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Nursing Therapeutics 3

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Mina Lau

on 21 January 2014

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Transcript of Nursing Therapeutics 3

Nursing Therapeutics 3
Hepatic Encephalopathy

Presented by Group AB1, Class 2012
TMH12-004 Chan Choi Wan
TMH12-005 Chan Chui Ting
TMH12-009 Chan Kit Ying
TMH12-038 Lau Cho Yan
TMH12-090 Chan Ka Chai
TMH12-092 Chung Tsz Him *

Introduction
What is Hepatic Encephalopathy?
GENERAL MANAGEMENT (ACUTE PHASE)
Nursing Diagnoses (ACUTE STAGE)
Excess Fluid Volume
Ineffective Breathing Pattern
Imbalanced nutrition: less than body requirement
Discharge Management -
Non-compliance
What is
Hepatic Encephalopathy
?
a worsening of
brain function
that occurs when the
liver
is no longer able to
remove toxic substances
in the blood. (MedlinePlus, 2014)

Reversible
condition for
minor attack
Pathogenesis
Clinical Manifestations
Hepatic Encephalopathy:
Changes in personality
Intellectual impairment
Poor coordination
Disorientation
Confusion
Coma
Assessment on HE
1. Glasgow Coma Scale (GCS)

Grade 1
1. Inverted sleep-wake pattern
2. Mild decrease in awareness
3. Euphoria or anxiety
4. Decreased attention time
Case Scenario
Mr. Chan, 62/M
Brought to AED by family due to
confusion
since that day morning,
claimed that had joined a wedding party two day before and
excessive alcohol and meats were consumed
.
Vital signs:

BP: 135/78 mmHg

Pulse: 75 bpm
RR: 32/mins
Temp: 36.2 C
GCS: E4
V4
M6
Tests for possible causes
1. Brain computed tomography (CT):
No intra-cerebral hemorrhage
No tumor & abscess
No stroke
Diagnosis
From above examinations and tests:

No hypertension
No Intracranial lesions
No hypoglycemia
No electrolytes imbalance

--> Impaired liver function
Learning Objectives
On completion of this seminar, all of us will be able to:

• 1.
Define
“Hepatic Encephalopathy”.
• 2. Describe the
pathogenesis
of hepatic encephalopathy.
• 3. Identify the
clinical manifestations
of hepatic encephalopathy.
• 4. Describe the
general treatments
for hepatic
encephalopathy.
• 5. Describe the
nursing managements
for a patient with hepatic encephalopathy associated with liver cirrhosis.
Case Scenario
--> Altered mental status
Clinical Manifestations
Liver Cirrhosis:
Jaundice
Hypoalbuminemia, ascites, dyspnea
Petechiae, bruising
Fatigue
Loss of appetite

Dietary Modification
Goal:
Decreased NH3 production
to decrease hepatic encephalopathy

Dietary modification:
High calories
diet
consume diet high in calories & carbohydrates
2500-3000 kcal/day

Lactulose
Surgical Treatment
Liver Transplant
Antibiotics
DIET
MEDICAL TREATMENT
1. To
lower the pH
of the lower bowel
reduce the activity of intestinal bacteria

2. To
increase the osmotic pressure
in the lower bowel
draw water from blood vessel into bowel
ammonia together is drawn out

Actions
Goal:
To
reduce the ammonia level
in bloodstream thus alleviate HE
To treat
constipation

Suggested Regimen:
PO, 15~30ml, twice daily

Lactulose
Side Effects
1. Stomach rumble
2. Abdominal cramping
3. Noisy and pungent flatulence
4. Diarrhea
5. Nausea and vomiting (rare)

Second line treatment

1. Neomycin
stop the production of essential proteins

needed by the bacteria to survive
250 mg PO 2-4 times a day

S/E:
Diarrhea
Nausea & Vomiting
Irritation/soreness of mouth and rectal area
Contact dermatitis
2. Rifaximin


fights bacterial infection
only in the
intestines
• 400 mg PO TDS

• S/E:
– Peripheral edema
– nausea
– Flatulence

CHECK for any S/S of allergy & AVOID prolong use/overdose !
Antibiotics
1. Altered Thought Process

2. Excess Fluid Volume

3. Ineffective Breathing Pattern

4. Imbalanced nutrition: less than body requirement
Altered Thought Process
Altered Thought Process
Related to:
cerebral toxicity

associated with

high serum ammonia level

resulting from
the
liver’s inability to convert ammonia to urea

As evidenced by:
confusion and disorientation
GCS: E4
V4
M6

Assessment
From significant others for:
patient's
usual
level of cognitive & emotional functioning

