Cerebral Edema

Postoperative edema of the neural tissue is almost inevitable after any degree of surgical manipulation, but in most cases, this is not clinically significant. Subtle cerebral edema may lead to delayed return of normal neurologic function, but in severe cases may manifest as worsening level of sensorium, seizures, and neurologic deficits. In severe cases, it is referred to as malignant cerebral edema, which may lead to cerebral herniation and also death. The pathogenesis of cerebral edema involves both the macro- and microcirculation. Hemodynamic changes after damage or thrombosis of draining veins, accompanied by cytotoxic changes of brain parenchyma due to direct damage or ischemia from prolonged retraction, form a vicious cycle that produce macroscopic cerebral edema. Multiple factors have been correlated with the development of cerebral edema, including excessive brain manipulation, prolonged retraction, and excessive bipolar coagulation with resultant venous edema. Incorrect positioning or excessive head rotation that leads to impaired venous return may also result in brain edema that itself may become obvious during surgery. Some of the anesthetic agents can also cause cerebral edema by various mechanisms; for example, isoflurane and nitrous oxide may increase cerebral blood volume, and enflurane and halothane may reduce CSF absorption. Cerebral venous thrombosis can also occur after an uneventful surgery because of dehydration and intraoperative hypotension. Patients with inherited coagulopathy are more prone to this complication. Cerebral edema is usually diagnosed in computed tomography (CT) scans as areas of hypodensity surrounding the surgical cavity with or without mass effect. Large areas of edema may be seen as loss of demarcation at gray-white matter interface. In magnetic resonance imaging (MRI), edema is more evident in T2 and fluid attenuation inversion recovery (FLAIR) sequences, where it appears as areas of hyperintensity due to increased water content. In most cases, postoperative edema is self-limiting and requires only careful observation and strict intake and output monitoring with maintenance of euvolemia and normotension. Resolution of edema becomes clinically evident with improvement in the sensorium and in neurologic deficits. In moderate cases, osmotic agents like mannitol and hypertonic saline as well as diuretics like furosemide are used to decrease the brain’s hydrostatic pressure. Mechanical ventilation in obtunded patients is usually helpful in reducing edema by improving brain oxygenation and cerebral vasoconstriction. In cases of severe malignant edema with impending herniation, surgical intervention may be required in the form of decompressive craniectomy or lobectomy. Surgical strategies that are suggested to prevent significant postoperative edema include proper positioning to decrease venous compression, avoidance of excessive brain retraction, adequate intraoperative hydration, minimal manipulation of the normal brain parenchyma, judicious use of bipolar coagulation, and avoidance of coagulation of draining veins.

Cerebral Hemorrhage

Postoperative hematoma is one of the most common and catastrophic complications after intracranial surgery and is an important cause of postoperative morbidity and mortality. The reported rates of postoperative hemorrhage vary in the literature depending on the practice patterns and definitions of postoperative hemorrhage. Many patients have a small amount of blood in the operative cavity, and such radiologic incidence of hemorrhage ranges from 10% to 50%. However, the incidence of hemorrhage having clinical implications that require some form of intervention is reportedly low, ranging from 0.8% to 6.9%. Many factors have been correlated with the formation of postoperative hemorrhage. The most important are perioperative factors, which include the inability to achieve hemostasis, and intraoperative factors such as hypertension and intraoperative severe bleeding causing disseminated intra-vascular coagulation (DIC). Important preoperative factors include older age, hypertension, and hematologic abnormalities such as thrombocytopenia and coagulation abnormality. Some of the intracranial lesions have a greater propensity for developing postoperative hemorrhage, notably vascular tumors like meningioma, glomus tumor, and hemangiopericytoma; arteriovenous malformations; and high-grade gliomas, especially after subtotal resection. Conditions such as chronic subdural hematomas also have a propensity for recurrence, though this is not evident in the immediate postoperative periods. Similarly, patients with traumatic hemorrhage or contusion tend to have increased incidence of postoperative hematoma because of trauma-induced coagulopathy.

