Causes of Delirium
List of causes of Delirium
Following is a list of causes or underlying conditions
(see also Misdiagnosis of underlying causes of Delirium)
that could possibly cause Delirium includes:
More causes:
see full list of causes for Delirium
Causes of Delirium (Diseases Database):
The follow list shows some of the possible medical causes of Delirium
that are listed by the Diseases Database:
Source: Diseases Database
Delirium Causes: Book Excerpts
- Differential Diagnosis - Dementia
- Differential Diagnosis - Hallucinations
- Differential Diagnosis - Syncope
- Differential Diagnosis - Delirium
- Differential Diagnosis - Hallucinations
- Differential Diagnosis - Syncope
- Differential Diagnosis - Delirium
- Medical causes - Agitation
- Medical causes - Confusion
- Medical causes - Level of consciousness, decreased
- Medical causes - Seizures, complex partial
- Medical causes - Syncope
- Causes and incidence - Malignant brain tumors
- Medical causes - Agitation
- Medical causes - Confusion
- Medical causes - Level of consciousness, decreased
- Medical causes - Seizures, complex partial
- Medical causes - Syncope
- Differential Overview - Dementia
- Differential Overview - Syncope
- Differential Overview - Delirium/Hallucinations
- Causes - Brain tumors, malignant
- Causes - Brain abscess
- Medical causes - Level of consciousness, decreased
- Medical causes - Syncope
- Medical causes - Agitation
- Medical causes - Confusion
- Medical causes - Level of consciousness, decreased
- Medical causes - Seizures, complex partial
- Medical causes - Syncope
- Principal Causes of Syncope and Dizziness - Syncope and Dizziness
- Medical causes - Agitation
- Medical causes - Confusion
- Medical causes - Level of consciousness, decreased
- Medical causes - Seizures, complex partial
- Medical causes - Syncope
Delirium as a complication of other conditions:
Other conditions that might have
Delirium as a complication may,
potentially, be an underlying cause of Delirium.
Our database lists the following as having
Delirium as a complication of that condition:
Delirium as a symptom:
Conditions listing Delirium
as a symptom may also be potential underlying causes of Delirium.
Our database lists the following as having
Delirium as a symptom of that condition:
Medications or substances causing Delirium:
The following drugs, medications, substances or toxins are some of the possible
causes of Delirium as a symptom.
This list is incomplete and various other drugs or substances
may cause your symptoms.
Always advise your doctor of any medications or treatments you are using,
including prescription, over-the-counter, supplements, herbal or alternative treatments.
See full list of 62
medications causing Delirium
Drug interactions causing Delirium:
When combined, certain drugs, medications, substances or toxins may react
causing Delirium as a symptom.
The list below is incomplete and various other drugs or substances may cause your symptoms.
Always advise your doctor of any medications or treatments you are using,
including prescription, over-the-counter, supplements, herbal or alternative treatments.
- Parnate and tranylcypromine sulfate interaction
- Amitriptyline and monoamine oxidase inhibitor interaction
- Clomipramine and monoamine oxidase inhibitor interaction
- Dothiepin and monoamine oxidase inhibitor interaction
- Doxepin and monoamine oxidase inhibitor interaction
- more interactions...»
See full list of 271
drug interactions causing Delirium
Medical news summaries relating to Delirium:
The following medical news items are relevant to causes of Delirium:
Related information on causes of Delirium:
As with all medical conditions,
there may be many causal factors.
Further relevant information on causes of Delirium may be found in:
Causes of Delirium: Online Medical Books
16 MEDICAL BOOKS ONLINE!
Review excerpts from medical books online, free, without registration,
for more information about the causes of Delirium.
Dementia:
Differential Diagnosis
(In a Page: Signs and Symptoms)
-
Alzheimer's disease is the most common cause of dementia
-
Lewy body dementia
-
Multi-infarct dementia
-
Parkinson's disease
-
Alcohol/drugs
-
Vitamin deficiency (B12, thiamine)
-
CNS infections
–HIV encephalitis
–Meningitis
–Herpes encephalitis
–Creutzfeldt-Jacob disease
–Cerebral abscess
–Neurosyphilis
-
Depression (pseudodementia)
-
Head trauma
-
Pick's disease
-
Chronic subdural hematoma
-
Huntington's disease
-
Chronic hydrocephalus
-
Paraneoplastic encephalitis
-
Hypothyroidism
-
Cerebral vasculitis
-
Systemic lupus erythematosus (lupus cerebritis)
-
Wilson's disease
-
Chronic hypoglycemia or hypocalcemia
-
Uremic encephalopathy
-
Dialysis dementia
-
Multiple sclerosis
-
Hydrocephalus
-
Postanoxic dementia
» READ BOOK EXCERPT ONLINE »
Source: In a Page: Signs and Symptoms, 2004
Hallucinations:
Differential Diagnosis
(In a Page: Signs and Symptoms)
- Delirium
–Develops over hours to days
–Fluctuates throughout the day
–Causes include dehydration, drug-induced, electrolyte imbalance, UTI, URI, hypoglycemia, and alcohol or drug withdrawal
–Occurs in 10–30% of hospital patients
–Drug-induced delirium (e.g., cocaine, β-blockers, alcohol, corticosteroids, pseudoephedrine, dopaminergic drugs)
- Alcohol withdrawal (delirium tremens)
–Often presents in hospitalized patients about 3 days after admission
–Commonly presents with tactile hallucinations (e.g., formication—the sense of insects crawling over body)
–May be accompanied by seizure activity
- Hallucinogenic syndromes (e.g., LSD, marijuana, mescaline, phencyclidine, mushrooms, amphetamines)
- Schizophrenia
–Auditory hallucinations are most frequent; visual hallucinations occur in about 50% of patients, tactile in 20%, olfactory in 6%
–Progresses to positive psychotic symptoms (e.g., hallucinations, delusions, thought disorder) and/or negative symptoms (e.g., anhedonia, poor concentration, flattened affect, poor social/personal function)
–1% incidence in the general population, males >females
-
Schizophreniform disorder
-
Schizoaffective disorder
-
Post-traumatic stress disorder
-
Dementia
-
Systemic lupus erythematosus
–Auditory hallucinations caused by corticosteroids; visual and tactile by lupus psychosis
-
Bipolar disorder
-
Psychotic depression
-
Postpartum major depression
-
Mass lesions
-
CNS infections/encephalitis
-
Seizures
-
Occipital lobe injury
-
Heavy metal ingestion
-
Lewy body dementia
» READ BOOK EXCERPT ONLINE »
Source: In a Page: Signs and Symptoms, 2004
Syncope:
Differential Diagnosis
(In a Page: Signs and Symptoms)
-
Vasovagal episode
–Most common cause of syncope
–May be triggered by heat, fatigue, stress,
hunger, alcohol, and severe pain
–Associated with diaphoresis, weakness, blurry vision, lightheadedness
–Almost always benign
-
Orthostatic hypotension
–Fall in blood pressure upon standing, due to failure of vasoconstrictor reflexes
–Precipitated by sudden standing from recumbent position
–Often associated with antihypertensive medications (diuretics, vasodilators, α
- or β-blockers) and dehydration/hypovolemia
–May occur with autonomic disorders (e.g., Shy-Drager syndrome)
-
Situational syncope
–Increased intrathoracic pressure (e.g., cough, micturition, defecation) leads to decreased venous return and resulting diminished blood flow to the brain
-
Cardiac arrhythmias
–Very slow (<30 bpm) or fast (>180 bpm) heart rates may result in decreased cardiac output and resulting diminished blood flow to the brain
-
Valvular disease
–Most commonly due to aortic stenosis
-
Myocardial disease
-
Cerebrovascular disease
–Usually due to carotid or vertebrobasilar atherosclerosis
-
Hypoglycemia
-
Anemia
-
Seizure
-
Anxiety attack
-
Migraine
-
Medications (e.g., anticholinergics)
-
CVA
-
Hemorrhage
-
Trauma
>
» READ BOOK EXCERPT ONLINE »
Source: In a Page: Signs and Symptoms, 2004
Delirium:
Differential Diagnosis
(In a Page: Signs and Symptoms)
-
Dementia
-
Medical etiologies
–Infections (e.g., UTI, pneumonia,
encephalitis, meningitis)
–Drug toxicity, including alcohol
–Drug withdrawal (especially
benzodiazepines)
–Fluid, electrolyte, and metabolic disorders (e.g., hyponatremia, hypoglycemia, hypercalcemia, uremia, hypercarbia)
–CHF
–Hypoxia (multiple causes, including CHF)
–Medications (e.g., antiarrhythmics,
antidepressants, neuroleptics, analgesics, GI
medications)
–Stroke
–Cerebral ischemia (multiple causes)
–Complex partial seizure disorder is
associated with an alteration of awareness
- Psychiatric etiologies
–Depression
–Psychotic illness
–“Sundowning”: Behavioral deterioration
occurs during evening hours (typically occurs in demented institutionalized patients)
» READ BOOK EXCERPT ONLINE »
Source: In a Page: Signs and Symptoms, 2004
Hallucinations:
Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)
-
Hallucinogenic drugs
–LSD, “mushrooms,” mescaline, and PCP are primarily hallucinogens
–Amphetamines, cocaine, inhalants, and marijuana may also produce hallucinations
-
CNS acute events
–Trauma
–CNS infection
–Hypoxic events
- Psychosis
–Defined as a mental state with significant impairment in cognition, interpersonal relations, and reality testing
–Hallucinations may be a major or minor component
–Psychosis may be psychiatric or organic (secondary to CNS insult)
- Schizophrenia
–A disorder of impaired perception, cognition, interpersonal relations, and behavior with illogical and disordered thought content
–Hallucinations (most often auditory) and
delusions are common findings
–Onset is frequently in adolescence
–Frequently a positive family history
-
Seizure disorders
–Prominent auras may manifest as perceptual disturbances; visual and olfactory are the most common; tactile may also occur
-
Narcolepsy
–Hypnagogic hallucinations are hallucinations that occur while falling asleep; they may be visual or auditory
-
Medications
–Antipsychotics, anticholinergics, and
corticosteroids can rarely cause
hallucinations
» 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
Delirium:
Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)
-
Acute systemic infection
–May be viral or bacterial cause
–Often associated with high fever
-
Hypoglycemia, diabetic ketoacidosis
-
Central nervous system infection
–Meningitis, encephalitis, brain abscess
- Drugs
–Alcohol: Acute intoxication
–Amphetamines: Also tremors, dry mouth, tachycardia, hyperactivity
–Hallucinogens (LSD, mescaline, PCB) also tremors, dilated pupils, nausea, and abdominal pain
–Phencyclidine (a.k.a. Angel Dust) with atxia,
nystagmus, hyperreflexia, and hypertension
–Opiates: Also with pinpoint pupils
–Antihistamines
–Phenothiazines
–Organic solvents
–Salicylates
–Glucocorticoids
-
Head injury
-
Rocky Mountain spotted fever (RMSF)
–Delirium and hallucinations may precede rash; fever, headache, myalgias, chills
-
Malaria
-
Rabies
-
Syphilis
–Tertiary syphilis is rare in children
-
Hyponatremia
-
Uremia
-
Migraine
-
Hypoxia
-
Heat stroke
-
Hepatic failure
-
Systemic lupus erythematosus
–Delirium is due to cerebral vasculitis
-
Pellagra
–Due to niacin deficiency
–Also with diarrhea, dermatitis, dementia
-
Hartnup disease
–Rash, ataxia, psychological disturbance
–Symptoms may be intermittent
-
Porphyria
–Attacks of abnormal behavior do not begin until late adolescence
» READ BOOK EXCERPT ONLINE »
Source: In A Page: Pediatric Signs and Symptoms, 2007
Agitation:
Medical causes
(Handbook of Signs & Symptoms (Third Edition))
❑ Alcohol withdrawal syndrome. Mild to severe agitation occurs in alcohol withdrawal syndrome, along with hyperactivity, tremors, and anxiety. With delirium, the potentially life-threatening stage of alcohol withdrawal, severe agitation accompanies hallucinations, insomnia, diaphoresis, and a depressed mood. The patient’s pulse rate and temperature rise as withdrawal progresses; status epilepticus, cardiac exhaustion, and shock can occur.
❑ Anxiety. Anxiety produces varying degrees of agitation. The patient may be unaware of his anxiety or may complain of it without knowing its cause. Other findings include nausea, vomiting, diarrhea, cool and clammy skin, frontal headache, back pain, insomnia, and tremors.
❑ Dementia. Mild to severe agitation can result from many common syndromes, such as Alzheimer’s and Huntington’s diseases. The patient may display a decrease in memory, attention span, problem-solving ability, and alertness. Hypoactivity, wandering behavior, hallucinations, aphasia, and insomnia may also occur.
❑ Drug withdrawal syndrome. Mild to severe agitation occurs in drug withdrawal syndrome. Related findings vary with the drug, but include anxiety, abdominal cramps, diaphoresis, and anorexia. With opioid or barbiturate withdrawal, a decreased level of consciousness (LOC), seizures, and elevated blood pressure, heart rate, and respiratory rate can also occur.
❑ Hepatic encephalopathy. Agitation occurs only with fulminating encephalopathy. Other findings include drowsiness, stupor, fetor hepaticus, asterixis, and hyperreflexia.
❑ Hypersensitivity reaction. Moderate to severe agitation appears, possibly as the first sign of a reaction. Depending on the severity of the reaction, agitation may be accompanied by urticaria, pruritus, and facial and dependent edema.
