Cns infections


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Cns infections

  1. 1. 1
  2. 2. 2 CNS infections By Dr Muhammad Saleem Laghari MBBS(KEMU), MCPS, FCPS (Paed) Gold Medalist FCPS-I Associate Professor Department of pediatrics SMC,RYK
  3. 3. 3 CNS INFECTIONS  MENINGITIS: I) Acute Bacterial (Pyo) Viral (Aseptic) ii) Sub acute (Chronic) TB, Fungal, Neoplastic, Parasitic, Rickettsial iii) Partially treated iv) Chemical  ENCEPHALITIS  CEREBRAL ABSCESS
  4. 4. 4 Case Scenario A 2 years old boy presented with history of fever, irritability & vomiting. Examination revealed semiconscious child having temp.102F0 decrebrate posturing .Rest of systemic examination unremarkable. Q - write 3 differential diagnosis.
  5. 5. 5 Key. 1- pyomeningitis 2- Encephalitis 3- cerebral malaria
  6. 6. 6 Case Scenario A 7 year old boy brought to emergency with high grade fever, headache for 2 days & projectile vomiting since morning. Examination revealed semiconscious child with positive neck stiffness. 1- What is the most likely diagnosis? 2- Write 3 relevant investigations to reach final diagnosis. 3- Write steps in the management of this case.
  7. 7. 7 Key: 1- Acute – pyogenic meningitis 2- (i) CSF examination & culture (after fundoscopy) (ii) CBC (iii) Blood culture 3- Steps of Treatment a. General Supportive Measures Maintain I/V line, Monitor vitals, Fluids balance, IOP record, Control of fever. b. Specific treatment (i) Either combination of B. Penicillin + Chloramphenicol or (ii)Vancomycin + Cefotaxime / Ceftriaxone (iii)Duration of Treatment: 7 – 10 days c. Steroids: Dexamethasone 0.6 mg/kg/day in 2 – 4 divided doses for 2- 4 days d.Monitor and treatment of complications.
  8. 8. 8 Case Scenario 8 year old girl presented to emergency department with complaint of progressive loss of weight & low grade fever for 2 months, lethargy, off & on headache & vomiting for 2 weeks and now unconsciousness for last 5 days. Examination revealed unconscious, emaciated girl having 10 Kg weight. No BCG scar. CNS examination revealed right sided uncrossed hemiplegia. Her grand father died 2 months back. 1- What is most likely diagnosis? 2- Mention 4 investigations to reach final diagnosis? 3- Write 4 steps of treatment of above disease?
  9. 9. 9 Key: 1- TBM 2- (i) CSF examination & Culture (ii) CBC + ESR (iii) Chest X-ray (iv) Mantoux test (v) CT Scan Brain 3- (i) General measures (ii) Anti tuberculosis treatment (INH, PZA, Rifampicin, Streptomycin) (iii) Corticosteroids (iv) Monitor & treatment of complication (v) Follow up
  10. 10. 10 MENINGITIS Meningitis is defined as inflammation of the membranes surrounding the brain & spinal cord.
  11. 11. 11 Meningoencephalitis Inflammation of both the meninges & cortex of brain.
  12. 12. 12 ROUTES OF INFECTION  Nasopharyngeal.  Paranasal sinuses.  Blood stream Septicemia Pneumonia, Osteomyelitis  Skull Fracture, Meningocele, Encephalocele  Middle Ear Infection/ Mastoiditis.  VentriculoPeritoneal Shunts  Pilonidal Sinus
  13. 13. 13 ETIOLOGY Organisms  0-2months: E.coli, Group B streptococci, staylococcus aureus, Listeria monocytogenes.  2months -2 years: Hib, S. pneumoniae, Neisseria meningitidis  2 years - 21 years :N. meningitidis, S. pneumoniae ,Hib.
