Practicum Material 9: Stroke Cases

PRACTICUM MATERIAL 9: STROKE CASES Pathophysiology Strokes Ischemic Strokes Ischemia involves 3 basic mechanisms that occur The causes are thrombosis, embolism, and decreased perfusion pressure. Thrombosis occurs due to changes in the characteristics of blood vessels and the formation of blood clots. Pathologies that cause blood clots include atherosclerosis, fibromuscular dysplasia, arteritis, blood vessel dissection and bleeding in atherosclerotic plaques. Atherosclerosis is the most frequent main cause of thromboembolism with the mechanism of blockage of intracranial blood vessels. Emboli form in the heart's large arteries (aorta, carotid, vertebral) or veins. Emboli can be blood clots, vegetations, or intracardiac tumors. A decrease in perfusion pressure can be caused by failure of the heart to pump blood or insufficient (intravascular) blood volume. Pathophysiology Strokes Hemorrhagic Strokes Hemorrhagic has typical clinical manifestations in that the process is not indicated, the sudden occurrence of bleeding from blood vessels into brain tissue. Process Strokes Hemorrhage occurs dynamically and complexly involving other body organs. Strokes hemorrhagic disease requires fast, precise and careful treatment.Strokes Hemorrhagic hemorrhages are divided into three types, namely intracerebral hemorrhage, subarachnoid hemorrhage and subdural hematoma. Subarachnoid hemorrhage occurs when blood flow enters the subarachnoid space due to trauma, rupture of an intracranial aneurysm, or rupture of an arteriovenous malformation.Strokes intracerebral hemorrhage occurs whenblood vessels rupture within the brain parenchyma and form a hematoma.Strokes Intracerebral hemorrhage can occur due to hypertensioncontrolled and is usually caused by trauma. General Therapy Strokes a. Stabilization of the airway and breathing. b. Hemodynamic stabilization (crystalloid infusion). c. Control of intracranial pressure (mannitol, furosemide, if necessary). d. Seizure control (anti-seizure therapy if necessary). e. Analgesics and antipyretics, if necessary. f. Gastroprotector, if necessary. g. Nutrition management. h. Prevention of DVT and pulmonary embolism: heparin or LMWH. 2. Specific Therapy Strokes Ischemic a. Intravenous Thrombolysis: Alteplase dose 0.6-0.9 mg/kgBW, atStrokes ischemic onset <6 hours. b. Endovascular therapy: Mechanical thrombectami, onStrokesischemia with occlusion of internal carotid or intracranial vessels, onset <8 hours. c. Hypertension management (ARB, ACEInhibitors, CCBs, Beta Blockers, Diuretics). d. Blood sugar management (insulin or oral antidiabetics). e. PreventionStrokessecondary (antiplatelets: acetosal, clopidogrel, cilostazol or anticoagulants: warfarin, dabigatran, rivaroxaban). f. Neuroprotectors (citicolin, piracetam, pentoxyfiline, DLBS 1033). g. In-unit maintenanceStrokes. Supporting investigationStrokesIschemic a. CT Scan + CT Angiography / MRI + Brain MRA. b. EKG. c. Carotid Doppler. d. Transcranial Doppler. e. TCD Bubble Contrast & VMR. f. Lab: Routine hematology, instant blood sugar, kidney function (urea, creatinine), Activated Partial Thrombin Time (APTT), prothrombin time (PT), INR, fasting blood sugar and 2 hour PP, HbA1C, lipid profile, C-reactive protein (CRP), erythrocyte sedimentation rate, and examination for indications such as: cardiac enzymes (troponin / CKMB), serum electrolytes, hepatic analysis and electrolyte examination. g. Thorax photo. h. Urinalysis. i. Echocardiography (TTE/TEE). j. Neurobehavior Examination (Higher Function). k. Cerebral DSA Supporting investigationStrokesHemorrhagic a. CT Scan/MRI Brain. b. CT/MR Brain Angiography. c. EKG. d. Carotid Doppler. e. Transcranial Doppler. f. Labs: Routine hematology, instant blood sugar, kidney function (urea, creatinine), Activated Partial Thrombin Time (APTT), prothrombin time (PT), INR, fasting blood sugar and 2 hour PP, HbA1C, lipid profile, C-reactive protein (CRP), erythrocyte sedimentation rate, and examination for indications such as: cardiac enzymes (troponin / CKMB), serum electrolytes, hepatic analysis and electrolyte examination. g. Thorax photo Implementation of CASE Practicum Mr. A (57 years old) was taken by his son to the emergency room at 10 am. From his son's statement, it was discovered that his father had difficulty speaking, numbness in his left arm and dizziness. While playing tennis this morning at 9.30, his father suddenly knelt down and dropped his tennis racket. Previously, at 8 am his father complained of slight dizziness and tingling in his left hand which went away by itself. The patient had no previous history of stroke or TIA. From the results of the anamnesis, physical and supporting examination, the doctor diagnosed the patient as suffering from an ischemic stroke. Patient's disease history: Hypertension and hyperlipidemia since 10 years ago Family history: 62 year old sister also has hypertension, 31 year old son suffers from type 2 DM Social history: has a wife and 3 children, does not smoke The patient's current therapybefore admission to hospital: amlodipine 5 mg orally in the morning every day, simvastatin 10 mg orally every day in the evening before bed Physical examination:BP: 192/100 mmHg, Pulse: 70, Respiration: 19, Temperature: 360C ECG examination results: Normal CT scan results: infarction in the right midbrain, no signs of hemorrhage. Laboratory examination results Sodium 140 mEq/L WBC 5.9 x 103/mm3 cabbage. total 200 mg/dL K 4.2 mEq/L Hgb 16.4 d/dL LDL 118 mg/dL Cl 103 mEq/L Hct 49.6% TG 160mg/dL CO2 28 mEq/L Plt 310 x 103/mm3 HDL 50 mg/dL BUN 10 mg/dL aPTT 25.3 s Scr 0.6 mg/dL GDP 98 mg/dL