Paediatrics Flashcards
Paediatric life support routine
- Safety (MRI)
- Stimulate
- Shout for help
- Assessment 10secs - look,listen, feel
- Not breathing - 5rescue breaths (neutral head for babies and tilted back for infants and odler). C to E grip tehcnique and dont cover eyes
- assess for signs of life
- CPR 15c:2breaths
- assess for signs of life
- Repeat
Descrieb Chronic asthma, the patho, exam and mamagement
- Asthma = chronic inflammatory disorder of airways
- Diagnosis: Episodic symptoms. Wheeze confirmed by healthcare professional, diurnal variability, atopic history, nothing suggestive of alternative diagnosis.
- Red flags – Failure to thrive, focal signs, abnormal cry, dysphagia, stridor, nasal polyps, persistent wet cough, frequent infections, murmur, present since birth, FH, severe attack.
- Patho: Chronic inflammation of the bronchial mucosa associated with mucosal oedema, secretions and constriction of airway smooth muscle narrows the airway.
- Focus on: Pattern symptoms, triggers, severity, personal/family history atrophy
- Examination: Hyper expansion, pigeon chest, Harrison sulcus.
- Management: Aim is No daytime symptoms or waking at night, no exacerbations, no need for relievers, no limitations, normal lung function and minimal side effects.
Prevent brown, reliever blue
Acute Asthma
- Commonly from attack triggers
- Requires hospital when you havent repsonded dequately clinically so become exhausted and reduced O2 sats or reduced PEFR or FEV1 (<50%)
- Clinical - PEF<33% predicted, O2 sats <92% in high flow oxygen, silent chets, hypotension, fatigue, poor repsiraotry effort, reduced consciousness, agitation
- Management:
Bronchiolitis - Dx, management
- Bronchiolitis = Inflammation of bronchioles, in repsonse to viral infection, most commonly RSV. Less common are adenovirus, influenza, parainfluenza, mycoplasma pneumoniae.
- Major cuase of LRTi in infants with increased risk if premature, congenital cardiac or respuratory disease, downs syndrome and exposure to ciagerrette smoke.
- Clinical - – coryza, dry cough, breathing difficulties, poor feeding, end inspiratory crackles, wheeze, recessions, nasal flaring
- Investigations =Pulse oximetry, clunical diagnosis but possible CXR
- Management - humidified oxygen, CPAP may be used if ventilation required and feeding support (NG feeds or IV fluids)
- DDx - GORD, congenitla malformations,sasthma, foreign body apsiration.
Most make full recovery in 2weeks, but some have recurrent episodes cough and wheeze over few years and some may develop asthma.
80% caused by RSV
90% infants affected are 1-9
What is croup?
- Croup = acute laryngotracheobronchitis.
- Most caused by parainfluenza virus (respiratory synctital virus also) and bacterial infection.
- More common in winter and pea at 2 years old (6m-6rs)
- Clinical = symptoms LRTi (cough, fever) usually few days then characetristic barking cough, hoarse voice, stridor. Symptoms tpyiclaly start and worse at night
- MX = All with mild, mdoerate corup should get single dose oral dexamethasone (or oral prednisolone) and if too unwell to receive inhaled budesonide or IM dexamethasone. If severe then nebulised epinephrine (adrenaline) qith oxygen by face mask abd closely observe for 2-3hours after effects worn off.
The causative organisms of Pneumonia
Pneumonia - inflammation of the lung parenchyma with consolidation within alveoli. Can be caused by virsuses (More under 2 years) and bacteria.
- Newborn – GBS, gram negative enterococci
- Infants + young children – Viruses 9RSV/Adenovirus/rhinovirus. Influenza/parainfluenza. Bacteria – strep.pneumoniae (most common), H.influenzae (unvacc), bordatella pertussis, chlamydia trachomatis. S.Aureus in CF
- Every 5 years old – Bacteria, mycoplasma pneumoniae, streptococcus pneumoniae and chlamydia pneumoniae
- Always consider mycobacterium tuberculosis.
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Pneumonia - Inflammation of the lung parenchyma with consolidation within alveoli. Can be caused by viruses (more in under 2years) and bacteria.
Presentation: Fever, cough, increased work of breathing, tachypnoea, lethargy, poor feeding.
Exam: Tachypnea, coarse crackles, reduced 02 sats, nasal flaring, recessions.
DDx - Otitis media, Rhinnorrhea, Nasal polyps, Pharyngitis, Upper respiratory infections, asthm, bronchiolitis, Bronchitis
Investigations – CXR may confirm diagnosis, NPA aspirate for viral PCR, Bloods – generally helpful.
Management:
- Indications for admission – O2 sats<92%, apnoeas/grunting, unable to maintain fluids
- Antibiotics (newborn-broad s, older amoxicillin, over 5 amocixillin or oral macrolide)
- Small parapneumonic effusions in some and may resolve with antibiotics but persistent fever after 48hours antibiotics suggests pleural collection which needs drainage.
- With lobar collapse or atelectasis then consider 4-6weeks faster, CXR
- Complications – sepsis, acute respiratory distress syndrome, pleural effusion, empyema.
Chest Xray basics
Assess image quality: Rotation, inspiration (ribs), picture and projections (assume PA), exposure
Systematic approach:
- Airways and lungs + tracheal deviation
- Bones and soft tissues (scoliois, rib fractures, lytic lesions)
- Cardiac - size,borders, mediastinal masses
- Diaphragm - clear and crisp
- Extra body equipment
Used for checking NG placement.
Cystic fibrosis
CF = Autosomal recessive disease from mutations in a gene on chromosome 7 that encodes cystic fibrosis transmembrane regulator (CFTR) protein. Mmebrane chloride channel affects sodium transportation = thickened, sticky secretions
CF – abnormal ion transport across epithelia l cells. Dysregulation oof inflammation and defence against infection. Pancreatic ducts become blocked. And abnormal function ins sweat glands.
Clinical features: Most picked up via screening (heel prick) .
- Neonates – meconium ileus
- Children – frequent infection, failure to thrive, wheeze, cough, steatorrhea.
In most, def of pancreatic co-enzymes leads to malabsorption, steatorrhea, and failure to thrive.
Investigations – Part of new-born blood spot test with immunoreactive trypsinogen. Gold standard is sweat test with pilocarpine iontophoresis as failure of normal reabsorption of sodium and chloride by sweat duct leads to abnormally salty sweat (high chloride). A CF genotype using DNA analysis is also available for more common mutations to help confirm diagnosis (DeltaF508)
Management: Prevent progression and maintain adequate nutrition and growth.
- Respiratory management – recurrent and persistent chest infections (prophylactic antibiotics). Physiotherapy to clear airway continuous prophylactic antibiotics. Bilateral lung transplant is end stage treatment. Vaccines, Mucolytics
- Nutritional management – pancreatic replacement therapy, high calorie diet. Annual OGTT and creon replacement
- Targeted – Lvacaftor/Lumacaftor
- Teens and adults – treating more complications etc.
Given monoclonal antibodies in winter to try to stop them developing bronchiolitis.
Bacterial Meningitis
-
Patho = Usually followes bactaraemia and msot damage is from the response to infection,a nd leads to cerebral oedema, raised intracranial pressure and decreased cerebral blood flow.
- Neonatal -3m = GBS, E.Coli, listeria monocytogens
- 1M-6y = Neisseria meningitides, streptococcus pneumonias, haemophilus influenza
- >6y = neisseria meningitides, streptococcus pneumonia
- Presentation = Headache, neck stiffnes, photophobia. Some may have sepsis so tachycardia, tachypnoea, prolonged capillary refill time and hypotension (shock)
- Investigations = lumbar punctue for CSF for antibiotic sensitives and organism, blood culture, throat swabs
- Management - antibiotics and supportive therapy. 3rd gen cephalosporin (ceftriaxone). Dexamethasone might help long temr complication risk.
- Complications = Hearign impairment, local vascultitis, local cerebral infarction, subdural effusion, hydrocpehalus, cerebral abscess.
- Prophylaxis = Rifampicin or ciprofloxacin to eradice nasopharyngeal carriage in household contacts for meningococal or Hib or vaccinated if group C
Viral Meningitis
- Usually less severe, most make full recovery
- organisisms - mostly viral (enterovirus, EBV, adenovirus, mumps). Uncommon is thing slike mycoplasma species or borell aburddorferi (lymes), particularly in immunocomprimised.
Acute otitis media
- Acute otitis media = infeciton of the middle ea,r often following iral URTI but can also be caused by bacterial infection. Very common in preschool children.
- Pathogens - Viruses, especially RSV and rhinovirus including strep pneumonia, haemophilus influenza and Moraxella catarrhalis
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Clinical:
- Often non specific with fever, tahcycardia, vomtiing and distress although older choldren may localise pain to right ear
- O/E- otosocpy reveals red, bulging eardrum with loss of light reflex. Perforation of eardrum may occur, with purulent discharge.
- Recurrent ones can lead to otitis media with effusion “glue ear”. Hearing loss and developmental delay, may be treated with grommets.
- Recurrent infections are asosicated with otitis media with effusion (OME). Mastoiditis and meningitis are now incommon complications of acute otitis media
- Mx = Mx – reassurance (usually self resolves in 3/5days, analgesia and fluids and antibiotics not usually required unless not resolving. Kids get more ear infectiosn due to shorter, more horizontal eustachian tubes that let bacteria nad viruses find their way in more easily and tubes are narrower so more likely to get blocked.
Impetigo
- Impetigo = highly contagious skin infection commonly on the face in infants and oyung children, espeically if pre-existing skin disease.
