treatment of raised icp.pdf

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SYMPOSIUM ON PICU PROTOCOLS OF AIIMS

Management of Raised Intracranial Pressure

Naveen Sankhyan & K. N. Vykunta Raju &Suvasini Sharma & Sheffali Gulati

Received: 3 August 2010 /Accepted: 18 August 2010 /Published online: 7 September 2010# Dr. K C Chaudhuri Foundation 2010

Abstract Appropriate management of raised intracranial

pressure begins with stabilization of the patient andsimultaneous assessment of the level of sensorium and the

cause of raised intracranial pressure. Stabilization is

initiated with securing the airway, ventilation and circula-

tory function. The identification of surgically remediable

conditions is a priority. Emergent use of external ventricular

drain or ventriculo-peritoneal shunt may be lifesaving in

selected patients. In children with severe coma, signs of

herniation or acutely elevated intracranial pressure, treat-

ment should be started prior to imaging or invasive

monitoring. Emergent use of hyperventilation and mannitol

are life saving in such situations. Medical management

involves careful use of head elevation, osmotic agents, and

avoiding hypotonic fluids. Appropriate care also includes

avoidance of aggravating factors. For refractory intracranial

hypertension, barbiturate coma, hypothermia, or decom-

pressive craniectomy should be considered.

Keywords Coma . Critically ill child . Intracranial

hypertension . Traumatic brain injury

Introduction

Raised intracranial pressure (ICP) is a common neurolog-

ical complication in critically ill children. The cause may be

either an increase in brain volume, cerebral blood flow, or

cerebrospinal fluid (CSF) volume. Despite its high inci-dence, there are few systematically evaluated treatments of

intracranial hypertension. Most management recommenda-

tions are based on clinical experience and research done in

patients with traumatic brain injury.

Intracranial Pressure: Normal Values

Intracranial pressure is the total pressure exerted by the

brain, blood and CSF in the intracranial vault. The Monroe-

Kellie hypothesis states the sum of the intracranial volumes

of brain (≈80%), blood(≈10%), and CSF(≈10%) is constant,

and that an increase in any one of these must be offset by

an equal decrease in another, or else pressure increases. The

ICP varies with age and normative values for children are

not well established. Normal values are less than 10 to

15 mm Hg for adults and older children, 3 to 7 mm Hg for

young children, and 1.5 to 6 mm Hg for term infants [1].

ICP values greater than 20 to 25 mm Hg require treatment

in most circumstances. Sustained ICP values of greater than

40 mm Hg indicate severe, life-threatening intracranial

hypertension [2].

Cerebral Pressure Dynamics

Cerebral perfusion pressure (CPP) is a major factor that

affects cerebral blood flow to the brain. CPP measurement

is expressed in millimeters of mercury and is determined by

measuring the difference between the mean arterial pressure

(MAP) and ICP (CPP = MAP – ICP). It is apparent from

the formula that, CPP can reduce as a result of reduced

MAP or raised ICP, or a combination of these two. CPP

N. Sankhyan : K. N. Vykunta Raju : S. Sharma : S. Gulati (*)

Child Neurology Division, Department of Pediatrics, All India

Institute of Medical Sciences,

New Delhi 110029, India

e-mail: [email protected]

Indian J Pediatr (2010) 77:1409 – 1416

DOI 10.1007/s12098-010-0190-2


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measurements aid in determining the amount of blood

volume present in the intracranial space. It is used as an

important clinical indicator of cerebral blood flow and

hence adequate oxygenation. Normal CPP values for

children are not clearly established, but the following

values are generally accepted as the minimal pressure

necessary to prevent ischemia: adults CPP>70 mm Hg;

children CPP>50 – 60 mm Hg; infants/toddlers CPP>40 – 50 mm Hg [3].

Causes of Raised ICP

The various causes of raised ICP (Table 1) can occur

individually or in various combinations. Based on the

Monroe-Kellie hypothesis, raised ICP can result from

increase in volume of brain, blood, or CSF. Frequently it is

a combination of these factors that result in raised ICP. The

causes of raised ICP can also be divided into primary or

secondary depending on the primary pathology. In primarycauses of increased ICP, normalization of ICP depends on

rapidly addressing the underlying brain disorder. In second-

ary causes of raised ICP the underlying systemic or

extracranial cause has to be managed.

Assessment and Monitoring

Identify children at risk for raised ICP (Table 1). Those at

greater risk are children with head trauma, suspected

neuroinfections, or suspected intracranial mass lesions.

Raised pressure usually manifests as headache, vomiting,

irritability, squint, tonic posturing or worsening sensorium.

