TB Meningitis

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  • Dear Cristal,Can you please mail me the presentation on drgoyaddc@gmail.com
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  • @AgustinaWulandari Thank you! Glad it helped. Unfortunately, the laptop with that file was stolen.
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  • you may send to this e-mail address: agustinaw81@gmail.com
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  • dear cristal ann laquindanum

    I really like your presentation
    i also have patient with the same case
    would you mind to share your power point to me
    cos i can get it from slide share
    thank you

    sincerely your
    Agustina Wulandari
    Indonesia
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  • CHANGE TITLE
  • CHANGE TO HEAD
  • CHANGE TO HEAD
  • CHANGE TO HEAD
  • CHANGE TO HEAD
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  • CT Plain axial images of head 5mm (posterior fossa) 10mm (suprasellar region) An ill-defined area of low attenuation is seen involving the head of the caudate nucleus, anterior limb of the internal capsule, lentiform nucleus, corona radiata and superior temporal lobe, all in the left. The adjacent frontal horn of the left lateral ventricle is partly compressed. The rest of the brain parenchyma appears normal with no other distinct lesion seen, the grey white matter interface is maintained. No acute intracranial hemorrhage or abnormal extra-axial fluid accumulation is noted. The ventricles are normal in size and configuration The cerebral sulci, sylvian fissures and basal cistern are intact. The midline structures are undisplaced. The sellaturcica and pineal gland are not unusual. The included paranasal sinuses, orbit, petromastoid, and bony calvaria are unremarkable. Impression: Non-specific area of hypodensity in the left as detailed above. Acute infarct may be considered (stroke in the young). Follow-up contrast CT or MRI is suggested.
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  • CT Plain and contrast enhanced (50 cc IV lopamino) There is an intense enhancement in the region of the basal cistern (more on the left side). Irregular enhancements are also noted in the left frontotemporal lobe and left basal ganglia conforming the previous seen areas of ill-defined hypodensities. The overlying sulci and left sylvian fissure are effaced. No new parenchymal lesion is identified. The grey white matter interface is maintained. No acute intracranial hemorrhage or abnormal extra-axial fluid accumulation is noted. The frontal horn of the left lateral ventricles is minimally displaced. The midline structure are undisplaced. The rest of the neurocranium remain essentially unremarkable.Impression: AV Malformation, differential diagnosis: meningitis and early cerebritis
  • CT Plain and contrast enhanced (50 cc IV lopamino) There is an intense enhancement in the region of the basal cistern (more on the left side). Irregular enhancements are also noted in the left frontotemporal lobe and left basal ganglia conforming the previous seen areas of ill-defined hypodensities. The overlying sulci and left sylvian fissure are effaced. No new parenchymal lesion is identified. The grey white matter interface is maintained. No acute intracranial hemorrhage or abnormal extra-axial fluid accumulation is noted. The frontal horn of the left lateral ventricles is minimally displaced. The midline structure are undisplaced. The rest of the neurocranium remain essentially unremarkable.Impression: AV Malformation, differential diagnosis: meningitis and early cerebritis
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  • Because of the inherent chronicity of the disease, signs of cranial nerve involvement (usually ocular palsies, less often facial palsies or deafness) and papilledema may be present at the time of admission to the hospital (in 20 percent of the cases). Occasionally the disease may present with the rapid onset of a focal neurologic deficit due to hemorrhagic infarction, with signs of raised intracra- nial pressure or with symptoms referable to the spinal cord and nerve roots. Hypothermia and hyponatremia have been additional presenting features in several of our cases.
  • Usually, the prodrome is nonspecific, including headache, vomiting, photophobia, and fever. In one study, only 2% of patients reported meningitic symptoms. The duration of presenting symptoms may vary from 1 day to 9 months, although 55% presented with symptoms of less than 2 weeks in duration.
