Alternative Resuscitative Fluids

 Hypertonic saline solutions (3.5% and 5%) – used for

correction of severe sodium deficits

 Hypertonic saline solution (7.5%) – used as treatment

modality in patients with closed head injuries
- increases cerebral perfusion and decreases
intracranial pressure, thus decreasing brain edema

 Colloids – volume expanders (confined to intravascular

space due to their MW) but in sevee hemorrhagic
shock, increased capillary permeability allows colloids
to enter interstitial space leading to edema and
impaired tissue oxygenation
o 4 major types: albumin, dextrans, hetastarch, gelatins
Correction of Life-Threatening Electrolyte Abnormalities
1. Sodium
a. Hypernatremia – usually, treatment of associated water deficit
 if hypovolemic: restore volume first with normal saline
 once volume is adequate: replace water deficit with hypotonic fluid (D 5W, D5 1/4NS, enteral water)
 formula: Water deficit (L) = serum Na+ – 140 x TBW
140
 est. TBW – 50% of lean body mass in men; 40% in women
 for acute symptomatic hypernatremia (onset within < 48hrs): titrate decrease Na + concentration of no
more than 1 mEq/h or 12 mEq/d
 for chronic hypernatremia (onset within > 48hrs): no more than 0.7 mEq/h as rapid correction may
lead to cerebral edema and herniation
 for severe hypernatremia associated with volume deficit: slow correction with 0.45% saline or lactated
Ringer’s solution rather than 5% dextrose alone
 frequent evaluation of neurologic status and serum sodium levels

b. Hyponatremia – most cases can be treated by free water restriction

 if severe: administration of sodium
 for patients with normal renal function, symptomatic hyponatremia occurs with serum Na +< 120
mEq/L
 if neurologic symptoms are present: 3%NaCl used to increase Na + by no more than 1 mEq/L/h
until serum Na+ reaches 130 mEq/L or neurologic symptoms improve
 for asymptomatic hyponatremia: increase Na+ by no more than 0.5 mEq/L/h to max. 12 mEq/L/day
 for chronic hyponatremia: slower infusion as rapid correction can lead to pontine myelinolysis
2. Potassium
a. Hyperkalemia – goals of therapy include reducing total body K +, shifting K+ from extracellular to intracellular
space, and protecting the cells from effects of increased potassium
 for potassium removal
 Oral Kayexelate (for alert patients) - 50-30 g in 50-100 mL of 20% sorbitol
 Rectal Kayexelate – 50 g in 200 mL of 20% sorbitol
 Dialysis (for severe hyperkalemia)
 for shifting potassium
 Glucose – 1 amp of D50 and 5-10 ‘u’ RI IV
 Bicarbonate – 1 amp IV
 Nebulized albuterol – 10-20 mg
 for counteracting cardiac effects (when ECG changes present)
 Calcium gluconate 5-10 mL of 10% solution
 WOF: circulatory overload and hypernatremia in Kayexelate and Bicarbonate administration in pts.
with fragile cardiac function
 WOF: digitalis toxicity for calcium infusion in pts. receiving digitalis

b. Hypokalemia – treatment consists of potassium repletion

 Serum potassium level <4.0 mEq/L
 Asymptomatic, tolerating enteral nutrition: KCl 40 mEq per enteral access × 1 dose
 Asymptomatic, not tolerating enteral nutrition: KCl 20 mEq IV q2h × 2 doses
 Symptomatic: KCl 20 mEq IV q1h × 4 doses (no more than 10 mEq/h if unmonitored, can be
increased to 40 mEq with continuous ECG monitoring, even more in case of imminent cardiac
arrest from malignant arrhythmia-associated hypokalemia)
 Recheck potassium level 2 h after end of infusion; if <3.5 mEq/L and asymptomatic, replace as
per above protocol
3. Calcium
a. Hypercalcemia – treatment required when symptomatic (usually at serum Ca ++ >12 mg/dL (critical level >15
mg/dL)
 Initial treatment aimed repleting associated volume deficit and then inducing brisk diuresis with NS.

