MARIANO MARCOS STATE UNIVERSITY

COLLEGE OF HEALTH SCIENCES

Department of Nursing
Batac, Ilocos Norte

FLUIDS & ELECTROLYTES

DISORDERS

Submitted by:
John Clements D. Galiza
BSN III-A

November 6, 2017
 Hypermagnesemia
I. Brief Description
 Hypermagnesemia is an uncommon laboratory finding and symptomatic
hypermagnesemia is even less common.
 This disorder has a low incidence of occurrence, because the kidney is able to eliminate
excess magnesium by rapidly reducing its tubular reabsorption to almost negligible amt.
 Hypermagnesemia is a serum magnesium concentration > 2.6 mg/dL (> 1.05 mmol/L).
 Rare electrolyte abnormality, because the kidneys efficiently excrete magnesium.
 A serum Mg level can appear falsely elevated if blood specimens are allowed to hemolyze
or are drawn from an extremity with a tourniquet that was applied too tightly.

II. Pathophysiology

Magnesium is one of the body's major electrolytes. As the second most common
intracellular cation, it plays a vital role in many cellular metabolic pathways. Magnesium is
required for deoxyribonucleic acid (DNA) and protein synthesis. It is a necessary cofactor for most
enzymes in phosphorylation reactions. It is also important for parathyroid hormone synthesis.

The total body content of this central cation is 2000 mEq, or 24 g. The magnesium is distributed
in bone (67%), intracellularly (31%), and extracellularly (a mere 1%).The intracellular
concentration is 40 mEq/L, while the normal serum concentration is 1.5-2.0 mEq/L. Of this serum
component, 25-30% is protein bound, 10-15% is complexed, and the remaining 50-60% is
ionized.

Magnesium is absorbed in the ileum and excreted in stool and urine. The minimum daily
requirement of magnesium is 300-350 mg, or 15 mmol; this amount is easily obtainable with a
normal daily intake of fruits, seeds, and vegetables because magnesium is a component of
chlorophyll and is present in high concentrations in all green plants.

The kidney is the main regulator of magnesium concentrations. Absorption occurs primarily in the
proximal tubule and thick ascending limb of the loop of Henle.

III. Risk Factors

 Untreated diabetic ketoacidosis- when catabolism causes the release of cellular
magnesium that cannot be excreted because of profound fluid volume depletion and
resulting oliguria
 Excessive use of magnesium based antacids or laxatives and medications that
decrease GI Motility, including opioids and anticholinergics- can also increase serum Mg
levels.
 Intestinal hypomotility- decreased elimination of Mg or its increased absorption
 Lithium intoxication
 Extensive soft tissue injury or necrosis- as with trauma, shock, sepsis, cardiac arrest.
IV. Manifestations
 Flushing
 Hypotension
 Muscle weakness
 Drowsiness
 Hypoactive reflexes
 Depressed respirations
 Cardiac arrest and coma
 Diaphoresis
 ECG: Tachycardia  Bradycardia
 Prolonged PR interval and QRS, peaked T waves

V. Medical and Nursing Management

a) Diagnosis
 Serum magnesium concentrations >2.6 mg/dL (> 1.05 mmol/L)
 The ECG shows prolongation of the PR interval, widening of the QRS complex, and
increased T-wave amplitude.
b.) Medical Management

 Calcium gluconate may reverse many of the magnesium-induced changes,

including respiratory depression.
 Diuresis or dialysis - Hemodialysis may be valuable in severe hypermagnesemia,
because a relatively large fraction (about 70%) of blood magnesium is not protein
bound and thus is removable with hemodialysis. When hemodynamic compromise
occurs and hemodialysis is impractical, peritoneal dialysis is an option.
 Avoiding administration of Mg to patients with renal failure.
 Administration of IV furosemide can increase magnesium excretion when renal
function is adequate; volume status should be maintained.
 Administration of loop diuretics and sodium chloride or lactated Ringer’s IV solution
enhances Mg excretion in patient with renal failure

c.) Nursing Management

 Nurse monitors vs, noting hypertension, and shallow respirations. T

 Nurse also observes for decreased deep tendon reflexes (DTRs) and changes in level
of consciousness.
 Medications that contains Mg are not administered to patients with renal failure or
compromised renal function.
 Patients with renal function are cautioned to check with their HCP before taking OTC
medications.
 Caution is essential when preparing and administering Mg-containing fluids
parenterally, because available parenteral Mg solutions differ in concentration.
 VI. Nursing Diagnosis and Possible Intervention