With anaphylactic shock, a potentially life-threatening reaction, agitation occurs rapidly along with apprehension, urticaria or diffuse erythema, warm and moist skin, paresthesia, pruritus, edema, dyspnea, wheezing, stridor, hypotension, and tachycardia. Abdominal cramps, vomiting, and diarrhea can also occur.
❑ Hypoxemia. Beginning as restlessness, agitation rapidly worsens. The patient may be confused and have impaired judgment and motor coordination. He may also have tachycardia, tachypnea, dyspnea, and cyanosis.
❑ Increased intracranial pressure (ICP). Agitation usually precedes other early signs and symptoms, such as head-ache, nausea, and vomiting. Increased ICP produces respiratory changes, such as Cheyne-Stokes, cluster, ataxic, or apneustic breathing; sluggish, nonreactive, or unequal pupils; widening pulse pressure; tachycardia; a decreased LOC; seizures; and motor changes such as decerebrate or decorticate posture.
❑ Post-head trauma syndrome. Shortly after, or even years after injury, mild to severe agitation develops, characterized by disorientation, loss of concentration, angry outbursts, and emotional lability. Other findings include fatigue, wandering behavior, and poor judgment.
❑ Vitamin B6 deficiency. Agitation can range from mild to severe. Other effects include seizures, peripheral paresthesia, and dermatitis. Oculogyric crisis may also occur.
Other causes
❑ Drugs. Mild to moderate agitation, which is commonly dose related, develops as an adverse reaction to central nervous system stimulants — especially appetite suppressants, such as amphetamines and amphetamine-like drugs; sympathomimetics, such as ephedrine; caffeine; and theophylline.
❑ Radiographic contrast media. Reaction to the contrast medium injected during various diagnostic tests produces moderate to severe agitation along with other signs of hypersensitivity.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Confusion:
Medical causes
(Handbook of Signs & Symptoms (Third Edition))
Brain tumor.
In the early stages of a brain tumor, confusion is usually mild and difficult to detect. As the tumor impinges on cerebral structures, however, confusion worsens and the patient may exhibit personality changes, bizarre behavior, sensory and motor deficits, visual field deficits, and aphasia.
Cerebrovascular disorders.
Cerebrovascular disorders produce confusion due to tissue hypoxia and ischemia. Confusion may be insidious and fleeting, as in a transient ischemic attack, or acute and permanent, as in a stroke.
Decreased cerebral perfusion.
Mild confusion is an early symptom of decreased cerebral perfusion. Associated findings usually include hypotension, tachycardia or bradycardia, an irregular pulse, ventricular gallop, edema, and cyanosis.
Fluid and electrolyte imbalance.
The extent of imbalance determines the severity of the patient's confusion. Typically, he'll show signs of dehydration, such as lassitude, poor skin turgor, dry skin and mucous membranes, and oliguria. He may also develop hypotension and a low-grade fever.
Head trauma.
Concussion, contusion, and brain hemorrhage may produce confusion at the time of injury, shortly afterward, or months or even years afterward. The patient may be delirious, with periodic loss of consciousness. Vomiting, a severe headache, pupillary changes, and sensory and motor deficits are also common.
Heatstroke.
Heatstroke causes pronounced confusion that gradually worsens as the patient's body temperature rises. Initially, he may be irritable and dizzy; later, he may become delirious, have seizures, and lose consciousness.
Hypothermia.
Confusion may be an early sign of hypothermia. Typically, the patient displays slurred speech, cold and pale skin, hyperactive deep tendon reflexes, a rapid pulse, and decreased blood pressure and respirations. As his body temperature continues to drop, his confusion progresses to stupor and coma, his muscles become rigid, and his respiratory rate decreases.
Hypoxemia.
Acute pulmonary disorders that result in hypoxemia produce confusion that can range from mild disorientation to delirium. Chronic pulmonary disorders produce persistent confusion.
Infection.
Severe generalized infection, such as sepsis, typically produces delirium. Central nervous system (CNS) infections, such as meningitis, cause varying degrees of confusion along with a headache and nuchal rigidity.
Metabolic encephalopathy.
Hyperglycemia and hypoglycemia can produce sudden confusion. A patient with hypoglycemia may also experience transient delirium and seizures. Uremic and hepatic encephalopathies produce gradual confusion that may progress to seizures and coma. Usually, the patient also experiences tremors and restlessness.
Nutritional deficiencies.
Inadequate dietary intake of thiamine, niacin, or vitamin B12 produces insidious, progressive confusion and possible mental deterioration.
Seizure disorders.
Mild to moderate confusion may immediately follow any type of seizure. The confusion usually disappears within several hours.
Other causes
Alcohol.
Intoxication causes confusion and stupor, and alcohol withdrawal may cause delirium and seizures.
Drugs.
Large doses of CNS depressants produce confusion that can persist for several days after the drug is discontinued. Opioid and barbiturate withdrawal also causes acute confusion, possibly with delirium. Other drugs that commonly cause confusion include lidocaine, a cardiac glycoside, indomethacin, cycloserine, chloroquine, atropine, and cimetidine.
HERB ALERT:Herbal remedies, such as St. John's wort, can cause confusion, especially when taken in conjunction with an antidepressant or other serotonergic drug.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Level of consciousness, decreased:
Medical causes
(Handbook of Signs & Symptoms (Third Edition))
Adrenal crisis
A decreased LOC, ranging from lethargy to coma, may develop within 8 to 12 hours of its onset
Early associated findings include progressive weakness, irritability, anorexia, a headache, nausea and vomiting, diarrhea, abdominal pain, and a fever. Later signs and symptoms include hypotension; a rapid, thready pulse; oliguria; cool, clammy skin; and flaccid extremities. The patient with chronic adrenocortical hypofunction may have hyperpigmented skin and mucous membranes.
Brain abscess
A decreased LOC varies from drowsiness to deep stupor, depending on the abscess size and site
Early signs and symptoms — a constant intractable headache, nausea, vomiting, and seizures — reflect increasing ICP. Typical later features include ocular disturbances (nystagmus, vision loss, and pupillary inequality) and signs of infection such as a fever. Other findings may include personality changes, confusion, abnormal behavior, dizziness, facial weakness, aphasia, ataxia, tremor, and hemiparesis.
Brain tumor
The patient’s LOC decreases slowly, from lethargy to coma
He may also experience apathy, behavior changes, memory loss, a decreased attention span, a morning headache, dizziness, vision loss, ataxia, and sensorimotor disturbances. Aphasia and seizures are possible, along with signs of hormonal imbalance, such as fluid retention or amenorrhea. Signs and symptoms vary according to the location and size of the tumor. In later stages, papilledema, vomiting, bradycardia, and a widening pulse pressure also appear. In the final stages, the patient may exhibit decorticate or decerebrate posture.
Cerebral aneurysm (ruptured)
Somnolence, confusion and, at times, stupor characterize a moderate bleed; deep coma occurs with severe bleeding, which can be fatal
The onset is usually abrupt, with a sudden, severe headache and nausea and vomiting. Nuchal rigidity, back and leg pain, a fever, restlessness, irritability, occasional seizures, and blurred vision point to meningeal irritation. The type and severity of other findings vary with the site and severity of the hemorrhage and may include hemiparesis, hemisensory defects, dysphagia, and visual defects.
Diabetic ketoacidosis
Diabetic ketoacidosis produces a rapid decrease in the patient’s LOC, ranging from lethargy to coma, commonly preceded by polydipsia, polyphagia, and polyuria
The patient may complain of weakness, anorexia, abdominal pain, nausea, and vomiting. He may also exhibit orthostatic hypotension; a fruity breath odor; Kussmaul’s respirations; warm, dry skin; and a rapid, thready pulse. Untreated, this condition invariably leads to coma and death.
Encephalitis
Within 24 to 48 hours after onset, the patient may develop changes in his LOC ranging from lethargy to coma
Other possible findings include an abrupt onset of a fever, a headache, nuchal rigidity, nausea, vomiting, irritability, personality changes, seizures, aphasia, ataxia, hemiparesis, nystagmus, photophobia, myoclonus, and cranial nerve palsies.
Encephalomyelitis (postvaccinal)
Postvaccinal encephalomyelitisis a life-threatening disorder that produces rapid deterioration in the patient’s LOC, from drowsiness to coma
He also experiences a rapid onset of a fever, a headache, nuchal rigidity, back pain, vomiting, and seizures.
Encephalopathy
With hepatic encephalopathy, signs and symptoms develop in four stages: in the prodromal stage, slight personality changes (disorientation, forgetfulness, slurred speech) and slight tremor; in the impending stage, tremor progressing to asterixis (the hallmark of hepatic encephalopathy), lethargy, aberrant behavior, and apraxia; in the stuporous stage, stupor and hyperventilation, with the patient noisy and abusive when aroused; in the comatose stage, coma with decerebrate posture, hyperactive reflexes, a positive Babinski’s reflex, and fetor hepaticus.
With life-threatening hypertensive encephalopathy, the LOC progressively decreases from lethargy to stupor to coma
Besides markedly elevated blood pressure, the patient may experience a severe headache, vomiting, seizures, vision disturbances, transient paralysis and, eventually, Cheyne-Stokes respirations.
With hypoglycemic encephalopathy,the patient’s LOC rapidly deteriorates from lethargy to coma. Early signs and symptoms include nervousness, restlessness, agitation, and confusion; hunger; alternate flushing and cold sweats; and a headache, trembling, and palpitations. Blurred vision progresses to motor weakness, hemiplegia, dilated pupils, pallor, a decreased pulse rate, shallow respirations, and seizures. Flaccidity and decerebrate posture appear late.
Depending on its severity, hypoxic encephalopathyproduces a sudden or gradual decrease in the LOC, leading to coma and brain death. Early on, the patient appears confused and restless, with cyanosis and increased heart and respiratory rates and blood pressure. Later, his respiratory pattern becomes abnormal, and assessment reveals a decreased pulse, blood pressure, and deep tendon reflexes (DTRs); a positive Babinski’s reflex; an absent doll’s eye sign; and fixed pupils.
With uremic encephalopathy,the LOC decreases gradually from lethargy to coma. Early on, the patient may appear apathetic, inattentive, confused, and irritable and may complain of a headache, nausea, fatigue, and anorexia. Other findings include vomiting, tremors, edema, papilledema, hypertension, cardiac arrhythmias, dyspnea, crackles, oliguria, and Kussmaul’s and Cheyne-Stokes respirations.
Heatstroke
As body temperature increases, the patient’s LOC gradually decreases from lethargy to coma
Early signs and symptoms include malaise, tachycardia, tachypnea, orthostatic hypotension, muscle cramps, rigidity, and syncope. The patient may be irritable, anxious, and dizzy and may report a severe headache. At the onset of heatstroke, the patient’s skin is hot, flushed, and diaphoretic with blotchy cyanosis; later, when his fever exceeds 105° F (40.5° C), his skin becomes hot, flushed, and anhidrotic. Pulse and respiratory rate increase markedly, and blood pressure drops precipitously. Other findings include vomiting, diarrhea, dilated pupils, and Cheyne-Stokes respirations.
Hypernatremia
Hypernatremia, life threatening if acute, causes the patient’s LOC to deteriorate from lethargy to coma
He is irritable and exhibits twitches progressing to seizures. Other associated signs and symptoms include a weak, thready pulse; nausea; malaise; a fever; thirst; flushed skin; and dry mucous membranes.
Hyperosmolar hyperglycemic nonketotic syndrome
LOC decreases rapidly from lethargy to coma
Early findings include polyuria, polydipsia, weight loss, and weakness. Later, the patient may develop hypotension, poor skin turgor, dry skin and mucous membranes, tachycardia, tachypnea, oliguria, and seizures.
Hypokalemia
LOC gradually decreases to lethargy; coma is rare
Other findings include confusion, nausea, vomiting, diarrhea, and polyuria; weakness, decreased reflexes, and malaise; and dizziness, hypotension, arrhythmias, and abnormal electrocardiogram results.
Hyponatremia
Hyponatremia, life threatening if acute, produces a decreased LOC in late stages
Early nausea and malaise may progress to behavior changes, confusion, lethargy, incoordination and, eventually, seizures and coma.
Hypothermia
With severe hypothermia(temperature below 90° F [32.2° C]), the patient’s LOC decreases from lethargy to coma. DTRs disappear, and ventricular fibrillation occurs, possibly followed by cardiopulmonary arrest. With mild to moderate hypothermia, the patient may experience memory loss and slurred speech as well as shivering, weakness, fatigue, and apathy. Other early signs and symptoms include ataxia, muscle stiffness, and hyperactive DTRs; diuresis; tachycardia and decreased respiratory rate and blood pressure; and cold, pale skin. Later, muscle rigidity and decreased reflexes may develop, along with peripheral cyanosis, bradycardia, arrhythmias, severe hypotension, a decreased respiratory rate with shallow respirations, and oliguria.
Intracerebral hemorrhage
Intracerebral hemorrhage is a life-threatening disorder that produces a rapid, steady loss of consciousness within hours, commonly accompanied by a severe headache, dizziness, nausea, and vomiting. Associated signs and symptoms vary and may include increased blood pressure, irregular respirations, a positive Babinski’s reflex, seizures, aphasia, decreased sensations, hemiplegia, decorticate or decerebrate posture, and dilated pupils.
Listeriosis
If listeriosis spreads to the nervous system and causes meningitis, signs and symptoms include a decreased LOC, a fever, a headache, and nuchal rigidity
Early signs and symptoms of listeriosis include a fever, myalgia, abdominal pain, nausea, vomiting, and diarrhea.
Gender cue
Infections during pregnancy may lead to premature delivery, infection of the neonate, or stillbirth.
