Answers 1, 2 and 5 are appropriate treatments for dumping syndrome or postgastrectomy, but the question is focused on initial management, so the most appropriate answer seems to be 2.

Answers 1, 2 and 5 are appropriate treatments for dumping syndrome or postgastrectomy, but the question is focused on initial management, so the most appropriate answer seems to be [HIDDEN].

A 45-year-old man undergoes a truncal vagotomy and antrectomy with Billroth II reconstruction for chronic peptic ulcer disease with pyloro-duodenal stricture. Six weeks after the surgery she reports that shortly after (less than half an hour) after ingestions she presents nausea, asthenia and sweating, dizziness and abdominal cramps usually accompanied by diarrhea. Which of the following is the most appropriate approach for her initial management?

Apply treatment with a somatostatin inhibitor (octreotide).

Search for a probable neuroendocrine tumor (e.g. carcinoid).

Indicate surgical treatment to perform an antiperistaltic Roux-en-Y gastrojejunostomy.

[Peptic ulcer: late complications of the surgical treatment].

The incidence of surgical treatment of peptic ulcer decreased in the last two decades. The majority of procedures for surgical management of peptic disease impairs the ability of the stomach to receive and to store food. The intake of high protein-caloric content diets can improve some nutritional deficits expressed by loss of body weight and anemia. The mechanism responsible for diarrhea is unknown, but truncal vagotomy has the highest incidence. It is usually episodic, lessens over the first year after operation and rarely remains a severe problem. The decreasing levels of colecistokinin response after meal in gastrectomy and the division of hepatic branch of anterior vagus can cause gallbladder sludge and stone formation. Alkaline reflux explains gastritis and esophagitis after partial gastric resection. Surgical duodenal diversion, like a Roux-en-Y limb, have been successful in its control. The mechanism that leads to the dumping syndrome are loss of gastric reservoir function and rapid emptying of hyperosmolar meals into small intestine. Somatostatin analogues improve the symptoms caused by abnormal release of neurohormonal agents responsible of the behaviour of the gastrointestinal tract after meals. Cancer of gastric remanent may be due to increased bacterial overgrowth and nitrosation formation. The endoscopic follow-up is essential for early diagnosis of the stump cancer. In spite of all complications, the surgeon cannot have hesitations by carrying out radical approach meanly during catastrophic emergencies of peptic disease i.e. in elderly aged patients. Nowadays, the control of chronic sequelas is easy with conservative therapeutic.

Diagnosis and treatment of gastrinoma in the era of proton pump inhibitors.

The Zollinger-Ellison syndrome is characterized pathophysiologically by a significant hypergastrinemia derived from a gastrin-secreting neuroendocrine tumor with a primary location in the pancreas or duodenum. Chronic hypergastrinemia in turn triggers gastric acid hypersecretion yielding in chronic or recurrent or refractory peptic ulcer disease and/or chronic diarrhea. One half of patients with ZES will have distant metastases in the liver by the time the diagnosis is established and one half of all patients with ZES will experience chronic diarrhea as chief complaint rather than peptic ulcer-related symptoms and signs. Gastrinomas have been reported to either manifest sporadically or to occur in conjunction with the genetic background of the MEN-I syndrome. Diagnosis is based on the patients history which is typically characterized by recurrent episodes of peptic ulcer disease or by severe reflux esophagitis and/or diarrhea or by acid-related symptoms which fail to respond to standard treatment regimens. Upper gastrointestinal tract endoscopy will provide evidence for peptic ulcer disease in anatomical regions located aborally the duodenal bulb within the descending part of the duodenum or even farther distally within the jejunum. Peptic ulcers frequently occur in groups indicating some substantial acid hypersecretion. A gastric pH > 2 is mutually exclusive for ZES. Increased serum gastrin levels confirm the diagnosis biochemically. Gastrin secretion can be determined in the basal state or following stimulation with secretin or calcium. High sensitivity and specificity for the diagnosis of ZES is provided by determining the ratio of basal versus pentagastrin-stimulated gastric acid secretion: The ratio of BAO / MAO > 0.6 is highly specific for gastrinoma. To localize the gastrin-secreting tumor computer-assisted tomography, endoscopic ultrasound, and somatostatin receptor scintigraphy provide useful help but most recently, endoscopic ultrasound with high resolution transducers appear to improve preoperative site localization. If modern imaging techniques fail to elucidate the site of the tumor, intraoperative diaphany may help to detect gastrinomas within the duodenal wall. Definitive treatment will only be achieved by total surgical resection of the gastrin-producing tumor in the pancreas or duodenum including dissection of the regional lymph nodes. Control of symptoms will have to be achieved by administration of highly potent proton pump inhibitors in up to 2-3-fold increased standard doses to inhibit gastric acid hypersecretion. Elevation of gastric pH > 4 will be the therapeutic target to protect the mucosa of the upper gastrointestinal tract. Basal acid output should be reduced to less than 10 mEq H(+) per hour which requires administration of highly potent proton pump inhibitors with a recommended starting dose of 60 mg omeprazole equivalents per day.

Octreotide improves early dumping syndrome potentially through incretins: a case report.

Dumping syndrome, or rapid gastric emptying, is a frequent complication after gastric surgery. In this case, the patient was a 47-year-old woman who 10 years previously had undergone distal gastrectomy with Billroth I reconstruction for early-stage gastric cancer. She presented with symptoms of weakness, headache, palpitation, sweating, dizziness and significant fatigue between one and two hours after a meal. Because a 75 g oral glucose tolerance test (75 g-OGTT) induced both acute postprandial tachycardia (within 1 hour) and postprandial hypoglycemia, we diagnosed this patient with early and late dumping syndrome. Dietary measures and acarbose improved symptoms of late dumping syndrome but did not prevent the symptoms of early dumping syndrome such as postprandial tachycardia, weakness, headache, palpitation, and dizziness. We therefore used the somatostatin analogue octreotide, which has been reported as an effective therapy for early dumping syndrome. Octreotide prevented the symptoms of early dumping syndrome, especially postprandial tachycardia, but caused postprandial hyperglycemia. Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) were completely suppressed during the 75 g-OGTT following subcutaneous injection of octreotide. No change was observed in vasoactive intestinal polypeptide (VIP), which is the gastrointestinal peptide hormone generally responsible for early dumping syndrome, suggesting possible contribution of incretins in early dumping syndrome of this patient.

Post-vagotomy diarrhea

Post-vagotomy diarrhea is a form of diarrhea which occurs in 10% of people after a truncal vagotomy, which can range from severe to debilitating in approximately 2% to 4% of patients. However, the occurrence of post-vagotomy diarrhea is significantly reduced after proximal selective vagotomy, specifically when celiac and hepatic branches of the vagus are retained. Diagnosis Treatment Surgical treatment for refractory post-vagotomy diarrhea is rarely needed and at least one year from the occurrence of symptoms should be allotted to ensure all non-surgical treatments have been appropriately explored. Under severe cases, where surgical intervention does become necessary, a 10 cm reverse jejunal interposition is usually the procedure of choice. References Neurosurgery Diarrhea

Gastric outlet obstruction

Treatment Treatment of gastric outlet obstruction depends on the cause, but is usually either surgical or medical. Medication In most people with peptic ulcer disease, the oedema will usually settle with conservative management with nasogastric suction, replacement of fluids and electrolytes and proton pump inhibitors. Surgery Surgery is indicated in cases of gastric outlet obstruction in which there is significant obstruction and in cases where medical therapy has failed. Endoscopic balloon therapy may be attempted as an alternative to surgery, with balloon dilation reporting success rates of 76% after repeat dilatons. The operation usually performed is an antrectomy, the removal of the antral portion of the stomach. Other surgical approaches include: vagotomy, the severing of the vagus nerve, the Billroth I, a procedure which involves anastomosing the duodenum to the distal stomach, or a bilateral truncal vagotomy with gastrojejunostomy. References External links

Treatment of severe postvagotomy/postgastrectomy symptoms with the somatostatin analogue octreotide.

Fourteen patients with severe and persistent postvagotomy/postgastrectomy symptoms were entered into a trial of treatment with the somatostatin analogue octreotide, 50 micrograms twice daily 30 min before meals being self-administered by subcutaneous injection. Six of the seven patients completing the 3-month trial showed sustained overall improvement of symptoms. The remaining patients were unhelped by treatment or developed unwanted effects. Six of eight patients with dumping syndrome showed sustained improvement of dumping symptoms during treatment. Bile vomiting was relieved in three of four patients with this complaint. Diarrhoea accompanying dumping showed a variable response to treatment, with improvement in three patients and no change or worsening of this symptom in five. Two patients with severe postvagotomy diarrhoea alone showed no improvement. Four patients with unwanted effects and three patients who found no benefit stopped the trial medication early. Four further patients reported mild or transient side-effects. For patients with severe postvagotomy/postgastrectomy symptoms, a trial of octreotide seems justified when significant dumping symptoms are present and other treatment options have been exhausted.

Vagotomy

All types of vagotomy can be performed at open surgery (laparotomy) or using minimally invasive surgery (laparoscopy). For the management of PUD, vagotomy is sometimes combined with antrectomy (removal of the distal half of the stomach) to reduce the rate of recurrence. Reconstruction is performed with gastroduodenostomy (Billroth I) or gastrojejunostomy (Billroth II). It is left intact in highly selective vagotomy so the function of gastric emptying remains intact. Applications Truncal vagotomy is a treatment option for chronic duodenal ulcers. It was once considered the gold standard, but is now usually reserved for patients who have failed the first-line "triple therapy" against Helicobacter pylori infection: two antibiotics (clarithromycin and amoxicillin or metronidazole) and a proton pump inhibitor (e.g., omeprazole). It is also used in the treatment of gastric outlet obstruction.

[Diarrhoea, nausea and vomiting].

