Asfixia Perinatal

How is everyone? Okay, now we're going to

talk about perinatal asphyxia.

Asphyxia will be defined as the

aggression produced to the fetus or

newborn due to lack of oxygen or lack

of adequate tissue perfusion. It is

generally associated with

respiratory depression, cyanosis and pallor, and

usually results in a

hypotonic newborn at birth with

metabolic acidosis.

To talk about asphyxia, we have to take

into account some

perinatal history and some data at the

time of birth. Generally,

the resignation of the suffocated child

includes what was previously called

fetal distress, which is now called

risk of loss of fetal well-being,

which can be evidenced by an

alteration in the cardiographic recording

or in the fetal pH

that translates into a non-reassuring fetal state

or also called

hypoxic sentinel episodes,

such as, for example, tachycardia

or decelerations of the heart rate.

Um, at the time of birth,

obviously, this non-reassuring fetal state

, the history of the

non-reassuring fetal state and the

requirement for advanced animation

can indicate asphyxia. If

we talk about concepts, we have

neonatal depression, mild neonatal asphyxia

, moderate asphyxia, and severe asphyxia.

Within the depression, we are dealing with

a baby with a history of

fetal well-being, both the

non-reassuring fetal episode or the

hypoxic sentinel episodes.

Uh, this is associated with an Apgar score of

less than six at one minute, but

equal to or greater than seven at five minutes. So, the child

required resuscitation measures, he

was received, everything

that had to be done with the baby was done, within

5 minutes he was already in

recovery and 99% of the time he did not

present neurological signs.

mild asphyxiation. However, we are already going to

have a baby with an agar

less than three at one minute and less than 7 at

5 minutes. He failed to recover the gar. If

we take a cord blood gas analysis, we will

find a pH in the

umbilical artery less than 7.21.

However, we still have an absence of

neurological signs.

These children may already have some

degree of long-term health problems.

In patients with moderate asphyxia, the

pH at 5 minutes is between

three and five, and in a small child with

greater asphyxia, there is

greater evidence of hypoxia and therefore

an umbilical pH greater than

7.21 is obtained.

In the patient with severe asphyxia

, the Apgat score remains less than

three at 5 minutes. Uh, we already have

frank acidosis in the umbilical artery with

a pH less than 7. And the

clinical manifestations of asphyxia can be evidenced

by means of

hypoxic-ischemic encephalopathy,

which will be the functional alteration of the

central nervous system attributed to a

hypoxic region.

At what point does asphyxiation occur?

Generally,

70% of asphyxia cases

occur during childbirth.

There are multiple causes, starting with

cord compression. I choose AM is a

prolonged labor.

However, there is also a 30% that is

divided between alterations prior to

labor, such as

placental abruption, or a 10%

that occurs after the

neonatal period, such as crushing

or suffocation.

Physiopathologically, asphyxia

can occur in two ways: by a

total, acute, rapid interruption of

blood flow and oxygen, or by a

gradual or intermittent alteration.

Within the acute interruption are

cord prolapse,

placental detachment,

uterine rupture, which is evidenced in the

brain by the absence of

adaptive changes. We

are going to have clear alterations

in the trunk, the basal ganglia, the

gray matter, and obviously the result will be

death and neurological damage.

However, in gradual alterations,

such as in a

non-asphyxiating nuchal cord,

intrauterine growth retardation, or

maternal hypertension, there are

adaptive changes, changes due to

brain neuroplasticity that cause

the alteration to be mainly in

basal nuclei and in the gray matter

of the brain,

mainly resulting in

pyramidal alterations and

multisystemic involvement.

However, unfortunately, we cannot

say how much

the child will be affected immediately

after birth, but we have to

wait for an evaluative assessment.

If we talk a little bit about the

pathophysiology itself, let's remember that the

damage is caused by this

sentinel event. uh the

placental expulsion,

uh the previous base,

maternal hypertension. This damage then

blocks the flow of blood and oxygen

to the brain tissue, which can be

reversed. We can have reperfusion

for up to about 30 minutes, which,

mind you, will also cause injury.

Then we have a temporary improvement.

Yes, after this impact there is the

latent phase in which we have

low electrical activity and apoptosis and

the release of cytokines begin

with the subsequent third phase of the

establishment of brain damage, which occurs

between 6 and 15 hours

after the damage. That's where the

neurological clinic will take effect:

the seizures, the cytotoxic edema,

right? Excitotoxins and finally we will

have the tertiary phase or

permanent damage phase mainly associated with

brain death, which can be

evidenced from 3 days to 7

days after the damage. However,

let us remember that hypoxia

not only affects the brain,

but we also have

multisystemic lesions associated with hypoxia,

ranging from cardiovascular,

respiratory, renal,

gastrointestinal alterations or

coagulopathies.

For example, the most frequent thing in the

brain is

toxic-ischemic encephalopathy, but in the

kidney we can have

ischemic necrosis, kidney failure, in the

cardiopulmonary part a transient myocardial ischemia

, persistent pulmonary hypertension

of the newborn,

pulmonary edema and even

progressive respiratory failure.

