Approach To An Unconscious Patient 385w2x
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Approach to
Contents
Clinical Evaluation History Examination
Lab Evaluation
Management
Basics
Wakefulness depends on the integrity of both cerebral hemispheres and the ascending reticular activating formation of the brain stem.
Cont..
The management of an unconscious patient is never an easy task in clinical practice
The duty of physician is Arrive at diagnosis Predict the eventual outcome
History
i)
Onset of coma
(abrupt, gradual)
ii) Recent complaints ( headache, depression, focal weakness, vertigo ) iii) Recent injury
iv) Previous medical illness ( diabetes,uraemia, heart disease ) v) Access to drugs ( sedatives,psychotropic drugs )
Examination
General physical Examination i) Vital signs ii) Evidence of trauma iii) Evidence of acute or chronic system illness iv) Evidence of drug ingestion ( needle marks alcohol breath ) v) Nuchal rigidity (examine with care)
Neurological Examination
State of consciousness Obtundation; responds-to verbal stimuli although slow and inappropriate.
Stupor; the subject can be aroused only by vigorous and repeated noxious stimuli. Coma; unarousable and unresponsive.
Respiratory pattern a ) Hyperventilation - midbrain and upper pons lesion metabolic diseases e.g. hepatic coma, diabetes and generalised raised intracranial pressure in its early stages. ( b ) Hypoventilation - medullary, upper cervical spinal lesion Drug overdose and later stages of cerebral herniation. ( e ) Cheyne-Stoke respiration – usually diencephalic lesion central transtentorial herniation and obstructive hydrocephalus.
( d ) Ataxic respiration (completely irregular breathing) brain-stem dysfunction of a diffuse nature
Pupillary size and reaction Medium to dilated symmetrical pupils fixed to light structural disease of the brain stem. Small symmetrical pupils reactive to light metabolic diseases and drug overdose. Unequal pupil fixed to light intracranial mass lesion producing 3rd nerve palsy e.g in unilateral uncal herniation.
Eye movements Vestibulo-ocular reflexes – douching of one ear with cold water produces ipsi-lateral deviation of both eyes with a contralateral quick phase nystagmus lasting for 1—2 minutes. Use of hot water produces the opposite effect i.e. contralateral deviation with ipsilateral quick phase nystagmus. Bilateral douching with cold water gives rise to downward deviation with upward nystagmus and with hot water the opposite response. Absence or abnormal response indicates brainstem dysfunction.
Oculo-cephalic reflexes (Doll's eye movement ) -
Normal response consist of deviation of both eyes to the opposite direction of head rotation. Again absence or abnormal response indicates brain-stem dysfunction.
Motor Responses This is elicited by applying peripheral noxious stimuli e.g. pinching of limbs rubbing the sternum to elicit pain. ( a ) Appropriate response – brushing away the source of stimulus. { b ) Inappropriate response - decerebrate or decorticate rigidity. Motor response is also of localising value. Paralysed limb will show no response and presence of hemiplegia can therefore be evident. Decerebrate rigidity indicates brain-stem damage and if bilateral is usually associated with a very poor prognosis. Complete flaccidity with no response to noxious stimuli is often indicative of severe central nervous system depression due to drug overdose.
Laboratory Evaluation
Supratentorial lesions
Skull radiograph Computerised tomographic scan CTscan) Carotid angiography EEG ( electroencephalogram )
Infratentorial lesions
Skull radiograph CT scan Vertebral angiography EEG Ventriculography
Diffuse neuronal lesions
Examination of CSF ( cerebro spinal fluid ) Serum glucose, calcium, Na, K, magnesium Blood gases and PH Liver and renal functions Drug levels
Management
Initial Management
Airway Breathing Circulation Deformity Exposure
Definitive Management
In general, management of the comatose patient depends on the cause. However, while the patient is undergoing evaluation, it is essential to : pressure area care care of the mouth, eyes and skin physiotherapy to protect muscles and ts risks of deep vein thrombosis risks of stress ulceration of the stomach nutrition and fluid balance urinary catheterization monitoring of the CVS infection control maintenance of adequate oxygenation, with the assistance of artificial ventilation
You are in emergency department when an unconscious patient land in emergency with B.P 90/50 pulse 92/min and attendants tell u that the patient suddenly fell unconscious, how will you approach ?
