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Emergency and Acute Medicine – Labyrinthitis
Basic description
Labyrinthitis is an inflammatory disorder of the inner ear that results in unilateral vestibular dysfunction. Inflammation decreases afferent firing from the affected labyrinth, which the central nervous system interprets as head rotation away from the diseased side. This imbalance produces spontaneous nystagmus with the fast phase directed away from the pathologic ear. Labyrinthitis typically causes vertigo and balance disturbance and may be associated with hearing loss and tinnitus. Peak onset is between 30 and 60 years of age, and approximately half of patients report a recent upper respiratory tract infection. Symptoms are often worsened by head movement but may persist at rest, with gradual recovery over weeks to months.
Etiology
The three most common causes of peripheral vertigo are benign paroxysmal positional vertigo (BPPV), Ménière disease, and labyrinthitis. Labyrinthitis may be serous (viral or bacterial), suppurative (bacterial), autoimmune (e.g., Wegener granulomatosis or polyarteritis nodosa), vascular ischemic, traumatic, or medication-related. Ototoxic agents include aminoglycosides, loop diuretics, and antiepileptics such as phenytoin. Allergies and chronic BPPV may also contribute. Chronic BPPV may result from idiopathic otoconia dislodgement, post-traumatic causes, sequelae of labyrinthitis, or ischemic injury.
Pediatric considerations
In children, suppurative and serous labyrinthitis are usually secondary to acute otitis media, mastoiditis, or meningitis. BPPV may occur between 1 and 5 years of age, presenting with abrupt crying, nystagmus, diaphoresis, emesis, and ataxia, with recurrences for up to three years. Migraine–BPPV complex is the most common cause of pediatric vertigo. Ménière disease is rare before 10 years of age.
Diagnosis: signs and symptoms
Patients typically present with sudden-onset peripheral vertigo that is positional or movement-associated and described as a spinning sensation or imbalance. Nausea and vomiting are common. Hearing impairment may be unilateral or bilateral and range from mild to profound. Tinnitus suggests Ménière disease, while otorrhea or otalgia raises concern for otitis media, tympanic membrane perforation, mastoiditis, or cholesteatoma. Symptoms often follow recent infections or sick contacts. Risk factors include prior ear surgery, diabetes mellitus, stroke, migraine, and trauma.
Physical examination
A complete head and neck examination is essential. The external ear, ear canal, tympanic membrane, and middle ear should be inspected for erythema, swelling, vesicles, effusion, perforation, or cholesteatoma. Mastoid tenderness suggests mastoiditis. Ocular examination assesses extraocular movements, pupils, and fundi for papilledema. Nystagmus is typically horizontal with a rotational component, constant in direction, augmented by head movement, fatigable, and suppressed by fixation. A full neurologic and cardiac examination is required to exclude central causes, including assessment of cranial nerves, cerebellar function, gait, orthostatic vitals, and vascular bruits. Facial weakness may suggest Ramsay Hunt syndrome or stroke, while neck stiffness suggests meningitis.
Caloric testing may demonstrate partial or complete loss of response in the affected ear, but should only be performed after confirming an intact tympanic membrane. The Dix–Hallpike maneuver is used to evaluate for BPPV.
Essential workup
The priority is exclusion of central vertigo and serious underlying conditions. A careful neurologic examination is mandatory. Clinicians should evaluate for associated infections such as acute otitis media, meningitis, mastoiditis, and Ramsay Hunt syndrome. Orthostatic vitals and basic auditory assessment are recommended.
Diagnostic tests and interpretation
Laboratory testing is generally unnecessary unless evaluating for central vertigo or unusual peripheral causes. Basic labs, including electrolytes and glucose, may be obtained in patients with significant vomiting or dehydration. Lumbar puncture is indicated when meningitis or subarachnoid hemorrhage is suspected. Imaging is warranted when features suggest central vertigo, such as nonpositional symptoms, vertical or direction-changing nystagmus, nonfatigable nystagmus, focal neurologic deficits, or high cardiovascular risk. MRI with MRA of the posterior fossa and vertebrobasilar circulation is preferred, while CT may be used acutely to evaluate for hemorrhage. Brain imaging should be strongly considered in patients over 45 years of age, children, and those with vascular risk factors.
Differential diagnosis
Peripheral causes include vestibular neuritis, otitis media, acoustic neuroma, autoimmune inner ear disease, BPPV, cholesteatoma, Ménière disease, otosyphilis, ototoxic medications, herpes zoster oticus (Ramsay Hunt syndrome), perilymphatic fistula, post-traumatic vestibular concussion, suppurative labyrinthitis, and temporal bone fracture. Central causes include brainstem or cerebellar ischemia or hemorrhage, tumors, Chiari malformation, multiple sclerosis, vestibular migraine, Wallenberg syndrome, seizures, arrhythmias, hypoglycemia, hypotension, cervicogenic vertigo, hypothyroidism, and alcohol or drug intoxication.
Treatment
Prehospital care includes cardiac monitoring, finger-stick glucose assessment, evaluation for acute stroke, antiemetics, intravenous fluids for dehydration, and fall precautions. Initial ED management focuses on bed rest, hydration, and prevention of falls. Medications provide symptomatic relief but should be limited to short-term use, generally no more than 48 hours, to promote vestibular compensation. Vestibular suppressants such as meclizine, diazepam, or scopolamine and antiemetics such as ondansetron, prochlorperazine, or promethazine may be used. Corticosteroids have limited evidence of benefit. Canalith repositioning maneuvers, particularly the Epley maneuver, are the primary treatment for BPPV and provide relief in most patients. Surgery is reserved for refractory cases.
Disposition and follow-up
Admission is indicated for patients with concern for stroke or central causes, intractable nausea and vomiting, severe dehydration, or unsteady gait. Patients may be discharged if they can tolerate oral intake, ambulate safely, and have a normal neurologic examination, with counseling to avoid driving, heights, and hazardous activities. Neurology or otolaryngology referral is recommended for recurrent or persistent symptoms. Vestibular rehabilitation is beneficial for chronic symptoms.
Pearls and pitfalls
Always exclude life-threatening conditions such as meningitis, cerebrovascular ischemia, or intracranial tumors. Counsel patients regarding fall risk and occupational hazards. Use caution with positional maneuvers, as aggressive cervical hyperextension may precipitate vertebral artery dissection.
Basic description
Labyrinthitis is an inflammatory disorder of the inner ear that results in unilateral vestibular dysfunction. Inflammation decreases afferent firing from the affected labyrinth, which the central nervous system interprets as head rotation away from the diseased side. This imbalance produces spontaneous nystagmus with the fast phase directed away from the pathologic ear. Labyrinthitis typically causes vertigo and balance disturbance and may be associated with hearing loss and tinnitus. Peak onset is between 30 and 60 years of age, and approximately half of patients report a recent upper respiratory tract infection. Symptoms are often worsened by head movement but may persist at rest, with gradual recovery over weeks to months.
Etiology
The three most common causes of peripheral vertigo are benign paroxysmal positional vertigo (BPPV), Ménière disease, and labyrinthitis. Labyrinthitis may be serous (viral or bacterial), suppurative (bacterial), autoimmune (e.g., Wegener granulomatosis or polyarteritis nodosa), vascular ischemic, traumatic, or medication-related. Ototoxic agents include aminoglycosides, loop diuretics, and antiepileptics such as phenytoin. Allergies and chronic BPPV may also contribute. Chronic BPPV may result from idiopathic otoconia dislodgement, post-traumatic causes, sequelae of labyrinthitis, or ischemic injury.
Pediatric considerations
In children, suppurative and serous labyrinthitis are usually secondary to acute otitis media, mastoiditis, or meningitis. BPPV may occur between 1 and 5 years of age, presenting with abrupt crying, nystagmus, diaphoresis, emesis, and ataxia, with recurrences for up to three years. Migraine–BPPV complex is the most common cause of pediatric vertigo. Ménière disease is rare before 10 years of age.
Diagnosis: signs and symptoms
Patients typically present with sudden-onset peripheral vertigo that is positional or movement-associated and described as a spinning sensation or imbalance. Nausea and vomiting are common. Hearing impairment may be unilateral or bilateral and range from mild to profound. Tinnitus suggests Ménière disease, while otorrhea or otalgia raises concern for otitis media, tympanic membrane perforation, mastoiditis, or cholesteatoma. Symptoms often follow recent infections or sick contacts. Risk factors include prior ear surgery, diabetes mellitus, stroke, migraine, and trauma.
