Peads - Acute Abdominal Pain Flashcards
How common is haematemesis in children?
Uncommon
(often due to Mallory-Wiss tear but need to consider other causes)
What questions are important regarding vomiting & stool?
Vomit:
- Frequency, volume, triggers, timeline
- Blood?
- Haematemesis
- Bile?
- Bilious vomiting = always abnormal
Stool:
- Frequency, consistency / form, timeline, Bristol stool chart
- Blood?
- Stool - fresh on wiping (?peri-anal pathology), on outside of hard stool (?constipation), mixed in with soft stool (?infection - likely bacterial blood in stool)
- Mucus - possible infection
What are functional GI disorders?
Functional GI disorders are common disorders characterised by persistent & recurring GI symptoms due to ‘abnormal functioning’ of the GI tract
(I.e. NOT due to structural or biochemical abnormalities - thus scan and blood tests often appear normal)
Examples:
- Irritable Bowel Syndrome (IBS)
- Functional dyspepsia
- Functional abdominal pain
- Functional constipation or diarrhoea
In a paediatric GI case what ‘red flag’ features can you name that would prompt further investigation?
History:
- Age < 5yrs
- Systemic symptoms: weight loss, fever, dysphagia, vomiting (?blood, bilious)
- Nocturnal symptoms - that wake child from sleep
- Persistent RU or RL abdo pain
- Dysuria / haematuria / flank pain
- Chronic NSAID use
- FHx of IBD / coeliac / peptic ulcer disease
Examination:
- Growth deceleration
- Delayed puberty
- Jaundice or Pallor
- Rebound / guarding / organomegaly
- Perianal disease
- Blood in stool
Investigations:
- ↑ WCC
- ↑ inflammatory markers
- anaemia or hypoalbuminaemia
Abdominal tenderness / pain can be difficult to evaluate when examining a child, what other observation can provide information as to whether the child is in pain?
Behaviour
- Walking normally / normal play / climb onto bed without discomfort = likely not in serious pain
What are some common causes of malaena in children?
- Infection - e.g. bacterial diarrhoea ( e.g. campylobacter, salmonella)
- IBD - Crohn’s or UC
- Tearing of anal vein
- Polyp
- Intussusception - child will be acutely unwell
What investigation can be done on stool if suspecting IBD?
Faecal Calprotectin Test
- Faecal calprotectin ↑↑ (up to 10 times) in IBD
- Not specific for IBD!! - can be ↑ due to polyps or infection
- Faecal calprotectin = normal in IBS
How does the Faecal Calprotectin Test work?
- Calprotectin = complex of proteins, which in the presence of Ca2+ can sequester metals; iron, manganese and zinc –> this gives antimicrobial properties
- Calprotectin comprises up to 60% of soluble content of cytosol of neutrophils –> which secrete it during inflammation
- IBD –> causes migration of neutrophils into intestinal mucosa –> which secrete calprotectin, which moves into the intestinal lumen = faecal calprotectin –> thus faecal calprotectin is ↑ inflammatory bowel diseases (UC and Crohn’s can have 10x ↑ in faecal calprotectin)
What features are common to both UC and Crohn’s, including ‘extra-intestinal’ symptoms?
- Abdominal pain
- Diarrhoea
- Fever
- Weight loss (more so in Crohn’s)
- Arthralgia / arthritis in large joints (most common extra-instestinal features of both UC and Crohn’s)
- Ulcers in mouth and vagina - (more common in Crohn’s)
- Anterior uveitis - inflammation of iris (pain, photophobia, redness, irregular pupil)
- Skin:
- Erythema Nodosum - painful itchy raised round lumps (1-5cm), commonly on legs (more common in UC)
- Pyoderma gangrenosum - dead black pus necrotic tissue, commonly on legs or around stoma
- Primary sclerosing cholangitis (more common in UC)
What are the key features of Ulcerative Colitis?
Define:
- UC is a relapsing-remitting disease characterised by;
- Colon inflammation (lead-pipe appearance on barium enema)
- Rectal bleeding
- Ulcers interspersed with preserved mucosa –> producing pseudo-polyps
Signs/Symptoms:
- Bloody diarrhoea
- Mucus in stool
- Tenesmus - feeling of incomplete defecation
- Feacal urgency
- Abdominal pain (particularly LLQ)
- Extra-intestinal features
Physiology of Inflammation:
- Inflammation is worse/starts distally in the rectum and can progress proximally BUT rarely passes ileocecal valve
- No inflammation beyond submucosa (confined to mucosa + submucosa)
- Neutrophils migrate into glandular lumens forming ‘crypt abscesses’
-
40-50% Proctitis = inflammation of anus/rectum (only first 6 inches of rectum)
- Proctosigmoiditis = inflammation of rectum + sigmoid colon
- 30-40% Left-sided colitis = Inflammation can spread in proximal direction i.e. from rectum/sigmoid backwards through descending colon
- 20% extensive colitis = Inflammation can spread further proximally to involve transverse colon
- Pancolitis = inflammation of entire colon
Prognosis:
- NO ↓ in mortality, 10-30% need colectomy (within 10yrs post onset)
Flares of Ulcerative Colitis can be classified as; Mild, moderate and severe - what are the features of each?
-
Mild:
- < 4 stools / day (with/without blood)
- No systemic disturbance
- Normal ESR + CRP
-
Moderate:
- 4-6 stools / day (with/without blood)
- Minimal systemic disturbance
-
Severe:
- > 6 stools / day - contains blood
- Evidence of systemic disturbances e.g.
- Fever
- ↑ HR (tachy)
- ↑ ESR
- Abdo pain, distension or reduced bowel sounds
- Anaemia
- Hypoalbuminaemia
What tests might you want to do in a patient with UC?
Beside:
- Obs - ↑ temp, ↑ HR, ↑ RR in severe flare of UC
- Abdominal exam - LLQ pain, clubbing, erythema nodosum, pyoderma gangrenosum, iritis
- PR exam - may show blood on glove
- Stool sample - ↑ WBCs suggestive of infective cause
Bloods: - in flare
- FBC:
- ↑ WCC
- ↑ platelets
- ↓ Hb (iron-deficient anaemia)
- ↑ ESR
- ↑ CRP
- pANCA - may be positive in UC (usually negative in Crohn’s)
Other tests:
- Flexible sigmoidoscopy - often shows inflammation, ulceration and bleeding mucosa (is rare rectum/sigmoid are clear in UC)
- AXR - may show air in colon + colonic dilation (often only needed in acute emergency presentations)
-
Barium Enema: - in UC:
- Loss of haustrations
- Superficial ulceration
- Long standing UC: shortened + narrow colon ‘leadpipe’
- Colonoscopy:
- Should not be used during actue attacks of IBD
- Can be used during remission to assess; extent of IBD, perform biopsies to rule out malignancy
What are 4 potential complications associated with UC?
- Bleeding
- Perforation
- Toxic megacolon
- Colorectal cancer
What drugs are used to induce remission of UC and which are used for maintiaining remission?
Induce Remission:
- Acute mild:
- 1st line = Topical (suppository or enema) mesalazine
- 2nd line = Topical (suppository or enema) mesalazine + oral prednisolone
- Acute moderate:
- Topical (suppository or enema) mesalazine (aminosalicylate anti-inflammatory) + oral prednisolone
- Acute Severe:
- 1st line = IV steroids e.g. hydrocortisone
- 2nd line = Ciclosporin (immunosuppresant) or Infliximab (monoclonal antibody - not advised due to lack of evidence but is more effective in Crohn’s)
- 3rd line = surgery (colectomy)
Maintaining Remission:
- Oral aminosalicylates e.g. Mesalazine
- Thiopurines e.g. azathipurine or mercatopurine (immunosuppresants)
What are the key features of Crohn’s Disease?
Define:
- Relapsing-remitting disease
- Can affect any part of GI tract (mouth-anus) often present as ‘skip lesions’ = areas of pathology with gaps of healthy GI tract in-between
- Often involves all layers of bowel + pattern of inflammation gives cobblestone appearances
- Rectum is rarely affected BUT anus often is (fistulae + perianal abscesses)
Signs/symptoms:
-
Diarrhoea (usually non-bloody)
- Can cause constipation if blockage forms e.g. stricture
- Weight loss - crohn’s often affects small intestine (failure to thrive in children)
- Abdominal pain (can mimic appendicitis i.e. umbilical –> LRQ)
- Right iliac fossa mass - 70% of Crohn’s affects the terminal ileum - can produce an abscess
- Fistulae + Abscesses - results from full thickness ulceration of GI tract
- Perianal disease - e.g. skin tags or ulcers
- Non-necrotising granulomas
- Gallstones + renal stones - more common in Crohn’s secondary to reduced bile acid reabsorption (Crohn’s affects small intestine)
- Fat wrapping - mesentery becomes thickened and wraps around bowel to anti-mesenteric border
- Extra-intestinal symptoms
Physiology of Inflammation:
- 40% ileocecal area (ileum + cecum)
- 30-40% small intestine - inflammation appears in segments (skip lesions)
- 20% Crohn’s Colitis = skip lesions in colon (large intestine)
- <10% Perianal inflammation
Prognosis:
- Slight ↓ mortality
- ~50% need surgery (within 10yrs post diagnosis)
What are the 4 main complications of Crohn’s Disease?
- Stricture - can cause obstruction, presents as ‘acute abdomen’ can mimic appendicitis
- Fistulas = abnormal connnection between 2 organs e.g. bladder-bowel
- Adhesions
- GI cancer - commonly adenocarcinomas of terminal ilieum
What test might you do for a patient with Crohn’s Disease?
Bedside:
- Abdominal exam - acute abdomen, LRQ pain/mass, clubbing, erythema nodosum, pyoderma gangrenosum, mouth ulcers, iritis
- PR exam - may have blood on glove, identify perianal abscess / skin tags
- Stool samples - to exclude infective diarrhoea (↑ WBCs)
Bloods:
- FBC:
- ↑ WCC (if disease active)
- ↓ Hb (anaemia)
- Serum Iron + B12 if anaemic on FBC - ↓ B12 anaemia
- ↑ CRP
- ↑ ESR
- LFTs - may be deranged if gallstones are present
- U+Es - may be deranged if renalstones are present
Other tests:
- Faecal calprotectin test
- CT - can show fistuals, fistulas and bowel wall changes
- Barium swallow - shows; strictures, mucosal changes and fistulas and picture of skip lesions
How is smoking advice potentially different in UC vs Crohn’s?
- Potentially don’t stop smoking in UC –> protective in UC, stopping smoking ↑ risk of relapse
- Stop smoking in Crohn’s –> it can be enough to maintain remission
How is Crohn’s Disease managed?
Crohn’s is NOT treated if asymptomatic (unlike UC)!!
Lifestyle:
- Low residue diet (↓ high-fibre foods e.g. nuts, seeds, fruit and veg) is advised in those with stricture
Pharmacological:
- Acute flares:
- 1st line = Glucocorticoids
- 2nd line = aminosalicylates (5-ASA drugs) e.g. Mesalazine
- Adjunct: Thiopurines e.g. azathipurine or mercatopurine (immunosuppresants) or Methotrexate
- Last line prior to surgery: Infliximab (monoclonal antibody)
- Surgery
- Maintaining remission:
- Stop smoking!!
- Azathipurine or mercatopurine
If you were to draw the colon and small intestine to demonstrate affected areas in UC vs Crohn’s how would each look?
Clostridium Difficle is an organism which is part of normal gut flora.
Abx can make it more predominate by killing competing organisms. This can present with what symptoms?
And what complications?
Symptoms of C.Diff infection:
- Diarrhoea
- Fever
- Nausea
- Abdominal pain
- ↑ WCC
Complications:
- C.Diff colitis
-
Toxic megacolon
- Acute form of colonic distension/dilation, which is often accompanied by paralysis of peristalsis, which can lead to accumulation of faeces in the immotile segment. Also characterised by
- Very distended colon
- Abdo pain
- Fever
- Bloating
- Colon perforation
- Sepsis
How do you manage a C.Diff patient?
- Discontinue offending Abx
- Oral vancomycin or fidaxomicin or metronidazole
- Isolate pt in side-room
- Gown + glove interaction with patient
- Fluid support if dehydrated due to diarrhoea
How do Aminosalicylate (5-ASA) drugs work?
5-aminosalicylic acid acts as a local anti-inflammatory agent
(mechanism not fully understood - may inhibit prostaglandin synthesis)
More effective in UC and less effective in Crohn’s management!
What is Azathioprine?
It is an immunosuppresive medication
Commonly used in:
- Crohn’s - for maintaining remission or as adjunct to steroids or mesalazine in inducing remission
- RA
- SLE
- Myasthenia Gravis
What are the adverse side-effects of Azathioprine?
- bone marrow supression
- nausea / vomiting
- pancreatitis
- ↑ risk of non-melanoma skin cancer
What are the common side effects of Mesalazine?
- GI upset
- headache
- agranulocytosis
- interstitial nephritis
- pancreatitis (7 x more common for mesalazine than sulfasalazine)
10 year old Hannah presents with a 6 week history of increased stool frequency, pale & bulky stools, weight loss, fatigue and pallor. Her full blood count shows a microcytic anaemia.
Which investigation is likely to be diagnostic?
