complications

Cardiac Complications After Subarachnoid Hemorrhage

Cardiac Complications After Subarachnoid Hemorrhage

Subarachnoid hemorrhage (SAH) is a serious condition, and a myocardial injury or dysfunction could contribute to the outcome.

Acute cardiac complications frequently occur after subarachnoid hemorrhage (SAH). These complications include electrocardiogram (ECG) abnormalities, the release of cardiac biomarkers, and the development of acute stress-induced heart failure resembling Takotsubo cardiomyopathy 1) 2) 3) 4) 5) 6)

non-ST elevation myocardial infarction, ST-elevation myocardial infarction and cardiac arrest, but their clinical relevance is unclear.

Lång et al. assessed the prevalence and prognostic impact of cardiac involvement in a cohort with SAH in a prospective observational multicenter study. They included 192 patients treated for non traumatic subarachnoid hemorrhage. They performed ECG recordings, echocardiogram, and blood sampling within 24 h of admission and on days 3 and 7 and at 90 days. The primary endpoint was the evidence of cardiac involvement at 90 days, and the secondary endpoint was to examine the prevalence of a myocardial injury or dysfunction. The median age was 54.5 (interquartile range [IQR] 48.0-64.0) years, 44.3% were male and the median World Federation of Neurosurgical Societies grading for subarachnoid hemorrhage score was 2 (IQR 1-4). At day 90, 22/125 patients (17.6%) had left ventricular ejection fractions ≤ 50%, and 2/121 patients (1.7%) had evidence of a diastolic dysfunction as defined by mitral peak E-wave velocity by peak e’ velocity (E/e’) > 14. There was no prognostic impact from echocardiographic evidence of cardiac complications on neurological outcomes. The overall prevalence of cardiac dysfunction was modest. They found no demographic or SAH-related factors associated with 90 days cardiac dysfunction 7).

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).

1)

Zaroff JG, Rordorf GA, Newell JB, Ogilvy CS, Levinson JR. Cardiac outcome in patients with subarachnoid hemorrhage and electrocardiographic abnormalities. Neurosurgery. 1999;44:34–39. doi: 10.1097/00006123-199901000-00013.
2)

Tung P, Kopelnik A, Banki N, et al. Predictors of neurocardiogenic injury after subarachnoid hemorrhage. Stroke. 2004;35:548–551. doi: 10.1161/01.STR.0000114874.96688.54.
3)

Banki N, Kopelnik A, Tung P, et al. Prospective analysis of prevalence, distribution, and rate of recovery of left ventricular systolic dysfunction in patients with subarachnoid hemorrhage. J Neurosurg. 2006;105:15–20. doi: 10.3171/jns.2006.105.1.15.
4)

Lee VH, Connolly HM, Fulgham JR, Manno EM, Brown JRD, Wijdicks EFM. Tako-tsubo cardiomyopathy in aneurysmal subarachnoid hemorrhage: an underappreciated ventricular dysfunction. J Neurosurg. 2006;105:264–270. doi: 10.3171/jns.2006.105.2.264.
5)

Oras J, Grivans C, Bartley A, Rydenhag B, Ricksten SE, Seeman-Lodding H. Elevated high-sensitive troponin T on admission is an indicator of poor long-term outcome in patients with subarachnoid haemorrhage: a prospective observational study. Crit Care (Lond, Engl) 2016;20:11. doi: 10.1186/s13054-015-1181-5.
6)

van der Bilt IA, Hasan D, Vandertop WP, et al. Impact of cardiac complications on outcome after aneurysmal subarachnoid hemorrhage: a meta-analysis. Neurology. 2009;72:635–642. doi: 10.1212/01.wnl.0000342471.07290.07.
7)

Lång M, Jakob SM, Takala R, Lyngbakken MN, Turpeinen A, Omland T, Merz TM, Wiegand J, Grönlund J, Rahi M, Valtonen M, Koivisto T, Røsjø H, Bendel S. The prevalence of cardiac complications and their impact on outcomes in patients with non-traumatic subarachnoid hemorrhage. Sci Rep. 2022 Nov 22;12(1):20109. doi: 10.1038/s41598-022-24675-8. PMID: 36418906.
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.

Ventriculoperitoneal Shunt Complications

Ventriculoperitoneal Shunt Complications

see External ventricular drainage complications

see also Cerebrospinal fluid shunt complications.

Ventriculoperitoneal shunt is the most common treatment to manage hydrocephalus; It is unfortunately burdened by up to 25% of complications. The peritoneal approach may expose patients to many complications.

Patients with a ventriculoperitoneal shunt tend to develop epidural fluid accumulation after cranioplasty and also have a higher frequency of syndrome of the trephined after bone flap removal. Thus treatment of patients with postcranioplasty infection and a VP shunt is often challenging.

The management of ventriculoperitoneal shunt complication or failure is a common problem in neurosurgical practice. On occasion, extraperitoneal sites for CSF diversion are required when shunting to the peritoneal cavity has failed after multiple attempts.

Complications frequently associated with a VP shunt: includes shunt obstruction, infection, overdrainage of CSF, and perforation of the gastrointestinal tract, gallbladder, vagina, and abdominal wall at the umbilicus… 1).

Despite procedural and equipment advances, the procedure it is accompanied by frequent complications and malfunctions. Some studies have shown an overall shunt failure rate as high as 59%, with the majority of failures occurring within the first 6 months after shunt placement 2).

Endoscopic placement of ventriculoperitoneal (VP) shunt catheters in pediatric patients has been increasingly used in an attempt to minimize the unacceptably high rates of revision. Although this procedure carries an increased expense, there is currently no evidence to support an improved long-term outcome.

Endoscopic assisted ventricular catheter placement decreased the odds of proximal obstruction but failed to improve overall shunt survival in a 6 year experience 3).

Diagnosis

The evaluation of children with suspected ventriculoperitoneal shunt (VPS) malfunction has evolved into a diagnostic dilemma. This patient population is vulnerable not only to the medical risks of hydrocephalus and surgical complications but also to silent but harmful effects of ionizing radiation secondary to imaging used to evaluate shunt efficacy and patency. The combination of increased medical awareness regarding ionizing radiation and public concern has generated desire to reduce the reliance on head computed tomography (CT) for the evaluation of VPS malfunction. Many centers have started to investigate the utility of low dose computed tomography and alternatives, such as fast magnetic resonance imaging for the investigation of VP shunt malfunction in order to keep radiation exposure as low as reasonably achievable.

A pilot study demonstrates that utilization of limited head CT scan in the evaluation of children with suspected VP shunt malfunction is a feasible strategy for the evaluation of the ventricular size 4).

In the study of Afat et al., low-dose computed tomography (LD-CT) provides excellent sensitivity and higher diagnostic confidence with lower radiation exposure compared with radiographic shunt series (SS) 5).

Ventriculoperitoneal shunt infection

see Ventriculoperitoneal shunt infection.

Ventriculitis

Intraventricular administration of proper antibiotics is a reliable and effective way to treat ventriculitis associated with ventriculoperitoneal shunts.

