Paediatrics Flashcards
Developmental Milestones 2 months
- hearing/language
- social/emotional
- cognitive/visual/fine motor
coos and gurgles. turns head to sound
Begins to smile at people. Tries to look at parents. Sucks on hand to sooth
Begins to follow things with eyes
Begins to act bored
Developmental Milestones 8 months
- hearing/language
- social/emotional
- cognitive/visual/fine motor
Understands no. Mamama/dadada sounds
Stranger awareness. Has favourite toy
Transfers from one hand to another
Picks up cereal between thumb and index finger
Plays peek a boo
Developmental Milestones 18 months
- hearing/language
- social/emotional
- cognitive/visual/fine motor
Says 10 words
Says no and shakes head
Temper tantrums
Points to show something interesting
Follows 1 step verbal command
Scribbles on own
Developmental Milestones 3 years
- hearing/language
- social/emotional
- cognitive/visual/fine motor
Understands words such as in/on/under
Carries on a conversation using 2 to 3 sentences
Copies adults and friends
Takes turns in games
Shows concern friend crying
Does jig saw 3-4 pieces
Copies a circle with a pencil
cpr in children
15 compression s to 2 breaths
Croup (laryngotracheobronchitis) presentation and management
Common cause of acute respiratory distress in children 6 months to 3 years
Acute onset of seal-like barky cough in moderate to severe cases accompanied by stridor and sternal/intercostal indrawing
Fever
Viral cause (parainfluenza usually)
note majority of cases mild but if needed…
- oral dexamethasone 0.15 mg/ kg as a single dose
- Nebulised Adrenaline 5mls 1:1000 (mod or severe)
- senior input
symptoms and management of foreign body aspiration
sudden onset of respiratory distress associated with coughing, gagging, or stridor. Unilateral wheezing suggests partial obstruction of the main or distal bronchi
management with flexible bronchoscopy or rigid if fails
signs of respiratory distress
- increased RR
- stridor
- tracheal tug; retraction at the suprasternal notch
- intercostal recession
- subcostal recession
- head bobbing
- grunting
- posture
impending respiratory failure and exhaustion will develop a low respiratory rate (for their age) and breath sounds including added sounds can diminish
differentials child in upper respiratory distress
Viral Croup
Epiglottitis (unlikely with haemophilia influenza vaccine)
Foreign body aspiration
Anaphylaxis
Bacterial tracheitis
laryngeal capillary haemangioma
slowly progressive airway obstruction / stridor since birth, particularly if the child has other capillary haemangiomas
gastro-oesophageal reflux disease in infants
silent symptoms or intermittent distress commonly after feeds and on lying flat, intermittent breathing difficulty with symptoms including stridor, episodes of colour change and / or recurrent chest infections, and behavioural changes such as back arching
stridor present since birth
Laryngomalacia or floppy larynx
soft stridor that worsens with feeds
monitor feeding and growth
epiglottitis
very rare cause of airway obstruction seen most in children 2-7
sudden onset of distressed child with muffled cough and voice, normal temp, drooling and leaning forward
needs emergency airway management
usually bacterial cause
bacterial tracheitis
differenital for epiglottis
younger age; 6 months to 14 months
fever present
sudden onset
hoarse voice and cough
drooling
needs emergency airway
broad spec Abx once airway secured
anaphylaxis presentation
Hypotension, Bronchoconstriction or Airway compromise in the setting of an allergic reaction
child pale and sweating (hypotensive), wheeze, stridor
what type of allergic reaction is a food allergy
type I hypersensitivity
sensitisation to allergen
for an allergy to occur a child must have previously encountered the allergen
Following exposure to an antigen the protein causes cross binding of two bound IgE molecules on the Mast Cell or Basophil surface. This process results in degranulation of the Mast Cell.
Histamine is released immediately causing the reaction
actions of histamine
localised irritation
vasodilation
bronchoconstriction
endothelial cell separation - resulting in urticarial rash
criteria for prescribing an Adrenaline Pen
- History of Anaphylaxis
- Previous cardiovascular / Respiratory involvement
- Evidence of airway obstruction
- Poorly controlled Asthma requiring regular inhaled corticosteroids
- Reaction to a small amount of allergen
- Ease of allergen avoidance
in less severe allergy, having antihistamine available can be sufficient
what is bronchiolitis
acute inflammation of the bronchioles usually caused by RSV
affects infants
initially subtle symptoms which worsen over 3-4 days
usually self limiting and needs supportive care but infants can become more unwell and need admission
symptoms of bronchiolitis
initial coryzal symptoms
progress to some or all of (day3-6)
- increased work of breathing
- typical cough
- poor/reduced feeding
- pallor
- exhaustion
- widespread wheeze and crackles
- fever (low grade)
- apnoea
- reduced oxygen sats
- tachycardia of bradycardia (more worrying)
symptoms bronchiolitis requiring admission
- 50% feeding intake
- pre-existing condition such as prematurity, CF
- RR>70
- O2 sats <92%
- moderate resp distress
- apnoeas
- clinical dehydration
management of bronchiolitis in hospital
maintain oxygen sats
NG feed
if severely worsening; NBM, FBC, blood gas, biochem
IV fluids
orogastric decompression
consider CPAP if very severe
PICU?
consider Abx ?concurrent bac infection
accurate assessment of feeding in an infant
calculate the amount in mls/kg/day not ounces as reported by parents
minimum milk requirement for growth
150ml/kg/day in first month
100ml/kg/day after as long as meeting growth requirements
antenatal Hx
important in early childhood illness
maternal health
delivery
post delivery
systolic paediatric murmurs
Tetralogy of Fallot
VSD
pul/aortic stenosis
diastolic murmurs
pul or aortic valve regurge
mitral stenosis
symptoms/signs of HF in children
shortness of breath; tachypnoea and dyspnoea
poor feeding; can’t breathe and feed comfortably
tachycardia
hepatomegaly
poor pulses
acidosis
sweating
oedema only in children 3years+
management of HF in children
diuretics
ACEi
oxygen; with caution can close ducts
prostaglandins; prostin, to keep duct open
monitor diet/fluid intake
inotropes such as dopamine
sometimes catheter interventions, surgery last resort
diet in infants in HF
have higher energy requirements but need to control volume - high calorie feeds, supplements, frequent feeds less volume
sometimes need NG or if long term gastronomy
embryology of heart
forms from mesenchymal cells
4 chamber heart forms by 40 days
types of heart problems in children
congenital
- cyanotic
- acyanotic
acquired (rare)
- myocarditis (coxsackie B virus)
- viral pericarditis
- rheumatic heart disease
inherited
- HOCM
- marfans etc
presentation of congenital heart disease
antenatal; routine scan or FHx initiated scan
postnatal; routine check, symptomatic (cyanotic)
acyanotic CHD
majority septal defects; VSD, ASD
also
- aortic/pulmonary stenosis
- PDA
- coarctation of aorta
- mitral/tricuspid stenosis rare
VSD murmur
pansystolic
PDA murmur
continuous + bounding pulses
coarctation (narrowing) of aorta presentation
femoral pulses weak/absent
hypertension upper limbs
commonly associated with other heart defects
in newborns risk of necrotising enterocolitis
presents around 3 days. needs surgery and give prostin to keep a PDA open
cyanotic CHD
many but most important are
- fallot’s tetralogy
- transposition of great arteries (TGA)
- complete atria-ventricular septal defects
atrial-ventricular septal defect
atrial and ventricular septal defect
can be partial (no ventricular) or complete
higher incidence in trisomy 21
LAD on ECG
CHD and chromosomal syndromes
trisomy 21; 40% have CHD
trisomy 13 (Patau’s); 80% have CHD
trisomy 18 (Edward’s; 80-100% have CHD
DiGeorge syndrome
autosomal dominant condition. DiGeorge syndrome is associated with congenital heart disease.
