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SHIP Cases

SHIP Cases. Beverly M. Wilson, MD August 18, 2011. Presentation. 32 year old CF presents your ER with rapidly developing pain and visual impairment in her Left eye Pain worse with eye movement Blurred vision Also notices a change in color perception Has transient flashes of light

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SHIP Cases

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  1. SHIP Cases Beverly M. Wilson, MD August 18, 2011

  2. Presentation • 32 year old CF presents your ER with rapidly developing pain and visual impairment in her Left eye • Pain worse with eye movement • Blurred vision • Also notices a change in color perception • Has transient flashes of light • No ocular discharge, no erythema • Recently had URI with RN and ST in the last week.

  3. PMH: • Depression • Allergic Rhinitis • Migraines • RLS • DDD & Back pain secondary to Car accident as teen • PSH: • Tubal ligation • Thumb surgery

  4. Soc Hx: • Divorced • Has three children • Currently unemployed • Former smoker • No drug use • Rare etoh • Family Hx: • No family history of ocular or neurological disease

  5. Home Meds: • Maxalt • Claritin • ProAir • Flexeril • Gabapentin • Phentermine • Fluoxetine • Amitriptyline • Lortab • Fluticasone Allergies NKDA

  6. ROS: • General: Fevers, Fatigue, Usual Migraines • HEENT: as in HPI plus runny nose last week • CV: none • Resp: none • GI: none • GU: none • Musk: occ weakness in left hand • Skin: none • Neuro: occ numbness in left hand

  7. Vitals: • Ht: 5’5” Wt: 239 lbs • Temp: 101.2 • BP: 109/74 • Pulse: 104 • Sat: 97% RA

  8. Physcial Exam: • Snellen40/20 L eye. 20/20 R eye • Tonometry: 14mmHg (Normal 10 mm Hg to 21 mm Hg) • General: A&Ox3. NAD. overweight • HEENT: nmlfundus, normal exam except EOM difficult to ascertain and mild afferent pupillary defect • CV: RRR • Resp: CTAB • ABD: ND, NTTP, soft, +BS, No HSM • Musk: 4/5 grip strength L hand • Skin: no rashes

  9. Lab & Imaging • CBC : normal • CMP: normal • B12, ESR, ANA, TSH, RPR all normal • Imaging?

  10. Differential Diagnosis ???????????

  11. Differential Diagnosis • Retinal Artery Occlusion • Glaucoma, angle closure vs open angle • Ocular HSV • Viral Optic Neuropathy • Sarcoidosis Associated ON • Optic Neuritis

  12. Optic Neuritis • Optic neuritis (ON) is a demyelinating inflammation of the optic nerve. • Many cases of ON are associated with multiple sclerosisbut ON can occur in isolation. • In cases associated with MS, ON is commonly the first manifestation of the chronic demyelinating process. • Up to 75% of female patients initially presenting with ON ultimately develop MS. • Occasionally, can be due to an infectious process involving the orbits or paranasal sinuses or occur in the course of a systemic viral infection

  13. Special Testing • MRI (brain and orbit MRI) • Enhancement of Left Optic Nerve and very subtle few millimeter solitary focus of right parietal lobe with enhancement. • To test for lesions and examine the optic nerve and orbits, an MRI should be performed routinely within the first 2 weeks of symptom onset. • Lumbar puncture? • A lumbar puncture is useful — especially in patients with normal findings on brain MRI — to test for oligoclonal banding of proteins in CSF. The presence of oligoclonal banding of proteins in the CSF is predictive of a high risk of MS.

  14. LP: • clear fluid • Glucose: 65 (normal 50-80mg/dl) • Protein: 60 (normal 15-45mg/dl) (oligoclonal bands present on EP) • Cells: 0-3 rbc, 0-3 wbc

  15. Optic neuritis • In the Optic Neuritis Treatment Trial (ONTT), patients recovered visual function regardless of whether they were treated with oral prednisone, intravenous methylprednisolone (IVMP), or placebo. • However, although it did not change the final visual outcome, IVMP hastened the rate of recovery. It also seemed to decrease the incidence of the development of MS over a 2-year period, but this effect was not sustained after year 3. • IV immunoglobulin (IVIG) treatment of acute ON has been shown to have no beneficial effect.

  16. Multiple Sclerosis • Multiple sclerosis (MS) typically presents in adults who are 20 to 45 years of age. Occasionally, the disease presents in childhood or late middle age. • Twice as many women are affected as men, and persons of Northern European descent appear to be at highest risk for the disease.

  17. Multiple Sclerosis • Clinical: • Episodic, relapsing-remitting neurologic symptoms in a young adult (typically) • Neurological symptoms disseminated in time & space • Common presentations: monocular visual disturbances (optic neuritis), paresthesias/weakness (myelitis), incoordination (cerebellar), and/or diplopia (brainstem) • Labs:Oligoclonal bands positive, MBP (myelin basic protein) elevated • Not specific, new tests improving sensitivity/specificity • MBP elevated in various disease processes • MRI: T2 intense foci in white matter, periventricular lesions, involve corpus collosum

  18. Multiple Sclerosis • Relapsing-remitting MS (RRMS): • Most common • 85% of MS initially diagnosed • Partial or total recovery between attacks • Secondary-progressive MS (SPMS): • RRMS course, but becomes gradually progressive • Attacks & partial recoveries may continue to occur • Over 60% initially RRMS progress to SPMS in 10 yrs • Does not seem to be responsive to Disease modifying agents