  • The 1st stage, which typically lasts 1–2 wk, is characterized by nonspecific symptoms, such as fever, headache, irritability, drowsiness, and malaise. Focal neurologic signs are absent, but infants may experience a stagnation or loss of developmental milestones. The 2nd stage usually begins more abruptly. The most common features are lethargy, nuchal rigidity, seizures, positive Kernig or Brudzinski signs, hypertonia, vomiting, cranial nerve palsies, and other focal neurologic signs. The accelerating clinical illness usually correlates with the development of hydrocephalus, increased intracranial pressure, and vasculitis. Some children have no evidence of meningeal irritation but may have signs of encephalitis, such as disorientation, movement disorders, or speech impairment. The 3rd stage is marked by coma, hemiplegia or paraplegia, hypertension, decerebrate posturing, deterioration of vital signs, and eventually death. The prognosis of tuberculous meningitis correlates most closely with the clinical stage of illness at the time treatment is initiated. The majority of patients in the 1st stage have an excellent outcome, whereas most patients in the 3rd stage who survive have permanent disabilities, including blindness, deafness, paraplegia, diabetes insipidus, or mental retardation. The prognosis for young infants is generally worse than for older children. It is imperative that antituberculosis treatment be considered for any child who develops basilar meningitis and hydrocephalus, cranial nerve palsy, or stroke with no other apparent etiology. Often the key to the correct diagnosis is identifying an adult in contact with the child who has infectious tuberculosis. Because of the short incubation period of tuberculous meningitis, the ill adult contact has not yet been diagnosed in many cases.
  • The 1st stage, which typically lasts 1–2 wk, is characterized by nonspecific symptoms, such as fever, headache, irritability, drowsiness, and malaise. Focal neurologic signs are absent, but infants may experience a stagnation or loss of developmental milestones. The 2nd stage usually begins more abruptly. The most common features are lethargy, nuchal rigidity, seizures, positive Kernig or Brudzinski signs, hypertonia, vomiting, cranial nerve palsies, and other focal neurologic signs. The accelerating clinical illness usually correlates with the development of hydrocephalus, increased intracranial pressure, and vasculitis. Some children have no evidence of meningeal irritation but may have signs of encephalitis, such as disorientation, movement disorders, or speech impairment. The 3rd stage is marked by coma, hemiplegia or paraplegia, hypertension, decerebrate posturing, deterioration of vital signs, and eventually death. The prognosis of tuberculous meningitis correlates most closely with the clinical stage of illness at the time treatment is initiated. The majority of patients in the 1st stage have an excellent outcome, whereas most patients in the 3rd stage who survive have permanent disabilities, including blindness, deafness, paraplegia, diabetes insipidus, or mental retardation. The prognosis for young infants is generally worse than for older children. It is imperative that antituberculosis treatment be considered for any child who develops basilar meningitis and hydrocephalus, cranial nerve palsy, or stroke with no other apparent etiology. Often the key to the correct diagnosis is identifying an adult in contact with the child who has infectious tuberculosis. Because of the short incubation period of tuberculous meningitis, the ill adult contact has not yet been diagnosed in many cases.
  • Someone gets sick from TB every four seconds and someone dies of TB every ten seconds according to WHO.
  • Someone gets sick from TB every four seconds and someone dies of TB every ten seconds according to WHO.
  • aerobic gram-positive rod that stains poorly because of its thick cell wall that contains lipids, peptidoglycans, and arabinomannans.acid-fast Ziehl-Neelsen stain; Magnified 1000 X.
  • Tuberculin skin test is nonreactive in up to 50% of cases, and 20–50% of children have a normal chest radiograph. The most important laboratory test for the diagnosis of tuberculous meningitis is examination and culture of the lumbar CSF
  • Tuberculin skin test is nonreactive in up to 50% of cases, and 20–50% of children have a normal chest radiograph. The most important laboratory test for the diagnosis of tuberculous meningitis is examination and culture of the lumbar CSF
  • In any case suspected of meningitis based on the clinical signs, a lumbar puncture is essential. Sometimes parents are afraid of the procedure and fear it is harmful to the child. It should be emphasized to them that treatment is highly dependent on CSF results. A lumbar puncture may be postponed or withheld in the following situations: presence of significant cardiac or respiratory distress and shock, sign of increased intracranial pressure, infection in the area that the spinal needle will traverse to obtain CSF, and hematologic problems such as thrombocytopenia and coagulation defects.
