Ординатура / Офтальмология / Английские материалы / Risk Prevention in Ophthalmology_Kraushar_2008

Nontraditional Treatment for Glaucoma

Glaucoma is a disorder whose etiology is still only partially understood, making treatment challenging and not always successful with consequences that are potentially debilitating to the patient. As a result, patients are often attracted to nontraditional treatment because of frustration with the limited results or with the difficulty in using their current treatment, because of their dissatisfaction with the physician, or a combination of these. The patient in such a situation may turn to nontraditional therapy such as special diets, exotic treatments, or the use of herbs or other botanicals, including cannabis, all of which have been touted for the treatment of glaucoma. This decision may be suggested or reinforced by information obtained from nonprofessional sources. The patient is likely to incur vision loss when using alternative treatments despite their glowing claims to preserve or enhance vision, and the physician should be especially on guard, without being offensive or appearing dogmatic, to avoid any perception of encouragement in unproven or untested treatments.10,11

Consider the following situation. A patient complained to her physician of her lack of faith in his prescribed remedies. He responded by pointing out that her pressures had remained under good control, and the progressive damage to her optic nerves had been stopped. The patient wanted not control but a cure and questioned the direction and adequacy of the treatment. She announced that she wanted to try a botanical treatment that was advertised in the media. The physician in his frustration said she was free to do what she felt was best but to let him know the result if she tried the botanical. The patient had not been seen for several years before being examined once again by the original physician. By then she had sustained increased damage to the optic nerves with a corresponding loss in visual field. The patient sued the physician because he gave no warning of the risk of damage if she pursued her plans for alternative treatment. The court held for the patient, saying that under the circumstances the physician erred by not warning the patient more emphatically and in a manner by which the patient would likely understand the potential risks of the alternate treatment, and for vaguely implying that the unorthodox treatment might be useful.

The question arises whether the patient is actually aware of the risk that is being assumed. In the situation in which the patient knowingly fails to comply with the physician’s instructions or selects a course of treatment different from the one recommended by the physician, the law considers the patient to have accepted the consequences of his own actions. Legally this is termed the assumption of risk. The physician’s duty is to inform the patient of the potential risks for glaucomatous damage arising from the failure to follow customary practices. The physician must also point out any risk, if known, arising from the patient’s choice of alternative treatment. To be legally protected the physician should always place in the patient’s record information about the patient’s actions and decisions that may affect treatment.12

Management of the Noncompliant Patient

The physician–patient relationship may occasionally experience a strain or tension that interferes with good glaucoma care. This is particularly true because primary open angle glaucoma is a life-long condition that, although controllable, requires good communication and interaction to form a workable partnership between physician and patient. Like any long-term relationship, the effectiveness of the relationship may weaken because of interpersonal factors. If it becomes obvious to the physician that, despite the best efforts at reaching a workable accommodation, the treatment goals are not being reached because the patient is not cooperating, it is often advisable to terminate the professional relationship. The patient will usually find another ophthalmologist who can provide a workable situation. To continue in a negative relationship is to risk visual loss for the patient and potential liability to the ophthalmologist. There is a specific manner by which this can be accomplished, and the physician is advised to follow this protocol.13

Glaucoma Research and the Physician’s Professional Interests

The physician who is treating glaucoma may sometimes be engaged in basic glaucoma research or clinical evaluation of an experimental medication, device, or procedure. Although the U.S. Food and Drug Administration (FDA) is authorized by law to investigate and approve for use additions to the treatment armamentarium, the individual physician may still be involved in the development of new treatments and as a result may make them available for a particular patient. Providing experimental treatment to the patient can also create a personal benefit for the physician that may be monetary or may advance his reputation or career in a nonmonetary way. In these situations the physician has the duty to inform the patient that he may also receive a potential benefit in addition to any benefit that may accrue to the patient. This is an extension of the doctrine of informed consent and in these circumstances it must be communicated to the patient.14

