Acute Lung Injury Is an Independent Risk Factor for Brain Hypoxia After Severe Traumatic Brain Injury

Oddo, Mauro; Nduom, Edjah K.; Frangos, Suzanne; MacKenzie, Larami; Chen, Isaac; Maloney-Wilensky, Eileen; Kofke, W. Andrew; Levine, Joshua M.; LeRoux, Peter D.

doi:10.1227/01.neu.0000371979.48809.d9

Cited by 59 publications

(38 citation statements)

References 42 publications

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“…Its severity is related to the magnitude of the brain injury and it is associated with high morbidity rates and up to 7% mortality. 8,10,25 NPE may be triggered by different brain conditions, including seizures, stroke and traumatic brain injury ( Figure 3). NPE is most common in seizures during the post-critical period, affecting to up to one third of patients in status epilepticus.…”

Section: Neurogenic Pulmonary Edema (Npe)mentioning

confidence: 99%

Pulmonary Complications in Patients with Brain Injury

Alvarez¹,

Quevedo²,

Furelos³

et al. 2015

Pulm Res Respir Med Open J

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Section: Neurogenic Pulmonary Edema (Npe)mentioning

confidence: 99%

Pulmonary Complications in Patients with Brain Injury

Alvarez¹,

Quevedo²,

Furelos³

et al. 2015

Pulm Res Respir Med Open J

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“…Based on the formula PbtO 2 = CBF ∙ AVTO 2 , reduced PbtO 2 occurs frequently because of low CBF. However, PaO 2 also is an important determinant of PbtO 2 [42] and additional pathological events (e.g., impaired lung function [43] or impaired O 2 extraction due to increased gradients for oxygen diffusion in injured brain tissue [17]) might reduce PbtO 2 , in the absence of reduced CBF. Hemoglobin concentration also affects PbtO 2 and reduced hemoglobin concentration below 9 g/dl may aggravate brain hypoxia [44].…”

Section: Bedside Clinical Approachmentioning

confidence: 99%

Beyond intracranial pressure: optimization of cerebral blood flow, oxygen, and substrate delivery after traumatic brain injury

Bouzat

Sala

Payen

et al. 2013

Ann. Intensive Care

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106

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Monitoring and management of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) is a standard of care after traumatic brain injury (TBI). However, the pathophysiology of so-called secondary brain injury, i.e., the cascade of potentially deleterious events that occur in the early phase following initial cerebral insult—after TBI, is complex, involving a subtle interplay between cerebral blood flow (CBF), oxygen delivery and utilization, and supply of main cerebral energy substrates (glucose) to the injured brain. Regulation of this interplay depends on the type of injury and may vary individually and over time. In this setting, patient management can be a challenging task, where standard ICP/CPP monitoring may become insufficient to prevent secondary brain injury. Growing clinical evidence demonstrates that so-called multimodal brain monitoring, including brain tissue oxygen (PbtO2), cerebral microdialysis and transcranial Doppler among others, might help to optimize CBF and the delivery of oxygen/energy substrate at the bedside, thereby improving the management of secondary brain injury. Looking beyond ICP and CPP, and applying a multimodal therapeutic approach for the optimization of CBF, oxygen delivery, and brain energy supply may eventually improve overall care of patients with head injury. This review summarizes some of the important pathophysiological determinants of secondary cerebral damage after TBI and discusses novel approaches to optimize CBF and provide adequate oxygen and energy supply to the injured brain using multimodal brain monitoring.

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“…High altitude is a low-pressure and hypoxic environment and it has been demonstrated that acute hypoxia can cause injury to a number of organs (1–3). The specialized blood supply and anatomical structure of the intestine increases its sensitivity to hypoxia, which makes the intestine vulnerable to the effects of hypoxic stress (4–6).…”

Section: Introductionmentioning

confidence: 99%

Establishment and evaluation of an experimental rat model for high-altitude intestinal barrier injury

Luo

Zhou

Chen

et al. 2016

Experimental and Therapeutic Medicine

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In the present study an experimental high-altitude intestinal barrier injury rat model was established by simulating an acute hypoxia environment, to provide an experimental basis to assess the pathogenesis, prevention and treatment of altitude sickness. A total of 70 healthy male Sprague-Dawley rats were divided into two groups: Control group (group C) and a high-altitude hypoxia group (group H). Following 2 days adaptation, the rats in group H were exposed to a simulated 4,000-m, high-altitude hypoxia environment for 3 days to establish the experimental model. To evaluate the model, bacterial translocation, serum lipopolysaccharide level, pathomorphology, ultrastructure and protein expression in rats were assessed. The results indicate that, compared with group C, the rate of bacterial translocation and the apoptotic index of intestinal epithelial cells were significantly higher in group H (P<0.01). Using a light microscope it was determined that the intestinal mucosa was thinner in group H, there were fewer epithelial cells present and the morphology was irregular. Observations with an electron microscope indicated that the intestinal epithelial cells in group H were injured, the spaces among intestinal villi were wider, the tight junctions among cells were open and lanthanum nitrate granules (from the fixing solution) had diffused into the intestinal mesenchyme. The expression of the tight junction protein occludin was also decreased in group H. Therefore, the methods applied in the present study enabled the establishment of a stable, high-altitude intestinal barrier injury model in rats.

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Acute Lung Injury Is an Independent Risk Factor for Brain Hypoxia After Severe Traumatic Brain Injury

Abstract: After severe TBI, PbtO2 correlates with PF ratio. Acute lung injury is associated with an increased risk of compromised PbtO2, independent from intracerebral and systemic injuries. Our findings support the use of lung-protective strategies to prevent brain hypoxia in TBI patients.

Cited by 59 publications

References 42 publications

Pulmonary Complications in Patients with Brain Injury

Pulmonary Complications in Patients with Brain Injury

Beyond intracranial pressure: optimization of cerebral blood flow, oxygen, and substrate delivery after traumatic brain injury

Establishment and evaluation of an experimental rat model for high-altitude intestinal barrier injury

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