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Abstract

The risk of lumbar puncture (LP) to precipitate brain herniation in acute bacterial meningitis (ABM) was reviewed in this journal in 2007. We report the case of an infant with ABM who had acute apnea requiring intubation and tonic posturing (mistaken for seizure), and then had brain herniation within four hours of an LP. The case prompted this updated narrative review, from 2007 to 2024, focused on the twelve points made in 2007. The review included 14 case reports of brain herniation shortly after LP in ABM, 23 observational studies or systematic reviews, 28 narrative reviews, and 9 guidelines, each with evidence, advice, or recommendations important for the decision to perform LP in ABM. We found evidence to support, and did not find convincing evidence to refute, the twelve points. We found five additional claims made that were meant to refute some of the original points; however, these were based upon data that did not support the claims made. Limitation of the evidence reviewed was the absence of randomized trials to prove whether those patients who herniated may have been destined to herniate regardless of whether they had an LP. Reasons why ABM may be a unique circumstance where normal CT scan cannot determine the risk of herniation after an LP were discussed. We argue that the preponderance of evidence supported the conclusion that, in a patient with strongly suspected ABM who is clinically considered at high risk for herniation, interventions to control ICP and antibiotics administration should be the priority, followed secondarily by an urgent CT scan and, even with a normal CT, not an LP. The case report emphasized that respiratory arrest or suspected tonic seizure can be due to early herniation, and indicate CT scan, and prolonged LP deferral (for 3-4 days) even with a normal CT.

Keywords

acute bacterial meningitis herniation lumbar puncture computed tomographic scan

Introduction

A crucial decision in practice is when to consider delaying a lumbar puncture (LP) in suspected acute bacterial meningitis (ABM) due to the risk of the LP precipitating or worsening brain herniation.¹ One of us reviewed the literature on this topic in 2007, supplemented with another related review in 2010.^1,2 Twelve important points relevant to this risk were made in those two papers, summarized in Table S1.^1,2 The general conclusion was that, in those considered at high risk for herniation, interventions to control intracranial pressure (ICP) and antibiotics administration should be the priority, followed secondarily by an urgent computed tomographic (CT) scan and not an LP.¹ This was because clinical signs of ‘impending herniation’ were found to be the best indicators of who should not have an LP done [even with normal CT scan] in the setting of ABM due to the risk that the LP can precipitate or complete herniation.¹ These clinical signs included significant alterations in level of consciousness (often increasing in degree), seizure within 30 min (which often precedes a terminal respiratory arrest during herniation), decerebrate or decorticate posturing (that may be mistaken for a tonic seizure), respiratory abnormalities (Cheyne-Stokes, hyperventilation, or apnea), and pupillary changes.¹ Importantly, evidence was reviewed that demonstrated that a CT scan cannot reliably detect high ICP or risk of herniation in ABM.¹

A recent case of ABM having brain herniation shortly after an LP prompted us to update the review. The objective was to determine evidence published since the 2007 review that supported or not the twelve important points previously made. The case report and updated narrative review led us to re-emphasize the important points previously made, and also to draw attention to points that were not sufficiently emphasized in the previous reviews.

Case Report

Signed informed consent to publication of this case report was provided by the patient's legal guardian. An 18-month-old previously healthy fully immunized male presented to a rural hospital emergency department (ED) with a 3-day history of fever, cough, irritability, loose stools, and emesis. He was diagnosed with bilateral acute otitis media, started on oral clarithromycin, and discharged home. Over the next day at home he experienced increasing lethargy, refusal to walk, and poor appetite, and therefore returned to the rural ED. At that time, he received 40 ml/kg of intravenous (IV) fluids for dehydration, blood culture was drawn, and ceftriaxone IV given. He was then transferred to a regional ED for further management, where, upon arrival, his HR was 190 and capillary refill 4 s. There he received another 10 ml/kg IV fluid, and an epinephrine infusion at 0.1 mcg/kg/min was started. Approximately 15 min after arrival he had sustained apnea requiring bag-valve mask ventilation, unresponsiveness, and tonic posturing thought to be a tonic seizure. He was intubated with ketamine anesthetic, with initial end tidal carbon dioxide of 70–90 mm Hg, and was loaded with levetiracetam (60 mg/kg IV). Due to the tachycardia, he was given one dose of adenosine. At this time the pediatric intensive care unit (PICU) transport team was dispatched to transfer the patient to our children's hospital.

On arrival of the transport team, he was hemodynamically stable, ventilation was optimized (pH 7.3 and PCO₂ 40 mm Hg on capillary blood gas), sedation was adjusted to a propofol infusion, vancomycin and acyclovir IV were administered, and he was transported to our PICU. Upon arrival to PICU the epinephrine infusion was discontinued, and the propofol stopped. Approximately 3 h after stopping propofol his Glasgow Coma Scale (GCS) was 9, with localization to stimuli, opening eyes to pain, equal reactive pupils, and no focal neurological deficits. No CT scan was performed at any point prior to the LP. An LP was done with anesthesia (using ketamine) on the first attempt approximately 17 h after the episode of apnea and intubation. Cerebrospinal fluid (CSF) analysis showed protein 1.05 g/L, glucose 1.0 mmol/L, RBC 150 × 10⁶/L, WBC 2669 × 10⁶/L with 72% neutrophils, and gram-positive cocci in pairs on gram stain, confirming ABM. Opening pressure was not measured. Blood Culture grew Streptococcus pneumonia sensitive to penicillin, and CSF culture was negative.

Less than 4 h after the LP he developed decerebrate posturing, decreased GCS to 4, and sunset eyes. Mannitol and 3% saline were administered. An urgent head CT performed less than 1 h later showed marked cerebellar edema concerning for ischemia with tonsillar herniation, early uncal herniation, and acute obstructive hydrocephalus due to occlusion at the foramen magnum (Figure 1).

Figure 1.

Noncontrast head CT performed just under 4 h after the LP. A) Sagittal image shows severe downward cerebellar tonsil herniation (red dotted line) that occludes the foramen magnum and causes acute obstructive hydrocephalus at the level of the foramen magnum with dilation of the fourth ventricle (4) and the aqueduct of sylvius (white arrow), as well as mass effect on the brainstem and effacement of the pre-pontine cistern. B) Axial image shows dilation of the lateral ventricles (asterisk) with effacement of the sulci/gyri along the cerebral convexities indicative of increased intracranial pressure from the acute obstructive hydrocephalus. The third ventricle was also dilated (not shown). Parasagittal cuts through the right C) and left D) cerebellar hemispheres show evolving early hypoattenuation involving the posterior inferior aspects of the cerebellar hemispheres bilaterally (dashed white line), indicative of early ischemic change in the posterior inferior cerebellar artery (PICA) vascular territories. This pattern of ischemic injury is seen specifically with acute, severe downward tonsillar herniation through the foramen magnum, which causes compression/compromise of the bilateral PICA's as they come off the high vertebral arteries.

Within one hour after the head CT, the patient underwent emergent insertion of an external ventricular drain (EVD). The ICP initially measured 25 cmH₂O, and decreased to 12 cmH₂O with CSF drainage. An MRI immediately after the operation showed improved but still significant tonsillar herniation and hydrocephalus, as well as diffuse ischemia in the posterior inferior cerebellar hemispheres bilaterally corresponding to the posterior inferior cerebellar artery vascular territories (Figure 2).

Figure 2.

MRI of the brain with and without IV contrast performed immediately after external ventricular drain placement, 2.25 h after CT scan, and 6 h after LP. Axial diffusion-weighted imaging (DWI) (A) and corresponding Apparent Diffusion Coefficient (ADC) map (B) show diffuse signal abnormality (dashed white line) indicative of cytotoxic edema from ischemia involving the posterior inferior cerebellar hemispheres bilaterally, again corresponding to the bilateral PICA territories. Coronal T2-weighted image (C) shows ongoing dilation of the lateral ventricles (asterisk) immediately post EVD placement with corresponding abnormal T2-hyperintense signal in the cerebellar PICA territories at the sites of ischemia (white dashed line). Sagittal post-contrast T1-weighted image (D) shows improved but still severe cerebellar tonsil herniation (red dotted line), with ongoing mild mass effect on the pons (star) and pre-pontine cistern, as well as dilation of the fourth ventricle (4) and the aqueduct of sylvius (arrow). Additional minor scattered DWI signal abnormality was noted in the cortex of the bilateral parietal and occipital regions, as well as along the ventricular lining, in keeping with changes from meningitis-related sites of cerebritis and ventriculitis. No additional large territorial vascular injury related to herniation was identified.

Four days after EVD placement, upon weaning of sedation, he again developed an increased ICP (15-20 cmH₂O). The GCS remained at 7–8 and there was now left hemiparesis (arm worse than leg). Repeat CT and MRI at this time demonstrated severely increased edema and bulkiness of the ischemic cerebellum with resultant significantly worsened hydrocephalus, now with trans-ependymal flow of CSF, and progressive severe compression of the brainstem (Figure 3). Within hours he underwent a second emergent neurosurgery for posterior fossa decompression, and resection of both the infarcted cerebellar tonsils and portions of infarcted cerebellum.

Figure 3.

MRI of the brain performed 4 days after LP and external ventricular drain placement. Axial (A), coronal (B), and sagittal (C) T2-weighted images show worsened T2-hyperintense edema at site of posterior inferior cerebellar artery territory infract in the bilateral cerebellar hemispheres (dashed white line), with worsening mass effect in the posterior fossa where there is increasing tonsillar herniation (red dotted line), increased flattening of the brainstem, and worsening of obstructive hydrocephalus (asterisk) in spite of EVD placement (yellow arrow).

Ten days after his arrival at our PICU he was extubated. He was discharged from PICU with left hemiparesis, swallowing dysfunction, no verbal communication, and poor neck and truncal tone. Four weeks later, he was discharged to the rehabilitation hospital, where he continued to demonstrate improvements. At discharge from the rehabilitation hospital he had ataxia, was crawling, self-feeding, interactive and speaking some sentences, without residual hemiparesis.

