Metabolic Acidosis: Clinical Approach

Introduction

In this chapter, our goal is to provide a bedside approach to the patient with metabolic acidosis. This approach focuses not only on diagnosing the cause of metabolic acidosis but also (and importantly) on identifying and managing emergencies that are present and anticipating and preventing risks that are likely to arise during therapy.

An important component of our approach is to deduce whether there is a risk of excessive binding of H ⁺ ions to intracellular proteins in vital organs (e.g., the brain and the heart). We discuss how this may occur and how it can be reversed.

Metabolic acidosis can be caused by the gain of acids or the loss of sodium bicarbonate (NaHCO ₃ ). We describe the clinical approach to determine the basis of metabolic acidosis by finding new anions in blood or the urine and examining the renal response to the presence of chronic metabolic acidemia by assessing the rate of excretion of ${NH}_{4}^{+}$ ${NH}_{4}^{+}$ ions in the urine.

Objectives

▪
To emphasize the following issues in the clinical approach to the patient with metabolic acidosis:
- 1.
  Deal with emergencies first: Our first step is to recognize and manage threats to the patient’s life and to anticipate and prevent risks that may arise during or because of therapy.
- 2.
  Assess the effectiveness of the bicarbonate buffer system (BBS): Measurement of brachial venous PCO ₂ provides a means to evaluate the effectiveness of the BBS in skeletal muscle, where the bulk of this buffer system exists, in removing the H ⁺ ion load.
- 3.
  Determine whether the basis of the metabolic acidosis is the addition of acids and/or the loss of NaHCO ₃ : Look for the presence of new anions in plasma and urine, and assess the rate of excretion of ${NH}_{4}^{+}$ ${NH}_{4}^{+}$ ions in the urine.

Abbreviations

BBS, bicarbonate buffer system
NaHCO ₃ , sodium bicarbonate
P _Glucose , concentration of glucose in plasma
P _Albumin , concentration of albumin in plasma

Case 3-1: Stick to the Facts

A 28-year-old man with a known history of sniffing glue presented to the emergency room with profound muscle weakness and a very unsteady gait, which had become progressive over the last 3 days. On physical examination, his blood pressure was 100/60 mm Hg and his pulse rate was 110 beats per minute while lying flat. When he sat up, his blood pressure fell to 80/50 mm Hg and his pulse rate rose to 130 beats per minute. Neurological examination revealed severe muscle weakness but no other findings. His arterial blood pH was 7.20, PCO ₂ was 25 mm Hg, and $P_{{HCO}_{3}}$ $P_{{HCO}_{3}}$ was 10 mmol/L. His P _Glucose was 3.5 mmol/L (63 mg/dL), his P _Albumin was 6.0 g/dL (60 g/L), and his hematocrit was 0.50. Other laboratory measurements in brachial venous blood and the urine are shown in the following table:

		Venous Blood	Urine
pH		7.00	6.0
PCO ₂	mm Hg	60	—
${HCO}_{3}^{-}$ ${HCO}_{3}^{-}$	mmol/L	15	<5
Na ⁺	mmol/L	120	50
K ⁺	mmol/L	2.3	30
Cl ⁻	mmol/L	90	0
Creatinine	mg/dL (μmol/L)	1.7 (150)	3.0 mmol/L
BUN (urea)	mg/dL (mmol/L)	14 (5.0)	150 mmol/L
Osmolality	mOsm/kg H ₂ O	250	400

Questions

What dangers were present on admission?
What dangers should be anticipated during therapy?
What is the basis for the metabolic acidosis?

Part A

Clinical Approach

The first step in the clinical approach to the patient with metabolic acidosis is to deal with emergencies on presentation and anticipate and prevent risks that may arise during therapy.
The next two steps are: (1) Determine whether H ⁺ ions were buffered appropriately by the BBS. (2) Determine whether the basis of the metabolic acidosis is the addition of acids and/or the loss of NaHCO ₃ .

