| Postoperative Complications | Respiratory Care| Cardiovascular Therapy| Fluid Management| Nutrition in Critical Patients |Traumatic Brain Injury-Stroke-Brain Death |

I. Complications after operation for supratentorial tumor

Increased intracranial pressure (ICP). The cranial cavity has a limited capacity to accommodate increased intracranial volume without a significant increase in pressure. Increased volume of any of the three components of the intracranial cavity ”brain cells, blood, and cerebrospinal fluid (CSF)” may increase ICP. Increased ICP causes injury to the brain by compression, herniation, and ischemia. Brain ischemia in turn enhances brain edema, propagating a cycle of vascular insufficiency and swelling.
Intracranial hemorrhage, hydrocephalus, and cerebral edema are the most common postoperative causes of increased ICP. Intracranial hypertension leads to headache, nausea, vomiting, decreased level of consciousness, and neurologic dysfunction. These signs are not specific for increased ICP and are not uncommon postoperatively. Detection of increased ICP relies on clinical signs and symptoms, direct measurement of ICP, and imaging studies such as computed tomographic (CT) scanning. Prevention and treatment seek to avoid and alleviate factors that can aggravate intracranial hypertension such as arterial hypertension, impaired cerebral venous drainage, blocked or malfunctioning surgical drains, postoperative pain, respiratory depression, nausea and vomiting, shivering, and seizures.
Cerebral edema is minimized by intraoperative and postoperative use of dexamethasone, loading dose 10 to 20 mg intravenously (i.v.); then 4 mg i.v. every 6 hours and mannitol, loading dose 0.25 to 2 g/kg i.v. over 30 minutes; then every 6 hours as needed, with careful monitoring of fluid intake and output and control of blood pressure and central venous pressure.
Cerebral venous drainage is facilitated by head elevation to 30°, blood pressure permitting.
Postoperative ventilation and oxygenation should be monitored and supplemental oxygen and ventilatory support should be provided as needed.
Pain is treated with small doses of fentanyl, 0.5 to 1 mcg/kg i.v. every 1 to 2 hours; morphine, 0.025 to 0.05 mg/kg i.v. every 1 to 2 hours; or hydromorphone, 0.2 to 1 mg i.v. every 2 to 3 hours.
Postoperative nausea and vomiting are minimized by intraoperative use of dexamethasone and 5HT3 receptor antagonists such as dolasetron, 12.5 mg i.v. in adults and 0.35 mg/kg i.v. in children; or ondansetron, 4 mg i.v. over 4 minutes for adults and children weighing >40 kg and 0.1 mg/kg i.v. over 4 minutes for children weighing <40 kg.
Postoperative shivering is treated by gradually rewarming the patient and administering small doses of meperidine, 12.5 mg i.v.
Postoperative seizures are treated with phenytoin, loading dose 10 to 20 mg/kg i.v. no faster than 50 mg/minutes (1,000 mg over 20 minutes in typical adults) and then 5 to 7 mg/kg/day; or fosphenytoin, loading dose phenytoin equivalent (PE) 15 to 20 mg/kg i.v. no faster than 100 to 150 mg/minute (1,000 mg PE over 10 minutes in typical adults) and then 4 to 6 PE mg/kg/day.

