Perinatal risk factors for neonatal encephalopathy: an unmatched case-control study

Tann, Cally J; Nakakeeto, Margaret; Willey, Barbara; Sewegaba, Margaret; Webb, Emily L.; Oke, Ibby; Mutuuza, Emmanuel Derek; Peebles, Donald; Musoke, Margaret; Harris, Kathryn; Sebire, Neil J.; Klein, Nigel; Kurinczuk, Jennifer J; Elliott, Alison M.; Robertson, Nicola J.

doi:10.1136/archdischild-2017-312744

Cited by 58 publications

(70 citation statements)

References 32 publications

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“…In line with findings from another Ugandan study [24], we observed that FHR was not monitored in the second stage of labor. One of the reasons could be that although the WHO guidelines recommend listening to FHR every 5 min during the second stage of labor, the Ugandan clinical guidelines do not give guidance regarding FHRM during this stage [6,17].…”

Section: Discussionsupporting

confidence: 91%

Fetal heart rate monitoring practices at a public hospital in Northern Uganda – what health workers document, do and say

Ayebare

Jonas

Ndeezi

et al. 2020

Global Health Action

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Background: In Uganda, perinatal mortality is 38 per 1000 pregnancies. One-third of these deaths are due to birth asphyxia. Adequate fetal heart rate (FHR) monitoring during labor may detect birth asphyxia but little is known about monitoring practices in low resource settings. Objective: To explore FHR monitoring practices among health workers at a public hospital in Northern Uganda. Methods: A sequential explanatory mixed methods study was conducted by reviewing 251 maternal records and conducting 11 interviews and two focus group discussions with health workers complemented by observations of 42 women in labor until delivery. Quantitative data were summarized using frequencies and percentages. Content analysis was used for qualitative data. Results: FHR was assessed in 235/251 (93.6%) of records at admission. Health workers documented the FHR at least once in 175/228 (76.8%) of cases during the first stage of labor compared to observed 17/25 (68.0%) cases. Median intervals between FHR monitoring were 30 (IQR 30-120) minutes in patients' records versus 139 (IQR 87-662) minutes according to observations. Observations suggested no monitoring of FHR during the second stage of labor but records indicated monitoring in 3.2% of cases. Reported barriers to adequate FHR monitoring were inadequate number of staff and monitoring devices, institutional challenges such as few beds, documentation problems and perceived non-compliant women not reporting for repeated checks during the first stage of labor. Health workers demonstrated knowledge of national FHR monitoring guidelines and acknowledged that practice was different. Conclusions: When compared to national and international guidelines, FHR monitoring is sub-optimal in the studied setting. Approximately one in four women was not monitored during the first stage of labor. Barriers to appropriate FHR monitoring included shortage of staff and devices, institutional challenges and mother's negative attitudes. These barriers need to be addressed in order to reduce neonatal mortality.

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Section: Discussionsupporting

confidence: 91%

Fetal heart rate monitoring practices at a public hospital in Northern Uganda – what health workers document, do and say

Ayebare

Jonas

Ndeezi

et al. 2020

Global Health Action

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“…Fetal inflammation (funisitis) and early neonatal bacteraemia have been shown to be independent risk factors for encephalopathy (Tann et al . ). Late onset bacteraemia (due to factors such as long‐term indwelling catheters) in preterm infants during postnatal weeks 2–4 is associated with a greater risk of neurocognitive limitations at age 10 years (Bright et al .…”

Section: The Global Burden Of Hypoxic–ischaemic Brain Injurymentioning

confidence: 97%

The fetus at the tipping point: modifying the outcome of fetal asphyxia

Dhillon

Lear

Galinsky

et al. 2018

The Journal of Physiology

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Brain injury around birth is associated with nearly half of all cases of cerebral palsy. Although brain injury is multifactorial, particularly after preterm birth, acute hypoxia-ischaemia is a major contributor to injury. It is now well established that the severity of injury after hypoxia-ischaemia is determined by a dynamic balance between injurious and protective processes. In addition, mothers who are at risk of premature delivery have high rates of diabetes and antepartum infection/inflammation and are almost universally given treatments such as antenatal glucocorticoids and magnesium sulphate to reduce the risk of death and complications after preterm birth. We review evidence that these common factors affect responses to fetal asphyxia, often in unexpected ways. For example, glucocorticoid exposure dramatically increases delayed cell loss after acute hypoxia-ischaemia, largely through secondary hyperglycaemia. This critical new information is important to understand the effects of clinical treatments of women whose fetuses are at risk of perinatal asphyxia.

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“…A plausible hypothesis might be that the inflammatory activation in the absence of marked temperature changes lowers the threshold to cellular injury from an HI insult, without leading to neuronal necrosis, and thereby maintaining susceptibility to hypothermic rescue. The increased rate of infection (6–13%) among HIE neonates, compared to 0.5–1% in the general term-born neonatal population, supports the theory of elevated susceptibility to HI [39, 40]. HT reduces mortality and severe neurological morbidity in asphyxiated neonates, even though the investigated cohorts include infants with severe encephalopathy of HI origin both with and without infectious pre-exposure [1, 41].…”

Section: Discussionmentioning

confidence: 81%

Hypothermia Is Neuroprotective after Severe Hypoxic-Ischaemic Brain Injury in Neonatal Rats Pre-Exposed to PAM<sub>3</sub>CSK<sub>4</sub>

et al. 2018

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Background: Preclinical research on the neuroprotective effect of hypothermia (HT) after perinatal asphyxia has shown variable results, depending on comorbidities and insult severity. Exposure to inflammation increases vulnerability of the neonatal brain to hypoxic-ischaemic (HI) injury, and could be one explanation for those neonates whose injury is unexpectedly severe. Gram-negative type inflammatory exposure by lipopolysaccharide administration prior to a mild HI insult results in moderate brain injury, and hypothermic neuroprotection is negated. However, the neuroprotective effect of HT is fully maintained after gram-positive type inflammatory exposure by PAM₃CSK₄ (PAM) pre-administration in the same HI model. Whether HT is neuroprotective in severe brain injury with gram-positive inflammatory pre-exposure has not been investigated. Methods: 59 seven-day-old rat pups were subjected to a unilateral HI insult, with left carotid artery ligation followed by 90-min hypoxia (8% O₂ at T_rectal 36°C). An additional 196 pups received intraperitoneal 0.9% saline (control) or PAM_{1 mg/kg}, 8 h before undergoing the same HI insult. After randomisation to 5 h normothermia (NT₃₇_°_C) or HT₃₂_°_C, pups survived 1 week before they were sacrificed by perfusion fixation. Brains were harvested for hemispheric and hippocampal area loss analyses at postnatal day 14, as well as immunostaining for neuron count in the HIP CA1 region. Results: Normothermic PAM animals (PAM-NT) had a comparable median area loss (hemispheric: 60% [95% CI 33–66]; hippocampal: 61% [95% CI 29–67]) to vehicle animals (Veh-NT) (hemispheric: 58% [95% CI 11–64]; hippocampal: 60% [95% CI 19–68]), which is defined as severe brain injury. Furthermore, mortality was low and similar in the two groups (Veh-NT 4.5% vs. PAM-NT 6.6%). HT reduced hemispheric and hippocampal injury in the Veh group by 13 and 28%, respectively (hemispheric: p = 0.048; hippocampal: p = 0.042). HT also provided neuroprotection in the PAM group, reducing hemispheric injury by 22% (p = 0.03) and hippocampal injury by 37% (p = 0.027). Conclusion: In these experiments with severe brain injury, Toll-like receptor-2 triggering prior to HI injury does not have an additive injurious effect, and there is a small but significant neuroprotective effect of HT. HT appears to be neuroprotective over a continuum of injury severity in this model, and the effect size tapers off with increasing area loss. Our results indicate that gram-positive inflammatory exposure prior to HI injury does not negate the neuroprotective effect of HT in severe brain injury.

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Perinatal risk factors for neonatal encephalopathy: an unmatched case-control study

Cited by 58 publications

References 32 publications

Fetal heart rate monitoring practices at a public hospital in Northern Uganda – what health workers document, do and say

Fetal heart rate monitoring practices at a public hospital in Northern Uganda – what health workers document, do and say

The fetus at the tipping point: modifying the outcome of fetal asphyxia

Hypothermia Is Neuroprotective after Severe Hypoxic-Ischaemic Brain Injury in Neonatal Rats Pre-Exposed to PAM<sub>3</sub>CSK<sub>4</sub>

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