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Shigella infection in children 1 Clinical manifestations and diagnosis of Shigella infection in children Rabia Agha, Marcia B Goldberg, MD Up to date on line 16.1 This topic last updated: Fevereiro, 2006 http://www.uptodate.com/online/content/ acessado em 04 de junho de 2008. Modificado por Jefferson P Piva (Julho 2008) INTRODUCTION — Shigella species are a common Frequency of stools typically is 8 to 10 per day but may cause of bacterial diarrhea worldwide, especially in increase to up to 100 per day. The stools are of small developing countries. The organism is less susceptible volume, so significant fluid loss typically does not occur to acid than many other bacterial pathogens; thus, as (average approximately 30 mL/kg per day) [7]. These few as 10 to 100 organisms can cause disease, in part findings are characteristic of diarrhea caused by because the organisms can survive transit through the infection of the colon (the major site of infection with stomach [1]. Thus, ingested bacteria pass into the small Shigella) because the colon functions as a storage intestine where they multiply, so that several logs more organ. This is in contrast to small bowel infections in bacteria pass into the colon, where the organisms enter which the diarrhea typically is watery; of large volume; the colonic cells. and associated with abdominal cramping, bloating, gas, Intermediate bacterial replication in contaminated food and weight loss. or water is not required to achieve this low infectious The spectrum of severity of disease varies according to dose. As a result, Shigella transmission can occur the serogroup of the infecting organism. Shigella sonnei through direct person-to-person spread, as well as from commonly causes mild disease, which may be limited contaminated food and water; the former accounts for to watery diarrhea, although Shigella dysenteriae 1 or most cases in the United States, whereas the latter is Shigella more important in the developing world. symptoms (bloody diarrhea) [8]. The course of disease CLINICAL MANIFESTATIONS — Shigella is a flexneri commonly causes dysenteric in a normal healthy host generally is self-limited, lasting pathogen that primarily infects the lower intestinal tract. no more than seven days when left untreated. Patients with Shigella gastroenteritis typically present The typical course of disease varies with age group. In with high fever, abdominal cramps, and bloody, mucoid a review of 318 infants and children hospitalized with diarrhea. The approximate prevalence of these signs shigellosis in Bangladesh, infants had fewer days with and symptoms is [2-5] : diarrhea (four versus six) and were more likely to have Fever (30 to 40 %); abdominal pain (70 to 93%),mucoid watery (as opposed to bloody) stools, hyponatremia, diarrhea (70 to 85%), bloody diarrhea (35 to 55%), abdominal distension, and acidosis than were older watery diarrhea (30 to 40%), vomiting (35%). children [9] . Older children were more likely to have a The incubation period ranges from one to seven days, leukemoid reaction than were infants. The mortality rate with an average of three days [6]. The disease typically for infants was twice that of older children. Infants who begins with constitutional symptoms such as fever, were breast fed were less frequently infected and had a anorexia, and malaise; diarrhea initially is watery, but milder illness than infants who were not breast fed [2]. subsequently may contain blood and mucus. Tenesmus Intestinal complications: is a common complaint. Rectal prolapse - The severe inflammation of the rectum and distal colon that is induced by invasion of Shigella infection in children 2 the organism into the colonic mucosa may lead to diarrhea caused by S. dysenteriae 1 [13]. Generally, proctitis or rectal prolapse. hyponatremia is caused by the syndrome of Toxic megacolon - Toxic megacolon occurs primarily inappropriate ADH secretion, not by volume depletion in the setting of S. dysenteriae 1 infection. The [1,13]. Several consequences of shigellosis contribute pathogenesis is unclear; it occurs in the setting of to malnutrition, such as: Increased catabolism pancolitis and seems to be related to the intensity of secondary to fever, stool protein loss, decreased intake inflammation rather than being mediated by Shiga toxin. caused by anorexia, Malabsorption The incidence of toxic megacolon in children with Leukemoid reaction — A leukemoid reaction (defined diarrhea is low (3%) [1]. as a white blood cell count of 50,000/mm3 or more) has Intestinal obstruction — Severe colonic disease may been noted in approximately 4% of patients, most result in intestinal obstruction. The incidence in one commonly in children between 2 and 10 years of age series of 1211 patients with shigellosis was 2.5%[10]. and not at all in children younger than 1 year of age The patients with obstruction were more likely to be [15]. The WBC count in these patients ranged from infected with S. dysenteriae 1 and were more severely 50,000 to 195,000/mm3 and was accompanied by an ill, as evidenced by a significantly higher white blood increased number of immature forms. The mortality rate cell sodium also was increased (21 versus 7.4% in those without a concentration than patients without evidence of leukemoid reaction). In contrast, an earlier study obstruction. conducted in the United States found no association Colonic perforation — Colonic perforation is an between disease severity and a high WBC count [3]. unusual complication of shigellosis. It occurs principally Neurologic disease — Seizures, the most common in infants or severely malnourished patients and is neurologic complication associated with Shigella associated with infection caused by S. dysenteriae 1 or infection, are always associated with fever (usually S. flexneri (1.7% of fatal cases) [11]. greater than 39ºC), are generalized, uncomplicated, Systemic complications . nonrecurring, and not associated with neurologic Bacteremia — Bacteremia occurs in approximately 4% deficits [16] . Seizures can be seen with all serotypes of of patients with Shigella gastroenteritis and is Shigella infection, but are least common with S. associated with an increase in mortality [12]. Young, dysenteriae 1. malnourished children are at greatest risk. Bacteremia The reported prevalence of seizures in children with with another gram-negative organism is seen in shigellosis has ranged from 12 to 45% [16] and, in approximately 5% of patients who have a stool culture patients of all ages hospitalized with shigellosis, is positive for Shigella. approximately 10% [1]. In hospitalized children, the (WBC) Metabolic count and lower serum disturbances — Substantial volume most common age group in which seizures occur is that depletion is uncommon in shigellosis because the stool between 6 months and 4 years, the same group most volume usually is low. In a review of 412 patients with likely to have simple febrile seizures [17]. Analysis of shigellosis, 36% had mild, 12% had moderate, and 2% cerebrospinal fluid obtained by lumbar puncture had severe dehydration [2]. In another series, typically is normal, although as many as 15% of these hyponatremia (defined as serum sodium below 120 patients may have mild lymphocytic pleocytosis with as meq/L) was noted in 29% of patients hospitalized with many as 12 cells [16]. Shigella infection in children 3 In the past, neurologic complications of Shigella accompanied by fever. Nausea and vomiting are infection were thought to be induced by circulating notably absent in most patients. The presence or Shiga toxin, which is produced by S. dysenteriae 1 [18]. absence of leukocytes in the stool can be determined Shiga toxin was not detected in serum or spinal fluid rapidly and simply by microscopic examination. The and was present in stool at levels that were 1000-fold constellation of the above symptoms and increased below that of cultured S. dysenteriae 1in children with numbers of fecal leukocytes is strongly suggestive of seizures[19]. However, there are no conclusive studies infection with Shigella, Salmonella, Campylobacter, demonstrating relationship between Shiga toxin and Yersinia, enteroinvasive E. coli, or Clostridium difficile, seizures. Furthermore, the majority of patients who or of noninfectious inflammatory bowel disease [33]. have seizures are infected with S. flexneri or S. sonnei, Fecal leukocytes — In a study that examined the neither of which expresses Shiga toxin. Taken together, usefulness of fecal leukocytes in predicting the etiology these data suggest that other Shigella enterotoxins of diarrhea, the presence of fecal leukocytes was might contribute to the induction of seizures, although associated with a bacterial cause of acute diarrhea in this possibility has not as yet been proved [22] . 