VP shunts

Cite this article as:
Angharad Griffiths. VP shunts, Don't Forget the Bubbles, 2020. Available at:
https://doi.org/10.31440/DFTB.25996

Rhiannon is a 2 year old with spina bifida who had a VP shunt inserted during the first month.  It was revised because of a “blockage” at 18 months.  She has not been herself for the last 24hours; more lethargic than usual- especially this morning when she woke up where she also felt hot.  She vomited in the car on the way to the Emergency Department.  She has had previous urinary tract infections.

Rhiannon was afebrile on presentation in ED.  In triage, she was observed as being awake and drinking from a bottle but wasn’t perturbed by having her observations taken or finger-prick glucose.  Overall she was a little quiet in the ED and her mum was concerned that this was absolutely different from her baseline.  Her urine microscopy was not concerning.  She had a mild neutrophilia and a normal CRP.  Subcutaneous examination of her shunt, from her skull to the right clavicle was normal.  She vomited once in the ED.

 

This is a common presentation and one that can be challenging to manage. Missing a shunt problem can have catastrophic consequences. This post will take you through some pearls and pitfalls of managing children with VP shunts presenting to the ED.

 

What is a VP shunt?

A ventriculoperitoneal (VP) shunt is a medical device used to drain fluid via a pressure gradient, away from the brain for conditions of excessive cerebrospinal fluid (CSF).  The intention is to shunt fluid away and avoid excessive pressure on the brain.  It is one of the commonest performed neurosurgical procedures and is the treatment of choice for the vast majority of patients with hydrocephalus.

 

Shunts drain according to the differential pressure gradient between the ventricle and the tip of the distal catheter.  The ventricular end of the catheter is inserted through a burr hole in the right parietooccipital region and the valve often sits behind the right ear.  The distal portion is subcutaneously tunneled down into the abdomen where it’s positioned inside the peritoneal cavity.

The diagnosis of raised intracranial pressure in children with VP shunts is challenging.  The symptoms are non-specific and the commonest causes often benign.  Rhiannon could easily have a simple viral illness or her symptoms could be associated with rising intracranial pressure. Missing a shunt malfunction in these patients can be catastrophic.

 

Physiology of CSF circulation and drainage

  • CSF  is produced at a rate of approximately 20ml/h in children and adults. In normal circumstances, in a normal adult, CSF is recycled three times a day. The normal adult volumes of CSF (approximately 150mls) are reached by age 5.  The volume in a neonate can be estimated at  2ml/kg.
  • Around 50% of CSF is created by the choroid plexus of the lateral, third and fourth ventricles.  The rest of the CSF arises from the extracellular fluid of the brain.  CSF travels out of the foramen of Lushka and foramen of Magendie (at the level of the fourth ventricle), and heads through to the subarachnoid spaces, along the spinal cord to the cerebral hemispheres.  Over the cerebral hemispheres, the CSF is reabsorbed by arachnoid villi and then into the venous sinuses which drain into the jugular (internal) veins.
  • Intracranial pressure (ICP) rises when CSF production exceeds absorption.
  • Hydrocephalus is the consequence of the excessive accumulation of CSF. This could be from disruptions in formation, flow or absorption.
  • As hydrocephalus worsens and intracranial pressure increases, the temporal and frontal horns dilate, sometimes asymmetrically; and there’s elevation of the corpus callosum and stretching of white matter tracts.

 

Lateral = Lushka — Median = Magendie

 

Shunting CSF is an effective way to avoid the neurological damage that ensues if the build-up of CSF is left untreated.

Three shunts types are mainly used to shunt CSF: Ventriculoperitoneal (VP), ventriculopleural (VPL), and ventriculoatrial (VA). By far, the commonest are VP shunts.

 

Reasons for shunt placement

There is a myriad of reasons as to why a VP shunt should be placed.  They can be categorized into congenital or acquired causes.

