CONFIRMING DIAGNOSIS In many cases, a definitive diagnosis follows a tissue biopsy performed by stereotactic surgery. In this procedure, a head ring is affixed to the skull, and an excisional device is guided to the lesion by a computed tomography (CT) scan or magnetic resonance imaging (MRI).
Other diagnostic tools include a patient history, a neurologic assessment, skull X-rays, a brain scan, a CT scan, MRI, and cerebral angiography. An EEG may reveal focal abnormalities. Lumbar puncture shows increased pressure and protein levels, decreased glucose levels and, occasionally, tumor cells in cerebrospinal fluid (CSF).
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Agitation:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
Determine the severity of the patient’s agitation by examining the number and quality of agitation-induced behaviors, such as emotional lability, confusion, memory loss, hyperactivity, and hostility. Obtain a history from the patient or a family member, including diet, known allergies, and use of prescribed or over-the-counter drugs, including supplements and herbal medicines.
Ask if the patient is being treated for any illnesses. Has he had any recent infections, trauma, stress, or changes in sleep patterns? Check for signs of drug abuse, such as needle tracks and dilated pupils, and ask about alcohol intake. Obtain baseline vital signs and neurologic status for future comparison.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Confusion:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
When you take his history, ask the patient to describe what’s bothering him. He may not report confusion as his chief complaint but may complain of memory loss, persistent apprehension, or the inability to concentrate. He may be unable to respond logically to direct questions. Check with a family member or friend about the onset and frequency of the patient’s confusion. Find out, too, if the patient has a history of head trauma or a cardiopulmonary, metabolic, cerebrovascular, or neurologic disorder. Which medications is he taking, if any? Ask about any changes in eating or sleeping habits and in drug or alcohol use.
Perform an assessment to determine the presence of systemic disorders. Check vital signs, and assess the patient for changes in blood pressure, temperature, and pulse.
Next, perform a neurologic assessment to establish the patient’s level of consciousness.
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Source: Professional Guide to Signs & Symptoms (Fifth 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.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Seizures, complex partial:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
If you witness a complex partial seizure, never attempt to restrain the patient. Instead, lead him gently to a safe area. (Exception: Don’t approach him if he’s angry or violent.) Calmly encourage him to sit down, and remain with him until he’s fully alert. After the seizure, ask him if he experienced an aura. Record all observations and findings.
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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.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Confusion:
History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
. Collateral information is valuable with confused patients.
A. Characteristics. Is there an altered level of consciousness? Is so, consider urgent factors. Is the patient easily distractible or having difficulty keeping track of what is said? Is there an altered sleep–wake cycle; do symptoms fluctuate and are there changes in psychomotor behavior? If so, delirium is likely. Is thinking disorganized or incoherent? Is speech rambling, irrelevant, or frequently switching subjects? Is the patient disoriented? Do memory problems exist? Are there perceptual disturbances, including hallucinations or thought broadcasting, insertion, or withdrawal? The presence of visual hallucinations suggests organic causes. Are delusions present? Is there an indifference to the symptoms? If so, consider conversion disorder. Are there nightmares or increased startle response? If so, acute or posttraumatic stress disorders should be considered (Chapter 3.1).
B. Chronology of symptoms. Is the onset acute? In dementia, a chronic degree of confusion exists; however, acute confusion can herald the onset of delirium, warranting further evaluation (Chapter 4.1). Is the course fluctuating and do symptoms occur more often at night? If so, this suggests delirium. Have such symptoms occurred in the past? If so, what caused them then?
C. Medical history. Confusion is more likely in patients with multiple medical problems, longer lists of medications, or recent medication changes. Medications that can induce confusion include anticholinergics, sedatives, steroids, metronidazole, and digoxin, among others.
D. Psychiatric history. Are there any prior diagnoses and treatments, or a psychotropic medication history? If so, do current symptoms match prior psychiatric episodes? If so, consider a psychiatric recurrence. Have there been any recent psychosocial stressors? If so, consider the possibilities of dissociative and stress syndromes. It is important to note that a prior psychiatric history does not necessarily imply the confusion is caused by a psychiatric exacerbation; conversely, the absence of a psychiatric history does not rule out a psychiatric cause. Psychotic disorders tend to occur in younger patients, whereas delirium is more likely in older patients.