We saw a 54-year-old patient who had been treated for gastrointestinal ulcerations with bleeding complications now presenting with nausea, vomiting and diarrhoea. The patient has been suffering from recurrent diarrhea for years. The suspicion of a neuroendocrine tumor had been made but could not be confirmed intraoperatively in the past. As suspicion was still high with high levels of chromogranin A and high gastrin levels the diagnosis now could be confirmed with a somatostatin scintigraphy. Finally the confirmed spot was identified to be a metastasis of a gastrinoma of still unknown primary localisation.

Early and late results after antrectomy, selective vagotomy and Roux-en-Y reconstruction for severe peptic ulcer disease.

The Roux-en-Y gastrojejunostomy has become an increasingly used method for gastrointestinal tract reconstruction, and is advocated in the treatment of alkaline reflux gastritis. Since 1979 we have used selective vagotomy, antrectomy and Roux-en-Y reconstruction as the primary method in treating gastric ulcer and complicated duodenal ulcer in 25 patients. In a follow-up study we have evaluated the postoperative course and the long term results. All patients were operated on between 1979 and 1984. Nine patients had a gastric ulcer (GU), 11 a prepyloric ulcer (PPU) and 5 patients had a complicated duodenal ulcer (DU). The clinical results showed a grade Visick I in 48%, Visick II in 44%, Visick III in 4% and a grade Visick IV in 4%. There were no postoperative deaths, but other early complications occurred in 9 patients (36%). At follow-up, endoscopy showed signs of delayed emptying in 5 patients, but only 1 had corresponding symptoms. Mild to moderate symptoms of dumping were found in 1 patient. There was no case of severe diarrhea. The overall results were satisfactory, indicating that selective vagotomy and antrectomy with Roux-en-Y reconstruction is a valuable alternative as a primary method in the surgical treatment of severe peptic ulcer disease.

[Endosonographic demonstration of extrapancreatic and extraintestinal gastrinoma].

No cause had been found for chronic diarrhoea in a 57-year-old man. Up to 15 watery stools daily had been without relation to food intake and without blood admixture. But muscular cramps had developed, especially in the legs. The patient had a history of recurrent peptic ulcers for which a selective proximal vagotomy had been performed 13 years ago. Physical examination was unremarkable. Alkaline phosphatase activity (182 U/l) and C-reactive protein (9.3 mg/l) were slightly raised; serum iron was 42 micrograms/dl, while all other routine laboratory tests, including protein electrophoresis, blood picture and differential count were within normal limits. Gastroscopy revealed ulcerative duodenitis, gastritis with erosions and numerous ulcers and reflux oesophagitis, grade III-IV. Endosonography showed enlarged gastric mucosal relief as sign of foveolar hyperplasia and a ca. 4 x 3 cm tumour next to the duodenal bulb. Gastrin level was 7537 pg/ml (normal < 150 pg/ml). Computed tomography and somatostatin receptor scintigraphy confirmed the site and size of the gastrinoma. Treatment with omeprazole (40 mg three times daily) slightly improved the symptoms. The tumour was excised a week after diagnosis. The patient has been symptom-free since then. Chronic diarrhoea of unknown aetiology can be caused by an endocrine tumour; endosonography can often provide information on the diagnosis and location of such a tumour.

Carcinoid

Cause Carcinoid syndrome involves multiple tumors in one out of five males. The incidence of gastric carcinoids is increased in achlorhydria, Hashimoto's thyroiditis, and pernicious anemia. Treatment Surgery, if feasible, is the only curative therapy. If the tumor has metastasized (most commonly, to the liver) and is considered incurable, there are some promising treatment modalities, such as radiolabeled octreotide (e.g. Lutetium (177Lu) DOTA-octreotate) or the radiopharmaceutical 131I-mIBG (meta iodo benzyl guanidine) for arresting the growth of the tumors and prolonging survival in patients with liver metastases, though these are currently experimental. Chemotherapy is of little benefit and is generally not indicated. Octreotide or lanreotide (somatostatin analogues) may decrease the secretory activity of the carcinoid, and may also have an anti-proliferative effect. Interferon treatment is also effective, and usually combined with somatostatin analogues.

Experience with vagotomy--antrectomy and Roux-en-Y gastrojejunostomy in surgical treatment of duodenal, gastric, and stomal ulcers.

Gastroduodenostomy (Billroth I) is our reconstruction of choice following gastric resection for gastroduodenal ulcer. Dissatisfaction with a Billroth II anastomosis has led us in recent years to employ a Roux-en-Y diversion in selected cases, particularly those in which the pathologic state of the pyloroduodenal canal would render a Billroth I anastomosis unsafe. During the past 7 years, truncal vagotomy-antrectomy and Roux-en-Y (VARY) has been carried out in 50 selected patients: duodenal ulcer (DU) 13 patients, gastric ulcer (GU) 11 patients, and stomal ulcer (SU) 26 patients. Fourteen patients (28%) developed postoperative complications, of which nine (18%) were of major degree and five (10%) of a lesser degree. No hospital death occurred among the 50 patients. Five patients (10%) developed postoperative delayed gastric emptying and two of the five required revision of the Roux. Forty-five patients had no clinical problems with delayed emptying. Overall results showed a Visick grading of I in 72%, Visick II in 24%, and Visick III in 4%. Further analysis revealed that of the 13 patients with DU who had VARY, 62% were Visick I, 30% Visick II, and 8% Visick III. The 11 GU patients with VARY were graded Visick I 73% and Visick II 27%. Of 26 patients with SU who underwent VARY, 77% were Visick I, 19% Visick II, and 4% Visick III. Mild to moderate dumping took place in 8% of the 50 patients, mild diarrhea 10%, weight loss 10%, and no patient experienced alkaline reflux gastritis. Long-range postoperative gastric emptying studies among nine patients using a radionuclide revealed varying patterns of emptying. Overall clinical results have been satisfactory and we are continuing to use VARY in selected cases, particularly those in which a Billroth I reconstruction appears contraindicated.

The early diagnosis of gastrinoma.

Despite the increasing awareness of gastrinoma and its lethal peptic ulcer sequelae, the diagnosis is often initially missed or made as a terminal event. The authors screened all patients with peptic ulcer symptoms serious enough to warrant hospital admission or those associated with diarrhea, nephrolithiasis, hypercalcemia, or pituitary abnormality. In a one-year period (1979-1980) nine (of 14 suspected) new gastrinoma patients were identified using a sensitive and specific gastrin radioimmunoassay in combination with provocative tests including IV secretin, calcium, and food. Conventional upper GI series, CAT scan, arteriography, and endoscopy provided no additional information other than to confirm the presence of ulcer disease. Basal plasma gastrin levels were more than 200 pmol L-1 in only three of the nine (normal fasting plasma gastrin levels are less than 25 pmol L-1). Three patients presented with acute ulcer perforation, and the diagnosis of gastrinoma was suspected because of multiple ulcers and pancreatic masses. In three other patients, previous duodenal ulcer surgery had failed. One patient with dyspepsia, high basal plasma gastrin, negative secretin and calcium infusion studies, and a positive meal test was diagnosed as having G-cell hyperplasia; this was confirmed by biopsy and antral gastrin extraction. Antrectomy alone resulted in cure. In all patients tested, a positive calcium infusion or secretin bolus (greater than 100% rise over basal) strongly suggested the diagnosis of gastrinoma, which was confirmed at surgery. In the acute perforations, initial management with omental patch and cimetidine therapy allowed survival of two patients, while emergency total gastrectomy in the third resulted in death due to esophagojejunal leak. Elective patients were treated with cimetidine initially for at least two weeks before total gastrectomy. In this group there were no operative mortalities, and postoperative morbidity was minimal. This series illustrates three important points: (1) careful screening of an ulcer population using gastrin radioimmunoassay and provocative tests has enabled a high yield of gastrinomas while conventional investigations are of minimal values; (2) a high index of suspicion in appropriate cases is necessary; and (3) total gastrectomy performed under elective circumstances is safe and allows the patients to resume a normal and healthy life without the sequelae of aggressive peptic ulceration or daily drug administration.

Surgical treatment of peptic ulcer disease.

Elective surgery for peptic ulcer disease has diminished significantly over the past 15 years. However, emergency surgery has not shown a decline. Some series have even reported an increase in hospitalizations and operations for hemorrhage. The appropriate surgical procedure for peptic ulcer disease must be tailored to the specific needs of the individual patient. During emergency operations for hemorrhage from duodenal ulcer, we recommend suture ligature of the bleeding vessel and vagotomy-pyloroplasty for high-risk patients, or vagotomy-antrectomy for the lower-risk patient. Bleeding gastric ulcers should be resected, if possible. For massive hemorrhage from stress ulceration requiring surgery, near-total or total gastrectomy should be performed. Perforated duodenal ulcers are best managed by closure and a definitive ulcer operation, such as vagotomy-pyloroplasty. Perforated gastric ulcers are best excised but may be simply closed if conditions do not favor resection. In these situations, biopsy should be performed. We recommend truncal vagotomy-antrectomy for patients presenting with obstruction. Vagotomy (truncal or proximal gastric) with drainage is an acceptable alternative in this situation. For patients with intractable ulcer disease or for those who are noncompliant, proximal gastric vagotomy is the preferred operation. However, other operations may need to be considered, depending on the specific situation. Recurrent ulceration needs appropriate work-up to determine the possible cause. Although patients with ulcer recurrence initially may be placed on medical treatment, about 50% will require reoperation. The most effective procedure for peptic ulcer disease is truncal vagotomy-antrectomy, which has a recurrence rate of less than 1%. The procedure with the least morbidity and the fewest undesirable side effects is proximal gastric vagotomy. Ulcer recurrence after proximal gastric vagotomy or truncal vagotomy-pyloroplasty is in the range of 10% to 15%.

[10 years' results following proximal selective vagotomy in duodenal ulcer disease. A prospective study].