However the symptoms depend on the age, cause, andevolution of the raised ICP.

Initial Assessment

As with any sick child, one begins with assessment and

maintenance of the airway, breathing and circulatory function.

An immediate priority is to look for potentially life threatening

signs of herniation (Table 2). If these signs are present then

measures to decrease intracranial pressure should be rapidly

instituted. Cushing’s triad (bradycardia, hypertension and

irregular breathing) is a late sign of herniation.

Neurological Assessment

After the initial stabilization, a thorough history and clinical

examination is performed to determine the possible etiology

and further course of management. Pupillary abnormalities and

abnormalities in ocular movements as determined by sponta-

neous, dolls eye or cold caloric testing are important clues to the

localization of brainstem dysfunction. The examination of

fundus is focused on detection of papilledema, keeping in mind

that its absence does not rule out raised ICP. The motor system

examination focuses on identifying posturing or flaccidity due

to raised ICP or focal deficits. Findings on the general physical

and systemic examination may provide clues to the underlying

cause for raised ICP (e.g. jaundice/hepatomegaly in hepatic

encephalopathy, rash in viral encephalitis etc.).

Neuroimaging

The imaging study of choice for the patient with raised

intracranial pressure presenting to the emergency room is a

computed tomography (CT) scan. A contrast study is

helpful to identify features of infection (meningeal en-

hancement, brain abscess etc.) and tumors. If CT scan is

normal, and the patient has clinical features of raised ICP,

then an MRI with MR venogram must be obtained once the

patient is stabilized. MRI can pick up early stroke, venous

thromboses, posterior fossa tumors and demyelinating

lesions which might be missed on CT.

Invasive ICP Monitoring

ICP monitoring is used mainly to guide therapy, such as

in d etermining when to d rain C SF o r admin ister

Table 1 Causes of raised intracranial pressure

Increased brain volume

Intracranial space occupying lesions

Brain tumors

Brain abscess

Intracranial hematoma

Intracranial vascular malformation

Cerebral edema

Encephalitis (viral, inflammatory)

Meningitis

Hypoxic ischemic encephalopathy

Traumatic brain injury

Hepatic encephalopathy

Reye’s syndrome

Stroke

Reye’s syndrome

Increase in CSF volume

Hydrocephalous

Choroids plexus palpilloma

Increased blood volume

Vascular malformations

Cerebral venous thrombosis

Meningitis, encephalitis

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mannitol or sedation. In addition, invasive monitoring

allows for observation of the shape, height, and trends

of individual and consecutive ICP waveforms that may

reflect intracranial compliance, cerebrovascular statusand cerebral perfusion. Guidelines for ICP monitoring

are availab le for traumatic b rain injury [4]. ICP

monitoring is indicated for a patient with Glasgow Coma

Scale (GCS) score of 3 – 8 (after resuscitation) with either

an abnormal admission head CT or motor posturing and

hypotension [4]. The role and benefit of ICP monitoring

in other conditions such as subarachnoid hemorrhage,

hydrocephalus, intracranial infections, and Reyes syn-

drome remains unclear. Also, the availability of this

modality is limited. In other brain injuries, such as

hypoxic and ischemic injuries, monitoring ICP has not

been shown to improve outcome [5].

Management of Intracranial Hypertension

The goal for patients presenting with raised ICP is to identify

and address the underlying cause along with measures to

reduce ICP (Fig. 1, Table 3). It is important not to delay

treatment, in situations where identifying the underlying cause

will take time. When elevated ICP is clinically evident, the

situation is urgent and requires immediate reduction in ICP.

Avoidance of factors aggravating or precipitating raised ICP is

an important goal for all children with intracranial hyperten-

sion. The availability of ICP monitors is not universal and

should not come in the way of emergent therapy.

ABCs

The assessment and management of the airway, breathing

and circulation (ABCs) is the beginning point of manage-

ment. Early endotracheal intubation should be considered

for those children with GCS


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Osmotherapy

Mannitol

Mannitol has been the cornerstone of osmotherapy in raised

ICP. However, the optimal dosing of mannitol is not

known. A reasonable approach is to use an initial bolus of

0.25 – 1 g/kg (the higher dose for more urgent reduction of

ICP) followed by 0.25 – 0.5 g/kg boluses repeated every 2 –

6 h as per requirement. Attention has to be paid to the fluid

balance so as to avoid hypovolemia and shock. There is

also a concern of possible leakage of mannitol into the

damaged brain tissue potentially leading to “rebound” rises

in ICP [13]. For this reason, when it is time to stop

mannitol, it should be tapered and its use should be limited

to 48 to 72 h. Apart from hypotension, rebound rise in ICP,

mannitol can also lead to hypokalemia, hemolysis and renal

failure.

