应该是病毒性腹泻，早治疗

秋季腹泻低钾

支持病毒性腹泻，还是以对症处理为主

是腹泻呕吐导致低钾的吧

病毒性腹泻，对症支持疗法为主

给点具体的治疗方案

2岁的孩子每天补500ml，有点不太理解。每公斤体重才补40ml啊。

腹泻多代酸，低钾代碱确要考虑巴特氏

摘录emedicine Bartter syndrome, originally described by Bartter and colleagues in 1962, represents a set of closely related autosomal recessive renal tubular disorders characterized by hypokalemia, hypochloremia, metabolic alkalosis, and hyperreninemia with normal blood pressure. The underlying renal abnormality results in excessive urinary losses of sodium, chloride, and potassium. Bartter syndrome has traditionally been classified into 3 main clinical variants: neonatal Bartter syndrome, classic Bartter syndrome, and Gitelman syndrome. Advances in molecular diagnostics have revealed that Bartter syndrome results from mutations in numerous genes that affect the function of ion channels and transporters that normally mediate transepithelial salt reabsorption in the distal nephron segments. A modern, and more clinically relevant, classification of Bartter syndrome takes into account the 3 main anatomic and pathophysiologic disturbances that lead to the salt-losing tubulopathy. The first type involves distal convoluted tubule dysfunction that leads to hypokalemia; this is currently known as classic Bartter syndrome or Gitelman syndrome, which can be caused by defects in the NCCT and CLCNKB genes, respectively. The second type involves polyuric loop dysfunction that is more severe; this is referred to as antenatal Bartter syndrome or neonatal Bartter syndrome, which is characterized by defects in the NKCC2 and ROMK genes. The third type involves the most severe combined loop and distal convoluted tubule dysfunction and is now referred to as antenatal Bartter syndrome with sensorineural deafness; this is caused by defects in the chloride channel genes CLCNKB and CLCNKA or their beta subunit BSND. The neonatal and classic types of Bartter syndrome are discussed in detail below, and the differentiating features of Gitelman syndrome are highlighted. Pathophysiology Whereas 60% of the filtered sodium chloride is reabsorbed in the proximal tubule, an additional 30% must be reabsorbed by the thick ascending limb of the Henle loop in order to maintain fluid and electrolyte homeostasis. The reabsorption of sodium in the ascending Henle loop primarily occurs by an electroneutral bumetanide-sensitive sodium-chloride potassium-chloride cotransporter (encoded by the gene NKCC2), with a function driven by the low intracellular concentration of sodium. The low sodium concentration in the cell is maintained by the basolateral membrane sodium-potassium pump, which extrudes sodium. Chloride exits the cell through a basolateral channel or a potassium chloride cotransporter; potassium is secreted in the luminal fluid through the apical ATP-regulated potassium channel (encoded by the ROMK gene) See Media file 1. Defects in either the sodium-chloride potassium-chloride cotransporter or potassium channel affect the transport of sodium, potassium, and chloride in the thick ascending limb of the loop of Henle. The result is the delivery of large volumes of urine with a high content of these ions to the distal segments of the renal tubule, where only some sodium is reabsorbed and potassium is secreted. In the subset of patients with neonatal Bartter syndrome, at least 2 genotypes have been identified. Type I results from mutations in the sodium-chloride potassium-chloride cotransporter gene (NKCC2 gene). See Media file 2. Type II results from mutations in the ROMK gene. See Media file 3. In the classic form of Bartter syndrome, the defect in sodium reabsorption appears to result from mutations in the chloride-channel (CLCNKB) gene; this constitutes type III. The consequent inability of chloride to exit the cell inhibits the sodium-chloride potassium-chloride cotransporter (see Media file 4). Increased delivery of sodium chloride to the distal sites of the nephron leads to salt wasting, polyuria, volume contraction, and stimulation of the renin-angiotensin-aldosterone axis, with resultant hypokalemic metabolic alkalosis. The hypokalemia, volume contraction, and elevated angiotensin levels increase intrarenal prostaglandin E2 synthesis, which contributes to a vicious cycle by further stimulating the renin-aldosterone axis and inhibiting sodium chloride reabsorption in the thick ascending loop of Henle. Studies have identified a novel type IV Bartter syndrome.7, 8, 19 This is a type of neonatal Bartter syndrome associated with sensorineural