents such as hypertonic saline (HTS) and mannitol, sedatives such as fentanyl and propofol, benzodiazepines, and barbiturates. Hypertonic saline is associated with faster resolution of intracranial hypertension and restoration of optimal cerebral hemodynamics, although these advantages did not translate into long term benefits in morbidity or mortality. In patients refractory to treatment with hyperosmolar therapy, induction of a barbiturate coma can reduce ICP, although requires close monitoring to prevent adverse events.
Conclusion:
Current research suggests that the use of hypertonic saline following TBI is the best option for immediate decrease in intracranial pressure. A better understanding of the efficacy of each treatment option can help to direct treatment algorithms during the critical early hours of trauma care and continue to improve morbidity and mortality following TBI.
... Aucun agent hypnotique ou morphinique n'a fait la preuve de sa supériorité chez le patient cérébrolésé. Une hypotension artérielle peut être provoquée par des barbituriques [110], des bolus de midazolam [111] ou des fortes doses de morphiniques en bolus [112], ce qui peut être délétère sur l'hémodynamique cérébrale. La priorité doit être donnée au contrôle de l'hémodynamique systémique dans le choix des drogues et de leurs modalités d'administration. ...
... Aucun agent hypnotique ou morphinique n'a fait la preuve de sa supériorité chez le patient cérébrolésé. Une hypotension artérielle peut être provoquée par des barbituriques [110], des bolus de midazolam [111] ou des fortes doses de morphiniques en bolus [112], ce qui peut être délétère sur l'hémodynamique cérébrale. La priorité doit être donnée au contrôle de l'hémodynamique systémique dans le choix des drogues et de leurs modalités d'administration. ...
Numerous studies indicate that outcomes for pediatric patients are improved when the anesthesia caregiver has advanced training and knowledge of pediatric anesthesiology. Essentials of Pediatric Anesthesiology is a unique new handbook, providing a clinically relevant and easy-to-read review of all key topics in this important field. Written and edited by leading pediatric anesthesia physicians, each chapter takes a consistent approach, guaranteeing this book is user-friendly and authoritative throughout. Topics include physiology, anatomy, equipment, a comprehensive overview of relevant disease states, and special topics such as regional anesthesia, complications, and anesthesia for remote locations. Numerous diagrams, tables and figures help to organize the information for easy reference. Whether you choose to dip into a particular chapter or read the book cover to cover, Essentials of Pediatric Anesthesiology is a valuable review book for all residents, fellows and clinical practitioners needing to improve or refresh their understanding of pediatric anesthesia management.
Numerous studies indicate that outcomes for pediatric patients are improved when the anesthesia caregiver has advanced training and knowledge of pediatric anesthesiology. Essentials of Pediatric Anesthesiology is a unique new handbook, providing a clinically relevant and easy-to-read review of all key topics in this important field. Written and edited by leading pediatric anesthesia physicians, each chapter takes a consistent approach, guaranteeing this book is user-friendly and authoritative throughout. Topics include physiology, anatomy, equipment, a comprehensive overview of relevant disease states, and special topics such as regional anesthesia, complications, and anesthesia for remote locations. Numerous diagrams, tables and figures help to organize the information for easy reference. Whether you choose to dip into a particular chapter or read the book cover to cover, Essentials of Pediatric Anesthesiology is a valuable review book for all residents, fellows and clinical practitioners needing to improve or refresh their understanding of pediatric anesthesia management.
Numerous studies indicate that outcomes for pediatric patients are improved when the anesthesia caregiver has advanced training and knowledge of pediatric anesthesiology. Essentials of Pediatric Anesthesiology is a unique new handbook, providing a clinically relevant and easy-to-read review of all key topics in this important field. Written and edited by leading pediatric anesthesia physicians, each chapter takes a consistent approach, guaranteeing this book is user-friendly and authoritative throughout. Topics include physiology, anatomy, equipment, a comprehensive overview of relevant disease states, and special topics such as regional anesthesia, complications, and anesthesia for remote locations. Numerous diagrams, tables and figures help to organize the information for easy reference. Whether you choose to dip into a particular chapter or read the book cover to cover, Essentials of Pediatric Anesthesiology is a valuable review book for all residents, fellows and clinical practitioners needing to improve or refresh their understanding of pediatric anesthesia management.
Numerous studies indicate that outcomes for pediatric patients are improved when the anesthesia caregiver has advanced training and knowledge of pediatric anesthesiology. Essentials of Pediatric Anesthesiology is a unique new handbook, providing a clinically relevant and easy-to-read review of all key topics in this important field. Written and edited by leading pediatric anesthesia physicians, each chapter takes a consistent approach, guaranteeing this book is user-friendly and authoritative throughout. Topics include physiology, anatomy, equipment, a comprehensive overview of relevant disease states, and special topics such as regional anesthesia, complications, and anesthesia for remote locations. Numerous diagrams, tables and figures help to organize the information for easy reference. Whether you choose to dip into a particular chapter or read the book cover to cover, Essentials of Pediatric Anesthesiology is a valuable review book for all residents, fellows and clinical practitioners needing to improve or refresh their understanding of pediatric anesthesia management.
Numerous studies indicate that outcomes for pediatric patients are improved when the anesthesia caregiver has advanced training and knowledge of pediatric anesthesiology. Essentials of Pediatric Anesthesiology is a unique new handbook, providing a clinically relevant and easy-to-read review of all key topics in this important field. Written and edited by leading pediatric anesthesia physicians, each chapter takes a consistent approach, guaranteeing this book is user-friendly and authoritative throughout. Topics include physiology, anatomy, equipment, a comprehensive overview of relevant disease states, and special topics such as regional anesthesia, complications, and anesthesia for remote locations. Numerous diagrams, tables and figures help to organize the information for easy reference. Whether you choose to dip into a particular chapter or read the book cover to cover, Essentials of Pediatric Anesthesiology is a valuable review book for all residents, fellows and clinical practitioners needing to improve or refresh their understanding of pediatric anesthesia management.
Numerous studies indicate that outcomes for pediatric patients are improved when the anesthesia caregiver has advanced training and knowledge of pediatric anesthesiology. Essentials of Pediatric Anesthesiology is a unique new handbook, providing a clinically relevant and easy-to-read review of all key topics in this important field. Written and edited by leading pediatric anesthesia physicians, each chapter takes a consistent approach, guaranteeing this book is user-friendly and authoritative throughout. Topics include physiology, anatomy, equipment, a comprehensive overview of relevant disease states, and special topics such as regional anesthesia, complications, and anesthesia for remote locations. Numerous diagrams, tables and figures help to organize the information for easy reference. Whether you choose to dip into a particular chapter or read the book cover to cover, Essentials of Pediatric Anesthesiology is a valuable review book for all residents, fellows and clinical practitioners needing to improve or refresh their understanding of pediatric anesthesia management.
Numerous studies indicate that outcomes for pediatric patients are improved when the anesthesia caregiver has advanced training and knowledge of pediatric anesthesiology. Essentials of Pediatric Anesthesiology is a unique new handbook, providing a clinically relevant and easy-to-read review of all key topics in this important field. Written and edited by leading pediatric anesthesia physicians, each chapter takes a consistent approach, guaranteeing this book is user-friendly and authoritative throughout. Topics include physiology, anatomy, equipment, a comprehensive overview of relevant disease states, and special topics such as regional anesthesia, complications, and anesthesia for remote locations. Numerous diagrams, tables and figures help to organize the information for easy reference. Whether you choose to dip into a particular chapter or read the book cover to cover, Essentials of Pediatric Anesthesiology is a valuable review book for all residents, fellows and clinical practitioners needing to improve or refresh their understanding of pediatric anesthesia management.
Numerous studies indicate that outcomes for pediatric patients are improved when the anesthesia caregiver has advanced training and knowledge of pediatric anesthesiology. Essentials of Pediatric Anesthesiology is a unique new handbook, providing a clinically relevant and easy-to-read review of all key topics in this important field. Written and edited by leading pediatric anesthesia physicians, each chapter takes a consistent approach, guaranteeing this book is user-friendly and authoritative throughout. Topics include physiology, anatomy, equipment, a comprehensive overview of relevant disease states, and special topics such as regional anesthesia, complications, and anesthesia for remote locations. Numerous diagrams, tables and figures help to organize the information for easy reference. Whether you choose to dip into a particular chapter or read the book cover to cover, Essentials of Pediatric Anesthesiology is a valuable review book for all residents, fellows and clinical practitioners needing to improve or refresh their understanding of pediatric anesthesia management.
