Saint Louis University

Baguio City
School Of Nursing
S.Y 2017-2018

FLUID AND ELECTROLYTE DISORDERS

1. What are electrolyte disorders?
An electrolyte disorder occurs when the levels of electrolytes in your body are either too high or too low.
Electrolytes are naturally occurring elements and compounds in the body. They control important physiologic
functions.

Examples of electrolytes include:

 calcium
 chloride
 magnesium
 phosphate
 potassium
 sodium
These substances are present in your blood, bodily fluids, and urine. They’re also ingested with food, drinks,
and supplements.

Electrolytes need to be maintained in an even balance for your body to function properly. Otherwise, vital body
systems can be affected. Severe electrolyte imbalances can cause serious problems like coma, seizures, and
cardiac arrest.

Symptoms of electrolyte disorders

Mild forms of electrolyte disorders may not cause any symptoms. Such disorders can go undetected until they
are discovered during a routine blood test. Symptoms usually start to appear once a particular disorder becomes
more severe.

Not all electrolyte imbalances cause the same symptoms, but many share similar symptoms.

Common symptoms of an electrolyte disorder include:

 irregular heartbeat
 fast heart rate
 fatigue
 lethargy
 convulsions or seizures
  nausea
 vomiting
 diarrhea or constipation
 abdominal cramping
 muscle weakness
 muscle cramping
 irritability
 confusion
 headaches
 numbness and tingling
Call your doctor right away if you’re experiencing any of these symptoms and suspect you might have an
electrolyte disorder. Electrolyte disturbances can become life-threatening if left untreated.

Causes of electrolyte disorders

Electrolyte disorders are most often caused by a loss of bodily fluids through prolonged vomiting, diarrhea, or
sweating. They may also develop due to fluid loss related to burns. Certain medications can cause electrolyte
disorders as well. In some cases, underlying diseases are to blame.

The exact cause may vary depending on the specific type of electrolyte disorder.

Types of electrolyte disorders

Elevated levels of an electrolyte are indicated with the prefix “hyper-.” Depleted levels of an electrolyte are
indicated with “hypo-.”

Conditions caused by electrolyte level imbalances include:

 calcium: hypercalcemia and hypocalcemia

 chloride: hyperchloremia and hypochloremia
 magnesium: hypermagnesemia and hypomagnesemia
 phosphate: hyperphosphatemia or hypophosphatemia
 potassium: hyperkalemia and hypokalemia
 sodium: hypernatremia and hyponatremia
Calcium

Calcium is a vital mineral that your body uses to stabilize blood pressure and control skeletal muscle
contraction. It’s also used to build strong bones and teeth.

Hypercalcemia is when you have too much calcium in the blood. This usually happens due to:

 hyperparathyroidism
  kidney disease
 thyroid disorders
 lung diseases, such as tuberculosis or sarcoidosis
 certain types of cancer, including lung and breast cancers
 excessive use of antacids and calcium or vitamin D supplements
 medications like lithium, theophylline, or certain water pills
Hypocalcemia is a lack of adequate calcium in the bloodstream. Causes can include:

 kidney failure
 hypoparathyroidism
 vitamin D deficiency
 pancreatitis
 prostate cancer
 malabsorption
 certain medications, including heparin, osteoporosis medicine, and antiepileptic drugs
Chloride

Chloride is necessary for maintaining the proper balance of bodily fluids.

Hyperchloremia occurs when there is too much chloride in the body. This can happen as a result of:

 severe dehydration
 kidney failure
 dialysis
Hypochloremia develops when there is too little chloride in the body. This is often caused by sodium or
potassium problems, as discussed below. Other causes can include:

 cystic fibrosis
 eating disorders, such as anorexia
 scorpion stings
 acute kidney injury
Magnesium

Magnesium is a critical mineral that regulates many important functions, such as:

 muscle contraction
 heart rhythm
 nerve function
Hypermagnesemia means excess amounts of magnesium. This is a disorder that primarily affects people
with Addison’s disease and end-stage kidney disease.

Hypomagnesemia means having too little magnesium in the body. Common causes include:

 alcohol use disorder

 malnutrition
 malabsorption
 chronic diarrhea
 excessive sweating
 heart failure
 certain medications, including some diuretics and antibiotics
Potassium

Potassium is particularly important for regulating heart function. It also helps maintain healthy nerves and
muscles.

Hyperkalemia may develop due to high levels of potassium. This condition can be fatal if left undiagnosed and
untreated. It’s typically triggered by:

 severe dehydration
 kidney failure
 severe acidosis, including diabetic ketoacidosis
 certain medications, including some blood pressure medications and diuretics
 adrenal insufficiency, which is when your cortisol levels are too low
Hypokalemia occurs when potassium levels are too low. This often happens as a result of:

 eating disorders
 severe vomiting or diarrhea
 dehydration
 certain medications, including laxatives, diuretics, and corticosteroids
Sodium

Sodium is needed in the body to maintain fluid balance and is critical for normal body function. It also helps to
regulate nerve function and muscle contraction.

Hypernatremia happens when there is too much sodium in the blood. Abnormally high levels of sodium may
occur due to:

 inadequate water consumption

 severe dehydration
  excessive loss of bodily fluids as a result of prolonged vomiting, diarrhea, sweating, or respiratory illness
 certain medications, including corticosteroids
Hyponatremia develops when there is too little sodium. Common causes of low sodium levels include:

 excessive fluid loss through the skin from sweating or burns

 vomiting or diarrhea
 poor nutrition
 alcohol use disorder
 overhydration
 thyroid, hypothalamic, or adrenal disorders
 liver, heart, or kidney failure
 certain medications, including diuretics and seizure medications
 syndrome of inappropriate secretion of antidiuretic hormone (SIADH)
Phosphate

The kidneys, bones, and intestines work to balance phosphate levels in the body. Phosphate is necessary for a
wide variety of functions and interacts closely with calcium.

Hyperphosphatemia can occur due to:

 low calcium levels

 chronic kidney disease
 severe breathing difficulties
 underactive parathyroid glands
 severe muscle injury
 tumor lysis syndrome, a result of cancer treatment
 excessive use of phosphate-containing laxatives
Low levels of phosphate, or hypophosphatemia, can be seen in:

 acute alcohol abuse

 severe burns
 starvation
 vitamin D deficiency
 overactive parathyroid glands
 certain medication use, such as intravenous (IV) iron treatment, niacin, and some antacids
Diagnosing electrolyte disorders

A simple blood test can measure the levels of electrolytes in your body. A blood test that looks at your kidney
function is important as well. Your doctor may want to perform a physical exam or order extra tests to confirm
a suspected electrolyte disorder. These additional tests will vary depending on the condition in question.

For example, hypernatremia can cause loss of elasticity in the skin due to significant dehydration. Your doctor
can perform a pinch test to determine whether dehydration is affecting you. They may also test your reflexes, as
both increased and depleted levels of some electrolytes can affect reflexes. An electrocardiogram (EKG), an
electrical tracing of your heart, may also be useful to check for any irregular heartbeats, rhythms, or EKG
changes brought on by electrolyte problems.

Treating electrolyte disorders

Treatment varies depending on the type of electrolyte disorder and on the underlying condition.

In general, certain treatments are used to restore the proper balance of minerals in the body. These include:

IV fluids

IV fluids, typically sodium chloride, can help rehydrate the body. This treatment is commonly used in cases of
dehydration from vomiting or diarrhea. Electrolyte supplements can be added to IV fluids to correct
deficiencies.

Certain IV medications

These can help your body restore electrolyte balance quickly. They can also protect from negative effects while
you’re being treated by another method.

Oral medications

Oral medications are often used to correct mineral abnormalities in the body that are chronic. This occurs
especially in people with ongoing kidney disease. Common oral medications treat electrolyte imbalances, like
high potassium, calcium, or phosphate.

Hemodialysis

This is a type of dialysis that uses a machine to remove waste from your blood. One way to get the blood to
flow to this artificial kidney is for a doctor to surgically create a vascular access, or an entrance point, into your
blood vessels. This entrance point will allow a larger amount of blood to flow through your body during
hemodialysis treatment.

This means more blood can be filtered and purified. Hemodialysis can be used when an electrolyte disorder is
caused by sudden kidney damage and other treatments aren’t working. Your doctor may also decide on
hemodialysis treatment if the electrolyte problem has become life-threatening.
Supplements

Supplements can help replace depleted electrolytes on a short- or long-term basis, depending on the cause.

Once the imbalance has been corrected, your doctor will treat the underlying cause.

Risk factors for electrolyte disorders

Anyone can develop an electrolyte disorder. Certain people are more at risk because of their medical history.
Conditions that increase risk for an electrolyte disorder include:

 alcohol use disorder

 cirrhosis
 congestive heart failure
 kidney disease
 eating disorders, such as anorexia and bulimia
 trauma, such as severe burns or broken bones
 thyroid and parathyroid disorders
 adrenal gland disorders
Preventing electrolyte disorders

1. Visit a doctor if you’re experiencing common symptoms of an electrolyte disorder.

2. If the electrolyte disorder is caused by medications or underlying conditions, your doctor will adjust
your medication and treat the cause. This will help prevent future electrolyte imbalances.
3. Stay hydrated if you’re experiencing prolonged vomiting, diarrhea, or sweating.

https://www.healthline.com/health/electrolyte-disorders#overview1

2. Why does hemodialysis prevent a person to urinate?

Dialysis, a procedure that uses a special machine to replace the kidneys in filtering waste from the bloodstream,
may reduce the daily urine output that a person normally produces. This happens because as the blood is filtered
during dialysis, fluid is removed, thus reducing the kidneys' traditional role. As a result many dialysis patients
produce very small amounts of urine. However, dialysis does not prevent someone from urinating normally; it
only reduces the total urine output, so that he or she may only need to urinate once a day, which is not
dangerous. Some dialysis patients produce as little as one cup or less of urine each day, though urine volume is
usually dependent on the underlying cause of kidney failure. Some patients continue to produce normal volumes
of urine, which helps to manage their fluid balance. You should be able to get more information from your
grandmother's doctor, a nephrologist. This medical specialist is experienced in treating kidney disease and can
provide insight into the cause of your grandmother's kidney failure.
https://www.everydayhealth.com/urology-specialist/dialysis-trouble.aspx

The decreased urine amount is directly related to the loss in kidney function. In other words, dialysis treatment
is unable to stop the kidney function being lost, though it is very necessary and important sometimes. When
kidney disease patients undergo dialysis treatment, the blood flow in kidneys will become less briefly, which
causes further damage to kidneys. What is more, in addition that dialysis help remove wastes and excessive
fluid out of body and relieve some symptoms or complications, it is unable to do anything to repair kidney
damage and recover renal function. That is the reason why kidney function is still lost and dialysis patients
experience decreased urine amount with the treatment.
http://www.kidneyfailureweb.com/dialysis-knowledge/1678.html

3. Benign Prostatic Hyperplasia (Enlarged Prostate)

Benign prostatic hyperplasia (BPH) is one of the most common diseases in aging men. It can cause
bothersome lower urinary tract symptoms that affect quality of life by interfering with normal daily activities
and sleep patterns (AUA, 2006; Kaplan, 2006). BPH typically occurs in men older than 40 years of age. By the
time they reach 60 years of age, 50% of men have BPH. It affects as many as 90% of men by 85 years of age.
BPH is the second most common cause of surgical intervention in men older than 60 years of age.

Pathophysiology

The cause of BPH is not well understood, but testicular androgens have been implicated. Dihydrotestosterone
(DHT), a metabolite of testosterone, is a critical mediator of prostatic growth. Estrogens may also play a role in
the cause of BPH; BPH generally occurs when men have elevated estrogen levels and when prostate tissue
becomes more sensitive to estrogens and less responsive to DHT. Smoking, heavy alcohol consumption,
obesity, reduced activity level, hyper- tension, heart disease, diabetes, and a Western diet (high in animal fat and
protein and refined carbohydrates, low in fiber) are risk factors for BPH (Parsons, 2007).

BPH develops over a prolonged period; changes in the urinary tract are slow and insidious. BPH is a result of
complex interactions involving resistance in the prostatic urethra to mechanical and spastic effects, bladder
pressure during void- ing, detrusor muscle strength, neurologic functioning, and general physical health
(McCance & Huether, 2005). The hypertrophied lobes of the prostate may obstruct the bladder neck or urethra,
causing incomplete emptying of the bladder and urinary retention. As a result, a gradual dilation of the ureters
(hydroureter) and kidneys (hydronephrosis) can oc- cur. Urinary retention may result in UTIs because urine that
remains in the urinary tract serves as a medium for infective organisms.

Clinical Manifestations

BPH may or may not lead to lower urinary tract symptoms; if symptoms occur, they may range from mild to
severe. Severity of symptoms increases with age, and half of men with BPH report having moderate to severe
symptoms. Ob- structive and irritative symptoms may include urinary fre- quency, urgency, nocturia, hesitancy
in starting urination, decreased and intermittent force of stream and the sensa- tion of incomplete bladder
emptying, abdominal straining with urination, a decrease in the volume and force of the urinary stream,
dribbling (urine dribbles out after urina- tion), and complications of acute urinary retention (more than 60 mL of
urine remaining in the bladder after urina- tion), and recurrent UTIs. Ultimately, chronic urinary retention and
large residual volumes can lead to azotemia (accumulation of nitrogenous waste products) and renal failure.

Generalized symptoms may also be noted, including fa- tigue, anorexia, nausea, vomiting, and pelvic
discomfort. Other disorders that produce similar symptoms include ure- thral stricture, prostate cancer,
neurogenic bladder, and uri- nary bladder stones.

4. PROBLEMS IN URINATION
Urinary incontinence - A lack of voluntary control over micturition is called urinary incontinence (in-KON-
ti-nens). In infants and children under 2–3 years old, incontinence is normal because neurons to the external
urethral sphincter muscle are not completely developed; voiding occurs whenever the urinary bladder is
sufficiently distended to stimulate the micturition reflex. Urinary incontinence also occurs in adults. There are
four types of urinary incontinence—stress, urge, overflow, and functional.

Stress incontinence is the most common type of incontinence in young and middle-aged females, and results
from weakness of the deep muscles of the pelvic floor. As a result, any physical stress that increases abdominal
pressure, such as cough- ing, sneezing, laughing, exercising, straining, lifting heavy objects, and pregnancy,
causes leakage of urine from the urinary bladder.

Urge incontinence is most common in older people and is charac- terized by an abrupt and intense urge to
urinate followed by an in- voluntary loss of urine. It may be caused by irritation of the urinary bladder wall by
infection or kidney stones, stroke, multiple sclerosis, spinal cord injury, or anxiety.

Overflow incontinence refers to the involuntary leakage of small amounts of urine caused by some type of
blockage or weak contractions of the musculature of the urinary bladder. When urine flow is blocked (for
example, from an enlarged prostate or kidney stones) or when the urinary bladder muscles can no longer
contract, the urinary bladder becomes overfilled and the pressure inside increases until small amounts of urine
dribble out.

Functional incontinence is urine loss resulting from the inability to get to a toilet facility in time as a result of
conditions such as stroke, severe arthritis, or Alzheimer's disease. Choosing the right treatment option depends
on correct diagnosis of the type of incontinence. Treatments include Kegel exercises (see Clinical Connection:
Injury of Levator Ani and Urinary Stress Incontinence in Chapter 11), urinary bladder training, medication, and
possibly even surgery. •

5. ASCITES
What is ascites? - Ascites is the buildup of an abnormal amount of fluid inside the abdomen (belly). This is a
common problem in patients with cirrhosis (scarring) of the liver. Approximately 80% of patients with cirrhosis
of the liver develop ascites.

What are the symptoms of ascites? - Most people who develop ascites develop a large belly and experience a
rapid gain in weight. Some people also develop swelling of the ankles and shortness of breath.

What causes ascites? - Ascites is the end result of a series of events. Cirrhosis of the liver is the most common
cause of ascites. When cirrhosis occurs, blood flow through the liver is blocked. This blockage causes an
increase in the pressure in the main vein (the portal vein) that delivers blood from the digestive organs to the
liver. This condition is called portal hypertension. Ascites occurs when portal hypertension develops. The
kidneys cannot rid the body of enough sodium (salt) through urine. Not being able to rid the body of salt causes
fluids to build up in the abdomen, resulting in ascites.

What are the risk factors for development of ascites? - Common risk factors for the development of ascites
are any diseases that can cause cirrhosis of the liver. These include hepatitis B, hepatitis C, and
alcoholism/alcohol abuse. Other diseases that lead to fluid buildup are congestive heart failure and kidney
failure. Cancers of organs in the abdomen also may lead to ascites.

How is ascites diagnosed? - Ascites is diagnosed based on physical exam medical history, blood tests,
ultrasound or CT scan, and paracentesis. Paracentesis is a procedure in which a needle is inserted through the
abdominal wall (after local anesthesia and fluid is removed. This fluid is examined for signs of infection,
cancer, or other medical problems.

What are the complications of ascites? - Abdominal pain, discomfort and difficulty breathing: These
problems may occur when too much fluid builds up in the abdominal cavity. This may limit a patient's ability to
eat, walk and perform daily activities.
Infection: The fluids that build up in the gut as a result of ascites could become infected with bacteria. When
this happens, the condition is called spontaneous bacterial peritonitis. It usually causes fever and abdominal
pain. The diagnosis is generally made by taking a sample from the abdominal cavity as described above (ie, by
performing a paracentesis). Spontaneous bacterial peritonitis is a serious condition that requires treatment with
IV antibiotics. After recovery from this infection, long-term treatment with oral antibiotics is needed to keep the
infection from recurring.
Fluid in the lungs: This condition is called hepatic hydrothorax. Abdominal fluid fills the lung (mostly on the
right side). This results in shortness of breath, cough, hypoxemia (lack of oxygen in the blood) and/or chest
discomfort. Hepatic hydrothorax is best treated by removing the abdominal ascites by paracentesis.

Kidney failure: Worsening of cirrhosis of the liver can lead to kidney failure. This condition is called
hepatorenal syndrome. It is rare, but is a serious condition and may lead to kidney failure.

What are the best treatments for ascites?

Limit the amount of salt in your diet. The most important step to treating ascites is to drastically reduce your
salt intake. Recommended limits are 2,000 mg or less a day. Seeing a nutritional specialist (dietitian) is helpful
especially because the salt content in foods is difficult to determine. Salt substitutes – that do not contain
potassium -- can be used. Often, patients will require diuretics ("water pills") to treat ascites. Take these pills as
prescribed. Common diuretics are spironolactone (Aldactone®) and/or furosemide (Lasix®). These water pills
can cause problems with your electrolytes (sodium, potassium) and kidney function (creatinine). Taking water
pills is not a substitute for reducing your salt intake. Both are needed to treat ascites.

Other, increasingly more aggressive treatments include:

Paracentesis as a treatment: Sometimes fluids continue to build up in the abdomen despite use of diuretics and a
restricted salt diet. In these cases, patients may need paracentesis to remove this large amount of excess fluid.

Surgery: Surgical placement of a shunt between the main vein (portal vein) and smaller veins is sometimes used
as a treatment. A radiologist can place a shunt directly through the liver, thereby relieving portal hypertension
and diminishing ascites. By increasing blood flow, all organs of the body are better able to perform their
function. For example, in patients with ascites, improved kidney function helps rid the body of excess sodium
(salt) and prevent the buildup of fluids.

Liver transplant. This approach is reserved for patients with very severe cirrhosis whose livers are failing.

What can I do to control my ascites?

Weigh yourself daily. Call your doctor if you gain more than 10 lbs (or more than 2 lbs per day on 3
consecutive days).

Limit the amount of alcohol you drink. Better yet, do not drink any alcoholic beverages at all. Reducing the
amount of alcohol you drink reduces the risk of developing ascites.

Limit use of nonsteroidal anti-inflammatory drugs (NSAIDs) Ibuprofen (Advil®, Motrin®), aspirin,
indomethacin, sulindac are examples of NSAIDs. These drugs affect the kidneys, causing water and salt to be
retained by the body.
Follow guidelines for a low-salt diet. Recommended limits are 2,000 mg or less a day.

Ascites is the excessive accumulation of fluid in the abdominal cavity. For fluid to be detectable by clinical
examination there has to be at least 1500 ml present (slightly less in a small, thin person, but significantly more
in an obese person). Ultrasound can detect much smaller volumes (≤500 ml). Ascites that is not infected and not
associated with hepato-renal syndrome may be graded as follows:[1]
• Grade 1 is mild ascites and is only detectable by ultrasound examination.
• Grade 2 is moderate ascites causing moderate symmetrical distension of the abdomen.
• Grade 3 is large ascites causing marked abdominal distension.
Refractory ascites can be divided into two groups:
• Diuretic-resistant ascites is refractory to dietary sodium restriction and intensive diuretic treatment for at least
one week.
• Diuretic-intractable ascites is refractory to therapy due to the development of diuretic-induced complications
that preclude the use of an effective dose of diuretic.
Causes of ascites
• Cirrhosis:
Ascites is the most common manifestation in cirrhotic patients and is associated with a reduced survival rate.[2]

Approximately 75% of patients presenting with ascites have underlying cirrhosis and about 50% of patients
with cirrhosis will develop ascites over a 10-year period of follow-up.[1]

Fluid retention (primarily ascites but also peripheral oedema and pleural effusions) is the most frequent
complication of end-stage liver disease. It significantly impairs the quality of life of patients with cirrhosis and
is associated with poor prognosis - one-year and five-year survival rates of 85% and 56% respectively.[3]

Beware the patient with a very long history of stable cirrhosis who then develops ascites - hepatocellular
carcinoma must be excluded.

• Malignancy accounts for around 15%. The usual causes are:

Malignancies of the gastrointestinal tract (carcinoma of stomach, colon, pancreas; primary hepatocellular
carcinoma and metastatic liver cancer).

Carcinoma of ovary: Meigs' syndrome is a rare complication of ovarian cancer and produces ascites out of all
proportion to the size of the tumour and pleural effusions, often unilateral.

Hodgkin's lymphoma and non-Hodgkin's lymphoma.

Metastatic carcinoma within the abdominal cavity.

• Heart failure.
• Nephrotic syndrome.
• Protein-losing enteropathy.
• Tuberculosis.
• Pancreatitis.
• Other rare causes, including hypothyroidism.
• Iatrogenic - eg, ovarian hyperstimulation as a consequence of IVF procedures.

Presentation
• Abdominal distension.
• Weight gain as a result of water retention.
• Discomfort: tense ascites is very uncomfortable but prior to this stage there is simply abdominal distension
with only very mild discomfort. Malignancy-related ascites is frequently painful.
• Nausea and appetite suppression: tense ascites presses on the stomach and bowel.
• Increasing dyspnoea: due to limited venous return from the lower limbs (pressure on the inferior vena cava)
and impaired expansion of the lungs (pressure on the diaphragm).
• There may be other symptoms related to the cause of the ascites.
• Consider risk factors for liver disease:
• Alcohol consumption.
• History of jaundice.
• History of chronic hepatitis B or hepatitis C (or risk factors for these diseases).
• Obesity, hypercholesterolaemia and type 2 diabetes mellitus are causes of non-alcoholic
steatohepatitis, which can progress to cirrhosis.[4]

6. Examination - full abdominal examination.

• Look at the patient, both with them lying down and standing up. The shape of the abdomen often suggests
fluid. On lying down, the flanks are full but on standing the fluid accumulates in the lower abdomen.
• The high intra-abdominal pressure may push out an umbilical hernia or even an inguinal hernia.

There may be stigmata of other diseases. Look for signs of liver disease and cirrhosis including:
-Jaundice
-Muscle wasting
-Gynaecomastia
-Spider naevi
-Palmar erythema

Rarely, a firm nodule in the umbilicus (known as Sister Mary Joseph's nodule) is found and suggests peritoneal
carcinomatosis originating from gastric, pancreatic, or hepatic primaries. A left-sided supraclavicular node, or
Virchow's node, suggests the presence of upper abdominal malignancy.

Examination for ascites

1. Shifting dullness is used to detect ascites. One study found the absence of flank dullness to be the most
accurate predictor against the presence of ascites - the probability of ascites without flank dullness was
less than 10%.[5]
2. Percuss from the level of the umbilicus and repeat moving laterally towards one side.
3. When the sound becomes dull, keep your fingers there to mark the spot and ask the patient to move on
to the opposite side.
4. Wait briefly for the fluid to sink and percuss again. If it is now resonant, that is a positive sign. Percuss
down until dullness is reached again.
5. Repeat on the other side.
6. False positives do occur, probably from dilated coils of small intestine reacting to gravity.
7. At least 1500 ml of fluid must be present for a result. An ultrasound scan will detect much less fluid
with greater certainty.
8. Large ascites can be detected by a 'fluid thrill'. This test requires two examiners. One person places the
side of the palm of one hand firmly on the centre of the abdomen, with the fingers pointing towards the
groin. The second person places the palm of one hand on one flank and then flicks the other flank. In
large ascites, a palpable fluid thrill can be felt by the palm resting on the opposite flank.

Monitoring
Simple assessment of the progress of ascites may be made by:
• Serial measurements of the abdominal girth - ensure the tape measure is placed in the same position each
time.
• Serial measurement of weight - rapid changes indicate fluid gain or loss which are much faster than gain or
 loss of fat or lean body mass.

Differential diagnosis
The differential diagnosis of ascites is with other causes of abdominal mass, especially large cysts, although
sometimes plain obesity may seem like ascites. The essential feature is the fluidity and shifting with position.

Investigations
The cause of the ascites is often apparent after an adequate history and examination. The aims of investigation
for ascites are:
• Confirming the presence of ascites.
• Finding the cause for the ascites.
• Assessing any complication due to the ascites.

Blood tests
• FBC
• Renal function tests
• LFTs
• Clotting screen
• TFTs
If cirrhosis is confirmed, further tests will be required to elucidate the cause - eg, antibody tests for hepatitis B
or C.

Imaging studies
• Abdominal ultrasound is a very sensitive way of assessing ascites and may also show the causative pathology
such as carcinoma of ovary or metastatic liver disease.
• CXR may show pleural effusion, evidence of pulmonary metastases or heart failure.
• If ultrasound has failed to reveal a cause then MRI scanning may be used.

Management[
• Treatment of any underlying cause.
• A diet with salt intake restricted to <90 mmol/day (5.2 g of salt/day) is useful, especially in cirrhosis but is
unlikely to be effective in other aetiologies such as malignancy.

Drugs - The first line of management of ascites is medical treatment (sodium restriction and diuretic therapy)
and is effective in the majority of cirrhotic patients with non-refractory ascites.
-Diuretics:
1. Spironolactone is the best initial choice in cirrhosis: it increases sodium excretion and potassium
reabsorption in the distal tubules. 100 mg/day can gradually be increased to 400 mg as necessary. Serum
potassium levels need monitoring, as hyperkalaemia frequently limits spironolactone's use.
2. Loop diuretics may be used as an adjunct to spironolactone, generally only when maximum doses of the
latter have been reached.[1] Start cautiously with, for example, furosemide 40 mg/day, although up to
160 mg/day may be used. High doses cause severe electrolyte disturbance, particularly hyponatraemia.

Therapeutic paracentesis
• Patients with large or refractory ascites generally benefit from therapeutic paracentesis.[1]
• This needs to be a sterile procedure.
• Paracentesis of <5 litres of uncomplicated ascites should be followed by plasma expansion with a synthetic
plasma expander
• Larger-volume paracenteses should be be followed by volume expansion using human albumin solution.
7. Total Parenteral Nutrition
Nutrition - When TPN is indicated - A multidisciplinary approach to the management of patients receiving
TPN is recommended to reduce complications.
Total parenteral nutrition is the aseptic delivery of nutrients into the circulatory system via a central venous
catheter or the peripheral veins. TPN is used when the gut is not functioning and there are several indications
that may suggest its use (see Table 1).

Indications for total parenteral nutrition

 Inadequate absorption resulting from short bowel syndrome

 Gastrointestinal fistula
 Bowel obstruction
 Prolonged bowel rest
 Severe malnutrition, significant weight loss and/or hypoproteinaemia when enteral therapy is not
possible
 Other disease states or conditions in which oral or enteral feeding are not an option

Access-routes-and-duration
Establishing and maintaining suitable access to the circulation is essential for the successful management of
TPN. The route used is dependent on the anticipated duration of feeding and the osmolarity of the solution.

Central vein cannulation is the most commonly used route, however peripheral feeding is an acceptable
alternative for short-term feeding. A single dedicated lumen should be used for administration of TPN.

Nutritionalassessment
Prior to commencement of TPN the patients nutritional requirements are assessed. Energy and nitrogen
requirements can vary, depending on age, sex, body composition, clinical status and activity. A baseline
biochemical assessment should identify any abnormal plasma electrolyte levels, liver function tests, renal
function tests, glucose levels or lipid screen.

Nutritional requirements

Fluid - TPN may be the sole source of fluid or used in combination with other sources such as iv fluids, iv
antibiotics and blood products. The fluid balance chart is an informative summary of determining adequacy of
input versus output.

Acute changes in fluid can also be determined by monitoring acute changes in biochemical parameters such as
albumin, haemoglobin, mean cell volume, urea and sodium. To maintain fluid levels, the following is required:

 18-60 years old 35ml/kg/day

 > 60 years old 30ml/kg/day

Plus replacement of ongoing fluid losses, eg. pyrexia, urine, drains, excess wound exudates, stomas and high GI
losses.

Energy - Energy requirements are most commonly estimated using predictive equations. 1 These are based on
population data, taking into account activity and stress factors.
It is imperative that these equations are not used in isolation and that monitoring of the patient occurs to assess
efficacy. Indirect calorimetry may be used. However, this is not practical in the acute setting.

Nutritional requirements are also affected by medical conditions, thus alternate evidence based predictive
equations exist for certain conditions such as liver disease, renal failure and the critically ill obese.

Nitrogen - Patients do not have a requirement for nitrogen per se, but for amINO acids, which are the substrates
needed for protein synthesis (1g nitrogen = 6.25g protein).

The aim of nutritional support is to achieve a state of nitrogen balance using nitrogen balance data where
available or general recommendations.2 The nitrogen in parenteral nutrition is provided in the form of an
amINO acid solution.

Electrolytes - The normal daily electrolyte requirements are:

 Sodium 1-1.5 mmol/kg

 Potassium 1-1.5mmol/kg
 Calcium 0.1-0.15mmol/kg
 Magnesium 0.1-0.2 mmol/kg
 Phosphate 0.5-0.7mmol/kg.

Vitamins and trace elements

 Water soluble (Pabrinex), fat soluble (Vitlipid) and combined preparations (Cernevit Multibionta) of
vitamins are available.
 Additrace contains trace elements, eg. iron, zinc, manganese, copper, chromium, selenium,
molybdenum, fluoride and iodine.

Monitoring - Regular monitoring is essential to detect and minimise complications and determine response to
nutritional support.

Patients receiving TPN should have their nutritional requirements reviewed regularly, taking into account
clinical condition, treatments (eg. dialysis), drug therapy, nutritional status, response to TPN and supporting
laboratory data.

Clinical assessment of the patient can reveal ascites, oedema, impaired wound healing or loss of muscle mass
that may not be evident from monitoring weight and biochemical indices (see Table 2).

Monitoring patients receiving TPN

Fluid balance Monitor daily

Glucose tolerance Initially levels checked every 4-6 hours; daily when stable

Weight Daily weights can show fluid changes

Long term trends determine changes in tissue mass

Venous access Venous access site regularly checked for signs of infection, phlebitis
Routine
Serum Na, K, urea and creatinine checked daily initially
biochemistry

Ca, Mg and P checked at least twice a week initially

Trace elements zinc, copper, selenium checked monthly

Vitamins B12, Folate, Vitamin A, Vitamin E checked monthly

Urinary levels of electrolytes useful when determining clinical significance of plasma

Urinalysis
levels

Complications
Mechanical, infectious and nutritional complications can arise, including:

 Mechanical pneumothorax, malposition, embolism

 Infectious sepsis, thrombophlebitis
 Nutritional complications including
o fluid overload/dehydration
o electrolyte imbalance
o hyperglycaemia/hypoglycaemia
o over feeding
o re-feeding syndrome
o nutrient deficiency
o hepatobiliary dysfunction.

Standard-versus-tailored-regimens
TPN can be provided by a standard or patient specific prescription. Many factors influence this decision such as
frequency of use, patient types, local compounding facilities and cost.

Patients on TPN that are metabolically stable can tolerate slight under or over provision of nutrients, fluid or
electrolytes with no complications.

It is the careful assessment that will identify those patients who are likely to be substrate intolerant and require
frequent manipulations or specifically tailored regimens.

Albumin
A low plasma albumin level is occasionally used as a reason for nutrition support. Albumin is a negative acute
phase protein, levels dropping within six hours of an acute injury, decreasing by up to 50% in severe cases. This
is due to the increased transcapillary escape rate and a reduced return via the lymphatic system. Albumin is not
a useful indicator of nutritional status, but is a useful prognostic marker.

Novel-substrates
The principal novel substrate with the most clinical evidence is glutamine. It should be reserved for critically ill
and surgical patients with anticipated prolonged length of stay.

After injury/hypercatabolic conditions, profound intracellular glutamine depletion has been found, thus is
regarded as a conditionally essential amINO acid. Studies have shown improvements in the clinical outcome of
hypermetabolic patients.
Optimal-management
Parenteral nutrition is the most complex and expensive form of artificial nutrition support. A multidisciplinary
approach to the management of these patients can optimise this therapy and reduce complications.

8. Diarrhea
CONSEQUENCES OF WATERY DIARRHEA
Diarrhea stool contains large amounts of sodium, chloride, potassium, and bicarbonate. All the acute effects of
watery diarrhoea result from the loss of water and electrolytes from the body in liquid stool. Additional amounts
of water and electrolytes are lost when there is vomiting, and water losses are also increased by fever. These
losses cause dehydration (due to the loss of water and sodium chloride), metabolic acidosis (due to the loss of
bicarbonate), and potassium depletion. Among these, dehydration is the most dangerous because it can cause
decreased blood volume (hypovolaemia), cardiovascular collapse, and death if not treated promptly. Three types
of dehydration are considered below.

Isotonic dehydration
This is the type of dehydration most frequently caused by diarrhoea. It occurs when the net losses of water and
sodium are in the same proportion as normally found in the ECF. The principal features of isotonic dehydration
are:
 there is a balanced deficit of water and sodium;
 serum sodium concentration is normal (130-150 mmol/l);
 serum osmolality is normal (275-295 mOsmol/l);
 hypovolaemia occurs as a result of a substantial loss of extracellular fluid.

Isotonic dehydration is manifested first by thirst, and subsequently by decreased skin turgor, tachycardia, dry
mucous membranes, sunken eyes, lack of tears, a sunken anterior fontanelle in infants, and oliguria. The
physical signs of isotonic dehydration begin to appear when the fluid deficit approaches 5% of body weight and
worsen as the deficit increases. As the fluid deficit approaches 10% of body weight, dehydration becomes
severe and anuria, hypotension, a feeble and very rapid radial pulse, cool and moist extremities, diminished
consciousness, and other signs of hypovolaemic shock appear. A fluid deficit that exceeds 10% of body weight
leads rapidly to death from circulatory collapse.

