ST. ANTHONY COLLEGE OF ROXAS CITY, INC.

San Roque Extension, Roxas City, Capiz, Philippines 5800

Member, DC-SLMES Philippines
Empowering Communities, Building Futures
+
COLLEGE OF NURSING
SY 2020-2021

READING SYNTHESIS # 2
Do some readings about fluid and electrolytes disturbances such as volume impairment, osmotic
imbalances and ionic concentration problems using any references. This activity pulls together your
background knowledge, newly learned ideas, connections, inferences and summaries into a complete
and original understanding of the topic. 

1. Hypocalcemia
 Cause:
Hypoalbuminemia is the most common cause of hypocalcemia. Causes include cirrhosis, nephrosis,
malnutrition, burns, chronic illness, and sepsis.
 Clinical manifestations:
Patients with hypocalcemia may be asymptomatic or experience milder symptoms such as muscle
cramps and paresthesias. The paresthesias, described as “pins and needles” sensations in the hands,
feet, and around the mouth, are episodic and often occur at times of stress, vomiting, or
hyperventilation. This can be explained by the fact that metabolic or respiratory alkalosis increases the
binding of serum calcium to albumin and decreases the concentration of free ionized calcium that
interacts with cells.
Symptoms of hypocalcemia are also more likely to occur when the serum calcium level has fallen
abruptly; chronic hypocalcemia, in contrast, can be asymptomatic with very low levels of serum calcium.
Asymptomatic hypocalcemia must be differentiated from the low total serum calcium concentration
(with a normal ionized calcium level) that occurs with hypoalbuminemia. The corrected total serum
calcium concentration can be calculated by measuring the serum albumin level and adding 0.8 mg/dL to
the total serum calcium level for each 1 g/dL reduction in the serum albumin level from 4 g/dL
(corrected calcium = 0.8 × [4.0 − patient’s albumin] + serum calcium).

Tetany can be elicited in patients with no overt signs of hypocalcemia by inducing the Chvostek and
Trousseau signs. The Chvostek sign is produced by tapping the facial nerves at the angle of the jaw,
which causes contracture of the ipsilateral facial muscles. The Trousseau sign is elicited by applying a
blood pressure cuff to the upper arm and inflating it to just above the systolic blood pressure for 3
minutes. The resulting carpopedal spasm, with contractions of the fingers and inability to open the
hand, is a result of increased neuromuscular irritability caused by hypocalcemia and aggravated by
ischemia. This may be painful for the patient if sustained for too long but is believed to be a more
specific marker of hypocalcemia than the Chvostek sign.

Other nonspecific signs and symptoms of hypocalcemia are lethargy, psychomotor depression, and
impaired cognitive function with poor school performance in children. Hypocalcemia also decreases the
contractility of the heart muscle, which can provoke or aggravate congestive heart failure in patients
with heart disease. In these patients, heart failure can improve with administration of calcium.
Hypocalcemia also leads to prolongation of the rate-corrected QT interval on an electrocardiogram. An
unusual ocular manifestation of chronic hypocalcemia is papilledema, caused by increased pressure of
the cerebrospinal fluid, which improves with reversal of hypocalcemia.

 Management:
o Ask the patient to relax his facial nerves. Next. Stand directly in front of him and tap the facial
nerve either just anterior to the earlobe or below the zygomatic arch and the corner of the
mouth. A positive response varies from twitching of the lip at the corner of the mouth spasm to
all facial muscles, depending on the severity of hypocalcemia.

Mild Hypocalcaemia: serum adjusted calcium 1.9 - 2.2mmol/L and asymptomatic

Commence oral calcium supplement e.g. Calcichew Forte Chewable, 2 tablets twice a day* (unlicensed
dose) and adjust to patient's individual requirements.

If post-thyroidectomy, repeat serum calcium 24 hours later. Then if:

Serum adjusted calcium >2.2mmol/L, patient may be discharged with plan to re-check serum calcium
within one week.

Serum adjusted calcium remains between 1.9-2.2mmol/L, increase Calcic hew Forte Chewable to three
tablets twice a day (unlicensed dose)*.
Patient remains in mild hypocalcemia range 72 hours post-operatively despite calcium
supplementation, start alfacalcidol oral 0.25microgram daily. Alfacalcidol is restricted to specialist
initiation; contact a senior member of medical staff to discuss use.
If vitamin D deficient, commence oral vitamin D supplementation: load with colecalciferol 300,000units
over 6-10 weeks e.g. 50,000units weekly for 6 weeks followed by a maintenance dose of 800-1000units
daily.
If patient has hypomagnesaemia, stop any precipitating drug and administer IV magnesium
   *This is an unlicensed dose of Calcic hew Forte Chewable tablets. Review on discharge and if
appropriate prescribe the licensed dose (1 tablet daily).

