Delayed recovery of consciousness

after anaesthesia

Dr. Shaiq Hameed

 Key points
 Delayed recovery from anaesthesia is often
multifactorial.
 Consider drug interactions with neuromuscular blocking
agents.
 Metabolic abnormalities will not present with the usual
signs and symptoms in the anaesthetized patient.
 Organic causes of prolonged unconsciousness may have
important sequelae that should be managed
appropriately.
 Rarely, disassociative states may present with episodes
of unconsciousness with no other identifiable cause.
 DEFINITIONS
 A conscious individual, is ‘awake and aware
of their surroundings and identity’.

 Coma from the Greek word "koma,"

meaning deep sleep.

 It is defined medically as ‘a state of

unresponsiveness from which the patient
cannot be aroused’.
 DEFINITIONS (contd.)
 Clouding of consciousness-Impaired capacity to think
clearly and remember current stimuli

 Delirium -disturbed consciousness with motor

restlessness, disorientation and hallucination

 Obtundation-reduced alertness, appears to be sleep

but responds to verbal or tactile stimuli

 Stupor-reduced alertness, person only responds to

noxious stimuli

 Coma-no response to noxious stimuli

 Glasgow Coma Scale
 Developed to define outcome in adult
patients with head injury

 Coma: score of 8 or less

 A useful tool to assess conscious state

regardless of the causative factor.
 Glasgow Score
 Eye opening Motor Response
 Spontaneous 4 obeys commands 6
 To command 3 localizes pain 5
 To pain 2 withdraws to pain 4
 None 1 abnormal flexion 3
 Verbal abnormal extension 2
 Oriented 5 none 1
 Confused 4
 Inappropriate words 3 TOTAL 3-15
 Incomprehensible sounds 2
 None 1
 Causes of prolonged
unconsciousness after anaesthesia
 The time taken to emerge to full consciousness
is affected by patient factors, anaesthetic
factors, duration of surgery and painful
stimulation.

 Non-pharmacological causes may have serious

sequelae; thus, recognizing these organic
conditions is important.
 Pharmacological
The residual effects of a drug (after administration has
ceased) are influenced by a number of factors as ;
Drug Factors
 Dose
 Absorption
 Distribution
 Metabolism
 Excretion
 Context-sensitive half-life
 Pharmacodynamic interactions (summation, potentiation,
synergism)
 Pharmacokinetic interactions (distribution, metabolism,
excretion)
Patient factors
 Age (especially extremes)
 Genetic variations
 Disease processes: renal, hepatic failure

Surgical factors
 Requirement for muscle relaxation
 Duration of surgery
 Utilisation of regional techniques
 Degree of pain/stimulation
 Metabolic Causes

 Hypoglycaemia
 Hyperglycaemia
 Hyponatraemia
 Hypernatraemia
 Hypothermia
 Central anticholinergic syndrome
 Hypothyroidism
 Hepatic or renal failure (uraemia)
 Sepsis
 Other causes

 Respiratory Failure
 Central drive
 Muscular/ventilatory disorders
 Pulmonary pathology
 Neurological Causes
 Intracerebral event
 Seizures
 Central hypoxia
 Central ischaemia
 Local anaesthetic toxicity
Benzodiazepines

 Used alone, benzodiazepines are unlikely to cause

prolonged unconsciousness except in susceptible,
elderly patients or when given in overdose.

 CNS depression can prolong the effects of other

anaesthetic agents.

 Benzodiazepines combined with high-dose opioids

can have a pronounced effect on respiratory
depression, producing hypercapnia and coma.
Opioids
There are two major mechanisms resulting in coma,
respiratory depression and direct sedation via opioid receptors;

1. The sensitivity of the brainstem chemoreceptors to

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

2. The direct opioid receptor effect which varies with drug

potency, half-life, metabolism and patient sensitivity.
Neuromuscular block
 Neuromuscular block in the conscious patient can mimic
unconsciousness.

 Neuromuscular blockers may result in prolonged

unconsciousness if a residual block causes hypoventilation.

 A large number of pharmacological interactions with

neuromuscular blocking agents prolong neuromuscular
block.

 The majority of drug interactions with nondepolarizing

neuromuscular blocking agents prolong blockade by
interfering with calcium, the second messenger involved in
acetylcholine release.
Neuromuscular block(contd.)

 Electrolyte disturbances cause cell wall hyperpolarization

and prolonged block.

 Hypothermia decreases metabolism and acidosis donates

protons to tertiary amines, increasing receptor affinity.

