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Neurosurgical and Neurologic Emergencies 

Neurosurgical and Neurologic Emergencies
Chapter:
Neurosurgical and Neurologic Emergencies
Author(s):

Kellie A. Park

DOI:
10.1093/med/9780199377275.003.0007
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date: 26 October 2020

Autonomic Hyperreflexia or Dysreflexia

Definition

An abrupt and profound autonomic discharge from sympathetic neurons caused by stimulation, such as distention of hollow viscous, distal to the level of a spinal cord injury resulting in severe hypertension and an impending medical emergency.

Presentation

  • In an awake patient, autonomic hyperreflexia causes an abrupt onset of headache and visual changes, such as blurred vision or scotoma, consistent with a rapid and significant elevation in blood pressure.

  • Elevated blood pressure may cause a reflex baroreceptor-mediated bradycardia.

  • In either an asleep or awake patient, skin erythema, diaphoresis, and/or piloerection above the dermatome of spinal injury may also occur.

Pathophysiology

As little as 2 weeks after injury to the spinal cord, descending control of preganglionic sympathetic neurons below the level of injury is lost. Uninhibited spinal circuits can then produce massive sympathetic discharge after stimulation from bladder distention, bowel distention, or skin incision. The discharge causes release of catecholamines, dramatically elevated blood pressure, and reflex bradycardia in 50% to 70% of individuals with cord injury at or above T6. Spinal anesthesia can decrease the risk of sympathetic discharge.

Differential Diagnosis

  • Light anesthesia

  • Untreated chronic hypertension

  • Pheochromocytoma

Immediate Management

  • Place patient in the head-up position if possible.

  • Immediately discontinue surgical stimulation and release the pressure in a distended hollow viscus (e.g., empty the bladder)

  • If the patient is awake, direct him or her to “bite and swallow” a nifedipine capsule.

  • In the anesthetized patient, deepen anesthesia and consider beginning intravenous nitroglycerine (20–40 mcg bolus at 3- to 5-minute intervals or 0.5 mcg/kg/min) or nitroprusside (3–4 mcg/kg/min titrated to effect up to 10 mcg/kg/min) to rapidly treat dangerous systolic hypertension.

Subsequent Management

If subsequent procedures are required, prophylaxis may be indicated. Oral therapy with prazosin (1–3 mg by mouth two or three times per day) or phenoxybenzamine (10–40 mg by mouth two or three times per day) may reduce the risk for later events.

Risk Factors

  • Spinal cord injury above T6 with distension of hollow viscous

  • Male gender (four times more likely than females)

Prevention

If feasible, spinal anesthesia with local anesthetic can be used to prevent sympathetic discharge with stimulation.

Further Reading

Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC, Ortega J, eds. Clinical anesthesia. 7th ed. Philadelphia: Lippincott Williams & Wilkins; 2013:1024.Find this resource:

Bycroft J, Shergill IS, Chung EA, Arya N, Shah PJ. Autonomic dysreflexia: a medical emergency. Postgrad Med J. 2005; 81(954): 232–235.Find this resource:

Intracranial Hypertension

Definition

Intracranial hypertension (ICH) in adults is defined as an elevation in ICP >15 mm Hg. Values above 20–25 mm Hg generally require intervention to reverse symptoms and restore cerebral perfusion. Sustained values >25 mm Hg cause significant injury, and values >40 mm Hg are life threatening. In general, normal values are considered to be 10–15 mm Hg for adults, 4–7 mm Hg for young children, and 1.5–6 mm Hg for full-term infants.

Presentation

  • In the awake patient, symptoms include headache, visual changes, nausea, and vomiting.

  • As ICH is sustained or increases, alterations in mental status, with confusion and decreased responsiveness occur.

  • Cushing’s triad of elevated blood pressure, reflex bradycardia, and irregular respiration can be observed with ICH and are late and ominous signs.

  • Papilledema can be observed with ICH, but its absence does not rule out the presence of ICH.

  • Pupillary dilation unreactive to light and decorticate posturing are associated with brain herniation; they are late and ominous signs.

