|Year : 2018 | Volume
| Issue : 1 | Page : 4-11
Neurocritical Care of Intracranial Brain Tumor Surgery: An Overview
Alexis R Narvaez-Rojas1, Joulem Mo-Carrascal2, Johana Maraby2, Guru D Satyarthee3, Samer Hoz4, Andrei F Joaquim5, Luis R Moscote-Salazar6
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 Publication||27-Mar-2018|
Luis R Moscote-Salazar
Facultad de Medicina, Campus de Zaragocilla, Universidad de Cartagena, Cartagena de Indias
Source of Support: None, Conflict of Interest: None
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 2018 Oct 20];4:4-11. Available from: http://www.mamcjms.in/text.asp?2018/4/1/4/228659
| Introduction|| |
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|| |
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.
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.
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. 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.
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., 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.,
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.,,,
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.,
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.
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.,, 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.,,
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.,
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 without randomized control trials available to date; it has shown some degree of improvement and, combined with troxerutin for acute cerebral infarction, 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.
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.,
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.
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.,
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, 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). Refer general measure in [Table 2].
| Syndrome of Inappropriate Antidiuretic Hormone|| |
The syndrome of inappropriate antidiuretic hormone (SIADH) or vasopressin causes hyponatremia, plasma hyperosmolality, inappropriately high urine osmolality, and high natriuresis., 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.
| Cerebral Salt-Losing Syndrome|| |
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.
| Sodium Homeostasis|| |
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.
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.
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.,
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.
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.
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., Refer [Table 3] for hyponatremia treatment.
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.,
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.
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.
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.
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.
Hypernatremia: It occurs when sodium concentration exceeds 145 mmol/L serum. 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:
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.,
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. Hypernatremia is common in hospitalized patients as an iatrogenic consequence and, therefore, considered a risk factor for hospital mortality.,, 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.
Anticonvulsants: The incidence of seizures in patients with supratentorial tumors is around 25–40%. In patients with low-grade astrocytoma, the rate of preoperative seizures can reach up to 75%. 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. 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. Refer [Table 4] for postoperative seizure prophylaxis.
Fever: Postoperative fevers are common after cerebral hemispherectomy, occurring in 30–82% of patients., There are no studies regarding postcraniectomy fever among adult populations, although multiple studies have been published regarding postoperative fever [Table 5].,,,
| Nutrition|| |
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. 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.
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, which can be used because no specific score has been designed for postsurgical patients after brain tumor surgery.
| Respiratory Complications|| |
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.
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:
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|| |
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.
| Prevention of Deep Vein Thrombosis|| |
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. 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.
| Postcraniotomy Pain|| |
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, which has been divided into the following four grades:
- 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. Acute pain can be managed with gabapentin, which is considered to decrease the posterior horn neuronal hyperexcitability induced by lesions, though effective to a small degree, decrease postoperative analgesic consumption, and may contribute to delayed extubation and increase the level of sedation postoperatively. When coadministered with dexamethasone, it may decrease the 24-h incidence of postoperative vomiting and nausea, postoperative pain, and the consumption of opioids.,,
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. When the American Society of Anesthesiologists compared paracetamol, sufentanil, and morphine, the best result was yielded by sufentanil, followed by morphine and paracetamol. 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.
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. COX-2 inhibitors including parecoxib do not have antiplatelet properties. Nowadays, its use is restricted due do important cardiovascular side effects. 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. 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.,
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. Preemptive scalp infiltration using 1% lidocaine and 0.5% ropivacaine is more efficacious before skin closure than postoperatively following craniotomies.,
| Conclusion|| |
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.
| References|| |
Ostrom QT, Gittleman H, Fulop J, Liu M, Blanda R, Kromer C et al.
CBTRUS statistical report: Primary brain and central nervous system tumors diagnosed in the United States in 2008–2012. Neuro Oncol 2015;17(Suppl 4):iv1-2.
Whitfield PC. Neuroprotection. Surgery 2004;22:63-6.
