Normal Digestive Tract Phenomena



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Normal Digestive Tract Phenomena :

Gastrointestinal function varies with maturity; what is a physiologic event in a newborn or infant might be a pathologic symptom at an older age. A fetus can swallow amniotic fluid as early as 12 wk of gestation, but nutritive sucking in neonates 1st develops at about 34 wk of gestation. The coordinated oral and pharyngeal movements necessary for swallowing solids develop within the 1st few months of life .

The recommendation to begin solids at 6 mo of age is based on nutritional and cultural concepts rather than maturation of the swallowing process. A number of normal anatomic variations may be noted in the mouth:


  • short lingual frenulum (tongue-tie) may be worrisome to parents but only rarely interferes with eating or speech, generally requiring no treatment.

  • Surface furrowing of the tongue (a geographic or scrotal tongue) is usually a normal finding.

  • bifid uvula may be normal or associated with a submucous cleft of the soft palate.

  • Regurgitation, the result of gastroesophageal reflux, occurs commonly in the 1st year of life. Effortless regurgitation can dribble out of an infant's mouth but also may be forceful. Episodes can occur from <1 to several times per day. Regurgitation gradually resolves in 80% of infants by 6 mo of age and in 90% by 12 mo. If complications develop or regurgitation persists, gastroesophageal reflux is considered pathologic rather than merely developmental and deserves further evaluation and treatment.

The number, color, and consistency of stools can vary greatly in the same infant and between infants of similar age without apparent explanation. The earliest stools after birth consist of meconium, a dark, viscous material that is normally passed within the 1st 48 hr of life. With the onset of feeding, meconium is replaced by green-brown transition stools, often containing curds, and, after 4-5 days, by yellow-brown milk stools.

Stool frequency is extremely variable in normal infants and can vary from none to 7 per day. Breast-fed infants can have frequent small, loose stools early (transition stools), and then after 2-3 wk can have very infrequent soft stools. Some nursing infants might not pass any stool for 1-2 wk and then have a normal soft bowel movement.

The color of stool has little significance except for the presence of blood or absence of bilirubin products (white-gray rather than yellow-brown).

The presence of vegetable matter, such as peas or corn, in the stool of an older infant or toddler ingesting solids is normal and suggests poor chewing and not malabsorption.

A protuberant abdomen is often noted in infants and toddlers, especially after large feedings. This can result from the combination of weak abdominal musculature, relatively large abdominal organs, and lordotic stance.

In the 1st yr of life, it is common to palpate the liver 1-2 cm below the right costal margin. The normal liver is soft in consistency and percusses to normal size for age. A Riedel lobe is a thin projection of the right lobe of the liver that may be palpated low in the right lateral abdomen. A soft spleen tip might also be palpable as a normal finding. In thin young children, the vertebral column is easily palpable,

and an overlying structure may be mistaken for a mass. Pulsation of the aorta can be appreciated. Normal stool can often be palpated in the left lower quadrant in the descending or sigmoid colon.

Blood loss from GIT is never normal, but swallowed blood may be misinterpreted as GI bleeding. Maternal blood may be ingested at the time of birth or later by a nursing infant if there is bleeding near the mother's nipple. Nasal or oropharyngeal bleeding is occasionally mistaken for GI bleeding . Red dyes in foods or drinks can turn the stool red but do not produce a positive test result for occult blood.

Jaundice is common in neonates, especially among premature infants, and usually results from the inability of an immature liver to conjugate bilirubin.It could be physiological or pathological.

Major Symptoms and Signs of GIT Disorders:

Disorders of organs outside GIT can produce symptoms and signs that mimic GIT disorders and should be considered in the differential diagnosis.

Dysphagia:

Difficulty in swallowing . Painful swallowing is termed odynophagia. Globus is the sensation of something stuck in the throat without a clear etiology.

It is classified as: Oropharyngeal dysphagia(transfer dysphagia) occurs when the transfer of the food bolus from the mouth to the esophagus is impaired . The striated muscles of the mouth, pharynx and upper esophageal sphincter are affected in oropharyngeal dysphagia. Neurologic and muscular disorders can give rise to oropharyngeal dysphagia . The most serious complication of oropharyngeal dysphagia is life-threatening aspiration. Esophageal dysphagia occurs when there is difficulty in transporting the food bolus down the esophagus. Esophageal dysphagia can result from neuromuscular disorders or mechanical obstruction.

Regurgitation(spitting): effortless movement of stomach contents into the esophagus and mouth.

Anorexia: prolonged lack of appetite.

Vomiting:

highly coordinated reflex process that may be preceded by increased salivation and begins with involuntary retching. Violent descent of the diaphragm and constriction of the abdominal muscles with relaxation of the gastric cardia actively force gastric contents back up the esophagus.

Vomiting caused by obstruction of the GI tract is probably mediated by intestinal visceral afferent nerves stimulating the vomiting center. If obstruction occurs below the 2nd part of the duodenum, vomitus is usually bile stained. Emesis can also become bile stained with repeated vomiting in the absence of obstruction when duodenal contents are refluxed into the stomach. Nonobstructive lesions of the digestive tract can also cause vomiting as diseases of the upper bowel, pancreas, liver, or biliary tree. CNS or metabolic derangements can lead to severe, persistent emesis.

Cyclic vomiting is a syndrome with numerous episodes of vomiting interspersed with well intervals.
Diarrhea :

Diarrhea is best defined as excessive loss of fluid and electrolyte in the stool. Acute diarrhea is defined as sudden onset of excessively loose stools of >10 mL/kg/day in infants and >200 g/24 hr in

older children, which lasts <14 days. When the episode lasts >14 days, it is called chronic or persistent diarrhea. Steatorrhea signifies an excess of fat in the stool and is a symptom of malabsorption.

Disorders that interfere with absorption in the small bowel tend to produce voluminous diarrhea( Under normal circumstances, approximately 90% of fluid absorption takes place in the small bowel), whereas disorders compromising colonic absorption produce lower-volume diarrhea.



Dysentery (small-volume, frequent bloody stools with mucus, tenesmus, and urgency) is the predominant symptom of colitis.

Movement of water across the gastrointestinal tract mucosa is passive, following osmotic gradients created by electrolytes and other osmotically active solutes such as glucose and amino acids.

Many nutrients, including glucose and most amino acids, are absorbed by active, carrier-mediated transport, which is coupled with sodium transport. The osmotic gradient created promotes the absorption of water. Movement of water, in turn, also carries small solutes such as sodium and chloride. This process is known as solvent drag and appears to be an important route for sodium absorption during normal digestion. These mechanisms of sodium movement associated with carrier-mediated nonelectrolyte transport are important to preserve normal fluid and electrolyte balance during some episodes of diarrhea (and this is the base for oral rehydration).

The pathophysiologic mechanisms for diarrhea fall into 4 basic groups:



  1. osmotic diarrhea:

The ingestion of a poorly absorbable, osmotically active substance and its presence in the bowel lumen create an osmotic gradient that encourages movement of water into the lumen and subsequently into the stool. Electrolyte losses increase because electrolytes will follow water into the lumen through solvent drag and will tend not to be reabsorbed because of unfavorable electrochemical gradients. Two main groups of poorly absorbed solutes exist, the ingestion of which result in osmotic diarrhea.

The first group includes normal dietary components that may be malabsorbed either transiently or permanently. For example, disaccharides are usually hydrolyzed to monosaccharides before they are absorbed. If a mucosal disaccharidase (eg, lactase) is deficient, then the disaccharide (in this case lactose) will be malabsorbed and will represent an osmotic load that will produce diarrhea. Medium-chain triglycerides are also osmotically active, Malabsorption of long-chain triglycerides (LCTs) does not lead to osmotic diarrhea because LCTs are large hydrophobic molecules,however, may lead to secretory diarrhea. Protein malabsorption does not appear to be associated with diarrhea except in the rare instance of congenital trypsinogen or enterokinase deficiency.



The second group of poorly absorbed solutes includes substances that are transported in limited amounts, even by healthy individuals. This group includes magnesium, phosphates, and sulfates. Because these ions invariably lead to diarrhea when given in large enough quantities, they are used as cathartics. The introduction of lactulose in the treatment of hepatic encephalopathy takes advantage of its being a nondigestible disaccharide that leads to acidification of colonic contents by bacterial fermentation of nonabsorbed sugar.

The key characteristic of an osmotic diarrhea is its association with the ingestion of the offending solute. When a patient who has an osmotic diarrhea is given no oral or enteral feeding, the



diarrhea will stop dramatically within 24 hours or less. If the agent is reintroduced, the diarrhea will reappear. The diarrhea is of a moderate volume compared with that in secretory diarrhea. The sodium and potassium ion concentrations in the stool fluid are useful in establishing a diagnosis. As ileal and colonic sodium absorption continue to function against a concentration gradient, stool sodium concentration will be lower than it is in the plasma. Normally, the electrolyte concentration in the stool is roughly twice its combined sodium and potassium concentration. When this number is much less than the total stool osmolality (usually approximately 290 mOsm/kg), osmotically active nonelectrolytes must be in the stool, and osmotic diarrhea is present. An osmotic gap of more than 100 mOsm/kg indicates osmotic diarrhea. In some instances, the clinician may be able to find the osmotic component in the stool, such as a reducing substance in lactose malabsorption.

Ion(osmotic) gap =stool osmolality-[(stool Na+stool K)×2]

  1. diarrhea resulting from secretion or altered absorption of electrolytes(secretory diarrhea):

occurs when a physiologic electrolyte secretory process is pathologically stimulated. Under such circumstances, a net increase in luminal electrolytes and, subsequently, a secondary increase in water occur. In addition, an associated decrease in absorptive processes may occur. The electrolytes that have been implicated are sodium, chloride, and perhaps bicarbonate. Itis usually of large volume and persists even with fasting. The ion gap is 100 mOsm/kg or less & stool osmolality is normal. The prototype for a secretory diarrhea is cholera. Cholera enterotoxin increases intestinal secretion of chloride and inhibits the absorption of sodium by stimulating surface epithelial adenylate cyclase.Another examples, Toxigenic Escherichia coli, congenital chloride diarrhea&bile salt malabsorption.



  1. exudative diarrhea:

A break in the integrity of the mucosal surface of the intestine can result in water and electrolyte loss, driven by hydrostatic pressure in blood vessels and lymphatics. The exudate contains mucus, protein, and blood cells. Examples include infectious(Salmonella, Shigella, infection; amebiasis; Yersinia, Campylobacter ), allergic, or ulcerative colitis.

  1. diarrhea resulting from abnormal intestinal motility:

The intestine has a cyclical, orderly pattern of motility. Increased, decreased, or disordered movement can lead to diarrhea. Rapid intestinal transit often occurs in association with osmotic and secretory diarrheas. Increased intraluminal volume has been implicated in stimulating increased peristaltic action. Increased motility may cause diarrhea by allowing less time for the contact of intraluminal contents with absorptive surfaces. Slowed transit and severely disordered motility lead to intraluminal stasis which leads to the development of bacterial over-growth.Best

examples are short-bowel syndrome, irritable bowel syndrome. Disordered motility frequently is an associated factor in chronic inflammatory bowel disease. Stools associated with motility diarrhea, except those secondary to fatty acid malabsorption, tend to be small in volume. The response to feeding is variable, and the gastrocolic reflex may be heightened. Patients who have chronic inflammatory bowel disease may find that meals stimulate intestinal activity, resulting in postprandial abdominal cramps and bowel movements.



ACUTE GASTROENTERITIS :

It denotes infections of the gastrointestinal (GI) tract caused by bacterial, viral, or parasitic pathogens. Many of these infections are foodborne illnesses. The most common manifestations are diarrhea and vomiting, which can also be associated with systemic features such as abdominal pain and fever. The term diarrheal disorders is more commonly used to denote infectious diarrhea in public health settings, although several noninfectious causes of GI illness with vomiting and/or diarrhea are well recognized. It is common in children, transient and usually self-limited. The role of the physician is to rule out causes that require specific treatment, to advise parents in supportive management, and to provide follow-up for possible complications.



