Coma

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Coma is a state of unconsciousness in which one can not be awakened; fails to respond normally to painful stimuli, light, or sound; does not have a normal sleep-up cycle; and does not initiate voluntary action. Someone in a coma is described as a comma . Differences are made in the medical community between actual coma and medical coma, the first being the outcome of circumstances beyond the control of the medical community, while the second is the way that medical professionals can use to heal the wounds of the patient in a controlled environment.

A comatose person shows no consciousness and can not consciously feel, speak, hear, or move. For a patient to maintain awareness, two important neurological components must function. The first is the cerebral cortex - the gray matter that forms the outer layer of the brain. The other is a structure located in the brainstem, called the reticular activating system (RAS).

Injury to one or both of these components is sufficient to cause the patient to go into a coma. The cerebral cortex is a group of solid and dense "gray matter", composed of a nucleus of axon whose axon forms "white matter", and is responsible for perception, sensory input relay through the thalamic path, and many other neurological functions, including complex thinking.

RAS, on the other hand, is a more primitive structure in the brainstem that includes reticular (RF) formation. The brain RAS area has two channels, a channel up and down. Formed from an acetylcholine-producing neuron system, rising route, or an elevated reticular activation system (ARAS), it works to awaken and awaken the brain, from RF, through the thalamus, and finally to the cerebral cortex. Failure of ARAS function can cause coma. The word is derived from the Greek ???? a comma , which means "deep sleep."

Video Coma

Signs and symptoms

Generally, a person who can not voluntarily open his eyes, does not have a sleep-wake cycle, is unresponsive despite strong stimuli (painful) or verbal stimulation, and a generally score between 3 and 8 on the Glasgow Coma Scale is considered comatose. Coma may have grown in humans in response to injuries that allow the body to stop body action and heal the wound most quickly before awakening. Therefore it can be a state of compensation in which the body's energy expenditure is not excessive. The severity and coma onset mode depends on the underlying cause. For example, severe hypoglycemia (low blood sugar) or hypercapnia (elevated levels of carbon dioxide in the blood) initially cause mild agitation and confusion, but develops into obtundation, fainting, and finally, total unconsciousness. Conversely, coma resulting from severe traumatic brain injury or subarachnoid hemorrhage may occur instantaneously. Therefore, the onset mode can be an indication of underlying causes.

Causes of commas

Coma can be produced from a variety of conditions, including poisoning (such as drug abuse, overdose or abuse of over-the-counter drugs, prescribed drugs, or controlled substances), metabolic disorders, central nervous system diseases, acute neurologic injuries such as stroke or herniation, hypoxia, hypothermia, hypoglycemia, eclampsia or traumatic injuries such as head trauma caused by falls, drowning accidents, or vehicle crashes. It may also be intentionally induced by pharmaceutical agents during major neurosurgery, to maintain higher brain function after brain trauma, or to save patients from severe pain during the healing of injury or illness.

Forty percent of the coma results from drug poisoning. Drugs damage or weaken synaptic function in ARAS and keep the system from functioning properly to generate the brain. Secondary effects of drugs, including abnormal heart rate and blood pressure, as well as abnormal breathing and sweating, may also indirectly damage the function of ARAS and cause coma. Seizures and hallucinations have been shown to also play a major role in ARAS malfunction. Since drug poisoning is the cause of most patients in a coma, the first hospital tests all comatose patients by observing pupil size and eye movements, via vestibular-ocular reflexes.

The second most common cause of coma, which causes about 25% of comatose patients, is oxygen deprived, commonly caused by a heart attack. Central nervous system (CNS) requires a lot of oxygen for its neurons. Lack of oxygen in the brain, also known as hypoxia, causes extracellular sodium and decreased neuronal calcium and increased intracellular calcium, which compromises neuron communication. Lack of oxygen in the brain also causes fatigue of ATP and cell damage from cytoskeleton damage and nitric oxide production.

Twenty percent of coma conditions result from side effects of stroke. During a stroke, blood flow to the brain is restricted or blocked. Ischemic stroke, cerebral hemorrhage, or tumor can cause cessation of blood flow. Lack of blood to the cells in the brain prevents oxygen from entering the neurons, and consequently causes the cell to become disturbed and eventually die. When brain cells die, brain tissue continues to worsen, which can affect the function of ARAS.

The remaining 15% of coma cases are due to trauma, excessive blood loss, malnutrition, hypothermia, hyperthermia, abnormal glucose levels, and many other biological disorders.

