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Nursing 272: Final Semester > Unit 3: Acute Pancreatitis > Flashcards

Unit 3: Acute Pancreatitis Flashcards

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1
Q

Pancreatitis

A
  • inflammation of the pancreas
  • acute or chronic
  • hospitalization in ICU
  • mild to severe
  • w/ severe acute pancreatitis may develop SIRS and end-organ dysfunction
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2
Q

Chronic Pancreatitis

A

persistent inflammation that causes scarring and damage to the pancreas and surrounding tissue

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3
Q

Causes of Acute Pancreatitis

A
  • Alcohol
  • Gallstones
  • Trauma
  • Medication reactions
  • Hypertriglyceridemia
  • Bile Duct abnormalities or obstruction (tumor)
  • Surgery
  • Infectious organisms
  • Parasites
  • Spider bites
  • Scorpion stings
  • Idiopathic (unidentified cause)
  • Pancreas divisum (congenital anomaly where pancreatic duct is divided into 2 parts)
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4
Q

Most Prevalent Causes of Acute Pancreatitis

A
  • Gallstones

- Alcohol

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5
Q

Gallstone Pancreatitis

A
  • due to presence of gallstones obstructing the bile duct or located near the area where the bile duct and pancreatic duct empty into the duodenum
  • causes alteration in the flow of bile and pancreatic enzymes leading to inflammation of the pancreas
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6
Q

Pathophysiology of Acute Pancreatitis

A
  • reversible process involving inflammation of the pancreas secondary to the release of pancreatic enzymes that “autodigest” the pancreas, peripancreatic tissue, and adjacent areas
  • may occur as an isolated event, or may be recurrent
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7
Q

Autodigestion

A

occurs when the pancreatic enzymes digest the pancreas and surrounding tissue

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8
Q

Clinical Manifestations

A
  • sudden onset of epigastric pain that is felt in the LUQ or mid-abdomen; can radiate to back or shoulder blades
  • pain is deep and very sharp
  • pain becomes more intense within minutes of eating foods high in fat
  • pain constant and severe
  • pain lasts several days
  • complain of severe pain when lying flat or bending forward
  • pain associated w/ nausea, vomiting, and anorexia
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9
Q

General Clinical Presentation of Pancreatitis

A
  • abdominal fullness from gas or bloating
  • hiccups
  • indigestion
  • fever
  • tachycardia
  • hypotension
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10
Q

What does the Physical Exam Reveal?

A

-tender abdomen with localized guarding and rebound tenderness

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11
Q

Cullen’s Sign

A

periumbilical bruising

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12
Q

Grey Turner’s Sign

A

flank bruising

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13
Q

What Indicates Retroperitoneal Hemorrhage?

A
  • Cullen’s Sign and Grey Turner’s sign
  • take 24 to 48 hours to develop
  • can be a predictor of acute pancreatitis w/ pancreatic necrosis and retroperitoneal or intra-abdominal bleeding
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14
Q

Laboratory Tests Used in Diagnosis of Pancreatitis

A
  • Metabolic Panel
  • Hematology Studies
  • Serum amylase
  • Serum Lipase
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15
Q

Amylase

A

enzyme that aids in digestion of carbohydrates

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16
Q

Lipase

A

enzyme that aids in the digestion of fats

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17
Q

What is the most specific test for pancreatitis?

A
  • Serum Lipase (elevated)

- lipase only produced by the pancreas

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18
Q

Diagnostic Imaging Tests For Pancreatitis

A

-Abdominal CT scan
-Abdominal MRI
-Abdominal Ultrasound
>these evaluate for inflamed pancreas, gallstones, and bile duct obstruction or distention

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19
Q 
Connection Check: The most specific laboratory result in in the patient with acute pancreatitis is an elevation in which laboratory value?
A. Serum bilirubin
B. Serum Lipase
C. Serum trypsin
D. Serum lactase
A

