Perioperative Management of Patients With Brain Tumours

Figure 80.1. Before surgery (A) and after surgery (B).

In intra-axial infiltrating tumours, mostly originating from the glia, surgery allows histological diagnosis and provides a means of temporal control; surgery can reduce mass effect and intracranial hypertension. Because of their locally aggressive nature, malignant brain tumours are not currently curable and their control requires multimodal strategies. Despite discussion on the role of aggressive surgery in the treatment of these lesions, most neuro-oncologists agree that “cytoreduction” and elimination of the tumoural mass are the goals of surgical resection, when they are obtained without causing neurological impairment [4,5].

Morbidity and mortality after brain surgery has decreased consistently in the last decades. The 30-year mortality rate after brain tumour removal is generally <3%. The number of surgical complications depends on the nature of the tumour and its location. Severe complications (perioperative hemorrhage, infection and permanent neurological lesions) occur in <10% of patients [6].

80.6.4 Radiotherapy

The efficacy of radiotherapy has been demonstrated in the treatment most malignant brain tumours. Once the anatomopatologic diagnosis has been established and surgical resection completed, radiotherapy is usually indicated. Although different histological tumour types have different sensitivity to radiation, the improvement in 1-5-year survival obtained with this technique makes its use incontestable in most CNS tumours. The main limiting factor of its long-term effects is the level of the dose or radiation exposure, which can be higher than the CNS can tolerate. Even with exposure to radiation doses within the established limits (40-60 Gy), the brain is vulnerable to many toxic effects. Acute reactions immediately after radiation ensure from acute brain tumefaction and manifest as an increase in neurological deficit. Fortunately, such reactions respond well to steroids and are generally reversible. Within 1-3 months after irradiation, a similar but late syndrome, also reversible with steroids, may appear. A less common brain reaction is radiation necrosis, which can appear months or years after radiotherapy. It is a progressive brain reaction that is probably caused by direct toxicity in the brain and its microvascularization. Patients will present with insidious and progressive deterioration, focal neurologic signs and dementia. Radiation necrosis can be difficult to distinguish from tumour recurrence, because they share similar clinical and image features. In such cases, they can be differentiated by stereotactic biopsy or brain SPECT. Therapy can include steroids or decompressive treatment. Many patients have already arrived at a terminal stage, so that the most adequate treatment is conservative and palliative in most cases.

When survival is prolonged, different additional complications of long-term radiation appear that are increasingly worrying: hypopituitarism, occlusive arterial disease and radiation-induced oncogenesis. Tumours associated with radiation (meningiomas, sarcomas and gliomas) are a rare and late complication that can appear decades after irradiation to the brain. More worrying are the risk of radiation in small children, leading to learning difficulties, hypophyseal insufficiency, myelopathies and spinal cord deformities, accompanied by the adverse events due to medications. Since myelinisation of the CNS is completed between 2-3 years of age, radiotherapy before this age is particularly hazardous and should be avoided.

80.6.5 Chemotherapy

Following brief episodes of optimism, chemotherapy has brought about no important improvement in the treatment of malignant brain tumours. Practically all the available anti-cancer agents for the treatment of hematologic or systemic malignant neoplasms have also been studied in brain tumours. Apart from recent discoveries in paediatric tumours such as germinoma and medulloblastoma, chemotherapy has shown no efficacy in improvement. In oncologic terms, brain tumours, with their highly defined localization, relatively small tumoural mass and non-metastatic nature, could well be responsive to chemotherapy. Nonetheless, these factors are contrasted by the peculiar complexity of the CNS, where the blood-brain barrier limits the access of most anti-cancer agents. Even if the blood-brain barrier’s integrity can be altered by different brain tumours, penetration by most chemotherapeutic agents is still limited. Nonetheless, a few liposoluble, low-molecular-weight and apolar agents exist that can pass across an intact blood-brain barrier. Among these, nitrosoureas, hydroxyurease and diazoquinon (AZQ).

The access of other less permeable agents (methotrexate, vincristine, cisplatin) can be improved by the rupture of the osmotic blood-brain barrier or with intrathecal or intracerebral administration. Among these agents, nitrosoureas and hydroxyurea are the most extensively studied. A recent analysis of prospective studies performed during the last 10 years demonstrated that chemotherapy administered after surgery and radiation therapy for malignant gliomas obtained a small improvement in survival. The 24-month median survival rate was 23.4% in the patients treated with chemotherapy and 15.9% in those treated with radiotherapy and surgery. This improvement, small but statistically significant, can be masked by other variables, such as age and functional status at tumour onset.

80.7 Complications and Postsurgical Management

As mentioned, variability in brain tumour is common, so that it is difficult to establish general rules for their management, depending as it does on tumour type, localization, and procedure among others. So we have patients who only undergo stereotactic biopsy and those who require therapy in order to go on breathing sensors for measuring intracranial pressure (ICP.)

Analogously, the same control should be maintained in a patient operated for a tumour of the posterior fossa, where edema can rapidly decompensate the patient, to a patient treated for a small convex meningioma with a Glasgow Coma Scale (GCS) score of 15.

Some general criteria and complications that can present in all operated tumours exist, as well as criteria that can be applied to all neurocritically ill patients.

