Case studies of chirrosis patient
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About This Presentation
Mohamed Anwer Naleef, I am Nurse at Hemas Hospital,
This is about care of patient with Cirrhosis Disease Condition. As a Nurse three days my Nursing Process, observation, Nursing care Plan, Nursing Care and Help to patient manage and adjust the disease condition. Because the Cirrhosis is majority o...
Slide Content
Care Study
Nursing Care of the patient with
Cirrhosis
Medical Nursing
Submitted to: Tutor
Mr. Mohamed Anwer Naleef
AUC/Nur/2011/0028
Faculty of Nursing
Aquinas University College, Colombo
Nursing Care of the patient with
Cirrhosis
Medical Nursing
Submitted to: Tutor
Mr. Mohamed Anwer Naleef
AUC/Nur/2011/0028
Faculty of Nursing
Aquinas University College, Colombo
Cirrhosis
Medical Nursing
Care Study
Submitted to: Tutor
Submitted by: Mohamed Anwer Naleef
Nursing Student 2011/2014
AUC/Nur/2011/0028
Faculty of Nursing
Aquinas University College
Colombo
Medical Nursing
Care Study
Submitted to: Tutor
Submitted by: Mohamed Anwer Naleef
Nursing Student 2011/2014
AUC/Nur/2011/0028
Faculty of Nursing
Aquinas University College
Colombo
Care Study of Patient with
Liver Cirrhosis
Mr. Mohamed Anwer Naleef
Nursing Student 2011/2014
AUC/Nur/2011/03/0028
Faculty of Nursing
Aquinas university College
Srilanka
Liver Cirrhosis
Mr. Mohamed Anwer Naleef
Nursing Student 2011/2014
AUC/Nur/2011/03/0028
Faculty of Nursing
Aquinas university College
Srilanka
Acknowledgement
I express my heartfelt gratitude, sincere appreciation
and profound regards to the following people who, gave
guidance, strength, and encouragement in making this case
presentation possible. First of all, Thanks to God, for
granted us the knowledge and skills. To their family,
friends, and classmates, for their consideration and
unending support, emotionally, spiritually and financially.
To their clinical instructor, Madam. for guiding us in the
course of making this case presentation and giving them tips
on how to have a good presentation. Thanks to all Lectures
of Aquinas University and School of Nursing and all
medical personnel and staff members of Hospital Wattala,
A Ward, for sharing ideas, cooperating and giving full effort
in making the case presentation successful Lastly, to our
client and his family for their acceptance and willingness to
share time, effort and giving us the essential information
needed for this case presentation.
Thank you Very Much
I express my heartfelt gratitude, sincere appreciation
and profound regards to the following people who, gave
guidance, strength, and encouragement in making this case
presentation possible. First of all, Thanks to God, for
granted us the knowledge and skills. To their family,
friends, and classmates, for their consideration and
unending support, emotionally, spiritually and financially.
To their clinical instructor, Madam. for guiding us in the
course of making this case presentation and giving them tips
on how to have a good presentation. Thanks to all Lectures
of Aquinas University and School of Nursing and all
medical personnel and staff members of Hospital Wattala,
A Ward, for sharing ideas, cooperating and giving full effort
in making the case presentation successful Lastly, to our
client and his family for their acceptance and willingness to
share time, effort and giving us the essential information
needed for this case presentation.
Thank you Very Much
Contents:-
1. Objectives of Care Study
2. Introduction
2.1. Liver
2.2. Liver Cirrhosis
3. Anatomy and Physiology of Liver
3.1. Anatomy of Liver
3.2. Physiology of Liver
4. Assessment of the Patient
4.1. Patient History and Physical Assessment
4.2. Care plan of the Patient
4.3. Vital Signs Chart
4.4. Intake and Output Chart
4.5. Medication Chart
4.6. Discharge and Follow Up Care
5. Disease Condition ( Cirrhosis)
5.1. Introduction/Definition
5.2. Etiology
5.3. Pathophysiology
5.4. Clinical Manifestation
5.5. Investigations
5.6. Management
5.7. Complications
5.8. Prognosis
6. Nursing Care of Patient with Cirrhosis
6.1. Nursing Assessment
6.2. Nursing Diagnosis
6.3. Nursing Interventions
7. Summary and Conclusion
8. References
1. Objectives of Care Study
2. Introduction
2.1. Liver
2.2. Liver Cirrhosis
3. Anatomy and Physiology of Liver
3.1. Anatomy of Liver
3.2. Physiology of Liver
4. Assessment of the Patient
4.1. Patient History and Physical Assessment
4.2. Care plan of the Patient
4.3. Vital Signs Chart
4.4. Intake and Output Chart
4.5. Medication Chart
4.6. Discharge and Follow Up Care
5. Disease Condition ( Cirrhosis)
5.1. Introduction/Definition
5.2. Etiology
5.3. Pathophysiology
5.4. Clinical Manifestation
5.5. Investigations
5.6. Management
5.7. Complications
5.8. Prognosis
6. Nursing Care of Patient with Cirrhosis
6.1. Nursing Assessment
6.2. Nursing Diagnosis
6.3. Nursing Interventions
7. Summary and Conclusion
8. References
1. Objectives
Short term Objectives:-
1. To relieve Pain.
2. To promote Nutritional Level
3. To give Health Education.
4. Provide Comfort.
5. To prevent complication.
6. To maintain optimal fluid level.
Long term Objectives:-
1. To prevent Complications.
2. To give Health Education.
3. To give the knowledge of the health promotion and taking health
decision.
4. To maintain normal nutritional level.
5. To continue Follow up Care.
Short term Objectives:-
1. To relieve Pain.
2. To promote Nutritional Level
3. To give Health Education.
4. Provide Comfort.
5. To prevent complication.
6. To maintain optimal fluid level.
Long term Objectives:-
1. To prevent Complications.
2. To give Health Education.
3. To give the knowledge of the health promotion and taking health
decision.
4. To maintain normal nutritional level.
5. To continue Follow up Care.
Section 2
Introduction
Introduction
2. Introduction
2.1. The Liver
The liver is one of the largest and most complex organs in the body. It stores vital
energy and nutrients, manufactures proteins and enzymes necessary for good
health, protects the body from disease, and
breaks down (or metabolizes) and helps
remove harmful toxins, like alcohol, from
the body. It is one of the most important
organs in the body since it has many
significant functions. A lack or failure to
provide proper care of it may lead to an
abnormality or disorder.
2.2. The Liver Cirrhosis
Cirrhosis is defined histologically by septal fibrosis with nodular parenchymal
regeneration. Only 60% of patients with
alcoholic cirrhosis have signs or
symptoms of liver disease, and most
patients with cirrhosis have no clinical
history of alcoholic hepatitis. Liver
enzyme levels may be relatively normal
in cirrhosis without alcoholic hepatitis.
Concomitant HCV infection is common
in patients with alcoholic liver disease.
The prognosis of alcoholic cirrhosis
depends on whether patients continue to
consume alcohol and whether there are
signs (jaundice, ascites, or gastrointestinal tract bleeding) of chronic liver disease.
The 5-year survival rate for patients who have ascites, jaundice, or hematemesis and
abstain from alcohol is 89% and for those who have signs and continue to consume
alcohol, 34%. Liver transplant is an option for patients with end-stage alcoholic liver
disease if they demonstrate that they can maintain abstinence from alcohol.
2.1. The Liver
The liver is one of the largest and most complex organs in the body. It stores vital
energy and nutrients, manufactures proteins and enzymes necessary for good
health, protects the body from disease, and
breaks down (or metabolizes) and helps
remove harmful toxins, like alcohol, from
the body. It is one of the most important
organs in the body since it has many
significant functions. A lack or failure to
provide proper care of it may lead to an
abnormality or disorder.
2.2. The Liver Cirrhosis
Cirrhosis is defined histologically by septal fibrosis with nodular parenchymal
regeneration. Only 60% of patients with
alcoholic cirrhosis have signs or
symptoms of liver disease, and most
patients with cirrhosis have no clinical
history of alcoholic hepatitis. Liver
enzyme levels may be relatively normal
in cirrhosis without alcoholic hepatitis.
Concomitant HCV infection is common
in patients with alcoholic liver disease.
The prognosis of alcoholic cirrhosis
depends on whether patients continue to
consume alcohol and whether there are
signs (jaundice, ascites, or gastrointestinal tract bleeding) of chronic liver disease.
The 5-year survival rate for patients who have ascites, jaundice, or hematemesis and
abstain from alcohol is 89% and for those who have signs and continue to consume
alcohol, 34%. Liver transplant is an option for patients with end-stage alcoholic liver
disease if they demonstrate that they can maintain abstinence from alcohol.
3. Anatomy and Physiology of Liver
3.1. Anatomy of Liver
The liver largest organ in the body. It weight between 1.0 – 2.5kg (2.2 – 5.5lb) and is
heavers’ in the male than the female. It is a wedge shaped organ, lying immediately
below the diaphragm in the right hypochondrium and epigastrium.
There are two distinct sources that supply blood to the liver, including the following,
Oxygenated blood flows in from the hepatic artery.
Nutrient – rich blood flows in from the hepatic and portal vein.
The liver is described as having right and left lobes, and superior, inferior,
anterior, and posterior surfaces. The right and left main lobes are made up of
thousands of lobules. These lobules are connected to small ducts that connect with
larger ducts to ultimately form the hepatic duct. The hepatic duct transports the bile
produced by the liver cells to gallbladder, and Duodenum.
Blood Supply of the Liver
The liver receives blood from two sources and is an extremely vascular organ.
The hepatic artery, which is a branch of the Coeliac axis from the abdominal
aorta, conveys oxygenated blood to the liver cells.
The Portal Vein conveys venous blood, poor in oxygen but rich in nutrients,
frm the Stomach and Intestines.
Venous drainage from the liver is by the Hepatic Veins which empty into the
inferior vena cava.
Due to its great vascularity, lacerations of the liver are very dangerous and
results in profuse haemorrhage.
3.1. Anatomy of Liver
The liver largest organ in the body. It weight between 1.0 – 2.5kg (2.2 – 5.5lb) and is
heavers’ in the male than the female. It is a wedge shaped organ, lying immediately
below the diaphragm in the right hypochondrium and epigastrium.
There are two distinct sources that supply blood to the liver, including the following,
Oxygenated blood flows in from the hepatic artery.
Nutrient – rich blood flows in from the hepatic and portal vein.
The liver is described as having right and left lobes, and superior, inferior,
anterior, and posterior surfaces. The right and left main lobes are made up of
thousands of lobules. These lobules are connected to small ducts that connect with
larger ducts to ultimately form the hepatic duct. The hepatic duct transports the bile
produced by the liver cells to gallbladder, and Duodenum.
Blood Supply of the Liver
The liver receives blood from two sources and is an extremely vascular organ.
The hepatic artery, which is a branch of the Coeliac axis from the abdominal
aorta, conveys oxygenated blood to the liver cells.
The Portal Vein conveys venous blood, poor in oxygen but rich in nutrients,
frm the Stomach and Intestines.
Venous drainage from the liver is by the Hepatic Veins which empty into the
inferior vena cava.
Due to its great vascularity, lacerations of the liver are very dangerous and
results in profuse haemorrhage.
3.2. Functions of the Liver
Secretion of bile
Storage of glycogen
Metabolism of fat
Deamination of amino acids
Production of the plasma protein
Storage of vitamins
Storage of irons
Production of clotting factors
Production of heat
Detoxification
Secretion of bile
Storage of glycogen
Metabolism of fat
Deamination of amino acids
Production of the plasma protein
Storage of vitamins
Storage of irons
Production of clotting factors
Production of heat
Detoxification
Section 4
Assessment of the Patient
Assessment of the Patient
4. Assessment of the Patient with Cirrhosis
Data gathering at 2013/02/20 at 10am
Bio Graphic Data
Patient Name : Mr.
Age : 58 years
Sex : Male
Address :
Civil Status : Divorced
Religion : Buddhist
Contact No :
BHT No : 30848
Ward & Room No :
Consultant Name :
Admission Date :
Chief Complaint
Inadequate urine output since 3 days
Vomiting 4 times today
Vomits are water and light Brown color content.
Swelling in Abdomen and Scrotum since 10 days
Generalized swelling in the abdomen and Scrotum, Tenderness
when palpating the abdomen and Scrotum.
Poor oral Feeding 10 days (Loss of Appetite)
Data gathering at 2013/02/20 at 10am
Bio Graphic Data
Patient Name : Mr.
Age : 58 years
Sex : Male
Address :
Civil Status : Divorced
Religion : Buddhist
Contact No :
BHT No : 30848
Ward & Room No :
Consultant Name :
Admission Date :
Chief Complaint
Inadequate urine output since 3 days
Vomiting 4 times today
Vomits are water and light Brown color content.
Swelling in Abdomen and Scrotum since 10 days
Generalized swelling in the abdomen and Scrotum, Tenderness
when palpating the abdomen and Scrotum.
Poor oral Feeding 10 days (Loss of Appetite)
History of Present Illness
Patient is a 58 years old Mr. Rmale, who was in his usual state of health until
Saturday 16/01/2013, when noticed diffuse Swelling throughout his abdomen and
lower extremities. Swelling increased throughout the Saturday and Sunday. Patient
reports Discomfort, Pain and Tenderness. During this time patient attempted to
reduce the swelling by applying ice to affected region.
On Monday, 18/02/2013, the patient came to the Hospital, for a scheduled
appointment to monitor his Diabetes Mellitus condition. That time he presented with
Abdominal Distention, Diffuse Oedema of the lower extrimities and Swollen of the
Scrotum.
At that time Dr. (VP) admitted him. Since admission, he has been treated with
withdrawing peritoneal Cavity fluid (Paracentesis), NG Insertion, and Administration
of Diuretics ( Lasix 40mg IV), which has reduced the sowelling in his abdomen and
scrotum. Patient reports reduced discomfort, tenderness and pain.
Patient has a history of Diabetes Mellitus since 10 years and Hypertension
since 6 years which was controlled. Today the patient’s abdomen shows distended and
scrotal edema, Poor oral intake, inadequate urine output, and Vomiting.
Past Medical History
Liver Alcoholic Cirrhosis since two years.
Diabetes Mellitus since 10 years patient on Treatment.
Hypertension since 6 years patient on Treatment.
No Known history of Tuberculosis, Cancer, Coronary Artery Disease, Asthma, and
Anemia………………
Past Surgical History
Herniotomy in 2008
After surgery Blood transfusion done, Blood Group is O+.
After Surgery no Surgical Complications.
Patient is a 58 years old Mr. Rmale, who was in his usual state of health until
Saturday 16/01/2013, when noticed diffuse Swelling throughout his abdomen and
lower extremities. Swelling increased throughout the Saturday and Sunday. Patient
reports Discomfort, Pain and Tenderness. During this time patient attempted to
reduce the swelling by applying ice to affected region.
On Monday, 18/02/2013, the patient came to the Hospital, for a scheduled
appointment to monitor his Diabetes Mellitus condition. That time he presented with
Abdominal Distention, Diffuse Oedema of the lower extrimities and Swollen of the
Scrotum.
At that time Dr. (VP) admitted him. Since admission, he has been treated with
withdrawing peritoneal Cavity fluid (Paracentesis), NG Insertion, and Administration
of Diuretics ( Lasix 40mg IV), which has reduced the sowelling in his abdomen and
scrotum. Patient reports reduced discomfort, tenderness and pain.
Patient has a history of Diabetes Mellitus since 10 years and Hypertension
since 6 years which was controlled. Today the patient’s abdomen shows distended and
scrotal edema, Poor oral intake, inadequate urine output, and Vomiting.
Past Medical History
Liver Alcoholic Cirrhosis since two years.
Diabetes Mellitus since 10 years patient on Treatment.
Hypertension since 6 years patient on Treatment.
No Known history of Tuberculosis, Cancer, Coronary Artery Disease, Asthma, and
Anemia………………
Past Surgical History
Herniotomy in 2008
After surgery Blood transfusion done, Blood Group is O+.
After Surgery no Surgical Complications.
Medication History
Metformin 850mg bd
Furosemide 40mg nocte
Spironolactone 25mg bd
Tolbutamide 500mg bd
Atrovastatin 10mg nocte
Family History
Father, Uncles and Brother died at 57 from Myocardial infarction.
Family history of Diabetes Mellitus on both sides.
His daughter (20years old) in good health.
Does not know where about of his mother.
Social History
Living arrangement
Divorced and lives alone
Residence
Resides in an apartment, No identified harmful
environmental exposure.
Occupation
Retired Bank Manager
Tobacco, Alcohol and other Drug Use
One pack per day smoking history until 2010, 20 years of
Alcohol use until 2012 June.
Diet and Exercise
Patient maintains a low sodium diet and gets moderate
exercise.
Education
He is a University Graduate
Metformin 850mg bd
Furosemide 40mg nocte
Spironolactone 25mg bd
Tolbutamide 500mg bd
Atrovastatin 10mg nocte
Family History
Father, Uncles and Brother died at 57 from Myocardial infarction.
Family history of Diabetes Mellitus on both sides.
His daughter (20years old) in good health.
Does not know where about of his mother.
Social History
Living arrangement
Divorced and lives alone
Residence
Resides in an apartment, No identified harmful
environmental exposure.
Occupation
Retired Bank Manager
Tobacco, Alcohol and other Drug Use
One pack per day smoking history until 2010, 20 years of
Alcohol use until 2012 June.
Diet and Exercise
Patient maintains a low sodium diet and gets moderate
exercise.
Education
He is a University Graduate
Physical Assessment of the Patient
VITAL Signs
Temperature 98.5 F/Axilla
Pulse Rate 81/bpm
Respiratory Rate 24/bpm
Blood Pressure 120/80mmHg
Pain 6/10 in pain Scale
Height 174cm
Weight 78 kg
MBI
General Appearance
Patient is appropriately groomed for the environment, is oriented for Place,
Time, and Person, and in No apparent Distress. He appears jaundiced and
underweight.
Head
Head is regular shape, with no apparent lesion, Masses, or Foreign bodies.
Scalp shows no evidence of skin condition or infestation, and exhibited no
tenderness on palpation.
Eyes
Lids are normal, No evidence of discharge, Ptosis or edema.
Direct and consensual reactivity of light.
Visual fields are normal
Left 6/6, Right 6/6
Ears/ Nose/ Throat
External ears and nose are of symmetric regular shape and size.
No scars, lesions, masses or foreign bodies.
No tenderness to palpation of ears and nose.
Nasal mucosa is moist and pink with no discharge.
No allergic Rhinitis.
No Ear discharge.
Sense of smell is good.
VITAL Signs
Temperature 98.5 F/Axilla
Pulse Rate 81/bpm
Respiratory Rate 24/bpm
Blood Pressure 120/80mmHg
Pain 6/10 in pain Scale
Height 174cm
Weight 78 kg
MBI
General Appearance
Patient is appropriately groomed for the environment, is oriented for Place,
Time, and Person, and in No apparent Distress. He appears jaundiced and
underweight.
Head
Head is regular shape, with no apparent lesion, Masses, or Foreign bodies.
Scalp shows no evidence of skin condition or infestation, and exhibited no
tenderness on palpation.
Eyes
Lids are normal, No evidence of discharge, Ptosis or edema.
Direct and consensual reactivity of light.
Visual fields are normal
Left 6/6, Right 6/6
Ears/ Nose/ Throat
External ears and nose are of symmetric regular shape and size.
No scars, lesions, masses or foreign bodies.
No tenderness to palpation of ears and nose.
Nasal mucosa is moist and pink with no discharge.
No allergic Rhinitis.
No Ear discharge.
Sense of smell is good.
Mouth/Dental
Lips, Teeth, and gums all appear healthy with no lesions and ulceration.
Oral mucosa, tonsils, and palate appear healthy. No appear masses, lesions,
foreign bodies or other abnormalities.
Sense of taste is good.
Loss of Appetite in 10 days.
Neck
Neck is symmetric with no any lesions or ulceration.
There is no tenderness to palpation.
Skin
Skin appears is yellow color and there are no apparent rashes lesions or
ulcers.
Face
No scars in the face.
No wrinkles and patient facial appearance is normal.
Respiratory System
Chest is regular shape and size.
Chest girth is 34cm.
There is no apparent use of accessory muscle for normal breathing.
No reported respiratory related symptoms.
No cough, Dyspnoea, and Hemoptysis.
Cardiovascular System
No chest pain.
Patient has a 4 years history of hypertension, patient on treatment, regular
check up and using drugs such as Spironolactone and Frusemide.
Nails are Normal.
No cyanosis
CRFT (capillary refilling time) 2 seconds.
No oedema in the body and other extremities.
Extremities are Warm.
Lips, Teeth, and gums all appear healthy with no lesions and ulceration.
Oral mucosa, tonsils, and palate appear healthy. No appear masses, lesions,
foreign bodies or other abnormalities.
Sense of taste is good.
Loss of Appetite in 10 days.
Neck
Neck is symmetric with no any lesions or ulceration.
There is no tenderness to palpation.
Skin
Skin appears is yellow color and there are no apparent rashes lesions or
ulcers.
Face
No scars in the face.
No wrinkles and patient facial appearance is normal.
Respiratory System
Chest is regular shape and size.
Chest girth is 34cm.
There is no apparent use of accessory muscle for normal breathing.
No reported respiratory related symptoms.
No cough, Dyspnoea, and Hemoptysis.
Cardiovascular System
No chest pain.
Patient has a 4 years history of hypertension, patient on treatment, regular
check up and using drugs such as Spironolactone and Frusemide.
Nails are Normal.
No cyanosis
CRFT (capillary refilling time) 2 seconds.
No oedema in the body and other extremities.
Extremities are Warm.
Abdomen
Abdominal walls shows/ appearing distended and round.
Pain in the right upper quadrant of the abdomen, this pain is on and off
occurring an exertion.
Abdominal girth is 65cm.
Umbilicus is protruded.
Tenderness to palpation of Abdomen.
Nutritional Assessment
Patient non vegetarian.
No Anemic signs in the patient.
Vomiting 4times a day, vomits content are water.
No Nausea.
10 days history of Anorexia.
No Heart burn.
Elimination
Bladder
No Incontinence
4days history of Urinary Retention.
No Hematuria.
No Burning Sensation during pass Urine.
Bowel
No Constipation/diarrhea.
Patient taking Lactulose 30cc use in Ward.
No Malena
No difficulty passing Stool.
Neurological Assessment
No Syncope
No Confusion
Headache on the Morning
No Convulsive signs.
Abdominal walls shows/ appearing distended and round.
Pain in the right upper quadrant of the abdomen, this pain is on and off
occurring an exertion.
Abdominal girth is 65cm.
Umbilicus is protruded.
