Our Lady of Fatima University

120 McArthur Highway

Valenzuela City, Philippines

NURSING CARE OF CLIENTS WITH LIFE THREATENING CONDITIONS, ACUTELY ILL, MULTI-ORGAN
PROBLEMS HIGH ACUITY & EMERGENCY SITUATIONS (ACUTE & CHRONIC) 
Case Study Presented to the
Faculty of the College of Nursing

In Partial Fulfillment of the Requirements in NCMB 418 RLE

ACUTE LIVER FAILURE

Submitted by:
Angeles, Floren Anne N.
Briñas, Rogielyn Blessilda A.
Bustos, Christian Art R.
Cruz, Paola Luz R.
Gantang, Warddah G.
Maglaoy, Susan Jillian T.
Peralta, Melchizedek N.
Riedel, Lyka N.

GROUP 1

Submitted to:

Sharon B. Cajayon RN, MAN

Evangeline Orata RN, MAN
Learning Objectives

General Objective

To broaden the students’ understanding of a client with acute hepatic failure.

Specific Objectives

The learner will be able to:

o Discuss the epidemiology, statistics and factors that can contribute to acute hepatic
failure.
o Review the anatomical structures and physiological processes of the gastrointestinal
tract, specifically the liver.
o Trace the pathophysiology along with the precipitating and predisposing factors
that may lead to acute hepatic failure..
o Analyze ways that will prevent further complications to clients with acute
hepatic failure.
o Develop proper nursing care plans using appropriate nursing interventions from
evidence-based practice.
o Determine appropriate therapeutic management for a client with acute hepatic failure.
Case Scenario
Koko Melo Yellow (Adapted from Taylor & Vieder, 2019)

A 64-year-old man, Mr. Koko Melo, with a significant medical history of chronic obstructive pulmonary
disease, alcohol abuse, and depression presented to the intensive care unit (ICU) of FUMC as a
transfer from the emergency department for acute hepatic failure. Melo had reportedly ingested 50
tablets of hydrocodone/acetaminophen (10-325 mg; 16.2 g of acetaminophen) in an attempted
suicide 6 hours before arrival at Hospital M.

His initial laboratory evaluation was notable for the following:

• Ethanol level: 320 mg/dL
• Acetaminophen level: 430 μg/mL
• Aspartate aminotransferase (AST) level: 2066 U/L
• Alanine aminotransferase (ALT) level: 1321 U/L
• Potassium level: 5.6 mEq/L
• Creatinine phosphokinase (CPK) level: 62,530 IU/L

Orders at the ED was to place Mr. Melo on a continuous norepinephrine

infusion at 20 μg/h. He was intubated secondary to being obtunded. He
underwent treatment for hyperkalemia and was started on intravenous N-
acetylcysteine (NAC) 200mg/mL as follows:
- Loading dose of 150 mg/kg IV; mix in 200 mL of 5% dextrose in water
and infuse over 1hour
- Dose 2: 50 mg/kg IV in 500 mL D5W over 4 hours
- Dose 3: 100 mg/kg IV in 1000 mL D5W over 16 hours

Upon admission at the ICU, the patient was afebrile, blood pressure was 94/57mmHg, heart rate of
92 bpm, and respiratory rate at 22 breaths/min. He weighs 87 kg. His oxygen saturation was 96%
on the ventilator.

On examination, Mr. Melo exhibited diffuse jaundice, smelled of alcohol and tobacco, and appeared
much older than his stated age. He was in no acute distress. He had bilateral scleral icterus. His

cardiopulmonary examination findings were unremarkable for any acute changes. His abdominal
examination revealed a fluid wave with the absence of any peritoneal signs.

