GROUP 4
Del Rosario, Peter Shan T.
Laquindanum, John Paul E.
Moreno, Darwin Leonardo B.
Ramos, Valenrose R.
Sabaulan, Crestine D.
Sanchez, Angela B.
Visaya, Liahona J.
Acute Gastrointestinal Bleeding
Intra-abdominal HTN & Abdominal Compartment
Syndrome –Disorder
Liver Failure
Acute Pancreatitis
Bariatric Surgery
Diabetic Ketoacidosis
Hyperglycemia Hyperosmolar Non-Ketotic Acidosis
Acute and Chronic Renal Failure
Acute Gastrointestinal Bleeding
DISORDER
ACUTE
GASTROINTESTINAL
BLEEDING :
Gastrointestinal (GI) bleeding can
originate anywhere from the
mouth to the anus and can be
overt
or
occult.
The
manifestations depend on the
location and rate of bleeding.
KEYPOINTS:
 Rectal bleeding may result
from upper or lower GI
bleeding.
 Orthostatic changes in vital
signs are unreliable markers
for serious bleeding.
 Hematemesis, hematochezia,
or
melena
should
be
considered an emergency and
managed in an intensive care
unit or other monitored
setting.
 IV fluid resuscitation should
begin immediately and may
require transfusion with blood
products.
 About 80% of patients stop
bleeding
spontaneously;
various endoscopic techniques
are usually the first choice for
the remainder.
CLASSIFICATION:
OVERT GI BLEEDING:
otherwise known as acute GI
bleeding, is visible and can
present
in
the
form
of
hematemesis,
“coffee-ground”
Etiology/
Risk Factors/
Diagnostic Test/
Complications
Upper GI bleeding
Causes can include:

Peptic ulcer. This is the most common
cause of upper GI bleeding. Peptic
ulcers are sores that develop on the
lining of the stomach and upper portion
of the small intestine. Stomach acid,
either from bacteria or use of antiinflammatory drugs, damages the lining,
leading to formation of sores.
 Tears in the lining of the tube that
connects your throat to your stomach
(esophagus). Known as Mallory-Weiss
tears, they can cause a lot of bleeding.
These are most common in people who
drink alcohol to excess.
 Abnormal, enlarged veins in the
esophagus (esophageal varices). This
condition occurs most often in people
with serious liver disease.
 Esophagitis. This inflammation of the
esophagus is most commonly caused by
gastroesophageal
reflux
disease
(GERD).
Lower GI bleeding
Causes can include:

Diverticular disease. This involves the
development of small, bulging pouches
in the digestive tract (diverticulosis). If
one or more of the pouches become
inflamed or infected, it's called
PATHOPHYSIOLOGY
Helicobacter pylori →
mucosal barrier→ inflammation →
mucosa (stomach and duodenum) →
ulcer progresses →
weakening and necrosis of arterial walls→
pseudoaneurysm formation →
rupture and hemorrhage.
CLINICAL MANIFESTATION
NURSING RESPONSIBILITY
Symptoms of gastrointestinal (GI) bleeding may include
 black or tarry stool
 bright red blood in vomit
 cramps in the abdomen
 dark or bright red blood mixed with stool
 dizziness or faintness
 feeling tired
 paleness
 shortness of breath
 vomit that looks like coffee grounds
 weakness
Attaining Normal Fluid Volume:
 Maintain NG tube and NPO
status to rest GI tract and
evaluate bleeding.
 Monitor intake and output as
ordered to evaluate fluid status.
 Monitor vital signs as ordered.
 Observe for changes indicating
shock, such as tachycardia,
hypotension,
increased
respirations, decreased urine
output, change in mental
status.
Acute bleeding symptoms

Administer I.V. fluids and
You may go into shock if you have acute bleeding. Acute
blood products as ordered to
bleeding is an emergency condition. Symptoms of shock
maintain volume.
include




a drop in blood pressure
little or no urination
a rapid pulse
unconsciousness
Attaining Balanced Nutritional
Status:
 Weigh daily to monitor caloric
status.
 Administer I.V. fluids, TPN if
ordered to promote hydration
and nutrition while on oral
restrictions.
 Begin liquids when patient is
no longer NPO. Advance diet
as tolerated. Diet should be
high-calorie,
high-protein.
Frequent, small feedings may
be indicated.
 Offer snacks; high-protein
supplements.
Education:
 Discuss
the
cause
and
treatment of GI bleeding with
patient.
 Instruct patient regarding signs
emesis, melena, or hematochezia.

OCCULT OR CHRONIC GI:
bleeding as
a result of
microscopic hemorrhage can
present as Hemoccult-positive
stools with or without iron
deficiency anemia

OBSCURE GI BLEEDING:
refers to recurrent bleeding in
which a source is not identified
after upper endoscopy and
colonoscopy. Obscure bleeding
may be either overt or occult




diverticulitis.
Inflammatory
bowel
disease
(IBD). This includes ulcerative colitis,
which causes inflammation and sores in
the colon and rectum, and Crohn's
disease, and inflammation of the lining
of the digestive tract.
Tumors. Noncanerous (benign) or
cancerous tumors of the esophagus,
stomach, colon or rectum can weaken
the lining of the digestive tract and
cause bleeding.
Colon polyps. Small clumps of cells
that form on the lining of your colon can
cause bleeding. Most are harmless, but
some might be cancerous or can become
cancerous if not removed.
Hemorrhoids. These are swollen veins
in your anus or lower rectum, similar to
varicose veins.
Anal fissures. These are small tears in
the lining of the anus.
Proctitis. Inflammation of the lining of
the rectum can cause rectal bleeding.
Complications:
A gastrointestinal bleed can cause:



Shock
Anemia
Death
DIAGNOSTIC TEST:
 Stool test inspection of stool, having a
black, tarry appearance; analysis of the
sample to for fecal occult blood test to
determine any GI bleeding

Blood tests complete blood count (CBC)

and symptoms of GI bleeding:
melena, emesis that is bright
red or coffee ground color,
rectal bleeding, weakness,
fatigue, shortness of breath.
Instruct patient on how to test
stool or emesis for occult
blood, if applicable.
may reveal a low hemoglobin count;
hematinics or iron studies may show low
iron levels; biochemistry, may show poor
liver function and kidney function.

Nasogastric lavage – insertion of an NG
tube from the nose into the stomach in
order to aspirate stomach contents and
analyze them

Imaging – abdominal CT scan can be
used to visualize the abdomen

Endoscopy, colonoscopy, and flexible
sigmoidoscopy -– insertion of a long tube
with a small camera on its end in order to
visualize the GI tract Capsule

Endoscopy – swallowing a small capsule
containing a camera that takes pictures
while it travels down the GI tract

Balloon-assisted enteroscopy – used to
visualize parts of the small intestines that
the doctor cannot view using endoscopy

Angiography – insertion of a contrast in
an artery and taking X-rays to look and
treat the bleeding blood vessels
References:

“Gastrointestinal
GI
Bleed
Nursing
Diagnosis
Interventions
and
Care
Plans.”
NurseStudy.net,
3
Oct.
2020,
nursestudy.net/gi-bleed-care-plan-nclex-
review/?fbclid=IwAR3Lpoo956MAq48GSQtdBFXC040MtfI3py1UkIJpw2RTQf_iHHI53gcZIv0. Accessed 17 Sept. 2021.

Kim, Bong Sik Matthew. “Diagnosis of Gastrointestinal Bleeding: A Practical Guide for Clinicians.” World Journal of Gastrointestinal Pathophysiology, vol. 5, no. 4, 2014, p. 467, 10.4291/wjgp.v5.i4.467.

Mayo Clinic. “Gastrointestinal Bleeding - Symptoms and Causes.” Mayo Clinic, 15 Oct. 2020, www.mayoclinic.org/diseases-conditions/gastrointestinal-bleeding/symptoms-causes/syc-20372729.