Numerous studies indicate that outcomes for pediatric patients are improved when the anesthesia caregiver has advanced training and knowledge of pediatric anesthesiology. Essentials of Pediatric Anesthesiology is a unique new handbook, providing a clinically relevant and easy-to-read review of all key topics in this important field. Written and edited by leading pediatric anesthesia physicians, each chapter takes a consistent approach, guaranteeing this book is user-friendly and authoritative throughout. Topics include physiology, anatomy, equipment, a comprehensive overview of relevant disease states, and special topics such as regional anesthesia, complications, and anesthesia for remote locations. Numerous diagrams, tables and figures help to organize the information for easy reference. Whether you choose to dip into a particular chapter or read the book cover to cover, Essentials of Pediatric Anesthesiology is a valuable review book for all residents, fellows and clinical practitioners needing to improve or refresh their understanding of pediatric anesthesia management.
Numerous studies indicate that outcomes for pediatric patients are improved when the anesthesia caregiver has advanced training and knowledge of pediatric anesthesiology. Essentials of Pediatric Anesthesiology is a unique new handbook, providing a clinically relevant and easy-to-read review of all key topics in this important field. Written and edited by leading pediatric anesthesia physicians, each chapter takes a consistent approach, guaranteeing this book is user-friendly and authoritative throughout. Topics include physiology, anatomy, equipment, a comprehensive overview of relevant disease states, and special topics such as regional anesthesia, complications, and anesthesia for remote locations. Numerous diagrams, tables and figures help to organize the information for easy reference. Whether you choose to dip into a particular chapter or read the book cover to cover, Essentials of Pediatric Anesthesiology is a valuable review book for all residents, fellows and clinical practitioners needing to improve or refresh their understanding of pediatric anesthesia management.
Numerous studies indicate that outcomes for pediatric patients are improved when the anesthesia caregiver has advanced training and knowledge of pediatric anesthesiology. Essentials of Pediatric Anesthesiology is a unique new handbook, providing a clinically relevant and easy-to-read review of all key topics in this important field. Written and edited by leading pediatric anesthesia physicians, each chapter takes a consistent approach, guaranteeing this book is user-friendly and authoritative throughout. Topics include physiology, anatomy, equipment, a comprehensive overview of relevant disease states, and special topics such as regional anesthesia, complications, and anesthesia for remote locations. Numerous diagrams, tables and figures help to organize the information for easy reference. Whether you choose to dip into a particular chapter or read the book cover to cover, Essentials of Pediatric Anesthesiology is a valuable review book for all residents, fellows and clinical practitioners needing to improve or refresh their understanding of pediatric anesthesia management.
Numerous studies indicate that outcomes for pediatric patients are improved when the anesthesia caregiver has advanced training and knowledge of pediatric anesthesiology. Essentials of Pediatric Anesthesiology is a unique new handbook, providing a clinically relevant and easy-to-read review of all key topics in this important field. Written and edited by leading pediatric anesthesia physicians, each chapter takes a consistent approach, guaranteeing this book is user-friendly and authoritative throughout. Topics include physiology, anatomy, equipment, a comprehensive overview of relevant disease states, and special topics such as regional anesthesia, complications, and anesthesia for remote locations. Numerous diagrams, tables and figures help to organize the information for easy reference. Whether you choose to dip into a particular chapter or read the book cover to cover, Essentials of Pediatric Anesthesiology is a valuable review book for all residents, fellows and clinical practitioners needing to improve or refresh their understanding of pediatric anesthesia management.
Numerous studies indicate that outcomes for pediatric patients are improved when the anesthesia caregiver has advanced training and knowledge of pediatric anesthesiology. Essentials of Pediatric Anesthesiology is a unique new handbook, providing a clinically relevant and easy-to-read review of all key topics in this important field. Written and edited by leading pediatric anesthesia physicians, each chapter takes a consistent approach, guaranteeing this book is user-friendly and authoritative throughout. Topics include physiology, anatomy, equipment, a comprehensive overview of relevant disease states, and special topics such as regional anesthesia, complications, and anesthesia for remote locations. Numerous diagrams, tables and figures help to organize the information for easy reference. Whether you choose to dip into a particular chapter or read the book cover to cover, Essentials of Pediatric Anesthesiology is a valuable review book for all residents, fellows and clinical practitioners needing to improve or refresh their understanding of pediatric anesthesia management.
Numerous studies indicate that outcomes for pediatric patients are improved when the anesthesia caregiver has advanced training and knowledge of pediatric anesthesiology. Essentials of Pediatric Anesthesiology is a unique new handbook, providing a clinically relevant and easy-to-read review of all key topics in this important field. Written and edited by leading pediatric anesthesia physicians, each chapter takes a consistent approach, guaranteeing this book is user-friendly and authoritative throughout. Topics include physiology, anatomy, equipment, a comprehensive overview of relevant disease states, and special topics such as regional anesthesia, complications, and anesthesia for remote locations. Numerous diagrams, tables and figures help to organize the information for easy reference. Whether you choose to dip into a particular chapter or read the book cover to cover, Essentials of Pediatric Anesthesiology is a valuable review book for all residents, fellows and clinical practitioners needing to improve or refresh their understanding of pediatric anesthesia management.
Numerous studies indicate that outcomes for pediatric patients are improved when the anesthesia caregiver has advanced training and knowledge of pediatric anesthesiology. Essentials of Pediatric Anesthesiology is a unique new handbook, providing a clinically relevant and easy-to-read review of all key topics in this important field. Written and edited by leading pediatric anesthesia physicians, each chapter takes a consistent approach, guaranteeing this book is user-friendly and authoritative throughout. Topics include physiology, anatomy, equipment, a comprehensive overview of relevant disease states, and special topics such as regional anesthesia, complications, and anesthesia for remote locations. Numerous diagrams, tables and figures help to organize the information for easy reference. Whether you choose to dip into a particular chapter or read the book cover to cover, Essentials of Pediatric Anesthesiology is a valuable review book for all residents, fellows and clinical practitioners needing to improve or refresh their understanding of pediatric anesthesia management.
Numerous studies indicate that outcomes for pediatric patients are improved when the anesthesia caregiver has advanced training and knowledge of pediatric anesthesiology. Essentials of Pediatric Anesthesiology is a unique new handbook, providing a clinically relevant and easy-to-read review of all key topics in this important field. Written and edited by leading pediatric anesthesia physicians, each chapter takes a consistent approach, guaranteeing this book is user-friendly and authoritative throughout. Topics include physiology, anatomy, equipment, a comprehensive overview of relevant disease states, and special topics such as regional anesthesia, complications, and anesthesia for remote locations. Numerous diagrams, tables and figures help to organize the information for easy reference. Whether you choose to dip into a particular chapter or read the book cover to cover, Essentials of Pediatric Anesthesiology is a valuable review book for all residents, fellows and clinical practitioners needing to improve or refresh their understanding of pediatric anesthesia management.
Numerous studies indicate that outcomes for pediatric patients are improved when the anesthesia caregiver has advanced training and knowledge of pediatric anesthesiology. Essentials of Pediatric Anesthesiology is a unique new handbook, providing a clinically relevant and easy-to-read review of all key topics in this important field. Written and edited by leading pediatric anesthesia physicians, each chapter takes a consistent approach, guaranteeing this book is user-friendly and authoritative throughout. Topics include physiology, anatomy, equipment, a comprehensive overview of relevant disease states, and special topics such as regional anesthesia, complications, and anesthesia for remote locations. Numerous diagrams, tables and figures help to organize the information for easy reference. Whether you choose to dip into a particular chapter or read the book cover to cover, Essentials of Pediatric Anesthesiology is a valuable review book for all residents, fellows and clinical practitioners needing to improve or refresh their understanding of pediatric anesthesia management.
Numerous studies indicate that outcomes for pediatric patients are improved when the anesthesia caregiver has advanced training and knowledge of pediatric anesthesiology. Essentials of Pediatric Anesthesiology is a unique new handbook, providing a clinically relevant and easy-to-read review of all key topics in this important field. Written and edited by leading pediatric anesthesia physicians, each chapter takes a consistent approach, guaranteeing this book is user-friendly and authoritative throughout. Topics include physiology, anatomy, equipment, a comprehensive overview of relevant disease states, and special topics such as regional anesthesia, complications, and anesthesia for remote locations. Numerous diagrams, tables and figures help to organize the information for easy reference. Whether you choose to dip into a particular chapter or read the book cover to cover, Essentials of Pediatric Anesthesiology is a valuable review book for all residents, fellows and clinical practitioners needing to improve or refresh their understanding of pediatric anesthesia management.