deafness and has been shown to be caused by mutations in the BSND gene.2, 5, 8 This gene encodes barttin, an essential beta-subunit that is required for the trafficking of the chloride channel CLC-K (both ClC-Ka and ClC-Kb) to the plasma membrane in both the thick ascending limb and the marginal cells in the scala media of the inner ear that secrete potassium ion-rich endolymph.7 Thus, loss-of-function mutations in barttin cause Bartter syndrome with sensorineural deafness. Therefore, in contrast to other Bartter types, the underlying genetic defect in type IV is not directly in an ion-transporting protein but is instead due to indirect interference with the barttin-dependent insertion in the plasma membrane of chloride channel subunits ClC-Ka and ClC-Kb. Other observations have identified type V Bartter syndrome. This is a type of neonatal Bartter syndrome associated with sensorineural deafness but with no mutations in the BSND gene. Type V Bartter syndrome has been shown to be a digenic disorder due to loss-of-function mutations in the genes that encode the chloride channel subunits ClC-Ka and ClC-Kb.9 The specific genetic defect includes both a large deletion in the gene that encodes ClC-Kb (ie, CLCNKB) and a point mutation in the gene that encodes ClC-Ka (CLCNKA). A summary of currently identified genotype-phenotype correlations is in the table below. For completion, the gene defect in Gitelman syndrome (the thiazide-sensitive sodium-chloride cotransporter, encoded by the gene NCCT) is also appended. Bartter Syndrome Genotype-Phenotype Correlations Genetic Type Defective Gene Clinical Type Bartter type I NKCC2 Neonatal Bartter type II ROMK Neonatal Bartter type III CLCNKB Classic Bartter type IV BSND Neonatal with deafness Bartter type V CLCNKB and CLCNKA Neonatal with deafness Gitelman syndrome NCCT Gitelman syndrome A more clinically relevant terminology and classification of Bartterlike syndromes has recently been proposed, based on the underlying genetic cause and the anatomic location that leads to the salt-losing tubulopathy.15 Using this terminology, 3 major types of salt-losing tubulopathies can be identified Frequency United States The history of patients with Bartter syndrome may include the following: Neonatal Bartter syndrome Maternal polyhydramnios, secondary to fetal polyuria, is evident by 24-30 weeks' gestation. Delivery often occurs before term. The newborn has massive polyuria (rate as high as 12-50 mL/kg/h). The subsequent course is characterized by life-threatening episodes of fluid loss, clinical volume depletion, and failure to thrive. A subset of patients with neonatal Bartter syndrome (types IV and V) develop sensorineural deafness. Classic Bartter syndrome Patients have a history of maternal polyhydramnios and premature delivery. Symptoms include polyuria, polydipsia, vomiting, constipation, salt craving, tendency for volume depletion, failure to thrive, and linear growth retardation. Other symptoms, which appear during late childhood, include fatigue, muscle weakness, cramps, and recurrent carpopedal spasms. Developmental delay and minimal brain dysfunction with nonspecific electroencephalographic changes are also present. Physical Findings with Bartter syndrome include the following: Neonatal Bartter syndrome Patients are thin and have reduced muscle mass and a triangularly shaped face, which is characterized by a prominent forehead, large eyes, protruding ears, and drooping mouth. Strabismus is frequently present. Blood pressure is within the reference range. A subset of patients with Bartter syndrome (types IV and V) develop sensorineural deafness, which is detectable with audiometry. Classic Bartter syndrome: The patient's facial appearance may be similar to that encountered in the neonatal type. However, this finding is infrequent. Causes Causes of Bartter syndrome include the following: Neonatal Bartter syndrome An autosomal recessive mode of inheritance is observed in some patients, although many cases are sporadic. In type I Bartter syndrome, loss-of-function mutations in the sodium-chloride potassium-chloride cotransporter gene NKCC2 (locus SLC12A1 on chromosome bands 15q15-21) have been detected. In type II Bartter syndrome, mutations occur in the ROMK gene (locus KCNJ1 on chromosome bands 11q24-25). Newly described genetic defects include type IV (in the BSND gene) and type V (digenic, in both CLCNKB and CLCNKA genes). Classic Bartter syndrome Some patients have an autosomal recessive mode of inheritance, although many cases are sporadic. A subset of patients display mutations in the chloride-channel gene CLCNKB (locus CLCNKB on chromosome band 1p36). These represent type III Bartter syndrome. Blood and urine chemistries Evaluation of hypokalemia, hypochloremia, and metabolic alkalosis is essential for diagnosis. Hypokalemia is usually severe (1.5-2.5 mEq/L). Hypomagnesemia may be present and necessitates exclusion of Gitelman syndrome, in which hypomagnesemia is a cardinal finding. The differentiation is made by measuring the urinary excretion of magnesium (which is high in Gitelman syndrome and within the reference range in Bartter syndrome) and calcium (which is high in Bartter syndrome and within the referencer range in Gitelman syndrome). Hyperuricemia is present in 50% of patients with Bartter syndrome, whereas in Gullner syndrome (familial hypokalemic alkalosis with proximal tubulopathy), hypouricemia, secondary to impaired proximal tubular function, is present. Renin and aldosterone levels are elevated, but BP remains normal. ** count: Polycythemia may be present from hemoconcentration. Renal function The glomerular filtration rate is preserved during the early stages of the disease; however, it may decrease as a result of chronic hypokalemia. Increases in the fractional urinary excretion of sodium, potassium, and chloride are typical. Patients with Bartter syndrome have high urinary excretion of calcium and normal urinary excretion of magnesium. Patients with Gitelman syndrome have low urinary excretion of calcium and high urinary excretion of magnesium. The urinary excretion of prostaglandin E2 is elevated in both neonatal and classic forms of the disease. Amniotic fluid: If the diagnosis is being made prenatally, assess the amniotic fluid. The chloride content may be elevated in either Gitelman or Bartter syndrome. Imaging Studies Renal ultrasonography may reveal nephrocalcinosis in neonatal Bartter syndrome. Hydronephrosis and hydroureter secondary to chronic polyuria may also be evident. Other Tests An ECG may reveal changes characteristic of hypokalemia such as flattened T waves and prominent U waves. Procedures • Although renal biopsy is not usually required, histologic findings may be useful in confirming the diagnosis. Histologic Findings • In both neonatal and classic Bartter syndrome, the cardinal finding is hyperplasia of the juxtaglomerular apparatus. Less frequently, hyperplasia of the medullary interstitial cells is present. • Glomerular hyalinization, apical vacuolization of the proximal tubular cells, tubular atrophy, and interstitial fibrosis may be present as a consequence of chronic hypokalemia. • Neonatal Bartter syndrome • o Correct dehydration and electrolyte abnormalities immediately after birth. o The cornerstones of medical therapy are the administration of indomethacin and potassium supplementation. • Classic Bartter syndrome • o Supplementation with potassium chloride is always necessary but often insufficient. o The addition of a potassium-sparing diuretic may be effective initially, but the effect is transient. o Correction of hypokalemia is best achieved with prostaglandin synthetase inhibitors, such as indomethacin, acetylsalicylic acid, ibuprofen, or ketoprofen. Indomethacin is prescribed most frequently and is usually well tolerated. Surgical Care One approach involves preemptive nephrectomy and renal transplantation in children with severe Bartter syndrome.3 The rationale for this approach lies in the fact that Bartter syndrome is an incurable genetic disease, and the poorly controlled forms may result in frequent life-threatening episodes of dehydration and electrolyte imbalances. Preemptive bilateral nephrectomies and successful kidney transplantation prior to the onset of end-stage renal disease (ESRD) has resulted in correction of metabolic abnormalities and excellent graft function. Consultations Consult a pediatric nephrologist to assist with the initial diagnosis and for periodic outpatient evaluation of growth, development, renal function, serum electrolytes, and response to therapy. Diet Patients should consume foods and drinks that contain high levels of potassium (eg, tomatoes, bananas, orange juice). Activity No restriction on general activity is required, but precautions against dehydration should be taken. Patients should avoid strenuous exercise avoided because of the danger of dehydration and functional cardiac abnormalities secondary to potassium imbalance.

:( 我认为是秋季腹泻。碱中毒 依据。1：病毒性腹泻的表现 2：血气分析 3：尿糖**可能是不合里输液引起 建议做大便常规检查。

那楼上的怎么考虑其它的电介质基本恢复，而血钾持续性降低？

先不考虑巴特综合征，仍以轮状病毒肠炎，水电解质酸碱平衡紊乱为主

巴特综合征是一种难治性疾病。是因肾小球球旁细胞增生，分泌大量的肾素引起的继发性醛固酮增多症候群。临床表现主要为肌无力，周期性麻痹，心律失常，肠麻痹等低钾症状及烦渴，夜尿增多，骨质疏松等。 　　【诊断】 　　液体，电解质和激素同时异常，其特点是肾钾，钠及氯的消耗，低钾血症，醛固酮过多症，高肾素血症和血压正常。 　　【治疗】 　　钾补充再加用安体舒通，氨苯蝶啶，阿米洛利，一种ACEI类药物或消炎痛可纠正大多数症状，但没一个药物能完全消除钾的丢失。服消炎痛每日1～2mg/kg常使血浆钾浓度保持在接近正常低限。 　　【病因学】 　　本综合征常见于儿童期，散发或家族性多为常染色体隐性遗传疾病。其病因是Henle袢的上升支粗段及远端肾小管NaCl的转运紊乱。钾，钠，氯的消耗**肾素释放并伴球旁细胞的增生。醛固酮水平增高，纠正醛固酮过多症并不能改善钾的丢失。钠的损耗引起长期血浆容量低，表现为虽有肾素和血管紧张素的增多，但血压正常，对注入血管紧张素的加压反应受损。常发生代谢性碱中毒。血小板聚集受到抑制。可有高尿酸血症及低镁血症。激肽-前列腺素轴受到**，尿中前列腺素及血管舒缓素排出增多。 　　【症状体征】 　　主要为肌无力、周期性麻痹、心律失常、肠麻痹等低钾症状及烦渴、夜尿增多、骨质疏松等。儿童发病率较高，生长发育延迟，智力下降。本病的治疗主要还是服富含氯化钾的饮食，口服消炎痛等。目前还没有其它特殊治疗方法。Batter综合征与其他伴醛固酮增多症的疾病所不同处在于没有高血压(原发性醛固酮增多症有高血压)和水肿(继发性醛固酮增多症有水肿)。成人需排除：神经性贪食症，呕吐或私用利尿剂或轻泻药。这些情况下，尿氯常是低的(＜20mmol/L)。

抗病毒方面更昔洛韦，调节免疫力西咪替丁，左旋咪唑，黄芪，4天后可试用一下654-2等，注意液体疗法很重要。

是不是考虑一下抗病毒治疗: 1.病毒唑 2.莪术油

推拿是治疗腹泻最佳方案.及灌肠

不觉得肝大，感觉不大不小

患儿肝大怎么解释

1.秋季腹泻 2.低血钾 3.代谢性碱中毒

补充诊断：考虑该患儿是否合并心肌炎？ 应该查血生化（包括肝肾、电解质、心肌酶、血脂等） ]