HEAD INJURY Mohammed EL-Metaafy Consultant Neurosurgeon Riyadh National Hospital Prof.Of Neurosurgery Suez Canal University, Egypt

CLASSIFICATION OF HEAD INJURY SKULL FRACTURE; BY MORPHOLOGY 1-VAULT: a- Linear or Stellate.b-Depressed or non Depressed. 2- BASE A- with /without CSF leak B- with/without nerve VII palsy.

INTRACRANIAL LESIONS FOCAL; 1-EPIDURAL HEMATOMA 2- SUBDURAL HEMATOMA 3- INTRACEREBRAL HEMATOMA DIFFUSE; CONCUSSION CONTUSION DIFFUSE AXONAL INJURY

BY SEVERITY MILD;GCS 13 – 15 MODERATE; GCS 9 – 12 SEVERE ; GCS 8 OR LESS, COMMATOSED

BY MECHANISM CLOSED; 1- HIGH VELOCITY(AUTO ACCIDENT). 2- LOW VELOCITY (FALLS,ASSULT). PENETRATING a-GUNSHOT WOUNDS b-OTHER OPEN INJURIES

CLASSIFICATION EPIDURAL(EXTRADURAL) HEMATOMA SUBDURAL HEMATOMA INTRACEREBRAL HEMATOMA SUBARACHNOID HEMORRHAGE INTRAVENTRICULAR HEMORRHAGE

EPIDURAL HEMATOMA

EPIDURAL HEMATOMA 1% of all head injury admission Male: female=4:1 Rare before 2 years and after 60years 85% arterial bleeding (middle meningeal artery),many of the remainder from middle meningeal vein or dural sinus. 70% occur laterally over the hemisphere the rest occur frontal,occipital and posterior fossa(5-10% each).

Presentation With EDH Brief loss of consciousness Lucid interval for several hours Contralateral hemiparesis,ipsilateral pupillary dilatation Bradycardia always late EDH suspected if there is 10% reduction in hematocrit after admission

Diagnosis Plain x-rays skull; no fracture seen in 40% of EDH CT scan MRI

Mortality with EDH 20-50% (higher rate in older series) Optimal diagnosis and treatment within few hours result in 5-10% estimated mortality Bilateral Babiniski’s or decerebration pre-operative worse prognosis 20% of patient with EDH have ASDH at autopsy or operation. Mortality with both lesions 25-90%

treatment EDH volume >30ml should be evacuated regardless of GCS EDH with all of the following characteristics can be managed non surgically with serial CT scans and close neurological observation in a neurosurgical center: volume less than 30ml Thickness <15mm MLS <5mm GCS>8 No focal neuorological deficits

Timing of surgery It is strongly recommended that patient with EDH and GCS <9 and anaisocoria undergo surgical evacuation as soon as possible

Posterior Fossa Extradural Hematoma Comprise 5% of EDH .more common in the 1st two decade of life. Although as many as 84% have occipital skull fractures ,only 3% of children with occipital skull fractures develop EDH Mortality rate 26%

Acute Subdural Hematoma

Acute Subdural Hematoma Acute subdural hematoma (ASDH) is a common neurosurgical disorder that often requires surgical intervention. ASDH is a type of intracranial hemorrhage that occurs beneath the dura and may be associated with other brain injuries. SDHs are usually caused by trauma but can be spontaneous or caused by a procedure, such as a lumbar puncture. Anticoagulation, such as with heparin or warfarin (Coumadin)

Acute SDHs are less than 72 hours old and are hyperdense compared with the brain on CT scan. Subacute SDHs are 3-20 days old and are isodense or hypodense . Chronic SDHs are 21 days (3 wk) or older and are hypodense . However, SDHs may be mixed in nature, such as when acute bleeding has occurred into a chronic SDH.

Acute SDH is commonly associated with extensive primary brain injury Acute SDH is commonly associated with extensive primary brain injury. In one study, 82% of comatose patients with acute SDH had parenchymal contusions.The severity of the diffuse parenchymal injury correlates strongly (inverse correlation) with the outcome of the patient. In recognition of this fact, an SDH that is not associated with an underlying brain injury is sometimes termed a simple or pure SDH, whereas the term complicated has been applied to SDHs in which a significant injury of the underlying brain has also been identified.

Frequency Acute subdural hematomas (SDHs) have been reported to occur in 5-25% of patients with severe head injuries, depending on the study. Chronic SDH has been reported to be 1-5.3 cases per 100,000 people per year. More recent studies have shown a higher incidence, probably because of better imaging techniques.