- Eryhtematous macules develop into characteristic honey-coloured cursted lesions.
- Sometimes due to streptococcal infection
- Topical antibiotics can be used for mild xases (mupirocin) but fo rmoe severe then systemic Abs like flucloxacillin.
- Nasal carriage is important source of reinfection and can be eradictaed by nasal cream with chlorhexidine and neomycin.
- Complications – cellulitis, lymphadenitis and rarely scarlette fever, glomerulonephritis, staph scalded skin syndrome (SSSS)
Chicken Pox - Varicella Zoster virus
- Common childhood disease caused by primary infection with the varicella zoster virus. Highly infectious transmission occurring by droplet infection, direct contact or contact with soiled materials. Average incubation period is 2weeks. The infectivity is from 2days before eruption of the rash until all lesions have crusted over.
- Clinical =brief coryzal period, then eruption of an itchy rash which progresses from macules to papules to vesicles before crusting over. This starts on scalp or trunk and spread centrifugally; mucous membranes may be involved and typically new crops develops over 3-5days.
- Complications – unusual in immunocompetent children but can include secondary bacterial infection of skin with staphylyococci or streptococci and encephalitis which appears 3-6days after onset o the rash. Chickenpox can be very serious if immunocompromised child and in the newborn infant if mother develops chickenpox just before deliver. Persisting fever after the typical chickenpox rash has erupted should prompt evaluation for secondary infection
- Mx – clinical diagnosis but can isolate virus from fluid and identified. Generally symptomatic treatment but for severe or immunosuppressed can give acyclovir. Varicella zoster immune globulin provides passive immunity and should be given to immunosuppressed or newborn if mother develops chickenpox or shingles in 7days before or after birth. Live, attenuated vaccine exists but not given routinely in UK.
UTIs
Symptoms and signs: Usually non-specific.
- Infants – Fever, vomiting, lethargy, poor feeding, irritability
- Older children – fever dysuria, increased frequency, abdominal pain, vomiting, incontinence.
Investigations: Urinanalysis + Urine culture and sensitivity – E.Coli and klebsiella. No further ones unless concerned about sepsis.
Mx:
- If good clinical evidence or <3m then start antibiotics
- Upper UTI/Pyelonephritis = Cefalexin or Co-Amoxiclav
- Lower UTI – trimethoprim
- Under 3m – IV antibiotics
Further investigations after first ab confirmed diagnosis UTI:
<1 = For children do ultrasound (check structural things, within 6wks), DMSA (4-6m after to check renal parenchymal defects), MCUG- micturating cystorethrogram (check renal reflux). Also prophylactic antibiotics
1-3yrs = US, DMSA
3+ = US
Explanation: Caused by microorganisms in urinary tract. Usually UTIs are caused by bacteria from GIT.
Urinalysis: When suspected UTI or health problem that can cause abnormality in urine.
Presence RBC/WBC, presence bacteria/organisms, presence substances like glucose, pH, concentration.
Treatment: 5 days: Cefalexine trimethoprim, nitrofurantoin amoxicillin. (Depends on culture)
UTI: pus clel, nitrites
Microscopy >100/microlitre/100000/ml/10^8 of single type bacteria.
Culture: bacterial growth 100/microlitre/100000/ml/10^8 per litre.
Immunsiation schedule for children
Gastroenteritis
Gastroenteritis = Infection of the GIT. Rotavirus is most common cause in developed countries, particularly winter and early spring.
- Presentation – diarrhoea, vomiting, fever, poor feeding, shock. Green vomit (bile stained) is intestinal obstruction till proven otherwise.
Investigations: not usually indicated.
- Stool culture – if septic or blood in stools
- U+Es – If IV fluids required
- Glucose
- Blood culture (if started on Antibiotics)
- Assess dehydration.
Mx – correct dehydration (oral/IV fluid replacement). No place for antidiarrheal drugs (loperamide, Lomotil) and antiemetics as prolong bacteria excretion in stools etc, Antibiotics only if suspected sepsis/malnourished/ immunocompromised etc)
Causes: Most are viral (rotavirus), adeno or Campylocbacter (CB produces gripes an dbloody diarrhoea). E.Coli 157 (mostly for children on farms). If bloody diarrhoea send stool to check for CB as notifiable disease.
Abdominal pain and blood or mucus in stool suggests invasive bacterial pathogen. Toxic with high fever appearance is more likely bacterial.
Examine for signs of dehydration and fever, abdominal distention, hernia orifices and genitalia. Weight is a big determinant of dehydration as clinical dehydration is usually 5-10% weight lost and shock is >10%.
Assessment dehydration
Isonatraemic and hyponatraemic dehydration – when have ltos of water or hypotonic substances theres more loss of sodium than water so shift of water from ECF to ICF. This leads to increase in brain volume and can lead to seizures. More so in poorly nourished infants in developing countries.
Hypernatraemic dehydration – water loss eceeds sodium loss and plasma sodium concentration increases, Water goes ECF->ICF. Depression of fontonelle, reduced tissue elasticity and sunken eyes.
Full management schematic of dehdration due to gastroenteritis
Mnagement of dehdryation
Management: Rehydration with correction of fluid and electrolyte imbalance.
- No signs dehydration then encourages normal fluid intake and oral rehydration salts as supplemental fluids if worsens.
- Evidence clinical dehydration – give 50mL/kg ORS over 4hours in addition to maintenance fluids as ORS.
- Evidence shock (decreased conscious levels, poor perfusion, hypotension) then give 20mL/kg 0.5% saline rapidly and repeat if needed then continue with IV rehydration with 0.9% saline adding 100mL/kg to maintenance requirements.
Calculating maintenance fluids:
- 100mL/kg/24h for 0-10kg bodyweight
- 50mL/kg/24h for 10-20kg bodyweight
- 20mL/kg/24h for >20kg bodyweight
- If diarrhoea continues, give additional 5mL/kg ORS for each large watery stool.
GORD
Gastro-oesophageal reflux = involuntary passage of gastric contents into oesophagus
- Functional immaturity of lower esophageal sphincter
- Predominately fluid diet
- Mainly horizontal posture
- Short intra-abdominal length of oesophagus.
Reflux is common in infancy and usually benign and self-limitinglimiting but when termed ‘GORD’ it causes significant problems and is treated.
Clinical:
- Infants: Recurrent vomiting or regurgitation after feeds, Discomfort lying flat after feed, Usually well and normal growth
- Older children: Heartburn, Epigastric pain, Vomiting
Investigations: Most can be diagnosed clinically with no investigations. More common in those with cerebral palsy or neurodevelopmental disorders. Some techniques to confirm:
- 24h esophageal pH monitoring in older children or impedance studies in infants
- Barium studies – might be to exclude underlying anatomical abnormalities
- Endoscopy – for those with suspected esophagitis.
Management: Mostly reassurance and 95% resolve by 12/18m.
- Feeding assessment and smaller, more frequent and thicker feeds
- Alginate therapy (Gaviscon)
- 4 week trial PPI/H2 receptor antagonist
Complications – faltering growth from severe vomit, oesophagitis, recurrent pulmonary aspiration, dystonic neck posturing etc.
Coeliac Disease
What is it: Autoimmune disease where gluten ingestion results in dagame to the mucosa of the proximal small intestine with subsequent atrophy of the villi and loss of absorptive surface.
Gliadin + Glutenin = Gluten
Gliadin causes damaging immune response in proximal small intestinal mucosa.
Family predisposition with approx. 10% of 1st degree relative affected, HLA-DQ2 found in 95%. More common in Caucasian people and association with other autoimmune disease, downs syndrome and Turners syndrome.
Clinical features:
Classical presentation:
- Malabsorption at 8-24 after weaning
- Faltering growth and buttock wasting
- Abdominal pain and distention
- Abnormal stools
Often: Non-specific GI symptoms, anaemia (iron and/or folate deficiency)
Investigations:
- Bloods: Serological screening tests
- Anti-tTG (immunoglobulin A tissue transaminase antibodies)
- EMA (Endomysial antibodies)
- Biopsy = mucosal changes of small intestine.
Mx –Gluten free diet under dietician supervision. Adhere for life as otherwise you risk micronutrient deficiency, osteopenia, risk of increased bowel malignancy and mall bowel lymphoma.
Obesity in children
- Aetiological factors: excess caloric intake, reduced activity levels, prevalence of obesity in family and rarely endocrine or chromosomal cause like Cushing’s, hypothyroidism or Prader-Willi.
- Consequences: long term health risks (diabetes, hypertension, ischaemic heart disease), emotional disturbance, obstructive sleep apnoea.
BMI = weight in kilograms/ height^2 (m). Age and sex specific in children so plot on BMI chart.
Overweight = BMI over 91st centile
Obese = GMI over 98th centile.
- Prevention – decreased fat intake, increased fruit + veg, reduction in screen time, more physical activity and education.
- Mx – drug treatment for over 12 and BMI>40 (extreme obesity) or >35 and complications. Orlistat (reduces abrosption dietary fat and get steatorrhea), bariatric surgery – unless mature,
Faltering weight gainc causes
Faltering weight gain = Sustained dorp down two centile spaces. SLower weight gain than expected for age and sex in infants and preschool children and mostly due to inadequate nutritional intake. Compelx an dmultifactoria
- inadequate nutritioal intake - lakc healthy food, maltreatment, lack knowledge
- Inadequate absroption nutrients - vomiting, GORD, coeliac
- Psychological deprivation
- neglect or child abuse
- Undelryign patho - imapired suck/swallow
- Excessive energy expenditure from udnelryign problems
- Inadequate retention
- Malabsroptipn
- Failrue to utilise nutrient
- Increased requirements
Hepatomegaly causes
- Infection – congenital, infectious mononucleosis, hepatitis, malaria, parasitic infection
- Hematological – sickle cell anemia, thalassemia
- Liver disease – chronic active hepatitis, portal hypertension, polycystic disease
- Malignancy – leukaemia, lymphoma, neuroblastoma, Wilms tumour, hepatoblastoma
- Metabolic – glycogen and lipid storage disorders
- CV – heart failure
- Apparent – chest hyperexpansion from bronchiolitis or astma.