Nursing Intervention Rationale

Instruct in methods to conserve energy To assist patient to cope with fatigue and
manage within individual limits of ability

Discuss routines to promote restful sleep To assist patient to cope with fatigue and
manage within individual limits of ability

Instruct in stress-management skills of To assist patient to cope with fatigue and

visualization, relaxation, and biofeedback manage within individual limits of ability
when feedback.

Instruct patient in ways to monitor responses To promote wellness

to activity and significant signs/symptoms

Assist patient to identify appropriate coping Promotes sense of control and improves self-
behaviors esteem
 Hypomagnesemia
I. Brief Description
 Refers to a below- normal serum Mg concentration (1.3 mg/dl [o.62 mmol/L] and is
frequently associated with hypokalemia and hypocalcemia.
 Mg is similar to calcium in 2 aspects
 It is the ionized fraction of Mg that is primarily involved in neuromuscular activity
and other physiologic processes
 Mg levels should be evaluated in combination with albumin levels.

II. Pathophysiology
An important route of Mg loss is the GI tract; such loss can occur with nasogastric
suction, diarrhea, or fistulas. Because fluid from the lower GI tract has a higher
concentration of Mg (10-14 mEq per liter) than fluid from upper tract (1 to 2 mEq
per L), losses from diarrhea and intestinal fistulas are more likely to induce Mg
deficit than are those from gastric suction. Hypomagnesemia may occur with
withdrawal of alcohol and administration of tube feedings or parenteral nutrition.

III. Risk Factors

 Chronic Alcohol abuse
 Diabetic ketoacidosis, secondary to increased renal excretion during osmotic diuresis
and shifting of Mg into the cells with insulin therapy
 Patients who are receiving parenteral or enteral feedings: the major cellular
electrolytes move from the serum to newly synthesized cells
 Administration of aminoglycosides, cyclosporine, cisplatin, diuretics, digitalis, and
amphotericin as well as the rapid administration of citrated blood, especially to patient
with renal or hepatic disease.

IV. Manifestations
 Neuromuscular irritability
 Positive Trousseau’s sign and Chvostek’s sign
 Insomnia
 Mood changes
 Anorexia
 Vomiting
 Increased tendon reflexes
 Increased BP
 ECG: PVC’s flat or inverted T waves, depressed ST segment , prolonged PR interval,
and widened QRS
 V. Medical and Nursing Management
a. Diagnosis
 Urine Mg may help identify the cause of Mg depletion, and levels are measured after
a loading dose of Mg sulfate is administered
 Nuclear Magnetic Resonance Spectroscopy and the Ion-selective electrode- are
sensitive and direct means of measuring ionized serum Mg levels.
b. Medical Management
 Diet- green leafy vegetables, nuts, seeds, legumes, seafood, peanut butter, cocoa
 Mg salts can be administered orally in an oxide or gluconate form to replace continuous
losses but can produce diarrhea.
 Patient receiving parenteral nutrition require Mg in the IV solution to prevent
hypomagnesemia
 A bolus dose of Mg sulfate given too rapidly can produce alteration in cardiac
conduction leading to heart block or asystole
 VS must be assessed frequently during administration of Mg to detect cardiac rate and
rhytm.
 Monitoring urine output is essential before, during and after administration of Mg; the
physician is notified if urine volume decreases to less than 100 ml over 4 hours.
 Calcium gluconate must be readily available to treat hypocalcemic tetany or
hypermagnesemia.
c. Nursing Management
 Nurse should be aware of patients at risk for hypomagnesemia and observe them for
its signs and symptoms
 Patients receiving digitalis is closely monitored; because a deficit of Mg can predispose
them to digitalis toxicity
 If hypomagnesemia is severe, seizure precautions are implemented
 Patient education plays a major role in treating Mg deficit especially diet

VI. Nursing Diagnosis and Possible Intervention

Diagnosis; Sleep Deprivation

Nursing Intervention Rationale

Instruct in methods to conserve energy To assist patient to cope with fatigue and manage
within individual limits of ability

Discuss routines to promote restful sleep To assist patient manage within individual limits
of ability

Instruct in stress-management skills of To assist patient to cope with fatigue and manage
visualization, relaxation, and biofeedback when within individual limits of ability
feedback.

