closed spinal cord injury
Introduction
Introduction to closed spinal cord injury Closed spinal cord injury refers to compression or edema, hemorrhage, contusion or rupture of the spinal cord or cauda equina caused by spinal fracture or dislocation. It is not accompanied by a wound that communicates with the outside world. 14% of spinal fractures have spinal cord injury, most of which are Single segment injury. Spinal cord injury can be divided into primary spinal cord injury and secondary spinal cord injury. The former refers to the damage caused by external forces acting directly or indirectly on the spinal cord. The latter refers to the spinal cord edema caused by external force, hemorrhage caused by small blood vessel hemorrhage in the spinal canal, compression fracture and broken disc tissue to form further damage to the spinal cord caused by spinal cord compression. basic knowledge The proportion of illness: 0.001% Susceptible people: no specific people Mode of infection: non-infectious Complications: atelectasis phlebitis pulmonary embolism
Cause
Cause of closed spinal cord injury
(1) Causes of the disease
The cause of closed spinal cord injury is that violence indirectly or directly acts on the spine and causes fracture and/or dislocation, resulting in spinal cord, cauda equina compression, injury, and about 10% of spinal cord injury without obvious fractures and dislocations. It is a spinal cord injury without radiographic abnormalities. It is more common in children with strong spinal column elasticity and the elderly with original spinal stenosis or hyperosteogeny.
Direct violence is relatively rare, seen in heavy objects hitting the back of the neck, back, waist, corresponding parts of the lamina, spinous process fractures, fracture pieces into the spinal canal.
Indirect violence accounts for the vast majority of injuries, which are common in traffic accidents, falling from heights, collapse of buildings, collapse of tunnels, and sports. Violence acts on other parts of the body and then transmits to the spine to stretch beyond normal limits. , rotation, lateral flexion, vertical compression or traction (mostly mixed motion), resulting in ligament injury, fracture, vertebral fracture and/or dislocation, facet fracture and/or dislocation, accessory fracture , disc herniation, wrinkles of the ligamentum flavum, etc., causing compression and damage to the spinal cord.
Factors affecting the type of spinal fracture or ligament injury are: 1 strength and direction of external force, 2 points of action of external force, 3 posture of body when injured, and anatomical and biomechanical characteristics of 4 different segments.
Spinal cord injury usually occurs at the junction of a more active spinal segment and a less active segment. The cervical segment and thoracolumbar junction (thorax 11 to waist 2) are the most frequently affected spinal cord injuries. The incidence of regional, thoracic or lumbar regions is closely followed by the following types of common injury types in different segments:
1. The cervical segment has poor mechanical stability and is more vulnerable than other segments. The proportion of spinal cord injury is also high (40%), and cervical spinal cord injury accounts for 50% of all spinal cord injury.
(1) Flexion type injury: more common in sudden braking or crash, the head moves forward by inertia, the posterior ligament complex is damaged, and the front part of the vertebral body is compressed into a wedge shape. At this time, it is usually stable, but the overflexion movement It can cause extensive injury or joint protrusion including intervertebral disc and joint capsule, interlocking, shearing force to make the vertebral body in the upper part of the injury level slip forward, and the spinal cord is squeezed or even broken by the posterior upper part of the next vertebral body.
(2) Stretch type injury: When the jaw is dropped or the forehead touches the ground or when the vehicle is hit by the vehicle, the back of the vehicle collides and the head is reclined. The damage is mostly at the neck 4 to the neck 5, the anterior longitudinal ligament is broken, and the front part of the vertebral body can be avulsed. The vertebral arch can be broken. In severe cases, the vertebral body is dislocated backward. The spinal cord is subjected to the anterior vertebral body, the intervertebral disc and the posterior lamina, and the ligamentum flavum is compressed. Those with cervical spondylosis are prone to such damage.
(3) Vertical compression type injury: The longitudinal force is applied to the top of the head when the neck is straight, and burst fractures or vertebral arch fractures may occur at the neck 4 and neck 5 .
