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Diseases » Coma » Diagnosis

Diagnosis of Coma

Coma Diagnosis: Book Excerpts

Diagnosis of Coma: medical news summaries:

The following medical news items are relevant to diagnosis and misdiagnosis issues for Coma:

Diagnostic Tests for Coma: Online Medical Books

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

DELIRIUM: Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

Is there associated fever? Delirium with fever may simply indicate a self-limited infectious process, but it should bring to mind encephalitis and meningitis as well as cerebral abscess and cerebral hemorrhage.
Is there a history of trauma? A history of head trauma would make one suspect a subdural or epidural hematoma and concussion.
Is there a history of drug or alcohol ingestion? This is probably the most important single question to ask in the average case coming into the emergency room these days without a good history. Very often, the problem is alcoholism or various popular drugs such as cocaine, lysergic acid diethylamide (LSD), and phencyclidine (PCP).
Are there focal neurologic signs? Focal neurologic signs along with the delirium would make one think of subdural or epidural hematoma, cerebral abscess, or cerebral hemorrhage. Remember, a cerebral thrombosis or embolism may present with delirium also.
Is there nuchal rigidity? If there is nuchal rigidity, the patient may have meningitis or subarachnoid hemorrhage.
Is there a sweet odor to the breath? A sweet odor to the breath should make one think of diabetic coma or alcoholism.
What is the response to intravenous thiamine? If the patient responds to intravenous thiamine, the diagnosis is usually Wernicke's encephalopathy or Korsakoff's syndrome.
Intermittent delirium should suggest psychomotor epilepsy and transient global amnesia.

DIAGNOSTIC WORKUP

Routine laboratory tests include a CBC, sedimentation rate, ANA, chemistry panel including electrolytes and BUN and VDRL tests, a blood alcohol level, urinalysis, and urine drug screen. A CT scan of the brain and EEG is usually indicated also. Acute delirium may be an indication to administer intravenous glucose and thiamine. If there is fever, blood cultures and a spinal tap for analysis and culture need to be done. Arterial blood gases and carboxyhemoglobin should be determined. Generally, a neurologist or neurosurgeon should be consulted early.

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

SYNCOPE: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

Are there convulsive movements or incontinence? The presence of convulsive movements should suggest convulsions, and the differential diagnosis of this is discussed on page 88 . Convulsive movements can occur with other forms of syncope, however.
Is the pulse slow or absent? The presence of a slow or absent pulse would suggest heart block, vasovagal syncope, and carotid sinus syncope.
Is the pulse rate normal? The presence of a normal pulse rate would suggest anemia, aortic stenosis, aortic insufficiency, and cyanotic congenital heart disease.
Is the pulse rate rapid? The presence of a rapid pulse would suggest the various types of ventricular and supraventricular tachycardias, including auricular fibrillation and flutter, and it should also suggest heat exhaustion or heat stroke.
If the pulse is rapid, is it regular? The presence of a rapid regular pulse should suggest supraventricular or ventricular tachycardia, heat exhaustion, or heat stroke.
Is there a heart murmur? The presence of a heart murmur should suggest aortic stenosis, aortic insufficiency, and cyanotic congenital heart disease.
Is there pallor? The presence of pallor should suggest shock or severe anemia and acute bleeding.
Are there focal neurologic signs? The presence of focal neurologic signs should suggest cerebral vascular insufficiency, hypoglycemia, and transient ischemic attacks.

DIAGNOSTIC WORKUP

The diagnostic workup includes a CBC, sedimentation rate, urinalysis, chemistry panel, VDRL test, thyroid profile, glucose tolerance test, EKG, and chest x-ray. Several blood pressure recordings in the recumbent and upright positions should be made. If hypoglycemia is suspected, a 72-hr fast and a tolbutamide tolerance test should be done. The drug history should always be reviewed. A toxicology screen may be helpful.

Most cases will require 24-hr Holter monitoring or event Holter monitoring. In addition, other cardiovascular studies, such as echocardiography and His' bundle studies, may need to be done. Exercise tolerance testing is useful when the syncope seems to be exercise induced. An upright-tilt test is helpful when vasodepressor syncope is suspected, especially when combined with isoproterenol infusion. Signal-averaged EKG can be useful if a ventricular arrhythmia is suspected. If transient ischemic attacks are suspected, a carotid scan and cerebral angiography may be necessary. If the syncopal attacks are thought to be due to epilepsy, a wake-and-sleep EEG may need to be done. A CT scan or MRI of the brain may need to be done.

A cardiologist or neurologist should be consulted before ordering expensive diagnostic tests. A psychiatrist may also need to be consulted.

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

COMA: Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

Is there a history of drug or alcohol ingestion? This is a very important question to ask, as many cases of coma are due to acute alcohol intoxication, delirium tremens, opium poisoning, barbiturate poisoning, and other toxic cerebral depressants.
Is there a history of trauma? Most of the time it will be obvious that the patient has suffered a blow to the head. However, there are many times when one must contact the family or other people who witnessed the onset of the coma to determine if there was trauma.
Are there focal neurologic signs? Focal neurologic signs would make one think of a stroke, brain abscess, brain tumor, or epidural or subdural hematoma.
Is there papilledema? Papilledema certainly would indicate a possible space-occupying lesion such as a brain tumor, brain abscess, or subdural hematoma.
Is there a sweet odor to the breath? A sweet odor to the breath should make one think of a diabetic coma or alcoholism.
Is there fever? If there is fever, one should be thinking of meningitis, subarachnoid hemorrhage, or acute encephalitis. However, aspiration pneumonia, urinary tract infection (UTI), or septicemia may explain the fever.
Is there nuchal rigidity? The presence of nuchal rigidity suggests a meningitis or subarachnoid hemorrhage.
Are there sibilant or crepitant rales on examination of the lung? Sibilant rales would suggest the possibility that pulmonary emphysema is responsible for the coma, whereas crepitant rales would suggest that there is congestive heart failure or possibly pneumonia.

DIAGNOSTIC WORKUP

When one encounters a patient with coma, the first thing to do is to establish an airway. Next, the blood pressure is taken. If there are any signs of shock, an intravenous access is established, and the shock is treated appropriately. A cardiology and surgical consult are obtained. Blood should then be drawn for a CBC, type and cross-match, sedimentation rate, chemistry panel, electrolytes, blood ammonia level, and blood alcohol levels. Before removing the syringe, 50 cc of 50% dextrose is given unless the patient is suspected of having hyperosmolar nonketotic diabetic coma. A urinalysis and urine drug screen must be done also. Arterial blood gas analysis should be done. If the situation is urgent or emergent, a CT scan is done before the results of the laboratory tests are available. If the laboratory tests are inconclusive, a CT scan must be done anyway.

If all of the above studies are negative, a spinal tap is done for cell count, protein, glucose, VDRL test, smear, and culture and sensitivity. This is especially true when there is fever or nuchal rigidity.

If the diagnosis is still in doubt, blood tests for other toxic materials, such as the lead level, and blood cultures and EEG are done. A neurologist or neurosurgeon is usually consulted as soon as one is available.

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

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)
Workup and Diagnosis
- History should include evaluation of memory difficulties, disorientation, incoherent speech, and level of attention, and a discussion with patients’ family caregivers
  –Risk factors include advanced age, cognitive impairment (including dementia), psychiatric conditions, and severe chronic medical illness
  –Mini-mental status examination
- Physical examination should include vitals, state of hydration, infectious foci, and neurologic exam, with complete investigation into possible medical etiologies
- Initial labs may include serum electrolytes, BUN/creatinine, glucose, calcium, magnesium, CBC, and urinalysis
- Pulse oximetry and/or arterial blood gas may be indicated to screen for hypoxia and/or hypercarbia
- Thyroid function tests and vitamin B₁₂/folate levels
- Imaging studies (e.g., head CT, chest X-ray), blood and urine cultures, and/or lumbar puncture may be indicated
- EEG is indicated if suspect seizure disorder
  –Slowing of α rhythms and unusual slow-wave activity are common in delirium

» 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

Workup and Diagnosis

History and physical exam will often suggest the underlying etiology
–Note pre- and postsyncopal symptoms (e.g., chest pain, dizziness, lightheadedness, nausea/vomiting, headache, diaphoresis, blurry vision, blindness)
–Full HEENT, neurologic, and cardiovascular exam
–Examine for trauma following syncope
–Record BP in supine, sitting, standing, and in both arms
–Strategically attempt to reproduce syncope by Valsalva maneuver (e.g., coughing, deep breathing for 2–3 min)
Initial labs should include CBC, electrolytes, calcium, magnesium, glucose, toxicology screens, and ECG
Further cardiovascular testing may include cardiac enzymes if ischemia is suspected, 24-hour Holter monitor, echocardiogram, stress testing, and/or invasive cardiac monitoring
Head CT to rule out cerebral disease
Doppler ultrasound of carotids if bruit is heard
EEG may be useful if seizure disorder is suspected
Tilt table test may induce vasovagal episode
Plasma aldosterone/mineralocorticoid levels to evaluate for hypovolemia due to adrenocortical insufficiency

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Delirium: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Acute systemic infection
–May be viral or bacterial cause
–Often associated with high fever
Hypoglycemia, diabetic ketoacidosis
Central nervous system infection
–Meningitis, encephalitis, brain abscess

Drugs
–Alcohol: Acute intoxication
–Amphetamines: Also tremors, dry mouth, tachycardia, hyperactivity
–Hallucinogens (LSD, mescaline, PCB) also tremors, dilated pupils, nausea, and abdominal pain
–Phencyclidine (a.k.a. Angel Dust) with atxia, nystagmus, hyperreflexia, and hypertension
–Opiates: Also with pinpoint pupils
–Antihistamines
–Phenothiazines
–Organic solvents
–Salicylates
–Glucocorticoids

Head injury

Rocky Mountain spotted fever (RMSF)
–Delirium and hallucinations may precede rash; fever, headache, myalgias, chills

Malaria
Rabies
Syphilis
–Tertiary syphilis is rare in children
Hyponatremia
Uremia
Migraine
Hypoxia
Heat stroke
Hepatic failure
Systemic lupus erythematosus
–Delirium is due to cerebral vasculitis
Pellagra
–Due to niacin deficiency
–Also with diarrhea, dermatitis, dementia
Hartnup disease
–Rash, ataxia, psychological disturbance
–Symptoms may be intermittent
Porphyria
–Attacks of abnormal behavior do not begin until late adolescence

Workup and Diagnosis

History
–Duration of delirium
–Exposure to excessive heat
–Ingestion of drugs
–Associated signs and symptoms (fever, diarrhea, vomiting, rashes, sweating)
–Recent head trauma
–Unusual or fad diets (diets that are mainly corn-based can lead to pellagra)

Physical exam
–Vital signs
–Pupil size and reactivity
–Nuchal ridgidity, Kernig and Brudzinski sign
–Head exam for signs of trauma
–Scaling rashes (pellagra), petechiae of palms and soles (RMSF), sun sensitivity scars (porphyria)
–Ataxia, asterixis (flapping at wrists with uremia)

Labs
–All patients should have a glucose measurement
–Strongly consider toxicology evaluation for all patients (typically do both blood and urine)
–Serum electrolytes, BUN, creatinine
–Liver testing (ALT, AST, bilirubin, PT/PTT)
–Specific testing of enzyme levels (porphyries), urinary amino acids (Hartnup disease), niacin levels (pellagra)
- Studies
  –Consider LP and head imaging (CT or MRI)

» 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
Workup and Diagnosis
- History: Most important aspect to guide diagnostic workup
  –Vasovagal syncope: Prodromal symptoms (e.g., cold, clammy skin; pallor; nausea; blurry vision; yawning; dizziness; lightheadedness; palpitations; hyperventilation)
  –Duration: Vasovagal syncope is short (seconds to minutes)
  –Inciting situations
  –Lightheadedness: In orthostatic hypotension
  –Syncope at rest or recumbent in seizure or arrhythmia; syncope without prodrome or with exercise/exertion in cardiac etiology
  –Auras in migraine headaches
  –Seizures may have incontinent or post-ictal state or generalized tonic-clonic movements
  –Family history: Sudden or unexplained deaths, cardiac abnormalities, seizures, or deafness
- Physical exam
  –Orthostatic blood pressures and pulse
  –Perform a thorough cardiac and neurologic exam
- Extensive laboratory workup is not usually needed
  –Most clinicians would do an ECG
  –Tilt-table testing to diagnose vasovagal syncope is controversial as it is not very reproducible
  –Labs might include CBC, glucose, electrolytes, drug screen, carboxyhemoglobin, EEG, or head CT as guided by history; if cardiac abnormalities are suspected, may get a chest X-ray, Holter monitoring, or exercise testing

