Key points

Introduction

Sudden neurologic worsening in the neurosurgical patient is a complex topic due to the considerable diversity of procedures requiring postoperative intensive care unit (ICU) admission. Interventions may include open cranial procedures, endovascular procedures, and spine surgeries. The following discussion—framed by 4 clinical scenarios—will highlight some of the common pathologies to anticipate in the critical care management of postoperative neurosurgical patients. While these scenarios are not exclusive to patients with neurotrauma, they illustrate the importance of engaging in a systematic process for assessment that is applicable to any surgical patient with neurocritical illness.

Clinical scenario

Evaluating a patient with acute postoperative neurologic worsening

Each neurosurgical procedure offers a unique profile for potential complications. Every time the calvarium is opened, the potential exists to develop an epidural hematoma. Opening the dura may lead to the accumulation of blood within the subdural space and/or pneumocephalus. Manipulation of brain tissue creates the potential for intraparenchymal hematoma and seizures. With vessel manipulation, vasospasm, stroke, and acute bleeding may follow. Discerning the etiology of an acute neurologic examination change after a spinal surgery is predicated on the type of operation as well as perioperative and postoperative management. The differential diagnosis for acute neurologic worsening in a postoperative patient can be narrowed based on symptoms, key elements related to the operation, and patient history.

The journey to a diagnosis starts at the bedside, with the patient; a thorough neurologic examination is important to elucidate the etiology of an examination change and the appropriate steps for management.

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  Level of consciousness. Is the patient lethargic, or alert with a focal deficit? Whereas somnolence suggests a more global or brainstem-level structural process such as elevated ICP, a more focal finding may localize to the cranium or spine.

  
  
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  Forced gaze, aphasia, twitching/tremoring of face/extremities. Note any epileptiform activity, focal or generalized, and any evolution of symptoms. Determine whether depressed consciousness or focal weakness (eg, Todd’s paralysis) was preceded by seizure-like activity.

  
  
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  Pupillary abnormalities. Anisocoria of up to 1 mm is physiologic in up to 20% of the population and is accompanied by preserved accommodation and pupillary light reflex, ^, whereas a unilateral “blown pupil” (eg, fixed and dilated) may portend more ominous pathology such as herniation. Note that dilated, nonreactive pupils may be seen with hypoxia, seizures, or as a medication side effect. ^,

  
  
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  Speech deficits. Aphasia could suggest seizure, stroke, or a perfusion deficit.

  
  
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  Isolated cranial nerve deficits. These tend to suggest brainstem pathology but may be caused by lesions causing mass effect on a cranial nerve.

  
  
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  Isolated motor abnormalities. Focal weakness suggests a small stroke or nerve root impingement, whereas hemiplegia suggests large vessel (eg, middle cerebral artery [MCA]) involvement. Isolated bilateral lower extremity weakness with preserved upper extremity strength is more consistent with spinal pathology, especially with concurrent bowel or bladder involvement.

  
  
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  Nausea/emesis beyond expected postanesthetic effect. While raised ICP may present with nausea, it tends to be associated with somnolence when severe, although these symptoms are nonspecific. Nausea can also be seen with posterior fossa pathology.

An understanding of the patient’s clinical course, both prior to admission and during the hospital stay, can further delineate the cause of a change.

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  Symptom timing and progression. Were the new symptoms noted immediately postoperatively, or did they appear a few days later? Did they progress rapidly? Rapid progression suggests a more acute pathology that may need to be addressed urgently. In contrast, delayed and gradually progressing symptoms suggests a broader differential, including nonstructural causes such as metabolic derangement.

  
  
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  History of trauma. Coagulopathy is common in trauma, whether secondary to thromboplastin release, hemodilution after resuscitation, hypothermia, or acidosis. A phenomenon known as trauma-induced coagulopathy can also occur independently of these factors. Other pathologies, such as evolution of parenchymal contusions, ischemic infarcts from noncranial sources (eg, vascular dissection), and delayed cerebral edema should also be considered.

  
  
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  History of seizures or antiseizure medication (ASM) use. Seizures can be a symptom of brain tumors, especially those that are cortically based, ^, and may appear de novo postoperatively. Patients with a history of seizures will typically be on ASMs. Determine the timing of the most recent ASM dose. Sodium levels, particularly in patients with traumatic brain injury, or who are receiving certain medications (diuretics, ASMs, and mood stabilizers), may be helpful.

