32 Gastrointestinal Disorders

Nancy Barber Starr, Catherine G. Blosser, Margaret A. Brady, Catherine E. Burns, Ardys M. Dunn, Ann M. Petersen-Smith

The gastrointestinal (GI) system, also known as the digestive system, is essential for lifelong health. This system provides the nutrients that give the body’s cells the energy needed to function. Sustained operation and maintenance of this system are essential for normal growth and development and for the effective functioning of other organ systems.

The pediatric primary care provider plays an integral role in the care of children with GI dysfunction. A thorough understanding of the anatomy, physiology, and common disorders of the GI system is needed to appropriately assess and treat pediatric GI problems. This chapter focuses on pathologic GI disorders commonly seen in children. Other problems of the GI system, such as obesity, anorexia, bulimia, encopresis, and constipation, are discussed in Chapters 10, 12, and 19.

Anatomy and Physiology

The GI system begins to develop during the third week of gestation. The primitive gut is initially formed and then divides into the foregut, midgut, and hindgut. The structures further develop in an intricate and complex fashion to become the digestive tract and accessory organs.

The GI tract extends from the mouth to the anus. It includes the organs of digestion and accessory organs, such as the liver, pancreas, and gallbladder. The system provides the following functions: ingestion of food, movement of food from the mouth toward the rectum, mechanical dissolution of food, chemical dissolution of food, absorption of nutrients, and expulsion of waste products. The mouth serves as the site for ingestion, chewing, and mixing of food with saliva. The tongue senses the texture and taste of foods, which initiates salivation and the release of gastric juices in the stomach. The esophagus transports food from the mouth to the stomach by peristalsis, the sequential contraction and relaxation of the musculature in the esophagus. The upper esophageal sphincter prevents air from being swallowed while breathing. The lower esophageal sphincter (LES) prevents food from being regurgitated from the stomach, which is important because intraabdominal pressure exceeds intrathoracic and atmospheric pressures. The stomach serves as a reservoir for ingested foods. It secretes digestive juices, mixes food with the gastric fluids, and propels the liquid material into the small intestine. The small intestine’s primary function is absorption of nutrients (carbohydrates, fats, proteins, minerals, and vitamins) into the systemic circulation. Absorption occurs through villi, which cover the mucosal folds and serve as the functional unit of the intestine. Each villus contains an artery, a vein, and a lymph vessel that transport nutrients from the intestine into the systemic circulation. The villi are covered with enterocytes, whose major role is the digestion of carbohydrates and proteins. Enterocytes secrete proteins and enzymes known as brush border enzymes, which assist in digestion.

Carbohydrates must be converted to monosaccharides before their absorption is possible. This process begins in the mouth, where the salivary enzyme amylase breaks down complex starches into disaccharides. The brush border enzymes in the small intestine convert disaccharides into monosaccharides (sucrose to glucose and fructose, lactose to glucose and galactose, and maltose to glucose). When this process is hindered, disaccharides remain osmotically active and can cause diarrhea.

Fat absorption, which occurs mainly in the jejunum, is accomplished through the addition of lipases secreted by the pancreas. Lipases break down fats into particles that are easily absorbed by the villi. Fats then rely on the lymphatic system for absorption.

Proteins are converted to amino acids by pancreatic enzymes. The resulting amino acids are further divided into smaller amino acid particles that are absorbed via the brush border into the systemic circulation. After appropriate absorption of nutrients, the small intestine is left with the initial fecal liquid. This liquid is then propelled by peristalsis into the large intestine. The large intestine removes water from the fecal liquid and allows for short-term storage. The fecal mass, which consists of waste products, bacteria, intestinal secretions, and shed cells, is pushed into the sigmoid colon.

Entry of feces into the rectum stimulates the defecation reflex. This reflex stretches the rectal wall, relaxes the internal anal sphincter, and thereby creates the need to defecate. If this urge is ignored, further fluid resorption occurs as the stool is retained, resulting in an increase in stool mass and dryness. Excessive stretching of the colon from the hard, dry stool bolus can lead to decreased peristalsis, further complicating the retention of stool.