  14. 14. 14
  15. 15. 15 CLINICAL FEATURES NEONATES Sick Baby /Septicemia Subtle INFANTS  Fever, Vomiting, Stiffness, Sensorial disturbance, Irritability, Excessive Cry, Seizures,  Anterior Fontanel Full/Bulging.  Neck Retraction.  Meningeal signs Less Reliable  Papillodema  Tone/Reflexes Brisk
  16. 16. 16 CLINICAL FEATURES IN CHILDREN  Fever. Vomiting. Headache, Drowsiness  Seizures  Neck Stiffness  Kernings, Brudzinki signs  Rash (Petechial, purpural )  Vitals instability  Cranial nerve palsy, hemiplegia, ataxia  Infection Source e.g. otitis media.
  17. 17. 17
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  19. 19. 19 MENINGOCOCCIMIA  Fulminant Septicemia.  Acute Febrile Illness.  Petechial Haemorrhages.Purpura.  DIC.  Adrenal Haemorrhage.  Peripheral Circulatory Failure.  Shock
  20. 20. 20
  21. 21. 21
  22. 22. 22 DIAGNOSIS  CBC  Blood Culture  CSF examination  X-Ray chest  C T Scan brain  Rapid Diagnostic Test  Counter current immuno electrophoresis  Latex particle agglutination  ELISA  CSF, LDH  Gram Staining / Smears of Petechial / Purpural Lesions.
  23. 23. 23 CSF EXAM  Color.  Pressure.  Cells.  Gram staining  Proteins.  Glucose  Culture.
  24. 24. 24
  25. 25. 25 COMPLICATIONS  Seizures. Epilepsy.  Cranial Nerve Palsies. Deafness (sensoneural). Blindness, Oculomotor, Abducent, Facial ..  Raised ICP. Brain Herniation.  In Appropriate ADH syndrome  Stroke. Cerebral Infarcts.  DIC.  Hydrocephalus.  Subdural Effusion.  Mental & Physical Handicap.  Learning Disabilities.  Recurrences.
  26. 26. 26 MANAGEMENT SUPPORTIVE  Control Hyperpyrexia.  Seizures Diazepam iv slow, Midzolam i. v, Phenobarbitone .  Resticted Fluid 800-1000ml/m.sq./day.  Airway, Bowel & Bladder, Posture, Wt. H.C  Pupillary Reflex, Signs ICP, Fundoscpy..  Feeding.  IOP.
  27. 27. 27 Specific Therapy
  28. 28. 28
  29. 29. 29 CORTICOSTEROIDS Dexamethasone iv 0.15mg/kg/dose 6hr.2D. H Influenza type b. Inflammatory Mediators reduction. Cerebral edema.
  30. 30. 30 PROGNOSIS Considerable Age, Seizures, Coma Mortality 25% Pneumococcal. 15%Meningococcal. 8% H. Influenza type b. Morbidity 35% Neurological Deficit.
  31. 31. 31 PREVENTION  Vaccines. Pneumococcal polysaccharide. Meningococcal. H. Influenza.  Antibiotic Prophylaxis. Rifampicin oral Patient & contacts
  33. 33. 33 Definition It is inflammation of the lepatomenings (pia-arachnoid) by mycobacterium tuber-culosis.
  34. 34. 34 Incidence  Most serious complication of tuberculosis.  TBM complicates 1 of every 200 primary infections.  It is not reported in infants below 4 months of age.  The maximum risk of TBM is within 6 months of primary infection.  The highest incidence is recorded below 5 years of age.
  35. 35. 35 Pathogenesis  TMB is always a secondary lesion with primary usually in the lungs.  Meningitis results from the formation of a metastatic caseous lesion (seeding of the bacilli) in the cerebral cortex, meninges and choroid plexus during the process of initial occult lympho-hematogenous spread of the primary infection.
  36. 36. 36  Within a short period of time, caseous foci form on the surface of brain (Rich’s foci). They increase in size and discharge bacilli in the CSF (subarachnoid space).  A thick, gelatinous exudate may infiltrate the cortical or meningeal blood vessels, producing inflammation, obstruction, or infarction. Most commonly involved site is the brain stem causing frequent involvement of 3rd, 6th, and 7th cranial nerves.  Basal cisterns are obstructed causing communicating hydrocephalus. Accompany-ing inflammation may cause cerebral edema.