Although sedative use is near-ubiquitous in the acute management of moderate to severe traumatic brain injury (m-sTBI), the evidence base for these agents is undefined. This review summarizes the evidence for analgosedative agent use in the intensive care unit management of m-sTBI. Clinical studies of sedative and analgosedative agents currently utilized in adult m-sTBI management (propofol, ketamine, benzodiazepines, opioids, and alpha-2 agonists) were identified and assessed for relevance and methodological quality. The primary outcome was the effect of the analgosedative agent on intracranial pressure (ICP). Secondary outcomes included intracranial hemodynamic and metabolic parameters, systemic hemodynamic parameters, measures of therapeutic intensity, and clinical outcomes. Of 594 articles identified, 61 met methodological review criteria, and 40 were included in the qualitative summary; of these, 33 were prospective studies, 18 were randomized controlled trials, and 8 were blinded. There was consistent evidence for the efficacy of sedative agents in the management of m-sTBI and raised ICP, but the overall quality of the evidence was poor, consisting of small studies (median sample size, 23.5) of variable methodological quality. Propofol and midazolam achieve the goals of sedation without notable differences in efficacy or safety, although high-dose propofol may disrupt cerebral autoregulation. Dexmedetomidine and propofol/ dexmedetomidine combination may cause clinically significant hypotension. Dexmedetomidine was effective to achieve a target sedation score. De novo opioid boluses were associated with increased ICP and reduced cerebral perfusion pressure. Ketamine bolus and infusions were not associated with increased ICP and may reduce the incidence of cortical spreading depolarization events. In conclusion, there is a paucity of high-quality evidence to inform the optimal use of analgosedative agents in the management of m-sTBI, inferring significant scope for further research.
Sedation is frequently an integral part of treatment in brain-injured patients and has general and specific indications. Sedation may also have detrimental consequences for those patients. Hence, the choice of sedation is of utmost importance for their management and should be done on an individual basis. This choice should take account of the type and depth of needed sedation, and the eventual necessity of intermittent windows to assess the neurological status of the patient, the underlying brain injury and severity, the patient physical characteristics, his/her past medical history, and comorbidities, his/her hemodynamic, hepatic, and renal status, eventual interactions between medications or adverse reactions, and the locally available resources. In the first part of this chapter, we review the pharmacokinetic and pharmacodynamic properties of the most frequently used sedative agents, namely propofol, benzodiazepines, α2-adrenergic agonists, inhaled anesthetic agents, opioids, barbiturates, and ketamine. The second part of this chapter deals with the evidence-based practical use of each agent in the neuro-intensive care setting, their side effects, and their influence on specific outcomes. In the end, and based on the available information in the literature, we conclude by our view and pragmatic approach to sedation in neuro-intensive care patients.
Traumatic brain injury (TBI) is the leading cause of mortality and morbidity with a
high incidence in young people all over the world. Post-concussive syndrome (PCS)
is an international public health concern with 5–10% of mild TBI (mTBI) cases
experiencing concussion in their lives and about 20% of patients having persistent
PCS within 6 months to 1 year after mTBI. There are many advanced techniques
and methods for the investigation of brain changes and treatments in TBI patients
and each of these techniques provides important insights into pathophysiology due
to head injury but may not be limited to conventional methods. This new information emerges to give a broad picture of TBI research and clinical evaluation such as
cumulative mild head injury (CMHI), novel neuroimaging findings and biomarkers, neuroprotective treatments, brain cooling, and sedation in TBI patients, as well
as neuronal and glial biomarkers.
The first section of the book introduces disease neurobiology and PCS. Chapter 1
“Post-Concussion Syndrome” describes the definition of PCS, classification, and
association with brain dysfunction, blood flow regulation, intracranial pressure
change, and the role of neuroinflammation, as well as long-term sequelae such as
chronic traumatic encephalopathy and treatment. Discussing PCS problems in TBI
for the improvement of clinical diagnosis based on several definitions is challenging
given subjective and gross aspects of the assessments of PCS, e.g. Glasgow comma
scale and loss of conscious. This chapter provides many characteristics of PCS,
including classification, association with autonomic nervous system dysfunction,
brain changes, and treatment that could serve as a reference resource for further
research. Chapter 2 “Neuroprotection, Photoperiod, and Sleep” investigates the
neurobiological basis of neuroprotective activation, and correlation with PCS,
including sleep. The authors attempt to explain the neurobiological basis of neuro-
protective activation, adaptive response to photoperiod possibly due to injury of the
the suprachiasmatic nucleus, and correlation with post-traumatic symptoms, including
sleep, as well as limitations. This chapter provides clues to studying the relation-
ships between neuroprotection and sleep as well as the involved neurotransmission
systems.
The second section of the book covers the imaging diagnosis and biomarkers in
TBI. Chapter 3 “Cumulative Mild Head Injury (CMHI) in Contact Sports” provides
a CMHI review, brain changes, and risk factors. This chapter briefly overviews the
structure and neuroanatomy of brain change to illustrate the pathophysiological
mechanisms involved in primary and secondary head injuries. Some relatively new
imaging perspectives, including diffusion axonal injury, close-head injury, homeostasis irregulation, and tauopathy, are illustrated concisely. Risk factors for all types
of CMHI are described further with details for early prevention and cure. Chapter 4
“Neuronal and Glial Biomarkers Research for Traumatic Brain Injury” studies
multiple biomarkers, including S-100β, UCH-L1, and GFAP for blood–brain barrier
breakdown and neuronal injury. The sensitivity and specificity of each biomarker
from published articles as well as the ratio between GFAP and UCH-L1 are reported
with confirmative statistical results and table summaries. This chapter gives a full
overview of the most promising biomarkers studied as predictors of the severity of TBI, with a special focus on their nature, location, basal concentrations, and
methods by which they can be quantified efficiently in blood samples.
The third section refers to the treatment of and multiple therapeutic strategies in
TBI patients. Chapter 5 “Use of Neuroprotective Agents for Traumatic Brain Injury”
evaluates more than 12 neuroprotective agents from 32 studies with objective data
and statistical analyses. Complete descriptions of significance, improvements, and
side effects of each agent are covered in detail with the conclusion that a few agents,
including oxygen, cyclosporine A, and rivastigmine use for different phases of TBI,
show promising treatment effects. Authoritative statements, comprehensive citations, and confirmation with scientific and solid evidence are strong points of this
chapter. Chapter 6 “Direct Brain Cooling in Treating Severe Traumatic Head Injury”
addresses the interesting and promising topic of hypothermia as a neuroprotective
effect in TBI patients. The benefits of cooling, especially of mild cooling such as
brain oxygen level reaching desirable levels and a better Glasgow outcome scale at
6 months follow-up, are described and analyzed scientifically with a new cooling
machine D-Brain therapy. This chapter highlights the encouraging results of pilot
research on direct focal brain cooling therapy in severe head injury patients with
significant clinical outcome results in a mild cooling group due to elevations in oxygenation level of injured and decompressed brain tissues. The last chapter “Sedation
in TBI Patients” discusses sedation in TBI as a neurocritical and therapeutic strategy
with different assessments. The main pharmacological principles, neurophysiology,
and neuropathology of sedatives and analgesics, including propofol, benzodiazepines, and opioids, are outlined and evaluated. Several topics and properties based
on new technologies, including physiological indications, status epilepticus treatment, management, monitoring in the neuro-ICU with various scales and neuro-
logic examinations, are integrated for better diagnosis and treatment improvement.
Background:
Sedation/analgesia is a daily challenge faced by intensivists managing patients with brain injury (BI) in intensive care units (ICUs). The optimization of sedation in patients with BI presents particular challenges. A choice must be made between the potential benefit of a rapid clinical evaluation and the potential exacerbation of intracranial hypertension in patients with impaired cerebral compliance. In the ICU, a pragmatic approach to the use of sedation/analgesia, including the optimal titration, management of multiple drugs, and use of any type of brain monitor, is needed. Our research question was as follows: the aim of the study is to identify what is the current daily practice regarding sedation/analgesia in the management of patients with BI in the ICU in France?
Methods:
This study was composed of two parts. The first part was a descriptive survey of sedation practices and characteristics in 30 French ICUs and 27 academic hospitals specializing in care for patients with BI. This first step validates ICU participation in data collection regarding sedation-analgesia practices. The second part was a 1-day prospective cross-sectional snapshot of all characteristics and prescriptions of patients with BI.
Results:
On the study day, among the 246 patients with BI, 106 (43%) had a brain monitoring device and 74 patients (30%) were sedated. Thirty-nine of the sedated patients (53%) suffered from intracranial hypertension, 14 patients (19%) suffered from agitation and delirium, and 7 patients (9%) were sedated because of respiratory failure. Fourteen patients (19%) no longer had a formal indication for sedation. In 60% of the sedated patients, the sedatives were titrated by nurses based on sedation scales. The Richmond Agitation Sedation Scale was used in 80% of the patients, and the Behavioral Pain Scale was used in 92%. The common sedatives and opioids used were midazolam (58.1%), propofol (40.5%), and sufentanil (67.5%). The cerebral monitoring devices available in the participating ICUs were transcranial Doppler ultrasound (100%), intracranial and intraventricular pressure monitoring (93.3%), and brain tissue oxygenation (60%). Cerebral monitoring by one or more monitoring devices was performed in 62% of the sedated patients. This proportion increased to 74% in the subgroup of patients with intracranial hypertension, with multimodal cerebral monitoring in 43.6%. The doses of midazolam and sufentanil were lower in sedated patients managed based on a sedation/analgesia scale.
