Did they check for any biliary obstruction, like Gallstones or anything?
Here is the complete run-down of Pancreatitis, copied from the nutrition care manual. You have to be a member of the ADA to view it, so i'll copy and paste it here so that it can be read.
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Overview of Pancreatitis
Pancreatitis is a complex condition involving an inflammation of the pancreas. The condition can be both acute and chronic; can range from mild to severe; and, in the case of chronic pancreatitis, can take several years to evolve.
Acute pancreatitis is most often associated with alcoholism and biliary tract obstruction (Nagar, 2004). Pancreatitis may evolve from other medical conditions such as cystic fibrosis, hypertriglyceridemia, hypercalcemia, renal failure, or infectious causes such as hepatitis or mumps. Some medications such as diuretics (furosemide) or antibiotics (tetracycline); trauma; surgery; or other tests can lead to acute pancreatitis. Still,
alcohol abuse accounts for 70% to 80% of all cases.
Risk factors for acute pancreatitis include the following:
Previous gallbladder disease
Chronic alcohol ingestion
Obesity
Exposure to certain toxins or drugs
Cystic fibrosis, hereditary conditions, and chemical exposure can potentially lead to chronic pancreatitis.
Background Information
The pancreas, a gland lying posterior to the stomach and alongside the duodenum, performs both exocrine and endocrine functions.
Exocrine functions include the secretion of digestive enzymes, bicarbonate, and electrolytes. The pancreas may secrete up to 2.5 L secretions each day. The release of secretions are controlled by a host of neurohumoral factors, including the hormones gastrin and secretin. Neuropeptides involved in pancreatic function include somatostatin, vasopressin (vasoactive intestinal polypeptide), and gastrin-releasing peptide (bombesin).
Endocrine functions center on the secretion of insulin and glucagon, which are pivotal in the metabolism of glucose, fatty acids, and amino acids. When these normal processes of digestion and absorption are interrupted, the resulting signs and symptoms of acute pancreatitis occur. Pancreatitis can either be acute or chronic.
Chronic alcohol abuse is a leading contributing factor in acute and chronic pancreatitis, but these conditions differ from one another in several important ways:
Acute: The acute inflammation that occurs is generally associated with acute abdominal pain; nausea and vomiting; elevated serum levels of pancreatic enzymes; and C-reactive protein, and can be accompanied by infection. Except in very severe cases, the pancreatic function usually returns to normal after recovery from the acute episode.
Chronic: Chronic pancreatitis may be asymptomatic or may be characterized by intermittent, recurrent abdominal pain; serum levels of pancreatic enzymes are often normal. Chronic pancreatitis leads to permanent tissue damage with resulting permanent pancreatic insufficiency.
Disease Process
The exact mechanisms that lead to pancreatic injury are not fully understood. However, a common characteristic seems to be premature activation of trypsin within the pancreas, resulting in autodigestion of the pancreatic cells. The enzymes released by destroyed pancreatic cells eventually reach the bloodstream, causing elevated serum amylase and lipase levels. Systemic complications can include the following:
Shock
Respiratory failure
Sepsis
Signs and symptoms are as follows:
Abdominal pain radiating to the back
Nausea
Vomiting
Steatorrhea
Biochemical indices for diagnosis of pancreatitis incude the following:
Serum lipase
Serum amylase
Secretin stimulation test
Glucose tolerance test
Ranson's criteria (1977), computed tomography severity index, or Apache scores are used to grade the severity of the disease and can be additionally confirmed using the following procedures:
****Endoscopic retrograde cholangiopancreatography
****Computed tomography
****Ultrasound
Chronic pancreatitis is the result of irreversible damage to the pancreas that is caused by repeated inflammation and results in destruction of the exocrine and eventually the endocrine tissue.
The primary intervention for chronic pancreatitis is to minimize symptoms of pain and malabsorption by avoiding exacerbating factors (alcohol and high fat intake) and using pancreatic enzyme replacement as needed. In addition, endocrine abnormalities such as diabetes mellitus will need to be addressed.
For more information, see Pancreatitis–American Gastroenterological Association (accessed July 15, 2010).
Biochemical and Nutrient Issue
The primary intervention for acute pancreatitis is to prevent stimulation of the pancreas and thus reduce the release of its secretions. Thus, if the patient does not receive nutrition support, there will be risk for inadequate energy, protein, vitamins, and minerals.