sex chromosome aneuploidies
Turners 45XO
Klinefelters 47XXY
Triple X 47XXX
+ others
what is tested for on heel prick test
MCAD
HCU
Sickle cell
Isovalaric acidaemia
Cystic fibrosis
Hypothyroidism
Phenylketonuria
Kawasaki disease
inflammatory condition
swinging fevers resistant to paracetamol
lymphadenopathy
red eyes and tongue
rash
swollen feet and hands
platelet rise in 2 weeks
can cause coronary artery aneurysms; cardiac complications reduced by early aspirin and IV gammaglobulin
what can happen if VSD not treated
may close spontaneously but if left reversal of the shunt from L-R to R-L can occur which can lead to permanent pulmonary hypertension
VSD needs medical or surgical management
ASD management
needs closure
long term can result in arrhythmias or shunt reversal
pre term PDA
use NSAIDS for first 2-3 weeks
may close
if not surgery
4 components of tetralogy of fallot
pulmonary outflow obstruction
right ventricular hypertrophy
VSD
overriding aorta
baby presents with blue spells. needs surgery
innocent flow murmur
Many children will have an innocent flow murmur when they are pyrexic
differentials acutely breathless school age child
asthma
pneumonia
pneumothorax (unlikely)
foreign body aspiration
cardiac failure
acute severe asthma examination findings
Severe recession; sc/ic/ tracheal tug
Posture sitting forward; ‘Tripod’ position
Wheeze may be audible from end of bed
Hyperexpanded chest; Symmetrical expansion;
poor expansion if severe
trachea central cardiac apex in usual position
liver pushed down; edge palpable.
Resonant but equal
Air entry symmetrical; poor Air entry indicates increasing severity
severe pneumonia O/E
Respiratory distress with recession and tracheal tug
Wet cough; +/- Grunting
Expansion may be asymmetrical if severe unilateral pneumonia
Dullness over consolidation may be present
Reduced air entry +/-
Bronchial breathing / crackles over area of infection
what is Harrison’s sulcus
groove under ribcage seen in children with chronic respiratory disease e.g. severe asthma
sputum MC&S children
usually over 7 years can
if younger or cannot do a cough swab
investigations for chronic lung disease in a child e.g. bronchiectasis
CT chest
Measurement of serum immunoglobulin levels; assesses for primary immune deficiencies
Sweat chloride test; for CF
organs affected by cystic fibrosis
sinuses
lungs
skin - saltier sweat
liver
pancreas - exocrine and endocrine insufficiency
intestines - malabsorption
reproductive organs
CFTR protein
ion channel at cell membrane transporting ions such as chloride
loss of function results in altered secretions
diagnosis of CF
heel prick test approx day 5 in UK - measures a pancreatic trypsinogen elevated in CF babies
sweat test more accurate diagnosis esp in children >6 weeks
genetic testing analysis done to confirm
CF GI and liver complications
- Meconium ileus (often first sign)
- Constipation
- Distal Intestinal obstruction
- Neonatal cholestasis
- fatty liver
- cirrhosis
- gallstones
- cholecystitis
CF pulmonary management
Abx; oral/nebs/IV, prophylactic (start at birth) and treatment
mucolytics
physiotherapy
wheeze treatment
anti-fungals
extra pulmonary CF management
Creon for enzyme support + vitamins A, E, D, K (fat soluble)
management of constipation
insulin for CF diabetes
liver; ursodeoxycholic acid, vit K
salt supplements (lost in sweat)
presentation of CF if not diagnosed as neonate
poor growth and failure to thrive
fatty stools
recurrent respiratory problems (not in firth few months)
fetal circulation shunts
ductus arteriosus - between pulmonary artery and aorta to bypass lungs
foramen ovale - between R to L atria
ductus venosus - between umbilical vein and inferior vena cava to bypass liver
ducts are aided by high pulmonary vascular resistance in the foetus
how do fetal shunts change at birth
at first breath - alveoli fill with air and vascular resistance of the pulmonary circulation decreases
LA pressure exceeds RA pressure and the foramen ovale closes
circulating prostaglandins drop due to increased blood oxygenation - ductus arteriosus closes
ductus venous closes after cord clamped
PDA
- diagnosis
- management
may be picked up at birth with a murmur
can also present with failure to thrive, SoB, difficulty feeding - the L-R shunt causes increased pul pressure and HF
needs echo to diagnose
typically monitored until 1 year by which point may have closed or catheter surgery is performed
ASD symptoms/complicaitons
L-R shunt causes right heart strain and pul hypertension but is acyanotic because blood is always being oxygenated
eventually in Eisenmenger syndrome the pul pressure can exceed systemic and the shunt reverses to R-L causing cyanosis
murmur:mid-systolic, crescendo-decrescendo murmur loudest at the upper left sternal border with a fixed split second heart sound
may be picked up antenatally or later with symptoms/complciations
other complications are AF, stroke
VSD presentation
may be picked up antenatally or a murmur at newborn baby check
can also present with symptoms such as Poor feeding
Dyspnoea
Tachypnoea
Failure to thrive
CXR tetralogy of fallot
typically boot shaped heart due to RVH
“Tet spells” tetralogy of fallot
intermittent symptomatic periods where the right to left shunt becomes temporarily worsened, precipitating a cyanotic episode
usually when a child is physically exerting themselves, crying, laughing etc.
management: can try knees to chest/squatting. if failed
- oxygen
- IV fluids
- beta blockers/adrenaline/morphine
tetralogy of fallot management
prostaglandins can maintain ductus arteriosus
then heart surgery needed - mortality from surgery 5%
differentiating viral induced wheeze and asthma
factors favouring asthma
- personal or FHx of atopy
- interval symptoms (between viral infections ) of coughing at night, when playing or in cold
management of acute asthma child
Oxygen to maintain sats>94%
Salbutamol inhalers via a spacer device: starting with 10 puffs every 2 hours
Nebulisers with salbutamol / ipratropium bromide
Oral prednisone (e.g. 1mg per kg of body weight once a day for 3 days)
IV hydrocortisone
IV magnesium sulphate
IV salbutamol
IV aminophylline
if still not controlled contact ICU
work back down ladder as they get better
Antibiotics only if bacterial cause suspected
long term medical asthma therapy age <5
Start a short-acting beta-2 agonist inhaler (e.g. salbutamol) as required
Add a low dose corticosteroid inhaler or a leukotriene antagonist (i.e. oral montelukast)
Add the other option from step 2.
