These children are usually toddlers who have drunk the green liquid form of methadone.
Reassess ABC
• The sedative effect of the drug may reduce the conscious level sufficiently to put the airway at risk.
• These patients will usually hypoventilate.
• Support ventilation with bag-valve-mask before giving naloxone (see Chapter 5).
Opiate poisoning emergency treatment
Following stabilisation of airway, breathing and circulation, the specific antidote is naloxone. An initial bolus dose of 10 micrograms/kg is used but some children need doses as high as 100 micrograms/kg up to a maximum of 2 mg. Naloxone has a short half-life, relapse ofter occurring after 20 minutes. Further boluses, or an infusion of 10–20 micrograms/kg/min may be required.
It is important to normalise CO2before the naloxone is given as adverse events such as ventricular arrhythmias, acute pulmonary oedema, asystole or seizures may otherwise occur. This is because the opioid system and adrenergic system are interrelated. Opioid antagonists and hypercapnia stimulate sympathetic nervous system activity. Therefore if ventilation is not provided to normalise carbon dioxide prior to naloxone administration, the sudden rise in epinephrine (adrenaline) concentration can cause arrhythmias.
Transfer
After the child has been stabilised and conditions such as hypoglcaemia, meningitis and opiate poisoning treated as indicated some children will remain a puzzle.
These children and those in whom there is any suggestion of lateralisation or intra-cranial bleeding should have an urgent CT scan: get senior advice
Children who remain very ill and those in whom the cause of coma is as yet unidentified will require referral to a paediatric neurologist and may need transfer to a paediatric intensive care unit.
Patients may need paralysis, intubation, and ventilation for safe transfer (see Chapter 25). In such patients neurological assessment cannot be continued, and there should therefore be clear documentation of neurological signs before paralysis is commenced.
Raised intracranial pressure
The initial priority in the management of the unconscious child is the maintenance of adequate respiration, circulation, and metabolic homoeostasis. Once this has been done, the possibility of raised intracranial pressure should be considered.
In very young children, before the cranial sutures are closed, considerable intracranial volume expansion may occur if the process is slow. However, if the process is rapid and in children with a fixed volume cranium, increase in volume due to brain swelling, haematoma, or cerebral spinal fluid (CSF) blockage will cause raised intracranial pressure (ICP). Initially cerebrospinal fluid and venous blood within the cranium decrease in volume. Soon, this compensating mechanism fails and as the intracranial
THE CHILD WITH A DECREASED CONSCIOUS LEVEL
pressure continues to rise the cerebral perfusion pressure (CPP) falls and arterial blood flow is reduced.
CPP:MAP – ICP
where MAP is mean arterial pressure. Reduced CPP reduces cerebral blood flow (CBF). Normal CBF is over 50 ml/l00 g brain tissue/min. If the CBF falls below 20 ml/l00 g brain tissue/min, the brain suffers ischaemia.
Increasing intracranial pressure will push brain tissue against more rigid intracranial structures. Two clinical syndromes are recognisable by the site of localised brain compression.
Central syndrome
The whole brain is pressed down towards the foramen magnum and the cerebellar tonsils herniate through it (“coning”). Neck stiffness may be noted. A slow pulse, raised blood pressure, and irregular respiration leading to apnoea are seen terminally.
Uncal syndrome
The intracranial volume increase is mainly in the supratentorial part of the intracranial space. The uncus, which is part of the hippocampal gyrus, is forced through the tentorial opening and compressed against the fixed free edge of the tentorium. If the pressure is unilateral (for example, from a subdural or extradural haematoma), this
THE CHILD WITH A DECREASED CONSCIOUS LEVEL
Assess and stabilise ABC
URGENT Intubation and
ventilation
Establish IV access
Glucose stick test
Rapid assessment of conscious level
Identification and immediate treatment
of the treatable CONSIDER
Intubation and ventilation
Reassess Raised ICP
management Give dextrose 10%
5 ml/kg
Commence diagnostic workup Inform specialist teams
DEFINITIVE CARE
Insecure airway Inadequate
breathing
Unresponsive
Alert or responds to voice or pain
Signs of raised ICP
< 3 mmol/l
Give high-flow O2
Figure 12.1. Algorithm for the initial management of coma
APLS-136.QXD 8/2/01 3:28 PM Page 136
leads to third nerve compression and an ipsilateral dilated pupil. Next, an external oculomotor palsy appears, so the eye cannot move laterally. Hemiplegia may then develop on either or both sides of the body, depending on the progression of the herniation.
THE CHILD WITH A DECREASED CONSCIOUS LEVEL
Figure 12.2. Herniations of the brain
CHAP TITLE
BMJ Paediatrics 9/11/0 10:05 pm Page 138
CHAPTER
I 13 I
The convulsing child
INTRODUCTION
Generalised convulsive (tonic-clonic) status epilepticus (CSE) is currently defined as a generalised convulsion lasting 30 minutes or longer or when successive convulsions occur so frequently that the patient does not recover consciousness between them.
Although the outcome of CSE is mainly determined by its cause, the duration of the convulsion is also relevant. In addition, the longer the duration of the episode, the more difficult it is to terminate it. In general, convulsions that persist beyond five minutes may not stop spontaneously so it is usual practice to institute treatment when the episode has lasted between five and ten minutes.
Tonic-clonic status occurs in approximately 1–5% of patients with epilepsy. Up to 5%
of children with febrile seizures will present in status epilepticus.
Status epilepticus can be fatal, but mortality is lower in children than in adults at about 4%. Death may be due to complications of the convulsion, such as obstruction of the airway or aspiration of vomit, to overmedication, or to the underlying disease process.
