Download presentation
Presentation is loading. Please wait.
Published byJonathan Hancock Modified over 9 years ago
1
good morning
2
CNS Infection Dr. Ali Omar Saadoon Neurosurgeon 2013-2014
3
Brain abscess 8% of all intracranial space-occupying lesions %2 (most industrialized nations) Male: female ratio is 1.5-3:1
6
RISK FACTORS pulmonary abnormalities (infection, AV- fistulas..., congenital cyanotic heart disease bacterial endocarditis, penetrating head trauma chronic sinusitis or otitis media, immune compromise. dental procedures
7
The microorganism may reach the brain by different mechanisms: 1.Hematogenous spread from remote reservoir of infection( most common) Adults; lung abscess (the most common), bronchiectasis and empyema children; congenital cyanotic heart disease with R to L shunt Immunosuppression (AIDS-toxoplasmosis) pulmonary arteriovenous fistulas bacterial endocarditis dental abscess GI infections: pelvic infections may gain access to the brain via Batson's plexus In patients with septic embolization, the risk of cerebral abscess formation is elevated in areas of previous infarction or ischemia
8
2.Contiguous site of infection (infected sinus,naso/oropharynx) e.g. otitis media, mastoiditis,sinusitis,osteomyelitis,dental abscess. Rare in infants because they lack aerated paranasal and mastoid air cells. This route has become less common due to improved treatment of sinus disease. 3. Direct inoculation from penetrating trauma or during neurosurgical procedures.(trauma, iatrogenic…post operative, congenital defect….dermal sinus
9
Prior to 1980, the most common source of cerebral abscess was from contiguous spread. Now, hematogenous dissemination is the most common vector. In some cases no source can be identified
10
The responsible microorganism Otitis media : anaerobic streptococci, Haemophilus and Gram-negative anaerobic Sinusitis: streptococcus milleri and staphylococcus Traumatic: staphylococcus Hematogenous spread : various organism are involved
11
Clinical features features of raised intracranial pressure Seizure meningeal irritation focal signs rapid progression Systemic features of infection are frequently absent
12
Investigation leucocytosis, raised ESR, and C-reactive protein ( may initially be normal) CT and MRI of brain: may show ring enhancing mass lesion (differ with the stage of the abscess) CXR and chest CT (if indicated) to look for pulmonary source. Cardiac echo.
13
Treatment identify the bacterial organism IV antibiotics(6-8 wks) surgery (drain or excision) treat the cause anticonvulsant therapy
14
Surgical treatment Needle aspiration : may be performed under local anesthesia if necessary, may be the only surgical treatment required but some time must be followed with excision, recommended with multiple or deep lesion, or with thin walled Surgical excision: abscess is removed as any well-encapsulated tumor; the length of time on antibiotics can be shortened.
16
complications With abscess rupture : ventriculitis, meningitis, venous sinus thrombosis CSF obstruction…hydrocephalus Transtentorial herniation
17
prognosis Mortality with appropriate therapy—10% Permanent deficit ---50%
18
subdural empyemas uncommon sinusitis or mastoiditis these patients are systemically unwell with rapidly progressive neurological signs a depressed level of consciousness and hemiparesis Epilepsy
20
Treatment Like intracranial abscess, complications include refractory status epilepticus and cortical venous sinus thrombosis
21
Posttraumatic meningitis Occurs in 1-20% of patients with moderate to severe head injuries 75% of cases have basal skull fracture and 58% had CSF rhinorrhea.
22
Treatment Conservative treatment: antibiotics are used according to the culture and sensitivity tests. There is high rate of infection with organisms indigenous to the nasal cavity surgical treatment : repair of the dural tear.
23
Osteomyelitis of the skull The skull is very resistant to osteomyelitis, hematogenous infection is rare. usually due to infected air sinus, penetrating trauma or from scalp abscess
24
Treatment Antibiotics alone are rarely curative. Treatment is usually surgical debridement of infected skull (craniectomy). and 6-12 weeks of antibiotics. if no sings of infection a cranioplasty may be performed after 6 months. Post- operative.
25
Spinal infection
26
Spine infection 1. vertebral osteomyelitis(spondylitis) a. pyogenic b. nonpyogenic e.g. tuberculous spondylitis 2. epidural abscess 3. discitis a. spontaneous b. post-operative
27
Spinal tuberculosis Pott's disease more commone in third world countries. Is usually symptomatic for many months and affect more than one level.the most common levels involved are the lower thoracic and upper lumbar levels. Has a predilection for vertebral body, sparing the posterior elements. Psoas abscess is common. definitive diagnosis required a biopsy (may be done percutaneously) to identify the acid fast bacilli. Good results may be obtained with either medical treatment or surgery. Surgery is needed when definite cord compression is documented or for complication such as abscess or sinus formation.
32
Hydatid Cyst disease Caused by encysted larvae of the dog tapeworm Echinococcus granulosa CNS involvement occurs in only 3% Primary cysts are usually solitary, secondary cysts (e.g. from embolization from cardiac cysts that rupture or from iatrogenic rupture of cerebral cysts) are usually multiple. Presentation : ↑ ICP,seizures, or focal deficit. Treatment : surgical removal of intact cyst.
39
Brain Death Neurologically Determined Death
40
Brain death Brain death defined as total and irreversible loss of function of the cerebral hemispheres and the brainstem. The patient may continue to have some spinal reflex activity, which dose not rule out the patient brain death. If ventilation and circulation are maintained artificially, the heart, kidneys, and liver may continue to function for some hours or days, but after brainstem death has occurred cardiac arrest will follow within 2 weeks.
41
Diagnosis of brain death The reversible causes of coma should be excluded (like hypothermia(tempreture should be above 32C),no electrolyte/acid- base/endocrine disturbance, pentobarbital coma, neuromuscular blocking agents, shock or intoxications). A committee should perform the testes. The findings ….?
42
The findings no motor response to deep central pain fixed pupils : absent light reflex absent corneal reflex absent oculocephalic reflex(doll's eyes) absent oculovestibular reflex (cold water calorics) no motor responses within the cranial nerve distribution can be elicited by adequate stimulation of any somatic area. no cough and gag reflex no spontaneous respiration( disconnecting the patient from the respirator to allow the Pco2 to rise to 60 mmHg) EEG dose not detect brainstem activity brain arteriogram show total lack of cerebral blood flow
50
Thanks. Questions ?
Similar presentations
© 2024 SlidePlayer.com. Inc.
All rights reserved.