Abbreviations

ECF, extracellular fluid
ICF, intracellular fluid
EABV, effective arterial blood volume
GFR, glomerular filtration rate
GI, gastrointestinal
RTA, renal tubular acidosis
P _{Anion gap} , anion gap in plasma
P _{Osmolal gap} , osmolal gap in plasma
DKA, diabetic ketoacidosis
P _K , concentration of potassium (K ⁺ ) ions in plasma

The initial steps in our approach to the patient with metabolic acidosis are illustrated in Flow Chart 3-1 . The diagnosis of metabolic acidosis is based on one of the following criteria: (1) a low plasma pH and $P_{{HCO}_{3}}$ $P_{{HCO}_{3}}$ and (2) an appreciable decrease in the content of ${HCO}_{3}^{-}$ ${HCO}_{3}^{-}$ ions in the extracellular fluid (ECF) compartment in the patients who are ECF volume contracted. A quantitative estimate of the ECF volume is needed. Because one cannot obtain a quantitative estimate of the ECF volume with physical examination, we recommend using the hematocrit or the concentration of total protein in plasma to obtain this information (see the discussion of Case 2-1 ).

Flow Chart 3-1, Initial Steps in the Evaluation of the Patient with Metabolic Acidosis.

Emergencies in the Patient With Metabolic Acidosis

The common clinical practice is to begin the assessment of a patient with metabolic acidosis with an emphasis on diagnosis. We, however, recommend a different approach; our initial focus is to deal with threats to the patient’s life that may be present, and to anticipate and prevent dangers that may arise during or because of therapy ( Table 3-1 ). The diagnostic category of metabolic acidosis is made up of two major subgroups: one where the basis of the disorder is the addition of acids and the other where its basis is the loss of NaHCO ₃ . Although the emergencies may be different depending on the cause for the disorder, nevertheless, dealing with emergencies should take precedence over diagnostic issues.

TABLE 3-1

Threats to Life Associated With Metabolic Acidosis

On Presentation

Hemodynamic instability
- Marked decrease in myocardial contractility (e.g., cardiogenic shock)
- Very low intravascular volume (e.g., NaCl loss, hemorrhage)
- Decreased peripheral vascular resistance (e.g., sepsis)
Cardiac arrhythmia
- Most frequently seen in patients with hyperkalemia or hypokalemia
Respiratory failure (e.g., respiratory muscle weakness caused by hypokalemia)
Presence of toxins (e.g., methanol, ethylene glycol)
Presence of reactive oxygen species (e.g., pyroglutamic acidosis)
Nutritional deficiency (especially of B vitamins)

During Therapy

Development of cerebral edema during therapy of DKA in children
- Administration of a bolus of insulin
- Overly rapid or excessive administration of saline
- Failure to prevent an appreciable fall in the effective plasma osmolality during therapy
Pulmonary edema (e.g., in patients with severe diarrhea if the ECF volume is expanded and NaHCO ₃ is not given)
Too rapid a rise in the P _Na in patients with chronic hyponatremia
Development of a more severe degree of acidemia in a patient with metabolic acidosis
Acute shift of K ⁺ into cells (e.g., administration of NaHCO ₃ or glucose to patients with hypokalemia, administration of insulin to patients with DKA and hypokalemia
Wernicke’s encephalopathy caused by failure to give thiamin (vitamin B ₁ ) to a patient with chronic alcoholism and alcoholic ketoacidosis

Emergencies at Presentation

Hemodynamic emergency

The most common example is the patient with L-lactic acidosis because of cardiogenic shock caused by a massive myocardial infarction. Survival in this setting depends on whether the cardiac output can be improved very quickly. In most of the other settings of metabolic acidosis caused by added acids, true hemodynamic emergencies are not common, with the exception of some patients with sepsis and others with DKA caused by the marked degree of decreased effective arterial blood volume (EABV) because of glucose-induced osmotic natriuresis and diuresis.

