Gastro Flashcards
(78 cards)
1
Q
How do GI conditions present in a child?
A
- vomiting,
- abdominal pain,
- diarrhoea,
- crying, etc.
2
Q
What is posseting?
What is regurgitation?
What is vomiting?
A
- Posseting: non-forceful return of small amounts of milk that often accompanies the return of swallowed air (wind) à occurs in all babies from time to time
- Regurgitation: non-forceful return of larger amounts of milk
- Vomiting: forceful ejection of gastric contents
3
Q
What are the red flag features of vomiting?
A
- Bile stained vomit (intestinal obstruction)
- Haematemesis (peptic ulcer, varices)
- Projectile vomiting in first few weeks (pyloric stenosis)
- Paroxysmal coughing (pertussis)
- Abdo tenderness (surgical abdomen)
- Hepatosplenomegaly (liver disease, inborn error of metabolism)
- Blood in stool (intussusception, bacterial gastroenteritis)
- Severe dehydration, shock (severe gastroenteritis, systemic infection, DKA)
- Bulging fontanelle or seizures (raised ICP)
- Faltering growth (GORD, coeliac)
4
Q
What are the DDx of abdo pain in a child?
A
5
Q
Why might a child be crying?
A
- Usually due to hunger and discomfort
-
Sudden-onset crying:
- UTI,
- otitis media,
- meningeal infection,
- unrecognised fracture,
- oesophagitis,
- testicular torsion,
- constipation etc.
- Infant ‘colic’:
6
Q
Summarise infant colic
A
- Paroxysmal, inconsolable crying or screaming often accompanied by drawing up of the knees and passage of flatus, which takes place several times a day
- Lasts >3hrs/day and occurs >3days/week for at least 1 week
- Occurs in 40% babies, usually in first few weeks of life, and resolves from 3-12 months
- It is benign but frustrating and worrying for parents à support and reassurance
- If severe and persistent it may be due to cows milk protein allergy or GORD
7
Q
What is appendicitis?
A
Inflammation of the appendix (a narrow blind-ended tube connected to the posteromedial end of the caecum)
8
Q
Aetiology of appendicitis in a child?
A
Inflammation is due to obstruction of the lumen of the appendix (by a faecolith, normal faecal matter or lymphoid hyperplasia due to viral infection)
- Obstruction causes a cycle of progressive inflammation and bacterial overgrowth
- Leads to ischaemia → may progress to necrosis à risk of perforation
- Takes around 72hrs for perforation to occur
- May occur sooner in preschool children (omentum immature so fails to surround appendix)
- Perforation releases bacteria into abdominal cavity à peritonitis
- Takes around 72hrs for perforation to occur
9
Q
RFs of appendicitis in a child?
A
RFs: poor dietary fibre, prolonged bowel transit time
10
Q
Epidemiology of appendicitis in a child?
A
Most common cause of abdominal pain in childhood requiring surgical intervention
Most common in 10-19yo; uncommon in children <3yo
11
Q
Symptoms of appendicitis in child?
A
Classical presentation:
- Abdominal pain
- Initially central and colicky, then localises to RIF
- Umbilical initially because inflammation of visceral peritoneum is poorly localised; localises when parietal peritoneum becomes irritated (which is innervated by the same region of abdo wall that lines it)
- Aggravated by movement (walking, bumps during car journey)
- Initially central and colicky, then localises to RIF
- Anorexia, nausea, vomiting, diarrhoea
- Low-grade fever (high if rupture)
Atypical presentation:
- Especially likely in young children (can’t verbalise where the pain is)
- Vomiting and diarrhoea
- Different sites of pain if abnormal appendix position, e.g. retrocaecal appendix causes pain in RUQ and absence of peritoneal irritation signs
12
Q
Signs O/E of appendicitis in a child?
A
- Tachycardia, pyrexia, reluctance to move (esp if rupture)
- Tenderness and guarding at McBurney’s point (guarding may not occur in children); percussion pain
- Rovsing’s sign: RIF pain reproduced with palpation in LIF
- Psoas and obturator sign (rarely done): pain is elicited by extending R thigh in L lateral position (psoas) and by internal rotation of flexed thigh (obturator)
13
Q
Ix for appendicitis?
