Chapter 767 The culprit of the disease
Acute liver damage, severe acidosis, chronic anemia...
Xu Qiu tried to find clues to the culprit of the disease.
However, the next moment, the patient's condition took a sharp turn for the worse again.
Ugh!
Ding Tao felt a strong pressure rushing out of her stomach, and the muscles of the digestive tract seemed to spasm from bottom to top. She vomited painfully and retched with big mouthfuls.
"Didn't you have lunch?" Xu Qiu asked when he saw this.
It was more than three o'clock in the afternoon. If she had eaten at lunch time, she would definitely not have time to digest it completely at this time, so she would not be unable to vomit anything.
"Yes, she is more than twenty pounds heavier than before after giving birth. She said she wanted to lose weight." Ding Tao's husband's eyes were full of heartache. Although it didn't work, he still patted his wife's back.
Beep beep--
Soon, the monitor began to alarm, and the patient's condition began to deteriorate again.
Xu Qiu frowned slightly... As expected, as he predicted, before the root cause of the disease was found, all the improvements were just illusions. The patient could still be critically ill at any time, and only staying in the ICU could save his life.
Forced to stay in the ordinary ward, there is a lack of life-sustaining equipment, and the various life-saving facilities are not as complete as those there. By the time he was sent to the ICU, he was already dead.
"Transfer to the ICU." Xu Qiu said lightly.
This also means that the real burning of money to prolong life has begun.
On the first day alone, the startup fee of several important equipment cost 40,000 yuan, and this was without the use of ECMO. If ECMO, blood filtration, etc. were added, the medical expenses on the first day would easily exceed 200,000 yuan.
That is not a life-saving method that ordinary people can afford.
"It's a bit like IgA nephropathy."
In the office, Xu Qiu repeatedly checked Ding Tao's medical records and made a guess.
Shi Lian opened her mouth slightly and said, "The patient had no history of upper respiratory infection before, and there was no hematuria..."
IgA nephropathy has two characteristics.
One is that the onset is often one to three days after the upper respiratory tract infection.
The second is that the patient has macroscopic hematuria or microscopic hematuria.
But Ding Tao did not meet the two requirements.
Xu Qiu shook his head: "The textbooks teach the typical manifestations of classic diseases."
The patient's main problem is acute liver damage, but he still grasped the fact that the blood creatinine exceeded the standard in the renal function test.
Kidney disease progresses to renal insufficiency, and then induces metabolic acidosis.
If IgA nephropathy can be diagnosed, at least the acidosis can be explained.
"Arrange a renal biopsy pathology, and then do immunofluorescence."
These two tests, if they follow the routine process, will take about a week to get the results.
But Linyi has already opened a green channel to make way for urgent patients.
The next morning, two results came out.
The renal biopsy pathology showed that the patient had diffuse mesangial hyperplasia and focal segmental proliferative glomerulonephritis.
Another immunofluorescence showed that immune complex deposition dominated by IgA was found in the mesangial area!
These two results directly locked IgA nephropathy, even if the patient did not have a typical history of upper respiratory tract infection or hematuria.
This made the doctors in the emergency department and urology department a little excited for a moment.
Could it be that the culprit of the disease comes from the IgA nephropathy that has been hidden for so many years?
Xu Qiu is not sure.
Faced with an unknown and complex disease, he can only adapt to the situation.
The current task is to control the IgA nephropathy first and see if Ding Tao's condition is relieved. If the treatment is effective, the root of the disease is likely to be related to the IgA nephropathy.
...
However, the treatment of IgA nephropathy is also a major difficulty.
There is no special treatment for this disease. We can only formulate personalized plans based on experience according to the patient's symptoms, disease classification and course of the disease.
For example, IgA nephropathy with isolated microscopic hematuria is a blessing in disguise. Most of them have no clinical manifestations and do not require special treatment. Regular follow-up is sufficient.
On the contrary, recurrent macroscopic hematuria or abnormal urine test types are basically controlled by triple therapy of tripterygium wilfordii polyglycosides, rhubarb and ACEI/ARB.
Ding Tao's is the third type: vasculitis type.
This is also the most complex classification of IgA nephropathy.
It is precisely because he has not thoroughly studied the mechanism, manifestations, and pathogenic mechanism of this classification that Xu Qiu cannot determine whether it is IgA nephropathy that caused Ding Tao's critical illness.
"Use the MMF plan."
After considering for more than ten minutes, Xu Qiu confirmed the doctor's order.
Methylprednisolone shock treatment lasts for three days.
After that, continue treatment with 36mg of prednisone every day.
If it is just ordinary IgA nephropathy, this treatment plan will last at least half a year, reducing the dose of prednisone by 5mg every two weeks until it is maintained at 10mg per day...
But Ding Tao is different.
She is still lying in the ICU, her life is hanging by a thread, and it is naturally impossible to treat IgA nephropathy slowly.
The safest way is to see if methylprednisolone shock treatment can relieve the condition. If it can, continue to treat IgA nephropathy. If there is no improvement in the body, then the priority of kidney disease will be ranked very low.
On the first day of the MMF treatment plan, Ding Tao's condition was not much different from before.
On the second day of shock treatment, the internal environment was still in a disordered state, and the medication could only ensure that it would not endanger life.
On the third day, kidney damage continued to progress, and liver damage also did not improve.
Xu Qiu's face changed.
The patient did have IgA nephropathy, but this could only explain the abnormality of renal function indicators and had nothing to do with the patient's severe acidosis and acute liver damage.
Last year, he also diagnosed a patient with acute liver damage and chronic anemia.
That was a college student who was doing micro-business. He bought a batch of meal replacements and diet pills. He also ate meal replacements and also took the diet pills he sold.
As a result, the meal replacements had a serious nutritional imbalance, and the diet pills contained the banned ingredient sibutramine. The combination of the two made the patient step into the gates of hell in a short period of time.
But Ding Tao was completely different. She was pregnant some time ago. For the sake of the baby in her belly, she had not taken any medicine for more than a year, and had not touched any medicine for nearly a month after giving birth.
In this case, the most easily traceable cause of liver damage was ruled out.
"What is the connection between chronic anemia, acute liver damage and severe acidosis?" Xu Qiu fell into deep thought.
This is the key to diagnosing the disease.
The patient has heart failure, which is definitely related to chronic anemia.
But, is chronic anemia and the other two diseases causal or parallel?
And, is it acute liver damage that causes severe acidosis, or does the progression of acidosis damage the liver?
Different order, representing completely different diseases.
If it is the former…
The liver participates in the regulation of acid-base balance through four pathophysiological mechanisms, including lactate metabolism, albumin homeostasis, ketone body production, and urea production.
Although the kidney is the most important organ for maintaining acid-base balance, more than 70% of lactate is metabolized in the liver.
