What weird folk remedies have you tried to cure illnesses?

Let me tell you about a case I encountered in the emergency room.

The patient found a folk remedy to apply on his skin because of itchy skin, and ended up being admitted to the ICU, and then suffered a cardiac arrest…

I was on duty in the emergency room that day and a young girl came in.

He is 32 years old and said he has been vomiting and having diarrhea for a day and is in great pain. He wants to have an IV drip to see if he can get better faster.

The patient was an employee of a real estate company. He was very busy with a lot of work. He was supposed to come to the hospital in the morning, but he delayed it until noon.

The vomited out things were all stomach contents. Basically, he vomited whatever he ate. He also had frequent diarrhea, seven or eight times a day.

At first, the stool was formed, but later it became yellow, watery stool.

I felt almost exhausted, very tired, and my hands and feet were numb.

After assessing the situation, I considered it to be acute gastroenteritis, which was too obvious.

Because she said that she had had similar experiences before, and that eating slightly unclean food would cause this, and her intestines were particularly sensitive, but this time it was particularly serious, otherwise she would not have come to the emergency room.

I performed an abdominal color ultrasound on her and drew blood, and ruled out common acute abdominal diseases such as acute appendicitis, pancreatitis, and cholecystitis.

I also asked about her menstruation and sex life. She said she was still single and had no sex life, so it was impossible for her to be pregnant. A urine pregnancy test later confirmed that what she said was true.

So she really, just had acute gastroenteritis.

Then I felt at ease giving her antibiotics and a few bottles of fluids.

There was no way. Due to severe vomiting and diarrhea, she was very dehydrated and had to replenish her water in time.

The blood test results showed that she had hypokalemia, with blood potassium only 3.3mmol/L (normal 3.5-5.5mmol/L), which could explain the numbness in her limbs.

There is a lot of potassium ions in the digestive tract fluid. Severe diarrhea will cause the loss of potassium ions, and hypokalemia will inevitably occur.

Potassium ions have a great impact on muscle activity, so numbness in the limbs is considered mild.

Some severe hypokalemia may cause fatal arrhythmias or even cardiac arrest.

She went to the bathroom twice more and asked me if she could have some anti-diarrhea medicine.

I said that diarrhea will also excrete bacteria and viruses, which is conducive to recovery of the disease, so we can observe further.

Sure enough, after giving her regular fluid and potassium supplements, her condition improved.

She said she had an appointment with a client in the afternoon and couldn’t stay in the hospital, so she had to go back.

I mean wait until the blood test results come out before deciding.

But she was determined and joked with me, saying that if I couldn’t make the deal, my year-end bonus would be gone.

I saw that her condition had improved significantly and ruled out other more serious problems. It was just acute gastroenteritis, so I agreed to her request and let her go home.

Before leaving, I told her to go back and have a good rest, not to overwork, eat a light diet, take medicine on time, and come back for a follow-up visit if her condition worsens.

I say this to patients on a regular basis, and in fact I think she will not come back.

Because an acute gastroenteritis can be gradually relieved after taking medication.

Even if it doesn’t get better in a short time, it will get better after two days of rest.

But it turned out that I was too optimistic.

In the evening, the patient came back.

This time she was brought here by a colleague and was helped into the emergency room.

The patient had a painful expression and covered his stomach. He told me that his vomiting and diarrhea had improved a little after he went home, but his stomach started to hurt.

At first I thought I could just bear it, but I couldn’t bear it anymore. The pain was so severe that I couldn’t even straighten my back and couldn’t work at all.

When her colleagues saw her like this, they thought she had dysmenorrhea, so they gave her brown sugar water and took ibuprofen tablets, but it didn’t work.

The pain was so severe that I was sweating all over, so I was rushed back to the emergency room.

When I touched her limbs, they were all wet and cold. The situation was not good, so I quickly asked the resident doctor to help take her to the emergency room.

The nurses came over and quickly connected her to the ECG monitor.

Measure his blood pressure immediately, he might be in shock.

At the same time, I asked the nurse to open an intravenous access for her. Judging from the situation, she had to speed up the fluid replacement.

Because the patient suffers from vomiting and diarrhea and has a poor appetite, he does not eat much and is still dehydrated, and may even be in shock.

The blood pressure was measured and was basically normal, but the heart rate was very fast, 130 beats per minute.

No wonder she said her chest felt uncomfortable. With such a fast heart rate, she must be uncomfortable.

I roughly auscultated the patient’s heart and lungs, and found a few moist rales in both lungs.

