Management of raised intracranial pressure in children at emergency department

Authors: Vishwa CR1, Ramachandran Rameshkumar2, Arun Bansal1

Department and Institute:

1Division of Pediatric Critical Care, Department of Pediatrics, Advanced Paediatrics Centre,

Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh

2Division of Pediatric Critical Care, Department of Pediatrics, Jawaharlal Institute of

Postgraduate Medical Education & Research (JIPMER), Pondicherry

Corresponding author:

Arun Bansal, Professor, Division of Pediatric Critical Care, Department of Pediatrics, Advanced

Pediatrics Centre, Postgraduate Institute of Medical Education and Research (PGIMER),

Chandigarh, India - 160012. P: +919815455002; Email: drarunbansal@gmail.com

Financial assistance: None

Conflict of interest: None
Word count: Abstract: 145; Manuscript: 3925

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Abstract

Intractable raised intracranial pressure (ICP) is a potentially devastating complication of

traumatic or non-traumatic brain injury. It is associated with significant morbidity and

mortality. Prompt recognition and therapy directed at both reducing ICP and reversing its

underlying cause is needed to prevent complications and death. High index of suspicion is

necessary for early recognition as the signs and symptoms are non-specific. Main goal of

management is to prevent or reverse herniation and to maintain adequate cerebral perfusion

pressure. Appropriate management includes prompt stabilization and concomitant

identification of underlying etiology. Medical management includes stabilization of airway,

breathing and circulation along with general measures including maintaining head in midline,

head end elevation by 30 degrees, minimal stimulation, adequate sedation and analgesia and

hyperosmolar therapy. Surgically amenable conditions require early surgical intervention.

Short-term hyperventilation using bag ventilation can be resorted to if signs of impending

herniation are present.

Key words:

Intracranial pressure, Mean arterial pressure, Systolic blood pressure, Diastolic blood pressure,

Cerebral perfusion pressure, Traumatic brain injury, Cerebrospinal fluid, Glasgow coma scale,

Drug assisted intubation, Central nervous system, hyperventilation, decompressive

craniectomy

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Introduction

The causes of raised ICP in children can be divided into traumatic and non-traumatic causes.

Raised ICP in children is most commonly due to Traumatic Brain Injury (TBI). Worldwide, the

incidence of pediatric TBI varies from 47 - 280 per 100,000 children(1). The common non

traumatic causes leading to raised ICP in low middle income countries (LMIC) include CNS

infections, hydrocephalus, hypoxic/ ischemic brain injury, intraparenchymal bleed of vitamin K

deficiency, metabolic encephalopathy, brain tumors and cerebral infarction(2). Table 1 enlists

the causes of raised ICP in children.

Definitions and normal values

Intracranial pressure (ICP) – It is the pressure within the craniospinal compartment. The

normal pressure ranges between 5 to 15 mmHg(3). In newborn term infants it is 1.5 – 6 mmHg,

in young children 3–7 mmHg and in older children 10–15 mmHg. Any increase of ICP more

than the normal value for age is defined as raised ICP.

Cerebral perfusion pressure (CPP) – It is the pressure difference between mean arterial

pressure (MAP) and ICP. It is the pressure gradient which drives the cerebral blood flow.

Normal CPP in children is 40 to 60 mmHg.

Mean arterial pressure (MAP) – It is the average arterial pressure throughout one cardiac cycle.

MAP is given by the formula MAP = DBP + 1/3 (SBP - DBP) or MAP = DBP + 1/3(PP) (Where DBP

is Diastolic blood pressure, SBP is Systolic blood pressure and PP is pulse pressure). 50th

percentile MAP (for 50th percentile height) is given by the formula (1.5 x Age in years) + 55

mmHg.

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Pathophysiology of raised ICP

ICP is the total pressure exerted by the brain, blood and cerebrospinal fluid (CSF) in the

intracranial vault. According to Munroe Kellie hypothesis, the sum of the intracranial volumes

of brain (≈80%), blood(≈10%), and CSF(≈10%) is constant(4). Normally these 3 components

occupy the cranial vault at a low pressure, generally <10 mm Hg. In case of an expanding mass

lesion or brain edema, the initial compensatory mechanisms (leading to reduced CSF and

venous blood volumes) come into play and ICP remains low. However, further expansion of

the lesion or increase in cerebral edema, leads to an uncompensated state and exponential

increase in ICP.

