Intracranial hematomas

Intracranial hematomas

1. Intracranial hematomas Dr. Sachit Koirala Resident, 2 nd Year Department of Surgery, KISTMCTH

2. Intracranial hemorrhage ( ie , the pathological accumulation of blood within the cranial vault) may occur within brain parenchyma or the surrounding meningeal spaces. Intracerebral hemorrhage is more likely to result in death or major disability than ischemic stroke. May occur within brain parenchyma or the surrounding meningeal spaces.

3. Types Traumatic Non traumatic

4. Traumatic intracranial hematoma

5. Biomechanical basis of TBI

6. Clinical classification of brain injuries 3 distinct categories 1. Skull fracture may not involve damage to the underlying brain the fracture is often not a direct cause of neurological disability 2. Focal injury visible damage to the parenchyma that is generally limited to a well-circumscribed region injuries occur in nearly half of all patients with severe brain injuries responsible for approximately two-thirds of brain injury–related deaths include contusions to the cortex and subdural, epidural, and intracerebral hematomas 3. Diffuse brain injury often occur without producing macroscopic structural damage approximately 40% of patients with severe brain injuries

7. Diffuse brain injury 1/3 rd deaths from brain injury most prevalent cause of disability in survivors of traumatic brain injury. In its mildest form (concussion), diffuse brain damage may not necessarily be structural and may involve only alterations in neural excitability, neurotransmission, or long-term changes in receptor dysfunction. In more severe cases, diffuse brain injury manifests as prolonged coma without mass lesion and involves some degree of structural derangement at the microscopic level. Diffuse brain injury includes damage from both brain swelling and ischemic injury. The most commonly injured substrate in diffuse brain injury is the axons within the white matter; for this reason, the prominent form of diffuse brain injury is termed diffuse axonal injury

8. Biomechanical mechanisms Static or quasi-static loading Uncommon occurrence Force applied to the head very slowly >200ms 2. Dynamic loading Dynamic loading is applied rapidly <50ms Three types: impulsive, impact, or blast overpressure

9. Impulsive loading: head is set into motion indirectly by a blow to another body region or by the sudden motion of another body region (e.g., torso). Impact loading: result of motor vehicle accidents, falls, or sports collisions. Impact loading usually results from a combination of contact forces and inertial (acceleration) forces. For objects larger than approximately 2 square inches, localized skull bending occurs immediately beneath the impact point. If the skull deformation exceeds the tolerance, skull fracture occurs. Blast overpressure loading: delivery of a rapid-onset, very short (<5 ms ) pressure wave to the brain that travels at the speed of sound within the tissue. The pressure wave may reflect at different interfaces in the brain (e.g., blood/tissue; cerebrospinal fluid/tissue) and cause microscopic damage at these interfaces.

10. Impact can cause local contact effects Two additional effects contribute to the lesions observed clinically Brain slides in relation to the inner skull surface (circular arrow), and cortical vessels connecting the brain to the dural membrane may tear. Inertial loading delivered to the brain, coupled with its soft material properties, leads to a deformation of the brain contents.

11. Types of head acceleration

12. Epidural hematoma Generally a complication of linear skull fracture (91% of adults. 75% of children) May occur without bone fracture Typically occurs during the fracture initiation or propagation period Vessels in the underlying dural membrane are torn, and bleeding ensues in the epidural space Generally arterial Most EDHs result from arterial bleeding from a branch of the middle meningeal artery Epidural hematoma is an impact-based phenomenon No head motion or inertial effects cause an epidural hematoma.

13. Epidural hematoma Less common than subdural hematomas better prognosis than other mass lesions approximately one-fifth (22%) of patients with severe TBI; 31% mortality Only one-third of patients with an epidural hematoma are unconscious from the time of injury, one-third have a lucid interval, and one-third are never unconscious

14. Epidural hematoma On CT scan, an epidural hematoma is characterized by a biconvex, uniformly hyperdense lesion Presence of low-density areas within EDH and/or evidence of contrast extravasation into the hematoma on postcontrast head CT are indications of hyperacute/active bleeding into the hematoma EDH generally does not cross suture lines. Exception: EDH at the vertex which, can readily cross the midline sagittal suture In adults, approximately 75% occur in the temporal region Less common in children: Skull more compliant, MMA not/shallowly indented into the inner table Less common in elderly: Dura is more tightly adherent to skull

