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   Table of Contents      
Year : 2018  |  Volume : 4  |  Issue : 1  |  Page : 4-11

Neurocritical Care of Intracranial Brain Tumor Surgery: An Overview

1 Department of Neurosurgery, Latin America Foundation of Neurotrauma & Neuro Critical Care, Red Latino, Colombia
2 Researcher, Universidad Nacional Autonoma de , Managua, Nicaragua
3 All Institute of Medical Sciences, New Delhi, India
4 Neurosurgeon, Neurosurgery Teaching Hospital, Baghdad, Iraq
5 Department of Neurology, State University of Campinas, Campinas, Sao Paulo, Brazil
6 Department of Neurosurgery, Latin America Foundation of Neurotrauma & Neuro Critical Care, Red Latino; Cartagena Neurotrauma Research Group, University of Cartagena, Cartagena, Colombia

Date of Web Publication27-Mar-2018

Correspondence Address:
Luis R Moscote-Salazar
Facultad de Medicina, Campus de Zaragocilla, Universidad de Cartagena, Cartagena de Indias
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/mamcjms.mamcjms_79_17

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The principal aim of neurointensive care in patients with intracranial tumor surgery is prevention, prediction, early detection, and the prompt treatment of postoperative complications. Maintenance of proper hemodynamic and adequate respiratory support is necessary to prevent postoperative mass effect due to cerebral edema, hydrocephalus, hematoma, and infarct causing cerebral herniation syndromes. Invasive blood pressure monitoring is usually recommended along with measuring intracranial pressure to allow the proper evaluation of cerebral perfusion pressure and an effective cerebral blood flow. For the effective neurocritical intensive care of surgical patients with brain tumors, good harmony, interaction, and communication between the neurosurgeon and the neurointensive team is of paramount importance.

Keywords: Brain tumor surgery, cerebral edema, cerebral ischemia, hydrocephalus, neurocritical care, respiratory support

How to cite this article:
Narvaez-Rojas AR, Mo-Carrascal J, Maraby J, Satyarthee GD, Hoz S, Joaquim AF, Moscote-Salazar LR. Neurocritical Care of Intracranial Brain Tumor Surgery: An Overview. MAMC J Med Sci 2018;4:4-11

How to cite this URL:
Narvaez-Rojas AR, Mo-Carrascal J, Maraby J, Satyarthee GD, Hoz S, Joaquim AF, Moscote-Salazar LR. Neurocritical Care of Intracranial Brain Tumor Surgery: An Overview. MAMC J Med Sci [serial online] 2018 [cited 2020 Aug 3];4:4-11. Available from: http://www.mamcjms.in/text.asp?2018/4/1/4/228659

  Introduction Top

A very successfully executed intracranial surgery in the operation theatre may have an unfavorable outcome with improper and inadequate neurointensive management during the postoperative period. The proper management of alterations in homeostasis may halt or even altogether completely prevent the development of complications that may have potential to alter brain function and generate collateral cerebral injuries.

  Primary Intracranial Surgery of Cerebral Tumors Top

The incidence of tumors in the brain and central nervous system (CNS) (both malignant and nonmalignant) has an average annual age-adjusted incidence of 28.57 per 100,000 population.[1]

Neuroprotection strategies: Initial injury can be prevented by reducing primary risk factor magnitudes such as primary cerebral injury or accidental ischemic and hemorrhagic cerebrovascular incidents. These risk factors may include applying the rule for vehicle speed limits, the use of seat belts, avoiding drinking, smoking reduction and control of blood pressure, diabetes, and other comorbid illness.[2]

Physiological neuroprotective strategies

The physiological neuroprotective strategies have been directed to monitor and control blood pressure, cerebral oxygenation, and core body temperature. The result of traumatic brain injury (TBI) is relatively worse in patients with hypoxia, hypotension, or hyperpyrexia. The cerebral perfusion pressure (CPP) is the mean arterial pressure less the intracranial pressure (ICP). Patients with elevated ICP and reduced CPP have a worse prognosis.[2] Therefore, it is vitally important to maintain CPP >60 or 70 mmHg.

ICP control is a neuroprotective factor: An elevated ICP occurs after stroke, and head injury and causes reduced cerebral blood flow due to a decrease in CPP, which leads to cerebral ischemia and the initiation of events that may result in neuronal cell death.[2]

Reperfusion: Cerebral thrombolytic therapy can benefit patients with acute stroke if administered within key hours after stroke. However, in most patients who die from ischemic stroke soon, hemorrhagic transformation is usually evident. The use of thrombolytic agents leads to increased bleeding, which is secondary to reperfusion. Most patients die within 2 weeks of giving thrombolytics compared to those patients who did not receive thrombolytic therapy.[2],[3] However, patients who survived thrombolysis were comparatively less disabled than those who failed to receive treatment.

