Subdural empyema
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]; Anthony Gallo, B.S. [3]
Synonyms and keywords: Circumscript meningitis; Pachymeningitis interna; Purulent pachymeningitis; Subdural abscess; SDE
Overview
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]; Anthony Gallo, B.S. [3]
Overview
Subdural empyema is a life-threatening infection, consisting of a localized collection of purulent material, usually unilateral, between the dura mater and the arachnoid mater. Subdural empyema may be classified according to location of the infection into 2 groups: intracranial and spinal, with intracranial being the more common of the two groups, accounting for 95% of subdural empyema patients.[1][2] Subdural empyema accounts for approximately 15-25% of focal central nervous system infections. In 2014, the incidence of subdural empyema was estimated to be less than 1 case case per 100,000 individuals, with a male predominance.[3] The most common pathogens in intracranial subdural empyema are anaerobic and microaerophilic Streptococci, compared to spinal subdural epmyema, which can be caused by either Streptococci or Staphylococcus aureus.[2] If left untreated, subdural empyema frequently evolves into severe fever, headache, nausea, vomiting, seizures, coma, and subsequent mortality. Complications to subdural empyema include status epilepticus, neurological deficits, and thrombosis. Prognosis is generally good with antimicrobial therapy. Physical examination of patients with subdural empyema is usually remarkable for fever, facial pain, and altered mental status.[4][5][6] MRI is the primary imaging study of epidural abscess, with CT scan as a secondary alternative. Treatment of subdural empyema requires a combined medical and surgical approach. In order to evacuate the pus, burr hole placement or craniotomy may be used to treat the subdural empyema. The preferred surgical mainstay of treatment for subdural empyema is craniotomy.
Historical Perspective
In 1869, subdural empyema was first operated on by François Gigot de la Peyronie.[7] The first detailed description of the disease was by Cyril Brian Courville in 1939.
Classification
Subdural empyema may be classified according to location of the infection into 2 groups: intracranial and spinal.[1][2]
Pathophysiology
Subdural empyema is a localized collection of pus between the dura mater and arachnoid mater, occurring in either the intracranial space or the spinal canal.[8][1][2] Subdural empyema generally follows the same progression for both intracranial and spinal subtypes, spreading via blood or from nearby infection. Bacterial infections of the skull or air sinuses can spread to the subdural space, producing a subdural empyema. The underlying arachnoid and subarachnoid spaces are usually unaffected, but a large subdural empyema may produce a mass effect.
Causes
Common causes of subdural empyema include Streptococci, Staphylococci, and other Gram-negative bacilli.[1] In children, the majority of cases of subdural empyema occur due to meningitis, while in adults the most common causes are sinusitis, otitis media, mastoiditis, and trauma.[1][9]
Differentiating Subdural Empyema from Other Diseases
Subdural empyema must be differentiated from other diseases that cause fever, headache, focal neurological signs, seizures, and altered mental status, such as subdural hematoma, brain abscess, and bacterial meningitis. These conditions may be distinguished from subdural empyema by their clinical findings, brain imaging findings, and laboratory studies.
Epidemiology and Demographics
Subdural empyema accounts for approximately 15-25% of focal central nervous system infections. In 2014, the incidence of subdural empyema was estimated to be less than 1 case per 100,000 individuals.[3] Prior to antibiotics, the case fatality rate of subdural empyema was estimated to be near 100%. However, with antibiotics, the current rate is estimated between 10-20%.[10] The disease usually occurs in children and young adults (70% cases occurring in the second and third decades of life), being more frequent in men than women, possibly due to sex-related differences in sinus anatomy.
Risk Factors
Common risk factors in the development of subdural empyema are meningitis, sinusitis, otitis, mastoiditis, immunodeficiency, head trauma, and lumbar puncture.
Natural History, Complications, and Prognosis
If left untreated, subdural empyema frequently evolves into severe fever, headache, nausea, vomiting, seizures, coma, and subsequent mortality. Complications to subdural empyema include status epilepticus, neurological deficits, and thrombosis. Prognosis is generally good with antimicrobial therapy.
