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Electrolyte Concept Map

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by William Ogello on 18 January 2013

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Transcript of Electrolyte Concept Map

Electrolyte Concept Map Nur 311 Created for Professor Evinrude
By William Ogello Hypernatremia Hyponatremia Sodium When the serum sodium levels are >145 mEq/L it is known as hypernatremia. This can occur whenever there is excess sodium in relation to water (Lewis, Dirksen, Heitkemper & Bucher, 2011, p 313). This is mostly caused when there is excessive water loss or excessive sodium gained. Dietary causes can be too much sodium intake without adequate water intake. Hypertonic tube feedings without adequate water compensation may also cause hypernatremia as well as excessive sweating and diarrhea. Certain diseases such as hyperaldosteronism, Cushing syndrome, and diabetes insipidus can also cause hypernatremia.
It is important to establish an onset. In acute (less than 24 hours) hypernatremia, "correct the serum sodium at an initial rate of 2-3 mEq/L/h (for 2-3 h) (maximum Total, 12 mEq/L/d)" according to Ackley (2008, p. 215). With chronic (greater than 24 hours) hypernatremia with no or mild symptoms should be "corrected at a rate not to exceed 0.5 mEq/L/h and a total of 8-10 mEq/d (eg, 160 mEq/L to 152 mEq/L in 24 h)" according to Ackley (2008, p. 215).


Signs and symptoms include the following: lethargy, twicking, weakness, intense thirst, postural hypotension, weight loss, irritability, neuromuscular excitability, and edema. Severe elevations of the sodium level can cause seizures and coma (Lewis et al., 2011, p 313). Sodium is the most abundant cation in the extracellular fluid. The normal serum values range from 135-145 mEq/L (Marieb & Hoehn, 2010, p. 1002-1004). Sodium is kept in higher concentrations via a sodium potassium pump which requires ATP to pump sodium against its concentration gradient. It is easily lost in sweat, urine, and feces but is easily replaced by a normal diet. The body maintains the correct serum level mostly by antidiuretic hormone (ADH) and Aldosterone which are released in response to a lowered blood osmolality (Huether & McCance, 2008, p. 106-109). These both act on the kidney’s to reabsorb sodium and in turn water. Sodium’s positive ionization has a major effect on osmolality because of waters negative polar charge. This is why water will follow sodium between the intracellular and the extracellular compartments. When sodium moves into a cell it generates and propagates an electrical signal that allows the cells to communicate with each other. This facilitates muscle contractions as well as general nerve conduction. Sodium also plays a vital role in the regulation of bloods acid-base balance. (Marieb & Hoehn, 2010, p. 1002-1004) Clients who are at risk for developing hypernatremia include those who take corticosteroid medicines, who have hyperaldosteronism, kidney disease, diabetes, or heart disease. Also clients with the inability to drink water (conscious impairments) or have excessive intake of salty foods are all at risk (Huether & McCance, 2008, p. 106-109).
Specifically the geriatric patient is at risk also. Elderly people have decreased thirst, and therefore ingest less amounts of water. Along with a general decrease in total body water and decreased ADH production the geriatric patient is at risk for hypernatremia (Huether & McCance, 2008, p. 106-109). Hyponatremia h Lab test may include the following.
•Comprehensive metabolic panel (includes blood sodium)
•Osmolality blood test
•Urine osmolality
•Urine sodium
(Le fever Kee, 2005, p.111) In the assessment of a patient the nurse must ask about the patient’s daily fluid and salt intake. It’s also important to ask about daily urine output and if the urine appears concentrated. The nurse must also obtain a complete list of medication and chronic illnesses. Question the patient about events that might lead to dehydration such as excessive exercising, fever, diarrhea, and vomiting. It's also important to assess the patient to determine if the are a fall risk from altered mobility. Finally the nurse must obtain vitals. Out of range vitals may help lead the nurse to different implementations.
(Ackley & Ladwig, 2008, p. 212-215) Possible Physician’s orders:
•Oral ingestion of water
•Sodium restriction
•Iv solution that is hypotonic or contains no sodium (.45 saline and 5% dextrose respectively) (Lewis et al., 2011, p 313) Nursing implementations:
•If ordered start IV fluid of the ordered solution and monitor for desired affects.
•First step is to rehydrate the patient and encourage liquid consumption.
•Offer fluids frequently avoiding drinks with sodium content.
•Monitor the patient for signs and symptoms of cerebral edema. (Ackley & Ladwig, 2008, p. 215-218)
•Educate the patient on dietary sources of sodium and the importance of staying hydrated.
•Provide oral care as per the facilities policies. (Ackley & Ladwig, 2008, p. 215-218) Hyponatremia is measured by a serum level of < 135 mEq/L and is the most common electrolyte imbalance in the United States. Hyponatremia is mostly when a patient ingest a high volume of water, when the severely restrict sodium consumption, or a combination of the two (Lewis et al., 2011, p 313). In some extreme cases cancer may affect the organs that regulate sodium levels which can lead to hyponatremia. Acute hyponatremia develops over 48 hours or less, and patients are subject to more severe cerebral edema than those with chronic hyponatremia, which develops over more than 48 hours. If the serum sodium decreases slowly, or if it is greater than 125 mEq/L, the patient may be symptom free. If the serum sodium level drops below 115 mEq/L, cerebral edema and increased brain cell volume occur that could result in death.

