drugs, opiate receptor agonists (e.g., loperamide), reduce intestinal mobility and delay transit time, thereby prolonging course of illness Toxic side effects of these medications include lethargy and paralytic ileus Antisecretory drugs like bismuth subsalicylate have limited efficacy and have potential for salicylate toxicity Adsorbents (e.g., hydrated aluminomagnesium silicates and kaolin-pectin), while having potential to bind digestive mucus and reduce water loss, have not been shown to reduce diarrheal duration, frequency, or volume Suggested Readings and Key References Bryant K, McDonald LC Clostridium difficile infection in children Pediatr Infect Dis J 2009;28:145–146 Centers for Disease Control and Prevention Delayed onset and diminished magnitude of rotavirus activity—United States, November 2007–May 2008 MMWR Morb Mortal Wkly Rep 2008;57(25):697–700 Denno DM, Shaikh N, Stapp JR, et al Diarrhea etiology in a pediatric emergency department: a case control study Clin Infect Dis 2012;55:897–904 Freeman SB, Williamson-Urquhart S, Farion KJ, et al Multicenter trial of a combination probiotic for children with gastroenteritis N Engl J Med 2018;379:2015–2026 Gerber A, Karch H, Allerberger F, et al Clinical course and the role of Shiga toxin-producing Escherichia coli infection in hemolytic-uremic syndrome in pediatric patients, 1997–2000 in Germany and Austria: a prospective study J Infect Dis 2002;186:493–500 Goldman RD, Friedman JN, Parkin PC Validation of the clinical dehydration scale for children with acute gastroenteritis Pediatrics 2008;122:545–549 Gorelick MH, Shaw KN, Murphy KO Validity and reliability of clinical signs in the diagnosis of dehydration in children Pediatrics 1997;99:E6 Lochhead A, Jamjoom R, Ratnapalan S Intussusception in children presenting to the emergency department Clin Pediatr (Phila) 2013;52(11):1028–1033 Schnadower D, Tarr PI, Casper TC, et al Lactobacillus rhamnosus GG versus placebo for acute gastroenteritis in children N Engl J Med 2018;379:2002– 2014 Shane AL, Mody RK, Crump JK, et al 2017 Infectious Disease Society of America Clinical Practice Guidelines for the Diagnosis and Management of Infectious Diarrhea Clinical Infectious Diarrhea 2017;65(12):e45–e80 Vecchio AL, Vandenplas Y, Benninga M, et al An international consensus report on a new algorithm for the management of infant diarrhea Acta Paediatrica 2016;105:e384–e389 CHAPTER 24 ■ DIZZINESS AND VERTIGO SOFIA CHAUDHARY, THERESA A WALLS INTRODUCTION Dizziness can be a vague term that patients use to describe nonvertiginous disturbances (pseudovertigo) such as lightheadedness, presyncope, intoxication, ataxia, visual disturbances, unsteadiness, weakness, stress, anxiety, hyperventilation, depression, and fear True vertigo is the perception that the environment is rotating relative to the patient or that the patient is rotating relative to the environment It can be immensely disturbing, even frightening, to patients and their families Preverbal children, unable to articulate the sensation, may be irritable, may vomit, or may prefer to lie still Even older children and adults may have difficulty describing the sensation of vertigo Patients may present with dizziness as an isolated complaint or as part of a constellation of symptoms related to an underlying illness When evaluating a child complaining of dizziness, the practitioner should listen carefully to the details of the history as these may allow distinguishing true vertigo from pseudovertigo The key element in the history that strongly suggests true vertigo is the subjective sense of rotation Often, the best response to a chief complaint of being dizzy is to say, “Tell me what you mean by ‘dizzy.’” Initial vague complaints often become more concrete, and the underlying diagnosis may become increasingly clear PATHOPHYSIOLOGY True vertigo arises from a disturbance in either the peripheral or central components of the vestibular system The two peripheral sensory organs of the system (together known as the labyrinth) are the semicircular canals (stimulated by rotary motion of the head) and the vestibule (stimulated by gravity) Both organs lie near the cochlea within the petrous portion of the temporal bone The proximity of the vestibule and cochlea explains the frequent association of vertigo with hearing impairment Afferent impulses from these organs travel via the vestibular portion of the eighth cranial nerve to the vestibular nuclei in the