 

Having a VP shunt in itself is a cause for concern for patients and caregivers.  Common areas for concern in paediatric patients include:

  • Flying and travel: there is no evidence that flying is dangerous but patients have concern over access to neurosurgical help should they need it. Shunt alert cards displaying the type of shunt are available.  The need for augmented travel insurance is also an area of concern.
  • Sports: Contact sports such as boxing are contra-indicated, and the US paediatric neurosurgeons named wrestling and football (soccer) as the commonest sports with adverse events.  Neurosurgeons in the UK are advising that football and rugby wearing a skullcap are acceptable.  You can still go scuba diving.
  • Future employment: in the UK, the Royal Air Force, Royal Navy and Police Force are the only services that preclude entry.
  • Programmable shunts and magnets: Background magnetic fields of household objects such as microwaves etc are safe as are walk-through metal detectors.  Post MRI check is advised with some programmable shunts but all are MRI safe.  The iPad2 has a strong magnetic field and can re-program some shunt valves, thus important to keep them at safe distances.
  • Shunt length: reassurance that placing sufficient length inside the abdomen will suffice and allow for growth.
  • Weight: Obesity is a risk factor for failure of VP shunts and dislodgement.

 

Shunt related complications

Failure rates are quoted as 30-40% at 1 year and 50% at 2 years in the paediatric cohort. A patient can expect to have 2-3 shunt revisions over the course of 20 years and the median time to shunt failure is just 1 and a half years. Paediatric revisions are more commonplace than adult revisions.

 

Risk factors for shunt failure include:

  • Younger patients (<6months), particularly neonates
  • Complex comorbidities, for example, cardiac, myelomeningocele, IVH’s, tumour and post-meningitic hydrocephalus, spinal dysraphism, and congenital hydrocephalus
  • Prior shunt failure and short time intervals between revisions
  • Male sex
  • Low socioeconomic status

 

Causes of shunt failure

Obstruction, blockage or occlusion

The commonest cause of shunt malfunction is proximal occlusion. There’s no clear data on whether programmable or non-programmable shunts are less likely to occlude.

It’s hypothesized that on insertion, the lumen can be obstructed with brain parenchyma from the cerebral cortex before reaching the ventricle, or choroid plexus when inserted near to the foramen of Monroe. It can also be occluded with blood following choroid plexus haemorrhage along with other cellular matter such as macrophages, giant cells, connective tissue, fibrin networks, debris, neoplastic cells.

Distal catheter blockage tends to occur later and when it occurs, it should raise the suspicion for an intra-abdominal pseudocyst or adhesions which may affect future peritoneal catheter placements.

Shunt infection

Shunt infection is the second most common reason for malfunction. The data is mixed, particularly as some older papers use data from before the time of antibiotic-impregnated catheters, skewing the data. Risk factors include young age (including neonates), post-op CSF leak, previous shunt infections, and the presence of a gastrostomy tube.

The vast majority of shunt infections are acute.  Far fewer late-onset infections have been reported. They can be attributed, mostly, to peritonitis, abdominal pseudocyst, bowel perforation, and haematogenous inoculation.

Shunt infection is associated with an increased risk of seizure disorder, decreased intellectual performance, and a two-fold increase in long term mortality. Re-infection occurs in one-quarter of children.

The proportion of shunt infections falls off rapidly after the first several months following implantation. The vast majority occur during the first 6 months. Children will present with signs of shunt failure, as well as systemic infection.  Fever is common and if we were to sample CSF (which is not often done in the ED), the presence of >10% neutrophils in the ventricular fluid is highly specific and sensitive of infection.

The commonest organisms are skin flora, including Staphylococcus epidermidis, Staph. aureus and gram-negative rods.  Infections with Staph. aureus and epidermidis are associated with an earlier onset as they are skin commensals. Infections with Staph. aureus are associated with a significantly increased likelihood of subsequent shunt infection.

Shunt fracture

This is often a late complication and almost always occurs along the distal portion between the valve and peritoneum.  With age, fibrous tissue becomes calcified and does not slide freely within the subcutaneous tissue then the tubing can crack.  This is more likely to happen in the neck where most movement occurs.

Tension can also form along areas of calcification causing tethering and stretching as the child grows.  It is important to note that early shunt fracture can occur and this could be a consequence of trauma to the tubing during surgery.

CSF can still drain resulting in an insidious duration of symptoms, clouding and confusing the diagnostic process.

Shunt series radiographs should always be sought in this cohort, though frequently fractures and disconnections are incidental findings during surveillance exams.

VP shunt fracture. Reused with permission from Education and Practice, Archives of Disease of Childhood

 

Shunt disconnections

Catheters are generally multi-component and hubbed together so disconnections can occur soon after surgery. The disconnection impedes the flow of CSF and it may still leak.  The onset of these symptoms may be slow.  Disconnections can happen at either the proximal or distal aspect of the valve.

