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Diseases » Benign Paroxysmal Positional Vertigo » Diagnosis

Diagnosis of Benign Paroxysmal Positional Vertigo

Benign Paroxysmal Positional Vertigo Diagnosis: Book Excerpts

Diagnostic Tests for Benign Paroxysmal Positional Vertigo: Online Medical Books

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

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

Is it true vertigo? True vertigo is characterized by the fact that the subject feels he or his environment is turning. One other form of true vertigo is lateral pulsion, in which the subject feels as if he is moving to the left or right or may be moving forward or backward. True vertigo is a sign of neurologic or otologic disease, whereas dizziness that is not true vertigo is more likely a sign of cardiovascular disease.
Is there associated tinnitus or deafness? The presence of tinnitus or deafness, especially if the ear examination is negative, is a sign of a more serious otologic or neurologic condition. Such disorders as cholesteatoma, acoustic neuroma, and Ménière's disease must be considered. On the other hand, vertigo without tinnitus or deafness should prompt consideration of benign positional vertigo and vestibular neuronitis.
Are there other neurologic findings? The finding of abnormalities of other cranial nerves or the long tracts, such as the pyramidal tracts, would suggest multiple sclerosis, an advanced brain stem tumor, acoustic neuroma, or basilar artery insufficiency.
Are there findings on otoscopic examination? A normal neurologic examination with an abnormal ear exam would suggest otitis media, cholesteatoma, or petrositis.
Is there tachypnea during the attack? If there is hyperventilation during the attack, then hyperventilation syndrome should be considered.
Is there a history of trauma? A history of trauma would suggest a postconcussion syndrome.
Are there abnormalities of the blood pressure? If the dizziness is really lightheadedness, hypertension may be present, but hypertension may also cause true vertigo. Hypotension is more likely to cause lightheadedness, which is not true vertigo. Be sure to take the blood pressures while the patient is lying down and again after rapidly arising to the standing position.
Are there abnormal cardiac findings? A thorough cardiovascular examination should be done. Irregularities of the heartbeat, heart murmurs, or cardiac enlargement will suggest cardiac arrhythmia, aortic stenosis and insufficiency, mitral stenosis, prolapse of the mitral valve, and congestive heart failure.
Is there pallor? Moderate to severe anemia will cause lightheadedness and dizziness, but usually not true vertigo.

DIAGNOSTIC WORKUP

If there is true vertigo, an audiogram and a caloric test or electronystagmography should be done. Hallpike's maneuver should be done also. If these are abnormal, an x-ray of the mastoids, petrous bones, and internal auditory canals should be done. At this point a neurologist should be consulted. If an acoustic neuroma is strongly suspected, an MRI of the brain stem and auditory canals should be done. If the MRI of the brain is negative, a spinal fluid examination can be done to exclude such disorders as central nervous system lues and multiple sclerosis. An MRI of the brain needs to be done to distinguish multiple sclerosis. BSEPs, VEPs, and SSEPs will also be helpful in making the diagnosis of multiple sclerosis, along with the spinal fluid analysis mentioned above. A wake-and-sleep EEG needs to be done to exclude temporal lobe epilepsy. If migraine or migraine equivalents are suspected, perhaps a trial of beta-blockers would help make this diagnosis. If vertebral basilar artery ischemia is suspected, magnetic resonance angiography may be indicated.

If the dizziness is not true vertigo, a CBC and chemistry panel should be done at the outset. Additional studies in the form of 24-hr blood pressure monitoring, Holter monitoring, and echocardiography all have a valuable place in the diagnostic workup of dizziness without true vertigo. However, a referral to a cardiologist is wise before undertaking these expensive studies. If all studies are negative, perhaps a psychiatrist should be consulted.

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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

ABDOMINAL PAIN, CHRONIC RECURRENT: Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

Is there a family history of migraine or epilepsy? Migraine and epilepsy both present with abdominal pain.
Is the pain colicky or persistent? Chronic colicky abdominal pain may be due to chronic cholecystitis, cholelithiasis, renal calculus, or partial intestinal obstruction.
What is the location of the pain? If the pain is located in the upper abdomen, then one should consider peptic ulcer disease, pancreatitis, cholecystitis, and cholelithiasis. If the pain is located in the flanks, one should consider renal calculus and pyelonephritis. If the pain is located in the lower abdomen, one should consider diverticulitis, salpingitis, endometritis, and chronic appendicitis. Regional ileitis also may be located in the lower abdomen, particularly in the right lower quadrant.
What is the relationship to meals? Abdominal pain relieved by food may be due to a peptic ulcer. Abdominal pain brought on by food may be due to abdominal angina. If the pain comes on 2 to 3 hr after a meal, it may be due to a peptic ulcer. On the other hand, pain that comes on 1 to 2 hr after meals, especially if it's a fatty meal, may be related to cholecystitis and cholelithiasis.
Is there fever associated with the abdominal pain? Fever and abdominal pain may be due to pyelonephritis, diverticulitis, or appendicitis.
Is there a history of chronic alcoholism? The history of chronic alcoholism suggests acute and chronic pancreatitis.
Is there blood in the stool? The presence of blood in the stool would, of course, suggest peptic ulcer disease and diverticulitis.
Is there an abdominal mass? The presence of an abdominal mass, particularly in the midepigastrium, suggests a pancreatic cyst related to chronic pancreatitis. A mass in the right lower quadrant might be related to regional ileitis or salpingitis. A mass in the left lower quadrant may be related to diverticulitis and salpingitis.

DIAGNOSTIC WORKUP

Routine laboratory tests include a CBC, sedimentation rate, urinalysis, urine culture, sensitivity, colony count, chemistry panel, serum amylase and lipase, pregnancy test, stool for occult blood, and stools for ovum and parasites. A chest x-ray, EKG, and flat plate of the abdomen should also be done. A urine porphobilinogen will help exclude porphyria.

If these tests are negative, then an upper gastrointestinal (GI) series, esophagogram, and gallbladder ultrasound would be done for upper abdominal pain; an IVP would be done for flank pain; and a barium enema and sigmoidoscopy would be performed for lower abdominal pain.

If these studies are inconclusive, a gastroenterologist should be consulted for endoscopic procedures. If there is upper abdominal pain, esophagoscopy, gastroscopy, and duodenoscopy would be performed. Endoscopic retrograde cholangiopancreatography (ERCP) may be required to diagnose cholangitis or common duct stones. If there is lower abdominal pain, colonoscopy would be performed. A CT scan of the abdomen and pelvis is a useful diagnostic tool also. Gallium scans may detect a diverticular abscess or other localized area of chronic inflammation. Pelvic ultrasound may be useful in lower abdominal pain, especially in females. Aortography and angiography will be useful in abdominal angina. Lymphangiography can be helpful in discovering retroperitoneal tumors. Ultimately, exploratory laparotomy may still be necessary in some cases.

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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

Dizziness/Lightheadedness & Vertigo: Differential Diagnosis
(In a Page: Signs and Symptoms)

Dizziness/lightheadedness

Transiently decreased cerebral blood flow
–Hyperventilation
–Vasovagal response
–Congestive heart failure
–Aortic stenosis
–Hypertrophic cardiomyopathy
–Hemorrhage
–Dehydration or hypotension
–Carotid sinus pressure
–Cerebral artery thrombosis or embolism
–Cardiac arrhythmia
–Autonomic dysfunction (e.g., Shy-Drager syndrome)
–TIA
–Hypoxemia
–Anemia

Primary CNS dysfunction not associated with decreased blood flow
–Migraine
–Seizure
–Severe electrolyte disturbance
–Elevated intracranial pressure
Panic attack
Hyperventilation and/or anxiety
Ictal aura
Basilar migraine
Drug intoxication (e.g., alcohol, sedatives, centrally-acting α-blockers)
Allergic reactions
Postconcussion syndrome
Carbon monoxide poisoning
Vertigo
Peripheral vertigo (inner ear pathology)
–Benign positional vertigo (>20% of cases)
–Ménière's disease
–Labyrinthine trauma
–Labyrinthitis (viral)
–Nonspecific or recurrent vestibulopathy
–Bilateral vestibular loss
–Acoustic neuroma
–Autoimmune inner ear disease
Central vertigo (CNS pathology)
–Multiple sclerosis
–Brainstem tumors
–Labyrinthine trauma
–Epileptic vertigo
–Vertebrobasilar insufficiency
–Tabes dorsalis
–Friedreich's ataxia

Workup and Diagnosis

A complete history and physical exam should include signs of dehydration, questions about excessive pressure on the neck, headaches, palpitations, history of heart disease, hearing loss, cardiac auscultation, orthostatic blood pressures, and complete ENT (including Weber's and Rinne's tests) and neurologic exams (gait)
Laboratory evaluation may include CBC, electrolytes, calcium, glucose, BUN/creatinine, BNP, ESR, carbon monoxide level, pulse oximetry and/or arterial blood gas, eosinophil count, and stool occult blood testing
Further testing may include ECG, 24-hour ECG monitoring, echocardiography, electronystagmography, hearing evaluation, head CT, EEG, MRI (head and/or labyrinth) and/or MRA (head or vertebrobasilar circulation)
Vertigo may be evaluated with several specific maneuvers
–Dix-Hallpike maneuver: Patient is sitting; rapidly move to supine position with head over back of table; observe for nystagmus (type and duration); repeat with head facing to the left and right (nystagmus that does not fatigue or is vertical is unlikely to be BPV)
–Barany maneuver (Nylan-Barany maneuver) is similar to the Dix-Hallpike maneuver, but less sensitive

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

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

Benign paroxysmal positional vertigo (BPPV)
–Each episode lasts seconds to minutes
Vestibular neuritis
–Viral infection of the vestibular nerve
Otitis media

Migraine
–Vertigo may precede, follow, or present with the headache and aura

Acute labyrinthitis
–Acute onset with nausea and vomiting
–Lasts for days and slowly resolves
–45% cluster with viral infections

Posttraumatic
–Perilymphatic fistula
–Labyrinthine concussion
–Associated with postconcussive syndrome
–Worsened by change in head position, cough, sneeze, swallow, straining, and airplane travel

Cerebellar tumors
–Tumors may be associated with tinnitus, facial weakness, and nystagmus

Toxins/drugs: Antibiotics (aminoglycosides), salicylates, alcohol, phenytoin, quinine, arsenic, tricyclic antidepressants
Autoimmune: Collagen vascular disease, Wegener granulomatosis

Posterior circulation dissection
–Often associated with a history of neck extension or rotational injury

Cerebellar hemorrhage: Acute onset of vertigo, headache, nausea, and vomiting
Multiple sclerosis
–Vertigo is the presenting symptom in 5%
–Hearing loss rare
–Most common in young women
Temporal lobe or complex partial seizures
Ménière disease

Familial periodic ataxia syndromes
–Recurrent bouts of vertigo brought on by emotional stress or physical exertion

CNS infection: Syphilis, Lyme disease
Motion sickness
Vertigo mimics: Presyncope, disequilibrium from decreased vision or proprioception
Psychogenic
–Panic or anxiety disorder

Workup and Diagnosis

History
–Duration, headache, nausea, vomiting, worsening with activity or movement (postural hypotension, hyperventilation)
–Nausea and vomiting are classically more prominent with peripheral vertigo
–Associated neurologic deficits (extremity weakness, numbness, incoordination, dysarthria, diplopia, tinnitus, hearing loss, loss of consciousness)
–Facial numbness/weakness
–History of autoimmune disease, hyperlipidemia, stroke, migraine, seizure, cancer, prior ear surgery

Physical exam may be normal in asymptomatic periods
Cardiac and peripheral vascular examination for murmurs, arrhythmias, orthostatic changes in pulse and blood pressure (±ECG, Holter, Echo, Doppler)
Nystagmus, truncal ataxia, and limb incoordination are sometimes found in cerebellar infarction or neoplasm
Vertigo of a panic attack can sometimes be elicited by having the patient hyperventilate
Dix-Hallpike maneuver: Rapidly lay the patient down from sitting allowing the head to hang over the side of the bed while turning to the left or right; positive test shows vertigo with rotatory nystagmus within 30 seconds; if the etiology is peripheral, the nystagmus shows extinction with positioning maneuvers
MRI and MRA can help evaluate the posterior circulation

» READ BOOK EXCERPT ONLINE »

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

Fever – Recurrent: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Repeated viral infections
–Most common cause of recurrent febrile episodes in childhood
–Start of day care or change of geographic location may be related

Urinary tract infection (UTI)
–May be self-limited but recur especially if underlying anomaly exists

Epstein-Barr virus (EBV)
–May present with recurrent febrile episodes due to one initial infection

Other specific viral syndromes
–Parvovirus B19
–CMV

Immunodeficiency
–Repeated bacterial infections should lead to investigation of immune status

Dental abscess (non-dental abscesses typically present with prolonged daily fever)
Chronic meningococcemia
Acute rheumatic fever
Inflammatory bowel disease (IBD)
Juvenile rheumatoid arthritis (JRA)
Behçet disease

Tumor necrosis factor receptor-associated periodic syndrome (TRAPS) or Hibernian Fever
–Autosomal dominant disease with fever, myalgias with migratory pattern, conjunctivitis and rash

Familial cold autoinflammatory syndrome or familial cold urticaria
–Rash, fever, arthralgia, and conjunctivitis
–Precipitated by exposure to cold

Muckle-Wells syndrome
–Similar presentation to familial cold urticaria
–Symptoms not triggered by cold

Brucellosis
–Most prevalent around the Mediterranean and Arabic countries, also present in South America and India

Yersiniosis
Typhoid fever
Rat-bite fever
Malaria
Factitious fever

Workup and Diagnosis

History
–Documentation of fever
–Duration of episodes and fever-free intervals
–Symptoms associated with the fever
–Symptoms during the fever-free intervals
–Weight loss
–Recent documented infections, medications
–Travel, animal and insect exposure
–Specific conditions related to episodes (e.g., cold)

Physical exam
–Vitals, growth parameters (failure to thrive can be a presentation of UTI and immunodeficiency)
–Rash (transient pink rash in JRA)
–Ophthalmologic exam: Uveitis (IBD and Behçet), conjunctivitis (TRAPS)
–Hepatosplenomegaly, lymphadenopathy
–Genital ulcers (Behçet)
–Perianal skin tags (IBD)
–Mouth ulcers, pharyngitis
–Arthritis

CBC with differential
ESR or CRP
Urine culture
Blood culture
Serology for EBV, CMV, or Parvovirus B19
Low levels of serum type 1 TNF receptor in TRAPS
Documentation of fever in the office should exclude the possibility of factitious fever

» READ BOOK EXCERPT ONLINE »

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

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

The patient who does not experience true vertigo should have a syncope workup (see page 497). Narrowing the differential diagnosis of true vertigo depends on the presence or absence of other symptoms and signs. If there are other cranial nerve or long tract signs on neurologic examination, the patient may have a space-occupying lesion of the brain or brainstem or a hemorrhage, thrombosis or embolism in the vertebral–basilar artery distribution. A neurology consult should be obtained.

If there is true vertigo, tinnitis, and deafness, one would consider inner ear pathology such as Ménière disease, syphilis, petrositis, mastoiditis, and acoustic neuroma. If there is vertigo without tinnitis or deafness or focal neurologic signs, the clinician should suspect acute labyrinthitis, vestibular neuronitis, benign positional vertigo, and drug toxicity. If there are rapid respirations during the attack of vertigo, one would consider hyperventilation syndrome. If there are significant findings on otoscopic examination, a diagnosis of otitis media, cholesteatoma, or mastoiditis should be considered.

The workup will depend on whether the patient has objective findings on otoscopic or neurologic examination. If local pathology is suspected, perhaps a tympanogram, x-ray of the mastoids and petrous bones, audiogram, or referral to an otolaryngologist are required. If there are neurologic findings, perhaps a CT scan or MRI of the brain and auditory canal is indicated along with a referral to a neurologist.

It is wise to have a specialist on board before ordering an expensive workup.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

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

Ask about a history of diabetes and cardiovascular disease. Is the patient taking drugs prescribed for high blood pressure? If so, when did he take his last dose?

If the patient's blood pressure is normal, obtain a more complete history. Ask about myocardial infarction, heart failure, kidney disease, or atherosclerosis, which may predispose the patient to cardiac arrhythmias, hypertension, and a transient ischemic attack. Does he have a history of anemia, chronic obstructive pulmonary disease, anxiety disorders, or head injury? Obtain a complete drug history.

Next, explore the patient's dizziness. How often does it occur? How long does each episode last? Does the dizziness abate spontaneously? Does it lead to loss of consciousness? Find out if dizziness is triggered by sitting or standing up suddenly or stooping over. Does being in a crowd make the patient feel dizzy? Ask about emotional stress. Has the patient been irritable or anxious lately? Does he have insomnia or difficulty concentrating? Look for fidgeting and eyelid twitching. Does the patient startle easily? Also, ask about palpitations, chest pain, diaphoresis, shortness of breath, and chronic cough.

