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Published on March 20, 2014

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© 2013 Neurocritical Care Society Practice Update PERIOPERATIVE NEUROSURGICAL CRITICAL CARE Chris Zacko Penn State Hershey Medical Center Department of Neurosurgery Hershey, Pennsylvania Peter LeRoux MD, FACSMain Line Healthcare MLHS and Spine Center Wynnewood, PA CLINICAL CASE A 73 year old male with poorly controlled diabetes, coronary artery disease with cardiac stents, atrial fibrillation (non-therapeutic on Coumadin), bilateral carotid stenosis, hypertension, hyperlipidemia, hypothyroidism and morbid obesity has just returned to your ICU after a decompressive craniectomy for malignant MCA infarction. He is on a ventilator and muscle relaxation was not reversed by the anesthesia team. His sodium is 132, blood pressure is 90/45, glucose is 245, and he lost 750 cc of blood during surgery. What post-operative challenges do you face when balancing this patient’s medical co-morbidities, fresh surgical wounds, and need for cerebral perfusion? OVERVIEW All patients who undergo neurosurgical procedures, even a well-performed operation, are in a potentially unstable cardiopulmonary state and at risk for secondary neuronal injury. Depending on the specific operation performed these patients can also have fresh surgical incisions, delicate vascular anastomoses, friable resection beds, brittle patency of newly open vessels, and/or tenuous hemostasis. All of these factors leave these patients especially vulnerable to post-operative complications. The object of postoperative neurosurgical care is to resuscitate, stabilize, prevent/minimize secondary neuronal damage, and to optimize functional central CNS recovery. Therefore, the basic goals of postoperative neurosurgical care are: Provide smooth emergence from anesthesia Optimize post-operative hemodynamic, volume, and electrolyte status, Optimize airway and respiratory status, Treat coagulopathic states and hemostatic disorders, Optimize management of post-operative complications, Have reliable and appropriate systemic and neuromonitoring tools Use subtle and reproducible neurological examination methods

© 2013 Neurocritical Care Society Practice Update These goals depend on many variables and important questions to ask and answer include: What was status (medical and neurological) of the patient before surgery? What neurological disease is being treated? What other neurological disorders does the patient have? What position was the patient in during surgery? What procedure was performed (procedure specific and expected complications)? What happened during surgery, e.g. blood loss, vascular injury? What anesthetic technique was used? To manage a postoperative neurosurgical patient the neurointensivist requires knowledge of how the CNS reacts to stress and anesthesia as well as the potential complications associated with each specific procedure. This chapter will focus on the following topics: 1) Who goes to and who stays in the NCCU 2) The effects of anesthetic agents on the CNS and neurosurgical patients 3) Basic complications after neurosurgical procedures 4) Emergence from anesthesia in neurosurgical patients 5) Extubation in neurosurgical patients 6) Post-operative pain 7) Postoperative nausea and vomiting 8) Basic post-operative neurosurgical care 9) Postoperative monitoring WHO GOES TO AND WHO STAYS IN THE NEUROCRITICAL CARE UNIT (NCCU)? Postoperative neurosurgical cases account for numerous NCCU admissions. Traditionally, patients who had craniotomies and other invasive neurosurgical procedures were nursed postoperatively and overnight in the NCCU as a precaution. This practice is changing somewhat as most NCCU’s also have well-developed “step-down” or intermediate care units that can often manage routine uncomplicated cases. Among those patients admitted to the NCCU primarily for precautionary/observational purposes, very few “patient days” are created. It is estimated that only ~15% actually require/receive active treatment. Furthermore, when a patient stay in the NCCU is <24h, ~50% require no interventions beyond post-anesthetic care and frequent neurologic exams. Lastly, two-thirds of these patients require no further interventions of any kind after the first 4 hrs. The decision to admit a given patient to the NCCU can be subjective and surgeon specific but is often based upon: age, co-morbidities, pre-operative condition, intra-operative details (difficult hemostasis, unexpected cerebral edema), and need for post-operative respiratory and hemodynamic support. That said, a patient's risk for prolonged ICU stay (>1 day) can be anticipated by: a) preoperative radiologic findings (e.g. tumor location, mass effect), b)

© 2013 Neurocritical Care Society Practice Update significant intraoperative blood loss, c) substantial intra-operative fluid requirements, and d) the decision to keep the patient intubated at the end of surgery [1]. EFFECT OF ANESTHETIC AGENTS ON THE CNS AND NEUROSURGICAL PATIENTS An important aspect of postoperative neurosurgical care is to distinguish residual effects of anesthetic agents (e.g. drowsiness or confusion) from signs that indicate intracranial pathology. While it often is believed that patients with neurological disease are prone to anesthetic effects, this is not universally true – particularly in those patients who are fully awake preoperatively. Confusion or dementia can undoubtedly be exacerbated by anesthetic agents. That said, some note this is a bit more unusual (but not unheard of) for focal deficits to be aggravated by anesthesia. Excessive benzodiazepine use can be an exception and in some situations are even felt to unmask deficits. As a general rule, however, any progressive or fluctuating deterioration should be assumed to be a complication from the operative procedure rather than an anesthetic effect. The effects of anesthetic agents are complex and can depend on the agent used. For example, increased reflexes and extensor plantar responses may be observed in 50-60% of patients who receive enflurane or ethrane, in <30% who receive halothane, and almost never with a nitrous- narcotic mix [2]. Anesthetic associated abnormalities should return to normal when the patient is fully awake. Non-depolarizing neuromuscular blockers may be associated with persistent weakness or opthalmoplegia (especially in patients with underlying neuromuscular disorders) but usually the rest of the exam is benign. However, opthalmoplegia should never be attributed to drugs alone. Occasionally anticonvulsant toxicity, particularly Dilantin, may cloud recovery although this is uncommon with typical therapeutic dosing. This can be considered if a patient received excessive loading doses of certain AED’s. It is beyond the scope of this review to address all anesthetic agents. In addition the ‘‘best’’ anesthetic regimen for neurosurgery still is debated. Anesthetics with a short context-sensitive half-time (i.e. the time required for the effect-site concentration of an IV drug to decrease by 50% at steady state), such as the opioids remifentanil and sufentanil, are suitable for anesthesia when early neurologic assessment is preferred. Several studies have compared in a randomized fashion different drug combinations, balanced anesthesia e.g. sevoflurane-fentanyl, total intravenous anesthesia (TIVA) or inhalational anesthesia to examine impact on recovery [3, 4]. The results are varied and anesthetic effects may depend more on the way an agent is used rather than the specific agent itself. BASIC COMPLICATIONS AFTER NEUROSURGICAL PROCEDURES Between 20-50% of neurosurgical patients may develop early postoperative complications and about 25% will have more than one complication [5,6]. Many of these complications are “minor”, the commonest being nausea/vomiting (30%), or shivering (18%). The incidence of other complications is difficult to determine and in part depends on the procedure as well as how the complications are classified. These include: respiratory (3%), airway trauma (4%), cardiovascular (7%), and neurological (6%). Respiratory impairment (PaO2<90 mm Hg or