No further findings were made.

The resident doctor showed me the patient’s blood test results at noon. Except for the slightly higher white blood cell count, there were no other major abnormalities.

Does the patient really have acute gastroenteritis?

Why is there such severe abdominal pain?

Are there other hidden problems that have not been discovered?

My mind raced, thinking about all the possibilities.

My intuition told me that the condition of this young girl in front of me was not simple and I had misjudged her before.

She covered her stomach and told me that it hurt a lot and asked me to give her painkillers.

Her colleague also begged me to give her painkillers first, saying that it was not a good idea to continue suffering like this.

Before I could say anything, the resident doctor said that the cause of the abdominal pain was unknown and that painkillers were not appropriate as they might mask the cause and only treat the symptoms rather than the root cause.

I basically agree with what the resident doctor said because that’s what I taught him.

But I really don’t have any more ideas about this patient.

I carefully examined her stomach and found active bowel sounds, indicating that the intestines were moving faster. There was tenderness in the entire abdomen, but no rebound pain.

And the abdominal muscles are not too tense, so there is definitely no plank abdomen.

Is the abdominal pain caused by stomach problems?

If so, why didn’t the previous color ultrasound show any abnormalities?

“Let’s do an abdominal CT scan first to see it more clearly,” I told the patient.

When the cause of abdominal pain is unknown, abdominal CT must be done because it is much clearer than color ultrasound and can reveal many details that color ultrasound may miss.

The patient agreed to undergo CT.

I told the resident doctor that he had to go and come back quickly. The patient was already in shock and the slightest mistake could cost his life.

The resident doctor was puzzled and said that the blood pressure just measured was fine, so how could he go into shock?

I explained to him that by the time the blood pressure collapses, it is already in the late stage of shock.

The patient’s heart rate is so fast, his limbs are cold, he is sweating so much, and he is vomiting and having diarrhea. He is already in shock.

Her organ tissues are already suffering from oxygen deprivation. If we cannot reverse the condition in time, the next step will be a collapse in blood pressure, and by then I’m afraid it will be too late.

We, the emergency doctors, must nip the shock in the bud, quickly find the cause, and actively deal with it to prevent subsequent tragedies from happening.

For safety reasons, I brought a first aid kit and personally sent the patient to do a CT scan.

The patient endured the abdominal pain and asked me on the way if she would die.

Of course not. It’s hard for you to die in the hospital, let alone you are in my hands.

I said this to comfort her.

If a family member asks me whether the patient will die, I will definitely tell her that it is possible.

With such a serious illness and an unclear diagnosis, I naturally cannot guarantee that the patient will not die.

But in front of patients, I can only say good things.

I finally finished the CT scan.

I thought an abdominal CT scan would reveal some clues, or at least tell which organ had the problem.

After all, abdominal pain, vomiting, and diarrhea are basically stomach problems. As long as they are stomach problems, CT can detect them in most cases.

但让我捉急的是，腹部 CT 没看到明显异常，肝胆胰脾、阑尾、结肠等都没看到显著改变。

I’m confused.

I am wondering whether I should go further and do CT angiography.

Angiography requires the injection of contrast agent into the patient’s blood vessels, which then allows the condition of the blood vessels to be visualized.

In rare cases, if blood clots form in the abdominal blood vessels, causing intestinal ischemia, severe vomiting, diarrhea, and abdominal pain may also occur, but in this case the diarrhea will be bloody rather than yellow, watery stools.

Moreover, the patient is so young and has no history of underlying diseases, so it is unlikely that he has abdominal vascular thrombosis.

So I didn’t consider making a CTA for her at first.

After returning to the emergency room, what was even more unexpected to me was that the patient began to tremble, and his whole body, including his lips, was shaking.

This is a chill!

It should be a serious infection, sepsis, so there is chills.

But strangely, the patient’s body temperature was basically normal.

If it is really an infection, it is most likely an intestinal infection. CT scan cannot show intestinal infection because it is a problem with the intestinal mucosa. The lesions are very subtle and cannot be seen clearly on CT scan.

This is not uncommon in the emergency department. I quickly prescribed antibiotics for the patient and contacted the gastroenterology department, preparing to have them come for a consultation and admit them to the gastroenterology department for further treatment.

The patient’s lips seemed to be slightly cyanotic, and the blood oxygen saturation monitored on her fingers was very unstable, fluctuating, which might be related to the colder skin temperature at the extremities of her limbs.