Signs and symptoms: Headache, Confusion, Loss of energy, Fatigue, Restlessness and irritability, Muscle weakness, spasms or cramps, Seizures, Unconsciousness, Coma (Lewis et al., 2011, p 313). Patients who are at risk for hyponatremia include athletics and burn victims. Patients that have diarrhea, vomiting, excessive diuresis, or on fasting diets are at risk (Huether & McCance, 2008, p. 106-109). Patients with medical conditions such as CHF, kidney disease, liver cirrhosis (alcoholics, hepatitis, etc.) and syndrome of inappropriate antidiuretic hormone secretion (SIADH) are all at risk. Pregnant women are likely to be at risk. Lastly patients on diuretic medications and SSRI's can develop hyponatremia. The geriatric patient usually become ill with hyponatremia due to age related causes that affect the way the body handles the balance of sodium and water. Changes in kidney function, such as decreased kidney size or decreased blood flow through the kidneys (Huether & McCance, 2008, p. 106-109). The elderly are more prone to developing a chronic disease that affects your body's sodium balance. Underactive thyroid (hypothyroidism) and Addison’s disease can also affect the elderly’s sodium levels (Huether & McCance, 2008, p. 106-109). Lab test may include the following.
•Comprehensive metabolic panel (includes blood sodium)
•Osmolality blood test
•Urine osmolality
•Urine sodium
(Le fever Kee, 2005, p.111) The nurse assessment must include any prescribed or OTC medications. Ask about nausea, vomiting, diarrhea, abdominal cramps, headache, or dizziness. The nurse should have the patient recall their diet over the last three days to determine sodium content. The nurse should ask about weight loss which can be attributed to anorexic symptoms cause by hyponatremia. The nurse should assess a change in mental status or behavior such as confusion, a flat affect, and personality changes. (Ackley & Ladwig, 2008, p. 221-231) The nurse should assess the patient's level of orientation and ability to communicate needs. The main effects of hyponatremia are neurological so the nurse should assess the patient’s support systems outside of the healthcare facility. It’s important to know if diet supervision is required. During the physical exam it’s important to check the patient’s vitals a weak pulse may be noted as well as a low diastolic blood pressure, tachycardia, and orthostatic hypotension. (Ackley & Ladwig, 2008, p. 221-231) Note the skin turgor and peripheral vein refilling time which can be altered from edema. Because the legs are usually the first muscles affected by hyponatremia muscle strength and risk for falling should be assessed. In regards to cellular edema lung fields should be auscultated as well as bowel sounds which can become hyperactive. (Ackley & Ladwig, 2008, p. 221-231) Possible physician’s orders:
•Hypovolemic hyponatremic patients should be treated with isotonic saline to correct the volume deficit.
•Hypervolemic or edematous (diluted patients) patients are treated with a fluid restriction: 800 to 1,000 mL
•For severe hyponatremia an infusion of 3% to 5% sodium chloride solution.
•A diuretic may be given concurrently to avoid the occurrence of circulatory overload.
•Euvolemic patients may only need a water restriction without a sodium restriction. Nursing implementations
•If an IV solution is ordered begin the infusion with the proper solution. Report the signs and symptoms of water intoxication to the physician immediately.
•Monitor vitals and the effectiveness of fluid administration by following the serum sodium and osmolality levels, as well as daily weights and intake and output. (Ackley & Ladwig, 2008, p. 232)
•Be aware of clients risk for falls and implement the appropriate measures, as well as seizure precautions.
•In patients with hypervolemic or euvolemic hyponatremia offer cold liquids as they fulfill thirst mechanisms better than hot liquids. (Ackley & Ladwig, 2008, p. 232) Potassium + Potassium is the most abundant cation in the intracellular fluid. Potassium normal concentration in the EFC is 3.5-5.0 mEq/L which is kept in higher concentrations within the cell by a sodium-potassium pump. Potassium is necessary for adequate muscle contraction, healthy electrical activity in the heart and rapid transmission of nerve impulse throughout the body. Potassium is also exchanged for a hydrogen ion in times when the blood is becomes acidic. This function always it to be a key element in maintaining blood pH. (Marieb & Hoehn, 2010, p. 1002-1004) Hyperkalemia Hypokalemia Hyperkalemia is distinguished by a serum value of > 5.00 mEq/L. The three aspects that can cause hyperkalemia are: excessive intake of potassium, impaired renal excretion, and shift of potassium form the ICF to the ECF (Lewis et al., 2011, p 314). While the major cause of hyperkalemia is renal failure; it can also be caused by medications, tissue trauma, and a lowered blood pH.

Signs and symptoms: Hyperkalemia has symptoms that manifest as the following: anxiety, abdominal cramping, diarrhea, weakness of the lower extremities, paresthesias, irregular pulse, and with sudden or severe hyperkalemia cardiac arrest. An ECG can also show a tall peaked T wave. (Lewis et al., 2011, p 314) Risk for hyperkalemia Patients who are at risk for hyperkalemia include the following:
•Patients with renal insufficiency or kidney disease.
•Patients who are on blood pressure medications such as ACE inhibitors, angiotensin receptor blockers, and potassium-sparing diuretics.
•Patients with adrenal gland issues like addison's disease or an aldosterone deficiency.
•Patients who may have suffered excessive tissue damage (burn victims, crush injuries, etc.).
•Patients who receive blood transfusions and type 1 diabetic patients.
(Huether & McCance, 2008, p. 110-112) Geriatrics The geriatric patient is at risk for hyperkalemia because of two main factors. The first factor is the diminished functioning of the kidneys which leads to lower clearance of potassium. With diminished kidney function the production of renin and aldosterone is diminished (Huether & McCance, 2008, p. 802-803). These two hormones regulate K+ EFC concentration. The second factor attributed to the elderly is the medications they take to treat comorbidities. High blood pressure can be treated by lowering the total volume circulating in the body. The drugs used to facilitate this lead to higher concentrations of K+ in the EFC (salt substitutes, ACE inhibitors, potassium-sparing diuretics.) (Huether & McCance, 2008, p. 802-803) The following test may be ordered to check for hyperkalemia.
