1st-Degree Burn. This Minor Burn Affects Only The Outer Layer of The Skin 2nd-Degree Burn. This Type of Burn Affects Both The Epidermis and The Second

Claire Maurice G.
Juanero
BSN III-C
A. BURNS
ETIOLOGY
Burns are tissue damage that results from heat, overexposure to the sun or other
radiation, or chemical or electrical contact. Burns can be minor medical problems or life-
threatening emergencies.
Burns are caused by:
 Fire
 Hot liquid or steam
 Hot metal, glass or other objects
 Electrical currents
 Radiation, such as that from X-rays
 Sunlight or other sources of ultraviolet radiation, such as a tanning bed
 Chemicals such as strong acids, lye, paint thinner or gasoline
 Abuse
SIGNS & SYMPTOMS
Burn symptoms vary depending on how deep the skin damage is. It can take a day or
two for the signs and symptoms of a severe burn to develop.
 1st-degree burn. This minor burn affects only the outer layer of the skin
(epidermis). It may cause redness and pain.
 2nd-degree burn. This type of burn affects both the epidermis and the second
layer of skin (dermis). It may cause swelling and red, white or splotchy skin.
Blisters may develop, and pain can be severe. Deep second-degree burns can
cause scarring.
 3rd-degree burn. This burn reaches to the fat layer beneath the skin. Burned
areas may be black, brown or white. The skin may look leathery. Third-degree
burns can destroy nerves, causing numbness.
DIAGNOSTIC PROCEDURE
If you go to a doctor for burn treatment, he or she will assess the severity of your burn
by examining your skin. He or she may recommend that you be transferred to a burn
center if your burn covers more than 10 percent of your total body surface area, is very
deep, is on the face, feet or groin, or meets other criteria established by the American
Burn Association.
Your doctor will check for other injuries and might order lab tests, X-rays or other
diagnostic procedures
MEDICAL/SURGICAL MANAGEMENT
Most minor burns can be treated at home. They usually heal within a couple of weeks.
For serious burns, after appropriate first aid and wound assessment, your treatment
may involve medications, wound dressings, therapy and surgery. The goals of treatment
are to control pain, remove dead tissue, prevent infection, reduce scarring risk and
regain function. People with severe burns may require treatment at specialized burn
centers. They may need skin grafts to cover large wounds. And they may need
emotional support and months of follow-up care, such as physical therapy.
Medical treatment
After you have received first aid for a major burn, your medical care may include
medications and products that are intended to encourage healing.
 Water-based treatments. Your care team may use techniques such as ultrasound
mist therapy to clean and stimulate the wound tissue.
 Fluids to prevent dehydration. You may need intravenous (IV) fluids to prevent
dehydration and organ failure.
 Pain and anxiety medications. Healing burns can be incredibly painful. You may
need morphine and anti-anxiety medications — particularly for dressing changes.
 Burn creams and ointments. If you are not being transferred to a burn center,
your care team may select from a variety of topical products for wound healing,
such as bacitracin and silver sulfadiazine (Silvadene). These help prevent
infection and prepare the wound to close.
 Dressings. Your care team may also use various specialty wound dressings to
prepare the wound to heal. If you are being transferred to a burn center, your
wound will likely be covered in dry gauze only.
 Drugs that fight infection. If you develop an infection, you may need IV
antibiotics.
 Tetanus shot. Your doctor might recommend a tetanus shot after a burn injury.
Physical and occupational therapy
If the burned area is large, especially if it covers any joints, you may need physical
therapy exercises. These can help stretch the skin so that the joints can remain flexible.
Other types of exercises can improve muscle strength and coordination. And
occupational therapy may help if you have difficulty doing your normal daily activities.
Surgical and other procedures
You may need one or more of the following procedures:
 Breathing assistance. If you've been burned on the face or neck, your throat may
swell shut. If that appears likely, your doctor may insert a tube down your
windpipe (trachea) to keep oxygen supplied to your lungs.
 Feeding tube. People with extensive burns or who are undernourished may need
nutritional support. Your doctor may thread a feeding tube through your nose to
your stomach.
 Easing blood flow around the wound. If a burn scab (eschar) goes completely
around a limb, it can tighten and cut off the blood circulation. An eschar that goes
completely around the chest can make it difficult to breathe. Your doctor may cut
the eschar to relieve this pressure.
 Skin grafts. A skin graft is a surgical procedure in which sections of your own
healthy skin are used to replace the scar tissue caused by deep burns. Donor
skin from deceased donors or pigs can be used as a temporary solution.
 Plastic surgery. Plastic surgery (reconstruction) can improve the appearance of
burn scars and increase the flexibility of joints affected by scarring.
NURSING MANAGEMENT
Nursing care of a patient with burn injury needs to be precise and effective.
 Promoting Gas Exchange and Airway Clearance
 Restoring fluid and Electrolyte Balance
 Maintaining Normal Body Temperature
 Minimizing Pain and Anxiety
 Monitoring and Managing Potential Complications
 Restoring Normal fluid Balance
 Preventing Infection
 Monitor culture results and white blood cell counts.
 Maintaining Adequate Nutrition
 Promoting Skin Integrity
 Relieving Pain and Discomfort
 Encourage patient to use analgesic medications before painful procedures.
 Promoting Physical Mobility
 Strengthening Coping Strategies
 Supporting Patient and Family Processes
 Monitoring and Managing Potential Complications
 Promoting Activity Tolerance
 Improving Body Image and Self-Concept
 Teaching Self-care
B.LIVER CIRRHOSIS
ETIOLOGY
A wide range of diseases and conditions can damage the liver and lead to cirrhosis.
Some of the causes include:
 Chronic alcohol abuse
 Chronic viral hepatitis (hepatitis B, C and D)
 Fat accumulating in the liver (nonalcoholic fatty liver disease)
 Iron buildup in the body (hemochromatosis)
 Cystic fibrosis
 Copper accumulated in the liver (Wilson's disease)
 Poorly formed bile ducts (biliary atresia)
 Alpha-1 antitrypsin deficiency
 Inherited disorders of sugar metabolism (galactosemia or glycogen storage
disease)
 Genetic digestive disorder (Alagille syndrome)
 Liver disease caused by your body's immune system (autoimmune hepatitis)
 Destruction of the bile ducts (primary biliary cirrhosis)
 Hardening and scarring of the bile ducts (primary sclerosing cholangitis
 Infection, such as syphilis or brucellosis
 Medications, including methotrexate or isoniazid
SIGNS & SYMPTOMS
Cirrhosis often has no signs or symptoms until liver damage is extensive. When signs
and symptoms do occur, they may include:
 Fatigue
 Easily bleeding or bruising
 Loss of appetite
 Nausea
 Swelling in your legs, feet or ankles (edema)
 Weight loss
 Itchy skin
 Yellow discoloration in the skin and eyes (jaundice)
 Fluid accumulation in your abdomen (ascites)
 Spiderlike blood vessels on your skin
 Redness in the palms of the hands
 For women, absent or loss of periods not related to menopause
 For men, loss of sex drive, breast enlargement (gynecomastia) or testicular
atrophy
 Confusion, drowsiness and slurred speech (hepatic encephalopathy)
People with early-stage cirrhosis of the liver usually don't have symptoms. Often,
cirrhosis is first detected through a routine blood test or checkup. To help confirm a
diagnosis, a combination of laboratory and imaging tests is usually done
Tests
Your doctor may order one or more tests that may suggest a problem with your liver,
including:
 Laboratory tests. Your doctor may order blood tests to check for signs of liver
malfunction, such as excess bilirubin, as well as for certain enzymes that may
indicate liver damage. To assess kidney function, your blood is checked for
creatinine. You'll be screened for the hepatitis viruses. Your international
normalized ratio (INR) is also checked for your blood's ability to clot.
Based on the blood test results, your doctor may be able to diagnose the underlying
cause of cirrhosis. He or she can also use blood tests to help identify how serious your
cirrhosis is.
 Imaging tests. Magnetic resonance elastography (MRE) may be recommended.
This noninvasive advanced imaging test detects hardening or stiffening of the
liver. Other imaging tests, such as MRI, CT and ultrasound, may also be
done.Biopsy. A tissue sample (biopsy) is not necessarily needed for diagnosis.
However, your doctor may use it to identify the severity, extent and cause of liver
damage.
If you have cirrhosis, your doctor is likely to recommend regular diagnostic tests to
monitor for signs of disease progression or complications, especially esophageal
varices and liver cancer. Noninvasive tests are becoming more widely available for
monitoring.
Treatment for cirrhosis depends on the cause and extent of your liver damage. The
goals of treatment are to slow the progression of scar tissue in the liver and to prevent
or treat symptoms and complications of cirrhosis. You may need to be hospitalized if
you have severe liver damage.
Treatment for the underlying cause of cirrhosis
In early cirrhosis, it may be possible to minimize damage to the liver by treating the
underlying cause. The options include:
 Treatment for alcohol dependency. People with cirrhosis caused by excessive
alcohol use should try to stop drinking. If stopping alcohol use is difficult, your
doctor may recommend a treatment program for alcohol addiction. If you have
cirrhosis, it is critical to stop drinking since any amount of alcohol is toxic to the
liver.
 Weight loss. People with cirrhosis caused by nonalcoholic fatty liver disease may
become healthier if they lose weight and control their blood sugar levels.
 Medications to control hepatitis. Medications may limit further damage to liver
cells caused by hepatitis B or C through specific treatment of these viruses.
 Medications to control other causes and symptoms of cirrhosis. Medications may
slow the progression of certain types of liver cirrhosis. For example, for people
with primary biliary cirrhosis that is diagnosed early, medication may significantly
delay progression to cirrhosis.
Other medications can relieve certain symptoms, such as itching, fatigue and pain.
Nutritional supplements may be prescribed to counter malnutrition associated with
cirrhosis and to prevent weak bones (osteoporosis).
Treatment for complications of cirrhosis
Your doctor will work to treat any complications of cirrhosis, including:
Excess fluid in your body. A low-sodium diet and medication to prevent fluid buildup in
the body may help control ascites and swelling. More-severe fluid buildup may require
procedures to drain the fluid or surgery to relieve pressure.
 Portal hypertension. Certain blood pressure medications may control increased
pressure in the veins that supply the liver (portal hypertension) and prevent
severe bleeding. Your doctor will perform an upper endoscopy at regular
intervals to look for enlarged veins in the esophagus or stomach (varices) that
may bleed.
If you develop varices, you likely will need medication to reduce the risk of bleeding. If
you have signs that the varices are bleeding or are likely to bleed, you may need a
procedure (band ligation) to stop the bleeding or reduce the risk of further bleeding. In
severe cases, you may need a small tube — a transjugular intrahepatic portosystemic
shunt — placed in your vein to reduce blood pressure in your liver.
 Infections. You may receive antibiotics or other treatments for infections. Your
doctor also is likely to recommend vaccinations for influenza, pneumonia and
hepatitis.
 Increased liver cancer risk. Your doctor will likely recommend periodic blood tests
and ultrasound exams to look for signs of liver cancer.
 Hepatic encephalopathy. You may be prescribed medications to help reduce the
buildup of toxins in your blood due to poor liver function.
Liver transplant surgery
In advanced cases of cirrhosis, when the liver ceases to function, a liver transplant may
be the only treatment option. A liver transplant is a procedure to replace your liver with a
healthy liver from a deceased donor or with part of a liver from a living donor. Cirrhosis
is one of the most common reasons for a liver transplant. Candidates for liver transplant
have extensive testing to determine whether they are healthy enough to have a good
outcome following surgery.
Historically, those with alcoholic cirrhosis have not been liver transplant candidates
because of the risk that they will return to harmful drinking after transplant. Recent
studies, however, suggest that carefully selected people with severe alcoholic cirrhosis
have post-transplant survival rates similar to those of liver transplant recipients with
other types of liver disease.
For transplant to be an option if you have alcoholic cirrhosis, you would need:
 To find a program that works with people who have alcoholic cirrhosis
 To meet the requirements of the program, which would include lifelong
commitment to alcohol abstinence as well as other requirements of the specific
transplant center
Potential future treatments
Scientists are working to expand current treatments for cirrhosis, but success has been
limited. Because cirrhosis has numerous causes and complications, there are many
potential avenues of approach. A combination of increased screening, lifestyle changes
and new medications may improve outcomes for people with liver damage, if started
early.
Researchers are working on therapies that will specifically target liver cells, helping to
slow or even reverse the fibrosis that leads to cirrhosis. While no targeted therapy is
quite ready, the framework for developing such treatments is in place, and progress is
accelerating.
NURSING MANAGEMENT
 Observe stools and emesis for color, consistency, and amount, and test each
one for occult blood.
 Monitor fluid intake and output and serum electrolyte levels to prevent
dehydration and hypokalemia, which may precipitate hepatic encephalopathy.
 Maintain some periods of rest with legs elevated to mobilize edema and ascites.
Alternate rest periods with ambulation.
 Encourage and assist with gradually increasing periods of exercise.
 Encourage the patient to eat high-calorie, moderate protein meals and
supplementary feedings. Suggest small, frequent feedings.
 Encourage oral hygiene before meals.
 Administer or teach self-administration of medications for nausea, vomiting,
diarrhea or constipation.
 Encourage frequent skin care, bathing with soap, and massage with emollient
lotions.
 Keep the patient’s finger nails short to prevent scratching from pruritus.
 Keep the patient quiet and limit activity if signs of bleeding are evident.
 Encourage the patient to eat foods high vitamin C content.
 Use small gauge needles for injections and maintain pressure over injection site
until bleeding stops.
 Protect from sepsis through good handwashing and prompt recognition and
management of infection.
 Pad side rails and provide careful nursing surveillance to ensure the patient’s
safety.
 Stress the importance of giving up alcohol completely.
 Involve the person closest to the patient, because recovery usually is not easy
and relapses are common.
C.BUERGER’S DISEASE
ETIOLOGY
The exact cause of Buerger's disease is unknown. While tobacco use clearly plays a
role in the development of Buerger's disease, it's not clear how it does so. It's thought
that chemicals in tobacco may irritate the lining of your blood vessels, causing them to
swell.
Experts suspect that some people may have a genetic predisposition to the disease. It's
also possible that the disease is caused by an autoimmune response in which the
body's immune system mistakenly attacks healthy tissue.
SIGNS & SYMPTOMS
Buerger's disease symptoms include:
 Tingling or numbness in the hands or feet.
 Pale, reddish or blue-tinted hands or feet.
 Pain that may come and go in your legs and feet or in your arms and hands. This
pain may occur when you use your hands or feet and eases when you stop that
activity (claudication), or when you're at rest.
 Inflammation along a vein just below the skin's surface (due to a blood clot in the
vein).
 Fingers and toes that turn pale when exposed to cold (Raynaud's phenomenon).
 Painful open sores on your fingers and toes.
DIAGNOSTIC PROCEDURES
While no tests can confirm whether you have Buerger's disease, your doctor will likely
order tests to rule out other more common conditions or confirm suspicion of Buerger's
disease brought on by your signs and symptoms. Tests may include:
Blood tests
Blood tests to look for certain substances can rule out other conditions that may cause
similar signs and symptoms. For instance, blood tests can help rule out autoimmune
diseases such as scleroderma or lupus, blood-clotting disorders, and diabetes.
The Allen's test
Your doctor may perform a simple test called the Allen's test to check blood flow
through the arteries carrying blood to your hands. In the Allen's test, you make a tight
fist, which forces the blood out of your hand. Your doctor presses on the arteries at
each side of your wrist to slow the flow of blood back into your hand, making your hand
lose its normal color.
Next, you open your hand and your doctor releases the pressure on one artery, then the
other. How quickly the color returns to your hand may give a general indication about
the health of your arteries. Slow blood flow into your hand may indicate a problem, such
as Buerger's disease.
Angiogram
An angiogram helps to see the condition of your arteries. An angiogram can be done
non-invasively with the use of CT or MRI scans.
Or it may be done by threading a catheter into an artery. During this procedure, a
special dye is injected into the artery, after which you undergo a series of rapid X-rays.
The dye helps make any artery blockages easier to see on the images.
Your doctor may order angiograms of both your arms and your legs — even if you don't
have signs and symptoms of Buerger's disease in all of your limbs. Buerger's disease
almost always affects more than one limb, so even though you may not have signs and
symptoms in your other limbs, this test may detect early signs of vessel damage.
Smoking cessation
Although no treatment can cure Buerger's disease, the most effective way to stop the
disease from getting worse is to quit using all tobacco products. Even a few cigarettes a
day can worsen the disease.
Your doctor can counsel you and recommend medications to help you stop smoking
and stop the swelling in your blood vessels. You'll need to avoid nicotine replacement
products because they supply nicotine, which activates Buerger's disease. There are
non-nicotine products that you can use.
Another option is a residential smoking cessation program. In these programs, you stay
at a treatment facility, sometimes a hospital, for a set number of days or weeks. During
that time you participate in daily counseling sessions and other activities to help you
deal with the cravings for cigarettes and to help you learn to live tobacco-free.
Other treatments
Other treatment approaches exist for Buerger's disease, but are less effective than
quitting smoking. Options include:
 Medications to dilate blood vessels, improve blood flow or dissolve blood clots
 Intermittent compression of the arms and legs to increase blood flow to your
extremities
 Spinal cord stimulation
 Amputation, if infection or gangrene occurs
 Potential future treatments
 Nerve surgery. Surgery to cut the nerves to the affected area (surgical
sympathectomy) to control pain and increase blood flow, although this procedure
is controversial and long-term results haven't been well-studied
 Growing new blood vessels. Medications to stimulate growth of new blood
vessels (therapeutic angiogenesis), an approach that is considered experimental
 Bosentan (Tracleer). This medication has been approved for treating high blood
pressure in the lungs. The drug improved blood flow in small studies of people
with Buerger's disease.
 Blood vessel procedure. A thin catheter threaded into the blood vessels may be
able to open blood vessels, restoring blood flow. However, this procedure —
called endovascular therapy — isn't widely used because it hasn't been very
successful in the past. Newer techniques may help improve the success of this
procedure in the future.
NURSING MANAGEMENT
 Patient teaching, instruct the patient to do the following several times a day:
 Lie flat on a bed with both legs elevated above the level of the heart for two to
three minutes.
 Next sit on the edge of the bed with the legs dependent for three minutes
 Then exercise the feet and toes by moving them up, down, inward, then outward.
 Lastly, return to the first position and hold for five minutes.
 Provide for ulcer debridement and healing
 Remove dead or damaged material from the wound, using wet-to-dry dressing
with saline solution and coarse-mesh gauze filled with cotton.
 Use whirlpool therapy to debride the ulcer bed.
 Consider using an enzymatic debrider to aid removal of debris.
 Provide additional intervention to promote venous return and healing, maximize
comfort and provide client education for measures to prevent venous stasis ulcer.
 Administer medications which may include antibiotics.
 The patient is encouraged to make the lifestyle changes necessitated by the
onset of a chronic disease, including pain management and modifications in diet,
activity, and hygiene (skin care).
 The nurse assists the patient in developing and implementing a plan to stop
using tobacco.
D.RAYNAUD’S DISEASE
ETIOLOGY
Doctors don't completely understand the cause of Raynaud's attacks, but blood vessels
in the hands and feet appear to overreact to cold temperatures or stress.
Blood vessels in spasm
With Raynaud's, arteries to your fingers and toes become narrow and briefly limit blood
supply when exposed to cold or stress. Over time, these small arteries can thicken
slightly, further limiting blood flow.
Cold temperatures are most likely to trigger an attack. Exposure to cold, such as putting
your hands in cold water, taking something from a freezer or being in cold air, is the
most likely trigger. For some people, emotional stress can trigger an episode.
Primary vs. secondary Raynaud's
There are two main types of the condition.
 Primary Raynaud's. Also called Raynaud's disease, this most common form isn't
the result of an associated medical condition. It can be so mild that many people
with primary Raynaud's don't seek treatment. And it can resolve on its own.
 Secondary Raynaud's. Also called Raynaud's phenomenon, this form is caused
by an underlying problem. Although secondary Raynaud's is less common than
the primary form, it tends to be more serious.
Signs and symptoms of secondary Raynaud's usually appear around age 40, later than
they do for primary Raynaud's.
Causes of secondary Raynaud's include:
 Connective tissue diseases. Most people who have a rare disease that leads to
hardening and scarring of the skin (scleroderma) have Raynaud's. Other
diseases that increase the risk of Raynaud's include lupus, rheumatoid arthritis
and Sjogren's syndrome.
 Diseases of the arteries. These include a buildup of plaques in blood vessels that
feed the heart, a disorder in which the blood vessels of the hands and feet
become inflamed, and a type of high blood pressure that affects the arteries of
the lungs.
 Carpal tunnel syndrome. This condition involves pressure on a major nerve to
your hand, producing numbness and pain in the hand that can make the hand
more susceptible to cold temperatures.
 Repetitive action or vibration. Typing, playing piano or doing similar movements
for long periods and operating vibrating tools, such as jackhammers, can lead to
overuse injuries.
 Smoking. Smoking constricts blood vessels.
 Injuries to the hands or feet. Examples include a wrist fracture, surgery or
frostbite.
 Certain medications. These include beta blockers for high blood pressure,
migraine medications that contain ergotamine and sumatriptan, attention-
deficit/hyperactivity disorder medications, certain chemotherapy agents, and
drugs that cause blood vessels to narrow, such as some over-the-counter cold
medications.
SIGNS & SYMPTOMS
Signs and symptoms of Raynaud's disease include:
 Cold fingers or toes
 Color changes in your skin in response to cold or stress
 Numb, prickly feeling or stinging pain upon warming or stress relief
During an attack of Raynaud's, affected areas of your skin usually first turn white. Then,
they often turn blue and feel cold and numb. As you warm and your circulation
improves, the affected areas may turn red, throb, tingle or swell.
Although Raynaud's most commonly affects your fingers and toes, it can also affect
other areas of your body, such as your nose, lips, ears and even nipples. After you
warm up, the return of normal blood flow to the area can take 15 minutes.
Your doctor will ask about your symptoms and medical history and perform a physical
examination. Your doctor might also order tests to rule out other medical problems that
can cause similar signs and symptoms.
Sorting out primary vs. secondary Raynaud's
To tell the difference between primary and secondary Raynaud's, your doctor might do
a test called nailfold capillaroscopy. During the test, the doctor looks at the skin at the
base of your fingernail under a microscope or magnifier to look for deformities or
swelling of the tiny blood vessels.
If your doctor thinks that another condition, such as an autoimmune disorder or a
connective tissue disease, may be causing Raynaud's, he or she will likely order blood
tests, such as:
 Antinuclear antibodies test. Testing positive for these antibodies might be a sign
of a stimulated immune system, common in people who have connective tissue
diseases or other autoimmune disorders.
 Erythrocyte sedimentation rate. This test determines the rate at which red blood
cells settle to the bottom of a tube. A faster than normal rate might signal an
underlying inflammatory or autoimmune disease.
No one blood test can diagnose Raynaud's. Your doctor might order other tests, such
as those that rule out diseases of the arteries, to help pinpoint a condition that can be
associated with Raynaud's.
Dressing for the cold in layers and wearing gloves or heavy socks usually are effective
in dealing with mild symptoms of Raynaud's. Medications are available to treat more-
severe forms of the condition. The goals of treatment are to:
 Reduce the number and severity of attacks.
 Prevent tissue damage
 Treat the underlying disease or condition
 Medications
Depending on the cause of your symptoms, medications might help. To widen blood
vessels and increase blood flow, your doctor might prescribe:
 Calcium channel blockers. These drugs relax and open small blood vessels in
your hands and feet, reducing the severity and number of attacks in most people
with Raynaud's. These drugs can also help heal skin ulcers on your fingers or
toes. Examples include nifedipine (Adalat CC, Procardia), amlodipine (Norvasc),
felodipine and isradipine.
 Vasodilators. These drugs, which relax blood vessels, include nitroglycerin cream
(Nitro-Dur) applied to the base of your fingers to help heal skin ulcers. Other
vasodilators include the high blood pressure drug losartan (Cozaar), the erectile
dysfunction medication sildenafil (Viagra, Revatio), the antidepressant fluoxetine
(Prozac, Sarafem) and a class of medications called prostaglandins.
Surgeries and medical procedures
If you have severe Raynaud's, your doctor may recommend surgery or injections.
 Nerve surgery. Sympathetic nerves in your hands and feet control the opening
and narrowing of blood vessels in your skin. Cutting these nerves interrupts their
exaggerated responses.
Through small incisions in the affected hands or feet, a doctor strips these tiny nerves
around the blood vessels. This surgery, if successful, might lead to fewer and shorter
attacks.
 Chemical injection. Doctors can inject chemicals such as local anesthetics or
onabotulinumtoxinA (Botox) to block sympathetic nerves in affected hands or
feet. You might need to have the procedure repeated if symptoms return or
persist.
NURSING MANAGEMENT
 Assess the patient for the blood circulation, color, and sensation to the
extremities.
 Apply warm compress at the affected area.
 Administer the medication as prescribed by doctor such as vasodilator, calcium
channel blockers, and alpha blockers.
 Monitor the blood circulation to the extremities every two hourly(circulation char)
 Encourage patient to perform extremities exercises while sitting or during work.
 Assess the patient’s anxiety level by observing clients behavior
 Reinforce doctor’s explanations to the patient by using the non medical term.
 Provide moral and emotional support to the patient.
 Encourage diversional therapy e.g watching tv, listening songs
 Assess client knowledge level
 Advise patient to stop smoking
 Advise patient not to wear tight wrist band or watch and clothings.
E.ANEMIA
ETIOLOGY
Causes
Anemia occurs when your blood doesn't have enough red blood cells. This can happen
if:
 Your body doesn't make enough red blood cells
 Bleeding causes you to lose red blood cells more quickly than they can be
replaced
 Your body destroys red blood cells
What red blood cells do
Your body makes three types of blood cells — white blood cells to fight infection,
platelets to help your blood clot and red blood cells to carry oxygen throughout your
body.
Red blood cells contain hemoglobin — an iron-rich protein that gives blood its red color.
Hemoglobin enables red blood cells to carry oxygen from your lungs to all parts of your
body and to carry carbon dioxide from other parts of the body to your lungs to be
exhaled.
Most blood cells, including red blood cells, are produced regularly in your bone marrow
— a spongy material found within the cavities of many of your large bones. To produce
hemoglobin and red blood cells, your body needs iron, vitamin B-12, folate and other
nutrients from the foods you eat.
Causes of anemia
Different types of anemia have different causes. They include:
 Iron deficiency anemia. This most common type of anemia is caused by a
shortage of iron in your body. Your bone marrow needs iron to make hemoglobin.
Without adequate iron, your body can't produce enough hemoglobin for red blood
cells.
Without iron supplementation, this type of anemia occurs in many pregnant women. It is
also caused by blood loss, such as from heavy menstrual bleeding, an ulcer, cancer
and regular use of some over-the-counter pain relievers, especially aspirin, which can
cause inflammation of the stomach lining resulting in blood loss.
 Vitamin deficiency anemia. Besides iron, your body needs folate and vitamin B-
12 to produce enough healthy red blood cells. A diet lacking in these and other
key nutrients can cause decreased red blood cell production.
Also, some people who consume enough B-12 aren't able to absorb the vitamin. This
can lead to vitamin deficiency anemia, also known as pernicious anemia.
 Anemia of inflammation. Certain diseases — such as cancer, HIV/AIDS,
rheumatoid arthritis, kidney disease, Crohn's disease and other acute or chronic
inflammatory diseases — can interfere with the production of red blood cells.
 Aplastic anemia. This rare, life-threatening anemia occurs when your body
doesn't produce enough red blood cells. Causes of aplastic anemia include
infections, certain medicines, autoimmune diseases and exposure to toxic
chemicals.
 Anemias associated with bone marrow disease. A variety of diseases, such as
leukemia and myelofibrosis, can cause anemia by affecting blood production in
your bone marrow. The effects of these types of cancer and cancer-like disorders
vary from mild to life-threatening.
 Hemolytic anemias. This group of anemias develops when red blood cells are
destroyed faster than bone marrow can replace them. Certain blood diseases
increase red blood cell destruction. You can inherit a hemolytic anemia, or you
can develop it later in life.
 Sickle cell anemia. This inherited and sometimes serious condition is a hemolytic
anemia. It's caused by a defective form of hemoglobin that forces red blood cells
to assume an abnormal crescent (sickle) shape. These irregular blood cells die
prematurely, resulting in a chronic shortage of red blood cells.
SIGNS & SYMPTOMS
Anemia signs and symptoms vary depending on the cause. If the anemia is caused by a
chronic disease, the disease can mask them, so that the anemia might be detected by
tests for another condition. Depending on the causes of your anemia, you might have
no symptoms. Signs and symptoms, if they do occur, might include:
 Fatigue
 Weakness
 Pale or yellowish skin
 Irregular heartbeats
 Shortness of breath
 Dizziness or lightheadedness
 Chest pain
 Cold hands and feet
 Headaches
At first, anemia can be so mild that you don't notice it. But symptoms worsen as anemia
worsens.
To diagnose anemia, your doctor is likely to ask you about your medical and family
history, perform a physical exam, and run the following tests:
 Complete blood count (CBC). A CBC is used to count the number of blood cells
in a sample of your blood. For anemia, your doctor will be interested in the levels
of the red blood cells contained in your blood (hematocrit) and the hemoglobin in
your blood.
Normal adult hematocrit values vary among medical practices but are generally
between 40% and 52% for men and 35% and 47% for women. Normal adult
hemoglobin values are generally 14 to 18 grams per deciliter for men and 12 to 16
grams per deciliter for women.
 A test to determine the size and shape of your red blood cells. Some of your red
blood cells might also be examined for unusual size, shape and color.
Additional diagnostic tests
If you receive a diagnosis of anemia, your doctor might order additional tests to
determine the cause. Occasionally, it can be necessary to study a sample of your bone
marrow to diagnose anemia.
Anemia treatment depends on the cause.
 Iron deficiency anemia. Treatment for this form of anemia usually involves taking
iron supplements and changing your diet. If the cause of iron deficiency is loss of
blood — other than from menstruation — the source of the bleeding must be
located and the bleeding stopped. This might involve surgery.
 Vitamin deficiency anemias. Treatment for folic acid and vitamin C deficiency
involves dietary supplements and increasing these nutrients in your diet. If your
digestive system has trouble absorbing vitamin B-12 from the food you eat, you
might need vitamin B-12 shots. At first, you might have the shots every other day.
Eventually, you'll need shots just once a month, possibly for life, depending on
your situation.
 Anemia of chronic disease. There's no specific treatment for this type of anemia.
Doctors focus on treating the underlying disease. If symptoms become severe, a
blood transfusion or injections of a synthetic hormone normally produced by your
kidneys (erythropoietin) might help stimulate red blood cell production and ease
fatigue.
 Aplastic anemia. Treatment for this anemia can include blood transfusions to
boost levels of red blood cells. You might need a bone marrow transplant if your
bone marrow can't make healthy blood cells.
 Anemias associated with bone marrow disease. Treatment of these various
diseases can include medication, chemotherapy or bone marrow transplantation.
 Hemolytic anemias. Managing hemolytic anemias includes avoiding suspect
medications, treating infections and taking drugs that suppress your immune
system, which could be attacking your red blood cells. Depending on the cause
or your hemolytic anemia, you might be referred to a heart or vascular specialist.
 Sickle cell anemia. Treatment might include oxygen, pain relievers, and oral and
intravenous fluids to reduce pain and prevent complications. Doctors might also
recommend blood transfusions, folic acid supplements and antibiotics. A cancer
drug called hydroxyurea (Droxia, Hydrea, Siklos) also is used to treat sickle cell
anemia.
 Thalassemia. Most forms of thalassemia are mild and require no treatment. More
severe forms of thalassemia generally require blood transfusions, folic acid
supplements, medication, removal of the spleen, or a blood and bone marrow
stem cell transplant.
NURSING MANAGEMENT
The nursing interventions for a child with iron deficiency anemia are:
 Administer prescribed medications, as ordered:
 Administer IM or IV iron when oral iron is poorly absorbed.
 Perform sensitivity testing of IM iron injection to avoid risk of anaphylaxis.
 Advise patient to take iron supplements an hour before meals for maximum
absorption; if gastric distress occurs, suggest taking the supplement with meals
— resume to between-meals schedule if symptoms subside.
 Inform patient that iron salts change stool to dark green or black.
 Advise patient to take liquid forms of iron via a straw and rinse mouth with water.
 Reduce Fatigue
 Assist the client/caregivers in developing a schedule for daily activity and rest.
 Stress the importance of frequent rest periods.
 Monitor hemoglobin, hematocrit, RBC count, and reticulocyte counts.
 Educate energy-conservation techniques.
 Encourage patient to continue iron therapy for a total therapy time (6 months to a
year), even when fatigue is no longer present.
 Educate the client and caregivers about iron deficiency anemia:
 Explain the importance of the diagnostic procedures (such as complete blood
count), bone marrow aspiration and a possible referral to a hematologist.
 Explain the importance of iron replacement/supplementation.
 Educate the client and the family regarding foods rich in iron (organ and other
meats, leafy green vegetables, molasses, beans).
 Prevent Infection
 Assess for local or systemic signs of infection, such as fever, chills,
swelling, pain, and body malaise.
 Monitor WBC count; anticipate the need for antibiotic, antiviral,
