HEALTH Conspiracy

Wednesday, October 19, 2011

HEMANGIOMA

<div class="MsoNormal" style="text-align: justify; text-indent: 36pt;">By Deden Sura Agung</div><div class="MsoNormal" style="text-align: justify; text-indent: 36pt;"> </div><div class="MsoNormal" style="text-align: justify; text-indent: 36pt;">Hemangioma is a lesion that growth can be predicted, these lesions can be evoluted, and also aimed at vascular lesions found in adults who do not experience regression and sometimes experienced progression. The origins of the terminology on the basis of the appearance of abnormalities and maternal impressions, such as strawberry hemangiomas, cherry angiomas, port-wine stains and salmon patches. Virchow then make a histopathological classification of the first, divided into three: angioma simplex, angioma cavernosum, and angioma racemosim, and ambiguous terminology is still survive in the modern medical books until now. Diagnosis for these lesions is really not easy to do because naming of the description of ambiguous and not appropriate proficiency level, therefore, clinical correlation is needed to make a final diagnosis.</div><div class="MsoNormal" style="text-align: justify; text-indent: 36pt;"> 
</div><div class="MsoNormal" style="text-align: justify; text-indent: 36pt;"></div><div class="MsoNormal" style="margin-bottom: 0cm; text-align: justify;">CLASSIFICATION<a class="cssButton" href="javascript:void(0)" id="publishButton" target=""></a> 
<div class="cssButtonOuter"><div class="cssButtonMiddle"><div class="cssButtonInner"><a class="cssButton" href="javascript:void(0)" id="publishButton" target=""></a></div></div></div></div><div class="MsoNormal" style="text-align: justify;"><div style="text-align: left;"></div>Mulliken and Glowacki in 1982 proposed a classification system for vascular birthmarks that connects the history of the emergence of these birthmarks and physical examination with the cellular picture. They divided the vascular lesions of infancy and the kids into two major types: hemangiomas, with endothelial hyperplasia, and malformations, with normal endothelial changes. The key of the terminology is the word "oma" is derived from the Greek language, which was originally meaning "a lump or tumor". When this suffix is used for a term that describes lesions that grow from the cell proliferation. Most of hemangioma during infancy did not appear at birth but appear postnatally. Grew rapidly during the first year (proliferative phase), slowed, then regresses spontaneously in childhood (involuting phase), and then stabilized (involuted phase). 
 Histologically, proliferative phase has the character of an increase in mitotic activity, whereas in apoptotic phase of involution occurs, fibrosis occurs slowly and infiiltrasi fat. While the vascular malformation is a wrong morphogenesis that appear at 40-10 weeks in intrauterine life. Most of the vascular malformations appear at birth, or not appear at birth but appear a year later. If it has appeared it will continue to grow in proportion with the growth of the patient, however, rapid growth can grow due to trauma, hormonal changes, thrombosis, infection, or surgical intervention. In histology, vascular malformations have kareakteristik canal dilated, with an abnormal vascular wall, and endothelial quiet. There are classifies hemangiomas as follows: Superficial, Deep, Mixed, based on the location of the skin and subcutaneous tissue. It would be more appropriate terminology for these two disorders based on the use classification of vascular anomalies.</div><div class="MsoNormal" style="text-align: justify;"> 
</div><div class="MsoNormal" style="text-align: justify;">FREQUENCY 
Eighty percent growth as a single tumor, 20% multiple. Hemangiomas appear more in women than in men, with a ratio of 3-5:1. Incidence is more on baby as much as 10-12% were white, and about 22% found in premature infants weighing less than 1000 grams.</div><div class="MsoNormal" style="text-align: justify;"> 
</div><div class="MsoNormal" style="text-align: justify;">PATHOPHYSIOLOGY 
Hemangioma is a vascular network consisting of endothelial cells to proliferate. Proliferation is not regular at first, but over time become a regular form blood vessels in the form of lobules with lumen containing blood cells. Growth properties of endothelial cells is benign and has a thin basal membrane. </div><div class="MsoNormal" style="text-align: justify;">Proliferation is slowed and eventually stopped. The hypothesis of Takahashi stated that in the last trimester of pregnancy, the fetus is formed in the immature endothelial cells with pericyte is also immature, have the ability to perform limited proliferation began at age 8 months to 18 months of the first period of life after being born so there was hemangioma. During the proliferative activity of the endothelium occurs influx of a number of mast cells (as a proliferative stimulus endothelium) and tissue inhibitors of metalloproteinase (TIMP or tissue growth inhibitors). Endothelium proliferation returned to normal after stopping the proliferation phase (involution).</div><div class="MsoNormal" style="text-align: justify;"> 
</div><div class="MsoNormal" style="margin-bottom: 0cm; text-align: justify;">RESULT AND PROGNOSIS</div><div class="MsoNormal" style="text-align: justify;">Most hemangiomas occur during the early months of life, proliferates and peaked at age 1 year, and after it undergoes involution slowly. 50% experienced a complete involution by age 5 years. Seventy percent at age 7 years, and continued improvement until the age of 10-12 years. The exception of congenital hemangioma, which appear at birth usually regresses by age 1 year. Unlike vascular malformations, hemangiomas rarely cause distortion of the bones and excess growth except for a large facial hemangioma.</div>

