Serious central nervous system traumas occur in most of the traffic accidents that are quite common in our country. In many countries of the world, trauma is one of the leading causes of death and disability in children, adolescents and young adults. As a result of motor vehicle accidents, falls and beatings, which constitute the majority of accidents, serious injuries may occur in the brain, spinal cord and their supporting structures.
Head Traumas
Scalp Injury:
If a scalp injury is not treated promptly, it can cause bleeding and subsequent shock. Bleeding can usually be controlled with a pressure dressing or clamp on the scalp. Incisions in the scalp should be closed as soon as possible. Scalp lacerations covering compression fractures or penetrating skull injuries should be cleaned and sealed in the operating room. Simple scalp incisions should be cleaned, washed profusely, and closed primarily, paying attention to the approximation of the galea and skin layers. If the galea layer is closed well, excellent bleeding control is achieved. Scalp avulsions typically involve all layers other than the periosteum. If the avulsion is minor, primary closure of the wound margins is usually successful. In large scalp avulsions, if the ruptured tissues are preserved correctly and the surgery is not delayed, suturing the ruptured part by applying microsurgical technique is the preferred method.
In cases where the injured scalp has lost its vitality but the periosteum is intact, the defect can be closed with grafts. In such cases, the periosteum should be kept moist before surgery. Since the outer bone provides the blood supply to the tabula through the periosteal layer, repair is more difficult in a situation where the periosteum is absent or dissected. It is appropriate for any scalp incision to be evaluated by a neurosurgeon.
Skull Fractures
Skull fractures; whether the skin over the fracture is intact (closed fracture) or torn (open or compound fracture), a single fracture line (linear fracture), multiple fracture lines radiating from a single focus (stellate fracture), or comminuted (comminuted fracture) and It is classified according to whether the fracture line edges are below the level of the surrounding intact bones (collapse-depressed fracture) or not (non-depressed fracture).
Simple skull fractures (linear, stellate or comminuted non-depressed) require no special treatment. However, they are potentially dangerous if they cross vascular channels within the skull, such as the arteria meningia media or dural venous sinuses. If these structures rupture, an epidural or subdural hematoma may occur. Simple skull fractures that extend into the nasal sinuses or mastoid air cells due to exposure to air are also defined as “open fractures”.
Compression fractures often require surgical intervention to remove inwardly sinking bone fragments. If there are no neurological signs and the fracture is closed, surgery can be performed in elective conditions. During surgery, the dura should be examined and repaired if necessary.
Open skull fractures also require surgical intervention. Linear or stellate non-depressed open fractures can be treated by simply closing them after they are completely cleared. Compound open fractures with severe injury to the underlying bone should be repaired in the operating room where effective debridement can be performed. The dura should be carefully examined so that tears of the dura are not overlooked. Dural tears should be closed primarily or with fascia grafts to reduce the risk of infection and prevent CSF leakage. Considering that better visualization of the underlying dura and/or brain tissue may be necessary, open compression fractures should be cleaned and removed in the operating room after preparations for craniotomy are completed.
Base fractures may show bruising around the eyes (symptom of raccoon eyes) or behind the ear (sign of bat). These clinical signs are more frequently observed in anterior and middle fossa fractures. In this type of fracture, isolated cranial nerve lesions may be seen, since the exit holes of the cranial nerves are located at the base of the skull. The facial nerve is the nerve most commonly affected by skull fractures, often due to laceration or edema. Most facial nerve lesions resolve spontaneously and do not require any treatment. On the other hand, complete incisions of the facial nerve are usually explored surgically, but the timing of surgery is controversial.
It is expected to be treated in cases with rhinorrhea or otorrhea, that is, brain fluid coming from the nose and ears. Traumatic CSF leaks typically stop within the first 7 to 10 days. However, this treatment must be done under the supervision of a neurosurgery clinic.
Brain Laceration (crushing):
Brain laceration occurs as a result of deceleration, acceleration, rotation, or a combination of these, due to a blow to the head. During the first impact, neuronal and axonal tears may occur, which constitutes the primary injury. Any subsequent complications, such as intracranial hematoma, cerebral edema, hypoxia, hypotension, hydrocephalus, or endocrine disorders, constitute secondary injury.