 Deficiencies of plasma cholinesterase prolong block

produced by succinylcholine; therapeutic plasma
concentrations persist because of decreased metabolism.
 Interactions with non-depolarising muscle relaxants

Drug Interactions Metabolic Causes Genetic

Volatile anaesthetic Hypothermia Myasthenia gravis

agents
Acidosis Eaton Lambert/Myasthenic
Aminoglycosides syndrome
Hypokalaemia
Lithium
Hypermagnesaemia
Diuretics

Calcium channel
antagonists
 Interactions with depolarising muscle relaxants

Genetic Acquired acetylcholinesterase

deficiency

Succinylcholine apnoea Pregnancy

Liver Disease
Myotonic Dystrophy Renal failure
Cardiac failure
Thyrotoxicosis
Drugs (ecothiopate, ketamine, OCP’s,
lidocaine, neostigmine, ester local-
anaesthetics)
I.V. anaesthetic agents

 The termination of action of i.v. agents given as a bolus

for induction is predominantly determined by
redistribution and should not delay recovery.

 Propofol has a large volume of distribution at steady-

state and a relatively long elimination half-life. The
effect of propofol after total i.v. anaesthesia (TIVA) is
prolonged.

 Duration of unconsciousness is affected by context-

sensitive half-life, amount of drug, co-administration
with other drugs, and patient factors.
Volatile anaesthetic agents
 Emergence from volatile agent anaesthesia
depends upon pulmonary elimination of the drug
and MACawake (the end-tidal concentration
associated with eye-opening to verbal
command).

 MACawake is consistently and approximately 30%

of MAC.

 Pulmonary elimination is determined by alveolar

ventilation, blood–gas partition co-efficient and
dose (MAC-hours).
Volatile anaesthetic agents(contd.)

 Using an agent with low blood–gas solubility

results in a quicker emergence.

 Alveolar hypoventilation lengthens the time taken

to exhale the anaesthetic and delays recovery.

 Time to emergence increases with increasing

duration of anaesthesia (i.e. context-sensitive
half-life increases), but does not change MACawake.
 Metabolic causes

Hypoglycaemia
 Neuroglycopenia manifests as confusion, abnormal
behaviour, seizures and coma.
 In the elderly population, lateralizing neurological signs
are commonly seen.
 Postoperative hypoglycaemia most often results from
poorly controlled diabetes, starvation and alcohol
consumption.
 Other causes of hypoglycaemia include Sepsis, Liver
failure, Paediatrics, Sulphonylureas, Endocrine tumours,
Hypoadrenalism
Hyperglycaemia
 Severe hyperglycaemia can prolong
unconsciousness after anaesthesia.

 A venous blood glucose >14 mmol/litre causes an

osmotic diuresis and dehydration in the untreated
patient.

 The effects of dehydration range from drowsiness

to acidosis.

 Blood hyperosmolality and hyperviscosity

predispose to thrombosis and cerebral oedema.
Hyperglycaemia(contd.)

 Intraoperative cerebrovascular accident may

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

 Causes include; Ketoacidosis, Hyperosmolar non

ketotic acidosis (HONK), Lactic acidosis,
Gestational diabetes, Insulin resistance
(acromegally, Cushing’s), Pancreatitis, Inherited
syndromes.
Hyponatraemia
 Mild hyponatraemia is usually asymptomatic, but serum
sodium concentration <120 mmol/litre will cause
confusion and irritability. Serum sodium concentration
<110 mmol/litre causes seizures, coma and increased
mortality.

 The causes of hyponatraemia are multiple; however,

those pertinent to anaesthesia are the conditions that
may develop during operation.

 Inappropriate anti-diuretic hormone secretion (SIADH) can

result from brain trauma, subarachnoid haemorrhage and
administration of drugs (e.g. opioids, haloperidol,
vasopressin).
Hyponatraemia(contd.)

 Cerebral salt-wasting syndrome may also occur in the

brain injured patient, and infusion of mannitol can
dehydrate.

 Fluid overload and hyponatraemia may occur when large

volumes of irrigation fluid (glycine solution) are absorbed
by open venous sinuses during trans-urethral resection of
the prostate (TURP), that is TURP syndrome. The result is
hyponatraemia, pulmonary oedema and cerebral oedema
causing variable cerebral signs, including coma.
Hyponatraemia and water excess
 Na deficient i.v. fluids
 TURP syndrome
 Excessive drinking
 SIADH
 Drugs
 Nephrotic syndrome

Hyponatraemia and dehydration

 Diuretics
 Hypoadrenalism
 Cerebral salt-wasting
 Nephritis
 Diarrhoea, vomiting
 Pancreatitis
 Renal tubular acidosis
Hypernatraemia

 Extreme hypernatraemia is less likely to occur in

the postoperative environment.

