Medical ICU Patient with Severe Acute Pancreatitis

A 49-year old man presented to the emergency department with severe abdominal pain,
anorexia, and vomiting. His history included poorly controlled type 2 diabetes mellitus,
obesity, and hypertriglyceridemia (baseline triglycerides 1000-2000mg/dL). He had no
history of pancreatitis, and his social history was negative for alcohol. His medications
included fenofibrate 80mg, glipizide 5mg/d, and glargine insulin 60 units each evening.
His diet history was significant for 2 days of inability to tolerate solid food, with
vomiting and minimal fluid intake. His height was 68 inches, and weight 250 pounds. He
had previously gained 5 pounds in the last month.

On presentation to the ED, the patient’s labs were as follows:

Blood glucose: 425 mg/dL

Triglycerides: 4420 mg/dL
Lipase: 11200 U/L
Lactate: 2.7 mmol/L

An abdominal computer tomography (CT) scan showed a marked peripancreatic fat

stranding and fluid, mild enhancement of the head of the pancreas raised the possibility
of necrotizing pancreatitis with moderate thickening involving the duodenum, suggestive
of reactive changes due to the surrounding inflammation. He was admitted to the acute
medical ward from the ED with IV fluids and an insulin infusion. On the ward, he
became somnolent with respiratory depression, sinus tachycardia, and marginal blood
pressure of 90/50 mmHg. His lab values were checked again:

Lactate 8.6 mmol/L

Creatinine 2.6 mg/dL

The rapid response team was called and he was transferred to the ICU for aggressive
fluid resuscitation and monitoring. During nasogastric tube placement, he had a
cardiopulmonary arrest. He was intubated, received CPR, and had return of spontaneous
circulation. He required multiple vasoactive agents (norepinephrine, vasopressin, and
milrinone) to maintain mean arterial pressure (MAP) about 65 mmHg, as well as ongoing
fluid resuscitation. Medications administered included dexmedetomidine, fentanyl, and
meropenem. After surgical intervention was ruled out, a nasogastric tube was placed and
a nutrition consult ordered. Answer the following questions and complete the ADIME
template to your fullest extent with the information provided.

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1. Describe the normal exocrine and endocrine functions of the pancreas.

The pancreas consists of two glands, each with a different function.1 The
exocrine gland has digestive functions. It produces different enzymes that
combine with bile to make up digestive juices to break down food in the small
intestine. Trypsin and chymotrypsin digests proteins, amylase digests
carbohydrates and lipase is released to break down fats. These digestive enzymes
travel down the pancreatic duct into the bile duct and are inactive until they reach
the duodenum. Exocrine cells also secrete bicarbonate which is used to neutralize
stomach acid in the duodenum.

The endocrine gland has hormonal functions. It is composed of small islands of

cells called the islets of Langerhans, which secretes hormones to regulate blood
glucose levels. Insulin is released and lowers blood sugar, and glucagon is
released which acts to raise blood sugar.

2. Determine the potential etiology of both acute and chronic pancreatitis.

What information provided in the physical assessment supports the diagnosis
of acute pancreatitis?

Pancreatitis is a condition that occurs when it becomes inflamed. The pancreatic

enzyme secretions build up and starts digesting the pancreas itself.2 Causes can
be metabolic or structural.

Acute pancreatitis develops suddenly. Causes are due to gallstones, alcohol

consumption, medications such as estrogen supplements and diuretics, trauma,
and bacterial or viral infections. Symptoms include severe, steady pain in the
upper-middle abdomen which can also radiate to the back, abdominal bloating or
tenderness, nausea or vomiting, jaundice, and low-grade fever. Elevated levels of
amylase and lipase can indicate a diagnosis of acute pancreatitis.

Chronic pancreatitis occurs when there is ongoing inflammation that does not heal
or gets worse. The pancreas loses its function over time due to persistant damage.
Heavy alcohol use, autoimmune disease, genetic mutations due to cystic fibrosis,
or structural problems like a blocked pancreatic or bile duct are causes.
Symptoms include abdominal and/or back pain, weight loss, nausea and vomiting,
onset of diabetes, pale colored, oily stools.

This patient has severe abdominal pain and vomiting, which indicate acute
pancreatitis.

3. What laboratory values or other tests support this diagnosis? List the
abnormal values and explain the likely cause of each abnormal value.

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  Lipase: 11200 U/L is elevated, indicating that digestive enzymes for fats
are not functioning well.

