Intracranial Hemorrhage Intracranial Hemorrhage:  Intracerebral if in the parenchyma, can be traumatic or non-traumatic  Epidural hematoma, subdural hematoma

, and subarachnoid hemorrhage if in surrounding meningeal spaces Pathophysiology:  Hypertensive damage to blood vessel walls due to eclampsia, hypertension, and drug abuse  Autoregulatory dysfunction with excessive cerebral blood flow reperfusion injury, hemorrhagic transformation, and cold exposure  Rupture of an aneurysm or ateriovenous malformation  Arteriopathy due to cerebral amyloid angiopathy or moyamoya  Altered hemostasis due to thrombolysis, anticoagulation, and bleeding diathesis Predilection sites:  Highest frequency in the basal gangliaLobar RegionThalamusPonsCerebellum Manifestations:  Older than 50 years  Usually during activity  Progressive development of alteration in level of consciousness, nausea and vomiting, headache, seizures, and focal neurological defects Clinical Manifestations (Determined by size and location of hemorrhage):  Hypertension, fever or cardiac arrhythmias  Nuchal rigidity  Altered level of consciousness  Anisocuria  Focal neurological deficits Location: Putamen (Most common site of hypertensive ICH):  Contralateral hemiparesis, sensory loss and conjugate gaze  Homonymous hemianopia  Aphasia and ataxia and neglect Thalamus:  Contralateral sensory loss and confusion  Contralateral hemiparesis and homonymous hemianopia if extended to Internal Capsule  Fever and coma if secondary ventricular hemorrhage  High fever, miosis and upper gastrointestinal hemorrhage if extended to hypothalamus/brainstem  Aphasia Lobar:  Rupture of aneurysm and arteriovenous malformation in younger people  Cerebral amyloid angiopathy and arteriosclerosis in older people  Coma is rare, seizures are common  Neuropsychiatric symptoms and contralateral hemiparesis in frontal lobe  Contralateral hemiparesis and sensory loss in Parietal lobe  Sensory aphasia, neuropsychiatric symptoms and homonymous hemianopia in temporal lobe  Homonymous hemianopia and quadrantalanopia in occipital lobe Midbrain:  Consicousness disorders in reticular formation  Ventrical gaze paresis in corpora quadrigemina  Weber syndrome decerebrate in midbrain  Quadriparesis hemiparesis in pyramidal tract Pons:

and vomiting in vestibular nucleus  Conjugate gaze paresis in medial longitudinal fasciculus  Pinpoint pupils and high fever in sympathetic fibers  Quadriparesis hemiparesis in pyramidal tract Medulla Oblongata:  Very rare. miosis. nausea. and decreased level of consciousness Ventricle Hemorrhage:   Can be primary or secondary  Symptoms include headache. and a positive Kernig sign Imaging Studies:  CT scan shows acute hemorrhages with hyperdense signal intensity  MRI not highly sensitive to hemorrhage in the first few hours . skew deviation. vomiting. Vertigo. with Wallenberg syndrome and results in central respiratory and circulatory function failure Cerebellum:  Ataxia (usually beginning in trunk)  Ipsilateral facial weakness and sensory loss  Gaze paresis. nausea.

those with lobar hemorrhage or without a clear cause of hemorrhage and history of hypertension  Lumbar puncture for increased CSF pressure and haemic CSF Diagnosis: Differential Diagnosis: .Phase Hyperacute Acute Early subacute Late subacute Chronic   Time <24 hours 1-3 days >3 days >7 days >14 days Hemoglobin Oxyhemoglobin (intracellular) Deoxyhemoglobi n (intracellular) Methemoglobin (intracellular) Methemoglobin (extracellular) Hemosiderin (extracellular) T1 Iso or hypo Iso or hypo Hyper Hyper Iso or hypo T2 Hyper Hypo Hypo Hyper Hypo CTA/MRA permits screening of large and medium-sized vesels for arteriopathies Catheter angiography assesses all vessels for AVMs. vasculitis. and other arteriopathies. mostly for young patients.

ventricle puncture drainage) Complications:  Upper gastrointestinal hemorrhage  Pulmonary infections  Cardiovascular damage  Deep venous thrombosis Increased ICP Risk:  Major contributor to mortality  Correlation with poor outcome  Increased risk of herniation and decreased cerebral perfusion  Controlling ICP is essential (Using Osmotherapy. head elevation)  Surgical care If Putamen>30ml.Principles of Treatment:  General treatment (rest. hyperventilation. and barbiturate coma) Management:  Osmotherapy (Decreases Cerebral fluid volume)  Head of bed Elevation  Endotracheal intubation (not required)  Lidocaine (Depresses cough reflex)  Sedation (Prevents ICP Spikes)  Barbiturate Coma (Lowers Cerebral metabolism)  BP management (Decreases risk of ongoing bleeding from ruptured arteries)  Fever management (Cooling blanket and acetaminophen)  Seizure therapy (Consider prophylactic antiepileptic therapy)  Medical Therapy (Euvolemia and Electrolyte stabilization) Prognosis:  Better in patients with volume < 30cm and GCS 9 or higher  Worse in patients with volume > 60cm and GCS < 9 ICH Surgical Indications:  Cerebellar hemorrhage > 3cm with deterioration or brain stem compression  Vascular malformation if lesion is surgically accessible  Young patients with large lobar hemorrhage with clinical deterioration  Surgery not needed if hemorrhages are small with minimal neurological deficits and GCS < 4 Poor outcome Risk Factors:  Large. sedation. Thalamus/Cerebellar>10ml. antiepileptic drugs)  Control hypertension (Monitor BP)  Control intracranial hypertension (Osmotherapy. increasing hematoma vlume . Lobar>40ml. steroids. clot evacuation. Obstructive hydrocephalus (Craniotomy.

and the preferred first diagnostic study  Lumber puncture if patient has possible SAH and negative CT scan findings  Treatment include general therapy. nausea vomiting. seizures (25%). lumber puncture drainage. Hemostasis. fever. hydrocephalus. vision loss). and meningeal irritation  Complications include rebleeding. Low GCS on admission  Interventricular clot extension  Anticoagulation agents  Relative edema Subarachnoid Hemorrhage:  Can be traumatic or non-traumatic (Primary or secondary)  Common causes include intracranial aneurysms (Willis Circle) and Arteriovenous Malformation  Common in young age  Symptoms include sudden severe headache. dehydration. and avoiding cerebral vasospasm . and loss of consciousness  Syndromes of cranial nerve compression may be present (Nerve palsy. cerebral artery spasm  CT Scan is sensitive.

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