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General Data

General Data. 24 years old Female Single Marilao , Bulacan Chief Complaint Weakness of both lower extremities. History of Present Illness. History of Present Illness. History of Present Illness. ADMISSION. Past Medical History.

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General Data

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  1. General Data • 24 years old • Female • Single • Marilao, Bulacan • Chief Complaint Weakness of both lower extremities

  2. History of Present Illness

  3. History of Present Illness

  4. History of Present Illness ADMISSION

  5. Past Medical History • (+) Primary complex at 2 years old, treated for 3 months only • No DM, HPN, asthma • No allergies • No previous surgeries

  6. Obstetrical History • G0P0 • Menarche: 12 years old • Interval: 28-30 days • Duration: 4-5 days • Amount: 3 pads per day, fully soaked • Symptoms: Occasional dysmenorrhea • LMP: November 20, 2008 • PMP: October 22-25, 2008 • 1st sexual contact at 18 years old • 2 sexual partners • No post coital bleeding, no dyspareunia, no family planning methods used

  7. Family History • (+) HPN, asthma, PTB – father • No DM, cancer

  8. Personal & Social History • Non-smoker • Occasional alcohol beverage drinker

  9. Physical Examination • Conscious, coherent, not in distress • BP 110/70mmHg PR 85bpm RR 20cpm T37.3°C • Warm, moist skin, no active dermatoses • Pink palpebral conjunctivae, anicteric sclera • Supple neck, no palpable cervical lymphadenopathies • Adynamic precordium, AB 5th LICS MCL, no murmurs • Symmetrical chest expansion, clear breath sounds

  10. Physical Examination • Globular abdomen, NABS, bulging flanks, (+) fluid wave, (+) shifting dullness, soft, non-tender, no palpable masses • Abdominal circumference: 87cm • DRE: No fissures/anal lesions, tight sphincteric tone, no pararectal tenderness, smooth rectal mucosa, lower pole of masses cannot be appreciated, no blood on examining finger

  11. Physical Examination • External genitalia: No gross lesions • IE • Cervix firm, long, closed; • Uterus normal sized, pushed posteriorly; • (+) 6x5cm firm, slightly fixed, non-tender mass, right, seemingly anterior to the uterus • (+) 5x4cm firm, slightly fixed, non-tender mass, left, seemingly anterior to the uterus

  12. Neurologic Examination • Conscious, coherent, oriented to 3 spheres • Pupils 2-3mm ERTL, (+) direct and consensual light reflex • EOMs full and equal, no visual field cuts • No gross facial asymmetry, can frown, puff cheeks, raise eyebrows • (+) gag reflex • Can turn head side to side with resistance, tongue midline on protrusion • No atrophy, no fasciculations, no spasticity • MMT 5/5 on both upper extremities; 0/5 on both lower extremities • Can do FTNT and APST with ease • DTRs ++ both upper extremities, hyperreflexia on both lower extremities • 100% sensory deficit T9 below, 20% sensory deficit T8, 30% sensory deficit T7; intact sensory T6 and above • (+) Babinski, bilateral

  13. Salient Features

  14. Course in the Ward

  15. Course in the Ward

  16. Course in the Ward

  17. Course in the Ward

  18. Course in the Ward

  19. Course in the Ward

  20. Course in the Ward

  21. Course in the Ward

  22. Laboratories & Ancillaries

  23. Peripheral Smear (D25): hypochromic RBC with anisocytosis, no abnormal WBC seen • D5: AFP – 2.67 ng/mL (0-7) Beta HCG – 0 mIU/mL (non-pregnant: 0-2.9) CA 125 – 297.6 U/mL (0-35) • Sputum GS (D26): g(+) cocci singly in pairs and in clusters: ++ g(-) bacilli: +++ g(+) yeast-like cells: few PMNs: >25/lpf Squamous epithelial cells: >25/lpf

  24. MRI of the Whole Spine • Epidural soft tissue mass at level of C7-T8 producing severe compression of the spinal cord • Paravertebral soft tissue densities observed at level of lower cervical, mid and lower thoracic, lower lumbar and sacrum • Patchy areas of abnormal marrow signals seen in vertebrae, iliac bone, and femoral heads

  25. MRI of the Whole Spine • Solid soft tissue masses demonstrated, largest measuring 5.1 x 5.6 in transverse and vertical dimensions • Visualized portion of stomach thickened • Cervical alignment straightened, unremarkable craniocervical junction, visualized brain shown no abnormality, normal alignment of thoracic and lumbar spine, conusmedullaris ends at L1 • No abnormal enhancement in the pelvis and spine

  26. TransvaginalSonography • Normal sized uterus • Proliferative endometrium • Adnexal masses, bilateral; consider ovarian newgrowths • Minimal ascites

  27. Single-contrast barium enema Upper GI series with small intestinal series Unremarkable UGIS with small intestinal follow through • No significant findings

  28. Differential Diagnosis

  29. CaudaEquina Syndrome • Caudaequina (CE) – formed by nerve roots caudal to the level of spinal cord termination • Caudaequina syndrome (CES) – results from mechanical compression of cauda • Nerve root lesion (peripheral nerve injury) • Irreversible • Presents with the following: • Back pain • Unilateral or usually bilateral sciatica • Saddle sensory disturbances • Bladder and bowel dysfunction • Variable lower extremity motor and sensory loss

