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Diseases » Syncope » Diagnosis
 

Diagnosis of Syncope

Syncope Diagnosis: Book Excerpts

Diagnosis of Syncope: medical news summaries:

The following medical news items are relevant to diagnosis and misdiagnosis issues for Syncope:

Diagnostic Tests for Syncope: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about diagnostis of Syncope.


COMA: Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

  1. Is there a history of drug or alcohol ingestion? This is a very important question to ask, as many cases of coma are due to acute alcohol intoxication, delirium tremens, opium poisoning, barbiturate poisoning, and other toxic cerebral depressants.
  2. Is there a history of trauma? Most of the time it will be obvious that the patient has suffered a blow to the head. However, there are many times when one must contact the family or other people who witnessed the onset of the coma to determine if there was trauma.
  3. Are there focal neurologic signs? Focal neurologic signs would make one think of a stroke, brain abscess, brain tumor, or epidural or subdural hematoma.
  4. Is there papilledema? Papilledema certainly would indicate a possible space-occupying lesion such as a brain tumor, brain abscess, or subdural hematoma.
  5. Is there a sweet odor to the breath? A sweet odor to the breath should make one think of a diabetic coma or alcoholism.
  6. Is there fever? If there is fever, one should be thinking of meningitis, subarachnoid hemorrhage, or acute encephalitis. However, aspiration pneumonia, urinary tract infection (UTI), or septicemia may explain the fever.
  7. Is there nuchal rigidity? The presence of nuchal rigidity suggests a meningitis or subarachnoid hemorrhage.
  8. Are there sibilant or crepitant rales on examination of the lung? Sibilant rales would suggest the possibility that pulmonary emphysema is responsible for the coma, whereas crepitant rales would suggest that there is congestive heart failure or possibly pneumonia.

DIAGNOSTIC WORKUP

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.

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

DELIRIUM: Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

  1. Is there associated fever? Delirium with fever may simply indicate a self-limited infectious process, but it should bring to mind encephalitis and meningitis as well as cerebral abscess and cerebral hemorrhage.
  2. Is there a history of trauma? A history of head trauma would make one suspect a subdural or epidural hematoma and concussion.
  3. Is there a history of drug or alcohol ingestion? This is probably the most important single question to ask in the average case coming into the emergency room these days without a good history. Very often, the problem is alcoholism or various popular drugs such as cocaine, lysergic acid diethylamide (LSD), and phencyclidine (PCP).
  4. Are there focal neurologic signs? Focal neurologic signs along with the delirium would make one think of subdural or epidural hematoma, cerebral abscess, or cerebral hemorrhage. Remember, a cerebral thrombosis or embolism may present with delirium also.
  5. Is there nuchal rigidity? If there is nuchal rigidity, the patient may have meningitis or subarachnoid hemorrhage.
  6. Is there a sweet odor to the breath? A sweet odor to the breath should make one think of diabetic coma or alcoholism.
  7. What is the response to intravenous thiamine? If the patient responds to intravenous thiamine, the diagnosis is usually Wernicke's encephalopathy or Korsakoff's syndrome.
  8. Intermittent delirium should suggest psychomotor epilepsy and transient global amnesia.

DIAGNOSTIC WORKUP

Routine laboratory tests include a CBC, sedimentation rate, ANA, chemistry panel including electrolytes and BUN and VDRL tests, a blood alcohol level, urinalysis, and urine drug screen. A CT scan of the brain and EEG is usually indicated also. Acute delirium may be an indication to administer intravenous glucose and thiamine. If there is fever, blood cultures and a spinal tap for analysis and culture need to be done. Arterial blood gases and carboxyhemoglobin should be determined. Generally, a neurologist or neurosurgeon should be consulted early.

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

DIZZINESS: Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

  1. Is it true vertigo? True vertigo is characterized by the fact that the subject feels he or his environment is turning. One other form of true vertigo is lateral pulsion, in which the subject feels as if he is moving to the left or right or may be moving forward or backward. True vertigo is a sign of neurologic or otologic disease, whereas dizziness that is not true vertigo is more likely a sign of cardiovascular disease.
  2. Is there associated tinnitus or deafness? The presence of tinnitus or deafness, especially if the ear examination is negative, is a sign of a more serious otologic or neurologic condition. Such disorders as cholesteatoma, acoustic neuroma, and Ménière's disease must be considered. On the other hand, vertigo without tinnitus or deafness should prompt consideration of benign positional vertigo and vestibular neuronitis.
  3. Are there other neurologic findings? The finding of abnormalities of other cranial nerves or the long tracts, such as the pyramidal tracts, would suggest multiple sclerosis, an advanced brain stem tumor, acoustic neuroma, or basilar artery insufficiency.
  4. Are there findings on otoscopic examination? A normal neurologic examination with an abnormal ear exam would suggest otitis media, cholesteatoma, or petrositis.
  5. Is there tachypnea during the attack? If there is hyperventilation during the attack, then hyperventilation syndrome should be considered.
  6. Is there a history of trauma? A history of trauma would suggest a postconcussion syndrome.
  7. Are there abnormalities of the blood pressure? If the dizziness is really lightheadedness, hypertension may be present, but hypertension may also cause true vertigo. Hypotension is more likely to cause lightheadedness, which is not true vertigo. Be sure to take the blood pressures while the patient is lying down and again after rapidly arising to the standing position.
  8. Are there abnormal cardiac findings? A thorough cardiovascular examination should be done. Irregularities of the heartbeat, heart murmurs, or cardiac enlargement will suggest cardiac arrhythmia, aortic stenosis and insufficiency, mitral stenosis, prolapse of the mitral valve, and congestive heart failure.
  9. Is there pallor? Moderate to severe anemia will cause lightheadedness and dizziness, but usually not true vertigo.

DIAGNOSTIC WORKUP

If there is true vertigo, an audiogram and a caloric test or electronystagmography should be done. Hallpike's maneuver should be done also. If these are abnormal, an x-ray of the mastoids, petrous bones, and internal auditory canals should be done. At this point a neurologist should be consulted. If an acoustic neuroma is strongly suspected, an MRI of the brain stem and auditory canals should be done. If the MRI of the brain is negative, a spinal fluid examination can be done to exclude such disorders as central nervous system lues and multiple sclerosis. An MRI of the brain needs to be done to distinguish multiple sclerosis. BSEPs, VEPs, and SSEPs will also be helpful in making the diagnosis of multiple sclerosis, along with the spinal fluid analysis mentioned above. A wake-and-sleep EEG needs to be done to exclude temporal lobe epilepsy. If migraine or migraine equivalents are suspected, perhaps a trial of beta-blockers would help make this diagnosis. If vertebral basilar artery ischemia is suspected, magnetic resonance angiography may be indicated.

If the dizziness is not true vertigo, a CBC and chemistry panel should be done at the outset. Additional studies in the form of 24-hr blood pressure monitoring, Holter monitoring, and echocardiography all have a valuable place in the diagnostic workup of dizziness without true vertigo. However, a referral to a cardiologist is wise before undertaking these expensive studies. If all studies are negative, perhaps a psychiatrist should be consulted.