Hypertonic Saline

Hypertonic saline has a clear advantage over mannitol in

children who are hypovolemic or hypotensive. Other

situations where it may be preferred are renal failure or

serum osmolality >320 mosmol/Kg. It has been found

effective in patients with serum osmolality of up to

Surgical intervention

Evacuation of hematoma

CSF diversionNeuroimaging : Suggestive of

surgically remediable cause;

hydrocephalous, large hematoma, etc

“Yes”

“No” or delay

Immediate Measures*

Maintain airway and adequate

ventilation and circulation

Head end elevation-15-

Hyperventilation: (target PCO2 : 30-35mm Hg ) To be

used in emergent situations like herniation to bridge more

definitive therapy. Not to be used for more than a few

Osmotherapy**

Child with signs/symptoms of raised ICP

Decompressive craniectomy

BP Normal: Mannitol Hypotension, Hypovolemia Serum osmolality >320

mOsm/kg, Renal failure: Hypertonic Saline

Other options;***

Heavy sedation and paralysis

Barbiturate coma

Hypothermia

Special situations

Steroids: Intracranial tumors with perilesional edema, neurocysticercosis withhigh lesion load,

ADEM, pyomeningitis,TBM, Abscess

Acetazolamide: Hydrocephalus, Benign intracranial, high altitudei llness

Ongoing care

Sedation and analgesia

Avoid noxious stimuli

Control fever

Prevention andtreatment of

seizures

Maintain euglycemia

No hyotonicfluid infusions

Maintain Hb above 10gm%

.

.

.

.

.

.

.

(*- May be initiated immediately after brief evaluation if situation is urgent. Measures also used in children awaiting surgical/radiologial

procedures, ** -Preferable to monitor ICP, ***- undertake only with ICP monitoring)

Fig. 1 Algorithmic approach to

a child with raised ICP

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360 mosmol/Kg [14]. Concerns with its use are bleeding,

rebound rise in ICP, hypokalemia, and hyperchloremic

acidosis, central pontine myelinolysis, acute volume over-

load, renal failure, cardiac failure or pulmonary edema [15 –

17]. Despite these concerns, current evidence suggests that

hypertonic saline as currently used is safe and does not

result in major adverse effects [18]. In different studies the

concentration of hypertonic saline used has varied from

1.7% to 30% [18]. The method of administration has also

varied and hence, evidence based recommendations are

difficult. It would be reasonable to administer hypertonic

saline as a continuous infusion at 0.1 to 1.0 mL/kg/hr, to

target a serum sodium level of 145 – 155 meq/L [19, 20].

Serum sodium and neurological status needs to be closely

monitored during therapy. When the hypertonic saline

therapy is no longer required, serum sodium should be

slowly corrected to normal values (hourly decline in serum

sodium of not more than 0.5 meq/L) to avoid complications

associated with fluid shifts [6]. Monitoring of serum

sodium and serum osmolality should be done every 2 – 4 h

till target level is reached and then followed up with 12

hourly estimations. Under careful monitoring, hypertonic

saline has been used for up to 7 days [21].

Other Agents

Acetazolamide (20 – 100 mg/kg/day, in 3 divided doses, max

2 g/day) is a carbonic anhydrase inhibitor that reduces the

production of CSF. It is particularly useful in patients with

hydrocephalous, high altitude illness and benign intracranial

hypertension. Furosemide (1 mg/kg/day, q8hrly), a loop

diuretic has sometimes been administered either alone or in

combination with mannitol, with variable success [22, 23].

Glycerol is another alternative osmotic agent for treatment of

raised ICP. It is used in the oral (1.5 g/kg/day, q4 – 6hrly) or

intravenous forms. Given intravenously, it reduces ICP with

effect lasting for about 70 min without any prolonged effect

on serum osmolality [24]. Glycerol readily moves across the blood brain barrier into the brain. Though not proven, there

is concern of rebound rise in ICP with its use.

Steroids

Glucocorticoids are very effective in ameliorating the

vasogenic edema that accompanies tumors, inflammatory

conditions, infections and other disorders associated with

increased permeability of blood brain barrier, including

surgical manipulation [25]. Dexamethasone is the preferred

agent due to its very low mineralocorticoid activity (Dose:

0.4 – 1.5 mg/kg/day, q 6 hrly) [26]. Steroids are not routinely

indicated in individuals with traumatic brain injury [27].