Case courtesy of Dr Adam Eid Ramsey, Radiopaedia.org. From the case rID: 71794

 

Abdominal pseudocyst

This is a rare complication of VP shunts and is usually a late complication occurring years after initial placement. A pseudocysts is a fluid-filled sac that collects at the distal tip of the catheter.  It is thought that they form because of inflammation or due to abdominal adhesions.  It can present with abdominal pain or distention with, or without, a palpable abdominal mass.  Neurological symptoms occur when there is elevated ICP.

Shunt migration

The proximal or distal catheter tip may migrate.  With growth, the proximal catheter can withdraw from the ventricle (extremely rare), or the distal catheter can shift away from the peritoneum.  The distal tubing can become tethered and cause traction on some of the components causing a disconnection.  Distal migration occurs as the child grows.

 

Over-drainage

It is possible that a VP shunt can over-drain as well and ‘under-drain’.  With rapid over-drainage, the dura can be stressed and subdural haematomas and/or extra-axial fluid collections can form.

A slit ventricular syndrome occurs when gravitational forces exert a siphoning effect on the ventricles.  This effect is generally amplified by pressure.

 

Clinical presentation of shunt malfunction

Children with a blocked shunt can present with a myriad of symptoms including:

  • headache
  • nausea
  • vomiting
  • fever
  • irritability
  • abnormal level of consciousness

Infants and older children may present differently.

Infants

  • difficulty feeding
  • bulging fontanelle

Older children may present more specifically with

  • Nausea, somnolence, lethargy, cognitive difficulties, or eye pain.

 

Predictably, fever is commoner in children with shunt infections. Those with shunts because of myelomeningoceles may present with symptoms such as:-

  • weakness,
  • difficulty walking
  • bowel/bladder dysfunction
  • lower cranial nerve palsies.

Children present with these symptoms all the time to the ED. They are clearly not specific to a shunt problem.  As a consequence, diagnosing shunt malfunction on clinical grounds alone is incredibly difficult. Patients with shunt fracture or disconnection can present with a slow onset of symptoms.  They may have pain/tenderness localized to the area of fracture/disconnection or an area of calcification of an area of fluctuant swelling.

 

Diagnosis, evaluation, and imaging

The diagnosis of a shunt malfunction requires a combination of CT, shunt series radiographs, and occasionally (though seldom in the ED), CSF sampling.

A CT is likely to show an increase in ventricular size and occasionally, periventricular lucency representing oedema.  There may be increasing ventricular size on cross-sectional imaging but up to 15% will have “such profound alterations on brain compliance that their ventricles will not enlarge in the face of shunt failure and increased ICP”.  Ventricular size doesn’t appear to reach a plateau until approximately 14months after placement of the shunt (regardless of type implanted).

A lumbar puncture (LP) may demonstrate increased opening pressures, but not always.  It is also used for evidence of infection.  This not performed commonly in the ED in the context of possible shunt malfunction.

Shunt series (SS) radiographs are used to check the overall course of the catheter, looking for disconnection or disruption.  The series will not show obstructions, only damage to the catheter. It can rarely demonstrate complications such as a CSF pseudocyst (abnormal separation of bowel loops near the catheter tip) but shouldn’t be relied upon for this.

The number of radiographs needed varies according to the size of the child.  It is usually 3-4 radiographs, including two views of the skull and the continuous trajectory of the shunt tubing down the neck, chest, and then looping into the abdomen.

If a series is performed after the scan, theoretically a 2 view skull radiographs can be eliminated, provided that the chest x-ray includes the base of the neck. Unnecessary radiation may then be avoided.

The use of ultrasound is an area of ongoing research and has been largely unvalidated in children with VP shunts.

 

No clear cause for Rhiannon’s symptoms was found following a thorough examination.  A CT was performed because of concern over shunt failure. Her ventricles were noted to be slightly larger than a CT performed previously.  Shunt series radiographs showed continuous, non-kinked tubing.  She was admitted under the care of the Neurosurgeons and her shunt was revised.  No physical reason for shunt obstruction was found.

 

Selected references

Mansson PK, Johansson S, Ziebell M, Juhler M. Forty years of shunt surgery at Rigshospitalet, Denmark: A retrospective study comparing past and present rates and causes of revision and infection. BMJ Open. 2017;7(1).

