GI: Pyloric Stenosis, Gastroenteritis & Coeliac Disease Flashcards

1
Q

What is the pyloric sphincter?

A

A ring of smooth muscle that forms the canal between the stomach and the duodenum.

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2
Q

What is pyloric stenosis?

A

Hypertrophy of circular and longitudinal muscle layers in the pylorus.

This leads to narrowing of the pylorus - results in gastric outlet obstruction.

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3
Q

What is the classic presenting feature of pyloric stenosis?

A

Postprandial projectile non-bilious vomiting

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4
Q

Risk factors for pyloric stenosis?

A

There are no strongly associated risk factors of pyloric stenosis.

Some may include:
- Male
- First born
- FH
- Maternal smoking

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5
Q

Is the vomiting in pyloric stenosis bilious or non-bilious?

A

Non-bilious

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6
Q

What causes projectile vomiting in pyloric stenosis?

A

After feeding, there is increasingly powerful peristalsis in the stomach as it tries to push food into the duodenum.

Eventually it becomes so powerful that it ejects the food into the oesophagus, out of the mouth and across the room. This is called “projectile vomiting”.

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7
Q

When does pyloric stenosis typically present?

A

In the first few weeks of life.

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8
Q

When does the vomiting in pyloric stenosis typically occur?

A

Immediately following a feed, and the child is often extremely hungry and irritable after the episode.

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9
Q

Clinical features of pyloric stenosis?

A

1) Increasingly forceful and ultimately projectile non-bilious vomiting

2) Haematemesis (10%)

3) Weight loss or inadequate weight gain, failure to thrive

4) Dehydration

5) Stool changes; often small and hard, sometimes the child passes little to no stool

6) Visible peristalsis (may become more prominent following a feed)

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10
Q

What are some signs of dehydration in infants?

A
  • sunken fontanelles
  • sunken eyes
  • dry mucous membranes
  • poor skin turgor
  • decreased tearing
  • lethargy
  • tachycardia
  • prolonged CRT
  • decreased urine output
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11
Q

What metabolic changes can vomiting in pyloric stenosis result in?

A
  • severe hypochloraemia
  • hypokalaemic dehydration with metabolic alkalosis
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12
Q

What may be felt in the abdomen in pyloric stenosis?

A

Firm, non-tender 1-2cm mass in the right upper quadrant of the abdomen.

This is a result of the thickening of the pylorus muscles, often described as an ‘olive’.

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13
Q

Classic triad in pyloric stenosis?

A

1) palpable pyloric mass
2) visible peristalsis
3) projectile vomiting

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14
Q

Relevant investigations in pyloric stenosis?

A

1) Test feed with dextrose water

2) ABG

3) U&Es

4) Abdo US

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14
Q

One bedside investigation in pyloric stenosis is a test feed with dextrose water.

What does this involve?

A

This causes the pylorus to contract, making an epigastric mass more obvious on examination. This may also result in projectile vomiting.

If the pylorus was palpable from this test feed, no further imaging is required, and the diagnosis can be confirmed.

If the test is inconclusive, an ultrasound will be required.

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15
Q

What will an ABG show in pyloric stenosis?

A

Hypochloraemic hypokalaemic metabolic alkalosis caused by the loss of fluid, hydrogen and chloride through excessive vomiting.

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16
Q

What are the requirements for diagnosing pyloric stenosis on an abdo US?

A

1) Pyloric stenosis must be >4mm in thickness and;

2) Pyloric muscle length must be >18mm

3) There must be an obstruction preventing the passage of fluid beyond the pylorus, despite gastric peristalsis.

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17
Q

What sign is often described on US in pyloric stenosis?

A

A ‘target sign’ - this is due to hypertrophied hypoechoic muscle surrounding echogenic mucosa

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18
Q

What is the management of pyloric stenosis?

A

1) NG tube insertion

2) Preoperative rehydration and correction of electrolyte abnormalities

3) Ramstedt’s pyloromyotomy - definitive surgical management

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19
Q

What is the definitive management of pyloric stenosis?

A

Ramstedt’s pyloromyotomy

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20
Q

What is the role of NG tube insertion in pyloric stenosis?

A

This decompresses the stomach and allows accurate recording & replacement of gastric losses.

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21
Q

What is Ramstedt’s pyloromyotomy?

