The document provides an outline for approaching patients in a coma state, beginning with initial assessment of airway, breathing, and circulation. It discusses anatomy of consciousness and conditions that mimic coma such as persistent vegetative state. Common causes of coma including traumatic brain injury, stroke, and drug overdose are reviewed. The summary describes key components of examination such as vital signs, neurological assessment including brainstem reflexes, and initial investigations and management priorities like airway protection and monitoring of ICP.
👉 Amritsar Call Girls 👉📞 8725944379 👉📞 Just📲 Call Ruhi Call Girl Near Me Amri...
Approach to Coma.pptx
1. APPROACH TO COMA
Presenter :- Dr. Wondwosen M. (R1)
Moderator:- Dr. Desalegn Y. (Assistant Professor & Consultant Neuologist)
Arsi University
Dep’t Of Internal Medicine
1st August, 2023
2. OUT LINE
Introduction
Anatomy of Consciousness
Coma Mimics
Causes of Unconsciousness
Approaches to Unconscious Patients
Investigations
Management
Prognosis
References
3. Introduction
• Coma is among the most common neurologic emergencies encountered in
general medicine and requires an organized approach
• Consciousness: a state of awareness of self and Environment
Has two domains:
Arousal ( Level of consciousness)
• sustained by deep brainstem and medial thalamic structures.
Cognition (Content of consciousness)
• through integrity of the cerebral cortex and its subcortical structures
• A full function of consciousness (arousal) requires the stimulation of the caudal
brainstem reticular activating system (RAS) to the cerebral cortices
4. Introduction
• Levels of consciousness are classified into four levels, these being alert, drowsy,
stupor, and coma
• Drowsiness simulates light sleep and is characterized by easy arousal and the
continuation of alertness for a brief period
• Stupor refers to a state of near unresponsiveness that needs strenuous or
repeated stimulus to elicit a response
• Coma is a deep sleep like state with eyes closed, from which the patient cannot
be aroused, failure in responding to external stimuli,incapability in responding to
inner needs, and incompetence of interaction with the environment
5. Anatomy of Consciousness
• Arousal requires the interplay of both: ARAS and The cerebral hemispheres
• The RAS consists of multiple neuronal
networks, including the locus coeruleus,
raphe nuclei, posterior
tuberomammillary hypothalamus, and
pedunculopontine tegmentum, linking
the brain stem to the cortex
6. Coma Mimics
• There are also Several conditions that render patients unresponsive and
simulate coma :-
– Persistent vegetative state
– Minimal conscious state
– Locked in syndrome
7. Persistent Vegetative State
Unresponsiveness wakefulness syndrome
Patients have lost cognitive neurological function but retain vegetative
Patients are awake but unaware
They display no speech, comprehension, or purposeful movement
Yawning, sneezing, bruxism, and occasional meaningless smiles may occur
Display no interactive behavior and no ability to express emotion
The pathology invariably entails massive bilateral hemispheric damage with a
spared and intact brainstem
8. Minimal Conscious State
• Criteria for a diagnosis of MCS include:
following simple commands
responding with verbal or gestural yes/no answers
Understandable verbalization, and purposeful behavior
• Patients recovering at better rates than those in PVS
• Intermittent, behavioral evidence of awareness of self or environment
9. Locked in syndrome
Ventral brainstem destruction sparing the RAS renders the patient mute and
quadriplegic but not comatose
Patient is awake but speechless and motionless, with little response to stimuli
Lesion usually involves the mid pons and results in paralysis of facial movement and
horizontal gaze
There is preservation of vertical eye movements and the patient may be able to blink
Sensory pathways, hearing and vision are largely spared
The principal cause of locked-in syndrome is brainstem stroke (86%), but it may
