ANSWER
Unconsciousness is typically caused by a temporary or permanent impairment of the brainstem’s reticular activating system, both cerebral hemispheres, or bilateral thalami. The causes of an unconscious patient can be classified as either structural pathology of the brain or systemic pathology. This activity discusses the risk factors, evaluation, and management of unconscious patients, as well as the role of the interprofessional team in improving care for affected patients.

Objectives:

Describe the types and frequency of tests that should be performed on unconscious patients regularly.
Explain how to assess the unconscious patient.
Review the considerations for managing unconscious patients.
To improve the prompt and thorough delivery of care to unconscious patients, summarize the importance of improving care coordination, emphasizing communication between interprofessional medical teams.
Get free multiple-choice questions on this subject.
Go to:
Introduction
Consciousness is the awareness of oneself and one’s surroundings and the ability to respond to external stimuli.
[1] Impaired consciousness is diminished alertness, the ability to be aroused, or awareness of oneself and one’s surroundings. [2] A patient who appears unconscious at first can eventually manifest various clinical states. Some patients will regain full consciousness independently, while others require intensive management and complex diagnostic testing. Persistent unconsciousness can have reversible or permanent causes. The patient loses all protective reflexes and sensation responses while unconscious, making them vulnerable to aspiration and skin ulcers. [1]

A coma is a severe and sometimes persistent state of unconsciousness. According to Plum and Posner, a coma is “a state of unresponsiveness in which the patient lies with eyes closed and cannot be aroused to respond appropriately to stimuli, even with vigorous stimulation.” [3] Coma has also been objectively defined as a Glasgow coma scale (GCS) of less than 8.

Visit: Etiology
Unconsciousness is typically caused by a temporary or permanent impairment of the brainstem’s reticular activating system, both cerebral hemispheres, or bilateral thalamus. The three main mechanisms are structural brain lesions, diffuse neuronal dysfunction caused by a systemic pathology, and, in rare cases, psychiatric causes. [4]

Causes of Structure

These factors destroy an area entirely or cause indirect damage through compression or increased intracranial pressure. Increased intracranial pressure reduces cerebral blood flow and can cause tissue distortion and brain herniation. [2] [3]

Traumatic brain injury caused by a stroke (TBI)
Hemorrhages in the intracranial, epidural, and subdural spaces
Tumors of the intracranial cavity
Inflammation
Thrombosis of the veins
Hydrocephalus (acute)
Systemic Root Causes

Hypoglycemia
Hyperglycemia
Hyponatremia
Hypernatremia
Hypercalcemia
Seizures
Infections that affect the entire body (sepsis)
Meningitis
Encephalitis
Adrenaline rush
Pituitary apoplexy in conjunction with pituitary hormonal insufficiency
Abnormalities in the endocrine system
Coma from myxedema
Overdose of medications
Use of illegal drugs
Malignant neuroleptic syndrome
Excessive alcohol consumption
Encephalopathy of the liver
Uremia
Metals of a high melting point (lead poisoning)
Malaria
Fungemia (aspergillosis) (aspergillosis)
Herbicides
Gases (carbon monoxide) (carbon monoxide)
Anesthesia
Psychiatric Roots

Catatonia
Severe Depression
Conversion syndrome
Malingering
Visit: Epidemiology
The prevalence and relative causes of unconsciousness differ depending on the institution and patient population. A high-volume trauma center will almost certainly see many unconscious patients due to traumatic brain injury. The most common cause of non-traumatic coma was ischemic or hemorrhagic stroke (6–54%), followed by anoxia injury (3–42%), poisoning (1–39%), and metabolic (1–29%). Although stroke is the most common cause of non-traumatic coma, the total non-structural reasons (37 to 75%) outnumbered the structural causes (28 to 64%). [5]

The overall mortality rate is 25-87%. Stroke and anoxic coma had the highest mortality rates, ranging from 60 to 95% and 54 to 89%, respectively. Epilepsy and poisoning had the lowest mortality rates, both of which were less than 10%. [5]

Pathophysiology is an excellent place to start.
The pathophysiology of unconsciousness involves neuronal dysfunction caused by a decrease in the brain’s supply of glucose or oxygen.
[6] Coma may result from the direct destruction of arousal areas of the brain or from secondary damage caused by shifting intracranial structures, vascular compression, or increased intracranial pressure. [6]

The ascending reticular activating system in the brainstem is the anatomical seat of arousal. This system’s neurons originate in the dorsal pons and midbrain, connect in the thalamus, and project to various areas of the cortex. The cortex processes, integrate, and contextualizes the information presented, resulting in awareness. [4] To be aware of the environment, the reticular activating system receives impulses from the spinal cord and cortex. [1] [7]

The various causes of an unconscious patient can be divided into three major areas of the brain:

[3]

Damage/Effect on Both Hemispheres

Neuronal death and de-innervation of cortical regions result from extensive damage to the bilateral cerebral cortex, which can result from hypoxic-ischemic injury or brain trauma. Such patients lose the ability to process and respond to stimuli consciously. Systemic causes of coma fall into this category as well because they create an abnormal physiologic environment that inhibits neuronal function. If the systemic abnormality can be corrected, this pattern is usually reversible.

