M. Gorky Donetsk National Medical University Department No. 2 of Pediatrics Head of the Department Dr. Churilina A. V., Ph. D. Diarrhea icon

M. Gorky Donetsk National Medical University Department No. 2 of Pediatrics Head of the Department Dr. Churilina A. V., Ph. D. Diarrhea




НазваM. Gorky Donetsk National Medical University Department No. 2 of Pediatrics Head of the Department Dr. Churilina A. V., Ph. D. Diarrhea
Дата19.09.2012
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M.Gorky Donetsk National Medical University Department No. 2 of Pediatrics Head of the Department Dr. Churilina A.V., Ph.D. Diarrhea

  • Associate professor Masyuta D.I.


  • Frequent passage of watery stool is a common manifestation of gastrointestinal disturbances which may occur due to gastrointestinal infections or infestations (gastroenteritis), non-infective irritation or inflammation of the mucosa of the intestine, certain drugs or psychogenic factors.

  • There is predisposition to diarrhea in childhood due to anatomic and physiological peculiarities of gastrointestinal tract such as low pH of gastric juice, low level of secretory immunoglobulin A, decreased immunity if a baby is formula fed, decreased desintoxicative liver function, etc.

  • Diarrhea is probably the most common cause of death in infancy and childhood in tropical countries. Children below three years of age are the common victims, and about one-third of the total deaths in this age group may be ascribed to diarrhea.





Etiology

  • A. INFECTIONS. Majority of cases of acute diarrheas (50 %) are due to infections with wide spectrum of microorganisms.

    • 1. Bacterial infections — E. coli, Shigella, Salmonella, Staphylococci, Klebsiella, Proteus, Pseudomonas, Campylobacter enteritis, and V. cholera.
    • 2. Viral infections—Recently "ROTA" virus has been identified as the most virulent of all the viruses causing gastroenteritis. 30-40 % of diarrhea episodes is caused by viruses.
    • 3. Parasitic infestations and infections. Entameba histolytica, giardia lamblia, roundworms, tapeworms, hookworms and strongyloides are well known to cause gastroenteritis and diarrhea in children residing in overcrowded unhygienic area.
    • 4. Fungal infections. Candida albicans is the most common fungal etiological agent for diarrhea in neonates and small infants.
    • 5. Infections in other organs of the body (parenteral diarrhea). Infections. in the urinary tract, lungs, meninges, middle ear, mastoid process etc. have been found to cause diarrhea in small babies.


Etiology

  • ^ B. NON-INFECTIVE GASTROINTESTINAL DISORDERS

    • 1. Allergic disorder. Allergy to milk, wheat gluten, fish, egg, groundnut, tomato, some spices and condiments etc. is quite well known in pediatric practice as a causative factor for diarrhea. These antigens not only cause inflammation of the gut mucosa but also may cause secondary disaccharidase deficiency.
    • 2. Food intolerance. Foods containing excessive spices, sugars or fat can also give rise to bowel disorder. Some children cannot tolerate certain fruits which, when eaten, can cause bowel upset.
    • 3. Endocrinal disturbances. —Hyperthyroidism, excessive thyroid extract, hyperparathyroidism, adrenocortical hyperplasia or tumour, pheochromocytoma, ganglioneuroma, islet cell tumours are often responsible for acute diarrhea along with characteristic features of the respective disorders.


Etiology

  • ^ C. DRUGS.

    • Broad-spectrum antibiotics, theophylline, some heavy metals, some chemotherapeutic and antineoplastic drugs may cause diarrhea.
  • D. PSYCHOGENIC FACTOR.

    • Tension, excitement, fatigue, fear, depression all are known to cause excessive bowel movement in children with personality development problems. Ulcerative colitis secondary to emotional disturbances has been reported.


