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Keywords:

  • cardiac;
  • neonate;
  • non-accidental injury;
  • sepsis;
  • shock

Abstract

  1. Top of page
  2. Abstract
  3. Assessment
  4. Airway and breathing
  5. Circulation
  6. Correction of hypoglycaemia, anaemia and coagulopathy
  7. Treatment of possible causes
  8. Summary
  9. References

The shocked neonate often causes anxiety in the ED. This article aims to provide a systematic, practical approach to recognition and initial management of these patients. Their resuscitation should follow a pattern of provision of oxygen, fluid resuscitation, blood glucose correction, inotropic support and ventilation. Practical tips for intravenous access and the rationale behind choice of inotrope and anaesthetic induction agent are discussed. The major underlying causes – sepsis, cardiac disease, metabolic disease and non-accidental injury – along with their investigation and management are considered.

As maternity units discharge mothers and babies earlier unwell neonates are increasingly likely to present to the ED. The shocked neonate often causes anxiety. Most staff are well drilled in management of cardiorespiratory arrest; it is the peri-arrest situation that causes confusion. Early recognition and aggressive resuscitation is known to improve outcome; every hour shock persists increases the odds of mortality greater than twofold.[1] This article aims to provide a systematic, practical approach to initial management of these patients from resuscitation to treatment of the four major pathologies.

Assessment

  1. Top of page
  2. Abstract
  3. Assessment
  4. Airway and breathing
  5. Circulation
  6. Correction of hypoglycaemia, anaemia and coagulopathy
  7. Treatment of possible causes
  8. Summary
  9. References

Assessment should follow a standard ‘Airway, Breathing, Circulation’ approach. Paediatric advanced life support should be commenced in respiratory or cardiac arrest. Table 1 shows signs indicating neonatal shock, not all need to be present, in particular hypotension is a worrying and late sign in neonates.

Table 1. Signs suggestive of neonatal shock, modified from[2] and normal values
Heart rate>180 or <100/min
Respiratory rate>60 breaths/min
Systolic blood pressure<65 mmHg under 1 week
<75 mmHg 1 week to 1 month
Capillary refill time>3 s
Lethargy or GCS<12/15

Airway and breathing

  1. Top of page
  2. Abstract
  3. Assessment
  4. Airway and breathing
  5. Circulation
  6. Correction of hypoglycaemia, anaemia and coagulopathy
  7. Treatment of possible causes
  8. Summary
  9. References

Oxygenation

Any shocked patient should receive 100% oxygen. Neonates benefit from the application of positive end expiratory pressure (PEEP) via T-piece resuscitator or anaesthetic circuit especially if they are ‘grunting’. In grunting the neonate expires against a closed glottis to produce PEEP in the lower airways. This improves oxygenation and augments cardiac output by reducing afterload in a failing heart. Taking over provision of PEEP reduces neonatal work of breathing.

Ventilation

Ventilation is required if 60 mL/kg fluid resuscitation and inotropes do not rapidly improve signs of shock, in impaired mental status, respiratory failure (i.e. hypoxia and/or hypercarbia) or hypoventilation. Ventilation serves many purposes. Up to 40% of neonatal cardiac output is expended on work of breathing. Sedation reduces oxygen consumption and allows safe establishment of central and invasive haemodynamic monitoring. Controlling oxygenation and carbon dioxide by ventilation reduces pulmonary vascular resistance avoiding a persistent fetal circulation.

Cardiovascularly stable anaesthetic induction agents should be used. Ketamine with atropine premedication and a short acting muscle relaxant is the recommended combination in the American College of Critical Care Medicine Guidelines for paediatric and neonatal septic shock.[3] The disadvantage to ketamine is the transient rise in pulmonary vascular resistance it produces. Many neonatal units use fentanyl or morphine rather than ketamine. Propofol and thiopentone vasodilate and moderately drop cardiac output and so are avoided. It is useful to prepare a fluid bolus and a resuscitation dose of adrenaline before intubation.

Circulation

  1. Top of page
  2. Abstract
  3. Assessment
  4. Airway and breathing
  5. Circulation
  6. Correction of hypoglycaemia, anaemia and coagulopathy
  7. Treatment of possible causes
  8. Summary
  9. References

Intravenous access

Peripheral intravenous access can be challenging in neonates with decreased peripheral perfusion. Options for intravenous access include the femoral vein. This can be accessed with a 22 Gauge cannula just medial to the femoral arterial pulsation. A small nappy positioned under the hips brings the vein superficially. The external jugular vein is useful and can be made more prominent by placing a nappy under the baby's shoulders, turning the head and placing a finger above the clavicle to obstruct venous return. Often one external jugular vein is much larger than the other. Ensure blood can be aspirated easily before use as a small-volume fluid extravasation in the neck area can cause airway compromise. Clinical series and case reports suggest the intraosseous route is useful in neonates; access can be challenging because of the fragility of small bones and small intraosseous space. An umbilical venous catheter or, if unavailable, a 5 French feeding tube passed into the umbilical vein is an option in the first few days of life. The umbilical vein can rarely be accessed after day 4.