Vancomycin is the preferred antibiotic for ventriculitis, but other kind(s) of some antibiotics are necessary in a few patients in addition to or instead of vancomycin 6).

Ventriculoperitoneal shunt malfunction

Ventriculoperitoneal shunt overdrainage

see Ventriculoperitoneal shunt overdrainage

Ventriculoperitoneal shunt obstruction

see Ventriculoperitoneal shunt obstruction

Shunt calcification

see Shunt calcification

Abdominal complications

see Ventriculoperitoneal shunt abdominal complications.

Silicone allergy

Ventriculoperitoneal shunt complications have rarely been attributed to silicone allergy, with only a handful of cases reported in literature. The classic presentation of allergy to silicone ventriculoperitoneal shunt, i.e., abdominal pain with recurrent skin breakdown along the shunt tract, is nonspecific and difficult to distinguish clinically from other causes of shunt-related symptoms. It can be diagnosed by detection of antisilicone antibodies and is treated with removal of the shunt and replacement, if needed, with a polyurethane shunt system.

Kurin et al. report the first case of suspected silicone allergy presenting as clinical peritonitis without overt colonic perforation 7).

Progression of Normal-Tension Glaucoma 8).

Case series

Merkler et al., performed a retrospective cohort study of adult patients hospitalized at the time of their first recorded procedure code for VPS surgery between 2005 and 2012 at nonfederal acute care hospitals in California, Florida, and New York. We excluded patients who during the index hospitalization for VPS surgery had concomitant codes for VPS revision, CNS infection, or died during the index hospitalization. Patients were followed for the primary outcome of a VPS complication, defined as the composite of CNS infection or VPS revision. Survival statistics were used to calculate the cumulative rate and incidence rate of VPS complications.

17,035 patients underwent VPS surgery. During a mean follow-up of 3.9 (±1.8) years, at least one VPS complication occurred in 23.8% (95% CI, 22.9-24.7%) of patients. The cumulative rate of CNS infection was 6.1% (95% CI, 5.7-6.5%) and of VPS revision 22.0% (95% CI, 21.1-22.9%). The majority of complications occurred within the first year of hospitalization for VPS surgery. Complication rates were 21.3 (95% CI, 20.6-22.1) complications per 100 patients per year in the first year after VPS surgery, 5.7 (95% CI, 5.3-6.1) in the second year after VPS surgery, and 2.5 (95% CI, 2.1-3.0) in the fifth year after VPS surgery.

Complications are not infrequent following VPS surgery; however, the majority of complications appear to be clustered in the first year following VPS insertion 9).

Case reports

2015

A extremely rare and potentially severe complication of vesical calculi formation on the slit valves of distal end of VP shunt which erosively migrated into the urinary bladder. Suprapubic cystolithotomy performed, peritoneal end of the tube found to be eroding and entering into the bladder with two calculi firmly stuck to slit valves in the distal end of the tubing were removed. Shunt was functional, therefore, it was pulled out and repositioned on the superior aspect of the liver; the urinary bladder was repaired. Patient did well postoperatively. This complication was revealed 1.5 years after the shunt was implanted. Although there were symptoms of dysuria and dribbling of urine of short duration, the patient did not show obvious peritoneal signs; suggesting that, penetration of a VP shunt into the urinary bladder can remain asymptomatic for a long period of time, disclosed late and can lead to considerable morbidity. Careful follow-up is important and management should be individualized 10).

2009

An unusual case of perforation of the distal end of the VP shunt into the bladder, with vesical calculus formation 11).

2002

A bladder stone formed secondary to the erosion of a ventriculoperitoneal shunt through a normal bladder wall 12).

1)

Blount JP, Campbell JA, Haines SJ. Complications in ventricular cerebrospinal fluid shunting. Neurosurg Clin N Am. 1993;4:633–56.
2)

Reddy GK, Bollam P, Shi R, Guthikonda B, Nanda A. Management of adult hydrocephalus with ventriculoperitoneal shunts: long-term single-institution experience. Neurosurgery. 2011;69(4):774–781.
3)

Villavicencio AT, Leveque JC, McGirt MJ, Hopkins JS, Fuchs HE, George TM. Comparison of revision rates following endoscopically versus nonendoscopically placed ventricular shunt catheters. Surg Neurol. 2003 May;59(5):375-9; discussion 379-80. PubMed PMID: 12765808.
4)

Park DB, Hill JG, Thacker PG, Rumboldt Z, Huda W, Ashley B, Hulsey T, Russell WS. The Role of Limited Head Computed Tomography in the Evaluation of Pediatric Ventriculoperitoneal Shunt Malfunction. Pediatr Emerg Care. 2016 Jun 14. [Epub ahead of print] PubMed PMID: 27299297.
5)

Afat S, Pjontek R, Hamou HA, Herz K, Nikoubashman O, Bamberg F, Brockmann MA, Nikolaou K, Clusmann H, Wiesmann M, Othman AE. Imaging of Ventriculoperitoneal Shunt Complications: Comparison of Whole Body Low-Dose Computed Tomography and Radiographic Shunt Series. J Comput Assist Tomogr. 2016 Aug 16. [Epub ahead of print] PubMed PMID: 27529684.
6)

Li XY, Wang ZC, Li YP, Ma ZY, Yang J, Cao EC. [Study on treatment strategy for ventriculitis associated with ventriculoperitoneal shunt for hydrocephalus]. Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2005 Sep;17(9):558-60. Chinese. PubMed PMID: 16146606.
7)

Kurin M, Lee K, Gardner P, Fajt M, Umapathy C, Fasanella K. Clinical peritonitis from allergy to silicone ventriculoperitoneal shunt. Clin J Gastroenterol. 2017 Mar 6. doi: 10.1007/s12328-017-0729-0. [Epub ahead of print] PubMed PMID: 28265895.
8)

Chen BH, Drucker MD, Louis KM, Richards DW. Progression of Normal-Tension Glaucoma After Ventriculoperitoneal Shunt to Decrease Cerebrospinal Fluid Pressure. J Glaucoma. 2014 Oct 27. [Epub ahead of print] PubMed PMID: 25350819.
9)

Merkler AE, Ch’ang J, Parker WE, Murthy SB, Kamel H. The Rate of Complications after Ventriculoperitoneal Shunt Surgery. World Neurosurg. 2016 Nov 5. pii: S1878-8750(16)31137-8. doi: 10.1016/j.wneu.2016.10.136. [Epub ahead of print] PubMed PMID: 27826086.
10)

Gupta R, Dagla R, Agrawal LD, Sharma P. Vesical calculi formation on the slit valves of a migrated distal end of ventriculoperitoneal shunt. J Pediatr Neurosci. 2015 Oct-Dec;10(4):368-70. doi: 10.4103/1817-1745.174444. PubMed PMID: 26962346.
11)

Ramana Murthy KV, Jayaram Reddy S, Prasad DV. Perforation of the distal end of the ventriculoperitoneal shunt into the bladder with calculus formation. Pediatr Neurosurg. 2009;45(1):53-5. doi: 10.1159/000204904. Epub 2009 Mar 4. PubMed PMID: 19258730.
12)

Eichel L, Allende R, Mevorach RA, Hulbert WC, Rabinowitz R. Bladder calculus formation and urinary retention secondary to perforation of a normal bladder by a ventriculoperitoneal shunt. Urology. 2002 Aug;60(2):344. PubMed PMID: 12137842.