Pathogenesis

  • Any offending agent after ingestion induces hyperperistalsis in the following ways:

    • It is the natural tendency of the human system to drive out any ingested harmful agent by hyperperistalsis.
    • Some foods, drugs or chemicals increase the osmotic tension in the gut lumen and thereby imbibe more fluid from the intestinal mucosa. As a result the bulk of the intestinal contents increases which ultimately causes hyperperistalsis (osmotic diarrhea).
    • Recently it has been postulated that intestinal hyperperistalsis initiated by any agent leads to increased bile secretion in the intestine. Excess bile acids exert their irritating effect on the colon resulting in further hyperperistalsis and persistence of diarrhea.
    • The enterotoxins produced by E. coli induce fluid and electrolyte secretion when they come in contact with the intestinal mucosa. These toxins evoke the secretory activity (fluid and electrolyte) of the intestinal mucosa probably by stimulating adenyl cyclase system (CAMP) and guanyl cyclase system (CGMP).






The severity of dehydration

  • In acute diarrhea, large amounts of water and electrolytes are lost, which if not promptly taken care of may ultimately lead to progressive dehydration, circulatory collapse and oligemic renal failure. Therefore, a pediatrician must be alert and vigilant, and should assess this dangerous complication as quickly as possible for immediate remedy.

  • The severity of dehydration may be graded into three types. It is represented as the percentage of body weight lost.

  • Grade I. Up to 5% loss of body weight. Mild dehydration may be manifested only by thirst and occasionally by changes in behavior.



The severity of dehydration

  • Grade II. 5% to 10% loss of body weight.

    • The anterior fontanel is sunken, reflecting the depletion in cerebrospinal fluid.
    • Mucous membranes (such as lips and tongue) are dry from depletion of transcelluiar fluids.
    • Skin demonstrates tenting due to decreased interstitial fluid. It means loss of skin turgor. Tenting of the skin, often improperly evaluated, should be tested by pinching and gently twisting the skin of the abdominal or thoracic wall. Tented skin remains in a pinched position rather than springing quickly back to normal.
    • Eyes are sunken because of the decreased vitreous humor.
    • With hypovolemia due to contraction of plasma volume, the patient may have hypotension, cool extremities, and activation of the sympathetic nervous system, accompanied by tachycardia.
    • Oliguria is found.


The severity of dehydration

  • Grade III. More than 10% loss of body weight.

    • With very severe dehydration, circulatory collapse occurs, with cool, cyanotic, sweating extremities; a rapid, thready pulse; mottled skin; and severe lethargy or coma.
    • Delayed capillary refill often occurs in patients with severe dehydration. Capillary refill, measured by compressing the ball of the thumb or large tou and estimating or measuring the time for return of blood flow or a blush, is greater than 3 sec with profound volume depletion.
    • Tear production may be lacking in severe dehydration.
    • Severe diarrhea causing excessive fluid and water loss may be followed by oligemic shock, often in association with renal failure and intravascular thrombosis.




Assessment of Dehydration







Isotonic dehydration

  • The composition of fluid lost is the same as that of the extracellular fluid in terms of mEq of sodium. Except signs of dehydration no other complications are usually observed.

  • Serum sodium levels are 130-150 mmol/L.

  • This type of dehydration is seen in about 80% cases of acute gastroenteritis.

  • The severity of isotonic dehydration depends on the duration of diarrhea and the net amount of fluid and electrolyte lost.



Hypertonic (hypernatremic) dehydration

  • The body loses proportionately more water in stools than sodium. The hypertonicity of the extracellular fluid draws out more fluid from the intracellular compartment leading to shrinkage of cell mass, irritation to the CNS, intracerebral and intraventricular hemorrhages, and occasionally subdural hematoma.

  • There is usually excessive thirst, irritability, fever, often followed by convulsion.

  • Patients tend to be hypertonic and hyperreflexic.

  • The skin is warm and has a doughy feel.

  • Urine flow is diminished.

  • The potential for hypernatremia increases with the presence of fever, high environmental temperatures, and hyperventilation, each of which increases evaporative water loss significantly, and with decreased availability of clean free water.

  • Serum sodium levels are greater than 150 mmol/L.

  • This type of dehydration is observed in about 15% cases of diarrhoea.



Hypertonic (hypernatremic) dehydration

  • Signs of extracellular fluid depletion are less per unit of fluid loss, and depression of the fontanelle, reduced tissue elasticity and sunken eyes are less obvious.