The results 10 years after proximal gastric vagotomy for chronic duodenal ulcer disease in a prospective trial are presented. Among 76 patients 5 were lost to follow-up, 3 had died from causes unrelated of ulcer disease. 80.3% of the patients remained clinically free from recurrence. 92.2% had a Visick grade I or II. The symptomatic recurrence rate was 19.7%, total recurrence rate including asymptomatic recurrences having been 25.3%. 6 patients (8.4%) had to be reoperated, 12 (16.9%) were treated medically. 3/4 of the medically treated patients only had 1 recurrence throughout 10 years. The rate of mild dumping and diarrhea was 2% each. Patients with recurrence showed no more significant reduction of BAO or pentagastrin stimulated maximal acid output (MAO) 10 years postoperatively. Patients without recurrence had a significant reduction of BAO and MAO of 42%. Based upon the results presented, the indication for proximal gastric vagotomy for chronic duodenal ulcer is still justified.

Alkaline reflux gastritis.

Any surgical procedure that ablates the pyloric sphincter mechanism permits increased reflux of duodenal fluid into the stomach or gastric remnant. Although it is reported as most common with Billroth II gastrectomy, our experience indicates that reflux is nearly as frequent after Billroth I gastroduodenostomy and is not at all infrequent after pyloroplasty. The precise constituents of duodenal fluid which damage the gastric mucosa remain controversial. The best present evidence is that the bile acids are probably essential, but that one or more other constituents of duodenal content are also necessary. The clinical history differs significantly from chronic afferent loop syndrome in that the quality of pain is different, pain tends to be more continuous and less closely related to food-taking, and bile vomiting does not provide dramatic relief, often containing food due to coexistent interference with gastric emptying. Diagnosis is confirmed by gross endoscopic findings and characteristic histopathologic changes in the endoscopic biopsies. Treatment with an interposed isoperistaltic jejunal segment has been disappointing. Only four of ten patients experienced lasting relief, indicating that the relatively short 10 to 12 cm. of jejunum does not adequately prevent duodenogastric reflux. We have, therefore, shifted to the Roux-en-Y duodenal diversion implanting the afferent limb 40 cm. caudad to the gastrojejunostomy. Results have been excellent in 24 of 25 cases with prompt improvement in gastric emptying, absence of bile vomiting, progressive regression in abdominal distress and progressive improvement in nutrition. Endoscopic evaluation at three to four months has indicated marked gross improvement and striking histologic improvement in 23 of 25 cases. The question is raised whether the Roux-en-Y reconstruction should not be used primarily, particularly if both vagotomy and antrectomy are to be performed for peptic ulcer. Both the afferent loop syndrome and alkaline reflux gastritis would be prevented, and it is doubted that the incidence of marginal ulcer would increase appreciably.

The use of the long-acting somatostatin analogue, octreotide acetate, in patients with islet cell tumors.

Octreotide lowers plasma concentrations of the marker peptide in the majority of patients with islet cell tumors. However, as described above the effect of octreotide on plasma concentrations of marker peptides is not necessarily related to the effect on symptoms. Nevertheless octreotide is capable of producing symptomatic relief in a large proportion of patients with islet cell tumor syndromes. The data on the effect of octreotide on the symptoms due to VIPoma and due to the carcinoid syndrome (presumably including some who have islet cell tumors) are strong and the drug has been approved for these indications by the Food and Drug Administration. With respect to the other islet cell tumor syndromes, the published data suggest that the utility of octreotide differs in the different syndromes. Insulinomas are usually single, benign, and can and should be removed surgically, resulting in cure. Octreotide therefore has no role to play in such patients, particularly since the response of insulinomas is variable. However in the 10 per cent of insulinomas that are malignant octreotide is certainly effective in at least a portion of cases, although as yet the true response rate and efficacy compared with diazoxide is not clear. Although octreotide is effective at reducing acid output, and thus improving symptoms in patients with Zollinger-Ellison syndrome, because of the effectiveness of histamine H2-receptor antagonists and omeprazole, there is no need for octreotide in this syndrome. For patients with glucagonoma, GHRHoma, Cushing's syndrome, and other rare islet cell tumor syndromes octreotide may well be of benefit and should be considered. The current data do not support the use of octreotide for an antitumor effect.

[Laparoscopic truncal vagotomy, antrectomy with Billroth-II reconstruction for complicated duodenal ulcer (Case report and literature review)].

Today surgeons are performing fewer elective ulcer surgeries, as H2 receptor blockers and the eradication of Helicobacter pylori represent a major step in treatment of this disease. Nevertheless, patients with complications and those resistant to medical therapy should be offered surgical options. The laparoscopic management of these complications is an alternative to open surgery, if applied with appropriate patient selection. The authors report a case with repeated bleeding and duodenal narrowing due to a duodenal ulcer. The patient was treated by totally intraabdominal laparoscopic truncal vagotomy, antrectomy and Billroth-II reconstruction--this probably being the first performed and publicized operation in Hungarian literature. The technique this operation and common perioperative problems based on existing literature are reviewed. The benefits of the minimally invasive approach were clearly evident. The authors believe that minimally invasive approaches will renew the interest in definitive surgery for the treatment of ulcer disease.

Primary peptic ulcerations of the jejunum associated with islet cell tumors. Twenty-five-year appraisal.

A review of 42 patients with gastrinoma, who either survived five years or longer or who died during this period of evaluation, was carried out to define the surgical principles which might be combined with the recent trend toward cimetidine therapy. Thirty-four (80%) of the patients had total gastrectomy with an operative mortality rate of 2.3%, and eight patients (20%) had less than total gastrectomy. No tumor was found in six patients with hypergastrinemia and an abnormal secretin bolus whose five-year survival rate was 100%. Of the thirty-six patients having tissue proof of gastrinoma, twenty-two (61%) had complete resection of all gross tumor resulting in a 76% five-year survival rate. Fourteen patients had unresectable tumor or partial resection with a five-year survival rate of 21%. Complete gross tumor resection increased mean survival by six years (p < 0.01), but resulted in persistent eugastrinemia in only two patients. Long-term survival was possible with a combination of vagotomy, lesser gastric procedures, tumor resection, and cimetidine, seven of eight patients living more than five years. Surgical management of gastrinoma should be directed toward aggressive tumor resection and vagotomy, with reliance on cimetidine therapy postoperatively to control the gastric hypersecretion. Total gastrectomy should be reserved for cimetidine failures and those who do not wish to take cimetidine for the rest of their lives.

A comparative study of gastrectomy without vagotomy with either Roux-en-Y or Billroth II anastomosis in peptic ulcer.

Since recent small uncontrolled studies have suggested that surgery for peptic ulcer comprising partial gastrectomy with Roux-en-Y anastomosis without vagotomy effectively prevents postoperative enterogastric reflux without increasing ulcer recurrence rate, we have compared mortality, ulcer recurrence rate, and complaints in ulcer patients who had undergone partial gastrectomy with either Roux-en-Y (n = 47) or Billroth II anastomosis (n = 47). The groups were comparable with regard to age, sex, ulcer localisation, indication for surgery and number of emergency procedures. During postoperative follow-up, seven patients with Roux-en-Y have died, compared with nine patients with Billroth II gastrectomy. In two of the seven patients who died after Roux-en-Y gastrectomy, but in none of the nine who died after Billroth II resection, death was unequivocally related to postoperative ulcer recurrences. At 1, 2, 3 and 4 years postoperatively, 90 vs. 100% (not significant), 78 vs. 98% (p < 0.01), 72 vs. 95% (p < 0.01) and 72 vs. 95% (p < 0.01) of the patients were in remission after Roux-en-Y and Billroth II gastrectomy, respectively. All ulcers were localized at or just distal to the anastomosis, and were diagnosed within the first 3 postoperative years. We conclude that in peptic ulcer patients the ulcer recurrence rate after Roux-en-Y gastrectomy without vagotomy is considerably higher than after Billroth II resection. Thus, gastrectomy with Roux-en-Y anastomosis without vagotomy cannot be recommended as the primary procedure in patients undergoing partial gastrectomy for peptic ulcer disease.

Ten-year follow-up of a prospective, randomized trial of selective proximal vagotomy with ulcer excision and partial gastrectomy with gastroduodenostomy for treating corporeal gastric ulcer.

Between 1975 and 1980, 30 patients with type I corporeal gastric ulcer were randomly allocated to undergo selective proximal vagotomy with ulcer excision or partial gastrectomy with gastroduodenostomy. Sixteen patients underwent selective proximal vagotomy (1 was excluded from the follow-up since microscopic examination of the excised ulcer revealed an early gastric cancer) and 14 underwent partial gastrectomy. No significant differences in the clinical results were found 3 years after surgery. During a median follow-up of 10 years, ulcer recurred in 3 patients after selective proximal vagotomy and in 2 after partial gastrectomy. One patient in each group had recurrent ulcer without symptoms and received no treatment. Two selective proximal vagotomy patients and three partial gastrectomy patients had epigastric pain with or without ulcer. One patient with selective proximal vagotomy underwent a second operation because of epigastric pain and recurrent ulcer. Bowel habits remained unchanged in all but one patient in each group, and mild or moderate dumping was recorded for two patients in each group. Very good or good results (modified Visick scale) were recorded for 11 of 15 patients after selective proximal vagotomy and for 10 of 14 patients after partial gastrectomy. Except for one patient in each group who had moderate dumping, patients classified as Visick III or IV had no symptoms during treatment with antacids or H2-blockers, or had asymptomatic ulcers and needed no treatment. Selective proximal vagotomy reduced the median acid response to insulin hypoglycemia and to pentagastrin by 100% and 80%, respectively, for at least 3 to 5 years, and partial gastrectomy reduced the median acid response to pentagastrin by 97%. In our opinion, selective proximal vagotomy with ulcer excision is an alternative to partial gastrectomy for surgically treating type I gastric ulcer.

