Delayed recovery of consciousness

after anaesthesia

Delayed recovery of consciousness

after anaesthesia

Dr. Shaiq HameedDr. Shaiq Hameed

Dr. Shaiq HameedDr. Shaiq Hameed

Key pointsKey points Delayed recovery from anaesthesia is often Delayed recovery from anaesthesia is often

multifactorial.multifactorial. Consider drug interactions with neuromuscular Consider drug interactions with neuromuscular

blocking agents.blocking agents. Metabolic abnormalities will not present with the Metabolic abnormalities will not present with the

usual signs and symptoms in the anaesthetized usual signs and symptoms in the anaesthetized patient.patient.

Organic causes of prolonged unconsciousness may Organic causes of prolonged unconsciousness may have important sequelae that should be managed have important sequelae that should be managed appropriately.appropriately.

Rarely, disassociative states may present with Rarely, disassociative states may present with episodes of unconsciousness with no other episodes of unconsciousness with no other

identifiable causeidentifiable cause..

DEFINITIONSDEFINITIONS A conscious individual, is ‘awake and A conscious individual, is ‘awake and

aware of their surroundings and aware of their surroundings and identity’.identity’.

Coma Coma from the Greek word "koma," from the Greek word "koma," meaning deep sleep.meaning deep sleep.

It is defined medically as ‘a state of It is defined medically as ‘a state of unresponsiveness from which the unresponsiveness from which the patient cannot be aroused’.patient cannot be aroused’.

DEFINITIONS (contd.)DEFINITIONS (contd.)

Clouding of consciousness-Clouding of consciousness-Impaired capacity to Impaired capacity to think clearly and remember current stimuli think clearly 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 -reduced alertness, appears to be sleep but responds to verbal or tactile stimulisleep but responds to verbal or tactile stimuli

StuporStupor-reduced alertness, person only responds -reduced alertness, person only responds to noxious stimuli to noxious stimuli

ComaComa-no response to noxious stimuli-no response to noxious stimuli

Glasgow Coma Scale Glasgow Coma Scale

Developed to define outcome in Developed to define outcome in adult patients with head injury adult patients with head injury

Coma: score of 8 or lessComa: score of 8 or less

A useful tool to assess conscious A useful tool to assess conscious state regardless of the causative state regardless of the causative factor.factor.

Glasgow Score 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 2 To 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

Causes of prolongedunconsciousness after

anaesthesia

Causes of prolongedunconsciousness after

anaesthesia

The time taken to emerge to full The time taken to emerge to full consciousness is affected by patient consciousness is affected by patient factors, anaesthetic factors, duration of factors, anaesthetic factors, duration of surgery and painful stimulation.surgery and painful stimulation.

Non-pharmacological causes may have Non-pharmacological causes may have serious sequelae; thus, recognizing these serious sequelae; thus, recognizing these organic conditions is important.organic conditions is important.

Pharmacological Pharmacological The residual effects of a drug (after The residual effects of a drug (after

administration has ceased) are influenced by a administration has ceased) are influenced by a number of factors as ;number of factors as ;

Drug Factors Drug Factors DoseDose Absorption Absorption Distribution Distribution Metabolism Metabolism ExcretionExcretion Context-sensitive half-lifeContext-sensitive half-life Pharmacodynamic interactions (summation, Pharmacodynamic interactions (summation,

potentiation, synergism)potentiation, synergism) Pharmacokinetic interactions (distribution, Pharmacokinetic interactions (distribution,

metabolism, excretion)metabolism, excretion)

Patient factors Patient factors Age (especially extremes)Age (especially extremes) Genetic variations Genetic 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

Metabolic Causes Metabolic Causes

HypoglycaemiaHypoglycaemia HyperglycaemiaHyperglycaemia HyponatraemiaHyponatraemia HypernatraemiaHypernatraemia HypothermiaHypothermia Central anticholinergic syndromeCentral anticholinergic syndrome HypothyroidismHypothyroidism Hepatic or renal failure (uraemia)Hepatic or renal failure (uraemia) SepsisSepsis

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

BenzodiazepinesBenzodiazepines

Used alone, benzodiazepines are unlikely to Used alone, benzodiazepines are unlikely to cause prolonged unconsciousness except in cause prolonged unconsciousness except in susceptible, elderly patients or when given in susceptible, elderly patients or when given in overdose. overdose.

CNS depression can prolong the effects of CNS depression can prolong the effects of other anaesthetic agents. other anaesthetic agents.

