INFARCTION STROKE

Case Report

Name	Mrs. B
Age	74 years 6 months
Gender	Female

  

II. ANAMNESIS

Alloanamnesis (November, 25^th 2015)

Chief Complaint

The weakness on the right arm and leg

Present Illness History

§  Since a day before admission, the patient has complained the weakness on her right arm and leg. At first, the patient has complained the numbness and then weakened suddenly when she woke up on the morning. She never complained the numbness before.

§  Furthermore, the patient’s speech became slurred and nonfluent. The patient also can’t control her urination and defecation.

§  No history of headache, vomiting, losing of vision and decreasing of consciousness. No history of trauma.

Past Illness History

§  Unknown history of Hypertension, Diabetes mellitus and Cardiovascular disease

§  No history of obesity

Family Illness History

§  No history of Hypertension

§  No history of Diabetes mellitus

§  No history of Cardiovascular disease

Socioeconomic History

§  Menopause on 52 years old.

§  No history of oral contraception used

THE SUMMARY OF ANAMNESIS

Mrs. B, 74 years old admitted to the hospital on November, 24^th 2015. The patient has complained the sudden weakness on the right arm and leg since a day before admission. The patient’s speech became slurred and nonfluent and she also can’t control her urination and defecation. There were unknown history of hypertension, diabetes mellitus and cardiovascular disease.

III. PHYSICAL EXAMINATION

A.    General status

Blood Pressure   : 170/80 mmHg

Heart Rate          : 98 bpm

Respiratory Rate            : 20 times per minute

Temperature       : 37.8°C

B.     Neurological status

1)      Consciousness               :  Alertness                     GCS   :   E4M6Vaphasia          

2)      Cognitive Function       :  Cognitive Impairment

3)      Neck Stiffness               :  Negative

Cranial Nerves                    : Dysarthria

Motoric                                : Hemiparesis (UMN Type)

Sensory                                : Can’t be assessed

Coordination                      : Can’t be assessed

Autonomy                            : Abnormal urination and defecation

Reflex                                   : Normal

Gajah Mada Algorithm     : Infarction stroke

Siriraj Score                        : Infarction stroke

XI. WORKING DIAGNOSIS

CLINICAL DIAGNOSIS                  : Stroke

TOPICAL DIAGNOSIS                    : Carotid system

ETIOLOGICAL DIAGNOSIS         : Infarction stroke

DIFFERENTIAL DIAGNOSIS        : Hemorrhagic stroke

XII. SUGGESTION EXAMINATION

§  Blood routine

§  Blood chemistry

§  Electrocardiography : LVH

§  Chest X-ray : Normal Limits

§  Head CT Scan : --

XIII. SUGGESTION FOR MANAGEMENT THERAPY

§  General

-          Immobilization and head up 30°

-          Monitoring of vital sign

-          Medical rehabilitation

-          IVFD (30ml/kgBB/day) à Ringer Lactate 20 dpm

§  Special

-          Neuroprotector      : Citicoline 2 x 500 mg per IV

-          Antiplatelets          : Aspilet 3 x 500 mg per oral

XIV. LABORATORY AND RADIOLOGY FINDINGS

1.      Blood Routine (November, 24^th 2015)

-          Hemoglobin                : 12.2 g/dL

-          Hematocrit                  : 34 %

-          Leukocyte                   : 6.600/mm³

-          Thrombocyte               : 247.000/mm³

Interpretation: Normal

2.      Blood Chemistry

(November, 24^th 2015)

-          Glucose                             : 155 mg/dL

-          Ureum                        : 38.4 mg/dL

-          Creatinin                    : 0.96 mg/dL

-          AST                            : 19.6 U/L

-          ALT                           : 12 U/L

Electrolite:

-          Sodium                       : 144.8 mmol/L

-          Potassium                   : 2.89 mmol/L

-          Chloride                     : 115.9 mmol/L

 (November, 25^th 2015)

-          Chor                            : 165 mg/dL

-          HDL                            : 46.0 mg/dL

-          Triglyceride                 : 75 mg/dL

-          Uric acid                     : 6.3 mg/dL

-          LDL Cholesterol         : 104 mg/dL

 