  37. 37. 37 Clinical features  In a classical case, onset is insidious but may be fulminant in certain cases.  A more rapid progression of the disease may occur in young infants in whom symptoms develop for only several days before the onset of acute hydrocephalus, brain infarction, or seizures.  Classically, the onset is gradual (over several weeks).  History of measles may precede the onset of TBM.  The clinical manifestations may be divided into 3 stages and each stage lasts approximately 1 week. There may be considerable overlap of the 3 stages.
  38. 38. 38 Stage-1 (Prodromal stage). (lasts for 1-2 weeks)  Initial symptoms are non-specific.  The child becomes listless or irritable, loses interest in play, have fever, anorexia, vomiting, constipation and weight loss.  Some children may complain of headache and drowsiness.  There are no focal neurologic signs.  There may be loss of or stagnation of the developmental milestones.
  39. 39. 39 Stage – 2  Onset of 2nd stage is more abrupt.  During this stage, signs of meningeal irritation (neck stiffness) appear with increased CSF pressure. Positive kerning and Brudzinski signs develop with increased tendon jerks and extensor plantar responses. There may be generalized hypertonia.  Headache is the cardinal symptoms in the 2nd week of illness in older children. Fever is constant and headache is severe, persistent and often occipital.  Vomiting and constipation may become severe.  Exudate develops at the base of brain involving cranial nerves and brain stem.
  40. 40. 40  Abducent nerve paralysis is common. Oculomotor lesion causes internal squint. Facial palsy is also common.  Some children may have disorientation, and speech and movement disorders.  In infants anterior fontanelle may be bulging and sutures become separated with “crackpot” sign.  In older children, papilledema develops. Head circumference starts enlarging rapidly.
  41. 41. 41  Choroid tubercles may be seen.  Child is semiconscious and may shriek loud noises and develops convulsions.  All the above clinical features are due to the development of hydrocephalus and increased intracanial pressure along with meningeal irritation.
  42. 42. 42 Stage – 3  Child rapidly becomes comatose during 3rd week.  He is emaciated with scybalous masses in the abdomen.  Child starts getting high-grade irregular fever and convulsions.  There may be hemiplegia or paraplegia.  With extreme neck stiffness opisthotonus develops with decerebrate rigidity and pupil becomes dilated and fixed.  There is deterioration of the vital signs especially hypertension.  Death may occur if treatment is started late during this stage.  Tache-cerebrale is sometimes seen in children.
  43. 43. 43 Diagnosis  Clinical suspicion + Fundoscopy.  CBC, ESR  X-ray chest  Mantoux / Acc. BCG  Lumber puncture (CSF examination)  Gastric lavage or sputum examination  Lymph node biopsy  CT scan / MRI brain
  44. 44. 44 Management General measures 1. Careful record of vital signs 2. Daily monitoring of the complications 3. Phenobarbitone: Dose 5mg/kg/day to control convulsions. 4. Antipyretics: Paracetamol 5. corticosteroids
  45. 45. 45 6. Pyridoxine 10mg daily to prevent polyneuritis. 7. Feeding: Give tube feeding according to the requirement. 8. Bed sores: Change posture every two hours to prevent bed sores. 9. Care of comatose patient 10. Care of bowel and bladder. 11. It is also important to screen to screen the family members for tuberculosis and treat the infected persons.
