Clinical - Shorts Flashcards
Left Thoracotomy Scar
Shunt e.g. BT PA banding Coarctation repair PDA ligation Non-heart related
Right Thoracotomy Scar
Shunt e.g. BT
PA banding
Non-heart related: TOF repair, CDH repair
Wide split S1
RBBB
Ebsteins
S1 ejection click
Valvular stenosis
- AS: LLSE or apex
- PS: LUSE
Heart sounds are valves closing -> S1 followed by click = opening of aortic/pulmonary valves
Split S2
EXCLUDES SINGLE OUTFLOW OR PULMONARY HTN
Fixed:
- ASD, PAPVR
- RBBB
- PS
- MR (early aortic closure - the others delay pulmonary closure)
Abnormal P2
Increased = PTHN Decreased = severe PS, TOF, TS
Third and fourth heart sounds
Third
- can be normal in children
Fourth
- rare and always pathological
Pan/holosystolic murmur (or early systolic)
VSD
MR
TR
Usually occur with semilunar valves closed
Won’t be AS/PS
Systolic murmur at LUSE
RVOT
- sub/supra/valvular stenosis
- pulmonary flow (innocent)
- ASD, PAPVR (relative stenosis)
- PDA, CoA
Mid-systolic murmur at RUSE
LVOT
- sub/supra/valvular stenosis
- click = valvular
- thrill = usually valvular/supravalvular
Mid-systolic murmur apex
MR, MVP
Still’s/vibratory (innocent, no thrill)
AS (click)
HOCM
Late systolic murmur
MVP
Diastolic murmur
AR or PR (early) most commonly
Can be TS or MS (late)
Continous murmur
Shunt
- BT
- central
PDA (machinery, pink, no clubbing, no scars)
Collaterals (PA-VSD)
Coarctation or PA (pulmonary artery) stenosis (unlikely)
Venous hum (occlude jugular vein)
Murmurs and Valsalva
Decreases intracardiac volume
HOCM - increases intensity
MVP - increases
Innocent outflow and Stills will decrease
ECG rate based on number of large boxes
1 = 300 2 = 150 3 = 100 4 = 75 5 = 60 6 = 50
Right axis deviation
RVH
RBBB
Left axis deviation
LVH
LBBB
Superior axis
AVSD TA Noonans LTGA ALCAPA
Deep Q wave
Hypertrophy
ALCAPA
Ischaemia
Look at leads 2 and 3, if more than 1 large box
S1Q3T3
Right heart strain
Deep S wave in lead I, Q wave in III, inverted T wave in III
U waves
Can be normal If prominent (>1-2mm) can be d/t antiarrhythmics, LVH If inverted = always abnormal, but non specific
Ventricular hypertrophy - approach
Don’t need to remember criteria - state that you would compare against age (?gender) matched normal tables.
RVH = RAD +:
- V1: Neonate R >25mm or pure R>10mm
- V1: R>S after 1 year of age
- V1 upright T wave after 1 week (usually upright at birth, invert after a few days, then upright again towards adolescence)
- V6 S >15mm at 1 week or >5mm at 1 year
LVH, LAD +:
- V6/II/III/aVF with R>4-5 large boxes
BVH
- large equiphasic QRS complexes
TWI
Strain
AKA wide QRS-T axis?
Long PR
Normal (Vagal)
Rheumatic heart disease
Myocarditis
AVSD, ASD, Ebstein
Compare to age matched table
Short PR
WPW
DMD
Friedrichs ataxia
Normal
Compare to age matched tables
Early repolarisation
STE with upright T waves
STD with negative T waves
Loud S1
TS/MS
Loud A2
HTN
AS
Loud P2
PHTN
Previous surgery and pink
ASD/VSD/AVSD repair Tetralogy repair (likely PS murmur at ULSE) Arterial switch TAPVD repair Fontan no fenestration
Previous surgery and blue
Basically palliative procedure for complex congenital cyanotic disease. Shunt.
“Palliative surgery for cyanotic congenital heart disease, this may be a staged procedure and patient remains blue” Shunted circulations Tetralogy / Pulmonary atresia Single ventricle with PS Norwood procedure TGA / LVOTO Single ventricle lesions (no shunt) “Many complex heart lesions may lead to single ventricle physiology” “Palliative surgery in many stages” Bidirectional cavopulmonary shunt Fontan with fenestration
Fontan - steps
= staged palliation of a univentricular system (palliative as opposed to corrective)
• 1 = modified BT shunt (3 days)
• 2 = BCPC (SVC -> pulmonary artery) (3 months)
• 3 = Fontan (3 years) - connect IVC to PA
At 3 days get a BT shunt (pulmonary pressure too high to have a veno-PA shunt hence need an arterio-PA shunt until pulmonary pressures drop). These children are extremely fragile as high likelihood of shunt blockage. 20% mortality before 3 months. Hence very unlikely to be in the exam.
