Essential Conditions (2) Flashcards
Causes of constipation?
Idiopathic - low fibre, lack of mobility and exercise, poor colonic motility
GI - Hirschsprung’s, anal disease, partial intestinal obstruction, food hypersensitivity, coeliac disease
Non-GI - hypothyroidism, hypercalcaemia, neuro disease, chronic dehydration (diabetes insipidus), drugs, sexual abuse
Red flag symptoms in constipation?
Failure to pass meconium - Hirschsprung’s
FTT - hypoT, coeliac
Gross distension - Hirchsprung, GI dysmotility
Perianal fistulae, abscesses or fissures - perianal Crohn’s disease
History features in constipation?
Straining and/or infrequent stools Anal pain on defecation (Crying) Fresh rectal bleeding (anal fissure) Abdominal pain Anorexia Growth failure
Management of constipation?
DIETARY
Increase fluid intake, increase fibre, natural laxatives (prune juice)
BEHAVIOUR
Toilet footrests, regular toilet time, don’t show concern to child
MEDICATION
Disimpaction and maintenance - consistency and adherence, treat for at least 3 months.
Disimpcation regieme?
Regular oral faecal softeners e.g. Movicol
Oral stimulant laxatives e.g. Senna
Marcogel laxative e.g. Polyethene glycol (PEG)
Escalating dose for 1-2 weeks until impaction resolves.
Long term treatment allows rectum to return to normal size –> sphincter function regained
Causes of gastroenteritis?
Viral - ROTAVIRUS, adenovirus, norovirus, coronavirus, astrovirus
Bacterial - CAMPYLOBACTER JEJUNI, shigella, salmonella, E.coli, cholera
Indications for stool sample in gastroenteritis?
blood in stools
dysentery (mucous + blood), immunocompromised child
recent foreign travel
uncertain diagnosis
Advice in gastroenteritis?
Little and often fluids better than regular
Appropriate hand hygiene
Avoid antidiarrhoeals
SAFETY NET = weeing/drinking <50% normal or difficulty in waking
Management of dehydration in gastroenteritis?
Mild (<5%) = oral rehydration
Moderate (5-10%) = ORS 50ml/kg over 4 hours –> IV therapy if necessary
Severe (>10%) = boluses 20ml/kg then IV therapy for rehydration (100ml/kg)
AND MAINTENANCE
When does GORD usually resolve by?
12 months
Presentation of GORD?
GI - Vomiting (non-billious), Faltered growth , Oesophagitis
Resp - Apnoea, hoarseness/cough/stridor, lower RT disease
Complications of GORD?
Failure to thrive
Oesophagitis - Haematemesis, Discomfort on feeding/heartburn, Iron deficiency anaemia (chronic blood loss)
Recurrent pulmonary aspiration - Recurrent pneumonia, Cough or wheeze, Apnoea in preterm infants
Dystonic neck posturing - Sandifer Syndrome
Investigations in GORD?
Usually none - of uncertain, complications or not responding to treatment
24-hour oesophageal pH monitoring - Can quantify degree of acid reflux – GORD = acid in oesophagus for >4% of day
24-hour impedance monitoring
Endoscopy and biopsy - Identify oesophagitis and exclude other causes of vomiting
Fluoroscopy - Barium swallow. Can identify things like – achalasia, oesophageal strictures, malrotation
Management of GORD?
GENERAL
• Sit baby upright when possible (30o head-up prone position post-feeding) – encourage papoose slings
• Small regular feeds – avoid feeds before sleep, avoid fatty foods, citrus juices, caffeine and carbonated drinks.
• Do not overfeed (stomach = child’s fist)
• Add gaviscon to feeds and thicken feeds
MEDICAL
GORD - gaviscon, omeprazole, ranitidne, domperidone - reassess after 4-6 weeks
SURGICAL
Nissen’s fundoplication - failed intensive treatment, Barrett’s oesophagus, stricture, severe oesophagitis, recurrent apnoea, LRT disease, FTT
Red flag symptoms of vomiting
Bile stained - obstruction
Haematemesis - oesophagitis, peptic ulcer, oral/nasal bleeding
Projectile in first weeks - pyloric stenosis
Vomiting at end of paroxysmal coughing - whooping cough
Abdo tenderness - surgical abdomen
Abdo distension - obstruction, strangulated hernia
Organomegaly - chronic liver disease
Bloody stool - Intussception, bacterial gastroenteritis
Severe dehydration/shock - severe gastroenteritis, systemic infection, DKA
Bulging fontanelle/seziures - raised ICP
FTT - GORD, coeliac
Presentation of TIDM?