Glucose: A high concentrations of glucose before and/or during an ischemic event causes worse neurologic outcome. This is probably due to lactic acidosis in the brain regions with increased anaerobic glycolysis, although other mechanisms have been hypothesized.[2],[4]

Neuroprotective pharmacological strategies

More than 50 pharmacological drugs targeted at specific target points in the pathophysiology of neuronal cell death cascade have been used in clinical trials in addition to patients with stroke or head injury.[5],[6],[7],[8]

Nimodipine: It reduces the risk of a poor prognosis in subarachnoid hemorrhage by about 30%. Nimodipine therapy may neither reduce the incidence of angiographic spasm, nor is it proven to be neuroprotective after a head injury or ischemic stroke.[2],[9]

Glutamate receptor antagonists: Glutamate binds to a variety of cell surface receptors. This process is believed to be involved in ischemic neuronal cell death. Currently, concerns have been raised regarding its psychiatric side effects and the vacuolation of the brain.[2]

Free radical scavengers: Tirilazad mesylate has been extensively tested in patients with head injury and stroke. Testing was performed in low (randomized trial of tirilazad mesylate in patients with acute stroke—RANTTAS) and high doses (high-dose tirilazad for acute stroke—RANTTAS II). However, randomized clinical trials concluded that the drug is not beneficial, and other free radicals (e.g., superoxide dismutase) have not proven to be of clinical benefit.[10],[11],[12] Other targets developed in many molecular processes involving cell death cascade are described in [Table 1].
Table 1: Molecular processes involving cell death cascade, which can be targeted with free to improve neurocritical outcomes

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Erythropoietin: Cerebral erythropoietin is produced in the hippocampus, internal capsule, cortex, endothelial cells, and astrocytes, and their receptors are expressed by neurons, microglia, astrocytes, and endothelial cells. Hypoxia and ischemia are recognized as important driving forces to produce erythropoietin, suggesting that erythropoietin is part of a physiological self-regulation. Besides that, it stimulates neurogenesis, neuronal differentiation, and active neurotrophic brain. It is antiapoptotic, antioxidant, and anti-inflammatory, allowing signaling.[2],[13],[14]

Statins: Hydroxymethylglutaryl-CoA synthase reductase inhibitors reduce morbidity and mortality in patients with stroke, peripheral vascular lesions, and cardiac events. Statins cause the modulation of nitric oxide synthesis, the stabilization of atherosclerotic plaque, and the attenuation of inflammatory cytokines and antioxidant effects.[2],[15]

Hypnotics: Propofol reduces infarct size and improves neurological outcome after focal or incomplete ischemia in the brain, when physiological variables are controlled during the experiments. In contrast, etomidate worsens the final neurological outcomes. There is no clinical evidence to support the use of hypnotics. Barbiturates may also be beneficial in patients with severe TBI and refractory intracranial hypertension. The infusion of barbiturate has shown to be effective in reducing ICP and probably mortality after TBI, providing systemic hemodynamic stability.

Cerebroprotein hydrolysates: It has been studied in TBI[16] without randomized control trials available to date; it has shown some degree of improvement and, combined with troxerutin for acute cerebral infarction,[17] yielded positive result in a multicenter randomized, single-blind, and placebo-controlled study. No studies are available post-craniectomy after brain tumor surgery.

Mechanical ventilation: At least one-third of the patients with acute brain injury develop acute lung injury (ALI). Pressure-controlled ventilation, high Positive End-Expiratory Pressure (PEEP), low tidal volumes, permissive hypercapnia, and hypovolemia are recommended for patients with an intracranial lesion to ensure adequate brain oxygenation and prevent atelectasis and associated pulmonary complications.[18]

Kinetic therapy: The patient’s head elevation at 30° ensures the return of venous and cerebrospinal fluid (CSF), increasing cerebral oxygenation and preventing pulmonary atelectasis and microaspirations, especially when combined with percussion therapy in the perioperative setting. Recent studies have shown how the position of patients improve cerebral oxygenation and CSF in patients with severe ALI.[19],[20]

Magnesium: It has shown benefit in patients with vasospasm following Subarachnoid Hemorrhage (SAH). Till date, magnesium is known to decrease the length of stay (LOS) in the intensive care unit (ICU) and mortality rate.[21]

Antibiotic prophylaxis in neurosurgery: Postsurgical infections have high mortality and are among the most difficult-to-manage infections. Till date, only general recommendations for clean neurosurgery and surgeries derivative have been reported. There is no consensus on the class of optimal antibiotic and the administration period.[22],[23]

Management of cerebral edema: Edema associated with brain tumors is usually vasogenic and caused by the alteration of the microvasculature. The edema produces a mass effect besides the increase in ICP, which leads to neurological disorders by interrupting tissue homeostasis and a reduction of the local blood flow.