Refer to a specialist.
long term medical asthma therapy age 5+
Start a short-acting beta-2 agonist inhaler (e.g. salbutamol) as required
Add a regular low dose corticosteroid inhaler
Add a long-acting beta-2 agonist inhaler (e.g. salmeterol). Continue salmeterol only if the patient has a good response.
Titrate up the corticosteroid inhaler to a medium dose. Consider adding:
Oral leukotriene receptor antagonist (e.g. montelukast)
Oral theophylline
Increase the dose of the inhaled corticosteroid to a high dose.
Referral to a specialist. They may require daily oral steroids.
whooping cough symptoms
URTI caused by pertussis (children and pregnant women are vaccinated against)
typically starts with mild coryzal symptoms, a low grade fever and possibly a mild dry cough.
more severe coughing fits start after a week or more
whooping cough diagnosis
A nasopharyngeal or nasal swab with PCR testing or bacterial culture can confirm the diagnosis within 2 to 3 weeks
later can be tested for anti-pertussis toxin immunoglobulin G
whooping cough management
notifiable disease
management usually supportive
macrolide Abx can be helpful in early stages
close contacts are given prophylactic Abx
usually resolves in 8 weeks but can be long lasting and key complication is bronchiectasis
pyrexia and sepsis in children
apyrexia does not exclude sepsis
septic children often have normal or low temperatures
investigations suspected shaken baby
CT head - intracerebral haemorrhage?
skeletal survey
ophthalmology review - retinal haemorrhages?
metabolic testing - exclude glutaric aciduria associated with ICH
coagulation
clinical features of non-accidental head injury
Irritability
Poor Feeding
Increasing head circumference
Seizures
Reduced GCS
Full fontanelle
Anaemia
Retinal Haemorrhages
how does shaking baby cause injury
esp in a child under 6 months shaking can cause rupture to the small vessels crossing the subdural space, causing a subdural haemorrhage
What action should a doctor take if they have a child protection concern?
Refer to Social Services
Social Services will consider whether the child (and potentially siblings) requires a child protection medical assessment and needs to be safeguarded from impending harm.
child with bruising differentials
accidental injury
non accidental injury
immune thrombocytopenia
meningococcal septicaemia
leukaemia
Haemophilia A
Von Willebrands Disease
child with fractures differentials
accidental injury
non accidental injury
Osteogenesis Imperfecta
Copper Deficiency
Vit D defiency
Vit C deficiency
Ehlers Danlos and other hypermobility syndromes
JOBs syndrome
child with burns/scalds differentials
Accidental Injury
Non accidental injury
Bullous Impetigo
Scalded Skin Syndrome
red flag symptoms that indicate unlikely to be functional GI disorder of childhood
age <5years
weight loss/poor growth
blood in stools
regularly waking at night due to symptoms
causes of blood in stool in children
Infective – bacterial diarrhea eg campylobacter, salmonella
Inflammatory bowel disease
Tearing from anal vein
Polyp
Intussusception – acutely unwell
investigations IBD suspected
Hx and examination
bloods; FBC, U+E, LFT, CRP/ESR
Coeliac tests
stool MC&S
faecal calprotectin
if still suggestive; colonoscopy +/- small bowel barium studies
what typically causes Haemolytic Uraemia Syndrome
classical history
E Coli
Hx of severe diarrhoea, progressing to anaemia, thrombocytopenia, haematuria and raised creatinine
Kartagner’s triad
describes the three key features of primary ciliary dyskinesia. Not all patients will have all three features.
Paranasal sinusitis
Bronchiectasis
Situs Inversus
surgical causes abdo pain children
Appendicitis causes central abdominal pain spreading to the right iliac fossa
Intussusception causes colicky non-specific abdominal pain with redcurrant jelly stools
Bowel obstruction causes pain, distention, absolute constipation and vomiting
Testicular torsion causes sudden onset, unilateral testicular pain, nausea and vomiting
abdominal migraine
more likely in children compared to traditional migraine
abdo pain lasting >1 hour with possible associated Nausea and vomiting
Anorexia
Pallor
Headache
Photophobia
Aura
management similar to migraine in adults
acute; analgesia, low stimulus environment, triptan
preventative; Pizotifen, a 5-HT antagonist, consider propranolol
causes of constipation
majority idiopathic but consider CF, Hirschprungs, hypothyroidism
idiopathic contributed to by lifestyle factors including diet, activity, psychosocial problems
Encopresis/faecal incontinence
not pathological until >4years
usually a sign of chronic constipation where rectum loses sensation
other rarer causes include learning disability, abuse, psychosocial stress, cerebral palsy
constipation red flags
Not passing meconium within 48 hours of birth (cystic fibrosis or Hirschsprung’s disease)
Neurological signs or symptoms, particularly in the lower limbs (cerebral palsy or spinal cord lesion)
Vomiting (intestinal obstruction or Hirschsprung’s disease)
Ribbon stool (anal stenosis)
Abnormal anus (anal stenosis, inflammatory bowel disease or sexual abuse)
Abnormal lower back or buttocks (spina bifida, spinal cord lesion or sacral agenesis)
Failure to thrive (coeliac disease, hypothyroidism or safeguarding)
Acute severe abdominal pain and bloating (obstruction or intussusception)
management idiopathic constipation
diagnose without investigations if red flags excluded
- correct reversible lifestyle factors
- laxatives (movicol first line) should be weaned off as returns to normal
- impaction may require disimpaction regime
- encourage and praise toiletting
causes of vomiting
Overfeeding
Gastro-oesophageal reflux
Pyloric stenosis (projective vomiting)
Gastritis or gastroenteritis
Appendicitis
Infections such as UTI, tonsillitis or meningitis
Intestinal obstruction
Bulimia
red flags of vomiting
Not keeping down any feed (pyloric stenosis or intestinal obstruction)
Projectile or forceful vomiting (pyloric stenosis or intestinal obstruction)
Bile stained vomit (intestinal obstruction)
Haematemesis or melaena (peptic ulcer, oesophagitis or varices)
Abdominal distention (intestinal obstruction)
Reduced consciousness, bulging fontanelle or neurological signs (meningitis or raised intracranial pressure)
Respiratory symptoms (aspiration and infection)
Blood in the stools (gastroenteritis or cows milk protein allergy)
Signs of infection (pneumonia, UTI, tonsillitis, otitis or meningitis)
Rash, angioedema and other signs of allergy (cows milk protein allergy)
Apnoeas are a concerning feature and may indicate serious underlying pathology and need urgent assessment
physical risks of rapid weight loss
Refeeding syndrome risk, hypoglycaemia, risk of infection, cardiac arrhythmia.
What conditions can cause rapid weight loss in adolescents?
Coeliac disease
Type 1 diabetes mellitus
Hyperthyroidism
Malignancy
Anorexia nervosa
Inflammatory bowel disease
Oesphageal problems eg achalasia
Severe depression/OCD/autism
Juvenile arthritis
Addisons
what assessments/tests would you want in a child with rapid weight loss?
