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Care of Unconscious patient
PRESENTEDBY:ANJALIARORA
M.SC.NURSING-1ST YEAR
COLLEGEOFNURSING
INSTITUTEOFLIVERANDBILIARYSCIENCES
Introduction
 The concept of “Time is Brain” has to be borne in mind, and a work up quick,
investigations for the cause of coma, will make a physician’s effort highly successful
one.
 Wide tracking of causes, by repeated patient questioning to the relatives, at the
same time, carrying out the emergency measures to recover the patient’s health is
imperative.
Terminologies
consciousness
Awareness
Semi-coma
And
Coma
Stupor
Lethargy
Vegetative state
And
Brain Death
Alertness
And fainting
Terminologies
 Consciousness is the state or quality of awareness, or, of being aware of an external object
or something within oneself.
 Awareness means the ability to combine the data in memory to the surrounding internal and
external stimuli. When a person is conscious, he or she is awake, responds to his or her
surroundings and behaves meaningfully.
 Unconsciousness is an abnormal state in which a patient is totally unaware of both self and
external surroundings, and unable to respond meaningfully to external stimuli
 Alertness: open eyes spontaneously, responds to stimuli appropriately.
 Lethargy: slow to respond but appropriate response; opens eyes to stimuli; oriented.
 Stupor: aroused by and opens eyes to painful stimuli; never fully awake; confused; unclear
conversation.
 Semi-coma: move in response to painful stimuli; no conversation; protective
blinking/swallowing; pupillary reflex present.
Terminologies
 Coma: unresponsive except to severe pain; no protective reflexes;
fixed pupils; no voluntary movement.
 Fainting, also known as Syncope, is a loss of consciousness and
muscle strength characterized by a fast onset, short duration, and
spontaneous recovery.
 Vegetative state-It is a clinical condition of complete
unawareness of self and environment with damage to CNS. No
chance to recover back.
 Brain death, wherein the brain function has ceased irreversibly, is
the deepest level of unconsciousness. (Puumalainen 2005.)
Difference Between Vegetative
State And Brain Death
Vegetative State Brain Death
Introduction
unconsciousness
“Unconsciousness means lack of awareness”
Definition
“Unconsciousness is an abnormal state in which a patient is totally
unaware of both self and external surroundings, and unable to
respond meaningfully to external stimuli”
 It can range from a brief episode of fainting to the prolonged
unconsciousness of coma from which the person cannot be aroused,
even with vigorous external stimuli.
Unconsciousness
When someone’s consciousness level decreases his or her state of alertness gradually
declines from somnolence to coma.
 Lethargy
 Stuporous
 Semi-Coma
 Coma
 Vegetative state
 Brain death
Case You were called into
resuscitation, where a 55
year old man onto the ED
stretcher. You were called
after his family found him
unconscious at home. His
current GCS is 3…
My Approach
 The differential diagnosis of altered mental status is huge and can be
overwhelming in the face of an acutely ill, undifferentiated emergency
department patient.
 I try to sort through diagnoses based on how quickly they could kill the
patient and how quickly I can treat them.
What could kill my patient
immediately?
 Cardiac arrest
 Airway obstruction
 Breathing (oxygenation)
 The immediate first step is to check for a pulse. At the same time, nurses are getting
the patient on the monitor and getting a full set of vital signs. Next, I assess airway
patency and breathing pattern. If necessary, I start with basic, temporizing airway
maneuvers, such as positioning, oral/nasal airways,
 (I don’t want to intubate a patient who only requires D50W)
 The need for spine precautions should also be considered.
 NOTE: Don’t forget to get the history before they leave. The patient can’t
communicate and the medics almost always have important information.
What could kill my patient in the
next few minutes?
 Hypoglycemia
 Overdose
 Intracranial hypertension and herniation
 My first priority is getting the glucose checked, primarily so it does not get overlooked. Next,
I ask my nurses to start working on vascular access while I perform a rapid, focused primary
survey:
 Neuro: Pupils, eye movements, corneal reflex, moving all 4 extremities, reflexes, muscle
tone, any asymmetry?
 Signs of impending herniation: Hypertension, bradycardia, and irregular respirations
 Breathing pattern: Regular, Cheyne-Stokes, irregular, apnea?
Cont…
 Signs of shock: Cap refill, skin warm or cold?
 Abdo: Any obvious pain or masses?
 Trauma: Any clear signs of trauma?