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 hypertension, hyponatremia, 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).

Intracranial hemorrhage

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).

Vasospasm

see Vasospasm after aneurysmal subarachnoid hemorrhage.

Brain edema

Brain edema after aneurysmal subarachnoid hemorrhage

Delayed cerebral ischemia

see Delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage

Rebleeding

see Aneurysm rebleeding

Pulmonary complications

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

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

Acute kidney injury

Hyponatremia

see Hyponatremia after aneurysmal subarachnoid hemorrhage

Hypokalemia

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).

Hydrocephalus

see Hydrocephalus after aneurysmal subarachnoid hemorrhage.

Intraventricular 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).

Cognitive disorder

see Cognitive disorder after subarachnoid hemorrhage.

Neuropsychiatric disturbance

Aneurysmal subarachnoid hemorrhage neuropsychiatric disturbance.

Deep-Vein Thrombosis

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).

Prevention

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.

Seizure

see Seizure after aneurysmal subarachnoid hemorrhage.

Cytotoxic Lesions of the Corpus Callosum

Cytotoxic Lesions of the Corpus Callosum.

Nonocclusive mesenteric ischemia

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).

References

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.

Anterior communicating artery aneurysm endovascular treatment complications

Anterior communicating artery aneurysm endovascular treatment complications

Intraprocedural aneurysm rupture and thrombus formation are serious complications during coiling of ruptured intracranial aneurysms, and they more often occur in patients with anterior communicating artery aneurysms.

It is associated with a high rate of complete angiographic occlusion. However, the procedure-related permanent morbidity and mortality are not negligible for aneurysms in this location 1).

Delgado Acosta et al. from Hospital Universitario Reina Sofía aimed to report the characteristics of patients suffering intra- or peri-procedural ruptures during embolization of cerebral aneurysms.

Between March 1994 and October 2021, 648 consecutive cerebral aneurysms were treated by the endovascular procedure. Medical records were reviewed retrospectively with emphasis on procedure description, potential risk factors, and clinical outcomes related to intra- or peri-procedural rupture.

Of the 648 patients, 17 (2.6%) suffered an intra- or peri-procedural hemorrhagic event. The most common location was the anterior communicating artery. There was no significant difference between previously ruptured and unruptured aneurysms in the incidence of bleeding. In four patients, bleeding was evident within 24 h after the procedure. The clinical evolution at three months was poor and only four patients presented a positive evolution. There were 11 deaths (64.71%). Balloon remodeling was associated with an increased frequency of ruptures, while stenting was a safer treatment.

Aneurysm rupture during endovascular therapy is unpredictable, and its occurrence can be devastating. The incidence is quite low although the outcome is frequently poor. Early detection and proper management, including prompt occlusion of the aneurysm, are important to achieve a positive outcome. Anterior communicating artery aneurysms and those treated with balloon catheters have a higher incidence of rupture. A small number of ruptures of uncertain origin occur that go unnoticed in digital subtraction angiograms 2).

The immediate and long-term outcomes, complications, recurrences and the need for retreatment were analyzed in a series of 280 consecutive patients with anterior communicating artery aneurysms treated with the endovascular technique. From October 1992 to October 2001 280 patients with 282 anterior communicating artery aneurysms were addressed to our center. For the analysis, the population was divided into two major groups: group 1, comprising 239 (85%) patients with ruptured aneurysms and group 2 comprising of 42 (15%) patients with unruptured aneurysms. In group 1, 185 (77.4%) patients had a good initial pre-treatment Hunt and Hess grade of I-III. Aneurysm size was divided into three categories according to the larger diameter: less than 4 mm, between 4 and 10 mm and larger than 10 mm. The sizes of aneurysms in groups 1 and 2 were identical but a less favorable neck to depth ratio of 0.5 was more frequent in group 2. Endovascular treatment was finally performed in 234 patients in group 1 and 34 patients in group 2. Complete obliteration was more frequently obtained in group 2 unlike a residual neck or opacification of the sac that were more frequently seen in group 1. No peri-treatment complications were recorded in group 2. In group 1 the peri-treatment mortality and overall peri-treatment morbidity were 5.1% and 8.1% respectively. Eight patients (3.4%) in group 1 presented early post treatment rebleeding with a mortality of 88%. The mean time to follow-up was 3.09 years. In group 1, 51 (21.7%) recurrences occurred of which 14 were minor and 37 major. In group 2, eight (23.5%) recurrences occurred, five minor and three major. Two patients (0.8%) presented late rebleeding in group 1. Twenty-seven second endovascular retreatments were performed, 24 (10.2%) in group 1 and three (8.8%) in group 2, seven third endovascular retreatments and two surgical clippings in group 1 only. There was no additional morbidity related to retreatments. Endovascular treatment is an effective method for the treatment of anterior communicating artery aneurysms allowing late rebleeding prevention. Peri-treatment rebleeding warrants caution in anticoagulation management. This is a single center experience and the follow-up period is limited. Patients should be followed-up in the long-term as recurrences may occur and warrant additional treatment 3).

Prolonged anterograde amnesia and disorientation after anterior communicating artery aneurysm coil embolization 4)

LVIS stent-assisted coiling for ruptured wide-necked ACoA aneurysms was safe and effective, with a relatively low rate of perioperative complications and a high rate of complete occlusion at follow-up 5)

1)

Fang S, Brinjikji W, Murad MH, Kallmes DF, Cloft HJ, Lanzino G. Endovascular treatment of anterior communicating artery aneurysms: a systematic review and meta-analysis. AJNR Am J Neuroradiol. 2014 May;35(5):943-7. doi: 10.3174/ajnr.A3802. Epub 2013 Nov 28. PMID: 24287090; PMCID: PMC7964525.
2)

Delgado Acosta F, Bravo Rey I, Jiménez Gómez E, Saucedo VR, Toledano A, Oteros Fernández R. Intra- or peri-procedural rupture in the endovascular treatment of intracranial aneurysms. Acta Neurol Scand. 2022 Aug 17. doi: 10.1111/ane.13686. Epub ahead of print. PMID: 35975464.
3)

Finitsis S, Anxionnat R, Lebedinsky A, Albuquerque PC, Clayton MF, Picard L, Bracard S. Endovascular treatment of ACom intracranial aneurysms. Report on series of 280 patients. Interv Neuroradiol. 2010 Mar;16(1):7-16. doi: 10.1177/159101991001600101. Epub 2010 Mar 25. PMID: 20377974; PMCID: PMC3277962.
4)

Al-Atrache Z, Friedler B, Shaikh HA, Kavi T. Prolonged anterograde amnesia and disorientation after anterior communicating artery aneurysm coil embolisation. BMJ Case Rep. 2019 Jul 30;12(7). pii: e230543. doi: 10.1136/bcr-2019-230543. PubMed PMID: 31366616.
5)

Xue G, Liu P, Xu F, Fang Y, Li Q, Hong B, Xu Y, Liu J, Huang Q. Endovascular Treatment of Ruptured Wide-Necked Anterior Communicating Artery Aneurysms Using a Low-Profile Visualized Intraluminal Support (LVIS) Device. Front Neurol. 2021 Jan 28;11:611875. doi: 10.3389/fneur.2020.611875. PMID: 33584512; PMCID: PMC7876256.

terior communicating artery aneurysm endovascular treatment complications

Percutaneous balloon compression trigeminal rhizotomy complications

Percutaneous balloon compression trigeminal rhizotomy complications

Percutaneous balloon compression trigeminal rhizotomy-related trigemino-cardiac reflex (TCR) can induce dramatic hemodynamic disturbances 1).

