Brain death declaration in children - PowerPoint Presentation

Slide1

Brain death declaration in children

Dr

Lokesh

Lingappa

Consultant

Paediatric

Neurologist

Rainbow Children’s

Hospital and

Perinatal

Centre, HyderabadSlide2

outline

Limitations of current guidelines

Testing process

Are there differences adult/pediatric

Problems of newborn testing

Fallacies in

intepretation

of signs and testing

resultsSlide3

Key message

The

diagnosis of brain death should remain a clinical one to be made at the bedside by knowledgeable physicians who, in concert with grieving families, make the most agonizing of all life’s events (the death of a child) as bearable as possible for all concerned.

Freeman JM, Ferry PC. New Brain Death Guidelines in Children Slide4

Understanding limitations of

pediatric

brain death guidelines

Guidelines are 20 years old

Relied heavily upon EEG testing

Guidelines did not specifically address the trauma population

Guidelines were based upon limited clinical experience at the time of publication

Guidelines were based upon age criteria

No guidelines for neurologic death in neonates

Waiting times have never been validatedSlide5

History

Determination of cause of death is necessary to ensure the absence of treatable or reversible conditions (

ie

, toxic or metabolic disorders, hypothermia, hypotension, or surgically remediable conditions).Slide6

Primary requirement

Irreversibility of brain function cessation is recognized

Cause of coma is established and is sufficient to account for the loss of brain function

Possibility of recovery of any brain function is excluded

Cessation of brain function persists for an appropriate period of observation or trial of

therapy Slide7

Diagnostic criteria

Cessation of all brain function is recognized.

Cerebral functions are absent (

ie

, unresponsiveness)

Brainstem

functions are absent:

Pupillary

light reflex

Corneal reflex

Oculocephalic

/

oculovestibular

reflex

Oropharyngeal

reflex

Respiratory (

apnea

using an accepted

apnea

testing procedure)Slide8

Confounding factors

Complicating conditions are

excluded

Drug and metabolic intoxication

Hypothermia

Circulatory

shock

The patient has been monitored for an appropriate observation

periodSlide9

Brainstem testingSlide10

Without confirmatory tests

12 hours when the

etiology

of the irreversible condition is well established

24 hours for anoxic injury to the brain

With confirmatory tests

EEG: Irreversible loss of cortical functions with ECS, together with the clinical findings of absent brainstem functions, confirms the diagnosis of brain death.

CBF: Absent CBF demonstrated by radionuclide scanning or intracranial 4-vessel cerebral angiography in conjunction with clinical determination of absence of all brain function for at least 6 hours is diagnostic of brain deathSlide11

Age dependent Observation period

age

Hours between 2 examination

Recommended

number of

EEGs

7 days to 2 months

48

2

2 months to 1 year

24

2

Beyond 1 year

12

None neededSlide12

Brain death and organ donation Slide13
Slide14

Rainbow data 2009 29/79

Head injury

3

Near Drowning

2

CNS infection

9

Asphyxia

1

Metabolic

disorders

9

Cerebrovascular

disorders

1

Miscellaneous

4Slide15

Neonatal brain deathSlide16

Neurologic death in the neonate

“Brain death can be diagnosed in the term infant, even at less than 7 days of age. An observation period of 48 hours is recommended to confirm the diagnosis. If an EEG is

isoelectric

or if a CBF study shows no flow, then the observation period can be shortened to 24 hours.”

Ashwal

. Brain death in the newborn. Clinics in

Perinatology

1997;24:859-879Slide17

Brain death in the neonate

The

younger the child, the more one needs to exercise caution in determining brain death

A second opinion from a colleague in

pediatric

critical care or someone who is specialized in the neurosciences is reasonable

Physical examination criteria may require a longer observation time based upon mechanism of cerebral injury

Use of ancillary test may be beneficial, but may also confuse the issue in the neonateSlide18

The absence of

any form

of repetitive, sustained,

purposeful activity

on serial

examinations must

be documented; likewise,

brain death

must be differentiated

from other

states of unconsciousness,

such as

the vegetative

stateSlide19

preterm and term neonates

several

of the cranial

nerve responses

are not fully developed.