Weight, height
HR, BP, BM, RR, CRT
ECG, U+E, phosphate, calcium, magnesium, LFTS, CRP, WCC, TFTS, coeliac screen, ESR.
course of action severe weight loss concerns of eating disorder
Admit to stabilise physically, commence vitamins (thiamine, Vitamin B complex, multivitamins) to prevent refeeding syndrome, regular observations + BM, monitoring bloods. Contact local eating disorders team, diet plan. IV fluids if hypoglycaemic or not drinking (10% dextrose+045% saline).
Lanugo hair
fine hair growth in anorexia in response to loss of insulating fat
short term treatment/weight gain plan anorexia nervosa
if weight height ratio <75% commence thiamine, Vitamin B complex and multivitamins
Aim for 0.5 kg-1kg per week weight gain
monitor blood especially phosphate; drop indicates refeeding syndrome
regular ECGs
Discharge when vital signs stable and weight gain occurring
medium term plan anorexia nervosa
Multi-disciplinary treatment package in the community
- child psychiatrist oversees care + role of antidepressants for comorbidities
- dietician
- therapists + family therapist
- paediatrician to mentor physical health (risks of osteopenia/porosis esp if amenorrhea)
main types of eating disorder young people
anorexia nervosa
bulimia nervosa
EDNOS - eating disorder not otherwise specified)
What is weight for height ratio?
A method of assessing how appropriate that persons weight is for their height at a given age.
more accurate in children than BMI
most significant mortality risks in anorexia nervosa
Sudden cardiac death
Suicide
Chronic emaciation + pneumonia
causes of short stature in children/adolescents
- familial note hypochondroplasia
- constitutional/delay
- psychosocial
- chronic physical disease
- malabsorption
- endocrine
- genetic/syndrome
short stature; approach to diagnosing cause
general Hx + Hx of family
?diarrhoea ?abdo pain ?energy
examination: ?dysmorphic, ?limb size, ?skin lesions
parental heights + mid parental centile
blood pressure - renal failure can be missed cause
investigations; thyroid, creatinine, bone and liver profiles, FBC, CRP, glucose, coeliac screen
chromosomes esp girl ?turners
bone age vs actual age; is there just delay
follow up short stature
usually not immediate medical diagnosis
follow up every 4 months and if cause identified can treat
keep safeguarding in mind
first signs of puberty girls/boys
girls; breast development then pubic hair
boys; testicular enlargement followed by genital changes. later age than girls
definition of delay puberty
no signs age 14 in boy or age 13 in girl
in boys testosterone to kickstart puberty sometimes offered
precocious puberty
any signs before age of 8 in girl and 9 in boy
more likely to be pathological if under age 6
can be psychological distressing and can stunt adult height
can offer blockade with GnRH antagonist e.g. zoladex every 12 weeks injection
thyroid disorders causing stunted growth
congenital hypothyroidism - should be detected on newborn heel prick test
2/3 of these have absent or ectopic thyroid gland - need lifelong replacement
other 1/3 gland is present but not producing - usually still needs replacing but sometimes starts producing thyroxine; trial cessation at age 3
acquired hypothyroidism - autoimmune condition can be seen in adolescent females
physical features of dehydration in an infant
Sunken anterior fontanelle
dry mucous membrane
tachycardia
reduced capillary refill time
reduced skin turgor
common causes of gastroenteritis in young children
- rotavirus - particularly winter and early spring
- adenovirus
if bacterial campylobacter is most common
what infections can cause blood in the stool associated with diarrhoea and vomiting
Rotavirus
Intussusception
E. coli
Campylobacter
Shigella
definition and typical presentation of intussusception
invagination of proximal bowel into a distal segment commonly involving invagination of ileum into caecum through the ileocecal valve
age 3 months to 2 years
paroxysmal severe colicky pain
pallor during painful episodes followed by lethargy
child may refuse to feed, vomit, and pass red currant jelly stools
what infection is associated with haemolytic uraemia syndrome
management
E.Coli
associated with diarrhoea and blood in stool
can progress to HUS which is the most common cause of acute renal failure in children
treatment is mainly supportive; may include dialysis +/- IVIG if severe
red flag features of vomiting
blood in vomit
bilious vomiting
projectile vomiting
abdominal tenderness or distention
blood in stool
bulging fontanelle
young child vomiting with persistent or associated fever
may be associated with infections such as urinary tract infection or meningitis
what does bilious vomiting indicate
intestinal obstruction
what does haematemesis indicate
Oesophagitis, gastric ulcer, oral or nasal bleeding and vomiting up swallowed blood
projectile vomiting under 2mo
pyloric stenosis
vomiting with abdominal distention/tenderness
Intestinal obstruction, strangulated inguinal hernia, surgical abdomen
vomiting with severe dehydration/shock
Severe gastroenteritis, systemic infection – UTI, meningitis, diabetes ketoacidosis
vomiting with bulging fontanelle or fits
Raised intracranial pressure due to meningitis/ hydrocephalus
vomiting with faltering growth
Gastroesophageal reflux, coeliac disease, chronic gastrointestinal conditions
vomiting with paroxysmal cough
whooping cough
what is a fluid challenge
if at risk of dehydration, give oral bolus of rehydration solution frequently in small amounts
5ml/kg of ORS after each large watery stool in children who are at risk of dehydration - consider giving via NG
continue to monitor input and output
continue breast feeding and other milk feeds
what children are at risk of dehydration
low birth weight, age less than 1 year, had more than 2 vomiting episodes and more than 5 diarrhoeal episodes in the previous 24 hours
usual duration of diarrhoea illness in children + how to manage simple illness
5-7 days and in most children, it stops in 2 weeks. The family should continue encouraging intake of usual fluids (breast milk or formula) and give 5ml/kg of ORS after passage or each loose stool
not attend nursery until 48 hours after last vomit or diarrhoea
safety net simple gastroenteritis
contact healthcare professionals if child becomes unwell, appears pale/mottled, starts to vomit again (vomiting should not last longer than 3 days) has decreased urine output/wet nappies, irritable/lethargic and has cold extremities.
mechanisms of infectious diarrhoea
Secretory mechanism: ↓ absorption, ↑ secretion & electrolyte transport –> Watery stool. caused by Cholera, E. coli , Clostridium difficile and cryptosporidium (in HIV infection)
Mucosal Invasion: Inflammation, ↓ mucosal surface area and/or colonic reabsorption and ↑ motility –> stool with Blood and ↑ WBC’s. Caused by Rotavirus, campylobacter, Salmonella, shigella, Yersinia
features of a gastroenteritis that suggest another diagnosis
- Fever – temperature >38 degrees or higher in children younger than 3 months & >39 degrees or higher in children aged 3 months and older
- Tachypnoea
- Altered consciousness level
-Neck stiffness - Bulging fontanelle in infants
- Non-blanching rash
- Blood and /or mucus in stool
- Bilious vomit
- Severe or localised abdominal pain
- Abdominal distension or rebound tenderness
mechanisms/causes of dehydration
isonatraemic - proportional loss of water and sodium
hyponatraemic - intake of large quantity of water, fall in serum sodium, resulting is shift of water form extracellular to intracellular compartment causes brain oedema and marked extracellular dehydration and shock
hypernatraemic - water loss exceeds the sodium loss with resultant increase in plasma sodium concentration. This can happen when there is low sodium diarrhoea or high insensible water loss. There is shift of water from intracellular to extracellular compartment and therefore less signs of dehydration and more features of hypertonia, hyperreflexia, convulsions, drowsiness
when is stool microscopy and culture indicated in gastroenteritis
what other investigations are done
Recent travel abroad
The diarrhoea is not improving by day 7
Suspected septicaemia
Blood and /or mucus in stool
Immunocompromised child
blood culture if starting Abx
U+Es and glucose if dehydrated/starting fluids
IV fluid treatment of shock
treat with fluid bolus 20 ml /kg of 0.9% sodium chloride by rapid intravenous infusion.
