Dr. Shahnawaz Alam, profile picture
Uploaded byDr. Shahnawaz Alam
PPTX, PDF1,106 views

Infections in neurosurgery

This document discusses infections in neurosurgery, including: 1. The basic science of central nervous system infections, how pathogens enter the CNS, and the roles of microglia and astrocytes in the immune response. 2. Postoperative infections, which are most commonly caused by Staphylococcus aureus and coagulase-negative staphylococci. Risk factors include poor wound healing and device implantation. 3. Empirical treatment regimens typically involve vancomycin, third-generation cephalosporins, and metronidazole to cover gram-positive, gram-negative and anaerobic bacteria. Source control is critical for resolving infections.

Embed presentation

Downloaded 75 times
Dr. Shahnawaz Alam Guided by:-Dr. Vikas Chandra Jha HOD Neurosurgery Moderated by:-Dr. Saraj kumar Singh Asst.Prof. (Dept. of Neurosurgery) Infections in Neurosurgery
Outline • Basic Science of CNS Infections • Postoperative Infections of CNS • Brain Abscess • Meningitis and Encephalitis • Use and Misuse of Antibiotics in Neurosurgery • AIDS & Parasitic Infections of CNS
• Immune effectors: astrocytes and microglia • Varying degrees of both structural and functional damage to CNS • Others: matrix metalloproteinases enzymes/Dysregulation of glutamate metabolism • Implicated in many CNS ds.-infections, ischemic or traumatic injury, and autoimmune disorders • BBB is rich in potential substrates for MMPs, including type IV collagen, fibronectin, and laminin; MMP degradation of the BBB may favor transmigration of leukocytes as well as the movement of macromolecules and water, thus contributing to brain edema • MMPs are potential targets for therapeutic interventions Basic Science of CNS Infections
CLASSIFICATION • Anatomy of the infection (parenchymal, meningeal, parameningeal) • Presence of space-occupying lesions (e.g. abscess, empyema) • Diffuse inflammation (e.g. meningitis, encephalitis) • Also a/c to etiology • Pathogens enter the CNS directly (e.g., through trauma, neurosurgery), /Via BBB/CSFB (e.g., bacterial meningitis caused by Escherichia coli), / via retrograde transport along neural structures (e.g., rabies) • Iatrogenic routes are more relevant to the neurosurgeon • Perioperative breeches in structural barriers protecting the CNS (scalp, cranium, meninges), implantation of foreign bodies (e.g., cerebrospinal fluid [CSF] shunts, dural implants, electrodes, spinal hardware), and breeches in mucosal defenses (e.g., intubation, vessel catheterization)
 MICROGLIA; several different states • Resting microglia -Small cells with few surface markers & prominent thin branches • Stimuli activate microglia-Cellular debris from CNS damage, particularly free ATP- Ameboid cells • Receptors expressed by microglia includes Toll-like receptors/a cytosolic “alarm system” exists in microglia in the form of nucleotide-binding oligomerization domain 2 (NOD2) • NOD2 recognizes a common motif in bacterial peptidoglycan from both gram -/+ • NO synthesis and a respiratory burst, leading to the formation of peroxynitrite (ONOO−), a highly toxic product capable of damaging both host and pathogen/superoxide anion (O2−) • Phagocytes in the CNS under both physiologic and pathophysiologic conditions • Microglia also produce factors that support glial and neuronal cells/APC • Downregulate these proinflammatory responses
 Astrocytes; Resident glial cells derived from neuroectoderm;“nurse” cells for neurons • star-shaped morphology & GFAP • Maintain BBB/participate in the immunologic processes/targets of bacterial invasion • Expression of OmpA by pathogenic E. coli strains significantly enhances E. coli invasion of astrocytes • GBS also invades astrocytes -death via expression of β-hemolysin/cytotoxin • Pneumolysin (Ply)-structural and functional changes-tissue injury and brain edema • Main source of IL-6 production in the CNS • HIV gp120 reduces astrocyte expression of glutamine synthase, and patients with HIV- associated dementia have higher brain glutamate levels • Balance of CNS protection/ destruction during infection by secretion of MMPs
Postoperative Infections of the Head and Brain • Diagnosis of infection after craniotomy is often challenging • superficial incisional infections-skin and s.c tissue • deep incisional infections-subgaleal space and bone flap • Deep organ space infections-subdural empyema, brain abscess /meningitis/ventriculitis • superficial infections-60% of SSIs after craniotomy/Meningitis-mc deep organ space infection,22% /others;subdural empyema and brain abscess-14% • Infections after craniotomy are most commonly associated with gram-positive bacteria-S. aureus, and conS
• Majority of post-op infections- patient’s skin • Host defense mechanisms impaired in pt. undergoing craniotomy • Brain-relatively immune privileged site/low levels of Abs & C -brain less efficient than other organs • Post-op CSF leakage and early subsequent reoperation • Placement of drains or icp monitors, poor neurological status, paranasal sinus entry, foreign body implantation RISK FACTORS FOR INFECTION AND PREVENTIVE STRATEGIES
Role of Pre-op antibiotics in reducing the incidence of SSIs after craniotomy • The Surgical Care Improvement Project (SCIP) outlines the following 3 performance measures for monitoring appropriate antimicrobial prophylaxis use: 1.selection of an appropriate antibiotic, 2.adminstration within 1 hour before incision 3.discontinuation within 24 hours after surgery is completed • Choice of an agent-narrow spectrum;guided by institutional data on frequently recovered pathogens and their resistance profiles • For clean neurosurgical procedures, a single dose of cefazolin is recommended • Vancomycin –MRSA/β-lactam allergy • Antibiotics with short t1/2 such as cefazolin should be readministered every 3 to 4 hrs during prolonged surgery • Risk factors for MRSA: male, malignancy, DM, prior MRSA infection, immunosuppressed & traumatic injury • Other: surgical site preparation and environmental control within the operating room • any hair removal that is performed should be done as close to the time of surgery as possible • use of high-efficiency particulate air (HEPA) filters
PRINCIPLES OF TREATMENT •Postoperative infections tend to be particularly difficult to resolve because of the complex anatomic changes resulting from craniotomy •Early and decisive intervention is critical to limit morbidity, and the keystone of successful treatment is effective source control (i.e., drainage of abscesses and infected fluid collections and debridement of necrotic tissue) •Bactericidal rather than bacteriostatic agents are generally preferred •Most antibiotic agents enter CNS mostly by passive diffusion down a concentration gradient, with physical barriers BBB and blood-CSF barriers functioning as the primary determinants of drug distribution •Inflammation at the site of infection may facilitate entry of drugs across these barriers and into the brain •Other inherent physiochemical properties: Mwt., lipophilicity, PPB & ionization state •Ultimately, adequate dosing - minimal bactericidal concentration [MBC]).
• Empirical regimens for postcraniotomy infections: vancomycin + 3rd /4th gen. cephalosporin with antipseudomonal activity (e.g., ceftazidime, cefepime) + metronidazole (anaerobic) • carbapenem (e.g., meropenem) may be substituted for the combination of a third-generation cephalosporin and metronidazole (Gram - & anaerobes) • Imipenem-increased seizure risk relative to meropenem (and other β-lactams) • β-Lactam antibiotics (penicillins, cephalosporins, carbapenems) have poor penetration into the CSF in the absence of meningeal inflammation, but higher systemic doses can result in therapeutic CSF concentrations • 3rd /4th gen. cephalosporin (specifically cefotaxime, ceftriaxone, and ceftazidime) are often used for the treatment of CNS and postcraniotomy infections because of their low toxicity and excellent activity • High-dose β-lactamase inhibitors such as sulbactam and tazobactam are also effective in protecting the coadministered penicillin agent • β-lactam antibiotics-proconvulsive- use via intraventricular injection not recommended • Intraventricular antibiotic administration bypasses BBB, can achieve much higher CSF concentrations than systemic administration;asst. with neurotoxicity
 CSF Shunt Infections: The Role of Biofilms • Perioperative contamination/Wound dehiscence over the shunt /Hematogenous seeding/Distal port contamination • Biofilm formation occurs with both infection and colonization of prosthetic medical devices • Biofilms are in a stationary phase of growth-less susceptible to antibiotics/less permeable to most antibiotics/prosthetic devices lack a vascular supply • Coagulase-negative staphylococci (CoNS)-notorious for their ability to form biofilm on prosthetic devices • Soon after placement, bioprosthetic materials are coated with host proteins, which serve as receptors for bacterial adhesins k/a “microbial surface components recognizing adhesive matrix molecules,” or MSCRAMMs- CoNS initiate biofilm formation almost immediately • Transition state between planktonic and sessile bacteria in biofilms known as quorum sensing • Dormant microbes (sessile) within the biofilm are up to a 1000 times more tolerant of [most] antimicrobial agents than their free-living (planktonic) S. epidermidis biofilm formation on a catheter surface. Note the deposition of extracellular matrix,manifested as a complex web of material around and between microcolonies
SUPERFICIAL INCISIONAL INFECTIONS • extend from the skin to the epidural space. • May extend to the underlying bone flap and through the dura • repeat operative intervention, poor tissue quality, impaired vascular supply, radiation injury, nutritional deficiencies, and the presence of foreign bodies • manifests as local erythema, swelling, and tenderness at the craniotomy site with possible suppurative drainage • With progressive infection, systemic signs such as malaise, fever, and chills may develop • The most common pathogenic agents of superficial wound infections are gram-positive cocci, including S. aureus, coagulase-negative staphylococci, and P. acnes • clinically apparent; however, CT or MRI reveal fluid collections in the subgaleal or epidural space/extension/bone flap osteomylitis/ identifying possible precipitating factors • Measurement of ESR/CRP concentration may provide some assistance in detecting infection and monitoring the response to therapy • normally elevated after craniotomy and return toward baseline by the 5th POD • nonspecific, prolonged elevation or a secondary increase in their levels may indicate the development of infection • Hyperbaric oxygen (HBO)/local rotational or pedicled flaps or vascularized myocutaneous free flaps -chronic postoperative infections
Purulent drainage from a superficially infected craniotomy incision with surrounding erythema Skin breakdown at the inferior aspect of the craniotomy incision with exposed titanium hardware A.Surgical debridement of a superficial postcraniotomy infection in a patient who had undergone multiple craniotomies and radiation treatments for malignancy. There is spread of infection to the underlying bone flap, with erosion and adjacent purulent material in the epidural space. B.Epidural infection with contamination of the undersurface of the devascularized bone flap.
 DEEP INCISIONAL INFECTIONS: SUBGALEAL SPACE AND BONE FLAP • A high index of suspicion • majority d/t commensal skin flora infection of autogenous cranioplasties after decompressive craniectomy; however, a significant proportion are due to nosocomial gram-positive and gram-negative organisms • CT and MRI studies may show the presence of subgaleal or epidural infection with bone flap destruction suggestive of osteomyelitis • Treatment options: antibiotic therapy alone/surgical debridement with removal of the bone flap/debridement with replacement of the bone flap or other cranioplasty material such as titanium mesh • Removal of the infected bone flap followed by delayed cranioplasty offers the best chance of clearing the initial infection/ multiple surgical interventions • Several case series have reported clinical resolution of infection with preservation of the bone flap • In Other study successful resolution of infection in patients treated with immediate titanium mesh cranioplasty at the time of initial surgical debridement
A, Axial computed tomography (CT) scan demonstrating erosion of bone flap (asterisk) indicative of osteomyelitis. B, Coronal CT scan showing failure of titanium screws with surrounding bone lucency (arrow) A, Debridement of the epidural infection and removal of the infected bone flap and hardware. B, Immediate titanium mesh cranioplasty performed at the time of infection debridement. A, T1-weighted axial magnetic resonance (MR) image reveals a hyperintense subdural fluid collection that developed after craniotomy for aneurysm repair. The fluid collection enhances peripherally with gadolinium (B) and, because of higher protein content, exhibits increased signal intensity on fluid-attenuated inversion recovery (FLAIR) MR sequences (C) relative to cerebrospinal fluid. A craniotomy was performed to drain the collection, and frank purulence was encountered in the subdural space.
 Subdural Empyema • spontaneously subdural empyema- fever and headache, followed by the rapid development of focal neurological deficits, altered mental status, and seizures/rarely in subdural empyema develops after craniotomy;Insidious course • Febrile 33%;seizure 25% & 85% without headache;/MC findings- superficial wound infection/In 50% ;occurr more than 1 month after the craniotomy Diagnostic Imaging and Laboratory Data • extra-axial fluid collections are commonly noted on postoperative imaging studies • NCCT demonstrates a crescent-shaped fluid collection that is slightly more dense than CSF and located beneath the craniotomy flap or adjacent to the falx • Increased signal intensity on T1-w and fluid-attenuated inversion recovery (FLAIR) MRI sequences because of the increased protein concentration of an empyema relative to CSF. Peripheral enhancement of the fluid collection is common • presence of restricted diffusion on MRI may be helpful • Progressive enlargement of the fluid collection or unexplained edema in adjacent cerebral cortex • Laboratory data –nonspecific; LP-C/I Treatment • Goals of surgery are to evacuate the purulent collection completely/adequate decompression of the brain • optimal surgical approach (craniotomy versus bur-hole drainage) is debated, craniotomy is generally advocated • Empirical antibiotic therapy should be started Early DEEP ORGAN SPACE INFECTIONS