and antifungaltherapy.
 Instruct the client to avoid contact with people with existing infections.
 Stress the importance of daily hygiene, mouth care, and perineal care.
 Prevent Bleeding
 Monitor platelet count; instruct the client/caregivers about bleeding precauBleedi
 Anticipate the need for a platelet transfusion once the platelet count drops to a
very low value.
 Assess the skin for bruises and petechiae.
F.POLYCYTHEMIA
ETIOLOGY
Polycythemia vera occurs when a mutation in a gene causes a problem with blood cell
production. Normally, your body regulates the number of each of the three types of
blood cells you have — red blood cells, white blood cells and platelets. But in
polycythemia vera, your bone marrow makes too many of some of these blood cells.
The cause of the gene mutation in polycythemia vera is unknown, but it's generally not
inherited from your parents.
SIGNS & SYMPTOMS
Many people with polycythemia vera don't have noticeable signs or symptoms. Some
people might develop vague symptoms such as headache, dizziness, fatigue and
blurred vision. More-specific symptoms of polycythemia vera include:
 Itchiness, especially after a warm bath or shower
 Numbness, tingling, burning, or weakness in your hands, feet, arms or legs
 A feeling of fullness soon after eating and bloating or pain in your left upper
abdomen due to an enlarged spleen
 Unusual bleeding, such as a nosebleed or bleeding gums
 Painful swelling of one joint, often the big toe
 Shortness of breath and difficulty breathing when lying down
Your doctor will take a detailed medical history and perform a physical exam.
Blood tests
If you have polycythemia vera, blood tests might reveal:
 More red blood cells than normal and, sometimes, an increase in platelets or
white blood cells
 A greater percentage of red blood cells that make up total blood volume
(hematocrit measurement)
 Elevated levels of the iron-rich protein in red blood cells that carries oxygen
(hemoglobin)
 Very low levels of a hormone that stimulates bone marrow to produce new red
blood cells (erythropoietin)
Bone marrow aspiration or biopsy
If your doctor suspects that you have polycythemia vera, he or she might recommend
collecting a sample of your bone marrow through a bone marrow aspiration or biopsy.
A bone marrow biopsy involves taking a sample of solid bone marrow material. A bone
marrow aspiration is usually done at the same time. During an aspiration, your doctor
withdraws a sample of the liquid portion of your marrow.
Specific gene testing
If you have polycythemia vera, analysis of your bone marrow or blood might show the
gene mutation that's associated with the disease.
There's no cure for polycythemia vera. Treatment focuses on reducing your risk of
complications. These treatments may also ease your symptoms.
Blood withdrawals
The most common treatment for polychythemia vera is having frequent blood
withdrawals, using a needle in a vein (phlebotomy). It's the same procedure used for
donating blood.
This decreases your blood volume and reduces the number of excess blood cells. How
often you need to have blood drawn depends on the severity of your condition.
Treatments to reduce itching
If you have bothersome itching, your doctor may prescribe medication, such as
antihistamines, or recommend ultraviolet light treatment to relieve your discomfort.
Medications that are normally used to treat depression, called selective serotonin
reuptake inhibitors (SSRIs), helped relieve itching in clinical trials. Examples
of SSRIs include paroxetine (Brisdelle, Paxil, Pexeva, others) or fluoxetine (Prozac,
Sarafem, Selfemra, others).
Drugs that reduce the number of red blood cells
If phlebotomy alone doesn't help enough, your doctor may suggest medications that can
reduce the number of red blood cells in your bloodstream. Examples include:
 Hydroxyruea (Droxia, Hydrea)
 Interferon alfa-2b (Intron A)
 Ruxolitinib (Jakafi)
 Busulfan (Busulfex, Myleran)
Heart medications
Your doctor will also likely prescribe medications to control risk factors for heart and
blood vessel disease, including high blood pressure, diabetes and abnormal cholesterol.
Your doctor may recommend that you take a low dose of aspirin to reduce your risk of
blood clots. Low-dose aspirin may also help reduce burning pain in your feet or hands.
NURSING MANAGEMENT
 Restrict visitors or medical personnel with bacterial or viral infections
 Provide instruction on handwashing to patient and visitors
 Monitor for signs and symptoms of infection
 Maintain standard precautions
 Utilize strict asepsis for procedures
 Avoid fresh flowers and plants
 Provide high-protein, high-vitamin, high-calorie soft diet to maintain nutritional
status
 Avoid raw foods, such as sushi, Caesar salad dressing(may have raw eggs),
blue cheese, and fruits that cannot be peeled or vegetables that cannot be well
cleaned
 Encourage increased fluid intake to prevent dehydration
 Monitor vital signs to assess for signs of infection
 Observe the patient for extreme fatigue, sore throat or mouth, and fever as signs
of infection
 Monitor laboratory values
 Relieve fever with tepid bath or cooling blanket
 Administer antibiotics as prescribed
 Provide hygiene with adequate rest periods.
G.HEMOPHILIA
ETIOLOGY
When you bleed, your body normally pools blood cells together to form a clot to stop the
bleeding. The clotting process is encouraged by certain blood particles. Hemophilia
occurs when you have a deficiency in one of these clotting factors.
There are several types of hemophilia, and most forms are inherited. However, about
30% of people with hemophilia have no family history of the disorder. In these people,
an unexpected change occurs in one of the genes associated with hemophilia.
Acquired hemophilia is a rare variety of the condition that occurs when a person's
immune system attacks clotting factors in the blood. It can be associated with:
 Pregnancy
 Autoimmune conditions
 Cancer
 Multiple sclerosis
 Hemophilia inheritance
In the most common types of hemophilia, the faulty gene is located on the X
chromosome. Everyone has two sex chromosomes, one from each parent. A female
inherits an X chromosome from her mother and an X chromosome from her father. A
male inherits an X chromosome from his mother and a Y chromosome from his father.
This means that hemophilia almost always occurs in boys and is passed from mother to
son through one of the mother's genes. Most women with the defective gene are simply
carriers and experience no signs or symptoms of hemophilia. But some carriers can
experience bleeding symptoms if their clotting factors are moderately decreased.
SIGNS & SYMPTOMS
Signs and symptoms of hemophilia vary, depending on your level of clotting factors. If
your clotting-factor level is mildly reduced, you may bleed only after surgery or trauma.
If your deficiency is severe, you may experience spontaneous bleeding.
Signs and symptoms of spontaneous bleeding include:
Unexplained and excessive bleeding from cuts or injuries, or after surgery or dental
work
 Many large or deep bruises
 Unusual bleeding after vaccinations
 Pain, swelling or tightness in your joints
 Blood in your urine or stool
 Nosebleeds without a known cause
 In infants, unexplained irritability
 Bleeding into the brain
A simple bump on the head can cause bleeding into the brain for some people who
have severe hemophilia. This rarely happens, but it's one of the most serious
complications that can occur. Signs and symptoms include:
 Painful, prolonged headache
 Repeated vomiting
 Sleepiness or lethargy
 Double vision
 Sudden weakness or clumsiness
 Convulsions or seizures
For people with a family history of hemophilia, it's possible to determine during
pregnancy if the fetus is affected by hemophilia. However, the testing poses some risks
to the fetus. Discuss the benefits and risks of testing with your doctor.
In children and adults, a blood test can reveal a clotting-factor deficiency. Depending on
the severity of the deficiency, hemophilia symptoms can first arise at various ages.
Severe cases of hemophilia usually are diagnosed within the first year of life. Mild forms
may not be apparent until adulthood. Some people first learn that they have hemophilia
after they bleed excessively during a surgical procedure.
Several different types of clotting factors are associated with different varieties of
hemophilia. The main treatment for severe hemophilia involves receiving replacement of
the specific clotting factor that you need through a tube placed in a vein.
This replacement therapy can be given to combat a bleeding episode that's in progress.
It can also be administered on a regular schedule at home to help prevent bleeding
episodes. Some people receive continuous replacement therapy.
Replacement clotting factor can be made from donated blood. Similar products, called
recombinant clotting factors, are manufactured in a laboratory and aren't made from
human blood.
Other therapies may include:
 Desmopressin. In some forms of mild hemophilia, this hormone can stimulate
your body to release more clotting factor. It can be injected slowly into a vein or
provided as a nasal spray.
 Clot-preserving medications. These medications help prevent clots from breaking
down.
 Fibrin sealants. These medications can be applied directly to wound sites to
promote clotting and healing. Fibrin sealants are especially useful in dental
therapy.
 Physical therapy. It can ease signs and symptoms if internal bleeding has
damaged your joints. If internal bleeding has caused severe damage, you may
need surgery.
 First aid for minor cuts. Using pressure and a bandage will generally take care of
the bleeding. For small areas of bleeding beneath the skin, use an ice pack. Ice
pops can be used to slow down minor bleeding in the mouth.
 Vaccinations. Although blood products are screened, it's still possible for people
who rely on them to contract diseases. If you have hemophilia, consider receiving
immunization against hepatitis A and B.
NURSING MANAGEMENT
The nursing interventions for a child with hemophilia are:
 Relieve pain. Immobilize joints and apply elastic bandages to the affected joint if
indicated; elevate affected and apply a cold compress to active bleeding sites,
but must be used cautiously in young children to prevent skin breakdown.
 Maintain optimal physical mobility. Provide gentle, passive ROM exercise when
the child’s condition is stable; educate on preventive measures, such as the
application of protective gear and the administration of factor products; and refer
for physical therapy, occupational therapy, and orthopedic consultations, as
required
 Assist in the coping of the family. Encourage family members to verbalize
problem areas and develop solutions on their own; encourage family members to
express feelings, such as how they deal with the chronic needs of a family
member and coping patterns that help or hinder adjustment to the process.
 Prevent bleeding. Monitor hemoglobin and hematocrit levels; assess for inhibitor
antibody to factor VIII; anticipate or instruct in the need for prophylactic treatment
before high-risk situations, such as invasive diagnostic or surgical procedures, or
dental work; and provide replacement therapy of deficient clotting factors.
 Prevent injury. Utilize appropriate toys (soft, not pointed or small sharp objects);
for infants, may need to use padded bed rail sides on crib; avoid rectal
temperatures; provide appropriate oral hygiene (use of a water irrigating device;
use of a soft toothbrush or softening the toothbrush with warm water before
brushing; use of sponge-tipped toothbrush); and avoid contact sports such as
football, soccer, ice hockey, karate.
H.DIC
ETIOLOGY
When the proteins used in your normal clotting process become overly active, it can
cause DIC. Infection, severe trauma (such as brain injuries or crushing injuries),
inflammation, surgery, and cancer are all known to contribute to this condition.
Some less common causes of DIC include the following:
 extremely low body temperature (hypothermia)
 venomous snake bites
 pancreatitis
 burns
 complications during pregnancy
You may also develop DIC if you go into shock.
SIGNS & SYMPTOMS
Bleeding, sometimes from multiple locations on the body, is one of the more common
symptoms of DIC. Bleeding from the mucosal tissue (in the mouth and nose) and other
external areas may occur. In addition, DIC may cause internal bleeding.
Other symptoms are:
 blood clots
 decreased blood pressure
 easy bruising
 rectal or vaginal bleeding
 red dots on the surface of the skin (petechiae)
If you have cancer, DIC generally begins slowly, and clotting in the veins is more
common than excessive bleeding.
DIC may be identified through various tests related to your levels of platelets, clotting
factors, and other blood components. However, there isn’t a standard procedure. The
following are some tests that may be conducted if your doctor suspects DIC:
 fibrin degradation product
 complete blood cell count from a blood smear
 complete blood cell count from a sample
 platelet count
 partial thromboplastin time
 D-dimer test
 serum fibrinogen
 prothrombin time
DIC treatment depends on what is causing the disorder. Treatment of the underlying
cause is the main goal. To treat the clotting problem, you may be given an anticoagulant
called heparin to reduce and prevent clotting. However, heparin may not be
administered if you have a severe lack of platelets or are bleeding too excessively
People with acute (sudden) DIC require hospitalization, often in an intensive care unit
(ICU), where treatment will attempt to correct the problem causing the DIC while
maintaining the function of the organs.
A transfusion may be needed to replace the platelets that you are missing. Plasma
transfusions have the ability to replace the clotting factors that you’re lacking.
NURSING MANAGEMENT
 Assess and monitor respiratory status; note rate, rhythm, cyanosis; auscultate
the lungs for areas of absent air movement
 Assess and monitor cardiac status; perform 12-lead ECG as indicated
 Assess for changes in level of consciousness
 Administer oxygen as necessary; monitor Arterial Blood Gas (ABG) and oxygen
saturation
 Provide wound care and pressure for external bleeding
 Provide wound care and pressure for external bleeding
 Monitor for blood in stool; administer stool softeners to avoid straining during
bowel movements
 Monitor for hemoptysis or blood in suctioning
 Monitor diagnostic tests (labs):Platelet count- decreased, PT / PTT- increased,
D-dimer level- markedly increased.
 Initiate bleeding precautions; no razors, soft toothbrush, limit needle sticks as
much as possible, limit BP readings
 Administer medications and blood products as necessary
I.BODY FLUID COMPOSITION
The composition of tissue fluid depends upon the exchanges between the cells in the
biological tissue and the blood. This means that fluid composition varies between body
compartments.
The compositions of the two components of the ECF—plasma and IF—are more similar
to each other than either is to the ICF. Blood plasma has high concentrations of sodium,
chloride, bicarbonate, and protein. The IF has high concentrations of sodium, chloride,
and bicarbonate, but a relatively lower concentration of protein. In contrast, the ICF has
elevated amounts of potassium, phosphate, magnesium, and protein. Overall, the ICF
contains high concentrations of potassium and phosphate (HPO42−HPO42−), whereas
both plasma and the ECF contain high concentrations of sodium and chloride.
Most body fluids are neutral in charge. Thus, cations, or positively charged ions, and
anions, or negatively charged ions, are balanced in fluids. As seen in the previous
graph, sodium (Na+) ions and chloride (Cl–) ions are concentrated in the ECF of the
body, whereas potassium (K+) ions are concentrated inside cells. Although sodium and
potassium can “leak” through “pores” into and out of cells, respectively, the high levels
of potassium and low levels of sodium in the ICF are maintained by sodium-potassium
pumps in the cell membranes. These pumps use the energy supplied by ATP to pump
sodium out of the cell and potassium into the cell.
The Sodium-Potassium Pump. The sodium-potassium pump is powered by ATP to
transfer sodium out of the cytoplasm and into the ECF. The pump also transfers
potassium out of the ECF and into the cytoplasm.
On the basis of evidence available from initial studies on body fluids and consensus:
 Total body water (60% of body weight in male adolescents) is divided into
extracellular fluid (ECF) and intracellular fluid (ICF). Blood volume (5% of body
weight) is responsible for ensuring circulatory flow to organs.
 Sodium is primarily present in the ECF and potassium in the ICF, but serum
concentrations of sodium or potassium do not reflect their respective total body
content.
 Two major mechanisms regulate water metabolism: thirst and arginine
vasopressin (also known as antidiuretic hormone). Sodium content, regulated by
complex mechanisms (juxtaglomerular apparatus, renin-angiotensin-aldosterone
system, glomerular filtration rate, and others), is responsible for maintaining the
ECF volume.
 Serum osmolality is calculated using sodium, glucose, and blood urea nitrogen
measurements.
 Hypernatremia or hyperosmolality is an indicator of relative deficiency of water to
solute in the ECF. This free water deficit is corrected slowly to prevent seizure
and cerebral edema.
 Hyponatremia or hypo-osmolality is an indicator of relative excess of water to
solute in the ECF (dilutional or total body deficit of solute). Rapid correction
causes osmotic shift of water from brain cells to the ECF and leads to central
pontine myelinolysis.
J.BODY FLUID DISTRIBUTION
The distribution of fluid throughout the body can be broken down into two general
categories: intracellular fluid and extracellular fluid. Intracellular fluid is approximately
40% of the total body weight. It is the total space within cells primarily defined as the
cytoplasm of cells. In general, intracellular fluids are stable and do not readily adjust to
rapid changes. This space is where much of chemical reactions occur, as such, it is
important to maintain an appropriate osmolality. The extracellular fluid comprises
approximately 20% of total body weight and further subcategorizes as plasma at
approximately 5% of body weight and interstitial space which is approximately 12% of
body weight. Additional fluid spaces are possible in pathological scenarios and are
categorized as a transudate or exudate based on location and etiology.
Intercellular Fluid
The ICF lies within cells and is the principal component of the cytosol/cytoplasm. The
ICF makes up about 60 percent of the total water in the human body, and in an
average-size adult male, the ICF accounts for about 25 liters (seven gallons) of fluid.
This fluid volume tends to be very stable, because the amount of water in living cells is
closely regulated. If the amount of water inside a cell falls to a value that is too low, the
cytosol becomes too concentrated with solutes to carry on normal cellular activities; if
too much water enters a cell, the cell may burst and be destroyed.
 Most of the water in the body is intracellular fluid. The second largest volume is
the interstitial fluid, which surrounds cells that are not blood cells.
Extracellular Fluid
The ECF accounts for the other one-third of the body’s water content. Approximately 20
percent of the ECF is found in plasma. Plasma travels through the body in blood
vessels and transports a range of materials, including blood cells, proteins (including
clotting factors and antibodies), electrolytes, nutrients, gases, and wastes. Gases,
nutrients, and waste materials travel between capillaries and cells through the IF. Cells
are separated from the IF by a selectively permeable cell membrane that helps regulate
the passage of materials between the IF and the interior of the cell.
The body has other water-based ECF. These include the cerebrospinal fluid that bathes
the brain and spinal cord, lymph, the synovial fluid in joints, the pleural fluid in the
pleural cavities, the pericardial fluid in the cardiac sac, the peritoneal fluid in the
peritoneal cavity, and the aqueous humor of the eye. Because these fluids are outside
of cells, these fluids are also considered components of the ECF compartment.
K.BODY FLUID MOVEMENT
Hydrostatic pressure, the force exerted by a fluid against a wall, causes movement of
fluid between compartments. The hydrostatic pressure of blood is the pressure exerted
by blood against the walls of the blood vessels by the pumping action of the heart. In
capillaries, hydrostatic pressure (also known as capillary blood pressure) is higher than
the opposing “colloid osmotic pressure” in blood—a “constant” pressure primarily
produced by circulating albumin—at the arteriolar end of the capillary.
This pressure forces plasma and nutrients out of the capillaries and into surrounding
tissues. Fluid and the cellular wastes in the tissues enter the capillaries at the venule
end, where the hydrostatic pressure is less than the osmotic pressure in the vessel.
Filtration pressure squeezes fluid from the plasma in the blood to the IF surrounding the
tissue cells. The surplus fluid in the interstitial space that is not returned directly back to
the capillaries is drained from tissues by the lymphatic system, and then re-enters the
vascular system at the subclavian veins.
Capillary Exchange. Net filtration occurs near the arterial end of the capillary since
capillary hydrostatic pressure (CHP) is greater than blood colloidal osmotic pressure
(BCOP). There is no net movement of fluid near the midpoint of the capillary since CHP
= BCOP. Net reabsorption occurs near the venous end of the capillary since BCOP is
greater than CHP.
Hydrostatic pressure is especially important in governing the movement of water in
the nephrons of the kidneys to ensure proper filtering of the blood to form urine. As
hydrostatic pressure in the kidneys increases, the amount of water leaving the
capillaries also increases, and more urine filtrate is formed. If hydrostatic pressure in the
kidneys drops too low, as can happen in dehydration, the functions of the kidneys will
be impaired, and less nitrogenous wastes will be removed from the bloodstream.
Extreme dehydration can result in kidney failure.
Fluid also moves between compartments along an osmotic gradient. Recall that an
osmotic gradient is produced by the difference in concentration of all solutes on either
side of a semi-permeable membrane. The magnitude of the osmotic gradient is
proportional to the difference in the concentration of solutes on one side of the cell
membrane to that on the other side. Water will move by osmosis from the side where its
concentration is high (and the concentration of solute is low) to the side of the
membrane where its concentration is low (and the concentration of solute is high). In the
body, water moves by osmosis from plasma to the IF (and the reverse) and from the IF
to the ICF (and the reverse). In the body, water moves constantly into and out of fluid
compartments as conditions change in different parts of the body.
For example, if you are sweating, you will lose water through your skin. Sweating
depletes your tissues of water and increases the solute concentration in those tissues.
As this happens, water diffuses from your blood into sweat glands and surrounding skin
tissues that have become dehydrated because of the osmotic gradient. Additionally, as
water leaves the blood, it is replaced by the water in other tissues throughout your body
that are not dehydrated. If this continues, dehydration spreads throughout the body.
When a dehydrated person drinks water and rehydrates, the water is redistributed by
the same gradient, but in the opposite direction, replenishing water in all of the tissues.
L.BODY FLUID REGULATION
The major hormones regulating body fluids are ADH, aldosterone and ANH.
Progesterone is similar in structure to aldosterone and can bind to and weakly stimulate
aldosterone receptors, providing a similar but diminished response. Blood pressure is a
reflection of blood volume and is monitored by baroreceptors in the aortic arch and
carotid sinuses. When blood pressure increases, more action potentials are sent to the
central nervous system, resulting in greater vasodilation, greater GFR, and more water
lost in the urine. ANH is released by the cardiomyocytes when blood pressure
increases, causing Na+ and water loss. ADH at high levels causes vasoconstriction in
addition to its action on the collecting ducts to recover more water. Diuretics increase
urine volume. Mechanisms for controlling Na+ concentration in the blood include the
renin–angiotensin–aldosterone system and ADH. When Na+ is retained, K+ is excreted;
when Na+ is lost, K+ is retained. When circulating Ca++ decreases, PTH stimulates the
reabsorption of Ca++ and inhibits reabsorption of HPO42−. pH is regulated through
buffers, expiration of CO2, and excretion of acid or base by the kidneys. The breakdown
of amino acids produces ammonia. Most ammonia is converted into less-toxic urea in
the liver and excreted in the urine. Regulation of drugs is by glomerular filtration, tubular
secretion, and tubular reabsorption.
Fluid and Electrolyte Balance
The kidneys are essential for regulating the volume and composition of bodily fluids.
This page outlines key regulatory systems involving the kidneys for controlling volume,
sodium and potassium concentrations, and the pH of bodily fluids.
A most critical concept for you to understand is how water and sodium regulation are
integrated to defend the body against all possible disturbances in the volume and
osmolarity of bodily fluids. Simple examples of such disturbances include dehydration,
blood loss, salt ingestion, and plain water ingestion.
Water balance
Water balance is achieved in the body by ensuring that the amount of water consumed
in food and drink (and generated by metabolism) equals the amount of water excreted.
The consumption side is regulated by behavioral mechanisms, including thirst and salt
cravings. While almost a liter of water per day is lost through the skin, lungs, and feces,
the kidneys are the major site of regulated excretion of water.
One way the kidneys can directly control the volume of bodily fluids is by the amount of
water excreted in the urine. Either the kidneys can conserve water by producing urine
that is concentrated relative to plasma, or they can rid the body of excess water by
producing urine that is dilute relative to plasma.
Direct control of water excretion in the kidneys is exercised by vasopressin, or anti-
diuretic hormone (ADH), a peptide hormone secreted by the hypothalamus. ADH
causes the insertion of water channels into the membranes of cells lining the collecting
ducts, allowing water reabsorption to occur. Without ADH, little water is reabsorbed in
the collecting ducts and dilute urine is excreted.
ADH secretion is influenced by several factors (note that anything that stimulates ADH
secretion also stimulates thirst):
1. By special receptors in the hypothalamus that are sensitive to increasing plasma
osmolarity (when the plasma gets too concentrated). These stimulate ADH secretion.
2. By stretch receptors in the atria of the heart, which are activated by a larger than
normal volume of blood returning to the heart from the veins. These inhibit ADH
secretion, because the body wants to rid itself of the excess fluid volume.
3. By stretch receptors in the aorta and carotid arteries, which are stimulated when
blood pressure falls. These stimulate ADH secretion, because the body wants to
maintain enough volume to generate the blood pressure necessary to deliver blood to
the tissues.
Sodium balance
In addition to regulating total volume, the osmolarity (the amount of solute per unit
volume) of bodily fluids is also tightly regulated. Extreme variation in osmolarity causes
cells to shrink or swell, damaging or destroying cellular structure and disrupting normal
cellular function.
Regulation of osmolarity is achieved by balancing the intake and excretion of sodium
with that of water. (Sodium is by far the major solute in extracellular fluids, so it
effectively determines the osmolarity of extracellular fluids.)
An important concept is that regulation of osmolarity must be integrated with regulation
of volume, because changes in water volume alone have diluting or concentrating
effects on the bodily fluids. For example, when you become dehydrated you lose
proportionately more water than solute (sodium), so the osmolarity of your bodily fluids
increases. In this situation the body must conserve water but not sodium, thus
stemming the rise in osmolarity. If you lose a large amount of blood from trauma or
surgery, however, your loses of sodium and water are proportionate to the composition
of bodily fluids. In this situation the body should conserve both water and sodium.
As noted above, ADH plays a role in lowering osmolarity (reducing sodium
concentration) by increasing water reabsorption in the kidneys, thus helping to dilute
bodily fluids. To prevent osmolarity from decreasing below normal, the kidneys also
have a regulated mechanism for reabsorbing sodium in the distal nephron. This
mechanism is controlled by aldosterone, a steroid hormone produced by the adrenal
cortex. Aldosterone secretion is controlled two ways:
1.The adrenal cortex directly senses plasma osmolarity. When the osmolarity increases
above normal, aldosterone secretion is inhibited. The lack of aldosterone causes less
sodium to be reabsorbed in the distal tubule. Remember that in this setting ADH
secretion will increase to conserve water, thus complementing the effect of low
aldosterone levels to decrease the osmolarity of bodily fluids. The net effect on urine
excretion is a decrease in the amount of urine excreted, with an increase in the
osmolarity of the urine.
2. The kidneys sense low blood pressure (which results in lower filtration rates and
lower flow through the tubule). This triggers a complex response to raise blood pressure
and conserve volume. Specialized cells (juxtaglomerular cells) in the afferent and
efferent arterioles produce renin, a peptide hormone that initiates a hormonal cascade
that ultimately produces angiotensin II. Angiotensin II stimulates the adrenal cortex to
produce aldosterone.
M. HYPONATREMIA
Hyponatremia occurs when the concentration of sodium in your blood is abnormally low.
Sodium is an electrolyte, and it helps regulate the amount of water that's in and around
your cells.
In hyponatremia, one or more factors — ranging from an underlying medical condition to
drinking too much water — cause the sodium in your body to become diluted. When this
happens, your body's water levels rise, and your cells begin to swell. This swelling can
cause many health problems, from mild to life-threatening.
Hyponatremia treatment is aimed at resolving the underlying condition. Depending on
the cause of hyponatremia, you may simply need to cut back on how much you drink. In
other cases of hyponatremia, you may need intravenous electrolyte solutions and
medications.
Symptoms
Hyponatremia signs and symptoms may include:
 Nausea and vomiting
 Headache
 Confusion
 Loss of energy, drowsiness and fatigue
 Restlessness and irritability
 Muscle weakness, spasms or cramps
 Seizures
 Coma
Causes
Sodium plays a key role in your body. It helps maintain normal blood pressure, supports
the work of your nerves and muscles, and regulates your body's fluid balance.
A normal blood sodium level is between 135 and 145 milliequivalents per liter (mEq/L).
Hyponatremia occurs when the sodium in your blood falls below 135 mEq/L.
Many possible conditions and lifestyle factors can lead to hyponatremia, including:
 Certain medications. Some medications, such as some water pills (diuretics),
antidepressants and pain medications, can interfere with the normal hormonal
and kidney processes that keep sodium concentrations within the healthy normal
range.
 Heart, kidney and liver problems. Congestive heart failure and certain
diseases affecting the kidneys or liver can cause fluids to accumulate in your
body, which dilutes the sodium in your body, lowering the overall level.
 Syndrome of inappropriate anti-diuretic hormone (SIADH). In this condition,
high levels of the anti-diuretic hormone (ADH) are produced, causing your body
to retain water instead of excreting it normally in your urine.
 Chronic, severe vomiting or diarrhea and other causes of dehydration. This
causes your body to lose electrolytes, such as sodium, and also increases ADH
levels.
 Drinking too much water. Drinking excessive amounts of water can cause low
sodium by overwhelming the kidneys' ability to excrete water. Because you lose
sodium through sweat, drinking too much water during endurance activities, such
as marathons and triathlons, can also dilute the sodium content of your blood.
 Hormonal changes. Adrenal gland insufficiency (Addison's disease) affects your
adrenal glands' ability to produce hormones that help maintain your body's
balance of sodium, potassium and water. Low levels of thyroid hormone also can
cause a low blood-sodium level.
 The recreational drug Ecstasy. This amphetamine increases the risk of severe
and even fatal cases of hyponatremia.
Risk factors
The following factors may increase your risk of hyponatremia:
 Age. Older adults may have more contributing factors for hyponatremia,
including age-related changes, taking certain medications and a greater
likelihood of developing a chronic disease that alters the body's sodium balance.
 Certain drugs. Medications that increase your risk of hyponatremia include
thiazide diuretics as well as some antidepressants and pain medications. In
addition, the recreational drug Ecstasy has been linked to fatal cases of
hyponatremia.
 Conditions that decrease your body's water excretion. Medical conditions
that may increase your risk of hyponatremia include kidney disease, syndrome of
inappropriate anti-diuretic hormone (SIADH) and heart failure, among others.
 Intensive physical activities. People who drink too much water while taking
part in marathons, ultramarathons, triathlons and other long-distance, high-
intensity activities are at an increased risk of hyponatremia.
Diagnosis
Your doctor will start by asking about your medical history and doing a physical
examination.
However, because the signs and symptoms of hyponatremia occur in many conditions,
it's impossible to diagnose the condition based on a physical exam alone. To confirm
low blood sodium, your doctor will order blood tests and urine tests.
Treatment
Hyponatremia treatment is aimed at addressing the underlying cause, if possible.
If you have moderate, chronic hyponatremia due to your diet, diuretics or drinking too
much water, your doctor may recommend temporarily cutting back on fluids. He or she
may also suggest adjusting your diuretic use to increase the level of sodium in your
blood.
If you have severe, acute hyponatremia, you'll need more-aggressive treatment.
Options include:
 Intravenous fluids. Your doctor may recommend IV sodium solution to slowly
raise the sodium levels in your blood. This requires a stay in the hospital for
frequent monitoring of sodium levels as too rapid of a correction is dangerous.
 Medications. You may take medications to manage the signs and symptoms of
hyponatremia, such as headaches, nausea and seizures.
Nursing Interventions
1. Strictly maintain fluid intake and output of patient hourly.
2. Check weight everyday to monitor the fluid volume status.
3. Monitor and observe skin turgor to identify dehydration and accurately record
state of hydration.
4. Monitor vital signs carefully and note respiratory rate and depth to indentify
pulmonary edema.
5. Check and monitor the hyponatremia patient for signs of edema and
hypertension.
6. Monitor for signs of circulatory overload, as indicated
7. Ensure high sodium containing food such as milk, meat, eggs, carrots, beets and
celery.
8. Ensure adequate dietary sodium intake of 90 to 250 mEq Day.
9. Monitor and observe for neuromuscular changes such as declining levels of
consciousness, fatigue and muscular weakness.
10. Give supplemental oxygen to lethargy or unconscious patient as needed.
11. Patient with sodium imbalances often are confused and act as crazy. So ensure
safety measure.
12. Maintain quiet environment.
13. Keep bed in low locked position.
14. Keep side rails up to prevent fall.
15. Keep nurse call within reach and instruct patient to call nurse for any assistance.
16. Carefully monitor hyponatremia patient for any sign of convulsion and notify to
physician.
17. Take seizure precautions as order.
18. Monitor laboratory serum sodium levels as order to determine the effectiveness
of IV fluids.
19. Administer prescribed medication as order.
20. Carefully administer the 3% or 5% sodium containing fluid by using infusion
pump as prescribed.
21. Monitor IV site for patency, signs of infiltration such as redness or irritation.
22. Identify the specific cause of hyponatremia such as sodium loss or fluid excess.
23. Give mouth care frequently as dry mouth and saliva production decreased.
24. Irrigate nasogastric tube with normal saline instead of plain water.
25. Prepare patient for dialysis as indicated.
26. Address acute life threatening conditions and initiate supportive care.
N. Hypernatremia
Hypernatremia is the medical term used to describe having too much sodium in the
blood. Sodium is an important nutrient for proper functioning of the body. Most of the
body’s sodium is found in the blood. It’s also a necessary part of the body’s lymph fluids
and cells.
In many cases, hypernatremia is mild and doesn’t cause serious problems. However, in
order to prevent or reverse problems caused by hypernatremia, it’s important to correct
high sodium levels.
Hypernatremia is a common electrolyte problem that is defined as a rise in serum
sodium concentration to a value exceeding 145 mmol/L. [1, 2, 3] It is strictly defined as a
hyperosmolar condition caused by a decrease in total body water (TBW) [4] relative to
electrolyte content. Hypernatremia is a “water problem,” not a problem of sodium
homeostasis.
Symptoms and Signs

