Perioperative Acid-Base Disturbances

An acid-base disturbance is a sign of an imbalance in acid-base physiology. In the perioperative setting, acid-base disturbances can be an early-warning sign and portend worse prognosis. Downstream effects of these disturbances can include vasodilatation with hypotension, arrhythmias, increased inflammation, vasopressor resistance, and increased mortality. Corresponding compensatory mechanisms, including sustained tachypnea, can mask impending respiratory arrest. Thus, timely identification and management of these disturbances are essential.

The topics in this rotation guide are organized as follows:

• Overview of Acidosis and Alkalosis

• Common Etiologies

• Workup and Assessment

• Treatment

• Compensatory Mechanisms

Overview of Acidosis and Alkalosis

Definitions

Acidemia and alkalemia refer to states in which the blood pH is abnormally low (acidic) or abnormally high (alkaline). The two types of acid-base disorders are:

• Acidosis is the process in which the hydrogen-ion concentration is increased.

• Alkalosis is the process in which the hydrogen-ion concentration is decreased.

Acid-base disorders are further categorized as follows:

• Metabolic acidosis is due to a metabolic process that reduces serum bicarbonate (HCO₃⁻) concentration and pH.

• Metabolic alkalosis is due to a metabolic process that elevates serum HCO₃⁻ concentration and pH.

• Respiratory acidosis is due to a respiratory process that elevates arterial partial pressure of carbon dioxide (PaCO₂) and reduces the pH.

• Respiratory alkalosis is due to a respiratory process that reduces arterial PaCO₂ and elevates the pH.

Common Etiologies

The evaluation of perioperative patients with acid-base abnormalities is focused on identifying the underlying etiology. In addition to traditional causes of acid-base disturbances (e.g., vomiting, diarrhea, medications, overdose, and many chronic conditions), surgery or surgical disease processes can significantly stress homeostasis.

The following table summarizes potential causes of acid-base disorders to consider in the workup of a patient with an acid-base disturbance in the perioperative period.

Workup and Assessment

The aim of the workup for perioperative patients with acid-base abnormalities is to identify the underlying cause and determine the appropriate treatment directed at the underlying cause. Details of the workup are as follows:

• Obtain a history:

  • comorbidities (e.g., diabetes)

  • medication history (e.g., opioid use, metformin, diuretics)

  • nutrition status

  • surgical history (what surgery was performed, how much time has passed since the patient left the operating room, and did the patient receive perioperative transfusions)

  • review of systems (pain, shortness of breath, nausea, vomiting, diarrhea, constipation)

• Complete a thorough but focused physical exam:

  • vital signs (temperature, tachypnea/bradypnea, tachycardia/bradycardia, hypotension, hypoxemia)

  • neurologic exam (abnormal pupil exam, orientation status, or Glasgow coma scale)

  • chest (irregular rate or rhythm, crackles, hyperresonance, unequal breath sounds, note the ventilator settings)

  • abdomen (peritonitis, distention, high ostomy output, decreased urinary output, presence of nasogastric tube)

  • surgical site exam (evidence of infection [redness, delayed healing, fever, pain, tenderness, warmth, or swelling], bleeding, hematoma)

  • lines, drains, tubes (inspect all for quality and quantity of output, and that they are functioning as they should)

  • volume status (peripheral edema, inferior vena cava ultrasound, weight, in/outs)

• Obtain initial labs:

  • basic metabolic panel (sodium, potassium, chloride, bicarbonate, glucose, creatinine, blood urea nitrogen [BUN; electrolyte derangements, hyper/hypoglycemia, kidney dysfunction])

  • additional electrolytes (magnesium, calcium, phosphate)

  • albumin (hypoalbuminemia)

  • arterial blood gas/venous blood gas (overall acid-base status)

  • complete blood count (infection or hemorrhage), cultures (infection)

  • lactate (malperfusion)

• Ancillary tests:

  • electrocardiogram (ECG)

  • chest x-ray

The following algorithms represent a stepwise approach to the assessment of acid-base disorders. Because current acid-base assessment methods are not without limitations, the diagnosis must correlate with patient presentation.

(Source: Physiological Approach to Assessment of Acid-Base Disturbances. N Engl J Med 2014.)