Causes of Acute Diarrhea:

USUALLY WITHOUT BLOOD IN STOOL

Viral enteritis : rotavirus, orbivirus, noroviruses (includes Norwalk virus), other caliciviruses, enteric adenovirus, astrovirus, sapoviruses

Enterotoxin : E coli, Klebsiella organisms, cholera, Clostridium perfringens, Staphylococcus organisms, Bacillus cereus, and Vibrio species

Parasitic : Giardia, Cryptosporidium, Cyclospora, Dientamoeba fragilis, and Blastocystis hominis organisms

Extraintestinal infection( parenteral) : otitis media and urinary tract infection

Antibiotic-induced and Clostridium difficile toxin (without pseudomembranous colitis)




COMMONLY ASSOCIATED WITH BLOOD IN STOOL

Bacterial : Shigella, Salmonella, and Campylobacter organisms, Yersinia enterocolitica, invasive E coli, gonococcus (venereal spread), enteroadherent E coli, enteroaggregative E coli, Aeromonas hydrophilia, and Plesiomonas shigelloides

Cytomegalovirus (especially in immunocompromised individuals)

Amebic dysentery, Trichuris trichiura (whipworm)

Hemolytic-uremic syndrome (enterohemorrhagic E coli—E coli O157:H7 and other Shiga toxin-producing E coli)

Henoch-Schonlein purpura

 Pseudomembranous enterocolitis (C difficile toxin)

Ulcerative or granulomatous colitis (acute presentation)

Necrotizing enterocolitis (neonates)

Pathogenesis of Infectious Diarrhea:

Enteropathogens elicit noninflammatory diarrhea through enterotoxin production by some bacteria, destruction of villus (surface) cells by viruses, adherence by parasites, and adherence and/or translocation by bacteria. Inflammatory diarrhea is usually caused by bacteria that directly invade the intestine or produce cytotoxins with consequent fluid, protein, and cells (erythrocytes, leukocytes) that enter the intestinal lumen. Some enteropathogens possess >1 virulence property. Some viruses, such as rotavirus, target the microvillus tips of the enterocytes and can enter the cells by direct invasion or calcium-dependent endocytosis. This can result in villus shortening and loss of enterocyte absorptive surface through cell shortening and loss of microvilli.



Risk Factors for Gastroenteritis :

Major risks include environmental contamination and increased exposure to enteropathogens. Additional risks include young age, immunodeficiency, measles, malnutrition, and lack of exclusive or predominant breast-feeding.

The risks are particularly higher with micronutrient malnutrition; in children with vitamin A deficiency, the risk of dying from diarrhea, measles, and malaria is increased by 20-24%. Zinc deficiency is estimated to increase the risk of mortality from diarrhea, pneumonia, and malaria by 13-21%.
Neonatal Diarrhea

Neonates with acute diarrhea must be considered differently from older infants and children because of both lower tolerance to the associated fluid shifts and the greater likelihood of severe infection or of a congenital anomaly. In addition, signs of necrotizing enterocolitis, including gastric retention (frequently bilious), distention, and occult or bright red blood in the stool, should raise concern. Although this disease usually occurs in premature infants, it also has been reported in full-term infants. The presence of pneumatosis intestinalis, gas in the portal vein, or free intraperitoneal gas seen on abdominal radiographs supports this diagnosis. Epidemics of diarrhea associated with rotavirus, enteropathogenic E coli, salmonellae, and other organisms, including Klebsiella organisms, have been reported in nurseries. If the onset of diarrhea is associated with initial feedings, then the clinician should consider congenital digestive defects, especially sugar intolerance. Hirschsprung disease may produce acute diarrhea and enterocolitis in the neonatal period and should be considered, especially in the infant who has not passed meconium in the first 24 hours. Bloody diarrhea that results from cow milk or soy protein intolerance may develop as early as the first few days of life. Resolution and exacerbation on removal and reintroduction of cow milk or soy formula, as well as an atopic family history, are clues to the diagnosis.



Differential Diagnosis in the Older Infant and Child:

Most episodes of acute diarrhea are transient and benign. On the initial visit, the physician must evaluate the course in terms of both possible causes and the status of hydration. The

diarrhea is usually the result of viral enteritis, typically occurring with low-grade fever, vomiting, and frequent watery stools. Generally, the stools are without blood or white blood cells. Enterotoxin-producing organisms (eg, toxigenic E coli) are associated with watery stools and are without evidence of mucosal invasion (no high fever or blood in the stool). G lamblia produces watery diarrhea associated with intestinal gas and crampy abdominal pain. Diarrhea in association with extraintestinal infections, most notably otitis media and pyelonephritis, has been called parenteral diarrhea; its mechanism is obscure. An associated viral enteritis may occur in some cases of otitis media. Certain antibiotics, especially ampicillin, have been associated with transient diarrhea. Less common but of greater danger is antibiotic-associated pseudomembranous colitis, which may occur acutely or as a more chronic illness of 1 or 2 months' duration. C difficile toxin, the cause of most cases of pseudomembranous colitis, may also be associated with chronic childhood diarrhea in the absence of colitis.

The presence of blood in the stool, especially with symptoms of colonic involvement (tenesmus, urgency, and crampy lower abdominal pain), should make the clinician think of infection with Campylobacter, Shigella, or Salmonella organisms or with C difficile toxin-associated pseudomembranous colitis. The symptoms of dysentery may be less striking with Salmonella. When the Shigella is an enterotoxin-producing organism, watery diarrhea may actually precede the onset of dysentery.

Patients who have Shigella organisms tend to appear severely ill and may have meningismus or seizures. The stools tend to be foul smelling. Up to 40% of individuals who have Guillain-Barre syndrome have evidence of a Campylobacter infection occurring before the onset of neurologic symptoms.Yersinia enterocolitis also may be associated with blood in the stool. E coli can produce diarrhea by several pathogenic mechanisms; the enteroadherent, enteroinvasive, enterohemorrhagic, and enteroaggregative forms can all be associated with blood in the stool. Hemolytic-uremic syndrome is the result largely of enterohemorrhagic E coli (especially serotype O157) and less commonly Shigella infections.