Technology in Glaucoma Treatment

The field of glaucoma over the past few decades has expanded widely its diagnostic and therapeutic capabilities. Whereas 30 years ago topical medicines were the mainstay of glaucoma treatment, newer technology has since then slowly been added to the treatment options available. Lasers were the first addition. Argon laser trabeculoplasty alters the microstructure of the trabecular meshwork, increasing outflow of aqueous from the eye, and has been in use now for a number of years. More recently selective laser trabeculoplasty using a pulsed neodymium-YAG

laser has been introduced and works in a similar manner. Mechanical drainage devices, such as the Krupin, the Ahmed, and the Baerveldt tube drains, have also become a regular part of glaucoma therapy.

Because newer treatments, despite extensive evaluation, can still have as yet undiscovered negative consequences, a question arises concerning the nature and extent of the physician’s responsibility and liability for these consequences. The physician’s duty to inform the patient must include anything that may affect the patient’s decision to accept or reject treatment. This includes the use of a new medicine, a new technique, or a new instrument. In the case of something that is experimental, this status must also be communicated to the patient, emphasizing the possibility that unknown negative consequences may occur. When the physician has fully communicated all the information that may influence the patient’s decision, the patient’s free acceptance of any risk will have been established.

When introducing new technology, it is important to stay within the parameters established by the manufacturer and by the FDA, which approves it use, and within any established and customary practices that would apply to the situation. As mentioned earlier, when departing from customary practice, the physician has the duty to fully inform the patient of this departure and to discuss possible risks that may occur. Everything necessary for the patient’s free decision must be provided in order to establish valid informed consent.15

Consider this situation. A glaucoma patient was advised of the availability of a new laser treatment that decreases the secretion of aqueous humor, and, following discussion of the treatment, the patient agreed to its use. The laser had been approved for this specific use by the FDA, and the physician used it according to the instructions provided by the manufacturer and within the purpose and guidelines established by the FDA. Following treatment with the new laser, the patient developed hypotony and a reduction in vision. She sued the manufacturer of the laser for failure of the instrument to control the intraocular pressure in the manner predicted, and she also brought suit against the physician for her loss of vision. The court in this case recognized that the physician had used the instrument according to the manufacturer’s established instructions as well as within the FDA guidelines and therefore held the manufacturer solely liable for the equipment failure and the resulting visual loss.

As the practice of medicine in general and glaucoma management in particular changes with the increase in knowledge of diagnosis and treatment, issues will arise that may have legal consequences. Evidence-based medicine relating to newer drugs and instrumentation will alter the balance of duty and responsibility between the manufacturer and the physician who uses them.16 Recent advances in technology have already influenced medicine, and practice support systems such as telemedicine and electronic records will cause even further change and raise additional questions. Situations in glaucoma management will surely occur that cannot be imagined in today’s practice of medicine but that will nonetheless affect the legal environment.

Especially in the area of glaucoma, keeping abreast of the latest knowledge and developments, always putting the patient’s best interests first, and giving consideration

and respect to the patient’s point of view are the best approach to reduce the physician’s legal risk. Established legal doctrines and duties can be expected to continue unchanged, but, as the options for diagnosis and treatment increase, these established duties will expand and become more narrowly defined, resulting in new duties and responsibilities for the physician. Because glaucoma is a life-long disorder, frequent and appropriate evaluation of the patient at risk and initiation of treatment at the earliest signs of glaucomatous change will continue to be the best protection for the patient’s vision throughout his life. Attention to the patient’s individual situation and personal risk factors will enable the physician to establish the best and most effective treatment program while minimizing legal risk and liability. Putting the patient’s interest first has long been a pillar of established medicine, and this is just as true today as it ever was.

References

1.Collaborative Normal-Tension Glaucoma Study Group. Comparison of glaucomatous progression between untreated patients with normal-tension glaucoma and patients with therapeutically reduced intraocular pressures. Am J Ophthalmol 1998;126:487–497.