also occur after trauma (14%)
10. Table: Behaioral state confused with Coma
Abulia severe aphaty, patient neither speaks no
moves spontaneously
Bilateral frontal medial
Pseudocoma Feigned coma
11. Brain Death
• Brain death is a condition in which systemic circulation is preserved but complete
and irreversible loss of cerebral and brainstem function
• Common causes : cerebral anoxia, ICH, aneurysmal SAH and TBI
• The diagnosis of brain death should ideally be after
– Identified underlying Cuase
– Exclusion of Confounding Medical conditions
– Neurologic examination must demonstrate
• Coma
• No brain-generated response to external stimuli
• Absent brainstem reflexes
• An apnea test
12. The Apnea Test
Prerequisites
• PaCO2 b/n 35 mmHg and 45 mmHg
• SBP ≥100mmHg with/out vasopressors
• Administer 100% oxygen for at least 10
minutes (ideal PaO2 >200 mmHg with
PEEP ≤ 5 cmH2O)
• Absence of clinical signs of
hypovolemia
Steps
• Disconnect the patient from the ventilator
• Deliver O2 at 6 L/min through a catheter
advanced through the tracheal tube until
close to the carina
• Look carefully for any respiratory mov’ts
while monitoring pulse oximetry and BP
• If no respiratory movements after ≈(8-10)’ ,
obtain arterial blood gases
• Apnea is established if PaCO2 ≥ 60
mmHg (or 20 mmHg greater than baseline)
13. Causes of Unconsciousness
• Brain lesions causing comatous conditions:-
Widespread dysfunction in both cerebral cortices from ischemia, trauma or
inflammation/infection, etc
Extrinsic agents suppressing cortical function toxins, hypoxia or internal
metabolic derangements such as hypoglycemia, azotemia, hepatic failure, or
hypercalcemia
Any brainstem lesions that cause impairment to the RAS from either primary
upper brainstem lesions or secondary lesions from hemispheres
• Bilateral hemispheric dysfunction and impairment of RAS lead to alteration of
consciousness
15. Herniation syndromes
• Due to shifting of brain structures caused by increased intracranial pressure
• They are evidence of severe disease, and are life-threatening
• The more common and important one are central transtentorial, lateral
transtentorial (uncal), and tonsillar (foramen magnum) herniation
• Signs of herniation tend to progress generally in a rostrocaudal manner
20. Causes Of Coma
• Traumatic brain injury (TBI) is the most common cause of coma in children
• Hypoxic-ischemic encephalopathy (HIE) and stroke are the most common cause
of nontraumatic coma in adults
21. Approaches To Unconscious Patients
Initial assesssment
• Three requirements for rescue treatments remain a priority for the initial assessment of
unconscious patients
Airway
Breathing
Circulation
– establishing IV access
– Blood should be withdrawn: estimation of glucose , other biochemical parameters , drug screening
22. History
The history will often be limited, sources may be relatives, friends,or witnesses if available
• The details of the present illness should include:-
– onset of unconsciousness (sudden or gradual)
– recent complaints (headaches, depression, focal weakness, or vertigo)
– recent injuries
– underlying medical illnesses(diabetes, uremia, or heart disease)
– possible exposure to drugs (sedatives or psychotropic drugs)
• Informative history-taking is crucial for the management of unconscious patients
23. Physical Examination
• Careful PE uncovers clues leading to the diagnosis of the cause of unconsciousness
• Evidence of trauma leads to suspicions of traumatic brain injury
• Signs of an acute or chronic systemic illness may be related to metabolic coma
• Evidence of needle marks or alcoholic breath, points to drug intoxication
• Examinations for nuchal rigidity should not be performed unless neck damage has
been excluded
27. Physical Examination
• Odour Of Breath
– Acetone: DKA
– Fetor Hepaticus: in hepatic coma
– Urineferous odour: in uremic coma
– Alcohol odour: in alcohol intoxication
28. Neurological examination
• The initial goal of the neurological examination is to determine whether it is from a
