A CT scan with IV contrast is needed because a scan without contrast will exclude a perforated viscus but will not be able to determine the presence of pancreatitis.

Acute pancreatitis may be mild or life-threatening but it usually subsides. Gallstones and alcohol abuse are the main causes of acute pancreatitis. Severe abdominal pain is the predominant symptom.

For diagnosis of acute pancreatitis, serum lipase is both more sensitive and specific than serum amylase.
Serum amylase levels do not correlate with disease severity and may give both false positive and negative results. Three scoring systems are used to assess the severity of the disease, which are Glasgow pancreatitis score, Ranson criteria, and APACHE II scoring system.

Management options are as follows:
1. There is very little evidence to support the administration of antibiotics to patients with acute pancreatitis. These may contribute to antibiotic resistance and increase the risks of antibiotic-associated diarrhoea.
2. Patients with acute pancreatitis due to gallstones should undergo early cholecystectomy.
3. Patients with obstructed biliary system due to stones should undergo early ERCP.
4. Patients with infected necrosis should undergo either radiological drainage or surgical necrosectomy.

Complications of ERCP include pancreatitis, duodenal perforation, duodenal haemorrhage, infection, stent migration, and complications secondary to endoscopy. CT is performed if patients have severe abdominal pain, jaundice, elevated white blood cell count, and fever after ERCP.

A gastrinoma is a gastrin-secreting tumour that can occur in the pancreas, although it is most commonly found in the duodenum. Duodenal wall gastrinomas have been identified in 40-50% of patients. These duodenal wall tumours are frequently small and multiple. Sporadic tumours occurring in the pancreas tend to be solitary and have a greater malignant potential as compared to duodenal gastrinomas.

Primary tumours also occur in a variety of ectopic sites, including the body of the stomach, jejunum, peripancreatic lymph nodes, splenic hilum, omentum, liver, gallbladder, common bile duct, and the ovary. Over 50% of gastrinomas are malignant and can metastasize to the regional lymph nodes and the liver. One fourth of gastrinomas are related to multiple endocrine neoplasia (MEN) type I and are associated with hyperparathyroidism and pituitary adenomas.

The symptoms in 90-95% of patients with gastrinomas are similar to the symptoms of common peptic ulcer disease. Usually, persistent abdominal pain exists that is less responsive to medical treatment.
Sometimes, symptoms may relate to a complication of peptic ulcer disease, such as bleeding (e.g., melena, hematemesis), gastric outlet obstruction (e.g., vomiting), and perforation (e.g., peritoneal irritation).
Other symptoms include gastroesophageal reflux, diarrhoea, steatorrhea, and weight loss, all of which are secondary to acid hypersecretion. Vitamin B-12 malabsorption, which is not correctable by oral intrinsic factor, may also be observed.

Somatostatin receptor scintigraphy (SRS) is very useful to identify the primary lesions preoperatively. SRS is the most sensitive non-invasive method for localizing the primary tumours and metastases. It also is helpful for detecting the presence of liver or bone metastasis.

Achalasia is an oesophageal motor disorder characterized by aperistalsis of the oesophageal body and lack of relaxation of the lower sphincter in response to swallows.
Achalasia cardia is one of the common causes of motor dysphagia. Pathophysiologically, achalasia cardia is caused by loss of inhibitory ganglion in the myenteric plexus of the oesophagus. In the initial stage, degeneration of inhibitory nerves in the oesophagus results in unopposed action of excitatory neurotransmitters such as acetylcholine, resulting in high amplitude non-peristaltic contractions (vigorous achalasia); progressive loss of cholinergic neurons over time results in dilation and low amplitude simultaneous contractions in the oesophageal body (classic achalasia).

An anal fissure is a painful linear tear or crack in the distal anal canal, which, in the short term, usually involves only the epithelium and, in the long term, involves the full thickness of the anal mucosa. Typically, the patient reports severe pain during a bowel movement, with the pain lasting several minutes to hours afterward. The pain recurs with every bowel movement, and the patient commonly becomes afraid or unwilling to have a bowel movement, leading to a cycle of worsening constipation, harder stools, and more anal pain. Approximately 70% of patients note bright-red blood on the toilet paper or stool. Occasionally, a few drops may fall in the toilet bowl, but significant bleeding does not usually occur with an anal fissure.
Second-line medical therapy consists of intra-anal application of 0.4% nitro-glycerine (NTG; also called glycerol trinitrate) ointment directly to the internal sphincter. Nitro-glycerine rectal ointment is approved by the US Food and Drug Administration (FDA) for moderate-to-severe pain associated with anal fissures and may be considered when conservative therapies have failed.

In patients with ulcerative colitis (UC) where medical management is not successful, surgical resection (pan-proctocolectomy) may offer a chance of cure. Those patients wishing to avoid a permanent stoma may be considered for an ileoanal pouch. However, this procedure is only offered in the elective setting.

Patients with inflammatory bowel disease (UC and Crohn’s disease) frequently present in surgical practice. Elective indications for surgery in UC include disease that requires maximal therapy or prolonged courses of steroids.

Long-standing UC is associated with a risk of malignant transformation. Dysplastic transformation of the colonic epithelium with associated mass lesions is an absolute indication for a proctocolectomy. Restorative options in UC include an ileoanal pouch. Complications of such a pouch include anastomotic dehiscence, pouchitis, and poor physiological function with seepage and soiling.
.
Emergency presentation of poorly-controlled colitis that fails to respond to medical therapy should usually be managed with a subtotal colectomy. Excision of the rectum is a procedure with a higher morbidity and is not generally performed in the emergency setting.

Rejection is related primarily to activation of T cells, which, in turn, stimulate specific antibodies against the graft. Various clinical syndromes of rejection can be correlated with the length of time after transplantation.

Hyperacute rejection
Hyperacute rejection of the renal allograft happens in the operating room within hours of the transplant, when the graft becomes mottled and cyanotic. This type of rejection is due to unrecognized compatibility of blood groups A, AB, B, and O (ABO) or to a positive T-cell crossmatch (class I human leukocyte antigen [HLA] incompatibility).
It is thought that IgG antibodies from the host bind to HLA-1 antigen of the donated organ.
No treatment exists, and nephrectomy is indicated.

Acute rejection
Acute rejection appears within the first 6 months after transplantation and affects approximately 15% of transplanted kidneys. Rejection is secondary to prior sensitization to donor alloantigens (occult T-cell crossmatch) or a positive B-cell crossmatch.
Acute tubular interstitial cellular rejection is the most common type of rejection reaction, with an incidence of approximately 20-25%. Typically, it occurs between 1 and 3 months after transplantation. It is T-cell mediated, and injury is directed to the renal tubules. The standard for diagnosis is renal allograft biopsy. Mild rejections may be successfully reversed with corticosteroids alone, whereas moderate or severe rejections may require the use of anti–T-cell antibodies, either polyclonal or monoclonal.
Late acute rejection is strongly correlated with the scheduled withdrawal of immunosuppressive therapy 6 months after transplantation.

Chronic rejection
Chronic rejection occurs more than 1 year after transplantation and is a major cause of allograft loss. It is a slow and progressive deterioration in renal function characterized by histologic changes involving the renal tubules, capillaries, and interstitium. Its precise mechanism is poorly defined and is an area of intense study. Diagnosis is by renal biopsy, and treatment depends on the identified cause if any. Application of conventional antirejection agents (e.g., corticosteroids or anti–T-cell antibodies) does not appear to alter the progressive course.

This patient is likely to have paralytic ileus and the administration of antiemetic drugs, in this situation, will have no effect. It is, therefore, important to decompress the stomach with a wide bore nasogastric tube.

Paralytic ileus is the obstruction of the intestine due to paralysis of the intestinal muscles. It commonly occurs after an abdominal surgery. Irrespective of the cause, paralytic ileus causes constipation, abdominal distention, nausea, and vomiting. It is a severe condition because if left untreated, an ileus can cut off blood supply to the intestines and cause tissue death.

Renal vein thrombosis (RVT) is the formation of a clot in the vein that drains blood from the kidneys, ultimately leading to a reduction in the drainage of one or both kidneys and the possible migration of the clot to other parts of the body.

Venous thrombosis is a rare occurrence, occurring in 0.5% of kidney transplants. With aggressive treatment,
i.e. thrombectomy, the chances of success are very poor, but treatment is successful in rare cases. More often, patients are treated with transplantectomy.

The left side is preferred for live donor transplants due to longer renal vein while right side has been associated with renal vein thrombosis and shorter vessels.

With the iliac artery anatomically located lateral to iliac vein, one would need a longer vein in the graft to enable the graft placement in the iliac fossa, its final location. Most renal transplant surgeons would intuitively prefer to implant a graft harvested from the left side. The right kidney has a simpler anatomy for retrieval, with no adrenal or lumbar veins to tackle. However, a long artery and short vein make this kidney’s anatomy skewed for grafting. Studies on cadavers have shown significantly shorter right renal vein length (average 13.7%) on the right side. With its weak posterior wall, there is an added risk of tear of the right renal vein if there is tension during anastomosis. Overzealous manoeuvres and stretching of a short vein during retrieval, or handling during allografting may also risk intimal damage, a possible aetiology for some early reports of right grafts lost to renal vein thrombosis following laparoscopic harvest.

Recommendations:
• On the right, lengthen the renal vein with the infra renal vena cava in order to avoid an anastomosis
under tension.
• Carry out a large venous anastomosis; at declamping, if the renal vein is tight, re-do the venous anastomosis.

Pelvic inflammatory disease (PID) is an infectious and inflammatory disorder of the upper female genital tract, including the uterus, fallopian tubes, and adjacent pelvic structures. Infection and inflammation may spread to the abdomen, including perihepatic structures (Fitz-Hugh−Curtis syndrome). The classic high-risk patient is a menstruating woman younger than 25 years who has multiple sex partners, does not use contraception, and lives in an area with a high prevalence of sexually transmitted disease (STD).
PID is initiated by an infection that ascends from the vagina and cervix into the upper genital tract. Chlamydia trachomatis is the predominant sexually transmitted organism associated with PID. Of all acute PID cases, less than 50% test positive for the sexually transmitted organisms such as Chlamydia trachomatis and Neisseria gonorrhoea.
Other organisms implicated in the pathogenesis of PID include Gardnerella vaginalis (which causes bacterial vaginosis (BV), Haemophilus influenzae, and anaerobes such as Peptococcus and Bacteroides species. Laparoscopic studies have shown that in 30-40% of cases, PID is polymicrobial.
The most common presenting complaint is lower abdominal pain. Abnormal vaginal discharge is present in approximately 75% of cases. Unanticipated vaginal bleeding, often postcoital, is reported in about 40% of cases. Temperature is higher than 38°C (found in 30% of cases), nausea, and vomiting manifest late in the clinical course of the disease. Abnormal uterine bleeding is present in more than one-third of patients.
Right upper quadrant tenderness, especially if associated with jaundice, may indicate associated Fitz-Hugh−Curtis syndrome.

Antibody-mediated rejection (AMR) is defined as allograft rejection caused by antibodies of the recipient directed against donor-specific HLA molecules and blood group antigens. Although the mechanism by which HLA I antibodies promote inflammation and proliferation has been revealed by experimental models, the pathogenesis of HLA II antibodies is less defined. Antibodies to HLA II frequently accompany chronic rejection in renal transplants. AMR has been recognized as the leading cause of graft loss after kidney transplant if there is a donor-host antigenic disparity. Antibodies can be produced against epitopes of the antigen that differ from self by as little as one amino acid. Pre-existing antibodies or the development of de novo antibodies after transplantation has become a biomarker for AMR graft loss. HLA antibodies are risk factors for hyperacute, acute, and chronic allograft rejections.

The specificity of HLA antibodies can be determined using single-antigen luminex beads that consist of fluorescent microbeads conjugated to single recombinant HLA class I and class II molecules. Complement-fixing ability would be assessed by the binding of C1q to HLA antibodies present in the serum. In several studies, C1q-positive DSA had associated with antibody-mediated rejection in renal transplantation compared with antibodies identified only by IgG. Complement-fixing ability is relevant to hyperacute and acute rejections. Hyperacute rejection is predominantly complement-mediated severe allograft injury occurring within hours of transplantation. It is caused by high titre of pre-existing HLA or non-HLA antibodies in presensitized patients. But the incidence of hyperacute rejection is reduced due to improved DSA detection methods and desensitization protocols.

Proctectomy with end stoma is the best operative strategy in severe perianal and/or rectal Crohn’s disease.

Surgical resection of Crohn’s disease does not provide a complete cure but it may produce substantial symptomatic improvement. Indications for surgery include complications such as fistulae, abscess formation, and strictures.

Colonoscopy and a small bowel study (e.g. MR enteroclysis imaging) are used to stage Crohn’s disease to facilitate decision-making regarding surgery.
Complex perianal fistulae are best managed with long-term draining seton sutures. Severe perianal and/or rectal Crohn’s disease usually require proctectomy with formation of end stoma. Ileoanal pouch reconstruction carries a high risk of fistula formation and pouch failure and is, therefore, not recommended. Terminal ileal Crohn’s remains one of the most common form of the disease, and it may be treated with limited ileocaecal resections.

Containment of fistula output and skin protection should be instituted as soon as the diagnosis is made as it will decrease local skin excoriation and inflammation, pain and infection. While low output fistulas may be controlled with a simple absorbent dressing, complex fistulas often require advanced techniques including barrier creams, powders, and sealants to protect the skin from auto-digestion as well as bridging for fistula isolation, topographical enhancements, and complex pouching systems with or without sump drainage
Fistulas arising from the oesophagus, duodenal stump after gastric resection, pancreaticobiliary tract, and jejunum are more likely to close without operative intervention. Additionally, those with long tracts and small enteric wall defects are associated with higher spontaneous closure rates. Fistulas in the colon show favourable rates of spontaneous resolution.

Acute cholangitis is a bacterial infection superimposed on an obstruction of the biliary tree most commonly from a gallstone, but it may be associated with neoplasm or stricture. The classic triad of findings is right upper quadrant (RUQ) pain, fever, and jaundice. A pentad may also be seen, in which mental status changes and sepsis are added to the triad.

A spectrum of cholangitis exists, ranging from mild symptoms to fulminant overwhelming sepsis. Thus, therapeutic options for patient management include broad-spectrum antibiotics and, potentially, emergency decompression of the biliary tree.
The main factors in the pathogenesis of acute cholangitis are biliary tract obstruction, elevated intraluminal pressure, and infection of bile. A biliary system that is colonized by bacteria but is unobstructed, typically does not result in cholangitis. It is believed that biliary obstruction diminishes host antibacterial defences, causes immune dysfunction, and subsequently increases small bowel bacterial colonization. Although the exact mechanism is unclear, it is believed that bacteria gain access to the biliary tree by retrograde ascent from the duodenum or from portal venous blood. As a result, infection ascends into the hepatic ducts, causing serious infection. Increased biliary pressure pushes the infection into the biliary canaliculi, hepatic veins, and perihepatic lymphatics, leading to bacteraemia (25-40%). The infection can be suppurative in the biliary tract.

Hyperacute rejection occurs almost immediately following organ implantation and necessitates immediate explant of the organ. Hyperacute rejection is uncommon with pre-transplantation cross-matches and screening. Hyperacute rejection (HAR) of the kidney was first recognized 20 years ago in cases of donor-recipient incompatibility for the major blood group and tissue antigen systems. Classic pathological changes described include early accumulation of PMNs in glomeruli and peritubular capillaries, progressive glomerular thrombosis, tubular necrosis, and eventual cortical necrosis. Reaction of host humoral antibodies with antigens on donor cells serves as one trigger of the clotting mechanism, which then proceeds in a nonspecific fashion.

Antigen systems other than the ABO groups that contribute to HAR reactions are leukocyte antigens, endothelial and monocyte antigens, and B cell antigens. It is also documented that glomerular thrombosis identical to HAR may occur secondary to endothelial damage after pulsatile perfusion. However, in such cases no specific deposition of immunoglobulins and complement is detected.

A history of weight loss and intermittent diarrhoea makes inflammatory bowel disease (IBD) the most likely diagnosis. Conditions such as appendicitis and infections have a much shorter history. Although Meckel’s diverticulum can bleed and cause inflammation, it seldom causes marked weight loss. Irritable bowel syndrome (IBS) presents with alternating episodes of constipation and diarrhoea along with abdominal pain, bloating, and gas.

Answer: Mittelschmerz

Mittelschmerz is midcycle abdominal pain due to leakage of prostaglandin-containing follicular fluid at the time of ovulation. It is self-limited, and a theoretical concern is treatment of pain with prostaglandin synthetase inhibitors, which could prevent ovulation. The pain of mittelschmerz usually occurs in the lower abdomen and pelvis, either in the middle or to one side. The pain can range from a mild twinge to severe discomfort and usually lasts from minutes to hours. In some cases, a small amount of vaginal bleeding or discharge might occur. Some women have nausea, especially if the pain is very strong.
Diagnosis of pelvic pain in women can be challenging because many symptoms and signs are insensitive and nonspecific. As the first priority, urgent life-threatening conditions (e.g., ectopic pregnancy, appendicitis, ruptured ovarian cyst) and fertility-threatening conditions (e.g., pelvic inflammatory disease, ovarian torsion) must be considered.
Many women never have pain at ovulation. Some women, however, have mid-cycle pain every month, and can tell by the pain that they are ovulating.
As an egg develops in the ovary, it is surrounded by follicular fluid. During ovulation, the egg and the fluid, as well as some blood, are released from the ovary. While the exact cause of mittelschmerz is not known, it is believed to be caused by the normal enlargement of the egg in the ovary just before ovulation. Also, the pain could be caused by the normal bleeding that comes with ovulation.
Pelvic inflammatory disease can be ruled out if the patient is not sexually active.

Answer: Bochdalek hernia

A Bochdalek hernia is one of two forms of a congenital diaphragmatic hernia, the other form being Morgagni hernia. A Bochdalek hernia is a congenital abnormality in which an opening exists in the infant’s diaphragm, allowing normally intra-abdominal organs (particularly the stomach and intestines) to protrude into the thoracic cavity. In the majority of patients, the affected lung will be deformed, and the resulting lung compression can be life-threatening. Bochdalek hernias occur more commonly on the posterior left side (85%, versus right side 15%).

In normal Bochdalek hernia cases, the symptoms are often observable simultaneously with the baby’s birth. A few of the symptoms of a Bochdalek Hernia include difficulty breathing, fast respiration and increased heart rate. Also, if the baby appears to have cyanosis (blue-tinted skin) this can also be a sign. Another way to differentiate a healthy baby from a baby with Bochdalek Hernia, is to look at the chest immediately after birth. If the baby has a Bochdalek Hernia it may appear that one side of the chest cavity is larger than the other and or the abdomen seems to be scaphoid (caved in).

Situs inversus (also called situs transversus or oppositus) is a congenital condition in which the major visceral organs are reversed or mirrored from their normal positions. The normal arrangement of internal organs is known as situs solitus while situs inversus is generally the mirror image of situs solitus. Although cardiac problems are more common than in the general population, most people with situs inversus have no medical symptoms or complications resulting from the condition, and until the advent of modern medicine it was usually undiagnosed. In the absence of congenital heart defects, individuals with situs inversus are homeostatically normal, and can live standard healthy lives, without any complications related to their medical condition. There is a 5–10% prevalence of congenital heart disease in individuals with situs inversus totalis, most commonly transposition of the great vessels. The incidence of congenital heart disease is 95% in situs inversus with levocardia.

Cystic fibrosis is a progressive, genetic disease that causes persistent lung infections and limits the ability to breathe over time. In people with CF, mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene cause the CFTR protein to become dysfunctional. When the protein is not working correctly, it’s unable to help move chloride — a component of salt — to the cell surface. Without the chloride to attract water to the cell surface, the mucus in various organs becomes thick and sticky. In the lungs, the mucus clogs the airways and traps germs, like bacteria, leading to infections, inflammation, respiratory failure, and other complications.

Necrotizing enterocolitis (NEC) is a medical condition where a portion of the bowel dies. It typically occurs in new-borns that are either premature or otherwise unwell. Symptoms may include poor feeding, bloating, decreased activity, blood in the stool, or vomiting of bile.
The exact cause is unclear. Risk factors include congenital heart disease, birth asphyxia, exchange transfusion, and premature rupture of membranes. The underlying mechanism is believed to involve a combination of poor blood flow and infection of the intestines. Diagnosis is based on symptoms and confirmed with medical imaging.

Morgagni hernias are one of the congenital diaphragmatic hernias (CDH), and is characterized by herniation through the foramen of Morgagni. When compared to Bochdalek hernias, Morgagni hernias are:
-anterior
-more often right-sided (,90%)
-small
-rare (,2% of CDH)
-at low risk of prolapse

Only ,30% of patients are symptomatic. New-borns may present with respiratory distress at birth similar to a Bochdalek hernia. Additionally, recurrent chest infections and gastrointestinal symptoms have been reported in those with previously undiagnosed Morgagni hernia.
The image of the transverse colon is herniated into the thoracic cavity, through a mid line defect and this indicates that it is a Morgagni hernia since the foramen of a Morgagni hernia occurs in the anterior midline through the sternocostal hiatus of the diaphragm, with 90% of cases occurring on the right side.

Clinical manifestations of congenital diaphragmatic hernia (CDH) include the following:

Early diagnosis – Right-side heart; decreased breath sounds on the affected side; scaphoid abdomen; bowel sounds in the thorax, respiratory distress, and/or cyanosis on auscultation; CDH can often be diagnosed in utero with ultrasonography (US), magnetic resonance imaging (MRI), or both
Late diagnosis – Chest mass on chest radiography, gastric volvulus, splenic volvulus, or large-bowel obstruction
Congenital hernias (neonatal onset) – Respiratory distress and/or cyanosis occurs within the first 24 hours of life; CDH may not be diagnosed for several years if the defect is small enough that it does not cause significant pulmonary dysfunction
Congenital hernias (childhood or adult onset) – Obstructive symptoms from protrusion of the colon, chest pain, tightness or fullness the in chest, sepsis following strangulation or perforation, and many respiratory symptoms occur.

