Acid–Base and Electrolyte Disturbances
Derangement of electrolytes and acid–base balance is commonly encountered in the PICU. This section highlights the approach to pediatric acid–base disorders and briefly reviews common electrolyte disturbances and their management.
Acid–base disturbance is frequently encountered in PICU patients, stemming from either primary metabolic or primary respiratory derangement. Often, correcting the acid–base disturbance is best achieved by addressing the underlying cause. Acid–base status is usually assessed by measuring the components of the bicarbonate–carbon dioxide buffer system in blood:
Acid-Base Status = Dissolved CO2 + H2O ↔ H2CO3 ↔ HCO3- + H+
Normal values for pH, bicarbonate, and pCO2 are affected by the site of sampling (venous versus arterial puncture).
- Arterial sample: Normal range for pH is 7.36 to 7.44; for bicarbonate (HCO3) concentration, 21 to 27 meq/L; and for PCO2, 36 to 44 mmHg.
- Peripheral venous sample: Normal pH is approximately 0.02 to 0.04 pH units lower than in arterial blood, the HCO3 concentration is approximately 1 to 2 mEq/L higher, and the PCO2 is approximately 3 to 8 mmHg higher.
A systematic approach to interpreting acid–base disturbances is key to diagnosing the underlying cause accurately.
|Systematic Approach to Interpreting Acid–Base Disturbances
||Determine the primary acid–base disturbance and the current compensation.
Assess the metabolic component.
- Acidosis: Determine if anion gap is present.
- Alkalosis: Determine urinary chloride concentration.
Consider mixed disturbances.
- Calculate delta-delta (magnitude of change in anion gap
compared to magnitude of change in bicarbonate).
||Determine serum osmolar gap for unexplained high anion-gap acidosis.
||Determine if respiratory component is acute or chronic.
The following algorithms detail the stepwise approach to assessment of acidosis and alkalosis:
Assessment of Acidosis
Assessment of Alkalosis
Commonly encountered electrolyte abnormalities include hypokalemia, hyperkalemia, hypocalcemia, hypomagnesemia, hyponatremia, and hypernatremia. Abnormalities should be corrected to prevent serious sequelae such as an arrhythmia, altered mental status, or seizure. Some common approaches to correction for potassium and sodium disturbances are discussed below.
The approach to treatment is dependent on whether the child is symptomatic. Urgent therapy is warranted in:
- patients with electrocardiogram (ECG) changes (other than isolated peaked T waves): widening of the QRS complex, loss of P waves, or arrhythmias
- patients with potassium levels >7 mEq/L regardless of symptoms
- high-risk patients with expected continued potassium rises, including those with tumor lysis syndrome and rhabdomyolysis
Urgent treatment involves first stabilizing cardiac membranes by administering calcium, either in the form of calcium gluconate or calcium chloride. Next, the shifting of extracellular potassium into cells helps mitigate the cardiac toxicity of extracellular potassium. This can be achieved by administering insulin concomitantly with glucose (to mitigate hypoglycemia), inhaled beta-adrenergic agonists, and/or sodium bicarbonate.
Hypokalemia in the PICU is common and can be caused by gastrointestinal losses, urinary losses, reduced dietary potassium intake (especially in patients receiving fluids only), and factors that cause the driving of potassium intracellularly, including beta-adrenergic therapy (especially in patients with asthma receiving continuous albuterol therapy) and alkalosis. Severe hypokalemia can cause arrhythmias, muscle weakness, and diaphragmatic paralysis. Enteral potassium replacement is preferred to IV because it is associated with fewer adverse effects. In patients who are unable to tolerate the enteral route or who are symptomatic from severe hypokalemia, IV administration is appropriate at rates not to exceed 0.5 to 1.0 mEq/kg of body weight per hour.
Hypernatremia in children is caused by an imbalance of the body’s handling of water, resulting in an excess of plasma tonicity to total body water. In children, it is typically caused by fluid losses from the gastrointestinal tract, urine, or skin. Rarely, it can be caused by excess salt intake from iatrogenic administration or salt poisoning. Chronic hypernatremia (>24 hours in duration) can result in cerebral adaptations to restore brain volume that can precipitate cerebral edema if excess free water is administered and correction occurs too rapidly. Therefore, the goal in correction of hypernatremia should be a rate of correction that does not exceed a fall of sodium >0.5 mEq/L per hour or 10 to 12 mEq/L per day. If the patient presents with marked volume depletion and hemodynamic instability, rapid fluid resuscitation should not be delayed.
Hyponatremia in children is caused by an imbalance in the body’s handling of water, resulting in a relative deficit of effective plasma osmolality (tonicity) to total body water. It is typically classified by the patient’s volume status (hypovolemic, euvolemic, or hypervolemic). The most common etiology in children is hypovolemic hyponatremia from gastrointestinal losses. In euvolemic patients, a syndrome of inappropriate antidiuretic hormone secretion (SIADH) can cause hyponatremia that is associated with many conditions in the ICU, including pulmonary and oncologic disorders, surgery, central nervous system injury, and certain medications. Hypervolemic hyponatremia can be caused by renal failure and conditions associated with a reduced effective circulating volume (e.g., cirrhosis, heart failure, and nephrotic syndrome). Treatment of hyponatremia requires treatment of the underlying condition and administration of replacement fluids to prevent overly rapid correction that can lead to osmotic demyelination. The usual approach is to avoid correcting the plasma sodium >6–8 mEq/L in 24 hours. In the case of patients with severe neurologic manifestations (e.g., seizures), administering hypertonic saline is indicated until symptoms improve.
Neurologic Consequences of Overly Rapid Sodium Correction