Paeds Flashcards
Developmental milestones - 6 weeks
Valentine’s day
Newborn bb check @ GP
GM: good head control
FM: tracking objects/face
S/L: startles to loud noice
S: social smile
<span><em>(In GP examining bb - check for head control, using steth and watching bb track is w eyes. Someone accidentally bangs room door and bb cries, then parents comforts them and they smile)</em></span>
Developmental milestones - 6 months
Summer
GM: sits unsupported with rounded back, rolls tummy (prone) to back (supine)
FM: palmar grasp and transfer hand to hand
S/L: turns head to loud sounds, understands bye bye, babbles
S: puts objects in mouth, shakes rattle, reaches for bottle
<span><em>(Imagine bb on beach in middle of summer. Can sit w rounded back bc 6 is curved - rolling from front to back catching sunrays. Palmar grasp under the palm trees and passing stuff between hands - turn to a loud squawking bird and babbling away, mum says “say bye bye birdie”)</em></span>
Developmental milestones - 9 months
End of September - autumn & falling leaves
GM: stands holding on, sits w straight back
FM/V: inferior pincer grip, object permanence
S/L: responds to own name, imitates adult sounds
S: stranger fear, hold and bites food
<em>(Autumn park able to sit up in autumn leaves or stand holding hand. Can pick up leaves w pincer grip. Dad calls name in park and responds. Stranger approaches and cries. Can play peekaboo bc of object permanence and hold and bite food at picnic)</em>
Developmental milestones - 12 months
Christmas time
GM: walks alone
FM: Casting bricks/toys (dropping them on the floor), can build a tower of 2 bricks
S/L: shows understanding of nouns “where’s Santa?”, speaks 3 words
S: waves bye bye, hand clapping, plays alone if someone nearby, drinks from beaker w lid
<em>(Walking to Xmas tree, putting small present on top of another. Could understand “Where’s Santa?” and will wave bye bye. 3word vocab “happy new year” - lol realisticlly mama, papa, santa. Claps to Xmas song and drinks festive drink w lid)</em>
Developmental milestones - 18 months
2nd summer
GM: runs (16), jumps (18)
FM: scribble to and fro, stack 4 bricks
S/L: shows understanding of nouns “show me the pool”, 1-6 words
S: imitates everyday activities
<em>(Posh resort - running and jumping by pool. Parents give crayon and paper to keep them occ whilst sipping beers - scribble back and forth. Can stack double no. suitcases (LOL) from Xmas. Copies parents.)</em>
Developmental milestones - 2years
2nd birthday - “2 themed party”
GM: runs on (2) tiptoes, walks upstairs (2) feet 1 step at a time, throws ball (2) someone
FM/V: draws vertical line, stacks 8 bricks (2 circles in 8), turns (2) pages of book
S/L: shows understanding of verbs, (2)-3 words sentences, 50 word vocab
S: eats skillfully with spoon (2os in spoon)
Developmental milestones - 3 years
GM: hops on one foot for (3) steps, walks upstairs 1 foot per step but downstairs 2 feet per step (1+2=3)
FM/V: draw a circle, build a bridge
S/L: understand negatives, understand adjectives
S: Begin share toys, eat alone w/o parents, use fork and spoon, bowel control
Developmental milestones - 4 years
Starting reception
GM: Walks up and down stairs in adult manner
FM/V: Draws a cross, build 12 blocks, cut paper in half
S/L: Understands complex instructions
S: Concern/sympathy for others, best friend, bladder control. eats w/o help. dress/undress
What can hand preference under the age of 2 suggest?
