voeding(bij(acute pancreatitis( - vvkvm · • anatomiepancreas •...

Voeding bij acute pancreatitis Karolien Dams, MD, intensieve zorgen UZA

Leerdoelen • Onderscheid milde/erns.ge pancrea..s •  Impact van adequate nutri.onele ondersteuning op klinische outcome

• Voor-‐ en nadelen van enterale nutri.e (EN) en parenterale nutri.e (PN)

• Beste approach bij erns.ge, gecompliceerde acute pancrea..s

Inhoud • Anatomie pancreas • Acute pancrea..s: classifica.e •  Enteraal of parenteraal? •  Toedieningsroute

ANATOMIE PANCREAS

Anatomie pancreas

Endocriene pancreasfunctie

Exocriene pancreasfunctie

Figure 2. Bicarbonate secretion response of the exocrine pancreas after nutrient intake

The vagus nerve and the hormones secretin and cholecystokinin (CCK) are responsible for stimulation of the exocrine pancreas. The pancreatic enzymes digest starch (amylase), lipids (lipase), and protein (trypsin and other proteolytic enzymes). The most important stimulus for pancreatic secretion is the presence of nutrients in the duodenal lumen.

Figure 3. Factors regulating exocrine pancreatic secretion

It is not only the quantity but also the composition of nutrients in the duodenal lumen which influences the pancreatic secretory response (Fig. 3).

3. Pathophysiology of chronic pancreatitis

Due to the loss of acinar and duct cells (Fig. 4) the secretory capacity of the exocrine pancreas decreases. The large physiological reserve of the pancreas is the reason why clinical signs of fat maldigestion occur late in the course of CP, typically when 80 % of the secretory capacity of the pancreas has been lost.

Fat maldigestion (steatorrhoea; > 10 g of stool fat per 24 hours) is the major problem in these patients. Steatorrhoea is caused by (i) reduced pancreatic bicarbonate secretion leading to more rapid and complete inactivation of lipase in the acidic duodenum; (ii) further impairment of lipid absorption by bile

Copyright © by ESPEN LLL Programme 2011

ACUTE PANCREATITIS: CLASSIFICATIE

Acute pancreatitis

• Mild (75-‐80%) ➙ erns.g necro.serend •  Systemische inflammatoire respons

•  op een lokaal proces van autodiges2e •  variabele aantas2ng van het peri-‐pancrea2sch weefsel en andere orgaansystemen

•  2 meest frequente oorzaken: •  galstenen •  alcohol

•  2 outcome predictors: ernst + nutri8onele status

Classi<icatie van ernst 1.  Klinische score systemen (Ranson, Glasgow,

APACHE II, Atlanta) 2.  Biochemisch (CRP, BUN) 3.  Radiologische criteria (Balthazar)

Mortaliteit: •  Mild-‐moderate: 1% •  Severe pancrea..s: 19-‐30%

•  > 50% necrose: 50% •  + sepsis: tot 80%

Ranson score

Classification of severity defines severe acute pancreatitis on the basis of standard clinical manifestations: a score of 3 or more in the Ranson Criteria (Table 1) (9), or a score of 8 or more in the APACHE II-Score, and evidence of organ failure and intrapancreatic pathological findings (necrosis or interstitial pancreatitis) (Tab. 2). This classification is helpful because it also allows the comparison of different trials and methodologies (11). The severity of acute pancreatitis based on imaging procedures is based on the Balthazar-Score, which predicts severity on CT appearance, including presence or absence of necrosis (Table 3) (10). Failure of pancreatic parenchyma to enhance during the arterial phase of intravenous contrast-enhanced CT indicates necrosis, which predicts a severe attack if more than 30% of the gland is affected. The measurement of concentrations of serum C-reactive protein (CRP) is very useful in clinical practice. CRP concentration has an independent prognostic value. A peak of more than 210 mg/l on day 2 to 4, or more than 120 mg/l at the end of the first week, is as predictive as multiple-factor scoring systems (12). Another predictive factor on mortality was recently published. The blood urea nitrogen levels (BUN) were persistently higher among nonsurvivors than survivors in the first 48 hours of hospitalisation. It seems that BUN is a new valuble marker for predicting mortality (13).

