ACUTE PANCREATITIS SiSx:

 Subjective Data
Inflammation of pancreas ranging from mild edema  Abrupt onset of aching, burning,
to extensive hemorrhage resulting from various stabbing of central epigastric pain that
insults to pancreas. may radiate to the shoulder, chest, and
back
May occur after bariatric surgery.  Abdominal tenderness
 Nausea
Common Sx:  Pruritus associated with Jaundice
 Discrete episode of abdominal pain  Objective Data
 ↑ Serum Enzymes  Elevated temperature
 Shallow respiration
Even if person is suffering from acute pancreatitis,  Vomiting
function and structure of the pancreas will  Wt loss
eventually return to normal state after acute attack.  Change in character of stools
 Shock
60% of patients suffering from Acute Pancreatitis  Tachycardia
dies.  Hypotension
 Jaundice
Classification of Pancreatitis  Grossly elevated serum amylase and
 Acute Pancreatitis lipase
 Does not usually lead to chronic  Decrease in Calcium Serum Level
pancreatitis unless complication  Board-like abd (if peritonitis is present)
develops.
 Chronic Pancreatitis Therapeutic Intervention
 Inflammatory disorder  Neutralize gastric secretions
characterized by progressive  Narcotics (morphine is contraindicated
destruction of the pancreas. as it causes spasm)
 Takes time to develop  Bed rest to increase metabolic demands
and wound healing
Common cause of Acute Pancreatitis  NPO to reduce stimulation of pancreas
 Alcohol use to secrete enzymes (decrease vomiting)
 Gallstone  Administer nasogastric decompression
 Hypertriglyceridemia to control nausea
 Anticolinergic – suppress vagal
Other causes may include: stimulation therefore decreases gastric
 Trauma motility and juvenile spasm
 Antibiotics – prevent secondary
 Smoking
infections and abscess formation
 Congenital anomalies
 Usually parenteral administration of fluid
and electrolytes
Acute pancreatitis is due to an organ injury with a
 Diet should be low in fats and proteins
subsequent inflammatory response that may involve
 No coffee and alcohol
both adjacent and distance fractures.
 Administer bile salts if necessary

Whatever the reason for acute pancreatitis, there is Surgical Intervention

an intra-acinar activation of pancreatic enzyme  Only if unresponsive to therapeutic
including Trypsin, Phospholipase A2, and treatment
Elastase. These three enzymes leads to injury of  If severe in jaundice, pseudocyst, and
pancreas itself. bleeds
 Type of surgery depends on the location
of inflammation

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 Nursing Assessment
 Look for the causative factors
 Recent wt loss
 Abd is rigid
 Guarding position
Nursing Diagnosis
 Pain r/t inflammation of the pancreas
 Ineffective breathing pattern
 Altered nutrition
 Fluid volume deficit
Nursing Intervention
 Provide care for a client with NGT
 Alert for hyperglycemic states
 Monitor VS
 Administer prescribed analgesic
 NPO especially during acute stage of
illness
 Semi-fowlers position to help w/
breathing
 Monitor parenteral therapy
 Teach for dietary modification
 Teach pt and family members what is
supposed to eat
 Advise what is the importance in taking
pancreatic enzymes medication
Desired Outcome
 ↓ Pain
 Nutritional status will be maintained
 Pt will demonstrate adequate depth of
respirations
 Maintains fluid and electrolyte balance
Bariatric Surgery resections and makes changes in
digestive system to loss wt. Advantage is that it
has a significant long term wt loss.
Pancreatitis may occur after Bariatric Surgery and
it is called Post Bariatric Pancreatitis.
DIABETIC KETOACIDOSIS (DKA)
Serious complication of DM that can be life
threatening.
Common in Type 1 DM (Juvenile Diabetes or
Insulin Dependent Diabetes)
DKA is the first sign of diabetes.
Usually develops slowly. If untreated, it would
develop to the following sx:
 Kussmaul Breathing
 Dry skin and mouth
 Flushed face
 Fruity smelling breath
 Headache
 Muscle stiffness/ aches
 Being very tired
 Nausea and vomiting
 Stomach pain
Causes
 Hyperglycemia (↑ blood sugar & ↓ insulin
levels)
 Certain antibiotics for infection
 Missed several insulin shots
 Clogged insulin pump
 Insufficient insulin
 Heart attack/ stroke
 Physical injury
 Alcohol/ drug use
 Diuretics and Corticosteroids (especially if pt
is treating for and inflammatory disease)
 Certain antibiotics
Treatment
 Fluid and electrolyte replacement
 Insulin administration
Nursing Diagnosis
 Risk for unstable blood glucose
Nursing Assessment
 Assess understanding of diabetes diagnosis
 Review lab work
 Assess patients’ understanding of insulin
Nursing Intervention
 Observe patients’ use of glucometer (might
be incorrect)
 Advise pt to use ketone kit
 Educate pt about causes of KDA
Nursing Diagnosis
 Acute confusion r/t delirium
 Acute confusion r/t cerebral edema
 Acute confusion r/t encephalopathy
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Nursing Assessment
 Pt is agitated
 Lethargy
 Headache
 Fluctuation in cognition
 Increased Intracranial Pressure (ICP) HYPERGLYCEMIC HYPEROSMOLAR
Nursing Plan NONKETOTIC SYNDROME (HHNS)
 Pt will remain alert and oriented with the
place and time Usually caused by an infection.
 Pt will not experience seizures, cerebral
If patient has pneumonia, UTI, poor management of
edema, or coma
glucose level, and not taking in diabetic
medications then he/ she is at risk for HHNS.
Nursing Diagnosis
 Risk for deficient fluid volume
Steroids/ Glucocortocoids/ Diuretics – decreases
Nursing Assessment
sugar levels. Alters glucose levels.
 Assess VS and respiration (because
dehydration may cause tachycardia and HHNS is a life threatening complications of
high BP called Kussmaul Breathing) uncontrolled DM.
 Monitor electrolytes (K levels may ↑ but can
drop heavily as fluid volume ↓). All Main Characteristics:
electrolyte should be replaced  Severe hyperglycemia
 Assess kidney function and output
 Increase in serum osmolality
Nursing Intervention
 Clinical evidence of dehydration (w/out the
 Administer isotonic solution initially (once
significant accumulation of ketone or
glucose has stabilized)
ketosis)
 If pt can drink by mouth, give oral fluids
 Educate sx for prevention Difference between DKA and HHNS is that
DKA does have ketosis and HHNS is a non-
Main concern in DKA is there is polyuria ketone.
which leads to kidney diseases and death.

SiSx (HHNS, w/ DKA)

 ↑ blood sugar levels
 Dry mouth
 Fast HR
 Thirst
 Frequent urination
 Nausea and vomiting
 Stomach ache
 Confusion, slurred speech, and weakness
on one side of the body

Causes of HHNS
 ↑ blood sugar level (unmanaged
Diabetic diabetes)
Ketoacidosis (DKA) - Pathogenesis and Clinical
Findings
 Substance misuse
 Comorbidity
Note: Infection (i.e. pneumonia, UTI, sepsis)
 In DKA, body K+ is lost via osmotic diuresis &
 Certain medications for psychosis
vomiting. But diffusion of K+ out of cells may cause
 Not [K+]
serum following
to diabetes treatment
be falsely plan
normal/elevated. To
3 IV
prevent hypokalemia, give IV KCI along with
insulin as soon as serum <5.0 mmol/L. But ensure
Treatment
 Fluids through IV
 Managing electrolyte
 Administer insulin through IV
 Diagnose and manage the cause of HHNS
 Determine if there is coexisting conditions