CASE PRESENTATION Liver Cirrhosis

Hepatic Encephalopathy Esophageal Varices

Chichan

Nico

April

Joseph
Marj

GROUP 4 O.N.S

Gab
Renz

Erickson

Clau

INTRODUCTION
NURSING as our future profession involves the risk of exploring the unseen and discovering the unknown. Part of our duty is the mesmerizing roller coaster discovery on the hospital, this is somewhat highfalutin but in reality this makes our Group become more dedicated to assist even in worse scenario.
Having the privilege to select our case to present, we have come up to study about Liver Cirrhosis leading to hepatic encephalopathy and esophageal varices. For others it seems that it's just an ordinary disease but for the patient himself and his family, it is an extraordinary experience that we, nursing students fortunately made a glance. Making the most out of everything is at the same time making a case study with effort and utilization of modern technology like internet in gathering information for this case.

LIVER CIRRHOSIS incidence in the country continues to rise every year due to the changing lifestyle and diet of Filipinos. It is a complex case in terms of the complications that it may bring when not treated. Making this as the number one reason why the group selected this case. In our case presentation you will find out how a simple alcohol drinking, excess fat intake, which facinates people, can lead to a worse disease where complicated conditions may branch out like ESOPHAGEAL VARICES and HEPATIC ENCEPHALOPATHY.

BIOGRAPHIC DATA

Name: Patient X Age: 56 years old Birthday: 09/15/1955 Religion: Catholic Citizenship: Filipino Address: San Pablo City

BIOGRAPHIC DATA

Name: Patient X Age: 56 years old Birthday: 09/15/1955 Religion: Catholic Citizenship: Filipino Address: San Pablo City

ADMITTING HISTORY
One day prior to admission the patient had black tarry stool for three times without episodes of vomiting.

CHIEF COMPLAINT
Melena

What is melena?
A black tarry stool caused by upper gastrointestinal bleeding.

HISTORY OF PRESENT ILLNESS

One day prior to admission the patient had black tarry stool and dizziness.

PAST HEALTH HISTORY

CHILDHOOD ILLNESS and IMMUNIZATION: This information had not Been taken, because the Patient was disoriented and Her daughter has no Idea about it.
ALLERGY:

The patient has no known allergy.

PREVIOUS HOSPITALIZATION
Three years ago the patient underwent endoscopy for four times in Philippine General Hospital. He also had surgical removal of the gall bladder or cholecystectomy in the same hospital.

PHYSICAL ASSESSMENT
Date: FEBRUARY 10, 2012 (Friday) Time: 10:00 am

NEUROLOGIC ASSESSMENT GLASGOW COMA SCALE

BEST EYE RESPONSE: Spontaneous To speech Pain No response BEST VERBAL RESPONSE Oriented 3x 5 2 1 4 3

DAY 1 -Weak in appearance -The patient's daughter verbalized that it took a long time before her father recognized her. The patient was disoriented. And hard to be awaken. GCS: 8

Conversion
Speech: inappropriate Sound incomprehensible No response 1

4
3 2

MOTOR RESPONSE
Obeys verbal command Localizes pain Flexion-withdrawal Flexion-abnormal Extension-abnormal No response 1 6 5 4 3 2

VITAL SIGNS
8 AM BP: 120/80 12 NN BP: 120/80

RR: 18
HR: 61 T: 35.3

RR: 21
HR: 70 T: 36.9

Vital Signs Progress

Feb. 10 BP: 120/80 RR: 18 Feb. 11 BP: 110/80 RR: 12 Feb. 17 BP: 130/80 RR: 15 Feb. 18 BP: 130/90 RR: 21

HR: 61
T: 35.3

HR: 81
T: 36.3

HR: 70
T: 36

HR: 78
T: 36.8

AREA ASSESED SKIN:

METHOD USED

NORMAL

ACTUAL FINDINGS

POSSIBLE REASON

Moisture Inspection Turgor Palpation Temperature Palpation NAIL: Nail bed Shape Capillary refill Inspection Inspection Inspection

Moist Dry < 2 sec. < 2 sec. Not too warm Cold not too cold Pinkish Convex < 3 sec. Light brow(Depending on the race) No lesion, scar or inflammation Smooth Pale Convex 3 sec.

Decrease hydration. Anemia rt bleeding

SKIN: Inspection Color/ pigmentation Inspection Lesion Palpation Texture

Yellowish disco-loration Impaired (Jaundice) liver function No lesion, scar or inflammation Rough

AREA ASSESED METHOD USED NORMAL

ACTUAL FINDINGS -Normocephalic -Circumference: 21-23 in. -round, symmetrical -no tenderness was noted upon palpation. No lesions or scars should be noted.- No tenderness nor masses on palpation. -Hair color is black. -Without presence of lice. - Evenly distributed.