E. Other information. Current or past use of alcohol or drugs, recent injuries (particularly head injuries), and exposure to toxins. A review of systems helps detect organic causes.
Physical examination
A. Focused physical examination. This should include vital signs, psychomotor characteristics, assessment of skin, hair, and nail beds; and
a funduscopic examination. A screening neurologic examination should include a check for nuchal rigidity, and an assessment of Kernig’s and Brudzinski’s signs. Positive findings warrant further testing. The Folstein Mini-Mental State examination (2) can help assess cognitive functioning (Chapter 4.5). The Confusion Assessment Method may be used to help detect delirium (3).
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Dementia:
History.
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A concerned family member will often bring patients into the office when obvious memory impairment occurs. The deficit will be sufficiently obvious to interfere with daily living, work, or social activities. When questioning the reliable historian, ask about the specific cognitive changes (language, judgment, abstract thinking, praxis, visual recognition, and constructional ability). Ask about the duration of symptoms, the mode of onset (insidious or abrupt), and the progression (slow or rapid, gradual or stepwise). Check on general risk factors (e.g., increasing age, atherosclerosis, head trauma, CNS infection), and family history. Specific risk factors for AD include increasing age, lower intelligence, small head size, history of head trauma (4), and Down’s syndrome.
Physical examination.
The patient should undergo a thorough general and neurologic examination and Mini-Mental Status Examination (MMSE). Look for focal neurologic deficits and assess cognitive function (memory, language, perception, praxis, attention, judgment, calculation and visuospatial function). Other neuropsychiatric testing is available.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Syncope:
History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. What are the symptoms or circumstances related to the syncope?
1. Dizziness preceding syncope is highly associated with a psychological cause (24%) versus syncope without preceding dizziness (5%) (3). Dizziness with syncope can also be associated with arrhythmia.
2. Important history includes palpitation, duration of prodrome and recovery, and presence of postural or exertional symptoms.
3. Related environmental factors include heat, dehydration, and alcohol.
B. Which disease, risk factor, or family history is present?
1. Organic heart disease is associated with arrhythmia and increased risk of death.
2. Psychiatric illnesses most commonly associated with syncope are major depression (12.2%), alcoholism (9.2%), generalized anxiety disorder (8.6%), and panic disorder (4.3%). These correlate with a higher rate of recurrent syncope, younger age, and a more benign course (4) (Chapters 3.1 and 3.3).
3. Older age (>60 years) is more highly associated with arrhythmias, orthostatic hypotension, medication side-effects, and situational (e.g., micturition) syncope.
4. Ask about diabetes mellitus, neuropathy, anemia, and other chronic diseases.
5. Inquire about a family history of sudden death, hypertrophic cardiomyopathy, or other organic heart disease.
C. What medicines does the patient take? The most commonly implicated are antihypertensives and antidepressants. Others include antianginals, analgesics, and sedatives.
Physical examination
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.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Delirium:
History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. Baseline. Perhaps the most important aspect of taking the patient’s history is establishing the individual’s baseline mental status and level of functioning. In addition to interviewing the patient, family, friends, and acquaintances must be interviewed as well. Other healthcare providers, such as nurses and doctors, who have dealt with the patient previously in an office, nursing home, or hospital setting, can be invaluable sources of information. Try to establish the presence or absence of the signs and symptoms of dementia or depression (section V).
B. Previous medical history. Look for previously existing medical problems that can precipitate delirium, such as CHF, diabetes, hypothyroidism, benign prostatic hypertrophy or HIV (section I.B). Evaluation of the medications is crucial, including prescription and over-the-counter medications. Is the patient taking them as directed? Is the patient on any medications that could be present in toxic levels (e.g., digoxin, phenytoin or theophylline)? Has there been any recent trauma or surgery? Are there symptoms of infection such as UTI or pneumonia? Be sure to interview friends and family.
C. Social history. Does the patient have a history of substance abuse? Is the patient currently using any alcohol or illegal substances? When was their last use? Be aware of potential withdrawal. If the patient is abusing alcohol, is there a history of delirium tremors with previous abstinence? Does the patient live alone? Is the patient at risk for poor nutrition?
Physical examination.
Because of the fluctuating nature of delirium, serial examinations are valuable.