» READ BOOK EXCERPT ONLINE »

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

Coma: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Infection
–Meningitis/encephalitis
–Bacteria, virus, fungi, spirochete
Increased intracranial pressure
–Tumor, abscess, hydrocephalus

Vascular
–Intracranial hemorrhage, stroke
–Hypoxic ischemic injury (hypotension, cardiac arrest, arrhythmia, near-drowning)
–Vasculitis

Toxins
–Uremia, ethanol, atropine, opiates, lead, substance abuse

Trauma: Concussion, contusion
Seizure
–Nonconvulsive status epilepticus
–Postconvulsive state (postictal state)
Electrolyte imbalance
–Hyponatremia, hypernatremia
–Hypomagnesimia
–Hypoglycemia, hyperglycemia
–Hypercalcemia, hypocalcemia

Postinfectious
–Acute disseminated encephalomyelitis (ADEM)

Endocrine disorders
–Adrenal insufficiency
–Thyroid disorders
Degenerative and metabolic diseases
–Urea cycle disorders
–Reye syndrome
–Mitochondrial disease
Systemic infection and sepsis
Hepatic encephalopathy
Psychogenic
The mnemonic AEIOU-TIPS has been used to recall portions of the differential diagnosis:
Alcohol ingestion and acidosis
Epilepsy and encephalopathy
Infection
Opiates
Uremia
Trauma
Insulin overdose or inflammatory disorders
Poisoning and psychogenic causes
Shock

Workup and Diagnosis

History
–Trauma, seizures, diabetes; cardiac, liver, renal disease
–Presence of delirium before the onset of coma
–Fever, neck stiffness, headache
–Possible toxins at home
Physical exam
–Vital signs, temperature
–Pattern of breathing (Cheyne-Stokes, apneustic, ataxic)
–Retinal hemorrhages, otorrhea, spinal fluid rhinorrhea
–Thyroid, cardiac rhythm, murmur
–Skin (cyanosis, petechiae, splinter hemorrhages)
–Hepatosplenomegaly, meningismus

Neuro exam: Response to voice and noxious stimulation
–Papilledema, pupillary size, and light reflex
–Eye movements (spontaneous, doll's, calorics), corneals
–Gag, motor response to pain, DTRs, Babinski
–Decerebrate or decorticate posturing, muscle tone

Labs
–Toxicology screen, glucose, electrolyes
–CBC, ABG, LFT, ammonia
–BUN, creatinine, TSH, blood culture
Studies
–Neuroimaging: CT or MRI
–Lumbar puncture (after herniation has been ruled out)
–If subarachnoid hemorrhage or infection is suspected
–EEG to rule out nonconvulsive status epilepticus, gives clues to a metabolic process (triphasic waves)

» READ BOOK EXCERPT ONLINE »

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

DELIRIUM: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

It is essential to get a history of drug or alcohol use from the patient or family and a drug screen may be done in most cases. The workup should also include a CBC, sedimentation rate, urinalysis, ANA analysis, chemistry panel, and electrolytes. A CT scan or MRI of the brain will be necessary in most cases. It may be wise to administer intravenous thiamine and glucose while awaiting the results of blood work. If there is a fever, blood cultures and possibly a spinal tap (after a CT scan or MRI has ruled out a space-occupying lesion) may be indicated. Arterial blood gas analysis and carboxyhemoglobin should be determined. A neurologist or neurosurgeon needs to be consulted early in the workup.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

SYNCOPE: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

Clinical differentiation of the various forms of syncope is made by combinations of symptoms. Thus, syncope with marked sweating and tachycardia is more likely due to hypoglycemia. Syncope with sweating and bradycardia is more likely due to vasovagal syncope. Focal neurologic signs during the attack suggest transient cerebral ischemia (TIA) and prompt a search for sources of emboli or thrombosis (sickle cell disease, polycythemia, or macroglobulinemia). A family history of syncope suggests migraine, epilepsy, or vasovagal attacks. Epilepsy is a strong possibility in the young, whereas heart block is more likely in the aged. Consequently, an EEG and Holter monitoring are useful in the workup.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

COMA AND SOMNOLENCE: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

It has been my experience that the neurologic examination is best performed simultaneously with the taking of a history from a relative or friend. In this way, various telltale neurologic signs can be found with alacrity. A unilateral dilated pupil (suggesting a subdural hematoma or aneurysm), acetone breath (suggesting diabetic acidosis), contusion of the skull (suggesting cerebral concussion or hematoma), and nuchal rigidity (suggesting a subarachnoid hemorrhage in meningitis) are just a few of the signs that can help identify the cause of the coma rapidly.

Coma without focal neurologic findings should suggest a metabolic or toxic cause. In that case, an intensive laboratory workup as listed below would be indicated. A spinal tap maybe indicated if there is fever as well. On the other hand, coma with focal neurologic signs suggests tumor, abscess, hematoma or cerebral embolism, thrombosis, or hemorrhage. The clinician should proceed with a skull x-ray film and CT scan immediately. When these are not available, immediate referral to a large medical center is necessary. Electroencephalography (EEG) and a spinal tap may identify the cause. A spinal tap should be considered with extreme caution even if there is no papilledema. Of course, a spinal tap is never done in the presence of papilledema unless a neurologist is consulted and CT findings are negative. One indication for a spinal tap under these circumstances might be meningitis. Another might be “benign intracranial hypertension.”

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Source: Differential Diagnosis in Primary Care, 2007

Level of consciousness, decreased: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

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

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

» READ BOOK EXCERPT ONLINE »

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

Syncope: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

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

Next, take the patient’s vital signs and examine him for any injuries that may have occurred during his fall.

» READ BOOK EXCERPT ONLINE »

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

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

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

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

» READ BOOK EXCERPT ONLINE »

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

Syncope: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

Next, take the patient’s vital signs and examine him for any injuries that may have occurred during his fall.

» READ BOOK EXCERPT ONLINE »

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

Delirium: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

A. Baseline. Perhaps the most important aspect of taking the patient’s history is establishing the individual’s baseline mental status and level of functioning. In addition to interviewing the patient, family, friends, and acquaintances must be interviewed as well. Other healthcare providers, such as nurses and doctors, who have dealt with the patient previously in an office, nursing home, or hospital setting, can be invaluable sources of information. Try to establish the presence or absence of the signs and symptoms of dementia or depression (section V).

B. Previous medical history. Look for previously existing medical problems that can precipitate delirium, such as CHF, diabetes, hypothyroidism, benign prostatic hypertrophy or HIV (section I.B). Evaluation of the medications is crucial, including prescription and over-the-counter medications. Is the patient taking them as directed? Is the patient on any medications that could be present in toxic levels (e.g., digoxin, phenytoin or theophylline)? Has there been any recent trauma or surgery? Are there symptoms of infection such as UTI or pneumonia? Be sure to interview friends and family.

C. Social history. Does the patient have a history of substance abuse? Is the patient currently using any alcohol or illegal substances? When was their last use? Be aware of potential withdrawal. If the patient is abusing alcohol, is there a history of delirium tremors with previous abstinence? Does the patient live alone? Is the patient at risk for poor nutrition?

Physical examination.

Because of the fluctuating nature of delirium, serial examinations are valuable.

A. Mental status. Observe the patient and take note of changes of level of consciousness, orientation, agitation, combativeness, hallucinations, or inability to concentrate. Evaluate the mental status by using the Mini Mental Status Examination (4) or a similar tool to standardize the findings (Chapter 4.5).

B. Physical status. Obtain vital signs and evaluate for clinical signs of dehydration, malnutrition, urinary retention, or fecal impaction. The physical examination should be guided by the history, keeping in mind the multifactorial nature of delirium. Evaluate for signs of infection, look for cardiopulmonary decompensation, and complete a thorough neurologic examination with special attention to identifying any focal neurologic deficit.

» READ BOOK EXCERPT ONLINE »

Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

Syncope: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

A. What are the symptoms or circumstances related to the syncope?

1. Dizziness preceding syncope is highly associated with a psychological cause (24%) versus syncope without preceding dizziness (5%) (3). Dizziness with syncope can also be associated with arrhythmia.

2. Important history includes palpitation, duration of prodrome and recovery, and presence of postural or exertional symptoms.

3. Related environmental factors include heat, dehydration, and alcohol.

B. Which disease, risk factor, or family history is present?

1. Organic heart disease is associated with arrhythmia and increased risk of death.

2. Psychiatric illnesses most commonly associated with syncope are major depression (12.2%), alcoholism (9.2%), generalized anxiety disorder (8.6%), and panic disorder (4.3%). These correlate with a higher rate of recurrent syncope, younger age, and a more benign course (4) (Chapters 3.1 and 3.3).

3. Older age (>60 years) is more highly associated with arrhythmias, orthostatic hypotension, medication side-effects, and situational (e.g., micturition) syncope.

4. Ask about diabetes mellitus, neuropathy, anemia, and other chronic diseases.

5. Inquire about a family history of sudden death, hypertrophic cardiomyopathy, or other organic heart disease.

C. What medicines does the patient take? The most commonly implicated are antihypertensives and antidepressants. Others include antianginals, analgesics, and sedatives.

Physical examination

What are the essential aspects to cover?

A. General: mental status, temperature, hydration status, pallor, or cyanosis.

B. Vital signs: tachycardia, bradycardia, irregularity, or orthostatic hypotension.

C. Cardiovascular: heart sounds, murmurs, bruits, edema, rales, and pulses.

D. Neurologic: cranial nerves, reflexes, strength and sensation, tremor, Romberg’s sign, gait, and cerebellar signs.

» READ BOOK EXCERPT ONLINE »

Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

Coma: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

A. Characteristics. Coma patients essentially behave in a reflex manner without spontaneous or purposeful movements, language cognizance or expression, or specific localizing responses (3).

B. Confounding conditions include some medications, mechanical ventilation, immobilized extremities, facial edema, and diurnal variations.

C. Differential diagnosis. Less severe conditions of altered consciousness include vegetative state, the minimally conscious state, akinetic autism, and locked-in syndrome (3).

Physical examination

A. General examination. A thorough general examination, including vital signs, helps to establish and rule out potential causes of coma. Look for evidence of head trauma or metabolic encephalopathy.

B. Neurologic examination. A detailed neurologic examination, including mental status; motor, sensory, reflex coordination; gait; and cranial nerve testing, will help distinguish the location and degree of dysfunction. Look for the following important features:

1. Level of consciousness. Is the patient responsive at all? To what degree?

2. Brainstem function

a. Pupils: assess cranial nerves (CN) 2 and 3 for anisocoria, miosis, pinpoint, mydriasis, or fixed, midposition pupils.

b. Eye movements: assess conjugate gaze, gaze deviation, nystagmus, and spontaneous movements (CN 3, 4, and 6).

c. Funduscopic examination: assess for papilledema and underlying diseases. Corneal reflexes (CN 5 and 7); gag and cough reflexes (CN 9 and 10).

3. Breathing patterns. Cheyne-Stokes respiration suggests cerebral hemispheric or diencephalic injury or an encephalopathy (hypoxic or metabolic). Central hyperventilation suggests brainstem injury. Ataxic or Biot’s respiration, which can progress to apnea, suggests injury to the reticular formation in the medulla and pons.

4. Sensorimotor activity. Are there spontaneous, volitional movements? Is there other motor activity such as choreoathetosis, decerebrate or decorticate activity, myoclonus, asterixis, or seizure activity? Is the muscle tone flaccid, rigid, spastic, or clonic? Is the response to painful stimuli purposeful, flexion withdraw, abnormal posturing, or no response at all?