POSSIBLE REASON

HEAD

Inspection/ Palpation

-Normocephalic -Circumference: 21-23 in. -round, symmetrical no tenderness was noted upon palpation. No lesions or scars should be noted.- No tenderness nor masses on palpation. Color and appearance depend on race -Without presence of lice. Evenly distributed

SCALP

Inspection/ Palpation

HAIR

Inspection

AREA ASSESED

METHOD USED

NORMAL

ACTUAL FINDINGS

POSSIBLE REASON

EYES

Inspection

Symmetrical Evenly placed in line. Non protruding Eyeballs are not sunken PERRLA Sclera is anicteric Conjunctiva is pinkish
-Symmetrical, should not have presence of discharge -Internal nose is pinkish.

Symmetrical Evenly placed in line. Non protruding Eyeballs are not sunken PERRLA noted - Sclera is icteric Conjunctiva is pale
-Symmetrical, did not have presence of discharge. -Internal nose is pinkish. -Frontal and maxillary sinuses are not tender to touch.

Impaired liver function Anemia rt bleeding

NOSE

Inspection

SINUS

Inspection/Palpation -Frontal and maxillary sinuses are not tender to touch. -Free from lumps and masses.

AREA ASSESED METHOD USED NORMAL

ACTUAL FINDINGS -Free from lumps and masses. -No bad odor has been noted.

POSSIBLE REASON

MOUTH

Inspection

-No bad odor has been noted.

GUMS

Inspection

-Pinkish, moist -Not swollen -Moist

-Pinkish -Does not show any fissures -No lump and mass have been palpated.

- Free from lumps and masses. -Pinkish -Not swollen

-Dry -Pale -Does not show any fissures -No lump and mass have been palpated. -Symmetrical upon expansion, no retraction was noted.

LIPS

Inspection

Anemia rt bleeding

NECK

Palpation

AREA ASSESED METHOD USED NORMAL

ACTUAL FINDINGS -Symmetrical upon expansion, no retraction was noted. -No adventitious sound - No abnormal sound heard -No abnormal sound heard Flabby -bowel sound heard every 2 minutes. -Flabby AC: 83 cm Edema grade 2

POSSIBLE REASON

CHEST

Inspection

-Symmetrical upon expansion, no retraction was noted. No adventitious sound - No abnormal sound heard -No abnormal sound heard -Flat -Bowel sound heard every 5-20 seconds -Tympany -Not soft, not hard -Circumference: 40-60 cm WITHOUT PRESENCE OF EDEMA

LUNGS HEART ABDOMEN

Auscultation Auscultation Inspection

-Immobility -Ascites

EXTREMETIES

Inspection Palpation

Fluid excess

GORDON'S FUNCTIONAL HEALTH PATTERN

FEBRUARY 10, 2012

HEALTH PERCEPTION AND HEALTH MANAGEMENT

Verbalization: Noong nakakausap ko pa sya alam naman nya kung ano yung sakit nya, kaso ngayon hindi ko na sya makausap then hirap din syang mag isa, kahit nga nakahiga lang sya hindi ko sya iniiwanan kasi nga medyo unconscious sya. as verbalized by the patient's daughter. Norms: He is aware of his medical condition and he complies to his drug regimen he is also independent with regards to health management. Change: The patient can longer care for himself because of altered level of consciousness. He is also unaware of what is happening to the surrounding.

DIAGNOSIS: Risk for fall

NUTRITIONAL AND METABOLIC PATTERN

Verbalization: Madalas wala syang ganang kumain, nangangayayat na nga s'ya. as verbalized by the patient's daughter. Norms: The patient eats 3 times a day and with afternoon snacks. According to his daughter, her father loves to eat fatty foods like meat. Change: According to his daughter the patient refuses his food. He eats only a little (3 tsp) from his food. DIAGNOSIS: Risk for imbalanced nutrition: Less than body requirements

ELIMINATION PATTERN
Verbalization: Nakadiaper si daddy, kasi nahihirapin syang umihi sabi ny dati, tapos yellow orange na ang ihi dahil daw 8 ang gamot na iniinum niya sabi ni Doc as verbalized by the patients daughter. Norms: The patient had ease in urination and usually urinates 45 times a day. According to the patient's daughter her father did not report any complaint of having colored urine. His daughter reported that the patient probably defecates once a day usually early in the morning. Change: The patient is wearing diaper and a catheter is inserted to him and his daughter stated that she changes it for 2-3 times, with semi solid stool, black in color. His urine is yellow orange, and he also have a catheter.

