11 Brain Tumor Postoperative Management

11.1 Introduction

11.1.1 Clinical Presentation

The clinical presentation of the patient varies and depends on the size and location of the tumor. Slow growing tumors can grow for years before a patient becomes symptomatic while a smaller metastatic tumor can be fast growing and have early signs and symptoms. ▶ Table 11.1 details some of the presenting symptoms. An understanding of involved cortical and subcortical structures, cranial nerves, vascular structures, and bony anatomy is important in identifying nuances in examination changes and allows for the neurointensivist to anticipate, mitigate, and manage potential complications in the perioperative period.

Table 11.1 Clinical presentation considerations and concerns

11.1.2 Tumor Classification

Primary brain tumors can be further classified into benign or malignant, with benign occurring almost twice as frequently as malignant. They can be classified as intra-axial, extra-axial, and intraventricular (see ▶ Table 11.2).

• Infra-axial tumors arise from cells within the brain parenchyma itself, i.e., glial cells.

• Extra-axial tumors arise from structures outside the brain, i.e., dura, cranial nerves, and bone.

• Intraventricular tumors arise from cells within the ventricles.

They can be further categorized into supratentorial and infratentorial. Distinctions between the two are important when considering associated anatomic structures and potential perioperative complications.

Table 11.2 Tumors by location

Supratentorial Tumors

• Higher incidence of pre- or postoperative seizures¹⁵

• May grow to larger sizes before exhibiting clinically significant mass effect

• Risk of venous injury causing venous infarction or possible catastrophic hemorrhage

• Potential for injury to anterior circulation arteries or branches causing hemorrhage or ischemia

Infratentorial Tumors

• Composed of the contents of the posterior fossa (cerebellum, brainstem, fourth ventricle, cerebral aqueduct, and origin of cranial nerves III–XII)

• Limited space available to accommodate postoperative swelling

• At risk for rapid clinical decompensation and cranial nerve involvement

• Potential for injury to posterior circulation arteries or branches causing hemorrhage or ischemia

• Tumors may invade or exhibit mass effect on the brainstem reticular activating system or the fourth ventricle potentially compromising a patient’s level of consciousness or causing hydrocephalus

11.2 Postoperative Care and Complications (▶ Table 11.3)

Most patients who undergo surgical intervention for brain tumors experience a relatively uneventful postoperative stay. The rate of postoperative complications is estimated to be around 3 to 4% based on National Inpatient Database sampling. Furthermore, certain at-risk populations may experience significantly higher rates of postoperative morbidity:^1,2

• Patients > 70 years of age

• Preoperative Karnofsky Performance score < 80

• High intraoperative blood loss (≥ 350 mL)

• Drop in hemoglobin of ≥ 2 g/dL preoperative to postoperative

11.2.1 Airway Management

Patients are typically extubated in the operating room once they are awake and following commands or exhibiting purposeful movement.³ However, prolonged operative times and brain retraction during surgery may result in an extended postanesthetic recovery period during which the patient might be at increased risk for respiratory compromise.³ Extended intubation times are not uncommon. In patients with delayed emergence from anesthesia, a screening computed tomography (CT) scan of the head is typically performed to rule out acute perioperative complications, such as a hematoma, followed by further monitoring if needed. Minimizing post-operative sedation and regular pulmonary toilet are important in preparing for extubation. Occasionally, patients develop airway edema which can delay extubation. Consider ear, nose, and throat (ENT) evaluation if concern. Patients with infratentorial lesions and suspected lower cranial nerve deficits require particular attention to limit the potential risk for aspiration due to insufficient airway protection.³ This also applies to patients with tumors of the pons, medulla, or fourth ventricle, as involvement of brainstem parenchyma or edema in this region may exacerbate vocal cord and pharyngeal muscle dysfunction. These patients require close monitoring to limit the risk for aspiration and further respiratory compromise.

Table 11.3 Postoperative management following brain tumor resection

11.2.2 Blood Pressure Control and Postoperative Hemorrhage

Postoperative hemorrhage is associated with a 3.3 times increased risk of inpatient hospital mortality and can be seen in 1.1 to 4.4% of cases, 88% of which occur within 6 hours of surgery.^1,4 While postoperative hemorrhage is often considered a result of insufficient intraoperative hemostasis, perioperative hypertension has been suggested to play a role as well by increasing dynamic stress on fragile bod vessels in the operative bed.^4,5 Patients aged > 40 years, with astrocytic tumors, giant tumors, and partially resected or biopsied tumors, especially highly vascularized, cystic, and/or malignant tumors, are at an increased risk of postoperative hemorrhage.^6,7,8 Minimally invasive procedures, such as stereotactic biopsies, may have hemorrhage rates as high as 5%, especially within high-risk locations, such as the pineal region.⁷ Furthermore, patients with a recurrent malignant gliomas and who have taken bevacizumab are also at an increased risk of perioperative hemorrhage.⁹

