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Severe brain injuries in children

Abstract

Injury is the leading cause of death or permanent disability in children up to 19 years of age and is one of the primary reasons for hospital treatment. Blunt injuries due to traffic accidents or falls and especially blunt head injuries are the most frequent child injuries.

Appropriate care and correct treatment of the injured child require multidisciplinary teamwork (medical emergency team, surgeons, radiologists, paediatric intensive care physicians and other specialists).

Key words: child, injury, treatment, intensive therapy

Introduction

In Europe, injuries and poisonings are the leading cause of death in children between 1 and 14 years of age. However, fatal injuries are only the tip of the iceberg. For every injury that results in the death of a child, between 160–200 children are hospitalized and 2,000 are examined by emergency service providers. Between the years 2007 and 2011, injuries were the cause of death in children between 1 and 3 years old in 30% of cases in Slovenia. In the age group from 15 to 19 years, injuries were the cause of death in as many as 70% of the cases. (1, 2)

Children typically suffer blunt injuries (80%), most frequently blunt head injuries. Falls and traffic accidents prevail as the main mechanisms of injuries. (3-6)

Most commonly, preschool children get injured at home, school children in traffic and in sports, while injuries in adolescents are usually a consequence of drug or alcohol abuse. (7-11)

Due to anatomical, physiological and psychological particularities of a child, mechanisms and causes of injuries in children and in adults often differ. A larger head and more exposed occiput in children are the reason why head injuries occur more often. Because of lower muscle mass, less subcutaneous fat and more elastic bones in children, more energy is transferred to internal organs (lung injury without rib fracture, damage to the organs in the abdominal cavity). (1, 3, 4)

A structured approach to the injured child and immediate reaction enable control over life threatening conditions, which helps to reduce mortality and morbidity. (1, 7, 10-12)

With the progress of emergency medicine and intensive care, preventive measures are crucial to reduce mortality and morbidity of children.

Driving speed limitations, bikeways and guard rails are some of the primary prevention measures. Secondary prevention measures focus on alleviating the immediate consequences of injuries in the event they occur. These include the use of safety belts, helmets, protective clothing, etc. Tertiary prevention measures are directed at limiting the progress and consequences of an injury that has already happened. (10, 11)

Severe brain injury in children and infants

Head injury and accompanying (severe) brain damage is one of the leading causes of death and disability in children and adolescents.

The primary purpose of modern intensive therapy treatment of children with severe brain injury is the prevention of secondary injuries. (13, 14)

Epidemiology

Severe brain injury is an important cause of death and disability in children admitted to the intensive care unit, especially in children who have reached less than 8 points according to the Glasgow Coma Scale (GCS). The incidence is 230 deaths per 100,000.

Pathophysiology

Brain injury occurs as a direct consequence of energy transmission and an indirect consequence of changes in biochemical parameters in the organism caused by an injury. In the first case, injuries are categorised as primary injuries and in the second as secondary injuries. The condition of an injured individual is a combination of both mechanisms. The transmission of energy to the brain causes primary brain injuries, such as contusions, conquassations and diffuse axonal injuries. Only secondary injuries can be treated, since they are susceptible to therapeutic measures. Mechanisms of secondary brain injuries are divided into intra and extracranial. The key intracranial mechanism of secondary injuries is increased intracranial pressure (ICP), which is sometimes accompanied by an infection. Among extracranial mechanisms, systemic hypotension and hypoxemia are the most important, followed by electrolytic disorders, hyperglycaemia and fever. A common denominator of secondary brain injury mechanisms is brain ischemia. If the brain is without oxygen for 7 to 10 minutes, it irreversibly damages. Oxygen deficiency leads to the lack of adenosine triphosphate (ATP) in neurons. Consequently, the sodium potassium adenosine triphosphatase (Na+/K+ ATPase) ceases acting on the neuron membrane. This triggers two mechanisms leading to cell death: firstly, an increased inflow of chlorine (Cl) and consequently water into the cell that causes cellular swelling, and secondly, an increased release of glutamate, which increases intracellular sodium levels (Na+) and calcium (Ca++). Although cell swelling is reversible, it causes a cerebral oedema.

Elevated (Ca++) levels in the cell trigger a sequence of events that lead to the necrosis of neurons and astrocytes. At the same time, the number of free radicals that damage the membrane arises under hypoxic conditions.

For the brain to survive, the key parameter is the cerebral perfusion pressure (CPP), defined as the difference between mean arterial pressure and intracranial pressure (CPP = MeanP – ICP). CPP is the force that drives the blood flow through the brain.