pupillary

light

reflex is

absent before 29 to 30 weeks’ gestation,

oculocephalic

reflex may

not be elicited before 32 weeks

’ gestation

Term and preterm

infants are

difficult to examine because

their smallness

makes it technically

difficult to

assess Slide20

Preterm and neonate

Assessment of

pupillary

reactivity can

be compromised

difficulties

in

gaining access –incubator,

by corneal injury,

retinal

hemorrhages

, and other

anatomical factors (swelling

or

partial

fusion of the

eyelids)

smaller

size of the pupils

in newborns- make

assessment of the loss of

pupillary

reactivity troublesomeSlide21

Preterm and neonate

Assessing the

caloric response adequately

more

difficult in neonates with

a small

external ear canal;

both

the

oculocephalic

(doll’s

eye)

and

oculovestibular

(caloric

) reflex

should always be

examined

corneal reflex-

easiest brain stem

reflex to

examine in neonates and infants

, it

is often the least

reliable

Contact irritation

, dehydration and

maceration of

the cornea, use of

lubricant drops

,

and use of analgesic medications often adversely affect tactile sensory informationSlide22

MRI and CT of Neonates -HIESlide23

Neuroimaging in Decision process

Neonatal CT

Follow up CT brainSlide24

Ancillary testingSlide25

Considerations when diagnosing brain death in children

Many

times the cause of the child’s neurologic demise is known

Based upon presentation and examination many times we know that there will be no hope for survival or if the child does survive, the outcome will be dismal

The waiting period may be extended or decreased depending upon social and family related

issuesSlide26

Ancillary testing

Ancillary test that may aid in the diagnosis of brain death

EEG

Cerebral angiography

Radionuclide Scans

Brainstem

evoked responses

Doppler

sonographySlide27

Ancillary testing

Ancillary tests may aid in the diagnosis of brain death

Ancillary tests can provide additional information to help confirm brain death in situations where clinical examination and

apnea

testing are not feasible or cannot be completed because of undue

circumstance

Facial

injury

Acute lung injury

Cardiovascular instabilitySlide28

Ancillary testing

Ancillary

tests are not mandatory

• Ancillary tests may provide another layer of comfort to the physician who is uncomfortable declaring brain death on clinical exam alone

• Ancillary tests may reduce observation periods thus increasing potential for retrieving viable transplant tissue

• Ancillary tests may also delay or prolong observation periodSlide29

Recommendation for EEG

the American Electroencephalographic Society retrospectively surveyed 1665 patients with

electrocerebral

silence (ECS), that is, no evidence of brain electrical activity greater than 2 µV between electrode pairs placed at a distance of 10 cm or more, who were in various levels of

coma

Only 3 of the 1665 patients recovered cerebral functionSlide30

EEG in

infants and

children

shorter

interelectrode

distances;

external

artifacts

in

newborn ICUs and PICUs;

Distances between

the heart and the brain

, making

the

electrocardiographic contribution disproportionately large

reduced amplitude of

cortical potentials in preterm

and term neonates

longer duration

of the

effect of depressant

medications

greater tendency for

suppression burst

patterns in infants with

neurological disordersSlide31

Need for EEG

Two cases of acute inflammatory

demyelinating

polyradiculoneuropathy

have

-at

satisfied the clinical criteria for brain death but had preserved EEG

activity

EEG

has an important role in the confirmation of brain death in such

casesSlide32

Electrocerebral silenceSlide33

EEG contd

EEG

patterns

may show

low-voltage

theta or

beta activity or intermittent

spindle activity

Such activity in

functionally dead

brains may persist

for days

Data from several studies

indicate that

the initial EEG in

brain dead children

is

isoelectric

in 51%

to 100

% of patients (mean 83

%).

In

most children

who initially have

EEG activity

, follow-up studies

usually show

evolution to

ECSTypically, when the initial EEGSlide34

EEG contd

ECS may occur soon after

an infant

or a child has had a

cardiac arrest

.

In

infants in whom the

initial EEG

(typically obtained 8-10

hours after

cardiac arrest) showed ECS,

a repeat

study 12 to 24 hours

later may

show diffuse low-voltage

activity

Most of these infants die of

complications - acute catastrophic

injury; the

remaining survivors permanent vegetative

or minimally

conscious stateSlide35

EEG and drugs

children, the most

common medications

causing reversible

loss of

brain

electrocortical

activity

include barbiturates

(

eg

,

phenobarbital

), benzodiazepines

, narcotics, and certain

intravenous (thiopental,

ketamine

,

midazolam

) and

inhalation (

halothane and

isoflurane

)

anesthetics

.