Next, perform a physical examination. Begin with a quick neurologic assessment, checking the patient's level of consciousness (LOC), motor and sensory functions, and reflexes. Then inspect for poor skin turgor and dry mucous membranes, signs of dehydration. Auscultate heart rate and rhythm. Inspect for barrel chest, clubbing, cyanosis, and use of accessory muscles. Also auscultate breath sounds. Take the patient's blood pressure while he's lying down, sitting, and standing to check for orthostatic hypotension. Test capillary refill time in the extremities, and palpate for edema.

» READ BOOK EXCERPT ONLINE »

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

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

Ask your patient to describe the onset and duration of his vertigo, being careful to distinguish this symptom from dizziness. Does he feel that he’s moving or that his surroundings are moving around him? How often do the attacks occur? Do they follow position changes, or are they unpredictable? Find out if the patient can walk during an attack, if he leans to one side, and if he’s ever fallen. Ask if he experiences motion sickness and if he prefers one position during an attack. Obtain a recent drug history, and note any evidence of alcohol abuse.

Perform a neurologic assessment, focusing particularly on eighth cranial nerve function. Observe the patient’s gait and posture for abnormalities.

» READ BOOK EXCERPT ONLINE »

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

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

Test the patient's motor and sensory functions. Evaluate pupil size, equality, and response to light. Then test cranial nerve function and deep tendon reflexes. Ask about headache, dizziness, nausea, changes in vision, and numbness or tingling. When did the patient first notice these symptoms? Is his family aware of behavioral changes? Also, ask about a history of cerebrovascular disease, cancer, meningitis, encephalitis, upper respiratory tract infection, bleeding or clotting disorders, or recent trauma.

» READ BOOK EXCERPT ONLINE »

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

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

Ask about a history of diabetes and cardiovascular disease. Is the patient taking drugs prescribed for high blood pressure? If so, when did he take his last dose?

If the patient’s blood pressure is normal, obtain a more complete history. Ask if he’s had a myocardial infarction, heart failure, kidney disease, or atherosclerosis, which may predispose him to cardiac arrhythmias, hypertension, and a transient ischemic attack. Does he have a history of anemia, chronic obstructive pulmonary disease, anxiety disorders, or head injury? Obtain a complete drug history.

Next, explore the patient’s dizziness. How often does it occur? How long does each episode last? Does the dizziness abate spontaneously? Does it lead to loss of consciousness? Find out if dizziness is triggered by sitting or standing up suddenly or by stooping over. Does being in a crowd make the patient feel dizzy? Ask about emotional stress. Has the patient been irritable or anxious lately? Does he have insomnia or difficulty concentrating? Look for fidgeting and eyelid twitching. Does the patient startle easily? Also, ask about palpitations, chest pain, diaphoresis, shortness of breath, and chronic cough.

Next, perform a physical examination. Begin with a quick neurocheck, assessing the patient’s level of consciousness (LOC), motor and sensory function, and reflexes. Then inspect for poor skin turgor and dry mucous membranes, signs of dehydration. Auscultate heart rate and rhythm. Inspect for barrel chest, clubbing, cyanosis, and use of accessory muscles. Also auscultate breath sounds. Take the patient’s blood pressure while he’s lying, sitting, and standing to check for orthostatic hypotension. Test capillary refill time in the extremities, and palpate for edema.

» READ BOOK EXCERPT ONLINE »

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

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

Perform a neurologic assessment, focusing particularly on eighth cranial nerve function. Observe the patient’s gait and posture for abnormalities.

» READ BOOK EXCERPT ONLINE »

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

Decorticate posture [Decorticate rigidity, abnormal flexor response]: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

Test the patient’s motor and sensory function. Evaluate pupil size, equality, and response to light. Then test cranial nerve function and deep tendon reflexes. Ask family members if the patient experienced headache, dizziness, nausea, changes in vision, numbness, or tingling. When did the patient first notice these symptoms? Is his family aware of any behavioral changes? Also, ask about a history of cerebrovascular disease, cancer, meningitis, encephalitis, upper respiratory tract infection, bleeding or clotting disorders, or recent trauma.

» READ BOOK EXCERPT ONLINE »

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

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

The patient should be allowed, in his or her own words, to describe what is meant by dizziness. A description of the first attack can be helpful. What is the time course of subsequent attacks? How long do the episodes last? How frequent are they? Do any particular positions or movements bring on episodes? Is there any associated nausea, headache, fever, hearing loss, ear pain, or tinnitus? Are there other neurologic symptoms? What medications is the patient taking?

Physical examination.

A focused physical examination usually confirms rather than makes the diagnosis. An otoscopic examination should be done looking for impacted cerumen or signs of infection. A focused neurologic examination should be done. The patient’s eyes should be observed for spontaneous, gaze-evoked or positional nystagmus. A Dix-Hallpike maneuver should be done when BPPV is suspected. The patient should be observed walking to assess cerebellar function and disequilibrium.

» READ BOOK EXCERPT ONLINE »

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

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

The patient’s age, underlying comorbidities, and symptom classification category will help limit the diagnostic possibilities. Further specificity is gained by eliciting the following:

A. Temporal pattern. Are the symptoms episodic or continuous? If episodic, how long do they last? Peripheral origin vertigo is often intermittent and of sudden onset compared with the usual, more gradual onset of central vertigo. A continuous history suggests CNS pathology, drug or toxin effects, metabolic dysfunction, or psychiatric disease. BBPV episodes last less than a minute; vertebrobasilar transient ischemic attacks last minutes to an hour; Ménière’s disease persists 1 to 24 hours; and vestibular neuronitis or acute labyrinthitis continues several days.

B. Precipitating or exacerbating factors. Has there been recent head trauma (implying perilympathic fistula) or viral illness (labyrinthitis)? What is the relationship to sudden head movement or turning over in bed (BPPV), coughing or sneezing (perilymphatic fistula), postural changes (orthostasis), exercise (arrhythmias), foods (salty meals exacerbating Ménière’s), walking and turning (multiple sensory deficits), micturition or pain (vasovagal reaction), and emotional upset (hyperventilation)?

C. Associated symptoms. Marked nausea, vomiting, diaphoresis, aural fullness, and recruitment (perception of sounds being too loud) are typical of peripheral vestibular disorders. Episodic vertigo associated with tinnitus and gradual (unilateral) hearing loss involving low frequencies preferentially suggests Ménière’s disease. Asymmetric weakness, cranial nerve or cerebellar dysfunction, diplopia, or dysarthria suggests brainstem or CNS disease. Headache, scotomata, or tunnel vision points to migraine. Numbness or paresthesias may indicate neuropathy contributing to multiple sensory deficits (Chapter 4.6). A single, abrupt episode of severe vertigo with negative Dix-Hallpike (DH) testing (section III.A) that gradually subsides over days implies labyrinthitis (if hearing is affected) or vestibular neuronitis (if hearing is unaffected). Mild vertigo with prominent tinnitus, unilateral hearing loss, and loss of corneal reflex is worrisome for an acoustic neuroma.

D. Medications or toxins. Many medications can cause “dizziness,” although few (aminoglycosides, lead, mercury) cause vertigo. Assess toxin exposure by exploring job and recreational activities.

Physical examination (PE)

This will emphasize orthostatic vital signs, the eyes, ears, and neurologic and cardiovascular systems.

A. Detection of nystagmus is critical because it is the only objective sign of vertigo (5). Nystagmus can occur spontaneously or in response to changes in eye or body position. Peripheral vestibular disorders usually cause horizontal or rotatory nystagmus, whereas CNS pathology is reflected by vertical nystagmus—an ominous sign. In true vertigo caused by BPPV, DH maneuvers will often confirm the diagnosis (sensitivity 60% to 90%, specificity 90% to 95%) (2,3). The patient is moved rapidly from a sitting to a supine position with the head turned at a 30-degree angle, first to one side and then to the other. A positive DH test includes precipitation of vertigo, latency of onset by a few seconds, rotational nystagmus, resolution within a minute, and lessened symptoms and nystagmus with prolonged latency on repeated testing (i.e., fatiguability). Lack of latency and fatiguability characterize vertigo caused by serious central lesions.

B. Neurologic examination serves to detect brainstem or CNS pathology.

C. Otoscopy can detect otitis media or cholesteatoma. Nystagmus with vertigo following positive or negative pressure applied to the tympanic membrane (pneumatic otoscopy) suggests a perilymphatic fistula.

D. Other provocative tests (forced hyperventilation, vestibulo-ocular reflex testing, vigorous horizontal head shaking) are not routinely helpful.

