Delayed Awake – Assessment of Extubation

Delayed Awake – Assessment of Extubation

Tracheal Extubation is a high risk procedure in anaesthesia and critical care .Up till now most guidelines or criteria mainly focus on intubation with little of extubation.

Consciousness implies “awake and aware of surroundings & identify “,With the general use of fast acting anaesthetic agents ,patients usually awaken quickly and extubated but sometimes recovery is prolonged and list of possible causes is long .Accurate diagnosis ,assessment before extubation and treating accordingly is key to institution of appropriate therapy.

Awakening results from elimination of anesthetic agents from the brain. Patients usually respond to verbal stimuli when alveolar anesthetic concentration is decreased to about 30% of minimum alveolar concentration if unimpeded by other factors. Recovery from intravenous (IV) opioids and hypnotics may be more variable and difficult to quantify than recovery from inhalational and neuromuscular blocking agents. Patients should not leave the operating room unless they have stable hemodynamic parameters, a patent airway, have adequate ventilation, and oxygenation. Since beginning of anaesthesia practice we are following certain criteria’s of adequate neuromuscular recovery (TOF ratio) and awakening from anaesthesia like Glassgow Coma scale ,Alderate score etc.

Delayed Awake

Definition

Delayed awake is defined as the failure to regain consciousness as expected within 20-30 minutes of the end of a surgical procedure or discontinuation of anaesthesia.

Failure to awaken promptly after general anaesthesia may be related to three basic causes: prolonged action of anaesthetic drugs, metabolic encephalopathy, and neurologic injury.

Table 1: Showing differential diagnosis of Prolonged Recovery and failure to regain consciousness

Residual Drug Effects:

1. Overdose. Too much drug has been given or the patient is unduly susceptible for the drug action. Debilitated, paediatric or elderly patients generally require lower doses than young, healthy adults. Hepatic and / or renal disease delays drug metabolism and thus requires smaller drug doses. Myasthenia gravis greatly increases the sensitivity to non- depolarizing muscle relaxants; requiring only 10 to 50 % of the normal dose.

2. Duration and type of anaesthetic given. For inhalational anaesthetics the speed of recovery is directly related to alveolar ventilation. Hence hypoventilation may cause delayed awakening. Speed of emergence is also inversely proportional to the blood gas solubility of the agent, so the less soluble agents are eliminated more rapidly. Recovery from ether anaesthesia is more prolonged than halothane and nitrous

For IV anaesthetic agents, immediate recovery depends mainly on redistribution from blood and brain into muscle and fat. It also depends on the metabolism of the drug in liver and other extrahepatic sites. Propofol metabolises rapidly in the liver and possibly at other sites also. So the patients receiving propofol recovers faster. Elimination half life of propofol is 10-70 minutes and it does not accumulate also. Initial drug effect of thiopental is terminated by redistribution within 5 to 15 minutes but the elimination half life is 3.4 to 22 hours and the drug has cumulative effects also when more than one dose is given. This may delays recovery. For most other IV anaesthetic drugs the termination of drug action depends on the time required for metabolism and excretion. Advanced age, renal or hepatic disease can prolong drug action.

3. Timing of the drug dose. Delayed recovery may occur if a long acting drug has been given towards the end of the procedure, or if the more soluble volatile agent has been continued until the end of surgery.

4. Potentiation by other drugs. Sedative premedication such as benzodiazepines, narcotics will potentiate the CNS depressant effects of the anaesthetic agents, and may delay recovery. Alcohol consumption may have similar effect.

5. Prolonged neuromuscular blockade. Overdose or incomplete reversal of non-depolarizing muscle relaxants may be perceived as unresponsiveness though the patient may be fully conscious and aware. This can be diagnosed clinically or by using nerve stimulator. Failure to maintain head lift for 5 seconds, twitchy muscle movements, agitated or depressed patient will suggest incomplete reversal.

