Scott G. Houghton

Surgical Management of Amiodarone-associated Thyrotoxicosis: Mayo Clinic Experience

Amiodarone-associated thyrotoxicosis (AAT) is often poorly tolerated owing to underlying cardiac disease, and it is frequently refractory to conventional medical treatment. The goal of this study was to describe the patient characteristics, management, and outcomes of all the patients treated surgically for AAT at a single institution. We conducted a retrospective chart review of all patients managed surgically for AAT (April 1985 through November 2002) at the Mayo Clinic in Rochester, Minnesota. Altogether, 29 men and 5 women, ages 39 to 85 years (median 60 years), treated with amiodarone for 3 to 108 months underwent near-total or total thyroidectomy. Frequent symptoms were worsening heart failure, fatigue, weight loss, and tremor. Altogether, 12 patients failed medical management of their AAT, and 21 received no preoperative medical therapy. One patient had been successfully managed medically but required definitive treatment. Common indications for operation were the need to remain on amiodarone, cardiac decompensation, medically refractory disease, and severe symptoms, both hyperthyroid and cardiac, necessitating prompt resolution. The median ± SD American Society of Anesthesiologists (ASA) classification (1 = healthy through 5 = moribund) was 3.00 ± 0.58. A total of 27 specimens had histology consistent with AAT. Complications included death (n = 3), rehospitalization (n = 3), symptomatic hypocalcemia (n = 2), pneumonia (n = 2), cervical hematoma (n = 1), prolonged ventilatory wean (n = 1), and stroke (n = 1); one patient developed hypotension, adult respiratory distress syndrome, and sepsis. Of the 31 surviving patients, 25 (80%) remained on amiodarone postoperatively. The median follow-up was 29 months, at which time all surviving patients were free of hyperthyroid symptoms. Thyroidectomy is an effective treatment for AAT but has a high incidence of perioperative morbidity and mortality. The cardiovascular co-morbidities and high operative risk in this group of patients may account for the increased complication rate.

Expression and function of intestinal hexose transporters after small intestinal denervation

BACKGROUND The role of neural regulation in expression and function of intestinal hexose transporters is unknown. The aim of this study is to determine the role of intestinal innervation in gene expression and function of the membrane hexose transporters, SGLT1, GLUT2, and GLUT5 in the enterocyte. We hypothesize that denervation of the small intestine decreases expression of hexose transporters, which leads to decreased glucose absorption. METHODS Six groups of Lewis rats were studied (n = 6 each) as follows: control, 1 week after sham laparotomy, 1 and 8 weeks after syngeneic (no immune rejection) orthotopic small-bowel transplantation (SBT) (SBT1 and SBT8) to induce complete extrinsic denervation, and 1 and 8 weeks after selective disruption of intrinsic neural continuity to jejunoileum by gut transection and reanastomosis (T/A1 and T/A8). All tissue was harvested between 8 AM and 10 AM. In duodenum, jejunum, and ileum, mucosal messenger RNA (mRNA) levels were quantitated by real-time polymerase chain reaction (PCR), protein by Western blotting, and transporter-mediated glucose absorption using the everted sleeve technique. RESULTS Across the 6 groups, the relative gene expression of hexose transporter mRNA and protein levels were unchanged, and no difference in transporter-mediated glucose uptake was evident in any region. The glucose transporter affinity (K(m)) and functional transporter levels (V(max)) calculated for duodenum and jejunum showed no difference among the 6 groups. CONCLUSION Baseline regulation of hexose transporter function is not mediated tonically by intrinsic or extrinsic neural continuity to the jejunoileum.

Combined Transabdominal Gastroplasty and Fundoplication for Shortened Esophagus : Impact on Reflux-Related and Overall Quality of Life

BACKGROUND Transabdominal gastroplasty for shortened esophagus at the time of fundoplication results in a segment of aperistaltic, acid-secreting neoesophagus above the fundoplication. We hypothesized that transabdominal gastroplasty impairs quality of life (QOL). METHODS This was a matched paired analysis with retrospective chart review and follow-up questionnaire of 116 patients undergoing transabdominal fundoplication with gastroplasty with 116 matched controls undergoing transabdominal fundoplication alone from January 1997 to June 2005. Medical Outcomes Study Short-Form 36-Item Health Survey (SF-36) and Quality Of Life in Reflux And Dyspepsia (QOLRAD) instruments were used to measure overall and reflux-related QOL. Overall response rate was 75%; including 65 matched pairs used for long-term follow-up and QOL analysis. RESULTS Groups were similar in age, sex, duration of hospitalization, and complications (p > 0.05). Gastroplasty patients had larger hiatal hernias and were more likely to have undergone a previous fundoplication (p < 0.01). No perioperative deaths or major morbidity occurred in 18% of both groups. Survey respondents were older than nonrespondents (p < 0.01). Complications did not impact response rates (p = 0.11). Median follow-up was 14 months in the gastroplasty group and 17 months in controls (p = 0.02). The groups had similar scores on the SF-36 and QOLRAD (p > 0.05) and similar overall frequency of patient satisfaction, perceived health status, and self-reported symptoms of reflux, dysphagia, bloating, diarrhea, and excessive flatus (p > 0.05). Control patients were more likely to require rehospitalization or reinterventions (p = 0.04). CONCLUSIONS Transabdominal gastroplasty and fundoplication for shortened esophagus is safe and results in similar overall and reflux-related QOL compared with fundoplication alone.

Postprandial Augmentation of Absorption of Water and Electrolytes in Jejunum Is Neurally Modulated: Implications for Segmental Small Bowel Transplantation

Postprandial augmentation of absorption of water and electrolytes is believed to occur in the jejunum. Neural mechanisms of control, however, have not been studied in the in situ jejunum or in the transplanted bowel. The aim of this study was to determine if postprandial augmentation of absorption occurs in the in situ jejunum and to evaluate neural mechanisms controlling postprandial jejunal absorption. Based on our previous work, we hypothesized that postprandial augmentation of absorption does not occur in the jejunum in situ and that extrinsic denervation of the jejunum is associated with decreased postprandial absorption. Absorption was studied in an 80 cm, in situ jejunal segment in six dogs by using an isosmolar electrolyte solution alone, or with 80 mmol/L glucose before and after jejunal transection to disrupt intrinsic neural continuity of the study segment with the remaining gut. Net absorptive fluxes of water and electrolytes were measured in the fasted state and after a 400-kcal meal. Another six dogs were studied 3 weeks after our validated model of extrinsic denervation of jejunoileum; identical fasting and postprandial absorptive states were evaluated. Postprandial augmentation of absorption of water and electrolytes did occur in the jejunum (P<0.03) both in the absence and in the presence of intraluminal glucose. After intrinsic neural transection or extrinsic denervation, no postprandial augmentation of absorption occurred, with or without glucose. Postprandial augmentation of absorption of water and electrolytes occurs in the in situ jejunum. Disrupting intrinsic neural continuity or extrinsic denervation (as after intestinal transplantation) abolishes postprandial augmentation.