Blood tests which include:
Electrolytes
Bicarbonate level
Full blood count
Renal function tests:
Urinalysis,
24 hour urine aldosterone (to detect Addison's disease)
(Le fever Kee, 2005, p. 157) Labs and Diagnostics Assessment Assess the history dietary patterns and of medications to determine if excess potassium is a result of excess ingestion. A medical history of both past and present diseases is important. The nurse should look for signs of nausea and diarrhea, and a complaint of general weakness is an early sign of hyperkalemia. A history of heart related problems should be obtained including irregular beats fast or slow, dizziness while changing positions, and postural hypotension. (Ackley & Ladwig, 2008, p. 236) The patients pulse should be assessed and heart sounds should be auscultated. An ECG should be performed to get a visual representation of the heartbeat. (Ackley & Ladwig, 2008, p. 236) Interventions •Following the orders of the physician the nurse should administer medications that move excess potassium from the ECF to the ICF. IV insulin will move potassium from the EFC to the ICF. (Ackley & Ladwig, 2008, p. 240)
•Correct the blood pH if acidosis is the cause of hyperkalemia. IV administration of sodium bicarbonate will neutralize the high acidity.
•The nurse should administer drugs that correct the membranes hyper excitability such as calcium gluconate.
•The nurse should eliminate sources of potassium whether they are from food or medications.
•Safety measures for clients with fall measures so be implemented.
•Education on foods and drugs with high potassium concentration should be given to the patient. (Ackley & Ladwig, 2008, p. 240) Providers prescriptions The provider may order the following drugs in order to reduce serum levels of potassium.
•Calcium gluconate
•Sodium bicarbonate
•Glucose plus insulin
•Nebulized albuterol
•Furosemide
(Wilson, Shannon, Shields & Stang, 2008, p.1513-1515) Hypokalemia is distinguished by a serum level of <3.5 mEq/L. This can be caused by potassium shifting from the EFC to the IFC, abnormal losses by the kidneys or GI track, and in rare cases inadequate diet consumption (Lewis et al., 2011, p 315). The most common cause is from diarrhea and vomiting. Patients on certain medications for high blood pressure have a potassium loss at the kidneys. Certain adrenal conditions can also cause a loss of potassium at the kidneys as well.

Signs and symptoms
When potassium levels are low, the cells can’t generate or pass along the electrical signal. This affects the muscles and nerves and causes them to function abnormally (Lewis et al., 2011, p 315).
•ECG will show a ST segment depression and flattened T wave (Lewis et al., 2011, p 315)
•Bradycarida and palpitations.
•Fatigue, nausea, vomiting, paralytic ileus, and polyuria.
•Muscle weakness and cramps (usually starting with legs), paresthesias, and decreased reflexes (Lewis et al., 2011, p 314). Risk for Hyopkalemia Geriatrics Labs and Diagnostics Assessment Providers Prescriptions Interventions Potassium is readily supplied in our diets; however people with eating disorders such as anorexia nervosa, bulimia, or even excessive use of laxatives may develop hypokalemia. Patients with AIDS, have alcoholism, or taking diuretics are at risk as well (Huether & McCance, 2008, p. 110-112). Patients who have Cushing syndrome or take corticosteroids are also at risk. Lastly patients with kidney disease, diabetes, and asthma are also at risk. In the elderly, one of the main contributing causes is the use of thiazide diuretics in treating high blood pressure. Another cause is a condition called hyperaldosteronism which causes retention of sodium with a simultaneous loss of potassium into the urine (Huether & McCance, 2008, p. 802-803). Diarrhea which is another common and recurring condition in older persons for various reasons may expedite the loss of potassium. Conversely to the overuse of laxatives and certain antacids in the elderly can also cause hypokalemia (Huether & McCance, 2008, p. 802-803). The doctor may order various test to both check electrolyte level and rule out conditions that cause hypokalemia.
•Blood tests check potassium level
•Kidney function (BUN and creatinine)
•Digoxin (Lanoxin) level if you are taking a digitalis preparation.
•Urinalysis
(Le fever Kee, 2005, p. 157) Assess the history dietary patterns and of medications to determine if the potassium deficit is a result of decreased ingestion of potassium products. Fluid intake and output should be assessed. A medical history of both past and present diseases is important as some illnesses can cause a lowered serum value of potassium. A complete list of medication should also be complied as certain medications lower potassium levels. The nurse should look for signs of mental status such as drowsiness and sensitivity to stimulation (noise, bright lights) (Ackley & Ladwig, 2008, p. 250). Muscle pain and weakness should be assess to protect the patient from falls. Respiratory muscles can be effected so respiration depth and effort should be noted. Auscultate lung fields for the presence of breath sounds. A hypokalemic effect on the GI system may lead to cramping and constipation and should be assessed (Ackley & Ladwig, 2008, p. 250). Cardiac problems such as hypotension, weak and or irregular pulse, and altered ECG should be addressed. The physician may order the following prescriptions.
•Spironolactone
•potassium chloride Oral
•potassium gluconate Oral
•potassium chloride IV
•potassium acetate IV
•D5 in 0.45%NaCl & potassium Cl IV
•0.45 % NaCl-potassium chloride IV
(Wilson et al., 2008, p. 978-981) Following the orders of the provider the nurse should implement the following interventions.
•Administer potassium supplements which can be given orally or IV in severe cases.
•When given IV assess the infusion site every hour for signs of infiltration or phlebitis (Ackley & Ladwig, 2008, p. 255).
•When given IV K+ rate should not be given greater than 20 mEq/L per hour.
•Provide foods rich in potassium with plenty of water.
•Ensure fall risk precautious have been implemented.
•Educate the client to report chest pain or an unusual heartbeat. Potassium infusions can be painful so education on pain management should be provided (Ackley & Ladwig, 2008, p. 255).
