Subdural hematomas: 

Dr. Krishna Sharma, 
Senior Neurosurgical Registrar,  Chennai , India.

An accumulation blood between the dura and the archnoid constitutes subdural haematoma. The classical view is that the subdural space is a preexisting space although, electron microscopy suggests no evidence of naturally occurring space at the dura-arachnoid junction.

Subdural hematoma (SDH) may accumulate on any site of the inner surface of the skull. Longitudinal cerebral fissure is a rare location.

Acute subdural hematoma (ASDH):


The incidence varies from 5 to 22% of severe head injuries; more common in men and those  above 40 years of age compared to extramural haematoma.


The ASDH results from high speed rotational acceleration injuries of the brain in relation to the fixed dural structure and can occur during deceleration also. This causes either tearing of surface or bridging veins between the cortical surface and venous sinuses. The bridging veins are 1-2 cm long and occur in the largest in the frontal and parietal regions.

If it is associated with extensive area of lobar contusion and ICH, this combination is often referred to as a burst lobe.

If it is above 100ml and the only cause of increased ICP, it is called true ASDH; it occurs mainly in small children, elderly and alcoholics. Almost ten times more common is a group of small volume hematomas, with disproportionate mass effect due to intrinsic brain injury.

The commonest site is the anterior temporal region but inferior frontal, parietal, bilateral haematomas are encountered. There may be a combination of EDH SDH & ICH also.

Rare causes are anticoagulants and coagulopathies. Rarer still,  are those due to rupture of an aneurysm.


Ischemic brain damage occurs below the haematoma. Haematoma as well the underlying brain releases vasoactive and neurotoxic substances. It is also found that autoregulation of brain is disturbed following the injury causing impaired cerebral blood flow. Decoupling of cerebral edema of the underlying brain aggravating the effect of direct actions of the neurotoxic and vasoactive substances. The substances are thought to be ghetamate, aspartate, free radicals, platelete aggravating factors, etc. These secondary auto destructive procedure play to greater role in the clinical manifestation, and prognosis of the patient than the damage due to primary injury. This was substantiated by the low morbidity & mortality (20%) in cases where the arachnoid matter was not breached. Ischemic brain damage is not reversible even after removing the clot.


Diffuse axonal injury may coexist since the etiopathogenesis of ASDH and DAI being the same. The clinical picture and the outcome is dominated mainly by DAI.

Clinical features:

They result from raised ICP. Loss of consciousness from the time of injury suggest underlying brain injury rather than ASDH alone; the patient deteriorates rapidly. In 60% brainstem damage is found with bilateral babinski sign, respiratory disorders, pulse and systemic blood pressure fluctuations.


Differentiating between EDH and ASDH is usually impossible. Early onset of impaired consciousness suggest ASDH. CT scan helps. and is the choice of imaging.

CT scan done immediately after the trauma may not reveal the hematoma, but reveals the signs of increased ICP, such as  narrowing of the ventricles, and obliteration of sulci.

       CT- large ASDH
Plain Xray - A limited value in presence of CT scan as it gives little information and delaysdiagnostic evaluation except in case of associated depressed fracture and localizing CSF fistula.

CT scan - The most important diagnostic aid. ASDH appear as a crescentric (cancavoconvex) mass of increased attenuation adjucent to inner table prominent surround edema, brain contusion.

        CT- shallow ASDH
 MRI scan is more sensitive and helpful in isodense haematoma & to defect parenchymal injury and DAI. Disadvantage takes too long to perform & has too many restriction.


The mode of treatment is influenced by

            CT-  ASDH

A. Contribution of ASDH to the overall neurological status of the patient & the part responsible by associated brain injury.

B. Associated raised intracranial pressure. In condition where all the potential spaces have been exhausted, decompressive procedure may play a significant role to reduce ICP.

C. General condition and neurological status of the patient. After aggressive resuscitation if the patient remains flacoid and brain stem reflexed are absent, it will not make any contribution by performing surgery. Patient with no/or minimal neurological deficit do better after surgery.

D. Size of haematoma :- More than 5 mm thick ASDH contributing significantly to the mass effect & shift have good surgical outcome. Smaller SDH with minimal mass effect in a neurologically intact patient may not require surgical swelling.

E. Age : >65 year old patient do not do well ever with timely and adequate surgery. Their mortality rate equating with those managing non surgically.

Thus decision to operate involves a critical analysis of the contribution of the hematoma to the overall condition of the patient.

In case of large hematomas, surgical evacuation and securrring the bleeding cortical vessels is mandatory. If required,  bone flap may be emoved. Post operatively, aggressive monitoring and treatment of brain injury is warranted.


It is usually poor in ASDH and depends on the primary brain injury. Despite medical efforts mortality is about 80%. Most of the survivers have protracted convalescence and effects of post traumatic syndrome and about 25% will develop seizure disorders.

Chronic subdural hematomas (CSDH):


The incidence varies from 1-2 per 100,000 people per year. Over 75% occur in patients over 50years of age. 25% to 50% of the patients have no significant history of head injury. Chronic alcoholics, epileptics, and those with coagulopathy are more prone. Reduction in ICP like after shunt surgery in infants and children also predispose to SDH.

Initial hemorrhage from a torn bridging vein, following head injury (often trivial), may be small and asymptomatic.