Postoperative morbidity included common side effects such as facial numbness in 66 (97.1 %) patients, masseter muscle weakness in 19 (27.9 %) patients, paresthesia in 7 (10.3 %) patients, and diplopia secondary to abducens nerve weakness in 1 (1.5 %) patient 2)

The main reason for ineffective or short-term recurrence of PBC in trigeminal neuralgia patients is the ineffectively compressed of trigeminal ganglion.According to the different types of patients,the use of individualized modified surgical scheme can improve the efficacy of PBC surgery 3).

Extracranial complications

Bloody saliva Stensen duct puncture

Facial hematoma/A-V fistula Puncture of internal MA and pterygoid plexus

Injury to ICA, jugular vein Excessively medial displacement of the needle causing injury to the ICA in the FL,

posterolateral displacement causing injury to the jugular vein

Injury to Eustachian tube Posterior displacement of the needle

Blindness Needle inserted anteriorly and medially passing through inferior orbital fissure to the orbital apex

Intracranial complications

Carotid-cavernous fistula ICA injury in the CS

Temporal lobe hematoma Dura mater penetration and intradural balloon inflation

Brainstem lesion Guiding stylet/balloon catheter far from the petrous ridge

Diplopia Compression of CN VI (most common) or CN IV

Meningitis Oral mucosa puncture, contamination or improper sterility 4).

Lichtor and Mullan from one hundred patients treated by this method that have been followed for 1 to 10 years; treatment has been technically successful in 97% of cases. Relief persisted at five years in 80%, and it is estimated that at 10 years the figure will be 70%. There were no deaths, no cerebral damage, no keratitis, and no analgesia dolorosa; 4% of the patients reported dysesthesia 5).

Most of the minor surgical complications observed were also related to avoidable technical errors 6)

1)

Wang CM, Guan ZY, Wang QC, Zhang J, Ma Y, Zhao P. The Effect of Depth of Anesthesia on Hemodynamic Changes Induced by Therapeutic Compression of the Trigeminal Ganglion. J Neurosurg Anesthesiol. 2019 May 27. doi: 10.1097/ANA.0000000000000612. [Epub ahead of print] PubMed PMID: 31145173.
2)

Du, YF., Gu, Q., Yang, DB. et al. Percutaneous balloon compression for primary trigeminal neuralgia in patients older than 80 years. Chin Neurosurg Jl 1, 8 (2015). https://doi.org/10.1186/s41016-015-0007-2
3)

Chong YL, Xu W, Wang J, Jiang CR, Liang WB. [The ineffective or short-term recurrence of trigeminal neuralgia after microballoon compression:different causes and management strategies]. Zhonghua Wai Ke Za Zhi. 2022 May 1;60(5):473-478. Chinese. doi: 10.3760/cma.j.cn112139-20210825-00391. Epub ahead of print. PMID: 35359090.
4)

https://www.reumatek.com/wp-content/uploads/Percutaneous_Balloon_Compression_for_Trigeminal.pdf
5)

Lichtor T, Mullan JF. A 10-year follow-up review of percutaneous microcompression of the trigeminal ganglion. J Neurosurg. 1990 Jan;72(1):49-54. doi: 10.3171/jns.1990.72.1.0049. PMID: 2294184.
6)

Lobato RD, Rivas JJ, Sarabia R, Lamas E. Percutaneous microcompression of the gasserian ganglion for trigeminal neuralgia. J Neurosurg. 1990 Apr;72(4):546-53. doi: 10.3171/jns.1990.72.4.0546. PMID: 2319312.

Vagus nerve stimulation complications

Vagus nerve stimulation complications

The most common side effects associated with Vagus nerve stimulation are hoarseness, throat pain and coughing. Cardiac arrhythmia has been reported during lead tests performed during implantation of the device, but few cases during regular treatment.

After implanting vagus nerve electrodes to the cervical vagus nerve, side effects such as voice alterations and dyspnea or missing therapeutic effects are observed at different frequencies. Cervical vagus nerve branching might partly be responsible for these effects.

Adverse events (AEs) are generally associated with implantation or continuous on-off stimulation. Infection is the most serious implantation-associated AE. Bradycardia and asystole have also been described during implantation, as has vocal cord paresis, which can last up to 6 months and depends on surgical skill and experience. The most frequent stimulation-associated AEs include voice alteration, paresthesia, cough, headache, dyspnea, pharyngitis and pain, which may require a decrease in stimulation strength or intermittent or permanent device deactivation. Newer non-invasive VNS delivery systems do not require surgery and permit patient-administered stimulation on demand. These non-invasive VNS systems improve the safety and tolerability of VNS, making it more accessible and facilitating further investigations across a wider range of uses.

VNS battery replacement, revisions, and removals account for almost one-half of all VNS procedures. The findings suggest important long-term expectations for VNS including expected complications, battery life, and other surgical issues. Review of the literature suggests that the first large review of VNS revisions by a single center was done by Couch et al. The findings are important to better characterize long-term surgical expectations of VNS therapy. A significant portion of patients undergoing VNS therapy will eventually require revision 1).

In a retrospective study over an 8-year period, 13 patients underwent revision surgery due to lead failure. Lead failure was classified as either lead intrinsic damage or lead pin disengagement from the generator header. In the X-ray image, Zhou et al., defined an RC ratio that represented the portion of rear lead connector in the header receptacle. It was used to quantitatively evaluate the mechanical failure of the lead-header interface. Optimal procedures to identify and manage lead failure were established.

All 13 patients presented with high lead impedance ≥ 9 kOhms at the time of revision. Seven of ten patients with lead damage presented with increased seizure frequency after a period of seizure remission. In contrast to lead damages occurring relatively late (> 15 months), lead pin disengagement was usually found within the early months after device implantation. A significant association was found between an elevated RC ratio (≥ 35%) and lead pin disengagement. The microsurgical technique permitted the removal or replacement of the lead without adverse effects.

The method of measuring the RC ratio developed in this study is feasible for identifying lead disengagement at the generator level. Lead revision was an effective and safe procedure for patients experiencing lead failure 2).

Vocal cord paralysis

Main risk of surgery is transient or permanent vocal cord paralysis.