© 2013 Neurocritical Care Society Practice Update PaCO2>45 mmHg) may occur in ~25% of patients usually within the first 30 to 60 minutes. About 1% of patients require re-intubation. Overall serious complications may occur in 10% of patients. In patients who undergo emergency surgery, or have a depressed preoperative level of consciousness (Glasgow Coma Scale ≤8), this risk is greater (>40%). Being aware of some common complications and associated management strategies is fundamental to the practice of neurocritical care. Craniotomies: Complications can be general or specific to the type of surgery. The most common complications are cerebral edema, seizures, vascular injury, and post-operative hemorrhage. General complications after craniotomy: a. Agitation and discomfort are common and now commonly treated quite successfully with dexmedetomidine. b. Cerebral Infarction: Can be due to arterial or venous injury. Venous occlusion and infarct can occur when a bleeding vein must be coagulated or when massive cerebral edema leads to a compressive occlusion of venous outflow. One should also be attentive to possible venous injuries after meningioma surgery located near venous sinuses (tentorial, parasagittal, convexity, and parafalcine). Arterial infarct can occur with either traumatic laceration or sacrifice of an artery for hemostasis. This can occur in TBI, glioma surgery with en passant vessels, and epilepsy surgery (i.e. anterior choroidal artery in temporal lobectomy). c. Seizures: particularly after penetrating TBI, epilepsy surgery, subdural empyema, and glial resection near motor cortex, but may occur in any patient post-operatively d. Pneumocephalus: air can be retained after craniotomy and act very much like mass lesions. Symptoms include lethargy, confusion, nausea/vomiting, and headache. Diagnosis is easily made with head CT. Once suspected one should actively investigate for the presence of tension pneumocephalus and CSF fistula as this will dictate management. Tension pneumocephalus can be urgent and is surgically evacuated. If there is a CSF leak, the leak should be managed in typical fashion before the pneumocephalus is addressed. Simple pneumocephalus can typically be managed expectedly as the air normally absorbs with time. Some advocate for the use of non-rebreathing mask with 100% oxygen for 24-48 hours. Brain sagging may be encountered as a related phenomenon – often seen after intraoperative over drainage of CSF (e.g. during aneurysm surgery). The clinical triad consists of pneumocephalus, midbrain crowding, and neurological symptom such as decreased mental status improving with reverse trendelenburg e. Postoperative hematomas: Approximately 2% of patients who undergo a cranial procedure will develop a postoperative hematoma (PICH) with 0.8% of patients developing a hemorrhage that requires surgical evacuation. The most common PICH presentations include: 60% present with a decreased level of consciousness (as a result PICH should be considered in all patients who do not recover or improve in the expected

© 2013 Neurocritical Care Society Practice Update manner after surgery). 33% of patients develop focal neurological deficits 90% will have elevated ICP (when ICP is being monitored). By contrast in the absence of a PICH, ICP is elevated in only 10% of post-operative patients. In most patients (50%) clinical deterioration associated with a postoperative hematoma occurs within 6 hours of surgery [7,8]. However, ~20% of PICH may develop after 24 hours. Those patients at particular risk for delayed hematomas are those who underwent posterior fossa surgery or emergency craniotomy. Once should consider longer periods of ICU observation in such cases. Risk factors for a PICH, particularly one that requires surgery include: meningioma surgery; intraoperative or immediate (12 hour) postoperative hypertension [9], intraoperative blood loss >500ml, age >70 years, hypoxia, coughing and hiccoughs, and laboratory signs of coagulopathy (high PT, low fibrinogen and platelet counts). Remote hemorrhages from the surgical site can also be problematic. Etiologies/risk factors include reperfusion hemorrhages, releasing the tamponade effect of a contralateral hemorrhage with debulking of a mass lesion, CSF drainage/hyperosmolar therapy causing shift of parenchyma (especially in cerebellum), and coagulopathic states (including patients with history of alcohol abuse). Reoperation: Reoperation is necessary in some patients. Removal of various types of hematomas is the most common surgical procedure at reoperation. Outcome is favorable in about half the patients indicating the importance of prevention. Factors associated with poor outcome include: histological type of the tumor, clinical state at admission, GCS score before urgent reoperation, time interval between primary surgery and urgent reoperation, and patient age [10]. Specific complications after craniotomy: Glioma: cerebral edema is more common after partial resection than with gross total resection. Epilepsy: hemiplegia can be seen if the anterior choroidal artery was injured. Word finding difficulties can be seen with injury to the left temporal lobe. Lastly, aseptic meningitis after depth electrode placement is a concern [11]. Pituitary and Transphenoidal Surgery: Complications to be aware of are diabetes insipidus (DI), neuroendocrine disorders from panhypopituitarism (adrenal insufficiency, central hypothyroid), CSF leaks, sinonasal injuries, hyponatremia, and alterations in visual function (acuity, fields, ocular movement). Posterior Fossa Surgery: air embolism is a classical, yet uncommon, complication of surgery in the seated position. It is typically diagnosed and managed in the operation room by flooding the filed with irrigation, applying bone wax to cut bone surfaces, lowering the head of bed, placing the patient in left lateral decubitus

© 2013 Neurocritical Care Society Practice Update position (if possible), aspirating air from the left atrium via CVP catheter, and achieving hemostasis as soon as possible. Another complication associated with posterior fossa surgery is accelerated hypertension. Any unexpected or refractory hypertension should warrant careful examination and a low threshold for imaging looking for post-operative hemorrhage. Other complications include obstructive hydrocephalus (if 4th ventricle compressed), upward herniation (via over drainage through and EVD when the 4th ventricle is compressed), cranial nerve injuries, and CSF leak and/or pseudomeningocele due to dependency of dural opening. Craniotomy for securing ruptured aneurysm: this will be covered in another chapter of this manual, but there are several strategies regarding the prevention and treatment of vasospasm. In general terms the patient should be kept euvolemic (please see appropriate chapter in this manual for a more complete discussion). Arteriovenous Malformation (AVM): these cases generally have especially tenuous and brittle hemostasis and very strict blood pressure control is crucial. In addition, liberal use of sedation to prevent coughing and straining against the ventilator may be critically important in the first few days after surgery. Seizures are also known to occur after AVM surgery as these patients often have pre-operative seizure disorders. Transient mutism can occur with bilateral retraction of the cingulate gyrus or division of the corpus callosum [12]. Carotid Endarterectomy (CEA) The need for ICU management after CEA is highly variable and is dependent on surgeon preference, anesthetic/surgical technique (local vs. general), pre-operative clinical presentation and the patient’s co-morbidities. Medical complications to be mindful of are: a) cardiac arrhythmias, b) myocardial ischemia (cardiac complications may be more common if the procedure done under general anesthesia), c) respiratory compromise (either from soft-tissue swelling after dissection or post-operative hematoma), d) seizures, e) hypertension (deranged sensitivity of carotid sinus baroreceptor reflex or injury to the Hering nerve, a branch of CN IX), and f) bradycardia (also from carotid baroreceptor injury). Surgical and neurologic complications include: a. Stroke: Etiologies: a) embolic from the endarterectomized surface, b) hemorrhagic from reperfusion injury (see below), or c) occlusive from re-stenosis of the ICA (most common cause of major stroke). If the stroke is noted directly after surgery, the patient is typically taken immediately back to surgery for exploration without further imaging. If the deficit is delayed, a workup is initiated and management options vary on the findings. Options include surgery, anticoagulation, augmentation of cerebral perfusion via blood pressure elevation, and observation with generous fluid administration and serial examinations/imaging. b. Post-operative hematoma: sources can be from venous bleeding in the operative bed or from disruption of arterial suture line. The latter is an emergent situation. If suspected, the surgeon and a dedicated team to manage the airway should

