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Neurocritical Care

Agent selection

First line therapy

Second line therapy

Prepared by

Dr. Rania Salah Nasr

PhD,Clinical diploma,TOT,

TQM,Hospital management diploma

Third line therapy(refractory)

Characteristics of Agents for Status Epilepticus

Super-refractory

status epilepticus

Non pharmacolgical

therapy

Main topics

INTRACRANIAL PRESSURE TREATMENT

First line therapy( emergency )

-Hyponatremia.

-Hypernatremia.

-Status epilepticus.

-CNS infection.

-Intracranial pressure treatment.

-Paroxysmal sympathetic hyperactivity.

-Acute ischemic stroke.

-Intracerebral hemorrhage.

-Subarachnoid hemorrahage.

-Interventional endovascular treatment.

-Acute spinal cord injury.

-Brain tumor.

-Citical illness polyneuropathy.

-Guillian-Biarre syndrome.

-Myasthenia crisis.

-Serotonin syndrome.

-Benzodiazepine therapy preferred

1- lorazepam 0.1 mg/kg IV (max : 4mg/dose).

2- Midazolam 5–10 mg IM (preferred for patients with no intravenous access).

3- Diazepam IV (0.15–0.2 mg/kg, max :10 mg/dose).

or rectally (0.2–0.5 mg/kg,max :20 mg/dose).

Not recommended as first line for hospitalized patient due to short duration of seizure.

ACUTE ISCHEMIC STROKE

Hyponatremia

-Serum normal level: 135-145 meq/L

-Epidemiology: Na less than 135.

-Diagnosis/Pathophysiology:

1. laboratory test.

2. Urine sodium, urine osmolality, serum osmolality, and measurement of intravascular volume.

*Causes:

- increase in salt-free water.

--or loss of serum sodium.

General Concepts

Clinical Impact

Second-line therapy (urgent)

*Initiate an anticonvulsant after benzodiazepine therapy if seizures persist

or if a maintenance therapy needs to be initiated to prevent future seizures.

* Can add anticonvulsants if the patient does not respond to treatment and is not intubated

1- Valproate 20–40 mg/kg IV.

2- (Fos)phenytoin 18–20 mg/kg IV.

3- Phenobarbital 20 mg/kg IV.

4- Levetiracetam 1-3 g IV.

1.Hyponatremia may result in increased brain edema and elevated ICP.

2.May cause neurologic symptoms such as delirium, agitation, tremor, seizure, or coma.

*Types of hyponatremia:

-Mild.

-Moderate.

-Sever.

Diagnosis

Normal level of ICP = 15- 20 mmHg

1. Elevated ICP decreases tissue perfusion and tissue oxygenation and worsens neurologic outcome.

2. Monro-Kellie doctrine:

ICP= cerebral blood volume (10%)+ CSF (10%)+ brain tissue (80%).

*Each therapy targeted at decreasing ICP acts on one or more of these components.

3. Most practitioners use a stepwise approach to treating elevated ICP, including the following interventions:

a. Head-of-bed elevation (30–45 degrees): Optimizes venous return from the brain, reducing venous pooling.

b. Osmotherapy (mannitol or hypertonic saline).

c. Acute hyperventilation: Reduction in PCO2 to around 32 mm Hg causes a compensatory vasoconstriction, which reduces cerebral blood volume (chronic hyperventilation should be avoided because of complications such as stroke).

d. Drainage of CSF by a ventriculostomy.

e. Sedation with or without neuromuscular blockade (avoid benzodiazepines, when possible).

f. Maintenance of CPP at 60–70 mm Hg .

g. Surgical decompression or hemicraniectomy (depending on the clinical scenario).

h. Pharmacologic coma (pentobarbital)

i. Hypothermia (33-36 )versus targeted temperature management for control of ICP.

Hyponatremia Clinical Symptoms by Severity of Hyponatremia

Serum [Na+] 130–135 mEq/L

Serum [Na+] 120–130 mEq/L

Serum [Na+] < 120 mEq/L

• Headache

• Restlessness

• Lethargy

• Seizures

• Brain stem herniation

• Respiratory arrest

• Death

• Asymptomatic

• Headache

• Nausea

• Vomiting

• Fatigue

• Confusion

• Anorexia

• Muscle cramps

•Depressed reflexes

• Malaise

• Unsteadiness

• Headache

• Nausea

• Vomiting

• Fatigue

• Confusion

• Anorexia

• Muscle cramps

Fifth leading cause of death.