 This all takes about 1 minute to complete. At this point, I am ready to consider if any
immediate therapeutic interventions are required:
 Hypoglycemia: D50W 1-2 amps IV
 Opioid toxidrome (or suspicion): Naloxone 0.2-0.4mg IV q2-3min. (If the patient is
stable, I will usually start with a much lower dose (0.04mg IV) to avoid precipitating rapid
opioid withdrawal.)
 Intubate; provide analgesia and sedation; elevated the head of the bed; respirate to a
target pCO2 of 35mmHg; Mannitol 0.5-1gram IV or 3% hypertonic saline 2-3ml/kg IV
bolus.
What could kill my patient in the
next 10 minutes?
 Still the ABCs
 Hypotension
 Anaphylaxis
 Hyperkalemia
 MI
 It’s easy to get lost in the differential. After the rapid primary survey and initial
interventions.
 I remind myself to reassess the ABCs. If a rapidly reversible cause hasn’t been
identified.
 I will start planning for a definitive airway. The next two diagnostic moves are an
ECG and the ultrasound machine.
Cont….
 The ECG will provide essential diagnostic information about ischemia, arrhythmias,
overdoses, and hyperkalemia. Ultrasound examination may be a RUSH exam for
hypotension, or a more focal exam based depending on the findings of the primary survey.
 Interventions at this point: For hypotension, I will start a fluid bolus or blood products
depending on the context.
 If there is any suspicion of anaphylaxis, I will give epinephrine 0.5mg IM.
 If there is reason to suspect hyperkalemia, or any bizarre appearing ECG, I will empirically
give calcium (2-3 amps of calcium gluconate IV).
What could kill my patient over
the next few hours?
 Sepsis
 Intracranial hemorrhage
 Alcohol Withdrawal
 Status epilepticus (presumably non-convulsive if I didn’t recognize it
immediately
 Metabolic problems (DKA, HHNK, hyponatremia, thyroid disorders,
adrenal disorders)
Cont..
 After the rapid assessment and management of immediate life threats, the next step is to
ensure the patient is adequately resuscitated before the inevitable trip to the CT scanner.
 A definitive airway should be in place before traveling to radiology.
 Any signs of shock are addressed with fluids, blood, and/or vasopressors. Blood work,
probably already drawn reflexively by the nurses, should be sent off. Unless there is a
clear alternative diagnosis, I start empiric antibiotics on everyone. (Acyclovir can also be
considered for herpes encephalitis.
 It is important to use all possible sources of information, including old charts, family,
friends, and I also specifically search for things like medic-alert bracelets, medication lists.
it is generally better to get therapy started empirically, and Finally, once the patient is
stabilized, I will get them to the CT scanner for images of their brain (and any other
organs indicated by the primary survey).
Causes of unconsciousness
Brain-derived causes
 Brain injury
 Cerebral hemorrhage
 Cerebral infarction
 Brain tumor
 Central nervous system infections
 Status epilepticus
Causes of unconsciousness
Systemic causes
 Metabolic causes (e.g. ketoacidosis, electrolyte imbalance)
 Cardiovascular causes (e.g. cardiac arrest, arrhythmia, shock)
 Hypoxic-ischemic (e.g. drowning, choking)
 Severe infections (e.g. sepsis)
 Pulmonary diseases (e.g. aspiration, foreign object in respiratory tract)
 Intoxication (e.g. carbon monoxide, medicines, ethanol, cyanide)
 Medicine disadvantage (e.g. opioids, antipsychotics)
Causes of unconsciousness
COMMON CAUSE-I
Interruption of energy substrate delivery
 Hypoxia
 Ischemia
 Hypoglycemia
Alteration of neurophysiologic responses of neuronal membranes
 Drug intoxication
 Alcohol intoxication
 Epilepsy
Causes of unconsciousness
COMMON CAUSE-II
Abnormalities of osmolarity
 Diabetic ketoacidosis
 Nonketotic hyperosmolar state
 Hyponatremia
 Hepatic encephalopathy
 Hypertensive encephalopathy
 Uremic encephalopathy
Causes of unconsciousness
COMMON CAUSE-III
 Hypercapnia
 Hypothyroidism
 Hypothermia
 Hyperthermia
Myxedema Coma: A New Look into an Old
Crisis
Journal of Thyroid Research
The term myxedema coma is a misnomer, and myxedema crisis may be an
apt term as quite a few patients are obtunded, rather than frankly
comatose. As the disease is rare and unrecognized, we only have a few
isolated case reports and case series, and there is a dearth of randomized
controlled trials in the field of myxedema crisis.
