Academe Learn
CBME Curriculum Preview

Page 48 of 48

PE27.1-14 | Central Nervous System — PBL Case

CLINICAL SETTING

District hospital emergency department, rural Maharashtra. It is 2:30 AM. Dr Priya Nair, the paediatric registrar on call, is managing a busy night when the emergency department doors burst open. A family — a mother, father, and grandmother — carry in 3-year-old Arjun, who is actively convulsing. The family has travelled 45 minutes by auto-rickshaw from their village. The grandmother is crying and repeating that the child 'went into a trance' and has not come out. The child's medical record from the village health centre shows no prior neurological illness, immunisations up to date (pentavalent ×3, OPV ×3, PCV ×3), and a weight of 12 kg at last visit. As Dr Priya assesses Arjun, she observes him to be febrile (axillary temperature 39.2°C), making tonic movements of all four limbs, eyes deviated to the right, oxygen saturation 94% on room air. He has been convulsing for approximately 8 minutes by the family's account.

Trigger 1: The Convulsing Child — Immediate Priorities

Dr Priya immediately calls for IV access to be established and oxygen administration. Within 90 seconds, a peripheral IV is secured. Arjun weighs approximately 13 kg on the emergency scale. His GCS is impossible to assess accurately during the seizure. His airway is maintained (lateral position), and oxygen is applied at 4 L/min by mask. The nurse asks: 'Doctor, what do we give first?' Dr Priya recalls the status epilepticus protocol. The seizure has now been running for 10 minutes. She has lorazepam, diazepam, phenobarbitone, and phenytoin available in the crash trolley.

DISCUSSION POINTS

  • Define status epilepticus (operational definition). At what duration does a seizure become status epilepticus requiring pharmacological intervention?
  • Which benzodiazepine would you choose as first-line and what is the correct dose in mg/kg for this 13 kg child? How does IV lorazepam differ from IV diazepam in terms of duration of action?
  • What are the sequential steps in managing status epilepticus if the first benzodiazepine dose fails? Name the second-line agents and their doses in mg/kg.
  • What immediate supportive care (airway, breathing, circulation, blood glucose) must accompany pharmacological treatment?
Click to reveal Trigger 2: Seizure Terminates — History and Examination Reveal More (discuss previous trigger first!)

Trigger 2: Seizure Terminates — History and Examination Reveal More

IV lorazepam 0.1 mg/kg (1.3 mg, given as 1.3 mg) is administered. After 4 minutes, the convulsion ceases. Arjun remains drowsy (post-ictal) but is arousable. His vital signs: HR 122/min, RR 28/min, temperature 39.4°C, BP 94/60 mmHg, SpO₂ 99% on oxygen. The mother, now calmer, gives the history. Arjun was completely well until 4 days ago when he developed a low-grade fever and became irritable. Yesterday evening he vomited twice and complained of headache (he pointed to his head). This morning he refused to walk, which the family attributed to tiredness. The neck appears stiff when Dr Priya gently flexes it. Kernig's sign is positive. There is no rash. The grandmother adds: 'Doctor, his head has been growing. We noticed it 3 months ago. The village doctor said it would settle.' On measuring the occipito-frontal circumference, Dr Priya finds it is 52 cm (>97th centile for age). The anterior fontanelle is closed (normal for a 3-year-old). The optic discs show blurred margins on fundoscopy.

DISCUSSION POINTS

  • What clinical signs of meningeal irritation are present? How do you elicit Kernig's and Brudzinski's signs and what do they indicate?
  • The combination of meningeal signs, subacute onset (4 days of fever), and an enlarged head is concerning. What are the two most likely diagnoses to consider, and how does the subacute onset help you distinguish between bacterial and tuberculous meningitis?
  • What is the significance of papilloedema (blurred optic discs) in the context of meningitis? Does this change your plan for lumbar puncture? What are the contraindications to LP?
  • The finding of progressive head enlargement over 3 months raises which additional diagnosis? What sign would you specifically look for on eye examination in a child with suspected hydrocephalus?
Click to reveal Trigger 3: CSF Analysis and a Family Question (discuss previous trigger first!)

