Delayed recovery from anesthesia can have multiple contributing factors and causes. It is important to consider potential drug interactions, metabolic abnormalities, and organic causes that may cause prolonged unconsciousness and have serious health implications. Signs and symptoms of metabolic issues may not present normally in an anesthetized patient. The Glasgow Coma Scale provides an objective measure of conscious state regardless of cause.

1. Delayed recovery of consciousness
after anaesthesia
Dr. Shaiq HameedDr. Shaiq Hameed

2. Key points
 Delayed recovery from anaesthesia is oftenDelayed recovery from anaesthesia is often
multifactorial.multifactorial.
 Consider drug interactions with neuromuscular blockingConsider drug interactions with neuromuscular blocking
agents.agents.
 Metabolic abnormalities will not present with the usualMetabolic abnormalities will not present with the usual
signs and symptoms in the anaesthetized patient.signs and symptoms in the anaesthetized patient.
 Organic causes of prolonged unconsciousness may haveOrganic causes of prolonged unconsciousness may have
important sequelae that should be managedimportant sequelae that should be managed
appropriately.appropriately.
 Rarely, disassociative states may present with episodesRarely, disassociative states may present with episodes
of unconsciousness with no other identifiable causeof unconsciousness with no other identifiable cause..

3. DEFINITIONS
 A conscious individual, is ‘awake and awareA conscious individual, is ‘awake and aware
of their surroundings and identity’.of their surroundings and identity’.
 ComaComa from the Greek word "koma,"from the Greek word "koma,"
meaning deep sleep.meaning deep sleep.
 It is defined medically as ‘a state ofIt is defined medically as ‘a state of
unresponsiveness from which the patientunresponsiveness from which the patient
cannot be aroused’.cannot be aroused’.

4. DEFINITIONS (contd.)
 Clouding of consciousness-Clouding of consciousness-Impaired capacity to thinkImpaired capacity to think
clearly and remember current stimuliclearly and remember current stimuli
 DeliriumDelirium -disturbed consciousness with motor-disturbed consciousness with motor
restlessness, disorientation and hallucinationrestlessness, disorientation and hallucination
 ObtundationObtundation-reduced alertness, appears to be sleep-reduced alertness, appears to be sleep
but responds to verbal or tactile stimulibut responds to verbal or tactile stimuli
 StuporStupor-reduced alertness, person only responds to-reduced alertness, person only responds to
noxious stimulinoxious stimuli
 ComaComa-no response to noxious stimuli-no response to noxious stimuli

5. Glasgow Coma Scale
 Developed to define outcome in adultDeveloped to define outcome in adult
patients with head injurypatients with head injury
 Coma: score of 8 or lessComa: score of 8 or less
 A useful tool to assess conscious stateA useful tool to assess conscious state
regardless of the causative factor.regardless of the causative factor.

6. Glasgow Score
 Eye openingEye opening Motor ResponseMotor Response
 Spontaneous 4Spontaneous 4 obeys commands 6obeys commands 6
 To command 3To command 3 localizes pain 5localizes pain 5
 To pain 2To pain 2 withdraws to pain 4withdraws to pain 4
 None 1None 1 abnormal flexion 3abnormal flexion 3
 VerbalVerbal abnormal extension 2abnormal extension 2
 Oriented 5Oriented 5 none 1none 1
 Confused 4Confused 4
 Inappropriate words 3Inappropriate words 3 TOTAL 3-15TOTAL 3-15
 Incomprehensible sounds 2Incomprehensible sounds 2
 None 1None 1

7. Causes of prolonged
unconsciousness after anaesthesia
 The time taken to emerge to full consciousnessThe time taken to emerge to full consciousness
is affected by patient factors, anaestheticis affected by patient factors, anaesthetic
factors, duration of surgery and painfulfactors, duration of surgery and painful
stimulation.stimulation.
 Non-pharmacological causes may have seriousNon-pharmacological causes may have serious
sequelae; thus, recognizing these organicsequelae; thus, recognizing these organic
conditions is important.conditions is important.

