Anestesia del paziente con aneurisma cerebrale

AZIENDA DI RILIEVO NAZIONALE E DI ALTA SPECIALIZZAZIONE

CIVICO- DI CRISTINA- BENFRATELLI

PALERMO

U.O.C. ANESTESIA E RIANIMAZIONE

Direttore: Dr. Romano Tetamo

Dott. Vincenzo Mazzarese

• Aneurismi Sacculari (più frequenti)

Estroflessioni sacculari § difetto congenito/stress emodinamico (biforcazioni e curvature vasali)

Caratteristiche Morfo-Strutturali

In base alledimensioni:

•piccoli (< 6 mm)

• medi (6-15 mm)

• grandi (15-25 mm)

• giganti (> 25 mm)

In base alla morfologiadella base di impianto

•an. con colletto stretto

•an. con colletto largo

• an. privi di colletto

• Nel lume della sacca aneurismatica (max se di cospicue dimensioni), si possonoriscontrare trombi che ne occupano il fondo – protezione alla rottura

• Il tipo di flusso nella sacca aneurismatica è turbolento(ristagnante/formazione di trombi – vorticoso/> rischio di rottura spontanea)

• Aneurismi Fusiformi (3-13% di tutti gli aneurismi)

Dilatazioni che interessano l’intera circonferenza del vaso §alterazioni aterosclerotiche, dissezione, cause infettive,

invasione neoplastica della parete arteriosa (sistema vertebro-basilare/cerebrale media e carotide interna)

Caratteristiche Morfo-Strutturali

Inquadramento Clinico

• Fisiopatologia della rottura aneurismatica

La sede della rottura è generalmente il punto più sottiledella parete aneurismatica (fondo)/> azione delle pulsazioni

del sangue

• Emorragia successiva a

rottura:

• Emorragia subaracnoidea (a)

• Emorragia cerebro-meningea

(b)

• Emorragia ventricolare (c) a bc

La rottura di verifica generalmente in coincidenza di sforzi fisici/in assenza di eventi scatenanti

• Quadro Clinico tipico: cefalea violenta (frontale/occipito-

nucale), vomito, malessere, vertigini, pallore, sudorazione

Mechanism of Action

• Initial Injury

– Aneurysm ruptures

• Releases blood into the CSF– Quickly

– Under arterial pressure

• Thus increasing ICP– Monroe Kellie Doctrine

Intracranial Pressure (ICP) Increases

■ Signs of elevated ICP:

■ Cushing’s Triad:

■ Hypertension

■ Bradycardia

■ Widening pulse pressure

■ Seizures

■ Nausea and vomiting

Iter Diagnostico

Metodica di riferimento per lo studio degli aneurismi intracranici

• Esame Angiografico (DSA)

Limiti

• esame invasivo

• elevate quantità di mdc iodato

• > durata del tempo d’esame

• RX (pz/operatore)

• Rischio di complicanze

• Angio-TC

• Angio-RM

“Gold Standard”

Aneurysm Grading Scales• Glasgow Coma Scale

• Hunt and Hess– Most widely used– Predicts clinical outcomes

• World Federation of Neurological Surgeons (WFNS)– Combines GCS and presence of motor deficits– Predicts clinical outcomes

• Fisher Scale– Vasospasm risk

• All scales have some issues with validity/ reliability

Trattamento

• Obiettivo

• Escludere la sacca aneurismatica dal circolo

• prevenire l’emorragia (aneurismi non rotti)

• prevenire il risanguinamento (ESA)

• Trattamento Endovascolare (occlusione con spirali/coils)

• Trattamento Chirurgico (craniotomia, clipping del colletto)

•Valutazione neurologica/Imaging

Nursing care preoperative• ABCs

• Neuro Checks

• BP management

– Systolic between 90-140mmhg

– AVOID Hypotension

• ICP Monitoring

– EVD if indicated

• Labs

– CMP, CBC, Cardiac Enzymes, Coags, T&C, ABGs if intubated, 12 lead EKG, Chest X-Ray

Preoperative Care• NPO

• IVF

• Maintain euvolemia

• 0.9 NS at 80-100ml per hour

• Fever management

• Hyponatriemia management

• DVT – No anticoagulation until aneurysm securement

• Teds, SCDs

Medications

• Nimodipine 60mg Q4 hrs

• Seizure prophylaxis

• Pain Management

• Antiemetics

• GI Protection

Inquadramento Clinico

• Complicanze Neurologiche

• Risanguinamento (frequente nelle prime ore e giorni)

• evento spesso fatale

• prevenzione (trattamento precoce

dell’aneurisma, stato di assoluto riposo)

• Vasospasmo cerebrale (40-50% dei casi/4ª-5ª giornata-II settimana) • fenomeno reattivo al sanguinamento

