HEALTH Conspiracy

Friday, September 23, 2011

PARKINSON'S

<div style="text-align: justify;">By <a href="https://www.djendrals.my.id/?m=1" target="_blank">djendrals</a></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 djendrals It is important to realize that not every person with Parkinson's develops all signs or symptoms of the disease. For exa...

Saturday, September 17, 2011

COMA is a state of unconsciousness

<div class="MsoNormal" style="line-height: normal; margin-bottom: 6pt; text-align: justify;">By <a href="https://www.djendrals.my.id/?m=1" target="_blank">djendrals</a></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 djendrals Coma is a medical condition that needs treatment sooner, because the basic course of the disease was the cause of 'coma...

SALMONELLA PARATYPHI - TYPHOID (TYPUS)

<div style="text-align: justify;">By Deden Sura Agung</div><div style="text-align: justify;"> </div><div style="text-align: justify;">Demam Enterik (Tifoid) adalah penyakit sistemik yang ditandai dengan demam dan nyeri pada abdomen yang disebabkan oleh penyebaran  Salmonella typhi atau Salmonella paratyphi. Pada awalnya penyakit ini disebut demam tifoid karena memiliki gejala klinis yang sama dengan typhus. Namun pada awal tahun 1800-an, demam typhoid secara jelas didefinisikan sebagai kelainan patologis berupa suatu penyakit yang berbeda (unik) dikarenakan dasar penegakan penyakit yang berhubungan dengan pembesaran Plak Peyeri dan nodus limfatikus mesenterik. Pada tahun 1869, berdasarkan tempat infeksi, istilah demam enterik diajukan sebagai istilah alternatif untuk membedakan demam tifoid dari tifus. Namun pada saat ini kedua istilah tersebut sering bertukar tempat.</div>Epidemiologi 
<div style="text-align: justify;"><div class="separator" style="clear: both; text-align: center;"></div>Beberapa hal yang mempengaruhi terjadinya penyebaran demam tifoid di negara sedang berkembang adalah kepadatan penduduk, sumber air minum, produksi makanan, strain resisten antibiotik, kesulitan menentukan identifikasi dan penatalaksanaan karier, keterlambatan membuat diagnosis pasti, patogenesis dan virulensi yang belum diketahui sepenuhnya, serta belum adanya vaksin, efektif aman dan murah.</div><div style="text-align: justify;">Bakteri S. typhi dapat bertahan hidup di lingkungan kering dan beku, peka terhadap proses klorinasi dan pasteurisasi pada suhu 630 C. Organisme ini mampu bertahan beberapa minggu di es, debu, sampah kering, dan pakaian, mampu bertahan di tempat sampah selama satu minggu dan dapat berkembang biak dalam susu, daging atau produknya tanpa merubah warna atau bentuknya. 
Manusia merupakan satu-satunya sumber penularan alami melalui kontak langsung maupun tidak langsung dengan seorang penderita tifoid atau karier kronis. Transmisi kuman terutama dengan cara menelan makanan atau air yang tercemar tinja manusia. Transmisi secara kongenital dapat terjadi dari seorang ibu yang mengalami bakteriemia kepada bayi dalam kandungan, atau tertular pada saat dilahirkan oleh seorang ibu merupakan karier tifoid dengan rute fekal oral.</div> 
Etiologi 
<div style="text-align: justify;">Salmonella Typhi adalah bakteri Gram negatif, mempunyai flagela, tidak berkapsul, tidak membentuk spora fakultatif anaerob. Mempunyai antigen somatik (O) yang terdiri dari oligosakarida, flagelar antigen (H) yang terdiri dari protein dan envelope antigen (K) yang terdiri dari polisakarida. Mempunyai makromolekular lipopolisakarida kompleks yang membentuk lapis luar dari dinding sel dan dinamakan endotoksin. Salmonella typhii juga dapat memperoleh plasmid faktor-R yang berkaitan dengan resistensi terhadap multipel antibiotik.</div> 
Patogenesis 
Jalur Masuknya Bakteri ke Dalam Tubuh 
