Table of Contents
Cerebral Hemorrhage within the Three Spaces
In the brain, bleeding can occur in the epidural, subdural, and subarachnoid spaces depending on the cerebral membranes (meninges). The subarachnoid space differs from the other 2 spaces to the extent that it also exists physiologically in the brain. The epidural and subdural spaces, however, are artificially created by the accumulation of blood between the internal lamina of the calvaria and the dura mater (epidural hemorrhage) or between the dura mater and the arachnoid mater (subdural hemorrhage).
Craniocerebral injuries are among the most common causes of death until early adulthood and require immediate treatment. Oxygen is not stored in the brain. Therefore, the brain depends on blood vessels for the supply of oxygen and essential nutrients. Hemorrhage in the brain cuts off this supply and cause death.
The clinical manifestations indicate the etiology. However, computer tomography (CT) is always indicated in emergency situations. The different types of bleeding can be distinguished based on radiological criteria.
Definition of Epidural Hemorrhage
Epidural hemorrhage (epidural = above the dura mater) or extradural hemorrhage refers to bleeding between the inside of the calvaria and the outer periosteal layer of the dura mater. The source is usually arterial bleeding, most commonly originating in the middle meningeal artery or any of its branches, which are especially vulnerable to fractures in the skull bound tightly to the cranial bone. Epidural hemorrhage is most commonly caused by head injury generally associated with fractures of the skull (85–95% of cases), which are associated with malfunction or injury to the brain. A plain injury to the head is known as a cranial contusion (bruise).
Symptoms of epidural hemorrhage
Based on clinical presentation, in approx. 30%–40% of the cases, the 2 phases of unconsciousness include initial loss of consciousness induced by the trauma itself and the second phase of unconsciousness triggered by arterial bleeding displacing brain parenchyma. Most often, it is accompanied by a severe headache.
The phase in between is referred to as the ‘free interval’ and is typical of epidural hemorrhage. The intracranial pressure is increased during the course of hemorrhage due to intracranial compression.
Symptoms associated with increased intracranial pressure include drowsiness, nausea and vomiting, seizure and a steady decline in consciousness. In addition, there may be a so-called ‘papilledema’ also known as optic disc swelling. Further, epidural hemorrhage leads to rapid compression of the 2 cerebral hemispheres resulting in contralateral symptoms including motor coordination disorder with symptoms of paralysis. The hemorrhage can lead to neurological damage, due to which the patient is conscious at one moment and comatose at another moment, and often death occurs in minutes.
Diagnosis of epidural hemorrhage
Epidural hemorrhage is a serious condition warranting emergency treatment. After stabilizing the patient, a computed tomography (CT) of the head is performed to detect or rule out any bleeding. Acute epidural hemorrhage appears in the CT as a hyperdense bi-convex patch with a swirl sign. Magnetic resonance imaging (MRI) is another diagnostic modality used to confirm epidural hemorrhage. X-rays are used to identify fractures and determine their impact on the dura mater. Angiography is also preferred to rule out laceration of the middle meningeal artery or extravasation of the artery into the middle meningeal vein generally known as ‘tram track sign’.
Treatment of epidural hemorrhage
Stabilization of the patient is the 1st priority, which may entail intubation of the patient depending on the level of consciousness. Advanced life support (ALS) protocol is focused on cervical spine control and airway breathing circulation (ABC). Another important element of the treatment approach involves a prompt reduction of increased brain pressure via neurosurgical removal of large hematomas (collection of blood) or solid blood clots. It is accomplished via craniotomy, clipping of the source of bleeding blood vessel (diathermy) or decompressive removal of hematoma. In this case, a hole is made in the calvaria (craniotomy) to relieve the pressure.
Intensive care to prevent or treat post-traumatic cerebral edema includes, among others, elevation in the upper body of the patient up to 30°, ventilation of the patient, administration of plasma expanders, osmotic therapy (= administration of hyperosmolar solutions such as mannitol) as well as the administration of barbiturates or saluretics. Administration of cortisone also lowers the intracranial pressure by reducing edema but is not indicated in traumatic brain injury. Edema increases the rate of complications.
