Repeat CT scans or MRIs are recommended every 1-2 weeks during antimicrobial therapy to monitor response. Scans should continue every 4-6 weeks for 3-6 months after completion of therapy to ensure resolution and check for recurrence. Earlier follow up scans may be needed if clinical deterioration occurs which could indicate treatment failure or recurrence.
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About ICH - Diagnosis and management, Discussed the clinical presentation, evaluation, radiological features and management including recent guidelines
Due to stretching forces placed on individual nerve cells
Pathology distributed throughout brain
Types
Concussion
Diffuse Axonal Injury (Moderate to Severe)
Gliomas are the commonest tumor of brain arising from the supportive cells of the brain with diverse form and presentation the treatment of which is surgical and demands adjuvant therapy for most of circumstances.
Intracerebral hemorhage Diagnosis and managementRamesh Babu
About ICH - Diagnosis and management, Discussed the clinical presentation, evaluation, radiological features and management including recent guidelines
Due to stretching forces placed on individual nerve cells
Pathology distributed throughout brain
Types
Concussion
Diffuse Axonal Injury (Moderate to Severe)
Gliomas are the commonest tumor of brain arising from the supportive cells of the brain with diverse form and presentation the treatment of which is surgical and demands adjuvant therapy for most of circumstances.
Magnetic resonance features of pyogenic brain abscesses and differential diag...Felice D'Arco
The aim of this presentation is to illustrate the potential of magnetic resonance imaging (MRI) in diagnosis, differential diagnosis, treatment planning and evaluation of therapy effectiveness of pyogenic brain abscesses, through the use of morphological (or conventional) and functional (or advanced) sequences.
Identify the most common parasitic diseases that affect the CNS.
Discuss the Imaging features of these diseases.
Clarify the significances of Imaging in diagnosis and assessment of pathological features of these diseases.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
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micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
1. Dr. Joe M Das
Senior Resident
Dept. of Neurosurgery
Brain abscess
2. History
Definition
Epidemiology
Pathogenesis
Clinical features
Investigations
Treatment
Special abscesses
3. History
Hippocrates – Purulent otorrhea and delerium
The first successful operation for brain abscess - S.F. Morand
(France) in 1752 on a temperoethmoidal abscess.
“Pyogenic Disease of the Brain and Spinal Cord, Meningitis,
Abscess of the Brain, Infective SinusThrombosis” (1893) -
William Macewen – Father of modern day abscess management
King (1924) – marsupialization
Dandy (1926) – aspiration
Sargent (1928) – enucleation
Vincent (1936) – complete excision
Heineman et al (1971) – successful medical management
4. Henry II, King of France
Death was predicted by
Nostradamus
Died from an orbital wound
The skull was not penetrated
but infection spread
intracranially
Infection had spread to the
brain along the orbital veins,
forming an abscess under the
cortex.
6. Definition
Mathisen GE, Johnson JP: Brain abscess. Clin Infect Dis
1997; 25:763-781.
A focal intracranial
infection that is initiated as
an area of cerebritis and
evolves into a collection of
pus surrounded by a
vascularized capsule.
7. Epidemiology
1500-2500 cases per year in the US
8% of ICSOL in developing countries
♂: ♀ = 2-3 : 1
Median age – 30 – 40 yrs
2° to otitic focus - <20 / > 40 yrs
2° to PNS infection – 30-40 yrs
25% in children – otitic focus / CHD
0.2% of cranial operations
Immunosuppression
9. Contiguous spread
Routes of contiguous spread:
Direct extension through osteitis / osteomyelitis
Retrograde thrombophlebitis via diploic or emissary vein
Via local lymphatics
Localisation:
Otitis media –Temporal lobe / cerebellum
PNS – Frontal lobe
Sphenoid sinusitis –Temporal lobe / sella
Dental infection (molars) – Frontal lobe (M.C) / temporal
10. India – M.C source –
Middle ear suppuration
Western countries – M.C
source – Spread from PNS
Sites of bone dehiscence:
Post wall of frontal sinus
Tegmen tympani
Trautmann’s triangle
11. Hematogenous
Multiple, multiloculated abscesses - ↑ mortality
M.C sources in adults – chronic pyogenic lung diseases (especially
lung abscess), bronchiectasis, empyema, and CF.