I asked the nurse to draw her blood for an arterial blood gas test to see if she was suffering from hypoxia and whether her internal environment was stable.

Then go deal with another patient.

He also instructed the resident doctor to keep a close eye on her and wait for the consulting doctor to come.

The patient collapsed right after his blood was drawn and the result wasn’t even out yet.

The resident doctor came running over to me in a hurry, and the patient said he felt dizzy and couldn’t see.

After hearing this, I rushed back to the emergency room and asked him if he had measured his blood pressure again and whether his blood pressure could be maintained. Low blood pressure can cause dizziness and blurred vision. If not, he would need to take blood pressure-raising drugs.

And, I have to report my serious illness again! Sign it!

The resident doctor told me that my blood pressure seemed to be okay.

I rushed back to the emergency room and found that the patient’s blood pressure was indeed normal, his heart rate was gradually slowing down, and his abdominal pain seemed to have eased.

But subjectively I felt very uncomfortable, with dizziness, blurred vision, and the feeling of about to pass out.

The nurse handed me the arterial blood gas results. Oops, the blood oxygen saturation was only 92% and the oxygen partial pressure was as low as 70 mmHg (normal is 90-100).

She was clearly suffering from lack of oxygen.

And his breathing is relatively rapid, very much like those patients with acute left heart failure.

But how could the patient, who is so young and has no history of hypertension or heart disease, suffer from left heart failure?

The resident doctor volunteered to do another electrocardiogram to see if there was anything found.

An electrocardiogram was quickly taken, and again no major findings were found, but the heart rate did slow down to around 90 beats per minute.

What we remember most vividly is that the patient was covered in sweat. Not only was his head sweating, but his torso and limbs were also wet.

I told the resident doctor that this was a sign of shock, and excessive sweating would aggravate the shock, so I had to continue to give fluids.

But I can’t add too much fluid because I heard that the patient’s moist rales in both lungs have increased compared to before.

Auscultation of the lungs reveals moist rales, which indicates an increase in lung water.

If there is more water in the tiny bronchi and alveoli, the gas flowing in and out will break these blisters, and the sound produced is called moist rales.

The number of moist rales in the lungs has increased, which indirectly reflects the increase in lung water, and large amounts of fluid can no longer be replenished.

This is a vexing therapeutic contradiction.

It seems that we need to call the ICU down for consultation. In addition to shock, the patient also has respiratory failure. The next step may be endotracheal intubation and ventilator-assisted ventilation.

When the patient’s colleagues heard that the patient was in critical condition, they became very nervous and said that they were just colleagues and could not help sign, and they had to contact the patient’s parents.

But the patient’s parents were thousands of miles away and it was impossible for them to rush to the scene immediately.

After much persuasion, they agreed to sign, but noted that they were colleagues behind their names.

I asked them to call the patient’s parents. After the call was connected, I briefly told them about the patient’s condition and asked them to find a way to come to the hospital.

Because there is indeed a risk to life.

As soon as the phone was hung up, the patient fainted.

Then, blood pressure also started to drop.

I expected the patient’s blood pressure to drop.

But what I didn’t expect was that this progress was so rapid.

Because we have been actively intervening.

Her situation is really unbelievable.

I have seen many cases of infectious shock and hypovolemic shock, but generally speaking, they give me time to react. This is the first time I have seen a patient progress so quickly.

更让我头疼的是，我甚至都不知道感染灶在哪里。

I told the resident doctor to quickly invite the ICU doctor down, and at the same time give the patient blood pressure-raising drugs and continue to give fluids to fight shock, at least to stabilize the blood pressure first.

My brain started working at high speed again, and I analyzed the patient’s strange condition:

Abdominal pain, vomiting, diarrhea, profuse sweating, hypotension, shortness of breath, moist rales in the lungs, shock, coma…but the CT scan did not reveal any major abnormalities.

Isn’t it a stomach problem?

Heart problems alone are not enough to explain the above symptoms.

Where exactly is the infection progressing so rapidly?

However, the patient’s body temperature did not rise significantly, and the level of procalcitonin (another infection marker) did not show any obvious abnormalities. No infection focus could be found, which did not seem to support the idea of ​​a severe infection.

If it’s not an infection, then what is it?

The resident doctor was also confused, but his words reminded me.

He said that he had seen patients with hyperthyroid crisis before, who also had profuse sweating, tachycardia, abdominal pain, and pulmonary edema. Could it be hyperthyroid crisis?