Meningitis
Confusion and irritability are expected; however, stupor, coma, and seizures may occur in the patient with severe meningitis
A fever develops early, possibly accompanied by chills. Associated findings include a severe headache, nuchal rigidity, hyperreflexia and, possibly, opisthotonos. The patient exhibits Kernig’s and Brudzinski’s signs and, possibly, ocular palsies, photophobia, facial weakness, and hearing loss.
Pontine hemorrhage
A sudden, rapid decrease in the patient’s LOC to the point of coma occurs within minutes and death within hours
The patient may also exhibit total paralysis, decerebrate posture, a positive Babinski’s reflex, an absent doll’s eye sign, and bilateral miosis (however, the pupils remain reactive to light).
Seizure disorders
A complex partial seizure produces a decreased LOC, manifested as a blank stare, purposeless behavior (picking at clothing, wandering, lip smacking or chewing motions), and unintelligible speech
The seizure may be heralded by an aura and followed by several minutes of mental confusion.
An absence seizure usually involves a brief change in the patient’s LOC, indicated by blinking or eye rolling, a blank stare, and slight mouth movements.
A generalized tonic-clonic seizure typically begins with a loud cry and sudden loss of consciousness. Muscle spasm alternates with relaxation. Tongue biting, incontinence, labored breathing, apnea, and cyanosis may also occur. Consciousness returns after the seizure, but the patient remains confused and may have difficulty talking. He may complain of drowsiness, fatigue, a headache, muscle aching, and weakness and may fall into a deep sleep.
An atonic seizureproduces sudden unconsciousness for a few seconds.
Status epilepticus,rapidly recurring seizures without intervening periods of physiologic recovery and return of consciousness, can be life threatening.
Shock
A decreased LOC — lethargy progressing to stupor and coma — occurs late in shock
Associated findings include confusion, anxiety, and restlessness; hypotension; tachycardia; a weak pulse with narrowing pulse pressure; dyspnea; oliguria; and cool, clammy skin.
Hypovolemic shock is generally the result of massive or insidious bleeding, either internally or externally. Cardiogenic shock may produce chest pain or arrhythmias and signs of heart failure, such as dyspnea, a cough, edema, jugular vein distention, and weight gain. Septic shock may be accompanied by a high fever and chills. Anaphylactic shock usually involves stridor.
Stroke
Changes in the patient’s LOC vary in degree and onset, depending on the lesion’s size and location and the presence of edema
A thrombotic stroke usually follows multiple transient ischemic attacks (TIAs). Changes in the LOC may be abrupt or take several minutes, hours, or days. An embolic stroke occurs suddenly, and deficits reach their peak almost at once. Deficits associated with a hemorrhagic stroke usually develop over minutes or hours.
Associated findings vary with the stroke type and severity and may include disorientation; intellectual deficits, such as memory loss and poor judgment; personality changes; and emotional lability. Other possible findings include dysarthria, dysphagia, ataxia, aphasia, apraxia, agnosia, unilateral sensorimotor loss, and vision disturbances. In addition, urine retention, incontinence, constipation, a headache, vomiting, and seizures may occur.
Subdural hemorrhage (acute)
Acute subdural hemorrhageis a potentially life-threatening disorder in which agitation and confusion are followed by a progressively decreasing LOC from somnolence to coma
The patient may also experience a headache, a fever, unilateral pupil dilation, decreased pulse and respiratory rates, a widening pulse pressure, seizures, hemiparesis, and a positive Babinski’s reflex.
Thyroid storm
The patient’s LOC decreases suddenly and can progress to coma
Irritability, restlessness, confusion, and psychotic behavior precede the deterioration. Associated signs and symptoms include tremors and weakness; vision disturbances; tachycardia, arrhythmias, angina, and acute respiratory distress; warm, moist, flushed skin; and vomiting, diarrhea, and a fever of up to 105 ° F (40.5° C).
TIA
The patient’s LOC decreases abruptly (with varying severity) and gradually returns to normal within 24 hours
Site-specific findings may include vision loss, nystagmus, aphasia, dizziness, dysarthria, unilateral hemiparesis or hemiplegia, tinnitus, paresthesia, dysphagia, or staggering or incoordinated gait.
West Nile encephalitis
West Nile encephalitis is a brain infection that’s caused by the West Nile virus, a mosquito-borne flavivirus commonly found in Africa, West Asia, and the Middle East and, less commonly, in the United States
Mild infection is common. Signs and symptoms include a fever, a headache, and body aches, commonly with a skin rash and swollen lymph glands. More severe infection is marked by a high fever, a headache, neck stiffness, stupor, disorientation, coma, tremors, occasional convulsions, paralysis and, rarely, death.
Other causes
Alcohol
Alcohol use causes varying degrees of sedation, irritability, and incoordination; intoxication commonly causes stupor.
Drugs
Sedation and other degrees of a decreased LOC can result from an overdose of a barbiturate, another central nervous system depressant, or aspirin.
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Source: Handbook of Signs & Symptoms (Third Edition), 2006
Seizures, complex partial:
Medical causes
(Handbook of Signs & Symptoms (Third Edition))
Brain abscess
If the brain abscess is in the temporal lobe, complex partial seizures commonly occur after the abscess disappears. Related problems may include a headache, nausea, vomiting, generalized seizures, and a decreased level of consciousness (LOC). The patient may also develop central facial weakness, auditory receptive aphasia, hemiparesis, and ocular disturbances.
Head trauma
Severe trauma to the temporal lobe (especially from a penetrating injury) can produce complex partial seizures months or years later. The seizures may decrease in frequency and eventually stop. Head trauma also causes generalized seizures and behavior and personality changes.
Herpes simplex encephalitis
The herpes simplex virus commonly attacks the temporal lobe, resulting in complex partial seizures. Other features include a fever, a headache, coma, and generalized seizures.
Temporal lobe tumor
Complex partial seizures may be the first sign of a temporal lobe tumor. Other signs and symptoms include a headache, pupillary changes, and mental dullness. Increased intracranial pressure may cause a decreased LOC, vomiting and, possibly, papilledema.
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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.
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Source: Handbook of Signs & Symptoms (Third Edition), 2006
Malignant brain tumors:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
The cause of most brain tumors is unknown, but exposure to ionizing radiation is a known environmental risk. Additionally, most malignant tumors of the brain are of metastatic origin; 20% to 40% of patients with cancer develop brain metastasis.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Agitation:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Affective disturbances
Agitation may occur in either the depressive or manic phase of affective disturbances and in personality disorders, such as borderline and antisocial personality disorders. The hallmark of the depressive form is depressed mood upon awakening, which eases during the day. Chronic anxiety may be mild or severe. Psychomotor agitation may be characterized by an inability to sit still, hand-wringing, pacing, and irritability. Other findings in the manic state may include decreased sleep, pressured speech, and grandiosity.
Alcohol withdrawal syndrome
Mild to severe agitation occurs with hyperactivity, tremors, and anxiety. In delirium tremens, the potentially life-threatening stage of alcohol withdrawal, severe agitation accompanies hallucinations, insomnia, diaphoresis, and depressed mood. Pulse rate and temperature rise as withdrawal progresses; status epilepticus, cardiac arrhythmias, and shock can occur.
Anxiety
Anxiety is a common symptom that produces varying degrees of agitation. The patient may be unaware of his anxiety or may complain of it without knowing its cause. Other findings may include nausea, vomiting, diarrhea, cool and clammy skin, frontal headache, back pain, insomnia, and tremors.
Chronic renal failure
Moderate to severe agitation occurs in chronic renal failure, which is marked by confusion and memory loss. The agitation is accompanied by diverse signs and symptoms, such as nausea, vomiting, anorexia, mouth ulcers, ammonia breath odor, GI bleeding, pallor, edema, dry skin, and uremic frost.
Dementia
Mild to severe agitation can result from many common dementia syndromes, such as Alzheimer’s and Huntington’s diseases. The patient may display a decrease in memory, attention span, problem-solving ability, and alertness. Hypoactivity, wandering behavior, hallucinations, aphasia, and insomnia may also occur.
Drug withdrawal syndrome
Findings vary with the drug but include mild to severe agitation, anxiety, abdominal cramps, diaphoresis, and anorexia. In opioid or barbiturate withdrawal, a decreased level of consciousness (LOC), seizures, and elevated blood pressure, heart rate, and respiratory rate can also occur.
Hepatic encephalopathy
Agitation occurs only in fulminating encephalopathy. Other findings include drowsiness, stupor, fetor hepaticus, asterixis, and hyperreflexia.
Hypersensitivity reaction
Moderate to severe agitation may be the first sign of a hypersensitivity reaction. Depending on the severity of the reaction, agitation may be accompanied by urticaria, pruritus, and facial and dependent edema.
In anaphylactic shock, a potentially life-threatening reaction, agitation occurs rapidly along with apprehension, urticaria or diffuse erythema, warm and moist skin, paresthesia, pruritus, edema, dyspnea, wheezing, stridor, hypotension, and tachycardia. Abdominal cramps, vomiting, and diarrhea can also occur.
Hypoxemia
Beginning as restlessness, agitation rapidly worsens in hypoxemia. The patient may be confused and have impaired judgment and motor coordination. He may also have tachycardia, tachypnea, dyspnea, and cyanosis.
Increased intracranial pressure (ICP)
Agitation usually precedes other early signs and symptoms, such as headache, nausea, and vomiting. Increased ICP produces respiratory changes, such as Cheyne-Stokes, cluster, ataxic, or apneustic breathing; sluggish, nonreactive, or unequal pupils; widening pulse pressure; tachycardia; decreased LOC; seizures; and motor changes, such as decerebrate or decorticate posture.
Organic brain syndrome
In organic brain syndrome, agitation is manifested as hyperactivity, emotional lability, confusion, and memory loss. Slurred or incoherent speech and paranoid behavior may also occur.
Post–head trauma syndrome
Shortly—or even years—after injury, mild to severe agitation develops, characterized by disorientation, loss of concentration, angry outbursts, and emotional lability. Fatigue, wandering behavior, and poor judgment are other findings.
Vitamin B6 Deficiency
Agitation can range from mild to severe. Other effects include seizures, peripheral paresthesia, and dermatitis. Oculogyric crisis may also occur.
Other causes
Drugs
Mild to moderate agitation, which is commonly dose related, is an adverse effect of central nervous system stimulants—especially appetite suppressants, such as amphetamines and amphetamine-like drugs; sympathomimetics such as ephedrine; caffeine; and theophylline.
Radiographic contrast media
Injection of a contrast medium during various diagnostic tests may produce moderate to severe agitation along with other signs of hypersensitivity.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Confusion:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Brain tumor
In the early stages of a brain tumor, confusion is usually mild and difficult to detect. As the tumor impinges on cerebral structures, however, confusion worsens and the patient may exhibit personality changes, bizarre behavior, sensory and motor deficits, visual field deficits, and aphasia.
Cerebrovascular disorders
These disorders produce confusion due to tissue hypoxia and ischemia. Confusion may be insidious and fleeting, as in a transient ischemic attack, or acute and permanent, as in a stroke.
Decreased cerebral perfusion
Mild confusion is an early symptom of decreased cerebral perfusion. Associated findings usually include hypotension, tachycardia or bradycardia, irregular pulse, ventricular gallop, edema, and cyanosis.
Fluid and electrolyte imbalance
The extent of the imbalance determines the severity of the patient’s confusion. Typically, he’ll show signs of dehydration, such as lassitude, poor skin turgor, dry skin and mucous membranes, and oliguria. He may also develop hypotension and a low-grade fever.
Head trauma
Concussion, contusion, and brain hemorrhage may produce confusion at the time of injury, shortly afterward, or months or even years afterward. The patient may be delirious, with periodic loss of consciousness. Vomiting, severe headache, pupillary changes, and sensory and motor deficits are also common.
Heatstroke
This disorder causes pronounced confusion that gradually worsens as body temperature rises. Initially, the patient may be irritable and dizzy; later, he may become delirious, have seizures, and lose consciousness.
Hypothermia
Confusion may be an early sign of this disorder. Typically, the patient displays slurred speech, cold and pale skin, hyperactive deep tendon reflexes, rapid pulse, and decreased blood pressure and respiratory rate. As his body temperature continues to drop, his confusion progresses to stupor and coma, his muscles become rigid, and his respiratory rate decreases.
Hypoxemia
Acute pulmonary disorders that result in hypoxemia produce confusion that can range from mild disorientation to delirium. Chronic pulmonary disorders produce persistent confusion.
Infection
A severe generalized infection, such as sepsis, commonly produces delirium. Central nervous system (CNS) infections, such as meningitis, cause varying degrees of confusion along with headache and nuchal rigidity.
Metabolic encephalopathy
Both hyperglycemia and hypoglycemia can produce sudden confusion. A patient with hypoglycemia may also experience transient delirium and seizures. Uremic and hepatic encephalopathies produce gradual confusion that may progress to seizures and coma. Usually, the patient also experiences tremors and restlessness.
Nutritional deficiencies
Inadequate dietary intake of thiamine, niacin, or vitamin B12 produces insidious, progressive confusion and possibly mental deterioration.
Seizure disorders
Mild to moderate confusion may immediately follow any type of seizure. The confusion usually disappears within several hours.
Thyroid hormone disorders
Hyperthyroidism produces mild to moderate confusion along with nervousness, inability to concentrate, weight loss, flushed skin, and tachycardia. Hypothyroidism produces mild, insidious confusion and memory loss; weight gain; bradycardia; and fatigue.
Other causes
Alcohol
Intoxication causes confusion and stupor, and alcohol withdrawal may cause delirium and seizures.
