2- Paediatrics Emergency Flashcards
paediatric shock background
- Life threatening condition caused by systemic failure of the circulatory system
- Causes inadequate perfusion of major organs that eventually leads to multi-organ failure due to ischaemia if not corrected
- Sepsis most common cause
red flags for children about to go into cardiac arrest
Big red flags
- Hypoxia
- Hypotension (last thing to go)
- Silent chest
- Unequal pupils
- Posturing
Adults vs children
- Deteriorate quicker
- Compensate well
- Smaller anatomy
- Physiology
- Psychology
- Pattern of pathology
- Emergency presentation
Types of shock
- Hypovolemic – consequence of inadequate circulating volume.
- Obstructive – obstruction of blood flow to and from the heart.
- Cardiogenic – pump failure.
- Distributive – maldistribution of the circulating volume (2).
pathophysiology of shock
- Caused by a failure of the circulatory system to adequately perfuse major organs
- Circulatory system requires
o A pump (heart)
o Reservoir (vascular blood volume)
o Pipes (vessels)
Mechanisms used in compensated shock (to maintain BP)
- Tachycardia to increase cardiac output
- Redistribution of blood flow to increase perfusion of most important organs at the expense of others e.g. skin. Involves vasodilation and vasoconstriction
- Tachypnoea to reduce anaerobic resp and reduce lactic acidosis
- If shock isnt treated these mechanisms become insufficient to maintain BP
Risk factors for shock
- Sepsis
- Anaphylaxis
- Dehydration
- Arrythmia
Reversible causes of cardiac arrest (Hs and Ts)
H’s
- Hypovolemia
- Hypoxia
- Hydrogen ion excess (acidosis)
- Hypokalaemia and hyperkalaemia
- Hypothermia
T’s
- Tamponade
- Toxins
- Tension pneumothorax
- Thrombosis (pulmonary)
- Thrombosis (coronary)
Distributive shock
Causes
- Sepsis
o Often caused by sepsis due to the release of many inflammatory cytokines in response to infection. - Anaphylaxis
- High spinal cord injury
Pathophysiology of distributive shock
- Inappropriate redistribution of normal intravascular blood due to systemic vasodilation – loss of sympathetic tone
- This reduces blood flow to major organs despite normal blood volume
Hypovolaemic shock
Reduced circulating blood volume decreases cardiac output through Starling’s law, decreasing perfusion of the major organs causing shock.
It is commonly caused by (4):
1) Dehydration e.g. diarrhoea, vomiting, burns, inadequate feeding in infants, or diuresis in diabetic ketoacidosis.
2) Third spacing – the movement of fluid from the intravascular compartment to an extracellular compartment i.e. the interstitial space. In both sepsis and anaphylaxis, the release of inflammatory mediators increases the permeability of capillaries, leading to fluid in the capillaries moving to the interstitial space.
3) Haemorrhage.
Obstructive shock
An obstruction to the outflow of blood from the heart itself or the great vessels decreases cardiac output and therefore perfusion of the major organs.
This the least common cause of shock in paediatrics but can be caused by coarctation of the aorta, cardiac tamponade, tension pneumothorax or massive pulmonary embolism.
Cardiogenic shock:
Causes of cardiac arrest
- Cardiomyopathy
- Primary arrhythmias
o Long QT syndrome
o Wolff-Parkinson-White syndrome - Congenital heart problems
- Myocarditis (viral)
- Chest trauma
Pathophysiology of cardiogenic shock
- When the heart itself fails, this decreases the cardiac output, resulting in reduced perfusion of the major organs.
- It should be suspected in a patient who is not responding to fluid therapy and BP remains low and/or is demonstrating signs of pulmonary overload (tachypnoea, respiratory distress, hepatomegaly) (4, 11).
This is uncommon in paediatrics and has a poor prognosis. Approximately a third of these children either die or require a heart transplant within a year (7).
presentation of shock
Often show very few signs of shock even after severe fluid depletion due to high physiological reserve
From History
Shock can present very subtly. The most sensitive symptom is change in mental state. This can be agitation, restlessness, sedation, confusion, or reduced GCS.
Ask about symptoms of any of the causes mentioned above that the parent may report e.g. cough, thirst, choking.
From Examination
Signs of causes include things like a non-blanching rash for sepsis or stridor for anaphylaxis.
