Liver Cirrhosis Case Presentation 4r423w

CASE PRESENTATION Liver Cirrhosis

Hepatic Encephalopathy Esophageal Varices

Chichan

Joseph Marj

Nico

GROUP 4 O.N.S

Erickson

Clau

April

Gab Renz

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 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

ITTING HISTORY One day prior to ission 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 ission 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

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.

BEST EYE RESPONSE: Spontaneous

4

To speech

3

Pain

2

No response

1

BEST VERBAL RESPONSE Oriented 3x

5

Conversion

4

Speech: inappropriate

3

Sound incomprehensible

2

No response

MOTOR RESPONSE Obeys verbal command

6

Localizes pain

5

Flexion-withdrawal

4

Flexion-abnormal

3

Extension-abnormal

2

No response

GCS: 8

1

1

VITAL SIGNS 8 AM

12 NN

BP: 120/80

BP: 120/80

RR: 18

RR: 21

HR: 61

HR: 70

T: 35.3

T: 36.9

Vital Signs Progress Feb. 10

Feb. 11

Feb. 17

Feb. 18

BP: 120/80

BP: 110/80

BP: 130/80

BP: 130/90

RR: 18

RR: 12

RR: 15

RR: 21

HR: 61

HR: 81

HR: 70

HR: 78

T: 35.3

T: 36.3

T: 36

T: 36.8

AREA ASSESED

METHOD USED

NORMAL

ACTUAL FINDINGS

POSSIBLE REASON

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

Inspection Inspection Inspection

SKIN: Inspection Color/ pigmentation Inspection Lesion Palpation Texture

Moist Dry < 2 sec. < 2 sec. Not too warm Cold not too cold

Decrease hydration.

Pinkish Convex < 3 sec.

Pale Convex 3 sec.

Anemia rt bleeding

Light brow(Depending on the race) No lesion, scar or inflammation Smooth

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

AREA ASSESED METHOD USED NORMAL

ACTUAL FINDINGS

HEAD

Inspection/ Palpation

-Normocephalic -Circumference: 21-23 in. -round, symmetrical no tenderness was noted upon palpation.

-Normocephalic -Circumference: 21-23 in. -round, symmetrical -no tenderness was noted upon palpation.

SCALP

Inspection/ Palpation

No lesions or scars should be noted.- No tenderness nor masses on palpation.

No lesions or scars should be noted.- No tenderness nor masses on palpation.

HAIR

Inspection

Color and appearance depend on race -Without presence of lice. Evenly distributed

-Hair color is black. -Without presence of lice. - Evenly distributed.

POSSIBLE REASON

AREA ASSESED

METHOD USED

NORMAL

ACTUAL FINDINGS

EYES

Inspection

Symmetrical Evenly placed in line. Non protruding Eyeballs are not sunken PERRLA Sclera is anicteric Conjunctiva is pinkish

Symmetrical Evenly placed in line. Non protruding Eyeballs are not sunken PERRLA noted - Sclera is icteric Conjunctiva is pale

NOSE

SINUS

Inspection

-Symmetrical, should not have presence of discharge -Internal nose is pinkish.

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

-Symmetrical, did not have presence of discharge. -Internal nose is pinkish. -Frontal and maxillary sinuses are not tender to touch.

POSSIBLE REASON

Impaired liver function Anemia rt bleeding

AREA ASSESED METHOD USED NORMAL

ACTUAL FINDINGS

MOUTH

Inspection

-No bad odor has been noted.

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

GUMS

Inspection

-Pinkish, moist -Not swollen -Moist

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

LIPS

Inspection

-Pinkish -Does not show any fissures

-Dry -Pale -Does not show any fissures

NECK

Palpation

-No lump and mass have been palpated.

-No lump and mass have been palpated. -Symmetrical upon expansion, no retraction was noted.