Amebiasis ( Entamoeba histolytica) can produce a picture of acute colitis. Causes of bloody diarrhea that are not obviously infectious include intussusception and immune deficiencies. Chronic inflammatory bowel disease can produce an initial episode of acute dysentery, although the history may reveal previous episodes; arthralgia or growth failure may have preceded the diarrhea. A history of recent similar diarrheal illness in family members or friends suggests an infectious diarrhea.

Food-borne spread of organisms or toxins is an important cause of acute diarrheal illness. Improperly prepared poultry and eggs are the major source for both campylobacteriosis and salmonellosis, and the major source for E coli O157 infection is ground beef.
Clinical Evaluation of Diarrhea :

The most common manifestation of GIT infection in children is diarrhea, abdominal cramps, and vomiting. Systemic manifestations are varied and associated with a variety of causes. The evaluation of a child with acute diarrhea includes:



HISTORY

1. Length of illness

2. Characterization of stools: frequency, looseness (watery versus mushy), and presence of gross blood

3. Oral intake: diet, quantity of fluids and solids taken

4. Presence of vomiting

5. Associated symptoms: fever, rash, and arthralgia

6. Urine output: frequency and qualitative amount

7. Possible exposure to diarrheal illness, child-care center attendance




PHYSICAL EXAMINATION

1. Hydration status: weight (stable or loss), mucosa (moist or dry), saliva and tears (present or absent), skin turgor (normal or poor), eyeballs and fontanelle (normal or sunken), and vital signs

2. Alertness

3. Infant: vigor of suck



LABORATORY (PERFORMED AS INDICATED)

1. Stool evaluation: culture, ova and parasites, smear for WBC, C. difficile toxin assay, occult blood & reducing substances

2. CBC: Hemoconcentration from dehydration causes an increase in PCV and Hb.

3. If hydration status is in question: blood urea nitrogen (BUN),serum creatinine & electrolytes

4. Urinalysis:the urine specific gravity is usually elevated (≥1.025) in cases of significant dehydration, but decreases after rehydration. With dehydration, a urinalysis may show hyaline and granular casts, a few white blood cells and red blood cells, and 30 to 100 mg/dL of proteinuria

5. If child is lethargic or has had a seizure, culture for sepsis: measure the BUN and serum electrolyte and glucose levels and examine and culture the cerebrospinal fluid.


A stool culture should be obtained if blood or leukocytes are noted in the stool and the child is severely ill. Examination of the stool for leukocytes is helpful in establishing the presence of colitis. In the presence of both infectious and noninfectious colitis, white blood cells (WBCs) are usually found in high numbers, frequently in sheets. The absence of WBCs in grossly bloody diarrheal stool occurs with enterohemorrhagic E coli infection but should also direct attention to entities such as intussusception and Meckel diverticulum when these diagnoses seem clinically appropriate.

Amebic colitis also may not be associated with WBCs in the stool, although the trophozoites and numerous red blood cells may be visible on a saline wet mount preparation of the stool. Invasive bacterial diarrhea frequently is associated with a peripheral blood leukocytosis.





Assessment of Degree of Dehydration:



 

Mild

Moderate

Severe

Infant(wt loss)

5%

10%

15%

Adolescent

3%

6%

9%

Infants and young children

Thirsty; alert; restless

Thirsty; restless or

lethargic but

irritable or drowsy


Drowsy; limp, cold, sweaty, cyanotic

extremities; may be

comatose


Older children

Thirsty; alert; restless

Thirsty; alert (usually)

Usually conscious

(but at reduced level), apprehensive

; cold, sweaty, cyanotic

extremities; wrinkled skin



on fingers and toes; muscle cramps



Signs and Symptoms

Tachycardia

Absent

Present

Present

Palpable pulses

Present

Present (weak)

Decreased

Blood pressure

Normal

Orthostatic hypotension

Hypotension

Cutaneous perfusion

Normal

Normal

Reduced and mottled

Skin turgor

Normal

Slight reduction

Reduced

Fontanel

Normal

Slightly depressed

Sunken

Mucous membrane

Moist

Dry

Very dry

Tears

Present

Present or absent

Absent

Respirations

Normal

Deep, may be rapid

Deep and rapid

Urine output

Normal

Oliguria

Anuria and severe oliguria




Calculation for correction of dehydration(deficit+maintenance+ongoing losses):

1.deficit



A child with dehydration has lost water; there is usually a concurrent loss of sodium and potassium. Most patients have isotonic dehydration . The following guidelines are used for calculating the deficits in isotonic dehydration secondary to gastroenteritis. The water deficit is the percentage of dehydration multiplied by the patient's weight (for a 10-kg child, 10% of 10 kg = 1 L deficit).The sodium and potassium deficits are derived from the water deficit .

Water deficit =%dehydration× weight

Sodium deficit = Water deficit × 80 mEq/L

Potassium deficit = Water deficit × 30 mEq/L


2.

Maintenance Therapy:





















Maintenance fluids are most commonly necessary in preoperative and postoperative surgical patients; many nonsurgical patients also require maintenance fluids. Maintenance fluids are composed of a solution of water, glucose, sodium, and potassium.

Sources of Water losses:

(Urine 60%,Insensible losses (skin and lungs)35%,Stool 5%)

 BODY WEIGHT METHOD FOR CALCULATING DAILY MAINTENANCE FLUID VOLUME



BODY WEIGHT

FLUID PER DAY

0-10 kg


100 mL/kg

11-20 kg


1,000 mL + 50 mL/kg for each kg >10 kg

>20 kg


1,500 mL + 20 mL/kg for each kg >20 kg*

*

The maximum total fluid per day is normally 2,400 mL.



Maintenance requirements of electrolytes:

  • Sodium: 2 - 3 mEq/kg/day

  • Potassium: 1 - 2 mEq/kg/day.