Give a second bolus of 20 ml /kg of 0.9% sodium chloride by rapid intravenous infusion if shock persists. Considers other causes of shock.
Once symptoms and signs of shock resolve, start rehydration using intravenous fluids
what fluid is generally used for maintenance
0.9 % sodium chloride and 5 % dextrose
how do you calculate volume of maintenance fluids for 24 hours
100ml/kg first 10kg
50ml/kg second 10kg
over 20kg 20ml/kg
how should weight and U+Es be monitored in fluid therapy
Weight and u&e’s should be measured prior to commencing intravenous fluids and then at least every 24 hours if u&e’s are normal.
Measure blood glucose when starting intravenous fluids and at least every 24 hours or more frequently if there is risk of hypoglycaemia.
when and what Abx are given for treatment of diarrhoea
Campylobacter – Erythromycin shortens the duration of illness and shedding of bacteria
Clostridium difficile – metronidazole or vancomycin
Nontyphoid salmonella, shigella , vibrio cholerae, Giardia, Yersinia and cryptosporidium
what fluid is typically used for acute resuscitation
0.9% saline
pyloric stenosis
- presentation
- investigation
- management
first few weeks of life, pale hungry baby with FTT and projectile vomiting + crying after feeds
diagnosis is by abdominal USS which shows pyloric hypertrophy
blood gas shows hypochloric metabolic alkalosis
treatment is laparoscopic pyloromyotomy (known as “Ramstedt’s operation“) - excellent prognosis
post-gastroenteritis complications
Lactose intolerance
Irritable bowel syndrome
Reactive arthritis
Guillain–Barré syndrome
coeliac disease presentation
can often be asymptomatic
may present when weaning starts
possible symptoms
Failure to thrive in young children
Diarrhoea
Fatigue
Weight loss
Mouth ulcers
Anaemia secondary to iron, B12 or folate deficiency
Dermatitis herpetiformis is an itchy blistering skin rash that typically appears on the abdomen
coeliac disease diagnosis
Investigations must be carried out whilst the patient remains on a diet containing gluten
Check total immunoglobulin A levels to exclude IgA deficiency before checking for coeliac disease specific antibodies:
Raised anti-TTG antibodies (first choice)
Raised anti-endomysial antibodies
Endoscopy and intestinal biopsy show:
“Crypt hypertrophy”
“Villous atrophy”
when to suspect IBD in children
children and teenagers presenting with perfuse diarrhoea, abdominal pain, bleeding, weight loss or anaemia. They may be systemically unwell during flares, with fevers, malaise and dehydration
may have extraintestinal features such as eye, joint and skin symptoms
when to suspect IBD in children
children and teenagers presenting with perfuse diarrhoea, abdominal pain, bleeding, weight loss or anaemia. They may be systemically unwell during flares, with fevers, malaise and dehydration
may have extraintestinal features such as eye, joint and skin symptoms
what is biliary atresia
when to suspect
management
where a section of the bile duct is either narrowed or absent resulting in cholestasis
babies with a persistent jaundice, lasting more than 14 days in term babies and 21 days in premature babies
measure the bilirubin and conjugated only will be elevated
management is surgical
causes of intestinal obstruction
Meconium ileus
Hirschsprung’s disease
Oesophageal atresia
Duodenal atresia
Intussusception
Imperforate anus
Malrotation of the intestines with a volvulus
Strangulated hernia
presentation of intestinal obstruction
Persistent vomiting. This may be bilious, containing bright green bile
Abdominal pain and distention
Failure to pass stools or wind
Abnormal bowel sounds. These can be high pitched and “tinkling” early in the obstruction and absent later
investigation is suspected intestinal obstruction
abdominal X-ray is first line - absence of air in rectum
initial management intestinal obstruction
emergency referral to paediatric surgical unit
NBM, insert NG tube, IV fluids
what is Hirschsprung’s disease
congenital condition where nerve cells of the myenteric plexus are absent in the distal bowel and rectum - absence of parasympathetic ganglion cells
length of lost innervation varies
what family pattern does Hirschsprung’s disease occur in
usually in isolation but does have genetic associations
Downs syndrome
Neurofibromatosis
Waardenburg syndrome (a genetic condition causing pale blue eyes, hearing loss and patches of white skin and hair)
Multiple endocrine neoplasia type II
how does Hirschsprung’s disease present
varies significantly depending on length of gut affected
can present with acute intestinal obstruction shortly after birth or more gradually developing symptoms:
- Delay in passing meconium (more than 24 hours)
- Chronic constipation since birth
- Abdominal pain and distention
- Vomiting
- Poor weight gain and failure to thrive
what is Hirschsprung-associated enterocolitis (HAEC)
inflammation and obstruction of the intestine occurring in around 20% of neonates with Hirschsprung’s disease.
It typically presents within 2-4 weeks of birth with fever, abdominal distention, diarrhoea (often with blood) and features of sepsis.
It is life threatening and can lead to toxic megacolon and perforation of the bowel.
It requires urgent antibiotics, fluid resuscitation and decompression of the obstructed bowel.
diagnosis and management of Hirschsprung’s
definitive diagnosis is with rectal biopsy
management is surgical removal of the affected bowel
Intussusception
- diagnosis
- management
- complications
diagnosis; USS or contrast enema
management; therapeutic enemas can be used. if failed, surgical management
Obstruction
Gangrenous bowel
Perforation
Death
appendicitis
- signs and symptoms
- diagnosis
- management
S&S
- anorexia, N&V
- Rovsing’s sign; palpation of LIF causes pain in RIF
- guarding
- rebound and percussion tenderness (suggest rupture and peritonitis)
diagnosis: clinical presentation and raised inflammatory markers but CT/USS can be used to rule out differentials
management: appendicectomy; better by laparoscopic
when to suspect Kawasaki’s disease
fever >5 days
additional features:
- bilateral conjunctival injection without exudate
- erythema and cracking of lips, strawberry tongue, or erythema of oral and pharyngeal mucosa
- oedema and erythema in the hands and feet
- polymorphous rash
- cervical lymphadenopathy
causes of non-blanching petechial/purpuric rash
meningococcal septicaemia
Henoch-Schonlein Purpura
Idiopathic thrombocytopaneia purpura
Non-accidental injury
suspected meningitis actions
A-E and sepsis 6
obtain IV access and call seniors
fluid, Abx and oxygen IN
blood cultures, lactate and urine output OUT
bloods for FBC, CRP, Blood culture, lactate, whole blood real-time PCR testing for Meningococcus and Pneumococcus
LP if not contraindicated but shouldn’t delay Abx being given - third gen cephalosporin
suspected meningitis Abx
- under 3 months
- over 3 months
under 3 mo - IV ceftriaxone with amoxicillin for listeria cover
over 3 mo - IV ceftriaxone
What bacterial causes of meningitis are more prevalent in
- under 3 mo
- 3 mo to 5 years
- over 5 years
under 3 mo - listeria, E. coli, Group B strep
3mo-5yrs; Niesseria Meningitides, Streptococcus pneumoniae, Haemophilus influenza B
over 5 (same as adults) - niesseria or strep pneumonia
what are the most likely viral causes of meningitis
enteroviruses (85%, especially coxsackie and echovirus).