15. Epidural hematoma 10% of EDHs are caused by venous bleeding, often from laceration of a dural venous sinus Venous EDHs occur most commonly along the anterior aspect of the middle cranial fossa, caused by laceration of the sphenoparietal sinus or a fracture of the greater sphenoid wing superficial to the transverse sinus, often caused by laceration of the sinus by an overlying occipital skull fracture at the vertex, caused by injury to the superior sagittal sinus resulting from either skull fracture or diastasis of the sagittal suture, crossing the midline because of the relatively weak attachment of the outer periosteal dural layer to the sagittal suture

16. Epidural hematoma Primary treatment of the epidural hematoma is prompt surgical evacuation. Indications of surgery: Volume greater than 30 cm3 regardless of the patient’s GCS score. >5mm midline shift Non-operative management An epidural hematoma less than 30 cm3 in volume less than 15 mm in thickness less than 5-mm midline shift GCS score more than 8 No focal deficit

17. Subdural hematoma Most common focal intracranial lesion (24% of patients with TBI) Three varieties 1. Most common form: vascular disruption Tearing of parasagittal bridging veins located along the superior margin of the brain During angular acceleration of brain Results entirely from inertial, not contact, forces Differential motion between the brain and dura cause concentrated shear strain fields along the outer margins where the parasagittal bridging veins reside.

18. Subdural hematoma 2. Associated with contusion 3. Associated with laceration Because of its similar mechanism, subdural hematoma may coexist with underlying hemispheric brain damage, usually diffuse axonal injury. This explains the frequency of cases in which the subdural hematoma is small but the underlying brain damage is greater than expected. Unlike EDHs, there is no known consistent association between SDH and skull fracture. Unlike EDHs, SDHs are more commonly located at the contrecoup site than at the coup site Complicated subdural hematomas

19. Subdural hematoma Typically located in the frontoparietal region Acute subdural hematoma, identified within 72 hours after trauma, usually appears on a CT scan as a high density, homogeneous crescent-shaped mass paralleling the calvarium. SDHs freely cross suture lines. Unlike EDHs, SDHs cannot cross the thick dural reflections formed by the falx cerebri and tentorium cerebelli.

20. Subdural hematoma The mortality rate in patients with subdural hematomas is high (47%) CT scan findings predictive of outcome: Hematoma thickness Midline shift Presence of underlying brain swelling or contusions Obliteration of basal cisterns Presence of traumatic subarachnoid hemorrhage

21. Subdural hematoma Subdural hematomas cause brain damage by: Increasing ICP and Shifting brain structures  Reductions in CBF below ischemic thresholds  Marked reductions in cerebral oxygenation

22. Treatment of SDH Indications for surgery with an acute subdural hematoma: Any subdural hematoma greater than 10 mm in thickness Midline shift greater than 5 mm Subdural hematoma less than 10 mm in thickness and with a midline shift less than 5 mm If the GCS score is less than 9 and decreases 2 or more points between the time of injury and the hospital admission and/or Asymmetrical or fixed and dilated pupils and/or - ICP exceeds 20 mm Hg.

23. Intracerebral hematoma Large traumatic intracerebral hematomas are uncommon Associated with extensive cortical contusions Contusions in which larger, deeper vessels have been disrupted. usually located in frontal and temporal lobes Expansion of the intracerebral hemorrhage occurs in one-half of patients within the initial 24 hours

24. Intracerebral hematoma Indications for surgery Signs of neurological deterioration referable to the parenchymal lesion Medically refractory intracranial hypertension or Signs of mass effect on CT scan Frontal or temporal contusions greater than 20 cm3 + Midline shift of 5mm and/or Cisternal compression in a patient with a GCS score of 6 to 8 Any parenchymal lesion with volume greater than 50 cm3

25. Coup contusions Arise principally from the local bending or fracture of the skull caused by an impact from a relatively small, hard object. Underlying cortical and pial vascular network to strains that, if excessive, cause bleeding at or near the brain surface. Damage is likely to occur when the skull is rebounding from the impact and the vessels are experiencing tensile deformations.