 Sodium excess results in cellular dehydration

including cerebral dehydration, ruptured vessels
and intracranial haemorrhage.

 Symptoms include thirst, drowsiness, confusion

and coma.
Uraemia
 Uraemia results in dehydration and cerebral effects
attributable to cellular damage and distortion.
 The clinical effects of uraemia are varied, but
intracerebral changes may produce drowsiness, confusion
and coma.

Hypothermia
 The effects of hypothermia are multiple and widespread
throughout the body.
 Neurological and respiratory changes occur with decreasing
temperature, e.g. confusion (<35C), unconsciousness
(<30C), apnoea (<24C), absent cerebral activity (<18C).
Respiratory failure

 Postoperative respiratory failure causes

hypoxaemia, hypercapnia, or both.

 The causes of respiratory failure are multiple and

may be classified into neurological, pulmonary,
and muscular.

 Central drive is lost during drug overdose, with

intracranial pathology and in patients with
chronic obstructive pulmonary disease or sleep
apnoea.
Respiratory failure(contd.)

 Ventilation is affected by primary muscle

problems, metabolic imbalance, obesity and
residual neuromuscular block.

 Pulmonary disease states result in venous

admixture, dead space, or both and include
pulmonary embolism, atelectasis, obstruction,
aspiration, consolidation, acute respiratory
distress syndrome and transfusion-related acute
lung injury.
Respiratory failure(contd.)

 Cerebral damage results from lactic acid

production, free radical accumulation, and
release of intracellular metabolites.

 Hypoxaemia, through resulting cerebral hypoxia,

will depress cerebral function.

 Hypoxaemia with continuing blood supply causes

less damage than complete interruption of
perfusion, because toxins are removed.
Respiratory failure (contd.)

 Hypercapnia, detected by central chemoreceptors,

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

 Hypercapnia in a head-injured patient with

impaired cerebral autoregulation causes
vasodilatation and a consequent increase in
intracranial pressure which may result in secondary
brain injury.
 Neurological causes

 Common mechanism is ischaemic brain

destruction.

 Carotid surgery and operations in sitting position

present a high risk of hypoperfusion.

 The outcome from ischaemic events varies

between discrete functional deficits, hemiparesis
and coma.
 In brain with impaired autoregulation, injury may
be caused by hypercapnia, hypoxaemia, low MAP
and increased metabolic rate.

 Cerebral hypoxaemia may result when epileptic

seizures are masked by neuromuscular block, and
from intraoperative air embolism.

 Finally, the spread of intracranial local anaesthetic

can cause unconsciousness.
 Uncommon causes

Central anticholinergic syndrome

 Symptoms range from cerebral irritation with delirium
and agitation to CNS depression with stupor and coma.

 These accompany peripheral anticholinergic effects that

is tachycardia, blurred vision, dry mouth and urinary
retention.

 The symptoms are rapidly reversed by physostigmine .

 Anti-Parkinsonian, antidepressant and antihistamine drugs

can cause central anticholinergic syndrome.
Disassociative coma
 A number of authors report cases and hypothesize
that, after exclusion of organic and
pharmacological causes, coma may be attributed
to a disassociative stupor.

 Reported delays in return to consciousness span

time periods from 2 to 30 h, and longer periods of
amnesia thereafter.

 Thyroid failure should be considered as a possible

cause of unconsciousness in the immediate
postoperative period.
 A stepwise approach to the patient with prolonged unconsciousness.
Rapid assessment of A B C 100% Oxygen, airway adjuncts, manual
ventilation, Is the airway protected?

Assess GCS
Stimulate the patient

Review anaesthetic chart

Consider: Naloxone, Flumazenil
Neostigmine, Doxapram
Drugs, timing, interactions
Take account of patient characteristics

Capillary blood glucose Correct glucose if low or high

Measure temperature Warm if temp < 35.5ºC

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

Full clinical examination, with

particular attention to respiratory Consider further diagnostic tests:
system and nervous system CXR, CT HEAD

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

If patient remains unconscious decide:

Where this patient should be managed?
Further course of action?
Consider a dissociative test where other
diagnoses absent
Thank you