Hernia is defined as protrusion of viscus or a part or viscus through a weakness or hole in other body tissue. Medically it is defined as a protrusion of a viscus or a part of a viscus through an abnormal opening in the walls of it  containing cavity. Hernia are see elsewhere in the body but the most common are inguinal, femoral and umbilical  hernias accounting for 75% of all cases.

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Primary sclerosing Cholangitis (PSC) is a cholestatic liver disease characterized by fibrotic strictures involving the intrahepatic and extrahepatic biliary tree in the absence of a known precipitating cause. It is a progressive disease that eventually results in biliary cirrhosis. PSC is a risk factor for cholangiocarcinoma which may occur in 4% to 20% of people.

What cause the primary sclerosing cholangitis?

The exact causes of PSC is unknown but believed that it is strongest associated with inflammatory bowel disease and ulcerative colitis.  PSC is more common in certain HLA haplotypes such as B8/DR3

What are the pathological changes in primary sclerosing cholangitis?

Liver biopsy shows periductal concentric fibrosis around the macroscopic bile ducts .Obliterative fibrosis cholangitis or concentric fibrosis with obliteration of the small ducts is virtually diagnostic but is seen in less than 10% of cases .Additional findings may include cholestasis, inflammation and secondary biliary sclerosis.

What are the sign and symptoms of primary sclerosing cholangitis?

• Male are more than female.
• Most patients can be asymptomatic.
• Mean age at presentation is 40 to 45 years.
• Jaundice
• Pruritus
• Fatigue
• Condition is characterized by relapses and remission with quiescent period.

How to diagnosed Primary sclerosing cholangitis?

Diagnosis relies on clinical findings, Labatory data, Imaging studies and Liver biopsy.

Laboratory studies reveled:

• Elevated alkaline phosphatase out of proportion to the bilirubin.
• Serum transaminase may be elevated.

Imaging studies:

ERPC and PTC show diffuse and irregular narrowing of the entire biliary tree and short annular strictures giving a beaded appearance. Cholangiography is the gold standard diagnosis of PSC.

If diagnosis is uncertain liver biopsy is needed.

How to managed primary sclerosing cholangitis (PSC)?

• Symptomatic management with use of various drugs aimed at reversing the presumed autoimmune etiology, including corticosteroids immunosuppressive agents, mehotrexate and D-penicillamine.
• Ursodeoxycholate lower serum bilirubin and transaminase.
• Antibiotic are used to manage recurrent biliary sepsis.
• PSC is effectively palliated with endoscopic or percutaneous dilatation of strictures.
• If above management fails operative intervention is required to placement of stent after dilatation.

1. Resection or bypass of localized strictures.
2. Extensive, diffuse stricture disease with end stage cirrhosis is an indication for orthotopic liver transplantation.

What is the prognosis of PSC?

Many patients have a course that progressive to cirrhosis and liver failure despite early palliative interventions. Median length of survival from diagnosis of death or liver transplantation is 10 to 12 years.

References:

1. Sabiston textbook of surgery 18th edition
2. Bailey and love, surgery 25th edition
3. The Washington manual of surgery, 5th edition.
4. emedicine.medscape.com

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Paralytic ileus is a condition characterized by the symptoms of abdominal bowel obstruction like nausea, vomiting, and vague abdominal discomfort due to neuromuscular failure, metabolic disturbance, and post abdominal surgery. Diagnosis is based on x-ray findings and clinical findings.

What causes the paralytic ileus?

1. Postoperative: ileus usually occurs after any abdominal procedure.
2. Infection: intra-abdominal sepsis may cause ileus.
3. Reflux ileus: due to facture spine or ribs, retroperitoneal hemorrhage.
4. Metabolic disturbance: hypokalemia, uremia are the most common contributory factors.

Sign and symptoms of paralytic ileus.

Irrespective of the cause ,paralytic ileus has the sign and symptoms of bowel obstruction which includes:

1. Abdominal distension
2. Vague abdominal discomfort and generalized abdominal pain.
3. Nausea and vomiting
4. No bowel sound during auscultation
5. No passage of stool and flatus.

