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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