GI Flashcards
What is the acute abdomen?
= sudden onset, severe abdominal pain which may indicate potentially life-threatening intra-abdominal pathology that requires urgent surgical intervention.
when can a pain free acute abdomen occur?
particularly in older people, in children, in the immunocompromised, and in the last trimester of pregnancy.
potential conditions causing pain in the right hypochondriac region
Gallstones Cholangitis Hepatitis Liver abscess Cardiac causes Lower lobe pneumonia
potential conditions causing pain in the epigastric region
Oesophagitis Peptic Ulcer Perforated Ulcer Pancreatitis MI
potential conditions causing pain in the left hypochondriac region
Spleen Abscess
Acute splenomegaly
Spleen rupture
Lower lobe pneumonia
potential conditions causing pain in the right lumbar region
Renal stones
Pyelonephritis
potential conditions causing pain in the umbilical region
AAA rupture Appendicitis (early) Meckel’s diverticulitis Small bowel obstruction Ischaemic bowel Peritonitis DKA
potential conditions causing pain in the left lumbar region
Renal stones
Pyelonephritis
potential conditions causing pain in the right iliac region
Appendicitis IBD Caecum obstruction Ovarian cyst/torsion Ectopic pregnancy Hernias
potential conditions causing pain in the hypogastric/suprapubic region
Testicular Torsion Urinary retention Cystitis Placental Abruption Large bowel obstruction PID Endometriosis
potential conditions causing pain in the left iliac region
Diverticilitis IBD Constipation Ovarian Cyst Hernias
Acute abdomen - BLEEDING
AAA rupture – most serious cause, requires immediate surgical intervention.
Ruptured ectopic pregnancy
Bleeding
Gastric ulcer
Trauma
What is there a risk of in an acutely bleeding patient?
Hypovolaemic shock:
- Hypotension
- Tachycardia
- Pale and clammy
- Cool to touch
Acute abdomen - PERITONITIS
Localised or generalised inflammation of the peritoneum
Patients lay completely still, with shallow breathing (pain made worse by movement/coughing/breathing).
Tachycardia and potential hypotension/pyrexia
Percussion/rebound tenderness
Involuntary guarding
Reduced or absent bowel sounds (paralytic ileus)
Localised peritonitis
when the inflammation is in a limited area (e.g. adjacent to inflamed appendix/diverticulum prior to rupture).
Generalised peritonitis
when the inflammation is widespread (e.g. after the rupture of an abdominal organ)
Why is there rebound tenderness in peritonitis?
movement of the peritoneum upon the removal of the palpating hand causes intense pain
Acute abdomen - ISCHAEMIC BOWEL
Any patient who has severe pain out of proportion to the clinical signs (i.e. the examination is unremarkable) has ischaemic bowel until proven otherwise
May have acidaemia with raised lactate on blood gases.
=> Due to impaired blood supply resulting in anaerobic respiration of the tissues
How do you diagnose ischaemic bowel?
CT scan with IV contrast
Inflammatory abdominal pain
Constant pain, supported by a raised temperature, pulse and leucocytosis.
Obstructive abdominal pain
COLICKY PAIN
Crescendos to become very severe and then completely goes away
Patients often agitated.
Pain may become constant with superimposed inflammation
Why is biliary colic not “true” colic?
the pain never goes away completely
Referred Visceral Pain in the abdomen
- Foregut pain is referred to the upper abdomen.
- Midgut pain is referred to the middle abdomen
- Hindgut pain is referred to the lower abdomen
Acute abdomen - bedside tests
Basic observations (NEWS2 score)
ECG
=> exclude MI
Urine dip
Pregnancy test
=> all women of reproductive age
BM
=> DKA can present as abdominal pain
Acute abdomen - bloods
FBC U&E LFTs and amylase/lipase CRP Coagulation G&S / XM ?Blood cultures
Acute abdomen - Imaging (basic and specialist)
?Erect CXR
?AXR
?USS
?CT scan
Amylase levels
Amylase 3x higher than upper limit to be diagnostic of pancreatitis
Values lower than this suggests other pathology – e.g. perforated bowel, ectopic pregnancy, DKA
Abdo imaging - use of erect CXR
will show bowel perforation (free air under the diaphragm)
Abdo imaging - use of AXR
Bowel obstruction
Toxic megacolon
Foreign body ingestion (if radio-opaque)
Abdo imaging - use of USS
Biliary pathologies
Kidneys, ureter and bladders
Gynae pathologies
Appendix
Appendicitis
= most common cause of an acute abdomen
inflammation of the appendix, usually caused by blockage within the lumen
Causes of appendicitis
Faecolith (a stone made of faeces) – most common.
Swollen lymphoid tissue in the wall – common in adolescence
Parasites
Tumours
Pathophysiology of appendicitis
Lumen is blocked => bacteria multiply
Appendix swells => blood supply becomes impaired.
ischaemia and necrosis
appendix can eventually perforate due to the raised intraluminal pressure, releasing bacteria into the abdominal cavity, leading to abscess, peritonitis and sepsis
Appendix mass
inflamed appendix with an adherent covering of omentum and small bowel
Appendicitis - Differential diagnoses
Gynae – ovarian cyst rupture, ectopic pregnancy, PID
Renal – UTI, pyelonephritis, ureteric stones
GI – mesenteric adenitis, diverticular disease, IBD
Urological – testicular torsion, epididymo-orchitis
Appendicitis - Symptoms
Abdominal pain
=> Starts dull and central
=> Then becomes localised and sharp in the RIF at McBurney’s point
=> Pain may not be severe until the appendix has ruptured!
Constipation (or sometimes diarrhoea).
Anorexia
Nausea and vomiting (after the pain starts).
Where is McBurney’s point?
1/3 of the way between the ASIS and the umbilicus
Appendicitis - Signs
Rebound and percussion tenderness in RIF (maximum at McBurney’s point)
Guarding (especially if perforated)
Rovsing’s Sign
Tachycardia, tachypnoea
Mild pyrexia
Rovsing’s sign
Pain in the RIF when the LIF is pressed
Appendicitis - investigations
Abdominal exam
PR
Pelvic examination in females
Pregnancy test
Bloods – FBC, U&E, CRP/ESR
Urinalysis
USS/CT – if diagnostic uncertainty
AXR/erect CXR – if questioning perforation
Appendicitis - management
Nil by mouth ready for appendectomy.
Resuscitation – IV fluids.
Appendectomy (laparoscopic is gold standard)
+ Wash out if ruptured
What are the complications of an appendectomy?
Early complications – haematoma, wound infections
Late complications – small bowel obstruction (adhesions) or incisional hernia.
Complications of appendicitis
Perforation – if left untreated, causes peritoneal contamination (peritonitis and sepsis).
Surgical site infection
Appendix mass – omentum and small bowel adhere to the appendix.
Pelvic abscess – fever with a palpable RIF mass, CT for confirmation
Adhesions – small bowel obstruction due to scarring.
Universal post-op complications – DVT/PE, bleeding, ileus, surgical damage to other organs, etc.
What is colorectal cancer?
a malignant neoplasm of epithelium in the large bowel, excluding the appendix and the anus
Most common variant is Adenocarcinoma
=> Squamous and adeno-squamous variants can be found in the distal rectum
Aetiology of colorectal cancer
Colon cancer: Male = Female
Rectal cancer: Male > Female
Age >50 years
3rd most common cancer in the UK
More common in the western world
Global mortality is 50%
non-modifiable risk factors for colorectal cancer
Ethnicity Age Sex T2DM IBD – Chron’s Disease, UC Family History
modifiable risk factors for colorectal cancer
Diet rich in red and processed meats Obesity Physical inactivity Smoking tobacco Heavy alcohol consumption
factors protective against colorectal cancer
diet rich in high fibre (and F&V),
exercise,
hormone replacement therapy,
aspirin/NSAIDs
HNPCC/Lynch syndrome
Autosomal dominant mutation affecting various mismatch repair genes
Responsible for ~3% of colorectal cancers
Familial Adenomatous Polyposis (FAP)
Autosomal dominant defect in tumour-suppressor APC gene.
Causes numerous colonic polyps to develop, with an increased chance of malignancy
MUTYH-associated polyposis
Autosomal recessive
Causes polyposis with increased risk of malignancy
Presentation of right-sided colon tumours
often asymptomatic;
may present with weight loss/iron-deficiency anaemia;
can present with abdominal discomfort and change in bowel habit
Presentation of left-sided colon tumours
PR bleeding/mucous,
altered bowel habit,
tenesmus,
obstruction,
Presentation of rectal tumours
PR bleeding,
pain,
changes in bowel habit,
masses/stricture
What signs/symptoms are common to all colorectal tumours (regardless of location)?
Weight loss, loss of appetite, N&V
abdominal mass, abdominal pain/discomfort,
Altered bowel habits/constipation/diarrhoea
haemorrhage, perforation, fistula
Where are colorectal tumours most commonly located?
- Sigmoid colon
- Rectum
- Ascending colon
- Descending/transverse colon
Complications of CRC
- Bowel Obstruction
- Bowel Perforation
- Iron Deficiency Anaemia
- Hepatic and Peritoneal Metastasis
- Bone and Lung Metastases
- Colo-vesical fistula
What symptoms can occur from the spread of CRC?
Hepatic Metastases: Jaundice, RUQ pain, early satiety
Peritoneal Metastases: Ascites or pain
Colo-vesical fistula: Pneumaturia or recurrent UTI
Weight loss
Screening for CRC in the UK
Routine regular colonoscopy – in high-risk groups (positive family history)
average-risk population => colonoscopy, CT colonography, and faecal occult blood (FOB) testing are conducted
CRC - investigations
BLOODS
- FBC, U&E, LFT, Magnesium, Calcium
- Carcinoembryonic antigen – tumour marker, can be used to monitor disease.
- Coagulation, G&S/XM
Colonoscopy to identify and obtain tissue for histology
=> For palliative patients – stent insertion.
Imaging for staging
=> CT abdomen-pelvis
=> CT chest
CRC TNM staging
T1-T4 = tumour spread
N0-N2 = nodal status
M0 - M1 = metastatic status
Stage I CRC
Grown through the inner lining of the bowel, or into the muscle wall. It has not spread to lymph nodes or distant body parts
Stage II CRC
Spread into the outer wall of the bowel or into tissue or organs next to the bowel. It has not spread to the lymph nodes or distant parts of the body
Stage III CRC
Spread to nearby lymph nodes, but hasn’t spread to distant body parts
Stage IV CRC
Spread to distant body parts, such as the liver or lungs
= advanced bowel cancer
Grading of CRC
The grades of bowel cancer cells are from 1 to 4 depending on histology:
- (Low grade) look most like normal cells
- Look a bit like normal cells
- Look very abnormal and not like normal cells
- (High grade) grade 4 looks completely different from normal cells
Treatment of CRC
wide resection of the growth and regional lymphatics
=> e.g. right/left hemicolectomy, sigmoid colectomy, high anterior resection
Total colectomy in FAP, HNPCC and synchronous cancers.
Dysplastic polyps and carcinoma in situ can be removed via colonoscopic excision
What is anal cancer?
mainly squamous cell carcinoma of the epithelium of the anus
Risk factors for anal cancer?
Ano-receptive sex
Syphilis infection
Anal warts/cervical cancer (HPV)
Immunosuppression
pectinate line
an embryological division between the upper 2/3rds and the lower 1/3rd of the anal canal
Anal cancer above the pectinate line
Columnar epithelium
Lymph draining to internal iliac nodes
Portal venous drainage (thus hepatic metastases).
More common in women, worse prognosis
Anal cancer below the pectinate line:
- type of epithelium
- lymph and venous drainage
- prognosis
Squamous epithelium
Lymph drainage to superficial inguinal nodes.
Caval venous drainage (thus pulmonary metastases)
More common in men, better prognosis
Mechanical vs functional bowel obstruction
mechanical - physical blockage of the passage of intestinal contents
functional - decreased bowel motility
What is bowel obstruction?
the mechanical of functional blockage of the bowel, resulting in absolute constipation. There will be dilatation of proximal bowel with sequestration of fluid into the intestinal lumen.
Absolute constipation
when the patient is not passing any flatus or faeces rectally
Differentials for bowel obstruction
Constipation
Paralytic ileus
Toxic megacolon
How does bowel obstruction typically present?
Abdominal pain (colicky in early obstruction, constant in perforation)
Vomiting
=> bilous - upper SBO
=> faeculent - lower SBO
=> Undigested food - suggests gastric outlet obstruction
Absolute constipation
Abdominal distension
Dehydration
Tinkling bowel sounds
Why does bowel obstruction cause dehydration?
How can you identify dehydration?
- Vomiting,
- Lack of fluid intake
- Fluid sequestration to the bowel/ “Third spacing”
Sleepiness, thirst, muscle weakness, headache, dizziness, dark urine, dry mouth, decreased JVP, low BP, tachycardia, sunken eyes, loss of skin turgor
Fluid sequestered to the bowel tends to be electrolyte rich, so the patient may be hypokalaemic and have an AKI.
How do LBO and SBO present differently?
LBO – absolute constipation and pain are more prominent early, vomiting often late
=> Symptoms are generally more gradual due to the large volume of colon.
=> Pain tends to be lower (suprapubic)
SBO – vomiting is the predominant early feature, constipation often late.
=> Pain tends to be peri-umbilical
Strangulating obstructions
interruption of the intestinal blood supply with simultaneous blockage of the intestinal lumen
Compromised blood supply may lead to infarction, perforation and peritonitis
Closed loop obstruction
an obstruction of two points in the bowel, causing a grossly distended loop of bowel in between those points.
This can grow until it becomes ischaemic and ultimately perforates. This is therefore a SURGICAL EMERGENCY
If the ileocaecal valve is competent, closed-loop obstruction forms with LBO.
If the ileocaecal valve is incompetent bowel content flows from large to small bowel
Volvulus
a twisting of a loop of bowel around its mesenteric axis, resulting in obstruction together with venous occlusion at the base of the mesentery
The bowel stretches, becomes ischaemic and is more likely to perforate
Sigmoid volvulus
Most common in elderly, constipated patients.
More common in men.
Classic “coffee bean” appearance on X-ray.
Treatment is insertion of a long flatus tube advanced into the sigmoid, which often untwists the volvulus (releases large amounts of faeces/gas).
If this is unsuccessful, there will be an emergency laparotomy
Caecal volvulus
Due to congenital malrotation, gives the classic “embryo” appearance of an ectopically placed caecum on AXR.
Treatment is untwisting during laparotomy
Causes of bowel obstruction
SBO (80%) Adhesions (~80%) Hernias Crohn’s disease Intussusception
LBO (20%) Carcinoma of the colon - considered til proven otherwise Diverticular disease Sigmoid volvulus Constipation
Bowel obstruction - bedside tests
Basic observations (NEWS2)
Abdominal Exam
Hernial Orifices
PR
Bowel obstruction - bloods
FBC U&E LFTs and Amylase CRP ABG/VBG
Bowel obstruction - Imaging
AXR Erect CXR (if perforation suspected)
CT scan (CAP)
Why would you do a blood gas in ?bowel obstruction ?
to look for metabolic derangement secondary to dehydration/excess vomiting,
or raised lactate in ?ischaemia
SBO on AXR
Dilated loops of bowel are >3cm in diameter.
Dilated loops of bowel are more central in the abdomen.
Valvulae conniventes/plicae circulares present (full crossings).
LBO on AXR
Dilated loops of bowel are >6cm in diameter (>9cm at caecum).
Dilated loops are more peripheral.
Haustra present (incomplete crossings).
Management of bowel obstruction
NBM, IV fluids, fluid balance, catheter
Analgesia, Antiemetics
SBO - usually drip and suck, hernias need surgery
LBO - usually requires surgery
Volvulus - initially flatus tube, may need surgery
ischaemia - urgent surgery
Red Flag Abdominal Symptoms suggesting upper GI malignancy
Dysphagia
Treatment resistant dyspepsia
Loss of appetite
Unintentional weight loss
Red Flag Abdominal Symptoms suggesting lower GI malignancy
Loss of appetite Unintentional weight loss Haematemesis Change in bowel habit Iron-deficiency anaemia Unexplained rectal bleeding
What is coeliac disease?
a gluten-sensitive enteropathy
involves inflammation of the jejunal mucosa in response to gluten
This ultimately results in decreased surface area for absorption, resulting in malabsorption
What is the pathophysiology of coeliac disease?
Alpha-gliandin (protein from gluten) is modified by tissue transglutaminase enzymes (TTG)
activates a T-cell mediated autoimmune reaction against the mucosa of the jejunum
How will a biopsy of duodenal mucosa appear in coeliac disease?
Biopsy of the duodenal mucosa will show flattened mucosa due to villous atrophy
There is hyperplasia of the crypts to compensate.
There will also be chronic inflammatory cells (lymphocytes) in the lamina propria
How many people are affected by coeliac disease in the UK?
~1 in 100
But only 10-20% of these people have a confirmed diagnosis
Peak age of incidence of coeliac disease
can be any age, but peak incidence is age 50-60
Risk factors for coeliac disease
Close association with human leucocyte antigens – 90% are positive for HLA DQ2
Family history
Increased risk if concurrent autoimmune illness (e.g. thyroid disorders, T1DM, etc.)
Symptoms/signs of coeliac disease
~1/3 are asymptomatic
Dermatitis herpetiformis is a recognised skin manifestation of coeliac disease
Non-specific: iron-deficient anaemia, weight loss, fatigue, aphthous ulcers.
Diarrhoea, steatorrhea, bloating, abdominal pain, N&V.
Failure to thrive in a child
Complications of coeliac disease
Malabsorption Anaemia Increased risk of GI malignancy and T-cell lymphoma Osteoporosis Hyposplenism
Investigations for coeliac disease
BLOODS
FBCs, LFTs, U&Es, bone profile, vitamin D, vitamin B12, haematinics and albumin
Serological blood sample
=> 1st line: total immunoglobulin A (IgA) and IgA tissue transglutaminase (tTG)
=> 2nd line: IgA endomysial antibody (EMA) can be used if IgA tTGA is unavailable, or in cases where it is weakly positive
Definitive diagnosis is made via upper GI endoscopy and biopsy of small bowel tissue
Management of coeliac disease
LIFELONG GLUTEN FREE DIET
Correct nutritional deficiency if indicated.
Verify that gluten-free diet is working by using endomysial antibody (EMA) tests
What is IBS?
a relapsing functional bowel disorder, with no discernible structural or biochemical cause.
It is shown to have a negative impact on quality of life, but it is not associated with the development of serious pathology
Suggested mechanisms of IBS?
Differences in the “brain-gut axis”, leading to increased visceral perception and decreased visceral pain threshold.
Abnormal GI motility
Changes in colonic microbiota
Abnormal GI immune function
Risk factors for IBS
Stress and other psychological factors
Dietary triggers (alcohol, caffeine, spicy foods)
Enteric infection
Diagnostic criteria for IBS
Consider the diagnosis if any of the following symptoms for at least 6 months:
=> Abdominal pain, or
=> Bloating, or
=> Change in bowel habit.
Make a diagnosis of IBS if a person has abdominal pain which is either:
=> Related to defecation, and/or
=> Associated with altered stool frequency (increased or decreased), and/or
=> Associated with altered stool form or appearance (hard, lumpy, loose, or watery)
AND at least 2 from the following:
=> Altered passage of stool (straining, urgency, tenesmus)
=> Abdominal bloating/ distension/ hardness
=> Symptoms aggravated by eating
=> Passage of rectal mucus
=> Associated gynaecological, urinary symptoms, or back pain.
Investigation and Diagnosis of IBS
History - ensure no red flag symptoms
Examination - signs of anaemia/masses?
Investigations:
=> CRP/ESR, faecal calprotectin to exclude IBD.
=> TTG/EMA antibodies to exclude coeliac disease
=> FBC for anaemia
In cases which meet the diagnostic criteria, no further investigations are required
Management of IBS - self-management/lifestyle
Advice on avoiding diet triggers, regular exercise, weight loss, stress management, regular meals and plenty of fluids.
Potentially low FODMAP diet
Management of IBS - Pharmacological
to target specific symptoms
Loperamide – 1st line for diarrhoea.
=> 2nd line – low-dose TCAs.
=> 3rd line – SSRI
Antispasmodics – abdominal pain/cramping.
Laxatives – constipation (but avoid lactulose as it cases bloating).
Peppermint oil.
Diverticulum
= an outpouching of the bowel wall
Diverticulosis
= presence of diverticula
Diverticular Disease
= Presence of diverticula + symptomatic
Where do diverticula occur?
anywhere in the GI tract but are more common in the sigmoid (95% of cases) and descending colon
Why is the sigmoid colon more prone to diverticula formation?
has smallest lumen and highest pressures, therefore more prone to diverticulum formation
True diverticulum
involving all layers of the intestine – serosa, muscle, submucosa, mucosa
e.g. Meckel’s diverticulum, the appendix
False/pseudo diverticulum
does not contain all layers – often mucosa pushed through muscle defect
Prevalence of diverticulosis
highest prevalence in Europe and the USA;
rare in Africa and Asia
occurs in 50% of over 50s and 80% of over 80s in the UK.
The majority of patients with diverticula are asymptomatic
Pathophysiology of diverticulosis
- Weakened bowel
- stool movement increases intraluminal pressure
- outpouching of the bowel wall
=> mucosa herniates through muscle layers, particularly at weak points close to penetrating vessels
Risk factors for diverticulosis
Western/low fibre diet
Age >50 years
Male
Obesity
Connective tissue disorders – e.g Marfans, Ehler-danlos; predisposition to weakened GI wall.
Smoking
Family history
NSAID use
Meckel’s Diverticulum
Congenital abnormality - an outpouching in the lower part of the small intestine (a remnant of the vitello-intestinal duct)
Most commonly presents in young (<2 years old) children with painless melaena, then followed by obstruction / intussusception
Can mimic appendicitis
Meckel’s Rule of 2s
Affects 2% of population 2 years old 2:1 M:F ratio 2 inches long 2 feet proximal to ileocaecal valve 2 types of ectopic tissue (gastric/pancreatic)
Diverticulitis
bacterial overgrowth within the gut causes inflammation of the diverticula
increased risk of complications such as perforation of the bowel and fistula formation
Presentation of diverticulitis
systemically unwell (N&V, pyrexia, tachycardia)
acute onset LIF pain
sometimes also loose stools
If perfortated - localised/generalised peritonitis
What can mask symptoms of diverticulitis?
if a patient is taking corticosteroids or immunosuppressants
Simple vs. complicated diverticulitis
Complicated – presence of abscess, formation of fistula, stricture, free perforation.
Simple – inflammation without any of these features
Diverticular bleed
when the diverticulum erodes into a submucosal blood vessel.
This causes haematochezia (the passage of bright red blood in the stool) but is generally painless.
Severe haemorrhage occurs in ~3-5% of patients with diverticulosis
Diverticular Disease - bedside tests
Basic observations (NEWS2) Abdominal Exam Urine Drip PR \+/- Faecal Calprotectin
Diverticular Disease - bloods
FBC
U&E
LFTs
CRP
All bloods should be normal in diverticular disease - but it is important to rule out other conditions
Diverticular Disease - imaging
Routine flexible sigmoidoscopy or colonoscopy
or CT colonogram if not fit
Faecal Calprotectin
used as a direct measure of bowel inflammation but is non-specific.
Raised in IBS, diverticular disease and IBD.
flexible sigmoidoscopy
involves using a fibre-optic endoscope to visualise the rectum, sigmoid and some parts of the descending colon
colonoscopy
involves using an endoscope to visualise the entire large bowel
Risks of colonoscopy/sigmoidoscopy in diverticular disease
perforation, haemorrhage, infection, diagnostic failure need to repeat procedure
Diverticulitis - bedside tests
Basic observations
=> tachycardia, pyrexia, hypotension
Abdominal Exam
=> palpable mass +/- localised peritonism
Urine dip
PR
+/- faecal calprotectin
Diverticulitis - bloods
FBC U&E LFTs CRP ABG/VBG Blood cultures
=> raised WBCs and CRP, and VBG/ABG may show raised lactate
Diverticulitis - imaging
AXR – ?bowel obstruction
Erect CXR – ?perforation
CT abdomen/pelvis
USS Abdomen/pelvis
What imaging is best to AVOID in diverticulitis?
endoscopic procedures - risk of perforation
plan these for after the acute episode
Diverticular bleed - bedside tests
Basic observations
=> tachycardia, increased RR, hypotension
Abdominal Exam
=> palpable mass +/- peritonitic abdomen
Urine dip
PR
+/- faecal calprotectin
Diverticular bleed - bloods
FBC U&E CRP ABG/VBG G&S/XM - for potential blood transfusion Blood cultures
Diverticular bleed - imaging
AXR – ?bowel obstruction
Erect CXR – ?perforation
CT abdomen/pelvis
Urgent colonoscopy to find source of bleeding and treat if indicated
Diverticulosis - management
no management needed
Prophylactic benefit of high fibre diet
Diverticulitis - management
Most patients will require hospital admission.
Encourage PO fluids (clear fluids only), reintroduce solids slowly.
Paracetamol for analgesia
Broad spectrum antibiotics (IV) and IV fluids.
Blood transfusion if haemorrhage.
Surgical management may be indicated in acute complicated diverticulitis.
=> Hartmann’s procedure or sigmoid resection with primary anastomoses are most likely.
What are the complications of diverticulitis?
Pericolic abscess - collection of pus within bowel wall
Fistulas (colovesical/colovaginal)
Perforation
Bowel obstruction
Which muscles maintain anal continence?
Levator Ani
Internal anal sphincter
External anal sphincter
What is the dentate line?
Divides the anal canal into two parts
Mucosa gathers into longitudinal folds containing the anal glands.
Anal canal above the dentate line - origin, epithelium, blood supply and drainage and innervation
from embryological hindgut.
Columnar epithelium.
Blood supply from superior rectal artery (from inferior mesenteric artery).
Venous drainage by superior rectal vein (branch of inferior mesenteric vein).
Internal iliac lymph nodes
Innervated by inferior hypogastric plexus – sensitive to stretch only.
Anal canal below the dentate line - origin, epithelium, blood supply and drainage and innervation
from ectoderm.
Non-keratinising stratified squamous epithelium.
Blood supply from the inferior rectal artery (from pudendal a., a branch of internal iliac a.)
Venous drainage by inferior rectal vein (branch of internal pudendal vein).
Superficial inguinal lymph nodes.
Innervated by pudendal nerve – sensitive to pain, temperature, touch and pressure.
What bedside test should anyone with palpable inguinal lymph nodes get?
PR exam - ?anal cancer.
What happens to the epithelium at the anal verge?
the epithelial cells become keratinised squamous (i.e. “true skin”)
What is Anal Fissure/ fissure-in-ano?
A longitudinal tear in the anal canal mucosa, distal to the dentate line
More common on males
Usually at 6 o’clock (90%) or 12 o’clock (10%)
Can be acute (present <6 weeks) or chronic (present >6 weeks)
What are the main causes of fissure-in-ano?
Mainly constipation.
Infections (syphilis/herpes) Trauma Crohn’s Anal cancer Psoriasis
Parturition – causes anterior/12 o’clock tears.
Clinical presentation of fissure-in-ano
Symptoms:
Severe pain post defecation
Fresh red PR bleeding
Itching
OE:
- Upon spreading the skin, can see breaks/ulcers in the mucosa.
- PR exam will be found very painful by the patient.
Management of fissure-in-ano
Conservative – dietary modification
Medical – laxatives, instillagel, topical diltiazem/GTN cream
Injection of botox sometimes used to relax the anal sphincter and allow healing.
May need examination under general anaesthesia if chronic.
What is a drawback of botox in management of anal fissure?
Injection of botox can cause transient incontinence (especially flatus) after the procedure
How does a perianal abscess occur?
= a collection of pus in the anal region
Plugging of the anal ducts (cryptoglandular plugging) causes bacteria overgrowth and cryptoglandular infection. Pus builds up and causes an abscess.
What pathogens are normally involved in a perianal abscess?
usually gut organisms – E. coli, bacteriodes spp., and enterococcus spp
Perianal abscess - presentation
Painful, hot, red lump in the perianal region
Discharging of pus
Maybe “fluctuance” in the area of abscess.
Sepsis – diabetic patients in particular can become septic very quickly from anal abscesses
Perianal abscess - management
Complicated patients might need a CT/MRI to delineate where the abscess is.
Incision and drainage of the abscess under spinal/general anaesthetic
=> to prevent rupture/possible formation of fistula.
Fistula-in-ano
= an abnormal connection between the anal canal and peri-anal skin.
This is commonly associated with peri-anal abscesses
(~1 in 3 abscess patients have a fistula).
Risk factors for fistula-in-ano
Peri-anal abscess IBD Systemic disease – HIV, TB, diabetes Trauma Pelvic radiation
Goodsall’s Rule
= the position of the external opening can give you clues as to the tract of the fistula
Anterior to transverse line – short, direct radicular tract to the interior opening.
Posterior to transverse line – curved/horseshoe tract to the interior opening
Presentation of fistula-in-ano
Maybe peri-anal abscess
Intermittent or continuous discharge of pus/blood/mucous from the perineum
Investigation of fistula-in-ano
PR exam
Proctoscopy under anaesthesia
(Complex cases – pelvic MRI)
Management of fistula-in-ano
Drain abscess in acute setting.
Seton-suture – an elastic band slung through the external opening into the internal opening in the anal canal and tied to make a loop that allows sepsis to drain, preventing abscess.
Fistulotomy – laying open of the tract, including the overlying skin and/or muscle.
Odynophagia vs dysphagia
- Dysphagia – swallowing difficulties
* Odynophagia – painful swallow
GI history - difficulty swallowing
Any pain?
Onset – how quickly did they start and how have they progressed?
Solids and liquids – difficulty with one or the other/both?
Progression – intermittent? Constant? Worsening?
GI history - N+V
Frequency and volume
Appearance - e.g. undigested, fresh bleed, coffee ground, bilous, faecal matter?
What would cause vomiting with fresh blood?
Mallory Weiss tear,
oesophageal variceal rupture
What would cause vomiting with “coffee ground” appearance?
peptic/duodenal ulcer
GI history - Weight loss
How much? Over how long? Intentional or unintentional? Anorexia? Dysphagia? Life stressors?
GI history - Dysuria
Urgency and frequency? Volume? Nocturia? Appearance? (haematuria/cloudy) Abdominal pain? Temperature?
GI history - Haematuria
Quantity? Thick blood or discoloured urine? Recent catheter? Anaemia symptoms? Occupation? Trauma?
GI history - abdominal distension
Any weight gain – eating more/decreased exercise/stress eating?
Alcohol intake?
Any systemic features of malignancy?
Bowel habits?
Any chance of pregnancy?
GI history - altered bowel habits
What is normal for the patient?
How often? Any urgency?
How long has this been happening?
Appearance – consistency, mucous, blood, melaena, pale?
Any recent antibiotics? Laxatives?
Recent suspicious food?
GI history - jaundice
Any dark urine/pale stools?
Any pain?
Itching? (Pruritis)
GI History - PMH
Previous medical conditions etc.
BUT ALSO
any pervious surgery?
previous colonoscopy/endoscopy?
GI History - FH
specifically history of polyps or bowel cancer?
what are the anal vascular cushions ?
highly vascular areas, formed of smooth muscle with subepithelial anastomoses of the rectal arteries/veins.
The 3 cushions act to assist the anal sphincter in maintaining continence
Where are the 3 anal cushions located?
positioned at the 3-, 7- and 11 o’clock positions when viewed from the lithotomy position
What are haemorrhoids?
disrupted/dilated anal vascular cushions
1st Degree Haemorrhoids
Remain in the rectum
2nd Degree Haemorrhoids
Prolapse through the anus on defecation but spontaneously reduce
3rd Degree Haemorrhoids
Prolapse through the anus on defecation but require digital reduction
4th Degree Haemorrhoids
Remain persistently prolapsed
Causes/risk factors for haemorrhoids
Idiopathic
Excessive straining/increased anal tone – chronic constipation, low-fibre diet.
Increasing age
Raised intra-abdominal pressure – pregnancy, chronic cough, or ascites.
Congestion of superior rectal veins – cardiac failure, rectal carcinoma, portal hypertension
Symptoms of haemorrhoids
Often asymptomatic
Painless rectal bleeding - on SURFACE of stool
Prolapse
Mucous discharge – pruritis ani due to chronic irritation.
Impaired continence
Rectal fullness/anal lump
Pain if the haemorrhoids are thrombosed.
Complications of haemorrhoids
Anaemia – if severe/continuous bleed.
Thrombosis
Ulceration/gangrene (secondary to thrombosis).
Perianal sepsis.
Thrombosis of haemorrhoids
When prolapsing haemorrhoids are gripped by the anal sphincter (“strangulated”).
Venous return is occluded, leading to thrombosis.
Haemorrhoids swell, become purple/blue and tense, cause significant pain/distress.
Often fibrose within 2-3 weeks, giving spontaneous cure.
Management is conservative – cold compresses, opioids and rest.
DDx for haemorrhoids
exclude other causes of rectal bleeding – malignancy, IBD, diverticular disease.
Other perianal DDx – fissure-in-ano, perianal abscess, fistula-in-ano
Haemorrhoids - investigations
PR exam – prolapsing haemorrhoids are obvious.
Protoscopy – can visualise the haemorrhoids and assess for any lesion higher in the rectum.
Abdominal exam – palpable mass, enlarged liver.
Colonoscopy/flexi-sigmoidoscopy – if symptoms suggest a different pathology (e.g. malignancy).
If significant/prolonged bleeding – FBC and coagulation screen.
Haemorrhoids - management
Normally always conservative/medical management:
- plenty of fluids, lots of fibre, try not to strain.
- ice packs
- Topical analgesia (e.g. instillagel)
- Bulk forming laxative.
Sometimes surgical management, particularly if bleeding:
- Banding
- Sclerotherapy
- Haemorrhoid artery ligation operation (HALO)
- Surgical haemorrhoidectomy
“Heartburn”
epigastric discomfort following a meal
Central, no radiation.
Worse with bending/lying down and when drinking hot liquids/alcohol.
Improves with sitting upright and Gaviscon
GORD
= Gastro-oesophageal Reflux Disease
A long-term condition where stomach contents rise up into the oesophagus - prolonged contact of the gastric contents with the oesophageal mucosa, leading to oesophagitis.
Results in either symptoms or complications.
Lower oesophageal sphincter - components and purpose
helps to prevent gastric contents reflux
Two muscular components – external and internal.
One physiological sphincter – angle of His
Symptoms of GORD
Heartburn. Acid reflux Oesophagitis – sore, inflamed oesophagus. Halitosis – bad breath Bloating and belching Nausea and/or vomiting Odynophagia and/or dysphagia
Risk factors for GORD
Obesity Hiatus hernia Pregnancy Connective tissue disorders Delayed stomach emptying
What can aggravate acid reflux?
Smoking
Eating large meals/late at night
Certain foods/drinks – e.g. fatty/fried foods, alcohol, coffee.
Certain medications, such as aspirin.
Complications of GORD
Oesophageal ulcers
Oesophageal strictures
=> Caused by repeated ulcers/inflammation
Barrett’s Oesophagus
Oesophageal Cancer
What are the Red Flag upper GI symptoms ?
ALARM55: Anaemia (iron deficient) Loss of weight Anorexia Recent onset, progressive symptoms Melaena or haematemesis Swallowing difficulties. >55 years of age
Diagnosis of GORD
Diagnosis is usually based on symptoms and treated empirically.
referral for endoscopy if red flag symptoms or symptoms are persistent/not controlled by medication.
