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KELAS C1 :
Zakiah Kurniasari – 173112540120475
Rochmawati – 173112540120456
Fitri Apriyanti – 173112540120202
Linda Kada – 173112540120221
Intan Mauludd – 173112540120382
Hidayati – 173112540120170
Monalisa – 173112540120270
Judul Jurnal :
Neonatal hipertermia dan stres termal di negara-negara
berpenghasilan rendah dan menengah: penyebab
tersembunyi kematian pada neonatus dengan berat
badan sangat rendah.
Amadi HO, Olateju EK, Alabi P, Kawuwa MB, Ibadin
MO, Osibogun AO.
(2015 Aug;35(3):273-81.Epub 2015 May 2.)
Metodologi :
Hasil : This article explores the concerns related to adverse
neurological out- comes associated with fetal and neonatal
hyperthermia. Maternal temper- ature is the most important
determinant of fetal temperature; here we draw attention to
the changing epidemiology of intrapartum maternal py-
rexia and consequent fetal hyperthermia, particularly its
association with labour epidural analgesia. The
implications of potential adverse neonatal outcomes
demand a greater understanding of the pathophysiology of
intrapartum maternal fever and exploration of monitoring,
preventative and therapeutic options encompassing the
modern obstetric, anaesthetic and neonatal practice.
Kesimpulan :
There is a need for heightened awareness among perinatal
cli- nicians about the potential harmful effects of
intrapartum maternal pyrexia on the fetus and the newborn
infant, including its association with epidural use. Epidural
analgesia is now so integral to pain relief in labour that it
will be unkind and impractical to suggest universal
limitation of its use. However, patients should be informed
of this adverse effect and its im- plications so that they are
able make an informed choice of the different available
modes of analgesia in labour. A greater vig- ilance of
maternal temperature in labour must be adopted and
traditionally available means of reducing temperature
instituted promptly until a more specific preventative or
therapeutic strategy is available. This may include a
prompt measurement of neonatal temperature at birth and
adoption of intentional passive cooling for the
hyperthermic newborns. Ongoing research in this area is
vital to resolve many of the unanswered
questions.
Latar Belakang : There are numerous studies that have assessed the
effect of hyperthermia on cerebral damage during a
period of ischemia, with or without hypoxia. It has
been repeatedly demonstrated that hyperthermia
exacerbates ischemic and/ or hypoxic-ischemic damage
and that avoidance of hyper- thermia in a patient at risk
for neurologic injury is imper- ative. Potential
mechanisms of injury include an increase in metabolic
demand, alterations in cerebral blood flow, and/ or an
increase in enzymes such as caspase-3, which is
important in the pathway leading to apoptosis [8,9,18].
Additionally, alteration of the blood-brain barrier may
occur with hypoxia and/or ischemia. A study of rats
exposed to 1, 2, and 7 days of hypobaric hypoxia
demonstrated a signifi- cant increase in sodium
fluorescein leak, which was used as a proxy for altered
blood-brain barrier permeability, into brain
parenchyma. There was also an associated reduction in
the expression of endothelial barrier antigen, a blood-
brain barriereassociated protein. When hypoxia was