Endotracheal Tube Electrode Neuromonitoring represents a safe adjunctive tool that can help localize the vagus nerve, particularly in the setting of varying anatomy or hazardous dissections. It may help reduce the potential for vagal trunk damage or electrode misplacement and potentially improve clinical outcomes 3).

1)

Couch JD, Gilman AM, Doyle WK. Long-term Expectations of Vagus Nerve Stimulation: A Look at Battery Replacement and Revision Surgery. Neurosurgery. 2016 Jan;78(1):42-6. doi: 10.1227/NEU.0000000000000985. PubMed PMID: 26678088.
2)

Zhou H, Liu Q, Zhao C, Ma J, Ye X, Xu J. Lead failure after vagus nerve stimulation implantation: X-ray examination and revision surgery. World Neurosurg. 2018 Dec 26. pii: S1878-8750(18)32893-6. doi: 10.1016/j.wneu.2018.12.070. [Epub ahead of print] PubMed PMID: 30593965.
3)

Katsevman GA, Josiah DT, LaNeve JE, Bhatia S. Endotracheal Tube Electrode Neuromonitoring for Placement of Vagal Nerve Stimulation for Epilepsy: Intraoperative Stimulation Thresholds. Neurodiagn J. 2022 Feb 28:1-12. doi: 10.1080/21646821.2022.2022911. Epub ahead of print. PMID: 35226831.

Idiopathic normal pressure hydrocephalus treatment complications

Idiopathic normal pressure hydrocephalus treatment complications

The rate of complications or readmission within 30 d of ventricular shunting for NPH is 25.15%. Preoperative comorbidities of myocardial infarction within 1 yr, cerebrovascular disease, and moderate/severe renal disease are independent risk factors for poor outcomes 1) 2).

Outcomes did not differ significantly among different CSF diversion techniques, and overall improvement was reported in more than 75% of patients. The use of programmable valves decreased the incidence of revision surgery and of subdural collections after surgery, potentially justifying the higher initial cost associated with these valves 3).

The goal is to avoid serious complications, such as subdural effusion or subdural hematoma. Adjustable pressure valves offer the advantage of being able to lower the pressure setting incrementally until symptoms improve and to raise the pressure setting if low-pressure symptoms or complications emerge. The introduction of adjustable valves has dramatically lowered the need for shunt revisions, and most complications can be handled by changing the shunt setting. Severe complications, such as subdural hematoma with mass effect, shunt infection, and shunt obstruction, typically require neurosurgical intervention. Adjustable shunts can be used to safely manage patients with Idiopathic normal pressure hydrocephalus who need chronic anticoagulation 4).

Subdural collections, shunt malfunction, and postoperative seizures constituted the most frequent complications 5).

see Shunt overdrainage in idiopathic normal pressure hydrocephalus.

The objectives of Larsson et al., from the Umeå University, in Sweden were to establish the frequencies of epilepsy, headache, and abdominal pain and determine their impact on patient quality of life (QOL), in long-term follow-up after shunt surgery for INPH.

One hundred seventy-six shunt-treated patients with Idiopathic normal pressure hydrocephalus (INPH) (mean age 74 years) and 368 age- and sex-matched controls from the population were included. The mean follow-up time after surgery was 21 months (range 6-45 months). Each participant answered a questionnaire regarding present frequency and severity of headache and abdominal pain. Confirmed diagnoses of epilepsy and all prescriptions for antiepileptic drugs (AEDs) before and after shunt surgery for INPH were gathered from national registries. Equivalent presurgical and postsurgical time periods were constructed for the controls based on the date of surgery (the division date for controls is referred to as virtual surgery). All registry data covered a mean period of 6 years (range 3-8 years) before surgery/virtual surgery and 4 years (range 2-6 years) after surgery/virtual surgery. Provoked epileptic seizures were excluded. Patient QOL was assessed with the EuroQoL 5-dimension 5-level instrument.

Epilepsy was more common in shunt-treated patients with INPH than in controls (4.5% vs 1.1%, respectively; p = 0.023), as was treatment with AEDs (14.8% vs 7.3%, respectively; p = 0.010). No difference was found between the populations before surgery/virtual surgery (epilepsy, 2.3% [INPH] vs 1.1% [control], p = 0.280; AED treatment, 8.5% [INPH] vs 5.4% [control], p = 0.235). New-onset epilepsy and new AED treatment after surgery/virtual surgery were more common in INPH (epilepsy, 2.3% [INPH] vs 0.0% [control], p = 0.011; AED, 8.5% [INPH] vs 3.3% [control], p = 0.015). At follow-up, more patients with INPH than controls experienced headache several times per month or more often (36.1% vs 11.6%, respectively; p < 0.001). Patients with INPH and unilateral headache had more right-sided headaches than controls (p = 0.038). Postural headache was experienced by 16% (n = 27 of 169) of the patients with INPH. Twenty percent (n = 35) of the patients with INPH had persistent abdominal pain. Headache was not correlated to lower QOL. The study was underpowered to draw conclusions regarding QOL in patients with INPH who had epilepsy and abdominal pain, but the finding of no net difference in mean QOL indicates that no correlation between them existed.

Epilepsy, headache, and abdominal pain are common in long-term follow-up in patients after shunt surgery for INPH and are more common among patients with INPH than in the general population. All adverse events, including mild and moderate ones, should be considered during postoperative follow-ups and in the development of new methods for shunt placement 6).

Transient or minimal improvement of symptoms

Di Rienzo et al. retrospectively collected data on a 10-year series of VP-shunted patients with Idiopathic normal pressure hydrocephalus showing transient or minimal improvement of symptoms within 3 weeks from surgery. A full workup (including noninvasive diagnostic, cognitive, and invasive tests) was performed. After ruling out mechanical ventriculoperitoneal shunt malfunction, they performed a tap test followed by a Katzman test 2 weeks later. The confirmed persistence of disturbance of cerebrospinal fluid dynamics was treated by shunt revision and, if found working, by its replacement into the atrial cavity.

Twenty patients were diagnosed with shunt insufficiency. At surgery, the distal end of the shunt was easily extruded and found working in all cases. It was then repositioned into the right atrium (the first 8 patients of the series also underwent failed contralateral abdominal replacement). Early postoperative clinical improvement was always confirmed. In 1 case, shunt overdrainage was corrected by valve upregulation.

Inadequate distal end placement of a shunt might be one of the reasons needing investigation in patients with iNPH failing improvement after surgery. In such situations, the conversion to a ventriculoatrial shunt proved to be a low-cost and successful treatment option 7).