Conclusions:
Midazolam and sufentanil are frequently used, often in combination, in French ICUs instead of alternative drugs. In our study, cerebral monitoring was performed in more than 60% of the sedated patients, although that proportion is still insufficient. Future efforts should stress the use of multiple monitoring modes and adherence to the indications for sedation to improve care of patients with BI. Our study suggests that the use of sedation and analgesia scales by nurses involved in the management of patients with BI could decrease the dosages of midazolam and sufentanil administered. Updated guidelines are needed for the management of sedation/analgesia in patients with BI.
Sedation and analgesia are used in the neurocritically ill patient to treat discomfort associated with routine ICU care and to minimize ICP elevations. Particularly important in this critically ill population is the use of short-acting agents to allow for frequent neurologic assessments. Pharmacologic coma is reserved for limited indications such as refractory intracranial hypertension and status epilepticus. The BPS and CPOT assessment scores have received limited validation in small studies, and are recommended for the assessment of pain in patients with neurologic injury who cannot self-report pain; the Nociception-Coma Scale-Revised may be useful in patients with prolonged comatose states. Opioids, including meperidine, have particular indications in the prevention and treatment of shivering in patients undergoing targeted temperature management (TTM). In patients undergoing TTM after cardiac arrest, impaired metabolism and clearance of medications – including fentanyl, morphine, and remifentanil – is proportional to the depth of hypothermia and may significantly increase serum drug levels. Accumulation of sedative doses received during TTM must be accounted for, and sufficient time allowed for awakening before accurate prognostication in patients who do not regain consciousness. Morphine and alternative opioids are also specifically indicated in the treatment of paroxysmal sympathetic hyperactivity to treat and reduce recurrence of storming episodes.
This article introduces the basic concepts of intracranial physiology and pressure dynamics. It also includes discussion of signs and symptoms and examination and radiographic findings of patients with acute cerebral herniation as a result of increased as well as decreased intracranial pressure. Current best practices regarding medical and surgical treatments and approaches to management of intracranial hypertension as well as future directions are reviewed. Lastly, there is discussion of some of the implications of critical medical illness (sepsis, liver failure, and renal failure) and treatments thereof on causation or worsening of cerebral edema, intracranial hypertension, and cerebral herniation.
Severe traumatic brain injury physiologically is a heterogeneous disorder that is characterized by a cascade of events from the “second-hit” phenomenon. The management of these patients is becoming increasingly sophisticated with the introduction of multimodal monitoring systems and better understanding of the complex interactions of the brain and other vital organs. Many of the traditional therapeutic options still lack level 1 evidence, however, this chapter is focused on the key therapeutic options that significantly impact the outcome of severe TBI patients.
Pain relief and the avoidance of stress and agitation may help to keep intracranial pressure (ICP) within acceptable levels. Sedatives and analgesics are thus an important part in the treatment of severe traumatic brain injury (TBI). In this chapter, the most common sedative and agents and analgesics are discussed in a setting with severe TBI. All available drugs used have their pros and cons, and the scientific evidence regarding which drugs to use is still scarce. Propofol has the advantage to be short-acting and therefore is recommended when using wake-up tests. The risk for propofol infusion syndrome (PRIS), however, must be considered, especially in children.
Das postoperative Delir tritt bei rund einem Drittel der älteren Patienten auf. Es handelt sich um eine schwere Komplikation, die für die betroffenen Patienten und ihre Angehörigen sehr belastend ist. Der Hausarzt, der zumindest bei elektiven Operationen für die Operationsvorbereitung verantwortlich ist, kann Maßnahmen treffen, um das Risiko für ein postoperatives Delir so gering wie möglich zu halten.
Supratentorial tumors account for approximately 80% of all brain tumors in adults and constitute the majority of neurosurgical conditions that present for craniotomy. The nature of the lesions varies from benign tumors like meningiomas, pituitary adenomas to highly malignant tumors like glioblastomas. An anesthesiologist may encounter a patient with a supratentorial tumor for an elective planned surgery, thus allowing adequate time for optimization or for an acute neurologic deterioration, requiring emergent intervention. Understanding supratentorial tumors’ pathophysiology and implications of their effects not only on the neurological system, but also on other bodily systems like the endocrine, is crucial for delivering a safe and optimal anesthetic. The perioperative goals for supratentorial tumor resection are to optimize cerebral perfusion, oxygenation, and operative conditions, bestow neuroprotection, facilitate rapid and smooth awakening for postoperative neurological evaluation, minimize postoperative pain, and improve the oncological outcomes. It is important to avoid any secondary systemic insults. An ideal anesthetic regimen should deliver adequate amnesia and analgesia while maintaining systemic and cerebral milieu along with reduction in CMR and ICP. The different stages of anesthesia, from induction to emergence, entail idiosyncrasies that calls for tailored medication delivery, special positioning and monitoring. Intracranial hypertension, brain edema, seizure, and sequelae of endocrinopathies like DI, SIADH, or CSW are features of some brain tumors that need to be considered as understanding of their effects can guide how and when hyperosmolar solutions, diuretics, steroids, antiepileptics, and/or colloids are administered.
Increased intracranial pressure (ICP) is frequently encountered in the neurosurgical setting. A multitude of tactics exists to reduce ICP, ranging from patient position and medications to cerebrospinal fluid diversion and surgical decompression. A vast amount of literature has been published regarding ICP management in the critical care setting, but studies specifically tailored toward the management of intraoperative acute increases in ICP or brain bulk are lacking. Compartmentalizing the intracranial space into blood, brain tissue, and cerebrospinal fluid and understanding the numerous techniques available to affect these individual compartments can guide the surgical team to quickly identify increased brain bulk and respond appropriately. Rapidly instituting measures for brain relaxation in the operating room is essential in optimizing patient outcomes. Knowledge of the efficacy, rapidity, feasibility, and risks of the various available interventions can aid the team to properly tailor their approach to each individual patient. In this article, we present the first evidence-based review of intraoperative management of ICP and brain bulk.
Traumatic brain injury is a cause of significant morbidity and mortality. TBI involves primary injury as a result of physical impact and secondary injury is delayed injury that occurs as a result of local and systemic mediators. Most of the treatment for TBI is directed at minimizing the effects of secondary injury. Treatment is focused on maximizing cerebral perfusion pressure and minimizing the effects of intracranial pressure.
Das Phänomen des Delirs ist mit vielen Komplikationen verbunden, die darüber hinaus betroffene Patienten in eine weitere Pflegebedürftigkeit bringen können. Die Risikofaktoren sind seit Jahren bekannt und erfordern ein besonderes Augenmerk, da hieraus weitere Handlungen zwangsläufig resultieren. Dies gilt besonders für Menschen im Krankenhaus höheren Alters mit multimorbiden Zuständen. Eine adäquate Delirtherapie kann jedoch nur gelingen, wenn dieses vorher erkannt wurde — damit ist klar, dass Screening- und Assessmentinstrumente routinemäßig eingesetzt werden müssen, um darauf aufbauend eine geeignete Therapie einzuleiten. Dabei wird deutlich, dass dieses Phänomen im interprofessionellen Kontext betrachtet werden muss und Angehörige ebenso einen elementaren Baustein in der Therapie darstellen.
In the neurointensive care setting, specific considerations of sedation are required; sedation may act as a therapeutic agent itself, when causing a reduction in cerebral metabolic rate of oxygen, cerebral blood flow, and intracranial pressure and in the incidence of seizures. However, the physician must be aware of the effects of every sedative agent on cerebral physiology, in order to obtain beneficial effects and avoid side effects. In this chapter, the need of sedation and its assessment and the effects of sedative agents are described in order to provide knowledge for an adequate sedative strategy.
Patients with brain injury of any etiology are at risk for developing increased intracranial pressure. Acute intracranial hypertension is a medical emergency requiring immediate intervention to prevent permanent damage to the brain. Intracranial pressure as an absolute value is not as valuable as when one investigates other important associated variables such as cerebral perfusion pressure and contributing factors for an adequate cerebral blood flow. This manuscript reviews a number of various interventions that can be used to treat acute intracranial hypertension and optimize cerebral perfusion pressure. Management options are presented in an algorithm-format focusing on current treatment strategies and treatment goals. In addition to the efficacy, clinicians must consider significant adverse events that are associated with each therapy prior to initiating treatment. The initial step includes elevation of head of the bed and adequate sedation followed by osmotic agents such as mannitol and hypertonic saline infusion. Hypothermia and pentobarbital therapy represent more aggressive steps, and utilize different mechanisms by which the pressure is controlled, likely causing significant reduction in metabolism. Surgical intervention may precede any medical therapy in order to provide more robust response in controlling intracranial hypertension in certain cases.