5. Tendon reflexes. Are the reflexes asymmetric, increased, or decreased?

6. Glasgow Coma scale. Measures the depth and duration of altered consciousness based on the best response to three actions: eye opening, verbal response, and motor response to commands or painful stimulus.

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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

Syncope: Differential Overview
(Field Guide to Bedside Diagnosis)

Orthostatic/Autonomic

❑ Neurally mediated hypotension

❑ Volume depletion

❑ Cough syncope

❑ Anemia

❑ Autonomic insufficiency

Cardiac/Obstructive

❑ Myocardial infarction

❑ Pulmonary embolism

❑ Aortic stenosis

❑ Hypertrophic obstructive cardiomyopathy

❑ Aortic dissection

❑ Cardiac tamponade

❑ Left atrial myxoma

Cardiac/Dysrhythmic

❑ Complete heart block

❑ Sick sinus syndrome

❑ Tachyarrhythmia

❑ Carotid sinus hypersensitivity

Neurologic

❑ Vertebrobasilar ischemia

❑ Hypoglycemia

❑ Unwitnessed seizure

❑ Subclavian steal syndrome

Psychologic

❑ Hyperventilation

❑ Hysterical faint

Diagnostic Approach

The cause of syncope is usually evident after a careful history and physical exam. Identification of a cardiac cause is critical because it portends a poor prognosis (1-year mortality 18% to 33%). In patients with heart disease, the most specific predictors of a cardiac cause are syncope in the supine position or during effort, blurred vision, and convulsive syncope. In patients without heart disease, palpitations are the only significant predictor of a cardiac cause.

Focus on preceding events and witness description. Sudden loss of consciousness without warning is usually due to an arrhythmia. Syncope with chest pain mandates that aortic dissection, myocardial infarction, and pulmonary embolism be ruled out. Syncope with exertion suggests aortic stenosis, hypertrophic obstructive cardiomyopathy, or bradycardia. Events after the syncope, such as confusion, lethargy, or neurological symptoms suggest a seizure.

Consider syncope as the cause of unexplained trauma such as hip fracture or MVA.

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Source: Field Guide to Bedside Diagnosis, 2007

Coma: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Alcohol intoxication

❑ Drug overdose

❑ Hypoglycemia

❑ Metabolic acidosis

❑ Subdural hematoma

❑ Hypothermia

❑ Heat stroke

❑ Meningitis

❑ Subarachnoid hemorrhage

❑ Head trauma

❑ Ischemic encephalopathy

❑ Epidural hematoma

❑ Pontine hemorrhage

❑ Cerebellar hemorrhage

❑ Psychogenic

Diagnostic Approach

Coma is a state of pathological unconsciousness, where the patient is unaware of their environment and unarousable. It is caused by dysfunction of either the reticular activating system above the level of the mid-pons or both cerebral hemispheres. It should be distinguished from brain death due to cessation of cerebral and cerebellar function, marked by absense of response to stimuli, respiratory drive, and central reflexes (although spinal reflexes may be preserved), and from persistent vegetative state, characterized by diurnal wakefulness but with unawareness and inability to interact with others.

Pupils: Pupillary responses are more sensitive than papilledema in detecting increased intracranial pressure. Normal pupils imply an intact midbrain and CNIII. Preserved pupillary light reflex with other signs of brainstem impairment suggests a toxic/metabolic cause. Asymmetric reactivity is consistent with an acute structural process. A unilaterally dilated pupil suggests ipsilateral uncal herniation. Hypothermia, barbiturates, and midbrain lesions produce midposition unreactive pupils. Pinpoint pupils occur with pontine lesions and opiates. Bilateral dilated unresponsive pupils occur with anoxia, severe midbrain damage caused by transtentorial herni-ation, or anticholinergic drugs. Large pupils that dilate and contract automatically (hippus) but do not react to light suggest a tectal lesion.

Eye deviation: Injection of ice water into the ear (calorics) normally causes deviation of both eyes toward the stimulated ear. Its absence implies dysfunction of the pons or medulla. Cortical mass lesions produce ipsilateral conjugate deviation that can be overcome with calorics. Brainstem and pontine lesions produce contralateral deviation that cannot be overcome with calorics. In metabolic coma or drug overdose coma, eyes move loosely side-to-side opposite the turning of the head. A pontine or cerebellar lesion causes skew deviation (separation of horizontal axes). Ocular bobbing (briskly down, slowly up) is a result of bilateral pontine lesions. Ocular dipping (slow arrhythmic downstroke, followed by a faster upstroke) with normal calorics is consistent with anoxic encephalopathy.

Posturing: Decorticate posturing (arm flexion and leg extension) is found with hemispheric lesions or metabolic derangement. Decerebrate posturing (extension of the legs and arms) implies dysfunction of the midbrain or upper pons on a structural or metabolic basis. In response to noxious stimuli, flexion, extension, and adduction reflexes are found. Shoulder and hip abduction involve cortical activity whereas withdrawal implies voluntary behavior.

Respiratory pattern: If the patient is yawning or swallowing, coma is not very deep and brainstem function is intact. Cheyne-Stokes respiration (crescendo-decrescendo pattern with apneic pauses) is seen with herniation, metabolic encephalopathy, and congestive heart failure. Central neurogenic hyperventilation (rapid deep breathing) indicates damage to the brainstem between the midbrain and pons. Ataxic respiration occurs with midbrain lesions. Apneustic respiration with inspiratory pauses occurs with pontine lesions and precedes respiratory arrest.

Asymmetric resting muscle tone, deep tendon reflexes, or Babinski response suggests a structural lesion. A toxic/metabolic cause is suggested by preceding confusion, disorientation, and somnolence. Myoclonic jerks or clonus provide further support.

The Glasgow Coma Scale is scored as follows: Best Motor Response: 6 obeys commands, 5 localizes pain, 4 withdraws to pain, 3 decorticate (flexion), 2 decerebrate (extension), 1 none. Best Verbal Response: 5 oriented, 4 confused conversational, 3 inappropriate words, 2 incomprehensible sounds, 1 none. Eye Opening: 4 spontaneous, 3 to speech, 2 to pain, 1 none.

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Source: Field Guide to Bedside Diagnosis, 2007

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

Diagnostic Approach

Delirium is characterized by gross disorientation in the presence of alertness and vigilance, disorders of perception with vivid illusions, and psychomotor and autonomic hyperactivity. It usually develops over a short time and is associated
with fluctuating mental status, decreased attention, disorganized thinking as indicated by rambling, irrelevant, or incoherent speech, and a decreased level of consciousness. The most sensitive findings are variability in level of arousal, impaired short-term memory (e.g., digit span), and disorientation to time. Relatives or friends are helpful sources of information about the tempo and degree of impairment.

Fever, tachycardia, or hypertension should prompt a careful evaluation for a medical cause. Infection is a common cause in the elderly, especially pneumonia or urinary tract infection. Visual hallucinations are organic in origin, due to factors such as drugs, rather than due to schizophrenia.

Confusion Assessment1) Change in mental state (from baseline) that is acute and fluctuates. 2) Difficulty focusing attention or trouble keeping track of what is said. 3) Disorganized thinking (rambling or irrelevant conversation, unpredictable switching between subjects, illogical flow of ideas). 4) Altered level of consciousness (lethargy, stupor, or hyperalert). A positive test requires 1 and 2 positive, and either 3 or 4.

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Source: Field Guide to Bedside Diagnosis, 2007

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

Physical examination

Because decreased LOC can result from a disorder affecting virtually any body system, tailor the remainder of your evaluation according to the patient’s associated symptoms. Perform a complete neurologic assessment and a physical assessment. Determine the patient’s baseline Glasgow Coma Scale score and evaluate on an ongoing basis.

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

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

Ask the patient for information about the fainting episode. Did he feel weak, light-headed, nauseous, or sweaty just before he fainted? Did he stand quickly from a sitting or prone position? During the fainting episode, did he have muscle spasms or incontinence? How long was he unconscious? When he regained consciousness, was he alert or confused? Did he have a headache? Has he fainted before? If so, how often does it occur?

Physical examination

Perform a complete cardiac and neurologic examination. Provide continuous cardiac monitoring. Next, take the patient’s vital signs and examine him for injuries that may have occurred during his fall.

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

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

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

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

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

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

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

Cardiovascular Syncope

Neurocardiogenic Syncope (Common Faint)

Most commontype of syncope in childhood and adolescence.

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

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

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

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

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

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

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

Seizures are unusual but may occurwith prolonged syncope.

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

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

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

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

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

Cardiac Syncope

Congenital and Acquired Heart Disease

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

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

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

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

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

Hypercyanotic Episodes

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

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

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

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

Arrhythmias in Structurally Normal Heart

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

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

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

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

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

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

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

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

Arrhythmias in Structurally Abnormal Heart

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

WPW syndrome and supraventricular tachycardiaare occasionally associated with Ebstein anomaly.

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

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

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

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

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

Vascular Syncope

Orthostatic Syncope

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

Possible causes include

Decreasedblood volume (blood loss, GI fluid loss, excessive diuretic use)

Failure of normal postural reflexes(suddenly standing up after prolonged bedrest, familial dysautonomia,spinal cord lesions)

Drugs (vasodilators, tricyclic antidepressants,sedatives, opiates, cocaine)

Supine and standing BPs should be measuredin any individual with unexplained syncope.

Cerebrovascular Syncope

This typeof syncope may be due to excessive vagal stimulation, which causessevere bradycardia or AV block.

Examples include intubation, placementof nasogastric tube or esophageal overdrive pacing catheter, removalof pleural or peritoneal fluid, and distention of viscera.

Excessive vagal tone also may occurin normal adolescents or well-trained athletes, and a further increasein vagal tone may worsen bradycardia or AV block enough to causesyncope.

Carotid Sinus Syncope

Pressure on baroreceptors in carotid sinusmay cause carotid sinus syncope. Uncommon in children but can occurwith excessive pressure on neck (e.g., wearing tight collar).

Noncardiovascular Syncope

Breath-Holding

Common inchildren 6 mos–6 yrs of age. Precipitating factors includepain, frustration, and anger.

Pallid breath-holding, which is nowthought to be variation of neurocardiogenic syncope, usually followsacute pain or injury. The infant or child becomes pale and losesconsciousness. Complete recovery occurs in 1–2 mins.

More common is cyanotic breath-holdingspell in which infant or child cries, holds breath during expiration,and turns dusky until breathing begins again. Loss of consciousnessand tonic-clonic movements may occur with prolonged episode.

Hyperventilation

Frequentcause of dizziness but rare cause of syncope.

Common in adolescent girls and usuallydue to emotional stress.

Frequent complaints include lightheadedness,blurred vision, difficulty breathing, choking, smothering, chesttightness, and numbness or tingling of fingers, toes, and face.Individuals who are hyperventilating appear anxious and have fastand deep respirations.

Rebreathing into paper bag and thoughtfulreassurance usually lessen hyperventilation, so that individualscan begin talking about what is upsetting them.

Migraine

Severe migraine headache may cause syncopalepisode, especially if basilar arterial system is affected (see Chap. 25, Headache).

Metabolic

Hypoxia Including Anemia

Severe hypoxia or severe anemia of any causemay result in syncope. See Chap.45, Pallor (Anemia), and Chap. 56, Respiratory Distress and Apnea.

Hypoglycemia

Often causesfaintness and dizziness, but syncope is exceedingly rare. Othermanifestations of hypoglycemia include headache, hunger, sweating,and jitteriness, which may progress to confusion, seizures, andcoma.

Low blood glucose level confirms presenceof hypoglycemia.

With administration of oral or intravenousglucose, symptoms resolve.

See further discussion of hypoglycemiain Chap. 59, Seizures.

Psychologic

Acute stressmay produce anxiety and syncope with or without hyperventilation. Commonstresses are witnessing a tragic event or hearing news of the deathof close friend or relative.

Hysteria is common cause of recurrentfainting in adolescents, especially in those with hysterical personalities.

In this typeof episode, which almost always occurs in presence of other people,hysterical person falls or slumps in dramatic way but avoids injury.Fainting also may occur while lying or sitting down. There is noprodrome or change in heart rate, BP, or skin color.