Distant sources – wound & skin infections, osteomyelitis, pelvic
intra-abdominal infections; after esophageal dilation or sclerosing
therapy for esophageal varices.
CCHD (TOF/TGV) – 5-15% of brain abscess cases.
<5% of patients with IE despite the presence of continuous
bacteremia
Hereditary hemorrhagic telangiectasia (with coexisting pulmonary
AVM) - allows septic emboli to cross the pulmonary circulation
without capillary filtration – 5-9% risk
12. How does TOF lead to brain abscess?
TOF Chronic hypoxemia Polycythemia
↑ viscosity Multiple infarcts at grey-white
junction Milieu for bacterial growth
13. Trauma
Open cranial fracture with dural breach / foreign body
injury / as a sequel of neurosurgery
Civilian population - 2.5-10.9 %
Includes those 2° to compound depressed skull
fractures, dog bites, rooster pecking, tongue piercing
Nosocomial brain abscess - halo pin insertion, electrode
insertion to localize seizure foci, and in malignant glioma
patients treated by placement of Gliadel wafers
14. In military populations - 3-17 %
Usually occur secondary to retained bone fragments or
contamination of initially uninfected missile sites with
bacteria from skin, clothes, or the environment
The retained foreign bodies did not seem to increase the
infection rate except in patients who suffered an in-
driven cluster of bone fragments or leakage of
cerebrospinal fluid.
19. Recommended Dosages of Antimicrobial
Agents in Adults with Brain Abscess and
Normal Renal and Hepatic Function
20. Stages of abscess formation
A canine model after inoculation of α-hemolytic Streptococci
Britt RH, Enzmann DR,YeagerAS. Neuropathological and computerized tomographic findings
in experimental brain abscess. J Neurosurg. 1981 Oct;55(4):590-603.
24. Histopathologic findings in the stages
of brain abscess formation
Data from Tunkel AR, Scheld WM. Pathogenesis and pathophysiology of bacterial infections. In: Scheld WM, Whitley RJ, Durack, DT, eds. Infections of the Central
Nervous System, tind ed. Philadelphia: Lippincott-Raven; 1997;297-312; and Britt RH, Enzmann DR, Yeager AS. Neuropathological and computerized tomographic findings in
experimental brain abscess. J Neurosurg. 1981;55:590-603.
25. Early cerebritis
Acute inflammatory
infiltrate
Marked edema
Invisible on CT OR
Poorly marginated cortical
/subcortical hypodensity
with mass effect with no
enhancement
26. Late cerebritis
Central necrosis
Macrophages and
fibroblasts
Vascular proliferation
Maximum edema
Irregular rim enhancing
lesion with
hypodense center, better
defined than early
cerebritis
27. Early capsule formation
Necrotic centre ↓
Collagenous capsule
Edema starts to regress
Well-defined rim
enhancing mass; an outer
hypodense and inner
hyperdense rim (double
rim sign)
28. Late capsule formation
Collagen capsule complete
↑ density and thickness
Rim enhancing lesion with
thickened capsule and
diminished hypodense
central cavity
31. Why does abscess often rupture
intraventricularly?
Difference in vascularity between cortical grey
and white matter
↑ fibroblast proliferation on cortical side
Capsule less formed on ventricular surface
Tendency for intraventricular rupture
33. Initial Findings in Patients with Brain
Abscess Based on Intracranial Location
Frontal >Temporal >
Parietal > Cerebellum >
Occipital
34. Classic triad of headache, fever, and focal neurologic
deficit is rarely seen (< 5-20% of cases in case series)
1/3rd – polymicrobial
Incidence of negative cultures - 25-30%
Sudden worsening of a preexisting headache
accompanied with meningismus may be indicative of a
catastrophic event—rupture of the abscess into the
ventricular space.
35. When there is no obvious source (up to 25% of cases),
upper respiratory tract flora and anaerobes are often
isolated.
Several sources have identified a patent foramen ovale by
echocardiogram in these cases and propose this as a
possible mechanism for seeding oral flora to the brain.
Khouzam RN, El-DoklaAM, Menkes DL. Undiagnosed patent foramen ovale
presenting as a cryptogenic brain abscess: case report and review of the literature. Heart
Lung. Mar-Apr 2006;35(2):108-11.