Drugs
Large doses of CNS depressants produce confusion that can persist for several days after the drug is discontinued. Opioid and barbiturate withdrawal also causes acute confusion, possibly with delirium. Other drugs that commonly cause confusion include lidocaine, cardiac glycosides, indomethacin, cycloserine, chloroquine, atropine, and cimetidine.
Heavy metal poisoning
Chronic ingestion or inhalation of heavy metals (such as lead, arsenic, mercury, and manganese) eventually produces confusion and, typically, weakness and drowsiness. The patient may also experience headache, vomiting, seizures, tremors, gait disturbances, and mental deterioration.
Herb Alert
Herbal medicines, such as St. John’s wort, can cause confusion, especially when taken in conjunction with an antidepressant or another serotonergic drug.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Level of consciousness, decreased:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Adrenal crisis
Decreased LOC, ranging from lethargy to coma, may develop within 8 to 12 hours of onset. Early associated findings include progressive weakness, irritability, anorexia, headache, nausea and vomiting, diarrhea, abdominal pain, and fever. Later signs and symptoms include hypotension; rapid, thready pulse; oliguria; cool, clammy skin; and flaccid extremities. The patient with chronic adrenocortical hypofunction may have hyperpigmented skin and mucous membranes.
Brain abscess
Decreased LOC varies from drowsiness to deep stupor, depending on abscess size and site. Early signs and symptoms—constant intractable headache, nausea, vomiting, and seizures—reflect increasing ICP. Typical later features include ocular disturbances (nystagmus, vision loss, and pupillary inequality) and signs of infection such as fever. Other findings may include personality changes, confusion, abnormal behavior, dizziness, facial weakness, aphasia, ataxia, tremor, and hemiparesis.
Brain tumor
LOC decreases slowly, from lethargy to coma. The patient may also experience apathy, behavior changes, memory loss, decreased attention span, morning headache, dizziness, vision loss, ataxia, and sensorimotor disturbances. Aphasia and seizures are possible, along with signs of hormonal imbalance, such as fluid retention or amenorrhea. Signs and symptoms vary according to the location and size of the tumor. In later stages, papilledema, vomiting, bradycardia, and widening pulse pressure also appear. In the final stages, the patient may exhibit decorticate or decerebrate posture.
Cerebral aneurysm (ruptured)
Somnolence, confusion and, at times, stupor characterize a moderate bleed; deep coma occurs with severe bleeding, which can be fatal. Onset is usually abrupt, with sudden, severe headache, nausea, and vomiting. Nuchal rigidity, back and leg pain, fever, restlessness, irritability, occasional seizures, and blurred vision point to meningeal irritation. The type and severity of other findings vary with the site and severity of the hemorrhage and may include hemiparesis, hemisensory defects, dysphagia, and visual defects.
Cerebral contusion
Usually unconscious for a prolonged period, the patient may develop dilated, nonreactive pupils and decorticate or decerebrate posture. If he’s conscious or recovers consciousness, he may be drowsy, confused, disoriented, agitated, or even violent. Associated findings include blurred or double vision, fever, headache, pallor, diaphoresis, tachycardia, altered respirations, aphasia, and hemiparesis. Residual effects include seizures, impaired mental status, slight hemiparesis, and vertigo.
Diabetic ketoacidosis
This disorder produces a rapid decrease in LOC, ranging from lethargy to coma, commonly preceded by polydipsia, polyphagia, and polyuria. The patient may complain of weakness, anorexia, abdominal pain, nausea, and vomiting. He may also exhibit orthostatic hypotension; fruity breath odor; Kussmaul’s respirations; warm, dry skin; and a rapid, thready pulse. Untreated, this condition invariably leads to coma and death.
Encephalitis
Within 24 to 48 hours after onset, the patient may develop LOC changes ranging from lethargy to coma. Other possible findings include abrupt onset of fever, headache, nuchal rigidity, nausea, vomiting, irritability, personality changes, seizures, aphasia, ataxia, hemiparesis, nystagmus, photophobia, myoclonus, and cranial nerve palsies.
Encephalomyelitis (postvaccinal)
This life-threatening disorder produces rapid LOC deterioration from drowsiness to coma. The patient also experiences rapid onset of fever, headache, nuchal rigidity, back pain, vomiting, and seizures.
Encephalopathy
With hepatic encephalopathy, signs and symptoms develop in four stages: in the prodromal stage, slight personality changes (disorientation, forgetfulness, slurred speech) and slight tremor; in the impending stage, tremor progressing to asterixis (the hallmark of hepatic encephalopathy), lethargy, aberrant behavior, and apraxia; in the stuporous stage, stupor and hyperventilation, with the patient noisy and abusive when aroused; in the comatose stage, coma with decerebrate posture, hyperactive reflexes, positive Babinski’s reflex, and fetor hepaticus.
With life-threatening hypertensive encephalopathy, LOC progressively decreases from lethargy to stupor to coma. Besides markedly elevated blood pressure, the patient may experience severe headache, vomiting, seizures, visual disturbances, transient paralysis, and eventually Cheyne-Stokes respirations.
With hypoglycemic encephalopathy, LOC rapidly deteriorates from lethargy to coma. Early signs and symptoms include nervousness, restlessness, agitation, and confusion; hunger; alternate flushing and cold sweats; and headache, trembling, and palpitations. Blurred vision progresses to motor weakness, hemiplegia, dilated pupils, pallor, decreased pulse rate, shallow respirations, and seizures. Flaccidity and decerebrate posture appear late.
Depending on its severity, hypoxic encephalopathy produces a sudden or gradual decrease in LOC, leading to coma and brain death. Early on, the patient appears confused and restless, with cyanosis and increased heart and respiratory rates and blood pressure. Later, his respiratory pattern becomes abnormal, and assessment reveals decreased pulse, blood pressure, and deep tendon reflexes (DTRs); Babinski’s reflex; absent doll’s eye sign; and fixed pupils.
With uremic encephalopathy, LOC decreases gradually from lethargy to coma. Early on, the patient may appear apathetic, inattentive, confused, and irritable and may complain of headache, nausea, fatigue, and anorexia. Other findings include vomiting, tremors, edema, papilledema, hypertension, cardiac arrhythmias, dyspnea, crackles, oliguria, and Kussmaul’s and Cheyne-Stokes respirations.
Epidural hemorrhage (acute)
This life-threatening posttraumatic disorder produces momentary loss of consciousness, sometimes followed by a lucid interval. While lucid, the patient has a severe headache, nausea, vomiting, and bladder distention. Rapid deterioration in consciousness follows, possibly leading to coma. Other findings include irregular respirations, seizures, decreased and bounding pulse, increased pulse pressure, hypertension, unilateral or bilateral fixed and dilated pupils, unilateral hemiparesis or hemiplegia, decerebrate posture, and Babinski’s reflex.
Heatstroke
As body temperature increases, LOC gradually decreases from lethargy to coma. Early signs and symptoms include malaise, tachycardia, tachypnea, orthostatic hypotension, muscle cramps, rigidity, and syncope. The patient may be irritable, anxious, and dizzy and may report a severe headache. At the onset of heatstroke, the patient’s skin is hot, flushed, and diaphoretic with blotchy cyanosis; later, when his fever exceeds 105° F (40.5° C), his skin becomes hot, flushed, and anhidrotic. Pulse and respiratory rate increase markedly, and blood pressure drops precipitously. Other findings include vomiting, diarrhea, dilated pupils, and Cheyne-Stokes respirations.
Hypercapnia with pulmonary syndrome
LOC decreases gradually from lethargy to coma (usually not prolonged). The patient becomes confused or drowsy and develops asterixis and muscle twitching. He may complain of headache and exhibit mental dullness, papilledema, and small, reactive pupils.
Hypernatremia
This disorder, life-threatening if acute, causes LOC to deteriorate from lethargy to coma. The patient is irritable and exhibits twitches progressing to seizures. Other associated signs and symptoms include a weak, thready pulse; nausea; malaise; fever; thirst; flushed skin; and dry mucous membranes.
Hyperosmolar hyperglycemic nonketotic syndrome
LOC decreases rapidly from lethargy to coma. Early findings include polyuria, polydipsia, weight loss, and weakness. Later, the patient may develop hypotension, poor skin turgor, dry skin and mucous membranes, tachycardia, tachypnea, oliguria, and seizures.
Hyperventilation syndrome
Brief episodes of unconsciousness follow stress-induced deep, rapid breathing associated with anxiety and agitation. Associated findings include dizziness, circumoral and peripheral paresthesia, twitching, carpopedal spasm, and arrhythmias.
Hypokalemia
LOC gradually decreases to lethargy; coma is rare. Other findings include confusion, nausea, vomiting, diarrhea, and polyuria; weakness, decreased reflexes, and malaise; and dizziness, hypotension, arrhythmias, and abnormal electrocardiogram results.
Hyponatremia
This disorder, life-threatening if acute, produces decreased LOC in late stages. Early nausea and malaise may progress to behavior changes, confusion, lethargy, incoordination and, eventually, seizures and coma.
Hypothermia
With severe hypothermia (temperature below 90° F [32.2° C]), LOC decreases from lethargy to coma. DTRs disappear, and ventricular fibrillation occurs, possibly followed by cardiopulmonary arrest. With mild to moderate hypothermia, the patient may experience memory loss and slurred speech as well as shivering, weakness, fatigue, and apathy. Other early signs and symptoms include ataxia, muscle stiffness, and hyperactive DTRs; diuresis; tachycardia and decreased respiratory rate and blood pressure; and cold, pale skin. Later, muscle rigidity and decreased reflexes may develop, along with peripheral cyanosis, bradycardia, arrhythmias, severe hypotension, decreased respiratory rate with shallow respirations, and oliguria.
Intracerebral hemorrhage
This life-threatening disorder produces a rapid, steady loss of consciousness within hours, commonly accompanied by severe headache, dizziness, nausea, and vomiting. Associated signs and symptoms vary and may include increased blood pressure, irregular respirations, Babinski’s reflex, seizures, aphasia, decreased sensations, hemiplegia, decorticate or decerebrate posture, and dilated pupils.
Listeriosis
If this serious infection spreads to the nervous system and causes meningitis, signs and symptoms include decreased LOC, fever, headache, and nuchal rigidity. Early signs and symptoms of listeriosis include fever, myalgias, abdominal pain, nausea, vomiting, and diarrhea.
Gender cue Infections during pregnancy may lead to premature delivery, infection of the neonate, or stillbirth.
Meningitis
Confusion and irritability are expected; however, stupor, coma, and seizures may occur in those with severe meningitis. Fever develops early, possibly accompanied by chills. Associated findings include severe headache, nuchal rigidity, hyperreflexia and, possibly, opisthotonos. The patient exhibits Kernig’s and Brudzinski’s signs and, possibly, ocular palsies, photophobia, facial weakness, and hearing loss.
Myxedema crisis
The patient may exhibit a swift decline in LOC. Other findings include severe hypothermia, hypoventilation, hypotension, bradycardia, hypoactive reflexes, periorbital and peripheral edema, impaired hearing and balance, and seizures.
Pontine hemorrhage
A sudden, rapid decrease in LOC to the point of coma occurs within minutes and death within hours. The patient may also exhibit total paralysis, decerebrate posture, Babinski’s reflex, absent doll’s eye sign, and bilateral miosis (however, the pupils remain reactive to light).
Seizure disorders
A complex partial seizure produces decreased LOC, manifested as a blank stare, purposeless behavior (picking at clothing, wandering, lip smacking or chewing motions), and unintelligible speech. The seizure may be heralded by an aura and followed by several minutes of mental confusion.
An absence seizure usually involves a brief change in LOC, indicated by blinking or eye rolling, blank stare, and slight mouth movements.
A generalized tonic-clonic seizure typically begins with a loud cry and sudden loss of consciousness. Muscle spasm alternates with relaxation. Tongue biting, incontinence, labored breathing, apnea, and cyanosis may also occur. Consciousness returns after the seizure, but the patient remains confused and may have difficulty talking. He may complain of drowsiness, fatigue, headache, muscle aching, and weakness and may fall into deep sleep.
An atonic seizure produces sudden unconsciousness for a few seconds.
Status epilepticus, rapidly recurring seizures without intervening periods of physiologic recovery and return of consciousness, can be life threatening.
Shock
Decreased LOC—lethargy progressing to stupor and coma—occurs late in shock. Associated findings include confusion, anxiety, and restlessness; hypotension; tachycardia; weak pulse with narrowing pulse pressure; dyspnea; oliguria; and cool, clammy skin.
Hypovolemic shock is generally the result of massive or insidious bleeding, either internally or externally. Cardiogenic shock may produce chest pain or arrhythmias and signs of heart failure, such as dyspnea, cough, edema, jugular vein distention, and weight gain. Septic shock may be accompanied by high fever and chills. Anaphylactic shock usually involves stridor.
Stroke
LOC changes vary in degree and onset, depending on the lesion’s size and location and the presence of edema. A thrombotic stroke usually follows multiple transient ischemic attacks (TIAs). LOC changes may be abrupt or take several minutes, hours, or days. An embolic stroke occurs suddenly, and deficits reach their peak almost at once. Deficits associated with a hemorrhagic stroke usually develop over minutes or hours.
Associated findings vary with stroke type and severity and may include disorientation; intellectual deficits, such as memory loss and poor judgment; personality changes; and emotional lability. Other possible findings include dysarthria, dysphagia, ataxia, aphasia, apraxia, agnosia, unilateral sensorimotor loss, and visual disturbances. In addition, urine retention, incontinence, constipation, headache, vomiting, and seizures may occur.