Adjustments in Maintenance Water:للاطلاع فقط


Source

Causes of Increased Water Needs

Causes of Decreased Water Needs

Skin

Radiant warmer

Mist tent

 

Phototherapy

Incubator (premature infants)

 

Fever

 

 

Sweat

 

 

Burns

 

Lungs

Tachypnea

Humidified ventilator

 

Tracheostomy

 

 

 

Mist tent

Gastrointestinal

Diarrhea

 

 

Emesis

 

 

Nasogastric suction

 

Renal

Polyuria

Oliguria/anuria

Miscellaneous

Surgical drain

Hypothyroidism

 

Third space losses(edema &ascites)















3.ongoing losses:

Adjusting Fluid Therapy for Gastrointestinal Lossesللاطلاع فقط




Average Composition

Approach to Replacement

Diarrhea

Replacement of Ongoing Stool Losses

Sodium: 55 mEq/L

Solution: 5% dextrose in ¼ normal saline + 15 mEq/L bicarbonate + 25 mEq/L potassium chloride

Potassium: 25 mEq/L

Replace stool mL/mL every 1-6 hr

Bicarbonate: 15 mEq/L

 

Gastric Fluid

Replacement of Ongoing Gastric Losses

Sodium: 60 mEq/L

Solution: 5% dextrose in half normal saline + 10 mEq/L potassium chloride

Potassium: 10 mEq/L

Replace output mL/mL every 1-6 hr

Chloride: 90 mEq/L

 



Fluid Management of Dehydration




1.Restore intravascular volume( fluid bolus or shoot):

  Normal saline or Ringer's lactate : 20 mL/kg over 20 min (repeat until intravascular volume restored, 3 times)

2.Calculate 24-hr water needs

  Calculate maintenance water

  Calculate deficit water

3.Calculate 24-hr electrolyte needs

  Calculate maintenance sodium and potassium

  Calculate deficit sodium and potassium

4.Select an appropriate fluid (based on total water and electrolyte needs) For a patient with isotonic dehydration, D5 half NS with 20 mEq/L of potassium chloride is usually an appropriate fluid. For a child weighing less than 10 to 20 kg with mild dehydration, a reduction of the sodium concentration is usually reasonable (1/4 NS) because the sodium deficit is small. Potassium usually is not included in the IV fluids until the patient voids, unless significant hypokalemia is present. So it will be:

D5 1/2NS   + 20 mEq/L KCl or D5 0.2NS + 20 mEq/L KCL



  Administer half the calculated fluid during the first 8 hr, first subtracting any boluses from this amount

  Administer the remainder over the next 16 hr

5.Replace ongoing losses as they occur

In all children, it is critical to carefully monitor vital signs, weight, urine output, and electrolytes to identify overhydration or underhydration, hyponatremia, and other electrolyte disturbances, and to then adjust the rate or composition of the intravenous solution accordingly.

Types of dehydration are 3 according to sodium level:

1.isotonic (isonatremic: S.Na 135-145mEq/L)

2.hypotonic(hyponatremic:S.Na <135 mEq/L)

3.hypertonic(hypernatremic:S.Na >145 mEq/L)



Hyponatremic dehydration occurs in children who have diarrhea and consume a hypotonic fluid (water or diluted formula). Volume depletion stimulates secretion of ADH, preventing the water excretion that should correct the hyponatremia. Hyponatremic dehydration produces a more substantial intravascular volume depletion owing to the shift of water from the extracellular space into the intracellular space. In addition, some patients develop symptoms, predominantly neurologic, from the hyponatremia . Most patients with hyponatremic dehydration do well with the same general approach outlined above. Overly rapid correction of hyponatremia (>12 mEq/L/24 hr) should be avoided because of the remote risk of central pontine myelinolysis.

Hypernatremic Dehydration

It is the most dangerous form of dehydration due to complications of hypernatremia and of therapy. Hypernatremia can cause serious neurologic damage, including central nervous system hemorrhages and thrombosis. This damage appears to be secondary to the movement of water from the brain cells into the hypertonic extracellular fluid, causing brain cell shrinkage and tearing blood vessels within the brain.It is usually a consequence of an inability to take in fluid, owing to a lack of access, a poor thirst mechanism (neurologic impairment), intractable emesis, or anorexia. The movement of water from the intracellular space to the extracellular space during hypernatremic dehydration partially protects the intravascular volume. Children with hypernatremic dehydration often appear less ill than children with a similar degree of isotonic dehydration. Urine output may be preserved longer, and there may be less tachycardia. Children with hypernatremic dehydration are often lethargic and irritable when touched. Hypernatremia may cause fever, hypertonicity, and hyperreflexia. Some infants have a high-pitched cry and hyperpnea. Alert patients are very thirsty, even though nausea may be present.

Probably because of intracellular water loss, the pinched abdominal skin of a dehydrated, hypernatremic infant has a “doughy” feel.

Too-rapid treatment of hypernatremic dehydration may cause significant morbidity and mortality. Idiogenic osmoles are generated within the brain during the development of hypernatremia. These idiogenic osmoles increase the osmolality within the cells of the brain, providing protection against brain cell shrinkage secondary to movement of water out of cells into the hypertonic ECF. These idiogenic osmoles dissipate slowly during correction of hypernatremia. With rapid lowering of the extracellular osmolality during correction of hypernatremia, there may be a new gradient created that causes water movement from the extra-cellular space into the cells of the brain, producing cerebral edema. Symptoms of the resultant cerebral edema can produce seizures, brain herniation, and death. To minimize the risk of cerebral edema during correction of hypernatremic dehydration, the serum sodium concentration should not decrease more than 12 mEq/L every 24 hours. The deficits in severe hypernatremic dehydration may need to be corrected over 2 to 4 days(based on initial sodium concentration).

N.B:The resuscitation phase (treatment of shock state ) is same in iso, hypo, & hypernatremic dehydration

Oral Rehydration:

Mild to moderate dehydration from diarrhea of any cause can be treated effectively using a simple, oral rehydration solution (ORS) containing glucose and electrolytes.Oral rehydration therapy(ORT) is less expensive than IV therapy and has a lower complication rate. IV therapy still may be required for patients with severe dehydration; patients with uncontrollable vomiting; patients unable to drink because of extreme fatigue, stupor, or coma; or patients with gastric or intestinal distention.