Injury to the Diencephalon (Thalamus)

Because the thalamus contains relay nuclei that direct afferent input to the cortex, bilateral thalamic lesions can mimic the outcome of bilateral cortical lesions.

Upper Brainstem Damage

The reticular activating system is located in the dorsal pons and midbrain. Lesions in this region can impair consciousness and cause a comatose state.

Supplementary data is used to create an unconscious patient’s history and physical history. It is preferable to question someone familiar with the patient’s recent history. [2] Knowing the patient’s medical history can help narrow down the diagnosis. Chronic cardiopulmonary, hepatic, or renal disease may have played a role. The use or availability of sedative or psychoactive drugs may indicate intoxication. [3]

The sudden onset of altered mental status suggests drug poisoning or acute structural lesions like trauma or stroke. Most metabolic disorders and compressive structural injuries develop gradually.

Neurological abnormalities or a headache in an unconscious patient indicate a structural lesion. Cranial nerve abnormalities may indicate involvement of the brainstem. Before unconsciousness or coma, metabolic disturbances usually cause diffuse forebrain dysfunction manifesting as confusion, delirium, or encephalopathy.

Go to: ABCs of Evaluation

The first step in evaluating an unconscious patient is looking for basic life signs. The American Heart Association suggests checking for a pulse and assessing airway patency and breathing pattern. Essential life support/advanced cardiovascular life support is indicated if the patient does not have a pulse or a regular breathing pattern.

The evaluation shifts to a detailed neurological examination for patients with a pulse and breathing normally. The purpose of the neurologic examination would be to determine the location and nature of the neurological lesion and the prognosis. The analysis is most beneficial when the patient is well-perfused, normothermic, normoglycemic, and free of neurologically active toxins or medications. [8]

Responsiveness

The first step is to assess reactivity using objective measures. Begin by speaking to the patient, then progress to light shaking, and finally to more intense mechanical stimulation. Sufficient supraorbital ridge, nail beds, or temporomandibular joint stimulation can cause pain without causing tissue damage. In the case of a focal spinal cord lesion, the response to these painful stimuli should be graded bilaterally. If these measures fail to elicit a response, vigorously pressing the examiner’s knuckles up and down the sternum should rouse any patient who is not profoundly unconscious. [3]

The best way to report the level of responsiveness is to specifically document how the patient reacted to the external stimulus provided for testing.

[3] Glasgow Coma Scale (GCS)[9] and Full Outline of Unresponsiveness (FOUR)[10] coma scales

[11] are available to assist in objectifying results for provider communication, trending, and prognosis. The physical exam should be performed in sequential order daily and meticulously documented. [8]

Pupils

The initial position and movement of the eyes should be recorded. In unconscious patients, nystagmus is uncommon, but it may indicate an irritating brain lesion or even occult seizure activity. The size of the pupils (as measured with a pupilometer) and reaction to light should be recorded. Because pupillary responses may be sluggish in unconscious patients, bright light should be used. [8]

The Cranial Nerves

A funduscopic exam, if available, may reveal significant findings such as papilledema or subhyaloid hemorrhage.

Oculocephalic or oculovestibular eye movement testing can provide information about cranial nerves III, IV, VI, and VIII. Patients with normal brainstem function should generally respond to these maneuvers. Oculovestibular testing using caloric stimulation should be performed in patients with a clear cervical spine.

The corneal reflex can be established by stimulating the cornea and watching for blinking. Stimulation should elicit both a direct and consensual response, indicating that the brainstem’s CN V and VII nuclei are functioning normally. To avoid corneal damage, it is advised to stimulate the cornea with drops of normal saline. Contact lenses will significantly reduce this reflex.

The gag and cough reflexes indicate that the brainstem’s cranial nerves IX and X nuclei are functioning normally.

[3]

Motor Ability

Muscular tone, movement patterns, and peripheral tendon reflexes are all used to assess motor function. Decerebrate or decorticate postures are dangerous.