B. Serum Lipase

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20
Q

Four Scoring Systems of Pancreatitis

A
  • Ranson’s Criteria
  • APACHE II score (Acute Physiology and Chronic Health Evaluation)
  • Balthazar CT severity index
  • Bedside Index Severity of Acute Pancreatitis (BISAP)
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21
Q

Ranson’s Criteria

A

measures severity of illness and the likelihood of mortality in patients w/ pancreatitis

  • evaluated upon admission, and then again within the first 48 hours according to the scoring criteria
  • if at 48 hours the patient has a score of greater than or equal to 3, severe pancreatitis is likely
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22
Q

Mortality Associated with Ranson’s Score

A
  • 0 to 2: 2% mortality
  • 3 to 4: 15 % mortality
  • 5 to 6: 40% mortality
  • 7 to 8: 100% mortality
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23
Q

Treatment

A
  • NPO status to prevent release of pancreatic enzymes responsible for autodigestion of the pancreas
  • IV hydration and pain medications
  • if has severe acute pancreatitis, managed in ICU
  • aggressive supportive therapy
  • if has necrotic pancreatitis, antibiotics are given
  • if pancreatitis caused by gallstones, undergo a cholecystectomy
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24
Q

Approved Agents for Acute Pancreatitis

A
  • Opioid Narcotics: Morphine Sulfate (for pain)
  • Anticholinergic agents
  • Spasmolytic
  • H2 (histamine) antagonist or proton pump inhibitor
  • Pancreatic enzymes
  • Antibiotics
  • Octreotide
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25
Q

Anticholinergic Agents

A

decreases intestinal motility and decrease pancreatic enzyme release

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26
Q

Spasmolytics

A

relaxes smooth muscle and relax sphincter of Oddi

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27
Q

H2 (Histamine) antagonist or proton pump inhibitor

A

decreases gastric acid secretions

28
Q

Pancreatic enzymes

A

aids in digestion of fats and proteins; take w/ meals

29
Q

Antibiotics

A

treats acute necrotizing pancreatitis

30
Q

Octreotide

A

decreases secretion of enzymes

31
Q

Diet for Acute Pancreatitis

A
  • IV fluids and parenteral nutrition, avoiding use of enteral nutrition in an effort to “rest” the inflamed pancreas and prevent the release of pancreatic enzymes
  • new guidelines: initiation of early enteral feeding
32
Q

Complications of Acute Pancreatitis

A
  • Necrotizing Pancreatitis
  • Pancreatic Hemorrhage
  • Pancreatic Pseudocysts
  • Pleural Effusions
33
Q

Necrotizing Pancreatitis

A
  • may present 1 or more weeks after initial onset of acute pancreatitis
  • diagnosed by CT scan; shows presence of air and gas surrounding the pancreas
  • caused by activation of pancreatic enzymes that basically “eat through” the tissue of the pancreas and enter the peritoneal cavity and surrounding tissue, causing extensive peripancreatic tissue breakdown, inflammation, and hemorrhage from the rupture of surrounding blood vessels
  • can develop sepsis, shock, and multiple-organ failure
34
Q

Two Types of Pancreatic Necrosis

A

-Sterile
-Infected
>type is determined through a needle biopsy and culture

35
Q

Sterile Necrosis

A

areas of necrosis that are free from bacteria

36
Q

Infected pancreatic necrosis

A

necrosis that is caused by bacteria

37
Q

How is Necrotizing Pancreatitis Treated?

A
  • medically in the basis of clinical presentation
  • drainage or surgical intervention that involves debridement of the necrotic tissue and infected debris via the step-up approach
  • if culture is positive; antibiotics
38
Q

Surgical Management for Necrotizing Pancreatitis

A

-pancreatic resection, open abdominal resection w/ open packing and serial debridement every 2 to 3 days, or necrosectomy (resection of necrotic tissue) with lavage or drainage

39
Q

Complication: Pancreatic Hemorrhage

A
  • hemorrhage as a result of pancreatic enzymes causing micro-rupture of the vascular system surrounding the pancreatic bed
  • experience increased pain, decreased BP, and elevated HR
  • abdominal exam may reveal Grey Turner’s sign or Cullen’s sign
  • if an active bleed is diagnosed, patients undergo embolization to stop the hemorrhage
40
Q