<div style="text-align: justify;">Infeksi didapat dengan cara menelan makanan atau minuman yang terkontaminasi dan dapat pula dengan kontak langsung jari tangan yang terkontaminasi tinja, urin, sekret saluran nafas, atau dengan pus penderita yang terinfeksi. Agar dapat menimbulkan gejala klinis, diperlukan S. typhi dalam dosis 106 - 109 . Pada fase awal demam tifoid biasa ditemukan adanya gejala saluran nafas atas. Ada kemungkinan sebagian kuman ini masuk ke dalam peredaran darah melalui jaringan limfoid di faring. Pada tahap awal ini penderita juga sering mengeluh nyeri telan. Lidah tampak kotor tertutup selaput berwarna putih sampai berwarna putih sampai kecoklatan yang merupakan akibat sel epitel mati oleh bakteri S. typhi. Bila terjadi infeksi dari nasofaring melalui saluran tuba eustachi ke telingah tengah dan hal ini dapat terjadi otitis media.</div><div style="text-align: justify;">Di lambung, organisme menemui suasana asam dengan pH dengan rendah dalam kuman dimusnahkan. Pengosongan lambung yang bersifat lambat merupakan pelindung fisiologis. Setelah melalui barier asam lambung mikroorganiusme sampai ke usus halus dan menemui dua mekanisme pertahanan tubuh, yaitu motilitas dan flora normal usus. Penurunan motilitas usus karena obat-obatan atau faktor anatomis meningkatkan derajat beratnya penyakit dan timbulnya komplikasi, serta memperpanjang keadaan karier konvalesens. </div><div style="text-align: justify;">Sebuah penelitian menunjukkan bahwa apabila kuman yang masuk sebanyak 103 atau kurang, belum dapat menimbulkan gejala pada penderita, tetapi jika jumlahnya lebih dari 105 atau lebih menimbulkan gejala pada 27% sukarelawan. Semakin tinggi jumlah kuman yang masuk, semakin besar kemungkinan seseorang terkena deman typhoid, apalagi apabila kuman tersebut termasuk jenis yang menghasilkan gen polisakarida kapsul atau Vi. 
Selanjutnya kuman akan menembus dinding usus halus, masuk ke kelenjar mesentrika, lalu ke duktus thoracicus dan masuk ke dalam peredaran darah, dan menimbulkan bakteriemi I. 
Kuman-kuman ini kemudian akan ditangkap oleh sel-sel RES dari limpa hati dan organ-organ lainnya. Setelah beberapa lama, kuman-kuman tersebut kembali masuk ke peredaran darah, dan menimbulkan bakteriemi II dan menyebar ke seluruh tubuh, termasuk melalui kantung empedu dan aliran empedu, masuk ke lumen usus lalu menembus hingga ke  plaque peyeri.</div> 
Manifestasi Klinis 
<div style="text-align: justify;">Pada anak, periode inkubasi demam tifoid antara 5-40 hari dengan rata-rata 10 – 14 hari. Gejala klinis demam tifoid sangat bervariasi, dari gejala klinis ringan dan tidak memerlukan perawatan khusus sampai dengan berat sehingga harus dirawat. Variasi gejala ini  disebabkan faktor galur Salmonella, status nutrisi, imunologi dan lama sakit di rumahnya. </div><div style="text-align: justify;">Semua pasien demam tifoid selalu menderita demam pada awal penyakit. Pada era pemakaian antibiotik belum seperti saat ini, penampilan demam pada kasus demam tifoid mempunyai istilah khusus yaitu step ladder temperature chart yang ditandai dengan demam timbul insidius, kemudian naik secara bertahap tiap harinya dan mencapai titik tertinggi pada akhir minggu pertama, setelah itu demam akan bertahan tinggi dan pada minggu ke-4 demam turun perlahan secara lisis, kecuali apabila terjadi fokus infeksi seperti kolesistitis, abses jaringan lunak maka demam akan menetap. Banyak orang tua pasien demam tifoid melaporkan bahwa demam lebih tinggi saat sore dan malam hari dibandingkan denga pagi harinya. Pada saat demam sudah tinggi, pada kasus demam tifoid dapat disertai gejala sistem saraf pusat; seperti kesadaran berkabut atau delirium atau obtundasi, atau penurunan kesadaran mulai apati sampai koma.</div><div style="text-align: justify;">Gejala sistemik lain yang menyertai timbulnya demam adalah nyeri kepala, malaise, anoreksia, nausea, mialgia, nyeri perut, dan radang tenggorokan. Pada kasus yang berpenampilan klinis berat, pada saat demam tinggi akan nampak toksik/sakit berat. Bahkan dapat juga ijumpai penderita demam tifoid yang datang dengan syok hipovolemik sebagai akibat kurang masukan cairan dan makanan. Gejala gastrointestinal pada kasus demam tifoid sangat bervariasi. Pasien dapat mengeluh obstipasi, obstipasi kemudian disusul episode diare, pada sebagian pasien lidah tampak kotor dengan putih di tengah sedang tepi dan ujungnya kemerahan. Banyak dijumpai gejala meteorismus, berbeda dengan buku bacaan Barat pada anak Indonesia lebih banyak dijumpai hepatomegali dibandingkan splenomegali. 
Rose spot suatu ruam makulopapular yang berwarna merah dengan ukuran 2-4 sering kali dijumpai pada daerah abdomen, toraks, ekstremitas dan punggung pada orang tua kulit putih, tidak pernah dilaporkan ditemukan pada anak Indonesia. Bronkhitis banyak dijumpai pada demam tifoid sehingga buku ajar lama bahkan menganggap sebagai bagian dari penyakit demam tifoid. Bradikardi relatif jarang dijumpai pada anak. 
 
