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The Correlations Between Early Enteral Nutrition and Intra-abdominal Pressure in Severe Acute Pancreatitis

The Correlations Between Early Enteral Nutrition and Intra-abdominal Pressure in Severe Acute Pancreatitis

Status
Completed
Phases
Phase 4
Study type
Interventional
Source
ClinicalTrials.gov
Registry ID
NCT01507766
Enrollment
60
Registered
2012-01-11
Start date
2010-09-30
Completion date
2011-09-30
Last updated
2012-11-16

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Acute Pancreatitis, Intra-abdominal Hypertension

Keywords

severe acute pancreatitis, intra-abdominal pressure, enteral nutrition

Brief summary

As an important management of severe acute pancreatitis (SAP), enteral nutrition (EN), especially early enteral nutrition (EEN) increases the blood flow of gut mucosa and stimulates the intestinal motility. Moreover, EEN maintains the gut integrity, prevents bacterial and endotoxin translocation and thereby theoretically reduces the incidence of infections. Therefore, EEN has the ability to reduce the infectious complications, length of hospital stay and mortality of patients with SAP. However, the role of EEN is considered to be influenced by intra-abdominal hypertension (IAH) in patients with SAP. The previous studies showed that gut was the most sensitive splanchnic organ to the increase of intra-abdominal pressure (IAP). When IAH occurs, it reduces the blood flow of gut, and then results in the development of intestinal ischemia and edema. The hypoxia and hypoperfusion of intestine leads to the increase of permeability of the intestinal mucosal barrier, and then leads to bacterial translocation. Therefore, IAH could result in the gastrointestinal dysfunction. Nevertheless, the different impacts of specific IAP values on the tolerance of EEN have not been reported. Furthermore, the effects of early enteral feeding on the IAP in SAP also remain unknown. Due to the severe inflammatory response of SAP, could EEN increase the burden of bowel, cause expansion of intestinal cavity, thus increase IAP? However, there were rare literatures up to date reporting the association between EEN and IAH in patients with SAP. Therefore, the present study aimed to investigate the influence of specific IAP on the tolerance of early enteral feeding, as well as the effects of EEN on IAP in SAP patients. Moreover, the impacts of EEN on the disease severity and clinical outcome of SAP were also researched.

Interventions

The enteral nutrition was started within 48h after admission

DRUGDelayed enteral nutrition

The enteral nutrition was started at the 8th day after admission

Sponsors

Jinling Hospital, China
CollaboratorOTHER
Nanjing University School of Medicine
Lead SponsorOTHER

Study design

Allocation
RANDOMIZED
Intervention model
PARALLEL
Primary purpose
TREATMENT
Masking
SINGLE (Subject)

Eligibility

Sex/Gender
ALL
Age
18 Years to 70 Years
Healthy volunteers
No

Inclusion criteria

* The diagnosis of acute pancreatitis accords with the Atlanta criteria in 1992 * Within 3 days from the onset of the disease * Hemodynamics stable

Exclusion criteria

* Decompressive measures and enteral nutrition was performed before admission * Ileus of lower digestive tract * Pregnant pancreatitis * Chronic organs dysfunction * Immunodeficiency

Design outcomes

Primary

MeasureTime frameDescription
Enteral nutrition14 daysThe caloric intake and tolerance of feeding were recorded daily after enteral nutrition was started
Intra-abdominal pressure14 daysThe value of intra-abdominal pressure (per 6 hours) and the incidence of intra-abdominal hypertension

Secondary

MeasureTime frameDescription
Clinical outcome variables14 daysHospital mortality; Duration of ICU stay; The development of multiple organ dysfunction syndrome and pancreatic infection; APACHEII score; SOFA score; CRP levels
Immune parameters14 daysIgA, IgG, IgM, CD4+/CD8+T cell and HLA-DR

Countries

China

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026