Superior Mesenteric Artery Syndrome^-www.drkeyurbhatt.in*

Superior mesenteric artery (SMA) syndrome is an uncommon but well recognized clinical entity characterized by compression of the third, or transverse, portion of the duodenum between the aorta and the superior mesenteric artery. 


This results in chronic, intermittent, or acute complete or partial duodenal obstruction.¹ Superior mesenteric artery syndrome was first described in 1861 by Von Rokitansky, who proposed that its cause was obstruction of the third part of the duodenum as a result of arteriomesenteric compression. 


The superior mesenteric artery usually forms an angle of approximately 45° (range, 38-56°) with the abdominal aorta, and the third part of the duodenum crosses caudal to the origin of the superior mesenteric artery, coursing between the superior mesenteric artery and aorta. 


Any factor that sharply narrows the aortomesenteric angle to approximately 6-25° can cause entrapment and compression of the third part of the duodenum as it passes between the superior mesenteric artery and aorta, resulting in superior mesenteric artery syndrome.

In addition, the aortomesenteric distance in superior mesenteric artery syndrome is decreased to 2-8 mm (normal is 10-20 mm).


In a review of the literature, approximately 0.013-0.78% of the findings from upper GI tract barium studies support a diagnosis of superior mesenteric artery syndrome.
surgery:

Surgical intervention is indicated when conservative measures are ineffective, particularly in patients with a long history of progressive weight loss, pronounced duodenal dilatation with stasis, and complicating peptic ulcer disease. A trial of conservative treatment should be instituted for at least 4-6 weeks prior to surgical intervention.

Choice of procedure is  duodenojejunostomy

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INSULINOMA^-www.drkeyurbhatt.in*

What is an insulinoma?

Insulinoma is a tumor of the pancreas that produces excessive amounts of insulin. Insulinomas are more common in women. The tumors are usually small (less than 2cm) and more than 90% of all insulinomas are benign (non-cancerous).

Insulinomas produce excessive amounts of insulin and this causes low blood sugar. The typical symptoms that patients complain about are related to the development of low bloods sugar and include tiredness, weakness, tremulous and hunger. Many patients have to eat frequently to prevent symptoms from the low blood sugar. Some patients may develop psychiatric symptoms because of the low blood sugar.

Workup

Laboratory Studies

• Failure of endogenous insulin secretion to be suppressed by hypoglycemia is the hallmark of an insulinoma. Thus, the finding of inappropriately elevated levels of insulin in the face of hypoglycemia is the key to diagnosis. Considering the reference range, the fasting plasma levels of insulin, C-peptide, and, to a lesser degree, proinsulin need not be elevated in insulinoma patients in absolute terms.
• The biochemical diagnosis is established in 95% of patients during prolonged fasting (up to 72 h) when the following parameters are found:
  • Serum insulin levels of 10 µU/mL or more (normal <6 µU/mL)
  • Glucose levels of less than 40 mg/dL
  • C-peptide levels exceeding 2.5 ng/mL (normal <2 ng/mL)
  • Proinsulin levels greater than 25% (or up to 90%) that of immunoreactive insulin
  • Screening for sulfonylurea negative
• Stimulation tests no longer are recommended. The intravenous application of tolbutamide, glucagon, or calcium can be hazardous, as they may induce prolonged and refractory hypoglycemia.
• Prolonged (ie, 72 h) supervised fast in hospitalized patients provides the most reliable results.
  • The calculation of ratios of insulin (µU/mL) to plasma glucose (mg/dL) is diagnostic.
  • Healthy patients maintain a rate of less than 0.25. Obese patients may have a slightly higher rate.
  • In patients with insulinoma, the ratio rises during fasting.
• In a study from the Netherlands, a positive Whipple triad on a prolonged fasting test, in combination with an insulin/C-peptide ratio <1, had a sensitivity of 88.9% and a specificity of 100% for the diagnosis of insulinoma.

