Primary damage: The effect of the initial event on the brain.
Secondary damage: If the primary damage is not recognized, the child can suffer even more brain damage. Causes of secondary injury include systemic hypotension, respiratory failure and hypoxia, cerebral edema or cerebral or brainstem herniation secondary to intracranial hemorrhage.
The most common causes of acute global neurological dysfunction in children are head trauma, hypoxia, central nervous system infections, encephalopathies due to endogenous metabolites or exogenous toxins. Idiopathic status epilepticus can also cause significant or severe encephalopathy.
Trauma-related secondary brain injury occurs at the beginning of the posttraumatic period or develops over the next few days. Secondary damage is associated with systemic hypertension, hypoxia, intracranial hemorrhages, or increased metabolic requirements. Cerebral edema is a significant secondary injury that can lead to further neuron damage, cerebral herniation and death. TBI can also initiate various events that can lead to neuronal death through the production of various mediators such as excitatory amino acids (EAA). It develops after a generalized neuron depolarization following primary brain injury. When this happens, cerebrovascular dysfunction (loss of autoregulation), cerebral edema, blood-brain barrier changes, free radical formation, mitochondria damage, and neuron death occur.
Clinical Findings:
Traumatic brain injury (TBI) is divided into three according to GCS: Severe (GCS 3-8), Moderate (GCS 9-12), Mild (GCS 13-15)
• The typical clinical manifestation of severe TBI is coma. Newly developed or exacerbated headache, confusion, hypertension, bradycardia, respiratory irregularity, 6th cranial nerve palsy (lateral rectus paralysis), or 3rd cranial nerve palsy (anisocoria, ptosis, inferior outward paralysis) in cerebral edema and secondary hernia developing in these patients eye characterized by gaze) can be observed. ICP increase can be successfully treated with continuous ICP monitoring. The development of cerebral edema is progressive. Severely increased ICP (>20 mm Hg) may occur shortly after TBIH, but usually peak ICP increase 48-72. It is seen in hours.
• In the case of epidural hematoma and diffuse edema, the clinical findings may worsen within hours while the child is initially fully conscious (talk and die scenario).
• Coma can be observed without increased ICP in axonal damage or brain stem damage.
Treatment in Severe TBI Cases:
1. Sequential serial intubation
2. Hemodynamics and blood gas stabilization
3. Euvolemia should be ensured with saline bolus (hypotonic fluids should be avoided), hypo- and hypervolemia should be avoided
4. ICP monitoring and herniation monitoring
5. In case of herniation, hyperventilation, 100% oxygen, thiopentalpentobarbital coma, mannitol or 3% Naci are given.
Treatment algorithm in severe TBI
Braindeath
Trauma and asphyxia are the most common causes of brain death in children.
For brain death, the following should be present: (1) Irreversible loss of consciousness, (2) Irreversible loss of brain stem reflexes, (3) Absence of any factor (drugs, hypothermia, etc.) that may cause damage to the central nervous system (4) Apnea
There are three important features in the diagnosis of brain death (1) coma, 2) loss of brain stem reflexes, (3) apnea.
Apnea
In a patient who is in a coma and does not have brainstem reflexes, an apnea test is performed to show the presence of apnea. If the patient has hypoxia or hypotension during the test, the test is stopped. Absence of respiratory effort during the test and an increase in pCO2 of 60 mmHg or 20 mmHg from baseline are in favor of brain death.
Clinical evaluation should be done 2 times with a certain time interval. This period is 24 hours in the neonatal period and 12 hours after the first month. It is recommended to wait 24-48 hours before starting brain death studies after severe traumatic brain injury or CPR.
Sequential Intubation
