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Delayed Recovery of Consciousness After Anaesthesia

Delayed Recovery of Consciousness After Anaesthesia

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A conscious individual, as defined in theOxford English Dictionary, is ‘awake andaware of their surroundings and identity’.However, consciousness represents a con-tinuum with varying depths of consciousness.Coma is derived from the Greek ‘koma’meaning a state of sleep; more specifically, itis defined medically as ‘a state of unrespons-iveness from which the patient cannot bearoused’.By convention we use the Glasgow comascale (GCS) to provide a rapid, reproduciblequantification of depth of unconsciousness.Although the GCS was developed for assess-ment and prediction of outcome in traumaticbrain injury, it remains a useful tool to assessconscious state regardless of the causativefactor. The GCS scores verbal, movementand visual responses to stimulation; a GCS
8 defines coma.
Causes of prolongedunconsciousness after anaesthesia
The causes of prolonged unconsciousnessafter anaesthesia are summarized in Table 1.The time taken to emerge to full consciousnessis affected by patient factors, anaestheticfactors, duration of surgery and painful stimu-lation. Non-pharmacological causes may haveserious sequelae; thus, recognizing theseorganic conditions is important.
The residual effects of a drug (after adminis-tration has ceased) are influenced by a numberof factors, as outlined in Table 1. With somany variables, it is not surprising thatadministration of an ideal dose to one patientcan have a very different effect on an appar-ently similar patient.
Benzodiazepines are used for anxiolysisand pre-medication; co-induction facilitatesthe hypnotic and sedative properties of otheragents. Used alone, benzodiazepines areunlikely to cause prolonged unconsciousnessexcept in susceptible, elderly patients or whengiven in overdose. However, central nervoussystem (CNS) depression can prolong theeffects of other anaesthetic agents. Benzo-diazepines combined with high-dose opioidscan have a pronounced effect on respiratorydepression, producing hypercapnia andcoma. Midazolam is metabolized by the sameP450 iso-enzyme as alfentanil, such that co-administration prolongs the actions of bothdrugs.
Opioids produce analgesia, sedation andrespiratory depression; the intensity of eachaction varies between subjects and can bedifficult to predict. As noted previously,dose–response is affected by co-administeredsedatives and analgesia and by patient factors.There are two major mechanisms resulting incoma: respiratory depression and direct seda-tion via opioid receptors. The sensitivity of the brainstem chemoreceptors to carbon dio-xide is reduced by opioids with consequentdose-dependant respiratory depression andresultant hypercapnia. This may affect clear-ance of volatile agents and carbon dioxide;both can cause unconsciousness. The directopioidreceptoreffectvarieswithdrugpotency,half-life, metabolism and patient sensitivity.Active metabolites of morphine and meperid-ine (pethidine) prolong the duration of action,especially in the presence of renal failure.
Neuromuscular block
Neuromuscular block in the conscious patientcan mimic unconsciousness. In addition, neur-omuscular blockers may result in prolongedunconsciousness after operation if a residualblock causes hypoventilation. A large numberof pharmacological interactions with neur-omuscular blocking agents prolong neuromus-cular block; these are outlined in Table 2.
The majority of drug interactions with non-depolarizing neuromuscular blocking agentsprolong blockade by interfering with calcium,the second messenger involved in acetylcholine
Key points
Delayed recovery fromanaesthesia is oftenmultifactorial.Consider drug interactionswith neuromuscular blockingagents.Metabolic abnormalities willnot present with the usualsigns and symptoms in theanaesthetized patient.Organic causes of prolongedunconsciousness may haveimportant sequelae thatshould be managedappropriately.Rarely, disassociative statesmay present with episodes of unconsciousness with noother identifiable cause.
Rhona C F Sinclair BMedSci BM BSMRCP
Senior House Officer Department of AnaesthesiaDerbyshire Royal Infirmary Derby DE1 2QYUK 
Richard J Faleiro BSc (Hons) DCHFRCA
Consultant in Anaesthesia andPain MedicineDepartment of AnaesthesiaDerbyshire Royal Infirmary Derby DE1 2QYUK Tel: 01332 347141 ext. 4747Fax: 01332 254963E-mail: richard.faleiro@nhs.net(for correspondence)
Continuing Education in Anaesthesia, Critical Care & Pain | Volume 6 Number 3 2006doi:10.1093/bjaceaccp/mkl020
The Board of Management and Trustees of the British Journal of Anaesthesia [2006].All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Delayed recovery of consciousnessafter anaesthesia
Rhona C F Sinclair B MedSci BM BS MRCPRichard J Faleiro BSc (Hons) DCH FRCA
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release. Electrolyte disturbances cause cell wall hyperpolarizationand prolonged block. Hypothermia decreases metabolism andacidosis donates protons to tertiary amines, increasing receptoraffinity.Deficiencies of plasma cholinesterase prolong block producedby succinylcholine; therapeutic plasma concentrations persistbecause of decreased metabolism. Extension of the block isvariable and depends upon the genotype.
