Mention and explain about EDH,SDH,ICH,SAH, IVH.

Factor in the Rural Environment The following factors are significant in rural trauma : asolation and distance, medical facilities, level of neurosurgical competence, delay in definitive care, administrative organisation, rural crash profiles, e.g., incidence of 40 fatality on admission, more severe injuries, multiple injuries, higher incidence of single vehicle crashes, road and environmental conditions, driver competence and fatigue and compliance with preventive measures such as alcohol, seatbelts, helmets and speed. Neurotrauma Clinical factors adversely influencing outcome [death and disability] - Severity of Primary Injury - Intracranial Complications - Hypoxaemia - Hypercarbia - Hypotension - Anaemia - Multiple Injuries - Age - Prolonged Prehospital Time - Admission To Inappropriate Hospital - Delayed Or Inappropriate Interhospital Transfer Retrieval - Delay In Definitive Surgical Treatment Learning Task Head Injury Female 40 years old a pedestrian was hit by motor bike , upon arrival to emergency department, she able to open her eye and say painfull while she withdrawn her hand , there are brill hematoma, rinorhea, and bloody discharge from her nose and mouth, respiratory rate 26xmnt gurgling, Blood pressure 8060 mmHG, and Heart rate 120xmnt. 1. What is the clinical diagnosis base on GCS. 2. Initial management 3. Sign of skull base fracture 4. Sign and symptom of intracranial hematoma

5. Mention and explain about EDH,SDH,ICH,SAH, IVH.

Self assessment 1. What is cushing respons 2. Craniotomy, craniectomy 3. Lucid interval 4. Lateralization or hemisyndrome 5. Brain death Learning resourse 1. Sri maliawan cedera kepala 2. American college of surgeon ; ATLS 3. The neurosurgical society of Australia; head injury an remote area Faculty of Medicine Udayana University, DME 56 DAY 9 th May 28 th 2014 STROKE dr. AABN. Nuartha, Sp.SK: Aims: Describe diagnosis, management and referral patients with stroke. Learning outcome: Describe pathogenesis, clinical aspect, examination, and management patient with stroke. Curriculum contents: 1. Ischemic stroke. 2. Haemorrhagic stroke. Abstract of lectures: Stroke is a clinical diagnosis made on the characteristic temporal profile of neurological symptoms and signs, as examplified by the WHO definition : Rapidly developing clinical signs of focal or global disturbance of cerebral function, with symptoms lasting 24 hours or longer, or leading to death, with no apparent cause other than of vascular origin. Stroke is the third most common cause of death worldwide after coronary heart disease and all cancers combined and the major cause of disability. The most frequent cause of stroke is a localized disturbance of cerebral circulation, i.e., cerebral ischemiainfarction ischemicnon haemorrhagic stroke. Ischemic stroke classification is base on five subtype: large artery atherothrombosis-thromboembolism, embolism from the heart, small vessel disease, uncertain cause, and rare causes. Less common are haemorrhagic stroke spontaneous intra cerebral haemorrhage and subarachnoid haemorrhage. Subarachnoid hemorrhage is the exception to this definition and usually presents without focal neurological deficits. Stroke typically manifect abruptly, resulting in a maximum deficit usually within hours and lasting longer than 24 hours. If a patient’s focal neurological deficit lasts less than 24 hours, it is arbitrarily defined as a TIA transient ischemic attack. Clinical history, examination and investigation will separate infarction and haemorrhage. When a clear account of symptoms is available, the clinical diagnosis of stroke works well and the risk of mistaking a nonvascular lesion for stroke is very small. When the history is not so clear, however, because the patient is unconscious, confused, or aphasic and the event has no reliable withness, the diagnosis is more difficult and the chance of misdiagnosis is high. In these situations, CT computed tomography or MRI magnetic resonance imaging is important to exclude non-stroke diagnoses such as traumatic subdural haematomas or malignancy. Treatment aims, prevent progression of present event, prevent immediate complication, prevent the development of subsequent event, rehabilitation and stroke prevention. Triggerscenario: A 53 years old women with a history of type 2 diabetes mellitus and atrial fibrillation pressents to the emergency room with slurred speech and right body weakness. The onset was sudden while she was swimming 1 hour ago, and she was brought immediately to the emergency room. Physical exam findings include blood pressure of 9570 and irregularly irregular heartbeat. GCS 15. Paralysed from the right side of the body, with the face and upper extremity being worse than the lower extremity. Routine chemistries and cell counts are normal Self assessment: 1. What is the possibility diagnosis of this patient ? Faculty of Medicine Udayana University, DME 57 2. What is the diagnosis tools you made to make definited diagnosis ? Learning Task 1. Pathogenesis of stroke. 2. Clinical aspect and diagnostic tool of stroke 3. Management and prevention of stroke. SURGICAL ASPECT OF CEREBROVASCULAR ACCIDENTS CVA dr. I Wayan Niryana, M.Kes, SpBSK AIMS: Provide initial assessment and management, established tentative diagnosis, proposed definitive management, and prognosis patient with CVA. LEARNING OUTCOME: The student know what is the surgical indication of CVA CURRICULUM CONTENTS: Cerebrovascular Accidents CVA 1. Etiology and Pathophysiology of Cerebrovascular disease 2. Clinical Features and Investigations of Cerebrovascular disease 3. Management and Surgical Indication for Cerebrovascular disease ABSTRACTS OF LECTURES Due to the improvement of the treatment of ischemic heart disease over ischemic or hemorrhagic brain disease over the last 10 years, more and more patients can benefit from non surgical and surgical intervention. The nineties have been called the decade of the brain in developed countries where brain attack has been treated as aggressively as heart attacks. Thus it is now the time for all developing countries to follow the same pathway. Next to heart disease and cancer, cerebrovascular disease is the most frequent cause of death in the western world. And at least one-half of all neurological patients in general have some type of cerebrovascular disease. The term cerebrocvascular disease denotes any abnormality of the brain resulting from a pathologic process of blood vessels, be they arteries, arterioles, capillaries, veins, or sinuses. The pathologic change in the vessels takes the form of occlusion by thrombus or embolus, or of rupture, and the resulting abnormalities in the brain are of two types: ischemia, with and without infarction, and hemorrhage. Rarer forms of cerebrovascular disease are those due to altered permeability of the vascular wall and increased viscosity or other changes in the quality of blood. The latter changes underlie the strokes that complicate diseases such as sickle-cell anemia and polycythemia and account for the headache, brain edema, and convulsions of hypertensive encephalopathy. From all of Cerebrovascular accidents 25 present with intracerebral haematoma ICH and account for 2-4 of all deaths. They are twice as common as SAH. Over two thirds are known to be fatal. The patients are usually middle aged or over, with a male preponderance. The incidence is about 1 per 10,000 with a 30day mortality of 44. Faculty of Medicine Udayana University, DME 58 Etiology: There are two categories, primary and secondary. PrimaryICH: It is associated with hypertension and distinct from hemorrhagic infarcts. It has been suggested that hypertensive changes in the arterial wall, such as, hyaline degeneration, and micro aneurysms are at fault. Another suggestion is the thin walled vessels such as lenticulostriates, originating directly from the main vessel are subjected to higher intravascular pressure than the cortical vessels and tend to rupture.Eighty percent of them are supratentorial. Mostly, the location is central and deep. SecondaryICH: It is associated with a medical condition other than hypertension, representing about 20 of all ICHs. They may be due to: Coagulopathies 10-15-Among these, platelet disorders are important. About 5 of those receiving heparin, irrespective of the dosage, develop thrombocytopenia. The platelet defects may be hereditary Von Willebrand’s disease or acquired through drugs Aspirin, penicillin, or new cephalosporin’s or through disease myeloproliferative and dysplastic disorders, uremia, cirrhosis, SLE, multiple myeloma. Arterio Venous Malformations AVMs 7 represent a heterogeneous group with different histological types cavernoma, AVMs, venous angioma and capillary telangiectosis. Vasculopathies 5, such as cerebral amyloid angiopathy, polyarterites nodosa and necrotizing vasculopathy in drug abusers, tend to produce multiple subcortical haematomas. Tumors 2 such as glioblastoma and metastasis tumors such as, melanoma, choriocarcinoma, renal cell carcinoma and bronchogenic carcinoma, are the most frequent tumors in producing ICH. Pathophysiology: The