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Electrolyte Imbalance
Electrolyte Imbalance
IMBALANCE
PRESENTED BY GROUP 11
AKELLO SARAH AND APENJURWOTH VISION
LEARNING OBJECTIVES
• Electrolytes: Electrolytes are minerals in the blood and other body fluids that carry an
electric charge that play a role in metabolic processes.
• Examples: sodium, potassium, chlorides, calcium, magnesium, phosphates and
bicarbonates.
• Electrolyte imbalance: deviation of electrolyte level within body fluids from the normal.
ELECTROLYTES
Sodium
• Deficit : hyponatremia
• Excess: hypernatremia
Potassium
• Deficit: hypokalemia
• Excess: hyperkalemia
CONT.
Calcium
• Deficit: hypocalcemia
• Excess: hypercalcemia
ROUTES OF GAINS AND LOSSES OF
ELECTROLYTES
• Kidney
• Skin
• Lungs
• Gi tracts
HYPONATREMIA
• Hyponatremia can be classified based on temporality (acute <48 hrs; chronic >48 hrs) or
based on serum sodium (mild 130-135 mEq/L (mmol/L); moderate 125-130 mEq/L
(mmol/L); severe <125 mEq/L (mmol/L).
PRESENTATION
Renal
• Diuretics.
• Mineralocorticoid deficiency.
• Salt losing nephropathies.
• Osmotic diuretics.
• Renal tubular acidosis.
CONT.
• The treatment aims at correcting both the underlying disorder as well as the plasma
concentration of Na+.
• Correction of plasma Na+ concentration to greater than 125mEq/L is usually sufficient to
alleviate symptoms.
• Desired value, the Na+ deficit can be estimated using :
Na+ deficit=TBW X (Desired [Na+]-present [Na+])
CONT.
• A plasma sodium concentration greater than 130mEq/L is usually considered safe for
patients undergoing general anesthesia.
• In most circumstances plasma sodium concertation should be corrected to greater than
130mEq/L for elective procedures even in the absence of neurological symptoms.
• This is because lower concentration may result in significant cerebral edema that can be
manifested intraoperatively and a decrease in MAC or postoperatively as agitation,
confusion or somnolence.
COMPLICATIONS
• Neurological manifestations predominate and are generally thought to result from cellular
dehydration.
Restlessness
Lethargy
Hyperreflexia
seizures
Coma, and ultimately death may occur
CAUSES
Correction should be done over 48hours with a hypotonic solution such as 5% dextrose in water.
NB: decrease in plasma Na+ concentration should not proceed at a rate faster than 0.5mEq/L/hr
ANESTHETIC CONSIDERATION
• Hypernatremia has been demonstrated to increase the MAC for inhalation anesthetics
• Elective surgery should be postponed in patients with significant hypernatremia (>
150mEq/L).
• Both water and isotonic fluid deficits should be corrected prior to elective surgery
COMPLICATIONS OF HYPERNATREMIA
• Cerebral edema
• Seizures
• Permanent neurological damage
• Muscle twitching
DIAGNOSTIC APPROACH OF HYPERNATREMIA
• Potassium <3.5 mEq/L (mmol/L) and can be life threatening if serum potassium <2.5
mEq/L (mmol/L).
• A vast majority of potassium is located intracellularly therefore hypokalemia is often due
to a large total body potassium deficit.
• The relationship between potassium level and total body potassium deficit is exponential;
as the potassium level falls progressively lower, this represents an exponentially larger
decrease in the total body potassium deficit.
CONT.
• Clinical features usually occur when serum potassium<2.5 mEq/L (mmol/L) and include:
muscle pain
Cramps
Weakness
Fatigue
Constipation
syncope and palpitations.
CAUSES OF HYPOKALEMIA
GI loss
• Vomiting
• Diarrhea
ECF – ICF shift
• Acute alkalosis
• Hypokalemic periodic paralysis
• Barium ingestion and insulin therapy
DIAGNOSTIC APPROACH OF HYPOKALEMIA
• Goals of treatment are to reduce further potassium loss, replenish potassium stores,
evaluate potential toxicities and treatment of the underlying cause
• Due to the intracellular nature of potassium deficit means that intravascular potassium
must be administered slowly, and time is required for potassium to enter the cells. Rapid
administration may cause serum levels to be elevated even though there is a total body
deficit leading to serum hyperkalemia.
CONT.
• Due to the intracellular nature of potassium deficit means that intravascular potassium
must be administered slowly, and time is required for potassium to enter the cells.
• Rapid administration may cause serum levels to be elevated even though there is a total
body deficit leading to serum hyperkalemia.
HYPERKALEMIA
• Neuromuscular weakness,
• Bradycardia and ventricular tachycardia/fibrillation.
• In practice however, most patients are asymptomatic
EKG FINDINGS
• Only a small portion of total body calcium and phosphate is located in the plasma and it
is the ionized calcium and inorganic phosphate that is regulated by hormones.
• Calcium balance is regulated by the parathyroid hormone and calcitriol which affects
intestinal absorption, bone formation/ resorption and urinary excretion.