• At 3 months get BCPC (AKA Glenn). Performed once pulmonary pressures drop. SVC to main PA. Can’t connect IVC at this point because there would be too much pulmonary blood flow.
• 3 years get definitive Fontan (SVC and IVC now connected to PA)
• In mid-late teen years get a transplant
Complications of Fontan:
• Chylothorax and pleural effusions are very common complications.
• Protein losing enteropathy common (and is an indication for transplant)
• Strokes – post-fontan all patients are on warfarin to prevent paradoxical embolus and stroke
• Cerebral abscesses
CXR: Lung fields: reduced/increased vascularity
Increased: VSD, TGA, TA, TAPVD
o Decreased: ToF, PA, TA, critical PS, Ebsteins
o (If the patient is blue they will have poor vascularity (dark lung fields) cf L-R shunt will have plethoric lung fields)
ECG axis
a) Birth → +60 to +180 degrees
b) 1 year → +10 to + 100 degrees
c) 10 years → +30 to +90 degrees
d) Also check p-wave axis (should be ↑ or +ve in avF/II/III)
ECG: LAH (bifid P wave)
- MR or MS
- Cardiomyopathy
- Large VSD/PDA
ECG: RAH (tall and tented wave)
ASD, TR, TA, PA, Pulm HTN, ToF, TAPVR/PAPVR, severe PS
ECG: LVH
Large R waves in V1 and V3
Large S waves in V5 and V6
↑ LV overload Aortic stenosis Mitral insufficiency VSD PDA
ECG: RVH
Large R waves in V1 and V3
Large S waves in V5 and V6
↑ RV over-load Pulmonary valve stenosis Tricuspid insufficiency Pulmonary HT VSD (L → R shunt)
ECG: Left axis deviation (↓ in III, evident when ↓ in II)
Tricuspid atresia ASD (primum) PS in Noonan’s esp if HCM Endocardial cushion defect Single ventricle LVH esp with volume overload Ebsteins WPW L-TGA
ECG: Right axis deviation (↓ in III, ↓ in I)
ASD (secundum)
RBBB
ECG: heart block
L-TGA (corrected TGA) Polysplenia syndrome AVSD Ebstein’s Acute rheumatic fever Congenital heart block with maternal SLE
ECG: Q wave in right chest leads Normal if in leads: II III AVF V5 and V6
LBBB RVH L-TGA HOCM Infarction
ECG: Q wave in lateral chest leads (infarction)
ALCAPA
ECG: RBBB
Partial
ASD
Ebstein’s anomaly
Complete
Post right-ventriculotomy (repair of VSD, tetralogy of Fallot)
Coarctation of the aorta (in infants<6mo)
Endocardial cushion defects
PAPVR
Occasionally in normal children
With left axis deviation → ostium primum ASD
With R axis deviation → ostium secundum ASD
With R atrial hypertrophy + delta waves → Ebstein’s
Complete RBBB → post-ventriculotomy
ECG: Dextrocardia
Normal – I, V6 +ve
Dextrocardia – 1, V6 –ve with inverted QRS
Norwood procedure
Aorta connected to RV (for HLHS) so that RV becomes main systemic ventricle
Global developmental delay
1. Static causes (No regression) o Cerebral Malformations o Chromosomal disorders o Intrauterine infection o Perinatal disorders o Antenatal toxins (alcohol, VPA, PHT) o Static encephalopathy with apparent regression (frequent seizures, AED side effects, depression, contractures, increased spasticity, progressive hydrocephalus)
2. Degenerative causes o Grey matter • Gangliosidoses (GM1, GM2 – i.e. Tay Sachs, Sandhoff) • Niemann-Pick o White matter • MLD • Krabbe (globoid cell leukodystrophy) • ALD
Isolated speech delay
- Hearing impairment
- Infantile Autism
- Bilateral hippocampal sclerosis
Isolated motor delay
- Ataxia
- Hemiplegia
- Paraplegia
- Hypotonia
- Neuromuscular disorders
IHUGVIDEP
Introduce Hands Unwell/well Growth Vitals Iatrogenic Dysmorphism Expose Pain
Primitive reflexes - rooting
Birth-4mo
Do: Light touch perioral area
Reaction: Turn toward stimulation & mouth should open
Primitive reflexes - sucking
Birth-4mo
Do: gloved finger or nipple in infant’s mouth
Reaction: coordinated, strong & symmetric suck
Primitive reflexes - asymmetrical tonic neck reflex
