gastroenterology Flashcards
define posseting
describes the small amounts of milk that often accompany the return of swallowed air (wind), whereas regurgitation describes larger, more frequent losses.
infant causes of vomitting
- Gastro-oesophageal 2. reflux
- feeding problems
- infection
- gastroeneteritis
- OM
- whooping cough
- urinary tract
- menigitis - food allergy and food intolerance
- eosinophilic oesophagitis
- intestinal obstruction
- pyloric stenosis
- atresia - duodenal
- intussusception
- malrotation
- volvulus
- dupilication cysts
- strangulated inguinal hernia
- hirschsprung disease - congenital adrenal hyperplasia
- renal failure
preschool children causes of vomiting
- gastroenteritis
- infection
- gastroeneteritis
- OM
- whooping cough
- urinary tract
- menigitis - intestinal obstruction
- intussusception
- malrotation
- volvulus - raised ICP
- coeliac disease
- renal failures
- torsion of testes
school age and adolescents causes of vomiting
gastroenteritis infection - pyelonephritis peptic ulceration appendicitis migraine raised ICP coeliac renal failure DKA alcohol drug ingestion BN/AN pregnancy torsion of testes
red flag clinical features
Bile-stained vomit -Intestinal obstruction
Haematemesis - Oesophagitis, peptic ulceration, oral/nasal bleeding, and oesophageal variceal bleeding
Projectile vomiting, in first few weeks of life Pyloric stenosis
Vomiting at the end of paroxysmal coughing Whooping cough (pertussis)
Abdominal tenderness/abdominal pain on movement - Surgical abdomen
Abdominal distension Intestinal obstruction, including strangulated inguinal hernia
Hepatosplenomegaly Chronic liver disease, inborn error of metabolism
Blood in the stool Intussusception, bacterial gastroenteritis
Severe dehydration, shock - Severe gastroenteritis, systemic infection (urinary tract infection, meningitis), diabetic ketoacidosis
Bulging fontanelle or seizures- Raised intracranial pressure
Faltering growth - Gastro-oesophageal reflux disease, coeliac disease and other chronic gastrointestinal conditions
factors contributing to the gastro-oesophageal reflux
relaxation of the lower oesophageal sphincter as a result of functional immaturity.
fluid diet
horizontal posture a short intra-abdominal length of oesophagus
what is gastro-oesophageal reflux
CFs
recurrent regurgitation or vomittung but are putting on weight normally
hoarse cry dehydration weight loss failure to thrive aspiration pneumonia
complications of gastro- reflux
faltering growth from severe vomiting
- Oesophagitis – haematemesis, discomfort on feeding or heartburn, iron-deficiency anaemia
- Recurrent pulmonary aspiration – recurrent pneumonia, cough or wheeze, apnoea in preterm infants
- Dystonic neck posturing (Sandifer syndrome)
- Apparent life-threatening events
who is more predisposed to gastro-oesophageal reflux
- children with cerebral palsy or other neurodevelopmental disorders
- preterm infants, especially in those with bronchopulmonary dysplasia
- following surgery for oesophageal atresia or diaphragmatic hernia.
Ix for gastro-oesophageal reflux
clinical diagnosis
- 24-hour oesophageal pH monitoring to quantify the degree of acid reflux - pH should be ABOVE 4
- 24-hour impedance monitoring which is available in some centres. Weakly acidic or nonacid reflux, which may cause disease, is also measured
- endoscopy with oesophageal biopsies to identify oesophagitis and exclude other causes of vomiting.
Mx of gastro oesophageal reflux
uncomplicated - parental reassurance, adding inert thickening agents to feeds (e.g. Carobel), and smaller, more frequent feeds.
trial of alginate therapy ie Gaviscon not the same time as thickening agents
- unexplained feeding difficulties (for example, refusing feeds, gagging or choking)
- distressed behaviour
- faltering growth - acid suppression with proton-pump inhibitors (e.g. omeprazole)
reduce the volume of gastric contents and treat acid-related oesophagitis
domeperidone - enhance gastric emptying - SEs arryhtmias
ABOVE FAILS
- cows milk protein allergy ???
surgical Mx only for children with complications unresponsive to intensive medical treatment or oesophageal stricture - Nissen fundoplication - fundus of the stomach is wrapped around the intra-abdominal oesophagus, is performed either as an abdominal or as a laparoscopic procedure.
what is pyloric stenosis
presents at what age
more common in who
hypertrophy of the pyloric muscle causing gastric outlet obstruction.