• Newer agents useful for the treatment of resistant staphylococcal infections include linezolid and daptomycin • It has excellent bioavailability, i.v ior orally; adr- myelosuppression and irreversible peripheral neuropathy • Rifampin is a broad-spectrum antimicrobial ;role in the adjunctive Rx of bone flap osteomyelitis or infections associated with foreign body implantation • Rifampin-penetrate biofilms and kill organisms in the sessile phase of growth/used in combination/cytochrome –p enzyme + • Fluoroquinolones (levofloxacin, ciprofloxacin, moxifloxacin) are attractive agents for the treatment of CNS infection because of their lipophilicity and low molecular weight./High resistant/increase seizure threshold • Aminoglycosides have excellent activity against aerobic gram-negative bacilli, including P. aeruginosa, as well as synergistic activity with β-lactams against aerobic gram-positive cocci
Brain Abscess: Pus in the Parenchyma • Space-occupying purulent infections within the substance of the brain • Clinically, the classic triad of headache, fever, and focal neurological deficit is rarely present; s/s of postop abscess nonspecific; expanding, irritative mass lesion-altered LOC, N/V & seizures 20% • Microbiology related to the primary source of the abscess • staphylococci and Enterobacteriaceae- direct inoculation from trauma or neurosurgical procedures
• Abrupt worsening of preexisting headache asst. with new onset of meningismus - Intraventricular rupture of a brain abscess (IVROBA) • manifest sudden neurological deterioration with obtundation or coma (widespread meningoencephalitis ; alterations in CSF flow ) • multiloculated abscesses/ decreased distance from the abscess capsule to the ventricular wall/ deep-seated abscesses have been correlated with increased risk • localized ventricular enhancement on CT - impending intraventricular rupture • diffuse ependymal and meningeal enhancement and the presence of debris within the ventricles- IVROBA • Hydrocephalus 50% & septation of the ventricles delayed complication
Diagnostic Imaging and Laboratory Data • CT cerebritis stage- poorly defined area of low attenuation with a mass effect and significant edema • capsule- peripheral enhancement increases and the center of the lesion becomes progressively hypodense • Corticosteroids- reduce the thickness of the abscess capsule and the extent of contrast enhancement on both CT and MRI • DwMRI -high degree of sp & sn in differentiating spontaneous abscess from other ring- enhancing lesions/ presence of restricted diffusion;non-specific • correlation with ADC & T2-w MRI sequences or CT is necessary to evaluate for blood products that may cause a “T2 shine-through effect,” in which the infection appears bright on diffusion-weighted images • Peripheral leukocytosis is frequently absent, and although the ESR and CRP concentration are usually elevated • Blood cultures seldom yield a causative organism/LP c/i
Axial CE T1-w mri ;two rim-enhancing masses of the left periventricular white matter that represent abscesses. The intraventricular enhancement is suggestive of ventriculitis. Axial fluid-attenuated inversion recovery (FLAIR) image of the same pt.- vasogenic edema surrounding each lesion.
Purulent drainage developed after craniotomy for a left frontal cavernous malformation A.T1-w axial MRI after gadolinium administration demonstrates enhancement within the extra-axial space and the resection cavity. A craniotomy with drainage of purulent material from the epidural and subdural compartments was performed, and treatment with intravenous antibiotics was started. Five days later, severe headache and worsened mental status developed B. MRI - IVROBA One month after resection of a right frontal glioma, this patient exhibited confusion and lethargy. T1-w axial MRI obtained before (A) and after (B) gadolinium administration demonstrate enhancement of the resection cavity and surrounding meninges, and the fluid-attenuated inversion recovery (FLAIR) sequence (C) shows significant surrounding edema. Abnormal restricted diffusion on DWMRI (D) suggests infection. Craniotomy confirmed the presence of purulent material in the subdural and intraparenchymal locations
Treatment • goals - to relieve the mass effect; improve clinical symptoms & fully resolve the infection • In most cases, a combination of sxl drainage (iopen operative drainage or excision of the lesion and stereotactic aspiration ) & a prolonged course of iv antibiotics (6-8 wks f/b oral) • Progressive enlargement of the abscess or failure of the abscess to become smaller- sxl • intraventricular administration of antibiotics, most commonly vancomycin, aminoglycosides, and colistin • Adjunctive corticosteroid - significant cerebral edema related to cerebral infections with signs of impending herniation/ seizure prophylaxis until infection resolved
 Postoperative Infections of the Spine • risks, symptoms & Rx depend on the region of the intervention (cervical, thoracic, or lumbar), the approach (anterior, posterior, or lateral) & instrumentation  Noninstrumented spinal surgery (anterior and posterior decompressive procedures) ;usually confined to short stretches of the spinal column; mostly single level • Lumbar diskectomy < 1% (ssi or muscle tissue, or in the disk space)/ laminectomy without fusion ~2%. • Backache with fever; elevation in ESR/CRP; later - radiographic changes with disk degeneration; progressive cases- end plate degeneration • Risks: longer operating times (>5 hrs), greater blood loss( >1L), no. of levels, greater soft tissue destruction,revision of sx, sx extending below sacrum, ≥2 resident surgeons, the placement of devascularized allograft, long hospital stay, traumatic spinbal injury / pt. comorbidities-obesity/DM/malignancy-20%/  Instrumented Spinal Procedures - posterior spinal procedures ~3% to 7%. • type of instrumentation - older steel implants v s newer titanium implants • Anterior instrumented spinal procedures -lower rates of infection • anterior-posterior approach - highest rates of infection • MIS- no reduction in wound infection • intrathecal drug delivery systems and spinal cord stimulators ~5% ;within the first 2 weeks to 2 months after surgery& treated by removal of the complete system
• Superficial-above the lumbodorsal fascia in the dermis and s.c tiss.;manifest in the immediate posto period with erythema, purulent drainage, local tenderness, and separation or dehiscence of the wound edges • low-grade fever; elevated ESR/CRP/WBC;variable • Deep - more variable manifestation; most manifesting 2 to 3 weeks posto or after several months to several years after surgery • acute manifestation-significant pain, fever, anorexia, and night sweats • wound overlying a deep infection-normal/track superfcially • delayed manifestation progressive backache, wound drainage, and erythema but may lack fever • serial ESR/CRP values with trends-useful in diagnosing and monitoring; tracking the response to treatment • If debridement is planned, specimens should be taken from both superficial and deep parts • blood cultures may aid in the diagnosis of a pathogen • CT- guided or open biopsy may be helpful; 30-50%
Sagittal CT of Pt. with discitis of L5- S1;end plate sclerosis,VB collapse & focal kyphosis. MRIs of thoracic discitis; A.Sagittal T1-w NC MRI; B.Sagittal T1-w CE MRI; hypointense SI in VB & avid enhancement ; C. Sagittal T2-w sequence MRI in a Pt. with postop L5-S1 discitis; hyperintense signal in adjacent end plates • Plain radiographs -assessment of spinal alignment, paravertebral soft tissue swelling;bony changes; integrity of spinal hardware/MRI-ioc • Early bone changes ~2 to 3 wks postop with evidence of disk space narrowing, bone destruction & blurring of end plates f/b VB collapse or sclerosis of end plates and bone ankylosis in the more chronic setting • Increased soft tissue swelling, especially in the retropharyngeal space after anterior spinal surgery- abscess • lucency around screws - loosening, hardware failure, or pseudoarthrosis
Nonoperative Treatment : • SSI, Postoperative discitis /Use of an external brace in postope discitis/iv antibiotics 6 wks f/b oral 6 wks Surgical treatment : • Goals -(1) diagnosis of the infective agent (2) débridement of nonviable tissue, and (3) assurance of stabilization • Preop imaging-extent of debridement; evidence of deep infection mandates opening of the lumbodorsal fascia • Opened only after thorough debridement and irrigation of the superficial compartment • Loose bone fragments, gel foam or fibrin sealant remnants, and necrotic muscle and fat should be meticulously removed • If instrumentation is found to be loose-an alternative means of fixation must be used • In the case of pedicle screw fixation, a screw of larger diameter can be used as a “rescue screw.” • Structural allograft tissue used in the initial construct may also be left in place, but loose chips of bone should be removed • Primary wound closure should be performed if possible • The wound should be closed in layers around a drain to eliminate dead space  Wound Vacuum-Assisted Closure  Irrigation-Suction Technique  Other Surgical Techniques : use of antibiotic beads and muscle flaps  Vancomycin Powder
Use and Misuse of Antibiotics in Neurosurgery • Antibiotics are an integral part of the daily life of the neurosurgeon GENERAL PRINCIPLES OF ANTIBIOTIC USE • Not only CNS but cranial soft tissues, skull, and paranasal sinuses; the spine, intervertebral disks, and paraspinal soft tissues; and the tissues • delivery not depend on physiology of either BBB/BCSFB; act as obstacles • active influx and efflux transporters located on the endothelial/epithelial cell surface alter the distribution of an antibiotic • goal : to deliver an adequate concentration of the drug to the proper compartment • Dose & choice of antibiotics/intraventricular drugs Pharmacokinetics of Antibiotic Delivery • Concentrations throughout CSF not constant (Ventricular < lumbar CSF) • Penetration depend of stage of abscess (blood-abscess barrier) • Most are not metabolized in the CSF/elimination by diffusion or CSF turnover • Generally, CSF t1/2 of antibiotics >> plasma t1/2 • CSF t1/2 increased in CNS infections (decreased turnover) • Pt. with CSF shunts or external CSF drains, CSF t1/2 the CSF quite (altered circulation)
CNS Toxicity of Antibiotic Therapy • include encephalopathy, seizures, psychiatric symptoms, cranial nerve injury, and ataxia • most commonly used intrathecal antibiotics, vancomycin and gentamicin- relatively low toxicity • Intraventricular vancomycin relatively free of toxicity, even at high CSF levels • Intraventricular gentamicin may have CNS toxicity, causing ototoxicity or epilepsy • Intraventricular administration of β-lactam similar to systemic ; seizures • infection rates range < 1% in clean wounds to 6% to 10% in dirty wounds, even with antibiotic treatment • Clean shunt implantations utilizing antibiotic prophylaxis ~ 8-10% infection rate • use of prophylactic antibiotics; irrigation of the wound and filling the shunt with antibiotic solution and antibiotic-impregnated ventricular drains
• Judicious use and adherence to basic principles • Basic principles : 1. Antibiotics only for the prevention or treatment of susceptible infections 2. choice of antibiotic guided by the most likely pathogen and directed by C/S results 3. used for their shortest effective duration 4. risks associated must be considered 5. Adequate Dose and frequency • Failure -antibiotic misuse; ineffective(MDR) to harmful(superinfection) • MC misuses of antibiotics in neurosurgery: Intraventricular administration of chloramphenicol/ Routine use of vancomycin for prophylaxis • appropriate consultation with specialists in infectious diseases
Meningitis and Encephalitis • Meningitis is defined as inflammation of the meninges, the lining of the brain and spinal cord • Encephalitis represents inflammation of the brain, and the pathogens typically responsible are quite different from those usually seen in meningitis • overlap between the two (meningoencephalitis) • Ventriculitis is focal or diffuse inflammation of the ependymal lining of the cerebral ventricular system • Community-Acquired Bacterial Meningitis;Streptococcus pneumoniae and Neisseria meningitidis • 30-50% of survivors sustaining neurological sequelae • 60% pneumococcal meningitis;triad consisting of fever, nuchal rigidity, and altered mental status • mortality associated with pneumococcal meningitis 15-25% for pediatric & 20-37% • Pneumococcal vaccines have been developed and proved to be very effective in the prevention of invasive pneumococcal disease, including meningitis • efficacy of the heptavalent pneumococcal conjugate vaccine ~97%
• uncommon after neurosurgical procedures; < 1% • clinical course of nosocomial meningitis tends to be less fulminant than that of community-acquired meningitis • typical symptoms- fever, headache, and neck stiffness/non-specific; without infection in posterior fossa sx/chemical irritation • aseptic (chemical) meningitis 60%-75% of postop meningitis; frequently in children and after posterior fossa surgery • Others : craniopharyngiomas/ Rathke’s cleft cysts/ epidermoid & dermoid cysts/ cholesteatomas • Release of the irritating element; chronic headache syndrome relieved by resection of the offending lesion • Diagnosis of aseptic meningitis- negative CSF Gram staining & sterile culture and full recovery without antibiotics • Corticosteroids- symptomatic relief in aseptic chemical meningitis
Diagnostic Imaging and Laboratory Data •no single clinical sign or diagnostic test distinguishes between the two entities •Neuroimaging studies rarely assist in the diagnosis of postop meningitis b/c the characteristic sign, meningeal enhancement in 80% of postcraniotomy pt. without infections •CT or MRI -secondary complications of meningitis;HCP, parameningeal abscess, and ischemia/ infarction related to vasculitis and thrombosis of superficial vessels •CSF culture data remain the “gold standard” •Newer diagnostic tests : CSF lactate/IL-1β- promising data