- Flexible sigmoidoscopy
- ESR
- Tumour markers
- MRI small bowel
- TTG antibody
TTG antibody
- Hx = classic for coeliac disease
- 1st line screen = tissue transglutaminase (TTG) antibodies (IgA)
- 2nd line = endomyseal antibody (IgA) - do this if patient has low IgA
- Coeliac disease = strongly associated with HLA-DQ2 (95% of patients) and HLA-DQ8 (80%)
-
Duodenal / Jejunal biopsy = diagnostic
- Not required IF … classic symptoms + very high TTG + HLA-DQ2 or HLA-DQ8
Managmenet:
- Gluten-free diet (life-long) > 90% respond well
What is haemolytic uraemic syndrome (HUS)?
Condition often seen in children /w a triad of:
- AKI
- microangiopathic haemolytic anaemia
- thrombocytopenia
Causes:
- E. coli - classically caused by Shiga toxin-producing Escherichia coli (> 90% of cases)
- pneumococcal infection
- HIV
Investigations:
- FBC - anaemia, thrombocytopenia, fragmented blood film (schistocytes)
- U&Es - AKI
- Stool culture - E.coli
Management = supportive e.g. fluids / blood transfusion / dialysis
What are some common causes of abdominal pain in children?
- Functional GI disorders e.g. functional abdominal pain
- Constipation
- Gastroenteritis
- Primary dysmenorrhoea (period pain)
- Cholelithiasis (gallstones) / cholecystitis
- Acute apendecitis
- UTI
What is Intussusception?
Cause of intestinal obstruction in young children, defined as prolapse of one part of intestine into the lumen of adjoining distal intestine
(Intestine within intestine!!)
This causes 1) venous obstruction 2) bowel-wall oedema –> can progress to bowel necrosis, perforation and death
In which area of the intestine is intussusception most common?
Ileo-caecal region
What can cause intussusception?
Lead point of intussusception is most often an enlarged lymph node (Peyer’s patch) in terminal ileum
Pathological lead points (due to a condition):
- luminal polyps
- mesenteric lymphadenopathy
- malignant tumours (e.g. lymphoma)
- benign masses e.g. lipomata, Mekel’s diverticulum or Henoch-Schonlein purpura
What age is intussusception most common?
More common in boys or girls?
6-18 months old
Boys 2 x risk
What are the features of intussusception?
- Age 6-12 months
- Male
-
Acute abdo pain - paroxysmal & colic in nature
- during paroxysm the infant will characteristically draw their knees up + turn pale
- Guarding - may indicate peritonitis due to perforation
- Pallor
- Vomiting
- Poor feeding
- Bloodstained stool - ‘red-currant jelly’ is a late sign - due to bleeding into intestine
- Sausage-shaped mass in the RU quadrant
- Hypovolaemic shock (uncommon)
How is intussusception investigated & managed?
Investigation:
- Ultrasound - showing ‘target’ or ‘doughnut’ sign (investigation of choice)
Management:
- 1st line = air sufflation (most cases) - involves rectal tube which shoots air into GI tract to force prolapse to correct
- 2nd line = surgery (if air sufflation fails or child has signs of peritonitis)
What is Meckel’s Diverticulum?
What is the rule of 2’s?
Meckel’s diverticulum is a congenital diverticulum of the small intestine
it is a remenant of the omphalomesenteric duct (also called the vitellointestinal duct) & is typically lined with ileal mucosa but can be ectopic gastric mucosa (risk of peptic ulceration)
- Diverticulum = a blind tube leading from a cavity / passage i.e. a small closed tube hanging from GI tract
Rule of 2’s:
- occurs in 2% of the population
- is 2 feet from the ileocaecal valve
- is 2 inches long
How does a Meckel’s diverticulum present?
Often asymptomatic!
Features can be:
- Abdo pain (mimicking appendicitis)
- Rectal bleeding
- Intestinal obstruction - secondary to an omphalomesenteric band (most commonly), volvulus and intussusception
Management:
- Removal - if narrow neck or symptomatic
What is Hirschsprung’s disease?
Hirschsprung’s disease is caused by an aganglionic segment of bowel (i.e. failure of parasympathetic Auerbach & Meissner plexuses locally)
Features:
- Rare (1 in 5000 births)
- 3 x more common in males
- Associated with Down’s syndrome
- Neonatal - failure / delay in passing meconium
- Children - constipation, abdominal distention
What is coeliac disease?