APPROACH
ABC
Immediate management
Examination
History
Investigations
ABC
ABC
A –Open the airway
B –breathing
C –circulation
Immediate management
Maintain i.v line, oxygen inhalation
Blood sample for RBS
Control seizures
Consider i.v glucose, thiamine, naloxone, flumazenil
Examination Examination
•Vitals •Skin petechial rash •Injection marks
•Neurological assessment •Neck rigidity •Fundoscopy •Brainstem reflexes
•Detailed medical examination
CONTD.
Vitals 1.Pulse
tachycardia Hypovolemia/haemorrhage hyperthermia Intoxication bradycardia Raised intracranial pressure Heart blocks
CONTD. 2.Temperature increased Sepsis Meningitis ,encephalitis Malaria ,Pontine haemorrhage Decreased Hypoglycemia Hypothermia (less than 31 C) Myxedema Alcohol, barbiturate ,sedative or phenothiazine intoxication.
CONTD. 3.Blood pressure increased Hypertensive encephalopathy Cerebral haemorrhage Raised intracranial pressure Decreased Hypovolemia /hgr Myocardial infarction Intoxication/poisoning Profound hypothyroidism, Addisonian crisis
CONTD. 4.Respiratory rate Increased(tachypnae) Pneumonia Acidosis (DKA, renal failure) Pulmonary embolism Respiratory failure Decreased Intoxication/poisoning
CONTD.
Skin petechial rash
Meningococcal meningitis
Endocarditis
Sepsis,thrombotic thrombocytopenic purpura
Rickettsial infection RMS (rocky mountain spotted fever)
CONTD.
Multiple injection marks
Drug addiction
Acute endocarditis
Hepatitis B /C with encephalopathy
HIV
CONTD.
Neurological assessment;
General posture
Level of conciousness
CONTD.
Posture;
Lack of movements on one side
Intermittent twitching
Multifocal myoclonus
DECORTICATION
DECEREBRATION
CONTD.
Level of conciousness Glasgow coma scale (GCS) Best motor response Best verbal response Eye opening GCS score 3 –severe injury less than or equal to 8 – moderate injury 9 to 12 – minor injury
CONTD. An abbreviated coma scale is used in the assessment of critically ill patient (primary servey) AVPU A –alert V – respond to voice stimulus P – respond to pain U - unresponsive
Brainstem reflexes
Pupillary responses to light Spontaneous and elicited eye movements
Corneal responses
Respiratory movements
CONTD. Ocular movements
Conjugate deviation of eyes to a side – ipsilateral hemisphere frontal leison or contralateral pontine leison. Rarely eyes may turn paradoxically away from the side of deep hemisphere leison (WRONG-WAY EYES) Downward conjugate deviation of eyes – mesencephalic leison.
CONTD.
Eyes turn down and inward in – thalamic hgr and upper midbrain leison. Ocular bobbing – is diagnostic of pontine hgr. Ocular dipping - indicates diffuse cortical anoxic damage. Dysconjugate ocular deviation – brainstem leison.
CONTD.
Oculocephalic reflex (Doll’s eyes response) – brisk in cortical depression ,lost in brainstem leison.
Oculovestibulo responses –two components 1.Conjugate ocular movement – loss in brainstem damage.
2.Nystagmus – loss in damage to cerebral hemisphere
CONTD. Pupillary changes; Sr no
pupils
causes
1
B/L Pin-point pupils ( less than 1mm)but responsive
Opiates poisoning ,extensive pontine hgr.
2
B/L small pupils but responsive
B/L diencephalon involvement or destructive pontine leison
3
B/L slightly small pupils(1 to 2.5 mm) but responsive
Metabolic encephalopathies ,deep B/L hemisphere leison or thalamic hgr.
4
B/L dilated and fixed
Severe midbrain damage, Overdose of atropine,scopolamine, glutethemide.
CONTD. Sr. no.
Pupil
cause
6
U/L small pupil
Horner syndrome
5
Ipsilateral dilated pupil with no direct or consensual reflexes
Compression of 3rd cranial nerve e.g, uncal herniation
7
U/L small and irregular pupil unresponsive
Leison in pretectal area of midbrain
CONTD. Respiratory movements
Has less localizing value then other brainstem reflexes. Cheyen-stokes respiration(classic cyclic form ending with a brief apneic period – B/L hemisphere damage or metabolic depression.
