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Microsoft word - shigella infection in children.doc

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 typical y is watery; of large volume; and associated with abdominal cramping, bloating, gas, Intermediate bacterial replication in contaminated food 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. Shigel a 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 symptoms (bloody diarrhea) [8]. The course of disease CLINICAL MANIFESTATIONS — Shigella is a
in a normal healthy host general y 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 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 il ness than infants who were not breast fed [2]. subsequently may contain blood and mucus. Tenesmus Intestinal complications:
Rectal prolapse - The severe inflammation of the
rectum and distal colon that is induced by invasion of the organism into the colonic mucosa may lead to diarrhea caused by S. dysenteriae 1 [13]. General y, 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 shigel osis 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. The incidence of toxic megacolon in children with Leukemoid reaction — A leukemoid reaction (defined
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 shigel osis 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 also was increased (21 versus 7.4% in those without a concentration than patients without evidence of leukemoid reaction). In contrast, an earlier study 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 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, 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 approximately 10% [1]. In hospitalized children, the Metabolic
disturbances — Substantial
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, typical y 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 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 Shigel a, 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 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 Shigel a 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 encephalopathy that were fatal, cerebral edema was experimental y, the presence of fecal leukocytes was a 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. Shigel a 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 optimal y 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 potential y 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 accounts for about 70 percent of cases in the United Other manifestations: In young girls, Shigella can
cause vulvovaginitis with or without diarrhea [30]. DIAGNOSIS — Shigel a should be suspected in any
patient with frequent, smal volume, bloody stools, abdominal cramps, and tenesmus, particularly if REFERENCES
Bennish, ML. Potential y lethal complications of shigel osis. Rev Infect Dis 1991; 13 Suppl 4:S319. Stol , BJ, Glass, RI, Huq, MI, et al. Epidemiologic and clinical features of patients infected with Shigel a who attended a diarrheal disease hospital in Bangladesh. J Infect Dis 1982; 146:177. Barrett-Connor, E, Connor, JD. Extraintestinal manifestations of shigel osis. Am J Gastroenterol 1970; 53:234. Echeverria, P, Sethabutr, O, Pitarangsi, C. Microbiology and diagnosis of infections with Shigel a 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 Shigel a flexneri 2a. J Infect Dis 1969; 119:296. Maurel i, AT, Lampel, KA. Shigel a. In: Foodborne Disease Handbook, Hui, YH, Gorham, JR, Murrel , KD, Cliver, DO (Eds), Marcel Dekker, New York 1994. p.321. Acheson, DW, Keusch, GT. Shigel a 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. Shigel osis. In: Tropical and Geographical Medicine, Warren, KS, Mahmoud, AA (Eds), McGraw-Hil , New York 1990. p.763. Huskins, WC, Griffiths, JK, Faruque, ASG, et al. Shigel osis in neonates and young infants. J Pediatr 1994; 125:14. 10. Bennish, ML, Azad, AK, Yousefzadeh, D. Intestinal obstruction during shigel osis: Incidence, clinical features, risk factors and outcome. Gastroenterology 1991; 101:626. 11. Azad, MA, Islam, M, Butler, T. Colonic perforation in Shigel a dysenteriae 1 infection. Pediatr Infect Dis 1986; 5:103. 12. Struelens, MJ, Patte, D, Kabir, I, et al. Shigel a septicemia: Prevalence, presentation, risk factors, and outcome. J Infect Dis 1985; 13. Keusch, GT, Bennish, ML. Shigel osis: Recent progress, persisting problems and research issues. Pediatr Infect Dis J 1989; 14. Bennish, ML, Salam, MA, Wahed, MA. Enteric protein loss during shigel osis. Am J Gastroenterol 1993; 88:53. 15. Butler, T, Islam, MR, Bardhan, PK. The leukemoid reaction in shigel osis. Am J Dis Child 1984; 138:162. 16. Ashkenazi, S, Dinari, G, Zevulunov, A, et al. Convulsions in childhood shigel osis. Am J Dis Child 1987; 141:208. 