Maps Coma

Diagnosis

A simple coma diagnosis, but diagnosing the underlying cause of the disease process is often challenging. The first priority in the treatment of coma patients is stabilization following basic ABC (standing for airway, breathing, and circulation). Once a person is in a stable coma, investigations are carried out to assess the underlying cause. The method of investigation is divided into findings of physical examination and imaging (such as CAT scan, MRI, etc.) and special studies (EEG, etc.)

Diagnostic steps

When an unconscious patient enters the hospital, the hospital uses a series of diagnostic steps to identify the cause of the unconscious. According to Young, the following steps should be taken when dealing with patients may be in a coma:

1. Perform a general checkup and medical history check
2. Make sure the patient is in an actual coma and/or not in a locked state (the patient can voluntarily move the eye or blink) or psychogenic responsiveness (caloric stimulation of the vestibular apparatus produces a slow deviation from the eye to the stimulus followed by a quick correction to the midline. This response can not be voluntarily suppressed, so if the patient does not have this response, the psychogenic coma can be ruled out.)
3. Find sites of the brain that may cause coma (ie brainstem, back of brain...) and coma severity with Glasgow coma scale
4. Take the blood to see if the medication is involved or whether it is due to hypoventilation/hyperventilation
5. Check the levels of "serum glucose, calcium, sodium, potassium, magnesium, phosphate, urea, and creatinine"
6. Perform brain scans to observe abnormal brain function using CT scan or MRI
7. Continue to monitor brainwaves and identify patient seizures using EEG

Initial assessment and evaluation

In the initial assessment of coma, it is common to measure the level of consciousness with spontaneously exhibited action, response to vocal stimuli ("Can you hear me?"), And painful stimuli; this is known as AVPU (warning, vocal stimulation, painful stimulation, unresponsive) scale. More complicated scales, such as Glasgow Coma Scale, measure individual reactions such as eye opening, movement, and verbal responses on a scale; Glasgow Coma Scale (GCS) is an indication of varying brain damage levels from 3 (showing severe brain injury and death) to a maximum of 15 (indicating mild or absent brain injury).

In those who are not consciously deep, there is a risk of shortness of breath as control over the muscles in the face and throat is reduced. As a result, those who come to the hospital with a coma are usually assessed for this risk ("airway management"). If the risk of asphyxia is considered high, the doctor may use various devices (such as the oropharyngeal ducts, nasopharyngeal or endotracheal airway) to maintain the airway.

Findings of physical examination

Physical examination is very important after stabilization. This should include vital signs, a general portion dedicated to making observations of the patient's breathing (breathing pattern), body movements (if any), and the patient's (physical) body's habitus; it should also include brainstem assessment and cortical function through special reflex tests such as oculocephalic reflex tests, oculovestibular reflex tests (cold calorific tests), tingling nose, corneal reflexes, and gag reflexes.

Vital signs in treatment are the most accurate (rectal) temperature, blood pressure, heart rate (pulse), respiratory rate, and oxygen saturation. It should be easy to evaluate these vital signs quickly to gain insights into the patient's metabolism, fluid status, heart function, blood vessel integrity, and tissue oxygenation.

The respiratory pattern (respiratory rhythm) is significant and should be noted in coma patients. Certain stereotype breathing patterns have been identified including Cheyne-Stokes, a form of breathing in which the patient's breathing patterns are described as episodes of alternating hyperventilation and apnea. This is a dangerous pattern and is often seen in delayed herniation, large cortical lesions, or brainstem damage. Another breathing pattern is apneustic breathing, which is marked by a sudden inhalation pause and caused by a pons lesion. Ataxic breathing is irregular and is caused by lesions (damage) of the medulla.

Assessment of posture and body habitus is the next step. This involves a general observation of the patient's position. There are often two stereotyped postures seen in coma patients. The attitude of deposition is a stereotypical attitude in which the patient has arms flexed at the elbow, and an adducted arm towards the body, with both legs extended. Decerebrate posture is a stereotypical stance in which the same legs are extended (stretched), but the arms are also stretched (extended at the elbow). Posture is very important because it shows where the damage in the central nervous system. Decortication posture shows lesions (points of damage) at or above the red nucleus, whereas decerebrate posture shows lesions at or below the red nucleus. In other words, the decorticate lesions closer to the cortex, as opposed to the decerebrate cortex that is closer to the brainstem.

