|Year : 2013 | Volume
| Issue : 3 | Page : 163-168
Common avoidable mistakes in the management of glaucoma
Barun K Nayak, Dhwani Shahanand
P.D. Hinduja Hospital, Mumbai, India
|Date of Submission||13-Mar-2013|
|Date of Acceptance||20-May-2013|
|Date of Web Publication||23-Aug-2013|
Barun K Nayak
P.D. Hinduja National Hospital, Veer Savarkar Marg, Mumbai - 400 016, Maharashtra
Source of Support: None, Conflict of Interest: None
Glaucoma is managed by most of the general ophthalmologists as well as by the glaucoma specialists. Two types of mistakes by the general ophthalmologists have been noticed quite frequently while managing glaucoma. The first one is the misdiagnosis of neuro ophthalmological cases as glaucoma or failure to recognize the coexistence of neuro- ophthalmological cases and glaucoma. The second error occurs is in prescription writing which is of paramount importance. The purpose of the present write up is to discuss these commonly occurring two mistakes while managing glaucoma patients. The knowledge of which can improve the patient care with a better outcome.
Keywords: Glaucoma, Medical negligence,neuro ophthalmology, prescription writing, misdiagnosis of glaucoma
|How to cite this article:|
Nayak BK, Shahanand D. Common avoidable mistakes in the management of glaucoma. J Clin Ophthalmol Res 2013;1:163-8
|How to cite this URL:|
Nayak BK, Shahanand D. Common avoidable mistakes in the management of glaucoma. J Clin Ophthalmol Res [serial online] 2013 [cited 2020 May 31];1:163-8. Available from: http://www.jcor.in/text.asp?2013/1/3/163/116857
In the current scenario of medical practice, there is a lot of consumer protection and incidents of patients suing the doctors for medical negligence. It is very important for the doctors to be well aware of the very common avoidable medical errors in management and should always be vigilant to make sure that such errors are not committed by them while managing their patients. Also making a correct diagnosis and giving the correct and most effective treatment to a patient is the responsibility of a clinician.
Medical error does take place in our clinical practice, which sometimes, may lead to medico legal cases. The term "medical error" itself, suggests that it should be prevented from occurring. Medical error is any deviation from the process of care, which may or may not cause harm to the patient. It could be an error of execution (failure of a planned action to be completed as intended), or an error of planning (application of inappropriate plan) or an unintended outcome resulting from an act of omission (forgetting a task or sub-task leading to injuries from the patients' underlying disease, which could have been prevented by optimal care) or an act of commission (doing a task incorrectly leading to injuries caused by a medical intervention).
Medical negligence, in law, is defined as failure to exercise the degree of care expected of a person of ordinary prudence in protecting others from a risk of harm. It may render one civilly and sometimes criminally liable for resulting injuries. The doctrine of negligence does not require the elimination of all risk, but rather only foreseeable and unreasonable risk.
It has been noticed by Institute of Medicine in the second report that our healthcare system fails with embarrassing frequency to provide medical interventions known to benefit patients.  Hayward et al. noticed that over 95% of medical errors were caused by patients receiving too little medical care. 
The two common mistakes in Glaucoma Management are in diagnosis, that is, confusing glaucoma patients with neuro-ophthalmological discs and writing incorrect prescriptions. This article deals with these errors so that preventive measures can be adapted to avoid them.
| Confusing Glaucoma cases with neuro-ophthalmological cases|| |
History taking is the most neglected aspect of glaucoma and ophthalmology in general since the physical findings are so apparent. However, sometimes a carefully taken history will make the difference between successfully managing the disease and failure.