The normal cerebral blood flow is from 50 to 65 ml / 100 g of brain tissue per minute. The flow is self-regulating in the mean pressure area between 60 and 140 mmHg. The physiological CPP is between 70 and 85 mmHg. Ischemic changes in the brain are observed when its value drops below 60 mmHg. A drop in CPP and concomitant impairment of the autoregulation of the blood flow are the basic levers for hypotension to act as a mechanism of secondary brain injury.

Hypoxemia causes brain ischemia; a less important factor than hypotension in the acute phase. Hypoxemia becomes more important if both lungs and head are injured and acute respiratory distress syndrome (ARDS) develops later on. The latter can also develop with isolated brain injury (especially severe). The probability of the development of ARDS is independent of the localisation of the injury.

Intracranial pressure (ICP) is the pressure inside the skull. Its normal values are: adults below 20 mmHg, children below 15 mmHg and newborns below 10 mmHg. The ICP is considered as increased when it exceeds normal values. After an injury, the ICP increases due to reduced cerebral circulation in the added volume that resulted from a cerebral oedema and bleeding. There are three conditions that lead to the development of a cerebral oedema after an injury: cell swelling (ischemia), interstitial damage (blood-brain barrier damage) and, consequently, osmotic imbalance between the vessels and the interstitium. Increased ICP exacerbates the neurological condition due to reduced CPP and possible herniations.

Herniation (abnormal protuberance) develops when the brain is displaced beneath the duplications of dura (falx and tentorium) and in foramen magnum. In subfalcine herniation, the gyrus cinguli is displaced beneath the lower edge of the falx cerebri, possibly resulting in the compression of the anterior cerebral artery branches. Transtentorial herniation can be unilateral or central. Both types involve the displacement of the medial part of the temporal lobe beneath the tentorium. Central herniation develops due to diffuse or advanced focal lesions. The consequences of a transtentorial herniation are the compressed III. cranial nerve (same-sided pupil dilation) and the pressure on the cerebri posterior arteries, which show as the visual field impairment due to partial ischemia of the visual cortex.

Tonsillar herniation is the most dangerous one. In this type of herniation, the cerebellar tonsils are displaced through the foramen magnum, which consequently compresses the respiratory centres in the prolonged spinal cord. It usually occurs due to transtentorial herniation or, more rarely, due to a hematoma in the posterior part of the cranial cavity. (15-18)

Severe brain injury management

First steps in treating a child with severe brain injury include clearing the airway, restoring adequate ventilation and preventing or treating the state of shock (with fluid and medication). Since hypoxia and hypotension are the key factors in the development of a secondary brain injury, these steps are particularly important. After clearing the airway and adding oxygen, the heart function and blood circulation are evaluated. Afterwards, the following measures are taken:

  • Two broad peripheral intravenous cannulas G 14 to 16 are inserted to every injured person. Their size depends on the age of a child (G 18–24). For children up to 6 years, after an unsuccessful insertion of the peripheral intravenous cannula, an intraosseous approach may be used.
  • The recommended systolic pressure for infants is 80 mmHg, for children up to 10 years 90 mmHg and after 10 years of age 100 mmHg.
  • If arterial hypotension occurs, we must first check whether the injured person has any other injuries apart from the head injury. Hypotension exists if:

the systolic pressure of a newborn is ≤ 60 mmHg;
– the systolic pressure of an infant up to 1 year is ≤ 70 mmHg;
– the systolic pressure of a child from 1 to 10 years is ≤ 70 + (years x 2) mmHg;
– the systolic pressure of child older than 10 years or an adult is < 90 mmHg.

  • Isotonic solutions for intravenous administration (physiological or Ringer’s solution) are administered. For the treatment of cerebral oedema, hypertonic solutions are used, most commonly mannitol and (3%) sodium chloride solution.
  • If hypotension persists despite adequate hydration, vasopressor agents can be used to normalise the blood pressure, usually dopamine (2 do 5 μg/kg of body weight per minute or until the desired effect). (17-20)

Neurological exam

Evaluation of:

  1. State of consciousness according to GCS, size and response of the pupils, mobility of the limbs and data on possible cramps. Head injury is severe if the GCS score is ≤ 8; moderate if the GCS is from 9 to 12 points and mild if the GCS is from 13 to 15 points.