Signs of compensated shock are often very subtle (4, 10):
* Altered mental state
* Tachycardia
* Tachypnoea
* Decreased urine output
* Increased capillary refill time (Note: in distributive shock peripheries are likely to remain warm due to peripheral vasodilation)
As shock progresses, these symptoms worsen. If not treated, this will progress to uncompensated shock. This has a much higher mortality and signs signify organ ischaemia (9, 10):
- Hypotension
- Decreased oxygen saturations
- Chest/abdominal pain
- Weak, thready pulse
- Cold, grey or mottled skin
- Decreased body temperature
If allowed to progress further, irreversible shock will occur. Signs of which include (9):
* Unconsciousness
* Slow, irregular pulse
* Unrecordable BP
* Progressing to cardiac arrest
Investigations for shock
DO NOT WAIT FOR INVESTIGATIONS BEFORE STARTING TREATMENT.
- Lactate and blood gases (lactic acidosis indicating ischaemia, and hypoxia) (1).
- Creatinine to look for acute kidney injury (a sign of uncompensated shock).
- U+Es to assess any electrolyte imbalances e.g. due to diarrhoea, and guide IV fluid management.
- Other investigations are guided by the suspected cause e.g. FBC, CRP, coagulation, blood cultures
- ECG
management of shock
A to E
Identification and treatment of underlying cause
IV fluid resus
- 10-20ml/kg bolus of crystalloids (blood if haemorrhage)
If adequate response fluid resus can be continued up to 60ml/kg - If child requires more, then blood products/ inotropes should be considered
- BEWARE IF CARDIOGENIC SHOCK- start with 5ml/kg fluid boluses and seek expert help
Secure airway
If IV access difficult- Intra-osseus (IO)
If not responding to fluids 0> vasoconstrictive agents such as IV adrenaline or dopamine
Sepsis 6(if cause is unknown)
presentation of cardiac arrest
- Unresponsiveness
- Lack of normal breathing (with only an occasional gasp)
- Low sats
- Weak/ undetectable pulse
o CPR should be started in children who become bradycardic (<60/min( with signs of inadequate perfusion
Causes of cardiac arrest:
cardiomyopathy, long QT syndrome, WPW, myocarditis, arrhythmia, congenital heart problems
management of cardiac arrest
1) Oxygenate, ventilate and start chest compression
- Give 5 rescue breaths: use bag-mask ventilation, using high concentration inspired oxygen 100% as soon as available
- Start chest compressions (100-120/min)
- Call for anaesthetist to intubate
*Pause compressions every 2 minutes for rhythm check
2) Attach a defibrillator or monitor
- Assess and monitor cardiac rhthm via ECG
- Assess rhythm
assesing rhythm
- Non-shockable - asystole, pulseless electrical activity (PEA), bradycardia
- Shockable – ventricular fibrillation (VF) or pulseless ventricular tachycardia (pVT).
management of Non-Shockable rhythm (asystole, PE, bradycardia)
- Perform CPR
- Ventilate with 100% oxygen
- Give adrenaline (IV 10mg /kg)
(If no IV – IO) - Consider and correct reversible causes e.g. hypoxia, hypovolaemia, tamponade, tension pneumo
management of Shockable (VF/pVT)
- Defibrillation should be immediately attempted – if in doubt consider the rhythm to be shockable (1 shock of 4 J/kg)
- Resume CPR
- Pause CPR after 2 mins, give second shock
- Resume CPR
- Pause CPR after 2 mins, give adrenaline 10mg/kg and amiodarone 5mg/kg
- Continue giving shocks every 2 mins
- Consider and correct reversible case
o Hypoxia
o hypovolaemia
Respiratory distress
Respiratory distress is defined as increased work of breathing that causes a sense of altered well-being. The hallmarks are use of accessory muscles and tachypnoea. Distress can be caused by disorders of gas exchange (O2 absorption, or CO2 elimination), respiratory drive, neuromuscular disease, and infection
Effort of breathing
* Rate
* Recession
* Accessory muscle
* Nasal flaring
* Child’s position
* Extra noises
* Wheezing
* Stridor
* Grunt
Effectiveness of breathing
* Chest expansion
* Air entry
* Pulse oximetry (sats)
* Exceptions
* Exhaustion
* Central
* Respiratory Depression
* Neuromuscular disease
Effects of respiratory inadequacy
* Heart rate
* Skin tone
* Mental state
causes of resp distress
Causes
- Epiglottitis
- Croup
- Asthma
- Bronchiolitis
- Pulmonary oedema
- Atelectasis
- Pleural effusion
- Pulmonary embolism
- Pneumothorax
- Duchenne muscular dystrophy
- CNS depression
Clinical assessment of resp distress
- Pallor or cyanosis
- Respiratory drive
- Inspiration and expiration
o Upper airway obstruction- stridor
o Lower airway obstruction leads to cough, wheeze and prolonged expiratory phase - Chest wall movement
o Flail chest
o Diaphragmatic palsy
o Pneumothorax
o Foreign body inhalation - Level of agitation
- Mental state
- HR and perfusion
investigations for resp distress
- Pulse oximetry
- ABG
o Acid-base, PaO2, PaCO2 - Bloods: FBC, electrolytes, glucose and cultures
- CXR e.g. severe pneumonia or pneumothorax
Monitoring resp distress
- Pulse oximetry.
