Spider Bleeding Part 4: Neurological Complications

Article by Dr Vu Duy Dung – General Internal Medicine Department – Share99 Times City International Health Hub

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Many serious neurological complications can occur after sage bleeding (SAH) such as re-bleeding, cerebral efficence, seizures, ishoma …

1. Re-bleeding

Re-bleeding is the most common immediate immediate life-threatening neurological complications after SAH. The best measure to reduce the risk of re-bleeding is the rapid treatment of unplugded ruptured aneurysms. Re-bleeding prevention through active blood pressure control should begin immediately during transportation before the hospital and in the emergency department.

2. Brain effer service

Hydrocephalus formed

Cerebral effusion, also known as myeloma, can still occur in SAH patients

Symptomatic emergency brain effuses occur in 20% of SAH patients, usually within minutes to several days after the oncage of SAH. Clinical signs of cerebral efficion are decreased consciousness, reduced ability to stare upwards, hypertension, and coma. Diagnosis is determined by clinical symptoms and ct scan of the head.

Brain efficence can regulate itself in 30% of patients but can also worsen rapidly. Placing a encesalye encephaes outward (EVD) can save the patient's life. Some centers place a lumbar conduction instead of an EVD in cases of circulating brain efficions, while some centers place both types of conduction. Obstacles to placing an EVD include the risk of infection, bleeding (in the brain or in the brain), and piercing pressure transformations that pose a risk of re-bleeding an unblemed aneurysm. The risk of bleeding and infection of evd placing is almost 8% for each type.

Rapid withdrawal of EVD is recommended after removal of the aneurysm or for 48 hours of drainage if the patient is neurologically stable. In patients who do not withdraw drainage (about 40%), placing a long-term ural and pericardic drainage may be necessary. A small resuscitation study in Germany has suggested dexamethasone doses of 12 mg/day for at least 5 days can reduce the risk of post-SAH brain effuse. Due to the lack of randomized controlled studies, routine use of corticosteroids in addition to the in addition to the management of headaches due to post-SAH meningeal chemical irritation is not recommended.

3. Seizures and seizure prevention

epilepsy

Seizures in SAH patients

Determining the true rate of seizures in SAH patients is difficult because many patients (up to 26%) manifestations of seizure-like attacks, but these are not easy to clearly identify when they occur at the on onslest of symptoms. If seizures occur before an aneurysm intervention, they are usually a sign of premature bleeding. Prolonged menopause is seen in 2% of SAH patients and is associated with greater severe levels of SAH. Rate of non-seizure seizures (7% to 18%) and non-convulsive seizures (3% to 13%) is more common in SAH patients who are in a coma and are accompanied by ischemia of the ischemia late and worse results. It is not yet fully understood that non-seizure seizures are the cause of late ischemia and bad end or a phenomenon of severe SAH with bad endings due to the severe level of SAH. Since non-convulsive seizures are treatable, continuous EEG monitoring should be considered in patients with severe SAH. A 2015 overview summarized non-convulsive seizures and non-convulsive seizure states in SAH. However, in some hospitals, the limitation lies in the ability to perform and read EEG continuously. Furthermore, recent findings show that surface EEG can detect non-convulsive seizures of only 8% of SAH patients, while they are present in 38% of patients when measuring EEG through electrolyses deep in the cerebral cortex placed through a hole in the skull. Such deep-written electrolyses, however, are more invasive, are used limitedly in very few centers, and are not currently considered therapeutic standards. Non-convulsive seizures should be thought of in SAH patients in a coma.

Currently, with the absence of randomized controlled clinical trials of anti-kinhtic drug treatment in SAH patients, treatment with anti-kinhal drugs should be limited only to pre-intervention treatment of aneurysms, considering the known side effects of anti-kinhal drugs , especially phenytoin, for post-SAH neurostopathic recovery.

Guidelines and experts recommend stopping anti-seizure drugs in patients who can be trusted clinically monitored as soon as the aneurysm has been sealed and not to last more than 3 to 7 days if the patient does not have an seizure at the onsl start of SAH. In the author's hospital, only patients in a coma and severe SAH patients were continued to take anti-seizure drugs after aneurysm intervention because of the high risk of non-seizure seizure seizures in these patients.

Levetiracetam is an anti-kinh drug commonly used because of its high bio-availability, favorable side effects data, and no drug interactions. However, it should be noted that there are no studies that show the advantages of levetiracetam over other anti-kinh drugs. In addition, levetiracetam has not been licensed by the U.S. Food and Drug Administration (FDA) for prescriptions for neuropyh therapy; therefore, no specific anti-kinh drugs may be recommended for the prevention of menopause in SAH patients.