“Overview of Gastrointestinal Bleeding - Gastrointestinal Disorders.” MSD Manual Professional Edition, 2020, www.msdmanuals.com/professional/gastrointestinal-disorders/gastrointestinal-bleeding/overview-of-gastrointestinalbleeding?fbclid=IwAR0Fe8Fb-4BrZsb9kyGoOZ3g31RORKKwh1hD6ekuThk--b2W0I01xoM9glU. Accessed 17 Sept. 2021.
Intra-abdominal HTN & Abdominal Compartment Syndrome – Disorder
Disorder
Intra-abdominal pressure (IAP)
=Is defined by a sustained repeated
pathological elavation in IAP 12MMhG
=is the pressure within the abdominal
cavity.
Intra-Abdominal hypertension(IAH)
Is the steady-state pressure concealed
within the abdominal cavity
Abdominal Compartment
Syndrome(ACS)
Sustained IAP >20mmHg(with or without
an APP <60mmHg) that is associated with
new organ dysfuction/failure.
Types of IAH/ACS
Primary IAH/ACS
=Injury/Disease of abdominal perlvic
region, “surgical”
=is a conition associated with injury or
disease in the abdominopelvic region that
frequently requires early surgical or
interventional radiological intervention
Secondary IAH/ACS
=Sepsis, capilliary leak, burns, “Medical”
=refers to conditions that do not originate
from the abdominopelvic region
Recurrent IAH/ACS
ACS develops despite surgical
intervention
Etiology/
Risk Factors/
Diagnostic Test/
Complications
Risk factors for IAH/ACS:
1. Diminished abdominal wall compliance
● Acute respiratory failure, especially w/
↑ intrathoracic pressure.
● Abdominal surgery w/ primary fascial
or tight closure
● Major trauma/ burns
● Prone positioning, head of bed >30
degrees
● ↑ BMI, central obesity
2. Increased intra-luminal contents
● Gastroparesis
● Ileus
● Colonic pseudo-obstruction
3. Increased abdominal contents
● Hemoperitoneum/pnuemoperitoneum
● Ascites/ Liver dysfunction
4. Capillary leak/ fluid resuscitation
● Acidosis (pH<7.2)
● Hypotension
● Hypothermia (<33℃)
● Polytransfusion (>10 units of
blood/24hr)
● Coagulopathy (platelets<55000/mm3
OR prothrombin time >15 secs. OR
partial thromboplastin time > 2 time
normal OR international standardised
ratio >1.5)
● Massive fluid resuscitation (>5L/24 hr)
● Pancreatitis
● Oliguria
● Sepsis
● Major trauma/burns
● Damage control laparotomy
Pathophysiology
Intra-abdominal Hypertension
Intra-abdominal pressure
Hypoperfusion and ischemia
Release of cytokines and O2 free radicals
Cellular production of adenosine
triphosphate
Translocation of bacteria to the gut and
intestinal edema
Multi-organ failure
Clinical Manifestation









Increase in abdominal girth
Difficulty breathing
Decreased urine output
Syncope
Melena
Alcohol abuse
Nausea and vomiting
History of pancreatitis
Difficulty of breathing
Nursing Responsibilities
Nursing Responsibility and Treatment
for Intra-abdominal HTN
-If there is an upward trend to a Grade
II or Grade III (IAP 16-20 mHg), the
patient should receive evencloser
monitoring. The following interventions
can be done:
• All previous listed
• Enteral nutrition at trophic levels only
• Colloids plus diuretics
• Hemofiltration/dialysis to remove excess
fluid
• Ultrasound or CT the abdomen to
identify free fluid, space occupying lesions
amenable to
drainage
• Paracentesis catheter to drain any free
fluid
• CT or US guided drainage or abscesses
or hematomas
-If the patient advances to a Grade IV
(IAP >20 mmHg), the following
interventions can be done:
• All previous listed
• Neuromuscular blockade and infusion
• Colonoscopy to decompress distended
colon
• Stop enteral nutrition
• Surgical evacuation of any tumors,
masses
•
Surgical
consultation
to
plan
decompressive laparotomy if the above
interventions fail, IAP
exceeds 25 mmHg or organ failure ensues
Important!
Like any hemodynamic number, it is
important to look at the trend of the
number and correlateit with the patient's
signs and symptoms.
Complications:
● Infection
● hemorrhage
● Renal failure
● Bowel ischemia
● Respiratory distress
● Increased cranial pressure
● Low cardiac output and shock
Risk factors for IAH/ACS:
1. Diminished abdominal wall compliance
● Acute respiratory failure, especially w/
↑ intrathoracic pressure.
● Abdominal surgery w/ primary fascial
or tight closure
● Major trauma/ burns
● Prone positioning, head of bed >30
degrees
● ↑ BMI, central obesity
2. Increased intra-luminal contents
● Gastroparesis
● Ileus
● Colonic pseudo-obstruction
3. Increased abdominal contents
● Hemoperitoneum/pnuemoperitoneum
● Ascites/ Liver dysfunction
4. Capillary leak/ fluid resuscitation
● Acidosis (pH<7.2)
● Hypotension
● Hypothermia (<33℃)
● Polytransfusion (>10 units of
blood/24hr)
● Coagulopathy (platelets<55000/mm3
OR prothrombin time >15 secs. OR
partial thromboplastin time > 2 time
normal OR international standardised
ratio >1.5)
● Massive fluid resuscitation (>5L/24 hr)
● Pancreatitis
● Oliguria
Nursing Responsibility for Abdominal
Compartment Syndrome
Because of tissue necrosis, patients with
abdominal compartment syndrome are at
risk for infection.
-Monitor the patient's vital signs and
surgical wound closely. Report signs and
symptoms of infection to the healthcare
provider.
-Be aware of all complications that can
occur systemwide with abdominal
compartment syndrome, and assess the
patient each shift; more frequently if
abnormalities occur.
-Assess the patient's pain using a valid and
reliable pain intensity rating scale.
-If the patient needs more analgesia than is
prescribed, notify the healthcare provider.
-Perform a gastrointestinal assessment
every shift or more frequently if needed,
assessing for abdominal distention,
discoloration, and firmness.
-Assess bowel sounds.
-Assess the patient's nutritional status and
ambulation status for changes from
baseline.
-For patients who had surgery, assessment
is essentially the same as for presurgery
patients with abdominal compartment
syndrome.
-Monitor for signs and symptoms of
infection (drainage, fever, abdominal
distension and firmness, increased pain);
monitor nutrition, ambulation, and bowel
sounds; and monitor intake and output,
particularly if the patient has wound
drainage, anorexia, or decreased fluid
intake.
● Sepsis
● Major trauma/burns
● Damage control laparotomy
Complications:
● Infection
● hemorrhage
● Renal failure
● Bowel ischemia
● Respiratory distress
● Increased cranial pressure
● Low cardiac output and shock
References:
 Newcombe, Jennifer & Mathur, Mudit & Ejike, Janeth. (2012). Abdominal Compartment Syndrome in Children. Critical care nurse. 32. 51-61. 10.4037/ccn2012761.

Newman RK, Dayal N, Dominique E. (2021).Abdominal Compartment Syndrome. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-.Retrieved from: https://www.ncbi.nlm.nih.gov/books/NBK430932/

Paula, R. (2021). Abdominal compartment syndrome workup: Approach considerations, CT and other imaging studies, intra-abdominal pressure measurement. Abdominal Compartment Syndrome Workup: Approach Considerations, CT
and Other Imaging Studies, Intra-abdominal Pressure Measurement. Retrieved from https://emedicine.medscape.com/article/829008-workup#showall.