Appendicitis
Appendicitis = inflammation of the appendix secondary to obstruction (usually by faecolith) or lymphoid hyperplasia. It is the most common surgical emergency and can occur at any age, although it is rare in infancy when lumen of appendix is wider and well drained.
Clinical features:
- Symptoms = Classically abdo pain which starts poorly localized, periumbilical pain and then becomes sharper and localized to RIF. Pain is usually severe and worse on movement to child may lie still. Commonly associated with anorexia, nausea, vomiting, diarrhea or constipation. Anorexia, vomiting.
- Signs = Fever, pain aggravated by movement, tenderness and guarding in RIF (McBurneys point- 1/3 RASIS to umbilicus). If unwell, signs peritonism like high temp, abnormal observations.
Red flag – Perforated gangrenous appendix can cause peritonitis. Suspect this if high fever >40, profuse vomiting, severe abdominal tenderness/guarding or absent bowel sounds.
Investigations – FBC (increased wcc), CRP, ultrasound scan
Management – monitor obs + analgesia with fluid resuscitation and IV antibiotics if concerns perforation and unwell. Appendicectomy (laparoscopic or open) with IV antibiotic cover. Complications are perforation, sepsis, abscess, appendiceal mass.
Pyloric stenosis
Pyloric stenosis – due to hypertrophy of smooth muscle of pylorus causing gastric outlet obstruction and more common in boys, commonly presenting in first 2-8weeks of life.
Clinical – persistent, projectile nonbilious vomiting after feeds. The infant remains hungry and eager to feed after vomiting. Weight loss, constipation, dehydration and mild jaundice develop after a few days. Hypochloraemic metabolic alkalosis with low plasma sodium and potassium occurs from the vomiting.
Dx
- Test feed: Gastric peristalsis wave moving form L->R. Pyloric mass Oliver shaped mass in RUQ.
- Capillary blood gas – Hypochloraemic metabolic alkalosis, low sodium and potassium
- Ultrasound
Mx – Rehydration correct electrolyte imbalances, pyloromyotomy.
Key gross motor milestones
Key fine motor and visual milestones
Key congitive and social milestones
Key speech and hearing milestones
Red flags for children
- Excessive head lag beyond 8w
- Persistence of primitive reflexes beyond 6m
- Hand preference before 18m
- Not interacting with other children at 3y.
Red Flags: Teaching
- 10 week old not smiling -could be visual problem, bell’s palsy, neglect, maternal mental health problems
- 9month old left-hand preference (hand preference should be normally after 1), could be birth injury (brachial plexus injury etc), muscle problems, spasticity (cerebral palsy). Could do physiotherapy
- 19month old not walking – worried about missing Duchenne muscular dystrophy (proximal muscle weakness, Trendelenburg gait), might just be children find bottom shuffling easier, could be DDH (development hip dysplasia). Blood test to check CK for DMD (would be really high), occupational therapy…
- 2 ½ year old not putting words together – could be autism spectrum disorder, cleft palate, tongue tied, refer to speech and language therapy.
What is a baby check and the further chekcups
Baby check – head to toe (head circumference, fontanelle, eyes, red light reflex, pallet, chest wall, heart (murmurs), hip (DDH), back (dimples, spina bifida), is there an anus and intact.
Hearing check, blood spot (heel prick) test.
- 1-2w old – health visitor check sleeping, vaccination, feeding, adjustment
- 6-8weeks – through physical exam by GP
- 2yrs and 3months – ASQ ages and stages questionnaire.
- Starting nursery check by health visitor
What age?
- Gross motor – wriggle + flex
- Fine motor + vision – move fingers, visual field very shallow
- Hearing + speech – startled to loud noise, newborn hearing screen
- Personal + social – cry
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NEWBORN
At 6 weeks – developed a couple of skills like hold head up (head control), start to see further (fix + follow), smile at 6weeks.
Sleep on back due to risk of sudden infant death syndrome. But to develop gross motor skills need time on tummy when playing. Helps them move on to moving and different positions.
What age am I
- Gross motor – tummy time, push up with arms, keep head up
- Fine motor + vision – might be grabbing for toys,
- Hearing + speech – more vocalization
- Personal + social – more giggling alongside smiling
3 months
WHat age am I
- Gross motor – sitting (6-9m), rolling (front to back first), usually everything goes in their mouth
- Fine motor + vision – palmar grasp, transfers toys one hand to another
- Hearing + speech – understand the word no
- Personal + social – more interested in playing, start to weane on to solid foods
6months
What age am I
- Gross motor – (9-12) crawling, might be able to hold on to furniture,
- Fine motor + vision – pincer grip for small objects,
- Hearing + speech – more repetitive sounds like faint sounding like mama, know their own name
- Personal + social – stranger awareness
9months
what age am i
- Gross motor – walking (furniture, hands held then without- 12-18months)
- Fine motor + vision – play more, casting (drop something, you pick up, they do it again), clap, wave, peekaboo
- Hearing + speech – mama/dada
- Personal + social – hold a cup with 2 handles and drink, might hold a spoon
12months
What age am I
- Gross motor – walking, running, climbing, jump (crawl up stairs), dancing (12-18)
- Fine motor + vision – scribbling, build tower with 3bricks,
- Hearing + speech – handful of single words, start to know body parts like point to tummy
- Personal + social –
18months
What age am I
- Gross motor – run, kick a ball, throw a ball but can’t catch usually
- Fine motor + vision – reading books, turn pages, copy line drawing
- Hearing + speech – 50 single words, put words together in simple phrases (eg. I want drink, don’t want)
- Personal + social – tantrums, meltdowns.
2 years
SOme children start toliet trainign 2 1/2
What age am I
- Gross motor – going to nursery (not legal obligation until 5) so tricycle, walking up and down stairs, hopping
- Fine motor + vision – copy circle, tower blocks 7/8, scissors, threading beads
- Hearing + speech – name friends, what they have done, short sentences.
- Personal + social – imaginative play, feeding babies, brushing hair on dolls…
3 years
15horus free per week nursery from 3 for all
WHat age am i
- Gross motor – start reception so catch, hop, up and down stairs in adult fashion
- Fine motor + vision – learning to write name.
- Hearing + speech – telling stories
- Personal + social – toilet trained, drink from open cup, dress and undress themselves, eat with knife and fork
4 years
line circle square triange = progression of drawing
Triangle at 4
Developmental assessment
clinical assessment of development
- History – birth, family hx, developmental skills, currently, social context, parenteral ICE, regression (in social skills could be autism and in motor etc could be progressive muscular dystrophy etc)
- Exam – general (dysmorphic, head size, growth, signs of neglect) and neuro (tone, power, asymmetry, reflexes)
- Investigations
- Management – MDT approach
Play with them, it is very opportunistic. Ask parents, formal assessment tools. Observe in more than one setting at more than one time. Start at where you expect and move back.
Causes for global developmental delay
- Genetic – downs, fragile X, chromosomal abnormalities
- Injury - pre, peri, post-natal
- CNS malformation neural tube defect hydrocephalus, structural abnormality brain
- Endocrine/metabolic – hypothyroidism
- Neurocutaneous- NF, tuberous sclerosis
- Idiopathic
Autism specturm disorder
- Autism spectrum disorder = pervasive developmental disorder which presents in early childhood and is lifelong. Qualitative differences in reciprocal social interaction and communication combined with restricted interest and repetitive behaviours. Usually presents by 3years old.
- More common with: 1st degree rel, parent with schizophrenia/affective disorder, maternal sodium valproate in pregnancy, gestational age <35weeks. Also in children with learning disability, congenital CNS malformation/CP/neonatal encephalopathy, downs syndrome and other genetic ones, tuberous sclerosis or neurofibromatosis, muscular dystrophy.
- Clinical:
- Impaired reciprocal social interaction – difficult forming relationships, avoiding eye contact + reduced response to others emotion
- Impaired communication – delayed speech, language development, repetitive use of language and difficulty initiating
- Restricted interests + repetitive behaviors
- Comorbidities – general learning and attention problems, seizures, affective disorders, mental health disorders.
- It is a spectrum so may not have significant impairment in all categories. Those with Asperger syndrome or ‘high-functioning’ autism may have normal intelligence quotient and speech development, having specific difficulties with social and communication skills or obsessional interests. 70^ coincidence of psychiatric conditions including ADHD, conduct disorders, depression and OCD.
ADHD
Attention deficit hyperactivity disorder.
3 hallmarks:
- Inattention – manifests as easily distracted child who changes activity frequently and doesn’t persist with tasks
- Hyperactivity – excess of movement with persistent fidgeting and restlessness
- Impulsiveness – Acting without reflection or prior thought
Physical exam – developmental delay, clumsiness deficits in hearing or vision and pecific learning difficulties, dysmorphic features.
Diagnosis: Current NICE guidelines suggests ADHD can be diagnosed where there is hyperactivity/impulsivitiy and/or inattention meeting either ICD-10 or DSM-5 criteria which:
- Are present for at least 6m
- Persist in 2 or more settings (ie, home and school)
- Impair function
Behaviour therapy, drug therapy (methylphenidate (Ritalin) or atomoxetine where tics and dexamfetamine where both failed.