II. Complications after operation for infratentorial tumor

Increased ICP. The elastance of the infratentorial compartment is greater than that of the supratentorial compartment, which means that it takes smaller increases in volume to produce significant increases in pressure. Furthermore, increased pressure in the posterior fossa is more life threatening because it can compress or herniate the brain stem, which contains the respiratory and vascular centers. Brain stem herniation can occur downward through the foramen magnum or upward through the tentorium, which is most common after resection of tumors of the cervical medullary junction. Brain stem compression is manifested by a decreased level of consciousness and respiratory and cardiovascular abnormalities including collapse. Measures to control ICP should be continued in the postoperative period: head elevation; prevention and treatment of hypertension; treatment of pain, nausea, and vomiting; prevention and treatment of shivering; and maintenance of adequate ventilation and oxygenation. Decreased level of consciousness or the development of respiratory or cardiovascular abnormalities should prompt surgical consultation.
Brain stem injury can occur intraoperatively. This presents postoperatively as failure to regain consciousness or resume spontaneous respiration with cardiovascular abnormalities such as bradycardia and hypertension/hypotension. Pharmacologic causes of such manifestations should be ruled out by ensuring adequate reversal of anesthetic agents and muscle relaxants. Supportive care in the form of mechanical ventilation and hemodynamic therapy is provided as needed.
Injury to cranial nerves IX, X, and XII may compromise the patient's ability to maintain a patent and protected airway due to difficulty in swallowing and clearing secretions. Tracheal extubation should be performed only after the integrity of protective upper airway reflexes is evident. After extubation, respiratory monitoring should continue with readiness to reintubate the trachea and reinstitute mechanical ventilation if the patient fails to maintain adequate ventilation and a patent and protected airway. Injury to the ophthalmic division of the trigeminal nerve (cranial nerve V) may impair protective reflexes of the cornea and require external protection with an eye patch.
Edema of the mucosa of the upper airway may occur after prolonged surgery, especially in the sitting position. It is more significant in children due to the small diameter of their airways. Tracheal extubation should be performed only after absence of airway edema is ascertained by deflating the cuff of the endotracheal tube and confirming the ability of the patient to breathe around the tube. If airway edema is suspected, the trachea should remain intubated and the patient sedated, if needed, until the edema resolves. Inhaled racemic epinephrine, 0.5 mL of 2% solution in 3 mL saline, decreases localized mucosal edema and might relieve upper airway obstruction. Macroglossia may accompany upper airway edema, causing complete airway obstruction. If this occurs, cricothyroidotomy, tracheotomy, or insertion of laryngeal mask airway may be the fastest way to reestablish the airway.
Pneumocephalus occurs after craniectomy, especially in the sitting position, and is usually of little clinical consequence. Tension pneumocephalus, which may decrease the level of consciousness due to brain compression, is more common in patients after ventricular shunting and aggressive drainage of CSF, which allows air trapping in the space that surrounds the brain that has been drained of CSF. Pneumocephalus is diagnosed by a CT scan or x-ray of the head and is effectively treated with a burr hole, which can be done under local anesthesia and usually produces rapid recovery of consciousness once the trapped air has been released.
Patients who develop intraoperative venous air embolism may subsequently develop postoperative pulmonary edema requiring mechanical ventilation and diuresis. Extubation is performed after resolution of pulmonary edema as documented by clinical examination, chest x-ray, and arterial blood gases. Patients with functionally patent foramen ovale may develop paradoxical air embolism, which is manifest postoperatively by neurologic deficits, decreased level of consciousness, and cardiac abnormalities.

III. Complications after operation for pituitary tumor

Endocrine complications include adrenocortical insufficiency, hypothyroidism, and diabetes insipidus (DI).
All patients receive corticosteroid coverage until testing indicates an intact pituitary-adrenal axis.
Thyroid hormone replacement is reserved for patients who were hypothyroid preoperatively.
DI occurs in 10% to 20% of patients, usually develops within 12 to 24 hours of surgery, and lasts for a few days. Decreased release of antidiuretic hormone results in the excretion of excessive amounts (4 to 14 L/day) of dilute urine and leads to dehydration, hypernatremia, increased serum osmolality (>300 mOsm/kg), decreased urine osmolality (<200 mOsm/kg), and decreased urine specific gravity (<1.005). Symptoms of hypernatremia are nonspecific and include decreased level of consciousness, tremulousness, muscle weakness, irritability, ataxia, spasticity, confusion, seizures, coma, and possibly intracranial bleeding due to increased serum osmolality. Treatment of DI consists of hydration and hormonal supplementation. The amount and content of intravenous fluids are guided by urine volume, serum electrolytes, and serum osmolality. Free water (H₂O) deficit can be estimated using the following formula:

If fluid is replaced early, it is not necessary to administer free water (D₅W). Rather, a hypotonic solution such as 0.45% sodium chloride (NaCl) or lactated Ringer's may be given. Insulin and potassium supplementation might be required when dextrose-containing fluids are used, especially if corticosteroids are used concomitantly. When hormonal replacement is required, 1-deamino-8-d-arginine vasopressin (DDAVP), a synthetic analog of the natural hormone arginine vasopressin, can be given intravenously, subcutaneously, orally, or intranasally. The latter might not be feasible after transnasal transsphenoidal pituitary surgery. The usual intravenous or subcutaneous dose is 0.3 mcg/kg/day, divided and given twice daily. The dose by mouth is 0.05 to 1.2 mg/day, divided and given two to three times a day. The intranasal dose is 10 to 40 mcg one to three times a day. The dose is adjusted according to the patient's sleep pattern and water turnover. Once intravascular volume has been restored, persistent hypernatremia may be treated with thiazide diuretics, such as hydrochlorothiazide, 50 to 100 mg/day i.v.
Rhinorrhea of CSF may develop after transnasal transsphenoidal operations. Spontaneous resolution occurs commonly, and clinical observation is sufficient in most cases. If signs of infection develop, antibiotic therapy and surgical repair are indicated.
Airway obstruction from bleeding and accumulation of blood and secretions in the pharynx sometimes occurs after transnasal transsphenoidal surgery. Frequent assessment of the patency of the airway and adequacy of ventilation is mandatory. Excessive bleeding might require reintubation and surgical consultation.
Postoperative nausea and vomiting might develop due to intraoperative swallowing of blood during transsphenoidal resection of pituitary tumors. To minimize the risk of postoperative nausea and vomiting, the pharynx and stomach are suctioned at the conclusion of surgery, and 5HT3 receptor antagonists are administered prophylactically: dolasetron, 12.5 mg i.v. in adults and 0.35 mg/kg i.v. in children; ondansetron, 4 mg i.v. over 4 minutes for adults and children weighing >40 kg and 0.1 mg/kg i.v. over 4 minutes for children weighing <40 kg, or granisetron, 0.1 to 1 mg i.v.