 Nursing interventions:
Nursing interventions for the calcium-deficient patient include monitoring serial lab values and
continuous cardiac monitoring. Nurses must assess for signs of neuromuscular excitability including
tetany and Chvostek's and Trousseau's signs. Close monitoring of the patient's respiratory status is
critical. Calcium replacement may be prescribed as orally or I.V. If administered orally, vitamin D is also
given to promote absorption. I.V. calcium can be caustic to the veins, and close monitoring is essential
related to possible extravasation.3,7,9 A dietitian may be consulted to assist with meal planning and
patient education.

2. Hypercalcemia 

2. Hypercalcemia Calcium is a mineral that is important in the regulation and processes of

many body functions including bone formation, hormone release, muscle contraction, and
nerve and brain function. Hypercalcemia is the term that refers to elevated levels of calcium
in the bloodstream. Causes: One of the most common causes of high calcium levels
(hypercalcemia), is an overproduction of parathyroid hormone, or hyperparathyroidism.
 Clinical Manifestations More-severe cases produce signs and symptoms related to the parts
of the body affected by the high calcium levels in the blood. Examples include: Kidneys.
Excess calcium makes your kidneys work harder to filter it. This can cause excessive thirst
and frequent urination. Digestive system. Hypercalcemia can cause stomach upset, nausea,
vomiting and constipation. Bones and muscles. In most cases, the excess calcium in your
blood was leached from your bones, which weakens them. This can cause bone pain and
muscle weakness. Brain. Hypercalcemia can interfere with how your brain works, resulting
in confusion, gue. It can also cause depression. Heart. Rarely, severe hypercalcemia can
interfere with your heart function, causing palpitations and fainting, indications of cardiac
arrhythmia, and other heart problems. Nursing Management and Interventions: Nursing
interventions include encouraging fluid intake and ambulation. Fluids containing sodium
should be used unless contraindicated as sodium increases calcium excretion. Cardiac
rhythm should be monitored. Calcium levels should be monitored as ordered, as well as
sodium and potassium levels due to use of diuretics. Intake and output measurement is also
critical to assess response to hydration and diuretic therapy.

3. Hypomagnesemia 
 Cause:
The causes hypomagnesemia are decreased gastrointestinal (GI) absorption and increased renal loss.
Decreased GI absorption is frequently due to diarrhea, malabsorption, and inadequate dietary intake.
Common causes of excessive urinary loss are diuresis due to alcohol, glycosuria, and loop diuretics.
Low magnesium is typically due to decreased absorption of magnesium in the gut or increased excretion
of magnesium in the urine. Low magnesium levels in otherwise healthy people are uncommon. This is
because magnesium levels are largely controlled by the kidneys. The kidneys increase or decrease
excretion (waste) of magnesium based on what the body needs.
Continually low dietary intake of magnesium, excessive loss of magnesium, or the presence of other
chronic conditions can lead to hypomagnesemia.
Remember “Low Mag”

Limited intake Mg+ (starvation)

Other electrolyte issues cause low mag levels (hypOkalemia, hypOcalcemia)

Wasting Magnesium kidneys (loop and thiazide diuretics & cyclosporine…stimulates the kidneys to
waste Mag)

Malabsorption issues (Crohn’s, Celiac, proton-pump inhibitors drugs “Prilosec, Nexium, Protonix”…drug
family ending in “prazole” Omeprazole, diarrhea/vomiting)

Alcohol (due to poor dietary intake, alcohol stimulates the kidneys to excreted mag, acute pancreatitis)

Glycemic issues (Diabetic Ketoacidosis, insulin administration)

  Clinical manifestations:
Early signs of low magnesium include:
o nausea
o vomiting
o weakness
o decreased appetite
As magnesium deficiency worsens, symptoms may include:
o numbness
o tingling
o muscle cramps
o seizures
o muscle spasticity
o personality changes
o abnormal heart rhythms
o Remember “Twitching” because the body is experiencing neuromuscular excitability. This is
the OPPOSITE in hypermagnesemia where everything system of the body is lethargic.
o Trouesseau’s (positive due to hypocalcemia)
o Weak respirations
o Irritability
o Torsades de pointes (abnormal heart rhythm that leads to sudden cardiac death…seen in
alcoholism) Tetany (seizures)
o Cardiac changes (moderate loss: Tall T-waves and depressed ST segments*** severe loss:
prolonged PR & QT interval (prolong of QT interval increases patient’s risk for Torsades de
pointes) with widening QRS complex, flattened t-waves, Chvostek’s sign (positive which goes
along with hypocalcemia)
o Hypertension, hyperreflexia
o Involuntary movements
o Nausea
o GI issues (decreased bowel sounds and mobility)

 Management:

o Teach patients the importance of proper nutrition, including dietary sources of magnesium like
whole grain cereals, fresh meat, fish, vegetables, and fruit.
o Encourage patients to avoid alcohol consumption.