Tenderness to palpation of Abdomen.
Nutritional Assessment
Patient non vegetarian.
No Anemic signs in the patient.
Vomiting 4times a day, vomits content are water.
No Nausea.
10 days history of Anorexia.
No Heart burn.
Elimination
Bladder
No Incontinence
4days history of Urinary Retention.
No Hematuria.
No Burning Sensation during pass Urine.
Bowel
No Constipation/diarrhea.
Patient taking Lactulose 30cc use in Ward.
No Malena
No difficulty passing Stool.
Neurological Assessment
No Syncope
No Confusion
Headache on the Morning
No Convulsive signs.
Musculoskeletal Assessment
No Numbness
No Myalgia
No Fracture/injury
Patient complain of Difficulty in Walking because abdominal distention, and
Dyspnoea on exertion.
Psychiatric Assessment
Patient Alert, and Oriented to Time, Place, and Person.
Patient Anxiety because of Disease Condition.
No Numbness
No Myalgia
No Fracture/injury
Patient complain of Difficulty in Walking because abdominal distention, and
Dyspnoea on exertion.
Psychiatric Assessment
Patient Alert, and Oriented to Time, Place, and Person.
Patient Anxiety because of Disease Condition.
Drug Treatment
Klean prep Enema bd Per Oral
IV Levofloxacin 500mg daily
IV Pantocid 40mg bd
Lactulose 30cc tds Per Oral
IV Metranindazole 200mg tds
IV Hartman 50cc/hr
Metformin 850mg bd Per Oral
Furosemide 40mg bd Per Oral
Spironolactone 25mg bd Per Oral
Tolbutamide 500mg bd Per Oral
Atorvatatin 10mg nocte Per Oral
Klean prep Enema bd Per Oral
IV Levofloxacin 500mg daily
IV Pantocid 40mg bd
Lactulose 30cc tds Per Oral
IV Metranindazole 200mg tds
IV Hartman 50cc/hr
Metformin 850mg bd Per Oral
Furosemide 40mg bd Per Oral
Spironolactone 25mg bd Per Oral
Tolbutamide 500mg bd Per Oral
Atorvatatin 10mg nocte Per Oral
Section 5
Cirrhosis
Cirrhosis
6. Disease Condition ( Cirrhosis)
6.1. Introduction/Definition
6.2. Etiology
6.3. Pathophysiology
6.4. Clinical Manifestation
6.5. Investigations
6.6. Management
6.7. Complications
6.8. Prognosis
5.1. Cirrhosis
Cirrhosis is a complication of many liver diseases that is characterized by
abnormal structure and function of the liver.
The diseases that lead to cirrhosis do so because they injure and kill liver cells,
and the inflammation and repair that is associated with the dying liver cells
causes scar tissue to form.
The liver cells that do not die multiple in an attempt to replace the cells that
have died. This results in clusters of newly formed liver cells (regenerative
nodules) within the scar tissue.
There are many causes of cirrhosis; they include chemicals, viruses, toxic
metals and autoimmune liver disease in which the body’s immune system
attacks the liver.
6.1. Introduction/Definition
6.2. Etiology
6.3. Pathophysiology
6.4. Clinical Manifestation
6.5. Investigations
6.6. Management
6.7. Complications
6.8. Prognosis
5.1. Cirrhosis
Cirrhosis is a complication of many liver diseases that is characterized by
abnormal structure and function of the liver.
The diseases that lead to cirrhosis do so because they injure and kill liver cells,
and the inflammation and repair that is associated with the dying liver cells
causes scar tissue to form.
The liver cells that do not die multiple in an attempt to replace the cells that
have died. This results in clusters of newly formed liver cells (regenerative
nodules) within the scar tissue.
There are many causes of cirrhosis; they include chemicals, viruses, toxic
metals and autoimmune liver disease in which the body’s immune system
attacks the liver.
5.2. Etiology
Alcohol
Is a very common cause of cirrhosis. The development of cirrhosis
depends upon the amount and regularity of alcohol intake. Chronic, high level
of alcohol consumption injures liver cells. Alcohol cause a range of liver
diseases; from simple and uncomplicated fatty liver, to the more serious fatty
liver with inflammation, to cirrhosis.
Chronic viral hepatitis
Is a condition where hepatitis B or hepatitis C virus infects the liver for
years. Most patients with viral hepatitis will not develop chronic hepatitis and
cirrhosis. For example, the majority of the patients infected with hepatitis A
recover completely within weeks, without developing chronic infection.
Inherited (genetic) disorders
Result in accumulation in toxic substance in the liver which lead to tissue
damage and cirrhosis. Examples include the abnormal accumulation of the iron
(hemochromatosis) or copper (wilson’s disease). In hemochromatosis, patients
inherit a tendency to absorb an excessive amount of iron from food. Over time iron
accumulation in different organs throughout the body causes cirrhosis, arthritis,
heart muscle damage leading to heart failure, and testicular dysfunction causing
loss of sexual drive. Over time copper accumulates in the liver, eyes, and brain.
Cirrhosis, tremor, psychiatric disturbances and other neurological difficulties
occur, if the condition is not treated.
Autoimmune hepatitis
Is a liver disease caused by a an abnormality of the immune system that is
found more commonly in women. The abnormal immune activity in autoimmune
hepatitis causes progressive inflammation and distruction of liver cells
(hepatocytes), leading ultimately to cirrhosis.
Primary biliary cirrhosis (PBC)
Is a liver disease caused by an abnormality of the immune system that is
found predominantly in women. The abnormal immunity in PBC causes
chronic inflammation and destruction of the small bile ducts within the liver. In
PBC, the destruction of the small bile ducts blocks the normal flow of the bile
into the intestine. As the inflammation continues to destroy more of the bile
ducts, it also spread to destroy nearby liver cells. As the destruction of the
Alcohol
Is a very common cause of cirrhosis. The development of cirrhosis
depends upon the amount and regularity of alcohol intake. Chronic, high level
of alcohol consumption injures liver cells. Alcohol cause a range of liver
diseases; from simple and uncomplicated fatty liver, to the more serious fatty
liver with inflammation, to cirrhosis.
Chronic viral hepatitis
Is a condition where hepatitis B or hepatitis C virus infects the liver for
years. Most patients with viral hepatitis will not develop chronic hepatitis and
cirrhosis. For example, the majority of the patients infected with hepatitis A
recover completely within weeks, without developing chronic infection.
Inherited (genetic) disorders
Result in accumulation in toxic substance in the liver which lead to tissue
damage and cirrhosis. Examples include the abnormal accumulation of the iron
(hemochromatosis) or copper (wilson’s disease). In hemochromatosis, patients
inherit a tendency to absorb an excessive amount of iron from food. Over time iron
accumulation in different organs throughout the body causes cirrhosis, arthritis,
heart muscle damage leading to heart failure, and testicular dysfunction causing
loss of sexual drive. Over time copper accumulates in the liver, eyes, and brain.
Cirrhosis, tremor, psychiatric disturbances and other neurological difficulties
occur, if the condition is not treated.
Autoimmune hepatitis
Is a liver disease caused by a an abnormality of the immune system that is
found more commonly in women. The abnormal immune activity in autoimmune
hepatitis causes progressive inflammation and distruction of liver cells
(hepatocytes), leading ultimately to cirrhosis.
Primary biliary cirrhosis (PBC)
Is a liver disease caused by an abnormality of the immune system that is
found predominantly in women. The abnormal immunity in PBC causes
chronic inflammation and destruction of the small bile ducts within the liver. In
PBC, the destruction of the small bile ducts blocks the normal flow of the bile
into the intestine. As the inflammation continues to destroy more of the bile
ducts, it also spread to destroy nearby liver cells. As the destruction of the
hepatocytes proceeds, scar tissue (fibrosis) forms and spreads throughout the
areas of destruction.
Non alcoholic fatty liver disease (NAFLD)
Refers to a wide spectrum of liver diseases that, like alcoholic liver
disease, ranges from simple steatosis, to nonalcoholic steatohepatitis (NASH),
to cirrhosis. All stages of NAFLD have in common the accumulation of fat in
liver cells. NAFLD is associated with the metabolic syndrome and diabetes
mellitus type 2. Obesity is the most important cause of insulin resistance,
metabolic syndrome, and type 2 diabetes mellitus.
Cryptogenic cirrhosis (cirrhosis due to unidentified cause)
Is a common reason for liver transplantation. Because Cryptogenic
cirrhosis is due to NASH (nonalcoholic steatohepatitis) caused by long
standing obesity, type 2 DM and insulin resistance.
Primary sclerosing cholangitis (PSC)
Is an infection and inflammation of the common bile duct and is an
uncommon disease found frequently in patients with ulcerative colitis. In PSC,
the large bile ducts outside of the liver become inflamed, narrowed and
obstructed. Obstruction to the flow of bile leads to infections of the bile ducts
and jaundice and eventually causes cirrhosis.
Infants can be born without bile ducts (biliary atresia)
Its ultimately develop cirrhosis. Other infants are born lacking vital
enzymes for controlling sugars that leads to the accumulation of sugars and
cirrhosis. On rare occasions, the absence of a specific enzyme can cause
cirrhosis and scarring of the lung (alpha 1 antitrypsin deficiency).
Less common cause of cirrhosis include unusual reactions to some drugs and
prolonged exposure to toxins, as well as chronic heart failure (cardiac
cirrhosis).
areas of destruction.
Non alcoholic fatty liver disease (NAFLD)
Refers to a wide spectrum of liver diseases that, like alcoholic liver
disease, ranges from simple steatosis, to nonalcoholic steatohepatitis (NASH),
to cirrhosis. All stages of NAFLD have in common the accumulation of fat in
liver cells. NAFLD is associated with the metabolic syndrome and diabetes
mellitus type 2. Obesity is the most important cause of insulin resistance,
metabolic syndrome, and type 2 diabetes mellitus.
Cryptogenic cirrhosis (cirrhosis due to unidentified cause)
Is a common reason for liver transplantation. Because Cryptogenic
cirrhosis is due to NASH (nonalcoholic steatohepatitis) caused by long
standing obesity, type 2 DM and insulin resistance.
Primary sclerosing cholangitis (PSC)
Is an infection and inflammation of the common bile duct and is an
uncommon disease found frequently in patients with ulcerative colitis. In PSC,
the large bile ducts outside of the liver become inflamed, narrowed and
obstructed. Obstruction to the flow of bile leads to infections of the bile ducts
and jaundice and eventually causes cirrhosis.
Infants can be born without bile ducts (biliary atresia)
Its ultimately develop cirrhosis. Other infants are born lacking vital
enzymes for controlling sugars that leads to the accumulation of sugars and
cirrhosis. On rare occasions, the absence of a specific enzyme can cause
cirrhosis and scarring of the lung (alpha 1 antitrypsin deficiency).
Less common cause of cirrhosis include unusual reactions to some drugs and
prolonged exposure to toxins, as well as chronic heart failure (cardiac
cirrhosis).
5.3. Pathophysiology
Liver cirrhosis occurs when the
regenerative capacity of the liver is
overwhelmed by alcohol consumption,
drug or chemical damage, long-term
infection brought upon by infection or
extra hepatic bile obstruction.
Numerous infiltrating inflammatory
cells stimulate fibrosis in response to such massive destruction. It will then
result in an ever increasing scarring until sheets of fibrous repair tissue from
throughout the liver. These are diffusely distributed thereby isolating areas of
the liver that still retains their regenerative capacity.
These detached areas are called nodules and are readily apparent in the
liver’s surface. This condition of modularity and fibrosis is called cirrhosis.
Cirrhosis is a non-specific end-stage disease towards which various pathologic
consequences converge. The differing degrees of functional loss of the
hepatocytes results in variable signs and symptoms. In certain instances, the
liver is able to compensate for necrosis that none or minimal symptoms appear.
This situation leads to an unnoticed and unresolved destruction of hepatocytes
until adequate function can no longer be maintained and reserves are
completely depleted leading to liver failure.
Liver cirrhosis is defined by two principal factors: Portal Hypertension and
Hepatic Dysfunction.
Portal hypertension is the result of restricted flow of blood through the liver to
the hepatic veins and then to the inferior vena cava. The resulting portal
congestion increases portal pressures and decreases blood flow to the liver.
With reduced blood flowing to the cirrhotic liver, the hepatocytes have minimal
accessed to blood, severely hampering their capacity to detoxify harmful
chemicals.
As a result, toxins become more concentrated in the blood producing damaging
effects particularly the production of ammonia (from amino acid breakdown).
Instead of being excreted, ammonia stays in the blood causing hepatic
encephalopathy and a noticeable foul breath.
Furthermore, the hepatocytes continue to die leading to a progressive
deterioration of the liver’s regulatory capabilities resulting in hypocoagulation
and hypoalbuminemia.
Liver cirrhosis occurs when the
regenerative capacity of the liver is
overwhelmed by alcohol consumption,
drug or chemical damage, long-term
infection brought upon by infection or
extra hepatic bile obstruction.
Numerous infiltrating inflammatory
cells stimulate fibrosis in response to such massive destruction. It will then
result in an ever increasing scarring until sheets of fibrous repair tissue from
throughout the liver. These are diffusely distributed thereby isolating areas of
the liver that still retains their regenerative capacity.
These detached areas are called nodules and are readily apparent in the
liver’s surface. This condition of modularity and fibrosis is called cirrhosis.
Cirrhosis is a non-specific end-stage disease towards which various pathologic
consequences converge. The differing degrees of functional loss of the
hepatocytes results in variable signs and symptoms. In certain instances, the
liver is able to compensate for necrosis that none or minimal symptoms appear.
This situation leads to an unnoticed and unresolved destruction of hepatocytes
until adequate function can no longer be maintained and reserves are
completely depleted leading to liver failure.
Liver cirrhosis is defined by two principal factors: Portal Hypertension and
Hepatic Dysfunction.
Portal hypertension is the result of restricted flow of blood through the liver to
the hepatic veins and then to the inferior vena cava. The resulting portal
congestion increases portal pressures and decreases blood flow to the liver.
With reduced blood flowing to the cirrhotic liver, the hepatocytes have minimal
accessed to blood, severely hampering their capacity to detoxify harmful
chemicals.
As a result, toxins become more concentrated in the blood producing damaging
effects particularly the production of ammonia (from amino acid breakdown).
Instead of being excreted, ammonia stays in the blood causing hepatic
encephalopathy and a noticeable foul breath.
Furthermore, the hepatocytes continue to die leading to a progressive
deterioration of the liver’s regulatory capabilities resulting in hypocoagulation
and hypoalbuminemia.
Congestion in the hepatic portal system causes blood to be diverted to the
collateral vessels forcing them to accommodate larger volumes. This
engorgement causes the veins to bulge producing easily visible hemorrhoids.
Another consequence of this diversion is the dilation of the thin-walled
esophagus causing esophageal varices. Esophageal varices are subjected to
trauma as food is swallowed and expose to gastric reflux. This poses a
potential threat of rupture and bleeding.
When the varices rupture it is usually asymptomatic and sudden, bringing forth
a large scale blood loss. Compounded by a prolonged bleeding time,
esophageal varices is a very serious complication of liver cirrhosis.
Portal hypertension in liver cirrhosis also causes ascites (accumulation of fluid
in the peritoneal cavity) and splenomegaly. Ascites is caused by hampered
albumin production, the osmotic pressure decreases reducing the return of
fluid to the blood from the tissues. It results in a significant and pronounced
abdominal distention, compressing the abdomen and compromising breathing.
collateral vessels forcing them to accommodate larger volumes. This
engorgement causes the veins to bulge producing easily visible hemorrhoids.
Another consequence of this diversion is the dilation of the thin-walled
esophagus causing esophageal varices. Esophageal varices are subjected to
trauma as food is swallowed and expose to gastric reflux. This poses a
potential threat of rupture and bleeding.
When the varices rupture it is usually asymptomatic and sudden, bringing forth
a large scale blood loss. Compounded by a prolonged bleeding time,
esophageal varices is a very serious complication of liver cirrhosis.
Portal hypertension in liver cirrhosis also causes ascites (accumulation of fluid
in the peritoneal cavity) and splenomegaly. Ascites is caused by hampered
albumin production, the osmotic pressure decreases reducing the return of
fluid to the blood from the tissues. It results in a significant and pronounced
abdominal distention, compressing the abdomen and compromising breathing.
Development of Liver Alcoholic Cirrhosis
Normal liver
Columns of hepatocytes 1–2
cells thick radiate from the portal
tracts (PT) to the central veins. The
portal tract contains a normal intra
lobular bile duct branch of the
hepatic artery and portal venous
radical
Bridging fibrosis (stained pink, arrows)
spreading out around the hepatic vein and
single liver cells (pericellular), and linking
adjacent portal tracts and hepatic veins.
A cirrhotic liver
The liver architecture is
disrupted. The normal arrangement
of portal tracts and hepatic veins is
now lost and nodules of proliferating
hepatocytes are broken up by strands
of pink/orange-staining fibrous tissue
(arrows) forming cirrhotic nodules
(CN).
Normal liver
Columns of hepatocytes 1–2
cells thick radiate from the portal
tracts (PT) to the central veins. The
portal tract contains a normal intra
lobular bile duct branch of the
hepatic artery and portal venous
radical
Bridging fibrosis (stained pink, arrows)
spreading out around the hepatic vein and
single liver cells (pericellular), and linking
adjacent portal tracts and hepatic veins.
A cirrhotic liver
The liver architecture is
disrupted. The normal arrangement
of portal tracts and hepatic veins is
now lost and nodules of proliferating
hepatocytes are broken up by strands
of pink/orange-staining fibrous tissue
(arrows) forming cirrhotic nodules
(CN).
5.4. Signs and Symptoms of Cirrhosis
Many people with cirrhosis have no symptoms during the early phases of the
disease. Symptoms are caused by either of 2 problems:
Gradual failure of the liver to carry out its natural functions.
Distortion of the liver’s usual shape and size because of scarring.
The most common symptoms of cirrhosis are as follows:
Tiredness (Fatigue) or even exhaustion.
weakness
Nausea, Vomiting
Loss of Appetite leading to weight loss
Loss of sex drive
Signs and Symptoms may not appear until complications of cirrhosis set in.
Many people do not know they have cirrhosis until they have a complication:
Jaundice – Yellowing of the skin and eyes from deposition of bilirubin in
these tissues. Bilirubin is a product of the breakdown of old blood cells
in the liver.
Fever
Diarrhea
Itching – from deposition in the skin of products of the breakdown of
bile.
Abdominal pain and Ascitis – from enlargement of the liver or formation
of gallstones.
Weight gain – from fluid retention
Swelling in ankles and legs (Edema) – from fluid retention
Difficulty breathing – from fluid retention
Sensitivity to medications – due to impairment of the liver’s ability to
filter medications from blood.
Confusion, Delirium, Personality changes, or Hallucinations
(Encephalopathy) – from buildup of drugs or toxins in the blood, which
then affect the brain.
Extreme sleepiness, Difficulty awakening, or Coma – other symptoms of
Encephalopathy
Bleeding from Gums or Nose – Due to impaired production of the
Clotting Factors.
Many people with cirrhosis have no symptoms during the early phases of the
disease. Symptoms are caused by either of 2 problems:
Gradual failure of the liver to carry out its natural functions.
Distortion of the liver’s usual shape and size because of scarring.
The most common symptoms of cirrhosis are as follows:
Tiredness (Fatigue) or even exhaustion.
weakness
Nausea, Vomiting
Loss of Appetite leading to weight loss
Loss of sex drive
Signs and Symptoms may not appear until complications of cirrhosis set in.
Many people do not know they have cirrhosis until they have a complication:
Jaundice – Yellowing of the skin and eyes from deposition of bilirubin in
these tissues. Bilirubin is a product of the breakdown of old blood cells
in the liver.
Fever
Diarrhea
Itching – from deposition in the skin of products of the breakdown of
bile.
Abdominal pain and Ascitis – from enlargement of the liver or formation
of gallstones.
Weight gain – from fluid retention
Swelling in ankles and legs (Edema) – from fluid retention
Difficulty breathing – from fluid retention
Sensitivity to medications – due to impairment of the liver’s ability to
filter medications from blood.
Confusion, Delirium, Personality changes, or Hallucinations
(Encephalopathy) – from buildup of drugs or toxins in the blood, which
then affect the brain.
Extreme sleepiness, Difficulty awakening, or Coma – other symptoms of
Encephalopathy
Bleeding from Gums or Nose – Due to impaired production of the
Clotting Factors.
Easy bruising – due to impaired production of the Clotting Factors.
Blood Vomit or Feces – due to bleeding of varicose veins caused by
liver congestion.
Hemorrhoids – varicose veins in Rectum due to liver congestion.
Loss of Muscle Mass (wasting)
In women, abnormal menstrual periods – Due to impairment of
hormone production and metabolism.
In men, enlargement of the breasts (Gynecomastia), Scrotal swelling or
small testes – Due to impairment in hormone production and
metabolism.
`
Blood Vomit or Feces – due to bleeding of varicose veins caused by
liver congestion.
Hemorrhoids – varicose veins in Rectum due to liver congestion.
Loss of Muscle Mass (wasting)
In women, abnormal menstrual periods – Due to impairment of
hormone production and metabolism.
In men, enlargement of the breasts (Gynecomastia), Scrotal swelling or
small testes – Due to impairment in hormone production and
metabolism.
`
5.5. Diagnostic Tests (Investigations)
The single best test for diagnosing cirrhosis is biopsy of the liver. Liver
biopsies, however, carry a small risk for serious complications, and, therefore, biopsy
often is reserved for those patients in whom the diagnosis of the type of liver disease
or the presence of cirrhosis is not clear. The possibility of cirrhosis may be suggested
by the history, physical examination, or routine testing. If cirrhosis is present, other
tests can be used to determine the severity of the cirrhosis and the presence of
complications. Tests also may be used to diagnose the underlying disease that is
causing the cirrhosis. The following are how to diagnose and evaluate cirrhosis:
In taking a patient's history, the physician may uncover a history of excessive
and prolonged intake of alcohol, a history of intravenous drug abuse, or a
history of hepatitis. These pieces of information suggest the possibility of liver
disease and cirrhosis.
Patients who are known to have chronic viral hepatitis B or C have a higher
probability of having cirrhosis.
Some patients with cirrhosis have enlarged livers and/or spleens. A doctor can
often feel (palpate) the lower edge of an enlarged liver below the right rib cage
and feel the tip of the enlarged spleen below the left rib cage. A cirrhotic liver
also feels firmer and more irregular than a normal liver.
Jaundice (yellowness of the skin and of the whites of the eyes due to elevated
bilirubin in the blood) is common among patients with cirrhosis, but jaundice
can occur in patients with liver diseases without cirrhosis and other conditions
such as hemolysis (excessive break down of red blood cells).