 Neisseria meningitidis; young adults and children (after the neonatal period);sporadic, and endemic- serogroups B, C, and Y • Assost. with smoking & deficiencies in the complement system, specifically the terminal components C5-8 • Four clinical syndromes have been described in meningococcal disease: (1) bacteremia without sepsis, (2) meningococcemia without meningitis, (3) meningitis with or without meningococcemia, and (4) meningoencephalitis. • classic meningitis triad- 27% • Prototypical skin lesions (purpura and petechiae-hemorrahagic rash; HALLMARK) - 60% of adults & 60-90% of children • mortality 4-8% in children and 7% in adults, with septicemia the MCC • 8-20% neurological sequelae;SNHL,MR,seizures • Other : Waterhouse- Friderichsen syndrome (a massive hemorrhage into the adrenal glands)& DIC • Current guidelines recommend the use of penicillin or ampicillin • conjugate vaccine 11-55 yrs • Asst. with a high risk of secondary infection in close contacts; rifampin 600 mg BD x 2 days; 20 mg/kg/day for children
 Diagnosis • Rapid diagnosis and treatment of bacterial meningitis are critical • LP should be done before institution of antibiotic therapy • Suspected increased ICP (h/o mass lesion, new-onset seizures, FND, papilledema, and severe impairment of consciousness) – CT/MRI head before LP • use a small-bore (25-gauge) needle • Severe HCP- require a ventriculostomy • CSF Gram stain-pathogen in 60-90% • CSF culture “gold standard”; 80-90% • CSF lactate >35 mg/dL; RDT with promising result Sn 93%/Sp 96% differentiating bacterial meningitis from aseptic meningitis;limited by other conditions- stroke/trauma • CRP >20 mg/L useful in discriminating bacterial from viral etiology • Procalcitonin (PCT) > 0.5 ng/mL with Sn 99%/Sp 83% distinguishing bacterial from aseptic meningitis • Blood cultures routinely done;50-80% • Others : PCR/ latex agglutination test (LAT)
 Radiologic Studies • X-ray chest, skull & sinuses • CT scans of the skull base - predisposing conditions such as sinus infection, mastoiditis, skull fractures & congenital anomalies • MRI is superior to CT; leptomeningeal enhancement and distention of subarachnoid space • diagnosis of meningitis is not based on imaging findings but allow delineate complications like HCP/abscess/subdural empyema or effusion/infarct • In straightforward cases of bacterial meningitis, early CT and MRI- normal • LP is still the most important diagnostic study  Treatment • Prompt clinical diagnosis of meningitis f/b rapid administration of antibiotics is a key factor • Delays- worse outcome. • After collection of CSF, empirical antibiotic therapy started ASAP
 Nosocomial bacterial meningitis • 0.5% ;serious complication of neurosurgical procedures, systemic infection & TBI • MC gram-negative rods (E. coli, Pseudomonas aeruginosa, Proteus mirabilis, Enterobacter, Acinetobacter), Propionibacterium acnes, streptococci, and Staphylococcus aureus) • prolonged hospital stays, multiple operations & increased morbidity  Postcraniotomy meningitis • 0.8-8.9% cranial surgery; MC S. aureus and Staphylococcus epidermidis; gram-negative • CSF results are altered by the operation/anesthesia/use of steroids • Risk: EVD/CSF leakage/periop steroids/incisional infection/male /operative time > 4 hrs. • 1/3rd within 1 wk of surgery, 1/3rd in 2nd wk & 1/3rd after 2 wks. • most powerful risk factor for postoperative CSF -early reoperation (within 1 month) • prophylactic antibiotic therapy reduced the incidence of incisional infection from 8.8% to 4.6% it didn’t prevent the development of meningitis
 EVD induced Meningitis/ ventriculitis; 8-23% • risk : greater frequency of CSF sampling/ >11 days; mc gram-positive cocci (S. aureus and S. epidermidis) consistent with skin flora • Intrathecal antibiotics administered through the EVD may be desirable, but this approach is not standardized  Lumbar Drain induced Meningitis ~5%  Posttraumatic Meningitis; 0.2-1.4% in moderate or severe head trauma • closed head trauma;mostly asst.with basilar skull fracture and subsequent CSF leakage • CSF rhinorrhea and otorrhea significant independent risk factors • Open (compound) cranial fractures ~5% • Trauma guidelines recommend that skull fractures depressed deeper than the thickness of the cranium be surgically debrided
 Recurrent bacterial meningitis : 2 separate episodes of meningitis separated by a period of full recovery; 6% • Risk : 1) anatomic factors (2) immunodeficiencies [(X-linked agammaglobulinemia (Bruton’s disease),HIV]& (3) chronic parameningeal infections (sinusitis, otitis media, and mastoiditis. ) • Anatomic factors -congenital (encephaloceles, congenital inner ear dysplasia,)/acquired (head trauma or skull fracture-csf leak ) • head trauma MCC • CT scan with thin cuts through the skull base on bone windows  Encephalitis or meningoencephalitis: gram-negative bacillus Legionella pneumophila/Mycoplasma pneumoniae/L. monocytogenes • Aseptic meningitis - nonbacterial inflammation of the tissues lining the brain;viruses/fungi/parasites/protozoa/Rickettsia species • noninfectious etiologies (e.g., drugs, collagen vascular disorders, sarcoidosis) • Viruses account for the vast majority of cases of aseptic meningitis • any age but most common in infants and children. • Enteroviruses are the most common cause of viral meningitis • include echovirus, coxsackievirus groups A and B & poliovirus • transmitted via the fecal-oral route
HSV : mcc of viral encephalitis; mainly HSV-1/HSV-2 4-6% • age distribution is bimodal;6M-20yrs,>50 yrs • primary infection (30%) or virus reactivation (70%) • Pathologically, herpes encephalitis- an acute focal, necrotizing encephalitis with inflammation and parenchymal swelling • predilection for the temporal lobe and limbic system/ olfactory hallucinations • Mollaret’s meningitis, a syndrome with recurrent bouts (≥3) of fever & S/S of aseptic meningitis, recovery is rapid & spontaneous; d/t an occult reservoir of HSV-1/HSV-2 • EEG shows paroxysmal lateralized epileptiform discharges • mortality ~ 80% in infants without treatment • I.V Acyclovir x for 2 weeks; mortality reduced to 20% • survivors -the risk of long-term neurological sequelae is 62%
• FLAIR MRI is most sensitive for showing areas of cerebral involvement and resulting inflammatory changes. • In this axial image, hyperintensity is visible in the right temporal lobe affecting the uncus and insular cortex as well as the subfrontal cortex. Although not present in this patient, foci of hemorrhage are common. •microglial nodules and cytoplasmic and intranuclear inclusion bodies
Tuberculous Meningitis • TBM begins with bacterial seeding of the brain with the formation of tubercles- rupture and cause seeding to adjacent subarachnoid space • military tuberculosis/generalized tuberculosis with a single area/any age (adult>children) • usual location- basal meninges • exudate obliterates the basal cisterns • not confined to SAS only as in bacterial meningitis, but instead spreads along pial vessels to invade adjacent brain • Headache 50%; stiff neck 75%, and lethargy/confusion/fever are typical. • chronicity leads to frequent cranial nerve involvement;20% at time of admission;poor outcome • glucose level, which is reduced but usually not to the very low as in bacterial meningitis • Currently the diagnostic of choice- PCR analysis • MRI- HCP as well as CE within the basal cisterns, subpial cortex, and subependymal areas/frank tuberculoma • self-limited meningitis k/A serous meningitis • meningeal signs are mild Role of Dexamethasone in TB meningitis
Tuberculous meningitis A.Axial T1-w: CE thick enhancement of the basal cistern (arrows), as well as abnormal enhancement in Rt. occipital horn (asterisk) B. sagittal T1-w CE: abnormal enhancement coating pituitary stalk & brain stem, continuing caudally along S.C (arrows) Tuberculoma;Pt. with seizure Axial T2-w (A) & T1-w CE MRI (B)- single ring-enhancing Rt. parietal lesion with moderate edema
• Occasionally an intracerebral tuberculoma- resection if it has mass effect or it fails to shrink with drug therapy • Neurological impairment 20-30% of survivors • Hyponatremia 49%/Hydrocephalus 42%/Stroke 33%/Cranial nerve palsies 29%/Epileptic seizures 28% • Diabetes insipidus 6%/Tuberculoma 3%/Myeloradiculopathy 3% /Hypothalamic syndrome 3% • The single most effective drug is isoniazid;neuropathy and hepatitis in alcoholics; Pyridoxine/Optic neuropathy- ethambutol; visual acuity & color discrimination • HRZS all enter CSF readily in the presence of meningeal inflammation • Ethambutol is less effective unless used in high doses • 2nd line drugs : Ethionamide, Cycloserine, Ofloxacin & PAS • 4 Drugs for 2 months f/b 2 Drugs (7 to 10 months)
Anti-Epileptic Drug in TB Meningitis •New onset seizures 50% of children & 5% of adults •Acute Management – Short acting Benzodaizapines & Phenytoin •Long Term Rx with Phenytoin, Valproate - Hepatotoxic as well as Enzyme inducer •Levetericetam-Safely given •Rx on lines of Symptomatic seizure disorder •neuroimaging and EEG-If normal give for 2 year seizure free •If tuberculoma or any other lesion present may be offered for longer period Role of Osmotic Agents in TBM •Short term use of Mannitol, Frusemide and Acetazolamide in Stage 1 & 2 Disease •Manitol can be given upto 72 hrs •Frusemide & Acetazolamide may be used for weeks • Only in Open Hydrocephalus
 Cryptococcal Meningitis : MC;C. neoformans (soil with bird feces) • common opportunistic infection in HIV • usually subacute/chronic course;headache & malaise,altered mental status 20% • basilar meningitis, miliary parenchymal nodules • infiltrate brain via the perivascular spaces • dilation of perivascular spaces c/a “gelatinous pseudocyst presentation” • mortality of HIV-associated cryptococcal meningitis 22-40% despite Rx Cryptococcosis HIV Pt.; Axial T2-w (A) & T1-w CE (B)- single small, enhancing lesion in left corona radiata with moderate associated edema
Protozoa  Toxoplasma gondii c/b obligate intracellular parasite Toxoplasma gondii/MC in HIV/ ingestion of contaminated cat feces/undercooked meat • CF: rash/myocarditis/polymyositis; meningoencephalitis (seizures/confusion/coma) • Lesions are scattered throughout the brain, and adjacent to the subarachnoid space cause the meningitis component of the meningoencephalitis • Diagnosis can be achieved by finding organisms in the CSF or in stereotactic biopsy specimens of brain lesions. • MRI :solid to ring enhancing lesions/combination; /any location/single or multiple • Positive response to medical Rx-diagnostic  Rx: combination of pyrimethamine (100-200 mg D1 f/b 50-75 mg/day x 6 wks) & sulfadiazine(4-6 g/day x 6 wks)- DOC  Folinic acid/Leucovorin (10-25 mg/day) to prevent pyrimethamine-induced hematologic toxicity HIV Pt. with seizures & CSF + for toxoplasma Ag; T2-w & T1-w CE of cerebral hemispheres (A & B) ; ring-enhancing lesion with an eccentric enhancing nodule
Acquired Immunodeficiency Syndrome • affect CNS/PNS both directly & indirectly • Direct infection CNS- acute retroviral syndrome/aseptic meningitis/transient & self-limited • Chronic HIV infection: HIV-associated encephalopathy/ myelopathy/ increased risk of stroke • highly active antiretroviral therapy (HAART)- robust immune response k/a the immune reconstitution inflammatory syndrome (IRIS);affect CNS • Toxoplasma/Cryptococcus/mycobacterial/viruses-JC virus & CMV/bacteria-Treponema & Bartonella species • CNS Lymphoma asst. with concomitant EBV infection CNS lymphoma A. coronal T1-w CE;solidly enhancing lesion infiltrating CC B. axial T1-w CE ; faintly rim-enhancing lesion Rt. frontal lobe immunocompetent - nonhemorrhagic, solidly enhancing lesion immunosuppressed -ring-enhancing lesion with cystic or hemorrhagic components
HIV associated encephalopathy (HAE) Coronal T2 w;ventricles & sulci markedly prominent-significant volume loss with minimal white matter signal abnormality Progressive multifocal leukoencephalopathy (PML) HIV pt.; CSF-JC virus; Axial T2-w: white matter signal abnormality involving Rt. frontal lobe & insula with spread across CC to involve Lt. frontal lobe;involvement of subcortical U fibers (arrows) & nearly complete lack of mass effect (classic) Immune reconstitution inflammatory syndrome (IRIS);HIV pt. on HAART  Axial T2-w: very extensive, confluent signal abnormality in the white matter of Lt. cerebral hemisphere & lesser degree of Rt.Hemisphere ;similar to that of PML In this patient but more mass effect
HELMINTHIC CNS INFECTIONS  Cysticercosis; humans intermediate hosts of Taenia solium; • neurocysticercosis (NCC);epilepsy-mc presentation; intracranial hypertension (obstructive HCP,mass effect)/FND • subacute course;difficult to differentiate NCC from neoplasia /other infections of CNS • intense inflammation around cysticerci & diffuse cerebral edema- cysticercotic encephalitis ; severe form of NCC • spinal cysticercosis –motor & sensory deficits, vary a/c to level of lesion • most typical imaging findings - cystic lesions showing the scolex & parenchymal brain calcifications • Others: ring-enhancing lesions/abnormal enhancement of leptomeninges/HCP/cerebral infarctions • CSF normal /CSF eosinophilia not consistent finding • subarachnoid & ventricular forms -CSF analysis-lymphocytic pleocytosis/increased protein/ normal glucose • most accurate serologic test is immunoblotting (ELISA) /also for Rx response
Treatment • cysticidal agents & corticosteroids with AED • Albendazole 15 mg/kg/day x 1 wk & praziquantel 50 mg/kg/day x 2 wks- preffered regimen • corticosteroids to prevent post-treatment seizure; routinely administered with cysticidal agents • dexamethasone 8 mg/day for 28 days, started early during antiparasitic treatment for viable parenchymal NCC • Pt. with cysticercotic encephalitis should not receive cysticidal drugs; managed with high doses of corticosteroids/osmotic diuretics/decompressive craniotomy if necessary • giant subarachnoid cysticerci (>5 cm); cysticidal drugs with caution ; occlude small leptomeningeal vessels ;stroke; concomitant steroid mandatory • Patients with calcifications alone should not receive cysticidal drugs because these lesions represent dead parasites • Temporal lobectomy can be safely performed in patients with temporal lobe epilepsy with hippocampal sclerosis caused by NCC without affecting cognitive outcomes and with a satisfactory long-term seizure control provided selected patients remain on chronic antiseizure medication • Hydrocephalus secondary to cysticercotic arachnoiditis requires placement of a ventricular shunt. • Hydrocephalus may also be managed with endoscopic foraminotomy and endoscopic third ventriculostomy
REFERENCES 1. Youmans and Winn Neurological Surgery; 7th edition 2. Ramamurthi & Tandon'S Textbook Of Neurosurgery; 3rd edition 3. Handbook of Neurosurgery. Mark S. Greenberg; 9th edition THANKYOU

More Related Content

PPTX
Colloid cyst
byRabailQazi
 
PPTX
Hemostasis in neurosurgery online.pptx
bykushal790662
 
PPT
CSF Shunt Infection: Diagnosis and Treatment
byLiew Boon Seng
 
PPTX
Shunt for hydrocephalus
byDr. Shahnawaz Alam
 
PPTX
Subdural empyema
byAdarsh Nath
 
PPT
043 Brain abscess
byNeurosurgery Vajira
 
PPT
392 Natural history of cavernous malformation
byNeurosurgery Vajira
 
PPTX
Cerebellar haematoma
bysuresh Bishokarma
 
Colloid cyst
byRabailQazi
 
Hemostasis in neurosurgery online.pptx
bykushal790662
 
CSF Shunt Infection: Diagnosis and Treatment
byLiew Boon Seng
 
Shunt for hydrocephalus
byDr. Shahnawaz Alam
 
Subdural empyema
byAdarsh Nath
 
043 Brain abscess
byNeurosurgery Vajira
 
392 Natural history of cavernous malformation
byNeurosurgery Vajira
 
Cerebellar haematoma
bysuresh Bishokarma
 

What's hot

PPTX
Clinoidal meningioma
byNeurosurgeon Mumtaz Ali Narejo
 
PPTX
Pterional craniotomy
byDr Fakir Mohan Sahu
 
PPT
370 MCA aneurysm
byNeurosurgery Vajira
 
PPTX
Primary and secondary head injury EDH and SDH
byDr. Ravi Bhushan
 
PPTX
cerebral metastasis
byDr. Shahnawaz Alam
 
PPSX
Brain abscess
byjoemdas
 
PPTX
Spontaneous intracerebral hemorrhage
byPratap Tiwari
 
PPTX
INSULAR GLIOMA SURGERY.pptx
byDr. Shahnawaz Alam
 
PPTX
Frontotemporal FTOZ craniotomy
byDr. Shahnawaz Alam
 
PPTX
Ependymoma
byInga Nalivaiko
 
PPTX
Cerebrovascular Vasospasm - Etiopathogenesis and Management
byDr. Rahul Jain
 
PPTX
Traumatic Brain Injury
byAngaihaMizo
 
PPTX
Herniation Syndromes
byCSN Vittal
 
PPTX
Anatomy of cerebral veins
byAmar Patil
 
PPTX
Parasagittal Meningioma
byFarrukh Javeed
 
PPTX
Brain stem glioma
bysuresh Bishokarma
 
PPTX
Approach to petroclival meningioma
byDr Himanshu Soni
 
PPT
Pathology of Head Injury
byShashidhar Venkatesh Murthy
 
PPTX
Cerebral Edema
byNikhil Chougule
 
PDF
Radiculopathy vs peripheral neuropathy
bySpinePlus
 
Clinoidal meningioma
byNeurosurgeon Mumtaz Ali Narejo
 
Pterional craniotomy
byDr Fakir Mohan Sahu
 
370 MCA aneurysm
byNeurosurgery Vajira
 
Primary and secondary head injury EDH and SDH
byDr. Ravi Bhushan
 
cerebral metastasis
byDr. Shahnawaz Alam
 
Brain abscess
byjoemdas
 
Spontaneous intracerebral hemorrhage
byPratap Tiwari
 
INSULAR GLIOMA SURGERY.pptx
byDr. Shahnawaz Alam
 
Frontotemporal FTOZ craniotomy
byDr. Shahnawaz Alam
 
Ependymoma
byInga Nalivaiko
 
Cerebrovascular Vasospasm - Etiopathogenesis and Management
byDr. Rahul Jain
 
Traumatic Brain Injury
byAngaihaMizo
 
Herniation Syndromes
byCSN Vittal
 
Anatomy of cerebral veins
byAmar Patil
 
Parasagittal Meningioma
byFarrukh Javeed
 
Brain stem glioma
bysuresh Bishokarma
 
Approach to petroclival meningioma
byDr Himanshu Soni
 
Pathology of Head Injury
byShashidhar Venkatesh Murthy
 
Cerebral Edema
byNikhil Chougule
 
Radiculopathy vs peripheral neuropathy
bySpinePlus
 

Similar to Infections in neurosurgery

PPTX
infectionsinneurosurgery-201007144543.pptx
byGeneralSurgeryNMC
 
PPT
040 Postoperative infection of the head and brain
byNeurosurgery Vajira
 
PPTX
CNS infections brain abscess meningitis.pptx
byNoorSaleh26
 
PPT
042 The use and misuse of antibiotic in neurosurgery
byNeurosurgery Vajira
 
PPT
ACUTE BACTERIAL MENINGITIS AND ANTI MICROBIALS.ppt
byRahul Rai
 
PDF
Pharmacotherapy of Central Nervous system infections
byTsegaye Melaku
 
PDF
Aspectos neuroqx de infeccion del snc 2012
byResidentes1hun
 
PPTX
Diagnosis of cns infections
byMahen Kothalawala
 
PPTX
Intracranial Infections in neuro surgery.pptx
bysofiyaabdulrafiu
 
PDF
SURGICAL SITE INFECTION (SSI). PPT .pdf
byMs.Shanmugapriya.K
 
PPTX
Brain abscess.pptxifjbigjhcjghjbhbbbbhhh
byDaluSaiLikhitha
 
PPT
Cns infection 2018
byPattaraphornSoot
 
PDF
17 Infections 1.pdf INFECTION BRAIN NEURO
byrizwanasalim3002
 
PPTX
Sepsis and antibiotic guidance in neurology wards
byDivya Shilpa
 
PPTX
surgery tutorial 1 PowerPoint presentation
byANGURAPHILLIPSBRIAN
 
PPT
Nursing Care: Meningitis and encephalitis
byAbdelrahman Alkilani
 
PPTX
Cerebral Abscess DVDFZVBSDBGDFNDFNDFGNDFNDFG
byRahul Rai
 
PPTX
4_6030689835172236525.pptx
byJibrilAliSe
 
PDF
Brain Abscess it's causes and treatment and sign symptoms
bywajidullah9551
 
PPTX
CNS disorders in pediatrics
byVirendra Hindustani
 
infectionsinneurosurgery-201007144543.pptx
byGeneralSurgeryNMC
 
040 Postoperative infection of the head and brain
byNeurosurgery Vajira
 
CNS infections brain abscess meningitis.pptx
byNoorSaleh26
 
042 The use and misuse of antibiotic in neurosurgery
byNeurosurgery Vajira
 
ACUTE BACTERIAL MENINGITIS AND ANTI MICROBIALS.ppt
byRahul Rai
 
Pharmacotherapy of Central Nervous system infections
byTsegaye Melaku
 
Aspectos neuroqx de infeccion del snc 2012
byResidentes1hun
 
Diagnosis of cns infections
byMahen Kothalawala
 
Intracranial Infections in neuro surgery.pptx
bysofiyaabdulrafiu
 
SURGICAL SITE INFECTION (SSI). PPT .pdf
byMs.Shanmugapriya.K
 
Brain abscess.pptxifjbigjhcjghjbhbbbbhhh
byDaluSaiLikhitha
 
Cns infection 2018
byPattaraphornSoot
 
17 Infections 1.pdf INFECTION BRAIN NEURO
byrizwanasalim3002
 
Sepsis and antibiotic guidance in neurology wards
byDivya Shilpa
 
surgery tutorial 1 PowerPoint presentation
byANGURAPHILLIPSBRIAN
 
Nursing Care: Meningitis and encephalitis
byAbdelrahman Alkilani
 
Cerebral Abscess DVDFZVBSDBGDFNDFNDFGNDFNDFG
byRahul Rai
 
4_6030689835172236525.pptx
byJibrilAliSe
 
Brain Abscess it's causes and treatment and sign symptoms
bywajidullah9551
 
CNS disorders in pediatrics
byVirendra Hindustani
 

More from Dr. Shahnawaz Alam

PPTX
DBS Advances.pptx
byDr. Shahnawaz Alam
 
PPTX
HIFU & LITT.pptx
byDr. Shahnawaz Alam
 
PPTX
peripheral nerve tumors.pptx
byDr. Shahnawaz Alam
 
PPTX
Decompressive Craniectomy.pptx
byDr. Shahnawaz Alam
 
PPTX
Trigeminal neuralgia
byDr. Shahnawaz Alam
 
PPTX
Trigeminal Schwannoma.pptx
byDr. Shahnawaz Alam
 
PPTX
Intraventricular tumors.pptx
byDr. Shahnawaz Alam
 
PPTX
natural history surgical decision aneurysm.pptx
byDr. Shahnawaz Alam
 
PPTX
endospine easygo system.pptx
byDr. Shahnawaz Alam
 
PPTX
Traumatic brain injury.pptx
byDr. Shahnawaz Alam
 
PPTX
SURGICAL PINEAL REGION TUMORS.pptx
byDr. Shahnawaz Alam
 
PPTX
NRC intraventricular sol.pptx
byDr. Shahnawaz Alam
 
PPTX
Management of Peripheral Nerve Entrapment (Carpal Tunnel Syndrome).pptx
byDr. Shahnawaz Alam
 
