Intrauterine growth restriction is one of the main diagnostic and therapeutic challenges in perinatal medicine. One in five perinatal deaths, the same number of preterm labours before 34 weeks of gestation and 1/3 of morbidity cases among newborns are associated with the occurrence of this pathology (1, 2). SGA (Small for Gestational Age) and IUGR (Intrauterine Growth Restriction) are used interchangeably. However, it should be emphasised that their meaning is different. The term SGA was first used by neonatologists in 1967 to describe a newborn with a birth weight below the 10^th percentile (3). Later, this term was adopted by obstetricians to describe foetuses with small birth weight regardless of aetiology. IUGR, in turn, refers to foetuses with growth rate reduction, and thereby the birth weight is causatively associated with the placental pathology. So far, there have been many definitions describing abnormal foetal growth. According to ASOG, these are foetuses with bodyweight below 10^th percentile, whereas the WHO defines in the same way foetuses under 3^rd percentile (4). The discrepancies in the definition make it difficult to determine the criteria for diagnosis and classification. The research on the natural course of intrauterine growth restriction poses a number of challenges. Firstly, the diagnosis often takes place after delivery. This concerns up to 3/4 of children born with intrauterine growth restriction (5). In the so-called low-risk populations, the diagnosis rate is only 15% (6). Such a low detection rate of foetuses with low birth weight is also observed in populations in which a routine reference test in the third trimester of pregnancy is performed (7, 8). It was shown that most intrauterine deaths that could have been avoided result from the failure to diagnose SGA prior to delivery (9). Secondly, IUGR diagnosis most often leads to earlier pregnancy termination, particularly in severe cases, and the greater the child’s maturity, the better the chance of extrauterine development. Most qualitative and quantitative evidence for the significance of IUGR diagnosis comes from retrospective analyses of post-delivery foetuses born alive or dead (10). The need to improve IUGR definition by implementing the concept of foetal growth potential is postulated. It is also important to differentiate between IUGR and SGA foetuses, whose lower birth weight is primarily due to constitutional factors and does not increase the risk of pathology in pregnancy, labour or the neonatal period. Selection of foetal subpopulations with pathologically restricted growth constitutes a challenge for modern perinatology. In recent years, two types of intrauterine foetal growth restriction have been distinguished – early and late (10). The first one occurs before the 34 weeks of pregnancy and is associated with difficulties in pregnancy monitoring and termination. The second type primarily constitutes a significant diagnostic problem. Innovating ultrasound techniques, with a view to a very detailed description of foetal anatomy, placental function and ultrasound assessment of uterine, placental and foetal blood flow, allow for a very detailed differentiation between small but healthy foetuses and the foetuses with restricted growth due to placental dysfunction.

An utmost care should be taken in the adequate diagnosis and managing a pregnancy characterised by disturbed foetal growth. Since most SGA cases are diagnosed in the third trimester of pregnancy and are associated with good prognostics, a precise analysis of risk factors should be performed (tab. 1) (11).

Determining the probable aetiology may reduce perinatal complications, in particular intrauterine death of anatomically normal foetuses. It should be noted that advanced age of the mother, diseases in the pregnancy and methods of assisted reproduction, which are well-known risk factors, have become more common. Intrauterine growth restriction is an important factor for intrauterine foetal death. The relative risk is 4.0 (95% CI = 2.8-5.7) when the pathology is diagnosed prenatally, and twice as high – 8.0 (95% CI = 6.5-9.9) if it is undiagnosed (2). In large population studies evaluating intrauterine deaths earlier growth retardation (weight < 10^th percentile) accounted for over 50% of deaths after the exclusion of congenital defects. As a result of the analysis, the number of unexplained intrauterine deaths decreased from 65-70% (Wigglesworth classification) to about 15% (12, 13).

Diagnostic management in determining SGA aetiology involves a detailed medical history, an evaluation of foetal anatomy, an assessment of markers for chromosomal aberrations, serological status of the patient and a Doppler analysis of maternal-foetal flows. This allows for an identification of the cause underlying the disturbed growth, differentiation between healthy and affected SGA infants and determination of IUGR. The exact diagnosis will influence adequate management aimed at minimising potential complications.

The potential risk of morbidity in foetuses with hypotrophy can be classified into two groups: early and late (tab. 2) (11).

In general, it can be stated that smaller foetuses run a higher risk of worse perinatal outcome, though this group should be divided into pathologically and physiologically (constitutionally) small foetuses. The latter group will be defined as SGA (small for gestational age). SGA are foetuses with estimated body weight (EFW) below the 10^th percentile. This group was selected from the population due to a significantly higher morbidity risk in term infants with body weight under the 10^th percentile compared to the average population risk (3). Foetuses with intrauterine growth restriction (IUGR) have a higher risk of intrauterine complications, such as hypoxia or death as well as low Apgar score at birth (7). They will comprise, to some extent, a subgroup of SGA in which the genetically programmed growth process was restricted by one or more risk factors connected with abnormal processes in the formation of maternal-foetal circulation. However, these are two separate groups, which is confirmed by a higher perinatal morbidity risk as compared to SGA. Therefore, IUGR should always be excluded in a group of foetuses with EFG < 10^th percentile. What should differentiate foetuses with restricted growth from constitutionally small ones is abnormal flow indicating centralised circulation that reflects adaptive foetal changes due to chronic malnutrition of varying degree will differentiate foetuses with restricted growth from constitutionally small foetuses. Macroscopic, histological and biochemical indicators of placental disease as well as an increased co-existence of preeclampsia will be observed in these pregnancies. For over 20 years, abnormal, elevated umbilical artery resistance was the main factor differentiating between these two forms. In recent years, it has been shown that although this was true for foetuses with severe placental pathology, in cases of moderate insufficiency this method does not allow for a diagnosis of a substantial part of early and virtually all late cases of hypotrophy (14-16).

Therefore, the division into early and late-onset IUGR seems justified. The widespread use of this division would be of a special value in attempts to compare the results from different centres. Clinically, this classification is important due to different methods for the monitoring and management in such pregnancies.

Early-onset IUGR accounts for approximately 20-30% of all pregnancies complicated by intrauterine growth restriction, while in almost 50% of cases it is associated with the co-existence of preeclampsia. In this form, the degree of placental failure is high and exceeds 30%. Moreover, in most cases it is characterised by an abnormal spectrum of flows in the umbilical artery (17). In these foetuses, a typical sequence of changes in Doppler flow spectra are observed: increased resistance in the umbilical artery, lower resistance in the middle cerebral artery, circulatory centralisation, gradual lowering of A-wave in the ductus venosus, disappearance of the diastolic wave in the umbilical cord, etc. These changes indicate foetal adaptation to chronic hypoxia and, in effect, may precede intrauterine death by weeks. The aim of the medical management is to balance between the risk of hypoxia-related complications and intrauterine death and the risk of complications and neonatal death as a result of prematurity.