Bedside Doppler Ultrasound Catches Hidden Brain Pressure Surge in Pneumococcal Meningitis

When a woman in her seventies arrived at the emergency department by ambulance, she was already fighting for her life. She had spent a week battling what seemed like a common cold, followed by two days of right-sided headache, ear pain, and discharge from the ear. Then, within a single day, her alertness collapsed. On arrival, her Glasgow Coma Scale score was just 6 out of a possible 15, she was burning with fever at 39 degrees Celsius, her heart raced at 119 beats per minute, and her blood pressure had climbed to 164 over 74 millimetres of mercury. She was breathing 15 litres of oxygen per minute through a non-rebreathing mask just to keep her saturation at 98 percent. The clinical picture pointed to one terrifying diagnosis: community-acquired bacterial meningitis, the kind that kills or cripples a large proportion of the adults it strikes.

Computed tomography of her head revealed the anatomy of the disaster. Communicating hydrocephalus had developed, with cerebrospinal fluid migrating across the ventricular walls in a pattern known as transependymal migration. The right mastoid air cells and middle ear were opacified, marking the otogenic route by which the infection had invaded the skull. There was no midline shift and no cortical herniation, which might have suggested the crisis was not yet at its peak. Empirical ceftriaxone, amoxicillin, and aciclovir were started immediately. But because she was vomiting and deteriorating, she was intubated for airway protection, and this is where the case became a lesson in the limits of bedside medicine.

Lumbar puncture is the standard method for measuring intracranial pressure at the bedside. A manometer attached to the spinal needle records the opening pressure of cerebrospinal fluid. But the technique depends on free communication between the fluid compartment, the needle, and the manometer column. In this patient, the cerebrospinal fluid was thick, turbid, blood-stained, and heavily proteinaceous. The manometer column could not be filled adequately. On reattempt, an opening pressure of 23 centimetres of water was recorded, with a closing pressure approaching zero. Both values were considered technically unreliable because adequate flow through the needle could never be established. The number could have appeared only modestly elevated, yet the flow dynamics told a different and more dangerous story.

Laboratory analysis of the cerebrospinal fluid confirmed the severity of the inflammatory burden. It contained 679 white cells per microlitre, almost all polymorphs, with protein at 10.42 grams per litre against a reference range of 0.15 to 0.45, glucose below 0.5 millimoles per litre, and lactate at 30.8 millimoles per litre against a reference range of 1.1 to 2.8. Gram stain showed Gram-positive cocci in pairs and chains, pneumococcal latex agglutination was positive, and cultures subsequently confirmed Streptococcus pneumoniae. Dexamethasone was commenced after the lumbar puncture, and neurosurgical review supported conservative management with close reassessment rather than immediate cerebrospinal fluid diversion, partly because the technically uncertain pressure measurement contributed to clinical equipoise.

Approximately five hours later, with the patient still comatose and sedated, the clinical team turned to transcranial Doppler ultrasonography. Using a point-of-care ultrasound system with a sector probe through the bilateral transtemporal acoustic windows, they insonated the middle cerebral arteries and examined the spectral waveforms. What they saw was striking. On colour-coded duplex imaging, the intracranial arterial colour signal was clearly visible during systole but markedly diminished or disappeared entirely during diastole, producing what the team described as a peek-a-boo appearance. On spectral Doppler, this corresponded to preserved systolic forward flow with markedly attenuated, near-absent diastolic flow bilaterally.

The physiology behind this warning pattern is elegant and unforgiving. Cerebral perfusion pressure equals mean arterial pressure minus intracranial pressure. As downstream pressure rises, forward flow is lost first during diastole, when the driving pressure is lowest. Progressive elevation of intracranial pressure produces reduced diastolic velocity, then near-absent diastolic flow, and eventually oscillating or reverberating flow associated with cerebral circulatory arrest. Transcranial Doppler does not directly measure intracranial pressure, and it cannot provide an exact numerical value. But a severely abnormal bilateral waveform, interpreted alongside persistent coma, CT-confirmed hydrocephalus, highly abnormal cerebrospinal fluid, and an earlier technically unreliable lumbar puncture, is a haemodynamic alarm that demands immediate action.