Congenital heart disease - overview
Normal foetal ciruclation
Transition at birth
Gas exchange changes from placenta to lungs
- Cord is clamped – cessation of blood flow from placenta and rise in systemic vascular resistance inside baby circulation. Increases left side pressure and Ductus venosus starts to close (3-10days).
-
Baby takes their first breath –
- Causes huge decrease in pulmonary vascular resistance (increases lung expansion and decreases hypoxic pulmonary constriction).
- Increase in pulmonary venous return to left atrium and red in right atrial pressure.
- Pressure in left atrium -> pressure in right atrial.
- Flap closure of foramen ovale in minutes (anatomical closures takes days)
- Systemic vascular resistance -> pulmonary vascular resistance reverse flow through ductus arteriosus
- Ductus arteriosus begins to close due to high partial pressure of 02 passing through it (2days)
- Over subsequent weeks, right ventricular wall muscle reduces and left ventricular wall thickens.
- If babies are born and exhibit significant hypothermia/hypoxia/acidosis can have persistent foetal circulation and won’t achieve this transition.
WHta is congenitla heart disease and general symptoms?
Congenital heart disease or congenital heart defects refers toa variety of malformations of the heart and/or its major blood vessels that are present at birth.
Some General Symptoms:
- Lagging physical development
- Cyanosis, pallor, SOB, anxiety in breastfeeding, rejection of the breast
- Cyanosis, pallor or of the skin and mucous membranes
- Heart murmurs from first days of lfie
- Increase in heart rate
- ECG signs of overload and hypertrophy of the heart (p-pulmonale, p-mitrale, left, right type of EOS)
- Echocardiography signs of hypertrophy of different parts of the heart
- Radiography – increase in heart size, depletion or enhancement of pulmonary pattern.
- 25% of cases have chromosomal abnormalities
- Trisomy 21, VACTERL, Digeorge, charge association
- Other risks = maternal infection and maternal teratogen exposure
- Commonest lesion = VSD
- Majority of cases picked up antenatally
- Can be subdivided into: Acyanotic and cyanotic.
Congenital cardiac associations
- Alcohol in utero – VSD, ASD, PDA, TOF
- Congenital Rubella – PDA, Pulmonary artery stenosis, septal defects
- Trisomy 21 (Downs) – ASD, VSD, AVSD (endocardial cushion defect)
- Mother has DM – TGA
- Marfan syndrome – MVP, Throacic aortic aneurysm and dissection, aortic regurgitation
- Prenatal lithium – ebstein anomaly
- Turner syndrome – Bicuspid aortic valve, coarctation of aorta
- Williams syndrome – supravalvular aortic stenosis
- 2Q11 (DiGeorge syndrome) – Truncus arteriosus, TOF
Acyanotic CHD - pink babies
Shunt left to right (no mixing of deoxygenated and oxygen bloods)
These can be divided into:
- Restrictive (allowing little flow left to right): Small ASDs/VSDs, PDAs. May close spontaneously
- Non restrictive (large defects, allow signficiant left to right flow): Moderate-Large asds, VSDs, AVSDs. Need surgical closure and carry risks of PHTN & Eisenmengers if untreated
- Obstructive (severity of lesion decides age of presentation): Aortic stenosis, co-arctation, pulmonary stenosis.
Ventricular septal defect
ATrial septal defect
Patent Ductus Arteriosus
Coarctation of aorta
Cyanotic chd - BLUE BABIES
Deoxygenated blood enters systemic circulation or mix of oxygenated and deozygenated blood entering systemic circulation.
5Ts of Cyanotic Disease: TOF, TGA, Truncus arteriosus, TAPVD, Tricuspid atresia (also HLHS)
- Tetralogy of Fallot
- Transposition of greater Arteries – aorta comes off right ventricle. PA comes of left (may be associated with ASD or VSD)
- Truncus arteriosus – pulmonary artery and aorta haven’t divided – single common overlying blood vessel
- Total anomalous pulmonary venous drainage – pulmonary veins do not connect to left atrium. 3 types described bu where the PVs connect (all have ASD otherwise not compatible with life).
- Supracardiac – PVs drain to right atrium
- Cardiac – PVs drain to right atrium through coronary sinus
- Infracardiac – PVs drain to right atrium through hepatic veins and IVC (has highest risk obstruction)
- Tricuspid atresia – tricuspid valve does not form (hypoplastic RV common). Similar defect affects left heart (Hypoplastic left heart syndrome HLHS.
- Ebstein anomaly – displaced tricuspid leaflets, artificially atrialising the RV.
Tetralogy of Fallot
Transposition of great vessels
total anomalous pulmonary venous drianage
Truncus arteriosus
Tricuspid atresia and hypoplastci left heart syndrome
Ebstein anomaly
Duct dependent lesions
Duct Dependent Lesions: If undiagnosed, classically presents days after birth.
- Systemic – Hypoxia/ respiratory distress, HF, Absent/reduced femoral pulses, severe metabolic acidosis.
- Pulmonary (not enough flow to lungs) – respiratory distress, cyanosis, normal pulses, no response to hyperoxia.
Treatment for suspected duct-dependent lesions is to keep patient with prostaglandin E2 (can cause apnoea, and may need intubation and ventilation.
Eisenmenger
Eisenmenger:
- When left to right becomes right to left
- Eissenmengers syndrome can result dorm untreated left to right shunts
- ASDs, VSDs, PDAs
- Over time, excess pulmonary blood flow from left to right hsunt causes pulmonary hypertension and right ventricular hypertension
- When pulmonary vascular resistance -> systemic vascular resistance, there is a functional reversal of flow from right to left
- Cyanosis now occurs
Heart murmurs amd grade
Common in children and most not associated with pathology.
Interpretation:
- Timing – Is it systolic or diastolic (most are systolic, diastolic is rare and pathological)
- Character – pansystolic or ejection systolic
- Loudness – Graded 1-6
- Radiation – A murmur that radiations from its site of maximal loudness is more likely significant.
Innocent heart murmur
- Murmurs produced by normal flow. Changing the flow should therefore change intensity of murmur.
- Maneuvers that decrease the flow of blood returning to the heart through the venous system will decrease the intensity of flow murmurs, suggesting that the murmur is flow related or innocent.
- Changing childs position form supine to sitting, then to standing and finally to squatting during exam will change flow and is useful in helping to define innocent murmur.
- Child may be asked to push out the abdomen or bear down to perform a Valsalva maneuver, which reduced venous blood flow to the heart and the intensity of innocent murmurs.
- Types – stills murmur, venous hum, turbulent flow in pulmonary artery bifurcation.
- 25% of full term neonates have a murmur.
- Features of an innocent murmur 10S: soft, systolic, short, S1&S2 normal, symptomless, special test (x-ray and ECG) normal, standing/sitting vary with position, sternal depression
- Stills murmur = soft vibratory murmur heard in LLSB most frequently in childhood when there is normal blood flow an dno cardiac lesion.
- Venous hum = continuous murmurs heard loudest over clavicles due to venous return form head and neck and this varies with position.
- Turbulent flow in pulmonary artery bifurcation = A soft ejection systolic murmur caused by turbulent flow in pulmonary artery (PA) bifurcation as the PA bifurcation and branches are small.
Significant heart murmur
- Symptoms = syncope, episodic cyanosis
- CVS sings = abnormal pulses, heart sounds, BP or cardiac impulse
- Murmur = diastolic, pansystolic, radiating to back or associated with a thrill
These can be difficult to distinguish from an innocent murmur. Refer for echocardiography if in doubt.
Kawasaki disease
Kawasaki disease = uncommon systemic vasculitis affecting small and medium vessels which can include the coronary arteries leading to aneurysm formation. Typically affects 6m-4y (peak at 1yr) and more common in children of Asian origin.
Clinical criteria for diagnosis: Fever for 5+ days or more with 4 of the following…
- Bilateral non-purulent conjunctivitis
- Polymorphous maculopapular rash
- Oral changes – red cracked lips or strawberry tongue
- Changes to extremities: reddening or oedema of hands and feet, or peeling of skin (classically a late sign)
- Cervical lymph nodes >1.5cm
May emerge sequentially and not be present all at once. Characteristically, the child is extremely miserable. Coronary aneurysms will occur in 230% f untreated cases an typically develop in first 4-6weeks of illness.
Investigations – FBC, CRP, ESR (raised), U&Es, LFTs (bilirubin + AST may be raised), throat swab and antistreptolysin 0 titre, blood culture + viral titres, Echocardiography, electrocardiogram.
DDx – measles, scarlet fever, rubella, roseola, fifth disease.
Management – single dose IV immunoglobulin to reduce incidence + severity of coronary artery aneurysm formation and aspirin.
Febrile seizure
Febrile convulsion = Seizure associated with a fever in a child between 6m-6y in absence of an intracranial infection or identifiable neurological disorder. Most common cause of seizures in childhood (5% children), might be familial predisposition and usually occur when body temp rises rapidly.
Clinical Features: Typically brief (1-2min), generalised, tonic-clonic seizures. Underlying infection causing fever may be vial/bacterial so need to identify fever cause and ensure no signs of meningitis.
- Simple febrile convulsion – <15mins, generalized, occurring once in 24hours.
- Complex - >15mins, focal or recurring within 24hours.
