Coma


A coma is a prolonged state of deep 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. People in a coma often require extensive medical care to maintain their health and prevent complications such as pneumonia or blood clots. Coma patients exhibit a complete absence of wakefulness and are unable to consciously feel, speak or move. Comas can be the result of natural causes, or can be medically induced, for example, during general anesthesia.
Clinically, a coma can be defined as the consistent inability to follow a one-step command. For a patient to maintain consciousness, the components of wakefulness and awareness must be maintained. Wakefulness is a quantitative assessment of the degree of consciousness, whereas awareness is a qualitative assessment of the functions mediated by the cerebral cortex, including cognitive abilities such as attention, sensory perception, explicit memory, language, the execution of tasks, temporal and spatial orientation and reality judgment. 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, a structure in the brainstem.

Etymology

'Coma' comes from the Greek word κῶμα koma.

Signs and symptoms

General symptoms of a person in a comatose state are:
Many types of problems can cause a coma. Forty percent of comatose states result from drug poisoning. Certain drug use under certain conditions can damage or weaken the synaptic functioning in the ascending reticular activating system and keep the system from properly functioning to arouse the brain. 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. Given that drug poisoning is the cause for a large portion of patients in a coma, hospitals first test all comatose patients by observing pupil size and eye movement, through the vestibular–ocular reflex.
The second most common cause of coma, which makes up about 25% of cases, is lack of oxygen, generally resulting from cardiac arrest. The central nervous system requires a great deal of oxygen for its neurons. Oxygen deprivation in the brain, or cerebral hypoxia, causes sodium and calcium from outside of the neurons to decrease and intracellular calcium to increase, which harms neuron communication. Lack of oxygen in the brain also causes ATP exhaustion and cellular breakdown from cytoskeleton damage and nitric oxide production.
Twenty percent of comatose states result from an ischemic stroke, brain hemorrhage, or brain tumor. During a stroke, blood flow to part of the brain is restricted or blocked. An ischemic stroke, brain hemorrhage, or brain tumor may cause restriction of blood flow. Lack of blood to cells in the brain prevents oxygen from getting to the neurons, and consequently causes cells to become disrupted and die. As brain cells die, brain tissue continues to deteriorate, which may affect the functioning of the ARAS, causing unconsciousness and coma.
Comatose cases can also result from traumatic brain injury, excessive blood loss, malnutrition, hypothermia, hyperthermia, hyperammonemia, abnormal glucose levels, and many other biological disorders. Furthermore, studies show that 1 out of 8 patients with traumatic brain injury experience a comatose state.
Heart-related causes of coma include cardiac arrest, ventricular fibrillation, ventricular tachycardia, atrial fibrillation, myocardial infarction, heart failure, arrhythmia when severe, cardiogenic shock, myocarditis, and pericarditis. Respiratory arrest is the only lung condition to cause coma, but many different lung conditions can cause decreased level of consciousness, but do not reach coma.
Other causes of coma include severe or persistent seizures, kidney failure, liver failure, hyperglycemia, hypoglycemia, and infections involving the brain, like meningitis and encephalitis.

Pathophysiology

Injury to either or both of the cerebral cortex or the reticular activating system is sufficient to cause a person to enter coma.
The cerebral cortex is the outer layer of neural tissue of the cerebrum of the brain. 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. White matter is responsible for perception, relay of the sensory input via the thalamic pathway, and many other neurological functions, including complex thinking.
The RAS, on the other hand, is a more primitive structure in the brainstem which includes the reticular formation. The RAS has two tracts, the ascending and descending tract. The ascending tract, or ascending reticular activating system, is made up of a system of acetylcholine-producing neurons, and works to arouse and wake up the brain. Arousal of the brain begins from the RF, through the thalamus, and then finally to the cerebral cortex. 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. 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. For instance, severe hypoglycemia or hypercapnia are examples of a metabolic diffuse neuronal dysfunction. Hypoglycemia or hypercapnia initially cause mild agitation and confusion, but progress to obtundation, stupor, and finally, complete unconsciousness. In contrast, coma resulting from a severe traumatic brain injury or subarachnoid hemorrhage can be instantaneous. The mode of onset may therefore be indicative of the underlying cause.
Structural and diffuse causes of coma are not isolated from one another, as one can lead to the other in some situations. For instance, coma induced by a diffuse metabolic process, such as hypoglycemia, can result in a structural coma if it is not resolved. Another example is if cerebral edema, a diffuse dysfunction, leads to ischemia of the brainstem, a structural issue, due to the blockage of the circulation in the brain.