By Deden Sura Agung Hemangioma is a lesion that growth can be predicted, these lesions can be evoluted, and also aimed at vascular lesions ...

Saturday, September 24, 2011

MENSTRUAL DISORDERS - MENORRHAGIA AND DYSMENORRHOEA

By Deden Sura Agung Abnormalities of menstruation is most reason for women to visit obstetricians and gynecology, and menorrhagia are the m...

Friday, September 23, 2011

PARKINSON'S

<div style="text-align: justify;">By Deden Sura Agung</div><div style="text-align: justify;"> </div><div style="text-align: justify;">It is important to realize that not every person with Parkinson's develops all signs or symptoms of the disease. For example, some people experience tremor as the primary symptom, while others may not have tremor but do have balance problems. Also, for some people the disease progresses quickly, and in others it does not. The following are descriptions of the most common primary symptoms of Parkinson's disease. 
Tremor: In the early stages of the disease, about 70 percent of people experience a slight tremor in the hand or foot on one side of the body, or less commonly in the jaw or face. It appears as a "beating" or oscillating movement. Because the Parkinson's tremor usually appears when a person's muscles are relaxed, it is called "resting tremor." This means that the affected body part trembles when it is not doing work, and it usually subsides when a person begins an action. The tremor often spreads to the other side of the body as the disease progresses, but remains most apparent on the original side of occurrence. 
Rigidity: Rigidity, also called increased muscle tone, means stiffness or inflexibility of the muscles. Muscles normally stretch when they move, and then relax when they are at rest. In rigidity, the muscle tone of an affected limb is always stiff and does not relax, sometimes resulting in a decreased range of motion. For example, a person who has rigidity may not be able to swing his or her arms when walking because the muscles are too tight. Rigidity can cause pain and cramping. 
Bradykinesia: Bradykinesia is the phenomenon of a person experiencing slow movements. In addition to slow movements, a person with bradykinesia will probably also have incomplete movement, difficulty initiating movements and sudden stopping of ongoing movement. People who have bradykinesia may walk with short, shuffling steps (this is called festination). Bradykinesia and rigidity can occur in the facial muscles, reducing a person's range of facial expressions and resulting in a "mask-like" appearance. 
Postural instability or impaired balance and coordination: People with Parkinson's disease often experience instability when standing or impaired balance and coordination. These symptoms, combined with other symptoms such as bradykinesia, increase the probability of falling. People with balance problems may have difficulty making turns or abrupt movements. They may go through periods of "freezing," which is when a person feels stuck to the ground and finds it difficult to start walking. The slowness and incompleteness of movement can also affect speaking and swallowing. 
 