S/S of altered thought process:
slowed verbal responses
decreased ability to concentrate
impaired memory
poor reasoning ability or judgment
apathy, agitation, and hallucinations


Monitor
Blood test
result closely
serum NH3 level
serum urea level

Conscious level
by GCS
for any change of conscious level
report immediately if significant change occurs

Actions
To
improve cerebral tissue oxygenation
:
Restrict activities
to lower O2 demands
Administer
O2
as prescribed
Breathing and coughing exercises
Avoid tight and heavy clothing
Reduce stress & anxiety
Address client by
name
Reorient
patient to ward environment, staff and his current situation
Avoid
repeatedly asking
questions
that patient
cannot answer
Approach patient in a
slow & calm
manner; allow
adequate time
for communication
Repeat instructions
as necessary using clear, simple language and short sentences

Goal:
Patient will experience
improvement on thought process


as evidenced by:
improved reasoning ability and judgment
state date, current season, time and place correctly
GCS score:
from 14 to 15(fully conscious)

within 14 days.
Altered Thought Process
Actions
Administer medications
as prescribed, monitor effect and side effect:
Lactulose
Antibiotics e.g. Neomycin, Rifaximin

Reduce stress & anxiety
Provide
quiet and calm
environment; promote adequate rest
Encourage
significant others
to be
supportive
of client;
instruct them in methods of dealing with client's altered thought process
Consult
appropriate health care provider if altered thought processes persist / worsen
Excess Fluid Volume
Related to:
decreased osmotic pressure
associated with
hypoalbinemia
secondary to
liver cirrhosis

As evidenced by:
increased body weight
increased abdominal girth
peripheral edema

Goal:
Patient will achieve
optimal fluid balance
,

as evidenced by:
stable weight
absence of peripheral edema
balanced intake and output,

by the time patient is discharged.
S/S of excess fluid volume:
Significant weight gain
Peripheral edema
Ascites
Dyspoea

Actions
Diet
modifications to
prevent fluid accumulation
by :
Restrict fluid
intake as prescribed
Restrict sodium
intake as prescribed
Provide appropriate diet for electrolyte imbalance

Maintain
bed rest
or encourage
lying down
to promote fluid back into vascular space

Assessment
Monitoring
Excess Fluid Volume
Patient’s
fluid status
by:
Daily body weight + abdominal girth
(same time everyday)
I&O

Vital signs for any
fluid overload
,
e.g. increased BP and pulse

Serum
albumin
and
electrolytes
level

Chest x-ray
results for pulmonary edema

Provide
medications
and monitor therapeutic and side effect:
Diuretics
, e.g. lasix, to reduce body fluid retension
Potassium-lowering agents
if hyperkalemia exist, e.g. resonium C
Phosphate binder
if hyperphosphatemia exist, e.g. calcium bicarbonate

Consult
MO if S/S of fluid imbalance is not improved

Actions
Ineffective Breathing Pattern
Related to:
restricted lung expansion
associated with pressure of
ascites
on the diaphragm

As evidenced by:
increased respiratory rate
Assessment
Monitor
Interventions
Goal:
Patient will resume the
normal breathing pattern
as evidenced by normal respiratory rate
before discharge
.
S/S of altered respiratory function:
Rapid & shallow respiration
Dyspnea
Orthopnea
Adventitious breath sounds
(crackles, wheezes, rhonchi)

Monitor and report for abnormalities:
Arterial blood gases
Oxygen saturation
Serum albumin level
Chest x-rays
level of consciousness
To Improve respiratory functions:

Semi-Fowler’s position
Encourage frequent repositioning and bed rest
Deep breathe & inspiratory exerciser
(every 2 hour)
Administer O2 if necessary
Diuretics / salt-free albumin
Assist doctor to perform abdominocentesis

Ineffective Breathing Pattern
Assessment
S/S of malnutrition:
Weight loss
Weakness and fatigue
Low serum albumin

Causes
of poor nutrition status:
Decrease of liver function
--> Liver Function Test
Nausea and vomiting

Amount of intake:
Keep I&O monitoring
Actions to maintain and improve nutritional status
Education
Avoid skipping meals

Dietary Modification:
High calories + carbohydrate (2500-3000kcal/day)
Vitamin B12, folic acid, iron
Avoid alcohol
Imbalanced Nutrition:
Less than body requirement
Related to:
decrease of metabolism and nutritional storage
by liver associated with a reduction of functional tissue
decrease oral intake associated with nausea and discomfort due to S/E of drugs

