Meningitis and Encephalitis — Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mr Williams is a 72-year-old retired engineer who presents with a 3-day history of fever, headache, and progressive drowsiness, found this morning unresponsive at home. He has type 2 diabetes, chronic lymphocytic leukaemia on rituximab, alcohol use disorder, and is on warfarin for atrial fibrillation. [1]

His main problems are:

1. Acute community-acquired bacterial meningitis, likely pneumococcal, in an immunocompromised and elderly patient — immediate empiric therapy required
2. Listeria risk (over 50, immunocompromised, alcoholic) — empiric therapy must include ampicillin
3. Encephalopathic presentation (GCS 11) — empiric aciclovir warranted until HSV PCR results
4. Septic shock (hypotensive, tachycardic) — requires ICU admission and resuscitation
5. Anticoagulation on warfarin — complicates LP and warrants reversal strategy
6. Risk of complications — SIADH, seizures, hearing loss, cognitive impairment, cerebral oedema [1]

My immediate plan is to start ceftriaxone, vancomycin, ampicillin, aciclovir, and dexamethasone, take blood cultures, perform CT then LP with reversal of anticoagulation, admit to ICU, and involve infectious diseases and haematology." [1]

Examiner probing questions and model answers

Q1: "Why are you giving ampicillin in addition to ceftriaxone?" [1]

"Because this patient is at high risk of Listeria monocytogenes meningitis. He is over 50, immunocompromised from chronic lymphocytic leukaemia and rituximab, and has alcohol use disorder — all independent risk factors for Listeria. Critically, Listeria is intrinsically resistant to all cephalosporins, including ceftriaxone. Ceftriaxone alone will not treat Listeria. Ampicillin, penicillin, or trimethoprim-sulfamethoxazole are the agents that cover Listeria. In my practice, I add ampicillin 2 g IV every 4 hours to ceftriaxone and vancomycin for any patient over 50 or immunocompromised with suspected bacterial meningitis. The risk of missing Listeria — with its high mortality — far outweighs the minimal additional risk of ampicillin." [1]

Q2: "You mentioned dexamethasone. What is the evidence and what is the timing?" [1]

"The de Gans and van de Beek trial, published in the New England Journal in 2002, randomised 301 adults with bacterial meningitis to dexamethasone 10 mg IV every 6 hours for 4 days or placebo, starting before or with the first antibiotic dose. Dexamethasone reduced unfavourable outcomes from 25 to 15 per cent overall and, in pneumococcal meningitis, from 52 to 26 per cent. The 2015 Cochrane review by Brouwer confirmed benefit in high-income countries, particularly for hearing loss and neurological sequelae. The mechanism is suppression of the subarachnoid inflammatory cascade triggered when antibiotics lyse bacteria and release cell wall products like teichoic acid and endotoxin. This is why the timing is critical — the dexamethasone must be given before or concurrently with the first antibiotic dose to suppress that inflammatory burst. If it is given hours after the first antibiotic, the benefit is largely lost. I give 10 mg IV immediately, then every 6 hours for 4 days, and I continue it only if the Gram stain or culture confirms pneumococcus. If the organism is Listeria or meningococcus, I stop it — there is no evidence of benefit in those organisms, and in Listeria (which is intracellular), steroids may impair clearance." [1]

Q3: "He is on warfarin with an INR of 2.5. How do you manage his lumbar puncture?" [1]

"The anticoagulation complicates the LP because of the risk of spinal epidural haematoma. My approach is risk-stratified. First, antibiotics and dexamethasone must not be delayed for any reason — I start them immediately after blood cultures. Second, because his GCS is 11, he needs a CT head before LP to exclude a mass lesion — that CT also buys me time to address the anticoagulation. I would reverse the warfarin with vitamin K 5 to 10 mg IV and, given the urgency, prothrombin complex concentrate (PCC) to bring the INR under 1.4 rapidly. PCC works faster than fresh frozen plasma and is preferred. Once the INR is under 1.4, I perform the LP. If the clinical picture is deteriorating rapidly and I cannot wait, I would treat empirically on the basis of blood cultures and clinical presentation, and defer the LP. The CSF findings will be altered by antibiotics given before the LP, but the meningitis/encephalitis multiplex PCR detects DNA and is less affected by prior antibiotics than culture." [1]

Q4: "His CSF shows lymphocytic pleocytosis with a very low glucose and very high protein. What is your differential, and how does it change your management?" [1]

"This CSF pattern — lymphocytic pleocytosis with very low glucose and very high protein — is atypical for acute pyogenic bacterial meningitis, which usually shows a neutrophilic predominance. This shifts my differential to three categories. First, tuberculous meningitis — subacute basal meningitis with lymphocytic CSF, very low glucose, and very high protein. I would send CSF for Xpert MTB/RIF (TB PCR) and AFB culture, and ask specifically about TB exposure, night sweats, and weight loss. Second, partially treated bacterial meningitis — if he received antibiotics from his GP before presentation, the CSF can shift from neutrophilic to lymphocytic and be culture-negative. Third, Listeria monocytogenes meningitis — which can produce a monocytic or lymphocytic CSF rather than the classic neutrophilic pattern of pneumococcus. The multiplex PCR will help here because it detects DNA regardless of the cellular pattern. If TB meningitis is confirmed or strongly suspected, I add four-drug anti-TB therapy (isoniazid, rifampicin, pyrazinamide, ethambutol) and adjunctive dexamethasone per the Thwaites trial, which showed a mortality benefit." [1]

Q5: "Two days into his admission, his sodium is 122 mmol/L. What is happening and what do you do?" [1]