 Nursing interventions:
o Monitor cardiac, GI, respiratory, neuro status. Place on a cardiac monitor (watching for any EKG
changes prolonging of PR interval and widening QRS complex)
o May administer potassium supplements due to hypokalemia (hard to get magnesium level up if
potassium level is down)
o Administering calcium supplements (oral calcium supplements w/ Vitamin-D or 10% Calcium
Gluconate)
o Administer Magnesium Sulfate IV route. Monitor Mg+ level closely because patient can become
magnesium toxic (***Watch for depressed or loss of deep tendon reflexes)
o Place patient in seizure precautions
o Oral forms of Magnesium may cause diarrhea which can increase magnesium loss so watch out
for this
o Watch other electrolyte levels like calcium and potassium
o Encourage foods rich in Magnesium:
 Avocado
 Green leafy vegetables
 Peanut Butter, potatoes, pork
 Oatmeal
 Fish (canned white tuna/mackerel)
 Cauliflower, chocolate (dark)
 Legumes
 Nuts
 Oranges
 Milk

4. Hypermagnesemia 
 Cause:
o Remember “MAG”
o Hypermagnesemia is less common than hypomagnesemia. It typically happens when you are
trying to correct hypomagnesemia with magnesium sulfate IV infusion. However, other causes
can include:
o Magnesium containing antacids and laxatives***(Mylanta, Maalox)
o Addison’s disease (adrenal insufficiency)
o Glomerular filtration insufficiency (<30mL/min) renal failure. This is because the kidneys are
keeping too much magnesium.

 Clinical manifestations:

 Remember: Every system of the body is “Lethargic” (opposite of hypomagnesemia

where the body systems are experiencing hyper-excitability)
 Note: You will typically only see symptoms in severe cases of hypermagnesemia (mild
cases patient will be asymptomatic)
 Lethargy (profound)
 EKG changes with prolonged PR & QT interval and widened QRS complex
 Tendon reflexes absent/grossly diminished
 Hypotension
 Arrhythmias (bradycardia, heart blocks)
 Respiratory arrest
 GI issues (nausea, vomiting)
 Impaired breathing (due to skeletal weakness)
 Cardiac arrest

 Management:
 o Monitor client risks.
o Watch for digitalis toxicity
o Cardiac monitoring
o Seizure precautions
o Monitor urine output

 Nursing interventions:
o Monitor cardiac, respiratory, neuro system, renal status. Put patient on cardiac monitor (watch
for EKG changes)
o Ensure safety due to lethargic/drowsiness
o Prevention:
o Avoid giving Magnesium containing antacids/laxative to patients with renal failure
o Assess for hypermagnesemia during IV infusions of magnesium sulfate for hypomagnesemia
(sign and symptom would be diminished/absent deep tendon reflexes)
o Withhold foods high in magnesium, such as:
Remember: “Always Get Plenty Of Foods Containing Large Numbers of Magnesium”
o Avocado
o Green leafy vegetables
o Peanut Butter, potatoes, pork
o Oatmeal
o Fish (canned white tuna/mackerel)
o Cauliflower, chocolate (dark)
o Legumes
o Nuts
o Oranges
o Milk
o Administer diuretics that waste magnesium (if patient is not in renal failure) such as Loop and
Thiazide diuretics
o Patient in renal failure patient prep for dialysis
o IV calcium may be order to reverse side effects of Magnesium (watch IV for infiltration…

5. Hypophosphatemia 

6. Hyperphosphatemia 
 Cause:
o Remember “PhosHi” (there is a drug called Phoslo (calcium acetate) which is prescribed for
patients in end stage renal failure (ESRF) to help keep phosphate levels low. Phoslo is a
phosphate binder and it prevents the GI system from absorbing phosphate.
o Phospho-soda overuse: phosphate containing laxatives or enemas (Sodium Phosphate/Fleets
Enema) ….do not administer to patients with renal failure
o Hypoparathyroidism due to under secretion of parathyroid hormone. The parathyroid plays a
role in maintaining calcium and phosphate levels and it normally inhibits reabsorption of
phosphate by the kidneys. In hypoparathyroidism, there is under secretion of PTH which causes
phosphate to become over absorbed by the kidneys.
o Overuse of Vitamin D (remember Vitamin D helps with phosphate absorption. Too much
vitamin-d would cause too much phosphate to be absorbed)
o Syndrome of Tumor Lysis is a metabolic problem that mainly occurs with treatment of cancer
with chemotherapy. It causes the electrolytes to imbalance due to the cell dying and releasing
intracellular contents into the blood, hence too much phosphate is released into the blood
o rHabdomyolysis is rapid necrosis of the muscles and this leads to myoglobin being released into
the bloodstream which affects the kidneys and causes renal failure. In renal failure, you start to
have phosphate excretion decreased.
o Insufficiency of Kidneys (end renal failure) causes phosphate to not be excreted

 Clinical manifestations:

o Will have many of the same symptoms as hypocalcemia because remember phosphate and
calcium function oppositely.
o Remember CRAMPS (same mnemonic used for hypocalcemia)
o Confusion
o Reflexes hyperactive
o Anorexia
o Muscle spasms in calves or feet, tetany, seizures
o Positive Trousseau’s Signs, Pruritis
o Signs of Chvostek

 Management:
o monitor renal function (blood urea nitrogen and serum creatinine levels)
o monitor for signs and symptoms of hypocalcemia.

 Nursing interventions:

o **Administer phosphate-binding drugs (PhosLo) which works on the GI system and causes
phosphorus to be excreted through the stool.*** NCLEX: Give with a meals or right after eating
meal
o Avoid using phosphate medication such as laxatives and enema
o Restrict foods high is phosphate ***eat, poultry, fish, dairy, nuts, sodas, oatmeal
o Prepare patient for dialysis if patient in renal failure

7. Hypochloremia 

8. Hyperchloremia 
 Cause:
o Loss of body fluids from prolonged vomiting, diarrhea, sweating or high fever (dehydration).
o High levels of blood sodium.
o Kidney failure, or kidney disorders.
 o Diabetes insipidus or diabetic coma.
o Drugs such as: androgens, corticosteroids, estrogens, and certain diuretics.

 Clinical manifestations:
 Many people do not notice any symptoms of hyperchloremia, unless they are experiencing very
high or very low levels of chloride in their blood.
 Dehydration, fluid loss, or high levels of blood sodium may be noted.
 You may be experiencing other forms of fluid loss, such as diarrhea, or vomiting when suffering
from hyperchloremia.
 You may be a diabetic, and have poor control over your blood sugar levels (they may be very
high).

 Management:
o Make sure you tell your doctor, as well as all healthcare providers, about any other medications
you are taking (including over-the-counter, vitamins, or herbal remedies).  Do not take aspirin or
products containing aspirin unless your healthcare provider permits this.
o Remind your doctor or healthcare provider if you have a history of diabetes, liver, kidney, or
heart disease. 
o Keep yourself well hydrated if you have hyperchloremia. Drink two to three quarts of fluid every
24 hours, unless you are instructed otherwise.
o Avoid caffeine and alcohol, as these can cause you to have electrolyte disturbances. 

 Nursing interventions:
monitor heart rate, I/O, low sodium diet

B. What nursing care management will you give to patients with the following imbalances? 

1. Fluid volume deficit

-Urge the patient to drink prescribed amount of fluid.

- Aid the patient if he or she is unable to eat without assistance, and encourage the family or SO to assist
with feedings, as necessary.

- If patient can tolerate oral fluids, give what oral fluids patient prefers. Provide fluid and straw at
bedside within easy reach. Provide fresh water and a straw.

- Emphasize importance of oral hygiene.

- Provide comfortable environment by covering patient with light sheets.

- Educate patient about possible cause and effect of fluid losses or decreased fluid intake
- Begin to advance the diet in volume and composition once ongoing fluid losses have
stopped.

2.

3. Hyponatremia 
o Watch cardiac, respiratory, neuro, renal, and GI status
o Hypovolemic Hyponatremia: give IV sodium chloride infusion to restore sodium and fluids (3%
Saline hypertonic solution….harsh on the veins…given in ICU usually through central line very
slowly…must watch for fluid overload)
o Hypervolemic Hyponatremia: Restrict fluid intake and in some cases administer diuretics to
excretion the extra water rather than sodium to help concentrate the sodium. If the patient has
renal impairment they may need dialysis.
o Caused by SIADH or antidiuretic hormone problems: fluid restriction or treated with an
antidiuretic hormone antagonists called Declomycin which is part of the tetracycline family
(don’t give with food especially dairy or antacids…bind to cations and this affect absorption).
o If patient takes Lithium remember to monitor drug levels because lithium excretion will be
diminished and this can cause lithium toxicity.
o Instruct to increase oral sodium intake and some physicians may prescribe sodium tablets. Food
rich in sodium include: bacon, butter canned food, cheese, hot dogs, lunch meat, processed
food, table salt

4. Hypernatremia 

5. Hypokalemia 
o Watch heart rhythm (place on cardiac monitor…most are already on telemetry), respiratory
status, neuro, GI, urinary output and renal status (BUN and creatinine levels)
o Watch other electrolytes like Magnesium (will also decrease…hard to get K+ to increase if Mag is
low), watch glucose, sodium, and calcium all go hand-in-hand and play a role in cell transport
o Administer oral Supplements for potassium with doctor’s order: usually for levels 2.5-3.5…give
with food can cause GI upset
o IV Potassium for levels less 2.5 (NEVER EVER GIVE POTASSIUM via IV push or by IM or subq
routes)
o -Give according to the bag instruction don’t increase the rate…has to be given slow…patients
given more than 10-20 meq/hr should be on a cardiac monitor and monitored for EKG changes
o -Cause phlebitis or infiltrations
o Don’t give LASIX, demadex , or thiazides (waste more Potassium) or Digoxin (cause digoxin
toxicity) if Potassium level low…notify md for further orders)
o Physician will switch patient to a potassium sparing diuretic Spironolactone (Aldactone),
Dyazide, Maxide, Triamterene

Instruct patient to eat Potassium rich foods

o Remember POTASSIUM to help you remember the foods
o Potatoes, pork
o Oranges
o Tomatoes
o Avocados
o Strawberries,
o Spinach
o fIsh
o mUshrooms
o Musk melons: cantaloupe
o Also included are: (carrots, raisins, bananas)

6. Hyperphosphatemia Cause: According to Lewis (2020), Causes include chronic kidney disease,
hypoparathyroidism, and metabolic or respiratory acidosis. Clinical features may be due to
accompanying hypocalcemia and include tetany. Clinical Manifestation: According to Lewis (2020),
Most patients with hyperphosphatemia are asymptomatic, although symptoms of hypocalcemia,
including tetany, can occur when concomitant hypocalcemia is present. Soft-tissue calcifications are
common among patients with chronic kidney disease; they manifest as easily palpable, hard,
subcutaneous nodules often with overlying scratches. Imaging studies frequently show vascular
calcifications lining major arteries. Nursing Management and Intervention According to Lederer
(2018), The major strategies for treating hyperphosphatemia are as follows: Diagnosis of the cause
in order to initiate specific therapy: For example, 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.
Limitation of phosphate intake: Patients with chronic kidney disease are advised to avoid foods that
are especially high in phosphate; high-phosphate foods include dairy products; meats, nuts, and
other high-protein foods; processed foods; and dark colas. Kidney Disease: Improving Global
Outcomes (KDIGO) guidelines note that it is reasonable to consider phosphate source in making
dietary recommendations, as approximately 40%-60% of animal-based phosphate is absorbed,
compared with 20%-50% of plant-based phosphate, and that fresh and homemade foods are
preferable to processed foods, which often contain inorganic phosphate additives. Enhancement of
renal excretion of phosphate: Hyperphosphatemia due to tumor lysis responds to enhancement of
urinary losses through forced saline diuresis The clinical condition most often requiring curtailment
of ingestion is renal failure. Because intestinal absorption of phosphate and phosphate content in a
typical diet is high, maintenance of phosphate homeostasis is dependent on renal excretion of the
ingested excess. Therefore, when renal failure develops and hyperphosphatemia ensues, the sole
means of controlling it is limitation of intake. Serum phosphate levels follow a circadian rhythm,
which must be considered when interpreting patient phosphate levels. Ix et al note a trough at 8
AM, with peaks at 4 AM and 4 PM. In patients with chronic kidney disease, these authors found that
differences in phosphate levels with lowest-phosphate versus highest-phosphate diets were smallest
at 8 AM and largest at 4 PM. The low-phosphate diet altered the circadian rhythm such that the 4
AM and 4 PM peaks were absent. Optimal phosphate control in dialysis patients is extremely
challenging. Despite the remarkable improvements made in dialysis techniques over the years,
phosphate control has not been substantially improved. In addition, variances in dialytic removal of
phosphate, enteral phosphate absorption unexplained by diet or vitamin D intake, and binder
efficacy may account for hyperphosphatemia in dialysis patients rather than nonadherence to
therapy. An alternative approach for dialysis-dependent patients that is presently being investigated
is daily nocturnal dialysis. Dialysis performed in this manner, as opposed to intermittent thrice-
weekly dialysis, seems to markedly decrease or even abolish the necessity for phosphate binders.
Dey et al reported achieving phosphate control with thrice-weekly sessions by using
hemodiafiltration, which combines diffusion and convection, rather than hemodialysis. Their
program consisted of nocturnal sessions lasting a median of 8 hours. In the 14 patients in their
study, pre-dialysis phosphate levels fell from a mean of 1.52 ± 0.4 to 1.06 ± 0.1 mmol/L (P< 0.05),
and use of phosphate binders became unnecessary. Surgical care Surgery may sometimes be
required for removal of large calcium phosphate deposits occurring in patients with tumoral
calcinosis or long-standing renal failure. Perform parathyroidectomy in patients with renal failure
who have tertiary (autonomous) hyperparathyroidism complicated by hypercalcemia,
hyperphosphatemia, and severe bone disease. Consultations The following consultations may be
required: Endocrinologist: To determine if the patient has hypoparathyroidism or one of the various
forms of pseudohypoparathyroidism Nephrologist: To evaluate and treat hyperphosphatemia
associated with renal failure Monitoring Calcium levels, phosphate levels, and renal function should
be monitored at intervals consonant with the severity of the underlying disorder. KDIGO guidelines
stress that in patients with chronic kidney disease (CKD), the development of metabolic bone
disease (MBD) involves a complex interaction of phosphate, calcium, and parathyroid hormone
(PTH). Consequently in patients with stage G3a–G5D CKD, the KDIGO recommends serial
assessments of all three parameters, considered together, in order to guide treatment of MBD.
KDIGO recommends monitoring serum levels of calcium, phosphate, PTH, and alkaline phosphatase
activity beginning in CKD stage G3a (in children, stage G2), at a frequency based on the presence
and magnitude of abnormalities, and the rate of progression of CKD. Reasonable monitoring
intervals would be as follows: CKD G3a–G3b – Serum phosphate and calcium, every 6–12 months;
PTH, based on baseline level and CKD progression CKD G4 – Serum phosphate and calcium, every 3–
6 months; PTH, every 6–12 months CKD G5, including G5D – Serum phosphate and calcium, every 1–
3 months; PTH, every 3–6 months Investigational therapy Tenapanor, an inhibitor of the
sodium/hydrogen exchanger isoform 3 (NHE3) that acts locally in the gut to reduce absorption of
sodium and phosphate, is being studied in the treatment of chronic kidney disease (CKD) patients
with hyperphosphatemia requiring dialysis. In a phase 1 study in healthy Japanese adults, tenapanor
treatment reduced intestinal absorption of sodium and phosphate. A trial evaluating tenapanor in
the treatment of hyperphosphatemia in end-stage renal disease patients on hemodialysis is
currently recruiting participants.
7. Hypochloremia
Cause: According to Seladi-Schulman (2018), Since the levels of electrolytes in your blood are
regulated by your kidneys, an electrolyte imbalance such as hypochloremia may be caused by a
problem with your kidneys. Hypochloremia can also be caused by any of the following conditions:
congestive heart failure prolonged diarrhea or vomiting chronic lung disease, such as emphysema
metabolic alkalosis, when your blood pH is higher than normal Certain types of drugs, such as
laxatives, diuretics, corticosteroids, and bicarbonates, can also cause hypochloremia. Clinical
Manifestation: According to Seladi-Schulman (2018), You often won’t notice symptoms of
hypochloremia. Instead, you may have symptoms of other electrolyte imbalances or from a
condition that’s causing hypochloremia. Symptoms include: fluid loss dehydration weakness or
fatigue difficulty breathing diarrhea or vomiting, caused by fluid loss Hypochloremia can also
frequently accompany hyponatremia, a low amount of sodium in the blood. Nursing Management:
According to Seladi-Schulman (2018), If your doctor detects an electrolyte imbalance such as
hypochloremia, they’ll investigate whether a condition, disease, or medication you’re taking is
causing the imbalance to occur. Your doctor will work with you to treat the underlying problem
that’s causing the electrolyte imbalance. If your hypochloremia is due to a medication or drug that
you’re taking, then your doctor may adjust the dosage, if possible. If your hypochloremia is due to
problems with your kidneys or an endocrine disorder, your doctor may refer you to a specialist. You
may receive intravenous (IV) fluids, such as normal saline solution, to restore electrolytes to normal
levels. Your doctor may also request that you have your electrolyte levels tested regularly for
monitoring purposes. If your hypochloremia is mild, then it can sometimes be corrected by an
adjustment to your diet. This could be as simple as consuming more sodium chloride (salt). Nursing
Intervention: According to Chase (2015), Nursing Interventions Hypochloremia Monitor I&O Monitor
bicarbonate & sodium level Assess LOC, muscle strength & movement Avoid bottled water (doesn’t
have any electrolytes, so large amts of chloride could be excreted in the kidneys. The water makes
you pee, and in this case, peeing a lot is bad) Pt education: food  in chloride –Tomato juice –
canned vegetables – broth, fruit, processed meat

8. Hyperchloremia
Cause: According to Cafasso (2018), Like sodium, potassium, and other electrolytes, the
concentration of chloride in your body is carefully regulated by your kidneys. The kidneys are two
bean-shaped organs located just below your rib cage on both sides of your spine. They are
responsible for filtering your blood and keeping its composition stable, which allows your body to
function properly. Hyperchloremia occurs when the levels of chloride in the blood become too high.
There are several ways that hyperchloremia can occur. These include: intake of too much saline
solution while in the hospital, such as during a surgery severe diarrhea chronic or acute kidney
disease ingestion of salt water extremely high ingestion of dietary salt bromide poisoning, from
bromide-containing drugs renal or metabolic acidosis, which happens when the kidneys don’t
properly eliminate acid from the body or the body makes an excess of acid respiratory alkalosis, a
condition that occurs when the amount of carbon dioxide in your blood is too low (such as when a
person hyperventilates) long-term use of drugs called carbonic anhydrase inhibitors, which are used
to treat glaucoma and other disorders. Clinical Manifestation: According to Cafasso (2018), The
symptoms that may indicate hyperchloremia are usually those linked to the underlying cause of the
high chloride level. Often this is acidosis, in which the blood is overly acidic. These symptoms may
include: fatigue muscle weakness excessive thirst dry mucous membranes high blood pressure Some
people may not experience any noticeable symptoms of hyperchloremia. The condition is
sometimes not even noticed until a routine blood test. Nursing Management: According to Cafasso
(2018)), The exact treatment for hyperchloremia will depend on its cause: For dehydration,
treatment will include hydration. If you received too much saline, the supply of saline will be
stopped until you recover. If your medications are causing the issue, your doctor might modify or
stop the medication. For a kidney problem, you’ll likely be referred to a nephrologist, a doctor
specializing in kidney health. You may need dialysis to filter your blood in place of your kidneys if
your condition is severe. Hyperchloremic metabolic acidosis may be treated with a base called
sodium bicarbonate. Nursing Intervention: According to Chase (2015); Monitor for those pt at risk
Monitor vital signs Monitor I&O Fluid restriction other than LR Monitor ABG Pt education: diet
restrictions Remember, IV fluid for Hyperchloremia is LR. And also remember, do this slowly! If you
have hyperchloremia, keep yourself well hydrated. Avoid caffeine and alcohol, as these can make
dehydration worse.

B.
What nursing care management will you give to patients with the following imbalances?
1.Fluid volume deficit -Monitor vital signs(compare with patients normal or previous readings
-Notes patients individual pshycological response to bleeding such as weakness,restlessness and
pallor. -Monitor intake and output -Maintain bedrest.Schedule the time of activities to provide
undisturbed rest period. -If necessary blood transfusion
2.Fluid volume excess - Instruct patient, caregiver, and family members regarding fluid restrictions,
as appropriate. - Elevate edematous extremities, and handle with care. - Place the patient in a semi-
 Fowler’s or high-Fowler’s position. - Educate patient and family members regarding fluid volume
excess and its causes. - Educate patient and family members the importance of proper nutrition,
hydration, and diet modification.
3.Hyponatremia - Strictly maintain fluid intake and output of patient hourly. -Check weight everyday
to monitor the fluid volume status. -Monitor and observe skin turgor to identify dehydration and
accurately record state of hydration. -Monitor vital signs carefully and note respiratory rate and
depth to indentify pulmonary edema. -Check and monitor the hyponatremia patient for signs of
edema and hypertension. -Monitor for signs of circulatory overload, as indicated 4.Hypernatremia -
Monitor the patient’s serum sodium levels daily as well to determine the effectiveness of IV fluids. -
Give oral care every 2 hours; avoid using lemon glycerin swabs and alcoholic mouthwashes because
they have a drying effect and can cause discomfort - Nursing management of a shocked patient
needs specialist input and close monitoring, preferably in a high dependency unit. Intravenous
normal saline should be used to correct the extracellular fluid depletion, with calculation of the free
water deficit to determine how much 5% dextrose to give. In patients with hypernatremia of longer
or unknown duration, reducing the sodium concentration more slowly is prudent.

