I. Clinical manifestations of epidural hematoma
1, trauma history of the cranial cap, especially the temporal part of the direct violence injury, local scars or scalp hematoma, cranial x-ray film found fracture line across the middle meningeal artery sulcus; or posterior occipital injury, there is soft tissue swelling, subcutaneous bruising, cranial x-ray summary film found fracture line across the transverse sinus; all should pay high attention to the possibility of epidural hematoma.
2, impaired consciousness hematoma itself caused by brain herniation, usually occurs within a few hours to 1-2 days after the injury. Since it is also affected by the primary brain injury, there can be three types of impaired consciousness.
①When the primary brain injury is very mild (concussion or mild cerebral contusion), the initial coma time is very short, and the formation of hematoma is not too rapid, there is a period of clear consciousness between the initial coma and the coma of brain herniation, mostly a few hours or a little longer, more than 24 hours is rare, called the “intermediate waking period”;
If the primary brain injury is severe or the hematoma formation is rapid, the intermediate wakefulness period is not seen, but there may be a “period of improvement in consciousness”, which may be aggravated before waking up, and may also be manifested as a continuous progressive worsening of the disorder of consciousness;
(3) A small number of hematomas occur in the absence of primary brain injury or with very limited cerebral contusions, with no early consciousness disturbance, and only when the hematoma causes brain herniation does consciousness disturbance occur. Most of the casualties had headache, vomiting, irritability or apathy, drowsiness, disorientation, urine loss, etc. before entering the coma of brain herniation, which is sufficient to suggest the occurrence of brain herniation.
In the early stage of cerebellar herniation, the affected side of the arteriolar nerve is stimulated by the address, and the affected side of the pupil may first shrink and become unresponsive to light; with the compression of the arteriolar nerve and midbrain, the side of the pupil immediately shows progressive enlargement, loss of response to light, lid ptosis, and the contralateral pupil also expands. It should be distinguished from primary articulatory nerve injury due to a simple anterior cranial fossa fracture, in which pupillary dilatation is present at the time of injury and does not progressively worsen. In the case of optic nerve damage, the pupil is dilated and an indirect response to light is present.
4, cone bundle sign early appearance of one limb muscle weakness, if there is no progressive aggravation performance, may be the focal signs of brain contusion; if it is slightly late or early appearance with progressive aggravation, it should be considered as a hematoma caused by brain herniation or hematoma compression of motor area. Deafferentation is a late manifestation of cerebral herniation.
5. Vital signs are often progressive increase in blood pressure, slowed heart rate and elevated body temperature. Because most of the hematomas in the temporal region first experience herniation of the cerebellar curtain and then combined with herniation of the foramen magnum, severe respiratory and circulatory disturbances often occur after a period of impaired consciousness and pupillary changes; while hematomas in the frontal or occipital regions may not experience herniation of the cerebellar curtain and occur directly with herniation of the foramen magnum, which may show that once there is impaired consciousness, pupillary changes and respiratory arrest occur almost simultaneously.
Subdural hematoma
Subdural hematoma refers to the accumulation of blood in the subdural cavity. It is the most common intracranial hematoma and often occurs in multiple cases or in combination with other hematomas.
(A) Clinical manifestations of acute subdural hematoma
Since most of them have cerebral contusions and secondary cerebral edema at the same time, the condition is generally more severe. If the cerebral contusion injury is severe or the hematoma formation is rapid, the coma of cerebral contusion injury and the coma of hematoma-induced brain herniation overlap, manifesting as progressive deepening of consciousness without intermediate wakefulness or improvement of consciousness. The increased intracranial pressure and other signs of brain herniation also tend to increase progressively within 1 to 3 days, making it difficult to distinguish them from other acute intracranial hematomas based on clinical manifestations alone.
If the cerebral contusion is relatively mild and the rate of hematoma formation is slow, a period of consciousness improvement may exist, and the signs of increased intracranial pressure and brain herniation may appear after 72 hours of injury, which is a subacute type, and it is difficult to distinguish such hematomas from secondary cerebral edema of cerebral contusion from clinical manifestations. In a few simple subdural hematomas without cerebral contusion, the course of impaired consciousness can be similar to that of epidural hematoma, with an intermediate waking period, except that the intermediate waking period can be longer because of pontine vein hemorrhage.
(B) Clinical manifestations of chronic subdural hematoma
1, chronic intracranial pressure increase symptoms such as headache, nausea, vomiting and optic papillary edema.
