Stenotrophomonas maltophilia meningitis

Stenotrophomonas maltophilia meningitis

Stenotrophomonas maltophilia treatment

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).

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.

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).

Vancomycin Indications.

see Vancomycin powder.

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.

Aneurysmal subarachnoid hemorrhage complications

Aneurysmal subarachnoid hemorrhage complications

Vasospasm is an important cause for mortality following aneurysmal subarachnoid hemorrhage aSAH affecting as many as 70% of patients. It usually occurs between 4th and 21st days of aSAH and is responsible for delayed ischemic neurological deficit (DIND) and cerebral infarction

It is one of the factors that can most significantly worsen the prognosis despite different treatments.

Transcranial doppler (TCD) evidence of vasospasm is predictive of delayed cerebral ischemia (DCI) with high accuracy. Although high sensitivity and negative predictive value make TCD an ideal monitoring device, it is not a mandated standard of care in aneurysmal subarachnoid hemorrhage (aSAH) due to the paucity of evidence on clinically relevant outcomes, despite recommendation by national guidelines. High-quality randomized trials evaluating the impact of TCD monitoring on patient-centered and physician-relevant outcomes are needed 1).


A greater proportion of aneurysmal subarachnoid hemorrhage patients, are surviving their initial hemorrhagic event but remain at increased risk of a number of complications, including delayed cerebral ischemia, epilepsy, nosocomial infections, cognitive impairment, shunt dependent hydrocephalus, and shunt related complications 2).

Intracranial complications including delayed cerebral ischemia (vasospasm), aneurysm rebleeding, and hydrocephalus form the targets for initial management. However, the extracranial consequences including hypertensionhyponatremia, and cardiopulmonary abnormalities can frequently arise during the management phase and have shown to directly affect clinical outcome.

Although the intracranial complications of SAH can take priority in the initial management, the extracranial complications should be monitored for and recognized as early as possible because these complications can develop at varying times throughout the course of the condition. Therefore, a variety of investigations, as described by this article, should be undertaken on admission to maximize early recognition of any of the extracranial consequences. Furthermore, because the extracranial complications have a direct effect on clinical outcome and can lead to and exacerbate the intracranial complications, monitoring, recognizing, and managing these complications in parallel with the intracranial complications is important and would allow optimization of the patient’s management and thus help improve their overall outcome 3).

Aneurysmal subarachnoid hemorrhage is complicated by intracerebral hemorrhage in 20—40 %, by intraventricular hemorrhage in 13-28%, and by subdural blood in 2-5% (usually due to posterior communicating aneurysm when over convexity, or distal anterior intracerebral artery (DACA) aneurysm with interhemispheric subdural).

The intracranial effects of aSAH causing death and disability are from vasospasm, direct effects of the initial bleed, increased intracranial pressure (ICP) and rebleeding 4).

Early brain injury and hydrocephalus (HCP) are important mediators of poor outcome in subarachnoid hemorrhage (SAH) patients. Injection of SAH patients’ CSF into the rat ventricle leads to HCP as well as subependymal injury compared with injection of control CSF 5).

Fever is a common occurrence (70%) especially in poor grades, contributes to adverse outcome and may not always respond to conventional treatment.

Persistent hyperglycemia (>200 mg/dl for >2 consecutive days) increases the likelihood of poor outcome after aSAH.

Management of patients following aSAH includes four major considerations:

(1) prediction of patients at highest risk for development of DCI,

(2) prophylactic measures to reduce its occurrence,

(3) monitoring to detect early signs of cerebral ischemia,

(4) treatments to correct vasospasm and cerebral ischemia once it occurs 6).

see Vasospasm after aneurysmal subarachnoid hemorrhage.

Brain edema after aneurysmal subarachnoid hemorrhage

see Delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage

see Aneurysm rebleeding

Subarachnoid hemorrhage (SAH) is often accompanied by pulmonary complications, which may lead to poor outcomes and death.