Threshold for treatment of raised ICP

ICP - Sustained increase of ICP ≥ 20 mm Hg for ≥ 5 minutes warrants treatment(5). For all

practical purposes, if symptoms and signs of raised ICP are present, one should consider that

ICP is > 20 mmHg and treat accordingly(6). Sustained ICP values >40 mmHg indicates severe life

threatening raised ICP.

CPP - The optimal CPP for therapy remains unknown. The minimal CPP values necessary to

prevent ischemia are: infants/toddlers: > 40–50 mmHg; children: > 50–60 mmHg. CPP<40

mmHg is a significant predictor of mortality in children with TBI (7).

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Clinical features

Early symptoms and signs of raised ICP are non-specific and vary with age and rapidity of

pressure rise (gradual or acute). Cushing reflex (hypertension, bradycardia, irregular

breathing), becomes evident only later in the course of illness. It may be absent in children less

than 6 years with severe raised ICP(8). Table 2 summarizes the signs of raised ICP in children.

Features that suggest progressive elevation of ICP due to a brain tumor include headache,

nausea/vomiting, gait disturbance, vision changes, seizures, change in behavior, cranial nerve

deficits, altered mental status, back/neck pain, sensory deficits, focal motor weakness, ptosis,

and growth abnormalities(9).

Approach in an Emergency Room

Examination

Initial Assessment - It includes assessment of airway, breathing and circulation. Signs of

herniation should be looked for, if present then measures to decrease ICP should be rapidly

instituted.

Neurological Assessment - After the initial assessment, a thorough history and clinical

examination is performed to determine the possible etiology and further course of

management.

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Level of consciousness is assessed using Glasgow coma scale (GCS). Other objective scales used

are AVPU (Alert, Verbal, Pain, Unresponsive) scale and FOUR score(10)(11).

Pupillary abnormalities can be due to oculomotor nerve or brainstem involvement. Miotic

pupils may be due to pontine lesions or drug/toxins (Opioids, OP compounds). Unilateral

mydriatic pupils suggest midbrain lesion or uncal herniation. Bilateral mydriatic pupils are due

to massive midbrain hemorrhage, hypoxic brain injury or drug / toxin induced (Atropine,

tricyclic antidepressants, sympathomimetics).

Fundus examination may reveal papilledema and provide clue to underlying diagnosis.

However, absence of papilledema does not rule out raised ICP(12).

Signs of brainstem dysfunction should be noted. Presence of oculocephalic, oculovestibular,

corneal, cough and gag reflexes indicate intact brainstem functions. Figure 1 shows the

features of various brain herniation syndromes based on the location of herniation.

The motor system examination focuses on identifying posturing or flaccidity due to raised ICP

and the presence of any focal deficits.

General physical examination

Findings on the general physical examination may provide clues to the underlying cause for

raised ICP (e.g. jaundice/hepatomegaly in hepatic encephalopathy, rash in viral encephalitis

etc.). Abnormal patterns of respiration should be noted. Cheyne Stokes breathing is due to any

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etiology which leads to hypoperfusion of the respiratory center, Biot’s breathing is due to

involvement of pons and apneustic & ataxic breathing are due to involvement of medulla.

Principles of Therapy

Goals of management include measures to reduce ICP and concomitantly identify and address

the underlying cause. Factors aggravating or precipitating raised ICP (fever, hypoxia,

hypoglycemia, hypotension and any noxious stimulation) should also be identified and

addressed. Surgically amenable conditions should prompt an emergent neurosurgical

intervention. Figure 2 shows the algorithm for the management of raised ICP in children.

Measures to bring down ICP are divided into first, second and third tier therapies. First-tier

includes elevation and positioning of head, sedation and analgesia, hyperosmolar therapy, mild

hyperventilation, steroids and acetazolamide if indicated and CSF diversion therapy. Second

tier includes moderate hyperventilation, barbiturate coma and moderate hypothermia. Third

tier includes decompressive craniectomy or temporal lobectomy and profound

hyperventilation (targeting PCO2 up to 28 mm of Hg). The treatment principles and guidelines

are extrapolated from studies on patients with TBI and adult patients. Few studies have directly

evaluated management of raised ICP in children.