A
- Clinical diagnosis (but Ix can help if in doubt)
-
Bloods:
- FBC: WBC (esp neutrophils) elevated in 70-90%
- U&Es (esp if vomiting)
- CRP and ESR
- Urine dip → rule out UTI (leukocytes may be present, but nitrite -ve)
- Pregnancy test if appropriate
-
USS
- May support diagnosis → thickened, non-compressible appendix with increased blood flow
- May show complications (appendix mass, abscess, perforation)
- Can exclude other diagnoses (ovarian torsion, ectopic pregnancy)
-
CT
- If diagnostic doubt; not usually done
14
Q
What score is used to assess appendicitis in a child?
A
- Paediatric appendicitis score (PAS) assesses the risk of appendicitis
- <4: low likelihood of appendicitis
- 4-6: further monitoring and clinical judgement; USS
- >6: refer to surgical team; higher risk of appendicitis
15
Q
Mx of appendicitis in a child?
A
Initial management:
- ABCDE approach, senior help
- IV access, IV fluids, NBM
- IV antibiotics (tazocin/cefoxitin)
-
Contact surgical team to discuss whether surgical intervention is needed
- Sometimes conservative management (IV antibiotics and monitoring) is used for early uncomplicated appendicitis or appendix mass, with later appendicectomy (after 6wks; sooner if deterioration)
Appendicectomy:
- In uncomplicated appendicitis (no mass)
- Usually laparoscopic
- IV antibiotics for 24hrs after; discharge in 24-36hrs
If suspected perforation:
- ABCDE approach (as above)
- Appendicectomy always done
16
Q
Complications and prognosis of appendicitis in a child?
A
Complications:
- Perforation (more common in young children) à peritonitis, sepsis
-
Appendix mass
- Greater omentum reduces spread of infection by surrounding and adhering to the appendix
-
Appendix abscess
- Treat by drainage; appendicectomy after 6wks if symptoms not resolved
Prognosis is excellent with treatment
17
Q
What is gastroenteritis?
A
Infection of the GI tract, usually by a virus
18
Q
Aetiology of gastroenteritis?
A
May be viral, bacterial or protozoal
- Viral:
- Most common in developed countries (80%)
- Rotavirus is most common (esp in winter and spring)
- Other viruses include adenovirus (type 40 and 41), norovirus, calicivirus, coronavirus, astrovirus
- Bacterial:
- More common in developing countries; uncommon in developed countries
- Campylobacter jejuni is most common in developed countries
- Protozoal:
- Uncommon in developed countries
- E.g. Giardia, Cryptosporidium
Spread is mainly by faecal-oral route (contaminated hands, utensils, food and drink)
19
Q
Name some other bacterial causes of gastroenteritis, other than the common ones
A
20
Q
What can diarrhoea and vomiting cause in gastroenteritis?
A
Diarrhoea and vomiting lead to dehydration
-
Isonatraemic and hyponatraemic dehydration:
- There is a total body deficit of sodium and water à these losses are usually proportional so plasma Na remains in normal range (isonatraemic dehydration)
- When children with diarrhoea drink large quantities of water or other hypotonic solutions (cola, fruit juices), there is greater net loss of sodium than water à fall in plasma sodium (hyponatraemic dehydration)
- This leads to a shift of water from extracellular to intracellular compartments
- Increased intracellular volume leads to seizures; decreased extracellular volume leads to shock
-
Hypernatraemic dehydration:
- Sometimes water loss exceeds the relative sodium loss à plasma sodium increases (hypernatraemic dehydration)
- Usually due to insensible water losses (high fever, hot environment) or from profuse, low sodium diarrhoea
- The extracellular fluid becomes hypertonic compared to the intracellular fluid à shift of water into the extracellular space from the intracellular compartment
- Signs of extracellular depletion are therefore less per unit of fluid loss (e.g. skin turgor, fontanelle depression) à harder to recognise clinically
- It is particularly dangerous because water is drawn out of the brain à cerebral shrinkage can cause jittery movements, increased muscle tone, altered consciousness, seizures
- Transient hyperglycaemia can occur
- Sometimes water loss exceeds the relative sodium loss à plasma sodium increases (hypernatraemic dehydration)
- Children at an increased risk of dehydration are:
- <1yo (esp <6mo),
- infants who were low BW,
- passed 6 or more diarrhoeal stools in past 24hrs,
- have not tolerated/been offered supplementary fluids,
- infants who have stopped breastfeeding,
- signs of malnutrition
21
Q
What are the RFs for dehydration e.g in gastroenteritis?
