Materiały źródłowe

• #1 Coma – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/sites/books/NBK430722/

  Coma reflects brain failure that may occur from a process originating in the central nervous system or may reflect a systemic metabolic process. […] Coma represents brain failure. It may be caused by neuronal dysfunction from many causes including structural or nonstructural processes affecting the central nervous system. […] The accepted pathophysiology of a coma involves neuronal dysfunction from a decrease in the supply of glucose or oxygen to the brain. A myriad of etiologies may lead to essential substrate disruption with diffuse central nervous system (CNS) dysfunction and coma as the extreme clinical condition. […] Structural lesions of the CNS, such as intracerebral hemorrhage, may lead to coma from direct destruction of arousal areas of the brain or from secondary damage from shifting of intracranial structures, vascular compression, or increased intracranial pressure. […] Increased intracranial pressure is a frequent cause of coma. Since the brain is enclosed in the closed skull, conditions that increase intracranial pressure may impair cerebral perfusion.

• #1 Overview of Coma and Impaired Consciousness – Neurologic Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/neurologic-disorders/coma-and-impaired-consciousness/overview-of-coma-and-impaired-consciousness

  Coma is unresponsiveness from which the patient cannot be aroused and in which the patient’s eyes remain closed. The mechanism for coma or impaired consciousness involves dysfunction of both cerebral hemispheres or of the reticular activating system (also known as the ascending arousal system). […] The mechanism of impaired consciousness must involve both cerebral hemispheres or dysfunction of the RAS. […] RAS dysfunction can result from a condition that has diffuse effects, such as toxic or metabolic disturbances (eg, hypoglycemia, hypoxia, uremia, overdose of a substance, illicit drug, or medication). RAS dysfunction can also be caused by focal ischemia (eg, certain upper brain stem infarcts), hemorrhage, or direct, mechanical disruption. […] Any condition that increases intracranial pressure (ICP) may decrease cerebral perfusion pressure, resulting in secondary brain ischemia.

• #1 Stupor and coma in adults – UpToDate

  https://www.uptodate.com/contents/stupor-and-coma-in-adults/print

  Stupor and coma are clinical states in which patients have impaired responsiveness (or are unresponsive) to external stimulation and are either difficult to arouse or are unarousable. Coma is defined as „unarousable unresponsiveness”. […] An alteration in arousal represents an acute, life-threatening emergency, requiring prompt intervention for preservation of life and brain function. […] The ascending reticular activating system (ARAS) is a network of neurons originating in the tegmentum of the upper pons and midbrain, believed to be integral to inducing and maintaining alertness. These neurons project to structures in the diencephalon, including the thalamus and hypothalamus, and from there to the cerebral cortex. Alterations in alertness can be produced by focal lesions within the upper brainstem by directly damaging the ARAS.

• #1 Coma – Wikipedia

  https://en.wikipedia.org/wiki/Coma

  The cerebral cortex is composed of gray matter which consists of the nuclei of neurons, whereas the inner portion of the cerebrum is composed of white matter and is composed of the axons of neuron. […] The RAS has two tracts, the ascending and descending tract. […] The ascending tract, or ascending reticular activating system (ARAS), is made up of a system of acetylcholine-producing neurons, and works to arouse and wake up the brain. […] Any impairment in ARAS functioning, a neuronal dysfunction, along the arousal pathway stated directly above, prevents the body from being aware of its surroundings. […] Without the arousal and consciousness centers, the body cannot awaken, remaining in a comatose state. […] The severity and mode of onset of coma depends on the underlying cause. […] There are two main subdivisions of a coma: structural and diffuse neuronal.

• #1 Coma – Wikipedia

  https://en.wikipedia.org/wiki/Coma

  A structural cause, for example, is brought upon by a mechanical force that brings about cellular damage, such as physical pressure or a blockage in neural transmission. […] By contrast, a diffuse cause is limited to aberrations of cellular function which fall under a metabolic or toxic subgroup. […] Toxin-induced comas are caused by extrinsic substances, whereas metabolic-induced comas are caused by intrinsic processes, such as body thermoregulation or ionic imbalances (e.g. sodium). […] For instance, severe hypoglycemia (low blood sugar) or hypercapnia (increased carbon dioxide levels in the blood) are examples of a metabolic diffuse neuronal dysfunction. […] In contrast, coma resulting from a severe traumatic brain injury or subarachnoid hemorrhage can be instantaneous. […] Structural and diffuse causes of coma are not isolated from one another, as one can lead to the other in some situations.

• #1 Stupor and coma in adults – UpToDate

  https://www.uptodate.com/contents/stupor-and-coma-in-adults

  Damage to the cerebral hemispheres can also produce coma, but in this case, the involvement is necessarily bilateral and diffuse, or if unilateral, large enough to exert remote effects on the contralateral hemisphere or brainstem. […] The mechanism of coma in toxic, metabolic, and infectious etiologies and hypothermia is less well understood and to some extent is cause specific. A simplified explanation is that these conditions impair oxygen or substrate delivery, which in turn alters cerebral metabolism or interferes with neuronal excitability and/or synaptic function.

• #1 Coma | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/19750

  Increased intracranial pressure is a frequent cause of coma. Since the brain is enclosed in the closed skull, conditions that increase intracranial pressure may impair cerebral perfusion. The equation that approximates this relationship is unforgiving CPP (cerebral perfusion pressure) = MAP (mean arterial pressure estimated as 1/3 systolic BP [blood pressure] + 2/3 diastolic BP) – ICP (intracranial pressure). As ICP approaches MAP, cerebral perfusion diminishes. It is essential to maintain CPP by reducing increased intracranial pressure while avoiding hypotension.

