Fluids & Electrolytes.pdf

Isotonic solution – equal concentration of solute and MODULE 6: FLUID & ELECTROLYTES IMBALANCES solvent Hypotonic solution – ther...

Isotonic solution – equal concentration of solute and MODULE 6: FLUID & ELECTROLYTES IMBALANCES solvent Hypotonic solution – there’s increase of solute in the BODY FLUID COMPARTMENTS cell; cell will swell, even ruptures (hemolyse); less INTRACELLULAR FLUID COMPARTMENT: consists of the concentrated fluid in the body’s cells and comprises 70% of the body Hypertonic solution – less solute in cell; SHRINKING fluids. there’s cell shrinking for fluid will move to extra Maintain normal body temperature compartments; more concentrated eg: D50 Water, given to pts who are dehydrated EXTRACELLULAR FLUID COMPARTMENT: is found in spaces between the cells and comprises 30% of body fluids. Maintain blood volume RENIN ANGIOTENSIN ALDOSTERONE SYSTEM (RAAS) STIMULI RENIN SUBSTRATE infant: 80% fluid male adult; 60% female; 50% Kidneys Renin Renin convers secrete travels to angiotensinogen 1. INTRAVASCULAR COMPARTMENT RENIN the liver to Angiotensin I 2. INTERSTITIAL COMPARTMENT Intravascular and interstitial fluids are separated by a Angiotensin II Angiotensin capillary endothelium that’s freely permeable to water, travels to Angiotensin I electrolytes, and other solutes; consequently, the Adrenal converted to I travels to Angiotensin II lungs composition of both types of extracellular fluid is similar. Gland The composition of intracellular fluid (ICF) differs from that of the extracellular fluid (ECF) - Sodium and water retention Adrenal Gland ICF has higher concentrations of protein, secretes - Increased Potassium potassium, magnesium, phosphate, and sulfate ALDOSTERONE excretion ICF has lower concentrations of sodium, calcium, chloride, and bicarbonate Stimulus or Triggers for RAA: maintain fluid balance Active transport helps maintain different - hyponatremia concentrations of sodium and potassium in the ICF - hyperkalaemia and ECF - decrease blood volume (haemorrhage) - Decrease Renal Blood flow inversely with body fat cause fat has no water - Decrease plasma intravascular: blood plasma & lymph; 5% interstitial: distributed diffusely through loose tissue ALDOSTERONE: retention of sodium surrounding the cell; 24% specialized compartment: 1% K+ & Na+ = inversely proportional BODY FLUID OSMOLARITY FLUID BALANCE When a semipermeable membrane separates two - The body gains & loses water daily through fluid intake solutions of unequal solute concentration, water shifts by & output. OSMOSIS. The ability of the more concentrated solution - Water enters the body via the GI tract and leaves via the to attract water is called OSMOTIC ACTIVITY. skin, lungs, GIT, and urinary tract. These gains and The OSMOTIC PRESSURE of a solution is usually balances must be balanced to stabilize the body's water measured in terms of OSMOLARITY content and to permit proper physiologic functioning Body fluids have low concentrations of dissolved 2 MECHANISMS OF FLUID BALANCE particles their osmolarity usually is expressed in 1. Thirst (conscious desire for water) primarily regulates milliosmols per liter (mOsm/L). fluid intake 2. Counter current mechanism, the kidneys can regulate *Osmolality expressed in osmolality/kilogram (osml/kg) fluid output by excreting urine of greater or lesser *Less concentration to more concentration = OSMOSIS concentration. Osmolarity – Concentration of solution, express in total NORMAL FLUID INTAKE AND LOSS IN ADULTS number of solute/L (osml/L) INTAKE OUTPUT NOTE: “Movement of water/fluid is from the area of less Water in 1,000 mL Skin 500 mL concentrated to the area of more concentrated. To maintain food a state of homeostasis” Water