© 2013 Neurocritical Care Society Practice Update immediately be called. The patient is assessed for pulsatile swelling, tracheal deviation and respiratory distress. If there is any hint of respiratory compromise this is managed by OPENING THE WOUND THEN INTUBATION. If not already in the operating room, the patient can now go to the OR and definitive repair can be accomplished. c. Cranial nerve injury: cited by some as the most common complication after CEA with incidence of 8-10% [13]. Nerves at risk are the a) hypoglossal (tongue deviation, chewing swallowing deficits); b) vagus (hoarseness, diminished cough); c) glossopharyngeal nerve (dysphagia, nasal regurgitation, hypertension if Hering nerve damaged); d) spinal accessory nerve (drooping shoulder), e) recurrent laryngeal (unilateral vocal cord paralysis), great auricular nerve, and mandibular branch of the facial nerve (asymmetry of upper lip). These injuries are generally self-limited and recover in time. d. Hoarseness: more likely from laryngeal edema than injury to recurrent laryngeal nerve e. Reperfusion Injury: a relatively rare occurrence that is possibly more prevalent after re-opening of a high-grade stenosis in hypertensive patients – especially if there is contralateral carotid occlusion. This abrupt re-establishment of flow into an area that is postulated to have impaired autoregulation can lead to microhemorrhages and large ICH’s. Symptoms include altered mental status, ipsilateral eye pain or headache [14]. This has also been known to lead to seizures. Endovascular Interventions This is an area of tremendous advancement in recent years for the management of stroke and vascular neurosurgery. Many of the complications to be aware of are inherent to the disorder being treated and are discussed elsewhere. The complications specific to endovascular procedures will be discussed below and are grouped into vascular access site and neurologic complications. Vascular access site complications due to the thrombogenic effect of the catheters used in these procedures, as well as the thromboembolic potential inherent to the conditions being treated, anti-coagulation is used much more readily in endovascular cases vs. open procedures. This can predispose the patient to hemorrhagic complications. Complications seen at the groin puncture site include arteriovenous fistulas, local bleeding, pseudoaneurysm, and local nerve injury. The latter can be emergent and require immediate attention. Any hypotension in a patient having undergone an endovascular procedure should warrant careful inspection for signs of pseudoaneurysm. This includes checking distal pulses, assessing for pallor in the extremity, and feeling for a palpable pulsatile mass at the access site. Pseudoaneurysm can lead to distal ischemia in the leg and be limb-threatening. Confirmation of a pseudoaneurysm triggers application of prolonged pressure to the site and consultation of a vascular surgeon.

© 2013 Neurocritical Care Society Practice Update Neurologic Complications The development of focal cerebral edema has been noted after coiling of aneurysms and embolization of AVM’s. This is typically managed with dexamethasone. Intracranial hemorrhage can be seen after these procedures and management is discussed elsewhere. Common sources of ICH include intra-operative rupture of an aneurysm, perforation of a vessel, and reperfusion hemorrhage. More unique to endovascular procedures are possible thromboembolic and thrombo-occlusive complications. The catheters used for these procedures can physically disrupt atherosclerotic plaques causing emboli, create a dissection, or generate thrombus due to their inherent thrombogenicity. Other sources of emboli include microthrombotic shower after mechanical thrombectomy and glue emboli after embolization. These emboli are often not noted until the post-operative period. Once symptoms are suspected, urgent MRI/MRA is advised with concomitant initiation of generous fluid administration. After diagnostic imaging is complete, treatment options include additional endovascular therapy, anticoagulation, and/or hypertensive therapy via pressors. Other complications of these procedures include arterial dissection, acute thrombus and perforation. These complications are almost always noted during the procedure and management options consist of blood pressure control, anticoagulation, and generous fluid administration (depending on the problem encountered). For acute thrombus noted in the procedure, treatment options include intra-arterial thrombolysis, mechanical thrombectomy, and Reopro. Reopro is a potent glycoprotein IIb/IIIA inhibitor and has been found to be quite effective in managing thrombo-occlusive events during endovascular procedures. The implication to the neurointensivist is that due to Reopro’s effective anti-platelet activity one need to carefully monitor for bleeding complications. Other complications It is important to recognize what may happen during surgery to best manage the patient after surgery. Complications depend in part on position or the procedure. Some specific examples include: a. Ocular: Periorbital and/or conjunctival edema, as well as chemosis, tend to occur more often in the prone position, during pterional approaches, or with orbitozygomatic craniotomies. Posterior ischemic optic neuropathy or central retinal artery occlusion also may occur (particularly with longer procedures). A third nerve palsy or blindness may result from posterior communicating artery or carotid ophthalmic artery surgery. b. Use of a lumbar drain may cause intracranial hypotension or remote hemorrhage distant to the surgical site c. Anterior cervical surgery: Soft tissue swelling can cause airway obstruction or swallowing abnormalities

© 2013 Neurocritical Care Society Practice Update EMERGENCE FROM ANESTHESIA IN NEUROSURGICAL PATIENTS Recovery from anesthesia and surgery is a period of intense stress for patients. The effects can be systemic or CNS-specific. Systemic effects There are several physiological responses as a patient emerges from anesthesia, including: an increase in oxygen consumption (VO2), sympathetic activation with catecholamine release, increases in blood pressure and/or heart rate, alterations in arterial blood gases, and hyperglycemia. Shivering, pain, and regaining awareness are additional stress factors encountered in recovery from anesthesia. 1) Shivering occurs in approximately 40% of patients recovering from general anesthesia with a body temperature of <36.5o C and is associated with a 200–400% increase in VO2. Mild intraoperative hypothermia can increase norepinephrine or epinephrine release, which may extend into the early postoperative period. Forced-air skin-surface warming may reduce the incidence and intensity of shivering. Precedex has also been used with success. 2) Pain is another stress factor and appropriate analgesic therapy may blunt the increase in plasma catecholamines both during and after surgery. Most patients will experience moderate or severe pain in the first two days following major intracranial surgery [15]. 3) Hypertension is frequent in the early postoperative period after neurosurgery. If a >20% blood pressure increase is considered a reasonable threshold for treatment, then 40-90% of patients require antihypertensive therapy during emergence. Analgesics, and particularly narcotics, reduce the sympathetic and catecholamine response to pain and extubation. Patients with PICH are 3.6 times more likely to be hypertensive than their matched controls. In particular there is a very strong association between intracranial hemorrhage and patients being normotensive intra-operatively but hypertensive postoperatively [9]. Hypertension after posterior fossa surgery should raise suspicions for possible post-operative hemorrhage. Postoperative blood pressure generally is managed in the range of 120–150 mmHg systolic. Cerebral effects Stressful events, including surgery and emergence from anesthesia, can alter CBF and CMRO2. Sympathetic stimulation acting through beta-adrenoreceptors may play a role in these effects. 1) CBF: Transcranial Doppler (TCD) studies suggest that CBF velocities increase significantly during emergence from anesthesia. The maximum increase is at extubation (as much as 60% over preoperative value) and return to normal in about 60 minutes [16]. The CBF increase is independent of anesthetic technique, PaCO2, or arterial pressure. This increase in CBF can cause cerebral edema, hemorrhage, and postoperative confusion. Changes in CBF are