Mild head trauma is usually not accompanied by primary brain injury, and neurological deficits are usually limited to transient loss of consciousness (concussion). On the other hand, moderate and severe head traumas typically result in reversible or irreversible neurologic deficits. Moreover, this degree of trauma is often accompanied by secondary brain damage.
Primary damaging blows can be severe enough to rupture intraparenchymal capillaries, superficial subdural bridging veins, or epidural arteries and veins, resulting in a hematoma with blood extravasated. Brain edema may occur as a result of vasodilation and disruption of the blood-brain barrier. Ischemia from hypotension and hypoxia can lead to cell death and cytotoxic edema. Mixing of CSF with blood may cause impaired absorption of CSF and hydrocephalus. Inappropriate release of antidiuretic hormone or diabetes insipidius may aggravate cerebral edema by disrupting fluid and electrolyte balance. Separately or together, these changes may result in elevation of ICP.
Rising ICP plays a role in secondary brain injury by decreasing cerebral perfusion pressure (CPP).
Intracranial hypertension is one of the most important factors affecting prognosis in head traumas. Therefore, when cerebral perfusion pressure drops, aggressive treatment is imperative to prevent secondary injury to the brain. If possible, early intervention should be made at the accident site using airway control and hyperventilation.
Rapid clinical assessment is essential. Although a comprehensive neurologic assessment is difficult in unresponsive and uncooperative patients, certain features are critical in trauma patients.
It is unlikely that a secondary complication from head trauma will develop in patients without headache, lethargy, or focal neurologic deficit. Imaging studies are generally not performed in the asymptomatic patient. On the other hand, CT (computerized tomography) examination should be performed in symptomatic patients with or without focal neurological deficit.
Spinal Cord Injury
Traumatic spinal cord injury can result from spinal fractures, fracture dislocations, hyperextension in cases with preexisting narrow canal, herniation of intervertebral disc material into the canal, and penetrating injuries such as gunshot or stabbing. Neurological deficits can be mild and temporary, or they can be serious and permanent. Whether or not coma develops, spinal fracture and spinal cord injury should be suspected in all cases with head trauma and multiple trauma. Assuming that the spine is unstable initially, it is best to keep the patient immobilized on a flat surface with a rigid collar until careful examination and diagnostic investigations are performed.
Clinical findings in spine or spinal cord injuries; It includes tenderness in the vertebrae, loss of strength in the extremities, numbness or paresthesia, respiratory disturbance and hypotension. Involvement of spinal nerve roots manifests itself as radiculopathy characterized by motor and sensory loss in the related myotoma and dermatome. Spinal cord involvement may give different and various clinical findings due to myelopathy.
A complete lesion typically presents as complete loss of motor and sensory functions below the level of injury and is indicative of a complete anatomic or physiological incision of the spinal cord. Acute incisions are characterized by areflexia, flaccidity, anesthesia, and autonomic paralysis below the level of the lesion. Arterial hypotension due to loss of sympathetic vascular tone is a constant finding in all cuts above T5.
Incomplete lesions of the spinal cord can cause Brown Sequard syndrome, which manifests itself as loss of pain and temperature sensation in the contralateral body, with loss of ipsilateral motor function and position/vibration sense below the level of injury. Anatomically, this is explained by the half-incision of the cord. Central cord syndrome is characterized by bilateral loss of motor function and sensation of pain and temperature in the upper extremities and relative preservation of these functions in the lower extremities. Typically, the distal upper extremities are more severely affected because the most medial portions of the corticospinal and spinothalamic systems carry fibers from these regions. Central cord syndrome is frequently seen following cervical hyperextension injury, with or without fracture. Anterior spinal artery syndrome; Below the level of the lesion, it includes bilateral loss of motor function and sensation of pain and temperature, while preserving position, vibration, and superficial tactile sensations. This incomplete lesion affects bilateral anterior and lateral columns due to ischemia in the spinal cord region fed by this artery as a result of injury to the anterior spinal artery. The most common cause of anterior spinal artery syndrome is acute cervical disc herniation.