Glasgow Coma Scale (GCS)

E. Eye response (4) spontaneous

to speech

to pain

no eye opening

4

3

2

1

V. Verbal responses (children*) oriented

confused

inappropriate words

incomprehensible sounds

no response

5

4

3

2

1

M. Motor responses obeys commands

localizes to pain

withdrawal from pain

flexion to pain

extension to pain

no motor response

6

5

4

3

2

1

Sum (E + V + M) 3-15

*Verbal responses are adapted for children age 4 or less:
Laughs, follows objects, detects sounds: 5 points
Cries or reacts inappropriately to objects
or sounds: 4 points
Cries inconsolably and moans: 3 points
Is agitated and cannot be calmed down: 2 points
No response: 1 point

  1. Shape, size, equality and responsiveness of pupils to illumination.
  2. Position of eyeballs and their spontaneous movement.
  3. Corneal reflex.
  4. Cough reflex, pharyngeal reflex.
  5. Type of breathing.
  6. Body and limb position.

Diagnostic examinations at the emergency room

Laboratory research

Blood samples are withdrawn to determine blood sugar, haemogram, urea and creatinine, electrolytes, liver tests, blood clotting, blood group and for arterial blood gas analysis. We can also test for alcohol level, sedatives and drugs or do a pregnancy test if there are indications for testing. Another blood sample is taken to determine lactate levels if an injured patient with severe head injury is in shock.

Radiological investigations

The following investigations are performed on an injured person with severe head trauma (computed tomography imaging – CT, X-ray imaging – X-ray, ultrasound imaging – US):

  • Head CT and a CT of the first cervical vertebra; a traumatologist will evaluate whether a CT of the other parts of the cervical spine is necessary;
  • In case the head CT was not performed, as usual with severe head injuries, a head X-ray in two projections is made;
  • Cervical spine X-ray in two projections if the CT was not performed;
  • Chest X-ray;
  • Pelvic X-ray;
  • Thoracic and lumbar spine X-ray in two projections;
  • X-ray of injured limbs;
  • US examination of abdominal organs for suspected bleeding in the abdomen – FAST.

In case of severe injuries and an unstable patient a full-body CT scan is performed according to protocol for polytraumatised patients.

Indication to perform a head CT

Emergency Head CT:

  • Every injured with GSC score of 8 points or less;
  • Injured with GCS score from 9 to 15 points who have:
  • neurological symptoms or signs or both;
  • deteriorating neurological condition;
  • cranial vault fracture visible on the X-ray images;

(Children with cranial vault fracture visible on the X-ray and a GCS score of 15 are not sent to the CT imaging straight away. They are hospitalised and observed for at least 5 days. If any clinical signs of exacerbation are observed, a CT scan is performed immediately.);

  • basilar fractures of the skull;
  • post-traumatic epileptic seizures;
  • depressed skull fracture;
  • perforating or penetrating head injury;
  • leaking of cerebrospinal fluid as a discharge from the nose or ear canal;
  • documented disorder of consciousness and are amnestic of the event;
  • signs of intoxication.

Control Head CT:

  • immediately after neurological deterioration or increased ICP, which remains elevated regardless of the treatment;
  • in 24 hours after emergency surgery;
  • in 24 hours after emergency CT during clinically stable condition and controlled artificial ventilation.

Neurosurgical treatment of children with head trauma

Emergency surgeries:

  • acute extra-axial hematoma (subdural, epidural) larger than 1 cm with the shift of central structures for more than 5 mm in an unconscious injured patient;
  • cortical haemorrhagic contusion or intracerebral hematoma with a larger diameter of 2 cm and central structures displacement of more than 5 mm in an unconscious injured patient;
  • depressed skull fracture that exceeds the cranial bone thickness;
  • depressed skull fracture in an injured patient with neurological damages regardless of the depth of the fracture;
  • open depressed skull fracture;
  • depressed skull fracture in an injured patient who has experienced post-traumatic epileptic seizures, regardless of the depth of the fracture;
  • perforating or penetrating head injuries.

Indications for inserting an ICP monitor:

  • injured patients with head injury and a GCS score of 8 points or less;
  • injured patients with head injury and a GCS score of more than 8 points with consciousness disorders and head CT with the signs of: increased ICP (compressed basal cistern, midline shift for > 5 mm); normal head CT and two positive signs at admission: unilateral or bilateral pathological motor response and hypotension.

Intensive treatment of severe brain injuries

When and how to react?

When treating an injured patient with severe traumatic brain injury (TBI), it is extremely important to maintain the optimal oxygenation and a normal blood pressure. (21, 22)

Desired levels of intracranial pressure (ICP):

– in newborns < 10 mmHg (< 1,33 kPa);
– in infants and children < 15 mmHg (< 2 kPa).