Myxedema (crisis) coma is a loss of brain function as a result of severe,
longstanding low level of thyroid hormone in the blood (hypothyroidism).
Myxedema com is considered a rare life-threatening complication
of hypothyroidism, and represents one of the more serious side of
of thyroid disease.
Causes of unconsciousness
Clinical Manifestations
 Alterations in LOC occur along a continuum, and the manifestations depend on where the
patient is on this continuum.
 As the patient's state of alertness and consciousness decreases, changes occur in the
pupillary response, eye opening response, verbal response, and motor response.
 However initial alterations in LOC may be reflected by subtle behavioural changes, such as
restlessness or increased anxiety.
 The pupils, normally round and quickly reactive to light, become sluggish (response is
slower); as the patient becomes comatose, the pupils become fixed (no response to light).
The patient in a coma does not open the eyes, respond verbally, or move the extremities in
response to a request to do so.
Pathophysiology
RAS - Anatomically located in Paramedian tegmental zone of dorsal midbrain-
responsible for arousal and cortical activation
Cerebral cortex-contains cognition centres determine content of consciousness
Impairment to cerebral cortex or brainstem can independently cause Coma:
vulnerable to Metabolic disturbances, toxins, Mechanical Injury
RAS is impaired, cerebral cortex cannot be aroused.
Assessment
 History Taking
 Physical Examination
 After the initial ABC assessment, the level of consciousness should be
formally measured and documented using the Glasgow Coma scale.
History
General Examination
Neuro Examination
Oculocephalic (doll’s Eye)
Response
Oculovestibular
(calorie testing ) Response
Glasgow coma scale
Glasgow coma scale
Glasgow coma scale
Glasgow coma scale
Pupillary
Reaction
Pupillary Reaction
Diagnostic findings
Common diagnostic procedures
Computed tomography (CT) scanning,
Magnetic resonance imaging (MRI),
Electroencephalography (EEG).
Less common procedures include
Positron emission tomography (PET)
Single photon Emission computed tomography (SPECT)
Laboratory tests include
Analysis of blood glucose
Electrolytes, serum ammonia, and liver function tests: blood urea nitrogen (BUN) levels; serum Osmolality:
calcium level; and partial thromboplastin and prothrombin time.
Other studies may be used to evaluate serum ketones, alcohol and drug concentrations, and arterial blood
gases.
Emergent Management
Initial assessment of the unconscious patient is done by
utilizing the ABCDE-protocol.
Assessment
Airway Management
Modified Mallampatti
Score
Breathing
Circulation
Medical Management
 The first priority of treatment for the patient with altered LOC is to obtain and maintain a
patent airway. The patient may be orally or nasally intubated, or a tracheostomy may be
performed. Until the ability of the patient to breathe is determined, a mechanical ventilator is
used to maintain adequate oxygenation and ventilation.
 The circulatory status (blood-pressure, heart rate) is monitored to ensure adequate perfusion
to the body and brain.
 An intravenous (IV) catheter is inserted to provide access for IV fluids and medications.
 Neurologic care focuses on the specific neurological pathology, if known.
 Nutritional support, via a feeding tube or a gastrostomy tube, is initiated as soon as possible.
In addition to measures designed to determine and treat the underlying causes of altered
LOC, other medical interventions are aimed at pharmacologic management and prevention of
complications.
Non-Invasive Hemodynamic
monitoring
Invasive Hemodynamic
monitoring
Resuscitation trolley
List of Emergency Drugs
Drug Calculation
Nursing
Management
of
Unconscious
Patient
Nursing Management
 Ineffective airway clearance related to inability to clear respiratory secretions as evidenced
by unclear lung sounds, unequal lung expansion, noisy respiration, presence of stridor, cyanosis
or pallor
 Ineffective cerebral tissue perfusion related to effects of increased ICP as evidenced by
papilledema, vomiting.
 Imbalanced nutrition – less than body temperature, related to inability to eat and swallow
as evidenced by weight and other nutritional parameters less than normal.
Nursing Management
 Altered oral mucous membrane related to ET insertion, absence of pharyngeal reflex,
inability to ingest fluid as evidenced by dryness, inflammation, crusting and halitosis.
