Harbingers of Poor Outcome the Day after Severe Brain Injury: Hypothermia, Hypoxia, and Hypoperfusion

Jeremitsky, Élan; Omert, Laurel; Dunham, C. Michael; Protetch, Jack; Rodríguez, Aurelio

doi:10.1097/01.ta.0000037876.37236.d6

Cited by 272 publications

(169 citation statements)

References 32 publications

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“…While hypothermia on admission is common in trauma patients with more severe injuries and poor prognoses (Little and Stoner, 1981;Little, 1985;Steinemann et al, 1990;Jeremitsky et al, 2003), it is currently unclear if hypothermia contributes to poor outcome or is simply correlative (Steinemann et al, 1990). We did not observe significant differences in any physiologic or neurologic outcome measures between the brain-injured animals that were hypothermic for 12 to 24 hours after injury and those that developed PTH.…”

Section: Discussionmentioning

confidence: 52%

“…The brain-injured patient often has multiple injuries, including fractures, hemorrhage, etc., that may present with hypotension and hypoxia as well as hypothermia (Statler et al, 2001). Although these factors have been shown to relate to poorer outcome after TBI (Jeremitsky et al, 2003), isolated hypothermia may or may not be causative of poor outcome. Because it has also been suggested that therapeutic postinjury hypothermia is neuroprotective (Clifton et al, 1991;Dietrich 1992;Marion et al, 1997;Kinoshita et al, 2002a, b), the findings of this study provide additional information to aid in the design of future preclinical neuroprotection studies.…”

Section: Discussionmentioning

confidence: 99%

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Development of Posttraumatic Hyperthermia after Traumatic Brain Injury in Rats is Associated with Increased Periventricular Inflammation

Thompson

Hoover

Tkacs

et al. 2005

J Cereb Blood Flow Metab

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Posttraumatic hyperthermia (PTH) is a noninfectious elevation in body temperature that negatively influences outcome after traumatic brain injury (TBI). We sought to (1) characterize a clinically relevant model and (2) investigate potential cellular mechanisms of PTH. In study I, body temperature patterns were analyzed for 1 week in male rats after severe lateral fluid percussion (FP) brain injury (n ¼ 75) or sham injury (n ¼ 17). After injury, 27% of surviving animals experienced PTH, while 69% experienced acute hypothermia with a slow return to baseline. A profound blunting or loss of circadian rhythmicity (CR) that persisted up to 5 days after injury was experienced by 75% of brain-injured animals. At 2 and 7 days after injury, patterns of cell loss and inflammation were assessed in selected brain thermoregulatory and circadian centers. Significant cell loss was not observed, but PTH was associated with inflammatory changes in the hypothalamic paraventricular nucleus (PVN) by one week after injury. In brain-injured animals with altered CR, reactive astrocytes were bilaterally localized in the suprachiasmatic nucleus (SCN) and the PVN. Occasional IL-1b þ / ED-1 þ macrophages/microglia were observed in the PVN and SCN exclusively in brain-injured animals developing PTH. In animals with PTH there was a significant positive correlation (r ¼ 0.788, Po0.01) between the degree of postinjury hyperthermia and the total number of cells positive for inflammatory markers within selected thermoregulatory and circadian nuclei. In study II, a separate group of animals underwent the same injury and temperature monitoring paradigm as in study I, but had additional physiologic data obtained, including vital signs, arterial blood gases, white blood cell counts, and C-reactive protein levels. All parameters remained within normal ranges after injury. These data suggest that PTH and the alteration in CR of temperature may be due, in part, to acute reactive astrocytosis and inflammation in hypothalamic centers responsible for both thermoregulation and CR.

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Section: Discussionmentioning

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Development of Posttraumatic Hyperthermia after Traumatic Brain Injury in Rats is Associated with Increased Periventricular Inflammation

Thompson

Hoover

Tkacs

et al. 2005

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

show abstract

“…Hypotension has been related with increased mortality, and hypoxia, hypocapnia, increased ICP, and acidosis were associated with poor outcome. 63 From the two prospective clinical trials of magnesium in TBI reported by Temkin et al 1 and Dhandapani et al, 2 it is evident that in clinical trials on brain injuries a study design with more stringent inclusion-exclusion criteria need to be considered, to account for secondary brain insults and parameters likely to adversely affect outcome, such as severity of head injury, multiorgan injury, age limits, renal function, pre-existing health conditions, concomitant medication, use of tobacco and alcohol, and history of substance abuse.…”

Section: Secondary Insults In Traumatic Brain Injurymentioning

confidence: 99%

Use of Magnesium in Traumatic Brain Injury

Sen¹,

Gulati

2010

Neurotherapeutics

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Summary: Depletion of magnesium is observed in animal brain and in human blood after brain injury. Treatment with magnesium attenuates the pathological and behavioral changes in rats with brain injury; however, the therapeutic effect of magnesium has not been consistently observed in humans with traumatic brain injury (TBI). Secondary brain insults are observed in patients with brain injury, which adversely affect clinical outcome. Systemic administration studies in rats have shown that magnesium enters the brain; however, inducing hypermagnesemia in humans did not concomitantly increase magnesium levels in the CSF. We hypothesize that the neuroprotective effects of magnesium in TBI patients could be observed by increasing its brain bioavailability with mannitol. Here, we review the role of magnesium in brain injury, preclinical studies in brain injury, clinical safety and efficacy studies in TBI patients, brain bioavailability studies in rat, and pharmacokinetic studies in humans with brain injury. Neurodegeneration after brain injury involves multiple biochemical pathways. Treatment with a single agent has often resulted in poor efficacy at a safe dose or toxicity at a therapeutic dose. A successful neuroprotective therapy needs to be aimed at homeostatic control of these pathways with multiple agents. Other pharmacological agents, such as dexanabinol and progesterone, and physiological interventions, with hypothermia and hyperoxia, have been studied for the treatment of brain injury. Treatment with magnesium and hypothermia has shown favorable outcome in rats with cerebral ischemia. We conclude that coadministration of magnesium and mannitol with pharmacological and physiological agents could be an effective neuroprotective regimen for the treatment of TBI.

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“…The optimal resuscitation constitutes the first step in the optimal treatment of the brain trauma patient, in virtue of the acknowledged deleterious role of secondary insults such as hypotension and hypoxia [125,126]. Maintaining SatP at a level >94%, the systolic blood pressure above 90 mm Hg, the mean arterial blood pressure above 70 mm Hg, and the PaCO 2 around 35 mm Hg seem reasonable goals [124].…”

Section: Initial Neurologic Evaluation Of the Trauma 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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Harbingers of Poor Outcome the Day after Severe Brain Injury: Hypothermia, Hypoxia, and Hypoperfusion

Cited by 272 publications

References 32 publications

Development of Posttraumatic Hyperthermia after Traumatic Brain Injury in Rats is Associated with Increased Periventricular Inflammation

Development of Posttraumatic Hyperthermia after Traumatic Brain Injury in Rats is Associated with Increased Periventricular Inflammation

Use of Magnesium in Traumatic Brain Injury

Critical Care Issues in the Early Management of Severe Trauma

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