  • Decreased glucoseLymphocyte predominanceIncreased WBCIncreased ProteinIncreased Pressure
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  • TB Meningitis

    1. 1. The Traitor Illness a TB Meningitis Case Presentation By: Cristal Ann G. Laquindanum Year Level 8 Ateneo School of Medicine and Public Health
    2. 2. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health Identifying data MF, 12 yr old female Pinagbuhatan, Pasig City Progressive weakness Informant reliability: <50%
    3. 3. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health History of Present Illne Chief complaint: progressive weakness MF, 12yF Pasig City > 3 weeks PTC •blurring of vision (diplopia) •headache not relieved by medications •Generalized weakness
    4. 4. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health History of Present Illne Chief complaint: progressive weakness MF, 12yF Pasig City > 3 weeks PTC •blurring of vision (diplopia) •headache not relieved by medications •Generalized weakness 3 weeks PTC •intermittent fever temporarily relieved by Paracetamol • difficulty in speaking (“ngo-ngo”) •strabismus noticed by the grandmother • consult done: CXR requested revealed Primary Koch’s infection given: Anti-Koch’s given (RMP, INH, PZA) Paracetamol 500 mg 1 tab for q4 hours >37.8 Ascorbic Acid 500mg 1 tab once a day Vitamin B complex 1 tab once a day
    5. 5. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health History of Present Illne Chief complaint: progressive weakness MF, 12yF Pasig City > 3 weeks PTC •blurring of vision (diplopia) •headache not relieved by medications •Generalized weakness 3 weeks PTC •intermittent fever •difficulty in speaking •strabismus • consult done: Primary Koch’s infection Few hours PTC •weakness right upper extremity •confusion (didn’t recognize his father)
    6. 6. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health History of Present Illne Chief complaint: progressive weakness MF, 12yF Pasig City > 3 weeks PTC •blurring of vision (diplopia) •headache not relieved by medications •Generalized weakness 3 weeks PTC •intermittent fever •difficulty in speaking •strabismus • consult done: Primary Koch’s infection Few hours PTC •weakness right upper extremity •confusion (didn’t recognize his father) Resolved to traditional medicine (hilot  albularyo  mangtatawas)
    7. 7. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health Review of System Weight loss (subjective assessment by father) Chronic back pain No cough and cold No rashes No changes in hair/nails No changes in color No tinnitus No nosebleeds No hemoptysis No chest pain No syncope No changes in bowel habits No history of trauma CC: progressive weakness Blurring of vision Headache Intermittent fever Difficulty in speaking Strabismus Diagnosed with PTB Weakness Confusion MF, 12yF Pasig City
    8. 8. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health Past Medical Histor History of Primary Koch’s Infection, currently being treated with Anti-Koch’s No history of pneumonia No history of trauma No history of past hospitalizations/surgeries MF, 12yF Pasig City CC: progressive weakness Blurring of vision Headache Intermittent fever Difficulty in speaking Strabismus Diagnosed with PTB Weakness Confusion Chronic back pain Weight loss No cough and cold
    9. 9. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health Family History PTB, paternal grandmother Hypertension, maternal grandmother No family history of the following: - diabetes - cancer - stroke - asthma - allergies MF, 12yF Pasig City CC: progressive weakness Blurring of vision Headache Intermittent fever Difficulty in speaking Strabismus Diagnosed with PTB Weakness Confusion Chronic back pain Weight loss No cough and cold On anti-Koch’s meds
    10. 10. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health Genogram MF, 12yF Pasig City I II III Hypertension CC: progressive weakness Blurring of vision Headache Intermittent fever Difficulty in speaking Strabismus Diagnosed with PTB Weakness Confusion Chronic back pain Weight loss No cough and cold On anti-Koch’s meds History of exposure to PTB
    11. 11. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health Genogram MF, 12yF Pasig City 6 I II III Hypertension employer CC: progressive weakness Blurring of vision Headache Intermittent fever Difficulty in speaking Strabismus Diagnosed with PTB Weakness Confusion Chronic back pain Weight loss No cough and cold On anti-Koch’s meds History of exposure to PTB
    12. 12. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health Birth and Nutritional Histo MF, 12yF Pasig City Born full term via NSD to a 24 year old G1P1 Birth weight unrecalled Attended by a physician (Fabella Hospital) No perinatal or neonatal complications More than 1 year of breastfeeding Interpretation: Unremarkable CC: progressive weakness Blurring of vision Headache Intermittent fever Difficulty in speaking Strabismus Diagnosed with PTB Weakness Confusion Chronic back pain Weight loss No cough and cold On anti-Koch’s meds History of exposure to PTB