Methods

We searched PubMed in October 2024 using the title/abstract terms ‘meningitis’ and ‘herniation’; ‘meningitis’ and ‘guideline’; and searched citations of Joffe 2007.¹ The search was from January 2007 to October 2024. Reference lists in relevant articles were screened for eligibility, and included publications’ reference lists were in turn screened for further relevant publications. We included any publication that was: i) a case report of brain herniation in ABM, or ii) a case series that presented data on brain herniation in ABM or on the risk of LP in ABM, or iii) a review article or guideline on AMB that discussed contraindications to LP. Study inclusion was determined by one of the authors after review of abstract and if necessary full text. Information from each included study was recorded according to its relevance to the previous 12 important points made. A narrative synthesis of this evidence was completed, as the outcomes (ie, relevance to each of the 12 points) were not amenable to meta-analysis. Evidence synthesis was first done by one of the authors, and then reviewed by all authors for accuracy.

Results

Case Reports of Brain Herniation in ABM

In addition to the 22¹ and 10² case reports of brain herniation occurring shortly after an LP in ABM previously reviewed,^1,2 there were 14 more cases, detailed in Table 1.^3–15 Most cases described pre-LP altered level of consciousness (10), and some reported recent seizure (1), anisocoria (1), apnea (1), repeated vomiting (6), or worsening headache (1). Pre-LP CT was normal in 5 and abnormal in 2.

Table 1.

Case Reports of Herniation Occurring Shortly After a Lumbar Puncture in Acute Bacterial Meningitis That Were not Included in the Previous Reviews.^1,2

Authors	Year	Age, Cause	Pre-LP	Post-LP	Comments
Feske et al³	1992	4 days old, Group B Streptococcus	Apneic episode, arching of back.	Irritable, opisthotonic posturing, bulging tense anterior fontanelle. Within 24 h irregular respirations, asymmetrical pupils, obtunded, ventilated. CT diffuse cerebral edema. Autopsy herniation.	Death.
Ibsen⁴	2002	16 years old, Neisseria meningitidis	1 day of fever, headache, lethargy. Vomited several times, disoriented, incontinent. Confusion and anisocoria.	OP 55 cmH₂0. Treated with mannitol. CT head normal. On arrival on transfer BP 168/100, HR 80, decerebrate posturing. ICP 80 mm Hg so given mannitol, pentothal, external ventricular drain, and dopamine to raise mean arterial pressure.	Normal neurologic examination on discharge.
Baussart et al⁵	2006	28 years old, Neisseria meningitidis	1 day of headache and vomiting, GCS 15.	30 min after LP GCS 4 and dilated left pupil. CT diffuse cerebral edema and both occipital and left temporal herniations. Elevated ICP was treated aggressively, including craniectomy.	Incomplete Broca's aphasia
Muralidharan et al⁶	2011	21 years old, Streptococcus pneumonia	3 days of headache followed by “acute stupor”, combativeness, and fever. CT mild generalized cerebral edema. Intubated and sedated.	Next morning, he did not awaken despite discontinued sedation (deeply comatose). Minimally reactive pupils without corneal, gag, or cough reflexes, and oculocephalic reflexes only present on one side, and no motor response. CT showed early cerebellar tonsillar herniation. Treated with dexamethasone and mannitol for ICP 80 mm Hg.	Long-term had walking with two-person assistance.
Kalay et al⁷	2011	22 day old	Progressive lethargy and feeding intolerance, bulging anterior fontanelle, hypoactive and hypotonic. Had high ammonia of 339 µmol/L.	15 min after LP “became hypotensive with shallow respirations and exhibited posture change. She was promptly intubated and stabilized with mechanical ventilation. The pupils were fixed and dilated with absent corneal and gag reflexes.” MRI diffuse cerebral edema and tonsillar herniation.	Not reported. Galactosemia diagnosed.
Adriani et al⁸	2012	43 years old, 29 weeks pregnant, Streptococcus pneumonia	Otitis, GCS 11	Brain herniation indicated by “deterioration of consciousness, bradycardia and fixed and dilated pupils.”	Death within 6 h [fetus good outcome on emergency Caesarean].
Adriani et al⁸	2012	36 years old, 36 weeks pregnant, Streptococcus pneumonia	Otitis, GCS 11	Brain herniation indicated by “deterioration of consciousness, bradycardia and fixed and dilated pupils.”	Death within 6 h [fetus good outcomes on emergency Caesarean].
Berkowitz et al⁹	2013	44 years old, Streptococcus pneumonia	1 day of headache and nausea. Developed fever and confusion, unable to answer questions or follow commands (GCS 13). CT normal.	Opening pressure 49 cmH20. 6 h after LP found to be apneic and intubated. Opened eyes to voice, but flaccid paralysis. Treated with hypertonic saline, mannitol, external ventricular drain, and decompressive suboccipital craniectomy.	Remained with quadriplegia, anarthria, and ventilator dependence.
Ramesh¹⁰	2013	Child, not reported	Acute onset worsening headaches and neck stiffness.	1 h after LP “she abruptly deteriorated.” Brain MRI 12 h later showed tonsillar herniation.	Modest recovery of quadriplegia.
Costerus et al¹¹	2018	48 years old, Streptococcus pneumonia	2 days of headache, nausea, fever, presented with GCS 3 and seizures, and CT generalized edema causing brain shift with partial obliteration of basal cisterns and hydrocephalus.	1 h after LP had fixed dilated pupils, and CT showed complete obliteration of basal cisterns and cerebral herniation.	Death.
Al Noaim¹²	2018	10 years old, Streptococcus pneumonia	2 days headache, recurrent vomiting. GCS 15. CT normal.	1 h 50 min after LP developed irregular respiration, GCS 3, fixed dilated pupils.	Death.
Chen et al¹³	2020	45 years old, Streptococcus pneumonia	Klippel-Feil syndrome. Headache, fatigue, vomiting, “inattentive, confused, and disoriented”. CT interpreted as normal, but “in retrospect revealed mild crowding of the foramen magnum owing to basilar invagination, platybasia, and cerebellar tonsillar ectopia”.	Shortly after LP rapidly deteriorated to locked-in syndrome and requiring ventilation. MRI tonsillar descent with cervicomedullary compression.	Locked-in state.
Yang et al¹⁴	2022	Adolescent, Neisseria meningitidis	Headache, vomiting, confused and not able to follow commands, GCS 13, CT normal.	LOC “subsequently deteriorated”, and she was intubated and ventilated. Within 48 h, had fixed dilated pupils, absent gag and corneal reflexes. CT diffuse edema and obliterated basal cisterns. Elevated ICP was treated aggressively.	Full recovery.
Stanley et al¹⁵	2024	6 years old, Streptococcus pneumonia	Vomiting, seizures, “opening his eyes intermittently to his voice, moving all extremities, and being post-ictal.” CT normal.	Shortly after LP GCS <12, left pupil dilated, EEG status epilepticus. Within 9 h dilated fixed right pupil, agitation, and respiratory depression, and after intubation fixed dilated pupils.	Death.

CT: computerized tomography scan of head; GCS: Glasgow Coma Score; ICP: intracranial pressure; LP: lumbar puncture; OP: opening pressure. Of note, anisocoria,⁴ and partial obliteration of basal cisterns with GCS 3,¹¹ may have indicated brain herniation that started prior to the LP.

Observational Studies with Data on Brain Herniation or Risk of LP in ABM

Since the original reviews, 23 relevant observational studies or systematic reviews were found.^16–40 These are presented in Table 2, organized by whether and how each supported one (or more) of the 10 points made in the previous review. Two additional claims were made in these case series that may appear to be contrary to our general point 10; however, limitations in the data used to support these claims make them unsupported by data (detailed in Table 2, Comments column).

Table 2.

Updated Observational Studies or Systematic Reviews with Relevant Evidence About When to do a Lumbar Puncture in Acute Bacterial Meningitis.

