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Comatose State

Coma is a clinical condition defined as a deep state of unconsciousness. A comatose patient is technically alive but unable to move and respond to any external stimuli introduced to him. Coma usually results as a complication of a metabolic disease or traumatic brain injury.


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
  • Farid Sadaka , Therapeutic Hypothermia for Brain Injury from Near Hanging: Review of the Literature , Therapeutic Hypothermia and Temperature Management , 3 , 1 , (13) , (2013) . Alexis A. Topjian, Robert A. Berg, Joost J. L. M.[doi.org]
  • This case describes a patient with myxoedema coma with severe hypothermia and cardiac involvement with development of multiorgan dysfunction all linked to the severe depletion of triiodothyronine.[ncbi.nlm.nih.gov]
  • Abstract A 62-year-old man was found to have bradycardia, hypothermia and respiratory failure 3 weeks after initiation of amiodarone therapy for atrial fibrillation.[ncbi.nlm.nih.gov]
  • We report a case of myxoedema coma in a woman presenting with respiratory failure, hypotension, hypothermia and a reduced level of consciousness, all of which are poor prognostic features in decompensated hypothyroidism.[ncbi.nlm.nih.gov]
  • Abstract We report a case of life-threatening myxoedema presenting with hypothermia, hypotension, bradycardia, pericardial effusion and deep coma. The condition was complicated by prolonged status epilepticus.[ncbi.nlm.nih.gov]
  • […] coma Approximate Synonyms Acute ischemic stroke with coma Intracerebral hemorrhage with brain compression and coma Intracerebral hemorrhage, coma Intracerebral hemorrhage, w coma and brain compression Ischemic stroke w coma Ischemic stroke with coma Myxedema[icd9data.com]
  • Hormonal disorders: Patients having physiologic decompensation with hypothyroidism will result into a myxedema coma. Diabetes: Severe hyperglycemic states or hypoglycemic states may cause a stroke or a diabetic coma.[symptoma.com]
  • Anemia ( low red blood cell count ) Toxins Poisons External poisons are those that are ingested or inhaled Internal poisons are by-products of the body's normal metabolism that for some reason cannot be excreted properly Endocrine disorders Myxedema coma[emedicinehealth.com]
  • Called also brain death. myxedema coma the mental stupor caused by severe hypothyroidism; seen most often in Doberman pinchers, it is associated with hypoventilation, hypothermia, hypotension and bradycardia. Death may occur.[medical-dictionary.thefreedictionary.com]
  • If thyroid hormone levels gradually drop too low over a period of time myxedema coma can occur because of the profound hypothyroidism. Ingestions can cause the brain to slow down, speed up or alter its perception of the world.[medicinenet.com]
  • Clinical data included time of no and low flow, CA rhythm, pupillary reflex, Glasgow motor score at admission and hyperthermia. Biological marker was the highest creatinine level.[ncbi.nlm.nih.gov]
  • Toxins/drugs Numerous causes including sedatives, narcotics, alcohol, psychotropics, carbon monoxide Organ failure Uremic encephalopathy, hepatic encephalopathy Metabolic hypoxia, hypercapnoea, hyponatraemia, hyperglycaemia, hypoglycaemia, hypothermia, hyperthermia[lifeinthefastlane.com]
  • The remaining 15% of comatose cases result from trauma, excessive blood loss, malnutrition, hypothermia, hyperthermia, abnormal glucose levels, and many other biological disorders.[en.wikipedia.org]
  • The clinical and laboratory assessments of the comatose patient are reviewed here, along with an analysis of how various conditions (structural brain lesions, metabolic and toxic disorders, trauma, infections, seizures, hypothermia, and hyperthermia)[doi.org]
Cheyne-Stokes Respiration
  • Long-cycle, Cheyne-Stokes respiration - damage at the diencephalon. Short-cycle, Cheyne-Stokes respiration - damage at the medulla. Central neurogenic hyperventilation - lesions in the low midbrain and upper pons.[patient.info]
Abnormal Breathing
  • Secondary effects of drugs, which include abnormal heart rate and blood pressure, as well as abnormal breathing and sweating, may also indirectly harm the functioning of the ARAS and lead to a coma.[en.wikipedia.org]
  • The syndrome is usually described in malignant hypertension, eclampsia, renal failure, immunosuppressive, and cytotoxic chemotherapies.[ncbi.nlm.nih.gov]
  • CONCLUSIONS Our results demonstrate that rural residence, higher HbA1c level, combined hypertension, and combined neural complications increase the incidence of hypoglycemic coma.[ncbi.nlm.nih.gov]
  • Subdural hemorrhage: bleeding inside the skull, and inside the dura, but not in the brain tissue itself Subarachnoid hemorrhage: bleeding in the space immediately adjacent to the brain tissue Causes of brain/skull hemorrhage include: High blood pressure ( hypertension[emedicinehealth.com]
  • Some medical causes of this form of bleeding include: Hypertension ( high blood pressure ): when blood pressure is too high, and not controlled, blood vessels in the brain may not be able to tolerate the high pressure and may leak blood into the brain[medicinenet.com]
Heart Disease
  • While tight control of blood glucose levels is important to prevent the long-term complications of diabetes, including heart disease, peripheral vascular disease, blindness, and kidney failure ; close monitoring is also required to prevent hypoglycemic[medicinenet.com]
  • While tight control of blood glucose levels is important to prevent the long-term complications of diabetes , including heart disease , peripheral vascular disease , blindness , and kidney failure ; close monitoring is also required to prevent hypoglycemic[medicinenet.com]
  • Immunohistochemical staining for CD45RO, CK-L, and M30 might be useful to observe sweat gland degeneration in the coma blister. Therefore, the apoptosis might be related to coma blisters and sweat gland degenerations.[ncbi.nlm.nih.gov]
  • […] word "coma" itself emerged from the Greek for "deep sleep" ( koma ) in around the 17th century, and methods throughout history for helping those in comas have included bloodletting from the head, emptying the stomach, cooling the body dramatically, blistering[bustle.com]
  • KEYWORDS: catatonia; coma; conversion disorder; factitious; functional neurologic disorder; psychogenic; stupor; unconsciousness[ncbi.nlm.nih.gov]
  • It is a rare condition which may sometimes present with severe symptoms such as stupor or coma. The standard treatment protocol includes conservative measures such as bed rest, hydration, and steroids.[ncbi.nlm.nih.gov]
  • These vary from a delirium, causing more or less anxiety, to definite meninjtis producing rapid and stupor and ultimately, coma . Metastatic cancer in-uences coma only indirectly, through brain tumour and increased total serum calcium.[dictionary.cambridge.org]
  • Stupor and coma in adults. . Accessed July 15, 2015. Daroff RB, et al. Bradley's Neurology in Clinical Practice. 6th ed. Philadelphia, Pa.: Saunders Elsevier; 2012. Accessed July 15, 2015. NINDS coma information page.[mayoclinic.org]
  • […] rupture or blockage of vessels supplying blood to the brain, can cause sudden loss of consciousness in some patients, while comas caused by metabolic abnormalities or cerebral tumours are characterized by a more gradual onset, with stages of lethargy and stupor[britannica.com]
  • Mydriasis is also common. This indicator can be used to include patients in one of two groups: V1: Autonomic responses to painful stimuli are present. V2: Absence of autonomic response to pain 9.[doi.org]
Unresponsive to Pain Stimuli
  • 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[symptoma.com]


