Book Text

Acid-Base Disturbances in Critical Illness

The emergence of the Stewart approach to acid-base balance in recent years owes much to the dissatisfaction of intensivists with the traditional approach. Critically ill patients may have many confounding acid-base disturbances that may not be revealed with a single quantitative measure such as BD. Patients frequently have perturbations of PCO₂ , SID, and A_TOT , and significant pathology may be overlooked because of apparently normal blood gas results.

The most important single disturbance in acid-base chemistry in critically ill patients is hypoalbuminemia.^[15] This condition is ubiquitous and causes an unpredictable metabolic alkalosis. It may mask significant alterations in the SID, such as lactic acidemia. Although Figge and colleagues^[19] presented a mechanism for adjusting the AG for albumin, this implies that the physician is aware of an acid-base abnormality. Likewise, the use of BD to predict lactate levels is unreliable in critical illness, particularly in patients undergoing secondary deterioration.^[18] Prolonged respiratory failure with associated hypercarbia leads to additional metabolic alkalosis because of chloride loss in urine.^[8] Mechanical ventilation increases the circulating volume of atrial natriuretic peptide and antiduretic hormone. The result is increased total body water, leading to dilutional acidosis. This may be further complicated by renal insufficiency or renal failure, with concomitant accumulation of metabolic by products, renal anions, and other UMAs. Polyuric renal failure may be associated with significant contraction alkalosis due to the loss of sodium, potassium, and free water.

Critically ill patients are vulnerable to significant changes in the SID and free water. Nasogastric suctioning causes chloride loss. Diarrhea causes loss of sodium and potassium. Surgical drains placed in tissue beds may remove fluids with various electrolyte concentrations (e.g., the pancreatic bed secretes fluid rich in sodium). Fever, sweating, oozing tissues, and inadequately humidified ventilator circuits lead to large-volume insensible loss and contraction alkalosis.

Infusions administered to patients may be responsible for stealth alterations in serum chemistry. Many antibiotics, such as piperacillin-tazobactam, are diluted in sodium-rich solutions. Others, such as vancomycin, are administered in large volumes of free water (5% dextrose). Lorazepam is diluted in propylene glycol, large volumes of which cause metabolic acidosis similar to that seen with ethylene glycol.^[41]

Continuous renal replacement therapy (CRRT) is used in critical illness for hemofiltration and hemodialysis of patients who are hemodynamically unstable. Rocktaschel and colleagues^[42] demonstrated that CRRT resolved the acidosis of acute renal failure by removing strong ions and phosphate. However, metabolic alkalosis ensued because of the unmasking of metabolic alkalosis due to hypoalbuminemia.

Other, seemingly innocuous therapies may cause significant disturbances in the acid-base balance. Loop diuretics are often administered to critically ill patients in

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the mistaken view that they can liberate sequestered fluids. These agents cause hypochloremic and contraction alkalosis. Similarly, the use of carbonic anhydrase inhibitors to treat patients with metabolic alkalosis is misguided. These agents increase tissue CO₂ levels, causing respiratory acidosis, and they cause diuresis, worsening contraction alkalosis. There is no treatment for hypoalbuminemic metabolic alkalosis except recovery. Contraction alkalosis is treated by correcting the free water deficit using the following formula:

Free water deficit = 0.6 × patient's weight (in kg) × ([patient's sodium level/140] − 1)

Hypochloremic alkalosis should be treated by correcting the chloride deficit, using normal saline.

CASE 2

A 56-year-old man is chronically critically ill. A serum chemistry panel and blood gas determinations are obtained. Consider the resulting data for the patient (in mEq/L unless otherwise stated): Na⁺ = 130, K⁺ = 4, Cl^- = 100, total CO₂ = 24, urea = 10, creatinine = 1.0, albumin = 1.0, lactate = 6.0, pH = 7.42, PCO₂ = 40, HCO₃ = 24, and BE = +1. Does he have any acid-base disturbances?

Using the Fencl-Gilfix^[31] ^[32] approach, correcting the base deficit or excess for acidifying and alkalinizing processes reveals a complex situation. Base deficit corrected (BDC) − base excess corrected (BEC) = 0.9.

Acidifying Processes	Magnitude	BDC	Alkalinizing Processes	Magnitude	BEC
Hyponatremia	130 mEq/L	-3	Hypoalbuminemia	1.0 g/dL	+11.9
Hyperchloremia	100 mEq/L	-3
Lacticemia	5 mEq/L	-5
Total		-11	Total		+11.9

In this example, the patient has three significant acidifying processes going on, and the presence of lactic acidosis is sinister. However, using traditional approaches would not reveal the abnormalities.

Neurosurgical patients are vulnerable to a variety of acid-base disturbances related to osmotherapy and brain injury (see Chapter 53 ). Mannitol, which is administered to reduce intracranial pressure, initially causes dilutional acidosis. A contraction alkalosis follows because of diuresis. Moreover, these patients are routinely treated with normal saline solution and frequently treated with hypertonic saline, both of which cause acidosis.^[43] Diabetes insipidus frequently occurs as a complication of severe head injury, usually in the terminal stages. It is caused by damage to or destruction of the pituitary gland or hypothalamus. In the absence of antiduretic hormone, the kidney is unable to concentrate the urine, and a massive diuresis follows. The disorder is characterized by an increase in plasma osmolality in the presence of a low urinary osmolality. It typically manifests as a contraction alkalosis. The treatment is hormonal replacement with vasopressin or desmopressin.