JOINT CARE FLOW-CHART FOR CHILDREN WITH SUPPURATIVE INTRACRANIAL INFECTIONS

Transcription

1 1 JOINT CARE FLOW-CHART FOR CHILDREN WITH SUPPURATIVE INTRACRANIAL INFECTIONS Suspected symptoms and examination All children should be managed under the joint care of Neurosurgery, General Paeds and Paediatric infectious diseases team. Depending on the suspected focus ENT should be also involved. - Admission to Nicholls ward. - All children should be handed over in the morning to the respective teams. - Refer to: - Neurosurgeons*: SHO 7223, SpR General paeds: SpR PID team: 6124, x ENT: SHO 6930 *Neurosurgeons should be contacted as soon as: The diagnosis of any suppurative collection or suspicion of it is made. Diagnosis: Bloods: FBC, LFT, CRP and blood cultures, G&S, clotting Imaging: - CT with contrast in case of: - Acute symptoms/out of hours. -MRI (first discussed with NS) (See text for further investigations to add/discussed) Cerebritis / Suppurative infection Surgical management if needed. DXM or anticonvulsant (levetiracetam) after discussion with NS. Consultants involved in the joint care: - NS: Miss. Hettige, Mr. Dabbous, MrStapleton - Hot week consultant - PID: consultant covering the week. - ENT: consultant Follow up: Ambulating (popat) on once daily iv treatment once clinically stable(2). - First MRI: 1-2 weeks after start of antibiotics. - Second MRI: 4-6 weeks after the start of treatment, before stopping or changing to orals (case of intracranial abscess) - Clinic follow up: NS and PID. (2) popat: Jaroslava.slobodova@stgeorges.nhs.uk Ceftriaxone ± Metronidazole(1) (1) Postoperative neurosurgical patients: Ceftriaxone + Vancomycin

2 2 1. INTRACRANIAL SUPURATIVE INFECTION. a. BRAIN ABSCESS Brain abscess is a focal collection within the brain parenchyma, which can arise as a complication of a variety of infections, trauma, or surgery. It requires prompt diagnosis and treatment. Neurosurgical consultation is required in all cases of brain abscesses. Pathogenesis Bacteria can invade the brain either by direct spread or through haematogenous seeding (bactereamic spread typically causes multiple lesions)(1,2). Direct spread include: - Subacute and chronic otitis media and mastoiditis (spread to the inferior temporal lobe and cerebellum) - Frontal, maxilar or ethmoid sinuses (frontal most commonly involved) - Dental infection (usually spreads to the frontal lobes) - Periorbital cellulitis. - Post-traumatic brain abscess can occasionally result from facial or dirty trauma. - Complications from neurosurgical procedures. Conditions that lead to haematogenous seeding of the brain include: - Chronic pulmonary infections, such as lung abscess and empyema, often within bronchiectasis or cystic fibrosis - Skin infections - Intra-abdominal infections - Bacterial endocarditis (brain abscess complicates 2 to 4 percent of cases) - Cyanotic congenital heart diseases (most common in children) - Intrapulmonary right-to-left shunting in patients with pulmonary arteriovenous malformations No primary site or underlying condition can be identified in 20 to 40 % of patients. There is a first stage of acute inflammation but no tissue necrosis, called cerebritis. After two to three weeks, necrosis and liquefaction occur. Microbiology Commonly isolates show multiple pathogens. Nevertheless, the most frequent causes of brain abscess are Streptococcus and Staphylococcus spp; among these species, Viridans group (S. milleri) and S. aureus (1,3,4). Gram negative bacteria are common in infants. The pathogens involved differ depending upon the site of the primary infection, the age and the immune status of the host (see table 1).