Diagnosis of psychologic causes ismade from history, physical exam, and clinical observation.

Diagnostic Approach

Neurocardiogenicsyncope, vascular syncope, breath-holding, hyperventilation, and psychologicdisturbances can usually be distinguished by history and physicalexam.

If syncopal episode occurs on assumingupright posture, BP should be measured in supine and upright positions.Postural difference in systolic pressure of >15 mm Hg confirmsdiagnosis of orthostatic syncope.

Individuals with recurrent syncope,family history of sudden death, or syncope occurring during intensiveexercise need further evaluation.

If recurrent syncope occurs, tilt testingmay determine whether syncope is neurocardiogenic.

Family history of syncope and suddendeath suggests hypertrophic cardiomyopathy or long QT interval syndrome.

Syncope during intense exercise mayoccur with hypertrophic cardiomyopathy, severe aortic stenosis,anomalous left coronary artery from pulmonary artery, primary pulmonaryhypertension, or exercise-induced atrial fibrillation associatedwith WPW syndrome.

Diagnosis of cardiac disorders canbe made from history, physical exam, chest radiograph, ECG, and2-D echocardiogram. Cardiac catheterization and angiography maybe necessary to make definitive diagnosis and to determine severityof lesion. Arrhythmia may be suspected from history, and routine ECGwith rhythm strip may be diagnostic. Otherwise, further testingmay be needed (e.g., Holter monitoring, maximal exercise testing,event recorder or implanted loop recorder monitoring, and electrophysiologictesting).

With syncopal episode of unknown cause,ECG should be initially performed searching for WPW syndrome, longQT interval syndrome, or LV hypertrophy with T-wave changes indicativeof cardiomyopathy.

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

Alteration in Consciousness: Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)

Head Trauma

Concussion

Definedas transient loss of neurologic function that usually involves lossof consciousness (seconds or minutes) after head trauma. Postconcussionsyndrome consisting of nausea, vomiting, headache, and lassitudemay last hours or days.

Diagnosis is made by the history, absenceof focal neurologic findings on physical exam, and normal brainimaging.

Brain Contusion

Definedas area of microscopic disruption of cellular architecture of brain.

May occur directly below area of injuryor as contrecoup lesion from acceleration-deceleration injury.

Some contusions increase in size infirst few days after injury and produce mass effect with contralateralshift of midline structures.

Small contusions usually resolve spontaneously.

CT or MRI is diagnostic.

Shearing Injury

Axonal injuryof white matter occurs.

Clinical spectrum varies from mildconcussion to coma.

CT is diagnostic, but MRI yields morespecific information, especially in individuals with unexplainedneurologic deficits or persistent loss of consciousness.

Cerebral Edema

Diffusecerebral edema is more common than focal lesion after head trauma.

Persistent loss of consciousness isusual clinical manifestation of severe cerebral edema.

CT findings of loss of gray-white interfacemay not be visible until 12–24 hrs after brain injury.

Intracranial Hemorrhage

Intraparenchymal Hemorrhage

Usuallyoccurs from direct blow to head or a penetrating injury.

Clinical manifestations include headache,vomiting, seizures, and alteration in consciousness.

CT is diagnostic.

Subdural Hematoma

Definedas collection of blood beneath dura.

Produced by tearing of cortical bridgingveins between dura and arachnoid.

Whether alteration of consciousnessoccurs depends on how severe injury is and size of hematoma.

Shaking injury in infants <1yr also may produce subdural hematoma, as well as seizures, bulgingfontanelle, retinal hemorrhages, and apnea.

CT is diagnostic.

Epidural Hematoma

Definedas collection of blood between dura and skull that occurs from bleedingfrom cerebral arteries or veins.

May be associated with overlying skullfracture.

Loss of consciousness may occur attime of injury or in 1–2 days, when hematoma enlarges. Vomiting,headache, and seizures also may occur.

CT is diagnostic.

Infection/Inflammation

Bacterial Meningitis

Most commonintracranial infection that produces alteration in consciousness.

Group B Streptococcus and gram-negativeenteric bacteria are most common pathogens in neonates, whereasS. pneumoniae and N. meningitidis are most common in infants andchildren. H. influenzae type b has become much less common sincedevelopment of H. influenzae vaccine.

Clinical findings include fever, irritability,headache, vomiting, stiff neck, bulging fontanelle, and seizures.Kernig and Brudzinski signs indicate meningeal irritation, but meningealsigns may not be present in infants.

Analysis of CSF reveals pleocytosisincluding many polymorphonuclear leukocytes, increased protein,and usually decreased glucose. Gram stain of spinal fluid is oftenpositive, and positive culture is diagnostic.

Detection of polysaccharide antigens(S. pneumoniae, N. meningitidis, group B Streptococcus) in CSF bylatex agglutination is also diagnostic.

Encephalitis

Definedas inflammatory process that involves brain. Pathogens include enteroviruses,measles virus, mumps virus, rabies virus, herpes simplex virus,varicella-zoster virus, Epstein-Barr virus, cytomegalovirus, arboviruses,M. pneumoniae, and rickettsiae.

Clinical findings include fever, headache,vomiting, ataxia, seizures, and alteration in consciousness.

CSF analysis usually reveals increasedcell count with primarily mononuclear cells, normal or mildly increasedprotein level, and normal glucose level.

MRI may demonstrate inflammation ofcerebral cortex, gray-white matter junction, or basal ganglia.

Diagnostic tests include appropriatecultures, polymerase chain reaction, and serologic methods.

Postinfectious encephalitis is autoimmuneprocess that usually follows preceding viral infection within 1–2wks. Clinical findings are similar to those that occur with infectiousencephalitis. MRI often shows demyelination in multiple areas ofbrain.

Septicemia

Ill childrenmay have alteration in consciousness.

Most common pathogens in neonates aregroup B Streptococcus and E. coli, whereas S. pneumoniae, N. meningitidis,group A Streptococcus, and S. aureus are most common in infantsand children.

Positive blood culture is diagnostic.

Focal Infection

Brain Abscess

Definedas localized collection of pus in cerebral hemispheres or cerebellum.

Predisposing factors are meningitis,sinusitis, chronic otitis media, mastoiditis, bacterial pneumonia,dental infection, endocarditis, congenital heart disease, and penetratinghead trauma.

Most common pathogens include Streptococcusspecies, Staphylococcus species, H. influenzae, N. meningitidis,Enterobacteriaceae, and anaerobes. Fungi and mycobacteria also maycause brain abscess.

Location of abscess and presence ofmass effect determine presentation.

Clinical manifestations include fever,headache, vomiting, seizures, ataxia, hemiparesis, visual fielddefects, papilledema, and alteration in consciousness.

CT or MRI is usually diagnostic.

Pathogens may be cultured from bloodor CSF in about 10% of cases. Yield of positive CSF culturesis higher in individuals with coexisting meningitis or rupture ofabscess into subarachnoid space. Lumbar puncture should not be performeduntil increased intracranial pressure has been excluded by CT orMRI.

Sometimes specific pathogen may beidentified by culturing abscess contents obtained from CT-guidedaspiration or surgical excision of abscess. These procedures mayneed to be performed when patients do not meet criteria for medicaltreatment alone.

Epidural Abscess

Occurs inepidural space between dura and skull.

Risk factors include sinusitis, otitismedia, orbital cellulitis, meningitis, and osteomyelitis.

Most common pathogens are same as thosethat cause brain abscess.

Clinical features include fever, headache,and sometimes alteration in consciousness.

CT or MRI is usually diagnostic.

Subdural Empyema

Usuallyoccurs from spread of infection from meninges, middle ear, or sinuses. Pathogenscausing this unusual infection are same as those causing brain abscess.

Fever, headache, vomiting, neck stiffness,papilledema, seizures, and alteration in consciousness are commonfindings.

CT or MRI can be diagnostic. Surgicaldrainage confirms diagnosis and is therapeutic.

Seizures

Status Epilepticus

Generalizedconvulsive status epilepticus is defined as single generalized seizurelasting >30 mins or recurrent seizures with failure toregain consciousness between them.

Predisposing factors include febrileillness, bacterial meningitis, viral encephalitis, head trauma,underlying brain disorders, and noncompliance with anticonvulsanttherapy.

Nonconvulsive generalized status epilepticusincludes absence status and almost always occurs in children withknown epilepsy.

Frequently recurring complex partialseizures with failure of recovery between seizures constitute partialnonconvulsive status.

Children with absence status or complexpartial status may be ambulatory but unable to follow complex commandsor converse appropriately.

Postictal State

After generalized or complex partial seizure,child may be confused and difficult to arouse. Normal consciousnessis usually regained in a few hours.

Brain Tumor

Alterationof consciousness may occur with brain tumors because of seizures,increased intracranial pressure, tumor invasion of reticular activatingsystem, or hemorrhage.

Location of tumor determines otherfindings.

Tumors above tentorium can cause seizures,hemiparesis, speech problems, and intellectual difficulties, whereastumors below tentorium usually cause vomiting and ataxia.

CT or MRI locates and defines extentof tumor.

Histologic diagnosis is definitive.

See Chap.25, Headache.

Cerebrovascular Disorders

Cerebral thrombosis, embolism, or hemorrhagemay interrupt cerebral blood flow to produce stroke and alterationof consciousness.

Cerebral Thrombosis

Cerebralinfarction from occlusion of major cerebral artery usually producesfocal neurologic deficit without loss of consciousness, unless cerebraledema or hemorrhage produces significant increase in intracranialpressure.

Common causes of stroke in pediatricpopulation are sickle cell disease, vasculitis, vascular dysplasia,and coagulopathy.

Clinical features depend on cerebralartery involved. Usual finding is acute hemiparesis, which may beaccompanied by seizures, aphasia, hemianopia, and sensory changes.Evolution of thrombotic stroke usually occurs over minutes to hours.

Thrombolytic therapy is only recommendedwithin 3 hrs of thrombotic or embolic stroke.

Exclusion of intracranial hemorrhageby CT is important consideration if thrombolytic therapy is beingconsidered. Diffusion-weighted imaging on MRI may show signal changewithin few hours, indicative of infarction, whereas T2-weightedMRI takes 12–24 hrs to show signal change from infarction. CTmay not show low-density changes from infarction for 24–72hrs. Once it has been determined that infarction has occurred, specificcause must be investigated.

Venous thrombosis (usually venous sinusthrombosis) leads to ischemia and sometimes infarction, usuallyhemorrhagic. Predisposing factors include infection (meningitis,sinusitis, mastoiditis, brain abscess), head trauma, dehydration,sickle cell disease, and drugs (L-asparaginase).

Clinical presentation depends on underlyingdisease process and its extent. Clinical features include vomiting,headache, seizures, hemiparesis, and alteration in consciousness.

CT or MRI can locate area of ischemiaor hemorrhage, but magnetic resonance venography is method of choiceto demonstrate venous thrombosis.

Cerebral Embolism

Emboli fromorganized thrombus, fat, air, bacteria, or tumor can occlude cerebralartery.

Causes include thrombosis (congenitalheart disease with right-to-left shunt lesions, atrial myxoma, cardiomyopathy,endocarditis, atrial fibrillation, arterial dissection), fat emboli(complications of fractures), air emboli (complications of cardiacor thoracic surgery), septic emboli (pneumonia or lung abscess),and tumor emboli that involve blood vessels.

Embolic strokes usually evolve overminutes. Seizures and transient loss of consciousness may occurinitially, and headache, vomiting, and lassitude can follow. Focalneurologic findings include hemiparesis, aphasia, hemianopia, andsensory changes, depending on which cerebral artery is involved. Mostfrequent vessel involved is middle cerebral artery.

CT or MRI can locate area of ischemiaor hemorrhage (see CerebralThrombosis). Specific cause must be investigated.

Cerebral Hemorrhage

Most commoncause of cerebral hemorrhage is head trauma. However, spontaneous hemorrhagecan occur from rupture of a cerebral aneurysm or arteriovenous malformation.

See Chap.25, Headache.

Hydrocephalus

Acute hydrocephaluswith increased intracranial pressure may occur as consequence ofobstruction of ventricular pathways (e.g., enlarging brain tumorin posterior fossa).