 

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

SYNCOPE: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

  1. Are there convulsive movements or incontinence? The presence of convulsive movements should suggest convulsions, and the differential diagnosis of this is discussed on page 88 . Convulsive movements can occur with other forms of syncope, however.
  2. Is the pulse slow or absent? The presence of a slow or absent pulse would suggest heart block, vasovagal syncope, and carotid sinus syncope.
  3. Is the pulse rate normal? The presence of a normal pulse rate would suggest anemia, aortic stenosis, aortic insufficiency, and cyanotic congenital heart disease.
  4. Is the pulse rate rapid? The presence of a rapid pulse would suggest the various types of ventricular and supraventricular tachycardias, including auricular fibrillation and flutter, and it should also suggest heat exhaustion or heat stroke.
  5. If the pulse is rapid, is it regular? The presence of a rapid regular pulse should suggest supraventricular or ventricular tachycardia, heat exhaustion, or heat stroke.
  6. Is there a heart murmur? The presence of a heart murmur should suggest aortic stenosis, aortic insufficiency, and cyanotic congenital heart disease.
  7. Is there pallor? The presence of pallor should suggest shock or severe anemia and acute bleeding.
  8. Are there focal neurologic signs? The presence of focal neurologic signs should suggest cerebral vascular insufficiency, hypoglycemia, and transient ischemic attacks.

DIAGNOSTIC WORKUP

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

Aura: Differential Diagnosis
(In a Page: Signs and Symptoms)

  • Epilepsy
    –Recurrent seizures
    –Strong family history
  • Migraine with aura
    –Usually visual aura (e.g., scotoma, flashing lights) lasting less than 60 minutes
    –Usually fully reversible with rare migrainous infarction (like CVA)
    –Migraine headache follows aura within 60 minutes and lasts 4–72 hours; however, aura may occur without headache
    • Partial seizure
      –60% of patients with focal seizures have an accompanying aura
      –Aura symptoms are associated with the brain area where they originate (e.g., occipital lobe seizure results in seeing lights)
      –Simple partial seizures result in focal tonic-clonic motor activity without loss of consciousness
      –Complex partial seizures progress to decreased consciousness and unresponsiveness
    • Tonic-clonic (grand mal seizure) seizures result in an abrupt loss of consciousness followed by stiffness (tonic); the patient then starts jerking (clonic) for an additional 2–3 minutes; rare aura
    • Pituitary adenoma or other underlying pathology that predisposes to migraines, seizures, or altered sensations (taste, smell)
    • Hallucinations (not actually an aura)
      • Physiologic nonepileptic seizures
        –Usually due to an underlying physiologic cause (e.g., fever, hypoglycemia, hypo- or hyperthyroidism, renal failure, cerebral anoxia)
    • Absence seizures (petit mal seizure) only rarely have an aura

    Workup and Diagnosis

    • History is very important
      –Type of aura (any of five senses)
      –Loss of consciousness
      –Associated activities and triggers (e.g., stress, medications, exertion, trauma, foods)
      –Postaura symptoms (e.g., headache, loss of consciousness, seizure)
      –History or family history of seizures or migraines
      –Review past medical history for head injury, stroke, dementia, intracranial infection, and alcohol or drug abuse
      –Full head, neck, and neurologic exam (look for one-sided features that suggest pathology on opposite side of brain)
      –Examine for trauma following loss of consciousness
    • Initial tests may include glucose, electrolytes, calcium, magnesium, CBC, BUN/creatinine, and toxicology screen
      • EEG may be indicated if seizure activity is suspected
        (provocative EEG with triggers gives higher yield)
        –Normal EEG does not rule out epilepsy
        –May be abnormal in migraines
      • MRI to rule out cerebral pathology
      • CT if physiologic seizure or trauma is involved (not indicated in patients with migraine and normal neurologic exam unless pattern of migraine has changed)

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Delirium: Differential Diagnosis
(In a Page: Signs and Symptoms)

  • Dementia
  • Medical etiologies
    –Infections (e.g., UTI, pneumonia, encephalitis, meningitis)
    –Drug toxicity, including alcohol
    –Drug withdrawal (especially benzodiazepines)
    –Fluid, electrolyte, and metabolic disorders (e.g., hyponatremia, hypoglycemia, hypercalcemia, uremia, hypercarbia)
    –CHF
    –Hypoxia (multiple causes, including CHF)
    –Medications (e.g., antiarrhythmics, antidepressants, neuroleptics, analgesics, GI medications)
    –Stroke
    –Cerebral ischemia (multiple causes)
    –Complex partial seizure disorder is associated with an alteration of awareness
    • Psychiatric etiologies
      –Depression
      –Psychotic illness
      –“Sundowning”: Behavioral deterioration occurs during evening hours (typically occurs in demented institutionalized patients)

    Workup and Diagnosis

    • History should include evaluation of memory difficulties, disorientation, incoherent speech, and level of attention, and a discussion with patients’ family caregivers
      –Risk factors include advanced age, cognitive impairment (including dementia), psychiatric conditions, and severe chronic medical illness
      –Mini-mental status examination
    • Physical examination should include vitals, state of hydration, infectious foci, and neurologic exam, with complete investigation into possible medical etiologies
    • Initial labs may include serum electrolytes, BUN/creatinine, glucose, calcium, magnesium, CBC, and urinalysis
    • Pulse oximetry and/or arterial blood gas may be indicated to screen for hypoxia and/or hypercarbia
    • Thyroid function tests and vitamin B12/folate levels
    • Imaging studies (e.g., head CT, chest X-ray), blood and urine cultures, and/or lumbar puncture may be indicated
    • EEG is indicated if suspect seizure disorder
      –Slowing of α rhythms and unusual slow-wave activity are common in delirium

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Syncope: Differential Diagnosis
(In a Page: Signs and Symptoms)

  • Vasovagal episode
    –Most common cause of syncope
    –May be triggered by heat, fatigue, stress, hunger, alcohol, and severe pain
    –Associated with diaphoresis, weakness, blurry vision, lightheadedness
    –Almost always benign
  • Orthostatic hypotension
    –Fall in blood pressure upon standing, due to failure of vasoconstrictor reflexes
    –Precipitated by sudden standing from recumbent position
    –Often associated with antihypertensive medications (diuretics, vasodilators, α - or β-blockers) and dehydration/hypovolemia
    –May occur with autonomic disorders (e.g., Shy-Drager syndrome)
    • Situational syncope
      –Increased intrathoracic pressure (e.g., cough, micturition, defecation) leads to decreased venous return and resulting diminished blood flow to the brain
    • Cardiac arrhythmias
      –Very slow (<30 bpm) or fast (>180 bpm) heart rates may result in decreased cardiac output and resulting diminished blood flow to the brain
  • Valvular disease
    –Most commonly due to aortic stenosis
  • Myocardial disease
    • Cerebrovascular disease
      –Usually due to carotid or vertebrobasilar atherosclerosis
  • Hypoglycemia
  • Anemia
  • Seizure
  • Anxiety attack
  • Migraine
  • Medications (e.g., anticholinergics)
  • CVA
  • Hemorrhage
  • Trauma

Workup and Diagnosis

  • History and physical exam will often suggest the underlying etiology
    –Note pre- and postsyncopal symptoms (e.g., chest pain, dizziness, lightheadedness, nausea/vomiting, headache, diaphoresis, blurry vision, blindness)
    –Full HEENT, neurologic, and cardiovascular exam
    –Examine for trauma following syncope
    –Record BP in supine, sitting, standing, and in both arms
    –Strategically attempt to reproduce syncope by Valsalva maneuver (e.g., coughing, deep breathing for 2–3 min)
  • Initial labs should include CBC, electrolytes, calcium, magnesium, glucose, toxicology screens, and ECG
  • Further cardiovascular testing may include cardiac enzymes if ischemia is suspected, 24-hour Holter monitor, echocardiogram, stress testing, and/or invasive cardiac monitoring
  • Head CT to rule out cerebral disease
  • Doppler ultrasound of carotids if bruit is heard
  • EEG may be useful if seizure disorder is suspected
  • Tilt table test may induce vasovagal episode
  • Plasma aldosterone/mineralocorticoid levels to evaluate for hypovolemia due to adrenocortical insufficiency
>

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Dizziness/Lightheadedness & Vertigo: Differential Diagnosis
(In a Page: Signs and Symptoms)

