includes details of major causes responsible for delayed awakening.

1. DELAYED RECOVERY OF
CONSCIOUSNESS
AFTER ANAESTHESIA
PRESENTER – DR. SOURAV MONDAL
MODERATOR – DR. ARVIND RATHIYA (MD)
DEPT. OF ANAESTHESIOLOGY ,SSMC, REWA , MP

2. INTRODUCTION
• Delayed awakening from anaesthesia remains one of
the biggest challenges involving an
anaesthesiologist.
• The principal factors responsible are anaesthetic
agents and medications used in the perioperative
period.
• Nonpharmacological causes may have a serious
sequel, hence recognizing these organic conditions is
important.

3. • Accurate diagnosis of the underlying cause is the key
for the institution of appropriate therapy, but
primary management is to maintain airway,
breathing and circulation

4. DEFINITIONS
• Recovery from anaesthesia may be defined as “a
state of consciousness of an individual when he is
awake or easily arousable and aware of his
surroundings and identity” .
• Coma is derived from the Greek ‘koma’ meaning a
state of sleep; & is defined medically as “a state of
unresponsiveness from which the patient cannot be
aroused”.

5. PHASES OF RECOVERY FROM
ANAESTHESIA
Divided into 3 phases :
• Immediate recovery
This consists of return of consciousness, recovery of
protective airway reflexes and resumption of motor
activity. Usually lasts for a short time.
• Intermediate recovery
During this stage, the patient regains his power of
coordination and the feeling of dizziness disappears.
This stage usually lasts for 1 hr.

6. • Long-term recovery
There is a full recovery of coordination and higher
intellectual function. May last for hours or even days

7. MONITORING RECOVERY FROM
ANAESTHESIA
GLASGOW COMA SCALE
By convention we use the GCS to provide a rapid,
reproducible quantification of depth of
unconsciousness.
Although the GCS was developed for assessment
and prediction of outcome in traumatic brain
injury, it remains a useful tool to assess conscious
state regardless of the causative factor.

8. GLASGOW SCORE

9. • Interpretation
 Best possible score - 15
 Worst possible score - 3
 Score of < 8 - coma
*When trachea is intubated then , verbal score
is designated as “T”
 Best possible score while intubated - 10T
 Worst possible score while intubated - 2T

10. DISCHARGE CRITERIA
A.PACU
Post Anaesthesia Aldrete Recovery Score

12. • Ideally , the pt should be discharged when the total
score is 10, but a minimum of 9 is required.
• In addition , pt receiving regional anaesthesia should
also be assessed for regression of both sensory and
motor blockade.

13. B.OUTPATIENTS
Post Anaesthesia Discharge Scoring System

15. • Score of ≥ 9 is required for discharge.
• Recovery of proprioception , sympathetic tone,
bladder function & motor strength are additional
criteria following regional anaesthesia.

16. CAUSES OF PROLONGED
UNCONSCIOUSNESS AFTER
ANAESTHESIA

18. PATIENT FACTORS

19. 1. EXTREMES OF AGE
• Geriatric patient
Elderly patients have increased sensitivity
towards general anaesthetics, opioids and
benzodiazepines, and slow return of
consciousness due to progressive decline in CNS
function
The decrease in volume of distribution, clearance
rate, and plasma protein binding results in high
free plasma concentration of drugs

20.  Furthermore, muscle relaxants if given on weight
basis delay onset of action and prolong drug effect.
• Paediatric patients
 Because of larger body surface area, heat loss is
greater in children resulting in hypothermia, slow
drug metabolism, and delayed return of
consciousness

21. 2. GENDER
 Men are 1.4 times more likely to have delayed
recovery than women.
 Lower sensitivity to the hypnotic effect of
anaesthetics in women may account for their faster
recovery.
 The female sex hormone was postulated to play a
role in the gender differences in recovery time.

22. 3. GENETIC FACTORS
 Unexpected responses and prolonged somnolence
after specific anaesthetic are commonly associated
with a genetic defect of the metabolic pathway of
the agent or its receptor.
 Polymorphic changes in gamma-aminobutyric acid 2
receptor can adversely affect the rapid reversal of
propofol anaesthesia.
 Also, variable prolongation of suxamethonium apnea
is due to abnormal or absent plasma cholinesterase
enzyme

23. 4. CO-MORBIDITIES
 Pre-existing cardiac and pulmonary disease require
adjustments in anaesthetic doses to avoid delayed
emergence.
 Significant lung disease decreases the ability to wash
out inhalational agents.
 Congestive heart failure and decreased cardiac
output prolong somnolence.

