Síndrome de Aspiración Meconial (SAM) RECIÉN NACIDO PATOLOGÍA RESPIRATORIA | Mentes Médicas

Hello, hello, how are you? How are you? Welcome to Mentes Médicas. My name is Juliana Parisi and today we are going to talk about a neonatal pathology. We are going to talk about the Meconial Aspiration Syndrome, known as SAM or also known as SALAM, which means Meconial Amniotic Liquid Aspiration Syndrome. Okay, so

Today we are going to talk about a pathology that affects newborns, one of the respiratory pathologies because they are the three main ones. One of them is that one and that's what we're going to talk about today.

It's also important to remind you that in my Patreon I have several summaries about newborns from the pathological clinical history, the physiological clinical history, the newborn poriculture, the pathologies like sepsis, like uterine cancer, there I have a little bit of everything and I will put them here in case you want to subscribe to the summary section in my Patreon, ok?

So, let's start. What does the Meconium Aspiration Syndrome mean? Well, this is a clinical picture that will be developed in the newborn, which will consist of a respiratory difficulty that he will present. And why is he going to present this respiratory difficulty? He will present it because he is aspirating amniotic fluid with meconium, ok?

So, it is one of the three main pathologies of respiratory diseases that we see in the newborn and it is important to highlight the fact that this will occur in mature newborns, that is, it has to be a newborn at the end

or a postterm or a newborn. Even this pathology, its incidence increases exponentially from 41 weeks of gestation. That is why this is a differential characteristic of other respiratory pathologies.

This is a newborn that will be term or post-term. So that's important to say. Why can't it be a newborn preterm? Notice that in a newborn preterm, his gastrointestinal system is not yet fully developed. So his gastrointestinal system does not produce his peristaltism and that is why he cannot have his meconium in the amniotic fluid. He cannot...

producir meconium, ok? Es por eso que esta patología no se va a producir en recién nacidos pretérminos.

Now let's talk about the incidence, look, from 4 to 22% of all pregnancies, only 4 to 22% will have meconium amniotic fluid. And from those who have meconium amniotic fluid 3 to 12% of newborns will develop SAM.

and from those 30 to 50% will require mechanical ventilation and a third of them will develop persistent pulmonary hypertension. That will be explained later what that pathology means, what it consists of. And mortality oscillates between 4 to 19%. So, let's continue with the physiopathology. What happens in this entity? Notice that everything starts with a fetal stress.

Everything begins, all the SAM, all the Meconium Aspiration Syndrome begins because there is a fetal stress. Why can there be a fetal stress? Well, for various situations that the fetus may be receiving in utero. Okay, like which ones? It may be that he is presenting hypoxia, okay, hypoxic phenomena. It may be that he has some inflammation or some infection. It may be that some of those three mechanisms are being produced.

So we see that an intrauterine hypoxia can be caused by a placental insufficiency where the mother is pregnant with a pregnancy, the mother is pregnant with gestational hypertension, the mother is a tobacco consumer during pregnancy and also consumes drugs, such as cocaine. All these situations can cause an intrauterine hypoxia and therefore a fetal stress.

Also, oligohydramniosis is associated with fetal stress and the common infection chorionitis also produces fetal stress. Not only that, but this fetal stress can also occur during labor. Why? Because there may be a compression of the head, that means a fetal stress, or a compression of the umbilical cord.

Now, another question I wanted to mention is that it is written that the appearance of meconium is not only produced by a fetal stress, but also indicates maturity. It indicates maturity in the fetus, it indicates maturity of its gastrointestinal tract. Why? Because remember that a mature fetus is the one that will produce meconium, so it is not always that the fetus is under stress, but it can also be simply due to maturity.

So, what is going to produce that fetal stress? Fetal stress will produce an activation of the parasympathetic nervous system, that is, an activation of the vagus nerve, which will give rise to two reactions. One is the increase of peristaltism and the other is the relaxation of the sphincter. And that's how it happens that there is meconium in the agnotic liquid.