Point made	Evidence provided	Comments
1. Brain herniation accounts for a significant proportion of deaths in ABM.	Koelman et al (2020) found brain herniation in 4.4% of cases, causing 21.5% of deaths.¹⁶ Weisfelt et al (2006) found brain herniation in 3.2% of cases, causing 10.3% of deaths.¹⁷ Weisfelt et al (2006) found brain herniation caused 23% of deaths in younger patients versus 2% of older patients (p = 0.004), likely attributed to age-related cerebral atrophy.¹⁸ Lucas et al (2014) found that, of those with GCS 3, mortality was 18/30 (60%), with acute brain herniation causing at least 4/18 (22%) of these deaths.¹⁹ Sharew et al (2020) found that, of 84 deaths, 8 (10%) were caused by herniation.²⁰	The studies included only patients having an LP, hence likely underestimating the risk of LP. Overlapping patients among studies.
2. Raised ICP is common in ABM.	Weisfelt et al (2006) found that, in 114 having OP measured, median was 40 cmH2O [range 7 to 70], and OP >40 cmH2O was associated with lower GCS.¹⁷ Costerus et al (2018) found that, in the 19/47 patients who had acute deterioration within 8 h of LP and had OP measured, the OP was >40 cmH2O in 15 (79%).²¹	Most patients did not have OP measured. Overlap in patients between the two studies.
3. With mass lesion, herniation after an LP may not be rare, may be gradual, and is likely due to focal or diffuse brain shift.	Niemantsverdriet et al (2015) and Engeborghs et al (2017): systematic review found post-LP-headache occurs in 1–40%, within 3 days after LP (and within 48 h in 66%), thought to be caused by “faster leakage of CSF through the dural puncture site into the epidural and paravertebral spaces than it can be compensated by its production rate… with resultant downward movement of the brain and traction.” Post-LP-headache was associated with cutting bevel needle [versus atraumatic needle] and large needle bore [≥22G].^22,23 Uppal et al^24,25: systematic review found post-LP-headache was lower with non-cutting needles [“by limiting CSF leakage after dural puncture”], cutting needle bevel parallel to the long axis of the spine [“limits the size of the subsequent dural tear”], lateral decubitus position [“sitting position… [the] higher CSF pressure may also result in a greater leak”], and with an intrathecal catheter [“leaving a catheter in situ reduces CSF leakage”]. MRI can show “manifestations of decreased CSF volume” including “sagging of the brainstem, enhancement of the dura, engorgement of venous structures, pituitary hyperemia, and subdural fluid collections.” Treatment by epidural blood patch “performed ideally at, or one space below” the site of previous dural puncture, likely occurs by “the clot sealing the dural hole and preventing CSF leakage.”	Supports the claim that ongoing CSF leakage after LP can lead to gradual and increasing brain shift.
4. When herniation occurs in ABM, it often occurs shortly after an LP.	Costerus et al (2018) found 3.1% had acute decline in consciousness or cardiorespiratory function within 8 h of LP and died within 7 days.²¹ McDowell & Chapman (2019) point out that according to European guidance on adverse drug reactions, and considering the severity of the reaction (ie, death), this rate of herniation after LP cannot be considered rare (0.01-0.1%), but rather was common (range 1-10%).²⁶ Sharew et al (2020) found that, of 8 deaths caused by herniation, death occurred at 2 [range 1 to 2.8] days.²⁰	In the studies reporting rates of herniation in ABM the herniation occurred after an LP in all cases [inclusion criteria included an LP to confirm a positive culture]. Studies included only deaths, and not morbidity associated with herniation.
5. CT cannot reliably detect the risk of elevated ICP (and hence of herniation) in ABM.	Costerus et al (2018) found that, of 47 patients who had acute deterioration within 8 h of LP, 43 had a prior CT which was normal in 17 (40%).²¹ Larsen et al (2017) found that, of 10 ABM patients with ICP measured ≥40 mm Hg, 6 (60%) had normal CT scan [including 1 with ICP 114 mm Hg 7 h after CT].²⁷ El-Hajj et al (2024) in a systematic review, found six studies that “confirmed that CT… could severely underestimate a raised ICP”, and two studies that found “once abnormal head CT findings were detected, clinical outcomes were remarkably worse.”²⁸	-
6. Focal neurological findings or significantly altered LOC are risk factors for abnormal CT scan that may contraindicate an LP.	Park et al (2022) found “only the IDSA guidelines did not miss any major intracranial abnormality [24 (11.8%): cerebral edema, hydrocephalus, intracranial hemorrhage, pneumocephalus, septic emboli] or any of the 9 patients that the CT scan prompted a neurosurgical intervention [7 EVD, 1 SAH with herniation, 1 empyema].” The main difference from UK, ESCMID, and Swedish guidelines was that IDSA included any “altered level of consciousness”.²⁹ O’Herlihy et al (2024) found the IDSA guideline (vs UK guideline) recommended more CT scans without detecting more “imaging-related contraindications to immediate LP”.³⁰ Salazar and Hasbun (2017): found CT with intracranial abnormalities in 25/193 (18.1%) with IDSA indication for CT, versus 2/356 (0.05%) without IDSA indication (p < 0.05).³¹	Park et al only included those who had a CT and LP; likely excluding those not having LP due to abnormal CT scan.²⁹ Herlihy et al had many limitations: i) only 11/196 had ABM; ii) only findings of “gyral flattening, obliteration of CSF spaces or cerebral herniation” were considered “abnormal with brain shift” and hence to contraindicate immediate LP [incorrectly referencing Joffe 2007¹], which was found in 2/196 (1%); and iii) only 66% of patients had an LP, including only 6/14 with “other abnormal” CT scans.³⁰ Salazar and Hasbun claimed “in this study, an LP was performed in 37 patients with abnormal CT findings with no complications.” Yet, i) patients not having an LP were excluded, ii) only 46/614 patients had ABM, and iii) those with CT indication had more adverse clinical outcomes of GOS 1–4 [59/207 (28.5%) versus 11/407 (2.7%) without CT indication].³¹
7. Clinical signs of ‘impending herniation’ are the best indicators of who should not have an LP done in the setting of ABM because of the risk that the LP can precipitate or complete herniation.	Weisfelt et al (2006) found an OP >40 cmH2O was associated with lower GCS.¹⁷ Costerus et al (2018) found that, of those having herniation within 8 h of LP, the median GCS was 9 [IQR 6, 11] before the LP and 3 [IQR 3, 3] after the LP.²¹ Sharew et al (2020) found the risk factors for fatal CNS complications were GCS <9, and focal neurological deficits. Of herniation cases, 4 had GCS <9, 3 had GCS 9–12, and 1 had GCS 15 prior to LP.²⁰	All patients in these studies had an LP, such that other clinical risk factors may not have been detected (ie, some high-risk patients may not have had an LP and hence not be included in the study).
8. If herniation occurs, it should be treated aggressively as the outcome is not necessarily dismal.	El-Hajj et al (2024) in a systematic review found invasive ICP monitoring and ICP management “may reduce mortality in selected cases of ABM” and “may reduce morbidity in selected cases of ABM” based on low or very low certainty evidence.²⁸	-
9. Delaying LP in those thought to be high risk for brain herniation in ABM would result in a very small proportion where Cefotaxime or Ceftriaxone alone for 10 days would not be adequate therapy.	Trujillo-Gomez et al (2022): in a systematic review and meta-analysis of CSF bacterial PCR panel the sensitivity among 15 studies was 92.1% (95% CI 86.8, 95.3), and not affected by pre-treatment with antibiotics among 2 studies (sensitivity 92.2%; 95% CI 76.5, 97.7).³² Brouwer et al (2010) review found CSF PCR for S. pneumonia, H. influenza, and N. meningitidis had high sensitivity of 61–100%, 72–92%, and 88–94% respectively, possibly lower with pre-treatment with antibiotics (for N. meningitidis sensitivity 81%). CSF culture pre-antibiotics was ∼85% sensitive.³³ Brink et al (2015) in 25 patients with 70 CSF samples found PCR was positive in 89% on days 1–3, 70% on days 4–6 and 33% on days 7–10. The CSF culture prior to antibiotics was positive in 70%. CSF polymorphonuclear and mononuclear leukocytes did not differ between day 0 and day 1–3 of antibiotics.³⁴ Nigrovic et al (2008) in 245 children with ABM found that, after adjustment for patient age, duration and severity of illness at presentation, and bacterial pathogen, longer duration of antibiotic pretreatment was not significantly associated with cerebrospinal fluid white blood cell count, or cerebrospinal fluid absolute neutrophil count. CSF culture pre-antibiotics was 88% sensitive.³⁵	Suggests that diagnosis of ABM can still be made reliably with a delayed LP until clinical signs have persistently resolved. This supports the recommendation to treat for ABM with antibiotic(s) urgently when LP is deferred.
10. In those considered at high risk for herniation, interventions to control ICP and antibiotics should be the priorities, followed by an urgent CT scan and not an LP. Additional claim 1 : Prompt LP regardless of level of consciousness or new onset seizures (that were not ongoing) improved favorable outcomes.^36,37 Additional claim 2 : Those having CT before LP may have delayed time to antibiotics and hence worse outcomes.^36,37,39	Gilmaker et al (2015) found comparing periods before and after revised Swedish guidelines [for prompt LP], the period after was associated with more favorable outcome and lower mortality. Effect was likely mediated by 1.2 h earlier adequate treatment, with relative increase in mortality of 12.6% per hour of delay in treatment.³⁶ Glimaker et al (2018) found adherence to Swedish guidelines associated with decreased mortality and increased favorable outcome. Effect likely mediated by significantly earlier treatment with antibiotics [aOR for treatment within 1 h 2.46 (95% CI 1.60 3.79) and for treatment within 2 h 2.12 (95% CI 1.45, 3.10)]. Antibiotics were started before CT in only half of patients having a CT.³⁷ Costerus et al (2020) found that, among those suspected of ABM (8% confirmed to have ABM), CT was done in 64%, and the start of antibiotic therapy between patients with and without CT before LP were not statistically significantly different, median 134 [IQR 58, 292] versus 141 [52, 227] minutes (p = 0.74) [also the case when restricted to those 16 with ABM].³⁸ Gulholm et al (2023) found that, among those suspected of meningitis, having CT prior to LP was associated with longer time to antibiotic administration.³⁹	Overlap of patients between the Glimaker et al studies.^36,37 Limitations of data for additional claim 1: i) All patients had an LP, no data was given on brain herniation, and the studies assumed CT (when done) excluded herniation risk of an LP. Therefore, no information was provided on the risk of LP in ABM, on risk factors for herniation after an LP in ABM, or on whether prompt LP in those with altered level of consciousness is better than delayed LP, immediate antibiotics, and CT if indicated; ii) observational data cannot demonstrate cause-effect, as claimed by the authors (“We demonstrated that LP in unconscious patients with AMB was not associated with any risks”)⁴⁰ and prompt-LP was likely confounded by the association with earlier antibiotics. Limitations of data for additional claim 2: i) Not confirmed in Costerus et al (2020);³⁸ and ii) unclear whether an emphasis on immediate antibiotics when LP is delayed would lead to the same or better outcomes.

ABM: acute bacterial meningitis; aOR: adjusted odds ratio; CNS: central nervous system; CT: computed tomography scan of head; GCS: Glasgow Coma Score; ICP: intracranial pressure; IQR: interquartile range; LP: lumbar puncture; OP: opening pressure measured on the lumbar puncture.

Narrative Review Articles on ABM That Discussed LP Contraindications in ABM

Since the original reviews, 28 relevant narrative reviews were found.^41–68 These reviews are presented in Table 3, organized by whether and how each review supported one (or more) of the 10 points made in the previous reviews. Three additional claims were made in these reviews that may appear to be contrary to our points 4, 9 and 10; however, limitations in the data used to support these claims make them unsupported by data (detailed in Table 4, Comments column). The narrative reviews often gave variable advice on indications for CT prior to LP, ambiguous advice on whether normal CT was sufficient to warrant an LP in the presence of risk factors, and often did not state that normal CT does not determine the safety of LP in ABM (Table 3).

