Transient Ischemic Attacks.

  • A ack (TIA) is an acute episode of temporary and focal loss of cerebral function of vascular (occlusive) origin. TIAs are rapid in onset; symptoms reach their maximal manifestation in fewer than 5 and typically last 2-15 minutes (rarely as long as 24 h).

 ETIOLOGY/ PATHOGENESIS

  • Blacks and men had significantly higher rates of TIA than whites and women.
  • TIAs are uncommon in persons younger than 60 years. Incidence of TIA is 4-8 cases per 1000 persons per year aged 50-59 years.
  • The majority of TIAs are caused by carotid and vertebral artery atherosclerotic disease. However, nonvascular causes occasionally produce TIA symptoms.
  • Other causes: Cerebral embolism, Embolic sources (Valvular disease, ventricular thrombus, and thrombus formation due to atrial fibrillation), Arterial dissection, Arteritis, Noninfectious necrotizing vasculitis (primary cause), Sympathomimetic drugs (eg, cocaine), Mass lesions (eg, tumors, subdural hematomas).
  • Death does not occur directly from a single episode of TIA. A TIA may be considered a sign of generalized atherosclerotic disease. The primary cause of death following a TIA is coronary artery disease.
  • The early risk of stroke following TIA could be as high as of 5-10% at 1 week and 10-20% at 3 months following a TIA.

PERTINENT HISTORICAL FINDINGS/ CLINICAL SYMPTOMS

  • A patient with a TIA may present to the ED with very subtle complaints.
  • Symptoms: sudden numbness or weakness of the face, arm or leg, especially on one side of the body, confusion, trouble speaking or understanding, trouble seeing in one or both eyes, trouble walking, dizziness, loss of balance or coordination, severe headache with no known cause
  • Attempt to isolate the CC into symptoms that are clues to a neurologic disorder.
  • As a TIA has a duration of fewer than 24 hours, question the presence of symptoms within the preceding 24 hours, 48 hours, or week.
  • Attempt to clarify when symptoms first occurred, how long they lasted, if the patient recovered completely (returned to baseline status), if a pattern of escalating symptoms is present, and if associated cardiac symptoms are present.
  • History of associated trauma or cardiac symptoms widens the differential diagnosis. Pertinent negative items in the review of systems also are important (eg, headache, chest pain, eye pain).
  • Determine the state of overall health of the patient and risk factors for various relevant diseases. Elicit any history of substance abuse. Use of sympathomimetic drugs (eg, cocaine) is associated with the following risk factors for TIAs: Hypercoagulable states, Platelet aggregation, Vasospasm, Dysrhythmia, Transient hypertension, Hyperdynamic states, Vasculitis

 PERTINENT PHYSICAL EXAM FINDINGS

  • A patient with a suspected TIA requires a complete physical examination with attention to a detailed neurologic examination.
  • Ideally, severity of neurologic deficits should be recorded with the aid of stroke scales (National Institutes of Health Stroke Scale ). A stroke scale prompts the examiner to be thorough and allows different examiners to reliably repeat the examination during subsequent phases of the evaluation.
  • Initial vital signs should include the following: Rectal temperature, Blood pressure recorded in each arm, Peripheral pulses compared to the apical pulse, Respiratory rate and pattern
  • The examiner should assess the patient’s overall health and appearance, making an assessment of the following: Attentiveness, Ability to interact with the examiner, Language and memory skills, Overall hydration status
  • Identify signs of vasculitis, sinusitis, mastoiditis, and meningitis. Carotid arteries are examined for pulse upstroke, bruit, and presence of carotid endarterectomy scars.
  • Perform funduscopy to identify retinal plaques, retinal pigmentation, and pupil reaction to direct and consensual light exposure.
  • In addition to performing standard auscultation, identify the presence of surgical scars or pacemaker or other clues that the patient may have a cardiac disorder and increased risk of a cardioembolic phenomenon.
  • Cardioembolic events are significant causes of TIAs. Identify unusual rhythms and rates, murmurs, or rubs that might suggest valvular disease, atrioseptal defects, or ventricular aneurysm (a source of mural thrombi).
  • A neurologic examination is the foundation of the TIA evaluation. Subsets of the neurologic examination include the following:Cranial nerve testing, Somatic motor strength, Somatic sensory testing, Cerebellar system
  • Mental status can be assessed formally (eg, Mini-mental Status Examination) or as part of the patient’s overall response to questions and interactions with the examiner.
  • The following signs may be present with cranial nerve dysfunction: Ocular dysmotility, Forehead wrinkling asymmetry, Incomplete eyelid closure, Asymmetrical mouth retraction, Loss of the nasolabial crease, Swallowing difficulty, Lateral tongue movement, Weak shoulder shrugging, Visual field deficits,
  • Test muscle stretch reflexes of biceps, triceps, and brachioradialis and patellar and Achilles reflexes using the standard grading system 0-4.
  • Inspect posture and presence of tremors. Formally test shoulder girdle, upper extremity, abdominal muscle, and lower extremity strength.
  • Test passive movement of major joints to look for spasticity, clonus, or rigidity.
  • The cerebellar system is tested by assessing ocular movement, gait, and finger-to-nose and heel-to-knee movements, looking for signs of past-pointing and dystaxia, hypotonia, overshooting, gait dystaxia, and nystagmus.

