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A coma is a profound unconscious state where the patient remains alive, yet is unable to move or respond to their environment. A coma is defined as a sleep-like state from which an individual has not yet been aroused. There are varying severities of coma that patients may progress through. The most severe coma involves the loss of all basic reflexes such as response to pain. A coma is not an illness unto itself but is a symptom of a variety of medical conditions.
A persistent vegetative state describes the condition of a patient that has been in coma for a month or more. The individual's eyes may be open and may blink but the person's stare is blank and no signs or awareness or purposeful responses are visible. A person in a persistent vegetative state has lost all conscious mental faculties yet the body continues non-cognitive functions such as regular blood pressures, digestion and elimination of foods and regular waking and sleeping cycles. Patients may open their eyes, make noises, laugh, cry or show facial expression yet the ability to relate to their surroundings is lost.
Brain death is often mistaken for comas and persistent vegetative states. Brain death is the complete and irreversible cessation of all brain activity, including breathing. Those who have undergone brain death cannot survive without the assistance of life support systems. Medical authorities define brain death as irreversible cessation of all brain activity. Simply put, this means that the brain is no longer alive and cannot possibly be brought back to life.
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Coma represents the last and lowest level of function of the brain prior to death.
A person in a coma may show varying degrees of responsiveness to stimuli. Progress of a coma is graded on what is known as the “Glasgow Coma Scale”. It grades three sorts of responses, Eye movement, Verbal response and Motor response. The lowest score on the scale is 3, which would be a deep coma. A fully conscious, responsive person would score 15. The Scale is as follows:
E1: No eye movement
E2: Eyes opens in response to pain
E3: Eyes opens in response to sound
E4: Eyes open spontaneously
V1: No verbal response
V2: Unintelligible noises
V3: Inappropriate words
V4: Speaking, yet confused
V5: Regular, oriented speaking
M1: No motor response to pain
M2: Decerebate Response (Involuntary extension of upper extremities)
M3: Decorticate Response (Involuntary flexing of upper extremities)
M4: Withdraws from pain
M5: Localizes pain (pulls examiner’s hand away)
M6: Obeys Commands
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Most people who enter a coma awaken in 2-4 weeks. However, there are those who do not recover so quickly, and stay in a coma for months, years or even decades. Some comas develop into a persistent vegetative state. After recovery, patients who have suffered comas often have emotional, physical or mental difficulties. When death occurs during a coma or persistent vegetative state, it is frequently from an infection, most commonly pneumonia. As a rule of thumb, if a coma patient survives the first seven to ten days following brain injury, chances of long-term survival is good.
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A coma can be caused by a myriad of injuries and conditions. Seizures, strokes, head injuries, allergies and intoxication from drugs or alcohol may result in a coma. However, metabolic abnormalities such as ketoacidosis, hypoglycemia and hyperglycemia are the most common causes. Severe nutritional deficiencies caused by general malnutrition or eating disorders may also result in comas.
Some of the causes of coma are treatable and reversible but some causes of coma are neither treatable nor reversible. Some causes are focal localized processes and abnormalities that exist only in one part of the brain and these may include:
- Coma caused by a brain tumor
- Coma after an ischemic stroke, a stroke due to the obstruction of a blood vessel in the brain
- Coma resulting from brain abscesses or infections in the brain
- Coma caused by a brain hemorrhage, an abnormal flow of blood affecting a specific part of the brain
Other causes of comas are diffused processes that affect large parts of the brain. These include:
- Coma brought about by severe hypertension
- Coma triggered by encephalitis, meningitis or other central nervous system infections
- Coma caused by head trauma associated with increased intracranial pressure
- Coma resulting from the Introduction of various toxins or poisons into the body
- Coma related to seizures and other seizure disorders
- Coma as a consequence of hypoxia (poor oxygenation)
- Coma induced by metabolic abnormalities leading to elevated or reduced glucose levels in the blood
- Coma associated with consumption of alcohol and other drugs including barbiturates, opiate narcotics, sedatives, amphetamines, cocaine, and aspirin
- Coma caused by liver or kidney failure
- Coma brought on by an imbalance of electrolytes, the salt substances (such as sodium and chlorine salts) found in the blood and tissues that play essential roles in normal body function
- Coma pursuant to a hemorrhage in one of the membranous layers covering the brain
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If the cause of Coma is unknown, what physicians call a "coma cocktail" is often administered to the patient. It's a mixture of thiamine, glucose (a sugar that can help diabetics who have developed a coma due to low sugar level) and naloxene (a substance that reverses the action of many narcotics and is used to treat overdoses).
