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Diagnosis of Stokes Adams syndrome

Stokes Adams syndrome Diagnosis: Book Excerpts

• Ask the following questions - COMA
• Ask the Following Questions - SYNCOPE
• Differential Diagnosis - Syncope
• Differential Diagnosis - Coma
• Differential Diagnosis - Syncope
• Approach to the Diagnosis - SYNCOPE
• Approach to the Diagnosis - COMA AND SOMNOLENCE
• History and physical examination - Level of consciousness, decreased
• History and physical examination - Syncope
• History and physical examination - Level of consciousness, decreased
• History and physical examination - Syncope
• History - Coma
• History - Syncope
• Differential Overview - Coma
• Differential Overview - Syncope
• History - Level of consciousness, decreased
• History - Syncope
• History - Level of consciousness, decreased
• History - Syncope
• Clinical Features and Diagnosis - Syncope and Dizziness
• History and physical examination - Level of consciousness, decreased
• History and physical examination - Syncope
• Approach to the Diagnosis - SYNCOPE
• Approach to the Diagnosis - COMA AND SOMNOLENCE

Diagnostic Tests for Stokes Adams syndrome: Online Medical Books

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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.

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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.

 

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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

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

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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)

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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

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

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

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

Level of consciousness, decreased: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

Try to obtain history information from the patient, if he’s lucid, and from his family. Did the patient complain of headache, dizziness, nausea, visual or hearing disturbances, weakness, fatigue, or any other problems before his LOC decreased? Has his family noticed any changes in the patient’s behavior, personality, memory, or temperament? Also ask about a history of neurologic disease, cancer, or recent trauma or infections; drug and alcohol use; and the development of other signs and symptoms.

Because decreased LOC can result from a disorder affecting virtually any body system, tailor the remainder of your evaluation according to the patient’s associated symptoms.

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

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

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

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.

» READ BOOK EXCERPT ONLINE »

Source: Field Guide to Bedside Diagnosis, 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.

» READ BOOK EXCERPT ONLINE »

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.

» READ BOOK EXCERPT ONLINE »

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

» READ BOOK EXCERPT ONLINE »

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?

» READ BOOK EXCERPT ONLINE »

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

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

Cardiovascular Syncope

Neurocardiogenic Syncope (Common Faint)

Most commontype of syncope in childhood and adolescence.

Often a response to anxiety, fear,pain, or other emotional stress.

Also may occur after extreme fatigue,prolonged standing, or fasting.

Pathogenesis involves vasodilatationof skeletal muscle vasculature and failure of heart rate and strokevolume to maintain cardiac output for adequate cerebral blood flow.

Dizziness, nausea, sweating, and abdominaldiscomfort may precede syncope. Interruption of cerebral perfusionfor 2–3 secs produces dizziness, but lying down duringpresyncopal phase may prevent syncopal episode.

If cerebral perfusion is interruptedfor >10 secs, syncope occurs.

Onset is sudden with hypotension (vasodepressorresponse), and BP decreases to ≤60 mm Hg. Bradycardia usuallyoccurs, and often junctional rhythm or period of asystole (cardioinhibitory response)may follow.

Most episodes are associated with uprightposition, and child becomes limp and falls to ground. Loss of consciousnessusually lasts <1 min.

Seizures are unusual but may occurwith prolonged syncope.

Once individual is horizontal, BP,heart rate, and color return toward normal.

History and physical exam are usuallydiagnostic. Individuals with this form of syncope do not need furthertesting unless syncope is recurrent, when tilt table testing mayconfirm its presence.

Both tussive and micturition syncopeare now considered forms of neurocardiogenic syncope.

Tussive syncopehas been attributed to large increase in intrathoracic pressure,which decreases venous return to the heart. It may occur after significantcoughing of any cause, but especially after severe paroxysmal coughingwith pertussis.

Micturition syncope is most commonin elderly men, but it can occur in older adolescents. Syncope usuallyoccurs at the end of micturition. The mechanism is unclear, buta full bladder causes peripheral vasoconstriction, and with emptying,peripheral vasodilatation occurs, which in the erect posture mayproduce syncope.

Cardiac Syncope

Congenital and Acquired Heart Disease

Syncopemay occur with outflow obstruction of left ventricle (LV) (valvar,subvalvar, or supravalvar aortic stenosis; hypertrophic cardiomyopathy),outflow obstruction of right ventricle (RV) (pulmonic stenosis,primary pulmonary artery hypertension, pulmonary vascular disease),inflow obstruction of LV (mitral stenosis, atrial myxoma), and inflowobstruction of RV (cardiac tamponade). More likely to occur duringor just after physical exertion, when cardiac output cannot increaseenough to meet demands of oxygen delivery to brain.

Syncope also may occur with cardiomyopathy,myocarditis, and endocarditis as a result of decreased cardiac output.

Another cause is myocardial ischemia,which may occur with coronary artery anomalies, especially anomalousorigin of left coronary artery from pulmonary artery and abnormalcourse of left coronary artery between aortic and pulmonary trunkswith compression of artery during exercise. Coronary artery aneurysmsand thrombosis found in Kawasaki disease also may produce myocardialischemia and syncope.

In most cases, history, physical exam,chest radiograph, ECG, and 2-D echocardiogram are diagnostic.

Diagnosis of primary pulmonary hypertensionusually requires lung biopsy to exclude pulmonary venoocclusivedisease. Although pulmonary vascular disease may be diagnosed clinicallywith support of echocardiography, cardiac catheterization and angiographycan confirm these findings.