36. Investigations
X-ray skull:
Often normal
Post-traumatic – air inside cranial cavity
Sinusitis/mastoiditis
CT brain:
Diagnosis, localisation and treatment
Sinisitis/mastoiditis
Staging, HCP, ↑ICP, edema, associated subdural empyema,
meningitis, ventriculitis, multiplicity
NCCT - Isodense / hyperdense
CECT - Smooth, thin, regular wall with decreased density both
in the centre and surrounding
37. MRI Brain
T1
Central low intensity (hyperintense to CSF)
Peripheral low intensity (vasogenic oedema)
Ring enhancement
Ventriculitis may be present, in which case hydrocephalus will commonly
also be seen
T2 / FLAIR
Central high intensity (hypointense to CSF, does not attenuate on FLAIR)
Peripheral high intensity (vasogenic oedema)
The abscess capsule may be visible as a intermediate to slightly low signal
thin rim
DWI / ADC
High DWI signal is usually present centrally
Low signal onADC
38. SWI
Low intensity rim
Complete in 75%
Smooth in 90%
Mostly overlaps with contrast enhancing rim
Dual rim sign - a hyperintense line located inside the low intensity
rim
MR perfusion - RCBV is reduced in the surrounding oedema
c.f. to both normal white matter and tumour oedema seen in high
grade gliomas
MR spectroscopy - elevation of a succinate peak is relatively
specific but not present in all abscesses ; high lactate,
acetate, alanine, valine, leucine, and isoleucine levels peak may be
present ; cho / crn and NAA peaks are reduced
49. Surgical therapy
The optimal approach to patients with bacterial brain abscess
Aspiration after bur-hole placement or complete excision after
craniotomy (no prospective trial comparing these two)
May be performed under stereotactic neuroimaging guidance
Stereotactic aspiration is a useful approach even for abscesses
located in eloquent or inaccessible regions; repeat aspiration
should be considered if the initial aspiration proves ineffective or
partially effective.
Intraoperative ultrasound - for the aspiration of small abscesses
and can delineate abscess pockets,
Recurrence rates after stereotactic aspiration range from 0-24 %.
50. Pus has been aspirated. What all
investigations are to be sent?
A. Stains
A. Gram stain
B. Acid-fast stain (AFB stain) for Mycobacterium
C. Modified acid-fast stain (for Nocardia) looking for branching acid
fast bacillus
D. Special fungal stains (e.g., methenamine silver, mucicarmine)
B. Cultures
A. Routine cultures: aerobic and anaerobic
B. Fungal culture: this is not only helpful for identifying fungal
infections, but since these cultures are kept for longer period and
any growth that occurs will be further characterized, fastidious or
indolent bacterial organisms may sometimes be identified
C. TB culture
51. What are the indications for initial
surgical treatment?
1. Significant mass effect exerted by lesion (on CT or MRI)
2. Difficulty in diagnosis (especially in adults)
3. Proximity to ventricle: indicates likelihood of intraventricular
rupture which is associated with poor outcome
4. Evidence of significantly increased intracranial pressure
5. Poor neurologic condition (patients responds only to pain, or
does not even response to pain)
6. Traumatic abscess associated with foreign material
7. Fungal abscess
8. Multiloculated abscess
9. Follow-up CT/MRI scans cannot be obtained every 1-2 weeks
52. What are the indications for complete
excision by craniotomy ?
Multiloculated abscesses in whom aspiration techniques have failed
Abscesses containing gas
Abscesses that fail to resolve
Posttraumatic abscesses that contain foreign bodies or retained
bone fragments to prevent recurrence
Abscesses that result from fistulous communications (e.g.,
secondary to trauma or congenital dermal sinuses)
Abscess localized to one lobe of the brain and contiguous with a
primary focus.
Cerebellar abscess in children
Difficulty in diagnosis
Suspected fungal abscess
53. What are the contraindications for
craniotomy and evacuation?
Abscess in the cerebritis stage
Deep-seated abscess in eloquent area
Multiple abscesses
54. Aspiration vs. Craniotomy
Craniotomy is now rarely practiced as the first line of treatment.
Aspiration repeated as necessary or with drainage, has widely replaced
attempts at complete excision.
Several reports have advocated excision as the procedure of choice
because it is often followed by a lower incidence of recurrence and
shorter hospitalization.
Xiao et al reported that favorable outcome was not significantly different
between the patients treated by excision or aspiration. However, the
mortality rate was significantly lower in the patients treated with
excision than the patients treated with aspiration.