© 2013 Neurocritical Care Society Practice Update associated with deleterious oxygen consumption (VO2) so prevention of agitation, shivering and coughing is important. 2) ICP: Up to 20% of patients who undergo intracranial surgery may develop increased ICP and when it occurs half will develop clinical deterioration in large part from edema or hemorrhage [17]. There is limited data on the specific effects of emergence and extubation on ICP. Endotracheal suctioning has been shown to increase ICP [18]. Similarly, extubation can increase ICP – particularly when associated with coughing. The ICP increase usually lasts 2 or 3 minutes, but is longer when intracranial compliance is reduced. 3) Hyperemia and normal perfusion pressure breakthrough (NPPB): The cerebral arteriovenous oxygen content difference (AVDO2) often is depressed immediately after craniotomy. This is suggestive of transient cerebral hyperemia (16). Hyperemia may result in hemorrhage or severe edema in 3–12.5% of cases. An especially at-risk group is patients undergoing craniotomy for AVM resection. Features of AVM’s associated with a high-risk for postoperative hyperemic complications, including “normal perfusion pressure breakthrough”, are: a) large and deep AVMs, b) low feeding-artery pressures, c) multiple arterial inflows but only a single venous draining vessel, and d) intense steal around the AVM nidus. Strategies used in the management of these precarious include staged therapies (embolization and surgical), barbiturate based anesthetic continued into the postoperative period, extremely rigorous blood pressure control after surgery, and either invasive or non-invasive cardiovascular monitoring to optimize filling pressure and cardiac performance EXTUBATION IN NEUROSURGICAL PATIENTS The goal of anesthetic emergence and subsequent extubation is to maintain stable respiratory and cardiovascular parameters while preventing adverse CNS effects. One must be cautious as even the physical act of extubation can cause sympathetic discharge via tracheal and laryngeal stimulation (although it relieves the endotracheal tube stimulation itself). On one hand, a delayed emergence with deferred extubation in the ICU may achieve better thermal and cardiovascular stability after major neurosurgical procedures (thereby limiting secondary insults). On the other hand, the timely diagnosis of neurosurgical complications is required to limit CNS damage. The diagnosis of complications relies on rapid neurological examination after early awakening and an awake patient is the best and the cheapest neuromonitoring available. However many factors may contribute to delayed emergence including: 1) perioperative opiate analgesia and anxiolytics, 2) metabolic disturbances (electrolyte or acid- base), 3) comorbidity, especially hepatorenal dysfunction that affect drug clearance, 4) stroke, 5) pneumocephalus or CSF hypotension and 6) seizures. Before extubation, airway and swallowing functions should be carefully evaluated and everything should be ready for a possible reintubation. For successful extubation, the patient should be 1) awake, 2) fully reversed from neuromuscular relaxation and spontaneously breathing, 3) hemodynamically stable, and 4) normothermic (Table 1 and 2).

© 2013 Neurocritical Care Society Practice Update Rapid awakening and recovery The rationale for "rapid-awakening" after craniotomy with general anesthesia is that an early diagnosis of postoperative neurological complications can limit potentially devastating consequences. But extubation must be balanced by the patient’s perioperative neurological status and prognosis, surgical concerns, and respiratory status. After uncomplicated surgery, normothermic and normovolemic patients generally recover from anesthesia with minimal metabolic and hemodynamic changes. Thus, early recovery and extubation in the operating room is the preferred method when the preoperative state of consciousness is relatively normal. Delayed recovery In the complicated or unstable patient, the risks of early extubation may outweigh the benefits. Delayed recovery/extubation is appropriate after: long (> 6 hours) surgery, surgery for large tumors or AVM resection, major intraoperative bleeding, preoperative altered consciousness, severe cardiac or respiratory impairment, posterior fossa surgery where there is possible injury to lower cranial nerves, and select cervical procedures where re-intubation may be difficult. It is, however, often possible to perform a brief awakening of the patient without extubation to allow early neurological evaluation, followed by delayed emergence and extubation. Alternatively to extubation, an immediate postoperative CT may be obtained or ICP monitor placed. Weaning strategies and extubation failure Standard weaning criteria includes normal mental status, and so these criteria are not always appropriate for neurosurgery patients. To be ready for extubation, the neurosurgical patient should successfully complete a spontaneous breathing trial. The initial trial should last at least 30 minutes and consist of either T-tube breathing or low levels of pressure support (≤8cmH20). A simple ‘‘leak test’’ with cuff deflation may help to identify laryngeal edema. Further details are provided in the recent report of the Task Force on Weaning from Mechanical Ventilation by the 6th International Consensus Conference on Intensive Care Medicine (Table 3). The GCS and partial pressure of arterial oxygen/fraction of inspired oxygen ratio are factors that may predict extubation. For example the success of extubation is >75% when the GCS is ≥8 but ~33% when GCS is <8 [19]. Extubation failure is diagnosed after extubation if the patient develops one or more of the following: tachypnea (respiratory rate >25/min for 2 hours), clinical signs of muscle fatigue or increased work of breathing, oxygen desaturation (SaO2 < 90%, PaO2 < 80 on FIO2 >0.5), hypercapnia (PaCO2 >45 mmHg, or an increase by >20%), and acidosis (pH <7.33). POSTOPERATIVE PAIN Surgery and the associated tissue injury and inflammation are almost always associated with postoperative pain. Recent evidence indicates that post-craniotomy pain is reported as moderate to severe in up to 80% of patients and may persist for several days postoperatively

© 2013 Neurocritical Care Society Practice Update [15]. Pain however often is underestimated and undertreated in neurosurgery patients. There are several reasons for this: 1) the patient may not be able to communicate because of aphasia, altered mental status, or cognitive impairment, 2) the side-effects of analgesic drugs are feared, 3) there is no consensus regarding the choice of the ‘‘best’’ anesthetic regimen for intracranial surgery, 4) there is a lack of standardized, proactive protocols to assess and evaluate post- craniotomy pain and pain therapy, and 5) few studies have examined this question or validated the benefits of post-operative pain control on outcomes and patient satisfaction. Management of post neurosurgery pain Analgesia needs will depend in part on the procedure. For example where there is extensive muscle dissection (suboccipital approach, thoracolumbar spine surgery) more analgesia will be required than procedures where there is little muscle dissection (anterior cervical discectomy and fusion (ACDF) or frontal craniotomy). Basic postoperative analgesia consists of opiates, non-steroidal inflammatory medicines, and acetaminophen-based preparations. Opioids are the mainstay of analgesia. All opioids blunt the respiratory response to hypercarbia and so there are concerns that opioid-induced carbon dioxide retention will trigger increases in cerebral blood volume with subsequent aggravation of cerebral edema and intracranial hypertension. In addition there are concerns that opioids may cause excessive sedation, miosis, and/or interfere with recovery from anesthesia and postoperative neurological assessment. For this reason codeine phosphate has traditionally been the most commonly used analgesic post-craniotomy [20]. However, there may be better choices. When properly titrated, morphine can be more efficacious and does not increase adverse side effects as compared with codeine [21,22]. Furthermore, codeine is an unpredictable pro-drug and most of its analgesic efficacy is derived from the 5–15% that is metabolized to morphine by hepatic CYP2D6. Inter- individual and ethnic differences in CYP2D6 can influence codeine’s efficacy e.g., because of genetic variation 15% of Caucasians do not experience any effect from codeine [23]. Consequently, morphine or fentanyl is recommended after surgery. With proper use, the benefits of analgesia (e.g. blood pressure control) outweigh the risks. The non-narcotics ketoprofen, tramadol, gabapentin, and acetaminophen-based agents (such as Fioricet) may be useful as supplemental, opioid-sparing drugs. Pain control is reviewed by Nemergut et al [24]. POST-OPERATIVE NAUSEA AND VOMITING (PONV) Postoperative nausea and vomiting are less common now that propofol is widely used an induction agent. However PONV remains a common complication after neurosurgical procedures. The incidence is uncertain since study design may influence the outcome and few studies have looked specifically at neurosurgery PONV. Nevertheless PONV may complicate between 30-70% of neurosurgical procedures [25]. While nausea is a source of patient discomfort, PONV can cause major complications in post-operative patients – particularly those undergoing craniotomy. Vomiting can lead to aspiration (particularly with a compromised swallowing reflex and impaired consciousness), electrolyte disturbances, ICP increases, and intracranial bleeding. During the pre-ejection phase of the vomiting reflex there is sympathetic stimulation. This can complicate control of blood pressure postoperatively. Furthermore, during

