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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypoxic-ischemic encephalopathy (HIE) in neonates is often difficult to diagnose in "real time" at the bedside because of the variety of disorders that can cause neonatal seizures and other nonspecific signs of encephalopathy. Standard interventions to support respiratory and cardiovascular disorders associated with HIE are appropriate, but none has been demonstrated to alter neurologic outcome. Anticonvulsants are indicated when seizures are observed, although they are considered a sign of HIE rather than a cause of injury. There is overwhelming evidence that the excitotoxic cascade that evolves during HIE extends over several days after the insult and is modifiable. Clinical trials of potentially neuroprotective interventions such as hypothermia are under way.
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PMID:Hypoxic-Ischemic Encephalopathy. 1109 41

Hypoxic-ischemic encephalopathy (HIE) remains one of the most important neurologic complications in the newborn. Several experimental and clinical studies have shown that hypothermia is the most effective means known for protecting the brain against hypoxic-ischemic brain damage. Furthermore, recent data have suggested that platelet-activating factor (PAF) could play a pathophysiologically important role in the progression of hypoxic-ischemic brain injury. The aim of the present study was to investigate the role of head cooling combined with minimal hypothermia in short-term outcome of infants with perinatal asphyxia. In addition, we have examined the effect of head cooling combined with minimal hypothermia on PAF concentrations in cerebrospinal fluid (CSF) after hypoxic-ischemic brain injury. The group of asphyxiated infants (Group 1) consisted of 21 full-term (gestational age >37 weeks). These infants were randomized and divided into either a standard therapy group (Group 1a; n=10) or cooling group (Group 1b; n=11). Head cooling combined with minimal hypothermia (rectal temperature 36.5-36 degrees C) was started as soon as practicable after birth. The infants were cooled for 72h and then were rewarmed at 0.5 degrees C/h. The control group (Group 2) consisted of seven full-term infants and none of these infants showed any sign of asphyxia. To measure PAF concentration in CSF, CSF with lumbar puncture was collected into tubes immediately before the cooling (1-3h after birth) and again after 36h. We had no evidence of severe adverse events related to hypothermia. In Group 1a, two infants died after 72h of life; however, all newborn infants in Group 1b survived. Convulsion required treatment in three infants of standard therapy group (1a); none of the infants in Group 1b had clinical seizure activity. Abnormal EEG patterns were found in four infants of Group 1a; no EEG abnormalities were noted in Group 1b (P<0.05). On admission (before cooling), PAF concentration in CSF of asphyxiated infants was found to be significantly higher when compared with that of control (P<0.001). Mean PAF concentration before initiation of the study was similar in the two asphyxiated groups (Group 1a vs. 1b) (P>0.05). Obtained PAF level in CSF after 36h, showed a profound decline in cooling group of infants compared to Group 1a infants (P<0.01). In conclusion, the present study suggests that cerebral cooling with minimal hypothermia started soon after birth has no severe adverse effects during 72-h cooling period and that short-term outcome of infants are encouraging. Our results also support the hypothesis PAF an important mediator in hypoxic-ischemic brain injury and demonstrate that head cooling combined with minimal hypothermia reduces the normal increase in PAF following hypoxic-ischemic brain injury in full-term infants.
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PMID:Selective head cooling with hypothermia suppresses the generation of platelet-activating factor in cerebrospinal fluid of newborn infants with perinatal asphyxia. 1287 50

Hypoxic-ischemic encephalopathy (HIE) is one of the most important complications found in the newborn period. It is the result of a deprivation of oxygen and glucose to the neural tissue, which may be the result of either hypoxemia or ischemia. Experimental animal research and clinical observations in humans have noted that the pattern of injury occurs in 2 phases. The first phase is a primary energy failure related to the insult, and then a second energy failure occurs some hours later. The combined effects of cellular energy failure, acidosis, glutamate release, intracellular accumulation of calcium, lipid peroxidation, and nitric oxide neurotoxicity destroy essential components of the cell, culminating in cell death. The clinical presentation depends on the severity, timing, and duration of the insult, with symptoms typically evolving over approximately 72 hours. Hypothermia strategies are aimed at targeting this narrow window of opportunity to ameliorate the brain injury.
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PMID:The chilling details: hypoxic-ischemic encephalopathy. 1920 61

Hypoxic-ischemic encephalopathy (HIE) is an important cause of acute neurologic injury at birth, affecting approximately two to three cases per 1000 full-term live births. Despite advancements in many aspects of neonatal intensive care, the outcome for infants with HIE remains poor. Interventions to improve outcomes in this population have been disappointing. The treatment of infants who have HIE is generally supportive and includes fluid and electrolytes homeostasis, correction of hypotension, and treatment of seizures. It is now known that severe hypoxia-ischemia may not necessarily cause immediate cell death, but can precipitate a complex biochemical cascade leading to the delayed neuronal loss. The key phases of injury include a latent phase after reperfusion, with initial recovery of cerebral energy metabolism, followed by a secondary phase characterized by accumulation of cytotoxins, seizures, cytotoxic edema, and failure of cerebral oxidative metabolism starting 6 to 15 h post insult. Studies designed around this conceptual framework have shown that moderate cerebral hypothermia initiated as early as possible before the onset of secondary deterioration, and continued for a sufficient duration has been associated with long-lasting neuroprotection. Three large controlled trials have demonstrated that post resuscitation cooling is generally safe and reduces death or disability at 18 months of age after neonatal encephalopathy. Hypothermia is now widely recommended as a standard of care for infants with HIE. However, national guidelines concerning regional organization and supportive care are necessary. A developmental follow-up must be organized. Neonatologists involved in this procedure must be encouraged joining a national data collection and registry.
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PMID:[Hypothermia for hypoxic-ischemic encephalopathy in fullterm newborns]. 2072 12

