Colorectal Flashcards
- How are anal fissures treated?
First line treatment involves conservative management. Surgical treatment is the other option and should only be considered if conservative management has failed after continuous treatment for 6-8 weeks.
For conservative management the treatment goal is to relax the internal anal sphincter, initiate and maintain atraumatic passage of stool, and relieve pain. This can be achieved by:
- fiber therapy to prevents hard bowel movements, which could reinjure a healing fissure.
- sitz baths which relaxes the anal sphincter and improves blood flow to anal mucosa
- stool softener or laxative to treat constipation and reduce straining
- topical nitroglycerin to promote healing of the fissure by increasing BF
- topical calcium channel blocker like nifedipine can reduce anal sphincter pressure
- topical analgesics like 2% lidocaine jelly for pain
• Local injection of botulinum toxin may also be useful to healing as a second line treatment before referral for a surgical opinion.
The gold standard surgical operation is lateral internal sphincterotomy
- What is an anal fissure? How does it develop? What causes it to persist?
- An anal fissure is a longitudinal tear in the mucosa and skin of the anal canal distal to the dentate line, Approx. 90% occur in the posterior midline due to poor perfusion of this portion, whereas secondary causes more associated with lateral tears.
- Primary fissures are due to local trauma and this may be due to:
- passage of hard stool
- prolonged diarrhea
- vaginal delivery
- repetitive injury or penetration such as in anal sex
Secondary fissures can be due to:
- IBD (chrons, UC)
- Infections (HIV/AIDS, syphillis)
- malignancy
- Anal fissures can persist and become chronic. This is due to:
- repeated tearing- “fear of defecation” can aggravate constipation and straining
- impaired healing- this is because the acute injury causes local pain and spasm of the internal anal sphincter that leads to reduced blood flow and poorer healing.
EXTRA
• Presentation:
- Severe tearing pain with the passage of faeces and sphincter spasm which persists for an hour or longer
- Small amount of bright red blood in the stool or toilet paper
- Fear of defecation, which worsens the constipation
- Examination is best performed in the lateral position and gently parting the buttocks – DRE is usually not needed and is usually contraindicated due to pain
Acute fissures – appear as a fresh laceration
Chronic fissures – have raised edges exposing the internal anal sphincter muscle fibres beneath, also often accompanied by an external skin tag (sentinel pile) and a hypertrophied anal papilla (benign growths of connective tissue that are covered by squamous cells) at the proximal end
o DDx: Haemorrhoid, anal fistula, solitary rectal ulcer
- How would you go about investigating a previously well 63 year-old man who presented to you with a short history of rectal bleeding?
I’d start of with a primary survey. If the pt is haemodynamically stable I would continue.
Patient’s >50 years old are at increased risk of Colorectal Ca, and in a patient presenting with PR bleeding it should be suspected and investigated.
I would start off by taking a detailed history focussing on the bleeding history, change in bowel habits, associated symptoms and the constituional signs for cancer. I’d also ask about PMHx, FHx, lifestyle and SHx for risk factors and differential diagnoses.
I would start of examination with a general exam by checking vitals, looking for signs of shock, signs of chronic bleeding (anemia- pallor, koilonychia, SOB) and signs of malignancy (cachexi or lymphadenopathy).
I’d then move on to an abdominal examination and rectal examination where I would examine the abdomen for mass and tenderness and other abnormalities and inspect the anus for anal fissure, skin tags, sentinel pile, haemorrhoids, fistulas, palpable masses and blood on the withdrawn gloved finger.
Investigations would include:
- FBC (anemia), UEC (hypokalemia), LFTs (mets), Coag studies, CRP
- a proctoscopy and rigid or a flexible sigmoidoscopy if in clinic
OR referral to colonoscopy as it is gold standard- can visualise and biopsy and remove polyps.
- CT scan can show diverticulitis or tumors.
- How would you go about investigating a previously well 63 year-old man who presented to you with a short history of anaemia?
A history focusing on the symptoms of anemia, blood loss and risk factors, medical conditions and previous surgeries (in particularly GI), diet, medications and Family history.
I would then follow this up with a general examination looking for signs of anemia or other conditions that can present with anemia. Then I would perform a targeted abdominal (PR exam, hepato-spleno-megaly, masses) and cardiovascular examination.
Investigations would include:
- FBC (Hb, WBC, blood film, reticulocyte count)
AND coagulation studies
Once anemia is confirmed and the RBC morphology is determines, focussed investigations can be aimed at the most likely causes for the anemia.
This includes:
- Iron studies (serum iron, ferritin, TIBC & transferrin)
- serum B12 and folate
- haemolytic parameters for haemolytic anemia (serum LDH, haptoglobin, bilirubin)
- Direct Coomb’s test for AI hemolytic anemia
- Hb Electrophoresis for thalasemias
- FOBT
- Urinalysis and Urine MCS- kidney problems affect EPO
- Gastroscopy and colonoscopy
- Small bowel capsule endoscopy- bleeds in small bowel.
MECHANISMS of ANEMIA
- Disorder of production
a) Bone marrow failure - e.g. aplastic anaemia, red cell aplasia
b) Decreased Erythropoeitin - e.g. Chronic Kidney Disease
- Disorder of maturation
a) Nuclear maturation defects - e.g. B12 or folate deficiency, OR Myelodysplasias- very active bone marrow but a low number of circulating blood cells due to poor maturation and early death
b) Cytoplasmic maturation defects - e.g. iron deficiency, thalassaemia
- Decreased Survival
a) Inherited defects - e.g. spherocytosis, G6PD deficiency, sickle-cell anaemia
b) Acquired defects - e.g. Autoimmune haemolysis, malaria, DIC, TTP= Thrombotic thrombocytopenic purpura
- Sequestration in spleen – hypersplenism
- Blood loss – e.g. GI haemorrhage, peri-operative bleeding
- How would you go about investigating a previously well 63 year-old man who presented to you with a short history of a change in bowel habit to more frequent evacuation of loose stools with mucus?
In a 63-year old male with a recent change in bowel habit, you need to exclude CR Ca, but other DDx may include inflammatory bowel disease, diverticulitis or infective colitis (campylobacter, salmonella, C.Difficle).
I’d start with a history that includes questions on:
- Bowel habits – duration, frequency, Bristol stool chart
- Associated Sx – bleeding, abdo pain, n/v/a, weight loss, fever
- Sick contacts, recent travel
- risk factors for CR cancer and other lifestyle factors
- medical conditions and medications
- FHx
On examination I’d assess:
- general appearance
- vitals
- fluid status - mucous membranes, cap refill
- a targetted abdo exam with PR
Investigations would include:
• FBC (+/- iron studies, folate and B12 as appropriate – i.e. anaemia)
• UEC- electro disturbance, LFT, CRP,
Coagulation studies
- Stool MCS (leukocytes, occult blood, ova/parasites)
- Stool PCR for Clostridium Difficile toxin
I'd also consider: - Colonoscopy +/- biopsy - upper GI endoscopy - barium studies - contrast CT if the previous tests were inconclusive or necessitated further investigations
- What are the major risk factors for colorectal cancer?
• Increasing Age (about 99% of cases in people > 40yrs) • Obesity • Inflammatory Bowel Disease • Personal or Family Hx of CRC or polyps • Lynch Syndrome • Polyposis Syndromes - smoking - alcohol consumption - diets with low fibre, high fat, high meat intake
- What method is used for population screening for colorectal cancer in Australia?
The National Bowel Cancer Screening Program is the population based screening program in Australia for colorectal cancer.
The screening test used in the Program is an immunochemical Faecal Occult Blood Test (iFOBT) which involves taking a tiny sample of faeces which is tested in a pathology laboratory for traces of blood.
People aged 50-74 years are sent a free Home Test Kit by mail to complete at home and send back to a laboratory for analysis.
Test results are sent directly to the participant and their nominated doctor. Participants with a positive test result are advised to see their doctor to discuss the result and referral to further diagnostic testing, usually colonoscopy.
Follow-up health services after a positive test result are provided through state and territory government health services or private health services.
- What is neoadjuvant therapy for rectal cancer?
Neoadjuvant therapy is treatment given prior to definitive surgery to shrink a tumour making it more easily resectable. This can be in the form of chemotherapy, radiotherapy and/or hormone therapy.
Neoadjuvant or induction chemoradiotherapy is an increasingly used strategy for patients with rectal adenocarcinomas.
The only definitive indication for neoadjuvant chemoradiotherapy, supported by the results of randomized trials, is the presence of a clinical T3 or T4 tumor.
Relative indications include:
- Clinically node positive T1/2 tumours staged with MRI or trans-rectal endoscopic US
- Distal rectal tumours requiring abdominopelvic resection (APR)
- Tumours that appear to invade the mesorectal fascia on pre-op imaging
The Advantages of neoadjuvant therapy include:
•Pre-operative tumour shrinkage
•Higher chance of resection
•Sphincter preservation
•Down staging by treating local Lymph Node involvement
•Decreased risk to small bowel
•Decreases the risk of pelvic recurrence with tumours extending through the bowel wall
Disadvantages:
- possible over treatment leading to unnecessary side eddects
- delayed wound healing
- delay in performing a potentially curative operation thus risking metastatic spread if the chemotherapy is ineffective.