A. Mental status. Observe the patient and take note of changes of level of consciousness, orientation, agitation, combativeness, hallucinations, or inability to concentrate. Evaluate the mental status by using the Mini Mental Status Examination (4) or a similar tool to standardize the findings (Chapter 4.5).
B. Physical status. Obtain vital signs and evaluate for clinical signs of dehydration, malnutrition, urinary retention, or fecal impaction. The physical examination should be guided by the history, keeping in mind the multifactorial nature of delirium. Evaluate for signs of infection, look for cardiopulmonary decompensation, and complete a thorough neurologic examination with special attention to identifying any focal neurologic deficit.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Dementia:
Differential Overview
(Field Guide to Bedside Diagnosis)
❑ Alzheimer disease
❑ Multi-infarct dementia
❑ Depression
❑ Drugs
❑ Parkinson disease
❑ Frontal lobe dementia
❑ Vitamin B12 deficiency
❑ HIV encephalopathy
❑ Korsakoff syndrome
❑ Brain tumor
❑ Normal pressure hydrocephalus
❑ Chronic subdural hematoma
❑ Neurosyphilis
❑ Creutzfeldt-Jakob
❑ Wilson disease
Diagnostic Approach
Many patients are concerned about age-related forgetting of details, a normal phenomenon. This usually results from decreased attention. The fact that they recognize and worry about this distinguishes them from patients with early dementia. Normal forgetting preserves vocabulary and spelling and improves with cues. For example, patients with Alzheimer disease cannot recall a list of related words any better than random words. Patients with dementia on the other hand have difficulty with one or more of the following: learning and retaining new information (e.g., remembering events); handling complex tasks (e.g., balancing a checkbook); reasoning (e.g., inability to cope with unexpected events); spatial orientation (e.g., getting lost in familiar places); language (e.g., word finding); and/or behavior.
Subtle impairments in memory, attention, and concentration are often easily compensated for and therefore hard to pinpoint. Impaired judgment and abstraction on increasingly simple matters and personality changes (notably irritability) are usually noted first. The time course of onset is helpful in distinguishing dementia from delirium, but acute exacerbations of an underlying dementia that mimic delirium are common with drugs and acute physical illness.
The Mini Mental State Exam (MMSE) measures across domains of cognitive function: memory, executive function, attention, language, praxis, and visuospatial ability. A total score of less than 24/30 suggests dementia or delirium. Scores of 20 to 24 suggest mild impairment; 16 to 19, moderate; and 15 or below, severe. It also provides a quantitative assessment useful in following the course of the disease or response to therapy.
Mini-Cog Repeat three objects, Clock Drawing Test (hands at 8:20), then recall three objects. Suggestive of dementia when either 0/3 objects are recalled or when 1 to 2 are missed and CDT is abnormal.
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Source: Field Guide to Bedside Diagnosis, 2007
Syncope:
Differential Overview
(Field Guide to Bedside Diagnosis)
Orthostatic/Autonomic
❑ Neurally mediated hypotension
❑ Volume depletion
❑ Cough syncope
❑ Anemia
❑ Autonomic insufficiency
Cardiac/Obstructive
❑ Myocardial infarction
❑ Pulmonary embolism
❑ Aortic stenosis
❑ Hypertrophic obstructive cardiomyopathy
❑ Aortic dissection
❑ Cardiac tamponade
❑ Left atrial myxoma
Cardiac/Dysrhythmic
❑ Complete heart block
❑ Sick sinus syndrome
❑ Tachyarrhythmia
❑ Carotid sinus hypersensitivity
Neurologic
❑ Vertebrobasilar ischemia
❑ Hypoglycemia
❑ Unwitnessed seizure
❑ Subclavian steal syndrome
Psychologic
❑ Hyperventilation
❑ Hysterical faint
Diagnostic Approach
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.