"This is the syndrome of inappropriate antidiuretic hormone secretion (SIADH), which is common in bacterial meningitis — the meningeal inflammation and the associated cerebral oedema trigger ADH release, causing water retention and dilutional hyponatraemia. The danger is cerebral oedema from hypo-osmolality compounding the existing intracranial pathology. My management: first, I stop all hypo-osmolar fluids and put him on fluid restriction if sodium is above 125. At 122, he needs active correction with hypertonic saline (3 per cent) — I would give 100 to 150 mL boluses and recheck sodium every 4 to 6 hours. The critical rule is to correct sodium no faster than 8 mmol/L in 24 hours, because rapid correction risks osmotic demyelination (central pontine myelinolysis). I also monitor urine sodium and osmolality to confirm the SIADH pattern and exclude cerebral salt wasting, which is treated with salt supplementation rather than fluid restriction." [1]

Q6: "What is his prognosis, and how would you discuss this with his family?" [1]

"The prognosis of bacterial meningitis in this context is guarded. His adverse prognostic factors include age over 60, reduced GCS at presentation (11), immunocompromise, and septic shock — all independently associated with worse outcome. Pneumococcal meningitis in this age group carries a mortality of 20 to 30 per cent and a significant risk of neurological sequelae including hearing loss (10 to 30 per cent), cognitive impairment, and seizures. With my family discussion, I would be honest but not nihilistic. I would explain that we have started the best available treatment immediately, that the next 48 hours will tell us how he responds, and that we are watching closely for complications. I would offer early and honest communication about goals of care, particularly if he does not improve or if devastating complications emerge. I would involve the palliative care team if the prognosis becomes clearly poor, and I would ensure the family understands the range of possible outcomes — from full recovery to severe disability to death." [1]

Short Case Discussion

Scenario: "Examine this patient's neurological system. She is a 35-year-old woman recovering from pneumococcal meningitis."

Candidate presentation (model): [1]

"I examined Ms Davies' neurological system. She is alert and cooperative but appears to have difficulty hearing when I speak to her from the right side. She has no overt facial asymmetry or limb weakness on general inspection. [1]

On mental state examination she is oriented in time, place, and person, with fluent speech and normal comprehension. Her GCS is 15. [1]

Cranial nerve examination reveals a right-sided sensorineural hearing loss — the Rinne test shows air conduction greater than bone conduction bilaterally, but the Weber test lateralises to the left, confirming a right sensorineural loss. The remaining cranial nerves, including fundoscopy (no papilloedema), are normal. [1]

Motor examination shows normal tone, power 5/5 in all four limbs, symmetric reflexes, and downgoing plantars. Sensation is intact to pinprick, light touch, vibration, and joint position. Coordination is intact on finger-nose and heel-shin testing. Her gait is normal. [1]

These findings — right sensorineural hearing loss in a patient recovering from pneumococcal meningitis — are consistent with post-meningitic cochlear damage. I would arrange formal audiometry to characterise the loss, inform the patient about the prognosis (which may be partial or complete recovery), and consider hearing rehabilitation if the loss persists." [1]

Examiner: "Why does pneumococcal meningitis cause hearing loss?" [1]

"The inflammation in the subarachnoid space extends along the eighth cranial nerve and into the cochlea via the cochlear aqueduct, causing inflammation of the cochlear hair cells and the stria vascularis. This is why the hearing loss is sensorineural rather than conductive. The cochlear aqueduct provides a direct pathway for the meningeal infection and inflammation to reach the inner ear. Dexamethasone reduces this inflammation and has been shown to reduce the incidence of severe hearing loss after bacterial meningitis, particularly in Haemophilus influenzae and pneumococcal meningitis. This is one of the reasons dexamethasone is part of the standard empiric regimen." [1]

Examiner: "What other complications of bacterial meningitis should you screen for at follow-up?" [1]

"At the 6-week follow-up I would screen for: sensorineural hearing loss with formal audiometry; cognitive impairment with a brief cognitive assessment (Montreal Cognitive Assessment or formal neuropsychology if deficits are suspected); seizures, which may require ongoing anticonvulsant therapy; and mood disorders, particularly depression and anxiety, which are common after critical illness and ICU admission. I would also ensure he has received the appropriate vaccinations (pneumococcal, meningococcal) to reduce the risk of recurrence, and I would review his immunosuppressive therapy with haematology to determine whether any changes are warranted." [1]

Examiner: "When would you consider autoimmune encephalitis in a patient who presented like this?" [1]

"I would consider autoimmune encephalitis in any patient with suspected encephalitis whose HSV PCR is negative or who is not improving on aciclovir after 48 to 72 hours. The Graus 2016 criteria define possible, probable, and definite autoimmune encephalitis, and they allow a clinical diagnosis of probable autoimmune encephalitis on the basis of subacute onset of psychiatric or cognitive symptoms, at least one supportive investigation (CSF pleocytosis, MRI inflammation, EEG abnormality), and exclusion of alternative causes — even before antibody results return. In that situation, I would send a panel of neuronal surface and intracellular antibodies (CSF and serum), screen for an occult tumour (CT chest/abdomen/pelvis, and pelvic ultrasound or MRI in a young woman to look for ovarian teratoma in suspected anti-NMDAR), and start empiric immunotherapy with high-dose methylprednisolone. The key antibody-mediated syndromes to recognise are anti-NMDAR (young women, psychiatric presentation, orofacial dyskinesias, ovarian teratoma), anti-LGI1 (older men, faciobrachial dystonic seizures, hyponatraemia), and anti-CASPR2 (neuromyotonia, Morvan syndrome)." [1]