Cerebral palsy
Traffic light system
Vaccination schedule
Key
Hib = Haemophilus influenzae B vaccine
PCV = Pneumococcal Conjugate Vaccine
Men B = Meningococcal B vaccine
Men C = Meningococcal C vaccine
Men ACWY = Meningococcal vaccine covering A, C, W and Y serotypes
MMR = Measles, Mumps, Rubella vaccine
HPV = Human Papilloma Vaccine
Mx upper airway in children
Signs of resp distress
3Es
Asthma
Wheezing inbetween viral infections and evidence of allergy
Asthma long term Mx
- Escalate asthma if:
- Using SABA>3x/week
- Syx > 3x/week
- Waking from syx
- Hospital admission –> steroid use
SABA = short acting beta agonist, i.e., albutamol inhaler (PRN)
ICS = inhaled cortico-steroid, i.e., beclometasone (regular)
LTRA = leukotriene receptor antagonist, i.e., montelukast
LABA = long acting beta agonist
MART = maintenance and reliever therapy (regularly + PRN in 1 inhaler)
*not often diagnosed until 5y/o unless wheezy despite lack of viral infx + strong family hx
*<5y/o if given ICS again - lower dose and long term
Asthma life threatening presentation
- PEFR <33% (peak expiratory flow rate)
- SpO2 <92%
- Altered consciousness
- Arrhythmia
- Hypotension
- Cyanosis
- Poor respiratory effort
- Silent chest
Acute asthma presentation
Asthma exacerbation levels
Acute asthma mx
- Salbutamol nebuliser
- Helps to open up airway and improve breathing
- Ipratroprium (Atrovent) nebuliser
- Short acting muscarinic antagonist helps relax smooth muscle around bronchi
- IV Magnesium sulphate + aminophylline + salbutamol
If life threatening: CALL FOR SENIOR HELP - consider intubation and ventilation
On D/C: Oral prednisolone (3-5 days)
(dampens down inflammation)
Acute epiglottitis presentation
- Stridor
- Drooling
- Rapid onset fever
Acute epiglottits cause
Haemophilus influenzae B
Bronchiolitis
Inflammation of bronchioles (small airways) due to respiratory syncytial virus (RSV) - lower airway problem -> inflamm and mucus narrows airway ->less airflow
Bronchiolitis presentation
Under 1 y/o!!
- Dry cough
- SOB
- Wheeze
- Crackles/crepitation
Bronchiolitis RF
- Formula milk
- Being younger than 3 months
- Premature
*Congenital heart disease can cause bronchiolitis to be more severe
Bronchiolitis Ix
Clinical diagnosis
- Resp exam
Bronchiolitis Mx
Conservative
- Self limting 5-7 days
- Simple analgesia
- Oxygen as required
- Intubate and ventilate if really worried
- Encourage reg feeds
- NG tube if normal feeds not tolerated
! Can be very severe in vulnerable children, e.g., pre term infant
- Palivizumab
- To prevent severe bronchiolitis infx
When to admit Bronchiolitis pt?
- oxygen saturation persistently <92%
- Feeding affected
Croup
Inflammation of the larynx and trachea (URTI) due to parainfluenza (upper airway problem)
Croup presentation
6 months - 2 years
- Barking cough
- Stridor
- SOB
- Fever
- Coryzal prodrome
OFTEN IN AUTUMN
Croup Ix
Clinical diagnosis
- Resp exam
Croup Mx
- Oral dexamethasone 0.15mg/kg
- Repeat if still mild stridor following day
If severe (significant airway compromise)
- Oxygen
- Nebulised adrenaline
- To try settle inflammation and open up airways
When to admit child with Bronchiolitis?
Consider if:
- RR >60
- Difficulty breastfeeding/ inadequate oral fluid intake (50–75% of usual volume)
- Clinical dehydration
When to admit child with croup?
If moderate- severe
Why are children so prone to wheezing?
