Paeds Flashcards
Normal resp rate for: Term-3 mo 4-12mo 1-4yrs 5-12yrs 12yrs+
Term-3 mo: 30-60 4-12mo: 30-40 1-4yrs: 20 5-12yr: 16 12yrs+: 16
HR MET criteria for: Term-3 mo 4-12mo 1-4yrs 5-12yrs 12yrs+
Term-3 mo: <100 >180 4-12mo: <100 >180 1-4yrs: <90 >160 5-12yrs: <80 >140 12yrs+: <60 >130
Normal signs of respiration in young children (4)
Chest in-drawing
Periodic respiration (not constant rate) BUT NO APNOEA
Incr rates of resp
Definition of apnoea in newborns
No respiratory effort for greater than 20 seconds.
No respiratory effort for shorter periods of time may also be classified as apnoea if accompanied by cyanosis or bradycardia
Causes of the following types of tachypnoea:
• Expiratory wheeze (lower airway obstruction with asthma, bronchiolitis)
• Exhaling with a closed glottis (pneumonia)
• Stridor (upper airway obstruction)
• Effortless (DKA)
other
- Expiratory wheeze (lower airway obstruction with asthma, bronchiolitis)
- Exhaling with a closed glottis (pneumonia)
- Stridor (upper airway obstruction)
- Effortless (DKA)
Other: anaemia, fever, cardiac failure, CNS pathology
Most common causes of bradycardia
Hypoxia MOST COMMON
Bradyarrhythmia
Drugs
Causes tachycardia
Fever Pain, Anxiety Hypoxia, hypercarbia, Hypovolaemia Anaemia Arrhythmia, cardiac failure Seizures Drugs
Causes of hypotension with
- Wide PP
- Narrow PP
- Wide PP (120/20)
- PDA
- AR
- Thyrotoxicosis
- Anaemia
- Sepsis - Narrow PP (70/50, weak thready pulse)
- Hypovolaemia
- Haemmhoragic shock
- Severe dehydration
- AS, coarctation of aorta
24 hours of fever, lethargy and vomiting in child.
- primary diagnosis and management
Bacterial sepsis until proven otherwise!
- A: Protect airway (sit up/safety position;; NG tube; yankee sucker)
- B: Give O2 >5L/min
- C: Give Hartmann’s or saline
- BSLs
- Reassess
- ORder: Blood cultures, blood gas
- Prophylactic antibiotics
- Call reg and PET service
Lump in children - what are the 3 main differential categories?
- Congenital
- Inflammatory
- Cancer
What is exomphalos?
What about this kills babies?
Exomphalosis a weakness of the baby’s abdominal wall where the umbilical cord joins it. This weakness allows the abdominal contents, mainly the bowel and the liver to protrude outside the abdominal cavity where they are contained in a loose sac that surrounds the umbilical cord.
It is the evaporative heat loss leading to hypothermia that kills babies
What is the most common DDX for a lump on the eyebrow at birth
Treatment
Exoid dermoid cyst (developmental remnant)
Treatment is surgical excision
How do you treat strawberry naevi
Propranolol accelerates their complete regression (would go away on their own by ~5 years)
What are the signs of hydrocephalous in infants?
Macrocephaly
Sun setting eyes (can only see upper half of iris)
Bulging fontanelle
Seizures
Causes of hydrocephalous in infants - what is the most common?
Congenital
Acquired
- Most common is medullary blastoma in 4th ventricle
- intraventricular haemmhorage
- SA haemmhorage
- meningitis
- SC lesion/tumour
- Traumatic head injury
- premature birth
What are you worried about when you see an absent anal cleft?
Sacrococcygeal teratoma -> tumor on coccyx that eventually grows to fill out the anal cleft and can grow larger than the baby. Turns malignant peri-natally
What is the functional consequence of cleft palate in babies?
Swallowing and sucking difficulties (can usually swallow but not suck)
What is the significance of an enlarged Virchow’s node in children? What does it drain?
What differentials you think of ?
Virchow’s node only enlarged with cancers, not inflame conditions. Drains the thoracic duct.
Hodgkins (10-15 year olds) or Neuroblastoma (very young children)
What is the most common anorectal malformation in females?
Symptoms
REctovestibular fistula. Abnormal connection between vagina and the rectum.