Patients with a significant degree of contraction of the EABV that causes hemodynamic instability require the urgent administration of a large volume of isotonic saline. In contrast, if the patient is not hemodynamically compromised, aggressive infusion of isotonic saline is not warranted because this may lead to serious complications (see the following discussion).

Cardiac arrhythmia

Patients with metabolic acidosis may develop a cardiac arrhythmia when there is a severe degree of hyperkalemia (e.g., patients with renal failure) or hypokalemia (e.g., certain patients with distal renal tubular acidosis [RTA], patients with metabolic acidosis caused by glue sniffing). In addition, hypokalemia may develop after therapy is initiated (see discussion of Case 3-1 ). The emergency treatment of hypokalemia and of hyperkalemia is discussed in Chapter 14, Chapter 15 , respectively.

Failure of adequate ventilation

A severe degree of hypokalemia may lead to respiratory muscle weakness and respiratory failure. A more severe degree of acidemia develops because of superimposed respiratory acidosis in a patient with metabolic acidosis. Enough KCl should be given to raise the concentration of potassium (K ⁺ ) ions in plasma (P _K ) to 3.0 mmol/L in this setting; mechanical ventilation may be needed.

Toxin-induced metabolic acidosis

Ingestion of methanol or ethylene glycol should always be suspected in a patient with metabolic acidosis, an elevated P _{Anion gap} , and no obvious cause for these findings, especially if the ECF volume is not significantly contracted (see Chapter 6 ). Failing to make this diagnosis can be devastating. If ingestion of these alcohols is suspected, one must calculate the P _{Osmolal gap} (see Chapter 2 ). If the P _{Osmolal gap} is considerably greater than 10 mosmol/kg H ₂ O, the diagnosis of ingestion of toxic alcohols should be confirmed by direct measurements of methanol and of ethylene glycol in plasma because the presence of ethanol in plasma also causes a high P _{Osmolal gap} . Because it is the products of the metabolism of these alcohols that create the danger rather than the parent compounds, inhibition of their metabolism via the enzyme alcohol dehydroenase with the administration of ethanol (alcohol dehydrogenase has a much higher affinity for ethanol than for methanol or ethylene glycol), or the administration of fomepizole (a direct inhibitor of alcohol dehydrogenase) is required until the facts become clear.

Dangers to Anticipate After Commencing Therapy

Several threats are anticipated during therapy in patients with metabolic acidosis.

Dangers related to overly aggressive administration of saline

Although enough saline should be given if there is evident hemodynamic instability, several complications may arise from excessive administration of saline. In the absence of hemodynamic instability, we use the brachial venous PCO ₂ as a guide to the amount of saline to be administered in the initial management of patients with metabolic acidosis (see the following). We also use the hematocrit to obtain a quantitative estimate of the ECF volume, and the P _Na on presentation to get an estimate of the deficit of Na ⁺ ions and avoid the excessive administration of saline (see chapter 5 for further discussion).

1 A more severe degree of acidemia

A large fall in the $P_{{HCO}_{3}}$ $P_{{HCO}_{3}}$ may occur when a large volume of saline without NaHCO ₃ is given to a patient who has metabolic acidosis caused by a large loss of NaHCO ₃ and a severe degree of ECF volume contraction due to a large loss of NaCl (e.g., the patient with severe diarrhea). When saline is infused very rapidly, some of these patients may develop pulmonary edema. This occurs even though they have not been given enough saline to sufficiently re-expand their ECF volume. It is interesting to note that the pulmonary edema in these patients can be treated, and its occurrence can be prevented with the administration of NaHCO ₃ (see [CR] ). Therefore, the fluid that is administered to these patients to achieve ECF volume expansion should contain NaHCO ₃ or anions that can be metabolized to produce ${HCO}_{3}^{-}$ ${HCO}_{3}^{-}$ anions (e.g., lactated Ringer’s solution).

Three mechanisms may lead to a more severe degree of acidemia with the infusion of a large amount of saline in these patients.

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