I.V. anaesthetic agents
The termination of action of i.v. agents given as a bolus forinduction is predominantly determined by redistribution andshould not delay recovery. Propofol has a large volume of distribution at steady-state and a relatively long eliminationhalf-life. The effect of propofol after total i.v. anaesthesia(TIVA) is prolonged. The context-sensitive half-life is the timetaken for the effect-site concentration of drug to reduce to 50%,and is dependent upon the duration of infusion (i.e. the context).A set of context-sensitive half-life curves can be constructedfor each drug allowing prediction of offset time. Typically,a reduction of 80% in the effect-site concentration is requiredfor emergence. For example, the time to emergence from a 2-hpropofol-only anaesthetic can be modelled and shows non-linearcontext-sensitive half-lives. An 80% decrease in effect-site con-centration after 2 h will take 36 min; if the dose of propofol isdoubled, the emergence time becomes 105 min, and if it is halved(sedation), the time decreases to 10 min.
Thus, duration of unconsciousness is affected by context-sensitive half-life, amount of drug, co-administration withother drugs, and patient factors.
Volatile anaesthetic agents
Emergence from volatile agent anaesthesia depends upon pul-monary elimination of the drug and MAC
(the end-tidalconcentration associated with eye-opening to verbal command).MAC
is consistently and approximately 30% of MAC.(MAC
: isoflurane 0.39%; desflurane 2.17%; sevoflurane0.61%). Pulmonary elimination is determined by alveolarventilation, blood–gas partition co-efficient and dose (MAC-hours). Using an agent with low blood–gas solubility resultsin a quicker emergence (e.g. sevoflurane 7 min; isoflurane11.5 min). Alveolar hypoventilation lengthens the time takento exhale the anaesthetic and delays recovery. Time to emer-gence increases with increasing duration of anaesthesia(i.e. context-sensitive half-life increases), but does not changeMAC
. Practically, once a patient has emerged fromanaesthesia any remaining volatile agent leaching from thebody stores is unlikely to cause an effect-site concentrationthat would cause unconsciousness.It is important to remember that drug overdoses are relative;they depend upon who receives them, what point in time relativeto cessation of general anaesthesia they occur, and what otheragents have been administered.
Table 1
Causes of prolonged unconsciousness after anaesthesia
Pharmacological EffectsDrug Factors Patient factors Surgical factorsDose Age (especiallyextremes)Requirement formuscle relaxation,Absorption Genetic variations Duration of surgery,Distribution Disease processes:renal, hepaticfailureUtilisation of regional techniques,Metabolism Degree opain/stimulationExcretionContext-sensitive half-lifePharmacodynamicinteractions (summation,potentiation, synergism)Pharmacokinetic interactions(distribution, metabolism,excretion)Respiratory FailureCentral driveMuscular/ventilatory disordersPulmonary pathologyNeurological CausesIntracerebral eventSeizuresCentral hypoxiaCentral ischaemiaLocal anaesthetic toxicityMetabolic CausesHypoglycaemiaHyperglycaemiaHyponatraemiaHypernatraemiaHypothermiaCentral anticholinergic syndromeHypothyroidismHepatic or renal failure (uraemia)Sepsis
Table 2
Interactions with neuromuscular antagonists.
