There are 2 major categories of IUGR: symmetrical and asymmetrical. Some conditions are associated with both symmetrical and asymmetrical growth restriction.

Asymmetrical IUGR is more common (70%). In asymmetrical IUGR, there is restriction of weight followed by length. The head continues to grow at normal or near-normal rates (head sparing). A lack of subcutaneous fat leads to a thin and small body out of proportion with the liver. Normally at birth the brain of the fetus is 3 times the weight of its liver. In IUGR, It becomes 5-6 times. In these cases, the embryo/fetus has grown normally for the first two trimesters but encounters difficulties in the third, sometimes secondary to complications such as pre-eclampsia. Other symptoms than the disproportion include dry, peeling skin and an overly-thin umbilical cord. The baby is at increased risk of hypoxia and hypoglycaemia. This type of IUGR is most commonly caused by extrinsic factors that affect the fetus at later gestational ages. Specific causes include:

- Chronic high blood pressure

- Severe malnutrition

- Genetic mutations, Ehlers–Danlos syndrome

Small for gestational age (SGA) newborns are those who are smaller in size than normal for the gestational age, most commonly defined as a weight below the 10th percentile for the gestational age.

Large for gestational age (LGA) is an indication of high prenatal growth rate.

LGA is often defined as a weight, length, or head circumference that lies above the 90th percentile for that gestational age. However, it has been suggested that the definition be restricted to infants with birth weights greater than the 97th percentile (2 standard deviations above the mean) as this more accurately describes infants who are at greatest risk for perinatal morbidity and mortality.

Macrosomia, which literally means "long body", is sometimes confused with LGA. Some experts consider a baby to be big when it weighs more than at birth, and others say a baby is big if it weighs more than . A baby is also called “large for gestational age” if its weight is greater than the 90th percentile at birth.

Tricho-hepato-enteric syndrome is one particular form of intractable diarrhea of infancy, presenting typically in the first month of life. These babies were usually born small for their age and continue to experience failure to thrive, usually with a final short stature. Typical facial features include prominent forehead and cheeks, a broad nasal root and widely spaced eyes (hypertelorism). Their hairs are woolly, easily removed and poorly pigmented. Liver disease is mainly present as cirrhosis or fibrosis, and staining might reveal high iron content of the liver cells (consistent with hemochromatosis). Most evaluated patients had some degree of decrease in intelligence.

LGA and macrosomia cannot be diagnosed until after birth, as it is impossible to accurately estimate the size and weight of a child in the womb. Babies that are large for gestational age throughout the pregnancy may be suspected because of an ultrasound, but fetal weight estimations in pregnancy are quite imprecise. For non-diabetic women, ultrasounds and care providers are equally inaccurate at predicting whether or not a baby will be big. If an ultrasound or a care provider predicts a big baby, they will be wrong half the time.

Although big babies are born to only 1 out of 10 women, the 2013 Listening to Mothers Survey found that 1 out of 3 American women were told that their babies were too big. In the end, the average birth weight of these suspected “big babies” was only . In the end, care provider concerns about a suspected big baby were the fourth-most common reason for an induction (16% of all inductions), and the fifth-most common reason for a C-section (9% of all C-sections). This treatment is not based on current best evidence.

Research has consistently shown that, as far as birth complications are concerned, the care provider’s perception that a baby is big is more harmful than an actual big baby by itself. In a 2008 study, researchers compared what happened to women who were suspected of having a big baby to what happened to women who were not suspected of having a big baby—but who ended up having one. In the end, women who were suspected of having a big baby (and actually had one) had a triple in the induction rate, more than triple the C-section rate, and a quadrupling of the maternal complication rate, compared to women who were not suspected of having a big baby but who had one anyway.

Complications were most often due to C-sections and included bleeding (hemorrhage), wound infection, wound separation, fever, and need for antibiotics. There were no differences in shoulder dystocia between the two groups. In other words, when a care provider “suspected” a big baby (as compared to not knowing the baby was going to be big), this tripled the C-section rates and made mothers more likely to experience complications, without improving the health of babies.

Developmental toxicity is any structural or functional alteration, reversible or irreversible, which interferes with homeostasis, normal growth, differentiation, development or behavior, and which is caused by environmental insult (including drugs, lifestyle factors such as alcohol, diet, and environmental toxic chemicals or physical factors). It is the study of adverse effects on the development of the organism resulting from exposure to toxic agents before conception (either parent), during prenatal development, or post-natally until puberty. The substance that causes developmental toxicity from embryonic stage to birth is called teratogens. The effect of the developmental toxicants depends on the type of substance, dose and duration and time of exposure.