  30. Intramedullary Spinal Cord Abscess • Mechanisms of infection: • Hematogenousspread from an extraspinal focus of infection • Contiguous spread from an adjacent focus of infection • Direct inoculation (i.e., penetrating trauma, post-neurosurgery) • Cryptogenic mechanisms (i.e., no documented extraspinal focus of infection) • Fever • Radiculopathic pain • Neurologic deficit

  31. Spinal Epidural Abscess • Hematogenous spread with seeding of epidural space is the suspected source of infection • The expanding suppurative infection can compress the spinal cord • Produces motor and sensory dysfunction • Depending on location it can ultimately lead to paralysis and even death • Staphylococcus aureus: most common pathogen

  32. Pott’sDisease • Also known as tuberculousspondylitis • Back pain is the earliest and most common symptom • Almost all have some spine deformity • The basic lesion is a combination of osteolyelitis and arthritis that usually involved more than one vertebra • Progressive bone destruction leads to vertebral collapse • Abscesses, granulation tissue or direct extension of lesion can compress spinal cord

  33. Amyotrophic Lateral Sclerosis • Familial (autosomal dominant) and sporadic forms (90-95% of cases) • Motor axons die by Wallerian degeneration, large motor neurons are affected to a greater extent • Death of the anterior horn cell body, leading to degeneration • F>M (2.1:1.5) • Peak age at onset occurs from 55-75 years (mean: 62) • Muscle weakness usually is asymmetric • Signs of mixed upper and lower motor neuron involvement • In patients with bulbar involvement, speech may be impaired

  34. Multiple Myeloma • Spinal cord compression is one of the most severe adverse effects • As many as 20% develop spinal cord compression • Symptoms include: back pain, weakness, paralysis in the legs, numbness, dysythesias in the legs • Frequent complication: pathological function

  35. Non-Pharmacologic Management

  36. Rehabilitation • Spinal Orthotics – stabilize patients spine and decrease spinal pain by limiting motion • Prophylactic fixation of upper extremity lesions to aid mobility and weight bearing

  37. Psychologic Interventions • Patient preparation • Patient may complain of issues such as loss of independence • Emotional support • Family participation

  38. Pharmacologic Management

  39. Symptomatic Therapy • Constipation, spinal instability, pain, and psychological and social distress • Constipation arises in these patients from autonomic dysfunction, inactivity, and opioids • Must be treated aggressively because the pain of cord compression increases with a Valsalvamaneuver, such as straining at stool • Osmotic agents, such as polyethylene glycol 3350 (MiraLax), are often needed in addition to stool softeners and stimulants to promote regular, soft stools

  40. Control of pain: opioidsand adjuvants for nerve and bone pain • Corticosteroids are effective adjuvants • NSAIDs for those unable to take corticosteroids

  41. Corticosteroids • Used most commonly in patients that develop spinal cord compression with neurologic deficits • Glucocorticoids with antioxidant or antioxidant-like activity (such as methylprednisolone) • Reduce the release of total free fatty acids (including arachidonic acid) and prostanoids and prevent lipid hydrolysis and peroxidation, thereby reducing injury from traumatic spinal cord injury • Dexamethasone I • Inhibits PGE2 and VEGF production and activity and, as a consequence, decreases ischemic edema, which is partially mediated by increased levels of PGE2 and VEGF

  42. Studies in animal models indicate a dose-dependent response of vasogenicedema to corticosteroids, even without radiation therapy • High doses of corticosteroids • better than low doses in reversing edema and improving neurologic function • Loading dose of 10 to 100 mg is administered, followed by a 16- to 96-mg/day maintenance dose • High doses have been recommended (100 mg loading dose followed by 24 mg every 6 hours × 3 days) to quickly restore ambulation, although may increase the incidence of serious adverse effects • Adverse effects of steroids • insomnia, increased appetite, edema, hyperglycemia, leukocytosis, increased risk of infection, and gastrointestinal bleeding

  43. 21-aminosteroids e.g. U-74006F • 21-aminosteroids that lack glucocorticoid or mineralocorticoid activity • These potent inhibitors of lipid peroxidation for the acute treatment of central nervous system trauma and ischemia • Inhibit the release of free arachidonic acid from injured cells

  44. Analgesics • Opioid and non-opioid • Mild pain • Nonsteroidalanti-inflammatory drugs (NSAIDs) and acetaminophen are • Acetaminophen-preferred in patients with thrombocytopenia, renal dysfunction, those receiving nephrotoxic agents, or at risk for gastrointestinal bleeds • In patients with liver dysfunction, NSAIDs are preferred for mild pain

  45. Analgesics • Moderate to severe pain • Opioid analgesics • begin with low doses of immediate release agents (typically 5-15 mg per os morphine or 2-4 mg intravenous morphine) • Reassess patient every 1 to 2 hours for effect • After 24 hours of pain control on a short-acting regimen, patients should be converted to a long-acting agent (morphine, oxycodone, fentanyl, or methadone).

  46. “ Radiation therapy is also the standard of care. Radiotherapy is delivered to the site of disease and to one or two levels above and below. It is typically given as 3,000 cGy in 10 300-Gy fractions. With this regimen, 50% of patients are able to walk again, Dr. Wen noted” management of spinal cord compression, journal of supportive oncology, volume 6, 2008

  47. Prognosis • Dependent upon histology • Better outcome with early diagnosis and treatment • Permanent disability is likely

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