- 1 Introduction
- 2 Epidemiology
- 3 Pathophysiology
- 4 Risk factors
- 5 Clinical features
- 6 Differential diagnosis
- 7 Investigations
- 8 Management
- 9 Complications
- 10 Summary
- 11 References
Shock is a life threatening condition caused by the systemic failure of the circulatory system. It causes inadequate perfusion of major organs that eventually leads to multi-organ failure due to ischaemia if not corrected (1).
Children often show few signs of shock even after severe fluid depletion due to high physiological reserves. This also means that when symptoms do occur, patients are likely to deteriorate rapidly (1).
There are four different types of shock, although there is overlap between them:
- 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).
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).
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)
It is important to first understand the physiology of cardiac output (11):
CO = HR X SV
MAP = CO X SVR
- HR & MAP can be easily measured at the patient’s bedside.
- SV can be estimated by assessing peripheral pulse volume and end organ perfusion (such as urine output & GCS).
- SVR can be estimated by assessing peripheral temperature and capillary refill time (11).
(CO= cardiac output, HR= heart rate, SV= stroke volume, MAP= mean arterial pressure, SVR= systemic vascular resistance)
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).
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.
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.
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).
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.
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
- Very young children
- Personal or family history of allergies or atopy
- Recent history of new medication (7)
- Young children (<6 months)
- Warm weather
- Concurrent illness (gastroenteritis, N+V and diarrhoea)
- Use of diuretics
- Cystic fibrosis
- Hirschsprung’s disease (8)
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.
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.
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
- 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):
- 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):
- Slow, irregular pulse
- Unrecordable BP
Progressing to cardiac arrest
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)
|Anaphylaxis||Third spacing||Cardiomyopathy||Pulmonary Embolism|
|High spinal injury||Bleeding||Arrhythmias||Tension pneumothorax|
|Sepsis||Congenital heart disease||Coarctation of the aorta|
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).
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.
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
- 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
|1||ATLS – Advanced Trauma Life Support – Student Course Manual (10 ed.). American College of Surgeons. 2018. pp. 43–52, 135. ISBN 978-78-0-9968267.|
|2||Wheeler DS, Basu RK. Pediatric Shock: An Overview. The Open Pediatric Medicine Journal. 2013;7(Suppl 1:M2):2-9.|
|3||Gobinathan S, Suresh Kannan K. Study of prevalence, etiology, response to treatment and outcome of paediatric shock in a tertiary care hospital. International Journal of Contemporary Paediatrics. 2018;5(3):1104-8|
|4||Pasman EA, Watson MC, Steele DW et al. Shock in Pediatrics [Internet] (2019). Medscape. [Accessed 21st December 2021]. Available from: https://emedicine.medscape.com/article/1833578-overview#a6|
|5||Carla de Souza D, Machado FR. Epidemiology of Pediatric Septic Shock. Journal of Paediatric Intensive Care. 2019;8(1):3-10.|
|6||Mayoclinic. Pediatric cardiogenic shock: What is the role of medical and mechanical circulatory support? (2018). [Accessed 21st December 2021]. Available from: https://www.mayoclinic.org/medical-professionals/cardiovascular-diseases/news/pediatric-cardiogenic-shock-what-is-the-role-of-medical-and-mechanical-circulatory-support/mac-20430722|
|7||Mustafa SS, Kaliner MA. What are the risk factors for anaphylaxis? [Internet] (2018). Medscape. [Accessed 21st December 2021]. Available from: https://www.medscape.com/answers/135065-52900/what-are-the-risk-factors-for-anaphylaxis|
|8||The Royal Children’s Hospital Melbourne. Dehydration [Internet] (2020). [Accessed 21st December 2021]. Available from: https://www.rch.org.au/clinicalguide/guideline_index/Dehydration/|
|9||Waltzman M. Initial Management of Shock in Children [Internet] (2011). [Accessed 21st December 2021]. Available from: https://somepomed.org/articulos/contents/mobipreview.htm?3/20/3393|
|10||Pittaway A. Paediatric shock [Internet] (2006) [Accessed 21st December 2021]. Available from: https://www.frca.co.uk/article.aspx?articleid=100571|
|11||Argent A et al. 2019, Shock, Paediatric BASIC manual. 3rd edition|