Restlessness or immobility, are all "nerves" to blame?

Conan Doyle, the author of the world-famous detective masterpiece Sherlock Holmes, was actually a clinician at first.

Why does a doctor have such careful thinking? In fact, in the process of exploring diseases, doctors often solve crimes like detectives, especially for complex neurological diseases.

Therefore, Yimaitong will launch a series of columns-"The "God" Medical Detective" column, which will analyze the complex diseases of the nervous system in the form of detectives, reveal the mystery of the disease, then follow us to explore now Case! At the beginning of the Year of the Ox, with the sound of firecrackers one after another, people are immersed in a happy and peaceful New Year, but the Central Hospital is staged a thrilling battle of life and death.

And my role on this day is the chief resident of God, participating in three contests with the god of death, and working closely with the brother department.

Two patients with severe restlessness and one patient who was dying motionless, both recovered and were discharged from the hospital.

Is the patient's restlessness or immobility caused by "nervous"? Let us find out.

Case 1: Male, 32 years old, had fever without obvious cause 4 days ago, the highest body temperature was 39.
0℃, accompanied by cough, white sputum, oral amoxicillin and antipyretic drugs, but fever repeated.

1 day ago, she had speech confusion, and the answer was not what was asked and the behavior was abnormal, so she came to our hospital for treatment, perfected related examinations and admitted to the ward with "mental disorder pending investigation".

No dizziness, headache, chest tightness, shortness of breath, frequent urination, urgency, dysuria, abdominal pain, poor eating, and sleep.

Previous physical fitness.

Physical examination: T 37.
5℃, P 102 times, Bp 155/86mmHg, trance, confusion, restlessness.

The pupils are of equal size and the diameter is 3.
0 mm, the light reflection is sensitive, the movement of the eyes is normal, and there is no nystagmus.The nasolabial folds are symmetrical, the tongue is in the center, the muscle strength and muscle tension of the extremities are normal, the sensory and mutual movement examinations are not cooperative, the bilateral knee tendon reflexes are symmetrical, the bilateral Pap sign is suspiciously positive, and there is no meningeal irritation.

Auxiliary examination: normal blood routine, Scr 182.
1umol/L, AST 415.
00IU/L, ALT 306 IU/L, LDH 989.
00 IU/L, CK 1403 IU/L, CK-MB53.
00 IU/L; ECG: sinus Tachycardia.

CT of the head and chest showed no abnormalities.

After admission, I wanted to improve the MRI, but at this time the patient's agitation became more serious, and he screamed like an arrow in the corridor.
He couldn't control it.
Urgently push the sedative medicine and call the security department for support.
The patient is placed in a single room with the doors and windows closed.
.

When the patient is quiet, perfect craniocerebral DWI shows that the corpus callosum pressure point is high signal, and the lumbar puncture cerebrospinal fluid pressure, routine, and biochemistry are normal.

Diagnosis: Reversible corpus callosum syndrome (viral infection), abnormal liver and kidney function.

Case 2: Male, 30 years old, developed weakness and soreness 4 days ago in the morning.
He thought that taking Analgin tablets and cold medicines for colds was ineffective.

Symptoms worsened in the afternoon 1 day ago.
During the local intravenous infusion of azithromycin, both upper and lower limbs were weakened, and gradually progressed to immobility of the limbs.
After 6 hours, he developed dyspnea and his symptoms worsened.
He called 120 and was sent to our hospital.

In the emergency room, the patient experienced decreased blood oxygen saturation and labored breathing.
The trachea was intubated, and the head and chest CT were completed and admitted to the ICU ward with acute respiratory failure.

There was no fever and abdominal pain, no syncope, no convulsions, no tearing pain, no nausea and vomiting, no dysphagia, poor diet and sleep, and normal stool.

He has previously denied a history of high blood pressure, diabetes, or heart disease.

Denies the history of food and drug poisoning.

Physical examination: T 36.
3℃, P 86 times, Bp 152/72mmHg, drowsiness (propofol sedation), tracheal intubation ventilator assisted breathing, questioning can indicate, cyanosis of the lips, no pale conjunctiva, no yellowing of the sclera, The pupils on both sides are of equal size with a diameter of 2.
5mm, light reflection is sensitive, the eyes are flexible, and the tongue and teeth can not cooperate.