Dizziness/lightheadedness

  • Transiently decreased cerebral blood flow
    –Hyperventilation
    –Vasovagal response
    –Congestive heart failure
    –Aortic stenosis
    –Hypertrophic cardiomyopathy
    –Hemorrhage
    –Dehydration or hypotension
    –Carotid sinus pressure
    –Cerebral artery thrombosis or embolism
    –Cardiac arrhythmia
    –Autonomic dysfunction (e.g., Shy-Drager syndrome)
    –TIA
    –Hypoxemia
    –Anemia
  • Primary CNS dysfunction not associated with decreased blood flow
    –Migraine
    –Seizure
    –Severe electrolyte disturbance
    –Elevated intracranial pressure
  • Panic attack
  • Hyperventilation and/or anxiety
  • Ictal aura
  • Basilar migraine
  • Drug intoxication (e.g., alcohol, sedatives, centrally-acting α-blockers)
  • Allergic reactions
  • Postconcussion syndrome
  • Carbon monoxide poisoning
    Vertigo
  • Peripheral vertigo (inner ear pathology)
    –Benign positional vertigo (>20% of cases)
    –Ménière's disease
    –Labyrinthine trauma
    –Labyrinthitis (viral)
    –Nonspecific or recurrent vestibulopathy
    –Bilateral vestibular loss
    –Acoustic neuroma
    –Autoimmune inner ear disease
  • Central vertigo (CNS pathology)
    –Multiple sclerosis
    –Brainstem tumors
    –Labyrinthine trauma
    –Epileptic vertigo
    –Vertebrobasilar insufficiency
    –Tabes dorsalis
    –Friedreich's ataxia

Workup and Diagnosis

  • A complete history and physical exam should include signs of dehydration, questions about excessive pressure on the neck, headaches, palpitations, history of heart disease, hearing loss, cardiac auscultation, orthostatic blood pressures, and complete ENT (including Weber's and Rinne's tests) and neurologic exams (gait)
  • Laboratory evaluation may include CBC, electrolytes, calcium, glucose, BUN/creatinine, BNP, ESR, carbon monoxide level, pulse oximetry and/or arterial blood gas, eosinophil count, and stool occult blood testing
  • Further testing may include ECG, 24-hour ECG monitoring, echocardiography, electronystagmography, hearing evaluation, head CT, EEG, MRI (head and/or labyrinth) and/or MRA (head or vertebrobasilar circulation)
  • Vertigo may be evaluated with several specific maneuvers
    –Dix-Hallpike maneuver: Patient is sitting; rapidly move to supine position with head over back of table; observe for nystagmus (type and duration); repeat with head facing to the left and right (nystagmus that does not fatigue or is vertical is unlikely to be BPV)
    –Barany maneuver (Nylan-Barany maneuver) is similar to the Dix-Hallpike maneuver, but less sensitive

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Coma: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

  • Infection
    –Meningitis/encephalitis
    –Bacteria, virus, fungi, spirochete
  • Increased intracranial pressure
    –Tumor, abscess, hydrocephalus
    • Vascular
      –Intracranial hemorrhage, stroke
      –Hypoxic ischemic injury (hypotension, cardiac arrest, arrhythmia, near-drowning)
      –Vasculitis
    • Toxins
      –Uremia, ethanol, atropine, opiates, lead, substance abuse
  • Trauma: Concussion, contusion
  • Seizure
    –Nonconvulsive status epilepticus
    –Postconvulsive state (postictal state)
  • Electrolyte imbalance
    –Hyponatremia, hypernatremia
    –Hypomagnesimia
    –Hypoglycemia, hyperglycemia
    –Hypercalcemia, hypocalcemia
    • Postinfectious
      –Acute disseminated encephalomyelitis (ADEM)
  • Endocrine disorders
    –Adrenal insufficiency
    –Thyroid disorders
  • Degenerative and metabolic diseases
    –Urea cycle disorders
    –Reye syndrome
    –Mitochondrial disease
  • Systemic infection and sepsis
  • Hepatic encephalopathy
  • Psychogenic
    The mnemonic AEIOU-TIPS has been used to recall portions of the differential diagnosis:
    Alcohol ingestion and acidosis
    Epilepsy and encephalopathy
    Infection
    Opiates
    Uremia
    Trauma
    Insulin overdose or inflammatory disorders
    Poisoning and psychogenic causes
    Shock

Workup and Diagnosis

  • History
    –Trauma, seizures, diabetes; cardiac, liver, renal disease
    –Presence of delirium before the onset of coma
    –Fever, neck stiffness, headache
    –Possible toxins at home
  • Physical exam
    –Vital signs, temperature
    –Pattern of breathing (Cheyne-Stokes, apneustic, ataxic)
    –Retinal hemorrhages, otorrhea, spinal fluid rhinorrhea
    –Thyroid, cardiac rhythm, murmur
    –Skin (cyanosis, petechiae, splinter hemorrhages)
    –Hepatosplenomegaly, meningismus
    • Neuro exam: Response to voice and noxious stimulation
      –Papilledema, pupillary size, and light reflex
      –Eye movements (spontaneous, doll's, calorics), corneals
      –Gag, motor response to pain, DTRs, Babinski
      –Decerebrate or decorticate posturing, muscle tone
  • Labs
    –Toxicology screen, glucose, electrolyes
    –CBC, ABG, LFT, ammonia
    –BUN, creatinine, TSH, blood culture
  • Studies
    –Neuroimaging: CT or MRI
    –Lumbar puncture (after herniation has been ruled out)
          –If subarachnoid hemorrhage or infection is suspected
    –EEG to rule out nonconvulsive status epilepticus, gives clues to a metabolic process (triphasic waves)

» READ BOOK EXCERPT ONLINE »

Source: In A Page: Pediatric Signs and Symptoms, 2007

Delirium: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

  • Acute systemic infection
    –May be viral or bacterial cause
    –Often associated with high fever
  • Hypoglycemia, diabetic ketoacidosis
  • Central nervous system infection
    –Meningitis, encephalitis, brain abscess
  • Drugs
    –Alcohol: Acute intoxication
    –Amphetamines: Also tremors, dry mouth, tachycardia, hyperactivity
    –Hallucinogens (LSD, mescaline, PCB) also tremors, dilated pupils, nausea, and abdominal pain
    –Phencyclidine (a.k.a. Angel Dust) with atxia, nystagmus, hyperreflexia, and hypertension
    –Opiates: Also with pinpoint pupils
    –Antihistamines
    –Phenothiazines
    –Organic solvents
    –Salicylates
    –Glucocorticoids
  • Head injury
    • Rocky Mountain spotted fever (RMSF)
      –Delirium and hallucinations may precede rash; fever, headache, myalgias, chills
  • Malaria
  • Rabies
  • Syphilis
    –Tertiary syphilis is rare in children
  • Hyponatremia
  • Uremia
  • Migraine
  • Hypoxia
  • Heat stroke
  • Hepatic failure
  • Systemic lupus erythematosus
    –Delirium is due to cerebral vasculitis
  • Pellagra
    –Due to niacin deficiency
    –Also with diarrhea, dermatitis, dementia
  • Hartnup disease
    –Rash, ataxia, psychological disturbance
    –Symptoms may be intermittent
  • Porphyria
    –Attacks of abnormal behavior do not begin until late adolescence