8.  PharmacologicalPharmacological
The residual effects of a drug (after administration hasThe residual effects of a drug (after administration has
ceased) are influenced by a number of factors as ;ceased) are influenced by a number of factors as ;
Drug FactorsDrug Factors
 DoseDose
 AbsorptionAbsorption
 DistributionDistribution
 MetabolismMetabolism
 ExcretionExcretion
 Context-sensitive half-lifeContext-sensitive half-life
 Pharmacodynamic interactions (summation, potentiation,Pharmacodynamic interactions (summation, potentiation,
synergism)synergism)
 Pharmacokinetic interactions (distribution, metabolism,Pharmacokinetic interactions (distribution, metabolism,
excretion)excretion)

9. Patient factorsPatient factors
 Age (especially extremes)Age (especially extremes)
 Genetic variationsGenetic variations
 Disease processes: renal, hepatic failureDisease processes: renal, hepatic failure
Surgical factorsSurgical factors
 Requirement for muscle relaxationRequirement for muscle relaxation
 Duration of surgeryDuration of surgery
 Utilisation of regional techniquesUtilisation of regional techniques
 Degree of pain/stimulationDegree of pain/stimulation

10.  Metabolic CausesMetabolic Causes
 HypoglycaemiaHypoglycaemia
 HyperglycaemiaHyperglycaemia
 HyponatraemiaHyponatraemia
 HypernatraemiaHypernatraemia
 HypothermiaHypothermia
 Central anticholinergic syndromeCentral anticholinergic syndrome
 HypothyroidismHypothyroidism
 Hepatic or renal failure (uraemia)Hepatic or renal failure (uraemia)
 SepsisSepsis

11.  Other causesOther causes
 Respiratory FailureRespiratory Failure
 Central driveCentral drive
 Muscular/ventilatory disordersMuscular/ventilatory disorders
 Pulmonary pathologyPulmonary pathology
 Neurological CausesNeurological Causes
 Intracerebral eventIntracerebral event
 SeizuresSeizures
 Central hypoxiaCentral hypoxia
 Central ischaemiaCentral ischaemia
 Local anaesthetic toxicityLocal anaesthetic toxicity

12. BenzodiazepinesBenzodiazepines
 Used alone, benzodiazepines are unlikely to causeUsed alone, benzodiazepines are unlikely to cause
prolonged unconsciousness except in susceptible,prolonged unconsciousness except in susceptible,
elderly patients or when given in overdose.elderly patients or when given in overdose.
 CNS depression can prolong the effects of otherCNS depression can prolong the effects of other
anaesthetic agents.anaesthetic agents.
 Benzodiazepines combined with high-dose opioidsBenzodiazepines combined with high-dose opioids
can have a pronounced effect on respiratorycan have a pronounced effect on respiratory
depression, producing hypercapnia and coma.depression, producing hypercapnia and coma.

13. OpioidsOpioids
There are two major mechanisms resulting in coma,There are two major mechanisms resulting in coma,
respiratory depression and direct sedation via opioid receptors;respiratory depression and direct sedation via opioid receptors;
1.1. The sensitivity of the brainstem chemoreceptors toThe sensitivity of the brainstem chemoreceptors to
carbon dioxide is reduced by opioids with consequentcarbon dioxide is reduced by opioids with consequent
dose-dependant respiratory depression and resultantdose-dependant respiratory depression and resultant
hypercapnia. This may affect clearance of volatile agentshypercapnia. This may affect clearance of volatile agents
and carbon dioxide; both can cause unconsciousness.and carbon dioxide; both can cause unconsciousness.
2.2. The direct opioid receptor effect which varies with drugThe direct opioid receptor effect which varies with drug
potency, half-life, metabolism and patient sensitivity.potency, half-life, metabolism and patient sensitivity.

14. Neuromuscular blockNeuromuscular block
 Neuromuscular block in the conscious patient can mimicNeuromuscular block in the conscious patient can mimic
unconsciousness.unconsciousness.
 Neuromuscular blockers may result in prolongedNeuromuscular blockers may result in prolonged
unconsciousness if a residual block causes hypoventilation.unconsciousness if a residual block causes hypoventilation.
 A large number of pharmacological interactions withA large number of pharmacological interactions with
neuromuscular blocking agents prolong neuromuscularneuromuscular blocking agents prolong neuromuscular
block.block.
 The majority of drug interactions with nondepolarizingThe majority of drug interactions with nondepolarizing
neuromuscular blocking agents prolong blockade byneuromuscular blocking agents prolong blockade by
interfering with calcium, the second messenger involved ininterfering with calcium, the second messenger involved in
acetylcholine release.acetylcholine release.

