Clinical and laboratory findings indicated numerous possible maladies. A CT scan eventually led to the correct diagnosis.
A 58-year-old truck driver presented to the clinic complaining of nausea and constant epigastric/right upper quadrant (RUQ) pain. The pain initially woke him in the middle of the night and continued for approximately 14 hours. The man tried taking simethicone (Mylanta), but his symptoms did not improve significantly. The last food he ate before feeling ill was a dinner of fast-food hamburgers and french fries.
The patient had no associated indigestion, jaundice, fever, vomiting, or change in bowel habits. A similar episode of abdominal pain six months earlier had been relieved with a GI cocktail consisting of phenobarbital/hyoscyamine/atropine/scopolamine (Donnatal), aluminum hydroxide/magnesium hydroxide (Maalox), and viscous lidocaine.
The man was obese and had type 2 diabetes and hyperlipidemia. Current medications included rosiglitazone (Avandamet) and rosuvastatin (Crestor). He reported no previous surgeries. The family history was positive for type 2 diabetes. He was married and did not use tobacco or drink alcoholic beverages.
The patient’s BP was 152/79 mm Hg, pulse 86 beats per minute, and temperature 98.4°F. Oxygen saturation on room air was 96%. He rated his epigastric pain at 8 on a 10-point scale. A head, eyes, ears, nose, and throat exam turned up nothing suspicious.
The man’s cardiovascular examination was normal, with a regular heart rate and rhythm. His lungs were clear on auscultation. The patient’s abdomen was mildly distended. Bowel sounds were heard, and an RUQ mass was tender to touch.
On examination, no hemorrhoids were found. The guaiac stool test was negative. There was no adenopathy detected in the neck, axilla, or inguinal region.
The patient’s skin was warm and dry and without rashes. We decided to investigate further.
Laboratory and CT findings
Laboratory evaluation revealed a WBC count of 11.4×103/µL, RBCs 4.05×106/µL, hemoglobin 12.6 g/dL, hematocrit 36%, platelets 167×103/µL, and mean corpuscular volume 89.0 fL.Urine was negative for leukocytes, protein, glucose, ketones, bilirubin, and blood; specific gravity was 1.025 and pH 7.0. Liver function tests revealed total bilirubin 0.9 mg/dL, direct bilirubin 0.2 mg/dL, indirect bilirubin 0.7 mg/dL, alkaline phosphatase 66 IU/L, aspartate aminotransferase 17 IU/L, alanine aminotransferase 21 IU/L, total protein 7.6 g/dL, and albumin 4.9 g/dL.A CT scan of the abdomen (Figure 1) showed the gallbladder measured 16 cm. Differential diagnoses included cholecystitis, gastroenteritis, hepatitis, pancreatitis, bowel obstruction, MI, peptic ulcer disease, and inflammatory bowel disease.
Gallbladder hydrops describes a gallbladder that is overdistended with mucoid or clear, watery contents >1,500 mL. The condition has been defined as gallbladder distension with an anteroposterior diameter >5 cm or enlargement >4×10 cm.1 This distension results from an outlet obstruction—commonly an impacted stone in the neck of the gallbladder or the cystic duct. Inflammation of the gallbladder can occur in the absence of gallstones.2 Other causes for hydrops include gallbladder polyps, malignancies of the liver or colon, prolonged total parenteral nutrition, congenital narrowing of the cystic duct, parasites, renal or pancreatic mass, or hepatomegaly.
Hydrops accounts for 3% of all pathologic gallbladders in adults.3 In children, hydrops has been reported with Kawasaki’s disease, strep pharyngitis, hepatitis, nephrotic syndrome, and mesenteric adenitis. The fluid buildup, seen in nearly all cases, is caused by long-standing obstruction. If distension continues to increase, gangrene or perforation may occur.
Clinical symptoms of gallbladder hydrops include RUQ/epigastric pain, nausea, and vomiting. Although less common, jaundice and fever may occur.Gallbladder hydrops can be diagnosed using ultrasound or CT scanning.
Magnetic resonance cholangiopancreatography may also be used to clearly visualize the biliary tree. Slight elevations in the WBC count are frequently seen, but liver enzymes are usually normal. Lipase/amylase are typically normal except with pancreatitis caused by an obstruction close to the ampulla of Vater.
Cholecystectomy is the definitive treatment for an obstructed gallbladder. Laparoscopic cholecystectomy is most commonly performed. However, open cholecystectomy may be the better option in patients whose gallbladders are very large or have greatly thickened walls.
Our patient underwent laparoscopic cholecystectomy. A large stone was discovered at the gallbladder neck. A cholangiogram of the cystic ducts showed normal filling of the biliary tree without evidence of other stones. Blood loss was minimal. He was discharged home and underwent an uneventful recovery. Ms. Meng is a primary-care/ER physician assistant at Kirby Hospital in Monticello, Ill.
1. Khothsymuong RR, Kaminski J. Gallbladder hydrops. J Diagn Med Sonography. 2004;20:256-259.
2. Shaffer EA. The biliary system. In: Thomson ABR, Shaffer EA, eds. First Principles of Gastroenterology. 3rd ed. Toronto, Ont.: Canadian Association of Gastroenterology; 1997:440-461.
3. Emedicine. Gallbladder mucocele. Available at www.emedicine.com/med/topic2817.htm. Accessed May 9, 2008.