Neonatal hypoglycaemia can be a stand-alone condition or a clinical manifestation of other conditions. Signs and symptoms
The way in which neonatal hypoglycemia symptoms may be presented is vague or hard to tell apart from other conditions. The symptoms can be confused with:

hypocalcemia
Sepsis
CNS disorders
Cardiorespiratory problemsNeonatal hypoglycemia can also show no symptoms in some newborns or may be life-threatening.Some observed symptoms are (these symptoms may be transient but reoccurring):

Jitteriness
hypothermia 
irritability 
pallor 
tremors
twitching
weak or high pitched cry
lethargy
hypotonia
generalized seizures
coma
cyanosis
apnea
rapid and irregular respirations
diaphoresis
eye rolling
refusal to feed
hunger

Causes
Risk Factors
Mother
Risk factors in the mother that increased the risk of developing hypoglycemia shortly after birth include:

Type 1 diabetes
Gestational diabetes mellitus (Transient)
Intrapartum glucose administration (Transient)
Gestational hypertension
Preeclampsia
Terbutaline administration (Transient)
Intrauterine growth restriction (Transient)
Perinatal stress or asphyxia (Transient)

Baby
Babies which have an increased risk of developing hypoglycemia shortly after birth are:

hypothermia (Transient)
polycythemia (Transient)
hyperinsulinism (Recurrent)
IEMs (Recurrent)
Beckwith-Wiedmann syndrome (Recurrent)
nesidioblastosis (Recurrent)
Rh isoimmunization (Recurrent)
Certain endocrine disorders (Recurrent)
fetal hydrops
Prematurity (Transient)
congenital malformations
small for gestational age (Transient)
Large for gestational age (Transient)

Hyperinsulinism
The most common cause on neonatal hypoglycemia is hyperinsulinism. Hyperinsulinism is also called persistent hyperinsulemic hypoglycemia of infancy (PHHI). This is seen very frequently to the neonates born from mothers with diabetes. Congenital hyperinsulinism is correlated with the abnormality of beta-cell regulation within the pancreas. Isolated islet adenoma, which is a focal disease, is often the cause of congenital hyperinsulism. Drug-induced hyperinsulisim is correlated with the administration insulin or use of hypoglycemic medication. In critical cases, a drug called Diazoxide is availed to stop any secretion of insulin. Limited glycogen stores
Limited glycogen storage occurs in premature newborns or newborns that had intrauterine growth retardation.
Syphilitic aortitis  is inflammation of the aorta associated with the tertiary stage of syphilis infection. SA begins as inflammation of the outermost layer of the blood vessel, including the blood vessels that supply the aorta itself with blood, the vasa vasorum. As SA worsens, the vasa vasorum undergo hyperplastic thickening of their walls thereby restricting blood flow and causing ischemia of the outer two-thirds of the aortic wall. Starved for oxygen and nutrients, elastic fibers become patchy and smooth muscle cells die. If the disease progresses, syphilitic aortitis leads to an aortic aneurysm. Overall, tertiary syphilis is a rare cause of aortic aneurysms. Syphilitic aortitis has become rare in the developed world with the advent of penicillin treatments after World War II. Signs and symptoms
The infection often has no symptoms until the patient develops an aneurysm because of the aortic dilatation. The disease is often discovered after a routine checkup of the heart and aorta. Although is easy to be overlooked, other symptoms of tertiary syphilis might appear such as gummas and symptoms of neurosyphilis (headache, stiff neck, gait abnormality, dementia etc). Additionally, in rare cases, chest pain and shortness of breath might appear as a result of the damage of the aorta and heart valve. Pathogenesis
Inflammatory involvement of tertiary syphilis begins at the adventitia of the aortic arch which progressively causes obliterative endarteritis of the vasa vasorum.