TPN and Acute Pancreatitis

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TPN and Acute Pancreatitis

Acute Pancreatitis

Stephen J D O’Keefe

University of Pittsburgh Medical

School


Learning Objectives

Upon completion of this session, you

should be able to:

1. Understand the pathophysiology of

acute pancreatitis

2. Know when to use nutritional support

3. Determine the best method of

nutritional support


Learning Assessment

Questions

1. The best way of meeting nutritional requirements

without stimulating the pancreas is to use jejunal

feeding (true/false)

2. The achievement of nutritional balance early in

the course of acute pancreatitis has been shown

to improve outcome (true/false)

3. Patients with acute pancreatitis are at higher risk

than other critically ill patients for developing

hyperglycemic complications (true/false)


Nutritional concerns

Elevated requirements

• Protein catabolism: increased 80%

• Energy expenditure: increased 20%

Nutritional risks

• Food stimulated pancreatic autodigestion

• Pancreatic endocrine impairment – hyperglycemia

and hypertriglyceridemia

Sepsis risk - immunoparesis


Enteral or Parenteral?

! Enteral is physiological

! Parenteral is not

! but enteral stimulates trypsin secretion

and may exacerbate acute

pancreatitis, while parenteral does not


Enteral Nutrition in Acute

Pancreatitis

! Pancreatic stimulation occurs in 3

phases

– Cephalic

– Gastric

– Intestinal


Ileal brake


Amylase Secretion in

Healthy Volunteers

i units/h

25000

22500

20000

17500

15000

12500

10000

7500

5000

2500

0

amyl

O’Keefe et al. Am J Physiol 2003

Oral

IV

Placebo


TPN and Acute

Pancreatitis

! Controlled study: TPN vs IV fluids; ; Sax

et al. Am J Surg 1987:

– 54 patients with mild disease (av(

RC=1),

TPN group did worse

! LOS 16 vs 10 days

! Catheter sepsis 11 vs 2%


Glycemic Response: Enteral

vs Parenteral

170

160

150

140

mg/dl

130

120

110

100

90

elemental

intravenous

80

Some of 0 Some of 120 Some of 240

O’Keefe et al. Am J Physiol 2003


Trypsin Secretion

1200

1000

i units/h

800

600

400

Elemental enteral

Complex enteral

200

0

true try

O’Keefe et al. Am J Physiol 2003


Trypsin Secretion

in health & disease

Units/hr

700

Group means (SE): p


Distal Jejunal Feeding

Vu et al. Eur JCI 1999


Why Enteral Feeding is

Superior

! Nutrients are needed in the

splanchnic, not the systemic

circulation

! Enteral feeding suppresses the

systemic inflammatory response


TPN enhances endotoxin-

induced cytokine production

Fong et al. Ann Surg 1989

! 12 healthy volunteers

! Randomized to enteral or parenteral

feeding for 7 days

! Arterial, hepatic vein and femoral

catheters

! IV E Coli endotoxin challenge


TPN enhances endotoxin

induced cytokine production

and hypermetabolism

TPN group:

! TNF alpha higher

! CRP higher

! Epinephrine levels higher

! Protein catabolism higher


9

8

7

6

5

4

3

2

1

0

patients

controls

umol/Kg/min

13C-leucine flux

D3-leucine flux

splanchnic leucine flux


Enteral vs Parenteral

Nutrition: mild

McClave et al: JPEN 1997

! 30 pts, 32 studies randomized to EN (jejunal

Peptimen) ) or PN after 48h.

! Mean Ranson’s 1.3 (0-5)

– i.e. mild

! Not intention to treat: 8 excluded for feeding

failure, 4 for failure to place or tolerate tubes

Results: No diff in nutrition days (5-7d), LOS,

infections

! Stress-hyperglycemia more common with PN

(p


Enteral vs Parenteral

Nutrition: mild-severe

Windsor et al: Gut 1998

! 34 patients, 16 EN, 18PN

! EN: severe pts (6/16) jejunal feeding, rest

oral!

