Infection

Intracranial hemorrhage from Dengue

Intracranial hemorrhage from Dengue

Dengue fever is a viral infection caused by the dengue virus, which is primarily transmitted by the Aedes mosquito. The virus belongs to the Flaviviridae family and has four different serotypes: DEN-1, DEN-2, DEN-3, and DEN-4. Dengue is prevalent in tropical and subtropical regions, particularly in urban and semi-urban areas.

Symptoms of dengue fever typically appear within 4 to 7 days after a person is bitten by an infected mosquito. They can range from mild to severe and may include high fever, severe headache, joint and muscle pain, rash, nausea, vomiting, and in some cases, bleeding manifestations.

Complications

Severe forms of dengue, known as dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS), can cause life-threatening complications such as severe bleeding, organ damage, and circulatory failure.

A rare but possibly dangerous consequence of dengue illness is intracranial hemorrhage (ICH). Currently, the pathogenesis of ICH is unknown.

Treatment

There is no specific antiviral treatment for dengue fever, and management mainly involves supportive care to relieve symptoms and prevent complications. Rest, hydration, and over-the-counter pain relievers such as acetaminophen can help alleviate fever and pain. It is important to avoid medications like aspirin, ibuprofen, and naproxen, as they can increase the risk of bleeding.

Studies have reported the use of emergency surgery while monitoring thrombocytopenia in the therapy of dengue ICH 1).

Prevention

Prevention is crucial in controlling the spread of dengue. Measures include eliminating mosquito breeding sites by emptying standing water containers, using insect repellents, wearing protective clothing, and using mosquito nets or screens. In some high-risk areas, mosquito control programs may be implemented to reduce the mosquito population.

If you suspect you have dengue fever or are in an area with a dengue outbreak, it is advisable to seek medical attention for diagnosis and appropriate management.

Bangladesh reported the highest number of annual deaths (n = 281) related to dengue virus infection in 2022 since the virus reappeared in the country in 2000. Earlier studies showed that >92% of the annual cases occurred between the months of August and September. The 2022 outbreak is characterized by late onset of dengue cases with unusually higher deaths in colder months, that is, October-December. Haider et al. present possible hypotheses and explanations for this late resurgence of dengue cases. First, in 2022, the rainfall started late in the season. Compared to the monthly average rainfall for September and October between 2003 and 2021, there was 137 mm of additional monthly rainfall recorded in September and October 2022. Furthermore, the year 2022 was relatively warmer with a 0.71°C increased temperature than the mean annual temperature of the past 20 yr. Second, a new dengue virus serotype, DENV-4, had recently reintroduced/reappeared in 2022 and become the dominant serotype in the country for a large naïve population. Third, the post-pandemic return of normalcy after 2 yr of nonpharmaceutical social measures facilitates extra mosquito breeding habitats, especially in construction sites. Community engagement and regular monitoring and destruction of Aedes mosquitoes’ habitats should be prioritized to control dengue virus outbreaks in Bangladesh 2).

Case reports

A 65-year-old man who presented with dengue fever symptoms and developed altered consciousness and focal neurological deficits. The findings of the tests showed thrombocytopenia, increased AST and ALT, positive anti-dengue IgG, and subdural hematoma on brain imaging. The urgent operations were completed satisfactorily.

Dengue-related intracerebral haemorrhage is still a complicated condition. Thrombocytopenia and leukopenia are the first symptoms that point to dengue. Some risk factors, such as thrombocytopenia and increased AST and ALT, have been identified as bleeding factors in dengue fever. For a possible intracerebral haemorrhage, radiological imaging should be performed. In an emergency neurosurgery setting, thrombocyte administration could be used to monitor thrombocytopenia.

Subdural hematoma is a possible dengue fever complication. If the patient’s symptoms with thrombocytopenia and elevated liver enzymes indicate the possibility of intracranial haemorrhage, immediate radiological imaging should be performed 3)

A 65-year-old male patient was admitted with high-grade febrile illness and diagnosed with dengue. The patient had no focal neurology and was managed adequately following the primary survey on admission but, then, developed severe thrombocytopenia and eventually the critical phase of dengue illness. On the 5th admission day, the patient collapsed. Glasgow Coma Score was 3/15 with bilaterally dilated, fixed pupils. Immediate computed tomography head revealed a large left SDH with a significant midline shift. SDH was emergently evacuated with two units of platelets transfused peroperatively and two additional units postoperatively. Thrombocytopenia resolved within 48 h, and interval scanning showed gradual resolution of SDH. The patient was discharged 18 days later. Five months later, on follow-up, the patient is well with mild left-sided weakness and an Extended Glasgow Outcome Score of 7.

Isolated SDH is a rare but life-threatening hemorrhagic complication of DHF. Even in the critical phase of illness, with severe thrombocytopenia, surgical evacuation should be considered if the SDH is present in isolation, within an accessible area, and can be operated on immediately 4).

A 48-year-old Indian woman presented with fever and body aches followed by acute onset of paraplegia with bladder and bowel dysfunction and loss of sensations below the level of the umbilicus. She had severe thrombocytopenia and positive dengue serology. Magnetic resonance imaging of the spine showed compression of the spinal cord due to intradural hematoma at the D7-D8 vertebral level. The patient received symptomatic treatment for dengue fever and steroids. Emergency D7-D8 laminectomy with excision of the clot and dural repair was done after stabilizing the platelet count with multiple platelet transfusions. The constitutional symptoms responded well to the treatment. There was good improvement in sensory symptoms but negligible improvement in paraplegia with a change in muscle power from grade 0/5 to grade 1/5 in the postoperative period. The patient was discharged from the hospital in a stable condition, but paraplegia showed little improvement during follow-up of 1 year.

Spontaneous spinal cord hemorrhage can present as acute paraplegia in dengue fever. Failure to recognize this complication can delay initiating appropriate treatment with permanent loss of neurologic function 5).

A 18-year-old Pakistani male, presented with fever, colicky abdominal pain, vomiting, diarrhea, dark-colored urine, and oliguria.

Diagnoses: Dengue rapid NS-1 test came back positive. Along with myoglobinuria both serum creatine phosphokinase and creatine levels were abnormal. Hence, the patient was diagnosed with rhabdomyolysis-induced acute kidney injury. On physical examination, his right arm was painful and tender with restricted movement at the elbow. A Doppler ultrasound of the arm revealed thickening of the skin and underlying muscles, as well as edematous abnormalities affecting the entire right upper limb, both of which are indications of compartment syndrome.

Interventions and outcome: The management included rehydration, administration of dextrose and bicarbonate (bicarbonate infusion) prepared by adding 150 mEq sodium bicarbonate in 850 mL dextrose 5%, pain killers, along with platelet, and packed red cell transfusions. Additionally, right upper limb was kept elevated at 90° for 30 minutes every 2 hours to reduce edema and crept bandages were applied. The patient was discharged after 11 days and the follow-up was uneventful.

Lesson: Physicians should be aware that rhabdomyolysis-induced acute kidney damage and limb compartment syndrome are also possible DF consequences, and they should be on the lookout for any indications pointing to these complications in DF. A prompt diagnosis can prevent further complications and fatality 6).

Four patients referred for neurosurgical intervention as sequelae to dengue coagulopathy. Among them, three had intracranial bleeds and one had spinal cord hematoma along with intracranial hemorrhages. This small series includes the youngest reported case of dengue coagulopathy with intracranial bleed and only the second case of spontaneous intraspinal hematoma sequelae to dengue hemorrhagic fever. The situations where patients contract dengue in a setting of neurosurgical intervention are grave. The margin of safety in the presence of dengue coagulopathy is narrow. The surgeon has to outweigh benefit against risk of surgery in each individual. A subdural and intramedullary spinal cord hematoma, which was summarized in the article “Burden of Dengue related neurosurgical emergencies during an epidemic- A tertiary care experience 7)

A report of quadriparesis in dengue fever due to hematomyelia 8).

The first report of intradural spinal hematoma secondary to dengue was reported by Kaur et al 9).

A patient with dengue fever with symptoms suggestive of acute flaccid paralysis, and on subsequent investigation he was diagnosed as a case of hypokalaemic quadriparesis. Clinicians in the endemic area should be aware of such association of acute pure motor reversible quadriparesis with dengue fever 10).

Dengue infection causing acute hypokalemic quadriparesis 11).

1)

Siahaan AMP, Tandean S, Nainggolan BWM, Tarigan J, Sitanggang JS. A Critical Analysis of Intracranial Hemorrhage (ICH) as a Fatal Complication of Dengue Fever. J Korean Neurosurg Soc. 2023 Jan 16. doi: 10.3340/jkns.2022.0205. Epub ahead of print. PMID: 36642946.
2)

Haider N, Hasan MN, Khalil I, Tonge D, Hegde S, Chowdhury MAB, Rahman M, Hossain Khan M, Ansumana R, Zumla A, Uddin MJ. The 2022 dengue outbreak in Bangladesh: hypotheses for the late resurgence of cases and fatalities. J Med Entomol. 2023 May 18:tjad057. doi: 10.1093/jme/tjad057. Epub ahead of print. PMID: 37202843.
3)

Siahaan AMP, Tandean S, Saragih EB, Nainggolan BWM. Spontaneous acute subdural hematoma in dengue fever: Case report and review of the literature. Int J Surg Case Rep. 2022 Sep;98:107512. doi: 10.1016/j.ijscr.2022.107512. Epub 2022 Aug 13. PMID: 35985111; PMCID: PMC9411658.
4)

Ashraf M, Hussain SS, Farooq M, Fatima L, Majeed N, Ashraf N. Isolated subdural hematoma due to dengue hemorrhagic fever: Surgical intervention and review of the literature. Surg Neurol Int. 2022 Jun 10;13:244. doi: 10.25259/SNI_334_2022. PMID: 35855175; PMCID: PMC9282807.
5)

Kaushik RM, Kumar R, Kaushik M, Saini M, Kaushik R. Spontaneous spinal intradural hemorrhage in dengue fever: a case report. J Med Case Rep. 2022 May 30;16(1):213. doi: 10.1186/s13256-022-03451-2. PMID: 35644613; PMCID: PMC9150361.
6)