On his 2nd hospital day, laboratory evaluation findings included the following:
• Hemoglobin level: 10.5 g/dL
• Platelet: 110 x 103/L
• Sodium level: 146 mmol/L
• Potassium level: 4.6 mmol/L
• Blood urea nitrogen level: 26 mg/dL
• Creatinine level: 3.02 mg/dL
• AST level: 2094 U/L
• ALT level: 1685 U/L
• Total bilirubin level: 0.4 mg/dL
• INR: 2.11
• Troponin level: 35.25 ng/mL (increasing to 44.66 ng/mL)
• Acetaminophen level: 237 μg/mL
• CPK level: 57,000 IU/L
• ABG: pH = 7.03, paCO2 = 41.26 mmHg, HCO3 = 6.0 mmol/L, paO2 = 112.53mmHg, and a
BE = –22.6 mmol/L

Ultrasonography of the abdomen revealed an increased hepatic echogenicity suggesting diffuse

hepatocellular disease, cirrhosis, and small amount of perihepatic ascites.

Given the Melo’s condition, conservative treatment was recommended. He was started on a low-
intensity heparin infusion (UFH 50,000units/5mL infusion rate of 12 units/kg/hr) for 48 hours.

By day 3, Melo’s creatinine level rose to 4.18 mg/dL, and he was anuric. His AST level increased to
3895 U/L, and his ALT level increased to 3215 U/L, despite intravenous NAC administration. His
lactic acid level increased from 2.2 to 8.2 mmol/L, with an anion gap of 25. He subsequently
underwent dialysis.

By day 4, vancomycin and piperacillin/tazobactam were initiated for healthcare-associated

pneumonia. Chest radiography revealed hazy opacities in the lung bases. The transplant surgery
team deemed him to be a poor candidate from a surgical perspective for a liver transplant.
Introduction 
Acute Liver Failure

Acute liver failure (ALF) is a rare life-threatening condition caused by severe injury and massive
necrosis of hepatocytes resulting in severe liver dysfunction that can lead to multi-organ failure and
death. It can occur in patients without preexisting liver disease and cause rapid deterioration of liver
function within days. ALF is commonly caused by metabolic disease, autoimmune disease, alcohol
abuse, hepatitis virus or overdose in drugs, such as acetaminophen.  Most patients who develop ALF
become ill rapidly, and the interval from onset of illness to near total liver collapse may be as short as a
week or less. Often the illness will begin with nonspecific symptoms, including malaise, ascites, fatigue,
nausea, abdominal pain and discomfort. Jaundice and scleral icterus are often present, but may not be
initially noted by patients or their families until relatively late in the course of the illness. Patients with
ALF often require admission to an intensive care unit and are probably best managed in a tertiary
referral center that performs liver transplantation. The current therapy of ALF is largely supportive such
as giving medications to reverse poisoning caused by acetaminophen overdose, providing nutritional
support, and etc. The goal is to anticipate, prevent, and treat complications, and facilitate the patient's
liver regeneration and repair.
Patterns of the progression from jaundice to encephalopathy have been identified and have led
to proposals of time-based classifications. However, no agreement about these classifications has been
reached. Three categories are frequently cited: hyperacute, acute, and subacute liver failure. In
hyperacute liver failure, the duration of jaundice before the onset of encephalopathy is 0 to 7 days; in
acute liver failure, it is 8 to 28 days; and in subacute liver failure, it is 28 to 72 days. The prognosis for
fulminant hepatic failure is much worse than for chronic liver failure. However, in fulminant failure, the
hepatic lesion is potentially reversible, and survival rates are approximately 20% to 50%, depending
greatly on the cause. Those who do not survive die of massive hepatocellular injury and necrosis. Viral
hepatitis is a common cause of fulminant hepatic failure; other causes include toxic medications like
acetaminophen and chemicals such as carbon tetrachloride, metabolic disturbances like Wilson disease,
a hereditary syndrome with deposition of copper in the liver, and structural changes such as Budd–
Chiari syndrome, an obstruction to outflow in major hepatic veins. Jaundice and profound anorexia may
be the initial reasons the patient seeks health care. Fulminant hepatic failure is often accompanied by
coagulation defects, kidney disease and electrolyte disturbances, cardiovascular abnormalities,
infection, hypoglycemia, encephalopathy, and cerebral edema.
Research into interventions for acute liver failure has begun to focus on techniques that
combine the efficacy of a whole liver with the convenience and biocompatibility of hemodialysis. The
acronyms ELAD (extracorporeal liver assist devices) and BAL (bioartificial liver) have been used to
describe these hybrid devices. These short-term devices, which remain experimental, may help patients
survive until transplantation is possible. The BAL device exposes separated plasma to a cartridge
containing porcine liver cells after the plasma has flowed through a charcoal column that removes
substances toxic to hepatocytes. The ELAD exposes whole blood to cartridges containing human
hepatoblastoma cells, resulting in removal of toxic substances. Research was conducted in the
Philippines about the incidence of acute liver failure. A hospital-based retrospective and prospective
surveillance study was conducted at Philippine General Hospital between January 2000 and December
2006. Blood samples were tested for viral hepatitis antibodies using ELISA (Abbott Lab). Acute liver
failure incidence rates were calculated with 95% confidence intervals (CI). Incidence of acute liver failure
was 11.05 per 100,000 subject years (95% CI 6.81-15.30). Jaundice was observed in 84.6% (22/26) of
subjects and encephalopathy on admission (any grade) was reported in 72.0% of subjects: Acute liver
failure was fatal in 84.6% (22/26) of subjects. Hepatitis A virus was the most common etiological agent
for acute liver failure. Another research from WHO says that the Philippines have 7,491 deaths from
liver disease that make up 1.23 percent of the population with a rate of 9.88 and in the 128th in the
world rank.
PATHOPHYSIOLOGY
ANATOMY AND PHYSIOLOGY