Headache, vomiting, lassitude, andalteration in consciousness are common findings. Increased intracranialpressure also may occur from malfunction of ventricular shunt.

CT is diagnostic. With increased intracranialpressure, shunt radiographic series and CT should be performed immediatelyand neurosurgical consultation requested.

Blood Pressure Disorders

Hypotension

May be dueto hypovolemia (diarrhea; vomiting; blood loss; plasma loss fromburns, hypoalbuminemia, or peritonitis; osmotic diuresis from diabetesmellitus), vasodilatation and pooling of blood in peripheral vasculature(septicemia, anaphylaxis, CNS or spinal injuries, drug ingestions),and depression of myocardial function (congenital heart disease,viral myocarditis, cardiomyopathy, arrhythmia, drug ingestion, complicationsof cardiac surgery).

Early signs include tachycardia, mildtachypnea, decreased capillary refill (>2–3 secs)and orthostatic changes in BP. Skin becomes cool and pale, and decreasedperfusion of brain results in confusion, agitation, and finallycoma.

Hypertensive Encephalopathy

Althoughthere is no absolute level of BP where hypertensive encephalopathyoccurs, rate of increase and level of BP are important determinants.After lowering BP, specific cause needs to be investigated.

Clinical findings include headache,vomiting, visual disturbance, seizures, and alteration in consciousnessthat may proceed to coma.

See Chap.32, Hypertension).

Metabolic Disorders

Hypoxic-Ischemic Encephalopathy

Producesloss of consciousness within seconds. If adequate ventilation andcardiac action are restored within 3–5 mins, recovery isusually complete. If hypoxia persists >5 mins, permanent neurologicdeficit usually occurs, unless subnormal body temperatures havediminished rate of cerebral metabolism and prolonged tolerated periodof hypoxia.

Most common cause in neonates is perinatalasphyxia. In infants and children, common causes include respiratoryarrest, near-drowning, strangulation, carbon monoxide poisoning,upper airway obstruction, aspiration of vomitus, and shock.

Diagnosis depends on history of hypoxicepisode and evidence of reduced oxygenation of arterial blood. Ingeneral a partial pressure of arterial O₂ of <50mm Hg causes confusion, and <20 mm Hg causes loss of consciousness.

Most severely affected patients requiremechanical ventilation and usually have flaccid limbs and recurrentseizures. They may die within 1–2 days or survive in irreversiblecoma for variable periods of time.

Acute Bilirubin Encephalopathy (Kernicterus)

Has becomemuch less common since anti-Rh immunoglobulin has been used to preventmaternal sensitization, but it still occurs.

Most cases in past decade have occurredin infants with G6PD deficiency, in ill newborns with low bilirubinlevels, and in apparently normal term and near-term newborns withbilirubin levels much >30 mg/dL. In latter group,infants were breast-fed but had weight loss secondary to decreasedcaloric intake or dehydration, and just about all of them were ≤40wks' gestation.

Initial manifestations include poorsucking, diminished movement, decreased muscle tone, and increasedsleepiness. Progression of illness causes irritability, minimalfeeding, high-pitched cry, and increased muscle tone, which mayinclude arching of neck (retrocollis) and back (opisthotonus). Severely illinfants have shrill cry, increased muscle tone, seizures, and coma.

Diabetic Ketoacidosis

Complicationof diabetes mellitus.

Possible causes in individuals withknown diabetes mellitus include inadequate insulin dosage, failureto take proper dose of insulin, and intercurrent infection.

Vomiting, abdominal pain, and hyperpneaare frequent findings. Alteration in consciousness occurs in severecases.

Presence of hyperglycemia, glycosuria,ketonuria, and metabolic acidosis (arterial pH <7.25 andserum bicarbonate <15 mEq/L) confirm diagnosis.

Hypoglycemia

Blood glucoseconcentration <30 mg/dL may produce confusionand seizures. If blood glucose falls to <10 mg/dL,loss of consciousness may occur.

Clinical presentation of hypoglycemiausually unfolds over 30–60 mins. If blood glucose is low,venous blood should be drawn for further studies and glucose shouldbe given immediately.

See Chap.59, Seizures.

Hypothermia

Definedas core temperature <35DEGC (95DEGF).

Common causes include exposure to lowenvironmental temperature, cold water immersion, septicemia, andanorexia nervosa.

Mental status may be normal with mildhypothermia but deteriorates until coma occurs at about 27DEGC.

Heat-Related Illness

Includesheat cramps, heat exhaustion, and heat stroke.

Heat cramps are muscle cramps occurringduring severe work.

Individuals with heat exhaustion experienceheadache, vomiting, and severe thirst from working in hot environmentwithout adequate replacement of water and salt. Body temperatureis usually <39DEGC.

With heat stroke, body temperatureis >41DEGC and CNS dysfunction (confusion, agitation, seizures,coma) and circulatory collapse may occur.

Hepatic Coma

May occurwith any form of severe acute or chronic liver disease. Intercurrentinfection, GI bleeding, and electrolyte imbalance with hypokalemiamay precipitate hepatic coma in those with severe liver disease.

Clinical findings include progressivejaundice, alteration in consciousness, and preceding asterixis.

Usual lab findings include elevationof serum aminotransferases and ammonia along with primarily conjugatedbilirubin. Prothrombin time is prolonged and serum albumin is decreased.Blood ammonia is usually >200 μmol/L,and severity of neurologic disturbance parallels ammonia levels.

Reye Syndrome

Due to diminisheduse of aspirin in recent years, incidence has decreased markedly.

Onset of persistent vomiting is usuallyfirst sign and occurs during week after viral illness or varicella.Confusion and listlessness may progress to disorientation and combativeness.Seizures may occur, but fever is unusual. Hypoglycemia is frequentfinding, especially in infants <1 yr. Decorticate or decerebrateposturing and loss of brainstem function due to cerebral edema mayoccur with disease progression.

Viral prodrome, behavior changes, unexplainedvomiting, and characteristic chemical profile (increase in serumaminotransferases, ammonia, and prothrombin time with minimal changein bilirubin) suggest diagnosis. Liver biopsy is usually diagnosticbut may not be necessary in mild cases. Certain metabolic disorders,such as defects in fatty acid oxidation, may mimic the condition.

Uremia

Alteration in consciousness may occur, butprecise mechanism is unknown.

Inborn Errors of Metabolism

Besides alteration of consciousness, clinicalfeatures include poor feeding, vomiting, seizures, and delayed neurologicdevelopment. Hyperammonemia occurs in many of these disorders.

Maple Syrup Urine Disease

Recognizedas autosomal-recessive disorder caused by deficiency in activityof branched-chain alpha-ketoacid dehydrogenase complex.

Onset of classic form is usually infirst or second week of life, with poor feeding, seizures, and alterationin consciousness.

Urine has characteristic odor of maplesugar and is positive for ketones.

Subsequent episodes of metabolic acidosisand disturbed consciousness may occur during catabolic period orwith excess protein intake.

Affected children usually have psychomotorretardation.

Analysis of plasma amino acids revealsincreased concentrations of isoleucine, leucine, and valine.

Enzyme assay of cultured fibroblastsor leukocytes is definitive.

Nonketotic Hyperglycinemia

Mutationsin several genes in glycine cleavage enzyme system can cause thisautosomal-recessive disorder.

Onset is typically in first few daysof life, with hypotonia, myoclonic jerks, alteration in consciousness,and often hiccups. Clinical course is characterized by intractableseizures and severe developmental delay.

Lack of hypoglycemia, metabolic acidosis,ketosis, hyperammonemia, hepatocellular dysfunction, and cardiac,renal, or hematologic abnormalities suggests diagnosis.

Though serum and urinary glycine concentrationsare usually increased, elevation of CSF glycine is considered diagnostic.

Hyperammonemic Disorders

Urea Cycle Defects

Urea cycleis major pathway for conversion of ammonia to urea. Enzyme deficiencies inthis pathway lead to production of excessive amounts of ammonia.

All are autosomal-recessive disordersexcept for ornithine transcarbamylase deficiency, which is X-linkeddisorder.

These defects commonly present duringfirst week of life, with poor feeding, vomiting, tachypnea, seizures,and alteration in consciousness, except for arginase deficiency,which usually appears in later infancy. Infants who survive neonatalperiod usually have developmental delay and psychomotor retardation.

Carbamyl Phosphate Synthetase Deficiency

Gene locushas been mapped to chromosome 2q35.

Serum levels of citrulline and arginineand urinary level of orotic acid are low.

Liver biopsy with enzyme assay is definitive.

Ornithine Transcarbamylase Deficiency

Althoughaffected boys become symptomatic in neonatal period, girls who arecarriers usually become symptomatic in childhood.

Clinical features include feeding difficulty,failure to thrive, intermittent ataxia, and alteration in consciousness.Plasma citrulline concentration is low, whereas urinary orotic acidconcentration is high.

Liver biopsy with enzyme assay is definitive.

Argininosuccinic Acid Synthetase Deficiency (Citrullinemia)

Gene locushas been mapped to chromosome 9q34.

3 clinical phenotypes have been described.

In neonates presentation is acute andsimilar to that of ornithine transcarbamylase deficiency.

In infants onset is gradual with poorfeeding, vomiting, hepatomegaly, and psychomotor retardation.

In children episodic hyperammonemiamay cause vomiting and seizures.

Marked increase in serum citrullineconcentration (>1,000 μM) is diagnostic. Enzymeassay of liver tissue or cultured fibroblasts is definitive.

Argininosuccinase Deficiency (Argininosuccinic Aciduria)

Gene locushas been mapped to chromosome 7.

Can present in neonatal period withacute encephalopathy or in infancy with hepatomegaly, seizures,ataxia, and developmental delay.

Some children have short brittle hair(trichorrhexis nodosa).

Plasma citrulline concentration ismoderately increased (100–300 μM).

Presence of high serum and urine concentrationsof argininosuccinic acid is diagnostic. Enzyme can be assayed inliver or skin fibroblasts.

N-Acetylglutamate Synthetase Deficiency

Catalyzesformation of N-acetylglutamate from glutamate and acetyl-CoA andis required activator of carbamyl phosphate synthetase. Only a fewcases have been reported.

Usual lab findings are absent or traceserum citrulline, low serum arginine and ornithine, increased serumalanine and glutamine, and decreased urinary orotic acid. Liverbiopsy that shows decreased enzyme activity confirms diagnosis.

Arginase Deficiency (Argininemia)

Gene locushas been mapped to chromosome 6q23.

Usually presents in infancy.

Characteristic features include recurrentvomiting, spastic diplegia, seizures, and developmental delay. Symptomatichyperammonemia may progress to encephalopathy.

Serum citrulline concentration is normalor mildly increased. High serum arginine concentration is diagnostic.Enzyme assay of erythrocytes or liver tissue is confirmatory.

Organic Acid Disorders

Propionic, Isovaleric, and Methylmalonic Acidemias

Autosomal-recessiveand clinically indistinguishable.

Hyperammonemia, metabolic acidosiswith anion gap, hypoglycemia, and urinary ketones usually occur.Psychomotor retardation occurs in most affected individuals.

Urinary organic acid analysis showstypical organic acid profile of specific disorder. Definitive diagnosisis made by analysis of specific enzyme activity in cultured skinfibroblasts or sometimes by specific mutation analysis.

Propionic acidemia is due to deficiencyin activity of propionyl-CoA carboxylase, which catalyzes conversionof propionyl CoA to methylmalonyl CoA.

Gene locus of type I has been mapped to chromosome13q32; gene locus of type II has been mapped to chromosome 3q21-22.

Excessive amounts of propionic acidand glycine in blood and urine suggest diagnosis. Presence of excessiveamount of methylcitrate in urine is diagnostic.

Deficiency in activity of isovalerylCoA dehydrogenase, which catalyzes conversion of isovaleryl CoAto 3-methylcrotonyl CoA, causes isovaleric acidemia.

Gene locushas been mapped to chromosome 15q14-q15.

Odor of sweaty feet produced by isovalericacid has been described.

Detection of excessive amounts of isovalerylglycineand 3-hydroxyisovaleric acid in urine is diagnostic.