© 2013 Neurocritical Care Society Practice Update the ejection phase increased intra-abdominal (>100 mmHg) and intra-thoracic pressures directly translates into elevated ICP [26]. General risk factors for PONV include: 1) female gender, 2) previous PONV or motion sickness, 3) non-smoker, 4) duration of surgery >60 minutes, and 5) early post-operative opioids [26]. Specific neurosurgical risk factors include: 1) surgery location (i.e., infratentorial surgery near the area postrema at the floor of the fourth ventricle), 2) CSF cisternal space opened (chemical meningitis), 3) awake procedure vs. general anesthesia, 4) intraoperative CSF leak and subsequent pneumocephalus, 5) use of a fat graft for a CSF leak, and 6) a lumbar intrathecal catheter and intracranial hypotension [27]. Management of PONV Various pharmaceutical agents can be used to manage PONV. Serotonin (5HT3) antagonists, such as ondansetron, are effective but expensive. Trimethobenzamide is another popular choice and is thought to inhibit the chemoreceptor trigger zone. Cyclizine is a cheap antihistamine commonly prescribed whenever opiates are given. Alternatives include dopamine antagonists, e.g. metoclopramide or droperidol. Steroids also work but there may be a ceiling effect (5-8mg). There are synergistic effects of dexamethasone and ondansetron. Intravenous ondansetron administration (4mg) at the time of dural closure can help reduce the incidence of PONV and the use of “rescue” antiemetics. Neufeld et al [25] preformed a recent meta-analysis of 7 prospective, randomized, placebo-controlled trials that together included 448 patients and found that ondansetron only had a significant impact on vomiting. BASIC POSTOPERATIVE NEUROSURGICAL CARE Basic postoperative neurosurgical management is centered on the ABCs of care: 1) Maintain a secure airway, 2) Adequate respiration to maintain oxygen saturation, 3) Hemodynamic stability and fluid management. “Normo-homeostasis” may be regarded as neuroprotective [28]. Other aspects of postoperative neurosurgical care (seizure control, prevention and management of infection, venous thromboembolism, ventriculostomy care) are beyond the scope of this review but clearly are fundamental to critical care. The typical postoperative patient probably does not require gastrointestinal prophylaxis unless they are on steroids or remain mechanically ventilated. Respiratory care Adequate oxygenation and ventilation are required to balance oxygen delivery to the brain, cerebral blood flow, cerebral perfusion pressure, and ICP. The Brain Trauma Foundation recommends maintaining PaO2 >60 mmHg and oxygen saturation >90% for traumatic brain injury (TBI) patients (BTF). These are sensible goals that have carried over into postoperative neurosurgical care of all patients. The following respiratory complications may be observed:

© 2013 Neurocritical Care Society Practice Update Airways obstruction: This may be caused by many factors e.g. laryngospasm, soft tissue swelling around the pharynx (especially children) or laryngeal or glottic edema (anterior cervical surgery, carotid endarterectomy), foreign bodies (loose teeth), hypotonia of pharyngeal muscles from the remaining anesthetic, and viscous fluids (blood after transphenoidal surgery). In all patients who develop airway obstruction, a patent airway must be achieved immediately (head tilt chin lift, airway adjuncts, or intubation). The signs of airway obstruction include stridor, tachypnea, tracheal tug (downward displacement of the trachea during inspiration), use of accessory muscles, Intercostal and supraclavicular muscle recession, and reduced oxygen saturation (late signs) Hypoventilation A reduced ventilatory capacity can be caused by a depressed neurogenic respiratory drive and neuromuscular disorders. Etiologies include opioid drugs, hypothermia, metabolic alkalosis secondary to intermittent positive pressure ventilation, or by mechanical difficulty in breathing. Impaired chest expansion may result from parenchymal lung disease (e.g. obstructive airways disease secondary to smoking), muscle weakness (e.g. electrolyte derangement, neuromuscular disorders), hindered diaphragm movement (pain, obesity), and the residual effect of paralyzing agents on the chest wall musculature. Hypoxemia The principal causes of hypoxemia include: 1) a reduced FiO2, 2) hypoventilation associated with a depressed consciousness or airway obstruction and 3) ventilation/perfusion mismatch (e.g. lung collapse, pneumonia, atelectasis, bronchospasm, pulmonary edema, pneumothorax, pulmonary embolism). Thoracic and abdominal surgery often may alter the chest expansibility, and contribute to decreased oxygen saturation. This cause is less frequent after neurosurgery (unless a thoracotomy was performed for thoracic disc or anterior decompression). Neurogenic pulmonary edema (NPE) NPE is a potential complication of CNS insults such as intracranial hemorrhage, SAH, uncontrolled generalized seizures, TBI, and tumors. The postulated cause is sympathetic discharge. The treatment is mainly supportive (mechanical ventilation possibly limiting PEEP, alpha-adrenergic blocking agents while managing ICP). Who should be ventilated? Intubation and mechanical ventilation is indicated in neurosurgical patients in the following conditions: inability to protect the airway or manage secretions; need to reduce ICP by ventilation control; PaO2 <60 mmHg despite supplemental O2; PaCO2 >50 mmHg, or pH <7.2; respiratory rate >40/minute or <10/minute; muscle fatigue; airway compromise; and hemodynamic instability. Orotracheal intubation with rapid sequence induction is the preferred technique. Nasotracheal intubation should be avoided particularly when there is a basilar skull fracture or skull base surgery. Maintenance of normocapnia is the major goal of ventilation therapy in neurosurgical patients. Whereas hypocapnia, achieved

© 2013 Neurocritical Care Society Practice Update through short periods of hyperventilation, is a potent cerebral vasoconstrictor (and can reduce ICP) it can exacerbate brain ischemia in patients with brain injury. Hyperventilation also decreases venous return, cardiac output, and PVO2 and may increase V/Q mismatch. Mechanical ventilation goals have changed from achieving normal blood gases to reducing the risks of ventilator-induced lung injury i.e. lung-protective ventilation strategy [29]. Positive- pressure ventilation with a tidal volume of 6 ml/kg (or less) of an ideal body weight is used to maintain a plateau pressure <30 cmH2O. Positive end-expiratory pressure (PEEP) is adjusted to keep FiO2 <0.6 to prevent oxygen toxicity, with an oxygenation goal of PaO2 >60 mmHg or SaO2 >90%. The risks and benefits of lung-protective ventilation in neurosurgical patients are unclear. One must be aware that lung-protective ventilation may lead to permissive hypercapnia that can be problematic in patients with elevated or borderline ICP. In addition, variable clinical responses to PEEP may occur in neurosurgical patients secondary to PEEP’s effect on hemodynamic and respiratory variables. High levels of PEEP may decrease CPP due to decreases in cardiac output and increases in ICP [30]. Fortunately, the influence of PEEP on ICP is less prominent in patients with stiff lungs (e.g., acute lung injury/ARDS) as they may be the patients who most need PEEP. PEEP should be applied carefully in patients with increased ICP, and ICP should be monitored simultaneously. Cardiovascular management Cardiovascular disturbances (e.g. hypotension, hypertension, dysrhythmias and myocardial failure) are common in patients who undergo neurosurgery. They occur as consequences of medical or surgical therapy, central neurogenic effects on the heart and the autonomic system, or from concurrently associated medical conditions that interact with CNS pathology. One challenge commonly encountered in the NCCU is balancing the risks/benefits of anti- platelet/anticoagulant agents used in acute coronary syndrome against the risk of post- operative hemorrhage. Each case needs to be carefully evaluated before a treatment strategy is initiated. Potential iatrogenic induced cardiovascular problems include: diuretic and steroid- induced hypovolemia and hypokalemia-induced ventricular irritation, bradycardia with low cardiac output caused by surgical stimulation of the vagal nucleus in the brainstem, and a Cushing’s-like response with poor venting of ventricular perfusate during endoscopic third ventriculostomy. Prone and seated positions are associated with low cardiac output, venous return and blood pressure. Blood pressure control Changes in blood pressure are common postoperative complications. Many times the surgeon will have specific BP parameters depending on where the goal is to prevent hematomas or preserve perfusion.

© 2013 Neurocritical Care Society Practice Update Hypotension Fluid loss from the intravascular space (bleeding) and extravascular space (e.g. vomiting, diarrhea, and sweating) can contribute to hypovolemia (Table 5). This may exacerbate cerebral ischemia. Fluid therapy is discussed below. Circulation support to influence CBF is achieved best by increasing blood pressure, as cardiac output appears not to vary with CBF. The drug of choice to increase blood pressure is phenylephrine. With active baroreflexes, bradycardia may occur. Careful anticholinergic administration then is necessary to augment the sympathomimetic hypertensive action. Patients with low myocardial reserve may require an inotrope, such as dopamine or epinephrine. Hypertension Increased blood pressure may be associated with pain, emergence from anesthesia, and the underlying disease which can lead to postoperative hemorrhage and exacerbate edema. Acute hypertension is associated with increased mortality in the NCCU (9). The precise level that represents a risk varies and depends on patient, disease, procedure, lesion size, traumatic disruption of vessels, and premorbid blood pressure. Strategies to limit commons irritants or triggers of hypertension include prevention and timely treatment of bladder distention, pain and shivering. Since sympathetic stimulation is responsible for the blood pressure increase, beta-blocker infusions are largely used. Esmolol and labetalol are effective agents since they have no significant effect on ICP. Cardene is a calcium-channel blocker that is used frequently with good success. Nitroglycerin, and sodium nitroprusside are cerebral vasodilators and these agents may increase cerebral blood volume. The specific agent used will depend on several factors including the perceived integrity of autoregulation and management strategy being employed for a given patient (i.e. Lund vs. Rosner theories regarding the relationship between ICP and MAP). In patients with severe hypertension post operatively, the elevated blood pressure also should considered to be a sign of intracranial pathology. This is particularly important after posterior fossa surgery. Lastly, one should always carefully consider a patient’s home medication regimen and be mindful of complications from that regimen being altered in the perioperative period (such as rebound phenomena from beta blocker withdrawal). Fluid status Osmolality is the primary determinant of water movement across the intact blood–brain barrier. Reduced serum osmolality can increase cerebral edema and ICP. The goals of fluid management after neurosurgery are: 1) maintain intravascular volume, 2) preserve CPP, and 3) minimize cerebral edema. In neurosurgical patients, and often in the postoperative period, intravascular volume is depleted (e.g. diuretic use, osmotherapy, or long spinal surgeries where large volume losses may be encountered). Systemic hypotension (MAP <70 mmHg) and negative fluid balance (<594 ml) independently aggravate outcome in TBI patients [31]. Basic fluid and electrolyte requirements must be considered in the postoperative period. In clinical practice, fluid management requires circulating blood volume assessment (Table 5). A patient generally is asymptomatic until the circulating volume has decreased by at least 10%. A

© 2013 Neurocritical Care Society Practice Update persistently low urine output (<0.5 ml/kg/hour) may indicate inadequate fluid replacement and thirst often is the first sign of reduced intravascular volume even though other vital signs are in the normal range. However when diuretics or mannitol are given, urinary output can be misleading. Lastly, thirst is not present if the patient is drowsy or sedated. New technologies have also become quite helpful in hemodynamic assessment, volume management, and the institution of more specific goal-directed therapy in ICU patients. One is arterial pulse contour wave analyses which require invasive arterial lines to obtain data. There are several manufacturers who make analogous equipment taking advantage of arterial pulse pressure (PP) waveform analysis to provide continuous assessments of volume status and cardiac hemodynamics. There is more than one methodological strategy employed to derive such parameters including: a) calibrated PP analysis relying on thermodilution for calibration (PiCCO®) and b) statistical analysis via computer-derived algorithms (Vigileo®). One of the more common variables assessed is stroke volume variation (SVV) which is used to optimize volume status in ICU patients such as those with subarachnoid hemorrhage. Non-invasive technologies also exist that assist in fluid management and hemodynamic monitoring. These include impedance cardiography (ICG) and a device that relies on bioreactivity and detecting phase shifts that occur when an alternating current is passed through the thorax (Cheetah NICOM®). Lastly, critical care ultrasound techniques such as IVC compressibility are also used to assess volume status. All of these technologies are crucial to the increasingly adopted goal-directed therapy with more restrictive use of crystalloid administration (unless contraindicated) in the perioperative period. Fluid therapy Complications can result from inadequate or excessive volume replacement. Inadequate volume can cause hypotension, perfusion deficits, and acute kidney injury. Excess fluid therapy can exacerbate heart failure, pulmonary function or cerebral edema. There are few human data about the impact of fluids on the brain that can guide rational fluid management in neurosurgical patients. The optimal fluid to prevent secondary brain damage after neurological insult also is unknown. Fluid administration that reduces osmolality should be avoided. Small volumes of lactated Ringer’s (1–3L) are unlikely to be detrimental and may be used. When larger volumes are needed a more isotonic fluid e.g. normal saline (0.9% NS) is preferred. Rapid NS infusion may cause a dose-dependent hyperchloremic metabolic acidosis (normal anion gap). When large volumes are needed, a combination of isotonic crystalloids and colloids should be considered. However Hetastarch and Dextran should be avoided since coagulation disorders, platelet dysfunction, and kidney injury may occur. While hypertonic saline is gaining popularity for treatment of intracranial hypertension it is not recommended for fluid resuscitation or volume replacement. One advantage HTS seems to have over mannitol in treating ICP is its ability to move fluid from the body's own extravascular space into the circulation across a sodium gradient without necessarily risking hypotension from diuresis [32]. Hyperglycemia is an independent predictor of poor outcomes, and so it is reasonable to avoid glucose-containing fluids.