Other viruses include adenovirus, mumps, EBV, CMV, Varicella zoster, Herpes Simplex virus, HIV.
risk factors for bacterial meningitis
- asplenia
- basal skull fracture
- attendance at daycare/crowding
- low family income
- children with facial cellulitis, periorbital cellulitis, sinusitis, and septic arthritis
- maternal infection and pyrexia at delivery
Indications for Dexamethasone in suspected/confirmed Meningitis
- Frankly purulent pus
- CSF wcc > 1000/microlitre
- Raised CSF wcc with CSF Protein > 1g/l
- Bacteria on Gram stain
give with first dose of Abx and never more than 12 hours after
usually given qds for 2-4 days under senior clinician
where should the needle enter in an LP
into the L4/L5 intervertebral space, With the child on his/her side with the child’s back in a vertical position then the L5 vertebrae is vertically below the iliac crest. The L4 L5 disc space is just above
when is LP contraindicated
- unstable child; signs of shock or respiratory insufficiency
- signs or symptoms of raised ICP
- extensive or spreading purpuric rash
- bleeding disorder
- after convulsions if not yet stabilised
- local infection at the LP site
acute complications of meningitis
- seizures
- raised ICP
- metabolic disturbance
- coagulopathies
- anaemia
- coma
- death
long term complications meningitis
- hearing impairment
- psychosocial problems
- epilepsy
- developmental/learnign difficulties
- neurological impairment
children need general paediatrician follow up + audiology assessment within two weeks
which pathogen in meningitis has the worst prognosis
group B streptococcus pneumonia
highest mortality and highest res of neurological complications
slapped cheek syndrome
fever and bright red clearly demarcated rash on cheeks
otherwise generally well
caused by parovirus
antenatal Hx and UTI risk
abnormalities such as renal pelvis dilatation, cysts, or poor production of amniotic fluid (oligohydramnios) may indicate antenatal renal abnormalities predisposing to infection.
Prematurity may indicate an increased overall infection risk
how can urine be obtained from an infant
clean catch sample is best method
if not possible can catheterise or suprapubic aspiration which should be ultrasound guided
management if UTI detected on dipstick
if nitrites and leukocytes +ve start antibiotics
if one positive start if clinical UTI
send samples for microscopy, culture and sensitivity (M,C&S)
what is checked for on a dipstick
- leukocytes
- nitrites
- blood (tumour, trauma, infection)
- protein (tubular or glomerular disease)
- ketones
In Renal disease, what are the significant levels of proteinuria?
> 20 mmol/ml - This may be significant, and may indicate tubular disease
> 200 mmol/mg - This is nephrotic range
complications of minimal change nephrotic syndrome are recognised in childhood?
- spontaneous bacterial peritonitis
- infection with streptococci
- recurrence
what parameters make a diagnosis of Minimal Change Nephrotic Syndrome less likely (meaning further investigations would be indicated)?
- abnormal renal function
- haematuria
- hypertension
when in gestation do the kidneys form?
5 weeks with glomeruli still forming until 34 weeks
What is the commonest congenital renal anomaly?
renal hypoplasia
Definition of atypical UTI; increased risk of renal screening
- seriously ill
- poor urine flow
- abdominal or bladder mass
- raised creatinine
- septicaemia
- failure to respond within 48 hours
- non E coli
Definition of recurrent UTI; requires investigations for an underlying cause
2 or more upper UTI
1 upper and 1 or more lower UTI
3 or more lower UTI
what features make an upper UTI more likely compared to lower?
Bacteriuria and fever of 38oC or higher +/- loin tenderness
Bacteriuria, loin pain/tenderness and fever of less than 38oC
Age less than 3 months
usually no systemic features in lower UTI
what developmental anomaly can underly UTIs
vesoureteric reflux - in 35% of cases in children
others; hydronephrosis, duplex system or obstructive lesions
management simple lower UTI
oral antibiotics for 3 days according to local guidelines, usually trimethoprim, nitrofurantoin, cephalosporin or amoxicillin. Parents should be asked to bring the children back if they remain unwell after 24-48 hours
management upper UTI
considered for admission to hospital. If not admitted oral antibiotics such as cephalosporin or co-amoxiclav should be given for 7-10 days
antibiotic prophylaxis UTI
not after first one but consider for recurrent or if structural abnormality such as VUR
investigations in atypical or recurrent UTI symptoms
3 investigations are used selectively depending on the age of the child and presence of atypical or recurrent UTI symptoms: Ultrasound scan, MCUG and DMSA.
indications for renal ultrasound in UTI
- Infants less than 6 months with confirmed UTI (acutely if infant has atypical or recurrent UTI)
- Children more than 6 months old only in the presence of atypical UTI
when is Micturating cystogram (MCUG) used in UTI
identify any vesicoureteric reflux (VUR), bladder abnormalities and posterior urethral valves within a few weeks after treatment of UTI
catheterizing the child in order to fill the bladder with a radio-contrast agent then taking x-rays as the infant voids urine..
Indications:
Infants younger than 6 months with atypical or recurrent UTI
Consider in children older than 6 months if dilatation on ultrasound, poor urine flow, non-E coli infection or family history VUR
when is DMSA used in UTI
DMSA in 4-6 months after infection
radionucleotide scan used to assess renal function and identify any scarring of the kidneys due to the UTI - predisposes to HTN
Healthy renal tissue takes up the isotope. Unhealthy or scarred tissue doesn’t take up the isotope and appears as a filing defect on DMSA scan. DMSA may be inaccurate if performed shortly after an infection.