Arif A, Abdul Razzaque MR, Kogut LM, Tebha SS, Shahid F, Essar MY. Expanded dengue syndrome presented with rhabdomyolysis, compartment syndrome, and acute kidney injury: A case report. Medicine (Baltimore). 2022 Feb 18;101(7):e28865. doi: 10.1097/MD.0000000000028865. PMID: 35363190; PMCID: PMC9281986.
7)

Kutty RK, Sreemathyamma SB, Sivanandapanicker JL, Mundhe V, Chhabra K, Peethambaran A. Burden of Dengue-related Neurosurgical Emergencies during an Epidemic: A Tertiary Care Experience. Asian J Neurosurg. 2019 Jan-Mar;14(1):211-218. doi: 10.4103/ajns.AJNS_318_17. PMID: 30937037; PMCID: PMC6417330.
8)

Kumar MS, Srinanthini KR, Gopal S. A report of quadriparesis in dengue fever due to hematomyelia. Neurol India. 2019 Mar-Apr;67(2):530-531. doi: 10.4103/0028-3886.258054. PMID: 31085871.
9)

Kaur J, Virk JS, Paul BS, Saggar K. Dengue fever presenting as cauda equina syndrome. BMJ Case Rep. 2017 Jul 24;2017:bcr2017221251. doi: 10.1136/bcr-2017-221251. PMID: 28739570; PMCID: PMC5624003.
10)

Gupta DK, Vaish AK, Arya RK, Chaudhary SC. Hypokalaemic quadriparesis: an unusual manifestation of dengue fever. BMJ Case Rep. 2011 Jun 17;2011:bcr1220103673. doi: 10.1136/bcr.12.2010.3673. PMID: 22692495; PMCID: PMC3118907.
11)

Gulati S. Dengue infection causing acute hypokalemic quadriparesis. Neurol India. 2011 Jan-Feb;59(1):143. doi: 10.4103/0028-3886.76887. PMID: 21339693.

Balamuthia amoebic encephalitis

Balamuthia amoebic encephalitis

Balamuthia mandrillaris is a free-living amoebae found in soil and water, which can cause a rare and potentially fatal infection in humans called Balamuthia amoebic encephalitis (BAE). The infection typically occurs when the amoeba enters the body through the nose, eyes, or broken skin, and travels to the brain, where it causes inflammation and damage to brain tissue.

Epidemiology

Balamuthia amoebic encephalitis is a very rare disease.

About 39% of the infected patients were found to be immunocompromised which is extremely rare clinically. The presence of trophozoites in diseased tissue is an important basis for the pathological diagnosis.

Clinical features

Symptoms of BAE typically develop over several weeks to months and can include headache, fever, nausea, vomiting, seizures, and neurological symptoms such as confusion, difficulty speaking, and weakness.

Treatment

Treatment of BAE typically involves a combination of antimicrobial drugs and supportive care to manage symptoms and prevent complications. However, the effectiveness of treatment can be limited, and many patients do not survive the infection.

Prevention of BAE involves avoiding exposure to potentially contaminated water and soil, and taking precautions to protect the nose and eyes from exposure, such as wearing a mask when working in dusty environments or swimming in freshwater lakes or rivers.

Nanotechnology was used to conjugate Zinc oxide with Ampicillin, Ceftrixon, Naringin, Amphotericin B, and Quericitin, and the amoebicidal activity and host cell cytotoxicity of these resulting compounds were investigated. The compounds ZnO-CD-AMPi, ZnO-CD-CFT, ZnO-CD-Nar, ZnO-CD-AMB, and ZnO-CD-QT were found to reduce N. fowleri viability to 35.5%, 39.6%, 52.0%, 50.8%, 35.9%, and 69.9%, respectively, and B. mandrillaris viability to 40.9%, 48.2%, 51.6%, 43.8%, and 62.4%, respectively, when compared with their corresponding controls. Furthermore, the compounds reduced N. fowleri-mediated and B. mandrillaris-mediated host cell death significantly. Additionally, the compounds showed limited cytotoxicity against human cells; cell toxicity was 35.5%, 36.4%, 30.9%, 36.6%, and 35.6%, respectively, for the compounds ZnO-CD-AMPi, ZnO-CD-CFT, ZnO-CD-Nar, ZnO-CD-AMB, and ZnO-CD-QT. Furthermore, the minimum inhibitory concentrations to inhibit amoeba growth by 50% were determined for N. fowleri and B. mandrillaris. The MIC50 for N. fowleri were determined to be 69.52 µg/mL, 82.05 µg/mL, 88.16 µg/mL, 95.61 µg/mL, and 85.69 µg/mL, respectively; the MIC50 of the compounds for B. mandrillaris were determined to be 113.9 µg/mL, 102.3 µg/mL, 106.9 µg/mL, 146.4 µg/mL, and 129.6 µg/mL, respectively. Translational research to further develop therapies based on these compounds is urgently warranted, given the lack of effective therapies currently available against these devastating infections 1)

Outcome

It is a serious condition with a high mortality rate and can be difficult to diagnose and treat. The infection can progress rapidly and can cause severe brain damage and death if left untreated.

Case reports

Liu et al. report clinical data from a patient with Balamuthia GAE to improve physician understanding of the disease and diagnostic accuracy of imaging and reduce misdiagnosis. A 61-year-old male poultry farmer presented with moderate swelling pain in the right frontoparietal region without obvious inducement three weeks ago. Head computed tomography(CT) and magnetic resonance imaging(MRI) revealed a space-occupying lesion in the right frontal lobe. Initially, clinical imaging diagnosed it as a high-grade astrocytoma. The pathological diagnosis of the lesion was inflammatory granulomatous lesions with extensive necrosis, suggesting amoeba infection. The pathogen detected by metagenomic next-generation sequencing (mNGS) is Balamuthia mandrillaris, and the final pathological diagnosis was Balamuthia granulomatous amoebic encephalitis.

When a head MRI shows irregular or annular enhancement, clinicians should not blindly diagnose common diseases such as brain tumors. Although Balamuthia GAE accounts for only a tiny proportion of intracranial infections, it should be considered in the differential diagnosis of intracranial lesions 2).

A 61-year-old woman with a history of an orthotopic heart transplant was hospitalized with a new-onset headache. Magnetic resonance imaging (MRI) of the brain revealed T2 hyperintense signal involving the left occipital lobe with leptomeningeal enhancement and mild vasogenic edema. Initial neurologic examination was normal; however, after 7 days she developed imbalance, visual disturbances, night sweats, bradyphrenia, alexia without agraphia, and right hemianopsia. Brain MRI showed enlargement of the left occipital mass and worsening edema. Stereotactic needle biopsy showed nondiagnostic necrosis. The patient continued to deteriorate despite dexamethasone. Cerebrospinal fluid (CSF) suggested infection, and cytomegalovirus CSF polymerase chain reaction (PCR) was positive. The patient received vancomycin, imipenem, and ganciclovir. After obtaining a positive serum beta-D-glucan (Fungitell), amphotericin was added. Despite the best medical efforts, the patient died. Postmortem broad-range PCR sequencing of the brain tissue was positive for rare amoeba Balamuthia mandrillaris 3).

A patient in California, USA, with rare and usually fatal Balamuthia mandrillaris granulomatous amebic encephalitis survived after receiving treatment with a regimen that included the repurposed drug nitroxoline. Nitroxoline, which is a quinolone typically used to treat urinary tract infections, was identified in a screen for drugs with amebicidal activity against Balamuthia 4).

An 80-year-old man presented with subacute mental status change, dizziness, and left-sided vision loss. Magnetic resonance imaging demonstrated a ring-enhancing right parietooccipital lesion.

Observations: Biopsy and laboratory testing demonstrated an amoebic Balamuthia mandrillaris infection. Fewer than 200 cases of this infection have been recognized in the United States, and no standardized treatment regimen currently exists.

Lessons: Rapid antimicrobial therapy with miltefosine, azithromycin, fluconazole, flucytosine, sulfadiazine, and albendazole was initiated. The pathophysiology, diagnosis, and management of this infection and the patient’s course were reviewed. The importance of biopsy for pathologic and laboratory diagnosis and rapid treatment initiation with a multidisciplinary team was reinforced 5).

1)

Siddiqui R, Boghossian A, Akbar N, Jabri T, Aslam Z, Shah MR, Alharbi AM, Alfahemi H, Khan NA. Zinc Oxide Nanoconjugates against Brain-Eating Amoebae. Antibiotics (Basel). 2022 Sep 20;11(10):1281. doi: 10.3390/antibiotics11101281. PMID: 36289939; PMCID: PMC9598189.
2)

Liu J, Zhang W, Wu S, Zeng T, Luo F, Jiang Q, Yang R. A clinical case report of Balamuthia granulomatous amoebic encephalitis in a non-immunocompromised patient and literature review. BMC Infect Dis. 2023 Apr 18;23(1):245. doi: 10.1186/s12879-023-08228-6. PMID: 37072710.
3)

Sakusic A, Chen B, McPhearson K, Badi M, Freeman WD, Huang JF, Siegel JL, Jentoft ME, Oring JM, Verdecia J, Meschia JF. Balamuthia mandrillaris Encephalitis Presenting as a Symptomatic Focal Hypodensity in an Immunocompromised Patient. Open Forum Infect Dis. 2023 Feb 21;10(3):ofad094. doi: 10.1093/ofid/ofad094. PMID: 37008568; PMCID: PMC10051015.
4)

Spottiswoode N, Pet D, Kim A, Gruenberg K, Shah M, Ramachandran A, Laurie MT, Zia M, Fouassier C, Boutros CL, Lu R, Zhang Y, Servellita V, Bollen A, Chiu CY, Wilson MR, Valdivia L, DeRisi JL. Successful Treatment of Balamuthia mandrillaris Granulomatous Amebic Encephalitis with Nitroxoline. Emerg Infect Dis. 2023 Jan;29(1):197-201. doi: 10.3201/eid2901.221531. PMID: 36573629; PMCID: PMC9796214.
5)

Levinson S, Kumar KK, Wang H, Tayyar R, Dunning M, Toland A, Budvytiene I, Vogel H, Chang A, Banaei N, Shuer L. Balamuthia mandrillaris brain infection: a rare cause of a ring-enhancing central nervous system lesion. Illustrative case. J Neurosurg Case Lessons. 2022 Apr 11;3(15):CASE2268. doi: 10.3171/CASE2268. PMID: 36303497; PMCID: PMC9379710.