Specialist investigations -
- Oesophageal manometry and ambulatory 24-hour oesophageal pH monitoring
- Barium swallow to rule out structural disorders
Management of GORD
LIFESTYLE
Weight loss and smoking cessation
Eat small and regular meals, >3h before bed.
Avoid hot drinks/alcohol.
Avoid drugs that exacerbate the condition/damage the mucosa (e.g. NSAIDs)
MEDICAL
Antacids +/- alginates
H2RAs/PPIs
Full-dose PPI for 8-weeks to heal severe oesophagitis.
What is Barrett’s oesophagus
= A pre-cancerous condition involving metaplasia in the mucosal cells lining the lower portion of the oesophagus.
occurs due to long-standing reflux
Cells transform from normal stratified squamous epithelium to gastric glandular columnar
Continued inflammation can lead to dysplasia and malignant changes
Diagnosis of Barrett’s Oesophagus
Diagnosis is with upper GI endoscopy
if present it will be visible and biopsies can be taken to confirm disease
Management of Barrett’s Oesophagus
Regular endoscopic surveillance
Biopsies to look for dysplasia/carcinoma in situ.
At what vertebral level is the oesophageal hiatus?
T10
Hiatus hernia
the protrusion of an organ (typically the stomach) through the oesophageal opening in the diaphragm, into the thoracic cavity.
What are the two types of hiatus hernia
Sliding
Rolling (para-oesophageal)
Sliding hiatus hernia
G-O junction slides through the hiatus to lie above the diaphragm.
Occurs in 30% of adults >50.
Usually of no significance, but symptoms may occur due to associated reflux.
Rolling hiatus hernia
A small part of the fundus rolls up through the hernia alongside the oesophagus, but the sphincter remains competent below the diaphragm.
Very occasionally can present with severe pain, requiring surgical intervention for gastric volvulus/ strangulation
What is a peptic ulcer?
a defect in the gastric or duodenal mucosa that extends through the muscularis mucosa
Gastric ulcers
Occur in older patients (>55)
Mainly on the lesser curve of the stomach
Pain is worse on eating
Relieved by antacids
May present with small bleed (iron deficiency anaemia) or major haemorrhage (haematemesis)
Peptic Ulcers
4x more common than gastric ulcers
90% located within 2cm of the pylorus.
Pain is at night and before meals.
Relieved by eating food/drinking milk.
May present with bleeding or perforation
Risk Factors/Causes of peptic ulcers
H. pylori infection
Long-term NSAIDs
Long-term/high-dose corticosteroids
Zollinger-Ellison Syndrome
Increased ICP (Cushing ulcers) Post severe burns (Curling ulcer)
Hepatic/renal failure
Zollinger-Ellison Syndrome
Excessive acid secretion due to a non-insulin secreting islet cell tumour of the pancreas which secreting gastrin-like hormone.
What can make peptic ulcers worse?
Smoking Alcohol Coffee consumption Stress Spicy foods
How does smoking impact peptic ulceration?
Smoking impairs gastric mucosal healing, and nicotine increases acid secretion.
How do NSAIDs impact peptic ulceration?
NSAIDs inhibit COX enzymes – inhibition of COX-1 in the stomach means that there is less production of prostaglandins which normally inhibit acid secretion and protect the mucosa.
Peptic Ulcers - Clinical Presentation
Nearly 75% of patients are asymptomatic
Symptoms can be:
- Burning epigastric pain, related to food intake.
- Feeling of fullness, bloating or belching.
- Appetite changes
- Unexplained weight loss
- Haematemesis/melaena
- Nausea
- Severe abdominal pain (?perforation)
Peptic Ulcers - management
If ALARMS55 symptoms – urgent referral for OGD (to be performed within 2 weeks).
If ALARMS symptoms not present:
1. Lifestyle measures – avoid food triggers, stop smoking.
- Medications
=> PPIs/H2Ras to reduce acid secretion
=> Stop NSAIDs if possible.
H. Pylori bacteria
Gram-negative, helical shaped rod bacteria
Produce a urease enzyme that will hydrolyse urea to form ammonium.
Ammonium neutralises the gastric acid in the surrounding environment to aid survival
What does H. Pylori infection cause?
- Direct mucosal injury via cytotoxins => mucosal damage.
- Increased gastrin release to make up for the neutralised environment => increased acidity.
This normally occurs in the antrum of the stomach and ulcer forms.
Also associated with duodenal ulcers
Management of H. Pylori infection
Eradication involves triple therapy:
= PPI + 2 antibiotics for 7 days.
Normally Omeprazole + 2 of clarithromycin/amoxicillin/metronidazole
Investigation of H. Pylori infection
Carbon-13 urea breath test
Stool antigen test
Laboratory-based serology (where its performance has been locally validated)
Biopsy of antral mucosa
Follow-up for peptic ulcers/H.pylori infection
Offer people with gastric ulcer and H. pylori repeat endoscopy 6 to 8 weeks after beginning treatment, depending on the size of the lesion
Perform re-testing for H. pylori using a carbon-13 urea breath test.
Globus
= a sensation of a lump/foreign body in the throat.
Dyspepsia
= a complex of upper GI tract symptoms, which are typically present for >4 weeks. Includes upper abdominal pain/discomfort, heartburn, acid reflux, nausea and/or vomiting.
Physical/obstructive causes of dysphagia
Foreign body (mainly in children) Tonsilitis Stricture Pharyngeal pouch Oesophagitis (GORD, infection, eosinophilic) Oesophageal malignancy Gastric malignancy Extrinsic pressure (lymph nodes, goitre, bronchial ca.)
Functional/neurological causes of dysphagia
CNS – Brain injury, Parkinson’s, MS, dementia
PNS – motor neurone disease, myasthenia gravis
Muscle – CREST syndrome, oesophageal spasm, achalasia
Functional – globus sensation
What infections can cause oesophagitis?
Bacteria
Candida (immunocompromised, poor steroid inhaler technique)
Dysphagia - duration of symptoms
Sudden – stroke
Rapidly progressive – cancer
Insidious – MND/MG
Longstanding – oesophageal spasm/achalasia.
Dysphagia - progressive vs. intermittent
Progressive – suspect benign/malignant stricture
Intermittent – motility disorders, spasms, achalasia
Dysphagia - solids/fluids/both?
Solids – suspect mechanical obstruction (benign/malignant stricture)
Fluids – suspect motility disorder (e.g. neuromuscular disease)
Dysphagia - is it difficult to make the swallowing movement?
If yes, suspect neurological cause.
Dysphagia - is swallowing painful?
If yes, suspect cancer, oesophageal ulcer, candida or spasm.
Dysphagia - associated symptoms
Gurgling Cough Hoarse voice Halitosis Weight loss (= red flag) Neurological symptoms
What is important PMHx in a history for dysphagia?
GORD – predisposes to oesophageal adenocarcinoma and also non-malignant strictures.
Peptic ulcers – scarring and strictures
Neurological condition
What is important DHx and SHx in a history for dysphagia?
any medications which increase the risk of GORD (e.g. NSAIDs, steroids, bisphosphonates)
Allergies
excess smoking and alcohol causes increased risk of gastric/oesophageal malignancy
Investigation of dyspepsia - Bedside tests
Basic observations Fluid status assessment Palpate neck Palpate abdomen Examine for Virchow’s node Examine for cachexia & anaemia Cranial nerves
Investigation of dyspepsia - Bloods
FBC
U&E
LFTs
Investigation of dyspepsia - Imaging
Key imaging = OGD +/- Biopsy
(CXR)
Barium swallow
Manometry
Staging CT if malignancy
What could be the cause of cachexia in dysphagia?