3 3 Clinical manifestations The manifestations of brain abscess initially tend to be nonspecific(1,2). Other symptoms include: - Headache (the most common symptom) - Neck stiffness (occipital lobe abscess) or changes in mental status (lethargy). - Fever (50% patients) - Focal neurologic deficits (50% patients). - Seizures (25% patients) Other signs such as third and sixth cranial nerve deficits indicate raised intracranial pressure. Papilloedema is a late manifestation usually takes several days to develop. The classic triad consisting of fever, headache, and focal neurologic deficits in brain abscesses is present in only 13-20% of patients(1,3). Diagnosis I. Imaging: - Computed tomographic (CT) scan with contrast. Include bony window. - Magnetic resonance imaging (MRI), more sensitive than CT.(3). - Echo. II. Further diagnosis: Treatment - Bloods: FBC, LFT, PCR and blood cultures (if meningitis is suspected). Laboratory tests are of limited value for the diagnosis of brain abscesses(2,5). - Lumbar puncture contraindicated in a patient with a space occupying lesion and mass effect (e.g. abscess or subdural empyema). Rarely, the CSF changes resembles bacterial meningitis, which indicates rupture of the abscess into the ventricle. Up to 24% of the patients can have a positive culture(3). - Drain cultures and histology. If risk factors, include Acid-fast bacilli (AFB) for Mycobacterium and modified AFB for Nocardia. - Serology Patients at risk, Anti-Toxoplasma, anticysticercal antibodies. - TST if risk of Tuberculosis. - Save a sample of CSF for 16S ribosomal sequencing. Drainage remains the treatment of choice for almost all brain abscesses. The choice of the type of surgical approach does not appear to be critical in determining outcome and should take into account the preference of the surgeon (6). Circumstances, drainage may be delayed or not required(2,3,7):

4 4 - Early cerebritis without evidence of cerebral necrosis - Abscesses located in vital regions of the brain or those inaccessible to aspiration. - Multiple small abscesses. - Small abscesses (< 2.5 cm) In patients treated solely medically, surgery should be reconsidered when the clinical condition is worsening or without clinical and radiological improvements within 1 2 weeks(6). Antibiotics a number of drugs can be chosen depending upon the likely origin of the abscess and the probable pathogen(s) involved. Depending on the source of infection, these antibiotics include(6,7): Source of infection Empiric therapy Oral, otogenic, or sinus source Ceftriaxone + Metronidazole Haematogenous spread (bacteraemia Ceftriaxone + Metronidazole or endocarditis) Postoperative neurosurgical patients Vancomycin + Ceftriaxone * Penetrating head trauma (unless 1 ) Ceftriaxone Unknown source Ceftriaxone + Metronidazole 1 High risk of MRSA infection Vancomycin *Meropenem if any deterioration/lack of response under the initial therapy, discusse with PID. Dosing: see table 2. Duration of therapy the duration of antibiotics for brain abscess is prolonged. U.K guidelines recommend four weeks parenteral treatment if the abscess has been drained or aspirated and six weeks if the abscess is treated without drainage(2,3,7). The duration of therapy should be guided by follow-up assessment of clinical course and imaging studies. Repeated MRI should be performed before stopping or changing to oral treatment. Unless resistances, co-amoxiclav should be the first option(1). Situations when longer treatment could be discussed: - Patients with an organized capsule with evidence of tissue necrosis - Multiloculated abscess - Lesions in vital locations such as the brain stem - Immunocompromised patient Adjuvant treatment: - Glucocorticoids (dexamethasone) can be used when substantial mass effect from oedema is demonstrated on imaging(2).

5 5 Dosing: a) Children under 35 kg body-weight: initially 16.7 mg, then 3.3 mg every 3 hours for 3 days, then 3.3 mg every 6 hours for 1 days, then 1.7 mg every 6 hours for 4 days, then decrease by 0.8 mg daily. b) Children under 35 kg body-weight: initially 20.8 mg, then 3.3 mg every 2 hours for 3 days, then 3.3 mg every 4 hours for 1 days, then 3.3 mg every 6 hours for 4 days, then decrease by 1.7 mg daily. - Antiepileptics may be required prophylactically if cortical lesions. Follow up: - Adverse outcomes are normally more common in younger children and those with low Glasgow Coma Scale at presentation (GCS <8)(1). - First MRI: 1-2 weeks after the start of treatment. - Second MRI: 4-6 weeks after the start of treatment, before stopping or changing to orals. b. SUBDURAL EMPYEMA Subdural empyema (SDE) results in a more systemic inflammatory reaction than brain abscess as there is no anatomical barrier preventing propagation within the subdural space. It is usually referred to an intracranial purulent material between the dura and arachnoid matter. Pathogenesis SDE can occur anywhere in the subdural space, but the majority are in the supratentorial compartment. Meningitis is the most common cause of SDE in infants and children under the age of 5. In older children, sinusitis and otitis media are the most common sources. When the source of SDE is sinusitis, then the frontal sinus is the most common (8 10). Microbiology There are many pathogens that can cause SDE and it depends on the route of the infection as well as the age of the patient. Under 5 years of age, the organisms are the same as for meningitis: pneumococci, meningococci, H.influezae and neonatal pathogens. Over 5 years of age, organisms are more similar to those causing brain abscesses. SDE could be also a kind of presentation of M.tuberculosis infection(5). Clinical manifestations

6 6 Infants and young children with SDE might present with high grade fever, altered mental status, meningeal irritation, seizures, and /or signs and symptoms of raised intracranial pressure or bulging fontanel(8,9). Diagnosis I. Imaging: - Computed tomographic (CT) scan with contrast shows an enhancing subdural collection. - Magnetic resonance imaging (MRI), again, more sensitive than CT, and can pick up very thin subdural empyemas. - Cranial ultrasonography is usually the first imaging mode to be done in infants (9). II. Further diagnosis: - Bloods: FBC, LFT, PCR and blood cultures, - Lumbar puncture: CSF culture is the gold standard for the diagnosis. But can be dangerous due to the mass effect of the collection and lead to brain herniation. - Serology or 16sPCR depending on diagnosis. Treatment Antibiotics-- The regimen should be chosen per route of infection; thereafter, narrow the coverage per culture identification and sensitivity, and rationalised when cultures available. If the organism is unknown, antibiotic treatment depends on the age and the suspected cause: a. Age under 5 and meningitis as the cause: Ceftriaxone 80 mg/kg/day iv. Likely already to be on antibiotics, and if sensitivities are known, change of antibiotics may not be appropriate (surgery may be what required). b. Age over 5 and caused by local spread or a de novo presentation, antibiotics should be the same as brain abscess: Ceftriaxone + Metronidazole The appropriate duration of therapy has not been studied in randomised, controlled trials, but available data suggest at least 2 weeks of intravenous therapy should be given; parenteral or oral therapy is frequently continued for up to a total of 6 weeks of antimicrobials (9,10); with or without associated osteomyelitis. Adjunctive care includes prophylactic anticonvulsants.

7 7 Surgery-- Surgical treatment is usually required. This is often in the form of craniotomy as access to the whole hemisphere. One of the surgical indications is progressive SDE accumulation despite antibiotic treatment. The other surgical indication would be the presence of high intracranial pressure due to the mass effect of SDE, requiring craniotomy. Washout of the adjacent pus filled sinus, e.g. frontal or mastoid air cells may also be required to help to treat the cause and to prevent recurrence. Follow up-- similar to abscess, a contrasted MRI scan should be performed in time to ensure resolution and no recurrence of the lesions. TABLES Table 1. Microbiology of brain abscesses t Source of infection Paranasal sinuses Odontogenic sources Otogenic sources Lungs Urinary tract Penetrating head trauma Neurosurgical procedures Endocarditis Cardiac malformations Immunocompromised Microorganisms Streptococcus spp (especially S. milleri), Haemophilus spp, Bacteroides spp, Fusobacterium spp Streptococcus spp, Bacteroides spp, Prevotella spp, Fusobacterium spp, Haemophilus spp Enterobacteriaceae, Streptococcus spp, Pseudomonas aeruginosa, Bacteroides spp Streptococcus spp, Fusobacterium spp, Actinomyces spp Pseudomonas aeruginosa, Enterobacter spp Staphylococcus aureus, Enterobacter spp, Clostridium spp Staphylococcus spp, Streptococcus spp, Pseudomonas aeruginosa, Enterobacter spp Viridans streptococci, S. aureus Streptococcus spp To consider: Toxoplasma gondii (cell-mediated immunedeficiencies, HIV); Listeria (corticosteroids); Nocardia asteroides, Aspergillus, Cryptococcus neoformans, and Coccidioides immitis Table 2. Antibiotic dosing Ceftriaxone Metronidazol Vancomycin Meropenem References: 80 mg/kg iv (max 4 g) daily 7.5 mg/kg iv (max. 400mg) TDS 15 mg/kg iv (max. 3g) QDS Levels should be above 15 (15-20). 40 mg/kg iv (max. 2g) TDS

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