from 300 mL Lungs 300 mL oxidation A solution of 1 Liter of water that contains 1 gram molecular Water as 1,200 mL Feces 200 mL weight of a substance that doesn't dissociate in solution liquid (such as glucose) has an osmolarity of 1 Osm/L = Kidneys 1,500 mL OSMORALITY TOTAL 2,500 mL TOTAL 2,500 mL A solution of 1 L of water that contains 1 gram molecular weight of an electrolyte that dissociates into 2 ions (such as sodium chloride) has an osmolarity of 2 Osm/L NOTES  FLUID VOLUME IMBALANCES SYNDROME OF INAPPROPRIATE ANTIDIURETIC VOLUME VOLUME HORMONE SECRETION (SIADH) DEFICIT OVERLOAD - Increase ADH ASSESSMENT ↑ temp No changes in Rapid and temp Assessment weak pulse ↑ pulse slightly Anorexia, nausea, ↑ RR ↑ RR, SOB, vomiting Lethargy Poor skin dyspnea, turgor – skin rales Headache cool, moist (crackles) ⬇deep tendon Peripheral reflexes Hypotension Edema Tachycardia Emaciation, wt. o ⬆ circulatory bld vol loss (bloated) HPN o ⬇ urinary output Dry eyes Analysis sockets, Muffled Heart Sounds ADH does fxn properly, ADH is released even when mouth and plasma hypoosmolalilty is present mucous Jugular vein Dx test: Anxiety, distention o Serum Na ⬇ apprehensio Urine specific o plasma osmolality ⬇ n, gravity o ⬆ specific gravity exhaustion, 1.030 BUN - lons may be positively (cations) charged or negatively ↓ urine output (anions) charged ↑ HCT Electrolytes ↓ Peripheral pulses Cations (+) Ca PLAN Force fluids Administer K /IMPLEMENTATION Provide diuretics Na isotonic IV Restrict fluids Mg fluids e.g. Na- restricted LR or PNSS diet Anions (-) I&O hourly (average Bicarbinate Daily wt (1L daily diet: 6- Chloride Fluid = 1kg 15 mg Na) Phosporus or 2.2 lbs) Daily wt Monitor VS Assess breath Cell: K (+) – P (-) Check skin sounds Outside the cell: Na (+) Cl (-) turgor Check Assess urine feet/ankle/s FUNCTIONS OF ELECTROLYTES specific acral region 1. Promote neuromuscular irritability gravity for edema 2. Maintain body fluid vol. & osmolality Semi-Fowler’s 3. Distribute body water between fluid compartments position if 4. Regulate acid-base balance dyspneic ICF AND ECF ELECTROLYTE COMPOSITIONS Elevated HOB ELECTROLYTE COMPOSITION (mEq/L) ADH Disorders ICF ECF DIABETES INSIPIDUS Sodium 10 135 - 145 - Decrease/deficient ADH Potassium 140 3.5 - 5.0 Calcium 10 4.5 - 5.8 Assessment: Magnesium 40 1.5 - 2.5 Excessive urine output Chloride 4 98 -108 Chronic severe dehydration Bicarbonate 10 24 - 28 Excessive thirst Phosphate 100 1 - 1.5 Anorexia, wt loss Weakness MECHANISMS OF ELECTROLYTE BALANCE Constipation - Electrolytes profoundly affect water distribution, osmolarity and acid-base balance Analysis - The body uses various mechanisms to maintain Deficiency of ADH electrolytes balance Dx test: o Low urine spec gravity o Urinary osmolality below plasma level o High serum Na NOTES  SODIUM is regulated chiefly by the kidneys through the *Potassium and sodium have an inversely proportional action of Aldosterone relationship o Sodium is absorbed readily from food by the small *Chloride and sodium have a directly proportional intestine relationship o It’s excreted through the skin and kidneys Sodium and water balances are closely interrelated SODIUM IMBALANCES 135-145 HYPONATREMIA OSMOTIC REGULATION OF SODIUM AND WATER GEN. INFO: Serum sodium level Excessive sodium loss Serum Sodium level decreases (water excess) increases (water Excessive water gain in extracellular fluid Inadequate deficit) sodium intake ECF osmolality decreases Serum osmolality falls Sodium moves out of ICF into ECF (water moves into Serum Osmolarity rises below 280 mOsm/kg more than 300 ICF) cellular swelling Eventually causes CNS changes mOsm/Kg - kidney disease (increase urination) Thirst diminishes, leading - Increase