A
Children at an increased risk of dehydration are:
- <1yo (esp <6mo),
- infants who were low BW,
- passed 6 or more diarrhoeal stools in past 24hrs,
- have not tolerated/been offered supplementary fluids,
- infants who have stopped breastfeeding,
- signs of malnutrition
22
Q
Signs and symptoms of gastroenteritis?
A
- Vomiting
- Diarrhoea
- Bloody stools suggests bacterial cause
- Mucous suggests bacterial cause or rotavirus
- Fever
- Low-grade seen in 50% children with viral gastroenteritis
- >39⁰C suggests bacterial
- Abdo cramps
- Anorexia
- Signs of dehydration
- Suspect hypernatraemic dehydration if jittery movements, increased muscle tone, hyperreflexia, convulsions, drowsiness/coma
23
Q
What are the clinical signs of dehydration (e.g. in gastroenteritis)?
A
24
Q
Ix for gastroenteritis?
A
- Clinical assessment of dehydration:
- Most accurate measure is weight loss (recent weight is not always available)
- History and examination are used to assess the degree of dehydration
- No clinically detectable dehydration (usually <5% loss of body weight)
- Clinical dehydration (usually 5-10% loss)
- Shock (usually >10% loss)
- Clinical diagnosis (usually no Ix needed)
- Stool microscopy and culture
- Indications: appears septic, blood/mucous in stool, immunocompromised, recent foreign travel, diarrhoea not improved by day 7
- Bloods:
- U&Es, creatinine, glucose, FBC: if IV fluids are needed or suspecting hypernatraemia
Blood culture: if antibiotics are started
25
Mx of gastroenteritis?
**_If no clinical dehydration:_**
* Aim is to prevent dehydration
* Continue breastfeeding and other milk feeds/age-appropriate diet
* Encourage fluid intake to compensate for increased GI losses
* Discourage fruit juices and carbonated drinks
* Give oral rehydration solution (ORS) as supplemental fluid if at increased risk of dehydration (see aetiology)
**_If there is clinical dehydration:_**
* Mainstay of therapy is oral rehydration
* ORS works by giving Na and glucose à these are absorbed which also causes water to be absorbed from intestine à absorption of solutes and water exceeds secretion à keeps the child hydrated until the infective organism is eradicated
* Give fluid deficit replacement (50ml/kg) over 4hrs as well as maintenance fluid requirement; give ORS often and in small amounts
* Continue breastfeeding/age-appropriate diet
* Consider supplementing ORS with usual fluids if inadequate intake of ORS
* If inadequate intake of fluid or vomits persistently, consider giving ORS via NG tube
* If deterioration or persistent vomiting à give IV fluids
**_If in shock:_**
* 20ml/kg 0.9% NaCl solution, repeat if necessary
* Then give IV fluids
**IV fluids:**
* Replace fluid deficit over 24hrs and give maintenance fluids
* 0.9% NaCl solution +/- 5% glucose
* Monitor plasma electrolytes, urea, creatinine and glucose; consider IV K supplementation
* Continue breastfeeding if possible
**_After rehydration:_**
* Reintroduce normal food
* Avoid fruit juices and carbonated drinks
* Advise parents: diligent hand washing, towels infected by child should not be shared, do not return to school until 48hrs after last episode
**Medication**:
* Do not give antidiarrhoeal drugs and antiemetics → ineffective and may prolong excretion of bacteria
* Antibiotics are not routinely given, even if there is a bacterial cause
* Only give for suspected/confirmed sepsis, extraintestinal spread of bacterial infection, salmonella gastroenteritis in children \<6 months, malnourished or immunocompromised children or for specific infections (e.g. C. diff with pseudomembranous colitis, cholera, shigellosis, giardiasis)
**_Hypernatraemic dehydration:_**
* Management can be difficult
* Use oral rehydration to rehydrate hypernatraemic children with clinical dehydration
* If IV fluids are needed they should be given slowly
* If given too quickly a rapid reduction in plasma Na conc and osmolality leads to a shift of water into cerebral cells à seizures and cerebral oedema
* Give 0.9% saline +/- 5% glucose over at least 48hrs to replace fluid deficit, measuring plasma Na regularly (aiming to reduce it at less than 0.5mmol/l/hr)
26
What is Crohn's disease?