Hormonal therapy (oncology)

Somatostatin analogs Octreotide is an analog of the peptide hormone somatostatin, which inhibits the production of the growth hormone as well as numerous peptide hormones of the gastrointestinal system, including insulin, glucagon, pancreatic polypeptide, gastric inhibitory polypeptide, and gastrin. Octreotide is used for suppression of the hormonal syndromes which accompany several pancreatic islet cell tumors, including the Zollinger-Ellison syndrome of gastrinoma and the chronic hypoglycemia of insulinoma. It is also effective in suppression of the carcinoid syndrome, caused by advanced or extra-gastrointestinal carcinoid tumors. Octreotide may also be used for treatment of severe diarrhea caused by 5-fluorouracil chemotherapy or radiation therapy.

Thoracoscopic truncal vagotomy.

Nowadays the only indications to truncal vagotomy is recurrent ulceration after previous gastric surgery. Truncal vagotomy allows us to obtain a reduction in acid production and to promote ulcer healing, but this technique causes pylorospasm in about 20% of cases and this requires further synchronous or metachronous pyloric drainage procedure. For this reason, videothoracoscopic truncal vagotomy is reserved to patients with gastroresection. The authors describe 15 patients treated with videothoracoscopic truncal vagotomy. In 12 patients, a gastrojejunostomy was done according to Roux technique in 2 patients, a reconstruction according Billroth II technique and in 1 patient, a gastroduodenostomy according to Billroth I technique. Videothoracoscopic bilateral truncal vagotomy was done in all patients; operation time was 45 minutes. During the postoperative period there were no complications. No patients underwent medical therapy for peptic ulcer. Only in 12 patients was it possible to execute an endoscopic follow-up in a period of 3 to 4 years. In all patients the ulcer was completely healed. Complete vagotomy in patients who present with recurrent gastrointestinal bleeding after previous gastroresection, is associated with significant risks. Videothoracoscopic bilateral truncal vagotomy as a simple and efficient procedure seems to be an alternative treatment for the management of recurrent ulceration after previous gastric surgery for peptic disease.

Octreotide

Octreotide, sold under the brand name Sandostatin (marketed by Novartis) among others, is an octapeptide that mimics natural somatostatin pharmacologically, though it is a more potent inhibitor of growth hormone, glucagon, and insulin than the natural hormone. It was first synthesized in 1979 by the chemist Wilfried Bauer, and binds predominantly to the somatostatin receptors SSTR2 and SSTR5. It was approved for use in the United States in 1988. Medical uses Tumors Octreotide is used for the treatment of growth hormone producing tumors (acromegaly and gigantism), when surgery is contraindicated, pituitary tumors that secrete thyroid-stimulating hormone (thyrotropinoma), diarrhea and flushing episodes associated with carcinoid syndrome, and diarrhea in people with vasoactive intestinal peptide-secreting tumors (VIPomas). Octreotide is also used in mild cases of glucagonoma when surgery is not an option.

Latest results (12-21 years) of a prospective randomized study comparing Billroth II and Roux-en-Y anastomosis after a partial gastrectomy plus vagotomy in patients with duodenal ulcers.

After a partial resection of the stomach, the continuity of the gastrointestinal tract can be restored either by a Billroth II gastrojejunal anastomosis or a Roux-en-Y gastrojejunostomy. Each procedure has its advantages and disadvantages. To determine through a prospective and random clinical trial, the clinical outcome and the endoscopic and histologic alterations of the distal esophagus and the gastric remnant in patients who received a partial distal gastrectomy due to duodenal ulcers and a Billroth II or Roux-en-Y reconstruction. In this prospective random trial, a total of 75 patients with duodenal ulcers were included. A bilateral selective vagotomy and partial distal gastrectomy were performed in all patients. A Billroth II or Roux-en-Y 60-cm-long loop was randomly used for reconstruction of the gastrointestinal tract. During the latest follow-up clinical evaluation, upper endoscopy and biopsy samples from the distal esophagus and gastric remnant were obtained. There was 1 operative mortality and 6 patients had some morbidity. The average follow-up period was 15.5 years (range, 11-21). Patients with Roux-en-Y gastrojejunostomy were significantly more asymptomatic and had greater Visick I grading than patients with Billroth II reconstruction (P < 0.001). In the distal esophagus, endoscopic findings were normal in 90% of the Roux-en-Y group, but only in 51% of the Billroth II group (P < 0.0009). Nearly 25% of the latter group had the appearance of a short-segment Barrett esophagus compared with 3% of the Roux-en-Y group (P < 0.0001). The gastric remnant endoscopic findings were normal in 100% of the Roux-en-Y group and in 18% of the Billroth II group (P < 0.02). Histologic analyses showed similar proportions of normal fundic mucosa and chronic active fundic gastritis. However, chronic atrophic fundic gastritis and intestinal metaplasia were significantly more frequent after Billroth II reconstruction (P < 0.008). Helicobacter pylorus was present in a similar proportion of patients. This prospective and random study showed that Roux-en-Y gastrojejunostomy is significantly better than a Billroth II reconstruction in patients with duodenal ulcers, through subjective and objective endoscopic and histologic evaluations during the latest follow-up evaluation.

[Changes in the diagnosis and treatment of Zollinger-Ellison syndrome (author's transl)].

A gastrinoma was found in 12 of 23 patients with Zollinger-Ellison syndrome. Those with gastrinoma were not different from those without as regarded fasting gastrin level, increased gastrin secretion after secretin and calcium, acid secretion, or survival time. Five of the 23 patients have died, four immediately postoperatively, the fifth of the metastasizing tumour. Treatment with the H2-receptor antagonist cimetidine avoided emergency operation and thus decreased operative mortality, giving time for localization by ultrasound, computed tomography and selective arteriography. The rate of false-negative results was high. Transhepatic selective catheterization of the pancreatic veins with gastrin determination gives localization of the tumour and identification of the secreted hormone. In three patients tumour resection was possible under cover of H2-receptor antagonist administration which normalized gastrin and acid secretion. There is a change in the treatment of the Zollinger-Ellison syndrome, away from total gastrectomy to conservative treatment with H2-receptor antagonists and an attempt of curative treatment by removal of the tumour.

[Somatostatin in gastroenterological therapy].

Somatostatin (SST) has been shown by several controlled studies to be effective in halting acute severe bleeding from ulcerative and erosive lesions of the upper intestinal tract. Its efficacy for the treatment of bleeding esophageal varices is less certain, and more controlled studies are necessary. Intravenous administration of SST or subcutaneous application of the new synthetic SST-analogues produces a decrease in serum hormone levels and abolition of symptoms in patients with endocrine-active tumors such as vipoma, glucagonoma and carcinoid. SST has no effect on the outcome of acute pancreatitis, and experience with SST in treating intestinal fistulas is very limited.

Gastrectomy

All patients lose weight after gastrectomy, although the extent of weight loss is dependent on the extent of surgery (total gastrectomy vs partial gastrectomy) and the pre-operative BMI. Maximum weight loss occurs by 12 months and many patients regain weight afterwards. History The first successful gastrectomy was performed by Theodor Billroth in 1881 for cancer of the stomach. Historically, gastrectomies were used to treat peptic ulcers. These are now usually treated with antibiotics, as it was recognized that they are usually due to Helicobacter pylori infection or chemical imbalances in the gastric juices. In the past a gastrectomy for peptic ulcer disease was often accompanied by a vagotomy, to reduce acid production. This problem is now managed with proton pump inhibitors. See also Finsterer-Hofmeister operation List of surgeries by type Roux-en-Y Sleeve gastrectomy References Digestive system surgery

VIPomas: an update in diagnosis and management in a series of 11 patients.

VIPoma is a rare pancreatic endocrine tumor (PET) which secretes excessive amounts of VIP (Vasoactive Intestinal Peptide) that causes a special clinical syndrome characterized by secretory diarrhea, hypokalemia and achlorhydria. Among a total number of 76 patients (pts) with PETs, we present in this study 11 pts with VIPoma syndrome focusing on our diagnostic and therapeutic approach, in parallel with a brief review of the literature. Eleven pts (7 males and 4 females), aged from 2 to 83 years (mean age 53.1 years) were included. The diagnosis was based upon compatible clinical features and serum VIP values and was supported by the estimation of other peptides and neuroendocrine markers such as gastrin, pancreatic polypeptide and chromogranin-A (CgA). In 10/11 pts, diagnosis was confirmed histopathologically. The primary or metastatic lesions were located by conventional imaging methods or by OCTREOSCAN or Endoscopic Ultrasound (EUS). The follow-up period ranged from 2.5-13.5 years (mean 4.8 years). Chronic secretory diarrhea, which persisted despite fasting, was the main symptom in all pts of our study. VIP levels at the time of diagnosis were more than 3 or 10 times the upper normal limit in 7/11 (63.6%) or 4/11 (36.4%) pts, respectively. The primary lesion was detected by CT scan or MRI in 6/11 (54.5%), with EUS or abdominal angiography in 4/11 (36.4%). OCTREOSCAN revealed a solitary lesion in the right hepatic lobe, not detected by all the previous studies, while it detected, as a whole, the primary lesion in 10/11 (91%), and the metastases in 3/4 (75%) pts. In 7/11 (63.6%) the primary lesion was located in the pancreas, whereas in the rest it was in the duodenum or retroperitoneum. A surgical resection was possible in 7/11 (63.6%) pts, while pts with metastatic disease already or poorly differentiated tumors also received additional treatment with somatostatin analogues and chemotherapy. Liver metastases and poor differentiation of tumors seemed to be negative prognostic factors. Clinical suspicion, early diagnosis and precise management may affect survival and improve the quality of life of patients. Also, surgical treatment, as extensive as possible, in combination with somatostatin analogues or chemotherapy when necessary, may also result in prolonged survival, also in patients with advanced disease.