haematomas may be massive 5cm with extension into the ventricles or may be small 1.5 cm. The extravagated blood forms a roughly circular or oval mass which grows in volume for a brief period. Adjacent brain tissue is displaced and compressed resulting in extensive edema and ischemia. Ischemic area may be much larger than the area of clot. Cerebellar and brainstem ICH may produce obstructive hydrocephalus which may add to the problems. In large hemorrhage, there is midline shift and the vital centers are compromised. Rebleeding is rare. Resolving haematomas may develop into a cyst over a period of months, with a gliotic wall which may be orange colored due to haemosiderin laden macrophages. Clinical features: It depends on the site and size of the hematoma.Sudden headache, vomiting with depressed level of consciousness and focal signs is the usual mode of presentation. Absence of neck stiffness may help to exclude SAH. The large ones are usually associated with LOC. In putaminal ICH, the patient develops sudden hemiplegia with conjugate horizontal gaze deviation towards the clot. Speech may be involved if the dominant hemisphere is involved. In thalamic ICH, the findings are as in putaminal ICH; in addition, there may be neck retraction, paralysis of vertical gaze with upward gaze palsy, inequality of pupils, and skew deviation with the contra lateral eye being displaced downward and medially. Cerebellar ICH presents with severe headache, nausea and vomiting and imbalance and depressed level of consciousness. Faculty of Medicine Udayana University, DME 59 Pontine ICH present with coma, pin point pupils and decerebrate rigidity. Cortical ICH may present with headache and seizures. Investigations: CTScan will reveal the clot and other associated features such as midline shift and hydrocephalus. A contrast CT may suggest a vascular problem, which may necessitate an angiography. MRI gives a better delineation of the above; in addition the age of the haematoma can be guessed. MRI may suggest an associated AVM. Angiography should be carried out whenever there is a suggestion of vascular malformation, in the absence of previous hypertension or coagulopathies before a life saving clot evacuation. When surgery is not planned, the angiography can wait for few weeks to avoid a false negative angiography. Coagulation studies must be done as a routine in addition to ECG, chest X-ray and other general investigations. Management: Supportive care control of hypertension, reduction of ICP without compromising the CPP and prevention of complications are the mainstay. Fluid and electrolytes and tissue oxygenation must be closely monitored. The aim is to avoid secondary events. An aggressive decrease of high BP may lead to cerebral ischemia. Ideally, it should not be lowered below 150mm Hg systolic and 100 mm of Hg diastolic. Should general measures to control the raising ICP fail, hyperventilation may help; but must be employed with careful watch on pCo2, arterial blood pressure and preferably with ICP monitoring as well. The CPP should not be compromised. Osmotherapy with mannitol may help only when the serum osmolality is lower than 300 mosmkg. Prophylactic anti convulsant therapy is advised by most physicians with no supporting evidence. The role of surgical intervention is controversial. Neurosurgeons and neurologistsadvocate that large cerebellar hemorrhages with compressionof the brain stem or obstruction of the fourth ventricle shouldbe surgically removed as soon as possible. Surgical removalof large lobar hemorrhages in young patients who are clinicallydeteriorating has also been recommended based on anecdotal experience. On the other hand, the results of such surgery in hematomas within the basal ganglia and other deep structures are unacceptable. Standard craniotomy for surgical removal of primary brainstem or thalamic hemorrhages has been all but abandoned becauseof the extremely poor outcomes in almost all patients. Craniotomy: Craniotomy and evacuation of the clot has been the standard approach for removal of intraparenchymal hemorrhage. In addition a decompressive craniectomy with a duraplasty is preferred by some.Its major advantage is adequate exposure to remove the clot. It is not difficult or time-consuming. The major disadvantageof a more extensive surgical approach is that it may lead tofurther brain damage, particularly in patients with deep-seated hemorrhages.In addition, the effectiveness of clot removal by craniotomyis far from ideal. There have been numerous nonrandomized series comparing craniotomy and bestmedical