(4) Special type of fracture: Jefferson fracture refers to the axial compression of the atlas, and the left and right arches are fractured at the same time. Therefore, the spinal canal is wide, generally no spinal cord injury, and the odontoid fracture is caused by overflexion or overextension of the neck. The fracture occurs at the tip of the odontoid, the body or the base, and the fracture of the sling or the fracture of the hangman is a pedicle fracture of the vertebral arch caused by extreme extension of the neck, which may be accompanied by separation of the neck 2 and neck 3 vertebral bodies.
2. Thoracic and lumbar chest 1 to 10 rib protection, relatively stable, low incidence of injury, but once it occurs, the injury is more complete, because the spinal canal is small, the upper thoracic spinal cord blood supply is poor, if the lower thoracic segment injury is involved Adamkiewicz artery, the ischemic plane can be raised to the chest 4, the lumbar vertebrae joint surface is vertical, the stability in the anterior-posterior direction is good, the lumbar spinal canal is wide, and the lumbar spine is below 1 to 2, so the damage is mostly incomplete, and the chest 12 to the waist 1 are relative. The stable thoracic vertebrae and the highly active lumbar vertebrae meet at the intersection, which is the most vulnerable.
(1) Flexion type injury: When the foot falls, the feet or the buttocks touch the ground. When the waist is bent, the weight is hit by the middle back, and the thoracolumbar flexion type damage is often caused. The anterior compression of the vertebral body is wedge-shaped, and the severe one is accompanied by dislocation or Separation damage to the posterior structure.
(2) Buckling-rotating injury: falling from a height, causing damage to the upper back and one shoulder, and involving the front, middle and rear three-column structure, anterior compression of the vertebral body, transverse fracture of the vertebral body, vertebrae Bow and transverse process fractures, often accompanied by dislocation, lead to severe spinal cord injury.
(3) Vertical compression type damage: the upper thoracic segment of the falling object or the ground of the feet or the buttocks when falling, can cause the chest 10 ~ waist 12 burst fracture.
(4) Buckling-separation injury: that is, seat belt fracture, the old-fashioned car seat belt is transverse to the front wall of the abdomen without shoulder protection. In the case of a car accident, the upper body of the person is used as an axis for the front curve. In severe cases, the three-column structure can be horizontally transected. , dislocation, and can be combined with abdominal visceral injuries.
(two) pathogenesis
The mechanism of acute spinal cord injury includes primary spinal cord injury and consequent secondary spinal cord injury. Primary injury refers to initial mechanical spinal cord injury due to local tissue deformation and trauma energy transfer; secondary spinal cord injury Refers to the chain reaction process including primary biochemical and cellular changes activated by primary injury, which can cause progressive and even death of nerve cell damage, and lead to autolysis of the spinal cord, irreversible damage to the intramedullary structure, spinal cord Progressive expansion of the damaged area.
Primary spinal cord injury
(1) Spinal cord turbulence: the mildest pathological injury in all spinal cord injuries, short-term recoverable spinal cord dysfunction after injury, microscopic focal hemorrhage of central gray matter, a small number of nerve cells or Axonal degeneration, usually a few weeks after the injury can return to normal, bleeding absorption.
(2) Spinal contusion: Early pathological changes are mainly hemorrhage, exudation, edema and neuronal degeneration. Microscopic rupture of small blood vessels, red blood cell overflow, neuronal swelling, Nissl disappearance, nerve axis The gap between the cord and the myelin sheath increases, and the myelin sheath separates. With the development of pathological process, necrosis, disintegration and disappearance of neuronal structure, glial infiltration and connective tissue cell proliferation, complete damage Pathological changes from central gray matter massive bleeding to white matter hemorrhage, from central gray matter necrosis to total spinal cord necrosis; incomplete lesions are mainly point hemorrhage, focal neuronal degeneration, disintegration and a few axonal degeneration Change, no central necrosis occurs, the pathological changes of the two have qualitative and quantitative differences.
(3) spinal cord compression injury: animal experiments have observed that long-term compression of the spinal cord will lead to vacuoles in the gray matter, phagocytic cells infiltrated by fibrous tissue around the cavity and cavity without obvious bleeding, and there is no obvious slight compression. change.