Berry JG, Hall MA, Ph D. A multi-institutional 5 year analysis of Initial and multiple ventricular shunt revisions in children. Neurosurgery. 2008;62(2):445–54.

Pople IK. Hydrocephalus and shunts: What the neurologist should know. Neurol Pract. 2002;73(1).

Paff M, Alexandru-Abrams D, Muhonen M, Loudon W. Ventriculoperitoneal shunt complications: A review. Interdiscip Neurosurg Adv Tech Case Manag. 2018;13(June 2017):66–70.

Gonzalez DO, Mahida JB, Asti L, Ambeba EJ, Kenney B, Governale L, et al. Predictors of Ventriculoperitoneal Shunt Failure in Children Undergoing Initial Placement or Revision. Pediatr Neurosurg. 2016;52(1):6–12.

Wu Y. V Entriculoperitoneal S Hunt C Omplications in C Alifornia : 1990 To 2000. 2007;61(3):557–63.

Brinker T, Stopa E, Morrison J, Klinge P. A new look at cerebrospinal fluid circulation. Fluids Barriers CNS. 2014;11(1):1–16.

Rochette A, Malenfant Rancourt MP, Sola C, Prodhomme O, Saguintaah M, Schaub R, et al. Cerebrospinal fluid volume in neonates undergoing spinal anaesthesia: A descriptive magnetic resonance imaging study. Br J Anaesth [Internet]. 2016;117(2):214–9. Available from: https://dx.doi.org/10.1093/bja/aew185

Desai KR, Babb JS, Amodio JB. The utility of the plain radiograph “shunt series” in the evaluation of suspected ventriculoperitoneal shunt failure in pediatric patients. Pediatr Radiol. 2007;37(5):452–6.

Stone JJ, Walker CT, Jacobson M, Phillips V, Silberstein HJ. Revision rate of pediatric ventriculoperitoneal shunts after 15 years: Clinical article. J Neurosurg Pediatr. 2013;11(1):15–9.

Brian W. Hanak et al. Cerebrospinal fluid shunting compliations in children. Pediatr Neur. 2017;52(6):381–400.

Hanak BW, Ross EF, Harris CA, Browd SR, Shain W. Toward a better understanding of the cellular basis for cerebrospinal fluid shunt obstruction: Report on the construction of a bank of explanted hydrocephalus devices. J Neurosurg Pediatr. 2016;18(2):213–23.

Khan F, Shamim MS, Rehman A, Bari ME. Analysis of factors affecting ventriculoperitoneal shunt survival in pediatric patients. Child’s Nerv Syst. 2013;29(5):791–802.

Shastin D, Zaben M, Leach P. Life with a cerebrospinal fluid (CSF) shunt. BMJ [Internet]. 2016;355(October):1–5. Available from: https://dx.doi.org/doi:10.1136/bmj.i5209

Simon TD, Butler J, Whitlock KB, Browd SR, Holubkov R, Kestle JRW, et al. Risk factors for first cerebrospinal fluid shunt infection: Findings from a multi-center prospective cohort study. J Pediatr [Internet]. 2014;164(6):1462-1468.e2. Available from: https://dx.doi.org/10.1016/j.jpeds.2014.02.013

Buster BE, Bonney PA, Cheema AA, Glenn CA, Conner AK, Safavi-Abbasi S, et al. Proximal ventricular shunt malfunctions in children: Factors associated with failure. J Clin Neurosci [Internet]. 2016;24:94–8. Available from: https://dx.doi.org/10.1016/j.jocn.2015.08.024

Mcgirt MJ, Zaas A, Fuchs HE, George TM, Kaye K, Sexton DJ. Factors Infecton for Pediatrc and Venticulopertoneal of Shunlt Predictors Infectous Patiogens. 2014;36(7):858–62.

Mcclinton D, Carraccio C, Englander R. Predictors of ventriculoperitoneal shunt pathology. Pediatr Infect Dis J. 2001;20(6):593–7.

Erol FS, Ozturk S, Akgun B, Kaplan M. Ventriculoperitoneal shunt malfunction caused by fractures and disconnections over 10 years of follow-up. Child’s Nerv Syst. 2017;33(3):475–81.

