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I. Routine IOPs, disc assessment and fields fail to detect glaucoma during a third of a century of eye care A. History and Chief Complaint: A 27 yo myopic f presented for CLs in the 1960’s. Other than blurred vision without her CLs, she reported no symptoms and no history or other risk factors for glaucoma. B. Clinical Findings: VA CC 20/20 or 20/25 R & L for third of a century. During over 100 visits, IOPs were never higher than 17 mm, CD was .2 or .3 w/o any change over time. fields WNL every several years. Last visit in 1999, no change and no indication of glaucoma. C . Diagnosis and Follow-up: Myopia was the Dx. 16 months after the last visit, the patient presented to a different doctor with complaints of blurred vision in the OS with dull orbital pain. VA CC was 20/30 R and 20/40 L and fields were abnormal OU with an arcuate defect in the L approaching fixation. MRI obtained & WNL. Doc diagnosed and treated for NTG since the IOP’s were only 16 OU on two visits. His CD was .8 to .9 in each eye. Corneal thickness around 500u in each eye and a GDx VCC revealed moderate to advanced NFL loss with NFI of 87 R and 73 L. At the present time, the treated IOPs are in the 10 mm range and glaucoma appears stabilized. D. Malpractice Allegation and Outcome: OD sued because he allegedly missed the glaucoma . Case settled just days before jury trial. E. Comment: The standard of care is constantly changing: IOPS, CDs and standard fields were adequate in the last millennium but may not be enough in this millennium. Pachymetry, field assessment with a more modern and sensitive system (such as the Matrix), nerve fiber layer assessment (with the GDx, OCT or perhaps the HRT) and objective disc assessment can often support a diagnosis even with normal IOPs, normal appearing discs and normal standard fields. This case is somewhat unusual in that the insurance carrier believed that the case would most likely be lost at trial, even though the doctor met the existing standard of care when the care was rendered. Sometimes, meeting the standard of care is not enough. Your best protection is to go beyond the standard of care and use new knowledge and technology when it becomes available. II. Poor outcome after cataract surgery in a patient with ICE syndrome A. History and Chief Complaint: a 55 yo f presented to an MD for the first time with a 10+ history of Irido-Corneal Endothelium (ICE) syndrome OD only. IOPS have been controlled for the last yr with 2 eye drops. She reported reduced vision OD relative to OS but had no new cc. B. Clinical Findings: VA (cc) 20/30 R 20/20- L. IOPs 18 R & 15 L. She reported good compliance. Slit lamp revealed irregular iris tissue R, lens changes R and gonio revealed zones PAS R. Fundus .4 CD R and .2 CD L. Fields and objective disc and NFL assessment were not obtained. C. Diagnosis: The new MD arrived at a diagnosis of cataract in the right eye (in addition to ICE) and recommended cataract extraction. D. Outcome: Vision worsened after surgery: marked corneal edema that failed to improve. IOPs increased to the high 30’s secondary to steroid eye drops in the post surgical period. A referral to a glaucoma specialist resulted in a surgical trab and then a shunt. Since the corneal edema never cleared, a referral to a corneal specialist was made and resulted in a first penetrating keratoplasty which failed and then a second. After 5 operations the patient still has not seen better than 20/400 since the first surgery and has had an “ugly red and often painful eye” ever since the first surgery. E. Malpractice Allegation and Comment: The MD who recommended and performed the cataract surgery should have realized that ICE by definition adversely affects the corneal endothelium. Although this MD never obtained a corneal endothelial cell count (ECC), eventual review of the old records revealed ECC of 850 in the right and 2100 in the left nearly 10 years earlier. Irreversible corneal decompensation after cat surgery is common with an ECC below 900 and was predictable in this case. Technology to obtain ECC in minutes is available and should have been obtained prior to surgery. The very considerable risks of cataract surgery in this unique case should have been explained to the patient. Note: Other cases of similar surgical mishaps will be briefly mentioned but even in surgical cases, the optometrist who refers the patient to a specific ophthalmologist is often sued as well. III. Diagnosis of Blurred Vision due to Cataracts Proves Wrong and Patient Dies A. History and Chief Complaint: A 45 yo presented for new glasses- reduced vision OU at D & N. He has no other symptoms or contributory history. B. Clinical Findings: VA cc 20/25- R & L with no change in lens prescription. Slit lamp exam revealed mild cataracts OU. IOPs and the fundus exam were unremarkable. Fields were not performed. C. Diagnosis: Doc advised patient that all is well except for very mild cataracts and that the patient should return in two years for the next exam. D. Follow-up: The patient presented 2 years later but this time he reported reduced vision OU, most evident in the “left eye to the left.” Although this latter comment was not recorded by the doctor, the obsessive compulsive patient recorded it in his health diary, an historical record of all his doctor’s appointments. Again the doctor diagnosed mild cataracts OU, a Dx that he made on 4 