What causes Parkinson's? 
Why an individual develops Parkinson's disease remains unclear. The cause is probably a combination of genetic and environmental factors, and may vary from person to person. Although the cause of Parkinson's remains unknown, scientists have identified factors that contribute to Parkinson's in some patients. For example, people over age 60 have a two-to-four percent risk of developing Parkinson's disease, compared with the one-to-two percent risk in the general population. 
Below is information on the two factors that scientists think are most likely to cause Parkinson's disease. 
Genetics About 15 to 25 percent of people with Parkinson's report having a relative with the disease. In large epidemiological studies (studies that deal with incidence, distribution and control of disease in a population), researchers have found that people with an affected first-degree relative, such as a parent or sibling, have a two-to-three fold increased risk of developing Parkinson's, as compared to the general population. This means that if your parent has Parkinson's, your chances of developing the disease are slightly higher than the risk in the general population. 
The vast majority of Parkinson's cases are not directly inherited, but researchers have discovered several genes that can cause the disease in a small number of families. Some of these genes involve proteins that play a role in dopamine cell functions. Because genetic forms of a disease can be studied in great detail in the laboratory, and because understanding the rare genetic forms of Parkinson's disease may help to understand more common forms of the disease, genetic aspects of PD are currently the subject of intense research. 
Environmental Factors Some scientists have suggested that Parkinson's disease may result from exposure to an environmental toxin or injury. Epidemiological research has identified several factors that may be linked to PD, including rural living, well water, herbicide use and exposure to pesticides. Also, a synthetic narcotic agent called MPTP can cause immediate and permanent parkinsonism if injected. These environmental factors are not useful in diagnosing the cause of Parkinson's disease in individual people. In fact, there is no conclusive evidence that any environmental factor, alone, can be considered a cause of the disease. However, these environmental factors have been helpful in studying laboratory models of Parkinson's disease. Scientists are continuing to pursue these clues to establish more concrete linkages. 
 
Parkinson’s Medications 
People with Parkinson’s disease often take a variety of medications in different doses in order to manage the symptoms of the disease.  These factors, combined with the frequency with which one must take their medicines, can be confusing.  People with Parkinson’s and their caregivers should become familiar with their medications in order to use them most effectively and avoid possible interactions. Understanding a medication regime and sticking to it will provide the greatest benefit from the drug and avoid unpleasant “off” periods due to missed doses or confusion. 
Although there are general guidelines that doctors use to choose a treatment regimen, each patient must be individually evaluated to determine which drug or combination of drugs is best for them.  For some, a “first choice” drug might be one of the levodopa preparations, and for others, an initial prescription may be given for one of the agonists, an MAO inhibitor or an anticholinergic.  The choice of drug treatment depends on many variables including symptom presentation, other concurrent health issues (and the medications being used to treat them) and a person’s age.  And while the suggested starting dosages (as indicated by the package insert) are listed here, remember that they too can vary greatly depending on a person’s needs and metabolism. 
 
Surgical Treatment for Parkinson's 
Surgery for Parkinson's disease has come a long way since it was first developed more than 50 years ago. The newest version of this surgery, deep brain stimulation or DBS, was developed in the 1990s and is now a standard treatment. Although it is certainly the most important therapeutic advance since the development of levodopa, it is not for every person with Parkinson's. It is most effective - sometimes, dramatically so - for individuals who experience disabling tremors, wearing-off spells and medication-induced dyskinesias. 
During deep brain stimulation surgery, electrodes are inserted into the targeted brain region using MRI and neurophysiological mapping to ensure that they are implanted in the right place. A device called an impulse generator or IPG (similar to a pacemaker) is implanted under the collarbone to provide an electrical impulse to a part of the brain involved in motor function. Patients have a controller, which allows them to check the battery and to turn the device on or off. An IPG battery lasts for about 3 to 5 years and is relatively easy to replace under local anesthesia. 
 