Abnormal or absent plasma cholinesterases may lead to prolonged apnoea after suxamethonium. Pregnancy, liver disease, starvation decrease the enzyme levels and may result in prolonged muscle relaxation. Repeated incremental doses may produce ‘dual block’ which is prolonged and very slow to recover. Non-depolarizing muscle relaxant mivacurium is also metabolized by plasma cholinesterase and similar effect may be observed.

There is increased sensitivity to muscle relaxants and to all respiratory depressant drugs in patients with muscular dystrophies. Longer acting relaxants should be avoided in such patients.

Patients receiving large doses of aminoglycoside antibiotics, polymixin B, calcium channel blockers can have delayed recovery.

Respiratory Failure:

Hypercarbia during anaesthesia may result in prolonged unresponsiveness. Underlying respiratory disease, high dose opioids, obstructed airway and inadequate reversal are the risk factors which causes raised CO₂. EtCO₂ and ABG estimation will give the clue towards diagnosis. It is important to note that patients receiving oxygen may have normal SpO₂ readings with significantly raised CO₂.

Metabolic Derangements:

Patients with metabolic abnormalities may have delayed emergence after anaesthesia. Conditions include:

1. Hypoglycaemia. It can occur in neonates, infants, and in those patients who are on insulin or oral hypoglycaemic agents. It may also be seen in alcoholics, in patients with hepatic failure, and in septicaemia. Several unusual drug interactions also predispose to hypoglycaemia. Salicylates, sulphonamides, and ethanol have known hypoglycaemic effects. Severe liver dysfunction can also contribute to hypoglycaemia by impairment of gluconeogenesis. Dangerous hypoglycaemia can occur intraoperatively in rare instances such as during manipulation of insulin producing tumours of the pancreas or retroperitoneal carcinomas.
2. Severe hyperglycaemia. May occur in poorly controlled diabetes i.e. hyperosmolar hyperglycaemic non-ketotic coma (HHNC), or diabetic ketoacidosis. Approximately half of these patients have no prior history of diabetes, but in most cases a severe concomitant illness, such as sepsis, pneumonia, pancreatitis, uraemia, CVA, or large surface area burns, is present. Hyperosmolar syndrome may occur following peritoneal or haemodialysis and cardiac surgery. Factors that tend to elevate the blood sugar, such as massive steroid therapy and IV administration of dextrose, may also precipitate it. The diagnosis of HHNC is confirmed by blood sugar level more than 600 mg/dl and elevated serum osmolarity in the absence of ketoacidosis. Azotemia and hypokalaemia are also frequently seen. Coma that accompanies HHNC is thought to result from cerebral intracellular dehydration due to hyperosmolarity. Damage to intracranial “bridging” veins may occur as a result of brain shrinkage.
3. Electrolyte imbalance. This may be due to the underlying illness or as a consequence of the surgical procedure e.g. hyponatraemia occurring after TURP. Hypocalcaemia (massive blood transfusion, pancreatitis, renal failure or after parathyroidectomy) and hypercalcaemia can delay recovery.
4. Hypothermia. A core temperature of less than 33OC has a marked anaesthetic effect itself and will potentiate the CNS depressant effect of anaesthetic drugs. Hypothermia also reduces the MAC value of inhalational anaesthetic agents, antagonizes muscle relaxant reversal and limits drug metabolism and thus may prolong the recovery.
5. Central anticholinergic syndrome. This rare event may result from the use of anticholinergic drugs especially hyoscine, but also with antihistamines, antidepressants, phenothiazines and pethidine. It has also been reported after inhalational agents, ketamine and benzodiazepines. Thought to be due to decrease in inhibitory anticholinergic activity in the brain, it may manifest as confusion, restlessness, hallucinations, convulsions and coma. This causes delayed awakening from anaesthesia. It can be treated with physostigmine 0.04mg/kg slow IV. Physostigmine acts within 5 minutes but symptoms may return after 60-90 minutes.
6. Endocrine disorders. Hypothyroidism is associated with decreased anaesthetic requirements. V. Vijay Kumar reported a case of subclinical hypothyroidism resulted in delayed recovery from anaesthesia. Patients with severe adrenal insufficiency may demonstrate prolonged unconsciousness in the postoperative period.
7. Deranged acid – base status. Alterations in the acid – base balance may result in delayed awakening or in coma.