Post-traumatic cerebral edema: It is also called “the concept of Lund” (LC). In the recent guidelines issued by the Brain Trauma Foundation in 2016,[24] a closer approach to the LC is found by the following concepts: CPP at 50–70 mmHg, the avoidance of osmotherapy (used but with caution), the avoidance of vasopressors (still used but not frequently), avoiding active cooling, and albumin as a volume expander (still not recommended).[25] Refer general measure in [Table 2].
Table 2: General measures proposed to aid in neuroprotection

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  Syndrome of Inappropriate Antidiuretic Hormone Top

The syndrome of inappropriate antidiuretic hormone (SIADH) or vasopressin causes hyponatremia, plasma hyperosmolality, inappropriately high urine osmolality, and high natriuresis.[26],[27] This can be associated with the use of selective serotonin reuptake inhibitors, tricyclic antidepressants, carbamazepine, oxcarbazepine, cyclophosphamide, ifosfamide, hydrochlorothiazide, thiazides, nonsteroidal anti-inflammatory drugs (NSAIDs), vincristine, neuroleptic agents, desmopressin, vasopressin, oxytocin, chlorpropamide, and clofibrate.[28]

  Cerebral Salt-Losing Syndrome Top

It is characterized by marked polyuria and natriuresis leading to hyponatremia and hypovolemia. Usually it occurs during the first 2 weeks after brain damage and resolves spontaneously after 2–4 weeks.[29]

  Sodium Homeostasis Top

Sodium is the major determinant of plasma osmolality, which regulates water movement in and out of the cell. Hyponatremia is frequent and highly deleterious in neurosurgical patients with brain damage. A close monitoring of serum sodium is required to monitor the levels of desired plasma sodium in patients with brain injury.[29]

Sodium level starts at 150–250 mEq/day but gradually decreases to 1–15 mEq/day. Changes in sodium and water metabolism may also result from changes in the potential of the plasma membrane consistent with starvation, reducing total body water content, and sodium accompanying the reduction of blood volume.[4]

Most acute lesions are accompanied by changes in electrolyte metabolism and acid-base status. Large changes occur because there is no intake of water and electrolytes, because injured patients do not perceive thirst because of sedation, anesthesia, or head injuries.[30],[31]

Alkalosis: Respiratory alkalosis is more frequent in patients with acid–base imbalance and mild-to-moderate injuries whose state is not deteriorated until renal or pulmonary circulatory decomposition.[32]

Hyponatremia: It is defined as a decrease in serum sodium concentration to a level <136 mmol/L. Acute hyponatremia bears the risk of cerebral edema with increased ICP and, in severe cases, cerebral herniation and death. In chronic hyponatremia, the brain uses adaptive mechanisms that prevent cerebral edema. However, in this case, an insufficient correction of hyponatremia wanting to reach the normal levels of sodium in a few hours can lead to osmotic demyelination syndrome.[9]

Management of hyponatremia: The presence of symptoms and their severity largely determine the pace of correction. Patients with symptomatic hyponatremia with concentrated urine (osmolality, <200 mOsm/kg H2O) and clinical euvolemia or hypervolemia require the infusion of hypertonic saline, thus achieving a rapid but controlled correction of hyponatremia. Hypertonic saline is generally combined with frusemide to limit the expansion of extracellular volume induced by treatment.[33],[34] Refer [Table 3] for hyponatremia treatment.
Table 3: Hyponatremia treatment

Click here to view

Although hypernatremia always denotes hypertonia, hyponatremia can be associated with a low, normal, or high tonicity. Effective osmolality or tonicity refers to the contribution to the osmolality of solutes such as sodium and glucose, which cannot move freely through the cell membranes, thereby inducing changes in the transcellular water.[13],[39]