Once we have meconium in amniotic fluid, the next thing we need to know is how the newborn is going to absorb that meconium amniotic fluid. It turns out that these hypoxic phenomena that were happening intrauterine make the newborn present some gasping movements. He is going to make mouth-to-mouth movements because he is hypoxic. So he is going to make those gasping mouth-to-mouth movements

And that will result in the aspiration of the meconium. Now we have the meconium in the respiratory tract. This happens in uterus, intrauterine, but it can also happen the aspiration of meconium in the birth. It may be that when he is born and he produces his first breaths, there he aspirates the meconium amniotic fluid. So those are the two ways he can aspirate the amniotic fluid.

So we have the aspiration of meconium. What is the meconium going to produce? And this is super, super important because from here basically derives everything. From here derives the clinic that he is going to present. Derives also the radiological manifestations that we are going to observe.

and also reminds us what treatment we are going to install this patient according to this physiophatology. Look, meconium in the respiratory tract is going to cause three main reactions. The first of them is a chemical pneumonia, which means that it is going to cause irritation of the parenchyma and irritation of the alveoli, it is going to result in a chemical irritation.

The second thing that will happen is an obstruction of the airway. We are talking about the meconium entering the airway, so it can be impacted and can obstruct this way. And it can be done in two ways. It can be a partial obstruction or it can be a total obstruction. If the obstruction is total, an atelictasis will occur. An atelictasis will occur and we can only observe it in the x-rays.

And if the obstruction is partial, what will happen is that the meconium will act, that space that will be, will act as a valve where air, where gases will be able to enter the alveoli but they will not be able to leave. So what happens? That an air trap is going to be generated. There will be alveoli that will be hyperinsulated.

In addition to this air capture, complications can occur. Why? Because if I am catching air, it may happen that at some point it escapes. So at that moment the four complications can occur, which are air escape. And there are four pathologies: a pulmonary enzima, a thorax pneumothorax, a mediastinum pneumothorax or a pericardium pneumothorax. Air can escape to all these places.

What else here? Yes, it was basically that And the diffusion of the surfactant That is the third reaction that meconium produces in the airways

What will happen? The meconium will produce a diffusion of the proteins A and B of the surfactant and that in turn not only is it that it inactivates the surfactant but it will also inactivate the cells that produce the surfactant, that is, the type 2 pneumocytes. It has a cytotoxic effect in the type 2 pneumocytes. So,

All of this, which are the main reactions that meconium produces in the airways, will cause an alteration of the BQ, the perfusion ventilation quotient. Why? Because we are going to have areas that are going to be well-perfused but poorly ventilated. So a shunt is going to be given where the blood is going to pass and oxygenation is not going to be able to happen. And if the blood does not oxygenate, we are going to have a hypoxemia.

And this hypoxemia will eventually lead to respiratory acidosis. Because the carbon dioxide will start to accumulate and it will give a hypercapnia and respiratory acidosis. As for this hypoxemia, look, if this hypoxemia is serious, if it is accentuated and is not solved, it can lead to persistent pulmonary hypertension. What does that mean? Remember that when the child

the fetus, when the fetus is inside the uterus of the mother, her lungs are full of liquid, therefore the vascular-pulmonary resistance is high, and in turn, as there is liquid, there is a vasoconstriction and well, that's how the lungs are maintained, while the peripheral resistance is decreased in relation to that vascular-pulmonary resistance.

Why? Because that's where he receives the blood from the placenta. What happens when he is born? When the baby is born, he is supposed to have to adapt to the environment and make some changes, some mechanisms of adaptation.

What are those mechanisms of adaptation? One of them is that when the baby is born, he will perform his first breathing and when he does, oxygen will enter the lungs and when oxygen enters the lungs, this oxygen will produce vasodilation and the vascular-pulmonary resistance, which was previously super high because there was liquid, is no longer high, but it will decrease.