2, focal symptoms and signs due to hematoma compression such as mild hemiparesis, aphasia and limited epilepsy, etc.
3, cerebral atrophy, cerebral blood supply insufficiency symptoms such as mental retardation, mental disorders and memory loss. This disease is easily misdiagnosed as neurosis, senile dementia, hypertensive encephalopathy, cerebrovascular accident or intracranial tumor, etc. Middle-aged and elderly people, regardless of the history of head trauma, should think of this disease if they have the above clinical manifestations.
Intracerebral hematoma
The clinical manifestations are mainly aggravated by progressive impairment of consciousness, which is very similar to acute subdural hematoma. The process of impaired consciousness is affected by the degree of primary brain injury and the speed of hematoma formation, and those caused by depression fracture may have an intermediate waking period.
Intraventricular hemorrhage and hematoma
In addition to the clinical manifestations of primary brain injury, cerebral edema and other intracranial hematomas, intracerebroventricular hematoma may block the cerebrospinal fluid circulation pathway and cause hydrocephalus, resulting in an acute increase in intracranial pressure, making the impairment of consciousness more severe; blood stimulation of the ventricles may cause hyperthermia and other reactions, generally lacking focal symptoms or signs. V. Delayed traumatic intracranial hematoma Delayed traumatic intracranial hematoma refers to the absence of hematoma at the first CT examination after injury, but the hematoma is found in subsequent CT examinations, or a new hematoma is found at the site where there was no hematoma, and this phenomenon can be seen in various traumatic intracranial hematomas. The clinical manifestation is the appearance of increased intracranial pressure after a period of post-injury stabilization, such as increased progressive impairment of consciousness, and the confirmation of the diagnosis depends on the comparison of multiple CT examinations. Delayed hematoma is common within 24 hours after injury, while the incidence is higher within 6 hours and less after 14 hours.
I. Epidural hematoma
The mechanism of formation is closely related to skull injury, where a fracture or transient deformation of the skull tears through the dural artery or venous sinus located within the bony sulcus causing bleeding, or bleeding from the plate barrier of the fracture. The blood accumulates between the skull and dura mater, and during the separation of the dura mater from the skull, some small vessels can be torn again, making the hematoma even larger. Since the dura mater in the skull cap is loosely attached to the skull bone and can be easily separated, and the dura mater at the base of the skull is tightly attached to the skull bone, epidural hematoma is usually seen in the skull cap. The amount of bleeding required to cause increased intracranial pressure and brain herniation may vary depending on the speed of bleeding, compensatory function, and the severity of the primary brain injury.
The source of hemorrhage is most commonly the middle meningeal artery, whose main trunk or anterior branch has a rapid hemorrhage rate and can become symptomatic within 6-12 hours or less; a few hematomas formed by bleeding from venous sinuses or plate barriers can become symptomatic later and can manifest as subacute or chronic types. Direct hematomas occur most often in the temporal region, mostly as a single hematoma, but a few may be multiple, located in one or both cerebral hemispheres, or above or below the cerebellar curtain. Clinical manifestations and diagnosis
1, trauma history of the cranial cap, especially the temporal part of the direct violence injury, local scars or scalp hematoma, cranial x-ray film found fracture line across the middle meningeal artery sulcus; or posterior occipital injury, soft tissue swelling, subcutaneous bruising, cranial x-ray summary film found fracture line across the transverse sinus; all should pay great attention to the possibility of epidural hematoma.
2, impaired consciousness hematoma itself caused by brain herniation, usually occurs within a few hours to 1-2 days after the injury. Since it is also affected by the primary brain injury, there can be three types of impaired consciousness.
①When the primary brain injury is very mild (concussion or mild cerebral contusion), the initial coma time is very short, and the formation of hematoma is not too rapid, there is a period of clear consciousness between the initial coma and the coma of brain herniation, mostly a few hours or a little longer, more than 24 hours is rare, called the “intermediate waking period”;
If the primary brain injury is severe or the hematoma formation is rapid, the intermediate waking period is not seen, and there may be a “period of improvement in consciousness”, which may be aggravated before waking up, or may be manifested as a continuous progressive worsening of the disorder of consciousness;
(3) A small number of hematomas occur in the absence of primary brain injury or with very limited cerebral contusions, with no early consciousness disturbance, and only when the hematoma causes brain herniation does consciousness disturbance occur. Most of the casualties had headache, vomiting, irritability or apathy, drowsiness, disorientation, urine loss, etc. before entering the coma of brain herniation, which is sufficient to suggest the occurrence of brain herniation.