Pathophysiology

Intracranial contents consist of brain tissue, cerebrospinal fluid (CSF), and blood contained within the non-compliant skull. Because the noncompliant skull does not allow for significant increases in volume, any increase in volume can increase pressure, causing ICH. Physiologic causes include increased abdominal or thoracic pressures (e.g., a Valsalva maneuver), head down position, seizure, hypoventilation, and some drugs (e.g., high-dose potent volatile anesthetics). Pathologic causes include intracranial hemorrhage, cerebral edema, tumor, and disturbances in CSF production, flow, or absorption. The rate at which the volume of blood, tissue, or CSF changes is critical. When the volume of one component changes rapidly, there is less time for compensation. Therefore, rapid changes are tolerated poorly. Very high ICP may ultimately cause herniation, in which parenchyma is displaced across the falx cerebri, the tentorium cerebelli, or the foramen magnum. Herniation generally occurs late and is associated with poor prognosis.

Differential Diagnosis

  • Headache of other etiology

  • Drug intoxication

  • Idiopathic intracranial hypertension (pseudotumor cerebri)

Immediate Management

  • Determine whether circulatory support and airway management are needed. (Patients with ICH may be unable to control their airway.)

  • Place the patient in the “head up” position of 30°–40° and facing straight ahead to prevent jugular venous occlusion.

  • Administer mannitol 20% 0.5–1.0 g/kg IV or hypertonic saline (3%–7.2% with total of 7–9 g given over 30 minutes to 1 hour) to decrease brain water content and ICP.

  • Control systemic blood pressure with phenylephrine (50–100 mcg boluses at 1- to 2-minute intervals or 100 mcg/min infusion), ephedrine (5–10 mg boluses), or labetolol (10-mg boluses at 1- to 2-minute intervals) to with a goal cerebral perfusion pressure of 60–70 mm Hg.

  • Provide sedation and analgesia as appropriate. Note: Reversible or short-acting drugs are preferred. Monitor the patient for signs of respiratory depression.

  • Control fever if present.

  • If ICH continues, intubate the trachea and initiate mechanical ventilation to induce mild cerebral vasoconstriction and reduce ICP as a bridge to definitive surgical treatment.

  • Consider seizure prophylaxis (e.g., Levetiracetam. Loading dose is 10 mg/kg IV over 15 minutes).

  • Maintain close communication with the neurosurgical team regarding imaging results and need for invasive intracranial pressure (ICP) monitoring, CSF drainage, or emergency craniotomy.

Diagnostic Studies

  • Computed tomography (CT) scan to diagnose surgical causes (e.g., hematoma, tumor), assess ventricular size, compression of basal cisterns, mass effect, edema.

  • Invasive ICP monitoring

  • Lumbar puncture to measure opening pressures (if CT scan shows absence of mass effect)

  • Note: Diagnostic studies should delay an urgent surgical intervention; coagulation panel should be obtained if immediate reversal of anticoagulation medications is required.

Subsequent Management

  • Identify and correct the underlying cause of ICH. Obtain a neurosurgical consultation if imaging is suggestive of a surgically correctible etiology.

  • Control blood glucose to avoid hypoglycemia and hyperglycemia to improve outcomes.

  • If required, administer continued ventriculostomy drainage and ICP monitoring.

Risk Factors

  • Intracranial hemorrhage

  • Severe serum hyponatremia or hypo-osmolality causing edema

  • Malignancy: primary or metastatic

  • Traumatic injury

  • Hydrocephalus

  • Infection (e.g., brain abscess)

  • Congenital anomalies

Special Considerations

  • Rapid recognition and initiation of treatment is critical for improving neurologic outcome in patients with ICH.

Further Reading

Rangel-Castillo L, Gopinath S, Robertson CS. Management of intracranial hypertension. Neurol Clin. 2008; 26(2): 521–541.Find this resource:

Ruskin, KJ, Rosenbaum SH, Rampil IJ, eds. Fundamentals of neuroanesthesia. 1st ed. Stony Brook, NY: Oxford University Press; 2014:16–25.Find this resource:

Spinal Cord Injury

Definition

Damage to spinal tissue caused by trauma, ischemia, hematoma, tumor, or other insult that causes temporary or lasting loss of sensory, motor, and/or autonomic function. The clinical signs and symptoms depend on the type and level of cord injury, ranging from paresthesias to complete sensory, motor, and autonomic paralysis.

