The first section of cerebral coma rescue treatment Jiao Hui, Department of Neurology, Beijing Military Region General Hospital
Cerebral coma includes: rescue treatment and wake-up promotion. Rescue treatment includes three parts: rescue treatment and wake-up promotion in the acute stage of cerebral coma, wake-up promotion treatment of micro-consciousness, and wake-up promotion treatment of vegetative state. Each part can be roughly divided into wake-up promotion treatment for traumatic brain injury and wake-up promotion treatment for closed cranial brain injury.
I. Acute cerebral coma treatment
1.Resuscitation: acute treatment includes: reducing cerebral edema, inhibiting cerebrospinal fluid secretion, restoring autonomic respiration and getting off the ventilator.
Micro-consciousness to promote awakening; drug, physical and herbal therapy; neural stem cell transplantation; appropriate hyperbaric oxygen therapy, transcranial magnetic stimulation therapy, cervical medulla and deep electrical stimulation and other comprehensive treatment.
The vegetative state is mainly the treatment of complications; complete recovery of consciousness, closure of tracheotomy, removal of urinary catheter and nasal feeding tube, early sitting, swallowing, standing, intelligence, language, etc.
In 2004, China established the brain coma promotion center and began to treat a large number of patients with different types of brain coma. At that time, research was focused on the treatment of traumatic brain injury. There was not much confidence in ischemic-hypoxic encephalopathy, which was considered “meaningless to treat”. The center became an outlet for the treatment of patients in cerebral coma, and also tried to become a platform for research into the promotion of cerebral coma.
After a patient in a coma is brought to the hospital emergency department and intensive care unit through onsite care, further treatment measures are required. Traumatic and ischemic-hypoxic encephalopathy brain coma generally routinely establishes five channels, one monitor and two pumps.
(i) Traumatic brain coma or cerebral hemorrhage coma.
1, tracheal intubation, oxygen tube, nasal feeding tube, urinary catheter, intravenous infusion tube, a class A multifunctional cardiac and blood pressure oximetry monitor and two pumps (nasal feeding pump, drug pump).
2, mild coma without tracheotomy, severe coma or coma unconscious for more than 7 seven days, do tracheotomy.
3.Oxygen continuous inhalation, if necessary, use tracheoscope to remove the misaspiration.
4.Decompression of debridement flap or minimally invasive hematoma removal.
5.Lower nasal feeding tube: pump in enteral nutrition solution and drugs.
6.The same day catheterization.
7.Multifunctional cardiac and blood pressure monitor to detect heart rate, blood pressure, oxygen saturation and cerebral pressure.
8.Rapidly establish infusion channel and infusion pump. Maintain blood pressure and vital signs.
9.Select surgery: debulking flap decompression, hematoma localization drilling, ventricular drainage, ventriculoscopic clot retrieval, etc.
(B) Closed cerebral coma (ischemic-hypoxic encephalopathy)
1, defibrillation and drug resuscitation to restore heartbeat and respiration. Tracheal intubation and ventilator-assisted breathing as soon as possible.
2, oxygen tube, laryngeal mask continuous oxygenation. Remove misaspirated material with tracheoscope if necessary.
3.Lower nasal feeding tube: pump in enteral nutrition solution and drugs.
4.Urinary catheter.
5.Intravenous infusion.
6.Class A multifunctional cardiac and blood pressure oximeter to detect heart rate, blood pressure, oxygen saturation and cerebral pressure.
7.For long coma time, tracheotomy after 7 days.
8.There are two methods to measure cerebral pressure within 24 hours of coma: lumbar puncture and automatic pressure-controlled subarachnoid placement, dynamic and continuous observation of cerebral pressure, implementation of reducing cerebral edema, lumbar puncture for 6 days 4 times lumbar puncture, automatic pressure-controlled subarachnoid placement continues 6-7 days of extubation.
Second, the emergency period to promote waking treatment
The acute phase of cerebral coma can be further divided into three phases.
Cerebral edema and brain swelling phase: Patients in cranial CT and MRI brain coma are the first to show cerebral edema. There is a difference between mild, moderate and severe edema on imaging, and brain herniation appears in severe cases. At this time, intracranial pressure is increased, respiratory depression or cessation, and ventilator-assisted breathing.
Epileptic phase: Coexisting with cerebral coma edema is the occult epileptic phase, which is characterized by the absence of typical epileptic convulsions and is mainly characterized by paroxysmal heart rate acceleration, increased blood pressure, binocular upward gaze, gaze, shortness of breath, and high muscle tone. Anti-epileptic drug therapy is effective.
Hydrocephalus phase: Most patients with open brain injury coma involving temporal lobe lesions found on cranial imaging can rapidly develop hydrocephalus in 1 month. Patients in coma with closed brain injury can develop hydrocephalus within 1 month. Coma with temporal lobe injury is more severe. Patients with left temporal lobe injury coma are difficult to promote awakening. These three stages of division are more in line with clinical practice.
Conventional treatment is generally.
① Water drugs mannitol, glycerol fructose, etc.
② Hormones: hydrogenated prednisone, methylprednisolone, dexamethasone, etc.
③ Human blood albumin.
④ Hypertonic sugar.
The patient has high intracranial pressure, compressing the respiratory center and no spontaneous breathing. Mild traumatic coma will quickly restore consciousness by intravenous dehydration, but patients with severe traumatic brain injury and ischemic-hypoxic coma will have many complications, commonly including urosepsis, decreased blood pressure, platelet hypotension, gastrointestinal bleeding, central hyperthermia, protruding eyes, fixed dilated pupils, electrolyte disorders, multi-organ failure, and platelet hypotension. It can cause brain herniation and even death at any time.
