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Gastrointestinal

Nutrition in Acute Pancreatitis

Dr Swapnil Pawar September 23, 2019 593


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Dr Jose Chacko & Dr Swapnil Pawar

Acute pancreatitis is the leading cause of acute hospital admission for gastrointestinal disorders in many countries, and its incidence continues to rise worldwide. The annual incidence of AP ranges from 13 to 45 cases per 100,000 population with the global estimate of 33.74 cases per 100,000 population, causing uneven burden across the globe. The health-care cost in the United States is reported to be $2.5 billion. The overall mortality ranges from 5 to 20% depending on severity. In patients who develop severe necrotizing pancreatitis, mortality is approximately 15%. In cases of infection of pancreatic necrosis and multi-organ failure, mortality can be as high as 30%. Up to date, a major challenge is to achieve nutritional targets, which is partly due to heterogeneous etiological factors and also due to varying clinical manifestations associated with this condition. So today we are going to discuss various controversies related to Nutrition in Acute pancreatitis.

The first controversy is when to start feeding?

In mild acute pancreatitis, intravenous hydration alone may be adequate, because rapid recovery is common, and oral intake is possible within a week. However, in moderate to severe acute pancreatitis, nutritional support is usually required as early oral intake is usually not possible. 

Mild diseaseConventionally, it was widely believed that enteral feeding may lead to worsening of pain and exacerbate acute pancreatitis. Gastric feeding may stimulate the release of pancreatic enzymes, worsen autodigestion, and aggravate the disease process. Hence, conventional management has been to place patients on strict bowel rest and use parenteral nutrition to bypass the stimulatory effects of oral feeding. Current evidence suggests a low-fat diet is safe and well-tolerated in most patients with acute pancreatitis. Hence, oral nutrition is advisable as tolerated when abdominal pain eases off, and there is a subjective feeling of hunger, regardless of complete resolution of pain and normalization of pancreatic enzyme levels.

Moderate to severe disease- severe pancreatitis leads to reduced contractility of the small bowel leading to bacterial overgrowth. Besides, reduced splanchnic blood flow increases intestinal permeability. Early commencement of enteral nutrition may have a trophic effect on gut wall integrity and may help reduce the inflammatory response.

As you said there is this myth that if we feed, that might worsen the situation. it is partly due to our understanding of the pathophysiology of the disease. Gut inflammation and barrier failure occur following systemic inflammatory responses, vascular disturbance, and ischemia/reperfusion injury secondary to pancreatic inflammation. Disrupted barrier function further leads to bacterial translocation, pancreatic infection and necrosis, and endotoxemia, ultimately responsible for multiple organ dysfunction syndromes (MODS) and death. But I guess if you don’t feed this leads to malnutrition which then results in the breakdown of the gut barrier and worsens translocation.

What is the evidence out there for commencing early nutrition in severe pancreatitis?

JC- Current evidence suggests a low-fat diet is safe and well-tolerated in most patients with acute pancreatitis. Hence, oral nutrition is advisable as tolerated when abdominal pain eases off, and there is a subjective feeling of hunger, regardless of complete resolution of pain and normalization of pancreatic enzyme levels. In the PYTHON trial, patients predicted to have severe acute pancreatitis were randomized to receive either early enteral nutrition through a nasoenteral feeding tube within 24 hours after presentation to the emergency department or placed on a nil-per-mouth regime for 72 hours followed by an oral diet. If the oral intake was insufficient after this period, a feeding tube was inserted, and enteral nutrition commenced. The primary endpoint was a composite of major infection (infected pancreatic necrosis, bacteremia, or pneumonia) or death during 6 months of follow-up. There was no difference in these outcomes between the two groups (30% in the early vs. 27% in the later feeding group).
A recent systematic review of 11 randomised controlled trials (RCT) compared early vs. delayed feeding in acute pancreatitis. This review suggested a reduced hospital length of stay with early enteral nutrition. None of the included studies showed a significant increase in the incidence of adverse events or worsening of symptoms with early feeding, regardless of disease severity.

So what we know so far is that immediate oral feeding in patients with  AP is feasible and safe and can lead to accelerated recovery without adverse gastrointestinal events. Still, there is hesitancy in commencing enteral feeding in severe pancreatitis with MODS. and I guess no trial will be able to answer this precise question. Also, whether we achieve nutritional targets early doesn’t add much mortality benefit in critically ill patients in general as per Target trial. So I guess even if start slow and then go up is okay. The idea is to prevent gut atrophy.

the next controversy – The route what’s the evidence for Enteral vs parenteral nutrition?