b. Hypocalcemia
 Asymptomatic (ionized calcium level < 4.0 mg/dL)
 With gastric access and tolerating enteral nutrition: Calcium carbonate suspension 1250 mg/5
mL q6h per gastric access; recheck ionized calcium level in 3 d
 Without gastric access or not tolerating enteral nutrition: Calcium gluconate 2 g IV over 1 h × 1
dose; recheck ionized calcium level in 3 d
 Acute symptomatic hypocalcemia: IV 10% calcium gluconate to achieve a serum concentration of 7 to
9 mg/dL
4. Phosphorus
a. Hyperphosphatemia - Phosphate binders such as sucralfate or aluminum-containing antacids for lowering
serum phosphorus levels
 with simultaneous hypocalcemia: calcium acetate tablets
 for pts. with renal failure: dialysis

b. Hypophosphatemia
 Phosphate level 1.0–2.5 mg/dL:
 Tolerating enteral nutrition: Neutra-Phos 2 packets q6h per gastric tube or feeding tube
 No enteral nutrition: KPHO4 or NaPO4 0.15 mmol/kg IV over 6 h × 1 dose
 Recheck phosphate level in 3 d
 Phosphate level <1.0 mg/dL:
 Tolerating enteral nutrition: KPHO4 or NaPO4 0.25 mmol/kg over 6 h × 1 dose
 Recheck phosphate level 4 h after end of infusion; if < 2.5 mg/dL, begin Neutra-Phos 2
packets q6h
 Not tolerating enteral nutrition: KPHO4 or NaPO4 0.25 mmol/kg (LBW) over 6 h × 1 dose;
recheck phosphate level 4 h after end of infusion; if < 2.5 mg/dL, then KPHO 4 or NaPO4 0.15
mmol/kg (LBW) IV over 6 h × 1 dose
5. Magnesium
a. Hypermagnesemia – Treatment consists of eliminating exogenous sources of magnesium, correcting
concurrent volume deficits, and correcting acidosis if present
 for acute symptoms: Calcium chloride (5-10 mL) administered immediately to antagonize
cardiovascular effects
 for persistent elevated levels and symptoms: hemodialysis

b. Hypomagnesemia
 Magnesium level 1.0–1.8 mEq/L:
 Magnesium sulfate 0.5 mEq/kg in normal saline 250 mL infused IV over 24 h × 3 d
 Recheck magnesium level in 3 d
 Magnesium level < 1.0 mEq/L (severe) or asymptomatic: 1-2 g Magnesium sulfate IV over 15 min or
over 2 min under ECG monitoring if necessary to correct torsades de pointes
 Magnesium sulfate 1 mEq/kg in normal saline 250 mL infused IV over 24 h × 1 d, then 0.5
mEq/kg in normal saline 250 mL infused IV over 24 h × 2 d
 Recheck magnesium level in 3 d
 Calcium gluconate may be given to counteract rapidly rising magnesium level and correct
hypocalcemia
 If patient has gastric access and needs a bowel regimen:
 Milk of magnesia 15 mL (approximately 49 mEq magnesium) q24h per gastric tube; hold for
diarrhea
Preoperative Fluid Therapy
 Absence of preexisting abnormalities:
o Administration of maintenance fluids whose volume is calculated with the following formula:
 For the first 0-10 kg Give 100 mL/kg per day
For the next 10-20 kg Give additional 50 mL/kg per day
For weight >20 kg Give an additional 20 mL/kg per day
o Alternative approach: replacing calculated daily water losses in urine, stool, and insensible loss with
hypotonic solution – allows kidney some sodium excess to adjust for concentration
o D5 1/4NS at 100 mL/h as initial therapy with potassium added

 Presence of volume deficit

o Prompt fluid replacement, usually with an isotonic crystalloid, depending on serum electrolyte values
o Pts. with cardiovascular signs: bolus of 1-2 L isotonic fluid followed by continuous infusion
o Resuscitation after reversal of the signs of volume deficit (e.g., acceptable VS values, adequate UO (0.5 to 1
mL/kg per hour adult), and after correction of base deficit
o Intensive ICU monitoring to be considered for pts. whose volume deficit is not corrected after initial
challenges, those with impaired renal function, and the elderly
Intraoperative Fluid Therapy
 Hypotension and hemodynamic instability during anesthesia – avoided by correcting known fluid losses, replacing
ongoing losses, and adequate maintenance fluid preoperatively
 Blood loss and ECF losses in major open abdominal surgeries in the form of bowel wall edema, peritoneal fluid,
and wound edema as well as third-space losses associated with large soft tissue wounds, complex fractures and
burns – restored by saline administration (500-1000 mL/h of balanced salt solution)