IV. Complications after operation for head trauma

Systemic sequelae of head trauma frequently become apparent in the postoperative period. These include adult respiratory distress syndrome, neurogenic pulmonary edema (NPE), cardiac arrhythmias, electrocardiographic (ECG) changes, disseminated intravascular coagulation, DI, syndrome of inappropriate antidiuretic hormone secretion (SIADH), hyperglycemia, nonketotic hyperosmolar hyperglycemic coma, and gastrointestinal ulcers and hemorrhage.
NPE is a fulminant form of pulmonary edema that progresses rapidly (within hours to days) toward either resolution or death. The pathologic characteristics of NPE are marked pulmonary vascular congestion, pulmonary arteriolar wall rupture, protein-rich edema fluid, and intra-alveolar hemorrhage. NPE results from a massive transient central sympathetic discharge due to an increase in ICP and is particularly associated with hypothalamic lesions. The pathophysiology includes systemic vasoconstriction and left ventricular failure, redistribution of blood from the systemic to the pulmonary vessels, pulmonary venous constriction, and increased pulmonary capillary permeability. Treatment is aimed at reducing ICP, reducing sympathetic hyperactivity, mainly by using alpha-adrenergic blockers such as diazoxide, 1 to 3 mg/kg i.v. every 5 minutes until blood pressure is controlled, up to 150 mg, or phentolamine, 5 mg i.v. increments, and providing respiratory supportive care and inotropic therapy as needed.
The syndrome of inappropriate antidiuretic hormone (SIADH) causes water retention with continued urinary excretion of sodium. This leads to dilutional hyponatremia, decreased serum osmolality, increased urine osmolality, and decreased urinary output. Water retention and serum hypo-osmolality might progress to water intoxication, which leads to nonspecific symptoms such as nausea, vomiting, headache, irritability, disorientation, seizures, and coma. Treatment consists of water restriction, loop diuretics, and hypertonic saline. In mild cases, fluid restriction (1 to 1.5 L/day) is sufficient to correct hyponatremia. Furosemide may be added because it impairs renal ability to concentrate urine. Hypertonic saline is usually reserved for serum sodium of <120 to 125 mEq/L. It is given in small amounts for a short time (1 to 2 mL/kg/hour for 2 to 3 hours), after which serum sodium and osmolality are measured. During the acute phase of SIADH, urine output is measured hourly and urine osmolality and specific gravity and serum sodium and osmolality are measured every 6 to 8 hours. Serum sodium should be increased at a rate of no more than 0.5 mEq/L/hour or 12 mEq/L/day. Faster rates of correction may cause osmotic demyelination, which develops over several days. It is associated with nonspecific signs such as behavioral changes, movement disorders, seizures, pseudobulbar palsy, quadriparesis, and coma.
Spinal cord injury occurring in conjunction with head injury might become apparent only in the postoperative period. Up to 15% of patients with head injury sustain cervical spine injury as well. Precautions to avoid exacerbation of spinal cord injury are continued in the postoperative period until cervical spine injury is ruled out or repaired. Pharmacologic therapy to ameliorate spinal cord injury may be given within 8 hours from injury in the form of methylprednisolone, loading dose 30 mg/kg i.v.; then 5.4 mg/kg/hour i.v. for 23 hours. Acute phase spinal shock (usually during the first week) is treated with fluids, inotropes, and pressors. During the chronic phase of spinal injury (after the first week), adequate analgesia is provided before somatic or splanchnic stimulation in patients with injury above T6 to avoid the risk of autonomic hyperreflexia.
Cardiovascular and respiratory monitoring, aided with the appropriate imaging and laboratory studies, is aimed at detecting extracranial injuries and complications such as pneumothorax, hemothorax, intra-abdominal or retroperitoneal hemorrhage, and fat embolism.
Prevention of secondary brain injury is continued in the postoperative period. Hypotension, hypoxia, hyperthermia, hyperglycemia, hypoglycemia, increased ICP, and any aggravating factors such as pain, nausea, vomiting, seizures, hypertension, hypercarbia, and impaired cerebral venous drainage should all be prevented and treated. Conscious, mechanically ventilated patients are sedated with short-acting agents, such as propofol, 10 to 30 mcg/kg/minute i.v., or dexmedetomidine, load 1 mcg/kg i.v. over 10 minutes; then 0.2 to 0.7 mcg/kg/hour for <24 hours, to allow intermittent neurologic assessment. Pain due to the operative procedure or the primary or associated injury is relieved with opioids such as morphine, 0.05 mg/kg i.v., or fentanyl, 0.5 to 1 mcg/kg i.v. Nausea and vomiting are treated with stomach suctioning (after ruling out skull base fracture) and pharmacologic means such as ondansetron, 4 mg i.v.; dolasetron, 12.5 to 25 mg i.v., or granisetron, 0.1 to 1 mg i.v. Seizure prophylaxis after head trauma is somewhat controversial. Phenytoin, loading dose 15 mg/kg i.v. over 20 minutes followed by 5 to 7 mg/kg/day, or fosphenytoin, loading dose PE 15 to 20 mg/kg i.v. and then 4 to 6 PE mg/kg/day, may be given for 2 weeks after head injury if there have been no seizures or longer if there have.
Clotting may be impaired because of the release of tissue thromboplastin and a trauma-induced decrease in platelets, prothrombin (factor II), proaccelerin (factor V), and plasminogen and increase in fibrin degradation products.