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

Dizziness: Differential Overview
(Field Guide to Bedside Diagnosis)

Vertigo

❑ Benign paroxysmal positional vertigo

❑ Vestibular neuronitis

❑ Toxic labyrinthitis

❑ Vertebrobasilar insufficiency

❑ Ménière disease

❑ Migraine

❑ Multiple sclerosis

❑ Acoustic neuroma

❑ Herpes zoster oticus (Ramsey–Hunt)

Disequilibrium

❑ Multifactorial disequilibrium

❑ Stroke

❑ Cerebellar disease

❑ Frontal lobe apraxia

Lightheadedness

❑ Orthostatic hypotension

❑ Common fainting (presyncope)

❑ Hyperventilation

❑ Panic attack

Diagnostic Approach

Differentiate between vertigo, disequilibrium, and lightheadedness. Each has its own non-overlapping differential:

• Vertigo is the illusory sensation of rotatory motion, either of the patient or the environment.

• Disequilibrium is a sensation of imbalance when standing and walking.

• Lightheadedness is a sensation of impending loss of consciousness.

Provide the patient with experiential examples to refine the history (e.g., vertigo after spinning around as a child).

Attempt to provoke dizziness with maneuvers to confirm a provisional diagnosis, such as observation of gait, ambulation, and turning; orthostatic vital signs; Dix–Hallpike maneuver; Romberg; and/or 3-minute hyperventilation. The Dix–Hallpike maneuver provokes vertigo and nystagmus by stimulation of the posterior semicircular canal with the head tilted toward the affected side at 30 degrees below the horizontal. Have the patient look straight ahead to observe nystagmus. The nystagmus will fatigue. These findings indicate posterior canalithiasis causing benign paroxysmal positional vertigo (BPPV). The Romberg maneuver is performed by observing the patient standing. Swaying with eyes closed suggests disordered proprioception and/or vestibular function. Swaying with eyes open or closed is cerebellar in origin.

Vertigo usually implies a vestibular lesion (rarely brainstem). Suspect a central lesion if symptoms are preceded by a headache and vomiting without tinnitus. Central dizziness is very sensitive to movement of the head and is usually constant. Other cranial nerve findings or long track signs are usually present. Tinnitus, pressure, or decreased hearing localizes the problem to the inner ear and indicates the involved side. Nystagmus may persist after vertigo clears. Spontaneous vertical nystagmus suggests a lesion at the vestibular nucleus or cerebellum. Nystagmus that reverses direction when the patient looks in the direction of the slow phase suggests a central lesion. Exertional lightheadedness occurs in severe anemia, aortic stenosis, pulmonary hypertension, pericardial disease, and hypertrophic cardiomyopathy.

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Source: Field Guide to Bedside Diagnosis, 2007

Chronic/Recurrent Abdominal Pain: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Irritable bowel syndrome

❑ Peptic ulcer disease

❑ Cholecystitis

❑ Chronic pancreatitis

❑ Inflammatory bowel disease

❑ Intermittent mesenteric ischemia

❑ Pancreatic cancer

❑ Gastric cancer

❑ Endometriosis

❑ Recurrent intestinal obstruction

❑ Sickle cell anemia

❑ Radiculopathy

❑ Adrenal insufficiency

❑ Lead poisoning

❑ Porphyria

Diagnostic Approach

Examining a patient during an episode of pain is important for diagnosis. A significant proportion of patients with chronic abdominal pain will remain undiagnosed despite extensive testing. For these patients, repeated history and examination, during which one looks for new symptoms or any change in the pattern of symptoms, may eventually yield a formulation.

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Source: Field Guide to Bedside Diagnosis, 2007

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

Ask about a history of diabetes and cardiovascular disease. Is the patient taking drugs prescribed for high blood pressure? If so, when did he take his last dose?

If the patient’s blood pressure is normal, obtain a more complete history. Ask about myocardial infarction, heart failure, kidney disease, or atherosclerosis, which may predispose the patient to cardiac arrhythmias, hypertension, and a transient ischemic attack. Does he have a history of anemia, chronic obstructive pulmonary disease (COPD), anxiety disorders, or head injury? Obtain a complete drug history.

Explore the patient’s dizziness. How often does it occur? How long does each episode last? Does the dizziness abate spontaneously? Does it lead to loss of consciousness? Find out if dizziness is triggered by sitting or standing up suddenly or stooping over. Does being in a crowd make the patient feel dizzy? Ask about emotional stress. Has the patient been irritable or anxious lately? Does he have insomnia or difficulty concentrating? Look for fidgeting and eyelid twitching. Does the patient startle easily? Also, ask about palpitations, chest pain, diaphoresis, shortness of breath, and chronic cough.

Physical examination

Perform a physical examination. Begin with a quick neurocheck, assessing the patient’s level of consciousness (LOC), motor and sensory functions, and reflexes. Then inspect for poor skin turgor and dry mucous membranes, signs of dehydration. Auscultate heart rate and rhythm. Inspect for barrel chest, clubbing, cyanosis, and use of accessory muscles. Also auscultate breath sounds. Take the patient’s blood pressure while he’s lying, sitting, and standing to check for orthostatic hypotension. Test capillary refill time in the extremities, and palpate for edema.

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

Decorticate posture [Decorticate rigidity, abnormal flexor response]: History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

Obtain a history from the patient (if possible) or his family. Did the patient complain about headache, dizziness, nausea, changes in vision, and numbness or tingling? When did he first notice these symptoms? Did the family observe any behavioral changes?

Ask about a history of cerebrovascular disease, cancer, meningitis, encephalitis, upper respiratory tract infection, bleeding or clotting disorders, or recent trauma.

Physical examination

Test the patient’s motor and sensory functions. Evaluate pupil size, equality, and response to light. Test cranial nerve function and deep tendon reflexes. Perform a complete neurologic examination and continue to perform frequent neurologic checks. Assess the patient’s respiratory function.

ALERT: Abnormal respirations may indicate a breakdown in the brain’s respiratory center and an impending tentorial herniation — a neurologic emergency.

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

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

If the patient’s blood pressure is normal, obtain a more complete history. Ask about a history of diabetes and cardiovascular disease. Is the patient taking drugs prescribed for high blood pressure? If so, when did he take his last dose? Also ask about myocardial infarction, heart failure, kidney disease, or atherosclerosis, which may predispose the patient to cardiac arrhythmias, hypertension, and a transient ischemic attack. Does he have a history of anemia, chronic obstructive pulmonary disease, anxiety disorders, or head injury? Obtain a complete drug history.

Next, explore the patient’s dizziness. How often does it occur? How long does each episode last? Does the dizziness abate spontaneously? Does it lead to loss of consciousness? Find out if dizziness is triggered by sitting or standing up suddenly or stooping over. Does being in a crowd make the patient feel dizzy? Ask about emotional stress. Has the patient been irritable or anxious lately? Does he have insomnia or difficulty concentrating? Look for fidgeting and eyelid twitching. Does the patient startle easily? Also, ask about palpitations, chest pain, diaphoresis, shortness of breath, and chronic cough.

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

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

Ask your patient to describe the onset and duration of his vertigo, being careful to distinguish this symptom from dizziness. Does he feel that he’s moving or that his surroundings are moving around him? How often do the attacks occur? Do they follow position changes, or are they unpredictable? Find out if the patient can walk during an attack, if he leans to one side, and if he has ever fallen. Ask if he experiences motion sickness and if he prefers one position during an attack. Obtain a recent drug history. Note any evidence of alcohol abuse.

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

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

Ask about headache, dizziness, nausea, changes in vision, and numbness or tingling. When did the patient first notice these symptoms? Is his family aware of any behavioral changes? Also, ask about a history of cerebrovascular disease, cancer, meningitis, encephalitis, upper respiratory tract infection, bleeding or clotting disorders, or recent trauma.

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

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

Peripheral Vestibular Dysfunction

Labyrinthitis

Acute otitismedia is most common cause of labyrinthitis in childhood. The infection mayextend directly into labyrinth, or inflammatory toxins may causelabyrinthine disturbance.

Viral infections (e.g., mumps, measles,and infectious mononucleosis) also may cause labyrinthitis.

History of infection followed by vertigoand hearing loss suggests diagnosis. Exam often reveals spontaneousnystagmus with fast component directed toward normal ear.

Motion Sickness

Can occur with land, sea, or air travel.Nausea and vomiting are common findings, but vertigo and nystagmusalso can occur.

Head Trauma

May causelabyrinthine injury with or without temporal bone fracture.

Frequent findings are falling towardaffected side and hearing loss.

Skull radiography and CT of temporalbone are useful in diagnosis. Caloric testing usually reveals decreasedlabyrinthine response on affected side.

Drugs

Several drugs, including aminoglycosides,ethacrynic acid, and quinine, may cause hearing loss, but rarelyvertigo.

Benign Paroxysmal Vertigo

Usuallyoccurs in children 2–6 yrs and is characterized by recurrentepisodes of vertigo that occur without warning.

Child appears pale, anxious, and unableto maintain upright position.