Note: NO physiologically occurring epidural space exists in the brain.
Definition of Subdural Hemorrhage
Subdural (below the dura mater) hemorrhage is defined as bleeding in the potential space created artificially by hemorrhage (see epidural hemorrhage) between the dura mater and the arachnoid mater. The subdural hemorrhage differs from the epidural hemorrhage in that venous bleeding from the bridging veins occurs between venous sinuses and cortex, whereas bleeding as such is usually also triggered by trauma. Due to the lower pressure, the bleeding in veins is slower and space fills much more slowly than in arterial epidural hemorrhage. Intracranial hypotension and dural metastases are the other causes of subdural hemorrhage.
Symptoms of subdural hemorrhage
Subdural hemorrhage clinically resembles epidural hemorrhage as it also leads to symptoms such as increased intracranial pressure, nausea or vomiting. However, due to the slower onset, these symptoms also occur during progression and are usually less pronounced than in epidural hemorrhage.
The most prominent clinical symptom is characterized by a rather slow-progressing so-called organic brain syndrome as well as hemiplegic symptoms with focal failures that lead to focal seizures. A change in personality and impaired intellectual functions are part of organic brain syndrome, prompting patients to seek psychiatric aid.
Fluctuating conscious level, sleepiness, headache, and confusion are the symptoms of subdural hemorrhage. Due to the slow development of subdural hematoma, it can become chronic and independent of previous trauma, and manifest acute symptoms. The resulting neurological deficits are limited to one part of the body (hemiplegic symptoms) and are often mistaken for an acute ‘stroke’.
Diagnosis of subdural hemorrhage
The emergency diagnosis used for subdural hemorrhage is similar to that of epidural hemorrhage based on a CT scan. Other diagnostic possibilities include MRI or angiography. In general, the acute subdural hemorrhage appears hyperdense and crescent-shaped in the CT. When bleeding lasts longer than a month, the detection of subdural hemorrhage is more likely with an MRI because the bleeding in CT often manifests as isodense areas bilaterally.
Treatment of subdural hemorrhage
The treatment of subdural hemorrhage is also based on the neurosurgical removal of hematoma using a burr twist drill and burr hole craniotomy. The faster the hematoma is removed, the better is the prognosis.
Note: There is NO subdural space in the brain.
Definition of Subarachnoid Hemorrhage
The most common cause of subarachnoid hemorrhage is a ruptured arterial aneurysm (blood vessel bulge) of the basilar arteries. 40–50% of aneurysms, and therefore, the majority of them can be found on the anterior communicating artery, followed by the posterior communicating artery and the ophthalmic aneurysm (20–30%). In addition to the innate (congenital) aneurysms, acquired aneurysms exist, for example, in connection with bacterial infection or trauma.
Other possible causes of subarachnoid hemorrhage include:
- Arteriovenous malformations
- Primary intracerebral hemorrhage
- Blood disorders such as hemophilia
- Anticoagulant therapy
- Cerebral venous sinus thrombosis
The bleeding occurs in the subarachnoid space, which also exists physiologically (= below the arachnoid). The bleeding itself can occur spontaneously or may be induced by trauma or other factors. Possible trigger factors include mainly activities that cause an increase in intra-abdominal pressure such as coughing, bending or lifting heavy loads.
However, bleeding occurs during resting phases. A number of risk factors are associated with subarachnoid hemorrhage: hypertension, nicotine, bleeding disorders, mycotic aneurysm or decrease in estrogen levels after menopause and alcohol abuse. Possible complications in the course of subarachnoid hemorrhage include vasospasm of the vessels (especially from day 3 to day 10 after the bleeding), recurrent bleeding and hydrocephalus aresorptivus.