PPTX
Imaging Cervico-vertebral junction: AAD with BI .pptx
byDr. Shahnawaz Alam
 
PPTX
Psychosurgery .pptx
byDr. Shahnawaz Alam
 
PPTX
Vertebrobasal Dolichoectesia.pptx
byDr. Shahnawaz Alam
 
PPTX
evaluation for epilepsy surgery.pptx
byDr. Shahnawaz Alam
 
PPTX
classification, pathophysiology and surgical management MOYAMOYA.pptx
byDr. Shahnawaz Alam
 
PPTX
TRAUMATIC CCF
byDr. Shahnawaz Alam
 
PPTX
APPROACH TO PETROCLIVAL MENINGIOMA
byDr. Shahnawaz Alam
 
DBS Advances.pptx
byDr. Shahnawaz Alam
 
HIFU & LITT.pptx
byDr. Shahnawaz Alam
 
peripheral nerve tumors.pptx
byDr. Shahnawaz Alam
 
Decompressive Craniectomy.pptx
byDr. Shahnawaz Alam
 
Trigeminal neuralgia
byDr. Shahnawaz Alam
 
Trigeminal Schwannoma.pptx
byDr. Shahnawaz Alam
 
Intraventricular tumors.pptx
byDr. Shahnawaz Alam
 
natural history surgical decision aneurysm.pptx
byDr. Shahnawaz Alam
 
endospine easygo system.pptx
byDr. Shahnawaz Alam
 
Traumatic brain injury.pptx
byDr. Shahnawaz Alam
 
SURGICAL PINEAL REGION TUMORS.pptx
byDr. Shahnawaz Alam
 
NRC intraventricular sol.pptx
byDr. Shahnawaz Alam
 
Management of Peripheral Nerve Entrapment (Carpal Tunnel Syndrome).pptx
byDr. Shahnawaz Alam
 
Imaging Cervico-vertebral junction: AAD with BI .pptx
byDr. Shahnawaz Alam
 
Psychosurgery .pptx
byDr. Shahnawaz Alam
 
Vertebrobasal Dolichoectesia.pptx
byDr. Shahnawaz Alam
 
evaluation for epilepsy surgery.pptx
byDr. Shahnawaz Alam
 
classification, pathophysiology and surgical management MOYAMOYA.pptx
byDr. Shahnawaz Alam
 
TRAUMATIC CCF
byDr. Shahnawaz Alam
 
APPROACH TO PETROCLIVAL MENINGIOMA
byDr. Shahnawaz Alam
 

Recently uploaded

PPTX
West Hatch High School - GCSE Art Presentation
byWestHatch
 
PPTX
The night at deoli - Ruskin bond's story of first love
byrajibhammar4
 
PDF
CAM, DHT11, GAS, ESP32, FLAME, IR, TEMP, LCD, PIR, SOIL, SOUND, RELAY, TURBID...
byPravinDhanrao3
 
PDF
Pratishta Educational Society., Courses & Opportunities
byGanapathiVankudoth
 
PPTX
West Hatch High School: Year 9 Art Course
byWestHatch
 
PPTX
Mohan - "A man of silence and authority"
bynidhibachauhan46
 
PPTX
Toba Tek Singh - Visualising Partition through Manto's Lens
bymiraljoshi48
 
PDF
Sharad Bisen_Irrigation Systems and Methods in Horticultural Crops.pdf
bybisensharad
 
PDF
Q4_LE_English 5_Lesson 1_Week 1.pdf learning instruction
byMichelleCajefe2
 
PDF
West Hatch High School - GCSE French Specification
byWestHatch
 
PPTX
How to Create & Automate Asset Model in Odoo 18 Accounting
byCeline George
 
PPTX
Biological source, chemical constituents, and therapeutic efficacy of the fol...
bySai Meer College of Pharmacy
 
PDF
Darwinism: Theory of Natural Selection and Origin of Species
byIPGDCWA,NAMPALLY
 
PDF
TỔNG HỢP 156 ĐỀ CHÍNH THỨC KỲ THI CHỌN HỌC SINH GIỎI TIẾNG ANH LỚP 12 CÁC TỈN...
byNguyen Thanh Tu Collection
 
PDF
Unit Plan and Unit Test-pdf-Dr. Rajashekhar Shirvalkar, Principal, SMRS B.Ed ...
byRajashekhar Shirvalkar
 
PDF
APPSC APPSC Forest Draughtsman GS Question paper.pdf
byssuser9d8e4e
 
PPTX
"Aristotle : Father Of Western Philosophy"
bymitalbarathod28
 
PPTX
'Colonial Mentality and Social Identity in Karma by Khushwant Singh'
byKrishnarajsinh Parmar
 
PPTX
That long silence - Novel by Shashi Deshapande
bysanjanavaghela65
 
PPTX
Appreciations - Jan 26 01.pptxkkkmmkmkmkmkm
bypreetheshparmar
 
West Hatch High School - GCSE Art Presentation
byWestHatch
 
The night at deoli - Ruskin bond's story of first love
byrajibhammar4
 
CAM, DHT11, GAS, ESP32, FLAME, IR, TEMP, LCD, PIR, SOIL, SOUND, RELAY, TURBID...
byPravinDhanrao3
 
Pratishta Educational Society., Courses & Opportunities
byGanapathiVankudoth
 
West Hatch High School: Year 9 Art Course
byWestHatch
 
Mohan - "A man of silence and authority"
bynidhibachauhan46
 
Toba Tek Singh - Visualising Partition through Manto's Lens
bymiraljoshi48
 
Sharad Bisen_Irrigation Systems and Methods in Horticultural Crops.pdf
bybisensharad
 
Q4_LE_English 5_Lesson 1_Week 1.pdf learning instruction
byMichelleCajefe2
 
West Hatch High School - GCSE French Specification
byWestHatch
 
How to Create & Automate Asset Model in Odoo 18 Accounting
byCeline George
 
Biological source, chemical constituents, and therapeutic efficacy of the fol...
bySai Meer College of Pharmacy
 
Darwinism: Theory of Natural Selection and Origin of Species
byIPGDCWA,NAMPALLY
 
TỔNG HỢP 156 ĐỀ CHÍNH THỨC KỲ THI CHỌN HỌC SINH GIỎI TIẾNG ANH LỚP 12 CÁC TỈN...
byNguyen Thanh Tu Collection
 
Unit Plan and Unit Test-pdf-Dr. Rajashekhar Shirvalkar, Principal, SMRS B.Ed ...
byRajashekhar Shirvalkar
 
APPSC APPSC Forest Draughtsman GS Question paper.pdf
byssuser9d8e4e
 
"Aristotle : Father Of Western Philosophy"
bymitalbarathod28
 
'Colonial Mentality and Social Identity in Karma by Khushwant Singh'
byKrishnarajsinh Parmar
 