Airway, Breathing and Circulation

Airway - Most children with raised ICP are unable to maintain their airway and therefore at risk

of central hypoventilation and aspiration. Hence, airway patency should be ensured by

maintaining position of the head or by positioning the patient on the side. Visible secretions

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must be gently suctioned with adequate sedation and analgesia. Oral or nasopharyngeal

airways may be used if gag reflex is absent.

Indications for endotracheal intubation include(13)

1. Hypoxemia (Failure of supplemental oxygen to increase PaO2 to 55-60 mm Hg)

2. Hypercarbia (PaCO2 >45 mm Hg) or hypocapnia (hyperventilation causing PaCO2 <25

mm Hg)

3. Glasgow coma scale (GCS) <9, a drop in GCS of 3 or more irrespective of initial GCS

4. Anisocoria >1 mm

5. Abnormal breathing due to cervical spine injury, chest wall dysfunction and loss of

protective airway reflexes

Drug assisted intubation (DAI) – Intubation increases ICP through several mechanisms(14).

Cerebroprotective DAI is the preferred method for securing airway in patients with suspected

raised ICP. The procedure should be gentle and controlled. Prolonged or multiple attempts at

intubation should be avoided. Pharmacologic adjuncts are used to prevent hypotension,

hypoxemia, intracranial hypertension and gastric aspiration. Table 3 shows drugs that are used

in DAI. Continuous cardiorespiratory and SpO2 monitoring should be done.

Breathing - Maintain normoxia and normocarbia. 100% oxygen should be started with non-

rebreathing mask and if needed, bag valve mask ventilation. If mechanically ventilated, titrate

FiO2 to achieve a threshold SpO2 greater than 92% and PaO2 of 90–100 mm Hg. PaCO2 should

be 35-40 mm Hg as part of 1st tier therapy and 30-35 mm Hg as part of second tier therapy.

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Circulation - Maintain euvolemia. If there are signs of poor perfusion, give a bolus of normal

saline 20mL/Kg. Maintain MAP to achieve desired CPP. If needed use fluids and vasoactive

agents (Noradrenaline). MAP should be targeted above the 50th centile for the age. Colloids

are not recommended in acute brain injury (except in acute ischemic stroke) due to their

adverse effect on survival.

Medical Management

First tier therapy

1. Head position - Elevate head end of bed by 30° and keep head in neutral position to promote

venous drainage via the external jugular veins(15). Avoid kinking of neck.

2. Minimization of stimulation - Attempt should be made to reduce interventions which would

be painful or cause excessive stimulation. Lignocaine should be used prior to ET suction.

Nebulized 4% Lidocaine 1-2 mg/Kg mixed in 0.9% saline or IV 1–2 mg/Kg as 1% solution is given

90 seconds prior to suction.

3. Sedation and Analgesia -No single sedative agent has been proven to be superior in the

treatment of raised ICP or with respect to mortality or functional outcome. A combination of

sedo-analgesia like midazolam and fentanyl/morphine infusions are used. If benzodiazepines

are used, measures must be instituted to prevent and correct hypotension. In the absence of

known adrenal insufficiency, etomidate may be the sedative of choice. For unstable or

hypotensive TBI patients, ketamine can be considered. Other alternatives include

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dexmedetomidine. Dose is titrated to achieve a state behavior scale (SBS) of -3 to -2 and

COMFORT Pain Score of 17.

Ketamine was initially contraindicated in patients with TBI or raised ICP. However, some studies

have shown that ketamine can be helpful as a sedative within these patient groups (16). Its use

has been associated with maintenance of CPP during stimulating interventions in critically ill

with brain injuries. An RCT conducted at our center in children with raised ICP due to CNS

infections comparing Midazolam-Fentanyl and Midazolam-Ketamine for sedo-analgesia

showed that both had similar cerebral hemodynamic parameters (17).

4. Temperature - Fever increases metabolic rate by 10 to 13% per degree Celsius and is a potent

cerebral vasodilator. Goal is to maintain normothermia, with an upper limit of less than 38°C.

If child is febrile, use paracetamol 15 mg/Kg/dose oral or IV every 6 hours and surface cooling.

5. Glucose control - Early hyperglycemia is associated with increased mortality, prolonged

duration of mechanical ventilation, and PICU stay in children with TBI (18). The optimal glycemic

target range is uncertain(19). It is advisable to maintain random blood sugar (RBS) between 120

and 150 mg/dL. Hypogycemia (<60 mg/dL) and hyperglycemia (>180 mg/dl) should be avoided.