    13. 13. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health Immunization History MF, 12yF Pasig City EPI until 9 months BCG 1 dose HepB 3 doses DTP 3 doses OPV 3 doses Measles 1 dose No immunization for the ff: HiB MMR Varicella Pneumococcal Rotavirus Hepa A Typhoid CC: progressive weakness Blurring of vision Headache Intermittent fever Difficulty in speaking Strabismus Diagnosed with PTB Weakness Confusion Chronic back pain Weight loss No cough and cold On anti-Koch’s meds History of exposure to PTB
    14. 14. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health Personal and Social Hist MF, 12yF Pasig City Went to school in Bicol from Grade 3 to 6 Currently in 1st year high school in Manila Living with her maternal grandmother and her employers (works as a househelp) She spent most of her life with her paternal grandmother (with PTB) in Bicol, doing household chores Recently, their house burnt down and by the request of the patient, she was sent to her maternal grandmother in Manila to study Even with her progressive symptoms, she still wants to go to school CC: progressive weakness Blurring of vision Headache Intermittent fever Difficulty in speaking Strabismus Diagnosed with PTB Weakness Confusion Chronic back pain Weight loss No cough and cold On anti-Koch’s meds History of exposure to PTB Vaccinated with BCG
    15. 15. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health Physical Examination MF, 12yF Pasig City Awake, ambulatory, not in cardiorespiratory distress Height = 151cm, Weight = 28.5 kg BMI: 12.5kg/m2 (less than 5th percentile) IBW = 39.5kg No stunting, severe wasting Acute malnutrition BP: 100/60 (normotensive) HR: 108 (normal) RR: 20 (normal) Temp: 37.0°C (afebrile)
    16. 16. Physical Examination Anicteric sclerae Pink conjunctivae No TPC, No CLAD Neck veins not dilated Intact tympanic membrane No ptosis Pupils 3mm equal brisk reactive to light Midline septum, no discharge No neck rigidity Dry lips, moist buccal mucosa Nonhyperemic pharynx HEENNT Severe wasting Vital signs: normal The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health MF, 12yF Pasig City
    17. 17. Physical Examination The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health MF, 12yF Pasig City Symmetrical chest expansion Resonant on percussion Equal tactile and vocal fremiti No retractions No rales No wheezes Chest/Lungs Severe wasting Vital signs: normal No nuchal rigidity
    18. 18. Physical Examination The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health MF, 12yF Pasig City Adynamic precordium No heaves or thrills Apex beat is at 5th ICS MCL Normal rate, regular rhythm No murmurs Heart Severe wasting Vital signs: normal No nuchal rigidity Normal chest/lungs findings
    19. 19. Physical Examination The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health MF, 12yF Pasig City Flat, soft abdomen No tenderness No organomegaly No masses Normoactive bowel sounds Abdomen Severe wasting Vital signs: normal No nuchal rigidity Normal chest/lungs findings Normal heart findings
    20. 20. Physical Examination The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health MF, 12yF Pasig City Full pulses No edema, no cyanosis Good turgor No rashes, no lesions Equally distributed hair No clubbing CRT <2sec Extremities Severe wasting Vital signs: normal No nuchal rigidity Normal chest/lungs findings Normal heart findings Normal abdomen findings
    21. 21. Physical Examination The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health MF, 12yF Pasig City Awake, cooperative, difficulty speaking (in phrases) Motor: 2/5 R upper, 5/5 the rest Sensory: 100% on all extremities Gait: normal, slow Nystagmus, right eye No meningeal signs GCS 14 (Verbal 4) Cranial Nerves: I-IV, VIII-XII intact VI right, lateral rectus weakness VII right, facial weakness Neuro Severe wasting Vital signs: normal No nuchal rigidity Normal chest/lungs findings Normal heart findings Normal extremities
    22. 22. Physical Examination The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health MF, 12yF Pasig City Neuro Right sided facial weakness Ocular palsy Severe wasting Vital signs: normal No nuchal rigidity Normal chest/lungs findings Normal heart findings Normal extremities Difficulty speaking Right upper motor weakness No sensory deficits Right eye nystagmus No meningeal signs GCS 14 Cranial nerve deficits (V,VII)
