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首页> 外文期刊>American journal of therapeutics >University of Miami Division of Clinical Pharmacology Therapeutic Rounds: the water-intolerant patient and perioperative hyponatremia.
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University of Miami Division of Clinical Pharmacology Therapeutic Rounds: the water-intolerant patient and perioperative hyponatremia.

机译:迈阿密大学临床药理学治疗学分部:不耐水的患者和围手术期低钠血症。

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Perioperative hyponatremia has been recognized as a serious in-hospital complication for many years. Because the kidney responds to changes in extracellular fluid tonicity by adjusting water excretion, a defect in any of several key elements of water excretion can lead to water retention and hyponatremia. Most cases of hyponatremia are caused by impaired renal water excretion in the presence of continued water intake. For the kidney to excrete excess free water and thereby protect the extracellular fluid against hyponatremia, there must be an adequate glomerular filtration rate (GFR), adequate delivery of glomerular filtrate to the diluting segments of the distal nephron, intact tubular diluting mechanisms, and appropriate inhibition of antidiuretic hormone (ADH) synthesis and release. Virtually all of the clinical disorders producing hyponatremia are based on abnormalities of these few mechanisms of water regulation. Finding the reason for impaired renal water excretion is the key to diagnosing the cause of hyponatremia. Impaired renal water excretion may be caused by impaired GFR (renal failure), impaired water delivery to the diluting segments of the distal nephron because of increased proximal reabsorption (decreased extracellular fluid volume and edematous states), impaired renal diluting mechanism (thiazide diuretics), the syndrome of inappropriate ADH (SIADH) due to a variety of causes including the perioperative state, and hypothyroidism or adrenal insufficiency. Any of the states that impair water excretion can produce hyponatremia in a patient with an initially normal serum sodium concentration if sufficient free water is supplied. Therefore, a patient who has one of the conditions listed above, including the perioperative state, may be considered "water intolerant" even if the serum sodium is normal. Such a patient is at risk for developing severe hyponatremia if given hypotonic IV fluids or a large oral water load. An understanding of the basic mechanisms leading to impaired water excretion and "water intolerance" is therefore an important key to avoiding perioperative hyponatremia.
机译:围手术期低钠血症已被公认为是一种严重的医院内并发症。因为肾脏通过调节水的排泄来响应细胞外液张力的变化,所以水排泄的几个关键要素中的任何一个缺陷都会导致水water留和低钠血症。低钠血症的大多数情况是由于在持续饮水的情况下肾排泄障碍。为了使肾脏排泄过量的游离水,从而保护细胞外液免于低钠血症,必须有足够的肾小球滤过率(GFR),将肾小球滤过剂充分输送到远端肾单位的稀释段,完整的肾小管稀释机制和适当的方法抑制抗利尿激素(ADH)的合成和释放。几乎所有产生低钠血症的临床疾病都基于这几种水调节机制的异常。找出肾水排泄受损的原因是诊断低钠血症原因的关键。肾水排泄障碍可能是由于GFR受损(肾衰竭),由于近端重吸收增加(减少的细胞外液量和水肿状态),输往远端肾的稀释段的水输送受损,肾脏稀释机制受损(噻嗪类利尿剂),由于各种原因引起的不适当的ADH综合征(SIADH),包括围手术期状态,甲状腺功能减退或肾上腺功能不全。如果提供足够的游离水,则任何会损害水分排泄的状态都会在患者血清钠浓度最初正常的情况下产生低钠血症。因此,即使血清钠正常,患有上述情况之一(包括围手术期状态)的患者也可能被视为“不耐水”。如果给予低渗静脉输液或大量口服水,此类患者有发生严重低钠血症的风险。因此,了解导致水分排泄受损和“水不耐受”的基本机制是避免围手术期低钠血症的重要关键。

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