Small airways so only takes small amount of inflammation to narrow airways a bit more to cause whistling sound as air passes through
Multiple trigger wheeze
Wheezing due to multiple stimuli (e.g., infection, dust, pollen, smoking, cold air)
Viral induced wheeze
Wheezing only during viral infx caused by bronchoconstiction
Usually <3yrs
Acute mx - asthma stairs exactly the same
Wheeze v stridor
Wheeze
Caused by small airways narrowing - causes rattling high pitched sound usually during (prolonged) expiratory phase
Stridor
Caused by upper airway obstruction/narrowing of some form - causes harsh sound primarily during inspiration
Laryngomalacia
Structural abnormality of the larynx which cause partial obstruction resulting in stridor/noisy breathing
Laryngomalacia mx
Self resolving
Pneumonia presentation
- Dyspnoea
- Fever
- Tachypnoea
Pneumonia Ix
- Resp exam
- Reduced air entry to specific area
- Creptitations ^
- O2 sats
- Lowered
- sputum culture
- Capillary blood gas
- CXR
- Consolidation
Cystic fibrosis
Autosomal recessive condition caused by mutation in CFTR gene on Cr7(cystic fibrosis transmembrance conductance regulator - Delta-F508 mutation most common)) leading to failure of chloride secretion.
Cl- important to get out of cells into extracellular space to places where you have secretions as Cl- draws water with it, making secretions less viscous and easier to move around/get out.
Main organ systems affected by CF
- Respiratory
- Thick airway secretions -> encourage bacterial colonisation -> more infx
- GI
- Thick pancreatic & biliary secretions -> blockage -> lack of digestive enzymes
- Endocrine
CF manifestations and mx
Respiratory
- Bronchiectasis
- Recurrent infx
Mx: Antibiotics (prophylactic flucox) + physiotherapy
GI
- Pancreatic exocrine insufficiency
- Diarrhoea
- Malabsorption
Mx: Vitamin supplementatin + nutritional support (high cal diet)
Endocrine
- Diabetes mellitus (due to pancreatic endocrine dysfunction)
- Random blood glucose >11
- Osteoporosis (due to lack of absorption of ca and other minerals)
Mx: Diabetes mx / Vit D + Ca supplementation
+ MDT input!
*CF itself - Ivacaftor/Lumacaftor
Tries to improve construction of CFTR genes and insertion into membrane
CF Ix
Sweat test
CF fertility
Male fertility affected as normal sperm but absence of vas deferens -> cant be released
Tracheitis and epiglottitis (the other upper airway disease)
Meconium aspiration syndrome presentation
- Born through thick meconium
- Breathing problems
Meconium aspiration CXR
hyper inflated lungs with areas of consolidation
Respiratory distress syndrome Ix
CXR: Ground glass
Transient tachypnoea of the newborn presentation
- Tachypnoea within 1st 2h of life
- Grunting
- Use of accessory muscles
- Goes within 24h
Transient Tachypnoea of the newborn Mx
Supportive care ± O2
Scarlet Fever cause
Group A Streptococcus
Scarlet fever presentation
- Fever
- Sore throat
- Strawberry tongue
- Petechiae (small red spots) visible on the hard and soft palate are called ‘Forchheimer spots’
- Blanching rash with rough, sandpaper-like texture
Scarlet fever Mx
10 day course of phenoxymethylpenicillin (penicillin V)
- Return to school 24h after commencing abx
- Notifiable disease
Whooping cough
Whooping cough is caused by bacteria bordella pertussis - attach to cillia of upper airway.
Whooping cause presentation
- Short period of coryzal symptoms followed by
- Onset of paroxysmal bouts of coughing
- Coughing intense, apnoeic, and may cause vomiting
Whooping cough mx
Presenting within 3 weeks start of cough
- Oral azithromycin or clarithromcyin
- Eradicate org and try reduce spread
(Admit and IV abx if pt clinically unstable)
Presenting >3 weeks start of cough
- Advice
Vomiting differentials
- Posset - small volumes, painless, common
- No cause for concern
- Cow’s milk protein allergy
- GORD - larger volume, relatively forceful
- No cause for concern if growth unaffected
- Intussusception
- Pyloric stenosis - forceful, projectile vomiting
- Red flag requiring further ix
Cow’s milk protein allergy
Abnormal immune reaction to a protein found in cow’s milk
Cow’s milk protein allergy presentation
- Vomiting
- Diarrhoea or constip
- ±PR bleed - red tinged nappy blood
- Rash!
