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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

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