Presentation

  • Quadraplegia with incomplete or complete loss of motor function is caused by a lesion at the level of the cervical spinal cord. Patients with C3 injury or above almost always require airway management and mechanical ventilation; C3-5 injuries vary in the degree of phrenic nerve paralysis.

  • Paraplegia with incomplete or complete loss of motor function of legs, torso, or pelvic organs is caused by injury to the thoracic cord. Motor function of the arms is preserved. Higher thoracic level injuries (T8 and above) may cause weakened intercostal muscles and affect coughing ability.

  • Neurogenic shock from loss of autonomic input from the thoracic spine causes hypotension, bradycardia, and hypothermia.

  • Spinal shock with loss of reflexes and motor function below the level of injury.

  • Anterior spinal artery syndrome presents with loss of pain and temperature with preservation of vibration, touch, and proprioception due to interruption of blood flow through the anterior spinal artery.

  • Brown-Sequard syndrome is defined as ipsilateral loss of motor function, vibration, touch, and proprioception with contralateral loss of tempterature and pain sensation secondary to hemi-cord injury.

  • Cauda equina syndrome presents with loss of bowel and bladder control and leg weakness cause by compression of the bundle of lumbosacral nerve roots.

  • Central cord syndrome presents with loss of motor function in the upper extremities greater than loss in lower extremities, and a variable loss of sensory function below the level of injury secondary to injury of the central portion of the spinal cord.

Pathophysiology

Primary injury to the spinal cord can be caused by compression, transection, or traction from hematoma, disk subluxation, hyperextension, or fractures of bony elements in the spinal column. Secondary injury results from interruption of vascular supply and tissue ischemia from edema and inflammation after the primary injury. Secondary injury may cause the injury to involve to higher cord levels, resulting in an evolving group of signs and symptoms. Injuries are divided into five classes based on impairments:

  • Complete transection with no sensory or motor function preserved in sacral segments S4-S5

  • Incomplete preservation of sensory but not motor function below the injured level, including sacral segments S4-S5

  • Incomplete preservation of motor function below the injured level with more than half of the muscles below the injury with strength <3/5

  • Incomplete preservation of motor function below the injured level with more than half of muscles below injury with strength ≥3/5

  • Sensory and motor function are not impaired.

Differential Diagnosis

  • Soft tissue injury of neck causing muscle spasm

  • Conversion motor paralysis disorder

Immediate Management

  • Assess the patient’s airway, breathing and circulation. Note: If intubation of the trachea is indicated in a patient with a cervical spine injury, a technique that maintains spinal alignment (e.g., in-line cervical spine stabilization or fiberoptic intubation) must be used.

  • Avoid hypoxemia; provide supplemental oxygen as required.

  • Rapidly examine the patient to identify additional life-threatening injuries.

  • Treat hypotension caused by neurogenic shock with vasopressors, phenylephrine (50- to 100-mcg boluses at 1- to 2-minute intervals or 100 mcg/min infusion), or ephedrine (5- to 10-mg boluses). This condition is relatively resistant to fluid resuscitation.

  • Administer steroids, such as methylprednisolone (30 mg/kg IV followed 5.4 mg/kg/h for 24 hours). This has been shown to reduce cord edema and improve outcome. Note: The specific protocol to be used should be discussed with the neurosurgery team if possible.

  • Therapeutic hypothermia is not recommended at this time.

  • Maintain close communication with the neurosurgical team regarding imaging results and the need for emergency surgical decompression.

Diagnostic Studies

  • Rapid total body CT to diagnose cord injury and other associated injuries; CT images are reformatted to assist in immediate diagnosis of injuries to vertebral column and spinal cord.

  • Depending on the stability of the patient, magnetic resonance imaging is useful to assess soft tissue and cord injury.

  • Note: Diagnostic studies should not delay emergency surgical intervention.

Subsequent Management

  • If subsequent procedures requiring anesthesia are needed, avoid succinylcholine in the period 24–72 hours after injury to avoid the development of life-threatening hyperkalemia.

  • Begin venous thromboembolism prophylaxis.

  • Pressure ulcer prophylaxis to prevent decubitus ulcers.

