Microbiology Induction for Neurosurgery trainees Kavita Sethi Consultant

Microbiology Induction for Neurosurgery trainees Kavita Sethi Consultant Microbiologist LTHT

LTHT Microbiology

Contact Details Duty Microbiologist for 0113 -392 -3962 or -8580 interpretative & clinical advice Ext 25034 if need to contact myself (Contact via switchboard for urgent queries) For laboratory assistance within normal working hours (e. g. l urgent samples) 0113 -392 -3499 Results will NOT normally be given out by telephone if the result is already available on the results server

LEEDS HEALTH PATHWAYS l Neurosurgery, Neurology, Rehabilitation Medicine Specialty Specific Treatment l l l Brain abscess and subdural empyema Deep spinal infection in adults Herpes Simplex Encephalitis in adults l l l General. Treatment Clostridium Difficile Infection Community Acquired Pneumonia Hospital Acquired Pneumonia (Non-ventilated Patients) Severe Sepsis Screening Tool and Resuscitation Care Bundle (Adults) Urinary Tract Infections (UTIs) including acute pyelonephritis in Adults (≥ 16 years of age

Restricted Antimicrobial Policy • To slow the development of resistance to a drug by limiting its use • There are more suitable alternatives that are less expensive or less toxic l DOCUMENTED approval from one of the Medical Microbiologists or infectious diseases physicians prior to prescribing (antimicrobial code)

How do you evaluate infection

NORMOTHERMIA l l An increase in body and brain temperature is associated with an increase in CBF, cerebral metabolic requirement for oxygen and oxygen utilisation, resulting in an increase in ICP and further cerebral ischaemia. Pharmacological antipyretics and surface cooling.

Evaluation of fever in Neurosurgical patients Nervous system is a sterile milieu. l Fever occurs in 25% of neurocritical care patients with 50% being noninfectious l Hypothalamic temp. l Majority of infections within the Neurocritical care units are nosocomial (device related infections) l

Total white cell count and C-reactive protein surgery

Risk Factors l l l Admission for more than 48 hours Mechanical ventilation Trauma Vascular catheterisation Urinary catheterisation Stress ulcer prophylaxis EPIC 1995

Nosocomial infections on NITU Respiratory infection l Early l Late l Bacteremia l GI infection l UTIs l l Haemophilus influenzae, Staphylococcus aureus, Streptococcus pneumoniae Pseudomonas, Coliforms, Acinetobacter, MRSA l l Neurosurgical device related infections l l l Clostridium difficile Asymptomatic bacteruria in catheterised patients Coagulase negative Staphylococcus, P. acnes, Staphylococcus aureus

Postoperative bacterial meningitis l Low overall incidence ¡ Variables l l l Clean or clean-contaminated Antibiotic prophylaxis Aetiology ¡ Aerobic GNB (60 -70%) l ¡ ¡ E. coli, K. pneumoniae, P. aeruginosa, Acinetobacter spp. S. aureus S. pneumoniae (dural defects/ CSF otorrhoea or rhinorrhoea) REMEMBER ASEPTIC MENINGITIS

Pathogenesis What is on the skin goes in the wound l Most cases are a result of surgical wound infection l Independent risk factors : l GCS < 10 l Emergency surgery l CSF leakage l External CSF drainage l

Diagnosis of bacterial meningitis post-neurosurgery Useful criteria Less helpful criteria high fever new neurological deficit active CSF leak CSF leukocytosis blood leukocytosis CSF glucose CSF protein type of operation presence of foreign material steroid use altered mental status neck stiffness headache / nausea Ross et al. Journal of Neurosurgery 1988; 69: 669 -74

Diagnosis of Nosocomial meningitis l l Challenging Clinical ¡ ¡ l Indistinguishable from community-acquired meningitis May be difficult to distinguish from neurological signs/ symptoms of underlying disease or associated with post-op period LP must be performed to confirm diagnosis (CT first to establish safety) ¡ ¡ CSF parameters may be altered due to surgery itself especially in the presence of SAH CSF leucocytosis not infrequent Antibiotics which achieve adequate CSF levels (guided by gram stain and culture) l Surgical management of wound infection/ persistent CSF leak l

CSF Penetration of antibiotics l Excellent l l Ceftazidime Meropenem Metronidazole Rifampicin Chloramphenicol l l Useless Macrolides l Aminoglycosides l Clindamycin

Additional points l Duration of therapy ¡ ¡ l S. aureus – 2 weeks AGNB – up to 3 weeks Vancomycin penetrates poorly into CSF and patient may fail to respond to systemic therapy ¡ Implant an Ommaya reservoir and instill vancomycin directly into ventricles every 3 rd day

Postoperative aseptic meningitis Thought to be the result of irritation caused either by blood/ degradation products introduced into SAS during surgery l Indistinguishable from postoperative bacterial meningitis (clinical & CSF cell count and chemistry) l ¡ l ? CSF lactate to distinguish Approach ¡ ¡ ¡ Empirical antibiotic therapy If CSF sterile – discontinue antibiotics Responds favourably to high dose corticosteroids