15. Neuromuscular block(contd.)Neuromuscular block(contd.)
 Electrolyte disturbances cause cell wall hyperpolarizationElectrolyte disturbances cause cell wall hyperpolarization
and prolonged block.and prolonged block.
 Hypothermia decreases metabolism and acidosis donatesHypothermia decreases metabolism and acidosis donates
protons to tertiary amines, increasing receptor affinity.protons to tertiary amines, increasing receptor affinity.
 Deficiencies of plasma cholinesterase prolong blockDeficiencies of plasma cholinesterase prolong block
produced by succinylcholine; therapeutic plasmaproduced by succinylcholine; therapeutic plasma
concentrations persist because of decreased metabolism.concentrations persist because of decreased metabolism.

16. Interactions with non-depolarising muscle relaxants
Drug Interactions Metabolic Causes Genetic
Volatile anaesthetic
agents
Aminoglycosides
Lithium
Diuretics
Calcium channel
antagonists
Hypothermia
Acidosis
Hypokalaemia
Hypermagnesaemia
Myasthenia gravis
Eaton Lambert/Myasthenic
syndrome

17. Interactions with depolarising muscle relaxants
Genetic Acquired acetylcholinesterase
deficiency
Succinylcholine apnoea
Myotonic Dystrophy
Pregnancy
Liver Disease
Renal failure
Cardiac failure
Thyrotoxicosis
Drugs (ecothiopate, ketamine, OCP’s,
lidocaine, neostigmine, ester local-
anaesthetics)

18. I.V. anaesthetic agentsI.V. anaesthetic agents
 The termination of action of i.v. agents given as a bolusThe termination of action of i.v. agents given as a bolus
for induction is predominantly determined byfor induction is predominantly determined by
redistribution and should not delay recovery.redistribution and should not delay recovery.
 Propofol has a large volume of distribution at steady-Propofol has a large volume of distribution at steady-
state and a relatively long elimination half-life. Thestate and a relatively long elimination half-life. The
effect of propofol after total i.v. anaesthesia (TIVA) iseffect of propofol after total i.v. anaesthesia (TIVA) is
prolonged.prolonged.
 Duration of unconsciousness is affected by context-Duration of unconsciousness is affected by context-
sensitive half-life, amount of drug, co-administrationsensitive half-life, amount of drug, co-administration
with other drugs, and patient factors.with other drugs, and patient factors.

19. Volatile anaesthetic agentsVolatile anaesthetic agents
 Emergence from volatile agent anaesthesiaEmergence from volatile agent anaesthesia
depends upon pulmonary elimination of the drugdepends upon pulmonary elimination of the drug
and MACand MACawakeawake (the end-tidal concentration(the end-tidal concentration
associated with eye-opening to verbalassociated with eye-opening to verbal
command).command).
 MACMACawakeawake is consistently and approximately 30%is consistently and approximately 30%
of MAC.of MAC.
 Pulmonary elimination is determined by alveolarPulmonary elimination is determined by alveolar
ventilation, blood–gas partition co-efficient andventilation, blood–gas partition co-efficient and
dose (MAC-hours).dose (MAC-hours).

20. Volatile anaesthetic agents(contd.)Volatile anaesthetic agents(contd.)
 Using an agent with low blood–gas solubilityUsing an agent with low blood–gas solubility
results in a quicker emergence.results in a quicker emergence.
 Alveolar hypoventilation lengthens the time takenAlveolar hypoventilation lengthens the time taken
to exhale the anaesthetic and delays recovery.to exhale the anaesthetic and delays recovery.
 Time to emergence increases with increasingTime to emergence increases with increasing
duration of anaesthesia (i.e. context-sensitiveduration of anaesthesia (i.e. context-sensitive
half-life increases), but does not change MAChalf-life increases), but does not change MACawakeawake..

21.  Metabolic causesMetabolic causes
HypoglycaemiaHypoglycaemia
 Neuroglycopenia manifests as confusion, abnormalNeuroglycopenia manifests as confusion, abnormal
behaviour, seizures and coma.behaviour, seizures and coma.
 In the elderly population, lateralizing neurological signsIn the elderly population, lateralizing neurological signs
are commonly seen.are commonly seen.
 Postoperative hypoglycaemia most often results fromPostoperative hypoglycaemia most often results from
poorly controlled diabetes, starvation and alcoholpoorly controlled diabetes, starvation and alcohol
consumption.consumption.
 Other causes of hypoglycaemia include Sepsis, LiverOther causes of hypoglycaemia include Sepsis, Liver
failure, Paediatrics, Sulphonylureas, Endocrine tumours,failure, Paediatrics, Sulphonylureas, Endocrine tumours,
HypoadrenalismHypoadrenalism