  • This makes this form of dehydration more difficult to recognise clinically, particularly in an obese infant.

  • It is a particularly dangerous form of dehydration as water is drawn out of the brain and cerebral shrinkage within a rigid skull may lead to multiple, small cerebral haemorrhages and convulsions.



Hypotonic (hyponatremic) dehydration

  • In approximately 5% cases body-sodium loss is comparatively more than the water loss. In an attempt to maintain the normal fluid and electrolyte ratio in the extracellular compartment fluid from the extracellular space is shifted into cells leading to cellular edema, rise in intracranial tension and convulsion.

  • Patients with dehydration, because of external losses and internal fluid shifts, may present with signs of profound volume depletion and shock.

  • It occurs more frequently with bacillary dysentery or cholera.

  • Serum sodium levels are less than 130 mmol/L.



Acidosis

  • It is most commonly associated with diarrheal disease because of stool bicarbonate losses and because of retention of anions from tissue catabolism and diminished renal function.

  • The most important physical sign is hyperventilation, the extreme of which is the deep, rapid respirations called Kussmaul breathing.

  • Severe acidosis itself may cause a decrease in peripheral vascular resistance and cardiac ventricular function, resulting in hypotension, pulmonary edema, and tissue hypoxia.

  • The laboratory findings are decreased serum pH and decreased levels of HCO2. (serum bicarbonate level less than 22 mEq/litre).



Hypopotassemia

  • Hypopotassemia, consequent to excess potassium loss in diarrheal stools, may lead to

    • muscular hypotonia (both skeletal muscles and smooth muscles),
    • weakness,
    • abdominal distention,
    • paralytic ileus,
    • sometimes poor myocardial contractility and cardiac arrhythmia.
  • The most observable cardiac manifestations of hypokalemia are electrocardiographic changes, including a prolonged QT interval and flattened T waves.

  • Severe hypokalemia may result in decreased function of the kidney.

  • Areflexia, paralysis, and death from respiratory muscle failure can develop.









Laboratory Evaluation

  • Laboratory tests can be useful in evaluating the nature and extent of dehydration and in guiding therapy, but they cannot substitute for careful bedside observation of the patient. Management of dehydration requires the clinical skills of the physician. In cases of serious dehydration, therapy should always be initiated promptly, even before receipt of the laboratory test results.

  • The etiological diagnosis may be made by the following investigations: microscopic stool examination, stool culture, blood culture.

  • Blood urea nitrogen and serum creatinine levels may be elevated in severe dehydration because of a decreased glomerular filtration rate.



Laboratory Evaluation

  • Identifying hemoconcentration, indicated by elevated hemoglobin, hematocrit, and plasma proteins, may help in estimating the severity of dehydration and in monitoring the response to rehydration. However, when hemoglobin and hematocrit appear normal despite severe dehydration, the physician should suspect that hemoconcentration exists and that the patient has an underlying anemia, often due to iron deficiency.

  • Stool specimens should be examined for mucus, blood, and leukocytes, the presence of which indicates colitis.

  • Urinalysis is most helpful in the measurement of urine specific gravity, which is usually elevated in cases of significant dehydration but which returns to normal after rehydration. With dehydration, urinalysis may show hyaline and granular casts, a few white cells and red cells, and 30-100 mg/dL of proteinuria. These findings usually are not associated with significant renal pathology, and they remit with therapy.



Management of Diarrhea

  • It should be started as early as possible with a careful and methodical approach.

  • The procedure may be guided by the following principles in order of clinical preference:

    • Assessment of severity of dehydration, and acidosis, and their prompt management.
    • Ascertain the cause of diarrhea and treat it.
    • Detection of complications and their management.
    • Prevention of sequele like malnutrition, vitamin deficiencies, anemia, and prevention of recurrence.
  • Similar therapeutic approaches are often used for patients with dehydration of different causes.



Management of Diarrhea

  • After careful assessment of the grade and the type of dehydration the following measures should be taken for its correction.