If a patient has hyperthyroidism (hyperthyroidism), when treatment is ineffective or the disease progresses, the hyperthyroidism will rapidly worsen and a large amount of thyroid hormone will be circulating in the blood.

The effects of these hormones on the human body are disastrous, and patients will experience the above-mentioned symptoms. This extremely serious hyperthyroidism is called hyperthyroid crisis.

Judging from the symptoms alone, thyroid crisis seems to explain the patient’s condition.

But we had asked the patient repeatedly before, and he had no history of any illness, nor did he mention having hyperthyroidism.

If there is no hyperthyroidism originally, it is impossible for a hyperthyroid crisis to occur suddenly.

I was afraid that the patient had hyperthyroidism but it had never been discovered or treated, and then it suddenly broke out tonight and a hyperthyroid crisis occurred.

If this is the case, then it would be really dangerous.

可我仔细看了，病人并无典型甲亢表现，比如双眼并不突出，看起来脖子也不粗，不像有显著甲状腺肿大，也没有高热（甲亢危象通常会有高热）。

These manifestations do not support hyperthyroid crisis.

If it is really a hyperthyroid crisis, immediate intervention is needed, including intravenous hormones and drugs that slow down metabolism.

Anti-hyperthyroidism drugs should be used at the same time, otherwise the patient may die within a short period of time.

In fact, the patient was in critical condition.

The consulting doctors rushed over, and everyone thought that the patient should have a serious infection, but the source of the infection was unknown, so they suggested continuing to treat the patient as suffering from septic shock.

The current condition is very serious and he needs to be sent to the ICU for treatment.

However, the patient’s relatives were not there, so the colleague was unable to make a decision. He had to call the family again and contact the medical department to let the people there know about the matter.

The head of the medical department said that they would give the patient first aid and they would be responsible for contacting the family.

This sentence gives us confidence.

As they were talking, the resident doctor ran out and shouted, the patient’s heart had stopped beating!

That’s fucked up.

Perform CPR immediately.

Fortunately, there were many people and several nurses immediately performed chest compressions.

One injection of epinephrine was given. Epinephrine is the most powerful cardiotonic and pressor drug and the most effective drug for rescuing cardiac arrest.

I immediately rushed to the patient’s bedside, intubated her in a few seconds, and then connected her to a ventilator for assisted ventilation.

I have to praise the nurse for this. She was very experienced and knew that the patient’s condition was not good. Without waiting for my instructions, she had already prepared the endotracheal intubation box at the patient’s bedside, which saved us time in the rescue.

After being connected to a ventilator and continuing compressions for about 2 minutes, the patient finally regained his spontaneous heartbeat.

Everyone breathed a sigh of relief when they saw the beating curve reappear on the ECG monitor.

My back was already soaked.

The patient’s heart stopped beating. What was the reason?

Several of us doctors began to analyze the matter.

The most likely cause is hypoxia. The patient has pulmonary edema, so hypoxia is possible.

Why does pulmonary edema occur? Is it caused by pneumonia, heart failure, or other causes? It is not clear yet.

At this moment, we must save his life first, and deal with the rest after he is in the ICU.

When a patient’s heart stops beating, we routinely open the patient’s eyes and look at the pupils to assess whether the brain has been severely damaged.

If the pupil is dilated and the light reflex disappears, it means that the patient has just suffered cardiac arrest, resulting in severe brain hypoxia, and the rescue is ineffective and the prognosis is poor.

However, if the pupil is not obviously dilated and still has a light reflex, it means that the brain damage may not be serious and the rescue is timely.

As I was looking at the patient’s pupils, I was stunned.

The patient’s pupils did not dilate, but were extremely small, as small as the tip of a needle.

The diameter of a normal person’s pupil is about 2-4mm, and if it is dilated, it can even reach 10mm.

But the patient’s pupil at this moment is not even 1mm, just like a needle tip, which means that the patient’s pupil is extremely constricted.

The resident doctor also exclaimed, isn’t this a pinpoint pupil?

What patients have pinpoint pupils?

Patients taking morphine (a powerful analgesic) may experience marked miosis, as may some sedatives.

But it is obvious that the patient had not used the above-mentioned drugs before.

Another common cause of pupil constriction or even pinpoint pupils is organophosphorus poisoning!

Organophosphate poisoning! This thought suddenly flooded into my brain and I couldn’t get rid of it.

Organophosphorus pesticides are the most widely used and largest amount of agricultural insecticides in my country.