The afferent loop syndrome.

The afferent loop syndromes result from obstruction to the afferent jejunal loop. Acute ALS results from complete obstruction, usually occurs early after surgery and runs a devastatingly lethal course unless promptly treated by reoperation. In chronic ALS the obstruction is intermittent and produces a clinical syndrome from which a diagnostic histroy can usually be obtained. Although the exact incidence is unknown, it is certainly not rare, especially in antecolic Billroth II gastrectomies. Treatment consists of doing away with the afferent loop. In gastroenterostomy alone takedown of the anastomosis with a Weinberg pyloroplasty is the treatment of choice. The safest and simplest treatment for patients whose original operation was Billroth II gastrectomy is conversion to a Roux-en-Y procedure. In all cases vagotomy should be added unless previously performed. No medical treatment is available and patients with no other contraindication should have revisional surgery if symptoms are clinically significant. Both acute and chronic afferent loop syndromes should be completely prevented by appropriate choice of the initial operative procedure. The vagotomized stomach should be drained by pyloroplasty, not gastrojejunostomy. Vagotomy and antrectomy should be reconstructed with a Billroth I gastroduodenostomy. The Braun enteroanastomosis should be utilized after subtotal gastrectomy for carcinoma. The wider application of parietal cell vagotomy for duodenal ulcer deserves close observation and further consideration.

Surgery_Schwartz

should prompt an evalu-ation for gastrinoma. Gastrinoma also should be considered in the differential diagnosis of recurrent or refractory peptic ulcer, secretory diarrhea, gastric rugal hypertrophy, esophagi-tis with stricture, bleeding or perforated ulcer, familial ulcer, peptic ulcer with hypercalcemia, and gastric neuroendocrine tumor (carcinoid). The majority of patients with ZES have been symptomatic for several years before definitive diagnosis and, 3Table 26-13Differential diagnosis of intractability or nonhealing peptic ulcer diseaseCancer Gastric Pancreatic DuodenalPersistent Helicobacter pylori infection Tests may be false-negative Consider empiric treatmentNoncompliant patient Failure to take prescribed medication Surreptitious use of NSAIDsMotility disorderZollinger-Ellison syndromeBrunicardi_Ch26_p1099-p1166.indd 113601/03/19 7:12 PM 1137STOMACHCHAPTER 26in general, patients with ZES and MEN1 are diagnosed in their 20s and 30s, while those with sporadic ZES more

Stasis syndromes following gastric surgery: clinical and motility features of 60 symptomatic patients.

We retrospectively reviewed the records of 60 patients who had been referred for gastrointestinal manometry because of stasis after gastric surgery. Nausea, vomiting, bloating, abdominal pain, and weight loss were the most common symptoms. Two thirds of these patients had a well-documented history of peptic ulcer before their initial operations; in others, surgery was performed for other reasons, such as obesity (5%) or reflux esophagitis (8%). Twelve patients had undergone truncal vagotomy and a "drainage operation" and 48 had received a partial gastrectomy with a gastroenterostomy: Billroth I (n = 8), Billroth II (n = 11), Roux-en-Y (n = 29). All patients had recordings of gastrointestinal manometry; 16 also had a scintigraphic measurement of gastric emptying. Measurements were compared with data from healthy controls. Gastric manometry, which could be assessed only in the group with an intact antrum, was characterized by antral hypomotility (p less than 0.05). Gastric emptying studies showed rapid early emptying of liquids and delayed emptying of solids (both p less than 0.05). In the whole group, fasting jejunal motility was characterized by absence of phase II in 13, presence of bursts of phasic activity in 18, and abnormal propagation of phase III in 8. A significantly increased frequency of phase III of MMC was noted in the patients after Billroth II and Roux-en-Y operations. Postprandially, 19 patients failed to develop a "fed pattern."(ABSTRACT TRUNCATED AT 250 WORDS)


Be careful with lithium. Intoxications have been seen with normal lithium. It is not rare -especially due to interactions-. A very effective drug if everyone is forewarned.

A 46-year-old man with bipolar disorder is brought to the emergency department after an over-ingestion of lithium carbonate. Examination reveals severe tremor, ataxia, dysarthria, myoclonus and fasciculations. Lithemia is 4.1 mEq/L (toxicity > 1.6 mEq/L). Which of the following therapeutic options would be most indicated?

Aminophylline associated with a cathartic.

[Acute intoxication with sustained-release lithium carbonate tablets. A propos of a case].

To describe the case of a patient who ingested 50 sustained release lithium carbonate 400 mg tablets, and reached a late peak concentration above 3 mEq/L. A 32-year-old male with bipolar mood disorder ingested 50 sustained-release lithium carbonate tablets. Upon admission to the emergency room, a gastric wash was performed,from which several tablet remnants were obtained, as well as an intestinal lavage using activated carbon. good general status, no fever, blood pressure 160/90 mm Hg, no edemas. Neurologic, pulmonary, and cardiac examinations were normal. CBC and the chemistry panel were normal. The patient's psychopathological examination suggested a stable status with no apparent manifestations arising from a decompensated mood disorder. Five hours after his massive lithium ingestion the drug's plasma levels were 0.75 mEq/L. At 22 hours post-ingestion a chemistry panel was obtained, which showed serum creatinin at 1.38 mg/dL and a lithium plasma concentration of 3.15 mEq/L. A hemodyalisis trial was attempted for 4 hours. At 73 hours post-ingestion, lithium plasma levels were 0.6 mEq/L, that is, within therapeutic range. The patient was hemodynamically stable and serial blood tests were normal; he was discharged. Acute lithium intoxication with plasma levels above 3 mEq/l can be fatal or result in irreversible neurologicsequelae in almost one third of cases, with persistent cerebellar dysfunction in association with dementia of variable degree, andrenal, blood, and liver disturbances. Sustained-release tablets may prolong absorption and delay peak plasma concentrations. In such cases, therefore, it is recommended that drug plasma concentrations be monitored during 48-72 hours post-ingestion.

Lithium intoxication presenting as altered consciousness and arrhythmia with cardiogenic shock: A case report.

Lithium has been used to treat bipolar disorder. Lithium has a narrow therapeutic index, with a therapeutic level between 0.6 and 1.5 mEq/L. The possible complications of lithium overdose include altered mental status, hand tremor, muscle weakness, nausea, vomiting, diarrhea, seizure, syncope, and arrhythmia. Lithium intoxication can be fatal and is difficult to diagnose in patients without a history of lithium intake. The occurrence of serious cardiac arrhythmias is rare in lithium intoxication. An 81-year-old man was brought to the emergency department because of consciousness disturbance for 2 days. According to his daughter, he had a history of hypertension and diabetes. Recently, his family also observed slurring of speech and easy choking. The physical examination findings were unremarkable. Blood examination only revealed impaired renal function. Twelve-lead electrocardiography revealed sinus rhythm with first-degree atrioventricular block. Chest radiography revealed mediastinal widening. The blood pressures obtained from the 4 limbs showed no significant differences. Subsequently, brain computed tomography revealed no obvious intracranial lesion. A neurologist was consulted, and a recent ischemic stroke could not be ruled out. While in the observation area, his systolic blood pressure decreased to <90 mm Hg and he showed bradycardia, and 12-lead electrocardiography revealed an AV block and long pulse. Contrast-enhanced chest computed tomography revealed no evidence of aortic dissection. Another family member reported a history of lithium intake for bipolar disorder for >30 years. Blood examination revealed a lithium concentration of 2.65 mEq/L. A nephrologist was consulted, and emergency hemodialysis was indicated. Dopamine was administered for his shock status via a right neck central venous catheter. His lithium level gradually declined after the hemodialysis, and blood pressure and consciousness level improved subsequently. The patient was discharged 9 days later in a stable condition. If an emergency physician encounters a patient with altered consciousness and arrhythmia with cardiogenic shock, the patient's drug intake history should be carefully reviewed to rule out cardiovascular problems on the basis of the patient's clinical condition.

Prolonged neurological burden in severe lithium intoxication.

A 53-year-old woman was brought to the Emergency Department for a persistent state of stupor, tremors, fever and oliguria. The patient had been under treatment for depression. The electrocardiogram showed a wider QRS complex; laboratory tests were as follows: urea 110 mg/dL, creatinine 3 mg/dL, sodium 135 mEq/L, potassium 4.5 mEq/L, and lithium 8.0 mEq/L. Renal replacement was initiated to normalize plasma lithium levels; both stupor and speech impairment persisted for several days after dialysis. Complete recovery was achieved several days afterwards.

[Difficulty in determining when to end continuous hemodialysis for lithium intoxication: case report].

The patient was a 26-year-old woman who ingested a total of 230 tablets, including 160 lithium carbonate tablets (200 mg), in a suicide attempt, and was brought to our hospital 5 hr later. After arriving at the hospital, her only complaint was mild nausea, and no neurological abnormalities or renal dysfunction was observed. We were unable to learn the blood concentration of lithium immediately. A forced diuresis was performed after admission, but the nausea persisted. Continuous hemodialysis (CHD) was performed for 23.5 hr starting 19 hr after ingesting the tablets because the patient had ingested a large amount of lithium carbonate, 32,000 mg. Since the nausea resolved after the CHD was started and no manifestations of lithium intoxication had developed as of 91 hr after ingestion, the patient was discharged. The blood lithium concentrations (mEq/L) revealed at a later date showed that the concentration 5 hr (at the time of the initial examination), 19 hr (start of CHD), 44.5 hr (end of CHD), and 91 hr after ingestion (at the time of discharge) was 4.08, 3.30, 1.09, and 0.38, respectively. Blood purification is said to be effective in treating serious lithium intoxication, but it is difficult to judge when to stop. A favorable outcome of treatment of acute lithium intoxication in a patient with normal renal function appears to have been achieved by performing CHD guided by the clinical manifestations, intravascular redistribution times, etc.

