| Title | Craniotomy in the Patient with Glioblastoma: A Case Report |
| Creator | Amy C. Lemmon |
| Subject | Glioblastoma; craniotomy; neuromonitoring; dexmedetomidine, MRI; MSNA |
| Description | Glioblastomas represent a unique challenge to anesthesia providers. They are an aggressive form of malignant tumors often causing change in the patient's ICP, blood flow and cerebral autoregulation. Grade IV glioblastomas accounts for 30% of all primary brain tumors and are more common between males 50-70 years old.1 Resection alone is usually inadequate because of microscopic invasion of tumor cells within the brain tissue.1 Treatment is generally a combination of chemotherapy, radiation and surgical debulking. Despite treatment, life expectancy can be measured in weeks and aim is towards palliative care.1 |
| Publisher | Westminster College |
| Date | 2014-12 |
| Type | Text; Image |
| Language | eng |
| Rights | Digital copyright 2014, Westminster College. All rights Reserved. |
| ARK | ark:/87278/s60s2xjj |
| Setname | wc_ir |
| ID | 1094113 |
| OCR Text | Show 1 CRANIOTOMY IN THE PATIENT WITH GLIOBLASTOMA: A CASE REPORT by AMY C. LEMMON, RN, MS A capstone project submitted in partial fulfillment of the requirement for the degree of Master of Science in Nurse Anesthesia Westminster College Salt Lake City, Utah December 2014 2 Keywords: Glioblastoma, craniotomy, neuromonitoring, dexmedetomidine, MRI Abstract Glioblastomas represent a unique challenge to anesthesia providers. They are an aggressive form of malignant tumors often causing change in the patient's ICP, blood flow and cerebral autoregulation. Grade IV glioblastomas accounts for 30% of all primary brain tumors and are more common between males 50-70 years old.1 Resection alone is usually inadequate because of microscopic invasion of tumor cells within the brain tissue.1 Treatment is generally a combination of chemotherapy, radiation and surgical debulking. Despite treatment, life expectancy can be measured in weeks and aim is towards palliative care.1 3 Case Report A 61-year-old male, 178 cm, 77 kg who presented to the emergency room with a new onset of tonic-clonic seizure. He presented signs of decreased mentation and cognition, difficulty reading and slurred speech. The patient also manifested signs of gait imbalance and one sided weakness. Magnetic Resonance Imaging (MRI) scan of the patient showed a large brain tumor in the left hemisphere pressing on Broca's region of the brain. His past medical history was significant for chronic obstructive pulmonary disease (COPD), smoking, hypertension, non-insulin dependent diabetes mellitus, gastroesophageal reflux disease (GERD), headaches, and depression. Current medications were budesonide and formoterol, lisinopril, hydrochlorothiazide, metformin, omeprazole and fluoxetine. Past surgical history consisted of a laparoscopic cholecystecomy, knee arthroscopy, esophagogastroduodenoscopy, and tonsillectomy with adenoidectomy. The laboratory values were unremarkable with the exception of mildly elevated liver enzymes. The patient was admitted to the intensive care unit for radiation treatment and surgical workup to undergo tumor removal through a craniotomy. However, within a short time, he lost the ability to speak or communicate. The patient was brought to the operating room, standard ASA monitors were applied and 10L/min of oxygen via facemask began with an FeO2 of 100%. Intravenous induction began with sublimaze 150 mcg, 2% lidocaine 60 mg, diprivan 150 mg, and cisatracurium 10 mg. The patient was intubated using a 2.0 miller blade and 7.5 mm tube. The endotracheal tube was placed and secured at a depth of 23 cm. End-tidal CO2 was achieved with equal bilateral breath sounds. Mechanical ventilation was maintained on volume 4 control with a tidal volume of 600 ml and a respiratory rate of 12/min. Isoflurane was started while a left radial arterial line was placed. The patient was disconnected from the ventilator and breathing was resumed with an ambu bag. Sedation was maintained with intermittent propofol doses and labile blood pressures were controlled with phenylephrine during transit to MRI. Blood pressure control in the MRI suite proved difficult due to limited monitoring capabilities. The patient was transported from MRI to the OR for surgical removal of glioblastoma. Imaging revealed a ring-enhancing lesion reflecting central necrosis and surrounding edema. Sedation was accomplished with propofol and remifentanil drips, while maintaining isoflurane at ½ MAC. Motor evoked potentials were performed. After the surgical procedure, the patient was left intubated and sedated while he was transported to the ICU. A repeat MRI one week postoperatively showed aggressive tumor regrowth. Unfortunately, the patient died as a result of the tumor two weeks after surgery. Discussion A family history of glioma is not seen often, but when it does exist, the risk doubles for developing glioblastoma.2 