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A few days ago, I was in charge of the resuscitation room and met a special postoperative patient
.
The patient, male, 31 years old, 65kg, was diagnosed as 1.
epilepsy 2.
hydrocephalus, and the operation was neuroendoscopic third ventriculostomy
.
When entering the recovery room, the patient was awake and talking freely.
The first impression was that he talked a lot; after connecting the monitor, it showed that the heart rate increased significantly, at about 110 beats/min, and the non-invasive blood pressure was about 140/78mmHg
.
At the request of the anesthesiologist in charge, the last blood gas analysis was collected, PH 7.
48, PO2 129mmHg (FiO2 30%), PCO2 23mmHg, BE -6.
5, Lac 6.
14, electrolytes and hemoglobin were normal, and he was instructed to slow down breathing, and no other treatment was done
.
About 20 minutes later, the patient complained of nausea, and then he vomited once, which was relieved after vomiting; the heart rate increased significantly after vomiting, up to 180 beats/min, and slowly decreased to about 150 beats/min after vomiting
.
At this point, we began to be vigilant, and urgently called the surgeon in charge of the operation to arrive.
At this time, in addition to the rapid heart rate, the breathing also increased faster than before, and the consciousness was unobstructed, but then there was a more serious situation
.
After about 5 minutes, the patient began to have a grand mal seizure, with loss of consciousness and rigidity of the limbs.
He was given propofol 80 mg intravenously, and the seizure stopped after 1-2 minutes.
In order to prevent the recurrence of seizures, 2 mg of midazolam was intravenously injected.
Light reflection is slow
.
During the epileptic seizure, the heart rate was as high as 200 beats/min, and it remained above 140 beats/min after intermittent bolus injection of esmolol
.
After communicating with the doctor in charge, the surgeon suggested that it may be a postoperative sympathetic storm, which is characterized by overexcited sympathetic nerves and induced epileptic seizures.
Finally, the patient will be transferred to the ICU for further observation and treatment after stabilization
.
Sympathetic storm, a very interesting complication, I quickly looked up the relevant knowledge and found that it does have this name, more officially called paroxysmal sympathetic hyperactivity (PSH)
.
It is an autonomic dysfunction regulation disorder that is most common in patients with acute brain injury, especially severe traumatic brain injury
.
The disease is characterized by recurrent episodes of sympathetic hyperactivity, which has a rapid onset, is often induced by stimulation, and can be relieved spontaneously after different periods of time or after abrupt medication
.
PSH has been called autonomic storm, sympathetic storm, hypothalamic dysregulation syndrome, autonomic dysfunction, paroxysmal autonomic instability with dystonia, and even diencephalic autonomic epilepsy
.
The pathophysiological mechanism of PSH is not fully understood
.
It is hypothesized that acute brain injury results in the disconnection of cortical inhibitory areas from sympathetic nerve centers located in the diencephalon (especially the hypothalamus), brainstem, and spinal cord
.
In theory, disruption of this descending inhibitory regulation could lead to sympathetic hyperresponsiveness to internal or external stimuli, as well as maladaptive changes at the level of the spinal cord, resulting in increased excitatory interneuron activity
.
As a result, non-noxious stimuli can trigger an overreaction in the spinal cord that is erroneously perceived as noxious by the higher-level central nervous system
.
In short, the inhibitory regulation of the high-level center fails, and the sympathetic nerves dominated by the low-level center are not regulated, and are particularly easily irritated and overreacted
.
This is similar to autonomic dysreflexia caused by damage to high spinal cord segments (above T6).
For details, please read Do patients with high paraplegia need anesthesia? PSH is usually seen in unresponsive patients with severe traumatic brain injury, and presents with repeated episodes of multiple symptoms, the most common symptoms include: almost all patients have tachycardia, usually sinus tachycardia
.
Hypertension, especially systolic hypertension, is often accompanied by elevated pulse pressure
.
Tachypnea with increased respiration and respiratory alkalosis
.
Dystonic postures are seen only in the most severe seizures and can be mistaken for tonic seizures, and abnormal postures in PSH patients are usually symmetrical
.
Treatment of PSH episodes requires a combination of abortive and prophylactic medications
.
The goal is to reduce the frequency and severity of attacks; if left unchecked, increased sympathetic activity can cause end-organ damage, most notably intracerebral hemorrhage
.
Some medicines, such as beta-blockers and clonidine, can be used as both abortive and preventive medicines
.
Other drugs are best used only as abortives (eg, morphine) or prophylactics (eg, gabapentin)
.
When I first encountered it, I was completely in a circle, and the severe vomiting was thought to be the manifestation of intracranial hypertension caused by hydrocephalus.
After I figured it out, I realized that it was true; because the sympathetic nerve center is located in the thoracolumbar spinal cord, it is higher than T6 and above.
Severe damage to the spinal cord or high center may block the inhibitory regulation of the descending high center, resulting in relative excitation of sympathetic nerves
.
Analgesic and sedative drugs during anesthesia can significantly reduce the occurrence of PSH, but severe PSH may occur after surgery due to the weakened sedative effect during the recovery phase
.
To sum up, for patients with severe craniocerebral injury, we should be alert to the perioperative paroxysmal sympathetic nerve hyperexcitability, and found that the heart rate, blood pressure, and breathing increased significantly.
PSH attacks should be considered, and esmolol and esmolol can be used.
Analgesic and sedative drugs, while preventing further development of dystonic postures
.
A little knowledge, I hope it will give you something to gain.
