Ventriculostomy related infection risk factors

Ventriculostomy related infection risk factors

Ventriculostomy related infection risk factors include prior brain surgerycerebrospinal 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).


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.

Pituitary apoplexy

Pituitary apoplexy

Pituitary apoplexy (PA) is a clinical condition characterized by a sudden increase in pituitary gland volume secondary to ischemia and/or necrosis.

● due to the expansion of a pituitary adenoma from hemorrhage or necrosis

● typical presentation: paroxysmal H/A with endocrinologic and/or neurologic deficit (usually ophthalmoplegia or visual loss)

● management: immediate administration of glucocorticoids, and transsphenoidal decompression within 7 days in most cases.

Pituitary apoplexy epidemiology.

It is important to note that pituitary apoplexy may be divided into hemorrhagic or ischemic, each with unique neuroimaging findings.

Pituitary apoplexy etiology.

Some postulate that a gradual enlarging pituitary tumor becomes impacted at the diaphragmatic notch, compressing and distorting the hypophyseal stalk and its vascular supply. This deprives the anterior pituitary gland and the tumor itself of its vascular supply, apoplectically causing ischemia and subsequent necrosis.

Another theory stipulates that rapid expansion of the tumor outstrips its vascular supply, resulting in ischemia and necrosis. This explanation is doubtful, since most tumors that undergo apoplexy are slow growing.

Cerebral ischemia due to pituitary apoplexy is very rare. It may be caused by vasospasm or direct compression of cerebral vessels by the tumor.

Pituitary apoplexy is characterized by a sudden onset of headache, visual symptoms, altered mental status, and hormonal dysfunction due to acute hemorrhage or infarction of a pituitary gland.

Diabetes insipidus may occur with pituitary apoplexy.

The clinical presentation varies widely and includes asymptomatic cases, classical pituitary apoplexy and even sudden death.

It is characterized by a sudden onset of headachevisual impairmentmental disorder, and hormone dysfunction due to acute hemorrhage or infarction of a pituitary gland.

Because of the acute symptomatology, many patients are referred to a neurosurgical department without prior endocrinological assessment.

Neurologists and neurosurgeons need to be aware of the endocrinological sequelae of pituitary apoplexy in order to avoid potentially lethal complications. Patients should be counselled to adhere to long-term endocrinological and neurosurgical follow-up 1).


An existing pituitary adenoma is usually present. The visual symptoms may include both visual acuity impairment and visual field impairment from involvement of the optic nerve or chiasm and ocular motility dysfunction from involvement of the cranial nerves traversing the cavernous sinus 2)


Paschou et al present a patient in his late 30s presented with sudden and severe frontal headachefeverblurred visionnauseaconfusion, as well as oculomotor nerve palsy (CN III) with partial ptosis of the left eyelid, dilated left pupil and left eye globe deviation inferiorly and laterally. The final diagnosis was acute pituitary apoplexy complicating a pituitary macroadenoma. In this setting, headache is usually present due to stretching and irritation of the dura mater, and fever due to meningeal irritation or upward expansion leading to hypothalamic dysfunction. Decreased visual acuity and defects in visual fields are caused by upward expansion, which compresses the optic chiasmOphthalmoplegia can also be observed due to lateral expansion with invasion of the cavernous sinus 3).

Pituitary apoplexy diagnosis.

Seung et al., present an unusual case of bitemporal hemianopsia caused by a large anterior communicating artery aneurysm.

A 41-year-old woman was admitted to our neurosurgical department with a sudden-onset bursting headache and visual impairment. On admission, her vision was decreased to finger counting at 30 cm in the left eye and 50 cm in the right eye, and a severe bitemporal hemianopsia was demonstrated on visual field testing. A brain computed tomography scan revealed a subarachnoid hemorrhage at the basal cistern, and conventional cerebral catheter angiography of the left internal carotid artery demonstrated an 18×8 mm dumbbell-shaped aneurysm at the ACoA. Microscopic aneurysmal clipping was performed. An ACoA aneurysm can produce visual field defects by compressing the optic chiasm or nerves.

Seung et al., emphasize that it is important to diagnose an aneurysm through cerebrovascular study to prevent confusing it with pituitary apoplexy 4).


