EM guidemap - Vertigo

Click on any of the headings or subheadings to rapidly navigate to the relevant section of the guidemap

Introduction

History of the present illness

Examination

Diagnostic testing Medical decision-making


Appendix

Introduction

- this guidemap is mainly focused on the clinical features that help differentiate acute peripheral vertigo (due to unilateral peripheral vestibular disease) from acute central vertigo (due to cerebellar or brainstem disease)

- this guidemap will also offer some guidance on how to approach the problem of recurrent episodic vertigo and acute positional vertigo

- the most important initial determination that needs to be made in a patient with acute dizziness is to determine whether the patient's dizziness represents true vertigo - rather than being due to some other specific/non-specific syndrome causing dizziness eg. non-specific lightheadeness or near-syncope/pre-syncope or dysequilibrium syndrome

- the patient should be asked to "describe his dizziness" without the use of leading questions

Vertigo = sensation of disorientation in space with a sensation of motion where no motion exists, and the sensation may be swaying, tilting or rotational in character

- mild vertigo may produce a feeling that the earth is moving or tilting slightly, or it may produce a vague sensation of motion-sickness, or a feeling that one is being pulled to the side; while severe vertigo may produce a distinct whirling sensation with prominent autonomic symptoms of nausea and vomiting and sweating and pallor

- vertigo is due to a mismatch of two-or-more of the vestibular, visual and proprioceptive inputs to the vestibular system and thus any unilateral lesion of the vestibular apparatus/pathways may produce vertigo

Oscillopsia = the visual (to-and-fro) illusion of enviromental movement, not accompanied by vertigo or a sensation of motion, and it signifies a bilateral decrease in vestibular function eg. secondary to ototoxic drugs (aminoglycosides, loop diuretics) or due to bilateral structural vestibular nerve damage eg. bilateral acoustic neuromas

- the patient with oscillopsia (due to bilateral vestibulopathy) does not complain of vertigo, although he may have a sensation of blurred vision or decreased visual acuity or spatial disorientation during head motion, especially when turning the head rapidly from side-to-side or when ambulating in a dark enviroment or spatial enviroment with too many blurring visual distractions eg. busy city street

- the patient with oscillopsia (due to bilateral vestibulopathy) may have difficulty reading street signs unless the head is held perfectly still, and he may have to stop walking to keep his head sufficiently still

- the patient with oscillopsia (due to bilateral vestibulopathy) may have poor balance when walking in the dark (when visual cues are absent) or on uneven surfaces such as gravel (which causes the head to lurch about)

Near syncope/pre-syncope = the sensation is that of "graying-out", lightheadedness, generalized weakness, or a sudden overwhelming feeling that one is going to "pass-out"

- the feeling can occur suddenly without warning in any postural position, or be precipitated by suddenly standing, or occur during heavy exertion

- cardiovascular pathology or volume depletion is responsible for the majority of cases

Dysequilibrium = a feeling of unsteadiness or imbalance, without an actual illusion of movement and without a sensation of faintness and usually more noticeable when the patient walks or stands unassisted eg. secondary to 'multi-sensory' deficits in elderly patients

(* Dysequilibrium and poor gait - without true vertigo - can also be caused by occult hydrocephalus, a chronic subdural hemorrhage, Parkinsons's disease or multi-infarct syndome)

Non-vestibular dizziness = a vague sensation of wooziness or wobbliness, floating sensations, feeling "spaced-out", feeling depersonalized or detached from one's body, feeling that "one is spinning inside one's head"

- the feelings may be precipitated by stressful conditions eg. driving on a busy highway or during a domestic argument

- many of these patients have "psychogenic dizziness"

- if the patient definitely has acute vertiginous symptoms, then the next most important determination that needs to be made in a patient with definite acute vertigo is to determine whether the acute vertigo fits into a particular clinical pattern, and whether the vertigo is:-

- each of these presentations has a different set of possible differential diagnoses and each presentation requires a different clinical approach

History of the present illness

- first confirm that the dizziness is vertiginous in nature, and not suggestive of near-syncope or non-vestibular dizziness

- secondly, confirm that the dizziness is affected by movements of the head, which suggests a peripheral vertigo

(* a sensation of acute vertigo can be precipitated in normal people - even with the head kept perfectly still - if there is sudden, extreme and continuous movement of visual targets; and this phenomenon of visual vertigo is different from acute peripheral vertigo, which is worsened by movements of the head and not by movements of the eyes or visual targets)