22. HyperglycaemiaHyperglycaemia
 Severe hyperglycaemia can prolongSevere hyperglycaemia can prolong
unconsciousness after anaesthesia.unconsciousness after anaesthesia.
 A venous blood glucose >14 mmol/litre causes anA venous blood glucose >14 mmol/litre causes an
osmotic diuresis and dehydration in the untreatedosmotic diuresis and dehydration in the untreated
patient.patient.
 The effects of dehydration range from drowsinessThe effects of dehydration range from drowsiness
to acidosis.to acidosis.
 Blood hyperosmolality and hyperviscosityBlood hyperosmolality and hyperviscosity
predispose to thrombosis and cerebral oedema.predispose to thrombosis and cerebral oedema.

23. Hyperglycaemia(contd.)Hyperglycaemia(contd.)
 Intraoperative cerebrovascular accident mayIntraoperative cerebrovascular accident may
occur as a result of cerebral vascular occlusion,occur as a result of cerebral vascular occlusion,
especially in diabetics with microvascular andespecially in diabetics with microvascular and
macrovasculardisease.macrovasculardisease.
 Causes include; Ketoacidosis, Hyperosmolar nonCauses include; Ketoacidosis, Hyperosmolar non
ketotic acidosis (HONK), Lactic acidosis,ketotic acidosis (HONK), Lactic acidosis,
Gestational diabetes, Insulin resistanceGestational diabetes, Insulin resistance
(acromegally, Cushing’s), Pancreatitis, Inherited(acromegally, Cushing’s), Pancreatitis, Inherited
syndromes.syndromes.

24. HyponatraemiaHyponatraemia
 Mild hyponatraemia is usually asymptomatic, but serumMild hyponatraemia is usually asymptomatic, but serum
sodium concentration <120 mmol/litre will causesodium concentration <120 mmol/litre will cause
confusion and irritability. Serum sodium concentrationconfusion and irritability. Serum sodium concentration
<110 mmol/litre causes seizures, coma and increased<110 mmol/litre causes seizures, coma and increased
mortality.mortality.
 The causes of hyponatraemia are multiple; however,The causes of hyponatraemia are multiple; however,
those pertinent to anaesthesia are the conditions thatthose pertinent to anaesthesia are the conditions that
may develop during operation.may develop during operation.
 Inappropriate anti-diuretic hormone secretion (SIADH) canInappropriate anti-diuretic hormone secretion (SIADH) can
result from brain trauma, subarachnoid haemorrhage andresult from brain trauma, subarachnoid haemorrhage and
administration of drugs (e.g. opioids, haloperidol,administration of drugs (e.g. opioids, haloperidol,
vasopressin).vasopressin).

25. Hyponatraemia(contd.)Hyponatraemia(contd.)
 Cerebral salt-wasting syndrome may also occur in theCerebral salt-wasting syndrome may also occur in the
brain injured patient, and infusion of mannitol canbrain injured patient, and infusion of mannitol can
dehydrate.dehydrate.
 Fluid overload and hyponatraemia may occur when largeFluid overload and hyponatraemia may occur when large
volumes of irrigation fluid (glycine solution) are absorbedvolumes of irrigation fluid (glycine solution) are absorbed
by open venous sinuses during trans-urethral resection ofby open venous sinuses during trans-urethral resection of
the prostate (TURP), that is TURP syndrome. The result isthe prostate (TURP), that is TURP syndrome. The result is
hyponatraemia, pulmonary oedema and cerebral oedemahyponatraemia, pulmonary oedema and cerebral oedema
causing variable cerebral signs, including coma.causing variable cerebral signs, including coma.

26. Hyponatraemia and water excessHyponatraemia and water excess
 Na deficient i.v. fluidsNa deficient i.v. fluids
 TURP syndromeTURP syndrome
 Excessive drinkingExcessive drinking
 SIADHSIADH
 DrugsDrugs
 Nephrotic syndromeNephrotic syndrome
Hyponatraemia and dehydrationHyponatraemia and dehydration
 DiureticsDiuretics
 HypoadrenalismHypoadrenalism
 Cerebral salt-wastingCerebral salt-wasting
 NephritisNephritis
 Diarrhoea, vomitingDiarrhoea, vomiting
 PancreatitisPancreatitis
 Renal tubular acidosisRenal tubular acidosis

27. HypernatraemiaHypernatraemia
 Extreme hypernatraemia is less likely to occur inExtreme hypernatraemia is less likely to occur in
the postoperative environment.the postoperative environment.
 Sodium excess results in cellular dehydrationSodium excess results in cellular dehydration
including cerebral dehydration, ruptured vesselsincluding cerebral dehydration, ruptured vessels
and intracranial haemorrhage.and intracranial haemorrhage.
 Symptoms include thirst, drowsiness, confusionSymptoms include thirst, drowsiness, confusion
and coma.and coma.

