Growth stunting is identified by comparing measurements of children's heights to the World Health Organization 2006 growth reference population: children who fall below the fifth percentile of the reference population in height for age are defined as stunted, regardless of the reason. The lower than fifth percentile corresponds to less than two standard deviations of the WHO Child Growth Standards median.

As an indicator of nutritional status, comparisons of children's measurements with growth reference curves may be used differently for populations of children than for individual children. The fact that an individual child falls below the fifth percentile for height for age on a growth reference curve may reflect normal variation in growth within a population: the individual child may be short simply because both parents carried genes for shortness and not because of inadequate nutrition. However, if substantially more than 5% of an identified child population have height for age that is less than the fifth percentile on the reference curve, then the population is said to have a higher-than-expected prevalence of stunting, and malnutrition is generally the first cause considered.

Three main things are needed to reduce stunting:

- a kind of environment where political commitment can thrive (also called an "enabling environment")

- applying several nutritional modifications or changes in a population on a large scale which have a high benefit and a low cost

- a strong foundation that can drive change (food security, empowerment of women and a supportive health environment through increasing access to safe water and sanitation).

To prevent stunting, it is not just a matter of providing better nutrition but also access to clean water, improved sanitation (hygienic toilets) and hand washing at critical times (summarised as "WASH"). Without provision of toilets, prevention of tropical intestinal diseases, which may affect almost all children in the developing world and lead to stunting will not be possible.

Studies have looked at ranking the underlying determinants in terms of their potency in reducing child stunting and found in the order of potency:

- percent of dietary energy from non-staples (greatest impact)

- access to sanitation and women's education

- access to safe water

- women's empowerment as measured by the female-to-male life expectancy ratio

- per capita dietary energy supply

Three of these determinants should receive attention in particular: access to sanitation, diversity of calorie sources from food supplies, and women's empowerment. A study by the Institute of Development Studies has stressed that: "The first two should be prioritized because they have strong impacts yet are farthest below their desired levels".

The goal of UN agencies, governments and NGO is now to optimise nutrition during the first 1000 days of a child's life, from pregnancy to the child's second birthday, in order to reduce the prevalence of stunting. The first 1000 days in a child's life are a crucial "window of opportunity" because the brain develops rapidly, laying the foundation for future cognitive and social ability. Furthermore, it is also the time when young children are the most at risk of infections that lead to diarrhoea. It is the time when they stop breast feeding (weaning process), begin to crawl, put things in their mouths and become exposed to faecal matter from open defecation and environmental enteropathies.

Measurements of a child’s growth provide the key information for the presence of malnutrition, but weight and height measurements alone can lead to failure to recognize kwashiorkor and an underestimation of the severity of malnutrition in children.

Measures have been taken to reduce child malnutrition. Studies for the World Bank found that, from 1970 to 2000, the number of malnourished children decreased by 20 percent in developing countries. Iodine supplement trials in pregnant women have been shown to reduce offspring deaths during infancy and early childhood by 29 percent. However, universal salt iodization has largely replaced this intervention.

The Progresa program in Mexico combined conditional cash transfers with nutritional education and micronutrient-fortified food supplements; this resulted in a 10 percent reduction the prevalence of stunting in children 12–36 months old. Milk fortified with zinc and iron reduced the incidence of diarrhea by 18 percent in a study in India.

In response to child malnutrition, the Bangladeshi government recommends ten steps for treating severe malnutrition. They are to prevent or treat dehydration, low blood sugar, low body temperature, infection, correct electrolyte imbalances and micronutrient deficiencies, start feeding cautiously, achieve catch-up growth, provide psychological support, and prepare for discharge and follow-up after recovery.

Among those patients who are hospitalized, nutritional support improves protein, colorie intake and weight.

As of 2016 is estimated that about 821,000 deaths of children less than five years old could be prevented globally per year through more widespread breastfeeding.

Physical examination to examine muscle wasting, laboratory investigations.

Novel zinc biomarkers, such as the erythrocyte LA:DGLA ratio, have shown promise in pre-clinical and clinical trials and are being developed to more accurately detect dietary zinc deficiency.

The diagnostic workup of a suspected iodine deficiency includes signs and symptoms as well as possible risk factors mentioned above. A 24-hour urine iodine collection is a useful medical test, as approximately 90% of ingested iodine is excreted in the urine. For the standardized 24-hour test, a 50 mg iodine load is given first, and 90% of this load is expected to be recovered in the urine of the following 24 hours. Recovery of less than 90% is taken to mean high retention, that is, iodine deficiency. The recovery may, however, be well less than 90% during pregnancy, and an intake of goitrogens can alter the test results.