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Source: Field Guide to Bedside Diagnosis, 2007
Delirium/Hallucinations:
Differential Overview
(Field Guide to Bedside Diagnosis)
Systemic
❑ Drugs/toxins
❑ Sepsis
❑ Hypoglycemia
❑ Hypercalcemia
❑ Hyponatremia
❑ Shock
❑ Delirium tremens
❑ Vitamin B12 deficiency
❑ Hypoxia
❑ Hypercapnia
❑ Thyrotoxicosis
❑ Uremia
❑ Hepatic encephalopathy
❑ Thiamine deficiency
❑ Heat stroke
❑ Hypothermia
❑ Lead intoxication
❑ Carbon monoxide poisoning
Neurologic
❑ Concussion
❑ Hypertensive encephalopathy
❑ Subdural hematoma
❑ Postictal
❑ Transient global amnesia
❑ Meningitis
❑ Right parietal stroke
❑ Encephalitis
❑ Vasculitis
❑ Carcinomatous meningitis
Hallucinations
❑ Drugs
❑ Schizophrenia
❑ Temporal lobe epilepsy
Diagnostic Approach
Delirium is characterized by gross disorientation in the presence of alertness and vigilance, disorders of perception with vivid illusions, and psychomotor and autonomic hyperactivity. It usually develops over a short time and is associated
with fluctuating mental status, decreased attention, disorganized thinking as indicated by rambling, irrelevant, or incoherent speech, and a decreased level of consciousness. The most sensitive findings are variability in level of arousal, impaired short-term memory (e.g., digit span), and disorientation to time. Relatives or friends are helpful sources of information about the tempo and degree of impairment.
Fever, tachycardia, or hypertension should prompt a careful evaluation for a medical cause. Infection is a common cause in the elderly, especially pneumonia or urinary tract infection. Visual hallucinations are organic in origin, due to factors such as drugs, rather than due to schizophrenia.
Confusion Assessment1) Change in mental state (from baseline) that is acute and fluctuates. 2) Difficulty focusing attention or trouble keeping track of what is said. 3) Disorganized thinking (rambling or irrelevant conversation, unpredictable switching between subjects, illogical flow of ideas). 4) Altered level of consciousness (lethargy, stupor, or hyperalert). A positive test requires 1 and 2 positive, and either 3 or 4.
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Source: Field Guide to Bedside Diagnosis, 2007
Brain tumors, malignant:
Diagnosis
(Handbook of Diseases)
In many cases, a definitive diagnosis follows a tissue biopsy performed by stereotactic surgery. In this procedure, a head ring is affixed to the skull, and an excisional device is guided to the lesion by a computed tomography (CT) scan or magnetic resonance imaging (MRI).
Other diagnostic tools include a patient history, a neurologic assessment, skull X-rays, a brain scan, a CT scan, MRI, and cerebral angiography. Lumbar puncture shows increased pressure and protein levels, decreased glucose levels and, occasionally, tumor cells in cerebrospinal fluid (CSF).
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Source: Handbook of Diseases, 2003
Brain abscess:
Diagnosis
(Handbook of Diseases)
A history of infection — especially of the middle ear, mastoid, nasal sinuses, heart, or lungs — or a history of congenital heart disease, along with a physical examination showing such characteristic indications as increased intracranial pressure (ICP), points to a brain abscess. An enhanced computed tomography (CT) scan and, occasionally, arteriography (which highlights the abscess by a halo) help locate the site.
Examination of cerebrospinal fluid can help confirm infection, but lumbar puncture is too risky because it can release the increased ICP and provoke cerebral herniation. A CT-guided stereotactic biopsy may be performed to drain and culture the abscess. Other tests include culture and sensitivity of drainage to identify the causative organism, skull X-rays, and a radioisotope scan.
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Source: Handbook of Diseases, 2003
Level of consciousness, decreased:
History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)
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.
Physical examination
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. Perform a complete neurologic assessment and a physical assessment. Determine the patient’s baseline Glasgow Coma Scale score and evaluate on an ongoing basis.
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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007
Syncope:
History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)
Ask the patient for information about the fainting episode. Did he feel weak, light-headed, nauseous, or sweaty just before he fainted? Did he stand quickly from a sitting or prone position? 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?
Physical examination
Perform a complete cardiac and neurologic examination. Provide continuous cardiac monitoring. Next, take the patient’s vital signs and examine him for injuries that may have occurred during his fall.
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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007
Agitation:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Determine the severity of the patient’s agitation by examining the number and quality of agitation-induced behaviors, such as emotional lability, confusion, memory loss, hyperactivity, and hostility. Obtain a history from the patient or a family member, including diet and known allergies.
