Acute scenarios Flashcards

(69 cards)

1
Q

Two aetiologies of heart failure in children

A

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

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2
Q

Definition of HF

A

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.

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3
Q

Causes of overcirculatory HF in children

A
  • 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)
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4
Q

Causes of pump failure HF in children

A
  • 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
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5
Q

Symptoms of HF in children

A

Infant: breathless, cold extremities, wheeze (cardiac asthma) , grunting, feeding difficulties, sweat, fail to thrive, recurrent chest infections

Older: fatigue, exercise intolerance, dizziness, syncope

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6
Q

Examination in HF in children

A

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

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7
Q

Investigations for HF in children

A

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

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8
Q

Management of HF in children

A

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.

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9
Q

Differentiating cardiogenic vs respiratory cyanosis in children

A

Hyperoxia test

The PaO2 is measured in the right radial artery (preductal) on room air and after 10 minutes of 100% oxygen supplementation.

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10
Q

Aetiology of Kawasaki disease

A

Epidemiological studies suggest infectious agent in genetically susceptible individuals
* Infectious hypothesis – winter spring seasonality, community outbreaks
* Genetic susceptibility: Japanese individuals more prone
* Superantigen hypothesis ?

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11
Q

DDX Kawasaki disease

A

Streptococcal disease (Scarlet fever) viral infection (measles, EBV, enterovirus) staphylococcal scalded skin syndrome, drug hypersensitivity, JIA,

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12
Q

Definition and criteria for KD

A

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.

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13
Q

Firstcardiac investigation on suspecting KD

A

Transthoracic echocardiography should be performed as soon as Kawasaki disease is suspected to evaluate for coronary artery aneurysms.

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14
Q

Treatment of KD

A

IVIG +/-
Consider corticosteroids for severe disease
ASPIRIN NOT RECOMMENDED

Long-term monitoring of coronaries

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15
Q

Causes of tachyarryhthmia in children

A

Sinus tachycardia
SVT
JET
Other atrial tachycardias (MAT/EAT)
VT

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16
Q

Management of SVT in children

A

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

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17
Q

PALS algorithm - non-shockable rhythm

A

Re-assess rhythm every 2 minutes
Adrenaline 10 mcg/kg immediately then on alternate 2-min rounds

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18
Q

PALS algorithm - shockable rhythm

A

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

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19
Q

Choking child with ineffective cough - conscious

A

5 back blows
5 chest thrusts
Assess and repeat

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20
Q

Choking child with ineffective cough - unconscious

A

Open aiwrway
2 breaths
CPR 15:2
Check for FB

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21
Q

Choking child with effective cough

A

Encourage coughing
Maintain ongoing assessment until resolved

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22
Q

Bradycardia - no shock

A

Monitor closely for symptoms
Seek opinion

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23
Q

Bradycardia with shock

A

Vagal overactivity? Atropine 20mcg/kg

No clear evidence of vagal overactivity? Adrenaline 10mcg/kg, consider adrenaline infusion, consider pacing

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24
Q

Blood and fluid therapy in trauma and massive blood loss

A

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

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25
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
26
What is pre-ductal SpO2
SpO2 taken from right arm (pre-ductal)
27
Causes of HF in utero
Severe valvular disease e.g., Ebstein Severe anaemia Paroxysmal SVT AV block Severe mitral insufficiency in AVSD
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Causes of HF in first day of life
II myocardial dysfunction (anaemia, sepsis, asphyxia, hypoglycaemia) Duct dependent lesions (TTTTP)
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Causes of HF in the first week of life
Duct dependent lesions (TTTTP) PDA Adrenal insufficiency due to enzyme deficiencies Arrhythtmias e.g., SVT
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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
31
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
32
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
33
Signs of heart failure in children with R>L failure
Hepatomegaly Ascites Pleural effusion Peripheral edema Weight gain JV distension rare in children
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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
35
Definition of failure to thrive
broadly defined as a faltering of growth from a previously established pattern of growth
36
Three key principles in assessment of child in shock
Primary ABCDE assessment and resuscitation Secondary assessment and emergency treatment Stabilisation and transfer
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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
38
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
39
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.
40
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
41
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
42
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.
43
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.
44
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.
45
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.)
46
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.
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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
48
AB shows Bubbling sound
Excessive secretions > Suctioning
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Harsh stridor and a barking cough
Croup > Oral dexamethasone Nebulised budesonide and adrenaline in severe cases
50
Soft stridor, drooling and fever in a sick looking child
Bacterial tracheitis or epiglottitis Intubation by anaesthetist followed by IV antibiotics
51
Sudden onset stridor with history of inhalation
Inhaled foreign body Laryngoscopy for removal
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Stridor following ingestion or injection of a known allergen
Anaphylaxis IM adrenaline
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Wheeze
Acute asthma Bronchodilators
54
Bronchial breathing
Pneumonia IV antibiotics
55
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
56
SVT
Vagal manoeuvres followed by a rapid bolus of IV adenosine or synchronous DC shock, depending upon the clinical status of the child.
57
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
58
Features of JET
Present with HF Usually regular but can be irregular conduction Origin near AV node
59
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
60
Management of JET
Amiodarone (note neg inotropic effect) Ivabradine Flecanide (with caution) BB (note neg inotropic effect) Ablation eventually
61
Types of JET
Post operative Congenital
62
Typical rate of AVRT/AVNRT in babies
300
63
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)
64
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
65
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
66
Second choice of vasoactive support post congenital surgery in addition to milrinone
Adrenaline or noradrenaline most commonly However lits of variability
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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
68
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)
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