Symptoms: Gas, faeces, pus passing through vagina
- Vulvar irritation, inflammation
- Gross smelling vaginal discharge
- Frequent UTIs
- Pain during sex if older
Clinical features of malrotation
Early signs
- Bilious vomiting (flour green)
- Poor feeding
Late signs include: PR bleeding, abdominal distention and tenderness
What causes malrotation?
Anatomical variation where base of mesentery is narrow which means DJ flexure and Ileocaecal flexure are next to each other, in RUQ which results in SHORT BASE OF MESENTERY and predisposes the mesentery to volvulus
With malrotation, at what point does venous and arterial supply become compromised and when is best to intervene?
- If mesentery twists 360deg, venous and lymphatic supply are compromised resulting in bile-stained vomiting. Surgical intervention here has good outcome.
- If gut rotates further, arterial supply can become compromised -> intestinal ischaemia and infarction
How do you diagnose malrotation?
What is the treatment?
Upper GI contrast study is gold standard - look for LOSS OF C-shaped duodenum to indicate malrotation
Or AXR changes: double bubble, gastric and proximal duodenal dilatation…
Urgent surgical referral and laparotomy -> LAdd’s procedure + appendicectomy
Child with bile stained vomiting - diagnosis
Malrotation +/- volvulus until proven otherwise
Non-bilious vomiting in neonates - differentials
Pyloric stenosis
Infection - Sepsis, Meningitis, UTI
Reflux
Overfeeding
Typical presentation of hypertrophic pyloric stenosis
PYLORIC STENSOSIS: Typically first born boys, with non-bilious projectile vomiting (vomit past their feet) after each feed who are HUNGRY after!
- family history of HPS
- visible gastric peristalsis
+/- palpable pyloric tumour (‘olive’) if stomach isn’t too distended
When does pyloric stenosis typically present?
Peak 3-6 weeks old
But can occur 10 days-11 weeks
What metabolic derangements do you see in pyloric stenosis and why?
Due to profuse vomiting -> losing water, HCL, NACL, K
Metabolic alkalosis
Hypochloraemia
Hypokalaemia
Normal serum na
Acidic urine (paradoxical change - kidneys conserve Na as compensation)
What is intussception and what generally causes it?
Invagination of proximal into distal bowel
- Peaks at 5-11 months
- Physiological/idiopathic cause is most common (hypothesised that as babies wean, new antigen exposure causes payer’s patches in terminal ileum to swell from inflammation and cause intussception)
Less commonly can be due to pathological lead points
Classic presentation of intussception
Crampy (intermittent, also known as colicky) Abdominal pain (infant pulls legs into stomach to relax abdo wall)
Vomiting
Bloody ‘red currant jelly’ stools (LATE sign)
Sausage shaped mass in RUQ and emptiness in RLQ.
What are ‘anatomic’ or ‘pathological’ lead points of intussception
Merkel’s diverticulum
Polyp
Vascular malformation
lymphoma
Complications of intussception if not treated early
Bowel obstruction,
Ischaemia, perforation, shock
How do you diagnose intussception?
Clinical suspicion -> US (‘target sign’) is first choice
or AXR (?soft tissue mass ?absence of gas in caecal region)
Treatment intussception
<48 hour history in otherwise stable child = air enema reduction
> 48 history or peritonitic/septic child = laparotomy
Treatment pyloric stenosis
Fluid rehydration therapy and electrolyte replacement
- 0.45% saline with 5% dextrose
- Add K when baby is urinating
Non-urgent surgical referral
Treatment exompathalous
Place baby in humidicrib wrapped in glad wrap (ensure blood supply of exposed bowel isn’t twisted/compromised)
NGT for GI decompression
Fluid resus
Urgent T/F to tertiary centre
DDX for acute scrotum (red, painful, tender scrotum)
Immediate management
- testicular torsion
- torsion of appendix testies
- epididymo orchitis
- idiopathic scrotal oedema
Urgent surgical referral ?surgical exploration
Classic presentation of appendicitis
Colicky periumbilical pain migrating to RLQ and becoming constant
Assoc w :
- anorexia
- fever
- nausea
- d&v
What are warning signs for appendicitis in kids?
abdo pain >24 hours
diarrhoea >24 hours
Infant preferring to lie still
Suspected peritonitis if child doesn’t allow abdo exam
What group most commonly have atypical presentations of appendicitis and how do you diagnose it?