Certain Pathogens are also included since the toxins they secrete are known to cause adverse effects on the development of the organism when the mother or fetus is infected. Developmental toxicology is a science studying adverse developmental outcomes. This term has widely replaced the early term for the study of primarily structural congenital abnormalities, teratology, to enable inclusion of a more diverse spectrum of congenital disorders. Typical factors causing developmental toxicity are radiation, infections (e.g. rubella), maternal metabolic imbalances (e.g. alcoholism, diabetes, folic acid deficiency), drugs (e.g. anticancer drugs, tetracyclines, many hormones, thalidomide), and environmental chemicals (e.g. mercury, lead, dioxins, PBDEs, HBCD, tobacco smoke). The first-trimester exposure is considered the most potential for developmental toxicity.

Once fertilization has taken place, the toxicants in the environment can pass through the mother to the developing embryo or fetus across the placental barrier. The fetus is at greatest risk during the first 14th to 60th day of the pregnancy when the major organs are being formed. However, depending on the type of toxicant and amount of exposure, a fetus can be exposed toxicant at any time during pregnancy. For example, exposure to a particular toxicant at one time in the pregnancy may result in organ damage and at another time in the pregnancy could cause death of the fetus and miscarriage. There are a number of chemicals, biological agents (such as bacteria and viruses), and physical agents (such as radiation) used in a variety of workplaces that are known to cause developmental disorders. Developmental disorders can include a wide range of physical abnormalities, such as bone or organ deformities, or behavioral and learning problems, such as a mental retardation. Exposures to some chemicals during pregnancy can lead to the development of cancer later in the life of the child and are called transgenerational carcinogens. Exposure to toxicants during the second and the third trimester of a pregnancy can lead to slow fetal grown and result in low birth weight.

Low birth weight (LBW) is defined by the World Health Organization as a birth weight of a

infant of 2,499 g or less, regardless of gestational age. Subcategories include very low birth weight (VLBW), which is less than 1500 g (3 pounds 5 ounces), and extremely low birth weight (ELBW), which is less than 1000 g (2 pounds 3 ounces). Normal weight at term delivery is 2500–4200 g (5 pounds 8 ounces – 9 pounds 4 ounces).

Tricho-hepato-enteric syndrome (THE), also known as syndromic or phenotypic diarrhea, is an extremely rare congenital bowel disorder which manifests itself as intractable diarrhea in infants with intrauterine growth retardation, hair and facial abnormalities. Many also have liver disease and abnormalities of the immune system. The associated malabsorption leads to malnutrition and failure to thrive.

It is thought to be a genetic disorder with an autosomal recessive inheritance pattern, although responsible genes have not been found and the exact cause remains unknown. Prognosis is poor; many patients die before the age of 5 (mainly from infections or cirrhosis), although most patients nowadays survive with intravenous feeding (parenteral nutrition).

Not all newborns that are SGA are pathologically growth restricted and, in fact, may be constitutionally small. If small for gestational age babies have been the subject of intrauterine growth restriction (IUGR), formerly known as intrauterine growth retardation, the term SGA associated with IUGR is used.

Intrauterine growth restriction (IUGR) refers to a condition in which a fetus is unable to achieve its genetically determined potential size. This functional definition seeks to identify a population of fetuses at risk for modifiable but otherwise poor outcomes. This definition intentionally excludes fetuses that are small for gestational age (SGA) but are not pathologically small. Infants born SGA with severe short stature (or severe SGA) are defined as having a length less than 2.5 standard deviation scores below the mean.

A related term is low birth weight (LBW), defined as an infant with a birth weight (that is, mass at the time of birth) of less than 2500 g (5 lb 8 oz), regardless of gestational age at the time of birth.

Related definitions include very low birth weight (VLBW) which is less than 1500 g, and extremely low birth weight (ELBW) which is less than 1000 g. Normal Weight at term delivery is 2500 g - 4200 g.

SGA is not a synonym of LBW, VLBW or ELBW.

Example: 35-week gestational age delivery, 2250g weight is appropriate for gestational age but is still LBW. One third of low-birth-weight neonates - infants weighing less than 2500g - are small for gestational age.