- Continuous ECG.
- BP.
- Temperature.
- Fluid balance.
- Conscious level.
Foreign-body inhalation
Foreign-body (FB) aspiration is more common in toddlers and infants, who tend to put objects in their mouths. FBs can be inhaled into the airway, or they may get caught in the oesophagus and compress the trachea.
Presentation of FB inhalation
- Larynx: usually causes hoarseness, cough, dysphonia, haemoptysis, stridor, wheezing, dyspnoea, cyanosis, or apnoea due to complete obstruction.
- Trachea and bronchus: can cause chest pain. After initial symptoms, there may be an asymptomatic period followed by features of pneumonia
- Oesophagus: will produce drooling, dysphagia, or vomiting and, if the trachea is compressed, may produce dyspnoea, stridor, respiratory failure, or apnoea
Investigations for FB inhalation
- Resp examination: A monophonic wheeze or absent breath sounds on one side of the chest may be noted on examination.
- Chest and neck X-ray, with lateral views, may be helpful in identifying the location of an object. Inspiratory and expiratory films may show an area of hyperinflation
- ABG analysis is indicated when the patient is in severe distress.
initial management of FB inhalation
- A to E
- FB removal: if the child is calm with good air exchange, removal of the FB should take place under controlled circumstances; manipulation may change the position of the object, inducing more severe obstruction. If the child is in distress, but maintaining good air exchange, back blows and chest thrusts may be performed as per the standard technique for paediatric advanced life support (ALS).
- An unconscious child with poor air entry should be given oxygen (FiO2 100%) via a face mask until rigid bronchoscopy and object removal can be performed.
Dehydration
Background
- Can occur with many illnesses
- Can be hard to assess in young children
- - If a child is haemodynamically unstable (e.g. in shock), prompt fluid resuscitation with fluid boluses must be given – sepsis should be considered
- Goal is to rehydrate enterally (orally or via NG), unless severe dehydration or shock
Best measure of dehydration
is weight loss – not always possible to get an accurate pre-morbid weight, therefore the best signs for predicting if a child is >5% dehydrates
o CRT
o Abnormal skin turgor
o Abnormal respiratory patter
Risk factors for dehydration
- Poor oral intake
- Increases losses e.g. diarrhoea or vomiting
- Child <6 months
Investigations for dehydration
- Intake output chart
- Electrolytes (capillary blood gas)
- Blood glucose (BM)
management of dehydration
- If mild/moderate dehydration enteral (oral or NG) rehydration preferable
o Can do oral glucose challenge if vomiting or refusing - If severe dehydration or cannot tolerate enteral rehydration use IV rehydration
- Rate of rehydration
o If gastroenteritis can be rapid
o Slower in other illness: resp infection, DKA, meningitis and hypernatremia - After treating shock replace remaining deficit slowly over 24-48 hours
- Rate of fluid admin should be adjusted according to ongoing clinical reassessment including fluid balance.
Clinical assessment of dehydration
1) Loss of bodyweight (pre-morbid compared to current body weight)
- eg a 10 kg child who now weighs 9.5 kg has a 500 mL water deficit and is 5% dehydrated
- Normal: no loss of body weight.
- Mild dehydration: 5-6% loss of body weight.
- Moderate: 7-10% loss of body weight.
- Severe: over 10% loss of body weight.