4. Late ischemia

Isthocemia

Late ischemia is one of the neurological complications

Late ischemia is one of the most ominous neurological complications after SAH, as a late ischemia-infarction is the leading cause of disability in patients who survive SAH. Late ischemia monitoring is the main reason for the recommendation to be in a long-term active treatment unit (ICU) for SAH patients. Late ischemia is defined as any neurodegenerative deterioration that persists for more than 1 hour that cannot be explained by other neurological or generalized disorders, such as fever, seizures, cerebral effrecies, infections, hypoxia, sedation, and other chemical causes. Late ischemia is diagnosed when other causes of neurodegenerative failure have been excluded or insufficient to cause neurodegenerative failure and therefore it is an exclusional diagnosis.

Historically, late ischemia is believed to be caused by brain vascular spasms. However, current evidence shows that pathogenesa of late ischemia consists of an interaction of early brain damage, microcular thrombosis, cortex spread decontamination, associated ischemia, and cerebral vascular spasms. Furthermore, some experts believe that brain vascular spasms are only a secondary phenomenon, and that biomedizing and biological changes that lead to late ischemia occur at the time of the oncage of SAH. This foundational change in the late ischemia approach was supported by a negative endothelin 1 edothelin test in SAH patients with clip clips or coil buttons.

Endothelin 1 has been considered the most powerful contraction intermediate in SAH. However, the in dinh of clazosentan, a strong inhibitor of endothelin receptor 1, leads to reduced brain vascular spasms but does not improve ischemia late and does not lead to an improvement in endoculation 3 months after SAH.

Late ischemia occurs an average of 3 to 14 days after SAH. The risk of late ischemia increases with thick SAH and bleeding in the vented brain, as illustrated in the revised Fisher scale. Added risk factors include severe clinical, loss of consciousness at the oncage, smoking, cocaine use, SIRS, increased blood sugar, cerebral effusion, and non-convulsive seizures. Predicting which patients will develop ischemia late has been proven to be very difficult but very important. Not only will such predictions have an impact on monitoring at the ICU, early diagnosis, and treatment, but also the provision of resources and early exit of the ICU with mild and low-risk SAH patients. The best predictive factors patients need to monitor less closely include advanced age (over 65 years old), low WFNSS scores of 1 to 3, and fisher scores with modifications below 3.

5. Late ischemia prevention

Nimodipine drugs

Nimodipine drugs help protect nerves

Blockage of calcium channels (nimodipine) and maintenance of normal epidemic status in the vessels has the strongest evidence in late is ischemia prevention intervention. Nimodipine (60 mg every 4 hours for 21 days) is a neurosyhical and has Group I evidence to reduce the risk of adverse functional outcome. However, it does not reduce the frequency of vascular spasms on the vascular image. A common side effect of nimodipine is a decrease in blood pressure, which can lead to a decrease in brain perfusion and a decrease in brain perfusion pressure. Therefore, in order to prevent hypotension, a reduction in the dose with an increased frequency to 30 mg every 2 hours may be necessary.

In all cases, reasonable maintenance of issentitic status in the vessel is recommended. Decreased volume in the vessels and a negative translational balance entail a higher rate of late ischemia and bad neurological endings.

How to monitor the status of an uns determined issymable. The trend of measuring central vein pressure has collapsed because it has pointed to a poor prediction of the epidemic response and volume in the vessel. Measuring vascular pressure variations or respiratory variations of the lower aortic vein diameter using bed-based ultrasound is easy to perform and is much more reliable monitoring techniques for the epidemic response of active treatment patients, including SAH. Increased volume of redity should be avoided, as this strategy does not show improvement in cerebral blood flow or a decrease in the frequency of late cerebral vascular spasms or ischemia but increases cardi lung complications.

Maintaining isspolypemia can be difficult with brain salt loss, an endococular neurological disorder commonly encountered in SAH (see hyponatremia follow-up). In patients with significant SAH and high urination and loss of sodiumuria, additional fludrocortisone may be useful in maintaining volume in the vessels and normal sodium values (fludrocortisone 0.2 mg to 0.4 mg orally every 12 hours).

6. Late diagnosis and monitoring of ischemia

CT scan

Experts have recommended that SAH patients receive a CT scan for accurate results

Diagnosing ischemia late is not easy. The combination of neurological examination and image exploration can increase the likelihood of early detection and reasonable treatment. Admitted to the neurological active treatment unit with regular neurological examinations by experienced nurses and doctors every 1 to 2 hours is necessary. Late ischemia should be suspected if SAH patients present with a localized or pervasive neurological deficiency or have a Glasgow score drop of 2 points or more and last at least 1 hour and cannot be explained by another cause.