References

1)

Nadel JL, Wilkinson DA, Linzey JR, Maher CO, Kotagal V, Heth JA. Thirty-Day Hospital Readmission and Surgical Complication Rates for Shunting in Normal Pressure Hydrocephalus: A Large National Database Analysis. Neurosurgery. 2020 Jun 1;86(6):843-850. doi: 10.1093/neuros/nyz299. PMID: 31420654.
2)

D’Antona L, Thompson SD, Thorne L, Watkins LD, Toma AK. Letter: Thirty-Day Hospital Readmission and Surgical Complication Rates for Shunting in Normal Pressure Hydrocephalus: A Large National Database Analysis. Neurosurgery. 2020 Sep 28:nyaa386. doi: 10.1093/neuros/nyaa386. Epub ahead of print. PMID: 32985659.
3)

Giordan E, Palandri G, Lanzino G, Murad MH, Elder BD. Outcomes and complications of different surgical treatments for idiopathic normal pressure hydrocephalus: a systematic review and meta-analysis. J Neurosurg. 2018 Nov 1:1-13. doi: 10.3171/2018.5.JNS1875. Epub ahead of print. PMID: 30497150.
4)

Goodwin CR, Kharkar S, Wang P, Pujari S, Rigamonti D, Williams MA. Evaluation and treatment of patients with suspected normal pressure hydrocephalus on long-term warfarin anticoagulation therapy. Neurosurgery. 2007 Mar;60(3):497-501; discussion 502. PubMed PMID: 17327794.
5)

Black PM. Idiopathic normal-pressure hydrocephalus. Results of shunting in 62 patients. J Neurosurg. 1980 Mar;52(3):371-7. PubMed PMID: 7359191.
6)

Larsson J, Israelsson H, Eklund A, Malm J. Epilepsy, headache, and abdominal pain after shunt surgery for idiopathic normal pressure hydrocephalus: the INPH-CRasH study. J Neurosurg. 2018 Jun;128(6):1674-1683. doi: 10.3171/2017.3.JNS162453. Epub 2017 Sep 8. PubMed PMID: 28885121.
7)

Di Rienzo A, Carrassi E, Dobran M, Colasanti R, Capece M, Aiudi D, Iacoangeli M. Ventriculoatrial Shunting: An Escape Option in Patients with Idiopathic Normal Pressure Hydrocephalus Failing Ventriculoperitoneal Drainage. World Neurosurg. 2022 Jan;157:e286-e293. doi: 10.1016/j.wneu.2021.10.073. Epub 2021 Oct 11. PMID: 34648991.

Cranioplasty complications

Cranioplasty complications

Complications include:

a) infection:≈8% risk

b) hematoma:under the cranioplasty flap(epidural or subdural)

c) seizures

d) brain injury

e) bone flap resorption

f) hydrocephalus

Risk of complication is increased with bifrontal bone defects.

The incidence of complications after cranioplasty is high, ranging from 12% to 50%.

The complication rate of cranioplasty is higher than for other elective neurosurgical procedures. Older age, poorer functional situation (worse Barthel index score) and early surgery (≤85 days) are independent risk factors for complications 1).

Cranioplasty after decompressive craniectomy (DC) is associated with increased morbidity, but the reported mortality rate is low.

Intracranial pressure (ICP) is a crucial factor that we need to take into account in all major pathophysiological changes of the brain after decompressive craniectomy (DC) and cranioplasty (CP). The purpose of a study was to check ICP values before and after cranioplasty and its relation to various parameters (imaging, demographics, time of cranioplasty, and type of graft) as well as its possible relation to postsurgical cranioplasty complications. The authors performed a prospective study in which they selected as participants adults who had undergone unilateral frontotemporoparietal DC and were planned to have cranioplasty. Intracranial pressure was measured with fiber-optic sensor in the epidural space and did not affect cranioplasty in any way.Twenty-five patients met the criteria. The mean vcICP (value change of ICP) was 1.2 mm Hg, the mean ΔICP (absolute value change of the ICP) was 2.24 mm Hg and in the majority of cases there was an increase in ICP. The authors found 3 statistically significant correlations: between gender and ΔICP, Δtime (time between DC and CP) and vcICP, and pre-ICP and ±ICP (quantitative change of the ICP).Μale patients tend to develop larger changes of ICP values during CP. As the time between the 2 procedures (DC and CP) gets longer, the vcICP is decreased. However, after certain time it shows a tendency to remain around zero. Lower pre-ICP values (close to or below zero) are more possible to increase after bone flap placement. It seems that the brain tends to restore its pre-DC conditions after CP by taking near-to-normal ICP values 2).

Epidural Fluid Collection

Epidural Fluid Collection.

Massive cerebral edema

Brain edema after cranioplasty.

Intracerebral Hemorrhagic Infarction

Cranioplasty infection

see Cranioplasty infection.

Bone flap resorption

see Bone flap resorption.

Epilepsy after cranioplasty

see Epilepsy after cranioplasty.

Case series

Morton et al., present the largest study to date on complications after cranioplasty, focusing specifically on the relationship between complications and timing of the operation.

They retrospectively reviewed all cranioplasty cases performed at Harborview Medical Center over the past 10.75 years. In addition to relevant clinical and demographic characteristics, patient morbidity and mortality data were abstracted from the electronic medical record. Cox proportional-hazards models were used to analyze variables potentially associated with the risk of infection, hydrocephalus, seizure, hematoma, and bone flap resorption.

Over the course of 10.75 years, 754 cranioplasties were performed at a single institution. Sixty percent of the patients who underwent these cranioplasties were male, and the median follow-up overall was 233 days. The 30-day mortality rate was 0.26% (2 cases, both due to postoperative epidural hematoma). Overall, 24.6% percent of the patients experienced at least 1 complication including infection necessitating explantation of the flap (6.6%), postoperative hydrocephalus requiring a shunt (9.0%), resorption of the flap requiring synthetic cranioplasty (6.3%), seizure (4.1%), postoperative hematoma requiring evacuation (2.3%), and other (1.6%). The rate of infection was significantly higher if the cranioplasty had been performed < 14 days after the initial craniectomy (p = 0.007, Holm-Bonferroni-adjusted p = 0.028). Hydrocephalus was significantly correlated with time to cranioplasty (OR 0.92 per 10-day increase, p < 0.001) and was most common in patients whose cranioplasty had been performed < 90 days after initial craniectomy. New-onset seizure, however, only occurred in patients who had undergone their cranioplasty > 90 days after initial craniectomy. Bone flap resorption was the least likely complication for patients whose cranioplasty had been performed between 15 and 30 days after initial craniectomy. Resorption was also correlated with patient age, with a hazard ratio of 0.67 per increase of 10 years of age (p = 0.001).

Cranioplasty performed between 15 and 30 days after initial craniectomy may minimize infection, seizure, and bone flap resorption, whereas waiting > 90 days may minimize hydrocephalus but may increase the risk of seizure 3).

2016

In 631 cranioplasty procedures (503 with autograft, 128 with bone substitute) by using a stepwise multivariable logistic regression model and discrimination analysis. There was a significantly higher risk for reoperation after placement of autograft than after placement of bone substitute; aseptic bone necrosis (n = 108) was the major problem (OR 2.48 [95% CI1.11-5.51]). Fragmentation of the flap into 2 or more fragments, younger age (OR 0.97 [95% CI 0.95-0.98]; p < 0.001), and shunt dependent hydrocephalus (OR 1.73 [95% CI1.02-2.92]; p = 0.04) were independent risk factors for bone necrosis. According to discrimination analysis, patients younger than 30 years old and older patients with a fragmented flap had the highest risk of developing bone necrosis.

Development of bone flap necrosis is the main concern in long-term follow-up after cranioplasty with autograft. Patients younger than 30 years old and older patients with a fragmented flap may be candidates for an initial artificial bone substitute rather than autograft 4).

2015

A retrospective analysis of 263 patients of all ages and both sexes who had undergone cranioplasty after craniectomy for traumatic brain injury (including chronic subdural hematoma), subarachnoidal hemorrhage (including intracerebral hemorrhage), ischemic stroke, and tumor surgery in one single center in 12 years from January 2000 to March 2012 has been carried out. A multiple logistic regression analysis was performed to identify potential risk factors (age, gender, used cranioplasty material, initial diagnosis, clipped or coil-embolized subarachnoidal hemorrhage (SAH) patients, time interval, complications especially hydrocephalus and seizures, mobility) upon the prognosis described as a dichotomized Glasgow Outcome Scale. Two hundred forty-eight patients met the study criteria. The overall complication rate after cranioplastic surgery was 18.5 % (46 patients). Complications included: surgical site infection, epidural hematoma, hydrocephalus with or without former SAH, and new-onset seizures. Logistic regression analysis identified significant correlation between a low GOS (2 or 3) and postoperative seizures (OR 2.37, CI 1.35-4.18, p < 0.05), shunt-depending hydrocephalus (OR 5.83, CI 3.06-11.11, p < 0.05), and age between 51 and 70 years (OR 2.4, 95 % CI 1.09-5.29, p = 0.029). However, gender, time interval between craniectomy and cranioplasty, initial diagnosis, and used cranioplasty material had no significant influence on post-cranioplasty complications as surgical site infections, hematoma, wound healing disturbance, seizures, or hydrocephalus. Evaluation of treatment modality in aneurysmal SAH clip vs. coil showed no significant relation to postoperative complications either. Complications after cranioplastic surgery are a common problem, as prognostic factors could identify a shunt-depending hydrocephalus and epilepsia to develop a major deficit after cranioplastic surgery (GOS 2 or 3). We detected a significant extra risk of people between the age of 51 and 70 years to end up in GOS level 2 or 3 5).

1)

Paredes I, Castaño-León AM, Munarriz PM, Martínez-Perez R, Cepeda S, Sanz R, Alén JF, Lagares A. Cranioplasty after decompressive craniectomy. A prospective series analyzing complications and clinical improvement. Neurocirugia (Astur). 2014 Dec 9. pii: S1130-1473(14)00145-6. doi: 10.1016/j.neucir.2014.10.001. [Epub ahead of print] PubMed PMID: 25497290.
2)

Tsianaka E, Singh A, Drosos E, Fountas K. Direct Consequences of Cranioplasty to the Brain: Intracranial Pressure Study. J Craniofac Surg. 2021 Nov-Dec 01;32(8):2779-2783. doi: 10.1097/SCS.0000000000007945. PMID: 34727479.
3)

Morton RP, Abecassis IJ, Hanson JF, Barber JK, Chen M, Kelly CM, Nerva JD, Emerson SN, Ene CI, Levitt MR, Chowdhary MM, Ko AL, Chesnut RM. Timing of cranioplasty: a 10.75-year single-center analysis of 754 patients. J Neurosurg. 2018 Jun;128(6):1648-1652. doi: 10.3171/2016.11.JNS161917. Epub 2017 Aug 11. PubMed PMID: 28799868.
4)

Schwarz F, Dünisch P, Walter J, Sakr Y, Kalff R, Ewald C. Cranioplasty after decompressive craniectomy: is there a rationale for an initial artificial bone-substitute implant? A single-center experience after 631 procedures. J Neurosurg. 2016 Mar;124(3):710-5. doi: 10.3171/2015.4.JNS159. Epub 2015 Sep 25. PubMed PMID: 26406796.
5)

Krause-Titz UR, Warneke N, Freitag-Wolf S, Barth H, Mehdorn HM. Factors influencing the outcome (GOS) in reconstructive cranioplasty. Neurosurg Rev. 2015 Dec 1. [Epub ahead of print] PubMed PMID: 26621678.

Vestibular Schwannoma Gamma Knife radiosurgery complications

Vestibular Schwannoma Gamma Knife radiosurgery complications

Patients treated with Stereotactic radiosurgery for vestibular schwannoma can have a similar complication profile to those treated with intracranial surgery. Vestibular Schwannoma Meta-analysis from early experience showed that 44% with serviceable hearing prior to treatment retained their ability after SRS, a statistically equivalent rate to the surgical data. This evidence also suggest that 37.9% of patients have other complications 1).

In the mid-1970s, early facial weakness occurred in 38% and facial numbness in 33%. This has gradually decreased to less than 2% in the 1990s. Preservation of hearing (unchanged or almost unchanged) is currently achieved in 65 to 70%. Tinnitus is rarely changed by the treatment. The risks of intracranial bleeding, infection, and CSF leak are avoided because of the non-invasive nature of the treatment. Hydrocephalus directly induced by the tumor occurred in 9.2% of patients. On the other hand, a treatment%related peritumoral reaction sufficient to block the CSF circulation and require shunt insertion was seen in only 1.4%. Based on experiences worldwide, the incidence of secondary neoplasia seems to be 0.1%. The effectiveness of GKR together with its low complication rate makes it a suitable treatment for anyone, regardless of age and general health 2).

Malignant transformation is possible 3). , and long-term post-SRS surveillance MRI is important 4).

Patients receiving > 13 Gy were significantly more likely to develop trigeminal neuropathy than those receiving < 13 Gy (p < 0.001) 5).

Case reports

Pollack et al. described an acute facial and acoustic neuropathy following gamma knife surgery (GKS) for vestibular schwannoma (VS). This 39-year-old woman presenting with tinnitus underwent GKS for a small right-sided intracanalicular VS, receiving a maximal dose of 26 Gy and a tumor margin dose of 13 Gy to the 50% isodose line. Thirty-six hours following treatment she presented with nausea, vomiting, vertigo, diminished hearing, and a House-Brackmann Grade III facial palsy. She was started on intravenous glucocorticosteroid agents, and over the course of 2 weeks her facial function returned to House-Brackmann Grade I. Unfortunately, her hearing loss persisted. A magnetic resonance (MR) image obtained at the time of initial deterioration demonstrated a significant decrease in tumor enhancement but no change in tumor size or peritumoral edema. Subsequently, the patient experienced severe hemifacial spasms, which persisted for a period of 3 weeks and then progressed to a House-Brackmann Grade V facial palsy. During the next 3 months, the patient was treated with steroids and in time her facial function and hearing returned to baseline levels. Results of MR imaging revealed transient enlargement (3 mm) of the tumor, which subsequently returned to its baseline size. This change corresponded to the tumor volume increase from 270 to 336 mm3. The patient remains radiologically and neurologically stable at 10 months posttreatment. This is the first detailed report of acute facial and vestibulocochlear neurotoxicity following GKS for VS that improved with time. In addition, MR imaging findings were indicative of early neurotoxic changes. A review of possible risk factors and explanations of causative mechanisms is provided 6).

