Diseases » Ménière's disease » Diagnosis

Diagnosis of Ménière's disease

Diagnostic Test list for Ménière's disease:

The list of medical tests mentioned in various sources as used in the diagnosis of Ménière's disease includes:

• Hearing tests
• Audiometry

Ménière's disease Diagnosis: Book Excerpts

• Ask the following questions - EARACHE
• Ask the following questions - ABDOMINAL PAIN, CHRONIC RECURRENT
• Differential Diagnosis - Dizziness/Lightheadedness & Vertigo
• Differential Diagnosis - Fever – Recurrent
• Differential Diagnosis - Vertigo
• Approach to the Diagnosis - EARACHE
• Approach to the Diagnosis - AURAL DISCHARGE (OTORRHEA)
• History and physical examination - Earache
• History and physical examination - Vertigo
• Diagnosis - Ménière's disease
• History and physical examination - Earache [Otalgia]
• History and physical examination - Vertigo
• History - Vertigo
• Differential Overview - Chronic/Recurrent Abdominal Pain
• History - Earache
• History - Vertigo
• Clinical Features and Diagnosis - Earache
• Clinical Features and Diagnosis - Recurrent Infection
• Clinical Features and Diagnosis - Vertigo
• History and physical examination - Earache [Otalgia]
• History and physical examination - Vertigo
• Approach to the Diagnosis - EARACHE
• Approach to the Diagnosis - AURAL DISCHARGE (OTORRHEA)

Diagnostic Tests for Ménière's disease: Online Medical Books

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

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

1. Are there abnormalities on the ear examination? The ear examination may reveal severe otitis externa, an epithelioma of the pinna, a foreign body, or impacted wax. It may also show inflammation and bulging of the eardrum. A vesicular rash of the drum and external auditory canal may indicate herpes zoster.
2. Is there pain on moving the pinna? Pain on moving the ear suggests otitis externa, foreign body, impacted wax, or keratosis obturans.
3. Is there hearing loss? Hearing loss with an abnormal drum would suggest serous or bacterial otitis media. It may also suggest a cholesteatoma. Hearing loss with a normal ear exam suggests aero-otitis.
4. Could the pain be a referred pain? Dental caries, dental abscesses, impacted teeth, tonsillitis, and temporomandibular joint syndrome may refer pain to the ear.

DIAGNOSTIC WORKUP

It should go without saying that diagnosis begins with an adequate otoscopic examination. If the drum is obscured by wax, gentle lavage after using Cerumenex will usually clear the canal. If there is an exudate, a culture and sensitivity should be ordered. Perhaps a throat culture should be done also. X-rays of the mastoids and petrous bones should be done if the exudate is believed to be from a deeper source. Perhaps a CT scan is also needed. If there is hearing loss, an audiogram needs to be done and a tympanogram will be useful in diagnosing serous otitis media. A trial of carbamazepine (Tegretol®) or phenytoin (Dilantin®) may be useful in diagnosing glossopharyngeal neuralgia or tic douloureux. If the discharge is thought to be cerebrospinal fluid, a CT scan and RISA study should be done.

Referral to an ear, nose, and throat specialist or neurologist should be considered before ordering expensive diagnostic tests.

 

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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)

1. Is there a family history of migraine or epilepsy? Migraine and epilepsy both present with abdominal pain.
2. Is the pain colicky or persistent? Chronic colicky abdominal pain may be due to chronic cholecystitis, cholelithiasis, renal calculus, or partial intestinal obstruction.
3. 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.
4. 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.
5. Is there fever associated with the abdominal pain? Fever and abdominal pain may be due to pyelonephritis, diverticulitis, or appendicitis.
6. Is there a history of chronic alcoholism? The history of chronic alcoholism suggests acute and chronic pancreatitis.
7. Is there blood in the stool? The presence of blood in the stool would, of course, suggest peptic ulcer disease and diverticulitis.
8. 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

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Source: In a Page: Signs and Symptoms, 2004

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

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

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

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

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

The approach to the diagnosis requires ear, nose, and throat examination, culture of any discharge, x-ray film of the mastoids, petrous bone, temporomandibular (TM) joints, and, in some cases, the sinuses and teeth. A careful neurologic examination is necessary in unexplained otalgia. Referral to an otolaryngologist or neurologist is probably best for the busy physician who is unable to find the cause on a routine examination.

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Source: Differential Diagnosis in Primary Care, 2007

AURAL DISCHARGE (OTORRHEA): Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

The approach to the diagnosis of an aural discharge is similar to the approach for discharges from any body orifice. After careful examination for a foreign body or obstruction, the discharge is cultured and appropriate therapy begun. A gram stain of the material often aids in the determination of the most appropriate antibiotic. If the discharge is chronic, x-rays of the mastoids and petrous bones may be necessary, as well as tomography. Obviously, referral to an otolaryngologist is wise at this point.

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Source: Differential Diagnosis in Primary Care, 2007

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

Ask the patient to characterize his earache. How long has he had it? Is it intermittent or continuous? Is it painful or slightly annoying? Can he localize the site of ear pain? Does he have pain in other areas such as the jaw? Does he experience any associated hearing loss?

Ask about recent ear injury or other trauma. Does swimming or showering trigger ear discomfort? Is discomfort associated with itching? If so, find out where the itching is most intense and when it began. Ask about ear drainage and, if present, have the patient characterize it. Does he hear ringing, “swishing,” or other noise in his ears? Ask about dizziness or vertigo. Does it worsen when the patient changes position? Does he have difficulty swallowing, hoarseness, neck pain, or pain when he opens his mouth?

Find out if the patient has recently had a head cold or problems with his eyes, mouth, teeth, jaws, sinuses, or throat. Disorders in these areas may refer pain to the ear along the cranial nerves.

Find out if the patient has flown, been to a high-altitude location, or been scuba diving.

Begin your physical examination by inspecting the external ear for redness, drainage, swelling, or deformity. Then apply pressure to the mastoid process and tragus to elicit tenderness. Using an otoscope, examine the external auditory canal for lesions, bleeding or discharge, impacted cerumen, foreign bodies, tenderness, or swelling. Examine the tympanic membrane: Is it intact? Is it pearly gray (normal)? Look for tympanic membrane landmarks: the cone of light, umbo, pars tensa, and the handle and short process of the malleus. (See Using an otoscope correctly.)

Perform the watch tick, whispered voice, Rinne, and Weber's tests to assess for hearing loss.

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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.

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

Ménière's disease: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Presence of all three typical symptoms suggests Ménière’s disease. Audiometric studies indicate a sensorineural hearing loss and loss of discrimination and recruitment. Selected studies such as electronystagmography, electrocochleography, computed tomography scan, magnetic resonance imaging, or X-rays of the internal meatus may be necessary for differential diagnosis.

Laboratory studies, including thyroid and lipid studies, may be performed to rule out other conditions such as Treponema pallidum.

Caloric testing may reveal loss or impairment of thermally induced nystagmus on the involved side. However, it’s important not to overlook an acoustic tumor, which produces an identical clinical picture.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Earache [Otalgia]: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

Ask the patient to characterize his earache. How long has he had it? Is it intermittent or continuous? Is it painful or slightly annoying? Can he localize the site of the pain? Does he have pain in any other areas, such as the jaw?

Ask about recent ear injury or other trauma. Does swimming or showering trigger ear discomfort? Is discomfort associated with itching? If so, find out where the itching is most intense and when it began. Ask about ear drainage and, if present, have the patient characterize it. Does he hear ringing, “swishing,” or other noises in his ears? Ask about dizziness or vertigo. Does it worsen when the patient changes position? Does he have difficulty swallowing, hoarseness, neck pain, or pain when he opens his mouth?

Find out if the patient has recently had a head cold or problems with his eyes, mouth, teeth, jaws, sinuses, or throat. Disorders in these areas may refer pain to the ear along the cranial nerves.

Finally, find out if the patient has recently flown, been to a high-altitude location, or been scuba diving.

Begin your physical examination by inspecting the external ear for redness, drainage, swelling, or deformity. Then apply pressure to the mastoid process and tragus to elicit any tenderness. Using an otoscope, examine the external auditory canal for lesions, bleeding or discharge, impacted cerumen, foreign bodies, tenderness, or swelling. Examine the tympanic membrane: Is it intact? Is it pearly gray (normal)? Look for tympanic membrane landmarks: the cone of light, umbo, pars tensa, and the handle and short process of the malleus. (See Using an otoscope correctly.) Perform the watch tick, whispered voice, Rinne, and Weber’s tests to assess for hearing loss.

» 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))

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.

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

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

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

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

Ask the patient to characterize the earache. How long has he had it? Is it intermittent or continuous? Is it painful or slightly annoying? Can he pinpoint the site of the ear pain? Does he have pain in any other areas such as the jaw?

Also ask the patient about recent ear injury or other trauma. Does swimming or showering trigger ear discomfort? Is discomfort associated with itching? If so, find out where the itching is most intense and when it began. Ask about ear drainage and, if present, have the patient characterize it. Does he hear ringing, “swishing,” or other noises in his ears? Ask about dizziness or vertigo. Do these symptoms worsen when the patient changes position? Does he have difficulty swallowing, hoarseness, neck pain, or pain when he opens his mouth?

Find out if the patient has recently had a head cold or problems with his eyes, mouth, teeth, jaws, sinuses, or throat. Disorders in these areas may refer pain to the ear along the cranial nerves. Also find out if the patient has recently flown, been to a high altitude location, or been scuba diving.

» READ BOOK EXCERPT ONLINE »

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

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

External Ear Including External Auditory Canal

Pain-sensitive structures of external earare skin and perichondrium of auricle and skin of external auditorycanal.

Infection/Inflammation

Otitis Externa

Producesinflamed, painful external auditory canal ± discharge.

Predisposingfactors include swimming, chronic otitis media with otorrhea, excessive cleaning,hearing aid use, and skin disorders (e.g., eczema).

Common pathogens include S. aureus,P. aeruginosa, and other gram-negative enteric bacteria. Fungalinfections with Aspergillus and Candida species are also common.

Culture of discharge is diagnostic.

Rare severe form is called invasive,necrotizing, or malignant otitis externa.

Usual pathogens are gram-negative entericbacteria, most commonly P. aeruginosa.

Has been reported in children withcancer, neutropenia, malnutrition, and immunosuppression.

Usual findings include ear pain, fever,otorrhea, and swelling of pinna. Tympanic membrane necrosis, ossiculardestruction, and involvement of temporal bone can occur.

CT shows extent of soft tissue andbone involvement.

Cellulitis

Inflammation of pinna or skin around earcan lead to cellulitis. Usual pathogens are S. aureus and groupA Streptococcus.

Furuncle or Abscess

S. aureusis pathogen most commonly responsible for furuncle or abscess, whichcan involve pinna, external auditory canal, or skin around ear.

Mass is tender, warm, and sometimesfluctuant.

Incision and drainage of abscess followedby Gram stain and culture are diagnostic.

Perichondritis of Pinna

Common causesof ear cartilage inflammation are trauma, burns, frostbite, or extensionof otitis externa.

Pinna is exquisitely tender and swollen.

Fluctuance may occur with bacterialperichondritis. Common pathogens are S. aureus and Pseudomonas species.Aspirate with Gram stain and culture may be diagnostic.

Cerumen Impaction

May causemild earache.

Impaction is readily visible by otoscopy,and earache resolves after its removal.

Trauma

Any traumato external ear may cause pain, swelling, and tenderness.

Hematoma of pinna may appear as purplish,boggy mass.

History and physical exam are diagnostic.

Foreign Body

Childrensometimes place beads, paper, erasers, cotton balls, and other smallobjects in external canal.

Ear pain, bleeding, and foul-smellingear discharge are frequent findings.

Otoscopy is diagnostic.

Neoplasm

Tumors ofexternal canal are usually visible, but extension can occur intomiddle ear, temporal bone, and temporomandibular joint.

Ear pain, otorrhea, and conductivehearing loss are common findings.

See Bellet et al. (1992) for discussionof tumors of external auditory canal.

Middle Ear, Eustachian Tube, and Mastoid Disorders

Infection/Inflammation

Acute and Chronic Otitis Media

Acute otitismedia is most common cause of ear pain in childhood.

Most common pathogens are S. pneumoniae,nontypeable H. influenzae, and M. catarrhalis. In infants <6wks of age, pathogens include S. aureus, group B Streptococcus,and gram-negative enteric bacteria (e.g., E. coli and P. aeruginosa).In some cases, respiratory syncytial virus, parainfluenza viruses, influenzaviruses, and enteroviruses can be cultured from middle ear fluid.

P. aeruginosa is most common causeof chronic otitis media, which involves nonintact tympanic membranewith either perforation or placement of tympanostomy tube.

Typically, child presents with upperrespiratory infection for 1–2 days and then develops ear pain.Nonspecific symptoms of acute otitis media in infancy include excessivecrying, irritability, vomiting, and diarrhea. Fever is variablefinding.

Visualization of tympanic membraneconfirms diagnosis. There is loss of or distortion of normal architectureof tympanic membrane, which appears opaque or bright red in color.Tympanic membrane loses its normal mobility with pus in middle earspace. With perforation of tympanic membrane, pus is seen in externalcanal. Large bulla or bullae (bullous myringitis) involving tympanicmembrane also signifies acute otitis media.

Acute otitis media is usually due tobacterial infection and requires antibiotic treatment. If resolutionof infection fails to occur after 2 or 3 courses of treatment withdifferent antibiotics, fluid should be drained and cultured.

Other indications for tympanocentesisor myringotomy and culture of middle ear fluid are critically illchild with otitis media, immunologically compromised child, or presenceof complication (e.g., facial paralysis or brain abscess).

Otitis Media with Effusion

Pathogenesisof persistent middle ear effusion is related to eustachian tubedysfunction. Predisposing factors include recurrent otitis media,enlarged adenoids and/or tonsils, allergic rhinitis, and,less commonly, nasopharyngeal tumors.

Sensation of ear discomfort or fullness,ear tugging, and irritability are frequent findings.

Otoscopic exam including pneumaticotoscopy usually confirms diagnosis. Retraction of tympanic membrane,air-fluid level, or bubbles in middle ear may be seen. Pneumaticotoscopy reveals decreased or absent mobility of tympanic membrane.If uncertainty exists about presence of effusion, tympanometry maybe diagnostic. This technique is more reliable in children who are≥6 mos of age.

Mastoiditis

Acute mastoiditisis usually complication of acute otitis media.

Same pathogens that cause acute otitismedia also cause mastoiditis. S. pneumoniae and nontypeable H. influenzaeare most common.

Usual findings include ear pain, postauricularswelling, tenderness over mastoid bone, and fever.

Radiographs of mastoid bone show evidenceof osteitis with destruction of bony trabeculae.

Chronic mastoiditis is usually complicationof chronic otitis media. S. aureus and gram-negative enteric bacteria(E. coli, P. aeruginosa, and Proteus species) are frequent pathogens.

Trauma

Acute headinjury may result in basilar skull fracture with hemotympanum. Ecchymosisbehind ear and in periorbital area may be seen.

Acute head injury or explosive blastalso can cause rupture of tympanic membrane and acute ear pain.

Injuries severe enough to rupture tympanicmembrane also can damage ossicular chain.

CT should be performed to determineextent of injury.

Barotrauma with sudden changes in middleear pressure sometimes occurs with flying in airplane or scuba diving.

In airplane,individuals experience positive middle ear pressure on ascent andnegative middle ear pressure on descent. Opposite happens in scubadiving.

If eustachian tube fails to open andequilibration of pressure fails to occur, negative pressure in middleear causes transudation of fluid, resulting in ear pain, conductivehearing loss, and sometimes bleeding.

Tympanic membrane also can rupture.Swallowing helps relieve pain by keeping eustachian tube open andenhancing pressure equilibration.

Neoplasm

Tumors arisingin middle ear or temporal bone are rare in pediatric population.

Conductive hearing loss, tinnitus,ear fullness, or facial nerve palsy may signal presence of middleear mass, which may or may not be visible by otoscopy.

Extension of tumor into external auditorycanal may produce otorrhea, whereas sensorineural hearing loss,tinnitus and vertigo may occur with inner ear involvement.

Temporal bone tumors may produce sensorineuralhearing loss, tinnitus, vertigo, and facial nerve palsy.

CT is initial imaging exam for massesin middle ear and temporal bone.

See Bellet et al. (1992) for discussionof tumors that arise in middle ear and temporal bone.

Referred Ear Pain from Cranial Nerves (V, VII, IX, X) orCervical Nerves (C2, C3)

Cranial Nerve V

Auriculotemporalbranch of mandibular division of trigeminal nerve (CN V) supplies tragus,anterior portion of auricle, anterior and superior auditory canalwalls, and anterior portion of tympanic membrane.

Pain from structures innervated bymaxillary and ophthalmic divisions of trigeminal nerve also canbe referred to those areas supplied by mandibular branch. Sinusitis,sialadenitis, parotitis, and tumors involving any of these areascan cause earache. Tooth (erupting teeth, impacted third molars,caries, dental abscess), gingival (gingivitis, stomatitis, aphthousulcers), jaw, and temporomandibular joint pain also can cause earpain.

Cranial Nerve VII

Sensoryportion of facial nerve (CN VII) supplies part of posterior wallof external auditory canal and posterior portion of tympanic membrane.

Herpes zoster can cause neuritis offacial nerve, with severe earache and vesicular eruption of auricle,external auditory canal, and occasionally tympanic membrane. Tumorsinvolving facial nerve during its intracranial or temporal bonecourse also can cause ear pain.

Cranial Nerve IX

Glossopharyngealnerve (CN IX) supplies pharynx, tonsils, nasopharynx, posterior one-thirdof tongue, and eustachian tube. Branch of this nerve supplies posteriorportion of external auditory canal and surface of tympanic membrane.

