Patients suffering from coma will commonly present with the following signs and symptoms:

• Diminished brainstem reflexes (i.e. pupillary response)
• Closed eyes
• Extremities does not respond to movement
• Unresponsive to painful stimuli
• Intact reflexes in the extremities
• Irregular patterns of breathing

A detailed clinical history is usually gathered from a reliable informant or a close family member in the case of a comatose patient. History regarding the events that surround the onset or the development of the coma is usually collected and chronologically assessed to determine the causative factor of the unconscious state. An extensive neurologic examination is done in all patients presenting with coma to determine the extent of the damage. Laboratory tests are also done to determine the exact causative factor of the disorder. The following laboratory tests are implored among patients with coma:

• Complete blood count (CBC)
• Blood pH levels [8]
• Electrolytes (Sodium and Calcium)
• Serum and intracranial glucose levels
• Thyroid function tests
• Liver enzymes 
• Alcohol levels in the serum
• Drug assays

Imaging techniques may elucidate the exact location of the pathology of the coma especially among patients with traumatic injuries:

• Computerized tomography (CT): A CT scan shows a detailed image of the brain demonstrating hemorrhage, tumors, and cerebrovascular ischemia.
• Magnetic resonance imaging (MRI): MRI renders a more enhanced view of the brain tissues damaged by ischemia, stroke, and hemorrhage.
• Electroencephalogram (EEG): This measures the electrical impulses of the brain and determine the presence of seizures as causative factor of the coma.

All patients that present as coma in the hospital are always treated as a medical emergency. The airways and breathing of the patient are initially secured. Fluid resuscitation or blood transfusion may be immediately indicated in the case of coma with shock. In cases of hypoglycemic shock, patients are given a glucose bolus to reverse the metabolic state [9]. Intravenous antibiotics are sometimes given in case of severe brain and systemic infections. Medications to decrease brain pressure may alleviate the symptoms of brain edema in the case of brain trauma and ketoacidosis [10]. Anti-seizure medications are also given to patients with seizure disorders that precipitated the coma.

The general outlook for patients in coma greatly depend on the location, cause, size, and extent of the neurologic damage. Coma that renders the patient in vegetative state for more than 5 weeks usually carries a poor prognosis. Some patients may emerge from coma with learning, physical, and psychological difficulties that fails to improve in time. The prompt identification and intervention of these problems will increase the chances for a full recovery. The time duration of the coma is currently revered as the best predictor of partial and full recovery among affected patients [7].

There are a number of medical conditions that can precipitate into a coma. The following conditions are common causes of coma:

• Cerebrovascular disease or stroke: This medical condition is characterized by the sudden cessation of blood flow in the brain or a ruptured brain vessel that can lead to coma.
• Brain tumors: Tumors located within the brain and the brainstem may result into coma.
• Traumatic brain injuries: Any direct trauma to the brain can initiate a comatose state.
• Hormonal disorders: Patients having physiologic decompensation with hypothyroidism will result into a myxedema coma [1].
• Diabetes: Severe hyperglycemic states or hypoglycemic states may cause a stroke or a diabetic coma [2].
• Seizures: Persistent and uncontrolled seizures can result in a vegetative state of consciousness.
• Toxins: Extrinsic toxins from the environment like lead and carbon monoxide can damage the brain and lead to coma.
• Drugs and alcohol: The elicit abuse of certain drugs like alcohol may lead to coma.
• Cerebral infections: Brain swelling due to meningitis or encephalitis can precipitate permanent brain damage and coma.
• Hypoxic states: Patients who has been resuscitated from a heart attack or rescued from drowning will experience low levels of oxygen to the brain and cause coma.

Coma is a result of a primary metabolic condition or a direct head trauma. Because coma is treated as a complication of a disease rather than a primary disorder, there are no available epidemiologic studies and statistics on the actual incidence and prevalence of coma. However, there are prospective studies conducted in the United Kingdom based on population about the general incidence of non-traumatic coma among children reaching an average rate of 30.8 cases per 100,000 children [3]. In Europe, non-traumatic coma has been an important source of pediatric mortality and morbidity [4].

