Diagnostic Tests for Stokes Adams syndrome
Stokes Adams syndrome Tests: Book Excerpts
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Stokes Adams syndrome Diagnosis: Book Excerpts
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COMA:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
When one encounters a patient with coma, the first thing to do is to establish an airway. Next, the blood pressure is taken. If there are any signs of shock, an intravenous access is established, and the shock is treated appropriately. A cardiology and surgical consult are obtained. Blood should then be drawn for a CBC, type and cross-match, sedimentation rate, chemistry panel, electrolytes, blood ammonia level, and blood alcohol levels. Before removing the syringe, 50 cc of 50% dextrose is given unless the patient is suspected of having hyperosmolar nonketotic diabetic coma. A urinalysis and urine drug screen must be done also. Arterial blood gas analysis should be done. If the situation is urgent or emergent, a CT scan is done before the results of the laboratory tests are available. If the laboratory tests are inconclusive, a CT scan must be done anyway.
If all of the above studies are negative, a spinal tap is done for cell count, protein, glucose, VDRL test, smear, and culture and sensitivity. This is especially true when there is fever or nuchal rigidity.
If the diagnosis is still in doubt, blood tests for other toxic materials, such as the lead level, and blood cultures and EEG are done. A neurologist or neurosurgeon is usually consulted as soon as one is available.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
SYNCOPE:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
The diagnostic workup includes a CBC, sedimentation rate, urinalysis, chemistry panel, VDRL test, thyroid profile, glucose tolerance test, EKG, and chest x-ray. Several blood pressure recordings in the recumbent and upright positions should be made. If hypoglycemia is suspected, a 72-hr fast and a tolbutamide tolerance test should be done. The drug history should always be reviewed. A toxicology screen may be helpful.
Most cases will require 24-hr Holter monitoring or event Holter monitoring. In addition, other cardiovascular studies, such as echocardiography and His' bundle studies, may need to be done. Exercise tolerance testing is useful when the syncope seems to be exercise induced. An upright-tilt test is helpful when vasodepressor syncope is suspected, especially when combined with isoproterenol infusion. Signal-averaged EKG can be useful if a ventricular arrhythmia is suspected. If transient ischemic attacks are suspected, a carotid scan and cerebral angiography may be necessary. If the syncopal attacks are thought to be due to epilepsy, a wake-and-sleep EEG may need to be done. A CT scan or MRI of the brain may need to be done.
A cardiologist or neurologist should be consulted before ordering expensive diagnostic tests. A psychiatrist may also need to be consulted.
» READ BOOK EXCERPT ONLINE »
Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
Level of consciousness, decreased:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
Try to obtain history information from the patient, if he’s lucid, and from his family. Did the patient complain of a headache, dizziness, nausea, vision or hearing disturbances, weakness, fatigue, or other problems before his LOC decreased? Has his family noticed changes in the patient’s behavior, personality, memory, or temperament? Also ask about a history of neurologic disease, cancer, or recent trauma or infections; drug and alcohol use; and the development of other signs and symptoms.
Because a decreased LOC can result from a disorder affecting virtually any body system, tailor the remainder of your evaluation according to the patient’s associated symptoms.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Syncope:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
If the patient reports a fainting episode, gather information about the episode from him and his family. Did he feel weak, light-headed, nauseous, or sweaty just before he fainted? Did he get up quickly from a chair or from lying down? During the fainting episode, did he have muscle spasms or incontinence? How long was he unconscious? When he regained consciousness, was he alert or confused? Did he have a headache? Has he fainted before? If so, how often does it occur?
Next, take the patient’s vital signs and examine him for any injuries that may have occurred during his fall.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Level of consciousness, decreased:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
Try to obtain history information from the patient, if he’s lucid, and from his family. Did the patient complain of headache, dizziness, nausea, visual or hearing disturbances, weakness, fatigue, or any other problems before his LOC decreased? Has his family noticed any changes in the patient’s behavior, personality, memory, or temperament? Also ask about a history of neurologic disease, cancer, or recent trauma or infections; drug and alcohol use; and the development of other signs and symptoms.