A

Involves longitudinally incising the muscle fibres of the hypertrophic pyloric muscle. This defect is left open, allowing the pyloric mucosa to bulge through the incision and providing a wider passage between the pylorus and the duodenum.

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22
Q

What are the 2 key pre-op complications of pyloric stenosis?

A

1) Electrolyte abnormalities

2) Dehydration

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23
Q

Is gastroenteritis more commonly bacterial or viral?

A

Viral

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24
Q

What is the most common cause of infantile gastroenteritis?

A

Rotavirus

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25
Q

What are the 3 most common viruses causing infantile gastroenteritis?

A

1) Rotavirus
2) Norovirus
3) Adenovirus

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26
Q

When is the rotavirus vaccination given?

A

At 8 and 12 weeks

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27
Q

Is rotavirus part of the national vaccination programme in the UK?

A

Yes

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28
Q

How is rotavirus spread?

A

By the faecal oral route or by environmental contamination, incidence peaks over the winter months.

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29
Q

What is the ommonest cause of gastroenteritis in ALL age groups in the UK?

A

Norovirus

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30
Q

What is the most commonly reported bacterial cause of gastroenteritis in the UK?

A

Campylobacter

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31
Q

Give 2 key bacterial causes of gastroenteritis

A

1) Campylobacter

2) E. coli

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32
Q

What are some key conditions to think about in young patients with loose stools?

A
  • Infection (gastroenteritis)
  • Inflammatory bowel disease
  • Lactose intolerance
  • Coeliac disease
  • Cystic fibrosis
  • Toddler’s diarrhoea
  • Irritable bowel syndrome
  • Medications (e.g. antibiotics)
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33
Q

Which E. coli strain can lead to haemolytic uraemic syndrome (HUS)?

A

E. coli 0157 –> produces the Shiga toxin

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34
Q

Presentation of infection with E. coli 0157 strain?

A
  • abdo cramps
  • bloody diarrhoea
  • vomiting
  • HUS (as Shiga toxin destroys RBCs)
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35
Q

What increases the risk of haemolytic uraemic syndrome?

A

Antibiotics !

Antibiotics should be avoided if E. coli gastroenteritis is considered.

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36
Q

What is the most common bacterial cause of gastroenteritis worldwide?

A

Campylobacter Jejuni

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37
Q

Clinical features of gastroenteritis?

A
  • Sudden onset of loose/watery stool with or without vomiting
  • Abdominal pain/cramps
  • Mild fever
  • Recent contact with someone with diarrhoea or vomiting.
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38
Q

What is a key complication of gastroenteritis?

A

Dehydration

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39
Q

Which children with gastroenteritis are at particularly risk of dehydration?

A

1) Young children (especially under 6months).

2) Children who have passed >5 diarrhoeal stools in the last 24 hours.

3) Children who have vomited >2x in the last 24 hours.

4) Children who have stopped breast feeding during the illness.

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40
Q

What are some signs of clinical dehydration?

A
  • Appears to be unwell or deteriorating
  • Altered responsiveness (for example, irritable, lethargic)
  • Decreased urine output
  • Sunken eyes
  • Dry mucous membranes (except for ‘mouth breather’)
  • Tachycardia
  • Tachypnoea
  • Reduced skin turgor
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41
Q

When should a stool sample should be sent in suspected infantile gastroenteritis?

A

1) Septicaemia is suspected or

2) blood and/or mucus is present in the stool or

3) the child is immunocompromised

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42
Q

Management of infantile gastroenteritis if the child is not clinically dehydrated?

A

1) Continue breast feeding/other milk feeds

2) Encourage fluid intake

3) Discourage fruit juices and carbonated drinks especially if the child is at risk of dehydration.

4) Offer oral rehydration salt solution (ORS) as supplemental fluid to those at risk of dehydration.

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43
Q

Management of infantile gastroenteritis if the child is clinically dehydrated?

A

Oral therapy for all children unless they have the indications for IV therapy:

1) Give ORS solution: 50 ml/kg over 4 hours to replace the defecit plus maintenance fluid.

2) Give the ORS solution frequently in small amounts e.g. 5ml every 5 minutes and consider supplementation with their usual fluids.

3) If the child is refusing the oral fluid then consider a NG tube.

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44
Q

When is IV therapy indicated in infantile gastroenteritis?