DIAGNOSIS: Impaired Urinary Elimination

ACTIVITY AND EXERCISE

Verbalization: Madalas siyang naglalaro noon ng basketball as verbalized by his daughter.
Norms: Basketball serves as his exercise,whenever he doesnt have a work he plays basketball with his friends. Change: His activity was limited lying on bed therefore he cannot do his self care. He looks weak and cant perform his normal norms. DIAGNOSIS: Activity intolerance

SLEEP AND REST PATTERN

Verbalization: Mahirap syang gisingin kapag natutulog, napapansin ko pati na ang haba ng tulog nya dito as verbalized by the patient's daughter.
Norms: The patient sleeps regular at night at 6 hours per day. Change: The patient usually sleeps more oftenly at 10 hours per day with naps in the afternoon for approximately 1 hour.

COGNITIVE AND PERCEPTUAL PATTERN

Verbalization: Hindi na nya ako makilala, hindi na din sya nakakausap ng matino tapos naging ganyan na sya unconscious.
Norms: Before hospitalization the patient was oriented and had no memory impairment. He was also not yet unconscious for the past 22 days of stay. Change: Since he was hospitalized he started to be hard to talk with, he also had memory impairment, as days pass by, he becomes more disoriented and last Feb. 18, 2011 he became unconscious and unresponsive to sternal rub. DIAGNOSIS: Impaired memory related to disease process.

ROLE RELATIONSHIP
Verbalization: Ako ang nagiisa nilang anak kaya malapit ang loob naming sa isat isa as verbalized by his daughter Norms: Watching tv and eating together serves as their bonding moments. Changes: Due to unnecessary circumstances, the patients wife is vulnerable in this event and the current situation and other relatives are busy with their own works. His daughter is currently has no job and can handle the situation. With this, she do the honors in attending the needs and all out support that is greatly needed.

COPING STRESS PATTERN

Verbalization: Madalas siyang maglaro ng basketball sabi nya dati pantanggal stress daw para makapaglibang naman daw as verbalized by the patient's daughter..

Norms: The patients daughter stated that her father used to play basketball whenever he feels stress it also serves as his exercise. He also sleeps and watches tv whenever she gets bored.
Change: The patient cannot play basket ball anymore due to his illness.

SELF PERCEPTION OR SELF CONCEPT

Verbalization: My dad, sa tingin ko ang tingin nya sa sarili nya is a father with a responsibility sa kanyang apo, at sa akin na anak nya. Norms: Based on his daughter's verbalization the patient sees himself as someone who cares for his family.
Changes: His daughter said, Based sa pagkakakilala ko sa daddy ko, feeling ko ang mga iniisip nya sa mga panahong ito is that he is so weak, kung dati sya ang nag aalaga ngayon sa naman ang mahina at dapat alagaan.

SEXUALITY REPRODUCTIVE

The patient has only one daughter. He is not sexually active because of his condition.

VALUE BELIEF
Verbalization: Alam ko namang hindi kame pababayaan ng Diyos as verbalized by the patient's daughter. Norms: He is a Roman Catholic. He always goes with her family every Sunday to go to mass. He was taught by his family to believe and have fear to GOD. They usually not believe in quack doctors and not using herbal meds.
Changes: Because of his hospitalization, he is now unable to attend mass. He has a rosary in his hand.

CLINICAL DISCUSSION

ANATOMY AND PHYSIOLOGY OF THE LIVER

ANATOMIC POSITION

T H E L I V E R

CIRCULATION

FUNCTIONS OF THE LIVER

1. GLUCOSE METABOLISM
MEAL DIGESTION OF FOOD GLUCOSE WILL BE CARRIED INTO PORTAL VEIN CONVERSION INTO GLYCOGEN STORAGE IN THE HEPATOCYTES

IN CASE OF GLUCOSE SHORTAGE (HYPOGLYCEMIA) GLYCOGEN GLUCOSE

GLYCOGENOLYSIS

2. AMMONIA CONVERSION

GLUCONEOGENESIS ---> AMINO ACIDS ---> AMMONIA----> UREA-----> EXCRETION IN URINE

3. PROTEIN METABOLISM
- Albumin - alpha and beta globulin - blood clotting factor - most of plasma lipoprotein - Vitamin K

4. FAT METABOLISM
- Limited glucose in the blood - Fatty acids will be broken down - Acetoacetic acid, beta- hydroxybutyric acid and acetone

5. VITAMIN/IRON STORAGE
- VITAMIN A,B,D and B complex - Iron storage

7. BILE FORMATION
-Hepatocytes- site for bile formation -Bile is necessary for the emulsification of fats

6. DRUG METABOLISM

- Drug conjugation

CLINICAL DISCUSSION

LIVER CIRRHOSIS

Cirrhosis is a complication of many liver disease 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 multiply 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 (such as alcohol, fat, and certain medications), viruses, metals (such as iron and copper that accumulate in the liver as a result of genetics), and autoimmune liver disease in which the body's immune system attacks the liver.

