Lower GI Flashcards
(138 cards)
1
Q
Abdo pain, bloating, vomiting post bowel surgery?
A
post op ileus
2
Q
Explain what anal fissures are?
A
- A tear in the sensitive skin-lined lower anal canal, distal to the dentate/pectinate line
- They can be primary or secondary
- Primary: no apparent cause
- Secondary: constipation, inflammatory bowel disease, STI, rectal malignancy
- In primary the exact aetiology is not understood
3
Q
Presentation of anal fissure?
A
- Severe pain on defaecation “like passing shards of glass”
- There may be bleeding on passing stools, if present it is seen as bright red blood on the stool or toilet paper
- The fissure can be seen on external examination of the anus
- Usually, it is in the form of a linear split of the mucosa
- Should not attempt DRE in acute as will be very painful but if think there is a need can get patient to return
4
Q
Investigation for anal fissure?
A
- Diagnosis can usually be made on history and physical examination
- Further investigations only required if there are features of an underlying pathology
5
Q
Management of anal fissures?
A
Primary Care
* Advise children and adults to take measures to keep stools regular and soft: adequate fluid intake, increase fibre content, consider use of laxative
* Pain relief e.g., paracetamol or ibuprofen, consider GTN ointment which relaxes smooth muscle and reduces anal tone, consider topical anaesthetic e.g. lidocaine for extreme pain
* Refer children with anal fissure that has not healed within 2 weeks, refer adults with ongoing pain which has not resolved within 6-8 weeks, refer adults who do not have symptoms but still have fissure after 12-16 weeks
* Consider earlier referral in elderly as it is less common in this group and there is a higher chance of malignancy
Secondary Care
* Topical diltiazem a CCB may be used
* Nifedipine another CCB may be used
* Botox may be used as a last resort
* Surgery might be done
6
Q
Define diverticula, diverticular disease, diverticulosis and diverticulitis?
A
- Diverticula are abnormal sacs or pockets in the GI tract thought to form due to increased luminal pressure and a low fibre diet
- Diverticulosis = presence of diverticula in the colon without symptoms
- Diverticular disease = the presence of diverticula with mild abdominal pain or tenderness and no systemic symptoms
- Diverticulitis = inflammation of diverticula
7
Q
Diverticula are most commonly found in what part of the colon?
A
sigmoid colon
8
Q
Who tends to get diverticula?
A
the elderly
9
Q
Presentation of diverticulosis, diverticular disease and diverticulitis?
A
- Diverticulosis is asymptomatic
- Diverticular disease presents with mild and intermittent left lower quadrant pain with constipation, diarrhoea or occasional rectal bleeds
- Diverticulitis presents with constant abdominal pain, usually severe and localising to the left quadrant, fever, sudden change in bowel habit, significant rectal bleeding, a palpable abdo mass or distension may be felt
10
Q
Investigations for diverticulosis, diverticular disease and diverticulitis?
A
- Those with diverticular disease do not need referred unless they have not been able to have routine endoscopic or radiological investigations in primary care, or they have cancer red flags or colitis
- Those with complicated acute diverticulitis suspected need referred to hospital for FBC, U and Es, CRP and a contrast CT
11
Q
Management for diverticulosis, diverticular disease and diverticulitis?
A
- Those with diverticulosis just need reassurance and advice on a high fibre diet
- Those with diverticular disease do not need antibiotics, they should be advised to stop smoking, weight loss, high fibre diet, can consider bulk forming laxatives, simple analgesia and/ or antispasmodics if needed
- Those with uncomplicated acute diverticulitis likely need antibiotics but in some cases can be sent home with simple analgesia to see if resolves
- Those with complicated will be given IV antibiotics (amoxicillin, metronidazole and gentamicin)
12
Q
What is Crohn’s disease?
A
- Inflammatory bowel disease that can affect any part of the GI tract from mouth to anus but most commonly affects the terminal ileum and colon
- Inflammation is discontinuous and occurs in skip lesions
- Inflammation is transmural meaning it extends down to the serosa
13
Q
Who gets crohn’s disease?
A
- Crohn’s disease is thought to be an immune-mediated condition caused by environmental triggering events in genetically susceptible people
- Risk factors include a family history of inflammatory bowel disease, smoking, previous infectious gastroenteritis, and drugs such as nonsteroidal anti-inflammatory drugs (NSAIDs)
14
Q
Presentation of Crohn’s disease?
A
- Depends on what part of the GI tract is affected
- Persistent diarrhoea with potential blood or mucus in the stool
- Abdominal pain and/ or discomfort
- Weight loss and failure to thrive in children
- Fatigue, malaise, anorexia or fever
- On examination may have abdo tenderness, perianal pain or tenderness as well as perianal skin tags, abscesses, fissures or fistulas
- May also see extra-intestinal manifestations
15
Q
Investigations for crohns disease?
A
- If suspected need referred to secondary care
- Initial investigations include FBC, CRP, ESR, U and Es, LFTs, stool culture and microscopy (inflammatory markers likely to be raised)
- Faecal calprotectin and lactoferrin are usually raised in active inflammatory intestinal disease
- Diagnosis generally needs biopsy from colonoscopy and/ or endoscopy
- May be ASCA positive
16
Q
Management of crohns disease?
A
- Give steroids to induce remission and manage flares
- Azathioprine or mercaptopurine can be used to maintain remission
- Anti-TNF e.g. infliximab and adalimumab are used in severe cases
- Surgery for Crohns can be done but is not curative and need to minimise the amount of bowel removed
17
Q
What are some extra-intestinal manifestations of crohns and UC?
A
- Enteropathic arthritis
- Skin rashes – erythema nodosum, pyoderma gangrenosum, anal skin tags, enterocutaneous fistulas, anal fissures
- Osteoporosis and osteomalacia (partially due to disease and also use of steroids)
- Uveitis and episcleritis
- Primary sclerosing cholangitis, gallstones, hepatitis, fatty liver disease
- Anaemia
18
Q
List some complications of crohns?
A
- Abscesses
- Strictures
- Fistulas
- Malnutrition and altered growth in children
- Cancer of the small and large intestine
19
Q
What is ulcerative colitis?
A
- Inflammatory bowel disease confined to the colon and rectum, inflammation is continuous and moves from the rectum upwards
- Can occur in the form of a proctitis (inflammation involving only the rectum), a left sided colitis (up to the splenic flexure), or as a pancolitis (the whole colon)
- Inflammation only extends to the submucosa and there are no granulomas
20
Q
Who gets ulcerative colitis?
A
- Thought to be autoimmune disease with environmental triggers in susceptibly genetic individuals
- Smoking has actually been shown to be protective
21
Q
Presentation of ulcerative colitis?
A
- Bloody diarrhoea
- Rectal bleeding
- Faecal urgency or incontinence
- Nocturnal defaecation
- Tenesmus (feeling that you need to pass stools even though bowels are already empty)
- Abdominal pain
- Fatigue, weight loss, anorexia or fever
- On examinations may find pallor, clubbing, abdominal distension, tenderness or mass
22
Q
Investigations for ulcerative colitis?
A
- May be PANCA positive
- Initial investigations include FBC, CRP, ESR, U and Es, LFTs, stool culture and microscopy (inflammatory markers likely to be raised)
- Faecal calprotectin and lactoferrin are raised in active intestinal disease
- Colonoscopy is usually done for diagnosis and biopsy taken
23
Q
Raised faecal ______ can suggest active inflammatory bowel disease
A
lactoferrin and calprotectin
24
Q
UC may be _______ positive and crohns may be ______ positive
A
uc - PANCA
crohns - ASCA
25
Management of uc?
* Aminosalicylates are first line for UC to induce and maintain remission e.g. delzicol, asacol HD, pentasa (can be topical first if not extensive disease then may convert to oral if not enough)
* If remission still not achieved use steroid
* Biologics and immunosuppressants can be used for severely active disease
* Surgery can be done in severe disease and in UC this is curative and also eliminates the risk of colorectal cancer
26
Complications of uc?
* Toxic megacolon
* Increased risk of primary sclerosing cholangitis and developing cholangiocarcinoma
27
8 differences between crohns and UC?
Crohns:
disease anywhere from mouth to anus
discontinuous skip lesions
granulomas present
inflammation is transmural
surgery is not curative
less increased risk of colorectal cancer
smoking aggravates disease
anal disease is common
Ulcerative colitis:
only the rectum and colon
continues inflammation from rectum upwards
granulomas absent
inflammation is confined to the mucosa and submucosa
surgery is curative
increased risk of colorectal cancer
smoking is protective against disease
PSC and cholangiocarcinoma increased risk
28
What is IBS?
* Functional GI disorder
* Characterised by abdominal discomfort, bloating or pain associated with defaecation or a change in bowel habit
29
Risk factors for IBS?
* It is not fully understood but thought to be some motor/ sensory dysfunction in the GI tract or changes in gut reactivity
* IBS is more common in middle aged women and is thought to be associated with emotional stimuli such as stress or abuse and is also linked to trauma
* Sometimes has initial trigger of gastroenteritis
* Related to other functional disorders e.g. fibromyalgia
30
Presentation of IBS?
* Abdominal pain and cramping
* Generally pain is relieved by defaecating
* Diarrhoea
* Constipation
* Food intolerance
* Can be classified as IBS with diarrhoea, IBS with constipation or mixed IBS
* Might get worse with stress
31
Diagnosis of IBS?
Need to exclude red flag symptoms for cancer:
* https://www.cancerreferral.scot.nhs.uk/lower-gastrointestinal-cancer/
* Bleeding – repeated rectal bleeding without an obvious anal cause or any blood mixed with stool
* Bowel habit – persistent (more than 4 weeks) change in bowel habit especially to looser stools (not so interested in constipation)
* Pain – abdominal pain with weight loss
* Iron deficiency anaemia – unexplained iron deficiency anaemia
Then need to exclude inflammatory bowel disease:
* Inflammatory markers blood test
Need to exclude Coeliac disease
Tests:
* QFit to check for blood in stool (sign of IBD or cancer)
* FBC (checking for anaemia and signs of a systemic disease)
* ESR AND CRP (for IBD)
* TTG (for coeliacs)
If all these tests come back negative can diagnose IBS
32
Management of IBS?
* Education and information on lifestyle, physical activity, diet and relaxation
* Diet and nutritional advice – general advice such as reducing caffeine and sugary drinks, reducing high fibre foods and resistant starch (recooked foods have this), if going to recommend the FODMAP diet should refer to a dietician
* Antispasmodic agents e.g. mebeverine hydrochloride, alverine citrate and peppermint oil
* Laxatives can be used and titrated to effect for those with constipation
* Loperamide can be used for acute diarrhoea
* Tricyclics and SSRIs can be used for pain
33
What is ascites? when will it be detected clinically?
* Excessive accumulation of fluid in the abdominal cavity
* To detect it clinically > 1500 ml needs to present
34
List some causes of ascites?
* Cirrhosis and hepatocellular carcinoma (sodium and water retention and hypoalbuminaemia)
* Malignancy – GI tract malignancies or metastatic disease in abdominal cavity, lymphoma, Meigs syndrome (benign ovarian tumour, ascites and pleural effusion) – generally get ascites if the cancer has spread to the liver or it is the peritoneum and making vessels leaky
* Heart failure (back up of blood in veins due to poor heart pumping power means fluid leaks out)
* Nephrotic syndrome (low albumin means fluid leaks)
* Pancreatitis (as a complication where there is leakage from the pancreatitis)
* Tuberculosis
35
How can you assess ascites?
* On examination look for shifting dullness – percuss abdomen when supine and find where at side it gets dull, then get patient to go on side and percuss again, should now be dull in centre but not dull at the sides as fluid has moved
* Abdominal ultrasound can be good for assessing ascites
* Other investigations are more for looking at underlying cause of ascites
* Ascites can be monitored by serial measurements of abdominal girth and of body weight
36
What is Meig's syndrome?
benign ovarian tumour, ascites and pleural effusion
37
Management of ascites?
* Treat underlying cause if possible
* 1st line management is to sodium restrict and give a diuretic, in cirrhosis use spironolactone, other diuretic that may be used is a loop
* Can do therapeutic paracentesis
* May do TIPS procedure in refractory ascites
38
Complications of ascites?
* Electrolyte imbalances
* Spontaneous bacterial peritonitis
39
Most colorectal cancers develop ______
difference between growth of right and left sided?
as a result of progression from normal mucosa to adenoma to invasive cancer (adenocarcinoma)
* Cancers on the right vs left tend to grow and present differently
* Right sided cancers tend to grow as a polyploid carcinoma, cancers on the left tend to grow as a stenosing carcinoma
40
Colorectal cancers most commonly metastasise to?
the liver or lungs
41
Staging for colorectal cancer?
tnm (dukes is no longer used)
42
Risk factors for colorectal cancer?
* 2 main genetic conditions can predispose to colorectal cancer:
1) Lynch Syndrome (AKA Hereditary Non-Polyposis Colorectal Cancer)
2) Familial Adenomatous Polyposis (FAP)
* Inflammatory bowel disease particularly ulcerative colitis increases risk of developing colorectal cancer
* Other risk factors are increasing age, male sex, diet high in red meat and fat, smoking, obesity, lack of physical activity
43
describe 2 genetic conditions that increase risk of colorectal cancer?
1) Lynch Syndrome (AKA Hereditary Non-Polyposis Colorectal Cancer)- this is caused by mutations in genes that are responsible for repair of DNA mismatches and is autosomal dominant and predisposes to cancer as a cell only then needs to lose one copy of mismatch repair genes before cancer can develop
2) Familial Adenomatous Polyposis (FAP)- this is an autosomal dominant condition that causes numerous adenomatous polyps to develop in childhood in the colon, in untreated individuals carcinoma is inevitable by 40 yrs, gene responsible is APC gene and this condition is more easily recognised compared to lynch syndrome as if do colonoscopy hundreds of polyps will be seen lining the bowel
44
Presentation of colorectal cancer?
* Left sided cancers (tend to present with symptoms of obstruction): altered bowel habit, worsening constipation, tenesmus, rectal bleeding
* Right sided cancers (vague symptoms): unexplained iron deficiency anaemia, persistent tiredness, persistent and unexplained change in bowel habit, unexplained weight loss, colicky abdominal pain, lump in the abdomen
Note: cancers in the transverse colon are very rare
45
Investigations for colorectal cancer?
* Diagnosed by colonoscopy or sigmoidoscopy
* Chest, abdo and pelvis CT is done to assess spread
46
Management of colorectal cancer?
* Treatment of cancer depends on stage, a total or partial colectomy can be done
* If cancer is advanced may do chemo or radiotherapy depending on location
* Palliation may involve stenting the colon or de-functioning the colon by leaving the cancer but bringing a stoma above to relieve symptoms of obstruction
47
Screening for colorectal cancer?
* In Scotland men and women aged 50-74 are offered screening for colorectal cancer
* A testing kit is sent to house called the FIT test every 2 years and this looks for blood in the stool, if it comes back positive people are usually offered a colonoscopy or sigmoidoscopy
48
Symptoms of ascites?
* Abdo distension and weight gain
* Nausea and anorexia
* Increasing dyspnoea
49
Explain what haemorrhoids are and internal and external haemorrhoids?
* Haemorrhoids are abnormally enlarged vascular mucosal cushions on the anal canal
* These mucosal cushions are normal findings and help to maintain continence but when they become enlarged and start to cause symptoms they are haemorrhoids
* Dentate (pectinate) line divides the anal canal into upper two thirds and lower one third, above and below are completely different neurovascular supplies and histology
* External haemorrhoids originate below the dentate line and are covered by modified squamous epithelium, which is richly innervated in pain fibres so external haemorrhoids can be painful and itchy, they may be visible on examination
* Internal haemorrhoids arise above the dentate line and are covered by columnar epithelium which have no pain fibres so are therefore not sensitive to touch, temperature or pain (unless they become strangulated)
* Internal and external haemorrhoids can co-exist
* Internal haemorrhoids are classified on their degree of prolapse
50
Risk factors/ who gets haemorrhoids?
Pretty common
Proposed risk factors include:
* Constipation
* Prolonged straining and time spent on the toilet
* Chronic diarrhoea
* Increased abdominal pressure e.g. ascites or pregnancy and childbirth
* Obesity
* Heavy lifting
* Chronic cough
* Injury to spinal cord or rectum
* IBD
* Ageing and hereditary factors
51
Presentation of haemorrhoids?
* Can be asymptomatic
* Bright red painless rectal bleeding with defecation – streaks on toilet paper or dripping into toilet – blood may coat stools but should not be mixed with it
* Anal itching and irritation
* Feeling of rectal fullness, discomfort or incomplete evacuation
* Lump at anal verge (if haemorrhoids have prolapsed)
* Soiling due to mucus discharge or impaired continence may be experienced
* Thrombosed haemorrhoids are painful
* On examination internal haemorrhoids are not evident on inspection and difficult to feel on PR
* Asking patient to strain may allow haemorrhoids to become visible
* Although internal haemorrhoids are not palpable on PR it is essential to do one to rule out other pathology
52
Investigations for haemorrhoids?
* A rigid anoscope, protoscope or rectoscope can be used to make diagnose of haemorrhoids, classify their severity and exclude sinister pathology, where the facilities or expertise are not available the person may need referred for assessment
53
Management of haemorrhoids?
* Consider admitting if extremely painful, acutely thrombosed external haemorrhoids or internal haemorrhoids which have prolapsed and become swollen, incarcerate and thrombosed
* Others may need referred for assessment if suspect other pathology or if haemorrhoids and complications too complicated to manage in primary care
* Secondary care treatments involves rubber band ligation, injection sclerotherapy, infrared coagulation, haemorrhoidectomy
General management:
* Ensure stools are easy to pass
* Lifestyle advice on anal hygiene – clean and dry, pat dry – advise against stool withholding and straining
* Manage any other symptoms e.g. simple analgesia, topic haemorrhoid preparations
54
What is necrotising enterocolitis?
* Most common GI emergency in neonates where there is inflammation and ischaemic necrosis
55
Who gets necrotising enterocolitis?
* Mainly affects premature infants who have survived a difficult neonatal period
* Thought to be due to immature GI tract and exaggerated immune response
56
Presentation of necrotising enterocolitis?
* Abdominal distension
* Visible intestinal loops
* Bloody mucoid stool and bilious vomiting
* Decreased bowel sounds with erythema of the abdomen
* Palpable abdominal mass or ascites
* Systemic signs: bradycardia, lethargy, shock, apnoea, respiratory distress and temperature instability
57
Investigations for necrotising enterocolitis?
* FBC
* Blood gas
* CRP
* Diagnosis confirmed by AXR supine and erect – bowel wall thickening, persistent loops that are filled with gas and overall gaseous distension may suggest NEC
* US may be useful
58
Management of necrotising enterocolitis?
* Nil by mouth to rest the bowel
* NG or orogastric tube to decompress the bowel with low intermittent orogastric suction
* IV fluids and TPN and IV antibiotics
* Analgesia
* Paracentesis for ascites may be necessary
* Surgery if deteriorating or necrotic bowel suspected
59
Complications and prognosis of necrotising enterocolitis?
* Substantial long term morbidity in survivors
* Perforation
* Acquired short bowel syndrome (following surgery)
* Stoma related complications
* DIC
* Sepsis and shock
* Intestinal strictures
* Enterocolic fistulae
* Abscess formation
60
Explain what hernia are and meaning of irreducible/ incarcerated and strangulation?
* Protrusion of abdominal contents through fascia of the abdominal wall
* If a hernia can no longer be reduced it is irreducible/ incarcerated, this can occur at any time as can strangulation
* Strangulation is when visceral contents of the hernia are twisted or entrapped by narrow opening, this causes ischaemia, infarction and bowel obstruction
61
List 5 types of abdominal hernia?
femoral
inguinal
incisional
epigastric
umbilical
62
Risk factors for inguinal hernia?
* Male gender
* Increasing age
* Raised intra-abdominal pressure e.g. chronic cough, heavy lifting or chronic constipation
* High BMI
63
Explain what happens in a direct inguinal hernia?
* The bowel enters the inguinal canal directly through a weakness in the posterior wall of the canal termed Hesselbach’s triangle i.e. hernia only goes through superficial ring
* These occur more commonly in older patients often secondary to abdominal wall laxity or a significant increase in intra-abdominal pressure
* Direct inguinal hernias are medial to the inferior epigastric vessels
64
Hernia that forms due to weakness in Hesselbach's triangle?
direct inguinal hernia
65
Direct inguinal hernias are ________
medial to inferior epigastric vessels
66
Explain what happens in an indirect inguinal hernia?
* Bowel enters the inguinal canal via the deep inguinal ring
* They arise from incomplete closure of the processus vaginalis, an outpouching of peritoneum allowing for embryonic testicular descent, they are therefore usually deemed congenital in origin
* Indirect hernias are lateral to inferior epigastric vessels
67
Hernia that is due to incomplete closure of the processus vaginalis?
indirect inguinal hernia
68
Indirect hernias are _________
lateral to inferior epigastric vessels
69
Clinical features of inguinal hernias?
* Most common PC is lump in groin, which for reducible hernia will initially disappear with minimal pressure or when the patient lies down
* May be mild to moderate discomfort
* If incarcerated the hernia may be painful
* Inguinal hernia are typically located above and medial to the pubic tubercle, contrast to femoral hernias which are typically located below and lateral to the pubic tubercle
* If it enters the scrotum have to see if can get above the lump and separate it from testis
70
Differentiating between direct and indirect inguinal hernia?
1. Locate the deep inguinal ring (midway between the ASIS and pubic tubercle)
2. Manually reduce the patient’s hernia by compressing it towards the deep inguinal ring starting at the inferior aspect of the hernia
3. Once the hernia is reduced apply pressure over the deep inguinal ring and ask the patient to cough
4. If hernia reappears it is more likely direct, if it doesn’t it is more likely indirect
71
Investigations for inguinal hernia?
* Typically, a clinical diagnosis, if diagnostic uncertainty would do an ultrasound
72
Management of inguinal hernia?
* Any patient with symptomatic inguinal hernia should be offered surgical intervention
* Any patient presenting with evidence of strangulation needs urgent surgical exploration
* A third of patients with inguinal hernia will never experience any symptoms
* Surgical repairs can be done open or laparoscopic
73
What is a femoral hernia?
* Femoral hernia occur when abdominal viscera or omentum pass through the femoral ring and into the potential space of the femoral canal
* They are relatively uncommon but important to know about due to their high risk of strangulation
74
Risk factors for femoral hernia?
* Female
* Pregnancy – higher incidence in multiparous women
* Raised intra-abdominal pressure
* Increasing age
75
Clinical features of femoral hernia?
* Commonly presents as a small lump in the groin
* When they are not obstructed/ strangulated they are generally asymptomatic and may not present because they are such small lumps
* 30% of femoral hernia present as an emergency
* Need to identify that it is a femoral hernia and not an inguinal hernia
* Femoral hernia: found infero-lateral to the pubic tubercle (and medial to the femoral pulse)
* Inguinal hernia: found supero-medial to the pubic tubercle
* The tightness of the femoral ring means the hernia is unlikely to be reducible, inguinal hernias are more likely to be reducible
76
Differentiate between inguinal and femoral hernia?
* Femoral hernia: found infero-lateral to the pubic tubercle (and medial to the femoral pulse)
* Inguinal hernia: found supero-medial to the pubic tubercle
* The tightness of the femoral ring means the hernia is unlikely to be reducible, inguinal hernias are more likely to be reducible
77
Investigations for femoral hernia?
* Whilst the diagnosis can be made clinically, additional imaging is often required
* Ultrasound scanning or CT can be used
78
Management of femoral hernia?
* All femoral hernias should be managed surgically, ideally within 2 weeks of presentation due to high risk of strangulation
79
Describe signs and symptoms of hernia strangulation?
* Emergency
* Symptoms/ signs of strangulated hernia: nausea, vomiting, fever, sudden pain that quickly intensifies, hernia bulge that turns red, purple or dark, inability to move bowels or pass gas
80
List some upper GI causes of GI perforation?
* Peptic ulcer disease
* Gastric or oesophageal cancer
* Foreign body ingestion
* Excessive vomiting
81
List some lower GI causes of GI perforation?
* Diverticulitis
* Colorectal cancer
* Appendicitis
* Foreign body insertion
* Severe colitis e.g. crohns
* Toxic megacolon (non-obstructive dilatation of the colon associated with systemic toxicity e.g. ulcerative colitis or C diff infection)
82
List any other causes of GI perforation?
* Iatrogenic e.g. from colonoscopy or gastroscopy
* Trauma
* Mesenteric ischaemia
* Obstructing lesions leading to obstruction, ischaemia and then necrosis
83
Clinical features of GI perforation?
* Abdominal pain
* Patients are systemically unwell with associated malaise, vomiting and lethargy
* On examination look unwell with symptoms and signs of sepsis
* May have localised or generalised peritonitis
84
Investigations for GI perforation?
* Urgent FBC, U and E, LFTs, CRP, clotting and group and save
* Raised WCC and CRP
* May show evidence of organ dysfunction e.g. AKI
* Gold standard for diagnosis is a CT scan with contrast confirming the presence of free air and also suggesting location
* Classically AXR and CXR were used but these are less specific
85
Management of GI perforation?
* Early resus, prompt diagnosis and definitive treatment
* Broad spectrum antibiotics should be started early
* Nil by mouth and NG tube should be inserted
* Analgesia
* Most patients will need to go to theatre
86
What is an anorectal abscess and what are common causes?
* Collection of pus in the anal or rectal region
* Can be caused by infection of an anal fissure, STIs or blocked anal glands
Can be classed anatomically
* Perianal abscess are most common (perianal area = skin that is around the anus that you can see if part buttocks)
* Ischiorectal abscess
* Intersphincteric abscess
* Supralevator abscess
* Postanal abscess
87
Risk factors for anorectal abscesses?
* High risk groups include diabetics, immunocomprimised patient, people who engage in receptive anal sex and patients with IBD
* Deep rectal abscess can occur due to intestinal disorders e.g. Crohns or diverticulitis
88
Presentation of anorectal abscesses?
* Painful, hardened tissue in the perianal area, discharge of pus from the rectum, a lump or nodule, tenderness at the edge of the anus, fever, constipation or pain associated with bowel movements
* Perianal pain is usually constant, throbbing and worse when sitting down
* Rectal exam may confirm the presence of an anorectal abscess
89
3 things you should rule out if someone is presenting with an anorectal abscess?
anal carcinoma, colorectal cancer and IBD
90
Investigations for anorectal abscess?
* DRE is usually sufficient for diagnosis and treatment planning
* Investigations will depend on presentation but likely to screen for STIs, IBD, diverticular disease or lower GI malignancy
* Protosigmoidoscopy may be performed to exclude associated diseases
* MRI if need to see fistulas or deep abscess
* Transperineal US can be useful
91
Fistula in ano, causes, presentation, management?
Fistula in Ano
* Fistula occur in approximately 40% of patients with anorectal abscesses
* These are fistula that develops between the end of the bowel and the skin near the anus
* This will cause skin irritation around the anus, pain, smelly discharge, mucus or blood in stool and potentially difficulties with bowel continence
* Needs a procedure to fix it
92
Management of anorectal abscesses?
outcome is good if abscess treated promptly
* Surgical drainage
* Analgesia
* Antibiotics
* Manage any fistula with surgery too
93
What is intussusception? Where does it often affect?
* Condition where one part of bowel telescopes into the other
* Often ileocaecal – so the ileum telescopes into the caecum
* The mesentery of the intussuscepted bowel becomes compressed, the bowel wall distends and obstructs the lumen, lymphatic and venous obstruction occurs causing ischaemia
94
Who tends to get intussusception?
* 2/3 of patients are under 1
* In children it might be related to lymphoid hyperplasia or viral infections, often no underlying cause is found
* If in adults it likely due to tumour of polyps in the bowel
95
Presentation of intussusception?
* Sudden onset
* Colicky abdominal pain
* Vomiting
* Palpable sausage shape mass often in right upper quadrant
* Dehydration, pallor, shock
* Later (as this is result of iscaemia and infarction) mucoid and bloody redcurrant stools
96
Investigations for intussusception?
* FBCs and U and Es
* AXR may show dilated gas filled proximal bowel
* Ultrasound may show doughnut or target sign
* Bowel enema – barium, air or water
* CT/ MRI scanning more often used in adults than in children
97
Management for intussusception?
* Resuscitation, NG tube and IV fluids
* Barium or air enema to fix the telescoping
* If unsuccessful or signs of peritonitis or shock they need surgery
98
Prognosis of intussusception?
with treatment prognosis is excellent
99
3 main types of bowel ischaemia?
acute mesenteric ischaemia
chronic mesenteric ischaemia
ischaemic colitis
100
What is acute mesenteric ischaemia and the types? Which artery is affected?
* This covers acute mesenteric arterial embolus and thrombus, mesenteric venous thrombus and non-occlusive mesenteric ischaemia (NOMI)
* Non-occlusive disease refers to systemic decreases in blood flow that result in ischaemia
* The SMA is the most commonly affected artery due to its size etc it is where emboli are more likely to end up
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Risk factors for acute mesenteric ischaemia?
* Conditions causing arterial emboli e.g. AF
* Conditions causing arterial thrombus e.g. atherosclerosis
* Non-occlusive disease may be caused by hypotension, certain drugs, low cardiac output following MI
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Presentation of acute mesenteric ischaemia?
* Moderate to severe colicky or constant poorly localised abdominal pain
* May be vomiting or bloody diarrhoea
* May have abdominal distension
* On examination abdomen may look normal until later stages where there will be rebound guarding and tenderness (so early on pain is outwith proportions of clinical findings)
* In later stages may have fever, oliguria, dehydration, confusion, tachycardia and shock
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Investigations for acute mesenteric ischaemia?
* ABG to assess degree of acidosis and serum lactate
* FBC, U and Es, clotting, amylase, LFTs
* CT angiography is gold standard and shows arterial blockages
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Management of acute mesenteric ischaemia?
* Initial resuscitation with IV fluids and oxygen
* NG tube should be sited
* Broad spectrum IV antibiotics
* Unfractionated heparin is also recommended
* Surgery to re-establish blood supply to bowel and remove any non-viable bowel
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What is chronic mesenteric ischaemia? What artery is involved?
* This is chronic atherosclerotic disease of the vessels supplying the intestine (AKA intestinal angina)
* Usually all 3 major mesenteric arteries are involved
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Risk factors for chronic mesenteric ischaemia?
* This is caused by factors predisposing to atherosclerosis e.g. smoking, hypertension, DM and hyperlipidaemia
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Presentation of chronic mesenteric ischaemia?
* Postprandial abdominal pain- described as dull and crampy located in the midepigastric region. Pain often occurs 15 to 45 minutes after a meal, develop “food fear”
* Progressive weight loss
* Physical examination findings are usually nonspecific
* Patients are commonly undernourished and cachectic
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Investigations for chronic mesenteric ischaemia?
* CT angiography is best investigation
* Mesenteric duplex US can be good as non-invasive but can be affected by obesity or respiratory movement
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Management of chronic mesenteric ischaemia?
* Asymptomatic patients are managed conservatively with smoking cessation and antiplatelet therapy
* Symptomatic chronic ischaemia is indication for open or endovascular revascularisation
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What is ischaemic colitis?
* Compromise of the blood circulation supplying the colon
* More often acute pathology than chronic
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Presentation of ischaemic colitis?
* Non specific acute abdomen
* Pain is most often in LIF
* Nausea and vomiting often occur
* In later stages loose stool containing dark blood
* Presence of peritonitis suggests full thickness ischaemia
* The acute onset suggests more it is ischaemic colitis compared to inflammatory or infective which has a more insidious onset
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Investigations for ischaemic colitis?
* Presence of metabolic acidosis
* Colonoscopy shows blue swollen mucosa
* AXR may show abnormal segment outlined with gas
* Barium enema shows thumb printing in early phase that may last for several days
* Occasionally CT scan, MRI scan and angiography
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Management of ischaemic colitis?
* Sometimes only supportive care needed if ischaemia transient
* CT angiography may be necessary if symptoms don’t improve in 24 – 48hrs and then may need surgery
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What is bowel obstruction?
* This refers to mechanical blockage of the bowel whereby a structural pathology physically blocks the passage of intestinal contents
* Once the bowel segment has become occluded, gross dilatation of the proximal limb of the bowel occurs
* There becomes an increased peristalsis of the bowel which in turn leads to secretion of large volumes of electrolyte rich fluid into the bowel (so urgent fluid replacement is needed)
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Aetiology of bowel obstruction?
* The most common cause depends on location
* Small bowel: adhesions or hernia
* Large bowel: malignancy, diverticular disease or volvulus
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Presentation of bowel obstruction?
Cardinal features of bowel obstruction:
* Abdominal pain – colicky or cramping in nature
* Vomiting – occurring early in proximal obstruction and late in distal obstruction
* Abdominal distension
* Absolute constipation
Ausculate for “tinkling bowel sounds”
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Investigations for bowel obstruction?
* Urgent bloods and group and save
* VBG can be useful to evaluate for end organ and for immediate assessment of any metabolic derangement
* CT scan with IV contrast is imaging of choice in suspected obstruction- shows obstruction and also the underlying cause
* AXR can be used in some settings where bowel appears dilated and valvulae conniventes or haustral lines are visible
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Explain what a closed loop obstruction is?
* In patients with a mechanical bowel obstruction if there is a second obstructing point proximally e.g. a large bowel obstruction with a competent ileocaecal valve (i.e. things cannot go forward due to obstruction and also cannot go backwards because the valve is still working and stops this)
* This is surgical emergency as the bowel will just keep distending stretching the wall until it becomes ischaemic and there may also be perforation
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Management of bowel obstruction?
* Depends on aetiology
* Everyone need urgent fluid resuscitation and should also have NG tube inserted
* If closed loop obstruction or evidence of ischaemia they need surgery
* Conservative management with drip and suck may work in some cases (nil by mouth, drip in IV fluids to hydrate and correct electrolyte imbalances, NG tube with dree drainage)
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What is an ileus?
lack of normal muscle contraction of the intestine
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What is a post op ileus?
* Deceleration or arrest in intestinal motility following surgery
* A functional bowel obstruction
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Risk factors for post op ileus?
* Increased age
* Electrolyte abnormalities
* Neurological disorders e.g. dementia or parkinsons
* Use of anti-cholinergic medication
* Surgical factors: use of opioids, pelvic surgery, extensive intra-operative intestinal handling, peritoneal contamination, intestinal resection
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Clinical features of post op ileus?
* Failure to pass gas or stool
* Sensation of bloating and distension
* Nausea and vomiting
* On examination there will be abdominal distension and absent bowel sounds (whereas in mechanical obstruction there is classically tinkling bowel sounds)
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Bowel sounds in post op ileus vs true obstruction
tinkling in true obstruction, absent in post op ileus
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Investigations for post op ileus?
* Need to rule out other more serious pathologies
* FBC, CRP, U and Es
* CT scan abdomen and pelvis will confirm the diagnosis and rule out any other intra-abdominal pathologies
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Management of post op ileus?
* Nil by mouth with IV fluids
* Daily bloods to look for electrolyte abnormalities and AKI
* Encourage mobilisation as tolerated
* Reduce opiate analgesia
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Prophylaxis of post op ileus?
* Minimise intra-operative intestinal handling
* Avoid fluid overload
* Minimise opiate use
* Encourage early mobilisation
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Why is fluid resuscitation important in bowel obstruction?
you start to make loads of fluid and secretions around the obstruction so lose lots of fluid and electrolytes
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In relation to a hernia what is meant by a cough impulse?
The cough impulse is a clinical sign that is elicited when examining a hernia. If the swelling expands upon coughing, it is said to have a 'cough' impulse
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Explain loop vs end ileostomy/ colostomy?
Loop - loop of bowel is brought to skin and then opened, this diverts contents from the rest of the bowel allowing healing/ rest. This is usually temporary
End- part of the bowel is separated and then brought to the skin, this is generally irreversible
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Explain what Hartmanns procedure is?
This is typically performed as an emergency due to sigmoid perforation as a result of diverticulitis or malignancy
Sigmoid colectomy with end colostomy formation, the rectal stump is then sutured shut
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In a non emergency, what surgery for sigmoid cancer?
high anterior resection
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Explain what an abdominoperineal resection is?
this is performed for very low rectal cancers or anal cancers or occasionally for severe perianal crohns
there is an abdominal approach to the remove the rectum and a end colostomy, then a perineal approach to remove the rest of the bowel
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What surgery is done for upper and mid rectal cancers?
anterior resection
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Right hemicolectomy?
removes the right side of the colon - up to just past the hepatic flexure
surgery for cancers of the caecum, ascending or proximal transverse colon
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Left hemicolectomy?
removes the left side of the colon and just past the splenic flexure
surgery for tumours of the distal transverse or descending colon
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What is a panproctocolectomy?
removal of all the colon, rectum and anus with end ileostomy - main indications are ulcerative colitis and familial adenomatous polyposis (FAP)
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What increases lifetime risk of bowel obstruction?
adhesions
any abdominal surgery no matter how long ago increases risk
