Causes of Stokes Adams syndrome
List of causes of Stokes Adams syndrome
Following is a list of causes or underlying conditions
(see also Misdiagnosis of underlying causes of Stokes Adams syndrome)
that could possibly cause Stokes Adams syndrome includes:
Stokes Adams syndrome Causes: Book Excerpts
Stokes Adams syndrome as a symptom:
Conditions listing Stokes Adams syndrome
as a symptom may also be potential underlying causes of Stokes Adams syndrome.
Our database lists the following as having
Stokes Adams syndrome as a symptom of that condition:
Related information on causes of Stokes Adams syndrome:
As with all medical conditions,
there may be many causal factors.
Further relevant information on causes of Stokes Adams syndrome may be found in:
Causes of Stokes Adams syndrome: Online Medical Books
16 MEDICAL BOOKS ONLINE!
Review excerpts from medical books online, free, without registration,
for more information about the causes of Stokes Adams syndrome.
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
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
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
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.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Syncope:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Aortic arch syndrome
With this syndrome, the patient experiences syncope and may exhibit weak or abruptly absent carotid pulses and unequal or absent radial pulses. Early signs and symptoms include night sweats, pallor, nausea, anorexia, weight loss, arthralgia, and Raynaud’s phenomenon. He may also develop hypotension in the arms; neck, shoulder, and chest pain; paresthesia; intermittent claudication; bruits; vision disturbances; and dizziness.
Aortic stenosis
A cardinal late sign, syncope is accompanied by exertional dyspnea and angina. Related findings include marked fatigue, orthopnea, paroxysmal nocturnal dyspnea, palpitations, and diminished carotid pulses. Typically, auscultation reveals atrial and ventricular gallops as well as a harsh, crescendo-decrescendo systolic ejection murmur that’s loudest at the right sternal border of the second intercostal space.
Cardiac arrhythmias
Any arrhythmia that decreases cardiac output and impairs cerebral circulation may cause syncope. Other effects—such as palpitations, pallor, confusion, diaphoresis, dyspnea, and hypotension—usually develop first. However, with Adams-Stokes syndrome, syncope may occur without warning. During syncope, the patient develops asystole, which may precipitate spasm and myoclonic jerks if prolonged. He also displays an ashen pallor that progresses to cyanosis, incontinence, bilateral Babinski’s reflex, and fixed pupils.
Carotid sinus hypersensitivity
Syncope is triggered by compression of the carotid sinus, which may be caused by turning the head to one side or by wearing a tight collar. The fainting episode is usually of short duration.
Hypoxemia
Regardless of its cause, severe hypoxemia may produce syncope. Common related effects include confusion, tachycardia, restlessness, and incoordination.
Orthostatic hypotension
Syncope occurs when the patient rises quickly from a recumbent position. Look for a drop of 10 to 20 mm Hg or more in systolic or diastolic blood pressure as well as tachycardia, pallor, dizziness, blurred vision, nausea, and diaphoresis.
Transient ischemic attacks
Marked by transient neurologic deficits, these attacks may produce syncope and decreased level of consciousness. Other findings vary with the affected artery but may include vision loss, nystagmus, aphasia, dysarthria, unilateral numbness, hemiparesis or hemiplegia, tinnitus, facial weakness, dysphagia, and staggering or uncoordinated gait.
Vagal glossopharyngeal neuralgia
With this disorder, localized pressure may trigger pain in the base of the tongue, pharynx, larynx, tonsils, and ear, resulting in syncope that lasts for several minutes.
Other causes
Drugs
Quinidine may cause syncope—and possibly sudden death—associated with ventricular fibrillation. Prazosin may cause severe orthostatic hypotension and syncope, usually after the first dose. Occasionally, griseofulvin, levodopa, and indomethacin can produce syncope.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Coma:
Differential Overview
(Field Guide to Bedside Diagnosis)
❑ Alcohol intoxication
❑ Drug overdose
❑ Hypoglycemia
❑ Metabolic acidosis
❑ Subdural hematoma
❑ Hypothermia
❑ Heat stroke
❑ Meningitis
❑ Subarachnoid hemorrhage
❑ Head trauma
❑ Ischemic encephalopathy
❑ Epidural hematoma
❑ Pontine hemorrhage
❑ Cerebellar hemorrhage
❑ Psychogenic
» READ BOOK EXCERPT ONLINE »
Source: Field Guide to Bedside Diagnosis, 2007
Syncope:
Differential Overview
(Field Guide to Bedside Diagnosis)
Orthostatic/Autonomic
❑ Neurally mediated hypotension
❑ Volume depletion
❑ Cough syncope
❑ Anemia
❑ Autonomic insufficiency
Cardiac/Obstructive
❑ Myocardial infarction
❑ Pulmonary embolism
❑ Aortic stenosis
❑ Hypertrophic obstructive cardiomyopathy
❑ Aortic dissection
❑ Cardiac tamponade
❑ Left atrial myxoma
Cardiac/Dysrhythmic
❑ Complete heart block
❑ Sick sinus syndrome
❑ Tachyarrhythmia
❑ Carotid sinus hypersensitivity
Neurologic
❑ Vertebrobasilar ischemia
❑ Hypoglycemia
❑ Unwitnessed seizure
❑ Subclavian steal syndrome
Psychologic
❑ Hyperventilation
❑ Hysterical faint
» READ BOOK EXCERPT ONLINE »
Source: Field Guide to Bedside Diagnosis, 2007
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)
- Cardiovascularsyncope
- Neurocardiogenicsyncope
- Cardiac syncope
- Congenitaland acquired heart disease
- Hypercyanotic episodes
- Arrhythmias in structurally normalheart
- Arrhythmias in structurally abnormalheart
- Vascular syncope
- Orthostaticsyncope
- Cerebrovascular syncope
- Carotid sinus syncope
- Noncardiovascular syncope
- Breath-holding
- Hyperventilation
- Migraine
- Metabolic
- Hypoxia including anemia
- Hypoglycemia
- Psychologic
» 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
While dehydration is a common concern for runners, especially during a marathon, experts now say that too much water can be worse. Learn the right...
A pacemaker is a battery-powered device that sends signals to the heart to help it beat properly. Tune in to find out more about these life-saving...
Germs are a fact of life and catching an infectious disease like a cold may seem inevitable. But there are simple ways to protect yourself against...
Sleep is necessary to feel refreshed, but now we know sleep actually impacts the way the body functions. Sleeping poorly can affect how often you get...
See full list of 4 related videos
» Next page: Symptoms of Stokes Adams syndrome
Rate This Website
What do you think about the features of this website?
Take our user survey and have your say:
Website User Survey
Medical Tools & Articles:
Next articles:
Tools & Services:
Medical Articles:
Forums & Message Boards
- Ask or answer a question at the Boards:
