TREATMENTS &
RESEARCH

Search the
latest
treatment
information
here.

Dr. Huntley's
Diagnosis
Checklist

Have a symptom?
See what questions
a doctor would ask.
 
Next Prev
Diseases » Syncope » Causes
 

Causes of Syncope

Contents
  1. Syncope: Introduction
  2. List of Causes
  3. Drugs/substances (614 causes)
  4. Drug interaction (114 causes)
  5. Hidden causes
  6. Excerpts from book chapters
  7. Complication causes
  8. Causes of symptoms
  9. News
  10. Related cause information

List of causes of Syncope

Following is a list of causes or underlying conditions (see also Misdiagnosis of underlying causes of Syncope) that could possibly cause Syncope includes:

More causes: see full list of causes for Syncope

Causes of Syncope (Diseases Database):

The follow list shows some of the possible medical causes of Syncope that are listed by the Diseases Database:

Source: Diseases Database

Syncope Causes: Book Excerpts

Syncope as a complication of other conditions:

Other conditions that might have Syncope as a complication may, potentially, be an underlying cause of Syncope. Our database lists the following as having Syncope as a complication of that condition:

Syncope as a symptom:

Conditions listing Syncope as a symptom may also be potential underlying causes of Syncope. Our database lists the following as having Syncope as a symptom of that condition:

Medications or substances causing Syncope:

The following drugs, medications, substances or toxins are some of the possible causes of Syncope as a symptom. This list is incomplete and various other drugs or substances may cause your symptoms. Always advise your doctor of any medications or treatments you are using, including prescription, over-the-counter, supplements, herbal or alternative treatments.

  • Chlorphenesin Carbamate
  • Maolate
  • Blanex
  • Chlorofon-F
  • Flexaphen
  • more drugs...»

See full list of 614 medications causing Syncope


Drug interactions causing Syncope:

When combined, certain drugs, medications, substances or toxins may react causing Syncope as a symptom.

The list below is incomplete and various other drugs or substances may cause your symptoms. Always advise your doctor of any medications or treatments you are using, including prescription, over-the-counter, supplements, herbal or alternative treatments.

  • Tamsulosin and beta-blocking drug interaction
  • Flomax and beta-blocking drug interaction
  • Nitroglycerin and alcohol interaction
  • Deponit and alcohol interaction
  • Minitran and alcohol interaction
  • more interactions...»

See full list of 114 drug interactions causing Syncope

Medical news summaries relating to Syncope:

The following medical news items are relevant to causes of Syncope:

Related information on causes of Syncope:

As with all medical conditions, there may be many causal factors. Further relevant information on causes of Syncope may be found in:

Causes of Syncope: Online Medical Books

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

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

» 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)

» 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
>

» 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

» 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

» 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

» 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

» 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

» READ BOOK EXCERPT ONLINE »

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

Aura: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

❑ Classic migraine headache. A migraine is preceded by a vague premonition and then, usually, a visual aura involving flashes of light. The aura lasts 10 to 30 minutes and may intensify until it completely obscures the patient’s vision. A classic migraine may cause numbness or tingling of the lips, face, or hands; slight confusion; and dizziness before the characteristic unilateral, throbbing headache appears. It slowly intensifies; when it peaks, it may cause photophobia, nausea, and vomiting.

❑ Seizure, generalized tonic-clonic. A generalized tonic-clonic seizure may begin with or without an aura. The patient loses consciousness and falls to the ground. His body stiffens (tonic phase), and then he experiences rapid, synchronous muscle jerking and hyperventilation (clonic phase). The seizure usually lasts 2 to 5 minutes.

» READ BOOK EXCERPT ONLINE »

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

Dizziness: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Anemia.

Typically, anemia causes dizziness that's aggravated by postural changes or exertion. Other signs and symptoms include pallor, dyspnea, fatigue, tachycardia, and a bounding pulse. The capillary refill time is increased.

Cardiac arrhythmias.

Dizziness lasts for several seconds or longer and may precede fainting in arrhythmias. The patient may experience palpitations; irregular, rapid, or thready pulse; and, possibly, hypotension. He may also experience weakness, blurred vision, paresthesia, and confusion.

Emphysema.

Dizziness may follow exertion or the chronic productive cough in patients with emphysema. Associated signs and symptoms include dyspnea, anorexia, weight loss, malaise, use of accessory muscles, pursed-lip breathing, tachypnea, peripheral cyanosis, and diminished breath sounds. Barrel chest and clubbing may be seen.

Generalized anxiety disorder

Generalized anxiety disorder produces continuous dizziness that may intensify as the disorder worsens. Associated signs and symptoms are persistent anxiety (for at least 1 month), insomnia, difficulty concentrating, and irritability. The patient may show signs of motor tension — for example, twitching or fidgeting, muscle aches, a furrowed brow, and a tendency to be startled. He may also display signs of autonomic hyperactivity, such as diaphoresis, palpitations, cold and clammy hands, dry mouth, paresthesia, indigestion, hot or cold flashes, frequent urination, diarrhea, a lump in the throat, pallor, and increased pulse and respiratory rates.

Hypertension.

With hypertension, dizziness may precede fainting, but it may also be relieved by rest. Other common signs and symptoms include a headache and blurred vision. Retinal changes include hemorrhage, sclerosis of retinal blood vessels, exudate, and papilledema.

Hyperventilation syndrome.

Episodes of hyperventilation cause dizziness that usually lasts a few minutes; however, if these episodes occur frequently, dizziness may persist between them. Other effects include apprehension, diaphoresis, pallor, dyspnea, chest tightness, palpitations, trembling, fatigue, and peripheral and circumoral paresthesia.

Hypovolemia.

Dizziness is caused by a lack of circulating volume and may be accompanied by other signs of fluid volume deficit (dry mucous membranes, decreased blood pressure, increased heart rate).

Orthostatic hypotension.

Orthostatic hypotension produces dizziness that may terminate in fainting or disappear with rest. Related findings include dim vision, spots before the eyes, pallor, diaphoresis, hypotension, tachycardia and, possibly, signs of dehydration.

Postconcussion syndrome.

Occurring 1 to 3 weeks after a head injury, postconcussionsyndrome is marked by dizziness, a headache (throbbing, aching, bandlike, or stabbing), emotional lability, alcohol intolerance, fatigue, anxiety and, possibly, vertigo. Dizziness and other symptoms are intensified by mental or physical stress. The syndrome may persist for years, but symptoms eventually abate.

Rift Valley fever

Typical signs and symptoms of Rift Valley fever include dizziness, a fever, myalgia, weakness, and back pain. A small percentage of patients may develop encephalitis or may progress to hemorrhagic fever that can lead to shock and hemorrhage. Inflammation of the retina may result in some permanent vision loss.

Transient ischemic attack (TIA)

Lasting from a few seconds to 24 hours, a TIA commonly signals an impending stroke and may be triggered by turning the head to the side. Besides dizziness of varying severity, TIAs are accompanied by unilateral or bilateral diplopia, blindness or visual field deficits, ptosis, tinnitus, hearing loss, paresis, and numbness. Other findings include dysarthria, dysphagia, vomiting, hiccups, confusion, a decreased LOC, and pallor.

Other causes

Drugs

Anxiolytics, central nervous system depressants, opioids, decongestants, antihistamines, antihypertensives, and vasodilators commonly cause dizziness.

Herb alert  

Herbal remedies, such as St. John's wort, can produce dizziness.

» READ BOOK EXCERPT ONLINE »

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

Level of consciousness, decreased: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Adrenal crisis

A decreased LOC, ranging from lethargy to coma, may develop within 8 to 12 hours of its onset

Early associated findings include progressive weakness, irritability, anorexia, a headache, nausea and vomiting, diarrhea, abdominal pain, and a fever. Later signs and symptoms include hypotension; a rapid, thready pulse; oliguria; cool, clammy skin; and flaccid extremities. The patient with chronic adrenocortical hypofunction may have hyperpigmented skin and mucous membranes.

Brain abscess

A decreased LOC varies from drowsiness to deep stupor, depending on the abscess size and site

Early signs and symptoms — a constant intractable headache, nausea, vomiting, and seizures — reflect increasing ICP. Typical later features include ocular disturbances (nystagmus, vision loss, and pupillary inequality) and signs of infection such as a fever. Other findings may include personality changes, confusion, abnormal behavior, dizziness, facial weakness, aphasia, ataxia, tremor, and hemiparesis.

Brain tumor

The patient’s LOC decreases slowly, from lethargy to coma

He may also experience apathy, behavior changes, memory loss, a decreased attention span, a morning headache, dizziness, vision loss, ataxia, and sensorimotor disturbances. Aphasia and seizures are possible, along with signs of hormonal imbalance, such as fluid retention or amenorrhea. Signs and symptoms vary according to the location and size of the tumor. In later stages, papilledema, vomiting, bradycardia, and a widening pulse pressure also appear. In the final stages, the patient may exhibit decorticate or decerebrate posture.

Cerebral aneurysm (ruptured)

Somnolence, confusion and, at times, stupor characterize a moderate bleed; deep coma occurs with severe bleeding, which can be fatal

The onset is usually abrupt, with a sudden, severe headache and nausea and vomiting. Nuchal rigidity, back and leg pain, a fever, restlessness, irritability, occasional seizures, and blurred vision point to meningeal irritation. The type and severity of other findings vary with the site and severity of the hemorrhage and may include hemiparesis, hemisensory defects, dysphagia, and visual defects.

Diabetic ketoacidosis

Diabetic ketoacidosis produces a rapid decrease in the patient’s LOC, ranging from lethargy to coma, commonly preceded by polydipsia, polyphagia, and polyuria

The patient may complain of weakness, anorexia, abdominal pain, nausea, and vomiting. He may also exhibit orthostatic hypotension; a fruity breath odor; Kussmaul’s respirations; warm, dry skin; and a rapid, thready pulse. Untreated, this condition invariably leads to coma and death.

Encephalitis

Within 24 to 48 hours after onset, the patient may develop changes in his LOC ranging from lethargy to coma

Other possible findings include an abrupt onset of a fever, a headache, nuchal rigidity, nausea, vomiting, irritability, personality changes, seizures, aphasia, ataxia, hemiparesis, nystagmus, photophobia, myoclonus, and cranial nerve palsies.

Encephalomyelitis (postvaccinal)

Postvaccinal encephalomyelitisis a life-threatening disorder that produces rapid deterioration in the patient’s LOC, from drowsiness to coma

He also experiences a rapid onset of a fever, a headache, nuchal rigidity, back pain, vomiting, and seizures.

Encephalopathy

With hepatic encephalopathy, signs and symptoms develop in four stages: in the prodromal stage, slight personality changes (disorientation, forgetfulness, slurred speech) and slight tremor; in the impending stage, tremor progressing to asterixis (the hallmark of hepatic encephalopathy), lethargy, aberrant behavior, and apraxia; in the stuporous stage, stupor and hyperventilation, with the patient noisy and abusive when aroused; in the comatose stage, coma with decerebrate posture, hyperactive reflexes, a positive Babinski’s reflex, and fetor hepaticus.

With life-threatening hypertensive encephalopathy, the LOC progressively decreases from lethargy to stupor to coma

Besides markedly elevated blood pressure, the patient may experience a severe headache, vomiting, seizures, vision disturbances, transient paralysis and, eventually, Cheyne-Stokes respirations.

With hypoglycemic encephalopathy,the patient’s LOC rapidly deteriorates from lethargy to coma. Early signs and symptoms include nervousness, restlessness, agitation, and confusion; hunger; alternate flushing and cold sweats; and a headache, trembling, and palpitations. Blurred vision progresses to motor weakness, hemiplegia, dilated pupils, pallor, a decreased pulse rate, shallow respirations, and seizures. Flaccidity and decerebrate posture appear late.

Depending on its severity, hypoxic encephalopathyproduces a sudden or gradual decrease in the LOC, leading to coma and brain death. Early on, the patient appears confused and restless, with cyanosis and increased heart and respiratory rates and blood pressure. Later, his respiratory pattern becomes abnormal, and assessment reveals a decreased pulse, blood pressure, and deep tendon reflexes (DTRs); a positive Babinski’s reflex; an absent doll’s eye sign; and fixed pupils.

With uremic encephalopathy,the LOC decreases gradually from lethargy to coma. Early on, the patient may appear apathetic, inattentive, confused, and irritable and may complain of a headache, nausea, fatigue, and anorexia. Other findings include vomiting, tremors, edema, papilledema, hypertension, cardiac arrhythmias, dyspnea, crackles, oliguria, and Kussmaul’s and Cheyne-Stokes respirations.

Heatstroke

As body temperature increases, the patient’s LOC gradually decreases from lethargy to coma

Early signs and symptoms include malaise, tachycardia, tachypnea, orthostatic hypotension, muscle cramps, rigidity, and syncope. The patient may be irritable, anxious, and dizzy and may report a severe headache. At the onset of heatstroke, the patient’s skin is hot, flushed, and diaphoretic with blotchy cyanosis; later, when his fever exceeds 105° F (40.5° C), his skin becomes hot, flushed, and anhidrotic. Pulse and respiratory rate increase markedly, and blood pressure drops precipitously. Other findings include vomiting, diarrhea, dilated pupils, and Cheyne-Stokes respirations.

Hypernatremia

Hypernatremia, life threatening if acute, causes the patient’s LOC to deteriorate from lethargy to coma

He is irritable and exhibits twitches progressing to seizures. Other associated signs and symptoms include a weak, thready pulse; nausea; malaise; a fever; thirst; flushed skin; and dry mucous membranes.

Hyperosmolar hyperglycemic nonketotic syndrome

LOC decreases rapidly from lethargy to coma

Early findings include polyuria, polydipsia, weight loss, and weakness. Later, the patient may develop hypotension, poor skin turgor, dry skin and mucous membranes, tachycardia, tachypnea, oliguria, and seizures.

Hypokalemia

LOC gradually decreases to lethargy; coma is rare

Other findings include confusion, nausea, vomiting, diarrhea, and polyuria; weakness, decreased reflexes, and malaise; and dizziness, hypotension, arrhythmias, and abnormal electrocardiogram results.

Hyponatremia

Hyponatremia, life threatening if acute, produces a decreased LOC in late stages

Early nausea and malaise may progress to behavior changes, confusion, lethargy, incoordination and, eventually, seizures and coma.

Hypothermia

With severe hypothermia(temperature below 90° F [32.2° C]), the patient’s LOC decreases from lethargy to coma. DTRs disappear, and ventricular fibrillation occurs, possibly followed by cardiopulmonary arrest. With mild to moderate hypothermia, the patient may experience memory loss and slurred speech as well as shivering, weakness, fatigue, and apathy. Other early signs and symptoms include ataxia, muscle stiffness, and hyperactive DTRs; diuresis; tachycardia and decreased respiratory rate and blood pressure; and cold, pale skin. Later, muscle rigidity and decreased reflexes may develop, along with peripheral cyanosis, bradycardia, arrhythmias, severe hypotension, a decreased respiratory rate with shallow respirations, and oliguria.

Intracerebral hemorrhage

Intracerebral hemorrhage is a life-threatening disorder that produces a rapid, steady loss of consciousness within hours, commonly accompanied by a severe headache, dizziness, nausea, and vomiting. Associated signs and symptoms vary and may include increased blood pressure, irregular respirations, a positive Babinski’s reflex, seizures, aphasia, decreased sensations, hemiplegia, decorticate or decerebrate posture, and dilated pupils.

Listeriosis

If listeriosis spreads to the nervous system and causes meningitis, signs and symptoms include a decreased LOC, a fever, a headache, and nuchal rigidity

Early signs and symptoms of listeriosis include a fever, myalgia, abdominal pain, nausea, vomiting, and diarrhea.

Gender cue

Infections during pregnancy may lead to premature delivery, infection of the neonate, or stillbirth.