A 52-year-old woman, previously diagnosed with asymptomatic Rathke cleft cyst (RCC), came with a severe headache, along with visual dysfunction and symptoms of pituitary insufficiency. Fluid-attenuated inversion recovery magnetic resonance imaging demonstrated diffuse hyperintensity in the cerebral cisterns, whereas watery clear cerebrospinal fluid was obtained by lumbar puncture. Surgery performed 1 month after onset revealed a nonhemorrhagic lesion, with a final diagnosis of nonhemorrhagic RCC rupture.

Yokota et al., conclude that nonhemorrhagic RCC rupture and subsequent leakage of the contents into subarachnoid space were the underlying pathogenesis in the present case of RCC resembling apoplexy 5).

Pituitary apoplexy treatment.

see Pituitary apoplexy outcome.

Lammert et al., analysed data from 24 patients (m:f/16:8) with a median age of 64 yrs (38 to 83yrs) that underwent surgery for pituitary apoplexy regardless of time from symptom onset. Apoplexies were necrotic in 14 cases and haemorrhagic in 10 cases.

Preoperatively, 7 patients (29.2%) showed complete anterior pituitary insufficiency, 16 patients (66.6%) had partial anterior pituitary insufficiency and one patient (4.17%) had normal pituitary functions. Persistent panhypopituitarism was found in 7 patients (29.2%), whereas an overall improvement of pituitary function was noted in 13 (57.1%) patients. Preoperative prolactin (PRL) levels were significantly associated with recovery of endocrine functions, whereas specifically all patients with preoperative PRL levels of at least 8.8 ng/ml recovered partially or fully. Time to surgery (0-7 days vs. 1-4 weeks vs.>4 weeks) was not significantly associated with outcome.

The data emphasize that normal and high preoperative PRL levels are associated with better endocrine outcome after surgery. They conclude that patients benefit from surgical intervention even after delayed diagnosis with the serum PRL levels is being a valid biomarker for clinical decision making 6).

Pituitary apoplexy case reports.

Nineteen cases of suspected Pituitary apoplexy were included. The majority of dogs showed behavioural abnormalities (11/19). Neurological signs more frequently identified were obtundation (7/19), vestibular signs (7/19) and epileptic seizures (6/19). The onset of neurological signs was per-acute in 14 out of 19 cases. Data regarding CT and MRI were available in 18 and 9 cases, respectively. Neurological signs resolved in less than 24 h in seven patients. The short-term prognosis was defined as favourable in the majority of the study population. The median survival time was of 7 months from the time of PA diagnosis. This is the first description of neurological signs, imaging findings and outcome in a large group of dogs with PA 7).


1)

Grzywotz A, Kleist B, Möller LC, Hans VH, Göricke S, Sure U, Müller O, Kreitschmann-Andermahr I. Pituitary apoplexy – A single center retrospective study from the neurosurgical perspective and review of the literature. Clin Neurol Neurosurg. 2017 Oct 10;163:39-45. doi: 10.1016/j.clineuro.2017.10.006. [Epub ahead of print] PubMed PMID: 29055223.
2)

Nawar RN, AbdelMannan D, Selman WR, Arafah BM. Pituitary tumor apoplexy: a review. J Intensive Care Med. 2008 Mar-Apr. 23(2):75-90.
3)

Paschou SA, Tzioras K, Trianti V, Lyra S, Lioutas VA, Seretis A, Vryonidou A. Young adult patient with headache, fever and blurred vision. Hormones (Athens). 2016 Oct;15(4):548-550. doi: 10.14310/horm.2002.1701. PubMed PMID: 28222415.
4)

Seung WB, Kim DY, Park YS. A Large Ruptured Anterior Communicating Artery Aneurysm Presenting with Bitemporal Hemianopsia. J Korean Neurosurg Soc. 2015 Sep;58(3):291-3. doi: 10.3340/jkns.2015.58.3.291. Epub 2015 Sep 30. PubMed PMID: 26539276; PubMed Central PMCID: PMC4630364.
5)

Yokota H, Ida Y, Wajima D, Nishimura F, Nakase H. Rathke Cleft Cyst with Evidence of Rupture into Subarachnoid Space. World Neurosurg. 2016 Oct 21. pii: S1878-8750(16)31061-0. doi: 10.1016/j.wneu.2016.10.072. [Epub ahead of print] PubMed PMID: 27777166.
6)

Lammert A, Walter MS, Giordano FA, Al Zhgloul M, Krämer BK, Nittka S, Schulte DM, Ratliff M, Hänggi D, Seiz-Rosenhagen M. Neuro-Endocrine Recovery After Pituitary Apoplexy: Prolactin as a Predictive Factor. Exp Clin Endocrinol Diabetes. 2018 Jul 2. doi: 10.1055/a-0640-2915. [Epub ahead of print] PubMed PMID: 29966153.
7)

Galli G, Bertolini G, Dalla Serra G, Menchetti M. Suspected Pituitary Apoplexy: Clinical Presentation, Diagnostic Imaging Findings and Outcome in 19 Dogs. Vet Sci. 2022 Apr 15;9(4):191. doi: 10.3390/vetsci9040191. PMID: 35448689.