Walker, J. (n.d.). Pathophysiology and management of abdominal compartment syndrome. PubMed. Retrieved September 18, 2021, from https://pubmed.ncbi.nlm.nih.gov/12882069/
Liver Failure
Disorder
LIVER FAILURE
Anatomy
and
Physiologic
Overview of Liver
٠Liver is the largest gland of the
body. It can be considered a
chemical
factory
that
manufactures, stores, alters and
excretes a large number of
substances
involved
in
metabolism.
٠The liver is a large, highly
vascular organ locate behind the
ribs in the upper right portion of
the abdominal cavity. It weighs
1200 and 1500 g and is divided
into four lobes.
-The liver is especially important
in the regulation of glucose and
protein metabolism.
Functions of the Liver:
-Glucose Metabolism
-Ammonia Conversion
-Protein Metabolism
-Fat metabolism
-Vitamin and Iron Storage
-Bile Formation
-Bilirubin Excretion
-Drug Metabolism
Etiology/
Risk Factors/
Diagnostic Test/
Complications
Risk Factors:
-heavy alcohol use
-type 2 diabetes
-exposure to other people’s blood and body
fluids
-Unprotected sex
-Family history of liver disease
-tattoos or body piercings
-injecting drugs using shared needles
-exposure to certain chemicals
-obesity
-individual who are taking drugs such as
acetaminophen
Diagnostic Test
-Liver function test (used to help diagnose
and monitor liver disease or damage. It
measures the level of certain enzymes and
protein in the blood.)
-Liver Biopsy (is the removal of a small
amount of liver tissue that is usually through
needle aspiration.
-Ultrasonography, computed tomography
(CT) scan
-magnetic resonance imaging (MRI)\
-Laparoscopy (used to examine thge liver
and other pelvic structures
Complications
-ascites
-spontaneous bacterial peritonitis
LIVER FAILURE
-It is the ability of the liver to -portal hypotension
perform its normal synthetic and -variceal bleeding
metabolic functions as part of -hepatorenal syndrome
-hepatic encephalopathy
normal physiology.
- Acute and Chronic is the the
type of liver failure. However, a *Liver failure is a life threatening
third form of this disease known condition that demands urgent medical
as acute on chronic liver failure care.
(ACLF)
Pathophysiology
Clinical Manifestation
Hepatitis and other viruses
Alcohol abuse
Prolonged use of medication
(acetaminophen)
↓
Injured the hepatocytes
↓
Accumulation of a cascade of
inflammatory cytokines
↓
Results in hepatic injury in the presence of
failure of hepatocyte
↓
Compromise in immune function and liver
decompensation
↓
Susceptibility to infections, multi-organ
failure and death
*The early symptoms of liver failure are often similar to those
of liver diseases and other conditions.
٠Early symptoms
-diarrhea
-loss of appetite
- nausea
-fatigue
Nursing Responsibilities
Treatment for Acute Liver Falure
(ALF)
-Patients require urgent treatment and
monitoring, including serial blood and
coagulation tests.
- To reduce the risk of aspiration
pneumonitis, patients with a decreased
level of consciousness are likely to be
*As a liver failure progresses, the symptoms become more intubated.
-Encephalopathy
necessitates
serious that needs the proper care.
treatment of fever and hyponatremia,
-jaundice
as well as sepsis screening.
-bleeding easily
-.High-grade encephalopathy warrants
-swollen belly
endotracheal intubation, with partial
-mental confusion (hepatic encephalopathy)
pressure of carbon dioxide maintained
-sleepiness
between 31 and 44 mm Hg and serum
-portal hypotension
sodium between 145 and 150 mmol/L.
-gynecomastia
-Intracranial hypertension calls for
-ascites
osmotherapy, temperature control, and
-pale stool
rescue therapy (such as indomethacin
and thiopentone).
-Antibiotic prophylaxis may be given
to patients at high sepsis risk.
Treatment for Chronic Liver
Failure (CLF)
-It focuses on stopping additional liver
damage and slowing
disease progression, as well as
managing symptoms.
-It includes a healthy, low-sodium
diet, abstaining
from alcohol and illicit drugs as well
as
addressing medical problems as they
occur. -The patients may
need a liver transplant.
NURSING CARE
-It focuses on supporting
body
TYPES:
1. ACUTE LIVER FAILURE
- It is loss of liver function that
occurs rapidly in days or weeks
that is usually in a person who has
no preexisting liver disease.
-It is most commonly caused by a
hepatitis virus or drugs such as
acetaminophen.
-It is also known as fulminant
hepatic failure that can cause
serious complications including
excessive bleeding and increasing
pressure in the brain.
2. CHRONIC
LIVER
FAILURE
-It may develops more slowly
that acute liver failure.
-It can take months or even years
before exhibit any symptoms.
-It is often the result of cirrhosis
which is usually caused by long
term alcohol use. Liver cirrhosis
occurs when healthy liver tissue is
replaced with scar tissue.
Three Types of Alcohol related
to Liver Failure:
-Alcoholic fatty liver disease (is
the result of fat cells deposited in
the liver and affects those who
drink a lot of alcohol and those
who are obese/
-Alcoholic
hepatitis
(characterized by fat cells in the
liver, inflammation and scarring.
According to the American Liver
Foundation, up to 35% of people
who drink heavily will develop
this condition.
-Alcohol cirrhosis (the most
advanced out of the three types
because ccording to American
Liver Foundation, that some form
of cirrhosis affects 10%-20%of
people who drink heavily.
Nursing care for patients with liver
failure focuses on supporting body
systems, managing signs and symptoms of
decreased liver function,
and avoiding worsening cerebral
edema.
• Monitor level of consciousness,
blood pressure, volume status,
blood and coagulation tests, and
signs and symptoms.
• Keep the head of the bed elevated 30
degrees, with the patient’s
head in the neutral position.
• Decrease stimulation, such as
frequent suctioning.
• Stay alert for hypercapnia and
hypoxia; correct these conditions
as indicated and ordered.
• Manage fever aggressively with a
fan, cooling blanket, or both.
• Watch for signs and symptoms of
infection and possible sepsis; administer
antibiotics, as needed
and ordered.
• Maintain strict glucose monitoring for
possible hypoglycemia or
hyperglycemia.
• Provide nutritional support as ordered.
Patients who reach an acuity
level that warrants close monitoring (such as
those in an intensive
care unit with grade 3 or 4 hepatic
encephalopathy) require ICP monitoring
systems,
managing
signs
and
symptoms of decreased liver function
and avoiding worsening cerebral
edema.
٠Monitor level of consciousness,
blood pressure, volume status,
blood and coagulation tests, and
signs and symptoms.
•Keep the head of the bed elevated 30
degrees, with the patient’s
head in the neutral position.
•Decrease stimulation, such as
frequent suctioning.
•Stay alert for hypercapnia and
hypoxia, correct these conditions as
indicated and ordered.
•Manage fever aggressively with a
fan, cooling blanket, or both.
•Watch for signs and symptoms of
infection
and
possible
sepsis,administer
antibiotics,
as
needed
and ordered.
•Maintain strict glucose monitoring for
possible hypoglycemia or
hyperglycemia.
•Provide nutritional support as
ordered.