Empiric therapy 1 st line therapy Cefotaxime 2 -3 g qds Confirmed Ceftazidime P. aeruginosa or recent broad spectrum antibiotic 2 g tds Suspected or confirmed Meropenem ESBL-producing Enterobacteriaceae or Acinetobacter spp. 2 g tds MSSA Flucloxacillin 2 -3 g qds MRSA Vancomycin PLUS Rifampicin 1 g bd 600 mg bd

Antibiotic Prophylaxis for Basilar Skull Fracture? Meta Analysis 12 studies, 1241 patients l 58% received antibiotics ¡ Antibiotics did not prevent meningitis RR 1. 15 (0. 68 - 1. 94) p=0. 68 l ¡ CSF leakage subset RR 1. 34 (0. 75 - 2. 41) p=0. 36

Brain abscess l l l Hematogenous spread from extracranial site Can arise from direct spread from mastoid and sinus infections Corticomedullary junction Frontal and parietal lobes most common Posterior fossa <5% l l Overall mortality rate has ranged from 0% to 24%. Prognosis the rapidity of progression before hospitalization mental status onadmission

Bacteriology l Streptococci (70%) l mixed infections (30% to 60%) Streptococcus milleri group l oral cavity, appendix, and female genital tract l otopharyngeal infections , l IE l l Staphylococcus aureus 10% to 15% cranial trauma l IE l Neurosurgical procedure l

Contd. l l l l Bacteroides and Prevotella in 20% to 40% mixed infection Enteric gram-negative bacilli (Proteus species, Escherichia coli, Klebsiella and Pseudomonas) in 23% to 33% otitic infection Septicemia neurosurgical procedures immunocompromised Rare pathogens : Nocardia, Mycobacterium tuberculosis, Listeria monocytogenes

Brain abscess l Blood cultures should be obtained when diagnosis is suspected l Lumbar puncture (LP) should be deferred in any case for which brain abscess is suspected because of the potential for CNS herniation and low likelihood of positive cultures l . Pus collected in a sterile universal container (NOT SWAB) should be sent to Microbiology for urgent microscopy, culture and sensitivity.

Cerebritis and abscess Early cerebritis – (3 -5 days) l Late Cerebritis -(4 to 14 days) l Early Capsule Stage (Begins at 2 weeks following initial infection) Late capsule stage

Initial approach to the patient with a suspected brain abscess l Contrast CT or MRI should be performed If single or multiple ring-enhancing lesions are found, the patient should taken urgently to surgery. l All lesions > 2. 5 cm in diameter should be excised or stereotactically aspirated. l For abscesses in the early cerebritis stage or when the abscesses are < 2. 5 cm in diameter, the largest lesionshould be aspirated for diagnosis and organism identification l

Antimicrobial therapy empirical antimicrobial therapy should be initiated on the basis of the patient’s predisposing conditions and the presumed pathogenesis of abscess formation Otitis media/mastoiditis/sinusitis Cefotaxime/ Metronidazole Post neurosurgical /trauma add anti-staphylococcal cover l l Use Ceftazidime as the 3 rd generation cephalosporin if Pseudomonas aeruginosa is suspected

Brain Abscess - Surgical treatment l l l significant mass effect exerted by lesion proximity to ventricle poor neurological condition Inability to obtain weekly CT scans In patient undergoing medical treatment ¡ Intervention, if neurological deterioration occurs, anatomic progression of abscess towards ventricles, or after 2 weeks of therapy if abscess is enlarged. Also consider if there is no decrease in abscess size by 4 weeks of treatment.

Shunt infections CSF shunts become infected by various routes: • Organisms directly colonize the shunt, usually at the time of surgery • Organisms reach the CSF and the shunt via haematogenous spread • Organisms travel along the shunt by retrograde spread (uncommon) l Coagulase-negative Staphylococci are isolated most commonly. Production of extracellular slime has been reported as being important in the pathogenesis of shunt infections

Clinical features l l l Variable Fever Signs of raised ICP Evidence of shunt malfunction Distal shunt infections can present with peritonitis

Shunt infections l l l CSF from shunt ( before antimicrobial therapy) SHUNT REMOVAL Proximal catheter, valve or shunt reservoir, distal catheter in three separate containers Intrathecal +/- systemic antibiotic Shunt replacement once the CSF sterile

EVD-related ventriculitis Incidence between 10 -17% l Risk ¡ Lowest risk 1 st 4 days that EVD is in-situ ¡ Rises over next 10 days ¡ Falls thereafter l Incidence not decreased by exchanging EVD at regular intervals l Aetiology ¡ CNS (predominant) l

Diagnostic approach Patient with EVD with symptoms and signs of ventriculitis CSF sample + Gram stain or + culture - Gram stain and culture 2 nd sample + Gram stain or + culture (same As 1 st) Treat No treatment

Additional points Collect CSF from EVD itself or the Ommaya reservoir, not the drainage bag l Treat CNS infections with intraventricular Vancomycin for 5 -7 days l ¡ ¡ ¡ Product license does not cover this route Not validated by clinical trials Guarantees max concentrations of vancomycin at the site of infection Avoids systemic toxicity Cheaper than systemic therapy No need to monitor levels

Hand Hygiene