Download MBBS Neuroanaesthesia PPT 14 Nosocomial Infection In Neurocritical Care Lecture Notes

Download MBBS (Bachelor of Medicine, Bachelor of Surgery) Neuroanaesthesia PPT 14 Nosocomial Infection In Neurocritical Care Lecture Notes

NOSOCOMIAL INFECTION IN NEUROCRITICAL

CARE

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OVERVIEW

? Introduction.
? Pneumonia.
? Bacteremia.
? Urinary tract infection.
? Ventriculitis.
? Subdural empyema.
? Brain abscess.
? Meningitis and encephalitis.

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INTRODUCTION

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? Nosocomial infections can be defined as those occurring within 48 hours of hospital admission, 3

days of discharge or 30 days of an operation.

? The reported incidence in the neurointensive care unit (NICU) ranges from 20% to 30%.

? The incidence of post neurosurgical wound infection is from <1 to 8%, with reported mortality as

high as 14%

? Infection risk is increased in NICU patients due to ?

?Medication side-effects
?Catheter and line placement
?External ventricular drains and ventilators
?Neurosurgical procedures
?Acquired immune suppression secondary to steroid/barbiturate use and brain injury itself.

? These infections are associated with increased length of hospital stay and increased morbidity

and mortality.

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? The blood?brain barrier presents a challenge to antimicrobial selection and infection treatment.

? Prevents large molecules from penetrating into cerebrospinal fluid (CSF).

? Limits the number of antimicrobials available for treating CNS infection.

? This makes it critical to identify whether a infection is intra-axial or extra-axial.

? Antibiotics that effectively enter the CNS are unfortunately often associated with CNS toxicities ?

?Encephalopathy are beta-lactam antibiotics (penicillins, cephalosporins, and carbapenems),

quinolones, and metronidazole.

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?Fortunately, the encephalopathy is reversible with discontinuation of the medication.

?Seizures have been reported with beta-lactams and fluoroquinolones.

?Aminoglycosides and polymyxins (colistin, polymyxin B) can cause a neuromuscular blockade

-like effect.

?Older age, renal failure, and higher doses are risk factors that increase neurotoxicity.

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PNEUMONIA

(Ventilator Associated Pneumonia)

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? Ventilator-associated pneumonia (VAP) is defined as pneumonia that occurs 48 hours after

endotracheal intubation.

? Early VAP occurs within 5?7 days of mechanical ventilation.

? Late VAP occurs more than 5?7 days of mechanical ventilation.

? It contributes to half of all cases of hospital acquired pneumonia (HAP).

? VAP is estimated to occur in 9?27% of all mechanically ventilated patients.

? All-cause mortality associated with VAP ranges from 20 to 50% in different studies, but the

attributable mortality is 9?13%.

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? The factors associated with increased mortality are:

?Bacteraemia,
?Shock,
?Coma,
?Respiratory failure,
?ARDS,
?Severe underlying comorbid disease, and
?Infection with MDR organisms.

? The risk of VAP is approximately 1%/day, being higher in initial days, and this decreases as time

passes to 3% in the first 5 days, then 2% between the fifth to tenth days, and then 1%/day of

mechanical ventilation.

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? The United States Centre for Disease Control and Prevention (CDC) has adopted a new method of

ICU surveillance.

? Employing ventilator-associated events (VAE) as a potential metric to assess quality of care in

ICU.

? VAE include ?

?Ventilator-associated complications (VAC),
?Infection-related ventilator-associated complications (IVAC),
?Possible and probable VAP.

? These definitions are used for surveillance and quality improvement of the ICUs.

? These definitions fail to detect many patients with VAP and do not aid in management at the

bedside level.

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? The presence of neurologic disease has been identified as an independent risk factor for

development of VAP and for failure of VAP resolution with initial antibiotic therapy.

? Neurologic patients are particularly vulnerable to pneumonia due to decreased consciousness,

dysphagia, and impaired protective airway reflexes.

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? Pathogenesis ?

?Micro and macro aspiration of the colonized oropharyngeal secretions across the tracheal tube

cuff.