1. Diagnostic tests

a. Neurologic examination.

b. Vital signs.

c. NIH Stroke Scale{national institute health}

(greater than 25 is severe, range 1–42).

d. CT scan or magnetic resonance imaging (MRI) of the brain.

e.Chest radiography ( if lung disease).

f.EEG (if seizure).

2. blood tests:

a. Blood glucose

b. INR, activated partial prothrombin time (consider thrombin time, anti–factor Xa [anti-Xa] activity for newer oral anticoagulants)

c. Complete blood cell count (CBC)

d. Tests for hypercoagulable state

Third-line therapy (refractory)

Differential Diagnosis for SIADH and CSWS

-Deffinition: seizures persist after first and second –line therapy, RSE should be treated aggressively with continuous infusion anesthetic agents.

-The patient should be intubated before starting therapy.

- RSE agents should be titrated to burst suppression (the almost total elimination of electrical activity on EEG, except for short “bursts” of cortical activity [typically therapy is titrated to 2–5 bursts/minute]) or termination of electrographic seizure activity, depending on provider preference.

-Treat RSE for 24–48 hours before trying to taper these continuous agents.

Serum sodium

(mEq/L)

Serum Osmolality

(mOsm/L)

Urine Osmolality

(mOsm/L)

Urine Sodium

(mEq/L)

Intravascular

Volume Status

> 200

Euvolemia

SIADH

> 25

<135

< 285

CSWS

> 200

< 285

> 25

<135

Hypovolemia

Treatment

Differentiating Between Syndrome of Inappropriate Antidiuretic Hormone (SIADH) and Cerebral Salt-Wasting Syndrome (CSWS)

1- osmotherapy is the first choice:

1. Typically made by assessing intravascular volume. Patients with SIADH tend to be euvolemic or hypervolemic with hyponatremia because of excessive antidiuretic hormone (ADH) release, whereas

patients with CSWS tend to be hypovolemic with hyponatremia because of inappropriate urinary excretion of Na & extracellular fluid.

2. Measure intravascular volume using a central venous pressure catheter or similar invasive monitoring.

3. Noninvasive hemodynamic monitoring devices.

4. Monitor fluid balance, weight & skin turgor.

5. Echocardiogram to estimate ventricular filling pressures.

Causes:

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

Euvolemic or hypervolemic due to ADH release.

Cerebral Salt Wasting Syndrome (CSWS)

Hypovolemic due to inappropriate urinary excretion & extracellular fluid.

-Metabolic acidosis may occur after several hypertonic saline doses as the result of hyperchloremia.

a. Combination of sodium chloride and sodium acetate may be considered to maintain the hyperosmolarity & decrease chloride provision.

b. Sodium bicarbonate 8.4% may also be considered for acute ICP elevations when other osmotherapy

options are not immediately available.

**Continuous infusion anesthetics for RSE

i. Midazolam high-dose infusion 0.05–2 mg/kg/hour (target burst suppression).

ii. Pentobarbital infusion (loading dose about 25 mg/kg total, continuous infusion 0.5–5 mg/kg/hour [target burst suppression]).

iii. Propofol infusion 20–200 mcg/kg/minute (target burst suppression).

**Other options for RSE in nonintubated patients

i. Valproate 20–40 mg/kg IV (if not already given).

ii. Lacosamide 200-400 mg IV.

iii. Topiramate 200–400 mg orally/nasogastrically.

iv. Other anticonvulsants listed earlier if not already given.

1. Cardioembolic (29.1%).

2. large-artery atherosclerosis(16.3%).

3. lacunar infarcts(15.9%).

4. Unknown (36.1%).

5. Other (2.6%).

Typical Causes of SIADH

*Medications:

Desmopressin/vasopressin

Selective serotonin reuptake inhibitors

Tricyclic antidepressants

Carbamazepine

Oxcarbazepine

Chlorpropamide

Cyclophosphamide/iphosphamide

Methylenedioxymethamphetamine

Nicotine

Opioids

Phenothiazine antipsychotic medications

Nonsteroidal anti-inflamatory drugs

TBI

Brain tumor

Stroke

Brain infection SAH

Intracerebral hemorrhage

Pneumonia/tuberculosis

Lung cancer

Treatment

Permissive hypertension

Super-refractory status epilepticus

Comparison of Osmotherapy Agents

Treatment – Updated guidelines for diagnosing and managing hyponatremia

Demeclocycline

Fluid restriction

Oral sodium intake

Secondary prevention

IV sodium

Vasopressin

antagonist

Seizure prophylaxis

Thrombolysis

Treatment Strategies for SIADH

Defined as failure to continous anesthetic agent after 24-48 hrs of burst suppression or termination of continuous EEG seizures.

A- Treatment is typically reinitiation of continuous anesthetic

Agents used for RSE:

B- Ketamine, an N-methyl-d-aspartate (NMDA) receptor antagonist, may also be considered. Ketamine may cause emergence psychosis and hallucinations, for which midazolam may help.

C- Patients should have a workup for causes of super-refractory status epilepticus (e.g., NMDA receptor antibody encephalitis, paraneoplastic syndromes, infectious encephalitis).

2-Metabolic Suppression by pentobarbital:

Mechanical thrombectomy

Calculation of Osmolar Gap

Monitoring osmolar changes with osmotherapy:

The traditional serum osmolality threshold was 320mOsm/L when using mannitol.

a. Theory was that serum osmolality values greater than 320 were associated with renal dysfunction.

b. Goal osmolar gap is less than 15–20 mOsm/kg.

Osmolar gap = measured osmolality-estimated osmolality

Osmolar gap = measured osmolality –{(2*Na)+(BUN/2.8)+(glucose/18)}

* Mechanism of action:

1.Suppression of electrical activity in brain (i.e., “burst suppression”) causes reduced cerebral metabolic rate of oxygen (CMRO2).

2. Reduced CMRO2 leads to decreased cerebral blood volume.

*pentobarbital is more effective & more harmful for first line therapy for ICP

than mannitol

– Early studies, clinicians begin using pentobarbital only in patients with refractory ICP elevation.

6. Typical pentobarbital dosage

a.25-30 mg/kg IV loading dose.given as 10mg/kg in dose,followed by 5mg/kg every hr in 3-4 doses to avoid hypotention with larg bolus dose.

b. 1- to 5-mg/kg/hour infusion after loading dose

1- Thrombolysis

Nonpharmacologic therapies

Alteplase

0.9 mg/kg (max. 90mg)within 4.5 hrs of symptoms onset.

-10% of total dose as IV bolus.

-followed by 90% as 60-minute intravenous infusion.

a. ketogenic diet : limiting medication and nutrition to low carbohydrate content.

-Exact mechanism of action is unknown, but may increase sequestration of glutamate and decrease reactive oxygen.

-benefits occure within 1-3 months.

-modify diet targeting fat to carbohydrate plus protein in a 4:1 or 3:1 ratio.

b. Vagus nerve stimulation.

c. Surgical management.

d. Hypothermia.

Titration

Some tips about treatment of SIADH

3-Sedation

a. Titrated to goal ICP (usually less than 20 mm Hg)

b. Burst suppression on continuous EEG (target usually is 2–5 bursts/minute) is a surrogate end point

for need of additional pentobarbital doses.

Monitoring

a. ICP

b. EEG and burst occurrence per minute

Adverse effects

a. Hypotension as the result of several different causes

i. Propylene glycol diluent

ii. Direct vasodilator

iii. Reduction in sympathetic tone because of metabolic suppression

iv. Cardiac depressant (particularly with high doses and duration greater than 96 hours)

b. Bradycardia

c. Decreased GI motility and ileus

i. difficulty with enteral nutrition .

ii. Caloric needs are around 80-90 % of basal energy needs.

enteral nutrition is permissible.

iii. Ideally, would use a low-residual nutrition product because stooling is rare on pentobarbital

infusion

d. Infection (particularly pneumonia)

e. Immunosuppression

f. Withdrawal seizures may occur.

Mechanism of action: decrease O2 delivery needs ,reduce agitation, decreased CMRO2.

1. Propofol is typically the preferred sedative – Quick onset, short acting, less accumulation with prolonged duration

*hypotention risk may be harmful in specific patients e.g. TBI & SAH.

* In contrast to midazolam, propofol is advantageous because of its short half-life and relative lack of residual sedative effects.

* Although dexmedetomidine has a short half-life similar to propofol, propofol has the added advantage of reducing CMRO2.

2. Benzodiazepines

a. Not preferred because of duration of action

b. Also associated with delirium and cognitive impairment

c. Potential for withdrawal effect, seizures

3. Dexmedetomidine

*Little evidence to use in neurocritical care.

*hypotention may be harmful in some patients e.g. TBI & SAH.

*May be particularly helpful in patients with paroxysmal sympathetic hyperactivity

Typical Inclusion/Exclusion Criteria for IV Alteplase

-Treatment of choice is fluid restriction.

-Treatment of SIADH can be difficult in some cases e.g. SAH & TBI.

-When treating ICP or cerebral vasospasm,the priority to maintain euvolmia to optimize CPP.

-Hypertonic saline solutions were commonly & most effectively increase serum sodium.

Considerations for Rapid Correction of Hyponatremia

1. Recommended increase in serum Na conc. Is 0.5 mEq/L/hr or less.

2. Patients with chronic hyponatremia may need to be corrected more slowly because of the equilibration of brain electrolytes.

3. Patients with acute hyponatremia may tolerate quicker correction.

4. Quicker correction in patients with severe symptoms (coma, seizures) may be prudent – Up to 1–2mEq/L/hr for first few hours.

5. Rapid correction necessitates frequent serum sodium monitoring (e.g., every 4 hours) to avoid overshoot or too rapid correction.

6. Too-rapid correction may result in osmotic demylination syndrome.

Routine approach should be limit Na increase to 12mEq/L in first 24 hours or less than 18 mEq/L in the first 48 hours.

4-Neuromuscular Blockade

CNS infection

Common Equations Used for Sodium Correction in Hyponatremia

*Mechanism of action: decrease O2 delivery needs , decreased CMRO2.

a. Neuromuscular blockers have no intrinsic value for reducing ICP, but they may be helpful in select

Patients with issues that increase ICP

i. Prevention of cough, ventilator dyssynchrony (both increase ICP)

ii. Control PCO2 (increased PCO2 may also increase ICP)

b. Prevention of shivering during therapeutic hypothermia or targeted temperature management

c. Reduces intrathoracic pressure

d. May be essential in patients requiring high positive end-expiratory pressure (increased intrathoracic pressure may increase ICP)

*Various agents may be useful – Depends on patient organ function, prescriber preference

a. Vecuronium (particularly if normal organ function)

b. Cisatracurium (particularly if end-organ dysfunction)

c. avoid atracurrium because of hypotention.

Patient Case

2- permissive hypertension

a. reduction in blood pressure after thrombolysis is needed in the first 24 hrs after the onset of stroke.but,catiously to avoid hypotension or underperfusion of infarcted area (less than 15% blood pressure lowering).

b. Recommended to treat blood pressure in patients who do not receive thrombolytics if it exceeds 220/120

Hypernatremia

Case Selection

1. recommended in adult with CSF shunt.

-or ventriculostomy infections for difficult to eradicate

pathogens .

-or for patients who cannot undergo the surgical component of therapy.

2. May be also in patients receiving systemic therapy who have not cleared CSF cultures after 3–4 days.

3. Not recommended for neonatal or infant central nervous system (CNS) infection

Epidemiology:

1. Na greater than 150 mEq/L.

2. SAH up to 22%.

3. TBI up to 21%.

Diagnosis :

Laboratory tests: serum Na, serum osmolality, urine Na, urine osmolality & urine volume.

3- Seizure prophylaxis:

Appropriate Dosing

Typical Causes:

PAROXYSMAL SYMPATHETIC HYPERACTIVITY

1.iatrogenic hypernatremia.

2. Diabetes insipidus:

a. Decreased secretion of ADH or vasopressin results in decreased retention of water.

b. dilute urinary output ( greater than 250 ml/ hr).

Use of anticonvulsant medications for seizure prophylaxis is not indicated after ischemic stroke.

4- Mechanical thrombectomy and neuroendovascular interventions for ischemic stroke:

a. Neuroendovascular devices may be used to remove or disrupt clot to facilitate recanalization.

b. No difference in safety outcomes when comparing usual care with usual care plus mechanical

thrombectomy

1. IV plus intraventricular is probably superior to intravenous or intraventricular alone.

2. Use preservative-free formulations.

3. Do not use diluents containing dextrose, whenever possible.

4. Do not use medications to lower the seizure threshold e.g. B-latams.

5. Daily dosing needs to adjust according to the amount of CSF drainage from external ventricular drain.

Treatment

Hypotonic solutions

Vasopressin analogs

1. Hypotonic solutions for free-water replacement:

a. Dextrose 5% in water.

b. 0.45% sodium chloride.

c. Water supplementation orally or by feeding tube.

2. Vasopressin analogs:

a. ADH supply to normal functional concentrations.

b. Desmopressin.

i. Intravenously or subcutaneously: 0.5–4 mcg every 8–12 hours (usual starting dose 1–2 mcg).

ii. Intranasally: 10–40 mcg/day divided into two or three doses (usual starting dose 10 mcg).

iii. Orally: 50–800 mcg divided into two doses (usual starting dose 50 mcg).

iv. May be dosed as needed, depending on initial laboratory values.

c. Patients after pituitary removal may more commonly require long-term therapy.

3.arginine vasopressin infusion 1-15 units/hr.

Arginine vasopressin

5- Secondary prevention

Diagnosis

Preventive and Abortive Therapies

Various Antimicrobials and Doses for Intraventricular Administration

Considerations for rapid correction of hypernatremia

Typically, three or more symptoms

1-Fever 2. Tachycardia 3. Hypertension

4. Tachypnea 5. Dyspnea 6. Diaphoresis

7. Muscle rigidity (posturing)

8. Common triggers

a. Pain

b. Bladder distension

c. Turning

d. Tracheal suctioning

e. Typically unprovoked

a. recommended decrease is 0.5 mEq/L or less.

b. Too-rapid correction of serum sodium may result in cerebral edema.

c. In general, neurocritical care patients should receive minimal amounts of dextrose or free water containing fluids.

Titrate therapy to normalized :

Urine output

Urine specific gravity

Na correction

a. initiate (325mg /day,then 81-325mg/day) ,highly intense statin & intensive blood pressure regimen is necessary.but, Aspirin should not be initiated within 24 hours of alteplase.

b. Clopidogrel 75 mg daily is also an option in patients whose aspirin therapy has failed or who have

an aspirin allergy.

c. Aggrenox (dipyridamole/aspirin) and ticagrelor plus aspirin (less than 100 mg) are also effective alternatives to aspirin for secondary prevention.

d. hypertension: threshold to treat high blood pressure is greater than 140/90 mmHg.

*typical blood pressure goal is less than 130/80 mm Hg.

e. atrial fibrillation

i. Rate or rhythm control.

ii. Anticoagulation (warfarin, direct-acting oral anticoagulants)

iii. Typically, anticoagulant therapy is delayed until at least 5–14 days after stroke to reduce the risk of hemorrhagic conversion.

iv. Avoid using loading doses of warfarin.

f. Carotid artery stenosis:

Stent versus endarterectomy (usually for patients with greater than 70% blockage and/or clinically evident symptoms)

i. Aspirin 81–325 mg daily after endarterectomy

ii. Dual antiplatelet therapy should be given for 3 months if stent placement is required, followed by one antiplatelet agent thereafter.

g. Control of diabetes mellitus

STATUS EPILEPTICUS

Deffintion

Diagnosis

Generalized convulsive

Nonconvulsive

Deffintion

1. laboratory tests:

Electrolyte abnormalities particularly Na,Mg & P.

2. EEG monitoring is necessary to identify and characterize seizures.

a. Continuous monitoring is preferred in patients with status epilepticus to capture intermittent or fluctuating seizure patterrns.

b. Typical recommended duration is at least 48 hours, and monitoring should be initiated as soon as possible after suggestion or diagnosis of seizure.

Intermittent seizures without regaining consciousness in between for more than 5 minutes.

Continous seizures for 5 miutes or more .

Typical Etiologies of Status Epilepticus

Clinical Impact

With onset of seizure activity

Occures in comatosed patients & seizures noted by EEG

Antiplatelets

1. Mortality rate ranges from:

- 9% (primarily in patients with preexisting epilepsy/anticonvulsant medication nonadherence).

-to 30% (in patients with a concomitant pathology such as TBI or stroke).

a. Mortality in nonconvulsive status epilepticus is about double that in more overt seizures.

b. Older adults have a higher mortality rate.

2. Discharge disposition: 14%–18% of patients presenting to the emergency department in status epilepticus have a resultant neurologic deficit.

CNS = central nervous system.

E.g. Asprin,clopidogrel,dipyridamol

-Platelet transfusion infusion (usefulness is uncertain).

-Consider desmopressin 0.4 mcg/kg IV.

S.E. Pulmonary edema or transfusionrelated

reaction.

Unfractionated heparin

Protamine (1 mg of protamine for each 100 units of heparin infused within the past 2–3 hr).

Low molecular weight heparins

Protamine 1 mg for each 1 mg of enoxaparin (within 8 hr of last dose).

S.E. Hypotension, hypersensitivity

Andexanet Alfa Dosing Based on Factor Xa Inhibitor Dose

Platelet transfusion:

INTRACEREBRAL HEMORRHAGE

Causes

*Two prospective studies suggest that platelet transfusion for patients taking antiplatelet agents with new ICH is harmful.

*Patients in these studies have small stable ICH , basal ganglia hemorrhage which non operative.

*Platelet transfusion is likely indicated for patients who:

i. Have an urgent need for surgery or a ventriculostomy and have abnormal platelet function tests.

ii. Have a large ICH, receiving antiplatelet agents and requiring neurosurgery.

iii. Have acute neurologic decline with an intracranial hemorrhage.

Direct thrombin inhibitor

Diagnosis

E.g. Argatroban,dabigatran,bivalurudin

Idarucizumab (praxbind) 5g IV once.

-repeat dose in patients with high DTI exposure or poor renal function

-If hemostasis is not achieved:

4F-PCC 25–50 units/kg or activated 4F-PCC (FEIBA) 25–50 units/kg.

S.E. -Idarucizumab approved in late 2015 –antibody spicific for dabigatran .

-thrombosis ,limited data.

1.Chronic/poorly treated hypertension

2. Oral anticoagulant use

3. Cocaine/other stimulant use

4. Ischemic stroke with hemorrhagic transformation

5. Chronic alcohol intake

6. Brain tumor

7. Arteriovenous malformation

8. Amyloid angiopathy

a. Neurologic examination

b. Vital signs

c. NIH Stroke Scale and/or GCS score

* Imaging and other tests

a. CT or MRI scan of the brain

b. CT angiography or contrast-enhanced CT (to help identify patients at risk of hematoma expansion and to evaluate for underlying structural lesions)

c. Medication history to identify agents that might produce coagulopathy

d. laboratory tests.

e. Blood glucose

f. INR

g. CBC

Factor Xa inhibitors

Clinical Impact:

Anticoagulant reversal​

Death or major disability occurs in around 50% of patients.

Treatment :

Platelet transfusion

Anticoagulant reversal

e.g.Apixaban,rivaroxaban ,fondaparinox

Andexanet alfa (Andexxa)

low dose(400 mg IV) or high dose(800 mg IV).

or 4F-PCC 25–50 units/kg.

or activated 4F-PCC (FEIBA) 25–50 units/kg.

S .E. -Rebound anti-Xa therapeutic concentrations within 2 hr of infusion completion.

-thrombosis ,limited data.

Argatroban,dabigatran,bivalurudin

Direct thrombin inhibitor

Apixaban,rivaroxaban ,fondaparinox

Factor x antagonist

Warfarin

Vit. K antagonist

Unfractionated heparin,low molecular weight heparin

Asprin,clopidogrel,dipyridamol

antiplatelets

Warfarin

INR < 4 4F-PCC(prothrombin complex concentrate e.g. cofact) 25 units/kg.

INR 4–6 35 units/kg.

INR > 6 50 units/kg + vitamin K 10 mg IV

Alternative :

FFP (fresh frozen plasma) 10-15 ml/kg+vitamin k 10 mg IV.

S.E. Thrombosis, anaphylactoid reaction(vitamin K), pulmonary edema, or transfusion-related reaction (FFP)

Neurocritical Care

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