This document discusses delayed recovery from anesthesia. It defines recovery as a state of consciousness where the patient is awake and aware of their surroundings. It then outlines several factors that can cause delayed recovery, including patient factors like age, comorbidities, and genetics, as well as drug factors like residual effects of anesthetic agents, drug interactions, and types of anesthetics used. Specific drugs that can cause delayed recovery, like opioids, benzodiazepines, propofol, and muscle relaxants are also discussed. Metabolic causes such as hypoglycemia, hyperglycemia, hyponatremia, hypernatremia, and hypokalemia are covered.

1. DELAYED RECOVERY FROM
ANAESTHESIA
MODERATOR - DR. B M CHANDRA KUMAR
PRESENTER - DR. VIJAY
DEPT. OF ANAESTHESIA, SNR DH, KOLAR

3. 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.

5. 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”.

6. 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. This stage 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.

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

8. MONITORING RECOVERY FROM
ANAESTHESIA
GLASGOW COMA SCALE
By convention we use the GCS to provide a
rapid,reproducible quantification of depth
ofunconsciousness.
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.

10. 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

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

14. B.OUTPATIENTS
Post Anaesthesia Discharge Scoring System

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

17. CAUSES OF PROLONGED
UNCONSCIOUSNESS
AFTER
ANAESTHESIA

19. PATIENT FACTORS

20. 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

21. • 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

22. 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.

23. 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

24. 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.

25. • 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.

26. 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.

27. 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.

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

29. 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.

30. DRUG FACTORS/
PHARMACOLOGICAL CAUSES

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

32. 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.

33. 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.
• lithium, ondansetron, metoclopramide,
codeine, fentanyl, and oxycodone are among
many others.

34. • 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,
polymyxinB, echothiophate, OCPs, LA etc., will
prolong neuromuscular block
• Neurotoxic effect of chemotherapeutic drugs such
as l-asparaginase and vincristine can also produce
CNS depression.

35. 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

36. 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.

37. • 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.

38. BENZODIAZEPINES
• Benzodiazepines are used for anxiolysis &
premedication; 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.

39. • 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 untildesired
degree of reversal is achieved . Usually total
dose is 0.6 – 1 mg.

40. INTRAVENOUS ANAESTHETIC AGENTS
• Propofol has a large volume of distribution at
steadystate 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.

41. 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.

42. • 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.

43. 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.

44. • 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.

45. • 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.

48. 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

49. METABOLIC CAUSES

50. 1. HYPOGLYCAEMIA
• Hypoglycemia can occur in children with
prolonged fasting.
• It may also occur in starvation, liver failure,
end-stage renal disease, alcohol intoxication,
septicemia, and malaria.
• As the brain is totally dependent on glucose for energy,
hypoglycemia may manifests as restlessness, sweating,
confusion, blurring of vision or diplopia, seizures, and coma.

51. • Diabetic patients on insulin and/or oral hypoglycemic may
sometimes present with hypoglycemia and delayed emergence.
• Salicylates and ethanol given preoperatively may exacerbate
hypoglycemia in starved patients.
• Hypoglycemia can occur during manipulation of insulin-producing
tumor of pancreas or retroperitoneal carcinoma.

52. Causes of hyperglycemia and
hypoglycemia

53. 2. HYPERGLYCAEMIA
• Hyperglycemia occurs in known diabetics as a result of
inadequate provision of insulin or injudicious glucose
supplementation.
• Hyperglycemia in hyperosmolar hyperglycemic nonketotic
acidosis causes an osmotic diuresis and intracellular
dehydration.

54. • The effects of dehydration range from drowsiness to acidosis.
• Intraoperative cerebrovascular accident may occur as a result of
cerebral vascular occlusion, especially in patients with micro..or
macrovascular disease.
• Diabetic ketoacidosis, stress response of prolonged surgery, and.
dexamethasone therapy can also lead to severe hyperglycemia.

55. 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.

56. • 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).

58. • 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

59. • 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)

60. 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.

61. Hypernatremia
Water and Na* loss Water loss. Increased Na+ content
Replace isotonic loss Replace water deficit Loop diuretic
Replace water deficit Replace anv water deficit
Algorithm for TT for
hypernatremia

62. • 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

63. 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.

64. • 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

65. • 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.

66. • Through central venous catheter , correction
@ 10-20 mEq/hr may be administered.
Max 240 mEq/day.

67. 6. OTHER ELECTROLYTE
IMBALANCE
• Hypocalcemia after thyroid or parathyroid
surgery, hypermagnesemia after MgSO4
therapy in preeclampsia, and severe
hypercalcemia produce CNS depression.

68. 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

69. 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.

70. • Cardiac output decreases with a decrease in
temperature and arrhythmias occur. Low
cardiac output affects circulation and drug
pharmacokinetics, as well as tissue perfusion.

71. 9. HYPERTHERMIA
• Temperature above 40°C leads to loss of
consciousness .
• Skeletal muscle destruction after malignant
hyperthermia can delay recovery from
anaesthesia.

72. RESPIRATORY FAILURE

73. • 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.

75. • 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.

76. • 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

77. NEUROLOGICAL CAUSES

78. • 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

79. • Intracranial haemorrhage, thrombosis or
infarction can occur in association with
intraoperativearrhythmias, 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

80. • 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

81. OTHER RARE CAUSES

82. 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.

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

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

85. DELAYED RECOVERY FROM
REGIONAL ANAESTHESIA

86. 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

87. 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.

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

89. A STEPWISE APPROACH TO THE
PATIENT WITH PROLONGED
UNCONSCIOUSNESS

90. Unresponsive patient
Stop all the anaesthetics and stimulate the patient
• Vaporizers switched off
• Change the iv set
• Change the breathing circuit
• Check machine and gas source
Basic care -Assess vital signs and GCS
• Airway - maintain clear airway
• Breathing - ensure adequate respiration ,continuous positive airway pressure
/intermittent positive pressure ventilation indicated
• Circulation - Assessed BP ,HR, ECG, Peripheral perfusion, urine output vasopressors as
indicated

91. looks for possible cause
• Review history and investigation - seizures ,diabetes mellitus,Renal or hepatic
disease
• Review anaesthetic chart - Drug dosage, timing of drug administration
• Other perioperative management
• Full clinical assessment, neurological examination,
Check pupillary response
Examination of remnanants of anaesthetics in the patients
• 100% O2 for 10-15 min
• Hyperventilation
• forced diuresis
warming the patient - Measure the temperature, warm if <35 cel
• Forced air warming ( warm/ Bair Hugger)
• wrapping in blanket / foil sheets
• the room is kept warm
• warm iv fluids

92. Correction of metabolic abnormalites:
Perform ABG - Check oxygenation,co2,blood sugar,electrolytes
• Hypogycemia IV dextrose if < 3mmol per liter
• hyperglycemia - Insulin
• Hyponatremia - 2 mmol/l/hr until the plasma sodium is 120 mmol/ l
• Acidosis
Reversal of residual NMB
• Neostigmine, sugammadex,ulinastetin,milrinone
• Amino acide infusion
• Substitution therapy - steroids, thyroxine,proteins,antibiotics,fresh blood
• Lipid emulsion therapy for local anaesthetic toxicity - 1.5 ml/ kg bolus
of 20% intralipid followed by 0.25 ml / kg/min for 10 min Max. 10ml/ kg
over 30 min

93. • Neurological opinion - Stroke therapy ( tissue plasminogen activator)
• Monitor the patient in intensive care unite with frequent neurolical examination
• Repeat CT scan in 6-8 hours if no improvement

94. 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.

95. • 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.

96. THANK YOU