! EN received less energy

Results: CRP & APACHE 2 down only with EN

! Endotoxin abs increased with PN

! MOF in 5 PN pts

! IA sepsis in 3 PN pts

! Only PN pts needed ICU management!


Enteral vs Parenteral

Nutrition: severe

Kalfarentzos et al: B J Surg 1997

! It took 5 years to accrue 40 patients with

necrotizing pancreatitis

! 72h IVI, imipenen

! Diets: jejunal peptide formula 25cc/h, inc

every 4h, TPN 40cc/h, inc every 4 h: target

1.5-2g

prot, , 30-35Kcal/kg/d

35Kcal/kg/d

Results: nitrogen balance achieved in both

! Septic and total complications higher with

TPN

! Cost x3 lower with EN


MCV Study: 12 month

evaluation of nutritional

management

All acute pancreatitis admissions

48hr IV fluids & analgesia

n=154

Improved

oral diet

n=102

No improvement

Randomized

Jejunal feeding

n=26

TPN & bowel rest

n=25

Abou-Assi, O'Keefe. Gastroenterol 2001


Hospitalization & Nutrition Support Days

22.5

days

20

17.5

15

12.5

10

7.5

5

2.5

*

* = p


Quantity of Feeds Received

100

90

% of requirements

80

70

60

50

40

***

***

ENTERAL

PARENTERAL

30

20

10

0

% Kcal % prot


Nutrition-Associated

Complications

! Hyperglycemia needing insulin: EN 2,

PN 7 (p


Summary

! Most patients (75%) do not need

nutritional support.

! duration of nutritional support is shorter

with enteral feeding

! TPN provides more nutrition, but causes

more hyperglycemic and septic

complications

! Enteral feeding saves $2,362/pt


Interventional Tube-

Feeding

! Nasogastic

! Nasojejunal

1. Fluoroscopic

2. Endoscopic

! Percutaneous

1. Surgical G and J

2. Endoscopic G with J extension

3. Direct endoscopic J


Transnasal Endoscopic

Placement of Feeding Tubes

in the ICU

51 ICU patients referred for TPN

– 29% respiratory failure, 28% head injury, 33%

acute pancreatitis

! Results:

– successful ‘StayPut‘

StayPut’ ’ placement in 46/51

– Perfect concordance between re-endoscopy endoscopy and

X-ray confirmation of placement

– Unrecognized esophageal and gastric pathology

revealed in 60%

TPN avoided in 77%

! O’Keefe et al. JPEN Sept 2003


Upper Abdominal Pain

Serum Enzymes >3x

Normal

NPO, IV Fluids, Analgesics

for 48 hrs

Jejunal Tube Placement

Elemental Diet 20 cc/hr

Progress to Goal over 48

hrs

Better

No improvement/

worse

Tolerated

Not

Tolerated

Improved Abdominal Pain

&

Serum Enzymes

Distal

jejunal

tube

Progressive Oral Diet

Discharge

TPN


Enteral Feeding in Necrotizing

Pancreatitis:

pt 1: 74 yr old man

! “when the tube feeding rate was

advanced to 60cc/h (65g protein,

1440 Kcal), abdominal pain

returned the following day,

associated with a dramatic

increase in WBC to 32.3 x10 9 /l. A

repeat CT suggested further

necrosis of the head, neck and

body, with marked fat stranding

and increased fluid collection.