?The bacteria can also adhere to the internal surface of the tube forming a biofilm and translocate

into the lungs with inspiration.

?Patients can be colonized either ?

?Exogenously from the hand, equipment, invasive devices and hospital environment, or

?Endogenously from the organisms present in the oropharynx, tracheal tube and

gastrointestinal tract.

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?In normal individuals, there are various defence mechanisms to prevent translocation of

pathogen in the lower airways like -

?Adduction of true and false vocal cords,
?Cough reflex,
?Mucociliary clearance in the upper airways.

?However, these body defence mechanisms are impaired in intubated patients.

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? Causative organisms ?

?Early-onset VAP, occurring within 4 days of
intubation, is usually attributed to antibiotic
sensitive pathogens.

?Late-onset VAP occurring later than 4 days
after intubation is more likely caused by multidrug
resistant (MDR) pathogens.

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? Diagnosis ?

?The clinical diagnosis of VAP is difficult because clinical findings are non-specific.

?At present, there is no universally accepted gold standard criteria for VAP.

?IDSA/ATS 2016 guidelines for management of VAP recommend clinical diagnosis of VAP based

upon -

?A new lung infiltrate PLUS
?Clinical features suggesting infectious nature of the infiltrate like new onset of fever, purulent

secretions, leukocytosis and decline in oxygenation.

?Unfortunately, in patients who are suspected of having VAP based on these clinical criteria, the

incidence of pneumonia on post-mortem exam is only 30% to 40%.

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?The limited diagnostic accuracy in VAP is primarily due to the nonspecific nature of pulmonary

infiltrates.

?Pneumonia accounts for only one-third of all pulmonary infiltrates in ICU patients.

?Differential diagnosis of pulmonary infiltrates includes ?

?Aspiration pneumonitis
?Pulmonary embolism
?Pulmonary hemorrhage
?Acute respiratory distress syndrome
?Infiltrative tumor
?Lung contusion
?Radiation pneumonitis
?Congestive heart failure.

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? The other limitation of chest radiography is a limited sensitivity for the detection of

pulmonary infiltrates.

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?Blood cultures have limited value in the diagnosis of VAP because organisms isolated from blood

in cases of suspected VAP are often from extrapulmonary sites of origin.

?Diagnosis is confirmed when lower respiratory tract sampling identifies a pathogen.

?Guidelines recommend obtaining lower respiratory tract samples for culture and microbiology,

ideally before antibiotics are started or when it is changed.

?There are two methods of sampling of the respiratory tract--invasive and non-invasive.

?Non-invasive sampling refers to endotracheal aspirates.

?Invasive involves bronchoscopic bronchoalveolar lavage (BAL), protected specimen brushing

(PSB) and blind bronchial sampling, i.e., miniBAL.

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? A positive microbiological sample in a patient with normal chest radiograph suggests

tracheobronchitis.

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?IDSA 2016 guidelines recommend using clinical criteria alone for starting antibiotics in patients

with suspected VAP and not on serum procalcitonin level plus clinical criteria.

?Procalcitonin levels can be useful -

?To stop/discontinue antibiotic therapy in patients with confirmed VAP, and
?Can also be used as a prognostic marker.

?Other diagnostic methods which have been in use to diagnose VAP include ?

?Clinical pulmonary infection score (CPIS),
?HELICS criteria, and
?Johannson criteria.

?Clinical pulmonary infection score (CPIS) ?

?The maximum score is 12 and a score > 6 is diagnostic of VAP.
?Sensitivity and specificity of only 65% and 64%, respectively.

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?The HELICS criteria are used for VAP

surveillance in Europe ?

?The Johannson criteria ?
?Sensitivity and specificity of these criteria are

69% and 75%, respectively.

?New/progressive infiltrates on chest X-ray

associated with at least 2 of 3 clinical features--

leucocytosis,

purulent

secretions

and

temperature greater than 38 ?C.

?The diagnosis of VAP is more problematic in

neuro-ICU due to ubiquitous nature of clinical

findings related to primary brain injury.

