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Case Management

Case Management. JC. 39/ F From Ermita , Manila DOA: December 8 2009 Married Right handed Roman Catholic Non-hypertensive, non-diabetic, non-asthmatic Chief complaint: Difficulty of breathing. JC’s Profile.

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Case Management

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  1. Case Management

  2. JC • 39/ F • From Ermita, Manila • DOA: December 8 2009 • Married • Right handed • Roman Catholic • Non-hypertensive, non-diabetic, non-asthmatic • Chief complaint: Difficulty of breathing

  3. JC’s Profile • Known case of Multiple Sclerosis (MS) in 2006 (PGH), supported by MRI and CSF studies • Had 3 admissions for MS relapse • Previous admissions: • July 2006 • November 2008 • November 2009 • Maintenance medication: • Polyneuro 1000 mg/tab OD • Gabapentin 400 mg/cap at HS

  4. History of Present Illness 3 days PTA • Patient noted sudden onset difficulty of breathing slightly relieved by O2 supplementation • (+) light-headedness, nonvertiguous dizziness, and anorexia • No headache, no weakness, no numbness, no vomiting, no chest pain, no blurring of vision, no slurring of speech

  5. History of Present Illness 2 days PTA • Persistence of previously mentioned symptoms • Inability to move right upper extremity up to the right hand and fingers • Dysphonia • Dysarthria • No numbness, paresthesia, shooting pain • Consult at PGH and admission

  6. Review of Systems • (-) headache, seizure, loss of consciousness • (-) fever, cough, colds • (-) vomiting, abdominal pain • (-) orthopnea, palpitations, PND • (-) dysuria, bowel changes • (-) petechiae, ecchymoses, edema, cyanosis, erythema, pruritus

  7. Past Medical History • (-) Hypertension • (-) Diabetes • (-) Bronchial Asthma • (-) PTB • 3 previous admissions in PGH for Multiple Sclerosis relapse • s/p Tracheostomy in 12/2008 for Acute respiratory failure

  8. Family History • No known case of Multiple Sclerosis • No family member presenting with similar symptoms • (-) Hypertension • (-) Diabetes • (-) BA • (-) PTB • (+) stroke - uncles

  9. Personal and Social History • Married and unemployed • Graduate of Commerce • Lives with husband and younger sister in Ermita Manila • Non-smoker • Non-alcoholic beverage drinker • Bed bound and wheelchair borne • Needs assistance on ADLs (self-care, transfer, bathing) • Able to feed herself

  10. Menstrual and Obstetric History • Menarche: 12 y/o • G 1 P 1 (1001), SVD • Menstruation : RMI interval, 3-5 duration, 3 pads per day, (+) dysmenorrhea

  11. Physical Examination • Awake, coherent, conversant • With tracheostomy tube, tracheostomy tube in place • MV setting: RR 16, PEEP 60, FiO2 40% • Can tolerate brief periods of room air, but still unable to tolerate weaning from MV • Dysphonic • Not in respiratory distress • Spontaneous eye opening, oriented, follows commands

  12. Physical Examination • BP 110-160 / 90-100 • HR 92-100 • RR 24 • T 38 – 39.5 ‘ C (since 5 days ago)

  13. Physical Examination

  14. Neurologic Examination • Awake, conscious, coherent, conversant but dysphonic • GCS 15: Spontaneous eye movement, oriented to time/place/person, follows commands • Good recent and remote memory • Scored 30/30 in MMSE • (-) dyscalculia, (-) Right to Left confusion

  15. Neurologic Examination Cranial Nerves: • II -VA – finger counting OU; 3 mm EBRTL D & C; (+) RAPD; Funduscopy: (+) ROR, clear media, (-) papilledema (-) disc atrophy, • III, IV, VI - 1˚ gaze midline, EOMS full and intact • V - good corneal reflex, intact sensory V1, V2, V3 • VII - no facial asymmetry • VIII - Good gross hearing • IX, X - Good gutturals, fair gag, midline uvula • XI – Weak shoulder shrug R>L • XII - Tongue midline

  16. 3++ 3+ 3+ 3++ Neurologic Examination • MMT • Sensory exam • Generalized atrophy, more extensive at Bilateral lower extremities • Hypertonic Right LEx, hypotonic Right UEx • ( - ) Babinski, ( - ) clonus • ( + ) abdominal reflex

  17. Neurologic Examination • (-) nystagmus • (-) dysmetria • (-) dysdiadochokinesia • (-) Kernig sign • (-) Brudzinski • (-) nuchal rigidity • (-) abnormal sweat pattern

  18. Past Working Impression Multiple Sclerosis in relapse Acute respiratory Failure 2’ MS • s/p MPPT (12/2009) • s/p Tracheostomy (12/2009)

  19. 12/8/09 Admitted Course in the Ward 12/25/09 MPPT 12/12/09 BT 1 pack pRBC 01/08/10 Unable to wean ETA CS: P. aeruginosa 02/01/10 Febrile 38-39 Ertapenem Ciprofloxacin January 12/10/09 Febrile rhonchi December • February 1/2/10 MRI: Patchy areas of intrinsic signal abnormalities within the cervico-medullary junction and cervical cord (@ C3-4 level), associated w/ patchy contrast enhancement consistent w/ M.S. No associated cord expansion. No evidence of cord compression 12/11/09 Self-extubated and reintubated 02/11/10 Given Doripenem 12/9/09 Intubated Referral to Pulmo and Rehab 02/08/10 U/A: WBC : 30-35 Urine GS: NG2D Trach CS: NG2D Blood CS : NG2D 12/13/09S s/p Tracheostomy

  20. Current Working Impression • Multiple Sclerosis, in relapse • Optic neuritis • t/c HAP, VAP, UTI • s/p MPPT (12/2009) • s/p Tracheostomy (12/2009)

  21. Discussion

  22. Multiple Sclerosis • Autoimmune disease • Inflammatory response on myelin sheath • Triad: Inflammation, demyelination and gliosis • Course • relapsing-remitting • Progressive • Initially remitting then becomes progressive

  23. ETIOLOGY • Cause is still unknown • Identified factors: • Autoimmune causes • Human Leukocyte Antigens • Viral causes • Roseola virus

  24. PATHOPHYSIOLOGY Viral infection and autoimmune CNS reaction resulting to abnormal expression of autoantigens (MBP) T-cell sensitization to myelin Demyelination Macrophage infiltration and adhesion to endothelial cells Astrocytes increase in number and size Think, matted fibroglial tissue Wallerian degeneration of axons Partial remyelination or cavitation

  25. Pathogenesis • Etiology • Neural antigens are processed by antigen presenting cells in lymph nodes and presented to T cells • Sensitized memory T cells migrate to the CNS, where they are reactivated by antigen presenting macrophages • Proinflammatory cytokines are secreted. Enhance expression of adhesion molecules by vascular endothelium, alter permeability of the blood-brain barrier, and induce a second wave of inflammatory cell recruitment • Inflammatory response leads to localized demyelination

  26. PATHOPHYSIOLOGY • Scattered areas of demyelination= • “Plaques” • Plaques are more common in: • Optic tracts • Spinal cord • Brain stem • Basal Ganglia • Neurologic Deficits of our patient: • VA at Counting finger, OU • MMT 4/5 for bilateral upper extremities • MMT 0/5 for bilateral lower extremities • Sensory loss 70% in upper extremities • Sensory loss 100% in lower extremities • Dyspnea and repeated respiratory failure • No tremors, chorea

  27. Neurologic Emergency • Multiple Sclerosis • typically progresses over decades • presenting with mild symptoms and some exacerbations • In some cases, however, it can progress so rapidly as to lead to major exacerbations and even sudden onset of symptoms and death in the course of a few days.