Neurological sequelae (persistent epilepsy, motor deficits, learning and behavioural difficulties) are age dependent, occurring in 6% of those over three years but 29% of those under one year.
A generalised convulsion increases the cerebral metabolic rate at least threefold. Initially, there is an increased sympathetic activity with release of catecholamines which lead to peripheral vasoconstriction and increased systemic blood pressure. There is also loss of cerebral arterial regulation and, following the increase in systemic blood pressure, there is a resulting increase in cerebral blood flow to provide the necessary oxygen and energy. If convulsions continue, the systemic blood pressure falls and this is followed by a fall in cerebral blood flow. Lactic acid accumulates and there is subsequently cell death, oedema, and raised intracerebral pressure resulting in further worsening of cerebral perfusion.
Cellular metabolism of calcium and sodium is also impaired, with further cell death.
PRIMARY ASSESSMENT
The first steps in the management of the patient who is convulsing are to assess and
CHAP TITLE
if necessary support airway, breathing and circulation. This will ensure that the convulsion is not secondary to hypoxia and/or ischaemia and that whatever the cerebral pathology it will not be worsened by lack of oxygenated blood supply to the brain.
Airway
Assess airway patency by the “look, listen, and feel” method.
If there is no evidence of air movement then chin lift or jaw thrust manoeuvres should be carried out and the airway reassessed. If there continues to be no evidence of air movement then airway patency can be assessed by performing an opening manoeuvre and giving rescue breaths (see Basic Life Support, Chapter 4).
Breathing
Assess the adequacy of breathing
Effort of breathing Recession Respiratory rate
Grunting. This may be caused by the convulsion and not be a sign of respiratory distress in this instance
Efficacy of breathing Breath sounds
Chest expansion/abdominal excursion
Effects of breathing Heart rate
Skin colour
Monitor oxygen saturation with a pulse oximeter.
Circulation
Assess the adequacy of circulation Cardiovascular status
Heart rate. The presence of an inappropriate bradycardia will suggest raised intracranial pressure
Pulse volume Capillary refill
Blood pressure. Significant (997th percentile for age) hypertension indicates a possible aetiology for the convulsion
Effects of circulatory inadequacy on other organs Pale, cyanosed or cold skin
Monitor heart rate/rhythm, blood pressure and core/toe temperature difference.
If heart rate is above 200 in an infant or above 150 in a child or if the rhythm is abnormal perform a standard ECG.
THE CONVULSING CHILD APLS-140.QXD 8/2/01 3:34 PM Page 140
Disability
Assess neurological function.
• The AVPU score cannot be measured meaningfully as the convulsing patient has an abnormal conscious level by virtue of the convulsion.
• Pupillary size and reaction should be noted. Very small pupils suggest opiate poisoning, large pupils amphetamines, atropine, tricyclic antidepressants and others (see page 156).
Note the child’s posture. Decorticate or decerebrate posturing in a previously normal child should suggest raised intracranial pressure. These postures can sometimes be mistaken for the tonic phase of a convulsion. Consider also the possibility of a drug-induced dystonic reaction or a psychogenic, pseudo-epileptic attack. All these movement disorders are distinguishable from tonic-clonic status epilepticus as long as they are considered.
Look for neck stiffness in a child and a full fontanelle in an infant which suggest meningitis.
Exposure
• Take the child’s core and toe temperatures. A fever is suggestive evidence of an infectious cause ( but its absence does not the suggest the opposite) or poisoning with ecstasy, cocaine or salicylates. Hypothermia suggests poisoning with barbiturates or ethanol.
• Look for a rash. If one is present, ascertain if it is purpuric as an indicator of meningococcal disease or non-accidental injury.
• Look for evidence of poisoning.
RESUSCITATION
Airway
• A patent airway is the first requisite. If the airway is not patent it should be opened and maintained with an airway manoeuvre and the child ventilated by bag-valve-mask oxygenation. An airway adjunct can be used. The airway should later be secured by intubation by experienced senior help.
• Even if the airway is open the oropharynx may need secretion clearance by gentle suction.
Breathing
• All convulsing children should receive high flow oxygen through a face mask with a reservoir as soon as the airway has been demonstrated to be adequate.
• If the child is hypoventilating, respiration should be supported with oxygen via a bag-valve-mask device and experienced senior help summoned.
Circulation
Gain intravenous or intraosseous access.
• Take blood for glucose stick test and laboratory test. Give 5 ml/kg of 10% dextrose to any hypoglycaemic patient. If possible, take 10 mls of clotted blood before giving the dextrose for later investigation of the hypoglycaemic state.
THE CONVULSING CHILD
• Give 20 ml/kg rapid bolus of crystalloid to any patient with signs of shock. Colloid and an antibiotic such as cefotaxime should be used for those in whom a diagnosis of septicaemia is made obvious by the presence of a purpuric rash after blood has been taken for culture.
• Give an antibiotic such as cefotaxime to any child in whom a diagnosis of meningitis is made obvious by a stiff neck or bulging fontanelle after blood has been taken for culture.
Key features
While the primary assessment and resuscitation are being carried out a focused history of the child’s health and activity over the previous 24 hours and any significant previous illness should be gained.
Specific points for history taking include:
• Current febrile illness
• Recent trauma
• History of epilepsy
• Poison ingestion
• Last meal
The immediate emergency treatment requirement, after ABC stabilisation and exclusion or treatment of hypoglycaemia is to stop the convulsion.
Reassess ABC