Imaging Studies

• Start imaging studies only after the diagnosis has been confirmed biochemically, because 80% of insulinomas are less than 2 cm in size and may not be visible by CT scan or transabdominal ultrasonography.
• Successful preoperative tumor localization is achieved in about 60% of patients.¹⁴
  • Some experienced surgeons perform only transabdominal ultrasound preoperatively.
  • Other surgeons argue that the preoperative localization of insulinomas is not necessary at all because surgical exploration and intraoperative ultrasonography identify more than 90% of tumors.¹⁵
  • Thus, the extent to which one attempts to define the anatomy of the beta cell lesion before surgery is a matter of judgment.
• Helical or multislice CT scan has 82-94% sensitivity. In one study, dual-phase helical CT proved more sensitive than single-phase for detection of insulinoma; in addition, image acquisition in the arterial phase proved more helpful than acquisition during the portal-venous phase.¹⁶
•  MRI with gadolinium can be helpful in detecting a tumor in 85% of cases. One case report suggests that diffusion-weighted MRI can be useful for detecting and localizing small insulinomas, especially for those with no hypervascular pattern.¹⁷
• The accuracy of selective arteriography is 82%, although affected by a false-positive rate of 5%. Many experts see it as the best overall preoperative localization procedure.
• Arteriography with catheterization of small arterial branches of the celiac system combined with calcium injections (which stimulate insulin release from neoplastic tissue but not from normal islets), and simultaneous measurements of hepatic vein insulin during each selective calcium injection localizes tumors in 47% of patients.
• The sensitivity of somatostatin receptor scintigraphy is 60%, although many insulinomas lack somatostatin receptor subtype 2 for successful identification.
• Endoscopic ultrasonography detects 77% of insulinomas in the pancreas.^18,19,20 The yield can be higher if it is done in combination with CT scan. A majority of sporadic insulinomas will be detected and localized by a combination of these two investigative means.
• Real-time transabdominal high-resolution ultrasonography has 50% sensitivity.
• Intraoperative transabdominal high-resolution ultrasonography with the transducer wrapped in a sterile rubber glove and passed over the exposed pancreatic surface detects more than 90% of insulinomas.
• Performing a preoperative study to localize the tumor followed by intraoperative ultrasonography and a physical examination is not unreasonable.
• Insulinomas have been shown to have a very high density of glucagon-like peptide-1 receptors (GLP-1R), and radiolabeling with an¹¹¹ In-labeled GLP-1R agonist (¹¹¹ In-DOTA-exendin-4) has successfully been used to localize small insulinomas both preoperatively and, with the use of a gamma probe, intraoperativel

Surgical Care

Because in Insulinoma resection achieves cure in 90% of 

patients, it is currently the therapy of choice.

• Preoperative management
  • Administer diazoxide on the day of surgery in patients who respond to it. Diazoxide reduces the need for glucose supplements and the risk of hypoglycemia.
  • Monitor blood glucose level throughout surgery.
  • Infuse 10% dextrose in water at a rate of at least 100 mL/h.
  • A preoperative trial with diazoxide is indicated to determine whether the patient is a responder. (Five to 10% of patients do not respond.) This information helps determine the intraoperative strategy if the tumor is not localized.
  • In MEN 1, hypercalcemia must be corrected first by parathyroidectomy before insulinoma resection.²⁴
• Successful tumor location
  • Fully expose the pancreas, including a wide Kocher maneuver to allow complete bimanual palpation.
  • A large study from Spain showed laparoscopic surgery to be safe and effective in benign and malignant tumor resection. It led to a shorter hospital stay compared to open resection.⁵
  • Laparoscopic enucleation techniques, also in combination with preservation of the spleen for distal pancreatic tumors, have been described recently.²⁵
  • Because of the small likelihood that a tumor that presents without metastatic spread is malignant, insulinomas may be removed by enucleation. Care should be taken to achieve total tumor capsule removal to prevent tumor recurrence. If enucleation is not possible, a larger pancreatic resection including pancreaticoduodenectomy may be necessary. This should only rarely be required. When metastatic insulinoma is found on a patient's initial presentation, the organ spread is to liver and sometimes to bone.
  • Avoid total pancreatectomy because of its high morbidity and mortality rates.
  • Major resections, such as the Whipple procedure, may become necessary when the tumor is found in the pancreatic head and local excision is not possible.
  • Resect all gross disease when multiple tumors or metastases are present.
  • If insulinoma is associated with MEN 1, the management strategy is modified because tumors are often multiple, diffusely spread in the pancreas, and of small size. Definite cure by surgery is rare.
  • Subtotal pancreatectomy with enucleation of tumors from the pancreatic head and uncinate processus often is recommended over simple enucleation because of frequent multiple tumors in MEN 1.
  • Intraoperative serum insulin measurements recently have been employed to ensure complete tumor removal. This may be important, particularly in patients with MEN 1 who harbor multiple insulinomas.
• Tumor is found to be metastatic at surgery in about 5-10% of patients. It would be extremely uncommon for metastases to develop in a case in which only a solitary lesion was found on initial presentation.
  • If the patient is responsive to diazoxide, continue it, while more invasive imaging studies are performed before repetitive surgery is considered.
  • If the patient is not responsive (5-10%) or if drug intolerance is present and ectopic disease is excluded, a blind distal two-thirds pancreatectomy may be performed. (This procedure has only a 25% success rate.)
  • Most authorities recommend serial sectioning during resection.
  • Tumors that are not found at surgery normally are located in the pancreatic head (54%), body (20%), and tail (14%).
• Metastatic disease found
  • Even when metastases are found, surgical excision is often feasible before any medical, chemotherapeutic, or other interventional therapy is considered.
  • Resect all gross disease, including wedge resections of hepatic metastases.
  • Avoid ligation of the hepatic artery in case further regional infusion therapy becomes necessary.