The Role of the Patient 
Treating Parkinson's disease is not exclusively the doctor's job; there are many things a person with Parkinson's can do to contribute. Regular exercise, joining a support group, maintaining a healthy diet and taking part in a clinical trial are just some of the things you might consider. 
•    Exercise 
•    Support Groups 
•    Diet 
•    A Healthy Patient / Doctor Relationship 
•    Physical, Speech and / or Occupational Therapy 
•    Clinical Trials 
Exercise: For people with Parkinson's, regular exercise or physical therapy is crucial for maintaining and improving mobility, flexibility, balance, range of motion and for warding off many of the disease's secondary symptoms such as depression and constipation. PDF offers Motivating Moves for People with Parkinson's, a unique program of 24 seated and stimulating exercises that were created especially for people with Parkinson's. Copies are available for ordering through the website, or you can call or email PDF for more information. As with every aspect of your care, always consult your doctor before starting an exercise program. 
Support groups: For many people, support groups play an important role in the emotional well-being of patients and families. They can provide a caring environment for asking questions about Parkinson's, for sharing stories and advice and for creating friendships with people who have experienced similar problems. To find a support group in your area, please call or email PDF. In addition to in-person support groups, many people also find online groups and list servs helpful. For a listing of list servs that serve the Parkinson's community, please request our publication, Web Resources for People with Parkinson's Disease. 
Diet: Many people with Parkinson's lose weight because of poor appetite and inadequate food intake. It is recommended to maintain a full diet that contains all the daily nutritional requirements, including extra fresh fruits and vegetables for fiber to help prevent constipation and plenty of fluids to keep hydrated. 
Some people who take levodopa find that protein may interfere with the medication's effect. Limiting protein intake or staggering the medication dosing to avoid conflicts with meals can help this problem. However, adjustments in protein intake are only worthwhile for those very few people whose response to levodopa is indeed sensitive to dietary protein. 
People with Parkinson's who lose weight for no clear reason should discuss this with a physician. 
A Healthy Patient/Doctor Relationship: Making an accurate diagnosis of Parkinson's - specifically in its early stages - is difficult, but a skilled practitioner can come to a reasoned conclusion that it is Parkinson's. Every person diagnosed with Parkinson's should consider getting a second opinion from a neurologist who specializes in movement disorders and is up-to-date on research and approaches to therapy. 
Locating a qualified physician is a first step; next is considering whether the physician is the right one. A person with Parkinson's will work with a physician for many years. Consider these questions: 
•    Are you comfortable speaking with your physician? 
•    Do you feel respected by your doctor? 
•    Are questions answered to your satisfaction or do you come away from a visit feeling that you have not been taken seriously? 
•    Can you get in touch with the doctor between visits? 
To find a neurologist or movement disorder specialist in your area: 
•    Ask your primary care physician for a referral 
•    Seek referrals from other living with Parkinson's 
•    Contact your insurance provider for a list of neurologists or movement disorder specialists in your network 
•    Contact PDF for a referral. 
Physical, Speech and/or Occupational Therapy: These therapies can help Parkinson's patients control their symptoms and make daily life easier. Physical therapy may increase muscle strength and flexibility and decrease the incidence of falls. Speech therapy can increase voice volume and assist with word pronunciation. The Lee Silverman technique is a special speech therapy that can be very beneficial to people with Parkinson's - for further information see www.lsvt.org. 
Occupational therapy gives people alternative methods of doing tasks that they can no longer perform with ease. These options may provide a stronger sense of control when living with Parkinson's disease. A neurologist should be able to provide recommendations for these therapies and, if needed, a referral. These therapies may or may not be covered by insurance. 
Clinical Trials: Clinical trials (also called medical research, clinical research or a clinical study) help researchers answer specific questions about the safety and efficacy of new treatments by studying its effects in people. They are an essential and necessary component of the scientific research process. Simply put, there is no other way for research to show that a proposed treatment works. In addition to contributing to research, joining a clinical trial can provide a person with early access to potentially-helpful Parkinson's treatments and drugs that are not yet on the market.</div>

By Deden Sura Agung It is important to realize that not every person with Parkinson's develops all signs or symptoms of the disease. ...