Diagnosis of Paralytic ileus

Diagnosis relies on patient history and physical examination. Abdominal x-ray, Ultrasound or CT, blood tests and serum electrolyte confirm the diagnosis.

How to managed paralytic ileus?

The essence of treatment is prevention, with the use of nasogastic tube and restriction of oral intake until bowel sound and passage of flatus return. Electrolyte must be substituted. Patients with intra abdominal sepsis are managed with giving broad spectrum antibiotics.

Early introduction of fluids and solids is, however, becoming popular.

Specific treatment is directed towards the cause, but the following general principle applies:

• The primary cause must be removed.
• Gastrointestinal distension must be relieved by decompression
• Close attention to fluid and electrolyte balance is mostly required.
• There is no role for the routine use of peristaltic stimulants
• If paralytic ileus is prolonged and threatens life, a laparotomy should be considered to exclude a hidden cause and facilitate bowel decompression.

References:

• Sabiston textbook of surgery 18th edition
• Bailey and love, surgery 25th edition
• The Washington manual of surgery, 5th edition.
• emedicine.medscape.com

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Juvenile polyposis syndrome is the autosomal dominantly inherited condition is characterized by the development of multiple rectal and colonic polyps around puberty. Polyps are non-neoplastic, hamartomatous which are the growth arising from the lumen of the stomach or colon. It is non cancerous but there is an increased risk of development of adenocarcinoma.

What causes the Juvenile polyposis syndrome?

Juvenile polyposis syndrome is caused by the mutation in the BMPR1A and SMAD4 gene on chromosome 5.

What are the symptoms and sign of Juvenile polyposis syndrome?

There is no any specific sign and symptoms for this condition but some people have

• Rectal bleeding
• Anemia
• Abdominal pain,
• Constipation
• Diarrhea

How to Diagnosed Juvenile polyposis syndrome?

Diagnosis of juvenile polyposis syndrome includes:

1. Family history of juvenile polyposis syndrome
2. On endoscopy, colonoscopy or Sigmoidoscopy presents of polyps that vary in shape of size.
3. Mutation of BMPR1A gene or the SMAD4 gene.

How to managed Juvenile polyposis syndrome?

Surgery is the only treatment option for this syndrome.  If the condition is pre-malignant, a total colectomy must be performed; often, the rectum can be preserved, but regular flexible endoscopy and removal of polyps before they developed carcinoma are required.If patients developed adenomas, colonoscopic polypectomy is required.

What is the prognosis of Juvenile polyposis syndrome?

Juvenile polyposis syndrome is the non cancerous condition but is considered to be at increased risk of developing stomach, colorectal, intestine and pancreatic cancers. 9% to 50% have the risk of developing cancer

References:

• Sabiston textbook of surgery 18th edition
• Bailey and love, surgery 25th edition
• The Washington manual of surgery, 5th edition.
• emedicine.medscape.com

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1. Exploding head syndrome

Short bowel syndrome is a condition of malabsorption (nutrients are not properly absorbed) due to extensive resection (<150cm of remaining) of small intestine or severe intestinal disease likes mesenteric ischemia, crohn disease, or necrotizing enterocolitis. The clinical presentation of patients with short bowel syndrome is dependent upon the nature and extent of intestinal resection.

What causes the Short bowel syndrome?

Short bowel syndrome is caused by:

1. Crohn’s disease
2. Volvulus
3. Necrotizing enterocolitis
4. Tumors of the small intestine
5. Intussusception
6. Injury of bowel
7. Surgical removal of small intestine

What is the Pathophysiolgy of Short bowel syndrome?

Physiologic of short-bowel syndrome is result form the loss of large amounts of intestinal absorptive surface area. The sequelae of this loss include malabsorption of electrolytes water, macronutrients like carbohydrates, fats, proteins and micronutrients include  vitamins, minerals,

What are the symptoms of Short bowel syndrome?