Pathophysiology

The GI tract can be affected by illness, injury, or other problems that prevent it from functioning normally. Dysfunction can be localized or systemic. Categories of dysfunction include the following: disorders of motility; infection; malabsorption syndromes; impairment of digestion, absorption, and nutrition; congenital malformations and genetic syndromes; metabolic disorders; behavioral problems; injuries and trauma; and food intolerances such as lactose and gluten intolerance.

Assessment

History

The history assesses the following:

• Family history of any GI disease (e.g., gallbladder disease, ulcers, or allergy to any food product)

• Past medical history related to the GI system (e.g., illnesses, surgeries, anatomic problems, such as cleft lip or palate, esophageal atresia)

• Feeding habits and nutrition history or current diet (what, when, how often, what tolerated)

• Changes in appetite

• Presence of pain (onset, location, type, quality, aggravating and alleviating factors)

Epigastric pain usually indicates pain from the liver, pancreas, biliary tree, stomach, and upper part of the small bowel (duodenum).

Periumbilical pain is generated from the distal end of the small intestine, cecum, appendix, and ascending colon.

Colonic visceral pain is lower abdominal pain that can be dull, diffuse, cramping, or burning.

Suprapubic discomfort indicates distal intestine, urinary tract, and pelvic organ dysfunction.

Referred pain is a diagnostic challenge. For example, because of convergent nerve pathways, inflammation of the diaphragm can generate pain that is perceived as shoulder or lower neck pain. When visceral pain is overwhelming, referred pain occurs.

Acute continuous pain is more indicative of an acute process.

Secondary autonomic nervous system stimulation associated with acute abdominal pain can produce symptoms of sweating, nausea, vomiting, pallor, and anxiety.

• Bowel habits (frequency, times per week, consistency, associated pain, the need for medications or enemas)

• Constipation and diarrhea (patient’s definition of each, how often they occur, treatment tried)

• Thirst level (increased or decreased)

• Food intolerance or allergy (what foods, symptoms, treatment)

• Heartburn, belching and flatulence, vomiting

• Other signs or symptoms (e.g., apnea or asthma that may be caused by gastroesophageal reflux [GER])

Physical Examination

When assessing a suspected GI problem, a head-to-toe physical examination is indicated.

• Plot growth parameters, including weight for height, to establish proportionality of the patient and exclude certain growth aberrations from the diagnosis.

• Determine body mass index (BMI). The BMI is one of the first indicators used to assess body fat and is a common method of tracking weight problems and obesity in children 2 years and older (see Chapter 10 for more details).

• Determine hydration status (skin turgor, mucous membranes, peripheral pulses, tears, capillary filling).

• Inspect the abdomen for visible peristalsis, rashes, lesions, asymmetry, masses, enlarged organs, and pulsations.

• Auscultate for frequency of bowel sounds (normal is 5 to 20 per minute).

• Percuss for density and to measure organs.

• Palpate both lightly and deeply.

• Assess peritoneal irritation:

Have the patient walk standing straight up or cough.

Have the patient stand on tiptoes and fall onto the heels or jump.

Palpate for rebound tenderness and a positive Rovsing sign.

Check for the obturator sign: A supine patient flexes the right thigh at the hip with the knee bent and internally rotates the hip. The sign is positive when it induces abdominal pain.

Check for the psoas sign: The patient lies on the left side and extends and then flexes the right leg at the hip. A positive sign is one that induces abdominal pain.

• Perform a rectal examination when intraabdominal, pelvic, or perirectal disease is suspected (the newborn examination should always routinely assess for anal stenosis). Include external inspection and internal palpation for masses, stool, or irregularities. The index finger is typically used because of its increased sensitivity; however, in infants and young children, use the fifth finger. Insert a gloved, lubricated finger into the rectum. Place the other hand on the abdomen for a bimanual examination. Young pediatric patients should be supine with their feet held together and knees and hips flexed, putting their legs over their abdomen. Adolescent males can be lying on their side or standing with the hips flexed and the upper part of the body on the examination table. Adolescent females can be lying on their side or, if a concurrent pelvic examination is to be done, in the lithotomy position.

• Perform a gynecologic examination if a pathologic pelvic condition is suspected (see Chapter 35).