Patients who reach an acuity level that
warrants close monitoring (such as
those in an intensive
care unit with grade 3 or 4 hepatic
encephalopathy)
require
ICP
monitoring.
*Postoperative Care
After the liver transplantation.
- Assess the patient for complications
such as bleeding, infection, and
rejection.
-Monitor the patient’s temperature,
urine output, neurologic status and
hemodynamic pressures.
-Provide
education
about
immunosuppressive drugs.
PATHOPHYSIOLOGY OF LIVER FAILURE
Hepatitis and other
viruses
Injured the hepatocytes
Accumulation of a cascade of
inflammatory cytokines
Alcohol abuse
Prolonged
use
of
medication (acetaminophen)
Susceptibility
to
infections,
multiorgan failure and
death
Compromise
in
immune function and
liver decompensation
Reference:
-Das, J., (2011),Liver Disease, Retrived from:https://pharmaceutical-journal.com/article/ld/liver-disease-pathophysiology
Results in hepatic injury in
the presence of failure of
hepatocyte regeneration.
Acute Pancreatitis
Etiology/
Risk Factors/
Diagnostic Test/
Complications
Disorder
Acute Pancreatitis
★ Causes:
“I GET SMASHED”
-Is a sudden inflammation of the
I- Idiopathic
pancreas.
- Pancreatitis is commonly
described as autodigestion of the G- Gallstones
E- Ethanol abuse
pancreas.
T- Trauma
★ Function of Pancreas
a. Endocrine cells that are
S- Steroids
specifically known as the islet of
M- Mumps virus
Langerhans cells that secrete
A- Auto-Immune Diseases
hormones to regulate the blood
S- Scorpion Stings
sugar.
H- Hypertriglyceremia & Hypercalcemia
- alpha Glucagon (↑ B.G)
E- Endoscopic retrograde
- beta Insulin (↓ B.G)
cholangiopancreatography (ERCP)
-delta cells Somastosin (inhibit
D- Drugs
the secretion of pancreatic
hormones)
★ Local Complications:
- Pseudocyst
b. Exocrine cells with the help of -Pancreatic cysts or abscesses, -Endocrine and
acinar cells that secretes inactive
exocrine dysfunction
digestive enzymes to the
- Fluid and electrolyte disturbances
pancreatic duct to break down
★ Systemic Complications:
foods into nutrients in the
-Pulmonary insufficiency with hypoxia
digestive system-Duodenum.
- Pneumonia
- Amylase (breaks carbs to
- Plural effusion
glucose)
-Atelectasis
- Trypsin (breaks ↓ protein)
- ARDS
- Lipase (breaks ↓fats)
- Hypotension
- Acute renal failure
- Pancreatic necrosis
★ 2 types of A. Pancreatitis
1. Mild (Edematous or interstitial -GI bleeding/hemorrhage
pancreatitis)
- Septic Shock
- affects the majority of the pt.
- The edema and inflammation are ★ Diagnostic Test:
confined to the pancreas itself.
- Serum amylase, lipase, glucose, bilirubin,
- return to normal. function
alkaline phosphatase, lactate dehydrogenase,
Pathophysiology
- Self-digestion of the pancreas caused by
its own proteolytic enzymes, particularly
trypsin, causes acute pancreatitis.
Entrapment
Gallstones enter the common bile duct and
lodge at the ampulla of Vater.
↓
Obstruction
The gallstones obstruct the flow of the
pancreatic juice or causing reflux of bile
from the common bile duct into the
pancreatic duct.
↓
Activation
The powerful enzymes within the pancreas
are activated.
↓
Enzyme activities
Activation of enzymes can lead to
vasodilation, increased vascular
permeability, necrosis, erosion, and
hemorrhage.
↓
Reflux
These enzymes enter the bile duct, where
they are activated and together with bile,
back up into the pancreatic duct, causing
pancreatitis.
Clinical Manifestation
●
●
●
●
●
●
●
Nursing Responsibilities
★ Medical Management
● Pain Management:
- Adequate administration of analgesia
Abdominal pain, usually constant, mid epigastric or
to minimize restlessness, which may
periumbilical, radiating to the back or flank.
stimulate pancreatic secretion further.
Nausea and vomiting
- Pain relief may require parenteral
Fever
opioids such as morphine, fentanyl
Involuntary abdominal guarding, epigastric tenderness.
(Sublimaze), or hydromorphone.
Dry mucous membranes, hypotension, cold clammy skin, - Antiemetic agents may be prescribed
cyanosis or tenderness, tachycardia, and mild to moderate to prevent vomiting.
dehydration.
- Cimetidine (Tagamet) is given to
Purplish discoloration of the flanks (Turner’s sign) or of
decrease hydrochloric acid secretion.
the periumbilical area (Cullen’s sign).
● Intensive care:
Shock with respiratory distress and acute renal failure.
- Nasogastric suction is used to relieve
nausea and vomiting, decrease painful
abdominal distention and paralytic
ileus and remove hydrochloric acid so
that it does not stimulate the pancreas.
- Correction of fluid and blood loss
and low albumin levels.
- Hemodynamic monitoring and
arterial blood gas monitoring.
- Antibiotic agents may be prescribed
if an infection is present.
- Insulin may be required if
hyperglycemia occurs.
● Respiratory Care
-is indicated because of the high-risk
elevation of the diaphragm, pulmonary
infiltrates and effusion, and atelectasis.
● Biliary Drainage
- Placement of biliary drains (for
external drainage) and stents
(indwelling tubes) in the pancreatic
duct to reestablish drainage of the
pancreas.
● Surgical Intervention
Diagnostic laparotomy
usually occurs within 6 months.
2. Severe (necrotizing
pancreatitis)
- presence of tissue necrosis in
either the pancreatic parenchyma
or in the tissue surrounding the
gland.
- Enzymes damage the local blood
vessels, and bleeding and
thrombosis can occur.
★ Classification
- Acute pancreatitis.
does not usually lead to chronic
pancreatitis unless complications
develop.
-Chronic pancreatitis.
is an inflammatory disorder
characterized by progressive
destruction of the pancreas.
AST, ALT, potassium, and cholesterol may
be elevated.
- Serum albumin, calcium, sodium,
magnesium, and potassium may be low due
to dehydration.
-Hematocrit and hemoglobin levels are used
to monitor the patient for bleeding.
- Abdominal x-ray to detect an ileus or
isolated loop of small bowel overlying
pancreas.
- CT scan is the most definitive study.
- Chest x-ray for detection of pulmonary
complications
- To establish pancreatic drainage; or
to resect or debrided an infected,
necrotic pancreas.
- The patient may have multiple drains
in place postoperatively, as well as a
surgical incision that is left open for
irrigation and repacking.
★ Nursing Management
● The patient should avoid oral
intake to inhibit pancreatic
stimulation and secretion of
pancreatic enzymes.
- Total parenteral nutrition is
administered to assist with metabolic
stress.
● Maintain fluid and electrolyte
balance
- Assess fluid and electrolyte status
(e.g. skin turgor, mucous membranes,
intake, and output); and provide
replacement therapy as indicated.
● Promote adequate nutrition
- Assess nutritional status; monitor
glucose levels; monitor IV therapy,
provide a high-carbohydrate, lowprotein, low-fat diet when tolerate; and
instruct the client to avoid spicy foods.
● Maintain optimal respiratory
status
- Place the client in semi-Fowler’s
position to decrease pressure on the
diaphragm.
-Teach the client coughing and deepbreathing techniques.
● Maintaining Skin Integrity
- Assess the wound, drainage sites, and
skin for signs of infection,
inflammation, and breakdown.
- The patient must be turned in every 2
hours.
References:

Belleza, M. (2021, February 20). Study guide for nurses: Pancreatitis nursing care and management. Nurseslabs. Retrieved from https://nurseslabs.com/pancreatitis/#pathophysiology.

RNpedia. (2017, July 9). Acute pancreatitis nursing care plan & management. Retrieved from https://www.rnpedia.com/nursing-notes/medical-surgical-nursing-notes/acute-pancreatitis-nursing-management/.

Brunner, L., & Smeltzer, S. (2010). Brunner & Suddarth's textbook of medical-surgical nursing. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.
Bariatric Surgery
Disorder
Bariatric Surgery
 Most common bariatric
procedures in US
 Limited to clients who
 Are morbidly obese
 Unable to lose weight via
diet/exercise Body weight ≥
45 kg/m2 or 100% above ideal
weight
 BMI > 40 kg/m2
 BMI ≥ 35 kg/m2 with medical
comorbidities (HTN,
metabolic syndrome, heart
disease)
 Can tolerate surgery
 Are free of drug/alcohol
addiction

Bariatric surgeries may
remove parts of the stomach
and small intestine or may
slow the entry of food into
stomach.
Three Basic Mechanisms
 Restrictive & Malabsorptive
and Combination
procedures :
 Laparoscopic Adjustable
Etiology/
Risk Factors/
Diagnostic Test/
Complications
Etiology:
 Obesity
Short term Risks :

Adverse reactions to anesthesia,
problems, Leaks in GI system,
Death (rare)
Longer term risks .
 Bowel obstruction, Dumping
syndrome,Gallstones , Hernias,
hypoglycemia, Malnutrition,
Ulcers, Acid reflux, Death (rare)
Complications:
 Adjustable gastric banding
•Low complication rate
• Some nausea and vomiting initially
• Problems with adjustment device •
Band may slip or erode into stomach
wall
• Gastric perforation
 Vertical sleeve gastrectomy
• Weight loss may be limited
• Leakage related to stapling
 Vertical banded gastroplasty
(VBG)
• High complication rate
• Slow weight loss
• Rupture of staple line
• Dilated pouch
Pathophysiology
Bariatric Surgery for morbid obesity
Ghrelin is known as the hunger
hormone
The stomach is empty
Ghrelin is secreted
The stomach is stretched
Ghrelin secretion decrease
This hormone works on the
hypothalamic brain cells
Both to increase hunger,
Increase gastric acid secretion
Known contributors include readily
Clinical Manifestation







Nursing Responsibility
Nausea/vomiting
Possibly syncope
Dehydration
 Monitoring and managing potential complications


 Dumping Syndrome (next slides)
 Dysphagia
 Bowel and Gastric Outlet Obstructions
 Obesity to occur:
 Diet of foods high in calories & fat, lack of exercise,
& over consumption of food
 Encourage the client to
express emotions about
eating behaviors, weight, and
weight loss to identify
psychosocial factors related to
obesity.
Arrange for availability of a
bariatric bed and mechanical
lifting devices to prevent
client/staff injury.
Assess pertinent lab results
(CBC, electrolytes, BUN,
creatinine, HbA1c, iron,
vitamin B12, thiamine, and
folate).
 Maintain Fluid Balance: Give
IV fluids until bowel sounds
return
Sugar Free Oral Fluids
Advance Diet as follows: clear
liquids, full liquids, soft solids,
and solid foods.
Discharge Teaching for the
Patient
Nutrition:
 Diet progression, nutrient
(including vitamin and
mineral) supplements,




gastric banding (LAGB) uses
a band to create a small
proximal gastric pouch.
Vertical sleeve gastrectomy
involves creating a sleeveshaped stomach by removing
about 80% of the stomach.
Vertical banded gastroplasty
(VBG) involves creating a
small gastric pouch.
Biliopancreatic diversion
(BPD) with duodenal switch
procedure creates an
anastomosis between the
stomach and the intestine.
Roux-en-Y gastric bypass
(RYGB) procedure involves
constructing a gastric pouch
whose outlet is a Y-shaped
limb of small intestine.
Types of bariatric surgery
 Roux-en-y gastric bypass
(rygb)
 Limits stomach size, &
duodenum & part of jejunum
are bypassed; limits
absorption of calories
 Biliopancreatic diversion w/a
duodenal switch
 Creates a more tubular gastric
“sleeve” W/connection to a
small part of duodenum.
 Vertical sleeve gastrectomy
 Removes at least half of
stomach, restricting dhrelin,
hormone that prompts
appetite; reduces hunger
more than other restrictive
surgeries.
• Dumping syndrome
 Biliopancreatic diversion (BPD)
• Abdominal bloating, diarrhea, and
foul-smelling gas (steatorrhea)
• Three or four loose bowel
movements a day
• Malabsorption of fat-soluble
vitamins
• Iron deficiency
• Protein-calorie malnutrition
• Dumping syndrome
 Roux-en-Y gastric bypass (RYGB)
•Leak at site of anastomosis
• Anemia: iron deficiency, cobalamin,
folic acid, Calcium deficiency
• Dumping syndrome
Diagnostic test:
 Screened for psychologic, physical,
and behavioral conditions.
 Height and weight chart:
 if more than 20% above ideal
body weight for age and body
 Measure waist & then hip
circumference.
 Calculate waist-to-hip rat
 A body mass index (BMI) of more
than 30 indicates obesity
 CBC, electrolytes (CMP test),
BUN, Cr.
available:
 High-calorie prepackaged foods
 Prevalence of high fructose corn
syrup in foods
 Consumption of sodas
 High fat fast food &
“supersized” Portions available in
restaurants.
hydration guidelines
Drug therapy:
 Analgesics and antiemetic
drugs, if needed; drugs for
other health problems
Wound care:
 Clean procedure for open or
laparoscopic wounds; cover
during shower or bath
Activity level:
 Restrictions, such as avoiding
lifting; activity progression;
return to driving and work
Signs and symptoms to report:
 Fever; excessive nausea or
vomiting; epigastric, back, or
shoulder pain; red, hot, and/or
draining wound(s); pain,
redness, or swelling in legs;
chest pain; difficulty breathing
Follow-up care:
 Health care provider office or
clinic visits, support groups
and other community
resources, counseling for
patient and family
Continuing education:
 Nutrition and exercise classes;
follow-up visits with dietitian
References:




Dhalla, N. S., Ramjiawan, B., Tappia, P. S., & Germans. (2020). Pathophysiology of obesity-induced health complications. Springer International Publishing.
Lewis, S. M., Collier, I. C., & Heitkemper, M. M. (1996). Medical surgical nursing assessment and management of clinical problems. Mosby.
Mayo Foundation for Medical Education and Research. (2020, January 22). Bariatric surgery. Mayo Clinic. Retrieved September 17, 2021, from https://www.mayoclinic.org/tests-procedures/bariatric-surgery/about/pac-20394258.
Hyperarts, R. M.-. (n.d.). Upper (GI) ENDOSCOPY. Bariatric Surgery - Upper (GI) Endoscopy. Retrieved September 17, 2021, from https://bariatricsurgery.ucsf.edu/conditions--procedures/upper-(gi)-endoscopy.aspx.
Diabetic Ketoacidosis
DISORDER
Etiology/
Risk Factors/
Diagnostic Test/
Complications
Diabetic Ketoacidosis
is a serious complication of diabetes  Have type 1 diabetes
that occurs when your body produces  Frequently miss insulin doses
high levels of blood acids called
Uncommonly, diabetic ketoacidosis can
ketones.
occur if you have type 2 diabetes. In some
cases, diabetic ketoacidosis may be the
Key Points:
-The condition develops when your first sign that you have diabetes.
body can't produce enough insulin.
-Insulin normally plays a key role in Complications:
helping sugar (glucose) — a major  Low
blood
sugar
source of energy for your muscles
(hypoglycemia). Insulin allows sugar
and other tissues — enter your cells.
to enter your cells, causing your blood
-Without enough insulin, your body
sugar level to drop. If your blood
begins to break down fat as fuel.
sugar level drops too quickly, you can
This process produces a buildup of
develop low blood sugar.
acids in the bloodstream called  Low potassium (hypokalemia). The
ketones, eventually leading to
fluids and insulin used to treat diabetic
diabetic ketoacidosis if untreated.
ketoacidosis can cause your potassium
level to drop too low. A low potassium
level can impair the activities of your
heart, muscles and nerves. To avoid
this, electrolytes, including potassium
are usually given along with fluid
replacement as part of the treatment of
diabetic ketoacidosis.
 Swelling in the brain (cerebral
edema). Adjusting your blood sugar
level too quickly can produce swelling
in your brain. This complication
appears to be more common in
PATHOPYSIOLOGY
Lack of Insulin - Decreased utilization of
glucose by muscle, fat, and liver increased production of glucose by liver Hyperglycemia - blurred vision, polyuria dehydration - weakness, headache,
increased thirst(polydypsia)
Lack of insulin - breakdown of fat increased fatty acids - increase ketone
bodies - Acetone breath, poor apetite,
nausea - acidosis - nausea, vomiting,
abdominal pain - increasing rapid
respirations.
CLINICAL MANIFESTATIONS