89% of cases [34] . Patients infected with Shigella had Encephalopathy with and fecal polymorphonuclear leukocytes in 70 to 100% of headache has been noted in as many as 40 percent of samples tested, with at least 10 to 25 cells/hpf in the children hospitalized with Shigella infection [23]. majority of patients [2,34] . In comparison, healthy Obtundation or coma and abnormal neurologic signs, controls and patients with cholera or viral diarrhea had including no posturing, lethargy, are rare. confusion, In cases of fecal leukocytes. In volunteers infected encephalopathy that were fatal, cerebral edema was experimentally, the presence of fecal leukocytes was a found at autopsy. more sensitive means of diagnosing infection with S. Hemolytic-uremic syndrome — Although relatively dysenteriae 1 than was stool culture [34] . uncommon, the hemolytic-uremic syndrome (HUS) can Stool culture — Confirmation of the infecting organism occur as a complication of infection caused by Shigella can be made only by culture of the stool. Shigella is a dysenteriae. Because HUS is mediated by Shiga toxin, fastidious organism; as a result, it requires prompt which is present in S. dysenteriae type 1, but not other handling and optimally should be inoculated onto agar species of Shigella, only S. dysenteriae type 1 can at the bedside. Culture from a stool sample may give a cause HUS. HUS is a potentially life-threatening illness better yield than culture from a rectal swab [35]. If that is characterized by a microangiopathic hemolytic transport of the sample is required, the best medium is anemia, thrombocytopenia, and acute renal failure. buffered glycerol saline (BGS) [36]. The best yield is Enterohemorrhagic Ecsherichia coli (EHEC) infection from a mucoid part of stool. accounts for about 70 percent of cases in the United States [28]. Other manifestations: In young girls, Shigella can cause vulvovaginitis with or without diarrhea [30]. DIAGNOSIS — Shigella should be suspected in any patient with frequent, small volume, bloody stools, abdominal cramps, and tenesmus, particularly if Shigella infection in children 4 REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 36. Bennish, ML. Potentially lethal complications of shigellosis. Rev Infect Dis 1991; 13 Suppl 4:S319. Stoll, BJ, Glass, RI, Huq, MI, et al. Epidemiologic and clinical features of patients infected with Shigella who attended a diarrheal disease hospital in Bangladesh. J Infect Dis 1982; 146:177. Barrett-Connor, E, Connor, JD. Extraintestinal manifestations of shigellosis. Am J Gastroenterol 1970; 53:234. Echeverria, P, Sethabutr, O, Pitarangsi, C. Microbiology and diagnosis of infections with Shigella and enteroinvasive Escherichia coli. Rev Infect Dis 1991; 13 Suppl 4:S220. DuPont, HL, Hornick, RB, Dawkins, AT, et al. The response of man to virulent Shigella flexneri 2a. J Infect Dis 1969; 119:296. Maurelli, AT, Lampel, KA. Shigella. In: Foodborne Disease Handbook, Hui, YH, Gorham, JR, Murrell, KD, Cliver, DO (Eds), Marcel Dekker, New York 1994. p.321. Acheson, DW, Keusch, GT. Shigella and enteroinvasive Escherichia coli. In: Infections of the Gastrointestinal Tract, Blaser, MJ, Smith, PD, Ravdin, JI, et al (Eds), Raven Press, New York 1995. p.765. Keusch, GT, Formal, SB, Bennish, ML. Shigellosis. In: Tropical and Geographical Medicine, Warren, KS, Mahmoud, AA (Eds), McGraw-Hill, New York 1990. p.763. Huskins, WC, Griffiths, JK, Faruque, ASG, et al. Shigellosis in neonates and young infants. J Pediatr 1994; 125:14. Bennish, ML, Azad, AK, Yousefzadeh, D. Intestinal obstruction during shigellosis: Incidence, clinical features, risk factors and outcome. Gastroenterology 1991; 101:626. Azad, MA, Islam, M, Butler, T. Colonic perforation in Shigella dysenteriae 1 infection. Pediatr Infect Dis 1986; 5:103. Struelens, MJ, Patte, D, Kabir, I, et al. Shigella septicemia: Prevalence, presentation, risk factors, and outcome. J Infect Dis 1985; 152:784. Keusch, GT, Bennish, ML. Shigellosis: Recent progress, persisting problems and research issues. Pediatr Infect Dis J 1989; 8:713. Bennish, ML, Salam, MA, Wahed, MA. Enteric protein loss during shigellosis. Am J Gastroenterol 1993; 88:53. Butler, T, Islam, MR, Bardhan, PK. The leukemoid reaction in shigellosis. Am J Dis Child 1984; 138:162. Ashkenazi, S, Dinari, G, Zevulunov, A, et al. Convulsions in childhood shigellosis. Am J Dis Child 1987; 141:208. Ashkenazi, S, Dinari, G, Weitz, R , Nitzan, M. Convulsions in shigellosis. Evaluation of possible risk factors. Am J Dis Child 1983; 