Kids <5 yo
Adolescent girls
Need U/S diagnosis
- May need to do bloods (CRP, WCC), but bloods are NOT ROUTINE in kids.
Long term effects of diptheria infection
Toxin causes nerve and heart damage
Mortality 1/15
Long term effects of tetanus infection
Toxin causes nerve and muscle changes resulting in paralysis, convulsions
Mortality 1/10
Pertussis - effects of infection
Whooping cough. M&M highest in infants
Poliomyelitis - effects on infection
Febrile illness followed by paralysis in many (may become permanent)
Mortality 1/20
HIB - effects of infection
Systemic infection - meningitis, epiglottitis, bone and joint infections
Mortality 1/20
MMR
Measles encephalitis 1/2000, mumps encephalitis 1/200
Where to give vaccines to children?
• Children under 1
○ Anterolateral thigh (if 3 vaccines given at once, space injections 2.5 cm apart with third vaccine in other thigh)
• Children >1
○ Mid-deltoid region of upper arm
• NOT BUTTOCKS -> risk damage to sciatic nerve
Side effects of vaccines
- Local superficial inflammatory response -> redness, swelling at injection site
- Mild transient systemic SX (crying, irritability, mild fever, febrile seizures)
- Measles may be followed by mild, transient measles like illness (fever and brief rash 7-10s post immunisation)
- anaphylaxis is v rare
What extra vaccines what an aboriginal/torres straight islander child receive?
BCG
Hep A vaccine
Vaccines given at 2,4,6 months
DTPa (Diptheria, tetanus, whooping cough)
HIB
IPV (inactive polio vaccine)
HBV
PCV (13v pneumococcal conjucate)
RV (Rotavirus)
Vaccines given at 12 months
MMR (measles, mumps, rubella)
HIB
MenCCV
Vaccines given at 18mo
VZV (chickenpox)
MMR (measles mumps rubella)
DTP
Vaccines given at 4 years
DTPa (diphtheria, tetanus, pertussis)
Polio
Vaccines given at 10-15years
DTPa (diphtheria, tetanus, pertussis)
VZV (chickenpox #2)
HPV
Vaccines given at birth
HBV
Pattern of generalised seizure vs focal seizure
Generalised: wide spread all over brain, symmetric activity bilaterally
Focal: starts in localised area of brain, unilateral
What is another term for focal seizure that is commonly used and how is this further classified based on consciousness?
Partial seizure
- Simple partial seizure: consciousness intact (motor, somatosensory, visual/auditoary, autonomic, dysphasic)
-Complex partial seizure
(consciousness not intact)
How are generalised seizures further classified?
Tonic clonic
Absence
Myoclonic
Atonic, Tonic etc
Do generalised seizures affect consciousness? Motor systems?
Yes, always involve consciousness AND motor manifestations!
What is the definition of a seizure vs of epilepsy
Seizure:
Transient occurrence of signs and/or SX due to abnormal, excessive or hypersynchronous neuronal activity in cerebral cortex
Epilepsy:
Tendency to have recurrent unprovoked seizures (2 or more AFEBRILE seizures)
What types of seizures aren’t included in the definition of epilepsies?
- Single seizure events
- Neonatal seizure
- Febrile seizures
- Acute symptomatic seizure (systemic illness, acute neurological insults)
Investigations for seizures in children
EEG (+/- video monitoring)
MRI if…
◊ Suspected underlying cerebral abnormality
◊ Significant developmental delay
◊ Abnormal neurological findings on exam
◊ History of prior ne◊ Poorly controlled seizures
CT only if suspected stroke, increased ICP, traumatic brain injury (never perform in otherwise well child)
Seizure mimics
○ Normal phenomenon
§ Sleep jerks
§ Tantrums
§ Inattention, day dreaming
○ Syncope and related episodes
§ Vasovagal
§ Breath-holding spells
§ Long QT syndrome
○ Parasomnias and related sleep disturbances
§ Night terrors, sleep walking, cataplexy, confusional arousals
○ Movement disorders
§ Tics, clonus, chorea, tremor
○ Behavioural and psychiatric disturbances
§ Mannerisms, psychogenic seizures, rage attacks
○ Migraine variants and NV episodes
§ TIA, complicated migraine, benign paroxysmal vertigo
How can absence seizures be provoked?
hyperventilation
what are febrile seizures often associated with?
