Answer: Haemorrhoidal disease

Haemorrhoids are a normal part of the anatomy of the anorectum. They are vascular cushions that serve to protect the anal sphincter, aid closure of the anal canal during increased abdominal pressure, and provide sensory information that helps differentiate among stool, liquid and gas. Because of their high vascularity and sensitive location, they are also a frequent cause of pathology. Contributing factors include pregnancy, chronic constipation, diarrhoea or prolonged straining, weight lifting, and weakening of supporting tissue as a result of aging or genetics.
Haemorrhoids are classified according to their position relative to the dentate line. External haemorrhoids lie below the dentate line, are covered by squamous epithelium and innervated by cutaneous nerves. If symptomatic, the only definitive therapy is surgical excision.
Internal haemorrhoids arise above the dentate line, are covered by columnar cells and have a visceral nerve supply. They are further categorized — and treated — according to their degree of prolapse:
-Grade I haemorrhoids bleed but do not prolapse; on colonoscopy, they are seen as small bulges into the lumen.
-Grade II haemorrhoids prolapse outside the anal canal but reduce spontaneously.
-Grade III haemorrhoids protrude outside the anal canal and usually require manual reduction.
-Grade IV haemorrhoids are irreducible and constantly prolapsed. Acutely thrombosed haemorrhoids and those involving rectal mucosal prolapse are also grade IV.

Most gastrointestinal and surgical societies advocate anoscopy and/or flexible sigmoidoscopy to evaluate any bright-red rectal bleeding. Colonoscopy should be considered in the evaluation of any rectal bleeding that is not typical of haemorrhoids such as in the presence of strong risk factors for colonic malignancy or in the setting of rectal bleeding with a negative anorectal examination.

Anal fissures are tears of the sensitive mucosal lining of the anus. Anal fissures often cause pain during and after a bowel movement, sometimes followed by throbbing pain for several hours. They are also often associated with itching and blood on toilet tissue, in the bowl, or on the surface of the stool. Anal fissures are caused by
trauma to the anal canal usually during bowel movements. Anal fissures are also sometimes caused by inflammatory bowel disease or infection.

Severe abdominal pain tends to favour infection with Campylobacter jejuni.

Infection with Campylobacter jejuni is one of the most common causes of gastroenteritis worldwide. In developed countries, the incidence of Campylobacter jejuni infections peaks during infancy and, again, during early adulthood. Most infections are acquired by the consumption and handling of poultry. A typical case is characterized by diarrhoea, fever, and severe abdominal cramps. Obtaining cultures of the organism from stool samples remains the best way to diagnose this infection. Complications of C. jejuni infections are rare, and most patients do not require antibiotics. Careful food preparation and cooking practices may prevent some Campylobacter infections.

This patient had endoscopy and biopsy done by different doctors and proton pump inhibitor therapy followed by repeat endoscopy and biopsy six months later which had no definite evidence of dysplasia.

British Society of Gastroenterology (BSG) guidelines state that for patients with Barrett’s oesophagus (BO) but without dysplasia, the recommended surveillance protocols are two yearly, four quadrant biopsies every 2 cm, but jumbo biopsies are not required.

The patient has a primary psoas abscess.

Psoas (or iliopsoas) abscess is a collection of pus in the iliopsoas muscle compartment. It may arise via contiguous spread from adjacent structures or by the haematogenous route from a distant site. Psoas abscesses may be either primary or secondary. Primary cases often develop in the immunosuppressed and may occur as a result of haematogenous spread. Secondary cases may occur as a complication of intra-abdominal diseases such as Crohn’s disease.

Patients usually present with lower back pain and if the abscess is extensive, a mass that may be localised to the inguinal region or femoral triangle. In most cases, the diagnosis can be made clinically. Where it is not clear, an ultrasound scan is often the most convenient investigation.

Smaller collections may be percutaneously drained. If the collection is larger, or the percutaneous route fails, then surgery (via a retroperitoneal approach) should be performed.

Hernia containing Meckel’s diverticulum is termed as Littre’s hernia.

Hernias occur when a viscus or part of it protrudes from within its normal anatomical cavity. A Littre’s hernia is an abdominal wall hernia that involves the Meckel’s diverticulum which is a congenital outpouching or bulge in the lower part of the small intestine and is a leftover of the umbilical cord.

Management of Littre’s hernia includes resection of the diverticulum followed by herniorrhaphy.

Melanosis coli may have occurred as a result of laxative abuse in this patient.

Melanosis coli, also pseudomelanosis coli, is a disorder of pigmentation of the wall of the colon, often identified at the time of colonoscopy. It is benign, and may have no significant correlation with the disease. The brown pigment seen is lipofuscin in macrophages, not melanin.

According to the World Health Organisation (WHO), chronic diarrhoea is defined as lasting for more than 14 days. It is very common in irritable bowel syndrome (IBS). Patients may be divided into those with diarrhoea-predominant IBS and those with constipation-predominant IBS. Along with diarrhoea/constipation, clinical features such as abdominal pain, bloating, weight loss, change in bowel habit, lethargy, nausea, backache, and bladder symptoms are also seen. Bloody diarrhoea is more common in ulcerative colitis than in Crohn’s disease.

Mirizzi syndrome is defined as common hepatic duct obstruction caused by extrinsic compression from an impacted stone in the cystic duct or infundibulum of the gallbladder. Patients with Mirizzi syndrome can present with jaundice, fever, and right upper quadrant pain. Mirizzi syndrome is often not recognized preoperatively in patients undergoing cholecystectomy and can lead to significant morbidity and biliary injury, particularly with laparoscopic surgery. Acute presentations of the syndrome include symptoms consistent with cholecystitis.
Surgery is extremely difficult as Calot’s triangle is often completely obliterated and the risks of causing injury to the common bile duct (CBD) are high.
Multiple and large gallstones can become impacted in the Hartmann’s pouch of the gallbladder, leading to chronic inflammation – which leads to compression of the CBD, necrosis, fibrosis, and ultimately fistula formation into the adjacent common hepatic duct (CHD). As a result, the CHD/CBD becomes obstructed by either scar or stone, resulting in obstructive jaundice. It can be divided into four types.
Type I – No fistula present
Type IA – Presence of the cystic duct
Type IB – Obliteration of the cystic duct
Types II–IV – Fistula present
Type II – Defect smaller than 33% of the CHD diameter
Type III – Defect 33–66% of the CHD diameter
Type IV – Defect larger than 66% of the CHD diameter

Simple cholecystectomy is suitable for type I patients. For types II–IV, subtotal cholecystectomy can be performed to avoid damage to the main bile ducts. Cholecystectomy and bilioenteric anastomosis may be required. Roux-en-Y hepaticojejunostomy has shown good outcome in some studies.

Goodsall’s rule can be used to clinically predict the course of an anorectal fistula tract. Imagine a line that bisects the anus in the coronal plane (transverse anal line). Any fistula that originates anterior to the line will course anteriorly in a direct route. Fistulae that originate posterior to the line will have a curved path. An exception to the rule are anterior fistulas lying more than 3 cm from the anus, which may open into the anterior midline of the anal canal.

Carcinoid tumours are of neuroendocrine origin and derived from primitive stem cells in the gut wall, especially the appendix.
Signs and symptoms of carcinoid tumours vary greatly. Carcinoid tumours can be non-functioning presenting as a tumour mass or functioning. The sign and symptoms of a non-functioning tumour depend on the tumour location and size as well as on the presence of metastases. Therefore, findings range from no tumour-related symptoms (most carcinoid tumours) to full symptoms of carcinoid syndrome (primarily in adults).
– Periodic abdominal pain: Most common presentation for a small intestinal carcinoid; often associated with malignant carcinoid syndrome
– Cutaneous flushing: Early and frequent (94%) symptom
– Diarrhoea and malabsorption (84%)
– Cardiac manifestations (60%): Valvular heart lesions, fibrosis of the endocardium; may lead to heart failure with tachycardia and hypertension
– Wheezing or asthma-like syndrome (25%)
– Pellagra
– Carcinoid crisis can be the most serious symptom of carcinoid tumours and can be life-threatening. It can occur suddenly, after stress, or following chemotherapy and anaesthesia.

Two surgical procedures can be applied to treat appendiceal Neuroendocrine Neoplasm (NEN): simple appendicectomy and oncological right-sided hemicolectomy.
– For T1 (ENETS) or T1a (UICC/AJCC) NEN (i.e. <1 cm), generally simple appendicectomy is curative and sufficient.
– For NEN >2 cm with a T3 stage (ENETS) or higher and T2 (UICC/AJCC) or higher respectively, a right-sided hemicolectomy is advised due to the increased risk of lymph node metastasis and long-term tumour recurrence and/or distant metastasis. The right-sided hemico- lectomy should be performed either as the initial surgical intervention should the problem be overt at that time, or during a second intervention.

Total parenteral nutrition (TPN) is usually indicated with suspected gastric, duodenal, or small-bowel fistula. When the fistula output is very high, discontinuance of oral intake is recommended because oral intake stimulates further losses of fluids, electrolytes, and protein via the fistula. A decrease in fistula output frequently occurs with the initiation of TPN.

Volume depletion from a proximal high-output fistula can be controlled with the use of the long-acting somatostatin analogue octreotide, which acts by inhibiting GI hormones. The administration of octreotide reportedly diminishes fistula output, but whether it shortens the time required for fistula closure remains to be determined.
Draus et al recommended a 3-day trial of octreotide, maintaining that if the fistula output is reduced during this time, then administration of the drug should be continued. Two meta-analyses showed that somatostatin and its analogues decreased the time for fistula closure and increased the closure rate.

Dysphagia that is episodic and nonprogressive and varies between solids and liquids is more likely to represent a motility disorder. It may also associated with retrosternal chest pain.

Motility disorder is a condition where the nerves and muscles in the gastrointestinal tract are not working together correctly, which cause difficulty in the digestive process. These conditions include chronic intractable constipation, gastroesophageal reflux disease (GERD), chronic intestinal pseudo-obstruction, gastroparesis, Hirschsprung’s disease, and oesophageal achalasia, among other disorders.

In addition to imaging studies, these conditions are usually evaluated with manometry studies which measure the pressure in different areas of the gastrointestinal tract.

The patient has a right groin hernia since he has a reducible lump and a history of carrying heavy objects.
Inguinal hernias present with a reducible lump in the groin.
A third of patients scheduled for surgery have no pain, and severe pain is uncommon (1.5% at rest and 10.2% on movement).
Inguinal hernias are at risk of irreducibility or incarceration, which may result in strangulation and obstruction; however, unlike with femoral hernias, strangulation is rare.
Inguinal hernias are often classified as direct or indirect, depending on whether the hernia sac bulges directly through the posterior wall of the inguinal canal (direct hernia) or passes through the internal inguinal ring alongside the spermatic cord, following the coursing of the inguinal canal (indirect hernia).

Surgery is the only curative treatment.
If patients with asymptomatic inguinal hernia are medically fit, they should be offered repair
Mesh repair is associated with the lowest recurrence rates of hernia
Laparoscopic repair is suggested for recurrent and bilateral inguinal hernias, though it may also be offered for primary inguinal hernia repair
The EuraHS recommendations:
– For Primary unilateral Hernia: Mesh repair, Lichtenstein or endoscopic repair are recommended. Endoscopic repair only if expertise is available.
– Primary bilateral: Mesh repair, Lichtenstein or endoscopic.
– Recurrent inguinal hernia: Mesh repair, modifying the technique with respect to the previous technique.
– If previously anterior: Consider open preperitoneal mesh or endoscopic approach (if expertise is present).
– If previously posterior: Consider an anterior mesh

In inguinal hernia tension-free repair, synthetic non-absorbable flat meshes (or composite meshes with a non-absorbable component) should be used.

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.

Advances in endoscopy have suggested wider use of ERCP, which in the past was mostly restricted to the treatment of biliary fistulas and to patients with associated medical disease. Several series in literature demonstrate that ERCP with stenting for major bile duct injuries in the form of incomplete strictures has comparable efficacy with surgery and lower rates of morbidity and mortality, but few give long-term results.

Bile duct injuries (BDI) can occur after many abdominal operations, e.g. liver surgery, gastrectomy, common bile duct (CBD) exploration. However, the majority of postoperative bile duct injuries (POBDI) occur during open or laparoscopic cholecystectomy. Despite increasing experience with laparoscopy, a review of 1.6 million cholecystectomies demonstrated an unchanging 0.5% incidence of bile duct injury, reported after many days post operation, of abdominal pain, bile leak, jaundice or cholangitis. Only 30% of injuries are recognized at the time of operation.
Bile duct injuries, particularly strictures, have traditionally been managed by surgical reconstruction (Roux-en-Y hepaticojejunostomy). The reported occurrence of symptomatic anastomotic strictures after long-term follow-up of surgical reconstruction ranges from 9-25 %. Surgery is definitely associated with significant morbidity and mortality. Endoscopic treatment has demonstrated results comparable to those achieved with surgery, with lower morbidity and mortality.

Anal fissure is a tear in the anoderm distal to the dentate line. It is the most common cause of severe anal pain. It is equally one of the most common reasons for bleeding per anus in infants and young children. The pain of an anal ulcer is intolerable and always disproportionate to the severity of the physical lesion. It may be so severe that patients may avoid defecation for days together until it becomes inevitable. This leads to hardening of the stools, which further tear the anoderm during defecation, setting a vicious cycle. The fissures can be classified into 1] Acute or superficial and 2] Chronic fissure in ano.

Initial therapy for an anal fissure is medical, and more than 80% of acute anal fissures resolve without further therapy.
The goals of treatment are to relieve the constipation and to break the cycle of hard bowel movement, associated pain, and worsening constipation. Softer bowel movements are easier and less painful for the patient to pass.

First-line medical therapy consists of therapy with stool-bulking agents, such as fibre supplementation and stool softeners. Laxatives are used as needed to maintain regular bowel movements. Mineral oil may be added to facilitate passage of stool without as much stretching or abrasion of the anal mucosa, but it is not recommended for indefinite use. Sitz baths after bowel movements and as needed provide significant symptomatic relief because they relieve some of the painful internal sphincter muscle spasm.
Recurrence rates are in the range of 30-70% if the high-fibre diet is abandoned after the fissure is healed. This range can be reduced to 15-20% if patients remain on a high-fibre diet.

Second-line medical therapy consists of intra-anal application of 0.4% nitroglycerin (NTG; also called glycerol trinitrate) ointment directly to the internal sphincter.
Some physicians use NTG ointment as initial therapy in conjunction with fibre and stool softeners, and others prefer to add it to the medical regimen if fibre and stool softeners alone fail to heal the fissure. NTG ointment is thought to relax the internal sphincter and to help relieve some of the pain associated with sphincter spasm; it also is thought to increase blood flow to the anal mucosa.
Unfortunately, many people cannot tolerate the adverse effects of NTG, and as a result, its use is often limited. The main adverse effects are headache and dizziness; therefore, patients should be instructed to use NTG ointment for the first time in the presence of others or directly before bedtime.
Analogous to the use of NTG intra-anal ointment, nifedipine ointment is also available for use in clinical trials. It is thought to have similar efficacy to NTG ointment but with fewer adverse effects.

Botulinum toxin has been used to treat acute and chronic anal fissures. It is injected directly into the internal anal sphincter, in effect performing a chemical sphincterotomy. The effect lasts about 3 months, until nerve endings regenerate. This 3-month period may allow acute fissures (and sometimes chronic fissures) to heal and symptoms to resolve. If botulinum toxin injection provides initial relief of symptoms but there is a recurrence after 3 months, the patient may benefit from surgical sphincterotomy.

Surgical therapy is usually reserved for acute anal fissures that remain symptomatic after 3-4 weeks of medical therapy and for chronic anal fissures.
Sphincter dilatation
Lateral internal sphincterotomy

Ileal resection may lead to bile acid malabsorption and an altered biliary lipid composition. A “bile acid deficiency” in the enterohepatic circulation with a relative excess of cholesterol and cholesterol supersaturated bile might ensue, causing cholesterol gallstone formation.

In patients with Crohn’s disease involving the small
intestine, the prevalence of gall-bladder stones is higher
than that in the general population. One hypothesis
for this increased risk is that bile acid malabsorption,
secondary to impaired active bile acid transport as a
consequence of ileal disease/resection, leads to a
reduction in the total bile acid pool size and an increase
in biliary cholesterol saturation. In patients with
ulcerative or Crohn’s colitis, or who have undergone
colectomy, the bile acid malabsorption is less than that
in those with ileal dysfunction or resection, but the risk
of gallstone formation is still increased, allegedly by the
same mechanism.

A cavernous liver haemangioma or hepatic haemangioma is a benign tumour of the liver composed of hepatic endothelial cells. It is the most common liver tumour, and is usually asymptomatic and diagnosed incidentally on radiological imaging. Liver haemangiomas are thought to be congenital in origin. Several subtypes exist, including the giant hepatic haemangioma, which can cause significant complications. This large, atypical haemangioma of the liver may present with abdominal pain or fullness due to haemorrhage, thrombosis or mass effect. It may also lead to left ventricular volume overload and heart failure due to the increase in cardiac output which it causes. Further complications are Kasabach-Merritt syndrome, a form of consumptive coagulopathy due to thrombocytopaenia, and rupture.

As one of the benign neoplasms, the AFP level of hepatic cavernous haemangioma patients is not usually outside the normal range.

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.

A pancreatic pseudocyst is a circumscribed collection of fluid rich in pancreatic enzymes, blood, and necrotic tissue, typically located in the lesser sac of the abdomen. Pancreatic pseudocysts are usually complications of pancreatitis, although in children they frequently occur following abdominal trauma. Pancreatic pseudocysts account for approximately 75% of all pancreatic masses.
Signs and symptoms of pancreatic pseudocyst include abdominal discomfort and indigestion.

Diagnosis of Pancreatic pseudocyst can be based on cyst fluid analysis:
Carcinoembryonic antigen (CEA) and CEA-125 (low in pseudocysts and elevated in tumours);
Fluid viscosity (low in pseudocysts and elevated in tumours);
Amylase (usually high in pseudocysts and low in tumours)

The most useful imaging tools are:

-Ultrasonography – the role of ultrasonography in imaging the pancreas is limited by patient habitus, operator experience and the fact that the pancreas lies behind the stomach (and so a gas-filled stomach will obscure the pancreas).
-Computerized tomography – this is the gold standard for initial assessment and follow-up.
-Magnetic resonance cholangiopancreatography (MRCP) – to establish the relationship of the pseudocyst to the pancreatic ducts, though not routinely used.

The patient mostly has an appendicular mass.
At present, the treatment of choice for uncomplicated acute appendicitis in adults continues to be surgical. The inflammation in acute appendicitis may sometimes be enclosed by the patient’s own defence mechanisms, by the formation of an inflammatory phlegmon or a circumscribed abscess. The management of these patients is controversial. An immediate appendectomy may be technically demanding. The exploration often ends up in an ileocecal resection or a right-sided hemicolectomy. Recently, the conditions for conservative management of these patients have changed due to the development of computed tomography and ultrasound, which has improved the diagnosis of enclosed inflammation and made drainage of intra-abdominal abscesses easier. New efficient antibiotics have also given new opportunities for nonsurgical treatment of complicated appendicitis. The traditional management of these patients is nonsurgical treatment followed by interval appendectomy to prevent a recurrence. The need for interval appendectomy after successful nonsurgical treatment has recently been questioned because the risk of recurrence is relatively small.
In patients with suspicion of contained appendiceal inflammation, based on a palpable mass or long duration of symptoms, the diagnosis should be confirmed by imaging techniques, especially CT scan. The patient should receive primary nonsurgical treatment with antibiotics and abscess drainage as needed. After successful nonsurgical treatment, no interval appendectomy is indicated in some cases, but the patient should be informed about the risk of recurrence especially in the presence of appendicolith. The risk of missing another underlying condition (cancer or CD) is low, but motivates a follow-up with a colon examination and/or a CT scan or US, especially in patients above the age of 40 years.

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.

Iron deficiency anaemia (IDA) is the most common form of anaemia worldwide and can be due to inadequate intake, decreased absorption (e.g., atrophic gastritis, inflammatory bowel disease), increased demand (e.g., during pregnancy), or increased loss (e.g., gastrointestinal bleeding, menorrhagia) of iron. Prolonged deficiency depletes the iron stores in the body, resulting in decreased erythropoiesis and anaemia.
Symptoms are nonspecific and include fatigue, pallor, lethargy, hair loss, brittle nails, and pica. Diagnostic lab values include low haemoglobin, microcytic, hypochromic red blood cells on peripheral smear, and low ferritin and iron levels. Once diagnosed, the underlying cause should be determined. Patients at risk for underlying gastrointestinal malignancy should also undergo a colonoscopy.
Iron deficiency anaemia is treated with oral (most common) or parenteral iron supplementation. Severe anaemia or those with concomitant cardiac conditions may also require blood transfusions. The underlying cause of IDA should also be corrected. IDA may manifest as Plummer-Vinson syndrome (PVS): triad of postcricoid dysphagia, upper oesophageal webs, and iron deficiency anaemia

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

Painful, bright red rectal bleeding is usually due to a fissure. Presence of pain and the sentinel tag suggests a posterior fissure-in-ano.

Anal fissures are a common cause of painful, bright red, rectal bleeding. Most fissures are idiopathic and present as a painful mucocutaneous defect in the posterior midline (90% cases). Fissures are more likely to be anteriorly located in females, particularly if they are multiparous. Diseases associated with fissure-in-ano include:
1. Crohn’s disease
2. Tuberculosis
3. Internal rectal prolapse

Diagnosis:
In most cases, the defect can be visualised as a posterior midline epithelial defect. Where symptoms are highly suggestive of the condition and examination findings are unclear, an examination under anaesthesia may be helpful. Atypical disease presentation should be investigated with colonoscopy and EUA with biopsies of the area.

Treatment:
1. Stool softeners are important as hard stools may tear the epithelium and result in recurrent symptoms. The most effective first-line agents are topically applied GTN (0.2%) or Diltiazem (2%) paste. Side effects of diltiazem are better tolerated.
2. Resistant cases may benefit from injection of botulinum toxin or lateral internal sphincterotomy. Advancement flaps may be used to treat resistant cases.

Answer: Fitz Hugh Curtis syndrome

Fitz-Hugh-Curtis syndrome is a rare disorder that occurs almost exclusively in women. It is characterized by inflammation of the membrane lining the stomach (peritoneum) and the tissues surrounding the liver (perihepatitis). The muscle that separates the stomach and the chest (diaphragm), which plays an essential role in breathing, may also be affected. Common symptoms include severe pain in the upper right area (quadrant) of the abdomen, fever, chills, headaches, and a general feeling of poor health (malaise). Fitz-Hugh-Curtis syndrome is a complication of pelvic inflammatory disease (PID), a general term for infection of the upper genital tract in women. Infection is most often caused by Neisseria gonorrhoeae and Chlamydia trachomatis.

Fitz-Hugh-Curtis syndrome is characterized by the onset of sudden, severe pain in the upper right area of the abdomen. Pain may spread to additional areas including the right shoulder and the inside of the right arm. Movement often increases pain. The upper right area may be extremely tender.

Additional symptoms may occur in some cases including fever, chills, night sweats, vomiting and nausea. Some affected individuals may develop headaches, hiccupping, and a general feeling of poor health (malaise).

Some affected individuals may have symptoms associated with pelvic inflammatory disease including fever, vaginal discharge, and lower abdominal pain. Lower abdominal pain may precede, follow, or occur simultaneously with upper abdominal pain.

Most cases of Fitz-Hugh-Curtis syndrome are caused by infection with the bacterium Chlamydia trachomatis, which causes Chlamydia or the organism Neisseria gonorrhoeae, which causes gonorrhoea. Chlamydia and gonorrhoea are common sexually transmitted diseases (STDs). Researchers believe that more cases of Fitz-Hugh-Curtis syndrome are caused by infection with Chlamydia trachomatis than with Neisseria gonorrhoeae.

The exact process by which such infections cause Fitz-Hugh-Curtis syndrome (pathogenesis) is not completely understood. Some researchers believe that it occurs because of infection of the liver and surrounding tissue, which may result from bacteria traveling from the pelvis directly to the liver or via the bloodstream or lymphatic system. Fitz-Hugh-Curtis syndrome is characterized by the developed of string-like, fibrous scar tissue (adhesions) between the liver and the abdominal wall or the diaphragm.

Laparoscopy is the gold standard for diagnosing FHCS and PID. In the setting of PID, laparoscopy can show oedema with exudates on tubal surfaces, ectopic pregnancy, or tubo-ovarian abscess. FHCS can be diagnosed directly via visualization of adhesions between the diaphragm and liver or liver and the anterior abdominal wall.

Achalasia is a failure of the lower oesophageal sphincter (LES) to relax that is caused by the degeneration of inhibitory neurons within the oesophageal wall. It is classified as either primary (idiopathic) or secondary (in the context of another disease). In patients with achalasia, the chief complaint is dysphagia to both solids and liquids, although regurgitation, retrosternal pain, and weight loss may also occur. Upper endoscopy, barium esophagram, and oesophageal manometry play complementary roles in the diagnosis of achalasia. While upper endoscopy and/or barium esophagram are often obtained initially, manometry usually confirms the diagnosis, and upper endoscopy is indicated to rule out a malignant underlying cause. In good surgical candidates, achalasia is usually treated with pneumatic dilation or myotomy. In most other cases, an injection of botulinum toxin is attempted. If these measures fail to provide relief, medical therapy (e.g., nifedipine) is indicated.

In patients with suspected gallstone complications, blood tests should include a complete blood cell (CBC) count with differential, liver function panel, and amylase and lipase. Up to 24% of women and 12% of men may have gallstones. Of these up to 30% may develop local infection and cholecystitis.

Acute cholecystitis is associated with polymorphonuclear leucocytosis. However, up to one third of the patients with cholecystitis may not manifest leucocytosis. In severe cases, mild elevations of liver enzymes may be caused by inflammatory injury of the adjacent liver.

Patients with cholangitis and pancreatitis have abnormal laboratory test values. Importantly, a single abnormal laboratory value does not confirm the diagnosis of choledocholithiasis, cholangitis, or pancreatitis; rather, a coherent set of laboratory studies leads to the correct diagnosis.

Choledocholithiasis with acute common bile duct (CBD) obstruction initially produces an acute increase in the level of liver transaminases (alanine and aspartate aminotransferases), followed within hours by a rising serum bilirubin level. The higher the bilirubin level, the greater the predictive value for CBD obstruction. CBD stones are present in approximately 60% of patients with serum bilirubin levels greater than 3 mg/dL.

If obstruction persists, a progressive decline in the level of transaminases with rising alkaline phosphatase and bilirubin levels may be noted over several days. Prothrombin time may be elevated in patients with prolonged CBD obstruction, secondary to depletion of vitamin K (the absorption of which is bile-dependent). Concurrent obstruction of the pancreatic duct by a stone in the ampulla of Vater may be accompanied by increases in serum lipase and amylase levels.

Repeated testing over hours to days may be useful in evaluating patients with gallstone complications. Improvement of the levels of bilirubin and liver enzymes may indicate spontaneous passage of an obstructing stone. Conversely, rising levels of bilirubin and transaminases with progression of leucocytosis in the face of antibiotic therapy may indicate ascending cholangitis with the need for urgent intervention. Blood culture results are positive in 30%-60% of patients with cholangitis.

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.

Oesophageal dysphagia occurs when there is a difficulty with the passage of solid or liquid material through the oesophagus, specifically the region between the upper and lower oesophageal sphincter. It results from either abnormal motility of this segment of the oesophagus or obstruction.
Common causes of dysphagia:
Gastro-oesophageal reflux—waterbrash, regurgitation, due to dysmotility or stricture
Achalasia—classically hold-up relieved by carbonated beverages
Motility disorders—may be associated with central chest pain, systemic disease (scleroderma, dermatomyositis)
Oesophageal cancer—progressive, weight loss
Head and neck cancer—pain, dysphagia, otalgia, >90% smokers, often excess alcohol consumption
Pharyngeal pouch—slowly progressive, regurgitation, gurgling
Web—able to swallow only small amounts, “can’t swallow tablets”
Stroke
Neurodegenerative disorders—parkinsonism, motor neurone disease, multiple sclerosis, myasthenia gravis
Presbyphagia

Endoscopy has the advantage of potentially yielding a histological diagnosis. The overall rate of oesophageal perforation after flexible endoscopy involving oesophageal instrumentation, biopsy, or dilatation is 2.6%

Oesophageal manometry remains the investigation of choice in suspected motility disorders. Manometry can classify oesophageal dysmotility into rare specific disorders such as achalasia and diffuse oesophageal spasm or more common non-specific motility disorders that do not respond directly to drug treatment but may improve if related reflux or psychiatric disturbances are treated. The symptoms of non-specific motility disorders may have an uncertain relation to the manometric abnormalities

Management is based on the history, findings of the clinical investigations, and prognosis for the individual patient. The underlying disorder is treated, but the impact of dysphagia on nutrition and hydration will compromise any intervention unless managed effectively. Poor physical condition from malnutrition or dehydration will lead to a suboptimal rehabilitation process, in both duration and completeness of recovery and inadequate management of dysphagia contributes to this. A malnourished person is at risk of decompensation of the swallow, leading to dysphagia. The clinical swallow assessment is used to determine safely modified diets that reduce malnutrition and dehydration. This may range from nil by mouth with total enteral support to full oral route or a balance of the two. Enteral feeding is essential to maintain nutritional status when oral feeding is suspended, even if only for a short time. Prompt involvement of a dietitian is thus essential.

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.