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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):
Etiopathogenesis:
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.
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Diagnosis:
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. |
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CT- large ASDH |
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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. |
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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.
Management: |
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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.
Prognosis:
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):
Etiopathogenesis:
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.
Management:
Nonoperative:
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.
Craniotomy:
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.
Complications:
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%.
Recurrence:
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.
Outcome:
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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