- Common in eczema!
- ±Wheezing
- ±Faltering growth
Cow’s milk protein allergy mx
If breast fed
- Mother to avoid dairy
If formula
- Extensively hydrolysed formula
*If growth still faltering -> lack of compliance or different diagnosis
*Most cases resolve by 5y/o
Duodenal atresia
The duodenum, which is the first part of the small intestine just beyond the stomach, is closed off/narrowed rather than being a tube
Duodenal atresia presentation
Low birth weight, premature, billious/non bilious vom, upper abdominal swelling
usually occurring within the first 24 to 38 hours of life after the first feeding
Duodenal atresia XR sign
double bubble
Duodenal atresia genetic syndrome association
Down’s
Duodenal atresia mx
NG tube + IV fluids –> surgery
GORD
Regurgitation of feed due to immaturity of lower oesophageal sphincter
Common in 1st year of life
GORD Mx
Breast fed
- Breast feeding assessed by midwife/health visitor
- Position upright after feeds
- Alginate therapy, e.g., Gaviscon infant
- small droplets given to baby - reacts w contents of stomach to form thickened, foam-like layer at top of stomach contents + generally
- PPI or H2 antagonist - omeprazole
- Paeds referral
Formula fed
- Review feeding hx - smaller and more frequent feeds
- Thickened formula or feed-thickeners
- Alginate therapy added to formula
- PPI or H2 antagonist (4 weeks)- omeprazole
- Paeds referral
Usually resolves spontaneously - early weaning may be recc
Intussusception
Telescoping of proximal bowel into distal bowel causing an obstruction
Intussusception presentation
3 months - 2years
- Paroxysmal, colicky pain
- Bouts of abdo pain causing significant distress -> screaming, drawing legs up
- Pallor
- Vomiting
- Non bilious at first, then once intestinal obstruction - vilious
- Sausage-shaped mass in abdo
- Red currant jelly stools (blood in stools - late stage feature)
Intussusception Ix
- Abdominal USS
- Target sign
- Abdominal XR
- If obstructed
- Contrast enema XR (gold standard)
Intussusception Mx
- Rectal air insufflation - pumping air into rectum and stretching out bowel allowing it to pop into place
Consider pathological lead point - an abnormality in tube where intussusception develops
Pyloric stenosis
Hypertrophy (narrowing) of pyloric muscle causing gastric outlet (opening from stomach to small intestine) obstruction
Pyloric stenosis presentation
2-8 weeks old, M>F
- Projectile vomiting (non-bile stained)
- Hungry after feeds
- Visible persistalsis LUQ
- stomach tries to push its contents past the obstruction
- Olive shaped mass o/e
Pyloric stenosis Ix
- VBG
- Hypochloraemic, hypokalaemic alkalosis due to persistent vomiting
- USS
- assess pyloric sphincter and see whether enlarged - donut sign
- Gold standard
Pyloric stenosis mx
- Fluid resus - NBM and NG tube
- Ramstedt pyloromyotomy
- Surgical intervention where pyloric sphincter is opened up and relaxed
Constipation differentials
- Foecal impaction
- Hirschsprung disease
- Hypothyroidism
- Hypercalcaemia
Impaction - where can mass most often be felt?
left iliac fossa
Constipation mx
If impaction -
Disimpaction!
- Movicol
* If unresolved 2 weeks/not tolerated* - Add stimulant laxative
If disimpacting not required/complete,
Maintenance dose movicol
Laxative classes (4)
- Softeners (more an oily material which infiltrates faecal masses and loosens them up)
- Lactulose
- Bulking agent (lend indigestible fibre to stool)
- Fybogel
- Osmotic laxatives (draw water into intestinal lumens and loosen up stools)
- Movicol
- Stimulants (augments intestinal contraction to help move things along)
- Senokot
Hirschsprung disease
Condition in which there is absence of ganglion cells of the myenteric and submucosal plexus -> leads to area of bowel that is unable to contract appropriately to expel contents
Hirschsprung disease is a birth defect in which some nerve cells are missing in the large intestine, so a child’s intestine can’t move stool and becomes blocked.