Pseudoprogression

see Vestibular Schwannoma pseudoprogression.

1)

Kaylie DM, Horgan MJ, Delashaw JB, McMenomey SO. A meta-analysis comparing outcomes of microsurgery and gamma knife radiosurgery. Laryngoscope. 2000 Nov;110(11):1850-6. doi: 10.1097/00005537-200011000-00016. PMID: 11081598.
2)

Norén G. Long-term complications following gamma knife radiosurgery of vestibular schwannomas. Stereotact Funct Neurosurg. 1998 Oct;70 Suppl 1:65-73. doi: 10.1159/000056408. PMID: 9782237.
3)

Yanamadala V, Williamson RW, Fusco DJ, Eschbacher J, Weisskopf P, Porter RW. Malignant transformation of a vestibular schwannoma after gamma knife radiosurgery. World Neurosurg. 2013 Mar-Apr;79(3-4):593.e1-8. doi: 10.1016/j.wneu.2012.03.016. Epub 2012 Apr 2. PubMed PMID: 22480982.
4)

Kawashima M, Hasegawa H, Shin M, Shinya Y, Katano A, Saito N. Outcomes of stereotactic radiosurgery in young adults with vestibular schwannomas. J Neurooncol. 2021 Jul 9. doi: 10.1007/s11060-021-03803-w. Epub ahead of print. PMID: 34241770.
5)

Sughrue ME, Yang I, Han SJ, Aranda D, Kane AJ, Amoils M, Smith ZA, Parsa AT. Non-audiofacial morbidity after Gamma Knife surgery for vestibular schwannoma. J Neurosurg. 2013 Dec;119 Suppl:E4. Review. PubMed PMID: 25077327.
6)

Pollack AG, Marymont MH, Kalapurakal JA, Kepka A, Sathiaseelan V, Chandler JP. Acute neurological complications following gamma knife surgery for vestibular schwannoma. Case report. J Neurosurg. 2005 Sep;103(3):546-51. doi: 10.3171/jns.2005.103.3.0546. PMID: 16235688.

Ventriculoperitoneal shunt abdominal complications

Ventriculoperitoneal shunt abdominal complications

Abdominal complications include peritonitis, ascites, bowel and abdominal wall perforation, and inguinal hernias.

Abdominal complications are reported in 5–47 % of ventriculoperitoneal shunt cases 1) 2).

Ascites

Abdominal pseudocyst

Bowel perforation

Hydrocele

Shunt extrusion

Shunt migration

CSF leaks

Viscous perforations

Protrusion of the catheter from the anus

Spontaneous knotting of the peritoneal catheter is a rare complication of the VP shunt 3).

Peritoneal catheter knot formation

Liver abscess

Pyogenic liver abscess in Taiwan is most commonly due to Klebsiella pneumoniae infection in diabetic patients, and less frequently due to biliary tract infections. Liver abscess caused by ventriculoperitoneal (VP) shunt is very rare. We report a case of liver abscess caused by methicillin-resistant Staphylococcus aureus (MRSA), which developed as a complication of an infected VP shunt. A 53-year-old woman, who had shad a VP shunt implanted 3 months previously for hydrocephalus due to intracranial hemorrhage, presented with fever off and on, drowsiness and seizure attacks for 1 week. Computed tomography (CT) of the brain showed only mild right-sided hydrocephalus, and was negative for intracranial hemorrhage and intracranial mass. Analysis of cerebrospinal fluid showed significant pleocytosis and hypoglycorrhachia. CT scan of the abdomen disclosed a huge abscess in the right lobe of the liver. Cultures of both the cerebrospinal fluid and aspirated liver abscess isolated MRSA. The patient was treated with intraventricular and intravenous vancomycin, intravenous teicoplanin and oral rifampicin, followed by oral chloramphenicol and rifampicin. Percutaneous drainage of the liver abscess and externalization of the VP shunt were performed. The liver abscess had resolved almost completely on ultrasonography after 2 weeks of therapy. Liver abscess in patients with a VP shunt should be considered a possible abdominal complication of the VP shunt, and may be caused by unusual pathogens. Diagnosis requires CT scan and direct aspiration and culture of the liver abscess. Treatment requires management of both the liver abscess and the infected shunt 4).

Liver pseudocyst

The formation of a liver pseudocyst is a rare occurrence, and its mechanisms are still largely unknown.

Mallereau et al. reported the case of a 69-year-old woman with a ventriculoperitoneal shunt, inserted for the management of hydrocephalus after aneurysmal subarachnoid hemorrhage, presenting to the Accident and Emergency for acute cholecystitis. Besides confirming the diagnosis, an ultrasound investigation revealed the presence of a hepatic cyst. Conservative treatment with antibiotics and non-steroidal anti-inflammatory drugs was performed with favorable outcomes and resorption of the cyst. Interestingly the patient kept on presenting several similar episodes managed well by non-steroidal anti-inflammatory drugs alone, each of them associated with transient symptoms and signs of ventriculoperitoneal shunt malfunction. Computerized Tomography brain and lumbar puncture were normal, whereas the CT abdomen showed the ventriculoperitoneal shunt distal catheter passing through the hepatic cyst. Given the ventriculoperitoneal shunt malfunction, in the context of an infective/inflammatory process, a conversion of the ventriculoperitoneal shunt into a ventriculoatrial shunt was carried out with a successful clinical outcome.

Based on current literature they propose a clinical and radiological classification of such pseudocysts related to ventriculoperitoneal shunt. Clinical presentation, diagnostic findings, and management options are proposed for each type: purely infective, spurious (infective/inflammatory), and purely inflammatory. In the absence of system infection, a simple replacement of the distal catheter seems to be the best solution 5).

References

1)

Chung J, Yu J, Joo HK, Se JN, Kim M. Intraabdominal complications secondary to ventriculoperitoneal shunts: CT findings and review of the literature. American Journal of Roentgenology. 2009;193(5):1311–1317.
2)

Murtagh FR, Quencer RM, Poole CA. Extracranial complications of cerebrospinal fluid shunt function in childhood hydrocephalus. American Journal of Roentgenology. 1980;135(4):763–766.
3)

Borcek AO, Civi S, Golen M, Emmez H, Baykaner MK. An unusual ventriculoperitoneal shunt complication: spontaneous knot formation. Turkish Neurosurgery. 2012;22(2):261–264.
4)

Shen MC, Lee SS, Chen YS, Yen MY, Liu YC. Liver abscess caused by an infected ventriculoperitoneal shunt. J Formos Med Assoc. 2003 Feb;102(2):113-6. PubMed PMID: 12709741.
5)

Mallereau CH, Ganau M, Todeschi J, Addeo PF, Moliere S, Chibbaro S. Relapsing-Remitting Hepatic Pseudo-Cyst: a great simulator of malfunctioning ventriculoperitoneal shunt. Case report and proposal of a new classification. Neurochirurgie. 2020 Oct 10:S0028-3770(20)30399-4. doi: 10.1016/j.neuchi.2020.08.001. Epub ahead of print. PMID: 33049283.