Benzodiazepines combined with high-dose Benzodiazepines combined with high-dose opioids can have a pronounced effect on opioids can have a pronounced effect on respiratory depression, producing respiratory depression, producing hypercapnia and coma.hypercapnia and coma.

OpioidsOpioids

There are two major mechanisms resulting in coma,There are two major mechanisms resulting in coma, respiratory depression and direct sedation via opioid respiratory depression and direct sedation via opioid

receptors;receptors;

1.1. The sensitivity of the brainstem chemoreceptors to The sensitivity of the brainstem chemoreceptors to carbon dioxide is reduced by opioids with carbon dioxide is reduced by opioids with consequent dose-dependant respiratory depression consequent dose-dependant respiratory depression and resultant hypercapnia. This may affect and resultant hypercapnia. This may affect clearance of volatile agents and carbon dioxide; clearance of volatile agents and carbon dioxide; both can cause unconsciousness.both can cause unconsciousness.

2.2. The direct opioid receptor effect which varies with The direct opioid receptor effect which varies with drug potency, half-life, metabolism and patient drug potency, half-life, metabolism and patient sensitivity.sensitivity.

Neuromuscular blockNeuromuscular block

Neuromuscular block in the conscious patient can Neuromuscular block in the conscious patient can mimic unconsciousness. mimic unconsciousness.

Neuromuscular blockers may result in prolonged Neuromuscular blockers may result in prolonged unconsciousness if a residual block causes unconsciousness if a residual block causes hypoventilation.hypoventilation.

A large number of pharmacological interactions with A large number of pharmacological interactions with neuromuscular blocking agents prolong neuromuscular neuromuscular blocking agents prolong neuromuscular block.block.

The majority of drug interactions with nondepolarizing The majority of drug interactions with nondepolarizing neuromuscular blocking agents prolong blockade by neuromuscular blocking agents prolong blockade by interfering with calcium, the second messenger interfering with calcium, the second messenger involved in acetylcholine release. involved in acetylcholine release.

Neuromuscular block(contd.)Neuromuscular block(contd.)

Electrolyte disturbances cause cell wall Electrolyte disturbances cause cell wall hyperpolarization and prolonged block.hyperpolarization and prolonged block.

Hypothermia decreases metabolism and acidosis Hypothermia decreases metabolism and acidosis donates protons to tertiary amines, increasing donates protons to tertiary amines, increasing receptor affinity.receptor affinity.

Deficiencies of plasma cholinesterase prolong block Deficiencies of plasma cholinesterase prolong block produced by succinylcholine; therapeutic plasma produced by succinylcholine; therapeutic plasma concentrations persist because of decreased concentrations persist because of decreased metabolism.metabolism.

Interactions with non-depolarising muscle relaxants

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

Interactions with depolarising muscle relaxants

Interactions with depolarising muscle relaxants

Genetic Acquired acetylcholinesterasedeficiency

Succinylcholine apnoea

Myotonic Dystrophy

PregnancyLiver DiseaseRenal failureCardiac failureThyrotoxicosisDrugs (ecothiopate, ketamine, OCP’s, lidocaine, neostigmine, ester local- anaesthetics)

I.V. anaesthetic agentsI.V. anaesthetic agents

The termination of action of i.v. agents given as a The termination of action of i.v. agents given as a bolus for induction is predominantly determined bolus for induction is predominantly determined by redistribution and should not delay recovery.by redistribution and should not delay recovery.

Propofol has a large volume of distribution at Propofol has a large volume of distribution at steady-state and a relatively long elimination half-steady-state and a relatively long elimination half-life. The effect of propofol after total i.v. life. The effect of propofol after total i.v. anaesthesia (TIVA) is prolonged.anaesthesia (TIVA) is prolonged.

Duration of unconsciousness is affected by Duration of unconsciousness is affected by context-sensitive half-life, amount of drug, co-context-sensitive half-life, amount of drug, co-administration with other drugs, and patient administration with other drugs, and patient factors.factors.

Volatile anaesthetic agentsVolatile anaesthetic agents Emergence from volatile agent anaesthesia Emergence from volatile agent anaesthesia

depends upon pulmonary elimination of the depends upon pulmonary elimination of the drug and MACdrug and MACawake awake (the end-tidal (the end-tidal concentration associated with eye-opening concentration associated with eye-opening to verbal command).to verbal command).