Table 1. Ranson’s criteria of severity for acute pancreatitis (9)

Admission criteria Age > 55 years WBC > 16.0x109/L Gucose > 10 mmol/l Lactate dehydrogenase (LDH) > 350 IU/L Aspartamine Transaminase (AST) >250 U/L

Following initial 48 hours Criteria Hematocrit decrease of >10% BUN increase of > 1.8 mmol/l Calcium < 2 mmol/l PaO2 < 60 mmHg Base deficit > 4 mEq/L Fluid sequestration >6 L

Table 2. Atlanta classification (11)

Atlanta Classification(Defining Severe Acute Pancreatitis)- Evidence of Organ Failure Shock (Systolic Blood Pressure <90 mm Hg) Pulmonary insufficiency (PaO2<60 mm Hg) Renal failure (creatinine > 2mg/dl) Gastrointestinal bleed (>500 ml/day)- Or Local Complications Pancreatic necrosis >30% Pancreatic abcess Pancreatic pseudocyst- With Unfavorable Prognostic Signs Ranson Criteria >3 or APACHE II score >8

Table 3. Computed tomography (CT) grading system of Balthazar (10)

CT gradeQuantityof necrotic pancreas


Atlanta classi<icatie

Balthazar score

Grade A = 0Grade B = 1Grade C = 2

Grade D = 3

Grade E= 4

Normal appearing pancreasFocal or diffuse enlargement of the pancreasPancreatic gland abnormalities accompanied by mild parapancreatic inflammatory changes

Fluid collection in a single location, usually within the anterior pararenal space

Two or more fluid collections near the pancreas or gas either within the pancreas or within parapancreatic inflammation

<33% = 233% - 50% = 4> 50% = 6

Total score = CT grade (0-4) + necrosis (0-6)

2.2. Nutritional status

Undernutrition and obesity are often seen in patients with acute pancreatitis. Both are well-known risk factors for more complications and higher mortality. Undernutrition is known to occur in 50-80% of chronic alcoholics and alcohol is a major etiological factor in acute pancreatitis patients (30-40%) (14). Patients with biliary pancreatitis have a high tendency to be overweight.For nutritional support it is therefore necessary to assess the severity of acute pancreatitis and the nutritional status at the time of admission and during the course of the disease. Both factors are necessary to plan nutrition interventions in patients with acute pancreatitis.

3. Energy and substrate metabolism during acute pancreatitis

Specific and non-specific metabolic changes occur during acute pancreatitis. A variety of proinflammatory cytokines increase the basal metabolic rate. This can result in increased energy consumption. The resting energy expenditure varies according to the severity and the duration of disease. If patients develop sepsis, 80% of them show an elevation in protein catabolism and an increased nutrient requirement. A prolonged negative nitrogen balance determines negative clinical outcome (15). Whether negative nitrogen balance is the principle factor for outcome is not clear. The relationship between nitrogen balance and outcome may only reflect the relationship between nitrogen balance and severity of disease. There is no study available in which patients were stratified according to the disease severity.

3.1. Metabolism of carbohydrates

Glucose metabolism in acute pancreatitis is determined by the SIRS response, oxidative stress, and insulin resistance. The resultant futile fluid cycling and milieu of inflammatory cytokines may cause an increase in energy demand. Endogenous gluconeogenesis is increased as a consequence of the metabolic response to the severe inflammatory process. Glucose is an important source of energy and can partially counteract the intrinsic gluconeogenesis from protein degradation. This can counteract, to a certain degree, the deleterious and unwanted effect of protein catabolism (16). The maximum rate of glucose oxidation is approximately 4 mg/kg/min. The administration of glucose in excess can be harmful, and even wasteful, because of lipogenesis and glucose recycling. Furthermore, hyperglycemia and hyperkapnia can occur. Hyperglycemia is a major risk factor for infections and metabolic complications. Monitoring and blood glucose control is therefore essential. Evidence of glucose intolerance occurs in the majority of cases (incidence 85%) (17).