Most cases of chronic open angle are asymptomatic while acute glaucoma by contrast will present with dramatic symptoms of pain, redness, and blurred vision. Sub-acute attacks of angle closure glaucoma may present with migraine like symptoms with intermittent attacks of pain and visual disturbance. A disease identical to chronic open angle glaucoma can be produced by previous trauma or steroid eye drops use, so a history of eye injury, often many years previously or of eye drops use, should be sought. Patients with significant myopia and glaucoma should prompt an examination for pigment dispersion as a cause of glaucoma. Anisometropia and amblyopia are often associated with asymmetrical optic disc appearance, if the congenital disc asymmetry is not recognized a false suspicion of glaucoma may be raised. History of refractive corneal surgery has implications since eyes with corneal thinning may have erroneously low intraocular pressure (IOP) readings with Goldman applanation tonometry.
General medical history of the patient is also very important to be asked. Bilateral adrenal hyperplasia is the only known medical condition to cause chronic glaucoma and is a very rare condition, whereas exogenous steroids are a much more frequent and is an overlooked cause.
Visual field examination can also provide with essential information for the diagnosis. A scotoma that obeys the vertical meridian almost always points to a neurological pathology rather than glaucoma. The field defects, which are typical of glaucoma, can also be produced by lesions such as anterior ischemic optic neuropathy, branch retinal vein occlusion, etc., hence clinical correlation is the most important key to glaucoma management. Purely central scotomas with preservation of peripheral fields are suggestive of neurological pathology rather than glaucoma, for example, optic neuritis. Rapidly progressive field loss and markedly asymmetric field loss also raise the possibility of neurological disease rather than glaucoma.
From the neuro-ophthalmic point of view, visual field defects could be divided in prechiasmatics, chiasmatics, and postchiasmatics. Prechiasmatic defects are strictly unilateral, do not respect the vertical meridian, often have a nasal step associated, and are usually accompanied by ocular pathology detectable in an ophthalmic examination. The characteristic perimetric pattern of chiasmal disease is bi-temporal hemianopsia. Homonymous contralateral defects are the characteristic perimetric pattern of postchiasmal disease, and their congruency increases when the lesions are closer to the occipital lobe. Neuro-image studies are mandatory in all patients with a perimetric defect pattern compatible with chiasmal or postchiasmal lesions.
Benign intracranial hypertension: The visual field defects that result from papilledema in benign intracranial hypertension (BIH) are "disc-related defects" and are similar to those found in glaucoma. The most common defects seen in BIH are blind spot enlargement, generalized constriction, and loss of the nasal visual fields, especially inferonasal, inferior altitudinal loss, and scotomas (central, cecocentral, and paracentral). ,,
Optic neuritis: Visual field defects in the affected eye at presentation included diffuse visual field loss (48%), altitudinal defects (15%), central or caecocentral scotoma (8.3%), arcuate or double arcuate (4.5%), and hemianopic defects (4.2%).  Patients with hemianopic field defects (13% during the first year) were more likely to show abnormalities on the brain magnetic resonance imaging (MRI) at baseline as compared with patients without these field defects, indicating the presence of demyelinating lesions and multiple sclerosis. A mean deviation cutpoint of ≤-15 dB at the 1-month follow-up correlated with moderate-to-severe visual loss (acuity, contrast, and field) at 6 months. 
Anterior ischemic optic neuropathy: Visual field defects in nonarteritic anterior ischemic optic neuropathy (NA-AION) include altitudinal field defect (classically occurring in the inferior hemifield), central scotoma, arcuate scotoma, and quadrantic defects.  Diffuse central field defects are more commonly seen on automated perimetery. While a superior or inferior arcuate defect was the most common defect, an additional central scotoma is seen in the eyes with visual acuity worse than 20/64 at baseline.  In patients with posterior ischemic optic neuropathy (PION), the most common type of field defect is also the central visual field loss. In patients with NA-AION, it is important to test both the central and peripheral fields.