© 2013 Neurocritical Care Society Practice Update Sodium balance: Sodium homeostasis is critical in neurosurgical patients. Disorders of sodium metabolism including diabetes insipidus, syndrome of inappropriate ADH secretion (SIADH) and cerebral salt wasting syndrome need to be diagnosed and treated. This important topic is discussed in a separate chapter of this manuscript. POSTOPERATIVE MONITORING Systemic and neuromonitoring are essential after neurosurgery to help identify patients who may deteriorate. However relatively few studies describe how postoperative monitoring influences outcome. Therefore, in most patients decisions about monitoring should be based on the patient’s presentation, the surgical procedure, and clinical judgment. The most important monitor after elective neurosurgical procedures is the repeated clinical examination. Neurological evaluation Postoperative neurological evaluation is focused on two characteristics - consciousness and focal neurologic findings. The procedure may determine the specific focal finding to concentrate upon. For example, assess for foot drop after an L4/5 discectomy. Objective scoring instruments are useful since they can limit inter - and intra-observer variability and objectify some examination findings making communication among practitioners easier. That said nothing replaces a detailed neurologic examination for detecting subtle changes in neurologic function. Common instruments include: the Glasgow Coma Score, Full Outline of UnResponsiveness (FOUR score), Reaction Level Score, and NIH Stroke Scale. Systemic Hypoxia and hypotension are the two most important systemic secondary insults in TBI patients, and it is reasonable to presume this also is true for postoperative neurosurgical patients. Therefore, oxygen saturation by pulse oximetry and blood pressure should be continuously monitored. Continuous EKG also should be considered (e.g. severe arrhythmias may occur after SAH). Other cardiovascular monitors (e.g. pulmonary artery catheters, invasive pulse pressure contour monitors, non-invasive impedance cardiography ) may be necessary for patients with pre-existing cardiac disease, neurogenic pulmonary edema, SAH with “stunned pericardium”, or Takatsubo’s cardiomyopathy. The arterial partial pressure of CO2 (PaCO2) is an important determinant of CBF. A PaCO2 change can be determined by blood gas analysis or estimated from end-tidal CO2 (ETCO2). There, however, is debate about ETCO2 reliability in neurosurgical patients. Intracranial Pressure The incidence of elevated ICP after neurosurgical procedures has had little study and most likely is underestimated. In addition, the impact of elevated ICP on outcome after neurosurgery has not been examined despite management of cerebral edema and elevated ICP being critical components of perioperative craniotomy care. Postoperatively elevated ICP can be expected in

© 2013 Neurocritical Care Society Practice Update about 15% of patients. An ICP monitor should be considered in the following circumstances: large vascular tumors, severe edema, trauma surgery, deeply sedated patients where an exam cannot be obtained (or a patient fails to wake up), known operative complications (e.g. aneurysm rupture, known vessel occlusion), and large fluid shifts are expected. Other monitors For most patients the extent of specialized neuromonitoring should be based on the clinical presentation and the experience of the responsible physician. This includes 1) bedside CBF assessment (e.g. jugular bulb oximetry, Transcranial Doppler sonography [TCD] Thermal diffusion flowmetry, Near infrared spectroscopy [NIRS]), 2) Microdialysis and brain tissue oxygen tension (PbtO2) and 3) Electroencephalography (cEEG). Imaging Imaging is a snap-shot in time. CT investigations in critically ill neurosurgical patients are useful to monitor the course of the illness and for the early detection of complications and should be considered when neurological deterioration occurs or the expected postoperative improvement does not occur. When early detection of ischemia is necessary MRI is superior to CT since diffusion weighted imaging (DWI) can recognize ischemic injury within 30-60 minutes of onset. In addition, CT-angiograms and CT-perfusion scans are rapidly improving technologies that are broadening diagnostic imaging options for practitioners. There is a well-documented risk of transporting patients to scanners and portable CT scanners are becoming increasingly adopted in NCCU’s. Surgical drains Many procedures require use of post-operative drains. This can entail hemovacs or JP drains left after craniotomy or lumbar drains left after spinal surgeries where there is a concern for CSF fistula formation. The neurointensivist should always communicate clearly with the surgical team to fully understand what compartment the drain was left in (subgaleal, epidural, subdural). This is crucial to evaluating both the quality (blood, CSF) and quantity of drain output. It is advisable to never remove a post-operative drain until you have specifically discussed its purpose with the surgeon. CONCLUSION Following a neurosurgical procedure, the patient remains vulnerable to secondary CNS injury because of the pathological changes associated with the disease, the nuances of the procedure itself, and the physiological changes associated with management. The level of care after surgery should be no less than that given during the procedure. Whereas the surgeon may influence patient's anatomy, it is the neurointensivist role in collaboration with the neurosurgeon to ensure the patient's physiological stability and to navigate the transition from pre- and intra-operative care through recovery and return to the ward.