Lithium toxicity precipitated by thyrotoxicosis due to silent thyroiditis: cardiac arrest, quadriplegia, and coma.

Lithium is widely used to treat bipolar disorders. Lithium toxicity is generally caused by inappropriately high doses of lithium or impaired lithium excretion. Most lithium is eliminated via the kidneys and, since thyroid hormone increases tubular reabsorption of lithium, thyrotoxicosis could contribute to the development of lithium toxicity. We report a case of severe lithium toxicity that was apparently precipitated by the onset of thyrotoxicosis resulting from silent thyroiditis and dehydration. The patient was a 64-year-old woman who was admitted for muscle weakness in the lower extremities, diarrhea, and palpitations. She had bipolar disorder and was being treated with lithium carbonate, which she discontinued one week before admission. Her circulating lithium levels had been monitored yearly. Early in her admission she was dehydrated and had febrile episodes, paroxysmal atrial fibrillation, and muscle weakness. Initially, fluid therapy was started, but she lost consciousness and had a cardiac arrest for 2 minutes due to prolonged sinus arrest. Chest compression and manual artificial ventilation were performed, and body surface pacing was started. Serum lithium was markedly elevated to 3.81 mEq/L (therapeutic range, 0.4-1.0 mEq/L), and thyroid hormone levels were increased (free triiodothyronine, 8.12 pg/mL; free thyroxine, 4.45 ng/dL), while thyrotropin (TSH) was suppressed (<0.01 μIU/mL). Hemodialysis was performed, and a temporary pacemaker was inserted for severe sinus bradycardia. The serum thyroglobulin was 4680 ng/mL (reference range, <32.7 ng/mL). A TSH receptor antibody test was negative. Glucocorticoid therapy and inorganic iodine (100 mg) were administered and continued until day 11. However, her neurological symptoms deteriorated with floppy quadriplegia and deep coma. She gradually recovered. On day 36, she was discharged without any neurological symptoms or thyrotoxicosis. A 64-year-old woman taking lithium for bipolar disorder developed lithium toxicity in the setting of what seemed likely to be a recent onset of thyrotoxicosis due to silent thyroiditis. Thyrotoxicosis may be a contributing cause of lithium toxicity, particularly if it is abrupt in onset and even with cessation of lithium therapy if renal function is compromised. Thyroid function should be assessed immediately in patients with suspected lithium toxicity.

[Reversible choreoathetosis associated with lithium intoxication].

Several reports have been published in the literature of choreoathetosis associated with lithium intoxication, but little is known about choreoathetosis without concurrent antipsychotic treatment. We report a 65-year-old woman with lithium intoxication whose choreoathetosis completely recovered without sequela following decrease of her serum lithium level. She had been treated elsewhere for bipolar II disorder and also for hypertension, chronic hepatitis type C and diabetes mellitus. As she became hypomanic, lithium carbonate at 600 mg/day was commenced, which was increased to 1200 mg/day due to unfavorable therapeutic response. She began to manifest disorientation and abnormal involuntary movement and was therefore referred to our Department of Psychiatry. Her clinical symptoms at admission included consciousness disturbance with marked bilateral symmetrical slow-wave activity in her EEG and choreoathetosis was observed in her face and upper and lower extremities. Cerebellar symptoms were minimal with only mild ataxic gait and finger-to-nose test did not show dysmetria or intention tremor. Her serum lithium level was 3.52 mEq/L, which was clearly in the toxic range. She demonstrated no metabolic abnormalities including hyperglycemia, and was diagnosed with lithium intoxication and treated with water loading and mannitol for forced diuresis. On the 14th day after admission her consciousness disturbance and choreoathetosis resolved, but EEG abnormalities still persisted. On the 23rd day after admission, she was discharged with clinical remission and normal EEG background activity. Although she developed mild renal dysfunction, hemodialysis was not indicated. Hypersensitivity of dopamine receptor in the nigrostriatal pathways may contribute to choreoathetosis in association with the patient's vulnerability. Choreoathetosis can be a sign of lithium intoxication and prompt treatment is required following careful differential diagnosis.

[Lithium sulfate poisoning treated with hemodialysis in a patient with normal renal function: a case report].

Lithium is the milestone of psychiatric patients' therapy, in particular in bipolar disorder. Despite its high therapeutic efficacy, there are several side effects (renal, thyroid, parathyroid, dermatological) and management problems linked to its narrow therapeutic range, which exposes patients to a high risk of toxicity. We describe the case of a male patient with bipolar disorder in therapy with lithium sulfate who developed a severe acute-on-chronic intoxication. He came to our attention in a somnolent state with lithemia >3 mEq/L and therefore underwent hemodialysis. In view of the high toxicity of lithium, a timely and correct therapeutic choice is important to improve the patient's outcome. In this context, considering lithemia, but also kidney function and the patient's clinical status, it is necessary to consider extracorporeal treatments, of which hemodialysis is the most preferable.

Lithium toxicity

Gastric lavage and whole bowel irrigation may be useful if done early. Activated charcoal is not effective. For severe toxicity hemodialysis is recommended. The risk of death is generally low. Acute toxicity generally has better outcomes than chronic toxicity. In the United States about 5,000 cases are reported to poison control centers a year. Lithium toxicity was first described in 1898. Signs and symptoms Symptoms of lithium toxicity can be mild, moderate, or severe. Mild symptoms include nausea, feeling tired, and tremor occur at a level of 1.5 to 2.5 mEq/L. Moderate symptoms include confusion, an increased heart rate, and low muscle tone occur at a level of 2.5 to 3.5 mEq/L. Severe symptoms include coma, seizures, low blood pressure and increased body temperature which occur at a lithium concentration greater than 3.5 mEq/L. When lithium overdoses produce neurological deficits or cardiac toxicity, the symptoms are considered serious and can be fatal.

Treatment of bipolar disorder

Potential side effects from lithium include gastrointestinal upset, tremor, sedation, excessive thirst, frequent urination, cognitive problems, impaired motor coordination, hair loss, and acne. Excessive levels of lithium can be harmful to the kidneys, and increase the risk of side effects in general. As a result, kidney function and blood levels of lithium are monitored in patients being treated with lithium. Therapeutic plasma levels of lithium range from 0.5 to 1.5 mEq/L, with levels of 0.8 or higher being desirable in acute mania. Lithium levels should be above 0.6 mEq/L to reduce both manic and depressive episodes in patients. A recent review concludes that the standard lithium serum level should be 0.60-0.80 mmol/L with optional reduction to 0.40-0.60 mmol/L in case of good response but poor tolerance or an increase to 0.80-1.00 mmol/L in case of insufficient response and good tolerance.

Antacid-induced hypermagnesemia in a patient with normal renal function and bowel obstruction.

To report a case of severe hypermagnesemia caused by magnesium hydroxide in a woman with normal renal function. A 42-year-old Hispanic woman with schizophrenia and bipolar affective disorder was transported from jail to the emergency department with confusion, abdominal pain, vomiting, and constipation. She had been treated in jail with magnesium hydroxide, ordered as milk of magnesia 30 mL po each night and Maalox 30 mL po three times daily. Additional medications included lithium carbonate 300 mg po three times daily, chlorpromazine 150 mg po three times daily, benztropine mesylate 1 mg po twice daily, and docusate sodium 100 mg po each morning. Her temperature was 35.1 degrees C, blood pressure 108/58 mm Hg, heart rate 112 beats/min, and respiratory rate 24 breaths/min. She would respond only briefly to voice or painful stimuli. Her abdomen was distended and diffusely tender. Laboratory tests included serum magnesium concentration 9.1 mEq/L (normal 1.3-2), blood urea nitrogen 16 mg/dL (8-22), creatinine 0.9 mg/dL (0.5-1.1), calcium 3.9 mEq/L (4.2-5.2), and lithium 1.0 mEq/L. A laparotomy was performed, and an adhesive band from a previous oophorectomy was found to be compressing the sigmoid colon. Hypermagnesemia, hypothermia, and hypotension continued in the intensive care unit. Despite successful treatment of the hypermagnesemia with calcium, intravenous fluids, and furosemide, the patient's cardiac rhythm degenerated into fatal, pulseless electrical activity on postoperative day 2. This case of severe hypermagnesemia from magnesium hydroxide ingestion illustrates many of the risk factors for hypermagnesemia in patients with normal renal function. People using magnesium-containing medications for relief of gastrointestinal distress may be at increased risk for hypermagnesemia. A brief review of magnesium physiology, clinical effects, and treatment is provided. Frequent use of the laboratory to identify hypermagnesemia is encouraged because it is often a clinically unexpected finding and responds well to early treatment.

[Diagnostic trap: Lithium neurotoxicity with normal lithemia].

We describe here the case of a 54-year-old bipolar woman, followed in psychiatry and treated with lithium and a selective serotonin reuptake inhibitor (escitalopram) and lamotrigine, presenting a lithium poisoning with an altered state of consciousness caused by a supposed mismanagement of her treatment. Lithium poisoning was suggested based on neurological clinical features, but the blood test brought out a lithium concentration within the therapeutic values at 1,2 mmol/L (N: 0,6-1,2 mmol/L). The classic biological complications related to lithium poisoning (hypercalcemia, diabetes insipidus) confirmed the diagnosis. The patient has been transferred to our nephrology department where she got two hemodialysis sessions conducting to clinical and biological improvement, confirming the diagnosis of lithium poisoning despite the normal blood levels. Later, she was transferred to the psychiatry department for follow-up and for treatment adjustment.

