Case Reports  |   March 2002
High Gastric Output as a Perioperative Sign of Carcinoid Syndrome
Author Affiliations & Notes
  • Pratik P. Pandharipande, M.D.
  • Peter S. Reichard, M.D.
  • Michael F. Vallee, D.O.
  • * Instructor in Anesthesiology, Vanderbilt University, Nashville, Tennessee.† Assistant Attending, ‡ Attending.
  • Received from the Department of Anesthesia, Saint Barnabas Medical Center, Livingston, New Jersey.
Article Information
Case Reports
Case Reports   |   March 2002
High Gastric Output as a Perioperative Sign of Carcinoid Syndrome
Anesthesiology 3 2002, Vol.96, 755-756. doi:
Anesthesiology 3 2002, Vol.96, 755-756. doi:
CARCINOID syndrome, although rare, may present dramatically secondary to the physiologic effects of the mediators carcinoid tumors secrete. Despite improvement in the tools for detection and treatment, carcinoid syndrome may still pose a diagnostic dilemma for the anesthesiologist.
Case Report
A 47-yr-old man with a history of persistent abdominal pain presented for elective resection of an ileal mass. The patient had no significant medical history and underwent small bowel resection for the ileal mass. At the time of surgery, nodules were noted on the omentum and the liver. His intraoperative course was uneventful. Pathologic examination of the specimens revealed metastatic adenocarcinoma of carcinoid origin with the primary in the ileum.
Postoperatively, the patient had 3–5 l/day of secretions via  his nasogastric tube, with minimal bowel activity. Abdominal films were consistent with a postoperative ileus or a small bowel obstruction. In view of these findings, the surgeon decided to reexplore the patient's abdomen on the seventh postoperative day.
During abdominal reexploration, a defasciculating dose of d-tubocurare was given before a rapid-sequence induction with succinylcholine. Anesthesia was maintained using 50% oxygen, 50% air, desflurane, and fentanyl. Although no signs of peritonitis or small bowel obstruction were noted, the surgeon revised the small bowel anastomosis. The patient remained hemodynamically stable throughout the procedure. Twenty milligrams morphine was gradually titrated, and the patient underwent extubation while awake and was brought to the recovery room.
In the recovery room, the patient was alert and oriented. During the next 45 min, the patient became agitated and combative, requiring 2 mg lorazepam and 2 mg midazolam intravenously. The complete blood count and electrolytes were within normal limits. Arterial blood gas showed a pH of 7.42, an arterial carbon dioxide tension (Paco2) of 33, and an arterial oxygen tension (Pao2) of 97 on 4 l oxygen. The patient was sedated through the night using a propofol (25–50 μg · kg−1· min−1) and lorazepam (1 mg/h) drip.
On the first postoperative day, the patient remained agitated despite having normal complete blood count, arterial blood gas, electrolytes, and computed axial tomography scan of the head. However, his blood glucose concentration was 295 mg/dl. During the course of the day, the patient became hypoxic (Pao2= 55 mmHg on 100% oxygen) and underwent reintubation and sedation. A ventilation/perfusion scan was read as low probability for a pulmonary embolus. The chest radiograph revealed bibasilar atelectasis and a right lower lobe infiltrate, and antibiotics were administered. More than 2 l gastric secretions continued to be suctioned from his nasogastric tube every 8 h.
Random urine 5 hydroxyindoleacetic acid (5HIAA), thyroid-stimulating hormone, T3, T4, and cortisol concentrations were taken on postoperative day 2. A presumptive diagnosis of carcinoid syndrome was made, and administration of octreotide, 50 μg subcutaneously every 8 h, was started. During the next several hours, nasogastric tube output decreased to approximately 0.4 l per each 8-h shift. The patient also became more alert and oriented.
The patient continued to show significant improvement and successfully underwent extubation on postoperative day 3. The hyperglycemia had resolved. The random 5HIAA concentration taken the previous day was 9.2 mg/l (normal value 0–6 mg per 24 h). All other hormonal concentrations were normal. The patient was alert and oriented, and nasogastric tube output was minimal. The patient was discharged home on the sixth postoperative day after abdominal reexploration.