Workup and Diagnosis

  • History
    –Duration of delirium
    –Exposure to excessive heat
    –Ingestion of drugs
    –Associated signs and symptoms (fever, diarrhea, vomiting, rashes, sweating)
    –Recent head trauma
    –Unusual or fad diets (diets that are mainly corn-based can lead to pellagra)
    • Physical exam
      –Vital signs
      –Pupil size and reactivity
      –Nuchal ridgidity, Kernig and Brudzinski sign
      –Head exam for signs of trauma
      –Scaling rashes (pellagra), petechiae of palms and soles (RMSF), sun sensitivity scars (porphyria)
      –Ataxia, asterixis (flapping at wrists with uremia)
  • Labs
    –All patients should have a glucose measurement
    –Strongly consider toxicology evaluation for all patients (typically do both blood and urine)
    –Serum electrolytes, BUN, creatinine
    –Liver testing (ALT, AST, bilirubin, PT/PTT)
    –Specific testing of enzyme levels (porphyries), urinary amino acids (Hartnup disease), niacin levels (pellagra)
    • Studies
      –Consider LP and head imaging (CT or MRI)

» READ BOOK EXCERPT ONLINE »

Source: In A Page: Pediatric Signs and Symptoms, 2007

Vertigo: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

  • Benign paroxysmal positional vertigo (BPPV)
    –Each episode lasts seconds to minutes
  • Vestibular neuritis
    –Viral infection of the vestibular nerve
  • Otitis media
    • Migraine
      –Vertigo may precede, follow, or present with the headache and aura
  • Acute labyrinthitis
    –Acute onset with nausea and vomiting
    –Lasts for days and slowly resolves
    –45% cluster with viral infections
    • Posttraumatic
      –Perilymphatic fistula
      –Labyrinthine concussion
      –Associated with postconcussive syndrome
      –Worsened by change in head position, cough, sneeze, swallow, straining, and airplane travel
    • Cerebellar tumors
      –Tumors may be associated with tinnitus, facial weakness, and nystagmus
  • Toxins/drugs: Antibiotics (aminoglycosides), salicylates, alcohol, phenytoin, quinine, arsenic, tricyclic antidepressants
  • Autoimmune: Collagen vascular disease, Wegener granulomatosis
    • Posterior circulation dissection
      –Often associated with a history of neck extension or rotational injury
  • Cerebellar hemorrhage: Acute onset of vertigo, headache, nausea, and vomiting
  • Multiple sclerosis
    –Vertigo is the presenting symptom in 5%
    –Hearing loss rare
    –Most common in young women
  • Temporal lobe or complex partial seizures
  • Ménière disease
    • Familial periodic ataxia syndromes
      –Recurrent bouts of vertigo brought on by emotional stress or physical exertion
  • CNS infection: Syphilis, Lyme disease
  • Motion sickness
  • Vertigo mimics: Presyncope, disequilibrium from decreased vision or proprioception
  • Psychogenic
    –Panic or anxiety disorder

Workup and Diagnosis

  • History
    –Duration, headache, nausea, vomiting, worsening with activity or movement (postural hypotension, hyperventilation)
    –Nausea and vomiting are classically more prominent with peripheral vertigo
    –Associated neurologic deficits (extremity weakness, numbness, incoordination, dysarthria, diplopia, tinnitus, hearing loss, loss of consciousness)
    –Facial numbness/weakness
    –History of autoimmune disease, hyperlipidemia, stroke, migraine, seizure, cancer, prior ear surgery
  • Physical exam may be normal in asymptomatic periods
  • Cardiac and peripheral vascular examination for murmurs, arrhythmias, orthostatic changes in pulse and blood pressure (±ECG, Holter, Echo, Doppler)
  • Nystagmus, truncal ataxia, and limb incoordination are sometimes found in cerebellar infarction or neoplasm
  • Vertigo of a panic attack can sometimes be elicited by having the patient hyperventilate
  • Dix-Hallpike maneuver: Rapidly lay the patient down from sitting allowing the head to hang over the side of the bed while turning to the left or right; positive test shows vertigo with rotatory nystagmus within 30 seconds; if the etiology is peripheral, the nystagmus shows extinction with positioning maneuvers
  • MRI and MRA can help evaluate the posterior circulation

» READ BOOK EXCERPT ONLINE »

Source: In A Page: Pediatric Signs and Symptoms, 2007

Syncope: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

  • Vasovagal
    –Most common etiology (more than 50%)
    –Also known as neurocardiogenic or vasodepressor syncope
    –Typical in adolescents; greater in females
    –Occurs after prolonged standing in a warm place; with emotional upset, pain, hunger, the sight of blood; crowded places
  • Postural/orthostatic hypotension
    –Occurs when standing up quickly
  • Micturation syncope (a rare form)
  • Breath-holding spells
    –Usually at ages 1–5 years
    –Two types: Cyanotic (80%) vs pale (20%)
    –Cyanotic spells start with crying
    –Provoked by anger, frustration, or pain, or used as an attention-getting behavior
    –May have generalized clonic jerks
    • Cardiac etiologies (less common)
      –Arrhythmias
      –Supraventricular tachycardia is the most common cause
      –Long QT syndrome (QTc >0.44 seconds): Causes ventricular arrhythmias, Romano-Ward (autosomal dominant), Jervell and Lange-Nielsen (autosomal recessive with deafness)
      –Medications (e.g., cisapride)
      –Sinus node dysfunction and atrioventricular block may lead to bradyarrhythmias
      –Post-op congenital lesions and dilated cardiomyopathy lead to arrhythmias
      –Structural cardiac disease
      –Severe obstructive lesions (e.g., hypertrophic obstructive cardiomyopathy, aortic stenosis, pulmonic stenosis, atrial myxomas, and pulmonary hypertension)
    • Hysterical fainting
    • Migraine
    • Hyperventilation
    • Pregnancy
    • Anemia or hypovolemia
    • Hypoglycemia
    • Carbon monoxide poisoning
    • Medications and drugs of abuse
    • Electrolyte abnormalities
    • Intracranial hypertension
    • Epilepsy may mimic syncope
    • Adrenal insufficiency

    Workup and Diagnosis

    • History: Most important aspect to guide diagnostic workup
      –Vasovagal syncope: Prodromal symptoms (e.g., cold, clammy skin; pallor; nausea; blurry vision; yawning; dizziness; lightheadedness; palpitations; hyperventilation)
      –Duration: Vasovagal syncope is short (seconds to minutes)
      –Inciting situations
      –Lightheadedness: In orthostatic hypotension
      –Syncope at rest or recumbent in seizure or arrhythmia; syncope without prodrome or with exercise/exertion in cardiac etiology
      –Auras in migraine headaches
      –Seizures may have incontinent or post-ictal state or generalized tonic-clonic movements
      –Family history: Sudden or unexplained deaths, cardiac abnormalities, seizures, or deafness
    • Physical exam
      –Orthostatic blood pressures and pulse
      –Perform a thorough cardiac and neurologic exam
    • Extensive laboratory workup is not usually needed
      –Most clinicians would do an ECG
      –Tilt-table testing to diagnose vasovagal syncope is controversial as it is not very reproducible
      –Labs might include CBC, glucose, electrolytes, drug screen, carboxyhemoglobin, EEG, or head CT as guided by history; if cardiac abnormalities are suspected, may get a chest X-ray, Holter monitoring, or exercise testing

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Source: In A Page: Pediatric Signs and Symptoms, 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. The workup should also include a CBC, sedimentation rate, urinalysis, 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

DIZZINESS: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

The first step is to determine if the patient has true vertigo. True vertigo is the experience of subjective or objective rotation with respect to the environment. In other words, either the patient or his or her environment is turning. One other form of true vertigo is lateral pulsion. This is the feeling that one is moving sideways when that is not the case.

The patient who does not experience true vertigo should have a syncope workup (see page 497). Narrowing the differential diagnosis of true vertigo depends on the presence or absence of other symptoms and signs. If there are other cranial nerve or long tract signs on neurologic examination, the patient may have a space-occupying lesion of the brain or brainstem or a hemorrhage, thrombosis or embolism in the vertebral–basilar artery distribution. A neurology consult should be obtained.

