This case study is about a neonate with severe Hypoxic-ischaemic encephalopathy, therefore it will take into account pathophysiological, diagnostic and grading issues surrounding HIE, and how these reflect on prognosis.

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This case study is about a neonate with severe Hypoxic-ischaemic encephalopathy, therefore it will take into account pathophysiological, diagnostic and grading issues surrounding HIE, and how these reflect on prognosis; consideration to the ethical issues associated with withdrawal of intensive care support will be made, encapsulating the infant’s predicted quality of life; finally, the impact that technology and medical/nursing interventions have upon the NICU environment will then be addressed, demonstrating how NICU’s and staff are responding to this.

Brain hypoxia and ischaemia from systemic hypoxaemia and reduced cerebral blood flow are the primary triggering events for HIE. A hypoxic-ischaemic insult occurring around the time of birth may result in an encephalopathic state characterised by the need for resuscitation at birth, neurological depression, seizures and electroencephalographic abnormalities, causing significant morbidity and mortality (Shankaran et al, 1991).

Hypoxic-ischaemic cerebral injury begins during an asphyxial insult and extends into a recovery period after resuscitation (the reperfusion interval). Asphyxia is impairment in gas exchange that results in both oxygen deficit and excess carbon dioxide, with ischaemia to vital organs (Rivkin, 1997). Subsequent tissue injury takes the form of apoptosis (i.e, programmed cell death). Experimental studies have shown that at a cellular level, (when cerebral perfusion is too low to provide adequate cerebral oxygenation), an evolving process of adverse biochemical events is initiated, including energy failure, acidosis, increased levels of excitatory neurotransmitters, free radical formation, increased intracellular calcium, and neurotoxicity from glutamate and nitric oxide (Edwards, 2003). These events disrupt cell structure and function ultimately causing cell death (Vannucci and Perlman, 1997). At the onset of reperfusion, several of these processes are further stimulated by the reintroduction of oxygen, so that injury is ongoing. Cerebral energy metabolism may initially recover only to deteriorate 6-24 hours later.  Although this secondary phase of impaired cerebral energy metabolism resolves after about 72 hours, a persistent disturbance may be detected for several months (Hanrahan et al, 1998;Robertson et al, 1999). This secondary insult (reperfusion injury) and its severity correlate well with the severity of long-term adverse neuro-developmental outcome and survival.

 It is during this interval after resuscitation that an intervention to reduce the severity of ongoing brain damage might prove effective. Mild selective brain hypothermia appears to be a promising option for encephalopathic infants following perinatal asphyxia. Positive results have been seen in adult human models (Marion et al, 1997; Schwab et al, 1998; Safar and Kochanek, 2002), and both adult and neonatal animal models (Wagner et al, 2002). However, a recent systematic review of treatment of head injury with whole body hypothermia failed to demonstrate benefit, but this could be due to inconsistencies in clinical management (Clifton et al, 2001 – see Appendix C – Clinical Care to see how TOBY guidelines aimed to address this issue). Presently, trials in human newborns are ongoing (such as the TOBY trial Ben was included in). Recent pilot studies in infants (Gunn et al, 1998; Azzopardi et al, 2000) have been reported with no noted complications, however only small groups were used making evaluations of benefit difficult.

Since no specific treatments are available for HIE as yet, current management remains reactive and early identification of the infants with asphyxia who are at highest risk for encephalopathy is critical if reperfusion injury is to be prevented. Therefore there is a need to have early markers of asphyxia such as: depressed Apgar scores, delay in establishing respiration, or evidence of significant metabolic acidosis on samples of cord blood (see Profile and Appendix A – TOBY Study Protocol inclusion criteria for Ben’s individual details).

Defence mechanisms contributing to neuronal preservation include a redistribution of cardiac output, with increased cerebral and myocardial blood flow at the expense of blood flow to less vital organs, a slower depletion of high-energy compounds during hypoxia-ischaema, and the use of alternative substrates (e.g., lactate and ketone bodies) as sources of energy (Perlman, 1997; Volpe, 2001).

Therefore the factors assessed during labour to identify Ben's risk of brain injury, included fatal heart rate monitoring and meconium monitoring in an attempt to identify fetal distress (see profile for details). Similarly a postnatal marker used to identify Ben’s risk of brain injury was the use of the Apgar score. In babies born of normal birth weight, the longer the Apgar score remains depressed, the more likely the baby is to die, but neurological prognosis is only well predicted if the score remains 0-3 at 20 minutes (Flavin, 2001). Other studies have suggested <5 at 15 minutes. (See profile for Ben’s Apgar scores).

Leeson et al (1995) considers analysis of umbilical cord gases to be a more effective means of assessment. Anaerobic metabolism, with the production of lactic acid, is a normal physiological response during periods of hypoxaemia. Although hypoxaemia may occur with accompanying hypercapnia (an abnormally high concentration of carbon dioxide in the blood), thus causing a respiratory acidosis, Ross et al (2002) claims that it is the cellular production of metabolic acids that reflects the degree of insult or injury. A marked metabolic acidosis was detected shortly after Ben’s birth; therefore the reporting of “base excess” assisted in providing a fuller understanding of Ben’s acid base assessments.

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There is an association between acidosis, acute physiological dysfunction in the neonate and longer-term neurodevelopment abnormalities. Whether the acidosis is causative or only an associated factor is less certain. Although umbilical artery cord pH has historically been used as a primary marker to hypoxic- ishaemic injury, most term infants with severe acidosis at the time of delivery have an uncomplicated neonatal course, reflecting in part the immense adaptive capacity of the fetus to withstand an asphyxia insult. In a study conducted by King et al (1998) the incidence of neonatal death and neonatal seizures did not increase until a ...

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