That long silence - Novel by Shashi Deshapande
bysanjanavaghela65
 
Appreciations - Jan 26 01.pptxkkkmmkmkmkmkm
bypreetheshparmar
 

Infections in neurosurgery

  • 1.
    Dr. Shahnawaz Alam Guidedby:-Dr. Vikas Chandra Jha HOD Neurosurgery Moderated by:-Dr. Saraj kumar Singh Asst.Prof. (Dept. of Neurosurgery) Infections in Neurosurgery
  • 2.
    Outline • Basic Scienceof CNS Infections • Postoperative Infections of CNS • Brain Abscess • Meningitis and Encephalitis • Use and Misuse of Antibiotics in Neurosurgery • AIDS & Parasitic Infections of CNS
  • 3.
    • Immune effectors:astrocytes and microglia • Varying degrees of both structural and functional damage to CNS • Others: matrix metalloproteinases enzymes/Dysregulation of glutamate metabolism • Implicated in many CNS ds.-infections, ischemic or traumatic injury, and autoimmune disorders • BBB is rich in potential substrates for MMPs, including type IV collagen, fibronectin, and laminin; MMP degradation of the BBB may favor transmigration of leukocytes as well as the movement of macromolecules and water, thus contributing to brain edema • MMPs are potential targets for therapeutic interventions Basic Science of CNS Infections
  • 4.
    CLASSIFICATION • Anatomy ofthe infection (parenchymal, meningeal, parameningeal) • Presence of space-occupying lesions (e.g. abscess, empyema) • Diffuse inflammation (e.g. meningitis, encephalitis) • Also a/c to etiology • Pathogens enter the CNS directly (e.g., through trauma, neurosurgery), /Via BBB/CSFB (e.g., bacterial meningitis caused by Escherichia coli), / via retrograde transport along neural structures (e.g., rabies) • Iatrogenic routes are more relevant to the neurosurgeon • Perioperative breeches in structural barriers protecting the CNS (scalp, cranium, meninges), implantation of foreign bodies (e.g., cerebrospinal fluid [CSF] shunts, dural implants, electrodes, spinal hardware), and breeches in mucosal defenses (e.g., intubation, vessel catheterization)
  • 5.
     MICROGLIA; severaldifferent states • Resting microglia -Small cells with few surface markers & prominent thin branches • Stimuli activate microglia-Cellular debris from CNS damage, particularly free ATP- Ameboid cells • Receptors expressed by microglia includes Toll-like receptors/a cytosolic “alarm system” exists in microglia in the form of nucleotide-binding oligomerization domain 2 (NOD2) • NOD2 recognizes a common motif in bacterial peptidoglycan from both gram -/+ • NO synthesis and a respiratory burst, leading to the formation of peroxynitrite (ONOO−), a highly toxic product capable of damaging both host and pathogen/superoxide anion (O2−) • Phagocytes in the CNS under both physiologic and pathophysiologic conditions • Microglia also produce factors that support glial and neuronal cells/APC • Downregulate these proinflammatory responses
  • 6.
     Astrocytes; Residentglial cells derived from neuroectoderm;“nurse” cells for neurons • star-shaped morphology & GFAP • Maintain BBB/participate in the immunologic processes/targets of bacterial invasion • Expression of OmpA by pathogenic E. coli strains significantly enhances E. coli invasion of astrocytes • GBS also invades astrocytes -death via expression of β-hemolysin/cytotoxin • Pneumolysin (Ply)-structural and functional changes-tissue injury and brain edema • Main source of IL-6 production in the CNS • HIV gp120 reduces astrocyte expression of glutamine synthase, and patients with HIV- associated dementia have higher brain glutamate levels • Balance of CNS protection/ destruction during infection by secretion of MMPs
  • 7.
    Postoperative Infections ofthe Head and Brain • Diagnosis of infection after craniotomy is often challenging • superficial incisional infections-skin and s.c tissue • deep incisional infections-subgaleal space and bone flap • Deep organ space infections-subdural empyema, brain abscess /meningitis/ventriculitis • superficial infections-60% of SSIs after craniotomy/Meningitis-mc deep organ space infection,22% /others;subdural empyema and brain abscess-14% • Infections after craniotomy are most commonly associated with gram-positive bacteria-S. aureus, and conS
  • 8.
    • Majority ofpost-op infections- patient’s skin • Host defense mechanisms impaired in pt. undergoing craniotomy • Brain-relatively immune privileged site/low levels of Abs & C -brain less efficient than other organs • Post-op CSF leakage and early subsequent reoperation • Placement of drains or icp monitors, poor neurological status, paranasal sinus entry, foreign body implantation RISK FACTORS FOR INFECTION AND PREVENTIVE STRATEGIES
  • 9.
    Role of Pre-opantibiotics in reducing the incidence of SSIs after craniotomy • The Surgical Care Improvement Project (SCIP) outlines the following 3 performance measures for monitoring appropriate antimicrobial prophylaxis use: 1.selection of an appropriate antibiotic, 2.adminstration within 1 hour before incision 3.discontinuation within 24 hours after surgery is completed • Choice of an agent-narrow spectrum;guided by institutional data on frequently recovered pathogens and their resistance profiles • For clean neurosurgical procedures, a single dose of cefazolin is recommended • Vancomycin –MRSA/β-lactam allergy • Antibiotics with short t1/2 such as cefazolin should be readministered every 3 to 4 hrs during prolonged surgery • Risk factors for MRSA: male, malignancy, DM, prior MRSA infection, immunosuppressed & traumatic injury • Other: surgical site preparation and environmental control within the operating room • any hair removal that is performed should be done as close to the time of surgery as possible • use of high-efficiency particulate air (HEPA) filters
  • 10.
    PRINCIPLES OF TREATMENT •Postoperativeinfections tend to be particularly difficult to resolve because of the complex anatomic changes resulting from craniotomy •Early and decisive intervention is critical to limit morbidity, and the keystone of successful treatment is effective source control (i.e., drainage of abscesses and infected fluid collections and debridement of necrotic tissue) •Bactericidal rather than bacteriostatic agents are generally preferred •Most antibiotic agents enter CNS mostly by passive diffusion down a concentration gradient, with physical barriers BBB and blood-CSF barriers functioning as the primary determinants of drug distribution •Inflammation at the site of infection may facilitate entry of drugs across these barriers and into the brain •Other inherent physiochemical properties: Mwt., lipophilicity, PPB & ionization state •Ultimately, adequate dosing - minimal bactericidal concentration [MBC]).
  • 11.
    • Empirical regimensfor postcraniotomy infections: vancomycin + 3rd /4th gen. cephalosporin with antipseudomonal activity (e.g., ceftazidime, cefepime) + metronidazole (anaerobic) • carbapenem (e.g., meropenem) may be substituted for the combination of a third-generation cephalosporin and metronidazole (Gram - & anaerobes) • Imipenem-increased seizure risk relative to meropenem (and other β-lactams) • β-Lactam antibiotics (penicillins, cephalosporins, carbapenems) have poor penetration into the CSF in the absence of meningeal inflammation, but higher systemic doses can result in therapeutic CSF concentrations • 3rd /4th gen. cephalosporin (specifically cefotaxime, ceftriaxone, and ceftazidime) are often used for the treatment of CNS and postcraniotomy infections because of their low toxicity and excellent activity • High-dose β-lactamase inhibitors such as sulbactam and tazobactam are also effective in protecting the coadministered penicillin agent • β-lactam antibiotics-proconvulsive- use via intraventricular injection not recommended • Intraventricular antibiotic administration bypasses BBB, can achieve much higher CSF concentrations than systemic administration;asst. with neurotoxicity
  • 12.
     CSF ShuntInfections: The Role of Biofilms • Perioperative contamination/Wound dehiscence over the shunt /Hematogenous seeding/Distal port contamination • Biofilm formation occurs with both infection and colonization of prosthetic medical devices • Biofilms are in a stationary phase of growth-less susceptible to antibiotics/less permeable to most antibiotics/prosthetic devices lack a vascular supply • Coagulase-negative staphylococci (CoNS)-notorious for their ability to form biofilm on prosthetic devices • Soon after placement, bioprosthetic materials are coated with host proteins, which serve as receptors for bacterial adhesins k/a “microbial surface components recognizing adhesive matrix molecules,” or MSCRAMMs- CoNS initiate biofilm formation almost immediately • Transition state between planktonic and sessile bacteria in biofilms known as quorum sensing • Dormant microbes (sessile) within the biofilm are up to a 1000 times more tolerant of [most] antimicrobial agents than their free-living (planktonic) S. epidermidis biofilm formation on a catheter surface. Note the deposition of extracellular matrix,manifested as a complex web of material around and between microcolonies
  • 13.
    SUPERFICIAL INCISIONAL INFECTIONS •extend from the skin to the epidural space. • May extend to the underlying bone flap and through the dura • repeat operative intervention, poor tissue quality, impaired vascular supply, radiation injury, nutritional deficiencies, and the presence of foreign bodies • manifests as local erythema, swelling, and tenderness at the craniotomy site with possible suppurative drainage • With progressive infection, systemic signs such as malaise, fever, and chills may develop • The most common pathogenic agents of superficial wound infections are gram-positive cocci, including S. aureus, coagulase-negative staphylococci, and P. acnes • clinically apparent; however, CT or MRI reveal fluid collections in the subgaleal or epidural space/extension/bone flap osteomylitis/ identifying possible precipitating factors • Measurement of ESR/CRP concentration may provide some assistance in detecting infection and monitoring the response to therapy • normally elevated after craniotomy and return toward baseline by the 5th POD • nonspecific, prolonged elevation or a secondary increase in their levels may indicate the development of infection • Hyperbaric oxygen (HBO)/local rotational or pedicled flaps or vascularized myocutaneous free flaps -chronic postoperative infections
  • 14.
    Purulent drainage froma superficially infected craniotomy incision with surrounding erythema Skin breakdown at the inferior aspect of the craniotomy incision with exposed titanium hardware A.Surgical debridement of a superficial postcraniotomy infection in a patient who had undergone multiple craniotomies and radiation treatments for malignancy. There is spread of infection to the underlying bone flap, with erosion and adjacent purulent material in the epidural space. B.Epidural infection with contamination of the undersurface of the devascularized bone flap.
  • 15.
     DEEP INCISIONALINFECTIONS: SUBGALEAL SPACE AND BONE FLAP • A high index of suspicion • majority d/t commensal skin flora infection of autogenous cranioplasties after decompressive craniectomy; however, a significant proportion are due to nosocomial gram-positive and gram-negative organisms • CT and MRI studies may show the presence of subgaleal or epidural infection with bone flap destruction suggestive of osteomyelitis • Treatment options: antibiotic therapy alone/surgical debridement with removal of the bone flap/debridement with replacement of the bone flap or other cranioplasty material such as titanium mesh • Removal of the infected bone flap followed by delayed cranioplasty offers the best chance of clearing the initial infection/ multiple surgical interventions • Several case series have reported clinical resolution of infection with preservation of the bone flap • In Other study successful resolution of infection in patients treated with immediate titanium mesh cranioplasty at the time of initial surgical debridement
  • 16.
    A, Axial computedtomography (CT) scan demonstrating erosion of bone flap (asterisk) indicative of osteomyelitis. B, Coronal CT scan showing failure of titanium screws with surrounding bone lucency (arrow) A, Debridement of the epidural infection and removal of the infected bone flap and hardware. B, Immediate titanium mesh cranioplasty performed at the time of infection debridement. A, T1-weighted axial magnetic resonance (MR) image reveals a hyperintense subdural fluid collection that developed after craniotomy for aneurysm repair. The fluid collection enhances peripherally with gadolinium (B) and, because of higher protein content, exhibits increased signal intensity on fluid-attenuated inversion recovery (FLAIR) MR sequences (C) relative to cerebrospinal fluid. A craniotomy was performed to drain the collection, and frank purulence was encountered in the subdural space.
  • 17.
     Subdural Empyema •spontaneously subdural empyema- fever and headache, followed by the rapid development of focal neurological deficits, altered mental status, and seizures/rarely in subdural empyema develops after craniotomy;Insidious course • Febrile 33%;seizure 25% & 85% without headache;/MC findings- superficial wound infection/In 50% ;occurr more than 1 month after the craniotomy Diagnostic Imaging and Laboratory Data • extra-axial fluid collections are commonly noted on postoperative imaging studies • NCCT demonstrates a crescent-shaped fluid collection that is slightly more dense than CSF and located beneath the craniotomy flap or adjacent to the falx • Increased signal intensity on T1-w and fluid-attenuated inversion recovery (FLAIR) MRI sequences because of the increased protein concentration of an empyema relative to CSF. Peripheral enhancement of the fluid collection is common • presence of restricted diffusion on MRI may be helpful • Progressive enlargement of the fluid collection or unexplained edema in adjacent cerebral cortex • Laboratory data –nonspecific; LP-C/I Treatment • Goals of surgery are to evacuate the purulent collection completely/adequate decompression of the brain • optimal surgical approach (craniotomy versus bur-hole drainage) is debated, craniotomy is generally advocated • Empirical antibiotic therapy should be started Early DEEP ORGAN SPACE INFECTIONS
  • 18.