  19. Multiple Sclerosis • Primary-progressive MS (PPMS): • Progressive from onset • Symptoms generally do not remit • Progressive disability w/o acute attacks • 10% of MS initially diagnosed • Primary-relapsing MS (PRMS): • Same as PPMS, but with acute attacks • Less than 5% of those with MS

  20. Multiple Sclerosis • The Uhthoff phenomenon • Exacerbation of symptoms induced by exercise, a hot meal, or a hot bath

  21. Treatment • Initiation of Early Therapy • Accumulating evidence indicates that the best time to initiate disease-modifying treatment is early in the course of MS. • Data indicate that irreversible axonal damage may occur early in relapsing-remitting MS and that drug therapies appear to be more effective in preventing new lesion formation than in repairing old lesions. • With disease progression, the autoimmune response of the disease may become more difficult to suppress. • The National Multiple Sclerosis Society supports the initiation of immunomodulating therapy at the time of diagnosis.

  22. Treatment • Adrenal Corticosteroids • Corticosteroids are the mainstay of symptomatic relief for an acute relapse of MS. • work through: • immunomodulatory and anti-inflammatory effects • restoration of the blood-brain barrier • reduction of edema • also may improve axonal conduction • Shortens the duration of acute relapses and accelerates recovery. • Not been shown to improve the overall degree of recovery or to alter the long-term course of MS.

  23. Treatment • Adrenal Corticosteroids • If a patient is having acute disability from an attack, the physician should consider treatment with a three- to five-day course of intravenous methylprednisolone (or equivalent corticosteroid) in a dosage of 1 g administered intravenously in 100 mL of normal saline over 60 minutes once daily in the morning.

  24. Treatment • DISEASE-MODIFYING THERAPIES • Four disease-modifying therapies: • intramuscular interferon beta-1a (Avonex) • subcutaneous interferon beta-1a (Rebif) • interferon beta-1b (Betaseron) • glatiramer acetate (Copaxone) • A fifth agent, mitoxantrone (Novantrone), has been approved by the U.S. Food and Drug Administration (FDA) for the treatment of worsening forms of relapsing-remitting MS and secondary progressive MS

  25. Treatment Symptomatic Therapies for Multiple Sclerosis Symptoms Spasticity • Baclofen (Lioresal), 10 to 40 mg three times daily; in high doses, can cause weakness and fatigue • Tizanidine (Zanaflex), 2 to 8 mg three times daily; in high doses, can cause weakness and fatigue • Gabapentin (Neurontin), 300 to 900 mg three or four times daily; in high doses, causes fatigue Bladder urgency • Oxybutynin (Ditropan), 5 mg once daily to 20 mg per day in divided doses; causes dry mouth and can exacerbate glaucoma or worsen urinary retention • Tolterodine (Detrol), 2 to 4 mg twice daily; causes dry mouth and can exacerbate glaucoma or worsen urinary retention (these side effects occur less often than with oxybutynin)

  26. Treatment Depression • SSRIs preferred because of activating properties; can have sexual side effects • Alternatives to SSRIs when sexual side effects occur: extended-release venlafaxine (Effexor) 75 to 225 mg per day, or sustained-release bupropion (Wellbutrin), 150 mg per day to 150 mg twice daily • Third-line drug or for use when a patient has a sleep disorder or concomitant headaches: amitriptyline, 10 to 150 mg per day at bedtime Fatigue • Amantadine (Symmetrel), 100 mg twice daily; can cause rash, edema, and anticholinergic effects • Modafinil (Provigil), 100 to 200 mg given in the morning; can cause jittery sensation and palpitations • SSRIs, can have sexual side effects

  27. Treatment Pain and paroxysmal disorders • Gabapentin, 300 to 900 mg three or four times daily; in high doses, causes fatigue • Carbamazepine (Tegretol), 100 to 600 mg three times daily; in high doses, causes rash and neurologic side effects; requires monitoring of complete blood count and liver function Other anticonvulsants • Amitriptyline (Elavil), 10 to 150 mg per day at bedtime

  28. ~90% of patients ultimately diagnosed with MS initially present with a clinically isolated syndrome (CIS), such as optic neuritis. • MRI can be valuable in differentiating. • American Academy of Neurology: on value of MRI predicting eventual conversion of a clinically isolated syndrome to clinically definite MS: • >3 white-matter lesions in T2 MRI is sensitive predictor (>80%) of clinically definite MS within 7-10 years • In Normal MRIs, <20% will have 2nd attack w/in 10y

  29. No single test helps to establish or exclude a diagnosis of MS. Instead, MS is a clinical diagnosis supported by laboratory studies and neuroimaging findings. • A common misconception is that any attack of demyelination means a diagnosis of acute MS. When a patient has a first attack of demyelination, the physician should not rush to diagnose MS, because the differential diagnosis includes a number of other diseases. • Clinicians who specialize in MS commonly see patients referred for multiple, ill-defined, vague complaints who had recent head or spinal MRI scans in which T2 hyperintense lesions have been demonstrated. • Careful questioning in these cases reveals that symptoms have been stereotyped and vague or do not truly qualify as exacerbations (eg, scintillating scotomas in a patient with concomitant migraines, or symptoms consistent with carpal tunnel syndrome).

  30. Traditionally, MS cannot be diagnosed after only a single symptomatic episode; diagnosis requires the appearance of lesions separated in time and space. In the past, treating physicians were content to "sit back and watch" after a single episode, as it was assumed the disease would "declare" itself.

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