Brain abscess

Brain abscess

J.Sales-Llopis

Neurosurgery Service, Alicante University General Hospital, Alicante Institute for Health and Biomedical Research (ISABIAL – FISABIO Foundation), Alicante, Spain.

A brain abscess is a focal area of necrosis starting in an area of cerebritis surrounded by a membrane.

Brain abscesses are suppurative infections of the brain parenchyma surrounded by a vascularized capsule.

see also Intracranial abscess.

It is a potentially life-threatening condition requiring prompt radiological identification and rapid treatment.

Classification

Brain abscess classification.

Epidemiology

The most frequent intracranial locations (in descending order of frequency) are: frontal-temporal, frontal-parietal, parietal, cerebellar, and occipital lobes.

In a article, Chen review the literature to find out how the epidemiology of this disease has changed through the years and re-visit the basic pathological process of abscess evolution and highlight the new research in the biochemical pathways that initiate and regulate this process 1).

The epidemiology of brain abscess has changed with the increasing incidence of this infection in immunocompromised patients, particularly solid organ and bone marrow transplant recipients, and the decreasing incidence of brain abscess related to sinusitis and otitis 2).

There have been several trends in the epidemiology of brain abscess over recent decades. One trend is that there appears to be a trend toward a decreasing incidence of brain abscess. In a population-based study of residents of Olmstead County, Minnesota, the incidence rate was 1.3 per 100,000 patient-years from 1935 to 1944 compared with 0.9 per 100,000 patient-years from 1965 to 1981 3).

Etiology

see Brain abscess etiology.

Clinical features

Clinical presentation is non-specific, with many cases having no convincing inflammatory or septic symptoms.

Abscess formation should be considered in case of clinical deterioration, headache, and any neurological deficit after febrile episodes.

Similar to any other mass lesion but tend to progress rapidly.

Symptoms of raised intracranial pressure, seizures and focal neurological deficits are the most common forms of presentation

Eventually, many abscesses rupture into the ventricular system, which results in a sudden and dramatic worsening of the clinical presentation and often heralds a poor outcome.

Pathology

Cerebral abscesses result from pathogens growing within the brain parenchyma. Initial parenchymal infection is known as cerebritis, which may progress into a cerebral abscess.

Cerebral infection is commonly divided into four stages with distinct imaging and histopathologic features:

early cerebritis (a focal infection without a capsule or pus formation,can resolve or develop into frank abscess) late cerebritis

early abscess/encapsulation – may occur 10 days after infection

late abscess/encapsulation – may occur >14 days after infection

Diagnosis

see Brain abscess diagnosis.

Differential diagnosis

see Brain abscess differential diagnosis.

Treatment

see Brain abscess treatment.

Management

see Brain abscess management.

Outcome

Significant advances in the diagnosis and management of bacterial brain abscess over the past several decades have improved the expected outcome of a disease once regarded as invariably fatal. Despite this, intraparenchymal abscess continues to present a serious and potentially life-threatening condition 4).

There has been a gradual improvement in the outcome of patients with brain abscess over the past 50 years, which might be driven by improved brain imaging techniques, minimally invasive neurosurgical procedures, and protocoled antibiotic treatment. Multicenter prospective studies and randomized clinical trials are needed to further advance treatment and prognosis in brain abscess patients.

Our understanding of brain abscesses has increased by meta-analysis on clinical characteristics, ancillary investigations, and treatment modalities. Prognosis has improved over time, likely due to improved brain imaging techniques, minimally invasive neurosurgical procedures, and protocoled antibiotic treatment 5).

Current evidences suggest that for encapsulated brain abscess in superficial non-eloquent area, abscess resection compared to abscess aspiration had lower post-operative residual abscess rate; lower re-operation rate; higher rate of improvement in neurological status within 1 month after surgery, shorter duration of post-operative antibiotics and average length of hospital stay. There was no statistically significant difference in the rate of improvement in neurological status at 3 months post-operative and the mortality 6).

Complications

Intraventricular rupture of brain abscess (IVROBA)

Strongly influences poor outcome in patients with cyanotic heart disease. The key to decreasing poor outcomes may be the prevention and management of IVROBA. To reduce operative and anesthetic risk in these patients, abscesses should be managed by less invasive aspiration methods guided by computed tomography. Abscesses larger than 2 cm in diameter, in deep-located or parieto-occipital regions, should be aspirated immediately and repeatedly, mainly using computed tomography-guided methods to decrease intracranial pressure and avoid IVROBA. IVROBA should be aggressively treated by aspiration methods for the abscess coupled with the appropriate intravenous and intrathecal administration of antibiotics while evaluating intracranial pressure pathophysiology 7).

Case series

Brain abscess case series.

Case reports

see Brain abscess case reports.

Brain abscess case reports from the General University Hospital Alicante

Known space-occupying lesion, centered in the right frontal anterior white matter, with estimated diameters of 3.5 x 3 x 3.5 cm. It shows well-defined contours and a practically spherical shape. A predominantly hypointense signal on T1 and homogeneously hyperintense on T2, with a wall with hypointense behavior on T2-weighted sequences. After contrast administration, only enhancement of its wall was observed, in a fine and linear way, without identifying solid poles. The lesion shows diffusion sequence restriction and low values ​​of rVSC in perfusion. Marked surrounding vasogenic edema, which causes a mass effect on the neighboring sulci, as well as mild subfalcian herniation, with a deviation from the midline of approximately 6 mm (significant improvement compared to previous CT control). The discrete mass effect is also on the knee of the corpus callosum and the frontal horn of the right ventricle. The findings are compatible with a brain abscess. A small solution of continuity is observed in its anterior wall, in contact with the meninge, which is thickened in a laminar manner in relation to inflammatory involvement, without clearly identifying empyema. Extensive occupation of the frontal sinus bilaterally, with an enhancement of its wall. Retrospectively, the CT study showed slight permeation on the posterior wall of one of the loculations of the frontal sinus close to the abscess. Small hyperintense foci in subcortical and periventricular white matter with a chronic ischemic profile of a small vessel, to a mild degree. Diagnostic impression: Findings compatible with a right frontal parenchymal abscess, 3.5 cm in diameter, with inflammatory changes and thickening of the adjacent pachymeninge, although without clear associated empyema.

Books

see Brain abscess books.

Latest news

1)

Chen M, Low DCY, Low SYY, Muzumdar D, Seow WT. Management of brain abscesses: where are we now? Childs Nerv Syst. 2018 Oct;34(10):1871-1880. doi: 10.1007/s00381-018-3886-7. Epub 2018 Jul 3. PubMed PMID: 29968000.
2)

Calfee DP, Wispelwey B. Brain abscess. Semin Neurol. 2000;20(3):353-60. Review. PubMed PMID: 11051299.
3)

Nicolosi A, Hauser WA, Musicco M, Kurland LT: Incidence and prognosis of brain abscess in a defined population: Olmsted County, Minnesota, 1935-1981. Neuroepidemiology 1991;10:122-131.
4)

atel K, Clifford DB. Bacterial brain abscess. Neurohospitalist. 2014 Oct;4(4):196-204. doi: 10.1177/1941874414540684. PubMed PMID: 25360205; PubMed Central PMCID: PMC4212419.
5)

Brouwer MC, van de Beek D. Epidemiology, diagnosis, and treatment of brain abscesses. Curr Opin Infect Dis. 2016 Nov 8. [Epub ahead of print] PubMed PMID: 27828809.
6)

Zhai Y, Wei X, Chen R, Guo Z, Raj Singh R, Zhang Y. Surgical outcome of encapsulated brain abscess in superficial non-eloquent area: A systematic review. Br J Neurosurg. 2015 Nov 16:1-6. [Epub ahead of print] PubMed PMID: 26569628.
7)

Takeshita M, Kagawa M, Yato S, Izawa M, Onda H, Takakura K, Momma K. Current treatment of brain abscess in patients with congenital cyanotic heart disease. Neurosurgery. 1997 Dec;41(6):1270-8; discussion 1278-9. PubMed PMID: 9402578.

Linezolid in Neurosurgery

Linezolid in Neurosurgery

Latest articles

Evidence for the effectiveness of linezolid in neurosurgical infections (NSIs) is growing. The comfortable oral dosage and tolerance of linezolid open the possibility for sequential antimicrobial treatment (SAT) in stable patients after a period of intravenous treatment 1).

Reviews

Relevant studies were identified through searches of the PubMed, Current Contents, and Cochrane databases (publications archived until October 2006).

Case reports, case series, prospective and retrospective studies, and randomized controlled trials were eligible for inclusion in our review if they evaluated the effectiveness and safety of linezolid for the treatment of patients with CNS infections.

In 18 (42.9%) of the 42 relevant cases identified, patients had undergone neurosurgical operations and/or had prosthetic devices. Meningitis was the most common CNS infection, accounting for 20 (47.6%) cases. Other CNS infections included brain abscesses (14; 33.3%), ventriculitis (5; 11.9%), and ventriculo-peritoneal shunt infection (3; 7.1%). In the 39 patients in whom the responsible pathogen was isolated, those predominantly responsible for the CNS infections were: penicillin-nonsusceptible Streptococcus pneumoniae (7; 17.9%), vancomycin-resistant enterococci (6; 15.4%), Nocardia spp. (5; 12.8%), methicillin-resistant Staphylococcus epidermidis (4; 10.3%), and methicillin-resistant Staphylococcus aureus (3; 7.7%). Of the 42 patients who received linezolid for the treatment of CNS infections, 38 (90.5%) were either cured or showed clinical improvement of the infection. The mean duration of follow-up was 7.2 months; no recurrent CNS infection was reported.

The limited published data suggest that linezolid may be considered for the treatment of patients with CNS infections in cases of failure of previously administered treatment or limited available options 2).