- > It presents at 2–8 weeks of age, irrespective of gestational age.
- > More common in boys (4 : 1), particularly firstborn, and there may be a family history, especially on the maternal side.
clinical features of pyloric stenosis
- vomiting, which increases in frequency and forcefulness over time, ultimately becoming projectile
- hunger after vomiting until dehydration leads to loss of interest in feeding
- weight loss if presentation is delayed.
hypokalaemic hypochloraemic metabolic alkalosis with a low plasma sodium and potassium occurs as a result of vomiting stomach contents.
Diagnosis of pyloric stenosis
examination features
test feed is performed
-> The baby is given a milk feed, which will calm the hungry infant, allowing examination
when feeding peristalsis may be seen as a wave moving from left to right across the abdomen
palpable in the right upper quadrant
tomach is overdistended with air, it will need to be emptied by a nasogastric tube to allow palpation.
US helpful to confirm prior to surgery
Mx of pyloric stenosis
correct any fluid and electrolyte disturbance with intravenous fluids
once everything is settled - PYLOROMYOTOMY -> division of the hypertrophied muscle down not mucosa
Postoperatively, the child can usually be fed within 6 hours and discharged within 2 days of surgery.
define colic
inconsolable crying or screaming often accompanied by drawing up of the knees and passage of excessive flatus takes place several times a day.
occurs in the first weeks of life
if its severe and persistent, protein hydrolysate formula (cow’s milk protein free) may be considered and continued if symptoms improve. If they do not, then a trial of gastro-oesophageal reflux treatment may be considered.
what is meckel diverticulum
presentation
2% of individuals ileal remnant of the vitello-intestinal duct, a Meckel diverticulum, which contains ectopic gastric mucosa or pancreatic tissue.
severe rectal bleeding
acute reduction in Hb
A technetium scan will demonstrate increased uptake by ectopic gastric mucosa in 70% of cases
Mx - surgical resection
what is malrotation
During rotation of the small bowel in fetal life, if the mesentery is not fixed at the duodenojejunal flexure or in the ileocaecal region, its base is shorter than normal, and is predisposed to volvulus. Ladd bands are peritoneal bands that may cross the duodenum, often anteriorly
presentations of malrotation
Ix
Mx
- high caecum at the midline
- High caecum at the midline
- Feature in exomphalos, congenital diaphragmatic hernia, intrinsic duodenal atresia
- May be complicated by the development of volvulus, an infant with volvulus may have bile stained vomiting
- Diagnosis is made by upper GI contrast study and USS
- Treatment is by laparotomy, if volvulus is present (or at high risk of occurring then a Ladd’s procedure is performed
Obstruction with bilious vomiting is the usual presentation in the first few days of life but can be seen at a later age
any child with dark green vomiting needs an urgent upper GI contrast study to assess intestinal rotation unless signs of vascular compromise are present, when an urgent laparotomy is needed.
what is recurrent abdominal pain
presentation
pain sufficient to interrupt normal activities and lasts for at least 3 months.
periumbilical pain
constipation
Ix of recurrent abdominal pain
urine microsopy adn culture is mandatory to exclude UTIs
abdominal US - excluding gall stones and pelvi-ureteric junction obstruction.
coeliac
TFTs
what is abdominal migraine
presentation
abdominal pain in addition to headaches
midline abdo pain w vomiting and facial pallor
long periods w no pain and shorter period with non specific abdo pain and pallor w or wo vomiting
what is IBS
altered gastrointestinal motility and an abnormal sensation of intra-abdominal events. Symptoms may be precipitated by a gastro-intestinal infection
experience pain on inflation of balloons in the intestine at substantially lower volumes than do controls.
presentation of IBS
- non-specific abdominal pain, often peri-umbilical, may be worse before or relieved by defaecation
- explosive, loose, or mucousy stools
- bloating
- feeling of incomplete defecation
- constipation (often alternating with normal or loose stools).