Instruct patient in ways to monitor responses to To promote wellness

activity and significant signs/symptoms

Assist patient to identify appropriate coping Promotes sense of control and improves self-
behaviors esteem
 Hyperphosphatemia
I. Brief Description
- Serum phosphorus level that exceeds 4.5mg/dL (1.45 mmol/L)
- Various conditions can lead to hyperphosphatemia; however the most common
is renal failure.
- Disorder that shifts intracellular phosphate to extracellular space.
- Morbidity In patients with this condition is more commonly associated with an
underlying disease than with increased phosphate values.

II. Pathophysiology
Phosphate is critical for a remarkably wide array of cellular processes. It is one of the
major components of the skeleton, providing mineral strength to bone. Phosphate is
an integral component of the nucleic acids that comprise DNA and RNA. Phosphate
bonds of ATP carry the energy required for all cellular functions. It also functions as a
buffer in bone, serum, and urine.
The addition and deletion of phosphate groups to enzymes and proteins are
common mechanisms for the regulation of their activity. In view of the sheer breadth
of influence of this mineral, the fact that phosphate homeostasis is a highly regulated
process is not surprising.

III. Risk Factors

 Increased Intake, decreased output, or a shift from the intracellular to extracellular
space.
 Excessive vitamin D intake
 Administration of total parenteral nutrition
 Chemotherapy for neoplastic disease
 hypoparathyroidism
 metabolic or respiratory ketoacidosis
 acute hemolysis
 high phosphate intake
 profound muscle necrosis
 increased phosphorus absorption
 Destruction of muscle tissue (rhabdomyolysis)
 Severe body wide infections

IV. Manifestations
 Tetany
 Tachycardia
 Anorexia
 Nausea and vomiting
 Muscle weakness
 s/s of hypocalcemia
 hyperactive reflexes
 soft tissue calcifications in lungs, heart, kidneys and cornea
 Positive Trousseau or Chvostek sign
 Hyperreflexia
  Carpopedal spasm
 Seizure
 Most people with hyperphosphatemia do not have symptoms. However, in people with
severe kidney dysfunction, calcium combines with phosphate, which lowers calcium
levels in the blood. Low calcium can cause muscle cramps and spasms but also causes
an increase in parathyroid hormone levels, resulting in bone weakness and other
problems. The calcium and phosphate also can form crystals (calcify) in body tissue,
including within the walls of the blood vessels. Severe arteriosclerosis (hardening of
the arteries) can result, leading to strokes, heart attacks, and poor circulation. Crystals
can also form in the skin, where they cause severe itching.

V. Medical and Nursing Management

a. Diagnosis
 Serum calcium level is useful for diagnosing the primary disorder and assessing
the effects of treatment
 X-rays may show skeletal changes with abnormal bone development
 PTH Levels are decreased in hypoparathyroidism
 BUN and Creatinine levels are used to assess renal failure
b. Medical Management
 Vitamin D Preparations – measures to decrease the serum phosphate level and
bind phosphorus in the GI tract such as calcitriol, which is both available in both
oral (Rocaltrol) and parenteral (Calcijex, paricalcitol) forms.
 Amphojel- with meals is effective but can cause bone and CNS toxicity with long
term use.
 Drugs that bind with phosphate, such as sevelamer,lanthanum, and calcium
compounds, should be taken with meals as prescribed by a doctor. By binding with
phosphate, these drugs make it harder to absorb, and more phosphate is
excreted. It is often used for people undergoing dialysis because calcium
compounds can make calcium-phosphate crystals more likely to form in tissues.
 Aluminum hydroxide - can be used to bind phosphate in your blood. However,
many do not use this, because of fear of aluminum toxicity.
 Calcium Carbonate tablets - This is the most common medication prescribed for
increased blood phosphate levels (hyperphosphatemia). These pills, taken 3 times
a day with meals, will bind to the phosphate in your bloodstream, and lower your
blood phosphate levels.
 Restriction of dietary phosphate, forced diuresis with a loop diuretic, volume
replacement with saline, and dialysis may also lower phosphorus.
 Surgery may be indicated for removal of large calcium and phosphorus deposits.
 Diagnosis of the cause in order to initiate specific therapy: Eg, patients with
hyperphosphatemia due to administration of liposomal amphotericin B who
continue to require antifungal therapy may be switched to the amphotericin B lipid
complex formulation, which contains less inorganic phosphate
 Enhancement of renal excretion of phosphate: Hyperphosphatemia due to
tumor lysis responds to enhancement of urinary losses through forced saline
diuresis
 c. Nursing Management
 Nurse monitors patients at risk for hyperphosphatemia
 If a low phosphorus diet is prescribed, the patient is instructed to avoid
phosphorus-rich foods such as hard cheeses, cream, nuts, meats, whole grain
cereals, dried foods, kidneys, sardines, foods made with milk/
 Nurse instructs the patient to avoid phosphate containing laxatives and enemas.
 Nurse educates patient about recognizing the signs impending hypocalcemia and
monitoring for changes in urine output.