Excessive thirst
Frequent urination
Nausea and vomiting
Stomach pain
Weakness or fatigue
Shortness of breath
Fruity-scented breath
Confusion
High blood sugar level
High ketone levels in your urine
NURSING RESPONSIBILITIES
Rehydration
In dehydrated patients, rehydration is
important for maintaining tissue
perfusion. In addition, fluid
replacement enhances the excretion of
excessive glucose by the kidneys.
Restoring Electrolytes
The major electrolyte of concern
during treatment of DKA is potassium.
The initial plasma concentration of
potassium may be low, normal, or
high, but more often than not, tends to
be high (hyperkalemia) from
disruption of the cellular sodiumpotassium pump (in the face of
acidosis).
Reversing Acidosis
Ketone bodies (acids) accumulate as a
result of fat breakdown. The acidosis
that occurs in DKA is reversed with
insulin, which inhibits fat breakdown,
thereby ending ketone production and
acid buildup.
Treatment:
 Fluid
replacement. You'll
receive fluids — either by mouth
children, especially those with newly
diagnosed diabetes.
Diagnostic Tests:
 Blood test,
 Arterial blood gas
 Urinalysis
 Electrocardiogram


or through a vein — until you're
rehydrated. The fluids will replace
those
you've
lost
through
excessive urination, as well as
help dilute the excess sugar in
your blood.
Electrolyte
replacement. Electrolytes
are
minerals in your blood that carry
an electric charge, such as
sodium, potassium and chloride.
The absence of insulin can lower
the level of several electrolytes in
your blood. You'll receive
electrolytes through a vein to help
keep your heart, muscles and
nerve cells functioning normally.
Insulin therapy. Insulin reverses
the processes that cause diabetic
ketoacidosis. In addition to fluids
and electrolytes, you'll receive
insulin therapy — usually through
a vein. When your blood sugar
level falls to about 200 mg/dL
(11.1 mmol/L) and your blood is
no longer acidic, you may be able
to stop intravenous insulin therapy
and
resume
your
normal
subcutaneous insulin therapy.
References:

Brunner & Suddarth's Textbook of Medical-Surgical Nursing (Textbook of Medical-Surgical Nursing- 13th ed) by Hinkle PhD RN CNRN Janice L. Cheever PhD RN Kerry H. (2013-11-18)

Mayo Foundation for Medical Education and Research. (2020, November 11). Diabetic ketoacidosis. Mayo Clinic. Retrieved September 18, 2021, from https://www.mayoclinic.org/diseases-conditions/diabetic-ketoacidosis/diagnosistreatment/drc-20371555.

Diabetic ketoacidosis. Diabetic ketoacidosis - Complications | BMJ Best Practice. (n.d.). Retrieved September 18, 2021, from https://bestpractice.bmj.com/topics/en-gb/3000097/complications.


