Medical conditions Flashcards
Clinical features of malrotation?
Can you also name some late signs?
Clinical features
- Normal baby with feeding difficulties
- Bile stained vomiting
- Grassy green (bilirubin > biliverdin via stomach acid)
- Mostly present within first month, nearly all present within first year of life
- Late signs
- PR bleeding
- Abdominal distension
- Abdominal tenderness
Investigation
- Investigate with a contrast swallow - look at the duodenum
- C shape = conservative management
- Screw shape = surgery
How does pyloric stenosis present?
Why does this rule out sepsis?
What would we expect to see in a blood test?
- Non bilious vomiting, pattern is projectile
- Stomach is a strong muscle, with the outlet blocked
- They will be hungry after they vomit, will imply not sepsis
- Metabolic derangement
- Hypochloremic, hypokalemic, metabolic alkalosis
- Vomit out double HCL, NaCl, and K
- No hyponatremia because hte body conserves it very well
- Kids have a paradoxic aciduria
- They’re trying to retain sodium so its a Na/H+ exchanger that results in loss of H+
- Need fluid resus before surgery
- Kids will die on the table otherwise
- Hypochloremic, hypokalemic, metabolic alkalosis
7 month old presents to ED with green vomitus, what do you do?
Green vomit = bile stained vomit = malrotation until proven otherwise
Investigate with contrast studies (upper GI)
Immediate surgical referral
What are 3 DDx for non-bilious vomiting?
- Pyloric stenosis
- Sepsis
- Meningitis
- UTI
- Reflux
- Overfeeding
What age does pyloric stenosis commonly present?
3-6 weeks
Management plan for kid with pyloric stenosis?
Presents with non-bilious projectile vomiting after every feed, scrawny and dehydrated, palpable olive in epigastrium.
- Resuscitate dehydrated infant
- Correct electrolytes
- 150ml/kg/day normal saline + 5% dextrose +/- 20mmol/L KCL after confirming K levels
- Replace ongoing fluid loss
- Surgical division of hypertrophic muscle
Age range of intususseption?
Peak? Why?
- 3m - 3y, peaks at 6m
- What happens at 6m? Immune system changes (loss of maternal immunity)
- Parental fatigue no longer sterilising
- Send to creche or grandparents, huge antigenic exposure
- Huge increase in mucosal associated lymphoid tissue, so it grows
- Theory is that lymph nodes get bigger, bowel picks some up and think its poo and pushes it along, and this snowballs
- Parental fatigue no longer sterilising
Clinical features of intususseption?
Investigation of choice?
Treatment?
CFt
-
Colicky abdominal pain, every 3 to 5 mins (rate or persistalsis)
- Pale, sweaty, hot feel like crap for 30 seconds then it seems to resolve for a bit
- As an adult you go down into the fetal position, a 6m old can’t do that so they pull their legs up while they’re in pain then they relax
- Vomit
- Mass is an early sign
- They back up with gas and it becomes hard to feel
-
Red current jelly stools in 40%
- Bit of blood in the mucus
Ix
- Plain XR - look for absence of gas in caecal region
- US - gold standard
- Look for target sign
Rx
- Gas enema
Match the CFt with the appendicitis presentation
- Vague non-localizing RIF pain with deep RIF tenderness (no guarding)
- Periumbilical pain with shift to RIF +/- N/V. Lying still, pale, low grade fever, guarding
- Generalised peritonitis
- Lower abdominal pain and tenderness, urinary symptoms, small volume diarrhoea
- ‘Medical student’ presentation
- Retrocaecal appendicitis
- Pelvic appendicitis
- Perforated appendicitis
- Retrocecal
- Medical student style
- Perforated appendicitis
- Pelvic appendicitis
Patient presents with appendicitis, how do you manage?
- Stabilise the patient
- Correct dehydration and electrolyte disturbance - most important step
- Appendicectomy
Define anaphylaxis clinically
- Any acute onset illness with typical skin features (urticarial rash or erythema/flushing, and/or angioedema) PLUS
- Respiratory and/or cardiovascular and/or persistent severe GI symptoms
What are 7 signs of IgE anaphylaxis?
- Tachy- / brady- cardia
- Hypotension
- Lower airway signs
- Cough, chest tightness, dyspnea, hoarse voice
- Difficult/noisy breathing
- Swollen tongue
- Swelling/tight throat/difficulty swallowing
- Hoarse voice
- Wheeze or persistent cough
- Persistent dizziness or collapse
- Pale and floppy infant/young child
Name 3 key risk factors for developing anaphylaxis
- History of anaphylaxis
- Multiple food and drug allergy
- Poorly controlled asthma
- Underlying lung disease
- Beta-blockers/ACE inhibitors
- Older age
Describe the key 3 investigations used to detect allergy.
- Skin prick test (SPT)
- Measure wheal at 15 mins
- Controls - histamine = +ve and saline = -ve
- +ve = SPT >/= 3mm (L+W/2) above saline control
- Before the test
- No antihistamines for 3-4 days
- SPT > 6 weeks after any anaphylaxis
- Issues with dermatographism (saline causes wheal)
- Correlate results with history
- +ve test and +ve history = allergy as more SPT +ve than allergic
- Measure wheal at 15 mins
- Serum specific IgE (previously RAST)
- Detects free antigen specific IgE in serum, results usually concordant with SPT
- Food challenges (gold standard)
- Confirms diagnosis of food allergy
- Non-IgE mediated reaction
- The only way to test
- IgE food reaction BUT
- Uncertain history with +ve RAST/SPT
- Good history but -ve RAST/SPT
- Non-IgE mediated reaction
- Confirms diagnosis of food allergy
What is food protein induced enterocolitis syndrome (FPIES)?
How does it normally present?
Management strategy?
- A type of non IgE mediated food allergy, mostly outgrown by ages 3-4
- Acutely unwell baby
- Vomiting 2-4 hours after allergen ingestion
- Bloody diarrhoea
- Can get CV collapse
- Redistributed body fluids > hypotension, pallor, floppiness
- May need IV resus
- Avoid allergen, challenge with an alternative (eg. soy milk), re-challenge when appropriate (age dependent)
What are the 4 key innocent murmurs?
These murmurs are clinically minimal, softer when erect adn vary with respiration. Typically heard at left sternal edge with minimal radiation.
- Still’s murmur (most common)
- Pulmonary flow murmur
- Branch pulmonary stenosis
- Venous hum
- What are the two congenital heart diseases that cause a left to right shunt?
- What is the key difference between the two?
- Which causes fixed S2 splitting, why?
- VSD, and ASD (secundum septum)
- VSD causes volume l oading on the left heart, while ASD loads teh right heart
- ASD because we get L > R shunting, which delivers preload to the right atrium and therefore ventricle, delaying closure of P2 thus causing fixed splitting.