Ординатура / Офтальмология / Английские материалы / Risk Prevention in Ophthalmology_Kraushar_2008

Case 4

A 65-year-old white female developed new-onset headache. She saw her family care doctor, who diagnosed “sinusitis” and treated the patient with antibiotics. Two weeks later the headache worsened, and she had blurred vision OD. The family practitioner referred the patient to an ophthalmologist. On examination, the visual acuity was 20/40 OD and 20/30 OS. The technician recorded “PERRLA.” The fundus examination was normal OU. The patient was referred back to the family practice physician. The next day, Friday, July 4th, the patient called the office at 4:50 PM with complaints of increasingly severe headache. The receptionist who took the call informed the patient that the doctor had already “left for the holiday.” The patient went to the emergency room that night and had a CT scan of the head and a lumbar puncture that were normal. The patient reported to the emergency room doctor that she has had several episodes of transient monocular visual loss OD and jaw claudication for the past 3 weeks but had already been seen by her ophthalmologist and family doctor for these problems. The emergency room physician called the ophthalmologist, who was watching the fireworks with his family downtown. The ophthalmologist told the emergency room doctor to schedule the patient to be seen on Monday. The patient was discharged from the emergency room with the diagnosis of “migraine.” The next day, Saturday, the patient lost vision OU to no light perception.

A second ophthalmologist saw the patient and diagnosed bilateral pallid disc edema consistent with arteritic anterior ischemic optic neuropathy. An erythrocyte sedimentation rate was normal at 15mm/hr, but the serum C-reactive protein was elevated at 16mg/dL. A temporal artery biopsy showed temporal arteritis, and the patient was treated with steroids without improvement in her vision. The family doctor, when notified of the impending lawsuit, altered the medical record to include a “negative review of systems” including “no jaw claudication.” The first ophthalmologist testified at deposition that he had asked the emergency room doctor on the phone about the presence of jaw claudication and recommended an erythrocyte sedimentation rate evaluation. There is no documentation in the emergency room record regarding this discussion. The family doctor, emergency room physician, and first ophthalmologist reach a substantial settlement with the patient.

What went wrong?

1.New-onset headache with or without visual loss in the elderly should be considered to be temporal arteritis until proven otherwise.

2.The standard of care does not change based on time of day, day of week, or holiday.

3.Patients with possible temporal arteritis should be evaluated urgently, as the natural history of untreated giant cell arteritis can lead to blindness. In the Kraushar and Robb series, the most frequent risk factors were altered records, poor documentation, informed consent problems, failure to see the patient promptly, and failure to obtain or follow the advice of a consultant.

Table 16.3 Common errors in evaluation of giant cell arteritis

•Failure to evaluate new-onset headache in the elderly

•Failure to triage or refer new diagnosis of temporal arteritis

•Failure to consider or to document appropriately pertinent positive or negative review of systems (e.g., headache, scalp tenderness, jaw claudication, polymyalgia rheumatica)

•Failure to consider occult giant cell arteritis in elderly patients with visual loss

•Failure to order erythrocyte sedimentation rate (ESR) or C-reactive protein in suspected giant cell arteritis

•Failure to consider that the ESR may be normal in temporal arteritis

•Failure to start or maintain adequate corticosteroid therapy in giant cell arteritis

•Failure to recognize the significance of “red flags” for giant cell arteritis (e.g., transient monocular visual loss preceding ischemic optic neuropathy, posterior ischemic optic neuropathy, bilateral visual loss, pallid disc edema, nonembolic central retinal artery occlusion, cilioretinal artery occlusion, ocular ischemic syndrome)

•Failure to perform temporal artery biopsy*

*I believe that establishing pathologic diagnosis is helpful in preventing inappropriate or too rapid tapering of the steroid treatment and for justifying continued treatment in the face of steroid related side effects.

Table 16.3 lists some common errors that can complicate evaluation of giant cell arteritis.