- determine whether the vertigo is positional in nature

(* benign paroxysmal vertigo of childhood may occur in young children (1 - 5 years of age) and be difficult to diagnose, and may present as paroxysmal torticollis - carefully inquire of the parents whether there are any abnormal eye movements during these paroxysmal episodes; patients with postural pre-syncope may develop dizziness with standing, but not with head turning when supine)

- establish whether associated autonomic symptoms are present

- determine the speed of onset and the duration of the vertigo

- sudden onset vertigo can be due to peripheral or central vertigo, and it may not be possible to differentiate between the two clinical syndromes if there are no associated otological or neurological symptoms to offer additional clinical clues

- the duration of the vertigo provides useful information

- a patient with acute peripheral vertigo secondary to vestibular neuronitis (the cause in 90% of cases in young patients with acute-subacute vertigo) often has dizziness that starts suddenly or gradually, and worsens over a few hours before spontaneously adapting/waning over a time period of 24 - 48 hours => the vertigo usually resolves completely over several weeks, although a variable sense of imbalance may persist for months

- a patient with acute central vertigo due to a posterior circulation stroke may have a lesser degree of dizziness that often has a more persistent course, and the vertigo does not necessarily adapt/wane within the next 12 - 48 hours; the patient often has accompanying posterior circulation neurological symptoms

- an acute episode of vertigo lasting only a few minutes suggests a vertebro-basilar artery TIA - especially if occurring in a patient with known cardiovascular risk factors (elderly, known vascular disease, CAD, AF, hypertension, smoker, diabetes mellitus) and especially when associated with posterior circulation neurological symptoms

- an isolated episode of sudden-onset vertigo that only lasts a few hours may be due to the first episode of Meniere's disease, which very rarely presents initially without the usual associated otological symptoms

- determine whether there are any associated otological or neurological symptoms

- associated otological symptoms (deafness and/or tinnitus) suggests peripheral vertigo

(* a patient with central vertigo due to a TIA or stroke only affecting the internal auditory artery - labyrinthine apoplexy - may present with vertigo + sensorineural hearing loss + no associated neurological symptoms, and can be nearly impossible to clinically differentiate from acute labyrinthitis)

- associated posterior circulation neurological symptoms suggest central vertigo

- posterior circulation stroke syndromes may present acutely and the stroke may be complete/incomplete, and the patient may have any of the following symptoms/signs:-

(* the absence of associated neurological symptoms does not exclude central vertigo because as many as ~ 25% of middle-aged/elderly patients with risk factors for stroke, who present to the ED with isolated severe vertigo +  postural instability may have an inferior cerebellar infarction)

- after determining the speed of onset and duration of the vertigo + presence of any otological or neurological symptoms => determine whether the patient has a history of previous episodes of vertigo

- a history of previous episodes of temporary dizziness lasting a few hours suggests Meniere's disease - especially if there is a history of associated ear fullness/pressure, poor speech discrimination in loud enviroments, fluctuating but progressive hearing loss (especially to low frequencies) and associated tinnitus; the recurrent attacks of vertigo may occur in clusters with long symptom-free intervals

- a history of previous episodes of temporary vertigo lasting minutes suggests vertebro-basilar artery TIAs, which may precede a full-blown stroke by days-to-weeks

- a patient with temporal lobe seizures will likely have associated symptoms - hallucinations, memory impairment, automatic behaviour, trance-like states and motor seizures (nystagmus is only seen when the seizure arises in the labyrinth = vestibulogenic seizure)

- a patient with basilar migraine is usually a young female and the patient will often develop a typical migraine headache concurrently with the vertigo, or after the onset of the vertigo, and the patient will usually have a previous history of recurrent attacks or a strong family history of basilar migraine (associated neurological symptoms - dysarthria, ataxia, blindness, deafness, tinnitus, confusion, sensorial clouding - are usually also present) => the diagnosis of basilar migraine can be missed if a typical migraine headache does not occur and the patient is then often incorrectly presumed to have a psychiatric condition

Examination

- vital signs and a detailed cardiovascular exam is required to exclude cardiac or vascular causes of near-syncope if the dizziness is not definitely vertiginous in character

- atrial fibrillation and secondary embolisation may be the cause of a cerebellar or brain stem stroke