The major symptom of hypernatremia is thirst. The absence of thirst in conscious
patients with hypernatremia suggests an impaired thirst mechanism. Patients with
difficulty communicating or ambulating may be unable to express thirst or obtain access
to water. Sometimes patients with difficulty communicating express thirst by becoming
agitated.
The major signs of hypernatremia result from central nervous system (CNS) dysfunction
due to brain cell shrinkage. Confusion, neuromuscular excitability, hyperreflexia,
seizures, or coma may result. Cerebrovascular damage with subcortical or
subarachnoid hemorrhage and venous thromboses have been described in children
who died of severe hypernatremia.
In chronic hypernatremia, osmotically active substances are generated in CNS cells
(idiogenic osmoles) and increase intracellular osmolality. Therefore, the degree of brain
cell dehydration and resultant CNS symptoms are less severe in chronic than in acute
hypernatremia.
When hypernatremia occurs with abnormal total body sodium, the typical symptoms
of volume depletion or volume overload are present. Patients with renal concentrating
defects typically excrete a large volume of hypotonic urine. When losses are extrarenal,
the route of water loss is often evident (eg, vomiting, diarrhea, excessive sweating), and
the urinary sodium concentration is low.
Epidemiology
Hypernatremia reflects a deficit of total body water (TBW) relative to total body sodium
content. Because total body sodium content is reflected by extracellular fluid (ECF)
volume status, hypernatremia must be considered along with status of the ECF volume:
 Hypovolemia
 Euvolemia
 Hypervolemia
Note that the ECF volume is not the same as effective plasma volume. For example,
decreased effective plasma volume may occur with decreased ECF volume (as with
diuretic use or hemorrhagic shock), but it may also occur with an increased ECF volume
(eg, in heart failure, hypoalbuminemia, or capillary leak syndrome).
Hypernatremia usually involves an impaired thirst mechanism or limited access to
water, either as contributing factors or primary causes. The severity of the underlying
disorder that results in an inability to drink in response to thirst and the effects of
hyperosmolality on the brain are thought to be responsible for a high mortality rate in
hospitalized adults with hypernatremia. There are several common causes of
hypernatremia.
Hypovolemic hypernatremia
Hypernatremia associated with hypovolemia occurs with sodium loss accompanied by a
relatively greater loss of water from the body. Common extrarenal causes include most
of those that cause hyponatremia and volume depletion. Either hypernatremia or
hyponatremia can occur with severe volume loss, depending on the relative amounts of
sodium and water lost and the amount of water ingested before presentation.
Renal causes of hypernatremia and volume depletion include therapy with diuretics.
Loop diuretics inhibit sodium reabsorption in the concentrating portion of the nephrons
and can increase water clearance. Osmotic diuresis can also impair renal concentrating
capacity because of a hypertonic substance present in the tubular lumen of the distal
nephron. Glycerol, mannitol, and occasionally urea can cause osmotic diuresis resulting
in hypernatremia.
The most common cause of hypernatremia due to osmotic diuresis is hyperglycemia in
patients with diabetes. Because glucose does not penetrate cells in the absence
of insulin, hyperglycemia further dehydrates the intracellular fluid (ICF) compartment.
The degree of hyperosmolality in hyperglycemia may be obscured by the lowering of
serum sodium resulting from movement of water out of cells into the ECF (translational
hyponatremia). Patients with renal disease can also be predisposed to hypernatremia
when their kidneys are unable to maximally concentrate urine.
Euvolemic hypernatremia
Hypernatremia with euvolemia is a decrease in TBW with near-normal total body
sodium (pure water deficit). Extrarenal causes of water loss, such as excessive
sweating, result in some sodium loss, but because sweat is hypotonic (particularly when
people are heat acclimatized), hypernatremia can result before significant hypovolemia.
A deficit of almost purely water also occurs in central diabetes
insipidus and nephrogenic diabetes insipidus.
Essential hypernatremia (primary hypodipsia) occasionally occurs in children with
brain damage and in chronically ill older adults. It is characterized by an impaired thirst
mechanism (eg, caused by lesions of the brain’s thirst center). Altered osmotic trigger
for vasopressin release is another possible cause of euvolemic hypernatremia; some
lesions cause both an impaired thirst mechanism and an altered osmotic trigger. The
nonosmotic release of vasopressin appears intact, and these patients are generally
euvolemic.
Hypervolemic hypernatremia
Hypernatremia in rare cases is associated with volume overload. In this case,
hypernatremia results from a grossly elevated sodium intake associated with limited
access to water. One example is the excessive administration of hypertonic sodium
bicarbonate during treatment of lactic acidosis. Hypernatremia can also be caused by
the administration of hypertonic saline or incorrectly formulated hyperalimentation.
Hypernatremia in older adults
Hypernatremia is common among older adults, particularly postoperative patients and
those receiving tube feedings or parenteral nutrition. Other contributing factors may
include the following:
 Dependence on others to obtain water
 Impaired thirst mechanism
 Impaired renal concentrating capacity (due to diuretics,
impaired vasopressin release, or nephron loss accompanying aging or other
renal disease)
 Impaired angiotensin II production (which may contribute directly to the impaired
thirst mechanism)
Diagnosis
 Serum sodium
The diagnosis is clinical and by measuring serum sodium. In patients who do not
respond to simple rehydration or in whom hypernatremia recurs despite adequate
access to water, further diagnostic testing is warranted. Determination of the underlying
disorder requires assessment of urine volume and osmolality, particularly after water
deprivation.
In patients with increased urine output, a water deprivation test is occasionally used to
differentiate among several polyuric states, such as central diabetes
insipidus and nephrogenic diabetes insipidus.
Treatment
 Replacement of intravascular volume and of free water
Replacement of both intravascular volume and free water is the main goal of treatment.
Oral hydration is effective in conscious patients without significant gastrointestinal
dysfunction. In severe hypernatremia or in patients unable to drink because of
continued vomiting or mental status changes, IV hydration is preferred. Hypernatremia
that has occurred within the last 24 hours should be corrected over the next 24 hours.
However, hypernatremia that is chronic or of unknown duration should be corrected
over 48 hours, and the serum osmolality should be lowered at a rate of no faster than
0.5 mOsm/L/hour to avoid cerebral edema caused by excess brain solute. The amount
of water (in liters) necessary to replace existing deficits may be estimated by the
following formula:
where TBW is in liters and is estimated by multiplying weight in kilograms by 0.6 for
men and by 0.5 for women; serum sodium can be in mEq/L or mmol/L. This formula
assumes constant total body sodium content. In patients with hypernatremia and
depletion of total body sodium content (ie, patients who have volume depletion), the free
water deficit is greater than that estimated by the formula.
In patients with hypernatremia and ECF volume overload (excess total body sodium
content), the free water deficit can be replaced with 5% dextrose in water (D/W), which
can be supplemented with a loop diuretic. However, too-rapid infusion of 5% D/W may
cause glucosuria, thereby increasing salt-free water excretion and hypertonicity,
especially in patients with diabetes mellitus. Other electrolytes, including serum
potassium, should be monitored and should be replaced as needed.
In patients with hypernatremia and euvolemia, free water can be replaced using either
5% D/W or 0.45% saline.
Treatment of patients with central diabetes insipidus and acquired nephrogenic diabetes
insipidus are discussed elsewhere.
In patients with hypernatremia and hypovolemia, particularly in patients with diabetes
with nonketotic hyperglycemic coma, 0.45% saline can be given as an alternative to a
combination of 0.9% normal saline and 5% D/W to replenish sodium and free water.
Alternatively, ECF volume and free water can be replaced separately, using the formula
given previously to estimate the free water deficit. When severe acidosis (pH < 7.10) is
present, sodium bicarbonate solution can be added to 5% D/W or 0.45% saline, as long
as the final solution remains hypotonic.
Nursing Interventions for Hypernatremia

