Here - American Geriatrics Society
Here - American Geriatrics Society
Here - American Geriatrics Society
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P OSTER<br />
A BSTRACTS<br />
Discussion/Conclusion<br />
Distress at the end of life may be from treatable factors such as<br />
urinary retention but often results from a complex interplay of delirium,<br />
pain and psychosocial factors. Effective palliation requires a<br />
multimodal approach targeting all sources of suffering. Geriatricians<br />
and palliative care experts have much to learn from each other and to<br />
teach trainees and hospitalists. To ease patients’ final hours and relieve<br />
the guilt of families, the <strong>American</strong> Academy of Hospice and Palliative<br />
Medicine and the <strong>American</strong> <strong>Geriatrics</strong> <strong>Society</strong> should collaborate<br />
on educational and clinical initiatives on end of life care<br />
C29<br />
Galantamine Induced Generalized Myoclonus.<br />
G. Luna, 1 N. Sharma, 2 J. Makela. 3 1. Geriatric, UIC, Chicago, IL; 2.<br />
Geriatric, UIC, Chicago, IL; 3. Geriatric, UIC, Chicago, IL.<br />
Supported By: No financial support provided<br />
Introduction: Myoclonus is a brief, involuntary twitching of a<br />
muscle or a group of muscles characterized by spastic-ballistic disabling<br />
jerking movements. It describes a medical sign and is not itself<br />
a diagnosis. While respiratory myoclonus associated with galantamine<br />
has been previously described, generalized myoclonus second to<br />
galantamine use has not been described before in the published geriatric<br />
literature.<br />
Case: A 87-year-old male with vascular dementia was started on<br />
galantamine for dementia. Four months later, at 16mg dosing, the<br />
caregiver reported that the patient started to experience a fine right<br />
hand tremor, but refused further work-up at the time. The patient<br />
continued on galantamine 16 mg. Nine months after galantamine<br />
therapy was started, the patient came to the clinic complaining of a<br />
new disabling movement disorder. The movements first started three<br />
months previous, as infrequent, short, brief jerks. These episodes did<br />
not follow a day cycle pattern or involve loss of consciousness. On<br />
clinical exam, high amplitude, frequent, multifocal myoclonus was observed.<br />
These jerks involved the whole body; however they were<br />
more prominent in the upper extremities. After discussion with a<br />
movement disorder specialist, who assisted in the assessment, galantamine<br />
was identified as a possible cause of myoclonus. Subsequent<br />
laboratory work-up for other causes was negative. Two weeks after<br />
stopping galantamine all movement symptoms had successfully disappeared,<br />
confirming the suspicion.<br />
Discussion:<br />
In the geriatric practice we see a number of conditions that can<br />
cause generalized myoclonus. Few of these conditions are reversible.<br />
This case report suggest that when we see a patient present with generalized<br />
myoclonus we should consider the possibility of galantamine<br />
induced myoclous, as it is easily reversible. It is important to note that<br />
the development of myoclonus was not abrupt, as might be expected<br />
in a drug reaction. Rather, the myoclonus worsened over the course<br />
of several months while on treatment. However, the rapid resolution<br />
of symptoms after galantamine withdrawal implicated it as a cause.<br />
The insidious onset and progression of myoclonus, as seen in this<br />
case, may hinder recognition of galantamine as a cause. We would encourage<br />
physicians treating generalized myoclonus to consider galantamine<br />
as a possible reversible cause.<br />
C30<br />
Bilateral pulmonary emboli in a patient with renal angiomyolipoma.<br />
G. Ratnarajah, D. Seminara, A. Szerszen . <strong>Geriatrics</strong>, Staten Island<br />
University Hospital, Staten Island, NY.<br />
Renal angiomyolipoma is a benign hamartoma that can rarely<br />
extend into the renal vasculature and subsequently into the inferior<br />
vena cava (IVC) . An even more rare occurrence is embolism of the<br />
tumor from the IVC into the pulmonary circulation<br />
A 72 year old lady with a history of hypertension was found to<br />
have renal insufficiency on routine evaluation by her private medical<br />