Dabdoub CB, Dabdoub CF, Chavez M, Villarroel J, Ferrufino JL, Coimbra A, et al. Abdominal cerebrospinal fluid pseudocyst: A comparative analysis between children and adults. Child’s Nerv Syst. 2014;30(4):579–89.

Boyle TP, Kimia AA, Nigrovic LE. Validating a clinical prediction rule for ventricular shunt malfunction. Pediatr Emerg Care. 2018;34(11):751–6.

Tuli S, O’Hayon B, Drake J, Clarke M, Kestle J. Change in ventricular size and effect of ventricular catheter placement in pediatric patients with shunted hydrocephalus. Neurosurgery. 1999;45(6):1329–35.

DeFlorio RM, Shah CC. Techniques that decrease or eliminate ionizing radiation for evaluation of ventricular shunts in children with hydrocephalus. Semin Ultrasound, CT MRI [Internet]. 2014;35(4):365–73. Available from: https://dx.doi.org/10.1053/j.sult.2014.05.002

Smyth MD, Narayan P, Tubbs RS, Leonard JR, Park TS, Loukas M, et al. Cumulative diagnostic radiation exposure in children with ventriculoperitoneal shunts: A review. Child’s Nerv Syst. 2008;24(4):493–7.

Pro tips for LPs in kids

Cite this article as:
Ben Lawton. Pro tips for LPs in kids, Don't Forget the Bubbles, 2015. Available at:
https://doi.org/10.31440/DFTB.7969

Though less commonly performed than it used to be, the lumbar puncture remains a key skill to master for anyone practising acute paediatrics. December’s Archives of Disease in Childhood Education and Practice contains an excellent paper entitled “How to use… lumbar puncture in children” (1), which flashes more pearls than a 4th of July garden party in the Hamptons. We share some of its wisdom below but highly recommend reading the paper to anyone who considers LP within their scope of practice.

How much is too much?

Adults have a CSF volume of about 150 mls and produce it at somewhere between 14-36 mls/hour. Neonates have about 50 mls of CSF, which they produce at a rate of 25 mls/day. Twenty drops of CSF equates to about 1 ml. How much CSF you need to take depends on what you want to do with it but 1.5 mls (or 30 drops) should be both safe and sufficient for your smallest patients.

It’s all about position

LP is commonly performed in the left lateral position in children. Hip flexion opens up the intervertebral spaces and makes the procedure easier. Neck flexion does nothing to help the procedure and will probably make it more uncomfortable for the child as well as making it harder for them to breathe. Supporting neonates in the sitting position with their hips flexed and their legs forward is associated with wider intervertebral spaces and less hypoxia than the left lateral position in this age group. Anecdotally I have recently changed my routine practice for neonatal LPs from left lateral to sitting and it also seems to be easier for holders with a wider range of experience to achieve an optimal position in relative comfort.

What am I aiming at?

The spinal cord in adults and older children ends around L1-L2, in neonates it extends down to L3. The sub-arachnoid space extends down to S2. L4-L5 is generally the best area to aim for (bearing in mind we are not always in the space we think we are) though L3-L4 is also OK. With the child in an appropriate position a line drawn between the most superior aspect of both Iliac crests (Tuffier’s line) crosses the midline over the body of L4 so the space just below this is ideal.

How deep do I need to go?

Medical folklore contains a few different answers to this question but the most scientific answer I have seen is following formula (2)

Depth (mm) = 0.4 x Weight (kg) + 20

So in a 10 kg child CSF should be found at a depth of 24 mm.

How can I make it more comfortable for the patient?

Use topical anaesthetic. EMLA has been shown to help in neonates(3). Post LP headache may be reduced by:

  • Using a smaller needle (25g in neonates, 22g in others)
  • Replacing stylet prior to needle withdrawal
  • Orientate the needle with the bevel parallel to the spine so it will separate the longitudinally running fibres of the Dura. (I think this feels natural in the left lateral position but requires more thought in the sitting position).

Have you thought about…

…CSF lactate? This is quite a good discriminator between viral and bacterial meningitis with levels over 3.5 suggestive of bacterial CNS infection. It’s not quite as accurate after antibiotic administration but may still be clinically useful.

…USS guidance? This is still waiting for a decisive trial in kids but small studies have shown it to be a promising option for further exploration.