  46. 46. 46 Specific management. 1. Isoniazid (INH) 2. Rifampicin 3. Pyrazinamide 4. Streptomycin /or 5. Ethambutol
  47. 47. 47 Complications  Mental retardation  Cranial nerve palsies (3rd, 6th & 7th)  Blindness (optic atrophy)  Deafness.  Hydrocephalus  Hemiplegia, paraplegia, or monoplegia.  Epilepsy  Endocrine disturbances (diabetes insipidus).  Tuberculoma
  48. 48. 48 Prognosis  It depends upon two factors: 1. Age of the patient 2. Stage of the disease at which treatment is started.  Without treatment it is invariably fatal.  In stage-1, 100% cure rate is expected.  Even with optimal therapy mortality ranges from 30- 50% and incidence of neurologic squelae is 75-80% especially in stage-3. there may be blindness, deafness, paraplegia, mental retardation and diabetes inspidus.  Infants and young children have poor prognosis as compared to older children.
  49. 49. 49 ENCEPHALITIS
  50. 50. 50 DEFINITION. The inflammation of the brain tissue is known as Encephalitis.
  51. 51. 51  It results in marked cerebral dysfunction and early loss of consciousness.  It is usually caused by viruses e.g. influenza, herpes simplex but brain tissue is also involved as part of bacterial meningitis (e.g. tuberculous meningoencephalitis, etc.)  Sometimes features of encephalitis occur after few days of known viral infection or vaccination and it is then called “Postinfectious” encephalitis.  Neuro-logic manifestations suggestive of encephalitis but occurring in the absence of inflammation indicate encephalopathy. General Consideration
  52. 52. 52 Etiology.  Encephalitis is mainly caused by viruses.  It is caused by direct viral infection of the brain via a hematogenous or neuronal route.  Arboviruses and enteroviruses are most commonly responsible for epidemics of acute encephalitis.  Herpes simplex is the most common cause of sporadic encephalitis.  Varicella virus commonly causes cerebellar ataxia.
  53. 53. 53 Table shows the Causes of Viral Meningitis / Encephalitis. Infections Post-infections Entero-viruses. Coxsackie. Polimyelitis. Echo-Virus. Myxovirus: Mumps Rabies. Herpes Virus. Herpes Simplex. Herpes Zoster. Arthropod-borne: Yellow Fever. Dengue Fever. Others. Lymphocytic Chriomeningitis. Psittacosis. Measles Rubella Varicella Pox virus Vaccinia
  54. 54. 54 Pathophysiology.  Following ingestion or mosquito bite, the virus infects several organs, where it multiples causing a systemic febrile illness.  CNS is involved in the secondary viraemia if the virus continues to multiply in the primary organs.  The neurologic damage occurs either (1) by direct invasion and destruction of neural tissues by actively multiplying viruses, (2) or by reaction of the patient tissues to antigens of the virus.
  55. 55. 55 Pathology.  The brain is swollen with marked vascular congestion, and initial polymorph response is followed by mononuclear, lymphocyte and plasma cells infiltration. There is degeneration of the neuronal cells and interanuclear inclusion bodies may be present.  Certain viruses appear to have an affinity for invading certain parts of the brain, e.g. herpes simplex for fronto-temporal lobe, mumps virus is often associated with transverse myelitis, chickenpox for cerebellum.
  56. 56. 56 Clinical Features.  All viruses, which cause encephalitis, can also cause meningitis. Encephalitic picture may predominate or a combined picture of meningo-encephalitis may occur if meninges are also inflamed. The clinical features are extremely variable.  A sudden onset of high fever and headache are the first signs of the illness.
  57. 57. 57 Features of encephalitis ` Most Common causes Herpes Measles Chicken Pox Polio. Clinical features Fever Disturbed Consciousness Convulsion Focal neurologic signs  Encephalitis; Direct invasion of gray matter by infectious agent.  Post-infectious; Delayed immunologicaly mediated demyelination.  Encephalopathy: Encephalitis like illness without fever or aseptic meningitis (inflammation) is called encephalopathy and is due to toxic or metabolic causes.