 Restrict sodium intake! Know foods high in salt such as bacon, butter, canned
food, cheese, hot dogs, lunch meat, processed food, and table salt.
 Keep patient safe because they will be confused and agitated.
 Doctor may order to give isotonic or hypotonic solutions such as 0.45%
NS (which is hypotonic and most commonly used). Give hypotonic fluids slowly
because brain tissue is at risk due to the shifting of fluids back into the cell
(remember the cell is dehydrated with hypernatremia) and the patient is at risk
for cerebral edema. In other words, the cell can lyse if fluids are administered
too quickly.
 Educate patient and family about sign and symptoms of high sodium level and
proper foods to eat.
O. Hypokalemia
Hypokalemia is when blood’s potassium levels are too low. Potassium is an important
electrolyte for nerve and muscle cell functioning, especially for muscle cells in the heart.
Your kidneys control your body’s potassium levels, allowing for excess potassium to
leave the body through urine or sweat.
Hypokalemia is also called:
 hypokalemic syndrome
 low potassium syndrome
 hypopotassemia syndrome
Mild hypokalemia doesn’t cause symptoms. In some cases, low potassium levels can
lead to arrhythmia, or abnormal heart rhythms, as well as severe muscle weakness. But
these symptoms typically reverse after treatment.
Causes
Typically, the potassium level becomes low because too much is lost from the digestive
tract due to vomiting, diarrhea, or excessive laxative use.
Sometimes too much potassium is excreted in urine, usually because of drugs that
cause the kidneys to excrete excess sodium, water, and potassium (diuretics).
In many adrenal disorders, such as Cushing syndrome, the adrenal glands produce too
much aldosterone, a hormone that causes the kidneys to excrete large amounts of
potassium.
Certain drugs (such as insulin, albuterol, and terbutaline) cause more potassium to
move from blood into cells and can result in hypokalemia. However, these drugs usually
cause temporary hypokalemia, unless another condition is also causing potassium to be
lost.
Hypokalemia sometimes occurs with or is caused by a low level of magnesium in the
blood (hypomagnesemia).
Hypokalemia is rarely caused by consuming too little potassium because many foods
(such as beans, dark leafy greens, potatoes, fish, and bananas) contain potassium.
Symptoms
A slight decrease in the potassium level in blood usually causes no symptoms.
A larger decrease can cause muscle weakness, cramping, twitches, and even paralysis.
Abnormal heart rhythms may develop. They may develop even when the decrease is
slight if people already have a heart disorder or take the heart drug digoxin.
If hypokalemia lasts for an extended time, kidney problems may develop, causing the
person to urinate frequently and drink large amounts of water.
Diagnosis
 Measurement of potassium level in the blood
 Electrocardiography
 Sometimes measurement of amount of potassium in urine
The diagnosis is made by measuring a low potassium level in the blood. Doctors then
try to identify what is causing the potassium level to decrease.
The cause may be clear based on the person’s symptoms (such as vomiting) or use of
drugs or other substances. If the cause is not clear, doctors measure how much
potassium is excreted in urine to determine whether excess excretion is the cause.
Because low potassium levels can cause abnormal heart rhythms, doctors usually
do electrocardiography (ECG) to check for abnormal heart rhythms.
Treatment
 Potassium supplements
If a disorder is causing hypokalemia, it is treated.
Usually, potassium can be replaced by taking potassium supplements by mouth.
Because potassium can irritate the digestive tract, supplements should be taken in
small doses with food several times a day rather than in a single large dose. Special
types of potassium supplements, such as wax-impregnated or
microencapsulated potassium chloride, are much less likely to irritate the digestive tract.
To treat hypokalemia more rapidly, potassium is given by vein (intravenously) in the
following situations:
 The potassium level is dangerously low.
 The low level causes abnormal heart rhythms.
 Supplements taken by mouth are ineffective.
 People continue to lose more potassium than can be replaced using
supplements taken by mouth.
Most people who take diuretics do not need to take potassium supplements.
Nevertheless, doctors periodically check the potassium level in blood so that
supplements can be given if necessary. Alternatively, diuretics that help the kidneys
conserve potassium (potassium-sparing diuretics), such
as amiloride, eplerenone, spironolactone, or triamterene can be used, but these drugs
are used only if the kidneys are functioning normally.
When hypomagnesemia occurs with hypokalemia, it too is treated.
Nursing Interventions for Hypokalemia