In the gastrointestinal tract there is frank

liver damage, ulcers,

intestinal perforation due to hypoxia and what we

call

necrotizing enterocolitis, which is much more frequent

in this group of patients. At the

endocrinological and hematological level,

disseminated intravascular coagulation is

something that is very common in

patients with moderate to severe

hemorrhagic dialysis,

predisposition to bleeding and the

syndrome of inappropriate

antibiuretic hormone response. In terms of

metabolism, these patients are very

prone to hypo- or hyperglycemia and

also to hypocalcemia, all

related to metabolism. We must

remember all these systemic injuries because, although the

most dramatic aspect of asphyxia is the

neurological one, we also have to

carry out different controls and

follow-ups in this type of patient.

And, for example, at 6 hours I have to

do a homogram and a coagulogram,

in addition to a blood gas analysis and

blood biochemistry to be able to evaluate all these

alterations.

An echocardiogram should be performed within the

first 48 hours, an

abdominal ultrasound within the first 48 hours to

demonstrate the lesions in these

systems

at 24, 48 or 72 hours, and

electroencephalographic monitoring is

continuous in a patient with a history

of asphyxia.

Let's remember then that to talk about

perinatal asphyxia

we have to have some criteria,

right?, from the non-reassuring fetal state

,

sustained radicardia, meconium-stained amniotic fluid

, bleeding due to detachment,

these hypoxic events, sentinels,

do a gastrometry in

cord blood, right? Or an arterial blood pressure reading of the

newborn, during the first hour of life.

where we will observe

pH alterations and an excess of bases. The Apgar score,

which has already been mentioned,

must be less than three to be considered severe,

three to five moderate, and one to three mild

at one minute, but less

than seven at five minutes. And obviously the

clinical picture ranges from multisystem damage

to moderate hypoxic-ischemic encephalopathy

.

If we talk a little more specifically about

hypoxic-ischemic encephalopathy, we can

see that 30% of children with

asphyxia, depending on the severity,

die in the neonatal period and up to

50% of them present abnormalities in

neurological development ranging from

cerebral palsy, decreased

intelligence quotient or decreased

learning. Here,

the criteria for asphyxia

that have already been mentioned

are also associated with these

potentially

ischemic events. There are essential criteria

such as evidence of acidosis,

early onset of severe encephalopathy, or the

presence of cerebral palsy that

has a characteristic of

[ __ ] quadriplegia or dyskinetic cerebral paralysis

. But we can also have

some non-specific disorders

that must be present in the

perinatal period, such as this

potentially hypoxic event, the

sudden deterioration of heart rate

after or during the hypoxic event,

alterations in the 5-

minute Aggar score, evidence of

early multi-organ dysfunction, and evidence of

brain alteration on neuroimaging.

All this data leads me to believe that the

patient's condition is caused by

perinatal asphyxia.

This sentinel event, then, the

non-reassuring fetal status, a

dystocic delivery, or anything related

to the criteria for AGGA,

advanced resuscitation, pH or

base excess, plus a neurological examination,

makes us think of

moderate to severe encephalopathy, which implies the

implementation of therapeutic measures.

Clinically, how are we going to view

hypoxic-ischemic encephalopathy?

For this purpose, scales are used,

primarily the Sarnat scale, which

evaluates different parameters to be

able to speak of encephalopathy, mild,

moderate or severe, or also called

stage 1, 2 and 3. If you look,

here is the level of consciousness, the

tone, spontaneous activity,

posture, the presence of primitive reflexes

such as Moro, alterations of the

autonomic system, such as the pupils,

heart rate, respiratory rate,

the presence of seizures,

alterations in the

electroencephalogram and obviously the

duration, the evolution of the patient.

Mild hypoxic-ischemic encephalopathy

usually lasts less

than 24 hours. Well, sometimes they seem

normal and in general the evolution is

good. Moderate encephalopathy can be

evident from 2 to 14 days and

varies greatly depending on the degree of

neuronal alteration; see prognosis,

evolution. And in severe encephalopathy, well, it

can last from days, from hours to

weeks, and in these cases, the most

frequent outcome is death or

complete disability. Unfortunately,

one of the first things we

notice when we

suspect

hypoxic-ischemic encephalopathy is seizures, and

the thing is that

neonatal seizures are very variable.

Here we can see, for example, the

presence of very subtle movements,

subtle convulsions. Here you can see the

sucking. Yes, look how

the baby moves its mouth trying to suck. Yes,

with very subtle, very slight movements.

Another form of subtle convulsion,

tonic extension,

yes, in flexion and deviation of the gaze

only with eye of with deviation of

gaze. Another type of subtle seizure.

We can have clonic seizures

with spasmodic movements.

In this case, only on my

body, look, just my little hand and foot.

The other is my body is immobile or

tonic convulsions.

with an extension of the entire

trunk and limbs.

Yes. In a brain-focused position.