(nerve fibres and ganglia help coordination contraction of bowels to keep things moving in one direction)
Hirschsprung disease presentation
Early in life
- Delayed/unable to pass meconium
- Abdominal distension
- Billious vomiting
Later
- Chronic hx constipation often later in childhood
Hirschsprung disease Ix
- Abdo XR
- dilated loops of bowel with fluid levels
-
Full thickness rectal biopsy
- Observe absence of ganglion cells
Hirschsprung disease Mx
Supprotive
- Bowel irrigation
- Allow baby to pass meconium
Definitive
- Anorectal pull-through
- Removing affected chunk of bowel and re-anastomosing the ends to maintain continence
Hirschsprung associated genetic condition
Down’s syndrome
Malrotation
Birth defect that occurs when the intestines do not correctly or completely rotate into their normal final position during development
Malrotation presentation
- Bile-stained vomiting
- Failure to thrive
- Painful/tender abdomen
- May also be paroxysmal w pulling up legs
- Bloating
- PR bleed/melaena
Usually <1 y/o at presentation
Malrotation Ix
upper GI contrast study (gold standard) and USS
Malrotation Mx
Laparoscopic Ladd procedure to reposition intestines.
Malrotation complication
Volvulus - A volvulus happens when the intestine becomes twisted. This causes an intestinal blockage.
Meckel’s diverticulum
Congenital diverticulum of the small intestine
Meckel’s diverticulum is an outpouching or bulge in the lower part of the small intestine. The bulge is congenital (present at birth) and is a leftover of the umbilical cord.
Meckel’s diverticulum presentation
Usually asyx
- Abdo pain mimicking appendicitis
- Rectal bleed
Meckel’s diverticulum Ix
Technetium scan
Meconium ileus
Meconium is blocking the last part of the baby’s small intestine (ileum) –> bowel obstruction.
Happens as meconium is more viscous and stickier than usual
What condition is meconium ileus often caused by?
Cystic fibrosis
Meconium ileus Ix
- Sweat test for CF
- Abdo XR
- distended coils of small bowel, but no fluid levels.
- PR contrast studies
- can be therapeutic
Meconium ileus Mx
- PR contrast studies
- May dislodge meconium plugs
- NG acetyl cysteine
- Liquifies meconium
If not, surgery
Mesenteric adenitis
Inflamed abdominal lymph glands
Mesenteric adenitis presentation
URTI and generalised abdominal pain
Necrotising enterocolitis
Intestinal tissue is inflamed and starts to die. This can lead to perforation, allowing intestinal contents to leak into abdomen.