Organophosphorus pesticides can inhibit the activity of multiple enzymes in the body, and the main mechanism of poisoning is the inhibition of cholinesterase.

Once cholinesterase is inhibited, the patient will experience a variety of clinical manifestations, especially effects on the brain, such as headache, ataxia, convulsions, coma, and in severe cases, respiratory and circulatory failure.

Organophosphate poisoning can also affect the peripheral nerves, manifesting as muscarinic (M-like) and nicotinic (N-like) symptoms.

M-like symptoms are mainly increased secretion of various glands (sweat glands, tear glands, salivary glands, etc.), contraction of smooth muscles, sweating, drooling, miosis (pinpoint pupils), blurred vision, nausea, vomiting, abdominal pain, diarrhea, dyspnea, moist rales in the lungs, slow heart rate, and decreased blood pressure.

The N-like symptoms are mainly that the skeletal muscles are first excited and then exhausted, manifested as muscle fiber tremors in the skeletal muscles throughout the body, similar to chills, and in severe cases there may be muscle spasms and paralysis.

From beginning to end, all of the patient’s symptoms could be explained by organophosphate poisoning.

I finally understood why she was sweating so much at the beginning!

I always thought it was a sign of shock, but it was probably increased glandular secretion caused by organophosphate poisoning.

Blurred vision, dizziness and headache are also manifestations of poisoning. My pupils may have shrunk at that time, but my attention was always attracted by the so-called septic shock.

The patient’s increased wet rales in both lungs are not caused by heart failure or pneumonia, but by increased secretion of glands in the trachea, resulting in an increase in lung water, which is also caused by organophosphorus poisoning.

I was also puzzled by the patient’s shivering (chills). He had no high fever, so why did he keep shivering? This time I finally understood it. It was the muscle fiber tremor caused by organophosphorus poisoning!

Also, the most typical pinpoint pupil is caused by contraction of the pupillary sphincter, which is also one of the signs of poisoning.

A drop in blood pressure and cardiac arrest may be manifestations of organophosphorus poisoning.

All the symptoms are linked together!

The patient was very likely to have organophosphate poisoning! I was extremely excited because logically speaking, this could be explained clearly.

But soon I was poured cold water on.

The patient lives in the city and works as a salesperson in a real estate company. It is impossible for him to be exposed to pesticides, so how could he have organophosphorus poisoning?

One of my colleagues told me that they lived together and had never been to farmland or come into contact with pesticides. Even if they had a few pots of plants in the apartment, they did not need to be fertilized, so it was impossible for them to be poisoned by pesticides.

Moreover, most cases of organophosphorus poisoning are suicides caused by oral ingestion of pesticides or accidental ingestion of pesticides, but the patient clearly showed no signs of this.

The ICU doctor also reminded me that if it was really organophosphorus poisoning, the gas exhaled by the patient would have a garlic smell, which was particularly pungent, but the patient in front of me did not have that.

But all the symptoms match!

Another colleague of the patient suddenly remembered that the patient’s skin had been itching for a while and no medicine was effective. Later, he got a prescription from somewhere and used some unknown medicine to wipe the skin.

That kind of medicine does have a rather pungent smell.

“What potion?” I asked her impatiently.

At the same time, I checked the patient’s skin. The rash was mainly distributed on the calves, thighs, and back. I couldn’t tell what specific skin disease it was.

As for what potion it was, they couldn’t explain clearly.

If you wipe your skin with a solution containing organophosphorus pesticides, it is entirely possible that you will get poisoned.

Organophosphorus pesticides can be absorbed through the gastrointestinal tract, respiratory tract, skin and mucous membranes. If the patient is poisoned by organophosphorus, absorption through the skin is most likely.

After being absorbed, pesticides are rapidly distributed throughout the body’s organs, causing various clinical manifestations.

I didn’t waste time asking questions and directly drew blood from the patient to test the cholinesterase level.

If it is really organophosphorus poisoning, the poison will inhibit the cholinesterase in the patient’s body, and the cholinesterase level in the blood will drop significantly.

This test only takes a few tens of minutes to get the results, it’s very fast.

We used medication to maintain the patient’s vital signs while waiting for the cholinesterase results.

At the same time, atropine and pralidoxime chloride are prepared. Once the cholinesterase results come out and confirm that it is organophosphorus poisoning, treatment will follow immediately.

没多久结果就出来了，胆碱酯酶只有 400U/L 左右（正常数值应该有几千到几万），这是显著降低了。

The resident doctor’s eyes widened, it turned out to be organophosphorus poisoning!