What ARENT they associated with?
Mostly assoc w URTI/UTI/viral exanthema
Family history of seizures (30%) - same mutation in neuronal ion channel gene
Age-limited predisposition to seizures (mostly 5mo-2yrs)
NOT ASSOC W: CNS illness, prev afebrile seizure, incr mortality or later intellectual impairment
Medications for epilepsy
Sodium valproate
Carbamazepine
Lamotrigine
Ethosuximide
DDX for generalised tonic clonic seizure (and what you would expect for each on history)
Focal seizure becoming generalised
□ Preceding aura (note: NO aura with generalised TC)
□ Todd’s paresis (transient unilateral postictal weakness)
□ Focal neurological deficits on exam
□ HX of prior CNS illness/cerebral trauma
Syncope
□ Vasovagal setting
□ Brief duration with rapid recovery
Psychogenic seizure
□ Eye closure during seizure
□ Resistance to passive eye opening
□ Intermittent or waxing and waning motor activity
what broad category of seizure if there is limb jerking/head turning/stiffening that is UNILATERAL?
Focal seizure! Not generalised because must be in one hemisphere only.
What type (lobe?) of focal seizure often gets confused for absence seizure?
Temporal lobe epilepsy
What type of (lobe?) focal seizure features hyperkinetic autisms (tapping, cycling, running in place)
Focal lobe epilepsy
Treatment of generalised vs focal epilepsies
Generalised seizures: Sodium valproate
Focal: Carbamazepine
What is the best method of measuring temp in children and what is the upper limit of normal (degC)
Electronic thermometer in axilla
Axillary > 37.2C
What is the definition of PUO?
Fever without focus for >2 weeks
What are the 3 main causes of PUO
- infection (?encapsulated bacteria)
- autoimmune
- malignancy
What 3 main encapsulated bacteria infect kids
HIB
Strep pneumonia
Neisseria meningiditis
What do you do if a child comes in with a fever?
If child is : > 3months non toxic fever <14 days It is likely viral so DON'T do septic screen (possibly check urine ex: if <6 months) and review to ensure they don't deteriorate.
Otherwise they get a septic screen
What comprises a septic screen?
FBE, blood film
Blood and urine cultures
LP +/- CXR (if resp SX/signs)
What questions to ask on HX when a child comes in with fever
Localising symptoms: cough coryza headache photophobia diarrhoea, vomiting abdominal pain joint symptoms
Travel history
Sick contacts
Immunisation hx
SX, signs suggestive of a ‘toxic’ or unwell child
Lethargic Poor interaction Inconsolability Tachycardia, tachypnoea, Cyanosis, poor peripheral perfusion
Presentation of meningococcus
Rapid onset
Fever
Flu-like SX (malaise, lethargy, vomiting, headache, myalgia, arthralgia)
Confusion
Rash (petechial/purpura)
Photophobia
Neck pain/stiffness
Differentials for child presenting with fever and petechial rash (previously well, onset this am)
Meningococcus if unwell/shocked/toxic
Viral infection (enterovirus, influenza)
HSP
ITP
15 month old presents with a non-itchy blanching erythematous rash (not on face) following 3 days of sudden-onset high-grade fever and a single febrile seizure.
What’s your top differential? Treatment?
HHV6 (roseola)
No treatment required - self limiting.
Child presents with ‘slapped cheek’ rash on face and lacy rash on trunk and limbs following low-grade fever, malaise, or a “cold” a few days before the rash broke out.
Differential? Treatment?
Parvovirus B19
No treatment required bc is viral
+/- Paracetamol to bring down fever
What is a rare complication of parvovirus B19 infection in pregnant women?
How common is this?
If exposed to ParvovirusB19 in first half of pregnancy, baby can get fetal anaemia hydrops fetalis and fetal death (miscarriage)
Occurs in 5% of pregnant women infected with parvovirus
What are the clinical features of measles?