defecation Thirst increases, to decreased water intake leading to increased May be classified according to ECF volume: water intake Abnormally decreased (Hypovolemic hyponatremia) ADH release is a.k.a DEPLITIONAL HYPONATRIMIA suppressed o sodium and water levels decreased in ADH release increases extracellular area o sodium loss is greater than water loss Renal water excretion *due to inadequate sodium intake increases * increase sodium loss than water. Renal water excretion diminishes Abnormally increased (Hypervolemic hyponatremia) a.k.a DILUTION o Sodium and water levels increase in extracellular Serum Osmolarity are normalizes o Water gain is greater than sodium gain *due to increase water intake; over fluid infusion Equal to ICF (Isovolemic hyponatremia) POTASSIUM is also regulated by the kidneys through o sodium levels may appear low because too the action of Aldosterone much fluid is in the body o Most of the body's potassium is absorbed from food o no physical fluid signs of fluid volume excess in the GIT o Total body sodium remains stable o The amount of potassium excreted in the urine normally equals dietary potassium intake CAUSES: Prolonged diuretic therapy CALCIUM in blood is in equilibrium with calcium salts in Excessive diaphoresis bone Insufficient sodium intake o Calcium is regulated primarily by Parathyroid hormone Excessive loss from trauma (severe burns) Severe Gl o Parathyroid hormone controls both calcium uptake fluid loss due to numerous causes from the intestinal tract and calcium excretion by the Hypotonic fluid administration kidneys Compulsive water drinking Labor induction with Oxytocin (Pitocin) MAGNESIUM is regulated by aldosterone Adrenal insufficiency Salt-losing nephritis o Aldosterone controls renal reabsorption of Cystic fibrosis magnesium Alcoholism o Magnesium is absorbed from the GIT and excreted SIADH in the urine, breastmilk, and saliva. Repeated tap water enemas CHLORIDE is regulated by the kidneys; chloride ions ASSESSMENT FINDINGS: move with sodium ions. Headache N/V BICARBONATE is regulated by the kidneys Muscle twitching o The kidneys may excrete, absorb, or form Tremors bicarbonate Weakness o Bicarbonate plays an important role in regulating Normal or increased weight acid base balance Irritability *alkaline in nature Hypotension Tachycardia PHOSPHATE is regulated by the kidneys Decreased urine output o Is absorbed well from food Decreased skin turgor o Is incorporated with calcium in bone Is regulated by Dry cracked mucous membranes parathyroid hormone along with calcium Seizures Coma NOTES DIAGNOSTIC FINDINGS: DIAGNOSTIC FINDINGS: Serum level less than 135 mEq/L, serum chloride level Serum Na greater than 145mEq/L less than 96 mEq/L Chloride levels elevated Urine specific gravity less than 1.010 Urine specific gravity greater than 1.030 Serum osmolality less than 280 m0sm/Kg (dilute) Serum osmolality greater than 300mOsm/Kg TREATMENT: TREATMENT: For mild hyponatremia: restricted fluid intake and Oral Oral or IV fluid replacement: fluids given gradually over sodium supplements 48 hrs For Hyponatremia r/t hypovolemia: Isotonic IVF to Sodium-free solutions should be used restore volume and High sodium foods Sodium restricted diet For severe hyponatremia (less than 120 mEq/L) Diuretic administration accompanied by oral or IV fluid o May require treatment in the ICU replacement to increase sodium excretion o Hypertonic saline solution infusion ( 3%-5% NaCl) ▪ Causes water to shift out of cells NSG MGT: ▪ May lead to intravascular water Monitor and record fluid intake and output overload and brain damage Monitor daily weight for changes Fluid volume overload may be prevented with slow Assess changes in LOC infusion of hypertonic