Ask if the patient is being treated for any illnesses. Has he had any recent infections, trauma, stress, or changes in sleep patterns? Ask the patient about prescribed or over-the-counter drug use, including supplements and herbal medicines. Ask about alcohol intake.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Confusion:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
When you take his history, ask the patient to describe what’s bothering him. He may not report confusion as his chief complaint but may complain of memory loss, persistent apprehension, or the inability to concentrate. He may be unable to respond logically to direct questions. Check with a family member or friend about onset and frequency. Find out, too, if the patient has a history of head trauma or a cardiopulmonary, metabolic, cerebrovascular, or neurologic disorder. Find out which medications he’s taking, if any. Ask about any changes in eating or sleeping habits and in drug or alcohol use.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Level of consciousness, decreased:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
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 or cancer; recent trauma or infection; drug and alcohol use; and the development of other signs and symptoms.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Seizures, complex partial:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
If you witness a complex partial seizure, never attempt to restrain the patient. Instead, lead him gently to a safe area. (Exception: Don’t approach him if he’s angry or violent.) Calmly encourage him to sit down, and remain with him until he’s fully alert. After the seizure, ask him if he experienced an aura. Record all observations and findings.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Syncope:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
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?
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Syncope and Dizziness:
Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Cardiovascular Syncope
Neurocardiogenic Syncope (Common Faint)
Most commontype of syncope in childhood and adolescence.Often a response to anxiety, fear,pain, or other emotional stress.Also may occur after extreme fatigue,prolonged standing, or fasting.Pathogenesis involves vasodilatationof skeletal muscle vasculature and failure of heart rate and strokevolume to maintain cardiac output for adequate cerebral blood flow.Dizziness, nausea, sweating, and abdominaldiscomfort may precede syncope. Interruption of cerebral perfusionfor 2–3 secs produces dizziness, but lying down duringpresyncopal phase may prevent syncopal episode.If cerebral perfusion is interruptedfor >10 secs, syncope occurs.Onset is sudden with hypotension (vasodepressorresponse), and BP decreases to ≤60 mm Hg. Bradycardia usuallyoccurs, and often junctional rhythm or period of asystole (cardioinhibitory response)may follow.Most episodes are associated with uprightposition, and child becomes limp and falls to ground. Loss of consciousnessusually lasts <1 min.Seizures are unusual but may occurwith prolonged syncope.Once individual is horizontal, BP,heart rate, and color return toward normal.History and physical exam are usuallydiagnostic. Individuals with this form of syncope do not need furthertesting unless syncope is recurrent, when tilt table testing mayconfirm its presence.Both tussive and micturition syncopeare now considered forms of neurocardiogenic syncope.Tussive syncopehas been attributed to large increase in intrathoracic pressure,which decreases venous return to the heart. It may occur after significantcoughing of any cause, but especially after severe paroxysmal coughingwith pertussis.Micturition syncope is most commonin elderly men, but it can occur in older adolescents. Syncope usuallyoccurs at the end of micturition. The mechanism is unclear, buta full bladder causes peripheral vasoconstriction, and with emptying,peripheral vasodilatation occurs, which in the erect posture mayproduce syncope. Cardiac Syncope
Congenital and Acquired Heart Disease
Syncopemay occur with outflow obstruction of left ventricle (LV) (valvar,subvalvar, or supravalvar aortic stenosis; hypertrophic cardiomyopathy),outflow obstruction of right ventricle (RV) (pulmonic stenosis,primary pulmonary artery hypertension, pulmonary vascular disease),inflow obstruction of LV (mitral stenosis, atrial myxoma), and inflowobstruction of RV (cardiac tamponade). More likely to occur duringor just after physical exertion, when cardiac output cannot increaseenough to meet demands of oxygen delivery to brain.Syncope also may occur with cardiomyopathy,myocarditis, and endocarditis as a result of decreased cardiac output.Another cause is myocardial ischemia,which may occur with coronary artery anomalies, especially anomalousorigin of left coronary artery from pulmonary artery and abnormalcourse of left coronary artery between aortic and pulmonary trunkswith compression of artery during exercise. Coronary artery aneurysmsand thrombosis found in Kawasaki disease also may produce myocardialischemia and syncope.In most cases, history, physical exam,chest radiograph, ECG, and 2-D echocardiogram are diagnostic.Diagnosis of primary pulmonary hypertensionusually requires lung biopsy to exclude pulmonary venoocclusivedisease. Although pulmonary vascular disease may be diagnosed clinicallywith support of echocardiography, cardiac catheterization and angiographycan confirm these findings. Hypercyanotic Episodes