Chronic granulomatous inflammatory disease that can affect any part of the GI tract from mouth to anus
27
Aetiology of Crohn's disease?
There is transmural, patchy inflammation affecting one or several segments of the GI tract
* Initially, there are areas of acutely inflamed, thickened bowel
* Leads to strictures of the bowel and fistulae (between adjacent loops of bowel, between bowel and skin, or to other organs (e.g. bladder, vagina)
Aetiology unknown; likely to be due to environmental factors (infections, medications) triggering a response in genetically susceptible patients (multiple genes identified)
28
Epidemiology of Crohn's disease?
Bimodal peak of onset: 15-30yo, 60-80yo
More common than UC in children
29
Signs and symptoms of Crohn's disease?
* Classical presentation (25%):
* Abdominal pain
* Diarrhoea (may be bloody but not always)
* Weight loss
* Extra-intestinal manifestations:
* Oral lesions or perianal skin tags/fistulae/abscesses
* Uveitis
* Arthralgia
* Erythema nodosum
* General ill health
* May be the presenting features, esp in older children
* Fever, lethargy, anorexia, weight loss
* Growth failure, delayed puberty
30
Ix for Crohn's disease?
* **Bloods**:
* FBC (low Hb, high WCC)
* Look for deficiencies due to malabsorption: iron, B12/folate
* High ESR/CRP
* Albumin (low)
* U&Es, LFTs
* pANCA negative (perinuclear antineutrophil cytoplasmic antibody)
* **Stool sample**
* Culture (exclude infection)
* Faecal calprotectin (raised in inflammation – non-specific)
* **Upper GI endoscopy and ileocolonoscopy and biopsy**
* Histological hallmark is presence of non-caseating granulomas (not seen in 30% at presentation)
* Cobblestone mucosa, transmural colonic inflammation with infiltration of macrophages/lymphocytes/plasma cells
* **Imaging**:
* CT/MRI (may be used to assess extent of disease)
* AXR, barium enema (strictures (string sign of Kantor), deep ulceration (rose thorn)
*NB endoscopy/colonoscopy and barium enema may be dangerous in acute exacerbation (perforation risk)*
31
Mx of Crohn's disease?
Specialist MDT
Inducing remission:
* Basic obs, fluid resuscitation, analgesia, TPN if necessary
* Monitor markers of disease activity (fluid balance, ESR/CRP, platelets, stool frequency, Hb, albumin)
* Polymeric diet (liquid diet consisting of hydrolysed nutrients)
* For 6-8wks in mild exacerbation; induces remission in 75%
* Oral budesonide (glucocorticoid)
* If polymeric diet ineffective or more severe exacerbation
* Fewer SEs than systemic corticosteroids
* Aminosalicylates (5-ASA), e.g. mesalazine
* If not controlled (add to budesonide or replace)
* Oral corticosteroid, e.g. prednisolone
* If still not controlled
* IV if severe disease
* Infliximab or surgery (if very severe and unresponsive)
Maintaining remission:
* Immunosuppressant therapy
* Azathioprine, mercaptopurine, methotrexate
* Anti-TNF agents if immunosuppressants failed
* Infliximab, adalimumab
* Very effective in maintaining remission
Long-term supplemental enteral nutrition
* May be needed to correct growth failure
* Overnight nasogastric or gastrostomy feeds
Surgery for complications
* Resection of affected bowel and stoma formation
* Risk of recurrence
32
Complications & prognosis of Crohn's disease?
Complications:
* Malabsorption, growth faltering
* Bowel strictures
* Perforation
* Fistulae (between bowel, bladder, vagina, skin)
* Perianal fistulae and abscesses
* Toxic megacolon (more common in UC)
Generally good prognosis à most patients lead normal lives with occasional relapses
2/3 require surgery at some stage
33
Prognosis and complications of gastroenteritis?
Complications:
* Dehydration → **shock, electrolyte abnormalities, AKI, metabolic acidosis**
* **Metabolic acidosis** (due to faecal loss of bicarbonate and impaired renal H+ excretion)
* **Postgastroenteritis syndrome:**
* Following gastroenteritis, the introduction of a normal diet may result in return of watery diarrhoea
* Treat by restarting oral rehydration therapy
Usually self-limiting in UK; 1% mortality in developing countries
34
What is ulcerative colitis?