Symptoms of subarachnoid hemorrhage
The most characteristic symptom of subarachnoid hemorrhage is the sudden onset of the so-called ‘thunderclap headache’, which is located in the neck and in the forehead region. Neck stiffness (meningism) may occur due to meningeal irritation. Other possible symptoms include nausea, vomiting, photophobia, collapse, seizures or a decreased level of consciousness, and coma, which are attributed to increased intracranial pressure. Headaches can also occur as a warning symptom of an impending aneurysm bleeding.
Diagnosis of subarachnoid hemorrhage
Bleeding occurs in the subarachnoid space containing the cerebrospinal fluid. Therefore, in case of subarachnoid hemorrhage, blood is present in the cerebrospinal fluid. Depending on the age of bleeding, this fluid has a salmon or xanthochromic discoloration.
The cerebrospinal fluid can be obtained via lumbar puncture. However, it is important that previous contraindications must be excluded. Xanthochromic blood is detected in CSF due to the presence of bilirubin from the breakdown of hemoglobin. Contraindications include increased intracranial pressure or a low platelet count. In addition to lumbar puncture, CT and angiography facilitate the diagnosis of subarachnoid hemorrhage. CT can be used to detect intraparenchymal or intraventricular hemorrhage as hyperdense areas. Angiography is especially indicated for the precise localization of the aneurysm.
Treatment of subarachnoid hemorrhage
Two options are available for the treatment of aneurysm: ‘clipping’, in which the aneurysm is neurosurgically eliminated externally, and ‘coiling’, in which metal spirals (coils) are inserted inside the aneurysm through the blood vessels via a catheter, to seal the aneurysm. Intracranial stents and balloon remodeling can be used to treat wide-necked aneurysms.
Summary of the Differences
|Bleeding location||Type of bleeding||Primary cause||Morphology based on CT scan|
|Epidural hemorrhage||Between the skullcap and the dura mater||Arterial||Traumatic||Lentiform, bi-convex|
|Subdural hemorrhage||Between the dura mater and the arachnoid||Venous||Traumatic||Crescent-shaped|
|Subarachnoid hemorrhage||Between the arachnoid and the pia mater||Arterial||Aneurysm||Detection of blood in the cisterns, between the sulci|
Possible Consequences of Cerebral Hemorrhage
The outcomes of cerebral hemorrhage depend on the type and size of bleeding and possible comorbidities. The precise localization of the bleeding also plays a crucial role in determining whether or not the damage is permanent. Pertinent examples may be the cause of permanent speech disorders (aphasia), motor dysfunction or sensory disturbances due to CNS deficit. Hydrocephalus and raised intracranial pressure are some of the complications. Early rehabilitation is critical to minimize the lasting damage. Patient rehabilitation is already initiated during the hospital stay and continued in specialized institutions.
Coma as a consequence of brain hemorrhage
Coma is a possible consequence of cerebral hemorrhage, which is one of the quantitative disorders of consciousness and is characterized by the inability to be awakened by any external stimulus. Consequently, coma may also be defined as brain death, the irreversible failure of the brain.
Cerebral hemorrhage occurs alongside cerebral ischemia, one of the main causes of coma. Other causes that result in coma include encephalitis or severe brain trauma. Initially, comatose conditions warranting immediate intervention, such as intoxication or related metabolic disorders (diabetes mellitus, uremia, and hepatic coma) are excluded. Therefore, laboratory examination is part of the diagnosis of a comatose patient, including the determination of blood count, blood sugar levels, liver and kidney parameters, electrolytes, thyroid levels and other parameters subject to clinical suspicion.
Third-party anamnesis to establish a tentative diagnosis is especially important because it can suggest the initial etiological insights into a coma. In addition, a neurological examination of the patient is conducted, which may indicate the severity and location of the injury. Based on the Glasgow coma scale (GCS), the severity of the disturbance of consciousness can be quantified based on a score ranging from 3 to 15. Further modalities such as CT or MRI may be indicated for definitive diagnosis.
Significant changes of re-bleeding in the cerebral spaces during the first two months can have life-threatening consequences.