4 day infectious prodrome (3 Cs) preceding rash:
Cough, coryza, conjunctivitis
Fever
Koplik’s spots
Rash (red, blotchy, starts on the head and then spreads to the rest of the body) - lasts ~7d
2 year old with incomplete immunisations at creche with fever and cough, coryza, conjunctivitis progressing to descending, blotchy raised (papular) rash
- diagnosis
Measles
Management for measles
MMR vaccine (2 doses) within 72 hours of exposure if >9mo
IVIG if <9mo or >9mo but >72 hours post exposure
Differentials for diffuse erythematous rash (sunburn-like) in child
Toxic shock syndrome (Staph or strep) Scarlet fever/Invasive GAS Kawasaki disease Enteroviral infection Antibiotics
what is the most severe complication of measles?
Encephalitis -> fatal in 15%
What causes Scarlet fever?
Exotoxins from Group A Strep (pyogenies)
What infections does GAS cause?
Scarlet Fever Pharyngitis Toxic shock Necrotising fasciitis Acute rheumatic fever GN
Clinical presentation of scarlet fever
Exudative tonsillitis +/- pharyngitis
Confluent erythematous sunburn-like rash
Strawberry tongue
Circumoral pallor
Treatment of scarlet fever
Penicillin (oral) - to treat GAS
What infectious agents cause toxic shock syndrome?
Exotoxins from staph aureus and strep pneumonia and strep progenies
Features of Kawasaki disease
Fever>5 days (unresponsive to antibiotics)
Polymorphous rash
Bilateral non-exudative conjunctivitis
Mucus membrane changes (oropharynx injected, strawberry tongue, swollen lips)
Swollen erythematous hands and feet with eventual desquamation
Unilateral cervical lymphadenopathy >1cm
Treatment of kawasaki disease
IVIG and low-dose aspirin
Complication of kawasaki disease
Coronary artery disease (aneurysm)
Higher risk of IHD
Features of infectious mononucleosis (glandular)
FEVER Exudative pharyngitis Tonsillitis Lymphadenopathy Splenomegaly Palatal petechiae Rash
Management of mono
None
Steroids only if airway obstructed due to tonsillar enlargement
What is TTN?
RF?
Tachypnoea of the newborn (TTN) = wet lung
retention of fetal long fluid
□ C-section without labour -> ‘Cold’ c-section = no maternal hormone surge hasn’t caused resorption of fluid yet
□ Breech delivery
□ Male sex
□ Birth asphyxiation
□ Heavy maternal analgesia
characteristic CXR for TTN
Coarse streaking w fluid in fissures
Mx TTN
most babies settle in 24-48 hours with minimal handling and cot O2.
CPAP if acidotic, low sats, working hard to breathe.
Signs of resp distress in a newborn
○ Tachypnoea (>60breaths/min)
§ In response to incr CO2 in order to breathe out and decr the CO2
○ Expiratory grunt
§ Produced by exhalation against a partially closed glottis in order to increase PEEP and therefore keep alveoli open
§ May be interpreted as crying or moaning
○ Recession of intercostal spaces and suprasternum; in drawing of subcostal margin
§ Due to the increased resp effort generating more negative intrapleural pressure which sucks in the softer/more compliant chest wall during inspiration
○ Nasal flare
§ Flare during inspiration decreases airway resistance
○ Central cyanosis
§ Note - polycythaemic babies will appear cyanosed at relatively high O2 sats but babies with low Hb will not appear cyanosed until saO2 is v low.
○ Deranged temperature control
○ Low O2 saturation
Ix for resp distress in a neonate
BSL CXR FBE, blood film, UEC Blood culture VBG
What is infant RDS? Another name for it?
Who gets it (RF)?
Treatment?
= hyaline membrane disease
§ Occurs in pre-term infants due to surfactant deficiency in the alveoli
Mx:
Empirical abx because looks similar to sepsis!
CPAP
If need more, intubate and give surfactant (need intubation).
Characteristic CXR appearance of RDS/HMD
Hypo aeration, diffuse ground-glass appearance, air bronchograms
RF for meconium aspiration?
Post-term (>40 weeks)
Births involving fetal distress
what is the pathophys behind meconium aspiration syndrome?