Defence against the dark arts

Many a mythical formula has been conjured up to interpret a white cell count in the context of bloodstained CSF. The authors of this paper suggest you can get a feeling by comparing the ratio of white cells to red cells in the peripheral blood and basing your maths on this, but wisely acknowledge that accurate interpretation is difficult in this context. It’s also worth highlighting the well described trap that a normal CT does NOT exclude raised intracranial pressure.

Though LP is a procedure I perform fairly frequently this paper has shone a spotlight into several dusky areas of my knowledge and I hope it will suitably illuminate yours. Finally, if I am asked to supply a question for next year’s Christmas quiz it may well be “Where can you find Tuffier’s line?”.

References

  1. Schulga P, Grattan R, Napier C, et al. How to use… lumbar puncture in children. Arch Dis Child Educ Pract Ed 2015;100: 264–271.
  2. Bailie HC, Arthurs OJ, Murray MJ, et al. Weight-based determination of spinal canal depth for paediatric lumbar punctures. Arch Dis Child 2013;98:877–80.
  3. Kaur G, Gupta P, Kumar A. A randomized trial of eutectic mixture of local anesthetics during lumbar puncture in newborns. Arch Pediatr Adolesc Med 2003;157:1065–70.

How many white cells v red cells do we allow in CSF?

Cite this article as:
Tessa Davis. How many white cells v red cells do we allow in CSF?, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.4722

Unless your skills are tip top, the chances are that you will have had a traumatic tap before (studies suggest up to 40% of lumbar punctures). Blood in the CSF on lumbar puncture can be a sign of a subarachnoid haemorrhage but more commonly is due to a traumatic tap (if the number of red cells in consecutive samples remains the same, it’s likely to be an SAH, but if they reduce then it’s likely due to a traumatic tap).

Do antibiotics affect CSF results?

Cite this article as:
Tessa Davis. Do antibiotics affect CSF results?, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3997

Paediatricians often have to make a decision about whether to just go ahead and give antibiotics in suspected meningitis, or wait for a lumbar puncture (LP) – this could be due to parental refusal, an unstable patient, or a failed attempt.

There is often a discussion about repeating the LP later that day, or even the following day. We all know that having had antibiotics might affect the results. But what effect does it actually have?

Here, I summarise three key papers looking at this very question – do antibiotics affect cerebrospinal fluid (CSF) results in bacterial meningitis?

Paper 1 - Michael et al (2010)

View paper

Who were the patients?

Patients were adults from a large UK district hospital and were identified retrospectively through a coding diagnosis of meningitis.

 

How was bacterial meningitis defined for inclusion criteria?

Patients had to have clinical features consistent with meningitis and had to have had an LP with a cell count of >4 cells/ml.

 

How many patients were included?

They had 92 patients included in the study.

They had been diagnosed with meningitis and had an LP with >4 cells/ml.

They all received antibiotics prior to the LP.

 

What did they find?

What they concluded from the analysis was that once antibiotics have been started, an LP within 4 hours of antibiotic administration is still likely to be culture positive.  After the 4 hour mark the proportion of positive CSF cultures dwindled. 

Paper 2 - Kengaye et al (2001)

View paper

Who were the patients?

The cohort was drawn from all patients discharged from San Diego Children’s Hospital during a 4 year period.

The patient group was identified by a coding diagnosis of bacterial or suspected bacterial meningitis.

 

How was bacterial meningitis defined for inclusion criteria?

CSF culture positive with bacteria; CSF WCC >10/mm3 + CSF antigen or Gram stain positive; CSF WCC >100/mm3 + blood culture positive; or CSF WCC >4000/mm3 in the absence of positive cultures.

 

How many patients were included?

There were 128 patients included.

43% had an LP both pre- and post-antibiotics, 30% had antibiotics prior to LP, and 27% had LP prior to antibiotics.

 

What did they find?

There were far less positive CSF cultures in post-antibiotic LPs.

In particular N. meningitides was sterilized earlier than Strep. penumoniae or Group B Strep. meningitis.

No N. meningitides CSF cultures were positive by 2 hours post-antibiotics.

Their conclusion was that negative cultures occurred in 44% of post-antibiotic LPs and only 8% of pre-antibiotic LPs.  And that meningococcal meningitis is very quick to sterilize.

Paper 3 - Nigrovic et al (2008)

View paper

Who were the patients?