Consistof intense cyanosis and hyperpnea. Occur most commonly with tetralogyof Fallot but also can occur with tricuspid atresia, transpositionof great arteries with pulmonary stenosis, and pulmonary vasculardisease.Children who can walk may squat duringepisode, which increases systemic vascular resistance and decreasesright-to-left shunt.Occasionally episodes may be prolongedand associated with syncope and seizures. During episode, murmuris less intense or disappears.Several factors seem to play a role:prolonged crying with decreased venous return, constriction of RVinfundibulum, decreased systemic vascular resistance secondary toimmobilization or spontaneous vasomotor changes, relative anemia,and increased physical activity with higher oxygen requirement. Arrhythmias in Structurally Normal Heart
Syncopemay occur from sinus bradycardia, junctional bradycardia, second-and third-degree (atrioventricular) AV block with low ventricularrate, supraventricular tachycardia, atrial flutter, or ventriculartachycardia.Atrial fibrillation with rapid ventricularresponse over the accessory pathway may be associated with syncopeor near syncope in Wolff-Parkinson-White (WPW) syndrome. Diagnosisis usually confirmed by ECG, which shows short PR interval and deltawave.Syncope also may occur with prolongedQT interval, in which variable recovery time with reentry depolarizationmay cause torsade de pointes ventricular tachycardia.ProlongedQT interval has a number of genetic causes. Hypokalemia, hypocalcemia, andhypomagnesemia also may cause QT interval prolongation. Tricyclicantidepressants and phenothiazines have been associated with prolongedQT interval, and so have overdoses of quinidine, procainamide, anddisopyramide.Prolonged QT interval can be diagnosedby measuring this interval on routine ECG, but it must be correctedfor heart rate. 1 method for correction of QT interval is to measureQT interval (in secs) and divide by the square root of the RR interval(in secs). In 95% of individuals, the corrected QT interval is <0.45secs. Sympathomimetic drugs when taken inlarge doses or from idiosyncratic reaction may produce supraventricularor ventricular tachycardia. Cocaine also may produce ventriculartachycardia and syncope. Metabolic derangements (e.g., hyperkalemia,hypoglycemia, and hypercalcemia) also may result in syncope by producingarrhythmias, but this is rare.ECG may be diagnostic of these arrhythmias.If syncopal episodes are frequent, Holter monitoring may be useful;if they occur during exercise, maximal exercise testing may be diagnostic.Otherwise, event recorder or implanted loop recorder should be considered.If syncope still remains unexplained,electrophysiologic studies should be performed. Arrhythmias in Structurally Abnormal Heart
Childrenwho have congenital or acquired heart disease are at risk for arrhythmias thatmay produce syncope. These include sinus bradycardia, sick sinussyndrome, supraventricular tachycardia, atrial fibrillation, atrialflutter, ventricular tachycardia, ventricular fibrillation, andcomplete heart block.WPW syndrome and supraventricular tachycardiaare occasionally associated with Ebstein anomaly.Complete heart block may be associatedwith ventricular inversion and transposition of great arteries.Ventricular tachycardia may occur fromarrhythmogenic RV dysplasia, although echocardiography may not bediagnostic because a heavily trabeculated RV may be indistinguishablefrom dysplasia. Recurrent ventricular tachycardia, especially exercise-induced,and left bundle branch pattern suggest this diagnosis, which canbe confirmed by MRI.Children who have had surgical repairof a cardiac defect are also at risk for development of arrhythmias.An incision in the ventricle is a risk factor for ventricular tachycardia.Supraventricular tachycardia, atrial fibrillation, atrial flutter,sick sinus syndrome, and ventricular tachycardia may occur after Mustardor Senning procedure for repair of transposition of great arteries.Surgical manipulation in the area of sinus or AV nodes in repairof AV canal defects, posterior ventricular septal defects, or tunnelaortic stenosis may predispose to development of sinus bradycardiaand heart block.ECG may be diagnostic of these arrhythmias.Holter monitoring and maximal exercise testing also may be helpfulin diagnosis.If these tests are normal consideringhigher risk of life-threatening events in children with structurallyabnormal hearts, electrophysiologic studies should be considered. Vascular Syncope
Orthostatic Syncope