This is probably due to the better general condition and/or more
favorable location of abscess that could be excised surgically in such
patients.
Stereotactic aspiration should be considered the treatment of choice in
all but the most superficial and the largest cerebral abscesses.
55. IV rupture with ventriculitis and HCP –
What to do?
Rapid evacuation and débridement of the abscess cavity via
urgent craniotomy
+
Ventricular drainage
+
Intravenous or intrathecal administration of appropriate
antimicrobial agents
56. When to opt for medical therapy alone?
Patients with medical conditions that increase the risk
associated with surgery
Multiple abscesses
Abscesses in a deep or dominant location
Coexisting meningitis or ependymitis
Early reduction of the abscess with clinical improvement
after antimicrobial therapy
Abscess size < 3 cm
57. What is the optimal duration of
medical treatment?
Bacterial brain abscess – 6-8 weeks IV → 2-3 months oral
antimicrobial therapy
Post-surgical excision - Courses of 3 to 4 weeks of antimicrobial
therapy
Medical therapy alone - up to 12 weeks with parenteral agents
A combination of surgical aspiration or removal of all abscesses
larger than 2.5 cm in diameter → 6 weeks or more of
antimicrobial therapy, and weekly neuroimaging to document
abscess resolution
Repeat neuroimaging studies - biweekly for up to 3 months after
completion of therapy
58. How will you follow up an abscess case
radiographically?
CT scans weekly during the course of therapy
One week after discontinuation of antibiotics
Scan one month later
Monthly or bimonthly till radiographic resolution
Time course for abscess resolution:
↓ in abscess size – 2-3 weeks after initiating therapy
Complete resolution of abscess cavity, mass effect – 3-4 months
Residual contrast enhancement – 6-9 months
60. Any role for steroids?
↓ host defense mechanisms and ↓ penetration of some antimicrobial
agents into the brain abscess cavity
May result in improvement of neurological symptoms and signs.
Therapy started in abscess patients with:
Associated edema and mass effect
Progressive neurological deterioration
Impending cerebral herniation.
Dose:
Dexamethasone, 10 mg every 6 hours is generally administered initially
and then tapered once the patient has stabilized.
The use of prolonged courses of corticosteroids is discouraged.
May also decrease contrast enhancement of the abscess capsule in the
early stages of infection, thereby being a false indicator of radiologic
improvement.
61. What is the role of anticonvulsants?
Initiated immediately and continued at least 1 year due to
high risk in the brain abscesses.
The treatment can be discontinued if no significant
epileptogenic activity can be shown in electroencephalogram
(EEG).
62. How to treat otogenic brain abscess?
Initial neurosurgical removal of abscess, which after
improvement of general condition of the patient should
be followed by radical otosurgical removal of the process
from the ear.
Otogenic brain abscess: diagnostic and treatment experience. D Djeric NArsovic V
Djukic. International Congress Series, 2003; 1240 (61-65)
Brain abscesses of otogenic origin. [Article in Serbian] NesićV1, Janosević L, Stojicić G,
Janosević L, Babac S, Sladoje R. SrpArh Celok Lek. 2002 Nov-Dec;130(11-12):389-93.
63. How to manage multiple brain
abscesses?
Incidence – 10-50%
Emergent stereotactic aspiration for all lesions > 2.5 cm diameter and
those causing mass effect, located deep in brain stem or close to
ventricular wall
If all the lesions are < 2.5 cm and not producing mass effect, the
largest one should be aspirated for diagnostic cultures.
Antibiotics withheld till culture results
Antibiotics for 3 months (Immunosuppressed – 1 yr)
Repeat surgical aspiration if
radiographic enlargement after 2 weeks of therapy
Failure to diminish in size after 4 weeks of antibiotics
Clinical deterioration
64. How to treat Nocardial brain abscess?
A sulfonamide ± trimethoprim, is recommended.
Alternative agents include minocycline,imipenem, amikacin, third-
generation cephalosporins, and linezolid
In immunocompromised patients or those in whom therapy fails
a third-generation cephalosporin or imipenem + a sulfonamide or
amikacin
Nocardia farcinica,a species that may be highly resistant to various
antimicrobial agents, successful treatment has included
moxifloxacin.
Craniotomy with total excision is difficult in patients with Nocardia
brain abscess because these abscesses are often multiloculated.