Case 5

A 65-year-old white female presented to her ophthalmologist with painless progressive visual loss OU. The past medical history was significant for Mycobacterium avium intracellulare infection of the lung treated by a pulmonary specialist with ethambutol 1,200mg per day for 3 months. The patient saw an ophthalmologist and reported the visual blurring. The visual acuity was 20/40 OU, and a mild cataract was detected. The technician reported no relative afferent pupillary defect. The fundus was normal. The ophthalmologist diagnosed “mild cataract” OU. The patient returned 3 weeks later with worsening vision OU at 20/100 OU. The ophthalmologist wrote, “No disc edema or optic atrophy—doubt toxicity. Schedule visual field next visit.” Two weeks later, the patient underwent a computerized Humphrey 30-2 visual field (HVF) test that was unreliable OU. The ophthalmologist noted “? Mild temporal pallor” and wrote “HVF—unreliable” and recommended referral to a neuroophthalmologist. The ophthalmologist wrote a note to the pulmonary doctor about the possibility of ethambutol toxicity but told the patient that he has to “check with the pulmonary doctor” before stopping the medicine. The pulmonary doctor is “on vacation,” and the phone message from the ophthalmologist and the letter regarding the possibility of toxicity remained on the desk of the pulmonologist.

Three weeks later the patient saw the neuroophthalmologist, who performed Goldmann perimetry that showed a dense cecocentral scotoma OU and counting fingers vision OU. The optic nerves showed bilateral temporal pallor. The ethambutol

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Table 16.4 Common errors in evaluating toxic optic neuropathy

•Failure to consider medications as a potential cause for visual loss (e.g., ethambutol, hydroxychloroquine, chloroquine, amiodarone)

•Failure to consider toxic retrobulbar optic neuropathy in differential diagnosis of unexplained visual loss (normal optic nerve initially)

•Failure to consider that bilateral and symmetric optic neuropathy may not have a RAPD

•Failure to perform formal visual field testing in patients with unexplained visual loss

•Failure to repeat or further evaluate patients with an “unreliable” automated perimetry

•Failure to communicate in a timely manner the need to discontinue potentially toxic medication to patient and prescribing physician

•Failure to consider referring a patient with unexplained optic neuropathy

•Failure to consider dose (mg/kg), duration of treatment, and risk factors for toxicity (e.g., body weight, renal or liver dysfunction)

was discontinued, but the patient did not recover her vision. The neuroophthalmologist scolds the patient for not discontinuing the medication sooner.

Table 16.4 lists common errors that can complicate the evaluation of toxic optic neuropathy

References

1.Ophthalmic Mutual Insurance Company. http://www.omic.com/resources/risk_man/deskref/ litigation/16.cfm.

2.Kraushar MF, Robb JH. Ophthalmic malpractice lawsuits with large monetary awards. Arch Ophthalmol 1996;114:333–337.

3.Kraushar MF, Turner MF. Medical malpractice litigation in ophthalmology: the New Jersey experience. Ophthalmic Surg 1986;17:671–674.

4.Kraushar MF. Recognizing and managing the litigious patient. Surv Ophthalmol 1992;37: 54–56.

5.Bettman JW. A review of 412 claims in ophthalmology. Int Ophthalmol Clin 1980;20:131–142.

6.Bettman JW. Office personnel and medicolegal claims. Surv Ophthalmol 1982;27:64–66.

7.Bettman JW. Seven hundred medicolegal cases in ophthalmology. Ophthalmology 1990;97: 1379–1384.

8.Bettman JW. Special problems in ophthalmic subspecialties. Ophthalmology 1979;86: 1246–1252.

9.Donin JF. Special risk areas in ophthalmology. Neuro-ophthalmology. Int Ophthalmol Clin 1980;20:93–107.

10. Donin JF. The neuro-ophthalmology trap: failure to diagnose. Ophthalmology 1979;86: 1240–1245.

11. Hepler RS. Ophthalmology personnel in risk management. What office personnel need to know to keep you out of trouble. Ophthalmology 1990;97:1385–1389.

12. Lanckton AV. How to avoid malpractice claims. Arch Ophthalmol 1996;114:339–340.

neoplasia of the conjunctiva, HIV disease must be ruled out. Again, there is no negative effect of biopsy in conjunctival lesions.

Orbital tumefactions and lesions that simulate them rarely lead to malpractice suits, although these can occur. Ironically, more commonly I have seen patients with undiagnosed thyroid orbitopathy than those with neoplastic processes sue an ophthalmologist for failure to diagnose and treat in a timely manner. The one area that can be problematic is childhood proptosis. Although most adults with orbital disease can be evaluated in a standard manner, children with proptosis require emergent evaluation to avoid preventable visual loss from either infections or tumors.