A

1) Shock is suspected

2) In a child with any red flag symptoms

3) If there is evidence of dehydration despite use of oral rehydration therapy

4) If the child persistently vomits when ORS solution is given either orally or via NG tube.

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45
Q

What is the fluid requirement for 24 hours in children weighing:

a) 0-10kg
b) 10-20kg
c) >20kg

A

a) 100ml/kg/day

b) Requirement for the 1st 10kg (i.e. 1000ml)+ 50ml/kg/day

c) Requirement for the 1st 20kg (i.e.1500ml) + 20ml/kg/day

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46
Q

Following rehydration in infantile gastroenteritis, what advice should be given?

A

Advise parents to give full strength milk straight away, and slowly re-introduce the child’s solid food. Suggest that fruit juices and carbonated drinks are avoided until the diarrhoea has resolved.

47
Q

What is HUS?

A

Rare but serious complication of acute infectious gastroenteritis that occurs mostly in young children and the elderly.

This can be a life-threatening complication causing:
- acute renal failure,
- haemolytic anaemia

48
Q

What are reactive complications associated with bacterial gastroenteritis?

A

Including arthritis, carditis, urticaria, erythema nodosum and conjunctivitis.

REMEMBER: Reiter’s syndrome i.e. reactive arthritis (the combination of urethritis, arthritis, and uveitis).

49
Q

What are some complications of infantile gastroenteritis?

A

1) HUS

2) Reactive complications e.g. reactive arthritis

3) Toxic megacolon (a rare but significant complication of rotavirus gastroenteritis).

4) Acquired /secondary lactose intolerance

5) Guillain–Barré syndrome

50
Q

What is a rare but significant complication of rotavirus gastroenteritis?

A

Toxic megacolon

51
Q

What causes acquired /secondary lactose intolerance following infantile gastroenteritis?

A
  • Occurs due to the lining of the intestine being damaged.
  • Leads to symptoms of bloating, abdominal pain, wind and watery stools after drinking milk.
  • Improves when infection resolves and gut lining heals
52
Q

What is coeliac disease?

A

An autoimmune condition where exposure to gluten causes an immune reaction that creates inflammation in the small intestine.

Autoantibodies are created in in response to exposure to gluten and these target the epithelial cells of the intestine and lead to inflammation.

This results in atrophy of the intestinal villi.

53
Q

Which part of the small intestine is most affected in Coeliac disease?

A

Jejunum

54
Q

What are the 2 key autoantibodies to remember in Coeliac disease?

A

1) Anti-tissue transglutaminase (anti-TTG)

2) Anti-endomysial (anti-EMA)

These antibodies correlate with disease activity and will rise with more active disease and may disappear with effective treatment.

55
Q

Presentation of coeliac disease in children?

A
  • Failure to thrive in young children
  • Diarrhoea
  • Fatigue
  • Weight loss
  • Mouth ulcers
  • Anaemia secondary to iron, B12 or folate deficiency
  • Dermatitis herpetiformis

Rarely coeliac disease can present with neurological symptoms:
- Peripheral neuropathy
- Cerebellar ataxia
- Epilepsy

56
Q

All patients with a new diagnosis of what are also tested for coeliac disease?

A

Type 1 diabetes - as the conditions are often linked.

57
Q

What is dermatitis herpetiformis?

A

An itchy blistering skin rash that typically appears on the abdomen

58
Q

Gluten is a protein found in what 3 three types of cereal?

A

1) Wheat
2) Barley
3) Rye

59
Q

What are some conditions related with coeliac disease?

A
  • T1D
  • Down syndrome
  • Turner syndrome
  • Other autoimmune diseases e.g. thyroid disease, rheumatoid arthritis & Addison’s disease.
60
Q

What is the most common age of presentation with coeliac disease?

A

9 months to 2 years.

61
Q

What is the ‘classic’ presentation of coeliac?

A
  • Features of malabsorption e.g. failure to thrive/ weight loss, loose stool, steatorrhea, anorexia, abdominal pain, abdominal distention, muscle wasting.
  • Child is often miserable with behavioral changes.
62
Q

What does histology show in Coeliac?

A

Histology reveals crypt hyperplasia and villous atrophy.

63
Q

What is the ‘atypical’ presentation of coeliac?