Blood tests

Blood tests are taken when intravenous access is established. Often a practical decision has to be taken when insufficient blood is obtained. Blood cultures and blood sugar are the important tests at this stage. If possible, also collect a group and hold, full blood count, clotting, renal and liver profile and a blood gas.

Fluid resuscitation

Aggressive fluid resuscitation in 20 mL/kg aliquots is first-line treatment. Stop fluid boluses if shock resolves. Begin preparing inotropes and if necessary calling for skilled airway assistance after 40 mL/kg. Ongoing signs of shock after three boluses (60 mL/kg) or development of hepatomegaly requires inotropes and ventilation. Continuing fluid resuscitation might be necessary. Evidence for rapid fluid resuscitation within the first hour of presentation is extrapolated from studies of neonatal and paediatric septic shock.[1] The optimal resuscitation fluid remains controversial, some studies favour colloid, whereas others find no difference between colloid and crystalloid.

Inotropes

If shock is unresolved after 60 mL/kg fluid resuscitation, commence drugs to increase cardiac contractility quickly. To prevent delay the most recent guidance from the American College of Critical Care Medicine for paediatric and neonatal septic shock[3] advises the use of peripheral inotropes if central access has not been obtained. The peripheral access site should be monitored for vascular injury and central access established as soon as feasible. Neonates die from a reduced cardiac output with normal or increased systemic vascular resistance. This differs from septic adults who die from refractory vasoplegia. Neonates are unique in that acidosis and hypoxia can cause failure of the usual drop in pulmonary vascular resistance after birth leading to a persistent fetal circulation and right heart failure. These differences mean the most appropriate initial inotrope for children is dopamine or adrenaline.

Correction of hypoglycaemia, anaemia and coagulopathy

  1. Top of page
  2. Abstract
  3. Assessment
  4. Airway and breathing
  5. Circulation
  6. Correction of hypoglycaemia, anaemia and coagulopathy
  7. Treatment of possible causes
  8. Summary
  9. References

Because of reduced glycogen stores and muscle mass for gluconeogenesis, neonates are likely to become hypoglycaemic when critically ill. Although there is no specific plasma concentration or duration of hypoglycaemia associated with neurological injury,[4] it is pragmatic to keep blood glucose greater than 3 mmol/L. Hypoglycaemia should be treated with an initial bolus dose of 2–3 mL/kg 10% dextrose, repeated if necessary, followed by an infusion containing dextrose. Failure of blood glucose to correct after 10 mL/kg of 10% dextrose might suggest liver failure or a metabolic disorder. Maintaining a haemoglobin level above 100 mg/dL enhances oxygen delivery and as part of a goal-directed therapy approach has been shown to reduce mortality.[5] Bleeding from puncture sites or mucous membranes is treated with 10 mL/kg fresh frozen plasma.

Treatment of possible causes

  1. Top of page
  2. Abstract
  3. Assessment
  4. Airway and breathing
  5. Circulation
  6. Correction of hypoglycaemia, anaemia and coagulopathy
  7. Treatment of possible causes
  8. Summary
  9. References

There are four major causes of neonatal shock. Awareness of the possibilities allows the clinician to look for the signs of each, but the important message is to suspect and treat all four until definitive investigation.

Sepsis

The commonest cause of neonatal shock is sepsis; antibiotics should be started in all. Microorganisms found in neonates in the first weeks of life are usually acquired from the maternal genital tract during birth. Group B streptococcal infection remains the leading cause of neonatal sepsis followed by Escherichia coli. As time from birth increases, the chance of more diverse organisms increases.[6] Most hospitals recommend a penicillin and gentamicin as first-line treatment. Neonatal herpes infection is less common but can cause a rapid deterioration. A severe coagulopathy manifest by bleeding from puncture sites and mucous membranes or a disturbance in liver function tests makes herpes more likely. Intravenous acyclovir should be commenced on suspicion.

Cardiac disease

The incidence of severe cardiac disease is three per 1000 live births;[7] however, the incidence of neonatal shock as first presentation is considerably lower than this. Most lesions are either detected by antenatal ultrasound or are not dependent on ductal flow. Congenital malformations can occur on the right or left side of the heart. While the ductus arteriosus is open, some blood might divert past the site of the lesion. In the first hours and days of life, the ductus will begin to close although it can remain patent for the first few weeks. Those babies reliant on this ‘bypass’ connection will become unwell. If the lesion is on the right side, there will be reduced flow to the lungs and the neonate will be cyanosed. If the lesion is on the left, systemic perfusion is reduced, with poor pulses, poor capillary refill and possibly hypotension, whereas cyanosis might be absent if pulmonary blood flow is normal. Therefore, lack of cyanosis does not rule out cardiac disease. Shock can be reversed with an infusion of prostaglandin E1 or 2 (prostin) to reopen the ductus arteriosus. It is difficult to differentiate a critically obstructed circulation from sepsis,[8] so infuse prostin until an echocardiogram rules out cardiac disease. Expert advice from a paediatric cardiologist should be sought as soon as possible. Prostin might cause hypotension and central apnoea.

