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Diabetes, milky serum and abdominal pain
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A 43-year-old woman with type 2 diabetes mellitus, hypertension, gastroesophageal reflux disorder and obesity presented to the ED with severe epigastric pain radiating to her back, nausea and vomiting for 1 day. She had not consumed alcohol for 3 months. Outpatient medications included: metformin 500 mg by mouth once daily; lisinopril 10 mg by mouth once daily; and omeprazole 20 mg by mouth once daily; each taken for 1.5 years prior to presentation. She was not taking a dipeptidyl peptidase IV inhibitor, glucagon-like peptide-1 analog or any other medications.
 Matthew Spitzer |
 Thomas Brahler |
 Stephanie L. Lee |
Physical examination disclosed a heart rate of 110 beats per minute; blood pressure of 167/108 mm Hg; respiratory rate of 18 respirations per minute (rpm) with oxygen saturation 100%; and temperature of 98°F. Skin and tendon exam were normal. Abdominal exam revealed moderate epigastric tenderness without rebound tenderness, normal bowel sounds and no masses. The biliary ducts and pancreas had a normal appearance on an ED sonogram of the abdomen.
The serum in a blood specimen was noted to be lipemic or lactescent (milky in appearance). Serum triglycerides were 5,080 mg/dL (reference range, 40-200 mg/dL). She had an elevated white blood cell count of 15,200 cells/mcL with 85% polymorphonuclear cells and a low hematocrit (28.6%). Other significant lab levels included elevated lipase, 82 U/L (normal 16-63 U/L); normal amylase, 64 U/L (normal 20-104 U/L); creatinine, 0.49 mg/dL; calcium, 8.6 mg/dL; bicarbonate, 24 mmol/L; thyroid-stimulating hormone, 1.14 mIU/mL; aspartate aminotransferase, 23 U/L; and alanine aminotransferase, 7 U/L. Her serum glucose was elevated at 178 mg/dL with HbA1c of 7.8% (normal, 4%-6%).
On admission, CT abdomen and pelvis revealed a mildly enlarged pancreas with a 1-cm hypodense lesion in the body of the pancreas, suggestive of an evolving pseudocyst, and stranding of the surrounding fat (Figures 1A, 1B). The absence of common bile duct dilation and recent alcohol use argued against cholelithiasis and alcohol as precipitants of her pancreatitis. Moreover, drug-induced pancreatitis seemed less likely as she had been on metformin, lisinopril, and omeprazole for more than a year. Consequently, she was assessed to have acute pancreatitis due to hypertriglyceridemia. Her CT severity index (CTSI) score of 2 for pancreatitis predicted a mortality of 3%. CTSI scores are determined by taking the sum of the CT grade and CT necrosis scores. The patient was admitted to the ICU for treatment with IV insulin drip and oral gemfibrozil 600 mg twice daily.
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Photo courtesy of: Stephanie L.
Lee, MD, PhD |
Fever develops
On day 1, the patient developed a fever of 102.2°F with an increase in creatinine to 2.1 mg/dL and the gemfibrozil was stopped. After 14 hours of IV insulin, her triglycerides decreased to 508 mg/dL and she was transitioned to subcutaneous insulin. Although afebrile and subjectively improved on days 2 and 3, her urine output decreased and she developed severe respiratory distress syndrome requiring intubation. Her temperature spiked to 103.2°F, but urine and blood cultures yielded no growth on day 6. Stool Clostridium difficile toxin tested positive, and she was treated with metronidazole.