28. UraemiaUraemia
 Uraemia results in dehydration and cerebral effectsUraemia results in dehydration and cerebral effects
attributable to cellular damage and distortion.attributable to cellular damage and distortion.
 The clinical effects of uraemia are varied, butThe clinical effects of uraemia are varied, but
intracerebral changes may produce drowsiness, confusionintracerebral changes may produce drowsiness, confusion
and comaand coma..
HypothermiaHypothermia
 The effects of hypothermia are multiple and widespreadThe effects of hypothermia are multiple and widespread
throughout the body.throughout the body.
 Neurological and respiratory changes occur with decreasingNeurological and respiratory changes occur with decreasing
temperature, e.g. confusion (<35C), unconsciousnesstemperature, e.g. confusion (<35C), unconsciousness
(<30C), apnoea (<24C), absent cerebral activity (<18C).(<30C), apnoea (<24C), absent cerebral activity (<18C).

29. Respiratory failureRespiratory failure
 Postoperative respiratory failure causesPostoperative respiratory failure causes
hypoxaemia, hypercapnia, or both.hypoxaemia, hypercapnia, or both.
 The causes of respiratory failure are multiple andThe causes of respiratory failure are multiple and
may be classified into neurological, pulmonary,may be classified into neurological, pulmonary,
and muscular.and muscular.
 Central drive is lost during drug overdose, withCentral drive is lost during drug overdose, with
intracranial pathology and in patients withintracranial pathology and in patients with
chronic obstructive pulmonary disease or sleepchronic obstructive pulmonary disease or sleep
apnoea.apnoea.

30. Respiratory failure(contd.)Respiratory failure(contd.)
 Ventilation is affected by primary muscleVentilation is affected by primary muscle
problems, metabolic imbalance, obesity andproblems, metabolic imbalance, obesity and
residual neuromuscular block.residual neuromuscular block.
 Pulmonary disease states result in venousPulmonary disease states result in venous
admixture, dead space, or both and includeadmixture, dead space, or both and include
pulmonarypulmonary embolism, atelectasis, obstruction,embolism, atelectasis, obstruction,
aspiration, consolidation,aspiration, consolidation, acute respiratoryacute respiratory
distress syndrome and transfusion-related acutedistress syndrome and transfusion-related acute
lung injury.lung injury.

31. Respiratory failure(contd.)Respiratory failure(contd.)
 Cerebral damage results from lactic acidCerebral damage results from lactic acid
production, free radical accumulation, andproduction, free radical accumulation, and
release of intracellular metabolites.release of intracellular metabolites.
 Hypoxaemia, through resulting cerebral hypoxia,Hypoxaemia, through resulting cerebral hypoxia,
will depress cerebral function.will depress cerebral function.
 Hypoxaemia with continuing blood supply causesHypoxaemia with continuing blood supply causes
less damage than complete interruption ofless damage than complete interruption of
perfusion, because toxins are removed.perfusion, because toxins are removed.

32. Respiratory failure (contd.)Respiratory failure (contd.)
 Hypercapnia, detected by central chemoreceptors,Hypercapnia, detected by central chemoreceptors,
initially stimulates respiration but thereafterinitially stimulates respiration but thereafter
depresses the regulatory respiratory centres of thedepresses the regulatory respiratory centres of the
brain causing hypoventilation and apnoea.brain causing hypoventilation and apnoea.
Respiratory acidosis results from hypoventilationRespiratory acidosis results from hypoventilation
rendering the patient acidaemic.rendering the patient acidaemic.
 Hypercapnia in a head-injured patient withHypercapnia in a head-injured patient with
impaired cerebral autoregulation causesimpaired cerebral autoregulation causes
vasodilatation and a consequent increase invasodilatation and a consequent increase in
intracranial pressure which may result in secondaryintracranial pressure which may result in secondary
brain injury.brain injury.