•Education on foods high in potassium should be given. This is even more true when the patient is on potassium wasting medications. Calcium Serum calcium is distinguished as a 8.6-10.2 mg/dL value (Marieb & Hoehn, 2010, p. 1002-1008). All cells need calcium in order to work. It is necessary for heart function, nerve signaling, muscle contraction, blood clotting, strong bones and teeth. It is mostly stored with phosphorus in the bones. The serum levels of calcium are controlled by PTH, calcitonin, and vitamin D. (Marieb & Hoehn, 2010, p. 1002-1008) Hypercalcemia Hypercalcemia is when serum calcium levels raise above 10.2 mg/dL. The main cause of hypercalcemia is over activity of the parathyroid glands (PTH) (Lewis et al., 2011, p 317). Other causes include cancer, some medications, excessive use of calcium, and vitamin D supplements. Lastly when a patient has a lowered blood pH it can force the calcium to unbind from proteins and become free calcium which raises serum levels. Signs and Symptoms: •Loss of appetite •Nausea and vomiting
•Excessive thirst •Frequent urination •Abdominal pain •Constipation
•Lethargy and fatigue •Muscle weakness •Confusion (Lewis et al., 2011, p 317) High Risk For Hypercalcemia Geriatrics Assessment Labs and Diagnostics Providers Prescriptions Interventions People who are at risk to develop hypercalcemia include people diagnosed with primary hyperparathyroidism. Patients with malabsorption like IBS or Crohn's disease are at risk.
Patients that have cancer are at risk because it can then force its way into the bone causing calcium displacement (Huether & McCance, 2008, p. 533). Another way cancer can raise your calcium levels is by creating proteins that mimic PTH. Patients with cancers such as multiple myeloma, breast cancer and lung cancer are at risk. Patients that have hypoalbuminemia are at risk because of the lack of carrier proteins in the blood allows for more free calcium ions. Tuberculosis can cause the over production of calcitriol which then causes greater absorption of calcium in the GI track. People who take lithium for bipolar disorder are also at risk. Thiazide diuretics that are used in people with high blood pressure can cause hypercalcemia as well. Lastly the elderly particularly elderly woman are at risk (Huether & McCance, 2008, p. 533). The primary cause of hypercalcemia is hyperparathyroidism which causes a greater release of PTH (Marieb & Hoehn, 2010, p. 613). The incidence of primary hyperparathyroidism is much higher in women therefore elderly woman are at the highest risk. The rate of malignancy increases with age (Marieb & Hoehn, 2010, p 799). This is a concern with the elderly patient because hypercalcemia is also cause by cancers. As the cancer works it's way into the bone it displaces calcium. Test that evaluate hormone levels may include
Blood tests: Such as PTH level and vitamin D level
Urinalysis
If these test reveal hormone levels to be normal the doctor may order test to check for cancer.
•Chest X-ray
•Computerized tomography (CT) scan
•Magnetic resonance imaging (MRI) scan
•Mammogram
(Le fever Kee, 2005, p. 313) Assess the history dietary patterns and of medications to determine if the hypercalcemia is a result of increased consumption of calcium containing items. Fluid intake and output should be assessed. A medical history of both past and present diseases is important as some illnesses can cause an elevated level of calcium. A complete list of medication should also be complied. The nurse should assess for a symptoms of hypercalcemia such as anorexia, constipation, polyuria, or polydipsia muscular weakness and muscle cramps. During the physical examination the nurse should assess for fluid volume deficit by checking skin turgor and mucous membranes. Auscultate the apical pulse to determine heart irregularities (Ackley & Ladwig, 2008, p. 212). As well as auscultate the lungs. The nurse should check for hypoflexia, and decreased muscle tone. The patient may have signs of confusion so the nurse should check the patients LOC. Hypercalcemia causes the GI to slow down when may cause abdominal cramps and constipation. Hypoactive bowel sounds may also be a result of this (Ackley & Ladwig, 2008, p. 212). The nurse should assess the GU system as well hypercalcemia may cause renal calculi to from causing pain on urination. An ECG reading may show a shortened ST and QT segment as well. The physician may order the following prescriptions to treat hypercalcemia.
•Furosemide •.9% saline IV •Prednisone
•Oral phosphate •Pamidronate and etidronate
•Calcitonin •Mithramycin
(Wilson et al, 2008, p. 251-254) The nurse following the orders of the physician would provide the prescribed medication in attempts to lower calcium levels. Depending on the type of hypercalcemia the treatment is varied.
•The nurse should administer furosemide.
•The nurse should encourage the patient to increase fluid consumption to 3000-4000 mL (Ackley & Ladwig, 2008, p. 214)
•Asses the patients risk for falls related to muscle weakness.
•The nurse should asses the patients vitals frequently.
•Educate the patient to call for help if bathroom assistance is needed (increased fluid and Lasix).
•Education and restriction of calcium in regards to diet should be in acted.
•The patient should be encouraged to perform weight baring exercises (Ackley & Ladwig, 2008, p. 212). Hypocalcemia Hypocalcemia: is defined as a serum calcium level < 8.6 mg/dL. It can be caused by various issues of both the parathyroid gland and the pancreases. When the patient’s PTH is diminished the body will not be able to regulate the serum calcium levels correctly (Lewis et al., 2011, p 318). Serum phosphorus levels are also a key player in calcium levels. Another issue is when calcium ions are bound up and no longer are free. This can occur from both excessive fatty acids and blood alkalosis (Lewis et al., 2011, p 318).

Signs and symptoms
Hypocalcemia causes the cell to become hyper excitable and the patient may have the following signs and symptoms.
•Classic signs are Chvostek’s and Trousseau’s signs •Cardiac dysrhythmias
•Laryngeal stridor, and dysphagia •A prickling sensation in the hands and feet.