Unless immediate postoperative CT scan is a norm, most postoperative hemorrhages are suspected based on clinical grounds, including lack of recovery from anaesthesia, deterioration of the sensorium, or development of focal neurologic deficits. Postoperative hemorrhages can be tumor bed hematomas or subdural or epidural hematomas. Although almost all postoperative hemorrhages are located in the primary surgical area, remote-site hemorrhages can occur in intraparenchymal, subdural, subarachnoid, and epidural locations and in different compartments as well. The incidence of remote-site hemorrhage is rare and has been estimated to be an average of 1 in 300 craniotomies. Important causes of remote-site hemorrhage include coagulation disorders, older patients with an atrophic brain, rapid decompression of the brain after ventricular shunts or evacuation of hematomas, brain shrinkage due to excessive mannitol use, sitting or remaining in a prone position for a prolonged period, and inappropriate placement of head holders with injury of epidural or subdural vessels. One study analyzing the NSQIP database reported that 1.5% of craniotomies required reoperation for hemorrhage. The most common site of hemorrhage was subdural or epidural, comprising 88.5% of cases, whereas only 11.5% of cases had intraparenchymal hemorrhage. Although repeat surgery decreases the mortality rate, the neurologic deficits are less likely to improve completely, giving rise to a significant morbidity. Therefore a preventive strategy is considered wiser; this includes meticulous hemostasis using bipolar coagulation and various commercially available topical hemostats. Maintaining perioperative and postoperative normotension and preventing and managing coagulation disorders are among the few general measures that help reduce the incidence of postoperative hematoma.

Cerebral Infarction

The incidence of postoperative stroke and coma after neurosurgical procedures is 0.73% as estimated by one study using the NSQIP database. Postoperative cerebral infarction can be arterial or venous. Arterial infarctions may occur due to intraoperative injury and sacrifice of major arteries, which are usually well delineated. Although sacrifice of a major artery almost definitely leads to the development of an infarction, in most cases the size of the infarction is limited due to the presence of collateral circulation. For this reason, watershed areas are more prone to the development of an infarction due to direct injury or even in the event of prolonged hypotension. Most of the arterial injuries are evident during surgery; however, in a few cases, injury of the perforating vessels may go unnoticed intraoperatively but give rise to significant postoperative deficits due to lacunar infarcts in the deep nuclear structures. Arterial injuries are dependent solely on the experience of the surgeons and on the type and extent of the lesions. Tumors with vascular encasements like meningiomas, chordomas, and hemangiomas are prone to arterial injury during dissection. Similarly, vascular lesions like aneurysms and arteriovenous malformations have an inherent tendency to induce vasospasm during/after surgery. Surgical experience has also been correlated with incidence of arterial injury. Inadequate knowledge of vascular anatomy, poor skills in microsurgery, inappropriate dissection techniques, and lack of expertise in vascular repairs are obvious surgeon-related factors associated with a higher incidence of vascular injuries. Arterial infarcts may develop in a delayed fashion due to vasospasm, most notably after subarachnoid hemorrhage due to aneurysm rupture. Some forms of vasospasm may be noted after resection of tumors from encased vessels and are related to prolonged dissection and manipulation of the vessel. In such cases arterial infarcts may not develop in all cases, but cerebral hypoperfusion can lead to altered sensorium and short-term neurologic deficits. Acute development of infarct is associated with some form of edema, which may give rise to mass effect and is therefore life-threatening. In such cases, intracranial pressure (ICP) reduction measures or even decompressive craniectomy may be required. The mortality risk decreases gradually once the infarct becomes well delineated; however, it carries a significant risk of permanent morbidity.