  • Consider management to prevent neuropathic pain when the patient is stable.

  • Control hypothermia.

Risk Factors

  • Male gender

  • Younger age

  • Risk-taking behavior

  • Elderly patients with increased risk for falling

Prevention

Avoid risk-taking behaviors. Modify risks in elderly with significant potential to fall.

Further Reading

Bonner S, Smith C. Initial management of acute spinal cord injury. Cont Educ Anaesthes Crit Care Pain. 2013.Find this resource:

Bracken MB. Steroids for acute spinal cord injury. Cochrane Database Syst Rev. 2012; Jan 18; CD001046.Find this resource:

Maynard FM, Bracken MB, Creasey G, et al. International standards for neurological and functional classification of spinal cord injury. Spinal Cord. 1997; 35: 266–274.Find this resource:

Miko I, Gould R, Wolf S, Afifi S. Acute spinal cord injury. Int Anesthesiol Clin. 2009; 47(1): 37–54.Find this resource:

Subarachnoid Hemorrhage

Definition

Subarachnoid hemorrhage (SAH) is a cerebrovascular accident in which bleeding occurs into the subarachnoid space. Extravasation of blood into the CSF can be caused by trauma or from nontraumatic bleeding of vascular defects, such as arteriovenous malformation (AVM) or from an arterial aneurysm.

Presentation

  • Sudden onset, severe, “thunderclap” headache is a classic sign of SAH. “Worst headache of my life.”

  • Nausea and vomiting are common.

  • Confusion or agitation, decreased level of responsiveness, or transient loss of consciousness may occur.

  • Nuchal rigidity may be present.

  • Photophobia and seizure may occur.

  • Hypertension and elevated temperature are common signs.

  • Focal deficits from ischemia, such as cranial nerve palsy, may occur.

Pathophysiology

Seventy to eighty-five percent of SAH events are secondary to aneurysmal bleeding, with the remainder of events caused by AVM, tumor, infection, or trauma. Arterial bleeding can rapidly increase ICP, potentially causing devastating neurologic impairment.

Differential Diagnosis

  • Headache of other etiology

  • Tumor

  • Infection or abscess

Immediate Management

  • Assess the patient’s airway, breathing, and circulation. Intubate the trachea and initiate mechanical ventilation if indicated.

  • Obtain large-bore peripheral IV access and insert an intra-arterial catheter for blood gas analysis and continuous blood pressure monitoring

  • Stabilize the blood pressure to achieve a CPP 60–70 mm Hg using vasopressors (e.g., phenylephrine 0.5- to 1-mcg/kg/minute infusion or 100-mcg boluses) or intravenous short-acting beta blockers (e.g., labetalol) and/or calcium channel blockers (e.g., nicardipine; starting dose 5 mg/hour).

  • Consider moderate hypocapnia (PaCO2 25–30 mm Hg) to reduce ICP until definitive treatment is achieved. Note: Hypercapnia decreases cerebral blood flow and worsens cerebral ischemia. This should only be used as a bridge to definitive treatment (e.g., surgical decompression).

  • Maintain euvolemia.

  • Mild hypothermia is not indicated and does not improve neurologic outcome.

  • Request a consultation from the neurosurgical team to plan definitive therapy, which may include intravascular therapy (i.e., coiling or embolization) or surgical management (i.e., aneurysm clipping or AVM resection).

Diagnostic Studies

  • Computed tomography scan without contrast, CT angiography: The Fisher grading scale, which describes the amount of blood observed on CT, helps to predict the occurrence of cerebral vasospasm.

  • Plasma electrolytes, complete blood count, coagulation profile, arterial blood gas analysis

  • Blood type and cross-match

  • Direct intravascular angiography

  • Electrocardiogram (often reveals repolarization abnormalities)

  • Note: Diagnostic studies should not delay urgent surgical intervention.

Subsequent Management

  • Close monitoring of neurologic status is imperative because re-bleeding may occur and carries a poor prognosis.

  • If vasospasm occurs, consider treatment with prophylaxis with nimodipine (60 mg by mouth or via nasogastric tube every 4 hours for 21 days), hypertensive hypervolemic hemodilution (“triple-H” therapy). Intravascular angioplasty, or stenting also should be considered.

