Placental insufficiency

Hypoxic ischaemic encephalopathy

Acute placental separation

Hypoxia, asphyxiation, ischaemia

Umbilical torsion/compression

Chest compression

Signs of prematurity at birth

Reduced surfactant production

Atelectasis

Neuronal cell damage due to lipid peroxidation, calcium influx into cells and neurotoxins such as nitric oxide and glutamate.

Neuronal cell death

Reperfusion injury from oxygen free radicals

Excessive

Insufficient

Rapid expulsion of fetus

Reduced time under pressure in birth canal

Lack of stimulus to inhibit secretion of sedative neurosteroids

Sedative effect on foal

Increased fetal and placental secretions of adenosine, pregnanolone and allopregnanolone

Hypoxic ischaemic encephalopathy

Perinatal asphyxia syndrome

Neonatal maladjustment syndrome

Abnormal behaviour, obtunded mentation

Increased recumbency

Hypersensitivity to stimuli

Anaerobic respiration and lactate synthesis

Increased exposure to pathogens

Metabolic acidosis

Increased risk of injury

Failure to suckle

SEPSIS

Increased risk of ischaemic ulceration of GIT

Impaired mucosal barrier

Increased risk of infection from enteric absorption

Increased risk of laryngeal cysts and DDSP

Abnormal breathing patterns and generalised weakness

Increased risk of aspiration pneumonia

Vasodilation

Hypotension

Reduced peripheral perfusion

Compensatory tachypnoea

Failure of passive transfer

Immunologically naive. Reduced ability to combat infection