Human liver development begins during the third week of gestation and does not achieve mature
architecture until about 15 years of age. It reaches its largest relative size, 10% of fetal weight, around
the ninth week. It is about 5% of body weight in the healthy neonate. The liver is about 2% of body
weight in the adult. It weighs around 1400g in an adult female and about 1800g in the male. 

The liver is located in the right upper quadrant of the abdomen, just below the diaphragm. It is almost
completely behind the rib cage but the lower edge may be palpated along the right costal margin during
inspiration. A connective tissue layer called Glisson's capsule covers the surface of the liver. The capsule
extends to invest all but the smallest the vessels within the liver. The falciform ligament attaches the
liver to the abdominal wall and diaphragm and divides the liver into a larger right lobe and a smaller left
lobe.

In 1957, the french surgeon Claude Couinaud described 8 liver

segments. Since then, radiographic studies describe an
average of twenty segments based on distribution of blood
supply. Each segment has its own independent vascular and
biliary branches. Surgeons utilize these independent segments
when performing liver resection for tumor or transplantation.
There are at least three reasons why segmental resection is
superior to simple wedge resection. First, segmental resection
minimizes blood loss because vascular density is reduced at the borders between segments. Second, it
results in improved tumor removal for those cancers which are disseminated via intrasegmental
branches of the portal vein. Third, segmental resection spares normal liver allowing for repeat partial
hepatectomy.

Each segment of the liver is further divided into lobules. Lobules are usually represented as discrete
hexagonal aggregations of hepatocytes. The hepatocytes assemble as plates which radiate from a
central vein. Lobules are served by arterial, venous and biliary vessels at their periphery. This model is
useful for teaching purposes but more closely resembles the adult pig lobule than the human. Human
lobules have little connective tissue separating one lobule from another. The paucity of connective
tissue makes it more difficult to identify the portal triads and the boundaries of individual lobules.
Central veins are easier to identify due to their large lumen and because they lack connective tissue that
invests the portal triad vessels.
Lobules consist of hepatocytes and the spaces between them. Sinusoids are the spaces between the
plates of hepatocytes. Sinusoids receive blood from the portal triads. About 25% of total cardiac output
enters the sinusoids via terminal portal and arterial vessels. Seventy-five percent of the blood flowing
into the liver comes through the portal vein; the remaining 25% is oxygenated blood that is carried by
the hepatic artery. The blood mixes, passes through the sinusoids, bathes the hepatocytes and drains
into the central vein. About 1.5 liters of blood exit the liver every minute.