  58. 58. 58  Signs of central nervous system involvement occur early which vary from mild drowsiness to deep coma.  Headache, fever, irritability, mental confusion or abnormal behavior may be marked.  Headache is common in older children whereas infants may have gross irritability and feeding difficulty.  Focal neurological signs may occur, cranial verve palsies (squint or facial palsy) speech, disturbances (aphasia), spastic palsies (hemiplegia, tetraplegia), cerebellar disturbances (ataxia) and abnormalities or various reflexes.  Meningeal infammation may produce neck rigidity and stiffness of back.
  59. 59. 59  some children may present with abnormal behavior screaming spells, irritability, confusion, tremors and stupor, muscle weakness and occasionally paralysis may occur.  Spastic paraplegia with loss of bowel and bladder control indicates spinal cord involvement.  Sensory disturbances may be present in some. Respiratory irregularities and visual disturbances may occur.  Occasionally myocarditis and hypotension may complicate the picture.
  60. 60. 60 The clinical features usually do not point to a specific viral etiology but some types of encephalitis present distinct clinical features e.g. Herpes simplex, since it is treatable it is described further.
  61. 61. 61 Herpes Simplex Encephalitis. Type-1:  infants and children typically present with fever, vomiting, and lethargy and proceed to coma and focal fits.  It usually produces features of a space- occupying lesion in the temporal lobe like hemiparesis, focal fits and raised intracranial pressure tentorial herniation, papilledema and decerebrate posturing may occur.  CSF examination may show xanthochromia and in some cases RBSs. Cell count varies between 50-5000, CSF protein is normal or moderately elevated with normal glucose.
  62. 62. 62 Type-2: Herpes virus type 2 causes encephalitis in the newborn following vaginal delivery. Virus is acquired from maternal birth canal and results in typical vesicular skin eruptions and encephalitis.
  63. 63. 63 Chicken Pox Encephalitis. (1 in 1000-5000). Occurs 4 – 6 days after the rash but it can produce the rash in some. CSF shows 10 – 15 cells/mm3 with polys initially and lymphos later. Protein is normal or moderately elevated with normal glucose.
  64. 64. 64 Measles Encephalitis. (1 in 600-1000 with a high mortality rate) It usually develops 2 days to 2 weeks after the appearance of rash, rarely even before. Spinal cord involvement with paraplegia and neurologic bladder may occur with inappropriate ADH secretion. CSF reveals lymphocytic pleocytosis of 20 – 250 cells with slightly raised protein and normal glucose.
  65. 65. 65 Polio – Encephalitis.  Occurs in 1 – 5 percent of patients showing neurological manifestation of polio infection.  Drowsiness, irritability, coarse tremors, coma and fits indicated encephalitis in addition to the usual symptoms of paresis of limbs or brain stem involvement.  Although sensory deficits are rare but these can occur in the presence of transverse myelitis or following involvement of the posterior hours of the gray mater.  CSF shows mild pleocytosis of 50 – 200 cells, initially polys and later lymphos. Protein in CSF is moderately elevated and glucose normal.  Polio-encephalitis should always be considered in differential diagnosis, as it is common here.
  66. 66. 66 Mumps Mumps is commonly associated with aseptic meningitis, which occurs 2 – 3 days after the onset of parotitis, but encephalitis occurs 7 – 10 days later with frequent convulsions and coma. Diagnosis is confirmed by virus isolation, serological methods and fluorescent antibody techniques
  67. 67. 67 Lymphocytic Choriomeningitis. This virus is thought to be transmitted to man by the inhalation or ingestion of dried mica excreta. After incubation period of 1 week there is malaise, headache and myalgia usually lasting 1 – 2 weeks. It is followed by meningo-encephalitis.
  68. 68. 68 Slow Viral Diseases Slow Viral Diseases are manifested months to years after the viral infection. Slow CNS infection is due to prions (Small protein-aceous particles). There is dementia, poor congnitive functions, and behavior changes. Most common viruses causing such type of disease are measles (subacute sclerosing panencephalitis or SSPE), rubella, HIV and HSV.
  69. 69. 69 Diagnosis. Diagnosis is essentially clinical and by exclusion of diseases such as meningitis, cerebral malaria, brain tumor, heat stroke and lead encephalopathy.