Ear pain can be due to lesions of oropharynx(pharyngitis, tonsillitis, foreign body, tumor, peritonsillar abscess,retropharyngeal abscess) and nasopharynx (nasopharyngitis, foreignbody, enlarged adenoids, tumor).

Cranial Nerve X

Sensoryfibers of vagus nerve (CN X) supply portion of posterior externalauditory canal and tympanic membrane. This nerve also supplies sensationto larynx, esophagus, trachea, and thyroid gland.

Although uncommonly seen in childhood,earache mediated by vagus nerve can be associated with lesions oflarynx (trauma, foreign body), esophagus (foreign body, causticburn), trachea (tracheitis), and thyroid gland (thyroiditis).

Cervical Nerves (C2 and C3)

Upper cervicalnerves, especially great auricular nerve, supply skin and musclesof neck as well as external ear and posterior auricular area.

Cervical lymphadenitis is common causeof ear pain. Unusual causes are infected branchial cyst and disordersof cervical spine (dislocation/subluxation, osteomyelitis,tumor).

Psychogenic

Ear painmay be psychogenic if otologic exam is normal and no lesion canbe found responsible for pain, including referred pain from cranialor cervical nerves.

Often these individuals have anxietyor depression.

Psychosocial history provides cluesto this diagnosis.

Diagnostic Approach

Most commoncauses of ear pain are acute and chronic otitis media, otitis externa, cerumenimpaction, foreign body, and trauma.

History and careful exam of externalear, external auditory canal, and middle ear are diagnostic. Ifexam of these structures is normal, possibility of referred earpain must be considered. Head, face, nose, mouth, pharynx, and neckshould be carefully examined.

Radiographs of temporal bone and mastoidregion, CT, and MRI are helpful in diagnosis of suspected neoplasmof external auditory canal, middle ear, mastoid, or temporal bone.

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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.

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

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

Earache [Otalgia]: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

Ask the patient to characterize his earache. How long has he had it? Is it intermittent or continuous? Is it painful or slightly annoying? Can he localize the site of ear pain? Does he have pain in other areas such as the jaw? Does he experience any associated hearing loss?

Ask about recent ear injury or other trauma. Does swimming or showering trigger ear discomfort? Is discomfort associated with itching? If so, find out where the itching is most intense and when it began. Ask about ear drainage and, if present, have the patient characterize it. Does he hear ringing, “swishing,” or other noise in his ears? Ask about dizziness or vertigo. Does it worsen when the patient changes position? Does he have difficulty swallowing, hoarseness, neck pain, or pain when he opens his mouth?

Find out if the patient has recently had a head cold or problems with his eyes, mouth, teeth, jaws, sinuses, or throat. Disorders in these areas may refer pain to the ear along the cranial nerves.

Find out if the patient has flown, been to a high-altitude location, or been scuba diving.

Begin your physical examination by inspecting the external ear for redness, drainage, swelling, or deformity. Then apply pressure to the mastoid process and tragus to elicit tenderness. Using an otoscope, examine the external auditory canal for lesions, bleeding or discharge, impacted cerumen, foreign bodies, tenderness, or swelling. Examine the tympanic membrane: Is it intact? Is it pearly gray (normal)? Look for tympanic membrane landmarks: the cone of light, umbo, pars tensa, and the handle and short process of the malleus. (See Using an otoscope correctly.) Perform the watch tick, whispered voice, Rinne, and Weber's tests to assess for hearing loss.

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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.

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Source: Nursing: Interpreting Signs and Symptoms, 2007

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

The approach to the diagnosis requires ear, nose, and throat examination; culture of any discharge; and x-ray film of the mastoids, petrous bone, TMJs; and, in some cases, the sinuses and teeth. A careful neurologic examination is necessary in unexplained otalgia. Referral to an otolaryngologist or neurologist is probably best for the busy physician who is unable to find the cause on a routine examination.

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Source: Differential Diagnosis in Primary Care, 2007

AURAL DISCHARGE (OTORRHEA): Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

The approach to the diagnosis of an aural discharge is similar to the approach for discharges from any body orifice. After careful examination for a foreign body or obstruction, the discharge is cultured and appropriate therapy begun. A gram stain of the material often aids in the determination of the most appropriate antibiotic. If the discharge is chronic, x-rays of the mastoids and petrous bones may be necessary, as well as tomography. Obviously, referral to an otolaryngologist is wise at this point.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

 » Next page: Signs of Ménière's disease

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