Leanna R. Miller, RN, MN, CCRN-CSC, PCCN-CMC, CEN, CNRN, CMSRN, NP
Education Specialist
LRM Consulting
Nashville, TN

inflammatory response and
potential necrosis of pancreatic
endocrine and exocrine cells
as the result of premature
activation of pancreatic
enzymes

Presenting Signs & Symptoms
pain (upper abdomen) – 95%
–edema and distension
–chemical burn
–release of kinin
–obstruction of biliary tree
Presenting Signs & Symptoms
Acute Abdomen
 protracted vomiting
 abdominal tenderness
 guarding
 distension
 tympany
Presenting Signs & Symptoms
 Severe disease
–hypovolemic shock
–Grey Turner’s sign
–Cullen’s sign

Diagnostics
Serum amylase
–elevated during 1st 24 hours
after onset of signs
–may remain elevated for only
2 days
–> 300 mcg/dL

Diagnostics
Serum lipase
–elevates within 24 to
48 hours of disease
–remains elevated for
5 - 7 days
–can indicate pseudocyst

Hypocalcemia
–free fatty acid-albumin
complexes bind calcium
–decreased PTH function
Radiographic Studies
 Computed tomography
(CT)
– gold standard for
diagnosis

Complications
Pancreatic Abscess
• high fever, palpable mass,
abdominal tenderness,
N & V, leukocytosis &
hyperglycemia
• surgery required

Complications
Pancreatic Pseudocyst
• abdominal pain, fever,
N & V > 1 week
• WBC or amylase
remains elevated
Medical Goals
 prevent & control shock
 relieve pain
 suppress pancreatic
stimulation
Medical Goals
 support the patient
 minimize the occurrence
of complications
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64 year old woman develops upper
abdominal pain late last night.
Band-like with radiation to back. Initially
not severe, but awoke and had several
episodes of non-bloody emesis.
The first 8 hours in ED/Hospital the
patient required 36 mg MSO4 to control
pain.
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PMHx: HTN,
Hyperlipidemia
MEDS: Estrace,
Plendil
SOCIAL: no
tobacco or ETOH
use
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BP: 94/45  160/90,
HR: 76, T: 97.9,
GEN: awake alert
HEENT: no icterus, mouth is
dry
CARDIO: ST
ABD: no rebound tenderness,
no bruising
•
ABD CT: marked
peri-pancreatic fluid,
streaking around
pancreas, normal
enhancement, no
clear gallstones,
CBD not dilated
LABS:
• AST/ALT both slightly
elevated.
• T.bilirubin normal
• Amylase 2620
• Lipase 26,625
• Hct normal
• WBC 14.8
Ranson’s Criteria
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Admission
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Age > 55
WBC > 16,000
Glucose > 200
LDH > 350
AST > 250
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During first 48 hours
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Hematocrit drop > 10%
Serum calcium < 8
Base deficit > 4.0
Increase in BUN > 5
Fluid sequestration > 6L
Arterial PO2 < 60
5% mortality risk with <2 signs
15-20% mortality risk with 3-4 signs
40% mortality risk with 5-6 signs
99% mortality risk with >7 signs
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At 36 hrs the patient has increased work
of breathing, crackles at bases of lungs.
She is 4 liters ahead on fluids.
What do you want to do?
•
“Vigorous intravenous hydration alone is
the best available option in the prevention
of pancreatic necrosis.”
• Pitchhumoni et al. “Mortality in Acute Pancreatitis,”
Journal of Clinical Gastroenterology
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AGGRESSIVE FLUID RESUSCITATION
• May require 250-500 cc/hr for first 48 hrs
– 6 L of fluid is sequestered in abdomen alone
– Third spacing can consume up to 1/3 of total plasma
volume
• 1/3 of people die in the first phase  50% of
these are associated to ARDS
•
PULMONARY EDEMA ≠ CHF
•
How do you know you have resuscitated
the patient?
• Blood pressure
• Heart rate
• Urine output
• SaO2/ABG’s show good oxygenation and
no acidemia
•
AGGRESSIVE FLUID RESSUCITATION
• may create electrolyte imbalances that need
to be corrected
• may need CVP monitoring (central line)
• CXRs help (CHF vs ARDS)
• ABGs help (still hypoxic  need more fluids?)
• 23% of SAP pts get ARF  80% mortality
• 0.5 cc/kg/hr urine output is goal (need a
Foley)
NECROSIS
• Starts to occur within 4 days of disease
• CT with oral & IV contrast is gold
standard
• necrotic areas do not enhance
• will NOT see it on CT before 48hrs
NECROSIS
• once diagnosis of necrosis is made mortality jumps
• 40-60% get secondary infection
• mortality then approaches 80%
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secondary infection symptoms:
• N/V, epigastric pain, distension, fever,
elevated WBC
diagnosis of sterile vs infected necrosis
• CT-guided needle aspiration
the most devastating complication and marks
the second peak in mortality (@ 2 weeks)
SECONDARY INFECTIONS
n
n
What bugs?
Gram (-) bacteria cross from gut
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E. coli (35%)
Klebsiella (24%)
Enterococcus (24%)
Staph (14%)
Pseudomonas, proteus, strep,
enterobacter, bacteroides, anaerobes
ANTIOBIOTICS
• Controversial
• DO decrease incidence of infection in necrosis,
but do NOT decrease mortality
• Gotta cover multiple bugs
• Gotta get into pancreas
• If you see necrosis  start antibiotics
NUTRITION
• normal pancreas secretes up to 2 liters/day of
secretions
• pancreatic stimulation during AP releases
proteolytic enzymes  autodigestion
• oral feeding increases release of secretin and
cholecystokinin  stimulates pancreas
• “rest the pancreas”  “NPO”
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ENTERAL vs TPN Feedings:
• If distal to Ligament of Treitz (nasojejunal tube
or J-tube) pancreatic secretion = basal rate
• Both started after 48 hours
– Easier to restart po feedings
– Average length of nutritional support
shorter
• 7 vs 11 days
– Fewer septic complications
– $23/day vs $222/day
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NEW THOUGHTS
• Meta-analysis of 15 randomized studies:
• Compared early vs delayed ENTERAL feedings in
753 critically ill pts
• Early was 36 hrs!
• Improved:
• Wound healing
• Host immune function
• Preservation of intestinal mucosal integrity
• Decreased infections
BUT, no decreased mortality
Case continues
• By 48 hours patient’s abdominal pain is
worsening
• HR is 140, afebrile, BP normal
• Abdomen shows very subtle guarding
• WBC: 27.6
• Ca++: 6.6
Case continues
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PO2: 61
Base deficit: 8
BUN rise: 9
LDH: 976
RANSON SCORE: 3
Case continues
• Patient transferred to ICU
• Central line & Arterial line
• Repeat Abdominal CT: new bilateral
pleural effusions, pancreas enhanced
in tail only.
• Patient died 5 weeks after admission
SUMMARY
• They may look good, but…
• Score severity early
• Use lots of IVF
• Go to ICU early
• Early enteral feedings work better