Management:
- Identify + treat underlying infections – may consider CXR, blood culture, microscopy + culture + LP
- Despite no evidence of reduction in seizures, regular antipyretics are recommended
- Prolonged convulsions are treated as per status epilepticus
- Parenteral education
Prognosis – v good in simple ones, but 1/3 children will have further ones in lifetime but usually grow out of this by 6yrs. Slightly higher risk of developing epilepsy in lifetime which is increased further by positive H or developmental/neurological abnormalities so EEG may be warranted in complex febrile convulsion or presence RFs.
Epilepsy
Epilepsy = Chronic disorder characterised by recurrent, unprovoked epileptic seizures. Diagnosis is made in a patient whom epileptic seizures recur spontaneously but an ‘epileptic seizure can be provoked in individuals who do not have epilepsy eg with fever.
DDx = Syncope, breath holding spell, aspiration, GERD, panic attack, daydreaming, conversion or pseudoseizures, benign sleep myoclonus benign paroxysmal vertigo, complicated migraine, motor tics, complex behaviours, decorticate posturing.
Causes Epilepsy – idiopathic, cerebral malformations, cortical dysgenesis, tumours, trauma, CNS infection, hypoxic ischaemic encephalopathy, chromosomal abnormalities, neurodegenerative conditions, neurocutaneous syndromes.
Diagnosis – careful history, distinguish epileptic seizures from the many causes of faints, fits and funny tums.
Investigations – EEG, neuroimaging, brain imaging (structural-CT/MRI and functional-PET/SPECT), metabolic investigations
Mx – anti-epileptic drug therapy. Other options like ketogenic diet, vagal nerve stimulation, epilepsy surgery.
Acute management – benzodiazepines if still convulsing except in neonates whoud shudl receive phenobarbitone.
Classification of seizures
Classification of seizures: initial division based on where electrical activity started in the brain.
- Generalized onset seizures – originate from network in both hemispheres. Can be motor (tonic-clonic and myoclonic_ or non motor (absence seizure)
- Tonic clonic: tonic phase (rigidity with loss of posture) and clonic phase (movements of all four limbs), loss of consciousness, postictal drowsiness. Can be in epilepsy but also in febrile seizures and meningoencephalitis.
- Absence seizures: brief unawareness lasting few seconds, no loss of posture, immediate recovery, might be very frequent, associated with automatisms (eg, blinking and lip smacking)
- Focal onset seizures – Thought to originate from one hemisphere, either localized point or more widespread. Can be subcategorized by level of self-awareness experienced:
- Involvement of only particular part of the body
- May be associated with aura
- Can have emotional, sensory or cognitive component
- Mya spread to involve entire body – focal onset to bilateral tonic-clonic.
- Frontal seizure = motor/pre-motor corte which may lead to clonic movements to a tonic seizure.
- Temporal lobe seizure – aura, with smell and taste, lip smacking etc.
- Occipital seizure– stereotypes visual hallucinations.
- Parietal lobe seizures – contralateral dysesthesias (altered sensation) or distorted body image.
- Unknown onset seizures
- ‘grand mal’, ‘petit mal’, ‘simple’, ‘partial’ are outdated and avoided now.
Cerebral Palsy ad the cause classification
Cerebral palsy = group of conditions affecting motor function and posture due to nonprogressive lesions of developing brain. Even though it isn’t nonprogressive lesion, the clinical manifestations evolve as the child gets older. Cause is uncommon in many but identified RFs can be categorised into antenatal, perinatal and postnatal insults. Perinatal asphyxia is an uncommon cause of cerebral palsy
- Antenatal.= cerebrovascular hemorrhage or ischaemia, cortical migration disorder, structural maldevelopment of brain in gestation osme linked ot gene deletions
- Birth – hypoxic ischaemic injury before or after deliver
- Preterm infants – vulnerable to damage from periventricular leukomalacia secondary to ischemia and or IV hemorrhage and venous infarction.
- Postnatal – meningitis/ encephalitis/ encephalopathy, head trauma, symptomatic hypoglycaemia, hydrocephalus and hyperbilirubinemia.
Types:
- Spastic = damage to UMN, spasticity with brisk deep tendon reflexes and extensory plantar responses. Unilateral, bilateral (quadriplegia), bilateral (diplegia).
- Dyskinetic = involuntary, uncontrolled movements. chorea, athetosis, dystonia.
- Ataxic = Hypotonic. Most genetically dertermined.
- Other.
Mx – MDT,novel - botulinum toxin injections to muscles, selective dorsal rhizotomy, intrathecal baclofen
Long term complications: Premature ageing, malnutrition, depression, anxiety, heart and lung disease, OA, chronic pain, scoliosis.
Clinical features and diagnosis of cerebral palsy
Cerebral palsy = group of conditions affecting motor function and posture due to nonprogressive lesions of developing brain.
Clinical features:
- Hypotonia in infancy
- Feeding dififuclties due to lack of oromotor coordination
- Delayed motor milestones
- Speech and language delay
- Motor disorders (eg, hypertonia, hemiplegia)
Effects can range from having little to no physical disability and thriving in mainstream school to children who are non verbal and have four limb spastic quadriplegia.
Diagnosis: Usually 1+
- Abnormal tone – hypertonia or hypotonia
- Abnormal power (eg delay in motor milestones)
- Abnormal reflexes
- Abnormal movements – athetosis or chorea
- Abnormal posture or gait
Girls vs boys Tanner stages of puberty
WHat is puberty?
Puberty = acquire secondary sex characteristics and reproductive capacity attained. Usually 8-13 females and 9-14 males.
- Girls: Average 10years, 1st signs breasts with peak height velocity breast stage 4- (12years). Menarche 11-13. first sign usually breasts begin to develop and pubic hair starts to grow with more hair on legs and arms. After 1 year…” breasts grown ore, first period (2years after), pubic hair coarser + curlier, underarm hair grows, sweat more, acne, more whit vaginal discharge, grwoth spurt, gain weight. After 4years breasts become adult like, pubic hair spread to inner thih, genitals fully developed, girls stop growing taller
- Boys: Av 12years, 1st sign 4mls testicular vol (from 2mls), peal heigh velocity 10-12mls testicular vol (14years). First sign testicle sbigger, scrotum thinns + reddens and pubic hair starts to appear at base of penis. After 1 year or so + continuing: penis _ testicles grow + scrotum darker, pubic hair thicket, udneramr hair, boys sweat more, breast can swell, boys have wet dreams, voice breaks and deeper, acne, growth spurt + muscular. After 4years, genitals look like adults and pubic hair spreads, facial hair, boys taller at slower rate then muscular.
Mood changes - unexplained mood swing, low self esteem, aggression, depression.
Precocious puberty - before 8years for girls or 9yrs boy. Assoicated growth spurt. most commonly ealry onset of nromal puberty in girls and in boy smostly paholoigcal.
Delayed - Absence of secondary sex characteristics at 13years of age in girls or 14years in boys. Can be hypogonadotropic hypogonadism (central delayed puberty) or hypergonadotropi hypogonadism(gonadal failure).
Diabetes Mellitus Type 1 : causes and presentation
Diabetes Mellitus = group of disorders of carbohydrate, fat and protein metabolism, caused by deficiency of or reduced efficacy of endogenous insulin.
T1DM:
- Autoimmune, lack of insulin. T-cell mediated autoimmune destruction of the B cells in pancreatic islets of Langerhans, perhaps triggered by environmental factors (eg, viruses) in people with genetic predisposition. Osmotic diuresis when blood glucose conc exceeds renal threshold. Ketoacidosis develops when insulin efficiency is severe. Associated with HLA-DR3/DR4
- Presentations: Hyperglycaemia, polydipsia/polyuria/polyphagia, weight loss, N/V/abdo pain (DKA)
- Mx: Lifelong insulin (high risk, measured in units) replacement, regular blood sugar checks, screen for complications and compliance. Normal BM is 4-7. Noncompliance is big issue for adolescent patients.
- Teach – how to treat hypos, sick day rules.
- Hyperglycemia – dry mouth, increased thirst, weakness, headache, blurred, frequent urination
- Hypoglycemia symptoms – sweating, pallor, irritability, hunger, lack of coordination, sleepiness.
DIabetes mellitus - invetsiagtions, managemnt and complications
- Invetsigations - WHO diagnosis: Fasting plasma glucose ?7mml/L or random plasma glucose of >11.1mmol/L in absence of other acute illness. If asymptomatic then needs to be confirmed on second occasion. In those with T1DM may be raised levels autoantibodies and in T2DM, raised C peptide.
- Management long term: Education + psychological support (diet), insulin replacement (basal bolus- long acting before bed, rapid before meals) or subcutaneous pump, diet, exercise, monitoring (finge rprick, fasting 4-7, post meals 5-9), management of acute compications and prveention long term
-
Complications:
- Hypoglycaemia - due to mismatch in insulin doe, time, carbs intake,e xercise etc. Initially faint, dizzy, wobbly, sweating, hunger and then more severe are lethargy, bizarre behavior, seizures etc. Need sugary drink, glucose tablet or glucose polymer gel followed by more complex carb and if severe or uncooperating then IV 10% dextrose or IM glucagon.
- Diabetic ketoacidosis – abdo pain, vomiting, features severe dehydration and ketoacidosis and can have severe complications including cerebral oedema.
- Late complications – CV disease, retinopathy, nephropathy, neuropathy.
Congenital Hypothyroidim
- Present at birth
- Developmental defects - thyroid agenesis or failure of migration
- Dyshormonogenesis - autosomal recessive inborn error of thyroid hormone synthesis
- Congenital pituitary lesion
- Transient congenital hypothyroidism in cases of materanl thyroid disease with passage of tyrou receptor antibodies or antithyroid medications.