As a guideline for oral rehydration, 50 mL/kg of the ORS should be given within 4 hours to patients with mild dehydration, and 100 mL/kg should be given over 4 hours to patients with moderate dehydration. Supplementary ORS is given to replace ongoing losses from diarrhea or emesis. An additional 10 mL/kg of ORS is given for each stool. Fluid intake should be decreased if the patient appears fully hydrated earlier than expected or develops periorbital edema. Breastfeeding should be allowed after rehydration in infants who are breastfed; in other patients, their usual formula, milk, or feeding should be offered after rehydration.




When rehydration is complete, maintenance therapy should be started, using 100 mL of ORS/kg/24 hr until the diarrhea stops.

The low-osmolality WHO oral rehydration solution (ORS) containing 75 mEq of sodium and 75 mmol of glucose per liter, with total osmolarity of 245 mOsm per liter, is more effective than other formulations in reducing stool output without the risk of hyponatremia, and it is now the global standard of care.

Zinc Supplementation :

There is strong evidence that zinc supplementation in children with diarrhea in developing countries leads to reduced duration and severity of diarrhea and could potentially prevent a large proportion of cases from recurring. In addition to improving diarrhea recovery rates, administration of zinc in community settings leads to increased use of ORS and reduction in the inappropriate use of antimicrobials.WHO and UNICEF recommend that all children with acute diarrhea in at-risk areas should receive oral zinc in some form for 10-14 days during and after diarrhea (10 mg/day for infants <6 mo of age and 20 mg/day for those >6 mo).



Additional Therapies :

The use of probiotic nonpathogenic bacteria for prevention and therapy of diarrhea has been successful in developing countries. In addition to restoring beneficial intestinal flora, probiotics can enhance host protective immunity.A variety of organisms (Lactobacillus, Bifidobacterium) have a good safety record.



Antimotility agents (loperamide) are contraindicated in children with dysentery and probably have no role in the management of acute watery diarrhea in otherwise healthy children. Similarly, antiemetic agents such as the phenothiazines are of little value. Nonetheless, ondansetron is an effective and less-toxic antiemetic agent. Because persistent vomiting can limit oral rehydration therapy, a single sublingual dose of an oral dissolvable tablet of ondansetron (4 mg 4-11 yr and 8 mg for children >11 yr [generally 0.2 mg/kg]) may be given.

Antibiotic Therapy:

are useful in specific situations: Shigella dysentery(Ciprofloxacin''˃18 yr age", ampicillin, ceftriaxone,

azithromycin, or TMP-SMX)

Yersinia(aminoglycoside, TMP-SMX,) or Campylobacter gastroenteritis(Erythromycin or azithromycin),

pseudomembranous colitis(Clostridium difficile) Metronidazole (first line), Discontinue initiating antibioticVancomycin (2nd line)



Salmonella infections in infants younger than 6 months, and Salmonella infections in older patients who have enteric fever, typhoid fever, or complications of bacteremia(same as shigella)

EPEC, ETEC, EIEC: TMP-SMX or ciprofloxacin



Entamoeba histolyticaMetronidazole followed by iodoquinol or paromomycin

Giardia lamblia Furazolidone or metronidazole or albendazole or quinacrine

Nitazoxanide, an anti-infective agent, has been effective in the treatment of a wide variety of pathogens including C. parvum, G. lamblia, E. histolytica, Blastocystis hominis, C. difficile, and rotavirus.

Prevention:

  1. Exclusive breast-feeding (administration of no other fluids or foods for the 1st 6 mo of life) protects very young infants from diarrheal disease through the promotion of passive immunity and through reduction in the intake of potentially contaminated food and water.

  2. Improved Complementary Feeding Practices:Contamination of complementary foods can be potentially reduced through caregivers’ education and improving home food storage. Improved vitamin A status has been shown to reduce the frequency of severe diarrhea

  3. Rotavirus Immunization(live-attenuated) associated with a significant reduction in severe diarrhea and associated mortality.

  4. Improved Water and Sanitary Facilities and Promotion of Personal and Domestic Hygiene

  5. Improved Case Management of Diarrhea:through prompt identification and appropriate therapy significantly reduces diarrhea duration, its nutritional penalty, and risk of death in childhood

Specific infective(foodborn) diarrheas:

1.bacterial:

  • Enterohemorrhagic Escherichia coli (EHEC) including E. coli O157:H7 and other Shiga toxin–producing E. coli (STEC):IP 1-8 days, Severe diarrhea that is often bloody; abdominal pain and vomiting Usually, little or no fever is present More common in children <4 yr old,duration of illness 5-10 ds,Dx stool culture Rx is supportive & monitor renal function,Hb platelet count as hemolytic uremic syndrome(HUS) is a possible complication[ which is triad of microangiopathic hemolytic anemia" MAHA",uremia & thrombocytopenia]. Studies indicate that antibiotics might promote the development of HUS



  • Shigella spp(bacillary dysentery).IP 1-2ds, Abdominal cramps, fever(that may cause fits), diarrhea( Stools might contain blood and mucus) or its toxins may cause fits( toxic encephalopathy),duration of illness 4-7 ds,Dx stool culture Rx Supportive care. TMP-SMX if organism is susceptible; nalidixic acid or other quinolones may be indicated if organism is resistant



  • Salmonella spp.IP 1-3ds, Diarrhea, fever, abdominal cramps, vomiting
    S. typhi and S. paratyphi produce typhoid with insidious onset characterized by fever, headache, constipation, malaise, chills, and myalgia; diarrhea is uncommon, and vomiting is not usually severe.duration of illness 4-7ds Dx stool culture Rx Supportive care




  • Other than for S. typhi and S. paratyphi, antibiotics are not indicated unless there is extra-intestinal spread, or the risk of extra-intestinal spread, of the infection




  • Consider ampicillin, gentamicin, TMP-SMX, or quinolones if indicated
    A vaccine exists for S. typhi