Because decreased LOC can result from a disorder affecting virtually any body system, tailor the remainder of your evaluation according to the patient’s associated symptoms.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Syncope:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
If the patient reports a fainting episode, gather information about the episode from him and his family. Did he feel weak, light-headed, nauseous, or sweaty just before he fainted? Did he get up quickly from a chair or from lying down? During the fainting episode, did he have muscle spasms or incontinence? How long was he unconscious? When he regained consciousness, was he alert or confused? Did he have a headache? Has he fainted before? If so, how often does it occur?
Next, take the patient’s vital signs and examine him for any injuries that may have occurred during his fall.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Coma:
Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. General examination. A thorough general examination, including vital signs, helps to establish and rule out potential causes of coma. Look for evidence of head trauma or metabolic encephalopathy.
B. Neurologic examination. A detailed neurologic examination, including mental status; motor, sensory, reflex coordination; gait; and cranial nerve testing, will help distinguish the location and degree of dysfunction. Look for the following important features:
1. Level of consciousness. Is the patient responsive at all? To what degree?
2. Brainstem function
a. Pupils: assess cranial nerves (CN) 2 and 3 for anisocoria, miosis, pinpoint, mydriasis, or fixed, midposition pupils.
b. Eye movements: assess conjugate gaze, gaze deviation, nystagmus, and spontaneous movements (CN 3, 4, and 6).
c. Funduscopic examination: assess for papilledema and underlying diseases. Corneal reflexes (CN 5 and 7); gag and cough reflexes (CN 9 and 10).
3. Breathing patterns. Cheyne-Stokes respiration suggests cerebral hemispheric or diencephalic injury or an encephalopathy (hypoxic or metabolic). Central hyperventilation suggests brainstem injury. Ataxic or Biot’s respiration, which can progress to apnea, suggests injury to the reticular formation in the medulla and pons.
4. Sensorimotor activity. Are there spontaneous, volitional movements? Is there other motor activity such as choreoathetosis, decerebrate or decorticate activity, myoclonus, asterixis, or seizure activity? Is the muscle tone flaccid, rigid, spastic, or clonic? Is the response to painful stimuli purposeful, flexion withdraw, abnormal posturing, or no response at all?
5. Tendon reflexes. Are the reflexes asymmetric, increased, or decreased?
6. Glasgow Coma scale. Measures the depth and duration of altered consciousness based on the best response to three actions: eye opening, verbal response, and motor response to commands or painful stimulus.
Testing
A. Clinical laboratory tests. Complete chemistry profile (including electrolytes, glucose, calcium, magnesium, creatinine, blood urea nitrogen), complete blood count, coagulation panel, arterial blood gas, toxicology screen (blood, urine, gastric contents), thyroid function tests, cortisol level, and select cultures (blood, urine, throat, rectal, spinal fluid). Consider performing lumbar puncture after obtaining a computed tomography (CT) scan.
B. Diagnostic imaging. Cerebral CT findings reliably suggest intracranial hemorrhage, cerebral edema, mass lesions, focal infection, or hydrocephalus as diagnoses. Magnetic resonance imaging is preferred for the detection of abscess, tumor, subdural empyema, inflammatory lesions, or demyelinating diseases.
C. Other testing. Electroencephalography rules out seizures, status epilepticus (SE), and nonconvulsive SE. Lumbar puncture, typically after diagnostic imaging, may help determine increased intracranial pressure as well as infectious causes. Evoked potentials, such as brainstem auditory or short-latency somatosensory, provide information about the physiologic state and response to therapy (4).
Diagnostic assessment.
The prognosis in comatose patients is typically poor except for those that are drug-related or result from traumas. In general, the longer the coma lasts, the poorer the prognosis. Coma rarely lasts longer than 4 weeks, after which, transition into a vegetative state or recovery occurs (3).
References
1. Plum F, Posner JB. The diagnosis of stupor and coma, 3rd ed. Philadelphia: FA Davis, 1983.
2. Feske SK. Coma and confusional states: emergency diagnosis and management. Neurol Clin North Am 1998;16:237–256.
3. Giacino JT. Disorders of consciousness: differential diagnosis and neuropathic features. Semin Neurol 1997;17:105–111.
4. Chiappa KH, Hill RA. Evaluation and prognostication in coma. Electroenceph Clin Neurophysiol 1998;106:149–155.
» READ BOOK EXCERPT ONLINE »
Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Syncope:
Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
What are the essential aspects to cover?