Table 3.

Updated Narrative Reviews Discussing Relevant Advice on When to do a Lumbar Puncture in Acute Bacterial Meningitis.

Point made	Details provided	Comments
4. When herniation occurs in ABM, it often occurs shortly after an LP. Additional claim 3 : Those who herniate after an LP may have been destined to herniate regardless of whether they have an LP.^41,42	April et al (2017) stated that “half of patients with intracranial mass effect not undergoing LP herniate”.⁴¹ Glimaker et al (2013) claimed that in 6/7 case reports in adults of fatal herniation after LP “had signs of extraordinarily high ICP indicating a possible herniation before LP”, based on the description in the original case reports of the patient being “desperately ill” [Dodge & Swartz], 4 with OP >50 cmH2O [Durand et al], and an “RLS 7” [Grande et al].⁴² Redetsky (2014) reviewed “fulminant” ABM, finding that this may occur in about 1% of AMB, and may be a situation where LP “might only accelerate an otherwise inevitable process”.⁴³ This was “not equivalent to meningitis with clinical brain herniation” in the “rapidity of deterioration [sudden onset with rapid neurological deterioration]” and “refractory nature of intracranial hypertension” [“evolves swiftly despite attempts to control ICP” with “irreversibility of the intracranial hypertension” and death within 36–48 h].⁴³ Giesbush et al (2024) note that “spinal coning [eg, 14% incidence, with symptoms such as rapid-onset paraplegia] has been observed following LP in patients with a complete spinal block, drawing parallels to the risks of brain herniation”.⁴⁴	Limitations of additional claim 3: not supported by the data provided. April et al⁴¹ limitations included: i) the claim was based on very limited data from Hasbun et al, where 4 patients had a CT suggestive of mass effect, did not have an LP, and 2 (50%) within one week herniated and died, and ii) this data had unclear relevance to LP in ABM, as these 4 patients did not have ABM, and the 2 that herniated were described as having “a severe mass effect [effacement of 50% or more plus a midline shift].”^1,41 Glimaker et al⁴² limitations included: i) did not consider important that, of those having non-fatal herniation after LP, the patient was described as “lethargy and confusion” [Ropper & Kanis], “confused” [Winkler et al], RLS 5 and 4 [Grande et al], and OP below 50 cmH2O in one [Durand et al],⁴² ii) missed some case reports in adults, including Raps et al (age 47yo with only “lethargy” prior to LP), O’Farrell et al (age 25yo with “coma” prior to LP followed by fatal herniation),² and the more recent 6 cases in Table 2,^{5,6,8,9,11,13} and iii) not clear whether any of the descriptions provided indicated the claimed “possible herniation before LP.”
5. CT cannot reliably detect the risk of brain herniation in ABM.	This was clearly stated in several reviews.^41,44–57 Examples of these statements over the years include: “also is important to note that normal findings on CT scan do not exclude increased intracranial pressure, and the patient [with normal CT] should be reassessed after LP is performed.”;⁴⁵ “a normal CT scan in ABM does not necessarily predict the outcome of a LP”;⁴⁷ “a normal CT does not disclose incipient cerebral herniation before LP”;⁵⁰ “a normal CT scan does not completely confirm that an LP is safe”;⁵² “up to 80% of patients with bacterial meningitis experiencing herniation have no CT abnormalities”;⁴¹ “important to recognize that normal CT does not exclude raised ICP in the context of these warning signs”;⁵⁴ “CT scan of the brain has consistently been shown to be nonpredictive of increased ICP in ABM”;⁵⁵ “clinical characteristics at admission can help to identify patients at risk for having an abnormal CT, but cannot identify who will have a higher risk for subsequent brain herniation;”⁵⁶ and “While CT can reveal brain shifts indicative of increased ICP, it is crucial to recognize that imaging may not always reflect elevated ICP levels”.⁴⁴	Yet, many other reviews did not mention this limitation of CT (see Limitations of Additional Claim 4 below). Some reviews recognized this limitation of CT, but still suggested doing the LP if no contraindication was found on CT. Examples include: “For patients who have signs of increased ICP, LP should be deferred until CT scan is performed. If a mass lesion, hemorrhage, midline shift, effacement of the basilar cisterns, or effacement of the sulci is noted, LP should be deferred and antimicrobial therapy started promptly;”⁴⁵ and “[if CT shows] no signs indicating increased risk of LP to proceed to LP (Figure 1).”⁴⁷
6. Focal neurological findings or significantly altered LOC are risk factors for abnormal CT scan that may contraindicate an LP.	Risk factors indicating a CT prior to LP were variable, and included: ‐Seizures: new onset,^{11,47,55,57–61} or continuous or uncontrolled^54,62,63 ‐Altered level of consciousness: GCS ≤9,¹¹ GCS ≤12,^54,62,63 moderate-to-severe impairment of consciousness,^47,57–61 or rapidly declining conscious level⁵⁴ ‐Severe immunocompromised state^{11,52,57–61} ‐Focal neurological deficits [presumably including pupillary changes, decerebrate or decorticate posturing]^{11,47,52,54,55,57–63} ‐Papilledema^{52,54,55,57–59,62} ‐History of selected CNS conditions (eg, CSF shunt, hydrocephalus, CNS trauma, neurosurgery, or space-occupying lesion)^52,57,59 ‐Signs of raised ICP;⁶³ bradycardia or irregular respirations⁵⁸ ‐Sedation or muscle paralysis⁵⁸	Almost all reviews suggested CT first in high-risk patients.
7. Clinical signs of ‘impending herniation’ are the best indicators of who should not have an LP done in the setting of ABM because of the risk that the LP can precipitate or complete herniation.	Some reviews simply state that “increased intracranial pressure” is a contraindication to LP.^{51,52,58,64,65} Some reviews state that clinical examination should guide appropriateness of LP.^49–51 Signs of concern were variable: ‐Altered level of consciousness: GCS <9 or drop of 3 or more,⁵¹ markedly decreased mental status to coma or semicoma,⁶⁶ rapidly deteriorating level of consciousness,⁴⁸ or decreased GCS^44,49 ‐Signs of possible (early) herniation: Cushing's triad in any combination,^51,66 decorticate or decerebrate posturing,^51,66 abnormal doll's eye movements,^51,66 dilated or fixed pupils,^44,48,66 or marked respiratory abnormalities^48,66 ‐Focal neurological signs^44,49,51,66 ‐Papilledema^44,49,51,66 ‐Seizures: until stabilized,⁵¹ recent^49,66	Some were still ambiguous whether CT was sufficient, with the following statements: “it is prudent to perform cranial CT imaging to assess for any such abnormalities prior to performing an LP if there is any concern for increased ICP”;⁶⁵ “[no LP until] resolution of increased ICP”, but when there are indications for head CT, if the CT is negative, “LP should be performed promptly”;⁵² “[signs suggesting raised ICP are] contraindications to performing immediate LP”;⁵¹ “head CT is commonly used before an LP to evaluate increased risks of brain herniation by detecting shift of brain compartments”;⁶⁶ “the use of CT prior to dural puncture is vital in patients with suspected increased ICP at risk for herniation”.⁴⁴ Some were clearer,⁴⁷ including the following statements: “may reasonably defer LP in such patients regardless of whether there is radiographic evidence of midline shift or impending herniation”;⁴⁶ “the best predictors of when to delay the LP because of risk of herniation were clinical signs of ‘impending’ herniation rather than findings on CT”.⁵⁵
9. Delaying LP in those thought to be high risk for brain herniation in ABM would result in a very small proportion where Cefotaxime or Ceftriaxone alone for 10 days would not be adequate therapy. Additional claim 4 : This may not apply in resource poor settings where CT availability is limited, and other causes are prevalent.^46,67	Scarborogh & Thwaites (2008): TB and Cryptococcal meningitis are common. Herniation risk “needs to be assessed in the context of the care available.” Omission of LP “for fear of complications carries a greater risk of death in a resource poor setting due to inaccurate diagnosis….”⁴⁶ Kestler et al (2014): HIV-associated neurological infections (eg, Cryptococcus, TBM) are common in Africa (HIV prevalence 25% in 15-49yo and >40% in 40-44yo), emergency CT investigations are not feasible in much of Africa (only the 2 largest referral hospitals in Botswana). Recommend CT for GCS ≤8, posturing, new onset seizures, suspected mass lesion, or unexplained altered mental status. In adults, if confusion or focal neurologic findings and after-hours, do “careful” LP for possible cryptococcus or TBM without CT.⁶⁷	Limitations of additional claim 4: This may be a reasonable clinical judgement in view of limited resources. The original review discussed the caveat when TBM or opportunistic infection (eg, in HIV) is suspected; even then, if resources allow, brain MRI, ventricular fluid obtained urgently by a neurosurgeon, or delayed LP may be better options when there are clinical signs of ‘impending herniation’.
10. In those considered at high risk for herniation, interventions to control ICP and antibiotics should be the priorities, followed by an urgent CT scan and not an LP. Additional claim 5 : Those with the above clinical risk factors should have CT done prior to an LP in order to exclude brain shift. If CT reveals no contraindication, then do immediate LP.^{11,55,59–63,68}	Brouwer et at. (2012): “[clinical findings can be used] to identify patients with suspected ABM who need imaging before LP.”⁵⁹ McGill et al (2016): Neuroimaging (CT) before LP indicated to “exclude significant brain swelling and shift”, and “if shift of brain compartments or herniation is found” LP should be delayed.⁶² Van de Beek et al (2016): CT might be indicated to “rule out” the possibility of “a space-occupying intracranial lesion or diffuse brain edema, which both cause substantial brain shift”.⁶⁰ Costerus et al (2018): Contraindications to LP to be excluded by CT include noncommunicating obstructive hydrocephalus, cerebral mass lesion, or “generalized edema causing brain shift and obliteration of basal cisterns”.¹¹ Young & Thomas (2018): recommend doing LP if CT does not show “raised ICP [Figure 1]”.⁶⁸ Van de Beek et al (2021): recommend cranial CT in order to “exclude brain shift” either from “a focal space-occupying lesion or severe diffuse brain swelling”.⁶¹ McEntire et al (2021): recommend “a CT scan should be obtained first in cases with [risk factors]… with poor examination and imaging concerns for diffuse edema or hydrocephalus, there may be a role for placement of an EVD…”⁵⁵ Brooke et al (2023): “Neuroimaging prior to LP should be performed where there is a clear indication.”⁶³	Limitations of additional claim 5: There was no mention or emphasis that a normal CT cannot exclude high ICP and risk of brain herniation after an LP [point 5]. Therefore, the reviews conflate that CT scan can exclude some cases of brain shift [eg, diffuse cerebral edema, acute obstructive hydrocephalus, and mass lesion] that may contraindicate an LP, with the claim that CT can exclude all cases of brain shift [eg, diffuse brain shift with tense brain] that may contraindicate an LP.

