Fluids & Electrolytes

Fluid Resuscitation

  • 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)
  • 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

Figure 1: Electrolyte Composition of Commonly Used Intravenous Fluids


Figure 2: Electrolyte makeup of common bodily fluids


Sodium Disorders

  • 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) 
NEJM Review Article (Adrogue NEJM 2000) 
  • 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. 


Potassium Disorders

  • 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, and ventricular arrhythmias
  • Treatment of hyperkalemia includes sodium polystyrene sulfonate (kayexlate) to bind potassium, Calcium chloride (20mg/kg) in a central IV to stabilize the cardiac membrane, insulin and dextrose (0.2 units/g glcuose and 1 g/kg glucose), sodium bicarbonate (1 mEq/kg IV), fuorsemide, albuterol, and renal replacement therapy

Figure 4: EKG changes in hypo and hyperkalemia


Magnesium Disorders

  • 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.

Phosphorous Disorders

  • 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


Calcium Disorders



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


References

1) Finfer S, Bellomo R, Boyce N, French J, Myburgh J, Norton R; SAFE StudyInvestigators. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med. 2004 May 27;350(22):2247-56. PubMed PMID: 15163774.

2)Raghunathan K, Shaw A, Nathanson B, Stürmer T, Brookhart A, Stefan MS,Setoguchi S, Beadles C, Lindenauer PK. Association between the choice of IV crystalloid and in-hospital mortality among critically ill adults with sepsis*. Crit Care Med. 2014 Jul;42(7):1585-91.

3) Au AK, Ray PE, McBryde KD, Newman KD, Weinstein SL, Bell MJ. Incidence ofpostoperative hyponatremia and complications in critically-ill children treated with hypotonic and normotonic solutions. J Pediatr. 2008 Jan;152(1):33-8.

4) Montañana PA, Modesto i Alapont V, Ocón AP, López PO, López Prats JL, ToledoParreño JD. The use of isotonic fluid as maintenance therapy prevents iatrogenic hyponatremia in pediatrics: a randomized, controlled open study. Pediatr Crit Care Med. 2008 Nov;9(6):589-97.

5) Finberg L. Hypernatremic (hypertonic) dehydration in infants. N Engl J Med.1973 Jul 26;289(4):196-8.

6) Gennari FJ. Hypokalemia. N Engl J Med. 1998 Aug 13;339(7):451-8.

7) Fiser RT, Torres A Jr, Butch AW, Valentine JL. Ionized magnesiumconcentrations in critically ill children. Crit Care Med. 1998 Dec;26(12):2048-52.

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