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An average adult whose entire intake is parenteral would require for maintenance 2500 3000 mL of 5% dextrose in 02% saline solution (34 mEq Na+ plus 34 mEq Cl /L) To each liter, 30 mEq of KCl could be added In 3 L, the total chloride intake would be 192 mEq, which is easily tolerated Guidelines for gastrointestinal fluid losses are shown in Table 21 18 Weight loss or gain is the best indication of water balance Insensible water loss should be further considered in febrile patients Water loss increases by 100 150 mL/d for each degree of body temperature over 37 C In situations requiring maintenance or maintenance plus replacement of fluid and electrolyte by parenteral infusion, the total daily ration should be administered continuously over the 24-hour period to ensure the best utilization by the patient If parenteral fluids are the only source of water, electrolytes, and calories for longer than a week, more complex fluids containing amino acids, lipids, trace metals, and vitamins may be indicated (See 29) For parenteral alimentation, 620 mg (20 mmol) of phosphorus is required for every 1000 nonprotein kcal to maintain phosphate balance and to ensure anabolic function For prolonged parenteral fluid maintenance, a daily ration is 620 1240 mg (20 40 mmol) of phosphorus
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A Symptoms and Signs
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In acute cases (hyperventilation), there is light-headedness, anxiety, paresthesias, numbness about the mouth, and a tingling sensation in the hands and feet Tetany occurs in more severe alkalosis from a fall in ionized calcium In chronic cases, findings are those of the responsible condition
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B Laboratory Findings
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Arterial blood pH is elevated, and PCO2 is low Serum bicarbonate is decreased in chronic respiratory alkalosis
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Treatment is directed toward the underlying cause In acute hyperventilation syndrome from anxiety, rebreathing into a paper bag will increase the PCO2 The processes are usually self-limited since muscle weakness caused by hyperventilation-induced alkalemia will suppress ventilation Sedation may be necessary if the process persists Rapid correction of chronic respiratory alkalosis may result in metabolic acidosis as PCO2 is increased in the setting of a previous compensatory decrease in HCO3
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Kidney Disease
Suzanne Watnick, MD Gail Morrison, MD
Renal disease presents in one of two ways: discovered incidentally during a routine medical evaluation or with evidence of renal dysfunction, such as hypertension, edema, nausea, and hematuria The initial approach in both situations should be to assess the cause and severity of renal abnormalities In all cases this evaluation includes (1) an estimation of disease duration, (2) a careful urinalysis, and (3) an assessment of the glomerular filtration rate (GFR) The history and physical examination, though equally important, are variable among renal syndromes thus, specific symptoms and signs are discussed under each disease entity Further diagnostic categorization is according to anatomic distribution: prerenal disease, postrenal disease, and intrinsic renal disease Intrinsic renal disease can be further divided into glomerular, tubular, interstitial, and vascular abnormalities
ASSESSMENT OF RENAL DISEASE Disease Duration
Renal disease may be acute or chronic Acute renal failure is worsening of renal function over hours to days, resulting in the retention of nitrogenous wastes (such as urea nitrogen) and creatinine in the blood Retention of these substances is called azotemia Chronic renal failure (chronic kidney disease) results from an abnormal loss of renal function over months to years Differentiating between the two is important for diagnosis, treatment, and outcome Oliguria is unusual in chronic renal insufficiency Anemia (from low renal erythropoietin production) is rare in the initial period of acute renal failure Small kidneys are most consistent with chronic kidney disease, whereas normal to large-size kidneys can be seen with both chronic and acute disease
stick examination followed by microscopic assessment if the dipstick has positive findings The dipstick examination measures urinary specific gravity, pH, protein, hemoglobin, glucose, ketones, bilirubin, nitrites, and leukocyte esterase Microscopy searches for all formed elements crystals, cells, casts, and infecting organisms Various findings on the urinalysis are indicative of certain patterns of renal disease A bland urinary sediment is common, especially in chronic kidney disease and prerenal and postrenal disorders The presence of hematuria with dysmorphic red blood cells, red blood cell casts, and proteinuria is indicative of glomerulonephritis Red blood cells are misshapen during passage from the capillary through the glomerular basement membrane into the urinary space of Bowman s capsule Casts are composed of Tamm-Horsfall urinary mucoprotein in the shape of the nephron segment where they were formed Heavy proteinuria and lipiduria are consistent with the nephrotic syndrome Pigmented granular casts and renal tubular epithelial cells alone or in casts suggest acute tubular necrosis White blood cells, including neutrophils and eosinophils, white blood cell casts, red blood cells, and small amounts of protein can be found in interstitial nephritis and pyelonephritis (Table 22 1); Wright s stain can detect eosinophiluria Pyuria alone can indicate a urinary tract infection Hematuria and proteinuria are discussed more thoroughly below
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