H.pylori causes what
Ix
antral gastritis, which may be associated with abdominal pain and nausea. It is usually identified in gastric antral biopsies. The organism produces urease, which forms the basis for a laboratory test on biopsies and the 13 C breath test following the administration of 13 C-labelled urea by mouth. Stool antigen for H. pylori may be positive in infected children
Mx of peptic ulceration
PPI - omeprazole
if investigations suggest they have an H. pylori infection, eradication therapy should be given (amoxicillin and metronidazole or clarithromycin
what is functional dyspepsia
Sx
Those who fail to respond to treatment or whose symptoms recur on stopping treatment should have an upper gastrointestinal endoscopy and, if this is normal
Sx
early satiety, bloating, and postprandial vomiting and may have delayed gastric emptying as a result of gastric dysmotility.
what is eosinophile oesophagitis
presentation
diagnosis
Mx
inflammatory condition affecting the oesophagus caused by activation of eosinophils within the mucosa and
submucosa.
presentation
vomiting, discomfort on swallowing or bolus dysphagia, when food “sticks in the upper chest”.
Diagnosis
endoscopy where macroscopically, linear furrows and trachealization of the oesophagus may be seen, and microscopically, eosinophilic infiltration is identified.
swallowed corticosteroids in the form of fluticasone or viscous budesonide.
what is gastroenteritis
common cause
other causes and presentation
- rotavirus infection under 2 esp during winter
- others
bacterial suggested by the presence of blood in the stools
campylobacter jejuni
Shigella and some salmonellae produce a dysenteric type of infection, with blood and pus in the stool, pain and tenesmus
Cholera and enterotoxigenic Escherichia coli infection are associated with profuse, rapidly dehydrating diarrhoea.
- protozoan - Giardia and Cryptosporidium .
severe abdo pain bilious vomit vom without diarrhoea temp >39 neck stiffness persistent diarrhoea >10 days blood or mucus in stool looks very unwell altered conscious state abdominal distension difficulty breathing
which children will be at an increased risk of rehydration
- infants, particularly those under 6 months of age or those born with low birthweight
- if they have passed six or more diarrhoeal stools in the previous 24 hours
- if they have vomited three or more times in the previous 24 hours
- if they have been unable to tolerate (or not been offered) extra fluids
- if they have malnutrition.
assessment of gastroenteritis
most accurate measure of dehydration is the degree of weight loss during the diarrhoeal illness
- no clinically detectable dehydration (usually <5% loss of body weight)
- clinical dehydration (usually 5% to 10% loss of body weight)
- shock (usually >10% loss of body weight; Fig. 14.9 and Table 14.1 ). Shock must be identified without delay.
red flag signs of shock
general appearance -> appears unwell or deteriorating
Altered responsiveness, e.g. irritable, lethargic
sunken eyes
tachycardia
tachypnoea
reduced skin turgor
what is isonatraemic and hyponatraemic dehydration
plasma sodium remains within normal range
loss of sodium more than water -> hyponatraemic
shift of water from extracellular to intracellular components
increase in brain volume -> seizures
extracellular depletion -> shock
what is hypernatraemic dehydration
plasma concetration increases
causes high fever or hot, dry environment) or from profuse, low-sodium diarrhoea.
ECF becomes hypertonic therefore water comes out of the
Signs
- jittery movements
- increased muscle tone
- hyperreflexia
- convulsions
- drowsiness or coma.
when is stool culture required for gastroenteritis
- septic
- if there is blood or mucus in the stools,
- immunocompromised
- recent foreign travel
- if the diarrhoea has not improved by day 7]- if the diagnosis is uncertain
Mx if clinical dehydration in gastroenteritis
ORS mechanism
shock
safety net
- oral rehydration solution
- 50ml/kg over 4 hours as well as maintenance fluid
adjunct to normal fluids or breastfeeding - deterioration or persisitent vomitting
- continue breastfeeding
ORS contains sodium and glucose which allows cotransport of SGLT 1 to work. increases salt and water uptake in the small intestinal lumen Na moving into lumen also pulls water too.