  
  
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  Changes in blood pressure. Systemic blood pressure and its association with acute neurologic change differs depending on the associated pathology. Hypotensive episodes may precede stroke-like symptoms or extremity weakness due to brain and spine hypoperfusion and may also beget altered mental status. Of note, significant blood pressure alteration is often a symptom of the process underlying the neurologic change rather than its cause. For example, hypotension with bradycardia may be a harbinger of neurogenic shock due to disruption of autonomic pathways after upper spinal cord injury. Alternatively, with SAH, ischemic stroke, or traumatic brain injury, patients developing vasospasm may “autopress” to counteract relatively decreased perfusion. With acutely elevated ICP, hypertension may develop as part of the “Cushing’s triad” of hypertension, bradycardia, and irregular respirations, signaling a potential herniation event in progress.

  
  
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  Balance of intake and output, trend in sodium levels, trend in transcranial Doppler (TCD) velocities. Vasospasm—a phenomenon often seen in the aftermath of aneurysmal SAH (but also occasionally after severe traumatic brain injury, particularly when diffuse traumatic SAH is present)—may be associated with increased urinary output, hyponatremia, and increased TCD velocities. If untreated, vasospasm may induce ischemia and rebound edema.

  
  
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  Trend in ICP. An ICP increase preceding a neurologic change may suggest a mass lesion (eg, hemorrhage) or worsening cerebral edema.

  
  
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  Presence of ventriculomegaly. Review preoperative and postoperative imaging for potential cerebrospinal fluid (CSF) pathway pathology—whether due to impaired absorption (eg, from diffuse subarachnoid blood), mechanical obstruction (eg, posterior fossa mass lesion), or hardware failure (eg, occluded EVD/lumbar drain and shunt malfunction). The presence of an interhemispheric hygroma in patients with severe traumatic brain injury (TBI) postcraniectomy has been associated with the development of external hydrocephalus as well as an increased likelihood to require permanent CSF diversion.

  
  
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  Endovascular considerations. Acute neurologic changes following endovascular interventions can be associated with thromboembolic events. Distal dislodgment of a thrombus, vessel dissection, vasospasm, inadvertent perforation and associated intracranial hemorrhage, or thrombosis of implanted hardware should be considered. Postoperative hypotension secondary to hemorrhagic shock may be seen with retroperitoneal hematoma after femoral access. Rarely, metabolic derangement secondary to contrast-induced nephropathy may lead to encephalopathy, especially in vulnerable patients (eg, those withchronic kidney disease [CKD]).

Key questions to be asked of the surgeon include:

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  Surgical approach. Did the operative trajectory traverse cortical tissue? Did the procedure compromise any major vascular structures?

  
  
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  Hemostasis. Was it difficult to achieve hemostasis?

  
  
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  Intraoperative medical interventions. Was the patient given an ASM? Was mannitol given? Were steroids administered? If so, were they given for cerebral edema or to reduce postoperative nausea?

  
  
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  Other surgical considerations. If neurophysiological monitoring was used, was there a change in signals?

  
  
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  Anesthesia considerations. Was there any difficulty maintaining blood pressure? Were blood products required in response to surgical blood loss or due to coagulopathy, baseline hematologic derangement, or preoperative antiplatelet or anticoagulant therapy?

  
  
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  Considerations unique to spine. In a patient with cervical spine instability, was an awake fiberoptic intubation used? Was perfusion optimized via MAP goal maintenance?

  
  
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  Considerations unique to endovascular. What access site was used (eg, radial, femoral)? Was the patient receiving antiplatelet or anticoagulant therapy? Was a closure device deployed? Was there concern for intraprocedural vasospasm, and if so, was it treated? In the case of mechanical thrombectomy for stroke, what degree of reperfusion was obtained?

Patients undergoing neurosurgical procedures often have underlying medical conditions that may be important in the perioperative period. Awareness of the patient’s medical history may inform the differential diagnosis.