This is what happens in normal cases and the peripheral vascular resistance increases because there is compression of the umbilical cord. So what happens if the fetus

The fetus, no, now the newborn because he was born, so if now the newborn is born and it turns out that he is not breathing well because he has meconium in his airways, he will not produce, he will not enter oxygen into his lungs and therefore there will be no vasodilation, then there will be hypoxemia because I am not receiving enough oxygen and at the same time that vasoconstriction will be maintained, that is why it is called persistent pulmonary hypertension.

and then vasoconstriction is maintained and there is even more vasoconstriction and in turn, remember that also that vasodilation effect also produced the closure of the short circuits, then the short circuits will be maintained and all this is like a vicious circle because with more hyperglycemia, more hypertension and all this will be even more complicated, ok? So that's why the importance of treating this pathology

Another thing that happens is infections and this is important because we know that meconium is a sterile substance, right? But it turns out that it contains abundant muco polysaccharides and what happens with those muco polysaccharides? Well, they serve as a cultivation stock, that is, they are the muco polysaccharides are great for cultivating bacteria like E. coli. So, let's get to this.

Clinical manifestations. Well, we are going to observe that our patient has signs of maturity, as I had told you at the beginning, it is a newborn who is going to be mature, ok? That we are going to observe meconial amniotic fluid and that we can see that the newborn is going to have meconium impregnation in the umbilical cord, in the casiox, ok? We are going to see that he has meconium in his skin, in his fetal parts, especially in the umbilical cord. Many times the umbilical cord looks green, green, green, green, green.

Of course, the respiratory difficulty syndrome will be moderate to severe, this is important, it is a serious picture, moderate to severe, which will start in the first hours, it will be early and it will also be progressive, that is, it will get worse. So, what do we have? That the newborn will have tachypnea, hypoxemia, prolonged exhalation, why?

the air trap that he has, he will present a thorax in the tunnel by the same air trap where the anterior-posterior diameters of the thorax will increase and at the occultation we can see extirpations and rashes.

Okay, radiological manifestations, what can be seen in a chest x-ray with SAM? Notice that what we can observe in a pattern that is not so serious, okay, is a patched and cotton pattern. What does this mean? That we are going to have areas that are going to be opaque due to the atelectasis, okay, notice how cotton

that will be at the same time with hyperinsulated or distended areas ok that is what is going to talk to me about the aereo entrapment yes then it is that alternation instead if it is a more serious patient notice that it will already be seen as a disease a respiratory syndrome sorry I was wrong

A type 1 respiratory difficulty syndrome, that is, the membrane and aline disease will look like this. Why? Because notice that there are diffuse opacities in both pulmonary fields, there is a smerulated glass pattern and that you can also see air bronchograms. Okay, well, those are going to be the radiological manifestations. The diagnosis, how are we going to do it?

Evidently, with the patient's clinic, the chest x-ray can help us. This one doesn't always show this way, but not all patients will have this, ok? That's what I want to tell you. Arterial gases, of course, we are going to evidence respiratory acidosis, hypoxemia, hypercapnia. And ok, we are going to talk about prevention now, about the prevention of SAM. From the obstetric point of view, of course,

The most convenient thing is to avoid the extension of pregnancy beyond 41 weeks. In that case, we are going to induce labor. In case the labor is already installed and present,

the pregnancy that we identify as meconium amniotic fluid, in that case we will evaluate the clinical state of the fetus and the mother with fetal maternal monitoring and we will determine if there is acute fetal suffering and of course if there is acute fetal suffering it will be required for a high-level solution, that is, by cesarean section.