         Head CT Scan without contrast

Interpretation: infarction on the left hemisphere cerebri

FINAL DIAGNOSIS

-          Infarction stroke

Discussion

INFARCTION STROKE

1.      Definition

Stroke is applied to a sudden focal neurologic syndrome, specifically the type due to cerebrovascular disease. The term cerebrovascular disease designates any abnormality of the brain resulting from a pathologic process of the blood vessels. Pathologic process is given an inclusive meaning namely, occlusion of the lumen by embolus or thrombus, rupture of a vessel, an altered permeability of the vessel wall, or increased viscosity or other change in the quality of the blood flowing through the cerebral vessels. The vascular pathologic process may be considered not only in its grosser aspects embolism, thrombosis, dissection, or rupture of a vessel but also in terms of the more basic or primary disorder, i.e., atherosclerosis, hypertensive arteriosclerotic change, arteritis, aneurysmal dilation, and developmental malformation. Equal importance attaches to the secondary parenchymal changes in the brain resulting from the vascular lesion. These are of two main types ischemia, with or without infarction, and hemorrhage and unless one or the other occurs, the vascular lesion usually remains silent. The only exceptions to this statement are the local pressure effects of an aneurysm, vascular headache (migraine, hypertension, temporal arteritis), multiple small vessel disease with progressive encephalopathy (as in malignant hypertension or cerebral arteritis), and increased intracranial pressure (as occurs in hypertensive encephalopathy and venous sinus thrombosis). Also, persistent acute hypotension may cause ischemic necrosis in regions of brain between the vascular territories of cortical vessels, even without vascular occlusion.¹

More than any other organ, the brain depends from moment to moment on an adequate supply of oxygenated blood. Constancy of the cerebral circulation is assured by a series of baroreceptors and vasomotor reflexes under the control of centers in the lower brainstem. Obstruction of an artery by thrombus or embolus is the usual cause of focal ischemic damage, but failure of the circulation and hypotension from cardiac decompensation or shock, if severe and prolonged enough, can produce focal as well as diffuse ischemic changes.¹

Focal cerebral ischemia differs fundamentally from global ischemia. In the latter state, if absolute, there is no cerebral blood flow of the entire brain and irreversible destruction of neurons occurs within 4 to 8 min at normal body temperature. In focal ischemia, there is nearly always some degree of circulation (via collateral vessels), permitting to a varying extent the delivery of oxygenated

blood and glucose.

The effects of a focal arterial occlusion on brain tissue also vary depending on the location of the occlusion in relation to available collateral and anastomotic channels. If the obstruction lies proximal to the circle of Willis (toward the heart), the anterior and posterior communicating arteries of the circle are often adequate to prevent infarction. In occlusion of the internal carotid artery in the neck, there may be anastomotic flow from the external carotid artery through the ophthalmic artery or via other smaller externalinternal connections. With blockage of the vertebral artery, the anastomotic flow may be via the deep cervical, thyrocervical, or occipital arteries or retrograde from the other vertebral artery. If the occlusion is in the stem portion of one of the cerebral arteries, i.e., distal to the circle of Willis, a series of meningeal interarterial anastomoses may carry sufficient blood into the compromised territory to lessen (rarely to prevent) ischemic damage. There is also a capillary anastomotic system between adjacent arterial branches, and although it may reduce the size of the ischemic field, particularly of the penetrating arteries, it is usually not significant in preventing infarction. Thus,

in the event of occlusion of a major arterial trunk, the extent of infarction ranges from none at all to the entire vascular territory of that vessel. Between these two extremes are all degrees of variation in the extent of infarction and its degree of completeness.¹

Additional ischemia-modifying factors determine the extent of necrosis. The speed of occlusion assumes importance; gradual narrowing of a vessel allows time for collateral channels to open. The level of blood pressure may influence the result; hypotension at a critical moment may render anastomotic channels ineffective. Hypoxia and hypercapnia are presumed to have deleterious effects. Altered viscosity and osmolality of the blood and hyperglycemia are potentially important factors but difficult to evaluate. Finally, anomalies of vascular arrangement (of neck vessels, circle of Willis, and surface arteries) and the existence of previous vascular occlusions must influence the outcome.¹

The specific neurologic deficit obviously relates to the location and size of the infarct or focus of ischemia. The territory of any artery, large or small, deep or superficial, may be involved. When an infarct lies in the territory of a carotid artery, as would be expected, unilateral signs predominate: hemiplegia, hemianesthesia, hemianopia, aphasia, and agnosias are the usual consequences. In the territory of the basilar artery, the signs of infarction are frequently bilateral and occur in conjunction with cranial nerve palsies and other segmental brainstem and cerebellar signs; quadriparesis, hemiparesis, and/or unilateral or bilateral sensory impairment are typical, coupled with diplopia, dysarthria, and vertigo in various combinations.¹

2.      Risk factor

            According to the American Heart Association (AHA), the risk factors of stroke are divided into two, that are not modifiable risks factors and modifiable risk factors. Not modifable risk factors include: age, sex, low birth weight, race or ethnicity, and genetic factors. Modifiable risk factors include: hypertension, smoking, diabetes, nutritional imbalance, lack of physical activity, alcohol consumption, and drug abuse. Incidence of stroke can occur with one or more risk factors (multifactor).^1-3