1. The symptoms of short bowel syndrome can include:
2. Fatigue
3. Diarrhea and steatorrhea
4. Abdominal pain
5. Fluid and electrolyte deficiency
6. Micro Nutrition (Iron, magnesium, zinc, copper and vitamins) deficiency

What are the complications of short bowel syndrome?

Complication caused by malabsorption of vitamins and minerals, complication include:

• Anemia
• Hyperkeratosis (scaling of the skin)
• Easy bruising
• Muscle spasms
• Poor blood clotting
• Bone pain

How to diagnosed short bowel syndrome?

Short bowel syndrome is diagnosed by history, clinical presentation, Blood albumin test, complete blood count and fecal fat test.

Is there a cure of Short bowel syndrome?

There is no cure of short bowel syndrome but some treatment available that can effectively reduce the symptoms and complication of the disease. Treatment includes:

• High-calorie diets
• Vitamins and mineral replacement
• Anti diarrheal medicine ( loperamide, codeine)
• H2 blocker and proton pump inhibitors to reduce stomach acid
• Parenteral nutrition

If above treatment fail to improve symptoms surgery likes intestinal transplantation or intestinal lengthening surgery may tired.

References:

• Sabiston textbook of surgery 18th edition
• Bailey and love, surgery 25th edition
• The Washington manual of surgery, 5th edition.
• emedicine.medscape.com

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1. Premenstrual syndrome(PMS)
2. HELLP Syndrome
3. Exploding head syndrome

Dumping syndrome is a group of symptoms that occurs following ingestion of a meal when who have undergone gastric bypass surgery. It is typically induced when the patient eats certain foods, such as sweets or carbohydrate sources. Dumping syndrome exists in either a late or an early form, with the early form occurring more frequently.

What is early dumping?

Early dumping usually occurs with in 20 to 30 minutes after ingestion of meal and accompanied by both GI and cardiovascular symptoms. The GI symptoms include nausea and vomiting, a sense of epigastric fullness, cramping abdominal pain, and often diarrhea. The cardiovascular symptoms include palpitation, tachycardia, diaphoresis, fainting, dizziness, flushing, and occasionally blurred vision. Usually GI symptoms are most common.

Although the exact sequence of events responsible fro this syndrome remains to be fully defined, it is generally agreed that it occurs because of the rapid passage of food of high osmolality from the stomach into the small intestine. The resultant hypertonic food bolus passes into the small intestine lumen to achieve isotonicity. After this shift extracelluar fluid, luminal distention occurs and induces the autonomic responses.

The symptoms associated with early dumping syndrome appear to be secondary to the release of several humoral agents, such as serotonin, bradykinin-like substance, neurotensin and enteroglucagon.

What is late dumping?

The syndrome of late dumping appears 2 to 3 hours after a meal and is far less common than early dumping syndrome. When carbohydrate rapidly delivers to small intestine, they are quickly absorbed, resulting in hyperglycemia, which triggers the release of large amounts of insulin to control the rising blood glucose. This results in an actual overshooting such that a profound hypoglycemia occurs in response to the insulin. The activates the adrenal gland to release catecholamines, which result in diaphoresis, tremulousness, light-headedness, tachycardia, and confusion. The symptoms complex is indistinguishable from insulin shock.

How dumping syndrome is diagnosed?

Usually, the symptoms of dumping are sufficiently obvious that the diagnosis can be on this basis alone; however if there is doubt, gastric emptying scans can be obtained that demonstrate rapid gastric emptying. Alternatively a provocation test can be done in the form of a 200 ml, meal of 50% glucose solution and water. Patients with this syndrome have their symptoms elicited after ingestion of this glucose solution.

Is there a treatment for dumping syndrome?

There is no any specific treatment for this syndrome, most however, experiences spontaneous relief and require no specific therapy. In those situations in which symptoms are prolonged, dietary measures are usually sufficient. These include avoiding foods containing sugar, frequent feeding on small meals rich in protein and fat. Recently the long acting somatostatin analogue octreotide acetate has been shown be highly effective in preventing the development of GI and cardiovascular symptoms.

In the fewer patients who fail to response to the conservative measures mentioned above, operative intervention may become necessary.