Coma induced by drugs accounts for 40% of the total cases seen in the clinics. Drugs damage or retard the synaptic function in the ascending reticular activating system (ARAS) which makes it hard for the brain to arouse from unconsciousness or from a vegetative state [5]. Other drugs that cause hallucinations, seizures and poisoning have been found to adversely affect the ARAS in the same way. Coma from brain hypoxia tallies to about 25% of the total coma cases seen in the hospitals. The progressive oxygen deprivation of the brain causes a decrease in the neuronal intracellular calcium and sodium which significantly hampers interneuron communications within the cerebrum [6]. Patients who sustain a stroke will have some form of blockage or thrombosis that prevents blood, oxygen, and nutrients from reaching certain areas of the brain resulting to cell death.

The best way to prevent the occurrence of coma is to actively prevent the events that may incite coma. The prudent practice of wearing helmet while driving motorcycles and bicycles can effectively prevent brain trauma significantly. Using of alcohol in moderation and abstinence from dangerous recreational drugs can prevent undue coma and death. Diabetics must achieve good glycemic control to avoid ketoacidotic coma and hypoglycemic coma. Mild seizures must be brought to proper medical care in soonest possible time to avoid coma as one of its serious complication.

Coma is a neurologic state of prolonged unconsciousness that results from various medical conditions like brain tumors, alcohol intoxication, diabetes mellitus, and cerebral infections. Coma is considered as a medical emergency, where all efforts are made to preserve life and brain functions as soon as the patient is brought to the emergency room. A number of tests are immediately done to determine its etiologic cause for the proper and prompt treatment of the medical condition. Coma usually last for several weeks, patients who stay comatose for more than a year will most likely stay in a persistent vegetative state.

Definition

Coma is a state of prolonged unconsciousness that may result from various medical factors like brain tumors, alcoholic intoxication, diabetes mellitus, trauma, and cerebral infections.

Cause

Majority of cases of coma is brought about by the intake drugs. Brain hypoxia and stroke are among the more common factors that triggers the clinical state. Sometimes seizures, diabetes, and hormonal imbalance may directly cause coma.

Symptoms

Patients are typically brought to the emergency room unconscious and eyes closed. They are usually not responsive to external stimuli like sound and pain but they maintain their deep tendon reflexes.

Diagnosis

A detailed clinical history is taken from the companion or witness. A complete physical examination and neurologic examination is also done on the patient. Blood tests for pH, CBC, thyroid and liver function test will be most helpful in the diagnostic process. Imaging modalities like CT and MRI may demonstrate bleeding and tumors within the brain.

Treatment and follow-up

The primary goal of treatment is to reverse the effects of the primary inciting factor that produces the coma. Glucose bolus with insulin for diabetic coma and fluid resuscitation for those with dehydration and electrolyte imbalance.

1. Wall CR. Myxedema coma: diagnosis and treatment. Am Fam Physician. Dec 1 2000; 62(11):2485-90.
2. Bowden SA, Duck MM, Hoffman RP. Young children (< 5 yr) and adolescents (>12 yr) with type 1 diabetes mellitus have low rate of partial remission: diabetic ketoacidosis is an important risk factor. Pediatr Diabetes. Jun 2008; 9(3 Pt 1):197-201.
3. Wong CP, Forsyth RJ, Kelly TP, Eyre JA. Incidence, aetiology, and outcome of non-traumatic coma: a population based study. Arch Dis Child 2001; 84:193-199 
4. Seshia SS, Seshia MM, Sachdeva RK. Coma in childhood. Dev Med Child Neurol 1977 19:614–628.
5. Young GB. Coma. Ann N Y Acad Sci 2009 1157 (1157): 32–47.
6. Busl KM, Greer DM. Hypoxic-ischemic brain injury: Pathophysiology, neuropathology and mechanisms. Neuro Rehabilitation 2010: 5–13.
7. Formisano R, Carlesimo GA, Sabbadini M et al. Clinical predictors and neuropleropsychological outcome in severe traumatic brain injury patients. Acta Neurochir (Wien) 2004 146 (5): 457–62.
8. Kitabchi AE, Umpierrez GE, Murphy MB, et al. Hyperglycemic crises in diabetes. Diabetes Care. Jan 2004; 27 Suppl 1:S94-102.
9. Savage MW, Dhatariya KK, Kilvert A, Rayman G, Rees JA, Courtney CH, et al. Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis. Diabet Med. May 2011; 28(5):508-15.
10. Wolfsdorf J, Craig ME, Daneman D, Dunger D, Edge J, Lee WR, et al. Diabetic ketoacidosis.Pediatr Diabetes. Feb 2007; 8(1):28-43.