Physical examination
A complete head and neck examination is essential. The external ear, ear canal, tympanic membrane, and middle ear should be inspected for erythema, swelling, vesicles, effusion, perforation, or cholesteatoma. Mastoid tenderness suggests mastoiditis. Ocular examination assesses extraocular movements, pupils, and fundi for papilledema. Nystagmus is typically horizontal with a rotational component, constant in direction, augmented by head movement, fatigable, and suppressed by fixation. A full neurologic and cardiac examination is required to exclude central causes, including assessment of cranial nerves, cerebellar function, gait, orthostatic vitals, and vascular bruits. Facial weakness may suggest Ramsay Hunt syndrome or stroke, while neck stiffness suggests meningitis.
Caloric testing may demonstrate partial or complete loss of response in the affected ear, but should only be performed after confirming an intact tympanic membrane. The Dix–Hallpike maneuver is used to evaluate for BPPV.
Essential workup
The priority is exclusion of central vertigo and serious underlying conditions. A careful neurologic examination is mandatory. Clinicians should evaluate for associated infections such as acute otitis media, meningitis, mastoiditis, and Ramsay Hunt syndrome. Orthostatic vitals and basic auditory assessment are recommended.
Diagnostic tests and interpretation
Laboratory testing is generally unnecessary unless evaluating for central vertigo or unusual peripheral causes. Basic labs, including electrolytes and glucose, may be obtained in patients with significant vomiting or dehydration. Lumbar puncture is indicated when meningitis or subarachnoid hemorrhage is suspected. Imaging is warranted when features suggest central vertigo, such as nonpositional symptoms, vertical or direction-changing nystagmus, nonfatigable nystagmus, focal neurologic deficits, or high cardiovascular risk. MRI with MRA of the posterior fossa and vertebrobasilar circulation is preferred, while CT may be used acutely to evaluate for hemorrhage. Brain imaging should be strongly considered in patients over 45 years of age, children, and those with vascular risk factors.
Differential diagnosis
Peripheral causes include vestibular neuritis, otitis media, acoustic neuroma, autoimmune inner ear disease, BPPV, cholesteatoma, Ménière disease, otosyphilis, ototoxic medications, herpes zoster oticus (Ramsay Hunt syndrome), perilymphatic fistula, post-traumatic vestibular concussion, suppurative labyrinthitis, and temporal bone fracture. Central causes include brainstem or cerebellar ischemia or hemorrhage, tumors, Chiari malformation, multiple sclerosis, vestibular migraine, Wallenberg syndrome, seizures, arrhythmias, hypoglycemia, hypotension, cervicogenic vertigo, hypothyroidism, and alcohol or drug intoxication.
Treatment
Prehospital care includes cardiac monitoring, finger-stick glucose assessment, evaluation for acute stroke, antiemetics, intravenous fluids for dehydration, and fall precautions. Initial ED management focuses on bed rest, hydration, and prevention of falls. Medications provide symptomatic relief but should be limited to short-term use, generally no more than 48 hours, to promote vestibular compensation. Vestibular suppressants such as meclizine, diazepam, or scopolamine and antiemetics such as ondansetron, prochlorperazine, or promethazine may be used. Corticosteroids have limited evidence of benefit. Canalith repositioning maneuvers, particularly the Epley maneuver, are the primary treatment for BPPV and provide relief in most patients. Surgery is reserved for refractory cases.
Disposition and follow-up
Admission is indicated for patients with concern for stroke or central causes, intractable nausea and vomiting, severe dehydration, or unsteady gait. Patients may be discharged if they can tolerate oral intake, ambulate safely, and have a normal neurologic examination, with counseling to avoid driving, heights, and hazardous activities. Neurology or otolaryngology referral is recommended for recurrent or persistent symptoms. Vestibular rehabilitation is beneficial for chronic symptoms.
Pearls and pitfalls
Always exclude life-threatening conditions such as meningitis, cerebrovascular ischemia, or intracranial tumors. Counsel patients regarding fall risk and occupational hazards. Use caution with positional maneuvers, as aggressive cervical hyperextension may precipitate vertebral artery dissection.
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