Analyzing its possible causes.
I. The amount of intravenous dehydration is not enough.
Second, no reasonable dehydration under cerebral pressure monitoring.
Third, insufficient knowledge or lack of experience in decompression under high cranial pressure. “Waiting for fate”.
(a) Desaturation is a must for rescue: there are two methods for decompression under high cranial pressure.
1, lumbar puncture: is the simplest and most effective decompression method. With the needle core slowly release pressure, tick release pressure. It is most appropriate to do it on the day of coma, because the patient has just appeared coma and there is no peak edema, decompression needs to be cautious.
2. Dynamic controlled pressure placement in the subarachnoid space: homemade. One end of the anesthesia tube is implanted in the subarachnoid space 50px, the other end is connected to a central venous pressure tube (with a tee, 5ml of cerebrospinal fluid in the tube), this port is connected to a miniature sensor line, and finally this line is inserted on the ICP port on the side of the polycardio monitor, which then displays the cerebrospinal fluid pressure. This method allows dynamic observation and regulation of cerebral pressure at any time and is superior to foreign intracranial pressure in vitro detectors.
(ii) Control of epilepsy
The presence of occult seizures in cerebral coma is common and is the main cause of promoting cerebrospinal fluid secretion and secondary cerebral hemorrhage. Therefore, seizure control is a key step in preventing deterioration and promoting awakening treatment. This is especially true for patients with left frontotemporal cerebral hemorrhage and left-sided ischemic-hypoxic encephalopathy. Most medical practitioners are more concerned with manifest convulsions, such as loss of consciousness, facial twitching, twitching of limbs, upturning of both eyes, incontinence and other seizure states, but more neglect the occult convulsions that occur in patients with cerebral coma, or even believe that the absence of the aforementioned external manifestations and spikes in the EEG means that there is no seizure. In fact shortness of breath, arrhythmias, and eyes that stare or float are caused by occult epilepsy.
In January 2012 Jack jallo, USA:Monitoring EEG changes in patients in neurological intensive care units for brain coma is primarily used to monitor epilepsy, which is an abnormal discharge of cortical neurons and is one of the primary concerns of comatose patients with severe cranial injury in the care unit and during recovery. Although sedative medications can be used to treat early post-traumatic seizures, they do not prevent the development of post-traumatic epilepsy. Approximately 50% of post-traumatic coma epilepsy is traced subcortically after cranial injury; 30% of traumatic coma is associated with brain contusions resulting from non-penetrating injuries.
Some of these mechanisms for the development of epilepsy may be related to the effects of hemoglobin degradation products on neuronal function. Closed brain injury coma may result in neuronal axonal shear injury, diffuse edema, and ischemia and can be caused by the release of excitatory amino acids, the
cytokines, secondary damage to cells by bioactive lipids or their toxic mediators leading to diffuse injury. The incidence of coma epilepsy after diffuse injury has not been fully determined, but patients with loss of consciousness for more than 24 hours have an approximately 10% probability of developing epilepsy after injury. The cause of epilepsy is a damaged brain region in the hippocampus.
The cause of non-awakening in comatose patients is the occurrence of non-convulsive epilepsy that triggers cerebral edema, which has been confirmed for experimental animal studies. In animal models, epilepsy can lead to increased intracranial pressure and aggravate brain cell damage. Therefore, aggressive treatment of acute seizures in comatose patients is essential in clinical practice. Prophylactic application of anti-convulsant drugs such as common sodium phenobarbital and levetiracetam is effective in reducing the occurrence of coma convulsive epilepsy after trauma, hemorrhage, and ischemia.
Some studies have found that prophylactic medication can improve neurological function in comatose patients, however, the dosage requires more precise administration. In recent years, zolpidem tartrate tablets have been reported in the United States to treat patients in a vegetative state, and it has been suggested that the effect is better if combined with amantadine hydrochloride tablets, but this is limited to the clinical trial stage.
Litt et al. found that the incidence of non-convulsive epilepsy was about 11%. Recently, Towne et al. found that the incidence of non-convulsive epilepsy was about 8% in 236 comatose patients, whose samples were mostly short-range EEG data of 30-60 s. Young et al. reported that 34% of 124 patients in monitored cerebral coma had non-convulsive epilepsy, and 76% of these patients had persistent status epilepticus. Patients with persistent epilepsy for >10 hours had a significantly increased risk of death and becoming vegetative, (dominance ratio 18, p=0.005). It has been studied that 570 patients with post coma epilepsy, 88% of them occurred within 24 hours of coma.
(iii) Timing of application of excitatory drugs in cerebral coma: It was previously believed that neuroexcitatory drugs, such as naloxone and cytarabine, were used to promote awakening of comatose patients as soon as possible. However, because the patient is always in an excited state, it can cause multiple episodes of manifest and occult epilepsy and even increased muscle tone. The use of neuroleptics in such patients may also accelerate cerebral edema and slow down the recovery of micro-consciousness. Therefore, it is believed that both appropriate use of neuroexcitatory drugs and appropriate amount of neuroinhibitory drugs are given to the patient, so that the patient has a normal pattern of excitement during the daytime and dormancy at night, and wakefulness is promoted in the process of alternating excitation and inhibition, and the clinical effect is often good.