    23. 23. Salient Features •12 year old female •Febrile episodes •Right upper extremity weakness •Cranial nerve deficit •Confusion •Difficulty speaking •Weight loss •No history of trauma •Currently diagnosed and treated with PTB Meds (RMP, INH, PZA) •Family history of PTB •History of exposure to person w/PTB The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health
    24. 24. Salient Features •12 year old female •Febrile episodes •Right upper extremity weakness •Cranial nerve deficit •Confusion •Difficulty speaking •Weight loss •No history of trauma •Currently diagnosed and treated with PTB Meds (RMP, INH, PZA) •Family history of PTB •History of exposure to person w/PTBClinical Impression: TB Meningitis The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health
    25. 25. Differential Diagnosis TB Meningitis Brain Mass Stroke (in the young) Age Common Any age Rare in this age group Febrile episodes + - - Focal Neurologic defects + + + Cranial Nerve deficits + + + Changes in sensorium + + + Positive history and exposure of PTB + - - Weight loss + - - Chronic back pain Potts? (Another extrapulmonary TB) - - The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health
    26. 26. Differential Diagnosis TB Meningitis Brain Mass Stroke (in the young) Age Common Any age Rare in this age group Febrile episodes + - - Focal Neurologic defects + + + Cranial Nerve deficits + + + Changes in sensorium + + + Positive history and exposure of PTB + - - Weight loss + - - Chronic back pain Potts? (Another extrapulmonary TB) - - The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health
    27. 27. At the ER The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health ER Orders • D5 0.3 NaCl (maintenance dose) • Paracetamol (10mkd) • CBG • NPO temporarily • CBC with platelet count • Urinalysis • Chest Xray • Na and K Admitting Orders • IVF PNSS (maintenance) for 3 cycles • Diagnostics: • CBC with platelet count • CXR-PA • Cranial CT-scan plain and contrast • For creatinine • Therapeutics: • Paracetamol (10mkd) for fever > 37.8 • KidKit 3 • INH 200mg/5mL (10mkd) • RMP 200mg/5mL (10mkd) • PZA 250 mg/5mL (20mkd)
    28. 28. At the ER The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health ER Orders • D5 0.3 NaCl (maintenance dose) • Paracetamol (10mkd) • CBG • NPO temporarily • CBC with platelet count • Urinalysis • Chest Xray • Na and K Admitting Orders • IVF PNSS (maintenance) for 3 cycles • Diagnostics: • CBC with platelet count • CXR-PA • Cranial CT-scan plain and contrast • For creatinine • Therapeutics: • Paracetamol (10mkd) for fever > 37.8 • KidKit 3 • INH 200mg/5mL (10mkd) • RMP 200mg/5mL (10mkd) • PZA 250 mg/5mL (20mkd) CXR: Normal CBG: INC (136mg/dL) CBC: Normal Urinalysis Normal Na DEC (132 mmol/L) Crea DEC (33umol/L) Potassium normal
    29. 29. Course in the WardDay1 SUBJECTIVE OBJECTIVE ASSESSMENT PLAN Febrile episodes (Tmax=38.6) No headache Good appetite Blurring of vision Difficulty speaking Right upper extremitiy weakness Stable VS Alert, ambulatory, cooperative Nystagmus, right eye No meningeal signs GCS14 CN deficit (6&7) No sensory deficit Right upper extremity weakness (2/5) DTRs intact TB Meningitis Sodium correction IVF: PNSS (maintenance) Repeat Na after 3 cycles For repeat urinalysis Start Mannitol (0.8g/kg/d)
    30. 30. Course in the Ward SUBJECTIVE OBJECTIVE ASSESSMENT PLAN Afebrile episodes No headache Good appetite Blurring of vision Difficulty speaking Right upper extremity weakness CT Plain: Non-specific area of hypodensity. Acute infarct may be considered (stroke in the young). Follow- up contrast CT or MRI is suggested Alert, ambulatory, cooperative Nystagmus, right eye No meningeal signs GCS14 CN deficit (6&7) No sensory deficit Right upper extremity weakness (2/5) DTRs intact TB Meningitis IVF:D5 0.3NaCl (maintenance) Continue medications Proceed with cranial CT with contrast Day2
    31. 31. Course in the Ward The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health Day2 An ill-defined area of low attenuation is seen involving the head of the caudate nucleus, anterior limb of the internal capsule, lentiform nucleus, corona radiata and superior temporal lobe, all in the left. The adjacent frontal horn of the left lateral ventricle is partly compressed. The rest of the brain parenchyma appears normal with no other distinct lesion seen, the grey white matter interface is maintained. Impression: Non-specific area of hypodensity, Acute infarct may be considered, follow up contrast CT or MRI
    32. 32. Course in the Ward SUBJECTIVE OBJECTIVE ASSESSMENT PLAN Febrile episodes (Tmax: 39.4) No headache Good appetite Blurring of vision Difficulty speaking Right upper extremity weakness Na DEC 130 mmol/L Stable vital signs Alert, ambulatory, cooperative Nystagmus, right eye No meningeal signs GCS14 CN deficit (6&7) No sensory deficit Right upper extremity weakness (2/5) DTRs intact TB Meningitis Sodium correction PNSS (maintenance) for 3 cycles Repeat Na after 3 cycles Continue medications Day3