Klein KU, Engelhard K. Perioperative neuroprotection. Best Pract Res Clin Anaesthesiol 2010;24:535-49.
Mesotten D, Van den Berghe G. Clinical benefits of tight glycaemic control: Focus on the intensive care unit. Best Pract Res Clin Anaesthesiol 2009;23:421-9.
Yuan J. Neuroprotective strategies targeting apoptotic and necrotic cell death for stroke. Apoptosis 2009;14:469-77.
Bansal S, Sangha KS, Khatri P. Drug treatment of acute ischemic stroke. Am J Cardiovasc Drugs 2013;13:57-69.
Xing C, Arai K, Lo EH, Hommel M. Pathophysiologic cascades in ischemic stroke. Int J Stroke 2012;7:378-85.
Auriel E, Bornstein NM. Neuroprotection in acute ischemic stroke—Current status. J Cell Mol Med 2010;14:2200-2.
Tomassoni D, Lanari A, Silvestrelli G, Traini E, Amenta F. Nimodipine and its use in cerebrovascular disease: Evidence from recent preclinical and controlled clinical studies. Clin Exp Hypertens 2008;30:744-66.
Haley EC. A randomized trial of tirilazad mesylate in patients with acute stroke (RANTTAS). The RANTTAS investigators. Stroke 1996;27:1453-8.
van der Worp HB, Kappelle LJ, Algra A, Bär PR, Orgogozo JM, Ringelstein EB et al.
The effect of tirilazad mesylate on infarct volume of patients with acute ischemic stroke. Neurology 2002;58:133-5.
STIPAS Investigators. Safety study of tirilazad mesylate in patients with acute ischemic stroke (STIPAS). Stroke 1994;25:418-23.
Tseng M-Y., Hutchinson PJ, Richards HK, Czosnyka M, Pickard JD, Erber WN et al.
Acute systemic erythropoietin therapy to reduce delayed ischemic deficits following aneurysmal subarachnoid hemorrhage: A phase II randomized, double-blind, placebo-controlled trial. J Neurosurg 2009;111:171-80.
Jerndal M, Forsberg K, Sena ES, Macleod MR, O’Collins VE, Linden T et al.
A systematic review and meta-analysis of erythropoietin in experimental stroke. J Cereb Blood Flow Metab 2010;30:961-8.
Vergouwen MD, de Haan RJ, Vermeulen M, Roos YB. Effect of statin treatment on vasospasm, delayed cerebral ischemia, and functional outcome in patients with aneurysmal subarachnoid hemorrhage: A systematic review and meta-analysis update. Stroke 2010;41:e47-52.
Karia S, Mahajan PT, Shah N, Sonavane S, De Sousa A. Cerebroprotein hydrolysate in traumatic brain injury. El Mednifico J 2013;2:34.
Liang K-S, Yin C-B, Peng L-J, Zhang J-L, Guo X, Liang S-Y et al.
Effect of troxerutin and cerebroprotein hydrolysate injection for the treatment of acute cerebral infarction: A multi-center randomized, single-blind and placebo-controlled study. Int J Clin Exp Med 2017;10:10959-64.
Muench E, Bauhuf C, Roth H, Horn P, Phillips M, Marquetant N et al.
Effects of positive end-expiratory pressure on regional cerebral blood flow, intracranial pressure, and brain tissue oxygenation. Crit Care Med 2005;33:2367-72.
Nekludov M, Bellander B-M., Mure M. Oxygenation and cerebral perfusion pressure improved in the prone position. Acta Anaesthesiol Scand 2006;50:932-6.
Raoof S, Chowdhrey N, Raoof S, Feuerman M, King A, Sriraman R et al.
Effect of combined kinetic therapy and percussion therapy on the resolution of atelectasis in critically ill patients. Chest 1999;115:1658-66.
Panahi Y, Mojtahedzadeh M, Najafi A, Ghaini MR, Abdollahi M, Sharifzadeh M et al.