saline in small volumes. Monitor V/S: BP, Pulse rate, and temperature Assess No hypertonic saline solutions are given except in rare skin and mucus membranes for signs of breakdown and instances of severe symptom producing hyponatremia. infection Provide oral hygiene NURSING MGT: Monitor I&O POTASSIUM IMBALANCES 3.5-5.0 Restrict fluid intake HYPOKALEMIA Administer parenteral fluids as ordered, sodium should Generally results from excessive excretion or be administered sparingly to prevent increases in fluid inadequate intake of potassium volume Potassium functions as: a major intracellular cation, Monitor and record VS, particularly BP balances sodium in the ECF maintaining Assess skin integrity at least every 8 hours electroneutrality of body fluids. Monitor sodium levels to determine treatment Freely excreted by the kidneys and hot stored by the effectiveness body Increased cellular uptake of potassium occurs in Monitor daily weight for increases linked to water excess insulin excess and certain disorders, such as chronic or decreases due to the success of fluid restrictions kidney disease. Teachings to prevent hyponatremia POTASSIUM HYPERNATREMIA - involved in cardiac rhythm - Indicates a water deficit in the ECF, which moves water - necessary for nerve transmission out of the ICF to equilibrate, cause could be increased - Gastric irritant salt intake - Usually results in ICF volume deficit; signs of HYPOKALEMIA hypervolemia may be present from increased ECF - use of Thiazide & Furosemide volume in the blood vessels - Alcoholism: decrease in potassium absorption - Possible result: cell shrinking - Mg and K are directly proportional - Impaired neurologic and cognitive function - Give KALIUM DURULES *Severe hypernatremia is not good; it can lead to neurologic CAUSES: and cognitive S&S Prolonged diuretic therapy with thiazides, Furosemide, - When you ingest lots of sodium, thirst center is activated or other drugs due to cell dehydration (water in cell moves out). Inadequate K intake Administration of potassium CAUSES: Severe diaphoresis Significantly decreased water intake Severe Gl fluid losses Hypertonic fluid administration, Hypertonic tube feedings Excessive insulin Excessive salt ingestion Excessive stress Severe watery diarrhea or severe insensible water Hyperaldosteronism losses (prolonged high fever) Acute alcoholism Cushing Syndrome (Endocrine disturbance specifically ASSESSMENT FINDINGS: thyroid) Extreme thirst Restlessness and agitation ASSESSMENT FINDINGS: Anorexia Anorexia N/V Nausea and vomiting Tachycardia Drowsiness Low grade fever Dry sticky tongue Leg cramps HTN Muscle weakness esp. in the legs Oliguria (less than 30 cc/hr) – Anuria (less than 10 cc/hr) Dereased/absent DTR Seizures Paresthesia Disorientations Decreased bowel sounds Hallucinations Decreased bowel motility (ileus) NOTES  Constipation Hyponatremia Cardiac arrythmias: premature atrial and ventricular Hypoaldosteronism *Aldosterone is used for excreting contractions potassium Metabolic/respi acidosis DIAGNOSTICS: Acute renal failure ECG changes o depressed ST segment, flattened/inverted T waves Metabolic acidosis: Bicarbonate is retained thus increasing o characteristic U waves Serum K less than 3.5 the potassium level (retained as well) mEq/L Elevated pH and bicarbonate levels (alkaline) Cell damage: the potassium leaks to extracellular due to cell Increased 2 urine level damage. Decreased serum magnesium levels DIAGNOSTIC FINDINGS: TREATMENT: Serum K>than 5.0 mEq/L A potassium low sodium diet Decreased arterial pH (acidosis) Oral potassium supplementation (Kalium Durule) ECG abnormalities that can lead to asystole if not o potassium salts, potassium chloride reversed IV potassium