(Source: Physiological Approach to Assessment of Acid-Base Disturbances. N Engl J Med 2014.)

Treatment

The following basic principles apply to the treatment of patients with acid-base disorders.

• Treat the underlying cause. Only by doing so will the acid-base disturbance resolve.

• Ensure appropriate respiratory status and intervene as needed.

• Correct electrolyte derangements and fluid status.

• Avoid premature closure on a diagnosis given that observed acid-base imbalances may be multifactorial.

Specific additional treatment considerations for the causes of common perioperative acid-base disorders are described below.

Acidosis

Severe acidosis: Severe acidosis is generally a sign of a life-threatening underlying condition. Thus, immediate intervention to stabilize patients is required.

• Supportive care includes respiratory support/hyperventilation and electrolyte management to prevent respiratory arrest, cardiac arrhythmias, and systemic vasoregulatory changes.

• The Surviving Sepsis Campaign guidelines make a weak recommendation against the use of sodium bicarbonate to improve hemodynamics or reduce vasopressor requirements. However, the guidelines note that the results from the BICAR-ICU trial support the use of intravenous (IV) sodium bicarbonate as a buffer in a subset of patients with septic shock, severe metabolic acidemia (pH ≤7.20), and acute kidney injury (with an AKIN score of 2 or 3).

• The use of hemodialysis or continuous renal replacement therapy (CRRT) should also be considered early in patients with acidosis and impaired renal function.

Metabolic Acidosis

• Lactic acidosis: Lactic acidosis is a common and potentially serious acid-base disturbance in the postoperative setting. Lactic acidosis is defined as an anion-gap metabolic acidosis, where the anion gap is explained by the presence of lactic acid (see Workup of Metabolic Acidosis algorithm above).

The differential for lactic acidosis is varied and includes the following:

• focal ischemia (local area of impaired perfusion due to injury, infection, vascular compromise)

• global ischemia (sepsis, shock)

• decreased hepatic clearance (liver dysfunction)

• other (ketosis, uremia, burns, and more)

In addition to supportive management (outlined above) for severe respiratory acidosis, the varied differential requires detailed inpatient evaluation via a focused physical exam or immediate imaging to examine the need for emergent surgical intervention for an underlying reversible cause (e.g., hollow viscous perforation with intra-abdominal sepsis, anastomotic leak, compartment syndrome, vascular ischemia).

• Hyperchloremic metabolic acidosis: Losses of fluid from the gastrointestinal system distal to the stomach (e.g., diarrhea, high ostomy output, enteroatmospheric fistula, or nasojejunal suctioning) can lead to hyperchloremic metabolic acidosis. The loss of bicarbonate results in an increase in extracellular chloride, referred to as hyperchloremic acidosis or a non-anion-gap acidosis. Resuscitation with a large volume of normal saline can also lead to relative hyperchloremia (e.g., in trauma patients with neurologic injuries).

  • Treatment involves addressing the underlying etiology and aggressive fluid and electrolyte repletion with caution taken in choice of resuscitative fluid.

    • Acute kidney injury (AKI): Patients with acute kidney injury (evidenced by increased levels of creatinine and oliguria) experience an exacerbation of acidosis with an accumulation of unmeasured anions and hyperphosphatemia.

  • Treatment may involve dose-adjusting or discontinuing medications, careful management of fluid status with diuresis, managing electrolyte imbalances (hyperkalemia), or dialysis in refractory cases.

• Ketosis (diabetic ketoacidosis or starvation ketosis): In patients who have underlying type 1 diabetes or are on nothing by mouth (NPO) orders, the physiological stress of surgery and pre/postop dietary restrictions can contribute to a ketone-driven metabolic acidosis as determined by glucose and serum/urine ketones. Determining the cause of ketosis is necessary to ensure the appropriate treatment.

  • Diabetic ketoacidosis (DKA) is more common and often associated with infection perioperatively.

  • Starvation ketosis is rare and managed with dextrose, volume resuscitation, and careful monitoring and correction of electrolyte abnormalities (especially in the setting of potential refeeding syndrome).

