In June 2023, we commenced a project to review and update the Maternity and Neonatal eHandbook guidelines with a view to completion in 2024. Please be aware that pending this review, some of the current guidelines may be out of date. In the meantime, we recommend that you also refer to more contemporaneous evidence.
Shock is a complex syndrome of circulatory dysfunction associated with reduced oxygen and nutrient delivery to peripheral systems and ultimately to central organs.
The aetiology of shock is multifactorial and the syndrome is frequently complicated by secondary involvement of many organ systems.
Systemic inflammatory response syndrome
The major secondary complication of severe shock, virtually universal in fatal shock, is a syndrome characterised as systemic inflammatory response syndrome (SIRS).
Key features of SIRS
The key features of SIRS are:
- circulatory failure
- endothelial dysfunction
- organ failure
- coagulation disturbances.
These secondary phenomena are responsible for much of the mortality and morbidity and early recognition and aggressive management are essentials of successful management.
Aetiology of neonatal shock
Antepartum or intrapartum, respiratory failure, impaired oxygen transport due to severe anaemia or haemoglobinopathy
Tension pneumothorax, excessive ventilator pressures, cardiac tamponade
Vasodilators, opiates, sedatives, maternal anti-hypertensives
Third space losses
|Antepartum or intrapartum,|
Impaired oxygen transport due to severe anaemia or haemoglobinopathy
Obstruction of venous return
Excessive ventilator pressures
|Obstructive lesions||Aortic stenosis|
Hypoplastic left heart
Likely clinical contexts
Clinical context of neonatal shock includes:
- feto-maternal haemorrhage
- vasa praevia
- cord accidents
- acute bleeding
- perinatal asphyxia
- ELBW infant
- severe sepsis
- metabolic diseases
- high fluid losses
- assisted ventilation (iatrogenic problems).
Clinical features of shock
Clinical features of neonatal shock include:
- peripheral vasoconstriction
- tachycardia (sometimes only bradycardia in ELBW)
- tachypnoea and/or apnoea
- metabolic acidosis
- CNS disturbance (lethargy, irritability)
- gastrointestinal disturbance
It is difficult to state meaningfully what a satisfactory blood pressure is in the context of the seriously ill infant for whom this is relevant in treatment. Issues to note include the following:
- 'Normal' values may not necessarily be helpful in defining a level of blood pressure below which the infant is compromised.
- Careful clinical judgement is important, beware blaming equipment as 'faulty' when baby is actually shocked.
- The levels below are based on the best available evidence but are probably higher than the level at which the infant is compromised.
- It is important to avoid over treatment and the lower end of these ranges should be used to guide treatment decisions.
The basic goal should be:
- Infant with good clinical perfusion and pulses. Beware that perfusion may appear normal when infants suffer from peripheral vasodilatation, especially in septic shock.
- Normal neurological behaviour
- Urine output of >0.5 mL/kg/hr
- No metabolic acidosis or lactate accumulation.
'Normal' ranges of neonatal blood pressure
See blood pressure.
Management of shock
Issues to note:
- Prevention, early diagnosis and aggressive management are the cornerstones of care.
- Once the secondary complications of shock (SIRS) are established it is very difficult to reverse.
- The key goal is the establishment of adequate tissue perfusion and oxygenation.
- Early consultation with PIPER is important once shock is diagnosed.
Key steps to manage shock
1. Establish airway, breathing and circulation
- Sick, clinically shocked neonates should be intubated and ventilated before they meet conventional ventilation criteria if this can be achieved safely (consider experience of operator).
- Intubation may precipitate decompensation in the critically ill infant.
- Perform intubation once circulation stabilised, especially if using induction agents.
- If using vasodilating agents (such as opiates), volume load first.
2. Stop any bleeding.
3. Monitor oxygen saturations.
4. Administer oxygen as required.
5. Establish reliable intravenous access.
Options for intravenous access include:
- peripheral IV - do not waste time on peripheral IV if insertion difficult
- umbilical venous catheter
- (5Fg for preterm, 5 - 8Fg for term or 5 8Fg sterile feeding tube)
6. Consider and treat causes (including iatrogenic problems).
Screening and treatment may include:
- screen for sepsis
- cover with broad spectrum antibiotics:
|Early onset (< 48 hrs)||Penicillin 60 mg/kg IV 12-hrly
Gentamicin 5 mg/kg stat, subsequent dosing according to weight and renal function
|Late onset (> 48 hrs) level 3-5 or has been home||Flucloxacillin 50 mg/kg/6-8 hrly
Gentamicin 5 mg/kg, subsequent dosing according to weight and renal function
|Late onset (> 48 hrs) level 6||Vancomycin 15-20 mg/kg
Gentamicin 5 mg/kg, subsequent dosing according to weight and renal function
- consider herpes and need for acyclovir
- consider use of immunoglobulin (Intragam) in established sepsis
- pericardial tamponade
- occult bleeding.