replacement therapy for certain patients o Tall T waves o those with severe hypoK o Widened QRS complex o those who can’t take oral supplements o prolonged PR interval Potassium sparing diuretics o depressed ST segment o Absent/flat P waves NSG MGT: Observe patients taking diuretics carefully because they ASYSTOLE: no heart rhythm are more at risk Monitor patients taking digoxin Note: Potassium moves into the serum as hydrogen ion Assess patient's respiratory rate, depth and pattern (acidic) moves into the cell. o hypokalemia may weaken and paralyze respiratory muscles Monitor I/O carefully TREATMENT: Check for signs of constipation (don't use laxatives that Administration of sodium polystyrene sulfonate promote potassium loss) (Kayexalate) Administer oral potassium replacements with plenty of o Onset of action usually delayed several hours, water to prevent gastric irritation. duration of action hours is 4-6 o Should be administered with Sorbitol or another NEVER administer IV potassium as bolus or IV push, osmotic substance to promote medicine's which could be fatal. excretion 1L of urine = 40 mEq/L of K+ Loop diuretics may be given Restricted dietary potassium intake HYPERKALEMIA KAYEXALATE: Cation exchange; given to excrete Results from impaired renal excretion of K or excessive potassium K intake Can also occur in metabolic acidosis For SEVERE CASES: Excessive serum potassium acts as myocardial Cardiac monitoring depressant 10% calcium gluconate and 10% Calcium chloride IV to Causes smooth muscle hyperactivity counteract the myocardial effects of hyperk Causes skeletal muscle weakness usually the initial Sodium bicarb for acidosis symptom that prompts pts to seek health care Insulin with IV hypertonic dextrose (D50 Water) assistance o happens particularly in the GIT * Potassium moves into the serum/blood as hydrogen moves o can result in diarrhea into the cell – hydrogen are acidic in nature Insulin: Opens the cell so glucose can enter the cell and *when you have an acid base balance, one of the first to potassium goes with the glucose. response is the kidney by excreting or retaining bicarbonate for bicarbonate is alkaline in nature which help in neutralizing NSG MGT: somehow to maintain balance Monitor patients at risk: those with acidosis, potassium sparing diuretics, those receiving potassium. ACID-BASE BALANCE - first to respond is KIDNEY (retaining or excreting Check adequacy of urine output before IV potassium BICARBONATE (alkaline or base)). administration Assess V/S CAUSES Monitor bowel sounds Increased dietary potassium intake, esp. with decreased Assess sensory and motor functions of extremities urine output Patients NOT on digoxin may receive calcium gluconate Excessive administration of potassium supplements Hyperkalemic pateints on digoxin may NOT take calcium Excessive use of salt substitutes gluconate Use of potassium-sparing diuretics Prepare for dialysis in acute cases Severe widespread cell damage from several possible Administer Kavexalate as ordered causes Administration of large volumes of blood nearing its CALCIUM GLUCONATE: exacerbate or potentiate the expiration date effects of DIGOXIN which could lead to cardiac arrest. Lysis of tumors cells from chemotherapy NOTES  CALCIUM IMBALANCES 4.5-5.8 TREATMENTS: HYPOCALCEMIA IV calcium gluconate IV calcium chloride - Results from abnormalities of PTH secretion or of Magnesium replacement may also be needed inadequate dietary intake or excessive losses of bound, Vitamin D supplements ionized (unbound) or total body calcium. Oral calcium supplements - Can cause skeletal and neuromuscular abnormalities. Aluminum hydroxide to bind with phosphorus - Impairs clotting mechanisms - 1/2 of ingested calcium is