MACMACawake awake is consistently and approximately is consistently and approximately 30% of MAC.30% of MAC.

Pulmonary elimination is determined by Pulmonary elimination is determined by alveolar ventilation, blood–gas partition co-alveolar ventilation, blood–gas partition co-efficient and dose (MAC-hours). efficient and dose (MAC-hours).

Volatile anaesthetic agents(contd.)Volatile anaesthetic agents(contd.)

Using an agent with low blood–gas solubility Using an agent with low blood–gas solubility results in a quicker emergence.results in a quicker emergence.

Alveolar hypoventilation lengthens the time Alveolar hypoventilation lengthens the time taken to exhale the anaesthetic and delays taken to exhale the anaesthetic and delays recovery. recovery.

Time to emergence increases with Time to emergence increases with increasing duration of anaesthesia (i.e. increasing duration of anaesthesia (i.e. context-sensitive half-life increases), but context-sensitive half-life increases), but does not change MACdoes not change MACawakeawake..

Metabolic causesMetabolic causes

HypoglycaemiaHypoglycaemia Neuroglycopenia manifests as confusion, abnormal Neuroglycopenia manifests as confusion, abnormal

behaviour, seizures and coma.behaviour, seizures and coma. In the elderly population, lateralizing neurological In the elderly population, lateralizing neurological

signs are commonly seen.signs are commonly seen. Postoperative hypoglycaemia most often results Postoperative hypoglycaemia most often results

from poorly controlled diabetes, starvation and from poorly controlled diabetes, starvation and alcohol consumption.alcohol consumption.

Other causes of hypoglycaemia include Sepsis, Other causes of hypoglycaemia include Sepsis, Liver failure, Paediatrics, Sulphonylureas, Endocrine Liver failure, Paediatrics, Sulphonylureas, Endocrine tumours, Hypoadrenalismtumours, Hypoadrenalism

HyperglycaemiaHyperglycaemia Severe hyperglycaemia can prolong Severe hyperglycaemia can prolong

unconsciousness after anaesthesia. unconsciousness after anaesthesia.

A venous blood glucose >14 mmol/litre A venous blood glucose >14 mmol/litre causes an osmotic diuresis and dehydration causes an osmotic diuresis and dehydration in the untreated patient.in the untreated patient.

The effects of dehydration range from The effects of dehydration range from drowsiness to acidosis.drowsiness to acidosis.

Blood hyperosmolality and hyperviscosity Blood hyperosmolality and hyperviscosity predispose to thrombosis and cerebral predispose to thrombosis and cerebral oedema. oedema.

Hyperglycaemia(contd.)Hyperglycaemia(contd.)

Intraoperative cerebrovascular accident Intraoperative cerebrovascular accident may occur as a result of cerebral vascular may occur as a result of cerebral vascular occlusion, especially in diabetics with occlusion, especially in diabetics with microvascular and macrovasculardisease.microvascular and macrovasculardisease.

Causes include; Ketoacidosis, Hyperosmolar Causes include; Ketoacidosis, Hyperosmolar non ketotic acidosis (HONK), Lactic acidosis, non ketotic acidosis (HONK), Lactic acidosis, Gestational diabetes, Insulin resistance Gestational diabetes, Insulin resistance (acromegally, Cushing’s), Pancreatitis, (acromegally, Cushing’s), Pancreatitis, Inherited syndromes.Inherited syndromes.

HyponatraemiaHyponatraemia Mild hyponatraemia is usually asymptomatic, but Mild hyponatraemia is usually asymptomatic, but

serum sodium concentration <120 mmol/litre will serum sodium concentration <120 mmol/litre will cause confusion and irritability. Serum sodium cause confusion and irritability. Serum sodium concentration <110 mmol/litre causes seizures, concentration <110 mmol/litre causes seizures, coma and increased mortality. coma and increased mortality.

The causes of hyponatraemia are multiple; The causes of hyponatraemia are multiple; however, those pertinent to anaesthesia are the however, those pertinent to anaesthesia are the conditions that may develop during operation. conditions that may develop during operation.

Inappropriate anti-diuretic hormone secretion Inappropriate anti-diuretic hormone secretion (SIADH) can result from brain trauma, subarachnoid (SIADH) can result from brain trauma, subarachnoid haemorrhage and administration of drugs (e.g. haemorrhage and administration of drugs (e.g. opioids, haloperidol, vasopressin).opioids, haloperidol, vasopressin).