Diagnosis
History and Symptoms
If possible, a detailed and thorough history from the patient is necessary. Specific areas of focus when obtaining a history from the patient include prior neurosurgery, sinusitis, or mastoiditis. Common symptoms of subdural empyema include headache, altered mental status, vomiting, and seizures.
Physical Examination
Physical examination of patients with subdural empyema is usually remarkable for fever, facial pain, and altered mental status.[4][5][6]
Laboratory Findings
Laboratory findings associated with subdural empyema are generally unspecific. Often, elevated inflammatory markers are present, including:[1][4]
Lumbar Puncture
Lumbar puncture is not diagnostic of subdural empyema. Lumbar puncture is an invasive procedure which is contraindicated in case of suspicion of subdural empyema and increased intracranial pressure, due to risk of brain herniation, and mortality.[2]
X ray
Generally, x ray is not helpful in the diagnosis of subdural empyema.
CT
Head CT scan may be helpful in the diagnosis of subdural empyema. CT scan is secondary to MRI for subdural empyema imaging. Findings on CT scan suggestive of subdural empyema include a crescentic shape, although collection pockets may appear bi-convex. A surrounding membrane that enhances intensely and uniformly following contrast administration is typically identified.[11]
MRI
MRI in the optimal imaging study in the diagnosis of subdural empyema. Findings on MRI suggestive of subdural empyema are similar to those on CT scan, and include a crescent or bi-convex shaped collection. A surrounding membrane that enhances intensely and uniformly following gadolinium enhancement is typically identified and may also demonstrate restricted diffusion.[11]
Treatment
Medical Therapy
Subdural empyema is a medical emergency and requires prompt treatment. Treatment of subdural empyema requires a combined medical and surgical approach. Empiric antimicrobial therapy depends on the location of the infection (intracranial vs. spinal) and whether it was community-acquired or hospital-acquired. The clinical symptoms may be mild and unspecific initially.
Surgery
Subdural empyema is a neurosurgical condition, which requires emergency surgical drainage and subsequent medical therapy. In order to evacuate the pus, burr hole placement or craniotomy may be used to treat the subdural empyema. The preferred surgical mainstay of treatment for subdural empyema is craniotomy. A wide craniotomy allows a wide exposure of the area, adequate exploration, and better evacuation of the infected material and decompression of the underlying cerebral hemisphere, thereby improving the outcome.[1][2]
Prevention
Effective measures for the primary prevention of subdural empyema include rapid treatment of inflammatory diseases of the head and prevention of trauma. Secondary prevention strategies following subdural empyema include treatment and management of existing infection.
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Agrawal, Amit; Timothy, Jake; Pandit, Lekha; Shetty, Lathika; Shetty, J.P. (2007). “A Review of Subdural Empyema and Its Management”. Infectious Diseases in Clinical Practice. 15 (3): 149–153. doi:10.1097/01.idc.0000269905.67284.c7. ISSN 1056-9103.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Greenlee JE (2003). “Subdural Empyema”. Curr Treat Options Neurol. 5 (1): 13–22. PMID 12521560.
- ↑ 3.0 3.1 French H, Schaefer N (2014). “Intracranial Subdural Empyema: A 10-Year Case Series”. Oschner J. 12 (2). doi:10.1002/bip.360240911. PMID PMC4052585 Check
|pmid=value (help). - ↑ 4.0 4.1 4.2 Hendaus, Mohammed A. (2013). “Subdural Empyema in Children”. Global Journal of Health Science. 5 (6). doi:10.5539/gjhs.v5n6p54. ISSN 1916-9744.
- ↑ 5.0 5.1 Bruner DI, Littlejohn L, Pritchard A (2012). “Subdural empyema presenting with seizure, confusion, and focal weakness”. West J Emerg Med. 13 (6): 509–11. doi:10.5811/westjem.2012.5.11727. PMC 3555596. PMID 23358438.
- ↑ 6.0 6.1 Mandell, Gerald L.; Bennett, John E. (John Eugene); Dolin, Raphael. (2010). Mandell, Douglas, and Bennett’s principles and practice of infectious disease. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0-443-06839-9.
- ↑ Khan M, Griebel R (1984). “Subdural empyema: a retrospective study of 15 patients”. Can J Surg. 27 (3): 283–5, 288. PMID 6144382.