no skl for 48 hours
Shock
- Bolus therapy 20ml/kg
- fluid deficit -> 100ml/kg/24hr
maintenacne fluids
- first 10kg -> 100ml/kg
- second 10kg -> 50ml/kg
- subsequent kg ->20ml/kg
safety net
Wash your hands (and your child’s) with soap and water after going to the toilet, changing nappies and before eating
Regularly clean the toilet at home with disinfectant/bleach
Do not share towels, flannels etc with your child
Wash soiled clothes separately- soiled clothing and bedding should be washed at high
temperatures (60°)
Keep children off school, playgroup etc until at least 48 hours after their last symptom
Your child should not use swimming pools for another two weeks after they are well.
Mx of hypernatraemic dehydration
you cant reduce sodium too quickly as it will lead to a shift of water into cerebral cells -> seizures and cerebral oedema
aim to reduce at less than 0.5 mmol/l per hour.
DD for diarrhoea
Infection (gastroenteritis) Inflammatory bowel disease Lactose intolerance Coeliac disease Cystic fibrosis Toddler’s diarrhoea Irritable bowel syndrome Medications (e.g. antibiotics)
postgastroenteritis syndrome
Infrequently, following an episode of gastroenteritis, the introduction of a normal diet results in a return of watery diarrhoea. In such cases, oral rehydration therapy should be restarted.
post gastroenteritis complications
Lactose intolerance
Irritable bowel syndrome
Reactive arthritis
Guillain–Barré syndrome
what is coeliac disease
exposure to gluten causes an immune reaction that creates inflammation in the small intestine. It usually develops in early childhood but can start at any age.
In coeliac disease autoantibodies are created in response to exposure to gluten. These autoantibodies target the epithelial cells of the intestine and lead to inflammation. There are two antibodies to remember: anti-tissue transglutaminase (anti-TTG) and anti-endomysial (anti-EMA). These antibodies correlate with disease activity and will rise with more active disease and may disappear with effective treatment.
Inflammation affects the small bowel, particularly the jejunum. It causes atrophy of the intestinal villi. The intestinal cells have villi on them that help with absorbing nutrients from the food passing through the intestine. The inflammation causes malabsorption of nutrients and disease related symptoms.
presentation of coeliac disease
faltering growth, abdominal distension and buttock wasting, abnormal stools, and general irritability
Diarrhoea
Fatigue
Weight loss
Mouth ulcers
Anaemia secondary to iron, B12 or folate deficiency
Dermatitis herpetiformis is an itchy blistering skin rash that typically appears on the abdomen
peripjeral neuropathy
cerebellar ataxia
epilepsy
HLA-DQ2
diagnosis of coeliac
increased intraepithelial lymphocytes
- villous atrophy
- crypt hypertrophy
endoscopically followed by the resolution of symptoms and catch-up growth upon gluten withdrawal.
Check total immunoglobulin A levels to exclude IgA deficiency before checking for coeliac disease specific antibodies:
Raised anti-TTG antibodies (first choice)
Raised anti-endomysial antibodies
ass w
type 1 diabetes mellitus, autoimmune thyroid disease, Down syndrome, primary scleorising cholangitis, primary biliary cirrhosis
turner
causes of chronic diarrhoea
- In an infant with faltering growth, consider coeliac disease and cow’s milk protein allergy.
- Following bowel resection, cholestatic liver disease or exocrine pancreatic dysfunction, consider malabsorption.
- In an otherwise well toddler with undigested vegetables in the stool, consider chronic non-specific diarrhoea.
clinical features of crohn’s disease
classical presentation
- abdominal pain
- diarrhoea
- weight loss
growth failure
puberty delayed
general ill health
- fever
- lethargy
- weight loss
extra-intestinal manifestations
- oral lesions or perianal skin tags
- uveitis
- arthralgia
- erythema nodosum
diagnosis of crohn’s
endoscopic and histological findings on biopsy. Upper gastrointestinal endoscopy, ileocolonoscopy and small bowel imaging are required. The histological hallmark is the presence of non-caseating epithelioid cell granulomata
Small bowel imaging may reveal narrowing, fissuring, mucosal irregularities and bowel wall thickening.