Interactions with non-depolarising muscle relaxantsDrug Interactions Volatile anaesthetic agentsAminoglycosidesLithiumDiureticsCalcium channel antagonistsMetabolic Causes HypothermiaAcidosisHypokalaemiaHypermagnesaemiaGenetic Myasthenia gravisEaton Lambert/Myasthenic syndromeInteractions with depolarising muscle relaxantsGenetic Succinylcholine apnoeaMyotonic DystrophyAcquired acetylcholinesterasedeficiencyPregnancyLiver DiseaseRenal failureCardiac failureThyrotoxicosisDrugs (ecothiopate, ketamine, oralcontraceptive pill (OCP), lidocaine,neostigmine, ester local anaesthetics)
Delayed recovery of consciousness after anaesthesia
Continuing Education in Anaesthesia, Critical Care & Pain | Volume 6 Number 3 2006
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Metabolic causes
Hypoglycaemia is diagnosed by confirmation of a venousblood glucose concentration of 
2.2 mmol litre
. The brain istotally dependent upon glucose as its energy source. The effectsof hypoglycaemia can be divided into those resulting fromthe sympathetic (catecholamine) response and those caused byneuroglycopenia. Neuroglycopenia manifests as confusion,abnormal behaviour, seizures and coma. In the elderly popula-tion,lateralizing neurologicalsignsarecommonly seen.Postoper-ative hypoglycaemia most often results from poorly controlleddiabetes, starvation and alcohol consumption. Alcohol impairsgluconeogenesis, and will exacerbate hypoglycaemia in starvedpatients or those with minimal energy reserves. Other causes of hypoglycaemia are listed in Table 3.
Severe hyperglycaemia can prolong unconsciousness afteranaesthesia. A venous blood glucose
14 mmol litre
causesan osmotic diuresis and dehydration in the untreated patient.The effects of dehydration range from drowsiness to acidosis.Furthermore, blood hyperosmolality and hyperviscosity pre-dispose to thrombosis and cerebral oedema. Intraoperativecerebrovascular accident may occur as a result of cerebralvascular occlusion, especially in diabetics with microvascularand macrovascular disease. An anaesthetized patient will notdisplay all the clinical signs of glucose abnormality.
Mild hyponatraemia is usually asymptomatic, but serum sodiumconcentration
120 mmol litre
will cause confusion andirritability. Serum sodium concentration
110 mmol litre
causes seizures, coma and increased mortality. The causes of ahyponatraemia are multiple; however, those pertinent to anaes-thesia are the conditions that may develop during operation.Inappropriate anti-diuretic hormone secretion (SIADH) canresult from brain trauma, subarachnoid haemorrhage andadministration of drugs (e.g. opioids, haloperidol, vasopressin).Cerebral salt-wasting syndrome may also occur in the brain-injured patient, and infusion of mannitol can dehydrate. Cerebralsalt-wasting syndrome describes sodium loss from the kidneys inassociation with intracranial pathology, thought to be mediatedby atrial natriuretic peptide secretion. Cerebral oedema resultsin cerebral irritation and coma.Fluid overload and hyponatraemia may occur when largevolumes of irrigation fluid (glycine solution) are absorbed byopen venous sinuses during trans-urethral resection of the pro-state (TURP), that is TURP syndrome. Glycine is a hypotonicsolution (220 mmol litre
). The result is hyponatraemia, pul-monary oedema and cerebral oedema causing variable cerebralsigns, including coma. Intensive resuscitation and managementis required.
Extreme hypernatraemia is less likely to occur in the post-operative environment; however, sodium excess results in acellular dehydration including cerebral dehydration, rupturedvessels and intracranial haemorrhage. Symptoms include thirst,drowsiness, confusion and coma.
Uraemia results in dehydration and cerebral effects attributableto cellular damage and distortion. The clinical effects of uraemiaare varied, but intracerebral changes may produce drowsinessconfusion and coma.
The effects of hypothermia are multiple and widespread through-out the body. Neurological and respiratory changes occur withdecreasing temperature, e.g. confusion (
C), unconsciousness(
C), apnoea (
C), absent cerebral activity (
C). Thedirect hypothermic effects on brain tissue are compounded bycardiovascular and respiratory disturbance at less profounddegrees of hypothermia.Cardiac output decreases with a decreasein temperature and arrhythmias occur. Low cardiac outputaffects circulation and drug pharmacokinetics, as well as tissueperfusion.
Table 3
Endocrine disturbances
Endocrine disturbance CausesHypoglycaemia DiabetesStarvationAlcoholSepsisLiver failurePaediatricsSulphonylureasEndocrine tumoursHypoadrenalismHyperglycaemia KetoacidosisHyperosmolar non ketotic acidosis (HONK)Lactic acidosisGestational diabetesInsulin resistance (acromegally, Cushing’s)PancreatitisInherited syndromesHyponatraemia and water excess Na deficient i.v. fluidsTURP syndromeExcessive drinkingSIADHDrugsNephrotic syndromeHyponatraemia and dehydration DiureticsHypoadrenalismCerebral salt-wastingNephritisDiarrhoea, vomitingPancreatitisRenal tubular acidosis
Continuing Education in Anaesthesia, Critical Care & Pain | Volume 6 Number 3 2006
Delayed recovery of consciousness after anaesthesia
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