- ↑ Longo, Dan L. (Dan Louis) (2012). Harrison’s principles of internal medici. New York: McGraw-Hill. ISBN 978-0-07-174889-6.
- ↑ Quraishi H, Zevallos JP (2006). “Subdural empyema as a complication of sinusitis in the pediatric population”. Int. J. Pediatr. Otorhinolaryngol. 70 (9): 1581–6. doi:10.1016/j.ijporl.2006.04.007. PMID 16777239. Unknown parameter
|month=ignored (help) - ↑ Nathoo N, Nadvi SS, van Dellen JR, Gouws E (1999). “Intracranial subdural empyemas in the era of computed tomography: a review of 699 cases”. Neurosurgery. 44 (3): 529–35, discussion 535–6. PMID 10069590.
- ↑ 11.0 11.1 Subdural empyema. Radiopaedia.org (2015). http://radiopaedia.org/articles/subdural-empyema Accessed on December 4, 2015.
Historical Perspective
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]; Anthony Gallo, B.S. [3]
Overview
In 1869, subdural empyema was first operated on by François Gigot de la Peyronie.[1] The first attempted detailed description of the disease was by Cyril Brian Courville in 1939.
Historical Perspective
- In 1869, subdural empyema was first operated on by François Gigot de la Peyronie[1]
- In 1939, the first attempted detailed description of the disease was by Cyril Brian Courville, who additionally referred to the disease as subdural abscess, pachymeningitis interna, purulent pachymeningitis, and circumscript meningitis[2]
- Historically, treatment was surgical, contrary to the present antimicrobial approach. Before the discovery of antibiotics, the mortality rate of patients with subdural empyema was near 100%, however the development of antimicrobial therapies have dramatically decreased the estimate to between 6-35%.[2]
References
- ↑ 1.0 1.1 Khan M, Griebel R (1984). “Subdural empyema: a retrospective study of 15 patients”. Can J Surg. 27 (3): 283–5, 288. PMID 6144382.
- ↑ 2.0 2.1 Agrawal, Amit; Timothy, Jake; Pandit, Lekha; Shetty, Lathika; Shetty, J.P. (2007). “A Review of Subdural Empyema and Its Management”. Infectious Diseases in Clinical Practice. 15 (3): 149–153. doi:10.1097/01.idc.0000269905.67284.c7. ISSN 1056-9103.
Classification
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]; Anthony Gallo, B.S. [3]
Overview
Subdural empyema may be classified according to location of the infection into 2 groups: intracranial and spinal.
Classification
Subdural empyema may be classified according to location of the infection into 2 groups: intracranial and spinal.[1][2]
Intracranial subdural empyema
Spinal subdural empyema
References
- ↑ 1.0 1.1 1.2 Agrawal, Amit; Timothy, Jake; Pandit, Lekha; Shetty, Lathika; Shetty, J.P. (2007). “A Review of Subdural Empyema and Its Management”. Infectious Diseases in Clinical Practice. 15 (3): 149–153. doi:10.1097/01.idc.0000269905.67284.c7. ISSN 1056-9103.
- ↑ 2.0 2.1 2.2 Greenlee JE (2003). “Subdural Empyema”. Curr Treat Options Neurol. 5 (1): 13–22. PMID 12521560.
Pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]; Anthony Gallo, B.S. [3]
Overview
Subdural empyema is a localized collection of pus between the dura mater and arachnoid mater, which occurs in either the intracranial space or the spinal canal.[1][2][3] Subdural empyema generally follows the same progression for both intracranial and spinal subtypes, spreading via blood or from nearby infection.
Pathophysiology
Subdural empyema is a localized collection of pus between the dura mater and arachnoid mater, which occurs in either the intracranial space or the spinal canal.[1][2][3]
Intracranial Subdural Empyema
Intracranial subdural empyema is usually unilateral, and affects the base of the brain, its convexity, the inter-hemispheric fissure along the falx cerebri, or the posterior fossa. The anatomy of the meningeal membranes dictate the course and characteristics of the disease. The dura mater and the arachnoid mater, which define the initial limits of the empyema, are joined only at the base of the brain, along the falx cerebri and at the tentorium cerebelli. This virtual space between these two meningeal membranes creates the potential for the infection to spread along the cerebral hemisphere, inter-hemispheric fissure, and posterior cranial fossa.
Intracranial subdural empyema’s origin generally depends on the age of the individual. In younger children, the empyema most commonly results from complications of purulent meningitis, while in older children and adults, it most commonly results from complications of sinusitis, otitis media, or mastoiditis. In the case of sinusitis, the frontal sinus is the most commonly affected sinus, followed by the ethmoidal, sphenoidal, and maxillary sinuses. The infection may then spread in two ways:[1][2][3][4][5][6]
- Blood, via retrograde infection, from thrombophlebitis of mucosal veins, which drain the sinuses
- Direct contact via:
- Bone erosion and Haversian canals in bone, as a complication of osteomyelitis
- Mastoid and middle ear by erosion of the tegmen tympani
- Frontal air sinus by erosion in its posterior wall
- Neurosurgical procedures, such as subdural hematoma drainage, craniotomy, and intracranial pressure monitoring
- Head trauma
- Bacteremic seeding of an previous subdural hematoma
The subdural empyema causes an inflammatory reaction in the subdural space, which may be accompanied by cerebrospinal fluid pleocytosis and encephalitis. The venous extension of the infection may lead to hemorrhagic infarction or superficial abscess. Next, cerebral edema and hydrocephalus may develop, which combined with the empyema, creates a mass effect that increases intracranial pressure, and leads to transtentorial herniation, brainstem compression, and death.[3][6] The most common pathogens in the intracranial type are:
Spinal Subdural Empyema
Spinal subdural empyema is more rare compared to intracranial. This type of infection follows a similar pathophysiology to intracranial subdural empyema. Potential sources of spread of infection include:
Spinal subdural empyemas are generally caused by Streptococci or Staphylococcus aureus.[3]
References
- ↑ 1.0 1.1 1.2 Longo, Dan L. (Dan Louis) (2012). Harrison’s principles of internal medici. New York: McGraw-Hill. ISBN 978-0-07-174889-6.
- ↑ 2.0 2.1 2.2 Agrawal, Amit; Timothy, Jake; Pandit, Lekha; Shetty, Lathika; Shetty, J.P. (2007). “A Review of Subdural Empyema and Its Management”. Infectious Diseases in Clinical Practice. 15 (3): 149–153. doi:10.1097/01.idc.0000269905.67284.c7. ISSN 1056-9103.
- ↑ 3.0 3.1 3.2 3.3 3.4 Greenlee JE (2003). “Subdural Empyema”. Curr Treat Options Neurol. 5 (1): 13–22. PMID 12521560.
- ↑ Hendaus MA (2013). “Subdural empyema in children”. Glob J Health Sci. 5 (6): 54–9. doi:10.5539/gjhs.v5n6p54. PMID 24171874.
- ↑ Kapu, Ravindranath; Pande, Anil; Ramamurthi, Ravi; Vasudevan, MC (2013). “Primary interhemispheric subdural empyemas: A report of three cases and review of literature”. Indian Journal of Neurosurgery. 2 (1): 66. doi:10.4103/2277-9167.110227. ISSN 2277-9167.
- ↑ 6.0 6.1 Courville, C. B. (1944). “SUBDURAL EMPYEMA SECONDARY TO PURULENT FRONTAL SINUSITIS: A CLINICOPATHOLOGIC STUDY OF FORTY-TWO CASES VERIFIED AT AUTOPSY”. Archives of Otolaryngology – Head and Neck Surgery. 39 (3): 211–230. doi:10.1001/archotol.1944.00680010224003. ISSN 0886-4470.
Causes
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]; Anthony Gallo, B.S. [3]
Overview
Common causes of subdural empyema include Streptococci, Staphylococci, and other Gram-negative bacilli.[1] In children, the majority of cases of subdural empyema occur due to meningitis, while in adults the most common causes are sinusitis, otitis media, mastoiditis, and trauma.[1][2]
Causes
Life Threatening Causes
Subdural empyema is a life-threatening condition and must be treated as such irrespective of the causes. Life-threatening conditions may result in mortality or permanent disability within 24 hours if left untreated.
Common Causes
Adults
Intracranial subdural empyema [1][3][4]
The most common cause of subdural empyema in adults is the complication of an infection of the air sinuses: frontal, ethmoid, sphenoid, and maxillary. The causative organisms of the empyema are similar to those causing the infection of the sinuses. Generally multiple organisms are present in the empyema, where anaerobes are almost always an important agent.[3][4] Common causative agents include:
Spinal Subdural Empyema [1][3]
Children
The most common cause of subdural empyema in children is occurs as a complication of meningitis. The agents isolated from the pus, are usually similar to the ones causing the meningitis.[3][5] Common causative agents include:
- Haemophilus influenzae
- Streptococcus pneumoniae
- Nontyphoidal Salmonella
Adults and Children
Common causative agents in trauma include:
- Coagulase negative strains of Staphylococcus
- Anaerobes
- Gram-negative microbes
Common causative agents in neurosurgical procedures include:
Causes by Organ System
Causes in Alphabetical order
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|
|
References
- ↑ 1.0 1.1 1.2 1.3 Agrawal, Amit; Timothy, Jake; Pandit, Lekha; Shetty, Lathika; Shetty, J.P. (2007). “A Review of Subdural Empyema and Its Management”. Infectious Diseases in Clinical Practice. 15 (3): 149–153. doi:10.1097/01.idc.0000269905.67284.c7. ISSN 1056-9103.
- ↑ Quraishi H, Zevallos JP (2006). “Subdural empyema as a complication of sinusitis in the pediatric population”. Int. J. Pediatr. Otorhinolaryngol. 70 (9): 1581–6. doi:10.1016/j.ijporl.2006.04.007. PMID 16777239. Unknown parameter
|month=ignored (help) - ↑ 3.0 3.1 3.2 3.3 Greenlee JE (2003). “Subdural Empyema”. Curr Treat Options Neurol. 5 (1): 13–22. PMID 12521560.
- ↑ 4.0 4.1 Yoshikawa TT, Chow AW, Guze LB (1975). “Role of anaerobic bacteria in subdural empyema. Report of four cases and review of 327 cases from the English literature”. Am J Med. 58 (1): 99–104. PMID 234678.
- ↑ Mandell, Gerald L.; Bennett, John E. (John Eugene); Dolin, Raphael. (2010). Mandell, Douglas, and Bennett’s principles and practice of infectious disease. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0-443-06839-9.
Differentiating Subdural Empyema from other diseases
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]; Anthony Gallo, B.S. [3]
Overview
Subdural empyema must be differentiated from other diseases that cause fever, headache, focal neurological signs, seizures, and altered mental status, such as subdural hematoma, brain abscess, and bacterial meningitis. These conditions may be distinguished from subdural empyema by their clinical findings, brain imaging findings, and laboratory studies.
Differential Diagnosis
Subdural empyema must be differentiated from other diseases that cause fever, headache, focal neurological signs, seizures, and altered mental status, including:[1][2]
| Disease | Findings |
|---|---|
| Subdural hematoma | Presents with an accumulation of blood in the subdural space, which frequently surges in the presence of trauma; it may cause an increase of intracranial pressure causing compression and damage to the brain. The acute form of this condition is considered a medical emergency. |
| Brain abscess | Presents with an abscess in the brain caused by the inflammation and accumulation of infected material from local or remote infectious areas of the body; the infectious agent may also be introduced as a result of head trauma or neurological procedures. |
| Bacterial meningitis | Presents with inflammation of the meninges, which may develop in the setting of an infection, physical injury, cancer, or certain drugs; it may have an indolent evolution, resolving on its own, or may present as an rapidly evolving inflammation, causing neurologic damage and possible mortality. |
| Viral encephalitis | Presents with acute inflammation of the brain, caused by a viral infection; it may complicate into severe brain damage as the inflamed brain pushes against the skull, potentially leading to mortality. |
