Nutritional Considerations in Failure to Thrive Clinical Presentation

Updated: Dec 02, 2016
  • Author: Simon S Rabinowitz, MD, PhD, FAAP; Chief Editor: Jatinder Bhatia, MBBS, FAAP  more...
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The most important part of the evaluation of a child with failure to thrive (FTT) is obtaining a careful, detailed history. Once identified, the history can reveal whether the failure to thrive is organic, nonorganic (no identifiable physical conditions contributing to the problem), [44, 45, 46] or has components of both. As suggested above, the keen clinician will strive to identify subtle organic problems that may influence eating in seemingly healthy but deprived children as well as psychosocial challenges that further compromise intake in sick children. [21, 16]

The next step is to establish whether the parent of a child with organic failure to thrive feels that it is related to decreased intake, increased losses (eg, diarrhea, emesis) or abnormal metabolism (chronic illnesses, especially cardiopulmonary illnesses that increase the basal metabolic rate). Often times, multiple factors can coalesce in a single patient.

The history should include the following:

  • Prenatal/perinatal history: This should include history, information regarding smoking, alcohol use, use of medications, illnesses (including rashes), gestational age, single or multiple births, parturition events and any data on prenatal growth.
  • A review of the events in the nursery: This should include feeding problems and medical conditions, especially those that delay discharge. Mothers of NICU infants or discharge summaries should be queried for oropharyngeal or gastrointestinal setbacks, as well as a timeline for the introduction of tube feeds, and the transition to oral feeds. 
  • Detailed feeding history (with a documentation of how many ounces or liters are consumed in a 24-hour period rather than 3 oz every 3 h): Breastfed babies should have 7 or more wet diapers per day and regular passage of stools.
  • Inquire as to when the rate of weight gain first become a concern. Was it present when being breast or formula fed or was it associated with the transition to solid food or afterwards?
  • Description of how the mother prepares any formula which is not ready to feed: Improperly prepared formula can result in failure to thrive and serious electrolyte imbalances. The use of any supplements to formulas and/or substitutes for formulas should be identified.
  • Description of the type of solid foods eaten (including the quantitative composition and frequency of meals and snacks): If a detailed history is difficult to obtain, parents should bring in a 3-day food diary, as well as the jars and/or labels from foods that the child is eating or if available photos on their cell phones. For infants and toddlers, include the amount of formula/milk or milk substitute the child is taking. Nutritionists are helpful in interviewing parents and calculating the exact number of calories consumed.
  • Previously charted growth: Previous documentation of anthropometric data from the primary physician, health station, clinic, or electronic medical records should be referred to when analyzing the data. If any changes in rate of weight gain are noted, the primary care taker should be asked about changes in feeding and additional changes, including introduction of new foods, change from breast milk to formula or between formulas, and changes in the primary individuals responsible for feeding the child. Finally, any changes in family dynamics should be investigated. Multiple modulations is a defined risk factor that may go unnoticed. [17]
  • Details about any illnesses that occurred since the neonatal period (particularly those that require hospitalization or are chronic and/or permanent) including weight changes during these events as well as weights at admission and discharge.
  • Medical problems that can compromise eating (eg,  cleft palatecerebral palsy, spasticity, seizures, delayed development, and low motor tone) require closer scrutiny regarding caloric intake.
  • Family and social history: This should include growth and eating pattern of other siblings, living conditions, stressors, and data on parents' growth history.
  • A drug history should be part of evaluating any adolescents who present with failure to thrive. A retrospective review of adolescent inhalant abuse found that the growth impairment in some of these individuals met the failure to thrive criteria. [47]


The first thing that pediatricians should do in all health assessments is to plot the head circumference, height, and weight on a growth chart. Previous growth parameters should be used to detect trends in growth rather than relying on measurements at one particular visit. If weight, height, and head circumference are all compromised, this suggests an in utero insult and/or genetic or chromosomal abnormality (see the image below).

Failure of growth in weight, length, and head circ Failure of growth in weight, length, and head circumference starting at birth, suggesting an organic etiology that occurred in utero.

If weight and height growth are delayed with a normal head circumference, endocrinopathies (see the first 2 images below) or constitutional delay (see the third image below) should be suspected.

