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Saturday, September 17, 2011

COMA is a state of unconsciousness

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.
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).

DEFINITION
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'.

ANATOMY AND PHYSIOLOGY
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.
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).
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.
The causes of 'coma' can be categorized into:
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).
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).
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).

CLINICAL APPROACH
As the algorithm approaches the patients 'coma' or loss of consciousness:
1.   ABC: in patients who experienced loss of consciousness, carried out the liberation of the airway, breathing and circulation should be checked and maintained.
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.
3.      Addressing a common cause of reversible: giving naloxone, thiamine, and dextrose 50% in patients with decreased consciousness and the cause is unknown.
4.      Neurology examination: check the brainstem and the search for focal lesions.

DIAGNOSIS
Physical Examination:
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.
Examination Neurolgic:
First of all examined the level of consciousness using the GCS - Glasgow Coma Scale which consists of:
EYE
-        Opening eyes spontaneously. (4)
-        Open the eyes with the sound stimuli. (3)
-        Open the eye with painful stimuli. (2)
-        Unable to open the eyes. (1)

MOTORIC
-        Moving according to the command. (6)
-        It can locate pain. (5)
-        avoidance reaction. (4)
-        Reaction dekortikasi / flexion. (3)
-        Directors deserebrasi / extension. (2)
-        There was no reaction. (1)

VERBAL
-        Good and no disorientation. (5)
-        'Confuse'. (4)
-        Talk is not appropriate. (3)
-        Can only groaned. (2)
-        There is no sound. (1)

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.
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.
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.

TREATMENT
The principle of treatment is generally required to be applied immediately although the diagnosis of the cause has not been enforced. Starting from:
1.      ABC: the liberation of the airway, breathing and circulation maintenance.
2.      Overcome state of shock, if any.
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.
4.      Giving Mannitol 50gr in a solution of 20% iv every 10 -20 minutes.
5.      Perform lumbar puncture if meningitis is suspected or subarakhnoi hemorrhage, or perform a CT-scan.
6.      Giving anticonvulsant such as phenytoin 500 - 1000mg iv, doses <50mg/mnt.
7.      Rinse and gastric lavage with normal saline is very useful if the coma is because taking drugs.
8.      The use of cooling mat to cope with hyperthermia.
9.      Installation of a catheter to help the urine output.
10.   Installation of stomach tube to assist the provision of food and drink.
11.   Changing the sleeping position of patients and restriction of oral fluids. Patient's legs should be checked to prevent phlebothrombosis.

CONCLUSION
'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.
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.
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:
1.   Remember ABC: the liberation of the airway, breathing and circulation maintenance.
2.   Find the clues of the cause of the reduction state of awareness. In this case, do diagnose, checking vital signs.
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.
4.   Check your brain stem reflexes and look for the symptoms / signs of focal lesions.

LITERATUR
1.         Adams R.D, Maurice V. Coma and Related Disorders of Consciousness, Principles of Neurology, 5th edition. McGraw-Hill Co,Inc. 1993: 300 – 318;
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;
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;
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;
5.         Gilroy J. Coma, Basic Neurology, 3rd edition, International edition. McGraw-Hill Co,Inc. 61 – 70;
6.         Listiono D. Koma dan Gangguan Kesadaran, Ilmu Bedah Saraf Satyanegara, edisi Ketiga. PT.Gramedia Pustaka Utama, Jakarta, 1998 : 130 – 143;
7.         Brust  J.C.M. Coma, Current Diagnosis & Treatment in Neurology, International edition. Lange Medical Books/McGraw-Hill Co,Inc. 2007: 29 – 34.

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