Steroids have not been found to be useful and may be

detrimental in ischemic lesions, cerebral malaria and

intracranial hemorrhage [26, 28, 29].

Sedation and Analgesia

Raised ICP is worsened due to agitation, pain, and patient-

ventilator asynchrony [8]. Adequate analgesia, sedation and

occasionally neuromuscular blockade are useful adjuvant in

the management of raised ICP. Appropriate Analgesia and

sedation is usually preferred over neuromuscular blockade,

as it is quickly reversible and allows for neurological

monitoring. For sedation it is preferable to use agents with

minimal effect on blood pressure. Short acting benzodiaze-

pines (e.g. midazolam) are useful for sedation in children. If

the sedatives are not completely effective, then a neuro-

muscular blocking agent (e.g. Pancuronium, atracurium,

vecuronium) may be required.

Table 3 Summary of measures to reduce intracranial pressure

1 Assessment and management of ABC’s (airway, breathing,

circulation)

2 Early intubation if; GCS 320 mOsm/kg, Renal failure,

Dose: 0.1 – 1 ml/kg/hr infusion, Target Na+−145 – 155 meq/L.

7 Steroids: Intracranial tumors with perilesional edema,

neurocysticerocosis with high lesion load, ADEM,

pyomeningitis, TBM, Abscess

Acetazolamide: Hydrocephalous, benign intracranial, high altitude

illness

8 Adequate sedation and analgesia

9 Prevention and treatment of seizures: use Lorazepam or midazolam followed by phenytoin as initial choice.

10 Avoid noxious stimuli: use lignocaine prior to ET suctioning

[nebulized (4% lidocaine mixed in 0.9% saline) or intravenous

(1 – 2 mg/kg as 1% solution) given 90 sec prior to suctioning]

11 Control fever: antipyretics, cooling measures

12 Maintenance IV Fluids: Only isotonic or hypertonic fluids (Ringer

lactate, 0.9% Saline, 5% D in 0.9% NS), No Hypotonic fluids

13 Maintain blood sugar: 80 – 120 mg/dL

14 Refractory raised ICP:

• Heavy sedation and paralysis

• Barbiturate coma

• Hypothermia

• Decompressive craniectomy

Indian J Pediatr (2010) 77:1409 – 1416 1413


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Minimization of Stimulation

Attempt must be made to reduce the number of elective

interventions that are likely to be painful or excessively

stimulating. Lidocaine instilled endotracheally has been

shown to prevent the endotracheal suctioning-induced

ICP increase and CPP reduction in adults with severe

traumatic brain injury [30]. It is recommended to instillidocaine at body temperature, slowly, and through a fine

tube advanced into the endotracheal tube within its length

(avoid direct contact with the mucosa) [30]. Lidocaine can

be given in nebulized (usually 4% lidocaine mixed in

0.9% saline) or intravenous forms (1 – 2 mg/kg as 1%

solution given 90 sec prior to suctioning) for the same

purpose [9].

Fluids

The main goal of fluid therapy is to maintain euvolemia,normoglycemia and prevent hyponatremia. Children with

raised ICP should receive fluids at a daily maintenance

rate, as well as fluid boluses as indicated for hypovole-

mia, hypotension, or decreased urine output. Mainte-

nance fluids usually consist of normal saline with daily

requirements of potassium chloride based on body

weight. All fluids administered must be isotonic or

hypertonic (e.g. Ringer lactate, normal saline) and

hypotonic fluids must be avoided (e.g. 0.18% saline in

5% dextrose, Isolyte P) [7]. Hyponatremia is to be

avoided and if it occurs, must be corrected slowly.

Blood Glucose

Blood glucose must be maintained between 80 – 120 mg/dL in

a child with raised ICP [7]. Studies in children with traumatic

brain injury have shown that hyperglycemia is associated

with poor neurological outcome and increased mortality [31].

On the other hand, hypoglycemia is known to induce a

systemic stress response and cause disturbances in CBF,

increasing the regional CBF by as much as 300% in severe

hypoglycaemia. Hypoglycemia can also lead to neuronal

injury and therefore, should be managed aggressively.

Temperature Regulation

Maintaining normothermia is important to prevent compli-

cations of temperature fluctuations. This is achieved by

frequent measurements of body temperature and correcting

any fluctuations using antipyretics, and assisted cooling or

heating per needed.

Prevention and Treatment of Seizures

Children with significant head injury and neuroinfections are at

risk for seizures. Seizures can increase CBF and cerebral blood

volume leading to increased ICP. They can also increase the

metabolic needs of the brain and predispose to ischemia [6].