A Spigelian hernia (or lateral ventral hernia) is a hernia through the Spigelian fascia, which is the aponeurotic layer between the rectus abdominis muscle medially, and the semilunar line laterally. These are generally interparietal hernias, meaning that they do not lie below the subcutaneous fat but penetrate between the muscles of the abdominal wall; therefore, there is often no notable swelling.

Spigelian hernias are usually small and therefore risk of strangulation is high. Most occur on the right side. (4th–7th decade of life.) Compared to other types of hernias they are rare.

Lynch syndrome, also known as hereditary non-polyposis colorectal cancer (HNPCC), is a type of inherited cancer syndrome associated with a genetic predisposition to different cancer types. People who have Lynch syndrome have a significantly increased risk of developing colorectal cancer. There is also an increased risk of developing other types of cancers, such as endometrial (uterine), stomach, breast, ovarian, small bowel (intestinal), pancreatic, prostate, urinary tract, liver, kidney, and bile duct cancers. Alterations in several genes involved in DNA mismatch repair that have been linked to Lynch syndrome. They include the genes of MLH1, MSH2, MSH6, PMS2, and EPCAM. A mutation (alteration) in any of these genes gives a person an increased lifetime risk of developing colorectal cancer and other related cancers.

Women also have an increased risk of developing endometrial and ovarian cancers. The safest operative strategy is a pancolectomy and end ileostomy.

The history of bloodstained vaginal discharge and lower abdominal tenderness makes ectopic pregnancy a strong possibility. Therefore, a pregnancy test (for beta hCG) and abdominal and pelvic USS should be performed. If the beta HCG is high, that is an indication for intrauterine pregnancy. If it is not, then an ectopic pregnancy is likely, and surgery should be considered.

Generally, the differential diagnosis of right iliac fossa (RIF) pain includes:
1. Appendicitis
2. Crohn’s disease
3. Mesenteric adenitis
4. Diverticulitis
5. Meckel’s diverticulitis
6. Perforated peptic ulcer
7. Incarcerated right inguinal or femoral hernia
8. Bowel perforation secondary to caecal or colon carcinoma
9. Gynaecological causes—pelvic inflammatory disease/salpingitis/pelvic abscess/ectopic pregnancy/ovarian torsion/threatened or complete abortion
10. Urological causes—ureteric colic/urinary tract infection/Testicular torsion
11. Other causes—tuberculosis/typhoid/ infection with herpes zoster

Treatment of Crohn’s disease is based on the disease site, pattern, activity, and severity. The general goals of treatment for Crohn’s disease are as follows:
To achieve the best possible clinical, laboratory, and histologic control of the inflammatory disease with the least adverse effects from medication.
To permit the patient to function as normally as possible.
Therapy for mild Crohn’s disease is typically administered in a sequential “step-up” approach, in which less aggressive and less toxic treatments are initiated first, followed by more potent medications or procedures if the initial therapy fails.
Patients are treated with preparations of 5-aminosalicylic acid (5-ASA), antibiotics, and nutritional therapy. However, the use of 5-ASA for the treatment of Crohn’s disease is controversial; only a small subset of patients may benefit from this agent. Although 5-ASA is effective for reducing disease activity in active Crohn’s disease, it typically has a lower efficacy for Crohn’s disease than for ulcerative colitis, and its efficacy for maintenance of remission remains unproven.

If no response occurs or if the disease is more severe than initially thought, corticosteroids and inhibitors of DNA synthesis (i.e., immunomodulators) with 6-mercaptopurine (6-MP)/azathioprine or methotrexate are administered. Finally, biologic agents (infliximab, adalimumab, certolizumab pegol, and natalizumab) and surgical therapies can be useful.

For the treatment of moderate to severe Crohn’s disease, current recommendations include the “top-down” approach, which differs from the conventional step-up approach in that more potent agents are administered initially. Top-down therapies include biologic agents and steroids as needed versus combination therapy with both biologic drugs and immunomodulatory agents.

Azathioprine or 6-MP is effective for maintenance of remission in Crohn’s disease; each is effective for avoiding surgery and for preventing postoperative and endoscopic relapse. Both agents can be used in combination with infliximab.

If medical therapy for active Crohn’s disease fails, surgical resection of the inflamed bowel, with the restoration of continuity, is indicated.

Recommended indications for surgical intervention include the following:
Failed medical therapy
Persistent symptoms despite high-dose corticosteroid therapy
Treatment-related complications, including intra-abdominal abscesses
Medically intractable fistulae
Fibrotic strictures with obstructive symptoms
Toxic megacolon
Intractable haemorrhage
Perforation
Cancer

For Rectal Crohn’s: Proctectomy is appropriate, and in published series, it is required in 10 to 20% of cases. Unfortunately, proctectomy can be complicated by poor wound healing and perineal sinus formation in up to 25 to 50% of patients. A gracillis flap can be helpful.

Surgical resection is the principal therapy for gastric cancer, as it offers the only potential for cure. A subtotal gastrectomy is usually performed for tumours of the distal stomach. Subtotal gastrectomy is the treatment of choice for middle and distal-third gastric cancer as it provides similar survival rates and better functional outcome compared to total gastrectomy, especially in early-stage disease with favourable prognosis. D2 dissections are recommended by the National Comprehensive Cancer Network over D1 dissections. A pancreas-and spleen-preserving D2 lymphadenectomy is suggested, as it provides greater staging information, and may provide a survival benefit while avoiding its excess morbidity when possible. Patients that undergo D2 lymphadenectomy as a standard part of surgical resection of gastric adenocarcinoma generally have better stage-for-stage overall survival figures compared to patients undergoing less extensive lymphadenectomies.
After partial gastrectomy, some patients report disorders such as reflux esophagitis and alkaline gastritis, as well as dumping syndrome, delayed gastric emptying and malabsorption, which are defined as functional dyspepsia. Duodenogastric reflux is recognized to be a major cause of clinical symptoms after resection.
Roux-Y reconstruction seems to be effective in reducing bile reflux into the stomach, compared to Billroth I and II procedure, and conversion to this procedure has been reported in patients with symptomatic uncontrolled reflux disease.

Typical pilonidal sinus disease (PSD) occurs in the natal cleft i.e. sacrococcygeal region.
However, some occupation related pilonidal sinuses occurs in webs of fingers e.g. hairdresser, sheep shearer, dog groomer, slaughterman or milker.
Other locations where pilonidal sinuses may occur include penis shaft, axilla, intermammary area, groin, nose, neck, clitoris, suprapubic area, occiput, prepuce, chin, periungual region, breast, face and umbilicus.

Although the pilonidal disease may manifest as an abscess, a pilonidal sinus, a recurrent or chronic pilonidal sinus, or a perianal pilonidal sinus, the most common manifestation of pilonidal disease is a painful, fluctuant mass in the sacrococcygeal region.
Initially, 50% of patients first present with a pilonidal abscess that is cephalad to the hair follicle and sinus infection. Pain and purulent discharge from the sinus tract is present 70-80% of the time and are the two most frequently described symptoms. In the early stages preceding the development of an abscess, only cellulitis or folliculitis is present. The abscess is formed when a folliculitis expands into the subcutaneous tissue or when a pre-existing foreign body granuloma becomes infected.
The diagnosis of a pilonidal sinus can be made by identifying the epithelialized follicle opening, which can be palpated as an area of deep induration beneath the skin in the sacral region. These tracts most commonly run in the cephalad direction. When the tract runs in the caudal direction, perianal sepsis may be present.

The ideal treatment for a pilonidal sinus varies according to the clinical presentation of the disease. First, it is important to divide the pilonidal disease into the following three categories, which represent different stages of the clinical course:
– Acute pilonidal abscess
– Chronic pilonidal disease
– Complex or recurrent pilonidal disease

Acute pilonidal abscess:
A pilonidal abscess is managed by incision, drainage, and curettage of the abscess cavity to remove hair nests and skin debris. This can be accomplished in the surgical office or the emergency department, using local anaesthesia.
If possible, the drainage incision should be made laterally, away from the midline. Wounds heal poorly in the deep, intergluteal natal cleft, for two reasons. The first is the frictional motion of the deep cleft, which creates continuous irritation to the healing wound; the second is the midline nature of the wound, which is a product of constant lateral traction during sitting.

Chronic pilonidal disease is the term applied when patients have undergone at least one pilonidal abscess drainage procedure and continue to have a pilonidal sinus tract. The term also refers to a pilonidal sinus that is associated with a chronic discharge without an acute abscess. Surgical options for management of a noncomplicated chronic pilonidal sinus include the following:
Excision and laying open of the sinus tract
Excision with primary closure
Wide and deep excision to the sacrum
Incision and marsupialization
Bascom procedure
Asymmetrical incisions
Skin flaps have also been described to cover a sacral defect after wide excision. Similarly, this keeps the scar off the midline and flattens the natal cleft.