Neuroimaging

Neuroimaging is extremely useful in evaluating the unconscious patient as an intracranial insult must be defined as soon as possible. The first study is usually a computed tomographic (CT) scan of the brain, revealing several key findings such as hemorrhage, infarction, space-occupying lesion, herniation, edema, and hydrocephalus. In cases where initial neuroimaging is inconclusive, magnetic resonance imaging is a worthwhile investigation. [2][4]

Laboratory Examination

Complete blood counts, serum electrolytes such as calcium and glucose, renal/hepatic functions, coagulation panel, and toxicology studies are all standard components of serum testing.

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Puncture of the Lumbar Spine

A lumbar puncture should be considered if the diagnosis is still unclear after the above tests or if a cerebral infection is suspected.

[2] If meningitis is suspected, the lumbar puncture procedure should not be used to delay the administration of empiric antibiotics and antivirals. Although the risk of herniation in patients with supratentorial mass effect is debatable, a CT scan should still be performed before lumbar puncture. [3] Opening pressure, cell count, gram stain, glucose, protein, culture, and viral testing should all be included in cerebrospinal fluid analysis. [8]

[9] Glasgow Coma Scale

Eye Reaction

4 = eyes open on their own
3 = eye-opening in terms of verbal command
2 = painfully awakening
1 = no startling revelations
Motor Reaction

6 = obey orders
5 = pain localization 4 = pain withdrawal 3 = flexion response to pain 2 = extension response to pain
One indicates that there is no motor response.
Verbal Reaction

5 = focused 4 = perplexed 3 = inappropriate words
2 = unintelligible sounds
1 denotes no verbal response
Four SCORE [10] [11]

Eye Reaction

4 = eyelids open or open, tracking or blinking in response to a command
3 = open eyelids but not tracking 2 = closed eyelids but open to a loud voice
1 = closed eyelids but open to pain
0 = closed eyelids due to pain
Motor Reaction

4 represents a thumbs-up, fist, or peace sign.
3 = pain localization
2 = pain-induced flexion
1 = pain extension response
0 = no pain response or generalized myoclonic status
Reflexes of the Brainstem

4 = present pupillary and corneal reflexes
3 = fixed and one pupil wide
2 = absent pupil or corneal reflexes 1 = absent pupil and corneal reflexes 0 = absent pupil, corneal, and cough reflexes
Respiration

4 = no intubation, regular breathing pattern
Three indicates that you are not intubated and have a Cheyne-Stokes breathing pattern.
2 = not intubated, breathing irregularly
1 = number of breaths taken more than the ventilator rate
0 = gusts at or below the ventilator rate
Please visit: Treatment / Management
Because the etiology of unconsciousness is frequently unknown initially, initial treatment paradigms are implemented before complete evaluation or diagnostics. Initial management principles for unconscious patients: [3][4]

Ensure adequate oxygenation
Continue to circulate
Maintain glucose control
Reduce intracranial pressure
Cessation of seizures
Infection treatment
Restore electrolyte and acid-base balance
Adjust your body temperature.
Thiamine should be given.
Think about specific antidotes (naloxone, flumazenil)
Agitation should be kept under control.
If the objectives mentioned above are met, management can be tailored based on diagnostic testing results. Patients who remain comatose despite initial interventions frequently require intensive care, such as an intensive care unit.

Visit Differential Diagnosis
The causes of unconsciousness have a wide range of differential diagnoses.

Some etiologies are apparent, such as anoxic brain injury, cerebrovascular accidents, seizures, and poisonings, but others have a wide range of severity. Hepatic encephalopathy, uremia, electrolyte abnormalities, and endocrine disorders are metabolic causes of coma. Infections, shock, temperature regulation problems, respiratory failure, or trauma can also cause a coma.

It is critical to distinguish organic causes of coma from disorders that cause psychiatric unresponsiveness, such as catatonia, severe depression, conversion disorder, and malingering, when examining an unconscious patient.

Active lid closure, reactive pupils, nystagmus, variable motor tone, eupnea or hyperventilation, the absence of pathologic reflexes, and a normal EEG are all signs of psychogenic unresponsiveness. [3] Structural brain disorders can also be confused with psychiatric illnesses. A psychogenic coma should be diagnosed after a thorough medical and neurological examination.