Penyulit (Komplikasi) 
Perforasi usus halus dilaporkan dapat terjadi pada 0,5-3 %, sedangkan perdarahan usus pada 1-10% kasus demam tifoid anak. Penyulit ini biasanya terjadi pada minggu ke-3 sakit, walau pernah dilaporkan terjadi pada minggu pertama. Komplikasi didahului dengan penurunan suhu, tekanan darah dan peningkatan frekuensi nadi. Pada perforasi usus halus ditandai oleh nyeri abdomen lokal pada kuadran kanan bawah akan tetapi dilaporkan juga nyeri yang menyelubung. Kemudian akan diikuti muntah, nyeri pada perabaan abdomen, dan hilangnya keredupan hepar.</div><div style="text-align: justify;">Pada komplikasi neuropsikiatri sebagian besar bermanifestasi gangguan kesadaran, disorientasi, delirium, obtudansi, stupor bahkan koma. Hepatitis tifosa asimtomatik dapat dijumpai pada kasus demam tifoid dengan ditandai peningkatan kadar transaminase yang tidak mencolok. Ikterus dengan atau tanpa disertai kenaikan kadar transaminase, maupun kolesistitis akut juga dapat dijumpai, sedang kolesistitis kronik yang terjadi pada penderita setelah mengalami demam tifoid dapat dikaitkan dengan adanya batu empedu dan fenomena pembawa kuman (karier). 
Sebagian kasus demam tifoid mengeluarkan bakteri Salmonella typhi melalui urin pada saat sakit maupun setelah sembuh. Sistitis bahkan pielonefritis dapat juga merupakan penyulit demam tifoid. Proteinuria transien sering dijumpai, sedangkan glomerunefritis yang dapat bermani9festasi sebagai gagal ginjal maupun sindrom nefrotik mempunyai prognosis yang buruk. 
Relaps yang didapat pada 5-10% kasus demam tifoid saat era pre antibiotik, sekarang lebih jarang ditemukan. Apabila terjadi relaps, demam timbul kembali seminggu setelah penghentian antibiotik. Pada umumnya relaps lebih ringan dibandingkan gejala demam tifoid sebelumnya. 
 