Diagnosis

Although diagnosis of coma is simple, investigating the underlying cause of onset can be rather challenging. As such, after gaining stabilization of the patient's airways, breathing and circulation various diagnostic tests, such as physical examinations and imaging tools are used to diagnose the underlying cause of the coma.
When an unconscious person enters a hospital, the hospital uses a series of diagnostic steps to identify the cause of unconsciousness. According to Young, the following steps should be taken when dealing with a patient possibly in a coma:
  1. Perform a general examination and medical history check
  2. Make sure the patient is in an actual comatose state and is not in a locked-in state or experiencing psychogenic unresponsiveness. Patients with locked-in syndrome present with voluntary movement of their eyes, whereas patients with psychogenic comas demonstrate active resistance to passive opening of the eyelids, with the eyelids closing abruptly and completely when the lifted upper eyelid is released.
  3. Find the site of the brain that may be causing coma and assess the severity of the coma with the Glasgow Coma Scale
  4. Take blood work to see if drugs were involved or if it was a result of hypoventilation/hyperventilation
  5. Check for levels of serum glucose, calcium, sodium, potassium, magnesium, phosphate, urea, and creatinine
  6. Perform brain scans to observe any abnormal brain functioning using either CT or MRI scans
  7. Continue to monitor brain waves and identify seizures of patient using EEGs

    Initial evaluation

In the initial assessment of coma, it is common to gauge the level of consciousness on the AVPU scale by spontaneously exhibiting actions and, assessing the patient's response to vocal and painful stimuli. More elaborate scales, such as the Glasgow Coma Scale, quantify an individual's reactions such as eye opening, movement and verbal response in order to indicate their extent of brain injury. The patient's score can vary from a score of 3 to 15.
In those with deep unconsciousness, there is a risk of asphyxiation as the control over the muscles in the face and throat is diminished. As a result, those presenting to a hospital with coma are typically assessed for this risk. If the risk of asphyxiation is deemed high, doctors may use various devices to safeguard the airway.

Imaging and testing

Imaging encompasses computed tomography scan of the brain, or MRI for example, and is performed to identify specific causes of the coma, such as hemorrhage in the brain or herniation of the brain structures. Special tests such as an EEG can also show a lot about the activity level of the cortex such as semantic processing, presence of seizures, and are important available tools not only for the assessment of the cortical activity but also for predicting the likelihood of the patient's awakening. In advanced cases, a technique called the Perturbational Complexity Index, which combines transcranial magnetic stimulation with EEG, has been developed to assess the capacity for consciousness by measuring the complexity of brain responses. PCI has shown promise in distinguishing between vegetative and minimally conscious states, even when behavioral signs are absent. The autonomous responses such as the skin conductance response may also provide further insight on the patient's emotional processing.
In the treatment of traumatic brain injury, there are four examination methods that have proved useful: skull x-ray, angiography, computed tomography, and magnetic resonance imaging. The skull x-ray can detect linear fractures, impression fractures and burst fractures. Angiography is used on rare occasions for TBIs i.e. when there is suspicion of an aneurysm, carotid sinus fistula, traumatic vascular occlusion, and vascular dissection. A CT can detect changes in density between the brain tissue and hemorrhages like subdural and intracerebral hemorrhages. MRIs are not the first choice in emergencies because of the long scanning times and because fractures cannot be detected as well as CT. MRIs are used for the imaging of soft tissues and lesions in the posterior fossa which cannot be found with the use of CT.