The role of magnesium sulfate in the intensive care unit. EXCLI J 2017;16:464-82.
Iacob G, Iacob S, Cojocaru I. [Prophylactic antibiotics in neurosurgery]. Rev Med Chir Soc Med Nat Iasi 2007;111:643-8.
Cacciola F, Cioffi F, Anichini P, Di Lorenzo N. Antibiotic prophylaxis in clean neurosurgery. J Chemother 2001;13:119-22.
Carney N, Totten AM, Hawryluk GW, Bell MJ, Bratton SL, Chesnut R et al.
Guidelines for the Management of Severe Traumatic Brain Injury, 4th ed. Neurosurgery 2017;80:6-15.
Grände P-O. Critical evaluation of the lund concept for treatment of severe traumatic head injury, 25 years after its introduction. Front Neurol 2017;8:315.
Pillai BP, Unnikrishnan AG, Pavithran PV. Syndrome of inappropriate antidiuretic hormone secretion: Revisiting a classical endocrine disorder. Indian J Endocrinol Metab 2011; 15(Suppl 3):S208-15.
Ellison DH, Berl T. The syndrome of inappropriate antidiuresis. N Engl J Med 2007;356:2064-72.
Gross P. Clinical management of SIADH. Ther Adv Endocrinol Metab 2012;3:61-73.
Moritz ML. Syndrome of inappropriate antidiuresis and cerebral salt wasting syndrome: Are they different and does it matter? Pediatr Nephrol 2012;27:689-93.
Frangiosa A, De Santo LS, Anastasio P, De Santo NG. Acid-base balance in heart failure. J Nephrol 2006;19(Suppl 9):S115-20.
Mazzaferro EM. Complications of fluid therapy. Vet Clin North Am Small Anim Pract 2008;38:607-19.
Reynolds RM, Padfield PL, Seckl JR. Disorders of sodium balance. BMJ 2006;332:702-5.
Sterns RH, Silver SM. Cerebral salt wasting versus SIADH: What difference? J Am Soc Nephrol 2008;19:194-6.
Hoyle GE, Chua M, Soiza RL. Volaemic assessment of the elderly hyponatraemic patient: Reliability of clinical assessment and validation of bioelectrical impedance analysis. QJM 2011;104:35-9.
Flear CT, Gill GV, Burn J. Hyponatraemia: Mechanisms and management. Lancet 1981;2:26-31.
Goldman MB, Luchins DJ, Robertson GL. Mechanisms of altered water metabolism in psychotic patients with polydipsia and hyponatremia. N Engl J Med 1988;318:397-403.
Vaidya C, Ho W, Freda BJ. Management of hyponatremia: Providing treatment and avoiding harm. Cleve Clin J Med 2010;77:715-26.
Verbalis JG, Goldsmith SR, Greenberg A, Schrier RW, Sterns RH. Hyponatremia treatment guidelines 2007: Expert panel recommendations. Am J Med 2007;120:S1-21.
Overgaard-Steensen C, Ring T. Clinical review: Practical approach to hyponatraemia and hypernatraemia in critically ill patients. Crit Care 2013;17:206.
Kahn A, Brachet E, Blum D. Controlled fall in natremia and risk of seizures in hypertonic dehydration. Intensive Care Med 1979;5:27-31.
Chassagne P, Druesne L, Capet C, Ménard JF, Bercoff E. Clinical presentation of hypernatremia in elderly patients: A case control study. J Am Geriatr Soc 2006;54:1225-30.
Moritz ML, Ayus JC. Preventing neurological complications from dysnatremias in children. Pediatr Nephrol 2005;20:1687-700.
Blum D, Brasseur D, Kahn A, Brachet E. Safe oral rehydration of hypertonic dehydration. J Pediatr Gastroenterol Nutr 1986;5:232-5.
Righini A, Ramenghi L, Zirpoli S, Mosca F, Triulzi F. Brain apparent diffusion coefficient decrease during correction of severe hypernatremic dehydration. Am J Neuroradiol 2005;26:1690-4.