Oculocephalic reflexes also known as pupal eyes are performed to assess the integrity of the brain stem. The patient's eyelids are gently elevated and the cornea is visualized. The patient's head is then moved to the patient's left, to observe whether the eye remains or deviates to the patient's right; The same maneuver is tried on the opposite side. If the patient's eyes are moving in the opposite direction of the head rotation, then the patient is said to have an intact brain stem. However, failure of both eyes to move to one side, may indicate damage or destruction of the affected side. In special cases, where only one eye is distorted and the other does not, this often shows a lesion (or damage) of the medial longitudinal fasciculus (MLF), which is a brainstem nerve stem. Caloric reflex tests also evaluate cortical and brainstem function; cold water is injected into one ear and the patient is observed for eye movement; if the patient's eyes slowly deviate toward the ear where the water is injected, then the brain stem is intact, but failure to deviate toward the injected ear indicates brain stem damage on the side. Cortex is responsible for rapid nystagmus away from this perverse position and is often seen in conscious or only lethargic patients.

An important part of physical examination is also the assessment of the cranial nerves. Because of the patient's unconscious status, only a small number of nerves can be assessed. These include cranial nerve number 2 (CN II), number 3 (CN III), number 5 (CN V), number 7 (CN VII), and cranial nerves 9 and 10 (CN IX, CN X). Gag reflex helps assess the cranial nerves 9 and 10. The pupillary reaction to light is important because it shows the intact retina, and the cranial nerve number 2 (CN II); if the student is reactive to light, then it also shows that the cranial nerve 3 (CN III) (or at least the parasympathetic fibers) is intact. The corneal reflex assesses the integrity of the cranial nerve number 7 (CN VII), and the cranial nerve number 5 (CN V). The cranial nerve 5 (CN V), and its ophthalmic branch (V ₁ ) are responsible for the reflex afferent arm, and the cranial nerve number 7 (CN VII) is also known to the facial nerve, responsible for the efferent arms, Orbicularis oculi muscle contractions result in eye closure.

Pupil assessment is often an important part of coma examination, as it may provide information about the cause of coma; the following tables are technical, medical guidelines for general student findings and possible interpretations of them:

Imaging and custom test findings

Imaging basically includes computed tomography (CAT or CT) brain scans, or MRIs for example, and is performed to identify specific causes of coma, such as bleeding in the brain or herniation of brain structures. Special tests such as EEG can also show much about the level of cortical activity such as semantic processing, seizures, and are important tools available not only for the assessment of cortical activity but also to predict the likelihood of the patient waking up. Autonomic responses such as skin conductance responses can also provide further insight into the patient's emotional processing.

History

When diagnosing neurological conditions, history and examination are fundamental. History is obtained by family, friends or EMS. Glasgow Coma Scale is a useful system used to check and determine the depth of coma, track patient progress and predict the best possible outcome. In general, correct diagnosis can be achieved by combining findings from physical examination, imaging, and history components and directing appropriate therapies.

Severity and classification

Coma can be classified as (1) supratentorial (above Tentorium cerebelli), (2) infratentorial (below Tentorium cerebelli), (3) metabolic or (4) spreads. This classification depends only on the position of the original damage that caused the coma, and not correlated with the severity or prognosis. The severity of coma disorders but categorized into several levels. The patient may or may not progress through this level. At the first level, the brain's response decreases, the normal reflex is lost, the patient no longer responds to pain and can not hear.

The Rancho Los Amigos scale is a complex scale that has eight separate levels, and is often used in the first few weeks or months of the coma while the patient is under closer observation, and when the shift between levels is more frequent.

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Treatment

Medical care

Hospital care used in coma patients depends on the severity and cause of the coma. Although the best treatment for comatose patients remains unknown, hospitals usually place comatose patients in the Intensive Care Unit (ICU) immediately. Attention should first be directed to maintaining the patient's breathing and circulation, using intubation and ventilation, administering intravenous fluids or blood and other supportive care as needed. Once a patient is stable and no longer in danger, medical staff can concentrate on maintaining the physical health of the patient. Concentrations are directed to prevent infections such as pneumonia, bedsores (decubitus ulcers), and provide balanced nutrition. Infection can arise from a patient who can not move, and is confined in bed. The nursing staff moves the patient every 2-3 hours from side to side and depending on the state of consciousness occasionally to the chair. The goal is to move patients as much as possible to try to avoid bedsores, atelectasis and pneumonia. Pneumonia can occur from a person's inability to swallow that leads to aspiration, lack of gag reflex or from a filler tube, (aspiration pneumonia). Physical therapy can also be used to prevent contractures and orthopedic defects that will limit recovery for patients awakened from coma.

A person in a coma can be restless, or embrace and require special care to prevent them from hurting themselves. Drugs can be given to soothe such people. The restless patient may also try to pull on a tube or clothing so a soft cloth wrist restrain may be worn. The side rails in the bed should be kept so that the patient does not fall.