On the basis of our experience, we recommend that the patient should stay for a minimum of 72 h in the intensive care unit (ICU); everybody knows the need for beds in our health system, but it is not uncommon that a patient who has performed well the first 24 hours will be transferred to a general ward, and then worsen again, and re-enter the ICU. In general, the cause is tumoural edema, which, as we will see, differs from traumatic edema which is sometimes present.

For example, we can operate metastasis in the posterior fossa, obtain a very immediate good postsurgical outcome, only to see edema develop days later when the patient is in the operating room. This edema can compress the brainstem and decompensate it rapidly, with the risk of late arrival because of not being in a place where it can be continuously monitored.

If the patient had a good neurological status before surgery and if the surgical procedure was not very invasive, administering therapy is recommended. On the contrary, if the operation lasted for many hours or in the case of large tumours, even if benign (basal meningiomas or others similar), it is sometimes recommended that the patient remain on assisted mechanical ventilation (AMV) and then be weaned gradually.

In such cases, or whenever the patient must remain on AMV, or when GCS cannot be assessed, a sensor to measure ICP should be placed. This highlights the need for close respiratory and hemodynamic monitoring in the first hours postoperatively, as well as monitoring the level of consciousness, electrolytes, coagulation and arterial blood gases, 24 hour-antibiotic prophylaxis, and control of arousal and pain.

Although neurological and extraneurological complications may arise, this chapter will cover only the first and most important, ones.

80.7.1 Convulsive Seizures

Almost 60% of patients with brain tumours can experience convulsive seizures or their first seizure episode after diagnosis or neurosurgery. Seizure is considered a consequence of craniotomy and occurs during the first week after surgery. The incidence of sudden seizures is between 4 and 19% in recent studies; the incidence of late attacks is 17-70%.

Seizures are complications exclusive of supratentorial lesions, particularly in the temporal, frontal, parasellar and parietal regions; even if some cases they have been reported after posterior fossa surgery, seizures most commonly occur in cortical tumours.

This complication can also be caused by indirect causes such as electrolyte abnormalities, hypoxia, or hypoglycaemia. The most common seizures in these cases are generalized, focal or simple and rare.

The consequences of seizure are severe neural lesions, increased intracranial pressure, and secondary increase in cerebral perfusion pressure; the systemic effect is hypoxia, metabolic acidosis and hyperthermia.

Prophylactic treatment is controversial. It is always necessary to take into consideration that medications can have adverse events and can interfere with steroids and chemotherapy [7].

A recent meta-analysis concluded that there is evidence both in favour and against prophylactic therapy; therefore, the decision to start anticonvulsive treatment for prophylaxis should be taken on the basis of individual risk factors, cortical localization and discussion with the patient.

The drug of first choice in adults is diphenylhydantoin, starting at a dose according to the patient’s body weight. The aim is to maintain blood levels to presurgical standard values, followed by postsurgical maintenance doses.

Also controversial is how long the patient should receive anticonvulsants after surgery. This choice depends on many factors: presence of seizures before surgery, type of pathology, type of resection (total, partial), surgery area, encephalographic and tomographic findings. On this one can decide when to start treatment, which in some cases can continue for years and in others for months.

80.7.2 Postsurgical Intracranial Hemorrhage

Postsurgical hemorrhage is quite a frequent complication and a potentially very severe one after this kind of surgery. In order to avoid it, careful surgical technique and careful pre-surgical and post-surgical control of coagulation and platelet function should be performed.

Postsurgical intracranial hemorrhage is estimated to occur in 2-10% of cases, extradural hemorrhage in 0.9-7.1%, and intracerebral in 3.9%.

The main causes of postsurgical intracerebral hemorrhage are: inadequate haemostasis, high arterial pressure both peri- and/or postsurgery, sudden ventricle decompression, difficulties in tumour dissection, direct arterial lesion, alteration in blood circulation, thrombocytopenia. A higher incidence of hemorrhage is observed in primary gliomas.

There are two peaks of presentation: the first and most important one occurs within the first 6 hours after surgery and the second starting after the first 24 hours; the second one is closely related to the occurrence of perilesional edema. Morbidity and mortality are high (almost 30%), with major complications in 60% of cases.

The prognosis is worse in the following cases: hematoma >3 cm, suprasellar hemorrhage, and cerebral hemorrhage associated with intraventricular extension. Almost 40% of these patients die during the following 48 hours.

Early diagnosis is essential to avoid complications. The key to early diagnosis is immediate postsurgical neurological control in the ICU with neuromonitoring when needed, and intracranial pressure monitoring.

Progressive deterioration in the level of consciousness and neurologic focality (pupils, motor, seizures, etc.) or a sudden increase in intracranial pressure should prompt immediate treatment.

Maintaining normal arterial pressure is important because it is one of the main risk factors for hemorrhage (tumours have neoformation of vessels with weaker walls). Besides the misconception of not lowering blood pressure to prevent secondary injury, it is essential not to apply criteria of other diseases to tumours since they can show a very specific behaviour. This concept is even more important in cerebral ischemia where the risk of hemorrhage is high.

80.7.3 Cerebral Edema

Cerebral edema can be defined as the increase of water in cerebral tissue sufficient to produce clinical symptoms. The brain has three anatomic compartments that can accumulate excessive amounts of liquids:

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