That is precisely what happened. The bilateral waveform abnormality acted as an escalation signal, prompting urgent reassessment. An immediate repeat lumbar puncture measured an opening pressure of 42 centimetres of water, confirming critical intracranial hypertension. Forty millilitres of turbid cerebrospinal fluid were drained therapeutically. Following urgent neurosurgical discussion and CT brain volumetry, a right frontal external ventricular drain was inserted on day 2, with turbid cerebrospinal fluid encountered under high pressure on the first pass. Source control was achieved with right tympanostomy tube insertion on day 2 and right cortical mastoidectomy on day 3, which identified two tegmen dehiscences providing the likely route of intracranial infection. Ceftriaxone was continued as definitive therapy for four weeks.

The patient survived despite several poor prognostic features at presentation, including a Glasgow Coma Scale score of 6, communicating hydrocephalus, multifocal intracranial disease, and cerebral venous sinus thrombosis. CT venography later demonstrated partially occlusive left transverse sinus thrombosis and a small right transverse sinus filling defect, consistent with septic lateral sinus thrombosis. Anticoagulation was commenced with low molecular weight heparin and subsequently transitioned to rivaroxaban after multidisciplinary hematology review. By day 5, CT showed mild reduction in ventricular size, the external ventricular drain was clamped and then removed on day 6, and she was extubated on day 7. By day 13, her Glasgow Coma Scale score was documented as 15, with improving alertness and speech.

Recovery has been real but incomplete. She experienced fluctuating consciousness, sleep-wake cycle disturbance, dysphonia, dysphagia requiring nasogastric feeding, and cognitive-linguistic impairment. She was transferred to specialist neurorehabilitation, where she has been improving in mobility, vocalization, and engagement with therapy. But she continues to experience marked short-term memory and concentration difficulties, with intermittent confusion. Discharge home is being planned. Her husband described the neurocritical care admission as traumatic and expressed gratitude to the teams involved, hoping that sharing the case would improve recognition and treatment of severe meningitis while encouraging clinicians to combine technical expertise with sensitive communication to families during life-threatening illness.

The central lesson of this case is reproducibility. In comatose bacterial meningitis with hydrocephalus, an apparently non-critical lumbar puncture opening pressure should not reassure when manometry is technically difficult or cerebrospinal fluid flow is poor. Bedside transcranial Doppler cannot measure intracranial pressure, but a severely abnormal bilateral waveform may provide an urgent, repeatable haemodynamic warning that should prompt integration with imaging and clinical findings, repeat measurement, and escalation to cerebrospinal fluid diversion when appropriate. The technique is operator-dependent, adequate transtemporal acoustic windows may not be obtainable in all patients, and waveform morphology is influenced by arterial pressure, carbon dioxide levels, cerebrovascular resistance, and other physiological factors. It is not a substitute for direct pressure measurement or invasive monitoring. But as this case demonstrates, when the numbers are unreliable and the patient is deteriorating, a striking waveform pattern at the bedside can be the difference between catching a pressure surge in time and missing it entirely.

Subject of Research: Bedside Transcranial Doppler as a Dynamic Warning Tool for Rapidly Evolving Intracranial Hypertension in Pneumococcal Meningitis

Article Title: Bedside Transcranial Doppler as a Dynamic Warning Tool for Rapidly Evolving Intracranial Hypertension in Pneumococcal Meningitis

Article References: Ahmed, M., Collins, V., & Lavinio, A. (2026). Bedside Transcranial Doppler as a Dynamic Warning Tool for Rapidly Evolving Intracranial Hypertension in Pneumococcal Meningitis. Clinical Case Reports, 14(10), Article e73733. https://doi.org/10.1002/ccr3.73733

Image Credits: AI Generated

DOI: 10.1002/ccr3.73733

Keywords: Bedside, Transcranial, Doppler, Dynamic, Warning, Tool, Rapidly, Evolving, Intracranial, Hypertension, Pneumococcal, Meningitis