After treating the root cause of the coma, care of the patient is geared towards protecting the body during the extended periods of inactivity. Patients are monitored for signs of infection, are regularly moved to prevent bedsores and kept on a balanced nutritional program. Physical therapy is often undertaken as well to prevent muscle atrophy and contractures (permanent muscle contractions), as well as bone and joint deformities.
Electrolytes are chemicals like sodium and chlorine salts found in the blood and tissues throughout the body and play an essential role in most physiological processes.
Depending on what has caused the coma, it may be necessary to correct electrolyte abnormalities. A renal dialysis, for example, is a process that removes toxins and maintains normal electrolyte balance in the kidneys.
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Comas must be treated by qualified medical personnel. However, non-traditional therapies for coma patients have shown signs of effectiveness. Musical and animal therapy have sped progress of coma recovery according to some studies.
Thiamin, or vitamin B1, is required for all tissues and is found in high concentrations in skeletal muscle, heart, liver, kidneys, and brain. The most common cause of a thiamine deficiency in affluent countries is alcoholism; however, a deficiency can also occur from unbalanced diets, rapid weight loss, hyperthyroidism, pregnancy, lactation, or fever. Thiamine serves as a cofactor for several enzymes involved primarily in carbohydrate catabolism. These enzymes are important in the biosynthesis of a number of cell constituents, including neurotransmitters, and for protection against oxidative stress.
Necropsy studies suggest that thiamine deficiency is under-diagnosed in life because classical clinical presentations are uncommon. The major manifestations of thiamine deficiency in humans involve failure of the cardiovascular and nervous (neuropathy) systems (forms of beriberi). Alcohol affects the uptake of thiamine utilization, and these affects may contribute to explain the increased prevalence of thiamin deficiency in alcoholics (Singleton et al. 2001). Supplementation with 100-500 mg of vitamin B1 prevents any type of deficiency.
A deficiency of thiamine causes a condition known as beriberi. Thiamine deficiency is most commonly seen in alcoholics, although it can occur in the presence of several diseases and in a pregnancy accompanied by severe vomiting. The major symptoms of beriberi or Vitamin B1 deficiency involve the nervous system causing sensory disturbances, muscle weakness, and impaired memory; and in functioning of the heart causing shortness of breath, palpitations, and, eventually, heart failure. Wernicke’s syndrome is a serious complication of alcoholism and thiamine deficiency that may manifest as impaired muscle coordination, impaired ability to move the eyes, and marked confusion. It may lead to Korsakoff’s psychosis, a chronic disorder in which memory and learning are impaired. A number of studies show the development of thiamine deficiency as a result of hospitalizations and especially in those on parenteral nutrition without the introduction of vitamins and minerals that are required by the body on a daily basis. Thiamine deficiency also results from overuse of alcohol, nutritional deficiencies and excessive vomiting and often goes unrecognized until the symptoms are dramatic such as a coma.
Research shows that dietary thiamin requirements are based on caloric intake, those individuals who consume more calories, such as athletes, are likely to require a higher than average intake of thiamin to help process the extra carbohydrates into energy. During acute periods of stress, thiamin needs may be increased. Food sources such as nuts, liver, brewer’s yeast and pork contain Thiamin.
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