DR. H. HOSSEINI MD

INTRACRANIAL ANEURYSEM

Definition of aneurysm; occurs at a weak spot in an artery. Once weakened, the artery wall bulges outward and fills with blood. This bulge is called an aneurysm. An aneurysm can burst,

spilling blood into the organ to which it supplies blood. When this happens, permanent damage, disability, or death may occur depending on the location and size of the aneurysm.

 

Signs and symptoms

A small, unchanging aneurysm will produce little, if any, symptoms. Before a larger aneurysm ruptures, the individual may experience such symptoms as a sudden and

unusually severe headache, nausea, vision impairment, vomiting, and loss of consciousness, or the individual may be asymptomatic, experiencing no

symptoms at all.

If an aneurysm ruptures, it leaks blood into the space around the brain. This is called a “subarachnoid hemorrhage.” Depending on the amount of blood, it can

produce:• a sudden severe headache that can last from several hours to days

• nausea and vomiting• drowsiness and/or coma• stiff neck• blurred vision

Signs and symptoms cont…

The ruptured aneurism (hemorrhage) may also damage the brain directly, usually from bleeding into the brain

itself. This is called a “hemorrhagic stroke.” This can lead to

•weakness or paralysis of an arm or leg•trouble speaking or understanding language•vision problems•seizures

Causes

-Hypertension-cigarette smoking

-cocaine abuse-female sex

- and use of oral contraceptives

-coarctation of the aorta,- polycystic kidney disease,

- and fibromuscular dysplasia, -as well as the occurrence of cerebral

aneurysms in first-degree relatives

Complications that can develop after the rupture of an aneurysm include

Re-bleeding. An aneurysm that has ruptured or leaked is at risk of bleeding again. Re-bleeding can cause further damage to brain cells.

Vasospasm. After a brain aneurysm ruptures, blood vessels in your brain may narrow erratically (vasospasm). This condition can limit blood flow to brain cells (ischemic stroke) and cause additional cell damage and loss.

Hydrocephalus. When an aneurysm rupture results in bleeding in the space between the brain and surrounding tissue (subarachnoid hemorrhage) — most often the case — the blood can block circulation of the fluid surrounding the brain and spinal cord (cerebrospinal fluid). This condition can result in hydrocephalus, an excess of cerebrospinal fluid that increases pressure on the brain and can damage tissues.

Hyponatremia. Subarachnoid hemorrhage from a ruptured brain aneurysm can disrupt the balance of sodium in the blood supply. This may occur from damage to the hypothalamus, an area near the base of the brain. A drop in blood sodium levels (hyponatremia) can lead to swelling of brain cells and permanent damage.

Development of vasospasm is likely triggered by many mechanisms, the most important being the contact of free hemoglobin with the abluminal surface of cerebral arteries. Not surprisingly, the incidence and severity of vasospasm correlate with the amount of subarachnoid blood seen on CT. Vasospasm typically occurs 3 to 15 days after subarachnoid hemorrhage

triple H therapy (hypertension, hypervolemia, passive hemodilution) is initiated. Specifically, colloid and crystalloid therapy is used, and pressor support may be needed. Nimodipine, a calcium channel blocker, has been shown to improve outcome when initiated on the first day and continued for 21 days after subarachnoid hemorrhage. Cerebral angiographic techniques can also be employed as a safe means to mechanically (via balloons) or chemically (via intra-arterial papaverine) dilate vasospastic arteries,

Management of Anesthesia

-prevent cerebral ischemia, and facilitate surgical exposure.-The goal during the induction of anesthesia is to prevent

increases in the transmural pressure of the aneurysmal sac

-avoid excessive decreases in ICP prior to dural opening, as seen with hyperventilation, such as not to decrease the tamponading force on the external surface of the aneurysm

-Patients with vasospasm pose a similar quandary in that systemic hypertension may improve flow through vasospastic vessels but may increase the risk of aneurysm rebleeding