Several investigations have shown that, in adults, the most common cause of unilateral or bilateral proptosis is thyroid orbitopathy. Any patient with proptosis or signs of optic nerve dysfunction (loss of color vision, afferent pupil defect, or changes in the nerve fiber layer or optic atrophy) should have good quality, thin section, orbital imaging. Ultrasonography in centers that manage many patients with ophthalmic oncologic problems is quite accurate, but, for the general ophthalmologist, high quality magnetic resonance imaging (MRI), preferably with thin sections and fat saturation gadolinium studies using a 3T magnet, is the best choice for imaging approach. The rational for this statement is that the quality of both computed tomography (CT) and MRI scans is really dependent on the equipment and on the patient’s cooperation. With excellent equipment and well-developed protocols, one can obtain as good a scan as those performed in a major ophthalmic oncologic center. In contrast, I have seen a number of suits where the ultrasound was diagnostic, but not correctly interpreted, even in large university centers without sufficient experience with ophthalmic oncologic processes.

Most patients with thyroid orbitopathy present within 18 months of the diagnosis of hyperthyroidism, but a minority of patients will present with just eye signs and no systemic symptoms. As described earlier, vision loss of unexplained origin mandates an imaging study. Many years ago Jonathan Trobe noted that up to 80% of patients with compressive thyroid optic neuropathy were not diagnosed by the primary ophthalmologist. The scans will obviously allow the correct diagnosis in such settings. In addition, over 95% of patients with thyroid orbitopathy can be diagnosed by simple thyroid blood tests. A serum thyroid stimulating hormone (TSH) level is the first-line test for hyperthyroidism because a 2-fold change in the serum thyroxin level produces a more than 50-fold change in the serum TSH. Hyperthyroid patients have immeasurably low TSH levels. Those whose thyroid gland has either spontaneously involuted or been destroyed by the autoimmune processes often have thyroid stimulating immunoglobins. Both types of studies should be performed when this diagnosis is suspected.

Intraocular tumors and lesions that simulate them generate the largest number of lawsuits I have seen. Most of the lawsuits regarding children are retinoblastoma cases and not initially diagnosed by the pediatrician. Frankly, I have not seen a retinoblastoma lawsuit directed against an ophthalmologist. As a profession we have been excellent when a child is referred with the possibility of an abnormal eye finding to have an appropriate evaluation in ophthalmic oncologic centers.

The two most common problems that have led to litigation involving adults have been failure to diagnose and treat uveal melanoma in a timely manner and a failure to diagnose and treat an intraocular lymphoma. Diagnosis and management of an atypical uveal melanoma can be difficult. Historically, 20% of the eyes removed with a clinical diagnosis of a uveal malignant melanoma contained a simulating lesion on histologic examination. Similarly, 10% of eyes with opaque media that were submitted to the Armed Forces Institute of Pathology, had unsuspected uveal melanoma. In 2006, the diagnostic accuracy with patients who have a melanoma large enough to require treatment approaches 100% in major ophthalmologic oncologic centers. How do we avoid missing a patient with a uveal malignant melanoma? One, it is imperative to be overly cautious in the evaluation of patients with a unilateral media opacity. About three to four times a year, I manage patients with a unilateral cataract who have had axial length measurements and placement of an intraocular lens. With several of these patients, the surgeons actually had difficulty inserting the lens because there was a <more than>10 mm thick ciliochoroidal melanoma that made lens implantation difficult. Any patient with unilateral media opacity requires diagnostic ultrasonography in addition to axial length measurements.

Another group of patients involved in litigation are those who have been seen with minimal retinal symptoms (flashes, floaters, visual field defect) or a sentinel vessel, were evaluated without dilation by an ophthalmologist, and then had the diagnosis of uveal melanoma made a year or two later in another office. Obviously, the lawyers query whether this could have been diagnosed earlier. The standard of care in most states requires a dilated fundus examination when the patient is seen for routine ophthalmic care, and it is imperative that this be documented on the chart. It is possible to defend the fact that a peripheral uveal melanoma was missed in the course of an ophthalmologic evaluation if there is documentation that the eye was dilated and the periphery was examined. What is much more difficult is the scenario when the patient has a tumor and there is no documentation that a dilated examination was performed. This becomes especially vexing with the patient who has symptoms of flashes, floaters, or a sentinel vessel peripherally and but for whom there is no evidence that a dilated examination had been performed.