The liver is central to a multitude of physiologic functions, including:

 Clearance of damaged red blood cells & bacteria by phagocytosis

 Nutrient management
 Synthesis of plasma proteins such as albumin, globulin, protein C,
insulin-like growth factor, clotting factors, etc.
 Biotransformation of toxins, hormones, and drugs
 Vitamin & mineral storage

The liver is the storage location for fat-soluble vitamins and handles

cholesterol homeostasis. It stores iron and copper. It plays a role in hematology with clotting factor and
protein synthesis. The liver plays a role in heme breakdown into unconjugated bilirubin and conjugates
it.

The liver regulates most chemical levels in the blood and excretes a product called bile. This helps carry
away waste products from the liver. All the blood leaving the stomach and intestines passes through the
liver. The liver processes this blood and breaks down, balances, and creates the nutrients and also
metabolizes drugs into forms that are easier to use for the rest of the body or that are nontoxic. More
than 500 vital functions have been identified with the liver. Some of the more well-known functions
include the following:

 Production of bile, which helps carry away waste and break down fats in the small intestine
during digestion

 Production of certain proteins for blood plasma

 Production of cholesterol and special proteins to help carry fats through the body

 Conversion of excess glucose into glycogen for storage (glycogen can later be converted back to
glucose for energy) and to balance and make glucose as needed 

 Regulation of blood levels of amino acids, which form the building blocks of proteins

 Processing of hemoglobin for use of its iron content (the liver stores iron)

 Conversion of poisonous ammonia to urea (urea is an end product of protein metabolism and is
excreted in the urine)
  Clearing the blood of drugs and other poisonous substances

 Regulating blood clotting

 Resisting infections by making immune factors and removing bacteria from the bloodstream

 Clearance of bilirubin, also from red blood cells. If there is an accumulation of bilirubin, the skin
and eyes turn yellow. 

When the liver has broken down harmful substances, its by-products are excreted into the bile or blood.
Bile by-products enter the intestine and leave the body in the form of feces. Blood by-products are
filtered out by the kidneys, and leave the body in the form of urine.
 DRUG STUDY