Meningitis

Confusion and irritability are expected; however, stupor, coma, and seizures may occur in the patient with severe meningitis

A fever develops early, possibly accompanied by chills. Associated findings include a severe headache, nuchal rigidity, hyperreflexia and, possibly, opisthotonos. The patient exhibits Kernig’s and Brudzinski’s signs and, possibly, ocular palsies, photophobia, facial weakness, and hearing loss.

Pontine hemorrhage

A sudden, rapid decrease in the patient’s LOC to the point of coma occurs within minutes and death within hours

The patient may also exhibit total paralysis, decerebrate posture, a positive Babinski’s reflex, an absent doll’s eye sign, and bilateral miosis (however, the pupils remain reactive to light).

Seizure disorders

A complex partial seizure produces a decreased LOC, manifested as a blank stare, purposeless behavior (picking at clothing, wandering, lip smacking or chewing motions), and unintelligible speech

The seizure may be heralded by an aura and followed by several minutes of mental confusion.

An absence seizure usually involves a brief change in the patient’s LOC, indicated by blinking or eye rolling, a blank stare, and slight mouth movements.

A generalized tonic-clonic seizure typically begins with a loud cry and sudden loss of consciousness. Muscle spasm alternates with relaxation. Tongue biting, incontinence, labored breathing, apnea, and cyanosis may also occur. Consciousness returns after the seizure, but the patient remains confused and may have difficulty talking. He may complain of drowsiness, fatigue, a headache, muscle aching, and weakness and may fall into a deep sleep.

An atonic seizureproduces sudden unconsciousness for a few seconds.

Status epilepticus,rapidly recurring seizures without intervening periods of physiologic recovery and return of consciousness, can be life threatening.

Shock

A decreased LOC — lethargy progressing to stupor and coma — occurs late in shock

Associated findings include confusion, anxiety, and restlessness; hypotension; tachycardia; a weak pulse with narrowing pulse pressure; dyspnea; oliguria; and cool, clammy skin.

Hypovolemic shock is generally the result of massive or insidious bleeding, either internally or externally. Cardiogenic shock may produce chest pain or arrhythmias and signs of heart failure, such as dyspnea, a cough, edema, jugular vein distention, and weight gain. Septic shock may be accompanied by a high fever and chills. Anaphylactic shock usually involves stridor.

Stroke

Changes in the patient’s LOC vary in degree and onset, depending on the lesion’s size and location and the presence of edema

A thrombotic stroke usually follows multiple transient ischemic attacks (TIAs). Changes in the LOC may be abrupt or take several minutes, hours, or days. An embolic stroke occurs suddenly, and deficits reach their peak almost at once. Deficits associated with a hemorrhagic stroke usually develop over minutes or hours.

Associated findings vary with the stroke type and severity and may include disorientation; intellectual deficits, such as memory loss and poor judgment; personality changes; and emotional lability. Other possible findings include dysarthria, dysphagia, ataxia, aphasia, apraxia, agnosia, unilateral sensorimotor loss, and vision disturbances. In addition, urine retention, incontinence, constipation, a headache, vomiting, and seizures may occur.

Subdural hemorrhage (acute)

Acute subdural hemorrhageis a potentially life-threatening disorder in which agitation and confusion are followed by a progressively decreasing LOC from somnolence to coma

The patient may also experience a headache, a fever, unilateral pupil dilation, decreased pulse and respiratory rates, a widening pulse pressure, seizures, hemiparesis, and a positive Babinski’s reflex.

Thyroid storm

The patient’s LOC decreases suddenly and can progress to coma

Irritability, restlessness, confusion, and psychotic behavior precede the deterioration. Associated signs and symptoms include tremors and weakness; vision disturbances; tachycardia, arrhythmias, angina, and acute respiratory distress; warm, moist, flushed skin; and vomiting, diarrhea, and a fever of up to 105 ° F (40.5° C).

TIA

The patient’s LOC decreases abruptly (with varying severity) and gradually returns to normal within 24 hours

Site-specific findings may include vision loss, nystagmus, aphasia, dizziness, dysarthria, unilateral hemiparesis or hemiplegia, tinnitus, paresthesia, dysphagia, or staggering or incoordinated gait.

West Nile encephalitis

West Nile encephalitis is a brain infection that’s caused by the West Nile virus, a mosquito-borne flavivirus commonly found in Africa, West Asia, and the Middle East and, less commonly, in the United States

Mild infection is common. Signs and symptoms include a fever, a headache, and body aches, commonly with a skin rash and swollen lymph glands. More severe infection is marked by a high fever, a headache, neck stiffness, stupor, disorientation, coma, tremors, occasional convulsions, paralysis and, rarely, death.

Other causes

Alcohol

Alcohol use causes varying degrees of sedation, irritability, and incoordination; intoxication commonly causes stupor.

Drugs

Sedation and other degrees of a decreased LOC can result from an overdose of a barbiturate, another central nervous system depressant, or aspirin.

» READ BOOK EXCERPT ONLINE »

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

Vertigo: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Acoustic neuroma

Acoustic neuroma is a tumor of the eighth cranial nerve that causes mild, intermittent vertigo and unilateral sensorineural hearing loss. Other findings include tinnitus, postauricular or suboccipital pain, and — with cranial nerve compression — facial paralysis.

Benign positional vertigo

With benign positional vertigo, debris in a semicircular canal produces vertigo on head position change, which lasts a few minutes. It’s usually temporary and can be effectively treated with positional maneuvers.

Brain stem ischemia

Brain stem ischemia produces sudden, severe vertigo that may become episodic and later persistent. Associated findings include ataxia, nausea, vomiting, increased blood pressure, tachycardia, nystagmus, and lateral deviation of the eyes toward the side of the lesion. Hemiparesis and paresthesia may also occur.

Head trauma

Persistent vertigo, occurring soon after injury, accompanies spontaneous or positional nystagmus and, if the temporal bone is fractured, hearing loss. Associated findings include headache, nausea, vomiting, and decreased (LOC). Behavioral changes, diplopia or visual blurring, seizures, motor or sensory deficits, and signs of increased intracranial pressure may also occur.

Herpes zoster

Infection of the eighth cranial nerve produces sudden onset of vertigo accompanied by facial paralysis, hearing loss in the affected ear, and herpetic vesicular lesions in the auditory canal.

Labyrinthitis

Severe vertigo begins abruptly with labyrinthitis, an inner ear infection. Vertigo may occur in a single episode or may recur over months or years. Associated findings include nausea, vomiting, progressive sensorineural hearing loss, and nystagmus.

Ménière’s disease

With Ménière’s disease, labyrinthine dysfunction causes abrupt onset of vertigo, lasting minutes, hours, or days. Unpredictable episodes of severe vertigo and unsteady gait may cause the patient to fall. During an attack, any sudden motion of the head or eyes can precipitate nausea and vomiting.

Multiple sclerosis (MS)

Episodic vertigo may occur early and become persistent. Other early findings include diplopia, visual blurring, and paresthesia. MS may also produce nystagmus, constipation, muscle weakness, paralysis, spasticity, hyperreflexia, intention tremor, and ataxia.

Seizures

Temporal lobe seizures may produce vertigo, usually associated with other symptoms of partial complex seizures.

Vestibular neuritis

With vestibular neuritis, severe vertigo usually begins abruptly and lasts several days, without tinnitus or hearing loss. Other findings include nausea, vomiting, and nystagmus.

Other causes

Diagnostic tests

Caloric testing (irrigating the ears with warm or cold water) can induce vertigo.

Drugs and alcohol

High or toxic doses of certain drugs or alcohol may produce vertigo. These drugs include salicylates, aminoglycosides, antibiotics, quinine, and hormonal contraceptives.

Surgery and other procedures

Ear surgery may cause vertigo that lasts for several days. Also, administration of overly warm or cold eardrops or irrigating solutions can cause vertigo.

» READ BOOK EXCERPT ONLINE »

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

Syncope: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Aortic arch syndrome

With aortic arch syndrome, the patient experiences syncope and may exhibit weak or abruptly absent carotid pulses and unequal or absent radial pulses. Early signs and symptoms include night sweats, pallor, nausea, anorexia, weight loss, arthralgia, and Raynaud’s phenomenon. He may also develop hypotension in the arms; neck, shoulder, and chest pain; paresthesia; intermittent claudication; bruits; vision disturbances; and dizziness.

Aortic stenosis

A cardinal late sign, syncope is accompanied by exertional dyspnea and angina. Related findings include marked fatigue, orthopnea, paroxysmal nocturnal dyspnea, palpitations, and diminished carotid pulses. Typically, auscultation reveals atrial and ventricular gallops as well as a harsh, crescendo-decrescendo systolic ejection murmur that’s loudest at the right sternal border of the second intercostal space.

Cardiac arrhythmias

Any arrhythmia that decreases cardiac output and impairs cerebral circulation may cause syncope. Other effects — such as palpitations, pallor, confusion, diaphoresis, dyspnea, and hypotension — usually develop first. However, with Adams-Stokes syndrome, syncope may occur without warning. During syncope, the patient develops asystole, which may precipitate spasm and myoclonic jerks if prolonged. He also displays an ashen pallor that progresses to cyanosis, incontinence, a bilateral Babinski’s reflex, and fixed pupils.

Hypoxemia

Regardless of its cause, severe hypoxemia may produce syncope. Common related effects include confusion, tachycardia, restlessness, and incoordination.

Orthostatic hypotension

Syncope occurs when the patient rises quickly from a recumbent position. Look for a drop of 10 to 20 mm Hg or more in systolic or diastolic blood pressure as well as tachycardia, pallor, dizziness, blurred vision, nausea, and diaphoresis.

Transient ischemic attack (TIA)

Marked by transient neurologic deficits, TIAs may produce syncope and a decreased level of consciousness. Other findings vary with the affected artery, but may include vision loss, nystagmus, aphasia, dysarthria, unilateral numbness, hemiparesis or hemiplegia, tinnitus, facial weakness, dysphagia, and a staggering or an uncoordinated gait.

Other causes

Drugs

Quinidine may cause syncope — and possibly sudden death — associated with ventricular fibrillation. Prazosin may cause severe orthostatic hypotension and syncope, usually after the first dose. Occasionally, griseofulvin, levodopa, and indomethacin can produce syncope.

» READ BOOK EXCERPT ONLINE »

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

Aura: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Migraine headache, classic

A classic migraine is preceded by a vague premonition and then, usually, a visual aura involving flashes of light. The aura lasts 10 to 30 minutes and may intensify until it completely obscures the patient’s vision. A classic migraine may cause numbness or tingling of the lips, face, or hands; slight confusion; and dizziness before the characteristic unilateral, throbbing headache appears. The headache slowly intensifies; when it peaks, the patient may experience photophobia, nausea, and vomiting.

Seizure, generalized tonic-clonic

A generalized tonic-clonic seizure may begin with an aura. The patient loses consciousness and falls to the ground. His body stiffens (tonic phase); then he experiences rapid, synchronous muscle jerking and hyperventilation (clonic phase). The seizure usually lasts 2 to 5 minutes.

» READ BOOK EXCERPT ONLINE »

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

Dizziness: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Anemia

Anemia typically causes dizziness that’s aggravated by postural changes or exertion. Other signs and symptoms include pallor, dyspnea, fatigue, tachycardia, bounding pulse, and increased capillary refill time.

Cardiac arrhythmias

Dizziness lasts for several seconds or longer and may precede fainting in arrhythmias. The patient may experience palpitations; irregular, rapid, or thready pulse and, possibly, hypotension. He may also experience weakness, blurred vision, paresthesia, and confusion.

Carotid sinus hypersensitivity

This disorder is characterized by brief episodes of dizziness that usually terminate in fainting. These episodes are precipitated by stimulation of one or both carotid arteries by seemingly minor sensations or actions, such as wearing a tight collar or moving the head. Associated signs and symptoms include sweating, nausea, and pallor.

Emphysema

Dizziness may follow exertion or the chronic productive cough that’s characteristic of this disorder. Associated signs and symptoms include dyspnea, anorexia, weight loss, malaise, use of accessory muscles, pursed-lip breathing, tachypnea, peripheral cyanosis, and diminished breath sounds. Barrel chest and clubbing may occur.

Generalized anxiety disorder

This disorder produces persistent anxiety (for at least 1 month), insomnia, difficulty concentrating, irritability and, possibly, continuous dizziness that may intensify as the anxiety worsens. The patient may show signs of motor tension—for example, twitching or fidgeting, muscle aches, a furrowed brow, and a tendency to be startled. He may also display signs of autonomic hyperactivity, such as diaphoresis, palpitations, cold and clammy hands, dry mouth, paresthesia, indigestion, hot or cold flashes, frequent urination, diarrhea, a lump in the throat, pallor, and increased pulse and respiratory rates.

Hypertension

In patients with hypertension, dizziness may precede fainting, but it may also be relieved by rest. Other common signs and symptoms include headache and blurred vision. Retinal changes include hemorrhage, sclerosis of retinal blood vessels, exudate, and papilledema.

Hyperventilation syndrome

Episodes of hyperventilation cause dizziness that usually lasts a few minutes; however, if these episodes occur frequently, dizziness may persist between them. Other effects include apprehension, diaphoresis, pallor, dyspnea, chest tightness, palpitations, trembling, fatigue, and peripheral and circumoral paresthesia.

Hypoglycemia

Dizziness is a central nervous system (CNS) disturbance that can result from fasting hypoglycemia. It’s generally accompanied by headache, clouding of vision, restlessness, and mental status changes.

Hypovolemia

Dizziness may be accompanied by other signs of fluid volume deficit, such as dry mucous membranes, decreased blood pressure, and increased heart rate.

Orthostatic hypotension

This condition produces dizziness that may terminate in fainting or disappear with rest. Related findings include dim vision, spots before the eyes, pallor, diaphoresis, hypotension, tachycardia and, possibly, signs of dehydration.

Panic disorder

Dizziness may accompany acute attacks of panic in patients with this disorder. Other findings include anxiety, dyspnea, palpitations, chest pain, a choking or smothering sensation, vertigo, paresthesia, hot and cold flashes, diaphoresis, and trembling or shaking. The patient may feel like he’s dying or losing his mind.

Postconcussion syndrome

Occurring 1 to 3 weeks after a head injury, this syndrome is marked by dizziness, headache (throbbing, aching, bandlike, or stabbing), emotional lability, alcohol intolerance, fatigue, anxiety and, possibly, vertigo. Dizziness and other symptoms are intensified by mental or physical stress. The syndrome may persist for years, but symptoms eventually abate.

Rift Valley fever

Typical signs and symptoms of this disorder include dizziness, fever, myalgia, weakness, and back pain. A small percentage of patients may develop encephalitis or may progress to hemorrhagic fever, which can lead to shock and hemorrhage. Inflammation of the retina may result in some permanent vision loss.

Transient ischemic attack (TIA)

Lasting from a few seconds to 24 hours, a TIA commonly signals an impending stroke and may be triggered by turning the head to the side. Besides dizziness of varying severity, TIAs are marked by unilateral or bilateral diplopia, blindness or visual field deficits, ptosis, tinnitus, hearing loss, paresis, and numbness. Other findings may include dysarthria, dysphagia, vomiting, hiccups, confusion, decreased LOC, and pallor.

Other causes

Drugs

Anxiolytics, CNS depressants, opioids, decongestants, antihistamines, antihypertensives, and vasodilators commonly cause dizziness.

Herb Alert

Herbal remedies, such as St. John’s wort, can produce dizziness.

» READ BOOK EXCERPT ONLINE »

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

Level of consciousness, decreased: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Adrenal crisis

Decreased LOC, ranging from lethargy to coma, may develop within 8 to 12 hours of onset. Early associated findings include progressive weakness, irritability, anorexia, headache, nausea and vomiting, diarrhea, abdominal pain, and fever. Later signs and symptoms include hypotension; rapid, thready pulse; oliguria; cool, clammy skin; and flaccid extremities. The patient with chronic adrenocortical hypofunction may have hyperpigmented skin and mucous membranes.