Methylmalonic acidemias are group ofdisorders in which methylmalonic acid accumulates in body fluidsbecause of deficiency in activity of methylmalonyl-CoA mutase. Thisenzyme requires cobalamin (vitamin B₁₂) ascofactor for activity.

Classic form of methylmalonic academia, whosegene locus has been mapped to chromosome 6p21, is not responsiveto pharmacologic doses of vitamin B₁₂.

In another milder form of disorderthat presents later in infancy with vomiting and delayed growthand development, pharmacologic doses of vitamin B₁₂ contributeto dramatic improvement.

In either form, excessive amount ofmethylmalonic acid is found in urine, which is diagnostic.

Glutaric Aciduria, Type II (Multiple Acyl-CoA DehydrogenaseDeficiency)

Can occurfrom deficiency in alpha or beta subunits of electron transfer flavoprotein ordeficiency of electron flavoprotein dehydrogenase.

Genetic transmission is autosomal-recessive,and gene locus for each defect has been mapped to different chromosomes.

Typical clinical features in neonatesare vomiting, tachypnea, hepatomegaly, sweaty feet odor, and alterationof consciousness.

Biochemical abnormalities include hyperammonemia,hypoglycemia, metabolic acidosis without ketosis, and large urinaryexcretion of glutaric, lactic, ethymalonic, butyric, isobutyric,2-methyl-butyric, and isovaleric acids.

Specific defects may be demonstratedin cultured fibroblasts.

Multiple Carboxylase Deficiency

2 basictypes of multiple carboxylase deficiency are holocarboxylase synthetasedeficiency and biotinidase deficiency.

Gene locus of former is chromosome21q22.1, whereas that of latter is chromosome 3p25.

Basic defect involves metabolism ofbiotin, vitamin necessary for action of carboxylases.

Onset of holocarboxylase synthetasedeficiency is in first week of life with tachypnea, vomiting, hypotonia,seizures, and alteration of consciousness.

Metabolic features include hyperammonemia,metabolic acidosis, ketosis, hypoglycemia, and organic acidemiawith increased serum concentrations of lactate, propionate, andbeta-methylcrotonate.

Enzyme defect can be demonstrated incultured fibroblasts and leukocytes.

Biotinidase deficiency typically presentsduring first 3 mos of life.

Clinical features are similar to those of holocarboxylasesynthetase deficiency. In addition, dry skin rash, alopecia, hearingloss, optic atrophy, developmental delay, and ataxia may occur.Diagnosis is confirmed by low serum biotinidase level.

Pyruvate Dehydrogenase Complex Deficiency

Deficiencyof any of enzymes involved in pyruvate dehydrogenase complex results inlactic acidosis and CNS dysfunction, including alteration in consciousness.

See Chap.4, Ataxia.

Pyruvate Carboxylase Deficiency

Pyruvatecarboxylase catalyzes conversion of pyruvate to oxaloacetate.

Clinical features in newborn includetachypnea, hypotonia, seizures, and alteration of consciousness.Survivors usually have episodic ataxia, seizures, and psychomotordelay.

Less severe form may occur in infancywith milder lactic acidosis and developmental delay.

Usual lab findings are increase inserum concentration of ammonia, lactate, pyruvate, alanine, citrulline,and lysine. Measurement of enzyme activity in skin fibroblasts orliver is diagnostic.

Fatty Acid Oxidation Defects

Most commonis medium-chain acyl-CoA dehydrogenase deficiency, but others includeshort-chain, long-chain, and very-long-chain acyl-CoA dehydrogenasedeficiencies.

May present with vomiting, hypotonia,seizures, cardiac dysfunction, and alteration of consciousness.

Usual metabolic findings include hyperammonemia,hypoglycemia without ketones, metabolic acidosis, and dicarboxylicaciduria (fatty acid intermediates).

Analysis of plasma acylcarnitine profilesin these disorders establishes diagnosis. Demonstration of enzymedefect in leukocytes or fibroblasts is definitive.

Respiratory Chain Disorders

Defectsin respiratory chain involving complexes I, III, and IV can causeseizures, weakness, hypotonia, developmental delay, and alterationin consciousness.

Hyperammonemia often occurs, and lactate/pyruvateratio is usually abnormally increased (>20).

Other mitochondrial disorders [e.g.,MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis,strokelike episodes)] may cause alteration of consciousnesswithout associated hyperammonemia. Other common presenting symptomsand signs of these disorders include developmental delay or regression,seizures, and hypotonia.

Muscle biopsy including electron microscopyand respiratory chain enzyme analysis is diagnostic.

Lysinuric Protein Intolerance

Definedas autosomal-recessive disorder caused by mutations in amino acidtransporter gene SLC7A7, whose locus has been mapped to chromosome14q11.2. As a result, intestinal membrane transport of lysine, arginine,and ornithine is defective.

Onset is usually in infancy or childhood,with poor feeding, vomiting, hypotonia, and alteration of consciousness.Hyperammonemia is prominent finding.

Serum concentrations of the above aminoacids are low, while their urinary excretion is high.

Hyperornithinemia-Hyperammonemia-Homocitrullinuria Syndrome

Definedas autosomal-recessive disorder with impaired transport of aminoacid ornithine into mitochondria via ornithine transporter protein.

Gene locus has been mapped to chromosome13q14.

May present in neonatal period or inchildhood with vomiting, seizures, and alteration in consciousnessrelated to hyperammonemia.

Diagnosis is confirmed by finding increasedserum concentration of ornithine and increased urinary concentrationof homocitrulline.

Transient Hyperammonemia of Prematurity

Usuallypresents on first or second day of life, often before any protein-containing feedingor IV solution has been given.

Usual findings include impaired eyemovements, fixed dilated pupils, seizures, alteration of consciousness,and marked hyperammonemia.

Spontaneous resolution usually occursover 1–2 wks.

Pathogenesis unknown.

Other Metabolic Disturbances

Hyponatremia,hypernatremia, hypocalcemia, hypercalcemia, hypomagnesemia, and hypermagnesemiamay cause alteration in consciousness.

Serum sodium, calcium, and magnesiumconcentrations should be measured.

See Chap.59, Seizures.

Poisoning, Drug Overdose, and Intoxication

Many substances in high enough doses cancause toxic reactions, including alteration in consciousness.

Carbon Monoxide

Should besuspected when individual has inhaled smoke from fire, automobileexhaust fumes in closed space, or fumes from faulty home heater.

Carbon monoxide binds much more tightlyto Hgb than does O₂ and thus decreases O₂-carryingcapacity of blood. Concentration of carboxyhemoglobin in blood ofnormal individuals is <1%. Levels of 20–40% produceconfusion, nausea, and vomiting. Incoordination, weakness, and lossof recent memory occur with levels of 40–60%,whereas seizures and coma are almost certain with levels >60%.

Simultaneous onset of similar symptomsin other individuals with same exposure is clue to this diagnosis.

Sedative-Hypnotic Drugs

Includebarbiturates and benzodiazepines, which depress CNS by depressingreticular activating system.

Overdose of up to 5 times hypnoticdose of barbiturate may produce headache, drowsiness, slurred speech,confusion, and ataxia. Ingestion of 10 times hypnotic close mayproduce decreased consciousness and respiratory depression.

Pupillary constriction is usual, butdilation sometimes occurs. Overdose of benzodiazepine (diazepam,chlordiazepoxide, flurazepam, lorazepam, triazolam) may producefindings similar to ethanol ingestion: euphoria, disinhibition,and ataxia. Severe overdose may cause bradycardia, hypothermia,miosis, hypotension, and coma.

History of ingestion or toxicologyurine screen confirms diagnosis.

Flumazenil, a benzodiazepine receptorantagonist, may be used to reverse benzodiazepine-induced coma andis important diagnostic and therapeutic agent in comatose childrenwith possible overdose.

Opiates

Definedas substances derived from the opium poppy. Codeine and morphineare natural derivatives. Heroin, oxycodone, hydromorphone, and oxymorphoneare semi-synthetic derivatives, whereas meperidine, methadone, propoxyphene,pentazocine, and fentanyl are completely synthetic derivatives.

Effects of opiates include analgesia,drowsiness, nausea and vomiting, constipation, and mood changes.Overdose may cause respiratory depression and alteration of consciousness.In the absence of history of ingestion, the combination of miosis,respiratory depression, and coma should suggest the diagnosis. Otherfindings may include bradycardia, hypothermia, hypotension, seizures,and pulmonary edema.

History, naloxone reversal of clinicalsigns, or toxicology screening of urine is diagnostic.

Alcohols

Intoxicationmay produce excitement, exhilaration, loquacity, slurred speech,loss of restraint, drowsiness, incoordination of movement and gait,and decreased consciousness.

Prototype alcohol ingestion is withethyl alcohol. Other alcohols that also may produce alteration ofconsciousness are ethylene glycol, isopropyl alcohol, and methylalcohol (methanol).

Ethyl Alcohol (Ethanol)

Distilledspirits contain 40–50% ethanol; wine, 10–20%;and beers, 2–6%. Many household products (e.g.,mouthwashes, colognes, after-shave lotions, and some liquid medications)also contain ethanol.

After significant ingestion, nauseaand vomiting occur. Ethanol concentrations in the blood of 100–150mg/dL produce slurred speech, incoherence, incoordination,ataxia, and impaired vision. Levels >300 mg/dLmay produce coma.

Infants and toddlers have a differentclinical course than older children and adolescents. Once ethanollevels are >50–100 mg/dL, hypoglycemia,hypothermia, and coma can develop.

History, smell of the breath, or quantitativeserum level is diagnostic.

Ethylene Glycol

Componentof windshield de-icer and automobile antifreeze solutions.

Ingestion produces ethanol-like intoxication,with nausea and vomiting, drowsiness, confusion, slurred speech,ataxia, and metabolic acidosis.

Production of oxalic acid from ethyleneglycol results in calcium oxalate crystal deposition throughoutthe body, including brain, heart, and kidney tubules.

Hypocalcemia may be significant enoughto produce tetany and disturbances of cardiac conduction.

History or quantitative serum levelis diagnostic.

Isopropyl Alcohol (Rubbing Alcohol)

Overdoseproduces ethanol-like intoxication, with nausea and vomiting, confusion, andataxia. Severe overdose may produce myocardial depression, hypotension,and shock.

Hypoglycemia may occur in young children.

Because the metabolite of isopropylalcohol is acetone and not an acid, acetonuria and absence of metabolicacidosis characterize this type of intoxication.

History or quantitative serum levelis diagnostic.

Methyl Alcohol (Methanol)

Used asantifreeze (windshield washer fluid and gasoline) and as solventin many industrial and home products (varnishes and paint thinners).

Its metabolites, formaldehyde and formicacid, are highly toxic.

Clinical effects usually occur within8–24 hrs of ingestion. Manifestations of severe overdoseinclude vomiting, abdominal pain, hyperpnea, impaired vision, seizures,coma, and metabolic acidosis with increased anion gap.

History or quantitative serum levelis diagnostic.

Anticonvulsants

Phenytoin

Drowsiness,slurred speech, nystagmus, and ataxia occur with mild ingestion.With more severe ingestion, tremor, choreoathetosis, and confusioncan occur, but coma is unusual.

History or quantitative serum levelis diagnostic.

Carbamazepine

Effectsof toxic ingestion include nystagmus, ataxia, and anticholinergicmanifestations, which may be followed by seizures and coma.

History or quantitative serum levelis diagnostic.

Valproic Acid

Toxic ingestionmay produce pinpoint pupils and drowsiness, which may progress to coma.

History or quantitative serum levelis diagnostic.

Phenothiazines

Commonlyprescribed major tranquilizers that are also used to treat nauseaand vomiting. Prototype is chlorpromazine.

In mild intoxication, slurred speech,sedation, and ataxia occur. Anticholinergic findings include constipation,blurred vision, and urinary retention. With more serious intoxication,muscle stiffness, dystonic reactions, arrhythmias, hypotension,and alteration of consciousness may occur.

Qualitative UA confirms diagnosis.

Tricyclic Antidepressants

Ingestionof 10–20 mg/kg of most tricyclic antidepressantsis moderate to severe exposure. Ingestion of 35–50 mg/kgmay result in death.