Hypoxic-ischemic encephalopathy (HIE) can lead to devastating neurodevelopmental consequences such as cerebral palsy, seizure disorders, and significant developmental delays. HIE in the newborn is often the result of a hypoxic event, such as uterine rupture, placental abruption, or cord prolapse. Biphasic brain injury occurs in HIE. The first phase involves activation of the sympathetic nervous system as a compensatory mechanism. The second phase, known as reperfusion brain injury, occurs hours later. Induced hypothermia, a neuroprotective strategy for treating HIE, targets the second phase to prevent reperfusion injury. NICU nurses are in a unique position to detect patient instability and to maintain the therapeutic interventions that contribute to the healing process. This article highlights the significant role nurses play in the management of infants diagnosed with HIE who are treated with induced hypothermia.
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PMID:Induced hypothermia for neonatal hypoxic-ischemic encephalopathy: pathophysiology, current treatment, and nursing considerations. 2131 95

Hypoxic-ischemic encephalopathy (HIE) is characterized as brain injury that results from lack of oxygen or blood flow to the brain in the perinatal period. Neonatal whole-body hypothermia and selective head cooling are becoming increasingly common care practices across the U.S. and Canada for infants with moderate-to-severe HIE because of the demonstrated ability of these approaches to reduce reperfusion injury to the brain. Health care professionals must develop a clinical care path for these fragile infants. For best results, induced hypothermia should be initiated within six hours of birth; therefore, care must be organized and provided without delay. This article provides bedside clinicians with care recommendations for infants being treated with these new interventions.
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PMID:"Caution! Contents should be cold": developing a whole-body hypothermia program. 2172 53

Hypoxic-ischemic encephalopathy (HIE) occurring during the perinatal period is one of the primary causes of severe, long-term neurological deficits in children. Initial systemic supportive therapy remains a critical aspect of HIE management. In addition to support therapy, the widespread use of hypothermia has demonstrated a reduction in death and neurodevelopmental disability in infants with moderate to severe HIE. Neonates with HIE born outside of tertiary care centers must be rapidly identified as hypothermia candidates and have emergent transport arranged. While waiting for the transport team to arrive, these neonates often require intensive stabilization, including meticulous temperature management. This article examines the need for HIE outreach teaching programs, assists in the identification of a neonate for hypothermia therapy, and supplies evidence-based recommendations for the initial stabilization and care of neonates delivered at nontertiary care facilities. The guidelines and materials supplied represent the outreach model used by our regional hypothermia center and disseminated to the surrounding referral hospitals.
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PMID:While waiting: early recognition and initial management of neonatal hypoxic-ischemic encephalopathy. 2430 Sep 60

Hypoxic-ischemic encephalopathy (HIE) due to neonatal asphyxia is an important cause of irreversible bad neurodevelopmental outcomes in children. Understanding the mechanisms causing the central nervous system cell death enabled the development of new treatment strategies that may decrease the severity of neurological damage. This survey includes data on epidemiology, pathogenesis, clinical features and diagnostic criteria of HIE. We discuss the neuro-protective mechanisms of therapeutic hypothermia and provide data on clinical studies conducted to investigate the impact and safety of this treatment in newborn infants affected by HIE. In addition, other therapeutic options of neuro-protective agents are mentioned.
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PMID:[Hypothermia as a treatment for hypoxic ischemic encephalopathy after neonatal asphyxia--update]. 2436 95

Hypoxic-ischemic encephalopathy (HIE) due to perinatal asphyxia remains an important cause of neonatal morbidity and mortality. The aim of this study was to investigate the predictive values of biochemical parameters, including serum creatine kinase (CK), lactate dehydrogenase (LDH), uric acid (UA), and lactate, in newborns with HIE. A total of 94 patients who were diagnosed with HIE were prospectively enrolled into the study. According to the Sarnat and Sarnat classification, 29 (30.9%) patients had Stage I, 36 (38.3%) Stage II, and 29 (30.9%) Stage III HIE. When CK, LDH, UA, and lactate were used together in order to determine the stage of HIE, specificity and sensitivity were calculated to be 87% and 94%, respectively. Measurement of serum CK, LDH, lactate, and UA levels together is a promising method in determining the stage of hypoxia in the laboratory before clinical manifestations occur so that hypothermia treatment can be initiated earlier.
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PMID:Can biochemical markers predict the severity of hypoxic-ischemic encephalopathy? 2482 49

Medical malpractice litigation in the USA and much of the developed world has reached near-epidemic proportions. Brain-damaged infants are among the most costly medical malpractice lawsuits, with the average indemnity for these cases being $524,047. Hypoxic-ischemic encephalopathy (HIE) is the most common birth injury claim, generally alleging that intrapartum asphyxia led to long-term neurologic sequelae, including cerebral palsy and/or developmental delay. Timing of injury is a key element in the legal arena. The plaintiff will try to prove that injury occurred in the intrapartum period, whereas the defense may argue that it occurred prenatally. A recent American Academy of Pediatrics/American College of Obstetricians and Gynecologists Task Force on Neonatal Encephalopathy developed a checklist that needs to be fulfilled in order to establish a reasonable causal link between an intrapartum asphyxial insult and subsequent long-term neurologic disability. Therapeutic hypothermia has been shown to benefit certain infants born with moderate to severe HIE by improving neurologic outcomes. Since the advent of hypothermic neuroprotection, new malpractice allegations have arisen, including the failure to refer a baby for cooling and failure to initiate cooling in a timely manner. In all cases, documentation of the status of the baby at birth, including a thorough neurologic exam, can be extremely helpful to the later defense of a malpractice claim, which might occur years later.
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PMID:Medico-legal implications of hypoxic-ischemic birth injury. 2515 Jul 92


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