  • A ventricular drain may be required for patients who develop obstructive hydrocephalus after SAH.

  • Additional management is guided by systemic complications, which catecholamine-induced cardiac abnormalities (e.g., dysrhythmia, myocardial infarction, heart failure), pulmonary hypertension and edema, and electrolyte disturbances (e.g., hyponatremia caused by syndrome of inappropriate anti-diuretic hormone [SIADH]).

Risk Factors

  • Uncontrolled hypertension

  • Smoking

  • Alcohol use

  • Family history of aneurysm

Special Considerations

  • Subarachnoid hemorrhage accounts for approximately 10%–15% of all strokes. Intraparenchymal hemorrhage is not considered SAH. The majority of aneurysms are not familial, but are instead associated with risk factors of uncontrolled hypertension, alcohol use, and smoking. Most ruptures are spontaneous. Sites of rupture are well defined, most commonly at the anterior communicating arteries, followed by posterior communicating/internal carotid arteries, then followed by the middle cerebral artery. The Hunt and Hess scale and the grading system of the World Federation of Neurological Surgeons are both acceptable predictors of morbidity and mortality after SAH. Vasospasm is a common and devastating complication after SAH.

Further Reading

Molyneux AJ, Kerr RS, Yu LM. International subarachnoid aneurysm trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomized comparison of effects on survival, dependency, seizures, rebleeding, subgroups. Lancet. 2005; 366: 809–817.Find this resource:

Priebe H. Aneurysmal subarachnoid haemorrhage and the anaesthetist. BJA. 2007; 99: 102–118.Find this resource:

Rosen DS, Macdonald RL. Subarachnoid hemorrhage grading scales: a systematic review. Neurocrit Care. 2005; 2: 110.Find this resource:

Traumatic Brain Injuries: Closed and Open Traumatic Injuries

Definition

An acute traumatic injury to the head and skull carrying a sudden concussive or shearing force transmitted to brain tissue. In addition to traumatic force, open traumatic injuries also involve fractures or penetration of the skull.

Presentation

  • Head injuries are widely variable in severity, mechanism, and presentation, depending on the nature of the injury sustained.

  • In the awake patient, one may elicit a history of sudden impact or acceleration/deceleration injury, followed by brief loss of consciousness. Other symptoms may include amnesia, confusion, headache, photophobia, or hemiparesis.

  • Individuals may exhibit lethargy or decreased responsiveness, with decreased pupillary light reflex.

  • Post-traumatic seizures may be present.

  • Patients with severe injuries may present with cardiovascular instability, including bradycardia, other dysrhythmia, and hypotension.

  • Epidural hematomas are associated with a severe head impact. The classical presentation consists of a brief loss of consciousness, followed by a lucid interval, followed by rapid progression to decreased level of consciousness and coma.

  • Subdural hematomas, traumatic subarachnoid hemorrhage, and intraparynchymal hemorrhage each can result from traumatic injuries, but typically do not have a lucid interval.

Pathophysiology

Traumatic brain injury is widely variable in type, severity, and associated injuries. Primary injury includes direct injury of brain parenchyma from contusion, shearing, or penetrating injury from bone or foreign body. Secondary injury is defined as tissue damage that is caused by ischemia, edema, and inflammation that leads to transient or more permanent brain dysfunction. Secondary injury is exacerbated by vascular injury, hypoventilation, and associated cardiovascular events with or without intracranial hypertension (ICH).

Differential Diagnosis

  • Rupture of pre-existing arteriovenous malformation or aneurysm

  • Chronic subdural hematoma

Immediate Management

  • Assess the patient’s airway, breathing, and circulation. Intubate the trachea and initiate mechanical ventilation if indicated. Note: If intubation of the trachea is indicated in a patient with a cervical spine injury, a technique that maintains spinal alignment (e.g., in-line cervical spine stabilization or fiberoptic intubation) must be used.

  • Provide supplemental oxygen if needed to avoid hypoxemia.

  • Rapidly examine the patient to identify additional life-threatening injuries.