Hyperglycemias are the most common cause of translocational hyponatremia. An increase of 100 mg/dL (5.6 mmol/L) in the serum glucose concentration decreases the volume of serum sodium by approximately 1.7 mmol/L, resulting in an increase in the serum osmolality of about 2.0 mOsm/kg H2O.[13]

The retention of mannitol, which occurs in patients with renal failure, has the same effect. In both conditions, the resulting hypertonicity can be aggravated by osmotic diuresis; the moderation of hyponatremia can develop frank hypernatremia, because the total of the concentrations of sodium and potassium in the urine falls short of this serum.[13]

As in hypernatremia, the manifestations of hypotonic hyponatremia are a largely related dysfunction of the CNS and become more noticeable when the decrease in serum sodium concentration is large or rapid (within a period of hours). Although most patients with higher serum sodium (125 mmol/L) are asymptomatic, those with lower values may have symptoms, especially if the disorder has developed rapidly.[39]

The complications of severe hyponatremia include convulsions, coma, permanent brain damage, respiratory failure, brainstem herniation, and death. Menstruating women seem to be particularly at risk.[39]

Hypernatremia: It occurs when sodium concentration exceeds 145 mmol/L serum.[39] Dysfunction in the CNS occurs in different intensities directly related to the severity of hypernatremia, being acute or chronic on its initiation. The water deficit in the hypernatremic patient can be estimated from the following formula:[40]

It may be asymptomatic; however, with sodium level >160 mmol/L, neurological symptoms such as lethargy, nausea, tremor, irritability, and confusion can occur. Subsequently, muscle stiffness, opisthotonus, convulsions, and coma (most severe in extreme old) also occur. Initially, especially in the elderly, thirst is prominent at the beginning. However, with long-standing hypernatremia (145–160 mmol/L), there is moderate but progressive loss of thirst.[41],[42]

The safe rate of correction is unknown, but by convention, the decrease should be 0.5 mEq/L/h and no more than by 12 mEq/L/day.[43] Hypernatremia is common in hospitalized patients as an iatrogenic consequence and, therefore, considered a risk factor for hospital mortality.[40],[44],[45] Chronic hypernatremia is characterized by the inappropriate loss of thirst despite high plasma osmolarity and mild hypovolemia. It is difficult to treat because no evidence has been found toward the use of vaptans.[46]

Anticonvulsants: The incidence of seizures in patients with supratentorial tumors is around 25–40%.[47] In patients with low-grade astrocytoma, the rate of preoperative seizures can reach up to 75%.[48] About 20–40% of the patients with brain tumors present with seizures as a symptom, and risk of convulsion varies according to the type of tumor, the degree, and location.[47] Levetiracetam has been proven to be the most effective drug for brain tumor seizure prophylaxis when compared to phenytoin. Studies evaluating the role of anticonvulsant prophylaxis in specific types of tumors, such as meningiomas, have not found any benefit in preventing early or late postoperative seizures.[49] Refer [Table 4] for postoperative seizure prophylaxis.
Table 4: Postoperative seizure prophylaxis

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Fever: Postoperative fevers are common after cerebral hemispherectomy, occurring in 30–82% of patients.[50],[51] There are no studies regarding postcraniectomy fever among adult populations, although multiple studies have been published regarding postoperative fever [Table 5].[52],[53],[54],[55]
Table 5: Fever in the postoperative period

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  Nutrition Top

Evidence-based nutritional support helps the patient to achieve better outcomes, with a decrease in 56% mortality in the ICU for patients starting nutritional support on Day 4 with change in the LOS.[56] The patient who is neurocritical tends to develop long LOS in the ICU, thereby becoming chronically critically ill patients, which puts this patient population at a risk of overfeeding.[57]

The NUTRIC score is the first nutritional risk assessment tool developed and validated specifically for patients in the ICU to discriminate which patient in the ICU will benefit more (or less) from aggressive protein-energy provision on the basis of age, acute physiology and chronic health evaluation (APACHE II) score, sequential organ failure assessment (SOFA), interleukin-6 levels, and the number of comorbidities and days from hospital to ICU admit,[58] which can be used because no specific score has been designed for postsurgical patients after brain tumor surgery.

  Respiratory Complications Top

It is recommended that patients stop smoking for at least 2 weeks before surgery and practice deep abdominal breathing. Large atelectasis requires bronchoscopy to remove the mucous plugs.[59]

The American College of Chest Physicians, the Society of Critical Care Medicine, and the American Association of Respiratory Care suggest that the patients who have the following criteria can be considered for mechanical ventilation withdrawal:[60]

The lung injury is stable/resolving and the gas exchange is adequate with positive end-expiratory pressure (5–8 cm H2O; fraction of inspired oxygen, 0.4–0.5).
  • Hemodynamic variables are stable.
  • The patient can initiate spontaneous breaths.
  • The same guidelines issued for anticipated need of the artificial airway for greater than 21 days, tracheostomy is preferred.

