Paeds Flashcards
Diagnosing T1DM in a child
Fasting glucose >/= 7
*Random blood glucose >/= 11.1
HbA1c >/= 48
Extra: Blood pH to exclude DKA Diabetes antibodies U&Es Autoimmune screen
1st presentation of T1DM1 management
Immediate
+
Long term
SAME DAY MDT paediatric diabetes team
Insluin ASAP
Admission for education + support
1) Insulin therapy: technique, dose adjustment
2) Nutritional: Complex carb high, <30% fat, 15-20% protein, refined sugar <25%
3) Monitoring of glucose: 4 x per day
Regualar management
- Avoid hypos
- Manage acute illness and avoid DKA
- Screen for micro and macrovascular complciations
Insulin need varies with age
Ongoing integrated package of care by MDT diabetes team
24 access to the team
Home-based care with support from local paediatric diabetes team
Initial inpatient management IF:
< 2 years
social/emotional factors
Home very far from hospital
Liase with school staff + education etc etc
Record details on Diabetes Register
Hypoglycaemia signs + cut off
Treatment
<4 blood glucose
Symptoms:
Hungry, dizzy, tummyache, faint, wobbly, progression to coma and seizures
Frequent episodes equals losing awareness of symptoms
Treating hypo
Early: sugary drinks or glucose tablet. Buccal if child unco-operative
Severe: glucagon injection kit if reduced consciousness (IM)
Unconscious: hospital to treat with IV glucose
After treatment biscuit/sandwich to prevent drop again
DKA management
Blood pH <7.3 + blood glucose >11.1, bicarb <15, capillary ketones >3mmol/l
A: Airway if coma. NGT if vom or coma
B: 100% oxgen face mask
C: Iv cannula, take bloods
- if shocked - 10ml/kg 0.9% saline bolus (Discuss more with consultant)
Diagnosis confirmation
Investigations: Blood glucose, Na, Cl, Ur, Cr, venous/cap blood gas
FLUIDS = requirement = deficit + maintenance
- Deficit 5% if ph>/= 7.1. 10% if <7.1.
- Maintenance if <10kg (2ml/kg/h), 10-40 (1ml/kg/h), more (fixed 40ml/hr)
FLUID = 0.9% NaCl (with 20 mmol/l KCl per 500ml)
Hourly rate = (10 x deficit/48) + maintenence/hour
BUT subtract boluses if >20ml/kg given before dividing
INSLUIN 1-2h after beginning IV fluid therapy
(dose 0.05-0.1 units/kg/hr)
Hourly monitoring: Cap glucose, fluid balance, GCS, vital signs
DKA risk
Cerebral oedema
Hypokalaemia
Aspiration pneumonia
T1DM follow up
4 x per year Regular dental Optician every 2 years Autoimmune screening Carry bracelet
Hypothyroid congenital vs acquired presentation
Congenital Usually asymptomatic and picked up on screening – faltering growth – feeding problems – prolonged jaundice – prolonged jaundice – constipation along – horse cry – delayed development – constipation along – hoarse cry – Congenital abnormalities e.g. heart defects
Acquired
SHORT STATURE
Classic
Females more than males
Why does neonatal hyperthyroidism occur
In infants of mothers with thyrotoxicosis from transplacental transfer of auntie TSH receptor antibodies – requires treatment as fatal but resolved with regression of maternal antibodies
CAH diagnosis
Presentation
Diagnosis
- 17-a-hydroxyprogesterone elevated for classical deficiency in 21 alpha hydroxylase
- 11-deoxycortisol if beta hydroxylase deficiency
DO blood gase \+ U&Es Genetic analysis Urinary steroids Pelvic and adrenal US for ambiguous genetalia at birth
Presentation
- F: At birth, virilisation
- M: salt losing crisis in the 80% that are salt loser ~ 1-3 weeks old = vom, weight loss, hypotonia, FTT
- -> Hypotension, hyponatraemia, hyperkalaemia, metabolic acidosis
Later features = Precocious puberty + final height below expected
Delayed puberty in female tests
Unlikely to be constitutional so do
- karyotyping
- TFTs
- Sex steroid hormones
- Consider eating disorder and pituitary pathology
Precocious puberty girl ultrasound
Uterus goes from tubular to pear shaped and can identify endometrial lining near menarche
Males causes of precocious puberty and how to differentiate
Differentiate based on testicular size
Bilateral enlargement (>l4m) = GDPP
