Acute scenarios Flashcards
Two aetiologies of heart failure in children
Over-circulation: more than expected flow in either side of the heart, muscle does not keep up
Pump failure: damage to heart muscle, fails to contract
Definition of HF
Failure of the heart to maintain adequate perfusion of body tissues.
Congestive heart failure term describes a situation of increased venous congestion in the pulmonary vasculature (LHF), or systemic (RHF) veins. This occurs when the mechanisms regulating CO are no longer adequate or overridden by excess demand. Common in syndromic children.
Causes of overcirculatory HF in children
- CHD: HLH, severe AS, interrupted AA/CoA, PDA, TAPVD, large VSD, TGA, truncus arteriosus.
- Postoperative CHD repair
- AV malformation (i.e. hepatic)
- Severe anaemia (i.e. hydrops fetalis)
Causes of pump failure HF in children
- Viral myocarditis/cardiomyopathy
- Metabolic cardiomyopathy (i.e. Pompe disease)
- Arrhythmias: SVT, VT, congenital heart block
- Ischemia: Kawasaki disease, early onset MI in FH, ALCAPA
- DMD
- Medications i.e. chemotherapy
Symptoms of HF in children
Infant: breathless, cold extremities, wheeze (cardiac asthma) , grunting, feeding difficulties, sweat, fail to thrive, recurrent chest infections
Older: fatigue, exercise intolerance, dizziness, syncope
Examination in HF in children
General: tachycardia (not in CHB), absence of heart murmur does not exclude this (TGA, HLH, COA)
Left HF: resp distress, gallop rhythma, displaced apex, tachypnea
Right HF: odema, hepatosplenomegaly, JV distension not often in child
Decompensated HF: hypotension, cool peripheries, shock, low urine output, thread pulse, high capillary refill time, renal and hepatic failure
Investigations for HF in children
Bloods: acid base balance, FBC, WCC, viral PCR, cultures for IE
CXR: cardiomegaly, signs of HF (Kerly B, pulmonary odema, increased markings, effusions, cardiomegaly)
ECG: rate, rhythm, hypertrophy or hypoplasia. Evidence of myocarditis or ischaemia
Echo is diagnostic in cases of CHD (see lesions), myocarditis/DCM (thin walled dilated LV), Kawasaki (if CA aneurysms seen)
Might require angiography, genetic testing, chromosomal type
Management of HF in children
ABCDE management. Emergency requiring admission to specialist unit.
Investigation of underlying cause and management
Newborn: Duct dependent CHD is most likely cause – IV PGE2 should be initiated.
General blanket principles: reduce preload (loop diuretics) enhance contractility (ionotropes) reduce afterload (ACEi), improve O2 delivery and nutrition.
Mechanical circulatory support as a bridge to cardiac transplantation may be considered.
Differentiating cardiogenic vs respiratory cyanosis in children
Hyperoxia test
The PaO2 is measured in the right radial artery (preductal) on room air and after 10 minutes of 100% oxygen supplementation.
Aetiology of Kawasaki disease
Epidemiological studies suggest infectious agent in genetically susceptible individuals
* Infectious hypothesis – winter spring seasonality, community outbreaks
* Genetic susceptibility: Japanese individuals more prone
* Superantigen hypothesis ?
DDX Kawasaki disease
Streptococcal disease (Scarlet fever) viral infection (measles, EBV, enterovirus) staphylococcal scalded skin syndrome, drug hypersensitivity, JIA,
Definition and criteria for KD
Childhood acute febrile illness with small and medium vessel vasculitis.
Classic features: high fever >=4days, presence of >=4 of:
* Erythema, odema of hands and feet
* Diffuse maculopapular rash (within 5 days)
* Bilateral non exudative oconjunctivitis
* Chapped erythemaotus lips and oral mucosa, strawberry tongue
* Cervical lymphadenopathy
Incomplete or atypical disease is suspected with fever of five days or more with two or three of the features.
Firstcardiac investigation on suspecting KD
Transthoracic echocardiography should be performed as soon as Kawasaki disease is suspected to evaluate for coronary artery aneurysms.