2) If pre recent weight is unavailable -> use clinical features and history to estimate degree of dehydration
History
* Take a detailed intake history regarding both food and fluid intake in comparison to normal feeding pattern
* Take a detailed output history regarding urine and stool, similarly in comparison to normal output pattern
* Ask about excessive losses (eg vomiting, frequent urination or diarrhoea)
* Recent use of potentially hypertonic/hypotonic fluids (eg diluted formula or soft drinks, water only, fortified feeds)
* Risk factors for severe dehydration and electrolyte disturbances
-> Infants <6 months old
-> Gastrointestinal pathology (eg short gut syndrome, ileostomy, colostomy, Hirschsprung disease)
-> Cystic fibrosis
-> Renal impairment
-> Use of diuretics
->Metabolic disorders
* Conditions where dehydration carries a high risk for children
-> Complex/cyanotic congenital heart disease (especially with cardiac shunts)
-> Slow weight gain
-> Immunocompromise
-> Use of nephrotoxic medications
-> Post-organ transplant
Examination
* Obtain vital signs
* Obtain weight
* Assess hydration level based on a combination of signs (see Assessment of severity table below)
o Children with mild dehydration have no clinical signs. They may have increased thirst and/or reduced urine output
o More numerous/pronounced signs indicate greater severity
o For clinical shock, one or more of these signs will be present – reduced conscious state, tachycardia, tachypnoea, hypotension, weak peripheral pulses, mottled/cold peripheries, acidosis
Clinical features of severe dehydration
- Abnormally sleepy or lethargic.
- Sunken eyes.
- Drinking poorly or not at all.
Pinch test (skin turgor): the sign is unreliable in obese or severely malnourished children.
* Normal: skin fold retracts immediately.
* Mild or moderate dehydration: slow; skin fold visible for less than 2 seconds.
* Severe dehydration: very slow; skin fold visible for longer than 2 seconds.
Other features of dehydration include dry mucous membranes, reduced tears and decreased urine output.
* Additional signs of severe dehydration include circulatory collapse (e.g. weak rapid pulse, cool or blue extremities, hypotension), rapid breathing, sunken anterior fontanelle.
Epiglottitis
Background
- Inflammation and swelling of the epiglottitis
o Haemophilus influenza type B most common - Life threatening emergency
- Now rare due to vaccination
epiglottitis pathophysiology
Pathophysiology
- The epiglottis can swell to the point of completely obscuring the airway within hours of symptoms developing.
Presentation of epiglottitis
- Patient presenting with a sore throat and stridor
- Drooling
- Tripod position, sat forward with a hand on each knee
- High fever
- Difficulty or painful swallowing
- Muffled voice
- Scared and quiet child
- Septic and unwell appearance
Investigations for epiglottitis
- Investigations of throat should not be performed- MAY STRESS PATIENT OUT AND MAKE BREATHING HARDER
- Lateral x-ray may show ‘thumb sign’ or ‘thumbprint sign’
o Soft tissue shadow which looks like a thumb pressed into the trachea
o Causes by oedematous and swollen epiglottitis - Useful for excluding a foreign body
management of epiglottitis
Emergency management
- Do not distress patient can cause prompt closure of the airway
- Alert senior paediatricians and anaesthetist
- Secure the airway
- Most patients do not acquire intubation, however preparations need to be made to perform intubation at any time
- Tracheostomy if airway is completely closed
- Transferred to ITU
Definitive management
- IV abx such as ceftriaxone
- Steroids i.e. dexamethasone
Croup
Background
croup pathophysiology
- URTI causing oedema in larynx
causes of croup
Causes
- Parainfluenza (most common)
- Influenza
- Adenovirus
- RSV
- Diphtheria – leads to epiglottitis (high mortality)
epiglottitis vs croup
epiglottitis
- inflammation of epiglottitis
- bacteria: HiB
Croup
-inflammation of the larynx
- viral
It can present in a similar way to croup, but with a more rapid onset. In you exams keep a lookout for an unvaccinated child presenting with a fever, sore throat, difficulty swallowing that is sitting forward and drooling and suspect epiglottitis.
Croup and epiglottitis share symptoms and signs including stridor, fever and respiratory distress. Croup uncommonly causes severe airway obstruction and has a slow course, whereas untreated epiglottitis rapidly culminates in complete obstruction, shock and may be fatal.
