Paediatric core conditions 5 Flashcards

1
Q

Testicular torsion- basics

A
  • twist of the spermatic cord resulting in testicular ischaemia and necrosis.
  • most common in males aged between 10 and 30 (peak incidence 13-15 years)
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2
Q

Testicular torsion- features

A
  • pain is usually severe and of sudden onset
  • the pain may be referred to the lower abdomen
  • nausea and vomiting may be present
  • on examination, there is usually a swollen, tender testis retracted upwards. The skin may be reddened
  • cremasteric reflex is lost
  • elevation of the testis does not ease the pain (Prehn’s sign)
  • Lie of the testis may be horizontal (bell-clapper position)
  • In neonatal torsion the patient may be asymptomatic and present as a firm, hard and enlarged testis in a blue scrotum
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3
Q

Testicular torsion: mangement

A
  • treatment is with urgent surgical exploration with fixation of the testicles with bilateral orchidoplexy
  • if a torted testis is identified then both testis should be fixed as the condition of bell clapper testis is often bilateral.
  • Manual detorsion can be performed if the patient presents early
  • Post operatively the patient is provided with scrotal support and advised bed rest for 24 hours and refrain from heavy lifting or exercise for the first few weeks
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4
Q

Testicular torsion: investigations and complications

A

Investigations
* Doppler ultrasound scan: shows lack of blood flow to the testis
* Surgical exploration confirms the diagnosis

Complications: atrophy or necrosis of the testis, infection, subfertility

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5
Q

Neonatal hypoglycaemia

A

Normal term babies often have hypoglycaemia especially in the first 24hrs of life but without any sequelae as they can utilise alternate fuels like ketones and lactate. Normally <2.6 mmol/L. Transient hypoglycaemia in the first few hours after birth is common.

Persistent/severe hypoglycaemia may be caused by: Preterm birth (<37 weeks), maternal diabetes mellitus, IUGR, Hypothermia, Neonatal sepsis, Inborn errors of metabolism.

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6
Q

Neonatal hypoglycaemia: features

A
  • May be asymptomatic
  • Autonomic (hypoglycaemia -> changes in neural sympathetic discharge)= jitteriness, irritable, tachypnoea, pallor
  • Neuroglycopenic= poor feeding/sucking, weak cry, drowsy, hypotonia, seizures
  • Other features: apnoea, hypothermia
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7
Q

Neonatal hypoglycaemia: management

A
  • Asymptomatic: encourage normal feeding (breast or bottle), monitor blood glucose
  • Symptomatic or very low blood gas: admit to the neonatal unit, intravenous infusion of 10% dextrose.
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8
Q

Transient tachypnoea of the newborn: pathophysiology

A
  • It is a parenchymal lung disorder characterised by pulmonary oedema resulting from delayed resorption and clearance of foetal alveolar fluid.
  • It is the commonest cause of respiratory distress in the term baby.
  • Commonly occurs after a C-section as passage through the birth canal applies external pressure on the thorax to help expel the fluid
  • Some babies have delayed resorption of the fluid due to suboptimal epithelial clearance
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9
Q

Transient tachypnoea of the neonate: presentation, diagnosis, management

A

Presentation= respiratory distress (tachypnoea, increased work of breathing and potentially desaturated/cyanotic)

Diagnosis= TTN is diagnosed both clinically an by hyperinflated lungs and fluid level on the chest x-ray

Management= oxygen support. Should resolve in a couple of days with resorption of lung fluid within the first 3 days of life

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10
Q

Respiratory distress syndrome: surfactant

A
  • Neonatal respiratory distress syndrome (NRDS) is caused by a lack of surfactant.
  • Surfactant is a phospholipid-containing fluid produced by type 2 pneumocytes.
  • It acts to lower the surface tension in the alveoli helping to keep them open. A lack of surfactant increases surface tension and causes alveoli to collapse, triggering respiratory distress.
  • Surfactant is made from around 26 weeks gestation, although adequate levels are not achieved until about 35 weeks. This means premature babies are at increased risk of NRDS.
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11
Q

RDS: diagnosis

A
  • Diagnosis of neonatal respiratory distress syndrome is principally through clinical evaluation.
  • A ‘ground glass’ appearance may be seen on chest x-ray.
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12
Q

RDS: management and complications

A

Management
* Treatment of neonatal respiratory distress syndrome is with intratracheal instillation of artificial surfactant.
* Additionally, if preterm delivery is suspected, giving the mother glucocorticoids before delivery can increase surfactant production in the baby.