  Noninvasive Ventilation in End-of-Life Patients Top

No specific trial has been developed for end-of-life patients after craniectomy for brain tumor surgery, although noninvasive ventilation has been compared to oxygen in reducing dyspnea and decreasing morphine use in the patient with end-stage solid tumors, thereby showing benefit. This data is hard to generalize.[61]

  Prevention of Deep Vein Thrombosis Top

Overall, it is considered that cancer increases the risk of deep vein thrombosis about 4.1 times, and chemotherapy does so by 6.5 times. This is a common complication and is one of the leading causes of death in patients with brain tumor.[62] About 30% of these patients develop venous thrombosis during their disease, particularly in those with high-grade glioma and in up to 20% of those with brain metastasis or primary CNS lymphoma.[63]

  Postcraniotomy Pain Top

The international classification of headache disorders (ICHD-3) has classified postcraniotomy headache and subdivided it into acute and persistent varieties. Acute occurs in up to 2/3 of all postcraniectomy patients, resolving within the acute postoperative period. This variety has a persistent headache, with pain starting within 7 days after craniotomy, as well as regaining of consciousness following the craniotomy or discontinuation of medication(s) that impairs the ability to sense or report a headache following the craniotomy. It persists for >3 months, and it cannot be explained by another ICHD-3 diagnosis,[64] which has been divided into the following four grades:[65]
  • Grade 1: a relatively minor annoyance.
  • Grade 2: a headache presents almost every day.
  • Grade 3: the patient requires medication every day.
  • Grade 4: the patient feels incapacitated.

The surgical routes with the highest incidence of postcraniectomy pain are the subtemporal and suboccipital.[66] Acute pain can be managed with gabapentin, which is considered to decrease the posterior horn neuronal hyperexcitability induced by lesions,[67] though effective to a small degree, decrease postoperative analgesic consumption, and may contribute to delayed extubation and increase the level of sedation postoperatively.[68] When coadministered with dexamethasone, it may decrease the 24-h incidence of postoperative vomiting and nausea,[69] postoperative pain, and the consumption of opioids.[70],[71],[72]

Opioids are useful for moderate-to-severe pain and can be used in the early period after craniectomy. Morphine is more effective than codeine beyond 60 min after recovery, requiring fewer doses than codeine.[73] When the American Society of Anesthesiologists compared paracetamol, sufentanil, and morphine, the best result was yielded by sufentanil, followed by morphine and paracetamol.[74] The use of tramadol, a weak μ-receptor agonist and an inhibitor of serotonin and norepinephrine reuptake, may decrease the final cost of craniectomy by decreasing the amount of analgesics required. This is attributed to earlier tolerance to oral intake, fewer opioids having adverse side effects, and more rapid ambulation.[75]

The usage of NSAIDs, especially cyclooxygenase 1 (COX-1) isomers is feared because of their increased risk of bleeding in patients after craniectomy due to their antiplatelet mechanism.[76] COX-2 inhibitors including parecoxib do not have antiplatelet properties. Nowadays, its use is restricted due do important cardiovascular side effects.[77] Parecoxib, a COX-2 inhibitor, decreases pain scores at 6 h and reduces the administration of morphine 6–12 h following the procedure, without a significant effect on analgesia postoperatively.[78] Paracetamol, a serotonergic activator, N-methyl-D-aspartate (NMDA) and substance P inhibitor in the spinal cord, and COX-3 inhibitor do not have the side effects of COXs.[79],[80]

Regional scalp block infiltrations with ropivacaine and lidocaine have shown to reduce opioid requirements, although small and of limited methodological quality randomized controlled trials are available, a meta-analysis showed consistent reduced postoperative pain.[81] Preemptive scalp infiltration using 1% lidocaine and 0.5% ropivacaine is more efficacious before skin closure than postoperatively following craniotomies.[82],[83]

  Conclusion Top

The neurointensive management of brain tumors guarantees a satisfactory evolution. The training of intensivists, neurologists, and neurosurgeons in intensive neurological management is a necessity for modern neurosurgery and using evidence-based strategies may aid in the development of more comprehensive care.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

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  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]

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[Pubmed] | [DOI]


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