  • Vibrio cholerae (toxin) IP 1-3ds, Profuse watery diarrhea and vomiting, which can lead to severe dehydration and death within hours duration of illness 3-7 ds,Dx Stool culture
    V. cholerae requires special media to grow; if V. cholerae is suspected, must request specific testing Rx Supportive care with aggressive oral and intravenous rehydration
    In cases of confirmed cholera, tetracycline or doxycycline is recommended for adults, and TMP-SMX for children <8 yr

2.viral:

Rotavirus (groups A-C):IP1-3ds, Vomiting, watery diarrhea, low-grade fever


Temporary lactose intolerance can occur
Infants and children, elderly, and immunocompromised are especially vulnerable.duration of illness 4-8 ds Dx Identification of virus in stool via immunoassay Rx Supportive care

Hepatitis A:IP 28 days average (15-50 days), Diarrhea, dark urine, jaundice, and flulike symptoms, i.e., fever, headache, nausea, and abdominal pain, duration of illness Variable 2 wk-3 mo,Dx Increase in ALT, bilirubin


Positive IgM and anti-hepatitis A antibodies,Rx Supportive care Prevention with immunization

3.parasitic:

Entamoeba histolytica (amebic dysentery),IP 2-3 days to 1-4 wk, Diarrhea (often bloody), frequent bowel movements, lower abdominal pain. , duration of illnessMay be protracted (several weeks to several months)Dx Examination of stool for cysts and parasites; may need at least 3 samples Serology for long-term infections Rx Metronidazole and a luminal agent (iodoquinol or paromomycin)

Giardia lamblia IP 1-2wk, Diarrhea, stomach cramps, gas, weight loss, duration of illness Days to weeks Dx Examination of stool for ova and parasites; may need at least 3 samples,Rx metronidazole

COMPLICATIONS OF GASTROENTERITIS:



  • Renal failure Dehydration,acute tubular necrosis,HUS,renal vein thrombosis"RVT"

  • Hypokalemia & paralytic ileus

  • 2ry lactose intolerance

  • Fluid overload & pulmonary edema

  • Convulsions( febrile,hyponatremia,hypernatremia,hypocalcemia,hypomagnesmia,hypoglycemia,meningitis & cerebral vascular thrombosis)


CHRONIC DIARRHEA

defined as a diarrheal episode that lasts for ≥14 days,itis often the result of an intestinal infection that lasts longer than expected. This syndrome is often defined as( protracted diarrhea), and there is no clear distinction between protracted and chronic diarrhea. The younger the infant is, the more likely he or she will be to enter the cycle of diarrhea and secondary malnutrition that leads to further diarrhea, malnutrition, and susceptibility to infection



Causes of chronic diarrhea:

Common :

Chronic enteric infection:Salmonella organisms; Yersinia enterocolitica; Campylobacter, Giardia, Clostridium difficile toxin; enteroadherent Escherichia coli; rotavirus (in immunodeficient patients); cytomegalovirus; adenovirus; and HIV

Food allergy(cow's milk or soy proteins, others)

Chronic non specific diarrhea(toddler's diarrhea, irritable colon of childhood)

Disaccharide intolerance(Congenital or acquired lactase deficiency)

Cystic fibrosis

Celiac disease

Inflammatory bowel disease(CD & UC)

UTI

Immunodeficiency



Postenteritis bile acid malabsorption

Less common:

toautoimmune enteropathy

adrenal insufficiency and hyperthyroidism

Inintestinal lymphangiectasia

A acrodermatitis enteropathica

Hirschsprung disease with enterocolitis

Congenital chloride-losing diarrhea

Immunodysregulation, polyendocrinopathy, enteropathy, X-linked syndrome (IPEX)


chronic nonspecific diarrhea
The most benign etiology that encompasses functional diarrhea (or toddler's diarrhea) in children <4 yr of age and irritable bowel syndrome in those ≥5 yr.

The disease is the same with a slightly different age presentation, in that abdominal pain is more common and clearly associated with the diarrhea in older children. The hallmark of the syndrome is diarrhea associated with normal weight growth in well-appearing subjects. In younger children diarrhea is often watery, at times containing undigested food particles. It is usually more severe in the morning.. If the dietary history suggests that the child is ingesting significant amounts of fruit juices, then the offending juices should be decreased.. In older children, irritable bowel syndrome is often associated with abdominal pain and may be related to anxiety, depression, and other psychologic disturbances.

Symptoms may begin initially after an apparent acute enteritis (postinfectious irritable bowel).

Treatment may include (1) restricting the frequency of feedings, whether liquids or solids, in an effort to decrease stimulation of the gastrocolic reflex (in the toddler, three meals and a bedtime snack with nothing by mouth in between); (2) restricting the volumes of fluids ingested when excessive.If the child's fluid intake is >150 mL/kg/24 hr, fluid intake should be reduced to no more than 90 mL/kg/24 hr. The child is often irritable in the first 2 days after the fluid restriction; however, persistence with this approach for several more days results in a decrease in the stool frequency and volume; (3) avoiding excessive intake of juices.Sorbitol, which is a nonabsorbable sugar, is found in apple, pear, and prune juices and it can cause diarrhea in toddlers. Apple and pear juices contain higher amounts of fructose than glucose, a feature postulated to cause diarrhea in toddlers; and (4) reassuring the parents of the benign nature of this entity. A high-fat diet may be helpful in some children, although probably is of less importance. Cholestyramine (2 g by mouth 1 to 3 times daily) is also effective at times; however, the duration of use should be restricted because of the potential for interference with fat-soluble vitamin absorption.

In any event, this condition is self-limited and typically resolves by 3.5 years of age.

Food Allergy & hypersensitivity

Defined as ‘an immune response to food proteins,it occurs in 4-8% children commonly with those of +ve family history of atopy or allergies. Food allergy may be IgE mediated or non-IgE mediated. If a non-immunological reaction to a specific food occurs this is called non-allergic food hypersensitivity or intolerance.

Presentation of food allergy varies with the agent and the child's age:

  • in infants the most common causes are milk, egg and peanut

  • in older children peanut, tree nut and fish.