Aspiration of substances leads to obstruction, atelectasis and chemical and mechanical pneumonitis
RF for neonate sepsis
Maternal GBS positive
Maternal fever
Prolonged rupture of membrane (>=18 hours)
Signs of pneumothorax
Most sensitive is transilluminator Tracheal deviation Chest asymmetry Unequal expansion Decr breath sounds unilaterally Resp distress
Abx coverage for neonatal sepsis (what bugs are you worried about?)
Gentamicin (listeria, e coli, HIB)
Benzyl-penicillin (GBS)
Differentials for resp distress
TTN/wet lung HMD/RDS Meconium aspiration syndrome Sepsis pneumothorax congenital pneumonia Cardiac (VSD, PDA, transposition, pulm HTN) Anatomical - although not usually in neonatal period (laryngomalacia etc) Drugs ?
RF for pneumothorax in neonates
Being on CPAP
Resp distress
Mx for MDS
NO evidence for suctioning airways
(UNLESS baby is floppy or has no/inadequate respirations then it is reasonable to suction under direct vision using laryngoscope)
Septic workup
CPAP if needed/intubation
metabolic disturbances causing apnoeic episodes in premmies
Hypoglycaemia, hypocalcaemia, hypo/hypermagnesaemia
Define apnoea in neonates
§ No air flow occurs for >=20sec
§ No air flow for >=10sec + bradycardia or desat
General management of Respiratory distress in neonates
Observation - admit to neonatal nursery, incubator
Monitor vital (HR, RR, saO2)
Septic workup (FBE, blood film, blood cultures, CXR, vBG)
Empiric antibiotics (gent and benpen)
IV fluids (10% dextrose at 60ml/kg daily)
Advice from senior physician!
Additional resp support (CPAP, intubation)
Definitions for
- term
- pre term
- post term
- term: ≥ 37 completed weeks’ gestation
- preterm: < 37 completed weeks’ gestation
- post-term: > 42 completed weeks’ gestation
Definitions for
- LBW
- VLBW
- appropriate weight for gestational age
• low birth weight (LBW): < 2500 g
• very low birth weight (VLBW): < 1500 g
- appropriate weight for gestational age; between 10th and 90th percentiles
3 things to look for on GI when examining a baby
- pink (well perfused)
- no incr WOB (resp effort)
- active, good tone
when is bronchiolitis most common?
Up to 2 years of age
In winter/rainy season
Risk factors for bronchiolitis
Maternal smoking, pre-term delivery, chronic lung disease of prematurity, allergy, CHD, immunodeficiency
common causative agents of bronchiolitis
VIRAL always Rhinovirus #1 cause of mild bronchiolitis RSV #1 cause of SeVere bronchiolitis HRV Parainfluenza, influenza A/B Adenovirus
SX and signs of Bronchiolitis
Low grade fever § Tachypnoea § Mild dry cough § Expiratory wheezing § Hyperinflation § WOB § Fine inspiratory crackles § Difficulty feeding if severe
Mx of bronchiolitis
○ Mx - supportive (O2, fluids, nutrition)
What is the most common cause of wheeze in the first 2 years of life?
Viral bronchiolitis
Complications of Pertussis (whooping cough)
who is most at risk?
Apnoea, severe pneumonia, encephalopathy, death
Most at risk is <6mo
Clinical signs and investigations : Pertussis
§ Prodrome of a few days: nasal discharge and mild dry cough
§ Cough becomes more pronounced and characteristically ‘whoop’ing
§ +/- severe vomiting and subconjunctival haemorrhages
§ Apnoea in young infants
Ix: nasopharyngeal specimen: immunofluorescent Ab, culture
Treatment of pertussis
§ Admission for supportive therapy
§ Macrolide antibiotics if early in course of disease or v severe Sx
§ Treat household contacts
§ Contact precaution (until 5 days of antibiotics or illness for 3 weeks)
Most common causes of viral pneumonia in kids
parainfluenza influenza RSV Human metapneumovirus (HMV) Adenovirus Human rhinovirus
What does an x ray of viral pneumonia look like?
CXR: patchy, widespread bilateral infiltrates rather than lobar involvement
Clinical présentation of viral pneumonia
Dry cough
Fever
LOA
Complications of HIB
Epiglottitis
Meningitis
Risk factors for HIB
Age <5yo Indigenous Lower SES Male sex Congenital and acquired immunodeficiency
Causative agents of bacterial pneumonia
- Strep pneumonia most common by far!