VI. Nursing Diagnosis and Possible Intervention

Diagnosis; Nausea

Nursing Intervention Rationale

Assess for presence of conditions of the GIT To determine contributing factor

Note systemic conditions that may result in To determine contributing factor

nausea

Determine if nausea is potentially self- Indicates degree of effect on fluid/ electrolyte

limiting or mild balance and nutritional status

Monitor response to medications that prevent To promote comfort

or relieve nausea

Encourage deep, slow breathing To promote relaxation

Review signs of dehydration and stress To promote wellness

importance of replacing fluids and
electrolytes
 Hypophosphatemia
I. Brief Description
- Is defined as a serum phosphate level of less than 2.5 mg/dL (0.8 mmol/L).
- Occurs in 2% of hospitalized patients but is more prevalent in certain populations
(eg, it occurs in up to 10% of hospitalized patients with alcoholism).
- Some people who survived concentration camps died because their already low
phosphate level suddenly fell when they began eating a normal diet, a
phenomenon called refeeding syndrome.
 Phosphorus, is similar to calcium, and is found in your teeth and bones. You need
Vit. D. in order to absorb phosphate. The kidneys excrete phosphate from our
bodies
 Significant hypophosphatemia (below 0.4 mmol/L) may occur due to redistribution
into cells, renal losses or decreased intake. Patients with low phosphate often also
have other electrolyte deficiencies.
 There are 3 major mechanisms by which hypophosphatemia can occur
●Redistribution of phosphate from the extracellular fluid into cells
●Decreased intestinal absorption of phosphate
●Increased urinary phosphate excretion
II. Pathophysiology
Excess phosphorus binding by antacids may decrease the phosphorus available
from the diet to an amount lower than required to maintain serum phosphorus balance.
The degree of hypophosphatemia depends on the amount of phosphorus in the diet
compared to the dose of antacid. Hypophosphatemia can occur with chronic diarrhea,
Crohn’s Disease, Vit. D deficiency, anorexia, malabsorption. Vitamin D regulates
intestinal Ion absorption; therefore, a deficiency of Vit. D may cause decreased Ca and
phosphate, which may lead to osteomalacia (softened, brittle bones)

III. Risk Factors

 Administration of calories to patients with severe protein calorie malnutrition
 Heat stroke
 Prolonged intense hyperventilation
 Alcohol
 Withdrawal
 Poor dietary intake; Malnutrition due to malabsorption or persistent vomiting.
 Diabetec ketoacidosis
 Respiratory alkalosis
 Hepatic encephalopathy
 Major thermal burns
 Increased urinary losses of phosphorus
 Osmotic diuresis
 Use of carbonic anhydrase inhibitors
 Theophylline intoxication
 Long-term diuretic use
 IV. Manifestations
Most of the manifestation of hypophosphatemia result from a deficiency of ATP, 2, 3-
diphosphoglycerate, or both. ATP deficiency impairs cellular energy resources,
impairs oxygen delivery to tissues resulting in a wide range of neurologic manifestation
 Bone pain and tenderness
 Paresthesia
 Chest pain
 Cardiomyopathy
 Respiratory Failure
 Seizures
 Tissue hypoxia
 Nystagmus
 Increased susceptibility to infection
 Confusion
 Muscle weakness