In the early stage of cerebellar herniation, the affected side of the arteriolar nerve is stimulated by the address, and the affected side of the pupil may first shrink and become unresponsive to light; with the compression of the arteriolar nerve and the midbrain, the pupil on that side immediately shows progressive enlargement, loss of response to light, lid ptosis, and the contralateral pupil also expands. It should be distinguished from primary articulatory nerve injury due to a simple anterior cranial fossa fracture, in which pupillary dilatation is present at the time of injury and does not progressively worsen. In the case of optic nerve damage, the pupil is dilated and an indirect response to light is present.
4, cone bundle sign early appearance of one limb muscle weakness, if there is no progressive aggravation performance, may be the focal signs of brain contusion; if it is slightly late or early appearance with progressive aggravation, it should be considered as a hematoma caused by brain herniation or hematoma compression of motor area. Deafferentation is a late manifestation of cerebral herniation.
5. Vital signs are often progressive increase in blood pressure, slowed heart rate and elevated body temperature. Because most hematomas in the temporal region first undergo herniation of the cerebellar curtain and then are combined with herniation of the foramen magnum, severe respiratory and circulatory disturbances often occur after a period of impaired consciousness and pupillary changes; hematomas in the frontal or occipital regions may not undergo herniation of the cerebellar curtain and directly herniate the foramen magnum, which may manifest as pupillary changes and respiratory arrest occurring almost simultaneously once there is impaired consciousness. CT examination can also be used to clearly localize, calculate the amount of hemorrhage, understand ventricular compression and displacement of midline structures, as well as cerebral contusion, hydrocephalus, and the coexistence of multiple or multiple hematomas.
Subdural hematoma
A subdural hematoma is an accumulation of blood in the subdural space. It is the most common intracranial hematoma and often occurs in multiple cases or in combination with other hematomas.
(A) Acute dural
Acute subdural hematoma is divided into compound hematoma and simple hematoma according to whether it is accompanied by cerebral contusion surface. The source of hemorrhage in compound hematomas can be cortical arterial or venous rupture due to cerebral contusion, or it can be an intracerebral hematoma that penetrates the cortex and flows into the subdural space. Most of these hematomas are caused by hedonic cerebral contusions and are more likely to occur at the tremor pole, the pole of the brain, and its base. Simple hematomas are less common and are the result of pontine vein injury. These hematomas may not be associated with cerebral contusions and are more extensive over the surface of the cerebral hemispheres.
Clinical presentation and diagnosis
Because most cerebral contusions and secondary cerebral edema are present at the same time, the condition is generally more severe. If the cerebral contusion is severe or the hematoma is formed rapidly, the coma of cerebral contusion and the coma of hematoma-induced brain herniation overlap, showing progressive deepening of consciousness without intermediate wakefulness or improvement of consciousness. The increased intracranial pressure and other signs of brain herniation also tend to increase progressively within 1 to 3 days, making it difficult to distinguish them from other acute intracranial hematomas based on clinical manifestations alone.
If the cerebral contusion is relatively mild and the rate of hematoma formation is slow, a period of consciousness improvement may exist, and the signs of increased intracranial pressure and brain herniation may appear after 72 hours of injury, which is a subacute type, and it is difficult to distinguish such hematomas from secondary cerebral edema of cerebral contusion from the clinical manifestations. A few simple subdural hematomas without cerebral contusions have a similar course of impaired consciousness as epidural hematomas, with an intermediate wakefulness period, which can be longer only because of pontine vein hemorrhage.CT examination: crescentic or semilunar shadows of high density, isointensity or mixed density between the intracranial plate and the brain surface can help confirm the diagnosis.
(ii) Chronic subdural hematoma
It may be a relatively independent disease from cranial injury, and its source of bleeding and pathogenesis are not fully understood. It occurs in elderly people over 50 years of age with only minor head trauma or no history of trauma, and in some patients with vascular or hemorrhagic disease. The hematoma may occur on one or both sides, mostly covering the temporal frontal surface of the brain, between the dura mater and the arachnoid, forming a complete envelope. The hematoma increases slowly, usually after 2 or 3 weeks, and causes clinical signs due to both direct pressure on the brain and increased intracranial pressure. Regarding the cause of hemorrhage, it may be related to the relative increase in intracranial space in senile brain atrophy, which, when encountering a slight inertial force, produces relative motion between the brain and the skull, causing hemorrhage by tearing the pontine vein entering the superior sagittal sinus.