Nystagmus also may occur.

Results of neurologic exam are normalbetween episodes.

Vestibular Neuronitis

Most frequentcause of vestibular neuronitis, which usually occurs in adolescents,is viral upper respiratory infection.

Onset is acute, with nausea, vomiting,vertigo, and nystagmus. Hearing loss does not occur.

Episodes are self-limited but may recur.

Caloric stimulation produces decreasedor absent response on affected side.

Middle Ear and Temporal Bone Masses

Middle earand temporal bone masses (e.g., cholesteatoma and acoustic neuroma) maydamage labyrinth and produce vertigo and hearing loss.

CT and MRI locate mass and define itsextent.

See Bellet et al. (1992) for furtherdiscussion.

Perilymphatic Fistula

Head trauma or sudden change in barometricpressure (flying or diving) may cause rupture of round or oval windowinto vestibule, creating fistula and producing vertigo and hearingloss (see Chap. 26, Hearing Lossand Deafness).

Ménière Disease

Uncommon disorder in children characterizedby recurrent episodes of vertigo, fluctuating hearing loss, andtinnitus. Caloric testing usually reveals reduced vestibular responseon involved side.

Central Vestibular Dysfunction

Head Trauma

Concussion or brain contusion with shearingforces may damage vestibular nuclei and produce vertigo. Calorictesting reveals diminished caloric responses.

Intracranial Infection

Vertigo may sometimes occur with meningitis,encephalitis, and brain abscess. These disorders are discussed in Chap. 3, Alteration in Consciousness.

Seizure Disorder

Vertigo may occur as part of initial manifestationof complex partial seizure.

Basilar Artery Migraine

In this type of migraine, vertigo may precedeor accompany throbbing occipital headache (see Chap. 25, Headache).

Neoplasm

Posteriorfossa tumors may cause vertigo, ataxia, and nystagmus, whereas brainstem gliomasmay cause vertigo, double vision, hearing loss, nystagmus, and cranialnerve dysfunction (III–VIII).

MRI is diagnostic study of choice.

Histologic diagnosis is definitive.

Psychologic Disturbance

Anxiety,depression, conversion reaction, or malingering may produce vertigo.

History and physical exam suggest diagnosis.Results of vestibular function testing, electroencephalography,and CT are normal.

Diagnostic Approach

Once presenceof vertigo has been established, next step is to determine whetherdisturbance is in peripheral or central vestibular system or whetherit is psychologic.

Important information is age of child;whether vertigo is acute, recurrent, or chronic; presence of hearingloss, ear pain, or tinnitus; and any history of recent trauma ordrug ingestion.

Complete physical exam should be performed,focusing on otologic and neurologic exams.

Vertigo caused by disturbance of peripheralvestibular system often occurs suddenly, lasts short time, and isunassociated with loss of consciousness. Sudden change in head positionfrequently precipitates episode. Nausea, vomiting, tinnitus, hearingloss, and swaying or falling toward affected side are common findings.Nystagmus is inhibited by visual fixation and may change with headposition.

Disturbance in central vestibular systemcan cause recurrent or chronic vertigo, which may be accompaniedby cranial nerve deficits, pyramidal signs, and cerebellar signs.If nystagmus occurs, it does not change with head position, noris it inhibited by visual fixation.

The history and physical exam are diagnosticin many cases of vertigo. Audiologic testing or brainstem evokedresponses should be performed with suspected hearing loss.

CT should be performed if there ishistory of acute head trauma. Otherwise, MRI is study of choiceif neuroimaging is indicated. Electroencephalography is useful ifseizures are suspected.

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

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

Recurrent Infection: Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)

Normal Host

The following are common recurrent infectionsthat occur in normal hosts.

Upper Respiratory Tract Infections (URIs)

Most commoncause of recurrent infection is viral URI because children are repeatedlyexposed to these pathogens at home, in day-care centers, in school,and in the community.

Infants <1 yr average 3–7respiratory illnesses/yr, whereas children 1–6yrs of age average 8 respiratory infections/yr. Childrenwho are >6 yrs of age have 5–6 respiratory illnesses/yrup to adolescence.

Otitis Media

Perhapsthe single most important factor contributing to recurrent acuteotitis media is eustachian tube dysfunction. Predisposing causesinclude allergic rhinitis, cleft palate, and enlarged adenoid glands.

For unexplained reasons, Native Americansand children with trisomy 21 have high incidence of eustachian tubedysfunction and recurrent otitis media.

Skin Infections

Recurrentimpetigo or cellulitis of lower extremities is usually due to traumaof skin with secondary excoriation.

As isolated finding, these skin infectionsdo not indicate primary immunodeficiency.

Urinary Tract Infections (UTIs)

RecurrentUTIs are frequent in girls, perhaps in part because of colonizationof short urethra by fecal flora. Usual pathogens are gram-negativeenteric bacteria.

Predisposing factors to UTI in bothgirls and boys are urinary tract obstruction and reflux.

Pneumonia

Factors that predispose to recurrent pneumoniainclude bronchopulmonary dysplasia, foreign body aspiration, reactiveairways disease, cystic fibrosis, and gastroesophageal reflux.

Meningitis

Fracture of basilar skull or cribriform plateor midline dermal defect may predispose to recurrent meningitis.

Foreign Body

Because chronic indwelling urinary cathetersand ventricular shunt catheters compromise skin and mucous membranebarriers to infection, they predispose to recurrent urinary tractand shunt infections, respectively.

Immunologically Compromised Host

Primary Immunodeficiency

Major clinicalmanifestation of primary immune deficiency is increased susceptibility toinfection, which can be manifested by increase in frequency, duration,or severity of infection; occurrence of unexpected or severe complications;or infection with unusual organisms.

Whether frequent infections indicatepresence of immunologic disorder depends on age of child, typesof infection, specific pathogens involved, associated findings,and family history of recurrent or unusual infections or childhooddeath.

Primary B-Cell Disorders

Antibody deficiency accounts for largestproportion of primary immunodeficiency disorders. There is increasein risk of recurrent pyogenic infection in children with defectsin B-cell function.

Transient Hypogammaglobulinemia of Infancy

Serum immunoglobulinG reaches its nadir at 3–4 mos of age in normal infantsas maternal IgG levels wane. Levels increase as infants begin toproduce their own IgG.

Transient hypogammaglobulinemia refersto delay in production of IgG beyond 6 mos of age.

Increase in incidence of otitis mediaand sinusitis may occur in affected children until IgG levels becomenormal at 18–36 mos of age. Number and function of B andT cells is normal.

X-Linked (Bruton) Agammaglobulinemia

Due to mutationsin gene at Xq22 that encodes for B-cell protein tyrosine kinase.

Affected individuals are well until6–9 mos of age, when they develop infections with encapsulatedorganisms (e.g., S. pneumoniae, H. influenzae, and S. aureus). Viralinfections are usually not a problem except for enteroviruses, whichcan cause persistent meningoencephalitis. Infections with fungi andP. carinii are unusual. Tonsils are small, and lymph nodes are rarelypalpable.

Diagnosis is confirmed by demonstrationof very low or undetectable serum concentrations of IgG, IgA, IgM,and IgE; absence or low numbers of circulating B cells; and failureof antibody production in response to antigenic stimulation (e.g.,immunizations).

Common Variable Immunodeficiency

Moleculardefect is unknown. Bacterial pathogens and types of infections aresimilar to those found with X-linked agammaglobulinemia.

Presentation is usually in later childhoodor adolescence with recurrent sinusitis, pneumonia, or GI infections.Tonsils and lymph nodes may be normal in size or enlarged.

Number of B-lymphocytes in peripheralblood is normal, but these cells are unable to differentiate normallyinto immunoglobulin-producing cells. Serum immunoglobulin levelsare decreased but higher than in those with X-linked agammaglobulinemia.T cell numbers are normal, but T-cell function may be depressed.

Selective Immunoglobulin A Deficiency

Basic defectleading to serum and secretory IgA deficiency is unknown. SerumIgA is <10 mg/dL, but serum IgG and IgM are normal.T-lymphocyte function is intact.

Some children have no obvious clinicalproblems, whereas others have recurrent infections (otitis media,sinusitis, pneumonia, gastroenteritis) caused by the same pathogensas in other antibody deficiency syndromes.

Some of these individuals may havedecreased IgG subclasses and abnormalities of specific antibodyproduction. Affected children also may have increased incidenceof allergic disorders (allergic rhinitis, eczema, asthma).

Immunoglobulin G Subclass Deficiencies

Despitenormal or increased serum IgG, deficiencies in ≥1 IgG subclassesmay occur.

Isolated or combined deficiency ofIgG1, IgG2, and IgG3 has been associated with increased risk ofinfection, usually otitis media, sinusitis, and pneumonia.