Swelling of the abdomen (ascites) and/or the lower extremities (edema) due to
retention of fluid is common among patients with cirrhosis, although other
diseases can cause them commonly, for example, congestive heart failure.
Patients with abnormal copper deposits in their eyes or certain types of
neurologic disease may have Wilson's disease, a genetic disease in which there
is abnormal handling and accumulation of copper throughout the body,
including the liver, which can lead to cirrhosis.
Esophageal varices may be found unexpectedly during upper endoscopy
(EGD), strongly suggests cirrhosis.
Computerized tomography (CT or CAT) or magnetic resonance imaging (MRI)
scans and ultrasound examinations of the abdomen done for reasons other than
evaluating the possibility of liver disease may unexpectedly detect enlarged
The single best test for diagnosing cirrhosis is biopsy of the liver. Liver
biopsies, however, carry a small risk for serious complications, and, therefore, biopsy
often is reserved for those patients in whom the diagnosis of the type of liver disease
or the presence of cirrhosis is not clear. The possibility of cirrhosis may be suggested
by the history, physical examination, or routine testing. If cirrhosis is present, other
tests can be used to determine the severity of the cirrhosis and the presence of
complications. Tests also may be used to diagnose the underlying disease that is
causing the cirrhosis. The following are how to diagnose and evaluate cirrhosis:
In taking a patient's history, the physician may uncover a history of excessive
and prolonged intake of alcohol, a history of intravenous drug abuse, or a
history of hepatitis. These pieces of information suggest the possibility of liver
disease and cirrhosis.
Patients who are known to have chronic viral hepatitis B or C have a higher
probability of having cirrhosis.
Some patients with cirrhosis have enlarged livers and/or spleens. A doctor can
often feel (palpate) the lower edge of an enlarged liver below the right rib cage
and feel the tip of the enlarged spleen below the left rib cage. A cirrhotic liver
also feels firmer and more irregular than a normal liver.
Jaundice (yellowness of the skin and of the whites of the eyes due to elevated
bilirubin in the blood) is common among patients with cirrhosis, but jaundice
can occur in patients with liver diseases without cirrhosis and other conditions
such as hemolysis (excessive break down of red blood cells).
Swelling of the abdomen (ascites) and/or the lower extremities (edema) due to
retention of fluid is common among patients with cirrhosis, although other
diseases can cause them commonly, for example, congestive heart failure.
Patients with abnormal copper deposits in their eyes or certain types of
neurologic disease may have Wilson's disease, a genetic disease in which there
is abnormal handling and accumulation of copper throughout the body,
including the liver, which can lead to cirrhosis.
Esophageal varices may be found unexpectedly during upper endoscopy
(EGD), strongly suggests cirrhosis.
Computerized tomography (CT or CAT) or magnetic resonance imaging (MRI)
scans and ultrasound examinations of the abdomen done for reasons other than
evaluating the possibility of liver disease may unexpectedly detect enlarged
livers, abnormally nodular livers, enlarged spleens, and fluid in the abdomen,
which suggest cirrhosis.
Advanced cirrhosis leads to a reduced level of albumin in the blood and
reduced blood clotting factors due to the loss of the liver's ability to produce
these proteins. Thus, reduced levels of albumin in the blood or abnormal
bleeding suggest cirrhosis.
Abnormal elevation of liver enzymes in the blood (such as ALT and AST) that
are obtained routinely as part of yearly health examinations suggests
inflammation or injury to the liver from many causes as well as cirrhosis.
Patients with elevated levels of iron in their blood may have hemochromatosis,
a genetic disease of the liver in which iron is handled abnormally and which
leads to cirrhosis.
Auto-antibodies (antinuclear antibody, anti-smooth muscle antibody and anti-
mitochondrial antibody) sometimes are detected in the blood and may be a clue
to the presence of autoimmune hepatitis or primary biliary cirrhosis, both of
which can lead to cirrhosis.
Liver cancer (hepatocellular carcinoma) may be detected by CT and MRI
scans or ultrasound of the abdomen. Liver cancer most commonly develops in
individuals with underlying cirrhosis.
If there is an accumulation of fluid in the abdomen, a sample of the fluid can be
removed using a long needle. The fluid then can be examined and tested. The
results of testing may suggest the presence of cirrhosis as the cause of the fluid.
which suggest cirrhosis.
Advanced cirrhosis leads to a reduced level of albumin in the blood and
reduced blood clotting factors due to the loss of the liver's ability to produce
these proteins. Thus, reduced levels of albumin in the blood or abnormal
bleeding suggest cirrhosis.
Abnormal elevation of liver enzymes in the blood (such as ALT and AST) that
are obtained routinely as part of yearly health examinations suggests
inflammation or injury to the liver from many causes as well as cirrhosis.
Patients with elevated levels of iron in their blood may have hemochromatosis,
a genetic disease of the liver in which iron is handled abnormally and which
leads to cirrhosis.
Auto-antibodies (antinuclear antibody, anti-smooth muscle antibody and anti-
mitochondrial antibody) sometimes are detected in the blood and may be a clue
to the presence of autoimmune hepatitis or primary biliary cirrhosis, both of
which can lead to cirrhosis.
Liver cancer (hepatocellular carcinoma) may be detected by CT and MRI
scans or ultrasound of the abdomen. Liver cancer most commonly develops in
individuals with underlying cirrhosis.
If there is an accumulation of fluid in the abdomen, a sample of the fluid can be
removed using a long needle. The fluid then can be examined and tested. The
results of testing may suggest the presence of cirrhosis as the cause of the fluid.
5.6. Management
Treatment of cirrhosis includes
1). Preventing further damage to the liver.
2) .Treating the complications of cirrhosis.
3). Preventing liver cancer or detecting it early.
4). Liver transplantation.
1. Preventing further damage to the liver
Consume a balanced diet and one multivitamin daily. Patients with PBC
(Primary Biliary Cirrhosis) with impaired absorption of fat soluble vitamins
may need additional vitamins D and K.
Avoid drugs (including alcohol) that cause liver damage. All patients with
cirrhosis should avoid alcohol. Most patients with alcohol induced cirrhosis
experience an improvement in liver function with abstinence from alcohol.
Even patients with chronic hepatitis B and C can substantially reduce liver
damage and slow the progression towards cirrhosis with abstinence from
alcohol.
Avoid no steroidal anti-inflammatory drugs (NSAIDs, for example, ibuprofen).
Patients with cirrhosis can experience worsening of liver and kidney function
with NSAIDs.
Eradicate hepatitis B and hepatitis C virus by using anti-viral medications. Not
all patients with cirrhosis due to chronic viral hepatitis are candidates for drug
treatment. Some patients may experience serious deterioration in liver function
and/or intolerable side effects during treatment.
Suppress the immune system with drugs such as prednisone and azathioprine
(Imuran) to decrease inflammation of the liver in autoimmune hepatitis.
Immunize patients with cirrhosis against infection with hepatitis A and B to
prevent a serious deterioration in liver function. There are currently no
vaccines available for immunizing against hepatitis C.
Treatment of cirrhosis includes
1). Preventing further damage to the liver.
2) .Treating the complications of cirrhosis.
3). Preventing liver cancer or detecting it early.
4). Liver transplantation.
1. Preventing further damage to the liver
Consume a balanced diet and one multivitamin daily. Patients with PBC
(Primary Biliary Cirrhosis) with impaired absorption of fat soluble vitamins
may need additional vitamins D and K.
Avoid drugs (including alcohol) that cause liver damage. All patients with
cirrhosis should avoid alcohol. Most patients with alcohol induced cirrhosis
experience an improvement in liver function with abstinence from alcohol.
Even patients with chronic hepatitis B and C can substantially reduce liver
damage and slow the progression towards cirrhosis with abstinence from
alcohol.
Avoid no steroidal anti-inflammatory drugs (NSAIDs, for example, ibuprofen).
Patients with cirrhosis can experience worsening of liver and kidney function
with NSAIDs.
Eradicate hepatitis B and hepatitis C virus by using anti-viral medications. Not
all patients with cirrhosis due to chronic viral hepatitis are candidates for drug
treatment. Some patients may experience serious deterioration in liver function
and/or intolerable side effects during treatment.
Suppress the immune system with drugs such as prednisone and azathioprine
(Imuran) to decrease inflammation of the liver in autoimmune hepatitis.
Immunize patients with cirrhosis against infection with hepatitis A and B to
prevent a serious deterioration in liver function. There are currently no
vaccines available for immunizing against hepatitis C.
2. Treating complications of Cirrhosis
Edema and ascites.
Retention of salt and water can lead to swelling of the ankles and legs
(edema) or abdomen (ascites) in patients with cirrhosis. Doctors often
advise patients with cirrhosis to restrict dietary salt (sodium) and fluid
to decrease edema and ascites. The amount of salt in the diet usually is
restricted to 2 grams per day and fluid to 1.2 liters per day. In most
patients with cirrhosis, however, salt and fluid restriction is not enough,
and diuretics have to be added.
Diuretics are medications that work in the kidneys to promote the
elimination of salt and water into the urine. A combination of the
diuretics spironolactone (Aldactone) and furosemide (Lasix) can reduce
or eliminate the edema and ascites in most patients. During treatment
with diuretics, it is important to monitor the function of the kidneys by
measuring blood levels of blood urea nitrogen (BUN) and creatinine to
determine if too much diuretic is being used. Too much diuretic can lead
to kidney dysfunction that is reflected in elevations of the BUN and
creatinine levels in the blood.
Sometimes, when the diuretics do not work (in which case the ascites is
said to be refractory), a long needle or catheter is used to draw out the
ascitic fluid directly from the abdomen, a procedure called abdominal
paracentesis. It is common to withdraw large amounts (liters) of fluid
from the abdomen when the ascites is causing painful abdominal
distension and/or difficulty breathing because it limits the movement of
the diaphragms.
Another treatment for refractory ascites is a procedure called
transjugular intravenous portosystemic shunting (TIPS, see below).
Bleeding from varices.
If large varices develop in the esophagus or upper stomach, patients
with cirrhosis are at risk for serious bleeding due to rupture of these varices.
Once varices have bleed, they tend to rebleed and the probability that a patient
will die from each bleeding episode is high . Therefore, treatment is necessary
to prevent the first (initial) bleeding episode as well as rebleeding.
Treatments include medications and procedures to decrease the
pressure in the portal vein, and procedures to destroy the varices.
Edema and ascites.
Retention of salt and water can lead to swelling of the ankles and legs
(edema) or abdomen (ascites) in patients with cirrhosis. Doctors often
advise patients with cirrhosis to restrict dietary salt (sodium) and fluid
to decrease edema and ascites. The amount of salt in the diet usually is
restricted to 2 grams per day and fluid to 1.2 liters per day. In most
patients with cirrhosis, however, salt and fluid restriction is not enough,
and diuretics have to be added.
Diuretics are medications that work in the kidneys to promote the
elimination of salt and water into the urine. A combination of the
diuretics spironolactone (Aldactone) and furosemide (Lasix) can reduce
or eliminate the edema and ascites in most patients. During treatment
with diuretics, it is important to monitor the function of the kidneys by
measuring blood levels of blood urea nitrogen (BUN) and creatinine to
determine if too much diuretic is being used. Too much diuretic can lead
to kidney dysfunction that is reflected in elevations of the BUN and
creatinine levels in the blood.
Sometimes, when the diuretics do not work (in which case the ascites is
said to be refractory), a long needle or catheter is used to draw out the
ascitic fluid directly from the abdomen, a procedure called abdominal
paracentesis. It is common to withdraw large amounts (liters) of fluid
from the abdomen when the ascites is causing painful abdominal
distension and/or difficulty breathing because it limits the movement of
the diaphragms.
Another treatment for refractory ascites is a procedure called
transjugular intravenous portosystemic shunting (TIPS, see below).
Bleeding from varices.
If large varices develop in the esophagus or upper stomach, patients
with cirrhosis are at risk for serious bleeding due to rupture of these varices.
Once varices have bleed, they tend to rebleed and the probability that a patient
will die from each bleeding episode is high . Therefore, treatment is necessary
to prevent the first (initial) bleeding episode as well as rebleeding.
Treatments include medications and procedures to decrease the
pressure in the portal vein, and procedures to destroy the varices.
Propranolol (Inderal)
A beta blocker is effective in lowering pressure in the portal vein
and is used to prevent initial bleeding and rebleeding from varices in
patients with cirrhosis.
Octreotide (Sandostatin)
Also decreases portal vein pressure and has been used to treat
variceal bleeding.
During upper endoscopy (EGD)
Sclerotherapy or band ligation can be performed to obliterate
varices and stop active bleeding and prevent rebleeding.
Transjugular intrahepatic portosystemic shunt (TIPS)
Is a non-surgical, radiolotic procedure to decrease the pressure
in the portal vein. TIPS are performed by a radiologist who inserts a
stent (tube) through a neck vein, down the inferior vena cava and into
the hepatic vein within the liver. The stent then is placed so that one end
is in the high pressure portal vein and the other end is in the low
pressure hepatic vein. This tube shunts blood around the liver and by so
doing lowers the pressure in the portal vein and varices and prevents
bleeding from the varices.
A surgical operation to create a shunt (passage)
From the high-pressure portal vein to veins with lower pressure
can lower blood flow and pressure in the portal vein and prevent varices
from bleeding.
Hepatic encephalopathy.
Patients with an abnormal sleep cycle, impaired thinking, odd behavior,
or other signs of hepatic encephalopathy usually should be treated with a low
protein diet and oral lactulose. Dietary protein is restricted because it is a
source of toxic compounds that cause hepatic encephalopathy. Lactulose,
which is a liquid, traps toxic compounds in the colon so they cannot be
absorbed into the blood stream, and causes encephalopathy. (Lactulose is a
laxative and the adequacy of treatment can be judged by loosening or
increasing frequency of stools).
A beta blocker is effective in lowering pressure in the portal vein
and is used to prevent initial bleeding and rebleeding from varices in
patients with cirrhosis.
Octreotide (Sandostatin)
Also decreases portal vein pressure and has been used to treat
variceal bleeding.
During upper endoscopy (EGD)
Sclerotherapy or band ligation can be performed to obliterate
varices and stop active bleeding and prevent rebleeding.
Transjugular intrahepatic portosystemic shunt (TIPS)
Is a non-surgical, radiolotic procedure to decrease the pressure
in the portal vein. TIPS are performed by a radiologist who inserts a
stent (tube) through a neck vein, down the inferior vena cava and into
the hepatic vein within the liver. The stent then is placed so that one end
is in the high pressure portal vein and the other end is in the low
pressure hepatic vein. This tube shunts blood around the liver and by so
doing lowers the pressure in the portal vein and varices and prevents
bleeding from the varices.
A surgical operation to create a shunt (passage)
From the high-pressure portal vein to veins with lower pressure
can lower blood flow and pressure in the portal vein and prevent varices
from bleeding.
Hepatic encephalopathy.
Patients with an abnormal sleep cycle, impaired thinking, odd behavior,
or other signs of hepatic encephalopathy usually should be treated with a low
protein diet and oral lactulose. Dietary protein is restricted because it is a
source of toxic compounds that cause hepatic encephalopathy. Lactulose,
which is a liquid, traps toxic compounds in the colon so they cannot be
absorbed into the blood stream, and causes encephalopathy. (Lactulose is a
laxative and the adequacy of treatment can be judged by loosening or
increasing frequency of stools).
Hypersplenism.
The filtration of blood by an enlarged spleen usually results in only mild
reductions of red blood cells (anemia), white blood cells (leukopenia) and
platelets (thrombocytopenia) that do not require treatment. Severe anemia,
however, may require blood transfusions or treatment with erythropoietin
hormone that stimulate the production of red blood cells.
No approved medication is available yet to increase the number of
platelets. As a necessary precaution, patients with low platelets should not use
aspirin or other no steroidal anti-inflammatory drugs (NSAIDS) since these
drugs can hinder the function of platelets. If a low number of platelets are
associated with significant bleeding, transfusions of platelets usually should be
given. Surgical removal of the spleen (splenectomy) should be avoided, if
possible, due to the risk of excessive bleeding during the operation.
Spontaneous bacterial peritonitis (SBP).
Patients suspected of having spontaneous bacterial peritonitis usually
will undergo paracentesis. Fluid that is removed is examined for white blood
cells and cultured for bacteria. Blood and urine samples also are often
obtained for culturing because many patients with spontaneous bacterial
peritonitis also will have infection in their blood and urine. In the infection may
have begun in the blood and the urine and spread to the ascitic fluid to cause
spontaneous bacterial peritonitis. Most patients with spontaneous bacterial
peritonitis are hospitalized and treated with intravenous antibiotics such as
cefotaxime.
In some patients oral antibiotics can be prescribed to prevent
spontaneous bacterial peritonitis. Not all patients with cirrhosis and ascites
should be treated with antibiotics to prevent spontaneous bacterial peritonitis,
but some patients are at high risk for developing spontaneous bacterial
peritonitis and warrant preventive treatment.
Patients with cirrhosis who are hospitalized for bleeding varices have a
high risk of developing spontaneous bacterial peritonitis and should be
started on antibiotics early during the hospitalization to prevent
spontaneous bacterial peritonitis.
Patients with recurring episodes of spontaneous bacterial peritonitis.
Patients with low protein levels in the ascitic fluid (Ascitic fluid with low
levels of protein is more likely to become infected.)
The filtration of blood by an enlarged spleen usually results in only mild
reductions of red blood cells (anemia), white blood cells (leukopenia) and
platelets (thrombocytopenia) that do not require treatment. Severe anemia,
however, may require blood transfusions or treatment with erythropoietin
hormone that stimulate the production of red blood cells.
No approved medication is available yet to increase the number of
platelets. As a necessary precaution, patients with low platelets should not use
aspirin or other no steroidal anti-inflammatory drugs (NSAIDS) since these
drugs can hinder the function of platelets. If a low number of platelets are
associated with significant bleeding, transfusions of platelets usually should be
given. Surgical removal of the spleen (splenectomy) should be avoided, if
possible, due to the risk of excessive bleeding during the operation.
Spontaneous bacterial peritonitis (SBP).
Patients suspected of having spontaneous bacterial peritonitis usually
will undergo paracentesis. Fluid that is removed is examined for white blood
cells and cultured for bacteria. Blood and urine samples also are often
obtained for culturing because many patients with spontaneous bacterial
peritonitis also will have infection in their blood and urine. In the infection may
have begun in the blood and the urine and spread to the ascitic fluid to cause
spontaneous bacterial peritonitis. Most patients with spontaneous bacterial
peritonitis are hospitalized and treated with intravenous antibiotics such as
cefotaxime.
In some patients oral antibiotics can be prescribed to prevent
spontaneous bacterial peritonitis. Not all patients with cirrhosis and ascites
should be treated with antibiotics to prevent spontaneous bacterial peritonitis,
but some patients are at high risk for developing spontaneous bacterial
peritonitis and warrant preventive treatment.
Patients with cirrhosis who are hospitalized for bleeding varices have a
high risk of developing spontaneous bacterial peritonitis and should be
started on antibiotics early during the hospitalization to prevent
spontaneous bacterial peritonitis.
Patients with recurring episodes of spontaneous bacterial peritonitis.
Patients with low protein levels in the ascitic fluid (Ascitic fluid with low
levels of protein is more likely to become infected.)
3. Prevention and early detection of liver cancer
Several types of liver disease that cause cirrhosis (such as hepatitis B
and C) are associated with a particularly high incidence of liver cancer. It
would be useful to screen for liver cancer in patients with cirrhosis, as early
surgical treatment or transplantation of the liver can cure the patient of
cancer. The difficulty is that the methods available for screening are only
partially effective, identifying at best only 50% of patients at a curable stage of
their cancer.
4. Liver transplantation
Cirrhosis is irreversible. Many patients' liver function will gradually
worsen despite treatment and complications of cirrhosis will increase and
become difficult to treat. Therefore, when cirrhosis is far advanced, liver
transplantation often is the only option for treatment. Recent advances in
surgical transplantation and medications to prevent infection and rejection of
the transplanted liver have greatly improved survival after transplantation.
Several types of liver disease that cause cirrhosis (such as hepatitis B
and C) are associated with a particularly high incidence of liver cancer. It
would be useful to screen for liver cancer in patients with cirrhosis, as early
surgical treatment or transplantation of the liver can cure the patient of
cancer. The difficulty is that the methods available for screening are only
partially effective, identifying at best only 50% of patients at a curable stage of
their cancer.
4. Liver transplantation
Cirrhosis is irreversible. Many patients' liver function will gradually
worsen despite treatment and complications of cirrhosis will increase and
become difficult to treat. Therefore, when cirrhosis is far advanced, liver
transplantation often is the only option for treatment. Recent advances in
surgical transplantation and medications to prevent infection and rejection of
the transplanted liver have greatly improved survival after transplantation.
5.7. Complications of Cirrhosis
The complications of cirrhosis are Edema and ascitis,
spontaneous bacterial peritonitis, Bleeding from esophageal vertices, Hepatic
encephalopathy, Hepatorenal syndrome, hepatopulmonary syndrome, Hypersplenism,
and Liver cancer
1. Edema and ascites
As cirrhosis of the liver becomes severe, signals are sent to the kidneys to retain salt
and water in the body. The excess salt and water first accumulates in the tissue
beneath the skin of the ankles and legs because of the effect of gravity when standing
or sitting. This accumulation of fluid is called edema or pitting edema. As cirrhosis
worsens and more salt and water are retained, fluid also may accumulate in the
abdominal cavity between the abdominal wall and the abdominal organs. This
accumulation of fluid (called ascites) causes swelling of the abdomen, abdominal
discomfort, and increased weight.
2. Spontaneous bacterial peritonitis (SBP)
Fluid in the abdominal cavity (ascites) is the perfect place for bacteria to grow.
Normally, the abdominal cavity contains a very small amount of fluid that is able to
resist infection well, and bacteria that enter the abdomen (usually from the intestine)
are killed or find their way into the portal vein and to the liver where they are killed.
In cirrhosis, the fluid that collects in the abdomen is unable to resist infection
normally. In addition, more bacteria find their way from the intestine into the ascites.
Therefore, infection within the abdomen and the ascites, referred to as spontaneous
bacterial peritonitis or SBP, is likely to occur. SBP is a life- threatening complication.
Some patients with SBP have no symptoms, while others have fever, chills, abdominal
pain and tenderness, diarrhea, and worsening ascites.
3. Bleeding from esophageal varices
In the cirrhotic liver, the scar tissue blocks the flow of blood returning to the heart
from the intestines and raises the pressure in the portal vein (portal hypertension).