If there is true vertigo, tinnitis, and deafness, one would consider inner ear pathology such as Ménière disease, syphilis, petrositis, mastoiditis, and acoustic neuroma. If there is vertigo without tinnitis or deafness or focal neurologic signs, the clinician should suspect acute labyrinthitis, vestibular neuronitis, benign positional vertigo, and drug toxicity. If there are rapid respirations during the attack of vertigo, one would consider hyperventilation syndrome. If there are significant findings on otoscopic examination, a diagnosis of otitis media, cholesteatoma, or mastoiditis should be considered.

The workup will depend on whether the patient has objective findings on otoscopic or neurologic examination. If local pathology is suspected, perhaps a tympanogram, x-ray of the mastoids and petrous bones, audiogram, or referral to an otolaryngologist are required. If there are neurologic findings, perhaps a CT scan or MRI of the brain and auditory canal is indicated along with a referral to a neurologist.

It is wise to have a specialist on board before ordering an expensive workup.

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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 cerebral ischemia (TIA) and prompt a search for sources of emboli or thrombosis (sickle cell disease, polycythemia, or macroglobulinemia). 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

COMA AND SOMNOLENCE: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

Obviously, the neurologic examination and a good history from a member of the family or friend are invaluable in the diagnosis of coma. However, one should not delay ordering laboratory work until the examination and history are accomplished. A CBC, BUN, fasting blood sugar (FBS), serum osmolality, electrolytes, blood gases, urinalysis, and drug screen are ordered immediately. If there is little or no history available and insulin shock is suspected, glucose or glucagon is administered before the laboratory reports are back, although this is done with more caution today for fear of aggravating a case of nonketotic, hyperosmolar diabetic coma.

It has been my experience that the neurologic examination is best performed simultaneously with the taking of a history from a relative or friend. In this way, various telltale neurologic signs can be found with alacrity. A unilateral dilated pupil (suggesting a subdural hematoma or aneurysm), acetone breath (suggesting diabetic acidosis), contusion of the skull (suggesting cerebral concussion or hematoma), and nuchal rigidity (suggesting a subarachnoid hemorrhage in meningitis) are just a few of the signs that can help identify the cause of the coma rapidly.

Coma without focal neurologic findings should suggest a metabolic or toxic cause. In that case, an intensive laboratory workup as listed below would be indicated. A spinal tap maybe indicated if there is fever as well. On the other hand, coma with focal neurologic signs suggests tumor, abscess, hematoma or cerebral embolism, thrombosis, or hemorrhage. The clinician should proceed with a skull x-ray film and CT scan immediately. When these are not available, immediate referral to a large medical center is necessary. Electroencephalography (EEG) and a spinal tap may identify the cause. A spinal tap should be considered with extreme caution even if there is no papilledema. Of course, a spinal tap is never done in the presence of papilledema unless a neurologist is consulted and CT findings are negative. One indication for a spinal tap under these circumstances might be meningitis. Another might be “benign intracranial hypertension.”

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Source: Differential Diagnosis in Primary Care, 2007

Aura: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

Obtain a thorough history of the patient’s headaches or seizure history, asking him to describe any sensory or motor phenomena that precede each headache or seizure. Find out how long each headache or seizure typically lasts. Does anything make it worse, such as bright lights, noise, or caffeine? Does anything make it better? Ask the patient about drugs he takes for pain relief.

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Dizziness: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

Ask about a history of diabetes and cardiovascular disease. Is the patient taking drugs prescribed for high blood pressure? If so, when did he take his last dose?

If the patient's blood pressure is normal, obtain a more complete history. Ask about myocardial infarction, heart failure, kidney disease, or atherosclerosis, which may predispose the patient to cardiac arrhythmias, hypertension, and a transient ischemic attack. Does he have a history of anemia, chronic obstructive pulmonary disease, anxiety disorders, or head injury? Obtain a complete drug history.

Next, explore the patient's dizziness. How often does it occur? How long does each episode last? Does the dizziness abate spontaneously? Does it lead to loss of consciousness? Find out if dizziness is triggered by sitting or standing up suddenly or stooping over. Does being in a crowd make the patient feel dizzy? Ask about emotional stress. Has the patient been irritable or anxious lately? Does he have insomnia or difficulty concentrating? Look for fidgeting and eyelid twitching. Does the patient startle easily? Also, ask about palpitations, chest pain, diaphoresis, shortness of breath, and chronic cough.

Next, perform a physical examination. Begin with a quick neurologic assessment, checking the patient's level of consciousness (LOC), motor and sensory functions, and reflexes. Then inspect for poor skin turgor and dry mucous membranes, signs of dehydration. Auscultate heart rate and rhythm. Inspect for barrel chest, clubbing, cyanosis, and use of accessory muscles. Also auscultate breath sounds. Take the patient's blood pressure while he's lying down, sitting, and standing to check for orthostatic hypotension. Test capillary refill time in the extremities, and palpate for edema.

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

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.

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Vertigo: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

Ask your patient to describe the onset and duration of his vertigo, being careful to distinguish this symptom from dizziness. Does he feel that he’s moving or that his surroundings are moving around him? How often do the attacks occur? Do they follow position changes, or are they unpredictable? Find out if the patient can walk during an attack, if he leans to one side, and if he’s ever fallen. Ask if he experiences motion sickness and if he prefers one position during an attack. Obtain a recent drug history, and note any evidence of alcohol abuse.

Perform a neurologic assessment, focusing particularly on eighth cranial nerve function. Observe the patient’s gait and posture for abnormalities.

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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.

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Aura: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

After providing emergency care, obtain a thorough history of the patient’s headaches or seizures, asking him to describe any sensory or motor phenomena that precede each headache or seizure. Find out how long each headache or seizure typically lasts. Does anything make it worse, such as bright lights, noise, or caffeine? Does anything make it better? Ask the patient about drugs he takes for pain relief.

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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Dizziness: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

Ask about a history of diabetes and cardiovascular disease. Is the patient taking drugs prescribed for high blood pressure? If so, when did he take his last dose?

If the patient’s blood pressure is normal, obtain a more complete history. Ask if he’s had a myocardial infarction, heart failure, kidney disease, or atherosclerosis, which may predispose him to cardiac arrhythmias, hypertension, and a transient ischemic attack. Does he have a history of anemia, chronic obstructive pulmonary disease, anxiety disorders, or head injury? Obtain a complete drug history.

Next, explore the patient’s dizziness. How often does it occur? How long does each episode last? Does the dizziness abate spontaneously? Does it lead to loss of consciousness? Find out if dizziness is triggered by sitting or standing up suddenly or by stooping over. Does being in a crowd make the patient feel dizzy? Ask about emotional stress. Has the patient been irritable or anxious lately? Does he have insomnia or difficulty concentrating? Look for fidgeting and eyelid twitching. Does the patient startle easily? Also, ask about palpitations, chest pain, diaphoresis, shortness of breath, and chronic cough.

Next, perform a physical examination. Begin with a quick neurocheck, assessing the patient’s level of consciousness (LOC), motor and sensory function, and reflexes. Then inspect for poor skin turgor and dry mucous membranes, signs of dehydration. Auscultate heart rate and rhythm. Inspect for barrel chest, clubbing, cyanosis, and use of accessory muscles. Also auscultate breath sounds. Take the patient’s blood pressure while he’s lying, sitting, and standing to check for orthostatic hypotension. Test capillary refill time in the extremities, and palpate for edema.

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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.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Vertigo: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

Ask your patient to describe the onset and duration of his vertigo, being careful to distinguish this symptom from dizziness. Does he feel that he’s moving or that his surroundings are moving around him? How often do the attacks occur? Do they follow position changes, or are they unpredictable? Find out if the patient can walk during an attack, if he leans to one side, and if he’s ever fallen. Ask if he experiences motion sickness and if he prefers one position during an attack. Obtain a recent drug history, and note any evidence of alcohol abuse.