Table 3. Stroke risk factors^1-3

Not Modifable

Modifable

1.    Age 2.    Gender 3.    Genetic 4.    Ethnic

1.    Stroke history                            10. Smoking 2.    Hypertension                             11. Alcohol 3.    Heart disease                             12. Drug abuse 4.    Diabetes melitus                        13. Hyperhomosisteinemia 5.    Carotid stenosis                         14. Antibody anti fosfolipid 6.    TIA                                                         15. Hyperurisemia 7.    Hypercholesterolemia                 16. Elevation of hematocrit 8.    Oral contraception                      17. Elevation of fibrinogen 9.    Obesity

3.      Clinical Manifestation

The specific neurologic deficit obviously relates to the location and size of the infarct or focus of ischemia. The territory of any artery, large or small, deep or superficial, may be involved. When an infarct lies in the territory of a carotid artery, as would be expected, unilateral signs predominate: hemiplegia, hemianesthesia, hemianopia, aphasia, and agnosias are the usual consequences. In the territory of the basilar artery, the signs of infarction are frequently bilateral and occur in conjunction with cranial nerve palsies and other segmental brainstem and cerebellar signs; quadriparesis, hemiparesis, and/or unilateral or bilateral sensory impairment are typical, coupled with diplopia, dysarthria, and vertigo in various combinations.^1,2

4.       Management

Stroke patients should be handled by a multidisciplinary team. Management stroke be done by improving the general state of the patient, treat the risk factors, and prevent complications.^3-6

4.1 Hyperacute stadium

            Action at this stadium is done at the Emergency Room, the aim is to prevent the widespread of brain tissue damaging. At this stage, patients were given oxygen 2 L / min and crystalloid/colloid fluid, avoid administration of dextrose. Brain CT scan examination, electrocardiography, chest X-ray, complete peripheral blood and platelet count, prothrombin time / INR, APTT, blood glucose, blood chemistry (including electrolytes), and if hypoxia, do the blood gas analysis. Other actions in the Emergency Room are providing mental support to patients and provide an explanation to the family to remain calm.^3-6

4.2              Acute stadium

4.2.1        General treatment

Place the patient’s head in 30^o positions, head an chest in a field, change the sleep position every 2 hours. Mobilization began gradually when hemodynamically stable. Furthermore, free the airway, give oxygen 1-2 liters / min. If necessary, intubation. Fever overcome with compresses and antipyretic, then look for the cause, when the bladder is full, emptied (preferably with intermittent catheters).^3-6

Fluid nutrition with 1500-2000 isotonic cristalloid or colloid and electrolyte as needed, avoid fluids containing glucose or isotonic saline. Nutrition orally only if swallowing function well, if there is swallowing disorders or decreased consciousness, nasogastric tube is recommended. ^3-6

Blood glucose levels > 150 mg% should be corrected with continuous intravenous drip insulin during 2-3 days. Hipoglikemia (blood glucose < 60 mg% or < 80mg% with symptoms) should be corrected immediatelywith dextrose 40% iv until return to normal and the cause must be sought. ^3-6

Headache, nausea, and vomiting treated according to the symptoms. Blood preassure doesn’t need taken down immediately, except when the systolic pressure ≥ 220 mmHg and diastolic pressure ≥120 mmHg, Mean Arterial Blood Pressure (MAP) ≥ 130 mmHg (the two measurements with an interval of 30 minutes), or obtained acute myocardial infarction, congestive heart failure as well as kidney failure. Maximal blood pressure reduction was 20%, and the recommended drugs are sodium nitroprusside, alpha-beta receptor blockers, ACE blockers, or antagonists calsium. ^3-6

If hypotension occurs, the systolic pressure ≤ 90 mmHg, diastolic ≤70 mm Hg, the patient should be given 250 mL of 0.9% NaCl for 1 hour, followed by 500 mL for 4 hours and 500 mL for 8 hours or until hypotension treated. If not corrected, that is systolic blood pressure still <90 mmHg, dopamine 2-20 mcg / kg / minute can be given until the systolic blood pressure ≥110 mmHg. ^3-6

If there is seizure, give diazepam 5-20 mg iv slowly for 3 minutes, the maximum dosage is 100 mg per day, followed by oral administration of anticonvulsants such as phenytoin, carbamazepine. If the seizure appeared after 2 weeks, given orally long-term anticonvulsant. ^3-6

If there is an increased of intracranial pressure, bolus mannitol were given an of 0.25 to 1 g / kg per 30 minutes intravenously, and if  rebound phenomenon suspected, or general condition deteriorated, followed by 0,25g / kg per 30 minutes every 6 hours for 3-5 days. Monitoring of the osmolarity should be performed (<320 mmol), alternatively can be administered hypertonic solutions (NaCl 3%) or furosemid. ^3-6