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.
  • Moving patients through the use of physical therapy also aids in preventing atelectasis, contractures or other orthopedic deformities which would interfere with a coma patient's recovery.Pneumonia is also common in coma patients due to their inability[en.wikipedia.org]
Burst Suppression
  • KEYWORDS: Awakening prognosis; Burst suppression; Levetiracetam; Overdose; Post anoxic coma[ncbi.nlm.nih.gov]
  • Variables recorded per minute included presence or absence of EEG burst suppression, burst count, BIS value over time, burst count, and SR.[ncbi.nlm.nih.gov]
  • This device works by automatically adjusting the infusion rate of propofol - a general anesthetic - in response to an electroencephalogram (EEG) pattern called burst suppression.[ncbi.nlm.nih.gov]
  • An isoelectric, low-voltage, or burst-suppression with identical bursts pattern at 24 hours invariably predicted poor outcome in both montages, with similar prognostic accuracy.[ncbi.nlm.nih.gov]
  • In contrast, continuous extremely low voltage, burst-suppression, or a flat tracing was correlated with poor 6-month neurological outcome with a sensitivity of 76.5% and specificity of 100%.[ncbi.nlm.nih.gov]
  • We present the case of a middle-aged woman diagnosed with myxoedema coma and severe hyponatremia.[ncbi.nlm.nih.gov]


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].

Sex distribution
Age distribution


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.

Patient Information


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.


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.


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.


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. 

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Last updated: 2017-08-09 18:25