Page 1399 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

972 PART 8: Renal and Metabolic Disorders

from hypermetabolism. In all cases, the SID is decreased and is expected TABLE 100-2 Causes of an Increased AG (Na − Cl − HCO )
36
−
+
−
to remain so unless some therapy is provided. Hemodialysis will permit 3
the removal of sulfate and other ions and allow normal Na and Cl bal- Renal failure
−
+
ance to be restored, thus returning the SID to normal (or near normal). Ketoacidosis
However, patients not yet requiring dialysis and those who are between Diabetic
treatments are often given other therapies to increase the SID. NaHCO
3
is used as long as the plasma [Na ] is not already elevated. Other options Alcoholic
+
include Ca , which usually requires replacement anyway. Ca replace- Starvation
2+
2+
ment cannot increase the SID much given the rather narrow range of Change in AG (usually small AG)
ionized Ca (0.975 − 1.125 mmol/L). Even though Ca is a divalent cation,
2+
2+
it is unreasonable to expect much effect on the SID by administering Ca . Lactic acidosis
2+
■ POISONS Toxins
Methanol
Metabolic acidosis with an increased AG and SIG is a major feature of Ethylene glycol
various types of drug and substance intoxications (Table 100-2; see also
Chap. 124). Again, it is generally more important to recognize these Salicylates
disorders so that specific therapy can be provided than to treat the acid- Toluene
base disorder itself. Critical illness a
■ MISCELLANEOUS AND UNKNOWN Sodium with weak anions
Table 100-2 lists several commonly and not so commonly recognized Decreased cation
causes of positive AG metabolic acidosis. It is important to recognize Hypomagnesemia
that unexplained anions have been found commonly in the plasma of Hypokalemia
critically ill and injured patients. The etiology or even identity of these Hypocalcemia
anions has not been established, nor has the clinical significance.
Alkalosis
NON-ANION-GAP (HYPERCHLOREMIC) ACIDOSES a Unexplained anions have been found in critically ill and injured patients, especially those with sepsis
and liver disease. The causative anions have not been identified.
Hyperchloremic metabolic acidosis occurs as a result of either the
increase in Cl relative to strong cations, especially Na , or the loss of
+
−
cations with retention of Cl . As seen in Figure 100-1, these disorders K excretion and may be used to unmask the defect and to probe K
−
+
+
can be separated by history and by examination of the urine [Cl ]. secretory capacity.
−
When acidosis occurs, the normal response by the kidney is to increase The mechanisms of RTA are not well established. It is likely that much
Cl excretion. Failure to do so identifies the kidney as the source of aci- of the confusion has occurred as a result of attempting to understand
−
dosis. Extrarenal hyperchloremic acidoses occur as a result of exogenous the physiology from the point of view of regulating [H ] and [HCO ].
+
−
3
Cl loads (iatrogenic acidosis) or because strong cations (Na or K ) are However, as we have discussed, this is simply inconsistent with the prin-
+
−
+
lost from the lower gastrointestinal tract disproportionally to the loss of ciples of physical chemistry. The kidney does not excrete H any more
+
strong anions (Cl ). as NH than it does as H O. The purpose of renal ammoniagenesis is
−
+
■ RENAL TUBULAR ACIDOSIS to allow the excretion of Cl , which balances the charge of NH . The
4
2
−
+
4
defect in all types of RTA is the inability to excrete Cl in proportion to
−
Examination of the urine and plasma electrolytes and pH and calcula- Na , although the reasons vary by type. Treatment is largely dependent
+
tion of the urine SIDa allow one to correctly diagnose most cases of on whether the kidney will respond to mineralocorticoid replacement or
renal tubular acidosis (RTA) (see Fig. 100-1). However, caution must there is loss of Na that can be replaced as NaHCO . 3
+
37
be exercised when the plasma pH is greater than 7.35 because this may Classic distal (type I) RTA responds to NaHCO replacement, and
3
turn off urine Cl excretion. In such circumstances, it may be necessary generally 50 to 100 mEq/d is required. K defects are also common in
+
−
to infuse sodium sulfate or furosemide. These agents stimulate Cl and this type of RTA, and K replacement is also required. A variant of
−
+
Urine SID (Na + K – CI)
(+) (–)
Renal tubular acidosis Non renal
latrogenic Parenteral
Urine pH <5.5 High serum K + Gastrointestinal diarrhea
Urine pH >5.5 Low serum K + Small bowel/pancreatic nutrition Saline
Distal (type I) Aldosterone deficiency Carbonic anhydrase inhibitors
Proximal (type II) (type IV) drainage Anion exchange resins
FIGURE 100-1. Differential diagnosis for a hyperchloremic metabolic acidosis. (Reproduced with permission from Kellum JA. Diagnosis and treatment of acid-base disorders. In: Grenvik
A, Shoemaker PK, Ayers S, et al, eds. Textbook of Critical Care. Philadelphia, PA: Saunders; 1999.)
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