Medical Care

Medical therapy is indicated in patients with malignant insulinomas and in those who will not or cannot undergo surgery. These measures are designed to prevent hypoglycemia and, in patients with malignant tumors, to reduce the tumor burden. In malignant insulinomas, dietary therapy with frequent oral feedings or enteral feedings may control mild symptoms of hypoglycemia. A trial of glucagon may be attempted to control hypoglycemia.

• Diazoxide is related to the thiazide diuretics and reduces insulin secretion. Adverse effects include sodium retention, a tendency to congestive cardiac failure, and hirsutism.
• Prescribe hydrochlorothiazide to counteract the edema and hyperkalemia secondary to diazoxide and to potentate its hyperglycemic effect.
• Of patients with insulinoma, 50% may benefit from the somatostatin analogue octreotide to prevent hypoglycemia.²²
  • The effect of the therapy depends on the presence of somatostatin receptor subtype 2 on insulinoma tumor cells.
  • As studies have shown, an OctreoScan is not a prerequisite before starting octreotide treatment. In patients with insulinoma and a negative scan finding, somatostatin decreased insulin levels significantly and lowered the incidence of hypoglycemic events.
• CT-guided radiofrequency ablation has been used successfully to treat insulinoma in an elderly patient whose hypoglycemia that was refractory to diazoxide, and who was not a candidate for surgery because of comorbidities and poor physical condition.

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Surgical versus nonsurgical management of pancreatic pseudocysts^-www.drkeyurbhatt.in*

J Clin Gastroenterol. 2009 Jul;43(6):586-90.

Johnson MD, Walsh RM, Henderson JM, Brown N, Ponsky J, Dumot J, Zuccaro G, Vargo J.

Department of General Surgery, Cleveland Clinic Foundation, Cleveland, OH 44195, USA.

Abstract

GOALS: Compare patient characteristics and outcome and also physician referral patterns between surgically and nonsurgically managed patients with pancreatic pseudocysts.

BACKGROUND: Treatment of pancreatic pseudocysts can be accomplished by surgical, endoscopic, or percutaneous procedures. The ideal treatment method has not yet been defined.

PATIENTS: All patients treated for pancreatic pseudocyst between 1999 and 2005 were identified in our health services database. Patients were treated with surgical, endoscopic, and percutaneous drainage procedures at the discretion of the treating physician. Main outcome measures included complications, pseudocyst resolution, and treatment modality as a function of the treating physician's specialty.

RESULTS: Thirty patients (49%) were treated surgically, 24 endoscopically (39%), and 7 (11%) with percutaneous drainage. The most common indications for treatment were symptoms of pain, and biliary or gastric outlet obstruction (81%). Patients treated surgically and endoscopically were similar in terms of age (49 vs. 52 y), mean cyst diameter (9.1 vs. 9.5 cm, P=0.74), incidence of chronic pancreatitis (50% vs. 32%, P=0.26) and complicated pancreaticobiliary disease (69% vs. 60%). There were no differences in complications (20% vs. 21%) or pseudocyst resolution (93.3% vs. 87.5%, P=0.39) between the surgical and endoscopic groups. There was no significant difference in the rate of surgical versus nonsurgical treatment in patients initially evaluated by surgeons versus nonsurgeons.