Desired levels of cerebral perfusion pressure (CPP):

– in infants and children CPP > 40 mmHg (> 6,67 kPa).
– in older children CPP > 50 mmHg

Measures are necessary if the levels of ICP and CPP are:

– > 10 mmHg (> 1,33 kPa) in newborns;
– > 15 mmHg (> 2 kPa) in infants and children;
– < 50 mmHg (< 6,67 kPa) CPP in infants and children.

Basic measures to lower the increased ICP:

  • deep sedation and analgesia (exceptionally muscular relaxation),
  • elevating the head of bed by 15°–30° (for normovolemic patients),
  • maintaining normothermia,
  • maintaining normocapnia.

Standard measures to lower the increased ICP:

  • hyperventilation; the recommended partial arterial carbon dioxide pressure should be attained – PaCO2 should be between 4 and 4.66 kPa (30 to 35 mmHg);
  • mannitol 0.25 to 0.3 g / kg of body weight in 20 minutes; the dose may be repeated depending on the patient’s neurological condition and the level of ICP. However, caution is advised due to the retroactive effect; serum osmolarity should be <360 mosmo / l;
  • ventricular drainage according to neurosurgeon’s evaluation.

Treatment when basic and standard measures fail:

  • Barbiturates, for example Nesdonal, at a single initial dose of 10 mg / kg of body weight in 30 minutes. The dose is repeated three times: 5 mg / kg of body weight every hour, then administered as an infusion of 1 mg / kg of body weight per hour. The preferred serum barbiturate concentration is 3 to 4 mg or 0.12 to 0.16 mmol / l. Electroencephalography (EEG) monitoring is recommended. Due to side effects, barbiturates are given only to hemodynamically stable patients.
  • Deep hyperventilation with the partial arterial carbon dioxide pressure (PaCO2) between 3.7 to 4 kPa (28 to 30 mmHg). Continuous monitoring of jugular bulb venous oxygen saturation (SjvO2), which should not fall below 55% of the normal value to avoid the consequences of excessive hyperventilation, such as brain ischemia, is recommended. The Doppler flow velocity measurements in the middle cerebral artery are not routinely taken in children. (20)
  • Decompressive craniectomy.

Measures for maintaining blood pressure in the brain by increasing the mean arterial pressure:

  • Maintaining normovolemia with isotonic crystalloid solution (0.9% NaCl solution, Ringer’s solution). The desired value of hematocrit is 0.28 to 0.3 (28 to 30%).
  • Increasing the mean arterial pressure with vasoactive substances to attain the level of CPP > 60 mmHg (> 8 kPa). Before using vasoactive substances, the injured patient must be sufficiently hydrated.
  • Noradrenaline is administered at an initial dose of 0.05 μg / kg of body weight per minute. The dose is increased to attain the desired level of blood pressure. If noradrenaline is administered in order to increase the mean arterial pressure, it is advisable to insert a pulmonary arterial catheter for invasive hemodynamic monitoring.
  • Dopamine is administered from2 do 5 μg / kg of body weight per minute (until the desired effect).

Infection prevention measures:

  • Antibiotics are used prophylactically only for injured patients with open depressed skull fracture and penetrating or perforating head injuries. For example, co-amoxiclav is administered to an infant at a normal intravenous dosage of 30 mg / kg of body weight per 8 hours. In case of an allergy to penicillin, a combination of first-generation cephalosporin (cefazolin) and metronidazole or a combination of vancomycin, gentamicin (garamycin) and metronidazole may be considered. If the injured patient has an impaired immune system, we consult an infectologist.
  • Infections must be controlled.
  • Surgical procedures are performed if necessary.

Epileptic spasms

  • Antiepileptic drugs are prescribed prophylactically for the first seven days to injured patients with depressed skull fracture, penetrating or perforating head injuries, cerebral contusions or after surgically removed traumatic hematoma.
  • Recommended dosage of medications to prevent early epilepsy:
  • Carbamazepine (Tegretol) 200 mg tablets; twice a day for the first three days 1/2 of the tablet (2 x 100 mg) per day, then 1/2 of the tablet (100 mg) in the morning and 1 tablet (200 mg) in the evening for three days, then continue with1 tablet (2 x 200 mg daily). Infants aged 3 months or older get Tegretol 15 do 20 mg / kg of body weight per day in two doses.
  • Phenobarbital 100 mg and 15 mg tablets may also be used. The recommended dosage is from 60 to 180 in the evening and 10 mg / kg of body weight per day in one dosage for infants up to 3 months.
  • Another possible medication is phenytoin (Epanutin) at an intravenous dosage of 17 mg / kg to a maximum of 20 mg / kg of body weight, injected at a rate of less than 50 mg per minute (the same for newborns, infants and children).
  • Phenytoin (Difetoin) tablets of 100 mg can be used. The recommended dosage for adults is 3 times 100 mg per day; and 4 to 8 mg / kg of body weight per day for children.
  • Therapeutic serum concentrations of antiepileptic drugs must be monitored.