For more detailed introduction, please
.
The patient, male, 31 years old, 65kg, was diagnosed as 1.
epilepsy 2.
hydrocephalus, and the operation was neuroendoscopic third ventriculostomy
.
When entering the recovery room, the patient was awake and talking freely.
The first impression was that he talked a lot; after connecting the monitor, it showed that the heart rate increased significantly, at about 110 beats/min, and the non-invasive blood pressure was about 140/78mmHg
.
At the request of the anesthesiologist in charge, the last blood gas analysis was collected, PH 7.
48, PO2 129mmHg (FiO2 30%), PCO2 23mmHg, BE -6.
5, Lac 6.
14, electrolytes and hemoglobin were normal, and he was instructed to slow down breathing, and no other treatment was done
.
About 20 minutes later, the patient complained of nausea, and then he vomited once, which was relieved after vomiting; the heart rate increased significantly after vomiting, up to 180 beats/min, and slowly decreased to about 150 beats/min after vomiting
.
At this point, we began to be vigilant, and urgently called the surgeon in charge of the operation to arrive.
At this time, in addition to the rapid heart rate, the breathing also increased faster than before, and the consciousness was unobstructed, but then there was a more serious situation
.
After about 5 minutes, the patient began to have a grand mal seizure, with loss of consciousness and rigidity of the limbs.
He was given propofol 80 mg intravenously, and the seizure stopped after 1-2 minutes.
In order to prevent the recurrence of seizures, 2 mg of midazolam was intravenously injected.
Light reflection is slow
.
During the epileptic seizure, the heart rate was as high as 200 beats/min, and it remained above 140 beats/min after intermittent bolus injection of esmolol
.
After communicating with the doctor in charge, the surgeon suggested that it may be a postoperative sympathetic storm, which is characterized by overexcited sympathetic nerves and induced epileptic seizures.
Finally, the patient will be transferred to the ICU for further observation and treatment after stabilization
.
Sympathetic storm, a very interesting complication, I quickly looked up the relevant knowledge and found that it does have this name, more officially called paroxysmal sympathetic hyperactivity (PSH)
.
It is an autonomic dysfunction regulation disorder that is most common in patients with acute brain injury, especially severe traumatic brain injury
.
The disease is characterized by recurrent episodes of sympathetic hyperactivity, which has a rapid onset, is often induced by stimulation, and can be relieved spontaneously after different periods of time or after abrupt medication
.
PSH has been called autonomic storm, sympathetic storm, hypothalamic dysregulation syndrome, autonomic dysfunction, paroxysmal autonomic instability with dystonia, and even diencephalic autonomic epilepsy
.
The pathophysiological mechanism of PSH is not fully understood
.
It is hypothesized that acute brain injury results in the disconnection of cortical inhibitory areas from sympathetic nerve centers located in the diencephalon (especially the hypothalamus), brainstem, and spinal cord
.
In theory, disruption of this descending inhibitory regulation could lead to sympathetic hyperresponsiveness to internal or external stimuli, as well as maladaptive changes at the level of the spinal cord, resulting in increased excitatory interneuron activity
.
As a result, non-noxious stimuli can trigger an overreaction in the spinal cord that is erroneously perceived as noxious by the higher-level central nervous system
.
In short, the inhibitory regulation of the high-level center fails, and the sympathetic nerves dominated by the low-level center are not regulated, and are particularly easily irritated and overreacted
.
This is similar to autonomic dysreflexia caused by damage to high spinal cord segments (above T6).
For details, please read Do patients with high paraplegia need anesthesia? PSH is usually seen in unresponsive patients with severe traumatic brain injury, and presents with repeated episodes of multiple symptoms, the most common symptoms include: almost all patients have tachycardia, usually sinus tachycardia
.
Hypertension, especially systolic hypertension, is often accompanied by elevated pulse pressure
.
Tachypnea with increased respiration and respiratory alkalosis
.
Dystonic postures are seen only in the most severe seizures and can be mistaken for tonic seizures, and abnormal postures in PSH patients are usually symmetrical
.
Treatment of PSH episodes requires a combination of abortive and prophylactic medications
.
The goal is to reduce the frequency and severity of attacks; if left unchecked, increased sympathetic activity can cause end-organ damage, most notably intracerebral hemorrhage
.
Some medicines, such as beta-blockers and clonidine, can be used as both abortive and preventive medicines
.
Other drugs are best used only as abortives (eg, morphine) or prophylactics (eg, gabapentin)
.
When I first encountered it, I was completely in a circle, and the severe vomiting was thought to be the manifestation of intracranial hypertension caused by hydrocephalus.
After I figured it out, I realized that it was true; because the sympathetic nerve center is located in the thoracolumbar spinal cord, it is higher than T6 and above.
Severe damage to the spinal cord or high center may block the inhibitory regulation of the descending high center, resulting in relative excitation of sympathetic nerves
.
Analgesic and sedative drugs during anesthesia can significantly reduce the occurrence of PSH, but severe PSH may occur after surgery due to the weakened sedative effect during the recovery phase
.
To sum up, for patients with severe craniocerebral injury, we should be alert to the perioperative paroxysmal sympathetic nerve hyperexcitability, and found that the heart rate, blood pressure, and breathing increased significantly.
PSH attacks should be considered, and esmolol and esmolol can be used.
Analgesic and sedative drugs, while preventing further development of dystonic postures
.
A little knowledge, I hope it will give you something to gain.
For more detailed introduction, please
