DClassification Aniongap AG metabolic acidosis

occurs with increased endogenous production of acid, as in lactic acidosis or diabetic ketoacidosis. The AG can be estimated by the following formula:

Normal AG is 11 ± 4, although there are several exceptions. AG acidosis can exist even with a normal AG in patients who are severely hypoalbuminemic or those who have pathologic paraproteinemias. For every 1 g/dL decrease in albumin, aG decreases by 2.5-3 mmol. Pathologic parapro-teinemias lower AG because immunoglobulins are largely cationic. AG may not reflect an underlying acidosis in a patient with significant alkalemia (pH > 7.5). In these circumstances, albumin is more negatively charged, which increases unmeasured anions.

Differential Diagnosis. In acutely ill patients, metabolic and respiratory acidosis commonly coexist.

A. Respiratory Acidosis. There are many possible causes of respiratory acidosis, including airway obstruction (foreign bodies, tongue displacement, laryngospasm, congenital malformations or airway malacia, severe bronchospasm), respiratory center depression (general anesthesia, sedatives, narcotics, CNS injury or ischemia, drugs or toxins, and electrolyte disorders), increased CO2 production (sepsis, seizures, malignant hyperthermia, shivering, hypermetabolic states, overfeeding with TPN), neuromus-cular diseases (spinal cord injuries, Guillain-Barre syndrome, myasthenia gravis, polymyositis, spinal muscular atrophy, muscular dystrophy, infantile botulism), intrinsic pulmonary disease (obstructive and restrictive conditions such as in chondrodystro-phies, acute lung injury, acute respiratory distress syndrome [ARDS], pulmonary edema), extrinsic pulmonary disease (hemothorax, pneumothorax, flail chest, pleural effusions, obesity), and issues related to mechanical ventilation (obstructed endotracheal tube, inadequate ventilatory support, permissive hypercapnia).

B. Metabolic Acidosis. May be associated with a normal or an increased AG. This division greatly facilitates diagnosis.

1. Elevated AG acidosis. Causes include lactic acidosis (tissue hypoxia, shock, cardiac arrest, sepsis, hematologic emergencies), ketoacidosis (diabetes, alcohol induced, starvation), renal failure (uremic metabolic acidosis), and toxins (salicy-lates, methanol, ethylene glycol).

2. Normal AG metabolic acidosis. Usually the result of HCO3 loss from bowel or kidneys but can occur from treatment with exogenous acids (eg, HCl). Normal AG acidoses are subcate-gorized on the basis of K+ level.

a. Hypokalemia. Associated with diarrhea, ureteral diversion, proximal renal tubular acidosis (RTA), type I RTA and hyper-alimentation.

b. Hyperkalemia. Can be found in hyperaldosterone states, ammonium chloride (NH4Cl) administration, and type IV distal RTA.

c. Differential diagnosis includes:

i. GI loss of HCO3 (from diarrhea, ileostomy, proximal colostomy, ureteral conduit).

ii. Renal loss of HCO3 (proximal RTA, carbonic anhydrase inhibitor).

iii. Renal tubular disease (acute tubular necrosis, chronic tubulointerstitial disease, distal RTA types I and IV, hypoaldosteronism, aldosterone inhibitors).

iv. Medications (NH4Cl, HCl, hyperalimentation, dilutional acidosis).

IV. Database. Clinical manifestations of acute respiratory acidosis and acute ventilatory failure are the same. They depend on the absolute increase in PaCO2, rate of rise of PaCO2, and severity of associated hypoxemia.

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