•Depression •Irritability •Lethargy or sluggishness •Muscle spasms •Seizures (Lewis et al., 2011, p 317) Risk for hypocalcemia Geriatrics Labs and Diagnostics Assessment Providers Prescriptions Interventions Labs and diagnostic for hypocalcemia include the following
•Ionized calcium •Phosphate
•Magnesium •Creatinine
•Vitamin D level •Intact PTH
•Comprehensive Metabolic Panel (CMP)
•Kidney Stone Analysis
(Le fever Kee, 2005, p. 313) Geriatrics Patients are at risk for both hypo and hypercalcemia with any form of cancer. As patients become older their ability to absorb calcium begins to diminish which can lead to hypocalcemia from the diet (Marieb & Hoehn, 2010, pp 191, 194, 244). The body will try to compensate for this by pulling calcium from the bones. This concept which is known as osteoporosis leads to fragile bones. Elderly women are particularly at risk because of the decline of estrogen with age (Marieb & Hoehn, 2010, pp 191, 194, 244). Another troubling factor is the reduced lean muscle in the elderly. The combined issue of weak bones and decreased lean muscles can lead to fractures and falls. This repair process and bone rebuilding leads to hypocalcemia. Risks for hypocalcemia include newborns particularly premature babies. One of the biggest risks is patients with hypoparathyroidism because they will have diminished PTH formations (Marieb & Hoehn, 2010, p 1008). Patients with acute pancreatitis are at risk because of the free fatty acids binding with calcium ions. A vitamin D deficiency is a risk and is common in people who do not get enough sunlight. As with all electrolytes chronic kidney disease also put a patient at risk for electrolyte imbalance. Certain medications can cause hypocalcemia. Patients with epilepsy are at risk do to anticonvulsant therapy. Patients who have tuberculosis are at risk because of the treatment associated with it (Marieb & Hoehn, 2010, p 1008). The nurse should inquire about past medical history that causes hypocalcemia. For example a prior diagnosis of hypomagnesemia, pancreatic insufficiency, and hypoparathyroidism can cause hypocalcemia (Ackley & Ladwig, 2008, p. 205). The nurse should assess the diet and fluid intake of the patient and whether or not proper calcium and vitamin D is being consumed. Along with that causes of magnesium and vitamin D deficiency should be assessed. Both poor diet and alkalosis can cause vitamin D and Mg deficiency. The physical assessment must include inspection of airway. Twitching around the mouth, laryngospasm, and dyspnea can be a severe issue with hypocalcemia. Auscultate for breath sounds such as wheezing. Auscultate heart sounds as hypocalcemia can cause ventricular tachycardia. The nurse should check for Trousseau’s sign and Chvostek’s sign. Lastly the nurse should monitor the ECG and look for a elongated ST and QT segment (Ackley & Ladwig, 2008, p. 205). The primary concern is to replace the low levels of calcium. Followed by treatment of the underlying cause of hypocalcemia. The initial treatment may include the following prescriptions.
•Calcium gluconate IV
•Tums Oral
•Calcium 600 Oral
•calcium chloride IV
•Citracal + vitamin D Oral
•calcium & magnesium carbonates Oral
(Wilson et al., 2008, pp. 251, 321, 342) •In response to the physician’s orders the nurse would administrate any prescribed medications.
•If the client is receiving intravenous calcium, the nurse needs to monitor the IV site for infiltration or phlebitis every hour.
•The nurse should frequently assess the patients vitals especially RES, HR, and O2sat (Ackley & Ladwig, 2008, p. 213).
•Education and implementation of calcium in regards to diet should be in acted.
•The nurse should monitor lab values of calcium as frequently as they are available.
•Assess the patient to determine if they are a fall risk and implement the appropriate safety implementations.
•Help the patient with management of anxiety to reduce stress and hyperventilation which can lead to alkalosis worsening hypocalcemia (Ackley & Ladwig, 2008, p. 213).
•Provide additional education on the disease process of hypocalcemia. Normal magnesium serum levels range between 1.5-2.5 mEq/L. It is the second most important electrolyte action in the ICF. Its primary action according to Marieb is “Energy metabolism, glucose utilization, protein synthesis, fatty acid synthesis/breakdown, muscle contraction, all ATPase functions, and for almost all hormonal reactions.” (2010, p. 1008) Many factors that control calcium levels also control magnesium levels which is why they are both assessed together . Hypermagnesemia Signs and Symptoms Risk for hypermagnesemia Geriatrics Labs and Diagnostics Assessment Providers Prescriptions Interventions Hypomagnesemia Signs and Symptoms Risk for Hypomagnesemia Geriatrics Labs and Diagnostics Assessment Providers Prescriptions Interventions Phosphorus Phosphorus Hyperphosphatemia Signs and Symptoms Risk for Hyperphosphatemia Geriatrics Labs and Diagnostics Assessment Providers Prescriptions Interventions Hypophosphatemia Signs and Symptoms Risk for Hypophosphatemia Geriatrics Labs and Diagnostics Assessment Providers Prescriptions Interventions Hypermagnesemia is when serum levels are > 2.5 mEq/L. The major cause of this is decreased renal excretion of magnesium. The second major cause is increased dietary intake (Lewis et al., 2011, p 319). Hypermagnesemia can lead to mild blocking of nerve impulses. This can cause a loss of deep tendon reflexes as well as flaccid paralysis. In severe cases mechanical ventilation if the patient has respiratory failure or a temporary pacemaker if the patient has symptomatic bradycardia might be needed. Its effect on smooth muscle results in urinary retention (Lewis et al., 2011, p 319). Hypermagnesemia can cause hypocalcemia because it inhibits the release of PTH. •Difficulty urinating •Nausea, Vomiting, Flushing
•Drowsiness •Lethargy •Muscle Weakness •Hypo/areflexia (Lewis et al., 2011, p 319)
•Paralysis •Respiratory failure •Hypotension •Bradycardia
•ECG Changes •Prolonged PR •Prolonged QRS •Prolonged QT
(Marieb & Hoehn, 2010, p 1003) Patients who are at risk for hypermagnesemia are patients with renal failure, adrenal insufficiency (Addison's disease), and patients who might have treatments that contain magnesium salts (Marieb & Hoehn, 2010, p 1003). These salts include antacids in people with heart burn or GERD. Patients taking laxatives for constipation are at risk. Magnesium maybe used as a pain relief for multiple patients especially in arthritis (Marieb & Hoehn, 2010, p 1003). The elderly is at risk primarily because of the aging process. Like most electrolytes Mg is excreted by the kidneys. The older people become the more the kidneys lose their functioning capabilities (Huether & McCance, 2008, p. 802-803). The decreased kidneys and comorbidities put the elderly at risk. The elderly typically use both antacids and laxatives on routine basics. The use of these two medications causes hypermagnesemia. Lastly the elderly might have arthritis pain which magnesium has been shown to help alleviate (Huether & McCance, 2008, p. 802-803). •Comprehensive Metabolic Panel (CMP)
•Urinalysis
•Creatinine
•24 hours the volume of urine magnesium
•Electrocardiogram
•The doctor will also want to check on both phosphate and calcium.
