Neurocritical Care

Introduction

• Life threatening deterioration occurs most often within first 48 hours after onset of symptoms in patients with MCA stroke.

• Patients should be closely monitored (continuous ECG, pulse oximetry, frequent NBP, hourly neurologic checks for the first 24-48 hours after the insult

Need for ICU/HDU

• Reduced or rapidly deteriorating consciousness

• Ventilatory support

• Control of HTN with infusions

• Hypotension

• Comorbidities (OSA, COPD with hypoxia, ACS, uncontrolled DM, CKD V.

Diagnosis & MonitoringICH SAH Isc Stroke

ECG/NBP/SpO2 Yes Yes Yes

Clinical Hourly Hourly Hourly

ICP Consider Ventriculostomy

Ventriculostomy for hydrocephalus

As needed

ECG On admission On admission On admission

CT Within 45 min Within 45 min Within 45 min

CXR As needed As needed As needed

Initial Assessment

• Airway, Breathing, Circulation

• Glasgow Coma Scale

• Pupillary size & reaction

• History

Initial Resuscitation

• Restore – Ventilation

- Oxygenation

- Circulating Volume

- Blood Pressure

- Avoid Secondary Insult

BASIC NEURO CRITICAL ISSUES

RESPIRATORY PROTECTIONCARDIOVASCULAR PROTECTION

EUVOLEMIA IN ICPHYPERVOLEMIA IN ISCHAEMIA/USE ISOTONIC & OCCASIONALLY ISOTONIC SOLUTIONSKEEP MABP AT 100-120 mm Hg

RENAL HOMEOSTASISK > 4.0 meq/LCa > 8.5 meq/LPhosphorus > 2.5 mg/dlMagnesium > 0.2 mg/dl

PAIN ALLEVIATIONMorphine 2-4 ml / 4 hrlyMidazolam 0.1 mg / kg in divided dosesOlanzapine 5-10 mg BDAtivan 1-2 mg QID 12/1M/ORAL

Basic Monitoring

• Basic monitoring – ECG, SpO2, NBP for 24 hours

• Neuro Exam every hour for 24-48 hours & then according to clinical course.

• Urinary Catheter for monitoring urine output & facilitating nursing care

Oxygenation & Ventilation

• Nasal cannula (max 4lit/min to avoid mucosal damage, O2 mask (> 6lit/min to avoid CO2 rebreathing.

• NIV

• Intubation for declining consciousness

• Head of bed raised 30 degree

• Regular mouth care with chlorhexidine

Intubation & Tracheostomy• Early Tracheostomy if brain stem lesions,

large hemisphere infarctions or hemorrhages who are unlikely to regain protective airway reflexes within 2 weeks

• Inpatients with reduced level of consciuosness but preserved protective airway reflexes (coughing & gaging) in whom clearing of secretions seems possible, an extubation trial may be attempted even if GCS is low

NEUROLOGICAL & SYSTEMIC MONITORING

1. SERIAL NEUROLOGIC EXAMINATION2. MULTIMODALITY NEURO-MONITORING (Andrews 2000, Casteillo 2001)

A. NON BRAIN MONITORINGBP

CONTINUOUS CORE BODY TEMP ABG

B. BRAIN MONITORINGICP

WHOLE BRAIN MONITORING ELECTRICAL

VENOUS O2

CBFVREGIONAL CBF

METABOLISM

O2

Electrolytes

• Isotonic full electrolyte for maintenance

• K monitored frequently

• Diabetes Insipidus – desmopressin

• SIADH & Cerebral Salt Wasting is difficult to differentiate. Sodium replenishment with isotonic/hypertonic saline is often started empirically.

Fever & Temperature Control

Seizure Prophylaxis

• Documented seizures treated aggressively with benzodiazepines & barbiturates

• Phenytoin or levetiracetam prophylaxis only in patients with clinical seizures or suspicion on EEG

• Phenytoin is associated with skin reactions & drug fever. Enterally given 30 min after feeds for adequate absorption.

WHOLE BRAIN MONITORING

INTRACRANIAL PRESSURE (ICP)

MONRO-KELLIE DOCTRINE

NORMAL MEAN ICP UPTO 10mm Hg

ICP THRESH HOLD FOR THERAPY 20mm Hg

CEREBRAL PERFUSION PRESSURE (CPP=70~200)

CPP IS VITAL

CPP IS DETERMINED BY ICP & MABP

CPP = MABP – ICP

CPP TO BE KEPT ABOVE 70 mm Hg.

REGULAR VENOUS OXYMETRY

ELECTRICAL MONITORING

Cerebral Blood Flow• CBF is relatively constant over MAP 60-150 mm

Hg• CPP of 60-90 mm Hg provides appropriate CBF• In acute cerebral injury CPP < 60 decreases CBF &

cause cerebral ischemia. Increase in CPP > 80 may increase CBF & cause vasogenic edema & increased ICP

• When CBF decreases below 20ml/100g/min electrical & chemical cellular functions are interrupted & ischemic symptoms develop

BASIC CRITICAL CARE APPROACH

SECURE ABC

CAUTIONS DURING ENDOTRACHEAL INTUBATION

CERVICAL SPINE INSTABILITY IF ANY

CONCERN OF AGGRAVATING ICP

(RAPID SEQUENCE INTUBATION)

NEUROPROTECTION

GLUCOSE 80-120 mg / dl ( Rodorf 2000)

KEEP CORE BODY TEMP < 37.5 C

INSTITUTE EARLY NUTRITION /HYDRATION

ISSUE OF ed ICP

• NORMAL ICP 5 – 10 mm Hg• DETERMINANTS OF NORMAL ICP

Monro kelle phenomena

Volumes of - Brain

- CBF

- CSF• MANAGEMENT (Saurez 1999)

Medical vs Surgical.

Indication of ICP monitoring

• GCS 3-8

• Abnormal CT

• Normal CT with age >40

• BP <90

MEDICAL MANAGEMENT FOR ELEVATED INTRACRANIAL PRESSURE

(ICP)

• Head up position at 30o

• Neck in a straight position• No ETT tape ties compressing

jugular veins• Gentle Chest Physiotherapy• Minimum PEEP

MEDICAL MANAGEMENT FOR ELEVATED INTRACRANIAL PRESSURE

(ICP)

CORRECTION OF FACTORS EXACERBATING ICP

HYPERCARBIA (aim PaCO2 34-37)HYPOXIA (aim PaO2>100)HYPERTHERMIA (<37o C)ACIDOSISHYPERTENSION (150-160/90-100)HYPERVOLEMIA

MEDICAL MANAGEMENT FOR ELEVATED

ICP • Endotracheal Intubation & Mechanical

Ventilation if- Glasgow coma scale <8 - ICP - Respiratory instability

• Controlled Hyperventilation to a PCO2 of 28-33 (if Herniating) otherwise normocapnia

• Sedation & Paralysis

Spontaneous or Induced Hyperventilation

• Causes cerebral vasoconstriction • This decreases cerebral blood volume & ICP• A steady state is established in 3-4 hours• Excessive hypocapnia may cause excessive

vasoconstriction & cerebral ischemia• Rapid return to baseline PCO2 may produce cerebral

vasodilatation causing increased CBV & rise in ICP• Lack of response to hyperventilation is a poor

prognostic sign

Medications that Influence ICP

• Vasodilators (NTG, SNP, Hydralaine) can induce cerebral vasodilation & increase ICP

• Labetalol & Propranolol have minimal minimal effect on CBF & ICP

• Labetalol may reduce sympathetically mediated large vessel vasoconstriction

• Barbiturates(Thiopental & Phenobarbitone) lower ICP but decrease BP

Medications that Influence ICP

• Catecholamines increase cerebral metabolic rate & CBF

• RL is hypoosmolar & may exacerbate brain edema in the setting of osmotic diuretic therapy

• Glucose solutions may produce hyperglycemia

MEDICAL MANAGEMENT FOR ELEVATED INTRACRANIAL PRESSURE

(ICP)

• Osmotherapy (Goal : Dehydrate brain not the patient)Mannitol (20%) 0.25-1 gm/kg over 30-60 minutes 4-6 hrly

Monitor - Chemical status - ICP measures - Serum osmolality (300-320) - Osmolar gap > 15 - Volume status

Looses effect if Osm >320 & Na >160• Fluid restriction

Choice fluid Isotonic saline Not Glucose• Replacement of urinary loss with NS in those receiving

mannitol • Reduce gradually to permit excretion of idiogenic osmoles

OSMOTHERAPY : MANNITOL

• The good, bad, ugly and unknown about it

• The dilemma persists

• Is it all about timing?

• Is monitoring essential?

Osmolality

ICP

Others

OSMOTHERAPY & HYPERTONIC SALINE

• Use of Hypertonic Saline in cerebral edema and intracranial hypertension

(critical care med; Quereshi et.al. 2000)

• Treatment of refractory intracranial hypertension with 23.4% saline (30-60ml bolus every 6 hours)

(Crit care med Suarez et.a.l 1998)

•  Protocol

•  Extreme Care

PROTOCOL GUIDELINE FOR ICP CONTROL IN SEVERE HEAD INJURY PATIENTS

• HYPERTONIC SALINE (3%)0.5-1 ml/kg/hr (frequent S.Na to obtain desired S.Na conc. & intra vascular volume)

• FUROSEMIDE0.05 – 0.25 mg/kg/hr to obtain desired protocol.

• MANNITOLbolus infusion 1/8 –1/2 gm/kg at 4-6 hrly intervals to obtain desired osmolality(Protocol 1985-1990, Critical Care Med, 2000)

Venticulostomy

AIM OF METICULOUS BP CONTROL

Cerebral perfusion pressure ( MABP – ICP) to be kept at or around 70 mm Hg

against an elevated ICP

(Rosner & Johnson – 1995)

ARTERIAL BLOOD PRESSURE (BP) MANAGEMENT

AIM :To keep BP within limits of auto-regulation. continuous BP measurement.

BENEFITS OBTAINED:Avoidance of lowered BP (Ischaemia ed)Avoidance of elevated BP(Hematoma ed ,

Increased risk of ICH in Thrombolysis.Guiding hypervolemic / induced hypertension

(in SAH to prevent vasospasm in critical vascular stenosis).Helping in early detection of autonomic instability.

ISSUE OF BP CONTROL (Adams, 1996)

• MONITOR BP FOR 24 HOURS

Every 15 Minutes X 2 hrs

Every 30 Minutes X 6 hrs

Every hour X 18 hrs

Is the patient Hypertensive?

• What to do?Type of fluidsType of vasopressorsAmount of fluids

(heart failure ? In association)• Should we induce Hypertension?

Yes, when possibility of intra or extra cranial arterial stenosis.

BP Control

ICH SAH Isc Stroke

Goal 120-160 120-140 <180

Drugs for BP control• Urapidil (0.1-1.5 mg/kg/hr)• Nicardipine (1-1.5 mg/hr)• Esmolol (0.05-0.4 mg/kg/hr)• Labetolol• Hydralazine• Diltiazem• Verapamil• Clonidine

Is the patient hypertensive?(contd.)

• Raised BP is a defensive auto regulatory process in acute setting

• Hypertension alone in the absence of excessive CBF or myocardial dysfunction should not be treated because it often reflects homeostatic response to acute cerebral ischemia

• Previously HTN – 180/100-105• Mild HTN – 160-180/90-100• BP 220/120 demand therapeutic intervention but

the fall in BP should be gradual

Issue of high BP & its control

• Diastolic BP 140 mm Hg (Two readings 5 min apart)

Nitroprusside 0.5 to 10 g /kg/min till DBP is lowered by 20%.

• Systolic BP 230 mm Hg (± DBP 121-140 mm Hg)

Labetalol 20 mg over 2 min (Dose may be doubled)

repeat or double every 10 min till 150 mg given

or BP controlled.

If not switch back to Nitroprusside.

If SBP is 180 – 230 mm Hg and/or DBP is 105-120 mm Hg at two readings 5-10 min apart, give Labetalol 10 mg IV over 2 min.

The dose may be repeated at 20 min upto 150 mg.

Monitor BP every 15 min to prevent hypotension.

• Avoid sublingual nifedipine

Analgesia & Sedation

Infarcts• Thrombolysis

• Decompressive Surgery – considered within 8 hours if ICP cannot be controlled conventionally, after careful discussion. (massive hemispheric strokes, malignant MCA infarcts & high ICP)

Surgery

• ICH – large >30 ml, close to surface with high ICP may be treated surgically (clot removal)

Poor Predictors of Outcome

• Absence of Pupillary reflexes at any time• Absence of corneal reflex• Absence of Motor response to pain at day 3• Absence of oculo-vestibular response at

24hrs• Post-anoxic status/myoclonic status

epilepticus• EEG – burst supression