  70. 70. 70 1- Lumber Puncture. Cerebrospinal fluid should be examined to exclude bacterial and tuberculous meningitis. In viral encephalitis CSF is generally clear. In viral encephalitis CSF is generally clear, leukocyte count varies from 10 – 5000 cells with polymorph initially and lymphocytes later. There is moderate elevation of protein with normal glucose. 2- Antibody titer. Serologic testing should be done twice 15 days apart or demonstrate rising titer (4 fold or more)
  71. 71. 71 3- Virus Isolation. Viruses can be isolated from blood, CSF, faces and throat swabs. 4- Brain CT Scan/MRI brain. These are helpful in localizing the process as in focal necrotizing encephalitis (Herpes simplex). 5- Brain Biopsy. The diagnosis is established and confirmed by brain biopsy. It is only indicated in cases, which are suspected to be having herpes encephalitis because specific antiviral chemotherapy is available. Virus is then identified by immuno- flouresecent technique from brain biopsy.
  72. 72. 72 6- EEG. infection of the brain causes very marked disorganization of the EEG with the development of large amplitude, slow waves. In herpes encephalitis there are large amplitude, slow waves at rate of 2 – 4 / Sec and these waves recur after every 2 sec on a background of very slow activity in the temporal region. 7- Blood Counts. these are done as routine to rule out bacterial infections.
  73. 73. 73 Complications. Early.  Hemiplegia.  Squints.  Deafness.  Intractable convulsions.  Bed Sores.  Aspirational Pneumonia, and  Urinary Tract infection from catheterization.
  74. 74. 74 Late.  Mental Retardation.  Hydrocephalus.  Epilepsy.  Learning Disabilities, and  Behavior Disorders.
  75. 75. 75 Management. 1- Nursing Care. Nursing a comatose child monitoring vital functions, frequent suctioning of airways, change of posture every ½-1 hours to avoid pressure sores and positional deformity. Attention should be paid to oral hygiene, eye care, and abdominal distension from bladder enlargement (urinary retention) and bowel care (ileus or severe constipation). 2- Anticonvulsants. Inj. Diazepam 0.2mg/kg I/V or Inj. Paraldehyde 0.15ml/kg PR. Once convulsions are controlled give phenobarbitone 5-8 mg/kg/day orally to prevent further convulsions.
  76. 76. 76 3- Cerebral Edema: Raised intra-cranial pressure and cerebral edema is present in most cases even without any evidence of papilledema and should be treated. (i). dexamethasone. (ii). Mannitol 4. Antiviral Drugs. For herpes simplex virus infections, acyclovir is the treatment of choice.
  77. 77. 77 5-Intravenous Fluids. Maintain fluid and electrolyte balance. Fluids should be restricted to 60% of the daily requirement and do not give dextrose water or 0.18% saline which results in cerebral edema. 6-Nutrition. Calories required are given through nasogastric tube in the from of liquid and semisolid diets e.g. milk, juices, soup, egg, etc.
  78. 78. 78 7-Antibiotics. Should be given until bacterial etiology is ruled out by blood and CSF examination. 8-Antipyretics. High fever should be controlled by antipyretics or tepid water sponging.
  79. 79. 79 Progonsis. Most patients survive and some may have residual focal defects. Mortality varies from 10-50%. The outcome is particularly poor in herpes simplex encephalitis (mortality rate > 70%) while better in enteroviral encephalitis. Encephalitis is usually severe in children > 1 year of age and in those presenting with coma.
  80. 80. 80 Cerebral Malaria
  81. 81. 81 Definition  It is a severe form of malaria caused by Plasmodium falciparum, manifesting as coma (GCS <11) convulsions, and/or hemoglobinuria. OR  Malaria with coma persisting for >30 min after a seizure.
  82. 82. 82 Etiology Plasmodium falciparum is transmitted from: 1. Bites of previously infected female anopheles mosquitoes. 2. Transfusion of infected blood. 3. Organ transplant and by hypodermic needles.