- auscultate the neck for bruits (vertebral artery insufficiency secondary to a subclavian steal syndrome, vertebral artery dissection or vertebral artery stenosis)

- auscultate the head for bruits in patients with pulsatile tinnitus (glomus tumor, aneurysm/dissection of the internal carotid artery)

- examine the ear for signs of cerumen impaction, an earcanal FB, evidence of otitis media or a choleastoma or a perforated eardrum or a hemotympanum (secondary to trauma) - they can all be associated with acute vertigo

- determine whether there is any hearing loss by determining how far from the ear a finger-rub can still be heard (compare sides)

- any hearing loss should be further differentiated as either a conductive or sensorineural hearing loss by doing the Rinne test (put a 256Hz tuning fork on the mastoid and determine for how many seconds the sound can be heard => repeat the test with the tuning fork held in the air about 1 inch from the external auditory meatus = > if bone conduction is better than air conduction = conductive hearing loss)

- the Weber test (performed by placing a tuning fork in the center of the forehead) confirms an unilateral conductive hearing loss by localising the sound to the affected side, but is referrred to the unaffected side when there is an unilateral sensorineural hearing loss

- perform the fistula test if you suspect a peri-lymphatic fistula (a simplified fistula test can be performed by pressing the tragus rapidly towards the earcanal so as to quickly occlude the earcanal opening => induced vertigo +/- nystagmus is a positive test = Hennebert's sign)

- perform a complete neurological examination including all the following observations:-

- checking for gait ataxia (= getting the patient to stand and then evaluating the patient's ability to walk) is a critical part of the neurological examination (* see the gait disorder, frequent falls, and drop attacks guidemap for further problem-solving information that can help differentiate the various causes of ataxia)

- carefully check for nystagmus

- if nystagmus is not present at rest or provoked by eccentric gaze => further provocative maneuvers should be utilized to try and induce vertigo and nystagmus (because the vertigo and nystagmus associated with benign positional vertigo may only be provoked in certain head positions)

- a common provocative test is the Dix-Hallpike maneuver
Differentiating between central and peripheral paroxysmal positional nystagmus
  Appearance Latentcy Duration Fatigability Localisation
Central  Pure vertical, usually downbeat Unusual Persistent Unusual Brainstem or cerebellum
Peripheral Torsional upbeat or horizontal geotropic Usual Brief Usual Posterior or horizontal semi-circular canal

- vertigo and nystagmus may also be induced in a patient with BPV affecting the horizontal semi-circular canals by suddenly turning the patient's head to the affected side while the patient is lying supine in the horizontal position and observing for induced vertigo +/- nystagmus => the nystagmus is horizontal, appears after a latent period of 1 - 10 seconds, and disappears after 1 minute with occasional reversal of the nystagmus prior to resolution

- head-shaking nystagmus can be induced in some patients with peripheral nystagmus by asking the patient to close his eyes and then shake his head from side-to-side at a rate of two cycles per second for about 15 - 30 seconds => after the patient opens his eyes, nystagmus occurs after a short latent period and is short-lived, and it suggests an unilateral vestibular disorder

- another bedside clinical test that can suggest peripheral vertigo is the head impulse test

- the test is performed by the examiner turning the patient's head as rapidly as possible ~ 15 degrees to one side while the patient continues to fixate on a distant target => the test is positive (and diagnostic of a peripheral vertigo) if the vestibulo-ocular reflex fails and the patient cannot continue to fixate on the target, so that he needs to make a rapid eye movement (a saccade) back to the target after the head impulse is completed

- the head impulse test is only positive in peripheral vertigo and it is only positive when the head is rapidly turned in the direction of the involved side; the patient should be able to maintain visual fixation on a distant target when passive rapid rotation to the opposite normal side is performed

(* see the appendix for further details on the evaluation of nystagmus in vertiginous patients)

Diagnostic testing

MRI of the head

- the imaging study-of-choice when central vertigo is suspected

- is indicated immediately if :-

- a MRI can be deferred for 24 - 48 hours if the patient has isolated acute vertigo without any neurological symptoms/signs, has peripheral-type nystagmus that is suppressed by visual fixation, and if the patient is only slightly unstable when walking