Chronic relapsing inflammatory disease involving the rectum, and extending proximally to affect a variable length of colon
35
Aetiology of ulcerative colitis?
There is diffuse inflammation of the rectal mucosa and submucosa, extending proximally
* Classified according to location (proctitis, proctosigmoiditis, L-sided colitis, extensive colitis)
Aetiology unknown; likely due to environmental factors triggering a response in genetically susceptible patients
36
Epidemiology of ulcerative colitis?
Common; peak onset 15-30yrs
Less common than Crohn’s in childhood
37
Signs and symptoms of ulcerative colitis?
* Rectal bleeding
* Diarrhoea (with blood and mucus)
* Colicky abdo pain
* Weight loss and growth failure (less frequent than Crohn’s)
* Extra-intestinal manifestations: erythema nodosum, arthritis, uveitis
38
Ix for ulcerative colitis?
* Bloods:
* FBC (low Hb, high WCC)
* Look for deficiencies due to malabsorption: iron, B12/folate
* High ESR/CRP
* Albumin (low)
* U&Es, LFTs
* pANCA positive (perinuclear antineutrophil cytoplasmic antibody)
* Stool sample
* Culture (exclude infection)
* Faecal calprotectin (raised in inflammation – non-specific)
* Upper GI endoscopy and ileocolonoscopy and biopsy
* Confluent colitis extending from the rectum proximally (variable length)
* 90% children have pancolitis (usually confined to distal colon in adults)
* Histology shows mucosal inflammation with granular appearance (pseudopolyps), crypt damage (cryptitis, architectural distortion, abscess, crypt loss) and ulceration
* Imaging:
* CT/MRI (may be used to assess extent of disease)
* AXR, barium enema
* NB endoscopy/colonoscopy and barium enema may be dangerous in acute exacerbation (perforation risk
39
Mx of ulcerative colitis?
Inducing remission:
* Basic obs, monitor fluid balance
* Aminosalicylates (5-ASA), e.g. mesalazine
* Topical if mild, oral if severe/extensive
* Corticosteroids
* Topical if mild (rectal hydrocortisone), oral if severe/extensive (prednisolone)
* Severe fulminating disease:
* Medical emergency
* IV fluids
* IV corticosteroids
* Ciclosporin or infliximab (if needed)
* Surgery (if no response)
Maintaining remission:
* Aminosalicylates
* If aggressive/extensive: immunomodulatory therapy (e.g. azathioprine) +/- low-dose corticosteroids
* In resistant disease biological therapies (e.g. infliximab) can be tried
Surgery
* Colectomy with ileostomy or ileorectal pouch
* For severe fulminating disease or chronic poorly controlled disease
Regular colonoscopic screening after 10yrs from diagnosis
40
Complications and prognosis of ulcerative colitis?
Complications:
* Toxic megacolon
* Perforation
* Colonic adenocarcinoma in adults
* Primary sclerosing cholangitis
* Ankylosing spondylitis
Generally good prognosis à most patients lead normal lives with occasional relapses
41
What is Meckel's diverticulum?
42
Aetiology of Meckel's diverticulum?
During embryogenesis the vitelline duct runs between the terminal ileum, the umbilicus and the yolk sac
* It usually regresses by the 5th week of development
* A Meckel’s diverticulum forms if it fails to regress
* It is a true diverticulum containing all 3 layers of the intestinal wall, and has its own blood supply
Symptoms arise from ectopic tissue within the diverticulum, or from residual bands that connect the apex of the diverticulum to the abdominal wall
Aetiology is unknown; no known RFs
43
Epidemiology of Meckel's diverticulum?
Rule of 2s:
* Affects 2% people (common)
* 2% are symptomatic
* Usually presents in \<2yo
* M:F 2:1
44
Signs and symptoms of Meckel's diverticulum?
* Usually **asymptomatic**
* **Intermittent painless rectal bleeding**
* **Bright red blood**
* Due to ulceration of ileal mucosa by acid production (from ectopic gastric cells)
* May cause anaemia
_O/E:_
* normal abdo exam
_Meckel diverticulitis_
* Peritoneal irritation which may localise to RIF (mimics appendicitis)
45
Ix for Meckel's diverticulum?