(Le fever Kee, 2005, p. 379) The nurse should inquire about past medical history that causes hypermagnesemia. A history of renal failure, adrenal insufficiency, laxative/antacid abuse, and acidosis related to diabetes or should be noted(Ackley & Ladwig, 2008, p. 265). The nurse should assess the diet and fluid intake of the patient and whether medication history maybe the cause. These include milk of magnesia and antacids that contain magnesium hydroxide. Assess the patients for the following illnesses: nausea or vomiting, flushed skin, and diaphoresis. The nurse should assess the patient’s vitals which may which may show bradycardia, or hypotension. The nurse should then auscultate the heart sounds. The nurse should note the depth and effort of respirations and auscultate the lung fields. A muscle weakness may be reported and a loss of deep tendon reflexes noted (Ackley & Ladwig, 2008, p. 265.) The physician may order the following prescriptions to help treat hypermagnesemia.
•furosemide (Lasix)
•calcium chloride IV
•calcium gluconate IV
•calcium gluconate in D5W IV
•calcium gluconate in 0.9% NaCl IV
(Wilson et al., 2008, pp. 251, 321, 342) •The nurse following the orders of the physician should administer the prescribed medications.
•The nurse should administer calcium gluconate to reverse severe symptoms of excess magnesium.
•The nurse should administer furosemide (Lasix) in patients who get enough fluids and whose kidneys are functioning properly to increase magnesium excretion (Ackley & Ladwig, 2008, p. 268).
•The nurse should monitor vital signs and LOC.
•The nurse should provide plenty of fluids for the patient.
•Assess the patient to determine if they are a fall risk and implement the appropriate safety precautions.
•Provide additional education on the disease process of hypermagnesemia. Especially on diet and medications that lead to hypermagnesemia.
•The nurse should advise clients who have renal disease to contact physician before taking OTC drugs (Ackley & Ladwig, 2008, p. 213.) •Following the orders of the physician the nurse should administer medication.
•The nurse should carefully administer magnesium salts as ordered.
•Iv should be given slowly to avoid cardiac complications and the infusion site should be assessed frequently (Ackley & Ladwig, 2008, p. 277).
•The nurse should carefully monitor vital signs, cardiac rhythm, and ECG.
•The nurse should take protective measures for clients with seizures.
•The nurse should assess the client’s ability to swallow.
•The nurse should provide foods high in magnesium.
•Assess the patient to determine if they are a fall risk and implement the appropriate safety precautions.
•Encourage active range-of-motion (ROM) exercises or perform passive ROM exercises several times a day to help prevent complications of inactivity (Ackley & Ladwig, 2008, p. 277).
•Provide additional education on the disease process of hypomagnesemia. Especially on diet and medications that lead to hypomagnesemia. The provider might prescribe the following prescriptions.
•magnesium citrate Oral
•magnesium sulfate IV
•magnesium chloride Oral
•magnesium sulfate in LR IV
•magnesium sulfate in D5W IV
•magnesium gluconate Oral
(Wilson et al., 2008, p 534-537) The nurse should inquire about past medical history that causes hypomagnesemia. Both poor diet and alkalosis can cause Mg deficiency. Ask the patient to describe bowel patterns, and note if the patient has diarrhea or a history of an eating disorder with laxative abuse (Ackley & Ladwig, 2008, p. 272). Ask about the patient's diet and drinking history, including the amount of alcohol intake on a usual day and an unusual day. Determine if the patient has experienced irregular heartbeats, lethargy, muscle weakness, tremors, mood alterations, anorexia, nausea, or dizziness. The patient's vital signs may reflect hypotension and tachycardia. When the nurse examine the patient's eyes nystagmus should be noted (Ackley & Ladwig, 2008, p. 272). •Comprehensive metabolic panel
•Magnesium blood test
•Urinalysis
•Urine magnesium test
•Test to rule out calcium and potassium deficit.
•ECG
(Le fever Kee, 2005, p. 379) The elderly is particularly at risk because of their lack of proper diet. This can manifest as both irregularity (diarrhea) and decrease Mg consumption (Marieb & Hoehn, 2010, p 904). The process of aging cause circulatory problems for which many patients turn to diuretics. Thiazides and loop diuretics both cause losses of Mg in the kidneys (Huether & McCance, 2008, p. 802-803). The elderly often isolate themselves from others which can lead to depression. That patient may then self-medicate on alcohol which can lead to hypomagnesemia. The major causes of hypomagnesemia outline which patients would be at risk to develop it. Patients with non-intentional mal absorption illnesses are at risk. Patients with IBS, Crohn’s disease, diarrhea, and vomiting are at risk (Lewis et al., 2011, p. 320). Other intentional illness such as anorexia nervosa and bulimia can lead to hypomagnesemia. Certain pregnant woman can develop toxemia that can lead to hypomagnesemia. Alcoholic are at risk because of alcohols diuretic effects (Lewis et al., 2011, p. 320). The signs and symptoms of hypomagnesemia resemble the signs of hypocalcemia. Another electrolyte deficiency hypomagnesemia resembles is hypokalemia. This is mostly causative because magnesium is needed for the sodium potassium pump to function properly.