Necrotising enterocolitis presentation
First 2 weeks life
- Feeding intolerance
- Abdominal distension
- Bilious vomiting
- Melaena
- ±signs of sepsis
- Common in premature infants
Necrotising enterocolitis Ix
- Abdo exam
- Reduced bowel sounds
- Abdo XR
- Dilated asymmetrical bowel loops
- Bowel wall oedema
- Air inside & outside bowel wall (Rigler sign)
- Air outlining falciform ligament (football sign)
Congenital diaphragmatic hernia
Herniation of abdominal organs into the chest cavity due to incomplete formation of the diaphragm
Congenital diaphragmatic hernia presentation
Respiratory distress
Congenital diaphragmatic hernia Ix
- Cardio + resp exam
- Heart sounds absent on LHS
- Tinkling sounds heard (bowel)
- Abdo exam
- Scaphoid abdomen (raised level of chest where abdo is)
- CXR
- Bowel loops can be seen in thoracic cavity
Congential diaphragmatic hernia Mx
Initial
- Intubation and ventilation
- NG tube with aim of keeping air out of gut
Definitive:
Surgical repair of diaphragm
Neonatal jaundice causes
<24 hours -> Pathological
Haemolytic
- Rhesus incompatibility
- ABO incompatibility
- G6PD deficiency
- Pyruvate kinase deficiency
- Hereditary spherocytosis
Congenital
- Toxoplasmosis
- Others (e.g., syphilis)
- Rubella
- CMV
- HSV
24 hours - 2 weeks
- Physiological
- Common
- Increased RBC breakdown following birth - trauma
- Decreased bilirubin metab due to immature liver
- Breast milk jaundice
- Pathological (causes as above and below)
>2 weeks
- Biliary atresia
- abnormal development of biliary tree
- pale sools, bruising
- abnormal development of biliary tree
- Congenital hypothyroidism
- Neonatal hepatitis
ABO incompatibility jaundice
mother has the blood type O (and therefore has antibodies against A and B cells) and her newborn is of blood type A or B
Neonatal jaundice Ix
<24 hours
- Serum bilirubin
- Group and save
- DAT test (Coombs’/direct antibody test)
- See whether antibody binding to neonate blood cells
- Autoimmune haemolytic anaemia
- FBC + CRP
- Blood culture
>2 weeks
- TSH
- LFTs
- Bilirubin
- Transcutaneous (TC) bilirubin
- Non invasive
- Less accurate - more for screening
- Used if jaundice >24h or born >35weeks (lower risk of pathological cause of jaundice)
- Serum bilirubin
- Used if jaundice at <24h or born <35 weeks gestation
- Transcutaneous (TC) bilirubin
- Hepatobiliary scintigraphy/nadionucleotide scan
- If considering biliary atresia
Neonatal jaundic Mx
- Phototherapy
- Light therapy (eyes protected and temp monitored) where unconjugated bilirubin converted to water-soluble pigment which can be excreted
- Bilirubin checked every 6-12h via heel prick test blood gas
- Intensified phototherapy
- +/- IVIG
- Primarily used in ABO or rhesus haemolytic disease
- +/- IVIG
*carry on until 5 boxes below line on trx threshold graph:)
or Exchange transfusion - removal of infant blood and replaced w donor blood
Biliary atresia presentation
jaundice, pale stools and dark urine
Biliary atresia Ix
- High levels conjugated bilirubin
- Liver is doing its thang but not able to excrete through biliary duct into bowel
- USS abdo - contracted/absent GB
- Liver biopsy
How is biliary atresia managed?
Surgical intervention - Kasai procedure
removing the blocked bile ducts and gallbladder and replacing them with a segment of child’s small intestine
Neonatal jaundice complx
Kernicterus
Unconj bilirubin can cross BBB and deposit in basal ganglia -> can result in cerebral palsy
Antenatal resp-cardio adaptation
- Oxygenated blood from umbilical vein
- Foramen ovale
- Right to left shunt (due to lower Pa on RHS)
- Ductus arteriosus
- Less resistance to go to aorta rather than pulm arteries
- Lungs are non functional (high pulmonary vascular resistance)
Innocent murmurs
- Systolic
- Soft / low amplitude
- Change position when breathing
- Single
- Short duration
2 types of congenital cyanotic heart diseases