26. Contrecoup contusions Predominant mechanism for contrecoup contusions is believed to be rotational acceleration. Cavitation effects and Inertial loading (More common) The theory of cavitation effects On impact, the brain moves toward the impact site Area of negative pressure develops directly opposite the point of loading. This negative pressure may in turn cause damage by exceeding the tensile strength of neural tissue Alternatively, can cause small gas bubbles to appear within the parenchyma The return to normal or positive pressures could then cause the small bubbles to collapse; this is termed cavitation. Translational OR angular head motion

27. Tissue tear hematoma Multiple areas of damage to blood vessels and axons occurring in combination with diffuse axonal injury. Caused by inertial head motion effects and therefore are not related to contact phenomena. Typically numerous, small, and located parasagittally and in the central portion of the brain.

28. Radiographic evaluation

29. Computed Tomography ATLS guidelines suggest a goal of 30 minutes between initial assessment and CT scan Any patient with moderate or severe TBI should undergo head CT

30. Indications of CT in mild TBI (IF 1 or more) Headache Vomiting Age >60 years Drug or alcohol intoxication Deficits in short-term memory Physical evidence of trauma above the clavicle Posttraumatic seizure GCS score <15 Focal neurologic deficit Coagulopathy

31. Plain radiographs Useful for imaging of calvarial fractures, penetrating injuries, and radiopaque foreign bodies Useful for diagnosis of other associated injuries

32. MRI Excellent visualization of hematomas and DAI Bony details are difficult to assess Long time required to perform Limited application in acute hematomas

33. Cerebral angiography CT angiography has largely replaced it for initial evaluation of TBI Intracranial vascular occlusion or dissection occurs in upto 10% Traumatic intracranial aneurysms become symptomatic days to weeks after trauma Angiography is not routinely indicated in initial assessment of TBI

34. Marshall score

35. Rotterdam score

36. Calculation of midline shift (A/2)-B A= Width of the intracranial compartment at the level of the foramen of Monro B= Shorter distance from the inner table to the septum pellucidum

37. Calculation of volume of hematoma

38. Surgical management in TBI

39. Non traumatic intracranial hematoma

40. Primary spontaneous ICH Represents only 15% of stroke Primary spontaneous ICH is associated with a higher rate of mortality Surviving patients having significant functional deficits Contributing epidemiologic factors: Age: Advancing age is clearly linked to an increased incidence of ICH Individuals older than 80 years being affected at an incidence 25 times greater than in the general population Hypertension: Most common causative factor. Cerebral Amyloid Angiopathy is 2 nd most common. African-American, Japanese, and Chinese populations Smoking, drug abuse, and heavy alcohol intake

41. Pathoetiology Parenchymal arteriole in the brain ruptures. Coagulopathy and drug abuse can contribute to ICH or its severity. Tumors , hemorrhagic transformation of an ischemic stroke, venous thrombosis, vasculitis, and vascular malformations (including cavernous angiomas, arteriovenous malformations (AVMs), aneurysms, or moyamoya vessels) are considered lesional causes.

42. Hypertension Most common cause of primary spontaneous ICH Elevated arterial pressures lead to vascular remodeling: neointimal hypertrophy, damage to the endothelial lining, and lipohyalinosis Histologically, these changes manifest as Charcot-Bouchard aneurysms, which are truly arteriolar dissections Occurs in deep locations like putamen, caudate, thalamus, brainstem, and deep cerebellar nuclei which are supplied by these small vessels.

43. Cerebral amyloid angiopathy Primarily found in the elderly population Typically >70 years typically in lobar locations Mostly sporadic, but familial forms have also been identified Amyloid deposition within the intracranial vessels, including cortical and leptomeningeal arterioles, capillaries, and veins. Histologic examination: amyloid β within the tunica media and adventitia. Gradual loss of smooth muscle cells results in fibrinoid necrosis and microaneurysm formation.

44. CAA- Microscopy with Congo red staining and birefringence under polarized light

45. Systemic anticoagulation and antiplatelet therapy 8- to 19-fold increased risk of ICH with the use of warfarin or other therapeutic anticoagulants Warfarin: Responsible for 90% of ICH in anticoagulated patients Larger hematomas Higher mortality rate Newer anticoagulant agents, the direct thrombin antagonists ( eg. Argatroban , Dabigatran), and factor Xa inhibitors ( eg. Fondaparinux) may be associated with a lower incidence of ICH when compared with Warfarin therapy.