Extremities muscle strength is grade 0, muscle tension is low, knee tendon reflex and Achilles tendon reflex disappear, meningeal irritation is negative, sensory examination lacks cooperation, no clear sensory plane is seen, and Pap's sign is negative.

Breath sounds in both lungs are clear, heart rhythm is uniform, and no murmur is heard, abdomen is soft without tenderness and rebound pain, and there is no edema in both legs.

Auxiliary examination: blood biochemistry: ALT: 136.
00IU/L, BUN 10.
29mmol/L, blood K 1.
6mmol/L, troponin T normal; blood routine: WBC 22.
08×109/L, NEUT# 19.
61×109/L, There is no abnormality in coagulation.

The new crown antibody was negative, the head CT showed no abnormalities, and the chest CT: the lower lobes of both lungs were drooping changes.

Blood gas: PH 7.
25, PCO2 38mmHg, PO2 165 mmHg, Lac: 3.
7mmol/L, FIO2: 50%, K: 1.
4mmol/L.

Diagnosis: hypokalemia; acute respiratory failure; metabolic acidosis.

Positioning: muscle, qualitative: low potassium.

At this time, the ICU doctor anxiously asked: Can only low potassium explain it? In the ICU for more than ten years, I have never encountered hypokalemic respiratory failure? Is there anything else, it won't be delayed.

While watching his puzzled eyes, he returned: Well, I have never seen a low-potassium decay in so many years, but the book says it's okay.

Seeing that I was about to leave, he chased after him, holding the blood qi that had just come out, the blood K had already reached 2.
5, or was he still motionless? Is there a possibility of myasthenia gravis or Guillain Barre? We just supplement potassium in this way, there is no other treatment, it will not be delayed, will it? Therefore, the two of us continue to analyze: 1.
Onset with weakness and pain in the whole body is not myasthenia gravis, because myasthenia gravis does not accompany soreness. 2.
Green Barley can indeed have quadriplegia and respiratory involvement.
Even if the diet is poor, the blood potassium will not be so low if there is no difficulty in swallowing.

3.
Low potassium can explain everything, why not explain it? 4.
Can the patient move out for EMG and MRI while the ventilator assists in breathing? Can I rush to C-ball and plasma exchange? Obviously not.

What we need to do now is to continue to supplement potassium, stay still, and observe the effect.

After the above-mentioned encouragement, he nodded, but still asked suspiciously: blood potassium has risen a lot, and it is still not good, limbs are 0 grade, how to explain? Well, I think it is a matter of time.

We came to the bed again.
At this time, there was a dramatic change.
The patient's limbs could be translated and his muscle strength returned to level 2.

Seeing the patient's horrified eyes, encouragement has improved, I returned to the ward safely.

Case 3: I ate lunch in a hurry, just wanted to drink some water, the phone rang, and the CCU had an emergency consultation.

An uncontrollable, restless patient needs support.

Female, 54 years old, with sudden frequent convulsions 5 hours ago, unconsciousness, shaking limbs, each lasting about 2 minutes, repeated dozens of episodes, underwent electrocardiogram examination at the local hospital, heart rate at least 30 beats/min, given atropine After Isopropyl Kidney, I came to our hospital and admitted to the CCU ward.

After admission, the patient developed restlessness, gibberish, and yelling.

I rushed to the CCU and saw that 6-7 medical staff were surrounding a patient who was "fluttering" in the bed.
They wanted to place a temporary pacemaker, but couldn't hold her.

The doctor on duty asked anxiously: Is there any neurology problem with the convulsions and restlessness who just came up? At first glance, it seems that there is something wrong with the "nerv".
Blood sugar and blood biochemistry are normal, blood HGB is normal, WBC 23.
15×109/L, NEUT# 19.
1×109/L.

At this time, you need to make a quick judgment, YES or NO, YES will be taken to the neurology department; NO will be left.

Notice that the monitor shows a heart rate of 17-26 beats/min and a blood pressure of 111/54mmHg.
Is it agitation caused by a slow heart rate, or a slow heart rate caused by encephalitis and intracranial hypertension? Pulling the crying daughter of the patient who lived next to her, she asked a few important words in the noise: there was only a history of heart disease in the past, no clear diagnosis, no fever, no headache, nausea, or vomiting recently.

To have a physical examination, the patient rolled left and right, beating, scolding, and kicking people.
He could barely check that there was no pathological reflex.

If it is encephalitis, headache, fever and vomiting must be the same.
In addition, intracranial hypertension usually has high blood pressure and low heart rate.