While there are no standardized parameters for blood pressure management, maintaining systolic blood pressure less than 140 mm Hg and mean arterial pressure less than 100 mm Hg have been reported to prevent spontaneous hematoma expansion, and are often used as guidelines for protection against postoperative bleeding following resection.^5,10 Furthermore, adequate control of postoperative pain and nausea, as well as an appropriate bowel regimen are recommended to limit blood pressure spikes from discomfort, retching, and Valsalva.³

11.2.3 Seizure Prophylaxis

Evidence based on a meta-analysis of high-quality randomized controlled trials suggests that seizure prophylaxis in the postoperative setting does not provide any significant benefit.¹¹ However, there are numerous criticisms to this assertion. Postoperative seizures have the greatest risk of occurring within 48 hours of surgery and can be present in 1 to 12% of cases. Furthermore, the potential consequences of postoperative seizure can be devastating, including malignant cerebral edema and hemorrhage.⁴ The vast majority of studies looking at perioperative seizure prophylaxis investigated older antiepileptic drugs (AEDs), such as phenytoin, which are known to have a more deleterious side effect profile, particularly in regards to their action on the cytochrome P450 enzyme complex.¹¹ Currently, there has been only one meta-analysis that has incorporated a study of more modern AEDs, specifically levetiracetam, which is known to have a far more limited side effect profile.¹² Levetiracetam is associated with rare behavioral disturbances, with dose limiting side effects seen in as few as 2.4% of patients.¹³ Additionally, newer agents, such as lacosamide, have yet to be studied regarding effectiveness for perioperative seizure prophylaxis in this population. Therefore, while there is limited data to suggests routine use of seizure prophylaxis following brain tumor resection, a thorough assessment of individual risks and benefits must be considered. Populations that are at an increased risk of seizures should be given additional consideration for starting seizure prophylaxis, namely patients with oligodendrogliomas, gangliogliomas, dysembryoplastic neuroepithelial tumors (DNET),⁸ glioblastomas (GBM) of the frontal lobe, non-skull base meningiomas, and meningiomas with significant peritumoral edema.^8,14,15 Generally, a short course of a recent generation AED, such as levetiracetam, is well-tolerated in patients for whom prophylaxis is deemed appropriate, and patients with history of seizure should have their AED maintained postoperatively.^4,11,12 Patients with posterior fossa lesions are unlikely to require any seizure protection due to the inherent lack of cortical involvement.

11.2.4 Venous Thromboembolism Prophylaxis

Venous thromboembolism (VTE) remains the most common adverse event affecting brain tumor patients in the postoperative setting, occurring in 3 to 26% of patients in the perioperative period.^4,16 Unfortunately, there is a dearth of literature to provide meaningful guidance on balancing this risk with the risk of postoperative hemorrhage. The use of sequential compression devices (SCDs) in neurosurgical patients has been well described and is currently recommended for all postoperative patients.¹⁷ The optimal timing and dose of chemical thromboprophylaxis with either heparin or low-molecular-weight heparins (i.e., enoxaparin) remain unclear; however, most practitioners agree that starting low-dose prophylactic anticoagulation in the acute postoperative period is generally acceptable. Patients with significantly increased risk of thromboembolic complications, such as those with a mechanical heart valve, hypercoagulability, or history of deep vein thrombosis, initiation of mechanical and chemical thromboprophylaxis should be started as soon as possible.^4,18 Patients with a paretic limb, patients on bevacizumab for recurrent GBM, and patients with malignant gliomas who are > 60 years old, are on active chemotherapy, and/or have a larger tumor burden, have also been showed to be at an increased risk for VTE.^19,20 Ultimately, the timing for restarting thromboprophylactic medication must be based on the individual patient’s risk profile for both hemorrhage and thromboembolism.^4,19,20

11.2.5 Antibiotic Prophylaxis and Postoperative Infection

Routine use of postoperative antibiotics has been shown to reduce the risk of surgical site infections, including a reduction in postoperative meningitis in neurosurgical patients.^21,22 Therefore, perioperative antibiotic use for approximately 24 hours postoperatively is universally recommended, with specific agents determined by institutional guidelines to account for local antibiotic resistances. Patients who undergo transsphenoidal surgery warrant special consideration, with studies suggesting up to 7 days of antibiotics, while nonabsorbable packing is in place, to prevent bacterial overgrowth and development of toxic shock syndrome.¹⁰ Other patients who may be at an increased risk for postoperative infection include those with advanced age, extended length of surgery, and factors that may affect wound healing such as obesity, diabetes/hyperglycemia, and poor nutritional status.²³