- Staph aureus
- Mycoplasma pneumonia
- HIB
Less common causes:
- Group A beta haemolytic strep (pyogenies)
- Klebsiella
Presentation of pneumococcal pneumonia
Typical CXR findings
fever sob pleuritic CP wet cough tachypnoea grunting nasal flaring Reduced expansion, dull to percussion, reduced breath sounds, bronchial breathing on affected side
CXR: lobal opacification although can be patchy
What antibiotics to use for pneumococcal pneumonia?
Penicillin and third gen cephalosporin
lung complications of pneumonia
what clinical features are the same, and what are different?
Pleural effusion
Pneumothorax
same - tracheal deviation
and reduced breath sounds
different - stony dull percussion and bronchial breathing above effusions.
what is the typical CXR appearance of mycoplasma pneumonia?
Central peribronchial opacification
Extensive opacification of 1+ lobes
Air bronchograms
Presentation of staph pneumonia
□ Shorter acute HX than other forms of pneumonia (acute onset, rapid course) □ Appears more toxic □ High fever □ Marked tachypnoea □ Significant resp distress □ Non-specific chest signs
Complications of staph pneumonia
LARGE pleural effusions Empyema Tracheal deviation Abscesses Air leaks (pneumothorax)
Antibiotics for staph pneumoniae
IV flucloxacillin and third generation cephalosporin (cefotaxime)
Vancomycin if MRSA suspected
RF for staph pneumonaie
Low SES
Indigenous b/g
Examples of ACYANOTIC heart defects
1. L->R shunt VSD PDA ASD AVSD
2. Obstructive heart defects Pulmonary stenosis Aortic stenosis Coarctation of aorta Hypoplastic L heart syndrome
Presentation of a VSD
Depends on the size
1. Small: pan systolic murmur @ L sternal edge rad to axilla BUT ASYMPTOMATIC at birth bc pressures between L and R heart are equal
- Large: left heart dilatation leads to displaced apex, parasternal heave
- SX of HF occur after lungs open up and L sided pressures > R.
(poor feeding, FTT, tachypnoea, incr WOB, hepatomegaly)
Note: L heart dilatation occurs because L heart has to work harder to generate the same CO w shunt present.
what are the 2 most common types of CHD in kids?
- VSD
2. PDA
What are SX of heart failure in a newborn?
tachypnoea
SOB and sweating when feeding
Failure to thrive
Incr WOB
Long-term complications of VSD
® Progressive AR if shunt is located close to aortic valve (aortic leaflets sucked/prolapses into defet due to high-velocity L->R flow)
Pulmonary HTN due to Increased pulmonary pressures (L-> R shunt)
What causes the ductus arterioles to close? when does this occur?
Closes in first 1-7 days post birth due to decreased circulating PGE2 and increased paO2, as well as muscle contraction
What can cause the ductus arteriosus to fail to close?
Prematurity
Congenital malformation
What is the treatment for a PDA in a premature infant?
Indomethacin or other NSAIDs (inhibit PGE2 to promote ductal constriction and closure)
Why do you treat small PDAs and how? How does this differ from treatment of large PDAs?
Small PDAs are treated to prevent endocarditis rather than to treat symptoms or complications. Via transcatheter duct occlusion.
Large PDAs need surgical ligation .
How do PDAs present?
Small PDAs generally asymptomatic. May have continuous murmur at upper L sternal edge.
Large PDAs present with L heart dilatation (displaced apex beat, parasternal heave) and progressive SX of heart failure.
+ Bounding pulses
+ Apical mid-diastolic murmur
What investigations do you do if you hear a murmur in a baby?
CXR
ECG
ECHO is diagnostic
Where do most ASDs occur?
fossa ovale (central part of atrial septum)
How do ASDs present?
Small ASDs go undetected (low pressure gradient across atria)
Large ASDs rarely symptomatic in childhood
-may cause Atrial arrhythmias in adulthood, and reduced exercise capacity
Because L->R shunt causes R heart enlargement ->
- parasternal heave
- ES murmur in pulmonary region with fixed splitting of A2 and P2
What might an ECG of ASD show?
partial RBBB
What is the treatment for ASD and when is it indicated?