visits over a 6 years. E. Outcome: During the 8th year following the initial complaint, the patient decided to have cataract surgery and is seen by a well-known cataract surgery. But the pre-surgical eval revealed only negligible cataracts and a field screening discovered a bitemporal hemianopsia. This led to an MRI, a diagnosis of a very large pituitary adenoma, a referral to a top neuro-surgeon, and a trans-sphenoidal route to remove the mass. This failed and the patient, after informed consent, had major neuro-surgery described to the patient as “cracking the skull.” One month after the “successful” removal of the mass, the patient died in the hospital due to complications of the second surgery. F. Malpractice Allegation and Comment: Although the patient died, his health diary clearly revealed reduced vision in the “left eye to the left” 6 yrs before Dx of the brain tumor. Expert stated that a several minute VF screening, never performed on any of the 4 exams, would have revealed a temporal field loss and would have led to a timely Dx of tumor. An expert witness in neurosurgery commented, “It is far easier to remove a grape than a grapefruit” and that “trans-sphenoidal surgery years earlier would have been successful” and “it is more probable than not that the patient would still be alive with virtually normal vision” if the diagnosis was made years earlier. The case is scheduled for a jury trial in April, 2006. IV. Choroidal Melanoma Masquerades as Central Serous Chorioretinopathy for several years with Dire Outcome A. History and Chief Complaint: A 35 yo m was referred by OD to a highly respected retinal specialist because of reduced vision in one eye for a month. Patient reported no other symptoms and no significant eye or health history. B. Clinical Findings: VA cc 20/50 R and 20/20 L. DFE revealed subtle fluid in the macula along with some minor pigment changes in RPE. The retinologist performed a FA which revealed some ill- defined areas of leakage in the posterior pole. C. Diagnosis: The MD diagnosed atypical central serous in the high strung patient. No treatment & patient was followed by both the OD and MD. D. Follow-up: About 6 repeat evals over 2 years failed to reveal any improvement. The patient reported that the vision was actually worsening. Another OD examined the patient at the end of the 2nd year and observed slight disc blurring and hyperemia in addition to the previously observed maculopathy. A review of the previous fundus photos confirmed a change in the disc appearance. The OD performed a B-scan, which revealed a mass lesion that included the macula and the disc. The patient was soon seen by an ophthalmic oncologist who diagnosed a malignant melanoma growing under the macula and around the optic nerve. No typical mushroom shaped lesion revealed by B-scan and MRI and hence the melanoma was growing backwards without ever breaking through Bruch’s membrane. E. Outcome: Based upon the size of the lesion and no evidence of metastasis on the extensive systemic work-up, the ophthalmic oncologist recommended enucleation. The patient agreed and the mass was confirmed histopathologically to be a mixed cell type MM. 5 years after uneventful ocular and systemic follow-ups, worsening liver enzymes were noted and a repeat liver scan revealed multiple, suspicious lesions. The prognosis at this point is very bleak since metastasis has been confirmed. F. Malpractice Allegations and Comment: Although the retinal specialist diagnosed atypical central serous and followed the patient, he never considered an underlying choroidal melanoma as the Dx. Although this retinal specialist was very experienced with B-scan & performs them daily, he never performed a Bcan in this case. B-scan appears to be an underutilized diagnostic procedure in that it reveals lots of info about structure in just minutes. Not all MMs break through BM &result in the classical mushroom-shaped lesion in the vitreous. V. A One Disc Diameter “Choroidal Nevus” Progressives to a Giant Amelanotic Melanoma in 12 Months A. History and Chief Complaint: A 45 yo myope presented for a routine exam. His only compliant was slightly blurred vision at near through his 2 yo scratched reading glasses. No eye or health history. he started wearing glasses after failing the vision screening back in the first grade. B. Clinical Findings: A minor change in prescription yielded 20/20 VA OU at D &N. DFE revealed a “one dd choroidal nevus” that was sketched the same size as the disc and located one dd temporal to the macula OD. When the patient was told about the little “freckle” he was surprised since no doctor had ever mentioned the “congenital lesion” during multiple exams over 4 decades. C. Diagnosis: The OD Dx’ed a small nevus OD and some mild peripheral thinning in the peripheral retina. New Rx & patient told RTC 2 yrs. D. Follow-up: Year later, patient experienced light flashes. He immediately reported this and was seen within a day by a retinal specialist in the practice who DX’ed a non-rhegmatogenous RD. B-scan: large mass was observed along with RD. Ophthalmic oncologist didproton beam irradiation for the large amelanotic MM. Although the patient did well for several years, metastasis led to death. E. Malpractice Allegation: Based upon the course of events, the 1 dd “nevus” must have been a small melanoma and year delay in diagnosis, more likely than not led to a premature death. The case was settled