Rapid ,deep breathing (Kussmaul) – in metabolic acidosis and in pontomesencephalic leison.
Neck rigidity;
Meningitis
Subarachnoid haemorrhage
Fundoscopy
Raised intracranial pressure
Hypertensive changes
Subarachnoid haemorrhage
Diabetic retinopathy
History
Onset of the symptoms
Antecedent symptoms
Use of medications
Chronic liver ,kidney ,lung or heart disease
CAUSES OF UNCONCIOUSNESS Thiamine deficiency
Brain tumor
epilepsy
metabolic disturbances Causes of unconciousness
infections
trauma
Cardiovascular disease
Causes of unconciousness Metabolic Drugs, poisoning e.g CO ,alcohol Hypoglcemia, hyperglycemia (keto acidoti or HONK) Hypoxia, carbondiaoxide narcosis (COPD) Septicemia Hypothermia Myxedema ,addisonian crisis Hepatic / uremic encephalopathy
CONTD. Neurological Trauma Infections – meningitis, encephalitis, malaria, typhoid, rabies, trypanosomiasis. Tumours – cerebral / meningeal tumors Vascular – subdural / subarachnoid hgr, stroke, hypertensive encephalopathy Epilepsy – nonconvulsive status / postictal state
Immediate investigations
RBS
Blood and ESR
LFTs
Urea and Creatnine
Blood and urine cultures
Other investigations
CRP
ABGs
Toxic screen , drug levels
Lumbar puncture and CXR
CT scan
Summary ABC of life
Oxygen and I.V access
Stabilize cervical spine
CONTD. Blood glucose
Control seizures
Consider I.V glucose, thiamine, naloxone, flumazenil
CONTD. Brief examination and obtain history
Investigate
Reassess the situation and plan further
Take home message
Early management
Prompt diagnosis
MCQ
Pupillary changes in opiate poisoning
1.B/L pinpoint
2.U/L pin point 3.B/L dilated
Answer
1. B/L pin point
MCQ
Myxoedema coma seen in
1.Euthyroid state
2.Hyperthyroid state 3. hypothyroid state
Answer
3. hypothyroid state
Contents
Clinical Evaluation History Examination
Lab Evaluation
Management
Basics
Wakefulness depends on the integrity of both cerebral hemispheres and the ascending reticular activating formation of the brain stem.
Cont..
The management of an unconscious patient is never an easy task in clinical practice
The duty of physician is Arrive at diagnosis Predict the eventual outcome
History
i)
Onset of coma
(abrupt, gradual)
ii) Recent complaints ( headache, depression, focal weakness, vertigo ) iii) Recent injury
iv) Previous medical illness ( diabetes,uraemia, heart disease ) v) Access to drugs ( sedatives,psychotropic drugs )
Examination
General physical Examination i) Vital signs ii) Evidence of trauma iii) Evidence of acute or chronic system illness iv) Evidence of drug ingestion ( needle marks alcohol breath ) v) Nuchal rigidity (examine with care)
Neurological Examination
State of consciousness Obtundation; responds-to verbal stimuli although slow and inappropriate.
Stupor; the subject can be aroused only by vigorous and repeated noxious stimuli. Coma; unarousable and unresponsive.
Respiratory pattern a ) Hyperventilation - midbrain and upper pons lesion metabolic diseases e.g. hepatic coma, diabetes and generalised raised intracranial pressure in its early stages. ( b ) Hypoventilation - medullary, upper cervical spinal lesion Drug overdose and later stages of cerebral herniation. ( e ) Cheyne-Stoke respiration – usually diencephalic lesion central transtentorial herniation and obstructive hydrocephalus.
( d ) Ataxic respiration (completely irregular breathing) brain-stem dysfunction of a diffuse nature
Pupillary size and reaction Medium to dilated symmetrical pupils fixed to light structural disease of the brain stem. Small symmetrical pupils reactive to light metabolic diseases and drug overdose. Unequal pupil fixed to light intracranial mass lesion producing 3rd nerve palsy e.g in unilateral uncal herniation.