The duration of therapy - 3 to 12 months, but it should probably
be continued up to 1 year in those who are immunocompromised.
65. What are the treatment options for
fungal brain abscess?
Patients with fungal brain abscess, especially those who are
immunocompromised, have a high mortality rate despite
combined medical and surgical therapy.
Candidal brain abscess -Amphotericin B preparation + 5-
flucytosine
The therapy of choice for Aspergillus brain abscess is voriconazole.
Alternative agents include an amphotericin B preparation,
posaconazole, and itraconazole.
Itraconazole - as an extension of successful treatment rather than
as primary therapy.
Excisional surgery or drainage is a key factor in the successful
management of CNS aspergillosis.
66. CNS mucormycosis - Amphotericin B deoxycholate or a lipid
formulation of amphotericin
Correction of the underlying metabolic derangements and
aggressive surgical débridement
The etiologic agents of mucormycosis invade blood vessels,
tissue infarction occurs and impairs the delivery of antifungal
agents to the site of infection; this often leaves surgery as the
only modality that may effectively eliminate the infecting
microorganism.
In patients not responding to or intolerant of an
amphotericin B formulation, posaconazole can be used as
salvage therapy.
HBO - useful adjunct
Surgery is the cornerstone of therapy for brain abscesses
caused by Scedosporium species
Voriconazole is the agent of choice.
67. What is meant by delayed “glue
abscess”?
Delayed multiloculated abscess after embolization ofAVM
nidus
The duration of the procedure and repeated handling of the
catheters along with use of large amount foreign material or
Hysto-acryl “glue” can precipitate infection.
Cure of the lesion can only be obtained by surgical excision
of the infected and partially embolizedAVM.
Antibiotic prophylaxis with all endovascular procedures is
recommended
Mourier L, Bellec C, Lot G, Reizine D, Gelbert F, Dematons C, et al. Pyogenic parenchymatous and nidus infection after embolization
of an arteriovenous malformation: an unusual complication. Case report. Acta Neurochir (Wien) 1993;122:130-3.
Pendarkar H, KrishnamoorthyT, Purkayastha S, GuptaAK. Pyogenic cerebral abscess with discharging sinus complicating an
embolized arteriovenous malformation. J Neuroradiol 2006;33:133-8
68. What are the factors to be considered in a patient
with cyanotic heart disease developing a brain
abscess?
5-18% population with CHD. 10 times more prone. M.C –TOF
Intracardiac right to left shunt by-pass allows direct entry of blood
containing bacteria to the cerebral circulation without pulmonary
filtration.
Anaerobic streptococci (Sterile cultures are reported in 16-68%)
Cardiopulmonary risk, coagulation defects and variable degree of
immunodeficient states
A deeply located parieto-occipital abscess larger than 2 cm
diameter which causes mass effect, should be aspirated
immediately even in late cerebritits stage using stereotactic or CT
guided methods to decrease intra-cranial pressure and avoid
intraventricular rupture of brain abscess.
Intravenous Beta-lactam antibiotics are started immediately.
69. Cerebellar abscess
6-35% of all brain abscesses
Often ominously silent and carry significant mortality
Can cause sudden total occlusion of CSF pathways early in
the course of disease.
Presence of periventricular lucency is an absolute indication
of immediate ventricular drainage regardless of level of
consciousness i.e. even if patient is fully conscious.
Burr hole aspiration has emerged as a satisfactory method
70. Sequelae
30-50% of survivors are found to have neurological sequelae.
The incidence of residual neural deficits - hemiparesis,
cognitive and learning deficits in children, is less with
aspiration than excision.
About 72% of patients can have epileptic seizures upto five
years of diagnosis.This incidence is less with aspiration than
excision.
5 to 10% abscesses recur due to inadequate or inappropriate
antibiotics, failure of removal of foreign body, dural fistula or
failure of eradication of primary source.
Hydrocephalus may also develop
71. What is the difference between otogenic and odontogenic
brain abscess?
Unlike otogenic abscess, odontogenic abscess occurs as a
sequel of acute rather than chronic infection
What is the most common site of metastatic abscess?
In the distribution of MCA – Parietal & frontal (left side)
Grey-white junction – capillary flow slowest
Does a high velocity bullet injury cause an abscess?
The fragments do not present a significant risk because of
heat sterilisation and do not require removal