A. General: mental status, temperature, hydration status, pallor, or cyanosis.
B. Vital signs: tachycardia, bradycardia, irregularity, or orthostatic hypotension.
C. Cardiovascular: heart sounds, murmurs, bruits, edema, rales, and pulses.
D. Neurologic: cranial nerves, reflexes, strength and sensation, tremor, Romberg’s sign, gait, and cerebellar signs.
Testing.
Which tests are useful in diagnosing syncope?
A. Electrocardiogram (ECG). The most important single initial test to evaluate syncope is the ECG; it is easy and inexpensive and can quickly identify life-threatening arrhythmias or ischemia. Although the diagnostic yield is only 5% (3), if the ECG is normal, ischemia, arrhythmias, and organic heart disease are very unlikely (5). If the ECG is abnormal but does not clearly demonstrate a likely cause for syncope (complete heart block or runs of ventricular tachycardia, for example), other tests are needed to clarify the underlying problem that may be related to the syncope. The result of the ECG, therefore, helps to direct the course of further workup.
B. Cardiac monitors
1. Holter monitor or telemetry performed for 24 hours. For patient with organic heart disease, this gives a diagnostic yield of from 2% for arrhythmias correlated to symptoms to 21% with unrelated arrhythmias. Extending this monitoring to 72 hours is not useful (5).
2. A loop event monitor is a portable, prolonged ambulatory event recorder indicating if there is recurrent syncope and no organic heart disease (yield = 24% to 47%) (4).
C. Electrophysiologic studies. This invasive cardiac monitoring and arrhythmia induction procedure gives a 50% diagnostic yield for those with organic heart disease or abnormal ECG (compared with 10% if no organic heart disease) (4). This is considered the gold standard for arrhythmia diagnosis but it is expensive and invasive. Powerful predictors of a positive test are an ejection fraction less than 40%, bundle branch block, or atrial fibrillation (5).
D. Tilt table testing is indicated for unexplained, recurrent syncope when arrhythmia or organic heart disease is excluded and neurocardiogenic syncope is suspected. In this setting, the sensitivity is 67% to 83% and specificity is 90% (4).
E. Echocardiogram and stress tests are used only to evaluate exertional symptoms (echo first in this case) or suspected organic heart disease.
F. Computed tomography scan is used to evaluate focal neurologic signs.
G. Electroencephalogram is indicated for seizure activity only (Chapter 4.7).
H. Carotid massage. Consider this if the patient is aged more than 60 years with unexplained syncope. Perform in the clinic if no bruits, ventricular tachycardia, recent stroke, or myocardial infarction.
I. Blood tests, including hematocrit, serum chemistries, and pregnancy test, are not for screening; order only if a specific medical condition is suspected.
J. Psychiatric evaluation is useful in the setting of a high recurrence rate in a young patient without resultant injuries and no evidence of organic heart disease.
Diagnostic assessment.
The keys to the diagnosis of syncope are the history, physical examination, and ECG, yielding a diagnosis 45% of the time. The history and physical should focus on cardiac, neurologic, and medication-related issues. Directed testing can add 8% to diagnosis (3). Further classification by age and presence of organic heart disease can help focus evaluation and treatment. If organic heart disease is present or the ECG is abnormal, inpatient telemetry monitoring and electrophysiologic studies are recommended. If organic heart disease is not evident, ambulatory loop ECG and psychiatric evaluations are indicated, as well as possible tilt table testing (4).
Although most syncope patients can be evaluated in the outpatient setting, hospitalization is recommended for those with organic heart disease, chest pain, a history or suspicion of arrhythmia, or presence of neurologic symptoms or signs suggesting transient ischemic attack or stroke. The extent of severity of the organic heart disease is the key determinant of mortality and should direct evaluation and therapy (2). Despite extensive evaluation and testing, the diagnosis may still be elusive in approximately 40% of patients with recurrent syncope, but fortunately these patients have a low incidence of morbidity and mortality.
References
1. Grubb BP, Kosinski D. Neurocardiogenic syncope and related syndromes of orthostatic intolerance. Cardiology in Review 1997;5:182–190.
2. Kapoor WN, Hanusa BH. Is syncope a risk factor for poor outcomes? Comparison of patients with and without syncope. Am J Med 1996;100:646–655.