References:

• Sabiston textbook of surgery 18th edition
• Bailey and love, surgery 25th edition
• The Washington manual of surgery, 5th edition.
• emedicine.medscape.com

Related posts:

1. HELLP Syndrome
2. Premenstrual syndrome(PMS)
3. Sweet’s syndrome

Hirschsprung’s disease is a developmental disorder that is present at birth but may not be diagnosed until later childhood. It is characterized by defecation difficulty of failure. The disease is often called congenital megacolon, because the proximal colon may become grossly enlarged with impacted feces, or congenital aganglionosis, because the ganglia of the intestine. Mutations in RET or endothelia genes account for the disease in some patients.

Enteric neurons may be absent in the rectosigmoid region only, in the descending colon, or in the entire colon. The aganglionic region appears constricted as a result of continuous contractile activity of the circular muscle, whereas the normally innervated intestine proximal to the aganglionic segment is distended with feces.

The constricted terminal segment of the large intestine in Hirschsprungs disease presents a functional obstruction to the forward passage of fecal material. Constriction and narrowing of the lumen of the segment reflects uncontrolled myogenic contractile activity in the absence of motor neurons.

Symptoms:
Symptoms appear right after a baby is born
1. Failure to pass stool within the first or second day of life.
2. Constipation of gas, which may a newborn
3. Vomiting
4. Diarrhea

In older children symptoms are
a. Swollen abdomen
b. Lack of weight gain

Pathology:
Pathologically by absent ganglion cells in the myenteric (Auerbach’s) & submucosal (Meissner’s) plexus. The neurogenic abnormality is associated with muscular spasms of the distal colon and internal anal sphincter resulting in a functional obstruction.
Diagnosis:
1. Radiology
2. Barium enema shows rectum is wider than the sigmoid colon.
3. Failure of the completely evacuate the installed contrast material after 24 hours would also consider with Hirschsprung’s disease.
4. Anorectal manometer shows failure of the internal sphincter to relax when the rectum is distended with a balloon.
5. Rectal biopsy is the gold standard for diagnosed Hirschsprung’s disease, absent ganglia, hypertrophied nerve trunks, & robust immunostaining for acetylcholinesterase are the pathologic criteria to make the diagnosis.

Management:
Multiple surgical options exist:
a. Diverting colostomy
b. Swenson procedure aganglionic bowel is removed and a coloanal anastomosis on the perineum.
c. Duhamel procedure.

Complication: Constipation is the most frequently post operative problem followed by soiling, incontinence, and enterocolitis.

References:
1. Short practice of surgery, Bailey and love 25th edition.
2. Short practice of surgery, Sabiston 18th edition.
3. Medical physiology, Lippincott Williams & Wilkins 3rd edition.

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Disorder of gastric motility can be divided into the broad categories of delay and rapid emptying. The generalized symptoms of both disorder overlap.

Delayed gastric emptying is common is diabetes mellitus and may be related to disorder of the vagus nerves, as part of a spectrum of autonomic neuropathy. Surgical vagotomy results in a rapid emptying of liquid and delayed emptying of solids. As mentioned later, vagotomy impairs adaptive relaxation and results in increased contractile tone in the reservoir. Increased pressure in the gastric antral pump. Paralysis with a loss of propulsive motility in the antrum occurs after a vagotomy. The result in gastroparesis, which can account for the delayed emptying of solids after a vagotomy. When selective vagotomy is performed as a treatment for peptic ulcer disease, the pylorus is enlarged surgically (pyloroplasty) to compensate for postvagotomy gastroparesis.

Delayed gastric emptying with no demonstrable underlying condition is common. Up to 80% of patients with anorexia nervosa have delayed gastric emptying of solids. Another such condition is idiopathic gastric stasis, in which no evidence of an underlying condition can be found. Motility-stimulating drugs are used successfully in treating these patients. In children, hypertrophic pyloric stenosis impedes gastric emptying. This is a thickening of the muscles of the pyloric canal associated with a loss of enteric neurons. The absence of inhibitory motor neurons and the failure of the circular muscles to relax account for the obstruction stenosis.

Rapid gastric emptying often occurs in patients who have had both vagotomy and gastric antrectomy for the treatment of peptic ulcer disease. These individuals have rapid emptying of solids and liquids. The pathological effects are referred to the dumping syndrome, which results form the dumping of large osmotic loads into the proximal small intestine.

References:

• Sabiston textbook of surgery 18th edition
• Bailey and love, surgery 25th edition
• The Washington manual of surgery, 5th edition.
• emedicine.medscape.com

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Intestinal pseudoobstruction is characterized by symptoms of intestinal intestine obstruction in the absence of a mechanical obstruction. The mechanisms for controlling orderly propulsive motility fail while the intestinal lumen is free form obstruction. This syndrome may result from abnormalities of the muscles of ENS. In general symptoms of colicky abdominal pain, nausea and vomiting, and abdominal distension simulate mechanical obstruction.Pseudoobstruction may be associated with degenerative changes is the ENS. Failure of propulsive motility reflects the loss of the neural networks that program and control the organized motility patterns of the intestine. This disorder can occur in varying lengths of intestine of in the entire length of the small intestine. Contractile behavior of the of the circular muscle is hyperactive but disorganized in the denervated segments. The behavior reflects the absence of inhibitory nervous control of the muscles, which are self-excitable when, released form the braking action of enteric inhibitory neurons.

Another form of pseudoobstruction is paralytic ileus characterized by prolonged motor inhibition .The electrical slow waves are normal but muscular action potentials and contractions are absent. Prolonged ileus commonly occurs after abdominal surgery. The illus. results form suppression of the synaptic circuits that organize propulsive motility in the intestine. A probable mechanism is presynaptic inhibition and the closure of the synaptic gates.Continuous discharge of the inhibitory motor neurons accompanies suppression of the motor circuits. This activity of the inhibitory motor neurons prevents the circular muscle form responding to electrical slow waves, which are undisturbed in ileus.

References:

1. Short practice of surgery, bailey and love, 25th edi.
2. Harrison’s Principles of Internal Medicine, 17th edition.
3. Davidson’s Principles and Practice of Medicine, 20th Edition
4. The Washington Manual of surgery, 5th edition.
5. Medical physiology, Lippincott Williams & Wilkins 3rd edi.

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Failure of peristalsis in the esophageal body or failure of the lower esophageal sphincter to relax will result in dysphagia or difficulty in swallowing. Some people show abnormally high pressure waves as peristalsis propagates past the recording ports on manometric catheters. This condition called nutcracker esophagus, is sometimes associated with chest pain that may be experienced as angina-like pain.

On diffuse spasm, organized propagation of the peristaltic behavioral complex fails to occur after a swallow. Instead, the act of swallowing results in simultaneous contraction all along the smooth muscle esophagus. On manometric tracings, this response is observed as a synchronous rise in intraluminal pressure at each of the recording sensors.

In achalasis of the lower esophagus sphincter, the sphincter fails to relax normally during a swallow. As a result, the ingested material does not enter the stomach and accumulates in the body of the esophagus. This leads to megaesophagus, in which distension and gross enlargement of the esophagus areevident. In advanced untreated cases of achalasis, peristalsis does not occur in response to a swallow.

Achalasis is a disorder of inhibitory motor neurons in the lower esophageal sphincter. The number of neurons in the lower esophageal sphincter is reduced, and the levels of the inhibitory neurotransmitter VIP and the enzyme NO synthase are diminished. This degenerative disease results in a loss of the inhibitory mechanism for relaxing the sphincter with appropriate timing for a successful swallow.

Symptoms of achalasis include progressive dysphagia, noted by essentially all patients; regurgitation immediately after meals (>70%); odynophagia (30%); and aspiration, with resultant bronchitis and pneumonia. Some patient experience chest pain due to esophageal spasms

The diagnosis is suggested by a chest x-ray, which often shows a fluid filled, dilated esophagus and absence of gastric air bubble. A barium esophagogram shows tapering (bird’s beak) of the distal esophagus and dilated proximal esophagus. Esophageal manometry is thedefinitive diagnostic test for the achalasis.

Achalasis is managed by medical and surgical method; medical treatment is aimed at decreasing the LES (lower esophageal sphincter) tone and includes nitrates, calcium channel blockers and endoscopic injection of botulism toxin.

Surgical treatment with a modified Heller esophagomotomy has been shown to produce excellent results in 95% of patients .Video-assisted thoracoscopic approaches have been tried. More recently, laparoscopic esophagomotomy combined with partial Fundaplication has been has been reported, and it is rapidly being adopted by most centers as the primary surgical option.

References:

1. The Washington Manual of surgery, 5th edition.
2. Medical physiology, Lippincott Williams & Wilkins 3rd edi.
3. Harrison’s Principles of Internal Medicine, 17th edition.
4. Davidson’s Principles and Practice of Medicine, 20th Edition

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Abstract

Background: Studies indicate that adjuvant 5-fluorouracil (5-FU) with folinic acid (FA) in colorectal cancer patients with completely resectable liver-limited metastases (LMCRC) offers clinical benefit over surgery alone. This phase III trial compared FOLFIRI with simplified 5-FU/FA in this setting.
Patients and methods: LMCRC patients were randomized to receive every 14 days, FA, 400 mg/m² infused over 2 h, followed by 5-FU as a 400 mg/m² i.v. bolus, followed by continuous 5-FU infusion, 2400 mg/m² over 46 h (LV5FUs) with or without irinotecan: 180 mg/m² infusion (FOLFIRI). The primary end point was disease-free survival (DFS); secondary end points included overall survival (OS) and safety.
Results: Treated patients (n = 306) were balanced for critical prognostic factors in each arm. Median DFS in patients receiving LV5FUs was 21.6 versus 24.7 months for FOLFIRI [hazard ratio (HR) 0.89, log-rank P = 0.44]. No significant differences were found in OS. A trend was observed for improved DFS in patients receiving FOLFIRI within 42 days of surgery (HR 0.75, P = 0.17). Grade 3/4 toxic effects were more common in patients treated with FOLFIRI versus LV5FUs (47% versus 30%) with neutropenia being most common (23% versus 7%).
Conclusion: FOLFIRI in the adjuvant treatment of LMCRC showed no significant improvement in DFS compared with LV5FUs.

Introduction

Colorectal cancer (CRC) is in the top four most common cancers worldwide and was responsible for over 500 000 deaths in 2002.^[1] Up to 25% of CRC patients present with metastatic disease (mCRC), with the most common site for metastases being the liver.^[2] An additional 35%–45% of patients will develop liver metastases during the course of their disease, with 20%–30% of patients having liver-limited metastases (LMCRC).^{[2, 3]} The prognosis for mCRC patients is poor with 5-year survival rates of 4% reported for untreated patients^[4] and 3-year survival rates of 5%–10% in patients treated with palliative 5-fluorouracil (5-FU) and folinic acid (FA).^[5] A proportion of LMCRC patients are eligible for surgery with curative intent, which if successful has been reported to achieve 5-year survival rates of between 25% and 40%.^[6–8] However, most treatment failures are due to local hepatic recurrences or metastases to the lungs, occurring within the first 2 years of surgery, raising the question of whether adjuvant therapy should be used in this setting.

Adjuvant 5-FU-based chemotherapy following surgery in patients suffering stage III CRC provides significant improvements in disease-free survival (DFS) and overall survival (OS) compared with surgery alone,^[9–11] providing a rationale for its use in the adjuvant treatment of LMCRC patients following complete resection of metastases. A number of small studies indicate that significant patient benefit may be obtained from such an approach.^[12–15] In a study in which LMCRC patients were randomized to receive postoperative local hepatic arterial infusion (HAI) of floxuridine in combination with i.v. continuous 5-FU or surgery alone, a significant improvement in 4-year recurrence-free rate (46% versus 25%) was reported in patients receiving adjuvant therapy.^[15] However, in a comparable larger study, adjuvant treatment was stopped due to toxicity associated with HIA.^[16] More recently, Portier et al.^[17] demonstrated in a multicenter randomized study, a significant improvement in 5-year DFS rate (33.5% versus 26.7%) in LMCRC following complete resection receiving systemic adjuvant 5-FU/FA compared with patients receiving surgery alone.

The combination of 5-FU/FA with irinotecan (FOLFIRI) has been reported to provide a significant improvement in the palliative treatment of mCRC patients compared with 5-FU/FA alone, with median survival times in excess of 20 months reported.^[18–21] A small phase II study reported tolerability of single-agent irinotecan in CRC patients previously treated with 5-FU following complete resection of colorectal hepatic metastasis.^[22] However, there are currently no published randomized studies on the use of FOLFIRI in the adjuvant treatment of completely resectable LMCRC patients. In the present study, we report the results from a multicenter, randomized, phase III trial comparing FOLFIRI versus simplified 5-FU with leucovorin (LV, also known as FA) (LV5FUs) as adjuvant treatment in LMCRC patients following complete resection of metastases.

Article taken from sciencedirect.com

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With the recent development of double-balloon endoscopy (DBE) and capsule endoscopy (CE), it has become possible to observe the entire small bowel endoscopically. DBE enables us to make detailed observations and at the same time takes biopsy samples. Single-balloon endoscopy (SBE), which has a balloon only at the tip of the overtube, has also been introduced. Since DBE and SBE are similar in the concept of insertion method, a general term ‘balloon-assisted endoscopy’ (BAE) is used when referring to these methods. Characteristic small bowel lesions observed with BAE in Crohn’s disease are aphthoid ulcers, round ulcers, irregular ulcers and longitudinal ulcers. These ulcers tend to be located on the mesenteric side of the small bowel. Since BAE can determine the location (mesenteric or antimesenteric side) of the ulceration, it is useful in distinguishing Crohn’s disease from other diseases that have ulcers in the small bowel. Strictures are a major clinical problem in the course of Crohn’s disease. Traditionally, surgery was the main choice for small bowel strictures. In some cases, strictures located in distal ileum or proximal jejunum have been dilated using standard enteroscopes. DBE now enables balloon dilatation to be performed endoscopically even in the deep small bowel.

Introduction

Crohn’s disease was first reported by Crohn et al. in 1932 as ‘regional ileitis’ with chronic granulomatous inflammation of the terminal ileum [Chron et al. 2000]. Today, Crohn’s disease is known to be a chronic inflammatory disease of unknown origin that can occur not only in the terminal ileum but anywhere in the gastrointestinal tract [Feagans et al. 2008].

Small bowel lesions occur frequently in Crohn’s disease. Traditionally, diagnosis and assessment of the small bowel lesions in Crohn’s disease has depended on X-ray tests, such as small bowel follow-through (SBFT) and computed tomography (CT). In recent years, however, new endoscopic modalities such as capsule endoscopy (CE) [Iddan et al. 2000] and balloon-assisted endoscopy (BAE) including both double-balloon endoscopy (DBE) [Monkemuller et al. 2007; Zhong et al. 2007; Heine et al. 2006; May and Ell, 2006; Yamamoto et al., 2001] and single-balloon endoscopy (SBE) have been developed. These instruments have enabled us to obtain clear endoscopic images of the small bowel which are useful in making more accurate diagnosis and evaluation of the small bowel lesions in Crohn’s disease [Oshitani et al. 2006]. Endoscopic-balloon dilation (EBD) for intestinal strictures has also become possible in a broader area of the small intestine with DBE [Fukumoto et al. 2007; Pohl et al. 2007]. In this report, we will discuss the diagnosis and treatment of small bowel lesions in Crohn’s disease, focusing on DBE, which was developed mainly in our hospital.

reff:

Ther Adv Gastroenterol. 2009;2(6) © 2009 Sage Publications, Inc

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Pre- and peri-operative strategies are becoming standard for the management of Localized gastro-esophageal cancer. For localized gastric/gastro-esophageal junction (GEJ) cancer there are conflicting data that a peri-operative approach with cisplatin-based chemotherapy improves survival, with the benefits seen in esophageal cancer likely less than a 5—10% incremental improvement. Further trends toward improvement in local control and survival, when combined chemotherapy and radiation therapy are given pre-operatively, are suggested by recent phase III trials. In fit patients, a significant survival benefit with pre-operative chemoradiation is seen in those patients who achieve a pathologic complete response. In esophageal/GEJ cancer, definitive chemoradiation is now considered in medically inoperable patients. In squamous cell carcinoma of the esophagus, surgery after primary chemoradiation is not clearly associated with an improved overall survival, however, local control may be better. In localized gastric/GEJ cancer, the integration of bevacizumab with pre-operative chemotherapy is being explored in large randomized studies, and with chemoradiotherapy in pilot trials. The addition of anti-epidermal growth factor receptor and anti-human epidermal growth factor receptor-2 antibody treatment to pre-operative chemoradiation continues to be explored. Early results show the integration of targeted therapy is feasible. Metabolic imaging can predict early response to pre-operative chemotherapy and biomarkers may further predict response to pre-operative chemo-targeted therapy. A multimodality approach to localized gastro-esophageal cancer has resulted in better outcomes. For T3 or node-positive disease, surgery alone is no longer considered appropriate and neo-adjuvant therapy is recommended. The future of neo-adjuvant strategies in this disease will involve the individualization of therapy with the integration of molecular signatures, targeted therapy, metabolic imaging and predictive biomarkers.

Introduction

Globally both gastric and esophageal cancers are significant health problems and account for approximately 1.4 million new cases per year with 1.1 million cancer-related deaths [Parkin et al. 2005]. This annual mortality is higher than that for both breast and colorectal cancers combined. In the United States, in 2008, an esti­mated 16,470 patients will be diagnosed with esophageal cancer resulting in 14,280 deaths, making this disease the seventh leading cause of cancer death in men, and 21,500 cases of gastric cancer will be diagnosed resulting in 10,880 deaths [Jemal et al. 2008].

The last three decades have seen a dramatic epi-demiologic shift in the location of both gastric and esophageal cancers as well as the histologic sub­type of esophageal cancers. Tumors of the lower esophagus and proximal stomach are classified as gastro-esophageal junction (GEJ) cancers and this cancer has been increasing in incidence by 5—10% per year since the mid 1970s and is the most rap­idly increasing cancer in many Western countries [Kamangar et al. 2006]. Distal esophageal and GEJ adenocarcinoma is now the predominant esophageal cancer subtype, and the majority of gastric cancers are now located in the proximal stomach [Pera et al. 1993].

The 5-year survival of patients with gastro-esophageal cancers (distal esophagus, GEJ, and proximal stomach making up the majority of cases) has not changed significantly over the last 25—30 years. Approximately 50—60% of patients present with distant metastatic disease and median overall survival (OS) with systemic chemotherapy has remained at less than one year [Van Cutsem et al. 2008]. However, progress has been made in the treatment of localized disease. Combinations of pre-operative (neo-adjuvant) chemotherapy, peri-operative chemotherapy or pre-operative (neo-adjuvant) chemoradiotherapy with surgery have resulted in R0 resection rates between 40 and 80% and 5-year survival rates from 20 to 40%.

A variety of combination chemotherapeutic agents have been used in the treatment of gastro-esophageal cancers over the last 30 years. These include fluoropyrimidines, anthracyclines, platinums, taxanes and campothecins. Combining different classes of drug exploits the different modes of action in the cancer cell and may allow lower doses of each individual drug to be given in the combination regimen thus reducing side effects. Work over the last decade has identified distinct molecular pathways lead­ing to tumorigenesis, angiogenesis and metasta­sis. Drug development has led to direct treatment at specific molecular targets. This review will focus on the integration of targeted therapy into the neo-adjuvant treatment of gastro-esophageal cancers.

reference:-

Ther Adv Med Oncol. 2009;1(3):145-165. © 2009

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