Neurological Complications:

• Cerebral hypoxia. result in reduced level of consciousness and initially present as delayed awakening from anaesthesia.
• Intracerebral complications such as haemorrhage, embolism or thrombosis which sometimes occur during neurosurgery, cardiac surgery and vascular surgeries delays recovery. Incidence: 0.1-0.4% in low-risk procedures; 2.5-5% in high-risk Procedures
  Patients who remain unresponsive for more than 2 hours after cessation of anaesthetic should be suspected to have serious intracranial pathology and deserve a thorough neurological evaluation. Obtaining a serial CT or MRI scan will help in the diagnosis.

Recognization & evaluation of Patient

It is very important to Recognize & evaluate patient before extubation .Patient should not extubated in haste and ventilatory and circulatory support should be provided as may be necessary till situation evaluated .Patient should be managed on table or well-equipped recovery room or icu.

We have to assess cause of delayed awakening and treat it and then extubate either on operating table or ICU as per extubation criteria mentioned.

Extubation criteria in operating room

1. Adequate Oxygenation
   SpO2 > 92%, PaO2 > 60 mm Hg
2. Adequate Ventilation
   VT > 5 ml/kg, spontaneous RR > 7 bpm, ETCO2 < 50 mm
   Hg, PaCO2 < 60 mm Hg
3. Hemo dynamically Stable
4. Full Reversal of Muscle Relaxation
   Sustained tetany, TOF ratio > 0.9
   Sustained 5-second head lift or hand grasp
   Clinical test of postoperative neuromuscular recovery
   • Unreliable criteria
     Sustained eye opening,Protrusion of tongue,Head lift to opposite shoulder,Normal tidal volume,normal or nearly normal vital capacity, maximum inspiratory pressure less than 40-50 cm of H2O
   • More reliable but still not excluding residual
     Sustained head lift for 5sec,sustained leg lift for 5 sec, sustained hand grip 5sec,sustained tongue depressor test,max inspiratory pressure 40-50cm of H2O or greater
   • TOF ratio less than 0.9 associated with functional impairment of pharyngeal and oesophageal muscle so chances of aspiration is more and also decrease in inspiratory airway pressure and vital capacity leading to pulmonary complication. > 0.9 TOF ratio ensures adequate recovery
5. Neurologically Intact
   Follows verbal commands
   Intact cough/gag reflex
6. Appropriate Acid-Base Status
   pH> 7.25
7. Normal Metabolic Status
   Normal electrolytes
   Normovolemic
8. Normothermic
   – Temp > 35.5°
9. Other Considerations
   Aspiration risk
   Airway edema

Extubation Criteria – ICU

• Subjective Criteria
  –- Underlying disease process improving.
  –Adequate cough
  –Absence of excessive secretions
  –Cardiovascular & haemodynamic stability
• Objective Criteria
  – Adequate mentation (GCS > 13, minimal sedation)
  – Hemodynamically stable, on minimal pressures (e.g. dopamine < 5 mcg/kg/min)
• Oxygenation Criteria
  – SaO₂ > 90% at FiO₂ up to 0.4
  — PaO₂ > 60 mm Hg, PaO₂/FiO₂ > 150 on PEEP < 5-8 cm H₂O and FiO₂ < 0.4-0.5
  — Qs/QT < 20%
  — P(A-a)O₂ < 350mm Hg at FiO₂ of 1.0
• Pulmonary Reserve
  Vital Capacity – > 10ml/kg
  Max. insp .pressure >- 30cm H₂O in 20sec
• Ventilator Criteria (during SBT)
  Spontaneous breathing trial tolerates 20-30mins
  – PaCO₂ < 50 mm Hg, pH > 7.25
  – RSBI (RR/VT) < 100, NIF > 20 cm H₂O
  – Spontaneous VT > 5 ml/kg, VC > 10 ml/kg
  – RR < 35bpm
  –f/vt < 100breaths/min/l
  — minute ventilation -< 10L with satisfactory ABG
• Pulmonary measurement
  Static Compliance > 30ml/cm H₂O
  Airway resistance stable or improving
  VD/VT < 60% while intubated