| Epidural abscess | Presents with an abscess in the epidural space, between the vertebrae and the dura mater of the spinal canal; it may complicate into spinal cord dysfunction, leading to paralysis. |
| Cerebral thrombophlebitis | Presents with inflammation of a cerebral vein, related to a blood clot or thrombus; it can cause chronic pain, leg swelling, and pulmonary embolism. |
| Superior sagittal sinus thrombosis | Presents with thrombosis affecting the dural venous sinuses, which drain blood from the brain; it can cause headaches, fever, and increased intracranial pressure. |
| Acute disseminated encephalomyelitis | Presents with scattered foci of demyelination and perivenular inflammation; it can cause focal neurological signs and decreased ability to focus. |
| Diseases | Diagnostic tests | Physical Examination | Symptoms | Past medical history | Other Findings | |||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Na+, K+, Ca2+ | CT /MRI | CSF Findings | Gold standard test | Neck stiffness | Motor or Sensory deficit | Papilledema | Bulging fontanelle | Cranial nerves | Headache | Fever | Altered mental status | |||
| Brain tumour[3][4] | ✔ | Cancer cells[5] | MRI | ✔ | ✔ | ✔ | ✔ | ✔ | ✔ | Cachexia, gradual progression of symptoms | ||||
| Delirium tremens | ✔ | Clinical diagnosis | ✔ | ✔ | ✔ | ✔ | ✔ | ✔ | Alcohol intake, sudden witdrawl or reduction in consumption | Tachycardia, diaphoresis, hypertension, tremors, mydriasis, positional nystagmus, | ||||
| Subarachnoid hemorrhage[6] | ✔ | Xanthochromia[7] | CT scan without contrast[8][9] | ✔ | ✔ | ✔ | ✔ | ✔ | ✔ | ✔ | ✔ | Trauma/fall | Confusion, dizziness, nausea, vomiting | |
| Stroke | ✔ | Normal | CT scan without contrast | ✔ | ✔ | ✔ | ✔ | ✔ | TIAs, hypertension, diabetes mellitus | Speech difficulty, gait abnormality | ||||
| Neurosyphilis[10][11] | ✔ | ↑ Leukocytes and protein | CSF VDRL-specifc
CSF FTA-Ab -sensitive[12] |
✔ | ✔ | ✔ | ✔ | ✔ | ✔ | Unprotected sexual intercourse, STIs | Blindness, confusion, depression,
Abnormal gait | |||
| Viral encephalitis | ✔ | Increased RBCS or xanthochromia, mononuclear lymphocytosis, high protein content, normal glucose | Clinical assesment | ✔ | ✔ | ✔ | ✔ | ✔ | ✔ | ✔ | Tick bite/mosquito bite/ viral prodome for several days | Extreme lethargy, rash hepatosplenomegaly, lymphadenopathy, behavioural changes | ||
| Herpes simplex encephalitis | ✔ | Clinical assesment | ✔ | ✔ | ✔ | ✔ | ✔ | History of hypertension | Delirium, cortical blindness, cerebral edema, seizure | |||||
| Wernicke’s encephalopathy | Normal | ✔ | ✔ | ✔ | History of alcohal abuse | Ophthalmoplegia, confusion | ||||||||
| CNS abscess | ✔ | ↑ leukocytes >100,000/ul, ↓ glucose and ↑ protien, ↑ red blood cells, lactic acid >500mg | Contrast enhanced MRI is more sensitive and specific,
Histopathological examination of brain tissue |
✔ | ✔ | ✔ | ✔ | ✔ | ✔ | ✔ | History of drug abuse, endocarditis, ↓ immune status | High grade fever, fatigue,nausea, vomiting | ||
| Drug toxicity | ✔ | ✔ | Lithium, Sedatives, phenytoin, carbamazepine | |||||||||||
| Conversion disorder | Diagnosis of exclusion | ✔ | ✔ | ✔ | ✔ | ✔ | Tremors, blindness, difficulty swallowing | |||||||
| Electrolyte disturbance | ↓ or ↑ | Depends on the cause | ✔ | ✔ | Confusion, seizures | |||||||||
| Febrile convulsion | Not performed in first simple febrile seizures | Clinical diagnosis and EEG | ✔ | ✔ | ✔ | ✔ | Family history of febrile seizures, viral illness or gastroenteritis | Age > 1 month, | ||||||
| Subdural empyema | ✔ | Clinical assesment and MRI | ✔ | ✔ | ✔ | ✔ | ✔ | ✔ | History of relapses and remissions | Blurry vision, urinary incontinence, fatigue | ||||
| Hypoglycemia | ↓ or ↑ | Serum blood glucose | ✔ | ✔ | ✔ | History of diabetes | Palpitations, sweating, dizziness, low serum, glucose | |||||||
References
- ↑ Agrawal, Amit; Timothy, Jake; Pandit, Lekha; Shetty, Lathika; Shetty, J.P. (2007). “A Review of Subdural Empyema and Its Management”. Infectious Diseases in Clinical Practice. 15 (3): 149–153. doi:10.1097/01.idc.0000269905.67284.c7. ISSN 1056-9103.