Indications:
All children with recurrent UTI
Children under 3 years with atypical UTI
how do urinary infections present in children
can be quite non-specific
more specific with age - older children more classic triad of dysuria, frequency and haematuria
Abdominal pain
Haematuria
Bedwetting/enuresis
Constipation
Febrile convulsion
Dysuria
definition of enuresis
involuntary discharge of urine by day or night or both, in a child aged 5 years or older, in the absence of congenital or acquired defects of the nervous system or urinary tract
how is nocturnal enuresis defined
primary - child never achieved continence
secondary - child was dry for at least 6 months before
possible underlying causes of enuresis
- neglect/abuse
- disturbed sleep/wake cycle
- constipation
- diabetes mellitus
- UTI if recent onset
- rarely neurological disease
enuresis management techniques
- general fluid intake management and toileting patterns
- reward systems for agreed behaviours (not for dry nights)
- enuresis alarm
- desmopressin can be used for short term eg. sleepovers
bilateral dilated kidneys in a neonate
in a male child can mean posterior urethral valves – this is a very serious condition which if untreated can cause renal failure due to obstruction
scarlet fever
presentation
immediate management
reaction to group A strep toxins
most common age 2-6 years
presentation:
fever: typically lasts 24 to 48 hours
malaise, headache, nausea/vomiting
sore throat
‘strawberry’ tongue
rash
commence Abx immediately 10 days of pen V
complications of scarlet fever
otitis media: the most common complication
rheumatic fever: typically occurs 20 days after infection
acute glomerulonephritis: typically occurs 10 days after infection
invasive complications (e.g. bacteraemia, meningitis, necrotizing fasciitis) are rare but may present acutely with life-threatening illness
presentation of immune thrombocytopenia purpura
petechial and purpura often after a viral illness
surgical sieve for anaemia
V-acute bleed? haemorrhgaic disease of newborn?
I- malaria, helminth infection, transient aplastic anaemia secondary to parvovirus, inflammatory bowel disease, severe cow’s milk protein enteropathy
T- acute bleed i.e. following an accident or non-accidental injury worsened by a clotting disorder
A- pernicious anaemia very rare in children , coeliac, haemolytic anaemia, haemolytic uraemic syndrome
M- G6PD deficiency
I- IDA
N- leukaemia
C- inherited pure red cell aplasia (Diamond Blackfan Anaemia), thalassaemia sickle cell, spherocytosis, fanconis anaemia, clotting disorders, congenital infectionsions ie parvo B19
D- physiological anaemia of the newborn
E - menstruation, medication ie nitrofurantoin
when does sickle cell disease present
after 6 months when fatal haemoglobin is replaced
what is Henoch Schonlein Purpura
an IgA vasculitis that presents with a purpuric rash affecting the lower limbs and buttocks in children
often triggered by a recent infection and most common under 10 years
4 main features:
- purpuric rash (100%)
- joint pain (75%)
- abdominal pain (50%)
- renal involvement (50%)
abdominal complications HSP
gastrointestinal haemorrhage, intussusception and bowel infarction
renal involvement HSP
affects the kidneys in around 50% of patients, causing an IgA nephritis.
This can lead to microscopic or macroscopic haematuria and proteinuria.
If there is more than 2+ of protein on the urine dipstick the child has developed nephrotic syndrome and will have a degree of oedema
HSP management
exclude other causes of purpura!
then supportive management:
- steroids debatable for abdo pain/renal involvement
- closely monitor urine dip and BP for 6 months
most fully recover 4-6 weeks. small proportion develop renal failure
what are Kernigs and Brudzinkis signs
Kernigs +ve = Pain on lower leg extension with hip flexed
Brudzinkis +ve = Involuntary flexion of the knees and hips with neck flexion
differentials child with seizure and reduced consciousness
febrile seizure
encephalopathy
encephalitis/meningitis
sepsis/shock
brain tumour
metabolic disorder
epilepsy
poisoning/intoxication
could be post ictal - only if returns to normal within an hour
Indications for urgent head CT or MRI in seizure
Encephalopathic or coma
Suspected raised intracranial pressure
Progressive neurological deficit
Indications for elective MRI head in seizure
- In a child under 2 year of age at onset
- hard focal neurological signs
- a focal epilepsy
- associated significant learning difficulties
- an epilepsy resistant to full doses of 2 appropriate drugs
EEG urgent and non urgent indications in seizure
Urgent Indications:
suspected non-convulsive status
Non traumatic encephalopathy
Coma of unknown cause
Elective standard EEG if:
strong suspicion of epilepsy (to support classification)
developmental or language regression
NOT generally after a first afebrile seizure or febrile seizures
causes of delayed walking
central - delayed maturation, global developmental delay, any cause of hemiplegia, cerebral palsy
peripheral - spinabifida
muscular and neuromuscular e.g. DMD
environmental
orthopaedic e.g. DDH
metabolic/hormonal - hypoT, rickets
what is cerebral palsy
Static brain injury pre or shortly post birth, causing a motor and coordination dysfunction, usually with neuroimaging changes
neonatal causes of tachypnoea
sepsis
cardiac
respiratory
metabolic
pain - either acidosis causing compensatory tachypnoea or a raised ammonia which acts as a respiratory stimulant causing tachypnoea
main groups of inborn errors of metabolism causing hyperammoniaemia
urea cycle disorders and the organic acidaemias
Urea cycle disorders
ammonia level is markedly raised and often over 1000 micromols/L and there is liver dysfunction
blood gas often shows a respiratory alkalosis due to the ammonia acting as a respiratory stimulant
organic acidaemia
mixed picture of metabolic acidosis and hyperammonaemia - less high than urea cycle disroders
The first pointer to diagnosis is a metabolic acidosis that does not respond to standard fluid resuscitation and then the finding of a raised anion gap caused by the presence of the abnormal organic acid.
Methylmalonic acidaemia and propionic acidaemia are the 2 most common organic acid disorders.
presentation in born errors of metabolism
presents neonatally
often reduced consciousness
blood gas abnormalities and often altered anion gap
can be very sick and need specialist review
definition of global developmental delay
A child has global developmental delay if they have a significant delay in milestones in two or more areas
definition of cerebral palsy
A disorder of tone, posture and movement, caused by a non-progressive brain lesion in a developing brain
types of cerebral palsy
spastic (UMN signs)
ataxic
dyskinetic aka choreoathetoid
in reality is often mixed
medications which can be used to help manage increase tone in children with cerebral palsy?
Baclofen
Diazepam
Botulinum toxin
what is Gower’s sign
pt uses hands and arms to walk to and then up the body in order to stand
sign of weakness of the proximal muscles
seen in Duchenne Muscular Dystrophy
Duchenne Muscular Dystrophy
most common muscular dystrophy in northern Europe and is due to an abnormality of the dystrophin gene
X linked disorder
measure CK +genetic testing to diagnose
Steroid treatment has been shown to delay the progression
can also present with early neurological signs due to expression of dystrophin protein in the brain
long term complications of conditions such as DMD
Reduced mobility, loss of ambulation
Scoliosis – spinal surgery will be needed if scoliosis significant
Feeding problems – may cause malnutrition – gastrostomy feeds may be required
Cardiac involvement (depending on condition, but common in DMD)
Respiratory weakness- nocturnal non-invasive ventilation may be required
side effects of steroids in children
Increased appetite – with weight gain
Behavioural deterioration – especially if pre-existing problems
Hypertension
Growth failure
Gastrointestinal irritation
Bone thinning
at what times are DKA most likely to occur in T1 DM
At diagnosis
During a growth spurt/puberty
Insulin omission for any reason
(DKA usually develops over 24 hours but can develop faster particularly in young children or patients on insulin pumps)
how does DKA present
may initially have polyuria, polydipsia, weight loss, excessive tiredness
more specific to DKA symptoms are nausea or vomiting, abdominal pain, hyperventilation, dehydration and reduced level of consciousness
when should a suspected DKA be sent immediately to an acute paediatric facility (HDU)
what needs measuring on arrival
child not known to have diabetes with glucose level is above 11 mmol/litre and suggestive symptoms
child known to have diabetes with any symptoms of DKA - but only need transfer if ketones elevated or can’t measure
on arrival measure
capillary blood glucose, capillary blood ketones (beta-hydroxybutyrate) capillary or venous pH and bicarbonate
DKA diagnostic criteria
- Acidosis (indicated by blood pH below 7.3 or plasma bicarbonate below 18 mmol/litre) and
- Ketonaemia (indicated by blood beta-hydroxybutyrate above 3 mmol/litre
Diagnose severe DKA in children and young people with DKA who have a blood pH below 7.1.