2.Heijl A, Leske MC, Bengtssen B, Hyman L, Hussein M. Reduction of intraocular pressure and glaucoma progression: results from the Early Manifest Glaucoma Trial. Arch Ophthalmol 2002;120:1268–1279.

3.Kass MA, Heuer DK, Higginbotham EJ, et al. The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol 2002;120:701–713, 829–830.

4.Lichter PR, Musch DC, Gillespie BW, et al. Interim clinical outcomes in the Collaborative Initial Glaucoma Treatment Study comparing initial treatment randomized to medications or surgery. Ophthalmology 2001;108:1943–1953.

5.Henderson v. Heyer-Schulte Corp. of Santa Barbara, 600 S.W.2d 844 (Tex. Cir. App.-Hous [1 Dist.] 1980), 28.

6.Restatement (Second) of Torts 282 (1965).

7.Helling v. Carey, 83 Wash.2d 514,519, 2d 981.

8.Preston v. Hubbell, 87 Cal App.2d 53, 196 P.2d 113 (Cal. App. 2 Dist. 1948), 98.

9.Kennedy v. Parrott, 243 N.C. 355, 90 S.E.2d 754 (N.C. 1956), 99.

10.Weil v. Seltzer, 873 F.2d 1453, 277. U.S. App. D.C. 196 (D.C. Cir. 1989), 161, 166.

11.Shorter v. Drury, 103 Wash.2d 645 P.2d 116 (Wash. 1985), 167.

12.Payton v. Weaver, 131 Cal.App.3d 38, 182 Cal Rptr. 225 (Cal. App. 1 Dist. 1982), 21, 24.

13.Lee PP. Medico-legal issues in glaucoma. In: Epstein DL, ed. Chandler and Grants Glaucoma. Baltimore: Williams & Wilkins; 1997:648–654.

14.Moore v. Regents of the University of California, 271 Cal. Rptr. 146, 793 P.2d 479 (Cal. 1990), 115, 284.

15.Kernke v. Menninger Clinic, Inc., 172 F.Supp.2d 1347 (D. Kan. 2001), 282.

16.Bujak JS, Lister E. Is the science of medicine trumping the art of medicine? Physician Executive 2006;32:18–21.

occur tend to result in higher payouts. Kraushar et al. reported 121 ophthalmic malpractice claims, and “failure or delay in diagnosis” represented 35% of claims and 63% of indemnification. The “failure to diagnose” retinal detachment was the most common cause.2–4 In Bettman’s review of 412 claims, 9 (2%) were “motility,” 9 (2%) were neuroophthalmologic procedures,” and 8 (1.9%) were “tumors.”5–8 In my consultative medicolegal practice, “failure to diagnose or delay in diagnosis” (“sin of omission”) for giant cell arteritis, compressive optic neuropathy (e.g., meningioma), sellar/chiasmal/pituitary tumor, and toxic medication effect (e.g., ethambutol and chloroquine/hydroxychloroquine toxicity) have been the most common. “Failure to treat” is a less common claim than “failure to diagnose” in my experience, but “failure to timely diagnose and treat visual loss from papilledema” (usually pseudotumor cerebri) is the leading culprit.9,10

Case 1: Optic Atrophy

A 55-year-old male with hypertension and diabetes presented with “acute awareness” of visual loss in his right eye (oculus dexter [OD]) while shaving the morning of presentation. An ophthalmologist examined the patient and found 20/50 OD and 20/20 OS (oculus sinister [left eye]). The pupil examination by the technician shows PERRLA (i.e., pupils equal, round, and reactive to light and accommodation). Slit-lamp examination discloses a “moderate nuclear cataract OD <more than> OS.” Ophthalmoscopy shows “possible mild optic atrophy OD and a normal optic nerve OS with a cup to disc ratio of 0.4.” The ophthalmologist writes the following: “Impression: ‘?’ mild optic atrophy and cataract OD. Plan: Return in 3 months.”