- Maternal iodide deficiency
- Clinical features - May be clinically normal at birth but if untreated then: Prolonged neonatal jaundice, sleepiness, feeding problems, constipation, umbilical hernia, bradycardia and poor peripheral perfusion, coarse facies/ wide posterior fontanelle, large tongue, hypotonia and learning difficulties and goitre.
- Testing is part of neonatal screening in the uK.. Most UK labs test for raised levels TSH
Acquire Hypothyroidism
- Causes include autoimmune disease (Hashimoto thyroiditis), iodide deficiency and iatrogenic (caused by thyroid surgery or meds).
- Clinical Presentation: Feeling cold, weakness + fatigue, low mood, constipation, menorrhagia, dry skin and coarse hair, bradycardia + heart failure, ataxia.
- Measures thyroid function tests and thyroid autoantibodies
Hyperthyroidism
Neonatal -
- Causes for neonatal – infants of mothers with Graves Disease or Hashimotos disease from transplacental transfer of thyroid stimulating immunoglobulins.
- Clinical presentation – may cause IUGR, tachycardia or fetal hydrops. Get goitre, increased appetite but faltering growth, diarrhea, CNS signs like irritability, CV signs like tachycardia, arrhythmias, hypertension and heart failure.
- Usually self-limiting within 1-3month but if severe may require treatment with propranolol or carbimazole.
Acquired –
- Most common by Graves disease(autoimmune) – TSH receptor antibodies
- Clinical – feeling hot, diarrhea, increased appetite but weight loss, tremor, tachycardia, palpitations, cardiomyopathy, eye signs like proptosis, cremosis, exposure keratitis and ophthalmoplegia.
- T4,T3 elevated, TSH depressed, thyroid autoantibodies. Carbimazole first line with B blockers for symptoms relief.
WHat is short stature and the causes
- Height below 0.4th centile for age
- Predicted height less than mid-parenteral arget height
- An abnormal growth velocity as indicated by heigh changing by more than the width of one centile band over 1-2years.
Causes:
- Familial short stature
- Constitutional delay of growth and puberty, ay be positive FH
- IUGR
- Endocrine disorder - GH deficiency,hypothyroidism, cushins
- Genetic:
- Achondroplasia - mutation in GFGR3 gene so other skeletal abnormalities
- Mucopolysaccharidosis - short stature, coarse faial features, assoicated learning difficulties
- Syndromes – Turner syndrome (45X0 kartotype), down syndrome, prader willi, russel silver syndrome.
- Malabsorption (CF/coeliacs)
- Any chronic disease (congenital heart disease, chronic kidney disease)
- Psychosocial deprivation/ neglect
History + exam of short stature
- Birth weight, length and head circumference
- Timeline of how they have grown and whether there has been any pubertal development
- Early childhood illness and systemic disorders
- Parenteral height – estimate target centile from mid parenteral height. (Father height + mother height)/2 then add 7 for boys and minus 7 for girls. Boys can then devite 10cm either way and girls 8.5cm either way. Can use chart where join mother and father heights and where cross centile line in middle. 9/10 childrens height centiles are within 2 centile spaces of mid parenteral centile. Can also then use adult height predictor.
- FH – inherited skeletal dysplasia’s
- Dietary and social history
Exam:
- Height – calculate growth velocity in cm/year (min2measurements 6m apart)
- Weight
- Head circumference
- Stage of puberty
- Dysmorphic features – might identify syndrome
- Visual fields and fundi – might indicate pituitary tumour.
Plotting of short stature
Iron Requirements
Fetus absorbs iron from mother across placenta. Term infants have adequate reserves for first4m life but preterm have limited stored and higher demands so utilise reserves by 8weeks. Reast milk and unmodified cow milk a=re low in iron but 50% of iron in breast milk is absorbed whereas only 10% from cows milk. Most formula milks are fortified with iron and have 10times concentration in breast milk but 4% absorbed.
Dietary sources – red meat, fortified breakfast cereals, dark green veg, bread. About 10-5% dietary iron absorbed by is enhanced by ascorbic acid (Vit C) and reduced by tannin in tea
95% iron supplies in adults is by recycling of broken RBCs but in infants they require 30% from dietary and this demand increases with age, especially with girls who loose iron through menstruation.
Iron deficiency anaemia
Main causes – : Inadequate intake (diet, growth spurt), malabsorption (coeliacs), blood loss (menstruation, meckels diverticulum)
Clincial features: Fatigue, slow feeding, Pica, Pallor (Conjuctiva, palmar creases)
O/E: only signs might be pallor of mucous membranes and if severe may be flow murmur due to hyperdynamic circulation. In infancy and childhood you get developmental delay and poor growth which is reversible by long term oral iron treatment. Severe anaemia can cause cardiac failure.
Invetsiagtions:
- FBS – Hb, MCV decreased (microcytic, hypochromic anaemia)
- Decreased serum ferritin
Management: : to prevent avoidance unmodified cow milk until 12m, iron supplementation in those vulnerable. Mild to mod then dietary counselling + oral iron supplements (dietician possible) and replacement for 3m after correction to replenish stores. For severe with cardiac compromise then may need transfusion.
ITP
Idiopathic thrombocytopenic purpura (ITP) = most common cause of thrombocytopenia in children. Immune destruction of platelets by autoantibodies. Autoimmune
Clinical Features: May be history of recent viral illness. ITP mainly affects children between 2-10, often 1-2 weeks after viral infection. Presentation is with purpura and minor bleeding eg, from mucosal surfaces like epistaxis. Spleen is palpable in minority of cases.
Diagnosis: Of exclusion (rule out more sinister causes): Acute leukaemia, aplastic anaemia. Organomegaly, lymphadenopathy, anaemia or neutropenia.
- FBC, low platelets
- Blood film
- (Bone marrow biopsy)
Treatment – Observation as usually self-resolves in 6-8 weeks. May need steroids or IV Ig.
DDx – acute leukaemia, nonaccidental injury, Henoch-Schonlein purpura.
Henoch Shonlein Purpura -
Henoch-Schönlein Purpura = commonest vasculitis in children. Multisystem vasculitis involving small blood vessels. Immune mediated IgA vasculitis, usually triggered by viral URTI. Common in boys and most are under 10 (2-10).
Clinical Features: Affects skin, joints, GI tract and kidneys. Painful, palpable purpura.
- Non-blanching rash (100%) – buttocks, extensor surfaces of legs/arms
- Painful, swollen joints (60-80%)
- Abdominal pain (80%)
- Hematuria (20-60%)
Investigations – Rule out other patho and measure extent of organ involvement. FBC, CRP, blood cultures, U&Es)
Estimated 2% with HSP develop renal failure.
Management – usually self resolves within6weeks, simple analgesia. Steroids sometimes used to treat joint pain.
Eczema and the types
Eczema = chronic inflammatory skin condition usually starting in childhood. 3 main variants: Atopic eczema, infantile seborrheic eczema and napkin dermatitis.
- Atopic
- Infantile seborrheic eczema
- napkin dermatitis
Atopic eczema
- Often FH of atopic disorders (eczema, asthma, allergic rhinitis), reflecting genetic predisposition that confers an abnormal immune response to environmental allergy.
- Clinical: Usually episodic but may be continuous in serious. Dry, red itchy rash usually on extensor surface and face and flexures in older children. Skin can vary from acute, weeping papulovesicular eruption to chronic, dry, scaly, thickened skin that develops in older children. Itching is often most problematic symptom.
- Investigations – clinical but IgE likely raised. Food and environmental allergens play role so exclusion diets or radioallergosorbent testing and skin pricks may be helpful.
- Management – regular use emollients even when under control and apply topical steroids. If not enough then topical therapies like tacrolimus and pimercrolimus may be used. Systemic therapy with immunsuppressive agents for severe. Education essential and many grow out of eczema by teens.
- Complictions – seocndayr infection with viruses or bacteria. Infection with herpes simplex is potentially serious and treat with aciclovir.
Infantile seborrheic Eczema:
Presents mostly in first 2m life with scaly, non itchy rash initially on the scalp (cradle cap) which might spread to involve the face, flexures and nappy areas. Treatment is emollients and mild topical steroids.
Napkin dermatitis
Rashes in nappy area are common and can be due:
Irritant contact dermatitis (nappy rash) – prolonged contact urine and faeces with ski. Include skin wetness and ammonia from breakdown or urine by faecal enzymes. Skin is red, moist and might ulcerate. Inguinal folds are spared. Can be prevented by frequent nappy changes and barrier creams. Exposure to air can hasten recovery.
Candidiasis – bright red skin with satellite lesions and involvement of ksin folds. Can be treated with topical and oral antifungal like nystatin
Seborrheic dermatitis.
Capillary gas interpretation
Used to monitor neonatal patients when collecting arterial sample is not practical. Lateral area of heel preferred but can use fingertip, earlobe, toe etc.
- Respiratory acidosis – excess carbonic acid as increased CO2. Eg from CNS depression (asphyxia), obstructed airways. Can be compensated (kidneys cnrease H+ secretion and bicarb reabsorption) when low normal pH with increased CO2/Bicarbonate
- Respiratory alkalosis – alveolar hyperventilation so deficiency carbonic acid. Cause eg, iatrogenic, hypoxemia, pain. Compensation is retain chloride and excrete fewer acid salts by kidneys decreased hydrogen secretion and when pH high normal with low CO2/bicarb
- Metabolic acidosis – deficiency in bicarbonate in ECF. Caused by any systemic disease that causes increased acid production or retention or anything caucusing excessive base losses (diarrhea, renal failure sepsis).Compensation if lungs blow off additional CO2 through hyperventilation and kidneys increased excreitona cid salts and reabsorption bicarbonate ions. pH below normal with low levels CO2/bicarb
- Metabolic alkalosis. Excess bicarbonate in ECF where problems lead to increased loss acid. Severe vomiting, diuretic therapy, iatrogenic etc. Compensate by retaining CO2 through hypoventilation so pH high normal, high co2 and bicarbonate
Lumbar puncture principles and interpretation
Needed to test the fluid around the brain and spinal cord. May be done to see if a child has meningitis.