V. Complications after operation for aneurysm

Vasospasm. Angiographic narrowing of blood vessels occurs in approximately 30% of patients between days 4 and 14 after subarachnoid hemorrhage (SAH). Neurologic dysfunction (disorientation, decreased level of consciousness, focal deficit) occurs in approximately 50% of patients who have angiographic narrowing. The risk for developing vasospasm correlates with the amount of blood around the circle of Willis, the preoperative use of antifibrinolytic therapy, and the postoperative development of the cerebral salt wasting (CSW) syndrome. Pharmacologic prophylactic therapy of vasospasm is initiated within 96 hours of SAH and consists of nimodipine, 60 mg by mouth every 4 hours for 21 days or longer. Triple-H therapy (hypervolemia, hypertension, and hemodilution) may be used to treat vasospasm following SAH. It consists of the administration of crystalloid and colloid solutions to achieve a pulmonary capillary wedge pressure of 15 mm Hg and hemoglobin level of 11 g/dL and the use of inotropes and vasopressors to achieve a mean arterial pressure of 120 mm Hg or more. Antidiuretic therapy with vasopressin is sometimes necessary to prevent the diuresis induced by volume loading. Hypotension, heart failure, myocardial ischemia, and pulmonary edema are occasional complications of triple-H therapy.
Obstructive hydrocephalus due to subarachnoid blood-induced disturbances in CSF circulation may occur after SAH. The resulting increase in ICP may manifest itself as a decreased level of consciousness. CT scan is diagnostic, and ventriculostomy with CSF drainage is the effective therapy.
Hyponatremia after SAH can be due to CSW syndrome or, less commonly, to SIADH. CSW syndrome is caused by increased secretion of atrial natriuretic peptide, brain natriuretic peptide, and C-type natriuretic peptide. These peptides suppress aldosterone synthesis and lead to natriuresis, diuresis, and vasodilatation. Hyponatremia in the CSW syndrome results from increased renal excretion of sodium (150 to 200 mEq/L), which is followed by water with resultant hypovolemia. Hyponatremia of SIADH is mainly due to water retention in conjunction with renal excretion of sodium in a range of 20 to 30 mEq/L. Treatment of the two forms of hyponatremia is completely different. Patients with CSW require sodium replacement and fluid administration, whereas patients with SIADH require fluid restriction and diuresis. Fluid restriction and diuresis in a patient with CSW can be fatal due to the possibility of severe hypovolemia and cerebral infarction; fluid and salt administered to a patient with SIADH may lead to osmotic demyelination. Hypertonic saline may be used with close monitoring of serum sodium in both CSW syndrome and SIADH.
DI occurs less frequently than CSW syndrome or SIADH after SAH. Treatment includes hypotonic fluids in the form of enteral free water or parenteral D5W, D5 0.2% NaCl, or 0.45% NaCl plus the administration of DDAVP, 0.3 mcg/kg/day i.v. or subcutaneously, divided and given twice a day; 0.05 to 1.2 mg/day by mouth; or 10 to 40 mcg one to three times a day by nasal spray.
Intracranial hematomas might develop at the operative site or at the bridging dural veins due to overzealous CSF drainage. Manifestations are those of increased ICP, which may be associated with focal deficit. CT scan is diagnostic, and treatment with surgical evacuation may be required.
Seizure prophylaxis is continued in the postoperative period due to the high risk of seizures after SAH, especially in hypertensive patients. Phenytoin is usually given for 3 to 6 months after SAH.
NPE occurs in some patients after SAH due to the sudden increase in ICP, which produces intense sympathetic activation, catecholamine release from the hypothalamus and the medulla, and increased pulmonary vascular pressure and permeability. Diagnosis depends on the exclusion of other causes of pulmonary edema such as triple-H therapy and aspiration pneumonia. Treatment includes supplemental oxygen, mechanical ventilation plus positive end-expiratory pressure, and reduction of ICP.
After SAH, patients are at moderate risk for developing deep venous thrombosis (DVT) and pulmonary embolus (PE). Mechanical DVT prophylaxis, in the form of graduated stockings or intermittent pneumatic compression of the lower extremities, is instituted in all patients after SAH. Anticoagulation is contraindicated in the acute postoperative phase. Insertion of an inferior vena cava filter may be necessary for the prevention of recurrent pulmonary embolization.
Cardiac complications are common after SAH. ECG changes of arrhythmia, ischemia, or infarction, which are detected in >50% of patients, occur within 48 hours of SAH but may be first noted in the early postoperative period. Echocardiography, thallium scintigraphy, and autopsy detect evidence of myocardial injury. These ECG changes may be due to hypothalamic injury and high catecholamine levels. Treatment depends on the severity of the complications, the hemodynamic stability of the patient, and concomitant vasospasm. Infarcted, stunned, or hibernating myocardium might exclude these patients from triple-H therapy.