Seizures, if clinically evident, must be treated. Given the lack

of studies in children and in patients with non traumatic raisedICP, evidence based recommendation regarding prophylactic

anti-epileptic therapy are not possible. But it is reasonable,

and a common practice is to use prophylactic anticonvulsants

for short term in children with raised ICP, unless indicated

otherwise [6, 26]. If available, it is prudent to use continuous

electroencephalography (EEG) to identify subclinical seizure

activity in children with increased risk for seizures.

Anemia

Theoretically, anemia would increase CBF and secondarilyraise ICP. There have been case reports of patients with severe

anemia presenting with symptoms of raised ICP and

papilledema [32]. Though not rigorously studied, it is

common practice to maintain hemoglobin above 10 g/dL

in patients with traumatic brain injury and raised ICP.

Surgical Therapy

Cerebrospinal Fluid Drainage CSF drainage using a

external ventricular drainage (EVD) or ventriculoperitoneal

shunt provides for an immediately effective means to lower

ICP. In addition EVD provides a method for continuously

monitoring ICP. CSF drainage is particularly useful in the

presence of hydrocephalus. But it may be considered even

in children without hydrocephalus. Its effectiveness in

lowering ICP has been shown to be comparable to

intravenous mannitol or hyperventilation [33]. However, it

is of limited utility in diffuse brain edema with collapsed

ventricles.

Resection of Mass Lesions Surgery should be undertaken

when a lesion amenable to surgical intervention is identified

as the primary cause of raised ICP. Common situations

where this neurosurgical intervention is preferentially

employed are acute epidural or subdural hematomas, brain

abscess, or brain tumors.

Target of Therapy

When facilities for ICP monitoring are available, the

management is tailored to maintaining an adequate CPP

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(i.e. Children >50 – 60, infants/toddlers >40 – 50 mm Hg)

and lower ICP to acceptable levels (i.e.


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nous corticosteroid in adults with head injury outcomes at 6

months. Lancet. 2005;365:1957 – 9.

28. Feigin VL, Anderson N, Rinkel GJ, Algra A, van Gijn J,

Bennett DA. Corticosteroids for aneurysmal subarachnoid

haemorrhage and primary intracerebral haemorrhage. Cochrane

Database Syst Rev 2005; CD004583.

29. Hoffman SL, Rustama D, Punjabi NH, et al. High-dose dexameth-

asone in quinine-treated patients with cerebral malaria: a double-

blind, placebo-controlled trial. J Infect Dis. 1988; 158:325 – 31.

30. Bilitta F, Branca G, Lam A, Cuzzone V, Doronzio A, Rosa G.Endotraceal lidocaine in preventing endotracheal suctioning

induced changes in cerebral hemodynamics in patients with

severe head trauma. Neurocrit Care. 2008;8:241 – 6.

31. Cochran A, Scaife ER, Hansen KW, Downey EC. Hyperglycemia

and outcomes from pediatric traumatic brain injury. J Trauma.

2003;55:1035 – 8.

32. Biousse V, Rucker JC, Vignal C, et al. Anemia and papilledema.

Am J Ophthalmol. 2003;135:437 – 46.

33. Fortune JB, Feustal PJ, Graca L, et al. Effect of hyperventilation,

mannitol, and ventriculostomy drainage on cerebral blood flow

after head injury. J Trauma. 1995;39:1091 – 9.

34. Schalen W, Sonesson B, Messeter K, et al. Clinical outcome

and cognitive impairment in patients with severe head injuries

treated with barbiturate coma. Acta Neurochir (Wien).

1992;117:153 – 9.

35. Hutchison JS, Ward RE, Lacroix J, et al. Hypothermia therapy

after traumatic brain injury in children. N Engl J Med.

2008;358:2447 – 56.

36. Clifton GL, Miller ER, Choi SC, Levin HS, et al. Lack of effect of

induction of hypothermia after acute brain injury. N Engl J Med.

2001;344:556 – 63.37. Adelson PD, Ragheb J, Kanev P, et al. Phase II clinical trial of

moderate hypothermia after severe traumatic brain injury in

children. Neurosurgery. 2005;56:740 – 54.

38. Berger S, Schwarz M, Huth R. Hypertonic saline solution and

decompressive craniectomy for treatment of intracranial hyper-

tension in pediatric severe traumatic brain injury. J Trauma.

2002;53:558 – 63.

39. Taylor A, Butt W, Rosenfeld J, et al. A randomized trial of very

early decompressive craniectomy in children with traumatic brain

injury and sustained intracranial hypertension. Child’s Nerv Syst.

2001;17:154 – 62.

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