24.  The renal or hepatic disease can prolong action of
anaesthetic agents dependent on hepatic
metabolism or renal excretion.
 Subclinical hypothyroidism may be diagnosed for the
first time as hypothermia and delayed emergence.
Response to l-thyroxin and thyroid profile will
confirm the diagnosis.
 Adrenal insufficiency can also present as delayed
recovery.

25. 5. BODY HABITUS
 Obesity with increased fat mass requires higher drug
doses to attain the same peak plasma concentration
than a standard sized person.
 Underweight patients are having a higher risk of slow
recovery after vascular surgery and cardiopulmonary
bypass graft surgery.

26. 6. COGNITIVE DYSFUNCTIONS
 Patients with Parkinson's disease are more prone
to postoperative confusion and hallucinations.
Inhaled anaesthetic agents have complex effects on
brain dopamine concentrations.
 Patients with Down's syndrome or mental
retardation are particularly susceptible to delayed
awakening.
 IV sedation in cerebral palsy increases the risk of
hypoxia, and delayed recovery of >60 min is
expected.

27. 7. SEIZURES
 A postictal state may well mimic unconsciousness.
 Antiepileptic drugs are known to reduce the
responsiveness of neuromuscular blocking agent
when given chronically

28. 8. STROKE
 Surgical procedures with increased risk of
embolization are coronary artery bypass graft,
orthopedic particularly joint replacement surgery,
peripheral vascular surgery, and valvular and aortic
surgery.
 Fat embolism from closed chest massage,
corticosteroid therapy, or tissue trauma may present
as delayed return to cognitive function.

29. DRUG FACTORS/
PHARMACOLOGICAL CAUSES

30. 1. RESIDUAL DRUG EFFECTS
 A heavy premedication or the relative overdose of
general anaesthetic agents may be the cause of
delayed awakening.

31. 2. POTENTIATION BY OTHER DRUGS
 Drugs such as tranquilizers, antihypertensives,
anticholinergics, clonidine, antihistamines,
penicillin-derived antibiotics, amphotericin B,
immunosuppressants, lidocaine, and alcohol will
potentiate the CNS depressant effects of anaesthetic
drugs and delay emergence from anaesthesia.

32. 3. DRUG INTERACTIONS
 Patient taking MAOIs or SSRIs may experience
severe drug interactions with IV agents that can
result in hyper/hypotension and postoperative coma
or a full-blown serotonergic syndrome.
 St. John's Wort, ginseng, lithium, ondansetron,
metoclopramide, codeine, fentanyl, and
oxycodone are among many others.

33.  Patients taking bromocriptine or pergolide are
prone to excessive vasodilatation exacerbating
hypotension
 Pharmacological interactions with neuromuscular
blocking agents such as aminoglycosides, diuretics,
calcium channel antagonists, lithium, polymyxin-
B, echothiophate, OCPs, LA etc., will prolong
neuromuscular block
 Neurotoxic effect of chemotherapeutic drugs such as
l-asparaginase and vincristine can also produce
CNS depression.

34. 4. DURATION AND TYPE OF
ANAESTHETIC USED
 The selection of anaesthetic technique and
anaesthetic drugs determines the duration of
unconsciousness
 Recovery may be delayed if soluble volatile agents
are continued until the end of surgery or long-acting
drugs are given toward the end of the procedure

35. OPIOIDS
 Opioids produce analgesia, sedation and respiratory
depression.
 Dose–response is affected by co-administered sedatives
and analgesia and by patient factors.
 There are two major mechanisms resulting in coma:
respiratory depression and direct sedation via opioid
receptors.
 The sensitivity of the brainstem chemoreceptors to CO2 is
reduced by opioids with consequent dose-dependant
respiratory depression and resultant hypercapnia.

36.  This may affect clearance of volatile agents and CO2;
both can cause unconsciousness.
 Active metabolites of morphine and meperidine
(pethidine) prolong the duration of action, especially
in the presence of renal failure.
 T/t – I.V. Naloxone @ 0.5-1 mcg/kg every 3-5 mins ,
until adequate ventilation or alertness is achieved.
Max 0.2 mg.

37. BENZODIAZEPINES
 Benzodiazepines are used for anxiolysis & pre-
medication; co-induction facilitates the hypnotic and
sedative properties of other agents.
 Used alone, benzodiazepines are unlikely to cause
prolonged unconsciousness except in susceptible,
elderly patients or when given in overdose.
 However, CNS depression can prolong the effects of
other anaesthetic agents.