Case series

To evaluate the efficacy and safety of SAT with oral linezolid in patients with NSI and to analyse the cost implications, an observational, non-comparative, prospective cohort study was conducted on clinically stable consecutive adult patients at the Neurosurgical Service. Following intravenous treatment, patients were discharged with SAT with oral linezolid.

A total of 77 patients were included. The most common NSIs were: 41 surgical wound infections, 20 subdural empyemas, 18 epidural abscesses, and 16 brain abscesses. Forty-four percent of patients presented two or more concomitant NSIs. Aetiological agents commonly isolated were: Propionibacterium acnes (36 %), Staphylococcus aureus (23 %), Staphylococcus epidermidis (21 %) and Streptococcus spp. (13 %). The median duration of the SAT was 15 days (range, 3-42). The SAT was interrupted in five cases due to adverse events. The remainder of the patients were cured at the end of the SAT. A total of 1,163 days of hospitalisation were saved. An overall cost reduction of €516,188 was attributed to the SAT. Eight patients with device infections did not require removal of the device, with an additional cost reduction of €190,595. The mean cost saving per patient was €9,179.

SAT with linezolid was safe and effective for the treatment of NSI. SAT reduces hospitalisation times, which means significant savings of health and economic resources 3).

Seventeen patients were included in the study. The main comorbidities among these patients included one or more of the following: subarachnoidal or intraventricular hemorrhage (n=8), solid neurological cancer (n=7), corticosteroids(n=9), and hydrocephalus (n=6). Eight patients underwent a craniotomy and fourteen patients had external ventricular drainage (EVD) as a predisposing factor for infection. Meningitis was the most common infection (11; 64.7%), followed by ventriculitis (4; 23.5%) and brain abscesses (2;11.8%). The main causative organisms were coagulase-negative Staphylococcus spp. (13; 76.5%). Linezolid was used as the initial therapy in 8 episodes, after therapy failure in 6, and for other reasons in 3. The oral route was used in 9 (52.9%) episodes; linezolid was initiated orally in 2 cases. The mean duration of treatment was 26.5 days (range 15-58). No adverse events were reported. Sixteen (94.1%) patients were considered cured. There was one recurrence. The mean length of hospital stay was 45.6 (range 15-112) days and the mean duration of follow-up was 7.2 (range 0.4-32) months. No related deaths occurred during active episodes.

Linezolid was mainly indicated in post-neurosurgical EVD-associated infections due to coagulase-negative Staphylococcus spp. It was used as initial therapy in most cases. A high rate of clinical cure was observed and no related adverse events were reported. More than half of the patients benefited from the advantages of the oral route of administration 4).

In order to study the penetration of this antimicrobial into the cerebrospinal fluid (CSF) of such patients, the disposition of linezolid in serum and CSF was studied in 14 neurosurgical patients given linezolid at 600 mg twice daily (1-h intravenous infusion) for the treatment of CNS infections caused by gram-positive pathogens or for prophylactic chemotherapy. Serum and CSF linezolid steady-state concentrations were analyzed by high-pressure liquid chromatography, and the concentration-time profiles obtained were analyzed to estimate pharmacokinetic parameters. The mean +/- standard deviation (SD) linezolid maximum and minimum measured concentrations were 18.6 +/- 9.6 microg/ml and 5.6 +/- 5.0 microg/ml, respectively, in serum and 10.8 +/- 5.7 microg/ml and 6.1 +/- 4.2 microg/ml, respectively, in CSF. The mean +/- SD areas under the concentration-time curves (AUCs) were 128.7 +/- 83.9 microg x h/ml for serum and 101.6 +/- 59.6 microg x h/ml for CSF, with a mean penetration ratio for the AUC for CSF to the AUC for serum of 0.66. The mean elimination half-life of linezolid in CSF was longer than that in serum (19.1 +/- 19.0 h and 6.5 +/- 3.6 h, respectively). The serum and CSF linezolid concentrations exceeded the pharmacodynamic breakpoint of 4 microg/ml for susceptible target pathogens for the entire dosing interval in the majority of patients. These findings suggest that linezolid may achieve adequate concentrations in the CSF of patients requiring antibiotics for the management or prophylaxis of CNS infections caused by gram-positive pathogens 5).

References

1)

Jahoda D, Nyc O, Pokorný D, Landor I, Sosna A. [Linezolid in the treatment of antibiotic-resistant gram-positive infections of the musculoskeletal system]. Acta Chir Orthop Traumatol Cech. 2006 Oct;73(5):329-33. Czech. PubMed PMID: 17140514.
2)

Ntziora F, Falagas ME. Linezolid for the treatment of patients with central nervous system infection. Ann Pharmacother. 2007 Feb;41(2):296-308. Epub 2007 Feb 6. Review. PubMed PMID: 17284501.
3)

Martín-Gandul C, Mayorga-Buiza MJ, Castillo-Ojeda E, Gómez-Gómez MJ, Rivero-Garvía M, Gil-Navarro MV, Márquez-Rivas FJ, Jiménez-Mejías ME. Sequential antimicrobial treatment with linezolid for neurosurgical infections: efficacy, safety and cost study. Acta Neurochir (Wien). 2016 Oct;158(10):1837-43. doi: 10.1007/s00701-016-2915-0. Epub 2016 Aug 13. PubMed PMID: 27520361.
4)

Sousa D, Llinares P, Meijide H, Gutiérrez JM, Miguez E, Sánchez E, Castelo L, Mena A. Clinical experience with linezolid for the treatment of neurosurgical infections. Rev Esp Quimioter. 2011 Mar;24(1):42-7. PMID: 21412669.
5)

Myrianthefs P, Markantonis SL, Vlachos K, Anagnostaki M, Boutzouka E, Panidis D, Baltopoulos G. Serum and cerebrospinal fluid concentrations of linezolid in neurosurgical patients. Antimicrob Agents Chemother. 2006 Dec;50(12):3971-6. doi: 10.1128/AAC.00051-06. Epub 2006 Sep 18. PMID: 16982782; PMCID: PMC1694012.

Stenotrophomonas maltophilia meningitis

Stenotrophomonas maltophilia meningitis

Treatment

Stenotrophomonas maltophilia treatment

Case series

The clinical characteristics of six Stenotrophomonas maltophilia ABM cases, collected during a study period of nine years (2001-2009) were included. In the related literature, 13 S. maltophilia ABM cases were reported, and their clinical data were also collected.

The 19 S. maltophilia ABM cases included 11 men and 8 women, aged 28-70 years. Of these 19 cases, 89.5% (17/19) had underlying neurosurgical (NS) conditions as the preceding event. Before the development of S. maltophilia ABM, 52.6% (10/19) of them had long stays in hospital and 63.2% (12/19) had undergone antibiotic treatment. Among the implicated S. maltophilia cases, three strains were found to have a resistance to sulfamethoxazole-trimethoprim (SMZ-TMP). Two of our five cases had resistant strains to levofloxacin. Among the antibiotics chosen for treatment, SMZ-TMP was the most common followed by quinolone (ciprofloxacin, levofloxacin, moxifloxacin). The therapeutic results showed 2 cases expired while the other 17 cases survived.

S. maltophilia ABM usually develops in patients with a preceding neurosurgical condition, a long hospital stay and antibiotic use. SMZ-TMP and quinolones, especially the ciprofloxacin, are the major antibiotic used. This study also shows the emergence of clinical S. maltophilia strains which are not susceptible to SMZ-TMP and quinolones and this development may pose a more serious threat in the near future because treatment options may become depleted and limited despite the mortality rate of this specific group of ABM not being high at this time 1).

Case reports

A young female patient with history of multiple shunt revisions in the past, came with shunt dysfunction and exposure of the ventriculoperitoneal shunt tube in the neck. The abdominal end of the shunt tube was seen migrating into the bowel during shunt revision. The cerebrospinal fluid analysis showed evidence of Stenotrophomonas maltophilia growth. This is the first reported case of Stenotrophomonas maltophilia meningitis associated with ventriculoperitoneal shunt migration into the bowel. 2).

A patient who developed C. utilis and S. maltophilia after undergoing neurosurgery and received effective nosocomial meningitis treatment. Multiple neurosurgeries were required for a 16-year-old girl due to complications. For probable nosocomial meningitis, she was treated with cefepime with vancomycin. Meropenem and liposomal amphotericin B were prescribed after her seizure and positive CSF culture for Candida utilis. Consequently, S. maltophilia was discovered in the CSF, and ceftazidime and trimethoprim-sulfamethoxazole were prescribed. The patient has been hemodynamically stable for the past two months, and consecutive CSF cultures have been negative. To the best of our knowledge, this is the first case of C. utilis and S. maltophilia co-infection that has been successfully handled. 3).

Two cases of S. maltophilia meningitis following neurosurgical procedures. The first patient was a 60-year-old female. She was admitted to the hospital with a left basal ganglia bleed and underwent placement of an external ventricular drain for the treatment of hydrocephalus. She developed S. maltophilia meningitis 20 days after surgery. She was successfully treated with a combination of trimethoprim-sulfamethoxazole and intravenous colistin and the removal of the drain. She successfully underwent a ventriculoperitoneal (VP) shunt placement at the therapeutic midway point. The second patient was a 35-year-old male with a history of intracranial aneurysm bleeding. He had undergone a craniotomy and placement of a ventriculoperitoneal shunt two years previously. His shunt was replaced twice due to blockage. The last replacement had occurred 15 days prior to the development of meningitis. He was treated with a combination of trimethoprim-sulfamethoxazole and ceftazidime (as well as undergoing another shunt replacement) and experienced an excellent recovery. S. maltophilia is a rare but important cause of nosocomial meningitis. It is strongly associated with prior hospitalization and neurosurgical intervention, which is also found in our case series. The management of S. maltophilia meningitis is a therapeutic challenge due to its high resistance to multiple antibiotics. Optimal therapy is based on antimicrobial sensitivity, and the trimethoprim-sulfamethoxazole-based combination has been shown to be successful. The duration of therapy is debatable, but like most gram-negative meningitis infections, therapy lasting up to three weeks appears to be adequate. 4).

Stenotrophomonas maltophilia CSF infection in infants after neurosurgery 5).