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  Underlying coagulopathy. Patients with hemophilia or other clotting factor deficiencies are at an increased risk of hemorrhage. ^,

  
  
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  Iatrogenic coagulopathy. Home antiplatelet (eg, aspirin and clopidogrel) or anticoagulant (eg, apixaban and warfarin) agents generally are held preoperatively for elective procedures, but this must be verified. These agents presumably increase the risk of postoperative bleeding after surgery. ^, In emergent situations—such a trauma—it may not be feasible to obtain this history preoperatively. Bear in mind that common preoperative laboratories such as complete blood count (CBC) or prothrombin time (PT), international normalized ratio (INR)/partial thromboplastin time (PTT) may only provide limited information. Advanced testing, such as a thromboelastographic (TEG) assay, may be pursued to identify hemostatic defects more specifically.

  
  
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  History of transient ischemic attack or stroke. Patients with a stroke history are at risk for additional ischemic events, and this risk may be increased perioperatively (particularly if antiplatelet or anticoagulant agents have been held). ^,

  
  
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  History of pre-existing respiratory conditions. Patients with conditions such as obstructive sleep apnea or chronic obstructive pulmonary disease may exhibit postoperative alterations in mental status secondary to hypoxemia or hypercapnia due to their respiratory disorder.

Diagnostic evaluation

In cases 1 and 4 , where there is concern for potential vascular compromise and ischemia, a noncontrast head computed tomography (CT) is a reasonable first step to exclude space-occupying lesions. With recent iodinated contrast administration, as in carotid artery stenting, a “dual-energy CT” can differentiate contrast extravasation from intracranial hemorrhage. If ischemia or infarction is suspected, CT angiogram, with or without perfusion, is indicated. These studies can demonstrate vascular narrowing or occlusion and potential associated perfusion defects and would provide the most expedient route to urgent endovascular therapy, if appropriate. Alternatively, a “stroke protocol” MRI of brain may be performed to confirm the diagnosis. The “gold standard” for diagnosing vasospasm is a catheter angiogram, which also offers the option for direct endovascular treatment.

In case 2 , where recurrent hemorrhage is suspected, a CT of the head enables rapid diagnosis. Obtaining laboratories, such as a PT/INR, PTT, and TEG, would also be helpful to identify any reversible coagulopathy present.

In case 3 , noncontrast CT of the spine can rule out bony pathology, hematoma, or hardware complication requiring emergent return to the operating room. This study may also provide limited information about compressive soft tissue lesions; however, MRI is more helpful for assessing these structures. MRI is the imaging of choice for diagnosing spinal cord ischemia or infarction.

Clinical decision-making and next steps

Accurately diagnosing the cause of acute neurologic worsening is crucial, as some entities may be managed medically, whereas others require operative intervention.

Seizure

In the acute setting, ASMs are the mainstay of treatment. Medical control of seizure and airway protection, if necessary, are imperative prior to pursuing imaging. An electroencephalogram should be obtained if subclinical status epilepticus is suspected. Operative intervention is dictated, in part, by the presence of a culprit lesion, if identified. Structural pathology—such as subdural hematoma, intraparenchymal hematoma, and residual tumor—and toxic-metabolic insults may be responsible for seizures.

Intracranial hematoma

A small amount of subdural hemorrhage or a small amount of hemorrhage within the tumor bed is not uncommon after craniotomy. Many hematomas do not cause significant mass effect or become symptomatic. Those causing clinical deterioration tend to occur within 6 hours of surgery. ^, Risk factors include intraoperative or postoperative hypertension and coagulopathy. If sudden neurologic worsening is attributable to a new space-occupying hematoma, surgical intervention is indicated. Correction of coagulopathy, strict blood pressure control, and seizure control should be performed in the interim.

Tension pneumocephalus

Urgent surgical intervention is required for symptomatic tension pneumocephalus. Bedside needle decompression through an existing burr hole could be considered if the pocket of air is accessible. Alternatively, bedside placement of a subdural evacuation port system drain has been described for acute decompression. Trace pneumocephalus, commonly seen after most procedures, does not require intervention and will resorb spontaneously. Large, but relatively asymptomatic pneumocephalus may also be managed expectantly; some recommend the use of a nonrebreather mask with 100% oxygen for 24 to 48 hours to aid in resorption. The amount of pneumocephalus can be monitored over time with serial skull radiographs.