• #1 Overview of Coma and Impaired Consciousness – Neurologic Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/neurologic-disorders/coma-and-impaired-consciousness/overview-of-coma-and-impaired-consciousness

  When brain damage is extensive, brain herniation may occur; it contributes to neurologic deterioration because it directly compresses brain tissue, blocks the blood supply to areas of the brain, increases ICP, may lead to hydrocephalus by obstructing the cerebral ventricular system, results in neuronal and vascular cell dysfunction, and may shift brain structures from one side of the brain to the other side. […] In addition to the direct effects of increased ICP on neuronal and vascular cells, cellular pathways of apoptosis and autophagy can become activated. Apoptosis has early and late phases that ultimately lead to the destruction of deoxyribonucleic acid (DNA) in cells. In autophagy, components of cell cytoplasm are recycled in an attempt to remove nonfunctional organelles and can sometimes lead to neuronal and vascular cell injury. […] Impaired consciousness may progress to coma and ultimately to brain death.

• #1 Coma | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/19750

  Structural lesions of the CNS, such as intracerebral hemorrhage, may lead to coma from direct destruction of arousal areas of the brain or from secondary damage from shifting of intracranial structures, vascular compression, or increased intracranial pressure. Herniation syndromes describe clinically recognizable physical examination features that may suggest the anatomic location of the CNS lesion. The most discussed of the herniation syndromes is uncal herniation, where the medial portion of the temporal lobes shifts with resulting loss of consciousness from brainstem compression. The pathophysiologic findings are often compression of the brainstem and cranial nerve III as it exits the brainstem and crosses the tentorium cerebelli. This results in impairment of the parasympathetic fibers (pupilloconstrictors) that travel with the third nerve, and in most cases pupillary dilatation on the same side (roughly 90%) of the mass lesion.

• #1 Acute Coma: Approach to Diagnosis and Management | RECAPEM

  https://recapem.com/acute-coma-approach-to-diagnosis-and-management/

  Coma can be caused by structural lesions or global acute physiologic derangement of brain function. […] Coma results from the disruption of pathways from the ascending reticular activating system. […] Coma is a state of complete unresponsiveness to any stimuli. Patients are not awake, not aware, and not arousable. […] If bihemispheric, it should cause diffuse bihemispheric damage or bilateral thalamic injury (e.g. vein of Galen thrombosis). […] Coma cannot be attributed to a unilateral cortical lesion alone. For example, for a unilateral cortical lesion to cause coma it must cause a herniation syndrome that results in damage to the upper midbrain. […] If brainstem lesion, primary brainstem lesion (e.g. brainstem infarction) vs. secondary brainstem injury (e.g. displacement)? […] In the central hernia, there is descent of the diencephalon, midbrain, and pons.

• #1 Prognosis and Therapy after Cardiac Arrest-Induced Coma | Journal of Ethics | American Medical Association

  https://journalofethics.ama-assn.org/article/prognosis-and-therapy-after-cardiac-arrest-induced-coma/2009-08

  The pathophysiology of hypoxic-ischemic cell death is that, as neurons are deprived of oxygen, the proteins and electrolytes necessary to maintain the membrane potentials are depleted, causing the cell to depolarize and the cell body to swell. The swelling results in irreversible damage to the cell’s contents, initiating cell autolysis. […] The precise mechanism by which cooling benefits patients is unknown, but it is thought to relate to decreased cerebral oxygen consumption, the inhibition of excitatory neurotransmitters, and a reduction in damaging free radicals and intracellular acidosis. […] Therapeutic hypothermia can provide real benefit to some patients and represents the first proven therapy to prevent brain damage after cardiac arrest.

• #1

  https://www.jci.org/articles/view/107803

  The mechanisms involved in the production of hypoglycemic coma were studied in rabbits. […] The data indicate that the seizures noted early in the course of insulin-induced hypoglycemia are temporally related to a rise in brain osmolality secondary to an increased net transport into brain of Na+ and K+, probably caused by insulin, per se. […] As hypoglycemia persists, there is also depletion of energy-supplying substrates (glucose, lactate, glutamate) in the brain, an event which coincides with the onset of coma.

• #1

  https://link.springer.com/article/10.1007/BF00965690

  Oxidation of [2,3-14C]succinate in the intramitochondrial Krebs cycle was used as a probe to investigate the effect of ammonia on protein incorporation and Krebs cycle oxidation of succinate carbons in isolated rat hepatocytes. […] The data presented in this paper lend strong support to the Krebs-cycle depletion theory of hepatic coma. […] They also suggest that reduced mitochondrial Krebs cycle activity caused by increased amphibolic depletion of substrates results in loss of insulin sensitivity in ammonia toxicity.

• #1 Diabetic coma – Wikipedia

  https://en.wikipedia.org/wiki/Diabetic_coma

  Diabetic coma is a life-threatening but reversible form of coma found in people with diabetes mellitus. […] Diabetic ketoacidosis (DKA), most typically seen in those with type 1 diabetes, is triggered by the build-up of chemicals called ketones. These are strongly acidic and a build-up can cause the blood to become acidic. […] If it progresses and worsens without treatment it can eventually cause unconsciousness, from a combination of a very high blood sugar level, dehydration and shock, and exhaustion. […] The diagnosis of diabetic ketoacidosis is usually suspected from the appearance and a history of 12 days of vomiting. The diagnosis is confirmed when the usual blood chemistries in the emergency department reveal a high blood sugar level and severe metabolic acidosis. […] Nonketotic hyperosmolar coma usually develops more insidiously than diabetic ketoacidosis because the principal symptom is lethargy progressing to obtundation, rather than vomiting and an obvious illness.