Brain abscess

Decreased LOC varies from drowsiness to deep stupor, depending on abscess size and site. Early signs and symptoms—constant intractable headache, nausea, vomiting, and seizures—reflect increasing ICP. Typical later features include ocular disturbances (nystagmus, vision loss, and pupillary inequality) and signs of infection such as fever. Other findings may include personality changes, confusion, abnormal behavior, dizziness, facial weakness, aphasia, ataxia, tremor, and hemiparesis.

Brain tumor

LOC decreases slowly, from lethargy to coma. The patient may also experience apathy, behavior changes, memory loss, decreased attention span, morning headache, dizziness, vision loss, ataxia, and sensorimotor disturbances. Aphasia and seizures are possible, along with signs of hormonal imbalance, such as fluid retention or amenorrhea. Signs and symptoms vary according to the location and size of the tumor. In later stages, papilledema, vomiting, bradycardia, and widening pulse pressure also appear. In the final stages, the patient may exhibit decorticate or decerebrate posture.

Cerebral aneurysm (ruptured)

Somnolence, confusion and, at times, stupor characterize a moderate bleed; deep coma occurs with severe bleeding, which can be fatal. Onset is usually abrupt, with sudden, severe headache, nausea, and vomiting. Nuchal rigidity, back and leg pain, fever, restlessness, irritability, occasional seizures, and blurred vision point to meningeal irritation. The type and severity of other findings vary with the site and severity of the hemorrhage and may include hemiparesis, hemisensory defects, dysphagia, and visual defects.

Cerebral contusion

Usually unconscious for a prolonged period, the patient may develop dilated, nonreactive pupils and decorticate or decerebrate posture. If he’s conscious or recovers consciousness, he may be drowsy, confused, disoriented, agitated, or even violent. Associated findings include blurred or double vision, fever, headache, pallor, diaphoresis, tachycardia, altered respirations, aphasia, and hemiparesis. Residual effects include seizures, impaired mental status, slight hemiparesis, and vertigo.

Diabetic ketoacidosis

This disorder produces a rapid decrease in LOC, ranging from lethargy to coma, commonly preceded by polydipsia, polyphagia, and polyuria. The patient may complain of weakness, anorexia, abdominal pain, nausea, and vomiting. He may also exhibit orthostatic hypotension; fruity breath odor; Kussmaul’s respirations; warm, dry skin; and a rapid, thready pulse. Untreated, this condition invariably leads to coma and death.

Encephalitis

Within 24 to 48 hours after onset, the patient may develop LOC changes ranging from lethargy to coma. Other possible findings include abrupt onset of fever, headache, nuchal rigidity, nausea, vomiting, irritability, personality changes, seizures, aphasia, ataxia, hemiparesis, nystagmus, photophobia, myoclonus, and cranial nerve palsies.

Encephalomyelitis (postvaccinal)

This life-threatening disorder produces rapid LOC deterioration from drowsiness to coma. The patient also experiences rapid onset of fever, headache, nuchal rigidity, back pain, vomiting, and seizures.

Encephalopathy

With hepatic encephalopathy, signs and symptoms develop in four stages: in the prodromal stage, slight personality changes (disorientation, forgetfulness, slurred speech) and slight tremor; in the impending stage, tremor progressing to asterixis (the hallmark of hepatic encephalopathy), lethargy, aberrant behavior, and apraxia; in the stuporous stage, stupor and hyperventilation, with the patient noisy and abusive when aroused; in the comatose stage, coma with decerebrate posture, hyperactive reflexes, positive Babinski’s reflex, and fetor hepaticus.

With life-threatening hypertensive encephalopathy, LOC progressively decreases from lethargy to stupor to coma. Besides markedly elevated blood pressure, the patient may experience severe headache, vomiting, seizures, visual disturbances, transient paralysis, and eventually Cheyne-Stokes respirations.

With hypoglycemic encephalopathy, LOC rapidly deteriorates from lethargy to coma. Early signs and symptoms include nervousness, restlessness, agitation, and confusion; hunger; alternate flushing and cold sweats; and headache, trembling, and palpitations. Blurred vision progresses to motor weakness, hemiplegia, dilated pupils, pallor, decreased pulse rate, shallow respirations, and seizures. Flaccidity and decerebrate posture appear late.

Depending on its severity, hypoxic encephalopathy produces a sudden or gradual decrease in LOC, leading to coma and brain death. Early on, the patient appears confused and restless, with cyanosis and increased heart and respiratory rates and blood pressure. Later, his respiratory pattern becomes abnormal, and assessment reveals decreased pulse, blood pressure, and deep tendon reflexes (DTRs); Babinski’s reflex; absent doll’s eye sign; and fixed pupils.

With uremic encephalopathy, LOC decreases gradually from lethargy to coma. Early on, the patient may appear apathetic, inattentive, confused, and irritable and may complain of headache, nausea, fatigue, and anorexia. Other findings include vomiting, tremors, edema, papilledema, hypertension, cardiac arrhythmias, dyspnea, crackles, oliguria, and Kussmaul’s and Cheyne-Stokes respirations.

Epidural hemorrhage (acute)

This life-threatening posttraumatic disorder produces momentary loss of consciousness, sometimes followed by a lucid interval. While lucid, the patient has a severe headache, nausea, vomiting, and bladder distention. Rapid deterioration in consciousness follows, possibly leading to coma. Other findings include irregular respirations, seizures, decreased and bounding pulse, increased pulse pressure, hypertension, unilateral or bilateral fixed and dilated pupils, unilateral hemiparesis or hemiplegia, decerebrate posture, and Babinski’s reflex.

Heatstroke

As body temperature increases, LOC gradually decreases from lethargy to coma. Early signs and symptoms include malaise, tachycardia, tachypnea, orthostatic hypotension, muscle cramps, rigidity, and syncope. The patient may be irritable, anxious, and dizzy and may report a severe headache. At the onset of heatstroke, the patient’s skin is hot, flushed, and diaphoretic with blotchy cyanosis; later, when his fever exceeds 105° F (40.5° C), his skin becomes hot, flushed, and anhidrotic. Pulse and respiratory rate increase markedly, and blood pressure drops precipitously. Other findings include vomiting, diarrhea, dilated pupils, and Cheyne-Stokes respirations.

Hypercapnia with pulmonary syndrome

LOC decreases gradually from lethargy to coma (usually not prolonged). The patient becomes confused or drowsy and develops asterixis and muscle twitching. He may complain of headache and exhibit mental dullness, papilledema, and small, reactive pupils.

Hypernatremia

This disorder, life-threatening if acute, causes LOC to deteriorate from lethargy to coma. The patient is irritable and exhibits twitches progressing to seizures. Other associated signs and symptoms include a weak, thready pulse; nausea; malaise; fever; thirst; flushed skin; and dry mucous membranes.

Hyperosmolar hyperglycemic nonketotic syndrome

LOC decreases rapidly from lethargy to coma. Early findings include polyuria, polydipsia, weight loss, and weakness. Later, the patient may develop hypotension, poor skin turgor, dry skin and mucous membranes, tachycardia, tachypnea, oliguria, and seizures.

Hyperventilation syndrome

Brief episodes of unconsciousness follow stress-induced deep, rapid breathing associated with anxiety and agitation. Associated findings include dizziness, circumoral and peripheral paresthesia, twitching, carpopedal spasm, and arrhythmias.

Hypokalemia

LOC gradually decreases to lethargy; coma is rare. Other findings include confusion, nausea, vomiting, diarrhea, and polyuria; weakness, decreased reflexes, and malaise; and dizziness, hypotension, arrhythmias, and abnormal electrocardiogram results.

Hyponatremia

This disorder, life-threatening if acute, produces decreased LOC in late stages. Early nausea and malaise may progress to behavior changes, confusion, lethargy, incoordination and, eventually, seizures and coma.

Hypothermia

With severe hypothermia (temperature below 90° F [32.2° C]), LOC decreases from lethargy to coma. DTRs disappear, and ventricular fibrillation occurs, possibly followed by cardiopulmonary arrest. With mild to moderate hypothermia, the patient may experience memory loss and slurred speech as well as shivering, weakness, fatigue, and apathy. Other early signs and symptoms include ataxia, muscle stiffness, and hyperactive DTRs; diuresis; tachycardia and decreased respiratory rate and blood pressure; and cold, pale skin. Later, muscle rigidity and decreased reflexes may develop, along with peripheral cyanosis, bradycardia, arrhythmias, severe hypotension, decreased respiratory rate with shallow respirations, and oliguria.

Intracerebral hemorrhage

This life-threatening disorder produces a rapid, steady loss of consciousness within hours, commonly accompanied by severe headache, dizziness, nausea, and vomiting. Associated signs and symptoms vary and may include increased blood pressure, irregular respirations, Babinski’s reflex, seizures, aphasia, decreased sensations, hemiplegia, decorticate or decerebrate posture, and dilated pupils.

Listeriosis

If this serious infection spreads to the nervous system and causes meningitis, signs and symptoms include decreased LOC, fever, headache, and nuchal rigidity. Early signs and symptoms of listeriosis include fever, myalgias, abdominal pain, nausea, vomiting, and diarrhea.

Gender cue  Infections during pregnancy may lead to premature delivery, infection of the neonate, or stillbirth.

Meningitis

Confusion and irritability are expected; however, stupor, coma, and seizures may occur in those with severe meningitis. Fever develops early, possibly accompanied by chills. Associated findings include severe headache, nuchal rigidity, hyperreflexia and, possibly, opisthotonos. The patient exhibits Kernig’s and Brudzinski’s signs and, possibly, ocular palsies, photophobia, facial weakness, and hearing loss.

Myxedema crisis

The patient may exhibit a swift decline in LOC. Other findings include severe hypothermia, hypoventilation, hypotension, bradycardia, hypoactive reflexes, periorbital and peripheral edema, impaired hearing and balance, and seizures.

Pontine hemorrhage

A sudden, rapid decrease in LOC to the point of coma occurs within minutes and death within hours. The patient may also exhibit total paralysis, decerebrate posture, Babinski’s reflex, absent doll’s eye sign, and bilateral miosis (however, the pupils remain reactive to light).

Seizure disorders

A complex partial seizure produces decreased LOC, manifested as a blank stare, purposeless behavior (picking at clothing, wandering, lip smacking or chewing motions), and unintelligible speech. The seizure may be heralded by an aura and followed by several minutes of mental confusion.

An absence seizure usually involves a brief change in LOC, indicated by blinking or eye rolling, blank stare, and slight mouth movements.

A generalized tonic-clonic seizure typically begins with a loud cry and sudden loss of consciousness. Muscle spasm alternates with relaxation. Tongue biting, incontinence, labored breathing, apnea, and cyanosis may also occur. Consciousness returns after the seizure, but the patient remains confused and may have difficulty talking. He may complain of drowsiness, fatigue, headache, muscle aching, and weakness and may fall into deep sleep.

An atonic seizure produces sudden unconsciousness for a few seconds.

Status epilepticus, rapidly recurring seizures without intervening periods of physiologic recovery and return of consciousness, can be life threatening.

Shock

Decreased LOC—lethargy progressing to stupor and coma—occurs late in shock. Associated findings include confusion, anxiety, and restlessness; hypotension; tachycardia; weak pulse with narrowing pulse pressure; dyspnea; oliguria; and cool, clammy skin.

Hypovolemic shock is generally the result of massive or insidious bleeding, either internally or externally. Cardiogenic shock may produce chest pain or arrhythmias and signs of heart failure, such as dyspnea, cough, edema, jugular vein distention, and weight gain. Septic shock may be accompanied by high fever and chills. Anaphylactic shock usually involves stridor.

Stroke

LOC changes vary in degree and onset, depending on the lesion’s size and location and the presence of edema. A thrombotic stroke usually follows multiple transient ischemic attacks (TIAs). LOC changes may be abrupt or take several minutes, hours, or days. An embolic stroke occurs suddenly, and deficits reach their peak almost at once. Deficits associated with a hemorrhagic stroke usually develop over minutes or hours.

Associated findings vary with stroke type and severity and may include disorientation; intellectual deficits, such as memory loss and poor judgment; personality changes; and emotional lability. Other possible findings include dysarthria, dysphagia, ataxia, aphasia, apraxia, agnosia, unilateral sensorimotor loss, and visual disturbances. In addition, urine retention, incontinence, constipation, headache, vomiting, and seizures may occur.

Subdural hematoma (chronic)

LOC deteriorates slowly. Other signs and symptoms include confusion, decreased ability to concentrate, and personality changes accompanied by headache, light-headedness, seizures, and a dilated ipsilateral pupil with ptosis.

Subdural hemorrhage (acute)

With this potentially life-threatening disorder, agitation and confusion are followed by progressively decreasing LOC from somnolence to coma. The patient may also experience headache, fever, unilateral pupil dilation, decreased pulse and respiratory rates, widening pulse pressure, seizures, hemiparesis, and Babinski’s reflex.

Thyroid storm

LOC decreases suddenly and can progress to coma. Irritability, restlessness, confusion, and psychotic behavior precede the deterioration. Associated signs and symptoms include tremors and weakness; visual disturbances; tachycardia, arrhythmias, angina, and acute respiratory distress; warm, moist, flushed skin; and vomiting, diarrhea, and fever to 105°F (40.5°C).

TIA

LOC decreases abruptly (with varying severity) and gradually returns to normal within 24 hours. Site-specific findings may include vision loss, nystagmus, dizziness, dysarthria, unilateral hemiparesis or hemiplegia, tinnitus, paresthesia, staggering or incoordinated gait, aphasia, or dysphagia.

West Nile encephalitis

This brain infection is caused by the West Nile virus, a mosquito-borne flavivirus commonly found in Africa, West Asia, and the Middle East and, less commonly, in the United States. Mild infection is common. Signs and symptoms include fever, headache, and body aches, commonly with skin rash and swollen lymph glands. More severe infection is marked by high fever, headache, neck stiffness, stupor, disorientation, coma, tremors, occasional seizures, paralysis and, rarely, death.

Other causes

Alcohol

Alcohol use causes varying degrees of sedation, irritability, and incoordination; intoxication commonly causes stupor.

Drugs

Sedation and other degrees of decreased LOC can result from an overdose of a barbiturate, another central nervous system depressant, or aspirin.

Poisoning

Toxins, such as lead, carbon monoxide, and snake venom, can cause varying degrees of decreased LOC. Confusion is common, as are headache, nausea, and vomiting. Other general features include hypotension, cardiac arrhythmias, dyspnea, sensorimotor loss, and seizures.

» READ BOOK EXCERPT ONLINE »

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

Vertigo: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Acoustic neuroma

This tumor of the eighth cranial nerve causes mild, intermittent vertigo and unilateral sensorineural hearing loss. Other findings include tinnitus, postauricular or suboccipital pain, and—with cranial nerve compression—facial paralysis.

Benign positional vertigo

In this disorder, debris in a semicircular canal produces vertigo lasting a few minutes when the patient changes head position. This type of vertigo is usually temporary and can be effectively treated with positional maneuvers.

Brain stem ischemia

This condition produces sudden, severe vertigo that may become episodic and later persistent. Associated findings include ataxia, nausea, vomiting, increased blood pressure, tachycardia, nystagmus, and lateral deviation of the eyes toward the side of the lesion. Hemiparesis and paresthesia may also occur.

Head trauma

Persistent vertigo, occurring soon after a head injury, accompanies spontaneous or positional nystagmus and, if the temporal bone is fractured, hearing loss. Associated findings include headache, nausea, vomiting, and decreased level of consciousness. Behavioral changes, diplopia or visual blurring, seizures, motor or sensory deficits, and signs of increased intracranial pressure may also occur.

Herpes zoster

Infection of the eighth cranial nerve produces sudden onset of vertigo accompanied by facial paralysis, hearing loss in the affected ear, and herpetic vesicular lesions in the auditory canal.