bound in protein NSG MGT: - 1/2 of ionized calcium is absorbed In the gut along with Carefully assess patient's risk for hypocalcemia Vit. D Monitor V/S - Results in increased neural excitability and spontaneous Monitor respiratory status stimulation of sensory and motor fibers Tracheostomy set and Calcium gluconate at bedside post thyroidectory/parathyroidectomy * Calcium main function: blood clotting and skeletal muscle Check Chvostek's and Trousseau's sign contraction – one of the clotting factors Initiate seizure precautions * Calcium level in the blood’s primary regulator is parathyroid hormone Reorient confused clients * Parathyroid hormone is necessary for both calcium uptake and calcium excretion Calcium & Phosphorus: Inversely proportional *Calcium, VIT D, & UV lights: connected Mg and Ca: Inversely proportional *calcium and phosphate: inversely proportional. Mg and Phosphorus: Direct relationship Mg and Potassium: Direct relationship CAUSES: Surgically induced or primary hypoparathyroidism HYPERCALCEMIA Acute renal failure - Occurs when rate of calcium entry in the ECF exceeds rate of renal calcium excretion Chronic malabsorption syndrome - Bone resorption and formation usually occurs at the Vit. D deficiency same rate Inadequate exposure to ultraviolet light - Causes a decrease in cell membrane excitability Insufficient dietary intake of calcium - Especially affects the tissues of skeletal muscle, heart Low magnesium levels (affects PTH secretion) muscle and nervous system Hypoalbuminemia - Increased intestinal absorption of calcium Hyperphosphatemia (interferes with calcium absorption) - Renal abnormalities that interfere with calcium secretion Anticonvulsants: phenobarbital and phenytoin and excretion. Loop duiretics - Patients with metastatic cancer at especially high risk Antineoplastic drugs RISK FOR FRACTURE: due to calcium is increase in the blood instead in the bone. ASSESSMENT FINDINGS: Muscle cramps and tremors CAUSES: Hyperactive DTR Primary hyperparathyroidism (most common cause) Paresthesia of fingers and toes Excessive intake of Ca supplements Tetany (unnecessary muscle contraction) Excessive use of calcium containing antacids o + Trousseau's sign – involuntary contraction of the Prolonged immobility muscles in the hand and wrist (i.e., carpopedal Use of lithium or thiazide diuretics spasm) that occurs after the compression of the Metastatic carcinoma upper arm with a blood pressure cuff. Thyrotoxicosis – due to hyperthyroidism o + Chvostek's sign – a twitch of the facial muscles Hypophosphatemia that occurs when gently tapping an individual's cheek, in front of the ear ASSESSMENT FINDINGS: Spasms: laryngeal and bronchial muscles Lethargy (may progress to coma) Brittle nails or dry hair and skin Increased risk of Fx Muscle weakness or flaccidity Irritability Hyporeflexia Seizures Constipation Polyuria TROUSSEAU'S SIGN: 2-5 min, use of BP cuff & inflated 20 Extreme thirst mmHg higher than the previous BP for 3 min. If there is Urinary calculi spasm, it is positive sign. Tetany or abnormal spasms. Pathologic fractures and bone pain CHVOSTEK'S SIGN: tap the facial nerve, 2 cm anterior the Metastatic calcifications earlobe below the zygomatic arc. If there is twitching of facial Arrythmias and cardiac arrest muscle means TETANY. SPASTIC PARALYSIS: HYPOCALCEMIA DIAGNOSTIC FINDINGS FLACCID PARALYSIS: HYPERCALCEMIA ECG: prolonged QT interval and ST segment DIAGNOSTICS: Serum calcium less than 4.5 mEq/L Serum calcium elevated Low albumin level Bone changes in Xray Prolonged prothrombin and partial thromboplastin time ECG changes: Albumin is a protein; 1/2 of calcium is bound in protein. Shortened QT interval Prolonged PR interval Flattened T waves Heart