Perform a neurologic assessment, focusing particularly on eighth cranial nerve function. Observe the patient’s gait and posture for abnormalities.

» 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.

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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Coma: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

 A. Characteristics. Coma patients essentially behave in a reflex manner without spontaneous or purposeful movements, language cognizance or expression, or specific localizing responses (3).

 B. Confounding conditions include some medications, mechanical ventilation, immobilized extremities, facial edema, and diurnal variations.

C. Differential diagnosis. Less severe conditions of altered consciousness include vegetative state, the minimally conscious state, akinetic autism, and locked-in syndrome (3).

Physical examination

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.

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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

Dizziness: History.
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

The patient should be allowed, in his or her own words, to describe what is meant by dizziness. A description of the first attack can be helpful. What is the time course of subsequent attacks? How long do the episodes last? How frequent are they? Do any particular positions or movements bring on episodes? Is there any associated nausea, headache, fever, hearing loss, ear pain, or tinnitus? Are there other neurologic symptoms? What medications is the patient taking?

Physical examination.

 A focused physical examination usually confirms rather than makes the diagnosis. An otoscopic examination should be done looking for impacted cerumen or signs of infection. A focused neurologic examination should be done. The patient’s eyes should be observed for spontaneous, gaze-evoked or positional nystagmus. A Dix-Hallpike maneuver should be done when BPPV is suspected. The patient should be observed walking to assess cerebellar function and disequilibrium.

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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

Vertigo: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

The patient’s age, underlying comorbidities, and symptom classification category will help limit the diagnostic possibilities. Further specificity is gained by eliciting the following:

A. Temporal pattern. Are the symptoms episodic or continuous? If episodic, how long do they last? Peripheral origin vertigo is often intermittent and of sudden onset compared with the usual, more gradual onset of central vertigo. A continuous history suggests CNS pathology, drug or toxin effects, metabolic dysfunction, or psychiatric disease. BBPV episodes last less than a minute; vertebrobasilar transient ischemic attacks last minutes to an hour; Ménière’s disease persists 1 to 24 hours; and vestibular neuronitis or acute labyrinthitis continues several days.

 B. Precipitating or exacerbating factors. Has there been recent head trauma (implying perilympathic fistula) or viral illness (labyrinthitis)? What is the relationship to sudden head movement or turning over in bed (BPPV), coughing or sneezing (perilymphatic fistula), postural changes (orthostasis), exercise (arrhythmias), foods (salty meals exacerbating Ménière’s), walking and turning (multiple sensory deficits), micturition or pain (vasovagal reaction), and emotional upset (hyperventilation)?

C. Associated symptoms. Marked nausea, vomiting, diaphoresis, aural fullness, and recruitment (perception of sounds being too loud) are typical of peripheral vestibular disorders. Episodic vertigo associated with tinnitus and gradual (unilateral) hearing loss involving low frequencies preferentially suggests Ménière’s disease. Asymmetric weakness, cranial nerve or cerebellar dysfunction, diplopia, or dysarthria suggests brainstem or CNS disease. Headache, scotomata, or tunnel vision points to migraine. Numbness or paresthesias may indicate neuropathy contributing to multiple sensory deficits (Chapter 4.6). A single, abrupt episode of severe vertigo with negative Dix-Hallpike (DH) testing (section III.A) that gradually subsides over days implies labyrinthitis (if hearing is affected) or vestibular neuronitis (if hearing is unaffected). Mild vertigo with prominent tinnitus, unilateral hearing loss, and loss of corneal reflex is worrisome for an acoustic neuroma.

 D. Medications or toxins. Many medications can cause “dizziness,” although few (aminoglycosides, lead, mercury) cause vertigo. Assess toxin exposure by exploring job and recreational activities.

Physical examination (PE)

This will emphasize orthostatic vital signs, the eyes, ears, and neurologic and cardiovascular systems.

 A. Detection of nystagmus is critical because it is the only objective sign of vertigo (5). Nystagmus can occur spontaneously or in response to changes in eye or body position. Peripheral vestibular disorders usually cause horizontal or rotatory nystagmus, whereas CNS pathology is reflected by vertical nystagmus—an ominous sign. In true vertigo caused by BPPV, DH maneuvers will often confirm the diagnosis (sensitivity 60% to 90%, specificity 90% to 95%) (2,3). The patient is moved rapidly from a sitting to a supine position with the head turned at a 30-degree angle, first to one side and then to the other. A positive DH test includes precipitation of vertigo, latency of onset by a few seconds, rotational nystagmus, resolution within a minute, and lessened symptoms and nystagmus with prolonged latency on repeated testing (i.e., fatiguability). Lack of latency and fatiguability characterize vertigo caused by serious central lesions.

 B. Neurologic examination serves to detect brainstem or CNS pathology.

C. Otoscopy can detect otitis media or cholesteatoma. Nystagmus with vertigo following positive or negative pressure applied to the tympanic membrane (pneumatic otoscopy) suggests a perilymphatic fistula.

D. Other provocative tests (forced hyperventilation, vestibulo-ocular reflex testing, vigorous horizontal head shaking) are not routinely helpful.

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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

Coma: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Alcohol intoxication

❑ Drug overdose

❑ Hypoglycemia

❑ Metabolic acidosis

❑ Subdural hematoma

❑ Hypothermia

❑ Heat stroke

❑ Meningitis

❑ Subarachnoid hemorrhage

❑ Head trauma

❑ Ischemic encephalopathy

❑ Epidural hematoma

❑ Pontine hemorrhage

❑ Cerebellar hemorrhage

❑ Psychogenic

Diagnostic Approach

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

Dizziness: Differential Overview
(Field Guide to Bedside Diagnosis)

Vertigo

❑ Benign paroxysmal positional vertigo

❑ Vestibular neuronitis

❑ Toxic labyrinthitis

❑ Vertebrobasilar insufficiency

❑ Ménière disease

❑ Migraine

❑ Multiple sclerosis

❑ Acoustic neuroma

❑ Herpes zoster oticus (Ramsey–Hunt)

Disequilibrium

❑ Multifactorial disequilibrium

❑ Stroke

❑ Cerebellar disease

❑ Frontal lobe apraxia

Lightheadedness

❑ Orthostatic hypotension

❑ Common fainting (presyncope)

❑ Hyperventilation

❑ Panic attack

Diagnostic Approach

Differentiate between vertigo, disequilibrium, and lightheadedness. Each has its own non-overlapping differential:

• Vertigo is the illusory sensation of rotatory motion, either of the patient or the environment.

• Disequilibrium is a sensation of imbalance when standing and walking.

• Lightheadedness is a sensation of impending loss of consciousness.

Provide the patient with experiential examples to refine the history (e.g., vertigo after spinning around as a child).

Attempt to provoke dizziness with maneuvers to confirm a provisional diagnosis, such as observation of gait, ambulation, and turning; orthostatic vital signs; Dix–Hallpike maneuver; Romberg; and/or 3-minute hyperventilation. The Dix–Hallpike maneuver provokes vertigo and nystagmus by stimulation of the posterior semicircular canal with the head tilted toward the affected side at 30 degrees below the horizontal. Have the patient look straight ahead to observe nystagmus. The nystagmus will fatigue. These findings indicate posterior canalithiasis causing benign paroxysmal positional vertigo (BPPV). The Romberg maneuver is performed by observing the patient standing. Swaying with eyes closed suggests disordered proprioception and/or vestibular function. Swaying with eyes open or closed is cerebellar in origin.