Peripancreatic fluid was aspirated

(70cc of chocolate fluid), and

shown to be non-infected. Tube

feeding was held and TPN was

restarted, allowing provision of full

nutritional requirements (i.e. 140g

protein, 2080 Kcal/day) within 3

days, with a dramatic improvement

in WBC from 32.3 to 9.3 x109/l”

! O’Keefe et al. Clin Gastro Hepatol

July 2003


Effects of Enteral Feeding in

Necrotizing Pancreatitis

7000

Enteral feeding

6000

5000

4000

3000

trypsin x 10 (iu/h)

amylase (iu/h)

lipase (iu/h)

2000

1000

0

30

60

90

120

150

180

210

240

270

300

330

360


Incorporation of 13 C-labeled Leucine

into Secreted Trypsin

9

8

7

atoms% excess

6

5

4

3

2

healthy voln 13C

acute pancreatitis 13C

1

0

Fig 4

minutes

0

30

60

90

120

150

180

210

240

270

300

330

360

370


Enteral Feeding in Necrotizing

Pancreatitis:

pt 2: 18 yr old woman

1400

22000

units/h

1200

1000

800

600

AMYLASE

units/h

20000

18000

16000

14000

12000

LIPASE

400

200

0

30

60

90

120

150

180

210

240

270

300

330

360

minutes

10000

8000

6000

4000

30

60

90

120

150

180

210

240

270

300

330

360

Minutes

IV......................Enteral..........................................................

IV......................Enteral..........................................................

180

160

140

120

units/h

100

80

60

TRYPSIN

40

20

0

-20

30

60

90

120

150

180

210

240

270

300

330

360

minutes

IV......................Enteral..........................................................


Conclusions

! The superiority of enteral feeding to

TPN in the management of acute

pancreatitis is due to

– Targeted delivery of nutrients to the

splanchnic bed and prevention of

bacterial overgrowth

– Avoidance of TPN complications


Learning Assessment

Questions: Answers

1. False it is difficult to meet nutritional

requirements with jejunal feeding, and only distal

jejunal feeding avoids pancreatic stimulation

2. False although this statement may be correct,

no controlled studies have been conducted to

prove it

3. True patients with acute pancreatitis have both

exocrine and endocrine damage, leading to a

relative insulin deficiency


References

1. O’Keefe

SJD, Lee RB, Anderson FP, Gennings C, Abou-Assi

Assi S, Clore JN, Heuman D,

Chey W. The Physiological Effects of Enteral and Parenteral Feeding on Pancreatic P

Enzyme Secretion in Humans. Am J Physiol 2003;284:27-36

36

2. Abou-Assi

Assi SA, O’Keefe SJD. Nutrition in Acute Pancreatitis. J Clin Gastroenterol

2001;32(3):203-209

209

3. McClave S, Greene L, Snider H, Makk LJ, Cheadle WG, Owens NA, Dukes LG,

Goldsmith LJ. Comparison of the safety of early enteral vs. parenteral nutrition in

mild acute pancreatitis. J Parent Ent Nutr 21, 014 – 020, 1997.

4. Windsor ACJ, Kanwar S, Li AGK, Barnes E, Guthrie JA, Spark JI, Welsh F, Guillou PJ,

Reynolds JV. Compared with parenteral nutrition, enteral feeding attenuates the

acute phase response and improves disease severity in acute pancreatitis. Gut 1998;

42: 431- 435.

5. Kalfarentzos F, Kehagias J, Mead N, Kokkinis K, Gogos CA. Enteral nutrition is

superior to parenteral nutrition in severe acute pancreatitis: results r

of a randomized

prospective trial. British Journal of Surgery 1997, 84, 1665 – 1669

6. Abou-Assi

Assi S, Craig K, O’Keefe SJD. Hypocaloric jejunal feeding is better than TPN in

acute pancreatitis: results of a randomized comparative study. Am J Gastroenterol.

2002;97(9): 2255-2262

2262

7. O'Keefe SJ, Foody W, Gill S. Transnasal endoscopic placement of feeding tubes in the

intensive care unit. J Parenter Enteral Nutr. . 2003 Sep-Oct;27(5):349

Oct;27(5):349-54. 54.

8. O’Keefe SJD, Broderick T, Turner MA, Stevens S, O’Keefe JS. Nutrition in the

Management of Necrotizing Pancreatitis. Clin Gastroenterol Hepatol. . 2003;1:315-321

321

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