As evidenced by:
Lethargy
Low serum albumin level
Imbalanced Nutrition:
Less than body requirement
Goal:
Patient can resume to
normal weight
for his age and height before discharge.
Nursing interventions
1.
Assessment

2.
Actions
to maintain and improve nutritional
status:
Dietary consult
Improve appetite
Provide conditions facilitating eating

3.
Education
on dietary recommendation
Actions to maintain and improve nutritional status
Actions to maintain and improve nutritional status
To
improve appetite
:

Provide
oral care
before meal

Provide
quiet and relax environment
to reduce stress
Provide
conditions facilitating eating:

Provide

rest
period before meals
Elevate head of bed
as tolerated for meals
help relieve dyspnea
Allow adequate time for meals
Reheat food if necessary
Reassess nutritional status
on
regular
basis
measure weight daily
same day, time and clothes

Consult physician about
alternative methods

of improving nutrition if patient does not consume enough food or fluids to meet the nutritional needs.
Monitor
Consult dietitian:
Obtain the dietary advices

Assist patient to select the foods and fluids
Meet nutritional needs
Patient’s preference
Level of understanding on disease and its related care
Reasons of non-compliance (difficulties?)
Family support
Concerns on lifestyle modification and drug treatment
Needs of professional guidance
Set
goals
with clients:
be flexible, realistic
Short and long term goals
not to force patient

Participation of family
Encourage self-monitoring + by significant others
Positive reinforcement
Solve the difficulties

Assist to relieve S/E of drugs

Help patient to deal with their individual difficulties in lifestyle modification
Assessment
Health Education
Diet - High calories;
Avoid alcohol intake
Drugs (uses? Effect? S/E?)
Stress the complications and the necessity for prevention
--> importance of lifestyle and drug compliance
Stress the importance of regular FU
Provide sources of help, e.g. GOPC
Non-compliance
Related to:
barriers to compliant the lifestyle modification,
secondary to the lack of
motivation

As evidenced by:
excessive intake of meats and alcohol
Goal:

Patient will
sustain
the compliance of drugs and lifestyle modification after discharge.
Encourage Positive Feelings
Assessment on HE
2. Mini-Mental State Examination

Problem List of Mr. Chan
Mild disorientation
Hyperammonemia
Hypoalbuminemia
Dyspnoea

Lethargy
Abdominal pain
Constipation

Grading & S/S
Protein ?
Anti-ulcer Drugs
Protein Restriction ?
NOT necessary
Protein restricted diet causes:
Higher protein breakdown
body requirement to protein cannot be achieved
increase skeletal muscle breakdown
nitrogen-containing amino acid released
increase serum ammonia production
prolong the course of HE
Malnutrition
: higher mortality rate

Past medical history:
Liver Cirrhosis with
portal hypertension
Esophagitis
Complain about:
Confusion
(claimed by relatives)
Constipation
Abdominal pain
Physical examinations:

Disorientation
(for time and place)
Lethargy
Muscle weakness
Jaundice
without skin rash
Severe
ascites
For Altered Mental Status....
Suspected --> Hepatic encephalopathy (HE)

Elevated serum ammonia level (NH3)
--> Not a tool to diagnose HE

Must include the
exclusion of alternate causes
of altered mental status !!!
2. Renal Function Test (RFT):
No imbalanced electrolytes
(normal level of Na, K, Ca & P)
Normal blood glucose level (5.8mmol/L)
3. Liver Function Test (LFT)

Serum albumin
:
1.3
g/dL
(Normal range:
3.4-5.4
g/dL)

Conjugated Bilirubin
:
1.6
mg/dL
(Normal level:
0-0.3
mg/dL)

Serum NH3
:
184
mcg/dL
(Normal range:
15-45
mcg/dL)
Tests for possible causes
(A.D.A.M., 2013)
Tests for possible causes
3. Liver Function Test (LFT)
(A.D.A.M., 2013)
Alanine transaminase (ALT)
:
86
IU/L
(Normal range:
10-40
IU/L)

Aspartate aminotransferase (AST)
:
76
IU/L
(Normal range:
10-34
IU/L)