Eye movements Vestibulo-ocular reflexes – douching of one ear with cold water produces ipsi-lateral deviation of both eyes with a contralateral quick phase nystagmus lasting for 1—2 minutes. Use of hot water produces the opposite effect i.e. contralateral deviation with ipsilateral quick phase nystagmus. Bilateral douching with cold water gives rise to downward deviation with upward nystagmus and with hot water the opposite response. Absence or abnormal response indicates brainstem dysfunction.
Oculo-cephalic reflexes (Doll's eye movement ) -
Normal response consist of deviation of both eyes to the opposite direction of head rotation. Again absence or abnormal response indicates brain-stem dysfunction.
Motor Responses This is elicited by applying peripheral noxious stimuli e.g. pinching of limbs rubbing the sternum to elicit pain. ( a ) Appropriate response – brushing away the source of stimulus. { b ) Inappropriate response - decerebrate or decorticate rigidity. Motor response is also of localising value. Paralysed limb will show no response and presence of hemiplegia can therefore be evident. Decerebrate rigidity indicates brain-stem damage and if bilateral is usually associated with a very poor prognosis. Complete flaccidity with no response to noxious stimuli is often indicative of severe central nervous system depression due to drug overdose.
Laboratory Evaluation
Supratentorial lesions
Skull radiograph Computerised tomographic scan CTscan) Carotid angiography EEG ( electroencephalogram )
Infratentorial lesions
Skull radiograph CT scan Vertebral angiography EEG Ventriculography
Diffuse neuronal lesions
Examination of CSF ( cerebro spinal fluid ) Serum glucose, calcium, Na, K, magnesium Blood gases and PH Liver and renal functions Drug levels
Management
Initial Management
Airway Breathing Circulation Deformity Exposure
Definitive Management
In general, management of the comatose patient depends on the cause. However, while the patient is undergoing evaluation, it is essential to : pressure area care care of the mouth, eyes and skin physiotherapy to protect muscles and ts risks of deep vein thrombosis risks of stress ulceration of the stomach nutrition and fluid balance urinary catheterization monitoring of the CVS infection control maintenance of adequate oxygenation, with the assistance of artificial ventilation
You are in emergency department when an unconscious patient land in emergency with B.P 90/50 pulse 92/min and attendants tell u that the patient suddenly fell unconscious, how will you approach ?
APPROACH
ABC
Immediate management
Examination
History
Investigations
ABC
ABC
A –Open the airway
B –breathing
C –circulation
Immediate management
Maintain i.v line, oxygen inhalation
Blood sample for RBS
Control seizures
Consider i.v glucose, thiamine, naloxone, flumazenil
Examination Examination
•Vitals •Skin petechial rash •Injection marks
•Neurological assessment •Neck rigidity •Fundoscopy •Brainstem reflexes
•Detailed medical examination
CONTD.
Vitals 1.Pulse
tachycardia Hypovolemia/haemorrhage hyperthermia Intoxication bradycardia Raised intracranial pressure Heart blocks
CONTD. 2.Temperature increased Sepsis Meningitis ,encephalitis Malaria ,Pontine haemorrhage Decreased Hypoglycemia Hypothermia (less than 31 C) Myxedema Alcohol, barbiturate ,sedative or phenothiazine intoxication.
CONTD. 3.Blood pressure increased Hypertensive encephalopathy Cerebral haemorrhage Raised intracranial pressure Decreased Hypovolemia /hgr Myocardial infarction Intoxication/poisoning Profound hypothyroidism, Addisonian crisis
CONTD. 4.Respiratory rate Increased(tachypnae) Pneumonia Acidosis (DKA, renal failure) Pulmonary embolism Respiratory failure Decreased Intoxication/poisoning
CONTD.
Skin petechial rash
Meningococcal meningitis
Endocarditis
Sepsis,thrombotic thrombocytopenic purpura
Rickettsial infection RMS (rocky mountain spotted fever)
CONTD.
Multiple injection marks
Drug addiction
Acute endocarditis
Hepatitis B /C with encephalopathy
HIV
CONTD.
Neurological assessment;
General posture
Level of conciousness
CONTD.
Posture;
Lack of movements on one side
Intermittent twitching
Multifocal myoclonus
DECORTICATION
DECEREBRATION
CONTD.