-Monitoring the systemic blood pressure via an intra---arterial catheter is desirable-Placing a CVP catheter is useful-A pulmonary artery catheter and a transesophageal echocardiography may be considered when patients have known cardiac disease-Electrophysiologic monitoring (electroencephalography, somatosensory or motor evoked potentials)

monitoring

Prophylaxis against systemic hypertension during direct laryngoscopy may be achieved by previous intravenous administration of the short-acting β-adrenergic antagonist esmolol, lidocaine, propofol, barbiturates, or short-acting opioids (fentanyl, sufentanil, remifentanil). Loss of consciousness is achieved with intravenous administration of thiopental, propofol, or etomidate

Maintenance of anesthesia

Cont.. Maintenance of anesthesia

Anesthesia is most often maintained with volatile anesthetics (isoflurane, desflurane, sevoflurane) with or without the addition of nitrous oxide, which may be supplemented with intermittent (fentanyl) or continuous infusion of opioids (remifentanil). Alternatively, a total intravenous anesthetic maintenance technique (propofol and short-acting opioid) can be used. Cerebral vasoconstricting anesthetics (e.g., barbiturates, propofol) help reduce brain volume and, in the case of barbiturates and possibly propofol, may provide some degree of neuronal protection against ischemia. Muscle paralysis is critical to prevent movement during clipping

the risk of intraoperative rupture is approximately 7% and most commonly occurs during the late stages of surgical dissection. Anesthetic management or rupture consists of aggressive volume resuscitation to maintain normovolemia combined with controlled hypotension (e.g., with nitroprusside) to temporarily limit hemorrhage and permit the neurosurgeon to gain control of the aneurysm. If a temporary clip on the feeding vessel is used to gain control of a ruptured aneurysm, systemic blood pressure is then returned to a normal or to a slightly elevated level to improve collateral blood flow

optimization of brain relaxation is an important part of anesthetic maintenance and combinations of lumbar CSF drainage, mild hyperventilation of the patient's lungs, administration of loop and/or osmotic diuretics, and proper patient positioning to facilitate cerebral venous drainage can help to optimize surgical exposurehyperthermia and fever should be avoided as they increase CMRO2 and CBVdrug-induced controlled hypotension has been used to decrease transmural pressure in the aneurysm, thereby decreasing the risk of aneurysm rupture during microscopic isolation and clippingregional controlled hypotension produced by placing a vascular clamp on the parent artery supplying the aneurysm provides protection against aneurysm rupture without the risk of global cerebral ischemia. Ideally, temporary occlusion of the parent artery does not exceed 10 minutes

At the conclusion of the surgical procedure

prompt emergence from anesthesia is desirable to facilitate immediate neurologic evaluation of the patient.

Incremental doses of antihypertensive drugs such as labetalol or esmolol may be needed as the patient emerges from anesthesia

Lidocaine may be administered intravenously to suppress airway reflexes and the associated responses to the presence of a tracheal tube. Tracheal extubation immediately after surgery is acceptable and encouraged in patients who are awake

with adequate spontaneous ventilation and protective upper airway reflexes.

Patients who were obtunded preoperatively are likely to require continued tracheal intubation and support of ventilation during the postoperative period. Likewise, patients who experience intraoperative rupture of intracranial aneurysms may recover slowly and benefit from postoperative airway and ventilation support.

Anesthesia for posterior fossa surgery in the sitting position and Venous Air Embolism

Craniotomy to remove a supratentorial tumor is usually performed in the supine position with the patient's head elevated 10 to 15 degrees to facilitate cerebral venous drainage. Infratentorial tumors have more unusual patient positioning requirements and may be performed in the lateral, prone, or sitting position

shoulder and thyroid,--often used for exploration of the posterior cranial fossa, which

may be necessary to resect intracranial tumors, clip aneurysms, decompress cranial nerves, or implant electrodes for cerebellar stimulation, as well as for surgery on the cervical spine and posterior cervical musculature

ADVANTAGES

Advantages of the sitting position over the prone positionare excellent surgical exposure, decreased blood loss in theoperative field, and possibly, reduced peri operative bloodloss. Advantages to the anesthesiologist are superior accessto the airway, reduced facial swelling, and improvedventilation, particularly in obese patients.