Ok, what are you going to do in the birth room once the baby is born? Well, notice that nasopharyngeal aspiration after birth and endotracheal aspiration according to the American Pediatrics Academy are not recommended. It is not recommended to aspire to these patients. Why? For three reasons. First, because it has not been evidenced that there are benefits of these techniques. Second, because we are prolonging the appropriate treatment that these patients who

And what is the treatment? Well, ventilation. You have to ventilate them. And third, because these maneuvers are not exempt from complications, such as injuries and infections. So that's why it's not recommended to breathe.

It is only recommended to aspirate in cases of an evident obstruction and to clear the life to be able to perform a positive compression ventilation to that patient. That is, in a case that we are seeing that there is amniotic fluid, meconia, at grade 3, that is very thick.

Ok, now we are going to the treatment of the SAM, we are going to talk first about a general management and then we are going to talk about the ventilatory management that this patient must receive. Ok, so let's start with where we are going to take this patient, of course this patient must be hospitalized, he must be in a neonatal intensive care unit, we are going to omit the oral life of this patient, of course we are facing a serious respiratory failure

Once the hemodynamic and respiratory stability is achieved, we can administer enteral feeding. The patient must receive their enteral maintenance hydration, must be in a neutral thermal environment that minimizes tactile, auditory, visual and nociceptive stimuli.

We must perform a continuous monitoring, a saturometer in a productive position, which means that we are going to place it on the right wrist. An electrocardiogram and an arterial tersion and first-line antibiotics. As I told you in the physiopathology, this entity can produce infections, so that is why we administer antibiotics.

As for patients who are already in mechanical ventilation, the umbilical artery will be catheterized and it is also best that in these patients who are already ventilated, to perform an invasive arterial pressure monitoring.

We continue with the laboratory exams, we are going to perform a complete hematology, also known as hemogram in other countries, arterial gasometry, of course, glycemia, electrolyte, renal function. And if you suspect infection, we are going to ask for a PCR and hemocultivation. The image, as I told you, it is important to perform a thorax radiography, an echocardiogram is going to be to detect the presence of a persistent pulmonary hypertension and well, urinary and diuretic urinary. As for respiratory management,

We are going to start with a controlled oxygen therapy, this is done by the halo, also known as the cephalic chamber. We are going to place this to achieve a preductal saturation of 92 to 95%. Remember that hypoxic episodes should be avoided, because hypoxemia can produce persistent pulmonary hypertension. So it is very important to administer oxygen to these patients.

The ventilation treatment itself consists of nasal CPAP, we are going to place the nasal CPAP at a pressure of 4 or 7 cm of water and you should be careful not to use very high values because also remember the risk of air escape, the patient already presents the air trap and has an air escape risk.

Mechanical ventilation is used in the event that the CPAP fails, that the estimated values do not reach, that there is acidosis with a pH lower than 7.25, hypercapnia with a partial pressure of carbon dioxide greater than 60 mmHg.

And if the mechanical ventilation fails, we will start a high-frequency ventilation. If the high-frequency ventilation fails, we will start the use of ECMO, which is oxygenation through the extracorporeal membrane.

And in cases of persistent pulmonary hypertension, other substances such as nitric oxide can be administered, but that treatment is already a matter of that pathology itself. Here we are talking about SAM, but I simply wanted to put them in so that they knew. Another of the questions that is thought with this pathology is whether we should administer surfactant or not. That is one of the unknowns.

So, notice that it has not been shown that mortality decreases, however, the severity of the respiratory frame decreases, of the respiratory difficulty that this patient presents and also reduces the need for ECMO. So, that is why the administration of a subfactor can be considered in case it is a newborn with severe SAM and in case it is a patient who is in mechanical ventilation.

How are we going to administer it? Well, it will be administered from 100 to 150 milligrams per kilogram every 6 hours up to 4 doses. And well guys, that has been all with this pathology.

I hope you liked it, I hope it was clear to you, if so please give me a like, give your like to this video, if you want to write a comment to see what you think and what other topics you would like me to do, what other pathologies you would like me to do and see you where? In the next video of my channel, your channel, Mentes Médicas, bye bye