* FBC (anaemia)
* Meckel’s scan
* Radionucleotide scan with IV technetium-99 pertechnetate
* Shows increased uptake by ectopic gastric mucosa in 70% cases
* Diagnostic (but negative scan doesn’t exclude diagnosis)
* AXR (if obstruction suspected)
46
Mx of Meckel's diverticulum?
If asymptomatic:
* No treatment if discovered incidentally on imaging
* Prophylactic excision if discovered intraoperatively in a child/young adult
If symptomatic:
* Excision of diverticulum and any bleeding section of ileum; lysis of any adhesions causing obstruction
* Blood transfusion if necessary
* IV antibiotics if perforation and peritonitis
47
Complications and prognosis of Meckel's diverticulum?
Complications:
* Anaemia
* Intussusception → obstruction
* Postoperative complications: intestinal leakage (from suture line at site of excision), infection, adhesions
Excellent prognosis with treatment of symptomatic patients
48
What is Hirschsprung's disease?
Congenital condition where there is absence of ganglion cells in the myenteric (Auerbach) and submucosal (Meissner) plexuses of part of the large bowel, resulting in a narrow, contracted segment
49
Aetiology of Hirschsprung's disease?
Affects the anus and extends for a variable distance proximally, ending in a normally innervated, dilated colon
* Confined to rectosigmoid colon in 75%; entire colon involved in 10%
Due to failure of the neural crest-derived ganglion cells to migrate from the proximal to distal bowel during embryonic development
* Leads to part of the rectum/colon with no parasympathetic nerve innervation
* The affected bowel has only sympathetic innervation à hypertonicity and lack of appropriate relaxation in response to proximal distension à narrow/contracted segment of bowel à functional obstruction
50
RFs for Hirschsprung's disease?
RFs:
* **Down’s,**
* MEN IIA,
* male,
* gene mutations (ch 10 and 21),
* FHx
51
Epidemiology of Hirschsprung's disease?
Uncommon à 1/5000 live births; 20% of all neonatal obstruction
M\>F
90% present in neonatal period; 95% present in 1st year
52
Signs and symptoms of Hirschsprung's disease?
* Neonatal presentation (most common):
* Failure to pass meconium in first 24-48hrs of life
* Signs of intestinal obstruction: abdominal distension, bilious vomiting
* Hirschsprung enterocolitis (rare, but life-threatening)
* DRE: may reveal narrowed segment; withdrawal of finger often releases gush of flatus and stool
* If presents in later childhood:
* Chronic constipation (usually profound) usually without soiling
* Associated abdo distension and pain
* Failure to thrive
53
Ix for Hirschsprung's disease?
* **AXR**
* Dilated colon with absent air in rectum
* Non-specific (difficult to differentiate between colon and small bowel in young children)
* **Contrast enema**
* The most valuable initial screening diagnostic test
* Shows contracted distal bowel and dilated proximal bowel
* **Suction rectal biopsy**
* Definitive diagnosis
* Must be taken at least 1.5cm above the pectinate line
* Shows absence of ganglion cells
* **Anorectal manometry**
* Usually not needed for diagnosis
* Normally when rectum is distended with a balloon, pressure in anal canal falls (due to sphincter relaxation) à this reflex is absent in Hirschsprung’s
54
Mx of Hirschsprung's disease?
Initial management:
* If enterocolitis: ABCDE approach, IV fluids, IV metronidazole
* Bowel irrigation
* Saline flushed into rectum through tube
* Used to manage the abdominal distension before surgery
Surgical:
* Initial colostomy, followed by anastomosing normally innervated bowel to the anus
* Usually in first week of life
Short-segment disease with only mild constipation in older children:
* Manage with stimulant laxatives alone (senna)
55
Complications and prognosis of Hirschsprung's disease?
Complications:
* Hirschsprung’s enterocolitis
* Ischaemic à necrosis and perforation proximal to the aganglionic segment
* 50% mortality
* Postoperative enterocolitis (enterocolitis can occur after a successful operation; usually disappears in \<1yr)
* Postoperative constipation
* Postoperative diarrhoea (esp if aganglionic segment is long)
Outcome is generally good à surgery works
56
What is intussusception?
Invagination (telescoping) of a portion of proximal bowel into the lumen of the adjoining distal segment
57
Aetiology of intussusception?
Usually involves the ileum passing into the caecum through the ileocaecal valve
* Leads to intestinal obstruction and mesenteric constriction à venous return obstruction à engorgement and oedema à bleeding à prevention of arterial perfusion à intestinal infarction and perforation
Aetiology is unclear; 90% idiopathic
* May be due to viral infection leading to enlargement of Peyer’s patches (lymphoid follicles in lamina propria) à act as lead point
* In older children there is usually a pathological lead point (e.g. Meckel diverticulum, polyp, tumours)
58
RFs for intussusception?
* adenovirus,
* HSP,
* FAP
59
epidemiology of intussusception?
Most common cause of intestinal obstruction in infants; rare in neonates
60
Signs and symptoms of intussusception?
* Usually presents at 3 months – 2yrs (can occur at any age)
* Triad:
* Severe colicky pain
* Episodes last 1-3mins; child become pale and draws up the legs
* There is recovery between the painful episodes
* Child may become increasingly lethargic
* Vomiting
* Initially non-bilious; becomes bilious as intussusception becomes more established
* PR bleeding
* Redcurrant jelly stools à late sign due to mucosal necrosis and sloughing
* On examination:
* Abdominal distension
* ‘Sausage shaped’ mass palpable in abdomen
* Signs of dehydration and shock (if severe)
61
Ix for intussusception?
* **AXR**
* Initial investigation when perforation or obstruction is suspected
* ‘Crescent sign’: curvilinear mass on R (esp in transverse colon distal to hepatic flexure) is pathognomonic
* **Abdo USS**
* To confirm diagnosis and check response to treatment
* ‘Donut’ or ‘target’ sign
62
Mx of intussusception?
Initial management:
* ABCDE approach
* IV fluid resuscitation (often hypovolaemia due to pooling of fluid in gut)
* NGT decompression
* IV antibiotics (e.g. gentamycin)
Therapeutic enema:
* Within 24hrs
* Air, water or contrast enema given for reduction of intussusception, by radiologist
* Usually 3 attempts (as risk of perforation)
Surgical reduction:
* If therapeutic enema fails or if there are signs of peritonitis
Laparoscopic or open
63
Complications and prognosis of intussusception?
Complications:
* Intestinal perforation à peritonitis, sepsis, shock
* Recurrence
Therapeutic enema has 75% success; recurrence rate is 10%
Surgery has 2-5% recurrence rate
64
What is malrotation and volvulus?
Malrotation is a spectrum of rotational and fixation disturbances that can occur during embryonic development
Volvulus is twisting of the intestine
65
aetiology of malrotation and volvulus?
In normal embryological development, the small bowel rotates around the superior mesenteric artery
* This happens in 3 stages: (I) herniation, (II) return to the abdomen with 270⁰ counter-clockwise rotation, (III) fixation
* If the rotation does not occur properly, fixation of the bowel is abnormal
* Non-rotation: midgut only rotates 180⁰; incomplete rotation (malrotation): duodenal loop lacks 90⁰ and caecocolic loop 180⁰ of the normal 270⁰ turn
* The most common form of malrotation is when the caecum remains high and fixed to the posterior abdominal wall
* Malrotation predisposes the patient to volvulus
* Usually when there is lack of fixation to the retroperitoneum and a narrow midgut mesenteric base à allows twisting of the intestine (volvulus)
* May obstruct the blood supply and lead to intestinal necrosis
* There may be abnormal peritoneal bands that cross the duodenum (Ladd’s bands)
* These create low-grade duodenal obstruction
66
RFs for malrotation and volvulus?
embryological abnormalities that disrupt rotation and fixation (gastroschisis, omphalocele, congenital diaphragmatic hernia, jejunoileal atresia)
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signs and symptoms of malrotation and volvulus?
* Usually presents in first 1-3d of life with intestinal obstruction (from Ladd bands) or volvulus, but can present later (with obstruction/volvulus)
* Acute mid-gut volvulus:
* Usually presents \<1yo
* Sudden onset bilious vomiting
* Abdo distension
* Severe pain
* Acute duodenal obstruction:
* Usually presents in infancy
* Forceful vomiting
* Abdo distension
* Gastric waves
* Diarrhoea, constipation, GOR
* Chronic mid-gut volvulus:
* Recurrent abdo pain
* Malabsorption
* May appear normal between volvulus episodes
* Chronic duodenal obstruction:
* Usually presents in infancy-preschool
* Bilious vomiting
* Failure to thrive
* May have intermittent abdo pain
* On examination:
* Acute obstruction: tachycardia, tachypnoea, abdo distension, tinkling bowel sounds
* Infarction/necrosis: tachycardia, pallor, pyrexia, signs of peritonitis
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Ix for malrotation and volvulus?
* Bloods: FBC, U&E, blood gas (metabolic acidosis with resp alkalosis)
* AXR
* Dilated loops of bowel or gasless abdominal fluid
* Urgent upper GI contrast study
* Diagnostic standard; should be performed on all infants with bilious vomiting
* Cork-screw appearance with volvulus, or duodenal-jejunal flexure to the R of the midline with malrotations
* If signs of vascular compromise or rupture à urgent laparotomy
* (Don’t do UGI)
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Mx for malrotation and volvulus?
Initial management (en route to theatre):
* ABCDE approach, senior help
* IV access, IV fluids
* NG tube decompression
* IV broad spectrum antibiotics
* UGI contrast study
Surgery:
* Open laparotomy and Ladd procedure
* Volvulus is untwisted, Ladd bands divided, placement of small bowel on R and large bowel on L (to broaden mesentery), appendicectomy (to avoid diagnostic confusion in the future)
* If non-acute presentation:
* Intermittent/partial volvulus or partial obstruction: timely (i.e. next day) open/laparoscopic Ladd procedure
* Asymptomatic finding of malrotation: elective open/laparoscopic Ladd procedure
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Complications and prognosis of malrotation and volvulus?
Complications:
* Bowel strangulation, necrosis and perforation à septic shock
* Short gut syndrome (if large amount of bowel removed due to ischaemia/necrosis) à malabsorption
* Recurrence of volvulus (because malrotation cannot be completely corrected)
* Adhesions
10% mortality in volvulus; volvulus survivors have 10% risk of recurrence
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What is necrotising enterocolitis?
Severe gastrointestinal illness usually seen in preterm babies, characterised by intestinal epithelial destruction
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What is the aetiology of necrotising enterocolitis?
* **Caused by impaired intestinal barrier function**
* This allows spread of commensal organisms into the mucosa, and potential colonisation by pathological organisms (E. coli, Klebsiella)
* This leads to inflammation (from immune response) → more cell damage → more bacterial invasion (cycle)
* Eventually leads to intestinal necrosis, perforation and sepsis
* **The exact cause of impaired barrier function is unknown**
* Thought to be due to a combination of immature intestinal epithelial barrier and immature mucosal immune system (leading to bacterial invasion)
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What are the RFs for necrotising enterocolitis?
* prematurity,
* low BW,
* formula feeding (breastmilk is protective)
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What are the signs and symptoms of necrotising enterocolitis?
Presents in the first few weeks of life
* Feed intolerance & vomiting (may be bile stained)
* Early signs
* May be a history of initially making progress on feeding
* Fresh blood in stool
**_Signs:_**
* Decreased bowel sounds
* Distended abdomen +/- visible intestinal loops
* Temperature instability, bradycardia, lethargy, respiratory distress
* Signs of shock (if severe)
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What are the Ix for ?necrotising enterocolitis?
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What is the Mx of necrotising enterocolitis?
Initial management:
* ABCDE approach
* Mechanical ventilation, IV fluids, circulatory support if needed
* Stop oral feeding (NBM)
* NG tube to decompress bowel (with suction)
* Broad spectrum antibiotics
* To cover aerobic and anaerobic organisms
* E.g. ampicillin/gentamycin + metronidazole/clindamycin
Surgery:
* For bowel perforation or if deteriorating; if extensive weigh up risks of short gut syndrome
* Needed in 20-40%
* Resection of necrotic bowel with formation of a stoma/anastomosis
Oral feeds can be restarted 7-10d after gas in the bowel wall (pneumatosis) clears
* TPN is always needed until then
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What are the complications of necrotising enterocolitis?
* Immediate:
* Bowel perforation
* Sepsis, shock, DIC
* Long-term:
* Strictures, fistulas
* Short gut syndrome (malabsorption due to extensive bowel resection)
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What is the prognosis of necrotising enterocolitis?
20% mortality (varies according to BW)