VI. Complications after ablation of arteriovenous malformation (AVM)

After surgery for AVM, patients are at risk of developing complications similar to those found after aneurysm surgery (vasospasm, hydrocephalus, and seizures). In addition, these patients are at high risk of developing hyperemic complications.
The syndrome of normal perfusion-pressure breakthrough or cerebral hyperperfusion is a hyperemic state characterized by cerebral edema, swelling, and/or hemorrhage that develops after resection of AVM. This condition results from the restoration of cerebral blood flow (CBF) to chronically hypoperfused areas or from venous outflow obstruction after AVM ablation. The ensuing cerebral swelling and hemorrhage cause neurologic dysfunction and are a major cause of postoperative morbidity and mortality. Patients who have ischemic rather than hemorrhagic symptoms preoperatively or certain angiographic features such as high or inverse flow in a large, deep, border zone AVM are particularly at risk. Staged repair and strict control of blood flow through the AVM may decrease the risk of hyperemic complications. Treatment of the manifestations of cerebral hyperemia includes mechanical hyperventilation, osmotic diuresis, and barbiturate coma.

VII. Complications after neuroradiologic procedures

Cerebral vascular embolization procedures may lead to complications such as SAH, intracerebral hemorrhage, cerebral ischemia, cerebral infarction, reperfusion syndrome, seizures, pulmonary embolism, and contrast reactions. The priority of treatment in all of these complications is to secure a patent and protected airway and maintain adequate cerebral perfusion pressure through the management of blood pressure and ICP.
Cerebral hemorrhage may occur either immediately due to vessel perforation by the catheter or guidewire or aneurysmal rupture or later due to hyperemic complications. Most small perforations can be managed conservatively by observation and follow-up. Alternatively, the catheter itself can be used to tamponade the source of bleeding and occlude the perforation. Other treatment measures include reversal of systemic anticoagulants, seizure prophylaxis, analgesic and antiemetic therapy, and insertion of large bore intravenous catheters for fluid resuscitation and possible blood transfusion. These measures should be instituted in consultation with the attending neuroradiologist or neurosurgeon. Large perforations with massive bleeding require emergent surgical intervention. However, the prognosis of extensive bleeding is grave because most of these patients exsanguinate prior to surgery owing to the inability to perform craniotomy and vascular repair in a timely manner, particularly because most of these vessels are situated deep in the cerebral parenchyma.
Cerebral ischemia may occur due to the obstruction of venous drainage, unintentional occlusion of surrounding arteries, or local injection of papaverine for treatment of vasospasm. Cerebral ischemia/infarction may manifest themselves as hemiplegia, hemiparesis, cranial nerve palsies, aphasia, nausea, vomiting, and seizures. Treatment of cerebral ischemia/infarction in this setting consists of maintaining adequate cerebral perfusion pressure by blood pressure and ICP management, airway protection, and other supportive care as needed. Intravenous thrombolytic therapy is contraindicated in this setting. Interventional neuroradiologic measures to reestablish perfusion can be attempted.
Seizures may occur in patients with preexisting seizure disorders or in patients with no such history. They may occur due to cerebral ischemia or infarction, which could be due to vessel obstruction or trauma, or localized cerebral edema, which could follow even successful embolization procedures; or they may be precipitated by the cerebral hyperperfusion syndrome. Management of seizures should include, in addition to pharmacologic therapy, identification and, when possible, treatment of precipitating factor(s), airway management, and stabilization of hemodynamic parameters. Anticonvulsant therapy includes midazolam, 0.1 to 0.2 mg/kg i.v.; lorazepam, 4 to 8 mg i.v.; thiopental, 3 to 5 mg/kg i.v.; phenytoin, loading dose 10 to 20 mg/kg i.v. no faster than 50 mg/minute (1,000 mg over 20 minutes in typical adult) and then 5 to 7 mg/kg/day; or fosphenytoin, loading dose PE 15 to 20 mg/kg i.v. no faster than 100 to 150 mg/minute (1,000 mg PE over 10 minutes in typical adult) and then 4 to 6 PE mg/kg/day.
Pulmonary embolism may occur due to either the release of embolization materials into the venous circulation, particularly in AVMs that contain large fistulae or those of the vein of Galen, or from vessels accessed en route to the AVM. Depending on the extent and source of embolism, treatment consists of securing a patent and protected airway, maintaining adequate oxygenation and ventilation, and, in case of cardiopulmonary collapse, performing surgical embolectomy.
Contrast media reactions may be allergic or nonallergic in nature. Allergic reactions manifest as generalized flushing, hives, hypotension, and bronchospasm. Treatment consists of supportive measures of airway, breathing, and circulation and pharmacologic therapy in the form of epinephrine, 0.5 to 1 mg i.v. or 3 to 5 mL intratracheally of 1:10,000 solution; hydrocortisone, 100 mg i.v. every 6 hours; and diphenhydramine, 25 to 50 mg i.v. every 4 to 6 hours. Nonallergic reactions occur due to the sheer volume of the contrast dye, which may lead to congestive heart failure in susceptible patients or to osmotic diuresis, which may lead to fluid and electrolyte imbalances in patients who are already hypovolemic due to diuretic therapy and/or restricted salt and water intake.
Cerebral hyperperfusion syndrome may occur in areas surrounding large AVMs due to diversion of blood flow to the AVM. These hypoperfused areas lose their ability to autoregulate blood flow and are usually maximally vasodilated. Following embolization, the large amount of blood flow flowing through the erstwhile AVM is now shunted back to these maximally dilated vessels leading to cerebral hyperemia, edema, and/or hemorrhage. Methods to prevent this sudden increase in blood flow include deliberate hypotension, pretreatment with barbiturates, clamping of the cervical carotid artery, and staged embolization of the feeding vessels to allow the surrounding tissues to regain their autoregulatory function. Pharmacologic treatment of cerebral edema includes administration of furosemide, 0.1 to 1 mg/kg i.v., and mannitol, 0.25 to 1 g/kg i.v. over 20 minutes.
Complications due to materials used for embolization. Glues such as normobutyl cyanoacrylate (NBCA) and isobutyl 2-cyanoacrylate may cause pulmonary complications manifesting as hemoptysis and pleural pain. Particulate materials such as polyvinyl alcohol (PVA), silicon beads, silk, steel and platinum microcoils, Gelfoam, and collagen may cause pulmonary or systemic embolism. Also, PVA is known to increase the risk of recanalization of the embolized AVM.

