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 patient is a case of fistula-in-ano.

A fistula-in-ano is an abnormal hollow tract or cavity that is lined with granulation tissue and that connects a primary opening inside the anal canal to a secondary opening in the perianal skin; secondary tracts may be multiple and can extend from the same primary opening. Fistulae usually occur following previous ano-rectal sepsis. The discharge may be foul smelling and troublesome.

Fistula-in-ano is classified into two groups based on its anatomical location.
1. Low fistula: relatively close to the skin and passes through a few or no sphincter muscle fibres, crosses <30% external sphincter
2. High fistula: passes through a large amount of muscle

Assessment of fistula-in-ano includes:
1. Examination of the perineum
2. Digital rectal examination (DRE)
Low, uncomplicated fistulas may not require any further assessment. Other groups will usually require more detailed investigation.
3. Endo-anal USS
4. Ano-rectal MRI scan

Treatment options include:
1. Seton suture
2. Fistulotomy: Low fistulas that are simple should be treated by fistulotomy once the acute sepsis has been controlled. Fistulotomy (where safe) provides the highest healing rates.
3. Anal fistula plugs and fibrin glue
4. Ano-rectal advancement flaps: primarily for high fistulae

Optimal physical assessment of an anorectal abscess may require anaesthesia to alleviate patient discomfort that would otherwise limit the extent of the examination.
Drainage should be carried out promptly to prevent the sepsis worsening. Perianal incisions to allow drainage of pus should be circumanal, thus reducing the likelihood of damage to the sphincters and thereby preventing faecal incontinence.

Passage of bloody diarrhoea together with mucus and a short history makes this a likely presentation of inflammatory bowel disease. Rectal malignancy in a young age would be a very unlikely event. Furthermore, the history is too short to be consistent with solitary rectal ulcer syndrome.

Rectal bleeding is a common cause for patients to be referred to the surgical clinic. In the clinical history, it is important to try and localise the anatomical source of the bleeding. Bright red blood is usually of rectal origin, whereas, dark red blood is more suggestive of a proximally located bleeding source. Blood which has entered the gastrointestinal tract from a gastroduodenal source will typically resemble melaena due to the effects of the digestive enzymes on the blood itself.

PR bleeding in ulcerative colitis (UC) is usually bright red and often mixed with stool. It is mostly associated with the passage of mucus as well. Other clinical features reported on history include diarrhoea, weight loss, and nocturnal incontinence. Proctitis is the most marked finding on examination and perianal disease is usually absent. Colonoscopy is carried out which shows continuous mucosal lesions.

Proctalgia fugax (PF) is a benign painful rectal condition that is defined as intermittent, recurring, and self-limiting pain in the anorectal region in the absence of organic pathology. The pain of proctalgia fugax is sharp or gripping and severe. Similar to other urogenital focal pain syndromes, such as vulvodynia and proctodynia, the causes remain obscure. Stress and sitting for prolonged periods often increase the frequency and intensity of attacks of proctalgia fugax. Patients often feel an urge to defecate with the onset of the paroxysms of pain . Depression often accompanies the pain of proctalgia fugax but is not thought to be the primary cause. The symptoms of proctalgia fugax can be so severe as to limit the patient’s ability to perform activities of daily living. Reassurance has proven to help in many cases as the condition has been linked to stress.

Since the most likely diagnosis is anal fissure, the correct treatment is topical nitrates.

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

Diagnostic options are as follows:
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 by colonoscopy and EUA, with biopsies of the area.

For management of anal fissure:
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.
2. Resistant cases may benefit from injection of botulinum toxin or lateral internal sphincterotomy. Advancement flaps may be used to treat resistant cases.

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.

Answer: Surveillance annual flexible sigmoidoscopy from age 13 years until age 30 years.

Familial adenomatous polyposis (FAP) is the most common adenomatous polyposis syndrome. It is an autosomal dominant inherited disorder characterized by the early onset of hundreds to thousands of adenomatous polyps throughout the colon. If left untreated, all patients with this syndrome will develop colon cancer by age 35-40 years. In addition, an increased risk exists for the development of other malignancies.
Most patients with FAP are asymptomatic until they develop cancer. As a result, diagnosing presymptomatic patients is essential.

Of patients with FAP, 75%-80% have a family history of polyps and/or colorectal cancer at age 40 years or younger.

Nonspecific symptoms, such as unexplained rectal bleeding (haematochezia), diarrhoea, or abdominal pain, in young patients may be suggestive of FAP.

In a minority of FAP families a mutation cannot be identified and so annual flexible sigmoidoscopy should be offered to at risk family members from age 13–15 years until age 30, and at three to five year intervals thereafter until age 60 years.

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.

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.

Presence of fever and severe pain point towards the diagnosis of an abscess rather than a fissure. Although fissures may be painful, they do not, in themselves, cause fever. Moreover, a case of fissure-in-ano typically presents with bright red PR bleed.

The management option for intersphincteric abscess includes examination of the ano-rectum under general anaesthesia and drainage of the sepsis.

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.

Solitary rectal ulcer syndrome is a rare disorder that involves straining during defecation, a sense of incomplete evacuation, and sometimes passage of blood and mucus by rectum.
The syndrome is poorly named because associated lesions may be solitary or multiple and ulcerated or nonulcerated; they range from mucosal erythema to ulcers to small mass lesions.
Lesions are typically located in the anterior rectal wall within 10 cm of the anal verge.
It is probably caused by localized ischemic injury or prolapse of the distal rectal mucosa. Diagnosis is clinical with confirmation by flexible sigmoidoscopy and biopsy. Treatment is a bowel regimen for mild cases, but surgery is sometimes needed if rectal prolapse is the cause.

The cardinal symptom of Fissure in ano is pain.

Subtotal colectomy with ileostomy remains a safe and effective treatment for patients requiring urgent surgery for severe inflammatory bowel disease. As the patient is not hemodynamically stable, any anastomosis like ileorectal or ileoanal should not be done. The patient should be fully resuscitated and given antibiotics and thromboprophylaxis preoperatively.

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.

The most appropriate management option to consider, after GTN or other topical nitrates have failed, is botulinum toxin injection. In males, a lateral internal sphincterotomy would be an acceptable alternative. In a female who has yet to conceive, this may predispose to an increased risk of sphincter dysfunction. Moreover, division of the external sphincter would result in faecal incontinence and is not a justified treatment for anal fissure.

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

Diagnostic options are as follows:
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 by colonoscopy and EUA, with biopsies of the area.

For management of anal fissure:
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.
2. Resistant cases may benefit from injection of botulinum toxin or lateral internal sphincterotomy. Advancement flaps may be used to treat resistant cases.

Answer: Measurement of faecal calprotectin

Based on Rome criteria, this patient has Irritable Bowel Syndrome (IBS). Irritable bowel syndrome (IBS) is a group of symptoms—including abdominal pain and changes in the pattern of bowel movements without any evidence of underlying damage. These symptoms occur over a long time, often years. It has been classified into four main types depending on whether diarrhoea is common or constipation is common, or both are common, or neither occurs very often (IBS-D, IBS-C, IBS-M, or IBS-U respectively). IBS negatively affects quality of life and may result in missed school or work. Disorders such as anxiety, major depression, and chronic fatigue syndrome are common among people with IBS.

The recommendations for physicians are to minimize the use of medical investigations. Rome criteria are usually used. They allow the diagnosis to be based only on symptoms, but no criteria based solely on symptoms is sufficiently accurate to diagnose IBS. Worrisome features include onset at greater than 50 years of age, weight loss, blood in the stool, iron-deficiency anaemia, or a family history of colon cancer, celiac disease, or inflammatory bowel disease. The criteria for selecting tests and investigations also depends on the level of available medical resources.

Rome criteria
The Rome IV criteria includes recurrent abdominal pain, on average, at least 1 day/week in the last 3 months, associated with two or more of the following criteria:

Related to defecation
Associated with a change in frequency of stool
Associated with a change in form (appearance) of stool.
Physicians may choose to use one of these guidelines or may simply choose to rely on their own anecdotal experience with past patients. The algorithm may include additional tests to guard against misdiagnosis of other diseases as IBS. Such red flag symptoms may include weight loss, gastrointestinal bleeding, anaemia, or nocturnal symptoms. However, red flag conditions may not always contribute to accuracy in diagnosis; for instance, as many as 31% of people with IBS have blood in their stool, many possibly from hemorrhoidal bleeding.

The diagnostic algorithm identifies a name that can be applied to the person’s condition based on the combination of symptoms of diarrhoea, abdominal pain, and constipation. For example, the statement 50% of returning travellers had developed functional diarrhoea while 25% had developed IBS would mean half the travellers had diarrhoea while a quarter had diarrhoea with abdominal pain. While some researchers believe this categorization system will help physicians understand IBS, others have questioned the value of the system and suggested all people with IBS have the same underlying disease but with different symptoms

The main diseases that cause an increased excretion of faecal calprotectin are inflammatory bowel diseases, coeliac disease, infectious colitis, necrotizing enterocolitis, intestinal cystic fibrosis and colorectal cancer.

Although a relatively new test, faecal calprotectin is regularly used as indicator for inflammatory bowel diseases (IBD) during treatment and as diagnostic marker. IBD are a group of conditions that cause a pathological inflammation of the bowel wall. Crohn’s disease and ulcerative colitis are the principal types of inflammatory bowel disease. Inflammatory processes result in an influx of neutrophils into the bowel lumen. Since calprotectin comprises as much as 60% of the soluble protein content of the cytosol of neutrophils, it can serve as a marker for the level of intestinal inflammation. Measurement of faecal calprotectin has been shown to be strongly correlated with 111-indium-labelled leucocytes – considered the gold standard measurement of intestinal inflammation. Levels of faecal calprotectin are usually normal in patients with irritable bowel syndrome (IBS). In untreated coeliac disease, concentration levels of faecal calprotectin correlate with the degree of intestinal mucosal lesion and normalize with a gluten-free diet.

Faecal calprotectin is measured using immunochemical techniques such as ELISA or immunochromatographic assays. The antibodies used in these assays target specific epitopes of the calprotectin molecule.

Gallbladder ultrasonography should be considered if the patient has recurrent dyspepsia or characteristic postprandial pain.

Abdominal computed tomography (CT) scanning is appropriate to screen for tumours, obstruction, and pancreatic disease if these are diagnostic possibilities.

CT and magnetic resonance (MR) enterography or wireless capsule endoscopy are employed if red flags exist to suggest enteritis (small bowel inflammation) or a tumour.

Colonoscopy is appropriate if alarm symptoms are present and in patients who otherwise qualify for screening colonoscopy.

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.

Neutropenic enterocolitis is a life threatening complication occurring most frequently after intensive chemotherapy in acute leukaemia and solid tumours. It is an acute life-threatening condition classically characterized by transmural inflammation of the cecum, often with involvement of the ascending colon and ileum, in patients who are severely myelosuppressed. Neutropenic enterocolitis has an incidence of 5% in patients typically undergoing chemotherapy for haematological malignancies. Mortality can be >50% in the presence of perforation and sepsis so patients must be identified quickly and treated.

Proctalgia fugax or functional recurrent anorectal pain is part of a spectrum of functional gastrointestinal disorders defined by the Rome III diagnostic criteria as episodes of sharp fleeting pain that recur over weeks, are localized to the anus or lower rectum, and last from seconds to several minutes with no pain between episodes. There is no diurnal variation. There are numerous precipitants including sexual activity, stress, constipation, defecation and menstruation, although the condition can occur without a trigger. It should be differentiated from chronic proctalgia, a functional anorectal pain disorder with a vague, dull ache or pressure sensation high in the rectum, often worse when sitting than when standing or lying down, and lasts at least 20 minutes.
Most treatments for proctalgia fugax (e.g., oral diltiazem, topical glyceryl nitrate, nerve blocks) act by relaxing the anal sphincter spasm, but the effectiveness of these treatments are supported only by case reports or case series, with the exception of a single randomized controlled trial of salbutamol, making the value of most treatment options, including salbutamol, difficult to judge.

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.

Colorectal cancer is one of the most common types of cancer in Western populations. The liver is the first location of metastatic disease; as the main mechanism of dissemination is through the portal system. In addition, the liver may be the sole site of metastasis in 30 to 40% of patients with advanced disease.

Unfortunately, 20% of these patients will develop metastasis in the lungs and >50% in liver. In 20 to 25% of patients at the time of diagnosis, hepatic metastatic disease can be identified clinically, and 40 to 50% will develop during the first 3 years after the primary tumour is diagnosed.
When metastatic lesions are localized in the liver, which corresponds to 30% of patients, there are several options for localized treatment, such as hepatic partial resection, localized ablative therapy, administration of chemotherapy by infusion of the hepatic artery, systemic chemotherapy, and isolated hepatic fusion for patients with high doses of chemotherapy. Surgical resection is the most effective treatment for hepatic metastasis in colorectal cancer, but only a few patients are candidates for initial surgery. Patients with hepatic metastasis that cannot be surgically resected are managed initially with chemotherapy and later are subject to surgery, and these patients present a similar survival rate to those undergoing surgery initially.
Prior to hepatic resection, patients with hepatic metastatic disease frequently receive neoadjuvant chemotherapy, which can aid in disappearing or hidden radiological lesions.
The 5-year survival rate after hepatic resection is 25-40%.

Answer: Inflammatory bowel disease

Inflammatory bowel disease (IBD) is an idiopathic disease caused by a dysregulated immune response to host intestinal microflora. The two major types of inflammatory bowel disease are ulcerative colitis (UC), which is limited to the colonic mucosa, and Crohn disease (CD), which can affect any segment of the gastrointestinal tract from the mouth to the anus, involves skip lesions, and is transmural. There is a genetic predisposition for IBD, and patients with this condition are more prone to the development of malignancy.

Generally, the manifestations of IBD depend on the area of the intestinal tract involved. The symptoms, however, are not specific for this disease. They are as follows:

Abdominal cramping

Irregular bowel habits, passage of mucus without blood or pus

Weight loss

Fever, sweats

Malaise, fatigue

Arthralgias

Growth retardation and delayed or failed sexual maturation in children

Extraintestinal manifestations (10-20%): Arthritis, uveitis, or liver disease

Grossly bloody stools, occasionally with tenesmus: Typical of UC, less common in CD

Perianal disease (e.g., fistulas, abscesses): Fifty percent of patients with CD

The World Gastroenterology Organization (WGO) indicates the following symptoms may be associated with inflammatory damage in the digestive tract [1] :

Diarrhoea: mucus or blood may be present in the stool; can occur at night; incontinence may occur

Constipation: this may be the primary symptom in ulcerative colitis, when the disease is limited to the rectum; obstipation may occur and may proceed to bowel obstruction

Bowel movement abnormalities: pain or rectal bleeding may be present, as well as severe urgency and tenesmus

Abdominal cramping and pain: commonly present in the right lower quadrant in Crohn disease; occur peri umbilically or in the left lower quadrant in moderate to severe ulcerative colitis

Nausea and vomiting: occurs more often in Crohn disease than in ulcerative colitis

The nocturnal diarrhoea and incontinence are important symptoms in diagnosis IBD.

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.

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

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.

The operation aims to remove most of your large bowel including the blood supply and associated lymph glands and leave the rectum behind. It is most commonly recommended for inflammatory bowel disease like ulcerative colitis and Crohn’s disease.

It is also recommended for other bowel conditions like familial adenomatous polyposis, and when there is more than one bowel cancer.

In inflammatory bowel disease such as ulcerative colitis the small bowel is brought out to the skin of the tummy as an ileostomy and the remaining bowel (rectum) is closed off and left inside. In other conditions where possible, the two ends of the remaining healthy bowel (small bowel to rectum) are re-joined (an anastomosis). Most
people therefore do not require a stoma. However some people benefit from having a stoma made depending on circumstances regarding:
1) Their general state of health (heart disease, lung disease, diabetes, vascular disease, smoking, steroid medications, being undernourished);
2) Factors which cannot be seen until the surgeon can see inside your tummy (more extensive disease than originally thought, extensive pelvic scarring from previous surgery or other treatment, excessive bleeding).
Temporary stomas are made to divert faeces away from the join (de-functioning) to give the best chance to heal if there is concern it may be slow to heal.

Emergency indications for surgical intervention in severe UC include free perforation, haemorrhage or systemic instability. An urgent indication for colectomy is a severe attack that is unresponsive to medical therapy.

In the setting of severe UC, the procedure of choice is subtotal colectomy and ileostomy. The residual rectal disease is controllable in most patients. In general, there are advantages to the subtotal colectomy approach, including a lower morbidity if pelvic dissection is not performed, preservation of the rectum so that reconstructive procedures can be performed later, and allowing the definitive procedure to be deferred to an optimal situation when the patient is off immunosuppressive medications and has improved nutritional status. Usually, the staged reconstruction with IPAA or definitive total proctocolectomy is performed several months later.

An anal fistula is an abnormal tract between the anal canal and the skin around the anus.
Anal fistulas can be classified according to their relationship with the external sphincter. A fistula may be complex, with several openings onto the perianal skin. Intersphincteric fistulas are the most common type and cross only the internal anal sphincter. Trans-sphincteric fistulas pass through both the internal and external sphincters.

The aim is to drain the infected material and encourage healing.
For simple intersphincteric and low trans-sphincteric anal fistulas, the most common treatment is a fistulotomy or laying open of the fistula tract.
For high and complex (deeper) fistulas that involve more muscle, with a high risk of faecal incontinence or recurrence, surgery aims to treat the fistula and preserve sphincter-muscle function. Techniques include a 1‑stage or 2‑stage seton (suture material or rubber sling) either alone or in combination with fistulotomy, ligation of an intersphincteric fistula tract, creating a mucosal advancement flap, injecting glue or paste, or inserting a fistula plug .

An Anal fissure is a cut or a tear in the anal canal typically caused by passing a hard stool. Patients often complain of severe anal pain and bleeding with bowel movements. On physical examination, you may see the fissure or just the sentinel tag. If the examination appears normal, you can elicit point tenderness. We recommend against continuing the digital rectal examination or anoscopy if the patient is having pain during the examination.
The primary goals of therapy are to properly bulk the stool with adequate fibre and relax the anal muscle. Specific steps include the following:
Properly bulk the stool with adequate fibre to minimize constipation and diarrhoea; both frequent bowel movements and hard bowel movements can lead to an anal fissure.
Temporary use of laxatives such as daily Miralax or senna. The dose of Miralax can be titrated up or down to achieve desired results. As the patient’s fibre supplementation increases, the need for Miralax will diminish.
Chronic use of laxatives should be avoided because it can lead to worsening colonic function and constipation.
Diltiazem 2% ointment is to be placed on the anal muscle 3 times daily—continue for a minimum of 8 weeks, even if symptoms improve earlier.
If a patient cannot tolerate diltiazem or is breastfeeding or pregnant, 0.2% nitroglycerin-compounded ointment can be prescribed. However, the proper dose of nitroglycerin is important as too high of a dose can cause severe headaches.
Do NOT prescribe haemorrhoid ointments or suppositories, especially steroid-based ones. Steroid ointments do not help. They do cause perianal skin thinning and dermatitis. At best, they act as a placebo, but they often are used chronically and cause unpleasant perianal skin changes.
Use mental anal muscle relaxation: Actively thinking about relaxing sphincter tone.
Consider sitz baths: Soaking the anal area in warm water induces relaxation. Warmer water induces more relaxation. No additives are needed.
Surgical intervention (such as Botox injections or sphincterotomy) is considered for patients whose symptoms do not improve with the above management strategies. It is imperative that the patient increases fibre and water intake so bowel movements are very soft before the surgical intervention to maximize chances of postoperative healing.

The patient has Haemorrhoid Disease
A total of 40% of individuals with haemorrhoids are asymptomatic.
For internal haemorrhoids, bleeding is the most commonly reported symptom. The occurrence of bleeding is usually associated with defecation and almost always painless. The blood is bright red and coats the stool at the end of defection.
Another frequent symptom is the sensation of tissue prolapse. Prolapsed internal haemorrhoids may accompany mild faecal incontinence, mucus discharge, a sensation of perianal fullness, and irritation of perianal skin. Pain is significantly less common with internal haemorrhoids than with external haemorrhoids but can occur in the setting of prolapsed, strangulated internal haemorrhoids that develop gangrenous changes due to the associated ischemia.
In contrast, external haemorrhoids are more likely to be associated with pain, due to activation of perianal innervations associated with thrombosis. Patients typically describe a painful perianal mass that is tender to palpation. This painful mass may be initially increasing in size and severity over time. Bleeding can also occur if ulceration develops from necrosis of the thrombosed haemorrhoid, and this blood tends to be darker and more clotted than the bleeding from the internal disease. Painless external skin tags often result from previous oedematous or thrombosed external haemorrhoids.

Lifestyle and dietary modification are the mainstays of conservative medical treatment of haemorrhoid disease. Specifically, lifestyle modifications should include increasing oral fluid intake, reducing fat consumptions, avoiding straining, and regular exercise. Diet recommendations should include increasing fibre intake, which decreases the shearing action of passing a hard stool.
Most patients with grade I and II and select patients with grade III internal hemorrhoidal disease who fail medical treatment can be effectively treated with office-based procedures.
For internal haemorrhoids, rubber band ligation, sclerotherapy, and infrared coagulation are the most common procedures but there is no consensus on optimal treatment. Overall, the goals of each procedure are to decrease vascularity, reduce redundant tissue, and increase hemorrhoidal rectal wall fixation to minimize prolapse.
Rubber band ligation is the most commonly performed procedure in the office and is indicated for grade II and III internal haemorrhoids.