137:985. Keusch, GT, Donohue-Rolfe, A, Jacewicz, M. Shigella toxin(s): description and role in diarrhea and dysentery. Pharmacol Ther 1981; 15:403. Ashkenazi, S, Cleary, KR, Pickering, LK, et al. The association of Shiga toxin and other cytokines with the neurologic manifestations of shigellosis. J Infect Dis 1990; 161:961. Noriega, FR, Liao, FM, Formal, SB, et al. Prevalence of Shigella enterotoxin 1 among Shigella clinical isotypes of diverse serotypes. J Infect Dis 1995; 172:408. Fasano, A, Noriega, FR, Maneval, DR, et al. Shigella enterotoxin 1: An enterotoxin of Shigella flexneri 2a active in rabbit small intestine in vivo and in vitro. J Clin Invest 1995; 95:2853. Nataro, JP, Seriwatana, J, Fasano, A, et al. Identification and cloning of a novel plasmid- encoded enterotoxin of enteroinvasive Escherichia coli and Shigella strains. Infect Immun 1995; 63:4721. Avital, A, Maayan, C, Goitein, KJ. Incidence of convulsions and encephalopathy in childhood Shigella infections. Clin Pediatr 1982; 21:645. Simon, G, Kaslow, RA, Rosenbaum, J, et al. Reiter's syndrome following epidemic shigellosis. J Rheumatol 1981; 8:969. Stieglitz, H, Lipsky, P. Association between reactive arthritis and antecedent infection with Shigella flexneri carrying a 2-Md plasmid and encoding an Hla-B27 mimetic epitope. Arthritis Rheum 1993; 36:1387. Granfors, K, Jalkanen, S, Toivanen, P, et al. Bacterial lipopolysaccharide in synovial fluid cells in Shigella triggered reactive arthritis. J Rheumatol 1992; 19:500. Hughes, RA, Keat, AC. Reiter's syndrome and reactive arthritis: A current view. Semin Arthritis Rheum 1994; 24:190. Siegler, RL. The hemolytic uremic syndrome. Pediatr Clin North Am 1995; 42:1505. Bennish, ML, Khan, WA, Begum, M, et al. Low risk of hemolytic uremic syndrome after early effective antimicrobial therapy for Shigella dysenteriae type 1 infection in Bangladesh. Clin Infect Dis 2006; 42:356. Murphy, TV, Nelson, JD. Shigella vaginitis: report of 38 patients and review of the literature. Pediatrics 1979; 63:511. Tobias, JD, Starke, JR, Tosi, MF. Shigella keratitis: a report of two cases and a review of the literature. Pediatr Infect Dis J 1987; 6:79. Rubenstein, JS, Noah, ZL, Zales, VR, Shulman, ST. Acute myocarditis associated with Shigella sonnei gastroenteritis. J Pediatr 1993; 122:82. DuPont, HL, Levine, MM, Hornick, RB, Formal, SB. Inoculum size in shigellosis and implications for expected mode of transmission. J Infect Dis 1989; 159:1126. Harris, JC, Du Pont, HL, Hornick, RB. Fecal leukocytes in diarrheal illness. Ann Intern Med1972; 76:697. Rahaman, MM, Huq, I, Dey, CR. Superiority of MacConkey's agar over Salmonella-Shigella agar for isolation of Shigella dysenteriae type 1. J Infect Dis 1975; 131:700. Farmer, JJ, Wells, JG, Griffin, PM. Enterobacteriaceae infections. In: Diagnostic Procedures for Bacterial Infections, Wentworth, BB (Ed), American Public Health Association, Washington, DC 1987. p.274. Shigella infection in children 5 Treatment and prevention of Shigella infections in children Shai Ashkenazi, This topic last updated: Maio 22, 2008 Modificado por Jeffferson Piva em Julho de 2008. SUPPORTIVE THERAPY — The mainstay of the of isolates are resistant to nalidixic acid [21-23]. treatment Resistance to nalidixic acid also been reported in of acute gastroenteritis in children, irrespective of the cause, which usually is not known at England [24] and the United States [20] . the time of presentation, is correction of fluid and Antimicrobial resistance is an increasing problem in the electrolyte losses [4] . Oral rehydration is preferred, United States. Between 1999 and 2002, the following when feasible [10], but intravenous fluids may be results were reported: necessary. (Ver texto inserido como apêndice ao final). All isolated Shigella were susceptible to ceftriaxone The use of intestinal antimotility drugs, such as and ciprofloxacin. diphenoxylate (Lomotil), should be avoided in children 78% of isolates were resistant to ampicillin, 46% to with suspected shigellosis. These drugs may prolong TMP-SMX, 38% to both ampicillin and TMP-SMX, duration of fever, diarrhea, and excretion of the and 1 percent to nalidixic acid. organism [11] . ANTIBIOTIC THERAPY Early restoration of oral intake, especially protein, is Rationale — The goals of antibiotic therapy for Shigella important, particularly in developing countries, to include improvement in symptoms and decreased prevent the exacerbation of malnutrition [12-14] . spread