It turns out that what we had always thought was acute gastroenteritis and infectious shock was actually organophosphorus poisoning.

This poisoning was not caused by oral ingestion of pesticides, but the patient may have used a folk remedy of organophosphorus pesticides to wipe his skin.

Although there is no evidence, this speculation is correct.

Adding together all the patient’s symptoms and the cholinesterase value, the diagnosis is very clear.

In any case, the antidote must be used immediately.

There are two most critical drugs for treating organophosphorus poisoning, one is atropine (symptomatic treatment) and the other is pralidoxime chloride (specific antidote).

Because the patient’s condition was critical, he was transferred to the ICU that night and received close monitoring and treatment in the ICU.

In addition to using special antidotes, he also received blood purification treatment to remove as much of the toxins inhaled into the body as possible.

Later I learned that the patient had already suffered cerebral edema that night.

The patient said he had blurred vision before he fell into a coma. This might not necessarily be caused by pinpoint pupils, but could also be papilledema. It was just that I had dealt with too few cases of organophosphorus poisoning and lacked experience, so I did not discover cerebral edema.

It really was a near-death experience.

The next day, the patient’s parents arrived and his colleagues also took the medicine used by the patient, and they found the ingredient dimethoate.

Dimethoate is a type of organophosphorus pesticide.

At this point, the truth is revealed.

The skin disease on the patient is actually psoriasis.

The patient tried many medications with little effect, so he later tried a folk remedy recommended by someone else. This remedy actually contained dimethoate (a type of organophosphorus pesticide), which is really dangerous.

Maybe they think it’s okay to apply dimethoate externally on the skin. In fact, the skin will also absorb pesticides, especially skin with wounds or bleeding, which can make drug toxins enter the blood more easily.

The patient eventually recovered and woke up.

We were always worried that the few minutes of cardiac arrest would have an impact on her brain. Subsequent observations proved that we were worrying too much. The patient recovered well, which also shows that our cardiopulmonary resuscitation was of high quality. We also performed tracheal intubation and connected her to a ventilator immediately, which quickly alleviated the problem of hypoxia.

Continuous chest compressions saved her life.

Popular Science Classroom: Don’t blindly follow folk remedies, as they may lead to poisoning

What is organophosphate poisoning and how common is it?

Organophosphorus pesticides (OPS) are the most widely used and largest amount of insecticides in my country, mainly including dichlorvos, parathion (1605), phorate (3911), chlorpyrifos (1059), dimethoate, trichlorfon, malathion (4049), etc.

Acute organophosphorus pesticide poisoning (AOPP) refers to a series of injuries, mainly damage to the nervous system, caused by large amounts of organophosphorus pesticides entering the human body in a short period of time.

There are three main ways for organophosphorus pesticides to enter the human body: entry through the mouth – accidental ingestion or voluntary oral ingestion (seen in people who commit suicide); entry through the skin and mucous membranes – often seen on hot days when organophosphorus falls on the skin when pesticides are sprayed. Due to sweating and expansion of pores, and the fact that most organophosphorus pesticides are fat-soluble, they are easily absorbed into the body through the skin and mucous membranes; entry through the respiratory tract – organophosphorus in the air enters the body through breathing.

After oral ingestion, symptoms usually develop within 10 minutes to 2 hours. Poisoning through skin absorption usually develops within a few hours to 6 days after exposure to organophosphorus pesticides.

The patient in this article used a solution containing organophosphorus pesticides to treat a skin disease, which eventually led to poisoning. This is not common, or even rare.

Young people generally will not suffer from related poisoning if they do not work with pesticides in farmland.

However, if you go on a picnic or work outdoors and accidentally enter a site that has just been sprayed with pesticides, and your skin comes into contact with too much pesticide, you may be poisoned, so you should take this as a warning.

Are folk remedies for skin diseases safe?

This cannot be generalized. In addition, folk remedies are not equivalent to traditional Chinese medicine. I can only say that many folk remedies are unsafe, but it cannot be denied that some folk remedies are effective. The key is that ordinary people (even doctors) have no ability to distinguish the safety and effectiveness of folk remedies, which is very dangerous.

Therefore, it is recommended that you go to a regular hospital for treatment when you have a difficult-to-treat skin disease. If the regular hospital cannot handle it well, you can go to another hospital to try again. You can also search for some authoritative textbooks or materials online to learn and increase your understanding of the disease, so as to avoid rushing to seek medical treatment.