VIII. Complications after carotid endarterectomy (CEA)

Cardiac ischemia and infarction are the leading cause of mortality after CEA. Coronary artery disease is common among patients undergoing CEA. Perioperative tachycardia, hypertension, and hypotension increase the risk of perioperative myocardial ischemia and infarction. The alpha-agonists, such as phenylephrine, are preferable in the treatment of hypotension in this setting because they raise blood pressure without significantly increasing heart rate. However, the ensuing hypertension may be detrimental. Combined alpha- and beta-agonists such as ephedrine increase heart rate and have been associated with myocardial ischemia and infarction in this setting.
Occlusion of the operated carotid artery should be suspected whenever new neurologic symptoms develop postoperatively. This is one cause of postoperative cerebral ischemia that is amenable to surgical intervention. Early diagnosis and treatment significantly alter outcome. A Doppler flow study can detect cessation of flow in the involved vessel, and angiography can confirm vascular occlusion. Surgical reexploration need not await angiographic confirmation but may be undertaken on the basis of the clinical picture and the ultrasound examination.
The cerebral hyperperfusion syndrome may develop after CEA due to the sudden increase in CBF in a maximally dilated vascular bed that has lost its ability to autoregulate because of longstanding hypoperfusion. This hyperperfusion may lead to cerebral edema or hemorrhage with headache, seizures, decreased level of consciousness, and focal neurologic deficit. Severe carotid stenosis and hypertension contribute to the development of this syndrome. Careful control of blood pressure is essential in preventing hyperperfusion. Mild elevation of blood pressure need not be treated in the postoperative period, whereas moderate to severe hypertension should be reduced to avoid the cerebral hyperperfusion syndrome. Titratable, short-acting agents such as sodium nitroprusside (SNP), 0.25 to 8 mcg/kg/minute i.v., and esmolol, loading dose 500 mcg/kg over 1 minute followed by 50 to 300 mcg/kg/minute i.v., are preferable in this setting. The beta-blocking effects of esmolol offset the sympathetic hyperactivity from SNP.
Hypotension is poorly tolerated by hypertensive patients who have a rightward shift in their autoregulatory curve. Hypotension can lead to cerebral and cardiac hypoperfusion and can increase the risk of thrombus formation in the operated vessel. Blood pressure is usually kept at 20% above baseline. Hypotension is treated with volume expansion and infusion of a short-acting alpha-agonist such as phenylephrine, 40 to 180 mcg/minute i.v., mixed as 20 mg in 250 mL D5W at 30 to 160 mL/hour.
Treatment of stroke after CEA consists of blood pressure management, supportive care, and treatment of complications. Intravenous thrombolytic therapy is contraindicated in the postoperative period. Intra-arterial thrombolytic therapy may be considered in institutions that have the expertise. Neuroprotective therapy, still the subject of clinical trials, has not been approved for clinical use.
Airway obstruction can result from hematoma formation and can be aggravated by laryngeal edema and cranial nerve injury. Reestablishing airway patency might require suture removal and drainage of the hematoma. This is best accomplished by a surgeon in conjunction with tracheal intubation and racemic epinephrine. If the patient is in extremis, the first person to reach the bedside opens the wound to secure the airway.