46. Antiplatelet therapy also contributes to the risk of ICH, but to a lesser extent than therapeutic anticoagulation. Recent studies showing clinical outcomes in ICH to be independent of antiplatelet therapy PATCH (Platelet Transfusion Versus Standard Care After Acute Stroke Due to Spontaneous Cerebral Haemorrhage Associated With Antiplatelet Therapy) trial did not confirm clinical benefit and raised the possibility of additional harm from platelet transfusion. BUT, included Aspirin only and didn’t include patients who underwent surgery.

47. Hematoma location in spontaneous ICH Putamen: most common location for spontaneous ICH. Putaminal hemorrhage is nearly always associated with hypertension About 15% of all primary spontaneous ICH arises from the thalamus, also a result of chronic hypertension. ICHs located in the caudate are relatively less common (<7% of all ICHs). Lobar hemorrhage : likely a result of CAA; most frequently found in the subcortical white matter of the parietal, temporal, and occipital lobes In younger patients, lobar hemorrhages almost always indicate an underlying vascular anomaly.

48. Hematoma location in spontaneous ICH Nonlesional cerebellar ICH accounts for 5% to 10% of ICH Perforating vessels supplying the dentate nucleus are the most common source of hemorrhage, particularly with hypertension Nonlesional brainstem ICH: result of chronic hypertension; rupture of small perforating branches arising from the basilar or long circumferential arteries (PICA or AICA) Pontine >> Midbrain/Medulla

49. Clinical presentation of intracranial hematoma

50. Putamen hemorrhage Abrupt onset of a severe headache May or may not be associated with nausea and vomiting. Neurological deficits develop over time as the hematoma expands, typically in the first 3 to 6 hours after symptom onset. Later hematoma expansion occurs less frequently, and rarely after 24 hours. Additional symptoms are variable and dependent primarily on the volume of the hemorrhage. Patients with small hemorrhages may have only minor deficits and remain fairly asymptomatic Putaminal hemorrhages extending to other deep structures result in contralateral progressive hemiparesis, hemisensory loss, and homonymous hemianopsia.

51. Thalamic hemorrhage Lateral extension into the internal capsule or superior dissection into the white matter tracts results in contralateral hemiparesis. Inferior extension into the midbrain may result in coma. Midbrain involvement is often associated with characteristic ocular findings of upward gaze palsy; miotic, unreactive pupils; retraction nystagmus

52. Lobar hemorrhage Depends on the size and location of the hematoma. Lower incidence of coma and fixed neurological deficits. Headache and vomiting Because of the superficial location of the hematoma, seizures are more frequently observed in this population

53. Cerebellar hemorrhage Extension of the hematoma into the surrounding white matter may dissect into the fourth ventricle and result in obstructive hydrocephalus Progressive course Headache, dizziness, neck stiffness, nausea and vomiting, and dysarthria Further deterioration consists of appendicular and truncal ataxia, peripheral facial palsy, ipsilateral sixth nerve palsy, and nystagmus If no surgical intervention occurs, patients with sizable cerebellar hematomas will become increasingly less responsive  Comatose

54. Brainstem hemorrhage Pontine ICH is among the most devastating of all ICHs, with a large number of patients comatose at presentation. In cases of hematoma extension into the midbrain and fourth ventricle, the vast majority of patients die within 48 hours, and the prognosis for survivors is extremely poor Awake patients complain of headache, nausea, and vomiting Diplopia, hemiparesis or quadriparesis, sensory deficits, and possibly deafness. Large hematomas result in coma with decorticate or decerebrate posturing, abnormal breathing patterns, pinpoint pupils, and ocular bobbing

55. Management of spontaneous ICH

56. Medical management Team of neurosurgeons, neurologists and critical care specialists ABC ICU/dedicated stroke unit Early CT angiography (CTA) to assess for a “spot sign” (active extravasation of contrast agent within the hematoma) – AHA Neuroimaging to prove stability (6-hour interval) and identify potential causes should be completed.