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? Differential diagnosis -

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? Treatment ?

? The duration of therapy is guided by clinical response.
?For early-onset VAP is 8 days.
?For late-onset VAP it is 8 to 14 days.

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? Prevention:

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BACTEREMIA

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? Bacteremia is the second most common HAI in the NICU.

? The crude mortality rate resulting from bacteremia has been estimated at 27%.

? Risk factors for bacteremia include ?

?Intravascular catheter placement
?Host factors such as immunosuppression, older age, malnutrition, and total parenteral

nutrition.

? The risk for catheter-related bacteremia (CRB) (per 1000 catheter days, with 95% confidence

intervals) has been estimated at ?

?2.7 (2.6?2.9) for noncuffed CVCs,
?1.7 (1.2?2.3) for arterial catheters,
?1.6 (1.5?1.7) for cuffed and tunneled CVCs, and
?1.1 (0.9?1.3) for peripherally inserted central catheters.

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? Aseptic technique is essential for avoidance of infection.

? A meta-analysis of randomized controlled trials favours the use of cutaneous chlorhexidine over

povidone-iodine for optimal antiseptic technique.

? Diagnosis and microbiology ?

?The most frequent pathogens associated with CRB are -

?Staphylococcus epidermidis (37%),
?S. aureus (13%),
?Enterococcus (13%),
?Enterobacter-Klebsiella (11%),
?Candida spp. (8%),
?Serratia (5%), and
?Others (Escherichia coli, Pseudomonas spp.).
?Gram-negative organisms are especially common in patients with malignancies

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?True confirmation of a catheter source requires the following:

?Same organism is grown from peripheral blood and the catheter tip culture with growth of

>15 CFUs; or

?Central blood sample is read as positive 2 hours earlier than a peripheral blood sample

inoculated at the same time; or

?Both catheter and peripheral cultures grow the same organisms and the colony count from

the catheter-drawn blood is three to five times greater than that drawn by venepuncture.

? Treatment ?

?Short- and long-term catheters should be removed from patients with CRB when associated with

any of the following conditions:

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?Hemodynamic instability or sepsis,
?Endocarditis,
?Suppurative thrombophlebitis, or
?Infections.

?Catheter tip culture should be performed when a catheter is removed for suspected CRB.

?For patients in whom catheter salvage is attempted, additional blood cultures should be

obtained.

?If blood cultures remain positive despite 72 hours of antimicrobial therapy, the catheter should

be removed.

?Antimicrobial therapy is often initiated empirically.

?Vancomycin is the empiric therapy of choice.

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?The addition of empiric therapy against Pseudomonas (e.g., cefepime, piperacillin-tazobactam,

meropenem) is indicated in patients who are ?

?Critically ill,
?Have sepsis or neutropenia, or
?Have a femoral catheter in place.

?If candidemia is suspected. Fluconazole or echinocandin (e.g., caspofungin) should be started.

?Blood cultures should be redrawn after initiation of therapy to assure clearance of bacteremia.

?The recommended duration of therapy is 14 days, with day 1 defined as the first day with

negative cultures.

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?Four to six weeks of therapy is recommended when ?

?Bacteremia or fungemia persists for more than 72 hours after catheter removal,

?Bacteremia resulting from infection with S. aureus in patients with diabetes,

immunocompromised state, or with a prosthetic intravascular device;

?Endocarditis, suppurative thrombophlebitis, or metastatic infectious foci are Identified.

?Antibiotic treatment is not recommended in some situations involving positive cultures

associated with an indwelling or recently removed CVC. These include ?

?Positive culture from a removed catheter tip not accompanied by clinical signs of infection,

?Positive cultures from an indwelling CVC associated with negative associated peripheral

blood cultures, and

?Phlebitis in the absence of infection (topical antimicrobials are preferred).

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URINARY TRACT INFECTIONS

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? Second most common HAI in patients admitted to ICUs.

? Third most common in patients admitted to NICUs, accounting for 22.7?36.6% of HAIs.

? Approximately 20% of hospital-acquired bacteremias, arise from the urinary tract, and the

mortality associated with this condition is 10%.