ABM: acute bacterial meningitis; CT: computed tomography scan of head; GCS: Glasgow Coma Score; ICP: intracranial pressure; LP: lumbar puncture; OP: opening pressure.

Table 4.

Updated Guidelines Discussing Relevant Recommendations on When to do an LP in ABM.^a

Guideline	Indication for CT Scan of head before LP	Neurologic contraindications to LP if CT is normal
EFNS guideline 2008⁶⁹	1. Absolute contraindication to LP: ‐signs of raised ICP: papilledema, decerebrate posturing ‐evidence of obstructive hydrocephalus, cerebral edema, or herniation on CT (or MRI) [evidence of intracranial mass lesion or midline shift] 2. Relative contraindication until CT (or MRI) is done: ‐focal neurological deficit, especially when posterior fossa lesion is suspected ‐GCS ≤8 ‐epileptic seizures	No LP if there are “signs of raised ICP: papilledema, decerebrate posturing.” ‐“A normal CT scan in a patient with clinical manifestations of cerebral herniation does not guarantee absence of risk from the procedure of LP [p. 651].”
Swedish guideline, 2013⁴²	1. Signs of a cerebral mass lesion: ‐focal neurological deficit (except cranial nerve palsy other than oculomotorius paresis) ‐new onset epileptic seizures if not associated with a clinical picture indicating ABM ‐long duration (>4 days) of cerebral symptoms 2. Ongoing or impending cerebral herniation: unconsciousness plus 1 or more of the following clinical findings: ‐Rigid dilated pupils ‐Increasing blood pressure and bradycardia ‐Disturbed breathing pattern ‐Opisthotonus ‐Loss of all reactions 3. Ongoing epileptic seizures 4. Papilledema (ophthalmoscopy is not mandatory before LP in cases with acute onset of ABM symptoms and short duration)	None. Yet, “it is also well-known that increased ICP and even impending cerebral herniation in ABM cannot be ruled out in patients with normal cerebral CT [p. 661].”
Australian guideline, 2015³⁹	‐Focal neurological signs ‐Papilledema ‐New-onset seizure ‐Abnormal or a rapidly deteriorating conscious state ‐Immunosuppression	Unable to ascertain
ESCMID 2016⁷⁰	CT to identify patients with an increased risk for space-occupying lesions associated with increased risk for cerebral herniation due to LP: ‐focal neurologic deficits (excluding cranial nerve palsies) ‐new-onset seizures ‐severely altered mental status (defined as a score on the GCS of <10) ‐severely immunocompromised state (eg, in organ transplant recipients and HIV-infected patients)	None. Yet, “the literature search identified 19 studies describing 74 bacterial meningitis patients in whom cerebral herniation occurred in timely association to the LP. However, a causal relationship is difficult to establish, as brain herniation also occurs during bacterial meningitis disease course, irrespective of LP [p. 547].”
UK joint specialist societies 2016⁷¹	CT “to exclude significant brain swelling and shift that may predispose to cerebral herniation post LP”: ‐focal neurological signs ‐papilledema [inability to view the fundus is not a contraindication to LP, especially in patients who have had a short duration of symptoms] ‐continuous or uncontrolled seizures ‐GCS ≤12	None: LP as soon as possible after CT unless: ‐CT reveals significant brain shift ‐an alternative diagnosis is established ‐the patient's condition precludes an LP by having continued seizures, rapidly deteriorating GCS or cardiac/respiratory compromise Yet, “these [brain swelling or shift] may occur in the context of a normal brain CT. The CT does not detect raised ICP [p. 414].”
French Infectious Diseases Society, 2018⁷²	1. Clinical signs potentially indicating intracranial expansion: ‐signs of localization: motor deficit (central facial palsy, oculomotor palsy, upper limb and/or lower limb impairment), hemi-body sensitive deficit, homonymous hemianopsia, cerebellar syndrome, aphasia] ‐focal AND recent [<4 days] seizures 2. Signs of brain herniation: ‐consciousness disorders AND one or more of pupillary abnormalities (fixed unilateral or bilateral mydriasis), dysautonomia (blood pressure and bradycardia, respiratory rate abnormalities), cerebellar tonic seizures, no reaction to stimuli, decortication or decerebration symptoms) 3. Persisting seizures (generalized motor seizures) preventing LP	None. Ambiguous statements [p. 414]: ‐“…however, in case of brain herniation signs, normal imaging results do not allow the LP to be performed.” ‐“Consciousness disorders associated with brain herniation… are absolute contraindications to LP without prior imaging test.” ‐Figure 1: shows that even with “signs and symptoms indicating brain herniation”, if brain CT scan does not show “LP contraindications”, LP should be done.
Canadian guidelines, 2021⁷³ [Children]	In the presence of the following signs, “LP should be deferred until imaging (a contrast-enhanced CT and/or MRI of the head) is performed, and the risk of potential herniation is ruled out. Although there are no specific studies involving children, herniation following an LP in meningitis is rare in the absence of focal CNS lesions.” ‐papilledema ‐new onset seizures ‐focal neurological deficits ‐decreased level of consciousness or coma	Unclear due to ambiguous statement [just prior to the statement about CT]: “An LP should always be attempted unless there are contraindications, such as coagulopathy, cutaneous lesions at the proposed puncture site, signs of herniation, or an unstable clinical status such as shock.” This makes it unclear whether CT can “rule out” the risk of herniation when there were “signs of herniation” other than new onset seizures, focal neurological deficits, or decreased level of consciousness.
German guidelines, 2023⁷⁴	CT “to rule out signs of increased ICP prior to LP [intracranial mass with midline displacement or herniation of brain tissue; hydrocephalus; (generalized) cerebral edema with reduced/abrogated grey and white matter differentiation; narrowed external CSF spaces (cortical sulci, basal cisterns), compression of ventricles]” ‐severely impaired consciousness ‐new onset focal neurological deficits (eg, hemiparesis) ‐newly occurring epileptic seizures	None
NICE Guideline, 2024⁷⁵	Recommendation 1.4.7: Perform imaging if the person has: risk factors for an evolving space-occupying lesion or any of these symptoms or signs, which might indicate raised intracranial pressure: ‐new focal neurological features (including seizures or posturing) ‐abnormal pupillary reactions ‐a GCS of 9 or less, or a progressive and sustained or rapid fall in level of consciousness.	Unclear due to ambiguous suggestions: ‐“Do not perform LP if there is [same indications as for imaging]…”, with the direction to “follow recommendation 1.4.7 on imaging”. Unclear whether a normal CT means to then immediately do an LP. ‐Imaging recommendation 1.4.7 writes “Do not perform a LP until these factors have been resolved.” Unclear whether “resolved” means by a normal CT, or clinically resolved. ‐Appendix B4 [Evidence review for factors associated with brain herniation] stated “the committee highlighted that raised ICP is a contraindication for LP due to the risk of brain herniation”, listed the risk factors for herniation after an LP, and then stated that with these risk factors “imaging should be performed prior to LP”.⁷⁶ Unclear whether a normal CT means to immediately do an LP.

ABM: acute bacterial meningitis; CNS: central nervous system; GCS: Glasgow Coma Scale; ICP: intracranial pressure; LP: lumbar puncture.

Most guidelines emphasize two other points: antibiotics must be started within 1 h, even if LP is deferred for CT or other reasons;^{42,70–73,75} and PCR for bacterial pathogens in CSF has a high sensitivity,^69,70,72,74 even with prior antibiotics.⁷¹

We did not include the “Consensus guidelines for LP in patients with neurological diseases” (Engelborghs et al 2017) as this did not focus on LP in ABM.²³ These guidelines seem to have stated that contraindications to LP without prior CT/MRI are “space-occupying lesion with mass effect, increase of ICP due to increased CSF pressure, tonsillar herniation is suspected, posterior fossa mass, or Arnold-Chiari malformation” indicated by focal neurological deficits, immune compromise, previous CNS disease, recent seizures, reduced consciousness, or papilledema.

Guidelines on ABM That Explain Contraindications to LP in ABM:

There were 9 different guidelines included, presented in Table 4, and organized by recommendations for CT and whether CT without imaging contraindications indicated immediate LP.^{39,42,69–76} There were differences in guideline listed indications for head CT prior to LP, mostly differing in the GCS level cut-off (with two only considering low GCS if other signs of brain herniation are present),^42,72 in whether immunocompromised status was relevant, and in whether recent (non-ongoing) seizure were indications (Table 4). Six of the guidelines recommended LP if head CT did not reveal an imaging contraindication to LP regardless of neurologic clinical findings,^{39,42,70–72,74} although one had ambiguous statements about this⁷²; two were unclear on this recommendation,^73–76 and one stated that even with normal CT “signs of raised ICP: papilledema, decerebrate posturing” contraindicate an LP.⁶⁹ Three of the guidelines stated that a normal head CT does not rule out high ICP or risk for herniation,^42,69,71 and two of these recommended that head CT without imaging contraindications indicated immediate LP regardless of clinical neurologic signs.^42,71 In general, the different guidelines emphasized the need for urgent LP for diagnosis, and to prevent delays in starting antibiotic(s) treatment.