3.2. Protein metabolism

A negative nitrogen balance is often seen in severe acute pancreatitis. The protein losses must be minimized and the increased protein turnover must be compensated. If acute pancreatitis is complicated by sepsis, up to 80% of the patients are in a hypermetabolic state with an increase of the resting energy expenditure. A negative nitrogen balance is associated with adverse clinical outcome. Nitrogen losses are as much as 20-40 g/day in some patients with acute pancreatitis.


Nutritionele status Ondervoeding en obesitas:

•  frequent •  risicofactoren:

•  meer complica.es •  hogere mortaliteit

Route, 8ming, hoeveelheid en samenstelling van nutri8e: belangrijke effect op ziekteverloop

ENTERAAL OF PARENTERAAL?

Voedingsdoelen • Voorzien in kcal met EN of PN:

•  Proteïne catabolisme omkeren •  Zonder s.mula.e van exocriene pancreas secre.e

• Het verbeteren/vermijden van malnutri.e • Morbiditeit en mortaliteit reduceren

ESPEN Guidelines Recommendations •  Enteral Nutri2on: Clinical Nutri2on Vol 25 (2), April 2006

• Parenteral Nutri2on: Clinical Nutri2on Vol 28, July 2009

•  www.espen.org/educa8on/ guidelines.htm

Enteraal of parenteraal? •  ENTERAAL •  Concept pancreasrust?

Spanier B

WM et a

l. Ga

stroen

terology Research and Prac.ce 2011.

Enteraal of parenteraal? Milde pancrea88s: •  geen effect als pa2ënt opnieuw eet binnen 5-‐7 d •  geen peroraal voedsel > 5-‐7d: start EN •  erns.ge abdominale pijn: EN <24h (MIMOSA

trial): goed verdragen, •  í intensiteit/duur pijn, nood aan opiaten •  írisico van orale voedselintoleran.e •  geen verschil in LOS

•  PN: •  te vermijden •  zo EN onmogelijk/onvoldoende •  meer complica.es en kosten hoger

Petrov M

S et al. Clinical Nutri.

on 32 (2013) 697-‐703

Enteraal of parenteraal? Erns8ge pancrea88s: •  eerst EN •  voordelen van vroege EN: start <24-‐48h

•  mucosale darmintegriteit •  preven2e bacteriële overgroei • í risico op infec.es, chirurgie • í ernst van ziekte en mortaliteit •  snellere genezing van het ziekte proces, í LOS

Bakker OJ e

t al. NEJM 2014;

371:1983-‐93

Welke enterale formule?

•  Start standaard polymere formule •  Zo intoleran.e ➙ switch naar semi-‐elementaire sondevoeding

•  Geen significant hoger risico van intoleran.e, infec.euze complica.es of mortaliteit

•  Goedkoper

Marik PE. Curr O

pin Crit Care 2009,

15: 131-‐8

Welke enterale voeding?

•  Immuun modulerende voeding? •  Arginine, glutamine, ω-‐3 poly-‐onverzadigde vetzuren, prebio.ca

•  Te weinig eviden8e

Hegazi RA

. et a

l. World J

Gastroen

terol 2014; 20 (43):

16101-‐5

Probiotica

Probio.ca = specifieke vezel-‐fermenterende melkzuurbacteriën

298 pt Meer orgaanfalen en hogere mortaliteit Non-‐occlusieve darmischemie

Besselink et al. Lancet 2008; 371: 651-‐59

Probiotica

Probio.ca = specifieke vezel-‐fermenterende melkzuurbacteriën

298 pt Meer orgaanfalen en hogere mortaliteit Non-‐occlusieve darmischemie

Poropat G

. et a

l. Co

chrane

Database of Systema.

c Re

view

s 2015, Issue

3.