Preventive measures, such as lifestyle changes, are ineffective in preventing glioblastomas. Unfortunately, early diagnosis and treatment do not improve outcomes, making it impossible to screen for this disease.2 Glioblastomas are a grade IV tumor that arises from astrocyte cells which are the supportive tissue of the brain. They appear as deep white matter and have a tendency to rapidly infiltrate into surrounding parenchyma.3 Glioblastoma has a mottled appearance, 5 reflective of the degree of necrosis and presence of hemorrhage. The tumor is confirmed by a craniotomy, allowing for maximum, feasible therapeutic resection.3 These tumors are usually malignant because the cells reproduce quickly and are nourished by a large network of blood vessels. Glioblastomas also contain a mix of cell types, such as: cystic mineral; calcium deposits; and dead cells within the center of the tumor. Hyperplasia of small vessel endothelium with vascular thrombosis, necrosis and hemorrhage distinguish glioblastomas from lower grade astrocytomas.3 Glioblastomas are prone to develop and live in the brain tissue because their progenitor cells originate in brain and spinal cord. Anesthesia is an ever-changing, adaptable science. While each anesthetic is individually tailored to suit a patient's specific health conditions and surgical needs, neurological cases present a unique challenge to the anesthesia provider. Neuromonitoring is a critical component of any neurological case. According to the Monro-Kellie doctrine the skull is a rigid, fixed compartment consisting of three main components: the brain tissue, cerebrospinal fluid, and blood.4 As a lesion begins to take up space in the skull another compartment must compensate, usually CSF decreases. Once the brain can no longer compensate for the growing mass, ICP begins to rise. As anesthesia providers the main component we can manipulate in regards to ICP involves blood flow. If an EVD is in place CSF can also be manipulated. Cerebral blood flow & volume, ICP, CMRO2, and cerebral compliance all must be taken into consideration on an individualized basis. All anesthetic agents decrease cerebrovascular resistance by causing dilation which increases ICP and CBV and decreases CMRO2.4 Inhalational agents decrease MAP, and increase ICP, reducing CPP.4 In addition, they may provide a neuroprotective 6 effect against ischemic insults by suppressing excitatory neurotransmission and potentiation of inhibitory activity. Hyperventilation can also lower ICP, although this effect is temporary and in some patients with malignant brain tumors this technique was found to increase ICP also.4 Dexmedetomidine, a selective alpha-2 agonist, has become a valid alternative for craniotomies by providing little respiratory depression and lack of impairment on electrophysiologic monitoring. It is more neuroprotective by reducing the number of delirium and ventilator days when likened to benzodiazepines. Compared to opioid induced sedation, dexmedetomidine preserves the hypercapnic arousal response which is a feature of natural sleep making it beneficial for a smooth wake up from a craniotomy procedure.5 Dexmedetomidine decreases the sedation level for volatile agents from 35% to 50%, but has an increased possibility for hypotension associated with a reduction of sympathetic outflow and increase in cardiac vagal activity.5 Upon review of this case, retrospectively, several aspects could have been handled differently. Doing a preoperative MRI rather than intraoperative MRI would have allowed monitoring during surgery to be continuous as well as providing a more suitable, uninterrupted environment for anesthesia care. MRI compatible monitoring should be available and part of the standard of care. Preoperative MRI would have provided a clear idea of what was causing the patient's symptoms and perhaps changed the operative plan. This case emphasizes the importance of planning, communication as a team and a thorough preoperative evaluation. 7 References 1. Hines, R.L. (2012) Stoelting's Anesthesia and Co-existing Disease (6th ed) (pp 225) Philadelphia, PA: Saunders Elsevier 2. Omuro A, DeAngelis LM. Glioblastoma and Other Malignant Gliomas: A Clinical Review. Journal of American Medical Association. November 2013, Vol 310, No. 17:1842-1850. 3. Ellor S, Pagano-Young T, Avgeropoulos N. Glioblastoma: Background, Standard Treatment Paradigms, and Supportive Care Considerations. Journal Of Law, Medicine & Ethics [serial online]. June 2014;42(2):171-182. Available from: CINAHL with Full Text, Ipswich, MA. Accessed August 8, 2014. 4. Nagelhout, J. & Plaus K. (2010) Nurse Anesthesia (4th ed) (pp 651-690) St. Louis MO: Saunders Elsevier 5. Barash P, Cullen B, Stoelting R, et al. Clinical Anesthesia (7th ed) (pp 392-393, 834) Philadelphia PA: Lippincott Williams & Wilkins Mentor: James Stimpson, CRNA, DNP jstimpson@westminstercollege.edu |
| Reference URL | https://collections.lib.utah.edu/ark:/87278/s60s2xjj |