Lie on side with knees tucked into chest and head bent forward. Babies will be curled in a ball to get a better position. Young children and babies will be held in place. Needle L4 level or lower as conus medullaris finishes near L3 at birth (L1-2 by adulthood). Preferable to get before antibiotics.
Interpretation: Normal CSF parameters vary with age. Any neutrophils present is unusual and should raise concern about bacterial meningitis. If CSF abnormal, safest course is to treat as bacterial meningitis.
Factors that can affect result – Ab prior, seizures, traumatic (blood stained) tap, tie between smapling and analysis
Growth parameter plotting
Measurements must be accurate for meaningful monitoring of growth. Groth parameters should be plotted on charts and dont assess a single growth parameter in isolation. The pattern of growth is essential when assessing the health of a child, consider genetics, nutrition, general health and hormones as potential causes of abnormal growth.
Measuring – remove footwear, without nappy using a length board or mat. Good to do 3 measurements and use average.
<2 years = length board or mat
>2years = rigid upright measure with T piece or stadiometer
Significant abnormalities:
- Measurements below the 0.4th or above the 99.6th centiles or outside the midparental height range
- If marked discrepant from weight
- Serial measurements, which cross growth centile lines after 1st year of life.
Short stature
height below 2nd centile (2SDs below mean). Most of these 1 in50 children will be normal as short parents but the further below centile, the more likely pathological. Measuring height velocity is a good indicator of growth failure.
Must compare heigh centile of a child with weight centile and expected genetic height. This is done by mean of father and mothers height with cm added for midparenteral height for boy and -7 for girl. The 9th to 91st centile range of this estimate is given by +/-10cm in boy and +/-8,5c, in a girl.
- Familial – may be small from parents to check parents and child odnt have inherited growth disorder like skeletal dysplasia
- Constitutional delay in growth and puberty – variation of normal growth with short stature in teens as delay in onset of puberty, bone age is delayed etc and onset of sexual secondary characteristics, but final height is normal.
- Small for gestational age and extreme prematurity
- Chromosomal disorder/syndromes – downs syndrome, turner, russell-silver, noonan.
- Nutritional/ Long term illness – coeliac, crohn’s, chronic kidney disease
- Psychosocial deprivation
- Endocrine – hypothyroidisim, GH deficiency, IGF-1 deficiency and associated with children beig relatively overweight.
- Extreme short staure – idiopathic short stature, abdnormlaities in SHOX gene
Tall stature:
Obesity fuels early growth but doesn’t increase final height. Secondary endocrine causes are rare. Both congenital adrenal hyperplasia and precocious puberty lead to early epiphyseal fusion so that eventual height is reduced after an early excessive growth rate. Marfan and Klinefelter’s syndrome cause long legged tall stature and in XXY there is infertility and learning difficulties. Excessive height in prepubertal or early pubertal adolescents can be treated with oestrogen therapy and testosterone therapy, but serious S/E and mixed results. Surgical destruction of epiphyses in extreme cases.
Weight measure and weight faltering
Measuring - Without clothes or nappies. Children over 2years can be weighed in a vest and pants but without shoes, footwear, or anything in their hand. Compare to the charts for growth standards which allow for lower weight of exclusively breast-fed infants, so they aren’t labelled as underweight and allow earlier identification of formula fed babies gaining weight too rapidly. Asses with things like height as small and a bit under isn’t as significant as tall and low weight.
Weight faltering – covered above and obesity.
HR,RR,BP, Temp, 02 sats, Capillary refill time – measure, interpret and explain
Capillary refill time: 2 or less when on finger, and if foot/chest then 4 or less seconds
- High HR – Hypovalaemia, sepsis, fever pain, hypoxia, anaemia
- Low HR – Hypothermia, hypothyroidism, anorexia nervosa, malnutrition, hypokalaemia, hypoxia.
- High RR – can be transient (less than 24hours), bronchiolitis, pneumonia, infection of lower airways.
- Low RR – hypothyroidism, opioids, toxins, head injury,
- High SBP – often related to other health conditions like heart defects, kidney disease, genetic conditions or hormone disorders and for older children it may be primary hypertension.
- Low SBP – anaphylaxis, arrhythmia, medications, dehydration, drinking alcohol, heart conditions, infections.
Urineanalysis
Paeds History taking
Pedigree symbols
PEWS
Non-epileptic conditions
- Benign neonatal sleep myoclonus
- Benign neonatal seizures
- Parasomias – sleep paralysis, sleepwalking, night terrors and confusional arousal.
- Syncope (vasovagal/reflex)
- Cyanotic Breath Holding spells (crying convulsions), blue spells.
- Reflex anoxic seizures (eg, pain (eg hit head),asystole, loose consciousness, fit), Pallid syncope
- Sandifer syndrome with GORD, apnoea, and dystonic reaction
- Hyperekplexia – whole body stiffening in response to sudden noise
- Daydreaming – occurs when bored or watching TV/screen, self-gratification (vs absent seizure, where in hyperventilation if its absent seizure they will stop and freeze)
- Febrile seizures, tics, infantile shudder, shivering due to excitement, cataplexy
Management of febrile seizures
Management at home:
- If it happens again, the plan…
- Place the child on a safe flat surface, no risk of falling (floor)
- Make sure nothing is close to child that can harm them while jerking
- Don’t panic
- Time and if beyond 5mins then 999
- Recovery position
- Most children are post-ictal so allow to recover (10-15mins)
- Then see GP – need to see what infection is causing it.
Acute Management:
- ABCD: airway, breathing, circulation, disability, exposure, glucose.
- Given oxygen (as most become cyanotic and hypoxic and body seizes)
- Note the time
- Check BM (blood glucose)
- Get IV access if possible then a benzodiazepine (if not then rectal diazepam). Can have 2 doses benzodiazepines ( eg, 1 paramedic, 1 hospital)
- APLS algorithm for convulsion child (tells you when to give next medication)
Describe, explain and demonstrate treatment for Dehydration
- Look at weight loss
- Loon at fontonelle
- Look at capillary refill time on chest
- Check for sunken eyes out
- Skin turgor on abdomen
Management: Rehydration with correction of fluid and electrolyte imbalance.
- No signs dehydration then encourages normal fluid intake and oral rehydration salts as supplemental fluids if worsens.
- Evidence clinical dehydration – give 50mL/kg ORS over 4hours in addition to maintenance fluids as ORS.
- Evidence shock (decreased conscious levels, poor perfusion, hypotension) then give 20mL/kg 0.5% saline rapidly and repeat if needed then continue with IV rehydration with 0.9% saline adding 100mL/kg to maintenance requirements.
Calculating maintenance fluids:
- 100mL/kg/24h for 0-10kg bodyweight
- 50mL/kg/24h for 10-20kg bodyweight
- 20mL/kg/24h for >20kg bodyweight
- If diarrhoea continues, give additional 5mL/kg ORS for each large watery stool.
breathlessness hisotry
Physical exam
RR,BP and HR expected at ages
Measles (Rubeola)
- Blanching
- Uncommon, few outbreaks, coryzal illness, cough + conjunctivitis, intense photophobia, rash starts at hairlines, spreads cephalo-caudally.
- Miserbale, high temperature.
- Diagnosis is clinical, Koplik spots in mouth (last only 1day or two, like salt sprinkled on cheek), morbilliform rash (maculo papula).
- Labs, measles IgM Ab. Complication are pneumonia and SPPE
- Begins face and behind ears spreading to trunk and extremities within 36hrs. Fades after 3-4days. Palmar sparing. Complications are otitis media (deafness), pneumonia and contact In pregnancy
Scarlatina (Scarlett fever):
- Blanching
- due to streptococcus spp, causing sore throat.
- Toxin mediated diseas.
- Red strawberry tongue, characteristic rash (maculo papula but sandpaper feel).
- High temp and miserable.
- Need 10days penicillin
- 2-4 day incubation, rash 12-48hrs after
German measles (Rubella)
- Blanching
- Self limiting, milder disease, similar to measles with upper respiratory features.
- Tender posterior cervical and occipital lymphadenopathy.
- Starts behind ears and spreads lower down.
- Infectious 7days before and 7days after. Pink/red macules lasting up to 5days. Severe if contact in pregnancy
staphylococcal scalded skin syndrome.
- blanching
- Usually in neonates, skin appears as scalded, around umbilical, flexural areas, toxin mediated.
- Mild fever, very painful rash when baby handled. Flucloxicillin
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Erythema Infectiousum:
- Blanching
- (5th disease) Parvovirus B19, common in winter and spring and often asymptomatic.
- 3 stages – slapped cheek, lacy rash on extremetiies, rash on trunk.
- Spares palms and soles, risk of miscarriage in pregnant contacts
Roseola Infantum:
- blanching
- exanthem subitem, caused by human herpes virus 6 and 7. High grade fever in relatively well playful child. After 3-4days, fever suddenly subsides and pink maculopapular rash breaks out
- High fever, runny nse, irritability 3days then rash. Complications ar every rare (liver involvement/encephalopathy)
Erythema Multiforme and Stephen Johnson syndrome:
Mild self-limiting rash usually associated with infections mycoplasma, herpes. Target lesions, symmetrical fixed urticarial. Abrupt onset. Last for good few weeks (2weeks) . Central zone dusky purple may develop into blister. Severe forms with mucosal (eyes, oral cavity, genitalia) involvement is Stephen Johnson syndrome.