Lactotroph adenoma treatment

Lactotroph adenoma treatment

Dopamine agonists such as bromocriptine and cabergoline have been found to be an effective treatment for hyperprolactinemia, not only inducing adenoma shrinkage but also lowering serum prolactin levels. Among known dopamine agonists, cabergoline is the drug of choice due to its enhanced tolerability compared with bromocriptine 1).


Surgical intervention may resurface as an alternative first-line treatment. When used in combination with cabergoline, surgery offers a higher disease remission rate than either drug or operation alone 2)


Lactotroph Adenoma Surgery is safe and efficient. It is particularly suitable for enclosed prolactinomas. The patient should be well informed of the pros and cons of the treatment options, which include dopamine agonist (DA) and transsphenoidal microsurgery, and the patient’s preference should be taken into account during decision-making 3).

In the absence of visual deficits, pituitary apoplexy in lactotroph adenomas is the only type of pituitary tumor for which medical therapy (Dopamine agonists) may be the primary treatment.


Issues and questions to be addressed in this approach to long-term management of prolactinomas include the frequency of radiographic monitoring, effect of pregnancy and menopause, safety of estrogen in women taking oral contraceptives, and the potential for discontinuation of dopamine agonist therapy 4).

see Dopamine agonist for Lactotroph adenoma.

see Lactotroph Adenoma Surgery

Although transsphenoidal surgery (TSS) is an option for prolactinoma treatment, it is less effective than medical management, carries considerably more risk, and is more expensive. The benefit/risk ratio for DA therapy compared to TSS actually becomes increasingly more favorable as tumor size increases. Therefore DA should remain the clear treatment of choice for essentially all patients with prolactinomas, reserving TSS as a second-line option for the very small number of patients that do not tolerate or are completely resistant to DA therapy 5).

Lactotroph adenoma radiosurgery.

The underlying decision to perform serial imaging in prolactinoma patients should be individualized on a case-by-case basis. Future studies should focus on alternative imaging methods and/or contrast agents 6).


1)

Krysiak R, Okopien B. Different Effects of Cabergoline and Bromocriptine on Metabolic and Cardiovascular Risk Factors in Patients with Elevated Prolactin Levels. Basic Clin Pharmacol Toxicol. 2014 Aug 13. doi: 10.1111/bcpt.12307. [Epub ahead of print] PubMed PMID: 25123447.
2)

Chen TY, Lee CH, Yang MY, Shen CC, Yang YP, Chien Y, Huang YF, Lai CM, Cheng WY. Treatment of Hyperprolactinemia: A Single-Institute Experience. J Chin Med Assoc. 2021 Jul 13. doi: 10.1097/JCMA.0000000000000584. Epub ahead of print. PMID: 34261980.
3)

Giese S, Nasi-Kordhishti I, Honegger J. Outcomes of Transsphenoidal Microsurgery for Prolactinomas – A Contemporary Series of 162 Cases. Exp Clin Endocrinol Diabetes. 2021 Jan 18. doi: 10.1055/a-1247-4908. Epub ahead of print. PMID: 33461233.
4)

Schlechte JA. Long-term management of prolactinomas. J Clin Endocrinol Metab. 2007 Aug;92(8):2861-5. Review. PubMed PMID: 17682084.
5)

Bloomgarden E, Molitch ME. Surgical treatment of prolactinomas: cons. Endocrine. 2014 Aug 12. [Epub ahead of print] PubMed PMID: 25112227.
6)

Varlamov EV, Hinojosa-Amaya JM, Fleseriu M. Magnetic resonance imaging in the management of prolactinomas; a review of the evidence. Pituitary. 2019 Oct 28. doi: 10.1007/s11102-019-01001-6. [Epub ahead of print] Review. PubMed PMID: 31659622.
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