Hypertonic (hypernatraemic) dehydration

Some children with diarrhoea, especially young infants, develop hypernatraemic dehydration. This reflects a
net loss of water in excess of sodium, when compared with the proportion normally found in ECF and blood. It
usually results from the ingestion during diarrhoea of fluids that are hypertonic (owing to their content of
sodium, sugar, or other osmotically active solutes, such as lactose in whole cow's milk) and not efficiently
absorbed, and an insufficient intake of water or other low-solute drinks. The hypertonic fluids create an osmotic
gradient that causes a flow of water from ECF into the intestine, leading to a decrease in the ECF volume and an
increase in sodium concentration within the ECF (see Figure 2.3, B). The principal features of hypernatraemic
dehydration are:
 there is a deficit of water and sodium, but the deficit of water is greater;
 serum sodium concentration is elevated (>150 mmol/l);
 serum osmolality is elevated (>295 mOsmol/l);
 thirst is severe and out of proportion to the apparent degree of dehydration; the child is very irritable;
 seizures may occur, especially when the serum sodium concentration exceeds 165 mmol/l.

Hypotonic (hyponatraemic) dehydration
Children with diarrhoea who drink large amounts of water or other hypotonic fluids containing very low
concentrations of salt and other solutes, or who receive intravenous infusions of 50% glucose in water, may
develop hyponatraemia. This occurs because water is absorbed from the gut while the loss of salt (NaCl)
continues, causing net losses of sodium in excess of water. The principal features of hyponatraemic dehydration
are:
 there is a deficit of water and sodium, but the deficit of sodium is greater;
 serum sodium concentration is low (<130 mmol/l);
 serum osmolality is low (<275 mOsmol/l);
 the child is lethargic; infrequently, there are seizures.

Base-deficit acidosis (metabolic acidosis)
During diarrhoea, a large amount of bicarbonate may be lost in the stool. If the kidneys continue to function
normally, much of the lost bicarbonate is replaced by the kidneys and a serious base deficit does not develop.
However, this compensating mechanism fails when renal function deteriorates, as happens when there is poor
renal blood flow due to hypovolaemia. Then, base deficit and acidosis develop rapidly. Acidosis also results
from excessive production of lactic acid when patients have hypovolaemic shock. The features of base-deficit
acidosis include:
 the serum bicarbonate concentration is reduced - it may be less than 10 mmol/l;
 arterial pH is reduced - it may be less than 7.10;
 breathing becomes deep and rapid, which helps to raise arterial pH by causing a compensating
respiratory alkalosis;
 there is increased vomiting.

Potassium depletion
Patients with diarrhoea often develop potassium depletion owing to large faecal losses of this ion; these losses
are greatest in infants and can be especially dangerous in malnourished children, who are frequently potassium-
deficient before diarrhoea starts. When potassium and bicarbonate are lost together, hypokalaemia does not
usually develop. This is because the metabolic acidosis that results from the loss of bicarbonate causes
potassium to move from ICF to ECF in exchange for hydrogen ion, thus keeping the serum potassium level in a
normal or even elevated range. However, when metabolic acidosis is corrected by giving bicarbonate, this shift
is rapidly reversed, and serious hypokalaemia can develop. This can be prevented by replacing potassium and
correcting the base deficit at the same time. The signs of hypokalaemia may include:
 general muscular weakness;
 cardiac arrhythmias;
 paralytic ileus, especially when drugs are taken that also affect peristalsis (such as opiates).

http://rehydrate.org/diarrhoea/tmsdd/2med.htm#CONSEQUENCES OF WATERY DIARRHOE

9. Burns
Consequences of BURNS
Electrolyte imbalance can be a serious complication experienced by burn victims. According to the December
2000 edition of “Annals of Burns and Fire Disasters,” fluid intake and electrolyte imbalance must be monitored
in burn victims. Due to the serious nature of this situation, hospitalization may be required.

When a person has major burns, there is a resultant damage to the intravascular volume and it is decreased in
both the damaged tissue as well as surrounding areas. This is caused due to increased permeability, changes in
interstitial osmotic pressure in burn tissue and cellular edema. This leads to an imbalance of all the necessary
minerals in the body and can prove lethal if not treated appropriately.

A decrease in sodium level or hyponatraema , decrease in potassium or hypokalaemia, imbalance of magnesium

or hypomagnesaemia, decrease in calcium ions or hypocalcaemia and altered phosphate ion levels or
Hypophosphataemia can cause heart failure, seizures, muscle spasms, renal and metabolic failure, damage to the
bones, and many other problems associated with a lack of proper ion balance in the body.
Types
The two types of electrolyte imbalances most likely to affect burn victims include hyponatremia and
hyperkalemia. Hyponatremia is a result of decreased sodium in the blood from the destroyed tissue caused by
burns on the body. Hyperkalemia occurs when the levels of potassium in the blood are higher than normal.
Hyperkalemia happens to burn victims as a result of the destruction of cells and tissues.

Symptoms
Electrolyte imbalances need to be managed by a physician immediately after the burns occur and until the
patient's condition stabilizes. The electrolyte imbalance that occurs after burns can create cardiac instability.
Symptoms may include muscle weakness, seizures, confusion, fatigue, vomiting, weakened pulse, irregular
heartbeat and nausea.
https://www.livestrong.com/article/298392-electrolyte-imbalance-in-kidney-failure/