Growth failure in length and weight with a normal Growth failure in length and weight with a normal head circumference in an infant with growth hormone deficiency.
Acquired hypothyroidism. Acquired hypothyroidism.
Constitutional delay of growth. Constitutional delay of growth.

This pattern also can occur in long-standing failure to thrive. Ultimately, head circumference is delayed, emphasizing the importance of following these growth parameters over time. When only weight gain is delayed, this usually reflects recent energy (caloric) deprivation (see the image below).

Failure to thrive secondary to caloric deprivation Failure to thrive secondary to caloric deprivation.

Vital signs are usually within the reference range, but blood pressure, respiration rate, pulse rate, and oxygen saturation may provide important clues regarding the etiology.




Failure to thrive can be organized into nonorganic failure to thrive, organic failure to thrive, and a combination of nonorganic and organic failure to thrive. The relative incidence of each category completely depends on the population that the study examines. A study from a pediatric endocrinology clinic in a US university hospital found that half of the patients had a purely nutritional deficiency and another quarter had short stature. [30] As indicated above, many of the children from older articles who were considered to have nonorganic failure to thrive actually had subtle organic problems that contributed to their poor growth.

While the authors believe that most children have contributions from both etiologies, guidelines are being composed to assist clinicians with unclear circumstances.  A retrospective review compiled by a national children's hospital in Korea concluded that in their population, children with organic failure to thrive had significantly lower gestational ages, birth weights, and weight percentiles at presentation than those with nonorganic failure to thrive. In addition, the children with organic failure to thrive were more likely to have severe weight decline. [48]

Nonorganic failure to thrive

Nonorganic failure to thrive, the most written about form of failure to thrive results from adverse environmental and psychosocial factors. [49] The onset is almost always prior to age 5 years. It is often associated with abnormal interactions between the caregiver and the infant or child. At times, it can be part of a more global pattern of child abuse. The result is an inadequate provision of food and/or inadequate intake of food. It is most common in the setting of poverty. When considering almost all of the individual entities associated with nonorganic failure to thrive, an organic process can frequently be identified as an accomplice. 

Prenatal causes of nonorganic failure to thrive include the following:

  • Some mothers who are malnourished during pregnancy can have babies who are malnourished and small. This is more common in teen pregnancies, in lower socioeconomic locations, and with multiple gestations.
  • Maternal eating disorders (eg, anorexia, bulimia) can affect the growth of fetuses as well. Whether the failure to thrive in these infants is related to hormonal factors in addition to nutrient deprivation is open to debate.

Postnatal causes of nonorganic failure to thrive include the following:

  • Traditionally, nonorganic postnatal causes of failure to thrive were thought to be due to maternal rejection or neglect. Skuse et al suggested that clinicians inquire about more than just the nutrition offered to children. [50] He found behavior at meals and psychosocial issues to be important variables that affected whether children obtained sufficient energy.
  • Poor parenting and family dysfunction can negatively affect a child's energy intake. Families characterized by less adaptive relationships, higher levels of family conflict, maternal drug abuse, maternal depression, lack of maternal education, and less emotional support for the mother have an increased rate of children with failure to thrive. The term psychosocial deprivation was created for these types of situations.
  • Other classical nonorganic reasons for failure to thrive in younger children include a failure to signal hunger, a poor suck, difficulty in weaning, or a refusal to eat. An organic basis that plays a large role in these behaviors is now noted. An appreciation of the role of sensory integration dysfunction in a subset of children with these suck and signaling problems highlights the difficulty in separating organic from nonorganic FTT. [21]
  • Rarely in infants and toddlers, but more common in older children, eating disorders (eg, anorexia, bulimia) may lead to severe growth disturbances. Although infants and toddlers do not have the classical disturbed body image that characterizes the adolescents with eating disorders, all are involved in a struggle over control with food as the medium.
  • A recent retrospective review from an Asian children's hospital found the most common history for children with nonorganic failure to thrive was a preceding intercurrent viral illness followed by adoption of ill-advised compensatory feeding measures by the care provider. [48]
  • In cohorts where the prevalence of FTT is high, efforts should be made to understand patterns of complementary feeding and to realize that complementary food choices are culturally dependent. [51]
  • Although the typical groups with nonorganic failure to thrive are infants and toddlers, the younger the child is, the more likely they are to have some organic pathology that contributes to the aberrant feeding behavior. Children who are slow or fussy feeders often result in parental frustration and a lack of persistence. Underlying mild dysphagia may be part of the cause of this behavior. Similarly, feeding aversion may start as a consequence of pain related to  gastroesophageal reflux, enteropathy or fear of micro-aspiration in an infant. Subsequently, the fear may persist even after effective medical therapy and become more consequential than the original organic problem. [52]
  • Mild dysphagia is present, the infant may be a slow or fussy feeder, which can lead to parental frustration and their lack of persistence. Conversely, pain related to gastroesophageal reflux or enteropathy or fear of aspiration may lead to feeding aversion by the infant that becomes a more significant problem than the organic one.