Prototype is amitriptyline hydrochloride.

Toxic effects produce drowsiness, slurredspeech, and ataxia. Anticholinergic signs (e.g., flushed skin, tachycardia,and dilated pupils) also may occur. Hallucinations, seizures, coma,and respiratory arrest can follow.

QRS duration of >100 msecsin the limb leads is indication of serious overdose; complete heartblock and ventricular tachycardia may occur.

History, quantitative serum level,or qualitative UA confirms diagnosis.

Anticholinergic Drugs

Block theaction of acetylcholine at CNS cholinergic receptors and at muscarinicreceptors (parasympathetic nerve endings and sympathetic nerve endingsto sweat glands). Some drugs (atropine, scopolamine, tricyclic antidepressants,phenothiazines, antihistamines) as well as certain plants and mushroomshave anticholinergic properties.

Clinical manifestations of mild overdoseinclude hyperpyrexia, tachycardia, mydriasis, flushing, dry mucousmembranes, hot dry skin, urinary retention, decreased sweating,drowsiness, excitement, confusion, disorientation, visual hallucinations,and anxiety. Large overdose may cause seizures, arrhythmias, coma,and shock.

History or qualitative UA confirmsdiagnosis.

Physostigmine can reverse mental statuschanges caused by anticholinergic drugs but should be used withcaution because it can produce bronchospasm, bradycardia, hypotension,and seizures.

Salicylates

Prototypeis acetylsalicylic acid (aspirin), although other chemical formsof salicylates exist in many different products.

Methyl salicylate (oil of wintergreen)is especially dangerous because of its high concentration of salicylate(1 mL contains 1.4 g of aspirin).

All forms of salicylates produce similarclinical picture. With mild poisoning, nausea and vomiting, fever,hyperpnea, and confusion occur. Severe poisoning produces seizures,coma, and respiratory or cardiovascular collapse.

Metabolic acidosis with increased aniongap and a respiratory alkalosis are characteristic of salicylateintoxication.

If <150 mg/kg ofsalicylate is acutely ingested, determination of serum level isunnecessary. History of single ingestion of 150–300 mg/kgsalicylate signifies mild intoxication, whereas ingestion of >300mg/kg signifies serious intoxication. With acute overdose,a nomogram may be used to estimate severity of poisoning. Bloodlevel >100 mg/dL is indicative of serious intoxication.

In chronic intoxication, impossibleto establish correlation between serum concentration and severityof illness.

Lead

Acute severepoisoning may cause encephalopathy but is rare now because of routine leadscreening.

Risk of acute encephalopathy increaseswith blood lead level >80 μg/dL.

Manifestations of encephalopathy includevomiting, ataxia, seizures, and impaired consciousness, which mayprogress to coma with increased intracranial pressure.

Organophosphates

Ingestion,inhalation, or skin exposure produce various toxic effects.

Organophosphates irreversibly phosphorylatethe enzyme acetylcholinesterase, which results in excessive accumulationof acetylcholine in CNS, at cholinergic junctions in autonomic nervous system(causing muscarinic effects), and in skeletal muscle or autonomicganglia (causing nicotinic effects).

Manifestations are CNS (headache, confusion,emotional lability, ataxia, seizures, coma), muscarinic (salivation,lacrimation, urinary incontinence, vomiting, diarrhea, abdominalcramping), and nicotinic (sweating, tremors, weakness, muscle twitching).Miosis, bradycardia, hypotension, rhinorrhea, and wheezing alsomay occur.

History of exposure and characteristicfindings are diagnostic. Decreased RBC cholinesterase level confirmsdiagnosis.

Amphetamines

Stimulaterelease of biogenic amines from presynaptic neurons and have agonistaction on postsynaptic catecholamine receptors.

Can cause nausea and vomiting, abdominalcramps, dry mouth, sweating, tremors, tachycardia, hyperpyrexia,hypertension or hypotension, dilated pupils, cardiac arrhythmias,excitation, confusion, hallucinations, paranoid delusions, seizures,and coma.

Peak serum level is 1–2 hrsafter acute ingestion.

History or toxicologic UA is diagnostic.

Cocaine

Importanteffects are interference with catecholamine, dopamine, and serotonintransmission in CNS and blocking of catecholamine reuptake at adrenergicnerve endings.

Clinical effects appear within minutesif injected or smoked and within 1 hr if ingested.

Effects on CNS include agitation, euphoria,tremor, twitching, and mydriasis. Severe overdose may produce respiratorydistress, hyperpyrexia, hypertension, stroke, myocardial infarction,seizures, and coma.

History or qualitative UA is diagnostic.

Hallucinogens (Psychedelics)

Commonlyused hallucinogens include phencyclidine (angel dust), lysergicacid diethylamide (LSD), and marijuana. Can produce illusions, hallucinations,delusions, and paranoid ideation as well as vivid and unusual visualexperiences with diminished control over what is experienced.

Phencyclidine can produce slurred speech,nystagmus, and staggering gait in small doses. Fever, hypersalivation,repetitive movements, and muscular rigidity can occur with moderatedoses. Severe intoxication can produce seizures, coma, and respiratoryarrest. History or qualitative UA is diagnostic.

Somatic effects of LSD are sympathomimeticand include pupillary dilatation, hypertension, tachycardia, hyperpyrexia,tachycardia, and hyperreflexia. CNS effects include euphoria, emotional lability,perceptual changes in vision and hearing, delusional ideation, andbody distortion. LSD is found in such low concentrations that identificationis difficult.

Most prominent symptoms of marijuanause involve CNS and cardiovascular system. Marijuana may produceconfused and disorganized thinking, impaired short-term memory,and euphoria followed by anxiety and panic. Larger doses may causehallucinations, delirium, and paranoid feelings. Tachycardia andhypertension also may occur. History or qualitative UA is diagnostic.

Iron

Ingestionof >20 mg/kg may produce symptoms, whereas >50mg/kg often produces toxic effects. Serum iron levels of >300 μg/dLare toxic; those >500 μg/dL are usuallyassociated with severe poisoning.

Overdose has GI, cardiovascular, andneurologic effects. Vomiting and diarrhea may be followed by GIbleeding, hypotension, pulmonary edema, renal tubular necrosis,liver dysfunction, coagulopathy, seizures, and coma.

History and serum iron level are diagnostic.

Hydrocarbons

Can be dividedinto 2 groups: aliphatic (petroleum distillates) and aromatic (benzene, xylene,toluene, turpentine, halogenated forms). Aliphatic hydrocarbonsare rapidly absorbed from respiratory tract but poorly absorbedfrom GI tract, whereas aromatic hydrocarbons are rapidly absorbedfrom either route.

Severe ingestion of aliphatic or aromatichydrocarbon may cause nausea and vomiting, cough, dyspnea, aspirationpneumonia, and fever. May produce alteration in consciousness rangingfrom confusion to coma.

History confirms diagnosis.

Clonidine

Acts centrallyas alpha₂ receptor agonist to reduce sympathetic outflow,which produces mild sedation and decrease in BP and heart rate.

Initial manifestations include changesin mental status that may range from lethargy to coma. Hypothermia,miosis, and respiratory depression also may occur. Clonidine-inducedhypertension is uncommon, and central effect may be overridden byalpha-adrenergic effects at peripheral vascular receptors.

No available blood tests.

Intoxication resembles opiate overdose,and lack of response to naloxone helps distinguish clonidine overdosefrom opiate overdose.

Diagnostic Approach

When individualpresents with alteration of consciousness, diagnosis and treatment mustproceed concurrently, not serially.

ABCs of resuscitation (airway, breathing,circulation) take precedence over other diagnostic and therapeuticmeasures. Airway must be cleared, and oxygen should be given bymask and bag ventilation.

Failure of adequate ventilation requiresintubation.

Hypotension or shock should be treatedwith volume expansion.

With suspected or known head or necktrauma, head should be stabilized until lateral cervical spine radiographcan be performed to determine whether cervical spine injury hasoccurred.

Level of consciousness and responsiveness,motor function, pupil size and responses, and extraocular movementsshould be evaluated. Presence or absence of meningeal signs as wellas focal hemispheric or brainstem findings also should be noted.

Unless diagnosis has been establishedby history and physical exam, a number of tests need to be performed.

Measurementof blood glucose should be done immediately at bedside.

Blood should be sent for CBC with differential;serum electrolytes, glucose, creatinine, calcium, magnesium, ammonia;blood urea nitrogen; liver function tests; blood culture; and toxicology screen.

Urine should be obtained for UA, urineculture, and toxicology screen.

Vital Signs

Respiratory Rate and Pattern

Dyspneaand/or tachypnea may occur with pneumonia, any cause ofmetabolic acidosis, and lesions of lower midbrain–upperpontine tegmentum.

Slow, irregular respirations may beassociated with drug intoxication, septicemia, and intracranialmass lesion. With acute head injury or diffuse brain damage of anycause, abnormal breathing patterns often overlap, making it difficultto relate specific pattern with discrete location of brain damage.

Heart Rate

Bradycardia,if associated with hypertension and periodic breathing, suggestsincreased intracranial pressure.

Tachycardia may occur with hypovolemicshock (dehydration, blood loss, diabetic ketoacidosis) and anticholinergicpoisoning.

Blood Pressure

Hypertensionmay occur with increased intracranial pressure and with drug overdoses (amphetamines,cocaine, phencyclidine).

Hypotension may occur with hypovolemia(fluid losses from gastroenteritis, acute blood loss, diabetic ketoacidosis),septicemia, adrenal insufficiency, and ingestion of alcohol or barbiturates.

Temperature

Hyperpyrexiamay indicate presence of infection (bacterial meningitis, septicemia, pneumonia),heat stroke, or cocaine overdose. Although uncommon, brain lesionthat has disturbed temperature-regulating center also may producehyperpyrexia.

Hypothermia may occur with severe hypovolemiaas well as with barbiturate or alcohol ingestion.

Level of Consciousness and Responsiveness

Level ofconsciousness can be determined by noting degree of arousability.

Response to name, simple commands,or painful stimuli (sternal pressure or pinching side of neck, innerarm, or thigh) can be used to evaluate degree of unresponsiveness.

Eye opening or any form of speakingincluding grunting or groaning suggests some degree of functionof reticular activating system.

Speech and purposeful withdrawal orlocalization of painful stimuli are signs of intact cortical function.

Motor Function

Restlessmovements of arms and legs, variable resistance to passive movement,complex avoidance movements, and discrete protective movements generallyindicate intact corticospinal tracts, whereas asymmetry of functionmay indicate hemiparesis.

Presence of posturing should be noted.Decorticate posturing consists of flexion of arms, wrists, and fingerswith adduction of upper extremities, and extension, internal rotation,and plantar flexion of lower extremities. Associated with diffusedamage to cerebral cortex and subcortical white matter or basalganglia. Decerebrate posturing, which consists of arm and hand extensionand back arching, is associated with extensive midbrain damage.

Flaccid extremities and absence ofany motor response indicate further depression of brainstem function.

Pupil Size and Responses

Exam ofpupils and their reactivity help determine level and location oflesions affecting reticular activating system in brainstem. Anyreactivity signifies intact parasympathetic and sympathetic pathwaysof oculomotor nerve. Bilateral lesions of midbrain that interruptthis pathway produce dilated unreactive pupils. Pontine lesionsproduce miotic pupils with only mild reaction to light. Unilateral pupillarydilatation suggests third nerve compression and impending uncalherniation.

Generally, pupils remain reactive withmetabolic or toxic causes of coma. Exceptions include atropine orscopolamine poisoning, which causes dilated unreactive pupils; glutethimidepoisoning, which may cause medium to large unreactive pupils; opiatepoisoning (morphine, heroin), which causes pinpoint pupils withonly slight constriction to light; and severe anoxia with cardiacarrest, which produces fixed and dilated pupils. Miosis is usuallyseen with opiate, organophosphate, or clonidine overdosage, whereasmydriasis is usually seen with anticholinergic poisoning (tricyclicantidepressants) or with stimulant overdosage (amphetamines, cocaine).

Extraocular Movements

Evaluationof eyes at rest, abnormal spontaneous eye movements, and ocularresponse to labyrinthine function provide important informationin assessment of alteration of consciousness.