The patient returns in 2 months with worsening vision OD to 20/100. The technician reports: “PERRLA.” Confrontation visual field testing shows an inferior altitudinal-type of visual field defect OD and is normal OS. The ophthalmologist records the following impression: “possible mild optic atrophy OD—likely old ischemic optic neuropathy due to inferior altitudinal defect” and “Return—3 months.” The patient calls the office and reports “worsening vision OD” and the ophthalmologist orders a “scan.” The patient returns 1 month later with a noncontrast head computed tomography (CT) scan that has been read as “normal.” The ophthalmologist tells the patient by phone that “there is nothing to worry about” and to keep the 3-month follow-up appointment.

The patient seeks a second opinion 2 months later from a second ophthalmologist. The vision is now hand motions only OD and 20/20 OS. A right afferent pupillary defect is detected. The formal (Goldmann) visual field test shows inferior and central loss OD and a superotemporal visual field defect respecting the vertical midline OS. The optic nerve is diffusely pale OD.

The second ophthalmologist tells the patient that he needs to have an “MR scan right away” and a postcontrast cranial magnetic resonance imaging (MRI) of the

sella shows a pituitary adenoma compressing the right optic nerve and the junction of the optic nerve and chiasm. The second ophthalmologist tells the patient and his family that he needed to see a “neuroophthalmologist” and “that if only they had come in sooner the vision might have been preserved.”

What went wrong?

1.I would recommend that the extremely common but insufficient clinical abbreviation for the pupil exam, “PERRLA,” should be avoided by the ophthalmologist. “PERRLA” makes no assessment of the relative afferent pupillary defect (RAPD), the single most important objective evidence for an optic neuropathy in a patient with unilateral visual loss.

2.“Optic atrophy” is not a diagnosis. It is an ophthalmoscopic description of a clinical examination finding and does not define the etiology. Describing the “optic atrophy” with adjectives such as “?,” “maybe,” or “possible” does not protect the ophthalmologist and does not obviate the need for differential diagnosis and evaluation. Patients with “optic atrophy” should have documentation of the presence or absence of clinical evidence for an optic neuropathy, including assessment for an RAPD, a formal visual field test, and possibly photographic or nerve fiber analysis (e.g., optical coherence tomography). Bettman in a review of 276 medicolegal cases disclosed the medical reasons for filing these claims were usually based on “sins of omission or commission in “basic ophthalmology” rather than the omission of sophisticated testing or procedures. The recommendations of Dr. Bettman included that physicians should plan for the care of emergencies, order imaging as needed, use consultants, stay well within one’s level of competence, and of course “document everything.”

3.Inferior altitudinal defect is common but not diagnostic in nonarteritic anterior ischemic optic neuropathy (NAION). The clinical diagnosis of NAION requires (i) a clinical history of acute unilateral visual loss, (ii) documentation of the initial optic disc edema phase (i.e., the “anterior” in NAION), and

(iii)stability over time with resolution of the disc edema. The presence of optic atrophy at the first visit is not compatible with the diagnosis of acute NAION. The small cup to disc ratio is the structural risk factor (i.e., “disc at risk”) for NAION, and the fellow eye should be examined for this finding. I would recommend that any patient with unexplained visual loss have consideration for formal perimetry. Patients with a visual field defect on confrontation testing should undergo formal visual field testing to exclude a subtle lesion in the contralateral eye (e.g., junctional scotoma as in this case) and to detect a vertical step if present (e.g., homonymous or bitemporal hemianopsia).

4.The second ophthalmologist inadvertently adds “fuel to the fire” by suggesting that “earlier diagnosis and treatment” would have made a difference in the case and criticizing the care of the first ophthalmologist. Many cases of medical malpractice are triggered by the comments or criticism from another provide.