In chronic pancreatitis, the symptoms of malabsorption and endocrine complications may lead to maldigestion and malabsorption of nutrients. Avoidance of food to decrease pain may result in malnutrition.
Implementation of the Nutrition Intervention - Oral Intake
Patients who undergo prolonged nutrition support or NPO (nil per os, or nothing by mouth) status may develop a fear of eating or aversions to specific foods that they associate an exacerbation of symptoms.
Feeding issues may present in the opposite manner—that is, patients may have a desire to eat when it is imperative that they maintain NPO status for recovery.
Close observation and counseling is necessary in both of these circumstances, and patients should be encouraged to discuss their issues with the health care team so that an appropriate plan of care can be determined and implemented.
As the patient's amylase and lipase begin to trend downwards, oral intake may be initiated. The historical progression from NPO to oral intake has included transition from clear liquids to a low fat solid food diet. Monitoring for any gastrointestinal complaints will alert the practitioner for any intolerance to the oral diet.
Biochemical Data, Medical Tests and Procedures
To diagnose pancreatitis, perform the following laboratory tests:
White blood cell count
Serum glucose
Serum lipase
Amylase
Lactic dehydrogenase (LDH)
Aspartate aminotransferase (AAST)
The degree of inflammation (and thus the severity of the disease) may be assessed by the following:
C-reactive protein
Evaluation using Ranson’s criteria, Apache score or Computed Tomography Severity Index
It is also common practice to use a combination of criteria that distinguish the severity of the disease. Common criteria include Ranson’s criteria, Apache score, and the Computed Tomography Severity Index. Ranson’s criteria (1977) are as follows:
Admission:
Age >55 years
White blood cell count >16,000/mm3
Blood glucose >200 mg/dL (especialy in nondiabetic patients)
LDH >350 IU/L
AAST >250
After initial 48-hour period:
Decrease in hematocrit by ≥10%
Increase in serum blood urea nitrogen by >5 mg/dL
pO2 of <60 mm Hg
Base deficit >4 mEq/L
Fluid sequestration >6 L
To follow hydration and acid-base status, monitor the following:
Serum electrolytes
Arterial blood gases
Other biochemical abnormalities may include the following:
Hypertriglyceridemia
Hypocalcemia (Rettally, 2003)
To determine presence of pseudocysts or necrosis, other diagnostic tests may include the following:
Computed tomography
Ultrasound
Endoscopic retrograde cholangiopancreatography
Laboratory Value Norms
Laboratory Normal Range: Adult Values
Amylase 25-125 U/L
Lipase 0-417 U/L
Lactate dehydrogenase 313-618 U/L
Serum glutamic-pyruvic transaminase 10-60 U/L
Serum glutamic-oxaloacetic transaminase 5-40 U/L
C-reactive protein 0
Hemoglobin 12-16 g/dL, women; 13.5-17.5 g/dL, men
Hematocrit 37% to 47% (women); 40% to 54% (men)
Glucose 70-110 mg/dL
Blood urea nitrogen 8-26 mg/dL
Creatinine 0.6-1.3 mg/dL
Sodium 135-155 mmol/L
Potassium 3.5-5.5 mmol/L
Phosphorous 2.5-4.5 mmol/L
Chloride 98-108 mmol/L
Calcium 8.7-10.2 mg/dL
Carbon dioxide 24-30 mmol/L
Osmolality 275-295 mOsm/kg H20
Vitamin D (25-hydroxy) 16-74 ng/dL
Nutrients Below Target Due to Nutrition Prescription
Carbohydrate, protein, and fat should be balanced according to standard guidelines when nutrition support is provided unless hyperglycemia, hypertriglyceridemia, or other metabolic complications necessitate substrate modification. Special attention to fat-soluble vitamin status may be needed when steatorrhea and other signs of malabsorption are present.
Dietary fat intake may be lower as a result of steatorrhea and malabsorption.
Standard multivitamin/mineral therapy should be considered during the recovery phase until normal eating habits have been well established and signs and symptoms of deficiency are not present.
Micronutrient deficiencies common in chronic alchoholism include thiamin; pyridoxine; folate; vitamins C, A, and K; zinc; and magnesium (Sucher, 2011 in press).