? Risk factors include ?

?Indwelling urethral catheters (80%),
?Diaabetes mellitus,
?Older age,
?Female sex,
?Severe underlying illness, and
?Bacterial colonization of the drainage bag.

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? Diagnosis and microbiology ?

?Most ICU-acquired catheter-associated UTIs (CAUTI) are monomicrobial (88?95%).

?The predominant pathogens are:

?E. coli (39%),
?P. aeruginosa (22%),
?Enterococcus (15%),
?Acinetobacter spp. (11%),
?Klebsiella spp. (11%), and
?Proteus (11%).
?Candida spp (account for one-third of all ICU-acquired UTIs).

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?CAUTI is defined as culture growth of > 1000 CFU/mL of uropathogenic bacteria in the presence

of symptoms or signs compatible with UTI with no other identified source of infection in a patient

with an indwelling urethral or suprapubic catheter, or intermittent catheterization.

?Signs and symptoms compatible with CAUTIs include ?

?New-onset or worsening fever,
?Rigors,
?Altered mental status,
?Malaise, or lethargy with no other identified cause.
?Flank pain,
?Costovertebral angle tenderness,
?Acute hematuria, and
?Pelvic discomfort.

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?Catheter associated asymptomatic bacteriuria is defined by culture growth of >10,000 CFU/mL of

uropathogenic bacteria in patients with an indwelling urethral or suprapubic catheter, or

intermittent catheterization in a patient without clinical symptoms.

?Pyuria (white blood cell count 10 cells/mL) can be present in catheterized patients with

asymptomatic bacteriuria, and has a low sensitivity.

?It is not recommended to use the degree of pyuria to differentiate CAUTI from catheter-

associated asymptomatic bacteriuria.

?A urine culture should be obtained prior to initiating treatment.

?The urine culture should be obtained from the freshly placed catheter prior to the initiation of

antimicrobial therapy in patients with long-term indwelling catheters.

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?In patients with short-term catheterization, it is recommended that ?

?Specimens be obtained by sampling through the catheter port using aseptic technique or,
?If a port is not present, by puncturing the catheter tubing with a needle and syringe.

?Culture specimens should not be obtained from the drainage bag.

? Treatment ?

?Uncomplicated UTI (not CAUTI) - Trimethoprim/sulfamethoxazole or ciprofloxacin.

?For empiric treatment of CAUTI with Gram-negative rods - third generation cephalosporins (e.g.,

ceftriaxone) or a fluoroquinolone (ciprofloxacin or levofloxacin) are recommended.

?Vancomycin is the drug of choice for empiric treatment of Gram-positive cocci.

?Attention to bacterial susceptibility is important. Follow-up of culture results is essential.

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?Candida albicans and C. glabrata are the most frequent uropathogens associated with CAUTI.

?Parenteral fluconazole for 14 days for C. albicans.

?Voriconazole is more effective against non-C. albicans.

?Severe illness who have uncomplicated UTI - 3?7 days of antibiotic treatment is sufficient.

?Ten to 14 days of therapy is recommended for those with a delayed response and in septic

patients.

?Colonized patients, without evidence of infection, do not require treatment.

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?However, the indwelling catheter should be changed or removed.

?Treatment is not necessary for asymptomatic bacteriuria and should be avoided due to concerns

of increasing antimicrobial resistance.

?Routine screening is not recommended.

? Prevention ?

?Indwelling catheters should be placed only when indicated,
?Should be removed as soon as possible,
?Sterility should be maintained.

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VENTRICULITIS

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? Bacterial ventriculitis (BV) is inflammation of the ventricular drainage system due to bacterial

infection of the cerebrospinal fluid (CSF).

? BV is associated with CSF shunts, EVD, or any other intracranial device.

? Hemorrhagic CSF further contributes to the increased incidence of EVD-associated Infections.

? Infection risk increases significantly after 5 days of placement and peaks at days 9?11 after

placement.

? CSF shunt-related infection is reported in 8?40% of patients, with most infections occurring

within 1 month of implantation.