There is an 8.1% incidence of low birth weight in developed countries, and 6–30% in developing countries. Much of this can be attributed to the health of the mother during pregnancy. One third of babies born with a low birth weight are also small for gestational age. Infants that are born at low birth weights are at risk of developing neonatal infection.

Both low and high maternal serum Vitamin D (25-OH) are associated with higher incidence SGA in white women, although the correlation does not seem to hold for African American women.

The specific problems produced differ according to the particular abnormal synthesis involved. Common manifestations include ataxia; seizures; retinopathy; liver fibrosis; coagulopathies; failure to thrive; dysmorphic features ("e.g.," inverted nipples and subcutaneous fat pads; and strabismus. If an MRI is obtained, cerebellar atrophy and hypoplasia is a common finding.

Ocular abnormalities of CDG-Ia include: myopia, infantile esotropia, delayed visual maturation, low vision, optic disc pallor, and reduced rod function on electroretinography.

Three subtypes of CDG I (a,b,d) can cause congenital hyperinsulinism with hyperinsulinemic hypoglycemia in infancy.

Neonatal hypocalcemia is an abnormal clinical and laboratory hypocalcemia condition that is frequently observed in infants.[1]

Healthy term infants go through a physiological nadir of serum calcium levels at 7.5 - 8.5 mg/dL by day 2 of life. Hypocalcemia is a low blood calcium level. A total serum calcium of less than 8 mg/dL (2mmol/L) or ionized calcium less than 1.2 mmol/L in term neonates is defined as hypocalcemia. In preterm infants, it is defined as less than 7mg/dL (1.75 mmol/L) total serum calcium or less than 4mg/dL (1 mmol/L) ionized calcium. [2]

Both early onset hypocalcemia (presents within 72h of birth) and late onset hypocalcemia (presents in 3-7 days after birth) require calcium supplementation treatment.

LBW is either caused by preterm birth (that is, a low gestational age at birth, commonly defined as younger than 37 weeks of gestation) or the infant being small for gestational age (that is, a slow prenatal growth rate), or a combination of both.

In general, risk factors in the mother that may contribute to low birth weight include young ages, multiple pregnancies, previous LBW infants, poor nutrition, heart disease or hypertension, untreated coeliac disease, drug addiction, alcohol abuse, and insufficient prenatal care. Environmental risk factors include smoking, lead exposure, and other types of air pollutions.

Other features include:

- Stunting

- Small hands and feet with long, tapering fingers and clinodactyly

- Dental anomalies in the form of malalignment and malocclusion

In another study of six patients, the patients were investigated further. They were found to have low levels of IGF-1 and markedly retarded bone age.

One of the principle symptoms of GAPO syndrome is growth retardation, caused by slow skeletal formation and results in individuals being below average height. Alopecia, or hair loss, is another key indication of GAPO syndrome. Their hair is typically thinly dispersed, and fragile, which often leads to baldness later in life. Similarly, tooth growth is stunted, with teeth failing to emerge form the gums or otherwise develop normally. Atrophy of the optic nerve occurs in approximately one third of individuals. This degradation leads to inhibited peripheral vision, and increased difficulty distinguishing colours.

While not a defining feature, most sufferers of GAPO syndrome have coarse facial features, and abnormal structure of the middle portion of their faces, typically coupled with a large forehead. Individuals with the disease tend to have depressed nose bridges, protruding ears, and abnormally thick lips, though these symptoms are not unique to this disorder.

No direct correlation has been found between GAPO syndrome and mental retardation, though cases of individuals having both have been reported.

Due to the severity of the phenotype, GAPO syndrome can be diagnosed very early on. Most cases can be diagnosed by 6 months of age, and most symptoms will be apparent by age 2.

Children with the Sanjad Sakati syndrome have a triad of:

a) hypoparathyroidism (with episodes of hypocalcemia, hypocalcemic tetany and hypocalcemic seizures.

b) severe mental retardation and

c) dysmorphism.

Typically, children with this syndrome are born low-birth-weight due to intrauterine growth retardation. At birth, there is dysmorphism, which is later typified into the features described below. The child is stunted, often with demonstrable growth hormone deficiency and has moderate to severe mental retardation, mainly as a consequence of repeated seizures brought on by the low blood ionic calcium levels. The immuno-reactive parathormone levels are low to undetectable, with low calcium and high phosphate levels in the blood.