If a 24-hour urine collection is not practical, a random urine iodine-to-creatinine ratio can alternatively be used. However, the 24-hour test is found to be more reliable.

A general idea of whether a deficiency exists can be determined through a functional iodine test in the form of an iodine skin test. In this test, the skin is painted with an iodine solution: if the iodine patch disappears quickly, this is taken as a sign of iodine deficiency. However, no accepted norms exist on the expected time interval for the patch to disappear, and in persons with dark skin color the disappeance of the patch may be difficult to assess. If a urine test is taken shortly after, the results may be altered due to the iodine absorbed previously in a skin test.

In order to avoid problems, the person must be rehabilitated with small but frequent rations, given every two to four hours. During one week, the diet, hyperglucidic, is gradually enriched in protein as well as essential elements: sweet milk with mineral salts and vitamins. The diet may include lactases - so that children who have developed lactose intolerance can ingest dairy products - and antibiotics - to compensate for immunodeficiency. After two to three weeks, the milk is replaced by boiled cereals fortified with minerals and vitamins until its mass is at least 80% of normal weight. Traditional food can then be reintroduced. The child is considered healed when his mass reaches 85% of normal.

Iodine deficiency is treated by ingestion of iodine salts, such as found in food supplements. Mild cases may be treated by using iodized salt in daily food consumption, or drinking more milk, or eating egg yolks, and saltwater fish. For a salt and/or animal product restricted diet, sea vegetables (kelp, hijiki, dulse, nori (found in sushi)) may be incorporated regularly into a diet as a good source of iodine.

The recommended daily intake of iodine for adult women is 150–300 µg for maintenance of normal thyroid function; for men it is somewhat less at 150 µg.

However, too high iodine intake, for example due to overdosage of iodine supplements, can have toxic side effects. It can lead to hyperthyroidism and consequently high blood levels of thyroid hormones (hyperthyroxinemia). In case of extremely high single-dose iodine intake, typically a short-term suppression of thyroid function (Wolff–Chaikoff effect) occurs. Persons with pre-existing thyroid disease, elderly persons, fetuses and neonates, and patients with other risk factors are at a higher risk of experiencing iodine-induced thyroid abnormalities. In particular, in persons with goiter due to iodine deficiency or with altered thyroid function, a form of hyperthyroidism called Jod-Basedow phenomenon can be triggered even at small or single iodine dosages, for example as a side effect of administration of iodine-containing contrast agents. In some cases, excessive iodine contributes to a risk of autoimmune thyroid diseases (Hashimoto's thyroiditis and Graves' disease).

Zinc deficiency can be classified as acute, as may occur during prolonged inappropriate zinc-free total parenteral nutrition; or chronic, as may occur in dietary deficiency or inadequate absorption.

A barium swallow test is often performed, where the child is given a liquid or food with barium in it. This allows the consulting medical practitioners to trace the swallow-function on an X-ray or other investigative system such as a CAT scan. An endoscopic assignment test can also be performed, where an endoscope is used to view the oesophagus and throat on a screen. It can also allow viewing of how the patient will react during feeding.

Fertilisers like ammonium phosphate, calcium ammonium nitrate, urea can be supplied. Foliar spray of urea can be a quick method.

Detecting phosphorus deficiency can take multiple forms. A preliminary detection method is a visual inspection of plants. Darker green leaves and purplish or red pigment can indicate a deficiency in phosphorus. This method however can be an unclear diagnosis because other plant environment factors can result in similar discoloration symptoms. In commercial or well monitored settings for plants, phosphorus deficiency is diagnosed by scientific testing. Additionally, discoloration in plant leaves only occurs under fairly severe phosphorus deficiency so it is beneficial to planters and farmers to scientifically check phosphorus levels before discoloration occurs. The most prominent method of checking phosphorus levels is by soil testing. The major soil testing methods are Bray 1-P, Mehlich 3, and Olsen methods. Each of these methods are viable but each method has tendencies to be more accurate in known geographical areas. These tests use chemical solutions to extract phosphorus from the soil. The extract must then be analyzed to determine the concentration of the phosphorus. Colorimetry is used to determine this concentration. With the addition of the phosphorus extract into a colorimeter, there is visual color change of the solution and the degree to this color change is an indicator of phosphorus concentration. To apply this testing method on phosphorus deficiency, the measured phosphorus concentration must be compared to known values. Most plants have established and thoroughly tested optimal soil conditions. If the concentration of phosphorus measured from the colorimeter test is significantly lower than the plant’s optimal soil levels, then it is likely the plant is phosphorus deficient. The soil testing with colorimetric analysis, while widely used, can be subject to diagnostic problems as a result of interference from other present compounds and elements. Additional phosphorus detection methods such as spectral radiance and inductively coupled plasma spectrometry (ICP) are also implemented with the goal of improving reading accuracy. According to the World Congress of Soil Scientists, the advantages of these light-based measurement methods are their quickness of evaluation, simultaneous measurements of plant nutrients, and their non-destructive testing nature. Although these methods have experimental based evidence, unanimous approval of the methods has not yet been achieved.