RISK FACTORS:
GENERAL Gender: the rate of chronic liver disease is twice in men compared to women. PATIENT /

Obesity
Weight gain High triglyceride level in the blood

Not proven
x x

Coronary artery disease

Intestinal bypass surgery Long term treatment with corticosteroid

/
x x

SIGNS AND SYMPTOMS

GENERAL SIGNS/SYMPTOMS FINDINGS

Jaundice
Fatigue

/
x

Loss of appetite
Itching

x
x

Bleeding

/ Esophageal varices

DIAGNOSTICS:

IMAGING

Ultrasound is routinely used in the evaluation of

cirrhosis, where it may show a small and nodular liver in advanced cirrhosis along with increased echogenicity with irregular appearing areas.

Abdominal CT scan Liver/bile duct MRI

Gastroscopy

Complications

Ascites: Salt restriction is often necessary, as cirrhosis leads to accumulation of salt (sodium retention). Diuretics may be necessary to suppress ascites. Diuretic options for inpatient treatment include aldosterone antagonists (usually spironolactone) and loop diuretics. Aldosterone antagonists are preferred for patients who can take oral medications and are not in need of an urgent volume reduction, with loop diuretics as additional therapy. Esophageal variceal bleeding: Bleeding esophageal varices are very swollen veins in the walls of the lower part of the esophagus (the tube that connects your throat to your stomach) that begin to bleed Hepatic encephalopathy: High-protein food increases the nitrogen balance, and would theoretically increase encephalopathy.

Management

Generally, liver damage from cirrhosis cannot be reversed, but treatment could stop or delay further progression and reduce complications. A healthy diet is encouraged, as cirrhosis may be an energy-consuming process. Close follow-up is often necessary. Antibiotics will be prescribed for infections, and various medications can help with itching. Laxatives, such as lactulose, decrease risk of constipation; their role in preventing encephalopathy is limited.

Preventing further liver damage: Regardless of underlying cause of cirrhosis, alcohol and paracetamol, as well as other potentially damaging substances, are discouraged. Vaccination of susceptible patients should be considered for Hepatitis A and Hepatitis B.
Transplantation: If complications cannot be controlled or when the liver ceases functioning, liver transplantation is necessary.

Decompensated cirrhosis: In patients with previously stable cirrhosis, decompensation may occur due to various causes, such as constipation, infection (of any source), increased alcohol intake, medication, bleeding from esophageal varices or dehydration. Patients with decompensated cirrhosis generally require admission to hospital, with close monitoring of the fluid balance, mental status, and emphasis on adequate nutrition and medical treatment often with diuretics, antibiotics, laxatives and/or enemas, thiamine and occasionally steroids, acetylcysteine and pentoxifylline. Administration of saline is generally avoided as it would add to the already high total body sodium content that typically occurs in cirrhosis.

Esophageal Varices
Bleeding from esophageal varices occurs approximately one third of patients with cirrhosis and varices. The mortality rate resulting from first bleeding episode is 45% to 50%; it is one of the major causes of death in patients with cirrhosis. (Pomier-Layrargues, Villeneuve, Deschenes et al., 2001). The mortality rate increases with each subsequent bleeding episode. In relation to bleeding the patient may exhibit melena/ hematochezia.

Hepatic Encephalopathy

Hepatic encephalopathy is a syndrome observed in patients with cirrhosis. Hepatic encephalopathy is characterized by personality changes, intellectual impairment, and a depressed level of consciousness. Subtle signs of hepatic encephalopathy are observed in nearly 70% of patients with cirrhosis. Symptoms may be debilitating in a significant number of patients and are observed in 24-53% of patients who undergo portosystemic shunt surgery. Approximately 30% of patients dying of end-stage liver disease experience significant encephalopathy, approaching coma.

RISK FACTORS:
GENERAL Hemorrhage in the GIT PATIENT / Esophageal varices

Excess protein in diet

Potassium depletion Alkalosis Trauma Infection Constipation Medications like: -furosemide -sedatives -analgesic

/
/ x x x x /

CLINICAL SYMPTOMS

CLINICAL SIGNS AND EEG SELECTED POTENTIAL CHANGES NURSING DIAGNOSES Activity intolerance Self Care deficit Disturbed sleep pattern

Normal level of consciousness Asterixis; impaired writing with periods of lethargy and and ability to draw line euphoria; reversal of day-night figures. Normal EEG sleep pattern.