Subdural hematoma (chronic)
LOC deteriorates slowly. Other signs and symptoms include confusion, decreased ability to concentrate, and personality changes accompanied by headache, light-headedness, seizures, and a dilated ipsilateral pupil with ptosis.
Subdural hemorrhage (acute)
With this potentially life-threatening disorder, agitation and confusion are followed by progressively decreasing LOC from somnolence to coma. The patient may also experience headache, fever, unilateral pupil dilation, decreased pulse and respiratory rates, widening pulse pressure, seizures, hemiparesis, and Babinski’s reflex.
Thyroid storm
LOC decreases suddenly and can progress to coma. Irritability, restlessness, confusion, and psychotic behavior precede the deterioration. Associated signs and symptoms include tremors and weakness; visual disturbances; tachycardia, arrhythmias, angina, and acute respiratory distress; warm, moist, flushed skin; and vomiting, diarrhea, and fever to 105°F (40.5°C).
TIA
LOC decreases abruptly (with varying severity) and gradually returns to normal within 24 hours. Site-specific findings may include vision loss, nystagmus, dizziness, dysarthria, unilateral hemiparesis or hemiplegia, tinnitus, paresthesia, staggering or incoordinated gait, aphasia, or dysphagia.
West Nile encephalitis
This brain infection is caused by the West Nile virus, a mosquito-borne flavivirus commonly found in Africa, West Asia, and the Middle East and, less commonly, in the United States. Mild infection is common. Signs and symptoms include fever, headache, and body aches, commonly with skin rash and swollen lymph glands. More severe infection is marked by high fever, headache, neck stiffness, stupor, disorientation, coma, tremors, occasional seizures, paralysis and, rarely, death.
Other causes
Alcohol
Alcohol use causes varying degrees of sedation, irritability, and incoordination; intoxication commonly causes stupor.
Drugs
Sedation and other degrees of decreased LOC can result from an overdose of a barbiturate, another central nervous system depressant, or aspirin.
Poisoning
Toxins, such as lead, carbon monoxide, and snake venom, can cause varying degrees of decreased LOC. Confusion is common, as are headache, nausea, and vomiting. Other general features include hypotension, cardiac arrhythmias, dyspnea, sensorimotor loss, and seizures.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Seizures, complex partial:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Brain abscess
If the brain abscess is in the temporal lobe, complex partial seizures commonly occur after the abscess disappears. Related problems may include headache, nausea, vomiting, generalized seizures, and a decreased level of consciousness (LOC). The patient may also develop central facial weakness, auditory receptive aphasia, hemiparesis, and ocular disturbances.
Head trauma
Severe trauma to the temporal lobe (especially from a penetrating injury) can produce complex partial seizures months or years later. The seizures may decrease in frequency and eventually stop. Head trauma also causes generalized seizures and behavior and personality changes.
Herpes simplex encephalitis
The herpes simplex virus commonly attacks the temporal lobe, resulting in complex partial seizures. Other features include fever, headache, coma, and generalized seizures.
Temporal lobe tumor
Complex partial seizures may be the first sign of this disorder. Other signs and symptoms include headache, pupillary changes, and mental dullness. Increased intracranial pressure may cause a decreased LOC, vomiting and, possibly, papilledema.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Syncope:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Aortic arch syndrome
With this syndrome, the patient experiences syncope and may exhibit weak or abruptly absent carotid pulses and unequal or absent radial pulses. Early signs and symptoms include night sweats, pallor, nausea, anorexia, weight loss, arthralgia, and Raynaud’s phenomenon. He may also develop hypotension in the arms; neck, shoulder, and chest pain; paresthesia; intermittent claudication; bruits; vision disturbances; and dizziness.
Aortic stenosis
A cardinal late sign, syncope is accompanied by exertional dyspnea and angina. Related findings include marked fatigue, orthopnea, paroxysmal nocturnal dyspnea, palpitations, and diminished carotid pulses. Typically, auscultation reveals atrial and ventricular gallops as well as a harsh, crescendo-decrescendo systolic ejection murmur that’s loudest at the right sternal border of the second intercostal space.
Cardiac arrhythmias
Any arrhythmia that decreases cardiac output and impairs cerebral circulation may cause syncope. Other effects—such as palpitations, pallor, confusion, diaphoresis, dyspnea, and hypotension—usually develop first. However, with Adams-Stokes syndrome, syncope may occur without warning. During syncope, the patient develops asystole, which may precipitate spasm and myoclonic jerks if prolonged. He also displays an ashen pallor that progresses to cyanosis, incontinence, bilateral Babinski’s reflex, and fixed pupils.
Carotid sinus hypersensitivity
Syncope is triggered by compression of the carotid sinus, which may be caused by turning the head to one side or by wearing a tight collar. The fainting episode is usually of short duration.
Hypoxemia
Regardless of its cause, severe hypoxemia may produce syncope. Common related effects include confusion, tachycardia, restlessness, and incoordination.
Orthostatic hypotension
Syncope occurs when the patient rises quickly from a recumbent position. Look for a drop of 10 to 20 mm Hg or more in systolic or diastolic blood pressure as well as tachycardia, pallor, dizziness, blurred vision, nausea, and diaphoresis.
Transient ischemic attacks
Marked by transient neurologic deficits, these attacks may produce syncope and decreased level of consciousness. Other findings vary with the affected artery but may include vision loss, nystagmus, aphasia, dysarthria, unilateral numbness, hemiparesis or hemiplegia, tinnitus, facial weakness, dysphagia, and staggering or uncoordinated gait.
Vagal glossopharyngeal neuralgia
With this disorder, localized pressure may trigger pain in the base of the tongue, pharynx, larynx, tonsils, and ear, resulting in syncope that lasts for several minutes.
Other causes
Drugs
Quinidine may cause syncope—and possibly sudden death—associated with ventricular fibrillation. Prazosin may cause severe orthostatic hypotension and syncope, usually after the first dose. Occasionally, griseofulvin, levodopa, and indomethacin can produce syncope.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Dementia:
Differential Overview
(Field Guide to Bedside Diagnosis)
❑ Alzheimer disease
❑ Multi-infarct dementia
❑ Depression
❑ Drugs
❑ Parkinson disease
❑ Frontal lobe dementia
❑ Vitamin B12 deficiency
❑ HIV encephalopathy
❑ Korsakoff syndrome
❑ Brain tumor
❑ Normal pressure hydrocephalus
❑ Chronic subdural hematoma
❑ Neurosyphilis
❑ Creutzfeldt-Jakob
❑ Wilson disease
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Source: Field Guide to Bedside Diagnosis, 2007
Syncope:
Differential Overview
(Field Guide to Bedside Diagnosis)
Orthostatic/Autonomic
❑ Neurally mediated hypotension
❑ Volume depletion
❑ Cough syncope
❑ Anemia
❑ Autonomic insufficiency
Cardiac/Obstructive
❑ Myocardial infarction
❑ Pulmonary embolism
❑ Aortic stenosis
❑ Hypertrophic obstructive cardiomyopathy
❑ Aortic dissection
❑ Cardiac tamponade
❑ Left atrial myxoma
Cardiac/Dysrhythmic
❑ Complete heart block
❑ Sick sinus syndrome
❑ Tachyarrhythmia
❑ Carotid sinus hypersensitivity
Neurologic
❑ Vertebrobasilar ischemia
❑ Hypoglycemia
❑ Unwitnessed seizure
❑ Subclavian steal syndrome
Psychologic
❑ Hyperventilation
❑ Hysterical faint
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Source: Field Guide to Bedside Diagnosis, 2007
Delirium/Hallucinations:
Differential Overview
(Field Guide to Bedside Diagnosis)
Systemic
❑ Drugs/toxins
❑ Sepsis
❑ Hypoglycemia
❑ Hypercalcemia
❑ Hyponatremia
❑ Shock
❑ Delirium tremens
❑ Vitamin B12 deficiency
❑ Hypoxia
❑ Hypercapnia
❑ Thyrotoxicosis
❑ Uremia
❑ Hepatic encephalopathy
❑ Thiamine deficiency
❑ Heat stroke
❑ Hypothermia
❑ Lead intoxication
❑ Carbon monoxide poisoning
Neurologic
❑ Concussion
❑ Hypertensive encephalopathy
❑ Subdural hematoma
❑ Postictal
❑ Transient global amnesia
❑ Meningitis
❑ Right parietal stroke
❑ Encephalitis
❑ Vasculitis
❑ Carcinomatous meningitis
Hallucinations
❑ Drugs
❑ Schizophrenia
❑ Temporal lobe epilepsy
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Source: Field Guide to Bedside Diagnosis, 2007
Brain tumors, malignant:
Causes
(Handbook of Diseases)
Some tumors are congenital, whereas others are hereditary. The cause of most brain tumors is unknown.
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Source: Handbook of Diseases, 2003
Brain abscess:
Causes
(Handbook of Diseases)
A brain abscess usually occurs secondary to some other infection, especially otitis media, sinusitis, dental abscess, and mastoiditis. Other causes include subdural empyema; bacterial endocarditis; human immunodeficiency virus infection; bacteremia; pulmonary or pleural infection; pelvic, abdominal, and skin infections; and cranial trauma, such as a penetrating head wound or compound skull fracture.
This condition also occurs in about 2% of children with congenital heart disease, possibly because the hypoxic brain is a good culture medium for bacteria. Common infecting organisms are pyogenic bacteria, such as Staphylococcus aureus and Streptococcus viridans. Penetrating head trauma or bacteremia usually leads to staphylococcal infection; pulmonary disease, to streptococcal infection. In up to 25% of patients, an original source isn’t discovered.
Pathophysiology
A brain abscess usually begins with localized inflammatory necrosis and edema, septic thrombosis of vessels, and suppurative encephalitis. This is followed by thick encapsulation of accumulated pus, and adjacent meningeal infiltration by neutrophils, lymphocytes, and plasma cells. Increasing pressure in the brain results in more damage.
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Source: Handbook of Diseases, 2003
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.
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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
Agitation:
Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Affectivedisturbance
Agitation may occur in depressed and manic phases of affectivedisturbance and in personality disorders, such as borderline and antisocial personality disorders. In its depressive form, chronic anxiety occurs with varying severity. The hallmark is depressed mood upon awakening, which eases during the day. Psychomotor agitation may be characterized by an inability to sit still, hand-wringing, pacing, and irritability. Other findings in manic states may include decreased sleep, pressured speech, and grandiosity.
Alcohol withdrawal syndrome
With alcohol withdrawal syndrome, mild to severe agitation occurs. It may be accompanied by hyperactivity, tremors, and anxiety. With delirium tremens, the potentially life-threatening stage of alcohol withdrawal, severe agitation accompanies hallucinations, insomnia, diaphoresis, and depressed mood. Pulse rate and temperature rise as withdrawal progresses; status epilepticus, cardiac exhaustion, and shock can occur.
Anxiety
Anxiety produces varying degrees of agitation. The patient may be unaware of his anxiety or may complain of it without knowing its cause. Other findings include nausea, vomiting, diarrhea, cool and clammy skin, frontal headache, back pain, insomnia, and tremors.
Chronic renal failure
Moderate to severe agitation occurs with chronic renal failure, marked especially by confusion and memory loss. The agitation is accompanied by diverse signs and symptoms, such as nausea, vomiting, anorexia, mouth ulcers, ammonia breath odor, GI bleeding, pallor, edema, dry skin, and uremic frost.
Dementia
Mild to severe agitation related to dementia can result from many common syndromes, such as Alzheimer’s and Huntington’s diseases. The patient may display a decrease in memory, attention span, problem-solving ability, and alertness. Hypoactivity, wandering behavior, hallucinations, aphasia, and insomnia may also occur.
Drug withdrawal syndrome
In drug withdrawal syndrome, mild to severe agitation occurs. Related findings vary with the drug but include anxiety, abdominal cramps, diaphoresis, and anorexia. With narcotic or barbiturate withdrawal, a decreased level of consciousness (LOC), seizures, and elevated blood pressure, heart rate, and respiratory rate can also occur.
Hepatic encephalopathy
Agitation occurs with fulminating hepatic encephalopathy. Other findings include drowsiness, stupor, fetor hepaticus (musty, sweet breath odor), asterixis, and hyperreflexia. Lethargy, aberrant behavior, and apraxia may also occur.
Hypersensitivity reaction
Moderate to severe agitation may be the first sign of a hypersensitivity reaction. Depending on the severity of the reaction, agitation may be accompanied by urticaria, pruritus, and facial and dependent edema.
With anaphylactic shock, a potentially life-threatening reaction, agitation occurs rapidly along with apprehension, urticaria or diffuse erythema, skin that’s warm and moist, paresthesia, pruritus, edema, dyspnea, wheezing, stridor, hypotension, and tachycardia. Abdominal cramps, vomiting, and diarrhea can also occur.
Hypoxemia
Beginning as restlessness, agitation rapidly worsens with hypoxemia. The patient may be confused and have impaired judgment and motor coordination. He may also have tachycardia, tachypnea, dyspnea, and cyanosis.
Increased intracranial pressure
With increased intracranial pressure (ICP), agitation usually precedes other early signs and symptoms, such as headache, nausea, and vomiting. ICP produces respiratory changes, such as Cheyne-Stokes, cluster, ataxic, or apneustic breathing; sluggish, nonreactive, or unequal pupils; widening pulse pressure; tachycardia; decreased LOC; seizures; and motor changes, such as decerebrate or decorticate posture.
Organic brain syndrome
With organic brain syndrome, agitation is manifested as hyperactivity, emotional lability, confusion, and memory loss. Slurred or incoherent speech and paranoid behavior may also occur.