33.  Neurological causesNeurological causes
 Common mechanism is ischaemic brainCommon mechanism is ischaemic brain
destruction.destruction.
 Carotid surgery and operations in sitting positionCarotid surgery and operations in sitting position
present a high risk of hypoperfusion.present a high risk of hypoperfusion.
 The outcome from ischaemic events variesThe outcome from ischaemic events varies
between discrete functional deficits, hemiparesisbetween discrete functional deficits, hemiparesis
and comaand coma..

34.  In brain with impaired autoregulation, injury mayIn brain with impaired autoregulation, injury may
be caused by hypercapnia, hypoxaemia, low MAPbe caused by hypercapnia, hypoxaemia, low MAP
and increased metabolic rate.and increased metabolic rate.
 Cerebral hypoxaemia may result when epilepticCerebral hypoxaemia may result when epileptic
seizures are masked by neuromuscular block, andseizures are masked by neuromuscular block, and
from intraoperative air embolism.from intraoperative air embolism.
 Finally, the spread of intracranial local anaestheticFinally, the spread of intracranial local anaesthetic
can cause unconsciousness.can cause unconsciousness.

35.  Uncommon causesUncommon causes
Central anticholinergic syndromeCentral anticholinergic syndrome
 Symptoms range from cerebral irritation with deliriumSymptoms range from cerebral irritation with delirium
and agitation to CNS depression with stupor and coma.and agitation to CNS depression with stupor and coma.
 These accompany peripheral anticholinergic effects thatThese accompany peripheral anticholinergic effects that
is tachycardia, blurred vision, dry mouth and urinaryis tachycardia, blurred vision, dry mouth and urinary
retention.retention.
 The symptoms are rapidly reversed by physostigmine .The symptoms are rapidly reversed by physostigmine .
 Anti-Parkinsonian, antidepressant and antihistamine drugsAnti-Parkinsonian, antidepressant and antihistamine drugs
can cause central anticholinergic syndrome.can cause central anticholinergic syndrome.

36. Disassociative comaDisassociative coma
 A number of authors report cases and hypothesizeA number of authors report cases and hypothesize
that, after exclusion of organic andthat, after exclusion of organic and
pharmacological causes, coma may be attributedpharmacological causes, coma may be attributed
to a disassociative stupor.to a disassociative stupor.
 Reported delays in return to consciousness spanReported delays in return to consciousness span
time periods from 2 to 30 h, and longer periods oftime periods from 2 to 30 h, and longer periods of
amnesia thereafter.amnesia thereafter.
 Thyroid failure should be considered as a possibleThyroid failure should be considered as a possible
cause of unconsciousness in the immediatecause of unconsciousness in the immediate
postoperative period.postoperative period.

37. A stepwise approach to the patient with prolonged unconsciousness.
Rapid assessment of A B CRapid assessment of A B C 100% Oxygen, airway adjuncts, manual100% Oxygen, airway adjuncts, manual
ventilation, Is the airway protected?ventilation, Is the airway protected?
Assess GCSAssess GCS
Stimulate the patientStimulate the patient
Review anaesthetic chartReview anaesthetic chart
Consider: Naloxone, FlumazenilConsider: Naloxone, Flumazenil
Neostigmine, DoxapramNeostigmine, Doxapram
Drugs, timing, interactionsDrugs, timing, interactions
Take account of patient characteristicsTake account of patient characteristics
Capillary blood glucose Correct glucose if low or highCapillary blood glucose Correct glucose if low or high
Measure temperature Warm if temp < 35.5ºCMeasure temperature Warm if temp < 35.5ºC

38. Clinical Approach (contd.)
Artrial blood gas analysis Correct hypoxia,Artrial blood gas analysis Correct hypoxia,
hypercapnia or acidosishypercapnia or acidosis
Full clinical examination, withFull clinical examination, with
particular attention to respiratory Consider further diagnostic tests:particular attention to respiratory Consider further diagnostic tests:
system and nervous system CXR, CT HEADsystem and nervous system CXR, CT HEAD
Blood TestsBlood Tests
U+E, FBC or haemocue, glucose, TFTU+E, FBC or haemocue, glucose, TFT
If patient remains unconscious decide:If patient remains unconscious decide:
Where this patient should be managed?Where this patient should be managed?
Further course of action?Further course of action?
Consider a dissociative test where otherConsider a dissociative test where other
diagnoses absentdiagnoses absent

39. Thank you