Chiasmatic disorders: Lesions of the optic chiasm can produce a variety of visual field defects including bitemporal hemianopia, junctional scotoma (anterior chiasmal defect), quadrantanopia and bitemporal, or unilateral temporal scotoma depending on the site and extent of the lesion. Visual field improvement following resection of the pituitary tumor occurs in three stages. Stage one is the early fast phase of recovery (days to a week) with complete normalization of the visual fields. Stage two is the phase of slow recovery (within a few weeks to a few months) where the visual fields show significant and slow and sustained improvement. Stage three is the late phase (a few months to a few years) with minimal improvement of the visual fields. Poor prognostic signs for improvement of visual fields include dense and extensive preoperative visual field deficit, pituitary tumor volume greater than 5 cc and the postoperative development of a surgically "empty sella" (which is associated with inflammatory scarring and descent of the chiasm into the empty sella). ,
Retrochiasmal disorders: They produce varied patterns of homonymous hemianopia, depending on the site of the lesion, which were used to localize a lesion in the visual pathway. Lesions anywhere along the retrochiasmal pathway can produce virtually any type of homonymous visual field deficit. Congruent homonymous hemianopias are produced by posterior pathway lesions and the chance that a congruent homonymous hemianopia is produced by a lesion involving the occipital lobe. However, unilateral loss of the temporal crescent and homonymous sector-anopia are produced exclusively by anterior occipital and geniculate lesions. Visual field improvement was defined as an improvement of the field defect by at least 10° horizontally and 15° vertically using similar isopters on the Goldmann visual fields and significant changes in mean and pattern deviations in Humphrey visual fields. It is important to detect and document improvement in the visual field to help prognosticate the patient's visual recovery.
Mills criteria  for subtle hemianopic defects:
If both criteria are met with, it is suggestive of early hemianopic defect and should be either investigated by neuroimaging or watched closely.
- Each threshold value in adjacent row on the either side of the vertical meridian should be compared in pairs (as mirror image). If at least three adjacent pairs show a unidirectional difference in sensitivity of at least 2 dB then it is considered significant.
- The corresponding points of the first column of defective points in the next column on both the sides should also show similar difference in the same direction.
The progressive nature of glaucoma should be borne in mind to differentiate it from an isolated ischemic event like AION. Also the appearance of the disc will be segmental or diffuse pallor of the disc as opposed to deep cup and loss of nerve fiber layer in glaucomatous discs. However, if there is rapid deterioration of the visual fields and visual acuity in spite of a tight control of IOP then a neurological lesion like pituitary adenoma compressing the optic nerve should be suspected. Baseline perimetry should always be done and glaucoma should not be diagnosed on the basis of Heidelberg retinal tomogram (HRT)/Scanning laser polarimetry (GDx)/Optical coherence tomography (OCT) only.
Optic nerve evaluation should always be in terms of
Warning signs for suspecting neuro-ophthalmological damage in cases of glaucoma:
- Overall impression of the disc
- Size and shape of the disc
- Evaluation of the neuroretinal rim keeping in mind the variability of its thickness in various zones mentioned in the text and also look for notch and neuroretinal rim hemorrhage.
- Peripappillary atrophy alpha and beta zones
- Nerve fiber layer abnormalities
- Vertical cup-disc ratio and asymmetry
- Stereoscopic evaluation of the optic nerve head with emphasis on changes of the neuroretinal rim and not estimation of cup-disc ratio will aid in early diagnosis of glaucoma.
Some interesting cases which were wrongly diagnosed as glaucoma are being described here [Case 1] [Additional file 1], [Case 2] [Additional file 2], [Case 3] [Additional file 3], [Case 4] [Additional file 4] and [Case 5] [Additional file 5].
- Loss of visual acuity - In glaucoma, visual acuity is not affected except in the advanced stages. If the visual acuity loss cannot be explained on the basis of other ocular conditions, suspicion of neurological condition should arise.
- Rapid progression of field loss and visual acuity - This indicates one may be dealing with something else than glaucoma.
- Cup to field mismatch - Field changes should corelate with the disc appearance, otherwise the diagnosis of glaucoma should be revised.
- Hemianopic visual field loss - Indicates a neurological disease.