Cyanotic heart failure = right to left shunt (deoxygenated blood in systemic circ)
- Transposition of the great arteries
- Tetralogy of fallot
Main features of cyanotic heart disease
Cyanosis onset
- Within days -> TGA
- Within months -> TOF (+murmur)
(When exerting themselves, e.g., feeding)
Transposition of the great arteries
Aorta and pulmonary trunk are switched around
Two completely separate circuits
- RHS (aorta) is systemic - goes to body and back
- LHS (pulm trunk) goes to lungs and back
*Ductus arteriosus maintains life by allowing blood from LHS (oxygenated) to mix with RHS and aorta -> rest of body
Abnormalities in tetralogy of fallot
- Pulmonary stenosis
- Narrowing of pulmonary valve -> lots of resistance going back towards RHS of heart
- Ventricular septal defect (VSD)
- Allows blood to mix between 2 sides of heart
- Overriding aorta
- Large proportion of outflow from heart going through aorta over pulmonary artery
- Right ventricular hypertrophy
- RHS having to pump against higher pressure than used to due 1) and 3)
TofF murmur
systolic ejection murmur at the left upper sternal border
Cyanotic heart disease ix
- Pulse oximetry
- TGA - suddenly profoundly hypoxic as DA is closing
- Hyperoxia test
- Sats probe placed on infant then + high flow O2 -> check if improvement
- TGA - no improvement as circuits are separate and sats probe only showing peripheral sat
- Sats probe placed on infant then + high flow O2 -> check if improvement
- CXR
- TGA: egg on a string
- TOF: boot shaped heart
Cyanotic heart disease mx
- IV prostaglandin infusion
- Maintain patency of DA
- Surgery
Acyanotic heart disease (4)
Defects in embryological development of heart or its major vessels (left to right shunt w/ exception of CoA)
- Ventricular septal defect (VSD)
- Hole in septum betwen ventricles
- Most common
- Atrial septal defect (ASD)
- Hole in spetum between atria
- Patent ductus arteriosus (PDA)
- Ductus arteriosis remains open beyond 1 month (usually shuts before 1 month)
- Coarctation of the aorta
- Narrowing of aorta
Acyanotic heart disease presentation
Asymptomatic, or HF signs:
- Fatigue
- SOB
- Exercise intolerance
- Poor feeding/failure to thrive
- (Systolic) murmur
Murmurs associated w/ ASD, VSD and PDA
- VSD: systolic murmur at left sternal border
- ASD: soft midsystolic murmur at the upper left sternal border with splitting of the 2nd heart sound (S2)
- PDA: continuous ‘machinery’ murmur over left clavicle
AVSD complx and association
May lead to pulmonary hypertension + associated with Down syndrome
PDA mx
- NSAIDs
- e.g., indomethacin
Coarctation of aorta specific sign
Brachio-femoral delay
Can feel strong brachial pulse, but delayed and v weak or even absent femoral pulse
Acyanotic heart disease complx
- Heart failure (SOB)
- Faltering growth
- Recurrent chest infx
- Infective endocarditis
Anaphylaxis
Severe allergic reaction
Anaphylaxis presentation
- Stridor
- Angioedema
- Urticaria
Anaphylaxis Mx
- Call for help +
- A to E
* 2 large bore cannulae - Lie patient flat
- Definitive (to carry on if anaphylaxis persists / refractory anaphylaxis)
- IM Adrenaline 1:1000
- age adjusted doses
- Repeat after 5 mins if needed
- IV fluid challenge - crystalloid
- IM or slow IV chlorphenamine + hydrocortisone
Upon d/c
- Safety net
- Avoiding allergen (if known)
- EpiPen
- Allergy clinic
Diabetic ketoacidosis
Pancreatic beta cells are not producing insulin -> serum glucose concentration increases considerably and increased ketone generation.
DKA presentation
- Polyuria -> dehydration
- N+V
- Thirsty
- Abdo pain
- Unexplained weight loss
- Coma
Ketones
- How are they produced?
- How are they useful?
- How are they harmful?
- Ketone bodies are produced during B-oxidation of fatty acids when body is low on glucose supply.
- Ketones allow brain to continue functioning in a time when glucose is scarce.