CT scan of the head

- same indications for testing as for MRI testing

- only indicated if a MRI is not readily available, because it lacks the sensitivity of a MRI in detecting posterior fossa pathology (it will at least exclude a cerebellar hemorrhage, even though it may not detect subtle posterior fossa or brain stem lesions or an early cerebellar infarct)

- fine cuts through the cerebellum should be obtained and clear visualization of the fourth ventricle is mandatory

- a repeat CT scan (or preferably a MRI) is indicated in 24 - 48 hours to exclude swelling from a cerebellar infarct if the initial CT scan is negative and the clinical suspicion of a posterior fossa infarct still exists

Medical decision-making

Acute vertigo of sudden onset

A patient with a sudden headache + acute vertigo + inability to ambulate => a cerebellar hemorrhage until proven otherwise (even in the absence of other neurological signs)

- any accompanying altered mental status signifies serious CNS pathology and the possibility of increased ICP in the infratentorial compartment

- acute vertigo (+/- posterior circulation-type neurological signs) followed by rapid coma + abnormal breathing patterns + bradycardia/hypertension suggests an acute posterior fossa bleed (or other rapidly expanding posterior fossa pathology) => rapid increase in ICP in the infratentorial compartment => brainstem/medulla compression and/or cerebellar tonsillar herniation

- a patient with acute vertigo, who has associated neurological signs and/or definite central nystagmus suggestive of an acute central vestibular syndrome, requires a stat MRI to r/o a  posterior fossa hemorrhage or infarct involving the cerebellum or brainstem

- consult a neurologist if a patient with acute vertigo has no associated neurological signs, but has equivocal, or definite, evidence of a central-type nystagmus

- an inferior cerebellar stroke patient may sometimes not have any associated posterior circulation-type neurological signs and the nystagmus may only be present in one direction of gaze - the clinical presentation may therefore closely resemble an acute peripheral vestibular syndrome

(* a subtle difference is that in patients with peripheral vertigo - the nystagmus, which is present in only one direction of gaze, intensifies when visual fixation is removed => see the appendix for further details)

- it is important to search diligently for any subtle clinical clues that could suggest an isolated inferior cerebellar infarct - i) any axial lateropulsion is towards the side of the rapid phase of the nystagmus, and ii) the degree of ataxia is slightly greater than would be expected in peripheral vertigo (in peripheral vertigo the axial lateropulsion is away from the rapid phase of nystagmus + the ataxia is usually of a lesser degree); iii) cerebellar infarct patients may also have slightly ataxic pursuit eye movements that may only be detectable using electro-oculography

- it is sometimes very difficult to properly test for nystagmus or gait ataxia if a patient with acute vertigo is very symptomatic and unwilling to ambulate => it may better to defer testing for nystagmus/ataxia and observe the patient in hospital for a number of hours before deciding whether early neuro-imaging is necessary - based on repeated clinical evaluations => if the patient still cannot ambulate after a few hours of observation, he may require a stat MRI to exclude an isolated inferior cerebellar infarct/hemorrhage that can mimic an acute peripheral vestibular syndrome (especially if the patient is middle-aged or elderly, and has multiple vasculopathic risk factors for stroke)

- a patient with typical features of acute peripheral vestibular syndrome, who remains persistently very symptomatic despite a few hours of IV treatment with droperidol and/or benzodiazepines, but has only mild imbalance when ambulating => hospital admission for continued IV therapy => MRI if not significantly improved within 24 - 48 hours

- a patient with typical features of acute peripheral vestibular syndrome can be treated with anti-emetics (eg. compazine or metoclopramide) +/- a sedative (eg. valium) +/- neuroleptic agents (eg. droperidol) while in the ED => discharged if symptomatically improved + able to ambulate + no abnormal neurological signs

- po medications can be continued for symptomatic, outpatient relief => follow-up with PMD, who can refer the patient prn for ENT evaluation +/- caloric testing/electronystagmography/audiometry

(* see the appendix for a list of some drugs used in the outpatient therapy of acute peripheral vertigo)

- a patient with vestibular neuronitis should be warned that a mild positional vertigo or a vague sense of imbalance may persist for many weeks-to-months

- a patient with a suspected peri-lymphatic fistulae can usually be treated conservatively => ENT consultation and outpatient referral (* except when secondary to barotrauma => immediate surgical exploration may be indicated)

- a patient with labyrinthine concusion secondary to head trauma may have positional vertigo that lasts for months => persistent symptoms require ENT evaluation to r/o an occult peri-lymphatic fistula