Thirsty
Toilet
Thinner
Tired
Diagnosis of TIDM?
Symptomatic AND
Random BM of >11.1 mmol/L
Other tests you should do in T1DM?
U&Es
Blood pH (to exclude DKA)
Diabetes antibodies (Anti-islet cell, Anti-insulin, Anti-GAD)
Autoimmune disease screen (TFTs, Tissue Transglutaminase (TTG), anti-gliadin and anti-endomysial)
Education on T1DM?
Pathophysiology
Injection (site rotation)
Sick day rules - extra monitoring when unwell, may need dose changing, maintain carbohydrate/fluid intake as much as possible - call diabetes team if vomiting/diarrhoea
Recognition of hypos
Voluntary groups (Diabetes UK)
Diet in T1DM?
o Reduced refined carbohydrates (low glycaemic index)
o No more than 30% fat intake
o Carbohydrate counting (1 unit per 20g of carbs)
Complex carbohydrates Adjustments of diet and insulin for exercise
BM monitoring in T1DM?
Regular monitoring when blood levels suspected to be high or low – adjust insulin regimen.
Aim = keep blood glucose as near to normal as possible (4-10 mmol/L in children, 4-8 mmol/L in adolescents)
Minimal testing 4 times a day (can be done with subcutaneous continuous glucose monitoring - CGM)
HbA1c to be checked at least 3 times a year.
Sites for insulin injection?
Injection sites – 45 degree angle – site rotation essential.
o Upper arm
o Anterior/lateral thigh
o Buttocks
o Abdomen
Management of hypos?
Hunger, sweatiness, faint/dizzy, irritability/ confusion, pallor
• Oral glucose
o Buccal gels
o Drinks (Lucozade)
o Tablets
If unconscious – IM glucagon injection..
What is mild and severe FTT?
Mild = falls across 2 centile lines
Severe = falls across 3 centile lines
Management of non-organic FTT?
MDT - carried out in primary care by increasing energy intake
Healthcare visitor - can assess eating behaviour and provide support
Dietary advice, behavioural modification, monitoring growth
Dietician, SALT, social services, nursery placement
Management of extreme cases of FTT?
Admission if <6 months requiring active refeeding - can observe and improve mother’s feeding skills and demonstrate that child will gain weight when fed appropriately.
If it continues despite dietary input - investigations for organic cause
Causes of FTT?
INADEQUATE INTAKE
Non-organic = inadequate availability of food, psychosocial deprivaiton, neglect or child abuse Organic = impaired suck/swallow, chronic illness --> anorexia
OTHERS
Inadequate retetnion (vomiting, severe GORD) Malabsorption (coeliac, CF, CM intolerance) Failure to utilise nutrients Increased requirements (thyroid, CF, malignancy, infection, CHD)
Why is vesico-ureteric reflux bad?
Can cause renal scarring –> HTN
Risk factors for UTI?
Constipation Female gender VUR CAKUT (posterior urethral valves, boys only) Previous UTIs Encopresis Nephrolithiasis Uncircumcised boys
Organisms causing UTI?
E.coli = most common
Klebsiella, proteus, pseudomonas, strep faecalis
Methods of urine collection?
Clean catch
MSU
Catheter (transurethral or suprapubic)
Urine bag
Definition of recurrent UTIs?
2 or more upper
1 upper and 1 lower
3 lower
Definition of atypical UTI?
Seriously ill Poor urine flow Raised creatinine Septicaemia Non-E.coli Failure to respond in 48 hrs
Criteria for UTI investigations?
<6 months - USS in 6 weeks (during infection if atypical), DMSA/MCUG if atypical/recurrent
6m - 3y - USS in 6 weeks if recurrent, DMSA 4-6 months if atypical/recurrent
3y + - USS in 6 wks if recurrent, DMSA in 4-6 months if recurrent
Prevention of UTIs?