Venous infarcts develop after sacrifice of major cortical draining veins or venous sinuses but are rarely permanent. Apart from direct venous injury, other significant causes for the development of venous infarcts include venous thrombosis or sinus thrombosis. Important factors responsible for this include prolonged cortical exposure without saline irrigation, intraoperative hypotension, and inappropriate use of pressure or hemostats for bleeding control or ligation of proximal veins. The venous thrombosis may manifest acutely or develop in a delayed fashion. Venous infarctions mostly manifest as the development of cerebral edema with or without venous hemorrhage. The edema and mass effect are more significant than with arterial infarcts and therefore need anti-ICP measures or surgery in almost all cases. The edema tends to be progressive, which requires prolonged clinical and radiologic monitoring. However, once the edema subsides, neurologic recovery is usually more complete as compared with arterial infarcts.

Seizures

Postoperative seizures can occur in the immediate postoperative period or late in the recovery course. Early postoperative seizures can occur in 10% to 20% of supratentorial surgeries due to cortical irritation after manipulation of brain tumors like gliomas and meningiomas or of vascular lesions like arteriovenous malformations or pneumocephalus. However, seizures can be the early manifestation of underlying severe complications like postoperative hematomas, venous edema, or infarction. Therefore all early postoperative seizures should be evaluated with brain imaging to rule out life-threatening events. Other causes of seizures during the postoperative period include recurrence in patients with previous seizures, electrolyte imbalance, hypoxia, and anaesthetic medication. Seizures may also occur during the late postoperative period due to cortical scarring or regrowth of the lesion. Postoperative seizures are usually managed conservatively with antiepileptic drugs, unless they are induced by life-threatening hematoma or edema. However, various systematic reviews as well as clinical trials have not proven any benefit of prophylactic use of antiepileptics for intracranial surgery. Intraoperative precautions that are helpful in reducing the incidence of seizures include minimization of retraction, avoidance of excessive coagulation, frequent irrigation, and maintenance of proper hemostasis.

Neurologic Deficits

Neurologic deficits are among the most feared complications. Many of the neurologic deficits especially affecting the higher mental functions go unnoticed unless checked specifically. Significant neurologic deficits causing limb weakness, numbness, or speech difficulties pose significant morbidity in the postoperative period. Most patients recover to a great extent in the long term; however, complete recovery is rare. Neurologic deficits are usually predictable because they are specific to the site of surgery. In the initial postoperative period, the deficits are denser and more widespread because of the involvement of surrounding neurons, called “neural stunning,” a condition that is usually transient. Once the neurons recover from the operative stress, the deficits gradually improve and become limited to the structures that were directly damaged. On the other hand, the deficits may appear in a delayed fashion with worsening of initial deficits; this is mostly due to damage to vascular structures, leading to gradual ischemia. The extent of damage required to produce a deficit greatly varies with the site involved. Sites with a great degree of plasticity like cerebral and cerebellar lobes require severe damage to produce deficits; however, deeper structures like the thalamus, internal capsule, and brainstem are less compliant, and small lesions may produce dense deficits. Cranial nerve deficits are not uncommon after posterior fossa surgery, especially around the cerebellopontine angle cistern. Sensory nerves are more prone to produce deficits as compared with motor nerves. Unfortunately, no specific therapy is available to treat neurologic deficits that have already occurred. However, physiotherapy and speech therapy are some interventions available to greatly improve the final outcome. The few intraoperative adjuncts available to decrease the incidence of postoperative deficits include cortical mapping, neuromonitoring, and intraoperative EEG. Other technical points that are important to prevent inadvertent injury include intratumoral dissection in lobar tumors, intraarachnoidal dissection in lesions around cisterns, and gentle manipulation of neural structures.

Hydrocephalus

Postoperative hydrocephalus is an important complication after surgeries around the third or fourth ventricles. Intraventricular surgeries for colloid cysts, central neurocytoma, ependymoma, thalamic tumors, medulloblastomas, and hemangioblastomas are a few examples where postoperative obstruction of the ventricular pathway can give rise to obstructive hydrocephalus. The cause of such obstruction may include intraoperative bleeding, debris, or postoperative edema of the surrounding tissues. Another important cause of postoperative hydrocephalus is subarachnoid hemorrhage, which impedes CSF absorption at the level of the arachnoid villi. Acute hydrocephalus in previously normal ventricles gives rise to a life-threatening increase in ICP and can be fatal unless addressed emergently. Patients with previously dilated ventricles may compensate to an extent before becoming symptomatic. Most patients with postoperative hydrocephalus are usually managed with an external ventricular drain (EVD), which may help in CSF diversion until the ventricular system clears up. A few patients may ultimately require permanent CSF diversion with insertion of shunts.

