Fluids and Electrolytes
Bolus of fluids defined as 20 cc/kg given over 5-10 minutes (Surviving Sepsis Guidelines). Hence, do not program 999 ml/hr on the pump. Pull and push directly or infuse via pressure bag.
No difference in outcomes whether one uses albumin vs. normal saline (SAFE Study, NEJM 2004)
Similar findings with other trials such as VISEP (10% pentastarch vs. LR), 6S (6% HES vs. Ringer's acetate), and CHEST (HES vs. NS) which generally showed worsened renal outcomes in the starch groups
Some recent evidence suggesting treatment with balanced fluids (lactated Ringer's) may be preferable to normal saline with associated improvements in outcome (Raghunathan, CCM 2014, Sankar J, CCM 2023). Other studies (Stenson et al, PCCM 2018) have shown hyperchloremia (i.e. from normal saline boluses) is independently associated with worse outcomes in pediatric sepsis.
Reasonable to limit overagressive resuscitation of patients with DKA as there may be some association of increased fluid administration with increased risk of cerebral edema- i.e. no fluid bolus or 10 cc/kg fluid bolus only unless other evidence of decompensated shock
Figure 1: Electrolyte Composition of Commonly Used Intravenous Fluids
Figure 2: Electrolyte makeup of common bodily fluids
Diuresis and Fluid Removal
Starling Equation describing net filtration out of the capillary (by convention) as determined by hydrostatic and oncotic pressures
The nephron and site of action for various diuretics
Common in the pediatric intensive care unit and hospitalized patients in general
Hyponatremia generally occurs as a result of increased ADH secretion (secondary to pulmonary or CNS pathology, pain, narcotic administration, etc) which promotes free water retention
This is the rationale for checking frequent sodiums on postoperative patients who have had a neurosurgical procedure such as a craniotomy or craniosynostosis repair
Due to the propensity of hospitalized patients to have increased ADH and free water retention, most patients in the PICU (with the exception of infants <1 yr, specific requests by specialty services, or in the case of unintentional iatrogenic hypernatremia) can be placed on isotonic (ie D5 normal saline) fluids as maintenance (vs. D5 1/2 normal saline). A RCT of 690 hospitalized pediatric patients (McNab et al, Lancet 2014) demonstrated a lower rate of hyponatremia (4 vs 11% p=0.001) with the use of isotonic saline vs. 1/2 normal saline. There were no significant differences in the rate of adverse events. The authors conclude isotonic saline should be used as maintenance fluid for hospitalized pediatric patients
Can also occur due to cerebral salt wasting (unclear pathophysiology but theory that neurologic injury leads to natriuretic peptide release that promotes loss of sodium and fluid). Treatment includes fluid/sodium repletion and potentially fludrocortisone
Workup of sodium disorders includes evaluation of fluid status, serum Na, urine output, and urine osmolality and can be differentiated by the table below:
Figure 3: Expected Changes for Common Sodium Disorders
Immediate life threatening hyponatremia (ie seizures, comatose) can be treated with hypertonic saline (3%) titrated to effect
Note there is a risk of central pontine myelinolysis with rapid correction of longstanding hyponatremia as fluid rushes out of neurons and into the intravascular space
Conversely, there is a risk of cerebral edema with overly rapid correction of chronic hypernatremia
In general, the recommendation is to correct chronic disorders of sodium no faster than 0.5-1 mEq/hr or a total of 12 mEq/L/day to avoid rapid shifts in tonicity. Careful and frequent monitoring with adjustment is critical.
Change in serum Na= Infusate Na -Serum Na/(Total body water +1) where TBW= 0.6(weight in kg)
Response in sodium to fluid depends on the underlying pathology and not just the amount of sodium in the fluid administered. For example, if a patient has SIADH, a urine osm of 600 and a serum Na of 125, giving them normal saline (Sodium of 154 mEq/L) will paradoxically decrease their serum Na and make the hyponatremia worse. This is because normal saline has an osm of ~300 and so the patient can excrete the 300 osm of solute you gave in 1/2 L of urine, leaving essentially 1/2 L of free water
Other causes of hyponatremia include adrenal insufficiency (generally accompanied by hyperkalemia), decreased effective circulating volume leading to appropriate ADH secretion (ie CHF, nephrotic syndrome), or hypothyroidism
3% hypertonic saline given in a dose of 5 cc/kg is expected to raise the serum sodium approximately 5 mEq/L.
Hypokalemia frequently occurs as a result of diuretics. Beta agonists, insulin, and alkalemia also promote entry of potassium into cells and thus relative serum hypokalemia. ECG changes include U waves or t wave flattening/inversion
Hypokalemia can lead to arrhythmias as well as skeletal muscle weakness
Significant risk of iatrogenic injury with overshoot hyperkalemia when treating hypokalemia
Hyperkalemia occurs with hemolysis, massive cell injury, acidemia, aldosterone deficiency (or spironolactone use), and renal failure
Hyperkalemia can lead to life threatening ECG changes and arrhythmias including peaked T waves, bradycardia, wide complex QRS complexes, sine wave pattern, and ventricular arrhythmias
Figure 4: EKG changes in hypo and hyperkalemia
Hypomagnesemia typically occurs in the PICU due to loop diuretics or transplant immunosupressives (i.e. tacrolimus or cyclosporine)
Hypomagnesemia is associated with ventricular arrhythmias, torsades de pointes, seizures, tetany, fasciculations, and coma. Repletion 25-50 mg/kg magnesium sulfate IV over 15-60 minutes
Hypermagnesemia occurs with renal failure or via iatrogenic administration. It is associated with decreased CNS responsiveness, depressed DTR's, and hypotension. IV calcium can be used to treat life threatening hypermagnesemia.
Hypophosphatemia generally associated with phsophate deficient TPN, refeeding syndrome, DKA, or severe respiratory alklalosis
Low phosphorous can lead to impaired energy utilization and diaphragmatic and respiratory muscle weakness, neuropathy and weakness, impaired cardiac output, tissue hypoxia due to reduced levels of 2-3 DPG, and impaired immune responses due to decreased available ATP. Generally treated with IV phosphorous repletion in the PICU (0.15 to 0.3 mmol/kg/dose)
Hyperphosphatemia generally associated with renal failure although phosphate containing enemas have also been reported as causes of hyperphosphatemia
Hyperhphosphatemia can be treated with sevelamer to beind phosphorous, mannitol diuresis, and renal replacement therapies
Figure 5: Calcium homeostasis
Hormonally regulated by PTH, viatmin D, and calcitonin
PTH inhibits phosphorous reabsorption and raises serum calcium levels by shifting it from bone to the ECF
Vitamin D stimulates intestinal absorption of calcium and phosphorous
Calcitonin is produced by c cells of the thyroid in response to elevated ionized Ca levels and leads to lower serum Ca levels
Hypocalcemia can be caused by PTH deficiency, vitamin D deficiency, hypercalcitoninemia, magnesium depletion, or iatrogenic causes such as significant blood product administration (citrate anticoagulant), or excessive citrate during renal replacement therapy
Hypocalcemia leads to tetany (Chovstek and Trousseau signs), seizures, hypotension
Treatment of hypocalcemia involves treating the underlying cause as well as oral/IV supplemenation (100 mg/kg calcium gluconate or 20 mg/kg calcium chloride)
Hypercalcemia can result from hyperparathyroidism, bone lysis, vitamin D intoxication
Hypercalcemia can lead to changes in CNS function, decreased QT interval, and impaired nerve conduction
Hypercalcemia is treated with fluid hydration and furosemide diuresis to promote calciuresis. Thiazides promote calcium retention and should not be used. Calcitonin has also been used to promote calciuria and prevent bone resporption
Electrolyte Derangement Chart
Courtesy of Richard Pierce, MD
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8) 140 mmol/L of sodium versus 77 mmol/L of sodium in maintenance intravenous fluid therapy for children in hospital (PIMS): a randomised controlled double-blind trial
McNab, Sarah et al. The Lancet , Volume 385 , Issue 9974 , 1190 - 1197