Definition
Subdural fluid accumulation is an accumulation of cerebrospinal fluid in the subdural space after trauma. It accounts for 0.5% to 1% of craniocerebral trauma, and often occurs in one or both frontal temporal areas, with bilateral frontal areas being the most common. Subdural fluid can be divided into acute and chronic, generally acute is rare and forms within a few hours, chronic can have envelope.
Mechanism of formation
1, “live flap” theory: after cranial injury, causing small rupture of the cerebral arachnoid,
The cerebrospinal fluid can only enter the subdural cavity without reflux, or after the fluid enters the subdural cavity, the arachnoid rupture is blocked by blood clots or edema, causing the cerebrospinal fluid to accumulate in the subdural cavity, resulting in the formation of subdural fluid.
2.Osmosis theory: After cranio-cerebral injury, the blood-brain barrier is destroyed, capillary permeability is enhanced, and a large amount of plasma components are leaked out, which increases the protein content and high osmotic pressure, which infiltrates the surrounding brain tissue and water in the subarachnoid space into the effusion, and the effusion continuously increases and forms.
3, pressure theory: craniocerebral injury due to trauma instantaneous pressure imbalance in various intracranial cavities, resulting in the rupture of the arachnoid membrane, cerebrospinal fluid to the low pressure area, the formation of subdural effusion.
Characteristics of the condition
1. The fluid accumulation mostly occurs in patients with primary craniocerebral injury with occipital landing and GCS score of 3-12 at the time of admission.
2.Most patients have cerebral contusions and subarachnoid hemorrhage, especially frontotemporal cerebral contusions.
3, the site of fluid accumulation is mostly in the frontotemporal area on the curtain or the adjacent parts, mostly occurring in the hedge part of the force, occurring in the subcurtain is very rare.
4, primary craniocerebral injury is relatively light, there may be no or only a short period of impaired consciousness after the injury, with the increase of fluid and coma or deepening of impaired consciousness.
Clinical typing and performance
1, receding type: young adults, generally no obvious symptoms of increased intracranial pressure, or only in the early symptoms of mild intracranial pressure increase, and then gradually improve, no positive signs of the nervous system. It can be explained by the theory of arachnoid rupture, that is, when the head is traumatized, the arachnoid membrane in the lateral fissure, the optic chiasm and the pterygoid crest are closely adhered to tear, resulting in the outflow of cerebrospinal fluid and accumulation in the subdural cavity, which is gradually absorbed and reduced later.
2, stable type: the majority of elderly people, most patients with dizziness, dizziness, nausea, vomiting, euphoria, apathy, depression, memory loss as the main manifestations, generally no subdural fluid-related positive signs of the nervous system. Long-term observation of this type can be transformed into a receding or evolving type.
3.Progressive type: common in children. The main manifestation is progressive intracranial pressure increase, the patient may have light hemiparesis, aphasia, mental abnormalities, infants and children may have similar hydrocephalus manifestations, if combined with brain parenchymal injury, can be accompanied by impaired consciousness and pathological signs.
4.Evolutionary type: The clinical characteristics are polarization of the age of onset, often occurring in children under 10 years old or in the elderly over 60 years old, which may be related to the larger subdural cavity in children and the elderly. It often occurs within 22-100 days after the effusion, and during the course of conservative treatment, the effusion may turn into a hydatid tumor, and the pericardial hemorrhage occurs after the formation of the pericardium, leading to a chronic hematoma, which often occurs after 1 month of the effusion. Since early surgery interrupts the process of fluid transformation into hydatid and pericardial formation, the evolution of traumatic subdural fluid into chronic subdural hematoma is not likely to occur in surgically treated cases.
Diagnosis
1.History of head trauma.
2.Signs and symptoms of the nervous system.
3, imaging can confirm the diagnosis. CT shows a crescentic hypodense area in the frontotemporal roof, often into the anterior part of the longitudinal fissure, brain tissue compression, CT value of 0-10Hu.
