Brain abscess and intracranial suppuration — branching viva

Examiner opening (Examiner)

You are the general paediatric registrar in the emergency department. A nine-year-old boy is brought in with a week of worsening frontal headache and low-grade fever, treated as sinusitis, who this morning is confused and dragging his right leg. His CT is on the screen — a 2.8 cm ring-enhancing left frontal-lobe lesion with oedema and midline shift. Talk me through your immediate assessment and plan. [1]

Exemplar opening (Candidate)

This is a febrile child with evolving focal neurology and a ring-enhancing lesion on CT — I am treating this as a suspected brain abscess, which is a neurosurgical emergency. My first priority is resuscitation and the brain. I will assess and secure his airway, breathing and circulation, treat any seizure with a benzodiazepine, and because he is drowsy with midline shift and signs of raised intracranial pressure, I will elevate the head of the bed to 30 degrees and give an osmotic agent — mannitol 0.25–0.5 g/kg IV or hypertonic 3% saline 2–5 mL/kg IV — for impending herniation. I will not perform a lumbar puncture, because a mass lesion is confirmed and it risks herniation. In parallel I will refer urgently to paediatric neurosurgery and infectious diseases, obtain a contrast MRI with gadolinium and diffusion-weighted imaging to characterise and date the lesion, take blood cultures, and arrange aspiration for pus and culture. [1] [2]

Branch 1 — imaging and the differential (Examiner)

Why MRI with diffusion-weighted imaging rather than just the CT you already have? And what are you trying to distinguish it from? [1]

Exemplar (Candidate)

Contrast MRI characterises the capsule, dates the lesion, detects small or multiple abscesses that CT may miss, and — decisively — diffusion-weighted imaging distinguishes a pyogenic abscess from a tumour. A pyogenic abscess restricts diffusion and appears bright on DWI because of the dense pus and inflammatory cells; a tumour or cystic necrosis usually does not restrict diffusion. I am trying to distinguish abscess from a ring-enhancing tumour (such as a low-grade glioma), a resolving haematoma or infarct, demyelination, and, depending on context, neurocysticercosis or tuberculoma. The combination of fever, a sinus source, raised inflammatory markers and diffusion restriction makes abscess the working diagnosis. [1] [2]

Branch 2 — microbiology and empiric therapy (Examiner)

He is going to theatre for aspiration. What do you want from the sample, and what empiric antibiotics will you start, and why? [6] [2]

Exemplar (Candidate)

I want the pus sent urgently for Gram stain, aerobic and anaerobic culture, and 16S ribosomal RNA PCR for organisms that are slow or fastidious — and I want it before antibiotics if the theatre delay is short, because prior antibiotics sterilise the culture. I will start empiric intravenous therapy with a third-generation cephalosporin, cefotaxime or ceftriaxone, plus metronidazole. This covers the streptococci — especially the Streptococcus anginosus group — and the anaerobes (Bacteroides, Prevotella, Fusobacterium) typical of a sinus source. I would add anti-staphylococcal cover, such as vancomycin, only if the source were trauma, neurosurgery or a shunt. I will then tailor the regimen to the organism and its sensitivities. [6] [2]

Branch 3 — the neurosurgical decision (Examiner)

He has a single 2.8 cm frontal abscess with midline shift. Aspiration, excision, or medical management — how do you decide? [1]

Exemplar (Candidate)

Aspiration via a burr-hole or stereotactic route is the usual first approach here: it is diagnostic, drains the collection, provides culture material, and can be repeated. Surgical excision is reserved for large, superficial, multiloculated or re-expanding lesions, and for posterior-fossa abscesses where aspiration alone is hazardous. Medical management alone is considered only for small lesions under about 2.5 cm, deep lesions, or multiple haematogenous abscesses when the organism is known and the child is improving — and that does not apply here, because he has a 2.8 cm lesion with mass effect. So this child goes for aspiration, with serial MRI afterwards and repeat aspiration if it re-expands or he fails to improve. [1]

Branch 4 — subdural empyema (Examiner)

If the MRI instead showed a subdural collection, how would your management change? [3]

Exemplar (Candidate)

Subdural empyema changes the urgency. The subdural space has no anatomical barrier, so pus spreads freely across the cortical surface and infected cortical veins develop septic thrombophlebitis — the collection can enlarge and cause herniation within hours. It is a neurosurgical emergency requiring urgent evacuation, not antibiotics and a repeat scan. If it were sinogenic in origin, I would also involve ENT for combined endoscopic sinus surgery to clear the source. The empiric antibiotics would be the same, but I would not delay surgery for them. [3]

Branch 5 — corticosteroids (Examiner)

The neurosurgeon asks whether to start dexamethasone. What is your answer, and what is the evidence? [4]

Exemplar (Candidate)

Not routinely. A systematic review and meta-analysis found that dexamethasone use was associated with higher mortality in brain abscess, although confounding by severity limits the causal inference. The consensus, reflected in the 2024 ESCMID guideline, is to reserve corticosteroids for significant mass effect or impending herniation, use the lowest effective dose, and taper as soon as the oedema settles — because routine use may dampen inflammation and delay capsule formation. For this boy with midline shift and drowsiness, I would consider a short, tapering course of dexamethasone to control the oedema in the acute period, and stop it as soon as the mass effect settles. [4] [2]

Branch 6 — duration and follow-up (Examiner)

How long will you treat him, and when will you consider switching to oral therapy? [2] [5]

Exemplar (Candidate)

The intravenous course is typically four to six weeks, and I would extend it to six to eight weeks for a lesion of this size with mass effect, guided by his clinical course, his inflammatory markers and serial MRI. I will monitor with serial MRI until the lesion resolves, watching for re-expansion or daughter lesions. I will consider a switch to oral therapy only when he is afebrile and clinically improved, his inflammatory markers are falling, source control is complete — meaning the sinus disease has been treated — and a suitable oral agent with good bioavailability and proven susceptibility is available. He also needs neurodevelopmental and seizure follow-up, because a substantial minority of survivors develop late epilepsy or cognitive sequelae that emerge over years. [2] [5]

Examiner wrap-up (Examiner)

Thank you. Summarise the three points you most want the examiner to remember. [1]

Exemplar (Candidate)

First, a febrile child with any new neurological sign is a scan, not reassurance — the classic triad is present in fewer than a quarter. Second, aspirate for pus before antibiotics when safe, because the culture guides weeks of therapy, and start a third-generation cephalosporin plus metronidazole. Third, subdural empyema is a neurosurgical emergency — the subdural space has no barrier — so urgent evacuation is mandatory, and lumbar puncture is contraindicated when a mass is present. [1] [3]