An autoimmune condition caused by sensitivity to the protein gluten
Details:
- ~ 1% of UK
- repeated exposure to gluten –> villous atrophy in small intestine, causing malabsorption
Which HLA serotypes is coeliac disease associated with?
HLA-DQ2 and HLA-DQ8
What conditions is coeliac disease associated with?
-
Dermatitis herpetiformis - autoimmune blistering skin condition
- Cause = IgA deposition in dermis
- Features = itchy, vesicular skin lesions on extensor surfaces (e.g. elbows, knees, buttocks)
- Diagnosed via skin biopsy + immunofluorescence
- Management = gluten-free diet + dapsone
-
Autoimmune disorders e.g.
- T1DM
- Autoimmune thyroid disease
- Autoimmune hepatitits
What are the presenting features of coeliac disease?
- Diarrhoea - chronic / intermittent
- Persistent / unexplained GI symptoms e.g.
- nausea & vomiting
- abdo pain
- cramping
- distention
- Fatigue - often prolonged e.g. ‘tired all the time’
- Weight loss - sudden or unexpected
- Anaemia - often iron-deficiency anaemia (or other unspecified anaemia folate-deficiency more common that B12)
- Hyposplenism - due to exxcessive loss of lymphocytes through a damaged GI mucosa (late symptom)
- Oesteoporosis
- ↓ fertility
In Children:
- Failure to thrive + symptoms above
- Many cases not diagnosed till adulthood
How is coeliac disease managed?
Gluten-free diet
Gluten is found in:
- Wheat - bread, pasta, pastry
- Barley - beer
- Rye & oats
Immunisation:
- Pts /w coeliac disease often have degree of functional hyposplenism –> offer pneumococcal vaccine /w booster every 5 years
What is pyloric stenosis?
At what age does it often present?
Pyloric stenosis is a narrowing of the opening from the stomach to the small intestine due to hypertrophy of the circular muscles of the pylorus / pyloric sphincter
- Age = 2nd - 4th week of life (can be up to 4 months)
- Most common cause of gastric outlet obstruction in 2-12 week old group
- 4 x more common in males
- 10-15% of infants have a +ve FHx
What are the features of pyloric stenosis?
- 2-12 weeks of age
- ‘projectile’ vomiting + non-bilious (typically ~ 30 mins after feeding)
- Hypochloraemic + hypokalaemic + metabolic alkalosis (due to vomiting)
- Palpable ‘olive shaped’ mass in right epigastrium
- Constipation
- Dehydration may occur - baby cries /wout tears, reduced urine output
- Can present /w weight loss & poor feeding (some have normal weight)
How is Pyloric Stenosis diagnosed?
Ultrasound
- Pyloric muscle thickness > 4 mm
- Pyloric canal length > 17 mm
How is pyloric stenosis managed?
-
IV fluid resuscitation
- Correct hypovolaemia and electrolyte disturbances
- Give fluid bolus of saline if severely volume depleted
- IV fluid at 1.5 x maintanence rate /w 5% dextrose + 0.45% saline
- No IV potassium until urine output is adequate –> then 10-20 mEq/L KCl can be added
-
Pyloromyotomy
- Laproscopic incision to muscles of pylorus
What are the 5 P’s of Ulcerative colitis?
- Pyrexia
- Pseudopolyps
- Lead Pipe radiological appearances
- Poo (bloody diarrhoea)
- Proctitis
What is Mesenteric Adenitis?
Mesenteric adenitis - is inflammation of lymph nodes in the abdomen
Features:
- Can be acute or chronic
- Often presents in children /w recent Hx of URTI
- Diffuse abdo pain - often able to move / jump (not the case in appendicitis)
- Generalised lymphadenopathy may be present (can be seen on US) - not localised to RIF (where appendicitis localises)
- Often mistaken for appendicitis!
What is Duodenal Atresia?
Congenital absence or complete closure of the lumen of the duodenum
Features:
- More common in Down’s syndrome
- Causes polyhydramnios (↑ amniotic fluid) during pregnancy
- occurs because fetus can’t swallow amnitoic fluid & absorb it via digestive tract
- Intestinal obstruction in newborns (few hrs after birth)
- Abdominal distension (absent in proximal atresia)
- Vomiting - bilious / non-bilious (depending on atresia proximal / distal to Ampulla of Vater)
- AXR shows:
- ‘double bubble’ sign - due to distended stomach + dueodenum (seperated by pyloric valve)
- absence of gas distal to obstruction
How do you manage duodenal atresia?
- Remove stomach fluid via NG-tube
- IV fluid replacement
- Duodenoduodenostomy or Duodenojejunostomy