• #1 Diabetes-Related Coma: What It Is, Symptoms & Treatment

  https://my.clevelandclinic.org/health/diseases/16628-diabetic-coma

  A diabetes-related coma is a life-threatening complication that can result from very high blood sugar (hyperglycemia) or very low blood sugar (hypoglycemia). […] Hyperosmolar hyperglycemic state (HHS) is a life-threatening complication of diabetes mainly Type 2 diabetes. HHS happens when your blood glucose (sugar) levels are too high for a long period, leading to severe dehydration and confusion. Blood sugar levels are usually over 600 milligrams per deciliter (mg/dL). If you dont get treatment for HHS in time, it can lead to a coma. […] Diabetes-related ketoacidosis (DKA) is a life-threatening complication that mainly affects people with diagnosed or undiagnosed Type 1 diabetes. But it sometimes affects people with Type 2 diabetes as well. DKA happens when your body doesnt have enough insulin (natural or synthetic). Your body needs insulin to make glucose in your blood enter your cells, where its used as fuel for energy. If theres no insulin or not enough insulin, your body starts breaking down body fat for energy instead. As your body breaks down fat, it releases ketones into your bloodstream.

• #1 Diabetic coma | Better Health Channel

  https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/diabetic-coma

  Uncontrolled diabetes may lead to a diabetic coma or unconsciousness. […] This type of coma is triggered by the build-up of chemicals called ketones. Ketones are strongly acidic and cause the blood to become too acidic. […] The kidneys respond to high levels of blood glucose by doing their best to remove it, along with a great deal of water. […] A diabetic hyperosmolar coma is caused by severe dehydration and very high blood glucose levels (hyperglycaemia). […] Hyperosmolar coma develops slowly over several days or weeks, so if the high blood glucose levels or dehydration are detected and treated early, coma can be prevented. […] If the blood glucose falls to very low levels, the person may become unconscious (hypoglycaemic coma) and seizures may occur. […] Prolonged or frequent coma should be avoided and hypoglycaemia needs to be treated quickly.

• #1 Hyperosmolar Hyperglycemic State: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1914705-overview

  The basic underlying mechanism of HHS is a relative reduction in effective circulating insulin with a concomitant rise in counterregulatory hormones. Unlike patients with DKA, most patients with HHS do not develop significant ketoacidosis. Insulin remains available in amounts sufficient to inhibit lipolysis and ketogenesis but insufficient to prevent hyperglycemia. Hyperosmolarity itself may also decrease lipolysis, limiting the amount of free fatty acids available for ketogenesis. […] Under normal circumstances, all of the glucose filtered by the kidneys is reabsorbed. When blood glucose levels reach approximately 180 mg/dL, proximal tubular transport of glucose from the tubular lumen into the renal interstitium becomes saturated, and further glucose reabsorption is no longer possible. The glucose that remains in the renal tubules continues to travel, passing into the distal nephron and, eventually, the urine, carrying water and electrolytes with it. Osmotic diuresis results, causing a decrease in total body water. Diuresis also leads to loss of electrolytes, such as sodium and potassium. Glucose concentration increases due to loss of circulating volume. In an insulinopenic state, hyperglycemia is exacerbated by continued gluconeogenesis and inability to clear glucose. Due to loss of circulating water volume, patients with HHS can have up to 9 L of water deficit because of hyperosmolarity and diuresis.

• #1 Hyperosmolar Hyperglycemic State: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1914705-overview

  The development of hyperosmolarity and hypotension can be accelerated by any process that accelerates water loss, such as diarrhea or severe burns. In a severely dehydrated and hyperosmolar state, hypotension causes a massive stimulation of the renin-angiotensin-aldosterone system and, eventually, renal shutdown. Oliguria precludes further excretion of glucose from the kidneys, which conserves circulating volume but exacerbates hyperglycemia. Hypotension also results in impaired tissue perfusion. Coma is the end stage of this hyperglycemic process, when severe electrolyte disturbances occur in association with hypotension.

• #1 Induced coma – Wikipedia

  https://en.wikipedia.org/wiki/Induced_coma

  An induced coma also known as a medically induced coma (MIC), barbiturate-induced coma, or drug-induced coma is a temporary coma (a deep state of unconsciousness) brought on by a controlled dose of an anesthetic drug, often a barbiturate such as pentobarbital or thiopental. Other intravenous anesthetic drugs such as midazolam or propofol may be used. […] Drug-induced comas are used to protect the brain during major neurosurgery, as a last line of treatment in certain cases of status epilepticus that have not responded to other treatments, and in refractory intracranial hypertension following traumatic brain injury. […] Barbiturates reduce the metabolic rate of brain tissue, as well as the cerebral blood flow. With these reductions, the blood vessels in the brain narrow, resulting in a shrunken brain, and hence lower intracranial pressure. The hope is that, with the swelling relieved, the pressure decreases and some or all brain damage may be averted. Several studies have supported this theory by showing reduced mortality when treating refractory intracranial hypertension with a barbiturate coma.