5.Hypokalemia - Record fluid intake and output hourly and observe for dehydration. -Check vitals
sign hourly in critical care unit with severe Hypokalemia. -Continue monitoring ECG and Identify ECG
changes such as depressed T waves, peaking P-waves. -Give mouth care to reduce vomiting
tendency. -Give antiemetic drugs as order. -Monitor for any complications such as paralysis, cardiac
arrest etc.

6. Hyperkalemia

Monitor intake and output.

- Monitor serum potassium and ECG closely during treatment.

• -Teach causes of hyperkalemia and the relationship between

hemodialysis and hyperkalemia.

• -Discuss the importance of avoiding foods high in potassium to

prevent or control hyperkalemia.

 References:
 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2413335/

 https://musculoskeletalkey.com/clinical-manifestations-of-hypocalcemia/

 https://www.mayoclinic.org/diseases-conditions/hypercalcemia/symptoms-
causes/syc-20355523#:~:text=Hypercalcemia%20is%20usually%20a
%20result,calcium%20and%20vitamin%20D%20supplements.
 https://journals.lww.com/nursingcriticalcare/Fulltext/2007/07000/Correct_that_cal
cium.3.aspx#:~:text=Nursing%20interventions%20include%20encouraging
%20fluid,Cardiac%20rhythm%20should%20be%20monitored.&text=Calcium
%20levels%20should%20be%20monitored,due%20to%20use%20of%20diuretics.

 https://www.mdedge.com/familymedicine/article/65567/gastroenterology/what-
are-causes-hypomagnesemia#:~:text=The%20causes%20of%20magnesium
%20depletion,malabsorption%2C%20and%20inadequate%20dietary%20intake.
 https://www.healthline.com/health/hypomagnesemia
 https://www.registerednursern.com/hypomagnesemia-nclex-review-notes-with-
mnemonics-quiz-fluid-electrolytes-for-nursing-students/

 https://www.registerednursern.com/hypermagnesemia-nclex-review-notes-with-
mnemonics-quiz-fluid-electrolytes-for-nursing-students/

 https://www.healthline.com/health/hypophosphatemia#symptoms
 https://www.registerednursern.com/hypophosphatemia-nclex-review-notes-with-
mnemonics-quiz-fluid-electrolytes-for-nursing-students/

 https://www.registerednursern.com/hyperphosphatemia-nclex-review-notes-with-
mnemonics-quiz-fluid-electrolytes-for-nursing-students/

 https://journals.lww.com/nursingmadeincrediblyeasy/Abstract/2004/11000/Phosph
orus__Here,_there,_everywhere.7.aspx

 https://www.healthline.com/health/hypochloremia#takeaway

 http://chemocare.com/chemotherapy/side-effects/hyperchloremia-high-
chloride.aspx
 https://www.coursehero.com/file/p7clq9an/3-nursing-interventions-for-high-and-
low-levels-High-hyperchloremia-monitor/

 https://nurseslabs.com/deficient-fluid-volume/
 https://nurseslabs.com/excess-fluid-volume/
 https://www.registerednursern.com/hyponatremia-nclex-review-notes-with-
mnemonics-quiz-fluid-electrolytes-for-nursing-students/
 https://nurseslabs.com/fluid-and-electrolytes/
 https://www.registerednursern.com/hypokalemia-mnemonics-class-notes-with-a-
fluid-electrolytes-quiz/
 Hyperphosphatemia:
 • Lewis, J. L., (2020), Hyperphasphatemia retrieved from
https://www.msdmanuals.com/professional/endocrine-and-metabolic-
disorders/electrolyte-disorders/hypophosphatemia#:~:text=Hypophosphatemia
%20is%20a%20serum%20phosphate,is%20by%20serum%20phosphate
%20concentration.
 • Lederer, E., (2018) Hyperphosphatemia Treatment & Management retrieved
from https://emedicine.medscape.com/article/241185-treatment
 Hypochloremia:
 • Seladi-Schulman, J., (2018), Hypochloremia: What Is It and How Is It Treated?
Retrieved from https://www.healthline.com/health/hypochloremia
 • Chase, R., (2015) Potassium Major electrolyte in intracellular fluid Normal serum
K+ is 3.5 to 5.0 mEq/L Influences both skeletal and cardiac muscle activity 2% is in
the. Retrieved from https://slideplayer.com/slide/6189458/
 Hyperchloremia:
 • Cafasso, J., (2018), Hyperchloremia (High Chloride Levels), retrieved from
https://www.healthline.com/health/hyperchloremia#treatment
 • Chase, R., (2015) Potassium Major electrolyte in intracellular fluid Normal serum
K+ is 3.5 to 5.0 mEq/L Influences both skeletal and cardiac muscle activity 2% is in
the. Retrieved from https://slideplayer.com/slide/6189458/