Post–head trauma syndrome
Shortly after — or even years after — head trauma, mild to severe agitation develops, characterized by disorientation, loss of concentration, angry outbursts, and emotional lability. Other findings include fatigue, wandering behavior, and poor judgment.
Vitamin B6 deficiency
With vitamin B6 deficiency, agitation can range from mild to severe. Other effects include seizures, peripheral paresthesia, and dermatitis. Oculogyric crisis may also occur.
Other causes
Drugs
Mild to moderate agitation, which is commonly dose related, develops as an adverse reaction to central nervous system stimulants — especially appetite suppressants, such as amphetamines and amphetamine-like drugs; sympathomimetics such as ephedrine; caffeine; and theophylline.
Radiographic contrast media
Reaction to the contrast medium injected during various diagnostic tests produces moderate to severe agitation along with other signs of hypersensitivity.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Confusion:
Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Brain tumor
In the early stages of a brain tumor, confusion is usually mild and difficult to detect. As the tumor impinges on cerebral structures, however, confusion worsens and the patient may exhibit personality changes, bizarre behavior, sensory and motor deficits, visual field deficits, and aphasia.
Decreased cerebral perfusion
Mild confusion is an early symptom of decreased cerebral perfusion. Confusion may be insidious and fleeting, as in a transient ischemic attack, or acute and permanent, as in stroke. Associated findings usually include hypotension, tachycardia or bradycardia, irregular pulse, ventricular gallop, edema, and cyanosis.
Fluid and electrolyte imbalance
A fluid and electrolyte imbalance can cause confusion. The extent of imbalance determines the severity of the patient’s confusion. Typically, he’ll show signs of dehydration, such as lassitude, poor skin turgor, dry skin and mucous membranes, and oliguria. He may also develop hypotension and a low-grade fever.
Head trauma
Such head trauma as concussions, contusions, and brain hemorrhages may produce confusion at the time of injury, shortly afterward, or months or even years afterward. The patient may be delirious, with periodic loss of consciousness. Vomiting, severe headache, pupillary changes, and sensory and motor deficits are also common.
Heatstroke
Heatstroke causes pronounced confusion that gradually worsens as body temperature rises. Initially, the patient may be irritable and dizzy; later, he may become delirious, have seizures, and lose consciousness.
Heavy metal poisoning
Chronic ingestion or inhalation of heavy metals (such as lead, arsenic, mercury, and manganese) eventually produces confusion and, typically, weakness and drowsiness. The patient may also experience headache, vomiting, seizures, tremors, gait disturbances, and mental deterioration.
Hypothermia
Confusion may be an early sign of hypothermia. Typically, the patient displays slurred speech, cold and pale skin, hyperactive deep tendon reflexes, rapid pulse, and decreased blood pressure and respirations. As his body temperature continues to drop, his confusion progresses to stupor and coma, his muscles develop rigidity, and his respiratory rate decreases.
Hypoxemia
Acute pulmonary disorders that result in hypoxemia produce confusion that can range from mild disorientation to delirium. In advanced stages, chronic pulmonary disorders produce persistent confusion as well as severe dyspnea, disability, cor pulmonale, and severe respiratory failure.
Infection
Severe generalized infection, such as sepsis, commonly produces delirium. Central nervous system (CNS) infections such as meningitis cause varying degrees of confusion along with headache and nuchal rigidity.
Metabolic encephalopathy
Both hyperglycemia and hypoglycemia can produce sudden confusion. A patient with hypoglycemia may also experience transient delirium and seizures. Uremic and hepatic encephalopathies produce gradual confusion that may progress to seizures and coma. Usually, the patient also experiences tremors and restlessness.
Nutritional deficiencies
Inadequate dietary intake of thiamine, niacin, or vitamin B12, which causes nutritional deficiencies, produces insidious, progressive confusion and possible mental deterioration. Associated CNS abnormalities may become severe enough to induce hallucinations and paranoia.
Seizure disorders
Mild to moderate confusion may immediately follow any type of seizure. The confusion usually disappears within several hours. The patient may have difficulty talking and may fall into deep sleep after the seizures.
Thyroid hormone disorders
Hyperthyroidism produces mild to moderate confusion along with nervousness, inability to concentrate, weight loss, flushed skin, and tachycardia. Hypothyroidism produces mild, insidious confusion and memory loss; weight gain; bradycardia; and fatigue.
Other causes
Alcohol
Intoxication causes confusion and stupor, and alcohol withdrawal may cause delirium and seizures.
Drugs
Large doses of CNS depressants produce confusion that can persist for several days after the drug is discontinued. Opioid and barbiturate withdrawal also causes acute confusion, possibly with delirium. Other drugs that commonly cause confusion include lidocaine, digoxin, indomethacin, cycloserine, chloroquine, atropine, and cimetidine.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Level of consciousness, decreased:
Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Adrenal crisis
Decreased LOC, ranging from lethargy to coma, may develop within 12 hours of adrenal crisis onset. Early associated findings include progressive weakness, irritability, anorexia, headache, nausea and vomiting, diarrhea, abdominal pain, and fever. Later signs and symptoms include hypotension; rapid, thready pulse; oliguria; cool, clammy skin; and flaccid extremities. The patient with chronic adrenocortical hypofunction may have hyperpigmented skin and mucous membranes.
Brain abscess
Decreased LOC varies from drowsiness to deep stupor, depending on abscess size and site. Early signs and symptoms — constant intractable headache, nausea, vomiting, and seizures — reflect increasing ICP. Typical later features include ocular disturbances (nystagmus, vision loss, and pupillary inequality) and signs of infection such as fever. Other findings may include personality changes, confusion, abnormal behavior, dizziness, facial weakness, aphasia, ataxia, tremor, and hemiparesis.
Brain tumor
In patients with brain tumors, LOC decreases slowly, from lethargy to coma. The patient may also experience apathy, behavior changes, memory loss, decreased attention span, morning headache, dizziness, vision loss, ataxia, and sensorimotor disturbances. Aphasia and seizures are possible, along with signs of hormonal imbalance, such as fluid retention or amenorrhea. Signs and symptoms vary according to the location and size of the tumor. In later stages, papilledema, vomiting, bradycardia, and widening pulse pressure also appear. In the final stages, the patient may exhibit decorticate or decerebrate posture.
Cerebral aneurysm (ruptured)
Somnolence, confusion and, at times, stupor characterize a moderate bleed; deep coma occurs with severe bleeding, which can be fatal. Onset of a ruptured cerebral aneurysm is usually abrupt, with sudden, severe headache, nausea, and vomiting. Nuchal rigidity, back and leg pain, fever, restlessness, irritability, occasional seizures, and blurred vision point to meningeal irritation. The type and severity of other findings vary with the site and severity of the hemorrhage and may include hemiparesis, hemisensory defects, dysphagia, and visual defects.
Cerebral contusion
Usually unconscious for a prolonged period, the patient may develop dilated, nonreactive pupils and decorticate or decerebrate posture. If he’s conscious or recovers consciousness, he may be drowsy, confused, disoriented, agitated, or even violent. Associated findings include blurred or double vision, fever, headache, pallor, diaphoresis, tachycardia, altered respirations, aphasia, and hemiparesis. Residual effects include seizures, impaired mental status, slight hemiparesis, and vertigo.
Diabetic ketoacidosis
Diabetic ketoacidosis produces a rapid decrease in LOC that ranges from lethargy to coma. It’s commonly preceded by polydipsia, polyphagia, and polyuria. The patient may complain of weakness, anorexia, abdominal pain, nausea, and vomiting. He may also exhibit orthostatic hypotension; fruity breath odor; Kussmaul’s respirations; warm, dry skin; and a rapid, thready pulse. Untreated, this condition invariably leads to coma and death.
Encephalitis
Within 48 hours of onset, the patient with encephalitis may develop LOC changes ranging from lethargy to coma. Other possible findings include abrupt onset of fever, headache, nuchal rigidity, nausea, vomiting, irritability, personality changes, seizures, aphasia, ataxia, hemiparesis, nystagmus, photophobia, myoclonus, and cranial nerve palsies.
Encephalopathy
With hepatic encephalopathy, signs and symptoms develop in four stages: in the prodromal stage, slight personality changes (disorientation, forgetfulness, slurred speech) and slight tremor; in the impending stage, tremor progressing to asterixis (the hallmark of hepatic encephalopathy), lethargy, aberrant behavior, and apraxia; in the stuporous stage, stupor and hyperventilation, with the patient noisy and abusive when aroused; in the comatose stage, coma with decerebrate posture, hyperactive reflexes, positive Babinski’s reflex, and fetor hepaticus.
With life-threatening hypertensive encephalopathy, LOC progressively decreases from lethargy to stupor to coma. Besides markedly elevated blood pressure, the patient may experience severe headache, vomiting, seizures, visual disturbances, transient paralysis, and eventually Cheyne-Stokes respirations.
With hypoglycemic encephalopathy, LOC rapidly deteriorates from lethargy to coma. Early signs and symptoms include nervousness, restlessness, agitation, and confusion; hunger; alternate flushing and cold sweats; and headache, trembling, and palpitations. Blurred vision progresses to motor weakness, hemiplegia, dilated pupils, pallor, decreased pulse rate, shallow respirations, and seizures. Flaccidity and decerebrate posture appear late.
Depending on its severity, hypoxic encephalopathy produces a sudden or gradual decrease in LOC, leading to coma and brain death. Early on, the patient appears confused and restless, with cyanosis and increased heart and respiratory rates and blood pressure. Later, his respiratory pattern becomes abnormal, and assessment reveals decreased pulse, blood pressure, and deep tendon reflexes (DTRs); Babin-ski’s reflex; absent doll’s eye sign; and fixed pupils.
With uremic encephalopathy, LOC decreases gradually from lethargy to coma. Early on, the patient may appear apathetic, inattentive, confused, and irritable and may complain of headache, nausea, fatigue, and anorexia. Other findings include vomiting, tremors, edema, papilledema, hypertension, cardiac arrhythmias, dyspnea, crackles, oliguria, and Kussmaul’s and Cheyne-Stokes respirations.
Epidural hemorrhage (acute)
Acute epidural hemorrhage, a life-threatening posttraumatic disorder, produces momentary loss of consciousness, sometimes followed by a lucid interval. While lucid, the patient has a severe headache, nausea, vomiting, and bladder distention. Rapid deterioration in consciousness follows, possibly leading to coma. Other findings include irregular respirations, seizures, decreased and bounding pulse, increased pulse pressure, hypertension, unilateral or bilateral fixed and dilated pupils, unilateral hemiparesis or hemiplegia, decerebrate posture, and Babinski’s reflex.
Heatstroke
As body temperature increases, LOC gradually decreases from lethargy to coma. Early signs and symptoms of heatstroke include malaise, tachycardia, tachypnea, orthostatic hypotension, muscle cramps, rigidity, and syncope. The patient may be irritable, anxious, and dizzy and may report a severe headache. At the onset of heatstroke, the patient’s skin is hot, flushed, and diaphoretic with blotchy cyanosis; later, when his fever exceeds 105° F (40.6° C), his skin becomes hot, flushed, and anhidrotic. Pulse and respiratory rate increase markedly, and blood pressure drops precipitously. Other findings include vomiting, diarrhea, dilated pupils, and Cheyne-Stokes respirations.
Hypernatremia
Hypernatremia, life-threatening if acute, causes LOC to deteriorate from lethargy to coma. The patient is irritable and exhibits twitches progressing to seizures. Other associated signs and symptoms include a weak, thready pulse; nausea; malaise; fever; thirst; flushed skin; and dry mucous membranes.
Hyperosmolar hyperglycemic nonketotic syndrome
LOC decreases rapidly from lethargy to coma in hyperosmolar hyperglycemic nonketotic syndrome (HHNS). Early findings include polyuria, polydipsia, weight loss, and weakness. Later, the patient may develop hypotension, poor skin turgor, dry skin and mucous membranes, tachycardia, tachypnea, oliguria, and seizures.
Hypokalemia
With hypokalemia, LOC gradually decreases to lethargy; coma is rare. Other findings include confusion, nausea, vomiting, diarrhea, polyuria, weakness, decreased reflexes, malaise, dizziness, hypotension, arrhythmias, and abnormal electrocardiogram results.
Hyponatremia
Hyponatremia, life-threatening if acute, produces decreased LOC in late stages. Early nausea and malaise may progress to behavior changes, confusion, lethargy, incoordination and, eventually, seizures and coma.
Hypothermia
With severe hypothermia (temperature below 90° F [32.2° C]), LOC decreases from lethargy to coma. DTRs disappear, and ventricular fibrillation occurs, possibly followed by cardiopulmonary arrest. With mild to moderate hypothermia, the patient may experience memory loss and slurred speech as well as shivering, weakness, fatigue, and apathy. Other early signs and symptoms include ataxia, muscle stiffness, and hyperactive DTRs; diuresis; tachycardia and decreased respiratory rate and blood pressure; and cold, pale skin. Later, muscle rigidity and decreased reflexes may develop, along with peripheral cyanosis, bradycardia, arrhythmias, severe hypotension, decreased respiratory rate with shallow respirations, and oliguria.
Intracerebral hemorrhage
Intracerebral hemorrhage, a life-threatening disorder, produces a rapid, steady loss of consciousness within hours, commonly accompanied by severe headache, dizziness, nausea, and vomiting. Associated signs and symptoms vary and may include increased blood pressure, irregular respirations, Babinski’s reflex, seizures, aphasia, decreased sensations, hemiplegia, decorticate or decerebrate posture, and dilated pupils.
