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Medicine 5th year, 4th lecture (Dr. Mohammed Tahir)


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The lecture has been given on May 14th, 2011 by Dr. Mohammed Tahir.

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Medicine 5th year, 4th lecture (Dr. Mohammed Tahir)

  1. 1. stroke is the clinical term for acute loss of circulation to an area of the brain, resulting in ischemia and a corresponding loss of neurologic function . Classified as either hemorrhagic or ischemic ,
  2. 2. <ul><li>strokes typically manifest with the acute onset of focal neurologic deficits, such as weakness, sensory deficit or speech difficulties . </li></ul><ul><li>Ischemic strokes have a heterogeneous group of causes, including thrombosis, embolism, and hypoperfusion, whereas hemorrhagic strokes can be either intraparenchymal or subarachnoid </li></ul>
  3. 3. Pathophysiology <ul><li>The brain is the most metabolically active tissue in the body . </li></ul><ul><li>While representing only 2% of the body's mass, it requires 15-20% of the total resting cardiac output to provide the necessary glucose and oxygen for its metabolism . </li></ul>
  4. 4. <ul><li>Ischemic strokes result from events that limit or stop blood flow, such as embolism, thrombosis in situ, or relative hypoperfusion . </li></ul><ul><li>As blood flow decreases, neurons cease functioning, and irreversible neuronal ischemia and injury begin at blood flow rates of less than 18 mL / 100 mg / min </li></ul>
  5. 5. Ischemic cascade <ul><li>The processes involved in stroke injury at the cellular level are referred to as the ischemic cascade . </li></ul><ul><li>Within seconds to minutes of the loss of glucose and oxygen delivery to neurons, the cellular ischemic cascade begins . </li></ul><ul><li>This is a complex process that begins with cessation of the electrophysiologic function of the cells . </li></ul><ul><li>The resultant neuronal and glial injury produces edema in the ensuing hours to days after stroke, causing further injury to the surrounding neuronal tissues </li></ul>
  6. 6. <ul><li>Ischemic penumbra </li></ul><ul><li>An acute vascular occlusion produces heterogeneous regions of ischemia in the dependent vascular territory . </li></ul><ul><li>The quantity of local blood flow is comprised of any residual flow in the major arterial source and the collateral supply, if any . </li></ul>
  7. 7. <ul><li>Regions of the brain without significant flow are referred to collectively as the core, and these cells are presumed to die within minutes of stroke onset . </li></ul><ul><li>Zones of decreased or marginal perfusion are collectively called the ischemic penumbra . </li></ul><ul><li>Tissue in the penumbra can remain viable for several hours because of marginal tissue perfusion, and currently studied pharmacologic interventions for preservation of neuronal tissue target this penumbra </li></ul>
  8. 8. Mechanisms of stroke <ul><li>-Embolic strokes </li></ul><ul><li>Emboli may either be of cardiac or arterial origin . Cardiac sources include:atrial fibrillation, recent myocardial infarction ( 1-3% of all acute myocardial infarctions [ AMIs ]) , prosthetic valves, native valvular disease, endocarditis, mural thrombi, dilated cardiomyopathy, or patent foramen ovale allowing passage of venous circulation emboli . </li></ul>
  9. 9. <ul><li>Arterial sources are atherothrombolic or cholesterol emboli that develop in the arch of the aorta and in the extracranial arteries ( ie, carotid and vertebral arteries ). Embolic strokes tend to have a sudden onset, and neuroimaging may demonstrate previous infarcts in several vascular territories </li></ul>
  10. 10. -Thrombotic strokes <ul><li>Thrombotic strokes include large - vessel strokes ( 70% ) and small - vessel or lacunar strokes ( 30% ). </li></ul><ul><li>They are due to in situ occlusions, characteristically on atherosclerotic lesions in the carotid, vertebrobasilar, and cerebral arteries, typically proximal to major branches . Thrombogenic factors include injury to and loss of endothelial cells exposing the subendothelium and platelet activation by the subendothelium, activation of the clotting cascade, inhibition of fibrinolysis, and blood stasis </li></ul>
  11. 11. <ul><li>Thrombotic strokes are thought to originate on ruptured atherosclerotic plaques . </li></ul><ul><li>Intracranial atherosclerosis may be the cause in patients with widespread atherosclerosis . </li></ul><ul><li>In other patients, especially younger patients, other causes should be considered, including coagulation disorders ( eg, antiphospholipid antibodies, protein C deficiency, protein S deficiency ) , sickle cell disease, fibromuscular dysplasia, arterial dissections, and vasoconstriction associated with substance abuse </li></ul>
  12. 12. -Lacunar stroke <ul><li>Lacunar strokes represent 20% of all ischemic strokes . </li></ul><ul><li>They occur when the penetrating branches of the middle cerebral artery ( MCA ) , the lenticulostriate arteries, or the penetrating branches of the circle of Willis, vertebral artery, or basilar artery become occluded . </li></ul><ul><li>Causes of lacunar infarcts include microatheroma, lipohyalinosis, fibrinoid necrosis secondary to hypertension or vasculitis, hyaline arteriosclerosis, and amyloid angiopathy . </li></ul><ul><li>The great majority are related to hypertension . </li></ul><ul><li>Of all stroke types, lacunar strokes have the best prognosis </li></ul>
  13. 13. -Watershed infarcts <ul><li>These infarcts, also known as border zone infarcts, develop from relative hypoperfusion in the most distal arterial territories and can produce bilateral symptoms . Frequently, these are associated with surgical procedures . </li></ul>
  14. 14. Frequency <ul><li>Approximately 750,000 strokes occur each year, approximately 500,000 are ischemic strokes . </li></ul><ul><li>stroke is the third leading cause of death and the leading cause of adult disability . </li></ul>
  15. 15. Mortality / Morbidity <ul><li>Stroke is the third leading cause of death in the United following cardiac diseases and cancer - related deaths . Approximately 29% of patients die within 1 year following a stroke; this percentage rises in patients older than 65 years . </li></ul><ul><li>Stroke is the leading cause of disability in the United States; 31% of stroke survivors need help in taking care of themselves after a stroke, 20% need some type of assistance for walking, and 16% need to be placed in some form of institution providing assisted living . </li></ul><ul><li>At least one third of stroke survivors have depression </li></ul>
  16. 16. Race <ul><li>stroke has a higher incidence in the black population than in the white population </li></ul><ul><li>In black males, the incidence is approximately 93 per 100,000, with a death rate of approximately 51% . </li></ul><ul><li>In black females, incidence is 79 per 100,000 with a death rate of 39.2% . </li></ul>
  17. 17. <ul><li>Young blacks have a 2-3 times greater risk of ischemic stroke than the white population of the same age, and they are 2.5 times more likely to die of stroke . </li></ul><ul><li>White males have a stroke incidence of 62.8 per 100,000, with death being the final outcome in 26.3% of cases, compared with women who have a stroke incidence of 59 per 100,000 and a death rate of 39.2% </li></ul><ul><li>Hispanics have a lower overall incidence of stroke than whites and blacks but more frequent lacunar strokes and stroke at an earlier age </li></ul>
  18. 18. <ul><li>Sex </li></ul><ul><li>In patients younger than 60 years, the incidence of stroke is greater in males ( 3:2 ratio) ) </li></ul><ul><li>Age </li></ul><ul><li>Stroke can occur in patients of all ages, including children </li></ul><ul><li>Risk of stroke increases with age, especially in patients older than 64 years, in whom 75% of all strokes occur </li></ul>
  19. 19. History <ul><li>The American Stroke Association advises the public to be aware of the symptoms of stroke . These symptoms are as follows </li></ul><ul><ul><li>1-Sudden numbness or weakness of face, arm, or leg, especially on one side of the body </li></ul></ul><ul><ul><li>2-Sudden confusion, difficulty in speaking or understanding </li></ul></ul><ul><ul><li>3-Sudden deterioration of vision of one or both eyes </li></ul></ul><ul><ul><li>4-Sudden difficulty in walking, dizziness, and loss of balance or coordination </li></ul></ul><ul><ul><li>5-Sudden, severe headache with no known cause </li></ul></ul>
  20. 20. <ul><li>Focus medical history on identifying risk factors for atherosclerotic and cardiac disease, including hypertension, diabetes mellitus, tobacco use, high cholesterol, and a history of coronary artery disease, coronary artery bypass, or atrial fibrillation </li></ul>
  21. 21. <ul><li>Consider stroke in any patient presenting with acute neurological deficit or any alteration in level of consciousness . </li></ul><ul><li>Common signs of stroke include the following: </li></ul><ul><ul><li>1-Acute hemiparesis or hemiplegia </li></ul></ul><ul><ul><li>2-Complete or partial hemianopia, monocular or binocular visual loss, or diplopia </li></ul></ul><ul><ul><li>3-Dysarthria or aphasia </li></ul></ul><ul><ul><li>4-Ataxia, vertigo, or nystagmus </li></ul></ul><ul><ul><li>5-Sudden decrease in consciousness </li></ul></ul>
  22. 22. <ul><li>In younger patients, elicit history of trauma, coagulopathies, illicit drug use ( especially cocaine ) , migraines, or use of oral contraceptives or over - the - counter medications ( especially those containing phenylpropanolamine </li></ul>
  23. 23. <ul><li>If the patient is a candidate for thrombolytic therapy, a thorough review of the inclusion and exclusion criteria from the NINDS trial must be performed . The exclusion criteria largely focus on identifying risk of hemorrhagic complication associated with thrombolytic use . </li></ul>
  24. 24. <ul><li>Physical examination is directed toward 5 major areas : </li></ul><ul><li>( 1 ) assessing the airway, breathing, and circulation ( ABCs ) , </li></ul><ul><li>( 2 ) defining the severity of the patient's neurologic deficits, </li></ul><ul><li>( 3 ) identifying potential causes of the stroke ( 4 ) identifying potential stroke mimics, and </li></ul><ul><li>( 5 ) identifying comorbid conditions </li></ul>
  25. 25. <ul><li>1-Vital signs </li></ul><ul><li>2-Head, ears, eyes, nose, and throat examination </li></ul><ul><li>3-Cardiac : Cardiac arrhythmias, such as atrial fibrillation </li></ul><ul><li>4-Extremities : Carotid or vertebrobasilar dissections, and less commonly, thoracic aortic dissections, may cause ischemic stroke </li></ul><ul><li>5 -The neurologic examination must be thorough. </li></ul><ul><li>A directed and focused examination can be performed in minutes and not only provides great insight into the potential cause of the patient's deficits, but also helps determine the intensity of treatment required . </li></ul>
  26. 26. <ul><li>A very useful tool in measuring neurological impairment is the National Institutes of Health Stroke Scale ( NIHSS ). </li></ul><ul><li>This scale can be used easily, is reliable and valid, provides insight to the location of vascular lesions, and can be correlated with outcome in patients with ischemic stroke . </li></ul><ul><li>It focuses on 6 major areas of the neurologic examination : </li></ul><ul><li>( 1 ) level of consciousness, ( 2 ) visual function, ( 3 ) motor function, ( 4 ) sensation and neglect, ( 5 ) cerebellar function, and ( 6 ) language </li></ul>
  27. 27. <ul><li>Risk factors for ischemic stroke comprise both modifiable and nonmodifiable characteristics . </li></ul><ul><li>Identification of risk factors in each patient can uncover clues to the cause of the stroke and the most appropriate treatment plan </li></ul>
  28. 28. <ul><li>Nonmodifiable risk factors include: </li></ul><ul><li>age, race, sex, ethnicity, </li></ul><ul><li>history of migraine headaches, sickle cell disease, fibromuscular dysplasia, and hereditory diseases. </li></ul>
  29. 29. Modifiable risk factors include the following: <ul><li>1-Hypertension ( the most important risk factor) </li></ul><ul><ul><li>2-Diabetes mellitus </li></ul></ul><ul><ul><li>3-Cardiac disease: atrial fibrillation, valvular disease, </li></ul></ul><ul><ul><li>mitral stenosis, structural anomalies allowing right to </li></ul></ul><ul><ul><li>left shunting, such as a patent foramen ovale, atrial </li></ul></ul><ul><ul><li>and ventricular enlargement </li></ul></ul><ul><ul><li>4-Hypercholesterolemia </li></ul></ul><ul><ul><li>5-Transient ischemic attacks ( TIAs) </li></ul></ul><ul><ul><li>6-Carotid stenosis </li></ul></ul><ul><ul><li>7-Hyperhomocystinemia </li></ul></ul><ul><ul><li>8-Lifestyle issues </li></ul></ul><ul><ul><li>9 - Excessive alcohol intake, tobacco use, illicit drug use, </li></ul></ul><ul><ul><li>obesity, physical inactivity </li></ul></ul><ul><ul><li>10-Oral contraceptive use </li></ul></ul>
  30. 30. Lab Studies: <ul><li>1-Glucose and Electrolyte disorders tests: Hypoglycemia is the most common electrolyte abnormality that produces stroke like symptoms . It is easily corrected, and correction leads to rapid resolution of symptoms . </li></ul><ul><li>Hyperglycemia and uremia should be considered carefully as the cause of ongoing mental and physical deficits. </li></ul>
  31. 31. <ul><ul><li>2-Complete blood count : provides key information regarding hemoglobin and hematocrit, thus evaluating for anemia and possible deficiencies in oxygen - carrying capacity . Additionally, sickle cell disease, polycythemia, and thrombocytosis increase the risk for stroke. </li></ul></ul>
  32. 32. <ul><ul><li>3-Prothrombin time ( PT ) and activated partial thromboplastin time ( aPTT ) tests : </li></ul></ul><ul><ul><li>many patients with acute stroke are on anticoagulants, such as heparin or warfarin . Treatment decisions, such as thrombolytic use, require data on coagulation status . </li></ul></ul><ul><ul><li>An elevated international normalized ratio ( INR ) may preclude patients from receiving thrombolytics </li></ul></ul>
  33. 33. <ul><ul><li>4-Cardiac enzymes : Not infrequently patients with acute stroke also experience acute myocardial ischemia . </li></ul></ul><ul><ul><li>In addition to ECG findings, increased cardiac enzymes might suggest concomitant cardiac injury. </li></ul></ul><ul><ul><li>5-Arterial blood gas ( ABG ) analysis : </li></ul></ul><ul><ul><li>In patients with suspected hypoxemia, ABG will define the severity of hypoxemia and may detect acid - base disturbances </li></ul></ul>
  34. 34. <ul><li>6-Additional laboratory tests may include rapid plasma reagent ( RPR ) , toxicology screen, fasting lipid profile, sedimentation rate, pregnancy test, antinuclear antibody ( ANA ) , rheumatoid factor and homocysteine. </li></ul>
  35. 35. <ul><li>7-In select patients with possible hypercoagulable states, protein C, protein S, antithrombin III, and Factor V Leiden testing may be required . These blood abnormalities mainly contribute to venous thrombosis but may be relevant in patients with cardiac shunts or cerebral venous thromboses </li></ul>
  36. 36. <ul><li>8-The anticardiolipin antibody and the lupus inhibitor, both antiphospholipid antibodies, correlate with arterial stroke, as well as with deep venous thrombosis, pulmonary embolism, myocardial infarction, and miscarriage </li></ul>
  37. 37. Imaging Studies <ul><li>CT is the most commonly used form of neuroimaging in evaluation of patients with apparent acute stroke . </li></ul><ul><li>Noncontrast CT is very sensitive in detecting intracerebral and subarachnoid hemorrhage, as well as subdural hematomas . </li></ul><ul><ul><li>Although CT is not very sensitive for early ischemia ( <6 h ) , several findings can suggest ischemic changes relatively early in the time course of stroke . </li></ul></ul><ul><ul><li>Loss of the gray - white matter interface, loss of sulci, and loss of the insular ribbon are subtle signs of early ischemia </li></ul></ul>
  38. 38. <ul><ul><li>Early mass effect and areas of hypodensity suggest irreversible injury and identify patients at higher risk of hemorrhage if given thrombolytics . </li></ul></ul><ul><ul><li>Significant hypodensity on the baseline scan should prompt the physician to question the time of onset . </li></ul></ul><ul><ul><li>Hypodensity in an area greater than one third of the MCA distribution is considered by some a relative contraindication for thrombolytics </li></ul></ul>
  39. 39. <ul><ul><li>A dense MCA sign suggests a clot in the MCA . These patients are at risk for significant hemispheric strokes . Some authorities believe that these patients may benefit most from aggressive thrombolytic therapy, including intra - arterial therapies, but this has not been specifically proven in double - blind randomized trials . </li></ul></ul>
  40. 40. <ul><ul><li>CT scan may demonstrate other causes of the patient's symptoms, including neoplasm, epidural and subdural hemorrhage, aneurysm, abscess, arteriovenous malformation, and hydrocephalus </li></ul></ul>
  41. 41. <ul><li>MRI ( MRA ) is a major advance in the neuroimaging of stroke . MRI not only provides great structural detail but also can demonstrate impaired metabolism .. </li></ul>
  42. 42. <ul><ul><li>Diffusion - weighted MRI ( DW - MRI ) can detect areas of ischemic brain injury earlier in the evolution of ischemia than standard T1 / T2-weighted MRI images or CT scan by detecting changes in water molecule mobility </li></ul></ul><ul><ul><li>Perfusion-weighted MRI ( PW - MRI ) uses injected contrast material to demonstrate areas of decreased perfusion . </li></ul></ul><ul><ul><li>These sequences in combination with DW - MRI yields areas of diffusion - weighted imaging / perfusion - weighted imaging ( DW - MRI / PW - MRI ) mismatch, theoretically identifying potentially salvageable tissues </li></ul></ul>
  43. 43. <ul><ul><li>MRA : This noninvasive technique demonstrates vascular anatomy and occlusive disease of the head and neck without the need for contrast material </li></ul></ul>
  44. 44. <ul><li>Echocardiography : Transthoracic echocardiography ( TTE ) and transesophageal echocardiography ( TEE ) are useful tools in evaluating patients with possible cardiogenic sources of their stroke . </li></ul><ul><li>TEE is more sensitive than TTE and can evaluate the aortic arch and thoracic aorta for plaques or dissections </li></ul>
  45. 45. <ul><li>ECG : Stroke and cardiovascular disease share many risk factors . ECG may demonstrate cardiac arrhythmias, such as atrial fibrillation, or may indicate acute ischemia . All patients with stroke should have an ECG as part of their initial evaluation </li></ul><ul><li>Chest radiography should be performed when clinically indicated </li></ul>
  46. 46. <ul><li>Digital subtraction angiography is considered the definitive method for demonstrating vascular lesions, including occlusions, stenoses, dissections, and aneurysms . </li></ul>
  47. 47. <ul><li>Carotid duplex scanning is one of the most useful tests in evaluating patients with stroke . </li></ul>
  48. 48. Management <ul><li>We should decide from the history, duration of onset and clinical presentation wither the case is anterior circulation (contralateral hemiparesis, dysphasia, apraxia, agnosia, preserved consciousness and visual field defect) or posterior circulation (vertigo, ataxia, dysphagia, diplopia, disturbed level of consciuosness, crossed hemiparesis and bilateral presentation) because if we received the patient within 160mins or less and there is no contraindications for thrombolytic therapy we decide this line of treatment accordingly. </li></ul>
  49. 49. Blood pressure managment <ul><li>Candidates for fibrinolysis </li></ul><ul><li>Pretreatment SBP >185 or DBP >110 mm Hg Labetalol 10-20 mg IVP 1-2 doses or Enalapril 1.25 mg IVP </li></ul><ul><li> </li></ul>
  50. 50. <ul><li>Posttreatment </li></ul><ul><li>DBP >140 mm Hg </li></ul><ul><li>Sodium nitroprusside ( 0.5 mcg / kg / min SBP >230 mm Hg or DBP 121-140 mm Hg </li></ul><ul><li>Labetalol 10-20 mg IVP and consider labetalol infusion at 1-2 mg / min or nicardipine 5 mg / h IV infusion and titrate SBP 180-230 mm Hg or DBP 105-120 mm Hg </li></ul><ul><li>Labetalol 10 mg IVP, may repeat and double every 10 min up to maximum dose of 150 mg </li></ul>
  51. 51. <ul><li>Noncandidates for fibrinolysis </li></ul><ul><li>DBP >140 mm Hg </li></ul><ul><li>Sodium nitroprusside 0.5 mcg / kg / min; may reduce approximately 10-20% SBP >220 or DBP 121-140 mm Hg or MAP >130 mm Hg </li></ul><ul><li>Labetalol 10-20 mg IVP over 1-2 min; may repeat and double every 10 min up to maximum dose of 150 mg or nicardipine 5 mg / h IV infusion and titrate SBP< 220 mm Hg or DBP 105-120 mm Hg or MAP <130 mm Hg Antihypertensive therapy indicated only if AMI, aortic dissection, severe CHF, or hypertensive encephalopathy present </li></ul>
  52. 52. <ul><li>If a case of anterior circulation and candidate for thrombolytic therapy (onset less than 160mins) </li></ul><ul><li>CT scan , no hemorrhage </li></ul><ul><li>Carotid Doppler, patent carotid arteries </li></ul><ul><li>IV infusion of Altiplase 0.9mg/kg not exceed 90mg </li></ul><ul><li>10% pulse IV and 90% IV infusion over 1 hour </li></ul>
  53. 53. <ul><li>Discharge patient to the ICU for close monitoring </li></ul><ul><li>Start heparine in the second day with antiplatelet </li></ul><ul><li>If there is underlying embolic source long term anticoagulant +/- antiplatelet +/- lipid-lowering agent </li></ul>
  54. 54. <ul><li>If a case of posterior circulation and candidate for thrombolytic therapy (onset within 160mins and in some studies less than 5 hours) </li></ul><ul><li>CT, no hemorrhage </li></ul><ul><li>Send patient to Cath lab. </li></ul><ul><li>Angiography to the posterior circulation </li></ul><ul><li>If no thrombus go out and keep patient on heparine. </li></ul><ul><li>If there is thrombus Insitu infusion of Altiplase </li></ul>
  55. 55. <ul><li>Discharge patient to the ICU for close monitoring </li></ul><ul><li>Start heparine in the second day with antiplatelet </li></ul><ul><li>If there is underlying embolic source long term anticoagulant +/- antiplatelet +/- lipid-lowering agent </li></ul>
  56. 56. <ul><li>If the patient is not a candidate for thrombolytic therapy </li></ul><ul><li>Keep on Antiplatelet (Asprine, Clopidogrile and Amibexicam) </li></ul><ul><li>Maintain BP (as above) and Blood Volume </li></ul><ul><li>In case of underlying embolization heparine for 5-7days and long term Warfarine with PT INR followup (range 2.5-4) </li></ul><ul><li>Heparine use is contraversy?? In case of thrombotic stroke. </li></ul>
  57. 57. <ul><li>-Blood glucose </li></ul><ul><li>Treat hypoglycemia with D50 </li></ul><ul><li>Treat hyperglycemia with insulin if serum glucose >200 mg / dL </li></ul>
  58. 58. <ul><li>-Cardiac monitor </li></ul><ul><li>Continuous monitoring for ischemic changes or atrial fibrillation </li></ul><ul><li>Intravenous fluids - </li></ul><ul><li>Avoid D5W and excessive fluid administration IV isotonic sodium chloride solution at 50 mL / h </li></ul>
  59. 59. <ul><li>-Oral intake </li></ul><ul><li>NPO initially; aspiration risk is great, avoid oral intake until swallowing assessed </li></ul><ul><li>-Oxygen Supplement if indicated </li></ul><ul><li>-Temperature </li></ul><ul><li>Avoid hyperthermia, oral or rectal acetaminophen as needed </li></ul>
  60. 60. <ul><li>-Diet therapy </li></ul><ul><li>-Treat hyperlipidemia </li></ul><ul><li>-Physiotherapy </li></ul><ul><li>-Treat convulsion, Fever, depression and complications </li></ul><ul><li>-Steroid when indicated (increase ICP, large infarction with midline shift on CT, CVT induced infarction and acute bacterial induced infarction. </li></ul>
  61. 61. Contraindication of thrombolytic therapy: <ul><li>1-Onset more than 160mins </li></ul><ul><li>2-age less than 18y </li></ul><ul><li>3-TIA or minor stoke </li></ul><ul><li>4-large infarction or Hm stroke. </li></ul><ul><li>5-DBP 120Hg or SBP 220Hg </li></ul><ul><li>6-IC surgery 3months ago </li></ul><ul><li>7-Major surgery 3wks ago </li></ul><ul><li>8-Previous ICH </li></ul><ul><li>9-Diabetic retinopathy </li></ul><ul><li>10-Low platelet </li></ul><ul><li>11-Sugar less than 60mg or more than 200mg </li></ul><ul><li>12-Bleedind tendency </li></ul><ul><li>13-morbid case </li></ul><ul><li>14-prolonged PT or PTT </li></ul>