Occurs whenindividual assumes upright posture and systolic arterial BP decreasesby ≥15 mm Hg.Possible causes includeDecreasedblood volume (blood loss, GI fluid loss, excessive diuretic use)Failure of normal postural reflexes(suddenly standing up after prolonged bedrest, familial dysautonomia,spinal cord lesions)Drugs (vasodilators, tricyclic antidepressants,sedatives, opiates, cocaine) Supine and standing BPs should be measuredin any individual with unexplained syncope. Cerebrovascular Syncope
This typeof syncope may be due to excessive vagal stimulation, which causessevere bradycardia or AV block.Examples include intubation, placementof nasogastric tube or esophageal overdrive pacing catheter, removalof pleural or peritoneal fluid, and distention of viscera.Excessive vagal tone also may occurin normal adolescents or well-trained athletes, and a further increasein vagal tone may worsen bradycardia or AV block enough to causesyncope. Carotid Sinus Syncope
Pressure on baroreceptors in carotid sinusmay cause carotid sinus syncope. Uncommon in children but can occurwith excessive pressure on neck (e.g., wearing tight collar). Noncardiovascular Syncope
Breath-Holding
Common inchildren 6 mos–6 yrs of age. Precipitating factors includepain, frustration, and anger.Pallid breath-holding, which is nowthought to be variation of neurocardiogenic syncope, usually followsacute pain or injury. The infant or child becomes pale and losesconsciousness. Complete recovery occurs in 1–2 mins.More common is cyanotic breath-holdingspell in which infant or child cries, holds breath during expiration,and turns dusky until breathing begins again. Loss of consciousnessand tonic-clonic movements may occur with prolonged episode. Hyperventilation
Frequentcause of dizziness but rare cause of syncope.Common in adolescent girls and usuallydue to emotional stress.Frequent complaints include lightheadedness,blurred vision, difficulty breathing, choking, smothering, chesttightness, and numbness or tingling of fingers, toes, and face.Individuals who are hyperventilating appear anxious and have fastand deep respirations.Rebreathing into paper bag and thoughtfulreassurance usually lessen hyperventilation, so that individualscan begin talking about what is upsetting them. Migraine
Severe migraine headache may cause syncopalepisode, especially if basilar arterial system is affected (see Chap. 25, Headache). Metabolic
Hypoxia Including Anemia
Severe hypoxia or severe anemia of any causemay result in syncope. See Chap.45, Pallor (Anemia), and Chap. 56, Respiratory Distress and Apnea. Hypoglycemia
Often causesfaintness and dizziness, but syncope is exceedingly rare. Othermanifestations of hypoglycemia include headache, hunger, sweating,and jitteriness, which may progress to confusion, seizures, andcoma.Low blood glucose level confirms presenceof hypoglycemia.With administration of oral or intravenousglucose, symptoms resolve.See further discussion of hypoglycemiain Chap. 59, Seizures. Psychologic
Acute stressmay produce anxiety and syncope with or without hyperventilation. Commonstresses are witnessing a tragic event or hearing news of the deathof close friend or relative.Hysteria is common cause of recurrentfainting in adolescents, especially in those with hysterical personalities.In this typeof episode, which almost always occurs in presence of other people,hysterical person falls or slumps in dramatic way but avoids injury.Fainting also may occur while lying or sitting down. There is noprodrome or change in heart rate, BP, or skin color. Diagnosis of psychologic causes ismade from history, physical exam, and clinical observation. Diagnostic Approach
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. >>
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Agitation:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
Determine the severity of the patient's agitation by examining the number and quality of agitation-induced behaviors, such as emotional lability, confusion, memory loss, hyperactivity, and hostility. Obtain a history from the patient or a family member, including diet, known allergies, and all medications, including the use of herbal medicine. Also ask the patient about substance abuse.
Ask if the patient is being treated for any illnesses. Has he had any recent infections, trauma, stress, or changes in sleep patterns? Observe the patient for signs of substance abuse, such as needle tracks, dilated pupils, jaundiced skin, or abdominal ascites. Ask him about alcohol intake. Obtain the patient's baseline vital signs and neurologic status for future comparison.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
Confusion:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
When you take his history, ask the patient to describe what's bothering him. He may not report confusion as his chief complaint, but may suffer from memory loss, persistent apprehension, or the inability to concentrate. He may be unable to respond logically to direct questions. Check with a family member or friend about its onset and frequency. Find out, too, if the patient has a history of head trauma or a cardiopulmonary, metabolic, cerebrovascular, or neurologic disorder. Which medications is he taking, if any? Ask about any changes in eating or sleeping habits and in drug or alcohol use.