- High fluid intake
- Regular voiding – ensure complete bladder emptying and encourage child to try second empty
- Perineal hygiene
- Prevent/treat constipation
Treatment of UTIs?
Oral = trimethoprim, cephalexin, co-amoxiclav
IV = cefuroxime, gentamicin
Repeat urine culture on completion of abx.
<3 months = Admit to hospital. IV abx until temperature settled then oral abx.
> 3 months upper = Oral abx for 7-10 days OR IV abx for 2-4 days then oral Abx for total treatment duration 10 days (i.e. 6 days oral)
> 3 months lower = Oral abx for 3 days. If still unwell after 24-48 hours –> reassess.
Where does infantile eczema affect?
Affects the face, neck, behind ears, scalp (cradle cap) and extensor surfaces. Nappy area mostly spared. Majority of cases clear within a few months but may progress.
Where does childhood eczema affect?
Mostly flexor surfaces – antecubital and popliteal fossae, volar aspect of wrists, neck and ankles. Less weepy and wet than infantile eczema but there is marked lichenification.
Complications of eczema?
Bacterial
• Golden crust and sometimes postulation (impetiginized eczema)
• Mild cases can be treated with antiseptic washes and topical antibacterial ointments. Oral abx and topical steroids for widespread infections.
Viral
• Chickenpox can be widespread and severe. Molluscum contagiousum more common.
• Eczema herpeticum = serious HSV complication. Monomorphic clusters of vesciles that erode and crust. Systemic acyclovir and same day dermatology referral.
General management of eczema?
Avoid irritants like soap and biological detergents. Clothing next to skin should be pure cotton where possible – avoid nylon and pure woollen garments.
Cut nails short to reduce damage from scratching.
Mittens at night in the very young
If specific allergen such as cow’s milk proven to be a precipitant –> avoid.
Can use antihistamines to stop itching
Emolients and steroids in eczema?
EMOLIENTS
Mainstay of treatment – apply liberally two or more times a day and after a bath. Can also use emollient oil as a soap substitute in bath - apply in direction of hair.
STEROIDS
Use with care – explain that benefits outweigh risks when used correctly. Prescribe lowest effective strength.
Apply thinly and use on the face should be avoided – excessive use can cause skin thinning and systemic side effects – should not deter from their use in exacerbations though.
Examples of topical steroids?
Mild = 1% hydrocortisone Moderate = 2.5% hydrocortisone Strong = Betnovate/dermovate
Most common cause of septic arthritis?
Staph aureus
Streptococci in neonates
Haematogenous spread
Direct innoculation from wound
Direct invasion from adjacent focus of infection (osteomyelitis)
Presentation of septic arthritis?
Warm, erythematous, swollen and acutely tender joint
Severely restricted joint movement (pseudoparalysis)
Joint effusion
Inability to weight bear – if hip involvement, leg is held flexed and abducted.
75% lower limb – Hip > knee > ankle
<10% will have more than one joint affected
Systemic features = Fever, rigors, tachycardia
Investigations in septic arthritis?
BLOODS
FBC - ↑WCC
CRP/ESR – both elevated
Blood cultures – take before abx commenced
IMAGING
X-ray
USS - effusion and can guide aspiration
ASPIRATION
Carried out under aseptic conditions by orthopaedic surgeon with US guidance can culture organisms guides Abx therapy.
Management of septic arthritis?
IV ABX
Start after joint aspirate and blood cultures taken – splint joint and start empirical broad-spectrum IV abx.
• Flucloxacillin – 3 weeks – until inflammatory markers normalise.
• Followed by oral abx for 4-6 weeks – tailor according to culture results.
SURGICAL
Irritgation/drainage/debridement – if resolution does not occur rapidly.
Prognosis and complicaitons of septic arthritis?
Prognosis is good with prompt recognition and treatment. <10% recurrence and develop chronic infection. Hip joint has worst prognosis.
- Joint stiffness – secondary to cartilage damage
- Septic dislocation – secondary to damage to the joint capsule and bone
- Osteonecrosis – secondary to ischaemia
- Shortening of limb – secondary to dislocation and osteonecrosis
- Secondary osteoarthritis – secondary to damage to joint capsule
Causes of cerebral palsy?