CONCLUSIONS: Surgical and endoscopic interventions for pancreatic pseudocysts are equally safe and effective with percutaneous drainage playing a less important role. Endoscopic drainage should be considered for initial therapy in appropriate patients.

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Clinical trial: a randomized trial comparing fluoroscopy guided percutaneous technique vs. endoscopic ultrasound guided technique of coeliac plexus block for treatment of pain in chronic pancreatitis^-www.drkeyurbhatt.in*

Santosh D, Lakhtakia S, Gupta R, Reddy DN, Rao GV, Tandan M, Ramchandani M, Guda NM.

Department of Anesthesiology, Asian Institute of Gastroenterology, Asian Institute of Gastroenterology, Hyderabad, India. sant_dari@yahoo.com

Abstract

BACKGROUND: Coeliac plexus block (CPB) is a management option for pain control in chronic pancreatitis. CPB is conventionally performed by percutaneous technique with fluoroscopic guidance (PCFG). Endoscopic ultrasound (EUS) is increasingly used for CPB as it offers a better visualization of the plexus. There are limited data comparing the two modalities.

AIM: To compare the pain relief in chronic pancreatitis among patients undergoing CPB either by PCFG technique or by EUS guided technique.

METHODS: Chronic pancreatitis patients with abdominal pain requiring daily analgesics for more than 4 weeks were included. Fifty six consecutive patients (41 males, 15 females) participated in the study. EUSG-CPB was performed in 27 and PCFG-CPB in 29 patients. In both the groups, 10 mL of Bupivacaine (0.25%) and 3 mL of Triamcinolone (40 mg) were given on both sides of the coeliac artery through separate punctures.

RESULTS: Pre and post procedure pain scores were obtained using a 0-10 visual analogue scale. Improvement in pain scores was seen in 70% of subjects undergoing EUS-CPB and 30% in Percutaneous- block group (P = 0.044).

CONCLUSIONS: EUS-guided coeliac block appears to be better than PCFG-CPB for controlling abdominal pain in patients with chronic pancreatitis.

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Surgical treatment of chronic pancreatitis--a 14 years experience^-www.drkeyurbhatt.in*

Stroescu C, Dima S, Scarlat A, Ivanov B, Bouaru O, Ionescu M, Vasilescu C, Popescu I.

Centrul de Chirurgie Generală si Transplant Hepatic, Institutul de Boli Digestive si Transplant Hepatic Fundeni, Bucureşti. cezar.stroescu@gmail.com

Abstract

BACKGROUND: Operative treatment of chronic pancreatitis is indicated for patients with intractable pain after failed medical and endoscopic treatment, or in the presence of complications of the disease.

AIMS: This study evaluates a single-center experience with operative management of chronic pancreatitis over a period of time of 14 years, regarding indication, surgical technique, early and late results.

PATIENTS AND METHODS: The records of 265 consecutive patients who underwent surgery for chronic pancreatitis between 1995 and 2008 were retrospectively reviewed and analyzed. Long-term outcomes were assessed by patient survey, with a median follow-up of 40 months.

RESULTS: 265 patients underwent 275 operations for chronic pancreatitis with the main indication abdominal pain (46.8%), followed by suspected malignancy in 24.8% and recurrent episodes of acute pancreatitis in 18.6%. Resection procedures 54.5% (150), drainage procedures 1.09% (3), bypass and denervation procedures 44.36% (122) and exploratory laparotomy 3.27% (9) were performed with an overall morbidity of 22% and an in-hospital mortality rate of 2.64%. After a median follow-up of 40 months survival information was available for 137 patients (51.69%) with a 5-and actuarial survival rate of 74.7% and quality of life improvement in most patients, especially in the resected group.

CONCLUSION: Our results suggest that in chronic pancreatitis the type of surgery has to be individualized in each patient (resection VS drainage) and organ preserving operations are safe and effective in providing long-term pain relief and in treating CP-related complications

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