Previously, parenteral nutrition was administered routinely in acute pancreatitis to prevent pancreatic stimulation. The traditional belief was that nutrition delivered proximal to the ligament of Treitz would stimulate the pancreas and worsen the severity of acute pancreatitis. Hence, parenteral nutrition seemed ideal for adequate nutritional support in acute pancreatitis. Enteral feeding may have immunomodulating effects, including preservation of the integrity of the gut mucosa; it may also stimulate intestinal motility, thereby reducing bacterial overgrowth. Besides, enteral feeding may also enhance splanchnic blood flow. All these may reduce bacterial translocation from the gut, which is one of the key factors that lead to infection in acute pancreatitis. Although there is no strong corroboratory evidence, enteral nutrition may prevent infection of the necrosis and reduce mortality. Two major RCTs have been carried comparing enteral with total parenteral nutrition. Wu et al., in a randomized controlled trial of 208 patients, showed a lower incidence of organ failure, infected necrosis, surgical intervention, and mortality with enteral nutrition. A smaller RCT of 70 patients also showed a lower incidence of infected necrosis, reduced organ failures, and lower mortality with enteral compared to parenteral nutrition. Three recent meta-analyses have also concluded that enteral nutrition significantly reduces infections, organ failure, and mortality in patients with acute pancreatitis compared with parenteral nutrition. Meta-analyses are limited by heterogeneous patient groups; inclusion of patients with mild disease may have resulted in reduced mortality. Despite these limitations, early enteral nutrition is recommended in acute pancreatitis; total parenteral nutrition is indicated only if enteral nutrition is not tolerated. 

Again for me, it’s about using the common sense approach. Start the feeding via natural route slow and steady. See how it goes. If there is a persistent problem in tolerating feeds, by all means, consider TPN. And again keep trying. if you get the opportunity to commence enteral nutrition, then go ahead and wean TPN.

Another popular controversy – which enteral route?? NG vs NJ Placement of a feeding tube beyond the ligament of Treitz is considered to reduce the risk of reflux of feeds back into the stomach and prevent stimulation of pancreatic enzyme release. However, it has been shown that pancreatic stimulation may be preventable only when enteral nutrition is given in the mid-distal jejunum.8 Three trials compared nasojejunal with nasogastric nutrition in patients with severe acute pancreatitis.9–11 These studies suggested that nasogastric feeding may be easier, well-tolerated, and equally efficacious as nasojejunal feeding. Infectious complications and duration of stay in hospital were also comparable. There was no difference in pain on refeeding, intestinal permeability, and endotoxemia. These studies were limited by small sample sizes, and included patients at different stages of the disease, with varying severity. A meta-analysis of these three randomized trials showed no differences in mortality, the incidence of tracheal aspiration, and attainment of calorie targets between the two groups.12 Although the quality of the evidence is limited, when tolerated, nasogastric nutrition appears to be safe. When nasogastric nutrition is not tolerated, or when the caloric requirement cannot be attained, nasojejunal feeding beyond the ligament of Treitz is recommended.

The last controversy – use of probiotics in AP
Probiotic bacteria may prevent infectious complications by inhibiting the overgrowth of pathogenic bacteria in the small bowel, restoration of gastrointestinal barrier function, and immune modulation. Hence, probiotic administration may potentially prevent pancreatic and extra-pancreatic bacterial infections. This was particularly of interest following the failure of prophylactic antibiotic therapy to prevent infections.  The PROPATRIA trial compared probiotic prophylaxis using six different strains of freeze-dried, viable bacteria with placebo in 298 patients who were predicted to have severe acute pancreatitis.13  No difference was observed in the incidence of infectious complications. Besides, there was a significant increase in mortality with the use of probiotics. Nine patients suffered non-occlusive mesenteric ischemia in the probiotic group compared to none in the placebo group. A subsequent retrospective study used the same type of probiotics in patients with acute pancreatitis without organ failure.14 This study revealed no evidence of benefit or harm, suggesting that the harmful effects of probiotics may occur in patients with evidence of organ failure. Based on these findings, the current recommendation is against the use of probiotics in acute pancreatitis.

Summary –

Keep It Simple – Enteral feeding is the best option. So commence enteral feeding as soon as feasible and keep trying to feed via NG route. If significant issues due to persistent ileus, consider the trial of TPN. Consider trophic feeding via NG or NJ route to prevent gut atrophy and bacterial translocation.

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