Prepubertal testes = GIPP e.g. Adrenal tumour/CAH
Unilateral enlargement equals gonadal tumour
Normal puberty males
First sign is testicular growth at around 12 years of age (range = 10-15 years)
testicular volume > 4 ml indicates onset of puberty
maximum height spurt at 14
Normal puberty girls
first sign is breast development at around 11.5 years of age (range = 9-13 years)
Height spurt reaches its maximum early in puberty (at 12) , before menarche
Menarche at 13 (11-15)
Increase of only about 4% of height following menarche
Precocious puberty males
Secondary sexual characteristics <9
Precocious puberty causes (broadly)
- Gonadotrophin dependent (‘central’, ‘true’)
Due to premature activation of the hypothalamic-pituitary-gonadal axis
FSH & LH raised - Gonadotrophin independent (‘pseudo’, ‘false’)
due to excess sex hormones
FSH & LH low
Thelarche
Premature breast development
Typically between six months to 2 years
Rarely be on stage three puberty
Non-progressive and self-limiting
Adrenarche
Premature appearance of androgen dependent secondary sexual hair development acne and exhilarate odour
- Less than eight years in females
- Less than nine years in males
Causes of HIE
Biochem picture
[1] fail of gas exchange across the placenta - abruption, uterine rupture, excess contactions
[2] Interruption of umbilical bloodflow - prolapse, compressionl
[3] Inadequate placental profusion perfusion - PET, HTN
[4] Compromised fetus - IUGR, anaemia
Hyperoxia hypercarbia metabolic acidosis
Due to cardiorespiratory depression
Classification of H I E
How to diagnose
Mild: hyperventilation, hypertonia, Impaired feeding, responds excessively to stimulation
Moderate: movement abnormalities, hypotonic, cannot feed,? Seizures
Severe: no spontaneously response to pain, tone fluctuates, prolonged seizures, multi organ failure
Diagnosis needs
- Asses for intrapartum problen (e.g. CTG, prolapse)
– Resp depression at birth + need to resuscitate (Five minute Apgar <5)
– ACIDOSIS soon after birth (pH less than 7.0)
– Encephalopathy within 24 hours of birth
– Other causes of encephalopathy excluded
Management
- Resp suppor, AVOID HYPERTHERMIA (33-34 degrees best), fluid restrict, treat hypotension, monitor electrolytes and glucose, CFAM
Prognosis
- Mild - expect full recovery
- Moderate and feeding by 2 weeks = good prognosis
- Abnormalities persiting beyond 2 weeks = unlikely recovery
30% mortality if severe
What is PVL
Periventricular white matter lesions - echogencity, cysts = diagnosis on cranial US or MRI
- Due to severe HIE, poor cerebral perfusion, ischaemia, inflammation
Risk factors Extreme prematurity Hypertension Severely ill Hypercarbia
Prognosis
CP - SPASTIC DIPLEGIA LIKELY
Define with cause
Caput secuccedaneum
Cephalhaematoma
Chignon
Caput secuccedaneum
- Bruising and oedema of presenting part
- ACROSS SUTURE LINES
- above periosteum
- Resolves in a few days
Cephalhaematoma
- Haematoma from bleed below periosteum
- Condfined so doesn’t cross sutures
- Centre feels soft
- Resolves over several weeks
Chignon
- Oedema and brusing from Ventouse
Respiratory distress syndrome
Risk factors
Cause
Presentation
Management
- Oxygen sats to aim for and why
Risk factors
- PREMATURITY
- Male
- C-section
- 2nd of premature twins
- Diabetic mum?
Cause
- Surfactant deficiency –> alveolar collapse + inadequate gas exchange
Presentation
- WITHIN 4h
- Tachypnoea >60, Recession, nasal flaring, expiratory grunting, cyanosis if severe
Management - Oxygen (21-30%) --> 91% to 95% <91% = NEC + DEATH risk >95% = ROP
May need surfactant therapy or additional resp support
Prematurity pneumothorax causes
Symptoms
Diagnosis
Management
1) Premature (RDS)
2) Meconium aspiration
3) Pulmonary hypoplasia
4) Pneumonia
5) TTN
6) Mechanical ventilation
Clinical picture
- Reduced breath sounds and chest movement on affected side
Dx: Transillumination with fibre optic light
Management
- Chest drain if tension
- Otherwise resolves alone
- prevent with lowest pressure ventilaton