  • Resuscitate the patient with normal saline or, if indicated, blood products. (Note: If massive transfusion is indicated for other injuries, consider infusing packed red blood cells, platelets, and fresh-frozen plasma in a 1:1:1 ratio.)

  • The cerebral perfusion pressure should be at least 60 mm Hg. Use vasopressors as necessary to achieve this goal (e.g., phenylephrine 100 mcg IV bolus or 0.5–1 mcg/kg/min). If ICH is suspected, increase the systemic blood pressure as needed to maintain CPP.

  • Administer mannitol 0.5–1.0 g/kg if ICH is suspected in the absence of disruption of blood-brain barrier.

  • If required, adjust mechanical ventilation to maintain PaCO2 30–35 mm Hg.

  • Request a consultation from the neurosurgic team to plan definitive therapy, including the need for ICP monitoring, CSF drainage, or emergency craniotomy.

Diagnostic Studies

  • Plasma electrolytes, complete blood count, coagulation profile

  • Arterial blood gas analysis as necessary to guide ventilator management

  • Computed tomography of the brain with and without contrast; cervical spine CT (to rule out concomitant cervical spine injury)

  • Worsening symptoms or level of critical illness will guide the clinician’s need for further diagnostic studies.

  • Note: Diagnostic studies should not delay urgent surgical intervention.

Subsequent Management

  • Continue supportive care.

  • Periodically re-evaluate the patient for injury progression; changes in neurologic status guide diagnostic studies and surgical referral.

  • Consider insertion of a ventriculostomy catheter to facilitate CSF drainage and control of ICH.

  • If appropriate, early referral to rehabilitation offers the patient the best chance for improvement of neurologic deficits resulting from the injury.

Risk Factors

  • Younger age and male gender

  • Pre-existing coagulopathy increases risk of delayed neuronal deficits.

  • Age >60 years increases risk of SDH.

Prevention

Avoidance of risk-taking behavior

Special Considerations

  • Suspect ICH if the patient has an altered mental status or symptoms such as headache, nausea, vomiting, or visual changes.

  • Suspect an epidural hematoma if the patient presents with a depressed skull fracture in the temporal-parietal region with trauma to the middle meningeal artery.

  • Subdural hematomas are classified as acute or chronic; acute hemorrhage is more likely to progress quickly to ICH and neurological deterioration. A chronic subdural hematoma progresses more slowly and is less likely to result in acute changes in ICP.

  • Glucose-containing solutions should be avoided to reduce hyperglycemia, which is associated with poorer outcomes.

  • Guidelines for surgical decompression include midline shift >5 mm, fixed pupils, ICP >20 mm Hg, hematoma thickness >1 cm, or severe mental status impairment.

  • High-dose corticosteroids and mild hypothermia have not been shown to improve outcomes and are not indicated.

  • Progesterone holds promise for improving neurologic outcome following traumatic brain injury, but is still considered experimental at this time.

Further Reading

Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of Neurological Surgeons. Guidelines for the management of severe traumatic brain injury. J Neurotrauma. 2007; 24(Suppl 1): S1–S106.Find this resource:

Gravel JL, D’Angelo A, Carrière B, Crevier L, Beauchamp MH, Chauny JM, Wassef M, Chaillet N. Interventions provided in the acute phase for mild traumatic brain injury: a systematic review. Syst Rev. 2013; 2: 63.Find this resource:

Ma J, Huang S, Qin S, You C. Progesterone for acute traumatic brain injury. Cochrane Database Syst Rev. 2012; 10.Find this resource:

Venous Air Embolism

Definition

Venous air embolism (VAE) is an iatrogenic, potentially life-threating emergency caused by the entrainment of atmospheric air into the systemic venous system.

Presentation

  • In an awake patient, such as during central line placement, early signs include coughing, chest pain, and possibly new neurologic deficits.

  • If air is entrained slowly, subtle changes in vital signs may be observed, including hypotension, tachycardia, or bradycardia. In a mechanically ventilated patient, peak airway pressure may be increased. Hypoxia may be seen on pulse oximetry or arterial blood gas analysis; hypercarbia may be noted on arterial blood gas analysis.

  • If a large volume of air is entrained, an abrupt decrease in end-tidal CO2 will be observed, coupled with an increase in PaCO2.