doctor. Her physical examination was unremarkable and workup of<br />
the renal insufficiency revealed a mass in the left kidney by ultrasound.<br />
Further inquiry of this renal mass was undertaken with abdominal<br />
computerized tomography ( CT ) scan which revealed a left<br />
sided renal mass with extension into the left renal vein; a preliminary<br />
diagnosis of renal angiomyolipoma was made. The scan also showed<br />
suspicion for a loculated effusion of the left lung. A chest CT scan was<br />
then performed to investigate the pleural effusion which incidentally<br />
revealed bilateral pulmonary emboli. In addition, the right sided embolus<br />
was seen to contain macroscopic fat.<br />
On admission to the hospital, the patient denied any chest pain,<br />
shortness of breath, abdominal pain, or hematuria. Her physical examination<br />
was unremarkable with no signs of tachycardia, fever, hypoxia,<br />
or petechiae. Her labs were significant for a glomerular filtration<br />
rate of 39 ml/min/1.73 m 2 . An echocardiogram was performed<br />
which revealed no signs of right ventricular strain pattern. The patient<br />
was started on intravenous heparin and the decision was made to<br />
bridge her with Coumadin therapy upon discharge. An open radical<br />
nephrectomy was planned on an outpatient basis.<br />
In conclusion, we present an asymptomatic elderly patient with<br />
bilateral pulmonary emboli from renal angiomyolipoma. The extension<br />
of renal angiomyolipoma into the renal vasculature is an uncommon<br />
entity. In these patients, clinicians should be aware of the complication<br />
of embolization and consider further workup to rule out<br />
pulmonary embolism.<br />
C31<br />
Cerebral Infarction: A Rare Presentation of Cryptococcal<br />
Meningoencephalitis in an Immunocompetent Patient.<br />
I. P. Resurreccion. Medicine, UAB Montgomery, Montgomery, AL.<br />
Cerebral cryptococcosis is common fungal opportunistic infection<br />
in immunocompromised, but a rare disease in immunocompetent<br />
patients. We report an unusual case of CNS cryptococcosis as<br />
cerebral infarction in an immunocompetent patient.<br />
A 78-year-old Caucasian male with hypertension, hyperlipidemia<br />
and osteoarthritis was admitted with confusion, left-sided<br />
weakness, dizziness, falls, headache and anorexia. No head trauma nor<br />
fever. On physical, he was disoriented to time and place and decreased<br />
strength on the left side with preserved sensation. Brain CT<br />
was negative. Brain MRI showed subacute infarct in anterior right<br />
middle cerebral territory. Lumbar puncture had normal opening pressure,<br />
showed 18 WBC with 100% mononuclears, high protein<br />
82.5mg/dL, low glucose 18mg/dL, positive India ink and cryptococcal<br />
antigen titer 1:1024. CSF culture grew Cryptococcus neoformans.<br />
HIV screening was negative. Induction therapy initiated with liposomal<br />
amphotericin and flucytosine. He continued to have altered mental<br />
status and headache. He was planned for another lumbar puncture<br />
every 2 weeks or earlier to relieve headaches. He continued to deteriorate<br />
with multi-organ failure and died.<br />
Cerebral infarction is an unusual presentation of CNS cryptococcosis.<br />
Rarely, cryptococcus can cause cerebral infection in immunocompetent<br />
patients. Manifestations include fever, headache, altered<br />
mental status, personality changes and memory loss. Lumbar<br />
puncture is useful for diagnostic and therapeutic. Opening pressure is<br />
elevated and CSF has elevated protein, low glucose with positive<br />
India ink stain, cryptococcal antigen titer and culture. Treatment includes<br />
induction therapy with amphotericin B and flucytosine. Duration<br />
in patients without neurological complications with a negative 2<br />
week CSF culture is 4 weeks and in patients with neurological complications<br />
is 6 weeks. Consolidation therapy with fluconazole is 8<br />
weeks. Maintenance therapy is 6-12 months. The incidence of cerebral<br />
infarction due to cryptococcal meningitis in HIV-negative patients is<br />
4%. Mechanisms include antigen-antibody complexes with vasculitis<br />
and direct toxic effects of viral antigen on vascular endothelium. Poor<br />
prognostic factors are cerebral infarcts, high opening pressure, CSF<br />
WBC