Indicated if patient has RH enlargement
Transcatheter or surgical closure
Which congenital heart defect is most assoc w down syndrome?
AVSD
How does AVSD present?
Partial AVSD - behaves physiologically and symptomatically like ASD
Complete AVSD - presents like severe VSD (FTT, feeding difficulties, tachypnoea, WOB)
Treatment of AVSD
almost always needs surgical closure
What is the most common type of Acyanotic obstructive heart defect?
What type of murmur is associated?
Pulmonary Stenosis
Ejection systolic @ L upper sternal edge
Radiating to back
Ejection click earlier than with AS
A2 and P2 widely split
how does pulmonary stenosis present?
usually asymptomatic in children and infants
Mild is benign, non-progressive finding
Severe can lead to heart-failure
What causes AS in children usually.
What type of murmur?
Bicuspid aortic valve
ES murmur over aortic area + radiation to carotids
Ejection click later than PS
Less splitting of A2 and P2 than PS
How might AS present in kids
ES murmur
Apical heave due to LV hypertrophy
Gradual progression of SX (syncope, angina, dizziness on exertion, sudden death)
Severe cases, HF evident at birth
When do you treat AS in kids? How?
If symptomatic or ECG changes w exercise
Balloon valvuloplasty (trans-acth) or aortic valvotomy (surgical)
what is coarctation of the aorta?
What can it result in?
Stricture at distal part of aortic arch (max obstruction site close to aortic end of Ductus arteriosus)
Can lead to severe cardiac failure in newborns with oliguria and acidosis
When does cardiac failure onset in newborns with coarctation of aorta?
How might this present on exam?
When ductus arteriosus closes because then there is NO blood flow to the rest of the body.
Diminished/absent femoral pulses
unequal BPs between L and R arm
Treatment of coarctation of aorta
surgical repair as early as possible!!
CXR findings of severe coarctation of aorta
Cardiomegaly
Pulmonary congestion
Abnormal appearance of aortic knuckle
Rib notching (due to enlarged IC arteries bypassing obstructed segment of aorta)
If a newborn has coarctation, what else might you expect?
other congenital heart defects such as :
VSD
PDA
valvular abnormalities
How does hypo plastic L heart syndrome present?
What is it?
§ Infants present w severe cardiac failure or shock within first few days of life
□ All periph pulses diminished or absent
Small left ventricle (hypoplasia) - Underdevelopment of left heart + valves (often assoc w severe MS and AS)
What is hypo plastic left heart syndrome always associated with
always assoc w PDA otherwise they would have died. Necessary to keep systemic circulation maintained
(R->L shunt due to R ventricular blood shunting via PDA into aorta )
Complications of Hypoplastic left heart syndrome
95% die within first few weeks of life if untreated
Neurodevelopment impairment if children survive due to marked hypoxia and cyanosis in early days of life
Treatment for Hypoplastic left heart syndrome
Immediate: PGE1 keeps PDA patient initially, until
SURGERY can be performed.
If untreated 95% die in first few weeks of life.
Examples of cyanotic heart defects
The 4 Ts:
- Tetralogy of ballot
- Transposition of great arteries
- Tricuspid atresia
- Truncus arteriosus
what is the most common cyanotic heart defect? What is it commonly assoc with?
tetralogy of fallot?
Syndromes -down syndrome
What is the tetralogy of fallot and what 4 things comprise it?
Obstruction to RV outlfow tract + septal defect below obstruction such that blood can flow from RV to LV (R->L shunting)
§ 4 anatomical defects: □ Overriding aorta □ RV hypertrophy □ Pulmonary stenosis □ VSD
Clinical picture of tetralogy of fallot
Kids:
Gradual, delayed development of cyanosis
Delayed exercise tolerance, finger clubbing, growth retardation
Development of compensatory polycythaemia
Babies:
‘tet’ spells: cyanosis more obvious when baby is upset, crying
(Baby may go floppy, lose consciousness)
What do you suspect if a baby becomes cyanosed only when upset and crying, and on one occasion goes floppy and loses consciousness during such an episode?
What do you do to manage this?
Tetralogy of fallot
Treatment - soothe the baby