Treatment of KD
IVIG +/-
Consider corticosteroids for severe disease
ASPIRIN NOT RECOMMENDED
Long-term monitoring of coronaries
Causes of tachyarryhthmia in children
Sinus tachycardia
SVT
JET
Other atrial tachycardias (MAT/EAT)
VT
Management of SVT in children
If signs of shock (chest pain, pulm oedema, hypoxia): Cardiac monitoring, NRB mask, insert IV, sedation, DCCV (1-2 J/kg)
If no signs of shock: Attempt manouvres( Valsalva, diving reflex). If no response, IV cannula and adenosine 100mcg/kg (then 200 then 300 if no response)
Record strips in all cases as this will help determine aetiology
In the long term: ablation, especially if AVRT
PALS algorithm - non-shockable rhythm
Re-assess rhythm every 2 minutes
Adrenaline 10 mcg/kg immediately then on alternate 2-min rounds
PALS algorithm - shockable rhythm
Re-assess rhythm every 2 minutes
Shock 4 J/kg
Adrenaline 10 mcg/kg at second shock, then every other
Amiodarone 5mg/kg after third shock, then every other
Choking child with ineffective cough - conscious
5 back blows
5 chest thrusts
Assess and repeat
Choking child with ineffective cough - unconscious
Open aiwrway
2 breaths
CPR 15:2
Check for FB
Choking child with effective cough
Encourage coughing
Maintain ongoing assessment until resolved
Bradycardia - no shock
Monitor closely for symptoms
Seek opinion
Bradycardia with shock
Vagal overactivity? Atropine 20mcg/kg
No clear evidence of vagal overactivity? Adrenaline 10mcg/kg, consider adrenaline infusion, consider pacing
Blood and fluid therapy in trauma and massive blood loss
15 mg/kg TXA IV/IO
Consider resuscitating with blood products (RBC:FFP 1:1) immediately. If not available, 10mL/kg warmed NaCl
If shock remains, repeat blood products or warmed NaCl
If shock remains, escalate hemorrage control + 5mL/kg blood product
After 20mL/kg of blood products, request major hemorrhage pack
Continue 5mL/kg boluses of blood products
After further 20mL/kg blood products, give 10-15mL/kg platelets and 0.1mL/kg of 10% Calcium chloride
Repeat blood product bolus loop if no resolution
Hyperkalaemia in child
Arrhythmia: as per arrhythmia protocol + Calcium 0.1mmol/kg IV
No arrhythmia:
- Nebulised salbutamol 2.5mg
- Repeat K
- If improving, Ca resonium 1g/kg PO
- If still high and pH<7.34, Na HCO3 1-2mmol/kg IV
- If still high and pH >7.35, Glucose 10% 5mL/kg and insulin 0.05u/kg/h IV + Ca resonium 1g/kg PO
Plan dialysis if necessary
What is pre-ductal SpO2
SpO2 taken from right arm (pre-ductal)
Causes of HF in utero
Severe valvular disease e.g., Ebstein
Severe anaemia
Paroxysmal SVT
AV block
Severe mitral insufficiency in AVSD
Causes of HF in first day of life
II myocardial dysfunction (anaemia, sepsis, asphyxia, hypoglycaemia)
Duct dependent lesions (TTTTP)
Causes of HF in the first week of life
Duct dependent lesions (TTTTP)
PDA
Adrenal insufficiency due to enzyme deficiencies
Arrhythtmias e.g., SVT
Causes of HF after 2nd week of life
Other congenital diseases that become symptomatic due to the reducing pulmonary pressures or due to worsening cardiac dysfunction
Cardiac causes of HF in children
Congenital
- Excessive preload
- Excessive afterload
- Complex congenital heart disease
Noncongenital
- Myocarditis
- Cardiomyopathy
- Sepsis
- Infarction (e.g., FH)
- Hypertension (renal)
- Acquired valve diseases
- Kawasaki
- Arrhythmia
Noncardiac
- Anaemia
- Sepsis
- Hyoiglycaemia
- DKA
- Hypothyroidism
- Other endocrinopathies
- AV fistula
- Renal failure
- Muscular dystrophies
Signs of heart failure in children with L>R failure
Tachypnea
Wheezing
Rales
nasal flaring or grunting
Retractions
Cough or chest congestion
Poor feeding
Irritability
Signs of heart failure in children with R>L failure
Hepatomegaly
Ascites
Pleural effusion
Peripheral edema
Weight gain
JV distension rare in children
Signs of heart failure in children with biventricular failure
Tachycardia with S3 gallop
Cardiomegaly
Decreased pulses
Delayed capillary refill
Fatigue
Pallor
Sweating
Poor weight gain
Dizziness
Altered consciousness
Syncope
Definition of failure to thrive
broadly defined as a faltering of growth from a previously established pattern of growth
Three key principles in assessment of child in shock
Primary ABCDE assessment and resuscitation
Secondary assessment and emergency treatment
Stabilisation and transfer
ABCDE in child
A + B - breathing effort, RR and rhythm, stridor or wheeze, ascultation, skin colour
C - HR, volume, cap refill, skin temp
D - Conscious level, posture, pupils
E - fever, rash, bruising
Airway assessment in child
Look, listen and feel for airway patency.