Visit: Prognosis
The prognosis of unconscious patients varies and is heavily influenced by the etiology, severity of brain injury, and individual patient factors. The GCS is used to evaluate outcomes in research. [15]

TBI has been the most researched cause of coma owing to its high prevalence and highly variable outcomes. TBI-related coma mortality is estimated to be between 40 and 50%. [16] Patient age, motor findings, neuro-ophthalmologic signs, secondary injuries, neuroimaging findings, and coma duration are all linked to outcomes. [3]

Patients who do not recover quickly from non-traumatic etiologies have an even worse prognosis than the TBI cohort. Non-traumatic coma mortality ranged from 25% to 87%. [5] [17] Patients who experienced a non-traumatic loss of consciousness that lasted more than six hours had a 76% one-month mortality rate. [18] Non-traumatic coma outcomes vary greatly depending on the cause. With adequate supportive care, non-traumatic unconsciousness caused by a depressant overdose, demyelinating disease, seizures, poisoning, or auto-immune encephalitis has an excellent prognosis. A large stroke or aneurysmal bleeding, as well as hypoxic-ischemic injury, has a poor prognosis. Neuro-ophthalmologic signs and motor function consistently predict long-term outcomes. [18]

Visit: Complications
Initial and permanent brain damage
Anoxia-related secondary brain injury
Aspiration pneumonia in a coma
Bowel and bladder dysfunction
Ulcers on the skin
Go to: Patient Education and Deterrence
Preventive measures are preferable to late interventions. Patients must be educated about their systemic illnesses and how to avoid complications. Some conditions that cause unconsciousness may allow for interventions before a coma develops. Closer monitoring and education of patients with poorly controlled diabetes may present a prevention opportunity. Early intervention and counseling for patients at risk of drug overdoses or illicit drug use intoxication will prevent many complications. Patients can be taught how to make decisions about their lives if they become unconscious.

Visit: Improving Healthcare Team Outcomes
Unconsciousness is caused by a temporary or permanent impairment of the bilateral forebrain (thalamus/cerebrum) or the brainstem’s reticular activating system. Because of the variety of causes for an unconscious patient, the condition is best managed by an interprofessional team that includes a neurologist, internist, intensivist, primary care provider, and neurosurgeon. A systematic assessment of the unconscious patient is advised. Because many cases of unconsciousness are reversible, managing unconscious patients necessitates a thorough history, patient evaluation, stabilizing treatment, and diagnostic testing, all taking place simultaneously. Patients who remain cold for an extended period have a mixed prognosis. Neuro-ophthalmologic responses and motor function are the most consistent predictive exam findings. [19] [Level 5]

To improve outcomes, the nurse assists the patient with absent protective reflexes, elimination, skin care, reorientation to the surroundings, and orientation for the family (problem-oriented approach).

[20] It is always necessary to communicate with the next of kin, family, or an appropriate advocate as soon as possible. When the prognosis is poor, these interprofessional discussions will include discussions about future treatment discontinuation and cardiopulmonary resuscitation. [2] Understanding the patient’s health status is critical before their presentation. Understanding that the prognosis in many comatose patients is poor and the presence of a pre-morbid condition will inform decisions about the escalation of care and the appropriateness of cardiopulmonary resuscitation. Decisions must be made following the patient’s stated preferences.
QUESTION
After studying the course materials located on Module 5: Lecture Materials & Resources page, answer the following:

Name some very important organs that are not vital organs.
List the functional description of all the normal vital organs, including today’s exceptions.
Is it possible to live without a vital organ? Why? Example?
Distinction between assisting or substituting vital organs. Bioethical analysis.
Do the following practices assist or substitute the vital organ? Why?
Dialysis
Respirator
Ventilator
Tracheotomy
CPR
Read and summarize ERD PART FIVE Introduction.
Unconscious state: Definition.
Clinical definitions of different states of unconsciousness: Compare and contrast
Benefit vs Burden: bioethical analysis.
Submission Instructions:
The submission is to be clear and concise and students will lose points for improper grammar, punctuation, and misspelling.
If references are used, please cite properly according to the current APA style.

Read and watch the lecture resources & materials below early in the week to help you respond to the discussion questions and to complete your assignment(s).

(Note: The citations below are provided for your research convenience. You should always cross reference the current APA guide for correct styling of citations and references in your academic work.)

Read
Ethical and Religious Directives (ERD) for Catholic Health Care Services (6th ed.). (2018).
PART FIVE: Introduction
PHI 3633 WK 5-A.pdfDownload PHI 3633 WK 5-A.pdf
PHI 3633 WK 5-B.pdfDownload PHI 3633 WK 5-B.pdf
DISTINCTION BETWEEN ASSISTING AND SUBSTITUTING VITAL ORGANS.pdfDownload DISTINCTION BETWEEN ASSISTING AND SUBSTITUTING VITAL ORGANS.pdf
Watch
Cioffi, A. (2019, March 9). BIO 603 VITAL ORGANS ASSIST SUBST 3 9 19 [Video file]. Retrieved fromBIO 603 VITAL ORGANS ASSIST SUBST 3 9 19

Cioffi, A. (2019, March 24). BIO 603 UNCONSCIOUS 3 23 19 [Video file]. Retrieved fromBIO 603 UNCONSCIOUS 3 23 19