Gambaran Darah Tepi 
Anemia normokrom normositik terjadi sebagai akibat perdarahan usus atau supresi pada sumsum tulang. Jumlah leukosit rendah, namun jarang di bawah 3.000/l3. Apabila terjadi abses piogenik maka jumlah leukosit dapat meningkat mencapai 20.000 – 25.000/l3. Trombositopenia sering dijumpai, kadang-kadang berlangsung beberapa minggu. 
 
Diagnosa dan Deteksi Pembawa Kuman 
Diagnosis ditegakkan berdasarkan gejala klinis berupa demam, gangguan gastrointestinal dan mungkin disertai perubahan atau gangguan kesadaran, maka seorang klinisi dapat dapat membuat diagnosis tersangka demam typhoid. Diagnosis pasti ditegakkan melalui isolasi S. typhi dari darah, atau dapat pula dari feces atau urine. Pada dua minggu pertama sakit, kemungkinan mengisolasi S. typhi dari dalam darah pasien lebih besar dari pada minggu berikutnya. Biakan yang dilakukan pada urin dan feses, kemungkinan keberhasilan lebih kecil. Biakan spesimen yang berasal dari aspirasi sumsum tulang mempunyai sensitivitas tertinggi, hasil positif didapat pada 90% kasus. Akan tetapi prcsedur ini sangat invasif, sehingga tidak dipakai dalam praktek sehari-hari. Pada keadaan tertentu dapat dilakukan biakan spesimen empedu yang diambil dari duodenum dan memberikan hasil yang cukup baik.</div><div style="text-align: justify;">Uji serologi Widal suatu metode serologik yang memeriksa antibodi aglutinasi terhadap antigen somatik (O), flagela (H) banyak dipakai untuk membuat diagnosis demam tifoid. Di Indonesia pengambilan angka titer O aglutinin > 1/40 dengan memakai uji Widal slide aglutination (prosedur pemeriksaan membutuhkan waktu 45 menit) menuniukkan nilai ramal positif 96%. Artinya apabila hasil tes positif, 96% kasus benar sakit demam tifoid, akan tetapi apabila negatif tidak menyingkirkan. Banyak pendapat apabila titer O aglutinin sekaii periksa > 1/200 atau pada titer sepasang terjadi kenaikan 4 kali maka diagnosis demam tit'oid dapat ditegakkan. Aglutinin H banyak dikaitkan dengan pasca imunisasi atau infeksi masa lampau, sedang Vi aglutinin dipakai pada deteksi pembawa kuman S. typhi (karier). Banyak peneliti mengemukakan bahwa uji serologik Widal kurang dapat dipercaya sebab dapat timbul positif palsu pada daerah endemis, dan sebaliknya dapat timbul negatif palsu pada kasus demam tifoid yang terbukti biakan darah positif. 
Akhir-akhir ini banyak dimunculkan beberapa jenis pemeriksaan untuk mendeteksi antibodi S.typhi dalam serum, antigen terhadap S. typhi dalam darah, serum dan urin bahkan DNA S. typhi dalam darah dan faeces. Walaupun laporan-laporan pendahuluan menunjukkan hasil yang baik namun sampai sekarang tidak salah satupun dipakai secara luas. Sampai sekarang belum disepakati adanya pemeriksaan yang dapat menggantikan uji serologi Widal. 
 