Patients with severe toxemia or suspected bacteremia, antimicrobial treatment of Shigella gastroenteritis underlying immune deficiency, and who are unable to reduces the duration of fever, diarrhea, and fecal take oral medications should be hospitalized. excretion [28-31] . It also may reduce the risk of ANTIBIOTIC RESISTANCE — The increasing of infection to contacts. Appropriate developing complications [32] . antimicrobial resistance of Shigella species is a major In randomized, placebo-controlled trials during the problem in treating shigellosis. The major route for 1960s and early 1970s (before the widespread dissemination of multiple resistance is by horizontal development of resistance to ampicillin), children with transfer of plasmids carrying antibiotic resistance (R- shigella infection who were treated with ampicillin had plasmids). A commonly isolated plasmid carries decreased duration of diarrhea, fever, and fecal resistance shedding than those who received placebo [28-31] . tetracycline, against ampicillin, sulfonamides, chloramphenicol, streptomycin, and The findings of the largest two studies are presented trimethoprim [17] . Ampicillin resistance also is below: mediated by beta-lactamases. In Children hospitalized with Shigella gastroenteritis, High rates of antimicrobial resistance were first reported those who received ampicillin (compared to placebo) in Asia, Africa, and South America, but antimicrobial had shorter duration of diarrhea (3.3 versus 6 days), resistance has rapidly spread to developed countries fever (1.3 versus 2.6 days), and fecal shedding [18-20] . In India and Bangladesh, 20 percent or more (positive stool culture for 2 versus 5 days) [28] . Shigella infection in children In another randomized study of 373 children with 6 the possibility of favoring emergence of resistant acute diarrhea who were treated as outpatients, 101 organisms [3] and potential adverse effects. children had stool cultures positive for Shigella [29]. Indications — Decisions Compared with those who received placebo, fewer antimicrobial therapy must consider the appearance of children with Shigella who were treated with the patient, the presence of host factors that predispose ampicillin had positive stool cultures after 48 hours (8 to versus 70 %) and fewer continued to have diarrhea considerations. after five days (5 versus 50 percent). None of the We recommend empiric antimicrobial therapy for patients who were treated with ampicillin required shigellosis in children and adolescents who present hospital admission or treatment with another with suspected shigellosis (bloody/mucousy diarrhea, antibiotic after completion of therapy (compared with high fever) and are immunocompromised or bacteremic one and five children in the placebo group, [33] . respectively). We recommend antimicrobial therapy for children and more severe regarding infection, and initiation public of health The decreased duration of shedding with antimicrobial adolescents with culture-proven Shigella who [33]: therapy reduces the risk of person-to-person spread of Have bacteremia, require hospitalization, attend day the infection. In the absence of specific antibiotic care, live in institutions or are involved in food handling. treatment, children with Shigella gastroenteritis shed Treatment of mild cases or of children who have the organism for up to four weeks, and children with recovered by the time the report of positive Shigella immune deficiency, for much longer periods, even if culture is available is controversial. Antimicrobial their symptoms have resolved [4,6,7,33] . treatment of such children is unlikely to significantly Shigella is highly contagious; ingestion of only 10 to affect the clinical course, but will shorten fecal excretion 100 organisms can produce disease. Therefore, and thus reduce the spread of this highly contagious treatment of an infected child at risk to transmit the bacterium. disease to others (eg, a day-care attendee, hospitalized Choice of regimen — The medication spectrum and patient) is particularly compelling. regimen (oral versus parenteral) are determined by The benefits of antimicrobial therapy discussed above severity of illness, local resistance patterns, and history outweigh the potential risks of therapy, which include of travel to an area of frequent resistance [3,35]. REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. Kotloff, KL, Winickoff, JP, Ivanoff, B, et al. 