Table 16.1 Common errors in evaluating optic atrophy

•Failure to document presence or absence of clinical evidence for optic neuropathy in suspected optic atrophy (e.g., relative afferent pupillary defect [RAPD], formal visual field, optic nerve assessment)

•Failure to document etiology for unexplained optic neuropathy (i.e., “optic atrophy” is not a diagnosis)

•Failure to check or document presence or absence of RAPD or delegating this task to the technician (e.g., pupils equal, round, and reactive to light and accommodation)

•Failure to perform, review, or interpret a visual field test (e.g., formal visual field), failure to confirm an abnormal confrontation visual field examination with formal perimetry, or failure to confirm with serial evaluation the stability of visual loss in a patient with suspected optic neuropathy

•Failure to recognize that any optic neuropathy can produce any visual field defect

•Failure to recognize a vertical step (e.g., hidden within diffuse depression or drift across the vertical meridian due to artifact, other superimposed causes of visual field loss, or poor test reliability)

•Failure to perform a timely and appropriate neuroimaging study in unexplained optic neuropathy, junctional visual field loss, bitemporal hemianopsia, or homonymous hemianopsia*

•Failure to order the correct neuroimaging study (e.g., for possible compressive optic neuropathy, in general postcontrast fat suppressed orbital and head MRI is superior to noncontrast CT scan for optic neuropathy)

•Failure to review the neuroimaging study (even with a “normal” report) with the neuroradiologist

•Failure to consider referral to a specialist (e.g., neuroophthalmologist) for unexplained, complex, and/or progressive optic neuropathy

*I would recommend orbit and head with fat suppression and gadolinium magnetic resonance imaging (MRI) for optic neuropathy. Sella sequence cranial MRI with and without contrast should be performed for junctional or bitemporal loss. Cranial MRI with and without contrast is recommended for homonymous hemianopsia. Magnetic resonance imaging is superior to computed tomography (CT) in the majority of neuroophthalmic conditions (except for need for a faster study; for examination of bone, acute blood, fracture, trauma, and some orbital conditions; and for patients who cannot undergo an MRI). Contrast for both MRI and CT should always be considered unless there is a contraindication.

Table 16.1 lists some common errors that can complicate the evaluation of optic atrophy.

Case 2

A 12-year-old white female presented with headache and blurred vision in both eyes (OU). An optometrist notes 20/60 vision OU and bilateral optic disc edema with a macular star figure of exudate in both eyes. No vitreous cells were noted. The patient had an esotropia of 30 prism diopters in primary position that was incomitant in lateral gaze with a moderate abduction deficit OU. The optometrist calls the ophthalmologist’s office and describes the findings. The ophthalmologist diagnoses “infectious neuroretinitis OU and sensory esotropia” on the telephone

and recommends laboratory testing with the pediatrician for cat scratch disease, Lyme disease, and tuberculosis and an appointment in 2 weeks in the office.

The patient’s mother calls the ophthalmologist’s office and “demands” that the appointment be “moved up.” The receptionist tells her that she will work on the scheduling but the mother is “frantic.” The office phone encounter form states “Anxious mother called about scheduling.” The patient’s mother calls 1 week later and reports that the vision is worsening and that the headache is increasing. The laboratory evaluation from the pediatrician returns as “negative.” The pediatrician records the negative results but does not call the patient or the ophthalmologist. The patient’s mother calls a second time 2 days later and the ophthalmic technician discusses the case with the ophthalmologist and reassures the patient’s mother to keep the scheduled appointment.

The patient develops worsening headache, does not keep the outpatient appointment, and instead is seen in the emergency room. A second ophthalmologist records the vision as hand motion OU with papilledema and bilateral sixth nerve palsies. A cranial CT scan shows a posterior fossa tumor. The blood pressure is normal. Urgent neurosurgical consultation and posterior fossa craniectomy with resection of tumor is performed at the second hospital, but the patient is left with no light perception vision and optic atrophy OU. The first ophthalmologist wonders why the patient did not show up for her appointment. A malpractice claim is filed 6 months later.