Weight loss due to inability to swallow
Weight loss due to malignancy
What could a CXR show in dysphagia ?cause ?
?gross dilatation of achalasia ?bronchial carcinoma ?hiatus hernia ?aspiration pneumonia ?mass impinging on oesophagus ?foreign body
Oesophageal malignancy - presentation
Initially asymptomatic – patients tend to present late
Progressive dysphagia
=> Starting with solids, then liquids and eventually difficulty swallowing saliva
Odynophagia Weight loss and anorexia. Retrosternal chest pain Coughing Hoarse voice Haemoptysis Vomiting Occasional lymphadenopathy.
Incidence of oesophageal cancer
What type of tumour is it normally?
3x more common in men than women
More common in age >55, but increasingly common in younger groups.
Mainly adenocarcinomas, with the remainder being mostly SCC
Oesophageal malignancy - adenocarcinoma
More common in UK and western Europe
Typically lower 1/3 of oesophagus
Risk factors:
• GORD – obesity/alcohol/medications
• Barrett’s Oesophagus
• Smoking
Metastasise earlier via lymphatics
Oesophageal malignancy - squamous cell carcinoma
More common worldwide
Typically middle and upper 1/3 oesophagus
Risk factors: • Alcohol • Smoking • Diet – high nitrates/nitrosamines • Chronic inflammation (e.g. Achalasia)
Regional lymph node spread.
Oesophageal malignancy - diagnosis
If suspected oesophageal malignancy – urgent OGD.
Staging CT CAP and PET-CT scan
Metastases are common at diagnosis (25%) in the liver/lungs/bones.
Oesophageal malignancy - management and prognosis
MDT management
Curative treatment = typically surgery +/- neoadjuvant chemotherapy or chemo-radiotherapy.
70% treated as palliative as the majority have advanced disease
Prognosis for both is poor (<10% 5-year survival), with SCC having a slightly better prognosis as it is more responsive to radiotherapy.
Incidence of gastric cancer
Falling incidence in the UK, but poor prognosis
75% of cases are in men
Most common in >55s
Risk factors for gastric cancer
- Hypochlorhydria
- H. pylori infection leading to metaplasia
- High salt/nitrate diet
- Smoking
- Genetic factors – blood group A, HNPCC, Japanese heritage
- Pernicious anaemia
- Adenomatous polyps
- Low socio-economic status.
Pathophysiology of gastric cancer and its spread
Most are adenocarcinomas, occurring in the antrum.
Metastases are local by direct invasion of abdominal viscera, lymphatic and then to the liver by portal dissemination.
Transcoelomic spread may cause peritoneal mets, including ovarian tumours.
More rare forms of cancer are stromal tumours (leiomyomas/leiomyosarcomas) arising from the interstitial cells of Cajal.
=> These are usually more slow-growing/benign.
Gastric cancer - clinical presentation
SYMPTOMS are frequently vague/non-specific symptoms.
Dyspepsia/epigastric pain Dysphagia Early satiety Nausea and Vomiting Anorexia, weight loss, anaemia, fatigue – late-stage symptoms
SIGNS are usually completely absent (esp. in early stages)
Anaemia
Jaundice
Hepatomegaly/jaundice/ascites – if liver metastases
Virchow’s node
Acanthosis nigricans
Palpable epigastric mass
Troisier Sign
Enlarged/hard left supraclavicular node (Virchow’s node)
This indicates intra-abdominal malignancy
Investigation of gastric cancer - bedside tests
Basic observations
Abdominal Exam
Lymph nodes
Investigation of gastric cancer - bloods
FBC - ?anaemia, ?raised platelet count
U&E
LFTs
Investigation of gastric cancer - imaging
OGD
=> Biopsies from suspected malignancy sent for histology, CLO testing and HER2
Staging CT CAP
Laparoscopy for peritoneal mets
Gastric cancer - management
Only ~1/3 have curable disease at presentation, the remainder are treated palliatively.
Treatment tends to be radical surgery, sandwiched between chemotherapy (neoadjuvant and adjunct).
Achalasia
= Failure of the lower oesophageal sphincter to relax during peristalsis (due to loss of ganglion cells).
Causes retention of a food bolus in the oesophagus.
There is consequential proximal inflammation, dilatation and muscle hypertrophy.
Chronic inflammation leads to a malignancy risk, particularly SCCs.
Achalasia - Clinical Features
Progressive, variable dysphagia on ingestion of both solids and liquids.
Regurgitation/vomiting
Nocturnal cough
Retrosternal discomfort – due to oesophageal inflammation
Weight loss
Achalasia - Investigations
OGD
=> rule out oesophageal malignancy
Mannometry (gold-standard diagnosis)
=> High resting pressure in the lower oesophageal sphincter
=> Incomplete relaxation on swallowing
=> Absent peristalsis
Barium swallow
=> Dilated tapering of oesophagus
Achalasia - Management
Conservative/lifestyle measures
=> Eat slowly, chew food well, always eat upright, drink lots with meals, etc.
Botulinum toxin injection (Temporary relief)
Endoscopic balloon dilation
Heller’s myotomy - Muscles of the cardia are divided.
Pharyngeal Pouch
an outpouching of posterior pharyngeal wall
typically at level C5-6
Incidence of pharyngeal pouch
Seen mostly in 60-80 year olds
more common in males (5:1)
Pharyngeal Pouch - Clinical Features
- Dysphagia - Solids AND liquids
- Regurgitation
- Chronic cough
- Gurgling on drinking
- Halitosis
- Globus
what is inflammatory Bowel Disease ?
= chronic, relapsing and remitting condition
Mainly due to an inappropriate immune activation in the mucosa.
Patients will have flare ups of symptoms and periods where they are completely symptom-free.
Mainly seen in teenagers/young adults.
More common in Caucasians, and Ashkenazi Jews
What are the types of IBD?
- Ulcerative colitis
- Crohn’s disease
- Indeterminate colitis (when it is not possible to distinguish between UC and Crohn’s)
What is Crohn’s disease?
Inflammation affects any part of the GI tract (mouth to anus).
Most commonly terminal ileum and proximal ascending colon.
Can affect just one area, or multiple areas leaving normal bowel in between (“skip lesions”).
pathophysiology of Crohn’s disease
The involved bowel is narrowed due to thickened wall, with deep ulcers.
“Rose thorn ulcers”
“Cobblestone” appearance on CT (specific to crohn’s, not seen on XR).
Due to inflammation, a lot of fat wrapping/stranding is seen around the intestine.
Inflammation extends through all layers of the bowel, so fistulas and strictures are common
Crohn’s disease - clinical presentation
Abdominal pain (varying in character)
Diarrhoea
=> Steatorrhoea in ileal disease
=> Bloody in colonic disease
Weight loss (or failure to thrive) – due to malnutrition
Severe apthous ulceration of the mouth (early sign)
Anal complications – fissure, fistula, haemorrhoids, skin tags, abscesses
Extra-GI manifestations of IBD
Can present with RIF pain/mass
Ileocolitis
inflammation of the terminal ileum and proximal ascending colon
pathophysiology of Ulcerative colitis
the inflammatory process is thought to be autoimmune in nature.
