Hypoxic brain injury

Becker R, Alberti O, and Bauer BL. Continuous intrathecal baclofen infusion in severe spasticity after traumatic or hypoxic brain injury. J Neurol 1997 244 160-166. 

A family physician/psychiatrist concludes that Sara has a history of hypoxic brain injury with consequent significant cognitive impairment, inability to perform activities of daily living, and impulse control problems (disinhibition because of her frontal lobe injury) in her role as a parent. Sara is given trazodone for her impulse-control problems. The therapist continues to work with Maria, Hector, and Sara to develop coping strategies for the family of this brain-injured woman. 

The therapist doesn t know much about hypoxic brain injury. How can collaboration help him address his concerns about his unfamiliarity with the diagnosis Dr. E has never treated someone with hypoxic brain injury. While he feels confident in his abilities to help set boundaries, establish a safety net for Hector, and encourage frequent communication between the clinic and the family, he is unsure about the course and prognosis of Sara s illness. He meets with the psychiatrist to learn some basic information. The psychiatrist is pleased to tell him what he knows and even has a few articles on brain injury for Dr. E to read. Together, they decide to do a quick literature review and share their findings with each other. 

CNS depression is the most frequently reported clinical effect. The typical overdose patient may present with extreme somnolence that may progress to frank coma. Miosis is usually present unless the individual is acidotic or has suffered hypoxic brain injury. Respiratory depression can occur and may progress to respiratory arrest. Pulmonary edema may be seen. Bradycardia, hypotension, and hyperthermia can develop. Hydrocodone is often combined in products with acetaminophen therefore, patients should be evaluated for hepatotoxicity secondary to acetaminophen overdose. Available opiate immunoassays cross-react unreliably with hydrocodone. Peak therapeutic serum levels are 0.024 mg 1 toxic levels have been reported to reach 0.1-1.3 pgml , but are of little prognostic or therapeutic value. 

Nervous system There was white matter vacuolation and intramyelinic edema in the brain of a child with quadriparetic cerebral palsy secondary to hypoxic brain injury following premature birth, who died 3 weeks after the start of a course of vigabatrin [421 ]. This increases concerns about the use of vigabatrin in individuals with preexisting abnormalities of myelin. 

Hypoxic cardiac arrest occurred before her airway was secured and she died of hypoxic brain injury 3 days later. The authors proposed that masseter muscle spasm may be associated with suxamethonium even late in the setting of carbamate poisoning. However masseter muscle spasm commonly occurs after suxamethonium and is occasionally life-threatening [9 ]. 

HYPOXIC-ISCHEMIC BRAIN INJURY AND OXIDATIVE STRESS 559... 

Hypoxic-Ischemic Brain Injury and Oxidative Stress... 

Akisu M, Kultursay N, Coker I, Huseyinov A. (1998). Platelet-activating factor is an important mediator in hypoxic ischemic brain injury in the newborn rat. Flunarizine and Ginkgo biloba extract reduce PAF concentration in the brain. Biol Neonate. 74(6) 439-44. 

Guan J, WiUiams CE, Skinner SJ, Mallard EC, Gluckman PD. 1996. The effects of insulin-like growth factor (IGF)-l, IGF-2, and des-IGF-1 on neuronal loss after hypoxic-ischemic brain injury in adult rats evidence for a role for IGE binding proteins. Endocrinology 137 893-898. 

D. Azzopardi, J. S. Wyatt, E. B. Cady, D. T. Delpy, J. Baudin, A. L. Stewart, P. L. Hope, P. A. Hamilton and E. O. Reynolds, Prognosis of newborn infants with hypoxic-ischemic brain injury assessed by phosphorus magnetic resonance spectroscopy. Pediatr. Res., 1989,25, U5-451. 

Until recently, the neonate has been a black box, an eminently valued patient, yet one that is difficult to study and treat effectively. Neonatal research, in particular, is often plagued by ethical problems of invasiveness of protocols, volume of blood to be drawn, inability of the patient to speak on his/her own behalf, etc. Even simple studies that try to address neonatal outcome often pose problems in these areas, requiring volumes of blood that subsequently need to be replaced by transfusion. Because the perceived benefit to both individual patients and to society as a whole is deemed to be highly valuable, such downsides to neonatal research are often accepted as inevitable. The introduction, however, of MS analysis, utilizing low volumes of blood for multiple biomarkers, appears to be a very attractive alternative with great potential. A number of critical areas have already begun to be addressed and include such diverse entities as hypoxic-ischemic brain injury, the infant of a diabetic mother, neonatal renal function, neonatal nutrition, neonatal sepsis, and pharmaceutical development. 

Assessment of the neonate with hypoxic-ischemic or other brain injury... 

Hypoxic-Ischemic Brain Injury, Perinatal Asphyxia, and Chronic Lung Disease The Potential for Proteomic Evaluation... 

In term infants, acute hypoxic-ischemic injury and birth trauma appear to be more significant events in the evolution of brain injury (64). It has been widely recognized, however, that although many neonates who ultimately develop CP sustain their injury during birth or in the NICU, most CP patients do not have evidence of acute neonatal events capable of producing permanent injury (65-67). In term neonates, the large majority of infants with CP have no clearly discernible asphyxial event to which the injury can be attributed. 

Several trials have confirmed the benefit of hypothermia following perinatal hypoxic-ischemic injury (76,77). It has been noted, however, that brain or body cooling has not produced improved outcomes that are as dramatic as those seen in animal studies, when the brain injury can be precisely timed. It is evident then that the most significant variable over which little control... 

Thornton JS, Ordidge RJ, Penrice J, Cady EB, Amess PN, Pun-wani S, Clemence M, Wyatt JS (1998) Temporal and anatomical variations of brain water apparent diffusion coefficient in perinatal cerebral hypoxic-ischemic injury relationships to cerebral energy metabolism. Magn Reson Med 39 920-927... 

Matsushita Y., BramlettH. M., Alonso O., and Dietrich W. D. (2001) Posttraumatic hypothermia is neuroprotective in amodel of traumatic brain injury complicated by a secondary hypoxic insult. Crit. Care Med. 29, 2060-2066. 

SirimanneE. S., Blumberg R. M., Bossano D., etal. (1996) The effect of prolonged modification of cerebral temperature on outcome after hypoxic-ischemic brain injury in the infant rat. Pediatr. Res. 39,591-597. 

Laptook A. R. and Corbett R. J. (2002) The effects of temperature on hypoxic-ischemic brain injury. Clin. Perinatol. 29, 623-649, vi. 

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