Complication: Pancreatic Pseudocyst

A
  • encapsulated areas of fluid that contain pancreatic enzymes and pancreatic tissue
  • usually form within 4 to 6 weeks after an episode of acute pancreatitis
  • vary in size and number
  • resolve spontaneously over several weeks
  • if pseudocyst becomes infected, it is known as a pancreatic abscess, and patient requires either percutaneous drainage or necrosectomy (excision of necrotic tissue) to drain or debride the infected fluid collection and surrounding tissue
  • with infected pseudocyst: chills, fever, N/V, and abdominal pain
  • monitor for rupture and impending shock
41
Q

Complications: Pleural Effusions

A
  • abnormal accumulation of fluid between the layers of the pleura in the lung
  • can occur in pancreatitis b/c of impaired capillary permeability or inflammation
  • typically located in left lung b/c of the proximity of the pancreas to the left hemidiaphragm but can be bilateral
  • may complain of SOB, hiccups, or pleuritic chest pain
  • pleural effusions are filled with exudates (high protein and blood) and have high amylase levels (> 30 times normal)
42
Q

Nursing Management: Assessment and Analysis

A 
>classic presentation of acute pancreatitis is sudden onset of acute unbearable abdominal pain
>other manifestations:
-elevated HR and respiratory rate
-low BP
-pain
-elevated serum lipase, amylase, and glucose values
-hypocalcemia
-steatorrhea, clay-colored stools
-hypovolemia
-hypoxia
-pleural effusions
-manifestations of adult respiratory distress syndrome (ARDS)
-multiple organ dysfunction
43
Q

Nursing Diagnoses

A
  • acute pain r/t inflammation, edema, and distention of the pancreas and surrounding tissue
  • ineffective breathing patterns r/t pain, pulmonary infiltrates, pleural effusions, and atelectasis
  • imbalanced nutrition, less than body requirements r/t decreased food intake and increased metabolic demands
44
Q

Nursing Assessments for Acute Pancreatits

A
  • Vital Signs
  • Oxygen Status
  • Pain location, intensity, duration
  • Abdominal assessment
  • Grey Turner’s and/or Cullen’s sign
  • Serum lipase and amylase
  • Serum glucose
  • Serum calcium, Trousseau sign or Chvostek sign
  • Stool color
  • Nutritional intake
  • Daily weight, monitoring of fluid intake and output
45
Q

Assessments: Vital Signs

A
  • fever and tachycardia may = inflammation
  • elevated respiratory rate may occur b/c of anxiety and pain
  • rate may be shallow and rapid as a result of pain
  • blood pressure may be low d/t dehydration and fluid shifts secondary to the inflammatory response
46
Q

Assessments: Oxygen status

A

-PaO2 may be decreased b/c of alveoli collapse and pleural effusion

47
Q

Assessment: Pain location, intensity, and duration

A
  • pain located in RUQ (head of pancreas) or LUQ (tail of pancreas) is r/t autodigestion of the pancreas d/t leaking of pancreatic enzymes into tissue surrounding the pancreas, leading to edema, distention of the pancreas, and peritoneal irritation
  • localized pain may = pseudocyst or abscess formation
48
Q

Assessment: Abdominal assessment

A

palpation may reveal rebound tenderness, muscle guarding, or rigid abdominal muscles

49
Q

Assessment: Grey Turner’s and/or Cullen’s sign

A

-Grey Turner’s sign is bruising noted on the flank d/t leaking of exudate stained with blood into the flank area
-Cullen’s sign is bruising around the umbilicus
>bruising in these areas indicates hemorrhage, severe inflammation, and tissue damage

50
Q

Assessment: Serum Lipase and Amylase

A
  • Elevated lipase and amylase are d/t inflammation of the pancreas, which interrupts its normal structure and function
  • Serum lipase is a useful biomarker b/c levels can remain elevated for up to 2 weeks
  • Elevated amylase levels that are three times normal are indicative of acute pancreatitis; elevated within 12 hours of the onset of inflammation, and can last 4 days
51
Q