Fruit allergy, although common, is usually mild, causing an itchy mouth but no systemic symptoms. This is called 'oral allergy syndrome' and is usually associated with spring hay fever due to cross-reaction with tree pollens. Kiwi fruit, however, can cause anaphylaxis.










Food hypersensitivity is not related to food aversion, where the person refuses the food for psychological or behavioural reasons.



Management








The management of a food allergic child involves avoidance of the food but, especially for milk and nuts, this is very difficult as they may be present in small quantities in many foods and food labels are often unclear. The advice of a paediatric dietician is essential.








In addition, the child and family must be able to manage an allergic attack. Written self-management plans and adequate training are essential.

Drug management for mild reactions (no cardiorespiratory symptoms) is with antihistamines.



If the child had a severe reaction or has asthma, treatment is with epinephrine (adrenaline) given intramuscularly by auto-injector (e.g. Epipen), which the child or parent should carry with them at all times.

Cow’s Milk Protein Allergy(CMPA):


  • Results from an immunological reaction to one or more of milk proteins,only 0.5% of exclusively breast fed infants are affected & 5-15% of infants show syggestive symptoms.It is either IgE- or non-IgE mediated.

  • 27% show symptoms within 45 minutes,58% within 2hrs

  • Its incidence 2-6% of children, Prevalence highest < 1 year

Cow’s Milk Intolerance:

  • A transient intolerance to lactose and/ or protein found in cow’s milk following an infective episode of diarrhoea

  • Carbohydrate intolerance is due to mucosal damage which results in reduced activity of disaccharide enzymes

  • Protein intolerance is an immunomediated reaction to cow’s milk protein following mucosal damag.

Clinical presentation:

  • Early reactions (within 45 minutes):

      • Urticaria

      • Angio-oedema

      • Vomiting

      • Acute flare up of atopic detmatitis

  • Medium (45 minutes to 20 hours)

      • Pallor

      • Gastro intestinal tract symptoms

  • Late reactions (after 20 hours)

      • Atopic dermatitis

      • Respiratory symptoms

      • Diarrhoea

IgE mediated (within 30mins)

  • Anaphylaxis

  • Skin (50-60%):

    • Angio-oedema

    • Urticaria

    • Pruritis

  • GI (50-60%):

    • Nausea/Vomiting

    • Colicky abdo pain



  • Resp (20-30%):

    • Wheezing

    • Rhinitis

    • Laryngeal oedema

    • Asthma

Non IgE Mediated (hours-days)

  • Skin: Dermatitis

  • GIT:

    • Chronic diarrhoea( intestinal protein loss produces edema and a protein-losing enteropathy)

    • Iron deficiency anaemia

    • Colic

    • Food refusal and poor growth

    • GORD

    • Blood in stool

    • Constipation

    • Enterocolitis

    • Eosinophilic oesophagogastroenteropathy

    • Respiratory:asthma

Evaluation of a child with suspected CMPA:

  • A comprehensive history:atopic one parent( risk 20-40%) or both(risk 40-50%) or sibling.

  • Symptoms:either GIT,skin or respiratory

CMPA in Breast fed Infants:

  • Symptoms include skin or GIT

  • Most of symptoms are mild to severe.

  • Infants with atopic dermatitis:

    • Risk of CMPA x 4

    • Risk of egg allergy x 8

Diagnosis:

  • Comprehensive allergy focused clinical history with careful & complete physical examination

  • IgE specific antibody (RAST)

  • Skin Prick Testing

  • Elimination Diet & Food Challenge

  • the diagnosis can be confirmed safely and easily by rectal mucosal biopsy; this shows eosinophilic inflammation of the mucosa. Visual findings at proctoscopy usually include mucosal friability and lymphoid hyperplasia, giving a lumpy, "mosquito-bitten" appearance to the rectal mucosa.

Treatment:

  • Breast fed infants: Maternal exclusion diet avoiding food containing CMP( dairy products)

  • Bottle fed infants: Cows Milk Free formula.

    • Extensively hydrolysed Formulae (e.g., Nutramigen, Pregestamil, or Alimentum).

    • Amino Acid based Formulae

Prognosis:

  • 50% resolve in first year of life

  • 60-70% resolve by second year of life

  • 80-90% resolve by fifth year of life

  • Parental reported rate 4x higher

Lactose intolerance:

It also called lactase deficiency and hypolactasia, is the inability to digest lactose, a sugar found in milk and to a lesser extent milk-derived dairy products. It is not a disorder as such, but a genetically-determined characteristic. Lactose intolerant individuals have insufficient levels of lactase, an enzyme that catalyzes hydrolysis of lactose into glucose andgalactose, in their digestive system. 

Lactase deficiency has a number of causes and is classified as one of three types:



  • Primary lactase deficiency(Primary adult type-hypolactasia) is genetic, only affects adults and is caused by the absence of a lactase persistence allele.  It is the most common cause of lactose intolerance as a majority of the world's population lacks these alleles. The brush border lactase is expressed at low levels during fetal life; activity increases in late fetal life and peaks from term to 3 yr, after which levels gradually decrease with age.

  • Secondary, acquired, or transient lactase deficiency is caused by an injury to the small intestine, usually during infancy, from acute gastroenteritis(rotavirus infection),celiac disease,chemotherapyintestinal parasites or other environmental causes.

  • Congenital lactase deficiency(CLD) is a very rare, autosomal recessive genetic disorder that prevents lactase expression from birth.  It is particularly common in Finland. People with congenital lactase deficiency cannot digest lactose from birth, and therefore cannot digest breast milk.

Lactose intolerance is not an allergy because it is not an immune response, but rather a problem with digestion caused by lactase deficiency. 

Clinical presentation:

The principal symptom of lactose intolerance is an adverse reaction to products containing lactose (primarily milk), including abdominal bloating and cramps, flatulence,diarrhea, nausea, borborygmi (rumbling stomach) and vomiting (particularly in adolescents). These appear thirty minutes to two hours after consumption.  The severity of symptoms typically increases with the amount of lactose consumed; most lactose-intolerant people can tolerate a certain level of lactose in their diet without ill-effect.
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