Comprehensive analysis is encephalopathy-severe arrhythmia caused by hypoxic-ischemic encephalopathy.

Consultation opinion: Stay in the CCU to increase heart rate, improve microcirculation, improve blood ammonia, vitamin B12, calcitonin, thyroid function, C-reactive protein, and head MRI when the condition permits.

Case analysis, sorting and outcome Case 1: There is abnormal liver, kidney function, and myocardial enzymes, can acyclovir be used for anti-virus? The answer is yes.

Give acyclovir antiviral, ceftriaxone anti-inflammatory, reduce cerebral edema, and protect the liver.

On the second day, the fever subsided and the renal function was normal; on the fifth day, the mental symptoms disappeared; when he was discharged from the hospital two weeks later, myocardial enzymes were basically normal, and the liver function transaminase was slightly higher.
Continue to take hepatoprotective drugs.

Two weeks after he was discharged from the hospital, he returned for a visit.
The DWI lesions disappeared, his liver function was basically normal, his speech was clear, and he worked normally.

The DWI on admission and 2 weeks after discharge is shown in the figure below.

Case 2: Potassium supplementation was given, and the ventilator assisted breathing.

TSH: 0.
01uIU/ml, FT4: 2.
51ng/dl, FT3: 5.
93pg/ml.

On the second day, the muscle strength of the limbs was level 4, the breathing was normal, and she was offline.

Blood potassium was normal on day 3, muscle strength was level 5 on day 4, and she got out of bed.

The nephrology department ruled out renal tubular acidosis.
After admission, the blood pressure was normal.
The endocrinology department perfected the aldosterone lying position test to exclude the original aldehyde.

Diagnosis: hypokalemia, hyperthyroidism.

He recovered and was discharged on the 8th day.

Case 3: Give atropine and isopropyl kidney to increase heart rate and improve microcirculation.

About 3 hours after admission, the patient's mental symptoms disappeared, and his restlessness and other symptoms were completely relieved that night.

Blood ammonia, calcitonin, C-reactive protein, and thyroid function were all normal.

There was no rebound afterwards, and the family members did not agree to do MRI.
The blood WBC 7.
79×109/L and NEUT# 3.
99×109/L were reviewed.
A permanent pacemaker was placed in the cardiology department.
He recovered and discharged after half a month.

 Case thinking, summary, and summary ➤The restless mental symptoms of cases 1 and 3 were cured quickly after symptomatic treatment, and they belonged to delirium.

➤Case 1 had liver and kidney function and myocardial damage at the time of admission.
What was the reason? ➤The white blood cells of Cases 2 and 3 were significantly higher than normal when they were admitted to the hospital.
Although chest CT showed penetrating changes, the patient's body temperature was normal, and there was no fever and lung infection symptoms before admission.
Obviously, it was not entirely due to the penetrating changes in the lungs.
What is the reason? ➤Differential diagnosis of case 2, what are the diseases of limb weakness and dyspnea? Expansion of case-related knowledge points ➤ Delirium: It is caused by a variety of reasons, a transient state of confusion, manifested as disturbance of consciousness and cognitive function changes, which are mainly manifested by mental symptoms.

Patients with delirium have different levels of consciousness, and the content of their consciousness is disorderly, which is the result of the joint effect of systemic disease and abnormal brain function.

Usually reversible, transient brain dysfunction, clinical manifestations of a variety of neuropsychiatric abnormalities, fluctuating symptoms, duration ranging from several hours to several days, but according to the tenth edition of the International Classification of Diseases (ICD-10), it may last Up to 6 months.

As many as 28% of patients with delirium after cardiac arrest hypoxic-ischemic encephalopathy.

The manifestations of delirium occur in the form of hypofunction, hyperfunction, or mixed forms.
It is a reversible brain insufficiency state, similar to the more familiar liver or kidney insufficiency.

Usually divided into (a) low activity subtype, characterized by reduced alertness, sedation, and reduced motor activity.

(b) High activity subtype, hyper-alertness, increased movement, and psychotic characteristics (hallucinations, delusions, restlessness).

(C) Mixed type.

➤Inflammatory storm: Also known as cytokine storm and cytokine waterfall cascade, it refers to the phenomenon that the body is infected with microorganisms and causes the rapid mass production of multiple cytokines in body fluids.
The body's excessive immunity to microorganisms causes damage to the body itself.
Phenomenon is an important cause of multiple organ failure.