7. Ensure adequate volume replacement.
- Administer 10-20 mL/kg N saline over 10 minutes.
- Repeat according to response.
- If clinical evidence of major blood or fluid loss, use appropriate higher volumes.
- Severe sepsis may require 40-60 mL/kg to establish adequate blood volume.
There is no evidence that colloid has any advantage over saline in initial resuscitation.
8. Use blood early if there is blood loss.
- Initially packed cells
- Urgently cross matched if available in time
- O negative uncross-matched blood
- Once initially stabilised consider need for other blood products
- Fresh frozen plasma
- These should be given on the basis of active bleeding or significant abnormality on investigation.
9. Consider treatment of acidosis.
- Primary goal is establishment of stable circulation, perfusion and ventilation.
- Once these are addressed and CO2 is normal, if significant metabolic acidosis is present (base deficit ≥ 10mEq/L) half-correction of acidosis using sodium bicarbonate (dose (m mol) = BE/2 X wt/4) can be given.
10-20 microgram/kg/min +/- Dopamine 2 microgram/kg/min (for Dopaminergic renal effect)
Raises cardiac output
Raises BP more
Choice conditioned by physiology and immediate goals of treatment.
Discuss use with PIPER consultant on 1300 137 650.
11. If response is poor
Take the following action if response to treatment is poor:
- check diagnosis
- transilluminate chest
- establish that ventilation and airway remain intact
- consider adequacy of volume replacement.
Consider adrenaline infusion:
- 0.05-1.0 microgram/kg/min
Consider use of steroids:
- especially in ELBW infants
- dose: Hydrocortisone 3 mg/kg 6-hourly
Noradrenaline should only be used in an ICU setting.
- A poor response to inotrope therapy can be due to an acquired catecholamine resistance. This is most commonly a problem in overwhelming sepsis or in the chronically hypoxically stressed or failing myocardium.
- Dopamine and dobutamine will not work well in this situation.
- Early use of adrenaline is advisable and urgent discussion with PIPER on 1300 137 650 should occur.
Management of secondary complications
Management of respiratory complications includes the following:
- Early stabilisation of airway breathing and circulation has been dealt with above. See resuscitation.
- Ongoing ventilation problems are commonly a feature of the sicker infant.
- Pulmonary oedema, hyaline membrane disease, acute respiratory distress syndrome (ARDS) and pneumonia may all be associated and need to be considered and treated in their own right.
- The combination of poor myocardial and circulatory performance with endothelial dysfunction commonly complicates respiratory management.
- End pressures used in ventilation should probably be higher because of this (6-8 cm) and careful attention needs to be paid to circulation.
- The early ventilator stabilisation of a critically ill patient may be associated with some understandable over-aggression, with the attendant risk of complications.
- It is important to reassess treatment quickly once stable to ensure that treatment is adequate but not excessive.
- Excessive low carbon dioxide levels are to be avoided because of concerns about CNS injury (especially in conjunction with sepsis).
- Ventilator stabilisation should be undertaken on the advice of the PIPER consultant.
- These guidelines are given as a starting point.
- See blood gas interpretation.
|Base deficit||> -8|
Management of renal complications includes the following:
- Renal impairment is a significant component of most shock syndromes in the neonate.
- Oliguria is the rule and may be associated with acute tubular necrosis or acute cortical necrosis.
- Complications include hyperkalaemia and fluid overload.
- The ELBW infant with renal impairment is particularly prone to hyperkalaemia, which may cause cardiac death.
- The hyperkalaemia may be the presenting feature of the renal impairment and may commence in the first two to three days of life.
- High-risk infants should have potassium levels
- If urine output is below 0.5 mL/kg/hr manage by:
- volume loading 10 mL/kg
- frusemide 2 mg/kg
- low-dose dopamine at 2-5 microgram/kg/min.
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First published: August 2013
Review by: August 2016