6. Anemia - Maintain hemoglobin concentration around 7g/dL, to help cerebral oxygen

delivery(20). In cases with severe anemia, a marked increase in CBF occurs to maintain cerebral

oxygen delivery.

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7. Osmotherapy- Hypertonic Saline (3% NaCl) – Hypertonic saline creates an osmotic force to

draw water from the interstitial space of the brain parenchyma into the intravascular space. It

promotes rapid CSF absorption, increases cardiac output, and expands intravascular volume

thereby augmenting the CPP with a positive inotropic effect. In different studies the

concentration of hypertonic saline used has varied from 1.7% to 30% (21). For continuous

infusion, 3% HS is preferred via central line. Usual dose is 5-10 mL/Kg as a loading followed by

0.1–1 mL/Kg/hour. In cerebral edema, the initial serum sodium goal is commonly set at 145–

155 mEq/L(22). It is intensified up to 160 mEq/L if clinically indicated. In general, it is well

tolerated and complications are rare. Monitor serum sodium and creatinine every 6 h. With

frequent monitoring hypertonic saline can be used up to 7 days (23). It is contraindicated if

serum osmolality >360 mOsmol/L.

Mannitol (20%) - It reduces blood viscosity and promotes plasma expansion and cerebral

oxygen delivery. This leads to cerebral vasoconstriction and reduced cerebral blood volume

(Rheological effect). It creates an osmotic gradient across the blood-brain barrier, leading to

the movement of water from the parenchyma to the intravascular space. Hence cerebral

volume is reduced. Mannitol also acts as an osmotic diuretic, leading to free water clearance

and an increase in serum osmolality. As a result, water moves from the intracellular to the

extracellular space, inducing a prolonged dehydrating effect. Reduction in ICP secondary to

mannitol administration is dose-dependent, occurring within 10 to 20 minutes with a peak

effect seen between 20 and 60 minutes and lasting between 4 to 6 hours. Dose ranges

between 0.5 to 1.5g/Kg/dose over 20-60 minutes. However, faster administration can be used

in acute ICP management. To prevent renal dysfunction, mannitol administration should be

avoided when serum osmolality is >320mOsm/L. Monitor the urine output and take care of

11
hypovolemia. Mannitol is contraindicated in decompensated shock, oliguria, anuria and heart

failure.

8. Seizure prophylaxis - Clinical seizures should be looked for and treated aggressively. There

are no clear guidelines for seizure prophylaxis in children with raised ICP. The committee for

TBI treatment guidelines in children also does not provide a consensus on the indications and

type or dosage of antiepileptic drugs. However, seizure prophylaxis may be considered in

patients at high risk of seizures such as those with severe head injury, impending brain

herniation, midline shift, focal symptoms and signs and CNS infections (meningitis and

encephalitis). Phenytoin or Levetiracetam can be used for the first 7 days. Comatose children

should also be considered for EEG monitoring and seizure prophylaxis as non-convulsive

seizures are not uncommon in them. The TBI guidelines also recommend use of continuous

EEG monitoring in all children with TBI especially when they are on neuromuscular blockade (24).

9. Antibiotics/Antiviral therapy - In a febrile child give empiric first dose of Ceftriaxone (50

mg/Kg IV 12 hourly) and Acyclovir (60 mg/Kg IV in 3 divided doses 8 hourly as infusion over 1–

2 hours) for herpes encephalitis. If child is a resident of P. falciparum endemic area, and has

hypoglycemia, elevated lactate, splenomegaly, anemia or absent meningeal signs then give

empiric IV Artesunate/Quinine.

10. Corticosteroids - Indications for corticosteroids include primary and secondary brain

tumors, tubercular meningitis, and neurocysticercosis. The most commonly used regimen is IV

dexamethasone 0.15 mg/Kg/dose every 6 hours (Maximum 16 mg/day). Routine use in TBI is

not recommended.

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11. Acetazolamide - It is used at a dose of 20-100mg/Kg/Day in 3 divided doses PO/IV

(Maximum dose of 2g/Day) in children with hydrocephalus.