- They are acidic -> enzyme dysfunction -> coma & death:(
Actions of insulin (2)
- Reduces serum glucose concentration via
- push glucose into hepatic glucose store
- push glucose into tissues
- Block ketone generation (within liver)
DKA Mx
- IV fluid resuscitation
- Shock
- Bolus 20ml/kg 0.9%NaCl over 15 mins
- Not in shock
- Bolus 10ml/kg 0.9% NaCl over 1h
- Deficit * weight (in kg) * 10 –> total deficit vol(ml) /48h
- pH>7.1 = 5%
- pH<7.1 = 10%
- Deficit * weight (in kg) * 10 –> total deficit vol(ml) /48h
- Maintenance fluids
- Shock
Fluid choice: 0.9% NaCl + 40mmol KCl, then once glucose <14mmol/L add 5-10% dextrose
- Insulin
Long term
- Education
- Family support
- Insulin rotating sites
- MDT care: diabetic nurse, dietician, paeds
- Annual r/v
IV Fluid resuscitation
Bolus (if in shock) + replacement fluid + maintenance fluid
How much bolus fluid for fluid resus?
20ml/kg/10mins
How much replacement fluid for fluid resus?
100ml/kg/24h
How much maintenance fluid for fluid resus?
100ml/kg for first 10kg +
50ml/kg for 2nd 10kg +
20ml/kg thereafter
CIs for LP
- Raised ICP
- Profoundly impaired consciousness
- Focal signs
- Focal or prolonged fits
- Cardio-pulmonary compromise (ie in shock or needing artificial ventilation)
- Local skin infection
Neonatal sepsis signs
- Respiratory distress (85%)
- Grunting
- Nasal flaring
- Use of accessory respiratory muscles
- Tachypnoea
- Tachycardia
- Apnoea
- Change in mental status/lethargy
- Jaundice
- Seizures
- if cause of sepsis is meningitis
- Poor/reduced feeding
- Abdominal distention
- Vomiting
- Temperature
*Frequently, the symptoms will be related to the source of infection (e.g. pneumonia + respiratory symptoms, meningitis + neurological symptoms)
Status Epilpeticus
Single continuous seizure or repetitive seizures ± recovery period of consciousness lasting 5 or less mins.
Status epilepticus Ix
- Glucose
- U&E
- Calcium
- Anticonvulsant levels
- Toxicology screen
Status epilepticus Mx
- IV Lorazepam
* If no IV access –> rectal diazepam or buccal midazolam*
* *after 10 mins** - IV Lorazepam (2nd dose)
- Phenytoin infusion
- General anaesthesia
Testicular torsion
Rotation of testicle leading to lack of blood supply as the spermatic cord which brings blood to scrotum is twisted
Testicular torsion presentation
- Severe testicular pain
- Nausea and vomiting
- Swelling of the testis with overlying erythema
- Absent cremaster reflex
Achondroplasia presentation
- Short stature
- Macrocephaly
- Bowing of legs
- Trident config of hands
(Dwarfism vibes)
Developmental dysplasia of the hip
Condition in neonates where acetabulum is shallow -> head of demur does not actually sit within acetabulum and can slip out quite easily
DDH presentation in non-neonates
Painles intermittent limp
DDH RF
- female sex: 6 times greater risk
- breech presentation
- family history
- firstborn children
- oligohydramnios
- birth weight > 5 kg
DDH Ix
- Barlow and Ortolani manoeuvres during newborn infant screening check
- USS at 6 weeks (if suspcion from B&O test)
- If present with possible DDH beyond 6/12, hip XR
DDH Mx
- Spontaneous resolution
- Pavlik harness
- Holds infant’s hips in a flexed position -> helps burrow head of femur into acetabulum
- Surgery
Duchenne muscular dystrophy
Duchenne muscular dystrophy (DMD) is a genetic disorder characterized by progressive muscle deterioration and weakness
DMD presentation
- Onset in early childhood
- Walking on tip toes
- Enlarged calves
- Calf pseudohypertrophy
DMD cause
Alterations of a protein called dystrophin which helps keep muscle cells intact
DMD Ix
- Gower’s sign
- +ve
- child uses arms to stand up from a squatted position
- CK
- Raised
- Genetic testing
What is the systemic onset of Juvenile Idiopathic Arthritis called?
Still’s disease