Saturday, September 17, 2011

COMA is a state of unconsciousness

<div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">By Deden Sura Agung</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">Coma is a medical condition that needs treatment sooner, because the basic course of the disease was the cause of 'coma' and direction of development of the disease can cause severe brain damage and irreversible. So rapid and systematic examination is needed to provide appropriate therapy and diagnostic work properly. Neurologic evaluation and management of patients 'coma' or loss of consciousness is very difficult, because patients in such conditions usually in critical condition and need help fast. 'Coma' is the result of brain dysfunction that can cause damage rekticular activation system such as loss of consciousness. </div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">In formulating a diagnosis of 'coma', there are two axioms that must be followed: (1) that found a single clue about the causes of 'coma' is not meant to prove the cause, (2) a complete Neurology examination itself is not efficient, because the examination of other organ systems should also be done . Disturbance of consciousness is a marker of nervous system disorders. In the examination must be distinguished from abnormalities in the level of consciousness (somnolence, stupor, coma) and / or the contents of consciousness (confuse, hallucinations).</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 0.0001pt; text-align: justify;"> 
</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">DEFINITION</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">Coma is a state of 'unresponsiveness' in which a person can not feel or react in the environment. Circumstances where a person looks like falling asleep and at the same time can not be awakened by external stimuli and the needs of the body in a state referred to as 'coma'.</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 0.0001pt; text-align: justify;"> 
</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">ANATOMY AND PHYSIOLOGY</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">State of human consciousness is a reflection of the level of 'arousal' and combined cognitive brain functions. 'Arousal' played by the integrity of the physiological mechanisms of formation rektikularis and structures located at the top of the brainstem, starting from the front until the mid-pons to the hypothalamus. Behavior 'conscious' tend in played by functional areas of the hemisphere cerebri each other and interact with each other is widely associated with the activation system that is more noble than the upper brain stem, hypothalamus, and thalamus. Moruzzi and Mogoun (1949), argued that the rektikularis formasio area located at the rostral brain stem, which when stimulated will cause a general activation of the non-specific in the cortex cerebri, which is referred to as 'Ascending Recticular Activating System'. This system includes areas in the middle of the brain stem, extending from the midbrain to the hypothalamus and thalamus, and describe these structures in transmitting the physiological effects of a diffuse to the cortex either directly or indirectly, in the role of the arousal of consciousness. Gellhorn (1953), suggests thinking about the process of 'consciousness', which is known as the hypothalamus or hypothalamic activation system controle system, which is composed of fibers of the projection between the hypothalamus with the front lobe of the piriformis, nucleus of the amygdala and hippocampus formasio rear, to deliver visceral feelings and impulses of organic sensations through the neocortex without direct contact with formasio rektikularis. In this case the activation of the cortex cerebri is controlled by a two-way through the hypothalamus, the activation / facilitation and inhibition systems. And this system is closely related to the setting instinktuil, emotional, autonomic, and hormonal.</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">Formasio rektikularis extends from the caudal medulla oblongata to the midbrain rostal, with no clear boundaries. In it lie many vital centers such as the respiratory center, blood pressure, heart rate, and other vegetative functions, and also contain components of ascending and descending pathways that play an important role in the regulation of endocrine secretion, reflex, sensory input, and awareness. 'Ascending Recticular Activating System' receiving stimulation by all the general somatic sensory pathways and specific. Rektikularis excitation system is a complex trajectory polisinaps, because apart from the sensory tract, also derived from the trigeminal system, hearing, sight, and smell. Conductive pathway talamikus spino-walk toward the medulla and pons tegmentum is a morphological pathway of the excitatory noksius of 'consciousness'. Some pathways of formasio rektikularis routed through the thalamus to the next projected evenly on the cortex cerebri (specific projections), while others will end up in nuckleus specific thalamus to then projected diffusely to the cortex (the projection of non-specific).