    • Newer agentsuseful for the treatment of resistant staphylococcal infections include linezolid and daptomycin • It has excellent bioavailability, i.v ior orally; adr- myelosuppression and irreversible peripheral neuropathy • Rifampin is a broad-spectrum antimicrobial ;role in the adjunctive Rx of bone flap osteomyelitis or infections associated with foreign body implantation • Rifampin-penetrate biofilms and kill organisms in the sessile phase of growth/used in combination/cytochrome –p enzyme + • Fluoroquinolones (levofloxacin, ciprofloxacin, moxifloxacin) are attractive agents for the treatment of CNS infection because of their lipophilicity and low molecular weight./High resistant/increase seizure threshold • Aminoglycosides have excellent activity against aerobic gram-negative bacilli, including P. aeruginosa, as well as synergistic activity with β-lactams against aerobic gram-positive cocci
  • 19.
    Brain Abscess: Pusin the Parenchyma • Space-occupying purulent infections within the substance of the brain • Clinically, the classic triad of headache, fever, and focal neurological deficit is rarely present; s/s of postop abscess nonspecific; expanding, irritative mass lesion-altered LOC, N/V & seizures 20% • Microbiology related to the primary source of the abscess • staphylococci and Enterobacteriaceae- direct inoculation from trauma or neurosurgical procedures
  • 20.
    • Abrupt worseningof preexisting headache asst. with new onset of meningismus - Intraventricular rupture of a brain abscess (IVROBA) • manifest sudden neurological deterioration with obtundation or coma (widespread meningoencephalitis ; alterations in CSF flow ) • multiloculated abscesses/ decreased distance from the abscess capsule to the ventricular wall/ deep-seated abscesses have been correlated with increased risk • localized ventricular enhancement on CT - impending intraventricular rupture • diffuse ependymal and meningeal enhancement and the presence of debris within the ventricles- IVROBA • Hydrocephalus 50% & septation of the ventricles delayed complication
  • 22.
    Diagnostic Imaging andLaboratory Data • CT cerebritis stage- poorly defined area of low attenuation with a mass effect and significant edema • capsule- peripheral enhancement increases and the center of the lesion becomes progressively hypodense • Corticosteroids- reduce the thickness of the abscess capsule and the extent of contrast enhancement on both CT and MRI • DwMRI -high degree of sp & sn in differentiating spontaneous abscess from other ring- enhancing lesions/ presence of restricted diffusion;non-specific • correlation with ADC & T2-w MRI sequences or CT is necessary to evaluate for blood products that may cause a “T2 shine-through effect,” in which the infection appears bright on diffusion-weighted images • Peripheral leukocytosis is frequently absent, and although the ESR and CRP concentration are usually elevated • Blood cultures seldom yield a causative organism/LP c/i
  • 23.
    Axial CE T1-wmri ;two rim-enhancing masses of the left periventricular white matter that represent abscesses. The intraventricular enhancement is suggestive of ventriculitis. Axial fluid-attenuated inversion recovery (FLAIR) image of the same pt.- vasogenic edema surrounding each lesion.
  • 24.
    Purulent drainage developedafter craniotomy for a left frontal cavernous malformation A.T1-w axial MRI after gadolinium administration demonstrates enhancement within the extra-axial space and the resection cavity. A craniotomy with drainage of purulent material from the epidural and subdural compartments was performed, and treatment with intravenous antibiotics was started. Five days later, severe headache and worsened mental status developed B. MRI - IVROBA One month after resection of a right frontal glioma, this patient exhibited confusion and lethargy. T1-w axial MRI obtained before (A) and after (B) gadolinium administration demonstrate enhancement of the resection cavity and surrounding meninges, and the fluid-attenuated inversion recovery (FLAIR) sequence (C) shows significant surrounding edema. Abnormal restricted diffusion on DWMRI (D) suggests infection. Craniotomy confirmed the presence of purulent material in the subdural and intraparenchymal locations
  • 25.
    Treatment • goals -to relieve the mass effect; improve clinical symptoms & fully resolve the infection • In most cases, a combination of sxl drainage (iopen operative drainage or excision of the lesion and stereotactic aspiration ) & a prolonged course of iv antibiotics (6-8 wks f/b oral) • Progressive enlargement of the abscess or failure of the abscess to become smaller- sxl • intraventricular administration of antibiotics, most commonly vancomycin, aminoglycosides, and colistin • Adjunctive corticosteroid - significant cerebral edema related to cerebral infections with signs of impending herniation/ seizure prophylaxis until infection resolved
  • 27.
     Postoperative Infectionsof the Spine • risks, symptoms & Rx depend on the region of the intervention (cervical, thoracic, or lumbar), the approach (anterior, posterior, or lateral) & instrumentation  Noninstrumented spinal surgery (anterior and posterior decompressive procedures) ;usually confined to short stretches of the spinal column; mostly single level • Lumbar diskectomy < 1% (ssi or muscle tissue, or in the disk space)/ laminectomy without fusion ~2%. • Backache with fever; elevation in ESR/CRP; later - radiographic changes with disk degeneration; progressive cases- end plate degeneration • Risks: longer operating times (>5 hrs), greater blood loss( >1L), no. of levels, greater soft tissue destruction,revision of sx, sx extending below sacrum, ≥2 resident surgeons, the placement of devascularized allograft, long hospital stay, traumatic spinbal injury / pt. comorbidities-obesity/DM/malignancy-20%/  Instrumented Spinal Procedures - posterior spinal procedures ~3% to 7%. • type of instrumentation - older steel implants v s newer titanium implants • Anterior instrumented spinal procedures -lower rates of infection • anterior-posterior approach - highest rates of infection • MIS- no reduction in wound infection • intrathecal drug delivery systems and spinal cord stimulators ~5% ;within the first 2 weeks to 2 months after surgery& treated by removal of the complete system
  • 28.
    • Superficial-above thelumbodorsal fascia in the dermis and s.c tiss.;manifest in the immediate posto period with erythema, purulent drainage, local tenderness, and separation or dehiscence of the wound edges • low-grade fever; elevated ESR/CRP/WBC;variable • Deep - more variable manifestation; most manifesting 2 to 3 weeks posto or after several months to several years after surgery • acute manifestation-significant pain, fever, anorexia, and night sweats • wound overlying a deep infection-normal/track superfcially • delayed manifestation progressive backache, wound drainage, and erythema but may lack fever • serial ESR/CRP values with trends-useful in diagnosing and monitoring; tracking the response to treatment • If debridement is planned, specimens should be taken from both superficial and deep parts • blood cultures may aid in the diagnosis of a pathogen • CT- guided or open biopsy may be helpful; 30-50%
  • 29.
    Sagittal CT ofPt. with discitis of L5- S1;end plate sclerosis,VB collapse & focal kyphosis. MRIs of thoracic discitis; A.Sagittal T1-w NC MRI; B.Sagittal T1-w CE MRI; hypointense SI in VB & avid enhancement ; C. Sagittal T2-w sequence MRI in a Pt. with postop L5-S1 discitis; hyperintense signal in adjacent end plates • Plain radiographs -assessment of spinal alignment, paravertebral soft tissue swelling;bony changes; integrity of spinal hardware/MRI-ioc • Early bone changes ~2 to 3 wks postop with evidence of disk space narrowing, bone destruction & blurring of end plates f/b VB collapse or sclerosis of end plates and bone ankylosis in the more chronic setting • Increased soft tissue swelling, especially in the retropharyngeal space after anterior spinal surgery- abscess • lucency around screws - loosening, hardware failure, or pseudoarthrosis
  • 30.
    Nonoperative Treatment : •SSI, Postoperative discitis /Use of an external brace in postope discitis/iv antibiotics 6 wks f/b oral 6 wks Surgical treatment : • Goals -(1) diagnosis of the infective agent (2) débridement of nonviable tissue, and (3) assurance of stabilization • Preop imaging-extent of debridement; evidence of deep infection mandates opening of the lumbodorsal fascia • Opened only after thorough debridement and irrigation of the superficial compartment • Loose bone fragments, gel foam or fibrin sealant remnants, and necrotic muscle and fat should be meticulously removed • If instrumentation is found to be loose-an alternative means of fixation must be used • In the case of pedicle screw fixation, a screw of larger diameter can be used as a “rescue screw.” • Structural allograft tissue used in the initial construct may also be left in place, but loose chips of bone should be removed • Primary wound closure should be performed if possible • The wound should be closed in layers around a drain to eliminate dead space  Wound Vacuum-Assisted Closure  Irrigation-Suction Technique  Other Surgical Techniques : use of antibiotic beads and muscle flaps  Vancomycin Powder
  • 31.
    Use and Misuseof Antibiotics in Neurosurgery • Antibiotics are an integral part of the daily life of the neurosurgeon GENERAL PRINCIPLES OF ANTIBIOTIC USE • Not only CNS but cranial soft tissues, skull, and paranasal sinuses; the spine, intervertebral disks, and paraspinal soft tissues; and the tissues • delivery not depend on physiology of either BBB/BCSFB; act as obstacles • active influx and efflux transporters located on the endothelial/epithelial cell surface alter the distribution of an antibiotic • goal : to deliver an adequate concentration of the drug to the proper compartment • Dose & choice of antibiotics/intraventricular drugs Pharmacokinetics of Antibiotic Delivery • Concentrations throughout CSF not constant (Ventricular < lumbar CSF) • Penetration depend of stage of abscess (blood-abscess barrier) • Most are not metabolized in the CSF/elimination by diffusion or CSF turnover • Generally, CSF t1/2 of antibiotics >> plasma t1/2 • CSF t1/2 increased in CNS infections (decreased turnover) • Pt. with CSF shunts or external CSF drains, CSF t1/2 the CSF quite (altered circulation)
  • 32.
    CNS Toxicity ofAntibiotic Therapy • include encephalopathy, seizures, psychiatric symptoms, cranial nerve injury, and ataxia • most commonly used intrathecal antibiotics, vancomycin and gentamicin- relatively low toxicity • Intraventricular vancomycin relatively free of toxicity, even at high CSF levels • Intraventricular gentamicin may have CNS toxicity, causing ototoxicity or epilepsy • Intraventricular administration of β-lactam similar to systemic ; seizures • infection rates range < 1% in clean wounds to 6% to 10% in dirty wounds, even with antibiotic treatment • Clean shunt implantations utilizing antibiotic prophylaxis ~ 8-10% infection rate • use of prophylactic antibiotics; irrigation of the wound and filling the shunt with antibiotic solution and antibiotic-impregnated ventricular drains
  • 33.
    • Judicious useand adherence to basic principles • Basic principles : 1. Antibiotics only for the prevention or treatment of susceptible infections 2. choice of antibiotic guided by the most likely pathogen and directed by C/S results 3. used for their shortest effective duration 4. risks associated must be considered 5. Adequate Dose and frequency • Failure -antibiotic misuse; ineffective(MDR) to harmful(superinfection) • MC misuses of antibiotics in neurosurgery: Intraventricular administration of chloramphenicol/ Routine use of vancomycin for prophylaxis • appropriate consultation with specialists in infectious diseases
  • 34.
    Meningitis and Encephalitis •Meningitis is defined as inflammation of the meninges, the lining of the brain and spinal cord • Encephalitis represents inflammation of the brain, and the pathogens typically responsible are quite different from those usually seen in meningitis • overlap between the two (meningoencephalitis) • Ventriculitis is focal or diffuse inflammation of the ependymal lining of the cerebral ventricular system • Community-Acquired Bacterial Meningitis;Streptococcus pneumoniae and Neisseria meningitidis • 30-50% of survivors sustaining neurological sequelae • 60% pneumococcal meningitis;triad consisting of fever, nuchal rigidity, and altered mental status • mortality associated with pneumococcal meningitis 15-25% for pediatric & 20-37% • Pneumococcal vaccines have been developed and proved to be very effective in the prevention of invasive pneumococcal disease, including meningitis • efficacy of the heptavalent pneumococcal conjugate vaccine ~97%
  • 35.
    • uncommon afterneurosurgical procedures; < 1% • clinical course of nosocomial meningitis tends to be less fulminant than that of community-acquired meningitis • typical symptoms- fever, headache, and neck stiffness/non-specific; without infection in posterior fossa sx/chemical irritation • aseptic (chemical) meningitis 60%-75% of postop meningitis; frequently in children and after posterior fossa surgery • Others : craniopharyngiomas/ Rathke’s cleft cysts/ epidermoid & dermoid cysts/ cholesteatomas • Release of the irritating element; chronic headache syndrome relieved by resection of the offending lesion • Diagnosis of aseptic meningitis- negative CSF Gram staining & sterile culture and full recovery without antibiotics • Corticosteroids- symptomatic relief in aseptic chemical meningitis
  • 36.
    Diagnostic Imaging andLaboratory Data •no single clinical sign or diagnostic test distinguishes between the two entities •Neuroimaging studies rarely assist in the diagnosis of postop meningitis b/c the characteristic sign, meningeal enhancement in 80% of postcraniotomy pt. without infections •CT or MRI -secondary complications of meningitis;HCP, parameningeal abscess, and ischemia/ infarction related to vasculitis and thrombosis of superficial vessels •CSF culture data remain the “gold standard” •Newer diagnostic tests : CSF lactate/IL-1β- promising data
  • 37.