Inflammation that starts at the rectum, extending proximally along the colon
The inflammation only affects the mucosa (i.e. superficial ulceration). Ulceration is extensive and continuous, with only very small portions of normal mucosa.
Mucosa is reddened, inflamed and bleeds easily.
Inflammation leads to loss of the colonic haustra.
Gives the adjacent mucosa the appearance of inflammatory polyps.
what is a protective factor in UC?
smoking!
Backwash ileitis
when UC also causes inflammation of the distal terminal ileum
The extent of UC in the colon
Proctitis – affects the rectum alone Proctosigmoiditis Distal colitis Extensive colitis Pancolitis – whole colon is affected
UC - clinical presentation
Crampy lower abdominal discomfort
Gradual onset diarrhoea (often bloody)
Urgency and tenesmus if disease confined to rectum
Extra-GI manifestations of IBD
What are the extra-GI manifestations of IBD?
Can be:
Skin disorders Joint pain Eye manifestations – conjunctivitis/episcleritis/iritis Venous thrombosis Fatty liver
What might appear on an AXR in UC?
may show dilated colon, with some thumb-printing of the bowel wall.
=> Indicates inflammation and thickening
Histological differentiation of Crohn’s and UC
Crohn’s – transmural inflammation, lymphoid hyperplasia, granulomas.
UC – mucosal inflammation, crypt abscesses, goblet cell depletion
Investigating IBD - bloods
FBC, U&E, LFT, CRP/ESR
Serum iron, B12, folate
Might see raised systemic inflammatory markers,
Anaemia, raised WCC, raised platelets
Investigations IBD - stool studies
Stool chart
MCS x3 to exclude infective causes
Calprotectin
Investigations IBD - radiology/endoscopy
AXR/CXR
Potentially CT in Crohn’s
Rigid/flexi-sigmoidoscopy
Colonoscopy
Endoscopic rectal biopsy
What are complications of IBD?
Bowel perforation
Lower GI haemorrhage
Toxic dilatation (more common in UC)
Colonic carcinoma (Higher risk in Crohn’s than UC)
Toxic dilatation of the colon
Features – persistent fever, tachycardia, loose blood-stained stools.
Investigations – falling albumin/potassium.
AXR – dilated (>6cm) colon with mucosal islands.
Perforation is imminent
Surgery often required
Management of IBD
Aim of treatment is to prolong the remission phase and prevent relapses with maintenance therapy.
The type of treatment used depends on the severity of the disease and the responsiveness to therapy
Options are:
- surgery
- biologics
- immunomodulators
- antibiotics
- corticosteroids
- aminosalcylates
The use of surgery in IBD
Surgery tends to only be effective in UC – colectomy provides cure.
In Crohn’s, surgery is never curative and patients still tend to develop recurrent disease
How does malnutrition impact hospital patients?
Increases length of stay
Impairs wound healing
Leads to a longer and more difficult recovery
Increases risk of poor outcome and reduced functioning after admission.
In which patients is malnutrition more common?
Long-term health conditions – particularly those that affect the gut such as Crohn’s disease
Swallowing difficulties
Social isolation
Recovery from injuries or burns.
How do you work out daily calorie requirements?
BMR x Activity level
Varies depending on age, weight, gender, activity, and medical conditions
What are the fat soluble vitamins?
A, D, E, K
What are the water soluble vitamins?
B, C
What is the issue with BMI?
Not accurate for patients of extreme sizes, amputees, etc.
What are the indications for NG tube insertion?
Unsafe swallow (e.g. result of stroke, motor neuron disease, head injury)
Altered level of consciousness (e.g. ventilated patients)
Supplement oral intake
Upper GI strictures (e.g. possible bowel obstruction)
How do you check the placement of an NG tube?
pH aspirate - pH >5.5 suggests presence of gastric acid
CXR if unsure
What is the issue with obesity?
Increases the risk of many conditions including: T2DM, HTN, CVA, Hyperlipidemia, Some cancers. OA
Obestity - conservative management
Diet - aim to be mildly hypocaloric.
Minimise alcohol.
Exercise
Obesity - pharmacological management
Orlistat - Pancreatic lipase inhibitor
Liraglutide - GLP-1 agonist
Very low calorie diet (<800 kcal/day)
What are some of the side effects of orlistat?
Can cause abdominal pain, diarrhoea and anal leakage
Obesity - surgical management
recommended in those who have a BMI >40, or >35 with complications (e.g. T2DM) after appropriate nonsurgical measures have been tried.
or option of choice for those with a BMI >50.
Broadly 2 types:
- Restrictive types – such as gastric bands and sleeve gastrectomy.
- Malabsorptive types – such as gastric bypass
Travel History
When and where did they travel?
Other relevant travel history in the last few years?
What did they do when they were there?
Personal questions - IV drug use, sex, tattoos
Timeline and location of when symptoms began.
Any hospital/doctor visits abroad?
pre-trip immunisations / malaria prophylaxis ?
What are the 4 main species causing malaria?
Plasmodium falciparum – more dangerous infection
P. vivax
P. ovale
P. malariae
Process of malaria infection
Infection is transmitted by mosquitos – their saliva can contain the sporozoite of the parasite.
After a period of infection in the liver, the parasite emerges into the bloodstream and infects the red blood cells.
Blood cells become increasingly infected and the parasitic burden increases.
In P. falciparum this tends to happen more in the microvasculature in organs (e.g. brain and kidneys).
=> This makes it harder for the spleen to remove parasites and makes the disease more severe.
Clinical Features of Malaria
Often non-specific symptoms: Fevers and rigors Malaise Headache GI upset
If severe: Reduced GCS Seizures ARDS Shock Jaundice Anuria/oliguria – due to severe AKI/renal failure. Severe anaemia (Hb <50) Acidosis DIC or spontaneous bleeding due to low platelets
Diagnosis of malaria
Diagnosis is via a blood film looking for parasites or a rapid diagnostic test.
Should also get parasite load (%) as higher percentage of parasitaemia is associated with risk of more severe illness (falciparum)
Important to also look for complications of severe disease with other investigations
Timings of infectious gastroenteritis
Bacterial and viral gastroenteritis - Onset tends to be acute.
Protozoal - often a more chronic onset.
Typhoid/paratyphoid – diarrhoea starts around week 3 of illness
Questions to ask about the appearance of traveller’s diarrhoea
Blood?
=> Dysentery is bloody diarrhoea and may be due to E. coli, campylobacter, shigella or amoebiasis.
Mucous?
=> Mucous is suggestive of large bowel pathology
=> Mucous + blood common in dysentery
Pus?
=> Increases likelihood of a bacterial cause
Is it watery?
=> E.g. cholera is classically a ‘rice water diarrhoea’
Colour?
=> C. diff often has a green tinge.
Diagnosis of traveller’s diarrhoea
Physical examination
Stool sample – may need more than one!
Blood cultures and malaria investigations if pyrexic
Causes of traveller’s diarrhoea
Normal causes - noro/rotavirus
Shigellosis Campylobacter E. coli Enteric fever/typhoid Parasitic causes
Potential causes of Jaundice in the returned traveller
Hepatitis A
Yellow Fever
Leptospirosis