In an unconscious baby or child, open the airway using the “head tilt chin lift”
The differences in airway anatomy as children mature, means that the desirable degrees of tilt is neutral in an infant and a ‘sniffing’ position in a child
If this manoeuvre is unsuccessful in establishing airway patency, a jaw thrust may be used
Airway management in a child
In an in-hospital setting, adjuncts such as naso-pharyngeal airways and Guedel airways may also be appropriate.
In a conscious child, stridor or hoarse voice may indicate a compromised airway and senior help must be sought promptly.
If there is any concern that a child’s airway is becoming compromised within the hospital, anaesthetic help must be requested urgently.
Breathing assessment in a child
A raised respiratory rate may be caused by airway or lung pathology or be driven by a metabolic acidosis (for example in diabetic ketoacidosis.)
Normal RR
<1: 30 to 40
1 to 2: 2 t o3
2 to 5: 2 to 30
5 to 12: 15 to 25
>12: 12 to 20
Other signs of respiratory distress include grunting, flaring of the nostrils, tracheal tug and accessory muscle use (intercostal, subcostal or at the most severe sternal recession). Gasping is a late sign of severe hypoxia.
Observe chest expansion and ascultate
Saturations
Breathing management in a child
high flow 15L oxygen mask with a reservoir bag
If there is also inadequate respiratory effort, then use a bag-valve mask and consider intubation and ventilation as appropriate
In a choking patient > choking APLS algrithm
Circulation assessment in a child
Record the patient’s heart rate, pulse volume, capillary refill time and blood pressure. Children are very good at compensating for alterations in their physiology and as such hypotension is a late sign. Assess the effect of any circulatory inadequacy on other organs. These may include a raised respiratory rate (driven by the resultant metabolic acidosis), reduced urine output, mottled skin with pale, cool peripheries (due to poor skin perfusion) or altered mental state.
Circulation management in child
If there are signs of circulatory compromise, establish venous or intraosseous access rapidly and give a 20ml/kg bolus of 0.9% sodium chloride. Further boluses should be guided by reassessment and inotropic support considered if more than two boluses are needed. Note in DKA, the initial bolus is 10ml/kg due to the risk of cerebral oedema. Venous access in seriously ill children is often difficult and fluid bolus administration should not be delayed by repeated attempts at cannulation – intraosseous access is rapid and effective and should be considered early.
Disability assessment in child
Assess the child’s conscious level using the AVPU score (where A is alert, V is responds to voice, P is responds to pain and U is unresponsive) or GCS. The AVPU scale is quicker to use with a response only to pain correlating with a GCS score of 8.
Many children suffering from a severe illness are floppy. Stiff posturing such as that in decorticate (flexed arms, extended legs) or decerebrate (extended arms and legs) suggests serious brain dysfunction.
Pupil size and response to light should be recorded. Bedside blood sugar testing should also be performed (although in reality this may have been checked with a blood gas at the time of obtaining IV or IO access). Consider raised intracranial pressure in any child with depressed conscious level. The presence of hypertension and bradycardia in such cases indicates impending coning.