38.  Benzodiazepines combined with high-dose opioids
can have a pronounced effect on respiratory
depression, producing hypercapnia and coma.
 T/t – I.V. Flumazenil @ 0.2 mg/min until desired
degree of reversal is achieved . Usually total dose is
0.6 – 1 mg.

39. INTRAVENOUS ANAESTHETIC AGENTS
 Propofol has a large volume of distribution at steady-
state and a relatively long elimination half-life. The
effect of propofol after TIVA is prolonged.
 Delayed emergence from thiopentone is observed in
Huntington's chorea
 Norketamine contribute in prolonging the effect of
ketamine
 Duration of unconsciousness is affected by context
sensitive half-life, amount of drug, co-administration
with other drugs, and patient factors.

40. VOLATILE ANAESTHETIC AGENTS
 Emergence from volatile agent anaesthesia depends
upon pulmonary elimination of the drug and
MACawake
 The speed of emergence is directly related to
alveolar ventilation and inversely related to blood gas
solubility.
 Hypoventilation lengthens the time taken to exhale
the anaesthetic agent and delays recovery.

41.  Prolonged duration of anaesthesia causes increased
emergence time due to tissue uptake depending
upon the concentration used and drug solubility.
 If vaporizers are not calibrated correctly, higher than
expected dose may be delivered, especially if end
tidal drug concentrations are not measured.
 Release of bromide ions after halothane anaesthesia
may produce postoperative drowsiness.

42. NEUROMUSCULAR BLOCKERS
 Occurs secondary to absolute or relative overdose or
incomplete reversal of nondepolarizing muscle
relaxants or in a patient with suxamethonium apnea
 The patient may become distressed or agitated,
typically twitchy movements of partial reversal may
also be seen.
 Electrolyte disturbances cause cell-wall
hyperpolarization and prolong block.

43.  Hypothermia decreases metabolism and acidosis
donates protons to tertiary amines, increasing
receptor affinity.
 Prolonged apnea following suxamethonium is due to
abnormal or absent plasma cholinesterase enzyme
 Acquired cholinesterase deficiency is seen in
pregnancy, liver disease, renal failure, starvation, and
thyrotoxicosis.

44.  Patients with myasthenia gravis are very sensitive to
nondepolarizing muscle relaxants.
 Increased sensitivity to muscle relaxants is also seen
in patients with muscle dystrophies
 T/t – Cholinesterase inhibitors for antagonism of
non-depolarising neuromuscular blockers.

46. DRUGS PROLONGING NEUROMUSCULAR
BLOCK

47. LOCAL ANESTHETIC SYSTEMIC TOXICITY
 Repeated doses of local anaesthetics in highly
vascular area, intracranial spread of local
anaesthetics after spinal anaesthesia, or accidental
subarachnoid injection during epidural or
interscalene brachial plexus block may cause
prolonged somnolence, seizures, coma, and
cardiorespiratory arrest

48. METABOLIC CAUSES

49. 1. HYPOGLYCAEMIA
 Hypoglycaemia is diagnosed when venous blood
glucose concentration is <2.2 mmol/litre.
 The brain is totally dependent upon glucose as its
energy source.
 The effects of hypoglycaemia can be divided into those
resulting from the sympathetic (catecholamine)
response and those caused by neuroglycopenia.
 Neuroglycopenia manifests as confusion, abnormal
behaviour, seizures and coma. In the elderly
population, lateralizing neurological signs are
commonly seen.

50.  Postoperative hypoglycaemia most often results from
poorly controlled diabetes, starvation and alcohol
consumption.
 Alcohol impairs gluconeogenesis, and will exacerbate
hypoglycaemia in starved patients.
 Other causes include :
– Sepsis
– Liver failure
– Paediatrics
– Sulphonylureas
– Endocrine tumours
– Hypoadrenalism

51. 2. 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.

52.  Intraoperative CVA may occur as a result of cerebral
vascular occlusion, especially in diabetics with
microvascular and macrovascular disease.
 Causes of hyperglycaemia include :
– Ketoacidosis
– Hyperosmolar non ketotic acidosis (HONK)
– Lactic acidosis
– Gestational diabetes
– Insulin resistance (acromegaly, Cushing’s)
– Pancreatitis

53. 3. HYPONATRAEMIA
 Mild hyponatraemia is usually asymptomatic, but
serum sodium concentration <120 mmol/litre may
cause confusion and irritability. Serum sodium
concentration <110 mmol/litre causes seizures, coma
and increased mortality.
 Cerebral salt-wasting syndrome may also occur in the
brain injured patient, and infusion of mannitol can
futher cause dehydration. Here, sodium loss from
the kidneys is thought to be mediated by ANP
secretion. Cerebral oedema results in cerebral
irritation and coma.