Infarction

The management of cerebral infarction focuses on preventing further strokes and addressing any postinfarct edema that may result. In the case of iatrogenic small vessel occlusion during aneurysm clipping, often no further management is required. In contrast, iatrogenic vessel occlusion secondary to stent thrombosis may require endovascular intervention to confirm the diagnosis, evaluate perfusion, administer medication (eg, intra-arterial eptifibatide, tissue-type plasminogen activator [tPA]), or mechanically open the vessel. Assessing a patient’s response to antiplatelet medication via aspirin function tests or P2Y12 levels can guide further management. This is particularly important in those receiving clopidogrel, a prodrug that requires enzymatic activation. Patients with loss-of-function alleles exhibited higher stroke recurrence rates and complications following carotid artery stenting.

In the setting of a traumatic vascular injury such as dissection, antiplatelet therapy could be considered; however, evidence is limited. Infarcts sustained due to vessel manipulation tend to be small; however, large, full territory infarctions can develop significant edema. Hypertonic saline is often employed to augment serum sodium levels and combat edema; alternatively, mannitol may be employed. In some cases, decompressive hemicraniectomy may be pursued as a lifesaving measure.

Vasospasm/delayed cerebral ischemia

At the initial appearance of symptoms, permissive hypertension or even blood pressure augmentation may be trialed, presuming the primary pathology has been addressed. If symptoms persist, return to the neurointerventional suite may be considered for angioplasty or intra-arterial injection of a spasmolytic, such as verapamil, or a vasodilator, such as milrinone.

Obstructive hydrocephalus

Symptomatic hydrocephalus warrants urgent intervention. Two broad approaches may be taken: addressing the cause (eg, removing an obstructive lesion), and thus secondarily treating the hydrocephalus, or addressing the hydrocephalus directly via placement of an EVD.

Spinal epidural or subdural hematoma

Symptomatic spinal epidural hematoma typically requires urgent surgical exploration and evacuation, both to relieve mass effect on the spinal cord, and to identify and address the source of the bleeding to prevent recurrence.

Spinal cord ischemia

Whereas infarcted spinal cord tissue is not salvageable, ischemic tissue may recover if perfusion is restored. Maintenance of perfusion is typically attained through blood pressure augmentation with a MAP goal of 85 to 90 mm Hg for a duration of 5 to 7 days. ^,

Discussion

In case 1 , the patient had undergone a craniotomy for clipping of a ruptured aneurysm. Mechanical manipulation of blood vessels intraoperatively risks direct injury, vasospasm, and/or occlusion (thrombotic or iatrogenic due to clip placement) resulting in stroke. This complication would manifest with acute neurologic findings attributable to the affected vascular territory. Ischemia or infarction secondary to vessel manipulation would typically be apparent in the immediate postoperative period. Studies identify the first 6 hours after surgery as a “critical period” for the development of clinically apparent postoperative hematomas, ^, but hemorrhages can also occur in a delayed manner. Surgery-specific factors also play a role: subtotal tumor resection and the presence of a large resection cavity have been associated with hemorrhage into the tumor bed, and failure to place epidural tacking stitches in patients with challenging epidural bleeding may increase the risk of postoperative hematoma.

Vasospasm is an entity somewhat unique to SAH, presenting several days after the initial insult and potentially resulting in delayed cerebral ischemia. Subarachnoid blood irritates vessels and leads to narrowing via incompletely understood mechanisms, ^, producing stroke-like symptoms. The risk of vasospasm is generally highest from postbleed day 4 to 14. One classic association is increased urinary output coupled with a decrease in serum sodium, often diagnosed as cerebral salt wasting. ^, The associated polyuria may lead to hypovolemia and worsen vasospasm. Syndrome of inappropriate antidiuretic hormone has also been associated with aneurysmal SAH. TCD may be performed to assess for vasospasm. An acute increase in TCDs, or an absolute value of greater than 120 cm/s in the MCA, is consistent with the diagnosis. While aneurysmal SAH is perhaps the most common associated condition, vasospasm may also occur in traumatic brain injury, where—if unrecognized—it may contribute to ischemia and rebound edema.

Case 2 addresses considerations specific to posterior fossa pathologies. Mass lesions can compress exiting cranial nerves or the brainstem. Posterior fossa lesions may also cause obstructive hydrocephalus through occlusion of the fourth ventricle. Pathology may manifest as nausea and emesis, similar to any postcraniotomy patient. In this case, however, the symptoms are concerning for increased ICP—whether due to direct compression from hematoma or swelling or due to secondary obstructive hydrocephalus. The constellation of worsening somnolence, extreme nausea, and hypertension is concerning for recurrent hemorrhage. Although infrequently associated with posterior fossa lesions, seizures can lead to an alteration in level of consciousness and should be considered in patients with depressed mental status after craniotomy.