A 4-year-old boy who developed meningitis associated with this organism, after several neurosurgical procedures and previous treatment with a broad-spectrum antibiotic. He was treated successfully with a combination of trimethoprim-sulfamethoxazole, ceftazidime and levofloxacin. Stenotrophomonas maltophilia should be considered as a potential cause of meningitis, especially among severely debilitated or immunosuppressed patients. Antimicrobial therapy is complicated by the high resistance of the organism to multiple antibiotics. 6).

A case of a six months old, male child who developed meningitis caused by Stenotrophomonas maltophilia, after he underwent a neurosurgical procedure. 7).

A 30-year-old male patient who developed meningitis associated with this organism after several neurosurgical procedures. A review of the literature revealed only 15 previous reports. Most cases were associated with neurosurgical procedures. Antimicrobial therapy is complicated by multiple drug resistance of the organism, and trimethoprim-sulfamethoxazole is the recommended agent for treatment. 8).

A case of generalized infection by S. maltophilia, including meningitis, bacteremia and respiratory tract infection, in a patient who had undergone multiple neurosurgical procedures and who was treated with trimethoprim-sulphamethoxazole 9).

Two cases of meningitis caused by Stenotrophomonas maltophilia in cancer patients following placement of an Ommaya reservoir for treatment of meningeal carcinomatosis. In addition, they review eight other cases of S. maltophilia that have been reported to date. Stenotrophomonas maltophilia meningitis is often associated with neurosurgical procedures; however, spontaneous infection may also occur, mainly in neonates. The disease’s clinical presentation is similar to that of other forms of meningitis caused by Gram-negative bacilli. The overall mortality rate of this disease is 20% and is limited to neonates with spontaneous meningitis in whom effective antibiotic therapy is delayed. Meningitis caused by S. maltophilia in the modern era should be considered in immunocompromised hosts with significant central nervous system disease who have undergone neurosurgical procedures and who do not readily respond to broad-spectrum antimicrobial coverage. 10).

1)

Huang CR, Chen SF, Tsai NW, Chang CC, Lu CH, Chuang YC, Chien CC, Chang WN. Clinical characteristics of Stenotrophomonas maltophilia meningitis in adults: a high incidence in patients with a postneurosurgical state, long hospital staying and antibiotic use. Clin Neurol Neurosurg. 2013 Sep;115(9):1709-15. doi: 10.1016/j.clineuro.2013.03.006. Epub 2013 Apr 20. PMID: 23611735.
2)

Manuel A, Jayachandran A, Harish S, Sunil T, K R VD, K R, Jo J, Unnikrishnan M, George K, Bahuleyan B. <i>Stenotrophomonas maltophilia</i> as a rare cause of meningitis and ventriculoperitoneal shunt infection. Access Microbiol. 2021 Oct 7;3(10):000266. doi: 10.1099/acmi.0.000266. PMID: 34816086; PMCID: PMC8604181.
3)

Mohzari Y, Al Musawa M, Asdaq SMB, Alattas M, Qutub M, Bamogaddam RF, Yamani A, Aldabbagh Y. Candida utilis and Stenotrophomonas maltophilia causing nosocomial meningitis following a neurosurgical procedure: A rare co-infection. J Infect Public Health. 2021 Nov;14(11):1715-1719. doi: 10.1016/j.jiph.2021.10.004. Epub 2021 Oct 13. PMID: 34700290.
4)

Khanum I, Ilyas A, Ali F. Stenotrophomonas maltophilia Meningitis – A Case Series and Review of the Literature. Cureus. 2020 Oct 28;12(10):e11221. doi: 10.7759/cureus.11221. PMID: 33269149; PMCID: PMC7704165.
5)

Mukherjee S, Zebian B, Chandler C, Pettorini B. Stenotrophomonas maltophilia CSF infection in infants after neurosurgery. Br J Hosp Med (Lond). 2017 Dec 2;78(12):724-725. doi: 10.12968/hmed.2017.78.12.724. PMID: 29240495.
6)

Correia CR, Ferreira ST, Nunes P. Stenotrophomonas maltophilia: rare cause of meningitis. Pediatr Int. 2014 Aug;56(4):e21-2. doi: 10.1111/ped.12352. PMID: 25252064.
7)

Sood S, Vaid VK, Bhartiya H. Meningitis due to Stenotrophomonas maltophilia after a Neurosurgical Procedure. J Clin Diagn Res. 2013 Aug;7(8):1696-7. doi: 10.7860/JCDR/2013/5614.3248. Epub 2013 Aug 1. PMID: 24086879; PMCID: PMC3782936.
8)

Yemisen M, Mete B, Tunali Y, Yentur E, Ozturk R. A meningitis case due to Stenotrophomonas maltophilia and review of the literature. Int J Infect Dis. 2008 Nov;12(6):e125-7. doi: 10.1016/j.ijid.2008.03.028. Epub 2008 Jun 24. PMID: 18579427.
9)

Platsouka E, Routsi C, Chalkis A, Dimitriadou E, Paniara O, Roussos C. Stenotrophomonas maltophilia meningitis, bacteremia and respiratory infection. Scand J Infect Dis. 2002;34(5):391-2. doi: 10.1080/00365540110080520. PMID: 12069028.
10)

Papadakis KA, Vartivarian SE, Vassilaki ME, Anaissie EJ. Stenotrophomonas maltophilia meningitis. Report of two cases and review of the literature. J Neurosurg. 1997 Jul;87(1):106-8. doi: 10.3171/jns.1997.87.1.0106. PMID: 9202275.

Vancomycin

Vancomycin

Vancomycin is a glycopeptide antibiotic medication.

Blood levels may be measured to determine the correct dose.

When taken by mouth it is poorly absorbed.

Vancomycin Cerebrospinal Fluid Pharmacokinetics

A study described the cerebrospinal fluid (CSF) exposure of vancomycin in 8 children prescribed intravenous vancomycin therapy for cerebral ventricular shunt infection. Vancomycin CSF concentrations ranged from 0.06 to 9.13 mg/L and the CSF: plasma ratio ranged from 0 to 0.66. Two of 3 children with a staphylococcal CSF infection had CSF concentrations greater than the minimal inhibitory concentration at the end of the dosing interval 1).

Cerebrospinal fluid (CSF) penetration and the pharmacokinetics of vancomycin were studied after continuous infusion (50 to 60 mg/kg of body weight/day after a loading dose of 15 mg/kg) in 13 mechanically ventilated patients hospitalized in an intensive care unit. Seven patients were treated for sensitive bacterial meningitis and the other six patients, who had a severe concomitant neurologic disease with intracranial hypertension, were treated for various infections. Vancomycin CSF penetration was significantly higher (P < 0.05) in the meningitis group (serum/CSF ratio, 48%) than in the other group (serum/CSF ratio, 18%). Vancomycin pharmacokinetic parameters did not differ from those obtained with conventional dosing. No adverse effect was observed, in particular with regard to renal function 2).

Ichinose et al. evaluated the concentration of Vancomycin in the plasma and CSF of postoperative neurosurgical patients with bacterial meningitis and evaluated the factors that affect the transferability of VCM to CSF. The concentrations of VCM in plasma (trough) and CSF were determined in eight patients (four males and four females) with bacterial meningitis who were treated with VCM using High-performance liquid chromatography. The ratio of the VCM concentrations in CSF/plasma was also calculated by estimating the blood VCM concentration at the same time as the VCM concentration in CSF was measured. The results showed that the VCM concentration in CSF was 0.9-12.7 µg/mL and the CSF/plasma VCM concentration ratio was 0.02-0.62. They examined the effect of drainage on the transferability of VCM to CSF, which showed that the VCM concentration in CSF and the CSF/plasma VCM concentration ratio were significantly higher in patients not undergoing drainage than in patients who were undergoing drainage. The CSF protein and glucose concentrations, which are diagnostic indicators of meningitis, were positively correlated with the VCM concentration in CSF and the CSF/plasma VCM concentration ratio. Thus, VCM transferability to CSF may be affected by changes in the status of the blood-brain barrier and blood-cerebrospinal fluid barrier due to drainage or meningitis 3).

Indications

Vancomycin Indications.

Vancomycin powder

see Vancomycin powder.

Intraventricular Vancomycin

Intraventricular Vancomycin

1)

Autmizguine J, Moran C, Gonzalez D, Capparelli EV, Smith PB, Grant GA, Benjamin DK Jr, Cohen-Wolkowiez M, Watt KM. Vancomycin cerebrospinal fluid pharmacokinetics in children with cerebral ventricular shunt infections. Pediatr Infect Dis J. 2014 Oct;33(10):e270-2. doi: 10.1097/INF.0000000000000385. PMID: 24776517; PMCID: PMC4209191.
2)

Albanèse J, Léone M, Bruguerolle B, Ayem ML, Lacarelle B, Martin C. Cerebrospinal fluid penetration and pharmacokinetics of vancomycin administered by continuous infusion to mechanically ventilated patients in an intensive care unit. Antimicrob Agents Chemother. 2000 May;44(5):1356-8. doi: 10.1128/AAC.44.5.1356-1358.2000. PMID: 10770777; PMCID: PMC89870.
3)

Ichinose N, Shinoda K, Yoshikawa G, Fukao E, Enoki Y, Taguchi K, Oda T, Tsutsumi K, Matsumoto K. Exploring the Factors Affecting the Transferability of Vancomycin to Cerebrospinal Fluid in Postoperative Neurosurgical Patients with Bacterial Meningitis. Biol Pharm Bull. 2022;45(9):1398-1402. doi: 10.1248/bpb.b22-00361. PMID: 36047211.

Cerebral venous sinus thrombosis after Vaccine-induced Immune Thrombotic Thrombocytopenia

Cerebral venous sinus thrombosis after Vaccine-induced Immune Thrombotic Thrombocytopenia

Health care providers should be familiar with the clinical presentations, pathophysiology, diagnostic criteria, and management consideration of this rare but severe and potentially fatal complication of the SARS-COV2 vaccine

Cerebral venous sinus thrombosis (CVT) prior to the COVID pandemic was rare, responsible for 0.5 of all strokes, at the onset of the pandemic on the East Coast, overall cross-sectional imaging volumes declined due to maintaining ventilation, high levels of care and limiting disease spread, although COVID-19 patients have a 30-60 times greater risk of CVT compared to the general population, and vaccination is currently the best option to mitigate severe disease. In early 2021, reports of adenoviral vector COVID vaccines causing CTV and Vaccine-induced Immune Thrombotic Thrombocytopenia (VITT), led to a 39.65% increase in cross-sectional venography, however, in this study unvaccinated patients in 2021 had a higher incidence of CVT (10.1%), compared to the vaccinated patients (4.5%). Clinicians should be aware that VITT CVT may present with a headache 5-30 days post-vaccination with thrombosis best diagnosed on CTV or MRV. If thrombosis is present with thrombocytopenia, platelets <150 × 109, elevated D-Dimer >4000 FEU, and positive anti-PF4 ELISA assay, the diagnosis is definitive. VITT CVT resembles spontaneous autoimmune heparin-induced thrombocytopenia (HIT) and is postulated to occur from platelet factor 4 (PF4) binding to vaccine adenoviral vectors forming a novel antigen, anti-PF4 memory B-cells, and anti-PF4 (VITT) antibodies. 1).

Outcome

Neurosurgical management involves treating intracranial hypertension however survival outcomes in a cohort were poor. In these series, decompression was performed in deteriorating patients however prophylactic decompression, in the presence of extensive venous sinus thrombosis, should be considered on a case-by-case basis. As vaccination programs accelerate across the world, neurosurgeons are likely to be increasingly involved in managing intracranial hypertension in patients with VITT-related sinus thromboses. 2).

A distinct clinical profile and a high mortality rate were observed in patients meeting the criteria for thrombocytopenia syndrome (TTS) after SARS-CoV-2 vaccination 3).

Non-heparin anticoagulants and immunoglobulin treatment might improve outcomes of VITT-associated cerebral venous thrombosis 4)

Systematic Review

Sixty-two studies reporting 160 cases were included from 16 countries. Patients were predominantly females with a median age of 42.50 (22) years. AZD1222 was administered to 140 patients (87·5%). TTS onset occurred in a median of 9 (4) days after vaccination. Venous thrombosis was most common (61.0%). Most patients developed cerebral venous sinus thrombosis (CVST; 66.3%). CVST was significantly more common in female vs male patients (p = 0·001) and in patients aged <45 years vs ≥45 years (p = 0·004). The mortality rate was 36.2%, and patients with suspected TTS, venous thrombosis, CVST, pulmonary embolism, or intraneural complications, patients not managed with non-heparin anticoagulants or IVIG, patients receiving platelet transfusions, and patients requiring intensive care unit admission, mechanical ventilation, or inpatient neurosurgery were more likely to expire than recover. 5)

Case series

Cerebral venous thrombosis caused by vaccine-induced immune thrombotic thrombocytopenia (VITT-CVT) is a rare adverse effect of adenovirus-based SARS-COV2 vaccines. In March 2021, after autoimmune pathogenesis of VITT was discovered, treatment recommendations were developed. This comprised immunomodulation, nonheparin anticoagulants, and avoidance of platelet transfusion. The aim of the study was to evaluate adherence to these recommendations and their association with mortality.

Scutelnic et al. used data from an international prospective registry of patients with CVT after adenovirus-based SARS-CoV-2 vaccination. They analyzed possible, probable, or definite VITT-CVT cases included until 18 January 2022. Immunomodulation entailed the administration of intravenous immunoglobulins and/or plasmapheresis.

99 VITT-CVT patients from 71 hospitals in 17 countries were analyzed. Five of 38 (13%), 11/24 (46%), and 28/37 (76%) of patients diagnosed in March, April, and from May onwards, respectively, were treated in-line with VITT recommendations (p<0.001). Overall, treatment according to recommendations had no statistically significant influence on mortality (14/44 (32%) vs 29/55 (52%), adjusted OR 0.43 (95%CI 0.16-1.19)). However, patients who received immunomodulation had lower mortality (19/65 (29%) vs 24/34 (70%), adjusted OR 0.19 (95%CI 0.06-0.58)). Treatment with non-heparin anticoagulants instead of heparins was not associated with lower mortality (17/51 (33%) vs 13/35 (37%), adjusted OR 0.70 (95%CI 0.24-2.04)). Mortality was also not significantly influenced by platelet transfusion (17/27 (63%) vs 26/72 (36%), adjusted OR 2.19 (95%CI 0.74-6.54)).

In VITT-CVT patients, adherence to VITT treatment recommendations improved over time. Immunomodulation seems crucial for reducing mortality of VITT-CVT 6).

During a 2-week period, we encountered five cases presenting with a combination of cerebral venous thrombosis (CVT), intracerebral hemorrhage, and thrombocytopenia. A clinical hallmark was the rapid and severe progression of disease in spite of maximum treatment efforts, resulting in fatal outcomes for 4 out of 5 patients. All cases had received the ChAdOx1 nCov-19 vaccine 1-2 weeks earlier and developed a characteristic syndrome thereafter. The rapid progressive clinical course and high fatality rate of CVT in combination with thrombocytopenia in such a cluster and in otherwise healthy adults is a recent phenomenon. Cerebral autopsy findings were those of venous hemorrhagic infarctions and thrombi in dural venous sinuses, including thrombus material apparently rich in thrombocytes, leukocytes, and fibrin. Vessel walls were free of inflammation. Extra-cerebral manifestations included leech-like thrombi in large veins, fibrin clots in small venules, and scattered hemorrhages on skin and membranes. CVT with thrombocytopenia after adenovirus vectored COVID-19 vaccination is a new clinical syndrome that needs to be recognized by clinicians is challenging to treat and seems associated with a high mortality rate 7)

Case reports

A patient was rapidly treated with steroids, immunoglobulin, and fondaparinux. She underwent within 6 h after hospital admission a mechanical thrombectomy in order to allow flow restoration in cerebral venous systems. Neuroendovascular treatment in cerebral venous thrombosis related to VITT has never been described before. It can represent a complementary tool along with the other therapies and a multidisciplinary approach 8).

Two cases of ChAdOx1 nCov-19 (AstraZeneca)-are associated with thrombotic thrombocytopenia syndrome (TTS) and cerebral venous sinus thrombosis (CVST). At the time of emergency room presentation due to persistent headache, blood serum levels revealed reduced platelet counts. Yet, 1 or 4 days after the onset of the symptom, the first MR-angiography provided no evidence of CVST. Follow-up imaging, performed upon headache refractory to nonsteroidal pain medication verified CVST 2-10 days after initial negative MRI. Both the patients received combined treatment with intravenous immunoglobulins and parenteral anticoagulation leading to an increase in platelet concentration in both individuals and resolution of the occluded cerebral sinus in one patient 9).

Rodriguez et al. reported the first described post Ad26.COV2.S (Janssen, Johnson & Johnson) vaccine-induced immune thrombocytopenia (VITT) case outside US. CASE DESCRIPTION: CA young woman without any medical history presented an association of deep vein thrombosis and thrombocytopenia at day 10 after vaccine injection. The patient was treated with low-molecular-weight heparin at a first medical institution. Twelve days post Ad26.COV2.S vaccination, the patient was admitted to the hospital for neurological deterioration and right hemiplegia. Medical imaging using MRI showed thrombosis of the major anterior part of the sagittal superior sinus with bilateral intraparenchymal hemorrhagic complications. Screening tests for antibodies against platelet factor 4 (PF4)-heparin by rapid lateral flow immunoassay and chemiluminescence techniques were negative. Platelet activation test using heparin-induced multiple electrode aggregometry confirmed the initial clinical hypothesis. Despite immediate treatment with intravenous immunoglobulin, dexamethasone, danaparoid, and attempted neurosurgery the patient evolved toward brain death.

Even though it is an extremely rare complication of vaccination physicians should maintain a high index of suspicion of VITT in patients who received an adenovirus-vector-based SARS-CoV-2 vaccine within the last 30 days with persistent complaints compatible with VITT or thromboembolic event associated with thrombocytopenia. The diagnosis should not be excluded if the rapid anti-PF4 immunological or chemiluminescence techniques yield negative results. An adapted functional assay should be performed to confirm the diagnosis. Early treatment with intravenous immunoglobulin and non-heparin anticoagulants is essential as delayed diagnosis and administration of appropriate treatment are associated with poor prognosis 10).

A case of VITT in a young female who presented 11 days after receiving the first dose of the Covishield vaccine, with severe headache and hemiparesis. She was diagnosed with CSVT with a large intraparenchymal bleed, requiring decompressive craniectomy and an extended period of mechanical ventilation.

The patient was successfully treated with intravenous immunoglobulin and discharged after 19 days in ICU. Although she was left with long-term neurological deficits, an early presentation and a multidisciplinary approach to management contributed to a relatively short stay in the hospital and avoided mortality 11).

1)

Franceschi AM, Petrover DR, McMahon TM, Libman RB, Giliberto L, Clouston SAP, Castillo M, Kirsch C. Retrospective review COVID-19 vaccine induced thrombotic thrombocytopenia and cerebral venous thrombosis-what can we learn from the immune response. Clin Imaging. 2022 Jul 15;90:63-70. doi: 10.1016/j.clinimag.2022.06.020. Epub ahead of print. PMID: 35926315; PMCID: PMC9283127.
2)

Eltayeb M, Jayakumar N, Coulter I, Johnson C, Crossman J. Decompressive craniectomy for intracranial hypertension in vaccine-induced immune thrombotic thrombocytopaenia: a case series. Br J Neurosurg. 2022 Aug 25:1-4. doi: 10.1080/02688697.2022.2115007. Epub ahead of print. PMID: 36004613.
3)

Sánchez van Kammen M, Aguiar de Sousa D, Poli S, Cordonnier C, Heldner MR, van de Munckhof A, Krzywicka K, van Haaps T, Ciccone A, Middeldorp S, Levi MM, Kremer Hovinga JA, Silvis S, Hiltunen S, Mansour M, Arauz A, Barboza MA, Field TS, Tsivgoulis G, Nagel S, Lindgren E, Tatlisumak T, Jood K, Putaala J, Ferro JM, Arnold M, Coutinho JM; Cerebral Venous Sinus Thrombosis With Thrombocytopenia Syndrome Study Group, Sharma AR, Elkady A, Negro A, Günther A, Gutschalk A, Schönenberger S, Buture A, Murphy S, Paiva Nunes A, Tiede A, Puthuppallil Philip A, Mengel A, Medina A, Hellström Vogel Å, Tawa A, Aujayeb A, Casolla B, Buck B, Zanferrari C, Garcia-Esperon C, Vayne C, Legault C, Pfrepper C, Tracol C, Soriano C, Guisado-Alonso D, Bougon D, Zimatore DS, Michalski D, Blacquiere D, Johansson E, Cuadrado-Godia E, De Maistre E, Carrera E, Vuillier F, Bonneville F, Giammello F, Bode FJ, Zimmerman J, d’Onofrio F, Grillo F, Cotton F, Caparros F, Puy L, Maier F, Gulli G, Frisullo G, Polkinghorne G, Franchineau G, Cangür H, Katzberg H, Sibon I, Baharoglu I, Brar J, Payen JF, Burrow J, Fernandes J, Schouten J, Althaus K, Garambois K, Derex L, Humbertjean L, Lebrato Hernandez L, Kellermair L, Morin Martin M, Petruzzellis M, Cotelli M, Dubois MC, Carvalho M, Wittstock M, Miranda M, Skjelland M, Bandettini di Poggio M, Scholz MJ, Raposo N, Kahnis R, Kruyt N, Huet O, Sharma P, Candelaresi P, Reiner P, Vieira R, Acampora R, Kern R, Leker R, Coutts S, Bal S, Sharma SS, Susen S, Cox T, Geeraerts T, Gattringer T, Bartsch T, Kleinig TJ, Dizonno V, Arslan Y. Characteristics and Outcomes of Patients With Cerebral Venous Sinus Thrombosis in SARS-CoV-2 Vaccine-Induced Immune Thrombotic Thrombocytopenia. JAMA Neurol. 2021 Nov 1;78(11):1314-1323. doi: 10.1001/jamaneurol.2021.3619. PMID: 34581763; PMCID: PMC8479648.
4)

Perry RJ, Tamborska A, Singh B, Craven B, Marigold R, Arthur-Farraj P, Yeo JM, Zhang L, Hassan-Smith G, Jones M, Hutchcroft C, Hobson E, Warcel D, White D, Ferdinand P, Webb A, Solomon T, Scully M, Werring DJ, Roffe C; CVT After Immunisation Against COVID-19 (CAIAC) collaborators. Cerebral venous thrombosis after vaccination against COVID-19 in the UK: a multicentre cohort study. Lancet. 2021 Sep 25;398(10306):1147-1156. doi: 10.1016/S0140-6736(21)01608-1. Epub 2021 Aug 6. PMID: 34370972; PMCID: PMC8346241.
5)

Waqar U, Ahmed S, Gardezi SMHA, Tahir MS, Abidin ZU, Hussain A, Ali N, Mahmood SF. Thrombosis with Thrombocytopenia Syndrome After Administration of AZD1222 or Ad26.COV2.S Vaccine for COVID-19: A Systematic Review. Clin Appl Thromb Hemost. 2021 Jan-Dec;27:10760296211068487. doi: 10.1177/10760296211068487. PMID: 34907794; PMCID: PMC8689609.
6)

Scutelnic A, Krzywicka K, Mbroh J, van de Munckhof A, Sánchez van Kammen M, Aguiar de Sousa D, Lindgren E, Jood K, Günther A, Hiltunen S, Putaala J, Tiede A, Maier F, Kern R, Bartsch T, Althaus K, Ciccone A, Wiedmann M, Skjelland M, Medina A, Cuadrado-Godia E, Cox T, Aujayeb A, Raposo N, Garambois K, Payen JF, Vuillier F, Franchineau G, Timsit S, Bougon D, Dubois MC, Tawa A, Tracol C, De Maistre E, Bonneville F, Vayne C, Mengel A, Michalski D, Pelz J, Wittstock M, Bode F, Zimmermann J, Schouten J, Buture A, Murphy S, Palma V, Negro A, Gutschalk A, Nagel S, Schoenenberger S, Frisullo G, Zanferrari C, Grillo F, Giammello F, Martin MM, Cervera A, Burrow J, Garcia Esperon C, Chew BLA, Kleinig TJ, Soriano C, Zimatore DS, Petruzzellis M, Elkady A, Miranda MS, Fernandes J, Hellström Vogel Å, Johansson E, Philip AP, Coutts SB, Bal S, Buck B, Legault C, Blacquiere D, Katzberg HD, Field TS, Dizonno V, Gattringer T, Jacobi C, Devroye A, Lemmens R, Kristoffersen ES, Bandettini di Poggio M, Ghiasian M, Karapanayiotides T, Chatterton S, Wronski M, Ng K, Kahnis R, Geeraerts T, Reiner P, Cordonnier C, Middeldorp S, Levi M, van Gorp ECM, van de Beek D, Brodard J, Kremer Hovinga JA, Kruip MJHA, Tatlisumak T, Ferro JM, Coutinho JM, Arnold M, Poli S, Heldner MR. Management of cerebral venous thrombosis due to adenoviral COVID-19 vaccination. Ann Neurol. 2022 Jun 10. doi: 10.1002/ana.26431. Epub ahead of print. PMID: 35689346.
7)

Wiedmann M, Skattør T, Stray-Pedersen A, Romundstad L, Antal EA, Marthinsen PB, Sørvoll IH, Leiknes Ernstsen S, Lund CG, Holme PA, Johansen TO, Brunborg C, Aamodt AH, Schultz NH, Skagen K, Skjelland M. Vaccine Induced Immune Thrombotic Thrombocytopenia Causing a Severe Form of Cerebral Venous Thrombosis With High Fatality Rate: A Case Series. Front Neurol. 2021 Jul 30;12:721146. doi: 10.3389/fneur.2021.721146. PMID: 34393988; PMCID: PMC8363077.
8)

Mirandola L, Arena G, Pagliaro M, Boghi A, Naldi A, Castellano D, Vaccarino A, Silengo D, Aprà F, Cavallo R, Livigni S. Massive cerebral venous sinus thrombosis in vaccine-induced immune thrombotic thrombocytopenia after ChAdOx1 nCoV-19 serum: case report of a successful multidisciplinary approach. Neurol Sci. 2022 Mar;43(3):1499-1502. doi: 10.1007/s10072-021-05805-y. Epub 2022 Jan 10. PMID: 35001190; PMCID: PMC8743093.
9)

Braun T, Viard M, Juenemann M, Struffert T, Schwarm F, Huttner HB, Roessler FC. Case Report: Take a Second Look: Covid-19 Vaccination-Related Cerebral Venous Thrombosis and Thrombotic Thrombocytopenia Syndrome. Front Neurol. 2021 Nov 22;12:763049. doi: 10.3389/fneur.2021.763049. PMID: 34880826; PMCID: PMC8645635.
10)

Rodriguez EVC, Bouazza FZ, Dauby N, Mullier F, d’Otreppe S, Jissendi Tchofo P, Bartiaux M, Sirjacques C, Roman A, Hermans C, Cliquennois M. Fatal vaccine-induced immune thrombotic thrombocytopenia (VITT) post Ad26.COV2.S: first documented case outside US. Infection. 2022 Apr;50(2):531-536. doi: 10.1007/s15010-021-01712-8. Epub 2021 Oct 9. PMID: 34626338; PMCID: PMC8501343.
11)

Kotal R, Jacob I, Rangappa P, Rao K, Hosurkar G, Anumula SK, Kuberappa AM. A rare case of vaccine-induced immune thrombosis and thrombocytopenia and approach to management. Surg Neurol Int. 2021 Aug 16;12:408. doi: 10.25259/SNI_689_2021. PMID: 34513173; PMCID: PMC8422498.

Ventriculoperitoneal shunt infection

Ventriculoperitoneal shunt infection

see also Shunt infection.

Ventriculoperitoneal shunt infection is the most common ventriculoperitoneal shunt complication, followed by abdominal pseudocyst, abscess, and infected fluid collection 1).

Epidemiology

see Ventriculoperitoneal Shunt Infection Epidemiology.

Types

see Methicillin resistant Staphylococcus aureus ventriculoperitoneal shunt infection.

see Staphylococcus epidermidis ventriculoperitoneal shunt infection

see Cryptococcus neoformans ventriculoperitoneal shunt infection.

Risk factors

Ventriculoperitoneal shunt infection risk factors.

Treatment

Ventriculoperitoneal shunt infection treatment

Outcome

Infection of ventriculoperitoneal shunt causes major morbidity and mortality in patients with cerebrospinal fluid shunts.

The prognosis of CSF shunt infections caused by Gram-negative bacteria (GNB) has been thought to be particularly poor.

Stamos et al. reviewed all GNB shunt infections treated at Children’s Memorial Hospital from January 1986 to January 1990 (n = 23). Of these infections 20 (87%) occurred within 4 weeks after shunt revision (median, 10 days). The most frequent symptoms were fever, lethargy, and irritability; the illness was not severe in the majority of these patients.

Escherichia coli was isolated from 12 of 23 patients (52%), Klebsiella pneumoniae from 5 (22%), and mixed GNB from 3 (13%) patients. Initial treatment always included immediate shunt removal, externalized ventricular drainage, and intravenous antibiotics. Extraventricular drainage revision and/or intraventricular antibiotics were required in four patients whose CSF cultures were persistently positive for GNB. At admission, these patients had CSF glucose levels of < 10 mg/dl and CSF positive for GNB by Gram’s stain. The overall cure rate was 100%, and no recurrence was observed; however, a subsequent infection with a different organism developed in four patients. Only 2 of 19 patients (11%) who were followed up suffered apparent CNS damage. One patient died of unrelated causes shortly after treatment. Our findings indicate that 1) patients with GNB CSF shunt infections often appear relatively well at presentation; 2) CSF positive for GNB by Gram’s stain and very low CSF glucose levels predict continued positive CSF cultures, despite appropriate antibiotic therapy; and 3) GNB CSF shunt infections can be successfully treated by prompt shunt removal, extraventricular drainage, and intravenous antibiotics 2).

