The child is 6 years old, sick for 2 months. The onset of the disease is with a rare cough, an increase in body temperature to 37.3 C, sweating at night. At home, I took cough syrup, augmentin. The dynamics showed headache, vomiting. The child was hospitalized in an infectious diseases hospital. A spinal puncture was performed: In the CSF analysis: the liquor is transparent, when the liquor was standing for 72 hours, a delicate fibrin film fell out, cytosis of 60 cells, lymphocytes 52% neutrophils 48%, glucose 1.8 mmol/l, protein 1.4 g/17 1. Interpretite analysis of liquor / ликвор анализіне талдау жасаныз/make interpretation liquor analysis 2. name the nosology / name the nosology with which forms ?
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I now have sufficient information from the textbook sources to provide a comprehensive answer. Let me compile the full analysis.
1. CSF Analysis Interpretation
Here is a systematic interpretation of each parameter:
| Parameter | Patient's Value | Normal Reference | Interpretation |
|---|---|---|---|
| Appearance | Transparent (clear) | Clear, colorless | Normal appearance — does NOT exclude TBM |
| Fibrin film | Delicate fibrin pellicle after 72 h standing | Absent | Highly characteristic "cobweb/fibrin clot" — a hallmark of TBM |
| Cytosis | 60 cells/mm³ | < 5 lymphocytes | Moderate pleocytosis |
| Differential | Lymphocytes 52%, Neutrophils 48% | Lymphocytes only | Mixed pleocytosis — mixed lymphocytic-neutrophilic; typical in early TBM |
| Glucose | 1.8 mmol/L (~32 mg/dL) | 2.2–3.9 mmol/L (45–100 mg/dL) | Markedly reduced (hypoglycorrhachia) |
| Protein | 1.4 g/L (140 mg/dL) | 0.15–0.45 g/L (15–45 mg/dL) | Markedly elevated (~3× upper limit) |
Summary interpretation:
The CSF picture shows subacute meningitis with hypoglycorrhachia characterized by:
- Transparent liquor — unlike bacterial meningitis where CSF is often turbid
- Delicate fibrin/pellicle film on standing — a classical sign in tuberculous meningitis; the fibrin web (pellicle) forms due to high fibrinogen content from protein-rich exudate
- Moderate mixed pleocytosis (60 cells) — early TBM characteristically shows a mixed polymorphonuclear + lymphocytic infiltrate; lymphocytes come to predominate later
- Sharply reduced glucose (1.8 mmol/L) — significant hypoglycorrhachia; in TBM glucose falls slowly over days (unlike acute bacterial meningitis where it drops rapidly)
- Markedly elevated protein (1.4 g/L) — consistent with TBM range of 100–200 mg/dL
"Early in the disease, there may be a more-or-less-equal number of polymorphonuclear leukocytes and lymphocytes, but after several days lymphocytes predominate in the majority of cases… The protein content of the CSF is always elevated, between 100 and 200 mg/dL in most cases… Glucose is reduced to levels below 40 mg/dL but rarely to the very low values observed in conventional bacterial meningitis." — Adams and Victor's Principles of Neurology, 12th Edition
2. Nosology and Clinical Form
Diagnosis: Tuberculous Meningoencephalitis (Meningitis tuberculosa)
Causative agent: Mycobacterium tuberculosis
Clinical reasoning:
- 6-year-old child — peak age for TB meningitis in children (following primary TB infection)
- Subacute onset over 2 months — low-grade fever (37.3°C), night sweats, rare cough → suggests a prodromal / primary pulmonary TB phase
- Gradual progression to headache, vomiting → signs of meningeal involvement and raised intracranial pressure
- CSF profile perfectly matches TBM: clear CSF, fibrin pellicle, moderate mixed pleocytosis, hypoglycorrhachia, elevated protein
- No response to Augmentin (amoxicillin-clavulanate) — this is expected since M. tuberculosis is intrinsically resistant to beta-lactams
Clinical Forms of Tuberculous Meningitis:
| Form | Description |
|---|---|
| Tuberculous serous meningitis (basilar meningitis) | Mild lymphocytic pleocytosis, slightly elevated protein, normal or mildly reduced glucose; often self-limited or prodromal |
| Tuberculous meningoencephalitis | (This patient's form) — Meningeal inflammation extending into brain parenchyma; involves basal cisterns, cranial nerves; headache, vomiting, fever, altered sensorium |
| Tuberculous meningomyelitis | Extension to spinal cord, with paraparesis/radiculopathy in addition to meningeal signs |
| Tuberculous meningitis with hydrocephalus | Thick basal exudate blocks CSF flow → communicating or obstructive hydrocephalus |
| Tuberculoma (space-occupying form) | Focal mass lesion(s) rather than diffuse meningitis; may cause focal deficits or seizures |
Staging (British Medical Research Council):
- Stage I — Alert, no neurological deficit (prodrome phase)
- Stage II — Confusion, minor neurological deficits (this child's likely stage)
- Stage III — Stupor/coma, severe neurological deficit, decerebrate posturing
Key diagnostic features confirming TBM in this child:
| Feature | Significance |
|---|---|
| 2-month subacute illness | Characteristic chronicity of TBM |
| Low-grade fever + night sweats + cough | Primary TB complex / pulmonary TB involvement |
| Failure of Augmentin | M. tuberculosis is beta-lactam resistant |
| Clear CSF with fibrin pellicle | Hallmark of TBM |
| Mixed pleocytosis (52% lymph / 48% PMN) | Early TBM — mixed picture before lymphocyte predominance |
| Glucose 1.8 mmol/L | Hypoglycorrhachia — characteristic of TBM |
| Protein 1.4 g/L (140 mg/dL) | Elevated, within TBM range |
In conclusion, this case represents Tuberculous Meningoencephalitis — the basal/diffuse form of CNS tuberculosis — in a 6-year-old child presenting after a 2-month subacute course with the classic CSF triad of clear CSF with fibrin pellicle + hypoglycorrhachia + elevated protein, with a mixed early pleocytosis.