Meningitis
Confusion and irritability are expected; however, stupor, coma, and seizures may occur in those with severe meningitis. Fever develops early, possibly accompanied by chills. Associated findings include severe headache, nuchal rigidity, hyperreflexia and, possibly, opisthotonos. The patient exhibits Kernig’s and Brudzinski’s signs and, possibly, ocular palsies, photophobia, facial weakness, and hearing loss.
Myxedema crisis
The patient experiencing myxedema crisis may exhibit a swift decline in LOC. Other findings include severe hypothermia, hypoventilation, hypotension, bradycardia, hypoactive reflexes, periorbital and peripheral edema, impaired hearing and balance, and seizures.
Pontine hemorrhage
With pontine hemorrhage, a sudden, rapid decrease in LOC to the point of coma occurs within minutes; death occurs within hours. The patient may also exhibit total paralysis, decerebrate posture, Babinski’s reflex, absent doll’s eye sign, and bilateral miosis (however, the pupils remain reactive to light).
Seizure disorders
A complex partial seizure produces decreased LOC, manifested as a blank stare, purposeless behavior (picking at clothing, wandering, lip smacking or chewing motions), and unintelligible speech. The seizure may be heralded by an aura and followed by several minutes of mental confusion.
An absence seizure usually involves a brief change in LOC, indicated by blinking or eye rolling, blank stare, and slight mouth movements.
A generalized tonic-clonic seizure typically begins with a loud cry and sudden loss of consciousness. Muscle spasm alternates with relaxation. Tongue biting, incontinence, labored breathing, apnea, and cyanosis may also occur. Consciousness returns after the seizure, but the patient remains confused and may have difficulty talking. He may complain of drowsiness, fatigue, headache, muscle aching, and weakness and may fall into deep sleep.
An atonic seizure produces sudden unconsciousness for a few seconds.
Status epilepticus, rapidly recurring seizures without intervening periods of physiologic recovery and return of consciousness, can be life-threatening.
Shock
Decreased LOC — lethargy progressing to stupor and coma — occurs late in shock. Associated findings include confusion, anxiety, and restlessness; hypotension; tachycardia; weak pulse with narrowing pulse pressure; dyspnea; oliguria; and cool, clammy skin.
Hypovolemic shock is generally the result of massive or insidious bleeding, either internally or externally. Cardiogenic shock may produce chest pain or arrhythmias and signs of heart failure, such as dyspnea, cough, edema, jugular vein distention, and weight gain. Septic shock may be accompanied by high fever and chills. Anaphylactic shock usually involves stridor.
Stroke
With stroke, LOC changes vary in degree and onset, depending on the lesion’s size and location and the presence of edema. A thrombotic stroke usually follows multiple transient ischemic attacks (TIAs). LOC changes may be abrupt or take several minutes, hours, or days. An embolic stroke occurs suddenly, and deficits reach their peak almost at once. Deficits associated with a hemorrhagic stroke usually develop over minutes or hours.
Associated findings vary with stroke type and severity and may include disorientation; intellectual deficits, such as memory loss and poor judgment; personality changes; and emotional lability. Other possible findings include dysarthria, dysphagia, ataxia, aphasia, apraxia, agnosia, unilateral sensorimotor loss, and visual disturbances. In addition, urine retention, incontinence, constipation, headache, vomiting, and seizures may occur.
CULTURAL CUE:The incidence of stroke is higher in Blacks than Whites. In fact, Blacks have a 60% higher risk for stroke than Whites or Hispanics of the same age. This is believed to be the result of an increased prevalence of hypertension in Blacks.
Subdural hematoma (chronic)
LOC deteriorates slowly in patients with chronic subdural hematomas. Other signs and symptoms include confusion, decreased ability to concentrate, and personality changes accompanied by headache, light-headedness, seizures, and a dilated ipsilateral pupil with ptosis.
Subdural hemorrhage (acute)
With acute subdural hemorrhage, a potentially life-threatening disorder, agitation and confusion are followed by progressively decreasing LOC from somnolence to coma. The patient may also experience headache, fever, unilateral pupil dilation, decreased pulse and respiratory rates, widening pulse pressure, seizures, hemiparesis, and Babinski’s reflex.
Thyroid storm
LOC decreases suddenly and can progress to coma. Irritability, restlessness, confusion, and psychotic behavior precede the deterioration. Associated signs and symptoms of a thyroid storm include tremors and weakness; visual disturbances; tachycardia, arrhythmias, angina, and acute respiratory distress; warm, moist, flushed skin; and vomiting, diarrhea, and fever to 105°F (40.6°C).
TIA
LOC decreases abruptly (with varying severity) and gradually returns to normal within 24 hours of a TIA. Site-specific findings may include vision loss, nystagmus, aphasia, dizziness, dysarthria, unilateral hemiparesis or hemiplegia, tinnitus, paresthesia, dysphagia, or staggering or incoordinated gait.
West Nile encephalitis
Signs and symptoms of this brain infection caused by the West Nile virus include fever, headache, and body aches, commonly with skin rash and swollen lymph glands. More severe infection is marked by high fever, headache, neck stiffness, stupor, disorientation, coma, tremors, occasional seizures, paralysis and, rarely, death.
Other causes
Alcohol
Alcohol use causes varying degrees of sedation, irritability, and incoordination; intoxication commonly causes stupor.
Drugs
Sedation and other degrees of decreased LOC can result from an overdose of a barbiturate, another central nervous system depressant, or aspirin.
Poisoning
Toxins, such as lead, carbon monoxide, and snake venom, can cause varying degrees of decreased LOC. Confusion is common, as are headache, nausea, and vomiting. Other general features include hypotension, cardiac arrhythmias, dyspnea, sensorimotor loss, and seizures.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Seizures, complex partial:
Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Brain abscess
If the brain abscess is in the temporal lobe, complex partial seizures commonly occur after the abscess disappears. Related problems may include headache, nausea, vomiting, generalized seizures, and a decreased level of consciousness (LOC). The patient may also develop central facial weakness, auditory receptive aphasia, hemiparesis, and ocular disturbances.
Head trauma
Severe trauma to the temporal lobe (especially from a penetrating injury) can produce complex partial seizures months or years later. The seizures may decrease in frequency and eventually stop. Head trauma also causes generalized seizures and behavior and personality changes.
Temporal lobe tumor
Complex partial seizures may be the first sign of a tumor in the temporal lobe. Other signs and symptoms include headache, pupillary changes, and mental dullness. Increased intracranial pressure may cause a decreased LOC, vomiting and, possibly, papilledema.
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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.
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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
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Agitation:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Alcohol withdrawal syndrome.Mild to severe agitation occurs in alcohol withdrawal syndrome, along with hyperactivity, tremors, and anxiety. With delirium, the potentially life-threatening stage of alcohol withdrawal, severe agitation accompanies hallucinations, insomnia, diaphoresis, and a depressed mood. The patient's pulse rate and temperature rise as withdrawal progresses; status epilepticus, cardiac exhaustion, and shock can occur.
Anxiety.Anxiety produces varying degrees of agitation. The patient may be unaware of his anxiety or may complain of it without knowing its cause. Other findings include nausea, vomiting, diarrhea, cool and clammy skin, frontal headache, back pain, insomnia, and tremors.
Dementia.Mild to severe agitation can result from many common syndromes, such as Alzheimer's and Huntington's diseases. The patient may display a decrease in memory, attention span, problem-solving ability, and alertness. Hypoactivity, wandering behavior, hallucinations, aphasia, and insomnia may also occur.
Drug withdrawal syndrome.Mild to severe agitation occurs in drug withdrawal syndrome. Related findings vary with the drug, but include anxiety, abdominal cramps, diaphoresis, and anorexia. With opioid or barbiturate withdrawal, a decreased level of consciousness (LOC), seizures, and elevated blood pressure, heart rate, and respiratory rate can also occur.
Hepatic encephalopathy.Agitation occurs only with fulminating hepatic encephalopathy. Other findings include drowsiness, stupor, fetor hepaticus, asterixis, and hyperreflexia.
Hypersensitivity reaction.Moderate to severe agitation appears, possibly as the first sign of a reaction. Depending on the severity of the reaction, agitation may be accompanied by urticaria, pruritus, and facial and dependent edema.
With anaphylactic shock,a potentially life-threatening reaction, agitation occurs rapidly along with apprehension, urticaria or diffuse erythema, warm and moist skin, paresthesia, pruritus, edema, dyspnea, wheezing, stridor, hypotension, and tachycardia. Abdominal cramps, vomiting, and diarrhea can also occur.
Hypoxemia.Beginning as restlessness, agitation rapidly worsens. The patient may be confused and have impaired judgment and motor coordination. He may also have tachycardia, tachypnea, dyspnea, and cyanosis.
Increased intracranial pressure (ICP).Agitation usually precedes other early signs and symptoms, such as headache, nausea, and vomiting. Increased ICP produces respiratory changes, such as Cheyne-Stokes, cluster, ataxic, or apneustic breathing; sluggish, nonreactive, or unequal pupils; widening pulse pressure; tachycardia; a decreased LOC; seizures; and motor changes such as decerebrate or decorticate posture.
Post-head trauma syndrome.Shortly after, or even years after a head injury, mild to severe agitation may develop, characterized by disorientation, loss of concentration, angry outbursts, and emotional lability. Other findings include fatigue, wandering behavior, and poor judgment.
Vitamin B6 deficiency.Agitation can range from mild to severe. Other effects include seizures, peripheral paresthesia, and dermatitis. Oculogyric crisis may also occur.
Other causes
Drugs.Mild to moderate agitation, which is commonly dose related, develops as an adverse reaction to central nervous system stimulants—especially appetite suppressants, such as amphetamines and amphetamine-like drugs; sympathomimetics, such as ephedrine; caffeine; and theophylline.
Radiographic contrast media.Reaction to the contrast medium injected during various diagnostic tests produces moderate to severe agitation along with other signs of hypersensitivity.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
Confusion:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Brain tumor.In the early stages of a brain tumor, confusion is usually mild and difficult to detect. As the tumor impinges on cerebral structures, however, confusion worsens and the patient may exhibit personality changes, bizarre behavior, sensory and motor deficits, visual field deficits, and aphasia.
Cerebrovascular disorders.Cerebrovascular disorders produce confusion due to tissue hypoxia and ischemia. Confusion may be insidious and fleeting, as in a transient ischemic attack, or acute and permanent, as in a stroke.
Decreased cerebral perfusion.Mild confusion is an early symptom of decreased cerebral perfusion. Associated findings usually include hypotension, tachycardia or bradycardia, an irregular pulse, ventricular gallop, edema, and cyanosis.
Fluid and electrolyte imbalance.The extent and type of fluid and electrolyte imbalance determines the severity of the patient's confusion. Typically, he'll show signs of dehydration, such as lassitude, poor skin turgor, dry skin and mucous membranes, and oliguria. He may also develop hypotension and a low-grade fever.
Head trauma.Concussion, contusion, and brain hemorrhage may produce confusion at the time of injury, shortly afterward, or months or even years afterward. The patient may be delirious, with periodic loss of consciousness. Vomiting, a severe headache, pupillary changes, and sensory and motor deficits are also common.
Heatstroke.Heatstroke causes pronounced confusion that gradually worsens as the patient's body temperature rises. Initially, he may be irritable and dizzy; later, he may become delirious, have seizures, and lose consciousness.
Hypothermia.Confusion may be an early sign of hypothermia. Typically, the patient displays slurred speech, cold and pale skin, hyperactive deep tendon reflexes, a rapid pulse, and decreased blood pressure and respirations. As his body temperature continues to drop, his confusion progresses to stupor and coma, his muscles become rigid, and his respiratory rate decreases.
Hypoxemia.Acute pulmonary disorders that result in hypoxemia produce confusion that can range from mild disorientation to delirium. Chronic pulmonary disorders produce persistent confusion.
Infection.Severe generalized infection, such as sepsis, typically produces delirium. Central nervous system (CNS) infections, such as meningitis, cause varying degrees of confusion along with a headache and nuchal rigidity.
Metabolic encephalopathy.Hyperglycemia and hypoglycemia can produce sudden confusion. A patient with hypoglycemia may also experience transient delirium and seizures. Uremic and hepatic encephalopathies produce gradual confusion that may progress to seizures and coma. Usually, the patient also experiences tremors and restlessness.
Nutritional deficiencies.Inadequate dietary intake of thiamine, niacin, or vitamin B12 produces insidious, progressive confusion and possible mental deterioration.
Seizure disorder.Mild to moderate confusion may immediately follow any type of seizure. The confusion usually disappears within several hours.
Other causes
Alcohol.Intoxication causes confusion and stupor, and alcohol withdrawal may cause delirium and seizures.
Drugs.Large doses of CNS depressants produce confusion that can persist for several days after the drug is discontinued. Opioid and barbiturate withdrawal also causes acute confusion, possibly with delirium. Other drugs that commonly cause confusion include lidocaine, a cardiac glycoside, indomethacin, cycloserine, chloroquine, atropine, cimetidine, and sleeping aids.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
Level of consciousness, decreased:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Adrenal crisis.A decreased LOC, ranging from lethargy to coma, may develop within 8 to 12 hours of the onset of adrenal crisis. Early associated findings include progressive weakness, irritability, anorexia, a headache, nausea and vomiting, diarrhea, abdominal pain, and a fever. Later signs and symptoms include hypotension; a rapid, thready pulse; oliguria; cool, clammy skin; and flaccid extremities. The patient with chronic adrenocortical hypofunction may have hyperpigmented skin and mucous membranes.