•neuromuscular irritability with tremors •increased reflexes •tremors & convulstions
•Trousseau's and Chvostek's signs •Tachycardia •Nystagmus •Increased BP •Dysrhythmias
•Disorientation •Confusion •Vertigo •Dysphagia •Respiratory difficulties (Lewis et al., 2011, p 320) Hypomagnesemia occurs when serum levels measure < 1.5 mEq/L. The primary cause hypomagnesemia is the diet. It occurs when fasting or starvation is an issue but can be caused by mal absorption illnesses. These illnesses include IBS, chronic pancreatitis, vomiting, and diarrhea (Lewis et al., 2011, p 320). Magnesium can also be lost in a patient with severe burns. Phosphorus is mostly a component of phosphate which is the most abundant anion in the ICF. The normal serum levels range from 2.4 to 4.4 mg/dL. Phosphate works as a buffer to maintain acid-base balance. It is also a key component in the body’s energy ATP. Phosphate is essential for cell membrane integrity, RBC function, teeth and bone structure. Lastly it helps with the metabolism of carbohydrates, proteins, and fats. There is a direct relationship between phosphorus and calcium in that when one is abnormally high the other will be low (Marieb & Hoehn, 2010, p. 1002-1008). Hyperphosphatemia occurs when the serum levels are > 4.4 mg/dL. The most common cause of this is renal failure as the kidneys won’t be able to filter out phosphate (Lewis et al., 2011, p 318-319). The relationship between phosphate and calcium means that issues that cause hypocalcemia will cause hyperphosphatemia (hypoparathyroidism). Other causes of hyperphosphatemia are rhabdomyolysis, lactic acidosis, ketoacidosis, and excessive use of laxatives containing phosphate (Lewis et al., 2011, p 319). •Calcification in soft tissues: blood vessels, cornea, skin, kidney, periarticular tissue
•Mimics hypocalcemia Chvostek’s and Trousseau’s signs (Lewis et al., 2011, p 319) •Cardiac dysrhythmias
•Laryngeal stridor, and dysphagia •A prickling sensation in the hands and feet.
•Depression •Irritability •Lethargy or sluggishness •Muscle spasms •Seizures
(Lewis et al., 2011, p 319) Patients at the highest risk are patients with acute or chronic renal failure. Patients with certain disease can cause elevated phosphate levels. Some of these diseases are leukemia, lymphoma, and bone tumors (Lewis et al., 2011, p. 318). Patients with endocrinopathies like hypoparathyroidism and Addison’s disease are at risk for hyperphosphatemia. Patients that have skin trauma or burns are at risk also. Ingestion of phosphate can put a patient at risk as well. Examples of ingested products are laxative and nutritional supplements (Lewis et al., 2011, p. 318-319). Lastly situations the lower blood pH (lactic acid, diabetic ketoacidosis) will increase phosphorus levels. The elderly patient is at risk for many reasons. The primary reason is a consequence of aging. The older people become the more the kidneys lose their functioning capabilities. The decreased kidneys and comorbidities put the elderly at risk (Huether & McCance, 2008, p. 802-803). The elderly typically use laxatives on routine basics. The use of this medications causes hyperphosphatemia. Another aging concern is a decreased immune system which normally keeps cancer in check. The process of aging increases the chance of developing cancer which can ultimately lead to hyperphosphatemia (Marieb & Hoehn, 2010, p 799). •Comprehensive Metabolic Panel (CMP)
•Urinalysis
•Serum and urine Phosphate
•Serum and urine Magnesium
•Serum and urine Calcium
•Creatinine and Bun
•Intact PTH
(Le fever Kee, 2005, p. 414) The nurse should assess the diet and fluid intake of the patient and whether or not medication linked hyperphosphatemia is the cause. The nurse should ask about the use of chronic laxative, enemas, and excess antacid use (Ackley & Ladwig, 2008, p. 282). The nurse should ask about a prior diagnosis of renal failure, hypoparathyroidism, and Addison’s disease. The nurse should assess the level of tetany or muscle spasms. The nurse should also check for Trousseau’s and Chvostek’s signs (Ackley & Ladwig, 2008, p. 282). Cardiopulmonary assessment may reveal tachypnea, decreased myocardial contractility, and vasodilation. With all electrolyte imbalances the nurse should assess the clients risk for falls. The physician may order the following prescriptions.
•Aluminum hydroxide
•Calcium carbonate •Calcium acetate
•Furosemide in patients without renal failure.
(Wilson et al., 2008, pp. 155, 315, 342) •Following the orders of the physician the nurse would administer the appropriate medications.
•The nurse would administer diuretics in patients without renal failure (Ackley & Ladwig, 2008, p. 286).
•The nurse would administer phosphate biding medications such as antacids (aluminum hydroxide) (Ackley & Ladwig, 2008, p. 286).
•Correcting the correlating hypocalcemia the nurse would administer calcium carbonate and monitor the infusion site.
•Dietary restriction and phosphorus containing medication substitutions with education should be implemented.
•The nurse would provide plenty of fluids for the patient.
•Assess the patient to determine if they are a fall risk and implement the appropriate safety precautions.
•Provide additional education on the disease process of hyperphosphatemia. Especially on diet and medications that lead to hyperphosphatemia. •Following the physicians orders the nurse would administer the prescribed medicine.
•The nurse would start an IV of potassium phosphate.
•The nurse would monitor the IV site for infiltration because potassium phosphate can cause tissue sloughing and necrosis (Ackley & Ladwig, 2008, p. 305).