Some 25% to 40% of young children are reported to have feeding problems—mainly colic, vomiting, slow feeding, and refusal to eat. It has been reported that up to 80% of infants with developmental handicaps also demonstrate feeding problems while 1 to 2% of infants aged less than one year show severe food refusal and poor growth. Among infants born prematurely, 40% to 70% experience some form of feeding problem.

The visual symptoms of nitrogen deficiency mean that it can be relatively easy to detect in some plant species. Symptoms include poor plant growth, and leaves that are pale green or yellow because they are unable to make sufficient chlorophyll. Leaves in this state are said to be chlorotic. Lower leaves (older leaves) show symptoms first, since the plant will move nitrogen from older tissues to more important younger ones. Nevertheless, plants are reported to show nitrogen deficiency symptoms at different parts. For example, Nitrogen deficiency of tea is identified by retarded shoot growth and yellowing of younger leaves.

However, these physical symptoms can also be caused by numerous other stresses, such as deficiencies in other nutrients, toxicity, herbicide injury, disease, insect damage or environmental conditions. Therefore, nitrogen deficiency is most reliably detected by conducting quantitative tests in addition to assessing the plants visual symptoms. These tests include soil tests and plant tissue test.

Plant tissue tests destructively sample the plant of interest. However, nitrogen deficiency can also be detected non-destructively by measuring chlorophyll content.

Chlorophyll content tests work because leaf nitrogen content and chlorophyll concentration are closely linked, which would be expected since the majority of leaf nitrogen is contained in chlorophyll molecules. Chlorophyll content can be detected with a Chlorophyll content meter; a portable instrument that measures the greenness of leaves to estimate their relative chlorophyll concentration.

Chlorophyll content can also be assessed with a chlorophyll fluorometer, which measures a chlorophyll fluorescence ratio to identify phenolic compounds that are produced in higher quantities when nitrogen is limited. These instruments can therefore be used to non-destructively test for nitrogen deficiency.

The condition is determined by birth weight and/or length.

A related condition, IUGR, is generally diagnosed by measuring the mother's uterus, with the fundal height being less than it should be for that stage of the pregnancy. If it is suspected, the mother will usually be sent for an ultrasound to confirm.

Rickets may be diagnosed with the help of:

- Blood tests:

- Serum calcium may show low levels of calcium, serum phosphorus may be low, and serum alkaline phosphatase may be high from bones or changes in the shape or structure of the bones. This can show enlarged limbs and joints.

- A bone density scan may be undertaken.

- Radiography typically show widening of the zones of provisional calcification of the metaphyses secondary to unmineralized osteoid. Cupping, fraying, and splaying of metaphyses typically appears with growth and continued weight bearing. These changes are seen predominantly at sites of rapid growth, including the proximal humerus, distal radius, distal femur and both the proximal and the distal tibia. Therefore, a skeletal survey for rickets can be accomplished with anteroposterior radiographs of the knees, wrists, and ankles.

Infants with rickets often have bone fractures. This sometimes leads to child abuse allegations. This issue appears to be more common for solely nursing infants of black mothers, in winter in temperate climates, suffering poor nutrition and no vitamin D supplementation. People with darker skin produce less vitamin D than those with lighter skin, for the same amount of sunlight.