Data from a

study

in 92

children indicated

that therapeutic levels

of

phenobarbital (ie, 15-40 μg/mL) do not affect the EEGSlide36

Need for repeat EEG

Data on 37 of 53

brain-dead newborns

in whom EEGs were performed

ECS

(n = 21), very low

voltage

(

n = 13),

burst

suppression (n = 1

),

seizure

activity (n = 1), and

normal activity

(n = 1

).

Almost all

patients whose

first EEG showed ECS

had ECS

on the second study, and

most patients

who did not show ECS

on the

first EEG did so on a repeat

study

The data suggest that only a

single EEG

showing ECS is necessary

to confirm

brain death, provided the results of the examination remain unchangedSlide37

Cerebral blood flow studies

The absence of CBF

in brain

death is due primarily to

low cerebral

perfusion pressure

and secondarily to

release of vasoconstrictors

from vascular smooth muscle Slide38

HMPO SPECTSlide39

Cerebral blood flow-neonatal issues

Newborns have

patent sutures and

an open

fontanel, increases in ICP

after acute

injury are

not

significant

cascade

of

herniation

from

increased ICP

and reduced cerebral

perfusion is

less likely to occur in newborns

Brain death

can be diagnosed in

newborns (

even when younger than 7 days)

if

physician is aware of the

limitations of

the clinical examination and

laboratory testingSlide40

Institutional Guidelines

Does

a policy regarding declaration of death exist in your institution

? Policy

should provide guidelines allowing flexibility and individuality for each child and their

family

Decisions regarding determination of brain death should be left to the physician’s discretion within evolving standards of medical

care

Who declares brain death in your institution

?

Concentrate

your efforts on educating these individuals and involve them in the establishment of institutional guidelinesSlide41
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Take home messages

Neurologic

death occurs in children

• There are no unique legal issues in determining neurologic death in children

• Neurologic death is a clinical diagnosis

• Ancillary studies are not mandatory, however they can assist in determining neurologic death in certain situations

• Ancillary studies can reduce or prolong the recommended observation period

• Observation periods have never been validated and are meant to serve as guidelines only

• Neurologic death can occur and be diagnosed in infants less than 7 days of ageSlide44

Thank youSlide45

One Class III study of 144 patients pronounced

brain dead found 55% (95% confidence interval

[CI] 47–63) of patients had retained plantar reflexes,

either flexion or “stimulation induced undulating toe

flexion.”22 Another study documented plantar flexion

and flexion synergy bilaterally that persisted for

32 hours after the determination of brain death.23Slide46

ApneaTesting

Absence of a breathing drive.

Prerequisites

: 1)

normotension

, 2)

normothermia

,

3)

euvolemia

, 4)

eucapnia

(PaCO2 35–45 mm Hg), 5) absence of

hypoxia, and

Procedure

:

• Adjust

vasopressors

to a systolic blood

pressure 100 mm Hg.

Neurology 74

8, 2010 Slide47

Preoxygenate

for at least 10

minutes with

100% oxygen to a PaO2

200 mm Hg

• 10 breaths

per

minute-

eucapnia

• Reduce

PEEP

to 5 cm H2O (oxygen

desaturation

with

decreasing PEEP

may suggest

difficulty with

apnea

testing).

•

SpO2> 95

%, obtain a baseline

blood gas

(PaO2, PaCO2, pH, bicarbonate,

base excess)

• Disconnect the patient from the

ventilatorSlide48

Preserve oxygenation (e.g., place an

insufflation

catheter

through the

endotracheal

tube

and close to the level

of the

carina and deliver 100% O2 at

6 L/min

).

•

Look

for respiratory

movements -

8–10 minutes.

•

Abort if systolic blood pressure

decreases to

90 mm Hg.

• Abort if oxygen saturation measured

by pulse

oximetry

is 85% for 30 seconds.

Retry procedure with T-piece

,

CPAP

10 cm H2O, and 100% O2

12

L/minSlide49

If no respiratory

drive- repeat

blood gas

after approximately 8

minutes.

• If respiratory movements are

absent and

arterial PCO2 is 60 mm Hg (

or 20

mm Hg increase in arterial

PCO2), the

apnea

test result is

positive

•

If test

is

inconclusive- patient is

hemodynamically

stable,

it may be repeated for

a longer

period of time (10–15 minutes)

after the patient is again

adequately

preoxygenated

.Slide50

Take home messages

Diagnosing brain death is not different in children as compared to adult

Newborn 34 week and above can be reliably

daignosed

to have brain death within first week of life

Most newborn withdrawal of care is based on future poor neurologic outcome rather than brain death

Most common ancillary testing required is EEGSlide51
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