High-dose barbiturate control of elevated intracranial pressure in patients with severe head injury

Eisenberg, Howard M.; Frankowski, Ralph F.; Contant, Charles F.; Marshall, Lawrence F.; Walker, Michael D.

doi:10.3171/jns.1988.69.1.0015

Cited by 543 publications

(135 citation statements)

References 24 publications

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“…Although their effect may be deleterious in the initial management compared with mannitol, barbiturates improve survival probability when used in patients with intracranial hypertension, refractory to other therapies [137]. The most commonly employed is pentobarbital sodium, at an IV load doses of 10 mg/kg over 30 minutes, followed by an infusion of 5 mg/kg/h, for 3 hours and then maintained at 1 to 3 mg/kg/h.…”

Section: Box 2 Management Of the Traumatic Brain Injury Patientmentioning

confidence: 99%

Critical Care Issues in the Early Management of Severe Trauma

García

2006

Surgical Clinics of North America

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Violent trauma and road traffic injuries kill more than 2.5 million people in the world every year. It has been calculated by the World Health Organization that in 2002 there occurred 1.6 million violent deaths [1] and 1.2 million deaths from traffic injury [2], for a combined mortality of 48 deaths per 100,000 population per year.Most trauma deaths occur at the scene or in the first hour after trauma, with a proportion from 34% to 50% occurring in hospitals [3]. These deaths could be prevented by optimization of trauma care. Preventability of trauma deaths has been reported as high as 76% [4] and as low as 1% in mature trauma systems [5,6].Prehospitalization procedures, elapsed time to hospital arrival are, of course, vital to the whole trauma scenario, but errors made in the in-hospital phase of care are responsible for one third to two thirds of the reported by different authors [7,8]. Of these, intensive care unit (ICU) errors are among the most frequent and significant. Errors in the ICU management of trauma patients were studied by Duke and colleagues [9]. They reported 165 ICU trauma deaths. Two hundred fifty-eight errors occurred in 81 patients (52%), and 134 of them contributed to death in 52 patients (34%). ICU errors were classified as management errors (82%), diagnostic (9%), technique (5%), and system inadequacies (4%). Davis and colleagues [10] identified critical care errors in 30% of 125 trauma deaths with errors. These errors contributed to 48% of all preventable deaths.The most common critical care errors are related to airway and respiratory management, fluid resuscitation, neurotrauma diagnosis and support, and delayed diagnosis of critical lesions [9,10].It is imperative for the general surgeon who takes care of trauma patients to know how to deal with these critical aspects, to reduce preventable morbidity and mortality. In the next segment, the situations in which the participation of the surgeon is crucial, during the initial phases of reanimation and stabilization of the critically traumatized patient will be discussed. Airway and ventilation managementAirway and respiratory management errors are the most common of those identified by several authors [9][10][11] The cardinal manifestation is a sudden or a rapidly progressing desaturation, frequently accompanied by tachycardia and arrhytmias, and occasionally by agitation. Hypertension announces the cardiovascular collapse, and bradicardia appears immediately after the total collapse [12]. The symptoms should not be attributed to agitation when it is present, and other possible causes must be ruled out before. Diagnosing the complication involves a directed physical examination, the analysis of the airway pressures and ventilator volumes, chest radiographs, and sometimes the measurement of arterial blood gases (ABG), and the urinary bladder pressure ( Table 1).The emergency conditions in which the access to the airways must be gained, the displacement to diagnosis areas or operating room and the agitation, often present, make the critical...

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Section: Box 2 Management Of the Traumatic Brain Injury Patientmentioning

confidence: 99%

Critical Care Issues in the Early Management of Severe Trauma

García

2006

Surgical Clinics of North America

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“…While many potential targeted therapies for TBI have shown promise in experimental models, disappointingly no therapies have shown benefit in human trials. [5][6][7][8][9][10][11][12][13][14] One potential culprit for failure of pharmacological agents targeting TBI is the unknown impact of drug transporters at the bloodbrain barrier (BBB) and brain-cerebrospinal fluid (CSF) barrier (BCSFB) in terms of entry into and elimination from injured brain, respectively. In addition to imposing physical barriers, the BBB and BCSFB represent dynamic barriers because they contain a vast number of energy-dependent membrane transporters.…”

Section: Introductionmentioning

confidence: 99%

Expression of ATP-Binding Cassette Transporters B1 and C1 after Severe Traumatic Brain Injury in Humans

Willyerd

Empey

Philbrick

et al. 2016

Journal of Neurotrauma

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Adenosine triphosphate-binding cassette (ABC) transport proteins ABCC1 and ABCB1 (also known as multidrug resistance-associated protein 1 and p-glycoprotein, respectively), are key membrane efflux transporters of drugs and endogenous substrates, including in the brain. The impact of traumatic brain injury (TBI) on ABCC1 and ABCB1 expression in humans is unknown. We hypothesized that ABCC1 and ABCB1 expression would be altered in brain tissue from patients acutely after severe TBI. Archived TBI samples (n = 10) from our Brain Trauma Research Center and control samples (n = 7) from our Alzheimer Disease Research Center were obtained under Institutional Review Board approval. Protein was extracted from fresh frozen cortical brain tissue for Western blot analysis and sections were obtained from fixed cortical tissue for immunohistochemistry. Relative abundance of ABCC1 was increased in samples from TBI versus controls (2.8 -2.5 fold; p = 0.005). ABCC1 immunohistochemistry was consistent with Western blot data, with increased immunoreactivity in cerebral blood vessel walls, as well as cells with the morphological appearance of neurons and glia in TBI versus controls. Relative abundance of ABCB1 was similar between TBI and controls ( p = 0.76), and ABCB1 immunoreactivity was primarily associated with cerebral blood vessels in both groups. These human data show that TBI increases ABCC1 expression in the brain, consistent with possible implications for both patients receiving pharmacological inhibitors and/or substrates of ABCC1 after TBI.

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“…Early experimental data suggested a neuroprotective effect in models of focal cerebral ischemia (Smith et al 1974); however, subsequent small-scale clinical trials were disappointing (Ward et al 1985;Kassell, Peerless et al 1980). Studies in brain injured patients indicate that barbiturates may be less effective than mannitol as an initial intervention, but nevertheless are useful in patients who have failed maximal osmotherapy (Eisenberg et al 1988;Schwartz et al 1984;Marshall et al 2010). Pentobarbital has a number of undesireable side-effects including systemic hypotension, decreased gastric motility, and bone marrow suppression ).…”

Section: Cerebral Edema Intracranial Hypertension and Cerebral Perfumentioning

confidence: 99%