Nonorganic causes of failure to thrive usually include combinations of the following:

  • Poverty
  • Dysfunctional family interactions (especially maternal depression or drug use)
  • Difficult parent-child interactions
  • Lack of parental support (eg, no friends, no extended family)
  • Lack of preparation for parenting
  • Family dysfunction (eg, divorce, spouse abuse, chaotic family style)
  • Difficult child (prior to this characterization, the provider should seek out explanations as to why, including subtle dysphagia)
  • Child neglect
  • Emotional deprivation syndrome
  • Inadequate understanding of age appropriate acquisition of mealtime feeding skills by the care provider (ie. failing to introduce chewable solid foods and finger feeding at critical periods).
  • Responding inappropriately in mealtime situations to the child's negative behaviors like tantrums, expelling or throwing food, and inadvertently ending the meal which allows the child to terminate eating and reinforces the behavior.
  • Feeding disorders (eg, anorexia, bulimia)

Organic failure to thrive

Prenatal onset of organic failure to thrive involves the following:

  • Prenatal causes of failure to thrive are often associated with complications of prematurity. Premature babies have an increased incidence of many medical conditions, including renal disease, heart disease, lung disease, and CNS disorders. All of these disorders can lead to intrauterine failure to thrive.
  • Most premature infants catch-up to the growth of term babies by the time they are aged 2-4 years. Intrauterine growth retardation (IUGR) is diagnosed when an infant is born below the expected weight (usually < 3%) for their gender and gestational age. Some premature (as well as full term) babies, particularly those with concomitant IUGR, have failure to thrive.
  • Whether premature babies are small because of prematurity or whether they have permanent failure to thrive is sometimes difficult to determine. If infants double their birth weight by age 4-6 months and triple their birth weight by 1 year, then full catch-up growth can be anticipated.
  • Other causes of the prenatal onset of failure to thrive include exposure to toxins, environmental influences, maternal factors, intrauterine infection, and placental or chromosomal abnormalities.
  • The most important prenatal exposures compromising growth are tobacco, which is known to produce placental insufficiency, and alcohol ingestion. Prenatal ingestion of drugs of abuse (eg, cocaine, amphetamines) can also play a role in the prenatal onset of failure to thrive. Because these drugs are often taken together, separating the effects of each drug may be difficult. Also, maternal exposure to certain medications (eg, hydantoin, phenobarbital) can lead to in utero failure to thrive.
  • Certain maternal illness (eg, hypertension, preeclampsia, heart disease, anemia, advanced diabetes mellitus) can lead to uteroplacental insufficiency and can result in smaller babies.

Although the differential diagnosis of postnatal organic failure to thrive is vast, dividing the etiology is useful. The etiology can be divided into the following 3 general areas: inadequate energy intake, compromised use (usually vomiting or malabsorption and/or excessive losses), and excessive metabolic demands. An astute mother recognizes the category to which her baby belongs. The astute physician recognizes patterns that encompass more than one of these categories.

Causes of inadequate energy intake include the following:

  • These causes can result from mechanical problems (eg, neuromuscular abnormalities, craniofacial abnormalities), lack of appetite, breathing difficulties, significant developmental delay, and primary GI disease or dysfunction. Medical therapy itself can sometimes significantly affect intake.
  • Mechanical problems can cause a poor suck or defective swallowing. Hypotonia (eg, Wernig-Hoffman syndrome, Prader-Willi syndrome), neuromuscular or CNS system disease, and CP (most commonly) lead to incoordination of feeding. Structural defects related to craniofacial abnormalities (eg, severe micrognathia, cleft palate, cleft lip) make coordinating an oral bolus difficult. Children with developmental disabilities are often malnourished.
    • A recently published analysis of growth data from a multicenter US neonatal research network concluded that children with hypoxic ischemic encephalopathy and moderate-to-severe CP had increased prevalence of weight, height, and head circumference greater than 10% at age 6-7 years compared with children without CP. [53]
    • However, a systematic approach can identify specific problems, including the need for supplemental gastrostomy tube feeds, and, once corrected, a considerable benefit is realized. [54]
  • Children who have chronic illnesses are often too sick or too apathetic to maintain good oral intake. A lack of appetite is seen in renal failure, malignancy, tuberculosis, and HIV infection, which are associated with increased circulating levels of cachectin (also known as tumor necrosis factor [TNF]).
  • Chronic cardiopulmonary compromise can make feeding exhausting and can attenuate caloric intake. Examples include congenital heart disease that leads to congestive heart failure (CHF) or chronic lung disease (eg, bronchopulmonary dysplasia, cystic fibrosis).
  • Conditions that cause abdominal pain with eating (eg, gastroesophageal reflux, celiac disease, inflammatory bowel disease, other enteropathies), and those that include impaired peristalsis (eg, achalasia, gastroparesis, pseudoobstruction) all decrease ingestion.
  • Children with developmental disabilities often have failure to thrive based on multiple physical and psychosocial contributions. 
  • The discovery of new hormones that appear to play a role in the control of appetite has led to investigations on their potential role in failure to thrive. However, to date, no definitive conclusions can be drawn. Ghrelin is an orexigenic (appetite-stimulating) hormone that enhances intake of calories, thus it would be anticipated to induce a positive energy balance.
    • An investigation that examined blood levels of ghrelin in children with failure to thrive revealed higher circulating concentrations but paradoxically lower appetite scores. [55] .
    • Another study that measured serum levels of ghrelin and obestatin (an anorexigenic, appetite-decreasing hormone) also found no differences when comparing children with failure to thrive to normal-weight controls. [56]
    • A third study followed ghrelin and leptin (another recently discovered anorexic peptide) levels in a single child with failure to thrive related to the diencephalic syndrome and found that leptin levels fell when tumor size decreased and weight increased. [57] Although the authors correctly concluded that this was unexpected because leptin (which is mainly secreted by adipocytes, fat cells) is expected to increase, an alternative hypothesis could be that tumor removal may have somehow increased gastric secretion of leptin, potentially leading to weight gain.

Inadequate use of ingested energy includes the following:

  • This can cause failure to thrive even when oral intake is adequate. This is usually secondary to emesis, or malabsorption, which is sometimes secondary to compromised digestion.
  • Children with metabolic diseases, drug toxicities, gastroesophageal reflux, and eosinophilic, viral, or traumatic esophagitis may experience considerable vomiting and may be unable to salvage adequate quantities of their ingested caloric intake.
  • Malabsorption may be secondary to compromised villous surface area, such as in celiac disease (gluten enteropathy), tropical sprue, cow's milk allergy and (less commonly) soy protein allergy, postviral enteropathy, chronic giardiasis and other chronic parasites, immunoglobin A (IgA) deficiency, radiation enteritis, Crohn disease, severe iron or zinc deficiency, acrodermatitis enteropathica, small bowel lymphoma, bacterial overgrowth, Zollinger-Ellison syndrome, Whipple disease, and abetalipoproteinemia.
  • An entity that has been receiving an increased amount of consideration that can result in poor weight gain if not recognized is food protein–induced enterocolitis syndrome (FPIES). [58] This non–IgE-mediated hypersensitivity is most often triggered by cow milk or soy protein, but it can be a reaction to rice, oat, or other dietary antigens. Children present with repetitive emesis, often with diarrhea, which can cause dehydration and be mistaken for acute viral gastroenteritis. A delay in diagnosis can result in multiple episodes that may lead to failure to thrive.
  • Anatomic defects of the small intestine (eg, short gut syndrome, blind loop syndrome, bacterial overgrowth, Hirschsprung disease) are frequently associated with failure to thrive.
  • Digestion must precede absorption and any diseases that compromise this process can lead to wasting of energy and failure to thrive. Examples include pancreatic insufficiency including cystic fibrosis and (less commonly) Shwachman-Diamond syndrome and chronic cholestasis (seen primarily in children with hepatobiliary disease, especially biliary atresia) and cirrhosis secondary to metabolic disease and intrauterine infection
  • Excessive losses of protein from the gut can disrupt growth and is discussed in the article Protein-Losing Enteropathy.