Sympathetic activation of the cardiovascular system in aneurysmal subarachnoid hemorrhage not only triggers the release of atrial and brain natriuretic peptides it can also lead to increased pulmonary venous pressures and permeability causing hydrostatic pulmonary edema 7).

see Neurogenic pulmonary edema.

Cardiac manifestations of intracranial subarachnoid hemorrhage patients include mild electrocardiogram variability, Takotsubo cardiomyopathy, non-ST elevation myocardial infarction, ST-elevation myocardial infarction and cardiac arrest, but their clinical relevance is unclear.

Among patients suffering from cardiac events at the time of aneurysmal subarachnoid hemorrhage, those with myocardial infarction and in particular those with a troponin level greater than 1.0 mcg/L had a 10 times increased risk of death 8).

Acute kidney injury

see Hyponatremia after aneurysmal subarachnoid hemorrhage

Hypokalemia is a common electrolyte disorder in the intensive care unit. Its cause often is complex, involving both potassium losses from the body and shifts of potassium into cells.

We present a case of severe hypokalemia of sudden onset in a patient being treated for subarachnoid hemorrhage in the surgical intensive care unit in order to illustrate the diagnosis and management of severe hypokalemia of unclear cause. The patient received agents that promote renal potassium losses and treatments associated with a shift of potassium into cells. Ibanez et al. outline the steps in diagnosis and management, focusing on the factors regulating the transcellular distribution of potassium in the body 9).

see Hydrocephalus after aneurysmal subarachnoid hemorrhage.

The clinical outcome after aneurysm rupture is at least in part determined by the severity of IVH. Knowledge of the effect of IVH may help guide physicians in the care of patients with aneurysmal bleeding 10).

see Cognitive disorder after subarachnoid hemorrhage.

Aneurysmal subarachnoid hemorrhage neuropsychiatric disturbance.

Overall rates of VTE (Deep-Vein Thrombosis Deep-vein thrombosis or PE), Deep-vein thrombosis, and PE were 4.4%, 3.5%, and 1.2%, respectively. On multivariate analysis, the following factors were associated with increased VTE risk: increasing age, black race, male sex, teaching hospital, congestive heart failure, coagulopathy, neurologic disorders, paralysis, fluid and electrolyte disorders, obesity, and weight loss. Patients that underwent clipping versus coiling had similar VTE rates. VTE was associated with pulmonary/cardiac complication (odds ratio [OR] 2.8), infectious complication (OR 2.8), ventriculostomy (OR 1.8), and vasospasm (OR 1.3). Patients with VTE experienced increased non-routine discharge (OR 3.3), and had nearly double the mean length of stay (p<0.001) and total inflation-adjusted hospital charges (p<0.001). To our knowledge, this is the largest study evaluating the incidence and risk factors associated with the development of VTE after aSAH. The presence of one or more of these factors may necessitate more aggressive VTE prophylaxis 11).

Short course (<48h) administration of EACA in patients with aneurysmal subarachnoid hemorrhage is associated with an 8.5 times greater risk of Deep-Vein Thrombosis (Deep-vein thrombosis) formation 12).

Routine compressive venous Doppler ultrasonography is an efficient, noninvasive means of identifying Deep-Vein Thrombosis (Deep-vein thrombosis) as a screening modality in both symptomatic and asymptomatic patients following aneurysmal SAH. The ability to confirm or deny the presence of Deep-vein thrombosis allows one to better identify the indications for chemoprophylaxis. Prophylaxis for venous thromboembolism in neurosurgical patients is common. Emerging literature and anecdotal experience have exposed risks of complications with prophylactic anticoagulation protocols. The identification of patients at high risk-for example, those with asymptomatic Deep-vein thrombosis-will allow physicians to better assess the role of prophylactic anticoagulation 13).

Deep-Vein Thrombosis (Deep-vein thrombosis) formation most commonly occurs in the first 2 weeks following aSAH, with detection in a cohort peaking between Days 5 and 9. Chemoprophylaxis is associated with a significantly lower incidence of Deep-vein thrombosis 14).

Patient should be ideally monitored in the NICU for at least 1st 24 h after surgery. Anticonvulsants, osmotherapy and nimodipine must be continued. Hydrocephalus, vasospasm, seizures, and electrolyte disturbances can occur necessitating close observation and prompt management. One of the major challenges in the management of aSAH is identifying potential or ongoing perfusion deficits. Ischemic insults can occur following ictus, or due to raised ICP, hypotension and vasospasm. Early identification and appropriate treatment of postictal intracranial (ICP, TCD flow velocities) and cardiovascular (cardiac output, ECG, BP, CVP) changes is possible in dedicated NICU and is crucial for improving outcomes. Heuer et al. observed that raised ICP (>20 mmHg) occurred in >50% of patients after aSAH and was associated with poor outcomes. Factors associated with raised ICP included poor clinical and radiological grades of aSAH, intraoperative brain swelling, parenchymal and intraventricular bleed and rebleeding.

see Seizure after aneurysmal subarachnoid hemorrhage.

Cytotoxic Lesions of the Corpus Callosum.

Koizumi et al. evaluated the incidence of NOMI in patients with subarachnoid hemorrhage (SAH) due to ruptured aneurysms, and they present the clinical characteristics and describe the outcomes to emphasize the importance of recognizing NOMI.

Observations: Overall, 7 of 276 consecutive patients with SAH developed NOMI. Their average age was 71 years, and 5 patients were men. Hunt and Kosnik grades were as follows: grade II, 2 patients; grade III, 3 patients; grade IV, 1 patient; and grade V, 1 patient. Fisher grades were as follows: grade 1, 1 patient; grade 2, 1 patient; and grade 3, 5 patients. Three patients were treated with endovascular coiling, 3 with microsurgical clipping, and 1 with conservative management. Five patients had abdominal symptoms prior to the confirmed diagnosis of NOMI. Four patients fell into shock. Two patients required emergent laparotomy followed by second-look surgery. Four patients could be managed conservatively. The overall mortality of patients with NOMI complication was 29% (2 of 7 cases).

NOMI had a high mortality rate. Neurosurgeons should recognize that NOMI can occur as a fatal complication after SAH 15).


1)

Kumar G, Shahripour RB, Harrigan MR. Vasospasm on transcranial Doppler is predictive of delayed cerebral ischemia in aneurysmal subarachnoid hemorrhage: a systematic review and meta-analysis. J Neurosurg. 2015 Oct 23:1-8. [Epub ahead of print] PubMed PMID: 26495942.
2)

Connolly ES Jr, Rabinstein AA, Carhuapoma JR, Derdeyn CP, Dion J, Higashida RT, et al: Guidelines for the manage- ment of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Asso- ciation/American Stroke Association. Stroke 43:1711–1737, 2012
3)

Hall A, O’Kane R. The Extracranial Consequences of Subarachnoid Hemorrhage. World Neurosurg. 2018 Jan;109:381-392. doi: 10.1016/j.wneu.2017.10.016. Epub 2017 Oct 16. Review. PubMed PMID: 29051110.
4)

Kassell MJ. Aneurysmal subarachnoid hemorrhage: An update on the medical complications and treatments strategies seen in these patients. Curr Opin Anaesthesiol. 2011;24:500–7.
5)

Li P, Chaudhary N, Gemmete JJ, Thompson BG, Hua Y, Xi G, Pandey AS. Intraventricular Injection of Noncellular Cerebrospinal Fluid from Subarachnoid Hemorrhage Patient into Rat Ventricles Leads to Ventricular Enlargement and Periventricular Injury. Acta Neurochir Suppl. 2016;121:331-4. doi: 10.1007/978-3-319-18497-5_57. PubMed PMID: 26463970.
6)

Dusick JR, Gonzalez NR. Management of arterial vasospasm following aneurysmal subarachnoid hemorrhage. Semin Neurol. 2013 Nov;33(5):488-97. doi: 10.1055/s-0033-1364216. Epub 2014 Feb 6. PubMed PMID: 24504612.
7)

Lo BW, Fukuda H, Nishimura Y, Macdonald RL, Farrokhyar F, Thabane L, Levine MA. Pathophysiologic mechanisms of brain-body associations in ruptured brain aneurysms: A systematic review. Surg Neurol Int. 2015 Aug 11;6:136. doi: 10.4103/2152-7806.162677. eCollection 2015. PubMed PMID: 26322246.
8)

Ahmadian A, Mizzi A, Banasiak M, Downes K, Camporesi EM, Thompson Sullebarger J, Vasan R, Mangar D, van Loveren HR, Agazzi S. Cardiac manifestations of subarachnoid hemorrhage. Heart Lung Vessel. 2013;5(3):168-78. PubMed PMID: 24364008; PubMed Central PMCID: PMC3848675.
9)

Ybanez N, Agrawal V, Tranmer BI, Gennari FJ. Severe hypokalemia in a patient with subarachnoid hemorrhage. Am J Kidney Dis. 2014 Mar;63(3):530-5. doi: 10.1053/j.ajkd.2013.07.005. Epub 2013 Aug 20. PubMed PMID: 23972266.
10)

Mayfrank L, Hütter BO, Kohorst Y, Kreitschmann-Andermahr I, Rohde V, Thron A, Gilsbach JM. Influence of intraventricular hemorrhage on outcome after rupture of intracranial aneurysm. Neurosurg Rev. 2001 Dec;24(4):185-91. PubMed PMID: 11778824.
11)

Kshettry VR, Rosenbaum BP, Seicean A, Kelly ML, Schiltz NK, Weil RJ. Incidence and risk factors associated with in-hospital venous thromboembolism after aneurysmal subarachnoid hemorrhage. J Clin Neurosci. 2014 Feb;21(2):282-6. doi: 10.1016/j.jocn.2013.07.003. Epub 2013 Oct 13. PubMed PMID: 24128773.
12)

Foreman PM, Chua M, Harrigan MR, Fisher WS 3rd, Tubbs RS, Shoja MM, Griessenauer CJ. Antifibrinolytic therapy in aneurysmal subarachnoid hemorrhage increases the risk for deep venous thrombosis: A case-control study. Clin Neurol Neurosurg. 2015 Sep 10;139:66-69. doi: 10.1016/j.clineuro.2015.09.005. [Epub ahead of print] PubMed PMID: 26378393.
13)

Ray WZ, Strom RG, Blackburn SL, Ashley WW, Sicard GA, Rich KM. Incidence of deep venous thrombosis after subarachnoid hemorrhage. J Neurosurg. 2009 May;110(5):1010-4. doi: 10.3171/2008.9.JNS08107. PubMed PMID: 19133755.
14)

Liang CW, Su K, Liu JJ, Dogan A, Hinson HE. Timing of Deep-Vein Thrombosis formation after aneurysmal subarachnoid hemorrhage. J Neurosurg. 2015 Oct;123(4):891-6. doi: 10.3171/2014.12.JNS141288. Epub 2015 Jul 10. PubMed PMID: 26162047; PubMed Central PMCID: PMC4591180.
15)

Koizumi H, Yamamoto D, Maruhashi T, Kataoka Y, Inukai M, Asari Y, Kumabe T. Relationship between subarachnoid hemorrhage and nonocclusive mesenteric ischemia as a fatal complication: patient series. J Neurosurg Case Lessons. 2022 Jul 18;4(3):CASE22199. doi: 10.3171/CASE22199. PMID: 36046708; PMCID: PMC9301345.
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