Diabetic ketoacidosis. Winchester Hospital. (n.d.). Retrieved September 18, 2021, from https://www.winchesterhospital.org/health-library/article?id=598176.
Mayo Foundation for Medical Education and Research. (2020, November 11). Diabetic ketoacidosis. Mayo Clinic. Retrieved September 18, 2021, from https://www.mayoclinic.org/diseases-conditions/diabetic-ketoacidosis/symptomscauses/syc-20371551.
Hyperglycemia Hyperosmolar Non-Ketotic Acidosis
DISORDER
Hyperosmolar Hyperglycemic
Nonketotic Syndrome (HHNS) - a
dangerous condition resulting from
very high blood glucose levels.
Key points:
❖ A clinical condition that
arises from a complication of
diabetes mellitus.
❖ .HHS is a serious and
potentially fatal complication
of type 2 diabetes.
❖ It is most commonly seen in
patients with obesity.
❖ The mortality rate in HHS
can be as high as 20% which
is about 10 times higher than
the mortality seen in diabetic
ketoacidosis.
Alternative names for HHNS:
❖ Hyperglycemic hyperosmolar
nonketotic coma (HHNK)
❖ Nonketotic hyperosmolar
syndrome (NKHS)
❖ Diabetic hyperosmolar
syndrome.
❖ Diabetic HHS.
❖ Hyperosmolar coma.
❖ Hyperosmolar hyperglycemic
state.
Etiology/
Risk Factors/
Diagnostic Test/
Complications
Pathophysiology
Clinical Manifestation
Nursing Responsibilities
Extreme thirst.
Frequent urination.
Confusion, or a change in your mental state.
Changes in your vision.
Fever (over 101 F)
High blood sugar level (over 600 mg/dL).
INTERVENTIONS:
1. Monitor blood glucose levels
Risk factors:
❖ A stressful event such as infection,
heart attack, stroke, or recent
surgery.
❖ Heart failure.
❖ Impaired thirst.
❖ Limited access to water (especially
in people with dementia or who are
bedbound)
❖ Older age. (Usually 60 or 70 older)
❖ Poor kidney function.
❖ Poor management of diabetes, not
following the treatment plan as
directed.
• HHNS is attributed to three factors
Complications:
❖ Seizures.
❖ Coma.
❖ Swelling of the brain.
❖ Organ failure.
❖ Death.
- Lack of ketoacidosis in HHNS attributed If the precipitating factor is a cardiac or vascular condition,
to:
signs and symptoms will include:
Diagnostic tests:
❖ Urinalysis
❖ ABG analysis
❖ CBC w/ differential
❖ Finger stick test - it is for
measuring blood glucose levels. A
blood glucose level of 600 mg/dL
and low ketone levels are the main
factors for diagnosis of HHNS.
❖ Serum osmolality - a test that
measures the body's
water/electrolyte balance. It
measures the chemicals dissolved
in the liquid part of blood (serum),
such as sodium, chloride,
• Decreased insulin utilization
•
Increased
glycogenolysis
gluconeogenesis
&
❖
❖
❖
❖
❖
❖
• Impaired renal excretion of glucose
If an infectious process precedes HHS, signs, and symptoms
include:
- End result - hyperglycemia and volume
● Fever
depletion through osmotic diuresis.
● Malaise
● General weakness
- Total body water losses can reach 8-12
● Tachypnea
liters
● Tachycardia
• Lower levels
hormones
of
counterregulatory
• High levels of endogenous insulin
inhibiting lypolysis
●
●
●
●
●
Chest pain
Chest tightness
Headache
Dizziness
Palpitations
• Hyperosmolar state inhibiting lypolysis
The most important distinguishing factor in HHS is the
presence of neurological signs. Decreased cerebral blood flow
from severe dehydration can cause:
●
●
●
●
Focal neurological deficit
Disturbance in visual acuity
Delirium
Coma
A system based approach is necessary for the physical
assessment:
The hallmark of HHNS is extremely
elevated blood glucose levels >600
mg/dL
2. Encourage optimal hydration
and administer IV fluids
(Normal Saline) to maintain
fluid balance.
Excessive urination can cause
dehydration. Encourage oral fluids as
tolerated and administer IV fluids to
re-establish tissue perfusion and
maintain electrolyte balance.
3. Insulin (Regular) infusion to
reduce blood glucose level.
Monitor for hypokalemia.
Monitor blood glucose levels and
serum potassium. As insulin is
administered, potassium is lost. Initiate
potassium supplementation as
necessary/
4. Frequently assess level of
consciousness and mentation
The brain is an insulin-dependent
tissue. With elevated glucose levels,
there is not enough insulin to
normalize and the patient becomes
confused, dizzy and may have changes
in level of consciousness. Patients
often experience drowsiness.
bicarbonate, proteins, and glucose.
The test is done by taking a sample
of blood from a vein.
★ General appearance: Patient with HHS are generally
ill-appearing with altered mental status
★ Cardiovascular: Tachycardia, orthostatic
hypotension, weak and thready pulse
5. Monitor for hyperthermia
and treat with antipyretics
(fever reducers), cool
compresses and cooled IV
fluids
★ Respiratory: Rate can be normal, but tachypnea might Thermoregulation is impaired as urine
be present if acidosis is profound
production decreases; sweating
decreases and electrolytes become
imbalanced.
★ Skin: Delayed capillary refill, poor skin turgor, skin
tenting might not be present even in severe
dehydration because of obesity
6. Monitor vitals for
hypotension and tachycardia
★ Genitourinary: Decreased urine output
Most likely related to dehydration and
★ Central Nervous System (CNS): Focal neurological
hypovolemia. Patient is at risk for
deficit, lethargy with low Glasgow Coma Score and in hypovolemic shock.
severe cases of HHS, the patient might be comatose
EDUCATION:
Educating diabetic patients and
their families is the most important
way to prevent HHS.
1. Importance of early
communication with a
healthcare provider when HHS
signs and symptoms appear
2. Importance of maintaining
insulin or oral diabetic
treatment during an illness
3. Appropriate serum glucose
goals
4. Proper use of supplemental
insulin or oral diabetics
5. Importance of keeping
medication on hand to suppress
a fever and getting early
treatment for infection
6. Starting an easily digested
liquid diet containing
carbohydrates and sodium
when nauseated
7. Appropriate sick-day
management, including
monitoring blood glucose
levels, urine output, oral intake,
daily weight, and insulin or
other drug administration.
MEDICATION:
Treatment
typically
involves
starting intravenous (IV) fluids
(saline solution delivered through a
needle into a vein) to rehydrate the
body quickly. It also may require IV
insulin to bring down blood sugar
levels.
-
10 to 15 units of regular human
insulin should be injected as a
bolus,
followed
by
a
continuous
infusion
of
approximately 0.1 U/kg/h.
Once the blood glucose
approaches 13.9 to 16.7
mmol/L (250 to 300) mg/dl,
5% dextrose should be added
to the intravenous fluids and
the rate of insulin infusion
reduced.
References:
 Understanding the presentation of Hyperglycemic Hyperosmolar Nonketotic syndrome. (2008, March 24). EMS1. https://www.ems1.com/ems-products/consulting-management-and-legal-services/articles/understanding-the-presentationof-hyperglycemic-hyperosmolar-nonketotic-syndrome-WzTcv28OOn9CdM1d/
 Hyperosmolar Hyperglycemic Nonketotic coma - StatPearls - NCBI bookshelf. (2021, May 12). National Center for Biotechnology Information. https://www.ncbi.nlm.nih.gov/books/NBK482142/
 Elwyn. (2012, August 1). Hyperosmolar Hyperglycemic Nonketotic syndrome. SlideServe. https://www.slideserve.com/elwyn/hyperosmolar-hyperglycemic-nonketotic-syndrome
 Avoiding Hyperglycemic Hyperosmolar Nonketotic syndrome. (n.d.). Verywell Health. https://www.verywellhealth.com/hyperglycemic-hyperosmolar-nonketotic-syndrome-3289614
 Hyperosmolar Hyperglycemic syndrome. (n.d.). Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/21147-hyperosmolar-hyperglycemic-syndrome
 Diabetic hyperosmolar syndrome - Symptoms and causes. (2020, July 25). Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/diabetic-hyperosmolar-syndrome/symptoms-causes/syc-20371501
Acute and Chronic Renal Failure
Disorder
Etiology/
Risk Factors/
Diagnostic Test/
Complications
Acute Renal Failure
Renal Failure
 Results when the kidneys
cannot remove the body’s
 Prerenal Failure
metabolic wastes or perform Volume depletion resulting from:
their regulatory functions.
- hemorrhage
Key Points:
- renal lossless (diuretics, osmotic
diuresis)
 Substances normally
- gastrointestinal losses (vomiting,
eliminated in the urine
diarrhea, nasogastric suction)
accumulate in the body
fluid as a result of:
Impaired cardiac efficiency resulting from:
- Impaired Renal
- myocardial infarction
Excretion
- heart failure
- Leading to a disruption
in endocrine and
- dysrhythmias
metabolic functions.
- Cardiogenic shock
- Fluid, electrolyte, and
acid-base balance
Vasodilation resulting from:
disturbances.
- sepsis
- anaphylaxis
 It is a systemic disease and
- antihypertensive medications or
final common pathway of
other medications that causes
many different kidney and
vasodilation.
urinary tract diseases.
Types of Renal Failure
 Intrarenal Failure
 Acute Renal Failure – is a Prolonged regional ischemia resulting
sudden and almost complete from:
loss of kidney function over
- pigment nephropathy (associated
a period of hours to days.
with the breakdown of blood cells
containing pigments that into an
 It has 4 phases the
occluded kidney structures)
initiation, oliguria, diuresis,
Myoglobinuria (trauma, crush
and recovery.
injuries, burns)
Acute Renal Failure has 3
hemoglobinuria (transfusion
categories.
reaction, hemolytic anemia)
1. Prerenal – result of
impaired blood flow that
Nephrotoxic agents such as:
leads to hypoperfusion of
- aminoglycoside antibiotics
the kidney.
(gentamicin, tobramycin,
2. Intrarenal – result of actual
radiopaque contrast agents)
parenchymal damage to the
glomeruli or kidney tubules.
- heavy metals (lead, mercury)
3. Postrenal – result of an
- solvents and chemicals (ethylene
Pathophysiology
Clinical Manifestation
Acute Renal Failure
Acute Renal Failure
Pre-renal:
↓ blood flow in the kidneys
↓
Impaired renal perfusion
↓
↓ glomerular filtration rate (GFR) →
activation of RAAS → release of
aldosterone → reabsorption of sodium,
water and urea
↓
↑ nitrogen containing compound in the
blood
↓
ARF
Patient may appear:
 Critically ill
 Lethargic
 w/ persistent nausea and vomiting
 Diarrhea
 Skin and mucous membranes are dry
 Uremic fetor (breath may have the odor of urine)
Intra-renal
Damaged renal tubules
Immune and inflammatory response
↓
Capillary fluid leakage and destruction
↓
↓ glomerular filtration rate (GFR) →
activation of RAAS → release of
aldosterone → reabsorption of sodium,
water and urea
↓
↑ nitrogen containing compound in the
blood
↓
ARF
Post-renal
Sudden obstruction of outflow
↓
Build-up of urine and pressure
↓
Increased renal tubule pressure
↓
Chronic Renal Failure






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Neurologic
Weakness and fatigue, disorientation, seizures,
disorientation, behavior changes.
Integumentary
Gray-bronze skin color, dry and flaky skin, brittle
nails, pruritis, thinning of hair
Cardiovascular
Hypertension, pitting edema, pericarditis, engorged
neck veins, pericardial effusion, hyperkalemia,
hyperlipidemia
Pulmonary
Crackles, thick, tenacious sputum, depressed cough
reflex, shortness of breath, tachypnea, Kussmaul-type
respirations, uremic lung
Gastrointestinal
Ammonia odor to breath, mouth ulcerations and
bleeding, anorexia, nausea and vomiting, hiccups,
constipation or diarrhea, bleeding GI tract.
Hematologic
Anemia, thrombocytopenia
Reproductive
Amenorrhea, testicular atrophy, infertility, decreased
libido
Musculoskeletal
Muscle cramps, loss of muscle strength, bone pain,
bone fractures
Nursing Responsibilities
Acute Renal Failure
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Monitoring Fluid and
Electrolyte Balance
Monitors the patient serum
electrolyte levels and physical
indicators of these
complications during all phases
of the disorder.
Hyperkalemia is the most
immediate life-threatening
imbalance seen in ARF.
The nurse monitors fluid status
by paying careful attention to
fluid intake and output
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Preventing Infection
Asepsis is essential with
invasive lines and catheters to
minimize the risk of infection
and increase metabolism.
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Providing skin care
The skin may be dry or
susceptible to break down as a
result of edema; therefore,
meticulous skin care is
important.
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Providing support
The patient and family need
assistance, explanation and
support during this time. ARF
requires certain treatments that
needs to be explained and
clarified.
The nurse plays an important role in
teaching the patient and family with
ARF.
obstruction somewhere
distal to the kidney.