Hepatic Failure
cirrhosis:
–alcoholic with malnutrition
–biliary cirrhosis
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
hepatitis
hepatatoxins
hypoperfusion
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Hepatic Failure
Signs & Symptoms
– asterixis
– jaundice
– obtundation
– distended abdomen & ascites
– renal failure
– GI bleed
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Hepatic Failure
Treatment
–encourage rest
–limit protein, amino
acids & fat
–prevent exposure to
stress

Hepatic Failure
Treatment: Monitor
–hemodynamic status
–serum drug levels
–lab tests

Hepatic Failure
Treatment
–monitor EEG
–maintain glucose
–monitor for  ICP

Hepatic Failure
Treatment
–jaundice = vitamin K
–thrombocytopenia = folic
acid & FFP, platelets
–DIC = fibrinogen & heparin

Hepatic Failure
Treatment for varicies
–saline lavage
–administer blood
–IV vasopressin or somastatin
–Sengstaken – Blakemore tube
–portacaval shunt
On May 3 (approx. 2200 hours) a 35 year old
alcoholic male began to take 2-3
acetaminophen 500 mg tablets per hour
because of a toothache. He continued this
through the night until 0800 hours.
What is the recommended therapeutic dose
for acetaminophen?
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Adults: 4 grams per day.
Children: 75 mg/kg/day to a
maximum of 4 grams per day.
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On May 4,the patient presented to the ED
because of his toothache and was
discharged home with Tylenol #3.
He went home and took 3-4 Tylenol #3 at
0900 hours.
At approx. 1100 hours he developed
abdominal pain and N/V and returned to
the ED.
His acetaminophen level was 212 umol/L and
his AST was 990 IU/L.
How do you interpret these numbers?
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Because it is a chronic ingestion you can not plot
it on the nomogram.
In instances where it is a chronic ingestion or the
time of ingestion is unknown, send an
acetaminophen level and an AST(ALT) and if
either are elevated start N-acetylcysteine
Rumack-Matthew Nomogram
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IV NAC is initiated.
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How does ethanol affect acetaminophen
toxicity?
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Chronic alcoholics are at increased risk with
an acetaminophen overdose.
Chronic ethanol consumption induces the
cytochrome P450 pathway resulting in
increased metabolism through this pathway
and therefore increased NAPQI formation.
Malnourishment decreases glutathione
stores.
On May 5 his acetaminophen level was nondetectable and his AST was 22,733 (2305 hours)
and his INR was 19.
Is his liver failure secondary to chronic alcohol
abuse or acetaminophen toxicity?
How long would you continue his NAC and why?
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Aminotransferase elevation in chronic ethanol
abuse rarely exceeds 1000 IU/L.
It is not unusual for severe acetaminophen
toxicity to have elevations in the 10,000’s
IU/L.
In alcoholics with acetaminophen overdoses
and elevated aminotransferases, err on the
side of caution and treat with IV NAC.
How long would you continue his NAC
and why?
• Continue IV N-acetylcysteine until his
INR is less than 2.
• N-acetylcysteine has antioxidant and
free radical scavenging effects which
have been shown to decrease mortality
in fulminant hepatic failure.
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When would you transfer this patient to a
hospital that could do liver transplants?
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What are the indications for a liver
transplant?
Transfer for transplant consideration!
• INR > 5 at anytime.
• Metabolic acidosis (pH <7.35 or CO2 <18)
• Hypoglycemia.
• Renal Failure (creatinine >200 umol/L)
• Encephalopathy
Indications for Transplant!
• pH <7.3 after adequate fluid replacement.
• Grade III or IV encephalopathy plus either:
• PT >100 seconds
• Creatinine > 292 umol/L
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The patient was continued on IV Nacetylcysteine and on May 14 his INR was
1.16.
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Will this patient have any chronic liver
damage from his acetaminophen
overdose?
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No, patients who recover from an
acetaminophen overdose go on to have
completely normal liver function with no
chronic sequelae