At the time of deposition, the patient’s mother testifies she felt “neglected and that no one would help her,” that the technician told her “not to worry and stop being a worry-wart” and that “two more days would not make a difference.” The physician testified that the ophthalmic technician had informed him of the patient’s mother’s phone call and included details of the patient’s vision, symptoms, and signs. The physician testified that the patient’s mother was told to bring the child in to the office if she was worsening. No documentation of this content for the phone encounter was available in the chart.

What went wrong?

1.Patients with bilateral optic disc edema should be presumed to have papilledema until proven otherwise. Optic disc edema from any cause (e.g., ischemic optic neuropathy, papilledema, malignant hypertension) may produce exudate in the macula and is not pathognomonic for infectious neuroretinitis.

2.Patients with a neuroophthalmic finding should be evaluated for other findings (i.e., “Is the finding isolated?”). Other symptoms (e.g., diplopia, headache) and signs (e.g., sixth nerve palsy) of increased intracranial pressure should trigger more aggressive and prompt evaluation, including neuroimaging.

3.Telephone triage may be appropriate in many circumstances. In general, however, objective neuroophthalmic findings should prompt further evaluation by an ophthalmologist or neuroophthalmologist rather than “diagnosis by phone.”

4.Communication among providers is important. If laboratory evaluation is performed and is positive or negative, then all of the physicians involved in the medical care of the patient should be informed.

5.Telephone calls should be documented, including persons involved, time and date of call, specific contents of the phone encounter, triage decision based on

the facts of the case, and the disposition of the call and any recommendations for further urgent or emergency evaluation. In general, patients with potentially serious conditions should discuss the findings with the physician rather than the technician. Hepler emphasized that risk factors for litigation associated with ophthalmic staff include improper triage of emergency patients, perceived abandonment, lack of confidentiality, improper maintenance of medical records, and perceived lack of compassion and skill on the part of staff members, pejorative comments and editorial comments.11,12 Bettman cited the following important ophthalmic office personnel factors: “friendly, courteous attitude, no matter how ‘trying’ the circumstance, and proper training of the personnel in handling of emergencies.”2

Case 3

A 35-year-old African-American female presented with neck pain and blurred vision to the emergency room. A cranial CT was normal. A lumbar puncture showed normal cerebrospinal fluid content with no evidence of subarachnoid hemorrhage or meningitis. No opening pressure was performed. No visual acuity was measured, and no documentation of the fundus examination was recorded. The emergency room physician diagnoses “migraine.” The patient was referred to a neurologist in 1 week. The neurologist treated the patient with migraine medicine, documented the emergency room encounter findings, and recommended an ophthalmology consultation in 1 or 2weeks for the blurred vision. The neurologist saw “possible blurred disc margins” and started the patient on acetazolamide 250 mg per day. The patient then lost vision to hand motions OU over the next few days. The ophthalmologist documented papilledema OU and performed an optic nerve sheath fenestration OU, but the vision did not recover. An MRI scan is normal, and a repeated lumbar puncture showed an opening pressure of 500 mm of water. A lumboperitoneal shunt was performed, but the vision remained hand motion and optic atrophy OU developed. Table 16.2 lists some common errors that can complicate the evaluation and treatment of papilledema.

Table 16.2 Common errors in evaluation and treatment of papilledema

•Failure to consider diagnosis of papilledema in bilateral optic disc edema

•Failure to perform timely and appropriate evaluation, including neuroimaging and lumbar puncture

•Failure to check blood pressure in bilateral optic disc edema for malignant hypertension

•Failure to consider urgent surgical treatment (e.g., optic nerve sheath fenestration) for patients with visual loss at presentation

•Failure to obtain an opening pressure at the time of lumbar puncture

•Failure to measure visual acuity or formal perimetry or to perform ophthalmoscopy in a patient with possible pseudotumor cerebri