administration of electrolytes in traumatic injuries

ELECTROLYTE

PRESENTED BY- DR. SUJAY S. PATILPART 1 RESIDENT

DEPT. OF OMFS

CATIONSCATIONS ANIONSANIONSNa- 135-145 m Eq/LNa- 135-145 m Eq/LK- 3.5 – 5.0 m Eq/LK- 3.5 – 5.0 m Eq/LCa- 4.5-5.5 mEq/LCa- 4.5-5.5 mEq/LMg -1.5 – 2.5 mEq/LMg -1.5 – 2.5 mEq/L

HCO3- 22-26 mEq/LHCO3- 22-26 mEq/LCl- 96-106 mEq/LCl- 96-106 mEq/LPO4 – 1.2 -3.0 mEq/LPO4 – 1.2 -3.0 mEq/L

Electrolytes – – These are chemical substances which when dissolved, dissociate into ions and pass electrical potential..

SODIUM

HYPONATREMIA (<135MEQ/L)

Contributing FactorsExcessive diaphoresisWound DrainageNPOCHFLow salt dietRenal DiseaseDiuretics


Assessment findings: Neuro - Generalized skeletal muscle weakness. Headache / personality changes.

Resp.- Shallow respirationsCV - Cardiac changes depend on fluid volumeGI – Increased GI motility, Nausea, Diarrhea (explosive)GU - Increased urine output


Interventions/TreatmentRestore Na levels to normal and prevent further decreases in Na.Drug Therapy – (FVD) - IV therapy to restore both fluid and Na. If severe may see 2-3% saline.

(FVE) – Administer osmotic diuretic (Mannitol) to excrete the water rather than the sodium.

Increase oral sodium intake and restrict oral fluid intake.

HYPERNATREMIA (>145MEQ/L)

Contributing FactorsHyperaldosteronismRenal failureCorticosteroidsIncrease in oral Na intakeNa containing IV fluidsDecreased urine output with increased urine concentration


Contributing factors (cont’d):DiarrheaDehydrationFeverHyperventilation

HYPERNATREMIA (>145MEQ/L) Assessment findings: Neuro - Spontaneous muscle twitches. Irregular contractions. Skeletal muscle weakness. Diminished deep tendon reflexes

Resp. – Pulmonary edemaCV – Diminished CO. HR and BP depend on vascular volume.


GU – Dec. urine output. Inc. specific gravity

Skin – Dry, flaky skin. Edema r/t fluid volume changes.


Interventions/TreatmentDrug therapy (FVD) .45% NSS. If caused by both Na and fluid loss, will administer NaCL. If inadequate renal excretion of sodium, will administer diuretics.

Diet therapyMild – Ensure water intake

POTASSIUM

Low concentrations in ECF

Normal 3.5-5.0 mEq/L

Major ICF cation

Normal daily intake : 40 -60 mEq/L

The rate of potassium excretion is regulated by aldosterone; aldosterone stimulates potassium ion excretion.

HYPOKALEMIA (<3.5MEQ/L)

Pathophysiology – Decrease in K+ causes decreased excitability of cells, therefore cells are less responsive to normal stimuli


Contributing factors:DiureticsShift into cellsDigitalisWater intoxicationCorticosteroidsDiarrheaVomiting


InterventionsAssess and identify those at riskEncourage potassium-rich foodsK+ replacement (IV or PO)Monitor lab valuesD/c potassium-wasting diureticsTreat underlying cause

HYPERKALEMIA (>5.0MEQ/L)

Pathophysiology – An inc. in K+ causes increased excitability of cells.


Contributing factors:Increase in K+ intakeRenal failureK+ sparing diureticsShift of K+ out of the cells


InterventionsNeed to restore normal K+ balance:Eliminate K+ administrationInc. K+ excretionLasixKayexalate (Polystyrene sulfonate)

Infuse glucose and insulinCardiac Monitoring

CHLORIDE Chloride (Cl-) - 95-103 mEq/liter

Major ECF anionhelps balance osmotic potential and electrostatic equilibrium between fluid compartments

plasma membranes tend to be leaky to Cl- anions

Regulation:aldosterone

HOMEOSTATIC IMBALANCES

Hypochloremia - results in muscle spasms, coma [usually occurs with hyponatremia] often due to prolonged vomiting

Causes:

metabolic alkalosis

Respiratory acidosis

emphysema

Adrenal cortical insufficiency

thiazides

diarrhea

HYPERCHLOREMIA

Causes: hyper chloremic acidosis

Respiratory alkalosisDehydrationDiabetes insipidus renal tubular acidosis

CALCIUM

Normal 4.5-5.5 mEq/L

99% of Ca in bones, other 1% in ECF and soft tissues

Total Calcium – bound to protein – levels influenced by nutritional state

Ionized Calcium – used in physiologic activities – crucial for neuromuscular activity

CALCIUM

Required for blood coagulation, neuromuscular contraction, enzymatic activity, and strength and durability of bones and teeth

Nerve cell membranes less excitable with enough calcium

Ca absorption and concentration influenced by Vit D, calcitriol (active form of Vitamin D), PTH, calcitonin, serum concentration of Ca and Ph.