Cauda equina compression symptoms and signs may occur as a result of lumbar spinal trauma. Many lumbosacral radioculopathies of varying severity may present themselves. Motor, sensory and reflex functions may be affected in the lower extremities. Various degrees of loss of strength, loss of sensation (all modalities in the areas of the specific distribution of the roots involved) and loss or decrease in reflexes occur. Bladder distension due to detrusor muscle paralysis, flaccidity in the anal sphincter, and loss of perineal sensation are common in severe injuries.
Ileus with gastric distension is common, requiring nasogastric drainage. Similarly, bladder distension occurs because the muscles at the base of the bladder and pelvis are flexed. Emptying the bladder will prevent excessive distension, which creates severe pressure in the inferior vena cava and pelvic veins, which may impair venous return to the heart and cause increased systemic hypotension.
If the spinal cord injury is above the T5 level, blood pressure is usually low. This causes denervation of the sympathetic nervous system leading to increased venous pooling and decreased venous return.
Tachycardia is a common compensatory response to hypotension, but is unavoidable in bradycardia when the cervical spinal cord is damaged and the heart’s sympathetic input is lost. This type of bradycardia does not require treatment unless the patient is symptomatic or is at risk for myocardial infarction or stroke due to age or other debilitating disease.
Spine radiographs are essential once the patient is in haemodynamic balance, but the patient must remain motionless on the back board with a rigid neck collar. Standard radiographs are taken, ensuring that the cervicothoracic junction is well visualized. Seriously injured patients in a coma and/or with multiple trauma should have a good, clear film showing the entire spine. Fracture sites can be examined in more detail with CT using both axial and sagittal images. If no abnormalities are found on CT or plain radiographs and the neurologic deficit is clearly present in the spinal cord, post-CT myelography or MRI should be used to identify other causes, such as traumatic intervertebral disc herniation or spinal epidural hematoma.
The goals of treatment are to correct the spinal alignment, preserve undamaged neural tissue, repair damaged neural tissue, and provide permanent stabilization of the vertebrae. Correction and fixation of any fracture or slippage must take priority in these purposes.
Misalignment in the cervical region can almost always be corrected with skeletal traction in the neutral position. Frequent radiographs are taken to ensure correct alignment.
In patients with thoracic and lumbar spine fractures, treatment is first initiated with stabilization. Stabilization is not very tight compared to cervical fractures, but in principle it is the same. While bending, stretching, side-tilting and rotational movements are avoided, patients are kept flat in bed without being moved. Typically, they have fewer systemic complications related to neurological damage, but vigilance is still necessary to ensure neurological recovery.
Indications for early surgery in patients with spinal cord injury are: fracture/dislocation cases that cannot be adequately corrected by closed methods; neurological deterioration in the patient with the incomplete lesion; A penetrating injury with or without severe spinal cord compression and CSF leakage caused by an intracanal mass lesion as demonstrated by myelography or MRI. In open wounds, eg stabs and gunshot wounds, the wound should be cleaned and closed, whether or not there is complete cord damage. Early surgery to stabilize the spine is justified. Because it allows early movement and rehabilitation. Depending on the nature of the spinal injury and the degree of instability, either an anterior or a posterior approach may be used.
If closed reduction is successful and the fracture is stable, at least 3 months of external immobilization is required to ensure adequate healing.
External immobilization is also indicated in cases where surgical reduction and/or stabilization is mandatory. After anterior and posterior metal plating applications, a rigid neck collar may be sufficient. In the thoracic and lumbar region, plastic body jacket or plastic plaster fixation is usually required for at least 3 months. Plain radiographs are used to monitor spinal alignment and degree of fusion throughout the recovery period.
If any function of the spinal cord is preserved immediately after the accident, some functions are usually restored if the cord and spine are not affected by secondary damage. In cases with complete cord lesion, functions below the level of the lesion rarely return. Rehabilitation for these cases is carried out in line with their own care and occupational adjustment. Long-term problems related to skin care and recurrent urinary tract infections are the causes of premature death.