Perform an assessment to determine the presence of systemic disorders. Check the patient's vital signs, and assess him for changes in blood pressure, temperature, and pulse.
Next, perform a neurologic assessment to establish the patient's level of consciousness.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
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.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
Seizures, complex partial:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
If you witness a complex partial seizure, never attempt to restrain the patient. Instead, lead him gently to a safe area. (Exception: Don't approach him if he's angry or violent.) Calmly encourage him to sit down, and remain with him until he's fully alert. After the seizure, ask him if he experienced an aura. Record all observations and findings. Obtain a history. Has the patient experienced a seizure in the past? Has he had a recent head injury? Has he experienced any fever, headaches, or periods of confusion? Obtain a complete drug history. Take his vital signs and perform a complete neurologic examination.
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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.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
HALLUCINATIONS:
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
In the workup of hallucinations, it is essential to get a drug history
from a relative or friend if not from the patient. Ask about a family
history of epilepsy or head trauma. A drug screen should be ordered. If
there is no mental deterioration, referral to a psychiatrist may be done but
an electroencephalogram (EEG) may
still be indicated. With mental deterioration, a neurologist should be
consulted. When there is doubt about mental deterioration, psychologic
testing may be done. Computed tomography (CT) scans, EEGs, skull x-ray
films, and arteriograms may be necessary in selected cases.
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Source: Differential Diagnosis in Primary Care, 2007
SYNCOPE:
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
Clinical differentiation of the various forms of syncope is made by
combinations of symptoms. Thus, syncope with marked sweating and tachycardia
is more likely due to hypoglycemia. Syncope with sweating and bradycardia is
more likely due to vasovagal syncope. Focal neurologic signs during the attack suggest
transient ischemia attack (TIA) and prompt
a search for sources of emboli or thrombosis (sickle cell disease,
polycythemia, or macroglobulinemia). Transesophageal echocardiography is the
procedure of choice to find a cardiac source. A family history of syncope
suggests migraine, epilepsy, or vasovagal attacks. Epilepsy is a strong
possibility in the young, whereas heart block is more likely in the aged.
Consequently, an EEG and Holter monitoring are useful in the workup.
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Source: Differential Diagnosis in Primary Care, 2007
MEMORY LOSS AND DEMENTIA:
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
Once again, the presence or absence of other neurologic signs and
symptoms is important. If one does not have the skills or the time for a
complete neurologic examination, immediate referral is indicated. Next, a
careful drug history is done. Withdrawal of all drugs may clear the
dementia. An electroencephalogram (EEG), skull x-ray film, computed
tomography (CT) scan or magnetic resonance imaging (MRI), spinal tap (if
there is no papilledema), and psychometric tests are basic to any workup. If
the CT scan or MRI shows dilated ventricles, a spinal fluid nuclear flow
study is indicated to exclude normal-pressure hydrocephalus. In the absence
of other neurologic signs and negative spinal fluid analysis for syphilis
and other chronic encephalopathies, one should do an endocrine workup and
look for systemic diseases such as porphyria. Drug screens for lead
intoxication and bromism should also be performed.
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Source: Differential Diagnosis in Primary Care, 2007
DELIRIUM:
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
It is essential to get a history of drug or alcohol use from the
patient or family, and a drug screen may be done in most cases. Infection is
another common cause. The workup should also include a CBC, sedimentation
rate, urinalysis, antinuclear antibody (ANA) analysis, chemistry panel, and
electrolytes. A CT scan or MRI of the brain will be necessary in most cases.
It may be wise to administer intravenous thiamine and glucose while awaiting
the results of blood work. If there is a fever, blood cultures and possibly
a spinal tap (after a CT scan or MRI has ruled out a space-occupying lesion)
may be indicated. Arterial blood gas analysis and carboxyhemoglobin should
be determined. A neurologist or neurosurgeon needs to be consulted early in
the workup.
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Source: Differential Diagnosis in Primary Care, 2007
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