    33. 33. Course in the Ward SUBJECTIVE OBJECTIVE ASSESSMENT PLAN No febrile episodes No headache Good appetite Blurring of vision Difficulty speaking Right upper extremity weakness Na Normal 135 mmol/L CT Plain and contrast: AV Malformation, differential diagnosis meningitis and early cerebritis Alert, ambulatory, cooperative Nystagmus, right eye No meningeal signs GCS15 CN deficit (6&7) No sensory deficit Right upper extremity weakness (2/5) DTRs intact TB Meningitis IVF:D5 0.3 NaCl (maintenance) Day4
    34. 34. Course in the Ward The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health Day4 There is an intense enhancement in the region of the basal cistern (more on the left side). Irregular enhancements are also noted in the left frontotemporal lobe and left basal ganglia conforming the previous seen areas of ill-defined hypodensities. The overlying sulci and left sylvian fissure are effaced. No new parenchymal lesion is identified. Impression: AV Malformation, differential diagnosis: meningitis and early cerebritis
    35. 35. Course in the Ward The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health Day4 There is an intense enhancement in the region of the basal cistern (more on the left side). Irregular enhancements are also noted in the left frontotemporal lobe and left basal ganglia conforming the previous seen areas of ill-defined hypodensities. The overlying sulci and left sylvian fissure are effaced. No new parenchymal lesion is identified. Impression: AV Malformation, differential diagnosis: meningitis and early cerebritis AV Malformation VS TB Meningitis
    36. 36. Course in the Ward The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health SUBJECTIVE OBJECTIVE ASSESSMENT PLAN No febrile episodes No headache Good appetite Blurring of vision Difficulty speaking Right upper extremity weakness Stable VS Urinalysis: normal Alert, ambulatory, cooperative Nystagmus, right eye No meningeal signs GCS15 CN deficit (6&7) No sensory deficit Right upper extremity weakness (2/5) DTRs intact TB Meningitis Continue medications IVF to follow D5 0.3NaCl (M) Start ceftriaxone 1g every 12h For PPD Start streptomycin (10mkd) Repeat CXR For lumbar tap Day5
    37. 37. Course in the Ward The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health SUBJECTIVE OBJECTIVE ASSESSMENT PLAN No febrile episodes No headache Good appetite Blurring of vision Difficulty speaking Right upper extremity weakness CXR: PTB, both apices; dextroscoliosis of the thoracic spine Alert, ambulatory, cooperative Nystagmus, right eye No meningeal signs GCS15 CN deficit (6&7) No sensory deficit Right upper extremity weakness (3/5) DTRs intact TB Meningitis Discontinue ceftriaxone Decrease mannitol to q12 Day6
    38. 38. Course in the Ward The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health SUBJECTIVE OBJECTIVE ASSESSMENT PLAN Febrile episodes (Tmax:38.1) No headache Good appetite Blurring of vision Difficulty speaking Right upper extremity weakness Alert, ambulatory, cooperative Nystagmus, right eye No meningeal signs GCS15 CN deficit (6&7) No sensory deficit Right upper extremity weakness (3/5) DTRs intact TB Meningitis For PPD For sputum AFB smear Refer to ophtha Continue medications Day7
    39. 39. Course in the Ward The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health SUBJECTIVE OBJECTIVE ASSESSMENT PLAN Afebrile episodes No headache Good appetite Blurring of vision Difficulty speaking Right upper extremitiy weakness Alert, ambulatory, cooperative Nystagmus, right eye No meningeal signs GCS15 CN deficit (6&7) No sensory deficit Right upper extremity weakness (3/5) DTRs intact TB Meningitis For PPD For sputum AFB smear Refer to ophtha Continue medications Day8
    40. 40. Course in the Ward The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health SUBJECTIVE OBJECTIVE ASSESSMENT PLAN Afebrile episodes No headache Good appetite Blurring of vision Difficulty speaking Right upper and lower extremity weakness Alert, ambulatory, cooperative Nystagmus, right eye No meningeal signs GCS15 CN deficit (6&7) No sensory deficit Right upper and lower extremity weakness (3/5) DTRs intact TB Meningitis IVF to follow: D5 0.3NaCl (M) Repeat Na serum Facilitate labs Discontinue mannitol Start prednisone (2mkd) Day9
    41. 41. Course in the Ward The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health SUBJECTIVE OBJECTIVE ASSESSMENT PLAN Afebrile episodes No headache Good appetite Blurring of vision Difficulty speaking Right upper and lower extremity weakness Na DEC 134 mmol/L Alert, ambulatory, cooperative Nystagmus, right eye No meningeal signs GCS15 CN deficit (6&7) No sensory deficit Right upper and lower extremity weakness (3/5) DTRs intact TB Meningitis Repeat CBC with platelet count Repeat Na IVF: D50.3NaCl (M) Day10
