Purpose: Hypertriglyceridemia-induced pancreatitis in pregnancy carries an increased risk of mortality. We report a case of a patient who refused plasmapheresis and was treated with supportive care only. A 34-week gestation 31-year-old female of Spanish descent presented to the ER with complaints of nausea, vomiting, and diffuse abdominal pain for 2 days. Past medical history was only significant for hypertension after her first pregnancy. She had no prior surgeries or pertinent family history. She denied ETOH or tobacco use. Her only medication was prenatal vitamins. On presentation to the hospital she appeared to be in moderate distress. She was pale and diaphoretic with a BP 99/47 mmHg, pulse 75 bpm, RR 18/min, temp 98.5 ° F. Fetal heart tones at baseline were in the 140s with moderate variability. Her conjunctiva were anicteric, mucous membranes were moist, skin was without eruptions, xanthomas, or ecchymosis. The abdominal exam revealed exquisite rebound tenderness with voluntary guarding mostly in the right lower quadrant and epigastric region. Lab specimens were lipemic and reveled a WBC of 21.5k and hct of 29.7. The renal and liver function tests were within normal limits. Lipid studies revealed a t. cholesterol of 1,165, HDL of 90, triglyceride of 13,357, lipase of 1,420, and amylase of 635. An abdominal CT demonstrated findings consistent with acute pancreatitis. Abdominal ultrasound was negative for cholelithiasis. On day two of admission the patient underwent emergent low transverse C-section. A viable 2,265 gram female infant was delivered. Ultrasound guided diagnostic and therapeutic paracentesis was done on day three and seven both of which were negative for SBP. She was treated with lasix and aldactone in addition to IV fluids, morphine pca, Omega 3, and Tricor. The hospital course was a total of 19 days and she was eventually discharged with a triglyceride level of 350. The most common cause of pancreatitis in pregnancy is cholecystitis followed by ETOH abuse, viral infection, and HLD accounting for only a small amount of the cases (1). Hypertriglyceridemia can be aggravated by pregnancy as increased levels of estrogen increases liver synthesis of triglyceride and VLDL-C (3). Pregnancy can also cause a secondary deficiency of lipoproteins, an enzyme that is needed for the removal of triglycerides from plasma (4). Authorities in the radiology community suggest ultrasound or MRI over abdominal CT, especially in the first trimester, but consult a radiologist when indicated (2). This case lends learning opportunities on the imaging studies which are recommended for pregnant women as well as a less common cause of pancreatitis during pregnancy.
Purpose: To evaluate the spectrum of Clostridium difficile associated diarrhea (CDAD) in African American (AA) patients. Methods: A retrospective age and sex adjusted case control study was performed after selecting cases of CDAD over a period of 11 years (1993–2003). Enzyme immunoassay (EIA) test to detect toxins A and B was used. Patient records, imaging studies and laboratory tests were retrospectively analyzed. Statistical analysis was performed by using T test for continuous variables and Chi square test for categorical variables. Results: A total of 301 cases of CDAD were identified over a period of 11 years. From these 301 cases, 54 records were reviewed and were compared with 47 age, sex and time of admission adjusted controls. All patients were African American. The mean age in those with CDAD was 58 whereas in the control group was 51. This age difference was statistically significant. Males comprised 65% of cases and 62% of controls. The number of cases increased by 24% from the first 6 years of study period (1994–1998) to the second half of the review period (1999–2003). HIV positive status was found in 24% of CDAD cases and 15% of controls. Patients who had CDAD were more likely to have tachycardia, leukocytosis, anemia, elevated BUN, low albumin and were older when compared to controls (Table 1). As expected there was an increased risk of CDAD in our hospital associated with antibiotic exposure (Odds ratio of 10.22, 95% CI 4.07–25.6). Flouroquinolone and cephalosporin use were found to be a major predictors of CDAD (OR 3.4 CI 1.02–11.3 and OR 25 CI 3.18–196 respectively). Toxic megacolon was not seen in our study patients.Table 1: Laboratory ValuesConclusions: Frequency of patients with CDAD continues to increase at a rapid phase. Continuous evaluation needs to be performed to single out high risk antibiotics. African American patients have similar risk factors to other racial groups. Whether this is due to increase use of antibiotics, better diagnosis, lack of infection control methods or increasing morbidity of patients needs to be studied further.
Introduction: Median arcuate ligament syndrome (MALS) is a controversial entity associated with postprandial epigastric pain, nausea, vomiting, and weight loss. It is due to external compression by the median arcuate ligament (MAL) on the celiac artery. Case Description: A 23 year old female military recruit presented with a 1 year history of severe abdominal pain, nausea, vomiting, and loose stools. Pain varied in intensity, worsened with food and exercise, and interfered with lifestyle and career. Studies by several physicians over one year including comprehensive metabolic panel, lipase, stool studies, ultrasound, CT scan, EGD, colonoscopy, and gastric emptying study were normal. Hepatobiliary iminodiacetic acid (HIDA) scan revealed an ejection fraction of 26%. A subsequent cholecystectomy failed to relieve symptoms and a functional GI disorder was considered. Medical regimens including anti-spasmotics, anti-depressants, narcotics, and a rectal sheath nerve block failed to improve symptoms. A magnetic resonance angiogram (MRA) revealed stenosis at the origin of the celiac artery suggesting MALS. Following group consensus, she underwent laparoscopic arcuate ligament release. Successful release of the MAL was confirmed with intra-operative doppler ultrasound. At 4 and 8 week follow-up, she remained asymptomatic. Discussion: MALS should be considered in patients with chronic abdominal pain, negative work-up, and failure to respond to medical therapy. The MAL is a fibrous band of tissue made up of the right and left crus of the diaphragm. It crosses superiorly to the celiac axis and in the case of low insertion or high celiac axis takeoff, has been thought to cause external compression of the celiac axis producing ischemia-related pain. Physical exam may reveal a mid-epigastric bruit which increases with inspiration. Diagnosis is generally obtained with angiography or duplex ultrasound. Surgical treatment is considered based upon certain clinical and radiographic findings. It involves surgical decompression of the celiac axis by division of the arcuate fibers surrounding the artery. Endovascular techniques (stenting, etc.) may be required when chronic external compression has damaged the intimal layers of the vessel.Figure: MRA of the abdomen revealing stenosis of the celiac artery.