When pressure in the portal vein becomes high enough, it causes blood to flow around
the liver through veins with lower pressure to reach the heart. The most common veins
through which blood bypasses the liver are the veins lining the lower part of the
esophagus and the upper part of the stomach.
As a result of the increased flow of blood and the resulting increase in pressure, the
veins in the lower esophagus and upper stomach expand and then are referred to as
esophageal and gastric varices.
The complications of cirrhosis are Edema and ascitis,
spontaneous bacterial peritonitis, Bleeding from esophageal vertices, Hepatic
encephalopathy, Hepatorenal syndrome, hepatopulmonary syndrome, Hypersplenism,
and Liver cancer
1. Edema and ascites
As cirrhosis of the liver becomes severe, signals are sent to the kidneys to retain salt
and water in the body. The excess salt and water first accumulates in the tissue
beneath the skin of the ankles and legs because of the effect of gravity when standing
or sitting. This accumulation of fluid is called edema or pitting edema. As cirrhosis
worsens and more salt and water are retained, fluid also may accumulate in the
abdominal cavity between the abdominal wall and the abdominal organs. This
accumulation of fluid (called ascites) causes swelling of the abdomen, abdominal
discomfort, and increased weight.
2. Spontaneous bacterial peritonitis (SBP)
Fluid in the abdominal cavity (ascites) is the perfect place for bacteria to grow.
Normally, the abdominal cavity contains a very small amount of fluid that is able to
resist infection well, and bacteria that enter the abdomen (usually from the intestine)
are killed or find their way into the portal vein and to the liver where they are killed.
In cirrhosis, the fluid that collects in the abdomen is unable to resist infection
normally. In addition, more bacteria find their way from the intestine into the ascites.
Therefore, infection within the abdomen and the ascites, referred to as spontaneous
bacterial peritonitis or SBP, is likely to occur. SBP is a life- threatening complication.
Some patients with SBP have no symptoms, while others have fever, chills, abdominal
pain and tenderness, diarrhea, and worsening ascites.
3. Bleeding from esophageal varices
In the cirrhotic liver, the scar tissue blocks the flow of blood returning to the heart
from the intestines and raises the pressure in the portal vein (portal hypertension).
When pressure in the portal vein becomes high enough, it causes blood to flow around
the liver through veins with lower pressure to reach the heart. The most common veins
through which blood bypasses the liver are the veins lining the lower part of the
esophagus and the upper part of the stomach.
As a result of the increased flow of blood and the resulting increase in pressure, the
veins in the lower esophagus and upper stomach expand and then are referred to as
esophageal and gastric varices.
4. Hepatic encephalopathy
Some of the protein in food that escapes digestion and absorption is used by bacteria
that are normally present in the intestine. While using the protein for their own
purposes, the bacteria make substances that they release into the intestine. These
substances then can be absorbed into the body. Some of these substances, for example,
ammonia, can have toxic effects on the brain. Ordinarily, these toxic substances are
carried from the intestine in the portal vein to the liver where they are removed from
the blood and detoxified.
When the toxic substances accumulate sufficiently in the blood, the function of the
brain is impaired, a condition called hepatic encephalopathy. Sleeping during the day
rather than at night (reversal of the normal sleep pattern) is among the earliest
symptoms of hepatic encephalopathy. Other symptoms include irritability, inability to
concentrate or perform calculations, loss of memory, confusion, or depressed levels of
consciousness. Ultimately, severe hepatic encephalopathy causes coma and death.
5. Hepatorenal syndrome
Patients with worsening cirrhosis can develop hepatorenal syndrome. This syndrome
is a serious complication in which the function of the kidneys is reduced. It is a
functional problem in the kidneys, meaning there is no physical damage to the
kidneys. Instead, the reduced function is due to changes in the way the blood flows
through the kidneys themselves. The hepatorenal syndrome is defined as progressive
failure of the kidneys to clear substances from the blood and produce adequate
amounts of urine while other important functions of the kidney, such as retention of
salt, are maintained.
6. Hepatopulmonary syndrome
Rarely, some patients with advanced cirrhosis can develop hepatopulmonary
syndrome. These patients can experience difficulty breathing because certain
hormones released in advanced cirrhosis cause the lungs to function abnormally.
7. Hypersplenism
The spleen normally acts as a filter to remove older red blood cells, white blood cells,
and platelets (small particles that are important for the clotting of blood.). The blood
that drains from the spleen joins the blood in the portal vein from the intestines. As the
pressure in the portal vein rises in cirrhosis, it increasingly blocks the flow of blood
from the spleen. The blood "backs-up," accumulating in the spleen, and the spleen
swells in size, a condition referred to as splenomegaly. Sometimes, the spleen is so
enlarged that it causes abdominal pain.
Some of the protein in food that escapes digestion and absorption is used by bacteria
that are normally present in the intestine. While using the protein for their own
purposes, the bacteria make substances that they release into the intestine. These
substances then can be absorbed into the body. Some of these substances, for example,
ammonia, can have toxic effects on the brain. Ordinarily, these toxic substances are
carried from the intestine in the portal vein to the liver where they are removed from
the blood and detoxified.
When the toxic substances accumulate sufficiently in the blood, the function of the
brain is impaired, a condition called hepatic encephalopathy. Sleeping during the day
rather than at night (reversal of the normal sleep pattern) is among the earliest
symptoms of hepatic encephalopathy. Other symptoms include irritability, inability to
concentrate or perform calculations, loss of memory, confusion, or depressed levels of
consciousness. Ultimately, severe hepatic encephalopathy causes coma and death.
5. Hepatorenal syndrome
Patients with worsening cirrhosis can develop hepatorenal syndrome. This syndrome
is a serious complication in which the function of the kidneys is reduced. It is a
functional problem in the kidneys, meaning there is no physical damage to the
kidneys. Instead, the reduced function is due to changes in the way the blood flows
through the kidneys themselves. The hepatorenal syndrome is defined as progressive
failure of the kidneys to clear substances from the blood and produce adequate
amounts of urine while other important functions of the kidney, such as retention of
salt, are maintained.
6. Hepatopulmonary syndrome
Rarely, some patients with advanced cirrhosis can develop hepatopulmonary
syndrome. These patients can experience difficulty breathing because certain
hormones released in advanced cirrhosis cause the lungs to function abnormally.
7. Hypersplenism
The spleen normally acts as a filter to remove older red blood cells, white blood cells,
and platelets (small particles that are important for the clotting of blood.). The blood
that drains from the spleen joins the blood in the portal vein from the intestines. As the
pressure in the portal vein rises in cirrhosis, it increasingly blocks the flow of blood
from the spleen. The blood "backs-up," accumulating in the spleen, and the spleen
swells in size, a condition referred to as splenomegaly. Sometimes, the spleen is so
enlarged that it causes abdominal pain.
8. Liver cancer (hepatocellular carcinoma)
Cirrhosis due to any cause increases the risk of primary liver cancer (hepatocellular
carcinoma). Primary refers to the fact that the tumor originates in the liver. A
secondary liver cancer is one that originates elsewhere in the body and spreads
(metastasizes) to the liver.
The most common symptoms and signs of primary liver cancer are abdominal pain
and swelling, an enlarged liver, weight loss, and fever. In addition, liver cancers can
produce and release a number of substances, including ones that cause an increased
in red blood cell count (erythrocytosis), low blood sugar (hypoglycemia), and high
blood calcium (hypercalcemia ).
Cirrhosis due to any cause increases the risk of primary liver cancer (hepatocellular
carcinoma). Primary refers to the fact that the tumor originates in the liver. A
secondary liver cancer is one that originates elsewhere in the body and spreads
(metastasizes) to the liver.
The most common symptoms and signs of primary liver cancer are abdominal pain
and swelling, an enlarged liver, weight loss, and fever. In addition, liver cancers can
produce and release a number of substances, including ones that cause an increased
in red blood cell count (erythrocytosis), low blood sugar (hypoglycemia), and high
blood calcium (hypercalcemia ).
5.8. Prognosis of Cirrhosis
The overall prognosis in cirrhosis is poor. Many patients present with
advanced disease and/or serious complications that carry a high mortality.
Overall, only 25% of patients survive 5 years from diagnosis but, where liver
function is good, 50% survive for 5 years and 25% for up to 10 years.
The prognosis is more favorable when the underlying cause of the cirrhosis
can be corrected, as in alcohol misuse, haemochromatosis and Wilson’s
disease.
Laboratory tests give only a rough guide to prognosis in individual patients.
Deteriorating liver function,as evidenced by jaundice, ascites or
encephalopathy, indicates a poor prognosis unless a treatable cause such as
infection is found.
Increasing bilirubin, falling albumin, marked hyponatraemia not due to
diuretic therapy, and a prolonged prothrombin time are all bad prognostic
features.
The overall prognosis in cirrhosis is poor. Many patients present with
advanced disease and/or serious complications that carry a high mortality.
Overall, only 25% of patients survive 5 years from diagnosis but, where liver
function is good, 50% survive for 5 years and 25% for up to 10 years.
The prognosis is more favorable when the underlying cause of the cirrhosis
can be corrected, as in alcohol misuse, haemochromatosis and Wilson’s
disease.
Laboratory tests give only a rough guide to prognosis in individual patients.
Deteriorating liver function,as evidenced by jaundice, ascites or
encephalopathy, indicates a poor prognosis unless a treatable cause such as
infection is found.
Increasing bilirubin, falling albumin, marked hyponatraemia not due to
diuretic therapy, and a prolonged prothrombin time are all bad prognostic
features.
Section 6
Nursing Care of Patient with
Cirrhosis
Nursing Care of Patient with
Cirrhosis
7. Nursing Care of Patient with Cirrhosis
Nursing Priorities:-
1. Maintain adequate nutrition.
2. Prevent complications.
3. Enhance self-concept and acceptance of situation.
4. Provide information about disease process, prognosis, potential
complications, and treatment needs.
Discharge Goals:-
1. Nutritional intake adequate for individual needs.
2. Complications prevented or minimized.
3. Deals effectively with current reality.
4. Disease process, prognosis, potential complications, and
therapeutic regimen understood.
5. Plan in place to meet needs after discharge.
Nursing Priorities:-
1. Maintain adequate nutrition.
2. Prevent complications.
3. Enhance self-concept and acceptance of situation.
4. Provide information about disease process, prognosis, potential
complications, and treatment needs.
Discharge Goals:-
1. Nutritional intake adequate for individual needs.
2. Complications prevented or minimized.
3. Deals effectively with current reality.
4. Disease process, prognosis, potential complications, and
therapeutic regimen understood.
5. Plan in place to meet needs after discharge.
7.1. Nursing Assessment
Monitor for signs and symptoms.
Fatigue
Weight loss, abdominal pain, and distention
Pruritus (severe itching of skin)
Confusion or difficulty thinking (due to the build-up of waste
products in the blood and brain that the liver is unable to get rid of).
Gastrointestinal bleeding (enlarged veins [varices] develop and
burst, causing vomiting and passing of blood in bowel movements)
Ascites (bloating or swelling due to fluid build-up in abdomen and
legs)
Jaundice (yellowing of skin) and icterus (yellowing of the eyes)
Petechiae (round, pinpoint, and red-purple lesions), ecchymosis
(large yellow and purple blue bruises), nose bleeds, hematemesis,
melena (decreased synthesis of prothrombin and deteriorating
hepatic function)
Palmar erythema (redness and warmth of the palms of the hands)
Spider angiomas (red lesions vascular in nature with branches
radiating onthe nose, cheeks, upper thorax, and shoulders)
Dependent peripheral edema of extremities and sacrum
Personality and mentation changes, emotional lability, euphoria,
and sometimes depression.
Asterixis (liver flapping tremor) is a coarse tremor characterized by
rapid,nonrhythmic extension and flexion of the wrists and fingers
Fetor hepaticus (liver breath) is a fruity or musty odor.
Monitor for signs and symptoms.
Fatigue
Weight loss, abdominal pain, and distention
Pruritus (severe itching of skin)
Confusion or difficulty thinking (due to the build-up of waste
products in the blood and brain that the liver is unable to get rid of).
Gastrointestinal bleeding (enlarged veins [varices] develop and
burst, causing vomiting and passing of blood in bowel movements)
Ascites (bloating or swelling due to fluid build-up in abdomen and
legs)
Jaundice (yellowing of skin) and icterus (yellowing of the eyes)
Petechiae (round, pinpoint, and red-purple lesions), ecchymosis
(large yellow and purple blue bruises), nose bleeds, hematemesis,
melena (decreased synthesis of prothrombin and deteriorating
hepatic function)
Palmar erythema (redness and warmth of the palms of the hands)
Spider angiomas (red lesions vascular in nature with branches
radiating onthe nose, cheeks, upper thorax, and shoulders)
Dependent peripheral edema of extremities and sacrum
Personality and mentation changes, emotional lability, euphoria,
and sometimes depression.
Asterixis (liver flapping tremor) is a coarse tremor characterized by
rapid,nonrhythmic extension and flexion of the wrists and fingers
Fetor hepaticus (liver breath) is a fruity or musty odor.
Assess/Monitor
ACTIVITY/REST
Weakness
Fatigue, exhaustion
CIRCULATION
History of or recent onset of heart failure (HF), pericarditis, rheumatic heart
disease, or cancer, causing liver impairment leading to failure
Easy bruising, nosebleeds, bleeding gums
ELIMINATION
Flatulence
Diarrhea or constipation
Gradual abdominal enlargement
FOOD/FLUID
Anorexia
Food intolerance, ingestion
Nausea, vomiting
Hematemesis
NEUROSENSORY
Significant other (SO)/family may report personality changes, depressed
mentation
PAIN/DISCOMFORT
Abdominal tenderness and right upper quandrant (RUQ) pain
Severe itching
Pins-and-needles sensation, burning pain in extremities (peripheral
neuropathy)
RESPIRATION
Dyspnea
SAFETY
Itching, dryness of the skin (pruritus)
SEXUALITY
Menstrual disorders (women)
Impotence (men)
TEACHING/LEARNING
ACTIVITY/REST
Weakness
Fatigue, exhaustion
CIRCULATION
History of or recent onset of heart failure (HF), pericarditis, rheumatic heart
disease, or cancer, causing liver impairment leading to failure
Easy bruising, nosebleeds, bleeding gums
ELIMINATION
Flatulence
Diarrhea or constipation
Gradual abdominal enlargement
FOOD/FLUID
Anorexia
Food intolerance, ingestion
Nausea, vomiting
Hematemesis
NEUROSENSORY
Significant other (SO)/family may report personality changes, depressed
mentation
PAIN/DISCOMFORT
Abdominal tenderness and right upper quandrant (RUQ) pain
Severe itching
Pins-and-needles sensation, burning pain in extremities (peripheral
neuropathy)
RESPIRATION
Dyspnea
SAFETY
Itching, dryness of the skin (pruritus)
SEXUALITY
Menstrual disorders (women)
Impotence (men)
TEACHING/LEARNING
History of long-term alcohol or injection drug use or abuse, alcoholic liver
disease, use of drugs affecting liver function
History of biliary system disease, hepatitis, exposure to toxins, liver trauma
DISCHARGE PLAN CONSIDERATIONS
May need assistance with self-care and other activities of daily living (ADLs),
homemaking and maintenance tasks
7.2. Nursing Diagnosis
1. Imbalanced Nutrition: Less than Body Requirements
May be related to:
Inadequate diet; inability to process, digest nutrients
Anorexia, nausea, vomiting, indigestion, early satiety (ascites)
Abnormal bowel function
Possibly evidenced by:
Weight loss, Changes in bowel sounds and functions,
Poor muscle tone, muscle wasting; fatigue
Imbalances in nutritional studies
2. Excess Fluid Volume
May be related to:
Compromised regulatory mechanism—syndrome of inappropriate anti
diuretic hormone (SIADH), decreased plasma proteins, malnutrition,
Excess sodium and fluid intake
Possibly evidenced by:
Edema, anasarca, weight gain
Intake greater than output, oliguria, changes in urine specific gravity
Dyspnea, adventitious breath sounds, pleural effusion
Blood pressure (BP) changes, altered central venous pressure (CVP)
JVD, positive hepatojugular reflex
Altered electrolyte levels
Change in mental status
3. Risk for impaired Skin Integrity
disease, use of drugs affecting liver function
History of biliary system disease, hepatitis, exposure to toxins, liver trauma
DISCHARGE PLAN CONSIDERATIONS
May need assistance with self-care and other activities of daily living (ADLs),
homemaking and maintenance tasks
7.2. Nursing Diagnosis
1. Imbalanced Nutrition: Less than Body Requirements
May be related to:
Inadequate diet; inability to process, digest nutrients
Anorexia, nausea, vomiting, indigestion, early satiety (ascites)
Abnormal bowel function
Possibly evidenced by:
Weight loss, Changes in bowel sounds and functions,
Poor muscle tone, muscle wasting; fatigue
Imbalances in nutritional studies
2. Excess Fluid Volume
May be related to:
Compromised regulatory mechanism—syndrome of inappropriate anti
diuretic hormone (SIADH), decreased plasma proteins, malnutrition,
Excess sodium and fluid intake
Possibly evidenced by:
Edema, anasarca, weight gain
Intake greater than output, oliguria, changes in urine specific gravity
Dyspnea, adventitious breath sounds, pleural effusion
Blood pressure (BP) changes, altered central venous pressure (CVP)
JVD, positive hepatojugular reflex
Altered electrolyte levels
Change in mental status
3. Risk for impaired Skin Integrity
Risk factors may include:
Altered circulation and metabolic state
Accumulation of bile salts in skin
Poor skin turgor, skeletal prominence, presence of edema, ascites
4. Risk for ineffective Breathing Pattern
Risk factors may include:
Intra-abdominal fluid collection (ascites)
Decreased lung expansion, accumulated secretions
Decreased energy, fatigue
5. Risk for Bleeding
Risk factors may include:
Abnormal blood profile; altered clotting factors—decreased production
of prothrombin, fibrinogen, and factors VIII, IX, and impaired vitamin K
absorption; and release of thromboplastin, Portal hypertension,
development of esophageal varices
6. Risk for acute Confusion
Risk factors may include:
Alcohol abuse
Inability of liver to detoxify certain enzymes and drugs
7. Self-Esteem [specify]/disturbed Body Image
May be related to:
Biophysical changes, altered physical appearance
Uncertainty of prognosis, changes in role function
Personal vulnerability
Self-destructive behavior—alcohol-induced disease
Possibly evidenced by:
Verbalization of change or restriction in lifestyle
Altered circulation and metabolic state
Accumulation of bile salts in skin
Poor skin turgor, skeletal prominence, presence of edema, ascites
4. Risk for ineffective Breathing Pattern
Risk factors may include:
Intra-abdominal fluid collection (ascites)
Decreased lung expansion, accumulated secretions
Decreased energy, fatigue
5. Risk for Bleeding
Risk factors may include:
Abnormal blood profile; altered clotting factors—decreased production
of prothrombin, fibrinogen, and factors VIII, IX, and impaired vitamin K
absorption; and release of thromboplastin, Portal hypertension,
development of esophageal varices
6. Risk for acute Confusion
Risk factors may include:
Alcohol abuse
Inability of liver to detoxify certain enzymes and drugs
7. Self-Esteem [specify]/disturbed Body Image
May be related to:
Biophysical changes, altered physical appearance
Uncertainty of prognosis, changes in role function
Personal vulnerability
Self-destructive behavior—alcohol-induced disease
Possibly evidenced by:
Verbalization of change or restriction in lifestyle
Fear of rejection or reaction by others
Negative feelings about body and abilities
Feelings of helplessness, hopelessness, or powerlessness
8. Deficient Knowledge [Learning Need] regarding condition, prognosis,
treatment, self-care, and discharge needs
May be related to:
Lack of exposure or recall; information misinterpretation
Unfamiliarity with information resources
Possibly evidenced by:
Questions, request for information, statement of misconception
Inaccurate follow-through of instructions, development of preventable
complications
Negative feelings about body and abilities
Feelings of helplessness, hopelessness, or powerlessness
8. Deficient Knowledge [Learning Need] regarding condition, prognosis,
treatment, self-care, and discharge needs
May be related to:
Lack of exposure or recall; information misinterpretation
Unfamiliarity with information resources
Possibly evidenced by:
Questions, request for information, statement of misconception
Inaccurate follow-through of instructions, development of preventable
complications
7.3. Nursing Interventions
IDEAL
Vital Signs monitored every 4 hours.
Intake and Output monitored every hour.
Monitored and documented Nasogastric tubing output every hour.
Medication given as prescribed by the physician.
Facilitate completion of NPO diet required.
NGT patency checking prior to medication done
Assessment for any alterations in body comfort and report
immediately to the physician.
NGT feeding done and medication.
Assessment for any profuse gum bleeding and note for the color
discharge, include odor.
Education for the significance of medication given
Encouraging the client to do exercise at a minimal level to promote
circulation.
Lifestyle modification: weight reduction (body mass index [BMI]
goal <25), reduction of dietary sodium to less than 2.4 g/day, DASH
diet (i.e., diet high in fruits and vegetables, reduced saturated and
total fat), aerobic physical activity >30 minutes most days of the
week, tobacco avoidance, increased dietary potassium and calcium,
moderation of alcohol consumption
.
Use of self BP monitoring. Home measurement device should be
checked regularly for accuracy. Mean self measured BP >135/85 is
generally considered to be hypertensive.
ACTUAL CARE GIVEN
Independent:
Assess for any significant findings on the abdominal size -to provide
a basis of proper and comfortable positioning
Assess for any discomfort related to pain at the right side of the
body- to provide a basis of proper and comfortable positioning.
Monitor intake and output closely (hourly)- to monitor any
improvement or worsening of patient’s condition
Regulate IVF to ordered flow rate- to prevent overload and under
load of fluid intake.
Provide side rails. - to promote patient’s safety
Encourage the client to urinate if feeling of voiding is present.- to
alleviate urinary distention
IDEAL
Vital Signs monitored every 4 hours.
Intake and Output monitored every hour.
Monitored and documented Nasogastric tubing output every hour.
Medication given as prescribed by the physician.
Facilitate completion of NPO diet required.
NGT patency checking prior to medication done
Assessment for any alterations in body comfort and report
immediately to the physician.
NGT feeding done and medication.
Assessment for any profuse gum bleeding and note for the color
discharge, include odor.
Education for the significance of medication given
Encouraging the client to do exercise at a minimal level to promote
circulation.
Lifestyle modification: weight reduction (body mass index [BMI]
goal <25), reduction of dietary sodium to less than 2.4 g/day, DASH
diet (i.e., diet high in fruits and vegetables, reduced saturated and
total fat), aerobic physical activity >30 minutes most days of the
week, tobacco avoidance, increased dietary potassium and calcium,
moderation of alcohol consumption
.
