K. J. Lee: Essential Otolaryngology and Head and Neck Surgery (IIIrd Ed) Chapter 31: Fluids, Electrolytes, and Acid-Base Balance
Critical disturbances in the fluid, electrolyte, or acid-base balance of the body may
have no outward signs or symptoms and only diagnosed by laboratory testing. It is importantto note that the body will try to maintain volume at the expense of osmolarity, electrolytes,or pH. Nonspecific signs such as somnolence, confusion, or weakness may be the only hintsof an underlying abnormality.
The otolaryngolic patient is particularly prone to such disturbances because of the
effects of anaesthesia, parenteral feeding, and underlying medical diseases such as diabetes,heart failure, or diuretic therapy. The following lists and tables review some of thesedisturbances. Therapy must be individualized based on all underlying conditions and theirpathophysiology. Nonspecific Signs of Fluid, Electrolyte, or Acid-Base Disturbances Signs of Fluid Disturbances Overhydration Dehydration Hyperkalaemia
Potassium-sparing diurecticsHypoaldosteronism - especially in diabeticsCrush injuryRenal failureIncreased intake (salt substitutes)AcidosisProstaglandin inhibitors
Decrease intakeCalcium gluconate: 1 ampule (10 mL = 940 mg) IV q 2 hrGlucose: 50 mL 50% dextrose plus insulin (crystalline zinc) 10 IU IV/SCSodium bicarbonate: 1.2 g TID PO or 1 ampule IV q 4 hr to keep bicarbonate level
Loop diuretics: 40-80 mg furosemide (Lasix) or 50-100 mg ethacrynic acid (Edecrin)
IV or PO. Do not use potassium-sparing diuretics such as spironolactone (Aldactone),hydrochlorthiazide and triamterene (Dyazide), or amiloride (Moduretic or Midamor).
Exchange resins: 25-50 mg sodium polystyrene sulfanate (Kayexelate) PO or by enema
Mineralocorticosteroids 0.1 mg fludrocortisone (Florinet) PO q 24 hrDialysis: peritoneal or hemodialysis. Table 31-1. Hyponatremia (Signs Are Those of Associated Fluid Status) Pathogenesis Volume Status Etiology Loss of sodium in excess of body water Volume depletion Renal losses: diuretics, nephritis, osmotic diuresis Normal saline: ± 1 L IV q 4-6 hr if cardiac status satisfactory Extra-renal losses: vomiting, diarrhea, thrid-space losses Normal saline: ± 1 L IV q 4-6 hr if cardiac status satisfactory Excess water Slight overhydration Addison's disease - Steroids Myxedema - Thyroxine Inappropriate anti-diuretic syndrome 1. Fluid restriction (1 L/24 hr) 2. Hypertonic saline 300 mL of 3% saline over 4 hr 3. Loop diuretics 4. Dilantin 100 mg t.i.d. 5. Lithium 300 mg p.o. q.i.d. 6. Demeclocycline 300 mg q.i.d. Excess sodium and excess water Overhydration with edema Congestive heart lung 1. Fluid restriction Nephrosis 2. Diuretics Cirrhosis Lasix 40-100 mg IV q 12-24 hr Renal failure Edecrin 50-100 mg IV q 12-24 hr. Table 31-2. Causes of Hypernatremia Therapy depends on fluid status and must be individualized. One should calculate the fluid deficit and replace fluids gradually over 1-2 days to avoid cerebral edema or congestive heart failure. Specific therapy must then be directed at the underlying condition. Water loss in excess of sodium loss Central or nephrogenic diabetes insipidus Vomiting Diarrhea Severe burns Osmotic diuresis (calcium, glucose, IVP dye) Excessive insensible losses Inadequate water intake Hypothalamic disease Stupor Administration of sodium in excess of water Excessive salt ingestion IV or p.o. Dialysis Sodium retention Cushing's syndrome Hyperaldosteronism Loss of renal concentration ability Uremia Hypokalemia Lithium therapy Methoxyflurane anesthesia Sickle cell anemia Multiple myeloma Hypercalcemia. Hypocalcemia
Hypoparathyroidism: iatrogenic, idiopathic. PseudohypoparathyroidismPancreatitisRenal failureHypomagnesemiaVitamin D deficiencyMalabsorptionHypoalbuminemia (does not need therapy).
1. Acute therapy: 10 mL of 10% calcium chloride or calcium gluconate IV repeat of
2. Chronic therapy: (a) calcium 1 g p.o. t.i.d.
(b) Vitamin D 50.000 units, or Dihydrotachysterol 0.125 mg to 0.4 mg/day
(c) Magnesium (if deficient) 2 mL magnesium sulphate IM p.r.n. Table 31-3. Hypercalcemia Hyperparathyroidism Ectopic parathyroid hormone secretion Bony metastases Milk alkali syndrome Vitamin D toxicity Sarcoid Tuberculosis Therapy (to be individualized) 1. Parathyroidectomy 2. Hydration: oral fluids as tolerated 3. Saline 1-2 L IV q 2-4 hr (watch cardiac status) 4. Loop diuretics Lasix 40 mg, Edecrin 50 mg IV or p.o. 5. Phosphate 250-500 mg p.o. q 6 hr (as Neutra-Phos) 6. Steroids 100 mg Solu-Cortef IV q 8 hr or 25 mg cortisone acet. q 6 hr 7. Mithramycin 15-25 microg/kg IV q 24-48 hr 9. Indomethacin 25 mg p.o. q 6 hr. Table 31-4. Acid-Base Disturbances Disturbance Hydrogen ion bicarbonate Metabolic acidosis Metabolic alkalosis Respiratory acidosis Respiratory alkalosis Normal range 7.35-7.45 36-45 mEq/L 35-45 mmHg 22-26 mEq/L. * Primary abnormality. Causes of Metabolic Alkalosis
DiureticsVomitingDiarrheaAntacid therapyHyperladosteronismGastrointestinal fistula.
Potassium chloride to maintain K level above 3.5 mEq/L, fluids, carbonic anhydrase
inhibitors (acetazolamide - Diamox - 250 mg p.o. q.i.d.). Treat underlying condition. Causes of Respiratory Acidosis
General anesthesiaCardiac arrestSedationPulmonary edemaSevere pneumoniaBronchospasmLaryngospasmForeign body aspirationMechanical ventilation.
Alveolar hypoventilationObstructive pulmonary diseaseBrain tumorRespiratory muscle weakness or nerve damageRestrictive lung disease.
Directed at improving respiratory gas exchange. Causes of Respiratory Alkalosis
AnxietyHysteriaOainFeverSalicylate intoxicationStrokeCNS trauma, infection, tumor. Congestive heart failurePneumoniaHypoxiaHepatic insufficiencyGram-negative sepsisMechanical ventilators.
Treat underlying condition, increase "dead space" if on ventilator. Causes of Metabolic Acidosis Increased Anion Gap Increased Organic Acid Production
lactic acidosisdiabetic ketoacidosisstarvation ketosisalcoholic ketoacidosis
Inability to Excrete Inorganic Acids Ingestion of Exogenous Acids
salicylatesmethanolparaldehideethylene glycol
Normal Anion Gap Loss of Bicarbonate
GI tract lossureterosigmoidostomyrenal tubular acidosisuremia (early)carbonic anhydrase inhibitor therapyhypoaldosteronismcorection of chronic respiratory alkalosis
Chloride Therapy
hyperalimentationammonium chloridelysine hydrochloridearginine hydrochloride
Administration of Acids with Rapid Renal Clearances of Unmeasured Ions
sulfuric acidphosphoric acidsulfur containing amino acids.
Bicarbonate therapy to raise pH above 7.3-7.35 and treat underlying abnormality. Electrocardiographic Abnormalities of Electrolyte Abnormalities Hyperkalemia
Peaked T waveProlonged QRSSinus arrestVentricular sine wave
Hypokalemia
Prolonged QT intervalST segment depressionU waves
Hypocalcemia
Lengthened QT segment (Normal T wave duration)
Hypercalcemia
G6PD Deficiency capable of producing the G6PD enzyme, resulting is an important element (enzyme) in the glucose in more severe symptoms. Females, on the other oxidation (oxygen utilization) process of red blood hand, inherit two X chromosomes, one from each cells (RBCs) and for maintaining their normal life parent. A mutation in one copy is compensated for span. G6PD deficiency is an inh
Objectives AFTER STUDYING THIS CHAPTER, THE STUDENT WILL BE ABLE TO: 1. Describe environmental and other major factors3. Discuss the drugs used to treat Pneumocystis in prevention and recognition of selected para- carinii pneumonia in clients with acquired 2. Discuss assessment and treatment of pinworm4. Teach preventive interventions to clients infestations and pediculosis in schoo