Therapeutics of neonatal asphyxia in production animals: a review

Abstract

The aim of this review is to assess the different treatments and therapeutic protocols used for neonatal asphyxia in animal production. Perinatal asphyxia is considered to be one of the main non-infectious causes of neonatal mortality in the majority of domestic mammals. However, its incidence in intensive animal production is increasing because of a series of implemented strategies aimed at improving and increasing production. For example, through the application of genetics, an increase in size and weight in newly born animals has been achieved. Nevertheless, this has resulted in a larger incidence of dystocia associated with oxygen restriction to thefoetus, which elicits metabolic and respiratory acidosis. Furthermore, aside from immediate financial implications when it comes to production, it also has an impact on the welfare of mother and offspring. Regarding the field of animal perinatology, several therapeutic strategies using respiratory and hormonal stimulants, as well as energetic supplements have been evaluated with the aim of preventing perinatal asphyxia and treating neonates with the condition, and also to diminish the incidence of stillbirths associated with it. However, during the last decades this condition has persisted mainly in porcine, equine, ovine and bovine production; for this reason, it continues to be studied extensively.

Treatments and therapeutic protocols for the recovery of an asphyxiated new-born: A review of pre-clinical and clinical studies in human neonates and in different animal models

“…The reduction in oxygen availability during asphyxiation in human neonates and foetuses and also in other mammals (for example: piglets, lambs, dogs, and foals) is classified into three types: Type 1) Hypoxaemia, which implies a reduction of oxygen in arterial blood without necessarily affecting the functions of the organs and cells (Sanchez-Salcedo et al 2019a). Type 2) Hypoxia, which results from a significant reduction of oxygen in the inhalation of air and, consequently, in the tissues.…”

“…Type 2) Hypoxia, which results from a significant reduction of oxygen in the inhalation of air and, consequently, in the tissues. Therefore, the oxygen (O 2 ) supply is inadequate for the oxygen requirements of the tissues and the aerobic metabolism is completed with the anaerobic metabolism to maintain the energy balance (Tsikouras et al 2017), and Type 3) asphyxiation, in which hypoxia spreads to the central organs and can lead to metabolic acidosis (Sanchez-Salcedo et al 2019a) because, when hypoxia is prolonged, blood is redistributed from the non-vital organs (liver, kidney) to the brain and anaerobic metabolism produces lactic acid (hence, metabolic acidosis). Since oxygen deficiency is accompanied by acidosis, the energy balance can no longer be maintained which leads to reduction in organ function eventually resulting in permanent tissue damage (Tsikouras et al 2017).…”

“…This injury is the result of the combination of a reduction in the cerebral oxygen (hypoxaemia) and/or a reduction of perfusion (ischaemia) and oxygenation to the brain. During the acute stage of brain damage, neuronal cell death occurs through necrosis, as a result of brain energy depletion, and even though metabolic energy levels recover in the brain after a few hours, a cascade of biochemical events is activated, resulting in neuronal apoptosis and, consequently, severe brain damage (Sanchez-Salcedo et al 2019a). Therefore, the early failure of the energy supply represents an important factor in the survival of the new-born.…”

“…During acute phases of hypoxic ischaemic encephalopathy (HIE), neuronal cell death by necrosis occurs because of a depletion of brain energy. Even at a few hours post-asphyxia, after the start of aerobic energy metabolism and replenishment of the glucose levels, the previously initiated apoptosis produces severe injury in the brain (Orozco-Gregorio et al 2008;Sanchez-Salcedo et al 2019a). Accordingly, one of the therapeutic agents studied for its possible neuroprotective effect is thiamine, a vitamin that exerts its metabolic action mainly through thiamine pyrophosphate (PPT), which is an indispensable cofactor in the activation of pyruvate dehydrogenase (PDH), alpha-keto glutarate dehydrogenase (α-CGDH), alpha-keto acid dehydrogenase and trancetolase; enzymes involved in energy generation processes through the Krebs cycle or the pentose pathway (Valenzuela-Peraza et al 2014).…”

Doenças na fase de aleitamento e práticas de manejo sanitário na criação de bezerras

“…15 Os animais com asfixia neonatal apresentam baixa pO 2 e desenvolvem hipertensão da artéria pulmonar, com persistência do forame oval e ducto arterioso, especialmente em bezerras clonadas . 16 A asfixia neonatal se caracteriza pela hipoxemia, hipercapnia e acidose mista, resultante da inadequada oxigenação do feto ou recém-nascido, descrita na literatura como Síndrome da Dificuldade Respira- 17,18 tória (SDR) ou Asfixia Perinatal . A asfixia neonatal pode ser classificada conforme sua etiologia e momento de seu aparecimento, em asfixia precoce, que ocorre durante ou imediatamente após o parto, e asfixia tardia, 13 observada nas primeiras horas de vida .…”