ACETYLCYSTEINE SOLUTION
Name of the Action Indication Contraindications Common Nursing Responsibilities
Drug S/S
Brand Name:  N- Acetylcysteine Contraindicated dry  Monitor signs of
N- Acetylcysteine is indicated for for those who mouth, bronchospasm and
Acetylcysteine is the drug of mucolytic have nausea, respiratory
choice for the therapy and in hypersensitivity vomiting, irritation, including
Generic Name: treatment of an the to the drug.  and wheezing, cough,
Acetylcysteine acetaminophen management diarrhea. dyspnea, increased
Solution  overdose. It is of secretions, and
thought to acetaminophe tightness in the
Drug Class:  provide n overdose chest and throat.
antidotes (for cysteine for Report excessive or
acetaminophe glutathione prolonged
n toxicity) synthesis and respiratory
possibly to form problems to the
Dosage & an adduct physician.
Frequency:  directly with  make sure the
200mg/mL  the toxic patient understands
metabolite of the purpose of drug
Route:  acetaminophen, therapy, and that
Intravenous the patient should
consult the
physician before
resuming use of
products containing
acetaminophen.
 Instruct patient and
family/caregivers to
report other
troublesome side
effects such as
severe or prolonged
drowsiness, chills,
fever, nasal
inflammation, or GI
problems (nausea,
vomiting, irritation
in/around the
mouth).
 HEPARIN
Name of the Action Indication Contraindications Common S/S Nursing Responsibilities
Drug
Brand Name:  In low Prophylaxis and Contraindicated GI: drug-  Assess for signs
Hep-Lock doses, treatment of to those who induced of bleeding and
prevents the various have hepatitis.  hemorrhage,
Generic Name: conversion thromboemboli hypersensitivity including
Heparin of c disorders to the drug. Derm: rashes, bleeding gums,
prothrombin urticaria. nosebleeds,
Drug Class:  to thrombin unusual
Anticoagulants by its effects Hemat: bruising,
Antithrombotics BLEEDING, black/tarry
anemia,  stools,
hematuria, and
Dosage & Misc: fever, fall in
Frequency:  hypersensitivity. hematocrit or
UFH 50,000 blood pressure.
units/ 5mL Notify physician
infusion rate at or nursing staff
12 units/kg/hr. immediately if
For 48 hours heparin causes
excessive
anticoagulation.
Route:   Monitor signs of
Intravenous allergic
reactions and
anaphylaxis
 Monitor and
report signs of
drug-induced
hepatitis
 Monitor signs of
allergic
reactions and
anaphylaxis,
 NOREPINEPHRINE
Name of the Action Indication Contraindication Common S/S Nursing
Drug s Responsibilities
Brand Name:  Vasoconstrictio indicated Contraindicated  Irregular  Cardiac
Levophed n of peripheral for blood for those who heartbeats monitors
arteries pressure have (arrhythmias should be
Generic Name: control in hypersensitivity ) used on
Norepinephrin Slight increase certain to the drug.   Confusion patients
e  in heart rate acute  Anxiety receiving
hypotensiv  Headache norepinephrin
Drug Class:  Increase in e states  Nausea and e IV infusions.
Alpha contractility in vomiting  Defibrillator
adrenergic low doses  Sweating and
agonist  Tremor resuscitation
 Restlessness cart should be
 Urinary close by
Dosage & retention during
Frequency:  infusion
20ug/h  Assess
patients
frequently for
Route:  headache,
Intravenous chest pain, or
other signs of
toxicity.
 Monitor blood
pressure and
apical pulse
continuously
during
norepinephrin
e therapy.
 VANCOMYCIN
DRUG ACTION INDICATION CONTRAINDICATION SIDE EFFECTS NURSING
CONSIDERATION
BRAND Vancomycin inhi Indicated for Vancomycin is  bitter taste • can cause
NAME: bits the second treatment of contraindicated in ototoxicity,
Mersa IV 500 stage of cell wall lower patients who have  reddish rash on nausea, vomiting,
synthesis in respiratory had an allergic face and upper nephrotoxicity,
GENERIC susceptible tract reaction to it. body anaphylaxis, red-
NAME: bacteria. infections (intravenously: man syndrome
Vancomycin Furthermore, due to: red neck or red • assess for
there is susceptible man infection
PHARMACOL evidence that isolates of syndrome, • obtain culture
OGIC CLASS: vancomycin also MRSA and related to prior to initiating
glycopeptide alters the coagulase infusion rate) therapy
antibiotics permeability of negative • monitor blood
ROUTE: the cell staphylococci,  low blood pressure
IV membrane and methicillin- pressure acco • dose
selectively susceptible mpanied by dependent draw
DOSE: inhibits staphylococci flushing serum trough
2 g divided ribonucleic acid in penicillin- levels frequently
either as 500 synthesis. allergic  nausea • administer over
mg q6hr or 1 patients, or at least 60
 vomiting
gram q12hr those minutes to avoid
patients who  chills skin irritation
cannot
receive or  drug fever
have failed to
respond to
other
therapies

PIPERACILLIN + TAZOBACTAM
DRUG ACTION INDICATION CONTRAINDICATION SIDE EFFECTS NURSING
CONSIDERATION
BRAND NAME: Piperacillin For Hypersensitivity to GI effects (e.g. Monitor signs of
Tazoget inhibits documented piperacillin sodium diarrhea, nausea, allergic reactions
bacterial multidrug- and tazobactam constipation), rash, and anaphylaxis,
 GENERIC NAME: septum resistant gram- sodium or to any of pruritus, fever, including
Piperacillin + formation and negative the components of headache, pulmonary
Tazobactam cell wall infections due Tazoget; or to any insomnia; symptoms
synthesis in to organisms other penicillin- Decreases in Hb (tightness in the
PHARMACOLOGI susceptible proven or antibacterial agent. and hematocrit, throat and chest,
C CLASS: bacteria. suspected to History of acute thrombocytopenia, wheezing, cough
penicillin/β- Tazobactam is be susceptible severe allergic increases in dyspnea) or skin
lactamase a penicillanic to piperacillin- reaction to any platelet count, reactions (rash,
inhibitor acid sulfone tazobactam other β-lactam transient pruritus,
combinations derivative w/ except central active substances eosinophilia, urticaria)
β-lactamase nervous system (eg, cephalosporin, leucopenia,
ROUTE: inhibitory (CNS) monobactam or neutropenia,
IV properties. In infections and carbapenem). prolonged
combination, for prothrombin time
DOSE: tazobactam polymicrobial and partial
Each vial contains enhances the infections (eg, thromboplastin
4.5 g (piperacillin activity of mixed aerobic time. Increases in
4 g and piperacillin & anaerobic serum
tazobactam 0.5 g): against β- infections) in concentrations of
4.5 g 6 hourly for lactamase- which other creatinine and
5-14 days by producing agents have BUN, changes in
infusion over 30 bacteria. insufficient serum electrolytes,
min. Piperacillin and activity or are transient increases
tazobactam has contraindicated in AST, ALT,
a wide range of due to toxic alkaline
activity and is potential. phosphatase and
active against bilirubin.
gm+ve and gm-
ve aerobic and
anaerobic
bacteria.