• Urinary diversion procedures: While the metabolic abnormalities in patients undergoing urinary diversion are often mild and able to be compensated, a subset of patients likely with impaired compensatory mechanisms may develop electrolyte abnormalities that can arise dependent on the gastrointestinal segment used for the diversion. Metabolic acidosis and electrolyte abnormalities including hypokalemia, hypocalcemia, hypomagnesemia, and hypochloremia can occur. Treatment includes alkalinizing oral therapy, including sodium bicarbonate or sodium citrate, and repletion of depleted electrolytes.

Respiratory Acidosis: Primary respiratory acidosis in the postoperative period is often related to two forms of hypoventilation. In both scenarios, reevaluation of the patient’s pain regimen is necessary.

• Opioid-induced respiratory depression: If opioid overdose is suspected, additional clinical findings include miosis, apnea/hypoventilation, or stupor. Treatment includes the immediate administration of naloxone (see dosing schema here) with bag mask ventilation and maintenance of the airway. Maintain subsequent observation with possible redosing as needed.

• Splinting: Splinting occurs when the patient’s tidal volume is reduced due to the pain of taking a deep breath and can lead to atelectasis and CO₂ retention.

Alkalosis

Metabolic Alkalosis

• Upper gastrointestinal losses of hydrogen ion: Vomiting or nasogastric tube suctioning/drainage can lead to metabolic alkalosis via hydrogen loss in gastric secretions. Appropriate fluid resuscitation (typically with IV isotonic sodium chloride) and electrolyte repletion (typically potassium) should be initiated. Antiemetics (including ondansetron) are often used to mitigate vomiting, taking care to confirm QTc interval prior to administration. Additionally, inhibition of gastric H⁺/K⁺-ATPase (e.g., with a proton pump inhibitor such as omeprazole) will limit acid loss and the development of a metabolic alkalosis and help ameliorate or reverse severe alkalosis.

• Renal loss of chloride (loop or thiazide use): A metabolic alkalosis is often seen in the setting of subacute to chronic hypovolemia from loop or thiazide diuretic use. These diuretics lead to distal delivery of chloride with accompanying loss of H⁺ as ammonium and K⁺. Secondary hyperaldosteronism from volume depletion in the perioperative setting can perpetuate this situation. If diuresis is still indicated, acetazolamide may be used instead or in combination with a lower dose of the offending diuretic.

Respiratory Alkalosis: Hyperventilation can result in primary respiratory alkalosis with eventual renal compensation.

• Pain, anxiety, or both are common causes of hyperventilation in the postoperative patient. An adequate pain regimen and addressing the patient’s anxiety are usually effective treatments.

• Pulmonary embolism (PE) without circulatory failure can lead to hypoxemia and subsequent respiratory alkalosis via tachypnea. In the event of circulatory failure, a mixed acidosis may be observed due to poor perfusion and subsequent lactic acidosis. Treatment requires rapid recognition of symptoms and further workup dependent on clinical suspicion. See the workup of suspected PE here.

• Ventilator settings may iatrogenically induce respiratory alkalosis. Management includes treatment of the underlying acidosis in addition to appropriate respiratory support and electrolyte repletion.

• Cirrhosis and pregnancy may cause respiratory alkalosis and no treatment is needed if other processes have been ruled out.

Compensatory Mechanisms

The body has compensatory mechanisms to try to maintain pH balance in the setting of acid-base disturbances.

• Respiratory compensatory mechanisms respond immediately to metabolic acidosis or alkalosis and may precede other clinical symptoms. However, If the compensation is not as expected, the possibility of a mixed respiratory-metabolic process should be explored.

• Metabolic (renal) compensation is slower than respiratory compensation, fully maturing 3 to 5 days after development of the initial respiratory alteration.

• Mixed respiratory-metabolic process: In certain instances, renal or respiratory compensation may prove insufficient, potentially necessitating patient intubation. For example, hyperventilation can occur as a secondary response to an underlying metabolic acidosis for compensatory purposes. In this critical setting, fatigue-induced respiratory compensation can precede respiratory arrest. This scenario, termed inadequate respiratory compensation or concomitant respiratory acidosis, requires patient intubation. (See algorithms above for evaluation and assessment of mixed processes).