Foetal Structural abnormalities (e.g. cerebral malformation), maternal hypothyroidism, chorioamnionitis.
Neonatal
Premature delivery, birth hypoxia, congenital infections.
Intraventricular haemorrhage, hyperbilirubinemia, hypoglycaemia, cerebral infarcts, meconium aspiration syndrome.
Infant
Hydrocephalus, hypoglycaemia, head injury secondary to non-accidental injury, CNS infection
Child Hypoxic events (e.g. drowning), head trauma, lead poisoning, CNS infections
Pathophysiology of spastic CP?
UMN lesion –> nerve receptors in spine don’t respond to GABA (inhibitory) properly –> hypertonia
Velocity dependent –> weakness, increased tone, brisk reflexes, clonus, bulbar palsy (dysphagia/dribbling)
Three types of spastic CP?
Spastic hemiplegia
Spastic diplegia
Spastic quadriplegia
How does spastic hemiplegia present?
Arm and leg on one side, arms affected more, sparing of face. Spasticity greatest in antigravity muscles.
Affected Arm = flexed, pronated, fisting of hand.
Affected leg = circumduction gait, toe-heel (tip toe) gait. Delayed walking.
May have growth arrest in extremities. Moderate incidence of seizure disorders and intellectual impairment.
How does spastic diplegia present?
Common in ex-prems (intra-ventricular haemorrhage)
Lower limbs (some involvement of ULs). ‘Paraplegia’ if no involvement of ULs.
Commando crawl (dragging legs) Scissoring of lower legs Severely delayed walking Toe-heel gait with feet held in equinovarus position. Legs severely underdeveloped compared to arms.
Disuse atrophy, impaired growth of lower extremities. Usually have normal intellectual development. Other learning difficulties and deficits in other neuro pathways (e.g. hearing). Minimal risk of seizures.
How does spastic quadriplegia present?
All four limbs
As for the others, but in all four limbs. Increased tone throughout, decreased spontaneous movements - worse on running
Swallowing difficulties (bulbar palsy). Weak suck. Tongue thrust. High incidence of seizure disorders, significant intellectual impairment, associated developmental abnormalities (speech, vision)
How does dyskinetic CP present?
- Movements are involuntary and uncontrolled. Become more evident with active movement or stress.
- Infants = initially hypotonic with poor head control. But show increased tone and dyskinetic movements as they develop.
- Oropharyngeal muscles are affected speech and feeding problems.
- Seizures uncommon, intellect usually preserved.
Three main features of dyskinetic CP?
DAC
DYSTONIA
Involuntary, sustained contractions of opposing muscle groups. Leads to abnormal posture, twisting movements and repetitive movements.
ATHEOSIS
Slow, involuntary writhing movements – distal (fingers)
CHOREA
Brief, irregular, non-repetitive/rhythmic movements. Appear to flow smoothly, giving the appearance of dance-like movements.
How does ataxic CP present?
Rare and poorly understood
Lack of voluntary co-ordinated movements of muscle. o Usually symmetrical o Hypotonia o Poor balance o Delayed motor development
Later signs
o Intention tremor
o Ataxic gait (staggering and broad-based)
o Poor co-ordination (dysdiadochokinesia, past-pointing)
Early features of CP?
Abnormal limb and/or trunk posture
Delayed motor milestones
o May be accompanied by delayed head growth
o Primitive reflexes may persist
Feeding difficulties
o Slow feeding, gagging, vomiting
Abnormal gait
o Once walking is achieved (usually 12-18 months)
Asymmetric hand function
o Before 12 years of age
Non-pharmacological management of CP?
Nutrition
At risk of malnutrition and faltering growth. May need NG or PEG feeding.
SALT
Promote use of language and improve swallowing.
Occupational Therapy/Physio
Promote mobility and physical activity for normal daily living.
Adaptive and Communicative Equipment Walkers, poles, frames, braces, splints, wheelchairs/special seats are useful aids.
Education
May need special needs education. Vocational training can help prepare adults for jobs.
Psychologist/Counsellor
Address emotional needs of child/family.
Pharmacological management of CP?
Anti-Muscarinics
Prevent drooling. Glycopyrronium bromide, hyoscine patches, botulinum injection into salivary gland.