InternalMed_Harrison

A 63-year-old man was admitted to the intensive care unit (ICU) with a severe aspiration pneumonia. Past medical history included schizophrenia, for which he required institutional care; treatment had included neuroleptics and intermittent lithium, the latter restarted 6 months before admission. The patient was treated with antibiotics and intubated for several days, with the development of polyuria (3–5 L/d), hypernatremia, and acute renal insufficiency; the peak plasma Na+ concentration was 156 meq/L, and peak creatinine was 2.6 mg/dL. Urine osmolality was measured once and reported as 157 mOsm/kg, with a coincident plasma osmolality of 318 mOsm/kg. Lithium was stopped on admission to the ICU. On physical examination, the patient was alert, extubated, and thirsty. Weight was 97.5 kg. Urine output for the previous 24 h had been 3.4 L, with an IV intake of 2 L/d of D5W.

Lithium intoxication-induced acute parkinsonism complicated with hyperparathyroidism and nephrogenic diabetes insipidus: report of a case.

To describe a patient with lithium intoxication presenting as acute parkinsonism, adverse metabolic effects and nephrogenic diabetes insipidus (DI). We report a case of a 67-year-old woman with a bipolar affective disorder who was treated with lithium for 10 years. Under concomitant renal insufficiency and urinary tract infarction, she experienced progressive hand tremor, bradykinesia, and unsteady gait. Laboratory results revealed hypercalcemia and hypermagnesiemia. A high serum lithium level (3.6 mEq/L) was found; thus lithium was discontinued. She was found to have a high serum level of intact parathyroid hormone: 135.0 pg/ml and a suspicious parathyroid adenoma. Polyuria with hypernatremia was also noted. A water deprivation test confirmed nephrogenic diabetes insipitces. After correction of electrolyte imbalance and reduction of lithium level, her consciousness recovered. Her parkinsonian features were responsive to levodopa 400 mg/day in 2 divided doses. One month later, apart from the residual extrapyramidal symptoms and mania, her condition was otherwise stationary. Tremor is the most frequent movement disorder associated with lithium therapy, while severe parkinsonism has been rarely reported. It should be kept in mind in differential diagnosis of acute parkinsonism especially in elder patients who receive a chronic lithium carbonate therapy.

[Reversible alterations in the dentate nuclei and rapid-onset cerebral atrophy due to neurotoxicity caused by lithium].

Treatment with lithium can cause several neurological side effects, even at therapeutic levels. We report the case of a 49-year-old woman, with bipolar disorder and depression, undergoing treatment with lithium, antidepressants and antipsychotics, who was admitted to hospital due to a clinical picture of visual hallucinations with an elevated lithaemia of 2.1 mEq/L (therapeutic range: 0.6-1.2 mEq/L). The patient developed a severe encephalopathy that required the use of assisted ventilation in the intensive care unit. Initial magnetic resonance imaging showed a reversible bilateral symmetrical hyperintensity in the dentate nuclei in T2 and T2-FLAIR sequences. Over the following months she gradually developed a pancerebellar syndrome with evidence of a marked loss of bilateral volume in the cerebellum, above all at the expense of the vermis, which was accompanied by a permanent and disabling cerebellar syndrome. Although treatment with lithium can cause a variety of neurological side effects, they are usually reversible. However, they occasionally give rise to permanent and disabling sequelae, as in the case of the patient reported here, with a marked and progressive cerebellar atrophy, accompanied by permanent sequelae in the form of a disabling cerebellar syndrome. The cerebellar neurotoxicity of lithium must be taken into account in the broad differential diagnosis of cerebellar ataxia in adults.

Use of the anion gap and intermittent hemodialysis following continuous hemodiafiltration in extremely high dose acute-on-chronic lithium poisoning: A case report.

A 35-year-old woman intentionally took 40,000 mg of lithium carbonate, and she was transferred to our hospital with nausea, vomiting, and diarrhea. She was diagnosed as having bipolar disorder 10 years ago and was receiving oral lithium therapy. Blood test results on arrival were remarkable for a negative anion gap of -2.1 and later, the serum lithium level turned out to be as high as 15.4 mEq/L. Intubation was required because of disrupted consciousness, and continuous hemodiafiltration (CHDF) was immediately started in the intensive care unit to obtain constant removal of lithium. After adding intermittent hemodialysis (IHD) twice during the daytime to accelerate the lithium clearance, CHDF became unnecessary on day 4, and she was extubated on day 6 with complete recovery of consciousness. Close monitoring of the patient data showed recovery of the decreased anion gap as indicator of the serum lithium level reduction. On day 36, she was discharged without any complication and sequela. The current case highlighted the effective use of CHDF between IHD sessions to prevent the rebound elevation of lithium and the role of the anion gap as a surrogate marker of serum lithium concentration during the treatment.

Mood stabilizer

Mineral Lithium – Lithium is the "classic" mood stabilizer, the first to be approved by the US FDA, and still popular in treatment. Therapeutic drug monitoring is required to ensure lithium levels remain in the therapeutic range: 0.6 or 0.8-1.2 mEq/L (or millimolar). Signs and symptoms of toxicity include nausea, vomiting, diarrhea, and ataxia. The most common side effects are lethargy and weight gain. The less common side effects of using lithium are blurred vision, a slight tremble in the hands, and a feeling of being mildly ill. In general, these side effects occur in the first few weeks after commencing lithium treatment. These symptoms can often be improved by lowering the dose.

Lithium (medication)

Lithium concentrations in whole blood, plasma, serum or urine may be measured using instrumental techniques as a guide to therapy, to confirm the diagnosis in potential poisoning victims or to assist in the forensic investigation in a case of fatal overdosage. Serum lithium concentrations are usually in the range of 0.5–1.3 mmol/L (0.5–1.3 mEq/L) in well-controlled people, but may increase to 1.8–2.5 mmol/L in those who accumulate the drug over time and to 3–10 mmol/L in acute overdose. Lithium salts have a narrow therapeutic/toxic ratio, so should not be prescribed unless facilities for monitoring plasma concentrations are available. Doses are adjusted to achieve plasma concentrations of 0.4 to 1.2 mmol /L on samples taken 12 hours after the preceding dose. Given the rates of thyroid dysfunction, thyroid parameters should be checked before lithium is instituted and monitored after 3–6 months and then every 6–12 months.

Lithium toxicity

Gastric lavage. A tube is placed through the nose or mouth into the stomach. The tube is used to remove lithium that has not been digested yet. It may also be used to put medicines directly into the stomach to help stop lithium from being absorbed. Use of an artificial kidney to clean the blood (dialysis). This is usually done only in the most severe cases. Diuretic medications such as furosemide and hydration via intravenous normal saline appear to be effective in speeding the removal of lithium and also rehydrate patients who've lost fluids. Hemodialysis. Hemodialysis is widely advocated as a means of reducing the risk of permanent neurological sequelae following lithium poisoning. Although hemodialysis clearly enhances the elimination of lithium, it is unclear whether this translates into improved patient outcomes. People may be sent home once their lithium level is less than 1.5 mEq/L and they have no symptoms. See also

InternalMed_Harrison

A stuporous 22-year-old man was admitted with a history of behaving strangely. His friends indicated he experienced recent emotional problems stemming from a failed relationship and had threatened suicide. There was a history of alcohol abuse, but his friends were unaware of recent alcohol consumption. The patient was obtunded on admission, with no evident focal neurologic deficits. The remainder of the physical examination was unremarkable. Na+ 140 meq/L K+ 5 meq/L Cl− 95 meq/L HCO3− 10 meq/L Glucose 125 mg/dL BUN 15 mg/dL Creatinine 0.9 mg/dL Ionized calcium 4.0 mg/dL Plasma osmolality 325 mOsm kg/H2O Urinalysis revealed crystalluria, with a mixture of envelope-shaped and needle-shaped crystals.

Neurology_Adams

With blood levels of lithium in the upper therapeutic range (therapeutic 0.6 to 1.2 mEq/L), it is not uncommon to observe a fast-frequency action tremor or asterixis, together with nausea, loose stools, fatigue, polydipsia, and polyuria. These symptoms usually subside with time. Above a level of 1.5 to 2 mEq/L, particularly in patients with impaired renal function or in those taking a thiazide diuretic, serious intoxication becomes manifest—clouding of consciousness, confusion, delirium, dizziness, nystagmus, ataxia, stammering, diffuse myoclonic twitching, and nephrogenic diabetes insipidus. Vertical (downbeating) nystagmus and opsoclonus (see Chap. 13) may also be prominent. A variety of skin problems is common including worsening of acne vulgaris. An uncommon toxic effect is the development of goiter but most patients remain euthyroid although the thyroid-stimulating hormone (TSH) levels may increase slightly. The goiter usually requires no treatment but it is possible to

Neurology_Adams

becomes effective, usually a matter of 4 or 5 days. The usual dosage of lithium is 1,200 to 2,400 mg daily in divided oral doses, which produces a desired serum level of 0.9 to 1.4 mEq/L. The serum level of lithium must be checked frequently, both to ensure that a therapeutic dose is being taken and to guard against toxicity (see later).

InternalMed_Harrison

In the treatment of acute mania, lithium is initiated at 300 mg bid or tid, and the dose is then increased by 300 mg every 2–3 days to achieve blood levels of 0.8–1.2 meq/L. Because the therapeutic effect of lithium may not appear until after 7–10 days of treatment, adjunctive usage of lorazepam (1–2 mg every 4 h) or clonazepam (0.5–1 mg every 4 h) may be beneficial to control agitation. Antipsychotics are indicated in patients with severe agitation who respond only partially to benzodiazepines. Patients using lithium should be monitored closely, since the blood levels required to achieve a therapeutic benefit are close to those associated with toxicity. Valproic acid may be better than lithium for patients who experience rapid cycling (i.e., more than four episodes a year) or who present with a mixed or dysphoric mania. Tremor and weight gain are the most common side effects; hepatotoxicity and pancreatitis are rare toxicities.