An important consideration regarding the workup for postoperative infection is the potential for aseptic (chemical) meningitis. The underlying etiology of this phenomenon is not clearly understood but is suspected to be an inflammatory response to the presence of external substances in the CSF such as blood, bone dust, tumor, and/or cystic contents. The clinical presentation of aseptic meningitis is highly variable, but largely mimics the symptoms of bacterial meningitis such as headache, neck stiffness, photophobia, and possibly fever. There are no clear risk factors for aseptic meningitis; however, resection of certain cystic tumors, such as epidermoid cysts and craniopharyngiomas, have been suggested to play a role in postoperative meningeal inflammation, especially if there is spillage of cystic contents intraoperatively or incomplete resection of the cyst wall.^24,25,26,27 Due to the largely ambiguous presentation of aseptic meningitis, patients exhibiting meningeal symptoms in the postoperative setting, particularly those with fever, CSF leak, or wound breakdown, should be expeditiously evaluated for bacterial meningitis with CSF sampling and started on broad-spectrum antibiotics while cultures are pending. There is no agreed upon standard for the diagnosis of aseptic meningitis based on CSF specimens. However, negative CSF cultures in low-risk patients may favor an aseptic etiology.²⁶ These patients may be treated conservatively for aseptic meningitis at the practitioners’ discretion with corticosteroids to reduce meningeal inflammation and possibly serial lumbar puncture or CSF diversion in cases of persistent symptoms or elevated intracranial pressure (ICP).²⁶

11.2.6 Cerebral Edema

Cerebral edema is commonly seen in patients harboring brain tumors and warrants careful management to avoid devastating complications. A more detailed discussion on the management of cerebral edema can be found in Chapter 6. therefore, only information as it pertains to brain tumor patients will be discussed. Vasogenic edema, which results from the disruption of the blood–brain barrier (BBB) and affects mostly the white matter, is the most common form of edema seen in brain tumors. Pathophysiologically, this is the result of the accumulation of inflammatory cytokines, leukotrienes, prostaglandins, vascular endothelial growth factor (VEGF), and matrix metalloproteinases (MMPs), which ultimately result in BBB breakdown and extravasation of plasma into the surrounding brain parenchyma.^{28,29,30,31,32,33} Surgical debulking relieves tumor mass effect and may improve surrounding edema. However, the timing of edema resolution is highly variable and may temporarily worsen following operative manipulation. Brain retraction and intraoperative venous compromise may also lead to venous congestion, worsening cerebral edema. Furthermore, cytotoxic edema from cerebral infarction my also occur in cases of injury to crucial draining veins, such as the veins of Trolard, Labbe, basal vein of Rosenthal, the dural sinuses, or in cases with intraoperative arterial compromise.

Symptomatic cerebral edema in the postoperative period is present in approximately 7.7 to 9.5% of patients.^4,34,35 Patients with cerebral edema require careful monitoring to mitigate the development of transient neurologic deficits and prevent potentially life-threatening elevations in ICP.³⁶ Early manifestations of elevated ICP secondary to cerebral edema include headaches, nausea, vomiting, diplopia (from cranial nerve VI palsy), and papilledema.³⁶ Focal neurologic deficits, impaired consciousness, aphasia, and seizures can also be seen as edema progresses. With the onset of any new neurologic deficit, emergent noncontrast CT of the head should be obtained to assess for alternative potential etiologies such as cerebral infarction or hemorrhage that may require emergent intervention.²⁸ Radiographic evidence of midline shift, sulcal effacement, and basal cistern obliteration can help assess the severity of the edema and potential for elevated ICPs. Magnetic resonance imaging (MRI) may also be used to better characterize the nature and extent of the edema, particularly T2 and fluid-attenuated inversion recovery (FLAIR) sequences.

Postoperatively, patients should have their head of bed elevated at a minimum of 30 degrees angle to increase venous outflow and decrease the hydrostatic pressure in the cranial vault to limit the potential for worsening edema.^37,38 Pharmacologically, steroids have been extensively used in the treatment of vasogenic edema, with dexamethasone being the most common agent. Corticosteroids can be administered 1 to 2 days before resection to reduce the edema preoperatively in symptomatic patients and are routinely administered intraoperatively. Steroids have been shown to result in neurologic improvement within the first 24 to 72 hours after initiation.^39,40 Postoperatively and/or upon improvement of symptoms, steroids should tapered to a low maintenance dose or weaned entirely as tolerated.⁴ Acute exacerbations in cerebral edema and ICP elevation should prompt interventions to improve cerebral perfusion and oxygenation, reduce the metabolic demands of the brain, and decrease ICP. Algorithms for the management of ICP crisis are beyond the scope of this chapter, but treatment should be initiated as soon as possible to limit the potential for permanent neurologic injury or death.