Illnesses that increase metabolic demands include the following:

  • Cancer, HIV, inflammatory bowel disease, certain collagen vascular diseases, and cardiopulmonary deficits that lead to tachypnea and hyperthyroidism can increase the amount of basal energy expenditure and thus increase the amount necessary to achieve normal growth.
  • Many illnesses simultaneously have 2-3 features that cause failure to thrive. Children with CHF or bronchopulmonary dysplasia have both decreased intake of nutrients and increased metabolic demands. In addition, right-sided heart failure leads to digestive tract edema that compromises digestion and absorption. Children with cystic fibrosis often have tachypnea, frequent intercurrent illnesses that rob them of their appetite, and fat malabsorption. These children may also suffer from depression, which introduces another important contributor to failure to thrive.

An important part of the evaluation of all children is observation of the infant while feeding. This elucidates maternal-infant interactions, the infant's ability to suck and swallow, and the general health, development and fatigability of the child.

Genetic short stature and constitutional delay of growth are 2 conditions associated with decreased growth that must be distinguished from failure to thrive. From birth to about age 2 years, a baby's weight changes to follow the genetic predisposition of the parents' height and weight. During this time of transition, children with genetic short stature may cross percentiles downward and still be considered normal. However, most children in this category find their true growth curve by age 3 years. Although children with genetic short stature are often below the third percentile on the growth chart, they have normal weight-to-height ratios and bone ages equal to their chronological ages.

The other condition associated with short stature that must be distinguished from failure to thrive is constitutional growth delay, another variation of normal growth. Children with short stature resulting from constitutional delay often have a family history of delayed growth and puberty. They have a deceleration of growth in the first 2 years that can be confused with failure to thrive, but then grow parallel to but below the third percentile. Puberty is delayed, but ultimate height may be normal. A distinguishing point from genetic short stature is that bone age is delayed.

Table 1. Summary of Organic Causes of Failure to Thrive (Open Table in a new window)

Prenatal causes
  • Prematurity with complications
  • Maternal malnutrition
  • Toxic exposure in utero
  • Alcohol, smoking, medications, infections
  • IUGR
  • Chromosomal abnormalities
Postnatal causes Inadequate intake

  • Lack of appetite (chronic illness)
  • Inability to suck or swallow
  • Vomiting
  • Therapy used to treat primary illness (eg, chemotherapy)
  • Developmental delay
  • GI pain or dysmotility
Poor absorption and/or use of nutrients

  • Malabsorption
  • Anatomical GI problems
  • Pancreatic and cholestatic conditions
  • Inborn errors of metabolism
  • Chronic GI infections
Increased metabolic demand

  • HIV infection
  • Malignancy
  • Cardiopulmonary diseases and inflammatory conditions
  • Renal failure
  • Hyperthyroidism

Combined organic and nonorganic failure to thrive

Failure to thrive is now becoming more commonly recognized as the result of both organic and nonorganic reasons. [14, 15]  In a recent multicenter study nearly one-half of children hospitalized for FTT had a complex chronic condition. However, the authors also realized that children with prematurity-related conditions and low median household income represent unique populations at higher risk for FTT readmissions. [59]  Among the many infants with psychosocial deprivation, those with growth compromise often exhibit subtle evidence of dysphagia.

Conversely, some children with chronic illnesses who have failure to thrive may have additional psychosocial issues that compromise adequate treatment for their primary organic disease. These would include poverty, lack of education, concurrent family emergencies or natural disasters, and dysfunctional or ill caretakers, who may have psychological or behavioral co-morbidities themselves. Illnesses in children, particularly chronic illnesses, may create insurmountable psychological, emotional, and financial burdens for certain families. Stresses from coping with chronic illnesses may lead to parental dysfunction, such as depression, alcohol or drug abuse, divorce, or chaotic home environments. Parental dysfunction and the resultant negative atmosphere in which children are reared affect their food intake. Among the many infants with psychosocial deprivation, those with growth compromise often exhibit subtle evidence of dysphagia.