structural cause or a metabolic abnormality, or possibly from both
• Two findings that strongly indicate a structural lesion include
persistent asymmetrical signs between right and left sides and
Abnormal reflexes that indicate specific areas with in the brainstem
29. Level of arousal
• The Glasgow Coma Scale (GCS)
– The GCS is generally helpful in evaluating consciousness levels in patients with
altering degrees of consciousness
•The FOUR (Full Outline of Unresponsiveness) score
– Has four components (eye, motor, brainstem, and respiration)
– Each component has a maximal score of four
– It may address some shortcomings of the GCS, especially in ventilated patients
– It can detect locked-in syndrome and is superior to the GCS due to the evaluation of brainstem
reflexes, breathing patterns, and the ability to recognize different stages of herniation
32. Brainstem Reflexes
• The brainstem reflexes that are examined are:-
– Pupillary reflex
– Ocular movements
– Corneal reflex
– Respiratory pattern
• As a rule, coma due to bilateral hemispheral disease preserves these brainstem activities
33. Pupillary Reflex
• Pupillary examination is beneficial to determine the localization of the lesions
• The pupils become small symmetrical & intact light reflex in Metabolic Uncsc
• Unilateral fixed dilated pupil suggests an ipsilateral oculomotor nerve compression
• Mid-position and non-reacting pupils suggest a Midbrain lesion
• Pinpoint pupils with poor reaction to light suggest a pontine tegmental lesion
• Opiates intoxication leads to pinpoint pupils
• Atropine intoxication leads to widely dilated and fixed pupils
35. Ocular Motility
The position of the eyes at rest
Presence of spontaneous eye movement
The reflex responses to oculocephalic and oculovestibular maneuvers
The eyes look toward a hemispheral lesion and away from a brainstem lesion
36. Oculocephalic Reflexes (Doll's eye movement)
• The intact reaction of oculocephalic reflexes (Doll’s eye movement) consists of the
deviation of both ocular globes towards the opposite direction of cephalic turning
• Once an unconscious patient does not express these symptoms, then a lesion must be
located at either the afferent or efferent arm of the reflex loop
• If the connective pathways b/n the afferent and efferent arms in the pons & medulla
become interrupted in unconscious patients, the doll’s eyes reflex will also be absent
37.
38. Oculovestibular Reflex
• Irrigating ear with cold water/saline introduces ipsilateral deviation of both eyes
with contralateral fast phase nystagmus lasting for one to two minutes
• The absence of any or abnormal responses indicates brainstem dysfunction
• Metabolic diseases & Structural diseases of the brainstem often give rise to
abnormal responses
• The presence of oculo-cephalic and vestibulo-ocular reflexes in unconscious
patients implies an intact connection between the pons and the midbrain
40. Corneal reflex
• The corneal reflex indicates the degree of intactness of the pathway from the
ophthalmic branch of 5th CN through the pons to the 7th & facial muscles
• Gently touching the cornea with a thin wisp of sterile cotton will lead to
– involuntary closure of the ipsilateral eye
– closing of the contralateral eye (consensual response)
• Bilateral loss of the corneal reflex with light unconsciousness indicates the influence
of drugs or local anesthetics in both eyes
• The unilateral loss of the corneal reflex indicates a focal neurological disease
• The existence of the corneal reflex in unconscious patients indicates that the lesion is
likely located outside the pons
41. Respiratory patterns
• Hyperventilation indicates midbrain or upper pons lesions and commonly occurs
in Metabolic disorders
• Hypoventilation indicates a Medullary or Upper cervical spinal lesion
• Normal respiration depends on:
A brainstem mechanism, located between the midpons and cervical medullary
junction, that regulates metabolic needs; and
Forebrain influences that subserve behavioral needs such as speech production
42.