57. Medical management Hypertension Hypertension at admission is associated with worse outcome SBP above 140 to 150 mm Hg after ICH has been shown to double the risk of subsequent death or dependency. Target blood pressure remains controversial AHA/ASA guidelines: ICH with SBP between 150 and 220 mm Hg and without contraindication to acute blood pressure treatment: lowering of SBP to 140 mm Hg is safe and may improve functional outcome ICH with SBP >220 mm Hg: aggressive reduction of blood pressure with a continuous intravenous infusion and frequent blood pressure monitoring

58. Medical management Blood glucose Limited data regarding optimal blood glucose Hyperglycemia is detrimental in this patient population. Hyperglycemia in animal models of ICH: More profound cerebral edema and increased perihematomal cell death. AHA/ASA guidelines: Both hyperglycemia and hypoglycemia should be avoided Kimura and colleagues: admission blood glucose level of 150 mg/dL to be the cutoff value for predicting early death Kazui and colleagues: fasting plasma glucose level of 141 mg/dL or higher combined with SBP of 200 mm Hg or higher independently increase the risk of hematoma expansion

59. Medical management Temperature Fever occurs commonly after ICH Duration of fever: independent prognostic factor in patients with ICH Maintenance of normothermia has not been clearly demonstrated as beneficial to outcome. AHA/ASA guidelines: treatment of fever after ICH may be reasonable

60. Medical management Systemic anticoagulation Normalization of the coagulation profile should be aggressively initiated (including stopping administration of anticoagulant medications). These goals hold true even in patients on systemic anticoagulation for thrombotic conditions with a risk of ischemic complications INR>3 :associated with larger hematoma volumes, a greater incidence of hematoma expansion, and poorer neurological outcomes Fresh frozen plasma (FFP) and vitamin K historically had the most widespread use

61. Medical management Systemic anticoagulation FFP: Thawing, blood typing and large volume required Each 30 min delay: 20% reduction in chance of correction at 24 hours Vitamin K: Slow onset ~6 hours AHA/ASA: Replacement of vitamin K–dependent factors along with IV vitamin K Prothrombin complex concentrates (PCCs) contains factor II,VII,IX,X Effect is achieved within minutes

62. Medical management Antiepileptic medications Seizures associated with ICH may be nonconvulsive rarely associated with spontaneous ICH Lobar hemorrhage, most likely caused by the close proximity to the cortical surface is significantly associated with the occurrence of early seizures AHA/ASA guidelines state that seizures that are uncontrolled lead to elevated ICP and elevated blood pressure and require intravenous antiepileptic therapy Prophylactic antiseizure medication is not recommended

63. Surgical management of ICH Minimally Invasive Surgery Plus rt-PA for ICH Evacuation (MISTIE) CLEAR trial Threshold of evacuation

64. International Surgical Trial in Intracerebral Hemorrhage (STICH) compare early surgery with initial conservative treatment in patients with supratentorial ICH The authors found no significant difference in the percentage of patients achieving a favorable outcome at 6 months (26% early surgery, 24% initial conservative management) For patients who were comatose at the time of randomization, early surgery increased the relative risk of poor outcome by 8%.

65. Endoscopic and Minimally Invasive Evacuations Patients treated with endoscopic evacuation achieved better outcome than those in the medically treated group Within 1 week of treatment: 14% mortality rate in the endoscopic group versus a 28% mortality rate in the medical treatment arm. At 6-month follow-up: 42% the mortality rate in the surgical group versus 70% in the medical group.

66. Stereotactic Aspiration and Thrombolysis Urokinase for lysis and catheter evacuation of ICH was then subsequently explored r-TPA is used at present Those treated with minimally invasive surgery had a better GCS score compared with those who underwent open craniotomy.

67. MISTIE trial image-guided cannula aspiration followed by catheter placement for delivery of r-tPA passive drainage of a hematoma MISTIE procedure achieved significantly lower mortality rates (6%–8% lower) than the medical arm at 1 year

68. Decompressive Hemicraniectomy With or Without Hematoma Evacuation For the treatment of malignant intracranial hypertension Patients with severe traumatic brain injury and hemispheric infarcts Bone removal allows the brain to swell outward  preventing downward herniation and relieving pressure on still healthy tissue Adequate decompression: improved tissue oxygenation, cerebral perfusion, and cerebral compliance Because of concerns regarding exacerbation of tissue damage during the removal of large hematomas, hemicraniectomy without clot evacuation has been explored as an alternate treatment. This option is of particular interest in the treatment of deep-seated lesions (e.g., basal ganglia and thalamus) and in large dominant hemisphere lesions.

69. Management of cerebellar hematomas Most suited to surgical treatment. Evacuation is performed without entering healthy tissue and with essentially no risk to motor and cognitive function. surgery is recommended for all hematomas greater than 3 cm in diameter (or 15 mL in volume) Hematomas smaller than 3 cm in diameter in awake and alert patients may be medically managed in a neurological intensive care unit with close clinical observation

70. Thank you