Use of self BP monitoring. Home measurement device should be
checked regularly for accuracy. Mean self measured BP >135/85 is
generally considered to be hypertensive.
ACTUAL CARE GIVEN
Independent:
Assess for any significant findings on the abdominal size -to provide
a basis of proper and comfortable positioning
Assess for any discomfort related to pain at the right side of the
body- to provide a basis of proper and comfortable positioning.
Monitor intake and output closely (hourly)- to monitor any
improvement or worsening of patient’s condition
Regulate IVF to ordered flow rate- to prevent overload and under
load of fluid intake.
Provide side rails. - to promote patient’s safety
Encourage the client to urinate if feeling of voiding is present.- to
alleviate urinary distention
Educated the client and the SO about the significance of urination.-
to provide information about the significance of voiding in relation
to its underlying condition
Bedside care done-to promote comfort and safety of the client’s
condition.
Position the patient in a Fowler’s or Semi Fowler’s position with
pillows - Relieves pressure on diaphragm. -Observe for
manifestations like crackles or increased respiration.- Identifies fluid
in the lungs
Monitor vital signs every 2 hours- to identify any changes in
patient’s health status.
Encourage the client to inhale and exhale exercise. - To alleviate
breathing difficulty.
Use light, cool clothing which promotes evaporation. Keep clothing
and bed dry. - Minimizes irritation and itching
Keeping the environment cool.- Minimizes itching
Avoid activities that promote sweating. Minimizes itching
Keep nails short and smooth.- Prevents breaking skin integrity when
scratching
Reposition patient every 2 hour.- Relieves pressure over bony
prominences
Dependent:
Medications were given as prescribed, lactulose 30 ml,
metronidazole 200mg 1 tab TID via NGT. To alleviate client’s
condition as prescribed by the physician.- to promote wellness and
alleviate the existing problem.
Instructed the So to maintain Nothing Per Orem Diet (NPO) as
recommended given since Gastrointestinal function are impaired due
to abdominal distention.- to reduce gastric irritation.
Administer Oxygen as ordered. - To alleviate breathing difficulty and
assist the need of air by the client.
to provide information about the significance of voiding in relation
to its underlying condition
Bedside care done-to promote comfort and safety of the client’s
condition.
Position the patient in a Fowler’s or Semi Fowler’s position with
pillows - Relieves pressure on diaphragm. -Observe for
manifestations like crackles or increased respiration.- Identifies fluid
in the lungs
Monitor vital signs every 2 hours- to identify any changes in
patient’s health status.
Encourage the client to inhale and exhale exercise. - To alleviate
breathing difficulty.
Use light, cool clothing which promotes evaporation. Keep clothing
and bed dry. - Minimizes irritation and itching
Keeping the environment cool.- Minimizes itching
Avoid activities that promote sweating. Minimizes itching
Keep nails short and smooth.- Prevents breaking skin integrity when
scratching
Reposition patient every 2 hour.- Relieves pressure over bony
prominences
Dependent:
Medications were given as prescribed, lactulose 30 ml,
metronidazole 200mg 1 tab TID via NGT. To alleviate client’s
condition as prescribed by the physician.- to promote wellness and
alleviate the existing problem.
Instructed the So to maintain Nothing Per Orem Diet (NPO) as
recommended given since Gastrointestinal function are impaired due
to abdominal distention.- to reduce gastric irritation.
Administer Oxygen as ordered. - To alleviate breathing difficulty and
assist the need of air by the client.
8. Summary and Conclusion
The significance of this study promulgates a comprehensive learning, skills and
responsibilities on the said case. It includes a thorough collaborative discussion and
interaction between me, as a student nurse and my client at the Medical Ward at
Hemas Hospital. Different nursing assessment and interventions, both ideal and
actual was presented in order to show a comparison and variability of each procedure
done. Not only on the nursing part was presented, a comprehensive medical and
diagnostic procedures was also compared, both actual and ideal to show the essence
of every care given. During the discussion of anatomy and physiology, and its
pathophysiology related to the condition, the case will thoroughly deviate from the
normal flow of the story and yet further analysis is required since no actual
Pathophysiology was thoroughly discussed to explain the theory presented. All the
essential data required are presented and tabularized in order to ease up the readers
upon reading.
The whole discussion will truly give innovations to the related education and field
studies and will somewhat aid the readers to enlighten their minds about Liver
Cirrhosis.
Thank you………….
The significance of this study promulgates a comprehensive learning, skills and
responsibilities on the said case. It includes a thorough collaborative discussion and
interaction between me, as a student nurse and my client at the Medical Ward at
Hemas Hospital. Different nursing assessment and interventions, both ideal and
actual was presented in order to show a comparison and variability of each procedure
done. Not only on the nursing part was presented, a comprehensive medical and
diagnostic procedures was also compared, both actual and ideal to show the essence
of every care given. During the discussion of anatomy and physiology, and its
pathophysiology related to the condition, the case will thoroughly deviate from the
normal flow of the story and yet further analysis is required since no actual
Pathophysiology was thoroughly discussed to explain the theory presented. All the
essential data required are presented and tabularized in order to ease up the readers
upon reading.
The whole discussion will truly give innovations to the related education and field
studies and will somewhat aid the readers to enlighten their minds about Liver
Cirrhosis.
Thank you………….
9. References
Saladin: Anatomy & Physiology: The Unity of Form and Function, Third
Edition, © the McGraw−HillCompanies
Marilynn E. Doenges, APRN, BC-Retired, Mary Frances Moorhouse, Alice C.
Murr (2010) Nursing Care Plans
Danielle Platt & Mary Moss, Adult Medical and Surgical Nursing
David A. Warrell (Editor), Timothy M. Cox (Editor), John D. Firth (Editor),
Edward J., J R., M.D. Benz, Oxford Textbook of Medicine 4th edition (March
2003), By Oxford Press.
Nicki R. Colledge, Brian R. Walker, Stuart H. Ralston,(2010), Davidson’s
Principles and Practice of Medicine, An imprint of Elsevier Limited.
Sondra G. Ferguson, Tracey Goldsmith, Constance J. Hirnle, Carol Ann
Barnett Lammon, Sandra Smith Pennington, Frank Romanelli.(2006), The
Clinical drug Therapy Rationales for Nursing Practice.
Saladin: Anatomy & Physiology: The Unity of Form and Function, Third
Edition, © the McGraw−HillCompanies
Marilynn E. Doenges, APRN, BC-Retired, Mary Frances Moorhouse, Alice C.
Murr (2010) Nursing Care Plans
Danielle Platt & Mary Moss, Adult Medical and Surgical Nursing
David A. Warrell (Editor), Timothy M. Cox (Editor), John D. Firth (Editor),
Edward J., J R., M.D. Benz, Oxford Textbook of Medicine 4th edition (March
2003), By Oxford Press.
Nicki R. Colledge, Brian R. Walker, Stuart H. Ralston,(2010), Davidson’s
Principles and Practice of Medicine, An imprint of Elsevier Limited.
Sondra G. Ferguson, Tracey Goldsmith, Constance J. Hirnle, Carol Ann
Barnett Lammon, Sandra Smith Pennington, Frank Romanelli.(2006), The
Clinical drug Therapy Rationales for Nursing Practice.
Vital Signs Chart
Patient Name: Mr. R
BHT No: 30848
Ward/Room No: A
Date Time Temperature Pulse Respiration BP Remarks
18/02/2013 On
admission
94.6 F/Axilla
80/bpm
22/bpm
130/70mmHg
10am 99.2/Axilla 86/bpm 24/bpm
02pm 100.4/Axilla 88/bpm 26/bpm 130/70 mmHg
06pm 98.6/Axilla 94/bpm 24/bpm
10pm 99.8/Axilla 86/bpm 22/bpm 120/80mmHg
19/02/2013 02am
06am 96.4/Axilla 80/bpm 22/bpm
10am 95.4/Axilla 84/bpm 24/bpm 120/85 mmHg
02pm 94.8/Axilla 82/bpm 28/bpm 130/80 mmHg
06pm 96.4/Axilla 82/bpm 26/bpm 120/80 mmHg
10pm 98.6/Axilla 86/bpm 24/bpm
20/02/2013 02am 98.9/Axilla 84/bpm 22/bpm
06am 99.1/Axilla 88/bpm 26/bpm 130/80 mmHg 96% on air
10am 98.2/Axilla 84/bpm 24/bpm 120/80 mmHg 98% on air
02pm 98.6/Axilla 86/bpm 20/bpm
06pm 92.4/Axilla 82/bpm 24/bpm 130/80 mmHg 99% on air
10pm 98.2/Axilla 80/bpm 20/bpm 135/65 mmHg
21/02/2013 02am
06am 92.4/Axilla 88/bpm 22/bpm 99% with O2
10am 98.6/Axilla 94/bpm 26/bpm 130/90 mmHg 98% with O2
02pm 96.6/Axilla 84/bpm 24/bpm 120/80 mmHg 99% with O2
06pm 98.4/Axilla 86/bpm 20/bpm 120/85 mmHg 96%with O2
10pm 97.8/Axilla 82/bpm 24/bpm
22/02/2013 02am
06am 98.8/Axilla 84/bpm 24/bpm 120/80 mmHg
10am 98.9/Axilla 80/bpm 26/bpm 98% on air
02pm 101/Axilla 88/bpm 26/bpm 130/80 mmHg 96% on air
06pm 99/Axilla 86/bpm 24/bpm
10pm 98.2/Axilla 82/bpm 20/bpm 140/70 mmHg
Patient Name: Mr. R
BHT No: 30848
Ward/Room No: A
Date Time Temperature Pulse Respiration BP Remarks
18/02/2013 On
admission
94.6 F/Axilla
80/bpm
22/bpm
130/70mmHg
10am 99.2/Axilla 86/bpm 24/bpm
02pm 100.4/Axilla 88/bpm 26/bpm 130/70 mmHg
06pm 98.6/Axilla 94/bpm 24/bpm
10pm 99.8/Axilla 86/bpm 22/bpm 120/80mmHg
19/02/2013 02am
06am 96.4/Axilla 80/bpm 22/bpm
10am 95.4/Axilla 84/bpm 24/bpm 120/85 mmHg
02pm 94.8/Axilla 82/bpm 28/bpm 130/80 mmHg
06pm 96.4/Axilla 82/bpm 26/bpm 120/80 mmHg
10pm 98.6/Axilla 86/bpm 24/bpm
20/02/2013 02am 98.9/Axilla 84/bpm 22/bpm
06am 99.1/Axilla 88/bpm 26/bpm 130/80 mmHg 96% on air
10am 98.2/Axilla 84/bpm 24/bpm 120/80 mmHg 98% on air
02pm 98.6/Axilla 86/bpm 20/bpm
06pm 92.4/Axilla 82/bpm 24/bpm 130/80 mmHg 99% on air
10pm 98.2/Axilla 80/bpm 20/bpm 135/65 mmHg
21/02/2013 02am
06am 92.4/Axilla 88/bpm 22/bpm 99% with O2
10am 98.6/Axilla 94/bpm 26/bpm 130/90 mmHg 98% with O2
02pm 96.6/Axilla 84/bpm 24/bpm 120/80 mmHg 99% with O2
06pm 98.4/Axilla 86/bpm 20/bpm 120/85 mmHg 96%with O2
10pm 97.8/Axilla 82/bpm 24/bpm
22/02/2013 02am
06am 98.8/Axilla 84/bpm 24/bpm 120/80 mmHg
10am 98.9/Axilla 80/bpm 26/bpm 98% on air
02pm 101/Axilla 88/bpm 26/bpm 130/80 mmHg 96% on air
06pm 99/Axilla 86/bpm 24/bpm
10pm 98.2/Axilla 82/bpm 20/bpm 140/70 mmHg
Intake and Output Chart
Patient Name: Mr. R
BHT No: 30848
Ward/Room No: A
Date Time Oral IV Fluids NG Feed Total Urine Other Total
18/2/2014 1pm-7pm 120ml 300ml 420ml 200ml 200ml
7pm-7am 140ml 600ml 1260ml 250ml 450ml
Total intake : 1260ml
Total output: 450ml
19/2/2014 Time Oral IV Fluids NG Feed Total Urine Other Total
7am-1pm 180ml 300ml 480ml 150ml 150ml
1pm-7pm 200ml 300ml 980ml 170ml 330ml
7pm-7am 300ml 600ml 1880ml 200ml 530ml
Total intake : 1880ml
Total output: 530ml
20/2/2014 Time Oral IV Fluids NG Feed Total Urine Other Total
7am-1pm 250ml 300ml 550ml 180ml 180ml
1pm-7pm 200ml 300ml 1050ml 200ml 380ml
7pm-7am 200ml 600ml 200ml 2050ml 300ml 680ml
Total intake : 2050ml
Total output: 680ml
Patient Name: Mr. R
BHT No: 30848
Ward/Room No: A
Date Time Oral IV Fluids NG Feed Total Urine Other Total
18/2/2014 1pm-7pm 120ml 300ml 420ml 200ml 200ml
7pm-7am 140ml 600ml 1260ml 250ml 450ml
Total intake : 1260ml
Total output: 450ml
19/2/2014 Time Oral IV Fluids NG Feed Total Urine Other Total
7am-1pm 180ml 300ml 480ml 150ml 150ml
1pm-7pm 200ml 300ml 980ml 170ml 330ml
7pm-7am 300ml 600ml 1880ml 200ml 530ml
Total intake : 1880ml
Total output: 530ml
20/2/2014 Time Oral IV Fluids NG Feed Total Urine Other Total
7am-1pm 250ml 300ml 550ml 180ml 180ml
1pm-7pm 200ml 300ml 1050ml 200ml 380ml
7pm-7am 200ml 600ml 200ml 2050ml 300ml 680ml
Total intake : 2050ml
Total output: 680ml
Intake and Output Chart
Patient Name: Mr. R
BHT No: 30848
Ward/Room No: A
21/2/2014 Time Oral IV Fluids NG Feed Total Urine Other Total
7am-1pm 100ml 120ml 300ml 420ml 200ml 200ml
1pm-7pm 50ml 120ml 300ml 890ml 250ml 450ml
7pm-7am 240ml 200ml 1330ml 270ml 720ml
Total intake : 1330ml
Total output: 720ml
22/2/2014 Time Oral IV Fluids NG Feed Total Urine Other Total
7am-1pm 100ml 120ml 200ml 420ml 350ml 350ml
1pm-7pm 100ml 120ml 200ml 840ml 300ml 650ml
7pm-7am 50ml 240ml 200ml 1330ml 350ml 1000ml
Total intake : 1330ml
Total output: 1000ml
Patient Name: Mr. R
BHT No: 30848
Ward/Room No: A
21/2/2014 Time Oral IV Fluids NG Feed Total Urine Other Total
7am-1pm 100ml 120ml 300ml 420ml 200ml 200ml
1pm-7pm 50ml 120ml 300ml 890ml 250ml 450ml
7pm-7am 240ml 200ml 1330ml 270ml 720ml
Total intake : 1330ml
Total output: 720ml
22/2/2014 Time Oral IV Fluids NG Feed Total Urine Other Total
7am-1pm 100ml 120ml 200ml 420ml 350ml 350ml
1pm-7pm 100ml 120ml 200ml 840ml 300ml 650ml
7pm-7am 50ml 240ml 200ml 1330ml 350ml 1000ml
Total intake : 1330ml
Total output: 1000ml
Diabetic Chart
Patient Name: Mr. R
BHT No: 30848
Ward/Room No: A
Date Time RBS Value Medication
18/02/2014 6am 180 mg/dl S. Insulin 15units SC given
19/02/2014 6am 125 mg/dl
12nn 110 mg/dl
6pm 117 mg/dl
20/02/2014 6am 132 mg/dl
12nn 128 mg/dl
6pm 118 mg/dl
21/02/2014 6am 96 mg/dl
12nn 84 mg/dl
6pm 70 mg/dl
22/02/2014 6am 90 mg/dl
12nn 84 mg/dl
6pm 99 mg/dl
23/02/2014 6am 120 mg/dl
Patient Name: Mr. R
BHT No: 30848
Ward/Room No: A
Date Time RBS Value Medication
18/02/2014 6am 180 mg/dl S. Insulin 15units SC given
19/02/2014 6am 125 mg/dl
12nn 110 mg/dl
6pm 117 mg/dl
20/02/2014 6am 132 mg/dl
12nn 128 mg/dl
6pm 118 mg/dl
21/02/2014 6am 96 mg/dl
12nn 84 mg/dl
6pm 70 mg/dl
22/02/2014 6am 90 mg/dl
12nn 84 mg/dl
6pm 99 mg/dl
23/02/2014 6am 120 mg/dl
Investigations
N
o
Investigation Name Normal
Value
18/02/
2013
19/02/
2013
20/02/
2013
21/02/
2013
22/02/
2013
1.
2.
Full Blood Count
WBC
Nutrophills
Lymphocytes
Monocytes
Eosinophills
Basophills
RBC
HGB
PCV
MCV
MCH
MCHC
RDW
Platelet Count
Serum Electrolytes
Sodium (Na+)
Potassium (K+)
Chloride (Cl-)
4000-11000 cumm
40-75%
20-40%
2-8%
1-6%
0-3%
4-6%
11.5-15.5g/dl
36-46%
83-101FL
27.5-32Pg
31.5-35g/dl
11.6-14.8%
150,000-450,000cumm
137-145mmol/L
3.5-5.1mmol/L
98-105mmol/L
8000 cumm
68%
20%
6%
4%
2%
6%
12.7g/dl
40%
88.1FL
32.4Pg
24.5g/dl
10.9%
198,0000cumm
141 mmol/L
3.5 mmol/L
99 mmol/L
6500 cumm
57%
38%
6%
5%
0%
4.25%
12.8g/dl
37.5%
88.1FL
29.8Pg
33.8g/dl
14.9%
257,000cumm
136 mmol/L
3.2 mmol/L
98 mmol/L
7800 cumm
64%
38%
6%
0%
0%
2.95%
10.4g/dl
30.5%
10.3FL
35.2Pg
34.1g/dl
18.8%
234,000cumm
N
o
Investigation Name Normal
Value
18/02/
2013
19/02/
2013
20/02/
2013
21/02/
2013
22/02/
2013
1.
2.
Full Blood Count
WBC
Nutrophills
Lymphocytes
Monocytes
Eosinophills
Basophills
RBC
HGB
PCV
MCV
MCH
MCHC
RDW
Platelet Count
Serum Electrolytes
Sodium (Na+)
Potassium (K+)
Chloride (Cl-)
4000-11000 cumm
40-75%
20-40%
2-8%
1-6%
0-3%
4-6%
11.5-15.5g/dl
36-46%
83-101FL
27.5-32Pg
31.5-35g/dl
11.6-14.8%
150,000-450,000cumm
137-145mmol/L
3.5-5.1mmol/L
98-105mmol/L
8000 cumm
68%
20%
6%
4%
2%
6%
12.7g/dl
40%
88.1FL
32.4Pg
24.5g/dl
10.9%
198,0000cumm
141 mmol/L
3.5 mmol/L
99 mmol/L
6500 cumm
57%
38%
6%
5%
0%
4.25%
12.8g/dl
37.5%
88.1FL
29.8Pg
33.8g/dl
14.9%
257,000cumm
136 mmol/L
3.2 mmol/L
98 mmol/L
7800 cumm
64%
38%
6%
0%
0%
2.95%
10.4g/dl
30.5%
10.3FL
35.2Pg
34.1g/dl
18.8%
234,000cumm
3.
4.
5.
6.
Serum Creatinine
CRP
Liver Profile
Total Protein
Albumin
Globulin
A/G Ratio
Total Bilirubin
Alkaline Phosphatese
ALT/SGPT
AST/SGOT
GAMMA GT
Renal Profile
Sodium
Potassium
Chloride
Urea
S. Creatinine
Calcium
Phosphorus
Uric acid
Male 0.5-1.5mg/dl
Female 0.6-1.2mg/dl
0-6 mg/L
6.4-8.2g/dl
3.4-5.0g/dl
2.5-3.5g/dl
1:1
0.2-1.2g/dl
50-136U/L
30-65U/L
15-37U/L
15-85U/L
137-145mmol/L
3.5-5.1mmol/L
98-105mmol/L
5-40mg/dl
0.5-1.5mg.dl
8.5-10.1mg/dl
2.5-4.5mg/dl
3.5-8.35mg/dl
1.1mg/dl
48.5mg/L
7.7 g/dl
3.1 g/dl
5.2 g/dl
1.1
10.58 g/dl
75 U/L
32 U/L
18 U/L
49 U/L
0.9mg/dl
42.5mg/L
7.6 g/dl
2.5 g/dl
5.1 g/dl
0.5
13.78 g/dl
122 U/L
33 U/L
60 U/L
40 U/L
134 mmol/L
4.7 mmol/L
96 mmol/L
23.54 mg/dl
0.8 mg/dl
8.9 mg/dl
3.3 mg/dl
2.8 mg/dl
1.1mg/dl
34.2mg/L
7.8 g/dl
2.2 g/dl
5.8 g/dl
1.1
10.2 g/dl
120 U/L
34 U/L
54 U/L
76 U/L
28.4mg/L
7.2 g/dl
3.0 g/dl
5.4 g/dl
0.5
9.4 g/dl
122 U/L
38 U/L
42 U/L
80 U/L
4.
5.
6.
Serum Creatinine
CRP
Liver Profile
Total Protein
Albumin
Globulin
A/G Ratio
Total Bilirubin
Alkaline Phosphatese
ALT/SGPT
AST/SGOT
GAMMA GT
Renal Profile
Sodium
Potassium
Chloride
Urea
S. Creatinine
Calcium
Phosphorus
Uric acid
Male 0.5-1.5mg/dl
Female 0.6-1.2mg/dl
0-6 mg/L
6.4-8.2g/dl
3.4-5.0g/dl
2.5-3.5g/dl
1:1
0.2-1.2g/dl
50-136U/L
30-65U/L
15-37U/L
15-85U/L
137-145mmol/L
3.5-5.1mmol/L
98-105mmol/L
5-40mg/dl
0.5-1.5mg.dl
8.5-10.1mg/dl
2.5-4.5mg/dl
3.5-8.35mg/dl
1.1mg/dl
48.5mg/L
7.7 g/dl
3.1 g/dl
5.2 g/dl
1.1
10.58 g/dl
75 U/L
32 U/L
18 U/L
49 U/L
0.9mg/dl
42.5mg/L
7.6 g/dl
2.5 g/dl
5.1 g/dl
0.5
13.78 g/dl
122 U/L
33 U/L
60 U/L
40 U/L
134 mmol/L
4.7 mmol/L
96 mmol/L
23.54 mg/dl
0.8 mg/dl
8.9 mg/dl
3.3 mg/dl
2.8 mg/dl
1.1mg/dl
34.2mg/L
7.8 g/dl
2.2 g/dl
5.8 g/dl
1.1
10.2 g/dl
120 U/L
34 U/L
54 U/L
76 U/L
28.4mg/L
7.2 g/dl
3.0 g/dl
5.4 g/dl
0.5
9.4 g/dl
122 U/L
38 U/L
42 U/L
80 U/L
Ultra Sound Scan Abdomen are Normal
Chest X ray, CT Scan Reports are Normal View.