12. Hypertension - Increase in blood pressure is common in response to raised ICP.

Characteristically rise in systolic-BP increase is greater than diastolic-BP. When autoregulation

is impaired, hypertension may increase CBF and ICP, and may exacerbate cerebral edema and

postoperative IC bleeds. Generally, it is left untouched in acute raised ICP unless underlying

cause is hypertensive encephalopathy. Treatment is also reasonable in patients with

impending congestive cardiac failure, those with evidence of rapidly worsening brain edema

on CT scan, and those with a persistent extreme surge in blood pressure. If it is decided to treat

hypertension, nifedipine, should be avoided; these could increase ICP. Sympathomimetic-

blocking drugs (esmolol, labetalol) or centrally acting alpha-receptor agonists (clonidine) are

preferred because they reduce BP without affecting ICP.

Second tier therapy

These options may be considered in hemodynamically stable patients with raised ICP

refractory to first tier measures, if continuous cardiovascular and electroencephalogram (EEG)

monitoring, and mechanical ventilation are available.

1. Barbiturate coma (Thiopental or pentobarbital) – Barbiturates can reduce the cerebral

metabolic rate and lower ICP. However, they also cause significant fall in systemic blood

pressure. Pentobarbital is given in a loading dose of 10 mg/Kg followed by 5 mg/Kg each for 3

doses. The maintenance dose is 1 to 2 mg/Kg/h, titrated to achieve a burst suppression pattern

on EEG.

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2. Moderate hypothermia (32–34°C) – It is a controversial second-tier therapy. Studies have

shown contrasting evidence with induced hypothermia in raised ICP. Neuromuscular blocking

agents and sedation must be used during hypothermia to prevent shivering. Prophylactic

moderate hypothermia is not indicated. However, it can be used as part of second tier measure

in raised ICP refractory to first tier measures. Whenever used, rewarming should be carried

out at a rate of 0.5–1.0°C every 12–24 hours or slower to avoid complications (24).

3. Hyperventilation - If there are signs of impending herniation (unequal pupils, posturing,

bradycardia, hypertension) mild short-term hyperventilation should be undertaken. This is

done by administering double the normal breathing rate for a given age for 10 minutes

duration. Look for reversal of unequal pupils, posturing and improvement in mentation. Target

a PaCO2 up to 28 mmHg. There is no role for prophylactic hyperventilation.

Third tier therapy

1. Decompressive craniectomy – Decompressive craniectomy may be a useful option for

control of increased ICP in children. Craniectomy performed within the first 24 h after severe

head injury, and in refractory raised ICP due to CNS infections may improve outcomes(25). A

study conducted at our center on decompressive craniectomy in pediatric non-traumatic

intracranial hypertension showed that it was beneficial in children with non-traumatic ICH due

to a focal pathology and midline shift (26).

Specific surgical management

CSF drainage should be considered in children with hydrocephalus. The means of CSF drainage

include external ventricular drainage (EVD) or Ventriculo-peritoneal (VP) shunt. Surgically

resectable mass lesions including tumors, hematoma or abscess should also be removed.

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Investigations

Baseline investigations

Complete blood count, Coagulogram, Serum electrolytes, Serum Calcium and Magnesium,

random blood sugar (RBS), Renal Function Test (RFT), Liver Function Test (LFT)

Specific investigations

Meningitis / encephalitis – CSF analysis for cells, protein, sugar and culture, triple antigen test,

Herpes Simplex Virus DNA PCR or Japanese B Encephalitis IgM antibody; Blood Culture

IEM – Arterial lactate, blood ketones, ammonia, Tandem Mass Spectroscopy (TMS), Gas

Chromatographic Mass Spectrometry (GCMS)

Tropical infections – Smear for malarial parasite, Dengue NS1 Ag or Serology, Widal serology,

scrub typhus serology

TB Meningitis – Chest X Ray, Mantoux test, Family screening, HIV serology, CSF analysis,

CBNAAT and ZN stain of gastric aspirate and/or CSF

Hepatic encephalopathy – LFT, Hepatitis A and E antibodies, Ammonia, ANA, Workup for

Wilsons disease

Diabetic ketoacidosis – HbA1c, RBS

Toxicology screen if indicated

Neuroimaging

Urgent neuroimaging may be needed, after initial stabilization and reversing potential or

clinically manifest herniation, to rule out surgically correctable causes of raised ICP. CT scan

will readily identify intracranial bleed, hydrocephalus, cerebral edema, compartmental shifts,

infarct, abscess or intracranial space occupying lesion (ICSOL). Non-contrast CT (NCCT) brain is