Experts have recommended that all SAH patients receive a ct scan of the head at 24 to 48 hours after aneurysm treatment to identify any infarction associated with treatment. Any reduction in new proportions not caused by EVD or bleeding in the cutic tissue should be considered as a late ischemia cerebral infarction regardless of clinical symptoms.

SAH patients should be monitored for physical and image monitoring regularly during the late is ischemia risk phase. Such monitoring is usually multidisciplinary and includes ICP measurements, brain perfusion pressure measurements, continuous EEG, and transcranial Doppler (TCD); DSA, CTA, and CT perfusence (CTP) are also used when in question as well as monitoring brain tissue oxygen saturation and microdialysis where possible.

TCD is used earliest and is best studied of all tracking methods. In the large blood vessels of the Willis ring, TCD has the appropriate sensitivity and specificity to detect an increase in the rate of secondary cerebral blood flow due to brain vascular spasms but is heavily dependent on the technical person and the skull bone window.

Practice workers need to be aware that TCD-specific sensitivity/specificity is good for the middle cerebral artery and the inner car carnous artery but much inferior to the frontal cerebral artery and the arteries of the later revascular ring. The thresholds for diagnosis of cerebral vascular spasms have been summed up.

In addition, the rate of cerebral blood flow may increase for other reasons (fever-in-fever convulsions, causing hypertension, anemia), and therefore a diagnosis of cerebral vascular spasms should be set only when the average rate of cerebral blood flow of blood vessels in the skull above the average cerebral blood flow rate of the care carnous artery in the outer cranial segment is high. Therefore, with the diagnosis of middle cerebral artery spasms, it would be prudent to regularly measure lindegaard ratio (average speed in the middle cerebral artery/average speed in the mediaction in the outer cranial segment of the same side). A score Lindegaard > 3 points of brain contraction. Similar ratios are available for other main blood vessels in the skull.

DSA remains the gold standard for detecting medium and large-sized arterial spasms. CTA can now be widely used and is generally applied to pre-DSA vascular spasm screening because of its high specificity and non-penetration. However, the CTA may over-estimate brain vascular spasms. CTP with increased average circulation time may be worth adding with the CTA to assess reduced brain perfusence, but further research into CTP application in SAH is needed.

Saturation of brain tissue oxygen, cerebral blood flow, and dialysis monitoring can provide additional information when used in the context of multimodal monitoring and potentially detecting brain vessel spasms early before it becomes symptomatic and before late ischemia occurs. Clinicians should always keep in mind the limitations of such monitoring, including limited to local monitoring rather than entire brain regions.

Scalp EEG consistently has the advantage of tracking across large areas of the brain. Continuous dosing EEG, if possible, can make the session easier than bedside data even by under-trained employees to read EEG. The price, and therefore less widely usable, currently limits the continuous use of dosing EEG as the standard of treatment.

It will be very important to distinguish between an anetic/TCD spasms and clinical symptomatic vascular spasms. The former occurs in the majority of SAH patients (70%) but not with consequences after SAH. Symptomatic vascular spasms, which occur in 30% of SAH patients, are accompanied by late ischemia and end up poor after SAH. Considering the risk of cerebral spasmodic endocular treatment, experts recommend that such treatment should be intended only for symptomatic spasms, while an anethortic/TCD spasms should be treated with caution and wait with a very low threshold to activate DSA and endocular treatment.

There are several other views on the timing and frequency of the application of different tracking methods. At the very least, SAH patient care needs to follow the regimen using a handwritten regimen and an algorithm. SAH patients should be admitted to the neurological active treatment unit and have an aneurysm sealed as soon as possible, at best in the first 6 to 12 hours from the time of entering the clinic.

Follow-up in the neurological active treatment unit includes daily TCD, although in low-risk patients it may be enough to monitor the day as long as neurological clinical monitoring can be done every 1 to 2 hours. Some centers perform routine CTA/CTP or DSA for all patients 5 to 7 days after hospitalization for screening for brain vascular spasms. Most centers, however, perform these photo tests only when symptomatic spasms are suspected.

In patients in coma or in response (inert), it may be difficult to conduct a reliable clinical examination, and therefore TCD and, in addition, CTA/CTP or DSA for vascular spasm screening may be necessary. Especially in severe SAH patients with severe neurological symptoms, late diagnosis and initiation of ischemia treatment can be difficult, slightly sensory, and mostly based on image monitoring results.