• #1 Induced coma – Wikipedia

  https://en.wikipedia.org/wiki/Induced_coma

  When barbiturates are given to brain injured patients for induced coma, they act by reducing the electrical activity of the brain, which reduces the metabolic and oxygen demand. Their action limits oxidative damage to lipid membranes and may scavenge free radicals. They also lead to reduced vasogenic edema, fatty acid release and intracellular calcium release. […] Controversy exists over the benefits of using barbiturates to control intracranial hypertension. Some studies have found that barbiturate-induced coma can reduce intracranial hypertension but does not necessarily prevent brain damage. Furthermore, the reduction in intracranial hypertension may not be sustained. Some randomized trials have failed to demonstrate any survival or morbidity benefit of induced coma in diverse conditions such as neurosurgical operations, head trauma, intracranial aneurysm rupture, intracranial hemorrhage, ischemic stroke, and status epilepticus. If the patient survives, cognitive impairment may also follow recovery from the coma. Due to these risks, barbiturate-induced coma should be reserved for cases of refractory intracranial pressure elevation.

• #1

  https://journals.lww.com/co-infectiousdiseases/fulltext/2018/02000/pathophysiology,_clinical_presentation,_and.11.aspx

  Cerebral impairment and acute kidney injury (AKI) are independent predictors of mortality in both adults and children with severe falciparum malaria. […] Common pathophysiological pathways include impaired microcirculation, due to sequestration of parasitized erythrocytes, systemic inflammatory responses, and endothelial activation. […] The direct causes of cerebral and kidney dysfunction remain incompletely understood. […] The majority of patients surviving these complications have complete recovery after appropriate treatment. […] The direct cause of coma and AKI complicating severe malaria are incompletely understood but likely share common pathophysiological mechanisms. […] Severe malaria is predominantly caused by Plasmodium falciparum because of its ability to induce infected red blood cell (RBC) cytoadherence to the vascular endothelium and consequent end-organ dysfunction.

• #1

  https://journals.lww.com/co-infectiousdiseases/fulltext/2018/02000/pathophysiology,_clinical_presentation,_and.11.aspx

  Cytoadhesion results in sequestration of parasitized RBCs in the capillaries and postcapillary venules causing heterogeneous blockage of the microcirculation and tissue hypoxia. […] Microvascular obstruction-induced tissue hypoxia is compounded by microvascular dysfunction and increased oxygen demand. […] Studies of patients with severe malaria having AKI show reduced renal cortical blood flow, increased kidney size, and endothelial changes in both glomerular and peritubular capillaries on histopathology. […] There is an imbalance of proinflammatory and anti-inflammatory responses in severe malaria. […] The role of cytokines and chemokines in the pathophysiology of AKI in severe malaria was recently highlighted. […] Microvascular obstruction and endothelial dysfunction are common mechanisms for both of these complications.

• #1 Sequestration and microvascular congestion are associated with coma in human cerebral malaria. – ORA – Oxford University Research Archive

  https://ora.ouls.ox.ac.uk/objects/uuid:914ca155-f1fd-4314-b92a-a7584ca95ae6

  The pathogenesis of coma in severe Plasmodium falciparum malaria remains poorly understood. Obstruction of the brain microvasculature because of sequestration of parasitized red blood cells (pRBCs) represents one mechanism that could contribute to coma in cerebral malaria. […] Quantitative postmortem microscopy of brain sections from Vietnamese adults dying of malaria confirmed that sequestration in the cerebral microvasculature was significantly higher in patients with cerebral malaria (CM; n = …

• #1 Defining the mechanism of coma in cerebral malaria – MESA

  https://mesamalaria.org/mesa-track/defining-mechanism-coma-cerebral-malaria/

  To define the role of pipecolic acid (PA) in coma induction and parasite biology to characterize a novel mechanism of coma in humans, potentially identify a biomarker of cerebral malaria (CM) etiology of coma, and characterize a potential novel target for improving the health outcomes of CM. […] The etiology of CM coma, which is reversible in survivors, remains unknown. High blood levels of pipecolic acid (PA) have been identified in children with CM compared to mild malaria. PA has been shown to induce coma in animal models, and this project will test the hypothesis that high blood levels in CM result in abnormally elevated PA central nervous system (CNS) concentrations to result coma in CM. […] The project will investigate the hypothesis that PA reduces consciousness through -aminobutyric acid (GABA) receptors, which has been suggested by prior studies using a rat model. PA has been shown by multiple groups to be produced by Plasmodium, and its role in parasite biology is unknown.

• #1 Myxedema coma pathophysiology – wikidoc

  https://wikidoc.org/index.php/Myxedema_coma_pathophysiology

  Myxedema coma occurs as a result of long-standing, undiagnosed, or untreated hypothyroidism. Myxedema coma is usually precipitated by a systemic illness. […] Thyroid hormone plays an important role in cellular metabolism. Long-standing hypothyroidism is associated with reduced metabolic rate and decreased oxygen consumption, which affects all organ systems. Reduced metabolism results in hypothermia. Reduced metabolism and decreased oxygen also result in decreased drug metabolism leading to overdosing of medications particularly sedatives, hypnotics, and anesthetic agents; this can precipitate myxedema coma. Even in severe hypothyroidism, a balance of metabolic homeostasis is achieved through adaptive neurovascular mechanisms. However, in conditions such as respiratory or urinary tract infections, cardiac, acute myocardial infarction or stroke interfere with this adaptive mechanisms by decreasing the blood volume and ventilation triggering myxedema coma.