Common Diagnostic Studies

Laboratory tests are performed as indicated:

Imaging of the abdomen may include the following (Clayton, 2010):

• Radiography

Abdominal x-ray, as the preliminary study; available, less expensive, with lower radiation

Upper and lower GI series with fluoroscopy demonstrate anatomy and function

Air contrast enema (diagnose and treat intussusceptions)

Bone age (to assess suspected growth abnormalities)

Chest radiographs (to rule out pneumonia)

• Ultrasound (US)—no ionizing radiation, noninvasive, relatively inexpensive (especially for pyloric stenosis, intussusceptions, appendicitis, cholelithiasis, trauma)

• Computed tomography (CT) scan—used only after other imaging studies; quick, but invasive, increased radiation, possible sedation (helpful in nephrolithiasis, appendicitis [the gold standard], intraabdominal masses, pancreatitis)

• Magnetic resonance imaging (MRI)—noninvasive and no ionizing radiation; more costly, sedation may be required (useful in a wide range of disorders)

• Nuclear medicine (scintigraphy)—provide functional and quantifiable data (especially with biliary disease, GER, and Meckel diverticulum)

Specialized tests may also be considered:

Management Strategies

Medications

Many common medications are used to treat various GI disorders:

• Antibiotics, antifungals, or anthelmintics for bacterial, fungal, or parasitic infections

• Antiemetics for nausea or vomiting

• Antidiarrheals occasionally for persistent diarrhea or diarrhea associated with chronic disease, but never for acute diarrheal diseases because toxins need to be excreted from the body

• Stool softeners, laxatives, and cathartics for acute treatment and long-term management of constipation and encopresis (see Chapter 12)

• Medications that alter GI motility or tone to treat GERD

• Oral steroids, parenteral steroids, and other immunosuppressants in the treatment of inflammatory bowel disease

• Pain medication and antispasmodics in selected acute and chronic GI conditions

• Medications that alter gastric acidity to treat GERD and ulcer disease

• Iron supplementation as supportive therapy for chronic disease

Probiotics and Prebiotics

Probiotics are foods or dietary supplements with viable microorganisms that alter the microflora of the host, stimulating favorable growth and/or activity of bacteria. Prebiotics are supplements or foods with nondigestible ingredients that benefit the host by stimulating favorable growth and/or activity of probiotic bacteria. Probiotics have been studied more extensively than prebiotics, with modest effectiveness shown in the prevention of acute infectious diarrhea as well as the treatment of acute viral gastroenteritis and in the prevention of antibiotic-associated diarrhea. There is also some evidence of effectiveness in preventing necrotizing enterocolitis in low birthweight infants, and in treating Helicobacter pylori gastritis, irritable bowel syndrome, chronic ulcerative colitis, and colic. Prebiotics may be of some benefit in preventing infection in healthy infants. Though these products seem to be safe in healthy infants and children, there is some concern about the safety of administering them to high-risk children including immunocompromised, ill preterm infants, and/or children with indwelling medical devices (Thomas et al, 2010; Weng and Walker, 2006). See Chapter 42 for further information about using probiotics.

Nutrition and activity

A nutritional plan that meets the recommended daily needs should be encouraged to promote normal GI function, growth, and development. Intake of fluids to ensure hydration is equally important. Dysfunction of the GI tract can be either short term or long term and can require alterations in dietary intake. Consultation with a registered dietitian is important in designing an adequate nutritional plan for a child with a long-term GI problem (see Chapter 10 for more detail).

Age-appropriate activity should be encouraged on a regular basis to help maintain normal GI function. Some GI maladies require short-term rest, but generally the system functions better when activity is regular and consistent.

Counseling and Education

It is important to spend time assessing and planning for the unique needs of a child with GI dysfunction. Helping the family understand the disease or disorder and its course, prognosis, and management is essential to normalize life for the child.

Upper Gastrointestinal Tract Disorders

Dysphagia

Description

Dysphagia, or difficulty swallowing, may be caused by a variety of disorders. Younger children may be unable to swallow, and older children can have awareness that something is wrong with their swallowing ability or may complain of something being stuck in their throat (globus). The physiology of swallowing is complex with oral, pharyngeal, and esophageal phases. The oral phase refers to ingestion, mastication, and the propulsion of food to the back of the mouth as a bolus. The pharyngeal phase includes the swallowing and transfer of food from the pharynx to the esophagus. Airway closure is critical during the pharyngeal phase, and the child needs to have intact motor and sensory pharyngeal protective mechanisms to prevent aspiration. The esophageal phase allows food to pass into the stomach.

Epidemiology

Dysphagia may occur as a result of a structural defect, neurologic or motor disorders, or mucosal injury. Structural defects make it more difficult to swallow solids than liquids. Common structural defects include esophageal narrowing (stricture, web, or tumor) or extrinsic obstruction (vascular ring). Nonstructural causes arise from motility disorders of the oropharynx or esophagus and are uncommon in children. Prematurity and neurologic impairment from disorders such as cerebral palsy or muscular dystrophy can be causes of dysphagia. Mucosal injury most commonly occurs from GERD or gastritis, but can also be due to caustic ingestion or medication. The number of children with swallowing difficulties has escalated because the advances in technology have increased the survival of children with special health care needs.

Clinical Findings

Vomiting and Dehydration

Description

Vomiting is the forceful emptying of gastric contents coordinated by the medullary vomiting center and/or the chemoreceptor trigger zone of the brain. It is differentiated from regurgitation, which is a passive reflux of gastric contents. It can be caused by GI or extraintestinal disorders that are either acute or chronic. Vomiting can be classified as projectile (often arising from the central nervous system [CNS]) or nonprojectile (often seen in GER), and bilious, bloody, nonbilious, or nonbloody.

The age of the child helps to formulate an appropriate list of potential diagnoses (Chandran and Chitkara, 2008).

• Newborn or young infant—infectious process, congenital gastrointestinal anomaly, CNS abnormality, or inborn errors of metabolism

• Infants and young children—gastroenteritis, GERD, milk/soy protein allergies, pyloric stenosis or obstructive lesion, inborn errors of metabolism, intussusception, child abuse, intracranial mass lesion

• Older children and adolescents—gastroenteritis, systemic illness, CNS (cyclic vomiting syndrome [CVS], abdominal migraine, meningitis, brain tumor), intussusception, rumination, superior mesenteric artery syndrome, pregnancy

Dehydration is the loss of water and extracellular fluid. Volume depletion or hypovolemia (loss of extracellular fluid) and dehydration are used interchangeably. Dehydration is classified by the Centers for Disease Control and Prevention (CDC) (2008) as minimal to none (<3%), mild to moderate (3% to 9%), or severe (>9%). It can also be differentiated between infants and older children respectively as mild (5% and 3%), moderate (10% and 6%), or severe (15% and 9%) (Mahajan, 2009).

Epidemiology

Vomiting

Vomiting is one of the most common symptoms in childhood. Nonbilious vomit is generally caused by infection, inflammation, and metabolic, neurologic, or psychological problems. An obstructive lesion generally causes bilious vomiting. Bloody vomit accompanies active bleeding in the upper GI tract (gastritis, peptic ulcer disease).

Following is a list of potential causes of vomiting by site of origin:

• Oropharynx: Cleft palate and laryngopharyngeal cleft

• Upper GI: Congenital stricture, foreign body, gastritis and/or esophagitis, gastric web, pyloric stenosis, tracheoesophageal fistula, vascular ring, peptic ulcer disease (PUD)

• Small intestine: Annular pancreas, choledochal cyst, intestinal atresias and stenosis, intestinal malrotation with volvulus, intestinal pseudo-obstruction

• Colon: Hirschsprung disease, intussusception, meconium ileus, necrotizing enterocolitis, fecal impaction

• Hepatobiliary or pancreatic dysfunction

• Infections: Bacterial enteritis, otitis media, sepsis, urinary tract infection (UTI), viral gastroenteritis (VGE), hepatitis

• Neurologic: Congenital anatomic malformation, gray and white matter degenerative disorders, hydrocephalus, kernicterus, brain tumors, migraine headache, head trauma

• Other: Cow’s-milk protein allergy (CMP intolerance), inborn errors of metabolism, maternal drug exposure and/or withdrawal, toxic ingestions, appendicitis, cyclic vomiting, pneumonia, drug or alcohol ingestion, eating disorders, pregnancy

Dehydration

Dehydration is overwhelmingly the result of an infectious process, primarily viral, that often causes diarrhea. Children are at increased risk due to their higher surface area–to–volume ratios, higher rate of insensible loss, and in younger children the inability to communicate or actively replenish losses. Depending on the cause of dehydration, water and salts (primarily sodium chloride) may be lost in physiologic proportion or disparately, producing one of three types of dehydration: isonatremic (isotonic), hypernatremic (hypertonic), and hyponatremic (hypotonic). When dehydration is caused by simple diarrhea, homeostatic mechanisms can usually maintain sodium concentrations in the serum, resulting in isonatremia. When vomiting occurs with diarrhea and water intake is less, there is greater water loss than salt loss, potentially resulting in hypernatremic dehydration. When there is massive stool loss of water and salt and only water is ingested, there is a large salt loss, potentially resulting in hyponatremia.

Clinical Findings

History

The vomiting history should assess the following:

The dehydration history should assess the following:

• Mental status and thirst

• Parental concern regarding decreased tearing or urination, or depressed fontanelle in infants

Physical Examination

• Growth parameters and vital signs

• Neurologic examination: Nuchal rigidity, decreased level of consciousness, and behavioral changes, which can include irritability or lethargy. Sensorium remains intact until there is greater than 6% of weight loss as a result of dehydration. Hypotension is a late manifestation of dehydration.

• Abdominal examination: Inspect for distention, abdominal scars from previous surgery (may be associated with obstruction and/or adhesions), or visible peristaltic waves. Auscultate bowel sounds (i.e., increased with gastroenteritis, decreased with obstruction, absent with ileus or peritonitis). Palpate the abdomen for pain and/or rebound tenderness. Assess abdominal organs (liver and spleen size, masses). Perform a rectal examination as indicated.

• Respiratory examination: Tachypnea, decreased oxygen saturation, stridor

• Assessment of dehydration (Table 32-1)

One of the most useful clinical signs of hydration is capillary refill time (CRT). Normal CRT is less than 2 seconds. CRT, skin turgor, and tachypnea, considered together, are most helpful in determining dehydration (Steiner et al, 2004).

A clinical dehydration scale (CDS) is a predictive tool regarding length of stay and need for intravenous fluids (Goldman et al, 2008). The four parameters used for assessment are general appearance, eyes (sunken or not), moistness of mucous membranes, and presence of tears.

Mahajan (2009) provides five points to assess the level of dehydration: volume deficit with history and physical, osmolar disturbance (serum sodium and osmolality), acid-base disturbance (blood pH, Pco₂, serum bicarbonate), potassium, and renal function (blood urea nitrogen [BUN]), creatinine, urine specific gravity.

TABLE 32-1 Assessment of Dehydration

Diagnostic Studies

Diagnostic studies are performed as indicated by the probable diagnosis:

• Complete blood count (CBC) with differential, blood culture

• Electrolytes, including BUN and creatinine, glucose, and liver function tests

Serum bicarbonate less than 17 mEq/L (differentiates mild from moderate/severe hypovolemia) (Mahajan, 2009)

Serum sodium less than 130 (hyponatremic) or more than 150 (hypernatremic)

• CRP and ESR

• Serum lactate, organic acids, ammonia for metabolic disorders (may only be abnormal during episodes of vomiting)

• UA and urine culture

• Toxicology screen

• Stool for culture and occult blood, leukocytes, parasites, fat, pH, reducing substances

• Rapid strep test and/or throat culture

• Pregnancy test

• Abdominal radiographs (suspected obstruction or foreign body ingestion, organomegaly, or a palpable mass)

• Chest radiograph (suspected pneumonia)

• US (abscesses, masses, stenoses, cysts, appendicitis, pyloric stenosis)

• Barium swallow or enema (malrotation, pyloric stenosis, GER, masses)

• Endoscopy (obstruction, hemorrhage, infection; collect biopsies)

• Esophageal pH probe analysis, scintiscan

• CT scan or MRI to diagnose masses, inflammation, herniations, perforations, and obstructions

• Electroencephalogram (EEG)

Differential Diagnosis

See Table 32-2.