Assessments: Serum Glucose

A

glucose elevations d/t the digestion of the pancreas, which leads to decreased production and availability of insulin

52
Q

Assessments: Serum Calcium, Trousseau sign, or Chvostek sign

A

> Hypocalcemia
-assess for neuromuscular irritability when calcium levels are low b/c of the accumulation of fatty acids, which chelate calcium salts, causing soapy deposits in the abdomen
Trousseau sign
-hand spasms with inflation of the blood pressure cuff 20 mm Hg above the patients systolic BP for 3 to 5 minutes; under these ischemic conditions, the nerves become irritable, and spams results
Chvostek’s sign
-facia twitching; tapping the skin over the facial nerve anterior to the external auditory meatus; in a patient w/ acute hypocalcemia, ipsilateral contraction of the facial muscles occurs

53
Q

Assessment: Stool color

A

steatorrhea, clay-colored stools due to obstruction of bile flow

54
Q

Assessment: Nutritional intake

A

patients exhibit loss of appetite b/c of pain; in alcoholic pancreatitis, patients may be malnourished at baseline

55
Q

Assessment: Daily weight, monitoring of fluid intake and output

A
  • monitor fluid status and prevent dehydration
  • hypovolemia occurs b/c of third-space losses in the retroperitoneum from autodigestion of the pancreas and capillary leak; these fluid shifts can impact weight, and with significant ascites formation, the weight increases as the fluid retention increases
56
Q

Nursing Actions for Acute Pancreatitis

A
  • Maintain NPO
  • NGT to low suction, as ordered
  • Administer analgesics, antiemetics, histamine blockers, sedatives, and antianxiety meds
  • Promote bedrest in semi-fowlers position or fetal position
  • Encourage coughing and deep breathing
57
Q

Actions: Maintain NPO status

A

decreases the secretion of digestive enzymes and prevents the contraction of the gallbladder and release of cholecystokinin

58
Q

Actions: NGT to low suction as ordered

A

decompresses stomach, prevents abdominal distention

59
Q

Actions: Administer analgesics

A

decreases symptoms of pain

60
Q

Actions: Administer antiemetics

A

decrease symptoms of N/V, which may occur for a prolonged time

61
Q

Actions: Administer histamine blockers

A

to decrease acid secretion and inhibit pancreatic enzyme activity

62
Q

Actions: Administer sedatives and anti-anxiety meds

A

help decrease spasms and subsequent enzyme secretions

63
Q

Actions: Promote bedrest in semi-Fowler’s position or fetal position

A
  • bedrest decreases the stimulation of pancreatic secretions and resulting pain
  • semi-Fowlers position relieves abdominal pressure and tension
  • fetal position is most comfortable
64
Q

Actions: Encourage coughing and deep breathing

A
  • prevents atelectasis and improve oxygenation

- patients commonly have pleural effusions

65
Q

Nursing Teaching

A
  • Appropriate diet and intake of small, frequent meals and vitamin supplements; carbohydrate-containing foods; avoid fat and protein-rich foods
  • Abstain from alcohol
  • Abstain from smoking
  • Disease symptoms, progression, diagnostic procedures, and interventions
66
Q

Evaluating Care Outcomes

A
  • acute pancreatitis is a serious, life-threatening disorder
  • b/c of the potential for sepsis and hypovolemia, monitoring of fluid and electrolytes, and CBC, is a priority for evaluating effectiveness of treatment plan
  • pain management and nutritional status are indicators of how the disease process is progressing
  • positive outcomes: stable vital signs, stable weight, serum electrolytes WNL, decreased pain, and decreased liver enzymes
  • may be hospitalized for weeks and require transitional care that focuses on reestablishing their weight and muscles mass, as well as understanding the disease process and lifestyle changes

Nursing 272: Final Semester (79 decks)

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