HYPOCALCEMIA (<9.0MG/DL)

Contributing factors:Dec. oral intakeLactose intoleranceDec. Vitamin D intakeEnd stage renal diseaseDiarrhea


Contributing factors (cont’d):

Acute pancreatitis

Hyperphosphatemia

Immobility

Removal or destruction of parathyroid gland

HYPOCALCEMIA (<9.0MG/DL) Assessment findings: Neuro –Irritable muscle twitches.Positive Trousseau’s sign. Positive Chvostek’s sign.

Resp. – Resp. failure d/t muscle tetany.CV – Dec. HR., dec. BP, diminished peripheral pulsesGI – Inc. motility. Inc. BS. Diarrhea


Interventions/TreatmentDrug TherapyCalcium supplementsVitamin D

Diet TherapyHigh calcium diet

Prevention of InjurySeizure precautions

HYPERCALCEMIA (>10.5MG/DL)

Contributing factors:Excessive calcium intakeExcessive vitamin D intakeRenal failureHyperparathyroidismMalignancyHyperthyroidism

HYPERCALCEMIA (>10.5MG/DL)

Assessment findings: Neuro – Disorientation, lethargy, coma, profound muscle weakness Resp. – Ineffective resp. movement CV - Inc. HR, Inc. BP. , Bounding peripheral pulses, Positive Homan’s sign. Late Phase – Bradycardia, Cardiac arrest GI – Dec. motility. Dec. BS. Constipation GU – Inc. urine output. Formation of renal calculi

HYPERCALCEMIA (>10.5MG/DL) Interventions/Treatment Eliminate calcium administration Drug Therapy Isotonic NaCL (Inc. the excretion of Ca) Diuretics Calcium reabsorption inhibitors (Phosphorus) Cardiac Monitoring

MAGNESIUM

Normal 1.5 to 2.5 mEq/L

Ensures K and Na transport across cell membrane

Important in CHO and protein metabolism

Plays significant role in nerve cell conduction

Important in transmitting CNS messages and maintaining neuromuscular activity

HYPOMAGNESEMIA (<1.4MEQ/L) Contributing factors: Malnutrition Starvation Diuretics Aminoglcoside antibiotics Hyperglycemia Insulin administration

HYPOMAGNESEMIA (<1.4MEQ/L)

Assessment findings:*Neuro - Positive Trousseau’s sign. Positive Chvostek’s sign. Hyperreflexia. Seizures*CV – ECG changes. Dysrhythmias. HTN*Resp. – Shallow resp.*GI – Dec. motility. Anorexia. Nausea

HYPOMAGNESEMIA (<1.4MEQ/L) Interventions: Eliminate contributing drugs IV MgSO4 Assess DTR’s hourly with MgSO4 Diet Therapy

HYPERMAGNESEMIA (>2.0MEQ/L) Contributing factors: Increased Mag intake Decreased renal excretion

HYPERMAGNESEMIA (>2.0MEQ/L) Assessment findings:Neuro – Reduced or weak DTR’s. Weak voluntary muscle contractions. Drowsy to the point of lethargyCV – Bradycardia, peripheral vasodilatation, hypotension. ECG changes.

HYPERMAGNESEMIA (>2.0MG/DL) Interventions Eliminate contributing drugs Administer diuretic Calcium gluconate reverses cardiac effects Diet restrictions

PHOSPHOROUS Normal 2.5-4.9 mg/dL

Intracellular mineral

Essential to tissue oxygenation, normal CNS function and movement of glucose into cells, assists in regulation of Ca and maintenance of acid-base balance

Influenced by parathyroid hormone and has inverse relationship to Calcium

HYPOPHOSPHATEMIA (<2.5MG/L) Contributing Factors: Malnutrition Starvation Hypercalcemia Renal failure Uncontrolled DM

HYPOPHOSPHATEMIA (<2.5MG/L) Assessment findings: (Chart 13-7)Neuro – Irritability, confusionCV – Dec. contractilityResp. – Shallow respirationsMusculoskeletal - RhabdomyolysisHematologic – Inc. bleeding

Dec. platelet aggregation

HYPOPHOSPHATEMIA (<2.5MG/L) Interventions Treat underlying cause Oral replacement with vit. D IV phosphorus (Severe) Diet therapy

Foods high in oral phosphate

HYPERPHOSPHATEMIA (>4.5MG/L) Causes few direct problems with body function. Care is directed to hypocalcemia. Rarely occurs

administration of electrolytes in traumatic injuries

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