Fistulotomy could achieve good results in terms of wound healing and incontinence in strictly selected patients with Crohn’s disease suffering from low-lying trans-sphincteric fistulae. For more high-lying or complicated fistulae, seton placement is more appropriate. For high transsphincteric fistulae, the only option is placement of loose seton.
Fistulae are classified into four main groups according to anatomical location and the degree of sphincter involvement. Simple uncomplicated fistulae are low and do not involve more than 30% of the external sphincter. Complex fistulae involve the sphincter, have multiple branches or are non cryptoglandular in origin

Answer: Sickle cell disease

An anal fissure is a painful linear tear or crack in the distal anal canal, which, in the short term, usually involves only the epithelium and, in the long term, involves the full thickness of the anal mucosa. Anal fissures develop with equal frequency in both sexes; they tend to occur in younger and middle-aged persons.

The exact aetiology of anal fissures is unknown, but the initiating factor is thought to be trauma from the passage of a particularly hard or painful bowel movement. Low-fibre diets (e.g., those lacking in raw fruits and vegetables) are associated with the development of anal fissures. No occupations are associated with a higher risk for the development of anal fissures. Prior anal surgery is a predisposing factor because scarring from the surgery may cause either stenosis or tethering of the anal canal, which makes it more susceptible to trauma from hard stool.

In rare cases, an anal fissure may develop due to:
-anal cancer
-HIV
-tuberculosis
-syphilis
-herpes

A study showed that a patient may exhibit severe, disabling, anorectal symptoms which are disproportionate to physical findings. Rarely leukaemia may be the cause, and the first signs of blood dyscrasia may appear in the anorectum. The diagnosis may not be suggested by the history, physical examination or routine laboratory data.

Crohn’s disease can also cause problems around the anus. These may include tiny but painful cracks in the skin known as anal fissures. Tunnelling sores called fistulas cause abnormal connections between the bowel and the skin; or an abscess, a pocket of inflamed or dead tissue that is usually very painful.

This individual has acute cholecystitis. This is demonstrated by well-localized pain in the right upper quadrant, usually with rebound and guarding; frequent presence of fever and peritonism. Ultrasonography is the procedure of choice in suspected gallbladder or biliary disease. A bile duct measuring 4mm is usually normal.
Once gallstones become symptomatic, definitive surgical intervention with cholecystectomy is usually indicated (typically, laparoscopic cholecystectomy is the first-line therapy at centres with experience in this procedure).

Lymphocele has been defined as a lymph-filled collection in the retroperitoneum without an epithelial lining. In kidney transplanted patients, lymphocele is a pseudocystic entity with lymph content covered with a hard fibrous capsule frequently localized around the graft. Lymphocele is one of the most common complications after kidney transplantation. It is usually asymptomatic, but can cause pressure on the kidney transplant, ureter, bladder, and adjacent vessels with deterioration of graft function, ipsilateral leg oedema, and external iliac vein thrombosis. Peritoneal fenestration is a well-established method for treatment.

Risk factors for Recurrent Inguinal Hernia with a moderate level of evidence include the presence of a sliding hernia, a diminished collagen type I/III ratio, increased systemic matrix metalloproteinase levels, obesity and open hernia repair under local anaesthesia by general surgeons.
The incorrect surgical technique is likely the most important reason for recurrence after primary IH repair.

According to the guidelines:
– Laparo-endoscopic recurred inguinal hernia repair is strongly recommended after failed anterior tissue or Lichtenstein repair (evidence: moderate; recommendation: strong).
– Anterior repair is recommended after a failed posterior repair (evidence: moderate; recommendation: strong).
– An expert hernia surgeon should repair a recurrent Inguinal Hernia after failed anterior and posterior repair. Choice of technique depends on patient and surgeon specific factors (evidence: low; recommendation: strong upgraded).

The EHS guidelines recommended for bilateral primary inguinal hernia repair, either a bilateral Lichtenstein or endoscopic approach.

Ulcer bleeding stops spontaneously in about 80% of patients. Only a small percentage require specific measures to stop bleeding. surgery remains the most definitive method of controlling ulcer haemorrhage, and is indicated when endoscopic haemostasis fails to control the bleeding, or when rebleeding occurs. The morbidity and mortality of emergency surgery for ulcer bleeding is high. In principle, the operation performed should be the minimum compatible with permanent haemostasis. The choice of operations is determined by the site and size of the ulcer as well as the experience and preference of the surgeon. Most bleeding duodenal ulcers may be managed by underrunning the bleeding vessel together with vagotomy and pyloroplasty.