    42. 42. Course in the Ward The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health SUBJECTIVE OBJECTIVE ASSESSMENT PLAN Afebrile episodes No headache Good appetite Blurring of vision Difficulty speaking Right upper and lower extremity weakness Alert, ambulatory, cooperative No meningeal signs GCS15 CN deficit (6&7) No sensory deficit Right upper and lower extremity weakness (3/5) DTRs intact TB Meningitis Continue medications Facilitate labs Day11-12
    43. 43. Course in the Ward The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health SUBJECTIVE OBJECTIVE ASSESSMENT PLAN Afebrile episodes No headache Good appetite Blurring of vision Difficulty speaking Right upper and lower extremity weakness Sputum AFB NEG Alert, ambulatory, cooperative No meningeal signs GCS15 CN deficit (6&7) No sensory deficit Right upper and lower extremity weakness (4/5) DTRs intact TB Meningitis Continue medications Facilitate labs Discontinue IVF Day13
    44. 44. Course in the Ward The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health SUBJECTIVE OBJECTIVE ASSESSMENT PLAN Afebrile episodes No headache Good appetite Blurring of vision Difficulty speaking Right upper and lower extremity weakness Alert, ambulatory, cooperative No meningeal signs GCS15 CN deficit (6&7) No sensory deficit Right upper and lower extremity weakness (4/5) DTRs intact TB Meningitis Continue medications Facilitate labs Day15-16
    45. 45. Course in the Ward The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health SUBJECTIVE OBJECTIVE ASSESSMENT PLAN Afebrile episodes No headache Good appetite Blurring of vision Difficulty speaking Right upper and lower extremity weakness PPD >10mm induration Alert, ambulatory, cooperative No meningeal signs GCS15 CN deficit (6&7) No sensory deficit Right upper and lower extremity weakness (4/5) DTRs intact TB Meningitis Continue medications Facilitate labs Day17
    46. 46. Signs and Symptom • Is a Mycobacterium tuberculosis infection of the meninges. It is the most common form of CNS tuberculosis • Symptoms may mimic space occupying lesions The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health
    47. 47. Signs and Symptom • occurs in all ages, most common between 6mo-4 years of age • Early manifestations: low grade fever, malaise, headache, lethargy, confusion, and stiff neck, with Kernig and Brudzinski signs • In young children and infants, apathy, hyperirritability, vomiting and seizures, stiff neck may not be prominent or may be absentThe Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health
    48. 48. Signs and Symptom • Symptoms evolve less rapidly compared to bacterial meningitis • because of the inherent chronicity, signs of cranial nerve involvement (usually ocular palsies, less often facial palsies or deafness) and papilledema may be present at the time of admission •Occasionally, there’s rapid onset of a focal neurologic deficit due to hemorrhagic infarction, with signs of raised intracranial pressure •Hypothermia and hyponatremia have been additional presenting features in several cases The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health
    49. 49. Signs and Symptom •In two thirds of patients, evidence of active TB elsewhere, usually in the lungs •In one study, only 2% of patients reported meningitic symptoms. The duration of presenting symptoms may vary from 1 day to 9 months, although 55% presented with symptoms of less than 2 weeks in duration. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health
    50. 50. Signs and Symptom The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health • 1-2 wks • Non-specific symptoms • Focal neurologic signs are absent 1st stage • Begin more abruptly • Focal neurologic signs are present: lethargy, nuchal rigidity, seizures, meningeal signs, hypertonia, vomiting, cranial nerve palsies • development of hydrocephalus, increased intracranial pressure, and vasculitis • signs of encephalitis: disoriention, speech impairment 2nd stage • coma, hemiplegia or paraplegia, hypertension, decerebrate posturing, deterioration of vital signs, and eventually death 3rd stage
    51. 51. Signs and Symptom The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health • 1-2 wks • Non-specific symptoms • Focal neurologic signs are absent 1st stage • Begin more abruptly • Focal neurologic signs are present: lethargy, nuchal rigidity, seizures, meningeal signs, hypertonia, vomiting, cranial nerve palsies • development of hydrocephalus, increased intracranial pressure, and vasculitis • signs of encephalitis: disoriention, speech impairment 2nd stage • coma, hemiplegia or paraplegia, hypertension, decerebrate posturing, deterioration of vital signs, and eventually death 3rd stage
    52. 52. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health Epidemiology Why should we care?