? The most common pathogens - Gram-positive organisms and fungi followed by gram negative

organisms.

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? Diagnosis ?

?Ventriculitis is diagnosed by the presence of clinical symptoms and a positive CSF analysis.

?The clinical symptoms of ventriculitis include fever and signs of meningitis (nuchal rigidity,

decreased mental status, seizures,etc.).

?A positive CSF culture with absent symptoms should lead the clinician to suspect colonization or

contamination.

?In patients who have already suffered a neurologic injury that causes inflammation and

breakdown of the blood?brain barrier, the diagnosis of ventriculitis can be challenging.

?CSF may already contain blood with increased protein, inflammatory cells, and decreased glucose

depending on the underlying pathology.

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?Determination of a high lactate concentration can assist with diagnosis.

?Factors that may elevate CSF lactate include ? cerebral hypoxia, vascular compromise.

?Current guidelines recommend that, in the postoperative neurosurgical patient, initiation of

empiric antimicrobial therapy should be considered if CSF lactate concentrations are 4.0

mmol/L, pending results of additional studies.

?Cranial sonography is useful in diagnosing this condition in infants and young children. Findings

include -

?Increased echogenicity of the ventricular wall,
?Increased thickness of the ventricular walls, and
?Presence of septations and debris in the ventricles.

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?Non-contrast CT ?

?Non-specific features,
?Hyperdense layering material may be seen dependently, particularly in the occipital horns of

the lateral ventricles.

?Hydrocephalus and periventricular low density (represents reactive edema).

?In contrast CT, thin regular enhancement of the ependymal lining of the ventricles may be seen.

?MRI findings include ?

?Ependymal enhancement and thickening,
?Dilated ventricles,
?Surrounding FLAIR signal hyperintensity, suggestive of parenchymal edema.
?Increased T2 hyperintensity in the ventricular wall, and
?Debris in the dependent portion of the ventricle (occipital horn) are other imaging findings.
?Restricted diffusion may be seen in the dependent purulent intraventricular fluid.

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? Treatment -

?Recommended empiric therapy are combination of ?

?Vancomycin and cefepime for adults, or
?Vancomycin plus ceftazidime, or
?Vancomycin plus meropenem.

?In most cases treatment is continued for 10?14 days.

?For aerobic Gram-negative bacilli, therapy may be continued for up to 21 days.

?A fungal infection with Candida species should be managed with voriconazole and the polyene

amphotericin B for 2 weeks since the last negative CSF culture.

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?In addition to antimicrobial therapy, infected hardware should be removed, replaced, or

externalized when appropriate.

?Intraventricular (IVT) administration of antibiotics may be effective in selected cases, although

indications remain controversial.

?IVT antibiotics can lead to rapid CSF sterilization in post neurosurgical patients with meningitis

and ventriculitis (mean time 2.9- 2.7 days, range 1?12 days).

?The relapse rate of ventriculitis is also very low among patients treated by IVT antibiotics.

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?The typical indications for intrathecal administration are:

?Failure to achieve adequate CSF antimicrobial concentrations with nontoxic drug doses, or

?Persistently positive CSF cultures despite intravenous dosing with an appropriate antibiotic,

and

?Exhaustion of all appropriate means of source control.

?Drug concentrations at least 10 times the MIC are recommended in CSF to achieve rapid

bactericidal activity.

?Intrathecal antibiotics are administered at 24-hour intervals and for 48?72 hours after

sterilization of the CSF in most cases.

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? Prevention ?

?Protocolized EVD insertion and nursing care.

?A recent meta-analysis found that both antibiotic- and silver-impregnated EVDs were more

effective than standard EVDs for the prevention of catheter-related infection.

?There is no conclusive evidence guiding preference of antibiotic or silver-impregnated EVDs.

?It is not recommended to exchange EVDs with the aim of preventing ventriculitis.

?Systemic antibiotic prophylaxis should be avoided in patients treated with antibiotic coated EVD.

?Prolonged systemic antibiotic therapy should be avoided in after placement of EVD.