43. The Motor System
• Resting posture
Head and eye deviation to one side, with contralateral hemiparesis, suggests a
supratentorial lesion where as Ipsilateral paralysis indicates a brainstem lesion
External rotation of the lower limb is a sign of hemiplegia or hip fracture
44. • Motor response for painful stimuli should be assessed carefully
– Particular attention should be directed towarad assymertry of tone and movement
• Asymmetric responses indicate structural lesions, either in the cerebral hemisphere
or brainstem
• Symmetric responses indicate more diffuse lesions (metabolic encephalopathy)
• Asymmetric motor response in unconscious patients indicates a focal lesion
The motor system
45. Adventitious movements
• Helps to differentiate metabolic from structural
Myoclonic jerk
Rhythmic myoclonus
Cerebellar fits
More subtle twitches, random or sustained
• Sensory examination
Look for asymmetry for painful stimuli
• Meningeal sign
The motor system
46. Sign of lateralization
• Unequal pupils
• Deviation of the eye to one side
• Facial asymmetry
• Turning of the head to one side
• Unilateral hypotonic/hypertonia
• Asymmetric deep tendon reflex
• Unilateral extensor plantar response
• Unilateral focal or jacksonian fits
47. Posturing
Decorticate rigidity
Flexion of the elbows and wrists and
supination of the arm
Bilateral damage rostral to midbrain
Decerebrate rigidity
Extension of the elbows and wrists
with pronation
Damage to motor tracts in the
midbrain or caudal diencephalon
48. • Laboratory studies remain primary for patients with potential diffuse lesions
– cerebrospinal fluids (CSF)
– serum glucose
– complete blood count (CBC)
– calcium, sodium, potassium, magnesium
– arterial blood gases and pH,
– liver and renal functions
– drug levels, and blood for metabolic panels and
– blood culture
Investigation
49. • In the case of potential focal lesions, Neuroimagings are the recommended
investigations include :-
– skull radiographs
– computer tomography (CT)/magnetic resonance imaging (MRI) of the brain
– ventriculography
– electroecephalography (EEG)
– electrocardiography (ECG)
– cardiac monitoring and
– carotid/vertebral angiography
Investigation
50. Management
General Mgm’t
• The ABCDE (A for airway, B for breathing, C for circulation, D for disability, and E
for exposure) approach to resuscitation must be applied
• The establishment of a clean airway includes
– maintaining an initial lateral position
– suction to remove secretions
– endotracheal intubation
– mechanical ventilation if patients cannot protect against aspiration, hypoxia, or
hypoventilation
51. Management
• Adequate respiration needs to be ensured throughout the course of management.
• Pulmonary embolism is a preventable cause of death in unconscious patients
• Feeding should not be delayed in unconscious patients
• The patients’ bowels, bladder, hygiene & skin care should not be ignored
52.
53. Monitoring and Management of ICP
• The treatment for ICP depends on the cause
• Regardless of the cause, ICP is a medical emergency, and treatment should be
undertaken as expeditiously as possible.
• If a diagnosis of elevated ICP is suspected and an immediately treatable proximate
cause is not present, then ICP monitoring should be instituted
• The goal of ICP monitoring and treatment should be to keep ICP < 20 mmHg
• Interventions should be utilized only when ICP is elevated above 20 mmHg for >5
to 10 minutes
54. ICP Monitors
• We Consider ICP Monitoring
When
• GCS < 8
• Significant IVH or Hydrocphalus
• Clinical evidene of Herniation
Monitoring and Management of ICP
57. Prognosis
• Targeted temperature management is an essential, acute treatment that may
improve outcomes in conscious-impairment patients after cardiac arrest
• In general, for patients who remain comatose for more than four weeks, the chance
of meaningful recovery is low
• A coma patient may still progress toward unresponsive wakefulness syndrome,
minimally conscious state or functional recovery
58. Prognosis
• In general, coma carries a serious prognosis
• This is dependent to a large extent on the underlying cause
• Coma due to depressant drugs carries an excellent prognosis provided that
resuscitative and supportive measures are available and no anoxia has been sustained
• Metabolic causes, apart from anoxia, carry a better prognosis than structural lesions
and head injury
• Length of coma and increasing age are of poor prognostic significance
• Brainstem reflexes early in the coma are an important predictor of outcome
59. References
• Harrison’s principles of Internal Medicine 21st edition
• Dejong’s The Neurologic Examination; 8th ed,
• Bradley and Daroff neurology in clinical practice 8th ed.
• Uptodate online
• Plum and Posner’s Diagnosis and Treatment of Stupor and Coma. 5th ed
• Winchana Srivilaithon, Sombat Muengtaweepongsa. Clinical approach to coma
patients: tips and tricks. Signa Vitae. 2022; 18(2): 8-18. doi:10.22514/sv.2021.230
Editor's Notes
Coma
A state of unresponsiveness in which the patient is not awake and cannot interact with the environment, even after vigorous stimulation.
Patients have lost cognitive neurological function but retain vegetative or noncognitive neurological function such as cardiac action, respiration, & maintenance of blood pressure
Display no interactive behavior and no ability to express emotion or engage another person on any level
# The locked-in state is frequently mistaken for coma.
#Appreciation that the patient is not comatose or vegetative but locked-in does not usually occur for 2 to 3 months (mean 79 days), and the average survival locked-in is 71 months
#Herniation refers to displacement of brain tissue by an overlying or adjacent mass into a contiguous compartment that it normally does not occupy
#A dreaded complication of lumbar puncture is herniation, especially cerebellar tonsillar herniation, due to removal of spinal fluid.