Methods to awaken coma patients include reversing the cause of coma (eg, glucose shock if sugar is low), giving medication to stop brain swelling, or trigger hypothermia. Inducing hypothermia in comatose patients provides one of the primary treatments for patients after suffering a heart attack. In this treatment, the medical officer exposes the patient to "external or intravascular cooling" at 32-34Ã, Â ° C for 24 hours; this treatment cools the patient down about 2-3 Â ° C less than normal body temperature. In 2002, Baldursdottir and his colleagues found that in hospital, more comatose patients survived after hypothermia induced than patients who remained at normal body temperature. For this reason, the hospital chooses to continue the induced hypothermia technique for all comatose patients who suffer from cardiac arrest.

Emotional Challenges

Coma has various emotional reactions from family members of affected patients, as well as primary care givers who care for patients. General reactions, such as despair, anger, frustration, and rejection can occur. The focus of patient care should be on creating friendly relationships with family members or comatose patients and creating relationships with medical staff.

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Prognosis

Comas can last from a few days to several weeks. In more severe cases, coma may last for more than five weeks, while some have lasted for several years. After this time, some patients gradually get out of the coma, some progress to a vegetative state, and others die. Some patients who have entered a vegetative state continue to regain consciousness. Others remain in a vegetative state for years or even decades (the longest recorded period is 42 years).

The results for coma and vegetative state depend on the cause, location, severity and extent of neurological damage. The deeper coma itself does not necessarily mean less recovery chances, as some people in coma recover well while others in so-called mild comas sometimes fail to improve.

People may emerge from comas with a combination of physical, intellectual, and psychological difficulties that need special attention. Recovery usually occurs gradually - the patient gains more ability to respond. Some patients have never progressed beyond a very basic response, but many have restored full awareness. Awareness is not instant: in the first days, the patient is only awake for several minutes, and the duration of waking time gradually increases. This is unlike the situation in many films where people who wake up from coma immediately can resume their normal life. In fact, coma patients are sometimes awake in confusion, not knowing how they got there and occasionally suffering from dysarthria, the inability to articulate any speech, and with many other defects.

The prediction of recovery possibilities varies because different techniques are used to measure the extent of neurological damage. All predictions are based on statistical levels with multiple levels of opportunity for recovery now: someone with a low likelihood of recovery can still be awakened. Time is the best general predictor of the possibility of recovery: after four months of coma caused by brain damage, the chance of partial recovery is less than 15%, and the possibility of full recovery is very low.

The most common cause of death for a person in a vegetative state is a secondary infection such as pneumonia, which can occur in patients who lie still for long periods of time.

There are reports of patients coming out of a coma after a long period of time. After 19 years in a state of minimal consciousness, Terry Wallis spontaneously began to talk and regain consciousness around him.

A brain-damaged man, caught in a coma like for six years, was brought back to consciousness in 2003 by a doctor who planted a deep electrode inside his brain. The method, called deep brain stimulation (DBS), successfully generates communication, complex movement and feeding abilities in 38-year-old American men with traumatic brain injury. His wounds make him in a minimally conscious state (MCS), a condition similar to a coma but characterized by occasional, but brief, environmental evidence and self-awareness that coma patients are lacking.

Comas seconds that last up to minutes produce post-traumatic amnesia (PTA) that lasts for hours to days; highland recovery occurs over several days to weeks. Comas that last hours until day produces PTA several days to weeks; highland recovery occurs for months. Comas last week produced PTA that lasted for months; highland recovery occurs for months to years.

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Society and culture

Research by Dr. Eelco Wijdicks on comatose depiction in the film was published in Neurology in May 2006. Wijdicks studied 30 films (made between 1970 and 2004) depicting actors in prolonged coma, and he concluded that only two films were accurately described. the circumstances of the victims of coma and suffering awaiting the patient to rise: Luck Reversals (1990) and The Dreamlife of Angels (1998). The remaining 28 were criticized for describing a stunning revival with no lasting side effects, unrealistic portrayal of treatments and equipment, and comatose patients who remained muscular and tanned.

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See also

• Brain death, lack of activity in both cortex, and lack of brainstem function
• Scaling the comma, the system for assessing the severity of the comma
• The syndrome is locked, paralysis of most muscles, except the eye muscles, while the patient is conscious
• Persistent vegetative conditions (vegetative coma), inner coma without consciousness that can be detected. Damage to the cortex, with an intact brain stem.
• Process Oriented Coma, for an approach to work with residual awareness in comatose patients.
• Pending animations, temporary suspension or main body decay.

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References

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External links

Source of the article : Wikipedia