Carcinoid tumors are tumors of amine precursor cells identified by silver staining of cytoplasmic granules within the cells. 1 These neoplasms tend to be found in a bimodal distribution occurring in patients between the third to fifth decade of life and then again after the age of 60 yr. Carcinoid tumors have an incidence of 1–10 per 100,000, with equal numbers among men and women. More than 75% of tumors originate in the gastrointestinal tract, with the highest incidence in the small bowel, followed by the appendix. The most commonly affected nongastrointestinal organ is the lung. 2 
Carcinoid syndrome is a constellation of signs and symptoms resulting from the direct release of bioactive substances into the circulation. Amines and peptides that have been implicated are serotonin, kinin peptide, gastrin, histamine, substance P, insulin, glucagon, prostaglandins, and bradykinins. 3 Calcitonin gene–related peptide, vasoactive intestinal peptide (VIP), and neurotensin are vasodilatory peptides synthesized by some carcinoid tumors. 3 Symptoms are generally caused by stress, strenuous physical activity, and tumor manipulation, as well histamine-releasing drugs, such as morphine and d-tubocurare. Most of these patients do not present with symptoms of the carcinoid syndrome because the liver metabolizes the active peptides.
Clinical manifestations include flushing (95%), diarrhea, nausea, vomiting, abdominal pain, autonomic instability, hyperglycemia, bronchospasm, and dermatosis. A prolonged time for recovery from anesthesia has also been seen in patients with high serum serotonin concentrations. 1 Mental status changes have infrequently been reported as symptoms seen in carcinoid syndrome. 4 
The syndrome is diagnosed with a 24-h urinary 5HIAA, which is a metabolic product of serotonin. However, 20% of patients with carcinoid syndrome may have a normal urinary 5HIAA concentration. 1 Diagnosis can be further confirmed by the finding of neuroendocrine cells with argyrophilic properties on pathology.
The gold standard in treating carcinoid syndrome is somatostatin or its synthetic analog, octreotide. 5 Somatostatin receptors, mostly subtype 2, have been found in many carcinoid tumors. This peptide has been shown to be responsible for reducing the production and release of gastropancreatic hormones. VIP release from VIPomas is normalized or significantly improved in 75% of patients. 6 
This case presented a dilemma because no perioperative diagnosis was made for the patient's high gastric output and mental status changes. The patient had definite carcinoid tumor confirmed by pathology. This tumor was found to produce serotonin, gastrin, and VIP. Random urinary 5HIAA concentration was increased compared with the lab reference for a 24-h urine 5HIAA concentration, which suggested the presence of carcinoid syndrome. Unfortunately, only this random urine 5HIAA concentration was obtained, and not a 24-h concentration.
No cases of perioperatively high gastric secretions associated with carcinoid syndrome have been reported in the literature, although diarrhea is a well-documented symptom of carcinoid syndrome. Stimulation of 5-hydroxytryptamine (5-HT) receptors has been shown to increase gastric secretions. 7 Serotonin also interacts with thyrotropin-releasing hormone to augment thyrotropin-releasing hormone–induced stimulation of gastric secretions. 8 The patient's increased glucose is also consistent with glucose intolerance seen with overproduction of VIP or serotonin. 9 The increased gastric secretions could also be due to a direct action of histamine or gastrin, both of which have been reported as substances released by carcinoid tumors.
Alteration in mental status, though infrequent with carcinoid tumors, has been shown to be associated with serotonin syndrome (hyperseratonergic state). 10 This is seen in patients receiving selective 5-HT blockers. An increase in drug-induced intrasynaptic 5-HT results in hyperstimulation of the 5-HT1Areceptor in the brain and spinal cord, causing altered mentation. A similar mechanism is possible for the mental status changes seen in this patient. Although we cannot be certain the improvement in mental status in this patient was definitively related to the administration of octreotide, his mental status and gastric output decrease occurred concurrently with the administration of octreotide.
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