Abdominal pain

The patient is a 55-year old Caucasian man who presented to an outside hospital with a chief complaint of abdominal pain and was admitted with acute pancreatitis. Abdominal ultrasound on admission only showed gallbladder sludge with no evidence of cholelithiasis. Serum triglycerides were 268. Three days later he was transferred to The Johns Hopkins Hospital for management of severe pancreatitis complicated by systemic inflammatory response syndrome, respiratory failure, and acute renal failure. This is the patient’s first episode of pancreatitis, and he was reportedly active and in relatively good health prior to this episode. His past medical history is significant for the diagnosis of primary hyperparathyroidism, and he is status post single-gland parathyroidectomy for parathyroid adenoma. He also has a history of hypertension, hypertriglyceridemia and depression. The patient denies alcohol use.

Primary hyperparathyroidism with parathyroid adenoma, status post resection
Hypertension
Hypertriglyceridemia
Hyperlipidemia
Basal cell carcinoma (remote)
Depression
Status post right inguinal hernia (1987)
Status post left mastoidectomy

The patient's family history is unremarkable.

The patient was working full time as an optician prior to his illness. He lives with his wife, and has a daughter and son. He does not consume alcohol, smoke or take illicit drugs.

Wellbutrin, 100 mg q8h

No known drug allergies.

Severe, continuous abdominal pain; fever; respiratory distress

Weight: 143 lbs. Height: 69 inches. T: 102.2 BP: 110/60 P: 100
General: Caucasian male, intubated
HEENT: Sclera anicteric. Extraocular movements intact.
CV: Regular rate and rhythm with no murmurs appreciated.
Lungs: Clear to auscultation bilaterally. No wheezes, rales or rhonchi.
Abdomen: Diffuse tenderness to palpation. Hypoactive bowel sounds
Lymph Node Exam: No lymphadenopathy appreciated.
Extremities: No cyanosis, clubbing, or edema.

Na 145; K 3.8 ; Cl 119 ; BUN 87 ; Glucose 167; Cre 5.7; Ca 6.6; Tot protein 4.0; Albumin 2.4; TBili 0.6; ALT 78; AST 102; Alk Phos 45; CO2 16; WBC 13740;Hct 34.4 Plt 128, 000;
PT 10.4
Ionized calcium 1.09 Lipase 250; Amylase 867
pH, arterial 7.29; pCO2, arterial 37; pO2, arterial 103
Bacterial culture, blood: No growth

Initial CT studies noted bilateral pleural effusions with associated compressive atelectasis and/or infiltrates. Marked edema and stranding were seen in the pancreatic bed, compatible with fulminant pancreatitis. Several indeterminate adrenal nodules were present bilaterally, and a stable, non-obstructing 1.5 cm stone was identified in the left kidney.

The patient was in respiratory failure and acute renal failure when he arrived and was admitted to the MICU. Imaging and laboratory tests were consistent with acute pancreatitis. He demonstrated a period of initial improvement and was eventually extubated, but two weeks after admission developed a high fever and acute respiratory decompensation. Repeat CT imaging revealed a pulmonary embolus in his main right pulmonary artery and pancreatic necrosis. Cultures of peripancreatic fluid grew Candida albicans, and the patient underwent three operations for pancreatic debridement. A cholecystectomy, gastojejunostomy tube placement, and inferior vena cava filter placement were also performed. Additional complications during his admission included Pseudomonas aeruginosa-positive sputum cultures and critical illness neuropathy/myopathy.

Prior to transfer to a rehabilitation facility, an endocrine consultation was obtained for hypercalcemia. Review of calcium levels revealed hypocalcemia in 6.6- 6.8 mg/dL range on presentation to JHH. However, as patient’s condition improved, calcium elevation in 10.7-12.1 mg/dL was noted persistently. Serum albumin during that time ranged between 1.8 and 2.5 g/dl. An initial biochemical evaluation included PTH of 255 pg/mL concurrently with calcium of 10.2 mg/dL, PTHrp of <2.5 pmol/L, Phosphorus 2.7 mg/dL, 1,25 OH-Vitamin D 27 pg/mL, 25 OH-Vitamin D 10 ng/mL, TSH 3.62.

While in rehabilitation, he experienced a gastrointestinal bleed, and was admitted to an outside hospital. Endoscopy revealed ulceration in the duodenum and at the gastroesophageal junction. Pseudomonas aeruginosa and vancomycin-resistant enterococcus were identified in urine cultures. He subsequently developed intraabdominal sepsis with a peripancreatic abscess. The abscess was drained, also revealing multi-drug resistant Pseudomonas aeruginosa. He was re-admitted to The Johns Hopkins Hospital for further management. At admission he was hemodynamically stable and afebrile, but presented with elevated white blood cell count, liver enzymes, alkaline phosphatase and amylase. He was treated with antibiotics and with discussion of further surgical intervention. Three days after admission, the patient was found in cardiopulmonary arrest and resuscitation attempts were unsuccessful.

Image 1 : CT Scan of the abdomen demonstrating bilateral enhancing adrenal nodules which are indeterminate by CT criteria, possibly adenomas. Moderate peripancreatric inflammation compatible with pancreatitis.

Image 2 : CT Scan of the abdomen demonstrating bilateral enhancing adrenal nodules which are indeterminate by CT criteria, possibly adenomas. Moderate peripancreatric inflammation compatible with pancreatitis with large pseudocyst formation in the region of the pancreatic body and tail. Hypoenhancement of the pancreatic body suspicious for necrosis.

Image 3 : CT Scan of the abdomen demonstrating atrophic left kidney consistent with prior infarcts which contains a large calculus in the collecting system.

Image 4 : CT Scan of the chest demonstrating a filling defect within the right main and right lower lobe pulmonary arteries compatible with a pulmonary embolus. Also seen are bilateral pleural effusions with bilateral lung consolidations.

1. Could hypercalcemia explain his acute pancreatitis?
2. What is the most likely cause of his initial hypocalcemia?
3. What is the most likely cause of his hyperparathyroidism and what additional studies would help determine the most likely cause?
4. What additional evaluation for other endocrine abnormalities may be indicated?