© 2013 Neurocritical Care Society Practice Update REFERENCES 1. Ziai WC, Varelas PN, Zeger SL, Mirski MA, Ulatowski JA. Neurologic intensive care resource use after brain tumor surgery: an analysis of indications and alternative strategies. Crit Care Med. 2003 Dec;31(12):2782-7. 2. Rosenberg H, Clofine R, Bialik O. Neurologic changes during awakening from anesthesia. Anesthesiology. 1981 Feb;54(2):125-30. 3. Frost EA, Booij LH. Anesthesia in the patient for awake craniotomy. Curr Opin Anaesthesiol. 2007;20:331-335. 4. Dinsmore J. Anaesthesia for elective neurosurgery. British Journal of Anaesthesia 2007; 99: 68–74. 5. Magni G, La Rosa I, Gimignani S, Melillo G, Imperiale C, Rosa G. Early postoperative complications after intracranial surgery: comparison between total intravenous and balanced anesthesia. J Neurosurg Anesthesiol. 2007 Oct;19(4):229-34. 6. Manninen PH, Raman SK, Boyle K, el-Beheiry H. Early postoperative complications following neurosurgical procedures. Can J Anaesth. 1999 Jan;46(1):7-14. 7. Zetterling M, Ronne-Engström E. High intraoperative blood loss may be a risk factor for postoperative hematoma. J Neurosurg Anesthesiol. 2004 Apr;16(2):151-5. 8. Taylor WA, Thomas NW, Wellings JA, Bell BA. Timing of postoperative intracranial hematoma development and implications for the best use of neurosurgical intensive care. J Neurosurg. 1995 Jan;82(1):48-50. 9. Basali A, Mascha EJ, Kalfas I, Schubert A. Relation between perioperative hypertension and intracranial hemorrhage after craniotomy. Anesthesiology 2000; 93: 48–54. 10. Chernov MF, Ivanov PI. Urgent reoperation for major regional complications after removal of intracranial tumors: outcome and prognostic factors in 100 consecutive cases. Neurol Med Chir (Tokyo). 2007 Jun;47(6):243-8 11. Widjicks E, The Practice of Emergency and Critical Care Neurology (2010), Chapter 42 Complications of Craniotomy and Biopsy, pgs. 629-641. Oxford University Press, Inc. New York, New York. 12. Rhoton AL, Yamamoto I, Pearce DA: Microsurgery of the third ventricle: Part I. Neurosurgery 1981 8: 334-56 13. Sajid MS, Vijaynagar B, Singh P, et al. Literature review of cranial nerve injuries during carotid endarterectomy. Acta Chir Belg 107 (1): Acta Chir Belg (2007): 25-8 14. Dolan JG, Mushlin AI. Hypertension, vascular headaches, and seizures after carotid endarterectomy. Arch Intern Med (1984) 144: 1489-91. 15. Gottschalk A, Yaster M. Pain management after craniotomy. Neurosurg Q. 2007;17:64-73. 16. Bruder N, Pellissier D, Grillot P & Gouin F. Cerebral hyperemia during recovery from general anesthesia in neurosurgical patients. Anesthesia and Analgesia 2002; 94: 650–654. 17. Constantini S, Cotev S, Rappaport Z et al. Intracranial pressure monitoring after elective intracranial surgery. A retrospective study of 514 consecutive patients. Journal of Neurosurgery 1988; 69: 540–544. 18. Gemma M, Tommasino C, Cerri M et al. Intracranial effects of endotracheal suctioning in the acute phase of head injury. Journal of Neurosurgical Anesthesiology 2002; 14: 50–54.

© 2013 Neurocritical Care Society Practice Update 19. Namen AM, Ely EW, Tatter SB, Case LD, Lucia MA, Smith A, Landry S, Wilson JA, Glazier SS, Branch CL, Kelly DL, Bowton DL, Haponik EF. Predictors of successful extubation in neurosurgical patients. Am J Respir Crit Care Med. 2001 Mar;163(3 Pt 1):658-64. 20. Roberts GC. Post-craniotomy analgesia: current practices in British neurosurgical centres--a survey of post-craniotomy analgesic practices. Eur J Anaesthesiol. 2005 May;22(5):328-32. 21. Stoneham MD, Cooper R, Quiney NF & Walters FJ. Pain following craniotomy: a preliminary study comparing PCA morphine with intramuscular codeine phosphate. Anaesthesia 1996; 51: 1176–1178. 22. Goldsack C, Scuplak SM & Smith M. A double-blind comparison of codeine and morphine for postoperative analgesia following intracranial surgery. Anaesthesia 1996; 51: 1029–1032. 23. Williams DG, Patel A & Howard RF. Pharmacogenetics of codeine metabolism in an urban population of children and its implications for analgesic reliability. British Journal of Anaesthesia 2002; 89: 839–845. 24. Nemergut EC, Durieux ME, Missaghi NB, Himmelseher S. Pain management after craniotomy. Best Pract Res Clin Anaesthesiol. 2007 Dec;21(4):557-73. 25. Neufeld SM, Newburn-Cook CV. The efficacy of 5-HT3 receptor antagonists for the prevention of postoperative nausea and vomiting after craniotomy: a meta-analysis. J Neurosurg Anesthesiol. 2007;19:10-17. 26. Andrews PLR. Physiology of nausea and vomiting. British Journal of Anaesthesia 1992; 69(Suppl 1): 2–19. 27. Apfel CC, Laara E, Koivuranta M et al. A simplified risk score for predicting postoperative nausea and vomiting. Anesthesiology 1999; 91: 693–700. 28. Fukuda S, Warner DS. Cerebral protection. Br J Anaesth. 2007;99:10-17. 29. Lowe GJ, Ferguson ND. Lung-protective ventilation in neurosurgical patients. Current Opinion in Critical Care 2006 Feb; 12(1): 3–7. 30. Muench E, Bauhuf C, Roth H et al. Effects of positive end-expiratory pressure on regional cerebral blood flow, intracranial pressure, and brain tissue oxygenation. Critical Care Medicine 2005 Oct; 33(10): 2367–2372. 31. Clifton GL, Miller ER, Choi SC et al. Fluid thresholds and outcome from severe brain injury. Critical Care Medicine 2002; 30: 739–745. 32. Ogden AT, Mayer SA, Connolly ES Jr. Hyperosmolar agents in neurosurgical practice: the evolving role of hypertonic saline. Neurosurgery. 2005 Aug;57(2):207-15; discussion 207-15.

© 2013 Neurocritical Care Society Practice Update Table 1. Systemic and brain conditions necessary for rapid postoperative awakening and extubation after a neurosurgical procedure Brain Conditions Systemic Conditions Normal pre-operative level of consciousness Normothermia (~36o C) Surgery < 6 hours Normovolemia, normotension (70 mmHg < MAP< 120 mmHg) No major CNS or vascular injury Spontaneous ventilation and PaCO2 <50 mmHg No brain swelling Normoglycemia (glucose 4-8 mmolL) Antiepileptic prophylaxis when indicated Normosmolality (>280 mOsm/kg) Intact lower cranial nerves (IX,X,XII) - airway protection Hemoglobin ~9g/dl Normal coagulation status No major swelling of face and tongue Table 2. Checklist before extubation of a neurosurgical patient. Discuss expected postoperative course and potential complications and agree with the neurosurgeon about postoperative management Check antiepileptic prophylaxis Infuse analgesics before the end of anesthesia Check respiratory and cardiovascular parameters Check adequate recovery of muscle strength if muscle relaxants were used Check pupil size and awareness Prepare IV antihypertensive agents for blood pressure control Check adequate spontaneous ventilation with end-tidal CO2 < 50 mmHg Check the vacuum system Be prepared to give supplemental oxygen after extubation Assess adequate recovery of neurologic function

© 2013 Neurocritical Care Society Practice Update Table 3. Factors associated with readiness to wean ventilator support in neurosurgical patients. Clinical assessment Adequate cough Absence of excessive tracheobronchial secretions Resolution of disease acute phase for which the patient was intubated; Normal intracranial pressure (ICP) Objective measurements Clinical stability o Stable cardiovascular status (i.e. heart rate ≤140beats/min; systolic BP 90-160 mmHg, no or minimal vasopressors) o Stable metabolic status Adequate oxygenation o SaO2 > 90% on FIO2 ≤0.4 (or PaO2/FIO2 ≥150 mmHg) o PEEP ≤8mmHg Adequate pulmonary function o Respiratory rate ≤35 breathes/minute o Maximal inspiratory pressure ≤ -20 to -25 cm H2O o VT >5 mL/kg o VC >10 mL/kg o Rapid shallow breathing index <105 breaths/min/L o No significant respiratory acidosis Abbreviations: BP = blood pressure; FIO2 = inspiratory oxygen fraction; PaO2 = arterial oxygen tension; PEEP = positive end-expiratory pressure; SaO2 = arterial oxygen saturation; Rapid shallow breathing index = respiratory rate/VT; VT = tid

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