POSSIBLE REASON

Anemia rt bleeding

AREA ASSESED METHOD USED NORMAL

ACTUAL FINDINGS

CHEST

Inspection

-Symmetrical upon expansion, no retraction was noted. No adventitious sound

-Symmetrical upon expansion, no retraction was noted. -No adventitious sound

LUNGS

Auscultation

- No abnormal sound heard

- No abnormal sound heard

HEART

Auscultation

ABDOMEN

Inspection

-No abnormal sound heard

-No abnormal sound heard

-Flat

Flabby

-Bowel sound heard every 5-20 seconds -Tympany -Not soft, not hard -Circumference: 40-60 cm

-bowel sound heard every 2 minutes. -Flabby AC: 83 cm

EXTREMETIES

Inspection Palpation

WITHOUT PRESENCE OF EDEMA

Edema grade 2

POSSIBLE REASON

-Immobility -Ascites

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 doesn’t 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 can’t 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 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 patient’s 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 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 patient’s 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.

Obesity

PATIENT /

Not proven

Weight gain

x

High triglyceride level in the blood

x

Coronary artery disease

/

Intestinal by surgery

x

Long term treatment with corticosteroid

x

SIGNS AND SYMPTOMS GENERAL SIGNS/SYMPTOMS

FINDINGS

Jaundice

/

Fatigue

x

Loss of appetite

x

Itching

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 ission 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. istration 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

PATIENT

Hemorrhage in the GIT

/ Esophageal varices

Excess protein in diet

/

Potassium depletion

/

Alkalosis

x

Trauma

x

Infection

x

Constipation

x

Medications like: -furosemide -sedatives -analgesic

/

CLINICAL SYMPTOMS

CLINICAL SIGNS AND EEG SELECTED POTENTIAL CHANGES NURSING DIAGNOSES

1

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.

Activity intolerance Self Care deficit Disturbed sleep pattern

2

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

3

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

4

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

Normal Range

Interpretation

Significance

Creatinine

2.6 mg/dL

0.7-1.4 mg/dL High

Sodium

133 mmol/L

135-145 mmol/L

Low

Extravasation of electrolyte and fluid due to decrease oncotic pressure.

10-20mg/dL

High

Impaired liver detoxification.

Urea Nitorgen 27 mg/dL

02-02-12 Result

Creatinine

1.9 mg/dL

Urea Nitorgen 25 mg/dL

Normal Range

Interpretation

Significance

0.7-1.4 mg/dL High 10-20mg/dL

High

Impaired liver detoxification.

02-04-12 Result

Normal Range

Interpretation

Significance

pH

7.419

7.350-7.450

Normal

pCO2

29.2 mmHg

35.0-45.0 mmHg

Low

PO2

113 mmHg

80-105 mmHg Low

HCO3 (Plasma Bicarbonate)

18.9 mmol/L

22-26 mmol/L Low

Metabolic Acidosis

Base Excess -6 mEq/L in Extracellular Fluid

-2-+2 mEq/L

Low

Metabolic Acidosis

Total CO2

20

23-27

Low

Saturated O2

99%

95-98%

High

Metabolic Acidosis

02-10-12 Result Glycosylated Hemoglobin

5.3%

Result Creatinine

1.5 mg/dL

Normal Range 4.2-6.5%

Normal Range

Interpretation

Significance

Normal

Interpretation

0.7-1.4 mg/dL High

Significance

02-13-12 Result

Normal Range

Interpretation

Significance

Hemoglobin

10.7 gm/dL

13-18 gm/dL

Low

Bleeding

Hematocrit

0.30

0.42-0.52

Low

Bleeding

Platelet

116.00/cu mm 150.00Low 450.00/cu mm

Liver Insufficiency

Mean Corpuscular Volume

97.70 fL

84-96 fL

High

Liver Disease

Mean Corpuscular Hemoglobin

34.60 pg

28-33 pg

High

Liver Disease

INTAKE AND OUTPUT Feb 10 6-2 2-10 10-6

ORAL 670 280 210

Feb 11 6-2 2-10 10-6

90 220 0

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

INFUSION 540 400 590

TOTAL 810 740 830

URINE 270 300 500

610 350 450

700 560 150

490 Diaper/stool 300

270 210 690

300 100 100

570 310 690

400 1220 2,780

90 0

100 100 330

100 190 330

500 400

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

330 400 770

610 460 120

400 330

Feb 16 6-2 2-10 10-6

180

410 418

180

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

GASTROINTES TINAL Ascites 85 cm AC Bowel sounds heard every 2 minutes

URINARY

Physical Exam

Intake: 810 cc Output 270 cc

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

NURSING CARE PLAN

DRUG STUDY