An infrequent but serious complication is tension pneumocephalus. A small amount of air is commonly seen in the cranial vault after craniotomy. However, when air continues to enter through a dural defect and becomes trapped via a ball-valve mechanism, it can exert mass effect. While seizures and focal neurologic deficits can be seen, a perhaps more common presentation is a declining level of conscious. Prompt recognition of this complication will prevent progression to herniation and death.

Case 3 illustrates acute worsening in the postoperative spine patient. In most individuals, the spinal cord terminates at the L1 vertebral body. Thus, procedures above L2 carry additional risk of direct cord injury, either at surgery or in a delayed manner secondary to recurrent disc or bone fragment impingement or hardware subsidence. Postoperative spinal epidural hematomas are rare but can also compress the cord and cauda equina. Another unique feature of the spinal cord, secondary to its vascular supply, is its relative susceptibility to ischemia; hypotensive infarction is a well-known entity. The region from T4 to T8 is at greatest risk in the “watershed zone” between the territories of the anterior spinal artery and the artery of Adamkiewicz. In the case presented earlier, the prolonged surgery, significant blood loss, and vasopressor requirements suggest that hypotension and consequent cord ischemia may underlie the patient’s new weakness.

Case 4 focuses on acute neurologic worsening after an endovascular procedure addressing symptomatic carotid artery stenosis. The unique set of complications associated with endovascular therapies include thromboembolic events, hemorrhage secondary to cerebral hyperperfusion syndrome (CHS), and arterial dissection. Space-occupying lesions, such as a hemorrhage from reperfusion injury, may generate stroke-like symptoms. Devices deployed into the vessel lumen may thrombose, leading to decreased or absent blood flow. Carotid artery stent occlusion itself is relatively rare and occurs in less than 1% of patients, typically secondary to antiplatelet noncompliance, medication resistance, or overlapping stent placement. Hyperperfusion following carotid stent placement occurs in 1.2% of patients, with ICH occurring in 0.74%. The diagnostic criteria for CHS include occurrence within 30 days postintervention, clinical features (eg, headache, seizure, hemiparesis, and Glasgow Coma Scale [GCS] <15), radiographic features (eg, cerebral edema or ICH, evidence of hyperperfusion), SBP greater than 180 mm Hg, and absence of new cerebral ischemia, postoperative carotid occlusion, or metabolic or pharmacologic cause. Traversing a vessel in itself risks dissection, atheroma dislodgement, and vessel perforation. Potential predisposing factors for carotid dissection include vessel tortuosity, excessive hardware manipulation, or postdilation of the distal stent edge. Perforation is an extremely rare event.

Summary

Care of the postoperative neurosurgical patient in the intensive care setting demands anticipation of a broad spectrum of potential secondary insults. Sudden neurologic worsening—whether following a cranial, spinal, or endovascular procedure—should trigger prompt bedside assessment, coupled with an awareness of the patient’s medical history, the procedure performed, and potential contributing factors, to generate a reasonable differential diagnosis and action plan. These principles are applicable whether the procedure was performed in the elective or emergent setting.

Clinics care points

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  Acute changes in vital signs, specifically blood pressure, are often the consequence of an underlying process (rather than the cause) and must be investigated promptly.

  
  
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  Important complications after craniotomy resulting in an acute neurologic change include postoperative hematoma, seizure, and, uncommonly, tension pneumocephalus.

  
  
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  Sudden neurologic worsening in the postoperative spine patient can occur due to direct injury to or compression of the spinal cord or due to spinal cord ischemia; the former is typically managed surgically, whereas the latter is typically managed medically.

  
  
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  Patients undergoing endovascular procedures are at risk for thromboembolic events that may lead to new onset acute neurologic deficits. Assessment with a noncontrast dual-energy CT, followed by CT angiography with or without perfusion, can guide further treatment.

  
  
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  Particularly in the ICU setting, it is important to consider nonstructural causes of sudden neurologic worsening; these are multiple and include electrolyte derangement, as well as metabolic, respiratory, and endocrine abnormalities.

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