Hyponatraemia(contd.)Hyponatraemia(contd.)

Cerebral salt-wasting syndrome may also occur in Cerebral salt-wasting syndrome may also occur in the brain injured patient, and infusion of mannitol the brain injured patient, and infusion of mannitol can dehydrate. can dehydrate.

Fluid overload and hyponatraemia may occur when Fluid overload and hyponatraemia may occur when large volumes of irrigation fluid (glycine solution) large volumes of irrigation fluid (glycine solution) are absorbed by open venous sinuses during trans-are absorbed by open venous sinuses during trans-urethral resection of the prostate (TURP), that is urethral resection of the prostate (TURP), that is TURP syndrome. The result is hyponatraemia, TURP syndrome. The result is hyponatraemia, pulmonary oedema and cerebral oedema causing pulmonary oedema and cerebral oedema causing variable cerebral signs, including coma.variable cerebral signs, including coma.

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

HypernatraemiaHypernatraemia

Extreme hypernatraemia is less likely to Extreme hypernatraemia is less likely to occur in the postoperative environment.occur in the postoperative environment.

Sodium excess results in cellular Sodium excess results in cellular dehydration including cerebral dehydration, dehydration including cerebral dehydration, ruptured vessels and intracranial ruptured vessels and intracranial haemorrhage. haemorrhage.

Symptoms include thirst, drowsiness, Symptoms include thirst, drowsiness, confusion and coma.confusion and coma.

UraemiaUraemia Uraemia results in dehydration and cerebral effects Uraemia 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, but The clinical effects of uraemia are varied, but

intracerebral changes may produce drowsiness, intracerebral changes may produce drowsiness,

confusion and comaconfusion and coma. .

HypothermiaHypothermia

The effects of hypothermia are multiple and The effects of hypothermia are multiple and widespread throughout the body. widespread throughout the body.

Neurological and respiratory changes occur with Neurological and respiratory changes occur with decreasing temperature, e.g. confusion (<35C), decreasing temperature, e.g. confusion (<35C), unconsciousness (<30C), apnoea (<24C), absent unconsciousness (<30C), apnoea (<24C), absent cerebral activity (<18C).cerebral activity (<18C).

Respiratory failureRespiratory failure

Postoperative respiratory failure causes Postoperative respiratory failure causes hypoxaemia, hypercapnia, or both. hypoxaemia, hypercapnia, or both.

The causes of respiratory failure are The causes of respiratory failure are multiple and may be classified into multiple and may be classified into neurological, pulmonary, and muscular.neurological, pulmonary, and muscular.

Central drive is lost during drug overdose, Central drive is lost during drug overdose, with intracranial pathology and in patients with intracranial pathology and in patients with chronic obstructive pulmonary disease with chronic obstructive pulmonary disease or sleep apnoea.or sleep apnoea.

Respiratory failure(contd.)Respiratory failure(contd.)

Ventilation is affected by primary muscle Ventilation is affected by primary muscle problems, metabolic imbalance, obesity and problems, metabolic imbalance, obesity and residual neuromuscular block.residual neuromuscular block.

Pulmonary disease states result in venous Pulmonary disease states result in venous admixture, dead space, or both and include admixture, dead space, or both and include pulmonary pulmonary embolism, atelectasis, embolism, atelectasis, obstruction, aspiration, consolidation, obstruction, aspiration, consolidation, acute acute respiratory distress syndrome and respiratory distress syndrome and transfusion-related acute lung injury. transfusion-related acute lung injury.

Respiratory failure(contd.)Respiratory failure(contd.)

Cerebral damage results from lactic acid Cerebral damage results from lactic acid production, free radical accumulation, and production, free radical accumulation, and release of intracellular metabolites.release of intracellular metabolites.

Hypoxaemia, through resulting cerebral Hypoxaemia, through resulting cerebral hypoxia, will depress cerebral function.hypoxia, will depress cerebral function.

Hypoxaemia with continuing blood supply Hypoxaemia with continuing blood supply causes less damage than complete causes less damage than complete interruption of perfusion, because toxins are interruption of perfusion, because toxins are removed.removed.

Respiratory failure (contd.)Respiratory failure (contd.)

Hypercapnia, detected by central Hypercapnia, detected by central chemoreceptors, initially stimulates respiration chemoreceptors, initially stimulates respiration but thereafter depresses the regulatory but thereafter depresses the regulatory respiratory centres of the brain causing respiratory centres of the brain causing hypoventilation and apnoea. Respiratory acidosis hypoventilation and apnoea. Respiratory acidosis results from hypoventilation rendering the results from hypoventilation rendering the patient acidaemic. patient acidaemic.