Discussion

Updated Literature Review Supported Previous Points

The updated literature review found further evidence to support, and did not find convincing evidence to refute, the original points made regarding the safety of performing LP in a patient with ABM (Table S1, Tables 1–4). This is important because, brain herniation accounts for a significant proportion of deaths in ABM (point 1),^1,16–20 raised ICP is common in ABM (point 2),^1,17,21 herniation after LP may be gradual due to ongoing CSF leakage from the LP site or cerebral vascular engorgement and edema after LP (point 3),^1,22,23 and when herniation occurs in ABM patients it most often occurs shortly after an LP (point 4),^{1,3–15,20,21,26} together providing a compelling logical pathophysiologic explanation for the risk of brain herniation precipitated by an LP in ABM. Furthermore, the original overarching general point 10, that in those considered at high risk for herniation, interventions to control ICP and administration of antibiotics should be the priority, followed secondarily by an urgent CT scan and not an LP, remained supported by the updated literature reviewed.^1,36–40 This is because the main rationales for this point were supported (beyond the pathophysiology mentioned above), that is, that a normal head CT cannot reliably detect an elevated ICP and therefore cannot determine the risk of herniation in ABM (point 5),^1,21,27,28 and that clinical signs of ‘impending herniation’ are the best indicators of who should not have an LP done [even with normal CT] in the setting of ABM because of the risk that the LP can precipitate or complete herniation (point 7).^1,17,20,21 Of note, in the narrative review articles these clinical signs were often framed as indications for CT prior to LP (point 6)^{11,47,52,54,55,58–63}; however, many of these narrative reviews ignored the fact that CT cannot exclude all cases of increased intracranial pressure and brain shift (eg, diffuse brain shift with tense brain and dura starting to displace brain from one intra-cranial compartment into another) indicated by these clinical risk factors and that may contraindicate an LP even with a normal CT (point 5).^{11,55,59–63,68} In other words, these clinical signs that indicate head CT were not recognized as stand-alone contraindications to LP even with a normal CT.

The updated literature review found five additional claims made that were meant to refute some of the original points.^36,42,46,67 These additional claims were based upon data that did not support the claims made (see Comments in Tables 3 and 4). Nevertheless, the main limitation of the data reviewed here remained the absence of any randomized controlled trial to prove whether those patients who herniated after an LP may have been destined to herniate regardless of whether they had an LP. Without an RCT, which in our view would be unethical, we are left to make the best use of observational data available. As argued above, we believe the preponderance of this evidence supports the overarching general point 10. Redetsky reviewed “fulminant” ABM where an LP “might only accelerate an otherwise inevitable process”.⁴³ Redetsky pointed out that fulminant meningitis may occur in up to 1% of ABM, and was “not equivalent to meningitis with clinical brain herniation.”⁴³ This was based on differences in the “rapidity of deterioration [sudden onset with rapid neurological deterioration],” and especially the “refractory nature of intracranial hypertension” and “irreversibility of intracranial hypertension” that “evolves swiftly despite attempts to control ICP” with death within 36–48 h.⁴³ These were not features in the majority of the reported cases of herniation after an LP in ABM (Table 1).^{1,2,4–6,9,10,13,14}

The 9 guidelines reviewed made some discordant recommendations on indications for head CT prior to LP.^{39,42,69–76} Guidelines often (though not always) recommended immediate LP after a head CT without an identified imaging contraindication, regardless of clinical findings.^{39,42,70–72,74} As reviewed in Table 2, we believe the best evidence available does not support this recommendation, as head CT cannot rule out high ICP or risk for herniation after LP in ABM (as three guidelines stated).^21,27,28 Reasons why ABM may be a unique circumstance for the risk of herniation after an LP despite normal CT include that purulent material may prevent the expected effacement of the extra-axial and ventricular spaces, meningeal hardening from inflammation may cause decreased meningeal compliance that then resists effacement, decreased CSF absorption may oppose the forces of cerebral edema, and, crucially, these factors may not be equally distributed throughout the brain, predisposing to unequal ICPs.¹ Again, this comes down to a judgment about the observational evidence for points 1–10, as discussed above.

The most common risk factor for herniation after LP in the described cases was a low or decreasing level of consciousness, without any other definitive clinical signs of herniation having occurred prior to an LP.^{6–9,13–15} Even so, as pointed out in the 2007 review, clinical risk factors identified in a minority of cases “seem to refer to patients that already have signs consistent with early uncal or central cerebral herniation… Doing an LP in that setting could complete the brain herniation. This makes pathophysiologic sense: an LP relieving pressure from below could allow a swollen brain with high ICP to develop more edema and to shift further and completely herniate.”¹

Some case series seemed to describe that rarely herniation was likely already starting prior to LP, eg, a case with decerebrate posturing,⁷⁷ dilated pupil before paralysis and intubation,⁷⁷ with obliterated basal cisterns and transient hemiparesis on admission,⁷⁸ and 4 cases with herniation “that reduced or cleared” after mannitol and then recurred after LP [no further details were provided].⁷⁹ The 14 case reports of herniation added in Table 1 included one patient with “anisocoria”,⁴ and one patient with “generalized edema causing brain shift with partial obliteration of basal cisterns [on CT]”,¹¹ both patients likely in the process of herniation prior to LP. Moreover, a seizure prior to LP, usually poorly described in the reported cases,^2,11,15 may actually have been posturing during herniation that was mistaken for a tonic seizure. Whether the decreased level of consciousness described in other case reports was indeed due to early herniation cannot be determined; however, that CT scan cannot detect the risk for brain herniation occurring shortly after the normal CT suggests otherwise, ie, the CT did not find early herniation.^9,12–15 In these cases the normal CT scan provided false reassurance, while the clinical signs suggested a high risk of herniation that subsequently occurred after LP was performed.

The Added Value of our Case Report

We reported our case because it made three points that may not have been adequately emphasized previously, or may have been misunderstood.

First, whether occurring before or after an LP, brain herniation often presents as a variable combination of apnea and quadriplegia (point 11 and 12),² often with a rapidly decreasing level of consciousness, and pupillary changes (unequal or fixed and dilated). These are clinical risk factors for abnormal CT,^{29–31,41,44–56} as well as for herniation or completion of herniation after an LP.^{11,17,20,21,47,52,54,55,58–63} The patient in our case report had an acute event of respiratory arrest and likely tonic (decerebrate) posturing (confused for a seizure), followed by rapid sequence intubation that later reversed these findings (ie, aborted the herniation episode). These initial findings were an indication of early herniation and indicated a head CT, which was not done and may have detected hydrocephalus, cerebral edema, or herniation.^{39,42,69–76} Therefore, our case emphasized that the clinical risk factors that indicate a head CT in suspected ABM include acute respiratory arrest or suspected tonic seizure as these can be due to early herniation from a very high ICP (due to diffuse cerebral edema, mass lesion, or acute hydrocephalus; point 6).¹

Second, within hours of the LP there was acute deterioration in the level of consciousness, and subsequent head CT indicated tonsillar herniation and acute obstructive hydrocephalus. The LP was done less than 17 h after intubation was done for signs compatible with early herniation. When ICP is elevated in ABM it is likely that the underling cerebral edema and hyperemia causing elevated ICP does not resolve for days.¹ In our case we cannot know whether a head CT would have detected diffuse cerebral edema or acute hydrocephalus that contraindicated an LP. However, even if a CT had been done, and the CT had been normal, the clinical risk factors indicating early herniation suggested a high risk of completed herniation to occur after an LP.^{1,17,20,21,44,48–52,58,64–66} Therefore, our case emphasized that clinical risk factors that indicate prolonged deferral of LP include acute respiratory arrest or suspected tonic seizure as these can be due to early herniation (point 7).

Third, the initial episode of herniation was aborted with anesthesia (ie, rapid sequence intubation), mechanical ventilation, and ongoing sedation (with propofol infusion). The second completed episode of herniation was reversed with mechanical ventilation, ongoing deep sedation, hyperosmolar therapy, and decompressive surgery. The initial treatment created the misleading impression that herniation had not occurred at all, and the improved clinical findings were why an LP was done. Treatment later led to survival with hemiplegia as an outcome at acute-care hospital discharge. Therefore, our case emphasized that if herniation occurs, this should be treated aggressively as the outcome is not necessarily dismal (point 8).^{1,2,4–6,9,14,28}

Limitations

This updated review has limitations. First, we only searched one database (PubMed), and could have missed papers indexed in other databases. The snowballing approach to reviewing references in identified publications mitigated this concern. Second, there were no randomized controlled trials, and inferences were made based on observational data. In particular, whether herniation would have occurred without having had an LP cannot be certain. Nevertheless, as argued above, we believe the preponderance of evidence supports the overarching general point 10. Third, adverse effects of delaying an LP in suspected ABM need to be considered. Early administration of antibiotics is crucial when LP is delayed. We found no updated information on potential effects of delayed LP after antibiotics on making diagnoses, and rely on point 9 in Table S1 and Table 2 to suggest this risk is very small.^1,32–35 The LP may be done later when the clinical course has suggested that elevated ICP is no longer suspected (eg, after peak edema resolves in at least 2-3 days,^80–84 with resolution of the clinical finding(s) that suggested elevated ICP), and PCR tests for bacterial pathogens are still reliable.^32–34 Treatment can also be based on clinical suspicion of ABM supplemented with blood culture results, or, if necessary, neurosurgically obtained CSF results from ventricular fluid.¹ A caveat is in poor resource countries, as discussed for additional claim 4 in Table 3.^1,46,67 Fourth, we did not include a systematic review and meta-analysis of the diagnosis of elevated ICP in critically ill adults that found isolated physical signs (dilated pupils, GCS ≤8, motor score ≤3) or CT findings (compression of basal cisterns, any midline shift) had inadequate sensitivity and specificity for ICP ≥20 mm Hg, and that sonography of optic nerve sheath diameter had high AUROC for ICP ≥20 mm Hg.⁸⁵ We did not include this review because there were no patients with ABM, and diagnostic accuracy was not determined for the very high ICP found in ABM,^17,21,27 nor for brain herniation.⁸⁵ Findings for sonography of optic nerve sheath diameter, while promising,⁸⁶ were limited by different optimal thresholds used across studies (with “variability in… sensitivity and specificity at any specific threshold”)⁸⁵; future study in ABM seems warranted.