• #1 New diabetic emergency; acute rhabdomyolysis complicating hyperglycemic hyperosmolar coma successful management and insight into pathogenesis | ICEECE2012 | 15th International & 14th European Congress of Endocrinology | Endocrine Abstracts

  https://www.endocrine-abstracts.org/ea/0029/ea0029p400

  We describe a case of severe rhabdomyolysis(peak CK 48897 /ml and massive myoglobinuria) complicating hyperglycemic hyperosmolar coma. […] Hyperglycemic hyperosmolar state precipitates rhabdomyolysis which aggravates acute renal failure. Pathogenesis of this nontraumatic rhabdomyolysis is multifactorial including, inhibition of the Na pump by hyperosmolar state, acidosis, hypernatremia, K deficiency, decrease in intramuscular energy supply from insulin deficiency. […] Resultant fall in transmembrane potential and elevated intracellular Ca, activates proteases with leakage of muscle enzymes resulting in rhabdomyolysis. […] We also hypothesize that the prothrombotic state induced by severe hyperglycemia causes muscle tissue infarction and elevated CK, confirmed in our case as 100% MM.

• #1 Coma due to drug intoxication | MedLink Neurology

  https://www.medlink.com/articles/coma-due-to-drug-intoxication

  Several drugs can cause coma (both alone and in combination with other drugs). […] Coma may be due to direct toxic effect of drugs on the brain or indirect effect due to disturbances of other systems. […] Coma may be due to direct toxic effect of drugs on the brain or indirect effect due to disturbances of other systems. […] Coma is associated with several drug-induced encephalopathies. Normal doses of some drugs may produce overdose effect in some circumstances, such as drug interactions and renal failure, impairing excretion of the drug. […] Opiates. Overdose of various opiates can cause coma, and this may occur in the hospital setting, such as with unintended overdose of morphine sulfate or with recreational drug use, such as with heroin use. […] Benzodiazepines. Enhancement of GABA activity at specific cerebral sites accounts for the clinical features of benzodiazepine-induced coma to a large extent.

• #1 Coma: Types, Causes, Treatments, Prognosis

  https://www.webmd.com/brain/coma-types-causes-treatments-prognosis

  A coma is caused by an injury to the brain that can be due to increased pressure, bleeding, loss of oxygen, or buildup of toxins. The injury can be temporary and reversible but can also be permanent and lead to death. […] More than 50% of comas are related to head trauma or disturbances in the brain’s circulatory system. […] Anoxic brain injury may result from heart attack (cardiac arrest), head injury or trauma, drowning, drug overdose, or poisoning. […] When the brain swells as a result of trauma, the fluid pushes up against the skull. The swelling may eventually cause the brain to push down on the brain stem, which can damage the reticular activating system (RAS) a part of the brain that’s responsible for arousal and awareness. […] Bleeding in the layers of the brain may cause a coma due to swelling and compression on the injured side of the brain. This compression causes the brain to shift, causing damage to the brainstem and the RAS (mentioned above).

• #1 Stupor and coma in adults – UpToDate

  https://www.uptodate.com/contents/stupor-and-coma-in-adults

  Stupor and coma are clinical states in which patients have impaired responsiveness (or are unresponsive) to external stimulation and are either difficult to arouse or are unarousable. Coma is defined as „unarousable unresponsiveness”. […] An alteration in arousal represents an acute, life-threatening emergency, requiring prompt intervention for preservation of life and brain function. […] The ascending reticular activating system (ARAS) is a network of neurons originating in the tegmentum of the upper pons and midbrain, believed to be integral to inducing and maintaining alertness. These neurons project to structures in the diencephalon, including the thalamus and hypothalamus, and from there to the cerebral cortex. Alterations in alertness can be produced by focal lesions within the upper brainstem by directly damaging the ARAS.

• #1

  https://pure.mpg.de/pubman/faces/ViewItemOverviewPage.jsp?itemId=item_2551969

  Millions of patients worldwide experience a coma every year due to trauma, stroke, and other severe brain injuries, but the mechanisms by which patients emerge from coma are incompletely understood. […] A major reason for this gap in knowledge is the absence of an animal model of coma, which would provide a means to study both the pathogenesis of coma and the mechanisms that enable reemergence of consciousness. […] Here, we develop a rat coma model to systematically study the progression of rat brain function and behavior after coma. […] This is, to our knowledge, the first report of a rat coma model that enables multimodality studies of the mechanisms underlying coma pathogenesis and recovery following brainstem injury. […] Ongoing studies using optogenetics and calcium imaging will investigate the role of specific brainstem-thalamo-cortical circuits in the comatose brain, which will help elucidate the mechanisms that underlie coma emergence.

• #1 Coma – Wikipedia

  https://en.wikipedia.org/wiki/Coma

  A coma is a deep state of prolonged unconsciousness in which a person cannot be awakened, fails to respond normally to painful stimuli, light, or sound, lacks a normal sleep-wake cycle and does not initiate voluntary actions. […] The person may experience respiratory and circulatory problems due to the body’s inability to maintain normal bodily functions. […] Comas can be the result of natural causes, or can be medically induced, for example, during general anesthesia. […] Neurologically, consciousness is maintained by the activation of the cerebral cortex the gray matter that forms the brain’s outermost layer and by the reticular activating system (RAS), a structure in the brainstem. […] Injury to either or both of the cerebral cortex or the reticular activating system (RAS) is sufficient to cause a person to enter coma.

• #1 Prognosis and Therapy after Cardiac Arrest-Induced Coma | Journal of Ethics | American Medical Association

  https://journalofethics.ama-assn.org/article/prognosis-and-therapy-after-cardiac-arrest-induced-coma/2009-08

  Consciousness is defined as an awareness of self and environment, although the boundaries of consciousness and how to definitively determine its presence are still debated in the neuroscientific, bioethical, and philosophical communities. Coma is defined as unarousable unresponsiveness, or the absence of any psychologically understandable response to external stimulus or inner need. […] Coma is not a permanent state, and comatose patients who do not die begin to awaken within several weeks, regardless of the severity of the underlying brain injury. Some patients may open their eyes and demonstrate limited movement without ever regaining consciousness or attaining higher mental functioning. The term for this condition is persistent vegetative state, and these patients can survive for decades without ever improving neurologically.

• #1 Coma and Locked-In Syndrome: Detailed Comparison

  https://rehabmodalities.com/the-difference-between-coma-and-locked-in-syndrome/

  A coma is a state of deep unconsciousness in which a person is unresponsive to their environment and unable to wake up. […] Causes of a coma results from severe brain damage or dysfunction, often caused by factors like head injury, stroke, lack of oxygen (hypoxia), drug overdose, or an underlying medical condition. […] Often caused by severe brain injury, stroke, lack of oxygen, or other conditions affecting brain function. […] In locked-in syndrome, while cognitive functions remain intact, the brainstem damage impairs motor control and voluntary muscle movement, leading to the paralysis of almost all voluntary muscles except for those controlling eye movements. This condition results in the person being fully aware but unable to communicate or move, except through eye movements or blinking.

• #1 Coma: Types, Causes, Treatments, Prognosis

  https://www.webmd.com/brain/coma-types-causes-treatments-prognosis

  Oxygen is essential for brain function. Cardiac arrest causes a sudden cutoff of blood flow and oxygen to the brain, called hypoxia or anoxia. […] Infections of the central nervous system, such as meningitis or encephalitis, can also cause a coma. […] Substances that are normally found in the body can accumulate to toxic levels if the body fails to dispose of them correctly. […] Continuous seizures called status epilepticus can prevent the brain from recovering in between seizures. This will cause prolonged unconsciousness and coma.

• #1 Causes of brain dysfunction in acute coma: a cohort study of 1027 patients in the emergency department | Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine | Full Text

  https://sjtrem.biomedcentral.com/articles/10.1186/s13049-019-0669-4

  Coma of unknown etiology (CUE) is a major challenge in emergency medicine. CUE is caused by a wide variety of pathologies that require immediate and targeted treatment. […] The data from our cohort show that the spectrum of conditions underlying CUE is broad and may include a surprisingly high number of coincidences of multiple coma-explaining pathologies. This finding has not been reported so far. […] Thus, significant pathologies may be masked by initial findings and only appear at the end of the diagnostic work-up. Furthermore, even transient CUE showed a significant mortality, thus rendering GCS cutoffs for selection of high- and low-risk patients questionable. […] Taken together, our data advocate for a standardized diagnostic work-up that should be triggered by the emergency symptom CUE and not by any suspected diagnosis. This standardized routine should always be completed – even when initial coma-explaining diagnoses may seem evident.

• #1 Coma | Description, Causes, & Types | Britannica

  https://www.britannica.com/science/coma-pathology

  Common causes of metabolic coma include diabetes, excessive consumption of alcohol, and barbiturate poisoning. In diabetes, low insulin levels allow the buildup of ketones, breakdown products of fat tissue that destroy the osmotic balance in the brain, damaging brain cells. Ingestion of large quantities of alcohol over a short period can cause a coma that may be treated by gastric lavage (stomach pump) in its early stages; alcohol combined with barbiturates is a common cause of coma in suicide attempts. Large doses of barbiturates alone will also produce coma by suppressing cerebral blood flow, thus causing anoxia. Gastric lavage soon after the drug is ingested may remove a sufficient amount of the barbiturate to allow recovery. […] For most metabolic comas, the first step in treatment is to protect the brain cells and attempt to eliminate the cause of coma. Assisted ventilation is often necessary. In some psychiatric conditions, such as catatonic schizophrenia, a comalike state may also occur. Electroencephalography (EEG) can be used to detect signs of consciousness in patients who are unresponsive; research suggests that EEG recordings potentially can be used to predict whether a patient will emerge from coma.

• #1 What is a Coma? Duration, Recovery, and Brain Damage Risk

  https://brainfoundation.org.au/disorders/coma/

  Initial treatment will depend on the cause of the coma and will be directed at preventing further damage to the brain. […] Once stable and no longer in immediate danger then further treatment will be directed at maintaining the patients physical condition and preventing complications. […] The chances of someone recovering from a coma largely depend on the severity and cause of their brain injury, their age and how long theyve been in a coma. […] Patients can gradually come out of the coma, some progress to a vegetative state (aka unresponsive wakefulness syndrome) and others die. Some patients who have entered a vegetative state go on to regain a degree of awareness (see Minimally Conscious State). The likelihood of significant functional improvement for coma patients diminishes over time.

• #2 Coma – Wikipedia

  https://en.wikipedia.org/wiki/Coma

  A coma is a deep state of prolonged unconsciousness in which a person cannot be awakened, fails to respond normally to painful stimuli, light, or sound, lacks a normal sleep-wake cycle and does not initiate voluntary actions. […] The person may experience respiratory and circulatory problems due to the body’s inability to maintain normal bodily functions. […] Comas can be the result of natural causes, or can be medically induced, for example, during general anesthesia. […] Neurologically, consciousness is maintained by the activation of the cerebral cortex the gray matter that forms the brain’s outermost layer and by the reticular activating system (RAS), a structure in the brainstem. […] Injury to either or both of the cerebral cortex or the reticular activating system (RAS) is sufficient to cause a person to enter coma.

• #2 Coma | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/19750

  The accepted pathophysiology of a coma involves neuronal dysfunction from a decrease in the supply of glucose or oxygen to the brain. A myriad of etiologies may lead to essential substrate disruption with diffuse central nervous system (CNS) dysfunction and coma as the extreme clinical condition. For example, any clinical process that causes circulatory collapse or profound hypoxemia may manifest as a coma. As little as fifteen seconds of circulatory collapse will result in loss of consciousness. If the cause of the circulatory collapse is brief and promptly restored, such as from a simple faint, consciousness is regained. If hypotension or hypoxemia continues, the altered mental state continues, and secondary CNS damage may occur. Hypoglycemia is encountered frequently in clinical practice most often in the association of treatment for diabetes mellitus or as a complication of alcoholism. Electrolyte abnormalities such as hyponatremia or hypercalcemia may disrupt normal neuronal metabolism. The pathophysiology of other causes of metabolic coma is not clear but may involve false neurotransmitters as is suggested in hepatic encephalopathy. Global depression of neuronal functioning is the most common mechanism of coma in toxins and poisonings.

• #2 Stupor and coma in adults – UpToDate

  https://www.uptodate.com/contents/stupor-and-coma-in-adults

  Stupor and coma are clinical states in which patients have impaired responsiveness (or are unresponsive) to external stimulation and are either difficult to arouse or are unarousable. Coma is defined as „unarousable unresponsiveness”. […] An alteration in arousal represents an acute, life-threatening emergency, requiring prompt intervention for preservation of life and brain function. […] The ascending reticular activating system (ARAS) is a network of neurons originating in the tegmentum of the upper pons and midbrain, believed to be integral to inducing and maintaining alertness. These neurons project to structures in the diencephalon, including the thalamus and hypothalamus, and from there to the cerebral cortex. Alterations in alertness can be produced by focal lesions within the upper brainstem by directly damaging the ARAS.

• #2 Coma – Wikipedia

  https://en.wikipedia.org/wiki/Coma

  The cerebral cortex is composed of gray matter which consists of the nuclei of neurons, whereas the inner portion of the cerebrum is composed of white matter and is composed of the axons of neuron. […] The RAS has two tracts, the ascending and descending tract. […] The ascending tract, or ascending reticular activating system (ARAS), is made up of a system of acetylcholine-producing neurons, and works to arouse and wake up the brain. […] Any impairment in ARAS functioning, a neuronal dysfunction, along the arousal pathway stated directly above, prevents the body from being aware of its surroundings. […] Without the arousal and consciousness centers, the body cannot awaken, remaining in a comatose state. […] The severity and mode of onset of coma depends on the underlying cause. […] There are two main subdivisions of a coma: structural and diffuse neuronal.

• #2 Coma | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/19750

  Increased intracranial pressure is a frequent cause of coma. Since the brain is enclosed in the closed skull, conditions that increase intracranial pressure may impair cerebral perfusion. The equation that approximates this relationship is unforgiving CPP (cerebral perfusion pressure) = MAP (mean arterial pressure estimated as 1/3 systolic BP [blood pressure] + 2/3 diastolic BP) – ICP (intracranial pressure). As ICP approaches MAP, cerebral perfusion diminishes. It is essential to maintain CPP by reducing increased intracranial pressure while avoiding hypotension.

• #2 Acute Coma: Approach to Diagnosis and Management | RECAPEM

  https://recapem.com/acute-coma-approach-to-diagnosis-and-management/

  The initial impairment of consciousness with supratentorial mass lesions usually relates to lateral rather than downward displacement. […] Hydrocephalus develops because of the compression of the cerebral aqueduct. […] The neurologic deficit is almost always symmetrical. […] Tremor, asterixis, and multifocal myoclonus strongly suggest metabolic coma. […] The pupillary response is generally preserved. […] The presence of decerebrate or decorticate posturing has relatively little utility in prognostication until the underlying etiology is found. […] The practice of empirically administering a battery of potential antidotes to patients presenting in a coma is no longer recommended.

• #2 Stupor and coma in adults – UpToDate

  https://www.uptodate.com/contents/stupor-and-coma-in-adults/print

  The mechanism of coma in toxic, metabolic, and infectious etiologies and hypothermia is less well understood and to some extent is cause specific. A simplified explanation is that these conditions impair oxygen or substrate delivery, which in turn alters cerebral metabolism or interferes with neuronal excitability and/or synaptic function.

• #2 Diabetic coma pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Diabetic_coma_pathophysiology

  People with type 1 diabetes mellitus who must take insulin in full replacement doses are most vulnerable to episodes of hypoglycemia. […] Unconsciousness due to hypoglycemia can occur within 20 minutes to an hour after early symptoms and is not usually preceded by other illness or symptoms. […] Diabetic ketoacidosis (DKA), if it progresses and worsens without treatment, can eventually cause unconsciousness, from a combination of severe hyperglycemia, dehydration and shock, and exhaustion. […] Coma from NKHC occurs most often in patients who develop type 2 or steroid diabetes and have an impaired ability to recognize thirst and drink.