InternalMed_Harrison

A 32-year-old man was admitted to the hospital with weakness and hypokalemia. The patient had been very healthy until 2 months previously when he developed intermittent leg weakness. His review of systems was otherwise negative. He denied drug or laxative abuse and was on no medications. Past medical history was unremarkable, with no history of neuromuscular disease. Family history was notable for a sister with thyroid disease. Physical examination was notable only for reduced deep tendon reflexes. Sodium 139 143 meq/L Potassium 2.0 3.8 meq/L Chloride 105 107 meq/L Bicarbonate 26 29 meq/L BUN 11 16 mg/dL Creatinine 0.6 1.0 mg/dL Calcium 8.8 8.8 mg/dL Phosphate 1.2 mg/dL Albumin 3.8 meq/L TSH 0.08 μIU/L (normal 0.2–5.39) Free T4 41 pmol/L (normal 10–27)

[Origin and treatment of the hypokalemic paresis (author's transl)].

The abuse of laxatives and a prolonged treatment with diuretics has to be brought into consideration as the most common cause for renal or intestinal loss of potassium. Besides characteristical alterations at the E.C.G. and besides intestinal disturbances there do occur again and again acute, life-threatening aspects of cases connected with tetraplegias and a respiratory failure. By means of 3 cases from our hospital and 27 casuistics in literature symptomatology and dynamic in the development of hypokaliemia is discussed. The mean of potassium in the serum of the 16 patients, those having quadriplegias, ran up to 1,7 mval/l (range 1,4-2,5). Paralysis develops peracutely in 4 of the cases within hours and in 12 of the cases within days. In the anamnesis symptoms of adynamia could be traced with nearly every patient. A functional psychosis (reversible physically founded psychosis) couldn't be detected in any of the cases. With the help of a administration of potassium one could achieve a total retrogression of the symptoms. Besides this a normalisation of the acide-base equilibrium is required because of a metabolic alkalosis, detectable in most of the cases.

[Aetiologies of lithium overdose: 10-year experience of Marseille poison centre].

Lithium is used for control of bipolar disorders. In order to precise the different circumstances at the origin of poisonings, the authors present the cases of lithium intoxication observed in the Marseille poison centre between January 1991 and December 2000. Retrospective study. Three hundred and four cases were observed during the studied period (1 patient a case), concerning 6 different circumstances. For 3 of them, the symptoms were mild: accidental ingestion with children (13 cases); mistakes on the quantities of ingested tablets (43 cases); elevation of lithium blood level due to diuretic therapy (8 cases). For 2 other circumstances, the clinical signs were more severe: treated patients who developed renal failure (15 cases, 6 patients managed in intensive care unit [ICU], 1 death) or dehydration (35 cases, 8 patients treated in ICU and 1 death). Finally, the most severe cases were collected with suicide attempts. Fifty-six percent of the patients were managed in ICU, 5% needed haemodialysis, 10% had cardiac (repolarization disturbances) or neurological (seizures) complications, 2% died. The severity of lithium poisonings depends of the circumstances. Ingestion of high quantities of sustained released tablets is the most dangerous situation. Accidental ingestion, even with children, must be considered as less severe situations.

Neurology_Adams

The myoclonic state, particularly when combined with confusion and sharp waves in the EEG, may mimic Creutzfeldt-Jakob disease (see Chap. 32) but there should be no problem in diagnosis if the setting of the illness and the administration of lithium are known. At blood lithium concentrations above 3.5 mEq/L, these symptoms are replaced by stupor and coma, sometimes with convulsions, and may prove fatal. Discontinuing lithium in the intoxicated patient, which is the initial step in therapy, does not result in immediate disappearance of toxic symptoms. This may be delayed by a week or two, and the diabetes insipidus may persist even longer. Fluids, sodium chloride, aminophylline, and acetazolamide promote the excretion of lithium. Lithium coma may require hemodialysis, which has proved to be the most rapid means of reducing the blood lithium concentration.

Lithium carbonate

Lithium carbonate is used as a psychiatric medication to treat mania, the elevated phase of bipolar disorder. Prescription lithium carbonate from a pharmacy is suitable for use as medicine in humans while industrial lithium carbonate is not since the latter may, for example, contain unsafe levels of toxic heavy metals or other toxicants. After ingestion, lithium carbonate is dissociated into pharmacologically active lithium ions (Li+) and (non-therapeutic) carbonate, with 300 mg of lithium carbonate containing approximately 8 mEq (8 mmol) of lithium ion. According to the Food and Drug Administration (FDA), 300–600 mg of lithium carbonate taken two to three times daily is typical for maintenance of bipolar I disorder in adults, where the exact dose given varies depending on factors such as the patient's serum lithium concentrations, which must be monitored by a physician to avoid lithium toxicity and potential kidney damage (or even failure) from lithium-induced nephrogenic diabetes

Lithium -- Toxicity -- Recommendations

The guidelines established by EXtracorporeal TReatments In Poisoning (EXTRIP) are listed below. Initiate extracorporeal treatment for patients with severe lithium poisoning presenting with coma, myoclonus, convulsions, or cardiopulmonary collapse. Initiate extracorporeal treatment when impaired kidney function is evident, and the lithium concentration surpasses 4 mEq/L. Hemodialysis is also indicated in patients with altered consciousness, seizures, or life-threatening dysrhythmias, regardless of the lithium concentration. Consider extracorporeal treatment if the lithium concentration exceeds 5 mEq/L, significant confusion is evident, or the projected duration for reducing the lithium concentration below 1 mEq/L extends beyond 36 hours. Continue extracorporeal treatment until clinical improvement or lithium concentration drops below 1 mEq/L. In cases where lithium concentration measurement is unattainable, maintain extracorporeal therapies for at least 6 hours.

Lithium toxicity

Lithium toxicity, also known as lithium overdose, is the condition of having too much lithium. Symptoms may include a tremor, increased reflexes, trouble walking, kidney problems, and an altered level of consciousness. Some symptoms may last for a year after levels return to normal. Complications may include serotonin syndrome. Lithium toxicity can occur due to excessive intake or decreased excretion. Excessive intake may be either a suicide attempt or accidental. Decreased excretion may occur as a result of dehydration such as from vomiting or diarrhea, a low sodium diet, or from kidney problems. The diagnosis is generally based on symptoms and supported by a lithium level of greater than 1.2 mEq/L.

Case report on lithium intoxication with normal lithium levels.

An 18-year old female was admitted to a psychiatric hospital with an initial episode of mania. Treated with routine dosages of lithium bicarbonate, her symptoms resolved after two weeks; she was discharged on a dosage of 250mg lithium bid. Five days after discharge she was taken to the emergency department of a general hospital with loss of appetite and disturbed consciousness. The general hospital physicians were unable to diagnose the problem so she was transferred back to the psychiatric hospital. At that time she had a lithium blood level of 0.57 mmol/L (i.e., at the lower end of the therapeutic range) but was, nevertheless, clearly experiencing lithium intoxication with anuria, trembling extremities, blurred speech, muscle rigidity and hyperactive tendon reflexes. Treated with intravenous mannitol, her acute symptoms resolved quickly. The case highlights the need to monitor clinical symptoms of intoxication in all patients taking lithium, regardless of their blood level, and to inform patients, family members, and general physicians about the symptoms and management of lithium intoxication.

[Analysis of the poisonings by lithium in a department of internal medicine].

Lithium salts have been mainly used in the treatment of bipolar disorder. Because of its narrow therapeutic range, and several well characterised adverse effects, serum lithium levels must be monitored regularly in patients given lithium treatment in order to prevent intoxication. To describe the clinic and toxic characteristics in inpatients at our Clinic Toxicologic Unit. Descriptive and retrospective study of lithium intoxications in 150 inpatients between 2003 and 2006. Patients were classified based on their neuropsychiathric symptom profile and serum lithium levels. Sixteen of 150 inpatients had lithium intoxication: 58.3% women and 43.8% men; 49.19% +/- 18.49% years old. Lithium was used as treatment of bipolar disorder in 87.5% of cases. The most frequent cause of intoxication was attempted suicide. Using neuropsychiatric parametres, intoxication was moderate in 50% of cases, and mild in 25% and severe or very severe in 25%. Using serum lithium levels, intoxication was very severe in 31.35%, severe in 25%, and slight-moderate in 43.7%. Conservative measures were used as the most frequent treatment (50%), and haemodialfiltration was needed in 37.5%. Mean stay was 4,8 days in acute intoxication, and 11.2 days in chronic. Sequelaes were found in two patients (ataxia). Death was not present. Lithium intoxications can involve severe complications, even death. Narrow control is encouraged in polymedicated and elderly patients, and in concommitant treatment with antidepressant and neuroleptics.

Lithium toxicity with prolonged neurologic sequelae following sleeve gastrectomy: A case report and review of literature.

Lithium is the first-line medication for bipolar disorder, given a narrow therapeutic window of 0.8 to 1.2 mEq/L. Change of lithium pharmacokinetics following bariatric surgery may lead to lithium toxicity, which is particularly concerned. We presented a 39-year-old man with morbid obesity and bipolar affective disorder for 20 years, who was treated with lithium. He developed serious lithium toxicity following sleeve gastrectomy and prolonged neurologic sequelae. He suffered from persistent watery diarrhea, general weakness, and then drowsy consciousness. Lithium level was checked immediately to be 3.42 mEq/L and lithium toxicity was diagnosed. After 3 courses of hemodialysis, his serum lithium level subsequently declined to 0.63 mEq/L, while his consciousness returned normal. Lithium was replaced by lamotrigine. The patient was discharged thirty-five days after admission, while his serum lithium declined to 0.06 mEq/L. Neurologic sequelae were noted by muscle weakness and pain sensation in both feet. The nerve conduction test revealed sensorimotor polyneuropathy with conduction block. He was advised to keep a passive range of motion exercise. Although the consensus guideline remains lacking, our report reviewed cases of relevance in the literature and highlighted the awareness of the potential risk of lithium toxicity following bariatric surgery. We suggest close monitoring of the lithium levels and perhaps a dosage adjustment for the postoperative period.