 Triglycerides: 4420 mg/dL is extremely high. Hypertriglycerdemia is a

known cause for acute pancreatitis.3
 Blood glucose: 425 mg/dL is extremely high and indicates uncontrolled
blood sugar. He is already diagnosed with diabetes mellitus, and there is
an association between diabetes and acute pancreatitis.4

4. What are the potential complications of acute pancreatitis?

Acute pancreatitis can be mild or life threatening. Common complications

include low blood pressure and shock. Since there is damage to the pancreas
activated enzymes and a cytokine flood are released into the bloodstream causing
low blood pressure.2 In severe cases when parts of the pancreas die
(necrotizing pancreatitis), decreased blood volume and large drops in blood
pressure can cause shock.2 This can also lead to other organs to fail like the
kidneys, lungs, or heart. If those organs fail to function it can lead to death.

5. Historically, the patient with acute pancreatitis was made NPO, why?

Consuming foods by moth stimulates enzyme production, causing further

inflammation. NPO minimizes pancreatic secretion.

6. A nutrition consult was order, using the most current literature and ASPEN
guidelines, explain the role of enteral feeding in acute pancreatitis. Do you
agree with the initiation of enteral feeding? Why or why not?

Nutritional support in acute pancreatitis is not always necessary since some cases
are short-lived.5 However malnutrition is also a common complication and since
he did not eat for 2 days he does have that risk. Enteral nutrition (EN) can
provide nutrition, preserve gut function and reduce pain.6,7 I do agree with the
initiation of EN feeding. In patients with acute pancreatitis, its efficacy has been
shown in providing nutrition and preventing complications when given during the
first 48 hours of admission when compared to parenternal feeding.6

7. Assess the patient’s height and weight, calculate his BMI and his percent
usual body weight.

BMI = weight (kg)/ [height (m)]2 = 38 (obese)

UBW: 245 lbs
%UBW = 102%

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8. Determine the patient’s energy and protein requirements. Explain the
rationale for the method used to calculate these requirements.

Caloric requirement
Using the Harris-Benedict Equation, his BMR is 2153.9.
 Sedentary lifestyle: 2153.9 x 1.2 = 2584.68 kCal to maintain weight
Using 22-25 kcal/kg
 22-25*113.4kg = 2494-2835 kCal/day

Protein requirement
1.5kg-2 g/113.4kg = 170.1-226.8g of protein daily

9. Determine the patient’s fluid requirements.

30-35ml/kg: 3.4L-4.0L/day

10. Given the current medications, identify any drug-nutrient interactions that
you should monitor. If none, list none.

Dexmedetomidine Highly selective α2-adrenergic

(Precedex) receptor (α2-AR) agonist8

Fentanyl Narcotic, synthetic opioid, used Avoid alcohol

for pain relief

Meropenem Antibiotic
(Merrum)

Fenofibrate 80mg Lipid regulating agent

(Tricor) Severe Hypertriglyceridemia

Glipizide 5mg/d Blood sugar control None

(Glucotrol)
Glargine insulin 60 units Blood sugar control None
each evening
(Lantus, Toujeo)

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 11. Identify the pertinent nutrition problems and the corresponding nutrition
diagnoses.

 Inadequate oral food intake - since he has not been able to eat solid food
for 2 days
 Impaired nutrient utilization – since he is vomiting and has high lipase
levels, indicating digestive enzyme dysfunction

12. Write your PES statement for each nutrition problem.

 PES #1: Inadequate oral intake, RT abdominal pain resulting in loss of

appetite, AEB not eating solids for 2 days

 PES #2: Impaired nutrient utilization, RT compromised pancreatic

function AEB excessive vomiting and elevated lipase levels (11200 U/L)

13. Determine your enteral feeding recommendations for the patient. Provide a
formula choice, goal rate, and instructions for initiation and advancement.

Research supports early EN in patients with severe acute pancreatitis (SAP).9

Jevity (1.2 Cal) @ 100 mL/hr

 Start at 20 mL/hr, titrate by 10-20 mL/hr every 4 hours to goal
 1 additional protein packets (Beneprotein) per day
 350 mL free water flushes every 4 hours (87.5 mL/hr)

The patient has been on your current nutrition order for 3 days, as you begin to
titrate toward your goal rate, the patient experiences worsening abdominal
distention, pain, and 2 episodes of vomiting, thus the tube feeding was stopped
overnight.

1. What do you recommend to the team? Do you feel that the tube should be
placed lower in the GI tract? Post-pyloric? If so why?
I would recommend nasojejunal/post-pyloric feeding to avoid stimulation of the
pancreas.5,10 It appears he is not tolerating gastric feeding. Post-pyloric feeding
significantly reduces the chance of vomiting as well.10

2. The team agrees that a post-pyloric tube is best. Determine your new enteral
feeding recommendations providing a formula choice, goal rate, and
instructions for advancement.

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 3. What recommendations can you make to the patient’s critical care team to
help improve tolerance to the enteral feeding?
The jejunum relies on controlled substance delivery. A sudden influx of EN can
lead to abdominal cramping, hyperperistalsis, diarrhea and other symptoms
similar to dumping syndrome. Post-pyloric feeds should be given continuously
by pump.10 The initial rate should be slow and then steadily increased very
gradually. Parenteral support is sometimes used to achieve caloric intake goals.

In severe acute pancreatitis, clinical studies recommend using EN formulas that

are peptide based and high medium chain triglycerides (MCT) to increase
tolerance.7 MCT has been shown to have anti-inflammatory effects in animal
models of inflammatory bowel diseases.

4. Does this patient’s cause indicate the use of an immune modulating formula?

Enteral nutrients play a major role in maintaining the integrity of the gut and can
have an immune modulating effect systemically as well as in the intestines.7
Since he denies alcohol use, I would recommend an immune modulating formula.

Duodenal infusion of the amino acid glutamine was shown to induce the
expression of heme-oxygenase-1 (HO-1).7 HO-e has anti-inflammatory effects
and is a major cytoprotective enzyme for immune homeostasis.

Prebiotics and probiotics can be added helpful for optimal function of the
intestinal epithelial cells (IEC) and in maintaining microbiome homeostasis.7

5. Are there any supplements or modulars you would consider adding to the
current tube feeding formula?

Although the evidence shows mixed results using probiotics, the data does not
show any harm. I would add probiotics to modulate the microbiota. Glutamine
has been shown to have anti-inflammatory effects and is an effective
immunomodulator, so I would add it as well.

1. Chronic Pancreatitis. The National Pancreas Foundation.

https://pancreasfoundation.org/patient-information/chronic-pancreatitis/. Accessed March
14, 2019.

2. Acute pancreatitis symptoms, treatment & causes - digestive disorders. Merck Manuals
Consumer Version Web site. https://www.merckmanuals.com/home/digestive-
disorders/pancreatitis/acute-pancreatitis. Accessed Mar 14, 2019.

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3. Kota SK, Kota SK, Jammula S, Krishna SVS, Modi KD. Hypertriglyceridemia-
induced recurrent acute pancreatitis: A case-based review. Indian J Endocrinol Metab.
2012;16(1):141-143. Accessed Mar 15, 2019. doi: 10.4103/2230-8210.91211.

4. Aura Diana Reghina, Silvia Craciun, Simona Fica. Severe transient hyperglycemia in a
prediabetic patient during mild acute pancreatitis. Case reports in medicine.
2015;2015:968593-3. doi: 10.1155/2015/968593.

5. Seminerio J, O’Keefe SJ. Jejunal feeding in patients with pancreatitis. Nutr Clin Pract.
2014;29(3):283-286. doi: 10.1177/0884533614529164.

6. Zarnescu NO, Barbu ST, Zarnescu Vasiliu EC, Costea R, Neagu S. Management of
acute pancreatitis in the early stage. Maedica. 2015;10(3):257.

7. Refaat A Hegazi Tiffany De Witt. Enteral nutrition and immune modulation of acute
pancreatitis. 世界胃肠病学杂志：英文版（电子版）. 2014;20(43):16101-16105. doi:
10.3748/wjg.v20.i43.16101.

8. Kaur M, Singh PM. Current role of dexmedetomidine in clinical anesthesia and

intensive care. Anesth Essays Res. 2011;5(2):128-133. Accessed Mar 15, 2019. doi:
10.4103/0259-1162.94750.

9. Petrov MS, Pylypchuk RD, Uchugina AF. A systematic review on the timing of
artificial nutrition in acute pancreatitis. Br J Nutr. 2009;101(6):787-793. doi:
10.1017/S0007114508123443.

10. Alkhawaja S, Martin C, Butler RJ, Gwadry-Sridhar F. Post-pyloric versus gastric tube
feeding for preventing pneumonia and improving nutritional outcomes in critically ill
adults. The Cochrane database syst rev. 2015(8):CD008875. doi:
10.1002/14651858.CD008875.pub2.