Complications= NRDS is a major cause of pre-term infant mortality and so prompt recognition and treatment is essential.

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13
Q

Overfeeding

A

Really common, uses feeding to settle babies. No sense of ‘fullness’

Signs:
* More than average weight gain
* 8 or more wet nappies per day
* Loose stool
* Milk regurgitation
* Irritability
* Sleep disturbances

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14
Q

What are the appropriate feeding volumes in babies

A
  • 60 ml/kg day 1
  • 90 ml/kg day 2
  • 120 ml/kg day 3
  • 150 ml/kg day 4 and onwards

Preemies and underweight babies may require more. Every 2-3h for 1st few weeks (up to 4h) then longer. Eventually they transition to feeding on demand (when hungry)

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15
Q

Self harm

A

Very common. 32% of 15 year old females, and 11% of 15yo males

Investigations= usually opportunistic. Full physical exam, opportunities to look for signs

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16
Q

PATHOS instrument to assess suicide risk after adolescent OD

A
  • Have you had Problems for over a month?
  • Were you Alone in the house at the time?
  • Did you plan the overdose for longer than Three hours?
  • Are you feeling HOpeless about the future?
  • Were you feeling Sad for most of the time before the overdose?

High risk >2 but use clinical judgment.

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17
Q

Suicide risk- management per BMJ best practise

A
  • ensure safety
  • treat any self-harm or underlying physical illness
  • determine treatment setting (opt for least restrictive that is also safe and effective)
  • safety plan - collaborative, will belong to the patient
  • psychotherapy (e.g. CBT, counseling, …)
  • treat any underlying psychiatric illness (e.g. depression, anxiety)
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18
Q

How is weight faltering defined

A
  • falling across 2 major weight centile lines
  • or being at a weight centile 2+ centiles below length/height
  • or head circumference or weight centile below 2nd centile for age
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19
Q

When is it normal for babies to loose weight

A

-Babies often lose up to 10% of birthweight in the first few days from fluid shifts but should have regained birthweight by 2 weeks.
-This is why the UK-WHO growth charts centile lines start at 2 weeks of age, rather than birth.
-Infants who become acutely ill often lose weight but usually regain their centile within 2-3w
-Some infants with severe IUGR remain small, though most exhibit catch-up growth

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20
Q

Weight faltering- investigations

A

Thorough feeding history
-Hx of milk feeding, age at weaning, range and type of foods, 3d food diary
-Mealtime routine, eating and feeding behaviors
Observed feeding if possible
Any psychosocial problems at home?

Further Ix only needed if faltering is severe and/or other comorbidities or red flags are identified:
-FBC, ferritin, U+E, coeliac screen, LFTs, bone panel, genetic, urinalysis/stools MCS
-Consider hospital admission to observe

21
Q

Weight faltering- psyhosocial causes

A

inadequate feeding - feeding problems, insufficient or unsuitable food offered, no regular feeding times, conflict over feeding, parental intolerance of normal feeding behavior, food unavailable

psychosocial deprivation - mother-infant interaction, maternal depression or other mental health disorder, poor maternal cognitive function

neglect or child abuse - includes factitious illness - deliberate underfeeding to generate weight faltering

22
Q

Psychosocial causes of weight faltering- management

A
  • health visitor - observations, food diaries
  • pediatric dietician or SALT may help
  • input from clinical psychologist, social services
  • nursery placement may help alleviate stress
  • mothers’ and parents’ groups may help
23
Q

Strategies for increasing food intake

A

Dietary
- 3 meals and 2 snacks /day
- Increase number + variety of foods
- Allow to self-feed, even if messy
- Increase energy density of foods (e.g. add cheese, butter, cream to fortify foods)
- Limit milk intake, use infant formula until 12 m
- Avoid XS fruit juice and diluted cordial drinks

Behavioral
- regular meal times
- praise when eating well, ignore when not
- limit mealtime to 30 min
- eat at same time as child
- avoid mealtime conflict
- never force feed