Labyrinthitis

Severe vertigo begins abruptly in this inner ear infection. Vertigo may occur in a single episode or may recur over months or years. Associated findings include nausea, vomiting, progressive sensorineural hearing loss, and nystagmus.

Ménière’s disease

In this disease, labyrinthine dysfunction causes abrupt onset of vertigo, lasting minutes, hours, or days. Unpredictable episodes of severe vertigo and unsteady gait may cause the patient to fall. During an attack, any sudden motion of the head or eyes can precipitate nausea and vomiting.

Motion sickness

This condition is characterized by vertigo, nausea, vomiting, and headache in response to rhythmic or erratic motions.

Multiple sclerosis (MS)

Episodic vertigo may occur early and become persistent in MS. Other early findings include diplopia, visual blurring, and paresthesia. MS may also produce nystagmus, constipation, muscle weakness, paralysis, spasticity, hyperreflexia, intention tremor, and ataxia.

Posterior fossa tumor

This type of tumor may produce positional vertigo that lasts for a few seconds as well as papilledema, headache, memory loss, nausea, vomiting, nystagmus, apneustic or ataxic respirations, and increased blood pressure. The patient may also fall sideways.

Seizures

Temporal lobe seizures may produce vertigo, usually associated with other symptoms of partial complex seizures.

Vestibular neuritis

In this disorder, severe vertigo usually begins abruptly, lasts several days, and isn’t accompanied by tinnitus or hearing loss. Other findings include nausea, vomiting, and nystagmus.

Other causes

Diagnostic tests

Caloric testing (irrigating the ears with warm or cold water) can induce vertigo.

Drugs and alcohol

High or toxic doses of certain drugs or alcohol may produce vertigo. These drugs include salicylates, aminoglycosides, antibiotics, quinine, and hormonal contraceptives.

Surgery and other procedures

Ear surgery may cause vertigo that lasts for several days. Administration of overly warm or cold eardrops or irrigating solutions can also cause vertigo.

» READ BOOK EXCERPT ONLINE »

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

Syncope: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Aortic arch syndrome

With this syndrome, the patient experiences syncope and may exhibit weak or abruptly absent carotid pulses and unequal or absent radial pulses. Early signs and symptoms include night sweats, pallor, nausea, anorexia, weight loss, arthralgia, and Raynaud’s phenomenon. He may also develop hypotension in the arms; neck, shoulder, and chest pain; paresthesia; intermittent claudication; bruits; vision disturbances; and dizziness.

Aortic stenosis

A cardinal late sign, syncope is accompanied by exertional dyspnea and angina. Related findings include marked fatigue, orthopnea, paroxysmal nocturnal dyspnea, palpitations, and diminished carotid pulses. Typically, auscultation reveals atrial and ventricular gallops as well as a harsh, crescendo-decrescendo systolic ejection murmur that’s loudest at the right sternal border of the second intercostal space.

Cardiac arrhythmias

Any arrhythmia that decreases cardiac output and impairs cerebral circulation may cause syncope. Other effects—such as palpitations, pallor, confusion, diaphoresis, dyspnea, and hypotension—usually develop first. However, with Adams-Stokes syndrome, syncope may occur without warning. During syncope, the patient develops asystole, which may precipitate spasm and myoclonic jerks if prolonged. He also displays an ashen pallor that progresses to cyanosis, incontinence, bilateral Babinski’s reflex, and fixed pupils.

Carotid sinus hypersensitivity

Syncope is triggered by compression of the carotid sinus, which may be caused by turning the head to one side or by wearing a tight collar. The fainting episode is usually of short duration.

Hypoxemia

Regardless of its cause, severe hypoxemia may produce syncope. Common related effects include confusion, tachycardia, restlessness, and incoordination.

Orthostatic hypotension

Syncope occurs when the patient rises quickly from a recumbent position. Look for a drop of 10 to 20 mm Hg or more in systolic or diastolic blood pressure as well as tachycardia, pallor, dizziness, blurred vision, nausea, and diaphoresis.

Transient ischemic attacks

Marked by transient neurologic deficits, these attacks may produce syncope and decreased level of consciousness. Other findings vary with the affected artery but may include vision loss, nystagmus, aphasia, dysarthria, unilateral numbness, hemiparesis or hemiplegia, tinnitus, facial weakness, dysphagia, and staggering or uncoordinated gait.

Vagal glossopharyngeal neuralgia

With this disorder, localized pressure may trigger pain in the base of the tongue, pharynx, larynx, tonsils, and ear, resulting in syncope that lasts for several minutes.

Other causes

Drugs

Quinidine may cause syncope—and possibly sudden death—associated with ventricular fibrillation. Prazosin may cause severe orthostatic hypotension and syncope, usually after the first dose. Occasionally, griseofulvin, levodopa, and indomethacin can produce syncope.

» READ BOOK EXCERPT ONLINE »

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

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

» READ BOOK EXCERPT ONLINE »

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

» READ BOOK EXCERPT ONLINE »

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

» READ BOOK EXCERPT ONLINE »

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

» READ BOOK EXCERPT ONLINE »

Source: Field Guide to Bedside Diagnosis, 2007

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

Anemia

Typically, anemia causes dizziness that’s aggravated by postural changes or exertion. Other signs and symptoms include pallor, dyspnea, fatigue, tachycardia, and bounding pulse. Capillary refill time is increased.

Cardiac arrhythmias

Dizziness lasts for several seconds or longer and may precede fainting in arrhythmias. The patient may experience palpitations; irregular, rapid, or thready pulse; and possibly hypotension. He may also experience weakness, blurred vision, paresthesia, and confusion.

Carotid sinus hypersensitivity.

Carotid sinus hypersensitivity is characterized by brief episodes of dizziness that usually terminate in fainting. These episodes are precipitated by stimulation of one or both carotid arteries by seemingly minor sensations or actions, such as wearing a tight collar or moving the head. Associated signs and symptoms include sweating, nausea, and pallor.

Emphysema

Dizziness may follow exertion or the chronic productive cough in patients with emphysema. Associated signs and symptoms include dyspnea, anorexia, weight loss, malaise, use of accessory muscles, pursed-lip breathing, tachypnea, peripheral cyanosis, and diminished breath sounds. Barrel chest and clubbing may be seen.

Generalized anxiety disorder

Generalized anxiety disorder produces continuous dizziness that may intensify as the disorder worsens. Associated signs and symptoms are persistent anxiety (for at least 1 month), insomnia, difficulty concentrating, and irritability. The patient may show signs of motor tension — for example, twitching or fidgeting, muscle aches, furrowed brow, and a tendency to be startled. He may also display signs of autonomic hyperactivity, such as diaphoresis, palpitations, cold and clammy hands, dry mouth, paresthesia, indigestion, hot or cold flashes, frequent urination, diarrhea, a lump in the throat, pallor, and increased pulse and respiratory rates.

Hypertension

With hypertension, dizziness may precede fainting, but it may also be relieved by rest. Other common signs and symptoms include headache and blurred vision. Retinal changes include hemorrhage, sclerosis of retinal blood vessels, exudate, and papilledema.

Hyperventilation syndrome

Episodes of hyperventilation cause dizziness that usually lasts a few minutes; however, if these episodes occur frequently, dizziness may persist between them. Other effects include apprehension, diaphoresis, pallor, dyspnea, chest tightness, palpitations, trembling, fatigue, and peripheral and circumoral paresthesia.

Hypoglycemia.

Dizziness is a central nervous system (CNS) disturbance that can occur due to fasting hypoglycemia. It’s generally accompanied by headache, clouding of vision, restlessness, and mental status changes.

Hypovolemia

Dizziness is caused by a lack of circulating volume and may be accompanied by other signs of fluid volume deficit (dry mucous membranes, decreased blood pressure, increased heart rate).

Orthostatic hypotension

Orthostatic hypotension produces dizziness that may terminate in fainting or disappear with rest. Related findings include dim vision, spots before the eyes, pallor, diaphoresis, hypotension, tachycardia and, possibly, signs of dehydration.

Panic disorder

Dizziness may accompany acute attacks of panic in patients with panic disorder. Other findings include anxiety, dyspnea, palpitations, chest pain, a choking or smothering sensation, vertigo, paresthesia, hot and cold flashes, diaphoresis, and trembling or shaking. The patient may have the sensation of dying or losing his mind.

Postconcussion syndrome

Occurring from the time of injury to 3 weeks after a head injury, postconcussion syndrome is marked by dizziness, headache (throbbing, aching, bandlike, or stabbing), emotional lability, alcohol intolerance, fatigue, anxiety and, possibly, vertigo. Dizziness and other symptoms are intensified by mental or physical stress. The syndrome may persist for years, but symptoms eventually abate.

Rift Valley fever

Typical signs and symptoms of Rift Valley fever include dizziness, fever, myalgia, weakness, and back pain. A small percentage of patients may develop encephalitis or may progress to hemorrhagic fever that can lead to shock and hemorrhage. Inflammation of the retina may result in some permanent vision loss.

Transient ischemic attack (TIA)

Lasting from a few seconds to 24 hours, a TIA commonly signals impending stroke. Besides dizziness of varying severity, TIAs are accompanied by unilateral or bilateral diplopia, blindness or visual field deficits, ptosis, tinnitus, hearing loss, paresis, and numbness. Other findings include dysarthria, dysphagia, vomiting, hiccups, confusion, decreased LOC, and pallor.

Other causes

Drugs

Anxiolytics, CNS depressants, opioids, decongestants, antihistamines, antihypertensives, and vasodilators commonly cause dizziness.

Herbal remedies

St. John’s wort can produce dizziness.

» READ BOOK EXCERPT ONLINE »

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

Level of consciousness, decreased: Medical causes
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

Adrenal crisis

Decreased LOC, ranging from lethargy to coma, may develop within 8 to 12 hours of onset. Early associated findings include progressive weakness, irritability, anorexia, headache, nausea and vomiting, diarrhea, abdominal pain, and fever. Later signs and symptoms include hypotension; rapid, thready pulse; oliguria; cool, clammy skin; and flaccid extremities. The patient with chronic adrenocortical hypofunction may have hyperpigmented skin and mucous membranes.

Brain abscess

Decreased LOC varies from drowsiness to deep stupor, depending on abscess size and site. Early signs and symptoms — constant intractable headache, nausea, vomiting, and seizures — reflect increasing ICP. Typical later features include ocular disturbances (nystagmus, vision loss, and pupillary inequality) and signs of infection such as fever. Other findings may include personality changes, confusion, abnormal behavior, dizziness, facial weakness, aphasia, ataxia, tremor, and hemiparesis.

Brain tumor

LOC decreases slowly, from lethargy to coma. The patient may also experience apathy, behavior changes, memory loss, decreased attention span, morning headache, dizziness, vision loss, ataxia, and sensorimotor disturbances. Aphasia and seizures are possible, along with signs of hormonal imbalance, such as fluid retention or amenorrhea. Signs and symptoms vary according to the location and size of the tumor. In later stages, papilledema, vomiting, bradycardia, and widening pulse pressure also appear. In the final stages, the patient may exhibit decorticate or decerebrate posture.

Cerebral aneurysm (ruptured)

Somnolence, confusion and, at times, stupor characterize a moderate bleed; deep coma occurs with severe bleeding, which can be fatal. Onset is usually abrupt, with sudden, severe headache, nausea, and vomiting. Nuchal rigidity, back and leg pain, fever, restlessness, irritability, occasional seizures, and blurred vision point to meningeal irritation. The type and severity of other findings vary with the site and severity of the hemorrhage and may include hemiparesis, hemisensory defects, dysphagia, and visual defects.

Cerebral contusion

Usually unconscious for a prolonged period, the patient may develop dilated, nonreactive pupils and decorticate or decerebrate posture. If he’s conscious or recovers consciousness, he may be drowsy, confused, disoriented, agitated, or even violent. Associated findings include blurred or double vision, fever, headache, pallor, diaphoresis, tachycardia, altered respirations, aphasia, and hemiparesis. Residual effects include seizures, impaired mental status, slight hemiparesis, and vertigo.

Diabetic ketoacidosis

Diabetic ketoacidosis produces a rapid decrease in LOC, ranging from lethargy to coma, commonly preceded by polydipsia, polyphagia, and polyuria. The patient may complain of weakness, anorexia, abdominal pain, nausea, and vomiting. He may also exhibit orthostatic hypotension, fruity breath odor, and Kussmaul’s respirations, as well as warm, dry skin and a rapid, thready pulse. Untreated, this condition invariably leads to coma and death.

Encephalitis

Within 24 to 48 hours after onset, the patient may develop LOC changes ranging from lethargy to coma. Other possible findings include abrupt onset of fever, headache, nuchal rigidity, nausea, vomiting, irritability, personality changes, seizures, aphasia, ataxia, hemiparesis, nystagmus, photophobia, myoclonus, and cranial nerve palsies.

Encephalomyelitis (postvaccinal)

Encephalomyelitis is a life-threatening disorder that produces rapid LOC deterioration from drowsiness to coma. The patient also experiences rapid onset of fever, headache, nuchal rigidity, back pain, vomiting, and seizures.

Encephalopathy

With hepatic encephalopathy, signs and symptoms develop in four stages: in the prodromal stage, slight personality changes (disorientation, forgetfulness, slurred speech) and slight tremor; in the impending stage, tremor progressing to asterixis (the hallmark of hepatic encephalopathy), lethargy, aberrant behavior, and apraxia; in the stuporous stage, stupor and hyperventilation, with the patient noisy and abusive when aroused; in the comatose stage, coma with decerebrate posture, hyperactive reflexes, positive Babinski’s reflex, and fetor hepaticus.

With life-threatening hypertensive encephalopathy, LOC progressively decreases from lethargy to stupor to coma. Besides markedly elevated blood pressure, the patient may experience severe headache, vomiting, seizures, vision disturbances, transient paralysis, and eventually Cheyne-Stokes respirations.

With hypoglycemic encephalopathy, LOC rapidly deteriorates from lethargy to coma. Early signs and symptoms include nervousness, restlessness, agitation, and confusion accompanied by hunger, alternate flushing and cold sweats, and headache, trembling, and palpitations. Blurred vision progresses to motor weakness, hemiplegia, dilated pupils, pallor, decreased pulse rate, shallow respirations, and seizures. Flaccidity and decerebrate posture appear late.

Depending on its severity, hypoxic encephalopathy produces a sudden or gradual decrease in LOC, leading to coma and brain death. Early on, the patient appears confused and restless, with cyanosis and increased heart and respiratory rates and blood pressure. Later, his respiratory pattern becomes abnormal, and assessment reveals decreased pulse, blood pressure, and deep tendon reflexes (DTRs); Babinski’s reflex; and fixed pupils.

With uremic encephalopathy, LOC decreases gradually from lethargy to coma. Early on, the patient may appear apathetic, inattentive, confused, and irritable and may complain of headache, nausea, fatigue, and anorexia. Other findings include vomiting, tremors, edema, papilledema, hypertension, cardiac arrhythmias, dyspnea, crackles, oliguria, and Kussmaul’s and Cheyne-Stokes respirations.

Epidural hemorrhage (acute)

Epidural hemorrhage is a life-threatening posttraumatic disorder that produces momentary loss of consciousness, sometimes followed by a lucid interval. While lucid, the patient has a severe headache, nausea, vomiting, and bladder distention. Rapid deterioration in consciousness follows, possibly leading to coma. Other findings include irregular respirations, seizures, decreased and bounding pulse, increased pulse pressure, hypertension, unilateral or bilateral fixed and dilated pupils, unilateral hemiparesis or hemiplegia, decerebrate posture, and Babinski’s reflex.

Heatstroke

As body temperature increases, LOC gradually decreases from lethargy to coma. Early signs and symptoms include malaise, tachycardia, tachypnea, orthostatic hypotension, muscle cramps, rigidity, and syncope. The patient may be irritable, anxious, and dizzy and may report a severe headache. At the onset of heatstroke, the patient’s skin is hot, flushed, and diaphoretic with blotchy cyanosis; later, when his fever exceeds 105° F (40.5° C), his skin becomes hot, flushed, and anhidrotic. Pulse and respiratory rate increase markedly, and blood pressure drops precipitously. Other findings include vomiting, diarrhea, dilated pupils, and Cheyne-Stokes respirations.

Hypercapnia with pulmonary syndrome

LOC decreases gradually from lethargy to coma (usually not prolonged). The patient becomes confused or drowsy and develops asterixis and muscle twitching. He may complain of headache and exhibit mental dullness, papilledema, and small, reactive pupils.

Hypernatremia

Hypernatremia, life-threatening if acute, causes LOC to deteriorate from lethargy to coma. The patient is irritable and exhibits twitches progressing to seizures. Other associated signs and symptoms include a weak, thready pulse, possibly accompanied by nausea, malaise, fever, thirst, flushed skin, and dry mucous membranes.

Hyperosmolar hyperglycemic nonketotic syndrome

LOC decreases rapidly from lethargy to coma. Early findings include polyuria, polydipsia, hyperglycemia, hyperkalemia, weight loss, and weakness. Later, the patient may develop hypotension, poor skin turgor, dry skin and mucous membranes, tachycardia, tachypnea, oliguria, and seizures.

Hyperventilation syndrome

Brief episodes of unconsciousness follow stress-induced deep, rapid breathing associated with anxiety and agitation. Associated findings include dizziness, circumoral and peripheral paresthesia, twitching, carpopedal spasm, and arrhythmias.

Hypokalemia

LOC gradually decreases to lethargy; coma is rare. Other findings include confusion, nausea, vomiting, diarrhea, and polyuria. The patient may also exhibit weakness, decreased reflexes, and malaise, along with dizziness, hypotension, arrhythmias, and abnormal electrocardiogram results.

Hyponatremia

Hyponatremia, life-threatening if acute, produces decreased LOC in late stages. Early nausea and malaise may progress to behavior changes, confusion, lethargy, incoordination and, eventually, seizures and coma.

Hypothermia

With severe hypothermia (temperature below 90° F [32.2° C]), LOC decreases from lethargy to coma. DTRs disappear, and ventricular fibrillation occurs, possibly followed by cardiopulmonary arrest. With mild to moderate hypothermia, the patient may experience memory loss and slurred speech as well as shivering, weakness, fatigue, and apathy. Other early signs and symptoms include ataxia, muscle stiffness, and hyperactive DTRs; diuresis; tachycardia and decreased respiratory rate and blood pressure; and cold, pale skin. Later, muscle rigidity and decreased reflexes may develop, along with peripheral cyanosis, bradycardia, arrhythmias, severe hypotension, decreased respiratory rate with shallow respirations, and oliguria.

Intracerebral hemorrhage

Intracerebral hemorrhage is a life-threatening disorder that produces a rapid, steady loss of consciousness within hours, commonly accompanied by severe headache, dizziness, nausea, and vomiting. Associated signs and symptoms vary and may include increased blood pressure, irregular respirations, Babinski’s reflex, seizures, aphasia, decreased sensations, hemiplegia, decorticate or decerebrate posture, and dilated pupils.

Listeriosis

If this serious infection spreads to the nervous system and causes meningitis, signs and symptoms include decreased LOC, fever, headache, and nuchal rigidity. Early signs and symptoms of listeriosis include fever, myalgias, abdominal pain, nausea, vomiting, and diarrhea.

Meningitis

Confusion and irritability are expected; however, stupor, coma, and seizures may occur in those with severe meningitis. Fever develops early, possibly accompanied by chills. Associated findings include severe headache, nuchal rigidity, hyperreflexia and, possibly, opisthotonos. The patient exhibits Kernig’s and Brudzinski’s signs and, possibly, ocular palsies, photophobia, facial weakness, and hearing loss.

Myxedema crisis

The patient may exhibit a swift decline in LOC. Other findings include severe hypothermia, hypoventilation, hypotension, bradycardia, hypoactive reflexes, periorbital and peripheral edema, impaired hearing and balance, and seizures.

Pontine hemorrhage

A sudden, rapid decrease in LOC to the point of coma occurs within minutes and death within hours. The patient may also exhibit total paralysis, decerebrate posture, Babinski’s reflex, absent doll’s eye sign, and bilateral miosis (however, the pupils remain reactive to light).

Seizure disorders

A complex partial seizure produces decreased LOC, manifested as a blank stare, purposeless behavior (picking at clothing, wandering, lip smacking or chewing motions), and unintelligible speech. The seizure may be heralded by an aura and followed by several minutes of mental confusion.

An absence seizure usually involves a brief change in LOC, indicated by blinking or eye rolling, blank stare, and slight mouth movements.

A generalized tonic-clonic seizure typically begins with a loud cry and sudden loss of consciousness. Muscle spasm alternates with relaxation. Tongue biting, incontinence, labored breathing, apnea, and cyanosis may also occur. Consciousness returns after the seizure, but the patient remains confused and may have difficulty talking. He may complain of drowsiness, fatigue, headache, muscle aching, and weakness and may fall into deep sleep.

An atonic seizure produces sudden unconsciousness for a few seconds.

Status epilepticus, rapidly recurring seizures without intervening periods of physiologic recovery and return of consciousness, can be life-threatening.

Shock

Decreased LOC — lethargy progressing to stupor and coma — occurs late in shock. Associated findings include confusion, anxiety, and restlessness; hypotension; tachycardia; weak pulse with narrowing pulse pressure; dyspnea; oliguria; and cool, clammy skin.

Hypovolemic shock is generally the result of massive or insidious bleeding, either internally or externally. Cardiogenic shock may produce chest pain or arrhythmias and signs of heart failure, such as dyspnea, cough, edema, jugular vein distention, and weight gain. Septic shock may be accompanied by high fever and chills. Anaphylactic shock usually involves stridor.

Stroke

LOC changes vary in degree and onset, depending on the lesion’s size and location and the presence of edema. A thrombotic stroke usually follows multiple transient ischemic attacks (TIAs). LOC changes may be abrupt or take several minutes, hours, or days. An embolic stroke occurs suddenly, and deficits reach their peak almost at once. Deficits associated with a hemorrhagic stroke usually develop over minutes or hours.

Associated findings vary with stroke type and severity and may include disorientation; intellectual deficits, such as memory loss and poor judgment; personality changes; and emotional lability. Other possible findings include dysarthria, dysphagia, ataxia, aphasia, apraxia, agnosia, unilateral sensorimotor loss, and vision disturbances. In addition, urine retention, incontinence, constipation, headache, vomiting, and seizures may occur.

Subdural hematoma (chronic)

LOC deteriorates slowly. Other signs and symptoms include confusion, decreased ability to concentrate, and personality changes accompanied by headache, light-headedness, seizures, and a dilated ipsilateral pupil with ptosis.

Subdural hemorrhage (acute)

With subdural hemorrhage — a potentially life-threatening disorder — agitation and confusion are followed by progressively decreasing LOC from somnolence to coma. The patient may also experience headache, fever, unilateral pupil dilation, decreased pulse and respiratory rates, widening pulse pressure, seizures, hemiparesis, and Babinski’s reflex.

Thyroid storm

LOC decreases suddenly and can progress to coma. Irritability, restlessness, confusion, and psychotic behavior precede the deterioration. Associated signs and symptoms include tremors and weakness; vision disturbances; tachycardia, arrhythmias, angina, and acute respiratory distress; warm, moist, flushed skin; and vomiting, diarrhea, and fever to 105°F (40.5°C).

Transient ischemic attack (TIA)

LOC decreases abruptly (with varying severity) and gradually returns to normal within 24 hours. Site-specific findings may include vision loss, nystagmus, aphasia, dizziness, dysarthria, unilateral hemiparesis or hemiplegia, tinnitus, paresthesia, dysphagia, or staggering or incoordinated gait.

West Nile encephalitis

This brain infection is caused by the West Nile virus, a mosquito-borne flavivirus commonly found in Africa, West Asia, and the Middle East and, less commonly, in the United States. Mild infection is common. Signs and symptoms include fever, headache, and body aches, commonly with skin rash and swollen lymph glands. More severe infection is marked by high fever, headache, neck stiffness, stupor, disorientation, coma, tremors, occasional convulsions, paralysis and, rarely, death.

Other causes

Alcohol

Alcohol use causes varying degrees of sedation, irritability, and incoordination; intoxication commonly causes stupor.

Drugs

Sedation and other degrees of decreased LOC can result from an overdose of a barbiturate, another central nervous system depressant, or aspirin.

Poisoning

Toxins, such as lead, carbon monoxide, and snake venom, can cause varying degrees of decreased LOC. Confusion is common, as are headache, nausea, and vomiting. Other general features include hypotension, cardiac arrhythmias, dyspnea, sensorimotor loss, and seizures.

» READ BOOK EXCERPT ONLINE »

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

Syncope: Medical causes
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

Aortic arch syndrome

With aortic arch syndrome, the patient experiences syncope and may exhibit weak or abruptly absent carotid pulses and unequal or absent radial pulses. Early signs and symptoms include night sweats, pallor, nausea, anorexia, weight loss, arthralgia, and Raynaud’s phenomenon. He may also develop hypotension in the arms, paresthesia, intermittent claudication, bruits, vision disturbances, dizziness, and neck, shoulder, and chest pain.

Aortic stenosis

A cardinal late sign, syncope is accompanied by exertional dyspnea and angina. Related findings include marked fatigue, orthopnea, paroxysmal nocturnal dyspnea, palpitations, and diminished carotid pulses. Typically, auscultation reveals atrial and ventricular gallops as well as a harsh, crescendo-decrescendo systolic ejection murmur that’s loudest at the right sternal border of the second intercostal space.

Cardiac arrhythmias

Any arrhythmia that decreases cardiac output and impairs cerebral circulation may cause syncope. Other effects — palpitations, pallor, confusion, diaphoresis, dyspnea, and hypotension — usually develop first. However, with Adams-Stokes syndrome, syncope may occur without warning. During syncope, the patient develops asystole, which may precipitate spasm and myoclonic jerks if prolonged. He also displays an ashen pallor that progresses to cyanosis, incontinence, bilateral Babinski’s reflex, and fixed pupils.

Carotid sinus hypersensitivity

Syncope is triggered by compression of the carotid sinus, which may be caused by turning the head to one side or by wearing a tight collar. The fainting episode is usually short.

Hypoxemia

Regardless of its cause, severe hypoxemia may produce syncope. Common related effects include confusion, tachycardia, restlessness, and incoordination.

Orthostatic hypotension

Syncope occurs when the patient rises quickly from a recumbent position. Look for a drop of 10 mm Hg or more in systolic or diastolic blood pressure as well as tachycardia, pallor, dizziness, blurred vision, nausea, and diaphoresis.

Transient ischemic attacks

Marked by transient neurologic deficits, these attacks may produce syncope and a decreased level of consciousness. Other findings vary with the affected artery, but may include vision loss, nystagmus, aphasia, dysarthria, unilateral numbness, hemiparesis or hemiplegia, tinnitus, facial weakness, dysphagia, and a staggering or an uncoordinated gait.

Vagal glossopharyngeal neuralgia

With this disorder, localized pressure may trigger pain in the base of the tongue, pharynx, larynx, tonsils, and ear, resulting in syncope that lasts for several minutes.

Other causes

Drugs

Quinidine may cause syncope — and possibly sudden death — associated with ventricular fibrillation. Prazosin may cause severe orthostatic hypotension and syncope, usually after the first dose. Occasionally, griseofulvin, levodopa, and indomethacin can produce syncope.

» READ BOOK EXCERPT ONLINE »

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

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

Classic migraine headache

A migraine headache is preceded by a vague premonition and then, usually, a visual aura involving flashes of light. The aura lasts 10 to 30 minutes and may intensify until it completely obscures the patient’s vision. A classic migraine may cause numbness or tingling of lips, face, or hands; slight confusion; and dizziness before the characteristic unilateral, throbbing headache appears. It slowly intensifies; when it peaks, it may cause photophobia, nausea, and vomiting.

Seizure, generalized tonic-clonic

A generalized tonic-clonic seizure may begin with or without an aura. The patient loses consciousness and falls to the ground. His body stiffens (tonic phase); then he experiences rapid, synchronous muscle jerking and hyperventilation (clonic phase). The seizure usually lasts 2 to 5 minutes.

» READ BOOK EXCERPT ONLINE »

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

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

Anemia

Typically, anemia causes dizziness that’s aggravated by postural changes or exertion. Other signs and symptoms include pallor, dyspnea, fatigue, tachycardia, and bounding pulse. Capillary refill time is increased.

Cardiac arrhythmias

Dizziness lasts for several seconds or longer and may precede fainting in arrhythmias. The patient may experience palpitations; irregular, rapid, or thready pulse; and possibly hypotension. He may also experience weakness, blurred vision, paresthesia, and confusion.

Carotid sinus hypersensitivity

Carotid sinus hypersensitivity is characterized by brief episodes of dizziness that usually terminate in fainting. These episodes are precipitated by stimulation of one or both carotid arteries by seemingly minor sensations or actions, such as wearing a tight collar or moving the head. Associated signs and symptoms include sweating, nausea, and pallor.

Generalized anxiety disorder

Generalized anxiety disorder produces continuous dizziness that may intensify as the disorder worsens. Associated signs and symptoms are persistent anxiety (for at least 1 month), insomnia, difficulty concentrating, and irritability. The patient may show signs of motor tension — for example, twitching or fidgeting, muscle aches, furrowed brow, and a tendency to be startled. He may also display signs of autonomic hyperactivity, such as diaphoresis, palpitations, cold and clammy hands, dry mouth, paresthesia, indigestion, hot or cold flashes, frequent urination, diarrhea, a lump in the throat, pallor, and increased pulse and respiratory rates.

Hypertension

With hypertension, dizziness may precede fainting, but it may also be relieved by rest. Other common signs and symptoms include headache and blurred vision. Retinal changes include hemorrhage, sclerosis of retinal blood vessels, exudate, and papilledema.

Hyperventilation syndrome

Episodes of hyperventilation cause dizziness that usually lasts a few minutes; however, if these episodes occur frequently, dizziness may persist between them. Other effects include apprehension, diaphoresis, pallor, dyspnea, chest tightness, palpitations, trembling, fatigue, and peripheral and circumoral paresthesia.

Hypoglycemia

Dizziness is a central nervous system (CNS) disturbance that can occur due to fasting hypoglycemia. It’s generally accompanied by headache, clouding of vision, restlessness, and mental status changes. Other signs and symptoms include irritability, trembling, hunger, cold sweats, and tachycardia.

Hypovolemia

Dizziness is caused by a lack of circulating volume and may be accompanied by other signs of fluid volume deficit (dry mucous membranes, decreased blood pressure, increased heart rate). Other signs and symptoms include orthostatic hypotension, thirst, poor skin turgor, and flattened neck veins.

Orthostatic hypotension

Orthostatic hypotension produces dizziness that may terminate in fainting or disappear with rest. Related findings include dim vision, spots before the eyes, pallor, diaphoresis, hypotension, tachycardia and, possibly, signs of dehydration.

Panic disorder

Dizziness may accompany acute attacks of panic in patients with panic disorder. Other findings include anxiety, dyspnea, palpitations, chest pain, a choking or smothering sensation, vertigo, paresthesia, hot and cold flashes, diaphoresis, and trembling or shaking. The patient may have the sensation of dying or losing his mind.

Postconcussion syndrome

Occurring 1 to 3 weeks after a head injury, postconcussion syndrome is marked by dizziness, headache (throbbing, aching, bandlike, or stabbing), emotional lability, alcohol intolerance, fatigue, anxiety and, possibly, vertigo. Dizziness and other symptoms are intensified by mental or physical stress. The syndrome may persist for years, but symptoms eventually abate.

Transient ischemic attack

Lasting from a few seconds to 24 hours, a transient ischemic attack (TIA) commonly signals impending stroke and may be triggered by turning the head to the side. Besides dizziness of varying severity, TIAs are accompanied by unilateral or bilateral diplopia, blindness or visual field deficits, ptosis, tinnitus, hearing loss, paresis, and numbness. Other findings include dysarthria, dysphagia, vomiting, hiccups, confusion, decreased LOC, and pallor.

Other causes

Drugs

Anxiolytics, CNS depressants, opioids, decongestants, antihistamines, antihypertensives, and vasodilators commonly cause dizziness. Herbal remedies such as St. John’s wort can also produce dizziness.

» READ BOOK EXCERPT ONLINE »

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

Level of consciousness, decreased: Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Adrenal crisis

Decreased LOC, ranging from lethargy to coma, may develop within 12 hours of adrenal crisis onset. Early associated findings include progressive weakness, irritability, anorexia, headache, nausea and vomiting, diarrhea, abdominal pain, and fever. Later signs and symptoms include hypotension; rapid, thready pulse; oliguria; cool, clammy skin; and flaccid extremities. The patient with chronic adrenocortical hypofunction may have hyperpigmented skin and mucous membranes.

Brain abscess

Decreased LOC varies from drowsiness to deep stupor, depending on abscess size and site. Early signs and symptoms — constant intractable headache, nausea, vomiting, and seizures — reflect increasing ICP. Typical later features include ocular disturbances (nystagmus, vision loss, and pupillary inequality) and signs of infection such as fever. Other findings may include personality changes, confusion, abnormal behavior, dizziness, facial weakness, aphasia, ataxia, tremor, and hemiparesis.

Brain tumor

In patients with brain tumors, LOC decreases slowly, from lethargy to coma. The patient may also experience apathy, behavior changes, memory loss, decreased attention span, morning headache, dizziness, vision loss, ataxia, and sensorimotor disturbances. Aphasia and seizures are possible, along with signs of hormonal imbalance, such as fluid retention or amenorrhea. Signs and symptoms vary according to the location and size of the tumor. In later stages, papilledema, vomiting, bradycardia, and widening pulse pressure also appear. In the final stages, the patient may exhibit decorticate or decerebrate posture.

Cerebral aneurysm (ruptured)

Somnolence, confusion and, at times, stupor characterize a moderate bleed; deep coma occurs with severe bleeding, which can be fatal. Onset of a ruptured cerebral aneurysm is usually abrupt, with sudden, severe headache, nausea, and vomiting. Nuchal rigidity, back and leg pain, fever, restlessness, irritability, occasional seizures, and blurred vision point to meningeal irritation. The type and severity of other findings vary with the site and severity of the hemorrhage and may include hemiparesis, hemisensory defects, dysphagia, and visual defects.

Cerebral contusion

Usually unconscious for a prolonged period, the patient may develop dilated, nonreactive pupils and decorticate or decerebrate posture. If he’s conscious or recovers consciousness, he may be drowsy, confused, disoriented, agitated, or even violent. Associated findings include blurred or double vision, fever, headache, pallor, diaphoresis, tachycardia, altered respirations, aphasia, and hemiparesis. Residual effects include seizures, impaired mental status, slight hemiparesis, and vertigo.

Diabetic ketoacidosis

Diabetic ketoacidosis produces a rapid decrease in LOC that ranges from lethargy to coma. It’s commonly preceded by polydipsia, polyphagia, and polyuria. The patient may complain of weakness, anorexia, abdominal pain, nausea, and vomiting. He may also exhibit orthostatic hypotension; fruity breath odor; Kussmaul’s respirations; warm, dry skin; and a rapid, thready pulse. Untreated, this condition invariably leads to coma and death.

Encephalitis

Within 48 hours of onset, the patient with encephalitis may develop LOC changes ranging from lethargy to coma. Other possible findings include abrupt onset of fever, headache, nuchal rigidity, nausea, vomiting, irritability, personality changes, seizures, aphasia, ataxia, hemiparesis, nystagmus, photophobia, myoclonus, and cranial nerve palsies.

Encephalopathy

With hepatic encephalopathy, signs and symptoms develop in four stages: in the prodromal stage, slight personality changes (disorientation, forgetfulness, slurred speech) and slight tremor; in the impending stage, tremor progressing to asterixis (the hallmark of hepatic encephalopathy), lethargy, aberrant behavior, and apraxia; in the stuporous stage, stupor and hyperventilation, with the patient noisy and abusive when aroused; in the comatose stage, coma with decerebrate posture, hyperactive reflexes, positive Babinski’s reflex, and fetor hepaticus.

With life-threatening hypertensive encephalopathy, LOC progressively decreases from lethargy to stupor to coma. Besides markedly elevated blood pressure, the patient may experience severe headache, vomiting, seizures, visual disturbances, transient paralysis, and eventually Cheyne-Stokes respirations.

With hypoglycemic encephalopathy, LOC rapidly deteriorates from lethargy to coma. Early signs and symptoms include nervousness, restlessness, agitation, and confusion; hunger; alternate flushing and cold sweats; and headache, trembling, and palpitations. Blurred vision progresses to motor weakness, hemiplegia, dilated pupils, pallor, decreased pulse rate, shallow respirations, and seizures. Flaccidity and decerebrate posture appear late.

Depending on its severity, hypoxic encephalopathy produces a sudden or gradual decrease in LOC, leading to coma and brain death. Early on, the patient appears confused and restless, with cyanosis and increased heart and respiratory rates and blood pressure. Later, his respiratory pattern becomes abnormal, and assessment reveals decreased pulse, blood pressure, and deep tendon reflexes (DTRs); Babin-ski’s reflex; absent doll’s eye sign; and fixed pupils.

With uremic encephalopathy, LOC decreases gradually from lethargy to coma. Early on, the patient may appear apathetic, inattentive, confused, and irritable and may complain of headache, nausea, fatigue, and anorexia. Other findings include vomiting, tremors, edema, papilledema, hypertension, cardiac arrhythmias, dyspnea, crackles, oliguria, and Kussmaul’s and Cheyne-Stokes respirations.

Epidural hemorrhage (acute)

Acute epidural hemorrhage, a life-threatening posttraumatic disorder, produces momentary loss of consciousness, sometimes followed by a lucid interval. While lucid, the patient has a severe headache, nausea, vomiting, and bladder distention. Rapid deterioration in consciousness follows, possibly leading to coma. Other findings include irregular respirations, seizures, decreased and bounding pulse, increased pulse pressure, hypertension, unilateral or bilateral fixed and dilated pupils, unilateral hemiparesis or hemiplegia, decerebrate posture, and Babinski’s reflex.

Heatstroke

As body temperature increases, LOC gradually decreases from lethargy to coma. Early signs and symptoms of heatstroke include malaise, tachycardia, tachypnea, orthostatic hypotension, muscle cramps, rigidity, and syncope. The patient may be irritable, anxious, and dizzy and may report a severe headache. At the onset of heatstroke, the patient’s skin is hot, flushed, and diaphoretic with blotchy cyanosis; later, when his fever exceeds 105° F (40.6° C), his skin becomes hot, flushed, and anhidrotic. Pulse and respiratory rate increase markedly, and blood pressure drops precipitously. Other findings include vomiting, diarrhea, dilated pupils, and Cheyne-Stokes respirations.

Hypernatremia

Hypernatremia, life-threatening if acute, causes LOC to deteriorate from lethargy to coma. The patient is irritable and exhibits twitches progressing to seizures. Other associated signs and symptoms include a weak, thready pulse; nausea; malaise; fever; thirst; flushed skin; and dry mucous membranes.

Hyperosmolar hyperglycemic nonketotic syndrome

LOC decreases rapidly from lethargy to coma in hyperosmolar hyperglycemic nonketotic syndrome (HHNS). Early findings include polyuria, polydipsia, weight loss, and weakness. Later, the patient may develop hypotension, poor skin turgor, dry skin and mucous membranes, tachycardia, tachypnea, oliguria, and seizures.

Hypokalemia

With hypokalemia, LOC gradually decreases to lethargy; coma is rare. Other findings include confusion, nausea, vomiting, diarrhea, polyuria, weakness, decreased reflexes, malaise, dizziness, hypotension, arrhythmias, and abnormal electrocardiogram results.

Hyponatremia

Hyponatremia, life-threatening if acute, produces decreased LOC in late stages. Early nausea and malaise may progress to behavior changes, confusion, lethargy, incoordination and, eventually, seizures and coma.

Hypothermia

With severe hypothermia (temperature below 90° F [32.2° C]), LOC decreases from lethargy to coma. DTRs disappear, and ventricular fibrillation occurs, possibly followed by cardiopulmonary arrest. With mild to moderate hypothermia, the patient may experience memory loss and slurred speech as well as shivering, weakness, fatigue, and apathy. Other early signs and symptoms include ataxia, muscle stiffness, and hyperactive DTRs; diuresis; tachycardia and decreased respiratory rate and blood pressure; and cold, pale skin. Later, muscle rigidity and decreased reflexes may develop, along with peripheral cyanosis, bradycardia, arrhythmias, severe hypotension, decreased respiratory rate with shallow respirations, and oliguria.

Intracerebral hemorrhage

Intracerebral hemorrhage, a life-threatening disorder, produces a rapid, steady loss of consciousness within hours, commonly accompanied by severe headache, dizziness, nausea, and vomiting. Associated signs and symptoms vary and may include increased blood pressure, irregular respirations, Babinski’s reflex, seizures, aphasia, decreased sensations, hemiplegia, decorticate or decerebrate posture, and dilated pupils.

Meningitis

Confusion and irritability are expected; however, stupor, coma, and seizures may occur in those with severe meningitis. Fever develops early, possibly accompanied by chills. Associated findings include severe headache, nuchal rigidity, hyperreflexia and, possibly, opisthotonos. The patient exhibits Kernig’s and Brudzinski’s signs and, possibly, ocular palsies, photophobia, facial weakness, and hearing loss.

Myxedema crisis

The patient experiencing myxedema crisis may exhibit a swift decline in LOC. Other findings include severe hypothermia, hypoventilation, hypotension, bradycardia, hypoactive reflexes, periorbital and peripheral edema, impaired hearing and balance, and seizures.

Pontine hemorrhage

With pontine hemorrhage, a sudden, rapid decrease in LOC to the point of coma occurs within minutes; death occurs within hours. The patient may also exhibit total paralysis, decerebrate posture, Babinski’s reflex, absent doll’s eye sign, and bilateral miosis (however, the pupils remain reactive to light).

Seizure disorders

A complex partial seizure produces decreased LOC, manifested as a blank stare, purposeless behavior (picking at clothing, wandering, lip smacking or chewing motions), and unintelligible speech. The seizure may be heralded by an aura and followed by several minutes of mental confusion.

An absence seizure usually involves a brief change in LOC, indicated by blinking or eye rolling, blank stare, and slight mouth movements.

A generalized tonic-clonic seizure typically begins with a loud cry and sudden loss of consciousness. Muscle spasm alternates with relaxation. Tongue biting, incontinence, labored breathing, apnea, and cyanosis may also occur. Consciousness returns after the seizure, but the patient remains confused and may have difficulty talking. He may complain of drowsiness, fatigue, headache, muscle aching, and weakness and may fall into deep sleep.

An atonic seizure produces sudden unconsciousness for a few seconds.

Status epilepticus, rapidly recurring seizures without intervening periods of physiologic recovery and return of consciousness, can be life-threatening.

Shock

Decreased LOC — lethargy progressing to stupor and coma — occurs late in shock. Associated findings include confusion, anxiety, and restlessness; hypotension; tachycardia; weak pulse with narrowing pulse pressure; dyspnea; oliguria; and cool, clammy skin.

Hypovolemic shock is generally the result of massive or insidious bleeding, either internally or externally. Cardiogenic shock may produce chest pain or arrhythmias and signs of heart failure, such as dyspnea, cough, edema, jugular vein distention, and weight gain. Septic shock may be accompanied by high fever and chills. Anaphylactic shock usually involves stridor.

Stroke

With stroke, LOC changes vary in degree and onset, depending on the lesion’s size and location and the presence of edema. A thrombotic stroke usually follows multiple transient ischemic attacks (TIAs). LOC changes may be abrupt or take several minutes, hours, or days. An embolic stroke occurs suddenly, and deficits reach their peak almost at once. Deficits associated with a hemorrhagic stroke usually develop over minutes or hours.

Associated findings vary with stroke type and severity and may include disorientation; intellectual deficits, such as memory loss and poor judgment; personality changes; and emotional lability. Other possible findings include dysarthria, dysphagia, ataxia, aphasia, apraxia, agnosia, unilateral sensorimotor loss, and visual disturbances. In addition, urine retention, incontinence, constipation, headache, vomiting, and seizures may occur.

CULTURAL CUE:The incidence of stroke is higher in Blacks than Whites. In fact, Blacks have a 60% higher risk for stroke than Whites or Hispanics of the same age. This is believed to be the result of an increased prevalence of hypertension in Blacks.

Subdural hematoma (chronic)

LOC deteriorates slowly in patients with chronic subdural hematomas. Other signs and symptoms include confusion, decreased ability to concentrate, and personality changes accompanied by headache, light-headedness, seizures, and a dilated ipsilateral pupil with ptosis.

Subdural hemorrhage (acute)

With acute subdural hemorrhage, a potentially life-threatening disorder, agitation and confusion are followed by progressively decreasing LOC from somnolence to coma. The patient may also experience headache, fever, unilateral pupil dilation, decreased pulse and respiratory rates, widening pulse pressure, seizures, hemiparesis, and Babinski’s reflex.

Thyroid storm

LOC decreases suddenly and can progress to coma. Irritability, restlessness, confusion, and psychotic behavior precede the deterioration. Associated signs and symptoms of a thyroid storm include tremors and weakness; visual disturbances; tachycardia, arrhythmias, angina, and acute respiratory distress; warm, moist, flushed skin; and vomiting, diarrhea, and fever to 105°F (40.6°C).

TIA

LOC decreases abruptly (with varying severity) and gradually returns to normal within 24 hours of a TIA. Site-specific findings may include vision loss, nystagmus, aphasia, dizziness, dysarthria, unilateral hemiparesis or hemiplegia, tinnitus, paresthesia, dysphagia, or staggering or incoordinated gait.

West Nile encephalitis

Signs and symptoms of this brain infection caused by the West Nile virus include fever, headache, and body aches, commonly with skin rash and swollen lymph glands. More severe infection is marked by high fever, headache, neck stiffness, stupor, disorientation, coma, tremors, occasional seizures, paralysis and, rarely, death.

Other causes

Alcohol

Alcohol use causes varying degrees of sedation, irritability, and incoordination; intoxication commonly causes stupor.

Drugs

Sedation and other degrees of decreased LOC can result from an overdose of a barbiturate, another central nervous system depressant, or aspirin.

Poisoning

Toxins, such as lead, carbon monoxide, and snake venom, can cause varying degrees of decreased LOC. Confusion is common, as are headache, nausea, and vomiting. Other general features include hypotension, cardiac arrhythmias, dyspnea, sensorimotor loss, and seizures.

» READ BOOK EXCERPT ONLINE »

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

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

Acoustic neuroma

Acoustic neuroma is a tumor of the eighth cranial nerve that causes mild, intermittent vertigo and unilateral sensorineural hearing loss. Other findings include tinnitus, postauricular or suboccipital pain, and — with cranial nerve compression — facial paralysis.

Benign positional vertigo

With benign positional vertigo, debris in a semicircular canal produces vertigo on head position change, which lasts a few minutes. It’s usually temporary and can be effectively treated with positional maneuvers.

Brain stem ischemia

Brain stem ischemia produces sudden, severe vertigo that may become episodic and later persistent. Associated findings include ataxia, nausea, vomiting, increased blood pressure, tachycardia, nystagmus, and lateral deviation of the eyes toward the side of the lesion. Hemiparesis and paresthesia may also occur.

Head trauma

Persistent vertigo, occurring soon after injury, accompanies spontaneous or positional nystagmus and, if the temporal bone is fractured, hearing loss. Associated findings include headache, nausea, vomiting, and decreased level of consciousness (LOC). Behavioral changes, diplopia or visual blurring, seizures, motor or sensory deficits, and signs of increased intracranial pressure may also occur.

Herpes zoster

Infection of the eighth cranial nerve with herpes zoster produces sudden onset of vertigo accompanied by facial paralysis, hearing loss in the affected ear, and herpetic vesicular lesions in the auditory canal.

Labyrinthitis

Severe vertigo begins abruptly with this inner ear infection. Vertigo may occur in a single episode or may recur over months or years. Associated findings of labyrinthitis include nausea, vomiting, progressive sensorineural hearing loss, and nystagmus.

Ménière’s disease

With Ménière’s disease, labyrinthine dysfunction causes abrupt onset of vertigo, lasting minutes, hours, or days. Unpredictable episodes of severe vertigo and unsteady gait may cause the patient to fall. During an attack, any sudden motion of the head or eyes can precipitate nausea and vomiting.

Motion sickness

Motion sickness is characterized by vertigo, nausea, vomiting, and headache in response to rhythmic or erratic motions. Headache, dizziness, fatigue, diaphoresis, hypersalivation, and dyspnea may also occur.

Multiple sclerosis

Episodic vertigo may occur early in multiple sclerosis and become persistent. Other early findings include diplopia, visual blurring, and paresthesia. Multiple sclerosis may also produce nystagmus, constipation, muscle weakness, paralysis, spasticity, hyperreflexia, intention tremor, and ataxia.

Seizures

Temporal lobe seizures may produce vertigo, usually associated with other symptoms of partial complex seizures. The seizures may be heralded by an aura and followed by several minutes of mental confusion.

Vestibular neuritis

With vestibular neuritis, severe vertigo usually begins abruptly and lasts several days, without tinnitus or hearing loss. Other findings include nausea, vomiting, and nystagmus.

Other causes

Diagnostic tests

Caloric testing (irrigating the ears with warm or cold water) can induce vertigo.

Drugs and alcohol

High or toxic doses of certain drugs or alcohol may produce vertigo. These drugs include salicylates, aminoglycosides, antibiotics, quinine, and hormonal contraceptives.

Surgery and other procedures

Ear surgery may cause vertigo that lasts for several days. Also, administration of overly warm or cold eardrops or irrigating solutions can cause vertigo.

» READ BOOK EXCERPT ONLINE »

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

Syncope: Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Aortic arch syndrome

With aortic arch syndrome, the patient experiences syncope and may exhibit weak or abruptly absent carotid pulses and unequal or absent radial pulses. Early signs and symptoms include night sweats, pallor, nausea, anorexia, weight loss, arthralgia, and Raynaud’s phenomenon. He may also develop hypotension in the arms; neck, shoulder, and chest pain; paresthesia; intermittent claudication; bruits; vision disturbances; and dizziness.

Aortic stenosis

A cardinal late sign of aortic stenosis, syncope is accompanied by exertional dyspnea and angina. Related findings include marked fatigue, orthopnea, paroxysmal nocturnal dyspnea, palpitations, and diminished carotid pulses. Typically, auscultation reveals atrial and ventricular gallops as well as a harsh, crescendo-decrescendo systolic ejection murmur that’s loudest at the right sternal border of the second intercostal space.

Cardiac arrhythmias

Any arrhythmia that decreases cardiac output and impairs cerebral circulation may cause syncope. Other effects — such as palpitations, pallor, confusion, diaphoresis, dyspnea, and hypotension — usually develop first. However, with Adams-Stokes syndrome, syncope may occur without warning. During syncope, the patient develops asystole, which may precipitate spasm and myoclonic jerks if prolonged. He also displays an ashen pallor that progresses to cyanosis, incontinence, bilateral Babinski’s reflex, and fixed pupils.

Carotid sinus hypersensitivity

With carotid sinus hypersensitivity, syncope is triggered by compression of the carotid sinus, which may be caused by turning the head to one side or by wearing a tight collar. The fainting episode is usually of short duration.

Hypoxemia

Regardless of its cause, severe hypoxemia may produce syncope. Common related effects include confusion, tachycardia, restlessness, and incoordination. The patient may also have tachypnea, dyspnea, and cyanosis.

Orthostatic hypotension

With orthostatic hypotension, syncope occurs when the patient rises quickly from a recumbent position. Look for a drop of 10 to 20 mm Hg or more in systolic or diastolic blood pressure as well as tachycardia, pallor, dizziness, blurred vision, nausea, and diaphoresis.

Transient ischemic attacks

Marked by transient neurologic deficits, transient ischemic attacks (TIAs) may produce syncope and decreased level of consciousness. Other findings vary with the affected artery but may include vision loss, nystagmus, aphasia, dysarthria, unilateral numbness, hemiparesis or hemiplegia, tinnitus, facial weakness, dysphagia, and staggering or uncoordinated gait.

Vagal glossopharyngeal neuralgia

With vagal glossopharyngeal neuralgia, localized pressure may trigger pain in the base of the tongue, pharynx, larynx, tonsils, and ear, resulting in syncope that lasts for several minutes.

Other causes

Drugs

Quinidine may cause syncope — and possibly sudden death — associated with ventricular fibrillation. Prazosin may cause severe orthostatic hypotension and syncope, usually after the first dose. Occasionally, griseofulvin, levodopa, and indomethacin can produce syncope.

» READ BOOK EXCERPT ONLINE »

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

Vertigo: Principal Causes of Vertigo
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)

  1. Peripheralvestibular dysfunction
    1. Labyrinthitis
    2. Motion sickness
    3. Head trauma
    4. Drugs
    5. Benign paroxysmal vertigo
    6. Vestibular neuronitis
    7. Middle ear and temporal bone masses
    8. Perilymphatic fistula
    9. Ménière disease
  2. Central vestibular dysfunction
    1. Head trauma
    2. Intracranial infection
    3. Seizure disorder
    4. Basilar artery migraine
    5. Neoplasm
  3. Psychologic disturbance

» READ BOOK EXCERPT ONLINE »

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

Syncope and Dizziness: Principal Causes of Syncope and Dizziness
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)

  1. Cardiovascularsyncope
    1. Neurocardiogenicsyncope
    2. Cardiac syncope
      1. Congenitaland acquired heart disease
      2. Hypercyanotic episodes
      3. Arrhythmias in structurally normalheart
      4. Arrhythmias in structurally abnormalheart
    3. Vascular syncope
      1. Orthostaticsyncope
      2. Cerebrovascular syncope
      3. Carotid sinus syncope
  2. Noncardiovascular syncope
    1. Breath-holding
    2. Hyperventilation
    3. Migraine
    4. Metabolic
      1. Hypoxia including anemia
      2. Hypoglycemia
    5. Psychologic

» READ BOOK EXCERPT ONLINE »

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

Aura: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Classic migraine headache.A migraine is preceded by a vague premonition and then, usually, a visual aura involving flashes of light. The aura lasts 10 to 30 minutes and may intensify until it completely obscures the patient's vision. A classic migraine may cause numbness or tingling of the lips, face, or hands; slight confusion; and dizziness before the characteristic unilateral, throbbing headache appears. It slowly intensifies; when it peaks, it may cause photophobia, nausea, and vomiting.

Seizure, generalized tonic-clonic.A generalized tonic-clonic seizure may begin with or without an aura. The patient loses consciousness and falls to the ground. His body stiffens (tonic phase), and then he experiences rapid, synchronous muscle jerking and hyperventilation (clonic phase). The seizure usually lasts 2 to 5 minutes.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Dizziness: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Anemia.Typically, anemia causes dizziness that's aggravated by postural changes or exertion. Other signs and symptoms include pallor, dyspnea, fatigue, tachycardia, and a bounding pulse. The capillary refill time is increased.

Cardiac arrhythmias.Dizziness may occur for several seconds or longer and may precede fainting in arrhythmias. The patient may experience palpitations; irregular, rapid, or thready pulse; and, possibly, hypotension. He may also experience weakness, blurred vision, paresthesia, and confusion.

Emphysema.Dizziness may follow exertion or the chronic productive cough in patients with emphysema. Associated signs and symptoms include dyspnea, anorexia, weight loss, malaise, use of accessory muscles, pursed-lip breathing, tachypnea, peripheral cyanosis, and diminished breath sounds. Barrel chest and clubbing may be seen.

Generalized anxiety disorder.Generalized anxiety disorder produces continuous dizziness that may intensify as the disorder worsens. Associated signs and symptoms are persistent anxiety (for at least 1 month), insomnia, difficulty concentrating, and irritability. The patient may show signs of motor tension—for example, twitching or fidgeting, muscle aches, a furrowed brow, and a tendency to be startled. He may also display signs of autonomic hyperactivity, such as diaphoresis, palpitations, cold and clammy hands, dry mouth, paresthesia, indigestion, hot or cold flashes, frequent urination, diarrhea, a lump in the throat, pallor, and increased pulse and respiratory rates.

Hypertension.With hypertension, dizziness may precede fainting, but it may also be relieved by rest. Other common signs and symptoms include a headache and blurred vision. Retinal changes include hemorrhage, sclerosis of retinal blood vessels, exudate, and papilledema.

Hyperventilation syndrome.Episodes of hyperventilation cause dizziness that usually lasts a few minutes; however, if these episodes occur frequently, dizziness may persist between them. Other effects include apprehension, diaphoresis, pallor, dyspnea, chest tightness, palpitations, trembling, fatigue, and peripheral and circumoral paresthesia.

Hypovolemia.A lack of circulating blood volume may cause dizziness and may be accompanied by other signs of fluid volume deficit (dry mucous membranes, decreased blood pressure, increased heart rate).

Orthostatic hypotension.Orthostatic hypotension produces dizziness that may terminate in fainting or disappear with rest. Related findings include dim vision, spots before the eyes, pallor, diaphoresis, hypotension, tachycardia and, possibly, signs of dehydration.

Postconcussion syndrome.Occurring 1 to 3 weeks after a head injury, postconcussion syndrome is marked by dizziness, a headache (throbbing, aching, bandlike, or stabbing), emotional lability, alcohol intolerance, fatigue, anxiety and, possibly, vertigo. Dizziness and other symptoms are intensified by mental or physical stress. The syndrome may persist for years, but symptoms eventually abate.

Rift Valley fever.Typical signs and symptoms of Rift Valley fever include dizziness, a fever, myalgia, weakness, and back pain. A small percentage of patients may develop encephalitis or may progress to hemorrhagic fever that can lead to shock and hemorrhage. Inflammation of the retina may result in some permanent vision loss.

Transient ischemic attack (TIA).Lasting from a few seconds to 24 hours, a TIA commonly signals an impending stroke and may be triggered by turning the head to the side. Besides dizziness of varying severity, TIAs are accompanied by unilateral or bilateral diplopia, blindness or visual field deficits, ptosis, tinnitus, hearing loss, paresis, and numbness. Other findings include dysarthria, dysphagia, vomiting, hiccups, confusion, a decreased LOC, and pallor.

Other causes

Drugs.Anxiolytics, central nervous system depressants, opioids, decongestants, antihistamines, antihypertensives, and vasodilators commonly cause dizziness.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Level of consciousness, decreased: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Adrenal crisis.A decreased LOC, ranging from lethargy to coma, may develop within 8 to 12 hours of the onset of adrenal crisis. Early associated findings include progressive weakness, irritability, anorexia, a headache, nausea and vomiting, diarrhea, abdominal pain, and a fever. Later signs and symptoms include hypotension; a rapid, thready pulse; oliguria; cool, clammy skin; and flaccid extremities. The patient with chronic adrenocortical hypofunction may have hyperpigmented skin and mucous membranes.

Brain abscess.With a brain abscess, decreased LOC varies from drowsiness to deep stupor, depending on the abscess size and site. Early signs and symptoms—a constant intractable headache, nausea, vomiting, and seizures—reflect increasing ICP. Typical later features include ocular disturbances (nystagmus, vision loss, and pupillary inequality) and signs of infection such as a fever. Other findings may include personality changes, confusion, abnormal behavior, dizziness, facial weakness, aphasia, ataxia, tremor, and hemiparesis.

Brain tumor.With a brain tumor, the patient's LOC decreases slowly, from lethargy to coma. He may also experience apathy, behavior changes, memory loss, a decreased attention span, a morning headache, dizziness, vision loss, ataxia, and sensorimotor disturbances. Aphasia and seizures are possible, along with signs of hormonal imbalance, such as fluid retention or amenorrhea. Signs and symptoms vary according to the location and size of the tumor. In later stages, papilledema, vomiting, bradycardia, and a widening pulse pressure also appear. In the final stages, the patient may exhibit decorticate or decerebrate posture.

Cerebral aneurysm (ruptured).Somnolence, confusion and, at times, stupor characterize a moderate cerebral bleed; deep coma occurs with severe bleeding, which can be fatal. The onset is usually abrupt, with a sudden, severe headache and nausea and vomiting. Nuchal rigidity, back and leg pain, a fever, restlessness, irritability, occasional seizures, and blurred vision point to meningeal irritation. The type and severity of other findings vary with the site and severity of the hemorrhage and may include hemiparesis, hemisensory defects, dysphagia, and visual defects.

Diabetic ketoacidosis.Diabetic ketoacidosis produces a rapid decrease in the patient's LOC, ranging from lethargy to coma, commonly preceded by polydipsia, polyphagia, and polyuria. The patient may complain of weakness, anorexia, abdominal pain, nausea, and vomiting. He may also exhibit orthostatic hypotension; a fruity breath odor; Kussmaul's respirations; warm, dry skin; and a rapid, thready pulse. Untreated, this condition invariably leads to coma and death.

Encephalitis.Within 24 to 48 hours after onset of encephalitis, the patient may develop changes in his LOC ranging from lethargy to coma. Other possible findings include an abrupt onset of a fever, a headache, nuchal rigidity, nausea, vomiting, irritability, personality changes, seizures, aphasia, ataxia, hemiparesis, nystagmus, photophobia, myoclonus, and cranial nerve palsies.

Encephalomyelitis (postvaccinal).Postvaccinal encephalomyelitis is a life-threatening disorder that produces rapid deterioration in the patient's LOC, from drowsiness to coma. He also experiences a rapid onset of a fever, a headache, nuchal rigidity, back pain, vomiting, and seizures.

Encephalopathy.With hepatic encephalopathy, signs and symptoms develop in four stages: in the prodromal stage, slight personality changes (disorientation, forgetfulness, slurred speech) and slight tremor; in the impending stage, tremor progressing to asterixis (the hallmark of hepatic encephalopathy), lethargy, aberrant behavior, and apraxia; in the stuporous stage, stupor and hyperventilation, with the patient noisy and abusive when aroused; in the comatose stage, coma with decerebrate posture, hyperactive reflexes, a positive Babinski's reflex, and fetor hepaticus.

With life-threatening hypertensive encephalopathy, the LOC progressively decreases from lethargy to stupor to coma. Besides markedly elevated blood pressure, the patient may experience a severe headache, vomiting, seizures, vision disturbances, transient paralysis and, eventually, Cheyne-Stokes respirations.

With hypoglycemic encephalopathy, the patient's LOC rapidly deteriorates from lethargy to coma. Early signs and symptoms include nervousness, restlessness, agitation, and confusion; hunger; alternate flushing and cold sweats; and a headache, trembling, and palpitations. Blurred vision progresses to motor weakness, hemiplegia, dilated pupils, pallor, a decreased pulse rate, shallow respirations, and seizures. Flaccidity and decerebrate posture appear late.

Depending on its severity, hypoxic encephalopathy produces a sudden or gradual decrease in the LOC, leading to coma and brain death. Initially, the patient appears confused and restless, with cyanosis and increased heart and respiratory rates and blood pressure. Later, his respiratory pattern becomes abnormal, and assessment reveals a decreased pulse, blood pressure, and deep tendon reflexes (DTRs); a positive Babinski's reflex; an absent doll's eye sign; and fixed pupils.

With uremic encephalopathy, the LOC decreases gradually from lethargy to coma. Initially, the patient may appear apathetic, inattentive, confused, and irritable and may complain of a headache, nausea, fatigue, and anorexia. Other findings include vomiting, tremors, edema, papilledema, hypertension, cardiac arrhythmias, dyspnea, crackles, oliguria, and Kussmaul's and Cheyne-Stokes respirations.

Heatstroke.With heatstroke, as body temperature increases, the patient's LOC gradually decreases from lethargy to coma. Early signs and symptoms include malaise, tachycardia, tachypnea, orthostatic hypotension, muscle cramps, rigidity, and syncope. The patient may be irritable, anxious, and dizzy and may report a severe headache. At the onset of heatstroke, the patient's skin is hot, flushed, and diaphoretic with blotchy cyanosis; later, when his fever exceeds 105° F (40.5° C), his skin becomes hot, flushed, and anhidrotic. Pulse and respiratory rate increase markedly, and blood pressure drops precipitously. Other findings include vomiting, diarrhea, dilated pupils, and Cheyne-Stokes respirations.

Hypernatremia.Hypernatremia, life-threatening if acute, causes the patient's LOC to deteriorate from lethargy to coma. He's irritable and exhibits twitches progressing to seizures. Other associated signs and symptoms include a weak, thready pulse; nausea; malaise; a fever; thirst; flushed skin; and dry mucous membranes.

Hyperosmolar hyperglycemic nonketotic syndrome (HHNS).LOC decreases rapidly from lethargy to coma with HHNS. Early findings include polyuria, polydipsia, weight loss, and weakness. Later, the patient may develop hypotension, poor skin turgor, dry skin and mucous membranes, tachycardia, tachypnea, oliguria, and seizures.

Hypokalemia.LOC gradually decreases to lethargy with hypokalemia; coma is rare. Other findings include confusion, nausea, vomiting, diarrhea, and polyuria; weakness, decreased reflexes, and malaise; and dizziness, hypotension, arrhythmias, and abnormal electrocardiogram results.

Hyponatremia.Hyponatremia, life-threatening if acute, produces a decreased LOC in late stages. Early nausea and malaise may progress to behavior changes, confusion, lethargy, incoordination and, eventually, seizures and coma.

Hypothermia.With severe hypothermia (temperature below 90° F [32.2° C]), the patient's LOC decreases from lethargy to coma. DTRs disappear, and ventricular fibrillation occurs, possibly followed by cardiopulmonary arrest. With mild to moderate hypothermia, the patient may experience memory loss and slurred speech as well as shivering, weakness, fatigue, and apathy. Other early signs and symptoms include ataxia, muscle stiffness, and hyperactive DTRs; diuresis; tachycardia and decreased respiratory rate and blood pressure; and cold, pale skin. Later, muscle rigidity and decreased reflexes may develop, along with peripheral cyanosis, bradycardia, arrhythmias, severe hypotension, a decreased respiratory rate with shallow respirations, and oliguria.

Intracerebral hemorrhage.Intracerebral hemorrhage is a life-threatening disorder that produces a rapid, steady loss of consciousness within hours, commonly accompanied by a severe headache, dizziness, nausea, and vomiting. Associated signs and symptoms vary and may include increased blood pressure, irregular respirations, a positive Babinski's reflex, seizures, aphasia, decreased sensations, hemiplegia, decorticate or decerebrate posture, and dilated pupils.

Listeriosis.If listeriosis spreads to the nervous system and causes meningitis, signs and symptoms include a decreased LOC, a fever, a headache, and nuchal rigidity. Early signs and symptoms of listeriosis include a fever, myalgia, abdominal pain, nausea, vomiting, and diarrhea.

Meningitis.Confusion and irritability are expected; however, stupor, coma, and seizures may occur in the patient with severe meningitis. A fever develops early, possibly accompanied by chills. Associated findings include a severe headache, nuchal rigidity, hyperreflexia and, possibly, opisthotonos. The patient exhibits Kernig's and Brudzinski's signs and, possibly, ocular palsies, photophobia, facial weakness, and hearing loss.

Pontine hemorrhage.A sudden, rapid decrease in the patient's LOC to the point of coma occurs within minutes and death within hours of pontine hemorrhage. The patient may also exhibit total paralysis, decerebrate posture, a positive Babinski's reflex, an absent doll's eye sign, and bilateral miosis (however, the pupils remain reactive to light).

Seizure disorders.A complex partial seizure produces a decreased LOC, manifested as a blank stare, purposeless behavior (picking at clothing, wandering, lip smacking or chewing motions), and unintelligible speech. The seizure may be heralded by an aura and followed by several minutes of mental confusion.

An absence seizure usually involves a brief change in the patient's LOC, indicated by blinking or eye rolling, a blank stare, and slight mouth movements.

A generalized tonic-clonic seizure typically begins with a loud cry and sudden loss of consciousness. Muscle spasm alternates with relaxation. Tongue biting, incontinence, labored breathing, apnea, and cyanosis may also occur. Consciousness returns after the seizure, but the patient remains confused and may have difficulty talking. He may complain of drowsiness, fatigue, a headache, muscle aching, and weakness and may fall into a deep sleep.

An atonic seizure produces sudden unconsciousness for a few seconds.

Status epilepticus, rapidly recurring seizures without intervening periods of physiologic recovery and return of consciousness, can be life-threatening.

Shock.A decreased LOC—lethargy progressing to stupor and coma—occurs late in shock. Associated findings include confusion, anxiety, and restlessness; hypotension; tachycardia; a weak pulse with narrowing pulse pressure; dyspnea; oliguria; and cool, clammy skin.

Hypovolemic shock is generally the result of massive or insidious bleeding, either internally or externally. Cardiogenic shock may produce chest pain or arrhythmias and signs of heart failure, such as dyspnea, a cough, edema, jugular vein distention, and weight gain. Septic shock may be accompanied by a high fever and chills. Anaphylactic shock usually involves stridor in response to an allergen.

Stroke.When a stroke occurs, changes in the patient's LOC vary in degree and onset, depending on the lesion's size and location and the presence of edema. A thrombotic stroke usually follows multiple transient ischemic attacks (TIAs) or an episode of atrial fibrillation. Changes in the LOC may be abrupt or take several minutes, hours, or days. An embolic stroke occurs suddenly, and deficits reach their peak almost at once. Deficits associated with a hemorrhagic stroke usually develop over minutes or hours.

Associated findings vary with the stroke type and severity and may include disorientation; intellectual deficits, such as memory loss and poor judgment; personality changes; and emotional lability. Other possible findings include dysarthria, dysphagia, ataxia, aphasia, apraxia, agnosia, unilateral sensorimotor loss, and vision disturbances. In addition, urine retention, incontinence, constipation, a headache, vomiting, and seizures may occur.

Subdural hemorrhage (acute).Acute subdural hemorrhage is a potentially life-threatening disorder in which agitation and confusion are followed by a progressively decreasing LOC from somnolence to coma. The patient may also experience a headache, a fever, unilateral pupil dilation, decreased pulse and respiratory rates, a widening pulse pressure, seizures, hemiparesis, and a positive Babinski's reflex.

Thyroid storm.The patient's LOC decreases suddenly with thyroid storm and can progress to coma. Irritability, restlessness, confusion, and psychotic behavior precede the deterioration. Associated signs and symptoms include tremors and weakness; vision disturbances; tachycardia, arrhythmias, angina, and acute respiratory distress; warm, moist, flushed skin; and vomiting, diarrhea, and a fever of up to 105º F (40.5º C).

TIA.When a TIA occurs, the patient's LOC decreases abruptly (with varying severity) and gradually returns to normal within 24 hours. Site-specific findings may include vision loss, nystagmus, aphasia, dizziness, dysarthria, unilateral hemiparesis or hemiplegia, tinnitus, paresthesia, dysphagia, or staggering or incoordinated gait.

West Nile encephalitis.Signs and symptoms of West Nile encephalitis include fever, headache, and body aches, commonly with a skin rash and swollen lymph glands. More severe infection is marked by high fever, headache, neck stiffness, stupor, disorientation, coma, tremors, occasional seizures, paralysis and, rarely, death.

Other causes

Alcohol.Alcohol use causes varying degrees of sedation, irritability, and incoordination; intoxication commonly causes stupor.

Drugs.Sedation and other degrees of a decreased LOC can result from an overdose of a barbiturate, another central nervous system depressant, or aspirin.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Vertigo: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Acoustic neuroma.Acoustic neuroma causes mild, intermittent vertigo and unilateral sensorineural hearing loss. Other findings include tinnitus, postauricular or suboccipital pain, and—with cranial nerve compression—facial paralysis.

Benign positional vertigo.With benign positional vertigo, debris in a semicircular canal produces vertigo with head position change, which lasts a few minutes. It's usually temporary and can be effectively treated with positional maneuvers.

Brain stem ischemia.Brain stem ischemia produces sudden, severe vertigo that may become episodic and later persistent. Associated findings include ataxia, nausea, vomiting, increased blood pressure, tachycardia, nystagmus, and lateral deviation of the eyes toward the side of the lesion. Hemiparesis and paresthesia may also occur.

Head trauma.Persistent vertigo, occurring soon after head injury, accompanies spontaneous or positional nystagmus and, if the temporal bone is fractured, hearing loss. Associated findings include headache, nausea, vomiting, and decreased (LOC). Behavioral changes, diplopia or visual blurring, seizures, motor or sensory deficits, and signs of increased intracranial pressure may also occur.

Herpes zoster.Herpes infection of the eighth cranial nerve produces sudden onset of vertigo accompanied by facial paralysis, hearing loss in the affected ear, and herpetic vesicular lesions in the auditory canal.

Labyrinthitis.Severe vertigo begins abruptly with labyrinthitis. Vertigo may occur in a single episode or may recur over months or years. Associated findings include nausea, vomiting, progressive sensorineural hearing loss, and nystagmus.

Ménière's disease.With Ménière's disease, labyrinthine dysfunction causes abrupt onset of vertigo, lasting minutes, hours, or days. Unpredictable episodes of severe vertigo and unsteady gait may cause the patient to fall. During an attack, a sudden motion of the head or eyes can precipitate nausea and vomiting.

Multiple sclerosis (MS).With MS, episodic vertigo may occur early and become persistent. Other early findings include diplopia, visual blurring, and paresthesia. MS may also produce nystagmus, constipation, muscle weakness, paralysis, spasticity, hyperreflexia, intention tremor, and ataxia.

Seizures.Temporal lobe seizures may produce vertigo, usually associated with other symptoms of partial complex seizures.

Vestibular neuritis.With vestibular neuritis, severe vertigo usually begins abruptly and lasts several days, without tinnitus or hearing loss. Other findings include nausea, vomiting, and nystagmus.

Other causes

Diagnostic tests.Caloric testing (irrigating the ears with warm or cold water) can induce vertigo.

Drugs and alcohol.High or toxic doses of certain drugs or alcohol may produce vertigo. These drugs include salicylates, aminoglycosides, antibiotics, quinine, and hormonal contraceptives.

Surgery and other procedures.Ear surgery may cause vertigo that lasts for several days. Administration of overly warm or cold eardrops or irrigating solutions can also cause vertigo.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Syncope: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Aortic arch syndrome.With aortic arch syndrome, syncope, weak or abruptly absent carotid pulses, and unequal or absent radial pulses may occur. Early signs and symptoms include night sweats, pallor, nausea, anorexia, weight loss, arthralgia, and Raynaud's phenomenon. He may also develop hypotension in the arms; neck, shoulder, and chest pain; paresthesia; intermittent claudication; bruits; vision disturbances; and dizziness.

Aortic stenosis.A cardinal late sign of aortic stenosis, syncope is accompanied by exertional dyspnea and angina. Related findings include marked fatigue, orthopnea, paroxysmal nocturnal dyspnea, palpitations, and diminished carotid pulses. Typically, auscultation reveals atrial and ventricular gallops as well as a harsh, crescendo-decrescendo systolic ejection murmur that's loudest at the right sternal border of the second intercostal space.

Cardiac arrhythmias.Any arrhythmia that decreases cardiac output and impairs cerebral circulation may cause syncope. Other effects—such as palpitations, pallor, confusion, diaphoresis, dyspnea, and hypotension—usually develop first. However, with Adams-Stokes syndrome, syncope may occur without warning. During syncope, the patient develops asystole, which may precipitate spasm and myoclonic jerks if prolonged. He also displays an ashen pallor that progresses to cyanosis, incontinence, a bilateral Babinski's reflex, and fixed pupils.

Hypoxemia.Regardless of its cause, severe hypoxemia may produce syncope. Common related effects include confusion, tachycardia, restlessness, and incoordination.

Orthostatic hypotension.Syncope occurs when the patient rises quickly from a recumbent position. Look for a drop of 10 to 20 mm Hg or more in systolic or diastolic blood pressure as well as tachycardia, pallor, dizziness, blurred vision, nausea, and diaphoresis.

Transient ischemic attack (TIA).Marked by transient neurologic deficits, TIAs may produce syncope and decreased level of consciousness. Other findings vary with the affected artery, but may include vision loss, nystagmus, aphasia, dysarthria, unilateral numbness, hemiparesis or hemiplegia, tinnitus, facial weakness, dysphagia, and a staggering or an uncoordinated gait.

Other causes

Drugs.Quinidine may cause syncope—and possibly sudden death—associated with ventricular fibrillation. Prazosin may cause severe orthostatic hypotension and syncope, usually after the first dose. Occasionally, griseofulvin, levodopa, and indomethacin can produce syncope.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Syncope: Syncope - pathophysiology
(The 5-Minute Pediatric Consult)

  • Most common mechanism is vasovagal or neurocardiogenic, in which a variety of stimuli and conditions—pain, dehydrated state, emotional upset, carotid pressure—trigger increased vagal tone, leading to slowed heart rate and peripheral vasodilation and decreased cerebral perfusion.
  • Rarer causes include cardiac arrhythmia (heart block or tachyarrhythmia) and intracranial hypertension.

Syncope - etiology

  • Underlying causes of syncope in any age group may include congenital heart malformations; arteriovenous malformation; pulmonary hypertension; intracranial hypertension due to hydrocephalus, mass, or pseudotumor; and tachyarrhythmia or heart block (Stokes–Adams).
  • Other causes of syncope by age group include the following:
    • Toddlers:
      • Pallid or cyanotic breath-holding spells; these occur in response to pain, excitement, or frustration, begin with a deep inspiration or exhalation, although the precipitating “gasp” may not be apparent. (Anemia may be associated.)
      • Mastocytosis: Syncope preceded by dyspnea
    • Older children:
      • Prolonged QT syndrome or arrhythmogenic right ventricular dysplasia; may be familial; may occur as unprovoked syncope or as exercise-induced syncope that may resemble an epileptic convulsion
      • Adrenal insufficiency
      • Dysautonomia, orthostatic hypotension

» READ BOOK EXCERPT ONLINE »

Source: The 5-Minute Pediatric Consult, 2008


 » Next page: Risk Factors for Syncope

Rate This Website

What do you think about the features of this website? Take our user survey and have your say:

Website User Survey

Medical Tools & Articles:

Next articles:

Tools & Services:

Medical Articles:

Forums & Message Boards
 
HONcode We subscribe to the HONcode principles

By using this site you agree to our Terms of Use. Information provided on this site is for informational purposes only; it is not intended as a substitute for advice from your own medical team. The information on this site is not to be used for diagnosing or treating any health concerns you may have - please contact your physician or health care professional for all your medical needs. Please see our Terms of Use.

Home | Symptoms | Diseases | Diagnosis | Videos | Tools | Forum | About Us | Terms of Use | Privacy Policy | Site Map | Advertise

Copyright © 2009 Health Grades Inc. All rights reserved.