Hypercyanotic Episodes

Consistof intense cyanosis and hyperpnea. Occur most commonly with tetralogyof Fallot but also can occur with tricuspid atresia, transpositionof great arteries with pulmonary stenosis, and pulmonary vasculardisease.

Children who can walk may squat duringepisode, which increases systemic vascular resistance and decreasesright-to-left shunt.

Occasionally episodes may be prolongedand associated with syncope and seizures. During episode, murmuris less intense or disappears.

Several factors seem to play a role:prolonged crying with decreased venous return, constriction of RVinfundibulum, decreased systemic vascular resistance secondary toimmobilization or spontaneous vasomotor changes, relative anemia,and increased physical activity with higher oxygen requirement.

Arrhythmias in Structurally Normal Heart

Syncopemay occur from sinus bradycardia, junctional bradycardia, second-and third-degree (atrioventricular) AV block with low ventricularrate, supraventricular tachycardia, atrial flutter, or ventriculartachycardia.

Atrial fibrillation with rapid ventricularresponse over the accessory pathway may be associated with syncopeor near syncope in Wolff-Parkinson-White (WPW) syndrome. Diagnosisis usually confirmed by ECG, which shows short PR interval and deltawave.

Syncope also may occur with prolongedQT interval, in which variable recovery time with reentry depolarizationmay cause torsade de pointes ventricular tachycardia.

ProlongedQT interval has a number of genetic causes. Hypokalemia, hypocalcemia, andhypomagnesemia also may cause QT interval prolongation. Tricyclicantidepressants and phenothiazines have been associated with prolongedQT interval, and so have overdoses of quinidine, procainamide, anddisopyramide.

Prolonged QT interval can be diagnosedby measuring this interval on routine ECG, but it must be correctedfor heart rate. 1 method for correction of QT interval is to measureQT interval (in secs) and divide by the square root of the RR interval(in secs). In 95% of individuals, the corrected QT interval is <0.45secs.

Sympathomimetic drugs when taken inlarge doses or from idiosyncratic reaction may produce supraventricularor ventricular tachycardia. Cocaine also may produce ventriculartachycardia and syncope. Metabolic derangements (e.g., hyperkalemia,hypoglycemia, and hypercalcemia) also may result in syncope by producingarrhythmias, but this is rare.

ECG may be diagnostic of these arrhythmias.If syncopal episodes are frequent, Holter monitoring may be useful;if they occur during exercise, maximal exercise testing may be diagnostic.Otherwise, event recorder or implanted loop recorder should be considered.

If syncope still remains unexplained,electrophysiologic studies should be performed.

Arrhythmias in Structurally Abnormal Heart

Childrenwho have congenital or acquired heart disease are at risk for arrhythmias thatmay produce syncope. These include sinus bradycardia, sick sinussyndrome, supraventricular tachycardia, atrial fibrillation, atrialflutter, ventricular tachycardia, ventricular fibrillation, andcomplete heart block.

WPW syndrome and supraventricular tachycardiaare occasionally associated with Ebstein anomaly.

Complete heart block may be associatedwith ventricular inversion and transposition of great arteries.

Ventricular tachycardia may occur fromarrhythmogenic RV dysplasia, although echocardiography may not bediagnostic because a heavily trabeculated RV may be indistinguishablefrom dysplasia. Recurrent ventricular tachycardia, especially exercise-induced,and left bundle branch pattern suggest this diagnosis, which canbe confirmed by MRI.

Children who have had surgical repairof a cardiac defect are also at risk for development of arrhythmias.An incision in the ventricle is a risk factor for ventricular tachycardia.Supraventricular tachycardia, atrial fibrillation, atrial flutter,sick sinus syndrome, and ventricular tachycardia may occur after Mustardor Senning procedure for repair of transposition of great arteries.Surgical manipulation in the area of sinus or AV nodes in repairof AV canal defects, posterior ventricular septal defects, or tunnelaortic stenosis may predispose to development of sinus bradycardiaand heart block.

ECG may be diagnostic of these arrhythmias.Holter monitoring and maximal exercise testing also may be helpfulin diagnosis.

If these tests are normal consideringhigher risk of life-threatening events in children with structurallyabnormal hearts, electrophysiologic studies should be considered.

Vascular Syncope

Orthostatic Syncope

Occurs whenindividual assumes upright posture and systolic arterial BP decreasesby ≥15 mm Hg.

Possible causes 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

Level of consciousness, decreased: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

Try to obtain history information from the patient, if he's alert, and from his family. Did the patient complain of a headache, dizziness, nausea, vision or hearing disturbances, weakness, fatigue, or other problems before his LOC decreased? Has his family noticed changes in the patient's behavior, personality, memory, or temperament? Also ask about a history of neurologic disease, cancer, or recent trauma or infections; drug and alcohol use; and the development of other signs and symptoms.

Because a decreased LOC can result from a disorder affecting any body system, tailor the remainder of your evaluation according to the patient's associated symptoms.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

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

If the patient reports a fainting episode, gather information about the episode from him and his family. Did he feel weak, light-headed, nauseous, or sweaty just before he fainted? Did he get up quickly from a chair or from lying down? During the fainting episode, did he have muscle spasms or incontinence? How long was he unconscious? When he regained consciousness, was he alert or confused? Did he have a headache? Has he fainted before? If so, how often does it occur? Obtain a complete drug history.

Next, take the patient's vital signs and examine him for any injuries that may have occurred during his fall. Place him on a cardiac monitor and assess his heart rhythm for abnormalities. Assess cardiac and respiratory status. Monitor pulse oximetry. Perform a neurologic examination.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

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

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.”

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Source: Differential Diagnosis in Primary Care, 2007

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