Etiology .1-Head trauma 2-Coagulopathy or medical anticoagulation (eg, warfarin [Coumadin], heparin, hemophilia, liver disease, .thrombocytopenia) 3-Nontraumatic intracranial hemorrhage due to cerebral aneurysm, arteriovenous malformation, or tumor (meningioma or .dural metastases)

Etiology 4-Postsurgical (craniotomy, CSF shunting) 5-Intracranial hypotension (e.g., after lumbar puncture, lumbar CSF leak, lumboperitoneal shunt, spinal epidural anesthesia 6-Shaken baby syndrome (in the pediatric age group) 7-Spontaneous or unknown (rare)

Chronic SDH Head trauma (may be relatively mild, e.g., in older individuals with cerebral atrophy) Acute SDH, with or without surgical intervention Spontaneous or idiopathic

Acute subdural hematoma Medical Therapy Acute subdural hematoma Emergency medical treatment of a patient with an acute subdural hematoma (SDH) that causes impending transtentorial herniation may include bolus administration of mannitol (in patients whose fluid levels have been adequately resuscitated and who have adequate blood pressure). Surgical evacuation of the lesion is the definitive treatment. Hyperventilation might be required but may decrease cerebral blood flow, thereby causing cerebral ischemia.

Surgical methods TIMING OF SURGERY ASDH meeting surgical criteria should be evacuated as soon as possible Surgical methods ASDH meeting surgical criteria should be evacuated via craniotomy with or without bone flap removal and duraplasty

Indication For surgery ASDH with thickness more than 10mm or midline shift more than 5mm should undergo surgical evacuation regardless of GCS ASDH with thickness less than 10mm or midline shift less than 5mm should undergo surgical evacuation if : GCS drop > 2points from injury to admission And or the pupils are asymetric or fixed and dilated And or ICP is > 20mmHg Monitor all patient with ASDH and GCS < 9

Surgical Therapy Surgery to manage an acute subdural hematoma (SDH) usually consists of a large craniotomy (centered over the thickest portion of the clot) to decompress the brain, to stop any active subdural bleeding, and if indicated, to evacuate intraparenchymal hematoma in the immediate vicinity of the acute SDH. An acute SDH usually has a consistency that is too firm to allow removal through burr holes alone.

Including the sylvian fissure in the craniotomy exposure should be considered, since this is a likely location of a ruptured cortical vessel. If brain injury and edema are associated with the SDH, an ICP monitor may need to be placed. Bullock and colleagues (2006) stated that "all patients with acute SDH in coma (Glasgow coma scale [GCS] score less than 9) should undergo intracranial pressure monitoring.

Craniectomy (ie, the removal of the bone plate or flap) is also sometimes required, such as when increased ICP is present or anticipated. Different methods for storing the bone flap for possible later replacement exist

Mortality Range 50-90%( a significant percentage of this mortality is from the underlying brain injury, and not the ASDH itself 90-100% in patient on anticoagulant

Intracerebral Hematoma

Intracerebral Hematoma The second most common form of stroke(15-30%),but the most deadly. The volume of the hematoma correlates highly with morbidity and mortality

surgery Lesions with marked mass effect, edema or midline shift Lesions where the symptoms ((hemiparesis/ plegia,aphasia,or sometimes just confusion or agitation))appear to be due to increased ICP or to mass effect of the clot or the surrounding edama Volume ;small clot<10cc mass effect is not significant

Large clot > 30cc:associated with poor outcome (only 1 of 71 patients could function independently at 30 days). >60cc with GCS< 8:91% 30-days mortality >85cc (diameter 5.5cm) no patient survived, regardless of treatment in one series

Persistent elevated ICP in spite of therapy but the effect in outcome is uncertain Rapid deterioration (especially with signs of brain stem compression) regardless of the location Favourable locations Lobar Cerebellar External capsule Non dominant hemisphere

Early intervention following hemorrhage: surgery after 24 hrs from onset of symptoms or deterioration may be of less benefit Young patients(especially age<50 years)

conclusion The usefulness of surgery is still controversial, but seems limited to some Cerebellar hemorrhages and select supratentorial hemorrhages that come within 1cm of the cortical surface.

Thank you

Thank you

INTRACRANIAL HEMORRHAGE Mohammed EL-Metaafy Consultant Neurosurgeon Riyadh National Hospital Prof.Of Neurosurgery Suez Canal University, Egypt