2. The concept of secondary injury secondary to spinal cord injury was first proposed by Allen in 1911. He observed in the animal experiments that the acute spinal cord injury dog had some improvement in neurological function after clearing the hematoma, and believed that there may be a source. Biochemical substances in local hematoma and necrosis can lead to further spinal cord injury. In the mid-1970s, Kobrine and Nelson proposed neurogenic theory and angiogenic theory for secondary spinal cord injury. The former considered neuronal damage. A series of pathophysiological metabolic changes were induced. The latter thought that spinal cord microvascular rupture, vasospasm, thrombosis and other causes spinal cord ischemia, eventually leading to central hemorrhagic necrosis. Since then, a large number of studies in the past 30 years have successively proposed various and subsequent Factors related to spinal cord injury include:
(1) vascular changes, including ischemia, microcirculatory disorders, vasospasm, embolism, loss of autoregulatory mechanisms.
(2) Ion disorders, including increased intracellular calcium, extracellular high potassium, and increased sodium ion permeability.
(3) Aggregation of neurotransmitters such as 5-hydroxy color saddle, catecholamines and excitatory amino acids, which can cause excitotoxic damage to neurons.
(4) Release of arachidonic acid, production of free radicals and lipid peroxidation.
(5) Endogenous opioids.
(6) Nitric oxide (N0).
(7) Edema.
(8) Inflammatory response.
(9) Abnormalities in cellular energy metabolism.
(10) Programmed cell death, ie apoptosis.
Despite this, the understanding of the mechanism of secondary spinal cord injury is still not very accurate, and the most important among these related factors is the ischemic changes caused by local microcirculation disorders and lipid peroxidation caused by free radicals. reaction.
Because secondary spinal cord injury is severely harmful, blocking early in the injury, reversing this process is extremely important for the treatment of spinal cord injury. Effective treatment should be directed to the pathophysiological mechanism of secondary spinal cord injury, protection The white matter conduction beam that has not been damaged, so as to achieve the purpose of preserving part of the nerve function.
Prevention
Closed spinal cord injury prevention
Pay attention to prevent traffic accidents and violent incidents, prevent accidental fall damage, and prevent work and sports related injuries.
Complication
Complications of closed spinal cord injury Complications, pulmonary atresia, pulmonary embolism
In patients with acute spinal cord injury, each system is affected. Chronic atelectasis and secretion of respiratory secretions often cause pneumonia and other respiratory complications. Deep vein thrombosis often occurs in the deposition of cardiovascular system. The literature reports that deep vein thrombosis causes phlebitis or There are 3% to 13% of cases of fatal pulmonary embolism. The skin compression without sensory area can cause hemorrhoids, ulcers, muscle incapacitation, muscle atrophy and severe soft tissue contraction around the joints. Siltation of the urinary tract system can cause frequent infection and calcification. Insufficient skeletal system causes calcium loss, urinary tract stones, ectopic bone, severe osteoporosis and eventually pathological fractures, gastrointestinal paralysis causes intestinal obstruction, ulcers, bleeding and chronic constipation, sometimes concurrent pancreatitis.
Patients with acute spinal cord injury over 40 years of age should have close cardiac monitoring when they have a history of heart disease or direct heart damage due to arrhythmia caused by neurogenic shock. For younger patients, generally better patients, give more than one Central venous catheter and peripheral venous access of the connector, continuous ECG monitoring has a great effect on reducing cardiovascular complications.
The most common complication of acute spinal cord injury is still involving the respiratory system. The function of the lungs is caused by the intercondylar muscle spasm. In the multiple trauma patients, direct trauma of the ribs and lung parenchyma can occur. For patients with high quadriplegia, it is often preventive. Intubation, oxygen should be given when the arterial blood oxygen is not enough or respiratory distress, 1 time chest physical therapy should be done every 4 hours, oxygen mask, nasal tube or end-expiratory positive pressure mask can be used to maintain blood gas level in normal Scope; tracheal intubation should be inserted through the nasal trachea as much as possible to avoid tracheotomy, patients with quadriplegia in the neck 1 ~ 4 injury, if there is no spontaneous breathing should be early tracheotomy, and do a good job of chronic airway, intermittent Ultrasonography, electrophysiological examination of the diaphragm and phrenic nerve, in addition, vital capacity, tidal volume and other respiratory parameters should be closely monitored. Patients with acute spinal cord injury, especially those with quadriplegia, such as premature tracheal extubation, may have mucus clogging, lung No, even respiratory distress.