The clot lyse (after about 60 hours); there is angioblastic invasion of clot (4-14 days). The clot breaks down and vascular sinusoids appear in the capsule(2-3 weeks), which become well developed (3-4 weeks) prior to liquefaction of the clot (4-6 weeks).

Some undergo spontaneous absorption, some clots get organized, and some enlarge.

The organized clot gets surrounded by a covering membrane. On the dural side efforts at absorption of the clot lead to the formation of vascular and often pigmented fibrous tissue, whereas the deeper layer adjacent to archnoid is thin. Compaction and fibrosis of the membranes of both sides occur (1-3 months). The membranes become fused consisting of mature fibrous tissue (3-12 months) and proceed to calcification and ossification (about 1 year).

The exact mechanism of enlargement of the hematoma is not known.

1) Osmotic gradient between the hematoma and the CSF space facilitates the enlargemet.Various theories exist:

Gardner (1932): The capsule acts as an osmotic membrane with CSF diffusing into hyperosmotic hematoma.     

Zollinger and Gross (1934): The flow across the membrane occurs as a result of an increase in osmotic pressure from a breakdown of hemoglobin molecules in red cells.     

Gitlin (1955): The albumin/gamma globulin and albumin/total protein ratios in the hematoma are higher than in serum. Because albumin is not found within red cells, the albumin has to diffuse across the membrane.    

Weir (1971): There is no significant difference in osmolality with increasing age of the hematoma and no significant difference in osmolality of blood and hematoma.  

Sato and Suzuki (1975): The capillary endothelial cells of chronic SDH capsule have cytoplasmic protrusions and fenestrations which are associated with high permeability and permit passage of protein moieties into the hematoma. 

Itoh (1978): The fibrionlytic enzymes in the hematoma membrane enhance the chance of recurrent hemorrhage into the hematoma cavity.  

Yamashima (1984): The most important factor for the development of Ch. SDH exists in the vessls of the capsule which have a marked proliferation potential and a fragile nature; the endothelial gap junctions of macrocapillaries in the outer membrane of SDH play a role in the leak of blood, causing enlargement of SDH.

2) Recurrent bleed from the outer membrane is a feasible theory. The content near the outer membrane is often shaggy and brighter in color. This also explains waxing and waning of the symptoms in patients with ch.SDH.

3) Periodic bleeding from a venous stump has been suggested by Furtado.

4) Low ICP has been suggested as a cause by Kopp.

5) Leakage of CSF from a rupture neighboring arachnoid granulations into the hematoma has also been  blamed.

There are three types:

Type I   -CSDH with a visible inner membrane: It is an expanding lesion.

Type II  -ASDH  in chronic healing stage: It is not an expanding lesion; lacks a visible inner membrane.

Type III -CSDH of hemorrhagic type: CSDH in which minimum amount of fresh blood is added to a maximum amount of xanthochromic fluids.

Clinical features:

The symptoms are variable. Impaired consciouness (53%), hemiparesis (45%), papilledema (24%), dysphasia (14%), 3rd nerve palsy (11%), and hemianopia (7%) are the common signs. Rare symptoms are  parkinsonism, and  monoparesis.


CT scan is the imaging of choice. After 3 weeks the majority of SDH will be hypodense and assume a lenticular appearance; because of recurrent hemorrhage, some may have heterodensity.  

MRI scan delineates the lesion better. CT- Bil. CSDH    in varying stages   CT- Bil CSDH   MRI- Bil. CSDH



In selected patients, with minimal signs and shallow SDH in a scan, nonoperative management with bed rest, cortico-steroids, and diuretics has been successful. But the treatment is prolonged, more expensive than surgical evacuation, and often unsuccessful.

Burr holes:

This is the most common mode of evacuation. Some prefer to place a drain to prevent a recollection. Some advocate intrathecal infusion of saline for reexpanding the brain in cases where the cortex do not surface after evacuation. Many feel such measures are of no use.


It provides access to solid components and the membrane thereby reduces the risk of recollection.

Twist-drill holes:

This may be performed at the bedside in an emergency. A catheter is passed into the subdural space and connected to a closed drainage system.


Rapid evacuation can cause brain shift and brainstem hemorrhages.

In bilateral hematomas, both should be evacuated simultaneously, otherwise the remaining hematoma can cause a rapid brain shift.

Seizures in the postoperative period are reported in up to 11%.


It has been reported that 78% of the post operative CTs show residual collection. However, evacuation of only a portion of the hematoma produces clinical improvement and the residual collection will gradually resolve. 

True reaccumulation has been reported in 8-45% of cases according to various reports.Recurrence was reported to occur more often (37%) following craniotomies than in burr-hole patients (20%).

Post operative re-evacuation is possible by needle aspiration or reoperation, if the patient deteriorates. Some may require a craniotomy and excision of the subdural membrane. Some suggest complete obliteration of the subdural space into epidural space; the subdural pocket is exteriorised so that it is in continuity with subgaleal space through a limited craniectomy. Some claim no difference with or without any of these procedures.

Recurrent SDH in a patient with shunt system may warrant blocking the system temporarily.


75% of patients resume normal activities. the preoperative neurological status is closely related to the outcome. Size of the hematoma does not influence the outcome.






































































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