3. Linzer M, Yang EH, Estes NA 3rd, et al. Clinical guideline: diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography. Ann Intern Med 1997;126:989–996.
4. Linzer M, Yang EH, Estes NA 3rd, et al. Clinical guideline: diagnosing syncope. Part 2: Unexplained syncope. Ann Intern Med 1997;127:76–86.
5. Meyer MD, Handler J. Evaluation of the patient with syncope: an evidence based approach. Emerg Med Clin North Am 1999;17:189–201.
» READ BOOK EXCERPT ONLINE »
Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Coma:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
Coma is a state of pathological unconsciousness, where the patient is unaware of their environment and unarousable. It is caused by dysfunction of either the reticular activating system above the level of the mid-pons or both cerebral hemispheres. It should be distinguished from brain death due to cessation of cerebral and cerebellar function, marked by absense of response to stimuli, respiratory drive, and central reflexes (although spinal reflexes may be preserved), and from persistent vegetative state, characterized by diurnal wakefulness but with unawareness and inability to interact with others.
Pupils: Pupillary responses are more sensitive than papilledema in detecting increased intracranial pressure. Normal pupils imply an intact midbrain and CNIII. Preserved pupillary light reflex with other signs of brainstem impairment suggests a toxic/metabolic cause. Asymmetric reactivity is consistent with an acute structural process. A unilaterally dilated pupil suggests ipsilateral uncal herniation. Hypothermia, barbiturates, and midbrain lesions produce midposition unreactive pupils. Pinpoint pupils occur with pontine lesions and opiates. Bilateral dilated unresponsive pupils occur with anoxia, severe midbrain damage caused by transtentorial herni-ation, or anticholinergic drugs. Large pupils that dilate and contract automatically (hippus) but do not react to light suggest a tectal lesion.
Eye deviation: Injection of ice water into the ear (calorics) normally causes deviation of both eyes toward the stimulated ear. Its absence implies dysfunction of the pons or medulla. Cortical mass lesions produce ipsilateral conjugate deviation that can be overcome with calorics. Brainstem and pontine lesions produce contralateral deviation that cannot be overcome with calorics. In metabolic coma or drug overdose coma, eyes move loosely side-to-side opposite the turning of the head. A pontine or cerebellar lesion causes skew deviation (separation of horizontal axes). Ocular bobbing (briskly down, slowly up) is a result of bilateral pontine lesions. Ocular dipping (slow arrhythmic downstroke, followed by a faster upstroke) with normal calorics is consistent with anoxic encephalopathy.
Posturing: Decorticate posturing (arm flexion and leg extension) is found with hemispheric lesions or metabolic derangement. Decerebrate posturing (extension of the legs and arms) implies dysfunction of the midbrain or upper pons on a structural or metabolic basis. In response to noxious stimuli, flexion, extension, and adduction reflexes are found. Shoulder and hip abduction involve cortical activity whereas withdrawal implies voluntary behavior.
Respiratory pattern: If the patient is yawning or swallowing, coma is not very deep and brainstem function is intact. Cheyne-Stokes respiration (crescendo-decrescendo pattern with apneic pauses) is seen with herniation, metabolic encephalopathy, and congestive heart failure. Central neurogenic hyperventilation (rapid deep breathing) indicates damage to the brainstem between the midbrain and pons. Ataxic respiration occurs with midbrain lesions. Apneustic respiration with inspiratory pauses occurs with pontine lesions and precedes respiratory arrest.
Asymmetric resting muscle tone, deep tendon reflexes, or Babinski response suggests a structural lesion. A toxic/metabolic cause is suggested by preceding confusion, disorientation, and somnolence. Myoclonic jerks or clonus provide further support.
The Glasgow Coma Scale is scored as follows: Best Motor Response: 6 obeys commands, 5 localizes pain, 4 withdraws to pain, 3 decorticate (flexion), 2 decerebrate (extension), 1 none. Best Verbal Response: 5 oriented, 4 confused conversational, 3 inappropriate words, 2 incomprehensible sounds, 1 none. Eye Opening: 4 spontaneous, 3 to speech, 2 to pain, 1 none.