Vertigo usually implies a vestibular lesion (rarely brainstem). Suspect a central lesion if symptoms are preceded by a headache and vomiting without tinnitus. Central dizziness is very sensitive to movement of the head and is usually constant. Other cranial nerve findings or long track signs are usually present. Tinnitus, pressure, or decreased hearing localizes the problem to the inner ear and indicates the involved side. Nystagmus may persist after vertigo clears. Spontaneous vertical nystagmus suggests a lesion at the vestibular nucleus or cerebellum. Nystagmus that reverses direction when the patient looks in the direction of the slow phase suggests a central lesion. Exertional lightheadedness occurs in severe anemia, aortic stenosis, pulmonary hypertension, pericardial disease, and hypertrophic cardiomyopathy.

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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

Dizziness: History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

Ask about a history of diabetes and cardiovascular disease. Is the patient taking drugs prescribed for high blood pressure? If so, when did he take his last dose?

If the patient’s blood pressure is normal, obtain a more complete history. Ask about myocardial infarction, heart failure, kidney disease, or atherosclerosis, which may predispose the patient to cardiac arrhythmias, hypertension, and a transient ischemic attack. Does he have a history of anemia, chronic obstructive pulmonary disease (COPD), anxiety disorders, or head injury? Obtain a complete drug history.

Explore the patient’s dizziness. How often does it occur? How long does each episode last? Does the dizziness abate spontaneously? Does it lead to loss of consciousness? Find out if dizziness is triggered by sitting or standing up suddenly or stooping over. Does being in a crowd make the patient feel dizzy? Ask about emotional stress. Has the patient been irritable or anxious lately? Does he have insomnia or difficulty concentrating? Look for fidgeting and eyelid twitching. Does the patient startle easily? Also, ask about palpitations, chest pain, diaphoresis, shortness of breath, and chronic cough.

Physical examination

Perform a physical examination. Begin with a quick neurocheck, assessing the patient’s level of consciousness (LOC), motor and sensory functions, and reflexes. Then inspect for poor skin turgor and dry mucous membranes, signs of dehydration. Auscultate heart rate and rhythm. Inspect for barrel chest, clubbing, cyanosis, and use of accessory muscles. Also auscultate breath sounds. Take the patient’s blood pressure while he’s lying, sitting, and standing to check for orthostatic hypotension. Test capillary refill time in the extremities, and palpate for edema.

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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

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

Aura: History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Obtain a thorough history of the patient’s headaches or seizure history, asking him to describe any sensory or motor phenomena that precede each headache or seizure. Find out how long each headache or seizure typically lasts. Does anything make it worse, such as bright lights, noise, or caffeine? Does anything make it better? Ask the patient about drugs he takes for pain relief.

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Dizziness: History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

If the patient’s blood pressure is normal, obtain a more complete history. Ask about a history of diabetes and cardiovascular disease. Is the patient taking drugs prescribed for high blood pressure? If so, when did he take his last dose? Also ask about myocardial infarction, heart failure, kidney disease, or atherosclerosis, which may predispose the patient to cardiac arrhythmias, hypertension, and a transient ischemic attack. Does he have a history of anemia, chronic obstructive pulmonary disease, anxiety disorders, or head injury? Obtain a complete drug history.

Next, explore the patient’s dizziness. How often does it occur? How long does each episode last? Does the dizziness abate spontaneously? Does it lead to loss of consciousness? Find out if dizziness is triggered by sitting or standing up suddenly or stooping over. Does being in a crowd make the patient feel dizzy? Ask about emotional stress. Has the patient been irritable or anxious lately? Does he have insomnia or difficulty concentrating? Look for fidgeting and eyelid twitching. Does the patient startle easily? Also, ask about palpitations, chest pain, diaphoresis, shortness of breath, and chronic cough.

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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

Vertigo: History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Ask your patient to describe the onset and duration of his vertigo, being careful to distinguish this symptom from dizziness. Does he feel that he’s moving or that his surroundings are moving around him? How often do the attacks occur? Do they follow position changes, or are they unpredictable? Find out if the patient can walk during an attack, if he leans to one side, and if he has ever fallen. Ask if he experiences motion sickness and if he prefers one position during an attack. Obtain a recent drug history. Note any evidence of alcohol abuse.

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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

Vertigo: Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)

Peripheral Vestibular Dysfunction

Labyrinthitis

  • Acute otitismedia is most common cause of labyrinthitis in childhood. The infection mayextend directly into labyrinth, or inflammatory toxins may causelabyrinthine disturbance.
  • Viral infections (e.g., mumps, measles,and infectious mononucleosis) also may cause labyrinthitis.
  • History of infection followed by vertigoand hearing loss suggests diagnosis. Exam often reveals spontaneousnystagmus with fast component directed toward normal ear.

    • Motion Sickness

    Can occur with land, sea, or air travel.Nausea and vomiting are common findings, but vertigo and nystagmusalso can occur.

    Head Trauma

  • May causelabyrinthine injury with or without temporal bone fracture.
  • Frequent findings are falling towardaffected side and hearing loss.
  • Skull radiography and CT of temporalbone are useful in diagnosis. Caloric testing usually reveals decreasedlabyrinthine response on affected side.

    • Drugs

    Several drugs, including aminoglycosides,ethacrynic acid, and quinine, may cause hearing loss, but rarelyvertigo.

    Benign Paroxysmal Vertigo

  • Usuallyoccurs in children 2–6 yrs and is characterized by recurrentepisodes of vertigo that occur without warning.
  • Child appears pale, anxious, and unableto maintain upright position.
  • Nystagmus also may occur.
  • Results of neurologic exam are normalbetween episodes.

    • Vestibular Neuronitis

  • Most frequentcause of vestibular neuronitis, which usually occurs in adolescents,is viral upper respiratory infection.
  • Onset is acute, with nausea, vomiting,vertigo, and nystagmus. Hearing loss does not occur.
  • Episodes are self-limited but may recur.
  • Caloric stimulation produces decreasedor absent response on affected side.

    • Middle Ear and Temporal Bone Masses

  • Middle earand temporal bone masses (e.g., cholesteatoma and acoustic neuroma) maydamage labyrinth and produce vertigo and hearing loss.
  • CT and MRI locate mass and define itsextent.
  • See Bellet et al. (1992) for furtherdiscussion.

    • Perilymphatic Fistula

    Head trauma or sudden change in barometricpressure (flying or diving) may cause rupture of round or oval windowinto vestibule, creating fistula and producing vertigo and hearingloss (see Chap. 26, Hearing Lossand Deafness).

    Ménière Disease

    Uncommon disorder in children characterizedby recurrent episodes of vertigo, fluctuating hearing loss, andtinnitus. Caloric testing usually reveals reduced vestibular responseon involved side.

    Central Vestibular Dysfunction

    Head Trauma

    Concussion or brain contusion with shearingforces may damage vestibular nuclei and produce vertigo. Calorictesting reveals diminished caloric responses.

    Intracranial Infection

    Vertigo may sometimes occur with meningitis,encephalitis, and brain abscess. These disorders are discussed in Chap. 3, Alteration in Consciousness.

    Seizure Disorder

    Vertigo may occur as part of initial manifestationof complex partial seizure.

    Basilar Artery Migraine

    In this type of migraine, vertigo may precedeor accompany throbbing occipital headache (see Chap. 25, Headache).

    Neoplasm

  • Posteriorfossa tumors may cause vertigo, ataxia, and nystagmus, whereas brainstem gliomasmay cause vertigo, double vision, hearing loss, nystagmus, and cranialnerve dysfunction (III–VIII).
  • MRI is diagnostic study of choice.
  • Histologic diagnosis is definitive.

    • Psychologic Disturbance

  • Anxiety,depression, conversion reaction, or malingering may produce vertigo.
  • History and physical exam suggest diagnosis.Results of vestibular function testing, electroencephalography,and CT are normal.