7.
8.
9.
ESR
Lipid Profile
Total Cholesterol
Triglyceride
HDL
LDL
VLDL
CHOL/HDL ratio
Prothrombin Time
Control
INR
0-20mm (1
st
Hour)
>200mg/dl
>150mg/dl
>40mg/dl
>129mg/dl
39seconds
13seconds
3.1
28mm
212 mg/dl
132 mg/dl
43 mg/dl
142.6 mg/dl
26.40
4.9
24mm
22mm
215 mg/dl
126 mg/dl
56 mg/dl
140 mg/dl
25.5
4.7
36seconds
15seconds
2.8
Chest X ray, CT Scan Reports are Normal View.
7.
8.
9.
ESR
Lipid Profile
Total Cholesterol
Triglyceride
HDL
LDL
VLDL
CHOL/HDL ratio
Prothrombin Time
Control
INR
0-20mm (1
st
Hour)
>200mg/dl
>150mg/dl
>40mg/dl
>129mg/dl
39seconds
13seconds
3.1
28mm
212 mg/dl
132 mg/dl
43 mg/dl
142.6 mg/dl
26.40
4.9
24mm
22mm
215 mg/dl
126 mg/dl
56 mg/dl
140 mg/dl
25.5
4.7
36seconds
15seconds
2.8
Medication Chart
No
Drug Name Route Action & Indications Contra Indications Side Effects Nursing Considerations
1.
Generic Name
Levofloxacin
Trade Name
Levofloxacin
Levaquin
Classification
Antibiotic
(Fluoroquinolone)
IV
Oral
Drugs
Action
Involve the inhabitation
of bacterial action and
fights bacterial in the
body.
Indications
Bacterial
infection of the
Skin, Sinuses,
Kidneys, Liver,
Bladder or
Prostate.
Bronchitis
Pneumonia
Anthrax or plaque
Hypersensitivity
of Levofloxacin
Pregnancy
Breast feeding
Diarrhea
Abdominal
pain/cramps
Agitation
Confusion
Fever
Redness &
Swelling of
skin
Burning on
the skin
Skin rash
itching
Hypersensitivity of
Levofloxacin
History of muscle
disorders
(myasthenia
gravis)
No
Drug Name Route Action & Indications Contra Indications Side Effects Nursing Considerations
1.
Generic Name
Levofloxacin
Trade Name
Levofloxacin
Levaquin
Classification
Antibiotic
(Fluoroquinolone)
IV
Oral
Drugs
Action
Involve the inhabitation
of bacterial action and
fights bacterial in the
body.
Indications
Bacterial
infection of the
Skin, Sinuses,
Kidneys, Liver,
Bladder or
Prostate.
Bronchitis
Pneumonia
Anthrax or plaque
Hypersensitivity
of Levofloxacin
Pregnancy
Breast feeding
Diarrhea
Abdominal
pain/cramps
Agitation
Confusion
Fever
Redness &
Swelling of
skin
Burning on
the skin
Skin rash
itching
Hypersensitivity of
Levofloxacin
History of muscle
disorders
(myasthenia
gravis)
No
2.
Drug Name
Generic Name
Pantaprazole
Trade Name
Pantacid
Pantodac
Classification
Proton Pump
inhibitor
Route
Oral
IV Drug
Action & Indications
Action
Suppress gastric acid
production
Indications
Sahort term
treatment of
erosive
oesophagitis
associated with
GERD
Duodenal Ulcer
Prophylaxis of
NSAID associated
gastric or
duodenal ulcer
Contra Indications
Hypersensitivity
of Pantaprazole.
Side Effects
Allergic
reactions
Constipation
Dry mouth
myalgia
Thrombocyt
openia
Generalized
oedema
Depression
Vertigo
pruritis
Nursing Considerations
Assess for side
effects.
Educate patient
about side effects.
2.
Drug Name
Generic Name
Pantaprazole
Trade Name
Pantacid
Pantodac
Classification
Proton Pump
inhibitor
Route
Oral
IV Drug
Action & Indications
Action
Suppress gastric acid
production
Indications
Sahort term
treatment of
erosive
oesophagitis
associated with
GERD
Duodenal Ulcer
Prophylaxis of
NSAID associated
gastric or
duodenal ulcer
Contra Indications
Hypersensitivity
of Pantaprazole.
Side Effects
Allergic
reactions
Constipation
Dry mouth
myalgia
Thrombocyt
openia
Generalized
oedema
Depression
Vertigo
pruritis
Nursing Considerations
Assess for side
effects.
Educate patient
about side effects.
3.
Drug Name
Generic Name
Metranidazol
e
Trade Name
Flagyle
Metranidazol
e
Classification
Antimicrobial
Drug
Route
Oral
drug,
Injec,
Action & Indications
Action
High action against
anaerobic bacteria and
protozoa to killing
Indications
Anaerobic
infection
Leg ulcers &
Pressure sores
Bacterial
vaginosis
Pelvic
inflammatory
disease
Acute ulcerative
gingivitis
Acute oral
infections
Surgical
prophylaxis
Contra Indications
Hepatic
impairment
Hepatic
encephalopathy
Pregnancy
Breast feeding
Side Effects
Nausea,
Vomiting
Taste
disturbance
Oral
mucositis
Drowsiness
Dizziness
Headache
Ataxia
Psychotic
disorders
Thrombocyt
openia
Myalgia
Visual
disturbance
Pruritis
Erythema
Nursing Considerations
Assess for contra
indications
Educate patient
about side effects
Drug Name
Generic Name
Metranidazol
e
Trade Name
Flagyle
Metranidazol
e
Classification
Antimicrobial
Drug
Route
Oral
drug,
Injec,
Action & Indications
Action
High action against
anaerobic bacteria and
protozoa to killing
Indications
Anaerobic
infection
Leg ulcers &
Pressure sores
Bacterial
vaginosis
Pelvic
inflammatory
disease
Acute ulcerative
gingivitis
Acute oral
infections
Surgical
prophylaxis
Contra Indications
Hepatic
impairment
Hepatic
encephalopathy
Pregnancy
Breast feeding
Side Effects
Nausea,
Vomiting
Taste
disturbance
Oral
mucositis
Drowsiness
Dizziness
Headache
Ataxia
Psychotic
disorders
Thrombocyt
openia
Myalgia
Visual
disturbance
Pruritis
Erythema
Nursing Considerations
Assess for contra
indications
Educate patient
about side effects
4
Drug Name
Generic Name
Metformin
Hydrochlorid
e
Trade Name
Glycomet
Metformin
Glymet
Classification
Biguanides
Route
Oral
Drugs
Action & Indications
Action
It exerts its effect mainly
decreasing
gluconeogenesis and by
increasing peripheral
utilization of glucose.
Indications
Diabetes Mellitus
Poly Cystic Ovary
syndrome
Contra Indications
Renal impairment
Ketoacidosis
Sepsis
Respiratory
failure
Hepatic
impairment
Pregnancy
Breast feeding
Side Effects
Anorexia
Nausea,
vomiting
Diarrhea
Abdominal
pain
Metallic
taste
Lactic
acidosis
Erythema
Pruritis
Urticaria
Decrease Vit
B12
absorption
Nursing Considerations
Assess the contra
indication before
administering
drug
Educate patient
about side effect
Assess Blood
Glucose level for
continuously
taking patients.
Drug Name
Generic Name
Metformin
Hydrochlorid
e
Trade Name
Glycomet
Metformin
Glymet
Classification
Biguanides
Route
Oral
Drugs
Action & Indications
Action
It exerts its effect mainly
decreasing
gluconeogenesis and by
increasing peripheral
utilization of glucose.
Indications
Diabetes Mellitus
Poly Cystic Ovary
syndrome
Contra Indications
Renal impairment
Ketoacidosis
Sepsis
Respiratory
failure
Hepatic
impairment
Pregnancy
Breast feeding
Side Effects
Anorexia
Nausea,
vomiting
Diarrhea
Abdominal
pain
Metallic
taste
Lactic
acidosis
Erythema
Pruritis
Urticaria
Decrease Vit
B12
absorption
Nursing Considerations
Assess the contra
indication before
administering
drug
Educate patient
about side effect
Assess Blood
Glucose level for
continuously
taking patients.
5.
Drug Name
Generic Name
Frusemide
Trade Name
Lasix
Frusemide
Classification
Loop Diuretic
Route
Oral,
inje
Action & Indications
Action
Loop diuretics inhibits
reabsorption from the
ascending limb of the
loop of Henle in the
renal tubule and are
powerful diuretic
Indications
Oedema
Oliguria due to
renal failure
Pulmonary
oedema
Chronic heart
failure
Contra Indications
Liver cirrhosis
Renal failure
Anuria
Side Effects
Hyponatrem
ia
Hypokalemi
a
Hypomagnes
imia
Hypochlorae
mic
alkalosia
Increase
calcium
exertion
Hypotension
GI
disturbance
Hyperglyce
mia
pancreatitis
Nursing Considerations
Administer in
night
Educate patient
about polyuria
Drug Name
Generic Name
Frusemide
Trade Name
Lasix
Frusemide
Classification
Loop Diuretic
Route
Oral,
inje
Action & Indications
Action
Loop diuretics inhibits
reabsorption from the
ascending limb of the
loop of Henle in the
renal tubule and are
powerful diuretic
Indications
Oedema
Oliguria due to
renal failure
Pulmonary
oedema
Chronic heart
failure
Contra Indications
Liver cirrhosis
Renal failure
Anuria
Side Effects
Hyponatrem
ia
Hypokalemi
a
Hypomagnes
imia
Hypochlorae
mic
alkalosia
Increase
calcium
exertion
Hypotension
GI
disturbance
Hyperglyce
mia
pancreatitis
Nursing Considerations
Administer in
night
Educate patient
about polyuria
6.
Drug Name
Generic Name
Spiranolacto
ne
Trade Name
Aldactone
Spiranolacto
ne
Classification
Potassium
sparing
Diuretics
Aldosterone
Antagonists
Route
Oral
drug
Action & Indications
Action
Antagonizing the
Aldosterone
Indications
Oedema
Ascitis in cirrhosis
Malignant
Cirrhosis
Nephritic
Syndrome
CHF
Primary
hyperaldoesteroni
sm
Contra Indications
Hyperglycemia
Hyponatremia
Addison’s disease
Side Effects
GI
disturbances
Impotence
Gynaecomes
tia
Menstrual
irregulation
s
Lethargy
Headache
Confusion
Rashes
Hyperkalemi
a
Hyponatrem
ia
Osteomalaci
a
Nursing Considerations
As with potassium
sparing diuretics,
potassium
supplements must
not be given with
aldosterone
antagonists.
Monitor serum
Electrolyte level.
Assess for GI
disturbances.
Drug Name
Generic Name
Spiranolacto
ne
Trade Name
Aldactone
Spiranolacto
ne
Classification
Potassium
sparing
Diuretics
Aldosterone
Antagonists
Route
Oral
drug
Action & Indications
Action
Antagonizing the
Aldosterone
Indications
Oedema
Ascitis in cirrhosis
Malignant
Cirrhosis
Nephritic
Syndrome
CHF
Primary
hyperaldoesteroni
sm
Contra Indications
Hyperglycemia
Hyponatremia
Addison’s disease
Side Effects
GI
disturbances
Impotence
Gynaecomes
tia
Menstrual
irregulation
s
Lethargy
Headache
Confusion
Rashes
Hyperkalemi
a
Hyponatrem
ia
Osteomalaci
a
Nursing Considerations
As with potassium
sparing diuretics,
potassium
supplements must
not be given with
aldosterone
antagonists.
Monitor serum
Electrolyte level.
Assess for GI
disturbances.
N
7.
Drug Name
Generic Name
Tolbutamide
Trade Name
Tolbutamide
Classification
Sulphonylure
as
Route
Oral
drug
Action & Indications
Action
The act by increasing
insulin release from the
beta cells in the
pancrease
Indications
Type 2 Diabetes
Mellitus
Contra Indications
Hepatic & Renal
impairment
Prophyria
Breast feeding
Ketoacidosis
Side Effects
Headache
Tinnitus
Nausea,
Vomiting
Diarrhea
Hypoglycemi
a
Fever
Jaundice
Photosensiti
vity
Thrombocyt
openia
Agranulocyt
osis
Anemia
Nursing Considerations
Assess patient for
hypoglycemia
Before use of this
drug patient
assess for RBS
7.
Drug Name
Generic Name
Tolbutamide
Trade Name
Tolbutamide
Classification
Sulphonylure
as
Route
Oral
drug
Action & Indications
Action
The act by increasing
insulin release from the
beta cells in the
pancrease
Indications
Type 2 Diabetes
Mellitus
Contra Indications
Hepatic & Renal
impairment
Prophyria
Breast feeding
Ketoacidosis
Side Effects
Headache
Tinnitus
Nausea,
Vomiting
Diarrhea
Hypoglycemi
a
Fever
Jaundice
Photosensiti
vity
Thrombocyt
openia
Agranulocyt
osis
Anemia
Nursing Considerations
Assess patient for
hypoglycemia
Before use of this
drug patient
assess for RBS
8.
Drug Name
Generic Name
Atorvastatin
Trade Name
Atorva
Atacor
Atrovastatin
Classification
Statin
Route
Oral
drug
Action & Indications
Action
Statins are lowering and
regulating LDL
cholesterol
concentration
Indications
Primary hyper
cholesterolaemia
Heterozygous
familial hyper
cholesterolaemia
Homozygous
familial hyper
cholesterolaemia
Prevention of
cardiovascular
events in patient
with Type 2 DM.
Contra Indications
Pregnancy
Breast Feeding
Side Effects
Chest pain
Angina
Insomnia
Dizziness
Hypoaesthes
ia
Arthralgia
Back pain
Headache
Altered liver
function test
Abdominal
pain
Flatulence
Constipation
Nausea &
vomiting
Hypersensiti
ve reaction.
Nursing Considerations
Assess for liver
function
Encourage patient
to take in night
time.
Educate patient
about side effects.
Drug Name
Generic Name
Atorvastatin
Trade Name
Atorva
Atacor
Atrovastatin
Classification
Statin
Route
Oral
drug
Action & Indications
Action
Statins are lowering and
regulating LDL
cholesterol
concentration
Indications
Primary hyper
cholesterolaemia
Heterozygous
familial hyper
cholesterolaemia
Homozygous
familial hyper
cholesterolaemia
Prevention of
cardiovascular
events in patient
with Type 2 DM.
Contra Indications
Pregnancy
Breast Feeding
Side Effects
Chest pain
Angina
Insomnia
Dizziness
Hypoaesthes
ia
Arthralgia
Back pain
Headache
Altered liver
function test
Abdominal
pain
Flatulence
Constipation
Nausea &
vomiting
Hypersensiti
ve reaction.
Nursing Considerations
Assess for liver
function
Encourage patient
to take in night
time.
Educate patient
about side effects.
Care Plan of the Patient
Nursing Assessment Nursing diagnosis Goal Planning Nursing Intervention Evaluation
20/02/2013,
Wednesday, 8.30am.
Subjective Data
Mr W A P Ranjith,
58years
Verbalized I have
1. Abdominal Distention
and Generalized
swelling of Abdomen
and Scrotum since two
weeks
2. Abdominal Pain
Right Upper Quadrent
site, On & Off type pain,
Pain on Exertion, and No
Radiation in other site.
3. Loss of Appetite sine
one Week
4. Vomiting 4 times its
watery contents.
1. Pain related to
Abdominal Distention
Reduce the
Pain
1. Assess the Pain noting
location, Characteristics,
intensity and Radiation.
2. Position the patient.
3. Provide comfort
measures such as mouth
care, back care and
repositioning.
4. Encourage the patient to
use of the relaxation
technique.
5. Monitor Vital Signs.
6. Provide Diversitional
Activities.
7. Administer Analgesics as
Prescribed.
8. Administer IV fluids as
Prescribed.
1. Assessed pain for location,
characteristic, intensity, and
radiation.
2. Positionate the patient for
Semi Fowlers position.
3. Provide comfort measures
such as mouth care and
Repositioning.
4. Educated patient for some
relaxation techniques.
5. Monitored and charted the
Vital Signs.
6. Provided some Divertional
Activities such as TV, Radio,
and Talked with patient.
7. Introduced Hospital
Environment, and ward
Staff.
After Nursing
interventions
patient
verbalized feel
comfortable.
Nursing Assessment Nursing diagnosis Goal Planning Nursing Intervention Evaluation
20/02/2013,
Wednesday, 8.30am.
Subjective Data
Mr W A P Ranjith,
58years
Verbalized I have
1. Abdominal Distention
and Generalized
swelling of Abdomen
and Scrotum since two
weeks
2. Abdominal Pain
Right Upper Quadrent
site, On & Off type pain,
Pain on Exertion, and No
Radiation in other site.
3. Loss of Appetite sine
one Week
4. Vomiting 4 times its
watery contents.
1. Pain related to
Abdominal Distention
Reduce the
Pain
1. Assess the Pain noting
location, Characteristics,
intensity and Radiation.
2. Position the patient.
3. Provide comfort
measures such as mouth
care, back care and
repositioning.
4. Encourage the patient to
use of the relaxation
technique.
5. Monitor Vital Signs.
6. Provide Diversitional
Activities.
7. Administer Analgesics as
Prescribed.
8. Administer IV fluids as
Prescribed.
1. Assessed pain for location,
characteristic, intensity, and
radiation.
2. Positionate the patient for
Semi Fowlers position.
3. Provide comfort measures
such as mouth care and
Repositioning.
4. Educated patient for some
relaxation techniques.
5. Monitored and charted the
Vital Signs.
6. Provided some Divertional
Activities such as TV, Radio,
and Talked with patient.
7. Introduced Hospital
Environment, and ward
Staff.
After Nursing
interventions
patient
verbalized feel
comfortable.
5. Decreased level of
Urine output since 3
days
Objective Data
1. Patient General
Appearance is good.
2. Patient oriented and
Alert for Time, Person,
and Place.
3. Patient Vision Normal
for L 6/6, R 6/6
4. Skin color is Yellow
color and Poor skin
Turgor.
5. Extremities are Warm.
6. Patient not complain
for Oedema and
Dysponea
7. CRFT <2 seconds
8. Patient's Abdomen is
Distended and
9. Monitor Intake & Output
Chart.
8. Monitored and Charted
the intake and output.
9. Administer Analgesics As
Prescribed.
Morphine SC
10. Administered the
Intravenous Fluid as
Prescribed.
Hartman 50cc/hr.
2. Risk for ineffective
breathing pattern
related to intra
abdominal fluid
collection.
Maintain
Effective
breathing
Pattern
1. Monitor Respiration rate
depth and effort.
2. Auscultate breathe sound
and Crackles.
3. Monitor Vital Signs.
4. Keep patient head of bed
elevated position client on
side.
5. Encourage patient
frequent repositioning.
6. Encourage patient to
deep breathing and
coughing exercises.
1. Monitored Respiratory
rate, depth and effort.
2. Auscultated the breathing
sound and crackles sound.
3. Monitored and charted
vital signs.
4. Kept patient head elevated
position.
5. Encouraged patient for
repositioning.
6. Educated the patient for
Deep breathing and
coughing exercises.
After Nursing
interventions
patient
breathing
pattern is normal
Urine output since 3
days
Objective Data
1. Patient General
Appearance is good.
2. Patient oriented and
Alert for Time, Person,
and Place.
3. Patient Vision Normal
for L 6/6, R 6/6
4. Skin color is Yellow
color and Poor skin
Turgor.
5. Extremities are Warm.
6. Patient not complain
for Oedema and
Dysponea
7. CRFT <2 seconds
8. Patient's Abdomen is
Distended and
9. Monitor Intake & Output
Chart.
8. Monitored and Charted
the intake and output.
9. Administer Analgesics As
Prescribed.
Morphine SC
10. Administered the
Intravenous Fluid as
Prescribed.
Hartman 50cc/hr.
2. Risk for ineffective
breathing pattern
related to intra
abdominal fluid
collection.
Maintain
Effective
breathing
Pattern
1. Monitor Respiration rate
depth and effort.
2. Auscultate breathe sound
and Crackles.
3. Monitor Vital Signs.
4. Keep patient head of bed
elevated position client on
side.
5. Encourage patient
frequent repositioning.
6. Encourage patient to
deep breathing and
coughing exercises.
1. Monitored Respiratory
rate, depth and effort.
2. Auscultated the breathing
sound and crackles sound.
3. Monitored and charted
vital signs.
4. Kept patient head elevated
position.
5. Encouraged patient for
repositioning.
6. Educated the patient for
Deep breathing and
coughing exercises.
After Nursing
interventions
patient
breathing
pattern is normal
Tenderness when
palpating abdomen.
9. abdominal Girth of the
Patient is 60cm
10. Decreased Urinary
output, today 150ml in
7am to 1pm.
11. Patient in R side 18G
IV Cannula and cannula
site normal.
12. Patient Weight is
78kg.
13. Vital Signs
Temperature 98.2
F/Axi
Pulse 84/bpm
Respiration 24/bpm
BP 120/80mmHg
SPO2 98% on air
14. Blood Investigations
Results.
* ESR 24mm (1st Hour)
* Full Blood Count
7. Assess the patient
coughing and coughing out
secretion.
8. Introduce the
Physiotherapist for chest
exercises as prescribed.
9. Monitor ABG and SPO2
level if needed.
10 Administer Supplement
O2 therapy.
11. Prepared patient for the
Paracentesis Procedure.
7. Assessed patient coughing
Secretion its light yellow
color.
8. Administered oxygen via
the face mask.
9. Prepared and send for the
patient for the Radiology
Department for Paracentesis
Procedure.
3. Imbalanced
Nutrition less than
body Requirements
related to Anorexia,
Nausea and Vomiting.
Maintain
normal
Nutrition
level
1. Assess and Evaluate
client's risk for
malnutrition.
2. Assess patient like and
dislike food and drink.
3. Administer patient like
food, in small amount
frequent interval.
4. Encourage patient to
increase oral intake.