2-6mo
Do: Rotate head to one side
Reaction: Should adopt “fencing position”
Reaction: Extension of ipsilateral limbs
Reaction: Flexion of contralateral limbs
Primitive reflexes - neck-righting
6mo-2yrs
Do: Rotate head to one side
Reaction: Trunk should rotate to same side
Primitive reflexes - palmar grasp
Birth-3mo
Primitive reflexes - stepping
Birth-1.5mo
Do: Touch feet to a flat surface
Reaction: Alternating stepping motion
Primitive reflexes - placing
Birth-1.5mo
Do: Contact dorsum of foot on edge of table
Foot should lift & place on table’s surface
Primitive reflexes - Landau reflex
Stage 1 (4mo-2yrs) o Do: Lie prone o Reaction: Should extend head, trunk & hips Stage 2 (9mo-2yrs) o Do: Flex head & neck o Reaction: Should flex trunk & hips
Primitive reflexes - Moro
Birth-4mo
Position: Supine
Do: Sudden downward mvmt of head & trunk
Reaction: Symmetric extension & abduction of arms
Reaction: Opening of hands
Reaction: Then flexion of UL (embracing movement)
Reaction: Then cries
Primitive reflexes - parachute reflex
9mo-persists
Position: Prone
Do: Move infant rapidly face downward
Reaction: Extension of UL (to break fall)
Look for asymmetry (hemiplegia)
Peripheral neuropathy
BITCHM
B12 deficiency Infective -> post infectious e.g. GBS Tumour -> lymphoma, NF1 Chemotherapy -> vincristine Hereditary sensory motor disease (CMT) Metabolic -> diabetes
UMN vs LMN
UMN
- Brain (metabolic, genetic prematurity/PVL, stroke/vascular, infection, space occupying lesion)
- Spine (spina bifida)
LMN
- Anterior horn (SMA
- Peripheral nerve (B12, GBS, tumour, chemo, CMT, diabetes)
- NMJ (myasthenia, botulism)
- Muscle (congenital myopathy, muscular dystrophy)
Hepatosplenomegaly
C – congenital hepatic fibrosis H – haematological (thalassemia) I – infection (EBV, TORCH) M – malignancy (leukaemia, lymphoma) S – storage diseases (MPS)
Hepatomegaly w/o splenomegaly
Malignancy - primary hepatic - secondary deposit: neuroblastoma, Wilms, gonadal - vascular malformation (cavernous haemangioma) Infective - viral Hep A-E, echovirus - bacterial - parasitic (hydatid, schistosomiasis) Metabolic - CHO: GSD, HFI, galactosemia, Cushing syndrome - protein: tyrosinemia, UCD - fatty acid oxidation defect Inflammatory - chronic active hepatitis - IBD associated liver disease - A1AT Structural - EHBA, choledochal cyst, Alagille Cardiac - CCF, constrictive pericarditis, obstructued IVC Congenital - polycystic disease Copper - Wilson Malnutrition Trauma
Splenomegaly w/o hepatomegaly
Haem - hereditary spherocytosis, G6PD Bacterial - SBE - typhoid - septicaemia Portal HTN Masses - cyst - hamartoma - haematoma
Example spiel:
H – haematological – such as HS, which is my leading differential as it causes splenomegaly in an otherwise well child
I – infective such as EBV – however tends to cause hepatosplenomegaly and Matthew is afebrile and well in himself
M – malignancy such as leukaemia however I’d expect to see other features to suggest thrombocytopenia or anemia
P – Portal hypertension however there were no stimata of CLD today
S – storage diseases such as MPS however Matthew does not have distinctive facial features
Complications of splenomegaly
Hypersplenism -> thrombocytopenia
Functional asplenism -> immunodeficiency, encapsulated organisms
Splenic infarct -> tenderness
Early satiety -> faltering growth
Causes cirrhosis
Primary biliary cirrhosis PSC (a/w IBD) AI hepatitis (ANA, anti smooth muscle antibodies, ANCA) Wilsons A1AT Congenital hepatic fibrosis (a/w PCKD) CF Chronic hep B/C
Unilateral flank mass
Tumour: Wilms, neuroblastoma, phaeochromocytoma Renal cyst RVT Hydronephrosis Hypertrophied solitary kidney