Key Words: Intracranial pressure; Intracranial hypertension; Cerebral perfusion pressure; Cerebral blood flow; Hypothermia; Osmotic agents
In order to evaluate the safety of the new synthetic opioids, alfentanil and sufentanil, in neurosurgical patients, we administered sufentanil 1 [mu]g/kg i.v., alfentanil 50 [mu]g/kg i.v. followed by an infusion of 1 [mu]g/kg/min, or fentanyl 5 [mu]g/kg i.v. to 30 patients with supratentorial tumors anesthetized with nitrous oxide (N2O), 60% in O2. Lumbar cerebrospinal fluid pressure (CSFP) and mean arterial pressure (MAP) responses were recorded for 10 min thereafter, while ventilation was held constant [mean PaCO2 = 36.1 +/- 1.0 mm Hg (SEM)]. There was no change in CSFP after fentanyl. In contrast, both sufentanil and alfentanil caused increases in CSFP, equal to 89 +/- 31 % SE (p < 0.05) and 22 +/- 5% (p < 0.05), respectively. MAP decreased after administration of each opioid. Peak decreases in cerebral perfusion pressure (MAP - CSFP) were 14 +/- 3% after fentanyl, 25 +/- 5% after sufentanil, and 37 +/- 3% after alfentanil. It is concluded that because sufentanil increased CSFP in patients who have brain tumors, it also may be contraindicated in other neurosurgical patients at risk for intracranial hypertension. Alfentanil may share this propensity, since CSFP increased despite a profound reduction in MAP. Among the three opioids evaluated, only fentanyl appears to be appropriate for supplementing N2O-2 anesthesia in patients who have compromised intracranial compliance.
Opioids, when administered in large doses, produce brain damage, primarily in the limbic system and association areas in rats.This investigation examined the relationship between opioid dose and severity and frequency of brain damage in rats. Forty male Sprague-Dawley rats were anesthetized with halothane/N2 O and underwent tracheal intubation, mechanical ventilation, arterial/venous cannulation, and insertion of a rectal temperature probe and biparietal electroencephalogram electrodes. After surgery, halothane was discontinued and O2/N2 O 30%/70% was administered for 1 h. Rats were then randomly assigned to one of eight groups. The control group received a loading dose (LD) of 4 mL/kg of 0.9% normal saline solution (NSS) and a maintenance dose (MD) of 4 mL [centered dot] kg-1 [centered dot] h-1 NSS. The other groups were given fentanyl lypophilized and reconstituted in NSS with the LD ranging from 50 to 3200 micro g/kg and the MD from 2 to 128 micro g [centered dot] kg-1 [centered dot] min-1. After 2 h of fentanyl or NSS infusion, all rats received 100% O2 and, when alert, their tracheas were extubated; after 7 days the rats underwent cerebral perfusion fixation, followed by light microscopic evaluation. Histopathologic lesions (primarily eosinophilic neuron degeneration) were subjectively graded by a pathologist unaware of the experimental treatment; the grades were based on the percentage of dead neurons. There were no lesions observed in the brain areas in any of the control or 200-8 (LD, micro g/kg; MD, micro g [centered dot] kg-1 [centered dot] min-1) groups. Eleven of 20 rats in the 400-16, 800-32, 1600-64, and 3200-18 groups showed evidence of brain damage primarily in limbic system structures and association areas (P < 0.05). Our data confirm that fentanyl produces limbic system brain damage in rats, and that the damage occurs over a broad range of doses. (Anesth Analg 1996;83:1298-306)
In order to evaluate the safety of the new synthetic opioids, alfentanil and sufentanil, in neurosurgical patients, we administered sufentanil 1 [mu]g/kg i.v., alfentanil 50 [mu]g/kg i.v. followed by an infusion of 1 [mu]g/kg/min, or fentanyl 5 [mu]g/kg i.v. to 30 patients with supratentorial tumors anesthetized with nitrous oxide (N2O), 60% in O2. Lumbar cerebrospinal fluid pressure (CSFP) and mean arterial pressure (MAP) responses were recorded for 10 min thereafter, while ventilation was held constant [mean PaCO2 = 36.1 +/- 1.0 mm Hg (SEM)]. There was no change in CSFP after fentanyl. In contrast, both sufentanil and alfentanil caused increases in CSFP, equal to 89 +/- 31 % SE (p < 0.05) and 22 +/- 5% (p < 0.05), respectively. MAP decreased after administration of each opioid. Peak decreases in cerebral perfusion pressure (MAP - CSFP) were 14 +/- 3% after fentanyl, 25 +/- 5% after sufentanil, and 37 +/- 3% after alfentanil. It is concluded that because sufentanil increased CSFP in patients who have brain tumors, it also may be contraindicated in other neurosurgical patients at risk for intracranial hypertension. Alfentanil may share this propensity, since CSFP increased despite a profound reduction in MAP. Among the three opioids evaluated, only fentanyl appears to be appropriate for supplementing N2O-2 anesthesia in patients who have compromised intracranial compliance.
(C) Lippincott-Raven Publishers.
The current study investigates the effects of sufentanil on cerebral blood flow velocity and intracranial pressure (ICP) in 30 patients with intracranial hypertension after severe brain trauma (Glasgow coma scale < 6).
Mechanical ventilation (FIO2 0.25-0.4) was adjusted to maintain arterial carbon dioxide tensions of 28-30 mmHg. Continuous infusion of midazolam (200 micrograms/kg/h intravenous) and fentanyl (2 micrograms/kg/h intravenous) was used for sedation. Mean arterial blood pressure (MAP, mmHg) was adjusted using norepinephrine infusion (1-5 micrograms/min). Mean blood flow velocity (Vmean, cm/s) was measured in the middle cerebral artery using a 2-MHz transcranial Doppler sonography system. ICP (mmHg) was measured using an epidural probe. After baseline measurements, a bolus of 3 micrograms/kg sufentanil was injected, and all parameters were continuously recorded for 30 min. The patients were assigned retrospectively to the following groups according to their blood pressure responses to sufentanil: group 1, MAP decrease of less than 10 mmHg, and group 2, MAP decrease of more than 10 mmHg.
Heart rate, arterial blood gases, and esophageal temperature did not change over time in all patients. In 18 patients, MAP did not decrease after sufentanil (group 1). In 12 patients, sufentanil decreased MAP > 10 mmHg from baseline despite norepinephrine infusion (group 2). ICP was constant in patients with maintained MAP (group 1) but was significantly increased in patients with decreased MAP. Vmean did not change with sufentanil injection regardless of changes in MAP.
The current data show that sufentanil (3 micrograms/kg intravenous) has no significant effect on middle cerebral artery blood flow velocity and ICP in patients with brain injury, intracranial hypertension, and controlled MAP. However, transient increases in ICP without changes in middle cerebral artery blood flow velocity may occur concomitant with decreases in MAP. This suggests that increases in ICP seen with sufentanil may be due to autoregulatory decreases in cerebral vascular resistance secondary to systemic hypotension.
Although opioids frequently are administered to patients with severe head trauma, the effects of such drugs on intracranial pressure are controversial. Nine patients with severe head trauma were studied for the effects of fentanyl and sufentanil on intracranial pressure (ICP). In all patients, ICP monitoring was instituted before the study. Full neuromuscular blockade was achieved with vecuronium bromide before the administration of either fentanyl (3 micrograms.kg-1) or sufentanil (0.6 microgram.kg-1) as an intravenous bolus over a 1-min period in a masked and random fashion. Patients received the other opioid in the same fashion 24 h later. Arterial blood pressure, heart rate, and ICP were recorded continuously for the 1 h after drug administration. Fentanyl was associated with an average ICP increase of 8 +/- 2 mmHg, and sufentanil with an increase of 6 +/- 1 mmHg. These increases were statistically significant. Both drugs produced clinically mild decreases in mean arterial blood pressure (fentanyl, 11 +/- 6 mmHg; sufentanil, 10 +/- 5 mmHg) that nevertheless were statistically significant. No significant changes in heart rate occurred. These results indicate that modest doses of potent opioids can significantly increase ICP in patients with severe head trauma.