block NOTES TREATMENTS: NURSING INTERVENTIONS: Dietary intake reduced Monitor patients at risk: esp. pts. On TPN with no D/C use of medications with calcium phosphorus supplements Calcium excretion measures: Monitor V/S and V/O: remember hypophosphatemia o Hydration lead to respi failure, low cardiac output, confusion, o NSS infusion seizures and coma Check neurologic status o Loop diuretics Monitor for evidence of heart failure and respi failure o Hemodialysis/peritoneal dialysis Assess frequently for evidence of decreased muscle o Calcitonin (Miacalcin) administration strength, such as weak hand grasps slurred speech. Administer prescribed phosphorus supplements Parathormone: From the bone towards the blood Infuse IV phosphorus solutions slowly (watch for signs Calcitonin: From the blood towards the bone for hypocalcemia and hyperphosphatemia) Be aware that potassium phosphate can cause tissue sloughing and necrosis if infiltrated. NSG MGT: Initiate safety precautions for pts, with altered LOC Monitor patients at risk: parathyroidism, cancer, long Reorient client term bed rest and immobility Assist with ADL Ambulate client ASAP if tolerated Monitor I&O HYPERPHOSPHATEMIA Encourage oral fluids (3-4 L) daily unless Most commonly results from the kidneys inability to contraindicated Strain all urine, check for flank pain excrete excess phosphorus along with increase release Ensure safety of phosphorus from damaged cells If pt. is taking digoxin watch for signs of toxicity Causes few clinical problems by itself (but may lead to Offer emotional support other imbalances such as hypocalcemia) Provide health teachings on recognizing S/Sx Signs and symptoms are usually associated with hypocalcemia effects PHOSPHORUS IMBALANCES 1.0-1.5 HYPOPHOSPHATEMIA CAUSES * Phosphate is regulated by the kidneys Acute renal failure/ chronic kidney disease * Phosphorus are redistributed from ECF to ICF during Excessive dietary intake glucose IV administration; also important as an aid to Excessive Vit. D use (results in increased Phosphorus calcium and regulated by parathyroid hormone absorption) Hypoparathyroidism CAUSES Cancer therapy Decreased intestinal absorption of phosphorus Excessive use of laxatives and phosphorus-based Wasting of phosphorus as a mechanism of acid balance enema IV glucose administration Ruptured abdominal viscera Prolonged vomiting Thiazide diuretics, loop diuretics ASSESSMENT FINDINGS: Alcoholism/ alcohol withdrawal Tetany Insulin administration/hyperglycemia Circumoral paresthesia High calcium intake Muscle spasms, cramps, pain, weakness Positive Trousseau's and Chvostek's signs ASSESSMENT FINDINGS: Decreased mental function, delirium seizures Paresthesia Soft tissue calcification (with long standing Profound muscle weakness hyperphosphatemia) Anorexia Rapid shallow respirations (potential for respiratory DIAGNOSTIC FINDINGS depression) Serum phosphorus greater than 1.5 mEq/L Altered LOC Serum calcium less than 4.5 mEq/L Loss of bone density Skeletal changes revealed in Xray studies (due to Bone pain osteodystrophy; seen in chronic cases) Fractures Increased BUN and creatinine levels which reflect worsening renal function ECG changes characteristic of * Calcium and phosphate in the body react in opposite ways: hypocalcemia (prolonged QT interval and ST segment) as blood calcium levels rise, phosphate levels fall. A hormone called parathyroid hormone (PTH) regulates the TREATMENT: levels of calcium and phosphorus in the blood. Reduce phosphorus intake Drug therapy: used to decrease absorption of DIAGNOSTIC FINDINGS: phosphorus in the GIT (aluminum, magnesium, calcium Serum phosphorus levels less than 1.0 mEq/L gel, phosphate binding antacids, calcium salts (Calcium