Fang C, Mao J, Dai Y, Xia Y, Fu H, Chen Y et al.
Fluid management of hypernatraemic dehydration to prevent cerebral oedema: A retrospective case control study of 97 children in China. J Paediatr Child Health 2010;46:301-3.
Bhandari S, Peri A, Cranston I, McCool R, Shaw A, Glanville J et al.
A systematic review of known interventions for the treatment of chronic nonhypovolaemic hypotonic hyponatraemia and a meta-analysis of the vaptans. Clin Endocrinol 2017;86:761-71.
Maschio M. Brain tumor-related epilepsy. Curr Neuropharmacol 2012;10:124-33.
Whittle IR, Beaumont A. Seizures in patients with supratentorial oligodendroglial tumours. Clinicopathological features and management considerations. Acta Neurochir (Wien) 1995;135:19-24.
Kerrigan S, Grant R. Antiepileptic drugs for treating seizures in adults with brain tumours. In: Kerrigan S, editor. Cochrane Database of Systematic Reviews. Chichester, UK: John Wiley & Sons Ltd; 2011. p. CD008586.
de Almeida AN, Marino R, Aguiar PH, Teixeira MJ. Postoperative fever after hemispherectomy: The role of non-infectious factors. Seizure 2006;15:340-3.
Kossoff EH, Vining EP, Pyzik PL, Kriegler S, Min K-S., Carson BS et al.
The postoperative course and management of 106 hemidecortications. Pediatr Neurosurg 2002;37:298-303.
Saavedra F, Myburg C, Lanfranconi MB, Urtasun M, De Oca LM, Silberman A et al.
[Postoperative fever in orthopedic and urologic surgery]. Medicina (B Aires) 2008;68:6-12.
Pile JC. Evaluating postoperative fever: A focused approach. Cleve Clin J Med 2006; 73(Suppl 1):S62-6.
Maday KR, Hurt JB, Harrelson P, Porterfield J. Evaluating postoperative fever. J Am Acad Physician Assist 2016;29:23-8.
Rzany B, Correia O, Kelly JP, Naldi L, Auquier A, Stern R. Risk of Stevens-Johnson syndrome and toxic epidermal necrolysis during first weeks of antiepileptic therapy: A case-control study. Study Group of the International Case Control Study on Severe Cutaneous Adverse Reactions. Lancet 1999;353:2190-4.
Barr J, Hecht M, Flavin KE, Khorana A, Gould MK. Outcomes in critically ill patients before and after the implementation of an evidence-based nutritional management protocol. Chest 2004;125:1446-57.
Boniatti MM, Friedman G, Castilho RK, Vieira SR, Fialkow L. Characteristics of chronically critically ill patients: Comparing two definitions. Clinics (Sao Paulo) 2011;66:701-4.
Heyland DK, Dhaliwal R, Jiang X, Day AG. Identifying critically ill patients who benefit the most from nutrition therapy: The development and initial validation of a novel risk assessment tool. Crit Care 2011;15:R268.
Massard G, Wihlm JM. Postoperative atelectasis. Chest Surg Clin N Am 1998;8:503-28.
MacIntyre NR. Evidence-based guidelines for weaning and discontinuing ventilatory support. Chest 2001;120:375S-95S.
Nava S, Ferrer M, Esquinas A, Scala R, Groff P, Cosentini R et al.
Palliative use of non-invasive ventilation in end-of-life patients with solid tumours: A randomised feasibility trial. Lancet Oncol 2013;14:219-27.
Fahrni J, Husmann M, Gretener SB, Keo HH. Assessing the risk of recurrent venous thromboembolism—A practical approach. Vasc Health Risk Manag 2015;11:451-9.
Jo J, Schiff D, Perry J. Thrombosis in brain tumors. Semin Thromb Hemost 2014;40:325-31.
HCC of the IHS. The international classification of headache disorders, 3rd edition (beta version). Cephalalgia 2013;33:629-808.