Recurrent episodic vertigo

- a patient with recurrent attacks of episodic vertigo lasting a few hours should have syphilitic or auto-immune labryrinthitis excluded before assuming that the patient may have Meniere's disease => outpatient workup (including electronystamography + audiometry) can be performed by the ENT consultant

- an elderly patient with risk factors for cerebrovascular disease + history of episodic vertigo lasting a few minutes may have vertebro-basilar artery TIA's => consult a neurologist to decide on inpatient-or-outpatient workup - which may include Doppler ultrasonography, a MRI and/or angiography

(* it is extremely difficult to make the diagnosis of a posterior circulation TIA if a multiplicity of associated neurological symptoms does not accompany any short-lived vertigo lasting < 30 minutes)

- recurrent episodes of vertigo precipitated by exertional straining (or a rapid change in air pressure), may be due to a peri-lymphatic fistula => refer the patient to an ENT specialist

Positional vertigo

- defined as short-lived vertigo lasting seconds, and occurring after a latent period when the head position is changed with respect to gravity

- consult a neurologist if the patient has evidence of a central positional vertigo; a patient with suspected central positional vertigo may need to be admitted for a neurological workup

- a patient with suspected benign positional vertigo can be treated by the Epley maneuvre and then referred to an ENT consultant for further testing (to r/o rare cases of a posterior fossa tumor or Arnold-Chiari malformation causing central positional vertigo that cannot be detected by the Dix-Hallpike maneuver in the ED) and further vestibular habituation therapy (Brandt-Daroff exercises) if still symptomatic and not responsive to a few rounds of repeat Epley maneuvers

(* see the appendix for details on performing the Epley maneuvre)

- 90 - 95% of patients with BPV have the posterior canal variant, but 5 - 10% of patients with BPV have the horizontal variant, which provokes vertigo with sudden turining of the head when lying in bed and not when sitting or looking up; this horizontal variant is usually unresonsive to the Epley maneuver

- a significant proportion of children with benign paroxysmal vertigo may develop migraine headaches in later life

Appendix

Evaluation of nystagmus in a patient with vertigo

- it is important to clearly understand the effect of visual fixation on nystagmus testing, because many cases of nystagmus may be missed or misinterpreted if testing for nystagmus is only performed using "visual fixation techniques" eg. asking the patient to fixate on the examiner's finger and instructing the patient to follow the finger as it is moved from side-to-side

- it is important to check for nystagmus not only when the patient is fixating, but also when he is not fixating, so that you do not miss subtle clues differentiating peripheral from central vertigo

Example number 1 - when the nystagmus is present in primary gaze, and in both directions of gaze

- the direction of the fast phase of the nystagmus is indicated by the direction of the arrows, and the intensity of the nystagmus is represented by the thickness of the arrows

- in peripheral vertigo, the direction of nystagmus is always in the same direction even if the direction of gaze changes from left-to-right, while in central vertigo the direction of the nystagmus can change direction when looking in the opposite direction

- also note that in peripheral vertigo that the intensity of the nystagmus increases when visual fixation is removed, while the intensity of the nystgamus in central vertigo is relatively unaffected by visual fixation

Example number 2 - when the nystagmus is only present in one direction of gaze

- note that there is no difference in the direction of the nystagmus, or the intensity of the nystagmus, when the patient is visually fixating - whether the cause of the nystagmus is peripheral or central

- note that the only clue to peripheral vertigo can be a slight increase in the intensity of the nystagmus when the patient is not visually fixating

- is is therefore very important to repeat testing for nystagmus using non-visual fixation techniques (fresnel lenses or darkened room + patient vaguely staring into the distance when instructed to look to the left and then to the right) to detect any subtle change in intensity of the nystagmus - a subtle increase in the intensity of the nystagmus when the patient is not visually fixating may be the only clue differentiating peripheral from central vertigo eg. inferior cerebellar infarct