Causes – hypersensitivity to drugs or infection (NSAIDs, baributrates, penicillins, HSV, Varicella, mycoplasma)
Meningitis vs meningococcal sepsis
Medicines, Procedures and Interventions:
bloog gas interpreation
Metabolic Acidosis = Decreased Ph, same PCO2, decreased bicarbonate
HCO2<22, DM ketoacidosis, urate acidosis (renal failure), lactic acidosis (decreased perfusion, severe hypoxemia/sepsis), drugs (eg, salicylates), anion gap.
Respiratory acidosis = decreased Ph, Increased PCO2, Noemal bicarbonate .
PACO2>6, hypoventilation, 12 RD-impaired gas exchange
COPD, heroin OD, Chest wall defect, respiratory muscle weakness eg, G.Barre
Metabolic alkalosis = Increased ph, normal PCO2, increased bicarbonate
Hco3 >26, XS loss (eg, vomiting), ingestion of alkali.
Respiratory Alkalosis = increased ph, decreased OCO2 and normal bicarbonate.
Alkalosis (PaCO2<4.7), hyperventilation
Bronchiolitis – pn
- Most common cause of LRTI in children under 2. Most commonly by Respiratory syncytial virus (RSV- incubation period 2-5days, shedding 6-21says after symptoms).
- RFs - <3yrs, premature, LWB, male, low socioeconomic group, parenteral smoking, chronic lug disease, CHD, NM disorders, immunodeficiency.
- Clinical – start subtle. Coryzal illness (wheeze etc) start then other symptoms pea at 3-5days. Typically apnoea, low grade fever, coryza + often significant nasal congestion, difficulty feeding, signs dehydration, tachypnoea, accessory muscles, fine end inspiratory crepitations + wheeze, hypoxia/cyanosis.
- Rapid viral antigen or nucleic acid amplification test of nasopharyngeal secretions can be used to confirm RSV.
- Clinical diagnosis
- Investigations – vital signs, pulse oximetry, viral throat swabs.
- Management – supportive care (antipyretics, airways, fluids, o2 etc) and CR monitoring.
- Will continue to cough for weeks after episode bronchiolitis, usually 2 weeks or so but can be up to6 weeks. This is normal and fine as long as not working hard and feeding okay.
Croup: (Laryngotracheitis or laryngotracheobronchitis)
- Common upper respiratory illness of childhood characterized by barking cough and inspiratory stridor. Most cases are self-limiting with full recovery.
- Most common in 6m-3y, boys more than girls.
- Parainfluenza type 1 virus is most common. May get secondary bacterial infection.
- Viruses infect nasopharyngeal mucosa and extend to larynx and subglottic airways.
- Clinical – corzyal symptoms, barking cough, stridor. Clinical diagnosis.
- Westley score for severity to mil d/ moderate/ severe to determine need for dexamethasone (bets treatment) , nebulized adrenaline, inpatient care and admission to PICU.
- On plain film radiograph is steeple sign (Pic)
- Management – based on severity and centres on administration of dexamethasone.
- NEVER EXAMINE THROAT IS SUPECT AS ditubrign child can cause full obstruction
Hands, foot + Mouth Disease:pn
- Acute viral illness, usually mild and self-limiting. Characterized by papulovesicular lesions on the distal limbs and vesicular eruptions in the mouth. Mostly late summer and early autumn and mostly in children under 10 (<4)
- Most commonly caused by Coxsackie A16 virus but can also be caused by other group A and B Coxsackie viruses or Enterovirus71. Transmitted between humans only.
- Not all get lesions on hand feet or mouth and has incubation of 3-7days. There is prodromal period 12-36hrs of fever, malaise, decreased appetite, cough, abdominal pain and myalgia. Mouth lesions which go to vesicles and erode. Distal limb lesions often elliptical with long axis parallel with skin lines. Atypical is nail shedding and widespread.
- Investigations + diagnosis- clinical
- Management – supportive and treatment of complications.
Henoch-Schönlein Purpura: pn
- IgA vasculitis commonly presenting in childhood. Commonly in 3-15years old. Precipitated by viral illness leading to immune mediated reaction In blood vessels.
- Immune mediated due to deposition of IgA immunoglobulin in blood vessels.
- Patho – inflammation of blood vessels.
- Clinical – Palpable purpura in symmetrical distribution over lower limb. Arthritis/arthralgia, GI upset, severe GI features, hematuria, nephritic syndrome, other…
- Diagnostic criteria - Based on EULAR and PRES diagnostic criteria. Must have palpable purpura in absence of thrombocytopenia or coagulopathy. Must have at least one of others like diffuse abdo pain, acute arthritis, renal involvement etc.
- DDx – sepsis, ITP, medication induced thrombocytopania, bone marrow failure, CT diseases
- Investigations – investigations help rule out things so do urine, protein/creatinine ratio, BP and bloods, imaging not routine
- Management – most make a fully recovery and monitored as outpatient. Most over 6weeks supportive therapy. Steroids can shorten duration symptoms but don’t affect clinical course
- Estimated up to 50% of children have preceding upper respiratory tract infections.
Meningitis
Viral induced wheeze
- Common causes – RSV, Rhinovirus, Coronaviruses, Parainfluenza, Influenza
- Remember to ask: Prior episodes, admissions, ITU trips, ever needed IV therapy, steroids given previously, FH atopy, use inhalers at home and hwo often, explore triggers.
Transient synovitis
- –“irritable hip syndrome”:
- Most common cause of acute hip pain in children
- Associated with viral infection
- Sudden onset hip pain or limp
- No pain at rest
- Reduced ROM – internal rotation
- Usually resolves within 1 week.
- Age 2-12
Slipped capital femoral epiphysis
- Displacement of epiphysis of femoral head postero-inferiorly
- Most commo at 10-15
- Commonly occurs during adolescent growth spurt
- Increased risk associated with obesity
- Restricted abduction and internal rotation
- Xray hip including frog lateral views
- Surgical management and should be prompty to prevent avascular necrosis.
IBD presentation
- A ¼ of cases of IBD present in childhood
- Crohn’s disease – affects any part of GI tract from mouth to anus. Non caseating epithelioid cell granulomata
- Ulcerative colitis – confined to colon. Mucosal inflammation and crypt cell damage
- Presentation – Abdo pai, diarrhoea, failure to thrive, weight loss, delayed puberty, extra-intestinal manifestations (oral lesions, uveitis, arthralgia, erythema nodosum)
- Investigations – FBC, CRP/ESR, Fecal elastase, Biopsy.
- Crohn’s Mx – nutritional therapy, systemic steroids, immunosuppressants, Anti-TNF (Infliximab)
- UC – Aminosalicylates (Mesalazine), topical or systemic steroids, immunosuppressants
Clinical guideline for presentation of first afebrile seizure + red flags
Red Flags:
- First seizure with accompanying fever, confusion, fluctuating consciousness, coma, or abnormal exam findings
- Rapidly recurring convulsive seizures without other accompanying symptoms/ signs
- A child who has sustained significant injury either before or as a result of the event
- Syncope with abnormal vital signs, cardiac exam and/or ECG
Fits/ faints/ funny turns referalls
Insulin + secretion
- Insulin = Stimulates glucose uptake into liver + muscle, stimulates liver + muscle to store glucose as glycogen. Stops production of glucose in liver
- Lack of insulin = stops uptake of glucose from blood into liver + muscle, stimulates breakdown of glycogen into FFA and ketones. Stimulates hepatic gluconeogenesis.
- Breakdown of glycogen/fat stores -> ketone body production -> acidosis
- Hyperglycemia -> glycosuria -> loss of water + electrolytes
Injectable Insulins:
- Short acting – Novorapid/Humalog (onset 15mins, peak action 2hrs, last at most 3/4hrs) and Actrapid (IV for DKA
- Long acting – Degludec (Tresiba- onset 2-4hr,lasts 24-48hrs), Levimir (Detemir-onset 2-4hrs,lasts 24hrs), Glargine (Lantus- onset 2-4hrs, lasts 24hrs)
- Basal Bolus/MDI: long acting at night, short acting with meals. More injections, more flexibility.
- Pumps: Variable basal rates, boluses with food and for correction of hights. Can programme temporary rates for eg, illness, but needs more monitoring. Short onset of DKA and always attached
Adrenal hormone synthesis
en do we measure children
Measuring children:
- Weight – birth, 2, 8, 12, 16weeks, 1 year, annually
- Length – until 2
- Height – until 2
- Centiel charts
- BMI = weight kg/ height^2 (M^2) for 2years+
SOme rashes
Blood gases
Feeding requirements/ problems in babies (term)
Breastfeeding or formula recommended until 12months. After 6m age breast milk isn’t enough so solid foods recommended ot be introduced between 17weeks – 26weeks
Milk aspiration – more frequent in preterm + respiratory distress or neuro damage. Those with bronchopulmonary dysplasa often have GORD which predisposes and cleft palate.
- Scabies
- Infestation with mites which burrow down epidermis along stratum corneum. Severe itching 2-6weeks after infestation and worse in warm conditions at night.
- Complciations – skin excoriated due to scratching anf secondary eczematous or urticarial reaction. Secondayr bacterial infections.
- Tx – whole family treted too. Permethrin cream below neck and washed off after 8-12hurs. Also malathion lotion is good.
FBC/U&E interpretation
Blood glucose, inflammatory markers etc