This was a retrospective cohort study across twenty Emergency Departments in US paediatric centres.

Paediatric patients were identified through a coding diagnosis of bacterial meningitis or unspecified meningitis; and a review of positive CSF cultures for bacteria.

 

How was bacterial meningitis defined for inclusion criteria?

CSF culture for positive for a bacterial pathogen; CSF WCC >=10 cells/microL with positive blood culture +/- positive CSF agglutination study results.

 

How many patients were included?

245 patients were included.

159 (65%) had the LP before antibiotic treatment and 85 (35%) had the LP after antibiotic treatment.

Of those who had received treatment prior to LP: 24% had oral antibiotics; 69% had IV antibiotics; 7% had both oral and IV antibiotics.

 

What did they find?

CSF culture results were significantly more likely to be negative after receiving antibiotics.

4 hours post-antibiotics: CSF WCC was not affected by the administration of antibiotics; but the CSF glucose was significantly higher; and the CSF protein lower (although not significantly).

This was more marked (and more significant) 12 hours post antibiotics.

What should we take from this for our daily practice?

I find it hard to draw any useful conclusions from the Benedict et al study. There are three major flaws with it:

  1. Every single patient had antibiotics before having their LP.  There is no comparison to the group that had the LP first (apparently there were none in this category) and so to draw any conclusion about the effect of the antibiotics on the CSF results seems a stretch.
  2. Patients were actually excluded if their CSF had <5 cells/ml and the culture was negative.  This seems to hugely skew the results.  It could be that there were thousands of (excluded) patients who had antibiotics prior to LP and that all their CSF sample showed no WCC and were culture negative.  This would vastly change the results.  It’s also in adults which makes it difficult to draw paediatric conclusions.
  3. The patients were split into viral and bacterial meningitis groups, and part of the way this decision was made was by looking at the CSF results.  It’s self-fulling spiral.

But, it is fair to say that in the patient group they looked at, the CSF cultures were still positive even after antibiotic administration as long as it was within 4 hours.  By the time there was an 8 hour gap post-antibiotics, none of the CSF cultures were positive.

All the studies were retrospective and relied on correct coding diagnosis.  The retrospective nature also made it difficult to accurately assess timing of lumbar puncture and antibiotics administration.  Deciding the inclusion criteria for bacterial meningitis in a study about the effect on CSF results is fraught with difficulties.

Kanageye’s paper, however, does indicate that CSF culture results are affected by antibiotic administration (even within a couple of hours) and so repeating the lumbar puncture the following day may well give false reassurance. And Nigrovic’s paper reinforces this finding, and adds that CSF glucose will increase, and CSF protein will decrease, post antibiotics (especially 12 hours post antibiotics).

Although the accuracy of the timing measurement is potentially flawed, this is something to bear in mind.  Often in paediatrics the LP is unsuccessful, the patient is treated anyway, and the LP will be repeated the following day.  This can give falsely reassuring results.  Be wary of making decisions around length or choice of antibiotic, based on a post-antibiotic lumbar puncture

 

References

Michael B, Menezes BF, Cunniffe J, Miller A, Kneen R, Francis G, Beeching NJ, Solomon T. Effect of delayed lumbar punctures on the diagnosis of acute bacterial meningitis in adults. Emerg Med J. 2010 Jun;27(6):433-8. 

Kanegaye JT, Soliemanzadeh P, Bradley JS. Lumbar puncture in pediatric bacterial meningitis: defining the time interval for recovery of cerebrospinal fluid pathogens after parenteral antibiotic pretreatment. Pediatrics. 2001 Nov;108(5):1169-74.

Nigrovic LE, Malley R, Macias CG, Kanegaye JT, Moro-Sutherland DM, Schremmer RD, Schwab SH, Agrawal D, Mansour KM, Bennett JE, Katsogridakis YL,Mohseni MM, Bulloch B, Steele DW, Kaplan RL, Herman MI, Bandyopadhyay S, Dayan P, Truong UT, Wang VJ, Bonsu BK, Chapman JL, Kuppermann N;American Academy of Pediatrics, Pediatric Emergency Medicine Collaborative Research Committee. Effect of antibiotic pretreatment on cerebrospinal fluid profiles of children with bacterial meningitis. Pediatrics. 2008 Oct;122(4):726-30.