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)
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
Administer oral Supplements for potassium with doctor’s order: usually for levels 2.5-
3.5…give with food can cause GI upset
IV Potassium for levels less 2.5 (NEVER EVER GIVE POTASSIUM via IV push or by IM
or subq routes)
-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
-Cause phlebitis or infiltrations
Don’t give LASIX, demadex , or thiazides (waste more Potassium) or Digoxin (cause
digoxin toxicity) if Potassium level low…notify md for further orders)
Physician will switch patient to a potassium sparing diuretic Spironolactone (Aldactone),
Dyazide, Maxide, Triamterene
Instruct patient to eat Potassium rich foods
Remember POTASSIUM to help you remember the foods
 Potatoes, pork
 Oranges
 Tomatoes
 Avocados
 Strawberries,
 Spinach
 fIsh
 mUshrooms
 Musk melons: cantaloupe
Also included are: (carrots, raisins, bananas)
P. Hyperkalemia
Hyperkalemia is the medical term that describes a potassium level in your blood that's
higher than normal. Potassium is a chemical that is critical to the function of nerve and
muscle cells, including those in your heart.
Your blood potassium level is normally 3.6 to 5.2 millimoles per liter (mmol/L). Having a
blood potassium level higher than 6.0 mmol/L can be dangerous and usually requires
immediate treatment.
Causes
The most common causes include:
 Kidney Disease. Hyperkalemia can happen if your kidneys do not work well. It is
the job of the kidneys to balance the amount of potassium taken in with the
amount lost in urine. Potassium is taken in through the foods you eat and the
liquids you drink. It is filtered by the kidneys and lost through the urine. In the
early stages of kidney disease, the kidneys can often make up for high
potassium. But as kidney function gets worse, they may not be able to remove
enough potassium from your body. Advanced kidney disease is a common cause
of hyperkalemia.
 A diet high in potassium. Eating too much food that is high in potassium can
also cause hyperkalemia, especially in people with advanced kidney disease.
Foods such as cantaloupe, honeydew melon, orange juice, and bananas are
high in potassium.
 Drugs that prevent the kidneys from losing enough potassium. Some drugs
can keep your kidneys from removing enough potassium. This can cause your
potassium levels to rise.
Other (less common) causes include:
 Taking extra potassium, such as salt substitutes or supplements.
 A disorder called “Addisons disease”, which can occur if your body does not
make enough of certain hormones. Hormones are chemicals produced by
different glands and organs, including the kidneys, to trigger certain responses in
your body.
 Burns or other severe injuries. This occurs because your body, in response to
severe burns or injuries releases extra potassium in your blood.
 Poorly controlled diabetes.
 When diabetes is not controlled, it has a direct effect on your kidneys which are
responsible for balancing potassium in your body.
Symptoms
Hyperkalemia can be asymptomatic, meaning that it causes no symptoms. Sometimes,
patients with hyperkalemia report vague symptoms including:
 nausea,
 fatigue,
 muscle weakness, or
 tingling sensations.
More serious symptoms of hyperkalemia include slow heartbeat and weak pulse.
Severe hyperkalemia can result in fatal cardiac standstill (heart stoppage). Generally, a
slowly rising potassium level (such as with chronic kidney failure) is better tolerated
than an abrupt rise in potassium levels. Unless the rise in potassium has been very
rapid, symptoms of hyperkalemia are usually not apparent until potassium levels are
very high (typically 7.0 mEq/l or higher).
Symptoms may also be present that reflect the underlying medical conditions that are
causing the hyperkalemia.
Diagnosis
Blood is withdrawn from a vein (like other blood tests). The potassium concentration of
the blood is determined in the laboratory. If hyperkalemia is suspected,
an electrocardiogram (ECG or EKG) is often performed, since the ECG may show
changes typical for hyperkalemia in moderate to severe cases. The ECG will also be
able to identify cardiac arrhythmias that result from hyperkalemia.
Treatment
Treatment of hyperkalemia must be individualized based upon the underlying cause of
the hyperkalemia, the severity of symptoms or appearance of ECG changes, and the
overall health status of the patient. Mild hyperkalemia is usually treated without
hospitalization especially if the patient is otherwise healthy, the ECG is normal, and
there are no other associated conditions such as acidosis and worsening kidney
function. Emergency treatment is necessary if hyperkalemia is severe and has caused
changes in the ECG. Severe hyperkalemia is best treated in the hospital, oftentimes in
the intensive care unit, under continuous heart rhythm monitoring.
Treatment of hyperkalemia may include any of the following measures, either singly or
in combination:
 A diet low in potassium (for mild cases).
 Discontinue medications that increase blood potassium levels.
 Intravenous administration of glucose and insulin, which promotes movement of
potassium from the extracellular space back into the cells.
 Intravenous calcium to temporarily protect the heart and muscles from the effects
of hyperkalemia.
 Sodium bicarbonate administration to counteract acidosis and to promote
movement of potassium from the extracellular space back into the cells.
 Diuretic administration to decrease the total potassium stores through increasing
potassium excretion in the urine. It is important to note that most diuretics
increase kidney excretion of potassium. Only the potassium-sparing diuretics
mentioned above decrease kidney excretion of potassium.
 Medications that stimulate beta-2 adrenergic receptors, such as albuterol and
epinephrine, have also been used to drive potassium back into cells.
 Medications known as cation-exchange resins, which bind potassium and lead to
its excretion via the gastrointestinal tract.
 Dialysis, particularly if other measures have failed or if renal failure is present.
Treatment of hyperkalemia also includes treatment of any underlying causes (for
example, kidney disease, adrenal disease, tissue destruction) of hyperkalemia.
Nursing Interventions for Hyperkalemia

