Other conditions may commonly co-occur with FAS, stemming from prenatal alcohol exposure. However, these conditions are considered alcohol-related birth defects and not diagnostic criteria for FAS.

- Heart: A heart murmur that frequently disappears by one year of age. Ventricular septal defect most commonly seen, followed by an atrial septal defect.

- Bones: Joint anomalies including abnormal position and function, altered palmar crease patterns, small distal phalanges, and small fifth fingernails.

- Kidneys: Horseshoe, aplastic, dysplastic, or hypoplastic kidneys.

- Eyes: Strabismus, optic nerve hypoplasia (which may cause light sensitivity, decreased visual acuity, or involuntary eye movements).

- Occasional problems: ptosis of the eyelid, microophthalmia, cleft lip with or without a cleft palate, webbed neck, short neck, tetralogy of Fallot, coarctation of the aorta, spina bifida, and hydrocephalus.

In terms of FASD, growth deficiency is defined as significantly below average height, weight or both due to prenatal alcohol exposure, and can be assessed at any point in the lifespan. Growth measurements must be adjusted for parental height, gestational age (for a premature infant), and other postnatal insults (e.g., poor nutrition), although birth height and weight are the preferred measurements. Deficiencies are documented when height or weight falls at or below the 10th percentile of standardized growth charts appropriate to the population.

Criteria for FASD are least specific in the IOM diagnostic system ("low birth weight..., decelerating weight not due to nutrition..., [or] disproportional low weight to height" p. 4 of executive summary), while the CDC and Canadian guidelines use the 10th percentile as a cut-off to determine growth deficiency. The "4-Digit Diagnostic Code" allows for mid-range gradations in growth deficiency (between the 3rd and 10th percentiles) and severe growth deficiency at or below the 3rd percentile. Growth deficiency (at severe, moderate, or mild levels) contributes to diagnoses of FAS and pFAS, but not ARND or static encephalopathy.

Growth deficiency is ranked as follows by the "4-Digit Diagnostic Code":

- Severe: Height and weight at or below the 3rd percentile.

- Moderate: Either height or weight at or below the 3rd percentile, but not both.

- Mild: Either height or weight or both between the 3rd and 10th percentiles.

- None: Height and weight both above the 10th percentile.

In the initial studies that discovered FAS, growth deficiency was a requirement for inclusion in the studies; thus, all the original people with FAS had growth deficiency as an artifact of sampling characteristics used to establish criteria for the syndrome. That is, growth deficiency is a key feature of FASD because growth deficiency was a criterion for inclusion in the study that defined FAS. This suggests growth deficiency may be less critical for understanding the disabilities of FASD than the neurobehavioral sequelae to the brain damage.

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

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).

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.

Slowed growth is well documented in fetuses, but it is not as clear whether older children remain smaller or catch up to their peers. Some studies show that growth remains slowed for as many as ten years. PCE may also interfere with the way the motor system matures. Motor effects that have been documented include poorer reflexes and quality of movement in infants. PCE may have an effect on the neuroendocrine system, but more study is needed to determine whether it does and what the effects are.

A review of the literature reported that cocaine use causes congenital defects between 15 and 20% of the time; however another large-scale study found no difference in rates of birth anomalies in PCE and non-PCE infants. It has been suggested that some birth defects could be due to cocaine's disruption of blood vessel growth.

Most PCE-related congenital defects are found in the brain, heart, genitourinary tract, arms and legs.

Cocaine use by pregnant mothers may directly or indirectly contribute to defects in the formation of the circulatory system and is associated with abnormalities in development of the aorta. Heart malformations can include a missing ventricle and defects with the septum of the heart, and can result in potentially deadly congestive heart failure. Genital malformations occur at a higher-than-normal rate with PCE.

The liver and lungs are also at higher risk for abnormalities. Cloverleaf skull, a congenital malformation in which the skull has three lobes, the brain is deformed, and hydrocephalus occurs, is also associated with PCE. Like birth defects, small head size, and stroke are risks in PCE.

Prenatal cocaine exposure (PCE), theorized in the 1970s, occurs when a pregnant woman uses cocaine and thereby exposes her fetus to the drug. "Crack baby" was a term coined to describe children who were exposed to crack (freebase cocaine in smokable form) as fetuses; the concept of the crack baby emerged in the US during the 1980s and 1990s in the midst of a crack epidemic. Other terms are "cocaine baby" and "crack kid". Early studies reported that people who had been exposed to crack in utero would be severely emotionally, mentally, and physically disabled; this belief became common in the scientific and lay communities. Fears were widespread that a generation of crack babies were going to put severe strain on society and social services as they grew up. Later studies failed to substantiate the findings of earlier ones that PCE has severe disabling consequences; these earlier studies had been methodologically flawed (e.g. with small sample sizes and confounding factors). Scientists have come to understand that the findings of the early studies were vastly overstated and that most people who were exposed to cocaine "in utero" do not have disabilities.

No specific disorders or conditions have been found to result for people whose mothers used cocaine while pregnant. Studies focusing on children of six years and younger have not shown any direct, long-term effects of PCE on language, growth, or development as measured by test scores. PCE also appears to have little effect on infant growth.