Clinical significance of IgG4 deficiencyis uncertain.

Primary T-Cell Disorders

Individuals with impaired T-cell functionhave increased susceptibility to opportunistic infection.

Thymic Hypoplasia (DiGeorge Syndrome)

Pathogenesisinvolves hypoplasia or aplasia of thymus and parathyroid glands.In >90% of cases, deletion of chromosome 22q11.2is found.

Typical facies consists of downwardslant of palpebral fissures, hypertelorism, low-set ears with notchedpinnae, short philtrum, and mandibular hypoplasia. Conotruncal defects(truncus arteriosus, interrupted aortic arch) are common. Hypocalcemicseizures may occur in first 1–2 wks of life. Other findingsinclude chronic rhinitis, recurrent pneumonia, thrush, and diarrhea.

Although serum immunoglobulin levelsare usually normal, specific antibody responses are decreased. T-cellnumbers are low, and lymphocyte responses to mitogens are usuallydiminished.

Combined B- and T-Cell Disorders

Defect in T-cell number or function impairscell-mediated immunity. Because B cells require helper T cells forproduction of IgG, IgA, and IgE, T-cell defect results in B-celldeficiency even when B cells are competent.

Combined Immunodeficiency

Characteristicmanifestations include recurrent pulmonary and skin infections,chronic diarrhea, oral and cutaneous candidiasis, and failure tothrive. Serum immunoglobulins may be normal, but impaired antibodyfunction usually occurs.

Cellular immune function studies showlymphopenia, profound decrease in T-cell number, and decreased lymphocyteresponses to mitogens and antigens in vitro.

Purine Nucleoside Phosphorylase Deficiency

Purine nucleosidephosphorylase is an enzyme that functions in purine salvage pathway,so that uric acid can be formed. Mutations in purine nucleosidephosphorylase gene on chromosome 14q13.1 lead to deficiency of thisenzyme and accumulation of toxic metabolites that affect immunefunction.

Spastic diplegia, psychomotor retardation,and autoimmune disorders are common. Serum uric acid concentrationis low.

Immune defects include significantlymphopenia, marked decrease in T cells, impaired T-cell function,and increase in natural killer cells.

Severe Combined Immunodeficiency

Differentmutations are responsible for various syndromes of severe combinedimmunodeficiency (SCID), which are the most severe of all immunodeficiencydisorders. X-linked SCID is most common form of SCID in U.S.

Skin infections, otitis media, pneumonia,chronic diarrhea, persistent candidiasis, and failure to thriveoccur in first few months of life. Infections with viruses, pyogenicbacteria, C. albicans, and P. carinii are common. There is absenceof lymph nodes and thymus.

Certain lab findings characterize SCID:lymphopenia; low or absent serum immunoglobulin levels; very lowor undetectable T cells; delayed cutaneous anergy; lack of antibodyformation after immunization; and absence of lymphocyte proliferativeresponses to antigens, mitogens, and allogenic cells in vitro.

Immunodeficiency with Thrombocytopenia and Eczema (Wiskott-Aldrich Syndrome)

X-linkeddisorder characterized by eczema, thrombocytopenic purpura, andrecurrent infections, including otitis media, pneumonia, meningitis,and septicemia.

Typical serum immunoglobulin patternconsists of normal to mildly decreased IgG, increased IgA and IgE,and low IgM. Antibody responses to polysaccharide antigens are poor.T-cell function is defective with cutaneous anergy and poor lymphocytemitogen response.

Parolini et al. (1998) have shown thatthis disorder also can occur in females by nonrandom inactivationof maternally derived X chromosome, but this is rare.

X-Linked CD-40 Ligand Deficiency

Previouslyreferred to as X-linked immunodeficiency with hyper-IgM. Mutationsin CD154 gene on X chromosome prevent T cells from signaling B cellsthrough CD40 pathway. Isotype switching does not occur, and increasedamount of IgM is produced.

Age of onset is usually from 6 mosto 2 yrs of age with recurrent infections (e.g., otitis media, sinusitis,and pneumonia) caused by pyogenic organisms or P. carinii. Lymphadenopathyand pancytopenia also may occur.

Frequency of autoimmune disorders andcancer is increased.

Although number of B lymphocytes inperipheral blood is normal, serum IgG, IgA, and IgE are very low,whereas serum IgM is normal or markedly increased. T-cell functionmay be normal or impaired. Molecular genetic analysis is confirmatory.

X-Linked Lymphoproliferative Disease

Infectionwith Epstein-Barr virus causes uncontrolled cytotoxic T-cell proliferation inchildren with this disorder. Gene has been mapped to Xq25 and proteinproduced by this gene is known as SAP (SLAM-associated protein).SAP inhibits upregulation of signaling lymphocyte activation molecule(SLAM) and thus prevents uncontrolled lymphoproliferation of Epstein-Barrvirus in normal persons.

Usual presentation is severe infectiousmononucleosis, which can be fatal, primarily because of severe liverinvolvement.

Identification of susceptible individualsbefore infection is possible by molecular genetic analysis.

Survivors have severe cellular immunedefects and may develop hypogammaglobulinemia, aplastic anemia,and lymphoma.

Ataxia-Telangiectasia

Gene locusof this autosomal-recessive disorder has been mapped to chromosome 11q22.3.

Characteristic manifestations includeprogressive cerebellar ataxia, telangiectasias of skin and bulbarconjunctivae, and recurrent sinus/pulmonary infections.

Usual immunologic abnormalities areselective absence of serum IgA, low serum IgG and IgE, decreasedor normal specific antibody titers, and diminished proliferativelymphocyte response to mitogens.

Hyper-IgE Syndrome

Autosomal-dominantdisorder, whose gene locus has been mapped to chromosome 4q21. Characterizedby recurrent staphylococcal abscesses (especially skin, lungs, andjoints), pruritic dermatitis, and marked increase in serum IgE.Number of eosinophils is increased in blood and sputum.

Antibody and cell-mediated responsesto antigens are poor.

Cartilage-Hair Hypoplasia

This autosomal-recessivedisorder is a form of short-limbed dwarfism characterized by presenceof fine, sparse, light hair and eyebrows; hyperextensible jointsof hands and feet with inability to extend elbows completely; andradiologic changes (costochondral junction flaring of ribs, scleroticor cystic changes of bone metaphyses).

Gene locus has been mapped to chromosome9p21-p12.

3 patterns of immune dysfunction mayoccur: defective antibody-mediated immunity, combined immunodeficiency,and severe combined immunodeficiency. Affected children are especiallyprone to severe and often fatal varicella infections.

Disorders of Phagocytic Function

Severe congenital neutropenia, cyclic neutropenia,chronic granulomatous disease of childhood, and Chediak-Higashisyndrome are discussed in this section. See Lekstrom-Himes and Gallin(2000) for discussion of other phagocytic defects.

Congenital Neutropenia

This autosomal-recessivedisorder is caused in many cases by mutation in neutrophil elastasegene located on chromosome 19p13.3.

Characterized by recurrent bacterialinfections and failure of myeloid cells to mature from promyelocytesto myelocytes. Absolute neutrophil count is <500 cells/mm³.

Cyclic Neutropenia

Mutationsin neutrophil elastase gene also cause this autosomal-dominant disorder.

Characterized by severe neutropeniathat typically occurs at intervals that last 3–6 days every3–4 wks. Children have fever and mucosal ulcers and maydevelop life-threatening infections during period of neutropenia.

Chronic Granulomatous Disease of Childhood

Genetictransmission is X- linked (most commonly) or autosomal-recessive.

Neutrophils and monocytes ingest butdo not kill catalase-positive microorganisms (S. aureus; S. marcescens;Proteus, Klebsiella, Candida, and Aspergillus species) because offailure to generate superoxide and other reactive oxygen radicals.

Recurrent abscess formation (skin,liver, lung), pneumonia, and osteomyelitis are characteristic findings.

Disease can be diagnosed by nitrobluetetrazolium test or by flow cytometry with dihydrorhodamine dye.

Chediak-Higashi Syndrome

Autosomal-recessivedisorder caused by mutations in lysosomal trafficking regulator gene,which has been mapped to chromosome 1q42.1-q42.2.

Characteristic findings include recurrentbacterial infections, partial ocular and cutaneous albinism, photophobia,nystagmus, peripheral neuropathy, platelet dysfunction with easybruising, and mental retardation. Life-threatening lymphoma-likesyndrome with fever, hepatosplenomegaly, lymphadenopathy, and pancytopeniaalso may occur.

Diagnosis can be established by presenceof giant cytoplasmic granules in neutrophils, monocytes, and lymphocytes.Molecular genetic analysis is definitive.