    • Diagnostic Approach

  • Once presenceof vertigo has been established, next step is to determine whetherdisturbance is in peripheral or central vestibular system or whetherit is psychologic.
  • Important information is age of child;whether vertigo is acute, recurrent, or chronic; presence of hearingloss, ear pain, or tinnitus; and any history of recent trauma ordrug ingestion.
  • Complete physical exam should be performed,focusing on otologic and neurologic exams.
  • Vertigo caused by disturbance of peripheralvestibular system often occurs suddenly, lasts short time, and isunassociated with loss of consciousness. Sudden change in head positionfrequently precipitates episode. Nausea, vomiting, tinnitus, hearingloss, and swaying or falling toward affected side are common findings.Nystagmus is inhibited by visual fixation and may change with headposition.
  • Disturbance in central vestibular systemcan cause recurrent or chronic vertigo, which may be accompaniedby cranial nerve deficits, pyramidal signs, and cerebellar signs.If nystagmus occurs, it does not change with head position, noris it inhibited by visual fixation.
  • The history and physical exam are diagnosticin many cases of vertigo. Audiologic testing or brainstem evokedresponses should be performed with suspected hearing loss.
  • CT should be performed if there ishistory of acute head trauma. Otherwise, MRI is study of choiceif neuroimaging is indicated. Electroencephalography is useful ifseizures are suspected.

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    Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006

    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 include

  • Decreasedblood 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.
    • >>

    » READ BOOK EXCERPT ONLINE »

    Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006

    Aura: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    Obtain a thorough history of the patient's headache or seizure history, asking him to describe any sensory or motor phenomena that precede each headache or seizure. Find out how long each headache or seizure typically lasts. Does anything make it worse, such as bright lights, noise, or caffeine? Does anything make it better? Ask the patient about drugs he takes for pain relief.

    Then perform a complete neurologic examination.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    Dizziness: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    Ask about a history of diabetes and cardiovascular disease. Is the patient taking drugs prescribed for high blood pressure? If so, when did he take his last dose?

    If the patient's blood pressure is normal, obtain a more complete history. Ask about myocardial infarction, heart failure, kidney disease, or atherosclerosis, which may predispose the patient to cardiac arrhythmias, hypertension, and a transient ischemic attack. Does he have a history of anemia, chronic obstructive pulmonary disease, anxiety disorders, or head injury? Obtain a complete drug history.

    Next, explore the patient's dizziness. How often does it occur? How long does each episode last? Does the dizziness abate spontaneously? Does it lead to loss of consciousness? Find out if dizziness is triggered by sitting or standing up suddenly or stooping over. Does being in a crowd make the patient feel dizzy? Ask about emotional stress. Has the patient been irritable or anxious lately? Does he have insomnia or difficulty concentrating? Look for fidgeting and eyelid twitching. Does the patient startle easily? Also, ask about palpitations, chest pain, diaphoresis, shortness of breath, and chronic cough.

    Next, perform a physical examination. Begin with a quick neurologic assessment, checking the patient's level of consciousness (LOC), motor and sensory functions, and reflexes. Then inspect for poor skin turgor and dry mucous membranes, signs of dehydration. Auscultate heart rate and rhythm. Inspect for barrel chest, clubbing, cyanosis, and use of accessory muscles. Also auscultate breath sounds. Take the patient's blood pressure while he's lying down, sitting, and standing to check for orthostatic hypotension. Test capillary refill time in the extremities, and palpate for edema.

    » READ BOOK EXCERPT ONLINE »

    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.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    Vertigo: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    Ask your patient to describe the onset and duration of his vertigo, being careful to distinguish this symptom from dizziness. Does he feel that he's moving or that his surroundings are moving around him? How often do the attacks occur? Do they follow position changes, or are they unpredictable? Find out if the patient can walk during an attack, if he leans to one side, and if he has ever fallen. Ask whether he experiences motion sickness and if he prefers one position during an attack. Obtain a recent drug history, and note evidence of alcohol abuse.

    Perform a neurologic assessment, focusing particularly on eighth cranial nerve function. Observe the patient's gait and posture for abnormalities.

    » 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

    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.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    DIZZINESS: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    The first step is to determine if the patient has true vertigo. True vertigo is the experience of subjective or objective rotation with respect to the environment. In other words, either the patient or his or her environment is turning. One other form of true vertigo is lateral pulsion. This is the feeling that one is moving sideways when that is not the case. The patient who does not experience true vertigo should have a syncope workup . Narrowing the differential diagnosis of true vertigo depends on the presence or absence of other symptoms and signs. If there are other cranial nerve or long tract signs on neurologic examination, the patient may have a space-occupying lesion of the brain or brainstem or a hemorrhage, thrombosis, or embolism in the vertebral–basilar artery distribution. A neurology consult should be obtained. If there is true vertigo, tinnitis, and deafness, one would consider inner ear pathology such as Ménière disease, syphilis, petrositis, mastoiditis, and acoustic neuroma. If there is vertigo without tinnitus, deafness, or focal neurologic signs, the clinician should suspect acute labyrinthitis, vestibular neuronitis, benign positional vertigo, and drug toxicity. If there are rapid respirations during the attack of vertigo, one would consider hyperventilation syndrome. If there are significant findings on otoscopic examination, a diagnosis of otitis media, cholesteatoma, or mastoiditis should be considered. The workup will depend on whether the patient has objective findings on otoscopic or neurologic examination. If local pathology is suspected, perhaps a tympanogram, x-ray of the mastoids and petrous bones, audiogram, or referral to an otolaryngologist are required. If there are neurologic findings, perhaps a CT scan or MRI of the brain and auditory canal is indicated along with a referral to a neurologist. It is wise to have a specialist on board before ordering an expensive workup.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    COMA AND SOMNOLENCE: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    Obviously, the neurologic examination and a good history from a member of the family or friend are invaluable in the diagnosis of coma. However, one should not delay ordering laboratory work until the examination and history are accomplished. A CBC, blood urea nitrogen (BUN), fasting blood sugar (FBS), serum osmolality, electrolytes, blood gases, urinalysis, and drug screen are ordered immediately. If there is little or no history available and insulin shock is suspected, glucose or glucagon is administered before the laboratory reports are back, although this is done with more caution today for fear of aggravating a case of nonketotic, hyperosmolar diabetic coma. It has been my experience that the neurologic examination is best performed simultaneously with the taking of a history from a relative or friend. In this way, various telltale neurologic signs can be found with alacrity. A unilateral dilated pupil (suggesting a subdural hematoma or aneurysm), acetone breath (suggesting diabetic acidosis), contusion of the skull (suggesting cerebral concussion or hematoma), and nuchal rigidity (suggesting a subarachnoid hemorrhage in meningitis) are just a few of the signs that can help to rapidly identify the cause of the coma. Coma without focal neurologic findings should suggest a metabolic or toxic cause. In that case, an intensive laboratory workup as listed below would be indicated. A spinal tap may be indicated if there is fever as well. In contrast, coma with focal neurologic signs suggests tumor, abscess, hematoma or cerebral embolism, thrombosis, or hemorrhage. The clinician should proceed with a skull x-ray film and CT scan immediately. When these are not available, immediate referral to a large medical center is necessary. Electroencephalography (EEG) and a spinal tap may identify the cause. A spinal tap should be considered with extreme caution even if there is no papilledema. Of course, a spinal tap is never done in the presence of papilledema unless a neurologist is consulted and CT findings are negative. One indication for a spinal tap under these circumstances might be meningitis. Another might be “benign intracranial hypertension.”

    » READ BOOK EXCERPT ONLINE »

    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.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007


     » Next page: Signs of Syncope

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