Cerebrospinal Fluid Fistula

CSF leak from the cranial wounds may complicate a significant number of craniotomies, but chronic fistula is rare. CSF leak in most cases is the result of faulty closure techniques including improper dural closure, dural tear due to stretching, and improper soft tissue and skin closure. In a few cases, increased CSF pressure due to hydrocephalus may give rise to wound dehiscence producing a leak. Similarly, wound breakdown due to ischemia after tight closure, closure of previously irradiated skin, or wound infection may produce CSF leakage. Posterior fossa craniotomies are especially prone to producing a CSF leak because of the thin and tight dura, which makes dural closure difficult. A CSF leak is manifested as clear discharge from the wound or wound bulge, which should be differentiated from benign wound seromas. Although CSF leaks are asymptomatic for the patient, persistent leakage may give rise to infectious complications like meningitis, empyema, or brain abscess. In few cases, CSF leak can manifest as CSF otorrhea or rhinorrhea instead of wound discharge. Notable examples include retromastoid craniotomies that produce CSF otorrhea or rhinorrhea due to CSF leakage through mastoid air cells into the middle ear cavity. Similarly, surgeries around the sella, especially endonasal approaches, can give rise to CSF rhinorrhea. Most postoperative CSF leaks are managed conservatively with revision of wound closure with or without CSF diversion. CSF rhinorrhea or otorrheas are managed with CSF diversion. Revision of dural closure with placement of dural substitutes that produce a watertight closure may be required for persistent leaks. Endonasal approaches are more prone to persistent leaks or delayed leaks, which may require reconstruction of the sellar floor using bone or fat-grafts along with dural substitutes. Most CSF leaks are due to technical failures and therefore are preventable. Meticulous watertight dural closure, adequate waxing of exposed air cells during the retromastoid or middle fossa approach, and proper reconstruction of the sellar floor are among the few important surgical steps that help in preventing CSF leak.

Infectious Complications

Postoperative infections are an important cause of postoperative morbidity and can complicate 0.7% to 1.1% of cranial procedures and 1.1% to 1.5% of spinal procedures. One of the retrospective longitudinal studies from the Statewide Planning and Research Cooperative System (SPARCS) database found postoperative infection to be the most common cause of unplanned readmission after neurologic surgery. Postoperative infections can be superficial surgical site infections, deeper infections like cranial osteomyelitis, meningitis, subdural empyema, or brain abscess. Another important site of infection is the hardware infection such as at the EVD, ventriculo-peritoneal shunt, bolts, or cranial or spinal implants. Surgical site infections manifest as erythema or edema around the incision site with or without purulent discharge. Postoperative meningitis can occur after 0.5% to 0.7% of neurosurgical procedures and is most commonly due to breach in antisepsis during surgery. Other causes include postoperative CSF leak and wound dehiscence with secondary contamination. Deeper infections are usually serious and can be life-threatening. Subdural empyema or abscess present as focal neurologic deficits with or without features of raised ICP. On imaging they present with enhancing walls with edema out of proportion to the size of the lesion. In some cases, necrosis of the residual tumor may simulate an abscess, which can be differentiated by diffusion-weighted MRI. The mainstay of postoperative infection is antibiotic therapy, so broad-spectrum antibiotics should be started in patients with clinical suspicion of infection. The surgical site of infection and meningitis can be treated with antibiotic therapy alone, although some cases may need surgical debridement of the wound or repair to treat CSF fistula. All deep infections like empyema or abscess are managed surgically, along with antibiotic therapy. Surgical drainage of the cavity is usually performed during a neurosurgical emergency both to decrease the raised ICP and to aid in isolating the organism for antibiotic sensitivity.