Symptom
Symptoms of closed spinal cord injury Common symptoms Flexor paraplegia reflexes disappeared spinal cord compression High fever Muscular atrophy Sensory disorder Urinary incontinence
1. After spinal cord injury, the spinal cord is completely delayed, the various reflexes, sensation and sphincter function disappear, and recovery begins within a few hours. It recovers completely within 2 to 4 weeks. The more severe injury has spinal shock. In the process, it usually takes 3 to 6 weeks to gradually develop spinal cord functional activity below the level of damage. It is difficult to judge whether the spinal cord injury is functional or organic during the spinal shock period, but the injury is complete at the time or within hours. Loss of sensation, especially the loss of vibration in the limbs, suggesting organic damage, the longer the spinal shock, indicating the more serious the degree of spinal cord injury.
2. Sensory Disorders All types of sensations are lost in the injured plane of the injured spinal cord. Some of the injured people retain some sensations depending on the degree of damage.
3. Transverse injury of motor function. After the spinal cord shock period, the motor function below the damaged plane still disappears completely, but the muscle tension is high and the reflex is hyperthyroidism. Some of the injured people gradually develop some muscle autonomic activity after the shock period, the spinal cord There is a significance of localization diagnosis when there is a sign of the injury of the damaged muscles, the atrophy and the disappearance of the tendon reflex, and the damage of the lower motor neuron.
4. After the shock period of reflex activity, the limb reflex below the damaged plane gradually changes from disappearing to hyperthyroidism, the tension changes from slow to sputum, the complete spinal cord injury is flexor paraplegia, and some lesions show extensor paraplegia, sometimes stimulating lower limbs can cause Unstoppable buckling and urination is called total reflex.
5. Bladder function The spinal cord shock stage is a tension-free neurogenic bladder; the spinal cord shock gradually recovers as a reflexive neurogenic bladder and interstitial urinary incontinence; when the spinal cord returns to reflex, the skin will be involuntarily reflected. Sexual urination, the late manifestation of the contracture neurogenic bladder.
6. Autonomic dysfunction can often occur abnormal penile erection, Horner syndrome, paralytic ileus, skin below the damaged plane does not sweat and have high fever.
7. Some patients have specific manifestations or syndromes after spinal cord injury for diagnosis. In 1985, Brown-Séquard syndrome was proposed. This type of injury is usually caused by a penetrating injury or a stab wound. The cut off, although the pure form of this type of injury is not common in clinical practice, but often patients have similar symptoms, functionally manifested as spinal cord hemisection, other more common syndromes include:
(1) Central spinal cord injury syndrome: It is the most common cervical syndrome, mainly found in older people, especially middle-aged and elderly men. These patients often have vertebral hypertrophy and spinal stenosis before injury. The injury is usually overextended. Sexuality, except for some primary changes such as vertebral hypertrophy, there are no or few abnormal manifestations on the X-ray. The clinical manifestations are quadriplegia, but the upper limbs are heavier than the lower limbs, the upper limbs are delayed, and the lower limbs are paralyzed. Hey, at the beginning, there are bowel movements and sexual dysfunction. Most patients can recover, and gradually improve to achieve a stable level of nerve function. During the recovery process, the lower limbs recover first, the bladder function is second, and the upper limbs, especially the fingers, recover slowly. .
The central spinal cord injury syndrome was originally proposed by Schneider. He believes that it is caused by central gray matter hemorrhage and surrounding white matter edema. According to autopsy studies, American University of Miami scholars believe that this is not absolute, and more is the scattered white matter damage on the backrest side. The new data is consistent with the magnetic resonance results of the patient before and after death, suggesting that the hypertrophy of the ligamentum flavum produces a cutting injury to the spinal cord tissue under overextension.
(2) anterior spinal cord injury syndrome: this type of injury is often caused by excessive flexion or spinal axial load mechanism, often accompanied by spinal fracture and / or dislocation and disc herniation, CT, myelography or magnetic resonance can often show The anterior and spinal cord of the spinal canal is compressed. The clinical manifestations are total motor function loss below the injury level, and loss of lateral beam sensory function (pain and temperature), while posterior bundle function (proprioception and positional awareness) is not affected. It is worse than the central spinal cord injury syndrome.
(3) Conical injury syndrome: Conic syndrome is often accompanied by thoracolumbar spinal cord injury, which is characterized by the involvement of the spinal cord and nerve roots (such as cone and horsetail damage), and the presence of upper motor neurons and lower motor neurons. Injury, conical injury is similar to the prognosis of superior spinal cord injury, ie, the prognosis of complete injury is poor, the prognosis of incomplete injury is better, the prognosis of cauda equina injury is better, like peripheral nerve injury, but complete Conus or spinal cord injury, incomplete cauda equina or nerve root injury is not uncommon. If these patients have sufficient decompression, they may return to their walking state, but if there is a long-term complete cone injury syndrome, the patient will Can not defecate and produce sexual dysfunction.
(4) cauda equina syndrome: the injury of conic injury syndrome is usually from the chest 11 to the waist 1 level, while the cauda equina syndrome is seen from the waist 1 to the level of injury. These patients present as simple lower motor neuron injury. Not only the lower extremity reflex is reduced, but also the intestinal and bladder reflexes are reduced. Clinically, incompleteness and asymmetry are often present, and there is a good prognosis. Patients with severe conus and cauda equina are often chronic intractable pain, which is higher than the high level. See more damage.
(5) Acute Dejerine onion-like syndrome: This type of injury is located in the high neck position due to damage to the spinal cord of the trigeminal nerve. The facial and frontal numbness, sensation loss and sensory loss surround the snout. The level of sensation of the body is still below the clavicle, and the limbs have varying degrees of paralysis.
According to the CT findings of thoracolumbar injuries, Denis l983 proposed the concept of the spine divided into anterior, middle and posterior collaterals. The anterior column includes the anterior longitudinal ligament, the anterior vertebral body and the anterior segment of the intervertebral disc. The middle column includes the posterior part of the vertebral body. Department, posterior longitudinal ligament and vertebral arch; posterior column including vertebral arch, facet joint and posterior ligament complex (spinous ligament, interspinous ligament, ligamentum flavum, joint capsule), when there are two columns or three When the column is damaged, it is considered unstable. The key is whether to maintain the integrity of the center column. This standard also applies to the lower cervical vertebra.
Examine
Examination of closed spinal cord injury
When the lumbar puncture finds blood or shed spinal cord tissue in the cerebrospinal fluid, it proves that the spinal cord is damaged, at least there is bleeding in the subarachnoid space. When the quinine test is obstructed, the spinal cord is under pressure. Both are early indications for surgery. .
1. X-ray film should usually be taken in the right position, side position and double oblique piece, but should prevent the patient from being overly moved for the pursuit of good image results. It is advisable to take the lateral position first.
1 The whole line of the spine is aligned;
2 vertebral fractures, the type of dislocation;
3 attachments have no fractures;
4 Whether there is stenosis or widening of the intervertebral space (revelation of disc herniation and anterior longitudinal ligament rupture, respectively), whether there is a widening of the spinous process gap (indicating the injury of the interspinous ligament), the first two of which have the greatest significance, but sometimes the injury is severely dislocated. Afterwards, the line can be restored, and the stability can be observed by stretching over the flexion position, but it should be used with caution.
2. CT scan axial CT can show the shape of the spinal canal, with or without fractures, and the CT can be injected into the lumbar puncture after injection of water-soluble contrast agent, which can clearly show the displacement of the intervertebral disc and spinal cord, when the spinal cord edema increases. When thick, the annular subarachnoid space can be narrow or disappear.
3. Spinal iodine angiography can show the presence or absence of obstruction in the subarachnoid space, the degree and direction of spinal cord compression, and the involvement of nerve roots.