At the author's hospital, the SAH regimen consists of tha, CT/CTA, and DSA scans when these patients have increased average speed on TCD and increased Lindegaard score (or other score). Other centers use information from multimodal monitoring (continuous EEG or even deep EEG in the cortex, brain tissue oxygen saturation, micro-dialysis, cerebral blood flow monitoring) to decide whether to reduce brain perfusence or vascular spasms and when to take a DSA scan. While randomly controlled data is missing on the value of multimedia monitoring for short- and long-term results in the treatment of SAH patients, resources in many hospitals can cause us, at least to some extent, to adopt a variety of advanced multi-method monitoring measures.

7. Complications Management

In the author's hospital, all patients are treated with nimodipine and issymodial. Low-risk patients with neurological examinations, TCD, and, if performed, unchanged CTA will be transferred to a lighter neurological unit under the treatment of a neuropsychial intensive care doctor between days 8 and 10 and given a sparse neurological examination (every 2 hours or for hours) than in the ICU. The patient will then be discharged home on the 14th day. High-risk patients with neurological examinations, TCD, and, if performed, the unchanged CTA will be transferred home or other mild treatment unit 14 days after SAH. If at any point the average cerebral blood flow rate is seen on TCD and abnormal CTA, the intensity of neurological monitoring increases.

If neurodegenerative patients suggest late ischemia, some de-cure therapy will be initiated. In case of symptomatic late cerebral vascular spasms and ischemia, tha-inquenation is inquenified according to current guidelines. Volumetric therapy, hypertension, and blood dilution (Triple H) are currently not supported by guidelines because of existing evidence of side effects that leave harmful consequences after blood dilution, and the current standard treatment is hypertension and mild volume gain (HHT). Many hospitals start with a dose of intravenous bolus (1 L to 2 L salt 0.9%) and maintaining translation for isthery or slight volume gain. The best hypertension is caused by the use of continuous intravenous α1 receptor co-operation (norepinephrine or phenylephrine). This group of drugs are the selected contractions in SAH, since cerebral blood vessels lack receptor α1, and therefore only contract the system and not the brain vessels. Hypertension should be carried out step by step with a periodical neurological assessment at each step.

At the author's hospital, the average arterial blood pressure (MAP) on the 20 mmHg background MAP is set for the first goal (usually MAP > 90 mmHg). Some facilities use sysysy blood pressure instead of map targets, and there is currently no evidence to guide clinicians which measure is better. At the base where sy blood pressure is set for causing hypertension, the original target should be approximately 20 mmHg to 40 mmHg on the sysysmous blood pressure base. This usually leads to a targeted sysysytenous blood pressure >180 mmHg or >200 mmHg.

If the clinical examination returns to its previous level, there is no need to raise blood pressure again, unless the clinical examination is more severe at the original blood pressure target. In the latter case, further increase in blood pressure should be tried. Although there is no maximum or optimal blood pressure target, heart and lung and brain side effects (e.g., self-conditioning side effects with increased ICP due to increased MAP or reversible posteri back syndrome[PRES]) should be considered in each patient.

In the author's hospital, myocardial drugs (milrinone, dobutamine) are intended for patients with known low heart supply due to an emergency or chronic cardicardiitis. If neurological deficiencies exist despite causing hypertension, the patient will receive a CT/CTA followed by DSA with endocular therapy if brain vascular spasms are identified. Ct head without injections of anti-ointed drugs before DSA scans is useful to exclude cerebral efficbolism and identify previous strokes before endovascular treatment. If other causes of neurodegenerative failure have been ruled out, and TCD suggests brain vascular spasms, the CTA can be ignored to limit radiation to patients, anti-iodine drugs, and to save time and allow patients to go for ASA scans immediately for treatment. Endovascular therapy using in-arterial dilated substances (nicardipine, milrinone, verapamil) or anthometry is supported by advanced and resuscitation observational data and recommended by the instructions. In the author's hospital, backup vascular forming is not performed if brain vascular spasms are detected in TCD or CTA without neurodegeneration because this practice is accompanied by a high rate of complications.

Source: Susanne Muehlschlegel. Subarachnoid hemorrhage. CONTINUUM (MINNEAP MINN) 2018;24(6, NEUROCRITICAL CARE): 1623–1657

SEE MORE:

  • Trans-skull doppler ultrasound in emergency resuscitation
  • Does a deep coma caused by a cerebral hematoma hope to regain normal wake?
  • Headache after more than 1 month of fall should I have a CT scan again?

About: John Smith

b1ffdb54307529964874ff53a5c5de33?s=90&r=gI am the author of Share99.net. I had been working in Vinmec International General Hospital for over 10 years. I dedicate my passion on every post in this site.

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