We evaluated the effect of alfentanil on hippocampal glucose utilization and histopathology associated with alfentanil-induced seizures. Three separate experiments were performed. First, anesthetized, paralyzed Long-Evans rats (n = 15; 5 rats per group) were mechanically ventilated and randomly assigned to three groups: (a) control, 70% N2O and 30% O2 continued for 1 h; (b) low-dose alfentanil (150 mug/kg IV bolus), followed by infusion at 15 mug.kg-1.min-1 for 1 h without N2O; or (c) high-dose alfentanil (1000 mug/kg IV bolus), followed by infusion at 100 mug.kg-1.min-1 for 1 h without N2O. After 1 h, [6-C-14]glucose was injected intravenously for autoradiography. With high-dose alfentanil, there was increased glucose utilization in the ventral hippocampus and the lateral septal nucleus. In the second experiment, anesthetized, paralyzed Sprague-Dawley rats (n = 12; 4 rats per group) were mechanically ventilated, underwent insertion of hippocampal depth electrodes, and were randomly assigned to three groups: (a) control, 70% N2O and 30% O2; (b) low-dose alfentanil (150 mug/kg IV bolus), with 70% N2O and 30% O2; or (c) high-dose alfentanil (1000 mug/kg IV bolus), with 70% N2O and 30% O2. An epileptiform pattern was observed on hippocampal and subdermal electroencephalographic recordings in both alfentanil groups. In the third experiment, anesthetized, paralyzed Sprague-Dawley rats (n = 20) were mechanically ventilated and assigned to two groups: (a) control, 70% N2O and 30% O2 (n = 5) or 100% O2 (n = 5) continued for 1 h; or (b) alfentanil (2000 mug/kg IV bolus), followed by infusion at 33.3 mug.kg-1.min-1 for 1 h with 100% O2. After tracheal extubation, the rats recovered overnight. Light-microscopic evaluation revealed hippocampal or amygdaloid damage in 6 of the 10 alfentanil-treated rats. High doses of alfentanil administered to rats can produce limbic system seizure activity with hypermetabolism associated with neuropathologic lesions.
mu opioids, such as morphine and certain enkephalin analogs, are known to modulate glutamate-evoked activity in dorsal horn neurons in the spinal cord and caudal brain stem. Yet the molecular mechanism by which this modulation occurs is not understood. We examined the interactions between glutamate and a selective mu opioid receptor agonist, D-Ala2-MePhe4-Gly-ol5-enkephalin (DAGO), in spinal trigeminal neurons in thin medullary slices of rats. DAGO caused a sustained increase in glutamate-activated currents that are mediated by N-methyl-D-aspartate receptors. Intracellularly applied protein kinase C (PKC) mimics the effect of DAGO, and a specific PKC inhibitor interrupts the sustained potentiation produced by DAGO. Thus, PKC plays a key role in mediating the action of mu opioid peptides.
The effects of sufentanil on intracranial pressure, mean arterial pressure, cerebral perfusion pressure and heart rate were studied in 20 neurosurgical intensive care unit patients. Epidural intracranial pressure probes were implanted in patients who suffered head injury, intracerebral haemorrhage or underwent tumour resection. Sufentanil was given intravenously in sequential doses of 0.5, 1.0 and 2.0 micrograms/kg. Fifteen minutes elapsed after each dose. The patients were allocated to either group 1 (baseline intracranial pressure less than 20 mmHg) or group 2 (baseline intracranial pressure greater than 20 mmHg). Intracranial pressure did not change significantly in either group. Therefore the falls in mean arterial pressure with the highest dose in both groups and with 1.0 micrograms/kg in group 2, closely reflect corresponding reductions in cerebral perfusion pressure. As sufentanil in itself exerts no effects on intracranial pressure, concomitant haemodynamic changes are the critical factor for an adequate cerebral perfusion pressure.
The effects of alfentanil on intracranial pressure in patients with diminished intracranial compliance has not been established. Ten patients with hydrocephalus of varying etiologies, ages 16 months to 20 yr, presenting for ventriculoperitoneal shunt revision were studied. Following induction of anesthesia with thiopental, nitrous oxide/oxygen, and isoflurane, the trachea was intubated and anesthesia was maintained with isoflurane (0.5%), nitrous oxide (70%), and oxygen. After a minimum of 30 min and after the new shunt was placed, alfentanil was administered in increments of 10, 20, and 40 micrograms/kg at 3-min intervals, and intracranial pressure was measured over 12 min via the new shunt. In these unstimulated, normocapnic (PETCO2 32-38 mmHg) patients, heart rate, mean arterial pressure, and cerebral perfusion pressure declined from 110 +/- 26 beats/min, 90 +/- 11 mmHg, and 71 +/- 14 mmHg, to 84 +/- 25 beats/min, 66 +/- 11 mmHg, and 45 +/- 16 mmHg (mean +/- SD), respectively, by 3 min after the third dose (P less than 0.001). Intracranial pressure did not change from baseline (19 +/- 14 mmHg vs. 21 +/- 11) after any dose of alfentanil. Contrary to earlier studies in adult patients with brain tumors, the authors found that alfentanil, in pediatric patients with hydrocephalus anesthetized with oxygen, nitrous oxide, and isoflurane, did not increase intracranial pressure within a 9-min study period. The significant decreases in cerebral perfusion pressure observed merit concern and further study.
The intracranial and systemic hemodynamic effects of sufentanil (20 micrograms/kg) were studied in 10 mongrel dogs. Baseline anesthesia was maintained with 0.7% end-tidal isoflurane and 50% nitrous oxide in oxygen. Catheters were inserted for blood pressure measurement, arterial and sagittal sinus blood sampling, radioactive microsphere injections, and intracranial pressure monitoring. Blood flow velocity was measured continuously in the middle cerebral artery using a transtemporal approach through a cranial window with a pulsed 8 MHz transcranial Doppler system (TCD). Cardiac output was measured using an electromagnetic flow probe on the pulmonary artery. After baseline measurements, sufentanil was injected and data were recorded at 5, 15, and 30 min. In group 1 (n = 5) blood pressure was not controlled, whereas in group 2 (n = 5) blood pressure was maintained at baseline levels with a phenylephrine infusion. Sufentanil decreased blood pressure from 120 +/- 10 mm Hg (mean +/- SEM) to 82 +/- 11 mm Hg in group 1. Cardiac output decreased 40%-50% in both groups. Intracranial pressure did not change. Cerebral blood flow (CBF) and TCD blood flow velocity decreased significantly (35%-40%) with no difference between groups. Relative decreases in CBF and TCD blood flow velocity were closely correlated (r = 0.82). The cerebral hemodynamic changes were associated with a 35%-40% decrease in cerebral oxygen consumption. We conclude that sufentanil decreases CBF in response to decreased metabolic demand without significantly affecting intracranial pressure. Relative changes in CBF can be reproducibly monitored using TCD.
