DEPARTMENT OF CARDIAC SURGERY CVA AFTER CABG DR .KAMBIZ ALIZADEH DR. M.TABARI DEPARTMENT OF CARDIAC SURGERY GHAEM HOSPITAL MASHAD UNIVERSITY OF MEDICAL SCIENCE

Major Neurologic Disorders After CABG Does off pump method reduce CVA?(elective patients). Many discussion about off pump method in mortality and morbidity . What about CVA?

Cerebral vascular Disease Definition of term: The term cerebrovascular disease designates any abnormality of the brain resulting from a pathologic process of the blood vessels. Sudden loss of neurological function is the hallmark of cerebrovascular disease. Cerebrovascular disease is the third most common cause of death and the most common disabling neurologic disorder in western civilized countries where an increasing proportion of people survive to old age. Its incidence increases with age and is somewhat higher in men than in women.

Risk factors for stroke Systolic or diastolic hypertension Diabetics Hypercholesterolemia Heart disease (afib) Cigarette smoking Heavy alcohol consumption High homocystine Oral contraceptive use

The major types of cerebrovascular disease Cerebral ischaemia and infarction Transient Ischemic Attacks Atherosclerotic thrombosis Lacunes Embolism Hemorrhage Hypertensive hemorrhage Ruptured aneurysms and vascular malformations Other

I、Cerebral ischaemia and infarction Anatomy and pathology The principal pathological process under consideration here is the occlusion of arteries supplying the brain. The two internal carotid arteries and the basilar artery form the Circle of Willis at the base of the brain, which acts as an efficient anatomotic device in the event of occlusion of arteries proximal to it.

Anatomy and pathology Occlusion leads to sudden severe ischaemia in the area of brain tissue supplied by the occluded artery, and recovery depends upon rapid lysis or fragmentation of the occluding material: Reversal of neurological function within minutes or hours gives rise to the clinical picture of a transient ischaemic attack.

Anatomy and pathology When the neurological deficit lasts longer than 24 hours, it may be called a reversible ischaemic neurological deficit ( RIND ) if it recovers completely in a few days, or a completed stroke if there is a persistent deficit. Sometimes recovery is very slow and incomplete.

Neurological symptoms and signs The loss of function that the patient notices, and which may be apparent on examination, entirely depends on the area of brain tissue involved in the ischaemic process.

Neurological symptoms and signs The following suggest middle cerebral territory: Dysphasia; Dyslexia, dysgraphia, dyscalculia; Loss of use of contralateral face and arm; Loss of feeling in contralateral face and arm.

Neurological symptoms and signs The following suggests anterior cerebral territory: Loss of use and/ or feeling in the contralateral leg. The following suggests posterior cerebral territory: Development of a contralateral homonymous hemianopia.

Neurological symptoms and signs The following suggests a deep-seated lesion affecting the internal capsule which is supplied by small perforating branches of the middle and posterior cerebral arteries close to their origins: Complete loss of motor and sensory function throughout the whole of the contralateral side of the body with a homonymous hemianopia.

Neurological symptoms and signs The following suggests ophthalmic artery territory (the ophthalmic artery arises from the internal carotid artery just below the Circle of Willis): Monocular loss of vision.

1. Transient Ischemic Attacks(TIA) Definition of term Current opinion holds that TIAs are brief, reversible episodes of focal, nonconvulsive ischaemic neurologic disturbance, Consensus has been that their duration should be less than 24 h.

Causes of cerebral embolism: Cardiac origin Noncardiac origin Undetermined origin

CARDAIC ORIGIN . LEFT SIDE CLOT (LV .LA) .AORTOIC CALCIFICATION . MITRAL VALVE OR AORTIC VALVE

CAN WE REDUCE CVA IN CABG ? FROM MARCH 2013 TO 2014 WE EVALUATE 100 OFF PUMP CABG THERE WAS NO DIFFERENCE IN CARDIAC MORTALITY BUT OVERAL MORTALITY WAS LOWER IN OFF PUMP GROUP BECAUSE OF LOWER RATE OF CVA

WHY LOWER RATE OF CVA IN OFF PUMP AORTIC CROSS CLAMP CANULATION SITE

EXEPTIONS IN OUR STUDY : IF THERE IS LV CLOT IF THERE IS CALCIFICATION IN LEFT SIDE VALVE USING CPB WOULD BE BETTER

Course and prognosis Most patients survive the initial insult, and in many the neurologic deficit may recede relatively rapidly, as indicated above. The eventual prognosis is determined by the occurrence of further emboli and the gravity of the underlying illness- cardiac failure myocardial infarction, bacterial endocarditis and so on.

Treatment and prevention Three phases of therapy : General medical management in the acute phase, Measures directed to restoring the circulation Physical therapy and rehabilitation These are much the same as described above the prevention of atherothrombotic infarction.

Intracranial Hemorrhage Intracranial hemorrhage is classified by its location as intracerebral, subarachnoid, subdural, or epidural, all of which- except subdural hemorrhage- are usually caused by arterial bleeding.

Intracranial Hemorrhage The bleeding occurs within brain tissue, and rupture of arteries lying in the subarachnoid space is practically unknown apart from aneurysms. The extravasation forms a roughly circular or oval mass that disrupts the tissue and grows in volume as the bleeding continues . Adjacent brain tissue is distorted and compressed. If the hemorrhage is large, midline structures are displaced to the opposite side and reticular activating and respiratory centers are compromised, leading to coma and death.

Treatment The management of patients with large intracerebral hemorrhages and coma includes the maintenance of adequate ventilation, use of controlled hyperventilation to a Pco2 of 25 to 30 mmHg, monitoring of intracranial pressure (ICP) in some cases and its control by the use of tissue-dehydrating agents such as mannitol (osmolality kept at 295 to 305 mosmol/L and Na at 145 to 150 meq), and limiting intravenous infusions to normal saline.

Treatment Rapid reduction in blood pressure, in the hope of reducing further bleeding , is not recommended, since it risks compromising cerebral perfusion in cases of raised intracranial pressure. On the other hand, sustained mean blood pressure of greater than 110mmHg may exaggerate cerebral edema and risk extension of the clot. It is at approximately this level of acute hypertension that the use of beta-blocking drugs(esmolol, labetalol) or angiotensin-converting enzyme inhibitory drugs is recommended.

Treatment In contrast to cerebral hemorrhage, the surgical evacuation of cerebellar hematomas is a generally accepted treatment and is a more urgent matter because of the proximity of the mass to brainstem and the risk of abrupt progression to coma and respiratory failure.

Course and Prognosis The immediate prognosis for large and medium-size cerebral clots is grave; some 30 to 35 percent of patients die in 1 to 30 days. Either the hemorrhage extends into the ventricular system or intracranial pressure is elevated to levels that preclude normal perfusion of the brain. Sometimes the hemorrhage itself seeps into vital centers such as the hypothalamus or midbrain.

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