TABLE 32-2 Differential Diagnosis of Vomiting in Infants and Children

Infant	Child	Adolescent
Common Conditions
Gastroenteritis	Gastroenteritis	Gastroenteritis
GERD	GERD	GERD
Overfeeding	Gastritis	Gastritis
Anatomic obstruction: pyloric stenosis, malrotation with intermittent volvulus, intestinal duplication, Hirschsprung disease, antral/duodenal web, foreign body, or incarcerated hernia	Toxic ingestion: lead, iron, or vitamins A and D	Toxic ingestion
Systemic infection: UTI, pneumonia, hepatitis	Systemic infection: UTI or pyelonephritis; pneumonia; hepatitis	Systemic infection
Pertussis syndrome	Pertussis syndrome	Pertussis syndrome
Otitis media	Otitis media, sinusitis	Sinusitis
	Appendicitis, small bowel obstructionMigraineMedication: ipecac, digoxin, theophylline, etc.	Appendicitis, small bowel obstruction, IBD
		Migraine
		Medication: ipecac abuse/bulimia
		Pregnancy, PID
Rare Conditions
• Other gastrointestinal disorders: achalasia, gastroparesis, peptic ulcer, food allergy or pancreatitis
• Neurologic: hydrocephalus, subdural hematoma, intracranial hemorrhage or mass, infant migraine, Chiari malformation, or meningitis
• Metabolic/endocrine: galactosemia, hereditary fructose intolerance, urea cycle defects, or amino and organic acidemias, congenital adrenal hyperplasia
• Renal: obstructive uropathy or renal insufficiency
• Cardiac: congestive heart failure or vascular ring
• Others: pediatric falsification disorder (Munchausen syndrome by proxy), child neglect or abuse, cyclic vomiting syndrome, or autonomic dysfunction

GERD, Gastroesophageal reflux disease; IBD, inflammatory bowel disease; PID, pelvic inflammatory disease; UTI, urinary tract infection.

Adapted from Blanchard S, Czinn S: Peptic ulcer disease in children. In Kliegman RM, Behrman RE, Jenson HB et al: Nelson textbook of pediatrics, ed 18, Philadelphia, 2007, Saunders, pp 1572-1574; Vandenplas Y, Rudolph C, Di Lorenzo C, et al: Pediatric gastroesophageal reflux clinical practice guidelines: joint recommendations of the North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition (NASPGHAN) and the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN), J Pediatr Gastroenterol Nutr 49(4):498-547, 2009. Used with permission of Lippincott Williams & Wilkins.

Management

Dehydration

• Determine the degree of dehydration.

If minimal, mild, or moderate, oral rehydration solution (ORS) with 70 to 90 mEq/L sodium, 25 g/L glucose, 20 mEq/L potassium, 30 mEq/L base (in the form of citrate, acetate, or lactate) with a defined osmolarity of 240 to 300 mOsm/L is recommended.

If severe, immediate and aggressive intervention is needed (e.g., intravenous [IV] fluids).

Pediatric subcutaneous rehydration using recombinant human hyaluronidase is an alternate method, effective when used in children with mild to moderate dehydration who require parenteral therapy (Allen et al, 2009).

• Initial rehydration, maintenance of fluids, and replacement of ongoing losses are stages of treatment (Table 32-3). Physiologically sodium and glucose are coupled in transport across the intestinal brush border into systemic circulation to maximize rehydration. Administration of fluid should be in frequent, small (5 mL or less) amounts. Larger amounts may be given as tolerated. Plain water, juices, soda, milk, and sports drinks should be avoided because these liquids are hyperosmolar and do not provide appropriate replacement of sugars and electrolytes. A pediatric emergency department using ORS in children with moderate dehydration showed not only successful rehydration, but also a decreased length of stay, less staff use, and more satisfied parents (Bell, 2010). Palatability of ORS does not affect the quantity consumed (Freedman et al, 2010). Homemade solutions can be used when premade ORS is not available (see http://rehydrate.org). Refeeding should resume as quickly as possible because the gut needs nutrition to facilitate mucosal repair following injury.

• Antiemetics. A single dose of an oral disintegrating tablet of ondansetron (2 mg for children 8 to 15 kg, 4 mg for children 15 to 30 kg, and 8 mg for more than 30 kg) reduces vomiting, decreases the chance of dehydration, and increases the success of oral hydration (Amir, 2007; Freedman et al, 2006; Roslund et al, 2006).

• Monitor urine output.

• Treat fever.

• Refer if the child has a toxic appearance, severe dehydration, projectile vomiting, abnormal examination, vomiting for greater than 12 hours, or vomiting of blood, bile, or fecal matter, or significantly decreased urine output.

TABLE 32-3 Treatment Based on Degree of Dehydration