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Distúrbios Hidroeletrolíticos na criança. IN: Piva J, Garcia PC (Eds). Medicina Intensiva em Pediatria. Rio de janeiro: Revinter. 2005. p317-333. O tratamento da desidratação inicia pela análise da osmolaridade séricos, além de creatinúria, glicosúria, história clínica, da diurese (se possível), da perda de cetonúria, pH urinário, osmolaridade e dosagem de peso e estimativas de perdas e aporte de líquidos. O eletrólitos na urina.(1-2) exame físico deve ser acurado, procurando detectar Na desidratação leve e em alguns casos sinais de comprometimento do intravascular. Os moderada, a reidratação deve ser realizada por via exames complementares devem incluir sódio, potássio, oral, pois, não há comprometimento dos espaços cálcio, hemograma, uréia, creatinina, glicose, pH, intravascular e intracelular. Nestes casos administra-se bicarbonato, podendo ainda ser indicados em casos 25-30 ml/kg/hora de solução de hidratação oral. A selecionados a dosagem sérica de albumina e solução de hidratação oral recomendada pela OMS foi Shigella infection in children 9 modificada em 2002. O conteúdo de Na foi reduzido de (melhora do pulso, diminuição da taquicardia, retorno 90 para 75 mEq/L, o K foi mantido em 20 mEq/L e o da diurese, etc.). bicarbonato mantido em 30 mEq/L, enquanto que a A fase de recuperação da reidratação por via glicose foi reduzida de 2 para 1,3%. Com estas endovenosa deve ser o mais breve possível, para que modificações a osmolaridade foi reduzida de 310 para utilize preferentemente a via oral. Entretanto, em um 245 mOsm/L. grande contingente de pacientes de UTI e de salas de Nos pacientes com desidratação de III grau e naqueles emergência, em razão de situações associadas (sepse, de II grau com menos de 3 meses, com alteração de pós-operatório, alterações do sensório, etc), esta fase estado de consciência, vômitos intratáveis, distensão de recuperação é mantida por via endovenosa e pode abdominal perdurar por cerca de 20 horas. Após a restauração da ou íleo adinâmico, o tratamento recomendado é a hidratação endovenosa (5,6). volemia, o objetivo é administrar a manutenção Existem vários esquemas de reidratação, que levam hidroeletrolítica adicionada das possíveis perdas e das em consideração a quantidade de líquido perdido, as deficiências eletrolíticas ainda existentes. A estimativa possíveis perdas posteriores e a quantidade de líquidos do volume a ser administrado depende da causa da de manutenção para cada indivíduo. Na prática, a desidratação, da resposta à infusão inicial e do próprio reidratação endovenosa deve ser um procedimento grau de desidratação. Utilizamos infundir a manutenção simples, eficaz e com controle clínico contínuo. De hídrica diária (~100 ml/kg/dia emlactentes) sob a forma forma que ao compensar o comprometimento de solução fisiológica (150 mEq/L de sódio) com 5% de intravascular retorna-se a hidratação pela via oral. glicose ou uma proporção de 50% de cada uma destas A reidratação endovenosa é constituída por duas soluções. Nesta etapa deve ser adicionado potássio na etapas: a fase de reposição ou de expansão proporção de 20 a 40 mEq/ para cada litro de solução. volumétrica e a fase de recuperação ou de No caso de haver perdas volumosas durante este estabilização. período (vômitos, drenagem volumos pela sonda A fase de expansão é rápida e agressiva, visando a gástrica, gastroenterites, etc), optamos por fazer novas restauração do volume intravascular nas primeiras expansões com Solução fisiológica (20 ml/kg em 20 horas (em média de 2 horas). Assim, quanto maior for minutos). a depleção de volume, mais agressiva e rápida deve Após as primeiras 24 horas de tratamento, a ser a reposição volumétrica. grande maioria dos pacientes apresenta reversão do Em crianças desidratadas de II e III grau, preconizamos quadro com melhora clínica e compensação fisiológica expansões com solução fisiológica (NaCl 0,9%) de 20 dos distúrbios hidroeletrolíticos e ácido-básicos. Nesta ml/kg a cada 20 minutos ou 30 minuto (40 a 60 fase de equilíbrio, a hidratação venosa pode ser ml/kg/hora) que podem ser repetidas tantas vezes reduzida, incentivando-se a administração por via oral. quanto necessárias para reverter a depleção volumétrica. É importante ressaltar que ao redor de 25% desta solução permanece dentro do espaço intravascular, sendo que os restantes 75% se distribuem no espaço intersticial. Repete-se estas expansões até que ocorra resposta hemodinâmica