15
done to look for intracranial hemorrhage. If meningoencephalitis, brain abscess or cerebral

vein thrombosis are suspected Contrast enhanced CT (CECT) brain should be done. CT scan

signs of brain swelling are predictive of increased ICP, but it may be normal even in the

presence of documented raised ICP. Initial normal CT does not rule out an evolving infection

or raised ICP. In herpes simplex encephalitis, CT head is abnormal in approximately 50% of

cases but may be normal in the first 4–5 days. The TBI guidelines in children recommends

repeat CT scan of brain in children with raised ICP refractory to first tier management. This is

done to identify any lesions that could be corrected surgically (24). MRI with or without MR

Venography / Angiography can be done if CT is noncontributory. It can detect viral

meningoencephalitis (HSV encephalitis – Frontotemporal lesions, Japanese encephalitis –

Thalamic involvement), meningitis, TB meningitis, brain abscess, intracranial tumors, stroke,

demyelinating disorders, cerebral venous thrombosis

Monitoring

Monitor continuously for all vital parameters (temperature, heart rate, respiratory rate, blood

pressure, mean arterial pressure, capillary refill time), and level of consciousness (hourly),

neurological status, brainstem signs, oxygenation (SpO2) and End tidal CO2 (EtCO2), ICP, CPP.

Also assess adequacy of sedation and analgesia, input and output and bowel sounds. Random

blood sugar should be monitored at least every 6 h, and if hypoglycemia or hyperglycemia is

detected, monitor blood sugar every 1–2 h. Serum sodium should be monitored every 4–6

hourly, if 3% saline is used. EEG should be monitored to look for non-convulsive seizure. It can

also give clue to etiological diagnosis (HSV encephalitis – Periodic Lateralized Epileptiform

Discharges)

16
Disposition

All patients with raised ICP (especially those requiring 2nd and 3rd tier measures) should be

transferred to PICU for continuous monitoring, including ventilation, ICP monitoring, further

diagnostic evaluation and treatment.

17
18
19
Table 1. Common causes of raised ICP

Non-traumatic Traumatic
A. Increase in brain volume Intracranial hemorrhage (Subdural,
Cerebral edema due to primary CNS epidural, or intraparenchymal
illness hemorrhage)
Encephalitis Ruptured aneurysm
Meningitis Diffuse axonal injury
Reye’s syndrome Arteriovenous malformation or other
Cerebral edema secondary to systemic vascular anomalies
illness
Hypoxic ischemic injury
(hypoventilation, shock)
Ischemic stroke/ infarct
Metabolic encephalopathy –
hyperpyrexia, hepatic failure, lead
intoxication
Space occupying lesions
Hematomas
Tumors
Abscesses

B. Increase in blood volume

Venous obstruction – Cerebral venous
sinus thrombosis
Vasodilatation – Hypoxia, drugs or
hypercapnia
Status epilepticus
Vascular malformations

C. Increases in CSF volume

Obstructive hydrocephalus
Communicating hydrocephalus
Choroid plexus papilloma

D. Idiopathic or benign intracranial

hypertension

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Table 2. Signs and symptoms of raised ICP according to age and duration of disease

Infants Children
Chronic raised ICP Poor feeding Nausea
Irritability Vomiting
Lethargy Headache
Shrill cry Visual disturbance
Vomiting Abnormal gait
Lack of interest in surroundings Poor coordination
Bulging anterior fontanel Gait disturbances
Downward deviation of the eyes Papilledema
("sun-setting” sign) Gaze abnormality
Macrocephaly

Acute raised ICP Headache, vomiting, altered mental status, papilledema*,

hypertension, bradycardia, seizures

Impending brain Abnormal posturing (decerebration or decortication), abnormal

herniation pupillary dilatation, hypertension, bradycardia, irregular breathing,
sixth nerve palsy, papilledema*

* - Papilledema is not seen in infants due to open fontanelle

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Table 3. Sedative agents for intubating a child with raised ICP

Hemodynamically stable Hemodynamically unstable

Sedation Midazolam (0.2-0.3mg/Kg IV) Avoid Midazolam

Etomidate (0.1-0.3mg/Kg)

Analgesia Fentanyl (5-10mcg/Kg IV) plus

Lignocaine (1-1.5mg/Kg IV)

Neuromuscular blockade Vecuronium 0.1mg/Kg IV or

Atracurium 0.5mg/Kg IV or
Rocuronium 0.6–1.2mg/Kg IV

22
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