Welke parenterale formule? •  PN voorbehouden voor:

•  Contraindica.e/intoleran.e voor EN •  Supplement bij EN

•  ω-‐3 vetzuren en glutamine •  íInfec.euze complica.es •  íLagere mortaliteit •  íLOS

1Ockenga et al, Clin Nutr 2002 2Xian-‐li et al, Clin Nutr Suppl 2004 3Sahin et al, Eur J Clin Nutr 2007 4Fuentes-‐Orozoco et al, JPEN 2008 5Xue et al, W J Gastroenterol 2008 6Wang et al, JPEN 2008; Inflamma.on 2009

Jafari T. et a

l. Clinical Nutri.

on 34 (2015) 35-‐43

TOEDIENINGSROUTE

Route

•  Nasogastrische voeding: mogelijk bij meerderheid van de pa.ënten (79%-‐90%)

•  Postpyloor: •  distaal (> 60cm) van het ligament van Treitz •  fluoroscopische/endoscopische/self-‐propelling/electromagne.c

•  Par.ële ileus is geen contra-‐indica.e •  Heelkunde: intra-‐opera.eve jejunostomie

Marik PE. Curr O

pin Crit Care 2009 (15): 131-‐8

Nally DM et a

l. Br J Nutr. 2014 Dec 14; 112 (1

1):1769-‐78

Gastrisch vs jejunaal •  Absolute noodzaak voor jejunale voeding? •  Gastrisch:

•  gemakkelijk •  ➘ .jd tot start van voeding •  kleinere kans op ileus

Postpylore sonde

Postpylore sonde

nutrition (ESPEN Guideline: Grade A). Several prospective studies have shown that jejunal tube feeding is possible in most patients with acute pancreatitis (42). Placing a jejunal feeding tube distally to the ligament of Treitz can easily be performed. The tubes are placed either with fluoroscopic help or more and more with the endoscope. Another way is also to use self-propelling nasojejunal feeding tubes. Normally, jejunal tubes are well tolerated (29,44-46). Very recently Hegazi et al reported that early initiation of distal jejunal feeding was associated with reduced mortality in patients with severe acute pancreatitis. The early achievement of the feeding goals was also associated with a shorter length in the ICU (47). Rarely, proximal migration of the feeding tube and subsequent pancreatic stimulation can aggravate acute pancreatitis (48). Partial ileus is not a contraindication for enteral feeding because these patients frequently tolerate continuous low-volume jejunal nutrients. Several single or multilumen tubes are available (Fig. 3). In case of surgery for pancreatitis an intra-operative jejunostomy (Fig. 4) for postoperative tube feeding is feasible (49).

Figure 3. Multilumen nasojejunal tube


Postoperatieve nutritie •  Jejunostomie: veilig en goede toleran.e

Bodoky et al, Am J Surg, 1991 Herandez-‐Aranda, Nutricion Hospitlaria, 1996 Weimann et al, JPEN, 2004

Jejunostomie

ESPE

N, G

uide

lines

200

6/20

09

Trea

tmen

t sev

ere

panc

reat

itis

Assessment of severity of acute pancreatitis

Severe

Early continuous EN (nasogastric/-jejunal tube) •  Elemental diet or •  Polymeric diet or •  Immune-enhancing diet?

EN is not possible

Add PN - All in one - or single component solutions (CH, AA, fat)

•  TPN and •  Con8nuous small amount of an enteral diet (10-‐30 ml/h) perfused to the jejunum

Nutri8onal goal not reached

Take home messages •  Beoordeel ernst + nutri.onele status •  Erns.ge/gecompliceerde pancrea..s:

•  adequate nutri.onele support cruciaal •  vroege EN verbetert het verloop

•  Gastrisch voeden: •  veilig alterna.ef voor jejunaal

•  Combina.e EN+PN als EN alleen niet succesvol •  Nutri.onele support = ac.eve therapeu.sche interven.e

•  Overweeg glutamine •  GEEN probio.ca

voeding(bij(acute pancreatitis( - vvkvm · • anatomie*pancreas* •...

Documents

voeding(bij(acute pancreatitis( - vvkvm · • anatomiepancreas •...