Traumatic Intracranial Haematoma

Traumatic Intracranial Haematoma

Types of intracranial haematoma can be classified into

Intracerebral or intraparenchymal which are hypodense on CT scan and small ones may enlarge and may need evacuation-1

2- Extradural or Epidural haematoma

3- Acute subdural haematoma

4- Chronic subdural haematoma

The various traumatic intracranial hematomas contribute to death and disability secondary to head injury. Hematomas can expand rapidly and cause brain shifting and subsequent herniation. Emer­gent neurosurgical evaluation and intervention are often necessary.

Extradural or Epidural Hematoma.

Epidural hematoma (EDH) is the ac­cumulation of blood between the skull and the dura. EDH usually
results from linear squamous temporal skull fractures with arterial disruption. especially of the middle meningeal artery. they can also arise from fractured bone edges or rarely from laceration of the dural venous sinuses the potential space between the dura and the bone is developed by the expanding haematoma allowing it take on the familiar convex lens configuration due to the adherence of the dura to the inside of the cranium the degree of trauma does not have to be severe and may in fact be trivial trauma there is classically a lucid interval following the trauma they are more likely to occur in the young age group as the dura is able to strip more readily off the underlying bone and also The dura is adherent to bone and some pressure is required to dissect between the two. EDH has a classic three-stage clinical presentation that is probably seen

in only 20% of cases. The pa­tient is initially unconscious from the concussive aspect of the head trauma. The patient then awakens and has a lucid interval while the hematoma subclinically expands. As the volume of the hematoma grows. the decompensated region of the pressure-volume curve is reached, the ICP increases, and the patient becomes lethargic and herniates. Uncal herniation from an EDH classically causes ipsilat­eral third nerve palsy and contralateral hemiparesis.

On head CT the clot is bright, biconvex (lentiform). and has a

well-defined border that usually respects cranial suture lines. the clot generally forms over the convexities, but may rarely occur in the posterior fossa as well

Open craniotomy for evacuation of the congealed clot and hemostasis is indicated for EDH. an extradural haematoma is a surgical emergency that will result in death if haematoma os not removed promptly except in selected cases of asymp­tomatic clots that are less than 1 cm in maximum thickeness, seen in patients with a negative neurologic examination. Prognosis after successful evacuation is better for epidural hematoma than subdural hematoma. EDHs are associated with lower-energy trauma with less resultant primary brain injury. Good outcomes may be seen in 85 to90% of patients, with rapid CT scan and intervention

Acute Subdural Hematoma.
An acute subdural hematoma (SDH) is the result of an accumulation of blood between the arach­noid membrane and the dura. Acute SDH usually results from ve­nous bleeding, usually from tearing of a bridging vein running from the cerebral cortex to the dural sinuses. The bridging veins are sub­ ject to stretching and tearing during acceleration/deceleration of the head. because the brain shifts in relation to the dura, which firmly adheres to the skull. Elderly and alcoholic patients are at higher risk: for acute SDH formation after head trauma due to the greater mobility of their atrophied brains within the cranial vault

On head CT scan. the clot is bright or hyperdens or mixed-density, crescent or concave­
shaped (lunate). may have a less distinct border, and does not cross the midline due to the presence of the falx. Most SDHs are over the cerebral hemispheres, but they may also layer on the tentorium or be interhemispheric

Open craniotomy for evacuation of the clot is indicated for any
acute SDH more than 1 cm in thickness, or smaller hematomas that are symptomatic. Symptoms may be as subtle as a contralat­ eral pronator drift, or as dramatic as coma. Smaller hematomas may stabilize and eventually reabsorb. or become chronic SDHs. Non op­eratively managed patients require frequent neurologic exams until stabilization of the clot if proven by serial head CT scans

The prognosis for functional recovery is significantly worse for
acute SDH than EDH. because it is associated with greater primray injury to brain parenchyma from high-energy impacts. Prompt recognition and intervention minimizes secondary injury.elderly patients, patients with low admission GCS, or high postoperative ICP do poorly, with as few as 5% attaining functional recovery

Chronic Subdural Hematoma

Chronic. SDH is a collection of blood breakdown products that is at least 3 weeks old. Acute hematomas are bright white (hyperdense on CT scan for approxi­mately 3 days. after which they fade to isodensity with brain, and then to hypodense after 2 to 3 weeks. A true chronic SDH will be as dark as CSF on CT.Traces of white are often seen due to
small hemorrhages into the collection. These small bleeds may ex­pand the collection enough to make it symptomatic. This is re­ferred to as acute-on-chronic SDH
appearance of an acute-on-chronic SDH. Vascularized membranes form within the hematoma as it matures. These membranes may be the source of acute hemorrhage.

Chronic SDHs often occur in patients without a clear history of
head trauma, as they may arise from minor trauma. Alcoholics. the elderly. and patients on anticoagulation are at higher risk for devel­oping chronic SDH. Patients may present with headache. seizure. confusion, contralateral hemiparesis, or coma.

A chronic SDH thicker than I cm, or any symptomatic SDH
should be surgically drained. Unlike acute SDH, which consists of a thick. congested clot, chronic SDH typically consists of a viscous fluid, with a texture and the dark brown color reminiscent of motor oil. As such, a simple burr hole can effectively drain most chronic SDHs. There remains controversy about the optimum treatment of chronic SDH, but most authorities agree that burr hole drainage should be attempted first, to obviate the risks of formal craniotomy. A single burr hole placed over the dependent edge of the collec­ tion can be made, and the space copiously irrigated until the fluid is clear. A second. more anterior, burr bole can then be placed if the collection does not drain satisfactorily due to containment by membranes. The procedure is converted to open craniotomy if the SOH is too congealed for irrigation drainage. the complex of mem­branes prevents effective drainage. or persistent hemorrhage occurs that cannot be reached with bipolar cautery through the burr hole. The required surgical prepping and draping are always performed

to allow simple conversion to craniotomy, and the incisions and burr holes placed to allow easy incorporation into question mark-shaped craniotomy flaps.

There are various strategies to prevent reaccumulation of blood.

Subdural or subgaleal drains may be left in place for I to 2 days. Mild hydration and bed rest with the head of bed flat may encourage brain expansion. High levels of inspired oxygen may help draw nitrogen out of the cavity. Regardless of the strategy used, follow-up head CT scans are required immediately postoperatively and approximately  month later to document resolution

Intraparenchymal Hemorrhage. Isolated hematomas within the brain parenchyma are more often associated with by­ pertensive hemorrhage or arteriovenous malformations. Bleeding may occur in a contused area of brain. Mass effect from develop­ing hematomas may present as delayed neurologic deficit. Delayed traumatic intracerebral hemorrhage is most likely to occur within the first 24 hours. Patients with contusion on the initial head CT scan should be reimaged 24 hours after the trauma to document stable pathology


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