Harner SG, Beatty CW, Ebersold MJ. Headache after acoustic neuroma excision. Am J Otol 1993;14:552-5.
Chattopadhyay S, Roy S, Rudra A, Saha P. Pain after craniotomy: A time for reappraisal? Indian J Pain 2013;27:7. [Full text]
Maneuf YP, Gonzalez MI, Sutton KS, Chung FZ, Pinnock RD, Lee K. Cellular and molecular action of the putative GABA-mimetic, gabapentin. Cell Mol Life Sci 2003;60:742-50.
Türe H, Sayin M, Karlikaya G, Bingol CA, Aykac B, Türe U. The analgesic effect of gabapentin as a prophylactic anticonvulsant drug on postcraniotomy pain: A prospective randomized study. Anesth Analg 2009;109:1625-31.
Misra S, Parthasarathi G, Vilanilam GC. The effect of gabapentin premedication on postoperative nausea, vomiting, and pain in patients on preoperative dexamethasone undergoing craniotomy for intracranial tumors. J Neurosurg Anesthesiol 2013;25:386-91.
Tiippana EM, Hamunen K, Kontinen VK, Kalso E. Do surgical patients benefit from perioperative gabapentin/pregabalin? A systematic review of efficacy and safety. Anesth Analg 2007;104:1545-56.
Wiffen PJ, Collins S, McQuay HJ, Carroll D, Jadad A, Moore RA. Anticonvulsant drugs for acute and chronic pain. In: Wiffen PJ, editor. Cochrane Database of Systematic Reviews. Chichester, UK: John Wiley & Sons Ltd; 2005, p. CD001133.
Kardash KJ, Sarrazin F, Tessler MJ, Velly AM. Single-dose dexamethasone reduces dynamic pain after total hip arthroplasty. Anesth Analg 2008;106:1253-7.
Goldsack C, Scuplak SM, Smith M. A double-blind comparison of codeine and morphine for postoperative analgesia following intracranial surgery. Anaesthesia 1996;51:1029-32.
Sane S, Tolumehr A, Hassani E, Mahoori A. Comparison the effects of paracetamol with sufentanil infusion on postoperative pain control after craniotomy in patients with brain tumor. Adv Biomed Res 2015;4:64.
] [Full text]
Rahimi SY, Alleyne CH, Vernier E, Witcher MR, Vender JR. Postoperative pain management with tramadol after craniotomy: Evaluation and cost analysis. J Neurosurg 2010;112:268-72.
Palmer JD, Sparrow OC, Iannotti F. Postoperative hematoma: A 5-year survey and identification of avoidable risk factors. Neurosurgery 1994;35:1061-4.
Pawlosky N. Cardiovascular risk. Can Pharm J/Rev Des Pharm Du Canada 2013;146:80-3.
Jones SJ, Cormack J, Murphy MA, Scott DA. Parecoxib for analgesia after craniotomy. Br J Anaesth 2009;102:76-9.
Anderson BJ. Paracetamol (acetaminophen): Mechanisms of action. Pediatr Anesth 2008;18:915-21.
Bertolini A, Ferrari A, Ottani A, Guerzoni S, Tacchi R, Leone S. Paracetamol: New vistas of an old drug. CNS Drug Rev 2006;12:250-75.
Guilfoyle MR, Helmy A, Duane D, Hutchinson PJ. Regional scalp block for postcraniotomy analgesia. Anesth Analg 2013;116:1093-102.
Katz J, Cohen L, Schmid R, Chan VWS, Wowk A. Postoperative morphine use and hyperalgesia are reduced by preoperative but not intraoperative epidural analgesia: Implications for preemptive analgesia and the prevention of central sensitization. Anesthesiology 2003;98:1449-60.
Song J, Li L, Yu P, Gao T, Liu K. Preemptive scalp infiltration with 0. 5% ropivacaine and 1% lidocaine reduces postoperative pain after craniotomy. Acta Neurochir (Wien) 2015;157:993-8.
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]