Anti-Reflux Medication Reflux a common feature – domperidone, ranitidine.
Bisphosphonates
Prevent osteoporosis – pamidronate.
Anti-spasmodics
Help relieve spasticity – benzos, baclofen (intrathecal), dantrolene, botulinum toxin.
Reserpine
Vesicular monoamine transporter (VMAT) blocker – good for hyperkinetic movements.
Causes of Down’s syndrome?
Majority = trisomy 21 due to non-disjunction during maternal oogenesis.
2% are Robertsonian translocation
2% are mosaic with normal cell line and trisomy 21 line.
How common is Down’s syndrome?
Most common autosomal trisomy. Most common genetic cause of severe learning disabilities.
1 in 1000 live births. 1 in 110 at maternal age 45.
Facial features in Down’s syndrome?
ROSEOLA • Round face • Occiput flattening • Speckled iris (brushfield spots) Epicanthic folds • Open mouth with protruding tongue • Low set ears • Almond (oval) upward slanting eyes
Hand/feet features in Down’s syndrome?
Hands
• Single palmar crease
• Short fingers
• Clinodactyly (Curved little finger)
Feet
• Sandal gap between big toe and other digit
Conditions associated with Down’s syndrome?
CARDIAC
• ASD/VSD/Complete AVSD
• Mitral/tricuspid regurgitation
Leads to Eisenmenger’s syndrome
GI
• Duodenal atresia
• Anal atresia
• Hirchsprung’s disease
OTHERS • Hypothyroidism • Eczema • Leukaemia (1%) • Developmental hip dysplasia • Deafness (sensorineural and conductive) • Alzheimer’s by 5th decade • Infection • Psychological – anxiety etc
Management of Down’s syndrome?
SCREENING Cardiac - Echo Hip US – Developmental hip dysplasia Audiology – deafness TFTs – acquired hypothyroidism In adulthood, annual health screening in primary care. “Personal health action plan” to address any health needs identified.
GENETIC COUNSELLING
Parents - only needed if Robertsonian translocation is the cause and are thinking of another baby.
MDT
Developmental paediatrician, child development centre, physiotherapy, dieticians, occupational therapists, SALT.
Almost all educated in mainstream schools with appropriate educational support.
Prognosis in Down’s syndrome?
Huge variability. Some lead active, semi-independent lives (education, employment).
Life expectancy better now – most live to be over 60. Many will develop Alzheimer’s by 40.
Types of squint?
Concomitant (Non-paralytic)
• Common
• Usually due to refractive error in one or both eyes.
• Can be treated with glasses but may require surgery.
• Squinting eye most often turns inwards (convergent) but there can be outwards (divergent), or rarely vertical deviation.
Non-Concomitant (Paralytic)
• Rare
• Usually due to paralysis of cranial nerves (III, IV, VI)
• Squint varies with gaze direction due to muscle paralysis
• Can be sinister as possibility of underlying brain tumour
Presentation of squint?
Convergent (esotropia) = bad eye turns inwards (COMMON)
Divergent (exotropia) = bad eye turns outwards
Latent = squint controlled by subconscious effort and is not always apparent. In situations such as fatigue, the control is lost and the squint will manifest. Only appears when fixation interrupted (cover test.
Pseudosquint = arises when epicanthic folds give the appearance of a squint which is excluded on testing.
Corneal light reflex test for squint?
Pen torch held at distance to produce reflections on both corneas simultaneously. Light reflection should appear in same position on both pupils – if not, they are misaligned.
Cover test for squint?
Ask child to fix on object 1 metre away. Cover each eye and look for movement of uncovered eye.
If manifest…
May correct and fix on object being focused on (NON-PARALYTIC)
May stay in same position (paralytic)
If latent…
Can only identify by looking through a semi-transparent ‘cover’ or by quickly removing the cover and looking for correction of the eye.
Management of squint?
Aim to get weaker eye ‘trained up’ • Correct refractive error – glasses o Hypermetropia = long-sighted – most common refractive error o Myopia = short sighted, common • Eye patch on good eye • Eye muscle exercises • Eye (muscle) surgery if large squint.
What can happen if you don’t correct a squint?
AMBLYOPIA
Signal from bad eye depressed to avoid double vision. Constant depression –> failure of visual development