The case report also has limitations. First, case reports provide a low level of evidence, and making strong inferences from a case report should be done with caution. This is why we presented the case report in the context of our previous and updated literature review. Second, how long to delay an LP when clinical risk factors are present is unknown. Since elevated ICP peaks in the first few days of ABM, this is likely for at least 2–3 days (and resolution of the clinical finding(s) that suggested elevated ICP if longer).^80–84 In the setting of an initial suspected herniation event, this may be longer to ensure resolution of the peak elevated ICP.

Conclusion

An updated literature review supported the general conclusion that, in a patient with strongly suspected ABM who is clinically considered at high risk for herniation, interventions to control ICP and antibiotics administration should be the priority, followed secondarily by an urgent CT scan and [even with a normal CT] not an urgent LP. The urgent CT scan may detect a contraindication to LP; however, a normal CT scan in the setting of ABM does not rule out very high ICP with risk for brain herniation after an LP.^{21,27,28,41,44–57,69} We report a case that led us to emphasize three points: clinical risk factors that indicate an urgent CT in suspected ABM include acute respiratory arrest or suspected tonic seizure as these can be due to early herniation, clinical risk factors that warrant prolonged (for 3-4 days) deferral of LP [even with a normal CT] include acute respiratory arrest or suspected tonic seizure as these can be due to early herniation, and if herniation occurs it should be treated aggressively as the outcome is not necessarily dismal.

Supplemental Material

sj-docx-1-jic-10.1177_08850666251337684 - Supplemental material for Lumbar Puncture and Brain Herniation in Acute Bacterial Meningitis: An Updated Narrative Review

Supplemental material, sj-docx-1-jic-10.1177_08850666251337684 for Lumbar Puncture and Brain Herniation in Acute Bacterial Meningitis: An Updated Narrative Review by Ari R. Joffe, Fernanda de Marzio Pestana Martins, Daniel Garros and Adrienne F. Thompson in Journal of Intensive Care Medicine

Footnotes

Author Contributions

All authors made substantial contributions to conception or design of the work, and interpretation of data for the work; reviewed the work critically for important intellectual content; made final approval of the version to be published; and agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. ARJ drafted the first version of the manuscript, FDMPM drafted the first version of the case report section, and AFT drafted the first version of the figures and figure legends.

Consent for Publication

Signed informed consent for publication of the case report was obtained from the legal guardian of the 18 months old patient.

Data Availability

All data used are given in the publication, and the original reference for that data provided.

Declaration of Conflicting Interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Ethics Approval

The University of Alberta health research ethics board does not review case reports. Approval was not required for the updated review as we used only already publicly available published data for review.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

ORCID iD

Ari R. Joffe

Supplemental Material

Supplemental material for this article is available online.

References

Joffe

. Lumbar puncture and brain herniation in acute bacterial meningitis: A review. J Intensive Care Med. 2007;22(4):194-207.

Joffe

Anton

Blackwood

. Brain death and the cervical spinal cord: A confounding factor for the clinical examination. Spinal Cord. 2010;48(1):2-9.

Feske

Carrazana

Kupsky

Volpe

. Uncal herniation secondary to bacterial meningitis in a newborn. Pediatr Neurol. 1992;8(2):142-144.

Ibsen

. Radiological case of the month. Arch Pediatr Adolesc Med. 2002;156(3):293-294.

Baussart

Cheisson

Compain

, et al. Multimodal cerebral monitoring and decompressive surgery for the treatment of severe bacterial meningitis with increased intracranial pressure. Acta Anesthesiol Scand. 2006;50(6):762-765.

Muralidharan

Rabinstein

Wijdicks

EFM

. Cervicomedullary injury after pneumococcal meningitis with brain edema. Arch Neurol. 2011;68(4):513-516.

Kalay

Oztekin

Tezel

Demirtas

Akcakus

Oygur

. Cerebellar herniation after lumbar puncture in galactosemic newborn. AJP Rep. 2011;11(1):43-46.

Adriani

Brouwer

van der Ende

van de Beek

. Bacterial meningitis in pregnancy: Report of six cases and review of the literature. Clin Microbiol Infect. 2012;18(4):345-351.

Berkowitz

Kimchi

Hwang

, et al. Clinical reasoning: A 44-year-old woman with headache followed by sudden neurologic decline. Neurology. 2013;80(13):e136-e141.

10.

Ramesh

. Diagnostic lumbar puncture in suspected acute bacterial meningitis: Avoiding catastrophe. Dev Med Child Neurol. 2013;55(12):1068.

11.

Costerus

Brouwer

van de Beek

. Technological advances and changing indications for lumbar puncture in neurological disorders. Lancet Neurol. 2018;17(3):268-278.

12.

Noaim

. Acute bacterial meningitis complicated by brain herniation shortly after lumbar puncture: A case report. Global J Health Science. 2018;10(3):121-124.

13.

Chen

Driver

Segar

Bernstock

Gupta

Bormley

. Medullary infarction leading to locked-in syndrome following lumbar puncture in a patient with basilar invagination. World Neurosurg. 2020;137:292-295.

14.

Yang

Sekhon

Griesdale

. Transtentorial herniation syndrome from meningococcal meningitis in a young woman: The case for neurocritical care. BMJ Case Rep. 2022;15(11):e253191.

15.

Stanley

Rizvi

Sahhar

. Rapidly progressive fatal pneumococcal meningitis in a fully immunized child with a history of facial bone fractures. Cureus. 2024;16(4):e59204.

16.

Koelman

Brouwer

Horsts

Bijlsma

Van der Ende

Van de Beek

. Clinical characteristics, prognostic factors, and causes of death in adults with community-acquired pneumococcal meningitis. Eur J Neurol. 2020;27(Suppl 1):449.

17.

Weisfelt

van de Beek

Spanjaard

Reitsma

de Gans

. Clinical features, complications, and outcome in adults with pneumococcal meningitis: A prospective case series. Lancet Neurol. 2006;5(2):123-129.

18.

Weisfelt

van de Beek

Spanjaard

Reitsma

de Gans

. Community-acquired bacterial meningitis in older people. J Am Geriatr Soc. 2006;54(10):1500-1507.

19.

Lucas

Brouwer

van der Ende

van de Beek

. Outcome in patients with bacterial meningitis presenting with a minimal Glasgow coma scale score. Neurol Neuroimmunol Neuroinflammation. 2014;1(1):e9.

20.

Sharew

Bodilsen

Hansen

Nielsen

Brandt

. The cause of death in bacterial meningitis. BMC Infect Dis. 2020;20:182.

21.

Costerus

Brouwer

Sprengers

MES

Roosendaal

van der Ende

van de Beek

. Cranial computed tomography, lumbar puncture, and clinical deterioration in bacterial meningitis: A nationwide cohort study. Clin Infect Dis. 2018;67(6):920-926.

22.

Niemantsverdriet

Struyfs

Duits

Teunissen

Engelborghs

. Techniques, contraindications, and complications of CSF collection procedures. In: Deisenhammer

Sellebjerg

Teunissen

Tumani

, eds. Cerebrospinal Fluid in Clinical Neurology. Springer; 2015:37-57.

23.

Engelborghs

Niemantsverdriet

Struyfs

, et al. CSF Biomarkers. Consensus guidelines for lumbar puncture in patients with neurological diseases. Alzheimer’s & Dementia. 2017;8:111-126.

24.

Uppal

Russell

Sondekoppam

, et al. Consensus practice guidelines on postdural puncture headache from a multisociety, international working group. A summary report. JAMA Netw Open. 2023;6(8):e2325387.

25.

Uppal

Russell

Sondekoppam

, et al. Evidence-based clinical practice guidelines on postdural puncture headache: A consensus report from a multisociety international working group. Reg Anesth Pain Med. 2024;49(7):471-501.

26.

McDowell

Chapman

ALN

. Cerebral herniation after lumbar puncture. Clin Infect Dis. 2019;69(7):1266-1267.

27.

Larsen

Poulsen

Nielsen

Nordstrom

Schulz

Andersen

. Use of intracranial pressure monitoring in bacterial meningitis: A 10-year follow up on outcome and intracranial pressure versus head CT scans. Infect Dis. 2017;49(5):356-364.

28.

El-Hajj

Pettersson

Gharios

, et al. Detection and management of elevated intracranial pressure in the treatment of acute community-acquired bacterial meningitis: A systematic review. Neurocrit Care. 2024;41(1):228-243.

29.

Park

Nigo

Hasbun

. Comparison of four international guidelines on the utility of cranial imaging before lumbar puncture in adults with bacterial meningitis. Clin Neuroradiol. 2022;32(3):857-862.

30.

O’Herlihy

Dempsey

Gorman

Muldoon

Gibney

. Comparison of international guidelines for CT prior to lumbar puncture in patients with suspected meningitis. Emerg Radiol. 2024;31(3):373-379.

31.

Salazar

Hasbun

. Cranial imaging before lumbar puncture in adults with community-acquired meningitis: Clinical utility and adherence to the Infectious Diseases Society of America guidelines. Clin Infect Dis. 2017;64(12):1657-1662.

32.

Trujillo-Gomez

Tsokani

Arango-Ferreira

, et al. Biofire FilmArray meningitis/encephalitis panel for the aetiological diagnosis of central nervous system infections: A systematic review and diagnostic test accuracy meta-analysis. eClinicalMedicine. 2022;44:101275.

33.

Brouwer

Tunkel

van de Beek

. Epidemiology, diagnosis, and antimicrobial treatment of acute bacterial meningitis. Clin Microbiol Rev. 2010;23(3):467-492.