- ↑ Longo, Dan L. (Dan Louis) (2012). Harrison’s principles of internal medici. New York: McGraw-Hill. ISBN 978-0-07-174889-6.
- ↑ Soffer D (1976) Brain tumors simulating purulent meningitis. Eur Neurol 14 (3):192-7. PMID: 1278192
- ↑ Invalid
<ref>tag; no text was provided for refs namedpmid3883130 - ↑ Weston CL, Glantz MJ, Connor JR (2011). “Detection of cancer cells in the cerebrospinal fluid: current methods and future directions”. Fluids Barriers CNS. 8 (1): 14. doi:10.1186/2045-8118-8-14. PMC 3059292. PMID 21371327.
- ↑ Yeh ST, Lee WJ, Lin HJ, Chen CY, Te AL, Lin HJ (2003) Nonaneurysmal subarachnoid hemorrhage secondary to tuberculous meningitis: report of two cases. J Emerg Med 25 (3):265-70. PMID: 14585453
- ↑ Lee MC, Heaney LM, Jacobson RL, Klassen AC (1975). “Cerebrospinal fluid in cerebral hemorrhage and infarction”. Stroke. 6 (6): 638–41. PMID 1198628.
- ↑ Birenbaum D, Bancroft LW, Felsberg GJ (2011). “Imaging in acute stroke”. West J Emerg Med. 12 (1): 67–76. PMC 3088377. PMID 21694755.
- ↑ DeLaPaz RL, Wippold FJ, Cornelius RS, Amin-Hanjani S, Angtuaco EJ, Broderick DF; et al. (2011). “ACR Appropriateness Criteria® on cerebrovascular disease”. J Am Coll Radiol. 8 (8): 532–8. doi:10.1016/j.jacr.2011.05.010. PMID 21807345.
- ↑ Liu LL, Zheng WH, Tong ML, Liu GL, Zhang HL, Fu ZG; et al. (2012). “Ischemic stroke as a primary symptom of neurosyphilis among HIV-negative emergency patients”. J Neurol Sci. 317 (1–2): 35–9. doi:10.1016/j.jns.2012.03.003. PMID 22482824.
- ↑ Berger JR, Dean D (2014). “Neurosyphilis”. Handb Clin Neurol. 121: 1461–72. doi:10.1016/B978-0-7020-4088-7.00098-5. PMID 24365430.
- ↑ Ho EL, Marra CM (2012). “Treponemal tests for neurosyphilis–less accurate than what we thought?”. Sex Transm Dis. 39 (4): 298–9. doi:10.1097/OLQ.0b013e31824ee574. PMC 3746559. PMID 22421697.
Epidemiology and Demographics
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]; Anthony Gallo, B.S. [3]
Overview
Subdural empyema accounts for approximately 15-25% of focal central nervous system infections. In 2014, the incidence of subdural empyema was estimated to be less than 1 case per 100,000 individuals.[1] Prior to antibiotics, the case fatality rate of subdural empyema was estimated to be near 100%. However, with antibiotics, the current rate is estimated between 10-20%.[2] The disease usually occurs in children and young adults (70% cases occurring in the second and third decades of life), being more frequent in men than women, possibly due to sex-related differences in sinus anatomy.