She continued to have severe abdominal pain and fever. A CT abdomen with contrast was performed on hospital day 9, revealing development of a 5.8-cm partially organized fluid collection near the tail of the pancreas (Figure 1C) and a stable, 1.3-cm intrapancreatic fluid collection. Piperacillin-tazobactam was started. On day 13, the patient was successfully extubated. CT abdomen (not shown) on day 14 revealed that the peripancreatic fluid collection had slightly decreased in size and the stable hypoattenuating lesion in the body of the pancreas. She slowly improved and was discharged on gemfibrozil 600 mg twice daily; lisinopril 10 mg by mouth once daily; and metformin 1,000 mg by mouth twice daily. MRI of the abdomen 34 days after presentation demonstrated near resolution of the peripancreatic fluid collection and a slight reduction in size of the 1.2-cm hyperintense pseudocyst (Figure 1D). As of 1 year later, the patient has not had any new episodes of pancreatitis.
Uncommon finding
Hyperlipidemic pancreatitis is uncommon and is the etiology of only 1% to 4% of cases of pancreatitis. A review of 70 patients with hyperlipidemic pancreatitis during 12 years revealed an average serum triglyceride of 4,587 ± 3,616 mg/dL, with a range of 600 mg/dL to 17,770 mg/dL. Pancreatitis is not associated with hypertriglyceridemia unless the triglyceride level is more than 500 mg/dL. Patients with type 2 diabetes are predisposed to elevated triglyceride levels because of reduced lipoprotein lipase activity and overproduction of very-low-density lipoprotein by the liver. Chylomicrons can be easily confirmed after overnight refrigeration of an upright tube of plasma (or serum) showing a creamy (lactescent) supernatant above the red blood cells. Forty-five percent of hyperlipidemic pancreatitis is associated with lactescent serum.
The diagnosis of acute pancreatitis hinges upon abdominal pain, elevated serum amylase and/or lipase at least three times the upper limit of normal, and CT scan evidence of pancreatitis. For this patient, diagnosis was initially questioned because the serum amylase and lipase levels were less than three times the upper limit of normal, besides normal pancreatic imaging on ultrasound. Review of the literature shows that the sensitivity and specificity of more than three-times elevated serum amylase with acute pancreatitis is only 50% and 99%, respectively. Similarly, serum lipase more than three times the upper limit of normal has a sensitivity and specificity of only 64% and 97%, respectively. This means amylase and/or lipase can be less elevated or normal in up to 50% of cases of acute pancreatitis. Therefore, a less than three-times elevated serum amylase and lipase does not exclude the diagnosis of acute pancreatitis.
CT scan with contrast is the gold standard for diagnosing acute pancreatitis. Pancreatic enlargement and peripancreatic fat stranding confirmed the diagnosis for this patient (Figure 1A). Acute peripancreatic fluid collections, also seen in this patient, are low attenuating and conform to peritoneal boundaries, but lack an inflammatory or fibrous capsule (Figure 1C). Acute peripancreatic fluid frequently resolves and requires no intervention. Pseudocysts are intrapancreatic fluid that persists for more than 4 weeks after the onset of pancreatitis and feature walls of fibrous or granulation tissue (Figures 1B, 1D).
This patient had acute pancreatitis without pancreatic necrosis. Pancreatic necrosis is visualized as non-enhancing portions of the pancreas after IV contrast. CT imaging findings of the pancreas can be used to predict mortality using a CTSI score. A CTSI score of 0 to 3, 4 to 6 and 7 to 10 predicts mortality of 3%, 6%, and 17%, respectively.
Matthew Spitzer, MD, is a fellow in endocrinology, section of endocrinology, diabetes and nutrition, at Boston Medical Center. Thomas Brahler, MD, is a resident, department of radiology, at Boston Medical Center. Stephanie L. Lee, MD, PhD, is director of the Thyroid Health Clinic at Boston Medical Center, associate professor of medicine at Boston University School of Medicine and is an Endocrine Today Editorial Board member.
For more information:
- Banks PA. Am J Gastroenterol. 2006;101:2379-2400.
- Bharwani N. Clin Radiol. 2011;66:164-175.
- Fortson MR. Am J Gastroenterol. 1995;90:2134-2139.
- Sutton PA. Ann R Coll Surg Engl. 2009;91:381-384.
Disclosures: The authors report no relevant financial disclosures.