Attention is then directed towards: Assessment of the patient
Severity of the coma
Diagnostic evaluation
All possible information from:
Relatives
Paramedics
Ambulance personnel
Bystanders particularly about the mode of onset
Also, a careful inspection of the skin and general appearance may be helpful.Bruises or contusions around the head and neck suggest traumatic brain injury
Cerebrospinalfluid(CSF)leakage from the ear or nose and periorbital hemorrhage may be connected to a skull fracture.
Profound anemia suggests internal bleeding. Jaundice with signs of liver disease suggests hepatic precoma.
Cyanosis may be associated with hypoxia
Bullous lesions are found in barbiturate intoxication.
Telangiectasia with hyperemia of the face and conjunctivae suggests alcoholism.
Puffy face suggests myxedema.Profuse sweating suggests hypoglycemia or shock.
Dry skin can be found in cases of diabetic ketosis and uremia.
Decreased skin turgor suggests dehydration.
The FOUR (Full Outline of Unresponsiveness) score:
has four components (eye, motor, brainstem, and respiration);
Each component has a maximal score of four.
It may address some shortcomings of the GCS, especially in ventilated patients.
It can detect locked-in syndrome and is superior to the GCS due to the evaluation of brainstem reflexes, breathing patterns, and the ability to recognize different stages of herniation
Oculocephalic maneuver (or doll's eyes) –
In the oculocephalic maneuver, the head is abruptly rotated from one side to the other in the horizontal plane.
When the oculocephalic reflex is present (positive doll's eyes), the eyes do not turn with the head, but in the opposite direction,
As if the patient is maintaining visual fixation on a single point in space.
The cervical spine must be cleared of fracture in any patient with suspected head trauma before this is performed.
This reflex is usually suppressed (and therefore not tested) in conscious patients.
Caloric testing –
Caloric testing of the oculovestibular reflex provides a stronger stimulus for reflex eye movements.
In this test, the head or upper torso is inclined 30 degrees up from the horizontal.
After inspecting the ears for obstruction from wax or a perforated drum, at least 50 mL of ice water is injected into the ear canal using a syringe with a small catheter attached.
This stimulus has the same effect on the horizontal semicircular canal as sustained turning of the head in the opposite direction, and results in sustained deviation of both eyes toward the ear being stimulated.
Five minutes should elapse before testing the other side.
A cold caloric response is also present in conscious people, producing not only deviation of the eyes toward the stimulated ear, but also nystagmus (with the fast phase away from the irrigated side), severe vertigo, nausea, and vomiting.
If nystagmus occurs, the patient is awake and not truly in coma;
a useful confirmatory test for psychogenic unresponsiveness.
However, the presence of nystagmus with caloric stimulation can also be seen in patients with akinetic mutism as well as in patients with less profound coma (eg, moderate metabolic encephalopathy).
Vertical eye movements can be tested:
Either by moving the head and neck in the vertical plane
Or by injecting ice water (causes the eyes to deviate downward in the unconscious patient) or warm water (seven degrees above body temperature; causes the eyes to deviate upwards) into both ear canals simultaneously.
With brainstem lesions, both VORs are often absent or abnormal.
If pupillary sizes and reflexes are normal and one eye abducts and the other fails to adduct, this indicates disruption of the medial longitudinal fasciculus in the pons.
Upper midbrain lesions, affecting the third cranial nerve nuclei, may also lead to abduction without adduction (but usually with pupillary involvement).
Pontine involvement of the sixth nerve nuclei may selectively affect abduction.
An abducens palsy can also occur when the sixth nerve is stretched by expanding mass lesions or trauma (a "false localizing" sign).
Profound toxic or metabolic pathology can also disrupt the VORs, usually the oculocephalic reflex primarily.
Abnormalities are generally symmetric and equally affect abduction and adduction.
Absent caloric responses with normal pupillary reflexes raises the possibility of Wernicke encephalopathy, which selectively involves the VOR, sparing other brainstem reflexes.
However, also seen in some cases of drug intoxication, especially with benzodiazepines.