Postoperative Fluid Therapy

 Should be based on patient’s current estimated volume status and projected ongoing fluid losses
 Isotonic solution on the initial postop period; resuscitation should be guided by restored acceptable VS and UO
 After initial 24 to 48 hrs: fluids can be changed to 5% dextrose in 0.45% saline if unable to tolerate enteral feeding
 Postop diuresis may need replacement of urinary potassium loss
 All measured losses (vomiting, NGT suctioning, drains, UO, insensible losses) - replaced with appropriate
parenteral solutions
Electrolyte Abnormalities in Specific Surgical Patients
 Syndrome of Inappropriate Secretion of Antidiuretic Hormone (SIADH)
o Etiology: head injury or CBS surgery; drugs (morphine, nonsteroidals, oxytocin), hypothyroidism,
glucocorticoid deficiency, malignancies (most often small cancer of the lung, Hodgkin’s dse, thymoma)
o Findings: euvolemic and hyponatremic with elevated urine sodium levels and urine osmolality
o Treatment: restriction of free water to improve hyponatremia (furosemide may induce free water loss)
 For chronic SIADH: demeclocycline and lithium to induce free water loss
 Diabetes Insipidus
o Etiology: central DI – from defect in ADH secretion (pituitary surgery, closed head injury); nephrogenic DI –
associated with hypokalemia, administration of radiocontrast dye, drugs (aminoglycosides, amphotericin B)
o Findings: dilute urine in the case of hypernatremia (diagnosed by documented paradoxical increase in urine
osmolality in response to a period of water deprivation)
o Treatment: free water replacement in mild cases; addition of vasopressin (5 U SQ q 6-8h) for severe cases
 Refeeding Syndrome
o Etiology: rapid and excessive feeding (enteral or parenteral) of patients with severe malnutrition results to
shift in metabolism from fat to carbohydrate substrate, stimulating insulin release and consequent cellular
uptake of electrolytes particularly Mg, K, and Ca.
o Findings: electrolyte abnormalities inducing cardiac arrhythmias, confusion, respiratory failure or death
o Treatment: Thiamine before initiation of feeding; caloric repletion gradually increased over the first week;
correction of electrolyte and fluid deficits
 Acute Renal Failure
o Prompt correction of prerenal azotemia
o Restriction of daily fluid intake in acute tubular necrosis (to match UO and insensible and GI losses)
o Close monitoring of serum K+ for oliguric renal failure
o Dialysis for severe hyponatremia, severe hyperphosphatemia and metabolic acidosis
o Phosphate binders for control of hyperphosphatemia; bicarbonate useful in metabolic acidosis
 Cancer
o Hypovolemic hyponatremia – due to renal loss of Na + caused by diuretics or salt-wasting nephropathy in
chemotherapeutic agents such as cisplatin
o Normovolemic hyponatremia – associated with SIADH from cervical cancer, lymphoma and leukemia
o Hypernatremia – from poor oral intake or GI losses as chemotherapy side effect; DI in CNS lesions
o Hypokalemia – from GI losses associated with diarrhea caused by radiation enteritis or chemotherapy
o Hyperkalemia – can be precipitated by tumor lysis syndrome from massive tumor cell destruction
o Hypocalcemia – can be seen after removal of thyroid or parathyroid tumor or after central neck dissection
that can damage the parathyroid glands; from prostate and breast cancer resulting in increased osteoblastic
activity which decreases serum calcium by increasing bone formation
o Hypomagnesemia – side effect of ifosfamide and cisplatin therapy
o Hypophosphatemia – can be seen in hyperparathyroidism due to decreased phosphorus reabsorption
o Acute hypophosphatemia – in acute leukemia and Tumor lysis syndrome as rapidly proliferating cells take
up phosphorus, or in use of biphosphonates to treat hypercalcemia
o Hypercalcemia – malignancy is the most common cause due to increased bone resorption or decreased
renal excretion
 Treatment: saline volume expansion (decreases renal reabsorption of calcium) then addition of loop
diuretic
 Drugs: biphosphonates (etidronate and pamidronate) – inhibit bone resorption and osteoclastic
activity (slow onset but effect last quickly); calcitonin – inhibites bone resorption and increases renal
excretion of calcium (acts quickly, within 2 to 4 hrs); gallium nitrates – bone resorption inhibitors and
has long duration of activity cause nephrotoxicity; mithramycin – blocks osteoclastic activity but
associated with liver, renal and hematologic abnormalities
o Tumor Lysis Syndrome
 Etiology: in poorly differentiated lymphomas and leukemias (and other malignancies), rapid release of
intracellular metabolites (uric acid, potassium, phosphorus); most commonly develops during
chemotherapy and radiotherapy
 Findings: marked hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia and ARF
 Treatment: volume expansion and correction of electrolyte abnormalities (hypocalcemia should not be
treated unless symptomatic to avoid metastatic calcifications); dialysis for impaired renal function