Trigger 3: CSF Analysis and a Family Question

CT head is performed first (given papilloedema): it shows mild generalised cerebral oedema and mild dilatation of the lateral and third ventricles. No posterior fossa mass. No midline shift. Dr Priya proceeds with LP. CSF results (simultaneous blood glucose 82 mg/dL): - Appearance: slightly turbid, yellowish tinge - Opening pressure: 280 mmH₂O - TLC: 320 cells/mm³ (82% lymphocytes, 18% neutrophils) - RBC: 4/mm³ (negligible) - Glucose: 28 mg/dL - Protein: 240 mg/dL - Gram stain: no organisms seen - India ink: negative - Ziehl-Neelsen stain: not yet reported - Culture sent Dr Priya is calculating the CSF:blood glucose ratio when the father tugs at her sleeve: 'Doctor, will my son survive? What is wrong with him? Should we have come sooner? Can this be prevented? My wife's brother had something similar at age 5 and died.' Dr Priya needs to answer with both compassion and clinical clarity.

DISCUSSION POINTS

  • Calculate the CSF:blood glucose ratio. What value do you get, and which type of meningitis does this CSF profile (subacute onset, lymphocytic pleocytosis, very low glucose ratio, high protein, turbid/slightly yellow, elevated pressure) most strongly support?
  • What is a cobweb clot and how is it formed in TBM? Name the three stages of TBM (British Medical Research Council / Bhatt stages) and state how staging influences prognosis.
  • What empirical treatment would you start while awaiting the ZN stain result? State the NTEP-recommended regimen, duration, and the role of adjuvant corticosteroids in TBM.
  • How would you communicate with the father — addressing prognosis, answering whether earlier presentation would have changed the outcome, and explaining preventability (BCG vaccine, contact tracing)? What key counselling points about drug compliance for 12 months must you convey?
Click to reveal Trigger 4: Week 3 — Complications and Discharge Planning (discuss previous trigger first!)

Trigger 4: Week 3 — Complications and Discharge Planning

Arjun is now in week 3 of ATT (isoniazid + rifampicin + pyrazinamide + ethambutol) plus dexamethasone. He is clinically improving — afebrile for 5 days, more alert, feeding better. However, repeat examination shows: Head circumference now 53 cm (increased 1 cm in 3 weeks). The setting-sun sign is present. A repeat CT head shows progressive dilatation of all four ventricles. The neurosurgery team has been consulted. They plan a ventriculo-peritoneal (VP) shunt. The mother asks: 'What caused the fluid in the brain — is it from the infection or was it always there?' She is also concerned because Arjun is not walking yet (he was walking normally before admission). The physiotherapy team has started passive exercises. The family lives in a village 45 km away with limited access to follow-up care.

DISCUSSION POINTS

  • Explain the mechanism by which TBM causes communicating hydrocephalus (exudate blocking basal cisterns and arachnoid granulations). How is this different from the non-communicating hydrocephalus seen with aqueductal stenosis?
  • What is the setting-sun sign — describe the mechanism and which part of the brain is affected? How does it relate to the ventricular dilatation on CT?
  • The child is not walking after TBM — what neurological deficits can TBM cause, and what rehabilitation interventions are appropriate? How would you monitor for sensorineural hearing loss (a known sequela) in a resource-limited setting?
  • Design a discharge plan that accounts for the family's rural location: which drugs (with doses in mg/kg), monitoring parameters, danger signs, follow-up interval, and how the DOTS programme (NTEP) can support medication adherence for the remaining ATT course?

Group Task Assignments

Group 1: Collaborative Task

Group 2: Collaborative Task

Group 3: Collaborative Task

Learning Issues

Research these questions and bring your findings to the discussion.

  1. [PE27.1] What are the age-specific bacterial pathogens for meningitis in children, and what is the complete empirical treatment regimen (drug names + mg/kg doses) for bacterial meningitis in a 3-year-old?
  2. [PE27.2] What is the NTEP-recommended drug regimen (with phases and duration) for TBM in children, and what is the evidence base for adjuvant corticosteroids in TBM?
  3. [PE27.3] How does CSF analysis (cell type, glucose ratio, protein, special stains) distinguish bacterial, TBM, viral, and fungal meningitis? What are the critical CSF:blood glucose ratio thresholds?
  4. [PE27.4] What are the mechanisms of hydrocephalus complicating meningitis (communicating vs non-communicating)? What are the indications and complications of VP shunt in children?
  5. [PE27.8] Define operational status epilepticus. What is the step-by-step pharmacological management algorithm (drug, dose in mg/kg, route, timing, escalation)?
  6. [PE27.13] What are the indications and contraindications for lumbar puncture in a child with suspected meningitis? How do you interpret opening pressure, cell count, glucose ratio, and protein in this CSF?
  7. [PE27.14] Describe the correct technique for lumbar puncture in a child (position, landmark, needle angle, what to check before withdrawing). What is the normal opening pressure range in children?