several weeks before a jury trial was to begin for a reported 2 million dollars. F. Comment: This case teaches us that an early melanoma can easily be misdiagnosed as a nevus and the first time a lesion is noted, it should be imaged with fundus photography or OPTOMAP . B-scan and even FA should be obtained in questionable cases and a re-eval in 3 months should be considered. Without any evidence of growth at 3 months, then a 6 month reevalshould be arranged and then yearly exams. Choroidal melanomas begin as small lesions and a timely diagnosis and treatment is arguably associated with reduced morbidity and mortality. VI. A Bottle of Nyquil for a Bad Cold Induces Bilateral Angle Closure in a Hyperopic Malpractice Attorney A. History and Chief Complaint: A 40 yo hyperopic malpractice attorney presented to an ER with a self diagnosed angle closure glaucoma in both eyes simultaneously. The history revealed a bad cold that was self -treated by ingesting an entire bottle of Nyquil over a period of several hrs. He reported that his last eye exam was about 3 years earlier and his glasses dated back to that evaluation. B. Clinical Findings: VA 20/60 OU, believed to be due to edematous corneas. IOPs around 70. Gonioscopy confirmed bilateral angle closure. C. Diagnosis: Bilateral, simultaneous angle closure in a hyperopic attorney secondary to Nyquil induced pupillary dilation. D. Follow-up: Laser PIs were successfully performed following the immediate treatment with Osmoglyn, Diamox and various eye drops. Even with patent PIs, pupillary dilation one occasion resulted in IOP spikes into the 50’s. Now appears to have normal discs but visual fields & NFL measurements with GDx and OCT reveal damage. After cat ext, IOPS normal w/o gtts OU. E. Malpractice Allegations: Although the previous doctor who prescribed the glasses for the hyperopia did not do gonioscopy and did not warn about possible pharmacologically induced angle closure, the most recent exam took place nearly 3 years earlier. In NYS, the statue of limitations in malpractice cases is 30 months from the last doctor patient contact. A frustrated malpractice attorney thus has no one to sue. F. Comment: Careful slit lamp exam for angle assessment as well as gonioscopy should be considered in all hyperopes, since these small eyes have a much higher risk of angle closure. Prophylactic LPI is recommended in such cases to prevent angle closure. Patients who are anatomically prone to angle closure should be told that many over- the -counter medicines contain (sympathomimetic) ingredients that can induce angle closure. Note- Another case of bilateral angle closure due to Topamax will briefly be reviewed. VII. Multiple doctors sued for failure to Diagnosis Wilson’s Hepatolenticular Degeneration A. History and Chief Complaint: A 25 yo school teacher presented because of irritation OD & no other history. B. Clinical Findings- Best correctable VA was 20/20 R and 20/20 L. Slit lamp exam revealed a misdirected lash touching the conjunctiva. The doctor also noticed a subtle, iridescent ring in the peripheral cornea of both eyes. C. Diagnosis: The symptom of irritation was proven to be due to the misdirected lash since the symptom immediately disappeared with the lash was removed. D. Follow-up: Six months later, the patient presented for new contact lenses. Again, the doctor noticed the iridescent ring but this time, he reviewed the corneal chapter in the Wills Eye Manual and realized that the rings were most likely Kayser-Fleischer rings secondary to Wilson’s Hepatolenticular degeneration. He then questioned the patient about liver problems and the patient revealed for the first time that she was being followed for abnormal liver enzymes, thought to be due to Acutane, by her physician. The doctor filled out an inter-professional referral form, and requested that the physician consider Wilson’s disease. The sheet was faxed to the doctor, and a copy was given to the patient with the recommendation to call her internist for an appointment. E. Malpractice Allegation: Unfortunately, the fax was received but then buried by a receptionist in the patient’s chart and was never seen by the internist until nearly two years later. In that period of time, the patient developed a whole series of somewhat bizarre symptoms, was under the care of two psychiatrists, who treated her with various medicines that were believed to be causing neurological-type side effects. About two years later, one of the doctors finally obtained an MRI. It revealed pathognomonic copper rings in the brain and the diagnosis of Wilson’s degeneration was finally made and the patient was treated. However, permanent brain and liver damage had already occurred. About 8 doctors provided some level of care over the past several years and all were sued, including the optometrist. The case was settled prior to a jury trial. The insurance companies for all the doctors who were sued contributed to the final settlement that ran into millions of dollars. F. Comment: Although the optometrist correctly identified the cause of the corneal abnormality, his attempt to convey this very important information never succeeded in initiating timely therapeutic intervention. The baseball analogy is that he “hit a triple but a run was never scored.” This case underscores the necessity to confirm that such vital information is received and acted upon. VIII. Other cases IX. Summary and Conclusions