X-rays revealing skeletal changes/fractures carbonate and calcium acetate) Abnormal electrolytes: decreased Magnesium and IV Saline solution infusion for severe cases increased Calcium levels Acetazolamide Hemodialysis/peritoneal dialysis TREATMENT Diet high in phosphorus (egg, nuts, whole grains, meat, fish, milk products) Oral phosphorus supplements: Neutra-Phos, Neutra- Phos-K IV phosphorus may be administered NOTES NURSING INTERVENTIONS: HYPERMAGNESEMIA Monitor patients at risk: those with hypocalcemia, - Usually results from acute renal failure or chronic kidney receiving phosphorus in IV infusions, enemas, or disease Produces sedative effect on the neuromuscular laxatives. junction Inhibits acetylcholine release Monitor V/S: keeping in mind signs and symptoms of - Can cause hypotension and cardiac arrest hypocalcemia. Monitor fluid intake and output. CAUSES: Monitor for neuromuscular irritability, which Acute renal failure and chronic kidney dse accompanies high phosphate levels. Excessive use of magnesium-containing antacids or Prepare patient for possible dialysis. laxatives Excessive administration of IV MgSO4 Hemodialysis with a magnesium-rich dialysate MAGNESIUM IMBALANCES 1.5-2.5 Untreated DKA HYPOMAGNESEMIA ASSESSMENT FINDINGS: * Normally, the parathyroid glands release a hormone that Lethargy and drowsiness increases blood calcium levels when they are low. Depressed neuromuscular activity Magnesium is required for the production and release of Depressed respirations parathyroid hormone, so when magnesium is too low, Sensation of warmth throughout the body insufficient parathyroid hormone is produced and blood Hypotension calcium levels are also reduced (hypocalcemia). Bradycardia Cardiac arrest CAUSES Poor dietary intake of magnesium DIAGNOSTIC FINDINGS: Poor magnesium absorption the GIT Serum magnesium greater than 2.5 mEq/L Excessive Mg loss from the GIT ECG changes: widened QRS complex, prolonged PR Excessive GIT excretion by the kidneys interval, and Tall T wave Increases muscle irritability and contractility Causes decreased BP and may result in ventricular TREATMENT: arrythmias Produces S/Sx similar to hypokalemia Oral or IV fluids (applies to patients with normal renal (conditions commonly occur simultaneously) function) Loop diuretics ASSESSMENT FINDINGS For Magnesium toxicity, 10% Calcium gluconate Tachycardia, anythmias, hypotension Hemodialysis for severe renal dysfunction Tremors/tetary Hypalactive DTR + Babinski reflex, + Chvostek's and NSG MGT: Trousseau's signs Monitor the patient at risk Confusion, dizziness, irritability Monitor V/S: particularly BP and respirations Seizures Check for flushed skin and diaphoresis Coma Monitor urine output Assess for changes in mental status DIAGNOSTIC FINDINGS: Check neuromuscular status Serum Mg less than 1.5 mEq/L Monitor lab tests and report abnormalities Hypocalcemia Monitor for hypocalcemia Hypokalemia ECG changes flattened T waves, slightly widened QRS complex, prominent U wave TREATMENT: Dietary magnesium intake increased Oral magnesium supplements encouraged IV or deep IM injections of MgSo4 used for severe cases NSG MGT: Monitor patients at risk. Closely monitor a pt. with hypomagnesemia who is also taking digoxin for signs and symptoms of toxicity Monitor patient's respi status, as magresium deficiency can cause laryngeal stridor and compromise airway Assess mental status Evaluate neuromuscular status regularly: hyperactive DTR, tremors, tetany. Check for Chvostek's and trousseau's sign Check for hypocalcemia and hypokalemia Check for dysphagia before giving food, meds, oral fluids Have calcium gluconate at hedside for patients receiving IV Ma HYPOMAGNESEMIA - give Mg Sulfate via the buttocks NOTES