DISADVANTAGES

•contraindication to the sitting position exists ( patent foramen ovale),

•decreases in systemic blood pressure and cardiac output produced by this position, and the potential hazard of venous air embolism.

The postoperative complications that may occur after posterior fossa craniotomy

-apnea due to hematoma formation,----tension pneumocephalus,-cranial nerve injuries- Macroglossia is also a possibility and is presumed due to impaired venous drainage from the tongue- Venous air embolism

Venous air embolism

-this complication is most often associated with neurosurgical procedures( veins in the skull may not collapse when cut)-operations involving the neck, thorax, abdomen, and pelvis -during open heart procedures, repair of liver and vena cava lacerations, -obstetric and gynecologic procedures, - total hip replacement

when air enters the right atrium and ventricle, there is interference with right-sided cardiac output and blood flow into the pulmonary artery. Air that eventually enters the pulmonary artery may trigger pulmonary edema and reflex bronchoconstriction.

Death is usually secondary to a vapor lock causing right-sided cardiac output to plummet, acute cor pulmonale, or arterial hypoxemia from combined cardiac and pulmonary insults.

-Small quantities of air can sometimes pass through pulmonary vessels to reach the coronary and cerebral circulations; -large quantities of air can travel directly to the systemic circulation through right-to-left intracardiac shunts created by a patent foramen ovale or true septal defects.- This passage of air from the right to left circulation is known as paradoxical air embolism. -For that reason, known foramen ovale or other cardiac defects that could possibly result in a right-to-left shunt are relative contraindications to use of the sitting position

Mid esophageal four-chamber view: TEE demonstrated that the right atrial and right ventricle were opacified with a massive amount of air.

When the likelihood of venous air embolism is increased, it is useful, but not mandatory, to place a right atrial catheter before beginning surgery. Death due to paradoxical air embolism results from obstruction of the coronary arteries by air, leading to myocardial ischemia and ventricular fibrillation. Neurologic damage may follow air embolism to the brain.

detection of venous air embolism

-A Doppler sonography transducer placed over the right-sided cardiac structures is one of the most sensitive indicators of intracardiac air-Transesophageal echocardiography, by comparison, is also useful for both detecting and quantifying intracardiac air.A sudden decrease in the end-expired PaCO2 may reflect increased alveolar dead space and/or diminished cardiac output resulting from air embolus-An increase in right atrial and pulmonary artery pressures reflects acute cor pulmonale and correlates with abrupt decreases in the end-expired CO2.-During controlled ventilation of the lungs, sudden attempts by patients to initiate spontaneous breaths (“gasp reflex”) may be the first indication of venous air embolism. Hypotension, tachycardia, cardiac arrhythmias, and cyanosis are late signs of venous air embolism. Certainly detection of the characteristic “millwheel” murmur, as heard through an esophageal stethoscope, is a late sign of catastrophic venous air embolism

Flat Air Emboli Monitoring Probe

TREATMENT-the surgeon should flood the operative site with fluid, apply occlusive material to all bone edges, and attempt to identify any other sources of air entry (e.g., perforation of a venous sinus). Aspiration of air should be attempted through the right atrial catheter-Nitrous oxide is promptly discontinued to avoid increasing the size of any venous air bubbles-oxygen is substituted for nitrous oxide-apply positive end-expiratory pressure or direct jugular venous compression to increase venous pressure at the surgical site-Extreme hypotension may require the support of perfusion pressure using sympathomimetic drugs as dopamine or dobutamine-Bronchospasm is treated with β2-adrenergic agonists by aerosol (metered-dose inhaler) or the intravenous route-placing the patient in the lateral position with the right chest uppermost-Hyperbaric therapy may be useful in the treatment of both severe venous as well as paradoxical air embolism within 8 hours-After successful treatment of small or modest venous air embolism, the surgical procedure can be resumed.