A

Usually no intestinal symptoms but associated extra-intestinal symptoms e.g. osteoporosis, peripheral neuropathy, anaemia and infertility.

64
Q

What are 5 extra-intestinal symptoms of coeliac?

A
  • osteoporosis
  • peripheral neuropathy
  • anaemia
  • infertility
  • dermatitis herpetiformis
65
Q

What 2 genes are associated with coeliac?

A

HLA-DQ2 gene (90%)

HLA-DQ8 gene

66
Q

What is it important to also test for when testing for autoantibodies in coeliac?

A

Important to test for total Immunoglobulin A levels as some patients have an IgA deficiency.

If total IgA is low the coeliac test will be negative even when they have the condition.

In this circumstance you can test for the IgG version of the anti-TTG or anti-EMA antibodies or do an endoscopy with biopsies.

67
Q

1st line investigation in coeliac?

A

Serology –> test for total immunoglobulin A (IgA) and IgA tissue transglutaminase (tTG)

68
Q

What is important to tell the patient when testing for coeliac disease?

A

Investigations for coeliac disease will be accurate only if the patient is having gluten in the diet at the period of the testing and for at least 6 weeks before testing.

69
Q

How long must patients be eating gluten for before testing for coeliac?

A

At least 6 weeks

70
Q

Which children should be offered serological testing for coeliac?

A

Children with any of the following:

  • persistent unexplained abdominal or GI symptoms
  • faltering growth
  • prolonged fatigue
  • unexpected weight loss
  • severe or persistent mouth ulcers
  • unexplained iron, vitamin B12 or folate deficiency
  • type 1 diabetes, at diagnosis
  • autoimmune thyroid disease, at diagnosis
  • irritable bowel syndrome (in adults)
71
Q

The diagnosis of which conditions indicates the need to test for coeliac disease?

A

T1DM & autoimmune thyroid disease

72
Q

When testing for coeliac, if IgA tTG is weakly positive, what should you test next?

A

use IgA endomysial antibodies (EMA)

73
Q

When testing for coeliac, if the patient is IgA deficient, what should you use?

A

Consider using IgG EMA, IgG deamidated gliadin peptide (DGP) or IgG tTG.

74
Q

What investigation is considered the gold standard to diagnose if a child has coeliac disease?

A

Duodenal biopsy

75
Q

What is the only treatment for coeliac disease?

A

Lifelong diet free of gluten.

76
Q

What are some complications of coeliac?

A
  • anaemia
  • osteopenia/ osteoporosis
  • refractory coeliac disease (symptoms persist despite diet, may need treatment with steroids)
  • malignancy
  • fertility problems / adverse events during pregnancy
  • depression/anxiety
77
Q

How can coeliac cause osteoporosis?

A

The release of pro-inflammatory cytokines, calcium malabsorption, and the activation of osteoclasts represent the main mechanisms responsible for bone derangement.

78
Q

When is vomiting bilious?

A

If obstruction is AFTER the junction of the duodenum (with the bile ducts at the ampulla of vater).

79
Q

Give some causes of bilious vomiting in infants (5)

A

1) Intestinal malrotation with volvulus

2) Intestinal atresia: duodenal/jejunal/ileal

3) Meconium ileus

4) Hirschsprung’s disease

5) NEC

80
Q

What happens in intestinal malrotation with volvulus?

A

There is twisting of the mesentery around the superior mesenteric artery.

Leads to intestinal obstruction, infarction and necrosis.

81
Q

Features of intestinal malrotation w/ volvulus?

A

1) Acute bilious vomiiting

2) Abdo distension

3) Bloody diarrhoea

4) Infarction

5) Can damage bowel wall –> sepsis

82
Q

Investigations in intestinal malrotation w/ volvulus?

A

1) US

2) AXR

3) Upper GI contrast

83
Q

Are air fluid levels seen on AXR in malrotation w/ volvulus?

A

Yes

84
Q

What does upper GI contast studies show in malrotation w/ volvulus?

A

Corkscrew/spiral shaped duodenum in the RLQ instead of LUQ (i.e. more medially placed).

85
Q

Mx of malrotation w/ volvulus?

A

1) Discontinue feedings

2) Fluid resus with saline

3) NG tube decompression

4) Broad spectrum Abx

5) ?emergency surgery

86
Q

What is intestinal atresia or stenosis?