34.

Brink

Welinder-Olsson

Hagberg

. Time window for positive cerebrospinal fluid broad-range bacterial PCR and Streptococcus pneumoniae immunochromatographic test in acute bacterial meningitis. Infect Dis. 2015;47(12):869-877.

35.

Nigrovic

Malley

Macias

, et al. Effect of antibiotic pretreatment on cerebrospinal fluid profiles of children with bacterial meningitis. Pediatrics. 2008;122(4):726-730.

36.

Glimaker

Johansson

Grindborg

Bottai

Lindquist

Sjolin

. Adult bacterial meningitis: Earlier treatment and improved outcome following guideline revision promoting prompt lumbar puncture. Clin Infect Dis. 2015;60(8):1162-1169.

37.

Glimaker

Sjolin

Akesson

Naucler

. Lumbar puncture performed promptly or after neuroimaging in acute bacterial meningitis in adults: A prospective national cohort study evaluating different guidelines. Clin Infect Dis. 2018;66(3):321-328.

38.

Costerus

Lemmens

CMC

van de Beek

Brouwer

. Cranial imaging and lumbar puncture in patients with suspected central nervous system infection. Clin Infect Dis. 2020;70(12):2469-2475.

39.

Gulholm

Kim

Lennard

, et al. Clinical variation in the early assessment and management of suspected community-acquired meningitis: A multicentre retrospective study. Internal Med J. 2023;53(12):2298-2306.

40.

Glimaker

Johansson

Grindborg

Bottai

Lindquist

Sjolin

. Reply to Brouwer and van de Beek. Clin Infect Dis. 2015;61(4):665-666.

41.

April

Long

Koyfman

. Emergency medicine myths: Computed tomography of the head prior to lumbar puncture in adults with suspected bacterial meningitis – due diligence or antiquated practice? J Emerg Med. 2017;53(3):313-321.

42.

Glimaker

Hohansson

Bell

, et al. Early lumber puncture in adult bacterial meningitis – rationale for revised guidelines. Scand J Infect Dis. 2013;45(9):657-663.

43.

Radetsky

. Fulminant bacterial meningitis. Pediatr Infect Dis J. 2014;33(2):204-207.

44.

Geisbush

Matys

Massoud

Hacein-Bey

. Dural puncture complications. Neuroimag Clin N Am. 2025;35(1):53-76.

45.

Mann

Jackson

. Meningitis. Pediatric in Review. 2008;29(12):417-430.

46.

Scarborough

Thwaites

. The diagnosis and management of acute bacterial meningitis in resource-poor settings. Lancet Neurol. 2008;7(7):637-648.

47.

Klein

Pfister

Leib

Koedel

. Therapy of community-acquired acute bacterial meningitis: The clock is running. Expert Opin Pharmacother. 2009;10(16):2609-2623.

48.

Somand

Meurer

. Central nervous system infections. Emerg Med Clin N Am. 2009;27(1):89-100.

49.

Hughes

Raghavan

Mordekar

Griffiths

Connolly

DJA

. Role of imaging in the diagnosis of acute bacterial meningitis and its complications. Postgrad Med J. 2010;86(1018):478-485.

50.

Nickerson

Richner

Santy

, et al. Neuroimaging of pediatric intracranial infection – part 1: Techniques and bacterial infections. J Neuroimaging. 2012;22(2):e42-e51.

51.

Schulga

Gratta

Napier

Babiker

MOE

. How to use… lumbar puncture in children. Arch Dis Child Educ Pract Ed. 2015;100(5):264-271.

52.

Swanson

. Meningitis. Pediatr Rev. 2015;36(12):514-526.

53.

Viallon

Botelho-Nevers

Zeni

. Clinical decision rules for acute bacterial meningitis: Current insights. Open Access Emerg Med. 2016;8:7-16.

54.

Ellis

LUintel

Chandna

Heyderman

. Community-acquired acute bacterial meningitis in adults: A clinical update. Br Med Bull. 2019;131(1):57-70.

55.

McEntire

CRS

Anand

Cervantes-Arslanian

. Neuroinfectious disease emergencies. Neurol Clin. 2021;39(2):565-588.

56.

Regina

Manuel

. Things we do for no reason^TM: Computed tomography of the head before lumbar puncture in low-risk adults and children. J Hosp Med. 2023;18(6):534-537.

57.

Hasbun

. Progress and challenges in bacterial meningitis. A review. JAMA. 2022;328(21):2147-2155.

58.

Ziai

Lewin

. Update in the diagnosis and management of central nervous system infections. Neurol Clin. 2008;26(2):427-468.

59.

Brouwer

Thwaites

Tunkel

van de Beek

. Dilemmas in the diagnosis of acute community-acquired bacterial meningitis. Lancet. 2012;380(9854):1684-1692.

60.

Van de Beek

Brouwer

Hasbun

Koedel

Whitney

Wijdicks

. Community-acquired bacterial meningitis. Nat Rev Dis Primer. 2016;2:1-20.

61.

Van de Beek

Brouwer

Koedel

Wall

. Community-acquired meningitis. Lancet. 2021;398(10306):1171-1183.

62.

McGill

Heyderman

Panagiotou

Tunkel

Solomon

. Acute bacterial meningitis in adults. Lancet. 2016;388(10063):3036-3047.

63.

Brooke

Patel

Agrawal

. Pneumococcal meningitis in children. Paediatrics Child Health. 2023;33(10):289-294.

64.

Bedetti

Marrozzini

Baraldi

, et al. Pitfalls in the diagnosis of meningitis in neonates and young infants: The role of lumbar puncture. J Maternal Fetal Neonatal Medicine. 2019;32(23):4029-4035.

65.

Bonadio

. Pediatric lumbar puncture and cerebrospinal fluid analysis. J Emergency Med. 2014;46(1):141-150.

66.

Davis

. Acute bacterial meningitis. Continuum (N Y). 2018;24(5):1264-1283.

67.

Kestler

Caruso

Chandra

Goldfarb

Haas

. CT Before lumbar puncture in suspected meningitis in Botswana: How established guidelines may not apply. African J Emergency Med. 2014;4(2):76-82.

68.

Young

Thomas

. Meningitis in adults: Diagnosis and management. Internal Med J. 2018;48(11):1294-1307.

69.

Chaudhuri

Martin

Kennedy

PGE

, et al. EFNS Guideline on the management of community-acquired bacterial meningitis: Report of an EFNS task force on acute bacterial meningitis in older children and adults. Eur J Neurol. 2008;15(7):649-659.

70.

Van de Beek

Cabellos

Dzupova

, et al. ESCMID Guideline: Diagnosis and treatment of acute bacterial meningitis. Clin Microbiol Infect. 2016;22(Suppl 3):S37-S62.

71.

McGill

Heyderman

Michael

, et al. The UK joint specialist societies guideline on the diagnosis and management of acute meningitis and meningococcal sepsis in immunocompetent adults. J Infect. 2016;72(4):405-438.

72.

Hoen

Varon

de Debroucker

, et al. Management of acute community-acquired bacterial meningitis (excluding newborns). long version with arguments. Med Mal Infect. 2019;49(6):405-441.

73.

Le Saux

. Guidelines for the management of suspected and confirmed bacterial meningitis in Canadian children older than 2 months of age. Canadian Pediatric Society Position Statement. 2021;19(3):141-146.

74.

Klein

Abdel-Hadi

Buhler

, et al. German Guidelines on community-acquired acute bacterial meningitis in adults. Neurol Res Pract. 2023;5:44.

75.

National Institute for Health and Care Excellence. Meningitis (bacterial) and meningococcal disease: recognition, diagnosis and management. NICE guideline. 2024;NG240:1-93.

76.

National Institute for Health and Care Excellence. Meningitis (bacterial) and meningococcal disease: recognition, diagnosis and management. [B4] Evidence review for factors associated with brain herniation. NICE guideline NG240. Evidence review underpinning recommendation 1.4.7 in the NICE guideline. March 2024.

77.

Rennick

Shann

de Campo

. Cerebral herniation during bacterial meningitis in children. Br Med J. 1993;306(6883):953-955.

78.

Cabral

Flodmark

Farrel

Speert

. Prospective study of computed tomography in acute bacterial meningitis. J Pediatr. 1987;111(2):201-205.

79.

Akpede

Ambe

. Cerebral herniation in pyogenic meningitis: Prevalence and related dilemmas in emergency room populations in developing countries. Dev Med Child Neurol. 2000;42(7):462-469.

80.

Goitein

Tamir

. Cerebral perfusion pressure in central nervous system infections of infancy and childhood. J Pediatr. 1983;103(1):40-43.

81.

Rebaud

Berthier

Hartemann

Floret

. Intracranial pressure in childhood central nervous system infections. Intensive Care Med. 1988;14(5):522-525.

82.

Lindvall

Ahlm

Ericsson

Gothefors

Naredi

Koskinen

LOD

. Reducing intracranial pressure may increase survival among patients with bacterial meningitis. Clin Infect Dis. 2004;38(3):384-390.

83.

Grande

Myhre

Nordstrom

Shliamser

. Treatment of intracranial hypertension and aspects on lumbar dural puncture in severe bacterial meningitis. Acta Anesthesiol Scand. 2022;46(3):264-270.

84.

Kumar

Singhi

Jayashree

Bansal

Bhatti

. Randomized controlled trial comparing cerebral perfusion pressure-targeted therapy versus intracranial pressure-targeted therapy for raised intracranial pressure due to acute CNS infections in children. Crit Care Med. 2014;42(8):1775-1771.

85.

Fernando

Tran

Cheng

, et al. Diagnosis of elevated intracranial pressure in critically ill adults: Systematic review and meta-analysis. Br Med J. 2019;366:14225.

86.

Yic

Pontet

Mercado

Munoz

Biestro

. Ultrasonographic measurement of the optic nerve sheath diameter to detect intracranial hypertension: An observational study. Ultrasound J. 2023;15(1):4.

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