•Monitor for over treatment which would have signs like tetany. The nurse would ensure the patient has an open airway, adequate breathing, normal circulation, and an adequate urine output (Ackley & Ladwig, 2008, p. 305).
•The nurse should have an artificial airway, manual resuscitator bag, at the bedside at all times (Ackley & Ladwig, 2008, p. 305).
•If linked to alcohol the nurse would watch for DT and withdrawal symptoms (Ackley & Ladwig, 2008, p. 305).
•The nurse should provide foods high in phosphorus.
•The nurse would provide plenty of fluids for the patient.
•Assess the patient to determine if they are a fall risk and implement the appropriate safety precautions.
•Provide additional education on the disease process of hypophosphatemia. Especially on diet and medications that lead to hypophosphatemia. The physician may order the following medications. •calcitriol Oral
•potassium phosphate dibasic IV
•calcitriol IV
•potassium & sodium phosphates Oral
•sodium phosphate IV
•potassium phosphate in D5W IV
•sodium phosphate in 0.9 % NaCl IV
(Wilson et al., 2008, p. 756-762) The nurse should assess the patients about their diet and if any anorexia, nausea, diarrhea, or vomiting. The nurse should ask if the patient has a history of eating disorders or is currently on any medications. Certain medications like diuretics, aluminum containing antacid, and bronchodilators can cause hypophosphatemia (Ackley & Ladwig, 2008, p. 298). A history of diabetes, cancer, alcoholism, a recent burn, or hyperparathyroidism should be assessed as well. The nurse should assess if the patient has any pain in their bones. The nurse should assess the patients concerns about the muscular weakness, paresthesia, and ability to perform ADL’s (Ackley & Ladwig, 2008, p. 298). The nurse should assess the patient's hand grasp and leg strength. The nurse should assess if deep tendon reflexes have been affected. Assessment of the pulse may result in a weak and irregular pulse. Assess the respiratory status noting the deep and effort because diaphragm muscles may be at risk. Muscle breakdown may occur so the nurse should assess the patient’s level of pain in the area of the kidneys (Ackley & Ladwig, 2008, p. 298). •Comprehensive metabolic panel.
•Urinalysis
•X-ray of the bone to check for bone disorders.
•The doctor may also want to check for hemolytic anemia or Rhabdomyolysis which are a result of hypophosphatemia.
•Electrocardiogram
•parathyroid hormone level
•urine amino acids
•blood urea nitrogen •creatinine
(Le fever Kee, 2005, p. 414) Many older people are undernourished and have inadequate diets. The idea refeeding to provide nourishment can lead to hypophosphatemia. Older woman on hormone replacement therapy are at risk because of estrogens link to hypophosphatemia (Marieb & Hoehn, 2010, p 1008). COPD which can occur in older adults can lead to hypophosphatemia because of its link to inhalers. Depression link alcoholism can be a larger factor in the elderly which can also cause lead to hypophosphatemia. The geriatric patient also has considerably less water weight compared to the rest of their body. This lower ratio can cause imbalances to occur much quicker (Marieb & Hoehn, 2010, p 1008). There are many patients that may be at risk for developing hypophosphatemia. Woman around child bearing age are at risk because of oral contraceptive (Marieb & Hoehn, 2010, p 1003). Patients that have issues absorbing foods can develop hypophosphatemia. These issues are IBS, Crohn’s disease, diarrhea, and vomiting. Patients with anorexia nervosa and bulimia are at risk as well (Lewis et al., 2011, p. 320). Some asthmatic patients will also be at risk from the use of certain inhalers. Patients that take antacids for heartburn are also at risk if they contain aluminum hydroxide. Diabetic patients who do not control their glucose levels are at risk as well. Individuals with alcoholism and parathyroid disease are also at risk (Lewis et al., 2011, p. 320). Lastly patients that have vitamin D deficiency will be at risk for hypophosphatemia.
•Impaired diaphragmatic function •Respiratory failure
•Weakness, Myopathy
•Osteomalacia •Osteopenia
•Cardiomyopathy •Arrhythmias •Paresthesias
•Hallucinations •Stupor, Coma •Seizures •Encephalopathy
(Marieb & Hoehn, 2010, p 1003) Hypophosphatemia is when serum levels measure < 2.4 mg/dL. The many causes of hypophosphatemia are changes in the diet as a result of malnutrition or alcoholism (Lewis et al., 2011, p 319). This can significantly reduce the serum phosphorus levels. Inadequate amounts of phosphorus in total parental nutrition may also lead to hypophosphatemia. Abnormal losses through vomiting and diarrhea can also cause hypophosphatemia (Lewis et al., 2011, p 319). Hypophosphatemia caused by medications are mostly are result from aluminum containing antacids and diuretics. Vaprisol (Lewis et al., 2011, p 313) References
Ackley, B. J., & Ladwig, G. B. (2008). Nursing diagnosis handbook, an evidence-based guide to planning care. (8th ed.). St. Louis, Missouri: Mosby.

Huether, S. E., & McCance, K. L. (2008). Understanding pathophysiology. (Fourth ed.). St. Louis, Missouri: Mosby.

Le fever Kee, J. (2005). Laboratory and diagnostic test with nursing implications. (7th ed.). Upper Saddle River, NJ: Pearson Prentice Hall.

Lewis, S. L., Dirksen, S. R., Heitkemper, M. M., & Bucher, L. (2011). Medical-surgical nursing, assessment and management of clinical problems. (8 ed.). St. Louis: Mosby.

Marieb, E. N., & Hoehn, K. (2010). Human anatomy and physiology. (8 ed., Vol. 8). San Francisco, CA: Pearson Benjamin Cummings.

Wilson, B. A., Shannon, M. T., Shields, K. M., & Stang, C. L. (2008). Nurse's drug guide. Upper Saddle River, NJ: Pearson Education Inc.
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