Diagnosis BandingPada stadium dini demam tifoid beberapa penyakit kadang-kadang secara klinis dapat merupakan diagnosis banding yaitu influenza, gastroenteritis, bronkitis dan bronkopneumonia. Beberapa penyakit yang disebabkan oleh mikroorganisme intraselular seperti tuberkulosis, infeksi Jamur sistemik, bruselosis, tularemia, shigelosis dan malaria juga perlu dipikirkan. Pada demam typhoid yang berat, sepsis, leukemia, limfoma, dan penyakit hodgkin dapat sebagai diagnosis banding.</div><div style="text-align: justify;"> 
</div><div style="text-align: justify;">Tatalaksana 
Sebagian besar pasien demam tifoid dapat diobati di rumah dengan tirah baring, isolasi yang memadai, pemenuhan kebutuhan cairan, nutrisi serta pemberian antibiotik. Sedangkan untuk kasus berat harus dirawat di rumah sakit agar pemenuhan cairan, elektrolit serta nutrisi disamping observasi kemungkinan timbul penyulit dapat dilakukan seksama.</div><div style="text-align: justify;">Kloramfenikol masih merupakn pilihan pertama pada pengobatan penderita demam tifoid. Dosis yang diberikan adalah 100 mg/kg Berat Badan/hari dibagi dalam 4 kali pemberian selama 10 sampai 14 hari sedang pada kasus dengan malnutrisi atau penyakit, pengobatan dapat diperpanjang sampai 21 hari. Salah satu kelemahan kloramfenikol adalah tingginya angka relaps dan karier. Namun pada anak hal hal tersebut jarang dilaporkan.</div><div style="text-align: justify;">Ampisilin memberikan respons perbaikan klinis kurang apabila dibandingkan dengan kloramfenikol. Dosis yang dianjurkan adalah 100-200 mg/kg Berat Badan/hari dibagi 4 kali  pemberian secara oral atau suntikan intravena. Amoksilin dengan dosis 100 mg/kg Berat Badan/hari dibagi 4 kali pemberian memberikan hasil yang setara dengan kloramfenikol walaupun penurunan demam lebih lama. Kombinasi trimetophin sulfametoksazol memberikan hasil yang kurang baik dibanding kloramfenikol. Di beberapa negara sudah dilaporkan kasus demam tifoid yang resisten terhadap kloramfenikol. Seftriakson dan sefoperazon dapat memberikan angka kesembuhan 90% dan relaps 0-4%. Akhir-akhir ini cefixime oral 15-20 mg/kgBB/hari pertama 10 kali dapat diberikan sebagai alternatif, terutama apabila jumlah leukosit <2000/ atau dijumpai resistensi terhadap S.typhi.</div><div style="text-align: justify;">Pada demam tifoid kasus berat seperti delirium, koma atau syok, deksametason dosis tinggi 1 – 3 mg/kg Berat Badan/hari disamping antibiotik yang memadai dapat menurunkan angka kematian. Demam tifoid edngan tifoid denga npenyulit perdarahan usus kadang-kadang memerlukan tranfusi darah. Sedangkan apabila diduga terjadi perforasi, adanya cairan pada peritoneum dan udara bebas pada foto abdomen dapat membantu menegakan diagnosis. Laparotomi segera harus dilakukan pada perfusi usus didertai penambahan antibiotik metronidazol dapat memperbaiki prognosis. 
Tiga persen penderita demam typhoid akan menjadi karier, kejadiannya meningkat sesuai dengan bertambahnya umur. Terjadinya penderita dengan karier biasanya disebabkan oloh infeksi kandung empedu yang kronis akibat batu empedu dan penderita mengeluarkan kumannya melalui kotoran ( kandung empedu dan saluran empedu  sebagai sumber infeksi), 
sehingga kolesistektomi dapal dipertimbangkan pada > 8 % karier, bahkan tanpa pemberian antibiotika. Pengobatan Karier tergantung ada tidaknya kelainan kandung empedu 
kantung empedu normal 
•    Ampisilin 500 mg (tiap 6 jam) selama 6 minggu, atau 
•    Ampisilin 200 mg (tiap 6 jam) selama 6 minggu, intravena, atau 
•    Ampsilin 100 - 200 mg/kg/hari, untuk 3 - 4 minggu. 
•    Amoksisilin 40 mg/kg/hari, peroral  (tiap 8 jam) + Probenezid 25 mg/kg dosis pertama (selanjutnya 40 mg), peroral (tiap 6 jam), selama 4 - 6 minggu. 
•    TMP 8 mg/kg/hari, SMZ 40 mg/kg/hari, uintuk 3 - 4 minggu. 
•    Norfloxazin / Ciprofloxacin. 
Merupakan golongnn quinolon, telah berhasil baik pada penderita dewasa. 
Karena pengaruhnya lerhadap perkeimbangan Tulang rawan, sehingga tidak dianjurkani untuk anakyang lebih muda dari 18 tahun. 
Disfungsi kandung empedu 
Obat dan dosis sama dengan untuk kandung empedu normal + Kolesistektomi + Amoksisilin untuk 30 hari kemudian. 
 