In a recent paper we published, approximately 35% of reasonable sized melanomas were not discovered on primary ophthalmologic examination. Those data can be interpreted two ways. One interpretation is that if this number of cases is missed, can you assume that it is not malpractice to be unable to diagnose a melanoma? The other interpretation is that a number of these cases should have been diagnosed (because the mean size of these tumors is over 5 mm in thickness), and perhaps we should be a little more judicious in our fundus examinations.

A more difficult diagnostic problem is in the patient who unfortunately is not diagnosed as having a tumor prior to the surgical management of another condition (usually a unilateral media opacity or vitreous hemorrhage and retinal detachment following an anterior segment procedure), meaning the diagnosis is established late in the disease course. I will give you two disturbing examples. One was a patient we saw several years ago who had cataract extraction with a nonclearing vitreous

hemorrhage. Vitrectomies were done on two separate occasions, and we were asked to see the patient when there were black masses growing out of the vitrectomy incisions. The second case was a patient who had intractable intraocular pressure elevation after cataract surgery and vitrectomy, and we were brought in after the patient had a Molteno valve with amelanotic growths around that area.

As clinicians, I think the most difficult problem we face diagnostically is when a patient has a very atypical response to therapy. I have always approached such patients with the assumption that we possibly have made an error and therefore have to start the evaluation again from “ground zero” because of the possibility of a missed diagnosis. Certainly for a patient who has had a cataract and now for some reason develops a hemorrhage, or especially has a nonclearing hemorrhage, the possibility of a tumor should be considered, and diagnostic ultrasound makes good sense.

Several rarer forms of malignancy can be difficult to diagnose, but because of their rarity they are less likely to initiate a lawsuit. We have seen a few patients present with a ring melanoma. Unfortunately, while these can be diagnosed with fine-needle biopsy, often they will present either as a unilateral glaucoma with just pigment present asymmetrically in the angle of one eye or, less commonly, as what appears to be a focal iris small tumor but with increased pressure in that eye. In either of these settings, the possibility of a melanoma that is a ring type should be considered and the patient referred for further evaluation.

Intraocular lymphomas have generated several lawsuits. Any older adult with diffuse uveitis (involvement of the vitreous as well as the anterior chamber), especially with yellowish-white choroidal-retinal infiltrates, should be presumed to have an intraocular lymphoma until you prove it otherwise. The management of these patients is obviously outside the purview of a general ophthalmologist, but the possibility of an intraocular lymphoma should be raised for patients over 50 years old with “diffuse uveitis.” Obviously, most patients in this age group with this presentation would not have intraocular lymphoma, but the failure to consider this diagnosis can place the clinician in legal jeopardy.

Several points are important to emphasize in commonality with other causes of ophthalmic malpractice litigation. I am impressed, having reviewed a number of cases, that the physician’s ability to be compassionate and caring are probably as important (and some would say more so) than the quality of their care in preventing or resulting in a malpractice case. There was a California physician who I thought was probably in the top 10% of practicing ophthalmologists but who I saw four different legal actions against mainly because, in each case, he managed to alienate patients who achieved less than perfect results (which certainly does happen to all of us). At the other extreme, there was another physician in Northern California who probably should have lost his license many times but was so charming that most patients did not initiate lawsuits against him even when they should have.

If you are asked to perform a definitive procedure for an ophthalmic oncology problem, it is imperative to provide appropriate informed consent. In eyelid or conjunctival tumors, even though we have <more than>98% local control rate, I always counsel patients about a possible false-positive or negative pathology result (for both diagnosis and tumor margins). In eyelid surgery we also counsel

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patients that it may be necessary to do more than one procedure to reconstruct the eyelid (even though this is necessary <less than>0.1% of the time). In cases with an intraocular tumor, the possibilities of false-positive or false-negative diagnosis, loss of vision, retinal detachment, cataract, and vitreous hemorrhage, as well as possible development of metastatic disease, should be discussed.

A final three points that are pertinent to all ophthalmic malpractice litigation are the following. One, if one is sued, it is imperative that the chart remain untouched and no attempt made to revise it. Revision of a chart basically will destroy any chance of successfully defending a lawsuit. Two, it is important when you are sued to inform your malpractice carrier immediately about it and ask the carrier to quickly suggest a possible consultant (to review the case). Three, in the setting of a malpractice suit, further discussion with either the patient or his or her representatives should be avoided.

Reference

1. Char DC. Tumors of the Eye and Ocular Adnexa. Hamilton, Ontario: BC Decker; 2001.