1. Assessed and Evaluate
client's risk for malnutrition.
2. Administered patient like
food, in small amount
frequent interval.
3. Encouraged patient to
increase oral intake.
4. Advised the patient for
limit the high salt food as
canned soups and
vegetables.
After nursing
patent get
normal diet
palpating abdomen.
9. abdominal Girth of the
Patient is 60cm
10. Decreased Urinary
output, today 150ml in
7am to 1pm.
11. Patient in R side 18G
IV Cannula and cannula
site normal.
12. Patient Weight is
78kg.
13. Vital Signs
Temperature 98.2
F/Axi
Pulse 84/bpm
Respiration 24/bpm
BP 120/80mmHg
SPO2 98% on air
14. Blood Investigations
Results.
* ESR 24mm (1st Hour)
* Full Blood Count
7. Assess the patient
coughing and coughing out
secretion.
8. Introduce the
Physiotherapist for chest
exercises as prescribed.
9. Monitor ABG and SPO2
level if needed.
10 Administer Supplement
O2 therapy.
11. Prepared patient for the
Paracentesis Procedure.
7. Assessed patient coughing
Secretion its light yellow
color.
8. Administered oxygen via
the face mask.
9. Prepared and send for the
patient for the Radiology
Department for Paracentesis
Procedure.
3. Imbalanced
Nutrition less than
body Requirements
related to Anorexia,
Nausea and Vomiting.
Maintain
normal
Nutrition
level
1. Assess and Evaluate
client's risk for
malnutrition.
2. Assess patient like and
dislike food and drink.
3. Administer patient like
food, in small amount
frequent interval.
4. Encourage patient to
increase oral intake.
1. Assessed and Evaluate
client's risk for malnutrition.
2. Administered patient like
food, in small amount
frequent interval.
3. Encouraged patient to
increase oral intake.
4. Advised the patient for
limit the high salt food as
canned soups and
vegetables.
After nursing
patent get
normal diet
WBC 6500cumm
RBC 4.25%
Hb% 12.8g/dl
PCV 37.5%
Plt Count 257,000
cumm
* Renal Profile
Na+ 134mmol/L
K+4.7mmol/L
Cl- 96mmol/L
Urea 23.54mg/dl
S. Creatinine 0.8mg/dl
Ca + 8.9mg/dl
Uric acid 2.8mg/dl
5. Assess and encourage
client eat, explain reasons
for the types of diet.
6. Advice the patient for
limit the high salt food as
canned soups and
vegetables.
7. Restrict intake of caffeine
and gas producing or spicy
and excessive hot or cold
foods.
8. Encourage and provide
frequent mouth care
especially before meals.
9. Administer Nutritional
Supplements as prescribed.
10. Administer IV fluids as
Prescribed.
11. Monitor Vital Signs.
12. Maintain Intake and
output.
5. Restricted intake of
caffeine and gas producing
or spicy and excessive hot or
cold foods.
6. Provided mouth care for
before meals.
7. Administered Nutritional
Foods such as Soup, juice
and Milk.
8. Administered Iv fluids
Hartmann 50cc/hr as
prescribed.
9. Monitor and Charted Vital
Signs.
10. Monitor and charted
intake and output chart.
RBC 4.25%
Hb% 12.8g/dl
PCV 37.5%
Plt Count 257,000
cumm
* Renal Profile
Na+ 134mmol/L
K+4.7mmol/L
Cl- 96mmol/L
Urea 23.54mg/dl
S. Creatinine 0.8mg/dl
Ca + 8.9mg/dl
Uric acid 2.8mg/dl
5. Assess and encourage
client eat, explain reasons
for the types of diet.
6. Advice the patient for
limit the high salt food as
canned soups and
vegetables.
7. Restrict intake of caffeine
and gas producing or spicy
and excessive hot or cold
foods.
8. Encourage and provide
frequent mouth care
especially before meals.
9. Administer Nutritional
Supplements as prescribed.
10. Administer IV fluids as
Prescribed.
11. Monitor Vital Signs.
12. Maintain Intake and
output.
5. Restricted intake of
caffeine and gas producing
or spicy and excessive hot or
cold foods.
6. Provided mouth care for
before meals.
7. Administered Nutritional
Foods such as Soup, juice
and Milk.
8. Administered Iv fluids
Hartmann 50cc/hr as
prescribed.
9. Monitor and Charted Vital
Signs.
10. Monitor and charted
intake and output chart.
4. Risk for fluid
volume deficit related
to vomiting and less
Urine Output
Maintain
normal
optimal
body fluids
1. Assess patient fluid status
and skin turgor.
2. Monitor intake and
output chart.
3. Daily weight measuring
and compare periodic
weight, as needed.
4. Administer IV fluids as
prescribed.
5. Assess and Record Vital
Signs.
6. Assess Skin color, Mucous
Membrane and CRFT.
7. Check the patient
Abdomen for Ascitis,
Oedema formation and
Measure Abdominal girth
as needed.
8. Encourage patient to
increase oral intake.
1. Assessed patient for fluid
status and skin turgor its
poor skin turgor.
2. Monitored and Charted
the intake and output chart.
3. Prescribed IV fluid
administered in 50cc/hr.
4. Monitored and Charted
Vital Signs.
5. Assessed patient CRFT <2
seconds.
6. Assessed patient ascitis
and Abdominal girth after
Paracentesis 40cm.
7. Encouraged patient to
increase oral intake as
frequently small interval.
8. Encouraged patient to
Ambulate and try passing
urine.
After Nursing
interventions
reduced vomiting
and patient have
normal Vital
Signs
volume deficit related
to vomiting and less
Urine Output
Maintain
normal
optimal
body fluids
1. Assess patient fluid status
and skin turgor.
2. Monitor intake and
output chart.
3. Daily weight measuring
and compare periodic
weight, as needed.
4. Administer IV fluids as
prescribed.
5. Assess and Record Vital
Signs.
6. Assess Skin color, Mucous
Membrane and CRFT.
7. Check the patient
Abdomen for Ascitis,
Oedema formation and
Measure Abdominal girth
as needed.
8. Encourage patient to
increase oral intake.
1. Assessed patient for fluid
status and skin turgor its
poor skin turgor.
2. Monitored and Charted
the intake and output chart.
3. Prescribed IV fluid
administered in 50cc/hr.
4. Monitored and Charted
Vital Signs.
5. Assessed patient CRFT <2
seconds.
6. Assessed patient ascitis
and Abdominal girth after
Paracentesis 40cm.
7. Encouraged patient to
increase oral intake as
frequently small interval.
8. Encouraged patient to
Ambulate and try passing
urine.
After Nursing
interventions
reduced vomiting
and patient have
normal Vital
Signs
9. Encourage patient to
frequently try to passing
urine.
10. Educate warn the
patient for risk of fluid
collection in the body and
its complications.
11. Administer Medication
as Prescribed, such as
Antiemetic, Antacid, and
Diuretics.
9. Administered Prescribed
medication, such as Antacid
(Pantocid 40mg), Diuretics
( Lasix 40mg, &
Spironolactone).
5. Risk for impaired
skin integrity related
to Poor skin turgor
and Accumulation of
bile in the Skin it
Evidenced by yellow
color skin
Maintain
skin
integrity in
normal
level
1. Assess patient skin color
and skin turgor.
2. Inspect patient skin
surface and pressure points
routinely.
3. Gently massage bony
prominences or areas and
Pressure point areas.
4. Provide bed bad and use
emollient lotion and limit
use of soap bathing.
1. Assessed patient skin color
and skin turgor.
2. Inspected patient skin
surface and pressure points
routinely for bedsores.
3. Administered pressure
point massages.
4. Administer emollient
lotion is back, thigh and
ankle such as baby cream
and Vaseline.
Maintained
normal skin
turgor
frequently try to passing
urine.
10. Educate warn the
patient for risk of fluid
collection in the body and
its complications.
11. Administer Medication
as Prescribed, such as
Antiemetic, Antacid, and
Diuretics.
9. Administered Prescribed
medication, such as Antacid
(Pantocid 40mg), Diuretics
( Lasix 40mg, &
Spironolactone).
5. Risk for impaired
skin integrity related
to Poor skin turgor
and Accumulation of
bile in the Skin it
Evidenced by yellow
color skin
Maintain
skin
integrity in
normal
level
1. Assess patient skin color
and skin turgor.
2. Inspect patient skin
surface and pressure points
routinely.
3. Gently massage bony
prominences or areas and
Pressure point areas.
4. Provide bed bad and use
emollient lotion and limit
use of soap bathing.
1. Assessed patient skin color
and skin turgor.
2. Inspected patient skin
surface and pressure points
routinely for bedsores.
3. Administered pressure
point massages.
4. Administer emollient
lotion is back, thigh and
ankle such as baby cream
and Vaseline.
Maintained
normal skin
turgor
5. Administer Morning and
Evening care to maintain
normal level of skin.
6. Encourage patient to
regular schedule while on
bed or chair and active or
passive range of motion
exercises.
7. Elevate the edematous
lower part if patient feel
comfort.
8. Keep linen dry and free of
wrinkles.
9. Position change the
patient 4 hourly as needed.
10. Encourage patient to
maintain Personal Hygiene
and perineal care following
urination and bowel
opening.
5. Provide morning and
evening care for maintain
normal skin care and
provide comfort.
6. Encouraged patient for
active and passive range of
motion.
7. Elevated patient
edematous leg part to
reduce edema.
8. Changed bed linen, kept
linen dry and free from
wrinkles.
9. Frequently change
position for prevent bed
sores.
10. Encouraged patient for
personal hygiene and
perineal care following
urination and bowel
opening.
Evening care to maintain
normal level of skin.
6. Encourage patient to
regular schedule while on
bed or chair and active or
passive range of motion
exercises.
7. Elevate the edematous
lower part if patient feel
comfort.
8. Keep linen dry and free of
wrinkles.
9. Position change the
patient 4 hourly as needed.
10. Encourage patient to
maintain Personal Hygiene
and perineal care following
urination and bowel
opening.
5. Provide morning and
evening care for maintain
normal skin care and
provide comfort.
6. Encouraged patient for
active and passive range of
motion.
7. Elevated patient
edematous leg part to
reduce edema.
8. Changed bed linen, kept
linen dry and free from
wrinkles.
9. Frequently change
position for prevent bed
sores.
10. Encouraged patient for
personal hygiene and
perineal care following
urination and bowel
opening.
Nursing Assessment Nursing Diagnosis Goal Planning Nursing Interventions Evaluation
21/02/2013 7.30am
Thursday
Subject Data
Mr. W A P Ranjith
Verbalized I have
1. Vomiting 3times in
morning its red color
with mixed watery.
2. Difficulty breathing
since morning 6am
3. Abdominal distention
and Discomfort
4. B/L Legs below Knee
Oedema
1. Risk for bleeding
related to development
of esophageal varices
it evidenced by
vomiting with blood.
Maintain
homeostasis
with absence of
GI bleeding
1. Assess for signs and
symptoms of GI bleeding.
2. Reassure the patient &
assess Vomitus for blood
stain.
3. Provide psychology
support.
4. Position the patient.
5. Assess & Monitor the
Vital Signs.
6. Assess for level of
Consciousness.
7. Assess for patient Full
Blood Count report as
prescribed.
8. Encourage patient to
increase oral intake.
9. Educate patient for
avoid irritable food in
1. Assessed for signs and
symptoms of GI bleeding.
2. Reassured the patient and
assed vomitus slight blood
stain in vomitus.
3. Position the patient in semi
fowler’s position.
4. Assessed & Charted Vital
signs.
5. Assessed patient LOC for
patient Conscious and
Rationale.
6. Assessed patient Blood
tests such as S. creatinine,
CRP, LFT, PT/INR, ESR, Lipid
Profile, and FBS.
7. Encouraged patient for
increase oral intake and
avoid irritable food in mouth.
8. Monitored and charted
intake and output chart.
After nursing
intervention
reduced
vomiting
21/02/2013 7.30am
Thursday
Subject Data
Mr. W A P Ranjith
Verbalized I have
1. Vomiting 3times in
morning its red color
with mixed watery.
2. Difficulty breathing
since morning 6am
3. Abdominal distention
and Discomfort
4. B/L Legs below Knee
Oedema
1. Risk for bleeding
related to development
of esophageal varices
it evidenced by
vomiting with blood.
Maintain
homeostasis
with absence of
GI bleeding
1. Assess for signs and
symptoms of GI bleeding.
2. Reassure the patient &
assess Vomitus for blood
stain.
3. Provide psychology
support.
4. Position the patient.
5. Assess & Monitor the
Vital Signs.
6. Assess for level of
Consciousness.
7. Assess for patient Full
Blood Count report as
prescribed.
8. Encourage patient to
increase oral intake.
9. Educate patient for
avoid irritable food in
1. Assessed for signs and
symptoms of GI bleeding.
2. Reassured the patient and
assed vomitus slight blood
stain in vomitus.
3. Position the patient in semi
fowler’s position.
4. Assessed & Charted Vital
signs.
5. Assessed patient LOC for
patient Conscious and
Rationale.
6. Assessed patient Blood
tests such as S. creatinine,
CRP, LFT, PT/INR, ESR, Lipid
Profile, and FBS.
7. Encouraged patient for
increase oral intake and
avoid irritable food in mouth.
8. Monitored and charted
intake and output chart.
After nursing
intervention
reduced
vomiting
Objective Data
1. Patient General
Appearance ill looking.
2. Patient Restlessness.
3. Skin color is yellow
color and poor skin
turgor
4. patient Weight 78kg
5. Patient Vision ability
normal R 6/6, L 6/6.
6. Patient on 18G IV
Cannula in R hand,
cannula site normal, no
signs of infection.
7. IV fluid progress in
20ml/hr
8. Patient in Difficulty in
Breathing, chest depth is
increase.
9. Abdomen distended ,
Abdominal girth 60cm
mouth.
10. Monitor & Maintain
intake and output chart.
11. Administer IV fluid as
prescribed.
12. Administer
medication as prescribed
such as Antiemetic &
Vitamins.
13. Administer stool
softeners to reduce
bleeding with rectum.
9. Administered prescribed IV
Fluid in 20ml/hr.
10. Administered Prescribed
stat dose Antiemetic
Doperidone 10mg stat.
11. Administered prescribed
stool softeners Lactulose 30cc
tds.
2. Excess fluid volume
related to
accumulation of fluid
in the body, evidenced
by B/L leg edema and
decreased urine
output.
Maintain
optimal body
fluid.
1. Assess patient for signs
of fluid overload.
2. Elevate the edematous
part.
3. Monitor Vital Signs 4
hourly.
4. Measure the patient
Weight daily as needed.
5. Assess for urinary
catheter patency and
1. Assessed patient for signs
of fluid over load as ascitis,
and Leg edema.
2. Elevated patient
edematous part such as both
legs to reduce edema.
3. Monitor and Charted Vital
signs.
4. Assessed patient urinary
catheter patency, no signs of
Slightly leg
Edema
reduced
1. Patient General
Appearance ill looking.
2. Patient Restlessness.
3. Skin color is yellow
color and poor skin
turgor
4. patient Weight 78kg
5. Patient Vision ability
normal R 6/6, L 6/6.
6. Patient on 18G IV
Cannula in R hand,
cannula site normal, no
signs of infection.
7. IV fluid progress in
20ml/hr
8. Patient in Difficulty in
Breathing, chest depth is
increase.
9. Abdomen distended ,
Abdominal girth 60cm
mouth.
10. Monitor & Maintain
intake and output chart.
11. Administer IV fluid as
prescribed.
12. Administer
medication as prescribed
such as Antiemetic &
Vitamins.
13. Administer stool
softeners to reduce
bleeding with rectum.
9. Administered prescribed IV
Fluid in 20ml/hr.
10. Administered Prescribed
stat dose Antiemetic
Doperidone 10mg stat.
11. Administered prescribed
stool softeners Lactulose 30cc
tds.
2. Excess fluid volume
related to
accumulation of fluid
in the body, evidenced
by B/L leg edema and
decreased urine
output.
Maintain
optimal body
fluid.
1. Assess patient for signs
of fluid overload.
2. Elevate the edematous
part.
3. Monitor Vital Signs 4
hourly.
4. Measure the patient
Weight daily as needed.
5. Assess for urinary
catheter patency and
1. Assessed patient for signs
of fluid over load as ascitis,
and Leg edema.
2. Elevated patient
edematous part such as both
legs to reduce edema.
3. Monitor and Charted Vital
signs.
4. Assessed patient urinary
catheter patency, no signs of
Slightly leg
Edema
reduced
10. CRFT < 2 Seconds
11. Patient on NG tube is
inserted yesterday night.
12. Patient on Urinary
Catheter is inserted
yesterday night.
13. Urinary catheter
normally drains and
urine color is dark color
and odor.
14. Patient
Psychologically confused
and worried about his
disease.
15. Vital Signs
Temper 98.6 F/Axilla
Pulse 90/bpm
Resp 26/bpm
BP 130/90mmHg
SpO2 98% with O2
16. Blood Investigation
Results
* S. Creatinine 1.1mg/dl
urine flow.
6. Assess NG tube
position and administer
Fluid prescribed time
interval.
7. Encourage patient to
take rest.
8. Educate patient for
Exercise of Extremities.
9. Monitor Serum
Electrolyte level as
needed
10. Educate patient for
Avoid & Restrict Sodium
and Potassium contain
diet as indicated.
11. Administer salt free
diet and juice.
12. Administer Diuretic
as prescribed.
heamaturia and infection.
5. Assessed NG tube position
and Administered liquid food
prescribed interval.
6. Encouraged patient to take
rest.
7. Educated patient for Leg
Exercises.
8. Avoided sodium and
potassium contain foods.
9. Administered salt free diet.
10. Administered prescribed
Diuretic.
*Frusimide 40mg bd
*Spironolactone mane
11. Patient on NG tube is
inserted yesterday night.
12. Patient on Urinary
Catheter is inserted
yesterday night.
13. Urinary catheter
normally drains and
urine color is dark color
and odor.
14. Patient
Psychologically confused
and worried about his
disease.
15. Vital Signs
Temper 98.6 F/Axilla
Pulse 90/bpm
Resp 26/bpm
BP 130/90mmHg
SpO2 98% with O2
16. Blood Investigation
Results
* S. Creatinine 1.1mg/dl
urine flow.
6. Assess NG tube
position and administer
Fluid prescribed time
interval.
7. Encourage patient to
take rest.
8. Educate patient for
Exercise of Extremities.
9. Monitor Serum
Electrolyte level as
needed
10. Educate patient for
Avoid & Restrict Sodium
and Potassium contain
diet as indicated.
11. Administer salt free
diet and juice.
12. Administer Diuretic
as prescribed.
heamaturia and infection.
5. Assessed NG tube position
and Administered liquid food
prescribed interval.
6. Encouraged patient to take
rest.
7. Educated patient for Leg
Exercises.
8. Avoided sodium and
potassium contain foods.
9. Administered salt free diet.
10. Administered prescribed
Diuretic.
*Frusimide 40mg bd
*Spironolactone mane
* CRP 34.2mg/L
3. Altered breathing
pattern related to
decreased lung
expansion and
accumulated secretion
it shows defaulting
Maintain
normal
breathing
pattern
1. Reassure the patient.
2. Provide psychological
support.
3. Position the patient in
semi fowler’s position.
4. Administer Oxygen as
needed.
5. Monitor Vital signs
especially patient
respiratory rate and
depth.
6. Assess patient
respiratory pattern for
using accessory muscle
for respiration.
7. Maintain a calm
attitude environment.
8. Encourage patient
deep breathing exercises.
9. Encourage patient for
express feeling.
10. Administer
Nebulization as
1. Reassured the patient.
2. Provided psychological
support and talked with
patient friendly.
3. Position the patient in semi
fowler’s position to reduce
difficulty breathing and
abdominal distention.
4. Administered Oxygen via
the face mask.
5. Monitored and charted
vital signs.
6. Assessed Respiratory rate,
depth and pattern for using
accessory muscle for
breathing.
7. Arranged calm and quiet
environment.
8. Encouraged patient for
deep breathing exercises.
9. Encouraged patient for
express feelings.
10. Administer Prescribed
medications.
After
Nursing
interventions
patient
breathing
pattern is
normal it
shown
normal
respiratory
rate and
depth.
3. Altered breathing
pattern related to
decreased lung
expansion and
accumulated secretion
it shows defaulting
Maintain
normal
breathing
pattern
1. Reassure the patient.
2. Provide psychological
support.
3. Position the patient in
semi fowler’s position.
4. Administer Oxygen as
needed.
5. Monitor Vital signs
especially patient
respiratory rate and
depth.
6. Assess patient
respiratory pattern for
using accessory muscle
for respiration.
7. Maintain a calm
attitude environment.
8. Encourage patient
deep breathing exercises.
9. Encourage patient for
express feeling.
10. Administer
Nebulization as
1. Reassured the patient.
2. Provided psychological
support and talked with
patient friendly.
3. Position the patient in semi
fowler’s position to reduce
difficulty breathing and
abdominal distention.
4. Administered Oxygen via
the face mask.
5. Monitored and charted
vital signs.
6. Assessed Respiratory rate,
depth and pattern for using
accessory muscle for
breathing.
7. Arranged calm and quiet
environment.
8. Encouraged patient for
deep breathing exercises.
9. Encouraged patient for
express feelings.
10. Administer Prescribed
medications.
After
Nursing
interventions
patient
breathing
pattern is
normal it
shown
normal
respiratory
rate and
depth.
prescribed.
11. Administer
Medication as prescribed.
4. Disturbed body
image related to
altered physical
appearance.
Understanding
changes &
acceptance of
self in the
present
situation.
1. Reassure the patient.
2. Provide psychological
support.
3. Discuss with patient
situation and encourage
verbalization of fears and
concerns.
4. Explain relationship
between nature of
disease and symptoms.
5. Support and encourage
client, provide care with
a positive friendly
attitude.
6. Encourage relation to
understanding patient
situation and participate
in care.
7. Assist client to cope
1. Reassured the patient.
2. Provided the psychological
support to the patient.
3. Discussed with patient
situation and encouraged
verbalized of fears and
concerns.
4. Explained relationship
between nature of disease
and symptoms.
5. Supported and Encouraged
client, provided care with a
positive friendly attitude.
6. Encouraged and Explained
family members to
understanding patient
situation and participate
patient care.
8. Assessed client to cope with
Patient
normally
adjusted his
condition.
11. Administer
Medication as prescribed.
4. Disturbed body
image related to
altered physical
appearance.
Understanding
changes &
acceptance of
self in the
present
situation.
1. Reassure the patient.
2. Provide psychological
support.
3. Discuss with patient
situation and encourage
verbalization of fears and
concerns.