24
Q

Caput succadeneum vs cephalohematoma

A

caput succedaneum - fluid collection on scalp outside periosteum. causes - pressure on an area of scalp during delivery. usually mild or no bruising. resolves in a few days, no treatment needed

cephalohematoma - blood collection below periosteum. center usually feels soft. resolves over w/m, risk of anemia and jaundice

25
Q

Chignon and Subaponeurotic haemorrhage- birth injury

A

Chignon- oedema and bruising from ventouse delivery

Subaponeurotic haemorrhage- very uncommon. Diffuse, boggy swelling of scalp. Blood loss may be severe, can lead to hypovolaemic shock and coagulopathy

26
Q

Facial paralysis and Erb’s palsy- birth injury

A

Facial paralysis- typically associated with forceps delivery. Normally function returns spontaneously within a few months. If it doesnt, may require neurosurgical input

Erb’s palsy- (C5/C6 injury) typically associated with shoulder dystocia, traumatic/instrumental delivery, large BW. Results in waiters tip

27
Q

Fractured clavicle- birth injury

A
  • Large shoulder dystocia, traumatic/instrumental delivery, large BW.
  • Conservative management (usually immobilization) – usually heals well
  • Main complication – injury to brachial plexus and subsequent nerve palsy
28
Q

What are some potential manifestations of HSV infections

A
  • Most are asymptomatic.
  • Gingivostomatitis – may need IV fluids and aciclovir.
  • Skin manifestations – mucocutaneous junctions, e.g. lips and damaged skin.
  • Eczema herpeticum – may result in secondary bacterial infection and sepsis.
  • Herpetic whitlows – painful pustules on the fingers.
  • Eye disease – blepharitis, conjunctivitis, and corneal ulceration.
  • CNS – aseptic meningitis, encephalitis.
  • Pneumonia and disseminated infection in the immunocompromised
29
Q

Chicken pox (VZV)- features and treatment

A
  • Clinical features – fever and itchy, vesicular rash, crops of lesions arising at different times for up to 7 days.
  • Treatment is mainly supportive; IV aciclovir for severe chickenpox and for immunocompromised children
  • Human varicella zoster immunoglobulin – if immunocompromised and in contact with chickenpox or if there is maternal chickenpox shortly before or after delivery
30
Q

Complications and transmission of chicken pox

A

Rare but serious complications incl.

Encephalitis, 2ndary bacterial infection, purpura fulminans, pneumonia, disseminated haemorrhagic chickenpox

Transmission: respiratory droplets, contact with lesions

31
Q

Chicken pox- red flags

A
  • Child with chickenpox whose fever settles but then recurs a few days later: Secondary bacterial infections
  • Beware of admitting a chickenpox contact to a clinical area with immunocompromised children: can disseminate and cause potentially fatal disease
32
Q

EBV

A
  • Infectious mononucleosis (aka glandular fever)
  • Also involved in Burkitt lymphoma, lymphoproliferative disease (immunocomp), and nasopharyngeal carcinoma
  • A lymphotropism of B cells (also epithelial cells of the oropharynx)
  • Transmission: saliva
33
Q

Features of infective mononucleosis

A

Main features:
- fever
- malaise
- lymphadenopathy
- tonsillitis/pharyngitis

Other features:
- petechiae on soft palate
- hepatosplenomegaly
- maculopapular rash
- jaundice

Sx may persist for 1 to 3m

34
Q

Infectious mononucleosis management

A

supportive
if airway compromised, corticosteroids

note= ampicillin or amoxicillin can cause a florid maculopapular rash in children infected with EBV and should therefore be avoided

35
Q

CMV: transmission, features and treatment

A
  • Transmission: saliva, genital secretions, breastmilk, rarely blood products, organ transplants and transplacentally
  • Features: may cause mild mononucleosis like syndrome. Main risk is congenital CMV infection and infection in the immunocompromised
  • Treatment: may include IV ganiclovir, oral valganiclovir, foscarnet or cidofovir
36
Q

HHV- 6 and HHV-7

A
  • Closely related and have similar presentations, although HHV-6 is more prevalent.
  • Most kids infected by age 2, usually from oral secretions of a family member.
  • Classically cause roseola infantum (aka exanthema subitum) - high fever, malaise lasting a few d, followed by generalized macular rash
  • Frequently misdiagnosed as measles or rubella - should confirm by PCR or serology.
37
Q