Correction and prevention of phosphorus deficiency typically involves increasing the levels of available phosphorus into the soil. Planters introduce more phosphorus into the soil with bone meal, rock phosphate,manure, and phosphate-fertilizers. The introduction of these compounds into the soil however does not ensure the alleviation of phosphorus deficiency. There must be phosphorus in the soil, but the phosphorus must also be absorbed by the plant. The uptake of phosphorus is limited by the chemical form in which the phosphorus is available in the soil. A large percentage of phosphorus in soil is present in chemical compounds that plants are incapable of absorbing. Phosphorus must be present in soil in specific chemical arrangements to be usable as plant nutrients. Facilitation of usable phosphorus in soil can be optimized by maintaining soil within a specified pH range. Soil acidity, measured on the pH scale, partially dictates what chemical arrangements that phosphorus forms. Between pH 6 and 7, phosphorus makes the fewest number of bonds which render the nutrient unusable to plants. At this range of acidity the likeliness of phosphorus uptake is increased and the likeliness of phosphorus deficiency is decreased. Another component in the prevention and treatment of phosphorus is the plant’s disposition to absorb nutrients. Plant species and different plants within in the same species react differently to low levels of phosphorus in soil. Greater expansion of root systems generally correlate to greater nutrient uptake. Plants within a species that have larger roots are genetically advantaged and less prone to phosphorus deficiency. These plants can be cultivated and bred as a long term phosphorus deficiency prevention method. In conjunction to root size, other genetic root adaptations to low phosphorus conditions such as mycorrhizal symbioses have been found to increase nutrient intake. These biological adaptations to roots work to maintain the levels of vital nutrients. In larger commercial agriculture settings, variation of plants to adopt these desirable phosphorus intake adaptations may be a long-term phosphorus deficiency correction method.

Being small for gestational age is broadly either:

- Being constitutionally small, wherein the state is basically a genetic trait of the baby.

- Intrauterine growth restriction, also called "pathological SGA"

Although GH can be readily measured in a blood sample, testing for GH deficiency is constrained by the fact that levels are nearly undetectable for most of the day. This makes simple measurement of GH in a single blood sample useless for detecting deficiency. Physicians therefore use a combination of indirect and direct criteria in assessing GHD, including:

- Auxologic criteria (defined by body measurements)

- Indirect hormonal criteria (IGF levels from a single blood sample)

- Direct hormonal criteria (measurement of GH in multiple blood samples to determine secretory patterns or responses to provocative testing), in particular:

- Subnormal frequency and amplitude of GH secretory peaks when sampled over several hours

- Subnormal GH secretion in response to at least two provocative stimuli

- Increased IGF1 levels after a few days of GH treatment

- Response to GH treatment

- Corroborative evidence of pituitary dysfunction

"Provocative tests" involve giving a dose of an agent that will normally provoke a pituitary to release a burst of growth hormone. An intravenous line is established, the agent is given, and small amounts of blood are drawn at 15 minute intervals over the next hour to determine if a rise of GH was provoked. Agents which have been used clinically to stimulate and assess GH secretion are arginine, levodopa, clonidine, epinephrine and propranolol, glucagon and insulin. An insulin tolerance test has been shown to be reproducible, age-independent, and able to distinguish between GHD and normal adults, and so is the test of choice.

Severe GH deficiency in childhood additionally has the following measurable characteristics:

- Proportional stature well below that expected for family heights, although this characteristic may not be present in the case of familial-linked GH deficiency

- Below-normal velocity of growth

- Delayed physical maturation

- Delayed bone age

- Low levels of IGF1, IGF2, IGF binding protein 3

- Increased growth velocity after a few months of GH treatment

In childhood and adulthood, the diagnosing doctor will look for these features accompanied by corroboratory evidence of hypopituitarism such as deficiency of other pituitary hormones, a structurally abnormal pituitary, or a history of damage to the pituitary. This would confirm the diagnosis; in the absence of pituitary pathology, further testing would be required.

The decision to treat is based on a belief that the child will be disabled by being extremely short as an adult, so that the risks of treatment (including sudden death) will outweigh the risks of not treating the symptom of short stature. Although short children commonly report being teased about their height, most adults who are very short are not physically or psychologically disabled by their height. However, there is some evidence to suggest that there is an inverse linear relationship with height and with risk of suicide.

Treatment is expensive and requires many years of injections with human growth hormones. The result depends on the cause, but is typically an increase in final height of about taller than predicted. Thus, treatment takes a child who is expected to be much shorter than a typical adult and produces an adult who is still obviously shorter than average. For example, several years of successful treatment in a girl who is predicted to be as an adult may result in her being instead.

Increasing final height in children with short stature may be beneficial and could enhance health-related quality of life outcomes, barring troublesome side effects and excessive cost of treatments.

Bed rest has not been found to improve outcomes and therefore is not typically recommended.

Mothers whose fetus is diagnosed with intrauterine growth restriction by ultrasound can use management strategies based on monitoring and delivery methods. One of these monitoring techniques is an umbilical artery Doppler. This method has been shown to decrease risk of morbidity and mortality before and after parturition among IUGR patients.

Time of delivery is also a management strategy and is based on parameters collected from the umbilical artery doppler. Some of these include: pulsatility index, resistance index, and end-diastolic velocities, which are measurements of the fetal circulation.