Kasus demam tifoid yang mengalami relaps diberi pengobatan sebagai kasus demam tifoid serangan pertama. 
Pencegahan 
Secara umum, untuk memperkecil kemungkinan tercemar S.typlii, maka setiap individu harus memperhatikan kualitas makanan dan minuman yang mereka konsumsi. Salmonella typhi di dalam air akan mati apabila dipanasi seting 57°C untuk beberapa menit atau dengan proses iodinasi/klorinasi. 
Untuk rnakanan, pemanasan sampai suhu 57°C beberapa menit dan secara merata juga dapat mematikan kuman Salmonella typhi. Penurunan endemisitas suatu negara/daerah tergantung pada baik buruknya pengadaan sarana air dan pengaturan pembuangan sampah serta tingkat kesadaran individu terhadap higiene pribadi. Imunisasi aktif dapat membantu menekan angka kejadian demam tifoid. 
Vaksin Demam Tifoid 
Saat sekarang dikenal (tiga macam vaksin untuk penyakit demam tifoid, yaitu yang berisi kuman yang dimatikan, kuman hidup dan komponen Vi dari Salmonella typhi. Vaksin yang berisi kuman Salmonella typhi, S. paratyphi A,  S. paratyphi B yang dimatikan (TAB vaccine) telah puluhan tahun digunakan dengan cara pemberian suntikan subkutan namun vaksin ini hanya memberikan daya kekebalan yang terbatas, disamping efek samping lokal pada tempat suntikan yang cukup sering. Vaksin yang berisi kuman Salmonella typhi hidup yang dilemahkan (Ty-21a) diberikan per oral tiga kali dengan interval pemberian selang sehari, memberi daya perlindungan 6 tahun. Vaksin Ty-21a diberikan pada anak berumur di atas 2 tahun. Pada penelitian di lapangan didapat hasil efikasi proteksi yang berbanding terbalik dengan derajat transmisi penyakit. Vaksin yang berisi komponen Vi dari Salmonella typhi diberikan secara suntikan intramuskular memberikan perlindungan 60 – 70 %.</div><div style="text-align: justify;"><a href="http://www.blogger.com/goog_1419315295"> 
</a></div><div style="text-align: justify;"><a href="http://adf.ly/104369/salmonella-paratyphi">Download artikel Salmonella Paratyphi - Typhoid (Typus) dalam bentuk Microsoft Word secara lengkap.</a></div><div style="text-align: justify;"> 
DAFTAR PUSTAKA 
1.Harrison’s Principles of Internal Medicine 16th edition .McGraw-Hill.2005 
2.Behrman KE. Kliegman RM, Nelson WE, Vaughan HI VC Typhoid fever. Nelson textbook of pediatrics, edisi ke-14 Philadelphia: WB Saunders Co, lS92.h.731-34. 
3.Butier T Typhoid fever. Dalanu Warren KS, Mahmoud AF (penyunting). Tropical 
and geographical medicine, edisi ke-2. New York: Me Graw-HiU Information 
Services Co, 1990 Ji.753-7. 
4.Hayani CH, Picketing LK. Salmonella infections. Dalam: Feigin RD, Cherry JD (penyunting). Textbook of pediatric infectious diseases, edisi ke-3, Tokyo: V/B Saunders Co, 1992.K620-33. 
5.Hoffman SL. Typhoid fever. Dalatn: Strickland GT penyunting. Hunter's tropical medicine, edisi ke-7. Philadelphia: WB Saunders Co. 1991.h.344-58. 
 
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By Deden Sura Agung Demam Enterik (Tifoid) adalah penyakit sistemik yang ditandai dengan demam dan nyeri pada abdomen yang disebabkan oleh ...

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SALMONELLA PARATYPHI - TYPHOID (TYPUS)

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