Disability management in a child
Consider intubation to stabilise the airway in any child with a conscious level graded as P or U.
Treat hypoglycaemia with a bolus of 2ml/kg 10% glucose IV or IO, followed by a glucose infusion to prevent recurrence.
In cases of suspected raised intracranial pressure consider mannitol and neuroprotective measures (see full guideline for further details.)
Exposure assessment in a child
A swift head to toe examination of the child may provide clues as to the aetiology of the illness, for example a purpuric rash may only be noted on full exposure or surgical scars may prompt you to consider particular histories. Be careful to ensure exposed areas are recovered to help maintain temperature control and preserve the child’s dignity.
Secondary assessment
Once immediately life threatening problems have been addressed, move on to assess the patient in further detail. This includes:
Reassessing the response to initial resuscitative measures
Taking a focused history
Performing detailed systems based examinations where appropriate
Further investigations – these may include laboratory blood tests, ECG, radiographs or other imaging such as CT
AB shows Bubbling sound
Excessive secretions > Suctioning
Harsh stridor and a barking cough
Croup > Oral dexamethasone
Nebulised budesonide and adrenaline in severe cases
Soft stridor, drooling and fever in a sick looking child
Bacterial tracheitis or epiglottitis Intubation by anaesthetist followed by IV antibiotics
Sudden onset stridor with history of inhalation
Inhaled foreign body Laryngoscopy for removal
Stridor following ingestion or injection of a known allergen
Anaphylaxis IM adrenaline
Wheeze
Acute asthma Bronchodilators
Bronchial breathing
Pneumonia IV antibiotics
duct dependent lesion is suspected
IV dinoprostone should be administered – this helps to keep the duct open, therefore allowing common mixing to occur until a definitive diagnosis and treatment
SVT
Vagal manoeuvres followed by a rapid bolus of IV adenosine or synchronous DC shock, depending upon the clinical status of the child.
Resuscitation of preterm cutoffs
Recommendations
Less than 23 weeks then resuscitation should not be performed
Between 23 and 23+6 weeks then there may be a decision not to start resuscitation in the best interests of the baby, especially if parents have expressed this wish.
Between 24 and 24+6 weeks, resuscitation should be commenced unless the baby is thought to be severely compromised. Response to initial measures should be considered before the decision is made to commence intensive care.
After 25 weeks, it is appropriate to resuscitate and start intensive care
Features of JET
Present with HF
Usually regular but can be irregular conduction
Origin near AV node
In post op patient, if JET suspected and they have pacing wires in, what can be helpful
A-wire ECG - to confirm whether atrial activity precedes QRS
Management of JET
Amiodarone (note neg inotropic effect)
Ivabradine
Flecanide (with caution)
BB (note neg inotropic effect)
Ablation eventually
Types of JET
Post operative
Congenital
Typical rate of AVRT/AVNRT in babies
300
DDx for tachycardia with retrograde p waves
AVNRT
AVRT
JET with origin very close to AVN (usually slower than AVRT/AVNRT and more in babies)
Narrow complex tachy with retrograde P’s with some missed retrograde P’s
More likely JET
If AVRNT/AVRT had a non conducted retrograde P they would usually revert to sinus
Post-op vasoactive for children who have had congenital surgery (PRIMACORP study)
Milrinone
PRIMACORP - Lower risk of low CO with high doses of milrinone vs without
Second choice of vasoactive support post congenital surgery in addition to milrinone
Adrenaline or noradrenaline most commonly
However lits of variability
Features of vasopressin as vasoactive
Pure vasoconstrictor and allows reducing noradrenaline doses
* Dose: 0.01 units/kg/min to 0.1 units/kg/min
* Use in refractory catecholamine shock
* Supports SVR without increasing PVR
* Be aware of severe peripheral ischaemia
Other interventions to support CO in addition to catecholamines, PD3 inhibitors and ADH
- Calcium infusion, optimal electrolytes, correct acidosis
- Hydrocortisone
- Control of temperature (control of SVR)
- Pacing for optimal output
- Levosimendan (controversial)