4. Explain relationship
between nature of
disease and symptoms.
5. Support and encourage
client, provide care with
a positive friendly
attitude.
6. Encourage relation to
understanding patient
situation and participate
in care.
7. Assist client to cope
1. Reassured the patient.
2. Provided the psychological
support to the patient.
3. Discussed with patient
situation and encouraged
verbalized of fears and
concerns.
4. Explained relationship
between nature of disease
and symptoms.
5. Supported and Encouraged
client, provided care with a
positive friendly attitude.
6. Encouraged and Explained
family members to
understanding patient
situation and participate
patient care.
8. Assessed client to cope with
Patient
normally
adjusted his
condition.
with change in
appearance, suggest
suitable clothing.
8. Introduce counselor
for Divert patient
worried mind.
9. Keep and observation
of patient in out of bed.
10. Educate the patient
about effect of Alcohol
consumption.
changes in appearance,
suggested suitable clothing.
9. Introduced Psychological
Counselor to divert patient
and family worried mind.
10. Kept and Observed
patient out of bed.
11. Educated patient for
effect of Alcohol and Smoking
consumption.
5. Acute confusion
related to disease
condition.
Maintain usual
level of
Consciousness
1. Observe patient for
changes in behavior,
drowsiness, slowing or
slurring speech and
confusion.
2. Provide psychological
support and talk with
friendly.
3. Keep the patient rest
and evaluate sleep and
rest schedule.
4. Maintain a pleasant,
1. Observed patient for
behavioral changes, patient
in drowsy and slight
restlessness.
2. Provided psychological
support and talked with
friendly.
3. Kept patient rest and
scheduled sleep time.
4. Maintained a pleasant,
quiet environment and
Patient
diverted in
his disease
condition
and satisfied
his nature of
disease.
appearance, suggest
suitable clothing.
8. Introduce counselor
for Divert patient
worried mind.
9. Keep and observation
of patient in out of bed.
10. Educate the patient
about effect of Alcohol
consumption.
changes in appearance,
suggested suitable clothing.
9. Introduced Psychological
Counselor to divert patient
and family worried mind.
10. Kept and Observed
patient out of bed.
11. Educated patient for
effect of Alcohol and Smoking
consumption.
5. Acute confusion
related to disease
condition.
Maintain usual
level of
Consciousness
1. Observe patient for
changes in behavior,
drowsiness, slowing or
slurring speech and
confusion.
2. Provide psychological
support and talk with
friendly.
3. Keep the patient rest
and evaluate sleep and
rest schedule.
4. Maintain a pleasant,
1. Observed patient for
behavioral changes, patient
in drowsy and slight
restlessness.
2. Provided psychological
support and talked with
friendly.
3. Kept patient rest and
scheduled sleep time.
4. Maintained a pleasant,
quiet environment and
Patient
diverted in
his disease
condition
and satisfied
his nature of
disease.
quiet environment and
approach slow, calm
manner.
5. Discuss with patient in
current situation and
future expectation of
disease and treatment
method.
6. Identify and provide
for safety needs, such as
bed in low position and
put side rails.
7. Monitor vital signs.
8. Administer IV fluids
and Nutritional food
supplements.
9. Provide continuity of
care for morning care,
evening care and mouth
care.
approach slow, calm manner.
5. Discussed patient current
situation and future
expectation of disease and
treatment method.
6. Provided Safety measures,
such as bed in low position,
and pt side rails every time.
7. Monitored and charted
vital signs.
8. Administered IV fluids and
Nutritional Food
supplements.
9. Provided continuity care of
Morning, Evening and Mouth
Care.
10. Administered Medication
in correct interval.
11. Encouraged patient for
express feelings.
approach slow, calm
manner.
5. Discuss with patient in
current situation and
future expectation of
disease and treatment
method.
6. Identify and provide
for safety needs, such as
bed in low position and
put side rails.
7. Monitor vital signs.
8. Administer IV fluids
and Nutritional food
supplements.
9. Provide continuity of
care for morning care,
evening care and mouth
care.
approach slow, calm manner.
5. Discussed patient current
situation and future
expectation of disease and
treatment method.
6. Provided Safety measures,
such as bed in low position,
and pt side rails every time.
7. Monitored and charted
vital signs.
8. Administered IV fluids and
Nutritional Food
supplements.
9. Provided continuity care of
Morning, Evening and Mouth
Care.
10. Administered Medication
in correct interval.
11. Encouraged patient for
express feelings.
Assessment Nursing Diagnosis Goal Planning Nursing Interventions Evaluation
22/02/2013,
02.00pm
Subjective Data
Mr. Ranjith verbalized
1. Fever since morning
2. Nausea
3. Tiredness due to
3days
4. Loss of Appetite due
to 10 days
Objective Data
1. Patient general
appearance is lethargy
and weakness.
2. Patient Conscious,
Rationale, and Alert to
1. Hyperthermia
related to infective
process
Maintain
normal body
temperature
1. Monitor QHT
2. Assess the patient for
chills and diaphoresis.
3. Monitor Vital signs.
4. Monitor and Adjust the
room temperature .
5. Apply Tepid sponge
bath if needed.
6. Provide cooling blanket
as needed.
7. Administer Antipyretic
as prescribed.
8. Administer Antibiotic as
prescribed.
9. Administer Cool drink.
10. Raise the bed side rails
of all time.
1. Monitored and maintained
the QHT chart.
2. Assessed patient chills and
diaphoresis.
3. Monitor and charted Vital
signs.
4. Adjusted the room
temperature in 67'C
5. Administered Prescribed
Antipyretic.
Paracetamol 1g
6. Administered Prescribed
Antibiotic.
IV Levofloxacin 500mg
7. Administered Slight cool
orange juice.
8. Raised patient bed rails to
prevent falling.
After nursing
interventions
patient body
temperature
was reduced
in
98.5F/axilla
22/02/2013,
02.00pm
Subjective Data
Mr. Ranjith verbalized
1. Fever since morning
2. Nausea
3. Tiredness due to
3days
4. Loss of Appetite due
to 10 days
Objective Data
1. Patient general
appearance is lethargy
and weakness.
2. Patient Conscious,
Rationale, and Alert to
1. Hyperthermia
related to infective
process
Maintain
normal body
temperature
1. Monitor QHT
2. Assess the patient for
chills and diaphoresis.
3. Monitor Vital signs.
4. Monitor and Adjust the
room temperature .
5. Apply Tepid sponge
bath if needed.
6. Provide cooling blanket
as needed.
7. Administer Antipyretic
as prescribed.
8. Administer Antibiotic as
prescribed.
9. Administer Cool drink.
10. Raise the bed side rails
of all time.
1. Monitored and maintained
the QHT chart.
2. Assessed patient chills and
diaphoresis.
3. Monitor and charted Vital
signs.
4. Adjusted the room
temperature in 67'C
5. Administered Prescribed
Antipyretic.
Paracetamol 1g
6. Administered Prescribed
Antibiotic.
IV Levofloxacin 500mg
7. Administered Slight cool
orange juice.
8. Raised patient bed rails to
prevent falling.
After nursing
interventions
patient body
temperature
was reduced
in
98.5F/axilla
Time, Person, and
Place.
3. Patient vision ability
normal.
4. Skin color is normal,
no itching and rashes.
5. No Allergies.
6.Patient sad mood and
worried about his
disease condition.
7. No respiratory
problem in patient.
8. Reduced extremities
edema.
9. CRFT <2 seconds.
10. Nails and
Extremities normal.
11. Peripheries are
warm.
12. Patient in 18G IV
cannula in L hand.
11. Monitor intake and
output chart.
12. Administer IV fluid as
prescribed.
13. Provide high calorie
diet as needed.
14. Educate the patient
for signs for Hypothermia.
9. Monitor and charted the
intake and output chart.
10. Administered prescribed
IV fluids.
11. Educated the patient for
signs of Hypothermia.
2. Imbalanced
Nutrition less than
body requirement
related to Loss of
appetite and Nausea
Maintain
normal body
nutrition level
1. Assess the patient for
like and dislike.
2. Administer the like food
or drink the patient.
3. Administer the fluid
drink 3 hourly.
4. Administer Nutritional
supplements and IV fluid
as prescribed.
5. Maintain intake and
output chart.
6. Educate the patient
1. Assessed the patient like
and dislike food.
2. Administered fluid via the
NG tube 3 hourly such as drink
and soup.
3. Educated the patient about
nutritional supplement.
4. Administer IV fluid as
prescribed.
5. Maintained intake and
output chart.
6. Educated the family about
Patient
satisfied
about
nursing care
Place.
3. Patient vision ability
normal.
4. Skin color is normal,
no itching and rashes.
5. No Allergies.
6.Patient sad mood and
worried about his
disease condition.
7. No respiratory
problem in patient.
8. Reduced extremities
edema.
9. CRFT <2 seconds.
10. Nails and
Extremities normal.
11. Peripheries are
warm.
12. Patient in 18G IV
cannula in L hand.
11. Monitor intake and
output chart.
12. Administer IV fluid as
prescribed.
13. Provide high calorie
diet as needed.
14. Educate the patient
for signs for Hypothermia.
9. Monitor and charted the
intake and output chart.
10. Administered prescribed
IV fluids.
11. Educated the patient for
signs of Hypothermia.
2. Imbalanced
Nutrition less than
body requirement
related to Loss of
appetite and Nausea
Maintain
normal body
nutrition level
1. Assess the patient for
like and dislike.
2. Administer the like food
or drink the patient.
3. Administer the fluid
drink 3 hourly.
4. Administer Nutritional
supplements and IV fluid
as prescribed.
5. Maintain intake and
output chart.
6. Educate the patient
1. Assessed the patient like
and dislike food.
2. Administered fluid via the
NG tube 3 hourly such as drink
and soup.
3. Educated the patient about
nutritional supplement.
4. Administer IV fluid as
prescribed.
5. Maintained intake and
output chart.
6. Educated the family about
Patient
satisfied
about
nursing care
13. Paracentesis
procedure done on
yesterday night, 500ml
peritoneal fluid
removed.
14. Patient feel
comfortably of without
abdominal distention.
Abdominal girth 45cm
15. Urinary Catheter
removed today
morning, no bleeding
from urethra after
removing catheter.
16. Patient urinary
sensation +.
17. Reduced patient
Scrotal edema.
18. Morning Bowel
opened normally, Dark
green color and no
blood stain.
19. No headache and
about nutritional Diabetic
diet.
7. Educate the family
members importance of
nutrition.
8. Assess the vital signs.
importance nutrition.
6. Assessed and charted vital
signs.
7. Educated the patient
simple relaxation techniques.
3. Anxiety related to
disease condition
Reduce Anxiety
1. Reassure the patient.
2. Provide psychological
support.
3. Communicate with
friendly and kindly.
4. Change the patient
position frequently.
5. Encourage the patient
for deep breathing and
exercises.
6. Educate simple
relaxation techniques.
7. Introduce the hospital
staff and environment for
the patient.
1. Reassured the patient.
2. Provided psychological
support to the patient to
reduce the anxiety.
4. Communicated with patient
friendly and kindly, to relieve
the anxiety.
5. Frequently changed patient
position.
6. Encouraged the patient for
deep breathing and exercises.
7. Educated the patient for
simple relaxation technique.
8. Introduced the hospital
environment and ward staff.
9. Done the some divertional
Patient
satisfied and
gained some
knowledge
about his
disease
condition
procedure done on
yesterday night, 500ml
peritoneal fluid
removed.
14. Patient feel
comfortably of without
abdominal distention.
Abdominal girth 45cm
15. Urinary Catheter
removed today
morning, no bleeding
from urethra after
removing catheter.
16. Patient urinary
sensation +.
17. Reduced patient
Scrotal edema.
18. Morning Bowel
opened normally, Dark
green color and no
blood stain.
19. No headache and
about nutritional Diabetic
diet.
7. Educate the family
members importance of
nutrition.
8. Assess the vital signs.
importance nutrition.
6. Assessed and charted vital
signs.
7. Educated the patient
simple relaxation techniques.
3. Anxiety related to
disease condition
Reduce Anxiety
1. Reassure the patient.
2. Provide psychological
support.
3. Communicate with
friendly and kindly.
4. Change the patient
position frequently.
5. Encourage the patient
for deep breathing and
exercises.
6. Educate simple
relaxation techniques.
7. Introduce the hospital
staff and environment for
the patient.
1. Reassured the patient.
2. Provided psychological
support to the patient to
reduce the anxiety.
4. Communicated with patient
friendly and kindly, to relieve
the anxiety.
5. Frequently changed patient
position.
6. Encouraged the patient for
deep breathing and exercises.
7. Educated the patient for
simple relaxation technique.
8. Introduced the hospital
environment and ward staff.
9. Done the some divertional
Patient
satisfied and
gained some
knowledge
about his
disease
condition
Confusion signs.
20. Patient on NG tube
3 hourly feeding to be
done.
21. Vital signs
Temperature
102F/Axilla
Pulse 88/bpm
Respiration 26/bpm
BP 130/80mmHg
Spo2 96% on air
21. Blood Investigation
Report Findings
* FBC
WBC 7800cumm
RBC 2.95%
Hb% 10.4g/dl
PCV 30.5%
Plt count
234,000cumm
*CRP 28.4mg/L
*Liver Profile
Total Protein 7.2g/dl
8. Encourage the patient
for express feelings.
9. Divert the patient
anxiety mind such as TV,
Radio and other activities.
10. Provide body wash to
increase comfort.
11. Educate the patient
for about his disease
condition, causes,
pathophysiology, and
treatment method.
12. Explain the patient for
doing every procedure
decrease fear.
13. Provide proper
information about drug
side effects of drugs.
activities to reduce anxiety
such as TV, and Radio.
10. Provided evening care of
the patient to induce comfort.
11. Educated the patient
about his disease condition
such as causes,
pathophysiology, and
treatment methods.
12. Before doing every
procedure explained briefly, to
reduce fear.
13. Provided proper
information about drug side
effects and interactions.
4. Deficient knowledge
regarding disease
condition, treatment,
and prognosis.
Increase
patient
knowledge
regarding
1. Educate the patient for
his disease condition, such
as pathophysiology,
clinical manifestation and
1. Educated the patient for his
disease condition such as
pathophysiology ,clinical
manifestation and treatment
Patient
satisfied and
gained some
knowledge
20. Patient on NG tube
3 hourly feeding to be
done.
21. Vital signs
Temperature
102F/Axilla
Pulse 88/bpm
Respiration 26/bpm
BP 130/80mmHg
Spo2 96% on air
21. Blood Investigation
Report Findings
* FBC
WBC 7800cumm
RBC 2.95%
Hb% 10.4g/dl
PCV 30.5%
Plt count
234,000cumm
*CRP 28.4mg/L
*Liver Profile
Total Protein 7.2g/dl
8. Encourage the patient
for express feelings.
9. Divert the patient
anxiety mind such as TV,
Radio and other activities.
10. Provide body wash to
increase comfort.
11. Educate the patient
for about his disease
condition, causes,
pathophysiology, and
treatment method.
12. Explain the patient for
doing every procedure
decrease fear.
13. Provide proper
information about drug
side effects of drugs.
activities to reduce anxiety
such as TV, and Radio.
10. Provided evening care of
the patient to induce comfort.
11. Educated the patient
about his disease condition
such as causes,
pathophysiology, and
treatment methods.
12. Before doing every
procedure explained briefly, to
reduce fear.
13. Provided proper
information about drug side
effects and interactions.
4. Deficient knowledge
regarding disease
condition, treatment,
and prognosis.
Increase
patient
knowledge
regarding
1. Educate the patient for
his disease condition, such
as pathophysiology,
clinical manifestation and
1. Educated the patient for his
disease condition such as
pathophysiology ,clinical
manifestation and treatment
Patient
satisfied and
gained some
knowledge
Albumin 3.0g/dl
Globulin 5.4g/dl
A/G ratio 0.5
Alkaline Phospata
122U/L
ALT(SGPT) 38U/L
AST(SGOT) 42U/L
disease
condition
treatment methods.
2. Educate the patient
about causes of cirrhosis.
3. Teach the patient
about avoid the risk
factors and worsening
factors.
4. Educate the patient
about maintain normal
life style.
5.Educate the patient
about warning signs of
severe conditions.
6. Educate the family
members about cirrhosis
disease condition.
7. Encourage the patient
for consult the Dietitian.
modalities.
2. Educated the patient about
causes of cirrhosis.
3. Encouraged the patient for
avoid risk factors and
worsening factors.
4. Encouraged the patient for
maintain normal life style
such as regular exercise,
restrict sodium intake, and
dietary management.
5. Educated the patient for
worsening signs.
6. Educated the family
members for cirrhosis and
how to care a cirrhosis patient
in home.
about his
disease
condition.
Globulin 5.4g/dl
A/G ratio 0.5
Alkaline Phospata
122U/L
ALT(SGPT) 38U/L
AST(SGOT) 42U/L
disease
condition
treatment methods.
2. Educate the patient
about causes of cirrhosis.
3. Teach the patient
about avoid the risk
factors and worsening
factors.
4. Educate the patient
about maintain normal
life style.
5.Educate the patient
about warning signs of
severe conditions.
6. Educate the family
members about cirrhosis
disease condition.
7. Encourage the patient
for consult the Dietitian.
modalities.
2. Educated the patient about
causes of cirrhosis.
3. Encouraged the patient for
avoid risk factors and
worsening factors.
4. Encouraged the patient for
maintain normal life style
such as regular exercise,
restrict sodium intake, and
dietary management.
5. Educated the patient for
worsening signs.
6. Educated the family
members for cirrhosis and
how to care a cirrhosis patient
in home.
about his
disease
condition.
Assessment Nursing Diagnosis Goal Planning Nursing Interventions Evaluation
23/02/2013 9.30am
Patient was
Discharged at 8am
Subjective Data
Mr. Ranjith 58yrs male
patient verbalized "I
am"
1. Feeling good.
2. Loss of Appetite and
loss of food taste
sensation.
Deficient Knowledge
regarding self and
Home care activities.
Educate self
and home care
interventions.
1. Educate the patient
about self and home care
activities of the cirrhosis.
2. Educate the patient
about how manage
symptoms in home
setting.
3. Follow up Care.
1.Educated the patient for stop
drinking alcohol if you stop all
alcohol intake, you may slow the
disease and feel better.
2. Avoid unnecessary medication
that may be harmful to your liver,
such as PCM or your kidneys such
as ibuprofen.
3. A low sodium diet helps relieve
that fluid retention problem.
4. Eat a balanced diet with
adequate calories and protein.
5. To do regular simple Exercises
to help maintain proper posture.
Patient
satisfied
the nursing
care.
23/02/2013 9.30am
Patient was
Discharged at 8am
Subjective Data
Mr. Ranjith 58yrs male
patient verbalized "I
am"
1. Feeling good.
2. Loss of Appetite and
loss of food taste
sensation.
Deficient Knowledge
regarding self and
Home care activities.
Educate self
and home care
interventions.
1. Educate the patient
about self and home care
activities of the cirrhosis.
2. Educate the patient
about how manage
symptoms in home
setting.
3. Follow up Care.
1.Educated the patient for stop
drinking alcohol if you stop all
alcohol intake, you may slow the
disease and feel better.
2. Avoid unnecessary medication
that may be harmful to your liver,
such as PCM or your kidneys such
as ibuprofen.
3. A low sodium diet helps relieve
that fluid retention problem.
4. Eat a balanced diet with
adequate calories and protein.
5. To do regular simple Exercises
to help maintain proper posture.
Patient
satisfied
the nursing
care.
3. Patient asked about
home care measures
and Drugs side effects.
Objective Data
1. Patient general
appearance is good.
2. Patient conscious ,
rationale and Alert to
Time, Place and Person.
3. Patient happy mood
in his discharge.
4. Skin color is normal
and no itching and
rashes.
5. Normal vision View.
6. Peripheries are warm.
7. No Extremities
edema.
8. IV cannula removed
and no bleeding in
cannula site.
6. Maintain optimal nutrition
level forget nutritional diet and
nutritional supplements such as
Vitamins A, B complex, D and K,
its help to reduce the Anemia.
7. Educated the patient deep
breathing and extremity
exercises.
8. Educated the patient about
drugs, such as side effects of
drugs.
9. Encouraged patient for proper
elimination habit.
10. Educate the patient about
worsening signs of his disease
condition. and that how to
manage and prevent further
damage.
11. Encouraged the patient
express the feelings.
12. Educated the patients
relatives and family members for
how to care cirrhosis patient in
home care measures
and Drugs side effects.
Objective Data
1. Patient general
appearance is good.
2. Patient conscious ,
rationale and Alert to
Time, Place and Person.
3. Patient happy mood
in his discharge.
4. Skin color is normal
and no itching and
rashes.
5. Normal vision View.
6. Peripheries are warm.
7. No Extremities
edema.
8. IV cannula removed
and no bleeding in
cannula site.
6. Maintain optimal nutrition
level forget nutritional diet and
nutritional supplements such as
Vitamins A, B complex, D and K,
its help to reduce the Anemia.
7. Educated the patient deep
breathing and extremity
exercises.
8. Educated the patient about
drugs, such as side effects of
drugs.
9. Encouraged patient for proper
elimination habit.
10. Educate the patient about
worsening signs of his disease
condition. and that how to
manage and prevent further
damage.
11. Encouraged the patient
express the feelings.
12. Educated the patients
relatives and family members for
how to care cirrhosis patient in
9.Patient discharge with
NG tube.
10.Urine output is good
and patient urine pass
with sensation.
11. Morning Bowel
opened without
lactulose.
12. Patient ambulate
morning without
restlessness and
discomfort.
13. Vital Signs
Temperature
98.6F/Axilla
Pulse 84/bpm
Respiration 24/bpm
BP 120/85mmHg
home settings.
13. Encouraged patient for get
adequate food and fluids as
frequent interval.
14. Encouraged the patient to
seek frequent medical follow up
from a physician and take
medicine on time.
15. Visits from a monthly clinics
to monitor the patient progress.
16. At lastly submitted the
patient Diagnosis card Drugs.
NG tube.
10.Urine output is good
and patient urine pass
with sensation.
11. Morning Bowel
opened without
lactulose.
12. Patient ambulate
morning without
restlessness and
discomfort.
13. Vital Signs
Temperature
98.6F/Axilla
Pulse 84/bpm
Respiration 24/bpm
BP 120/85mmHg
home settings.
13. Encouraged patient for get
adequate food and fluids as
frequent interval.
14. Encouraged the patient to
seek frequent medical follow up
from a physician and take
medicine on time.
15. Visits from a monthly clinics
to monitor the patient progress.
16. At lastly submitted the
patient Diagnosis card Drugs.
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