17. Ashkenazi, S, Dinari, G, Weitz, R , Nitzan, M. Convulsions in shigel osis. Evaluation of possible risk factors. Am J Dis Child 1983; 18. Keusch, GT, Donohue-Rolfe, A, Jacewicz, M. Shigel a toxin(s): description and role in diarrhea and dysentery. Pharmacol Ther 19. Ashkenazi, S, Cleary, KR, Pickering, LK, et al. The association of Shiga toxin and other cytokines with the neurologic manifestations of shigel osis. J Infect Dis 1990; 161:961. 20. Noriega, FR, Liao, FM, Formal, SB, et al. Prevalence of Shigel a enterotoxin 1 among Shigel a clinical isotypes of diverse 21. Fasano, A, Noriega, FR, Maneval, DR, et al. Shigel a enterotoxin 1: An enterotoxin of Shigel a flexneri 2a active in rabbit smal intestine in vivo and in vitro. J Clin Invest 1995; 95:2853. 22. Nataro, JP, Seriwatana, J, Fasano, A, et al. Identification and cloning of a novel plasmid- encoded enterotoxin of enteroinvasive Escherichia coli and Shigel a strains. Infect Immun 1995; 63:4721. 23. Avital, A, Maayan, C, Goitein, KJ. Incidence of convulsions and encephalopathy in childhood Shigel a infections. Clin Pediatr 24. Simon, G, Kaslow, RA, Rosenbaum, J, et al. Reiter's syndrome fol owing epidemic shigel osis. J Rheumatol 1981; 8:969. 25. Stieglitz, H, Lipsky, P. Association between reactive arthritis and antecedent infection with Shigel a flexneri carrying a 2-Md plasmid and encoding an Hla-B27 mimetic epitope. Arthritis Rheum 1993; 36:1387. 26. Granfors, K, Jalkanen, S, Toivanen, P, et al. Bacterial lipopolysaccharide in synovial fluid cel s in Shigel a triggered reactive 27. Hughes, RA, Keat, AC. Reiter's syndrome and reactive arthritis: A current view. Semin Arthritis Rheum 1994; 24:190. 28. Siegler, RL. The hemolytic uremic syndrome. Pediatr Clin North Am 1995; 42:1505. 29. Bennish, ML, Khan, WA, Begum, M, et al. Low risk of hemolytic uremic syndrome after early effective antimicrobial therapy for Shigel a dysenteriae type 1 infection in Bangladesh. Clin Infect Dis 2006; 42:356. 30. Murphy, TV, Nelson, JD. Shigel a vaginitis: report of 38 patients and review of the literature. Pediatrics 1979; 63:511. 31. Tobias, JD, Starke, JR, Tosi, MF. Shigel a keratitis: a report of two cases and a review of the literature. Pediatr Infect Dis J 1987; 32. Rubenstein, JS, Noah, ZL, Zales, VR, Shulman, ST. Acute myocarditis associated with Shigel a sonnei gastroenteritis. J Pediatr 33. DuPont, HL, Levine, MM, Hornick, RB, Formal, SB. Inoculum size in shigel osis and implications for expected mode of transmission. J Infect Dis 1989; 159:1126. 34. Harris, JC, Du Pont, HL, Hornick, RB. Fecal leukocytes in diarrheal il ness. Ann Intern Med1972; 76:697. 35. Rahaman, MM, Huq, I, Dey, CR. Superiority of MacConkey's agar over Salmonel a-Shigel a agar for isolation of Shigel a dysenteriae type 1. J Infect Dis 1975; 131:700. 36. Farmer, JJ, Wel s, JG, Griffin, PM. Enterobacteriaceae infections. In: Diagnostic Procedures for Bacterial Infections, Wentworth, BB (Ed), American Public Health Association, Washington, DC 1987. p.274. Treatment and prevention of Shigel a infections in children
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 of acute gastroenteritis in children, Resistance to nalidixic acid also been reported in 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 fol owing when feasible [10], but intravenous fluids may be necessary. (Ver texto inserido como apêndice ao final).  All isolated Shigel a were susceptible to ceftriaxone The use of intestinal antimotility drugs, such as diphenoxylate (Lomotil), should be avoided in children  78% of isolates were resistant to ampicil in, 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 ANTIBIOTIC THERAPY
Early restoration of oral intake, especial y protein, is Rationale — The goals of antibiotic therapy for Shigel a
important, particularly in developing countries, to include improvement in symptoms and decreased prevent the exacerbation of malnutrition [12-14] . 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
antimicrobial resistance of Shigella species is a major In randomized, placebo-controlled trials during the problem in treating shigel osis. 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 ampicil in had plasmids). A commonly isolated plasmid carries decreased duration of diarrhea, fever, and fecal shedding than those who received placebo [28-31] . The findings of the largest two studies are presented trimethoprim [17] . Ampicillin resistance also is  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] .  In another randomized study of 373 children with 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 regarding initiation of