Mx of crohn’s
remission is induced with nutritional therapy, when the normal diet is replaced by whole protein modular feeds (polymeric diet) for 6–8 weeks.
azathioprine, mercaptopurine or methotrexate maintain remission
if failed
biologics
infliximab or adalimumab
complications of crohns
obstruction, fistulae, abscess formation or severe localized disease unresponsive to medical treatment, often manifesting as growth failure
features of UC
ectal bleeding, diarrhoea and colicky pain. Weight loss and growth failure may occur
eryhtema nodosum
arthritis
diagnosis of UC
endoscopy (upper and ileocolonoscopy)
mucosal inflammation, crypt damage (cryptitis, architectural distortion, abscesses and crypt loss), and ulceration. Small bowel imaging is required to check that extracolonic inflammation suggestive of Crohn’s disease is not present.
Mx of UC
mild disease
- mesalazine induction and maintenance therapy
aggresive or extensive
- steroids acute exacerbations and immunomodulatory therapy, e.g. azathioprine alone to maintain remission or in combination with low-dose corticosteroid therapy. There is a role for biological therapies such as infliximab or ciclosporin in patients with resistant disease
severe
- IV fluids and steroids
FAILS -> ciclosporin
surgery
colectomy w ileostomy/ileorectal pouch severe complicated by a toxic megacolon or chronic poorly controlled disease
red flag symptoms/signs
Failure to pass meconium within 24 hours of life - Hirschsprung disease
Faltering growth/growth failure - Hypothyroidism, coeliac disease, other causes
Gross abdominal distension Hirschsprung disease or other gastrointestinal dysmotility
Abnormal lower limb neurology or deformity, e.g. talipes or secondary urinary incontinence Lumbosacral pathology
Sacral dimple above natal cleft, over the spine – naevus, hairy patch, central pit, or discoloured skin Spina bifida occulta
Abnormal appearance/position/patency of anus Abnormal anorectal anatomy
Perianal bruising or multiple fissures Sexual abuse
Perianal fistulae, abscesses, or fissures Perianal Crohn’s disease
Mx of constipation
faecal impaction
faecal impaction
stool softener - polyethylene glycol 3350 + electrolytes disimpaction regimen (escalating dose over 1-2 weeks)
after 2 weeks add stimulants
Not tolerated
Lactulose - osmotic laxative
Maintenance therapy
movicol first line
add a stimulant laxative
stools hard -> lactulose/docusate
mild constipation
same as above + stimualnt laxative ie sodium picosulphate
min of 6 months to ensure regular stooling titrating the dose
encouraged to sit on the toilet after mealtimes to utilise the physiological gastrocolic reflec
complciations of untreated coeliac disease
Vitamin deficiency Anaemia Osteoporosis Ulcerative jejunitis Enteropathy-associated T-cell lymphoma (EATL) of the intestine Non-Hodgkin lymphoma (NHL) Small bowel adenocarcinoma (rare)
what is biliary atresia
obliteration or discontinuity within the extrahepatic biliary system, which results in an obstruction in the flow of bile.