54.  Fluid overload and hyponatraemia may occur when
large volumes of glycine solution,is a hypotonic
solution (220 mmol /litre) is absorbed by open
venous sinuses during TURP, i.e. TURP syndrome
which results in pulmonary oedema and cerebral
oedema causing variable cerebral signs, including
coma.
 SIADH can result from brain trauma, subarachnoid
haemorrhage and administration of drugs (e.g.
opioids, haloperidol, vasopressin).

55. ALGORITHM FOR T/T OF HYPONATRAEMIA

56.  T/t –
Sodium deficit = total body water (TBW) × (desired
serum Na − measured serum Na), where TBW = body
weight (kg) × Y. ,
Y=
Children 0.6
Adult male 0.6
Adult women 0.5
Elderly male 0.5
Elderly women 0.45

57. Correction rates –
 Mild symptoms - @ 0.5mEq/L/hr or less
 Moderate symptoms - @1 mEq/L/hr or less
 Severe symptoms – @1.5 mEq/L/hr or less
Pharmacotherapy
 Demeclocycline
 Vaptans (conivaptan & tolvaptan)

58. 4. HYPERNATRAEMIA
 Hypernatremia (plasma Na+ >145 mmol/L) during
hepatic hydatid cyst removal may also hinder the
process of recovery from anesthesia due to cerebral
dehydration, vascular rupture, and intracerebral
hemorrhage.
 Symptoms include thirst, drowsiness, confusion, and
coma.

59. ALGORITHM FOR T/T OF HYPERNATRAEMIA

60. T/t -
Water deficit (L)= total body water(TBW) x
[(measured Na /140)-1]
 This deficit is replaced gradually over 48 hrs.
 Most commonly used fluid for correction of
hypernatraemia is 5% Dextrose in water

61. 5. HYPOKALEMIA
 Hypokalemia intensifies the effects of
nondepolarizing muscle relaxants.
 Respiratory alkalosis with PaCO2 <36 mmHg results in
reduced intracellular proton concentration and
draws K+ into the cells.
 There is a reduction of 0.5 mEq/L of K+ per 10 mmHg
reduction of PaCO2.

62.  Hypokalemia can also occur with perioperative use of
diuretics, calcium gluconate, sodium bicarbonate, β-
adrenergic agonists, glucose, and/or insulin without
K+ supplement
 Mild preoperative hypokalemia without any clinical
features could rapidly deteriorate after iatrogenic
hyperventilation or surgical stimulation and delays
recovery

63. • T/t –
Approximately 200 mEq potassium deficit is required
to decrease serum potassium by 1 mEq/L in the
chronic hypokalemic state.
 In acute situations, the serum potassium
concentration falls by approximately 0.27 mEq/L for
every 100 mEq reduction in total body potassium
stores.
Peripheral iv correction with KCl should not exceed 8
mEq/hr.

64. Through central venous catheter , correction @ 10-20
mEq/hr may be administered.
Max 240 mEq/day.
6. OTHER ELECTROLYTE IMBALANCE
 Hypocalcemia after thyroid or parathyroid surgery,
hypermagnesemia after MgSO4 therapy in
preeclampsia, and severe hypercalcemia produce
CNS depression.

65. 7. 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

66. 8. HYPOTHERMIA
 Neurological and respiratory changes occur with
decreasing temperature, e.g. confusion (<35°C),
unconsciousness (<30°C), apnoea (<24°C), absent
cerebral activity (<18°C).
 The direct hypothermic effects on brain tissue are
compounded by cardiovascular and respiratory
disturbance at less profound degrees of
hypothermia.

67.  Cardiac output decreases with a decrease in
temperature and arrhythmias occur. Low cardiac
output affects circulation and drug
pharmacokinetics, as well as tissue perfusion.
9. HYPERTHERMIA
 Temperature above 40°C leads to loss of
consciousness .
 Skeletal muscle destruction after malignant
hyperthermia can delay recovery from anaesthesia.

68. RESPIRATORY FAILURE

69.  Postoperative respiratory failure causes hypoxaemia,
hypercapnia or both.
 The causes of respiratory failure may be classified into
neurological, pulmonary, and muscular.
 Central drive is lost during drug overdose, with
intracranial pathology and in patients with COPD or sleep
apnoea.
 Ventilation is affected by primary muscle problems,
metabolic imbalance, obesity and residual
neuromuscular block.