 Monitor cardiac, respiratory, neuromuscular, renal, and GI status
 Stop IV potassium if running and hold any PO potassium supplements
 Initiate potassium restricted diet and remember foods that are high in potassium
 Remember the word POTASSIUM for food rich in potassium
Potatoes, pork
Oranges
Tomatoes
Avocados
Strawberries,
Spinach
fIsh
mUshrooms
Musk Melons: cantaloupe
Also included are carrots, cantaloupe, raisins, bananas.

o Prepare patient for ready for dialysis. Most patient are renal patients who
get dialysis regularly and will have high potassium.
o Kayexalate is sometimes ordered and given PO or via enema. This drug
promotes GI sodium absorption which causes potassium excretion.
o Doctor may order potassium wasting drugs like Lasix or
Hydrochlorothiazide
o Administer a hypertonic solution of glucose and regular insulin to pull the
potassium into the cell
Q. Hypocalcemia
Hypocalcemia is a condition in which there are lower-than-average levels of calcium in

the liquid part of the blood, or the plasma. Calcium has many important roles in your
body:
 Calcium is key to the conduction of electricity in your body.
 Your nervous system needs calcium to function properly. Your nerves need
calcium to relay messages between your brain and the rest of your body.
 Your muscles need calcium to move.
 Your bones need calcium to stay strong, grow, and heal.
Hypocalcemia may be the result of low calcium production or insufficient calcium
circulation in your body. A deficiency of magnesium or vitamin D is linked to most cases
of hypocalcemia.
Calcium is one of the body's electrolytes, which are minerals that carry an electric
charge when dissolved in body fluids such as blood (but most of the body's calcium is
uncharged). Although most of the body's calcium is stored in bones, some circulates in
the blood. About 40% of the calcium in blood is attached (bound) to proteins in blood,
mainly albumin. Protein-bound calcium acts as a reserve source of calcium for the cells
but has no active function in the body. Only unbound calcium affects the body’s
functions. Thus, hypocalcemia causes problems only when the level of
unbound calcium is low. Unbound calcium has an electrical (ionic) charge, so it is also
called ionized calcium.
Causes
Hypocalcemia most commonly results when too much calcium is lost in urine or when
not enough calcium is moved from bones into the blood. Causes of hypocalcemia
include the following:
 A low level of parathyroid hormone (hypoparathyroidism), as can occur when the
parathyroid glands are damaged during thyroid gland surgery
 Lack of response to a normal level of parathyroid hormone
(pseudohypoparathyroidism)
 No parathyroid glands at birth (for example, in DiGeorge syndrome)
 A low level of magnesium (hypomagnesemia), which reduces the activity of
parathyroid hormone
 Vitamin D deficiency (due to inadequate consumption or inadequate exposure to
sunlight)
 Kidney dysfunction, which results in more calcium excreted in urine and makes
the kidneys less able to activate vitamin D
 Inadequate consumption of calcium
 Disorders that decrease calcium absorption
 Pancreatitis
 Certain drugs, including rifampin (an antibiotic), antiseizure drugs (such
as phenytoin and phenobarbital), bisphosphonates (such
as alendronate, ibandronate, risedronate, and zoledronic
acid), calcitonin, chloroquine, corticosteroids, and plicamycin
Symptoms
The calcium level in blood can be moderately low without causing any symptoms. If
levels of calcium are low for long periods, people may develop dry scaly skin, brittle
nails, and coarse hair. Muscle cramps involving the back and legs are common. Over
time, hypocalcemia can affect the brain and cause neurologic or psychologic symptoms,
such as confusion, memory loss, delirium, depression, and hallucinations. These
symptoms disappear if the calcium level is restored.
An extremely low calcium level may cause tingling (often in the lips, tongue, fingers, and
feet), muscle aches, spasms of the muscles in the throat (leading to difficulty breathing),
stiffening and spasms of muscles (tetany), seizures, and abnormal heart rhythms.
Diagnosis
 Measurement of calcium level in the blood
Hypocalcemia is often detected by routine blood tests before symptoms become
obvious. Doctors measure the total calcium level (which includes calcium bound to
albumin) and the albumin level in blood to determine whether the level of
unbound calcium is low.
Blood tests are done to evaluate kidney function and to measure magnesium,
phosphate, parathyroid hormone, and vitamin D levels. Other substances in blood may
be measured to help determine the cause.
Treatment
 Calcium supplements
 Sometimes vitamin D
Calcium supplements, given by mouth, are often all that is needed to treat
hypocalcemia. If a cause is identified, treating the disorder causing hypocalcemia or
changing drugs may restore the calcium level.
Once symptoms appear, calcium is usually given intravenously. Taking vitamin D
supplements helps increase the absorption of calcium from the digestive tract.
Sometimes people with hypoparathyroidism are given a synthetic form of parathyroid
hormone.
Nursing Interventions for Hypocalcemia

 Safety (prevent falls because patient is at risk for bone fractures, seizures
precautions, and watch for laryngeal spasms)
 Administer IV calcium as ordered (ex: 10% calcium gluconate)….give slowly as
ordered (be on cardiac monitor and watch for cardiac dysrhythmias). Assess for
infiltration or phlebitis because it can cause tissue sloughing (best to give via a
central line). Also, watch if patient is on Digoxin cause this can cause Digoxin
toxicity.
 Administer oral calcium with Vitamin D supplements (given after meals or at
bedtime with a full glass of water)
 If phosphorus level is high (remember phosphorus and calcium do the opposite)
the doctor may order aluminum hydroxide antacids (Tums) to decrease
phosphorus level which in turn would increase calcium levels.
 Encourage intake of foods high in calcium:
Young Sally’s calcium serum continues to randomly mess-up.
 Yogurt
 Sardines
 Cheese
 Spinach
 Collard greens
 Tofu
 Rhubarb
 Milk
R. Hypercalcemia
Hypercalcemia is a condition in which the calcium level in your blood is above normal.
Too much calcium in your blood can weaken your bones, create kidney stones, and
interfere with how your heart and brain work.
Hypercalcemia is usually a result of overactive parathyroid glands. These four tiny
glands are situated in the neck, near the thyroid gland. Other causes of hypercalcemia
include cancer, certain other medical disorders, some medications, and taking too much
of calcium and vitamin D supplements.
Symptoms
You might not have signs or symptoms if your hypercalcemia is mild. More-severe
cases produce signs and symptoms related to the parts of your body affected by the
high calcium levels in your 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, lethargy and fatigue. 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.
Causes
Besides building strong bones and teeth, calcium helps muscles contract and nerves
transmit signals. Normally, if there isn't enough calcium in your blood, your parathyroid
glands secrete a hormone that triggers:
 Your bones to release calcium into your blood
 Your digestive tract to absorb more calcium
 Your kidneys to excrete less calcium and activate more vitamin D, which plays a
vital role in calcium absorption
This delicate balance between too little calcium in your blood and hypercalcemia can be
disrupted by a variety of factors. Hypercalcemia is caused by:
 Overactive parathyroid glands (hyperparathyroidism). This most common
cause of hypercalcemia can stem from a small, noncancerous (benign) tumor or
enlargement of one or more of the four parathyroid glands.
 Cancer. Lung cancer and breast cancer, as well as some blood cancers, can
increase your risk of hypercalcemia. Spread of cancer (metastasis) to your bones
also increases your risk.
 Other diseases. Certain diseases, such as tuberculosis and sarcoidosis, can
raise blood levels of vitamin D, which stimulates your digestive tract to absorb
more calcium.
 Hereditary factors. A rare genetic disorder known as familial hypocalciuric
hypercalcemia causes an increase of calcium in your blood because of faulty
calcium receptors in your body. This condition doesn't cause symptoms or
complications of hypercalcemia.
 Immobility. People who have a condition that causes them to spend a lot of time
sitting or lying down can develop hypercalcemia. Over time, bones that don't bear
weight release calcium into the blood.
 Severe dehydration. A common cause of mild or transient hypercalcemia is
dehydration. Having less fluid in your blood causes a rise in calcium
concentrations.
 Medications. Certain drugs — such as lithium, used to treat bipolar disorder —
might increase the release of parathyroid hormone.
 Supplements. Taking excessive amounts of calcium or vitamin D supplements
over time can raise calcium levels in your blood above normal.
Diagnosis
Hypercalcemia is easily diagnosed with a blood test. Diagnosing the causes of
hypercalcemia, however, is a more involved process; in addition to a detailed history
and physical examination, it may require further blood tests (such as a PTH level and
vitamin D level), urine evaluation, X-rays, and other imaging procedures.
Treatment
Treatment options for hypercalcemia depend on the severity of the condition and the
underlying cause.
Mild cases
You may not need immediate treatment if you have a mild case of hypercalcemia,
depending on the cause. However, you will need to monitor its progress. Finding the
underlying cause is important.
The effect that elevated calcium levels have on your body relate not just to the level of
calcium present, but how quickly it rises. Therefore, it’s important to stick to your
doctor’s recommendations for follow-up.
Even mildly elevated levels of calcium can lead to kidney stones and kidney damage
over time.
Moderate to severe cases
You will likely need hospital treatment if you have a moderate to severe case. The goal
of treatment is to return your calcium level to normal. Treatment also aims to prevent
damage to your bones and kidneys. Common treatment options include the following:
 Calcitonin is a hormone produced in the thyroid gland. It slows down bone loss.
 Intravenous fluids hydrate you and lower calcium levels in the blood.
 Corticosteroids are anti-inflammatory medications. They’re useful in the
treatment of too much vitamin D.
 Loop diuretic medications can help your kidneys move fluid and get rid of extra
calcium, especially if you have heart failure.
 Intravenous bisphosphonates lower blood calcium levels by regulating bone
calcium.
 Dialysis can be performed to rid your blood of extra calcium and waste when you
have damaged kidneys. This is usually done if other treatment methods aren’t
working.
Primary hyperparathyroidism
Depending on your age, kidney function, and bone effects, you might need surgery to
remove the abnormal parathyroid glands. This procedure cures most cases of
hypercalcemia caused by hyperparathyroidism.
If surgery isn’t an option for you, your doctor may recommend a medication called
cinacalcet (Sensipar). This lowers your calcium level by decreasing PTH production. If
you have osteoporosis, your doctor might have you take bisphosphonates to lower your
risk of fractures.
Nursing Interventions for Hypercalcemia