</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">Broadly speaking, the causes of 'coma' could be in for two, namely intracranial and metabolic. The cause of intracranial such as head trauma, infections, neoplastic, and vascular disorders. On the causes can be metabolic imbalance of electrolytes and acid-base, endocrine disorders, hepatic coma, uremic coma, anoxia encephalopathy, vitamin deficiency (thiamine, niacin, vitamin B12), toxins and intoksikan.</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">The causes of 'coma' can be categorized into:</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 21.3pt; text-align: justify; text-indent: -21.3pt;">a.      Dysfunction of the cerebral cortex of bilateral multifocal or diffuse, where the substantia grisea cortex is destroyed or depressed by acute and diffuse so that the curved trajectory of physiological feedback cortical-subcortical damage, the mechanism of autonomic arousal of the brain stem and cause shock terinhibisi acute rektikulaer below the level of lesion (eg : necrosis due to hypoxia-iskhaemia heavy, prolonged hipoleukhaemia, metabolic depression in ensefalopatia hepatica).</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 21.3pt; text-align: justify; text-indent: -21.3pt;">b.     Direct damage to the paramedian upper brain stem and posterior-inferior diencephalic ascending arousal system that is blocking the normal cortical activity (ie: encephalitis infrak or certain inflammatory lesions).</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 21.3pt; text-align: justify; text-indent: -21.3pt;">c.    Wide disconnection between the cortex and subcortical mechanisms of activity similar to the above two conditions (for example: dismielinisasi or extensive damage of the substantia alba severe cerebral hemisphere pascahipoperfusi-old cerebral hypoxemia due to CO poisoning). 
d. Diffuse abnormalities are usually caused by a metabolic disorder affecting competing cortical and subcortical arousal mechanisms (eg metabolic encephalopathy).</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 21.3pt; text-align: justify; text-indent: -21.3pt;"> 
</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">CLINICAL APPROACH</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">As the algorithm approaches the patients 'coma' or loss of consciousness:</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 21.3pt; text-align: justify; text-indent: -21.3pt;">1.   ABC: in patients who experienced loss of consciousness, carried out the liberation of the airway, breathing and circulation should be checked and maintained.</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 21.3pt; text-align: justify; text-indent: -21.3pt;">2.   Look for signs or clues about the cause of the decline in consciousness through anamnesa (a history of hereditary diseases, the state and condition of the patient is found, etc.), physical examination (odor breathing, signs of meningeal perangsagan, scar injections, etc.), laboratory and radiological examinations.</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 21.3pt; text-align: justify; text-indent: -21.3pt;">3.      Addressing a common cause of reversible: giving naloxone, thiamine, and dextrose 50% in patients with decreased consciousness and the cause is unknown.</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 21.3pt; text-align: justify; text-indent: -21.3pt;">4.      Neurology examination: check the brainstem and the search for focal lesions.</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 0.0001pt; text-align: justify;"> 
</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">DIAGNOSIS</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">Physical Examination:</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">Note vital signs like blood pressure, pulse, respiration and temperature, whether there are abnormalities or not. In general observations views posture, patient age, stigmata of chronic disease, breathing patterns, and skin color (jaundice, cyanosis, pallor, red cherry). Looking for signs of trauma to the head (skull fracture, laceration), seizures (myoclonic, deserebrasi), the smell of breathing (alcohol, acetone, ammonia), check the ears and nose (bleeding or discharge of cerebrospinal fluid), check the extremities body if there is a fracture or not, and palpation - percussion and auscultation of the thorax area, heart and abdomen.</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">Examination Neurolgic:</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">First of all examined the level of consciousness using the GCS - Glasgow Coma Scale which consists of:</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">EYE</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 0.0001pt 21.25pt; text-align: justify; text-indent: -21.25pt;">-        Opening eyes spontaneously. (4)</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 0.0001pt 21.25pt; text-align: justify; text-indent: -21.25pt;">-        Open the eyes with the sound stimuli. (3)</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 0.0001pt 21.25pt; text-align: justify; text-indent: -21.25pt;">-        Open the eye with painful stimuli. (2)</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 0.0001pt 21.25pt; text-align: justify; text-indent: -21.25pt;">-        Unable to open the eyes. (1)</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 0.0001pt 21.25pt; text-align: justify; text-indent: -21.25pt;"> 