A

When some of intestine is absent or narrowed.

87
Q

What condition is duodenal atresia associated with?

A

Down’s syndrome

88
Q

Pathophysiology of duodenal atresia vs other types (jejunal or ileal)?

A

Duodenal - failed canalisation of intestine in utero

Non-duodenal - lack of blood flow to developing gut

89
Q

Features of atresia?

A

1) Polyhydramnios (as foetus is less able to swallow amniotic fluid)

2) Bilious vomiting soon after birth

3) Abdominal distension

4) Absent bowel movements

90
Q

What feature can indicate intestinal atresia during pregnancy?

A

Polyhydramnios

91
Q

What will an AXR show in duodenal atresia?

A

‘Double bubble’ with gas filled distended stomach and duodenum with an absence of distal gas.

92
Q

Mx of intestinal atresia or stenosis?

A

1) Discontinue feeding

2) IV fluids

3) NG tube decompression

4) Surgery (removal and repair of affected segment)

93
Q

What is the surgery called in duodenal atresia?

A

Duodeno-duodenostomy –> attaching duodenum to duodenum.

94
Q

Presentation of Hirschsprung’s?

A

1) Bilious vomiting

2) Abdo distension

3) No meconium in first 48 hours of life

95
Q

What is the gold standard for diagnosis of Hirschsprung’s?

A

Rectal biopsy (of mucosa & submucosal layer)

96
Q

Mx of Hirschsprung’s?

A

Resection of aganglionic part and healthy end is connected to anus.

97
Q

Where is obstruction in non-bilious vomiting?

A

Obstruction above the junction w/ bile ducts and proximal to ampulla of vater.

98
Q

Give 2 causes of non-bilious vomiting in infants

A

1) Pyloric stenosis

2) Annular pancreas

99
Q

When do symptoms of pyloric stenosis typically first present?

A

2-6 weeks of life

100
Q

What can be felt on physical exam in pyloric stenosis?

A

1) Olive shaped mass in RUQ (felt during or at end of feeding)

2) Visible peristalsis of stomach

101
Q

What metabolic disturbance is seen in pyloric stenosis? (2)

A

1) Hypochloremic metabolic alkalosis (due to loss of HCl from stomach)

2) Low K+

102
Q

How is a definitive diagnosis of pyloric stenosis made?

A

Abdo US –> shows thickened pylorus.

103
Q

What pyloric wall thickness is seen in pyloric stenosis?

A

> 3mm

104
Q

Mx of pyloric stenosis?

A

1) Rehydration & correction of electrolyte disturbances:
- 5% dextrose in 0.45% NaCl with 40 mmol/L of K+

2) Surgical correction (pyloromyotomy)

105
Q

What is annular pancreas?

A

When a ring of pancreatic tissue surrounds and compresses the 2nd part of duodenum (like duodenal atresia).

106
Q

What condition is annular pancreas associated with?

A

Down’s syndrome

107
Q

How may annular pancreas present in prenatal US?

A

Polyhydramnios

108
Q

Is vomiting bilious or non-bilious in annular pancreas?

A

Non-bilious

109
Q

Investigations in annular pancreas?

A

1) AXR

2) Upper GI contrast series

3) Abdo CT scan (definitive)

110
Q

Causes of vomiting in infants >3 months or children?

A

1) Gastroenteritis (most common)

2) Intussusception

3) Gastroparesis

4) Cyclic vomiting syndrome

111
Q

Causes of vomiting in infants <3?

A

1) Malrotation w/ volvulus

2) Intestinal atresia

3) Hirschsprung’s

4) Pyloric stenosis

5) Annular pancreas

112
Q

3 broad categories of causes of gastroenteritis?

A

1) Virus:
- rotavirus
- norovirus

2) Bacterial:
- shigella
- salmonella
- e. coli
- yersinia
- campylobacter

3) Parasites:
- giardia lambli
- cryptosporidium

113
Q

Severity & duration of gastroenteritis caused by virsues vs bacteria?

A

Virus - sudden onset and quick resolution

Bacterial - prolonged & severe

114
Q

Abx in gastroenteritis are only indicated if a specific pathogen (like Shigella or Campylobacter) is isolated.

What is the Abx for Shigella or Campylobacter?

A

Oral azithromycin

115
Q
A