 Self-care deficit-bathing, feeding, grooming, toileting related to unconscious state as
evidenced by unkempt and poorly nourished look, bed soiling.
 Ineffective thermoregulation related to damage to hypothalamic centre as evidenced by
persistent elevation of body temperature, warm and dry skin, flushed appearance of skin.
Nursing Management
 Risk for complications – pressure sore, contractures, DVT, hypostatic pneumonia,
constipation – related to immobility.
 Risk of injury related to unconscious state.
 Risk for fluid volume deficit related to inability to ingest fluids, dehydration from osmotic
diuretics.
 Interrupted family process related to chronic illness of a family member as evidenced by
anger, grief, non-participation in client care.
Nursing Documentation
Points to remember
I. Put air way if Pt. is unconscious.
II. Tracheostomy – if air way obstruction.
III. Suction equipment available.
IV. Assess breath sound 1-2 hourly.
V. Never give fluid / food to shallow.
VI. Lateral position.
VII. Perineal care.
VIII. Examine abdomen for distention.
IX. Involve family in care (general wards).
Complications
 Skin: - Pressure sore, laceration.
 Respiratory: - pneumonia, pulmonary Embolism.
 C.V. system : - DVT, postural hypotension, thromboembolism.
 G.I. system: - Paralytic ileus, constipation, distention.
 Urological: - UTI
 Musculoskeletal: - Contracture, dystrophy, weakness.
 Neurological: - Foot drop.
 Psychological: - Anxiety, depression.
Research article
Continuous EEG Monitoring Predicts a Clinically Meaningful
Recovery Among Adult Inpatients.
Continuous EEG findings can be used to prognosticate survival and functional
recovery, and provide guidance in establishing goals of care.
Research articleHidden brain activity revealed in people with coma
Hospital patients who appear unresponsive after commands show evidence of brain
activity. Fifteen per cent of hospital patients with severe brain injuries exhibited
cognitive activity in response to commands — even though they did not react visibly.
Jan Claassen at Columbia University in New York and his colleagues studied 104
‘clinically unresponsive’ patients whose brains had been damaged by a stroke or other
trauma. None showed a visible response to verbal instructions; some were in a coma.
The researchers used a technique called electroencephalography (EEG) to study
electrical activity in the patients’ brains. When asked to move one hand, 15% of
patients showed brain patterns similar to those of healthy volunteers responding to the
same instructions. A year after their injury, 44% of patients whose brains responded to
commands could look after themselves for at least 8 hours, compared with only 14%
of those whose brains did not respond. Larger trials are needed to test the value of
EEG for prognosis, the authors say.
Summary
Conclusion
“Time is Brain”, an earliest intervention will
save the patient’s brain and life, to a great
extent.

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Care of unconscious patient

  • 1. Care of Unconscious patient PRESENTEDBY:ANJALIARORA M.SC.NURSING-1ST YEAR COLLEGEOFNURSING INSTITUTEOFLIVERANDBILIARYSCIENCES
  • 2. Introduction  The concept of “Time is Brain” has to be borne in mind, and a work up quick, investigations for the cause of coma, will make a physician’s effort highly successful one.  Wide tracking of causes, by repeated patient questioning to the relatives, at the same time, carrying out the emergency measures to recover the patient’s health is imperative.
  • 3.
  • 5. Terminologies  Consciousness is the state or quality of awareness, or, of being aware of an external object or something within oneself.  Awareness means the ability to combine the data in memory to the surrounding internal and external stimuli. When a person is conscious, he or she is awake, responds to his or her surroundings and behaves meaningfully.  Unconsciousness is an abnormal state in which a patient is totally unaware of both self and external surroundings, and unable to respond meaningfully to external stimuli  Alertness: open eyes spontaneously, responds to stimuli appropriately.  Lethargy: slow to respond but appropriate response; opens eyes to stimuli; oriented.  Stupor: aroused by and opens eyes to painful stimuli; never fully awake; confused; unclear conversation.  Semi-coma: move in response to painful stimuli; no conversation; protective blinking/swallowing; pupillary reflex present.
  • 6. Terminologies  Coma: unresponsive except to severe pain; no protective reflexes; fixed pupils; no voluntary movement.  Fainting, also known as Syncope, is a loss of consciousness and muscle strength characterized by a fast onset, short duration, and spontaneous recovery.  Vegetative state-It is a clinical condition of complete unawareness of self and environment with damage to CNS. No chance to recover back.  Brain death, wherein the brain function has ceased irreversibly, is the deepest level of unconsciousness. (Puumalainen 2005.)