This is a tonic seizure. We

also have

myoclonic seizures, just very

small movements marked in limbs,

hands, feet. These are

myoclonic seizures.

So, as you can see,

neonatal seizures are very, very

subtle. Sometimes we can't

differentiate in many cases whether it's a

seizure or not. One way to

tell is if the baby is

trembling; I grab their little hand and they stop

trembling. It was probably a

non-epileptic paroxysmal movement. Yes, it is

quite common in babies due to the

maturation of their brains. Yes, there are

movements in their little hands, jaws,

and feet, but if I grab them they give way

. If I hold her little hand and it keeps

shaking, it's probably a

seizure. There

may be some variables

that are predictive of a poor prognosis.

Yes. And this is generally what is associated

with moderate to

severe encephalopathies. We had already discussed the

Aggar score, the need for

peripartum resuscitation, and the delay in the

onset of spontaneous breathing; the

later the resuscitation, the worse

the degree of asphyxia,

severe neurological signs, the presence of

seizures in the first 12 hours or

seizures that are refractory

to treatment, severe alterations

in the electroencephalogram from the

seventh day onwards, or prominent lesions in the

basal ganglia.

or liguria or

altered neurological examination.

As already mentioned,

neuroimaging can be done, and here the image

we use most in neonatology is the

transfontanellar ultrasound. In this

ultrasound, hemorrhages can be seen

, as well as the presence of

leukomalacia, which is a thickening

of the lesion areas. Unfortunately, it doesn't give us

data on necrosis, but it

can show us

cerebral atrophy. Yes,

transfontanellar ultrasound is preferred because it

is easy, we don't need to sedate

the children, and it doesn't involve

ionizing radiation, but obviously it is

very operator-dependent.

Well, the CT scan, while it can

identify ischemic lesions,

hypodensities, and infarcts after

48 hours, the downside is that I

have to give up the patient and obviously there's

the risk of recurrence. What is

not present in the

magnetic resonance imaging, which would be ideal, since

here a diagnosis of

cytotoxicity can be made early, but

there are the problems that are

also seen with tomography, such as

sedation.

Within the treatment, we must keep

in mind that the management

is primarily with life support.

Good oxygenation and

adequate ventilation must be maintained. Maintain

blood pressure within

normal ranges. Avoid fluid overload.

Treat metabolic disorders and

multisystem involvement. And obviously,

to avoid these alterations, maintain

stable blood glucose levels. In cases of seizures,

which are the most dramatic, they have to be

managed and prevented. The

newborn with moderate to

severe asphyxia must have

continuous electroencephalogram monitoring.

And in the case of seizures,

phenobarbital is administered as the

first line of treatment for hypoxic-ischemic encephalopathy

with a loading dose of 20 mg per kilo

and then maintenance of 5 to 10. Yes,

the use of phenytoin or diazepam should be evaluated

in cases of hepatic or

renal dysfunction, but those are the options.

And another line of treatment,

especially for severe asphyxia,

is therapeutic hypothermia.

These are devices that

keep the body and head cool

to reduce metabolic activity.

Moderate hypothermia of

33.35

to 35ºC is used.

Ideally, it should be started before

6 hours and maintained for 72 hours. It can

be just the head or it can be

systemic therapeutic hypothermia

throughout the body, but the idea is to lower

the metabolic rate. It must be

remembered then that there will be

cardiovascular alteration

in 80% of cases with

severe encephalopathy. There will be

respiratory, renal, gastrointestinal,

hepatic and coagulation alterations. That's why it's

important to monitor the

clinical spectrum, the studies that should be

done on these patients, and the

treatment. He is an intensive care patient

. It needs to be in environments

where all the

medication it requires can be administered according to the

criteria that can be observed.

The prognosis depends a lot on the type

of encephalopathy, the type of asphyxia.

As we already mentioned, in

severe encephalopathy, 80% can

die and the remainder are left with sequelae,

right? This is different in

mild encephalopathy, where

up to 99% of people

may be

normal, including children. Always remember that

98% of patients with severe brain injury

develop cerebral palsy, the vast

majority of which is severe, characterized

mainly by

[ __ ] tetraparesis.

And these children with childhood brain damage

, with childhood cerebral palsy

, have problems with

feeding. The vast majority have

gluteal problems, so they

require a gastrostomy. In many

cases, 95% have speech problems,

most of them serious and

mainly associated with acoustic impairment. They do

n't listen. 75% have

visual impairment, right? Especially with

moderate to severe injury. Well, there will

be motor impairment and 75% of

asphyxiation cases have

residual seizures, always depending a lot on

the impairment in the cortex.

So, they are very traumatized kids.

For this we need to prevent

asphyxia, and this starts with the

obstetrics and gynecology team,

where

these situations that threaten

the newborn, the fetus, and the

infant must be detected in a timely manner, and once we can detect them, we must

perform

rapid and coherent neonatal resuscitation to avoid keeping the

child in hypoxia for a long time.

This is the bibliography.

Hey, any questions, I'll be waiting for you

in the comments section.

Thank you so much. M.