perinatal form presents in the first two weeks of life, and the postnatal form presents within the first 2-8 weeks of life
Sx
signs of biliary atresia
Ix
Mx
complications
- Jaundice >14 days
- Dark urine and pale stools
- Appetite and growth disturbance, however, may be normal in some cases
signs
- Jaundice
- Hepatomegaly with splenomegaly
- Abnormal growth
- Cardiac murmurs if associated cardiac abnormalities present
CONJUGATED BILIRUBIN HIGH
serum alpha-1 antritrypsin
sweat chloride test
US of biliary tree and liver - distension and tract abnormalities
Mx
surgical intervention - hepatoportoenterostomy
also called urgent kasai procedure -> bile drainage
blocked bile ducts are removed and replaced with a segment of the small intestine
- ursedeoxycholic acid -> adjuvant hepatoprotective and facilitates bile flow and it can be initiated following urinary bile acids being sent for analysis and continued until the resolution of jaundice
complications
- Unsuccessful anastomosis formation
- Progressive liver disease
- Cirrhosis with eventual hepatocellular carcinoma
what is intussusception
- Telescoping bowel
- Proximal to or at the level of, ileocaecal valve
- 6-18 months of age
features
- paroxysmal abdominal colic pain
- during paroxysm the infant will characteristically draw their knees up and turn pale
- vomiting
- bloodstained stool
- ‘red-currant jelly’ - is a late sign
- sausage-shaped mass in the right upper quadrant
Ix
US
-Mx: reduction with air insufflation
what is meconium ileus
- Usually delayed passage of meconium and abdominal distension
- The majority have cystic fibrosis
- X-Rays will not show a fluid level as the meconium is viscid, PR contrast studies may dislodge meconium plugs and be therapeutic
Infants who do not respond to PR contrast and NG N-acetyl cysteine will require surgery to remove the plugs
what is necrotising enterocolitis
- Prematurity is the main risk factor
- Early features include abdominal distension and passage of bloody stools
- X-Rays may show pneumatosis intestinalis and evidence of free air
- Increased risk when empirical antibiotics are given to infants beyond 5 days
- Treatment is with total gut rest and TPN, babies with perforations will require laparotomy
Sx of <1yr and >1 yrs constipation
< 1yr
Distress on passing stool
Bleeding associated with hard stool
Straining
> 1 yr
Poor appetite that improves with passage of large stool
Waxing and waning of abdominal pain with passage of stool
Evidence of retentive posturing: typical straight-legged, tiptoed, back arching
posture
Straining
Anal pain
possibel causes of constipation in children
dehydration low-fibre diet medications: e.g. Opiates anal fissure over-enthusiastic potty training hypothyroidism Hirschsprung's disease hypercalcaemia learning disabilities
features of idiopathic constipation
precipitating factors
starts after a few weeks of life
Generally well, weight and height within normal limits, fit and active
- no neuro problems in legs and normal locomotor dev
changes in infant formula weaning, insufficient fluid intake poor diet
Red flag signs of constipation
reported from birth or few weeks of life
> 48 hrs
ribbon stools
faltering growth AMBER flag
previously unknown or undiagnosed weakness in legs, locomotor delay
distension
define failure to thrive
when current weight or rate of weight gain is lower than that of children of the same age and sex
signs of dehydration
pale or mottled skin hypotension cold extremities reduce urine output sudden weight loss reduced skin turgor tachycardia prolonged capillary refill time tachypnoea eyes sunken dry mucous membranes sunken fontanelle decreased LOC
whos at increased risk of dehydration
- children younger than 1 year, particularly those younger than 6 months
- Low birth weight
- children who have passed more than five diarrhoeal stools in the previous 24 hours
- children who have vomited more than twice in the previous 24 hours
- can’t tolerate fluids
- stopped breastfeeding during the illness
- signs of malnutrition.
mesenteric adenitis
Aetiology: Inflammation of the mesenteric lymph nodes in response to infection, usually viral.
Epidemiology: True incidence unknown as easily missed or mistaken. Up to 20% of patients undergoing appendicectomy found to have mesenteric adenitis. More common in people <15 years old.
History: abdominal pain, fever, recent or current respiratory tract infection, diarrhoea, constipation, nausea, vomiting
Examination: diffuse abdominal tenderness, cervical lymphadenopathy, signs of URTI
Investigation: Abdominal USS
appendicitis
Aetiology: Inflammation of the appendix most commonly due to obstruction of the appendix lumen by faecolith, normal stool or lymphoid hyperplasia.
Epidemiology: Most cases between 15 & 59Y. Majority present as medical emergencies
History: Sharp abdominal pain, initially periumbilical moving to RIF, fever, loss of appetite (anorexia) nausea, vomiting
Examination: Pain brought on by movement, pain on palpation along McBurney’s point, rebound tenderness, guarding. Note not always seen in early presentation – can be vary varied.
Investigation: FBC, urinalysis, pregnancy test, abdominal USS