  • 7. Difference Between Vegetative State And Brain Death Vegetative State Brain Death
  • 9.
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  • 13. Definition “Unconsciousness is an abnormal state in which a patient is totally unaware of both self and external surroundings, and unable to respond meaningfully to external stimuli”  It can range from a brief episode of fainting to the prolonged unconsciousness of coma from which the person cannot be aroused, even with vigorous external stimuli.
  • 14. Unconsciousness When someone’s consciousness level decreases his or her state of alertness gradually declines from somnolence to coma.  Lethargy  Stuporous  Semi-Coma  Coma  Vegetative state  Brain death
  • 15. Case You were called into resuscitation, where a 55 year old man onto the ED stretcher. You were called after his family found him unconscious at home. His current GCS is 3…
  • 16. My Approach  The differential diagnosis of altered mental status is huge and can be overwhelming in the face of an acutely ill, undifferentiated emergency department patient.  I try to sort through diagnoses based on how quickly they could kill the patient and how quickly I can treat them.
  • 17. What could kill my patient immediately?  Cardiac arrest  Airway obstruction  Breathing (oxygenation)  The immediate first step is to check for a pulse. At the same time, nurses are getting the patient on the monitor and getting a full set of vital signs. Next, I assess airway patency and breathing pattern. If necessary, I start with basic, temporizing airway maneuvers, such as positioning, oral/nasal airways,  (I don’t want to intubate a patient who only requires D50W)  The need for spine precautions should also be considered.  NOTE: Don’t forget to get the history before they leave. The patient can’t communicate and the medics almost always have important information.
  • 18. What could kill my patient in the next few minutes?  Hypoglycemia  Overdose  Intracranial hypertension and herniation  My first priority is getting the glucose checked, primarily so it does not get overlooked. Next, I ask my nurses to start working on vascular access while I perform a rapid, focused primary survey:  Neuro: Pupils, eye movements, corneal reflex, moving all 4 extremities, reflexes, muscle tone, any asymmetry?  Signs of impending herniation: Hypertension, bradycardia, and irregular respirations  Breathing pattern: Regular, Cheyne-Stokes, irregular, apnea?
  • 19. Cont…  Signs of shock: Cap refill, skin warm or cold?  Abdo: Any obvious pain or masses?  Trauma: Any clear signs of trauma?  This all takes about 1 minute to complete. At this point, I am ready to consider if any immediate therapeutic interventions are required:  Hypoglycemia: D50W 1-2 amps IV  Opioid toxidrome (or suspicion): Naloxone 0.2-0.4mg IV q2-3min. (If the patient is stable, I will usually start with a much lower dose (0.04mg IV) to avoid precipitating rapid opioid withdrawal.)  Intubate; provide analgesia and sedation; elevated the head of the bed; respirate to a target pCO2 of 35mmHg; Mannitol 0.5-1gram IV or 3% hypertonic saline 2-3ml/kg IV bolus.
  • 20. What could kill my patient in the next 10 minutes?  Still the ABCs  Hypotension  Anaphylaxis  Hyperkalemia  MI  It’s easy to get lost in the differential. After the rapid primary survey and initial interventions.  I remind myself to reassess the ABCs. If a rapidly reversible cause hasn’t been identified.  I will start planning for a definitive airway. The next two diagnostic moves are an ECG and the ultrasound machine.
  • 21. Cont….  The ECG will provide essential diagnostic information about ischemia, arrhythmias, overdoses, and hyperkalemia. Ultrasound examination may be a RUSH exam for hypotension, or a more focal exam based depending on the findings of the primary survey.  Interventions at this point: For hypotension, I will start a fluid bolus or blood products depending on the context.  If there is any suspicion of anaphylaxis, I will give epinephrine 0.5mg IM.  If there is reason to suspect hyperkalemia, or any bizarre appearing ECG, I will empirically give calcium (2-3 amps of calcium gluconate IV).
  • 22. What could kill my patient over the next few hours?  Sepsis  Intracranial hemorrhage  Alcohol Withdrawal  Status epilepticus (presumably non-convulsive if I didn’t recognize it immediately  Metabolic problems (DKA, HHNK, hyponatremia, thyroid disorders, adrenal disorders)
  • 23. Cont..  After the rapid assessment and management of immediate life threats, the next step is to ensure the patient is adequately resuscitated before the inevitable trip to the CT scanner.  A definitive airway should be in place before traveling to radiology.  Any signs of shock are addressed with fluids, blood, and/or vasopressors. Blood work, probably already drawn reflexively by the nurses, should be sent off. Unless there is a clear alternative diagnosis, I start empiric antibiotics on everyone. (Acyclovir can also be considered for herpes encephalitis.  It is important to use all possible sources of information, including old charts, family, friends, and I also specifically search for things like medic-alert bracelets, medication lists. it is generally better to get therapy started empirically, and Finally, once the patient is stabilized, I will get them to the CT scanner for images of their brain (and any other organs indicated by the primary survey).
  • 24. Causes of unconsciousness Brain-derived causes  Brain injury  Cerebral hemorrhage  Cerebral infarction  Brain tumor  Central nervous system infections  Status epilepticus
  • 25. Causes of unconsciousness Systemic causes  Metabolic causes (e.g. ketoacidosis, electrolyte imbalance)  Cardiovascular causes (e.g. cardiac arrest, arrhythmia, shock)  Hypoxic-ischemic (e.g. drowning, choking)  Severe infections (e.g. sepsis)  Pulmonary diseases (e.g. aspiration, foreign object in respiratory tract)  Intoxication (e.g. carbon monoxide, medicines, ethanol, cyanide)  Medicine disadvantage (e.g. opioids, antipsychotics)
  • 26. Causes of unconsciousness COMMON CAUSE-I Interruption of energy substrate delivery  Hypoxia  Ischemia  Hypoglycemia Alteration of neurophysiologic responses of neuronal membranes  Drug intoxication  Alcohol intoxication  Epilepsy
  • 27. Causes of unconsciousness COMMON CAUSE-II Abnormalities of osmolarity  Diabetic ketoacidosis  Nonketotic hyperosmolar state  Hyponatremia  Hepatic encephalopathy  Hypertensive encephalopathy  Uremic encephalopathy
  • 28. Causes of unconsciousness COMMON CAUSE-III  Hypercapnia  Hypothyroidism  Hypothermia  Hyperthermia
  • 29. Myxedema Coma: A New Look into an Old Crisis Journal of Thyroid Research The term myxedema coma is a misnomer, and myxedema crisis may be an apt term as quite a few patients are obtunded, rather than frankly comatose. As the disease is rare and unrecognized, we only have a few isolated case reports and case series, and there is a dearth of randomized controlled trials in the field of myxedema crisis. Myxedema (crisis) coma is a loss of brain function as a result of severe, longstanding low level of thyroid hormone in the blood (hypothyroidism). Myxedema com is considered a rare life-threatening complication of hypothyroidism, and represents one of the more serious side of of thyroid disease.
  • 31. Clinical Manifestations  Alterations in LOC occur along a continuum, and the manifestations depend on where the patient is on this continuum.  As the patient's state of alertness and consciousness decreases, changes occur in the pupillary response, eye opening response, verbal response, and motor response.  However initial alterations in LOC may be reflected by subtle behavioural changes, such as restlessness or increased anxiety.  The pupils, normally round and quickly reactive to light, become sluggish (response is slower); as the patient becomes comatose, the pupils become fixed (no response to light). The patient in a coma does not open the eyes, respond verbally, or move the extremities in response to a request to do so.
  • 32. Pathophysiology RAS - Anatomically located in Paramedian tegmental zone of dorsal midbrain- responsible for arousal and cortical activation Cerebral cortex-contains cognition centres determine content of consciousness Impairment to cerebral cortex or brainstem can independently cause Coma: vulnerable to Metabolic disturbances, toxins, Mechanical Injury RAS is impaired, cerebral cortex cannot be aroused.
  • 33. Assessment  History Taking  Physical Examination  After the initial ABC assessment, the level of consciousness should be formally measured and documented using the Glasgow Coma scale.
  • 42.
  • 46. Diagnostic findings Common diagnostic procedures Computed tomography (CT) scanning, Magnetic resonance imaging (MRI), Electroencephalography (EEG). Less common procedures include Positron emission tomography (PET) Single photon Emission computed tomography (SPECT) Laboratory tests include Analysis of blood glucose Electrolytes, serum ammonia, and liver function tests: blood urea nitrogen (BUN) levels; serum Osmolality: calcium level; and partial thromboplastin and prothrombin time. Other studies may be used to evaluate serum ketones, alcohol and drug concentrations, and arterial blood gases.
  • 47. Emergent Management Initial assessment of the unconscious patient is done by utilizing the ABCDE-protocol.
  • 53. Medical Management  The first priority of treatment for the patient with altered LOC is to obtain and maintain a patent airway. The patient may be orally or nasally intubated, or a tracheostomy may be performed. Until the ability of the patient to breathe is determined, a mechanical ventilator is used to maintain adequate oxygenation and ventilation.  The circulatory status (blood-pressure, heart rate) is monitored to ensure adequate perfusion to the body and brain.  An intravenous (IV) catheter is inserted to provide access for IV fluids and medications.  Neurologic care focuses on the specific neurological pathology, if known.  Nutritional support, via a feeding tube or a gastrostomy tube, is initiated as soon as possible. In addition to measures designed to determine and treat the underlying causes of altered LOC, other medical interventions are aimed at pharmacologic management and prevention of complications.
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  • 71. Nursing Management  Ineffective airway clearance related to inability to clear respiratory secretions as evidenced by unclear lung sounds, unequal lung expansion, noisy respiration, presence of stridor, cyanosis or pallor  Ineffective cerebral tissue perfusion related to effects of increased ICP as evidenced by papilledema, vomiting.  Imbalanced nutrition – less than body temperature, related to inability to eat and swallow as evidenced by weight and other nutritional parameters less than normal.
  • 72. Nursing Management  Altered oral mucous membrane related to ET insertion, absence of pharyngeal reflex, inability to ingest fluid as evidenced by dryness, inflammation, crusting and halitosis.  Self-care deficit-bathing, feeding, grooming, toileting related to unconscious state as evidenced by unkempt and poorly nourished look, bed soiling.  Ineffective thermoregulation related to damage to hypothalamic centre as evidenced by persistent elevation of body temperature, warm and dry skin, flushed appearance of skin.
  • 73. Nursing Management  Risk for complications – pressure sore, contractures, DVT, hypostatic pneumonia, constipation – related to immobility.  Risk of injury related to unconscious state.  Risk for fluid volume deficit related to inability to ingest fluids, dehydration from osmotic diuretics.  Interrupted family process related to chronic illness of a family member as evidenced by anger, grief, non-participation in client care.
  • 75. Points to remember I. Put air way if Pt. is unconscious. II. Tracheostomy – if air way obstruction. III. Suction equipment available. IV. Assess breath sound 1-2 hourly. V. Never give fluid / food to shallow. VI. Lateral position. VII. Perineal care. VIII. Examine abdomen for distention. IX. Involve family in care (general wards).
  • 76. Complications  Skin: - Pressure sore, laceration.  Respiratory: - pneumonia, pulmonary Embolism.  C.V. system : - DVT, postural hypotension, thromboembolism.  G.I. system: - Paralytic ileus, constipation, distention.  Urological: - UTI  Musculoskeletal: - Contracture, dystrophy, weakness.  Neurological: - Foot drop.  Psychological: - Anxiety, depression.
  • 77. Research article Continuous EEG Monitoring Predicts a Clinically Meaningful Recovery Among Adult Inpatients. Continuous EEG findings can be used to prognosticate survival and functional recovery, and provide guidance in establishing goals of care.
  • 78. Research articleHidden brain activity revealed in people with coma Hospital patients who appear unresponsive after commands show evidence of brain activity. Fifteen per cent of hospital patients with severe brain injuries exhibited cognitive activity in response to commands — even though they did not react visibly. Jan Claassen at Columbia University in New York and his colleagues studied 104 ‘clinically unresponsive’ patients whose brains had been damaged by a stroke or other trauma. None showed a visible response to verbal instructions; some were in a coma. The researchers used a technique called electroencephalography (EEG) to study electrical activity in the patients’ brains. When asked to move one hand, 15% of patients showed brain patterns similar to those of healthy volunteers responding to the same instructions. A year after their injury, 44% of patients whose brains responded to commands could look after themselves for at least 8 hours, compared with only 14% of those whose brains did not respond. Larger trials are needed to test the value of EEG for prognosis, the authors say.
  • 80. Conclusion “Time is Brain”, an earliest intervention will save the patient’s brain and life, to a great extent.