Anterior temporal lobectomy complications

Anterior temporal lobectomy complications

Even though the mortality after Anterior temporal lobectomy (ATL) is minimal, the overall morbidity cannot be ignored. Psychiatric disturbances, visual field defects, and cognitive disorders are the most common postoperative complications, and should be considered during the preoperative planning and consultation 1).

Visual field defects

ATL is often complicated by quadrantanopia. In some cases this can be severe enough to prohibit driving, even if a patient is free of seizures. These deficits are caused by damage to Meyers loop of the optic radiation, which shows considerable heterogeneity in its anterior extent. This structure cannot be distinguished using clinical magnetic resonance imaging sequences.

Optic radiation tractography by DTI could be a useful method to assess an individual patient’s risk of postoperative visual deficit 2)3).

van Lanen et al., developed a score method for the assessment of postoperative visual field defects after temporal lobe epilepsy surgery and assessed its feasibility for clinical use. A significant correlation between VFD and resection size for right-sided ATL was confirmed 4).

Cranial nerve (CN) deficits following anterior temporal lobectomy (ATL) are an uncommon but well-recognized complication. The usual CNs implicated in post-ATL complications include the oculomotor nervetrochlear nerve, and facial nerves.

Injury to the trigeminal nerve leading to neuropathic pain are described in 2 cases following temporal lobe resections for pharmacoresistant epilepsy. The possible pathophysiological mechanisms are discussed and the microsurgical anatomy of surgically relevant structures is reviewed. 5).

Case reports

Dickerson et al., from the Department of Neurosurgery, University of Mississippi Medical Center, JacksonUSA report the third known case and first of diffuse vasospasm. A 48-year-old woman underwent a transcortical anterior left temporal lobectomy. Eleven days later, she had new-onset expressive aphasia with narrowing of the anterior, middle, and posterior cerebral arteries, and increased velocities via transcranial Doppler. She was treated with fluids, nimodipine, and permissive hypertension. At 6 months, her speech was near baseline. Cerebral vasospasm may represent a rare cause of morbidity after anterior temporal lobectomy; a literature review on the subject is presented 6).

References

1)

Brotis AG, Giannis T, Kapsalaki E, Dardiotis E, Fountas KN. Complications after Anterior Temporal Lobectomy for Medically Intractable Epilepsy: A Systematic Review and Meta-Analysis. Stereotact Funct Neurosurg. 2019 Jul 9:1-14. doi: 10.1159/000500136. [Epub ahead of print] Review. PubMed PMID: 31288240.
2)

Borius PY, Roux FE, Valton L, Sol JC, Lotterie JA, Berry I. Can DTI fiber tracking of the optic radiations predict visual deficit after surgery? Clin Neurol Neurosurg. 2014 Jul;122:87-91. doi: 10.1016/j.clineuro.2014.04.017. Epub 2014 May 5. PubMed PMID: 24908224.
3)

James JS, Radhakrishnan A, Thomas B, Madhusoodanan M, Kesavadas C, Abraham M, Menon R, Rathore C, Vilanilam G. Diffusion tensor imaging tractography of Meyer’s loop in planning resective surgery for drug-resistant temporal lobe epilepsy. Epilepsy Res. 2015 Feb;110:95-104. doi: 10.1016/j.eplepsyres.2014.11.020. Epub 2014 Nov 27. PubMed PMID: 25616461.
4)

van Lanen RHGJ, Hoeberigs MC, Bauer NJC, Haeren RHL, Hoogland G, Colon A, Piersma C, Dings JTA, Schijns OEMG. Visual field deficits after epilepsy surgery: a new quantitative scoring method. Acta Neurochir (Wien). 2018 Jul;160(7):1325-1336. doi: 10.1007/s00701-018-3525-9. Epub 2018 Apr 5. PubMed PMID: 29623432; PubMed Central PMCID: PMC5995984.
5)

Gill I, Parrent AG, Steven DA. Trigeminal neuropathic pain as a complication of anterior temporal lobectomy: report of 2 cases. J Neurosurg. 2016 Apr;124(4):962-5. doi: 10.3171/2015.5.JNS15123. Epub 2015 Oct 30. PubMed PMID: 26517768.
6)

Dickerson JC, Hidalgo JA, Smalley ZS, Shiflett JM. Diffuse vasospasm after transcortical temporal lobectomy for intractable epilepsy. Acta Neurochir (Wien). 2018 Jul 10. doi: 10.1007/s00701-018-3606-9. [Epub ahead of print] PubMed PMID: 29987392.

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).

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

Delayed cerebral ischemia

The risk of delayed cerebral ischemia is reduced with oral nimodipine and probably by maintaining circulatory volume 7).

Failure of cerebral autoregulation has been shown in patients with aSAH even before vasospasm sets in and contributes to delayed ischemic neurological deficits (DIND) along with vasospasm 8).

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 9).

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 10).

Acute kidney injury

Hyponatremia

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 11).

Hydrocephalus

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 12).

Cognitive disorder

Neuropsychiatric disturbance

Deep vein thrombosis

Overall rates of VTE (Deep vein thrombosis DVT or PE), DVT, 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 13).

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 (DVT) formation 14).

Routine compressive venous Doppler ultrasonography is an efficient, noninvasive means of identifying Deep vein thrombosis (DVT) as a screening modality in both symptomatic and asymptomatic patients following aneurysmal SAH. The ability to confirm or deny the presence of DVT 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 DVT-will allow physicians to better assess the role of prophylactic anticoagulation 15).

Deep vein thrombosis (DVT) 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 DVT 16).

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

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)

van Gijn J, Kerr RS, Rinkel GJ. Subarachnoid haemorrhage. Lancet. 2007 Jan 27;369(9558):306-18. Review. PubMed PMID: 17258671.
8)

Sriganesh K, Venkataramaiah S. Concerns and challenges during anesthetic management of aneurysmal subarachnoid hemorrhage. Saudi J Anaesth. 2015 Jul-Sep;9(3):306-13. doi: 10.4103/1658-354X.154733. Review. PubMed PMID: 26240552; PubMed Central PMCID: PMC4478826.
9)

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.
10)

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.
11)

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.
12)

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.
13)

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.
14)

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.
15)

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.
16)

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.
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