Chronic Renal Failure
(End-Stage Renal Disease)
- is a progressive,
irreversible deterioration in
renal function in which the
body’s ability to maintain
metabolic and fluid and
electrolyte balance fails,
resulting in uremia or
azotemia.
3 Stages of Chronic Renal
Failure.
 Stage 1 (Reduced renal
reserve) – characterized by
a 40% to 75% loss of
nephron function.
 Stage 2 (Renal
insufficiency) – occurs
when 75% to 90% loss of
nephron function.
 Stage 3 (End stage Renal
disease) – the final stage,
less than 10% nephron
function.
-
glycol, carbon tetrachloride,
arsenic)
Non-steroidal anti-inflammatory
drugs (NSAIDs)
Angiotensin converting enzyme
inhibitors (ACE inhibitors)
Infectious processes such as:
- Acute pyelonephritis
- Acute glomerulonephritis
 Postrenal failure
Urinary tract obstruction including:
- Calculi (stones)
- Tumors
- Benign prostatic hyperplasia
- Strictures
- Blood clots
Diagnostic Tests: (Acute & Chronic)
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Urine output measurement measuring how much you urinate in
24 hours may help your doctor
determine the cause of your kidney
failure.
Urine tests - Analyzing a sample of
your urine (urinalysis) may reveal
abnormalities that suggest kidney
failure.
Blood tests - A sample of your
blood may reveal rapidly rising
levels of urea and creatinine — two
substances used to measure kidney
function.
Imaging tests - Imaging tests such
as ultrasound and computerized
tomography may be used to help
your doctor see your kidneys.
Removing a sample of kidney
tissue for testing - In some
situations, your doctor may
recommend a kidney biopsy to
remove a small sample of kidney
tissue for lab testing.
↓ glomerular filtration rate (GFR)
↓
↑ nitrogen containing compound in the
blood
↓
ARF
Chronic Renal Failure
↓ nephron numbers
↓
Adoptive hyperfiltration at glomerulus
↓
↑ glomerular permeability; ↑ filtration of
proteins and macromolecules →
proteinuria and → ↑ RAAS; hypertension
↓
Nephrotoxic inflammation
↓
tubulointerstitial fibrosis and FSGS
↓
decrease GFR; decrease UO
↓
systemic complications
↓
CRF
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Nutrition. A referral to the
nutritionist is made because of
the dietary changes required.
Problems to report. The
patient and family must know
what problems to report to the
healthcare provider.
Follow-up examinations. The
importance of follow-up
examinations and treatment is
stressed to the patient and
family because of changing
physical status and renal
functions.
Medication and Treatment:
 Pharmacologic therapy.
Cation-exchange resins or
Kayexalate can reduce elevated
potassium levels; IV dextrose
50%, insulin, and calcium
replacement may be
administered to shift potassium
back into cells; diuretic agents
are often administered to
control fluid volume.
 Nutritional therapy.
Replacement of dietary
proteins is individualized to
provide the maximum benefit
and minimize uremic
symptoms; likewise, caloric
requirements are met with
high-carbohydrate meals,
because carbohydrates have a
protein-sparing effect; foods
and fluids containing
potassium or phosphorus are
restricted; and after diuretic
phase, the patient is placed on
a high-protein, high-calorie
diet.
Chronic Renal Failure
Nursing care is directed toward
Complications:
 ARF can affect the entire body
 infection
 hyperkalemia
 hyperphosphatemia
 hyponatremia
 water overload
 pulmonary edema
 reduced level of consciousness
 immune deficiency
assessing fluid status and identifying
potential sources of imbalance,
implementing a dietary program to
ensure proper nutritional intake within
the limits of the treatment regimen,
and promoting positive feelings by
encouraging increase self-care and
greater independence.
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Teaching Patients Self-Care
Because of the extensive
teaching needed, the home care
nurse, dialysis nurse, and nurse
in the outpatient setting all
provide ongoing education and
reinforcement while
monitoring the patient’s
progress and compliance with
the treatment regimen.
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Continuing Care
The importance of follow up
examination and treatment are
stressed to the patient and
family because of changing
physical status, renal function,
and dialysis requirements.
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Problems to report.
The patient and the family
need to know what problems to
report: nausea, vomiting,
change in usual urine output,
ammonia odor on breath,
muscle weakness, diarrhea,
abdominal cramps, clotted
fistula or graft, and signs of
infection.
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Home care referral.
Referral for home care gives
the nurse an opportunity to
assess the patient’s
environment and emotional
status and the coping strategies
Chronic Renal Failure
Signs and symptoms of chronic kidney
disease develop over time if kidney
damage progresses slowly. Loss of kidney
function can cause a buildup of fluid or
body waste or electrolyte problems.
Depending on how severe it is, loss of
kidney function can cause:
 Nausea
 Vomiting
 Loss of appetite
 Fatigue and weakness
 Sleep problems
 Urinating more or less
 Decreased mental sharpness
 Muscle cramps
 Swelling of feet and ankles
 Dry, itchy skin
 High blood pressure (hypertension)
that's difficult to control
 Shortness of breath, if fluid builds
up in the lungs
 Chest pain, if fluid builds up
around the lining of the heart
Risk Factors:
Factors that can increase your risk of
chronic kidney disease include:
 Diabetes
 High blood pressure
 Heart (cardiovascular) disease
 Smoking
 Obesity
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Being Black, Native American or
Asian American
Family history of kidney disease
Abnormal kidney structure
Older age
Frequent use of medications that
can damage the kidneys
Complications:
 Fluid Retention
 Hyperkalemia
 Anemia
 Heart disease
 Weak bones
 Decrease immune response
 Pericarditis
 Irreversible damage to the kidneys.
used by the patient and family.
The goal of management is to
maintain kidney function and
homeostasis for as long as possible.
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Pharmacologic therapy:
Calcium and phosphorus
binders treat
hyperphosphatemia and
hypocalcemia;
Antihypertensive and
cardiovascular agents (digoxin
and dobutamine) manage
hypertension;
Anti-seizure agents (IV
diazepam or phenytoin) are
used for seizures, and;
Erythropoietin (Epogen) is
used to treat anemia associated
ESRD.
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Nutritional therapy.
Dietary intervention includes
careful regulation of protein
intake, fluid intake to balance
fluid losses, sodium intake to
balance sodium losses, and
some restriction of potassium.
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Dialysis.
Dialysis is usually initiated if
the patient cannot maintain a
reasonable lifestyle with
conservative treatment.
References:
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Smeltzer, O. S. C. (2021). Brunner and Suddarth’s Textbook of Medical-Surgical Nursing 10th (tenth) edition Text Only (10th ed.). LWW.
Belleza, R. M. N. (2021b, February 20). Acute Renal Failure. Nurseslabs. https://nurseslabs.com/acute-renal-failure/#discharge_and_home_care_guidelines
Belleza, R. M. N. (2021c, February 20). Chronic Renal Failure. Nurseslabs. https://nurseslabs.com/chronic-renal-failure/#medical_management
Chaudhry, S. (n.d.). Chronic kidney disease (CKD). McMaster Pathophysiology Review. Retrieved September 17, 2021, from http://www.pathophys.org/ckd/
Chronic kidney disease - Symptoms and causes. (2021, September 3). Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/chronic-kidney-disease/symptoms-causes/syc-20354521
Chronic kidney disease - Diagnosis and treatment - Mayo Clinic. (2021, September 3). Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/chronic-kidney-disease/diagnosis-treatment/drc-20354527
Acute kidney failure - Diagnosis and treatment - Mayo Clinic. (2020, July 23). Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/kidney-failure/diagnosis-treatment/drc-20369053