The afferent arm includes the labyrinthine complex, vestibular nerve (CN VIII), and neck proprioceptors
The efferent arm includes the oculomotor nerve (CN III), trochlear (CN IV), and abducens nerve (CN VI), and their responsible muscles.
Conversely, switching to hot water produces the opposite reaction: contralateral deviation, with ipsilateral fast phase nystagmus.
Bilateral irrigating with cold water/saline gives rise to a downward deviation with upward nystagmus, and with hot water/saline, the opposite reaction occurs.
The corneal reflex usually remains intact until the level of unconsciousness becomes hugely impaired
Hyperventilation indicates midbrain or upper pons lesions and commonly occurs in metabolic disorders, such as hepatic or uremic encephalopathy, diabetic hyperosmolar, and early stages of generalized elevated ICP.
In contrast, hypoventilation indicates a medullary or upper cervical spinal lesion commonly found in drug overdoses and cerebral herniation in its later stages.
Cheyne-Stokes respiratory pattern indicates a lesion in the diencephalon commonly found in central transtentorial brain herniation and obstructive hydrocephalus.
Ataxic respiration (totally irregular breathing) usually indicates a brainstem dysfunction of a diffuse nature
#Reflex are less useful
#Coordination and active movement examination cannot be performed on unresponsive patients
#Flexion, extension, and adduction may be either voluntary or reflex in nature. In general, abduction is most reliably voluntary, with shoulder abduction stated to be the only definite non reflex reaction.
#Reflex flexor response to pain in the upper extremity consists of adduction of the shoulder, flexion of the elbow, and pronation of the arm
#triple flexion response in the lower extremities refers to reflex withdrawal,
Decorticate responses (adducted arm with flexion at elbow, flexion, and pronation at the wrist, extended at hip and knee) indicate lesions above the level of the red nucleus.
Decerebrate responses (arm is extended, adducted, and internally rotated; leg is extended) indicate lesions below the level of the red nucleus but unlikely to be severe metabolic disorders. Complete flaccidity without any response to pain stimuli usually indicates severe CNS depression due to drug overdose
ABCDE steps for emergency approach include clearing airways (A), breathing maintenance (B), sustaining circulation (C), assessing disability (D), and ensuring exposure
General Mgmt
The ABCDE (A for airway, B for breathing, C for circulation, D for disability, and E for exposure) approach to resuscitation must be applied
The preservation of a clear airway is mandatory.
The establishment of a clean airway includes maintaining an initial lateral position, suction to remove secretions, endotracheal intubation, and mechanical ventilation if patients cannot protect against aspiration, hypoxia, or hypoventilation.
Arterial blood gas should be evaluated and further monitored by oxygen saturation. If shock is presented, it needs to be managed immediately [48]. An IV line should be established. The level of consciousness should be immediately evaluated. Clothing should be removed to permit evaluation
Blood drawn for glucose, drugs, electrolyte, liver, and renal functions should be considered. Urine samples for glucose and ketone bodies may be helpful. Diagnostically and therapeutically, gastric lavage may also be helpful. If the patient does not immediately recover from unconsciousness, the patient’s ongoing requirements must be evaluated. The patient must be transferred to an intensive care unit (ICU) to allow for critical management
#Rational of glucose administration:
the frequent occurrence of alterations in arousal due to hypoglycemia and
the relatively good prognosis for coma due to hypoglycemia when it is treated expeditiously; and the potentially permanent consequences if it is not treated
the prognosis for anoxic or ischemic coma generally is poor and probably will remain poor regardless of glucose supplementation
Some of these techniques are generally applicable to all patients with suspected ICH; others (particularly glucocorticoids) are reserved for specific causes of ICH.
In addition to definitive therapy, there are maneuvers that can be employed to reduce ICP acutely
The best therapy for intracranial hypertension (ICH) is resolution of the proximate cause of elevated ICP. Examples include evacuation of a blood clot, resection of a tumor, cerebrospinal fluid (CSF) diversion in the setting of hydrocephalus, or treatment of an underlying metabolic disorder.
repositioning,
ventilator changes,
sedation,
analgesia
Therefore, future studies should focus on innovative tools or techniques to better predict outcomes in various types of patients with impairment of consciousness