V. Medical and Nursing Management

a. Diagnosis

 Kidney function tests

 Vitamin K blood test
 X-ray- may show skeletal changes of osteomalacia
 Serum phosphate levels
Exam and testing may show:
 Anemia due to too many red blood cells being destroyed (hemolytic anemia)
 Heart muscle damage (cardiomyopathy)
 PTH levels are increased
 Serum Mg may decrease due to increased urinary excretion of Mg
 Alkaline phosphate is increased with osteoblastic activity

b. Medical Management
 Electrolytes – The blood electrolyte levels are most likely low. Therefore, healthcare
provider may suggest magnesium or Vitamin D supplements, if phosphorous is low. It may
also be ordered a medication to lower your blood calcium levels, if it is elevated.
 Phosphate supplementation - Can be either intravenous (IV) with extremely low levels,
or it can be by mouth. Phosphate can be given in doses up to about 1 g PO TID in tablets
containing sodium phosphate or potassium phosphate. Oral sodium phosphate or
potassium phosphate may be poorly tolerated because of diarrhea. Ingestion of 1 L of low-
fat or skim milk provides 1 g of phosphate and may be more acceptable.
Parenteral phosphate is usually given IV. It should be administered in any of
the following circumstances:

 When serum phosphate is < 1 mg/dL (< 0.32 mmol/L)

 Rhabdomyolysis, hemolysis, or CNS symptoms are present
 Oral replacement is not feasible due to underlying disorder
  Treat underlying disorder are usually adequate in asymptomatic patients, even when
the serum concentration is very low
 Removal of the cause of hypophosphatemia may include stopping phosphate-binding
antacids or diuretics or correcting hypomagnesemia.

Parenteral treatment
IV administration of potassium phosphate (as buffered mix of K2HPO4 and KH2PO4) is
relatively safe when renal function is well preserved. Parenteral potassium phosphate
contains 93 mg (3 mmol) phosphorus and 170 mg (4.4 mEq) potassium per mL. The usual
dose is 0.5 mmol phosphorus/kg (0.17 mL/kg) IV over 6 h. Patients with alcoholism may
require ≥ 1 g/day during TPN; supplemental phosphate is stopped when oral intake is
resumed. If patients have impaired renal function or serum potassium > 4 mEq/L, sodium
phosphate preparations generally should be used; these preparations also contain 3
mmol/mL of phosphorus and are thus given at the same dose.

Serum calcium and phosphate concentrations should be monitored during therapy,

particularly when phosphate is given IV or to patients with impaired renal function. In most
cases, no more than 7 mg/kg (about 500 mg for a 70-kg adult) of phosphate should be given
over 6 h. Close monitoring is done and more rapid rates of phosphate administration should
be avoided to prevent hypocalcemia, hyperphosphatemia, and metastatic calcification due to
excessive calcium phosphate product.

c. Nursing Management
 Nurse identifies patients at risk for hypophosphatemia and monitors them- because
malnourished pt. receiving parenteral nutrition are at risk when calories are introduced too
aggressively
 Careful attention is given to preventing infection- because hypophosphatemia may alter the
granulocytes
 Reports early signs of hypophosphatemia
 If the pt. experiences mild hypophosphatemia, foods such as milk and milk products, organ
meats, nuts, fish and whole grains should be encouraged
 With moderate hypophosphatemia, supplements such as Neutra-Phos capsules, K-Phos,
and Fleet’s Phosphosoda may be prescribed

VII. Nursing Diagnosis and Possible Intervention Diagnosis: Confusion

Nursing Intervention Rationale

Identify factors present
Determine threat to safety of patient and
others
Evaluate extent of impairement
Orient patient to surroundings, staff,
necessary activities
Maintain calm environment and eliminate
extraneous noise
Provide for safety needs (siderails,
supervision)
Explain reason for confusion, if known
To determine contributing factor
To provide safety
To determine degree of impairment
To maximize level of function, prevent
further deterioration
To prevent over stimulation
To promote safety
To promote wellness