Level of conciousness Glasgow coma scale (GCS) Best motor response Best verbal response Eye opening GCS score 3 –severe injury less than or equal to 8 – moderate injury 9 to 12 – minor injury
CONTD. An abbreviated coma scale is used in the assessment of critically ill patient (primary servey) AVPU A –alert V – respond to voice stimulus P – respond to pain U - unresponsive
Brainstem reflexes
Pupillary responses to light Spontaneous and elicited eye movements
Corneal responses
Respiratory movements
CONTD. Ocular movements
Conjugate deviation of eyes to a side – ipsilateral hemisphere frontal leison or contralateral pontine leison. Rarely eyes may turn paradoxically away from the side of deep hemisphere leison (WRONG-WAY EYES) Downward conjugate deviation of eyes – mesencephalic leison.
CONTD.
Eyes turn down and inward in – thalamic hgr and upper midbrain leison. Ocular bobbing – is diagnostic of pontine hgr. Ocular dipping - indicates diffuse cortical anoxic damage. Dysconjugate ocular deviation – brainstem leison.
CONTD.
Oculocephalic reflex (Doll’s eyes response) – brisk in cortical depression ,lost in brainstem leison.
Oculovestibulo responses –two components 1.Conjugate ocular movement – loss in brainstem damage.
2.Nystagmus – loss in damage to cerebral hemisphere
CONTD. Pupillary changes; Sr no
pupils
causes
1
B/L Pin-point pupils ( less than 1mm)but responsive
Opiates poisoning ,extensive pontine hgr.
2
B/L small pupils but responsive
B/L diencephalon involvement or destructive pontine leison
3
B/L slightly small pupils(1 to 2.5 mm) but responsive
Metabolic encephalopathies ,deep B/L hemisphere leison or thalamic hgr.
4
B/L dilated and fixed
Severe midbrain damage, Overdose of atropine,scopolamine, glutethemide.
CONTD. Sr. no.
Pupil
cause
6
U/L small pupil
Horner syndrome
5
Ipsilateral dilated pupil with no direct or consensual reflexes
Compression of 3rd cranial nerve e.g, uncal herniation
7
U/L small and irregular pupil unresponsive
Leison in pretectal area of midbrain
CONTD. Respiratory movements
Has less localizing value then other brainstem reflexes. Cheyen-stokes respiration(classic cyclic form ending with a brief apneic period – B/L hemisphere damage or metabolic depression.
Rapid ,deep breathing (Kussmaul) – in metabolic acidosis and in pontomesencephalic leison.
Neck rigidity;
Meningitis
Subarachnoid haemorrhage
Fundoscopy
Raised intracranial pressure
Hypertensive changes
Subarachnoid haemorrhage
Diabetic retinopathy
History
Onset of the symptoms
Antecedent symptoms
Use of medications
Chronic liver ,kidney ,lung or heart disease
CAUSES OF UNCONCIOUSNESS Thiamine deficiency
Brain tumor
epilepsy
metabolic disturbances Causes of unconciousness
infections
trauma
Cardiovascular disease
Causes of unconciousness Metabolic Drugs, poisoning e.g CO ,alcohol Hypoglcemia, hyperglycemia (keto acidoti or HONK) Hypoxia, carbondiaoxide narcosis (COPD) Septicemia Hypothermia Myxedema ,addisonian crisis Hepatic / uremic encephalopathy
CONTD. Neurological Trauma Infections – meningitis, encephalitis, malaria, typhoid, rabies, trypanosomiasis. Tumours – cerebral / meningeal tumors Vascular – subdural / subarachnoid hgr, stroke, hypertensive encephalopathy Epilepsy – nonconvulsive status / postictal state
Immediate investigations
RBS
Blood and ESR
LFTs
Urea and Creatnine
Blood and urine cultures
Other investigations
CRP
ABGs
Toxic screen , drug levels
Lumbar puncture and CXR
CT scan
Summary ABC of life
Oxygen and I.V access
Stabilize cervical spine
CONTD. Blood glucose
Control seizures
Consider I.V glucose, thiamine, naloxone, flumazenil
CONTD. Brief examination and obtain history
Investigate
Reassess the situation and plan further
Take home message
Early management
Prompt diagnosis
MCQ
Pupillary changes in opiate poisoning
1.B/L pinpoint
2.U/L pin point 3.B/L dilated
Answer
1. B/L pin point
MCQ
Myxoedema coma seen in
1.Euthyroid state
2.Hyperthyroid state 3. hypothyroid state
Answer
3. hypothyroid state
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