Gamma-glutamyl transpeptidase (GGT)
:
106
IU/L
(Normal range:
0-51

IU/L)
--> Impaired liver function
(unable to
suffciently
convert ammonia into urea)
Most likely, the diagnosis is:
Hepatic encephalopathy (HE)
Grade 2
1. Lethargy
2. Mild disorientation of time or space
3. Mild personality change
4. Inappropriate behavior
Grading & S/S
Grade 3
1. Somnolence
2. Semi-stupor
3. Confusion
4. Disorientation
Grade 4
1. Coma
Patient
without
peptic ulcer:
Prevent occurrence
-->
Histamine-2 Receptor Antagonists

Patients
with
peptic ulcer
:
prevent GI bleeding
in gastrointestinal tract which may increase serum ammonia level
-->
Proton Pump Inhibitors


Histamine-2 Receptor Antagonists
Action:
Decrease gastric acid secretion

Indication:
When there is no evidence of peptic ulcer

Side effects:
Nausea and vomitting
Headache
Stevens-Johnson syndrome

Example: Pepcidine

Proton Pump Inhibitors
Action:
Decreasing gastric acid secretion through irreversible inhibition of enzymes in the gastric parietal cell

Indication:
When gastric-ulcer is evidenced

Side effects:
Diarrhea
Headache
Chest pain
Pruritus

Example: Pantoloc

Conclusion
Hepatic encephalopathy
Broad range of
neuropsychiatric abnormalities
e.g. alternation in intellectual and cognitive skill, and even coma

Varying severity
(Grading scales)

Resulted from:
hepatic insuffciency

Diagnosis of
exclusion of other causes

of altered mental status

May develop in irreversible cognitive impairment
Management
Identifying precipitating factors, such as:
Increased nitrogen load
(e.g. excessive dietary protein)
decreased toxin clearance
(e.g. constipation)

Drugs therapy:
Lactulose
and
Rifaximin
reduction of nitrogenous load in GI tract
Management
Supportive cares
to deal with the accompanied clinical manifestations
e.g. disorientation and ascites

Diet modification
e.g. high calories

Assess needs of
Liver transplant
Prevention
Avoid above precipitating factors

Continued drugs therapy

Reinforcement of compliance with the treatment and diet modification
Reference
Braissant, O., Mclin, V. A. & Cudalbu, C. (2013). Ammonia toxicity to the brain. Retrieved January 4, 2014 from National institutes of health, Web site: http://www.ncbi.nlm.nih.gov/pubmed/23109059

Caruana, P. & Shah, N. (2011). Hepatic Encephalopathy: Are NH4 Levels and Protein Restriction Obsolete?. Retrieved Month 3, 2014 from http://www.medicine.virginia.edu/clinical/departments/medicine/divisions/digestive-health/nutrition-support-team/nutrition-articles/Caruana%20Article.pdf

Longstreth, G. F. (2011). Hepatic encephalopathy: MedlinePlus Medical Encyclopedia. Retrieved January 3, 2014 from http://www.nlm.nih.gov/medlineplus/ency/article/000302.htm

Hepatic encephalopathy: MedlinePlus Medical Encyclopedia (2011). Retrieved January 10, 2014 from http://www.nlm.nih.gov/medlineplus/ency/article/000302.htm

Prakash, R. & Mullen, K. D. (2010). Mechanisms, diagnosis and management of hepatic encephalopathy. In Nature reviews: Gastroenterology & hepatology (pp. 515-525). Cleveland: Macmillan Publishers Limited.

Carpenito, L. J. (1997). Nursing Diagnosis --- Application to Clinical Practice. Philadelphia: Lippincott-Raven.

Wolf, D. C. (2013). Hepatic Encephalopathy. Retrieved January 11, 2014 from http://emedicine.medscape.com/article/186101-overview#aw2aab6b8

Ammonia - blood: MedlinePlus Medical Encyclopedia (2013). Retrieved January 10, 2014 from http://www.nlm.nih.gov/
medlineplus/ency/article/003506.htm

Hepatitis C oline Course-Management of Cirrhosis-Related Complications-Diagnosis and Management of Hepatic
Encephalopathy-Core Concepts (2013). Retrieved January 10, 2014 from http://hepatitisc.uw.edu/go/management-cirrhosis-related-complications/hepatic-encephalopathy-diagnosis-management/core-concept/all

Liver function tests: MedlinePlus Medical Encyclopedia (2013). liver function test. Retrieved January 10, 2014 from http://www.nlm.nih.gov/medlineplus/ency/article/003436.htm
Q & A
Which
GRADE
does Mr. Chan belongs to ?
GRADE 2 !
Full transcript