IX. Complications after vertebral column procedures

Complications after anterior cervical discectomy. The patient's trachea is usually extubated in the operating room after an uncomplicated discectomy. However, tracheal intubation may be maintained postoperatively if upper airway edema is anticipated after a prolonged operation or one associated with infusion of large volumes of fluid. It is important to prevent the patient from coughing and straining while the trachea is intubated. This may cause the newly placed bone graft to dislodge, which might compress the trachea or the esophagus and require reoperation. After extubation, the patient's voice is evaluated to detect recurrent laryngeal nerve injury, a benign complication that usually resolves over days to weeks.
Complications after cervical corpectomy and stabilization. These procedures are usually more invasive, more prolonged, associated with more fluid administration, and therefore more likely to cause airway edema at the conclusion of surgery. The patient's trachea usually remains intubated until the airway edema resolves, as evidenced by the ability of the patient to breathe around the endotracheal tube after the cuff has been deflated. Sedation is provided as needed while the trachea is intubated.
Complications after transoral resection of the odontoid and occipitocervical fusion. This operation is usually performed in two steps: anterior transoral resection of the odontoid and posterior occipitocervical fusion. Airway management involves either tracheotomy or an oral endotracheal tube draped out of the surgical field as for tonsillectomy. The procedure is associated with significant posterior pharyngeal swelling, which requires postoperative intubation for several days. The patient is usually awakened at the conclusion of surgery to undergo a neurologic examination and then sedated again. The degree of resolution of the airway edema is evaluated by deflating the cuff of the endotracheal tube and establishing the ability of the patient to breathe around the endotracheal tube.
Complications after posterior cervical spine procedures. Complications are related to the patient's intraoperative position and the degree of airway edema and respiratory dysfunction at the conclusion of surgery.
The operative positions include prone, sitting, and three-quarters prone. Complications of the prone position include injury at pressure points: eyes, cheeks, lips, breasts, and genitalia. Injury to these structures requires appropriate surgical consultation.
Airway edema depends on the duration of surgery, the amount of blood loss, and fluid administration.
Respiratory dysfunction may exist preoperatively due to involvement of C3-C5 nerve roots or may result from resection of intramedullary spinal cord tumors. These patients are evaluated before extubation to demonstrate the patency of the airway (lack of airway edema) and adequacy of respiratory function (tidal volume, vital capacity, negative inspiratory force). Postoperative intubation and mechanical ventilation might be required until airway edema resolves and respiratory function recovers.
Complications after scoliosis surgery. These procedures are performed with the patient in the prone or lateral position or a combination of a lateral-position operation followed immediately or 1 to 2 weeks later by a prone-position operation.
Complications related to the prone position are those of pressure point injury, particularly the eyes. Ischemic optic neuropathy (ION) is correlated with intraoperative hypotension and ischemia, regardless of position. Central retinal artery occlusion can occur during prone-position procedures due to improper protection of the eyes. Scoliosis surgery patients are therefore particularly vulnerable to ION, which is manifest postoperatively by varying degrees of unilateral or bilateral decreases in visual acuity or defects in the visual field. The decrease in visual acuity may resolve over time, but the defects in the visual field usually persist. Postoperative visual examination is performed routinely in these patients; ophthalmologic consultation is requested if any abnormality is detected.
Patients with scoliosis may have respiratory dysfunction preoperatively due to skeletal deformities, muscular weakness, central nervous system (CNS) dysfunction, or a combination of factors. This respiratory dysfunction might be aggravated postoperatively by the residual effect of anesthetics, inadequate reversal of muscle relaxants due to hypothermia, restrictive effect of pain, and pneumothorax. Airway edema from positioning, prolonged surgery, and administration of a large volume of fluids contributes to the respiratory compromise. Extubation of the trachea is undertaken only after airway patency and adequacy of respiratory function have been established. Pain control is essential for patient comfort and the maintenance of adequate respiratory function.
Postoperative hemorrhage can continue either externally from surgical drains or internally into the operative site. Monitoring of systemic blood pressure, urinary output, central venous pressure (if available), hemoglobin, and hematocrit is necessary. Excessive blood loss is treated with volume expansion, blood transfusion, hemodynamic support, and surgical consultation.
Central and peripheral neurologic function is monitored postoperatively. Patients might develop spinal cord injury due to instrumentation or hematoma formation and CNS dysfunction due to pharmacologic or hemodynamic factors. Neurologic dysfunction should prompt a thorough examination of the patient, review of medication, hemodynamic and laboratory workup, surgical consultation, and supportive therapy as needed.
Complications after lateral extracavitary and percutaneous endoscopic procedures. A factor common to these two operations is the intraoperative use of double-lumen endotracheal tubes or other forms of one-lung ventilation. Pulmonary edema may develop with reexpansion of the lung after one-lung ventilation for >3 hours, most likely within 1 hour of reexpansion. If mechanical ventilation is to be maintained in the postoperative period, the double-lumen tube is exchanged for a single-lumen one. Alternatively, a univent tube, which is a single-lumen tube with a movable endobronchial blocker, may be used intraoperatively and postoperatively during weaning and until extubation.