After the inflammatory storm occurs, the patient's condition often turns abruptly, and soon becomes unconscious, breathing speeds up, and even coagulation dysfunction, oliguria and anuria, elevated transaminases, and failure of various organs.

When viruses and bacteria invade the human body and activate the body’s immune system, the body will exert its own immune function, especially after the virus infects the human body, the immune system will make inflammatory factors (including tumor necrosis factor, granulocyte macrophages) through a series of mechanisms.
The release of colony stimulating factors, interleukins 6, 8), etc.
increases, leading to inflammation.

Inflammation is one of the common ways the body resists pathogens.
It helps to strengthen the body’s elimination of viruses, but at the same time it also enhances the permeability of blood vessel walls, triggers the release of a large amount of nitric oxide, destroys blood vessels, and causes organ function to be affected.
damage.

➤Leukocytosis: The white blood cell count in the adult peripheral blood exceeds 10.
0×109/L, which is called leukocytosis.
The production and release in the bone marrow increase; adherent white blood cells separate into the tissue; some microbial components or metabolites cause leukocytosis.

The white blood cell count is close to 100.
0×109/L, which is called a leukemia-like reaction.

The specific causes of leukocytosis are shown in the figure below.

➤ Hypoxic-ischemic encephalopathy (Hypoxic-ischemicencephalopathy, HIE): is a kind of acquired metabolic encephalopathy, caused by insufficient oxygen and glucose supply or insufficient brain metabolism.
It is caused by overall perfusion or insufficient oxygenation, not due to Cerebral vascular infarction in a specific area.

The most common cause is decreased cerebral blood flow, due to heart disease, ventricular arrhythmia, blood loss, drowning, hypotension, carbon monoxide poisoning, Guillain-Barré syndrome, amyotrophic lateral sclerosis, respiratory failure hypercapnia, etc.
Causes a decrease in oxygenated blood flow. Lack of cerebral blood flow quickly affects brain metabolism, especially in areas with high metabolic oxygen/sugar demand, including cortex, hippocampus, cerebellar deep chorion, thalamic reticular nucleus, and basal nucleus.
Insufficient metabolism, resulting in corresponding clinical symptoms .

The pathophysiological mechanism of hypoxic-ischemic encephalopathy is shown in the figure below.

➤ HIE causes the increase in the total number of white blood cells in the peripheral blood.
The reason: the body is stressed during HIE, the sympathetic nerve is excited, and the adrenaline is produced so that the blood flow is accelerated, and the granulocytes in the marginal pool enter the circulation pool.

The increase is temporary.

➤ Differential diagnosis of limb weakness with respiratory dysfunction includes myasthenia gravis (MG), juvenile myasthenia gravis (JMG), Lambert-Eaton myasthenia syndrome (LEMS), hyperthyroidism, Guillain-Barre syndrome ( GBS), polymyositis, muscular dystrophy, metabolic myopathy, botulism and beriberi.

➤ Beriberi: It is a disease of cardiovascular system and peripheral nerve damage caused by vitamin B1 (Vitamin B1, VitB1, also known as thiamine) deficiency.

Cardiovascular system damage is manifested as arrhythmia and heart failure.
Peripheral nerve damage is mainly manifested as limb numbness, pain and weakness, symmetrical peripheral nerve paralysis of limbs and muscle atrophy.

As early as the Sui and Tang Dynasties, China has recorded that beriberi occurred after eating white rice for a long time.

In the Tang Dynasty, Sun Simiao divided beriberi into swelling and non-swelling, and beriberi was in the heart.

VitB1 is an important component of the sugar metabolism process, and it also has a direct effect on nerve conduction.
Lack of glucose metabolism hinders the supply of energy and coenzymes.
The accumulation of lactic acid and pyruvate in blood tissue causes a series of symptoms.

Clinically, the symptoms of the cardiovascular system and the nervous system, which have the strongest metabolism and the most energy consumption, are prominent.

The main manifestation of circulatory system is wet beriberi, the main manifestation of peripheral nervous system is dry beriberi, and the main manifestation of central nervous system is cerebral beriberi.
Most people have mixed type.

VitB1 deficiency diseases include beriberi, Wernicke's encephalopathy, and Kosakov's psychosis.

Among them, Wernicke encephalopathy has been recognized by many doctors, but the lack of VitB1 can also cause beriberi.