CONT.
• Ionized calcium level < 4.4 mg/dl or total calcium level < 8.4 mg/dl (corrected by
albumin).
• Critically ill patients are commonly affected.
• Ionized calcium <0.65 is critically low which could cause hypotension.
CLINICAL PRESENTATION
• Chronic hypocalcemia (develops over years) is often asymptomatic however still possible
to cause neuromuscular irritability.
• Trousseaus sign is a hallmark sign of acute hypocalcemia in which 94% of patients will
have a positive sign.
CONT.
• First, IV loading dose can be given (1 g calcium chloride or 2-3 g calcium gluconate)
followed by maintenance doses if there is an ongoing process with smaller doses (for
example calcium gluconate 1 g q1h as needed).
• IV calcium increases ionized calcium in patients with hypocalcemia, but randomized
trials have not evaluated effect on clinical outcomes.
• IV calcium can eventually be transitioned to oral formulations.
CONT.
• For mild- moderate hypocalcemia, therapy can be started with oral calcium.
• Usual dose is calcium carbonate 1 g every 12 hours.
• Treatment of hypocalcemia is contraindicated in:
Hyperphosphatemia (could cause precipitation of calcium phosphate, calciphylaxis).
Ethylene glycol poisoning (calcium promotes calcium oxalate precipitation in the brain)
Digoxin poisoning.
COMPLICATIONS OF HYPOCALCEMIA
• Mild hypercalcemia may be asymptomatic however rapid increases are more likely is be
associated with symptoms than chronic hypercalcemia. This can present as :
bone pain,
delirium (which could progress to stupor/ coma),
paresthesia,
muscle weakness,
GI symptoms (abdominal pain, pancreatitis, constipation, ileus, nausea/vomiting).
CONT.
NOTE: Hypercalcemia does not commonly affect EKG or cardiac function however short
QT interval may be a common finding.
CAUSES OF HYPERCALCEMIA
• Osteoporosis.
• Kidney stones.
• Kidney failure.
• Arrythmias.
• Impaired nerve function.
EQUIPMENT FOR MANAGING PATIENTS WITH
ELECTROLYTE DISORDERS IN ICU
• Arterial Catheter.
• Balloon Tamponade Tubes.
• Bedside Monitors.
• BIPAP.
• Breathing Tube or Endotracheal Tube.
CONT.
• Epidural Catheter.
• Intra-Aortic Balloon Pump (IABP).
• Intracranial Pressure Monitoring.
• Nasogastric Tubes (NG Tube).
• Pacemaker.
• Pulmonary Artery Catheters.
CONT.
• Suction Catheters.
• Tracheostomy.
• Under Water Seal Drain & Chest Tube.
• Ventilators (Breathing Machines).
• Ventricular Assist Devices.
NURSING ASSESSMENT
Close monitoring should be done for patients with fluid and electrolyte imbalances.
• I&O. The nurse should monitor for fluid I&O at least every 8 hours, or even hourly.
• Daily weight. Assess the patient’s weight daily to measure any gains or losses.
• Vital signs. Vital signs should be closely monitored.
• Physical exam. Physical exam is needed to reinforce other data about a fluid or
electrolyte imbalance.
COMMON NURSING DIAGNOSES
• Excess fluid volume related to excess fluid intake and sodium intake as evidenced by
edema+++.
• Deficient fluid volume related to active fluid loss or failure of regulatory mechanisms
evidenced by reduced skin turgor.
• Imbalanced nutrition: less than body requirements related to inability to ingest food or
absorb nutrients as evidenced by visible muscle wasting.
• Imbalanced nutrition: more than body requirements related to excessive intake as
evidence by body mass index greater than 24.9.
NURSING INTERVENTION
• Monitor turgor. Skin and tongue turgor are indicators of the fluid status of the patient.
• Urine concentration. Obtain urine sample of the patient to check for urine concentration.
• Oral and parenteral fluids. Administer oral or parenteral fluids as indicated to correct the
deficit.
• Oral rehydration solutions. These solutions provide fluid, glucose, and electrolytes in
concentrations that are easily absorbed.
CONT.
• Central nervous system changes. The nurse must be alert for central nervous system
changes such as lethargy, seizures, confusion, and muscle twitching.
• Diet. The nurse must encourage intake of electrolytes that are deficient or restrict intake if
the electrolyte levels are excessive.
REFERNCES
• Fluids and Electrolytes Nursing Care Management and Study Guide (nurseslabs.com)
• Equipment Used in Intensive Care - Intensive Care Hotline
• Tazmini, K., & Ranhoff, A. H. (2020). Electrolyte outpatient clinic at a local hospital - Experience
from diagnostics, treatment and follow-up. BMC Health Services Research, 20(1), 1–7.
https://doi.org/10.1186/s12913-020-5022-0 (Tazmini & Ranhoff, 2020)
• Chapter Electrolytes in the ICU Syed Zaidi, Rahul Bollam and Kainat Saleem .