Tachy or bradyarrhythmias can precipitate neonatal collapse. The commonest cause of bradycardia is hypoxia; this should be excluded and an ECG performed to confirm dissociation of P wave and QRS complexes before congenital heart block is diagnosed. A constant heart rate of around 220/min unaffected by fluid boluses is a clue to neonatal supraventricular tachycardia. An ECG should be faxed urgently to a paediatric cardiologist for advice. Treatment includes adenosine, amiodarone and applying a cloth soaked in ice-cold water to the face.

Metabolic disease

Unexplained neonatal collapse raises the possibility of an inborn error of metabolism. Clues are hypoglycaemia, recurrent vomiting, congestive cardiac failure, jaundice or hepatosplenomegaly and seizures. Management includes prevention of catabolism with intravenous glucose (dextrose concentrations above 12.5% should be infused via a central line), correction of acidosis and removal of toxic metabolites. Initial investigations listed in Box 1 should be sent and the child discussed urgently with a metabolic specialist, as they might need transfer to a centre providing haemodialysis.

Box 1. Initial investigations for inborn errors of metabolism

  • Arterial blood gas
  • Blood glucose
  • Plasma ammonia
  • Plasma lactate
  • Plasma acylcarnitine
  • Plasma and urine amino acids
  • Urine organic acids
  • Urine ketones
  • Urine reducing substances

Non-accidental injury

Children less than 1 year make up the highest proportion of child protection substantiations in Australia.[9] Neonates can lose a large proportion of their blood volume into their abdomen or cranial vault causing hypovolaemic shock. Neurological signs might be absent; an open fontanelle allows significant bleeding before intracranial pressure rises. An index of suspicion plus a thorough examination for other signs of abuse is required. Head and abdominal CT, when haemodynamically stable, confirm the diagnosis.

Summary

  1. Top of page
  2. Abstract
  3. Assessment
  4. Airway and breathing
  5. Circulation
  6. Correction of hypoglycaemia, anaemia and coagulopathy
  7. Treatment of possible causes
  8. Summary
  9. References

A systematic approach to neonatal shock, summarised in Box 2, that includes aggressive fluid resuscitation, early inotropic support and ventilation followed by consideration and treatment of the four major causes of shock in this age group will reduce uncertainty surrounding management of these difficult patients.

Box 2. Steps in the practical management of neonatal shock

  • 100% oxygen, provide positive end expiratory pressure
  • Intravenous access and bloods
  • 20 mL/kg fluid bolus
  • Antibiotics, correct hypoglycaemia
  •       [DOWNWARDS ARROW]
  • Reassess – still shocked?
  • Up to 2 more fluid boluses 20 mL/kg
  •       [DOWNWARDS ARROW]
  • Reassess – still shocked?
  •       [DOWNWARDS ARROW]
  • Dopamine 10 mcg/kg/min or adrenaline 0.3 mcg/kg/min
  • Intubate and ventilate
  • Start prostin 10 ng/kg/min
  • Continue fluid resuscitation

Competing interests

None declared.

References

  1. Top of page
  2. Abstract
  3. Assessment
  4. Airway and breathing
  5. Circulation
  6. Correction of hypoglycaemia, anaemia and coagulopathy
  7. Treatment of possible causes
  8. Summary
  9. References
  • 1
    Han YY, Carcillo JA, Dragotta MA et al. Early reversal of pediatric-neonatal septic shock by community physicians is associated with improved outcome. Pediatrics 2003; 112: 793799.
  • 2
    Goldstein B, Giroir B, Randolph A et al. International Pediatric Sepsis Consensus Conference: definitions for sepsis and organ dysfunction in pediatrics. Pediatr. Crit. Care Med. 2005; 6: 28.
  • 3
    Briely J, Carcillo JA, Choong K et al. Clinical practice parameters for hemodynamic support of pediatric and neonatal septic shock: 2007 update from the American College of Critical Care Medicine. Crit. Care Med. 2009; 37: 666688.
  • 4
    Committee on Fetus and Newborn, Adamkin DH. Postnatal glucose homeostasis in late-preterm and term infants. Pediatrics 2011; 127: 575579.
  • 5
    de Oliveira CF, de Oliveira DS, Gottschald AF et al. ACCM/PALS haemodynamic support guidelines for paediatric septic shock: an outcomes comparison with and without monitoring central venous oxygen saturation. Intensive Care Med. 2008; 34: 10651075.
  • 6
    Schuchat A, Zywicki SS, Dinsmorr MJ et al. Risk factors and opportunities for prevention of early-onset neonatal sepsis: a multicentre case-control study. Pediatrics 2000; 105: 2126.
  • 7
    Hoffman JIE, Kaplan S. The incidence of congenital heart disease. J. Am. Coll. Cardiol. 2002; 39: 18901900.
  • 8
    Pickert CB, Moss MM, Fiser DH. Differentiation of systemic infection and congenital obstructive left heart disease in the very young infant. Pediatr. Emerg. Care 1998; 14: 263267.
  • 9
    Australian Institute of Heath and Welfare. Child Protection Australia 2010–2011. Child Welfare Series no. 53. Cat no. CWS 41. Canberra: AIHW, 2012.