    • For grade I dehydration total daily volume of fluid is 130-170 ml/kg.
    • For grade II dehydration it is 170-200 ml/kg.
    • For grade III dehydration - 200-220 ml/kg.




Management of Diarrhea

  • In grade I dehydration replacement of all fluild and electrolytes may be done by oral rehydration.

  • In grade II dehydration replacement of fluild and electrolytes may be done by two-third oral and one-third intravenous.

  • In grade II dehydration replacement of fluild and electrolytes may be done by two-third intravenous and one-third oral .



^ ORAL FLUID THERAPY (ORAL REHYDRATION)

  • Oral rehydration is used in many countries and significantly reduces the morbidity and mortality from acute diarrhea. In grade I dehydration without vomiting replacement of fluild and electrolytes may be done by oral sugar-salt-solution. Sodium and glucose facilitate absorption of water. A solution prepared accoding to the special formula serves as ideal replacement fluid. The ingredients are available in powder form in preweighed packages.

  • As a guideline for oral rehydration, 50 mL/kg of the ORS (oral rehydration solution) should be given within 4 hr to patients with mild dehydration and 100 mL/kg over 6 hr to those with moderate dehydration. The amounts and rates should be increased if the patient continues to have diarrhea or if rehydration does not appear complete. They should be decreased if the patient appears fully hydrated earlier than expected or develops periorbital edema.



^ ORAL FLUID THERAPY

  • Vomiting may occur during the first 2 hr of administration of ORS, but it usually does not prevent successful oral rehydration. To reduce vomiting, the ORS should be given slowly, in small amounts, with a teaspoon or in small sips, at short intervals. In this case it may be better to delay feeding for a few hours.

  • When rehydration is complete, maintenance therapy should be started. Patients with mild diarrhea usually can then be treated at home using 100 mL of ORS/kg/24 hr until the diarrhea stops. Patients with more severe diarrhea require continued supervision. The volume of ORS ingested should equal the volume of stool losses. If stool volume cannot be measured, an intake of 10 15 mL of QRS/kg/hr is appropriate.





^ PARENTERAL FLUID THERAPY

  • In grade II or grade III dehydration, in grade I dehydration with persistent vomiting, and in a state of metabolic acidosis restoration of hydration and correction of the metabolic acidosis can be successfully achieved by intravenous infusion of specific fluid. However, oral rehydration may be attempted for most patients with mild to moderate diarrheal dehydration if adequate supervision is available.



^ PARENTERAL FLUID THERAPY

  • Parenteral therapy has three phases.

    • Initial therapy is designed to expand extracellular fluid volume rapidly and improve circulatory and renal function.
    • Subsequent therapy is aimed at replacing deficits while providing for maintenance water, electrolyte requirements, and ongoing losses. During this phase, sodium and water losses are usually almost hilly corrected.
    • The final phase consists of returning the patient to normal composition, which is usually associated with a return to oral feedings and wish the more gradual correction of total body potassium deficits.




^ PARENTERAL FLUID THERAPY

  • The goal of initial therapy is to expand extracellular fluid volume rapidly, especially plasma volume, to prevent or treat shock. !n the initial phase, 20-30 mL/kg of body weight of isotonic solution should be given by bolus and repeated a second or, occasionally, a third time, until the patient is hemodynamically stable.

  • The subsequent phase of therapy is devoted to continued replacement of existing deficit, provision of maintenance fluid and electrolytes, and replacement of ongoing losses.



Replacement of the water and electrolyte deficits

  • The goal of deficit therapy is to replace past and continuing losses of water and electrolytes.

    • For isotonic dehydration a mixture of one part of physiologic saline and one parts 5% glucose solution may be administered.
    • For hypertonic dehydration one part of physiologic saline and two parts of 5% glucose solution make a useful mixture for correction.
    • For hypotonic dehydration a mixture of two parts physiological saline solution and one part 5% glucose solution should be administered.
  • In cases of moderate to severe dehydration, not hypertonic, half of the total requirement of fluid for the first 24 hrs should be administered in the first 8 hours; and the rest in the next 16 hours.

  • In hypertonic dehydration the replacement of the fluid should be slow and prolonged over a period to 24 to 48 hours to avoid cardiac failure.