</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">MOTORIC</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 0.0001pt 21.25pt; text-align: justify; text-indent: -21.25pt;">-        Moving according to the command. (6)</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 0.0001pt 21.25pt; text-align: justify; text-indent: -21.25pt;">-        It can locate pain. (5)</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 0.0001pt 21.25pt; text-align: justify; text-indent: -21.25pt;">-        avoidance reaction. (4)</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 0.0001pt 21.25pt; text-align: justify; text-indent: -21.25pt;">-        Reaction dekortikasi / flexion. (3)</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 0.0001pt 21.25pt; text-align: justify; text-indent: -21.25pt;">-        Directors deserebrasi / extension. (2)</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 0.0001pt 21.25pt; text-align: justify; text-indent: -21.25pt;">-        There was no reaction. (1)</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 0.0001pt 21.25pt; text-align: justify; text-indent: -21.25pt;"> 
</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 21.3pt; text-align: justify; text-indent: -21.3pt;">VERBAL</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 0.0001pt 21.25pt; text-align: justify; text-indent: -21.25pt;">-        Good and no disorientation. (5)</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 0.0001pt 21.25pt; text-align: justify; text-indent: -21.25pt;">-        'Confuse'. (4)</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 0.0001pt 21.25pt; text-align: justify; text-indent: -21.25pt;">-        Talk is not appropriate. (3)</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 0.0001pt 21.25pt; text-align: justify; text-indent: -21.25pt;">-        Can only groaned. (2)</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 0.0001pt 21.25pt; text-align: justify; text-indent: -21.25pt;">-        There is no sound. (1)</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 21.3pt; text-align: justify; text-indent: -21.3pt;"> 
</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">As a benchmark for 'coma' then according to GCS equal to 3, where there were no eye-opening response, verbal and motoric. Then note the pattern of breathing and motoric examination. </div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">On motoric examination, which is seen is the patient's posture and if there are seizures or not. Cranial nerves examination was conducted to assess the function of the brain stem. Where in the patients who experienced loss of consciousness or 'coma' will happen some decline in brain stem reflexes, then examined the pupillary reflex, corneal, okulocefalik (doll's eye), and vomiting.</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 0.0001pt; text-align: justify;">To help find out the causes of 'coma', then the examination can be performed with CT-scan or MRI, was conducted to determine abnormalities in the brain are like a tumor mass or increased intracranial fluid. If meningitis is suspected, then examination lumbar puncture. In laboratory tests that examined the levels of blood glucose, iodine, calcium, and urea nitrogen or creatinine; arterial pH, pO2, and PCO2; the concentration of ethanol in blood and urine; blood cultures and cerebrospinal fluid; and liver function.</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 0.0001pt; text-align: justify;"> 
</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">TREATMENT</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">The principle of treatment is generally required to be applied immediately although the diagnosis of the cause has not been enforced. Starting from:</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 21.3pt; text-align: justify; text-indent: -21.3pt;">1.      ABC: the liberation of the airway, breathing and circulation maintenance.</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 21.3pt; text-align: justify; text-indent: -21.3pt;">2.      Overcome state of shock, if any.</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 21.3pt; text-align: justify; text-indent: -21.3pt;">3.      Provision of naloxone 0.5 mg iv (if the cause is an overdose of narcotics), infusion of glucose 50% 25 50ml. And given the thiamine 50 - 100mg after administration of a bolus injection of glucose.</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 21.3pt; text-align: justify; text-indent: -21.3pt;">4.      Giving Mannitol 50gr in a solution of 20% iv every 10 -20 minutes.</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 21.3pt; text-align: justify; text-indent: -21.3pt;">5.      Perform lumbar puncture if meningitis is suspected or subarakhnoi hemorrhage, or perform a CT-scan.</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 21.3pt; text-align: justify; text-indent: -21.3pt;">6.      Giving anticonvulsant such as phenytoin 500 - 1000mg iv, doses <50mg/mnt.</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 21.3pt; text-align: justify; text-indent: -21.3pt;">7.      