Danh mục

Chapter 046. Sodium and Water (Part 5)

Số trang: 6      Loại file: pdf      Dung lượng: 14.09 KB      Lượt xem: 13      Lượt tải: 0    
Hoai.2512

Hỗ trợ phí lưu trữ khi tải xuống: 5,000 VND Tải xuống file đầy đủ (6 trang) 0
Xem trước 2 trang đầu tiên của tài liệu này:

Thông tin tài liệu:

Hypovolemia: TreatmentThe therapeutic goals are to restore normovolemia with fluid similar in composition to that lost and to replace ongoing losses. Symptoms and signs, including weight loss, can help estimate the degree of volume contraction and should also be monitored to assess response to treatment. Mild volume contraction can usually be corrected via the oral route. More severe hypovolemia requires intravenous therapy. Isotonic or normal saline (0.9% NaCl or 154 mmol/L Na+) is the solution of choice in normonatremic and most hyponatremic individuals and should be administered initially in patients with hypotension or shock. Hypernatremia reflects a proportionally greater...
Nội dung trích xuất từ tài liệu:
Chapter 046. Sodium and Water (Part 5) Chapter 046. Sodium and Water (Part 5) Hypovolemia: Treatment The therapeutic goals are to restore normovolemia with fluid similar incomposition to that lost and to replace ongoing losses. Symptoms and signs,including weight loss, can help estimate the degree of volume contraction andshould also be monitored to assess response to treatment. Mild volume contractioncan usually be corrected via the oral route. More severe hypovolemia requiresintravenous therapy. Isotonic or normal saline (0.9% NaCl or 154 mmol/L Na+) isthe solution of choice in normonatremic and most hyponatremic individuals andshould be administered initially in patients with hypotension or shock.Hypernatremia reflects a proportionally greater deficit of water than Na +, and itscorrection will therefore require a hypotonic solution such as half-normal saline(0.45% NaCl or 77 mmol/L Na+) or 5% dextrose in water. Patients with significanthemorrhage, anemia, or intravascular volume depletion may require bloodtransfusion or colloid-containing solutions (albumin, dextran). Hypokalemia maybe present initially or may ensue as a result of increased urinary K + excretion; itshould be corrected by adding appropriate amounts of KCl to replacementsolutions. Hyponatremia Etiology A plasma Na+ concentration Most causes of hyponatremia are associated with a low plasma osmolality(Table 46-2). In general, hypotonic hyponatremia is due either to a primary watergain (and secondary Na+ loss) or a primary Na + loss (and secondary water gain). Inthe absence of water intake or hypotonic fluid replacement, hyponatremia isusually associated with hypovolemic shock due to a profound sodium deficit andtranscellular water shift. Contraction of the ECF volume stimulates thirst and AVPsecretion. The increased water ingestion and impaired renal excretion result inhyponatremia. It is important to note that diuretic-induced hyponatremia is almostalways due to thiazide diuretics. Loop diuretics decrease the tonicity of themedullary interstitium and impair maximal urinary concentrating capacity. Thislimits the ability of AVP to promote water retention. In contrast, thiazide diureticslead to Na+ and K+ depletion and AVP-mediated water retention. Hyponatremiacan also occur by a process of desalination. This occurs when the urine tonicity(the sum of the concentrations of Na+ and K+) exceeds that of administeredintravenous fluids (including isotonic saline). This accounts for some cases ofacute postoperative hyponatremia and cerebral salt wasting after neurosurgery. Table 46-2 Causes of Hyponatremia I. PseudohyponatremiaA. Normal plasma osmolality 1. Hyperlipidemia 2. Hyperproteinemia 3. Posttransurethral resection of prostate/bladder tumorB. Increased plasma osmolality 1. Hyperglycemia 2. MannitolII. Hypoosmolal hyponatremia A. Primary Na+ loss (secondary water gain) 1. Integumentary loss: sweating, burns 2. Gastrointestinal loss: vomiting, tube drainage, fistula, obstruction, diarrhea 3. Renal loss: diuretics, osmotic diuresis, hypoaldosteronism, salt-wasting nephropathy, postobstructive diuresis, nonoliguric acute tubular necrosisB. Primary water gain (secondary Na+ loss) 1. Primary polydipsia 2. Decreased solute intake (e.g., beer potomania) 3. AVP release due to pain, nausea, drugs 4. Syndrome of inappropriate AVP secretion 5. Glucocorticoid deficiency 6. Hypothyroidism 7. Chronic renal insufficiencyC. Primary Na+ gain (exceeded by secondary water gain)1. Heart failure2. Hepatic cirrhosis3. Nephrotic syndrome

Tài liệu được xem nhiều: