B. Water Balance
C. Replacement Fluids
D. Acid-Base Disorders
1. Approach to Acid-Base Disorders
Table 9-2 describes acid-base abnlities and appropriate compensatory responses for simple disorders.
Box 9-1 Renal Fluid and Electrolyte Formulas
Calculation of Creatinine Clearance (CCr)
Calculation of Fractional Excretion of Sodium (FENa)
or
or
or
where UNa is urine sodium concentration, V is urine flow rate, PNa is plasma sodium concentration, UCr is urine creatinine concentration, and PCr is plasma creatinine concentration.
Sodium Formulas
Serum sodium correction in hyperglycemia:
Estimated sodium deficit in hyponatremia:
Estimated sodium excess in hypernatremia:
Serum sodium correction in hyperlipidemia and hyperproteinemia:
Potassium Formulas
Diagnostic equations for hyperkalemia:
| Fractional excretion of potassium (FEK) |  |
FEK <10% indicates renal cause FEK >10% indicates extrarenal cause Values can be increased in cases of chronic renal failure |
| Transtubular potassium gradient |  or  |
Gradient <6-8 indicates renal cause Gradient >6-8 indicates extrarenal cause Values can be increased in cases of chronic renal failure |
Osmolality Formulas
UK, Urine potassium; SK, serum potassium; UCr, urine creatinine; SCr, serum creatinine; Uosm, urine osmolality; Sosm, serum osmolality.
2. Metabolic Acidosis
Etiology
Metabolic acidosis w/AG (AG acidosis). The mnemonic MUDPILES is useful to remember the causes of AG acidosis:• Methanol
• Uremia
• DKA, alcoholic ketoacidosis (AKA), starvation ketoacidosis (SKA)
TABLE 9-1
Replacement Fluids
| Fluids | Na (mEq/L) | K (mEq/L) | Cl (mEq/L) | HCO3− (mEq/L) | Ca (mEq/L) | Kcal/L |
| ½ Nl saline | 77 | — | 77 | — | — | — |
| Nl saline | 154 | — | 154 | — | — | — |
| D5W | — | — | — | — | — | 170 |
| D10W | — | — | — | — | — | 340 |
| Lactated Ringer’s solution | 130 | 4 | 109 | 28∗ | 3 | 9 |
| Extracellular fluid | 141 | 4 | — | 27 | 5 | — |
∗ Lactate converted to HCO3− in liver.
From Nguyen TC, Abilez OJ (eds): Practical Guide to the Care of the Surgical Patient: The Pocket Scalpel. Philadelphia, Mosby, 2009.
Box 9-2 Water Balance
To estimate the amount of TBW, the following formula is frequently used:
The water deficit of a pt can be estimated by the following equation:
where PNa is plasma sodium concentration.
Alternatively, the free water deficit from the osmolality can be calculated as the following:
To calculate the free water clearance based on the osmolar clearance, the following formula can be used:
where the osmolar clearance is calculated as:
• Paraldehyde, phenformin (or metformin)
• Iron, isoniazid
• Lactic acidosis (cyanide, H2S, CO, methemoglobin)
• Ethylene glycol
• Salicylates
Metabolic acidosis w/nl AG (hyperchloremic acidosis)• RTA (including acidosis of aldosterone deficiency)
• Intestinal loss of HCO3− (diarrhea, pancreatic fistula)
• Carbonic anhydrase inhibitors (e.g., acetazolamide)
• Dilutional acidosis (as a result of rapid infusion of HCO3−-free isotonic saline)
• Ingestion of exogenous acids (ammonium chloride, methionine, cystine, CaCl)
• Ileostomy
• Ureterosigmoidostomy
• Drugs: amiloride, triamterene, spironolactone, β-blockers
Diagnosis (Fig. 9-3)
Measurement of urinary AG (UNa+ + UK+ − UCl−) and urinary pH is useful in the ddx of hyperchloremic metabolic acidosis:• (−) Urinary AG suggests GI loss of HCO3−.
• (+) Urinary AG suggests altered distal urinary acidification.
• ↓ Urinary pH and ↑ plasma K+ in pts w/(+) urinary AG suggest selective aldosterone deficiency.
• Urinary pH >5.5 and ↑ plasma K+ suggest hyperkalemic distal RTA.
• Urinary pH >5.5 and nl/↓ plasma K+ indicate classic RTA.
Treatment
3. Renal Tubular Acidosis (RTA)
Disorder characterized by an inability to excrete H+ or inadequate generation of new HCO3−. Four types:• Type 1 (classic, distal RTA): abnlity in distal hydrogen secretion resulting in hypokalemic hyperchloremic metabolic acidosis
• Type 2 (proximal RTA): ↓ proximal HCO3− reabsorption resulting in hypokalemic hyperchloremic metabolic acidosis
• Type 3 (RTA of glomerular insufficiency): normokalemic hyperchloremic metabolic acidosis as a result of impaired ability to generate sufficient NH3 in the setting of ↓ GFR (<30 mL/min). This type of RTA is described in older textbooks and is considered by many not to be a distinct entity.
• Type 4 (hyporeninemic hypoaldosteronemic RTA): aldosterone deficiency or antagonism resulting in ↓ distal acidification and ↓ distal Na+ reabsorption w/subsequent hyperkalemic hyperchloremic acidosis
Etiology
Type 2 RTA: Fanconi’s syndrome, primary hyperparathyroidism, MM, medications (acetazolamide)
Type 4 RTA: DM, sickle cell disease, Addison’s disease, urinary obstructionDiagnosis
Labs
ABGs: metabolic acidosis, with nl AG
Serum K+ ↓ in RTA types 1 and 2, nl in type 3, and high in type 4
Minimum urine pH >5.5 in RTA type 1 and <5.5 in types 2, 3, and 4
Urinary AG 0 or (+) in all types of RTATreatment
• Type 1 and type 2: PO NaHCO3 (1-2 mEq/kg/day in type 1 RTA, 2-4 mEq/kg/day in type 2 RTA) titrated to correct acidosis
• K+ supplementation in hypokalemic pts
• Type 4 RTA: furosemide to lower ↑ K+ levels and NaHCO3 to correct significant acidosis. Fludrocortisone 100 to 300 μg/day can be used to correct mineralocorticoid deficiency.
4. Respiratory Acidosis
Etiology
Pulmonary disease (COPD, severe pneumonia, pulmonary edema, interstitial fibrosis)
FIGURE 9-2 Map for acid-base disorders. (From Ferri F: Practical Guide to the Care of the Medical Patient, 8th ed. St. Louis, Mosby, 2011.)
Airway obstruction (foreign body, severe bronchospasm, laryngospasm)
Thoracic cage disorders (pneumothorax, flail chest, kyphoscoliosis)
Defects in muscles of respiration (myasthenia gravis, hypokalemia, muscular dystrophy)
Defects in PNS (amyotrophic lateral sclerosis, poliomyelitis, GBS, botulism, tetanus, organophosphate poisoning, spinal cord injury)
Depression of respiratory center (anesthesia, narcotics, sedatives, vertebral artery embolism or thrombosis, ICP)
Failure of mechanical ventilatorDiagnosis
Treatment
Correction of the underlying etiology5. Metabolic Alkalosis
Etiology
Divided into chloride-responsive (urinary chloride <20 mEq/L) and chloride-resistant (urinary chloride level >20 mEq/L) formsChloride Responsive
Vomiting
NG suction
FIGURE 9-3 Diagnostic approach to metabolic acidosis. (From Vincent JL, Abraham E, Moore FA, et al [eds]: Textbook of Critical Care, 6th ed. Philadelphia, Saunders, 2011.)
FIGURE 9-5 Workup of metabolic alkalosis. (From DuBose TD Jr: Acid-base disorders. In: Brenner BM [ed]: Brenner and Rector’s The Kidney, 8th ed. Philadelphia: Saunders, 2008, p. 513.)
Box 9-3 Common Causes of Mixed Disturbances Associated with Metabolic Acidosis
Mixed Anion Gap Acidosis
Ketoacidosis and lactic acidosis
Methanol or ethylene glycol intoxication and lactic acidosis
Uremic acidosis and ketoacidosis
Mixed Anion Gap and Hyperchloremic Acidosis
Diarrhea and lactic acidosis or ketoacidosis
Progressive renal failure
Type IV RTA and DKA
DKA during treatment
Mixed Hyperchloremic Acidosis
Diarrhea and RTA
Diarrhea and hyperalimentation
Diarrhea and acetazolamide or mafenide
Anion Gap Acidosis or Hyperchloremic Acidosis and Metabolic Alkalosis
Ketoacidosis and protracted vomiting or NG suction
Chronic renal failure and vomiting or NG suction
Diarrhea and vomiting or NG suction
RTA and vomiting
Lactic acidosis or ketoacidosis plus NaHCO3 Rx
Anion Gap Acidosis or Hyperchloremic Acidosis and Respiratory Alkalosis
Respiratory alkalosis
Lactic acidosis
Salicylate poisoning
Hepatic disease
Gram(−) sepsis
Pulmonary edema
Anion Gap Acidosis or Hyperchloremic Acidosis and Respiratory Acidosis
Cardiopulmonary arrest
Pulmonary edema
Respiratory failure in chronic lung disease
Phosphate depletion
Drug OD and poisoning
Modified from DuBose TD Jr: Clinical approach to patients with acid-base disorders. Med Clin North Am 67:799, 1983.
Diuretics
Posthypercapnic alkalosis
Stool losses (laxative abuse, cystic fibrosis, villous adenoma)
Massive blood transfusion
Exogenous alkali administrationChloride Resistant
Hyperadrenocorticoid states (Cushing’s syndrome, primary hyperaldosteronism, secondary mineralocorticoidism [licorice, chewing tobacco])
Hypomagnesemia
Hypokalemia
Bartter’s syndromeDiagnosis
Treatment
Chloride-responsive forms: saline administration and correction of accompanying hypokalemia
Chloride-resistant forms: correction of underlying cause and associated K+ depletion6. Respiratory Alkalosis
Etiology
Hypoxemia (pneumonia, PE, atelectasis, high-altitude living)
Drugs (salicylates, xanthines, progesterone, epinephrine, thyroxine, nicotine)
CNS disorders (tumor, CVA, trauma, infections)
Psychogenic hyperventilation (anxiety, hysteria)
Hepatic encephalopathy
Gram(−) sepsis
Sudden recovery from metabolic acidosis
Assisted ventilationDiagnosis
Treatment
Rx is aimed at its underlying cause; symptomatic pts w/psychogenic hyperventilation often require some form of rebreathing apparatus (e.g., paper bag, breathing 5% CO2 by mask).E. Disorders of Sodium Homeostasis
1. Hyponatremia
Etiology
Isovolemic
SIADH
Water intoxication (e.g., schizophrenic pts, primary polydipsia, Na+-free irrigant solutions, multiple tap-water enemas, dilute infant formulas). These entities are rare and often associated w/a deranged ADH axis.
Renal failure
Reset osmostat (e.g., chronic active TB, carcinomatosis)
Glucocorticoid deficiency (hypopituitarism)
Hypothyroidism
Thiazide diuretics, NSAIDs, carbamazepine, amitriptyline, thioridazine, vincristine, cyclophosphamide, colchicine, tolbutamide, chlorpropamide, ACEIs, clofibrate, oxytocin, SSRIs, amiodaroneHypovolemic
Renal losses (diuretics, partial urinary tract obstruction, salt-losing renal disease)
Extrarenal losses: GI (vomiting, diarrhea), extensive burns, third spacing (peritonitis, pancreatitis)
Adrenal insufficiencyHypervolemic
CHF
Nephrotic syndrome
Cirrhosis
Pregnancy
Isotonic hyponatremia (nl serum osmolality)
Pseudohyponatremia (↑ serum lipids and serum proteins). Newer Na+ assays eliminate this problem.
Isotonic infusion (e.g., glucose, mannitol)
Hypertonic hyponatremia (serum osmolality)
Hyperglycemia: each 100 mg/dL ↑ in blood glucose level above nl ↓ plasma Na+ concentration by 1.6 mEq/L
Hypertonic infusions (e.g., glucose, mannitol)Diagnosis
Treatment
Isovolemic Hyponatremia
SIADH: fluid restriction unless acutely symptomatic
Acute symptomatic pt: hypertonic 3% to 5% saline solution infusion; give 200 to 500 mL slowly, followed by fluid restriction to 750 mL/day for 24 to 48 hr. Hypertonic saline can be combined w/furosemide to limit Rx-induced expansion of the ECF volume.Hypovolemic Hyponatremia
0.9% NS infusionHypervolemic Hyponatremia
Na+ and water restriction. The combination of captopril and furosemide is effective in pts w/hyponatremia resulting from CHF.Chronic Hyponatremia
Correction of chronic hyponatremia should be kept at a rate <10 mEq/L (mmol/L) in any 24-hr period to prevent myelinolysis, a neurologic disorder that can occur after rapid correction of hyponatremia. Initially named central pontine myelinolysis, this disease is now known also to affect extrapontine brain areas and is known as osmotic demyelination syndrome. Manifestations of myelinolysis usually evolve several days after correction of hyponatremia. Typical features are disorders of UMNs, spastic quadriparesis and pseudobulbar palsy, and mental disorders ranging from mild confusion to coma. Death may occur. The motor and localizing signs of myelinolysis differ from those of the generalized encephalopathy that is caused by untreated hyponatremia.
FIGURE 9-7 Algorithm for treatment of hyponatremia. (From Cameron AM: Current Surgical Therapy, 10th ed. Philadelphia, Saunders, 2011.)
Clinical Pearls
In general, the serum Na+ should be corrected only halfway to nl in the initial 24 hr (but not >1 mEq/L/hr) to prevent complications from rapid correction (cerebral edema, myelinolysis, seizures). A slower correction rate is indicated in pts w/chronic hyponatremia.
In symptomatic pts w/hyponatremia, an ↑ in the serum Na+ concentration of 2 mEq/L/hr to a level of 120 to 130 mEq/L is considered safe by some experts; however, less rapid correction may be indicated in pts w/severe or chronic hyponatremia.2. Hypernatremia
Etiology
Isovolemic (↓ TBW, nl TBNa, and ECF)• DI (neurogenic and nephrogenic)
• Skin loss (hyperemia), iatrogenic, reset osmostat
Hypervolemic (TBW, TBNa, and ECF)• Iatrogenic (administration of hypernatremic solutions)
• Mineralocorticoid excess (Conn’s syndrome, Cushing’s syndrome)
• Salt ingestion
Hypovolemic: loss of H2O and Na+ (H2O loss > Na+)• Renal losses (e.g., diuretics, glycosuria)
• GI, respiratory, skin losses
• Adrenal deficiencies
Diagnosis
FIGURE 9-8 Algorithm for treatment of hypernatremia. (From Cameron AM: Current Surgical Therapy, 10th ed. Philadelphia, Saunders, 2011.)
Treatment
Isovolemic Hypernatremia
Fluid replacement w/D5W. Correct only half of estimated water deficit in initial 24 hr. The rate of correction of serum Na+ should not exceed 1 mEq/L/hr in acute hypernatremia or 0.5 mEq/L/hr in chronic hypernatremia.
Calculate water deficit in hypernatremic pts.
H2O deficit (in liters) = 0.6 × BW (kg) × ([measured Na+/140] − 1)Hypovolemic Hypernatremia
Fluid replacement is achieved w/isotonic saline solution.
The rate of correction of plasma osmolarity should not exceed 2 mOsm/kg/hr.Hypervolemic Hypernatremia
Fluid replacement w/D5W (to correct hypertonicity) is instituted after use of loop diuretics (to ↑ Na+ excretion).F. Disorders of Potassium Homeostasis
1. Hypokalemia
Etiology
Cellular shift (redistribution) and undetermined mechanisms• Alkalosis (each 0.1 ↑ in pH ↓ serum K+ by 0.4-0.6 mEq/L)
• Insulin administration
• Vitamin B12 Rx for megaloblastic anemias, acute leukemias
• Hypokalemic periodic paralysis: rare familial disorder manifested by recurrent attacks of flaccid paralysis and hypokalemia
• Beta adrenergic-Agonists, decongestants, bronchodilators, theophylline, caffeine
• Barium poisoning, toluene intoxication, verapamil intoxication, chloroquine intoxication
• Correction of digoxin intoxication w/digoxin Ab fragments (Digibind)
Renal excretion• Drugs: diuretics, including carbonic anhydrase inhibitors (e.g., acetazolamide); amphotericin B; high-dose Na+ PCN, nafcillin, ampicillin, or carbenicillin; cisplatin, AGs, corticosteroids, mineralocorticoids, foscarnet Na+
FIGURE 9-9 Diagnostic algorithm for hypokalemia. (From Ferri FF: Ferri’s Best Test: A Practical Guide to Clinical Laboratory Medicine and Diagnostic Imaging, 2nd ed. Philadelphia, Mosby, 2010.)
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