Evaluation and Management of Delayed

Awakening or Emergence From

Anaesthesia

Dr. Shagufta
Introduction

 Delayed emergence is failure to regain consciousness following general anesthesia. It commonly involves
altered mental status and respiratory compromise leading to increased morbidity, operating room delays,
and increased cost.

 At the end of surgery patient should be awake or easily rousable protecting their airway, maintaining adequate
ventilation and pain under control.
Recovery from Anaesthesia:
It’s a state of consciousness in which patient is awake, easily rousible and aware of his surroundings and identity.

Delayed Emergence:
Failure to regain consciousness following G/A, commonly involves alternative status and respiratory compromise
leading to increased morbidity, operating room delays and increase cost

Coma:
Phases of Recovery from Anaesthesia

 3-phases of recovery

 Immediate Recovery – Return of consciousness, recovery of protective airway reflexes &

resumption of motor activity. It last for short time.
 Intermediate Recovery – Patient regains power of coordination, feeling of dizziness disappear. It
last for 1 hour.
 Log Term Recovery – Full recovery of coordination and higher intellectual function
Causes of delayed awakening

 Residual drug effects:

 Overdose – Too much drug dose is given or patient is lightly susceptible.
 Frail, small or elderly patients require lower dose.
 Delayed drug metabolism in Renal and Hepatic failure
 Increased sensitivity to particular agent as in myasthenia, There is increased in sensitivity to non
depolarizing muscle relaxant.
Duration & Type of Anaesthesia given

 For Inhalational Anaesthetics – Speed of emergence related to alveolar ventilation. So

hypoventilation causes delayed emergence
 It is inversely related to blood gas solubility of agent.
 Less soluble agent i.e. Nitrous Oxide halothane rapidly eliminated than ether
 When duration prolongs emergence depends upon total tissue uptake of drug. This is
related to:
 Drug solubility
 Average concentration used
 Duration of Exposure
Duration & Type of Anaesthesia given

 For IV Anesthetic Agents:

 Immediate recovery depends upon redistribution from blood and brain into muscle and fat.
 Patient given propofol recovers faster as it is metabolized by liver and extrahepatic site.
 With thiopentone long elimination of life as 30% of dose may remain in the body as 24 Hrs.
 Patient with advanced age renal and hepatic failure can prolog drug action.

 Potentation by Other Drugs:

Prior ingestion of sedative premedication as benzodiazepines or alcohol will potentiate CNS
depressant effect of anesthetic and Analgesic drugs.
Prolonged Neuromuscular Blockade

 Residual NMB Results in Paralysis which is perceived as unresponsiveness.

 Occurs secondary to overdose or incomplete reversal of non-depolarizing NMB or in patient with
suxamethonium apnoea.
 Tested by nerve stimulator
 Inability to maintain head lift for 5 sec indicates 30% residual block
 Typical twitchy movement of partial reversal seen
 Scholine apnoea is due to abnormal or absent cholinesterase enzyme e.g. in pregnancy and liver
disease.
 Repeated doses of suxamethonium > 6-8 mg/Kg total dose produces dual block
 Mivacurium apnoea is rare (Metabolized by cholinesterase enzyme)
 In myasthenia Gravis long acting NMB should be avoided
 In renal failure, there is reduced elimination of non-depolarizing muscle relaxants.

Respiratory Failure

 Patient who do not breathe effectively during or after Anaesthesia may become hyperbaric
increased co2 that produce sedation or unconsciousness.
 Risk factors
 Underlying respiratory disease with co2 retention
 High dose opiods
 Obstructed airway
 Poor relaxant reversal
 diagnosed by arterial blood gases
Metabolic derangements

 Metabolic disorders may be responsible for delayed recovery

 Hypoglycemia – Occurs in small children in diabetics, liver failure, septicemia and malaria.
 Severe Hyperglycemia – In decompensated diabetes e.g. Hypersmolic Hyper glycemic
diabetic coma or DKA.
 Electrocyte Imbalance – Secondary to underlying illness or as consequence of surgical
procedure i.e. Hyponatremia following TURP.
 Hypothermia – Severe hypothermia leads to decrease conscious level.
 Temperature < 33 has marked anaesthetic effect and potentiate CNS depressant effect of anesthetic
drugs
 Hypothermia reduces MAC value of inhalational agents, antagonizes muscle relaxant reversal and
limits drug metabolism.
Central Anticholinergic Syndrome

 Rarely follow use of Anticholinergic drugs i.e. Hyoscine but also with antihistamines,
antidripesants, phenothiazine and pethidine.
 Also reported after vertile anesthetic agents, Ketamine and Benzodiazepines.
 Manifest as – Confusion, restlessness, hallucination, coma and convulsion and therefore as
delayed awakening from anesthesia.
 Peripheral anticholinergic effect i.e. dry mouth, tachycardia, blood vision may be seen.
 Treatment – Physostigmine 0.04 mg/Kg slowly IV acts within 5 minutes.
Neurological Complications

 Cerebral Hypoxia – causes reduced conscious level which present as delayed awakening
from anesthesia.
 Intracerebral Events – Hemorrhage, Embolism or thrombosis are rare except in
Neurosurgery, Cardiac surgery, cerebrosular or carotid surgery.
Evaluation and Management

 Immediate Care
 Airway – Maintain clear airway and give oxygen and reintubate, if indicated.
 Breathing – Ensure adequate respiration, if indicated ventilate patient with ETT, monitor SPO2.
 Circulation – Assess BP, HR, ECG, Peripheral perfusion, conscious level, and urine output.
Resuscitate, if indicated.
 Review – History, Investigations & Preoperative management including anaesthetic chart, timings
of drug administration, looking for possible caused of delay in recovery.
Assess for Persisting Neuromuscular
BlocKade

 Use nerve stimulator if available

 If patient awake command to lift his head off the pillow for 5 Sec
 If Patient is still paralyzed should be sedated, anesthetized and ventilated until block is reversed.
 Further dose of reversal agent may be tried,
 In Suxamethenium apnoea prolonged ventilation 12-36 Hrs may be required.
Look for signs of OPIOD NARCOSIS

 Pin point Pupils

 Slow R.R
 Test dose of Nalarone may be given i.e.
 IV increments of 100-200 mg are usually sufficient
 In children 10 mg/Kg, subsequent dost of 100 mg/ Kg, if no response.
 Duration of Action of Nalaxone 20 Minutes
 Subsequent doses or infusion of Naloxone 800 mg in 500 ml of N/S in 6 Hrs.
 When suspected delayed recovery of Benzodiazine (Diazepam or Midazolam) management
is supportive.
 Flumazenil can be tried IV increments of 0.1 mg – 1 mg.
Measure Patient Temperature

 And warm if necessary.

 Forced air warming with biar hugger. Most effective wrapping in blankets and tin foils
sheets
 Ensuring room temperature is warm
 Warm IV fluids
Check Blood Glucose

 Correct IV Dextrose if it is less than 3 mmol/L

 Hyperglycemia should also be managed
Measure & Correct Plasma Electrolytes

 Hyponatremine should be managed slowly, as there is risk of subdural hemorrhage, central

Pontine myelinolysis and cardiac failure if correction is too rapid.
 Max safe rate of5 – 10mmol/L/day has been suggested or upto
 2 mmol/L/Hour until plasma sodium is 120 mmol/L
If NO Cause

 Found an intracervical event may be suspected.

 Full neurological examination should be performed looking particularly for localizing
signs.
 Sometimes CT or MRI is required to confirm diagnosis.
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