• #2 Azthena logo with the word Azthena

  https://www.news-medical.net/health/Nonketotic-Hyperosmolar-Coma.aspx

  Nonketotic hyperosmolar coma is a life threatening metabolic derangement that can develop in people with diabetes mellitus, usually due to illness, infection or failure to monitor blood glucose levels. […] A relative deficiency in insulin levels caused by mismanagement of diabetes causes a rise in blood sugar levels. This triggers the kidneys to remove some of the glucose through urination, causing dehydration and more concentrated or hyperosmolar blood. This concentrated blood begins to draw water form other organs such as the brain and kidneys.

• #2 Diabetic coma – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/diabetic-coma/symptoms-causes/syc-20371475

  A diabetic coma is a life-threatening disorder that causes unconsciousness. If you have diabetes, dangerously high blood sugar (hyperglycemia) or dangerously low blood sugar (hypoglycemia) can lead to a diabetic coma. […] Blood sugar that’s either too high or too low for too long may cause the following serious health problems, all of which can lead to a diabetic coma. […] Diabetic ketoacidosis is most common in people who have type 1 diabetes. But it can also occur in people who have type 2 diabetes or gestational diabetes. […] If it isn’t treated, this can lead to life-threatening dehydration and a diabetic coma. […] In severe cases, low blood sugar (hypoglycemia) may cause you to pass out. Low blood sugar can be caused by too much insulin or not enough food. Exercising too vigorously or drinking too much alcohol can have the same effect. […] If it is not treated, a diabetic coma can lead to permanent brain damage and death. […] High levels of ketones can lead to diabetic ketoacidosis, which can lead to coma.

• #2 Myxedema Coma or Crisis: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/123577-overview

  Myxedema coma occurs because of long-standing, undiagnosed or undertreated hypothyroidism. […] Although any of the causes of hypothyroidism can lead to myxedema coma, the most common is chronic autoimmune thyroiditis. It can also occur in patients who had a thyroidectomy or who underwent radioactive iodine therapy for hyperthyroidism. Rare causes of myxedema coma include secondary hypothyroidism and medications such as lithium and amiodarone. […] Given the importance of thyroid hormones in cell metabolism, long-standing hypothyroidism is associated with a reduced metabolic rate and decreased oxygen consumption, affecting all body systems. […] Consequently, myxedema coma can also result when a hypothyroidism-induced decrease in drug metabolism leads to overdosing of medications, including sedatives, hypnotics, and anesthetic agents.

• #2 Coma due to drug intoxication | MedLink Neurology

  https://www.medlink.com/articles/coma-due-to-drug-intoxication

  Baclofen. Baclofen is a GABA-analogue that interacts with GABA-ergic spinal interneurons in low doses. […] Barbiturates. At high concentrations barbiturates dissolve in lipid membranes and interfere with ionic transfer and calcium uptake by nerve cell membrane. […] Cocaine. Cocaine is a psychostimulant and local anesthetic, which is sniffed, injected, or smoked. […] Methamphetamine overdose. This causes delirium, tachycardia, hypertensive crisis, malignant hyperthermia, cardiac arrhythmia, myoclonus, seizures, myoglobinuria, shock, coma, and death. […] Drug-induced cerebrovascular disorders. Drug-induced cerebral vasculitis, often associated with drug abuse, is an example of complications that may be associated with a comatose state. […] Drugs producing hypoglycemia. Glucose is the only nutrient that brain cells can utilize in sufficient quantity to meet their energy requirements. […] Drugs producing hyponatremia. Several drugs produce hyponatremia, which can lead to coma.

• #2 Stupor and coma in adults – UpToDate

  https://www.uptodate.com/contents/stupor-and-coma-in-adults/print

  Stupor and coma are clinical states in which patients have impaired responsiveness (or are unresponsive) to external stimulation and are either difficult to arouse or are unarousable. Coma is defined as „unarousable unresponsiveness”. […] An alteration in arousal represents an acute, life-threatening emergency, requiring prompt intervention for preservation of life and brain function. […] The ascending reticular activating system (ARAS) is a network of neurons originating in the tegmentum of the upper pons and midbrain, believed to be integral to inducing and maintaining alertness. These neurons project to structures in the diencephalon, including the thalamus and hypothalamus, and from there to the cerebral cortex. Alterations in alertness can be produced by focal lesions within the upper brainstem by directly damaging the ARAS.

• #2 Prognosis and Therapy after Cardiac Arrest-Induced Coma | Journal of Ethics | American Medical Association

  https://journalofethics.ama-assn.org/article/prognosis-and-therapy-after-cardiac-arrest-induced-coma/2009-08

  The pathophysiology of hypoxic-ischemic cell death is that, as neurons are deprived of oxygen, the proteins and electrolytes necessary to maintain the membrane potentials are depleted, causing the cell to depolarize and the cell body to swell. The swelling results in irreversible damage to the cell’s contents, initiating cell autolysis. […] The precise mechanism by which cooling benefits patients is unknown, but it is thought to relate to decreased cerebral oxygen consumption, the inhibition of excitatory neurotransmitters, and a reduction in damaging free radicals and intracellular acidosis. […] Therapeutic hypothermia can provide real benefit to some patients and represents the first proven therapy to prevent brain damage after cardiac arrest.

Zobacz więcej