• restringimento vasale localizzato o diffuso

➢ Prodotti di degradazione del sangue innescano una contrazione della muscolatura liscia della parete vasale mediata da ioni Ca e

prostaglandine (E2)

➢ La gravità del quadro neurologico varia a seconda del territorio interessato (asintomaticità, cefalea intensa, sonnolenza, emiparesi,

turbe fasiche, exitus)

Inquadramento Clinico

• Complicanze Neurologiche

• Idrocefalo (15-20% dei casi)

• Convulsioni

Prevenzione risanguinamento

Medical Measures to Prevent Rebleeding After aSAH: Recommendations

1. Between the time of aSAH symptom onset and aneurysm obliteration, blood pressure should be controlledwith a titratable agent to balance the risk of stroke, hypertension-related rebleeding, andmaintenance of cerebral perfusion pressure (Class I; Level of Evidence B). (New recommendation)

2. The magnitude of blood pressure control to reduce the risk of rebleeding has not been established, but adecrease in systolic blood pressure to <160 mm Hg is reasonable (Class IIa; Level of Evidence C). (Newrecommendation)

3. For patients with an unavoidable delay in obliteration of aneurysm, a significant risk of rebleeding,and no compelling medical contraindications, short term (<72 hours) therapy with tranexamic acid oraminocaproic acid is reasonable to reduce the risk of early aneurysm rebleeding (Class IIa; Level of

Evidence B). (Revised recommendation from previous guidelines)

Diringer, M., Bleck, T., et al. (2011). Critical Care Management of Patients Following Aneurysmal Subarachnoid Hemorrhage: Recommendations from the Neurocritical Care Society’s Multidisciplinary Consensus Conference

SAH-induced Vasospasm

• Occurs angiographically in 30-70% of patients

• Clinical symptoms seen in 20-45% of patients

• Adds 10-20% significant morbidity/mortality

• Smooth muscle constriction and vessel wall edema, infiltration and fibrosis leads to luminal narrowing and decreased compliance

• Time course

• Range: 4-14 days

• Peak: 7-10 days

Detection of Vasospasm

• Clinical exam

– Focal deficit

– Mental status changes

• Increasing TCDs

• CTA/CTP

• MRI/A/P

• Angio

Triple H Therapy (Modified)

• Hypertensive therapy– SBP >160 mm HG– Don’t treat BP – patients will usually auto regulate

• In symptomatic vasospasm vasopressors are used

• Hypervolemia– Maintain PCWP at 10 to 16 mm Hg– Urinary output >/= 250ml per hour

• Euvolumia– Using fluids and vasopressors for symptomatic patients

• Hemodilution– IV fluids at 100-150 ml per hour– Hematocrit <0.40

Vasospasm Treatment

• Nimodipine

– 60mg Q4hr for 21 days

• Cerebral Angiogram

– Intra arterial calcium channel blockers

• Verapamil

– Angioplast

– Stent

SEIZURE

• Seizures can occur in as many as 25% of patients

• Most common after MCA ruptures

• The use of prophylactic anticonvulsants may be considered in the immediate posthemorrhagic period (Class IIb; Level of Evidence B).

• The routine long-term use of anticonvulsants is not recommended (Class III; Level of Evidence B) but may be considered for patients with known risk factors for delayed seizure disorder, such as prior seizure, intracerebral hematoma, intractable hypertension,infarction, or aneurysm at the middle cerebral artery (Class IIb; Level of Evidence B)

FEVER

■ Patients are at risk for developing both infectious and non-infectious fever and often do not respond to treatment

■ Fever occurs in as many as 54% of patients recovering from SAH and is a predictor of poor prognosis

■ Fever increases cerebral metabolic rate, releases excitatory neurotransmitters, increases production of free radicals and breakdown of the blood-brain barrier – all result in an increased risk for ischemia

■ Aggressive control of fever to a target of normothermia by use of standard or advanced temperature modulating systems is reasonable in the acute phase of aSAH (Class IIa; Level of Evidence B). (New recommendation)

HYPONATREMIA■ Low sodium levels create a high risk for vasospasm when combined with

hypovolemia

■ Hyponatremia can be caused by SIADH (Syndrome of In-Appropriate Diuretic Hormone) or Cerebral Salt Wasting (CSW)

■ The cause must be distinguished because the treatment is so different: If caused by true SIADH – fluid restriction If caused by salt wasting – fluid replacement

■ Fluid restriction in a patient with salt wasting places them at high risk for vasospasm and ischemia

■ Monitoring volume status in certain patients with recent aSAH by some combination of central venous pressure, pulmonary wedge pressure, and fluid balance is reasonable, as is treatment of volume contractionwith crystalloid or colloid fluids (Class IIa; Level of Evidence B).

SIADH vs. Cerebral Salt Wasting

SIADH

■ Hyponatremia (dilutional)

■ Increased ECF

■ Increased plasma volume

■ Increased body weight

■ Low BUN

■ Low serum osmolality

■ Not necessarily negative salt balance

Salt Wasting

■ Hyponatremia (primary)

■ Decreased ECF

■ Decreased plasma volume

■ Decreased body weight

■ High BUN

■ High urine sodium

■ Negative salt balance (primary loss of sodium)

The use of fludrocortisone acetate and hypertonic saline solution is reasonable for preventing and correcting hyponatremia (Class IIa; Level of Evidence B)

Cardiac failure

• Cardiac Dysfunction

– Tako–tsubo Cardiomyopathy

• Neurogenic myocardial stunning

• Thought to be related to excessive release of catecholamine

• Left Ventricle

– Apical ballooning

• MUST rule out coronary artery disease first

Treatment of Myocardial Stunning

Supportive

• Unload the left ventricle

• Reduce vasopressors

• Started due to low BP (Results in increased SVR and afterload)

– Contractility Agents

• Dobutamine

– Address Pulmonary Edema

• Lasix

Intraoperatory care

• Prevent aneurysm rupture (avoid hypertension)

• Decrease ICP (surgical exposure, retraction)

• Maintain CPP (>70 mmHg)

• Prevent cerebral ischemia

• Good operating conditions (NO movement, brain relaxation for exposure)

Premedicazione

• Rupted aneurysm usually decreased mental status : no premedication

• Elective clipping: Premedicate with up to 2 mg of midazolam if normal mental status

• Adequate fluid loading

Monitoraggio

Parametri vitali (ECG, PAO,SPO2, EtCo2,Diuresi)

Avanzato:Pressione cruentaEGA CVCTOFTEG

Neurologic monitor

A. Monitor of brain electrical activity

1. Electroencephalography2. Evoked potentials:

I. Sensory evoked potentials

. Visual

. Somatosensory

. Auditory

II. Motor evoked potentials 3. Bispectral index

Monitors of blood flow dynamics

1.Transcranial doppler• Direct, noninvasive measurement of CBF

• Sound waves transmitted through

thin temporal bone contact blood,

are reflected, and detected

• Most easily monitor middle

cerebral artery

2. Cerebral Oximetry (Near infrared spectroscopy)

• determine cerebral saturation

• uses a similar principle to pulse oximetryby using multiple wave lengths of near infrared light , the absorption of this light by oxygenated and

deoxygenated haemoglobin determines

the overall saturation

of the blood present within

the brain tissues.

3. Jugular venous oxygen saturation (SjVO2)

The jugular bulb is the dilated portion of the jugular vein just below the base of the skull which contain blood with little extra cerebral contamination.

Measurement of oxygen saturation of the jugular bulb provide information about the global oxygenation state of the brain.

Induction

• Propofol

• Fentanyl 5 ug/kg in divided doses prior to intubation

• Muscle relaxant (roc)

• Avoid hypertension (rupture) and hypotension (CPP, vasospasm)

Maintenance

• TIVA infusion

• Muscle relaxation (roc)

• Moderate hyperventilation (ET CO2 30 mmHg)

• Euvolemia to 500 cc more (LR)

• BP 20% lower than baseline

Furosemide is an alternative for decreasing ICP and brain water content and can be used in combination with mannitol to achieve greater effect.65 Because of the combination of drugs’ greater effect, particular attention should be paid to the patient’s fluid volume, electrolytes, acid-base, and serum osmolality levels.

Mannitol is the drug of choice to decrease brain water content, and consequently ICP, by creating an osmotic gradient. The recommended dose ranges from 0.25-2 g/kg, and its peak effect occurs approximately 30-45 minutes after the start of infusion.

MaintenanceMild hyperventilation (30-35 mmHg PaCO2 with intact dura and 20-30 mmHg with open dura) can be employed to facilitate a reduction in brain-blood volume via cerebralvasoconstriction in patients with intact CO2 cerebrovascular activity. However, hyperventilation should be used only in patients with increased ICP and in moderation. Normoventilationis the general goal, because prolonged hyperventilation can cause cerebral ischemia

Clipping

• Temporary clips

• Permanent clips

• Aneurysm manipulation before clipping (bleed)

• Record clip on/off times

• Maintain CPP during temporary clipping

• Start more fluid loading after clipping

Burst supression ???

• When requested by surgeon

• Till 70-80% EEG burst supression

• Redose as needed

• Propofol infusion rate up

• Support CPP with phenylephrine infusion

Recovery

• Transport to ICU with monitor and oxygen

• Wake patient up as soon as possible

• Extubate if possible

• Prevent post op hypertension (bleed). Labetalol e nifedipine

• Head up position

Nursing Care Postoperative

• ABCs• Frequent Neuro exam Q1hr

– Or as exams dictate• HOB 30 degrees, neck midline• Reduce stimulation, quiet, dark room

– Headaches continue, until blood clears CSF

• BP Management– DO NOT TREAT BLOOD PRESSURE ONCE ANEURYSM IS SECURE

• Maintain perfusion to the brain• Allow BP to be 200mmhg systolic• CPP to be >60 to 70 mmHg

• Fever management• Daily Labs

– Electrolytes, CBC, Cardiac Enzymes (1st 5 days), ABGs, Chest X-Ray, Anticonvulsant levels

– Consider baseline 2D-Echo

Postoperative Nursing Care

• DVT prophylaxis

• Continue TEDs and SCDs

• SQ heparin/lovenox

• Trans cranial Doppler (TCDs)• Consistently measure MCA mean velocity

• <120 cm/sec = less risk of vasospasm

• >200 cm/sec = greater risk of vasospasm

• Used in conjunction with neuro exam

• Repeat Cerebral Angiogram

• Day 7-10

• Regardless of securement methodology

Medications

• Nimodipine 60mg Q4 hrs

• Seizure prophylaxis

• Pain Management

• Antiemetic

• GI Protection

Future Research

• Magnesium – Cerebral vasodilatory effects

• Ability to penetrate CNS

– Readily available, inexpensive

– Recent research• DNI

– 12/54 in the Magnesium Group = 22%

– 27/53 in the Control Group = 51%

• Mortality– 6/54 in the Magnesium Group = 11%

– 10/53 in the control Group = 19%

– Recommendations• Do not induce hypermagnesaemia

• Avoid hypomagnesaemia

• Further research is needed

Future Research

• Statins

– Several small randomized clinical trials

• Shown to reduce vasospasms and DNI

• Reactivation of the Stash Study– Multicenter study on the use of statins in aSAH

– Recommendation

• If patient is taking statin continue

• May consider in statin naive patients

• More research is recommended

Future Research

• Phenytoin Prophylaxis– Three day course of Phenytoin

• 1.9% of patients had seizures with 3 day prophylaxis– 1.3% in retrospective group

• 80% treated with craniotomy

– Drug Reaction• 8.8% to 0.5% with three day course• Hospital length of stay 14.2 to 13.1

– Recommendations• Use of anticonvulsants is not recommended• If anticonvulsant prophylaxis is used

– 3-7 days

• If patient presents with history of seizure– Institution’s protocol

Conclusioni

Evidence Based Care

References:AANN (2009). Care of the Patient with Aneurysmal Subarachnoid Hemorrhage. AANN Clinical Practice Guideline Series

Connolly, S., et al. (2012). Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage. Stroke

Bader, M., Littlejohns, L. (2004). AANN Core Curriculum for Neuroscience Nursing

Chumnanvej, S. (2007). Three day phenytoin prophylaxis is adequate after subarachnoid hemorrhage. Neurosurgery

Diringer, M., Bleck, T., et al. (2011). Critical Care Management of Patients Following Aneurysmal Subarachnoid Hemorrhage: Recommendations from the Neurocritical Care Society’s Multidisciplinary Consensus Conference

McDougall, C., et al. (2012). The Barrow ruptured aneurysm trial. Journal of Neurosurgery

Molyneux, A., et al. (2005). International subarachnoid aneurysm trial (ISAT) of neurosurgical clipping versus endovascular coilingin 2153 patients with ruptured intracranial aneurysms: a randomized comparison of effects on survival, dependency, seizures, rebleeding, subgroups, and aneurysm occlusion. The Lancet

Naidech, A., (2005). Phenytoin exposure is associated with functional and cognitive disability after subarachnoid hemorrhage. Stroke

Schmid-Elsaesser, R. et al. (2006). Intravenous Magnesium versus Nimodipine in the treatment of patients with aneurysmalsubarachnoid hemorrhage: A randomized study. Neurosurgery

Society for Critical Care Medicine. (2006). Ten things we hate about subarachnoid hemorrhage (or, the taming of the aneurysm. Critical Care Medicine

Up-to-date. Retrieved 8/30/2010. Etiology, clinical manifestations and diagnosis of aneurysmal subarachnoid hemorrhage. Subarachnoid hemorrhage grading scales

Westermaier, T., et al. (2010). Prophylactic intravenous magnesium sulfate for treatment of aneurysmal subarachnoid hemorrhage: A randomized, placebo-controlled, clinical study. Critical Care Medicine

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