4.2.2        Special treatment

The goal is to reperfusion by administration of antiplatelet agent such as aspirin and anticoagulant, or with trombolytic  rt-PA (combinant tissue Plasminogen Activator), and neuroprotective agent, such as citicoline or piracetam. ^3-6

4.3 Subacute Stadium

Medical measures may include cognitive therapy, behavior, swallowing, speech therapy, and bladder training (including physical therapy). Given the long course of the disease, it takes a special intensive treatment of post-stroke in the hospital with the goal of independence of the patient, understand, comprehend and implement primary and secondary prevention programs.⁶

Subacute phase treatment:⁶

-          Continuing the appropriate treatment of acute conditions before

-          The management of complications

-          Restoration / rehabilitation (as needed of patients), which is physiotherapy, speech therapy, cognitive therapy, and occupational therapy

-          Secondary Prevention

-          Family education and discharge planning

 

THE BASIC OF DIAGNOSIS

1. Basic clinical diagnosis

From the history taking, a 74 years old woman had a sudden weakness on the right arm and leg (Hemiparesis). And her speech became slurred and nonfluent.  She also can’t control her urination and defecation. No history of trauma. It is consistent with the WHO’s definition that clinical symptoms of stroke is cerebral disorders, either focal or global attack in 24 hours or more, no illness is found other than vascular disorders. And elderly is a risk factor of stroke.

2. Basic topical diagnosis

Carotid system had been considered in this patient because there is hemiparesis and aphasia. Hemiparesis and aphasia is symptoms of middle cerebral artery occlusion. Middle cerebral artery is the greatest branch of internal carotid artery. From the physical examination there is right hemiparesis, so the lesion is on the left hemisphere because a lesion in one side of carotid system will lead to contralateral neurological deficit.

3. Basic etiological diagnosis

Basic etiological diagnosis of this patient has been leaded to infarction stroke, because on this patient there are no losing of consciousness, no projectil vomiting, no headache, no increasing of diastolic blood pressure and hemiparesis. It is also supported by Siriraj score and Gajah Mada Algorithm that give the impression of the infarction stroke.

4. Basic differential diagnosis

            The gold standard examination for diagnosing the non hemorrhagic or hemorrhagic stroke is CT Scan. The consideration of the hemorrhagic stroke because of it almost has the same manifestation, like the immediate onset, the patient was not in severe activity, and there is neurological deficit.

5. Basic secondary diagnosis

            From the physical examination the blood pressure is 170/80 mmHg. This is appropriated with JNC 8 criteria that for patient’s >60 years old the diagnosis of hypertension is when the sistolic blood pressure ≥ 150 mmHg or the diastolic blood pressure ≥ 90 mmHg.

6. Basic final diagnosis

            The final diagnosis of this patient is infarction stroke. This diagnosis is based on history taking, physical examination and supporting examination.

7.      Basic treatment

a.       The aim of Bed rest with head position elevated 20-30⁰ is to maintain the adequate circulation to the brain.

b.      The aim of IVFD (30ml/kgbb/day)à Ringer Lactate 20 dpm is to maintain the euvolemic condition and glucose level needed.

c.       The aim of Inj aspilet 2 x 80 mg is to prevent from recurrent stroke attack

d.      The aim of Inj citicoline 2 x 500 mg is as the neuroprotector

 

REFFERENCE

1.      Ropper AH, Brown RH. Adams and Victor’s Principles of Neurology. 8th Ed. New York: McGraw-Hill Companies, Inc. 2005. Chapter 34, Cerebrovascular Disease; p.660-770.

2.      Rumantir CU. Gangguan Peredaran Darah Otak. Pekanbaru: SMF Saraf RSUD Arifin Achmad/FK UNRI. Pekanbaru. 2007.

3.      Warlow C, van Gijn J, Dennis M, Wardlaw J, Bamford J, Hankey G. Stroke Practical Management. 3th Ed. 2008. Blackwell Publishing. p.39-40.

4.      Guideline Stroke Tahun 2011. Pokdi Stroke. Perhimpunan Dokter Spesialis Saraf Indonesia (PERDOSSI). Jakarta. 2011.

5.      Powers WJ. AHA/ASA Guideline 2015 AHA/ASA Focused Update of the 2013 Guidelines for the Early Management of Patients With Acute Ischemic Stroke Regarding Endovascular Treatment. AHA journals. 2015;46:000-000.

6.      Setyopranoto I. Stroke: Gejala dan Penatalaksanaan. CDK 185/Vol.38 no.4/Mei-Juni 2011; hal.247-250.