Epidemiology and Demographics
Incidence
In 2014, the incidence of subdural empyema was estimated to be less than 1 case per 100,000 individuals.[1]
Case Fatality Rate
Prior to antibiotics, the case fatality rate of subdural empyema was estimated to be near 100%. However, with antibiotics, the current rate is estimated between 10-20%.[2]
Age
Subdural empyema may affect patients of any age group.[1] Subdural empyema most commonly affects individuals younger than 20 years of age, as approximately 70% of cases occur in the second and third decades of life.[3]
Gender
Males are more commonly affected with subdural empyema name than females. The male to female ratio is approximately 6 to 1.[2]
Race
There is no racial predilection to subdural empyema.
References
- ↑ 1.0 1.1 1.2 French H, Schaefer N (2014). “Intracranial Subdural Empyema: A 10-Year Case Series”. Oschner J. 12 (2). doi:10.1002/bip.360240911. PMID PMC4052585 Check
|pmid=value (help). - ↑ 2.0 2.1 2.2 Nathoo N, Nadvi SS, van Dellen JR, Gouws E (1999). “Intracranial subdural empyemas in the era of computed tomography: a review of 699 cases”. Neurosurgery. 44 (3): 529–35, discussion 535–6. PMID 10069590.
- ↑ Wu TJ, Chiu NC, Huang FY (2008). “Subdural empyema in center”. J Microbiol Immunol Infect. 41 (1): 62–7. PMID 18327428. Unknown parameter
|month=ignored (help)
Risk Factors
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]; Anthony Gallo, B.S. [3]
Overview
Common risk factors in the development of subdural empyema are meningitis, sinusitis, otitis, mastoiditis, immunodeficiency, head trauma, and lumbar puncture.
Risk Factors
Common risk factors in the development of subdural empyema include:[1][2]
References
- ↑ Agrawal, Amit; Timothy, Jake; Pandit, Lekha; Shetty, Lathika; Shetty, J.P. (2007). “A Review of Subdural Empyema and Its Management”. Infectious Diseases in Clinical Practice. 15 (3): 149–153. doi:10.1097/01.idc.0000269905.67284.c7. ISSN 1056-9103.
- ↑ Yip K, Gosling RD, Jones V, Hosein IK (2009). “An unusual case of meningococcal meningitis complicated with subdural empyema in a 3 month old infant: a case report”. Cases Journal. 2: 6335. doi:10.1186/1757-1626-0002-0000006335. PMC 2827145. PMID 20181146.
Natural History, Complications, and Prognosis
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]; Anthony Gallo, B.S. [3]
Overview
If left untreated, patients with subdural empyema may develop severe fever, headache, nausea, vomiting, and seizures. Untreated subdural empyema may also lead to coma and subsequent mortality. Complications of subdural empyema include status epilepticus, neurological deficits, and thrombosis. Prognosis is generally good with antimicrobial therapy.
Natural History
Subdural empyema is considered a neurosurgical emergency. If left untreated, subdural empyema frequently evolves into severe fever, headache, nausea, vomiting, seizures, coma, and subsequent mortality.
Complications
Complications to subdural empyema include:[1]
- Status epilepticus
- Neurological deficits
- Thrombosis
- Cerebritis
- Cerebral edema
- Cerebral infarction
- Hydrocephalus
- Osteomyelitis
- Damage to the bridging veins
Prognosis
Prognosis is generally good with antimicrobial thearpy. The outcome is dependent on:[1]
- Preoperative level of consciousness
- Commencement of treatment
- Treatment duration
- Disease progression
Patient education is imperative as failure to follow antibiotic therapy will adversely affect the outcome of the treatment. Identified prognostic factors associated with subdural empyema include:[1]
Unfavorable Prognostic Factors
- Presentation with encephalopathy or coma
- Age: younger than 10 years or elderly
- Delayed commencement of antibiotics
- Burr hole placement
- Sterile cultures
Favorable Prognostic Factors
- Craniotomy
- Early treatment
- Young age (optimal between 10-20 years)
- Patient presents awake, alert and oriented
- Source of infection: paranasal sinuses
- Aerobic Streptococci isolated in culture
- Aerobic Streptococci as single pathogen
References
Diagnosis
Diagnosis
History and Symptoms | Physical Examination | Laboratory Findings | Lumbar Puncture | X Ray | CT | MRI | Other Diagnostic Studies
Treatment
Treatment
Medical Therapy | Surgery | Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies
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