  83. 83. 83 Epidemiology  The infection is usually much more severe in young children.  A and B blood groups are more protective than O groups.  Hemoglobin E and C are also more protective.  Fetal hemoglobin, sickle cell trait and G6PD deficiency have lesser tendency of plasmodium falciparum infection.  Malnutrition is protective as immunity is decreased.
  84. 84. 84 Pathophysiology  First the Plasmodium falciparum enters the red blood cells.  After 8 – 18 hours, these cells become increasingly sticky and tend to adhere to the endothelial lining of blood sinuses and vessels especially when the circulation is slow. The fixed cells are unable to come back to the general circulation.  As more cells adhere, flow within the vessels is progressively impeded and occlusion or even rupture may occur.  The symptoms depend on the site and extent of the occlusion of the blood vessels. The lungs, brain and intestinal tract are usually more affected.  The parasites keep maturing in the infected cells even when they are fixed to the endothelium or
  85. 85. 85  The release of merozoites, where the circulation is slowed, facilitates the invasion of nearby red blood cells.  Plasmodium falciparum invades all erythrocytes irrespective of age and so parasitemia in a non-immune child may be very heavy.  One schizont yields 8 – 32 merozoites, the highest of all the species.
  86. 86. 86 Pathology  When the parasitized red blood cells attach to the endothelium of venules and capillaries, the inflammatory process start around them. There is hemorrhage and necrosis around these vessels.  All these lead to the blockage of vessels by parasitized red blood cells. Fibrin thrombi may also form in the arterioles and capillaries giving a picture of DIC. The same process in the brain lead to the cerebral edema.
  87. 87. 87  The immunofourescence has shown the deposition of plasmodium falciparum antigen and antibody complex in capillaries. There are two suggested ways to explain:  ICAM (Intercellular Adhesion Molecule) medicated increased adherence of RBC’s to the endothelium of cerebral vessels.  NO (Nitric oxide) mediated increased fragility and destruction of cerebral matter.
  88. 88. 88 Clinical Features  The characteristic adult pattern of cerebral malaria is not present in children especially under 5 years of age.  The clinical signs and symptoms usually start after 8-15 days of infection. Initially there are behavior changes like anorexia, fretfulness, unusual crying, drowsiness, or disturbance of sleep.  Fever may be absent or increase gradually for 1-2 days or the onset may be sudden with high-grade temperature with or without prodromal chill.  The complaints include headache, nausea, generalized aching, particularly of the back.  When the spleen has enlarged quickly and is
  89. 89. 89  Cerebral symptoms are evidenced by convulsions or coma. The neurologic signs in infants and children are those of increased intracranial pressure and symmetric upper motor neuron and brainstem disturbances such as disconjugate gaze and decerebrate and decorticate postures.  There is severe pallor and splenomegaly (or hepatosplenomegaly; liver may only be enlarged at times).  The classic picture of a child with high-grade fever who is unconscious and convulsing cannot be mistaken.  There is no neck rigidity (except abnormal posturing).
  90. 90. 90 Diagnosis 1. CBC  Leucopenia is variable.  Monocytosis is common.  Anemia  Reticulocyte count increased. 2. Thick and thin blood film: (most specific test)  Initially ring forms are seen and after 10 days crescents (gametocytes) are seen.  Up to 20 % of RBC’s may be infected.  Negative if antimalarials are given. 3. CSF:  Usually normal if no associated meningitis
  91. 91. 91 4. Serum electrolytes. 5. Blood sugar: hypoglycemia. 6. Detection of parasitic antigen: a. ICT – Malaria b. DNA / RNA are detected with probes. 7. Serological tests: Not very specific but species specific antibodies can be detected.
  92. 92. 92 Management Supportive treatment Anemia  Give blood transfusion if hemoglobin <6 gm %. (Pack cells 10 mlkg). Hypoglycemia:  Give 50 % glucose bolus I/V stat and then regular glucose supplements with 10 % dextrose water. Renal Failure:  Increase hydration  May require dialysis.  Decrease the dose of anti-malarial to 1/3.