Hypercapnia in a head-injured patient with Hypercapnia in a head-injured patient with impaired cerebral autoregulation causes impaired cerebral autoregulation causes vasodilatation and a consequent increase in vasodilatation and a consequent increase in intracranial pressure which may result in intracranial pressure which may result in secondary brain injury.secondary brain injury.

Neurological causesNeurological causes

Common mechanism is ischaemic brain Common mechanism is ischaemic brain destruction.destruction.

Carotid surgery and operations in sitting Carotid surgery and operations in sitting

position present a high risk of hypoperfusion. position present a high risk of hypoperfusion.

The outcome from ischaemic events varies The outcome from ischaemic events varies between discrete functional deficits, between discrete functional deficits, hemiparesis and comahemiparesis and coma..

In brain with impaired autoregulation, injury In brain with impaired autoregulation, injury may be caused by hypercapnia, hypoxaemia, may be caused by hypercapnia, hypoxaemia, low MAP and increased metabolic rate.low MAP and increased metabolic rate.

Cerebral hypoxaemia may result when Cerebral hypoxaemia may result when epileptic seizures are masked by epileptic seizures are masked by neuromuscular block, and from intraoperative neuromuscular block, and from intraoperative air embolism.air embolism.

Finally, the spread of intracranial local Finally, the spread of intracranial local anaesthetic can cause unconsciousness.anaesthetic can cause unconsciousness.

Uncommon causesUncommon causes

Central anticholinergic syndromeCentral anticholinergic syndrome Symptoms range from cerebral irritation with delirium Symptoms range from cerebral irritation with delirium

and agitation to CNS depression with stupor and and agitation to CNS depression with stupor and coma.coma.

These accompany peripheral anticholinergic effects These accompany peripheral anticholinergic effects that is tachycardia, blurred vision, dry mouth and that is tachycardia, blurred vision, dry mouth and urinary retention. urinary retention.

The symptoms are rapidly reversed by physostigmine The symptoms are rapidly reversed by physostigmine ..

Anti-Parkinsonian, antidepressant and antihistamine Anti-Parkinsonian, antidepressant and antihistamine drugs can cause central anticholinergic syndrome.drugs can cause central anticholinergic syndrome.

Disassociative comaDisassociative coma A number of authors report cases and A number of authors report cases and

hypothesize that, after exclusion of organic hypothesize that, after exclusion of organic and pharmacological causes, coma may be and pharmacological causes, coma may be attributed to a disassociative stupor. attributed to a disassociative stupor.

Reported delays in return to consciousness Reported delays in return to consciousness span time periods from 2 to 30 h, and longer span time periods from 2 to 30 h, and longer periods of amnesia thereafter. periods of amnesia thereafter.

Thyroid failure should be considered as a Thyroid failure should be considered as a possible cause of unconsciousness in the possible cause of unconsciousness in the immediate postoperative period.immediate postoperative period.

A stepwise approach to the patient with prolonged unconsciousness.

A stepwise approach to the patient with prolonged unconsciousness.

Rapid assessment of A B CRapid assessment of A B C 100% Oxygen, airway adjuncts, manual 100% Oxygen, airway adjuncts, manual ventilation, Is the airway protected? ventilation, Is the airway protected?

Assess GCSAssess GCS

Stimulate the patientStimulate the patient

Review anaesthetic chart Review anaesthetic chart

Consider: Naloxone, Flumazenil Consider: Naloxone, Flumazenil Neostigmine, Doxapram Neostigmine, Doxapram

Drugs, timing, interactionsDrugs, timing, interactions

Take account of patient characteristicsTake account of patient characteristics

Capillary blood glucose Correct glucose if low Capillary blood glucose Correct glucose if low or highor high

Measure temperature Warm if temp < Measure temperature Warm if temp < 35.5ºC35.5ºC

Clinical Approach (contd.)Clinical Approach (contd.)Artrial blood gas analysis Correct hypoxia,Artrial blood gas analysis Correct hypoxia,

hypercapnia or acidosishypercapnia or acidosis

Full clinical examination, with Full 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 HEAD system and nervous system CXR, CT HEAD

Blood TestsBlood Tests

U+E, FBC or haemocue, glucose, TFT U+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

Thank youThank you