Mild cases of Hypercalcemia
 Keep patient hydrated (decrease chance of renal stone formation)
 Keep patient safe from falls or injury
 Monitor cardiac, GI, renal, neuro status
 Assess for complaints of flank or abdominal pain & strain urine to look for stone
formation
 Decrease calcium rich foods and intake of calcium-preserving drugs
like thiazides, supplements, Vitamin D
To help you remember foods high in calcium remember the phrase:
“Young Sally’s calcium serum continues to randomly mess-up”
Yogurt
Sardines
Cheese
Spinach
Collard greens
Tofu
Rhubarb
Milk
Moderate cases of Hypercalcemia
Administer calcium reabsorption inhibitors: Calcitonin, Bisphosphonates, prostaglandin
synthesis inhibitors (ASA, NSAIDS)
Severe cases of Hypercalcemia
Prepare patient for dialysis
T. Hyperphosphatemia
Having a high level of phosphate — or phosphorus — in your blood is known as
hyperphosphatemia. Phosphate is an electrolyte, which is an electrically charged
substance that contains the mineral phosphorus.
Your body needs some phosphate to strengthen your bones and teeth, produce energy,
and build cell membranes. Yet in larger-than-normal amounts, phosphate can cause
bone and muscle problems and increase your risk for heart attacks and strokes.
A high phosphate level is often a sign of kidney damage. It’s more common in people
with chronic kidney disease (CKD), especially in those with end-stage kidney disease.
Causes
The usual cause of hyperphosphatemia is
 Decrease in renal excretion of phosphate
Advanced renal insufficiency (glomerular filtration rate [GFR] < 30 mL/minute) reduces
excretion sufficiently to increase serum phosphate. Defects in renal excretion of
phosphate in the absence of chronic kidney disease also occur
in pseudohypoparathyroidism, hypoparathyroidism, and parathyroid suppression (as
from hypercalcemia due to vitamin A or D excess or granulomatous disease).
Hyperphosphatemia occasionally results from a transcellular shift of phosphate into the
extracellular space that is so large that the renal excretory capacity is overwhelmed.
This transcellular shift occurs most frequently in
 Diabetic ketoacidosis (despite total body phosphate depletion)
 Crush injuries
 Nontraumatic rhabdomyolysis
 Overwhelming systemic infections
 Tumor lysis syndrome
Hyperphosphatemia can also occur with excessive oral phosphate administration and
occasionally with overzealous use of enemas containing phosphate.
Hyperphosphatemia can be spurious in cases of hyperproteinemia (eg, in multiple
myeloma or macroglobulinemia), dyslipidemia, hemolysis, or hyperbilirubinemia.
Symptoms
Most people with high phosphate levels don’t have symptoms. In some people
with chronic kidney disease, high phosphate levels cause calcium levels in the blood to
drop.
Symptoms of low calcium include:
 muscle cramps or spasms
 numbness and tingling around the mouth
 bone and joint pain
 weak bones
 rash
 itchy skin
Diagnosis
 Phosphate concentration > 4.5 mg/dL (> 1.46 mmol/L)
Hyperphosphatemia is diagnosed by phosphate concentration. When the etiology is not
obvious (eg, rhabdomyolysis, tumor lysis syndrome, renal failure, overingestion of
phosphate-containing laxatives), additional evaluation is warranted to exclude
hypoparathyroidism or pseudohypoparathyroidism, which is end-organ resistance to
parathyroid hormone (PTH). False elevation of serum phosphate also should be
excluded by measuring serum protein, lipid, and bilirubin concentrations.
Treatment
 Phosphate restriction
 Phosphate binders
 Sometimes saline diuresis or hemodialysis
The mainstay of treatment in patients with advanced chronic kidney disease is reduction
of phosphate intake, which is usually accomplished with avoidance of foods containing
high amounts of phosphate and with use of phosphate-binding drugs taken with meals.
Although quite effective, aluminum-containing antacids should not be used as
phosphate binding agents in patients with end-stage renal disease because of the
possibility of aluminum-related dementia and osteomalacia.
Calcium carbonate and calcium acetate are frequently used as phosphate binders. But
their use requires close monitoring because of the possibility of excessive
calcium × phosphate product causing vascular calcification in dialysis patients taking
calcium-containing binders.
A phosphate-binding resin without calcium, sevelamer, is widely used in dialysis
patients in doses of 800 to 2400 mg orally 3 times a day with
meals. Lanthanum carbonate is another phosphate binder that lacks calcium and is
used in dialysis patients. It is given in doses of 500 to 1000 mg orally 3 times a day with
meals.
Sucroferric oxyhydroxide combines the need many dialysis patients have for elemental
iron with phosphate binding. It is given in doses of 500 mg orally 3 times a day with
meals.
Hemodialysis does remove some phosphate, but not enough to allow most patients with
end-stage renal disease to avoid significant hyperphosphatemia without dietary
interventions.
Saline diuresis can be used to enhance phosphate elimination in cases of acute
hyperphosphatemia in patients with intact kidney function. Hemodialysis can lower
phosphate levels in cases of severe acute hyperphosphatemia.
Nursing Interventions of Hyperphosphatemia
 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
 Avoid using phosphate medication such as laxatives and enema
 Restrict foods high is phosphate ***eat, poultry, fish, dairy, nuts, sodas, oatmeal
 Prepare patient for dialysis if patient in renal failure
U. Metabolic acidosis
When your body fluids contain too much acid, it’s known as acidosis. Acidosis occurs
when your kidneys and lungs can’t keep your body’s pH in balance. Many of the body’s
processes produce acid. Your lungs and kidneys can usually compensate for slight pH
imbalances, but problems with these organs can lead to excess acid accumulating in
your body.
The acidity of your blood is measured by determining its pH. A lower pH means that
your blood is more acidic, while a higher pH means that your blood is more basic. The
pH of your blood should be around 7.4. According to the American Association for
Clinical Chemistry (AACC), acidosis is characterized by a pH of 7.35 or
lower. Alkalosis is characterized by a pH level of 7.45 or higher. While seemingly slight,
these numerical differences can be serious. Acidosis can lead to numerous health
issues, and it can even be life-threatening.
Metabolic acidosis starts in the kidneys instead of the lungs. It occurs when they can’t
eliminate enough acid or when they get rid of too much base. There are three major
forms of metabolic acidosis:
 Diabetic acidosis occurs in people with diabetes that’s poorly controlled. If your
body lacks enough insulin, ketones build up in your body and acidify your blood.
 Hyperchloremic acidosis results from a loss of sodium bicarbonate. This base
helps to keep the blood neutral. Both diarrhea and vomiting can cause this type
of acidosis.
 Lactic acidosis occurs when there’s too much lactic acid in your body. Causes
can include chronic alcohol use, heart failure, cancer, seizures, liver
failure, prolonged lack of oxygen, and low blood sugar. Even prolonged exercise
can lead to lactic acid buildup.
 Renal tubular acidosis occurs when the kidneys are unable to excrete acids
into the urine. This causes the blood to become acidic.
Symptoms and Signs

Symptoms and signs are primarily those of the cause. Mild acidemia is itself
asymptomatic. More severe acidemia (pH < 7.10) may cause nausea, vomiting, and
malaise. Symptoms may occur at higher pH if acidosis develops rapidly.
The most characteristic sign is hyperpnea (long, deep breaths at a normal rate),
reflecting a compensatory increase in alveolar ventilation; this hyperpnea is not
accompanied by a feeling of dyspnea.
Diagnosis
 Arterial blood gas (ABG) and serum electrolyte measurement
 Anion gap and delta gap calculated
 Winters formula for calculating compensatory changes
 Testing for cause
Recognition of metabolic acidosis and appropriate respiratory compensation are
discussed in Diagnosis of Acid-Base Disorders. Determining the cause of metabolic
acidosis begins with the anion gap.
The cause of an elevated anion gap may be clinically obvious (eg, hypovolemic shock,
missed hemodialysis), but if not, blood testing should include
 Glucose
 BUN (blood urea nitrogen)
 Creatinine
 Lactate
 Possible toxins
Salicylate levels can be measured in most laboratories, but methanol and ethylene
glycol frequently cannot; their presence may be suggested by presence of an osmolar
gap.
Calculated serum osmolarity (2 [sodium] + [glucose]/18 + BUN/2.8 + blood alcohol/5,
based on conventional units) is subtracted from measured osmolarity. A difference > 10
implies the presence of an osmotically active substance, which in the case of a high
anion gap acidosis is methanol or ethylene glycol. Although ingestion of ethanol may
cause an osmolar gap and a mild acidosis, it should never be considered the sole cause
of a significant metabolic acidosis.
If the anion gap is normal and no cause is obvious (eg, marked diarrhea), urinary
electrolytes are measured and the urinary anion gap is calculated as
[sodium] + [potassium] – [chloride]. A normal urinary anion gap (including in patients
with GI losses) is 30 to 50 mEq/L (30 to 50 mmol/L) ; an elevation suggests renal
HCO3− loss (evaluation of renal tubular acidosis is discussed elsewhere).
In addition, when metabolic acidosis is present, a delta gap is calculated to identify
concomitant metabolic alkalosis, and Winters formula is applied to see whether
respiratory compensation is appropriate or reflects a second acid-base disorder.
Treatment
 Cause treated
 Sodium bicarbonate (NaHCO3) primarily for severe acidemia—give with caution
Treatment is directed at the underlying cause. Hemodialysis is required for renal failure
and sometimes for ethylene glycol, methanol, and salicylate poisoning.
Treatment of acidemia with sodium bicarbonate (NaHCO3) is clearly indicated only in
certain circumstances and is probably deleterious in others. When metabolic acidosis
results from loss of HCO3− or accumulation of inorganic acids (ie, normal anion gap
acidosis), bicarbonate therapy is generally safe and appropriate. However, when
acidosis results from organic acid accumulation (ie, high anion gap acidosis),
bicarbonate therapy is controversial; it does not clearly decrease mortality in these
conditions, and there are several possible risks.
With treatment of the underlying condition, lactate and ketoacids are metabolized back
to HCO3−; exogenous HCO3− loading may therefore cause an “overshoot” metabolic
alkalosis. In any condition, sodium bicarbonate may also cause sodium and volume
overload, hypokalemia, and, by inhibiting respiratory drive, hypercapnia. Furthermore,
because HCO3− does not diffuse across cell membranes, intracellular acidosis is not
corrected and may paradoxically worsen because some of the added HCO 3− is
converted to carbon dioxide (CO2), which does cross into the cell and is hydrolyzed to
H+ and HCO3−.
Despite these and other controversies, most experts still recommend giving bicarbonate
IV for severe metabolic acidosis (pH < 7.0).
Treatment requires 2 calculations (same for both conventional and SI units). The first is
the level to which HCO3− must be raised, calculated by the Kassirer-Bleich equation,
using a target value for [H+] of 79 nEq/L (79 nmol/L), which corresponds to a pH of 7.10:
79 = 24 × Pco2/HCO3−
or
Desired HCO3−= 0.30 × Pco2
The amount of sodium bicarbonate needed to achieve that level is
NaHCO3 required (mEq/mmol) = (desired [HCO3−] − observed [HCO3−]) × 0.4 × body
weight (kg)
For example, a 70-kg man has severe metabolic acidosis with a pH of 6.92, PCO 2 40
mmHg and HCO3− of 8 mEq/L (8 mmol/L). The target bicarbonate level needed to
achieve a pH of 7.10 is 0.30 × 40 = 12 mEq/L (12 mmol/L). This level is 4 mEq/L (4
mmol/L) more than his current bicarbonate level of 8. To increase bicarbonate by 4,
multiply 4 by 0.4 times 70 (the body weight), giving a result of 112 mEq (112 mmol) of
HCO3−. This amount of sodium bicarbonate is given over several hours. Blood pH and
HCO3−levels can be checked 30 minutes to 1 hour after administration, which allows for
equilibration with extravascular HCO3−.
Alternatives to sodium bicarbonate include
 Lactate, either in the form of lactated Ringer's solution or sodium lactate (is
metabolized mEq for mEq to bicarbonate when liver function is normal)
 Sodium acetate (metabolized mEq for mEq to bicarbonate when liver function is
normal)
 Tromethamine, an amino alcohol that buffers both metabolic (H +) and respiratory
(carbonic acid [H2CO3]) acid
 Carbicarb, an equimolar mixture of sodium bicarbonate and carbonate (the latter
consumes CO2 and generates HCO3−)
 Dichloroacetate, which enhances oxidation of lactate
These alternatives do not offer a proven benefit over sodium bicarbonate alone and can
cause complications of their own.
Potassium (K+) depletion, common in metabolic acidosis, should be identified through
frequent serum K+ monitoring and treated as needed with oral or parenteral potassium
chloride.
Nursing Interventions & Considerations