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SUBDURAL EMPYEMA

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? SDE occurs after neurosurgery in 4% of cases.

? Signs and symptoms of SDE usually present within 1?8 weeks (mean 2 weeks).

? Staphylococci and Gram-negative bacilli are the most common pathogens.

? Pus can be found over the convexities, layering along the tentorium cerebelli, or in the

interhemispheric fissure, with 1?10% of SDEs located in the posterior fossa.

? Lumbar puncture is not recommended due to increased risk for cerebral herniation.

? The recommended management for SDEs includes surgical drainage and antibiotic therapy.

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? Empiric treatment - Vancomycin plus a fourth generation cephalosporin (i.e., cefepime).

? Cultures should be sent from the surgical drainage.

? Appropriate antibiotic therapy should be tailored accordingly.

? Duration of treatment ? 3 ? 6 weeks.

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CT Scan

DWI

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MRI ? T1

MRI ? T2

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BRAIN ABSCESS

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? Abscess formation is an uncommon but serious complication after neurosurgical procedures.

? Risk factors include -

?Immunocompromised patients,
?Head trauma patients with penetrating brain injury are at higher risk.

? Patients typically present 2 weeks post surgery with ?

?Headache,

?Low-grade fevers (present in over 50% of cases),

?Seizures and signs of increased intracranial pressure may be present.

?Focal neurologic deficit or altered level of consciousness (over 60% of cases).

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? The most common pathogens - Staphylococcus aureus and S. epidermidis, or Gram-negative

bacilli.

? Lumbar puncture should be performed only when there is clinical suspicion of meningitis or

abscess rupture into the ventricular system.

? Herniation is estimated to occur in 15?20% of patients who have a lumbar puncture with cerebral

abscess.

? When CSF analysis fails to identify a causative pathogen, surgical aspiration should be considered

to isolate the organism and to reduce the abscess diameter.

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? CT -
?Outer hypodense and inner hyperdense rim (double

rim sign) in most cases.

?Ring of iso- or hyperdense tissue, typically of

uniform thickness.

?Central low attenuation (fluid/pus).
?Surrounding low density (vasogenic edema).
?Ventriculitis may be present, seen as enhancement

of the ependyma.

?Obstructive hydrocephalus will commonly be seen

when intraventricular spread has occurred.

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? MRI -

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? D/D ? Metastasis, haemorrhage, infarction, demyelination lesion, radiation necrosis.

? Medical therapy alone may be appropriate in following conditions ?

?If the causative pathogen has been identified,

?Abscess measure less than 2.5 in diameter,

?When the abscess is located in deep or eloquent brai,

?Poor surgical candidacy,

?Concurrent meningitis, ventriculitis, or

?Concurrent hydrocephalus that requires CSF shunting which may become infected at the time

of abscess drainage.

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? Empiric treatment - vancomycin plus a fourth-generation cephalosporin (i.e., cefepime) and

metronidazole for 6?8 weeks.

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MENINGITIS AND ENCEPHALITIS

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? Meningitis and encephalitis are pathologically distinct syndromes but have extensive clinical

overlap.

? Diagnostic tools include ? general signs, imaging, CSF analysis, blood cultures.

? Differential diagnosis ? intracranial bleed, neuroinflammatory, and vasculitis disorders, post-ictal

patients.

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? Treatment ?

?In adult patients <50 years old, the most common pathogens are Neisseria meningitidis and

Streptococcus pneumoniae, and thus, recommended empiric therapy is vancomycin plus a

third-generation cephalosporin.

?Age >50 years, the risk of Listeria monocytogenes increases and prompts the addition of

ampicillin.

?In patients with suspected or confirmed pneumococcal meningitis, adjunctive

dexamethasone is recommended.

?The only commonly encountered viral meningoencephalitis with effective treatment is HSV,

and empiric acyclovir should be administered.

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? Antimicrobial prophylaxis for N.Meningitidis is recommended only for ``close contacts''.

?Chemoprophylaxis include ciprofloxacin, rifampicin, and ceftriaxone.

?Administered as soon as possible after exposure.

?Not effective after 14 days.

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