- Pallor >>> cupping (band atrophy) - Glaucomatous optic cup shows polar notching in the upper and lower pole, but nasal and temporal atrophy indicates neurological disease and not glaucoma. The optic disc after an attack of AION or disc swelling in the past may give it an appearance of glaucomatous disc.
- Retinochoroidal venous collateral ("Optociliary shunt vessel") - may represent other pathologies like meningioma or old ischemic event.
There are various criteria to establish whether a field change is glaucomatous or not. One among them is the structure and function evaluation (SAFE) criteria using standard automated perimetry (SAP) and short wavelength automated perimetry (SWAP).
For all criteria, confirmation on a second visual field was required for high specificity. The GHT "outside normal limits," two hemifield clusters worse than the normal 5% level and four abnormal (P <0.05) test locations on the pattern deviation probability plot provided the highest percentages of conversion from a normal to a glaucomatous visual field. 
- A pattern standard deviation (PSD) worse than the normal 1% level,
- A glaucoma hemifield test (GHT) "outside normal limits,"
- One hemifield cluster worse than the normal 1% level,
- Two hemifield clusters worse than the normal 5% level,
- Four abnormal (P <0.05) locations,
- Five abnormal locations (P <0.05) on the pattern deviation probability plot.
| Writing incorrect prescriptions|| |
A prescription is the most important form of communication between a patient, a pharmacist, and the doctor. A prescription should be completely understandable and accurate. Writing a correct prescription is a professional and ethical responsibility. A correctly written prescription should have the following essential elements as per the Texas State Law:
The prescription should be in the following format:
- Date of the order (especially the controlled drugs)
- Patients name and address
- Name of the drug
- Strength of the drug
- Quantity of drug
- Directions for use
- Intended use of drug unless practitioner feels indication is not in best interest of the patient
- Name, address, and telephone number of the prescribing practitioner.
Superscription : Containing name, age and address of patient, and the date of prescription.
Inscription : Containing name, amount and nature of each drug and its dosage and route of administration along with any specific precaution to be taken.
Subscription: Dispensing instructions.
Signatura : Should contain purpose of the drug and signature of the doctor along with his address and phone number.
Also it is very important to make sure that the prescription is written legibly, with adequate spacing in between the words and numbers to avoid confusion, have complete medication orders, and avoiding abbreviations.
It has been recommended by Joint Commission on Accreditation of Healthcare Organization (JCAHO) to avoid certain abbreviations some of which are as follows: OD - Right eye, OS - Left eye, OU - both eyes, HS - at bedtime (may be confused with half strength), trailing zero should be avoided as the decimal point may be missed or not seen, and a leading zero is necessary to be written to avoid missing a decimal point for a fraction. 
Look alike/Sound alike/Confusing drug names
Look-alike or sound-alike (LA/SA) health products refer to names of different health products that have orthographic similarities and/or similar phonetics. They sound similar when spoken or look similar when written. These similarities may contribute to medical errors in prescribing, documenting, dispensing, or administering a drug. Factors such as identical doses or routes of administration, similar packaging or labeling, incomplete knowledge of drug names, illegible handwriting, verbal order errors, and even lack of an appropriate knowledge contribute to such errors. Confusion regarding drug names is thought to account for 25% of all medication errors. 
Brand name : When a drug is developed and researched by a pharmaceutical company they market the product under a Brand Name.
Generic name : When the patent of the company is over the drug, is manufactured by other companies also, and its chemical name is the Generic name.
Many brand names of the drugs are confusing and do not give much information about the molecule in it, for example, Ganfort eye drops (bimatoprost + timolol).