  93. 93. 93 Convulsions:  Diazepam 0.3 – 0.5 mg IV slow;  Phenobarbitone (10 mg/kg PO/NG tube stat, then maintenance dose 5 mg/kg/day in 2 divided doses).  Paraldehyde (0. 15 ml/kg P/R). Lowering of high temperature.  Tepid sponging or paracetamol orally by N/G tube. Fluids:  5% dextrose saline 20-40ml/kg in 30 minutes or dextran 75%.  Late shift to 5% dextrose 1/5 saline.  Total fluid 100-150 ml/kg/day.
  94. 94. 94 Specific Treatment.  Start IV anti-malarial and then shift to oral when the patient becomes conscious. 1 injection quinine dihydrochloride (300 mg/1 ml vial).  20 mg/kg IV stat, then 10 mg/kg IV-8 hourly for 7 days (1 mg in 1 ml of 5% dextrose water over 2-4 hours.  8.3 mg quinine base = 10 mg quinine dihydrochloride. Injection Artemethrine:  It is also use in these days  Dose 3.2 mg/kg IM stat then 1.6 mg/kg/day for 2 days. 2 Injection Choloroquine dihydrochloride: (200 mg/5ml vial)  5 mg/kg in 10 ml/kg of isotonic saline in 3-4 hours, then repeat same dose at 6 hours, then give 5mg/kg daily for 3 days.
  95. 95. 95 Quinine Sulphate:  10 mg/kg/dose – 8 hourly for 4-7 days PO. Chloroquin phosphate / hydrochlorosuin sulphate:  10 mg/kg stat  Then 10 mg/kg next day  Then 5 mg/kg next day Injection chloroquin dihydrochloride: (200 mg/5ml vial)  5 mg/kg in 10 ml/kg of isotonic saline in 3-4 hours, then repeat same dose at 6 hours, then give 5mg/kg daily for 3 days.
  96. 96. 96 Differential Diagnosis.  Febrile Fits: Age 6 months – 6 years, patient is arousable, CSF clear.  Pyogenic meningitis: Toxic ill patient. Signs of meningeal irritation positive. CSF is turbid and abnormal.  Viral encephalitis: Anemia, coagulo-pathy and malarial parasite is absent. CSF may be normal with increased proteins and pleocytosis.  SOL: Increased ICP evidenced by vomiting, headache, diplopia and papill-edema.. Localizing signs and cranial nerve palsies are present. Malarial parasite is absent. MRI/CT scan confirm.
  97. 97. 97  Hepatic coma: Deep jaundice and less anemia. Liver is usually smaller. LFT’s gross abnormality. Coagulation defects. Decreased serum proteins and especially serum albumin. Malarial parasite is negative.  Hypoglycemic coma: Afebrile, cold and sweating. Jaundice, anemia, bleeding and MP are absent. Serum sugar is <40 mg%.  Uremia: H/o preceding edema, diarrhea, and vomiting. Hematuria, dysuria and recurrent abdominal pain. H/O previous UTI or renal stones.
  98. 98. 98 Criteria for cerebral malaria diagnosis CNS:  Unarousable or coma > 6 hours.  Focal or generalized fits.  Posture (opisthotonic, decerebrate, decorticate).  Conjugate deviation of the eyes.  Retinal hemorrhages. Renal:  Urine output < 400 ml/day.  Serum creatinine > 3 mg%.
  99. 99. 99 Prognosis  Mortality of cerebral malaria ranges from 10-30 %.  Death in most of the cases occur within 24 hours of admission / treatment.  Some children have a rapid and progressive recovery, but most of the time duration of impaired consciousness after treatment being started ranges form few hours to several days.  Majority of the surviving children had a full recovery but about 10% have a permanent neurologic deficit.
  100. 100. 100 Thank you