Compared with those who received placebo, fewer antimicrobial therapy must consider the appearance of children with Shigel a who were treated with the patient, the presence of host factors that predispose ampicillin had positive stool cultures after 48 hours (8 to more severe infection, and public health versus 70 %) and fewer continued to have diarrhea after five days (5 versus 50 percent). None of the We recommend empiric antimicrobial therapy for patients who were treated with ampicil in required shigellosis in children and adolescents who present hospital admission or treatment with another with suspected shigel osis (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, We recommend antimicrobial therapy for children and 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 Shigel a 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 Shigel a 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 disease to others (eg, a day-care attendee, hospitalized Choice of regimen — The medication spectrum and
regimen (oral versus parenteral) are determined by The benefits of antimicrobial therapy discussed above severity of il ness, local resistance patterns, and history outweigh the potential risks of therapy, which include of travel to an area of frequent resistance [3,35]. REFERENCES
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Lancet 1998; 352:522. 41. Khan, WA, Seas, C, Dhar, U, et al. Treatment of shigel osis: V. Comparison of azithromycin and ciprofloxacin. A double-blind, randomized, control ed trial. Ann Intern Med 1997; 126:697. 42. Basualdo, W, Arbo, A. Randomized comparison of azithromycin versus cefixime for treatment of shigel osis in children. Pediatr 43. Miron, D, Torem, M, Merom, R, Colodner, R. Azithromycin as an alternative to nalidixic acid in the therapy of childhood shigel osis. Pediatr Infect Dis J 2004; 23:367. 44. American Academy of Pediatrics. Antimicrobial agents and related therapy. In: Red Book: 2006 Report of the Committee on Infectious Diseases, 27th ed, Pickering, LK (Ed), American Academy of Pediatrics, Elk Grove Vil age, IL 2006. p. 735. 45. The use of systemic fluoroquinolones. Pediatrics 2006; 118:1287. 46. Burkhardt, JE, Walterspiel. JN. Schaad. UB. Quinolone arthropathy in animals versus children. Clin Infect Dis 1997; 25:1196. 47. Leibovitz, E, Janco, J, Piglansky, L, et al. Oral ciprofloxacin vs. intramuscular ceftriaxone as empiric treatment of acute invasive diarrhea in children. Pediatr Infect Dis J 2000; 19:1060. 48. Bhattacharya, K, Bhattacharya, MK, Dutta, D, et al. Double-blind, randomized clinical trial for safety and efficacy of norfloxacin for shigel osis in children. Acta Paediatr 1997; 86:319. 49. Rogerie, F, Ott, D, Vandepitte, J, et al. Comparison of norfloxacin and nalidixic acid for treatment of dysentery caused by Shigel a dysenteriae type 1 in adults. Antimicrob Agents Chemother 1986; 29:883. 50. Vinh, H, Wain, J, Chinh, MT, et al. Treatment of bacil ary dysentery in Vietnamese children: two doses of ofloxacin versus 5-days nalidixic acid. Trans R Soc Trop Med Hyg 2000; 94:323. 51. Ashkenazi, S, Amir, J, Waisman, Y, et al. A randomized, double-blind study comparing cefixime and trimethoprim- sulfamethoxazole in the treatment of childhood shigel osis. J Pediatr 1993; 123:819. 52. Helvaci, M, Bektaslar, D, Ozkaya, B, et al. Comparative efficacy of cefixime and ampicil in-sulbactam in shigel osis in children. 53. Prado, D, Lopez, E, Liu, H, et al. Ceftibuten and trimethoprim-sulfamethoxazole for treatment of Shigel a and enteroinvasive Escherichia coli disease. Pediatr Infect Dis J 1992; 11:644. 54. Martin, JM, Pitetti, R, Maffei, F, et al. Treatment of shigel osis with cefixime: Two days vs. five days. Pediatr Infect Dis J 2000; 55. Salam, MA, Seas, C, Khan, WA, et al. Treatment of Shigel osis: cefixime is ineffective in shigel osis in adults. Ann Intern Med 56. Islam, MR, Alam, AN, Hussain, MS, Mahalanabis, D. Effect of antimicrobial (nalidixic acid) therapy in shigel osis and predictive values of outcome variables in patients susceptible or resistant to it. J Trop Med Hyg 1995; 98:121. 57. Kagalwal a, AF, Khan, SN, Kagalwal a, YA, et al. Childhood shigel osis in Saudi Arabia. Pediatr Infect Dis J 1992; 11:215. 58. Bennish, M, Salam, MA, Wahed, MA. Enteric protein loss during shigel osis. Am J Gastroenterol 1993; 88:53. 59. Curtis, V, Cairncross, S. Effect of washing hands with soap on diarrhoea risk in the community: a systematic review. Lancet Infect 60. Gangaros, EJ. Annotation: a community-focused strategy for the control of day-care center shigel osis. Am J Public Health 1995; 61. Hoffman, RE, Shil am, PJ. The use of hygiene, cohorting, and antimicrobial therapy to control an outbreak of shigel osis. Am J Dis REIDRATAÇÃO
(texto extraído e modificado de: Bruno F et al. 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 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 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 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 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 perdurar por cerca de 20 horas. Após a restauração da 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 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 a depleção de volume, mais agressiva e rápida deve Após as primeiras 24 horas de tratamento, a 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

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