Differential diagnosis
Chronic subdural hematoma:
The hematoma is generally high signal in T1 and T2, and the effusion is consistent with the signal of cerebrospinal fluid, showing low signal in T1 and high signal in T2, which can be differentiated.
Chronic subdural hematoma.
Subdural effusion.
Treatment
I. Non-surgical treatment:
1, caution or do not use dehydrating agents, in order to avoid the increase of fluid accumulation due to low cranial pressure.
2, the application of neurotrophic drugs, cerebral vasodilators, drugs to inhibit the secretion of cerebrospinal fluid, hyperbaric oxygen therapy, in order to improve cerebral blood circulation and metabolism, for the brain tissue expansion reset to narrow the subdural space to provide the possibility.
Second, surgical treatment:
A. Principles:
① Eliminate the brain pressure of fluid accumulation;
② Eliminate the cause of fluid accumulation;
(3) Eliminate the cystic cavity of the effusion.
Only when the above three principles are met can we prevent the recurrence of effusion and achieve the purpose of complete cure.
B. Indications for surgery:
①If there are clinical symptoms of neurological compression or epileptic seizures, regardless of the amount of effusion, surgery should be used to remove the effusion and release the compression.
②If the volume of supratentorial fluid is >25ml or subratentorial fluid is >8ml, surgery should be performed even if there is no neurological compression to facilitate recovery.
③The occupying effect is more serious, there are obvious symptoms of cranial hypertension, and the imaging examination (CT or MRI) shows that the ventricle and brain pool are compressed, deformed, and the midline is shifted >10mm.
④ Infants and children with frontal space >6mm.
C. Surgical methods:
①Puncture and drainage.
②For patients with unclosed fontanelle, use a common venous 7-gauge trocar to percutaneously puncture the lateral corner of fontanelle for continuous drainage.
③In case of combined intracranial hematoma, severe cerebral contusion and brain herniation, early craniotomy should be performed to remove the hematoma and fluid and decompress the bone flap.
④Intracranial shunt: Although the clinical symptoms improve after external drainage, the effusion does not decrease or increases again after the drainage tube is removed or the clinical symptoms worsen.
D. The effect of surgery is:
①The drainage effectively reduces the intracranial pressure and interrupts the vicious cycle of increased pulsatile action due to intracranial hypertension.
②Removal of fluid with high protein content that cannot be easily absorbed.
③Subdural drainage facilitates the flow of exudate from brain tissue to the surface of the brain, without contributing to or aggravating cerebral edema by leakage into the interstitial space.
E. Surgical precautions:
1.Prevention of pneumocranial:
① Place a tube immediately after dural incision to avoid the outflow of cerebrospinal fluid and the entry of excessive gas;
② Not rushed to release fluid after placement, to close the incision and then connect the drainage bottle to close the drainage, otherwise there is still the possibility of intracranial gas because the incision is not closed;
③The drainage tube should not be elevated before connecting to the drainage bottle but should be clamped, otherwise there is a possibility of gas entering the skull from the drainage tube;
④Change the drainage bottle to pay attention to the clamped tube and keep the low position.
2, prevention of brain injury: drainage tube should be strictly biased towards the direction of the dura mater, do not adhere to the brain tissue, so as to avoid damage to brain tissue when intubating or extubating.
3, postoperative attention should be paid to replenish isotonic fluid, drainage tube elevated 15cm, to maintain normal cranial pressure, if necessary, lying down or head down position, conducive to brain tissue reset.
Prognosis
Regressive type: Generally no neurological abnormalities remain.
Stable type: Generally, the prognosis is also good, and most of the neurological system recovers well.
Evolutionary type: Almost all of them can be cured by early surgery and cranial drainage.
Progressive type: there may be some mortality due to combined parenchymal injury or postoperative complications, and the mortality rate of traumatic subdural effusion with combined parenchymal injury is reported to be 12%-25% in the literature.