Preventing stress ulcer:

  • Early enteral feeding,
  • Adequate sedation and analgesia,
  • Pharmacological protection with sucralfate: 30 minutes before the meal, 1 bag is given in the abdomen (venter) via gastric tube up to three times a day. H2 blockers are only administered exceptionally.

Nutrition of an injured patient with severe head trauma:

  • starting enteral feeding as soon as possible or
  • a combination of enteral and parenteral nutrition,
  • monitoring metabolism, electrolytes and fluid balance, as well as maintaining normal blood sugar levels. (17-19, 21)

Case study – a 12-year old girl with severe head trauma

Case history:

A 12-year-old girl fell off of a horse while riding and hit her head on a column. She was unconscious at the time of the event. Her father could not wake her up, so he placed her in the car (at the back seat) and took her to the nearest hospital. All this time, the girl was unconscious. Upon the arrival, the girl was still unconscious, did not open her eyes, did not speak and reacted to pain with the extension of the upper limbs. GCS = 4 (E1V1M2).

The girl was sedated and intubated. A head CT was taken as the basic emergency diagnostic measure. The CT scan showed a fracture of the right temporal and sphenoid bone, minor subdural hematoma and minor bleeding due to contusion in the left temporal lobe. (figure 1) In agreement with the neurosurgeon, she was transferred to the nearest tertiary institution together with an anaesthesiologist.

Figure 1.

Admission and treatment:
At the admission, the girl was brought directly into the operating theatre, where the ICP (intracranial pressure) transducer and external ventricular drain (EVD) were inserted. At the insertion of the drain, the ICP was about 10 mmHg, and occasionally increased to 40 mmHg. The girl was therefore deeply sedated with thiopental, and received a mannitol bolus of 20%, after which the ICP stabilized below 20 mmHg. The pupils were of medium size and were appropriately reactive.

The next day, the pupil reaction was slightly slower. The ICP increased to 26 and did not decrease despite all conservative measures. That is why, a bilateral decompressive craniectomy was performed. During the procedure, the ICP transducer was changed and EVD was removed (we did not decide to insert another one since the ventricles were practically blurred). At the end of the procedure, the pupils were wide and non-reactive. After that, the ICP was normal for two days, but then increased again. A new EVD was inserted and the ICP normalized.

On the eighth day, the sedation was withdrawn and on the tenth day tests for brain stem death were performed. Since the tests were positive, we sought confirmation with perfusion scintigraphy, which on the other hand showed good circulation of the entire brain. In the evening hours of the same day, the pupils began to react and the girl began to respond to tracheal aspiration.

In the following days, the girl was extubated and began breathing on her own. She only needed a minimum amount of added O2. A head MRI was made, which showed contusion and diffuse axonal injuries on both sides both frontally and temporally. (figure 2)

Figure 2.

Hospital care and discharge:

Approximately three weeks after the injury, spontaneous motor movements began to appear. A few days later, the girl began to follow with her eyes and after five weeks she started speaking slowly. By that time, we occasionally put her in a sitting position, however she still needed head support. After seven weeks, the percutaneous endoscopic gastrostomy (PEG) was inserted and rehabilitation continued. After eight weeks, the girl was walking with support. That is when a bilateral cranioplasty with her own bone was performed. We continued with rehabilitation and discharged the girl into home care after 89 days.

On the day of the discharge, a discrete left hemiparesis was present as well as walking abnormalities – spastic and scissors gait. Proprioception was preserved. When testing higher mental functions, she responded correctly in only ¼ cases. Rehabilitation was planned in the tertiary rehabilitation centre a month after she was discharged into home care. A check-up at our facilities is planned in three months for final assessment of the condition.

Conclusion

Injuries are the leading cause of death in children in the developed world. A structured approach and immediate reaction enable to control life-threatening conditions, which helps to reduce mortality and morbidity. In addition to the progress of emergency and intensive medicine, the preventive measures are crucial to reduce the morbidity and mortality of injured children.

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Corresponding author:
Mirjana Miksić
Paediatric intensive care and therapy unit
Paediatric Clinic, UMC Maribor,
Ljubljanska 5, 2000 Maribor, Slovenia
Phone: +386 40 328 426
E-mail: mima.miksic@gmail.com

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