NCP: IMPAIRED SPONTANEOUS VENTILATION

ASSESSMENT DIAGNOSIS INFERENCE PLANNING NURSING RATIONALE EVALUATION

INTERVENTIONS
Subjective Impaired Impaired After 8 hours Independent: Independent: After 8 hours of
Data: spontaneou liver function of nursing 1. Observed 1. Client may nursing
“Nag-aalala s ventilation ↓ intervention, overall be completely intervention, the
ako minsan related to Impairment the patient breathing dependent on patient was able to:
parang hindi metabolic in will be able pattern, the ventilator a. Display normal 
na siya factors detoxification to: distinguishing or able to take oxygen saturation,
humihinga.” secondary ↓ between breaths but and normal arterial
as verbalized to infection Toxins travel a. Display spontaneous have poor blood gases (ABGs)
by the and toxins to the brain normal  respirations and oxygen as evidenced by:
patient’s as and affect oxygen ventilator saturation  O2 Sat: 96%
daughter. evidenced brain saturation, breaths. without the  Arterial pH
by function and normal ventilator. = 7.35
Objective obtundation ↓ arterial 2. Verified that  Pao2 =
Data: and altered Patient is blood gases client’s 2. Decreases 98.51mmHg
(+) ABG levels. obtunded (ABGs) respirations are work of
Obtunded within client in phase with breathing; After 8 hours of
(+) Absence parameters. the ventilator. maximizes O2 nursing
of gag reflex delivery. intervention, the
3. Noted patient was not
Arterial pH = b. inspired 3. To liquify able to:
7.03 Demonstrate humidity and secretions, b. Demonstrate
Pao2 = spontaneous temperature; facilitating spontaneous gas
112.53mmHg gas maintain removal exchange. Patient
exchange. hydration remained to be
4. Suggestive obtunded.
4. Auscultated of other
breath sounds developing Goals were partially
periodically. complications met.
Investigated (atelectasis,
frequent acute
crackles or bronchospasm
rhonchi that do , pulmonary
not clear with edema).
coughing or
suctioning. Dependent:
5. To clear
Dependent: secretions and
5. Suctioned maintain
only as needed airway.
and as
prescribed, 6. Initiated for
using lowest healthcare-
pressure associated 
possible. Pneumonia.
Stops growth
6. Administered of bacterial
 prescribed infections.
medications a. Vancomycin
that promote b. Piperacillin /
airway patency tazobactam
and gas
exchange
as ordered by
the physician
and monitored
response to
medications.