Rinse and gastric lavage with normal saline is very useful if the coma is because taking drugs.</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 21.3pt; text-align: justify; text-indent: -21.3pt;">8.      The use of cooling mat to cope with hyperthermia.</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 21.3pt; text-align: justify; text-indent: -21.3pt;">9.      Installation of a catheter to help the urine output.</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 21.3pt; text-align: justify; text-indent: -21.3pt;">10.   Installation of stomach tube to assist the provision of food and drink.</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 21.3pt; text-align: justify; text-indent: -21.3pt;">11.   Changing the sleeping position of patients and restriction of oral fluids. Patient's legs should be checked to prevent phlebothrombosis.</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 0.0001pt; text-align: justify;"> 
</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">CONCLUSION</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">'Coma' is a state of reduced consciousness that causes people to look like falling asleep but can not be aroused by stimuli from the outside or the surrounding environment and by stimulation of the body. The causes of 'coma' can be divided into two, the first of abnormalities in the intracranial and the second by metabolic abnormalities. </div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">What makes 'coma' as a state of emergency is the cause of the disease course and progression of the disease that can cause severe brain damage and irreversible, and usually patients with a 'coma' was in critical condition.</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">Therefore, in treating patients with decreased consciousness or 'coma' should be quick and systematic, is intended to provide appropriate therapies and diagnostics work properly. In an effort to provide relief, then the following steps can be followed:</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 14.2pt; text-align: justify; text-indent: -14.2pt;">1.   Remember ABC: the liberation of the airway, breathing and circulation maintenance.</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 14.2pt; text-align: justify; text-indent: -14.2pt;">2.   Find the clues of the cause of the reduction state of awareness. In this case, do diagnose, checking vital signs.</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 14.2pt; text-align: justify; text-indent: -14.2pt;">3.   The management of circumstances that are still reversible, such as provision of naloxone, thiamine, and dextrose to patients with decreased awareness of the cause is unknown.</div><div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 6pt 14.2pt; text-align: justify; text-indent: -14.2pt;">4.   Check your brain stem reflexes and look for the symptoms / signs of focal lesions.</div><div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;"> 
LITERATUR</div><div class="MsoNormal" style="line-height: 150%; margin: 0cm 0cm 0.0001pt 21.3pt; text-align: justify; text-indent: -21.3pt;">1.         Adams R.D, Maurice V. Coma and Related Disorders of Consciousness, Principles of Neurology, 5th edition. McGraw-Hill Co,Inc. 1993: 300 – 318;</div><div class="MsoNormal" style="line-height: 150%; margin: 0cm 0cm 0.0001pt 21.3pt; text-align: justify; text-indent: -21.3pt;">2.         Drislane F.W, Benatar M, Chang B.S, et all. The Approach to Coma and Altered Consciousness, Blueprints Neurology, 2nd edition. Lippincott Williams & Wilkins. 2002: 20 – 26;</div><div class="MsoNormal" style="line-height: 150%; margin: 0cm 0cm 0.0001pt 21.3pt; text-align: justify; text-indent: -21.3pt;">3.         LeBlond R.F, DeGowin R.L, Brown D.D. Coma, DeGowin’s Diagnostic Examination The Complete Guide to Assessment Examination Differential Diagnosis, 8th edition, International edition. McGraw-Hill Co,Inc. 2004: 865 – 868;</div><div class="MsoNormal" style="line-height: 150%; margin: 0cm 0cm 0.0001pt 21.3pt; text-align: justify; text-indent: -21.3pt;">4.         Kasper D.L, Braunwald E, Fauci A.S, et all. Confusion, Stupor, and Coma, Harrison’s Manual of Medicine, 16th edition, International edition. McGraw-Hill Co,Inc. 2005: 54 – 58;</div><div class="MsoNormal" style="line-height: 150%; margin: 0cm 0cm 0.0001pt 21.3pt; text-align: justify; text-indent: -21.3pt;">5.         Gilroy J. Coma, Basic Neurology, 3rd edition, International edition. McGraw-Hill Co,Inc. 61 – 70;</div><div class="MsoNormal" style="line-height: 150%; margin: 0cm 0cm 0.0001pt 21.3pt; text-align: justify; text-indent: -21.3pt;">6.         Listiono D. Koma dan Gangguan Kesadaran, Ilmu Bedah Saraf Satyanegara, edisi Ketiga. PT.Gramedia Pustaka Utama, Jakarta, 1998 : 130 – 143;</div><div class="MsoNormal" style="line-height: 150%; margin: 0cm 0cm 0.0001pt 21.3pt; text-align: justify; text-indent: -21.3pt;">7.         Brust  J.C.M. Coma, Current Diagnosis & Treatment in Neurology, International edition. Lange Medical Books/McGraw-Hill Co,Inc. 2007: 29 – 34.</div>

By Deden Sura Agung Coma is a medical condition that needs treatment sooner, because the basic course of the disease was the cause of '...