  • Dysrhythmias, myocardial ischemia, right heart strain, and cardiovascular collapse may occur if significant air enters circulation.

  • The surgeon may note the presence of gas bubbles in the arterial blood supply.

Pathophysiology

During a surgical procedure or after trauma, veins are exposed allowing communication between the atmosphere and circulation. Air typically enters the venous circulation through open venous structures above the level of the heart. Air trapped in the right heart and pulmonary vasculature may then cause an “air-lock” and cardiovascular collapse as venous return decreases, or air may travel into the systemic circulation through right-to-left shunting in the heart, causing cerebral or myocardial ischemia.

Differential Diagnosis

  • Tension pneumothorax

  • Thrombotic pulmonary embolism

  • Ventricular dysrhythmia or myocardial infarction of other etiology

Immediate Management

  • Alert the surgeon to the suspected diagnosis of VAE. Ask him or her to flood the field with saline to inhibit further air entrainment.

  • Increase FiO2 to 100%.

  • If possible, place the patient in the head down (Trendelenburg) position.

  • Support blood pressure with vasopressors (e.g., phenylephrine) or inotropes as needed.

  • Administer isotonic crystalloid fluids to support blood pressure and increase right atrial pressure.

  • If possible, moving the patient to the left-lateral decubitus position may relieve the air-lock in the right heart.

  • If available, aspiration of air through a single- or multi-orifice catheter may decrease the amount of air in circulation.

  • If cardiovascular collapse occurs, begin Adult Cardiac Life Support (ACLS).

Diagnostic Studies

  • Transesphogeal echocardiolography is sensitive, and can detect both very small amount of air in circulation and right-to-left communication.

  • Precordial Doppler ultrasound also is sensitive and can detect small amounts of air.

Subsequent Management

  • If hemodynamically significant VAE occurs, a discussion with the surgeon regarding the continuation of the case is prudent.

  • If right-to-left shunting of air embolus has occurred, hyperbaric oxygen therapy will decrease the air bubbles and improve oxygenation to ischemic tissues.

  • Encourage liberal use of bone wax, soaking the field, and avoidance of large veins should be reiterated.

Risk Factors

  • Venous air embolism classically occurs in sitting craniotomy

  • Venous air embolism is a risk in many other surgical procedures, including but not limited to caesarean section, arthroscopic surgery of the shoulder, production of CO2 tension pneumoperitoneum for laparascopic surgery, central venous catheterization, thoracocentesis, chest trauma, high-pressure mechanical ventilation, and invasive vascular procedures.

Prevention

  • Avoid sitting, head-up positions.

  • Recommendation to surgeon of careful dissection of venous structures and judicious use of bone wax is critical.

  • Preoperative fluid loading may increase CVP and avoid large pressure gradients.

  • Use of positive end-expiratory pressure (PEEP) may increase CVP and decrease the incidence of VAE, but at the risk of increased risk of right-to-left shunting of bubbles.

Special Considerations

  • The volume of entrained air during the event determines, in part, the severity of cardiovascular compromise the patient will suffer. Although the size of a VAE is difficult to estimate, volumes as small as 20 mL of air have caused significant hemodynamic changes in the adult. If a right-to-left intracardiac communication exists (e.g., through a patent foramen ovale), as little as 0.5 to 2 mL of air can cause stroke or myocardial infarction if it becomes lodged in cerebral or coronary vessels. A large volume of air may become trapped in the right heart, decreasing blood flow to pulmonary circulation and increasing strain on the right ventricle. There is an increase in pulmonary artery pressures and a decrease in venous return to the left heart, causing decreased cardiac output and impending cardiovascular collapse.

Further Reading

Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC, Ortega J, eds. Clinical anesthesia. 7th ed. Philadelphia: Lippincott Williams & Wilkins; 2013:1004.Find this resource:

Mirski MA, Lele AV, Fitzsimmons L, Toung TJ. Diagnosis and treatment of vascular air embolism. Anesthesiology. 2007; 106: 164–177.Find this resource:

Ruskin, KJ, Rosenbaum SH, Rampil IJ, eds. Fundamentals of neuroanesthesia. 1st ed. Stony Brook, NY: Oxford University Press; 2014:212–214.Find this resource: