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Diseases » Coma » Causes
 

Causes of Coma

Contents
  1. Coma: Introduction
  2. List of Causes
  3. Drugs/substances (60 causes)
  4. Drug interaction (556 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 Coma

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

More causes: see full list of causes for Coma

Causes of Coma (Diseases Database):

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

Source: Diseases Database

Coma Causes: Book Excerpts

Coma as a complication of other conditions:

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

Coma as a symptom:

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

Medications or substances causing Coma:

The following drugs, medications, substances or toxins are some of the possible causes of Coma 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.

See full list of 60 medications causing Coma


Drug interactions causing Coma:

When combined, certain drugs, medications, substances or toxins may react causing Coma 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.

  • Phenelzine and tricyclic antidepressant interaction
  • Nardil and tricyclic antidepressant interaction
  • Parnate and tricyclic antidepressant interaction
  • Meperidine and monoamine oxidase inhibitor antidepressant interaction
  • Demerol and monoamine oxidase inhibitor antidepressant interaction
  • more interactions...»

See full list of 556 drug interactions causing Coma

Medical news summaries relating to Coma:

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

Related information on causes of Coma:

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

Causes of Coma: Online Medical Books

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

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

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

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

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

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

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

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.

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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.

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

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

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Source: Field Guide to Bedside Diagnosis, 2007

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

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Source: Field Guide to Bedside Diagnosis, 2007

Delirium/Hallucinations: Differential Overview
(Field Guide to Bedside Diagnosis)

Systemic

❑ Drugs/toxins

❑ Sepsis

❑ Hypoglycemia

❑ Hypercalcemia

❑ Hyponatremia

❑ Shock

❑ Delirium tremens

❑ Vitamin B12 deficiency

❑ Hypoxia

❑ Hypercapnia

❑ Thyrotoxicosis

❑ Uremia

❑ Hepatic encephalopathy

❑ Thiamine deficiency

❑ Heat stroke

❑ Hypothermia

❑ Lead intoxication

❑ Carbon monoxide poisoning

Neurologic

❑ Concussion

❑ Hypertensive encephalopathy

❑ Subdural hematoma

❑ Postictal

❑ Transient global amnesia

❑ Meningitis

❑ Right parietal stroke

❑ Encephalitis

❑ Vasculitis

❑ Carcinomatous meningitis

Hallucinations

❑ Drugs

❑ Schizophrenia

❑ Temporal lobe epilepsy

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Source: Field Guide to Bedside Diagnosis, 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

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

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

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

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

  1. Headtrauma
    1. Concussion
    2. Brain contusion
    3. Shearing injury
    4. Cerebral edema
    5. Intracranial hemorrhage
      1. Intraparenchymalhemorrhage
      2. Subdural hematoma
      3. Epidural hematoma
  2. Infection/inflammation
    1. Bacterialmeningitis
    2. Encephalitis
    3. Septicemia
    4. Focal infection
      1. Brainabscess
      2. Epidural abscess
      3. Subdural empyema
  3. Seizures
    1. Status epilepticus
    2. Postictal state
  4. Brain tumor
  5. Cerebrovascular disorders
    1. Cerebralthrombosis
    2. Cerebral embolism
    3. Cerebral hemorrhage
  6. Hydrocephalus
    1. Obstructive (tumor or other cause)
    2. Shunt malfunction
  7. Blood pressure disorders
    1. Hypotension
    2. Hypertensive encephalopathy
  8. Metabolic disorders
    1. Hypoxic-ischemicencephalopathy
    2. Acute bilirubin encephalopathy (kernicterus)
    3. Diabetic ketoacidosis
    4. Hypoglycemia
    5. Hypothermia
    6. Heat-related illness
    7. Hepatic coma
    8. Reye syndrome
    9. Uremia
    10. Inborn errors of metabolism
      1. Maplesyrup urine disease
      2. Nonketotic hyperglycinemia
      3. Hyperammonemic disorders
        1. Urea cycledefects
          1. Carbamylphosphate synthetase deficiency
          2. Ornithine transcarbamylase deficiency
          3. Argininosuccinic acid synthetase deficiency(citrullinemia)
          4. Argininosuccinase deficiency (argininosuccinicaciduria)
          5. N-acetylglutamate synthetase deficiency
          6. Arginase deficiency (argininemia)
        2. Organic acid disorders
          1. Propionic,isovaleric, and methylmalonic acidemias
          2. Glutaric aciduria, type II (multipleacyl-CoA dehydrogenase deficiency)
          3. Multiple carboxylase deficiency
          4. Pyruvate dehydrogenase complex deficiency
          5. Pyruvate carboxylase deficiency
          6. Fatty acid oxidation defects
          7. Respiratory chain disorders
        3. Lysinuric protein intolerance
        4. Hyperornithinemia-hyperammonemia-homocitrullinuriasyndrome
        5. Transient hyperammonemia of prematurity
    11. Other metabolic disturbances
  9. Poisoning, drug overdose, and intoxication
    1. Carbonmonoxide
    2. Sedative-hypnotic drugs
    3. Opiates
    4. Alcohols
      1. Ethyl alcohol (ethanol)
      2. Ethylene glycol
      3. Isopropyl alcohol
      4. Methyl alcohol (methanol)
    5. Anticonvulsants
      1. Phenytoin
      2. Carbamazepine
      3. Valproic acid
    6. Phenothiazines
    7. Tricyclic antidepressants
    8. Anticholinergic drugs
    9. Salicylates
    10. Lead
    11. Organophosphates
    12. Amphetamines
    13. Cocaine
    14. Hallucinogens (psychedelics)
    15. Iron
    16. Hydrocarbons
    17. Clonidine

» READ BOOK EXCERPT ONLINE »

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

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

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

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

Dysfunction of the reticular activating system in the brainstem or bilateral cerebral dysfunction

Coma - etiology

  • Trauma: Bleeds (epidural/subdural, intracerebral), cerebral swelling, diffuse axonal injury
  • Intoxication: Seizure or psychotropic medications, street drugs
  • Hypoxia/ischemia
  • Infection: Meningitis, encephalitis, toxic shock, subdural empyema, systemic shock
  • Metabolic disorders: Hypoglycemia (salicylate or ethanol intoxication, hyperinsulinemia); diabetic ketoacidosis (rarely neurologic deterioration on initiation of insulin therapy); Reye syndrome; electrolyte abnormalities (Na, K, Ca, Mg); hepatic/uremic encephalopathy; inborn errors of metabolism; hormonal abnormalities (thyroid, adrenal, pituitary); hypothermia/hyperthermia
  • Tumor
  • Seizure: Nonconvulsive status, spike and wave stupor
  • Vascular: Hezorrhage from arteriovenous malformation (AVM), aneurysm, coagulopathy, infarction, cerebral venous thrombosis, hypertensive encephalopathy
  • Hydrocephalus: Ventriculoperitoneal (VP) shunt obstruction, mass/bleed obstructing ventricular outflow

» READ BOOK EXCERPT ONLINE »

Source: The 5-Minute Pediatric Consult, 2008


 » Next page: Risk Factors for Coma

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