70.  Pulmonary disease states result in venous admixture,
dead space, or both and include pulmonary
embolism, atelectasis, obstruction, aspiration,
consolidation, ARDS and TRALI
HYPOXAEMIA
 Hypoxaemia, through resulting cerebral hypoxia, will
depress cerebral function, ultimately causing cell
death.
 Cerebral damage results from lactic acid production,
free radical accumulation, and release of intracellular
metabolites

71.  Hypoxaemia with continuing blood supply causes
less damage than complete interruption of
perfusion, because toxins are removed.
HYPERCAPNIA
 Detected by central chemoreceptors, initially
stimulates respiration but thereafter depresses the
regulatory respiratory centres of the brain causing
hypoventilation and apnoea.

72.  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

73. NEUROLOGICAL CAUSES

74.  The common mechanism is ischaemic brain
destruction.
 Periods of hypoxaemia or ischaemia may occur
during surgery; these are often a result of
inadequate cerebral perfusion secondary to MAP.
 Cerebral autoregulation in the normal brain occurs
between 60 and 160 mm Hg MAP.
 Carotid surgery and operations in a sitting position
present a high risk of hypoperfusion

75.  Intracranial haemorrhage, thrombosis or infarction
can occur in association with intraoperative
arrhythmias, hypo- or hypertension, or in patients
with abnormal cerebral vasculature.
 The outcome from ischaemic events varies between
discrete functional deficits, hemiparesis and coma.
 In the brain with impaired autoregulation, injury may
be caused by hypercapnia, hypoxaemia, low MAP
and increased metabolic rate

76.  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.
POSTOPERATIVE NEUROEXCITATORY SYMPTOMS
symptoms such as twitching, myoclonic movements,
opisthotonus, and seizures can present during
induction, maintenance as well as recovery from
anaesthesia

77. OTHER RARE CAUSES

78. CENTRAL ANTICHOLINERGIC
SYNDROME
 Historically, anticholinergic syndrome was a commonly
encountered sequel to anaesthesia
 It is thought to be due to a decrease in inhibitory
anticholinergic activity in the brain
 Symptoms range from cerebral irritation with delirium
and agitation to CNS depression with stupor and coma.
These accompany peripheral anticholinergic effects i.e.
tachycardia, blurred vision, dry mouth and urinary
retention.

79.  The symptoms are rapidly reversed by
physostigmine.
 Anti-Parkinsonian, antidepressant and antihistaminic
drugs can cause central anticholinergic syndrome

80. Other rare causes include :
– Dissociative coma,
– myxedema coma,
– thyroid failure,
– hunter syndrome (mucopolysaccharide storage
disease),
– valproate toxicity,
– drug abuse, and
– lidocaine infusion for arrhythmias

81. DELAYED RECOVERY FROM
REGIONAL ANAESTHESIA

82. CENTRAL NEURAXIAL BLOCK
 Vascular malformations and anticoagulant therapy
with increased pressure in the vertebral venous
plexus are common causative factors. Diagnosis is
established by MRI.
 Narrowed epidural spaces, migration of epidural
catheter, intrathecal migration of the drug, faulty
infusion pump, potentiation by fentanyl and
clonidine are possible mechanisms for prolongation
of block

83. PERIPHERAL NERVE BLOCK
 Patients with underlying nerve pathology such as
diabetic neuropathy, exposure to neurotoxic
chemotherapy, or disruption of neural blood supply
are more susceptible to peripheral nerve
complications.
 Neurological deficits may persist for days after high-
pressure intraneural injection of local anaesthetics.

84. WOUND INFILTRATION
 Brainstem paralysis due to bupivacaine wound
infiltration after foramina magnum decompression
and field block is also reported

85. A STEPWISE APPROACH TO THE
PATIENT WITH PROLONGED
UNCONSCIOUSNESS

86. 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 < 35.5°C

87. Arterial 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, CBC, 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

88. SUMMARY
 Delayed recovery from anaesthesia is often
multifactorial, and anaesthetic agents may not always be
the culprit.
 When other causes are excluded, the possibility of acute
intracranial event should be strongly considered.
 While the specific cause is being sought, primary
management is always support of airway, breathing, and
circulation.

89.  Good intraoperative care ensures the patient safety
 A calm, comprehensive, and timely management
with a systematic approach is highly rewarding.
 We, the anaesthesiologists, make the patient sleep,
so the recovery from anaesthesia is our
responsibility.