Assessment
Diagnosis
Early recognition of sepsis and prompt treatment is necessary to avoid further organ failure, deterioration and death.13 Consider sepsis in any child with an acute illness, or in any high-risk group (see box below), and initiate screening using the Queensland Paediatric Sepsis Pathway [PDF]. It is important to record a complete set of vital sign observations including blood pressure. The QPSP recognition tool supports clinicians to identify children with features of severe illness for early senior review with the question ‘could this be sepsis’?
A diagnosis of sepsis is made using clinical judgement, supported by laboratory testing. There is no single clinical finding or test that is diagnostic. A careful history and clinical examination paying attention to parental concerns may assist to reveal red flags. If sepsis is suspected, initiate investigations and treatment via the Queensland Paediatric Sepsis Pathway until sepsis can be excluded and therefore treatment de-escalated. Validated triage tools for early stages of paediatric sepsis based on vital signs are difficult to develop. Therefore, the emphasis is on senior medical review of the patient.15
Children at high risk for sepsis
- neonates and premature infants
- children of Aboriginal / Torres Strait Islander / Pacific Islander / Maori origin
- Immunocompromised patients:
- unimmunised or incomplete immunisation status
- malignancy and/or chemotherapy
- immune deficiency
- asplenia (surgical or functional e.g. sickle cell disease)
- long-term steroid use
- immunosuppressant drug therapy
- recent surgical procedure (within 6 weeks)
- intravenous recreational drug use
- indwelling lines or catheters (e.g. VP shunt or CVAD)
- Recent inpatient episode of sepsis (within 6-12 weeks)
Sepsis presentation varies with age. Infants and neonates commonly present with non-specific symptoms and signs, such as feeding difficulties and/or apnoea. Older children may present with a source of infection and/or a constellation of features including fever or hypothermia, vomiting, inappropriate and persistent tachycardia, altered mental state and reduced peripheral perfusion. Pain without an identified source can be a non-specific sign in children.13,15 Severe presentations can include seizures. Some infections present with a concerning purpuric rash. Deviations from pre-existing trends in vital signs (see table below) can be a red flag. The Paediatric sepsis pathway features of severe illness refer to the CEWT scores for the system examined e.g. the respiratory rate or heart rate; NOT the overall CEWT score which can be misleading.
Vital sign features of severe illness include:
- altered mental state
- severe tachypnoea, increased work of breathing, grunt, weak cry or apnoea
- marked and persistent tachycardia (including high normal in the absence of drivers i.e. fever, pain)
- hypotension
- poor skin perfusion
- indicators of moderate to severe dehydration
It is important to pay attention to concerns expressed by the caregiver, particularly changes in usual behaviour of the child.
Normal range for vital signs by age based on Childhood Early Warning Tool (CEWT)|
< 1 year old |
100-159
|
<75
|
21-45
|
1-4 year old |
90-139
|
<80
|
16-35
|
5-11 year old |
80-129
|
<85
|
16-30
|
12-17 year old |
60-119
|
<90
|
16-25
|
Laboratory sign features of severe illness include:
- lactate > 2 concerning, > 4
- glucose < 3 (note can be high with stress)
- low platelets
- elevated Creatinine
- elevated INR
- elevated bilirubin or ALT
Septic Shock
Septic shock is the progression of sepsis and can vary in presentation, oscillating from a child who is vasodilated with bounding pulses to a child who is cold and mottled 16 (see table below). Children with septic shock may have normal blood pressure. The way in which the child presents does not change management nor determine type of inotropic support.
Alert
Hypotension is a late, and often terminal, sign in paediatric septic shock.
Initiate treatment via the Queensland Paediatric Sepsis Pathway and immediately contact paediatric critical care (onsite or via RSQ) for child in septic shock.
Paediatric septic shock presentations Shock with vasodilation |
---|
- Distributive shock with capillary leak, vasoconstriction and relative myocardial depression
- common in infants and young children
- Constricted peripheral systemic vasculature: cold peripheries and prolonged capillary refill time
- Tachycardia is usually present; relative bradycardia is a pre-terminal sign
- Blood pressure can be maintained until late
| - Distributive shock with vasoplegia, capillary leak and often, preservation of cardiac function.
- More common in older children (and adults)
- Characterised by vasoplegia, in which the systemic vascular resistance is low with low diastolic blood pressure: brisk capillary refill time (‘flash’ capillary refill) and pulses are usually felt to be full or bounding
- Tachycardia is usually present: relative bradycardia is a pre-terminal sign
- Pulse pressure is high, often due to a low diastolic blood pressure
- Progression to low cardiac output can occur anytime
|
Clinical findings consistent with insufficient end-organ perfusion:
- Mental status: progressive lethargy, drowsiness or obtundation. Alternatively, restlessness and/or agitation are often seen and can be mistaken for “a vigorous child” but reflects compromised cerebral perfusion due to shock. Infants tend to have irritability and/or apnoeas. Parental concern for a change in behaviour can be an early warning sign.
- Skin: temperature gradient from core to extremities (note that either hyperthermia or hypothermia can be present), mottled colour, prolonged capillary refill time (more than 2 seconds but note that brisk capillary refill time can be seen), petechial or purpuric rash. Purpura fulminans is a widespread non-blanching purpuric rash classically seen in meningococcaemia but may also be associated with severe sepsis from Pneumococcus. A generalised erythematous rash is seen in toxic shock.
- Cardiovascular: tachycardia is usually one of the earliest signs. Mean arterial pressure (MAP) can be maintained and the pulse pressure typically is narrow (vasoconstriction to maintain MAP) but may be high (vasodilation). There may be evidence of cardiac failure (hepatomegaly, gallop rhythm and jugular venous distension) with myocardial depression. A classic pitfall in the recognition of shock is attributing difficulty in obtaining peripheral oxygen saturations and non-invasive blood pressure due to technical issues rather than recognising the presence of hypotension/hypoperfusion. Point of care testing of lactate and monitoring the trends in response to therapy (if abnormal) is also an important measure.
- Respiratory: rate is increased to compensate for metabolic acidosis including lactic acidosis (Kussmaul breathing) or if the respiratory system maybe the primary source of infection. Acute respiratory distress syndrome (ARDS) may develop with progressive worsening of respiratory distress (tachypnoea, increased work of breathing), hypoxia and focal chest signs (reduced breath sounds, inspiratory crepitations).
- Renal: reduced urine output.
Toxic Shock Syndrome
Toxic shock syndrome is a potentially life-threatening subset of paediatric sepsis, caused by superantigens from toxin-producing strains of Staphylococcus aureus or Streptococcal pyogenes.17 Symptoms may include high fever, vomiting, diarrhoea, myalgia, confusion, collapse and usually a widespread erythematous rash. It can occur in any patient. It is important to distinguish this entity as treatment requires the addition of further antibiotics (see AMS) and possibly IV immunoglobulin for their antitoxin properties.