How to Tackle delayed awake

Unresponsive patient

1. Stop all anaesthetic agents & Stimulate the patient
   -Vaporiser Switch Off/Change Iv Set/Change Breathing Circuit/Check Machine & Gas Resource
2. Ensure adequate oxygenation, ventilation, and hemodynamic
   • stability first
     Assess vital signs and GCS
   • Airway – Maintain clear airway /supplement O₂
   • Breathing – Ensure adequate respiration/continuous positive pressure ventilation/intermittent positive pressure ventilation
   • Circulation – Assess Blood pressure/heart rate/ECG/Peripheral perfusion/urine output/vasopressors if indicated Respiratory depression can lead to CO₂ narcosis. This may be more difficult to diagnose in PACU Where End Tidal CO₂ is not routinely monitored .Hypoxia resulting from depression & ventilation perfusion mismatching should be ruled out
3. Look for possible cause
   • Review history and investigations-seizures/diabetes mellitus/renal & hepatic disease
   • Review Anaesthetic chart :Dosage & Timings of drug administration
   • Other perioperative management
   • Full clinical assessment, Neurological assessment
4. Elimination of remnants of anaesthesia in the patients
   • Naloxone 0.40 mg – 2 mg IV Q 2-3 minutes.
   • If no response after 10 mg, reconsider narcotic overdose as cause of delayed emergency
   • Flumazenil 0.2 mg IV bolus Q 45-60 seconds over 15 seconds
   • May repeat doses. Maximum of 1 mg IV bolus. No more than 3 mg total in one hour.
   • 100%O2/Hyperventilation/ Forced diuresis
5. Warming of patients Measure Temperature warm if < 35c
   • Use Bair Hugger
   • Forced air warming/wrapping the blankest /foil sheets/warm iv fluids/kept room warm
6. Reversal of Residual neurological blockade
   • Administer “reversal agents”
   • Neostigmine/suggammadex/Amino acid infusion/Milirenone
   • Physostigmine 1-2 mg IV (for central cholinergic syndrome)
   • Neostigmine – maximum of 5 mg IV. Give with glycopyrrolate.
7. Substitution Therapy :steroids/antibiotics/Fresh blood/proteins etc
   Check ABG for PaO2, PaCO2, glucose, and electrolytes
8. Correction of metabolic abnormalities
   Hypoglycemia/Hypergycemia/Hyponitremia/Acidosis
9. Neurosurgical opinion/stroke therapy/Monitor patient in intensive care with frequent neurological examination.
   • Consider neurological insults
   • Perform pertinent neurologic exam
   • Consider further workup (e.g. CT, MRI, EEG)
   • Consider Neuro consult

Conclusion

Delayed awakening from anesthesia is often multifactorial, and anesthetic 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. Pre extubation assessment ,accurate diagnosis ,treatment 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 anesthesia is our responsibility.

References:

1. Millers Anaesthesia, 8TH Edition
2. Clinical Application Of Mechanical Ventilation ,4th edition David W. Chang
3. Differential Diagnosis of delayed awakening from general Anaesthesia : A Review, Elizabeth A.M.Frost ,MEJ ANESTH22(6)2014
4. Delayed recovery from anesthesia: A postgraduate educational review Ullhas Sudhakarrao Misal, Suchita Annasaheb Joshi, and Mudassir Mohd Shaikh Anaesth Essays Res:2016May-Aug 10(2)164-172
5. Delayed Emergence In Paediatric Patients, Hector F. Nicodemus and John B Rose, Pediatrics and Neonatology
6. Delayed Emergence, Deborah A.McClain, Special Topics, 885-887