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gastroenterology Flashcards

1
Q

define posseting

A

describes the small amounts of milk that often accompany the return of swallowed air (wind), whereas regurgitation describes larger, more frequent losses.

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2
Q

infant causes of vomitting

A
  1. Gastro-oesophageal 2. reflux
  2. feeding problems
  3. infection
    - gastroeneteritis
    - OM
    - whooping cough
    - urinary tract
    - menigitis
  4. food allergy and food intolerance
  5. eosinophilic oesophagitis
  6. intestinal obstruction
    - pyloric stenosis
    - atresia - duodenal
    - intussusception
    - malrotation
    - volvulus
    - dupilication cysts
    - strangulated inguinal hernia
    - hirschsprung disease
  7. congenital adrenal hyperplasia
  8. renal failure
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3
Q

preschool children causes of vomiting

A
  1. gastroenteritis
  2. infection
    - gastroeneteritis
    - OM
    - whooping cough
    - urinary tract
    - menigitis
  3. intestinal obstruction
    - intussusception
    - malrotation
    - volvulus
  4. raised ICP
  5. coeliac disease
  6. renal failures
  7. torsion of testes
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4
Q

school age and adolescents causes of vomiting

A 
gastroenteritis
infection - pyelonephritis
peptic ulceration
appendicitis
migraine
raised ICP
coeliac
renal failure
DKA
alcohol drug ingestion
BN/AN
pregnancy 
torsion of testes
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5
Q

red flag clinical features

A

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

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6
Q

factors contributing to the gastro-oesophageal reflux

A

relaxation of the lower oesophageal sphincter as a result of functional immaturity.

fluid diet
horizontal posture a short intra-abdominal length of oesophagus

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7
Q

what is gastro-oesophageal reflux

CFs

A

recurrent regurgitation or vomittung but are putting on weight normally

hoarse cry
dehydration
weight loss
failure to thrive
aspiration pneumonia
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8
Q

complications of gastro- reflux

A

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
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9
Q

who is more predisposed to gastro-oesophageal reflux

A
  • children with cerebral palsy or other neurodevelopmental disorders
  • preterm infants, especially in those with bronchopulmonary dysplasia
  • following surgery for oesophageal atresia or diaphragmatic hernia.
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10
Q

Ix for gastro-oesophageal reflux

A

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.
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11
Q

Mx of gastro oesophageal reflux

A

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.

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12
Q

what is pyloric stenosis
presents at what age
more common in who

A

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.
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13
Q

clinical features of pyloric stenosis

A
  • 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.

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14
Q

Diagnosis of pyloric stenosis

examination features

A

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

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15
Q

Mx of pyloric stenosis

A

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.

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16
Q

define colic

A

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.

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17
Q

what is meckel diverticulum

presentation

A

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

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18
Q

what is malrotation

A

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

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19
Q

presentations of malrotation

Ix
Mx

A
  • 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.

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20
Q

what is recurrent abdominal pain

presentation

A

pain sufficient to interrupt normal activities and lasts for at least 3 months.

periumbilical pain
constipation

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21
Q

Ix of recurrent abdominal pain

A

urine microsopy adn culture is mandatory to exclude UTIs

abdominal US - excluding gall stones and pelvi-ureteric junction obstruction.

coeliac
TFTs

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22
Q

what is abdominal migraine

presentation

A

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

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23
Q

what is IBS

A

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.

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24
Q

presentation of IBS

A
  • 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).
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25
Q

H.pylori causes what

Ix

A

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

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26
Q

Mx of peptic ulceration

A

PPI - omeprazole

if investigations suggest they have an H. pylori infection, eradication therapy should be given (amoxicillin and metronidazole or clarithromycin

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27
Q

what is functional dyspepsia

Sx

A

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.

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28
Q

what is eosinophile oesophagitis

presentation

diagnosis

Mx

A

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.

29
Q

what is gastroenteritis
common cause

other causes and presentation

A
  1. rotavirus infection under 2 esp during winter
  2. 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.

  1. 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
30
Q

which children will be at an increased risk of rehydration

A
  • 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.
31
Q

assessment of gastroenteritis

A

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.
32
Q

red flag signs of shock

A

general appearance -> appears unwell or deteriorating

Altered responsiveness, e.g. irritable, lethargic

sunken eyes
tachycardia
tachypnoea
reduced skin turgor

33
Q

what is isonatraemic and hyponatraemic dehydration

A

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

34
Q

what is hypernatraemic dehydration

A

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.
35
Q

when is stool culture required for gastroenteritis

A
  • 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
36
Q

Mx if clinical dehydration in gastroenteritis
ORS mechanism

shock

safety net

A
  • 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.

37
Q

Mx of hypernatraemic dehydration

A

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.

38
Q

DD for diarrhoea

A 
Infection (gastroenteritis)
Inflammatory bowel disease
Lactose intolerance
Coeliac disease
Cystic fibrosis
Toddler’s diarrhoea
Irritable bowel syndrome
Medications (e.g. antibiotics)
39
Q

postgastroenteritis syndrome

A

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.

40
Q

post gastroenteritis complications

A

Lactose intolerance
Irritable bowel syndrome
Reactive arthritis
Guillain–Barré syndrome

41
Q

what is coeliac disease

A

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.

42
Q

presentation of coeliac disease

A

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

43
Q

diagnosis of coeliac

A

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

44
Q

causes of chronic diarrhoea

A
  • 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.
45
Q

clinical features of crohn’s disease

A

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
46
Q

diagnosis of crohn’s

A

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.

47
Q

Mx of crohn’s

A

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

48
Q

complications of crohns

A

obstruction, fistulae, abscess formation or severe localized disease unresponsive to medical treatment, often manifesting as growth failure

49
Q

features of UC

A

ectal bleeding, diarrhoea and colicky pain. Weight loss and growth failure may occur
eryhtema nodosum
arthritis

50
Q

diagnosis of UC

A

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.

51
Q

Mx of UC

A

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

52
Q

red flag symptoms/signs

A

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

53
Q

Mx of constipation

faecal impaction

A

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

54
Q

complciations of untreated coeliac disease

A 
Vitamin deficiency
Anaemia
Osteoporosis
Ulcerative jejunitis
Enteropathy-associated T-cell lymphoma (EATL) of the intestine
Non-Hodgkin lymphoma (NHL)
Small bowel adenocarcinoma (rare)
55
Q

what is biliary atresia

A

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

56
Q

Sx
signs of biliary atresia

Ix

Mx

complications

A
  • 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
57
Q

what is intussusception

A
  • 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

58
Q

what is meconium ileus

A
  • 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
59
Q

what is necrotising enterocolitis

A
  • 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
60
Q

Sx of <1yr and >1 yrs constipation

A

< 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

61
Q

possibel causes of constipation in children

A 
dehydration
low-fibre diet
medications: e.g. Opiates
anal fissure
over-enthusiastic potty training
hypothyroidism
Hirschsprung's disease
hypercalcaemia
learning disabilities
62
Q

features of idiopathic constipation

A

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

63
Q

Red flag signs of constipation

A

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

64
Q

define failure to thrive

A

when current weight or rate of weight gain is lower than that of children of the same age and sex

65
Q

signs of dehydration

A 
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
66
Q

whos at increased risk of dehydration

A
  • 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.
67
Q

mesenteric adenitis

A

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

68
Q

appendicitis

A

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

Paediatrics (13 decks)

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