However, PCE is associated with premature birth, birth defects, attention deficit hyperactivity disorder, and other conditions. The effects of cocaine on a fetus are thought to be similar to those of tobacco and less severe than those of alcohol. No scientific evidence has shown a difference in harm to a fetus between crack and powder cocaine.

PCE is very difficult to study because it very rarely occurs in isolation: usually it coexists with a variety of other factors, which may confound a study's results. Thus, studies have failed to clearly show that PCE has negative cognitive effects, partly because such effects may be due to concurrent factors. Pregnant mothers who use cocaine often use other drugs in addition, or they may be malnourished and lacking in medical care. Children in households where cocaine is abused are at risk of violence and neglect, and those in foster care may experience problems due to unstable family situations. Factors such as poverty that are frequently associated with PCE have a much stronger influence on children's intellectual and academic abilities than does exposure to cocaine in isolation. Thus researchers have had difficulty in determining which effects result from PCE and which result from other factors in the children's histories.

Generally it is preferable to describe specific signs in lieu of declaring "fetal distress" that include:

- Decreased movement felt by the mother

- Meconium in the amniotic fluid ("meconium stained fluid")

- Non-reassuring patterns seen on cardiotocography:

- increased or decreased fetal heart rate (tachycardia and bradycardia), especially during and after a contraction

- decreased variability in the fetal heart rate

- late decelerations

- Biochemical signs, assessed by collecting a small sample of baby's blood from a scalp prick through the open cervix in labor

- fetal metabolic acidosis

- elevated fetal blood lactate levels (from fetal scalp blood testing) indicating the baby has a lactic acidosis

Some of these signs are more reliable predictors of fetal compromise than others. For example, cardiotocography can give high false positive rates, even when interpreted by highly experienced medical personnel. Metabolic acidosis is a more reliable predictor, but is not always available.

In most cases Ballantyne syndrome causes fetal or neonatal death and in contrast, maternal involvement is limited at the most to preeclampsia.

The problem of distinguishing (or not) between Ballantyne syndrome and preeclampsia is reflected in the diversity of terminology used and in the debate that surrounds the subject. It seems much more likely that an etiology of severe fetal hydrops may cause Ballantyne syndrome when the fetal status greatly worsens and that the syndrome is only a manifestation of the extreme severity of the fetus-placental pathology. Platelet count, aspartate transaminase, alanine transaminase, and haptoglobin are usually unaffected and may be used to distinguish mirror syndrome from HELLP syndrome.

Each year, ill health as a result of pregnancy is experienced (sometimes permanently) by more than 20 million women around the world. In 2013 complications of pregnancy resulted in 293,000 deaths down from 377,000 deaths in 1990. Common causes include maternal bleeding (44,000), complications of abortion (44,000), high blood pressure of pregnancy (29,000), maternal sepsis (24,000), and obstructed labor (19,000).

The following are some examples of pregnancy complications:

- Pregnancy induced hypertension

- Anemia

- Postpartum depression

- Postpartum psychosis

- Thromboembolic disorders. These are the leading cause of death in pregnant women in the US.

- PUPPP (Pruritic Urticarial Papules and Plaques of Pregnancy), a skin disease that develops around the 32nd week. Signs are red plaques, papules, and itchiness around the belly button that then spreads all over the body except for the inside of hands and face.

- Ectopic pregnancy, implantation of the embryo outside the uterus.

- Hyperemesis gravidarum, excessive nausea and vomiting that is more severe than normal morning sickness.

- Pulmonary embolism, blood clots that form in the legs that can migrate to the lungs.

There is also an increased susceptibility and severity of certain infections in pregnancy.

Neurodevelopmental disorder is a mental disorder. A narrower use of the term refers to a disorder of brain function which affects emotion, learning ability, self-control and memory and which unfolds as the individual grows.

Neurodevelopmental disorders are impairments of the growth and development of the brain or central nervous system. A narrower use of the term refers to a disorder of brain function that affects emotion, learning ability, self-control and memory and that unfolds as an individual develops and grows.

The term is sometimes erroneously used as an exclusive synonym for autism spectrum disorders.

In medicine (obstetrics), the term fetal distress refers to the presence of signs in a pregnant woman—before or during childbirth—that suggest that the fetus may not be well. Because of its lack of precision, the term is eschewed in modern American obstetrics.

A vanishing twin, also known as fetal resorption, is a fetus in a multi-gestation pregnancy which dies in utero and is then partially or completely reabsorbed. In some instances, the dead twin will be compressed into a flattened, parchment-like state known as "fetus papyraceus".

Vanishing twins occur in up to one out of every eight multifetus pregnancies and may not even be known in most cases. "High resorption rates, which cannot be explained on the basis of the expected abortion rate...suggest intense fetal competition for space, nutrition, or other factors during early gestation, with frequent loss or resorption of the other twin(s)."

In pregnancies achieved by IVF, "it frequently happens that more than one amniotic sac can be seen in early pregnancy, whereas a few weeks later there is only one to be seen and the other has 'vanished'."