 DIFFERENTIAL DIAGNOSIS

  • Bell Palsy
  • Headache, Migraine
  • Hypoglycemia
  • Neoplasms, Brain
  • Stroke, Hemorrhagic
  • Stroke, Ischemic
  • Subarachnoid Hemorrhage

 DIAGNOSTIC EVALUATIONS

  • Serum chemistry profile
  • Coagulation studies
  • Erythrocyte sedimentation rate (ESR)
  • Syphilis serology
  • Complete blood count
  • Platelet count
  • Antiphospholipid antibodies
  • Glucose level
  • Drug screens
  • Cardiac index markers (may be considered)
  • Other studies: Screening for hypercoagulable states (particularly in patients younger than 50 years), Levels of protein C and protein S, Antithrombin III level, Thrombin time, Hemoglobin electrophoresis, Serum protein electrophoresis,
  • Noncontrast cranial CT scan of the head: An area of infarction appropriate for the TIA symptoms has been identified in 29-34% of patients with TIA.
  • Magnetic resonance angiography: MRA provides noninvasive images of carotid and vertebral arteries.
  • Cerebral arteriography: Selective catheterization of the cerebral vessels is necessary to evaluate the carotid arteries prior to carotid endarterectomy, identify the vertebral and basilar arteries, and define intracranial stenosis or occlusion.
  • Cerebral arterial imaging: Carotid and vertebral artery ultrasound is required to identify the surgical candidate with high-grade carotid stenosis.
  • 12-lead ECG is indicated to assess the rhythm and guide case management.
  • Lumbar puncture (LP) is indicated if the diagnosis is in doubt and subarachnoid hemorrhage, infectious etiology, or demyelinating disease is to be excluded.

MEDICAL MANAGEMENT

  • If the patient is already taking aspirin, he or she may be a candidate to take aspirin plus extended-release dipyridamole. Recent reports suggest that this combination is more effective than aspirin alone at preventing stroke, particularly in patients at high risk for stroke. Although dual therapy carries the increased risk of GI bleeding.
  • A possible benefit may exist by administering antiplatelet therapy with aspirin and clopidogrel to patients who are showering the cerebral circulation with microemboli.
  • Outpatient management: Prescribe aspirin 325 mg orally per day. For crescendo TIA symptoms, eliminate aspirin and substitute clopidogrel 75 mg orally once a day OR ticlopidine 250 mg orally twice a day.
  • For patients with TIA who are diabetic, recent evidence indicates that BP treatment targets should be lower than previously recommended to less than 130/85 mm Hg.
  • Target levels for fasting blood glucose of less than 126 mg/dL are recommended for patients with TIA.

SURGICAL MANAGEMENT (when applicable)

  • Not applicable

EMERGENCY MANAGEMENT (when applicable)

  • Supporting the airway and restoring perfusion or a stable rhythm are tenets of emergency care. By definition, patients with TIA are hemodynamically stable and able to support their own airways. Rapid assessment excludes those conditions that mimic a TIA such as hypoglycemia or an intracranial hemorrhage.
  • Vital signs must be obtained promptly and addressed as indicated. Place the patient on a cardiac monitor and a pulse oximeter and establish an IV line (if one has not already been established by EMS).
  • Obtain a fingerstick glucose level and treat accordingly.
  • Obtain an ECG and initiate treatment for symptomatic rhythms or evidence of ischemia.
  • A significant area of controversy is whether to treat hypotension or hypertension during a stroke. For patients with TIA who are diabetic, recent evidence indicates that blood pressure (BP) treatment targets should be lower than previously recommended to less than 130/85 mm Hg.While BP and perfusion should be supported, cerebral perfusion pressure may respond inconsistently to antihypertensive therapy. Even a modest reduction in BP can extend a fragile ischemic penumbra.
  • If an antihypertensive agent is administered, closely monitor the patient’s response by repeating the physical examination.
  • Consensus suggests not treating hypertension during an acute stroke unless the mean arterial peripheral pressure exceeds 130 mm Hg. Mean pressure is calculated as (systolic BP + [2 x diastolic BP]) /3.
  • When a TIA is caused by large or small vessel arteritis, distinguishing between pure arteritis and arteritis that produces penetrating arterial disease is important. The former is treated with dexamethasone, often on an outpatient basis, but the latter is better treated with IV steroids and observation.

PATIENT EDUCATION/ MAINTENANCE – PREVENTION

  • Patients with TIAs have an increased risk of stroke and death from coronary artery disease (depending on risk factors in the study group, approximately 6-10%/y). Probability of stroke in the 5 years following a TIA is reported to be 24-29%.
  • Minimize risk factors: smoking, poorly controlled diabetes, high blood pressure, and high cholesterol.
  • Instruct patient to return to the ED if symptoms return.
  • Make sure patient understands the need for a complete workup through close follow-up care.

 Transient-Ischemic-Attacks

Dr. Zachary M. Lahlou

https://zacharylahlou.com

One thought on “Transient Ischemic Attacks.

  1. Pingback: Transient Ischemic Attacks. | Dr. Zachary Lahlou

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out /  Change )

Google+ photo

You are commenting using your Google+ account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

w

Connecting to %s