Using intracellular recording techniques, we characterized synaptic responses of CA3 pyramidal cells to mu and kappa agonists in hippocampal slices from rats and guinea pigs. In rat CA3 pyramidal cells, the mu selective agonist (N-MePhe3,D-Pro4)-morphiceptin (PLO17) inhibited both the early and the late inhibitory postsynaptic potentials (IPSPs) and increased excitatory postsynaptic potential (EPSP) amplitudes. Voltage clamp analysis of synaptic currents indicated that the excitatory postsynaptic current were not increased by PLO17, showing that the apparent increase in EPSPs was a result of a decrease in the underlying IPSP. The kappa agonists trans-(+)-3,4-dichloro-N-[2-(1-pyrrolidinyl)cyclohexyl]-benzeneacetamide methanesulfonate and dynorphin A (1-17) had no effect on EPSPs or IPSP conductances measured in rat pyramidal cells. Maximal inhibition of IPSPs by PLO17 resulted in a bursting response to stimulation in rat but not guinea pig CA3 pyramidal cells. In guinea pig CA3 pyramidal cells, PLO17 also inhibited IPSP conductances but did not affect EPSP amplitudes. In contrast to the lack of effect in rat pyramidal cells, trans-(+)-3,4-dichloro-N-[2-(1-pyrrolidinyl)cyclohexyl]-benzeneacetamide methanesulfonate (100 nM) inhibited the late IPSP conductance without influencing the EPSP or the early IPSP conductance of guinea pig pyramidal cells. Dynorphin A (1-17) (0.01-10 microM) did not affect resting membrane properties or evoked synaptic conductances in either preparation. Mu receptor activationin the CA3 of rats and guinea pigs results in the inhibition of inhibitory synaptic input to pyramidal cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Using a prospective, randomized, and double-blind study design, alfentanil (n = 15), fentanyl (n = 14), or sufentanil (n = 16), in combination with N2O, were administered to patients undergoing craniotomy for supratentorial tumor resection. Physicians were given two syringes, one of which was labeled as "load" for the initial loading dose and the other as "maintenance" for continuous infusion. The concentration of drug in each syringe was adjusted to permit administration on a milliliter per kilogram basis. The target loading doses for alfentanil, fentanyl, and sufentanil were 75, 10, and 1 microgram/kg, respectively, and initial infusion rates were 33.5, 2.0, and 0.3 microgram.kg-1.h-1, respectively. Additional supplementary boluses and changes in maintenance infusion rate were made according to predetermined guidelines. Isoflurane, in increasing 0.2% inspired increments, was used only when the maximum allowed opioid dose had been given (i.e., supplementary bolus doses equal to 75% of the calculated loading dose or supplementary bolus doses equal to 50% of the calculated loading dose combined with a 50% increase in the maintenance infusion rate). Opioid infusions were stopped at the time of bone flap replacement. Antihypertensive medications and naloxone were subsequently given at the discretion of the anesthesiologist. Group demographics were not different. Total volumes of drug were similar among groups indicating equipotent preparations. Administration of isoflurane, antihypertensive medications, and naloxone were not different among groups. Although decreases in blood pressure seen with induction were similar among groups, alfentanil-treated patients received ephedrine more frequently before intubation. Thirty minutes after entry into the postanesthesia recovery area, respiratory rate and pH were lowest in sufentanil-treated patients.(ABSTRACT TRUNCATED AT 250 WORDS)
The effects on the cerebrospinal fluid pressure (CSFP) of alfentanil and fentanyl were compared during nitrous oxide-oxygen (N2O-O2) anesthesia in 24 patients who had brain tumors. Monitored variables included CSFP (lumbar subarachnoid catheter), heart rate from electrocardiographic lead II, mean radial arterial blood pressure, and arterial blood gas tensions. General anesthesia was induced with thiopental, 5 mg/kg IV in divided doses, and maintained with 70% N2O in O2; ventilation was held constant (PaCO2 = 37.4 +/- 1.6 mm Hg [mean +/- SEM]). After baseline data were recorded, 16 subjects were randomly assigned to receive either 5 micrograms/kg fentanyl as an intravenous bolus or 50 micrograms/kg alfentanil as an intravenous bolus, followed by an infusion of alfentanil at 1 micrograms.kg-1.min-1. Monitored variables were continuously recorded for 15 min after opioid injection. A third group of 8 patients was studied subsequently; they received only N2O-O2 during a 15-min observation period and served as controls. Blood pressure was held constant with an intravenous infusion of 0.1% phenylephrine, as needed; noxious stimulation was carefully avoided. Cerebrospinal fluid pressure remained unchanged both in patients who received N2O-O2 alone and in those who received fentanyl-N2O-O2. By contrast, those who received alfentanil-N2O-O2 had a gradual increase in CSFP, reaching 30% above baseline values after 10 min and stabilizing thereafter. Although the absolute increase in CSFP during normocarbic alfentanil-N2O anesthesia was relatively small (9.5 +/- 1.3 mm Hg to 13.0 +/- 1.3 mm Hg [mean +/- SE], P less than 0.05), the absence of a similar effect after fentanyl administration suggests that precautionary measures such as hyperventilation are advisable if alfentanil is used for potentiating normocarbic N2O-O2 anesthesia in neurosurgical patients with intracranial mass lesions.
The cerebral and peripheral vascular effects of sufentanil (10-200 micrograms/kg) were examined in dogs. The cerebral blood flow (CBF) was measured continuously by an electromagnetic flow probe on the outflow of the posterior sagittal sinus. Sufentanil at all doses significantly increased CBF that lasted for approximately 20 min. The CBF then gradually decreased so that it was significantly below baseline levels by the end of the 60-min study period. The transient increase in CBF was accompanied by an equally transient statistically significant decrease in cerebrovascular resistance. Intracranial pressure did not change. Sufentanil produced an electroencephalographic pattern of deep anesthesia accompanied by a decrease in cerebral oxygen consumption significantly below baseline levels. At the end of the study tissue concentrations of metabolites taken from the cerebral hemispheres were within normal limits, indicative of a normal cerebral energy state. Sufentanil had little effect on systemic hemodynamics. The observation that sufentanil significantly increases CBF in the absence of seizure activity makes it unique among the narcotics. It is hypothesized that in the presence of decreased intracranial compliance, this sudden increase in CBF, although transient, may be detrimental if it is accompanied by an acute increase in intracranial pressure which could produce cerebral ischemia.
Under halothane anesthesia five dogs were prepared with both hindlimbs isolated from the systemic circulation to allow intermittent placement on extracorporeal perfusion at constant flow. One limb of each dog was surgically denervated. In this relatively anesthetic-free preparation, graded equivalent doses of alfentanil, fentanyl, and sufentanil were infused over 30 s, and vascular resistance was measured. Increasing opioid administration caused a progressive diminution in peripheral resistance. By the high dose level, alfentanil (500 micrograms/kg), fentanyl (50 micrograms/kg), and sufentanil (6 micrograms/kg) caused equal and significant decreases of 48%, 48%, and 44% in resistance, respectively. There was no difference among the opioids in effects on resistance at equivalent dosages. Neither pretreatment with naloxone nor denervation changed the response to the narcotics. We conclude that the three synthetic opioids produce vasodilation by direct action on the peripheral vascular smooth muscle.
The present study examines both the local and neurally mediated effects of sufentanil, a new synthetic opioid, on the vascular resistance of the isolated, separately perfused canine gracilis muscle. Infusions (50 micrograms/min) of sufentanil into the gracilis arteries of nine denervated gracilis muscles did not produce a direct vascular effect. Because morphine has been previously shown to produce a central sympatholytic effect, the neural effect of sufentanil was examined in 12 innervated muscles under conditions of either low or high background sympathetic activity produced by either hemorrhage or transfusion of the dog. After i.v. sufentanil (20 micrograms/kg), all dogs experienced a rapid parallel fall in gracilis vascular resistance (GVR) and mean arterial pressure. The GVR decreased under conditions of high and low sympathetic activity. With low sympathetic tone, the GVR decreased from a control value of 24.1 +/- 4.4 S.E.M. to 6.6 +/- 0.8 resistance units (RU), a value below the subsequently denervated level (13.2 +/- 2.5 RU) (P less than .05). In hemorrhaged animals with elevated control sympathetic tone, resistance declined from 38.4 +/- 9.1 to 26.1 +/- 4.4 RU (P less than .05) but did not reach the denervated level (12.4 +/- 2.7 RU). Local intra-arterial pharmacologic blockade of the gracilis muscle was performed in animals with low sympathetic tone. Intra-arterial atropine did not effect the neurogenic vasodilatory response to sufentanil, whereas prazosin abolished it. Intra-arterial H1 and H2 receptor blockade prevented the decline of GVR secondary to sufentanil below the denervated level. Thus, vasodilation associated with sufentanil administration is mediated solely through neurogenic mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)
The hypothesis that cerebral arteriovenous difference of oxygen content (AVDO2) can be used to predict cerebral blood flow (CBF) was tested in patients who were comatose due to head injury, subarachnoid hemorrhage, or cerebrovascular disease. In 51 patients CBF was measured daily for 3 to 5 days, and in 49 patients CBF was measured every 8 hours for 5 to 10 days after injury. In the latter group of patients, when a low CBF (less than or equal to 0.2 ml/gm/min) or an increased level of cerebral lactate production (CMRL) (less than or equal to -0.06 mumol/gm/min) was encountered, therapy was instituted to increase CBF, and measurements of CBF, AVDO2, and arteriovenous difference of lactate content (AVDL) were repeated. When data from all patients were analyzed, including those with cerebral ischemia and those without, AVDO2 had only a modest correlation with CBF (r = -0.24 in 578 measurements, p less than 0.01). When patients with ischemia, indicated by an increased CMRL, were excluded from the analysis, CBF and AVDO2 had a much improved correlation (r = -0.74 in 313 measurements, p less than 0.01). Most patients with a very low CBF would have been misclassified as having a normal or increased CBF based on the AVDO2 alone. However, when measurements of AVDO2 were supplemented with AVDL, four distinct CBF patterns could be distinguished. Patients with an ischemia/infarction pattern typically had a lactate-oxygen index (LOI = -AVDL/AVDO2) of 0.08 or greater and a variable AVDO2. The three nonischemic CBF patterns had an LOI of less than 0.08, and could be classified according to the AVDO2. Patients with a normal CBF (mean 0.42 +/- 0.12 ml/gm/min) had an AVDO2 between 1.3 and 3.0 mumol/ml. A CBF pattern of hyperemia (mean 0.53 +/- 0.18 ml/gm/min) was characterized by an AVDO2 of less than 1.3 mumol/ml. A compensated hypoperfusion CBF pattern (mean 0.23 +/- 0.07 ml/gm/min) was identified by an AVDO2 of more than 3.0 mumol/min. These studies suggest that reliable estimates of CBF may be made from AVDO2 and AVDL measurements, which can be easily obtained in the intensive care unit.