Sources: Adams and Victor's Principles of Neurology, 12th Ed. • Henry's Clinical Diagnosis and Management by Laboratory Methods • Neuroanatomy through Clinical Cases, 3rd Ed. (Table 5.7)
In short which proper answer
Short Answer
1. CSF Interpretation:
Subacute meningitis pattern — specifically:
- Clear CSF + fibrin pellicle after 72h → hallmark of TBM
- Cytosis 60 cells, mixed (lympho-neutrophilic) → early tuberculous pleocytosis
- Glucose 1.8 mmol/L → hypoglycorrhachia (markedly reduced)
- Protein 1.4 g/L → markedly elevated
2. Nosology:
Tuberculous Meningoencephalitis
(Neurotuberculosis — CNS tuberculosis)
Form → Basal tuberculous meningoencephalitis
Why?
| Clue | Points to TBM |
|---|---|
| 2-month subacute onset | Chronic course of TB |
| Fever 37.3°C + night sweats + cough | Primary pulmonary TB |
| No response to Augmentin | TB is beta-lactam resistant |
| Clear CSF + fibrin pellicle | Classic TBM sign |
| Mixed pleocytosis + low glucose + high protein | TBM CSF triad |
Is it polio?
No — this is NOT Polio.
Here's why polio doesn't fit:
Polio CSF profile:
| Parameter | Polio (typical) | This patient |
|---|---|---|
| Glucose | Normal | Low (1.8 mmol/L) ❌ |
| Protein | Mildly elevated | Markedly elevated (1.4 g/L) ❌ |
| Cells | 10–200, lymphocytes | 60, mixed lymph+neutrophil |
| Fibrin pellicle | Absent | Present ❌ |
| Course | Acute (days) | Subacute (2 months) ❌ |
Key differences:
- Polio is an acute illness — not 2 months of gradual onset
- Polio does not cause hypoglycorrhachia (low CSF glucose)
- Polio does not produce a fibrin pellicle
- Polio presents with flaccid paralysis — this child has headache + vomiting, not limb weakness
- Polio CSF glucose is normal
Bottom line:
The low glucose + fibrin pellicle + 2-month subacute course + night sweats + cough are absolutely incompatible with polio.
The diagnosis remains: Tuberculous Meningoencephalitis.
May be any form ?
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Yes — Could it be a form of Polio?
Polio has 4 forms:
| Form | Features | Matches this case? |
|---|---|---|
| Inapparent (subclinical) | No symptoms, virus in stool | ❌ No — child has meningeal symptoms |
| Abortive polio | Fever, headache, sore throat — NO paralysis, NO CSF changes | ❌ No — CSF is clearly abnormal |
| Non-paralytic (aseptic meningitis form) | Meningeal signs, CSF lymphocytosis, normal glucose, mildly elevated protein | ❌ No — glucose is LOW here |
| Paralytic polio | Flaccid asymmetric paralysis, anterior horn involvement | ❌ No — no paralysis described |
The non-paralytic (meningitic) form of polio is the closest — but still ruled out because:
- Glucose 1.8 mmol/L → LOW — polio never causes low CSF glucose
- Fibrin pellicle → never seen in polio
- Protein 1.4 g/L → too high for polio (usually 50–100 mg/dL)
- 2-month course → polio is acute, not subacute over months
- Night sweats + cough → classic TB prodrome, not polio
Final Answer:
No form of polio matches this clinical and CSF picture.
The diagnosis is Tuberculous Meningoencephalitis — the CSF triad of fibrin pellicle + low glucose + high protein over a subacute 2-month course is specific to TBM, not any form of polio.
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