X. Complications after spinal cord procedures

Complications after syringomyelia repair. Respiratory complications are the main concern. Preoperative respiratory dysfunction is due to skeletal deformities, autonomic dysfunction, and chronic aspiration (from depressed gag reflex and vocal cord paralysis). This respiratory dysfunction may be exacerbated in the postoperative period by airway edema, residual anesthetic effects, and incomplete reversal of muscle relaxants, which could be aggravated by the hypothermia of autonomic dysfunction. Extubation is performed only after the adequacy of respiratory function and airway patency have been established. Respiratory monitoring and support are maintained in the postoperative period as needed.
Complications after resection of spinal cord tumors. Significant cord edema may develop up to 24 hours after resection. The edema-induced respiratory dysfunction associated with the resection of upper cervical cord tumors might not become apparent in the immediate postoperative period. Respiratory monitoring of these patients in an intensive care setting for at least 24 hours postoperatively is therefore necessary.
Complications after spinal cord injury. Patients with spinal cord injury develop complications related to sympathectomy, skeletal muscle denervation, immobilization, chronic instrumentation, decreased respiratory force, and coexisting injuries involving other organs. Approximately 50% of patients with cervical spine injury have concurrent head trauma and approximately 25% have injuries to the chest, abdomen, or extremities.
The severity and mechanism of the initial spinal shock, which lasts for 2 to 3 weeks after injury, are related to the level of the injury. With mid-thoracic lesions (T6-7), hypotension may not be severe and is mainly due to vasodilatation. With higher lesions (T4 or above), hypotension may be profound when vasodilatation is added to a decrease in heart rate, contractility, and compliance from loss of cardiac accelerator fibers (T1-4).
Succinylcholine may cause hyperkalemia in patients who have denervated muscle because of the increased number and sensitivity of their neuromuscular cholinergic receptors. These receptor changes start 3 days after the injury and persist for 6 to 8 months. Succinylcholine is therefore avoided in spinal cord injury patients from 48 hours to 8 months after the injury.
Autonomic hyperreflexia is caused by noxious stimulation below the level of the lesion in a patient with a sympathectomy at or above T6.
1. The risk of autonomic hyperreflexia is highest during the fourth week after injury but continues thereafter. At this time, while the patient is recovering from the spinal shock phase, which lasts for 2 to 3 weeks after the initial injury, the flaccid paralysis changes to spastic paralysis because of the absence of the effect of central inhibitory pathways. The efferent sympathetic fibers recover from the initial injury but remain unaffected by central inhibitory input from the brain stem and hypothalamus.
2. The severity and manifestations of autonomic hyperreflexia are affected by the level of the sympathectomy. With mid-thoracic lesions below the level of cardiac accelerator fibers, hypertension is accompanied by reflex bradycardia transmitted via cardiac accelerator fibers and the vagus. In patients whose sympathectomy is above the level of the thoracic cardiac accelerator fibers, tachycardia may occur because cardiac accelerator fibers become part of the efferent sympathetic activity rather than part of the central inhibitory input from the brain stem and hypothalamus. Arrhythmias and occasionally heart block may accompany changes in heart rate. Clinical manifestations of autonomic hyperreflexia include vasodilatation, decreased sympathetic activity, and increased vagal activity above the level of the lesion such as nasal congestion, flushing, headache, dyspnea, nausea, and visceral muscle contraction. Vasoconstriction and increased sympathetic activity below the level of the lesion cause vasoconstrictive pallor, sweating, piloerection, and somatic muscle fasciculation. Patients also develop hypertension with headache, blurred vision, myocardial infarction, and retinal, subarachnoid, and cerebral hemorrhages that may lead to syncope, convulsions, and death.
3. Autonomic hyperreflexia may be prevented or attenuated by regional or deep general anesthesia, but this is usually impractical in the postanesthesia care unit. Pharmacologic means of preventing and treating autonomic hyperreflexia include alpha-blockers such as diazoxide, 1 to 3 mg/kg i.v. every 5 minutes up to 150 mg, or phentolamine, 5 mg i.v. increments, vasodilators such as SNP, 0.25 to 8 mcg/kg/minute i.v., and selective beta-blockers such as esmolol, loading dose 500 mcg/kg followed by 50 to 300 mcg/kg/minute i.v., for supraventricular tachycardia.