- Where are the common sites that metastatic disease from a colorectal primary are found?
Metastatic disease can result haematogenously, via direct invasion, via lymphatics and transperitoneally.
Metastatic disease from a colorectal primary are most commonly found in the liver. This is because the Sueprior and Inferior Mesenteric Veins drain into the splenic vein and subsequently the hepatic portal vein.
Colorectal cancers can also spread haematogenously to the lungs, bone, pertoneum and brain.
Anorectal tumors can directly invade the prostate (ant.) and sacrum (post.) in males and directly invade the vaginal wall and bladder in women.
EXTRA
- A tumor in the ascending colon or proximal 2/3 of the transverse colon drains into SM nodes
- distal 1/3 of transverse and descending colon drain into IM nodes.
- above the dentate line the sigmoid colon drains into inf. mesenteric (IM) nodes
- below the dentate line they drain into the inguinal nodes.
o SMN and IMN drains to para-aortic via cisterna Chyli into the thoracic duct
- What are the treatment options for liver metastases from a colorectal primary?
Treatment options include: - surgical hepatic resection - percutaneous radiofrequency ablation - selective internal radiation therapy - transarterial chemoembolisation AND - systemic management via chemotherapy
The surgical hepatic resection takes into consideration:
- PATIENT factors- such as comorbidities and their fitness for surgery
-TUMOR factors- right colon tumors from the midgut were associated with worse survival after resection than left colons of hindgut origin.
- ANATOMIC factors- Where there should be no extrahepatic metastasis,
No portal vein, hepatic artery or bile duct involvement AND
the preservation of two contiguous hepatic segments.
- percutaneous radiofrequency ablation can be done if pt is not eligible for surgery. It involves insertion of an image guided probe percutaneously into the tumour which emits high energy electrical currents effectively burning the cancer.
- Selective internal radiation therapy (SIRT) is an endovascular approach which involves the injection of radioactive beads the provide beta radiation to the liver.
- Trans-arterial chemoembolisation is also an endovascular approach where chemotherapy is injected directly into the liver vessels.
The treatment is based on the principle that hepatic cancers preferentially receive blood supply from the hepatic artery whilst normal parenchyma are supplied predominantly by the portal vein.
Chemotherapy can also be given neoadjuvantly, adjuvantly or palliatively to manage the patient.
- What is the adenoma-carcinoma sequence?
The adenoma-carcinoma sequence refers to a stepwise pattern of mutations in a cell or group of cells than results in cancer.
It is the process by which mutational activation of oncogenes and inactivation of tumour suppressor genes result in cancer.
In CR Ca, this is the process in which benign polyps undergo dysplastic change to become malignant adenocarcinomas. And this process takes approx. 5-10years
The mutations include:
- the activation of oncogenes from proto-oncogenes for example K-RAS
AND
- Inactivation of tumor suppresor genes such as p53 and APC
Normal mucosal cells of the intestine are continuously lost into lumen due to apoptosis and exfoliation, and are continually replaced by proliferation at the crypt base.
However, loss of one normal copy or inactivation of the tumor suppressor gene APC is the “first hit”. The loss of the second gene leads to the “second hit” at which point the mucosa is at risk and adenomas may form. Other mutations such as the mutation of K-RAS to a protooncogene and inactivation of p53 can then lead to the emergence of a carcinoma.
It does not follow a linear pathway, multiple mutations can occur in different order and it is the accumulation of mutations, as opposed to the the temporal sequence of change, that is more critical
- What is Crohn’s disease?
Chrons disease is is one of the two major entities of Inflammatory Bowel Disease (IBD), with Ulcerative Colitis (UC) being the other major entity.
It is a chronic, relapsing, immune-mediated inflammatory disorder that is transmural and can affect any part of the GIT. Most commonly the small or large bowel, and more particularly the terminal ileum (most affected site) and right colon.
It is a disorder of unknown aetiology, with incidence higher in ages between 13 to 30 and common clinical features can include:
- abdo pain- RIF pain
- diarrhea
- blood in the stools
- bowel obstruction due to stricture formation and luminal narrowing causing constipation
- fever maybe due to inflammatory process or abscess formation
- fatigue
- fistula formation- usually involving small bowel
- weight loss- due to malabsorption
- perianal lesions- fissure, abscess, fistulas
- aphthous ulcers or pain in the mouth and gums
- Esophageal involvement may present with odynophagia and dysphagia.
- Gallstones may form due to reduction in the bile acid
Chrons disease may also present with systemic features, affecting the skin, joints and eyes.
The diagnosis of Crohn disease (CD) is usually established with endoscopic findings or imaging studies in a patient with a compatible clinical history.
Routine laboratory tests may be normal or they may reveal anemia, iron deficiency, elevated white blood cell count, B12 deficiency, and/or elevated erythrocyte sedimentation rate or CRP. May also see a reduction in Hb and albumin due to protein losing enteropathy.
On colonoscopy, skip lesions (preserved mucosa between ulcers), transmural inflammation (thickened bowel), fat wrapping (mesenteric fat wraps around bowel due to chronic inflammation), abscess, fistulas, strictures and a cobblestone appearance may be noted.
Major findings on intestinal biopsy are focal ulcerations and acute and chronic inflammation. These findings are usually confirmatory rather than diagnostic. The focality of the inflammation differs from the diffuse pattern seen typically in ulcerative colitis. Granulomas may also be noted and if appropriate infections are ruled out it is diagnostic of chrons, however, not all patients with Chrons will have Granulomas (only 30% do)
Imaging studies are most useful to evaluate the upper gastrointestinal tract and allow documentation of the length and location of strictures in areas not accessible by colonoscopy. A CT can evaluate the small bowel, as well as extraintestinal complications, such as intraabdominal abscesses. MRI and endoscopic US can also show inflammatory findings.
- What is diverticular disease?
Diverticulosis, can be symptomatic or asymptomatic, and is the presence of sac like protusions of the colonic wall known as diverticula that develop at well defined points of weakness, usually where the vasa recta penetrate the circular muscle layer of the colon.
They are thought to be related to increased intraluminal pressure, which may be the result of low volume stool.
Colonic diverticula are most common in the sigmoid colon and to a lesser extent the descending colon but it can affect the whole colon.
The prevalence of diverticulosis is age-dependent, increasing from less than 20% at age 40 to 60% by age 60.
Diverticular Disease – is symptomatic diverticulosis, which can present as painless bleeding, altered bowel habit, or painful inflammation (diverticulitis). Bleeds more common on right sided (wall is thinner, bigger diverticula leads to more vessel damage) and diverticulitis more common L sided.
The aetiology is thought to involve both genetic and environmental factors.
Non modifiable risk factors include increasing age and being female. Modifiable RF include: - obesity - low fibre diet - alcohol and caffeine - NSAIDs and steroids,
- What is diverticulitis?
How does it present clinically?
Diverticulitis is the inflammation of one or more diverticulum.
It can be acute or chronic AND uncomplicated or complicated. They become complicated by:
- abscess formation
- fistulation
- perforation
- haemorrhage
AND bowel obstruction from chronic inflammatory strictures.
The clinical presentation of diverticulitis may include:
• Acute onset continuous LIF pain
• Nausea/ vomiting/ change in bowel habits (increased frequency and pellets)
• Fever
• Tachycardia
• LIF tenderness to obvious local peritonitis
• There may be a palpable mass in the LIF
• Leucocytosis
If it is complicated it can present with:
- peritonitis, sepsis and pneumoperitoneum if it is perforated
- swinging fever if theres an abscess formation
- haematochezia and hypovolemia if it haemorrhages
- severe constipation, colicky abdo pain and hyperresonant bowel sounds if it causes obstruction
- pneumaturia, severe uti or passage of faeces if it has led to a colovesical fistula
- purulent vaginal discharge if there is an entero-vaginal fistula
OR diarrhea if there is an colocolonic fistula.
EXTRA
Ix:
- Pathology:
o Leucocytosis
- Imaging
o AXR – exclude obstruction
o USS – allows percutaneous drainage if necessary
o Gold standard: CT – exclude concurrent issue - DO NOT sigmoidoscopy or barium enema as it can introduce air/contrast through the perforation
Mx:
- General measures:
o High fibre
o Increased fluid intake
o Stool softeners - Uncomplicated:
o Oral Co-Amoxiclav= amoxicillin and clavulanate
o Colonoscopy Follow Up after 6 weeks symptom free – exclude malignancy
Complicated=
bowel rest, intravenous fluids and intravenous antibiotic therapy= triple therapy= amoxycillin, gentamycin, metronidazole.
Consider surgery for perforation and uncontrolled abscess.
Recent studies have shown with anything up to a Hinchey III, a laparoscopic wash-out is a safe procedure, avoiding the need for a laparotomy and stoma formation.
- What are the major complications that can result from diverticulitis?
Major complications that can result from diverticulitis include:
- perforation
- peritonitis
- sepsis or septic shock
- pericolic abscess formation- serious if larger than 5cm
- fistulas
- strictures and bowel obstruction