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.

It has been suggested that shift work and exposure to bright light at night should be avoided at least during the last trimester of pregnancy to decrease the risk of psychological and behavioral problems in the newborn.

Neu-Laxova syndrome presents with severe malformations leading to prenatal or neonatal death. Typically, NLS involves characteristic facial features, decreased fetal movements and skin abnormalities.

Fetuses or newborns with Neu–Laxova syndrome have typical facial characteristics which include proptosis (bulging eyes) with eyelid malformations, nose malformations, round and gaping mouth, micrognathia (small jaw) and low set or malformed ears. Additional facial malformations may be present, such as cleft lip or cleft palate. Limb malformations are common and involve the fingers (syndactyly), hands or feet. Additionally, edema and flexion deformities are often present. Other features of NLS are severe intrauterine growth restriction, skin abnormalities (ichthyosis and hyperkeratosis) and decreased movement.

Malformations in the central nervous system are frequent and may include microcephaly, lissencephaly or microgyria, hypoplasia of the cerebellum and agenesis of the corpus callosum. Other malformations may also be present, such as neural tube defects.

Affected newborns generally have striking neurological defects and seizures. Severely impaired development is common, but disturbances in motor functions may not appear until later in life.

Infants with microcephaly are born with either a normal or reduced head size. Subsequently, the head fails to grow, while the face continues to develop at a normal rate, producing a child with a small head and a receding forehead, and a loose, often wrinkled scalp. As the child grows older, the smallness of the skull becomes more obvious, although the entire body also is often underweight and dwarfed. Development of motor functions and speech may be delayed. Hyperactivity and intellectual disability are common occurrences, although the degree of each varies. Convulsions may also occur. Motor ability varies, ranging from in some to spastic quadriplegia in others.

Genetic

- Inborn errors of metabolism

1. Congenital disorder of glycosylation

2. Mitochondrial disorders

3. Peroxisomal disorder

4. Glucose transporter defect

5. Menkes disease

6. Congenital disorders of amino acid metabolism

7. Organic acidemia

Syndromes

- Contiguous gene deletion

1. 17p13.3 deletion (Miller–Dieker syndrome)

- Single gene defects

1. Rett syndrome (primarily girls)

2. Nijmegen breakage syndrome

3. X-linked lissencephaly with abnormal genitalia

4. Aicardi–Goutières syndrome

5. Ataxia telangiectasia

6. Cohen syndrome

7. Cockayne syndrome

Acquired

- Disruptive injuries

1. Traumatic brain injury

2. Hypoxic-ischemic encephalopathy

3. Ischemic stroke

4. Hemorrhagic stroke

- Infections

1. Congenital HIV encephalopathy

2. Meningitis

3. Encephalitis

- Toxins

1. Lead poisoning

2. Chronic renal failure

- Deprivation

1. Hypothyroidism

2. Anemia

3. Congenital heart disease

4. Malnutrition

Genetic factors may play a role in causing some cases of microcephaly. Relationships have been found between autism, duplications of chromosomes, and macrocephaly on one side. On the other side, a relationship has been found between schizophrenia, deletions of chromosomes, and microcephaly. Moreover, an association has been established between common genetic variants within known microcephaly genes ("MCPH1, CDK5RAP2") and normal variation in brain structure as measured with magnetic resonance imaging (MRI)i.e., primarily brain cortical surface area and total brain volume.

The spread of Aedes mosquito-borne Zika virus has been implicated in increasing levels of congenital microcephaly by the International Society for Infectious Diseases and the US Centers for Disease Control and Prevention. Zika can spread from a pregnant woman to her fetus. This can result in other severe brain malformations and birth defects. A study published in The New England Journal of Medicine has documented a case in which they found evidence of the Zika virus in the brain of a fetus that displayed the morphology of microcephaly.

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.

Meronanencephaly is a rare form of anencephaly characterized by malformed cranial bones, a median cranial defect, and a cranial protrusion called area cerebrovasculosa. Area cerebrovasculosa is a section of abnormal, spongy, vascular tissue admixed with glial tissue ranging from simply a membrane to a large mass of connective tissue, hemorrhagic vascular channels, glial nodules, and disorganized choroid plexuses.

Neu–Laxova syndrome (also known as Neu syndrome or Neu-Povysilová syndrome, abbreviated as NLS) is a rare autosomal recessive disorder characterized by severe intrauterine growth restriction and multiple congenital malformations. Neu–Laxova syndrome is a very severe disorder, leading to stillbirth or neonatal death. It was first described by Dr. Richard Neu in 1971 and Dr. Renata Laxova in 1972 as a lethal disorder in siblings with multiple malformations. Neu–Laxova syndrome is an extremely rare disorder with less than 100 cases reported in medical literature.

The condition is characterised by aversive reactions to feeding and oral stimulation including Co-Symptoms. It can occur one week after tube insertion.

- Food refusal/Head turning

- Loss of appetite/disinterest

- Oversensitivity for touching, smelling, tasting food

- Nausea

- Gagging

- Retching

- Vomiting

- Anxiety attacks