"Dysmorphism" is most evident on the face, with the following features:

- Long narrow face

- Deep-set, small eyes

- Beaked nose

- Large, floppy ears

- Small head (microcephaly) and

- Thin lips with a long philtrum.

Mutations in several genes have been associated with the traditional clinical syndromes, termed muscular dystrophy-dystroglycanopathies (MDDG). A new nomenclature based on clinical severity and genetic cause was recently proposed by OMIM. The severity classifications are A (severe), B (intermediate), and C (mild). The subtypes are numbered one to six according to the genetic cause, in the following order: (1) POMT1, (2) POMT2, (3) POMGNT1, (4) FKTN, (5) FKRP, and (6) LARGE.

Most common severe types include:

About one third of children whose mothers are taking this drug during pregnancy typically have intrauterine growth restriction with a small head and develop minor dysmorphic craniofacial features and limb defects including hypoplastic nails and distal phalanges (birth defects). A smaller population will have growth problems and developmental delay, or intellectual disability. Methemoglobinemia is a rarely seen side effect.

Heart defects and cleft lip may also be featured.

Protein–energy malnutrition (PEM) refers to a form of malnutrition which is defined as a range of pathological conditions arising from coincident lack of protein and/or energy in varying proportions.The condition vary in forms ranging from mild through moderate to severe degrees.

Types include:

- Kwashiorkor (protein malnutrition predominant)

- Marasmus (deficiency in calorie intake)

- Marasmic Kwashiorkor (marked protein deficiency and marked calorie insufficiency signs present, sometimes referred to as the most severe form of malnutrition)

PEM is fairly common worldwide in both children and adults and accounts for 6 million deaths annually. In the industrialized world, PEM is predominantly seen in hospitals, is associated with disease, or is often found in the elderly.

Note that PEM may be secondary to other conditions such as chronic renal disease or cancer cachexia in which protein energy wasting may occur.

Protein–energy malnutrition affects children the most because they have less protein intake. The few rare cases found in the developed world are almost entirely found in small children as a result of fad diets, or ignorance of the nutritional needs of children, particularly in cases of milk allergy.

Symptoms include:

- intellectual disability (more than half of the patients have an IQ below 50)

- microcephaly

- sometimes pancytopenia (low blood counts)

- cryptorchidism

- low birth weight

- dislocations of pelvis and elbow

- unusually large eyes

- low ears

- small chin

Complications may include cord compression, musculoskeletal abnormalities such as facial distortion and clubfoot, pulmonary hypoplasia and intrauterine growth restriction. Amnion nodosum is frequently also present (nodules on the fetal surface of the amnion).

The use of oligohydramnios as a predictor of gestational complications is controversial.

Potter syndrome is a condition caused by oligohydramnios. Affected fetuses develop pulmonary hypoplasia, limb deformities, and characteristic facies. Bilateral agenesis of the fetal kidneys is the most common cause due to the lack of fetal urine.

Many of the physical features associated with the disorder are congenital. Characteristic craniofacial abnormalities typically include a long, narrow head that is disproportionate to the body size, a broad and prominent forehead, and a triangular-shaped face with a hypoplastic midface, pointed chin, prominent mouth, fleshy tipped upturned nose, large ears, and full lips. The teeth may be abnormally crowded together in some affected individuals.

Individuals with 3-M syndrome suffer from severe prenatal growth retardation due to growth delays during fetal development resulting in a low birth weight. Growth delays continue after birth throughout childhood and adolescence, ultimately leading to a short stature.

Risk factors of early neonatal hypocalcemia

- Prematurity

- Perinatal asphyxia

- Diabetes mellitus in the mother

- Maternal hyperparathyroidism

- Intrauterine growth retardation (IUGR)

- Iatrogenic

Risk factors of late neonatal hypocalcemia

- Exogenous phosphate load

- Use of gentamicin

- Gender and ethnic: late neonatal hypocalcemia occurred more often in male infants and Hispanic infants

- Others

Gestational pemphigoid or pemphigoid gestationis (PG) is a dermatosis of pregnancy, being an autoimmune blistering skin disease that occurs during pregnancy, typically in the second or third trimester, and/or immediately following pregnancy. It was originally called herpes gestationis because of the blistering appearance, although it is not associated with the herpes virus.