For patients with alcoholism and nutritional risk, when symmetrical peripheral nerve dysfunction occurs, pay attention to this disease.

 Classic case review Jegan et al.
reported that a 59-year-old man with previous hypertension, diabetes and hyperlipidemia had undergone coronary artery bypass surgery due to acute myocardial infarction.

During the operation, he did not have any complications related to surgery or anesthesia.

But after the operation, he felt irritable and lost his way of time, place and people, which lasted for 3 months.

He was transferred to a tertiary psychiatric hospital for treatment.

In the psychiatric ward, his clinical condition remained for several months.

9 months after the cardiac event, his delusional characteristics (including disorientation of people and places, impaired attention, visual and hearing, hallucinations and other perceptual disturbances, emotional instability and psychomotor disturbances) gradually improved.

But all basic activities in daily life (including going to the toilet and eating) need help.

He was later diagnosed with dementia, secondary to cardiac arrest-related HIE, with prolonged delirium.

Dementia begins after acute myocardial infarction and cardiac arrest, and it gets worse after heart bypass surgery.

Literature review misdiagnosed as Green Barley's beriberi.
Domestic literature reported that a middle-aged man had gone to work in Africa 7 months before he was admitted to the hospital.
He lost more than 10 kilograms because of his unaccustomed life.

One month before admission, he developed weakness, edema, palpitations, and oliguria in both lower limbs.
The edema of the lower limbs subsided with oral medication, but there was still weakness in the lower limbs.

After returning home, he went to a local hospital for treatment.
The cerebrospinal fluid was checked for protein 1.
2g/L (the rest was normal).
After the diagnosis of Guillain-Barre syndrome, he was given hormone therapy, and the weakness of both lower limbs became worse.

After the transfer, the cerebrospinal fluid protein 0.
4 g/L (more than normal) was rechecked, and the electromyogram was neurogenic damage, and the nerve conduction velocity slowed down.

The clinical diagnosis of beriberi was significantly improved after a large amount of VitB1 treatment.

 Do you know about pseudo-subarachnoid hemorrhage? Spiegel et al.
originally described the radiological signs of pseudo-SAH in 1986.

Initially, diffuse cerebral edema was the cause of the discovery.

Avrahami et al.
reported that, contrary to previous understanding, this is a rare phenomenon and is actually common; usually in the case of drug abuse, trauma or cardiopulmonary arrest, in young patients with larger brain volumes (40 years old) Below).

This is due to cerebral edema due to hypoxic-ischemic injury.

At present, multiple reports have proven other reasons for this discovery, including meningitis, subdural hemorrhage, cerebral infarction, use of contrast agents, spontaneous low intracranial pressure, polycythemia, and chronic hypoxemia.

The difference between pseudo-SAH and SAH: measure the CT value of the high-density area.
In patients with pseudo-SAH, the CT value of the high-density area is within 30-42 HU.

SAH patients have higher values, with CT values ​​ranging from 60 to 70 HU.

Among them, the most commonly mentioned pathogenic mechanism is compression of the dural sinus and obstruction of venous return, leading to superficial vein congestion, which appears as a high-density area under the background of low-density cerebral edema.

Secondly, pseudo-SAH is relatively symmetrical than SAH.

A case of pseudo-subarachnoid hemorrhage secondary to hypoxic-ischemic injury caused by bleeding from pulmonary arteriovenous malformations, as shown in the figure below.

  Epilogue During the emergency consultation, we encountered an imminent problem.
After the positioning was qualitative, we had to orientate.
At this moment, you are the commander.
The so-called "fighting", because life and death matter, the slightest difference is so ridiculous.

How to become a sharpshooter with perfect bullets is the goal of our persistent pursuit and hard training.

After half a month, all three of them recovered and were discharged from the hospital, returned to the vast crowd, and continued their lives.

Perhaps they will never forget it.
The Xinchou New Year of the Ox experienced a life-and-death tragedy and walked through the ghost gate.
Behind them, the Department of Pre-hospital First Aid, Emergency, ICU, CCU, Shennei, Renal, Endocrinology, and Radiology worked together for them.
The medical staff who fought a life-and-death struggle may have forgotten this thrilling struggle, because this is the bit of our daily work. Raise your head, spring returns to the earth, the distant mountains smile and the water flows long; look at your eyes, life continues, all people move forward calmly! References 1.
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