SA drugs with completely different molecules in them, for example, are:
Alphagan (Brimonidine), Lumigan (Bimatoprost), Betagan (Levobunolol), and Combigan (Brimonidine + Timolol)
Trusopt (Dorzolamide), Azopt (Brinzolamide), Cosopt (Dorzolamide + Timolol), Isopto (Pilocarpine), and Zioptan (Tafluprost - PG analogue)
Wrong dosing of the drug (timing and frequency)
The dosage of the prescribed drugs may be inappropriate, for example, prescribing a beta-blocker once a day dosing at night time is incorrect as the beta blocker is not effective in reducing pressure at night and may even cause nocturnal hypotension and further aggravate optic nerve damage. ,, A prostaglandin analogue is usually prescribed at night time for its maximal effect.  Errors of prescribing a prostaglandin analogue in morning, giving it twice a day, or prescribing two different prostaglandins are also commonly encountered. Also prescribing PG inhibitor in combination with beta blocker has to be used in morning instead of night time dosing to get the effect of the beta blocker optimally.
Optimal dosing of a carbonic anhydrase inhibitor is thrice a day but is very frequently prescribed twice a day. Carbonic anhydrase inhibitors reduce aqueous secretion only if more than 99% of carbonic anhydrase is inhibited in the ciliary epithelium. If the topical carbonic anhydrase inhibitor has produced effect, it indicates that more than 99% of carbonic anhydrase in the ciliary epithelium has been inhibited. Systemic carbonic anhydrase inhibitors do not add to the effect of topical carbonic anhydrase inhibitors but just cause more systemic adverse effects. Hence both systemic and topical carbonic anhydrase inhibitors are not recommended. 
While writing prescriptions five "R's" should be kept in mind:
Some of the wrong prescriptions are being reproduced with our comments [Table 1], [Table 2], [Table 3] and [Table 4].
- Right Patient
- Right Drug
- Right Dose
- Right Route
- Right Time
It should be emphasized that, in glaucoma overtreatment should be avoided and should follow the dictum, "No medication is Best medication and Least medication is Best alternative." According to the European glaucoma society (EGS) guidelines, it is unlikely that more than two pharmacological preparations, with maximum of three active molecules are going to be additive, effective or well tolerated and reliably taken by the patient.  However, the combination of the different drugs that are used should have a synergistic effect and not have same mechanism of action. For example, beta blockers and alpha adrenergic agonists have same mechanism of action, that is, decrease aqueous production and hence it will not have synergistic effect, in contrast, combination of drugs like PG inhibitors, which increase the uveo-scleral outflow, and the beta-blockers, which decrease the aqueous production, will have a maximal efficacy in reducing IOP as a combination. Prescriptions should not be too complex, which makes it difficult to comply with considering the fact that it is a disease that needs lifelong treatment without any apparent symptoms.
Resilience is transforming lessons from past failures into future success by understanding how humans bridge gaps. It is the ability to prevent something bad happening known as Foresight, ability to prevent something bad becoming worse known as Coping, and ability to recover from something bad once it has happened known as Recovery.
Mistakes and errors do happen and it is only about learning from them to make you wiser and help make better decisions. Reducing medical errors is a process of continuous quality improvement. Use of standard protocols and guidelines should be followed and should be backed up with proper academic education and encourage avoiding medical errors and framing a correct diagnosis, excluding various differential diagnosis, and prescribing correct medications right from the student level.