Intracranial pressure (ICP) was measured during alfentanil-induced rigidity in rats. Ten rats had arterial, central venous (CVP), and subdural cannulae inserted under halothane anesthesia. The animals were mechanically ventilated to achieve normocarbia (PCO2 = 42 +/- 1 mmHg, mean +/- SE). Following instrumentation, halothane was discontinued and alfentanil (125 mu/kg) administered iv during emergence from halothane anesthesia. In the five rats that developed somatic rigidity, ICP and CVP increased significantly above baseline (delta ICP 7.5 +/- 1.0 mmHg, delta CVP 5.9 +/- 1.3 mmHg). These variables returned to baseline when rigidity was abolished with metocurine. In five rats that did not become rigid, ICP and CVP did not change following alfentanil. These observations suggest that rigidity should be prevented when alfentanil, and, presumably, other opiates, are used in the anesthetic management of patients with ICP problems.
Laboratory observations made in cats with fluid-percussion head injuries have suggested that plateau waves or Lundberg “A-waves” are not independent of systemic circulatory events. Four distinct phases in the evolution of the plateau wave have been identified, and each related to a circulatory change in a causal manner. The first phase is the premonitory drift phase where intracranial pressure (ICP) gradually increases prior to the plateau proper. This phase is caused by a slow gradual decline in systemic arterial blood pressure (SABP) which increases ICP by autoregulatory vasodilation and reduces cerebral perfusion pressure (CPP) to a range of 70 to 80 mm Hg. The second phase is the plateau phase initiated at a CPP of about 70 to 80 mm Hg, and is characterized by a rapid increase in ICP as CPP falls further to 40 to 50 mm Hg. The plateau lasts as long as the CPP remains stable and above ischemic levels. The third phase is the ischemic response, characterized by CPP being returned toward normal by increases in SABP in response to very low CPP's. The fourth phase is the resolution, characterized by a rapid decline in the ICP to baseline levels with stabilization of the SABP and CPP, and is best explained by autoregulatory vasoconstriction.
Plateau waves appear to occur as the result of intact or mostly intact autoregulation responding to changes in CPP. The series of events that follow are best explained by what is known of normal autoregulation; the various properties of plateau waves are viewed and explained as the expected and logical consequences of an unstable CPP acting upon a generally intact cerebrovascular bed in the face of elevated ICP and decreased compliance.
Early results using cerebral perfusion pressure (CPP) management techniques in persons with traumatic brain injury indicate that treatment directed at CPP is superior to traditional techniques focused on intracranial pressure (ICP) management. The authors have continued to refine management techniques directed at CPP maintenance.
One hundred fifty-eight patients with Glasgow Coma Scale (GCS) scores of 7 or lower were managed using vascular volume expansion, cerebrospinal fluid drainage via ventriculostomy, systemic vasopressors (phenylephrine or norepinephrine), and mannitol to maintain a minimum CPP of at least 70 mm Hg. Detailed outcomes and follow-up data bases were maintained. Barbiturates, hyperventilation, and hypothermia were not used.
Cerebral perfusion pressure averaged 83 ± 14 mm Hg; ICP averaged 27 ± 12 mm Hg; and mean systemic arterial blood pressure averaged 109 ± 14 mm Hg. Cerebrospinal fluid drainage averaged 100 ± 98 cc per day. Intake (6040 ± 4150 cc per day) was carefully titrated to output (5460 ± 4000 cc per day); mannitol averaged 188 ± 247 g per day. Approximately 40% of these patients required vasopressor support.
Patients requiring vasopressor support had lower GCS scores than those not requiring vasopressors (4.7 ± 1.3 vs. 5.4 ± 1.2, respectively). Patients with vasopressor support required larger amounts of mannitol, and their admission ICP was 28.7 ± 20.7 versus 17.5 ± 8.6 mm Hg for the nonvasopressor group. Although the death rate in the former group was higher, the outcome quality of the survivors was the same (Glasgow Outcome Scale scores 4.3 ± 0.9 vs. 4.5 ± 0.7). Surgical mass lesion patients had outcomes equal to those of the closed head-injury group.
Mortality ranged from 52% of patients with a GCS score of 3 to 12% of those with a GCS score of 7; overall mortality was 29% across GCS categories. Favorable outcomes ranged from 35% of patients with a GCS score of 3 to 75% of those with a GCS score of 7. Only 2% of the patients in the series remained vegetative and if patients survived, the likelihood of their having a favorable recovery was approximately 80%. These results are significantly better than other reported series across GCS categories in comparisons of death rates, survival versus dead or vegetative, or favorable versus nonfavorable outcome classifications (Mantel—Haenszel χ ² , p < 0.001). Better management could have improved outcome in as many as 35% to 50% of the deaths.
Sufentanil is an intravenous opioid often used as a component of anesthesia during neurosurgical procedures. However, the effects of sufentanil on intracranial pressure in patients with diminished intracranial compliance are not well established, and remain controversial.
Ten patients with head trauma, in each of whom the trachea was intubated, were studied for the effects of sufentanil on intracranial pressure (ICP) and on cerebral perfusion pressure (CPP). In all patients, ICP monitoring was instituted before the study. Sedation was obtained using a propofol infusion, and paralysis was achieved with vecuronium. After obtaining control of ICP (between 15 and 25 mmHg) hemodynamic values and blood gas tensions (PaCO2 between 30 and 35 mmHg), the level of sedation was deepened with an intravenous injection of sufentanil (1 microgram/kg over 6 min), followed by an infusion of 0.005 microgram.kg-1min-1. Mean arterial pressure (MAP), ICP (fiberoptic intracranial pressure monitor), and end-tidal CO2 were continuously measured and recorded at 1-min intervals throughout the 30-min study period.
Sufentanil injection was associated with a statistically significant increase in ICP of 9 +/- 7 mmHg (+ 53%), which peaked at 5 min. Then ICP gradually decreased and returned to baseline after 15 min. This was accompanied by a significant decrease in MAP (24% decrease) and, thus, CPP (38% decrease). After 5 min, MAP and CPP gradually increased, but remained significantly decreased throughout the study.
The results of the current study indicate that caution should be exercised in the administration of sufentanil bolus to patients with abnormal intracranial elastance, particularly if ICP is significantly increased.
Opioids, when administered in large doses, produce brain damage, primarily in the limbic system and association areas in rats. This investigation examined the relationship between opioid dose and severity and frequency of brain damage in rats. Forty male Sprague-Dawley rats were anesthetized with halothane/N2O and underwent tracheal intubation, mechanical ventilation, arterial/venous cannulation, and insertion of a rectal temperature probe and biparietal electroencephalogram electrodes. After surgery, halothane was discontinued and O2/N2O 30%/70% was administered for 1 h. Rats were then randomly assigned to one of eight groups. The control group received a loading dose (LD) of 4 mL/kg of 0.9% normal saline solution (NSS) and a maintenance dose (MD) of 4 mL.kg-1.h-1 NSS. The other groups were given fentanyl lypophilized and reconstituted in NSS with the LD ranging from 50 to 3200 micrograms/kg and the MD from 2 to 128 micrograms.kg-1.min-1. After 2 h of fentanyl or NSS infusion; all rats received 100% O2 and, when alert, their tracheas were extubated; after 7 days the rats underwent cerebral perfusion fixation, followed by light microscopic evaluation. Histopathologic lesions (primarily eosinophilic neuron degeneration) were subjectively graded by a pathologist unaware of the experimental treatment; the grades were based on the percentage of dead neurons. There were no lesions observed in the brain areas in any of the control or 200-8 (LD, microgram/kg; MD, microgram.kg-1.min-1) groups. Eleven of 20 rats in the 400-16, 800-32, 1600-64, and 3200-18 groups showed evidence of brain damage primarily in limbic system structures and association areas (P < 0.05). Our data confirm that fentanyl produces limbic system brain damage in rats, and that the damage occurs over a broad range of doses.
The rate of cerebrospinal fluid (CSF) formation (Vf) and resistance to reabsorption (Ra) of CSF were determined in dogs at four doses of fentanyl (0.05, 0.18, 0.60, and 3.0 microg.kg. min), sufentanil (0.01, 0.04, 0.13, and 0.60 microg.kg min) and aflentanil (1.4, 4.0, 13.0, and 40.0 microg.kg min). Results were compared within and between groups and to previously reported normal values (obtained during a variety of background anesthetics) for Vf (0.030-0.054 ml/min) and Ra (220-253 cm H2O ml min) in dogs. At the two lower doses of fentanyl and at all doses of sufentanil and alfentanil, Vf values were not significantly different from previously reported normal values. At the two higher doses of fentanyl, Vf decreased by 24 and 49%, respectively. At the two lower doses of all three drugs, Ra was significantly decreased, with mean values 40-52% below previously reported normal values. At the two higher doses of alfentanil, Ra values were not significantly different from previously reported normal values, and at the two higher doses of fentanyl and sufentanil, Ra was unchanged or increased. It is concluded that, among these three narcotics, reduction of CSF volume (as determined by the balance between Vf and Ra) is favored most by fentanyl, and ease of CSF volume contraction (as determined by Ra) is favored most by alfentanil.
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