4. Magnetic resonance imaging is the only means to observe the shape of the spinal cord so far. It helps to understand the nature, extent, extent of the spinal cord injury, and the location of the bleeding and the traumatic syringomyelia. It can help to judge the prognosis, early lesion area of spinal cord injury. The relationship between magnetic resonance signal characteristics and pathological types and prognosis is shown in Table 1. Table 1 shows that the signals on T2-weighted images have characteristic changes in different types of injuries. T1-weighted images often only show thickening of the spinal cord and have localized significance. The obvious shortcoming is that the changes in bone structure by magnetic resonance imaging are unclear.
5. Somatosensory evoked potentials When electrical stimulation of peripheral nerves, potential changes can be recorded in the corresponding sensory areas of the cerebral cortex. The spinal cord injury can be used to determine the integrity of the spinal cord function and structure. After 24 hours of injury, the evoked potential cannot be induced. And after several weeks of continuous examination, there is still no recovery, indicating complete damage; after the injury can lead to evoked potential, or after a period of time can lead to abnormal potential wave, indicating incomplete damage, the disadvantage is that this test only Reflects sensory function and cannot evaluate motor function.
Diagnosis
Diagnosis and diagnosis of closed spinal cord injury
Diagnostic criteria
1. Diagnosis of closed spinal cord injury includes:
(1) The level of spinal injury, type of fracture, dislocation.
(2) Stability of the spine.
(3) The level and extent of spinal cord injury.
The level of spinal injury, dislocation usually only needs to be judged by X-ray film, and the type of fracture is fashionable to refer to CT film.
2. Maintaining the stability of the spine depends mainly on the complete clinical practice of the ligament tissue, and the factors that cause instability are combined:
(1) Front column: compression >50% (at this time, if the height of the middle column does not change, it indicates that the ligament structure is torn at the back).
(2) Middle column: damaged (the other two columns must have a structural incomplete).
(3) posterior column: destruction of bone structure: sagittal dislocation > 3.5 mm (neck) or > 3.5 mm (chest, chest and waist); sagittal angle > 11 ° (neck), > 5 ° (chest, Chest waist) or >11° (waist).
(4) Nerve tissue damage: It indicates that the spine is subjected to strong external force and deformed, displaced, and damaged.
(5) The original joint rigidity: the spine has no ligament support.
(6) Abnormal bones.
3. The standard of atlantoaxial instability
(1) The distance between the posterior edge of the anterior humerus and the anterior border of the odontoid is >3 mm.
(2) The total displacement of the lateral mass of the atlas was shifted to both sides by >7 mm.
The level of spinal cord injury refers to the last section of the spinal cord that retains intact sensation and motor function. Complete injury refers to the sensation including the lowest sacral ganglia, motor function disappears, and the light touch and pain sensation of the anal skin mucosal junction should be examined. And refers to the voluntary contraction function of the anal sphincter. Incomplete injury refers to partial sensation below the level of injury, and the motor function is retained, including the lowest sac.
Differential diagnosis
1. Intraspinal hemorrhage trauma, such as falling from the back or arm on the ground, direct force on the back, etc. can cause bleeding in the spinal canal; vascular malformation, anticoagulant therapy, blood disease and other patients can be mildly injured Hemorrhage (also spontaneous), hematoma can be located in the epidural, subdural, subarachnoid and intramedullary, more acute onset, often root pain, spinal cord compression symptoms, often involving several sections Segment, subarachnoid space and intramedullary hemorrhage, lumbar puncture cerebrospinal fluid was bloody, axial CT showed high density shadow in the corresponding part, MRI showed abnormal signal, early (2 days) T1 weighted image change was not obvious, T2 weighted The image shows a low signal; after that, as the methemoglobin in the red blood cells of the hematoma increases, the T1 time is shortened, and a high signal appears on the T1-weighted image; after about 1 week, the red blood cells rupture, and extracellular methemoglobin appears, which prolongs the T2 time. Therefore, T2 becomes a high signal (it is still a high signal on T1).
2. Tethered cord syndrome When the back of the lower back is directly hit or injured, the symptoms of the original tethered cord syndrome patients may be aggravated, legs may be weak, walking difficulties, sphincter dysfunction, cones can be seen on MRI Low, end silk thickening, more with spina bifida, intraspinal and/or subcutaneous lipoma.
