Paediatric Shock

Epidemiology

Shock is one of the most common life threatening presentations in paediatrics and accounts for 2% of all paediatric admissions to casualty worldwide.

Around 10 million children die of shock annually worldwide. The highest mortality is in under 5s in developing countries (3).

Sepsis is the cause in the majority of paediatric cases (57%) and has a high mortality rate ranging from 5% in developed countries to 35% in developing countries (4, 5).

Pathophysiology

Shock is caused by a failure of the circulatory system to adequately perfuse major organs. The circulatory system requires a functioning pump (heart), reservoir (vascular blood volume) and pipes (vessels). A failure of any of these can lead to shock. (2, 4)

When shock begins to develop, the body uses neural and hormonal mechanisms to compensate and increase blood pressure (BP) to perfuse the vital organs. This state is called compensated shock and BP is maintained (10).

Mechanisms used in compensated shock include:

• Tachycardia to increase cardiac output.
• Redistribution of blood flow to increase perfusion of more important organs at the expense of others (e.g. skin) through a combination of vasodilation and vasoconstriction.
• Tachypnoea to reduce anaerobic respiration and reduce lactic acidosis formation.

If the cause of shock is not treated, these mechanisms will become insufficient to maintain BP and therefore, vital organ perfusion. This state is called uncompensated or decompensated shock and is a bad prognostic sign (4, 10).

Distributive shock

This is a result of redistribution of a normal intravascular blood volume in the wrong vessels due to systemic vasodilation.

Ordinarily, there is a degree of sympathetic tone in all vessels to allow dilation and constriction depending on local circumstances; for example sending more blood to the skin for temperature control, or the muscles during exercise, at the expense of other areas. However, when all these vessels dilate simultaneously, it leads to shifts of blood flow within the vascular system, resulting in reduced blood flow to major organs despite a normal blood volume (4).

Systemic vasodilation is commonly caused by sepsis due to the release of many inflammatory cytokines in response to infection, but can also be caused by anaphylaxis or high spinal cord injury.

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):

• Dehydration e.g. diarrhoea, vomiting, burns, inadequate feeding in infants, or diuresis in diabetic ketoacidosis.
• 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.
• Haemorrhage.

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).

In paediatric patients, cardiogenic shock is commonly caused by viral myocarditis, or acute deterioration of heart failure secondary to cardiomyopathies or congenital heart defects.

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).

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. (4)

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.

Risk factors

Due to the variety of causes it is difficult to come up with a discreet list of risk factors for shock itself. However, they can be described based on the causes.

A few examples are included below:

Sepsis: Beware viral sepsis

• Immunocompromised
• Very young children

Anaphylaxis:

• Personal or family history of allergies or atopy
• Recent history of new medication (7)

Dehydration:

• Young children (<6 months)
• Warm weather
• Concurrent illness (gastroenteritis, N+V and diarrhoea)
• Use of diuretics
• Cystic fibrosis
• Hirschsprung’s disease (8)

Clinical features

Shock may present suddenly and obviously (e.g. major haemorrhage as a result of trauma), but more commonly it has an insidious onset (e.g. unrecognised meningococcal septicaemia) and features of shock are important to recognise before patients deteriorate.

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. (4)

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

Differential diagnosis               

When you have a patient you believe may be shocked, your differentials are for the types of shock and what may be causing them as explained above.

Below are some paediatric causes of shock (4)

Investigations

Shock often presents as an emergency and should be treated clinically. Do not wait for investigations before beginning treatment. However, investigations can be useful for assessing the severity of shock, the cause, and to monitor improvement.

• 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 (4).

Management

Initial management (9, 11):

An A to E assessment should be performed on all unstable patients. Early identification of the type of shock present, is important to guide management.

As shock in children is commonly as a result of dehydration or fluid shifts, the initial management of a shocked child is IV fluid resuscitation.  Start with 10-20ml/kg boluses of crystalloids (blood if haemorrhage). If there is an adequate response, fluid resuscitation can be continued up to 60ml/kg. If a child is requiring further fluid boluses, the use of blood products/ inotropes should be considered, in addition to methods of securing the airway. If IV access is difficult do not waste time, insert an intra-osseus line.

In children with suspected cardiogenic shock, be cautious with fluid resuscitation and start with 5ml/kg fluid boluses and seek expert help early.

Individual trusts may have their own guidelines for the management of shock or its causes e.g. septic shock.

If the cause of the shock is known, you should also begin treating this immediately e.g. sepsis 6. If the patient is not responding to fluids, the next step is vasoconstrictive agents such as IV adrenaline or dopamine.

Definitive and long-term management

Identification and treatment of the underlying cause. Even if the patient is responding to fluids, they should still be considered for PICU monitoring as they may need further treatment. If the patient does not seem to be improving, they should be escalated rapidly to a PICU.

Complications

There are many acute complications secondary to ischaemia (4):

• Central nervous system failure
• Respiratory failure (from muscle fatigue or acute respiratory distress syndrome)
• Acute kidney injury
• Gastrointestinal ischemia
• Disseminated intravascular coagulation (DIC)
• Metabolic derangements
• Death

Summary

• Shock is a common life threatening presentation in paediatrics
• It has many causes, the most common being sepsis
• It can be compensated or uncompensated
• It is treated with IV fluids with early goal-directed therapy
• Definitive management of the underlying cause is also needed

 References