 Keep sodium bicarbonate ampules handy for emergency administration.
 Monitor vital signs, laboratory results and level of consciousness frequently.
 Watch out for signs of decreasing level of consciousness.
 Record intake and output accurately to monitor renal function.
 For management of vomiting (common to metabolic acidosis), position the
patient to prevent aspiration.
 Prepare for possible seizures and administer appropriate precautions.
 Provide good oral hygiene after incidences of vomiting. Use sodium bicarbonate
washes to neutralize acid in the patient’s mouth.
V. Metabolic alkalosis
Metabolic alkalosis is a condition that occurs when your blood becomes overly alkaline.
Alkaline is the opposite of acidic.
Our bodies function best when the acidic-alkaline balance of our blood is just slightly
tilted toward the alkaline.
Alkalosis occurs when your body has either:
 too many alkali-producing bicarbonate ions
 too few acid-producing hydrogen ions
Many people don’t experience any symptoms of metabolic alkalosis, so you may not
know that you have it.
Metabolic alkalosis is one of the four main types of alkalosis. There are two kinds of
metabolic alkalosis:
 Chloride-responsive alkalosis results from loss of hydrogen ions, usually by
vomiting or dehydration.
 Chloride-resistant alkalosis results when your body retains too many
bicarbonate (alkaline) ions, or when there’s a shift of hydrogen ions from your
blood to your cells.
There’s also a condition called metabolic acidosis which occurs when your blood or
fluids become overly acidic.
Your body compensates for both alkalosis and acidosis mainly through your lungs. The
lungs change the alkalinity of your blood by allowing more or less carbon dioxide to
escape as you breathe. The kidneys also play a role by controlling the elimination of
bicarbonate ions.
Causes of metabolic alkalosis
Several different underlying conditions can cause metabolic alkalosis. These include:
Loss of stomach acids. This is the most common cause of metabolic alkalosis. It’s
usually brought on by vomiting or suction through a nose-feeding tube.
The gastric juices have a high content of hydrochloric acid, a strong acid. Its loss
causes an increase in the alkalinity of the blood.
The vomiting can result from any number of stomach disorders. By figuring out and
treating the cause of the vomiting, your doctor will cure the metabolic alkalosis.
Excess of antacids. Antacid use won’t normally lead to metabolic alkalosis. But if you
have weak or failing kidneys and use a nonabsorbable antacid, it can bring on alkalosis.
Nonabsorbable antacids contain aluminum hydroxide or magnesium hydroxide.
Diuretics. Some diuretics (water pills) commonly prescribed for high blood pressure
can cause increased urinary acid secretion. The increased secretion of acid in the urine
can make your blood more alkaline.
If alkalosis shows up when you’re taking drugs such as thiazide or loop diuretics, your
doctor may ask you to stop.
Potassium deficiency (hypokalemia). A deficiency of potassium can cause the
hydrogen ions normally present in the fluid around your cells to shift inside the cells.
The absence of acidic hydrogen ions causes your fluids and blood to become more
alkaline.
Reduced volume of blood in the arteries (EABV). This can come from both a
weakened heart and from cirrhosis of the liver. A reduced blood flow impairs your
body’s ability to remove the alkaline bicarbonate ions.
Heart, kidney, or liver failure. Metabolic alkalosis can be caused by failure of a major
organ, such as your heart, kidney, or liver. This leads to potassium depletion.
A standard saline solution (sodium chloride) can make things worse by causing your
body to retain fluids without getting rid of the excess of bicarbonate ions that are
causing the alkalosis.
Genetic causes. In rare cases, an inherited gene can be the cause of metabolic
alkalosis. Five inherited diseases that can cause metabolic alkalosis are:
 Bartter syndrome
 Gitelman syndrome
 Liddle syndrome
 glucocorticoid remediable aldosteronism
 apparent mineralocorticoid excess
Symptoms of metabolic alkalosis

Metabolic alkalosis may not show any symptoms. People with this type of alkalosis
more often complain of the underlying conditions that are causing it. These can include:
 vomiting
 diarrhea
 swelling in the lower legs (peripheral edema)
 fatigue
Severe cases of metabolic alkalosis can cause:
 agitation
 disorientation
 seizures
 coma
The severe symptoms are most common when the alkalosis is caused by chronic liver
disease.
Diagnosis
 Arterial blood gas (ABG) and serum electrolyte measurements
 Diagnosis of cause (usually clinical)
 Sometimes measurement of urinary Cl− and K+
Recognition of metabolic alkalosis and appropriate respiratory compensation is
discussed in Diagnosis of Acid-Base Disorders and requires measurement of ABG and
serum electrolytes (including Ca and Mg).
Common causes can often be determined by history and physical examination. If history
is unrevealing and renal function is normal, urinary Cl − and K+ concentrations are
measured (values are not diagnostic in renal insufficiency).
 Urinary Cl < 20 mEq/L (< 20 mmol/L) indicates significant renal Cl − reabsorption
and hence a Cl-responsive cause (see table Causes of Metabolic Alkalosis)
 Urinary Cl > 20 mEq/L (> 20 mmol/L) suggests a chloride-unresponsive form.
Urinary K and the presence or absence of hypertension help differentiate the chloride-
unresponsive alkaloses.
 Urinary K < 30 mEq/day (< 30 mmol/day) signifies hypokalemia or laxative
misuse.
 Urinary K > 30 mEq/day (> 30 mmol/day) in a patient without hypertension
suggests diuretic abuse or Bartter syndrome or Gitelman syndrome.
 Urinary K > 30 mEq/day (> 30 mmol/day) in a patient with hypertension requires
evaluation for hyperaldosteronism, mineralocorticoid excess, and renovascular
disease.
Tests in patients with hypertension typically include plasma renin activity and
aldosterone and cortisol levels (see Diagnosis of Cushing Syndrome and Diagnosis of
Primary Aldosteronism).
Treatment
 Cause treated
 IV 0.9% saline solution for chloride-responsive metabolic alkalosis
Underlying conditions are treated, with particular attention paid to correction of
hypovolemia and hypokalemia.
Patients with chloride-responsive metabolic alkalosis are given 0.9% saline solution IV;
infusion rate is typically 50 to 100 mL/hour greater than urinary and other sensible and
insensible fluid losses until urinary Cl rises to > 25 mEq/L (> 25 mmol/L) and urinary pH
normalizes after an initial rise from bicarbonaturia.
Patients with chloride-unresponsive metabolic alkalosis rarely benefit from rehydration
alone.
Patients with severe metabolic alkalosis (eg, pH > 7.6) sometimes require more urgent
correction of blood pH. Hemofiltration or hemodialysis is an option, particularly if volume
overload and renal dysfunction are present. Acetazolamide 250 to 375 mg orally or IV
once or twice a day increases HCO3− excretion but may also accelerate urinary losses
of K+ and phosphate (PO4−); volume-overloaded patients with diuretic-induced metabolic
alkalosis and those with posthypercapnic metabolic alkalosis may especially benefit.
In patients with severe metabolic alkalosis (pH > 7.6) and kidney failure who otherwise
cannot or should not undergo dialysis, hydrochloric acid in a 0.1 to 0.2 normal solution
IV is safe and effective but must be given through a central catheter because it is
hyperosmotic and scleroses peripheral veins. Dosage is 0.1 to 0.2 mmol/kg/hour.
Frequent monitoring of ABGs and electrolytes is needed.

 Dilute potassium when giving via I.V. containing potassium salts. Monitor the
infusion rate to prevent damage and watch out for signs of phlebitis.
 Watch for signs of muscle weakness, tetany or decreased activity. Monitor vital
signs frequently and record intake and output to evaluate respiratory, fluid and
electrolyte status.
 Observe seizure precautions.
W. Respiratory acidosis
Respiratory acidosis is a condition that occurs when the lungs can’t remove enough of
the carbon dioxide (CO2) produced by the body. Excess CO2 causes the pH of blood
and other bodily fluids to decrease, making them too acidic. Normally, the body is able
to balance the ions that control acidity. This balance is measured on a pH scale from 0
to 14. Acidosis occurs when the pH of the blood falls below 7.35 (normal blood pH is
between 7.35 and 7.45).
Respiratory acidosis is typically caused by an underlying disease or condition. This is
also called respiratory failure or ventilatory failure.
Normally, the lungs take in oxygen and exhale CO2. Oxygen passes from the lungs into
the blood. CO2 passes from the blood into the lungs. However, sometimes the lungs
can’t remove enough CO2. This may be due to a decrease in respiratory rate or
decrease in air movement due to an underlying condition such as:
 asthma
 COPD
 pneumonia
 sleep apnea
Forms of respiratory acidosis

There are two forms of respiratory acidosis: acute and chronic.
Acute respiratory acidosis occurs quickly. It’s a medical emergency. Left untreated,
symptoms will get progressively worse. It can become life-threatening.
Chronic respiratory acidosis develops over time. It doesn’t cause symptoms. Instead,
the body adapts to the increased acidity. For example, the kidneys produce more
bicarbonate to help maintain balance.
Chronic respiratory acidosis may not cause symptoms. Developing another illness may
cause chronic respiratory acidosis to worsen and become acute respiratory acidosis.
Symptoms of respiratory acidosis

Initial signs of acute respiratory acidosis include:
 headache
 anxiety
 blurred vision
 restlessness
 confusion
Without treatment, other symptoms may occur. These include:
 sleepiness or fatigue
 lethargy
 delirium or confusion
 shortness of breath
 coma
The chronic form of respiratory acidosis doesn’t typically cause any noticeable
symptoms. Signs are subtle and nonspecific and may include:
 memory loss
 sleep disturbances
 personality changes
Causes of respiratory acidosis

The lungs and the kidneys are the major organs that help regulate your blood’s pH. The
lungs remove acid by exhaling CO2, and the kidneys excrete acids through the urine.
The kidneys also regulate your blood’s concentration of bicarbonate (a base).
Respiratory acidosis is usually caused by a lung disease or condition that affects normal
breathing or impairs the lungs’ ability to remove CO2. Some common causes of the
chronic form are:
 asthma
 chronic obstructive pulmonary disease (COPD)
 acute pulmonary edema
 severe obesity (which can interfere with expansion of the lungs)
 neuromuscular disorders (such as multiple sclerosis or muscular dystrophy)
 scoliosis
Some common causes of the acute form are:
 lung disorders (COPD, emphysema, asthma, pneumonia)
 conditions that affect the rate of breathing
 muscle weakness that affects breathing or taking a deep breath
 obstructed airways (due to choking or other causes)
 sedative overdose
 cardiac arrest
Diagnosis
The goal of diagnostic tests for respiratory acidosis is to look for any pH imbalance, to
determine the severity of the imbalance, and to determine the condition causing the
imbalance. Several tools can help doctors diagnose respiratory acidosis.
Blood gas measurement
Blood gas is a series of tests used to measure oxygen and CO2 in the blood. A
healthcare provider will take a sample of blood from your artery. High levels of CO2 can
indicate acidosis.
Electrolytes
Electrolyte testing is a group of tests that measure levels of Na+ (sodium), K+
(potassium), Cl- (chloride), and bicarbonate. One or more of the electrolytes will be
increased or decreased in people with acid-base disorders such as respiratory acidosis.
Lung function tests
Many people with this condition have reduced lung function.
Chest X-ray
X-rays can help doctors see injuries or other problems likely to cause acidosis.
Other tests
Based on these tests, your doctor may also perform other tests to help diagnose the
underlying condition that’s causing the acidosis. (Another condition, known as metabolic
acidosis, may cause similar symptoms, and the doctor may order tests to be sure the
problem is solely respiratory. These tests measure the amount of acid in your body,
which may be caused by kidney failure, diabetes, or other conditions, and include
glucose, lactate, and ketones.) Other tests include drug testing, a complete blood count
(CBC), and a urinalysis (urine test).
Treating respiratory acidosis

There are several different treatments for respiratory acidosis.
Acute form
Treating acute acidosis usually means addressing the underlying cause. For example,
your airway may need to be cleared. This must be done as soon as possible. Artificial
ventilation may also be needed.
Chronic form
If you have the chronic form of this disease, your treatment will focus on managing any
underlying conditions. The goal is to improve airway function. Some strategies include:
 antibiotics (to treat infection)
 diuretics (to reduce excess fluid affecting the heart and lungs)
 bronchodilators (to expand the airways)
 corticosteroids (to reduce inflammation)
 mechanical ventilation (in severe cases)
Nursing Management
Nursing Priorities
1. Achieve homeostasis.
2. Prevent/minimize complications.
3. Provide information about condition/prognosis and treatment needs as
appropriate.
Discharge Goals
1. Physiological balance restored.
2. Free of complications.
3. Condition, prognosis, and treatment needs understood.

 Remain alert for critical changes in patient’s respiratory, CNS and cardiovascular
functions. Report such changes as well as any variations in ABG values or
electrolyte status immediately.
 Maintain adequate hydration.
 Maintain patent airway and provide humidification if acidosis requires mechanical
ventilation. Perform tracheal suctioning frequently and vigorous chest
physiotherapy, if ordered.
 Institute safety measures and assist patient with positioning.
 Continuously monitor arterial blood gases.
X. Respiratory alkalosis
Respiratory alkalosis occurs when the levels of carbon dioxide and oxygen in the blood
are not balanced.
Your body needs oxygen to function properly. When you inhale, you introduce oxygen
into the lungs. When you exhale, you release carbon dioxide, which is a waste product.
Normally, the respiratory system keeps these two gases in balance.
Respiratory alkalosis occurs when you breathe too fast or too deep and carbon dioxide
levels drop too low. This causes the pH of the blood to rise and become too alkaline.
When the blood becomes too acidic, respiratory acidosis occurs.
Hyperventilation is typically the underlying cause of respiratory alkalosis.
Hyperventilation is also known as overbreathing. Someone who is hyperventilating
breathes very deeply or rapidly.
Causes of hyperventilation
Panic attacks and anxiety are the most common causes of hyperventilation. However,
they’re not the only possible causes. Others include:
 heart attack
 pain
 drug use
 asthma
 fever
 chronic obstructive pulmonary disease
 infection
 pulmonary embolism
 pregnancy
Symptoms of respiratory alkalosis

Overbreathing is a sign that respiratory alkalosis is likely to develop. However, low
carbon dioxide levels in the blood also have a number of physical effects, including:
 dizziness
 bloating
 feeling lightheaded
 numbness or muscle spasms in the hands and feet
 discomfort in the chest area
 confusion
 dry mouth
 tingling in the arms
 heart palpitations
 feeling short of breath
Exams and Tests

Your health care provider will perform a physical exam. Tests that may be done include:
 Arterial blood gas, which measures oxygen and carbon dioxide levels in the
blood
 Basic metabolic panel
 Chest x-ray
 Pulmonary function tests to measure breathing and how well the lungs are
functioning
Treatment for respiratory alkalosis

The treatment for respiratory alkalosis depends on the underlying cause.
Panic and anxiety-related causes
Treating the condition is a matter of raising carbon dioxide levels in the blood. The
following strategies and tips are useful for respiratory alkalosis caused by overbreathing
due to panic and anxiety.
Breathe into a paper bag
1. Fill the paper bag with carbon dioxide by exhaling into it.
2. Breathe the exhaled air from the bag back into the lungs.
3. Repeat this several times.
Doing this several times can give the body the carbon dioxide it needs and bring levels
back up to where they should be.
Get reassurance
The symptoms of respiratory alkalosis can be frightening. This often causes faster and
deeper breathing, making things worse. Having a calm loved one provide reassurance
could help get your breathing under control.
Restrict oxygen intake into the lungs
To do this, try breathing while pursing the lips or breathing through one nostril. For the
second approach to be useful, the mouth and the other nostril need to be covered.
Other causes
The above strategies are very simple ways to address respiratory alkalosis. People who
often experience overbreathing due to anxiety can use these methods at home.
Anyone experiencing overbreathing and the symptoms of respiratory alkalosis
for the first time should go to the hospital right away. The strategies described in
the previous section should only be used if a doctor has confirmed the exact cause of
overbreathing. Overbreathing symptoms are very similar to the symptoms of other
serious health conditions.
Nursing Interventions for Respiratory Alkalosis

 Teach patient breathing techniques to slow down breathing, holding breath…”
rebreathing into a paper bag or re-breather mask
 Watch potassium levels (hypokalemia. Remember hyperkalemia in respiratory
acidosis & hypocalcemia) and for signs and symptoms of low calcium and
potassium levels.
 Closely watch patients on mechanical ventilation to ensure breaths are not
hyperventilating the patient

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Claire Maurice G.

Symptoms and Signs

Nursing Interventions for Hypernatremia

Nursing Interventions for Hypokalemia

Nursing Interventions for Hyperkalemia

Hypocalcemia is a condition in which there are lower-than-average levels of calcium in

Nursing Interventions for Hypocalcemia

Nursing Interventions for Hypercalcemia

Symptoms and Signs

Nursing Interventions & Considerations

Symptoms of metabolic alkalosis

Nursing Interventions & Considerations

Forms of respiratory acidosis

Symptoms of respiratory acidosis

Causes of respiratory acidosis

Treating respiratory acidosis

Nursing Interventions & Considerations

Symptoms of respiratory alkalosis

Exams and Tests

Treatment for respiratory alkalosis

Nursing Interventions for Respiratory Alkalosis

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