^ PARENTERAL FLUID THERAPY

  • In a state of shock and collapses. Intravenous drip should be started immediately with normal saline. Alternatively if possible, plasma or albumin (10 ml per kg) can be readily administered. The IV fluids should be administered as fast as possible till the signs of shock disappear, then continued more slowly.

  • Acidosis may reguire the administration of alkali ( 4 % sodium bicarbonate solution) One-fourth of the total fluid for the first 24 hours should be given as one-sixth molar sodium bicarbonate solution (50 ml. vial of molar + 250 ml 5% glucose solution). Only the required amount is to be infused).



^ PARENTERAL FLUID THERAPY

  • Hyperkalemia reguire the administration of 7,5 % potassium chloride solution or Panangin.

  • In cases of acute anuric renal failure, no potassium should be administered. It can be administered after the first observed urination. This order is necessary because potassium must move through the extracellular fluid compartment to reach the intracellular compartment in which most potassium is stored.

  • Large amounts of parenterally provided potassium can lead to hyperkalemia, which may have serious cardiac sequelae.



Drugs for Diarrheas

  • These have very limited use.

  • Antibiotics and Chemotherapeutics. It is neither necessary, nor desirable to use antibiotics. In infancy and childhood about 70 per cent of diarrheas are of viral origin where antibiotics have practically no role. They should be used only for the infectious agents such as Shigella, Salmonelle, E. Coli, Vibrio cholera, Entamoeba histolytica, and Giardia. Moreover misuse of these drugs may cause gut irritation and prolongation of diarrhea, may eliminate the residual flora which protects the gun and help in the growth of other non-susceptible bacteria or fungi. The following drugs are commonly used in pediatric practice: Nifuroxazid, Trimethoprim-sulphamethoxazole, Amikacin, Ceftriaxon. Parenteral administration of antibiotics may be required when there are evidences of systemic invasion of the organism.



Drugs for Diarrheas

  • Adsorbants and stool thickening agents. Formulas based on pectin, kaolin or bismuth salts are popular. So far there is little scientific evidence that they are useful. These agents do nof reduce excessive losses of fluids and electrolytes, even though the stool appears to be more solid and the mother is psychologically reassured.

  • Antiperistaltic drugs. Reduction of the gut motility may not abort the attack either. On the other hand, it may give more time for the harmful bacteria to multiply in the gut. Such wide spread drugs as loperamid (Imodium) or diphenoxylate hydrochloride (lomotil) also cause distention of the abdomen and other undesirable side effect of opiates. These may be given in some cases of chroic diarrhea and severe tenesmus or cramps.



Diet in diarrhea

  • It has been traditional to omit oral feedings initially when treating infants having more severe diarrhea. However, even during acute diarrhea, the small intestine can absorb various nutrients and may absorb up to 60% of the food eaten. Better weight gain has been documented in infants given a liberal dietary intake during diarrhea compared with others on a more restricted intake. Fasting has been shown to further reduce the ability of the small intestine to absorb nutrients, and because no physiologic basis exists for giving the bowel a "rest" during acute diarrhea. This approach may cause an increase in the volume of stool in most recipients, resulting in continuing large losses of fluid and electrolytes. This loss must be replaced and may require instituting or extending parenteral therapy for several days. Despite this unusual complication, studies have shown that rehydration occurs as rapidly with oral as with parenteral therapy in most patients.



Diet in diarrhea

  • After the first 24 hours, when dehydration has been corrected by oral or I.V. fluid, food should be reintroduced while the ORS is continued to replace ongoing losses from stools and for maintenance.

  • Breast-feeding in infants should be resumed as soon as possible. The child may be offered 10 ml of milk every 2 hours 10 times a day.

  • Oral feeding of one of the carbohydrate and electrolyte mixtures may be initiated if gastric distention and vomiting are absent. As soon as oralfeeding is tolerated without exacerbating the diarrhea, the caloric intake may be increased gradually by substituting mixtures that also contain fat and protein until the usual dietary intake is attained, which usually occurs within 7-8 days.



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