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Source: Field Guide to Bedside Diagnosis, 2007
Syncope:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
The cause of syncope is usually evident after a careful history and physical exam. Identification of a cardiac cause is critical because it portends a poor prognosis (1-year mortality 18% to 33%). In patients with heart disease, the most specific predictors of a cardiac cause are syncope in the supine position or during effort, blurred vision, and convulsive syncope. In patients without heart disease, palpitations are the only significant predictor of a cardiac cause.
Focus on preceding events and witness description. Sudden loss of consciousness without warning is usually due to an arrhythmia. Syncope with chest pain mandates that aortic dissection, myocardial infarction, and pulmonary embolism be ruled out. Syncope with exertion suggests aortic stenosis, hypertrophic obstructive cardiomyopathy, or bradycardia. Events after the syncope, such as confusion, lethargy, or neurological symptoms suggest a seizure.
Consider syncope as the cause of unexplained trauma such as hip fracture or MVA.
» READ BOOK EXCERPT ONLINE »
Source: Field Guide to Bedside Diagnosis, 2007
Level of consciousness, decreased:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Decreased LOC can result from a disorder affecting virtually any body system. After performing a complete neurologic examination, let the results of your history guide the rest of your physical assessment.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Syncope:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Take the patient’s vital signs and examine him for any injuries that may have occurred during his fall. Then perform a complete cardiac and neurologic assessment.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Syncope and Dizziness:
Diagnostic Approach
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Neurocardiogenicsyncope, vascular syncope, breath-holding, hyperventilation, and psychologicdisturbances can usually be distinguished by history and physicalexam.If syncopal episode occurs on assumingupright posture, BP should be measured in supine and upright positions.Postural difference in systolic pressure of >15 mm Hg confirmsdiagnosis of orthostatic syncope.Individuals with recurrent syncope,family history of sudden death, or syncope occurring during intensiveexercise need further evaluation.If recurrent syncope occurs, tilt testingmay determine whether syncope is neurocardiogenic.Family history of syncope and suddendeath suggests hypertrophic cardiomyopathy or long QT interval syndrome.Syncope during intense exercise mayoccur with hypertrophic cardiomyopathy, severe aortic stenosis,anomalous left coronary artery from pulmonary artery, primary pulmonaryhypertension, or exercise-induced atrial fibrillation associatedwith WPW syndrome. Diagnosis of cardiac disorders canbe made from history, physical exam, chest radiograph, ECG, and2-D echocardiogram. Cardiac catheterization and angiography maybe necessary to make definitive diagnosis and to determine severityof lesion. Arrhythmia may be suspected from history, and routine ECGwith rhythm strip may be diagnostic. Otherwise, further testingmay be needed (e.g., Holter monitoring, maximal exercise testing,event recorder or implanted loop recorder monitoring, and electrophysiologictesting).With syncopal episode of unknown cause,ECG should be initially performed searching for WPW syndrome, longQT interval syndrome, or LV hypertrophy with T-wave changes indicativeof cardiomyopathy.
» READ BOOK EXCERPT ONLINE »
Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Level of consciousness, decreased:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
Try to obtain history information from the patient, if he's alert, and from his family. Did the patient complain of a headache, dizziness, nausea, vision or hearing disturbances, weakness, fatigue, or other problems before his LOC decreased? Has his family noticed changes in the patient's behavior, personality, memory, or temperament? Also ask about a history of neurologic disease, cancer, or recent trauma or infections; drug and alcohol use; and the development of other signs and symptoms.
Because a decreased LOC can result from a disorder affecting any body system, tailor the remainder of your evaluation according to the patient's associated symptoms.
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
Syncope:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
If the patient reports a fainting episode, gather information about the episode from him and his family. Did he feel weak, light-headed, nauseous, or sweaty just before he fainted? Did he get up quickly from a chair or from lying down? During the fainting episode, did he have muscle spasms or incontinence? How long was he unconscious? When he regained consciousness, was he alert or confused? Did he have a headache? Has he fainted before? If so, how often does it occur? Obtain a complete drug history.
Next, take the patient's vital signs and examine him for any injuries that may have occurred during his fall. Place him on a cardiac monitor and assess his heart rhythm for abnormalities. Assess cardiac and respiratory status. Monitor pulse oximetry. Perform a neurologic examination.
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
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