Children may also undergo personality changes when they have chronic diseases. Medications (eg, steroids) are well known to cause behavioral changes, but the mere presence of a chronic illness can also result in resistance or noncompliance in many aspects of a child's life, including consumption of proper energy intake. This is most common when the chronic illness includes the GI tract (eg, Crohn disease) or is especially debilitating (eg, HIV, difficult to treat neoplasia). As psychologists identify a greater proportion of children with chronic diseases who have depression as a comorbidity, this possible cause of failure to thrive should not be overlooked.

Special concerns and medicolegal issues

A recently published systematic review of failure to thrive in affluent societies reveals expected conclusions in this population. [60] Since psychosocial deprivation is very rarely encountered in this cohort, the incidence of failure to thrive is less than anticipated in an unselected group of children. In addition, most measurements that fall below the defined cutoff represent transient events leading to temporary weight loss rather than significant chronic problems. The authors correctly recommend that children from this demographic should only be evaluated for failure to thrive when they meet the criteria over an extended period, rather than simply making this diagnosis based on a single set of measurements.

Failure to identify a child with a potentially treatable cause of organic failure to thrive that leads to permanent sequelae secondary to a delay in diagnosis is a pitfall. Conversely, failure to refer a child who requires protective services while being evaluated for nonorganic failure to thrive who sustains an inflicted complication is yet another potential pitfall.

Perhaps the greatest challenge for healthcare providers evaluating children with failure to thrive is to identify if the family seeking medical input is thinking of the best interest of the child. Medical child abuse (MCA), a form of Munchausen syndrome by proxy, is defined as a caretaker seeking unnecessary and harmful or potentially harmful medical care and/or procedures. A recent article published in Pediatrics provides the most cogent guidelines to date, and physicians should familiarize themselves with the risk stratification tool developed by this group. [61]

The review was based on a retrospective chart review comparing 17 cases of MCA to 68 controls from the same location and the same years with failure to thrive but without MCA. Features that distinguished MCA patients were involvement of multiple subspecialists in children without congenital anomalies, parents seeking input from multiple institutions, parents refusing services from a multidisciplinary feeding team or not allowing social workers into their homes, siblings with similar complaints, and children with multiple allergies restricting their caloric intake and leading to multiple formula changes.

The MCA cohort were also subjected to significantly more invasive procedures (1) to make a diagnosis (including upper endoscopy and muscle biopsy) and (2) to provide supplemental calories (nasogastric tube feedings, gastrostomy tube placement, Nissen fundoplication, and placement of a central line for parenteral nutrition).

Their model was able to predict MCA with a sensitivity of 100% and a specificity of 96%. However, this application was based on a small number of MCA cases, not all of whom were definitively identified as having this problem. In addition, it was derived from a specialized referral unit and may not be universally applicable.

The authors do agree with the conclusions from this review that the presence of inconsistencies over time and the pattern of increasingly more invasive investigations to identify a cause of the failure to thrive, or the necessity of increasingly more invasive procedures to provide adequate calories is alarming. Despite the trend to minimize hospitalization in general, including as part of the failure to thrive algorithm, there are certain circumstances in which the child must be observed to determine the precise nature of the problem. These become more compelling when the experienced clinician is faced with clinical events that stray further and further from what would be expected.


Physical Examination

The physical examination may reveal the following abnormalities in children with organic basis for failure to thrive:

  • Edema including  ascites - Renal disease, liver disease, protein-losing enteropathy
  • Wasting - Cancer, HIV, CP, poorly controlled inflammatory disease
  • Hepatomegaly - Liver infiltration by tumor, storage disease, or cirrhosis
  • Heart murmur, hepatosplenomegaly - Congenital heart disease
  • Hepatosplenomegaly - Infiltrative diseases, malignancy
  • Respiratory compromise - Cystic fibrosisbronchopulmonary dysplasia
  • Rash or skin changes - HIV,  congenital syphilis, cow's milk protein allergy, lupus
  • Hair color and texture changes - Zinc deficiency,  Menkes kinky hair disease
  • Mental status changes - CP
  • Signs of vitamin deficiency - Celiac disease, parasites, other enteropathy

Decreased weight secondary to marasmus (caused by insufficient caloric intake) should be distinguished from decreased weight secondary to acute dehydration. Only the latter is characterized by decreased skin turgor, sunken anterior fontanelle, dry mucous membranes, absence of tears, and acutely ill appearance.