Disorders of Complement System

Congenitaldeficiencies of all complement components of classical pathway have beendescribed (C1q, C1r, C1rs, C4, C2, C3, C5, C6, C7, C8, and C9) butare rare.

Complement deficiency predisposes topneumonia, cellulitis, abscesses, osteomyelitis, meningitis, andsepticemia caused by pyogenic bacteria. Individuals with C5, C6,C7, C8, or C9 deficiency are particularly susceptible to meningococcaland gonococcal infections.

Decreased total serum hemolytic complement(CH50) determination can be used as screening test for complementdeficiency. If CH50 is low, specific complement levels can be measured.

Secondary Immunodeficiency

Secondary immunodeficiency disorders aremuch more common than primary ones.

Immunosuppressive Agents

Corticosteroidsdepress immunoglobulin synthesis, delayed hypersensitivity response,and accumulation of leukocytes at site of inflammation.

Cyclosporine suppresses cell-mediatedimmunity and some humoral immunity.

Azathioprine and 6-mercaptopurine impairDNA and RNA synthesis and thus any immune response dependent oncell proliferation.

Antilymphocyte globulin diminishescutaneous delayed hypersensitivity reactions.

Therapeutic ionizing radiation significantlyimpairs cell-mediated immunity.

Sickle Cell Disease

Factors that increase risk of serious andrecurrent infection in children with sickle cell disease are diminishedsplenic function and decreased opsonic activity against encapsulatedorganisms (e.g., S. pneumoniae).

Nephrotic Syndrome

Septicemia and peritonitis are common recurrentinfections that occur in individuals with nephrotic syndrome. Thereis impaired antibody response to organisms (e.g., S. pneumoniae).

Burns

Becausenatural skin barrier to infection is destroyed in serious burns,septicemia is common complication.

Serum immunoglobulin levels decreasea few days after burn and return to normal in 1–2 wks.T-cell function is also diminished.

Uremia

There isincreased susceptibility to infections of skin, lung, urinary tract,and GI tract in individuals with uremia. Predominant immunologicdefect is impaired cell-mediated immunity.

Abnormal antibody responses to S. pneumoniaeand influenza virus as well as defective neutrophil function alsohave been described.

Asplenia Including Splenectomy

Because spleen plays major role in antibodysynthesis and in clearance of microorganisms from blood, individualswithout a spleen have increased susceptibility to infection. Commonpathogens infecting such individuals include S. pneumoniae, H. influenzaetype b, N. meningitidis, S. aureus, group A Streptococcus, and E.coli.

Neutropenia

Childrenwith severe neutropenia (absolute neutrophil count of <500cells/mm³) have increased susceptibilityto infection.

Causes include drugs (penicillins,sulfonamides, phenothiazines, anticonvulsants), immune neutropenia(isoimmune, autoimmune), hypersplenism, bone marrow replacement(especially malignancy), cancer chemotherapy, and radiation to bonemarrow.

S. aureus and gram-negative entericbacteria are most common pathogens isolated from neutropenic individuals.

Lymphoid Malignancy

Importantfactors in increased susceptibility of leukemic patients to infectionare decrease in number of circulating mature neutrophils and decreasedleukocyte mobilization.

Individuals with lymphoma have impairedantibody production and cell-mediated immunity. Defects of cell-mediatedimmunity often occur in Hodgkin disease.

Protein-Calorie Malnutrition

Bacterialinfections of GI tract, urinary tract, and blood are common in individuals withprotein-calorie malnutrition. So are fungal and parasitic infections.Most common immunologic abnormality is impaired cell-mediated immunity.

Dietary deficiencies of riboflavinand pyridoxine may lead to dermatitis and stomatitis that compromiseskin and mucous membrane barriers to infection.

HIV Infection

Causes spectrumof disease, and most severe form is AIDS.

Individuals at risk include male homosexuals,intravenous drug abusers, female sexual partners of carriers orindividuals with HIV infection, hemophiliacs who have received multipleblood transfusions, other recipients of blood products, and infantsborn to infected mothers.

Infected newborns are often small forgestational age and may develop clinical disease in first 6 mosof life.

Clinical manifestations include fever,diarrhea, failure to thrive, hepatosplenomegaly, generalized lymphadenopathy,parotitis, interstitial pneumonitis, persistent oral candidiasis,cardiomyopathy, hepatitis, nephropathy, lymphoid interstitial pneumonia,and encephalopathy. Recurrent infections (e.g., otitis media, sinusitis,pneumonia, and septicemia) also occur. Opportunistic infectionsare common with pathogens (e.g., P. carinii, cytomegalovirus, herpessimplex virus, varicella-zoster virus, M. tuberculosis, M. aviumcomplex, Cryptosporidium, T. gondii, and C. neoformans).

Principal immunologic abnormalitiesinclude

Diminishednumber of T cells, which is primarily due to decrease in T-helper CD4⁺ cells

Reversed T-helper:suppressor ratio(CD4⁺ to CD8⁺)

Decreased proliferative responses tomitogens (e.g., pokeweed mitogen, phytohemagglutinin, and concanavalinA)

Cutaneous anergy to delayed hypersensitivityantigens

Although there is increase in numberof B cells and immunoglobulin levels, especially IgG and IgA, theseindividuals are unable to generate adequate antibody responses afterexposure to new antigens.

Diagnosis is usually made by serumantibody tests (ELISA and Western blot or other confirmatory tests)in children >18 mos of age. In children <18 mosof age, diagnosis may be confirmed by positive viral blood cultureor demonstration of viral nucleic acids by polymerase chain reaction.

Diagnostic Approach

Recurrentviral URIs in otherwise normal child with normal growth and development occurbecause of recurrent exposure. Such infections rarely indicate underlyingimmune disorder with possible exception of selective IgA deficiency.

Localized defect is usually the problemwhen recurrent infections occur at single anatomic site (otitismedia, urinary tract infection, pneumonia, or meningitis). Tests(e.g., CBC and differential counts; UA; urine, blood, and spinalfluid cultures) and chest radiography are often diagnostic.

Primary or secondary immune deficiencyshould be suspected in children who have

≥2 serious bacterial infections(pneumonia, meningitis, septicemia, osteomyelitis, septic arthritis)

Infection with organisms of low virulence

Chronic sinopulmonary infection

Unusual infecting agents

Incomplete clearing between episodes

Incomplete response to treatment

Frequent findings in children withimmunodeficiency are impaired growth; recurrent or chronic diarrhea,eczema, or thrush; hepatosplenomegaly; recurrent abscesses; recurrentosteomyelitis; small or absent tonsils; and no palpable lymph nodes.Neutropenia, aplastic anemia, hemolytic anemia, and thrombocytopeniaare other common findings.

2 episodes of septicemia or meningitismay indicate asplenia or diminished splenic function, circulatingantibody deficiency, or complement deficiency. Recurrent meningococcalmeningitis or disseminated gonococcal infection may be due to deficiencyof C5, C6, C7, C8, or C9.

≥2 serious pyogenic skin infections(furunculosis, subcutaneous abscesses, or cellulitis), without otherexplanation, that are associated with recurrent otitis media orpneumonia suggest possible neutropenia, defective chemotaxis, ordefective phagocytosis.

Subcutaneous abscess or furunculosisassociated with lymph node, liver, or lung abscess suggests chronicgranulomatous disease.

Protracted diarrhea and persistentoral thrush associated with recurrent otitis media, sinusitis, orpneumonia suggest IgA deficiency or defect in cell-mediated immunity.

Single P. carinii pulmonary infection;L. monocytogenes infection occurring after newborn period; disseminatedor persistent herpes simplex, varicella, or cytomegalovirus infection;or chronic candidiasis of skin or mucous membranes may indicatedefective cell-mediated immunity.

Unusual associated physical exam findingsare suggestive of certain immunologic disorders:

Eczema andpetechiae (Wiskott-Aldrich syndrome)

Partial albinism (Chediak-Higashi syndrome)

Unusual facies with micrognathia, hypertelorism,malformed ears, and congenital heart defects (DiGeorge syndrome)

Ataxia and telangiectasia (ataxia-telangiectasia)

Fine hair with short extremities (cartilage-hairhypoplasia)

Recurrent skin abscesses and eczema(hyper-IgE syndrome)

The following diagnostic tests screenfor most primary immunologic defects. If any of these tests areabnormal, further investigations are necessary as outlined below.