what is the main cause of morbidity and mortality in childhood DKA
from cerebral oedema due to rapid correction
The aim of therapy is very gentle and slow correction to avoid cerebral oedema
initial management DKA
- inform senior clinician
- explain to child and parents
- fixed rate insulin infusion
- IV fluids
- may need potassium
- avoid hypo by adding dextrose when glucose is coming down
- monitor for signs of cerebral oedema
can give O2, consider ABX and consider NG tube
what is Kussmaul breathing
deep and labored breathing pattern often associated with severe metabolic acidosis, particularly diabetic ketoacidosis (DKA) but also kidney failure.
In metabolic acidosis, breathing is first rapid and shallow but as acidosis worsens, breathing gradually becomes deep, labored and gasping.
It is this latter type of breathing pattern that is referred to as Kussmaul breathing.
what needs recording once DKA diagnosed
blood gas - pH and pCO2, lactate
monitor ketones
level of consciouss
vital signs
clinical evidence of dehydration + weight
plasma sodium, potassium, urea and creatinine plasma bicarbonate
when should you think about sepsis in a child with DKA
has any of the following: fever or hypothermia, hypotension, refractory acidosis, lactic acidosis.
what fluids and when should be given in DKA
how much
only give oral fluids if alert, not nauseated or vomiting, and not clinically dehydrated
otherwise give IV and if IV don’t let them have oral until ketosis is resolving
give the fluid gradually - not a bolus unless can consider in severe
Use 0.9% sodium chloride without added glucose until the plasma glucose concentration is below 14 mmol/litre.
Ensure that all fluids (except any initial bolus) administered to children and young people with DKA contain 40 mmol/litre potassium chloride, unless they have renal failure.
first 48 hours adding the estimated fluid deficit to the fluid maintenance requirement
assume if pH>7.1 5% deficit
if <7.1 assume 10% deficit
maintenance if they weigh less than 10 kg, give 2 ml/kg/hour if they weigh between 10 and 40 kg, give 1 ml/kg/hour if they weigh more than 40 kg, give a fixed volume of 40 ml/hour - this is reduced volume to avoid cerebral oedema
when should insulin be started and how
fixed rate insulin infusion start 1-2 hours after fluids started
use a soluble insulin infusion at a dosage between 0.05 and 0.1 units/kg/hour
when should normal insulin be restarted
subcut at least 30 minutes before stopping intravenous insulin. For a child or young person with DKA who is using insulin pump therapy, restart the pump at least 60 minutes before stopping intravenous insulin
signs of cerebral oedema
when to treat and how
assess for oedema if any of headache, agitation/irritability, increased BP or fall in HR
treat with mannitol or hypertonic sodium chloride if a child with DKA has any of deterioration in level of consciousness abnormalities of breathing pattern (for example respiratory pauses), oculomotor palsies, pupillary inequality or dilatation
escalate
potassium in DKA
insulin moves potassium which can lead to hypokalaemia
if falls below 3mmol/L consider temporarily suspending the insulin infusion and discuss with ICU
potassium in DKA
insulin moves potassium which can lead to hypokalaemia
if falls below 3mmol/L consider temporarily suspending the insulin infusion and discuss with ICU
basic types of insulin regimen in T1DM
- Multiple daily injection basal–bolus insulin regimens: injections of short-acting insulin before meals, together with 1 daily injection of long-acting insulin.
- Continuous subcutaneous insulin infusion (insulin pump therapy): a programmable pump and insulin storage device that gives a regular or continuous amount of insulin (usually a rapid-acting insulin analogue or short-acting insulin) by a subcutaneous needle or cannula.
optimal target ranges for short-term plasma glucose control
Fasting plasma glucose level of 4–7 mmol/litre on waking
a plasma glucose level of 4–7 mmol/litre before meals at other times of the day
a plasma glucose level of 5–9 mmol/litre after meals
a plasma glucose level of at least 5 mmol/litre when driving
measure 5x a day - more in illness or activity
management of mild to moderate hypoglycaemia
Give fast-acting glucose (for example, 10–20 g) by mouth and recheck BM within 15 minutes
repeat if persists
once resolved give oral complex long-acting carbohydrate to maintain blood glucose levels
treatment of severe hypoglycaemia
if in hospital with IV access; give 10% intravenous glucose.
if no access give intramuscular glucagon or a concentrated oral glucose solution (for example Glucogel). Do not use oral glucose solution if the level of consciousness is reduced as this could be dangerous
what complications monitoring should children with T1DM have
Thyroid disease at diagnosis and annually thereafter until transfer to adult services
Diabetic retinopathy- annually from 12 years
Moderately increased albuminuria (albumin:creatinine ratio [ACR] 3–30 mg/mmol; ‘microalbuminuria’) to detect diabetic kidney disease- annually from 12 years
Hypertension- annually from 12 years.
Be aware of the following rare complications and associated conditions with type 1 diabetes:
Juvenile cataracts
Necrobiosis lipoidica
Addison’s disease.
In addition Children and Young People with Type 1 DM get screened for Coeliac Disease at diagnosis
what is Meckel’s diverticulum
congenital diverticulum of the small intestine
most common cause of massive GI bleeding requiring a transfusion in children between the ages of 1 and 2 years
presents with rectal bleeding, can cause obstruction and may be painful
investigation and management of Meckel’s diverticulum
‘Meckel’s scan’ should be used if haemodynamically stable
uses 99m technetium pertechnetate
mangamenet is surgical removal
traffic light system paediatric history
- colour
- activity; playing normally?
- respiratory; any difficulty breathing?
- hydration/circulation; feeding? drinking? nappies?
- other; have they felt hot? recorded temperatures? rashes?
APGAR score + what are the domains
assesses health of newborn baby at 1, 5 and 10 minutes looking at pulse, respiratory effort, colour, tone and irritability
A score of 0-3 is very low score, between 4-6 is moderate low and between 7 - 10 means the baby is in a good state
when is neonatal jaundice physiological or pathological
first 24 hours pathological
2-14 days physiological
> 14 days (21 in premature) pathological
if pathological screen for haemolytic anaemia and sepsis screen