11.2.7 CSF Leak

CSF leakage is a potential complication of brain tumor resection that can significantly prolong the postoperative ICU course. A variety of etiologies can lead to CSF leakage, including the presence of hydrocephalus, inadequate dural closure, and disruption of bony and soft tissue structures secondary to tumor invasion or extensive skull base surgical approaches.^4,41 Rates of CSF leak have been reported to range from 2 to 16% following transsphenoidal surgery^10,42,43 and up to 32% for posterior fossa surgeries.^44,45,46 High-flow CSF leaks occur when CSF cisterns and/or ventricles are entered during surgery and are much more likely to result in postoperative CSF leakage compared to low-flow leaks.¹⁰ Communication of operative factors between the surgeon and the ICU team is crucial in establishing the risk for postoperative CSF leak and the necessary treatment measures. For example, high-flow leaks may require more aggressive early intervention in order to resolve completely.^10,47

Depending on the site of surgical intervention, CSF leakage may manifest as clear fluid drainage from the wound or as rhinorrhea, with patients often complaining of a metallic or salty taste. Sampling of draining fluid for β2-transferrin can be helpful for establishing the presence of a CSF leak when the diagnosis is uncertain. β2-transferrin testing, however, typically does not yield rapid results and waiting for laboratory confirmation may lead to unnecessary delays in initiating treatment.⁴¹ In patients who have undergone transsphenoidal surgery, endoscopic exploration can sometimes be useful in isolating the source of the leak. Also, CT or MRI may be useful in identifying the site of an anatomical defect and potential CSF egress site, although small defects along the skull base may be missed on even thin-cut imaging. Other diagnostic tools available include radioactive cisternography, CT cisternogram, and intrathecal fluorescein administration, but these diagnostic interventions are used less frequently due to their invasive nature. Occasionally, a CSF leak may present solely as symptomatic intracranial hypotension, manifesting as positional headaches, nausea, and/or neck stiffness. Lastly, patients with prolonged CSF leaks may present with meningitis due to communication between the environment and the intracranial space. Therefore, patients with a CSF leak and clinical suspicion for meningitis should be evaluated emergently with CSF sampling and treated with antibiotics until the presence or absence of infection is confirmed.

Initial prevention of CSF leak involves patient positioning and basic postoperative care. Patients should be positioned with their head elevated and patients who have undergone a transsphenoidal resection should be placed on strict precautions to try and limit pressure gradients across the cranial defect into the sinonasal cavity. These precautions include sneezing with their mouth open and avoiding blowing their nose.¹⁰ Furthermore, all patients should be started on stool softeners and antiemetic medication to help avoid straining, which may result in transient ICP elevation and failure of intraoperative CSF leak repair.

Many patients with an established leak can be successfully managed with temporary CSF diversion, typically via a lumbar drain or external ventriculostomy, to allow the communicating defect to heal.^10,47 In patients with CSF leaks following posterior fossa surgery, several studies support the use of lumbar drainage for at least 5 days with good results.^10,48,49 On the contrary, in patients with CSF leaks following endoscopic transsphenoidal surgery, less than 24% are able to be treated conservatively with lumbar drainage alone, and many of these patients require operative intervention for definitive leak repair.^10,42,43 Patients with persistent CSF leaks should also be evaluated for the presence of hydrocephalus. Increased ICPs from hydrocephalus will not only prevent healing of dural defects but may also lead to long-term consequences if not managed appropriately. Diagnosis revolves around a constellation of clinical and radiographic findings, such as altered mental status, neurologic deficit, and ventriculomegaly; however, some patients may be asymptomatic. If hydrocephalus is suspected, alternative methods of CSF diversion, such as external ventricular drainage or ventriculoperitoneal shunt insertion, may be required.⁴¹

Tension pneumocephalus is a rare but potentially life-threatening condition in which air enters the cranial cavity via a one-way valve mechanism, resulting in progressively increased ICP as air enters and cannot escape. Tension pneumocephalus is frequently associated with a CSF leak, most commonly following transnasal surgery, and can exhibit a rapidly progressive course, resulting in severe clinical and neurologic sequelae.^50,51 Increased ICPs from tension pneumocephalus can result in brain herniation, air embolism, and/or cardiac arrest in cases where it is not recognized or treated rapidly.^51,52 On imaging, tension pneumocephalus may present as the “Mount Fuji sign” (▶ Fig. 11.1), seen when intracranial air compresses the bilateral frontal lobe convexities, exhibiting a “peak” at the frontal poles, or as the “air bubble sign” in which numerous air bubbles are found throughout the basal cisterns.^50,51,53 Management of tension pneumocephalus relies primarily on operative intervention. Burr hole decompression may allow release of the built-up air; however, ultimate treatment typically involves focal repair of the bony defect or site of CSF leak to prevent further air entry.^50,53,54

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