Increased drowsiness; disorientation; inappropriate behavior, mood swings, agitation.

Asterixis; fetor hepaticus. Abnormal EEG with generalized slowing.

Impaired social interaction Ineffective role performance Risk for injury

Stuporous; difficult to rouse, sleeps most of the time; marked confusion; incoherent speech.

Asterixis; increased deep tendon reflexes, rigidity of extremities. EEG markedly abnormal.

Impaired nutrition Impaired mobility Impaired verbal communication

Comatose; may not respond to Absence of asterixis; absence painful stimuli. of deep tendon reflexes, flacidity of extremities. EEG markedly abnormal.

Risk for aspiration Impaired gas exchange Impaired tissue integrity Disturbed sensory perception.

LABORATORY RESULTS

01-10-12

Chest X-Ray Poor inspiratory effort renders bronchovesicular and rule out underlying condition True cardiac size is difficult to assess but appears to have left ventricular cardiomegaly Aoral appears prominent

Both costophrenic sulci are obscured, to rule out minimal bilateral pleuric reactive change; effusion

02-01-12
Result Creatinine Sodium 2.6 mg/dL 133 mmol/L Normal Range Interpretation Significance 0.7-1.4 mg/dL High 135-145 mmol/L Low Extravasation of electrolyte and fluid due to decrease oncotic pressure.

Urea Nitorgen 27 mg/dL

10-20mg/dL

High

Impaired liver detoxification.

02-02-12
Result Normal Range Interpretation Significance Creatinine 1.9 mg/dL 0.7-1.4 mg/dL High 10-20mg/dL High Impaired liver detoxification.

Urea Nitorgen 25 mg/dL

02-04-12
Result pH pCO2 PO2 HCO3 (Plasma Bicarbonate) 7.419 29.2 mmHg 113 mmHg 18.9 mmol/L Normal Range 7.350-7.450 35.0-45.0 mmHg Interpretation Normal Low
Metabolic Acidosis

Significance

80-105 mmHg Low 22-26 mmol/L Low Metabolic Acidosis

Base Excess -6 mEq/L in Extracellular Fluid

Total CO2 Saturated O2 20 99%

-2-+2 mEq/L

Low

Metabolic Acidosis

23-27 95-98%

Low High

02-10-12
Result Glycosylated Hemoglobin 5.3% Normal Range 4.2-6.5% Interpretation Normal Significance

Result Creatinine 1.5 mg/dL

Normal Range

Interpretation

Significance

0.7-1.4 mg/dL High

02-13-12
Result Hemoglobin 10.7 gm/dL Normal Range 13-18 gm/dL Interpretation Low Significance Bleeding

Hematocrit
Platelet Mean Corpuscular Volume Mean Corpuscular Hemoglobin

0.30

0.42-0.52

Low

Bleeding
Liver Insufficiency
Liver Disease

116.00/cu mm 150.00Low 450.00/cu mm 97.70 fL 84-96 fL High

34.60 pg

28-33 pg

High

Liver Disease

INTAKE AND OUTPUT

Feb 10 6-2 2-10 10-6 ORAL 670 280 210 INFUSION 540 400 590 TOTAL 810 740 830 URINE 270 300 500

Feb 11 6-2 2-10 10-6 Feb 12 6-2 2-10 10-6 Feb 13 6-2 2-10 10-6

90 220 0 270 210 690

610 350 450 300 100 100 100 100 330

700 560 150 570 310 690 100 190 330

490 Diaper/stool 300 400 1220 2,780 500 400

90 0

Feb 14 6-2 2-10 10-6

300 230 0

330 400 770

630 630 770

810 420 400

Feb 15 6-2 2-10 10-6

280 230 0
180

330 400 770

410 418

610 460 120

180

400 330

Feb 16 6-2 2-10 10-6 Feb 17 6-2 2-10 10-6

150

540

PATHO PHYSIOLOGY

LETS SORT THE DATA!!!

DATA GATHERED LAST FEBRUARY 10, 2012

NEUROLOGIC RESPIRATORY GCS: 8 CARDIOVASCULAR

Gordon cognitve,perceptual DISORIENTED

URINARY GASTROINTES TINAL Ascites 85 cm AC Bowel sounds heard every 2 minutes Intake: 810 cc Output 270 cc

Physical Exam
-jaundice -Yellowish sclera -Ascites -Bipedal edema -weak in appearance

NURSING CARE PLAN

DRUG STUDY