Risk for Bleeding

ASSESSMEN DIAGNOSIS INFERENCE PLANNING INTERVENTION RATIONALE EVALUATIO
T N
Subjective: Risk for History of After 8 Independent Independent After 8 hours
“I’m feeling bleeding alcohol hours of of nursing
very weak related to abuse nursing 1. Determined the 1. Early intervention,
and dizzy”, impaired Hepatocyte intervention patient’s health identification of the patient
as verbalized liver injury , the patient history for signs possible risks for did not
by the client. function as Impaired will not that can be bleeding experience
evidenced liver function experience associated with a provides a bleeding but
Objective: by Decreased bleeding as risk for bleeding foundation for attained  
hypotension synthesis evidenced such as liver implementing ranges of:
BP 94/57 , abnormal Impaired by  disease. appropriate
hemoglobin production of normal preventive Blood
Hgb = 10.5 level and blood plasma ranges of: 2. Monitored measures. pressure =
g/dL range for proteins patient’s vital 120/80
coagulation Decreased Blood signs, especially
Platelet 110 profile. fibrinogen pressure = BP and HR. Hemoglobin
x 10^3 / L and 120-125/80- Looked for signs = 12.1
prothrombin 85 of orthostatic  2. g/dL
INR 2.11 Coagulopath hypotension. Hypotension an
y Hemoglobin d tachycardia Platelet =
Prolonged = 13.8 -17.2  3. Reviewed are initial 140 x 10^3 /
INR g/dL laboratory results compensatory L
Risk for for coagulation mechanisms
bleeding Platelet = status as usually noted INR < 1.5
150-450 x appropriate: with bleeding.
10^3 / L platelet count, Orthostasis (a Goal was
prothrombin drip of 20 mm partially met.
INR < 1.1 time/internationa Hg in systolic BP
l normalized ratio or 10 mm Hg in
(PT/INR), diastolic BP
activated partial when changing
thromboplastin from supine to
time (aPTT), sitting position)
fibrinogen, indicates
bleeding time, reduced
fibrin degradation circulating
products, vitamin fluids.
K, activated
coagulation time 3. These
(ACT). laboratory tests
provide
important
information
about the
patient’s
coagulation
status and
 bleeding
potential. The
specific
laboratory
values to be
monitored will
depend on the
patient’s specific
clinical
condition. For
patients
receiving
anticoagulants,
increased levels
of PT/INR and
aPTT above
therapeutic
values are
associated with
increased risk
for bleeding.
Reduced
platelet counts
may develop in
patients
receiving
heparin therapy.

Risk for Bleeding

ASSESSMEN DIAGNOSIS INFERENC PLANNING INTERVENTION RATIONALE EVALUATION
T E
Independent Independent After 8 hours of
nursing intervention,
4. Monitored 4. When bleeding the patient did not
hematocrit (Hct) is not visible, experience bleeding
and hemoglobin decreased Hgb but attained  
(Hgb). and Hct levels ranges of:
may be an early
5. indicator of Blood pressure =
Checked stool  bleeding. 120/80
(guaiac)
and urine  5. These tests are Hemoglobin = 12.1
(Hemastix) for used to g/dL
occult blood. distinguish
bleeding from Platelet = 140 x 10^3
6. Assessed skin the /L
and mucous gastrointestinal
membranes for or urinary tracts INR < 1.5
signs of that may not be
petechiae, visible. Goal was partially
bruising, met.
hematoma
formation, or 6. Patient with
oozing of blood. reduced platelet
counts or
impaired clotting
Dependent factor activity
may experience
7. Anticipated bleeding into
and prepared tissues that is out
the patient for of proportion to
blood the injury.
transfusion as Prolonged oozing
per doctor’s of blood from
order. When surgical incisions
laboratory or areas of skin
values are trauma is
abnormal, associated  with
administer coagulation
blood products abnormalities.
as prescribed.
Dependent

7. Blood product
transfusions
replace blood
clotting factors;
 RBCs increase
oxygen-carrying
capacity; FFP
replaces clotting
factors and
inhibitors;
platelets and
cryoprecipitate
provide proteins
for coagulations.

REFERRENCES

https://surgery.ucsf.edu/conditions--procedures/acute-liver-failure-(alf).aspx
https://my.clevelandclinic.org/departments/digestive/medical-professionals/hepatology/acute-liver-
failure#:~:text=Acute%20liver%20failure%20is%20a,a%20high%20morbidity%20and%20mortality.
Brunner & Suddarth's Textbook of Medical-Surgical Nursing, Fourteenth Edition Janice L. Hinkle; Kerry H. Cheever ISBN: 978-
1-4963-4799-2

https://pubmed.ncbi.nlm.nih.gov/23077857/

https://www.worldlifeexpectancy.com/philippines-liver-disease#:~:text=According%20to%20the%20latest%20WHO,Philippines
%20%23128%20in%20the%20world.