brainstem and in the cerebellum Efferent impulses travel through the vestibulospinal tract to the peripheral muscles (helping to maintain balance and position sense) and also within the medial longitudinal fasciculus to cranial nerves III, IV, and VI (accounting for the oculovestibular reflexes) Almost all patients complaining of true vertigo should have nystagmus, at least when the vertiginous symptoms are peaking The fast component of the nystagmus is almost always in the same direction as the perceived rotation DIFFERENTIAL DIAGNOSIS As discussed earlier, dizziness is best divided into vertiginous conditions (true vertigo) and nonvertiginous conditions (pseudovertigo) Table 24.1 lists the differential diagnosis of true vertigo and highlights the life-threatening causes Table 24.2 lists the most common causes of vertigo Table 24.3 lists numerous nonvertiginous conditions that may initially be described as dizziness Because the spectrum of nonvertiginous conditions is so broad, the following discussion will concentrate on true vertigo Vertigo follows a dysfunction of the vestibular system within the semicircular canals, vestibule, or vestibular nerve (peripheral vertigo), or within the brainstem, cerebellum, or cortex (central vertigo) It can also be divided into conditions in which hearing is impaired (usually peripheral causes) and into conditions in which hearing is spared (usually central causes) ( Table 24.1 ) Finally, vertigo can be divided into acute (usually infectious, postinfectious, traumatic, or toxic) and chronic-recurrent groups (usually caused by seizures, migraine, or benign paroxysmal vertigo of childhood) Infections Both acute and chronic bacterial and viral infections of the middle ear, with or without associated mastoiditis, may cause vestibular and auditory impairment (see Chapters 34 Hearing Loss and 58 Pain: Earache ) Severe, untreated, acute suppurative otitis media with effusion may extend directly into the labyrinth Even without direct invasion of pathogens, inflammation can cause labyrinthitis Chronic and recurrent otitis media can produce a cholesteatoma of the tympanic membrane, an abnormal growth of keratinizing squamous epithelium caused by repeated cycles of perforation and healing Cholesteatomas can erode the temporal bone and the labyrinth, producing a draining fistula from the labyrinth that presents as vertigo, nausea, and hearing impairment Computed tomography (CT) scan or magnetic resonance imaging (MRI) shows destruction of the temporal bone Viral infections can directly affect the labyrinth or the vestibular nerve; together these conditions are known as vestibular neuronitis Known pathogens include mumps, measles, and the Epstein–Barr virus Herpes zoster infection of the ear canal and facial palsy (Ramsay Hunt syndrome) may also involve the eighth nerve More commonly, a nonspecific upper respiratory tract infection may precede the illness Onset is usually acute and can be severe Nystagmus is usually present Patients prefer to lie motionless with their eyes closed Recovery is from to weeks Early use of prednisone may shorten the course Migraine Vertigo may be a prominent feature of classic migraine, or of a migraine equivalent, in which there is no associated headache (see Chapters 59 Pain: Headache and 97 Neurologic Emergencies ) Nearly 20% of children with migraine may have vertiginous symptoms during their aura Basilar migraine presents as a throbbing occipital headache following signs and symptoms of brainstem dysfunction (including vertigo, ataxia, tinnitus, and dysarthria) Vertigo from migraine equivalent (without pain) is typically seen in patients with a family history of migraine headache and is associated with other transient neurologic complaints (e.g., weakness, dysarthria) TABLE 24.1 CAUSES OF VERTIGO IN CHILDREN Peripheral causes Central causes Ingestions a , b Temporal bone fracture a , b Suppurative or serous labyrinthitis b External ear impaction (especially cerumen) Ramsay Hunt syndrome (Varicella zoster infection) Cholesteatoma b Perilymphatic fistula b Vestibular neuronitis Benign paroxysmal vertigo Posttraumatic vestibular concussion Ménière disease b Tumor a Meningitis a , b Encephalitis a Trauma a Stroke a , b Increased intracranial pressure a Life-threatening b May causes of vertigo have associated hearing impairment a Multiple sclerosis Seizure (usually complex partial) Migraine Motion sickness Paroxysmal torticollis of infancy