Differentials for croup
Differentials
- Anaphylaxis
- Smoke inhalation
- Trauma
croup presentation
- Increased work of breathing
- “Barking” cough, occurring in clusters of coughing episodes
- Hoarse voice
- Stridor (inspiratory)
- Low grade fever
- Drooling due to pain swallowing
scoring system for croup
Westley croup severity score
management of croup
Mild/ moderate
Can be managed at home with simple support
- Fluids and rest
- Sit child up
>Severe
Hospital management (stepwise)
- Oral dexamethasone
- Oxygen
- Nebulised budesonide
- Nebulised adrenaline
- Intubation and ventilation
febrile convulsions background
- A type of seizure which occurs in a child with a high fever
- By definition: only affects children between 6 months and 5 years
- Types: simple vs complex
simple vs complex febrile convulsion
Simple FC
* Generalised, tonic clonic seizures
* Last less than 15 mins
* Only occur once during a single febrile illness
Complex FC
* Partial or focal seizures
* Last more than 15 mins
* Occur multiple times during the same febrile illness
pathophysiology of febrile convulsion
- High fever is trigger
- Not caused by epilepsy or any neurological pathology such as meningitis, encephalitis or tumours
Presentation FC
- Typically in a child around 18 months presenting with 2-5 minute tonic clonic seizure during a high fever
o Bilateral seizure which involves both stiffening and twitching - Underlying viral or bacterial infection
investigations for febrile convulsion
Need to rule out other neurological pathology
- Epilepsy
- Meningitis, encephalitis, cerebral malaria
- SoL
o Haemorrhage
o Brain tumours
- Syncopal episodes
- Trauma
examination for FC
Examine from head to toe with special emphasis on:
- External ear examination with auroscope – to look for any signs of otitis externa or otitis media (red bulging tympanic membrane etc.)
- Throat examination – for signs of URTI (inflamed tonsils etc.)
- Full respiratory examination – looking for signs of LRTI
- Check fontanelles (raised anterior fontanelles with no pulsation felt in infants can be a sign of meningitis or raised ICP)
- Brudzinski’s or Kernig’s sign, (signs of meningitis, though less reliable in infants)
- Nuchal rigidity (neck stiffness)
- Mental status of the child (irritable, playful)
- Full neurological examination
- Cardiovascular examination
- Abdominal examination
- Urine dipstick and microscopy
- Any superficial infective skin lesions
Management FC
- Identify and manage source of underlying infection
- Analgesia- paracetamol and ibuprofen
PEWS
Paediatric early warning scores
Parameters
- Respiratory rate and effort
- Oxygen requirement
- Heart rate
- Level of consciousness
- Clinician/family concern
neurological failure- types of posturing
Decorticate
* Flexing to pain
* Primate response to pain
* Cortex no longer functioning, midbrain taken over
Decerebrate
* Extending to pain
* Spinal reflexes
* Worse
examples of peripheral nerve injury and palsy
Brachial plexus injury
- Erbs palsy – upper BP
- Klumpkes palys- lower BP
Erbs palsy
- upper BP injury
An Erbs palsy is the result of injury to the C5/C6 nerves in the brachial plexus during birth or other trauma - Upper brachial plexus injury
risk factors for brachial plexus injury- Erbs palsy
- Macrosomnia
- Mothers
Pelvic abnormality
Older age
Gestational diabetes
- Labour
Induction
Breech
Improper use of forceps
pathophysiology of Erbs palsy
Pathophysiology
- It is associated with shoulder dystocia (shoulder stuck in pelvis), traumatic or instrumental delivery and large birth weight.
- Due to stretching, compression and tearing of nerves away from spinor cord
- Damaged to the C5/C6 nerves leads to weakness of shoulder abduction and external rotation, arm flexion and finger extension.
Presentation of Erbs palsy
this leads to the affected arm having a “waiters tip” appearance:
* Internally rotated shoulder
* Extended elbow
* Flexed wrist facing backwards (pronated)
* Lack of movement in the affected arm
management of Erbs palsy
Management
- Function normally returns spontaneously within a few months.
- If function does not return then they may required neurosurgical input.
- PT
Klumpke’s palsy backgroun
lower brachial plexus injury
Result of an injury to C8/T1 nerves in the brachial plexus during birth or other trauma
risk factors for Klumpkes palsy
Childbirth -> especially breech
- Abducted arm during childbirth -> arm traction and pulling -> nerve stretching
- Avulsion injury- where nerves are torn away from spinal cord
- Stretch nerve
- Rupture
Grabbing things when falling from height e.g. falling from a tree
presentation of Klumpkes palsy
- Claw hand
–>Intrinsic hand muscle atrophy -> flexion of interphalangeal, extension of metacarpophalangeal joints - Involvement of T1 may result in Horners syndrome: ptosis, miosis and anhydrosis