  28. MS Variants Relapsing Remitting Multiple Sclerosis • Classic MS clinical pattern with exacerbations and improvement • 2/3 of cases are female

  29. MS Variants Secondary Progressive • 80% of relapsing remitting MS go on to this stage where there is disease progression and decreasing amounts of remission • Represents the late stage of the relapsing remitting MS type

  30. MS Variants Primary Progressive • Later onset (>40 years of age) • Insidious progression of disability affecting the spinal cord • MRI scans may show normal findings or only cord atrophy

  31. MS Variants Devic Syndrome (NeuromyelitisOptica) • Optic neuritis and transverse myelitisoccuring in a short time span • Little or no involvement of other parts of the CNS • May progress to relapsing remitting type • Unclear as to whether a variant of MS or a distinct disease

  32. MS Variants Marburg Disease • Acute Fulminant MS • Severe, unrelenting, progressive demyelinating disease • Leads to death in a few months or years

  33. MS Variants Balo Concentric Sclerosis • Agressive variant leading to death in a few weeks to months • Large plaques of demyelination with concentric bands of regenerated myelin • Regenerated myelin is only evident in very rapid disease

  34. MS Variants Acute Disseminated Encephalomyelitis • Monophasicdemyelinating disorder • Typically follows a viral infection • Rapid onset leading to confusion, fever and depressed consciousness • Can be fatal in days to weeks • Acute onset of motor, sensory, cerebellar, and cranial nerve dysfunction with encephalopathy, progressing to coma and eventual death in 30% of such cases

  35. Neurologic Emergency The majority of MS patients are sent to the emergency due to relapse of the previously managed condition or an acute exacerbation of the symptoms.

  36. Presentations Acute Transverse Myelitis Optic Neuritis Acute Disseminated Encephalitis

  37. Clinical Presentations Multiple Sclerosis Sensory Loss Motor (eg, muscle cramping secondary to spasticity) Autonomic (eg, bladder, bowel, sexual dysfunction) Cerebellar symptoms (eg, Charcot triad of dysarthria, ataxia, tremor) Constitutional symptoms (fatigue and dizziness) Subjective difficulties with attention span, concentration, memory, and judgment Depression 5-10% of patients develop an overt psychiatric disorder (eg, manic depression, paranoia, major depression) or dementia Eye symptoms (diplopia) Trigeminal neuralgia

  38. Clinical Presentations • Optic Neuritis • Demyelination of the optic nerve • 50% of patients with ON have MS • Unilateral blurring of vision, decreased acuity and color perception, discomfort • Phosphenes, Uhthoff phenomenon, Pulfrich effect

  39. Multiple Sclerosis as a Sole Symptom is Unusual • patients with MS often present with the other MS presentations such as • Aphasia or dysphasia • Hemianopsia • Seizures (5% of patients with MS) • Significant motor complaints without sensory deficits or dysautonomia (eg, bladder)

  40. Physical Examination • Eye Findings • Optic Neuritis • Impaired visual acuity • Optic atrophy • Papillitis • Afferent papillary defect in affected eye • Incomplete or slow eye movements • Nystagmus • Abnormal papillary responses

  41. Physical Examination • Spinal Cord Involvement • Acute transverse myelitis • Sphincter paralysis and unchanging level • Paralysis, spasticity and hyperreflexia • Decreased joint position and vibration sense • Decreased pain and temperature • Bladder, bowel and sexual dysautonomias

  42. Physical Examination • Cerebellar Findings • Disequilibrium • Truncal or limb ataxia • Scanning (ie, monotonous) speech • Intention tremor • Saccadic dysmetria • Lhermitte sign • Neck flexion results in an electric shocklike feeling in the torso or extremities

  43. Physical Examination • Acute disseminated encephalitis • Altered mental status and/or personality changes • Cranial nerve defects • Hemiparesis • Focal seizures • Autonomic dysfunction • Cranial nerve defects • Ataxia • Dysphasia • Meningismus –symptoms of meningeal irritation without actual inflammation

  44. Treatment Goals • Management of acute excaerbation • Modify disease progression • Symtomatic control • MS IS NOT CURABLE!

  45. Management of acute exacerbations • Glucocorticoids: reduce severity and shortens duration of attacks, suppress PML migration • IV methylprednisolone 500-1000mg/d 3-5 days ± oral prednisone 60-80 mgd • Plasmapheresis (7 exchanges: 54ml/kg every other day for 14 days • costly

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