CBC and differential

Analysis of blood smear

Quantitative serum immunoglobulins(IgG, IgA, IgM, IgE)

Functional antibody titers (polio,tetanus, diphtheria) for IgG function and isohemagglutinins (anti-Aand anti-B titers) for IgM function

Skin tests (Candida, tetanus toxoid)for delayed hypersensitivity and cell-mediated immunity

CH50

Chest radiograph (thymic shadow)

Evaluation of Humoral Deficiency

Serum immunoglobulinlevels should be measured (IgA, IgG, IgM) and compared with age-relatednormal values. Even though total serum IgG may be normal, subclassdeficiency may still occur and quantitative measurements of individualsubclasses can be performed.

Antibody function also should be assessed.Antibody responses to usual childhood immunizations (e.g., tetanusand diphtheria) can be determined. In children >18–24mos of age, antibody response to immunization with H. influenzaetype b capsular polysaccharide vaccine should be performed because somechildren respond normally to protein antigens but not to polysaccharideantigens.

If immunoglobulin levels and antibodytiters are decreased, next step is enumeration of B cells in peripheralblood by flow cytometry. Beyond these tests, immunologic consultationshould be requested. Studies (e.g., in vitro mitogen or antigendriven B-cell proliferation and immunoglobulin secretion) may beneeded to delineate functional B-cell defects.

Evaluation of Cell-Mediated Immunity

Should includeCBC, including absolute lymphocyte count, chest radiograph, anddelayed hypersensitivity skin tests. Presence of lymphopenia ishelpful because it occurs with T-cell disorders. Absence of thymussilhouette also may occur in some T-cell disorders, but thymus alsomay involute with stress.

Best screening test for delayed-typehypersensitivity testing is Candida skin test or standardized panelof antigens prepared for this purpose. Presence of ≥1 positivedelayed-type skin tests generally indicates intact cell-mediatedimmunity. However, prior exposure of the antigen is a prerequisite. Positiveresponse to some antigens does not ensure normal cell-mediated immunityto all antigens, and depression of reactivity may occur with acuteviral infections. Frequently, children <1 yr of age areunresponsive to all antigens on the panel.

Indirect assessment of T-cell functionmay be determined by enumeration of peripheral blood T-lymphocytesusing monoclonal antibodies to cell surface determinants. Otherspecialized tests measuring cell-mediated immunity include lymphocyteproliferation in vitro with mitogens, antigens, and allogenic cells.

Evaluation of Phagocytic Function

Number andfunction of phagocytic cells must be ascertained.

Number can be detected using WBC countand differential.

Function of phagocytic cells–cellmotility (chemotaxis), ingestion (phagocytosis), and intracellularkilling (bactericidal activity) can be determined by different assays.

An immunologist can help with selectionand interpretation of these tests.

Evaluation of Complement Deficiency

Complementdeficiencies C1–C9 can be detected by CH50 assay.

This assay depends on functional integrityof these complement components, and deficiency of any componentresults in marked decrease or absence of total hemolytic complementactivity.

If the assay is low, individual complementcomponents can be measured to determine which component is deficient.

>>>>>>

» READ BOOK EXCERPT ONLINE »

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

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

Ask about a history of diabetes and cardiovascular disease. Is the patient taking drugs prescribed for high blood pressure? If so, when did he take his last dose?

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

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

Ask your patient to describe the onset and duration of his vertigo, being careful to distinguish this symptom from dizziness. Does he feel that he's moving or that his surroundings are moving around him? How often do the attacks occur? Do they follow position changes, or are they unpredictable? Find out if the patient can walk during an attack, if he leans to one side, and if he has ever fallen. Ask whether he experiences motion sickness and if he prefers one position during an attack. Obtain a recent drug history, and note evidence of alcohol abuse.

Perform a neurologic assessment, focusing particularly on eighth cranial nerve function. Observe the patient's gait and posture for abnormalities.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Decorticate posture [Decorticate rigidity, abnormal flexor response]: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

Test the patient's motor and sensory functions. Evaluate pupil size, equality, and response to light. Then test cranial nerve function and deep tendon reflexes. Ask the patient about headache, dizziness, nausea, changes in vision, and numbness or tingling. When did the patient first notice these symptoms? Is his family aware of behavioral changes? Also ask about a history of cerebrovascular disease, cancer, meningitis, encephalitis, upper respiratory tract infection, bleeding or clotting disorders, or recent trauma.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

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

The first step is to determine if the patient has true vertigo. True vertigo is the experience of subjective or objective rotation with respect to the environment. In other words, either the patient or his or her environment is turning. One other form of true vertigo is lateral pulsion. This is the feeling that one is moving sideways when that is not the case. The patient who does not experience true vertigo should have a syncope workup . Narrowing the differential diagnosis of true vertigo depends on the presence or absence of other symptoms and signs. If there are other cranial nerve or long tract signs on neurologic examination, the patient may have a space-occupying lesion of the brain or brainstem or a hemorrhage, thrombosis, or embolism in the vertebral–basilar artery distribution. A neurology consult should be obtained. If there is true vertigo, tinnitis, and deafness, one would consider inner ear pathology such as Ménière disease, syphilis, petrositis, mastoiditis, and acoustic neuroma. If there is vertigo without tinnitus, deafness, or focal neurologic signs, the clinician should suspect acute labyrinthitis, vestibular neuronitis, benign positional vertigo, and drug toxicity. If there are rapid respirations during the attack of vertigo, one would consider hyperventilation syndrome. If there are significant findings on otoscopic examination, a diagnosis of otitis media, cholesteatoma, or mastoiditis should be considered. The workup will depend on whether the patient has objective findings on otoscopic or neurologic examination. If local pathology is suspected, perhaps a tympanogram, x-ray of the mastoids and petrous bones, audiogram, or referral to an otolaryngologist are required. If there are neurologic findings, perhaps a CT scan or MRI of the brain and auditory canal is indicated along with a referral to a neurologist. It is wise to have a specialist on board before ordering an expensive workup.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

» Next page: Signs of Benign Paroxysmal Positional Vertigo

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TREATMENTS & RESEARCH

Dr. Huntley's Diagnosis Checklist

Diagnosis of Benign Paroxysmal Positional Vertigo

Benign Paroxysmal Positional Vertigo Diagnosis: Book Excerpts

Diagnostic Tests for Benign Paroxysmal Positional Vertigo: Online Medical Books

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

DIAGNOSTIC WORKUP

ABDOMINAL PAIN, CHRONIC RECURRENT: Ask the following questions: (Algorithmic Diagnosis of Symptoms and Signs)

DIAGNOSTIC WORKUP

Dizziness/Lightheadedness & Vertigo: Differential Diagnosis (In a Page: Signs and Symptoms)

Workup and Diagnosis

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

Workup and Diagnosis

Fever – Recurrent: Differential Diagnosis (In A Page: Pediatric Signs and Symptoms)

Workup and Diagnosis

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

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

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

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

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

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

Decorticate posture [Decorticate rigidity, abnormal flexor response]: History and physical examination (Professional Guide to Signs & Symptoms (Fifth Edition))

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

Physical examination.

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

Physical examination (PE)

Dizziness: Differential Overview (Field Guide to Bedside Diagnosis)

Diagnostic Approach

Chronic/Recurrent Abdominal Pain: Differential Overview (Field Guide to Bedside Diagnosis)

Diagnostic Approach

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

Physical examination

Decorticate posture [Decorticate rigidity, abnormal flexor response]: History (Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

Physical examination

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

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

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

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

Peripheral Vestibular Dysfunction

Labyrinthitis

Motion Sickness

Head Trauma

Drugs

Benign Paroxysmal Vertigo

Vestibular Neuronitis

Middle Ear and Temporal Bone Masses

Perilymphatic Fistula

Ménière Disease

Central Vestibular Dysfunction

Head Trauma

Intracranial Infection

Seizure Disorder

Basilar Artery Migraine

Neoplasm

Psychologic Disturbance

Diagnostic Approach

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

Recurrent Infection: Clinical Features and Diagnosis (The Diagnostic Approach to Symptoms and Signs in Pediatrics)

Normal Host

Upper Respiratory Tract Infections (URIs)

TREATMENTS &
RESEARCH

Dr. Huntley's
Diagnosis
Checklist

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

ABDOMINAL PAIN, CHRONIC RECURRENT: Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

Dizziness/Lightheadedness & Vertigo: Differential Diagnosis
(In a Page: Signs and Symptoms)

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

Fever – Recurrent: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

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

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

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

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

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

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

Decorticate posture [Decorticate rigidity, abnormal flexor response]: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

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

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

Dizziness: Differential Overview
(Field Guide to Bedside Diagnosis)

Chronic/Recurrent Abdominal Pain: Differential Overview
(Field Guide to Bedside Diagnosis)

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

Decorticate posture [Decorticate rigidity, abnormal flexor response]: History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

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

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

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

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

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

Recurrent Infection: Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)

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

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

Decorticate posture [Decorticate rigidity, abnormal flexor response]: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

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

Symptom
Checker