Costs

Higher public expenditures were observed in the group of children undergoing ventriculoperitoneal shunt due to higher rates of ventriculoperitoneal shunt infections and mechanical complications requiring repeated hospitalizations and prosthesis replacements. Public policies must be tailored to offer the best treatment to children with hydrocephalus and to make judicious use of public resources without compromising the quality of treatment 3).

Case series

Ventriculoperitoneal shunt infection case series.

Case reports

Ventriculoperitoneal shunt infection case reports.

1)

Chung JJ, Yu JS, Kim JH, Nam SJ, Kim MJ. Intraabdominal complications secondary to ventriculoperitoneal shunts: CT findings and review of the literature. AJR Am J Roentgenol. 2009 Nov;193(5):1311-7. doi: 10.2214/AJR.09.2463. Review. PubMed PMID: 19843747.
2)

Stamos JK, Kaufman BA, Yogev R. Ventriculoperitoneal shunt infections with gram-negative bacteria. Neurosurgery. 1993 Nov;33(5):858-62. PubMed PMID: 8264883.
3)

Soriano LG, Melo JRT. Costs of pediatric hydrocephalus treatment for the Brazilian public health system in the Northeast of Brazil. Childs Nerv Syst. 2022 Aug 10. doi: 10.1007/s00381-022-05630-4. Epub ahead of print. PMID: 35948831.

Ventriculostomy related infection risk factors

Ventriculostomy related infection risk factors

Ventriculostomy related infection risk factors include prior brain surgery, cerebrospinal fluid fistula, and insertion site dehiscence. Walek et al. from Rhode Island Hospital found no significant association between infection risk and duration of external ventricular drainage placement 1).

A total of 15 supposed influencing factors includes: age, age & sex interactions, coinfection, catheter insertion outside the hospital, catheter type, CSF leakage, CSF sampling frequency, diagnosis, duration of catheterization, ICP > 20 mmHg, irrigation, multiple catheter, neurosurgical operation, reduced CSF glucose at catheter insertion and sex 2).

In a large series of patients, ventriculostomy related infection (VRI) was associated with a longer ICU stay, but its presence did not influence survival. A longer duration of ventriculostomy catheter monitoring in patients with VRI might be due to an increased volume of drained CSF during infection. Risk factors associated with VRIs are SAH, IVH, craniotomy, and coinfection 3).

A retrospective cohort study strengthens a growing body of works suggesting the importance of inoculation of skin flora as a critical risk factor in ventriculostomy related infections, underscoring the importance of drain changes only when clinically indicated and, that as soon as clinically permitted, catheters should be removed 4).

Associated with a longer ICU stay, but its presence did not influence survival. A longer duration of ventriculostomy catheter monitoring in patients with VAI might be due to an increased volume of drained CSF during infection. Risk factors associated with VAIs are subarachnoid hemorrhage (SAH), intraventricular hemorrhage IVH, craniotomy, and coinfection 5).

The risk of infection increases with increasing duration of catheterization and with repeated insertions. The use of local antibiotic irrigation or systemic antibiotics does not appear to reduce the risk of VAI. Routine surveillance cultures of CSF were no more likely to detect infection than cultures obtained when clinically indicated. These findings need to be considered in infection control policies addressing this important issue 6).

An increased risk of infection has been observed in patients with subarachnoid or intraventricular hemorrhage, in patients with concurrent systemic infections as well as with longer duration of catheterization, cerebrospinal (CSF) leakage, and frequent manipulation of the EVD system 7) 8) 9).

Many studies have been conducted to identify risk factors of EVD-related infections. However, none of these risk factors could be confirmed in a cohort of patients. Furthermore they not show any difference in infection rates between patients who were placed in single- or multibed rooms, respectively 10).

Interestingly no risk factor for EVD-related infection could be identified in a retrospective single center study 11).

References

1)

Walek KW, Leary OP, Sastry R, Asaad WF, Walsh JM, Horoho J, Mermel LA. Risk factors and outcomes associated with external ventricular drain infections. Infect Control Hosp Epidemiol. 2022 Apr 26:1-8. doi: 10.1017/ice.2022.23. Epub ahead of print. PMID: 35471129.
2)

Sorinola A, Buki A, Sandor J, Czeiter E. Risk Factors of External Ventricular Drain Infection: Proposing a Model for Future Studies. Front Neurol. 2019 Mar 15;10:226. doi: 10.3389/fneur.2019.00226. eCollection 2019. Review. PubMed PMID: 30930840; PubMed Central PMCID: PMC6428739.
3)

Bota DP, Lefranc F, Vilallobos HR, Brimioulle S, Vincent JL. Ventriculostomy-related infections in critically ill patients: a 6-year experience. J Neurosurg. 2005 Sep;103(3):468-72. PubMed PMID: 16235679.
4)

Katzir M, Lefkowitz JJ, Ben-Reuven D, Fuchs SJ, Hussein K, Sviri G. Decreasing external ventricular drain related infection rates with duration-independent, clinically indicated criteria for drain revision: A retrospective study. World Neurosurg. 2019 Aug 2. pii: S1878-8750(19)32121-7. doi: 10.1016/j.wneu.2019.07.205. [Epub ahead of print] PubMed PMID: 31382072.
5)

Bota DP, Lefranc F, Vilallobos HR, Brimioulle S, Vincent JL. Ventriculostomy-related infections in critically ill patients: a 6-year experience. J Neurosurg. 2005 Sep;103(3):468-72. PubMed PMID: 16235679.
6)

Arabi Y, Memish ZA, Balkhy HH, Francis C, Ferayan A, Al Shimemeri A, Almuneef MA. Ventriculostomy-associated infections: incidence and risk factors. Am J Infect Control. 2005 Apr;33(3):137-43. PubMed PMID: 15798667.
7)

Camacho E. F., Boszczowski Í., Basso M., Jeng B. C. P., Freire M. P., Guimarães T., Teixeira M. J., Costa S. F. Infection rate and risk factors associated with infections related to external ventricular drain. Infection. 2011;39(1):47–51. doi: 10.1007/s15010-010-0073-5.
8)

Kim J.-H., Desai N. S., Ricci J., Stieg P. E., Rosengart A. J., Hrtl R., Fraser J. F. Factors contributing to ventriculostomy infection. World Neurosurgery. 2012;77(1):135–140. doi: 10.1016/j.wneu.2011.04.017.
9)

Mayhall C. G., Archer N. H., Lamb V. A., Spadora A. C., Baggett J. W., Ward J. D., Narayan R. K. Ventriculostomy-related infections. A positive epidemiologic study. The New England Journal of Medicine. 1984;310(9):553–559. doi: 10.1056/NEJM198403013100903.
10)

Hagel S, Bruns T, Pletz MW, Engel C, Kalff R, Ewald C. External Ventricular Drain Infections: Risk Factors and Outcome. Interdiscip Perspect Infect Dis. 2014;2014:708531. Epub 2014 Nov 17. PubMed PMID: 25484896; PubMed Central PMCID: PMC4251652.
11)

Hagel S, Bruns T, Pletz MW, Engel C, Kalff R, Ewald C. External ventricular drain infections: risk factors and outcome. Interdiscip Perspect Infect Dis. 2014;2014:708531. doi: 10.1155/2014/708531. Epub 2014 Nov 17. PubMed PMID: 25484896; PubMed Central PMCID: PMC4251652.

Staphylococcus aureus

Staphylococcus aureus

Staphylococcus aureus is a gram positive coccal bacteria that is a member of the Firmicutes, and is frequently found in the human respiratory tract and on the skin. It is positive for catalase and nitrate reduction. Although S. aureus is not always pathogenic, it is a common cause of skin infections (e.g. boils), respiratory disease (e.g. sinusitis), and food poisoning. Disease-associated strains often promote infections by producing potent protein toxins, and expressing cell-surface proteins that bind and inactivate antibodies.

Implant failure is a severe and frequent adverse event in all areas of neurosurgery. It often involves infection with biofilm formation, accompanied by inflammation of surrounding tissue, including the brain, and bone loss. The most common bacteria involved are Staphylococcus aureus.

Classification

see Methicillin resistant Staphylococcus aureus.

see Methicillin sensitive Staphylococcus aureus.

Epidemiology

The epidemiology of invasive of S. aureus infections continues to evolve with Methicillin sensitive Staphylococcus aureus (MSSA) accounting for most of the infections in the series of Vallejo et al.

The majority of cases were associated with neurosurgical procedures; however, hematogenous S. aureus meningitis and spinal epidural abscess (SEA) occurred as community-acquired infections in patients without predisposing factors. Patients with MRSA CNS infections had a favorable response to vancomycin, but the beneficial effect of combination therapy or targeting vancomycin trough concentrations of 15-20 μg/mL remains unclear 1).

Prevention

Neurosurgical procedures and immunocompromisation are major risk factors for Staphylococcus aureus central nervous system infections. Hand hygiene, surveillance nasal swabs and perioperative prophylaxis are crucial points for effective SA infections prevention. In case of SA-CNS infections, pending microbiological results, anti-methicillin-resistant SA (MRSA) antibiotic, with good CNS penetration, should be included, with prompt de-escalation as soon as MRSA is ruled out. Consultation with an expert in antimicrobial therapy is recommended as well as prompt source control when feasible 2).

Treatment

Staphylococcus aureus treatment.

Complications

see Staphylococcus aureus brain abscess.

Outcome

Among central nervous system infections (e.g., meningitis, brain abscess, ventriculitis, transverse myelitis), those caused by Staphylococcus aureus (SA) are particularly challenging both in management and treatment, with poor clinical outcomes and long hospital stay 3).

Case series

Staphylococcus Aureus Case Series.

1)

Vallejo JG, Cain AN, Mason EO, Kaplan SL, Hultén KG. Staphylococcus aureus Central Nervous System Infections in Children. Pediatr Infect Dis J. 2017 Oct;36(10):947-951. doi: 10.1097/INF.0000000000001603. PubMed PMID: 28399057.
2) , 3)

Antonello RM, Riccardi N. How we deal with Staphylococcus aureus (MSSA, MRSA) central nervous system infections. Front Biosci (Schol Ed). 2022 Jan 12;14(1):1. doi: 10.31083/j.fbs1401001. PMID: 35320912.