Summary of the clinical features differentiating acute peripheral vestibular syndrome from acute central vestibular syndrome
  Peripheral Central
Onset of vertigo  Sudden/gradual  Sudden/Gradual
Severity of vertigo Often intense and disabling Less distinct and disabling
Pattern of vertigo Paroxysmal, constant, waxing-and-waning Constant
Vertigo aggravated by head or body movement/position Yes No
Associated nausea, vomiting, diaphoresis Frequent and prominent Infrequent and less severe
Nystagmus type Horizontal or torsional; or mixed horizonto-torsional, but never vertical or horizontal  Horizontal, torsional or vertical
Nystagmus direction Unidirectional with fast phase always away from the affected ear (irrespective of direction of gaze) May be bidirectional, and may change direction with changes in direction of gaze
Nystagmus intensity affected by fixation Intensity decreased or totally suppressed by visual fixation  Intensity unaffected by visual fixation
Nystagmus intensity affected by direction of gaze Nystagmus intensity may be increased when looking in direction of fast phase Nystagmus intensity is usually unaffected by direction of gaze
Nystagmus fatiguability Nystagmus decreases or disappears with repeat testing Nytagmus remains prominent despite repeat testing
Fatigue of vertigo symptoms over time Yes No
Hearing loss May be present Very infrequent
CNS symptoms/signs Absent Present
Gait Mild-moderate ataxia with tendency to fall towards one side - opposite to the direction of the fast phase of nystagmus  Moderate-severe ataxia with inability to walk, or tendency to fall to either side

Epley maneuver - Canalith re-postioning maneuver

- this maneuver can be used to treat patients with benign paroxysmal positional vertigo (BPPV)

- the maneuver is based on the theory that benign paroxysmal positional vertigo (canalolithiasis) is due the sudden movement of free-floating particles (otoconia) that accumulate in the posterior semi-circular canal => sudden head movements (looking up, rolling over in bed, leaning forward) cause the debris to move about en masse in the posterior semi-circular canal => vertigo lasting a few seconds

- treatment of BPPV can be undertaken in the ED by performing the Epley maneuver as follows:-

- seat the patient upright on the bed with his head extending over the edge of the bed (as in the Dix-Hallpike maneuver test) => tilt the patient's head gently 45 degrees towards the affected side => gently lower the head of the bed so that the patient is lying in the horizontal position with his head over the edge of the bed - his head should then be about 45 degrees below the horizontal level => wait about 30 - 60 seconds for the patient's vertigo to subside, and then keep the patient in that position for ~ 3 minutes => turn the patient's head gently to the midline => wait 30 seconds => turn the patient's head another 45 degrees to the opposite (unaffected) side => wait 30 seconds => let the patient slowly roll his torso towards that opposite side so that he is lying on that opposite shoulder, which should enable him to rotate his head another 45 degrees in that opposite direction so that his face is directed towards the floor => wait 30 seconds for any induced vertigo to resolve and keep the patient in that position for ~ 3 minutes => slowly bring the patient back up to the vertical position while he is still lying in that position => then gently turn his head back towards the midline  => when he is sitting upright, tilt the chin down about 30 degrees and keep the patient in that position for a few minutes

- if the patient is very vertiginous during the maneuver, anti-emetics may first have to be given in order to to successfully complete the maneuver

- the manuever may have to be repeated a few times and the patient should be told to sleep upright and minimize head movements during the next 24 - 48 hours; the patient should still expect to have a sense of dysequilibrium for a few days

- a clue to an unsuccessful canolith repositioning maneuver is nystagmus that changes direction during the maneuver (any nystagmus occurring during the maneuver should be in the same direction as the original nystagmus, which occurred when the patient was first placed flat with the affected ear undermost)

(* see section 9 of the emedicine.com chapter on Benign Positional Vertigo to see photographs of how to perform the Epley maneuver)

Drugs used in the outpatient treatment of acute peripheral vertigo
 Scopolamine - 0.5 mg transdermal patch qd
 Diphenhydramine - 25 - 50 mg qid
 Cyclizine - 25 - 50 mg qid
 Meclizine - 12.5 - 50mg tid
 Diazepam - 2.5 mg tid
 Flunarazine - 10mg qd

Disclaimer: My EM guidemaps reflect my personal approach to problem-solving/managing clinical cases in an ED setting and they should not be regarded as the standard of care. They merely represent the personal opinions of the author and they should only be used in clinical practice if the reader-user has substantial reason to believe that the clinical advice contained in the guidemaps is valid and accurate. The guidemaps are not meant to be "authoritative" and the reader-user should consult standard medical textbooks and expert opinion articles/guidelines for more authoritative advice. The reader-user should particularly confirm all drug doses, their indications and contra-indications, prior to their use.