Cerebral lesions (usually frontal lobe)usually produce conjugate deviation of eyes to side of lesion andnormal labyrinthine responses, whereas unilateral pontine lesionsusually produce eye deviation away from side of lesion as well asabnormal labyrinthine responses. Midbrain lesions that involve oculomotornucleus or nerve or pontine lesions involving abducens nucleus ornerve may cause abduction of ipsilateral eye.

Ocular response to vestibular stimulationalso helps evaluate integrity of brainstem function in childrenwith alteration of consciousness. Brainstem function is intact whenice water injection of 50 mL into external auditory canal with headflexed to 30 degrees produces conjugate horizontal eye deviationto side of injection and horizontal rapid nystagmus to oppositeside. Absence of such reflexes indicates severe brainstem dysfunction.

Oculocephalic (doll's eye)reflex is also used to produce vestibular stimulation, but it iscontraindicated with suspected cervical spine injury. Head is rotatedfrom side to side and positive response indicating intact brainstemfunction is conjugate horizontal eye movement in opposite directionfrom head turn.

Further Evaluation and Specific Diagnosis

Vital signsand assessments already described usually indicate whether any focal hemisphericor brainstem dysfunction exists. Final task is to make definitivediagnosis.

Focal neurologic signs including asymmetricmovements and abnormal postures usually signify structural lesionin cerebral hemisphere, which also may affect brainstem function.

Lesions above tentorium may cause alterationof consciousness by depression of large portions of both cerebralhemispheres, whereas lesions below tentorium (usually tumor or collectionof blood in posterior fossa) depress consciousness by compressionof brainstem structures.

Presence of increased intracranialpressure may lead to central or uncal cerebral herniation. Centralherniation refers to rostrocaudal pattern of deterioration withloss of consciousness and irregular respirations followed by bilateraldilated unresponsive pupils and either decorticate or decerebrateposturing. Uncal herniation occurs more suddenly with loss of consciousnessand unilateral dilated pupil occurring almost simultaneously.

Hemiparesis or hemiplegia may occurcontralateral to lesion.

In cases of suspected structural lesion ± historyof head trauma, CT should be performed immediately. When herniationor impending herniation is suspected, patient should be intubated,hyperventilated, and given mannitol to acutely decrease increasedintracranial pressure prior to CT.

Meningeal signs (stiff neck, Kernigor Brudzinski signs) commonly occur with bacterial meningitis andsubarachnoid hemorrhage. Lumbar puncture should be performed withsuspected bacterial meningitis or viral encephalitis. CT shouldbe performed first to rule out mass lesion in individuals with focalneurologic signs or symptoms of coma. If patient is unstable, appropriateantibiotic therapy should be given for suspected bacterial meningitisafter blood culture has been drawn, and lumbar puncture may be deferreduntil child is stable. In individuals with suspected subarachnoidhemorrhage and increased intracranial pressure, CT should be performedimmediately.

Individuals without meningeal or focalneurologic signs may have head injury, drug intoxication, seizure,or metabolic disorder. Precise drug history is important but oftenis unavailable. 3 specific antidotes are available:

Naloxone foropiate overdose

Physostigmine for anticholinergic poisoning

Flumazenil for benzodiazepine overdose

Metabolic causes of coma tend to producesymmetric hemispheric responses with normal brainstem function.

With hyperammonemia in neonatal period,urea cycle defects and organic acid disorders should be suspected. Fig.3.1 (Adapted from Batshaw ML. Inborn errors of ureasynthesis. Ann Neurol 1994;35:137, with permission.) provides schemeto determine cause of hyperammonemia in neonates. Measurement ofserum ammonia, amino acids, lactate, and pyruvate, as well as urinaryorganic acids and orotic acid, will identify virtually all of geneticcauses of hyperammonia in this age group. Plasma acylcarnitine profilecan help diagnose various fatty acid oxidation defects. In a fewinstances (carbamyl phosphate synthetase and N-acetylglutamate synthetasedeficiencies), specific enzyme analysis must be performed to confirmdiagnosis.

In infantsand children with hyperammonemia, scheme used for neonates can befollowed. However, if urinary organic acids are normal, prothrombintime and serum bilirubin should be measured. If these results areabnormal, liver disease, drugs, hepatotoxins, and Reye syndromeshould be considered. Also, if plasma citrulline is normal, plasmaarginine should be measured. Increase in plasma arginine signifiesarginase deficiency. Low or normal plasma arginine suggests 2 possibilities:lysine protein intolerance or hyperornithinemia-hyperammonemia-homocitrullinemiasyndrome. Increase in urinary lysine signifies lysine protein intolerance,whereas increase in plasma ornithine and urinary homocitrulline signifieshyperornithinemia-hyperammonemia-homocitrullinemia syndrome. Otherinvestigations depend on clinical findings and results of abovetests.

>>>'>>>>>>>>>

» READ BOOK EXCERPT ONLINE »

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

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

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

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

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

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

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

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

DELIRIUM: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

It is essential to get a history of drug or alcohol use from the patient or family, and a drug screen may be done in most cases. Infection is another common cause. The workup should also include a CBC, sedimentation rate, urinalysis, antinuclear antibody (ANA) analysis, chemistry panel, and electrolytes. A CT scan or MRI of the brain will be necessary in most cases. It may be wise to administer intravenous thiamine and glucose while awaiting the results of blood work. If there is a fever, blood cultures and possibly a spinal tap (after a CT scan or MRI has ruled out a space-occupying lesion) may be indicated. Arterial blood gas analysis and carboxyhemoglobin should be determined. A neurologist or neurosurgeon needs to be consulted early in the workup.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

SYNCOPE: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

Clinical differentiation of the various forms of syncope is made by combinations of symptoms. Thus, syncope with marked sweating and tachycardia is more likely due to hypoglycemia. Syncope with sweating and bradycardia is more likely due to vasovagal syncope. Focal neurologic signs during the attack suggest transient ischemia attack (TIA) and prompt a search for sources of emboli or thrombosis (sickle cell disease, polycythemia, or macroglobulinemia). Transesophageal echocardiography is the procedure of choice to find a cardiac source. A family history of syncope suggests migraine, epilepsy, or vasovagal attacks. Epilepsy is a strong possibility in the young, whereas heart block is more likely in the aged. Consequently, an EEG and Holter monitoring are useful in the workup.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

COMA AND SOMNOLENCE: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

Obviously, the neurologic examination and a good history from a member of the family or friend are invaluable in the diagnosis of coma. However, one should not delay ordering laboratory work until the examination and history are accomplished. A CBC, blood urea nitrogen (BUN), fasting blood sugar (FBS), serum osmolality, electrolytes, blood gases, urinalysis, and drug screen are ordered immediately. If there is little or no history available and insulin shock is suspected, glucose or glucagon is administered before the laboratory reports are back, although this is done with more caution today for fear of aggravating a case of nonketotic, hyperosmolar diabetic coma. It has been my experience that the neurologic examination is best performed simultaneously with the taking of a history from a relative or friend. In this way, various telltale neurologic signs can be found with alacrity. A unilateral dilated pupil (suggesting a subdural hematoma or aneurysm), acetone breath (suggesting diabetic acidosis), contusion of the skull (suggesting cerebral concussion or hematoma), and nuchal rigidity (suggesting a subarachnoid hemorrhage in meningitis) are just a few of the signs that can help to rapidly identify the cause of the coma. Coma without focal neurologic findings should suggest a metabolic or toxic cause. In that case, an intensive laboratory workup as listed below would be indicated. A spinal tap may be indicated if there is fever as well. In contrast, coma with focal neurologic signs suggests tumor, abscess, hematoma or cerebral embolism, thrombosis, or hemorrhage. The clinician should proceed with a skull x-ray film and CT scan immediately. When these are not available, immediate referral to a large medical center is necessary. Electroencephalography (EEG) and a spinal tap may identify the cause. A spinal tap should be considered with extreme caution even if there is no papilledema. Of course, a spinal tap is never done in the presence of papilledema unless a neurologist is consulted and CT findings are negative. One indication for a spinal tap under these circumstances might be meningitis. Another might be “benign intracranial hypertension.”

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

» Next page: Signs of Coma

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TREATMENTS & RESEARCH

Dr. Huntley's Diagnosis Checklist

Diagnosis of Coma

Coma Diagnosis: Book Excerpts

Diagnosis of Coma: medical news summaries:

Diagnostic Tests for Coma: Online Medical Books

DELIRIUM: Ask the following questions: (Algorithmic Diagnosis of Symptoms and Signs)

DIAGNOSTIC WORKUP

SYNCOPE: Ask the Following Questions: (Algorithmic Diagnosis of Symptoms and Signs)

DIAGNOSTIC WORKUP

COMA: Ask the following questions: (Algorithmic Diagnosis of Symptoms and Signs)

DIAGNOSTIC WORKUP

Delirium: Differential Diagnosis (In a Page: Signs and Symptoms)

Workup and Diagnosis

Syncope: Differential Diagnosis (In a Page: Signs and Symptoms)

Workup and Diagnosis

Delirium: Differential Diagnosis (In A Page: Pediatric Signs and Symptoms)

Workup and Diagnosis

Syncope: Differential Diagnosis (In A Page: Pediatric Signs and Symptoms)

Workup and Diagnosis

Coma: Differential Diagnosis (In A Page: Pediatric Signs and Symptoms)

Workup and Diagnosis

DELIRIUM: Approach to the Diagnosis (Differential Diagnosis in Primary Care)

SYNCOPE: Approach to the Diagnosis (Differential Diagnosis in Primary Care)

COMA AND SOMNOLENCE: Approach to the Diagnosis (Differential Diagnosis in Primary Care)

Level of consciousness, decreased: History and physical examination (Handbook of Signs & Symptoms (Third Edition))

Syncope: History and physical examination (Handbook of Signs & Symptoms (Third Edition))

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

Syncope: History and physical examination (Professional Guide to Signs & Symptoms (Fifth Edition))

Delirium: History (The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

Physical examination.

Syncope: History (The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

Physical examination

Coma: History (The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

Physical examination

Syncope: Differential Overview (Field Guide to Bedside Diagnosis)

Diagnostic Approach

Coma: Differential Overview (Field Guide to Bedside Diagnosis)

Diagnostic Approach

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

Diagnostic Approach

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

Physical examination

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

Physical examination

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

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

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

Cardiovascular Syncope

Neurocardiogenic Syncope (Common Faint)

Cardiac Syncope

Congenital and Acquired Heart Disease

Hypercyanotic Episodes

Arrhythmias in Structurally Normal Heart

Arrhythmias in Structurally Abnormal Heart

Vascular Syncope

Orthostatic Syncope

Cerebrovascular Syncope

Carotid Sinus Syncope

Noncardiovascular Syncope

Breath-Holding

Hyperventilation

Migraine

Metabolic

Hypoxia Including Anemia

Hypoglycemia

Psychologic

Diagnostic Approach

Alteration in Consciousness: Clinical Features and Diagnosis (The Diagnostic Approach to Symptoms and Signs in Pediatrics)

Head Trauma

Concussion

Brain Contusion

Shearing Injury

Cerebral Edema

Intracranial Hemorrhage

Intraparenchymal Hemorrhage

Subdural Hematoma

Epidural Hematoma

Infection/Inflammation

Bacterial Meningitis

TREATMENTS &
RESEARCH

Dr. Huntley's
Diagnosis
Checklist

DELIRIUM: Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

SYNCOPE: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

COMA: Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

Delirium: Differential Diagnosis
(In a Page: Signs and Symptoms)

Syncope: Differential Diagnosis
(In a Page: Signs and Symptoms)

Delirium: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Syncope: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Coma: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

DELIRIUM: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

SYNCOPE: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

COMA AND SOMNOLENCE: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

Level of consciousness, decreased: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

Syncope: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

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

Syncope: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

Delirium: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

Syncope: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

Coma: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

Syncope: Differential Overview
(Field Guide to Bedside Diagnosis)

Coma: Differential Overview
(Field Guide to Bedside Diagnosis)

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

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

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

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

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

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

Alteration in Consciousness: Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)