    53. 53. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health Epidemiology Why should we care? Someone gets sick from TB every four seconds and someone dies of TB every ten seconds (WHO, 2006)
    54. 54. Parents’ Worst Nightmare By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health EtiologyMycobacterium tuberculosis aerobic gram-positive rod that stains poorly because of its thick cell wall that contains lipids, peptidoglycans, and arabinomannans Acid fast Ziehl-Neelsen stain, Magnified 1000x
    55. 55. Pathophysiology Primary Infection of PTB Lympho- hematogenous dissemination formation of a metastatic caseous lesion in the cerebral cortex or meninges lesion increases in size & discharges small numbers of tubercle bacilli  subarachnoid space inflammation, obstruction, and subsequent infarction of cerebral cortex Cranial nerve involvement (usually CN III,VI,VII) interferes with the normal flow of CSF  communicating hydrocephalus Severe brain damage and eventual death
    56. 56. Diagnostics TUBERCULIN SKIN TEST • Nonreactive in up to 50% of cases CHEST RADIOGRAPH • 20-50% of children have a normal chest radiograph CSF ANALYSIS AND CULTURE • acid-fast stain of the CSF sediment is positive in up to 30% of cases • culture is positive in 50– 70% of cases CT or MRI • normal during early stages of the disease • basilar enhancement and communicating hydrocephalus with signs of cerebral edema or early focal ischemia
    57. 57. Diagnostics TUBERCULIN SKIN TEST • Nonreactive in up to 50% of cases • PATIENT: >10 mm induration CHEST RADIOGRAPH • 20-50% of children have a normal chest radiograph • PATIENT: PTB, both apices CSF ANALYSIS AND CULTURE • acid-fast stain of the CSF sediment is positive in up to 30% of cases • culture is positive in 50– 70% of cases • PATIENT: not yet done CT or MRI • normal during early stages of the disease • basilar enhancement and communicating hydrocephalus with signs of cerebral edema or early focal ischemia • PATIENT: basilar enhancement
    58. 58. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health DiagnosticsCSF Analysis
    59. 59. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health DiagnosticsCSF Analysis
    60. 60. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health •Stage I: 6 month regimen • Intensive Phase: 2 months of isoniazid, rifampicin, pyrazinamide with streptomycin or ethambutol •Continuation Phase: 4 months of isoniazid and rifampicin Treatment
    61. 61. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health •Stage II and III: 9 month regimen • Intensive Phase: 2 months of isoniazid, rifampicin, pyrazinamide with streptomycin or ethambutol •Continuation Phase: 7 months of isoniazid and rifampicin Treatment
    62. 62. Treatment The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health
    63. 63. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health •Adjunctive steroid therapy •All patients regardless of stage •To decrease neurologic sequelae and mortality Treatment
    64. 64. Treatment The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health Corticosteroid use… Corticosteroid inhibits the synthesis of interleukin 1 and TNF There is convincing evidence that corticosteroids decrease mortality rates and long-term neurologic sequelae in some patients with tuberculous meningitis by reducing vasculitis, inflammation, and, ultimately, intracranial pressure  Lowering the intracranial pressure limits tissue damage and favors circulation of anti-tuberculosis drugs through the brain and meninges.
    65. 65. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health Prognosis oIf left untreated, its course is characterized by confusion and progressively deepening stupor and coma, coupled with cranial nerve palsies, pupillary abnormalities, foci neurologic deficits, raised ICP, and decerebrate postures oFatal outcome then follows within 4 to 8 weeks at the onset
    66. 66. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health Prognosis •most patients in the 3rd stage who survive have permanent disabilities, including blindness, deafness, paraplegia, diabetes insipidus, or mental retardation •prognosis for young infants is generally worse than for older children
    67. 67. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health Prognosis •Overall Poor •Pts presenting in Stage I have 19% mortality •Pts presenting in Stage III have 69% mortality •Only 1/3 - 1/2 of patients demonstrate complete neurologic recovery •Up to 1/3 of patients have residual severe neurologic deficits such as hemiparesis, blindness, seizure DO
    68. 68. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health Preventive Measure BCG vaccination offers a protective effect (approximately 64%) against TB Meningitis the KEY TO DIAGNOSIS is identifying an adult in contact with the child who has infectious tuberculosis.
    69. 69. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health References oNelson’s Pediatrics oAdams and Victor’s Principle of Neurology oPhilippine CPG on Childhood Tuberculosis oPowerpoint slides of Dr. Mediadora Saniel on CNS infections oLectures from YL5 to YL7
    70. 70. The Traitor Illness By: Cristal Ann G. Laquindanum Year Level 8, Ateneo School of Medicine and Public Health

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