Brain abscess.With a brain abscess, decreased LOC varies from drowsiness to deep stupor, depending on the abscess size and site. Early signs and symptoms—a constant intractable headache, nausea, vomiting, and seizures—reflect increasing ICP. Typical later features include ocular disturbances (nystagmus, vision loss, and pupillary inequality) and signs of infection such as a fever. Other findings may include personality changes, confusion, abnormal behavior, dizziness, facial weakness, aphasia, ataxia, tremor, and hemiparesis.
Brain tumor.With a brain tumor, the patient's LOC decreases slowly, from lethargy to coma. He may also experience apathy, behavior changes, memory loss, a decreased attention span, a morning headache, dizziness, vision loss, ataxia, and sensorimotor disturbances. Aphasia and seizures are possible, along with signs of hormonal imbalance, such as fluid retention or amenorrhea. Signs and symptoms vary according to the location and size of the tumor. In later stages, papilledema, vomiting, bradycardia, and a widening pulse pressure also appear. In the final stages, the patient may exhibit decorticate or decerebrate posture.
Cerebral aneurysm (ruptured).Somnolence, confusion and, at times, stupor characterize a moderate cerebral bleed; deep coma occurs with severe bleeding, which can be fatal. The onset is usually abrupt, with a sudden, severe headache and nausea and vomiting. Nuchal rigidity, back and leg pain, a fever, restlessness, irritability, occasional seizures, and blurred vision point to meningeal irritation. The type and severity of other findings vary with the site and severity of the hemorrhage and may include hemiparesis, hemisensory defects, dysphagia, and visual defects.
Diabetic ketoacidosis.Diabetic ketoacidosis produces a rapid decrease in the patient's LOC, ranging from lethargy to coma, commonly preceded by polydipsia, polyphagia, and polyuria. The patient may complain of weakness, anorexia, abdominal pain, nausea, and vomiting. He may also exhibit orthostatic hypotension; a fruity breath odor; Kussmaul's respirations; warm, dry skin; and a rapid, thready pulse. Untreated, this condition invariably leads to coma and death.
Encephalitis.Within 24 to 48 hours after onset of encephalitis, the patient may develop changes in his LOC ranging from lethargy to coma. Other possible findings include an abrupt onset of a fever, a headache, nuchal rigidity, nausea, vomiting, irritability, personality changes, seizures, aphasia, ataxia, hemiparesis, nystagmus, photophobia, myoclonus, and cranial nerve palsies.
Encephalomyelitis (postvaccinal).Postvaccinal encephalomyelitis is a life-threatening disorder that produces rapid deterioration in the patient's LOC, from drowsiness to coma. He also experiences a rapid onset of a fever, a headache, nuchal rigidity, back pain, vomiting, and seizures.
Encephalopathy.With hepatic encephalopathy, signs and symptoms develop in four stages: in the prodromal stage, slight personality changes (disorientation, forgetfulness, slurred speech) and slight tremor; in the impending stage, tremor progressing to asterixis (the hallmark of hepatic encephalopathy), lethargy, aberrant behavior, and apraxia; in the stuporous stage, stupor and hyperventilation, with the patient noisy and abusive when aroused; in the comatose stage, coma with decerebrate posture, hyperactive reflexes, a positive Babinski's reflex, and fetor hepaticus.
With life-threatening hypertensive encephalopathy, the LOC progressively decreases from lethargy to stupor to coma. Besides markedly elevated blood pressure, the patient may experience a severe headache, vomiting, seizures, vision disturbances, transient paralysis and, eventually, Cheyne-Stokes respirations.
With hypoglycemic encephalopathy, the patient's LOC rapidly deteriorates from lethargy to coma. Early signs and symptoms include nervousness, restlessness, agitation, and confusion; hunger; alternate flushing and cold sweats; and a headache, trembling, and palpitations. Blurred vision progresses to motor weakness, hemiplegia, dilated pupils, pallor, a decreased pulse rate, shallow respirations, and seizures. Flaccidity and decerebrate posture appear late.
Depending on its severity, hypoxic encephalopathy produces a sudden or gradual decrease in the LOC, leading to coma and brain death. Initially, the patient appears confused and restless, with cyanosis and increased heart and respiratory rates and blood pressure. Later, his respiratory pattern becomes abnormal, and assessment reveals a decreased pulse, blood pressure, and deep tendon reflexes (DTRs); a positive Babinski's reflex; an absent doll's eye sign; and fixed pupils.
With uremic encephalopathy, the LOC decreases gradually from lethargy to coma. Initially, the patient may appear apathetic, inattentive, confused, and irritable and may complain of a headache, nausea, fatigue, and anorexia. Other findings include vomiting, tremors, edema, papilledema, hypertension, cardiac arrhythmias, dyspnea, crackles, oliguria, and Kussmaul's and Cheyne-Stokes respirations.
Heatstroke.With heatstroke, as body temperature increases, the patient's LOC gradually decreases from lethargy to coma. Early signs and symptoms include malaise, tachycardia, tachypnea, orthostatic hypotension, muscle cramps, rigidity, and syncope. The patient may be irritable, anxious, and dizzy and may report a severe headache. At the onset of heatstroke, the patient's skin is hot, flushed, and diaphoretic with blotchy cyanosis; later, when his fever exceeds 105° F (40.5° C), his skin becomes hot, flushed, and anhidrotic. Pulse and respiratory rate increase markedly, and blood pressure drops precipitously. Other findings include vomiting, diarrhea, dilated pupils, and Cheyne-Stokes respirations.
Hypernatremia.Hypernatremia, life-threatening if acute, causes the patient's LOC to deteriorate from lethargy to coma. He's irritable and exhibits twitches progressing to seizures. Other associated signs and symptoms include a weak, thready pulse; nausea; malaise; a fever; thirst; flushed skin; and dry mucous membranes.
Hyperosmolar hyperglycemic nonketotic syndrome (HHNS).LOC decreases rapidly from lethargy to coma with HHNS. Early findings include polyuria, polydipsia, weight loss, and weakness. Later, the patient may develop hypotension, poor skin turgor, dry skin and mucous membranes, tachycardia, tachypnea, oliguria, and seizures.
Hypokalemia.LOC gradually decreases to lethargy with hypokalemia; coma is rare. Other findings include confusion, nausea, vomiting, diarrhea, and polyuria; weakness, decreased reflexes, and malaise; and dizziness, hypotension, arrhythmias, and abnormal electrocardiogram results.
Hyponatremia.Hyponatremia, life-threatening if acute, produces a decreased LOC in late stages. Early nausea and malaise may progress to behavior changes, confusion, lethargy, incoordination and, eventually, seizures and coma.
Hypothermia.With severe hypothermia (temperature below 90° F [32.2° C]), the patient's LOC decreases from lethargy to coma. DTRs disappear, and ventricular fibrillation occurs, possibly followed by cardiopulmonary arrest. With mild to moderate hypothermia, the patient may experience memory loss and slurred speech as well as shivering, weakness, fatigue, and apathy. Other early signs and symptoms include ataxia, muscle stiffness, and hyperactive DTRs; diuresis; tachycardia and decreased respiratory rate and blood pressure; and cold, pale skin. Later, muscle rigidity and decreased reflexes may develop, along with peripheral cyanosis, bradycardia, arrhythmias, severe hypotension, a decreased respiratory rate with shallow respirations, and oliguria.
Intracerebral hemorrhage.Intracerebral hemorrhage is a life-threatening disorder that produces a rapid, steady loss of consciousness within hours, commonly accompanied by a severe headache, dizziness, nausea, and vomiting. Associated signs and symptoms vary and may include increased blood pressure, irregular respirations, a positive Babinski's reflex, seizures, aphasia, decreased sensations, hemiplegia, decorticate or decerebrate posture, and dilated pupils.
Listeriosis.If listeriosis spreads to the nervous system and causes meningitis, signs and symptoms include a decreased LOC, a fever, a headache, and nuchal rigidity. Early signs and symptoms of listeriosis include a fever, myalgia, abdominal pain, nausea, vomiting, and diarrhea.
Meningitis.Confusion and irritability are expected; however, stupor, coma, and seizures may occur in the patient with severe meningitis. A fever develops early, possibly accompanied by chills. Associated findings include a severe headache, nuchal rigidity, hyperreflexia and, possibly, opisthotonos. The patient exhibits Kernig's and Brudzinski's signs and, possibly, ocular palsies, photophobia, facial weakness, and hearing loss.
Pontine hemorrhage.A sudden, rapid decrease in the patient's LOC to the point of coma occurs within minutes and death within hours of pontine hemorrhage. The patient may also exhibit total paralysis, decerebrate posture, a positive Babinski's reflex, an absent doll's eye sign, and bilateral miosis (however, the pupils remain reactive to light).
Seizure disorders.A complex partial seizure produces a decreased LOC, manifested as a blank stare, purposeless behavior (picking at clothing, wandering, lip smacking or chewing motions), and unintelligible speech. The seizure may be heralded by an aura and followed by several minutes of mental confusion.
An absence seizure usually involves a brief change in the patient's LOC, indicated by blinking or eye rolling, a blank stare, and slight mouth movements.
A generalized tonic-clonic seizure typically begins with a loud cry and sudden loss of consciousness. Muscle spasm alternates with relaxation. Tongue biting, incontinence, labored breathing, apnea, and cyanosis may also occur. Consciousness returns after the seizure, but the patient remains confused and may have difficulty talking. He may complain of drowsiness, fatigue, a headache, muscle aching, and weakness and may fall into a deep sleep.
An atonic seizure produces sudden unconsciousness for a few seconds.
Status epilepticus, rapidly recurring seizures without intervening periods of physiologic recovery and return of consciousness, can be life-threatening.
Shock.A decreased LOC—lethargy progressing to stupor and coma—occurs late in shock. Associated findings include confusion, anxiety, and restlessness; hypotension; tachycardia; a weak pulse with narrowing pulse pressure; dyspnea; oliguria; and cool, clammy skin.
Hypovolemic shock is generally the result of massive or insidious bleeding, either internally or externally. Cardiogenic shock may produce chest pain or arrhythmias and signs of heart failure, such as dyspnea, a cough, edema, jugular vein distention, and weight gain. Septic shock may be accompanied by a high fever and chills. Anaphylactic shock usually involves stridor in response to an allergen.
Stroke.When a stroke occurs, changes in the patient's LOC vary in degree and onset, depending on the lesion's size and location and the presence of edema. A thrombotic stroke usually follows multiple transient ischemic attacks (TIAs) or an episode of atrial fibrillation. Changes in the LOC may be abrupt or take several minutes, hours, or days. An embolic stroke occurs suddenly, and deficits reach their peak almost at once. Deficits associated with a hemorrhagic stroke usually develop over minutes or hours.
Associated findings vary with the stroke type and severity and may include disorientation; intellectual deficits, such as memory loss and poor judgment; personality changes; and emotional lability. Other possible findings include dysarthria, dysphagia, ataxia, aphasia, apraxia, agnosia, unilateral sensorimotor loss, and vision disturbances. In addition, urine retention, incontinence, constipation, a headache, vomiting, and seizures may occur.
Subdural hemorrhage (acute).Acute subdural hemorrhage is a potentially life-threatening disorder in which agitation and confusion are followed by a progressively decreasing LOC from somnolence to coma. The patient may also experience a headache, a fever, unilateral pupil dilation, decreased pulse and respiratory rates, a widening pulse pressure, seizures, hemiparesis, and a positive Babinski's reflex.
Thyroid storm.The patient's LOC decreases suddenly with thyroid storm and can progress to coma. Irritability, restlessness, confusion, and psychotic behavior precede the deterioration. Associated signs and symptoms include tremors and weakness; vision disturbances; tachycardia, arrhythmias, angina, and acute respiratory distress; warm, moist, flushed skin; and vomiting, diarrhea, and a fever of up to 105º F (40.5º C).
TIA.When a TIA occurs, the patient's LOC decreases abruptly (with varying severity) and gradually returns to normal within 24 hours. Site-specific findings may include vision loss, nystagmus, aphasia, dizziness, dysarthria, unilateral hemiparesis or hemiplegia, tinnitus, paresthesia, dysphagia, or staggering or incoordinated gait.
West Nile encephalitis.Signs and symptoms of West Nile encephalitis include fever, headache, and body aches, commonly with a skin rash and swollen lymph glands. More severe infection is marked by high fever, headache, neck stiffness, stupor, disorientation, coma, tremors, occasional seizures, paralysis and, rarely, death.
Other causes
Alcohol.Alcohol use causes varying degrees of sedation, irritability, and incoordination; intoxication commonly causes stupor.
Drugs.Sedation and other degrees of a decreased LOC can result from an overdose of a barbiturate, another central nervous system depressant, or aspirin.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
Seizures, complex partial:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Brain abscess.If the brain abscess is in the temporal lobe, complex partial seizures commonly occur after the abscess disappears. Related problems may include headache, nausea, vomiting, generalized seizures, and decreased level of consciousness (LOC). The patient may also develop central facial weakness, auditory receptive aphasia, hemiparesis, and ocular disturbances.
Head trauma.Severe trauma to the temporal lobe (especially from a penetrating injury) can produce complex partial seizures months or years later. The seizures may decrease in frequency and eventually stop. Head trauma also causes generalized seizures and behavior and personality changes.
Herpes simplex encephalitis.Herpes simplex virus commonly attacks the temporal lobe, resulting in complex partial seizures. Other features include fever, headache, coma, and generalized seizures.
Temporal lobe tumor.Complex partial seizures may be the first sign of a temporal lobe tumor. Other signs and symptoms include headache, pupillary changes, and mental dullness. Increased intracranial pressure may cause decreased LOC, vomiting and, possibly, papilledema.
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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
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