treatment of ICH. Recently Morgenstern and colleagues reported a single-center, randomized trial STICH Trial ofstandard craniotomy versus best medical therapy in patientswithsupratentorial ICH; the goal was to perform surgery 12 hours after symptomonset. Patients had to have a supratentorial ICH with a volume10 cm 3 and a GCS score of 5 to 15. Of the 34 patients in therandomized trial, 17 were randomized to removal of the ICH bystandard craniotomy. The median time to surgery for the 17 patientswas 8.3 hours minimum 3.75 hours and maximum 26.1 hours. The6-month mortality for the surgical group was 17.6 comparedwith 23.5 for the medical group. The median 6-monthBarthel index score for survivors in the surgical group wasalso similar to the median Barthel index score for the medicalgroup. However, the groups were not balanced with regard to ICHlocation. Only 1 of the 17 patients 6 in the surgical grouphad a lobar hemorrhage compared with 7 of 17 patients 41of the medical group. Nonrandomized treatment series of patients with cerebellar hemorrhagereport good outcomes for surgically treated patients who havelarge 3 cm cerebellarhemorrhages or cerebellar hemorrhageswith Faculty of Medicine Udayana University, DME 60 brain stem compression or hydrocephalus. Inthese patients, medical management alone often results in badoutcomes. Smaller cerebellar hemorrhages without brain stemcompression that are managed medically do reasonably well. Outcome: The natural course of spontaneous ICH leads to a 30-day mortality rate of 45. The patients initial level of consciousness, hemorrhage size, and intraventricular extension of blood has proven to be accurate predictors of outcome. Less commonly, age, sex, hypertension, and mass effect may indicate harmful effects on outcome in patients with ICH. The author recommends that patients with smaller hematomas who are alert, stable, or improving should be treated medically and the patients with larger hematomas who show progressive neurological deficit, prolonged functional impairment, and intracranial hypertension should be treated surgically. Patientswith a GCS score 4 should also be treated medically because theyuniformly die or have extremely poor functional outcome that cannotbe improved by surgery. Easily accessible supratentorial hematomas with mass effect, especially in the young and in those with a GCS score 5, must be evacuated. The aim of surgery should be the removal of as much of the clot as possible, with minimal disruption of surrounding brain tissue. If possible,surgery should also remove the underlying cause of hemorrhage, suchas an arteriovenous malformation, and prevent complicationsof ICH such as hydrocephalus and mass effect of the blood clot. Morecomplete clot removal may decrease elevated ICP and local pressure effectsof the blood clot on the surrounding brain. Stereotacticaspiration may be associated with better outcomes than standardcraniotomy; but thishypothesis has yet to be tested in a randomized study. Ultra-earlyremoval of ICH by localized, minimally invasive surgical proceduresis promising but untested. Further study of the dynamics of hemorrhage and additional results are needed prior to making a decision on how to divide patient management into the two categories of surgical and nonsurgical treatment. SCENARIO Male patient, 50 years oldwas referred to the Emergency room on a face mask oxygenation, with Infusion lines at right arm with large caliber of needle, warmed crystalloids has been administered. The blood pressure is 180100 mmHg, heart rate 60xmnt, Respiration rate 20xmnt. Pupil round an equal, size: right side 5mm, left side 3mm, with left hemi paresis. His eyes are open with pain stimuli and his GCS was E2V2M4. History: When he was watching TV, suddenly he got severe headache, vomiting and then seizure. After that he looks decreased of consciousness. History of hypertension + since 5 years ago, regularly take medication. LEARNING TASKS 1. What is the clinical diagnosis and differential diagnosis? 2. What is the investigation that need for this patient? 3. How is the initial management for this patient? 4. When should you suggest to doing surgery for this patient? 5. How should you explain the prognosis of the patient to the family? SELF ASSESMENT 1. Explain the Cerebrovascular Anatomy that supplies the brain and cerebellum. 2. Learn about clinical features, investigations and differentials diagnosis of cerebrovascular disease. 3. Learn about emergency management: medical and surgical aspect of CVA.

4. Learn about how to explain the prognosis of CVA.