     Neisseria meningitidis;young adults and children (after the neonatal period);sporadic, and endemic- serogroups B, C, and Y • Assost. with smoking & deficiencies in the complement system, specifically the terminal components C5-8 • Four clinical syndromes have been described in meningococcal disease: (1) bacteremia without sepsis, (2) meningococcemia without meningitis, (3) meningitis with or without meningococcemia, and (4) meningoencephalitis. • classic meningitis triad- 27% • Prototypical skin lesions (purpura and petechiae-hemorrahagic rash; HALLMARK) - 60% of adults & 60-90% of children • mortality 4-8% in children and 7% in adults, with septicemia the MCC • 8-20% neurological sequelae;SNHL,MR,seizures • Other : Waterhouse- Friderichsen syndrome (a massive hemorrhage into the adrenal glands)& DIC • Current guidelines recommend the use of penicillin or ampicillin • conjugate vaccine 11-55 yrs • Asst. with a high risk of secondary infection in close contacts; rifampin 600 mg BD x 2 days; 20 mg/kg/day for children
  • 38.
     Diagnosis • Rapiddiagnosis and treatment of bacterial meningitis are critical • LP should be done before institution of antibiotic therapy • Suspected increased ICP (h/o mass lesion, new-onset seizures, FND, papilledema, and severe impairment of consciousness) – CT/MRI head before LP • use a small-bore (25-gauge) needle • Severe HCP- require a ventriculostomy • CSF Gram stain-pathogen in 60-90% • CSF culture “gold standard”; 80-90% • CSF lactate >35 mg/dL; RDT with promising result Sn 93%/Sp 96% differentiating bacterial meningitis from aseptic meningitis;limited by other conditions- stroke/trauma • CRP >20 mg/L useful in discriminating bacterial from viral etiology • Procalcitonin (PCT) > 0.5 ng/mL with Sn 99%/Sp 83% distinguishing bacterial from aseptic meningitis • Blood cultures routinely done;50-80% • Others : PCR/ latex agglutination test (LAT)
  • 39.
     Radiologic Studies •X-ray chest, skull & sinuses • CT scans of the skull base - predisposing conditions such as sinus infection, mastoiditis, skull fractures & congenital anomalies • MRI is superior to CT; leptomeningeal enhancement and distention of subarachnoid space • diagnosis of meningitis is not based on imaging findings but allow delineate complications like HCP/abscess/subdural empyema or effusion/infarct • In straightforward cases of bacterial meningitis, early CT and MRI- normal • LP is still the most important diagnostic study  Treatment • Prompt clinical diagnosis of meningitis f/b rapid administration of antibiotics is a key factor • Delays- worse outcome. • After collection of CSF, empirical antibiotic therapy started ASAP
  • 40.
     Nosocomial bacterialmeningitis • 0.5% ;serious complication of neurosurgical procedures, systemic infection & TBI • MC gram-negative rods (E. coli, Pseudomonas aeruginosa, Proteus mirabilis, Enterobacter, Acinetobacter), Propionibacterium acnes, streptococci, and Staphylococcus aureus) • prolonged hospital stays, multiple operations & increased morbidity  Postcraniotomy meningitis • 0.8-8.9% cranial surgery; MC S. aureus and Staphylococcus epidermidis; gram-negative • CSF results are altered by the operation/anesthesia/use of steroids • Risk: EVD/CSF leakage/periop steroids/incisional infection/male /operative time > 4 hrs. • 1/3rd within 1 wk of surgery, 1/3rd in 2nd wk & 1/3rd after 2 wks. • most powerful risk factor for postoperative CSF -early reoperation (within 1 month) • prophylactic antibiotic therapy reduced the incidence of incisional infection from 8.8% to 4.6% it didn’t prevent the development of meningitis
  • 41.
     EVD inducedMeningitis/ ventriculitis; 8-23% • risk : greater frequency of CSF sampling/ >11 days; mc gram-positive cocci (S. aureus and S. epidermidis) consistent with skin flora • Intrathecal antibiotics administered through the EVD may be desirable, but this approach is not standardized  Lumbar Drain induced Meningitis ~5%  Posttraumatic Meningitis; 0.2-1.4% in moderate or severe head trauma • closed head trauma;mostly asst.with basilar skull fracture and subsequent CSF leakage • CSF rhinorrhea and otorrhea significant independent risk factors • Open (compound) cranial fractures ~5% • Trauma guidelines recommend that skull fractures depressed deeper than the thickness of the cranium be surgically debrided
  • 42.
     Recurrent bacterialmeningitis : 2 separate episodes of meningitis separated by a period of full recovery; 6% • Risk : 1) anatomic factors (2) immunodeficiencies [(X-linked agammaglobulinemia (Bruton’s disease),HIV]& (3) chronic parameningeal infections (sinusitis, otitis media, and mastoiditis. ) • Anatomic factors -congenital (encephaloceles, congenital inner ear dysplasia,)/acquired (head trauma or skull fracture-csf leak ) • head trauma MCC • CT scan with thin cuts through the skull base on bone windows  Encephalitis or meningoencephalitis: gram-negative bacillus Legionella pneumophila/Mycoplasma pneumoniae/L. monocytogenes • Aseptic meningitis - nonbacterial inflammation of the tissues lining the brain;viruses/fungi/parasites/protozoa/Rickettsia species • noninfectious etiologies (e.g., drugs, collagen vascular disorders, sarcoidosis) • Viruses account for the vast majority of cases of aseptic meningitis • any age but most common in infants and children. • Enteroviruses are the most common cause of viral meningitis • include echovirus, coxsackievirus groups A and B & poliovirus • transmitted via the fecal-oral route
  • 43.
    HSV : mccof viral encephalitis; mainly HSV-1/HSV-2 4-6% • age distribution is bimodal;6M-20yrs,>50 yrs • primary infection (30%) or virus reactivation (70%) • Pathologically, herpes encephalitis- an acute focal, necrotizing encephalitis with inflammation and parenchymal swelling • predilection for the temporal lobe and limbic system/ olfactory hallucinations • Mollaret’s meningitis, a syndrome with recurrent bouts (≥3) of fever & S/S of aseptic meningitis, recovery is rapid & spontaneous; d/t an occult reservoir of HSV-1/HSV-2 • EEG shows paroxysmal lateralized epileptiform discharges • mortality ~ 80% in infants without treatment • I.V Acyclovir x for 2 weeks; mortality reduced to 20% • survivors -the risk of long-term neurological sequelae is 62%
  • 44.
    • FLAIR MRIis most sensitive for showing areas of cerebral involvement and resulting inflammatory changes. • In this axial image, hyperintensity is visible in the right temporal lobe affecting the uncus and insular cortex as well as the subfrontal cortex. Although not present in this patient, foci of hemorrhage are common. •microglial nodules and cytoplasmic and intranuclear inclusion bodies
  • 45.
    Tuberculous Meningitis • TBMbegins with bacterial seeding of the brain with the formation of tubercles- rupture and cause seeding to adjacent subarachnoid space • military tuberculosis/generalized tuberculosis with a single area/any age (adult>children) • usual location- basal meninges • exudate obliterates the basal cisterns • not confined to SAS only as in bacterial meningitis, but instead spreads along pial vessels to invade adjacent brain • Headache 50%; stiff neck 75%, and lethargy/confusion/fever are typical. • chronicity leads to frequent cranial nerve involvement;20% at time of admission;poor outcome • glucose level, which is reduced but usually not to the very low as in bacterial meningitis • Currently the diagnostic of choice- PCR analysis • MRI- HCP as well as CE within the basal cisterns, subpial cortex, and subependymal areas/frank tuberculoma • self-limited meningitis k/A serous meningitis • meningeal signs are mild Role of Dexamethasone in TB meningitis
  • 46.
    Tuberculous meningitis A.Axial T1-w:CE thick enhancement of the basal cistern (arrows), as well as abnormal enhancement in Rt. occipital horn (asterisk) B. sagittal T1-w CE: abnormal enhancement coating pituitary stalk & brain stem, continuing caudally along S.C (arrows) Tuberculoma;Pt. with seizure Axial T2-w (A) & T1-w CE MRI (B)- single ring-enhancing Rt. parietal lesion with moderate edema
  • 47.
    • Occasionally anintracerebral tuberculoma- resection if it has mass effect or it fails to shrink with drug therapy • Neurological impairment 20-30% of survivors • Hyponatremia 49%/Hydrocephalus 42%/Stroke 33%/Cranial nerve palsies 29%/Epileptic seizures 28% • Diabetes insipidus 6%/Tuberculoma 3%/Myeloradiculopathy 3% /Hypothalamic syndrome 3% • The single most effective drug is isoniazid;neuropathy and hepatitis in alcoholics; Pyridoxine/Optic neuropathy- ethambutol; visual acuity & color discrimination • HRZS all enter CSF readily in the presence of meningeal inflammation • Ethambutol is less effective unless used in high doses • 2nd line drugs : Ethionamide, Cycloserine, Ofloxacin & PAS • 4 Drugs for 2 months f/b 2 Drugs (7 to 10 months)
  • 48.
    Anti-Epileptic Drug inTB Meningitis •New onset seizures 50% of children & 5% of adults •Acute Management – Short acting Benzodaizapines & Phenytoin •Long Term Rx with Phenytoin, Valproate - Hepatotoxic as well as Enzyme inducer •Levetericetam-Safely given •Rx on lines of Symptomatic seizure disorder •neuroimaging and EEG-If normal give for 2 year seizure free •If tuberculoma or any other lesion present may be offered for longer period Role of Osmotic Agents in TBM •Short term use of Mannitol, Frusemide and Acetazolamide in Stage 1 & 2 Disease •Manitol can be given upto 72 hrs •Frusemide & Acetazolamide may be used for weeks • Only in Open Hydrocephalus
  • 49.
     Cryptococcal Meningitis: MC;C. neoformans (soil with bird feces) • common opportunistic infection in HIV • usually subacute/chronic course;headache & malaise,altered mental status 20% • basilar meningitis, miliary parenchymal nodules • infiltrate brain via the perivascular spaces • dilation of perivascular spaces c/a “gelatinous pseudocyst presentation” • mortality of HIV-associated cryptococcal meningitis 22-40% despite Rx Cryptococcosis HIV Pt.; Axial T2-w (A) & T1-w CE (B)- single small, enhancing lesion in left corona radiata with moderate associated edema
  • 50.
    Protozoa  Toxoplasma gondiic/b obligate intracellular parasite Toxoplasma gondii/MC in HIV/ ingestion of contaminated cat feces/undercooked meat • CF: rash/myocarditis/polymyositis; meningoencephalitis (seizures/confusion/coma) • Lesions are scattered throughout the brain, and adjacent to the subarachnoid space cause the meningitis component of the meningoencephalitis • Diagnosis can be achieved by finding organisms in the CSF or in stereotactic biopsy specimens of brain lesions. • MRI :solid to ring enhancing lesions/combination; /any location/single or multiple • Positive response to medical Rx-diagnostic  Rx: combination of pyrimethamine (100-200 mg D1 f/b 50-75 mg/day x 6 wks) & sulfadiazine(4-6 g/day x 6 wks)- DOC  Folinic acid/Leucovorin (10-25 mg/day) to prevent pyrimethamine-induced hematologic toxicity HIV Pt. with seizures & CSF + for toxoplasma Ag; T2-w & T1-w CE of cerebral hemispheres (A & B) ; ring-enhancing lesion with an eccentric enhancing nodule
  • 51.
    Acquired Immunodeficiency Syndrome •affect CNS/PNS both directly & indirectly • Direct infection CNS- acute retroviral syndrome/aseptic meningitis/transient & self-limited • Chronic HIV infection: HIV-associated encephalopathy/ myelopathy/ increased risk of stroke • highly active antiretroviral therapy (HAART)- robust immune response k/a the immune reconstitution inflammatory syndrome (IRIS);affect CNS • Toxoplasma/Cryptococcus/mycobacterial/viruses-JC virus & CMV/bacteria-Treponema & Bartonella species • CNS Lymphoma asst. with concomitant EBV infection CNS lymphoma A. coronal T1-w CE;solidly enhancing lesion infiltrating CC B. axial T1-w CE ; faintly rim-enhancing lesion Rt. frontal lobe immunocompetent - nonhemorrhagic, solidly enhancing lesion immunosuppressed -ring-enhancing lesion with cystic or hemorrhagic components
  • 52.
    HIV associated encephalopathy(HAE) Coronal T2 w;ventricles & sulci markedly prominent-significant volume loss with minimal white matter signal abnormality Progressive multifocal leukoencephalopathy (PML) HIV pt.; CSF-JC virus; Axial T2-w: white matter signal abnormality involving Rt. frontal lobe & insula with spread across CC to involve Lt. frontal lobe;involvement of subcortical U fibers (arrows) & nearly complete lack of mass effect (classic) Immune reconstitution inflammatory syndrome (IRIS);HIV pt. on HAART  Axial T2-w: very extensive, confluent signal abnormality in the white matter of Lt. cerebral hemisphere & lesser degree of Rt.Hemisphere ;similar to that of PML In this patient but more mass effect
  • 53.
    HELMINTHIC CNS INFECTIONS Cysticercosis; humans intermediate hosts of Taenia solium; • neurocysticercosis (NCC);epilepsy-mc presentation; intracranial hypertension (obstructive HCP,mass effect)/FND • subacute course;difficult to differentiate NCC from neoplasia /other infections of CNS • intense inflammation around cysticerci & diffuse cerebral edema- cysticercotic encephalitis ; severe form of NCC • spinal cysticercosis –motor & sensory deficits, vary a/c to level of lesion • most typical imaging findings - cystic lesions showing the scolex & parenchymal brain calcifications • Others: ring-enhancing lesions/abnormal enhancement of leptomeninges/HCP/cerebral infarctions • CSF normal /CSF eosinophilia not consistent finding • subarachnoid & ventricular forms -CSF analysis-lymphocytic pleocytosis/increased protein/ normal glucose • most accurate serologic test is immunoblotting (ELISA) /also for Rx response
  • 54.
    Treatment • cysticidal agents& corticosteroids with AED • Albendazole 15 mg/kg/day x 1 wk & praziquantel 50 mg/kg/day x 2 wks- preffered regimen • corticosteroids to prevent post-treatment seizure; routinely administered with cysticidal agents • dexamethasone 8 mg/day for 28 days, started early during antiparasitic treatment for viable parenchymal NCC • Pt. with cysticercotic encephalitis should not receive cysticidal drugs; managed with high doses of corticosteroids/osmotic diuretics/decompressive craniotomy if necessary • giant subarachnoid cysticerci (>5 cm); cysticidal drugs with caution ; occlude small leptomeningeal vessels ;stroke; concomitant steroid mandatory • Patients with calcifications alone should not receive cysticidal drugs because these lesions represent dead parasites • Temporal lobectomy can be safely performed in patients with temporal lobe epilepsy with hippocampal sclerosis caused by NCC without affecting cognitive outcomes and with a satisfactory long-term seizure control provided selected patients remain on chronic antiseizure medication • Hydrocephalus secondary to cysticercotic arachnoiditis requires placement of a ventricular shunt. • Hydrocephalus may also be managed with endoscopic foraminotomy and endoscopic third ventriculostomy
  • 55.
    REFERENCES 1. Youmans andWinn Neurological Surgery; 7th edition 2. Ramamurthi & Tandon'S Textbook Of Neurosurgery; 3rd edition 3. Handbook of Neurosurgery. Mark S. Greenberg; 9th edition THANKYOU