| References|| |
|1.||Crossing the Quality Chasm: A New Health System for the 21st Century. Institute of Medicine; 2001. Available from: http://www.nap.edu/books/0309072808/html [Last accessed on 2013 Mar 1]. |
|2.||Hayward RA, Heisler M, Adams J, Dudley RA, Hofer TP. Overestimating outcome rates: Statistical estimation when reliability is suboptimal. Health Serv Res 2007;42:1718-38. |
|3.||Wall M, George D. Idiopathic intracranial hypertension. A prospective study of 50 patients. Brain 1991;114:155-80. |
|4.||Salgarello T, Tamburrelli C, Falsini B, Giudiceandrea A, Colotto A. Optic nerve diameters and perimetric thresholds in idiopathic intracranial hypertension. Br J Ophthalmol 1996;80:509-14. |
|5.||Wall M, George D. Visual loss in pseudotumor cerebri. Incidence and defects related to visual field strategy. Arch Neurol 1987;44:170-5. |
|6.||Keltner JL, Johnson CA, Spurr JO, Beck RW; Optic Neuritis Study Group. Baseline visual field profile of optic neuritis. The experience of the optic neuritis treatment trial. Arch Ophthalmol 1993;111:231-4. |
|7.||Kupersmith MJ, Gal RL, Beck RW, Xing D, Miller N; Optic Neuritis Study Group. Visual function at baseline and 1 month in acute optic neuritis: Predictors of visual outcome. Neurology 2007;69:508-14. |
|8.||Hayreh SS, Zimmerman B. Visual field abnormalities in nonarteritic anterior ischemic optic neuropathy: Their pattern and prevalence at initial examination. Arch Ophthalmol 2005;123:1554-62. |
|9.||Feldon SE. Computerized expert system for evaluation of automated visual fields from the Ischemic Optic Neuropathy Decompression Trial: Methods, baseline fields, and six-month longitudinal follow-up. Trans Am Ophthalmol Soc 2004;102:269-303. |
|10.||Kerrison JB, Lynn MJ, Baer CA, Newman SA, Biousse V, Newman NJ. Stages of improvement in visual fields after pituitary tumor resection. Am J Ophthalmol 2000;130:813-20. |
|11.||Gnanalingham KK, Bhattacharjee S, Pennington R, Ng J, Mendoza N. The time course of visual field recovery following transphenoidal surgery for pituitary adenomas: Predictive factors for a good outcome. J Neurol Neurosurg Psychiatry 2005;76:415-9. |
|12.||Crabb D, Viswanathan A, McNaught A, Poinoosawmy D, Fitzke F, Hitchings R. Simulating binocular visual field status in glaucoma. Br J Ophthalmol 1998;82:1236-41. |
|13.||Johnson CA, Sample PA, Cioffi GA, Liebmann JR, Weinreb RN. Structure and function evaluation (SAFE): I. criteria for glaucomatous visual field loss using standard automated perimetry (SAP) and short wavelength automated perimetry (SWAP). Am J Ophthalmol 2002;134:177-85. |
|14.||Available from: http://www.jcaho.org/accredited+ organizations/ patient+ safety/04+ npsg.htm [Last accessed in 2004 Jan]. |
|15.||Lambert BL, Linn SJ, Chang KY, Gandhi SK. Similarity as a risk factor in drug-name confusion errors: The look-alike (orthographic) and sound-alike (phonetic) model. Med Care 1999;37:1214-25. |
|16.||Stewart WC, Konstas AG, Nelson LA, Kruft B. Meta-analysis of 24-hour intraocular pressure studies evaluating the efficacy of glaucoma medicines. Ophthalmology 2008;115:1117-22. |
|17.||Costagliola C, Parmeggiani F, Virgili G, Lamberti G, Incorvaia C, Perri P, et al. Circadian changes of intraocular pressure and ocular perfusion pressure after timolol or latanoprost in Caucasians with normal-tension glaucoma. Graefes Arch Clin Exp Ophthalmol 2008;246:389-96. |
|18.||Liu JH, Kripke DF, Weinreb RN. Comparison of the nocturnal effects of once-daily timolol and latanoprost on intraocular pressure. Am J Ophthalmol 2004;138:389-95. |
|19.||Lee AJ, McCluskey P. Clinical utility and differential effects of prostaglandin analogs in the management of raised intraocular pressure and ocular hypertension. Clin Ophthalmol 2010;4:741-64. |
|20.||Nesher R, Ticho U. Switching from systemic to the Topical Carbonic anhydrase inhibitor dorzolamide: Effect on the quality of life of glaucoma patients with drug related side effects. Isr Med Assoc J 2003;5:260-3. |
|21.||Available from: www.eugs.org/eng/EGS_guidelines.asp. [Last accessed on 2013 Mar 1]. |
[Table 1], [Table 2], [Table 3], [Table 4]