Human parvovirus B19 features and treatment

A
  • usually asymptomatic
  • if symptomatic, mild fever, coryza, myalgia, lethargy then slapped cheek rash spreading to limbs
  • supportive treatment; it is contagious so stay home
  • pregnant, immunocomp, hematological conditions are at risk
  • Slapped cheek syndrome
38
Q

Enterovirus: possible features

A
  • mostly asymptomatic and self-limiting with rash, which may be petechial
  • hand, foot, and mouth disease (coxsackie A16 - mild systemic upset, oral ulcers followed by vesicles on the palms and soles)
  • eczema coxsackium (affects kids with eczema; causes vesicles, bullae, erosions)
  • Supportive treatment
39
Q

Measles- clinical features

A
  • fever, cough, runny nose, conjunctivitis, marked malaise, Koplik spots, and maculopapular rash.
  • Viral resp illness with cold-like symptoms, conjunctivitis, cough, fever
  • Incubation 10-14d -> sx -> 2-3 d after sx onset Koplik spots -> 3-5d after sx onset measles rash
40
Q

Measles- investigations, management and complications

A
  • Investigations: measles specific IgM and IgG and PCR
  • Management: self-limiting, supportive, paracetaml/ibuprofin
  • Complications: Ear infections followed by HL, diarrhea, pneumonia, encephalitis, SSPE (years later, quite rare). Complications common if malnourished or immunocompromised, still major cause of death in low-income countries
41
Q

Mumps features

A

Acute infectious disease caused by paramyxovirus, spread by droplets, fomites, saliva
-Incubation – 2-3 w and then sx last about 9 days
-Not very common now due to MMR vaccine
-Sx – parotitis, tender glands, earache, difficulty chewing, systemic (fever, headache, appetite loss, fatigue)

42
Q

Mumps: investigations and management

A

-Ix – clinical diagnosis, confirmed by saliva sample (IgM)
-Mx – notifiable, self-limiting, supportive care, follow-up, isolation
-Complications – rare, epididymo-orchitis, oophoritis, meningitis, encephalitis, deafness, pancreatitis
-Dx – parotid duct obstruction, metabolic disorders

43
Q

Rubella- features and diagnosis

A
  • Respiratory spread - Incubation - 2-3 w
  • Mild disease - lymphadenopathy -> erythematous maculopapular rash (3-5d) (usually) and non-specific symptoms
  • Rash is face and neck then spreads down body
  • Infectious from 1w before sx to 4d after rash
  • Diagnosis: clinical suspicion and saliva swab to confirm
44
Q

Congenital rubella syndrome

A

Classic triad:
- congenital cataracts (white pupils)
- SN deafness
- Patent ductus arteriosus (could be pulmonary artery stenosis as well)

Could potentially also result in microcephaly and mental retardation - non-pregnant females should be vaccinated with the live MMR vaccine prior to pregnancy.

45
Q

Small bowel obstruction in neonates- causes

A

atresia or stenosis of duodenum, jejunum, or ileum- duodenal atresia is common in Down syndrome. associated with other congenital malformations

meconium ileus- almost all affected neonates have CF

malrotation with volvulus- dangerous, may lead to infarct of entire midgut

46
Q

Small bowel obstruction in neonates- presentation

A

May be recognized antenatally on US. Otherwise - persistent, vomiting, bilious (unless above the ampulla of Vater)

  • meconium may be passed initially
  • then no normal stool
  • abdominal distension

Depending on where the obstruction is, presentation may be soon after birth or some days after

47
Q

Small bowel obstruction in neonates- investigation, diagnosis and management

A
  • Diagnosis made on clinical features and AXR
  • If atresia, stenosis, malrotation: fluids and electrolytes then surgery
  • If meconium ileus: gastrografin contrast medium, surgery if unsuccessful
48
Q

Large bowel obstruction in neonates: causes

A

1) meconium plug - usually passes spontaneously
2) imperforate anus- complex anatomy requiring surgery - initially colostomy then reconstruction when older
3) Hirschsprung disease - absent myenteric nerve plexus in the rectum (may extend along colon). M>F, Down syndrome. Often don’t pass meconium in first 48h, then abdo distension

49
Q

Causes of bilious vomiting

A

1) Neonates: volvulus, Hirschsprungs disease, Necrotising enterocolitis, upper GI obstruction including duodenal atresia
2) Infants: upper GI obstruction including strangulated hernia, intussusception, adhesions