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Care of unconscious patient
- 1. UNCONSCIOUSNESS Presented by: Aruna Shastri MSC NURSING FIRST YEAR
- 2. Consciousness • It is defined as a state of awareness of one’s self and of one’s environment , as well as a state of responsiveness to that environment or adaptation to the external milieu.
- 3. UNCONSCIOUSNESS • Unconsciousness is a condition in which the patient is unresponsive and unaware of environmental stimuli.
- 4. CLASSIFICATION OF ALTERED LEVELS OF CONSCIOUSNESS 1. Confusional States 2. Delirium 3. Obtundation 4. Stupor 5. Coma
- 5. 1. CONFUSIONAL STATES People who do not respond quickly with information about their name, location, and the time are considered "confused". A confused person may be bewildered, disoriented, and have difficulty following instructions. The person may have slow thinking and possible memory loss. This could be caused by sleep deprivation, malnutrition, allergies, environmental pollution, drugs (prescription and nonprescription), and infection.
- 6. DELIRIUM: person may be restless or agitated and exhibit a marked deficit in attention. OBTUNDATION: a person has a decreased interest in their surroundings, slowed responses, and sleepiness. STUPOR: only respond by grimacing or drawing away from painful stimuli.
- 7. COMA • State in which a patient is totally unaware of both self and external surroundings, and unable to respond meaningfully to external stimuli touch, pain,light etc. Do not have sleep-wake cycles. • Coma usually lasts a few days to a few weeks. After this time, some patients gradually come out of the coma, some progress to a vegetative state, and some die
- 8. PERSISTENT VEGETATIVE STATE • Can result from diffuse injury to the cerebral hemispheres of the brain without damage to the cerebellum and brainstem . • Opens eyes spontaneously • Does not follow commands • No intentional movements • Demonstrate sleep -wake cycle
- 9. LOCKED IN SYNDROME Patient is listening to you • Caused by damage to specific portions of the lower brain and brainstem with no damage to the upper brain. Eye opening is well sustained • Basic cognitive abilities are evident on examination • Mode of communication is eye movements or clinking of the upper eyelid
- 10. AKINETIC MUTISM • Patients are immobile and usually lie with their eyes closed. • Sleep wake cycles exists. • There is little or no vocalization. • Motor response to noxious stimuli is absent or minimal • Command following or verbalization can be elicited but occur infrequently
- 11. ETIOLOGY • INTRA CRANIAL CAUSES • EXTRA CRANIAL CAUSES METABOLIC CAUSES RESPIRATORY INSUFFICIENCY DECREASED CARDIAC OUTPUT ENDOCRINE CAUSES DRUG ABUSE (drug poisoning) TOXINS PSYCHOGENIC CAUSES
- 12. • INTRA CRANIAL CAUSES • Head Trauma • SAH • Cerebral infarction • Intra cranial Neoplasm • CNS infection • Epilepsy
- 13. EXTRA CRANIAL CAUSES METABOLIC CAUSES Hepatic failure Uraemia Hypoglycaemia/ Hyperglycaemia
- 15. DECREASED CARDIAC OUTPUT MI Cardiac arrthymia Antihypertensive Blood loss
- 17. • DRUG ABUSE (drug poisoning)- sedatives ,hypnotics, Anti- depressants, Anticonvulsants, Anaesthetic agents . • TOXINS –alcohol ,carbon monoxide
- 19. PATHOPHYSIOLOGY -UNCONSCIOUSNESS Conscious state depends on intact cerebral hemisphere and RAS Exposure to etiological causes diffusely affects the cerebral hemisphere and RAS Impairment of consciousness
- 23. Head-eyes Occulocephalic reflex Normal : eyes turn together to side opposite the turn of head Abnormal : the eye do not change in conjugate manner.
- 24. Pupils assessment Size • Unilateral ,dilated .fixed pupil- intracranial mass lesion • Bilateral ,dilated fixed pupil- hydrocephalus Diffuse cerebral swelling • pinpoint pupils- drugs and pontine hemorrhage
- 25. Head –ears Assessment Battle sign redness in mastoid process .
- 27. Head –Nose Assessment CSF –Rhinorrhoea
- 28. MOUTH • Look for alcohol smell or poisons smell. • Smell of ketones -Diabetic coma • Uriniferous odour-Uremic coma • Musty smell-Hepatic coma • See for tooth's missing to prevent aspiration
- 30. CVS • Rate and rhythm of pulse • Rapid or slow rate may be associated with the cerebral hypo perfusion • Examination of the heart by auscultation • Absent peripheral pulse-peripheral vascular disease
- 31. skin • cyanosis→ hypoxia • Macculohaemorrhagic rash → meningococcal infection, Staph. Endocarditis, Rocky mountain spotted fever • Bullous lesion of barbiturate intoxication
- 32. SKIN • Cherry-red spot→CO poisoning • Telangiectasia & hyperemia of face & conjunctiva- alcoholism • Multiple bruises,bleeding,CSF leakage from ear,nose,periorbital haemorrhage→skull fracture
- 33. SKIN • Puffy face→myxoedema • ↑sweating→hypoglycaemia, shock • Dry skin→diabetic ketosis, uraemia • ↓Skin turgour →dehydration
- 34. ABDOMEN • Assessment of abdominal girth is very important -Since distended will impair respiration. • Tenderness and guarding – trauma or rupture of abdominal viscera. • Enlargement of liver- hepatitis
- 35. GENITOURINARY • Watch for bladder fullness • Urine characteristics
- 36. EXTREMITY • Watch for any injection marks –May be drug addiction
- 37. EXTREMITY • Assess for tone ,muscle size in both side • Assess for any contracture • Asymmetric limb response ( hemi/ mono paresis) – Focal brain damage, e.g. Tumour ,trauma, hematoma, • Symmetric limb response, suggest metabolic encephalopathy and drug toxicity.
- 38. DIAGNOSIS • X-ray- Skull • CT scan – coma raised ICP and focal neurologic signs
- 39. • Lumbar puncture- Meningitis without coma, focal neurologic sign and fever.
- 40. • 12-lead study • TRANSCRANIAL DOPPLER: to rule out vasospasm. • PET : if available
- 41. MANAGEMENT • Medical management- • Emergency management • Symptomatic management • Surgical management • Nursing management
- 42. Medical Management • Emergency management Circulation Airway Breathing
- 43. SYMPTOMATIC TREATMENT • Wernicke’s encephalopathy :thiamine100 mg IV as an initial dose followed by 50 to 100 mg/day IM or IV until the patient is on a regular, balanced, diet. • Opioid Drug overdose :Naloxone 0.4 to 2 mg/dose IV/IM/subcutaneously. May repeat every 2 to 3 minutes as needed.
- 44. SYMPTOMATIC TREATMENT • Seizures : antiepileptic • Infection :antibiotics • Poison ingestion: gastric lavage • Fever:antipyretics,cold sponge • Pain:analgesics
- 45. SURGICAL MANAGEMENT • Hematomas – Surgical evacuation •Hemorrhage ,tumor, cerebral abscess-Surgical decompression/ Partial or total resection •Cerebral aneurysm - surgically clipping or endovascular coiling
- 47. • Risk for aspiration R/T unconscious state • Keep NPO until risk assessment is complete • Do not feed if airway protection or swallowing is compromised • Position to facilitate oral drainage • Follow precautions to prevent enteral feed aspiration
- 48. • Ineffective airway clearance R/T unconsciousness • Lateral or semi prone position • Frequent position change • Suctioning • Elevating head end • Chest auscultation • Maintain patency of ET tube or TT • Chest physiotherapy and postural drainage • Ventilator settings
- 49. Risk for injury R/T unconsciousness Check dressings and casts for constriction. To protect the patient from self-injury and dislodging of tubes, use padded side rails or wrap the patient’s hands in mitts Prevent injury from invasive lines and equipment Careful suctioning
- 50. Ensure that oxygenation is adequate Ensure that the bladder is not distended. Enclosed or floor-level specialty beds may be indicated. Protect the patient from hypothermia and hyperthermia. Lubricate the skin with oil or emollient lotion to prevent irritation due to rubbing against the sheet. Minimize environmental stimuli
- 51. Risk for hyperthermia R/T brain damage • Monitor the body temperature • Environmental temperature control • Prescribed antipyretic • Cold sponge • Hyperthermia blanket • Prevent shivering
- 52. Risk for hypothermia R/T brain damage Assess body temperature frequently Provide a warm environment through use of heat shield, space blanket, heat lights, or blankets. Work quickly when any wounds exposed.
- 53. • Altered nutrition less than body requirement R/T unconsciousness Assess the Hydration status by examining tissue turgor and mucous membranes, assessing intake and output trends, and analysing laboratory data. Meet the fluid needs initially by giving the required fluids intravenously. However, intravenous solutions (and blood transfusions) for patients with intracranial conditions must be administered slowly
- 54. If the patient does not recover quickly and sufficiently enough to take adequate fluids and calories by mouth, a feeding tube will be inserted for the administration of fluids and enteral feedings
- 55. • Altered bowel elimination R/T immobility Assess abdominal distention No. and consistency of stool Rectal examination Measure abdominal girth Listen bowel sounds Stool softener Adequate fluid intake Dietary fibers
- 56. • Risk for contracture R/T immobility Proper positioning Use splints ROM
- 57. • Self care deficit R/T immobility and unconsciousness • Provide basic hygiene care • Dress and groom patient • Provide nutrition • Provide for elimination needs of patient
- 58. • Impaired skin integrity R/T immobility and nutritional deficit • Assess the skin specially on bony prominences for any color and temperature change • Position change • Avoid dragging • Correct body positioning • Use comfort devices • Trochanter role • Air mattress • Back care
- 59. • Sensory / perceptual alterations R/T unconsciousness • Communicate with patient • Orienting patient • Involve family members
- 60. • Altered family process related to disease state • Clarify doubts • Involve in patient care • Encourage ventilation of feelings • Supporting in decision making • Support groups
- 61. MAINTENANCE OF CORNEAL INTEGRITY Artificial tears Eye irrigation Cold compress Eye patch
- 62. Complications Convulsions Bladder and bowel distention
- 63. Complications The Failure of multiple organs, such as the kidneys, lungs, and heart. Fluid electrolyte imbalance
- 64. Complications pneumonia or other life-threatening infections osteoporosis
- 65. Complications bed or pressure sores of the skin Deep vein thrombosis/pulmonary embolism
- 67. CONCLUSION • An unconscious patient fully depends on us for his recovery as such it is our responsibility to always think critically before intervening. • The more the knowledge we have the greater the difference we can make to life of unconscious patients.
- 68. REFERENCES • Ramamurthi,tendon,Textbook of Neurosurgery,Vol 2, Page no.1225-1229. • Michael Swash,John Oxbury,Clinical Neurology,Vol1,Page no.184-203. • Luck Mann’ s “medical and surgical nursing” 4th edition, Saunders's publications .page no.673-670. • Barker’s “neuro sciences nursing” 2nd edition, mosby publications. Page no.698-712. • Hickey ,Neurological and Neurosurgical Nursing,5th edition ,Page no:345-357 • Smelzer.SC,Bare,BG,Medical Surgical Nursing,Lipincot Williams& Williams 10th edition,Page no: 1851-1856. • http//www.google.com • http//www.wikipedia.com
Editor's Notes
- Consciousness describes the set of neural processes that allow an individual to perceive ,comprehend ,and act on internal and extrnal stimuli..consciouness can b only descriptively approached nt directly observed.
- There are many different causes of unconsciousness. The causes of unconsciousness may dictate the length of the coma and the prognosis . Unconsciousness occurs when the RAS is damaged or inhibited, thus affecting the normal arousal mechanism (Pemberton 2000). Intrinsic factors that affect the nervous system directly can be seen as primary causes. secondary causes most often involve other body systems compromising metabolic and endocrine homeostasis. Unconsciousness may be sudden, for example, following an acute head injury, or it may be gradual, for example, with the onset of poisoning or a deranged metabolism, as in hypoxia or hypoglycaemia. It is also important to remember that unconsciousness may be induced, for example, the use of anaesthetics for surgical or medical intervention. Another example of this is in critical care units, such as intensive care, where an anaesthetist will intervene and induce unconsciousness pharmacologically to allow for emergency intervention to stop a decline in a patient’s condition.
- Total paralysis below the level of nucleus of cranial nerve 3 with the ability to open eyes and follow commands with the eyes.No other motor movement is possible.this syndromre is often result of b/l ventral pontine lesions or b/l destruction of medulla oblongata.
- Consciousness is a function of the reticular formation (RF), which has its origins in the brainstem . The RF is a network of neurones that connect with the spinal cord, cerebellum, thalamus and hypothalamus. All sensory pathways link into the RF . The reticular activating system (RAS) is a feature of the RF and is responsible for arousal from sleep and maintaining consciousness . The RAS has a large number of projections that are linked to the cerebral cortex (Pemberton 2000) and are concerned with the arousal of the brain during sleep and wakefulness . Awareness is the result of the combined activity of the RF, RAS and higher cortical function. The two main identified parts of the RAS are the mesencephalon (upper pons and mid-brain) and the thalamus. Signals from specific parts of the thalamus initiate activity in specific parts of the cerebral cortex, as opposed to the diffuse flow of impulses from the mesencephalon that causes generalised cerebral activity (Pemberton 2000). This process of selection prevents the cerebral cortex from receiving too much information at once, thus possibly playing a part in directing an individual’s attention to specific mental activities.
- Altered LOC is not a disorder itself; rather, it is a function and symptom of multiple pathophysiologic phenomena. The cause may be neurologic (head injury, stroke), toxicologic (drug overdose,alcohol intoxication), or metabolic (hepatic or renal failure, diabetic ketoacidosis) A disruption in the basic functional units (neurons) or neurotransmitters faulty impulse transmission, impeding communication within the brain or from the brain to other parts of the body Clinical features, complications Intact anatomic structures of the brain are needed for proper function. The two hemispheres of the cerebrum must communicate,via an intact corpus callosum, and the lobes of the brain (frontal, parietal, temporal, and occipital) must communicate and coordinate their specific functions Impairments of consciousness indicates dysfunction of ARAS .Regardless of etiology ,the common pathophysiology for all impairments in arousability is either a reduction in the cerebral metabolism or a reduction in cerebral blood flow.
- The GCS forms a quick, objective and easily interpreted mode of neurological assessment, avoiding subjective terminology, such as ‘stupor’ and ‘semi-coma’. As it is the internationally agreed common language in neurological assessment, it is essential that it is completed accurately, and that any uncertainties are reported immediately (Hickey 2003b). The GCS meas\ures the degree of consciousness under three distinct categories, and each category is further subdivided and given a scoreSource: redOrbit (http://s.tt/13Se7)
- The oculocephalic test evaluates extraocular muscle movements (controlled by CNs III and VI). The examiner moves the patient’s head from side to side forcefully and quickly; in an abnormal response (an ominous sign), the eyes remain stationary. This exam is contraindicated in patients with suspected cervical spinal cord injury.The vestibulo-ocular reflex (VOR) is a reflex eye movement that stabilizes images on the retina during head movement by producing an eye movement in the direction opposite to head movement, thus preserving the image on the center of the visual field. For example, when the head moves to the right, the eyes move to the left, and vice versa. Since slight head movement is present all the time, the VOR is very important for stabilizing vision: patients whose VOR is impaired find it difficult to read using print, because they cannot stabilize the eyes during small head tremors. The VOR does not depend on visual input and works even in total darkness or when the eyes are closed. However, in the presence of light, the fixation reflex is also added to the movement. For instance, if the head is turned clockwise as seen from above, then excitatory impulses are sent from the semicircular canal on the right side via the vestibular nerve (cranial nerve VIII) through Scarpa's ganglion and end in the right vestibular nuclei in the brainstem. From this nuclei excitatory fibers cross to the left abducens nucleus. There they project and stimulate the lateral rectus of the left eye via the abducens nerve. In addition, by the medial longitudinal fasciculus andoculomotor nuclei, they activate the medial rectus muscles on the right eye. As a result, both eyes will turn counterclockwise. Furthermore, some neurons from the right vestibular nucleus directly stimulate the right medial rectus motoneurons, and inhibits the right abducens nucleus. In comatose patients, once it has been determined that the cervical spine is intact, a test of the vestibulo-ocular reflex can be performed by turning the head to one side. If the brainstem is intact, the eyes will move conjugately away from the direction of turning (as if still looking at the examiner rather than fixed straight ahead). This is how a doll's eyes would move. So having "doll's eyes" is a sign that a comatose patient's brainstem is still intact.
- Pupil evaluation includes assessment of pupil size, shape, and equality before and after exposure to light. Normally, pupils are equal in size and about 2 to 6 mm in diameter, but they may be as large as 9 mm. Also, the pupils may be pinpoint, small, large, or dilated. Normal pupil shape is round; variations include irregular, keyhole, and ovoid. (See Visualizing a keyhole pupil.) To assess the patient’s pupils, hold both eyelids open and shine a light into the eyes. The pupils should constrict immediately and equally bilaterally; after you remove the light, they should immediately dilate back to baseline. Document the response: Is it brisk, sluggish, nonreactive, or fixed? Immediately report any changes from baseline. In many cases, a change in pupillary response, such as unequal or dilated pupils, results from a progressive neurologic condition. Fixed and dilated pupils are an ominous sign that warrant immediate physician notification (unless the patient’s pupils have just been dilated chemically). For true changes in pupillary response, expect the physician to order further diagnostic tests, such as a CT scan.
- Assess the patient’s neurologic function frequently. Keep him in a supine position to decrease pressure on dural tears and to minimize CSF leakage. Avoid nasogastric intubation and nasopharyngeal suction, which may cause cerebral infection. Also, caution the patient against blowing his nose, which may worsen a dural tear. The patient may need skull X-rays and a CT scan to help confirm a basilar skull fracture and to evaluate the severity of the head injury. Typically, a basilar skull fracture and associated dural tears heal spontaneously within several days to weeks. However, if the patient has a large dural tear, a craniotomy may be necessary to repair the tear with a graft patch. If the injury was due to abuse, notify the appropriate authority in the facility. Patient teaching Explain all procedures and tests. Inform the patient with a basilar skull fracture that he’ll require bed rest for several days to weeks. Explain the need to avoid placing pressure on the brain tissue, and advise him on proper positioning. Also tell him to refrain from blowing his nose. If the injury was due to an accidental fall, advise the patient’s family to assess the household for safety hazards and remove precipitating factors such as throw rugs
- As with any patient, give top priority to assessing the ABCs—airway, breathing, and circulation. Ask yourself: Is the airway patent? If so, is the patient able to maintain it? Next, check vital signs: Are her respirations adequate? Are her vital signs stable? Is her blood pressure high enough to perfuse the brain and other vital organs? Be aware that current or progressive injury to the brain and brain stem may make vital signs unstable, but this situation can be complex: Although unstable vital signs can reduce neurologic response, brain injury itself may cause unstable vital signs. To appropriately assess the patient’s peak neurologic status, be sure to evaluate oxygenation and circulation. Ideally, you should conduct the neuro exam when the patient’s blood pressure, temperature, heart rate, and heart rhythm are normal. Be aware that a temporary decline in neurologic status caused by insufficient oxygenation or circulation still represents a neurologic change—and leads to permanent neurologic loss unless the underlying problem is corrected.
- People with type 1 diabetes mellitus who must take insulin in full replacement doses are most vulnerable to episodes of hypoglycemia. It is usually mild enough to reverse by eating or drinking carbohydrates, but blood glucose occasionally can fall fast enough and low enough to produce unconsciousness before hypoglycemia can be recognized and reversed. Hypoglycemia can be severe enough to cause unconsciousness during sleep 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. Twitching or convulsions may occur. A person unconscious from hypoglycemia is usually pale, has a rapid heart beat, and is soaked in sweat: all signs of theadrenaline response to hypoglycemia. So there is no set limit below which the brain shall have a seizure but speaking in broader terms usually the brain does not tolerate blood sugar below 60mg/dl and below 40 mg/dl most patients shall be symptomatic (either have a convulsion or be confused and obtunded.
- Microbial keratitis is a severe complication of corneal exposure in unconscious patients. Without meticulous care, corneal exposure and its sequelae, sometimes with devastating consequences, is very likely. We emphasise the need for maintenance of lid closure in at risk patients. Early referral in suspicious circumstances is essential. Fluorescein aided examination may enhance the care of such patients by detecting an epithelial defect before the onset of superimposed corneal infection. In cases with an epithelial defect, particularly with exacerbating risk factors, early lid closure with a lower lid traction suture may be appropriate, as lid closure is maintained, but examination of the eye is still possible.